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An eight-year-old male presented with a mass in the right anterior neck that had been apparent for one week. Upon physical examination, blood pressure was recorded as 100/65 mmHg, heart rate was 80 beats per min, respiratory rate was 20 breaths per min and temperature was 36.1°C. A mass measuring ~4.0 cm in size, which caused difficulty in swallowing, was identified in the right anterior neck. The laboratory test results demonstrated a normal blood count and serum biochemistry, as well as normal levels of electrolytes and carcinoembryonic antigen. In addition, the test results for Epstein-Barr virus (EBV) viral capsid antigens immunoglobulin (Ig)M and IgG, human immunodeficiency virus (HIV) and hepatitis C virus antibodies, hepatitis B antigen and syphilis were negative. Furthermore, the thyroid hormone test results were as follows: Free thyroxine (FT) 4 levels of 11.8 pmol/l (normal range, 9–25 pmol/l); FT3 levels of 4.2 pmol/l (normal range, 3–9 pmol/l); thyroid-stimulating hormone levels of 0.720 μIU/ml (normal range, 0.34–5.60 μIU/ml); anti-thyroglobulin levels of 20 IU/ml (normal range, <115 IU/ml); and anti-thyroid peroxidase levels of 25 IU/ml (normal range, <34 IU/ml). The patient had no significant past medical or family history of disease. A B-mode ultrasound examination revealed a mass measuring 4.0×3.0×2.5 cm in the right lobe of the thyroid (), however, the lymph nodes surrounding the mass were normal (). The patient underwent a right lobe and isthmus thyroidectomy whereby two lymph nodes were excised simultaneously. Following the surgery, positron emission tomography-computed tomography scans showed normal metabolism in the left lobe of the thyroid and other parts of the body (). The patient’s bone marrow cytology was also normal, however, histological examination revealed diffuse infiltration of atypical lymphocytes and the observation of residual thyroid follicles and necrosis (). In addition, under low magnification, the ‘starry sky’ histology was observed in certain areas (). The atypical lymphocytes were medium-sized and consistent, with centrally located nuclei of irregular shape, displaying dispersed and deep basophilic chromatin and scanty cytoplasm. Additionally, certain neoplastic cells were visible, while varying numbers of nucleoli and apoptosis and mitosis were observed. Benign tissue cells engulfing apoptotic bodies were also observed under high magnification (), however, the isthmus of the thyroid was not infiltrated by the neoplastic cells. No reactive lymphocyte infiltration or fibrosis was identified in the stroma of the thyroid, and no oxyphilic change or squamous metaplasia was observed in the epithelial cells of the background thyroid tissues (). The only change in the two lymph nodes that were simultaneously excised, was the presence of reactive hyperplasia of the lymphoid follicles (). Immunohistochemical staining was then performed with the primary antibodies shown in (Zymed Corporation, Inc., San Francisco, CA, USA; Santa Cruz Biotechnology, Inc., Santa Cruz, CA, USA). The results showed that the neoplastic cells were diffusely positive for cluster of differentiation (CD)20 () and CD10 (), marginally positive for CD38, CD43 and B-cell lymphoma (Bcl)-6, but negative for Bcl-2 and terminal deoxynucleotidyl transferase (TDT). In addition, CD3 and CD5 stained the background T cells, and the Ki-67 proliferation index was >95% (). Analysis using an EBV-encoded small RNA (EBER) digoxin-labeled probe (PanPath B.V., Budel, Netherlands) was performed and revealed a negative result (), however, positive nuclei were observed in the nasopharyngeal carcinoma tissue, which was used as the positive control (). Analysis using the C-MYC break-apart detection probe (Guangzhou LBP Medical Science Technology Co., Ltd., Guangzhou, China) was also performed and the results revealed that ~90% of the neoplastic cells exhibited red and green signal separation, which indicated that chromosome breakage and translocation of the MYC gene had occurred in the neoplastic cells (). Immunoglobulin gene rearrangement assays were performed according to instructions of the Biomed-2 Polymerase Chain Reaction kit (Invivoscribe technologies, Inc., San Diego, CA, USA), followed by capillary electrophoresis, which was analyzed using Genemarker® v1.5. software (SoftGenetics, LLC, State College, PA, USA). Positive gene arrangements of IgH and IgK were observed in the tumor tissues, however, no positive gene rearrangements were observed for IgL (). Consequently, the patient was diagnosed with primary BL of the thyroid and underwent alternate R-B-NHL-BFM-90-A and R-B-NHL-BFM-90-B treatment, for four cycles each. The two regimens, including the dose and duration of chemotherapy, are described in . After almost four years of follow-up, the patient appears well and remains free of disease.

A 64-year-old man with a history of hypothyroidism and proven Hashimoto's thyroiditis presented with painless progressive asymmetric enlargement of the thyroid gland. Laboratory evaluation revealed an elevated erythrocyte sedimentation rate (ESR), elevated thyroid peroxidase antibody titer of 850 U/mL (normal <30 U/mL), free triiodothyronine (FT3) 2.34, free thyroxine (FT4) 0.97, and thyroid stimulating hormone (TSH) level of 22.11. A contrast enhanced CT (CECT) exam of the neck revealed a large heterogeneous mass lesion predominantly involving the left lobe of thyroid and partly involving the isthmus and anterior part of right lobe. A needle biopsy from the thyroid mass revealed features of non-Hodgkin's lymphoma (DLBCL) with the tumor cells staining positive for CD20, negative for cytokeratin (CK) and having a high proliferative index (MIB-1) of 35-40%. 18F-FDG PET/CT was performed for staging. It revealed a large heterogeneous mass lesion predominantly involving the left lobe of thyroid and partly involving the isthmus and anterior part of right lobe with intense radiotracer uptake in the thyroid mass (SUVmax-18.7) with no other abnormal identifiable areas [Figure –]. The patient underwent four cycles of combination chemotherapy (rituximab-cyclophosphamide, doxorubicin, vincristine, and prednisone) and was reevaluated with 18F-FDG PET/CT. Post therapy 18F-FDG PET/CT [Figure –] done 6 weeks after completion of chemotherapy revealed significant decrease in the size of the enlarged thyroid gland associated with no significant FDG avidity (SUVmax-2.0) of the residual thyroid mass (arrow), suggestive of complete metabolic response. The patient is in complete remission at 18 month follow-up.

Write a detailed clinical case vignette based on the following key phrases: Thyroid Lymphoma, Non-Hodgkin's Lymphoma, Primary Thyroid Malignancy

An eight-year-old male presented with a mass in the right anterior neck that had been apparent for one week. Upon physical examination, blood pressure was recorded as 100/65 mmHg, heart rate was 80 beats per min, respiratory rate was 20 breaths per min and temperature was 36.1°C. A mass measuring ~4.0 cm in size, which caused difficulty in swallowing, was identified in the right anterior neck. The laboratory test results demonstrated a normal blood count and serum biochemistry, as well as normal levels of electrolytes and carcinoembryonic antigen. In addition, the test results for Epstein-Barr virus (EBV) viral capsid antigens immunoglobulin (Ig)M and IgG, human immunodeficiency virus (HIV) and hepatitis C virus antibodies, hepatitis B antigen and syphilis were negative. Furthermore, the thyroid hormone test results were as follows: Free thyroxine (FT) 4 levels of 11.8 pmol/l (normal range, 9–25 pmol/l); FT3 levels of 4.2 pmol/l (normal range, 3–9 pmol/l); thyroid-stimulating hormone levels of 0.720 μIU/ml (normal range, 0.34–5.60 μIU/ml); anti-thyroglobulin levels of 20 IU/ml (normal range, <115 IU/ml); and anti-thyroid peroxidase levels of 25 IU/ml (normal range, <34 IU/ml). The patient had no significant past medical or family history of disease. A B-mode ultrasound examination revealed a mass measuring 4.0×3.0×2.5 cm in the right lobe of the thyroid (), however, the lymph nodes surrounding the mass were normal (). The patient underwent a right lobe and isthmus thyroidectomy whereby two lymph nodes were excised simultaneously. Following the surgery, positron emission tomography-computed tomography scans showed normal metabolism in the left lobe of the thyroid and other parts of the body (). The patient’s bone marrow cytology was also normal, however, histological examination revealed diffuse infiltration of atypical lymphocytes and the observation of residual thyroid follicles and necrosis (). In addition, under low magnification, the ‘starry sky’ histology was observed in certain areas (). The atypical lymphocytes were medium-sized and consistent, with centrally located nuclei of irregular shape, displaying dispersed and deep basophilic chromatin and scanty cytoplasm. Additionally, certain neoplastic cells were visible, while varying numbers of nucleoli and apoptosis and mitosis were observed. Benign tissue cells engulfing apoptotic bodies were also observed under high magnification (), however, the isthmus of the thyroid was not infiltrated by the neoplastic cells. No reactive lymphocyte infiltration or fibrosis was identified in the stroma of the thyroid, and no oxyphilic change or squamous metaplasia was observed in the epithelial cells of the background thyroid tissues (). The only change in the two lymph nodes that were simultaneously excised, was the presence of reactive hyperplasia of the lymphoid follicles (). Immunohistochemical staining was then performed with the primary antibodies shown in (Zymed Corporation, Inc., San Francisco, CA, USA; Santa Cruz Biotechnology, Inc., Santa Cruz, CA, USA). The results showed that the neoplastic cells were diffusely positive for cluster of differentiation (CD)20 () and CD10 (), marginally positive for CD38, CD43 and B-cell lymphoma (Bcl)-6, but negative for Bcl-2 and terminal deoxynucleotidyl transferase (TDT). In addition, CD3 and CD5 stained the background T cells, and the Ki-67 proliferation index was >95% (). Analysis using an EBV-encoded small RNA (EBER) digoxin-labeled probe (PanPath B.V., Budel, Netherlands) was performed and revealed a negative result (), however, positive nuclei were observed in the nasopharyngeal carcinoma tissue, which was used as the positive control (). Analysis using the C-MYC break-apart detection probe (Guangzhou LBP Medical Science Technology Co., Ltd., Guangzhou, China) was also performed and the results revealed that ~90% of the neoplastic cells exhibited red and green signal separation, which indicated that chromosome breakage and translocation of the MYC gene had occurred in the neoplastic cells (). Immunoglobulin gene rearrangement assays were performed according to instructions of the Biomed-2 Polymerase Chain Reaction kit (Invivoscribe technologies, Inc., San Diego, CA, USA), followed by capillary electrophoresis, which was analyzed using Genemarker® v1.5. software (SoftGenetics, LLC, State College, PA, USA). Positive gene arrangements of IgH and IgK were observed in the tumor tissues, however, no positive gene rearrangements were observed for IgL (). Consequently, the patient was diagnosed with primary BL of the thyroid and underwent alternate R-B-NHL-BFM-90-A and R-B-NHL-BFM-90-B treatment, for four cycles each. The two regimens, including the dose and duration of chemotherapy, are described in . After almost four years of follow-up, the patient appears well and remains free of disease.

A 70-year-old male presented a rapidly expanding mass of the neck associated with history of airway compression symptoms; progressive dyspnea and dysphonia lasting for 4 weeks, in a context of apyrexia and impairment of general condition. The patient was admitted to the hospital because of increasing dyspnea and urgently received a tracheostomy.\nA biopsy of the cervical mass was carried out and the histological examination showed diffuse infiltration of the thyroid gland by a monotonous population of atypical intermediate-sized lymphoid cells (Fig. ). These last possess scanty amphophilic to basophilic cytoplasm with centrally located nuclei of irregular shape, displaying dispersed basophilic chromatin, and frequent apoptotic figures (Fig. ). Scattered tingible body type macrophages were also present. Little residual thyroid follicles and some areas of necrosis was observed.\nImmunohistochemical staining was then performed and the tumour cells were positive for CD20, CD10 and BCL6. Ki-67 showed proliferation index approaching 100 %. CD3 and CD5 stained the background T cells (Fig. ). Immunoreactivity for Epstein-Barr virus (EBV) was negative. The diagnosis of BL was confirmed on fluorescence in situ hybridisation that showed tumour cell positivity for the t (8; 14) translocation. Bone marrow examination was normal.\nThe patient was transferred to the Clinical Haematology department. On physical examination, he was apyretic and hemodynamically stable with a cervical armouring by a huge mass of hard consistency. Neurological examination shows no sensorimotor deficits.\nOther systemic examinations were normal, without any palpable lymphadenopathy or organomegaly.\nThe computerized tomography (CT) scan showed a heterogeneous process of the thyroid gland measuring 10.5 × 8.2 × 6.5 cm in size, extending up towards the laryngeal region, infiltrating the right vocal cord and reducing the laryngeal lumen (Fig. ).\nThe thoraco-abdominal CT scan showed no other localization.\nThe examination of the cephalorachidian liquid showed no central nervous system involvement. The patient was diagnosed with thyroidal Burkitt lymphoma, stage I of Murphy [].\nAfter cardiac, renal and liver functions assessment, the patient received chemotherapy according to the LMBA02 protocol [], group A (Age > 60 years, no CNS nor bone marrow involvement), with a first course of COP (Cyclophosphamide, Vincristine and Prednisone) and intrathecal Methotrexate, followed a week after by a course of R-COPADEM (Rituximab at day 0 and day 6, Cyclophosphamide day 2,3 and 4, Prednisone from day 1 to 5, Doxorubicineat day 2, high dose Methotrexate at day 1 with folic acid rescue from day 2 to day 6 and intrathecal chemotherapy at day 2 and day 6).\nAt day 15 of chemotherapy, the patient developed febrile neutropenia, refractory to broad-spectrum antibiotics and antifungals. The evolution was marked by the installation of a septic shock with acute respiratory distress syndrome that led to his transfer to intensive care unit where he was intubated and ventilated. The patient died 2 days after.

Write a detailed clinical case vignette based on the following key phrases: Thyroid Lymphoma, Non-Hodgkin's Lymphoma, Primary Thyroid Malignancy

A 49-year-old woman with a history of Hashimoto’s thyroiditis presented with a rapidly growing neck mass and upper airway compression symptoms. No B symptoms were present. The hematological test showed a white blood cell count within the normal range (51.5 × 102/μL). Interleukin-2 receptor (801 U/mL) and lactate dehydrogenase (228 U/L) levels were elevated, although serum thyroxine and thyroid-stimulating hormone levels were within their normal ranges. An elevated thyroid peroxidase antibody of 271.4 IU/mL was detected. Ultrasonography revealed a mass measuring 2.0 × 1.0 × 1.0 cm in the right lobe of the thyroid; the border of the nodule was indistinct. The patient underwent a right thyroidectomy after a core needle biopsy revealed a diffuse large B-cell lymphoma. Following the final histological diagnosis of primary thyroid BL, the patient received rituximab, cyclosphosphamide, doxorubicin, vincristine, and prednisone for 2 weeks, as well as rituximab, hyperfractionated cyclophosphamide, vincristine, doxorubicin, and dexamethasone including prophylactic intrathecal methotrexate for 3 months. Adjuvant treatments involving 22 cycles of linear accelerator (LINAC) therapy, 40 Gy each, were administered after the chemotherapy. Thirty months after the initial diagnosis, the patient had no evidence of recurrent disease.\nThe tumor cells were composed of round, intermediate-sized lymphoid cells admixed with scattered tingible body macrophages imparting a “starry sky” appearance (Fig. ). The nuclei were uniform and round-to-oval-shaped. The chromatin was coarsely clumped and had medium-sized paracentral nucleoli, while the cytoplasm was basophilic. Mitotic figures (12 per high-power field) were identified; there was no coagulative necrosis, although extrathyroidal extension was observed. Hashimoto’s thyroiditis was identified in the non-tumoral thyroid tissue.\nDiffuse membranous immunostaining for CD10, CD20, and CD79α, as well as diffuse nuclear staining for MUM-1 (Fig. a) and p16 (Fig. b), were noted in the tumor cells. The expression of MDM2 was focal and confined to the tumor cell nuclei (Fig. c), although the cells were negative for Bcl-2, Bcl-6, and p53. The Ki-67 labeling index exceeded 90% (Fig. ). The EBER in situ hybridization test was negative (Fig. ). Ninety-six percent of the tumor cells were found to have MYC/IgH gene fusion as determined by FISH (Fig. ).\nThe clinicopathological features of 21 thyroid BLs are summarized in Table . The median age at diagnosis was 39.3 years with a male-to-female ratio of 13/8. The majority (94.4%) of these patients presented with a thyroid mass; patients also presented with a rapidly growing nodule (66.7%), dyspnea (61.1%), dysphagia (16.7%), and thyrotoxicosis (5.6%). Four of the 14 described patients (28.6%) showed B symptoms (e.g., systematic symptoms of fever, night sweats, or weight loss). None of the reported patients presented with immunosuppressive conditions or the endemic form of BL. Regarding the treatment modalities, all of the 20 patients for whom data were available (data for 1 were missing) received multidrug chemotherapy regimens; 12 received chemotherapy only, 7 received chemotherapy with combined surgery, and 1 was administered chemotherapy combined with surgery and adjuvant radiotherapy (LINAC).\nFive of 7 patients with thyroid BL (71.4%) had morphologic evidence of Hashimoto’s thyroiditis. Regarding immunohistochemical features, all patients who were tested for CD10 (n = 14), CD20 (n = 18), and CD79a (n = 5) were positive for these respective proteins. IgM was positive in the lone patient who was tested. Additional factors measured are shown in Table . The Ki-67 labeling index exceeded 90% in all 19 patients for whom such staining was performed. We demonstrated that our patient had focal immunoreactivity for MDM2, but none of the other patients had been tested for this protein. All 12 patients who were tested for EBER in situ hybridization showed negative results, and flow cytometry immunophenotyping demonstrated CD10-positive monotypic B-cell populations in all 5 tested patients; moreover, MYC gene translocation was detected using FISH in all 12 patients whose samples were tested.\nOf 19 patients with available clinical outcome data, 14 (73.7%) were alive with complete remission, 1 (5.3%) was alive with persistent disease, and 4 (21.1%) died of the disease. Three of the 19 patients lacked follow-up data; hence, the median follow-up of the 16 remaining patients was 46.5 months (range, 0.5–361 months). Kaplan-Meier survival analysis showed that the 12- and 60-month overall survival rates were 87.5 and 70.7%, respectively (Fig. ).

A 52-year-old woman presented to our Endocrinology Unit with a growing thyroid mass, which had enlarged so rapidly she had become unable to wear her motorcycle helmet in the weeks prior to her visit. She suffered from Hashimoto’s thyroiditis for which she was taking levothyroxine. There was no history of neck irradiation or family history of thyroid cancer. On examination, there was a large, firm thyroid nodule on the right side of the neck, without palpable cervical lymphadenopathy. TSH was 4.79 μU/mL with FT3 and FT4 within the reference range. Otherwise, there was only a mild thrombocytopenia. Thyroid ultrasonography showed a solid hypoechoic nodule in the right lobe of the gland, with significant internal vascularity and absence of calcifications (Figure ). FNA cytology with rapid on-site evaluation of the material adequacy showed that there were only atypical lymphoid cells with no thyrocytes and the specimens were considered suggestive of a lymphoproliferative disorder but insufficient to make a diagnosis, such that a CNB was scheduled for the following day.\nAfter checking the blood coagulation profile, the patient underwent a CNB, which allowed histological/morphological tissue analysis. This showed that normal thyrocytes were virtually all replaced by homogeneous medium-sized lymphocytes with scanty blue cytoplasm, round nuclei, coarse chromatin, and multiple small nucleoli. There were frequent mitotic figures and scattered macrophages ingesting apoptotic cells, giving to the tissue section the so-called ‘starry sky’ appearance (Fig. ). Overall, these features were consistent with the presence of a thyroid Burkitt’s lymphoma, and further investigations were ordered to confirm the diagnosis and evaluate the disease extent. A CT of chest and abdomen showed the 44x43x87 mm thyroid nodule with left tracheal deviation (Figure ) without other visible masses or lymph nodes. Bone marrow biopsy showed almost 100% lymphoid infiltration, consisting of a population of intermediate-sized blast-like cells, with prominent nucleoli, which were replacing all normal cells. These cells expressed CD10, CD20, and were negative for Bcl2, CD34, and TdT. Altogether these results led us to the final diagnosis of stage IV Burkitt’s lymphoma [].\nThe patient was admitted to our hospital’s Haematology Unit and was successfully treated with 3 cycles of Hyper-CVAD chemotherapy (cyclophosphamide, vincristine, doxorubicin and dexamethasone) completed in five months. The thyroid mass disappeared (Fig. ) and the platelets returned to baseline levels. At 60 months after diagnosis the patient is alive, and remains disease-free at regular follow-up.

Write a detailed clinical case vignette based on the following key phrases: Thyroid Lymphoma, Non-Hodgkin's Lymphoma, Primary Thyroid Malignancy

A 49-year-old woman with a history of Hashimoto’s thyroiditis presented with a rapidly growing neck mass and upper airway compression symptoms. No B symptoms were present. The hematological test showed a white blood cell count within the normal range (51.5 × 102/μL). Interleukin-2 receptor (801 U/mL) and lactate dehydrogenase (228 U/L) levels were elevated, although serum thyroxine and thyroid-stimulating hormone levels were within their normal ranges. An elevated thyroid peroxidase antibody of 271.4 IU/mL was detected. Ultrasonography revealed a mass measuring 2.0 × 1.0 × 1.0 cm in the right lobe of the thyroid; the border of the nodule was indistinct. The patient underwent a right thyroidectomy after a core needle biopsy revealed a diffuse large B-cell lymphoma. Following the final histological diagnosis of primary thyroid BL, the patient received rituximab, cyclosphosphamide, doxorubicin, vincristine, and prednisone for 2 weeks, as well as rituximab, hyperfractionated cyclophosphamide, vincristine, doxorubicin, and dexamethasone including prophylactic intrathecal methotrexate for 3 months. Adjuvant treatments involving 22 cycles of linear accelerator (LINAC) therapy, 40 Gy each, were administered after the chemotherapy. Thirty months after the initial diagnosis, the patient had no evidence of recurrent disease.\nThe tumor cells were composed of round, intermediate-sized lymphoid cells admixed with scattered tingible body macrophages imparting a “starry sky” appearance (Fig. ). The nuclei were uniform and round-to-oval-shaped. The chromatin was coarsely clumped and had medium-sized paracentral nucleoli, while the cytoplasm was basophilic. Mitotic figures (12 per high-power field) were identified; there was no coagulative necrosis, although extrathyroidal extension was observed. Hashimoto’s thyroiditis was identified in the non-tumoral thyroid tissue.\nDiffuse membranous immunostaining for CD10, CD20, and CD79α, as well as diffuse nuclear staining for MUM-1 (Fig. a) and p16 (Fig. b), were noted in the tumor cells. The expression of MDM2 was focal and confined to the tumor cell nuclei (Fig. c), although the cells were negative for Bcl-2, Bcl-6, and p53. The Ki-67 labeling index exceeded 90% (Fig. ). The EBER in situ hybridization test was negative (Fig. ). Ninety-six percent of the tumor cells were found to have MYC/IgH gene fusion as determined by FISH (Fig. ).\nThe clinicopathological features of 21 thyroid BLs are summarized in Table . The median age at diagnosis was 39.3 years with a male-to-female ratio of 13/8. The majority (94.4%) of these patients presented with a thyroid mass; patients also presented with a rapidly growing nodule (66.7%), dyspnea (61.1%), dysphagia (16.7%), and thyrotoxicosis (5.6%). Four of the 14 described patients (28.6%) showed B symptoms (e.g., systematic symptoms of fever, night sweats, or weight loss). None of the reported patients presented with immunosuppressive conditions or the endemic form of BL. Regarding the treatment modalities, all of the 20 patients for whom data were available (data for 1 were missing) received multidrug chemotherapy regimens; 12 received chemotherapy only, 7 received chemotherapy with combined surgery, and 1 was administered chemotherapy combined with surgery and adjuvant radiotherapy (LINAC).\nFive of 7 patients with thyroid BL (71.4%) had morphologic evidence of Hashimoto’s thyroiditis. Regarding immunohistochemical features, all patients who were tested for CD10 (n = 14), CD20 (n = 18), and CD79a (n = 5) were positive for these respective proteins. IgM was positive in the lone patient who was tested. Additional factors measured are shown in Table . The Ki-67 labeling index exceeded 90% in all 19 patients for whom such staining was performed. We demonstrated that our patient had focal immunoreactivity for MDM2, but none of the other patients had been tested for this protein. All 12 patients who were tested for EBER in situ hybridization showed negative results, and flow cytometry immunophenotyping demonstrated CD10-positive monotypic B-cell populations in all 5 tested patients; moreover, MYC gene translocation was detected using FISH in all 12 patients whose samples were tested.\nOf 19 patients with available clinical outcome data, 14 (73.7%) were alive with complete remission, 1 (5.3%) was alive with persistent disease, and 4 (21.1%) died of the disease. Three of the 19 patients lacked follow-up data; hence, the median follow-up of the 16 remaining patients was 46.5 months (range, 0.5–361 months). Kaplan-Meier survival analysis showed that the 12- and 60-month overall survival rates were 87.5 and 70.7%, respectively (Fig. ).

A 64-year-old man with a history of hypothyroidism and proven Hashimoto's thyroiditis presented with painless progressive asymmetric enlargement of the thyroid gland. Laboratory evaluation revealed an elevated erythrocyte sedimentation rate (ESR), elevated thyroid peroxidase antibody titer of 850 U/mL (normal <30 U/mL), free triiodothyronine (FT3) 2.34, free thyroxine (FT4) 0.97, and thyroid stimulating hormone (TSH) level of 22.11. A contrast enhanced CT (CECT) exam of the neck revealed a large heterogeneous mass lesion predominantly involving the left lobe of thyroid and partly involving the isthmus and anterior part of right lobe. A needle biopsy from the thyroid mass revealed features of non-Hodgkin's lymphoma (DLBCL) with the tumor cells staining positive for CD20, negative for cytokeratin (CK) and having a high proliferative index (MIB-1) of 35-40%. 18F-FDG PET/CT was performed for staging. It revealed a large heterogeneous mass lesion predominantly involving the left lobe of thyroid and partly involving the isthmus and anterior part of right lobe with intense radiotracer uptake in the thyroid mass (SUVmax-18.7) with no other abnormal identifiable areas [Figure –]. The patient underwent four cycles of combination chemotherapy (rituximab-cyclophosphamide, doxorubicin, vincristine, and prednisone) and was reevaluated with 18F-FDG PET/CT. Post therapy 18F-FDG PET/CT [Figure –] done 6 weeks after completion of chemotherapy revealed significant decrease in the size of the enlarged thyroid gland associated with no significant FDG avidity (SUVmax-2.0) of the residual thyroid mass (arrow), suggestive of complete metabolic response. The patient is in complete remission at 18 month follow-up.

Write a detailed clinical case vignette based on the following key phrases: Thyroid Lymphoma, Non-Hodgkin's Lymphoma, Primary Thyroid Malignancy

A 49-year-old woman with a history of Hashimoto’s thyroiditis presented with a rapidly growing neck mass and upper airway compression symptoms. No B symptoms were present. The hematological test showed a white blood cell count within the normal range (51.5 × 102/μL). Interleukin-2 receptor (801 U/mL) and lactate dehydrogenase (228 U/L) levels were elevated, although serum thyroxine and thyroid-stimulating hormone levels were within their normal ranges. An elevated thyroid peroxidase antibody of 271.4 IU/mL was detected. Ultrasonography revealed a mass measuring 2.0 × 1.0 × 1.0 cm in the right lobe of the thyroid; the border of the nodule was indistinct. The patient underwent a right thyroidectomy after a core needle biopsy revealed a diffuse large B-cell lymphoma. Following the final histological diagnosis of primary thyroid BL, the patient received rituximab, cyclosphosphamide, doxorubicin, vincristine, and prednisone for 2 weeks, as well as rituximab, hyperfractionated cyclophosphamide, vincristine, doxorubicin, and dexamethasone including prophylactic intrathecal methotrexate for 3 months. Adjuvant treatments involving 22 cycles of linear accelerator (LINAC) therapy, 40 Gy each, were administered after the chemotherapy. Thirty months after the initial diagnosis, the patient had no evidence of recurrent disease.\nThe tumor cells were composed of round, intermediate-sized lymphoid cells admixed with scattered tingible body macrophages imparting a “starry sky” appearance (Fig. ). The nuclei were uniform and round-to-oval-shaped. The chromatin was coarsely clumped and had medium-sized paracentral nucleoli, while the cytoplasm was basophilic. Mitotic figures (12 per high-power field) were identified; there was no coagulative necrosis, although extrathyroidal extension was observed. Hashimoto’s thyroiditis was identified in the non-tumoral thyroid tissue.\nDiffuse membranous immunostaining for CD10, CD20, and CD79α, as well as diffuse nuclear staining for MUM-1 (Fig. a) and p16 (Fig. b), were noted in the tumor cells. The expression of MDM2 was focal and confined to the tumor cell nuclei (Fig. c), although the cells were negative for Bcl-2, Bcl-6, and p53. The Ki-67 labeling index exceeded 90% (Fig. ). The EBER in situ hybridization test was negative (Fig. ). Ninety-six percent of the tumor cells were found to have MYC/IgH gene fusion as determined by FISH (Fig. ).\nThe clinicopathological features of 21 thyroid BLs are summarized in Table . The median age at diagnosis was 39.3 years with a male-to-female ratio of 13/8. The majority (94.4%) of these patients presented with a thyroid mass; patients also presented with a rapidly growing nodule (66.7%), dyspnea (61.1%), dysphagia (16.7%), and thyrotoxicosis (5.6%). Four of the 14 described patients (28.6%) showed B symptoms (e.g., systematic symptoms of fever, night sweats, or weight loss). None of the reported patients presented with immunosuppressive conditions or the endemic form of BL. Regarding the treatment modalities, all of the 20 patients for whom data were available (data for 1 were missing) received multidrug chemotherapy regimens; 12 received chemotherapy only, 7 received chemotherapy with combined surgery, and 1 was administered chemotherapy combined with surgery and adjuvant radiotherapy (LINAC).\nFive of 7 patients with thyroid BL (71.4%) had morphologic evidence of Hashimoto’s thyroiditis. Regarding immunohistochemical features, all patients who were tested for CD10 (n = 14), CD20 (n = 18), and CD79a (n = 5) were positive for these respective proteins. IgM was positive in the lone patient who was tested. Additional factors measured are shown in Table . The Ki-67 labeling index exceeded 90% in all 19 patients for whom such staining was performed. We demonstrated that our patient had focal immunoreactivity for MDM2, but none of the other patients had been tested for this protein. All 12 patients who were tested for EBER in situ hybridization showed negative results, and flow cytometry immunophenotyping demonstrated CD10-positive monotypic B-cell populations in all 5 tested patients; moreover, MYC gene translocation was detected using FISH in all 12 patients whose samples were tested.\nOf 19 patients with available clinical outcome data, 14 (73.7%) were alive with complete remission, 1 (5.3%) was alive with persistent disease, and 4 (21.1%) died of the disease. Three of the 19 patients lacked follow-up data; hence, the median follow-up of the 16 remaining patients was 46.5 months (range, 0.5–361 months). Kaplan-Meier survival analysis showed that the 12- and 60-month overall survival rates were 87.5 and 70.7%, respectively (Fig. ).

A 70-year-old male presented a rapidly expanding mass of the neck associated with history of airway compression symptoms; progressive dyspnea and dysphonia lasting for 4 weeks, in a context of apyrexia and impairment of general condition. The patient was admitted to the hospital because of increasing dyspnea and urgently received a tracheostomy.\nA biopsy of the cervical mass was carried out and the histological examination showed diffuse infiltration of the thyroid gland by a monotonous population of atypical intermediate-sized lymphoid cells (Fig. ). These last possess scanty amphophilic to basophilic cytoplasm with centrally located nuclei of irregular shape, displaying dispersed basophilic chromatin, and frequent apoptotic figures (Fig. ). Scattered tingible body type macrophages were also present. Little residual thyroid follicles and some areas of necrosis was observed.\nImmunohistochemical staining was then performed and the tumour cells were positive for CD20, CD10 and BCL6. Ki-67 showed proliferation index approaching 100 %. CD3 and CD5 stained the background T cells (Fig. ). Immunoreactivity for Epstein-Barr virus (EBV) was negative. The diagnosis of BL was confirmed on fluorescence in situ hybridisation that showed tumour cell positivity for the t (8; 14) translocation. Bone marrow examination was normal.\nThe patient was transferred to the Clinical Haematology department. On physical examination, he was apyretic and hemodynamically stable with a cervical armouring by a huge mass of hard consistency. Neurological examination shows no sensorimotor deficits.\nOther systemic examinations were normal, without any palpable lymphadenopathy or organomegaly.\nThe computerized tomography (CT) scan showed a heterogeneous process of the thyroid gland measuring 10.5 × 8.2 × 6.5 cm in size, extending up towards the laryngeal region, infiltrating the right vocal cord and reducing the laryngeal lumen (Fig. ).\nThe thoraco-abdominal CT scan showed no other localization.\nThe examination of the cephalorachidian liquid showed no central nervous system involvement. The patient was diagnosed with thyroidal Burkitt lymphoma, stage I of Murphy [].\nAfter cardiac, renal and liver functions assessment, the patient received chemotherapy according to the LMBA02 protocol [], group A (Age > 60 years, no CNS nor bone marrow involvement), with a first course of COP (Cyclophosphamide, Vincristine and Prednisone) and intrathecal Methotrexate, followed a week after by a course of R-COPADEM (Rituximab at day 0 and day 6, Cyclophosphamide day 2,3 and 4, Prednisone from day 1 to 5, Doxorubicineat day 2, high dose Methotrexate at day 1 with folic acid rescue from day 2 to day 6 and intrathecal chemotherapy at day 2 and day 6).\nAt day 15 of chemotherapy, the patient developed febrile neutropenia, refractory to broad-spectrum antibiotics and antifungals. The evolution was marked by the installation of a septic shock with acute respiratory distress syndrome that led to his transfer to intensive care unit where he was intubated and ventilated. The patient died 2 days after.

Write a detailed clinical case vignette based on the following key phrases: Thyroid Lymphoma, Non-Hodgkin's Lymphoma, Primary Thyroid Malignancy

A 52-year-old woman presented to our Endocrinology Unit with a growing thyroid mass, which had enlarged so rapidly she had become unable to wear her motorcycle helmet in the weeks prior to her visit. She suffered from Hashimoto’s thyroiditis for which she was taking levothyroxine. There was no history of neck irradiation or family history of thyroid cancer. On examination, there was a large, firm thyroid nodule on the right side of the neck, without palpable cervical lymphadenopathy. TSH was 4.79 μU/mL with FT3 and FT4 within the reference range. Otherwise, there was only a mild thrombocytopenia. Thyroid ultrasonography showed a solid hypoechoic nodule in the right lobe of the gland, with significant internal vascularity and absence of calcifications (Figure ). FNA cytology with rapid on-site evaluation of the material adequacy showed that there were only atypical lymphoid cells with no thyrocytes and the specimens were considered suggestive of a lymphoproliferative disorder but insufficient to make a diagnosis, such that a CNB was scheduled for the following day.\nAfter checking the blood coagulation profile, the patient underwent a CNB, which allowed histological/morphological tissue analysis. This showed that normal thyrocytes were virtually all replaced by homogeneous medium-sized lymphocytes with scanty blue cytoplasm, round nuclei, coarse chromatin, and multiple small nucleoli. There were frequent mitotic figures and scattered macrophages ingesting apoptotic cells, giving to the tissue section the so-called ‘starry sky’ appearance (Fig. ). Overall, these features were consistent with the presence of a thyroid Burkitt’s lymphoma, and further investigations were ordered to confirm the diagnosis and evaluate the disease extent. A CT of chest and abdomen showed the 44x43x87 mm thyroid nodule with left tracheal deviation (Figure ) without other visible masses or lymph nodes. Bone marrow biopsy showed almost 100% lymphoid infiltration, consisting of a population of intermediate-sized blast-like cells, with prominent nucleoli, which were replacing all normal cells. These cells expressed CD10, CD20, and were negative for Bcl2, CD34, and TdT. Altogether these results led us to the final diagnosis of stage IV Burkitt’s lymphoma [].\nThe patient was admitted to our hospital’s Haematology Unit and was successfully treated with 3 cycles of Hyper-CVAD chemotherapy (cyclophosphamide, vincristine, doxorubicin and dexamethasone) completed in five months. The thyroid mass disappeared (Fig. ) and the platelets returned to baseline levels. At 60 months after diagnosis the patient is alive, and remains disease-free at regular follow-up.

A 64-year-old man with a history of hypothyroidism and proven Hashimoto's thyroiditis presented with painless progressive asymmetric enlargement of the thyroid gland. Laboratory evaluation revealed an elevated erythrocyte sedimentation rate (ESR), elevated thyroid peroxidase antibody titer of 850 U/mL (normal <30 U/mL), free triiodothyronine (FT3) 2.34, free thyroxine (FT4) 0.97, and thyroid stimulating hormone (TSH) level of 22.11. A contrast enhanced CT (CECT) exam of the neck revealed a large heterogeneous mass lesion predominantly involving the left lobe of thyroid and partly involving the isthmus and anterior part of right lobe. A needle biopsy from the thyroid mass revealed features of non-Hodgkin's lymphoma (DLBCL) with the tumor cells staining positive for CD20, negative for cytokeratin (CK) and having a high proliferative index (MIB-1) of 35-40%. 18F-FDG PET/CT was performed for staging. It revealed a large heterogeneous mass lesion predominantly involving the left lobe of thyroid and partly involving the isthmus and anterior part of right lobe with intense radiotracer uptake in the thyroid mass (SUVmax-18.7) with no other abnormal identifiable areas [Figure –]. The patient underwent four cycles of combination chemotherapy (rituximab-cyclophosphamide, doxorubicin, vincristine, and prednisone) and was reevaluated with 18F-FDG PET/CT. Post therapy 18F-FDG PET/CT [Figure –] done 6 weeks after completion of chemotherapy revealed significant decrease in the size of the enlarged thyroid gland associated with no significant FDG avidity (SUVmax-2.0) of the residual thyroid mass (arrow), suggestive of complete metabolic response. The patient is in complete remission at 18 month follow-up.

Write a detailed clinical case vignette based on the following key phrases: Thyroid Lymphoma, Non-Hodgkin's Lymphoma, Primary Thyroid Malignancy

A 52-year-old woman presented to our Endocrinology Unit with a growing thyroid mass, which had enlarged so rapidly she had become unable to wear her motorcycle helmet in the weeks prior to her visit. She suffered from Hashimoto’s thyroiditis for which she was taking levothyroxine. There was no history of neck irradiation or family history of thyroid cancer. On examination, there was a large, firm thyroid nodule on the right side of the neck, without palpable cervical lymphadenopathy. TSH was 4.79 μU/mL with FT3 and FT4 within the reference range. Otherwise, there was only a mild thrombocytopenia. Thyroid ultrasonography showed a solid hypoechoic nodule in the right lobe of the gland, with significant internal vascularity and absence of calcifications (Figure ). FNA cytology with rapid on-site evaluation of the material adequacy showed that there were only atypical lymphoid cells with no thyrocytes and the specimens were considered suggestive of a lymphoproliferative disorder but insufficient to make a diagnosis, such that a CNB was scheduled for the following day.\nAfter checking the blood coagulation profile, the patient underwent a CNB, which allowed histological/morphological tissue analysis. This showed that normal thyrocytes were virtually all replaced by homogeneous medium-sized lymphocytes with scanty blue cytoplasm, round nuclei, coarse chromatin, and multiple small nucleoli. There were frequent mitotic figures and scattered macrophages ingesting apoptotic cells, giving to the tissue section the so-called ‘starry sky’ appearance (Fig. ). Overall, these features were consistent with the presence of a thyroid Burkitt’s lymphoma, and further investigations were ordered to confirm the diagnosis and evaluate the disease extent. A CT of chest and abdomen showed the 44x43x87 mm thyroid nodule with left tracheal deviation (Figure ) without other visible masses or lymph nodes. Bone marrow biopsy showed almost 100% lymphoid infiltration, consisting of a population of intermediate-sized blast-like cells, with prominent nucleoli, which were replacing all normal cells. These cells expressed CD10, CD20, and were negative for Bcl2, CD34, and TdT. Altogether these results led us to the final diagnosis of stage IV Burkitt’s lymphoma [].\nThe patient was admitted to our hospital’s Haematology Unit and was successfully treated with 3 cycles of Hyper-CVAD chemotherapy (cyclophosphamide, vincristine, doxorubicin and dexamethasone) completed in five months. The thyroid mass disappeared (Fig. ) and the platelets returned to baseline levels. At 60 months after diagnosis the patient is alive, and remains disease-free at regular follow-up.

A 70-year-old male presented a rapidly expanding mass of the neck associated with history of airway compression symptoms; progressive dyspnea and dysphonia lasting for 4 weeks, in a context of apyrexia and impairment of general condition. The patient was admitted to the hospital because of increasing dyspnea and urgently received a tracheostomy.\nA biopsy of the cervical mass was carried out and the histological examination showed diffuse infiltration of the thyroid gland by a monotonous population of atypical intermediate-sized lymphoid cells (Fig. ). These last possess scanty amphophilic to basophilic cytoplasm with centrally located nuclei of irregular shape, displaying dispersed basophilic chromatin, and frequent apoptotic figures (Fig. ). Scattered tingible body type macrophages were also present. Little residual thyroid follicles and some areas of necrosis was observed.\nImmunohistochemical staining was then performed and the tumour cells were positive for CD20, CD10 and BCL6. Ki-67 showed proliferation index approaching 100 %. CD3 and CD5 stained the background T cells (Fig. ). Immunoreactivity for Epstein-Barr virus (EBV) was negative. The diagnosis of BL was confirmed on fluorescence in situ hybridisation that showed tumour cell positivity for the t (8; 14) translocation. Bone marrow examination was normal.\nThe patient was transferred to the Clinical Haematology department. On physical examination, he was apyretic and hemodynamically stable with a cervical armouring by a huge mass of hard consistency. Neurological examination shows no sensorimotor deficits.\nOther systemic examinations were normal, without any palpable lymphadenopathy or organomegaly.\nThe computerized tomography (CT) scan showed a heterogeneous process of the thyroid gland measuring 10.5 × 8.2 × 6.5 cm in size, extending up towards the laryngeal region, infiltrating the right vocal cord and reducing the laryngeal lumen (Fig. ).\nThe thoraco-abdominal CT scan showed no other localization.\nThe examination of the cephalorachidian liquid showed no central nervous system involvement. The patient was diagnosed with thyroidal Burkitt lymphoma, stage I of Murphy [].\nAfter cardiac, renal and liver functions assessment, the patient received chemotherapy according to the LMBA02 protocol [], group A (Age > 60 years, no CNS nor bone marrow involvement), with a first course of COP (Cyclophosphamide, Vincristine and Prednisone) and intrathecal Methotrexate, followed a week after by a course of R-COPADEM (Rituximab at day 0 and day 6, Cyclophosphamide day 2,3 and 4, Prednisone from day 1 to 5, Doxorubicineat day 2, high dose Methotrexate at day 1 with folic acid rescue from day 2 to day 6 and intrathecal chemotherapy at day 2 and day 6).\nAt day 15 of chemotherapy, the patient developed febrile neutropenia, refractory to broad-spectrum antibiotics and antifungals. The evolution was marked by the installation of a septic shock with acute respiratory distress syndrome that led to his transfer to intensive care unit where he was intubated and ventilated. The patient died 2 days after.

Write a detailed clinical case vignette based on the following key phrases: Thyroid Lymphoma, Non-Hodgkin's Lymphoma, Primary Thyroid Malignancy

A 64-year-old man with a history of hypothyroidism and proven Hashimoto's thyroiditis presented with painless progressive asymmetric enlargement of the thyroid gland. Laboratory evaluation revealed an elevated erythrocyte sedimentation rate (ESR), elevated thyroid peroxidase antibody titer of 850 U/mL (normal <30 U/mL), free triiodothyronine (FT3) 2.34, free thyroxine (FT4) 0.97, and thyroid stimulating hormone (TSH) level of 22.11. A contrast enhanced CT (CECT) exam of the neck revealed a large heterogeneous mass lesion predominantly involving the left lobe of thyroid and partly involving the isthmus and anterior part of right lobe. A needle biopsy from the thyroid mass revealed features of non-Hodgkin's lymphoma (DLBCL) with the tumor cells staining positive for CD20, negative for cytokeratin (CK) and having a high proliferative index (MIB-1) of 35-40%. 18F-FDG PET/CT was performed for staging. It revealed a large heterogeneous mass lesion predominantly involving the left lobe of thyroid and partly involving the isthmus and anterior part of right lobe with intense radiotracer uptake in the thyroid mass (SUVmax-18.7) with no other abnormal identifiable areas [Figure –]. The patient underwent four cycles of combination chemotherapy (rituximab-cyclophosphamide, doxorubicin, vincristine, and prednisone) and was reevaluated with 18F-FDG PET/CT. Post therapy 18F-FDG PET/CT [Figure –] done 6 weeks after completion of chemotherapy revealed significant decrease in the size of the enlarged thyroid gland associated with no significant FDG avidity (SUVmax-2.0) of the residual thyroid mass (arrow), suggestive of complete metabolic response. The patient is in complete remission at 18 month follow-up.

A 70-year-old male presented a rapidly expanding mass of the neck associated with history of airway compression symptoms; progressive dyspnea and dysphonia lasting for 4 weeks, in a context of apyrexia and impairment of general condition. The patient was admitted to the hospital because of increasing dyspnea and urgently received a tracheostomy.\nA biopsy of the cervical mass was carried out and the histological examination showed diffuse infiltration of the thyroid gland by a monotonous population of atypical intermediate-sized lymphoid cells (Fig. ). These last possess scanty amphophilic to basophilic cytoplasm with centrally located nuclei of irregular shape, displaying dispersed basophilic chromatin, and frequent apoptotic figures (Fig. ). Scattered tingible body type macrophages were also present. Little residual thyroid follicles and some areas of necrosis was observed.\nImmunohistochemical staining was then performed and the tumour cells were positive for CD20, CD10 and BCL6. Ki-67 showed proliferation index approaching 100 %. CD3 and CD5 stained the background T cells (Fig. ). Immunoreactivity for Epstein-Barr virus (EBV) was negative. The diagnosis of BL was confirmed on fluorescence in situ hybridisation that showed tumour cell positivity for the t (8; 14) translocation. Bone marrow examination was normal.\nThe patient was transferred to the Clinical Haematology department. On physical examination, he was apyretic and hemodynamically stable with a cervical armouring by a huge mass of hard consistency. Neurological examination shows no sensorimotor deficits.\nOther systemic examinations were normal, without any palpable lymphadenopathy or organomegaly.\nThe computerized tomography (CT) scan showed a heterogeneous process of the thyroid gland measuring 10.5 × 8.2 × 6.5 cm in size, extending up towards the laryngeal region, infiltrating the right vocal cord and reducing the laryngeal lumen (Fig. ).\nThe thoraco-abdominal CT scan showed no other localization.\nThe examination of the cephalorachidian liquid showed no central nervous system involvement. The patient was diagnosed with thyroidal Burkitt lymphoma, stage I of Murphy [].\nAfter cardiac, renal and liver functions assessment, the patient received chemotherapy according to the LMBA02 protocol [], group A (Age > 60 years, no CNS nor bone marrow involvement), with a first course of COP (Cyclophosphamide, Vincristine and Prednisone) and intrathecal Methotrexate, followed a week after by a course of R-COPADEM (Rituximab at day 0 and day 6, Cyclophosphamide day 2,3 and 4, Prednisone from day 1 to 5, Doxorubicineat day 2, high dose Methotrexate at day 1 with folic acid rescue from day 2 to day 6 and intrathecal chemotherapy at day 2 and day 6).\nAt day 15 of chemotherapy, the patient developed febrile neutropenia, refractory to broad-spectrum antibiotics and antifungals. The evolution was marked by the installation of a septic shock with acute respiratory distress syndrome that led to his transfer to intensive care unit where he was intubated and ventilated. The patient died 2 days after.

Write a detailed clinical case vignette based on the following key phrases: Thyroid Lymphoma, Non-Hodgkin's Lymphoma, Primary Thyroid Malignancy

The patient is a forty-one-year-old man with an unremarkable medical history presented with a two-month history of scrotal swelling and discomfort. He denied a history of mal-descent, and there was no family history of testicular cancer. Physical exam was pertinent for an enlarged, nontender left testicle. An ultrasound revealed well-circumscribed hypo-echoic, heterogeneous lesions in both testicles (). The left testicular mass measured 3.0 × 2.6 × 4.3 cm, while the mass in the right testicle measured 2.1 × 3.1 × 0.5 cm. Doppler was suggestive of normal blood flow. Pertinent labs included (AFP) alpha fetoprotein 6.2 µg/L, (beta HCG) beta human chorionic gonadotropin <3 IU/L, (LDH) lactase dehydrogenase levels 572 U/L, and serum testosterone 375 ng/dL, and all prognostic markers are within normal limits. CT of the chest, abdomen, and pelvis was negative for evidence of metastatic disease or lymphadenopathy.\nHe underwent bilateral inguinal orchiectomy. Final pathology () revealed classical seminoma in both specimens. Both right and left tumors exhibited invasion of the rete testis. There was possible angiolymphatic space invasion noted within the left testicular mass. There was no tumor extension through the tunica albuginea, epididymis, or spermatic cord. Surgical margins were free. Both tumors were pathologically staged IA.\nThe patient did not have concerns regarding fertility and declined to consider an organ preserving approach. Our patient was uncomfortable with surveillance as an option. He declined medical oncology referral for discussion about systemic therapy and was therefore treated with external beam radiotherapy. He received 2550 cGy in 17 fractions at 150 cGy per fraction via 6 MV/18 MV photons with AP/PA fields. Field borders () included superior border at T10/11 interspace, inferior border at L5/S1 interspace, and lateral borders of vertebral transverse processes (field width approximately 10 cm). The patient did not have a history of previous pelvic surgery, and only the paraaortic lymph nodes were targeted. He tolerated treatment well, experiencing grade I nausea (as per Common Terminology Criteria for Adverse Events, version 3.0). He is currently disease-free, 18 months from completion of radiation therapy. His serum testosterone levels fell to 248 ng/dL after treatment, and he uses testosterone gel for hormone replacement.

A 29-year-old man developed a painless testicular lump, detected in auto-exam, and immediately sought medical assistance. An ultrasound examination showed a right testicle hypoechoic mass. AFP was above the superior limit of the normal value, and there was no evidence of metastatic disease in imagiological exams. Right inguinal radical orchiectomy was performed one day later, and histological exam revealed a teratoma with a low grade immature component. Pathological staging of pT1N0M0S0 – IA was done, and a surveillance program was implemented. Seven years later, during a routine scrotal ultrasound exam, a hypoechoic nodule of 11 mm was found. The patient was asymptomatic. Tumor markers were normal, as was the thoraco-abdomino-pelvian CT scan. A left inguinal radical orchiectomy was done. Histological exam revealed a TGCT with invasive classic seminoma with TIN component. He was staged as pT1N0M0S0 – IA, and a single carboplatin AUC7 session was done. 12 months later the patient remains disease free.

Write a detailed clinical case vignette based on the following key phrases: testicular cancer, germ cell tumors, orchidectomy

A 29-year-old man developed a painless testicular lump, detected in auto-exam, and immediately sought medical assistance. An ultrasound examination showed a right testicle hypoechoic mass. AFP was above the superior limit of the normal value, and there was no evidence of metastatic disease in imagiological exams. Right inguinal radical orchiectomy was performed one day later, and histological exam revealed a teratoma with a low grade immature component. Pathological staging of pT1N0M0S0 – IA was done, and a surveillance program was implemented. Seven years later, during a routine scrotal ultrasound exam, a hypoechoic nodule of 11 mm was found. The patient was asymptomatic. Tumor markers were normal, as was the thoraco-abdomino-pelvian CT scan. A left inguinal radical orchiectomy was done. Histological exam revealed a TGCT with invasive classic seminoma with TIN component. He was staged as pT1N0M0S0 – IA, and a single carboplatin AUC7 session was done. 12 months later the patient remains disease free.

A 40-year-old male presented at our outpatients department complaining about a testicular painless mass on the right testis, which had shown a gradual enlargement over the past two months. The only symptom the patient had was discomfort in the scrotum and a sensation of testicular heaviness. His medical history did not report any known risk factors for testis cancer, such as cryptorchidism, and he did not have any comorbidities. Physical examination revealed a firm and nontender mass both on the right and on the left testis, which were easily separable from the epididymis. No other constitutional signs were present. Laboratory workup revealed a moderately elevated b-hcG (24,7 mIU/mL) and CEA (1,97 ng/mL), a-FP (1,62 ng/mL), and LDH (180 IU/L) within normal levels. Firstly, he was submitted to a scrotal ultrasonography which revealed a testicular mass that measured approximately 2,3 × 3,1 cm on the right testis () and another testicular mass of 2,4 × 1,5 cm in size on the left testis (). The computer tomography (CT) of the abdomen did not demonstrate any enlarged retroperitoneal lymph nodes. The chest X-ray showed no abnormality. The patient was scheduled for operation and he did not want to have frozen storage of sperm, although he was fully informed about the consequences, since he was a father of two children and also was informed about the occurrence of hypogonadism after the operation and that he will have to be under a strict endocrinologist follow-up and hormone replacement. He chose bilateral orchiectomy for oncological reasons. Finally, he underwent bilateral orchiectomy with high ligation of the spermatic cord. The postoperative period was uneventful and the patient exited the hospital the next day. The elevated b-hcG on the postoperative measurement (the 15th day) was within normal values (0,3 mIU/mL). Histopathological evaluation of the specimens revealed the following: (a) an embryonal cell carcinoma of the right testis limited to the testis with lymphovascular invasion of pathological stage pT2 (): staining with antibodies showed CD30(+) and a-FP(−); (b) a seminoma of the left testis, limited to the testis without invasion of the tunica albuginea or vascular invasion of pathological stage pT1 (): staining with antibodies showed CD117(+), CD30(−), and a-FP(−). On both testicles intratubular germ cell neoplasia of unclassified type (IGCNU) was present. The patient was referred to an oncologist and was submitted to two cycles of adjuvant combined chemotherapy with bleomycin, etoposide, and cisplatin (BEP). His follow-up consisted of physical examination, serum markers, chest X-ray, and CT of the abdomen, according to the EAU Guidelines recommended follow-up schedule. Six months after the operation no residual tumor or recurrence was observed, neither local nor systematic. Finally the patient is under a strict endocrinologist follow-up for the management of his hypogonadism state.

Write a detailed clinical case vignette based on the following key phrases: testicular cancer, germ cell tumors, orchidectomy

A 29-year-old man developed a painless testicular lump, detected in auto-exam, and immediately sought medical assistance. An ultrasound examination showed a right testicle hypoechoic mass. AFP was above the superior limit of the normal value, and there was no evidence of metastatic disease in imagiological exams. Right inguinal radical orchiectomy was performed one day later, and histological exam revealed a teratoma with a low grade immature component. Pathological staging of pT1N0M0S0 – IA was done, and a surveillance program was implemented. Seven years later, during a routine scrotal ultrasound exam, a hypoechoic nodule of 11 mm was found. The patient was asymptomatic. Tumor markers were normal, as was the thoraco-abdomino-pelvian CT scan. A left inguinal radical orchiectomy was done. Histological exam revealed a TGCT with invasive classic seminoma with TIN component. He was staged as pT1N0M0S0 – IA, and a single carboplatin AUC7 session was done. 12 months later the patient remains disease free.

An 18-year-old man, without any known risk factor for testicular malignancy, presented to our hospital with a painful right testicular mass with 1 month of evolution. Physical examination detected a small lump, confirmed by testicular ultrasound as a hypoechoic nodule. A CT-scan revealed no metastatic disease. α-fetoprotein (AFP) and lactate dehydrogenase (LDH) were above the normal limit. A right inguinal orchiectomy was performed and the histological exam revealed a mixed germ cell testicular tumor (composed by embrionary carcinoma and mature teratoma). Tumoral markers normalized after surgery, and the tumor was staged as pT1N0M0S0 - IA, according to the American Joint Committee on Cancer guidelines. The patient remained under surveillance. Twelve years later he developed bilateral gynecomastia and a high human chorionic gonadotropin (HCG). CT-scan found a 1cm lateroaortic adenopathy and a PET-scan revealed hyperfixation in the referred adenopathy and left testicle. At that time a scrotal ultrasonography was done, and a voluminous testicle of 5 x 5 x 3 cm with hypoechogenic and hypervascularized areas were found. This was followed by a left radical inguinal orchiectomy with testicle prosthesis introduction. Histological exam revealed a mixed TGCT (with seminoma, embrionary carcinoma and immature teratoma components) and a pathological stage pT2N1M0S1 – IIA. Chemotherapy was started with BEP protocol (bleomycin, etoposide and cisplatin), administered every 21 days for 3 cycles. Retroperitoneal adenopathy disappeared, HCG normalized and a surveillance program was initiated. The patient was disease-free in the 5 months after having finished his treatment.

Write a detailed clinical case vignette based on the following key phrases: testicular cancer, germ cell tumors, orchidectomy

A 29-year-old man developed a painless testicular lump, detected in auto-exam, and immediately sought medical assistance. An ultrasound examination showed a right testicle hypoechoic mass. AFP was above the superior limit of the normal value, and there was no evidence of metastatic disease in imagiological exams. Right inguinal radical orchiectomy was performed one day later, and histological exam revealed a teratoma with a low grade immature component. Pathological staging of pT1N0M0S0 – IA was done, and a surveillance program was implemented. Seven years later, during a routine scrotal ultrasound exam, a hypoechoic nodule of 11 mm was found. The patient was asymptomatic. Tumor markers were normal, as was the thoraco-abdomino-pelvian CT scan. A left inguinal radical orchiectomy was done. Histological exam revealed a TGCT with invasive classic seminoma with TIN component. He was staged as pT1N0M0S0 – IA, and a single carboplatin AUC7 session was done. 12 months later the patient remains disease free.

We present the case of a 41-year-old male with repeated visits to outside emergency\ndepartments over a 3-month period with a waxing and waning pattern of worsening\ncognitive dysfunction as well as intermittent fevers. He also complained of\ngeneralized weakness and fatigue. His initial diagnosis was viral meningitis. He had\na negative workup for infectious etiologies, including negative CSF cultures,\nnegative Lyme titers, normal ACE level. Previous lumbar puncture was notable for\nelevated white blood cells, elevated protein, and glucose below 50g/dL. CT scan of\nthe abdomen at an outside hospital revealed a right pericaval lymph node measuring\n3.8 x 3.7 cm with central necrosis ().\nExternal genitalia were incompletely visualized on this scan. After transfer to our\ninstitution, the condition continued to worsen and after being admitted, the patient\nwas unable to speak and reported weakness in all four extremities that progressed to\nalteration of awareness, disorientation, and difficulty speaking. Labs at this time\nwere significant for phosphorous less than 2 mg/dL, which is known to precipitate\nseizures and altered mental status, however it was felt that the lower extremity\nshaking was not consistent with a seizure. He was placed on Keppra prior to arrival\nat our hospital. Based on this presentation, a CT of the head was obtained to rule\nout a primary central nervous system etiology. This imaging showed no acute process.\nFurther work up with MRI could not be obtained due to a non-compatible internal\npacemaker. Pacemaker analysis showed no abnormalities. Due to the para-aortic\nlocation of the mass, a 24-hour urine metanephrine was also performed to rule out a\nneuroendocrine tumor.\nAfter the negative initial workup, concern for distant metastasis led to the belief\ncurrent symptomatology was due to secondary to a paraneoplastic process.\nSpecifically, the presence of retroperitoneal lymphadenopathy with necrosis raised\nconcern for testicular origin. Sonographic evaluation of the testicles showed a\nright sided, ill-defined, multi-cystic 2.4 x 2.1 x 2.2cm mass (). Further laboratory evaluation revealed an\nelevated B-hCG of 49.9 mIU/mL, alpha fetoprotein level of 1.67 ng/mL and normal LDH\nlevel. A right radical orchiectomy was performed.\nGross pathology obtained from the right radical orchiectomy showed a 2.1 x 1.8 x 1.6\ncm tan-white, ill defined, soft, multicystic lesion in the medial and inferior pole\nof the testis, without hemorrhage or necrosis. Histologic evaluation revealed mixed\nrespiratory epithelium, gastrointestinal glands, and squamous epithelium with\nkeratinization consistent with a post-pubertal testicular teratoma with associated\ngerm cell neoplasia in situ (Figures , ).\nRepeat CT scan of the abdomen and pelvis showed continuous enlargement of the right\nperi-aortic lymph node, now measuring 5.6 cm in greatest dimension, as well as a new\nleft peri-aortic node measuring 2.2 cm in the largest dimension. After\nmultidisciplinary discussion, given the likelihood of a paraneoplastic syndrome that\nwould likely worsen with up front chemotherapy, the decision was made to proceed\nwith a primary retroperitoneal lymph node dissection. The large aortocaval mass was\nadherent to the inferior vena cava (IVC), but no invasion was noted. Measurement of\nthe extirpated mass was noted to be 7 x 6 x 4.5 cm in size cm in the largest\ndiameter. A complete bilateral template retroperitoneal lymph node dissection was\nperformed extending inferiorly from the renal veins to the bifurcation of the common\niliac arteries and to the ureters bilaterally.\nOn gross pathology, the aortocaval mass was well encapsulated with hemorrhagic and\nnecrotic cut surfaces. Microscopic evaluation displayed large anaplastic cells with\nepithelioid features, nuclear pleomorphism and frequent mitoses. Giant cells with\ngranular cytoplasm were also present. One node measuring 1.5 x 1.0 x 1.0 cm was\npositive for malignancy. Immunostaining of the mass and positive lymph node\ndisplayed positive staining for Pan-Keratin and OCT4, and negative staining for\nCD30, S-100, Desmin, pan-melanoma, and SOX2. The microscopic evaluation and\nimmunostaining combination led to the diagnosis of poorly differentiated embryonal\ncarcinoma ().\nThe patient’s neurological symptoms were managed with methylprednisolone, and Keppra\nwas continued for seizure prophylaxis. Following resection of the aortocaval mass,\nthe patient recovered well, and the diplopia and paralysis resolved. He was managed\npost-operatively with Bleomycin-Etoposide-Cisplatin (BEP) therapy. At the time of\npublication, he had received three cycles of BEP and has shown no evidence of tumor\nrecurrence.

Write a detailed clinical case vignette based on the following key phrases: testicular cancer, germ cell tumors, orchidectomy

A 35-year-old man with no known risk factors for testicular malignancy presented at the urology department with a right testicular mass causing painful swelling. He had been experiencing discomfort and heaviness for 10 days. His general practitioner had started antibiotic and anti-inflammatory treatment a week prior to his arrival at our department. The patient had no past medical history of testicular issues.\nPhysical examination revealed a lump, which testicular ultrasound confirmed as an 18 mm × 12 mm × 25 mm heterogeneous hypoechogenic mass localized to the upper pole of the right testis (Fig. ). A computed tomography (CT) scan showed no evidence of abdominopelvic or thoracic metastases. The blood serum tumor marker levels were as follows: human chorionic gonadotropin (HCG) < 1.20 U/ml (normal is < 5.01 U/ml); α-fetoprotein (AFP) = 3.4 ng/ml (normal is < 7 ng/ml); and lactate dehydrogenase (LDH) = 599 IU/l (normal is 313–618 IU/l).\nA right inguinal radical orchiectomy was performed in September of 2009. Histological examination revealed a pure seminoma of 4 cm × 2.5 cm, without lymphatic, vascular, or tunica albuginea infiltration. The tumor node metastasis (TNM) classification was pT1pNxpMx according to the Union for International Cancer Control (UICC) staging system, seventh edition. Two weeks after the surgery, this case was discussed during a multidisciplinary uro-oncology meeting. From October 21 to November 10 of 2009, the patient underwent adjuvant radiotherapy with doses of 25.2 Gy delivered to the paraaortic lymph nodes in 14 fractions.\nThe patient was considered to be disease-free and received follow-up in accordance with our standard protocol, which includes chest and abdominal CT, physical examination, and tumor marker assessment every 4 months for the first 2 years, and testicular ultrasound of the contralateral side once each year. A total-body CT scan at 1 year after radical surgical treatment showed a 16-mm lymph node under the patient’s left collarbone (Fig. ). The lesion was confirmed by positron emission tomography (PET) scan, and surgical node excision was performed. Histological examination revealed a typical seminoma (Fig. ). Chemotherapy was initiated with a bleomycin, etoposide, and cisplatin (BEP) protocol administered every 21 days for 2 cycles from October to December of 2010.\nFour years later, a follow-up ultrasound of the left testis revealed a 15 mm × 6 mm node with microcalcifications (Fig. ). Blood serum tumor markers were normal, and a CT scan showed no evidence of abdominopelvic or thoracic metastasis. The possibility of radical or partial orchiectomy was discussed with the patient. In March of 2014, the patient underwent left inguinal testicular exploration of the lesion with ultrasound image guidance and excisional biopsy. Analysis of frozen biopsy sections revealed a seminomatous tumor with an intense chronic granulomatous inflammatory lesion. Due to the diffuse nature of the tumor, radical left orchiectomy was performed. The final pathological diagnosis was a pure seminoma that presented as isolated and scattered neoplastic cells within an inflammatory and granulomatous reaction and multifocal intratubular germ cell neoplasia (IGGNU).\nThe patient remained under surveillance and received androgen replacement therapy with long-acting testosterone undecanoate every 12 weeks (Nebido®). A bilateral testicular prosthesis was proposed but was refused. Sperm cryopreservation was not performed because the patient had children and did not desire any additional offspring. Follow-up was performed following the standard protocol. At 2 years after left radical orchiectomy, the patient remained disease free. At the most recent visit, the patient reported maintenance of libido, no adverse effects from the androgen replacement therapy, and comfortable sexual activity and quality of life.\nReported TGCT incidence rates from multiple countries between 1991 and 2011 show geographical variations, with the highest rates observed in Denmark. Over recent decades, TGCT prevalence has gradually increased in most populations of European origin and in the USA [, ]. Some studies suggest an increased incidence of bilateral disease in the post-chemotherapy and radiotherapy era [, ]. A retrospective review shows a threefold higher incidence of bilateral testicular cancers in the post-chemotherapy era compared to the pre-chemotherapy era []. The apparent increase in the number of metachronous tumors may reflect the increased life expectancy of the general population as well as the prolonged survival associated with higher cure rates for initial tumors.\nA systematic literature review—including 50,376 men with TGCT between 1991 and 2011 from many countries—reported a BTGCT prevalence of 1.82 % []. Among those with BTGCT, 69.2 % had metachronous tumors and 30.8 % had synchronous tumors. Several studies indicate that metachronous testicular tumors seem to be more frequent than synchronous ones [, ]. Bilateral metachronous TGCT was first described in a case report in 1942. Metachronous testicular cancer is diagnosed when at least 6 months elapse between the appearance of the first tumor and the second tumor and when there is an ultrasound-documented absence of a contralateral mass at diagnosis of the first tumor.\nAmong patients with metachronous tumors, the mean age at diagnosis of the first tumor is 28 years old and the mean age at diagnosis of the second tumor is 35 years old []. Our present patient was 36 years old when the first tumor was diagnosed and 40 years old when the second tumor was diagnosed. In 70 % of cases, the second testicular malignancy arises within 5 years after the first TGCT []. Seminoma is the most common histological type of bilateral testicular cancer, comprising approximately 68 % of such cases [], as well as the most common histological type of metachronous tumor []. When the second tumor is a seminoma, the median interval between tumors seems to be longer (~10 years) []. There have been 25 reported cases of BTGCT in which the contralateral testicular tumor occurred 20 years or more after the original tumor. Within a series of 25 cases, 4 cases involved a second tumor that occurred at least 30 years after the original testicular tumor, with the longest interval being 40 years [, ]. Contralateral testicular seminoma can occur even at an advanced age, underscoring the importance of life-long follow-up for these patients [, ].\nThe incidence of metachronous germ cell tumors in patients diagnosed with a seminoma is influenced by the patient’s age at the time of the initial diagnosis. Evidence suggests that men who develop a seminoma when they are 30 years of age or younger may be at greater risk of developing a second tumor [, ]. Patients diagnosed with a seminomatous tumor at less than 30 years of age show an increased risk of relapse in the following 15 years compared to men who are over 30 years old at diagnosis (3.1 vs 1.2 %) [].\nAlthough the etiology of BTGCT remains unknown, both genetic and environmental causes are implicated. Presently known epidemiological risk factors for TGCT development include a history of cryptorchidism, Klinefelter syndrome, the presence of a contralateral tumor, infertility, and a history of testis cancer in first-degree relatives []. The elevated risk in family members and associations with inherited genotypes suggest genetic causes [, ]. On the other hand, testicular cancer incidence rates nearly doubled in industrialized countries between 1975 and 2007, suggesting an influence of environmental factors [, ]. Our present case involved no known genetic or environmental risk factors.\nIn our present case, serum markers were negative both at the diagnosis of the first tumor and at tumor recurrence. This is in accordance with the typical presentation of a seminoma. Most second tumors are discovered by the physician via scrotal ultrasonography or by the patient via testicular self-examination. Ultrasonography is a safe and simple screening procedure. One major difficulty regarding the diagnosis of second tumors is that patients may be reluctant to seek help due to fear of castration.\nUltrasound detection of microlithiasis in the contralateral testis is associated with a 30-fold increase in the risk of presenting with a second TGCT, and diagnosis of the first tumor is associated with a 5–8 % risk of testicular intraepithelial neoplasm (TIN) in the contralateral testis. These data highlight the need for long-term surveillance to support early detection of the second TGCT. Within 7 years, 70 % of all TINs will progress to invasive neoplasia [, ], although this risk is somewhat lower among patients who undergo chemotherapy for their first tumor. The 5-year survival rates for men with synchronous and metachronous bilateral testicular tumor are 88 and 95 %, respectively [], suggesting that metachronous tumors have a more favorable survival outcome than synchronous tumors. Synchronous tumors are also associated with more advanced disease than metachronous tumors []. Among patients with bilateral testicular cancer, 70 % present with stage I disease upon diagnosis of the second tumor. This is most likely due to close follow-up and increased patient awareness.\nThe optimal management of patients with intratubular germ cell neoplasms remains controversial. The choices include surveillance and irradiation of the contralateral testis. Since radiotherapy can result in infertility and may affect Leydig cell function [], surveillance is an important part of TGCT follow-up. Clear guidelines are also lacking for treatment of bilateral testicular tumors. Treatment of the second tumor is based on the stage and histology []. The incidence of contralateral testicular cancer is not significantly influenced by the use of radiation therapy for the initial testicular cancer [].\nTreatment for advanced germ cell tumors includes combination chemotherapy with bleomycin, cisplatin, and etoposide, followed by surgical salvage for residual disease. Depending of the patient’s risk profile, 3–4 cycles of chemotherapy are needed []. The patient in our present case received adjuvant radiation therapy after the onset of the first tumor as well as chemotherapy. Additionally, a metastatic lymph node was removed at relapse, which occurred long before the diagnosis of the second tumor. Notably, 5 years elapsed between diagnosis of the first and second tumors. A left radical orchidectomy was performed to eliminate the recurrent tumor due to its diffuse character and the history of metastases. Sparing the testis would have carried a risk of recurrence. Taking into account that he did not desire more children, the patient wanted radical surgery despite the need for hormonal replacement.\nIn the present case, the detection of a contralateral supradiaphragmatic lymph node 3 years prior to the contralateral testis diagnosis indicated metastatic relapse. A review by Cooper et al. reported that approximately 75 % of seminomas present as stage 1, with disease limited to the testis []. All tumors of germ cell origin have the propensity to metastasize via lymphatic pathways, which typically occurs in a sequential pattern, beginning with abdominal lymph node involvement, followed by successive involvement of lymph nodes in the chest and neck []. Wood et al. demonstrated that cervical metastasis is almost exclusively left-sided, with 21 of 23 patients showing disease in supraclavicular or scalene lymph nodes []. Metastatic tumors can also appear in locations outside of the direct line of spread from the primary site []. A review by Vledder reported that 4 % of seminoma patients showed cervical metastasis and that only 5 % of these patients had the neck mass as their initial disease sign []. Seminomas can metastasize to the supraclavicular lymph nodes, and tumors from the right testis can spread to the interaortocaval, precaval, and paraaortic regions, with crossover to left-sided lymph nodes. The left testis drains into the paraaortic and preaortic regions. Interaortocaval lymph node involvement occurs in higher-stage disease. From there, the tumors usually grow along the thoracic duct into the left supraclavicular lymph node and the subclavian vein and then show disseminated spread []. This hypothesis may be applicable to our present patient, since metastasis was not found elsewhere.

A 29-year-old man developed a painless testicular lump, detected in auto-exam, and immediately sought medical assistance. An ultrasound examination showed a right testicle hypoechoic mass. AFP was above the superior limit of the normal value, and there was no evidence of metastatic disease in imagiological exams. Right inguinal radical orchiectomy was performed one day later, and histological exam revealed a teratoma with a low grade immature component. Pathological staging of pT1N0M0S0 – IA was done, and a surveillance program was implemented. Seven years later, during a routine scrotal ultrasound exam, a hypoechoic nodule of 11 mm was found. The patient was asymptomatic. Tumor markers were normal, as was the thoraco-abdomino-pelvian CT scan. A left inguinal radical orchiectomy was done. Histological exam revealed a TGCT with invasive classic seminoma with TIN component. He was staged as pT1N0M0S0 – IA, and a single carboplatin AUC7 session was done. 12 months later the patient remains disease free.

Write a detailed clinical case vignette based on the following key phrases: testicular cancer, germ cell tumors, orchidectomy

A 29-year-old man developed a painless testicular lump, detected in auto-exam, and immediately sought medical assistance. An ultrasound examination showed a right testicle hypoechoic mass. AFP was above the superior limit of the normal value, and there was no evidence of metastatic disease in imagiological exams. Right inguinal radical orchiectomy was performed one day later, and histological exam revealed a teratoma with a low grade immature component. Pathological staging of pT1N0M0S0 – IA was done, and a surveillance program was implemented. Seven years later, during a routine scrotal ultrasound exam, a hypoechoic nodule of 11 mm was found. The patient was asymptomatic. Tumor markers were normal, as was the thoraco-abdomino-pelvian CT scan. A left inguinal radical orchiectomy was done. Histological exam revealed a TGCT with invasive classic seminoma with TIN component. He was staged as pT1N0M0S0 – IA, and a single carboplatin AUC7 session was done. 12 months later the patient remains disease free.

A 27 year old single male presented to our patient department with complaint of one month testicular swelling with left side preference. He has no complaints of pain in the testicles and abdomen. No problem in erectile function. He had no problems during puberty. He had no history of smoking and use of opioid in social habits. There is no family history and no evidence of risk factor for testicular cancer such as cryptorchidism or congenital abnormalities in the patient. Physical examination specified the left side testis with twice the normal volume swelling and without tenderness. The size of right side testis has increased slightly. Laboratory workup revealed azoospermia and an elevated a-FP (258.4IU/mL), and b-hcG (3.12mIU/mL) within normal levels. On ultrasound study the testes have 50mm×30mm in right side and 72mm×50mm in left side dimensions. No hydrocele was seen. Images of the right testis demonstrated 38mm×27mm hypoecho mass that accounting for (occupying) three-quarters of the volume of the parenchyma. Images of the left testis demonstrated approximately 70mm×47mm mixed echogenic mass, comprises almost the entire volume of the testis. Epididymis have normal parenchymal dimensions and echoes.\nThe ultrasound study of abdomen and pelvis showed no abnormality. The abdomen CT scan was not indicative of enlargement of the lymph nodes of retroperitoneum. The chest x-ray did not show evidence of metastasis. The patient underwent bilateral radical orchiectomy. Right testicular mass, excisional biopsy, for frozen section and intra-operative diagnosis, consists of a piece of creamy colored soft tissue specimen, with homogenous appearance, measured 45×35×22 mm in the largest diameters. Cryo and permanent sections of right testis mass, confirmed invasive, classic type seminoma that limited to the testis with intratubular and invasion to lympho-vascular tissues (tumor stage: at-least PT2) ().\nIn the left testis, in cut sections, almost all testicular volume replaced by tumoral tissue with heterogeneous appearance, containing solid and cystic, hemorrhagic and necrotic areas, measured 80×50×40 mm. the left side tumor was a malignant GCT with component of invasive, classic type seminoma (50-60%), yolk sac tumor (40-50%) and embryonal carcinoma (about 10%) (). Tumor extended to rete testis, tunica albuginea and tunica vaginalis. Epididymis was not involved. Intratubular and lympho-vascular invasion was present (tumor stage: PT2). Immunocytochemical study with AE1/AE3, CD30 and CD117 markers demonstrated a positive reaction (). The patient was discharged without problems and complications one day after surgery. The elevated a-FP on the postoperative measurement decreased to lower values (6,05mIU/mL). The patient was advised to go to an oncologist and was submitted to one cycle of adjuvant chemotherapy with bleomycin, etoposide, and cisplatin (BEP). As the follow-up physical examination, serum markers, chest X ray, and CT of the abdomen, were checked. Six months after the orchiectomy there was no residual tumor or recurrence, neither local nor systematic. Finally the patient is under a follow-up by an endocrinologist for the long-term management regarding the testosterone replacement therapy and he has been started on topical testrogel for life.

Write a detailed clinical case vignette based on the following key phrases: testicular cancer, germ cell tumors, orchidectomy

The patient is a forty-one-year-old man with an unremarkable medical history presented with a two-month history of scrotal swelling and discomfort. He denied a history of mal-descent, and there was no family history of testicular cancer. Physical exam was pertinent for an enlarged, nontender left testicle. An ultrasound revealed well-circumscribed hypo-echoic, heterogeneous lesions in both testicles (). The left testicular mass measured 3.0 × 2.6 × 4.3 cm, while the mass in the right testicle measured 2.1 × 3.1 × 0.5 cm. Doppler was suggestive of normal blood flow. Pertinent labs included (AFP) alpha fetoprotein 6.2 µg/L, (beta HCG) beta human chorionic gonadotropin <3 IU/L, (LDH) lactase dehydrogenase levels 572 U/L, and serum testosterone 375 ng/dL, and all prognostic markers are within normal limits. CT of the chest, abdomen, and pelvis was negative for evidence of metastatic disease or lymphadenopathy.\nHe underwent bilateral inguinal orchiectomy. Final pathology () revealed classical seminoma in both specimens. Both right and left tumors exhibited invasion of the rete testis. There was possible angiolymphatic space invasion noted within the left testicular mass. There was no tumor extension through the tunica albuginea, epididymis, or spermatic cord. Surgical margins were free. Both tumors were pathologically staged IA.\nThe patient did not have concerns regarding fertility and declined to consider an organ preserving approach. Our patient was uncomfortable with surveillance as an option. He declined medical oncology referral for discussion about systemic therapy and was therefore treated with external beam radiotherapy. He received 2550 cGy in 17 fractions at 150 cGy per fraction via 6 MV/18 MV photons with AP/PA fields. Field borders () included superior border at T10/11 interspace, inferior border at L5/S1 interspace, and lateral borders of vertebral transverse processes (field width approximately 10 cm). The patient did not have a history of previous pelvic surgery, and only the paraaortic lymph nodes were targeted. He tolerated treatment well, experiencing grade I nausea (as per Common Terminology Criteria for Adverse Events, version 3.0). He is currently disease-free, 18 months from completion of radiation therapy. His serum testosterone levels fell to 248 ng/dL after treatment, and he uses testosterone gel for hormone replacement.

A 40-year-old male presented at our outpatients department complaining about a testicular painless mass on the right testis, which had shown a gradual enlargement over the past two months. The only symptom the patient had was discomfort in the scrotum and a sensation of testicular heaviness. His medical history did not report any known risk factors for testis cancer, such as cryptorchidism, and he did not have any comorbidities. Physical examination revealed a firm and nontender mass both on the right and on the left testis, which were easily separable from the epididymis. No other constitutional signs were present. Laboratory workup revealed a moderately elevated b-hcG (24,7 mIU/mL) and CEA (1,97 ng/mL), a-FP (1,62 ng/mL), and LDH (180 IU/L) within normal levels. Firstly, he was submitted to a scrotal ultrasonography which revealed a testicular mass that measured approximately 2,3 × 3,1 cm on the right testis () and another testicular mass of 2,4 × 1,5 cm in size on the left testis (). The computer tomography (CT) of the abdomen did not demonstrate any enlarged retroperitoneal lymph nodes. The chest X-ray showed no abnormality. The patient was scheduled for operation and he did not want to have frozen storage of sperm, although he was fully informed about the consequences, since he was a father of two children and also was informed about the occurrence of hypogonadism after the operation and that he will have to be under a strict endocrinologist follow-up and hormone replacement. He chose bilateral orchiectomy for oncological reasons. Finally, he underwent bilateral orchiectomy with high ligation of the spermatic cord. The postoperative period was uneventful and the patient exited the hospital the next day. The elevated b-hcG on the postoperative measurement (the 15th day) was within normal values (0,3 mIU/mL). Histopathological evaluation of the specimens revealed the following: (a) an embryonal cell carcinoma of the right testis limited to the testis with lymphovascular invasion of pathological stage pT2 (): staining with antibodies showed CD30(+) and a-FP(−); (b) a seminoma of the left testis, limited to the testis without invasion of the tunica albuginea or vascular invasion of pathological stage pT1 (): staining with antibodies showed CD117(+), CD30(−), and a-FP(−). On both testicles intratubular germ cell neoplasia of unclassified type (IGCNU) was present. The patient was referred to an oncologist and was submitted to two cycles of adjuvant combined chemotherapy with bleomycin, etoposide, and cisplatin (BEP). His follow-up consisted of physical examination, serum markers, chest X-ray, and CT of the abdomen, according to the EAU Guidelines recommended follow-up schedule. Six months after the operation no residual tumor or recurrence was observed, neither local nor systematic. Finally the patient is under a strict endocrinologist follow-up for the management of his hypogonadism state.

Write a detailed clinical case vignette based on the following key phrases: testicular cancer, germ cell tumors, orchidectomy

The patient is a forty-one-year-old man with an unremarkable medical history presented with a two-month history of scrotal swelling and discomfort. He denied a history of mal-descent, and there was no family history of testicular cancer. Physical exam was pertinent for an enlarged, nontender left testicle. An ultrasound revealed well-circumscribed hypo-echoic, heterogeneous lesions in both testicles (). The left testicular mass measured 3.0 × 2.6 × 4.3 cm, while the mass in the right testicle measured 2.1 × 3.1 × 0.5 cm. Doppler was suggestive of normal blood flow. Pertinent labs included (AFP) alpha fetoprotein 6.2 µg/L, (beta HCG) beta human chorionic gonadotropin <3 IU/L, (LDH) lactase dehydrogenase levels 572 U/L, and serum testosterone 375 ng/dL, and all prognostic markers are within normal limits. CT of the chest, abdomen, and pelvis was negative for evidence of metastatic disease or lymphadenopathy.\nHe underwent bilateral inguinal orchiectomy. Final pathology () revealed classical seminoma in both specimens. Both right and left tumors exhibited invasion of the rete testis. There was possible angiolymphatic space invasion noted within the left testicular mass. There was no tumor extension through the tunica albuginea, epididymis, or spermatic cord. Surgical margins were free. Both tumors were pathologically staged IA.\nThe patient did not have concerns regarding fertility and declined to consider an organ preserving approach. Our patient was uncomfortable with surveillance as an option. He declined medical oncology referral for discussion about systemic therapy and was therefore treated with external beam radiotherapy. He received 2550 cGy in 17 fractions at 150 cGy per fraction via 6 MV/18 MV photons with AP/PA fields. Field borders () included superior border at T10/11 interspace, inferior border at L5/S1 interspace, and lateral borders of vertebral transverse processes (field width approximately 10 cm). The patient did not have a history of previous pelvic surgery, and only the paraaortic lymph nodes were targeted. He tolerated treatment well, experiencing grade I nausea (as per Common Terminology Criteria for Adverse Events, version 3.0). He is currently disease-free, 18 months from completion of radiation therapy. His serum testosterone levels fell to 248 ng/dL after treatment, and he uses testosterone gel for hormone replacement.

An 18-year-old man, without any known risk factor for testicular malignancy, presented to our hospital with a painful right testicular mass with 1 month of evolution. Physical examination detected a small lump, confirmed by testicular ultrasound as a hypoechoic nodule. A CT-scan revealed no metastatic disease. α-fetoprotein (AFP) and lactate dehydrogenase (LDH) were above the normal limit. A right inguinal orchiectomy was performed and the histological exam revealed a mixed germ cell testicular tumor (composed by embrionary carcinoma and mature teratoma). Tumoral markers normalized after surgery, and the tumor was staged as pT1N0M0S0 - IA, according to the American Joint Committee on Cancer guidelines. The patient remained under surveillance. Twelve years later he developed bilateral gynecomastia and a high human chorionic gonadotropin (HCG). CT-scan found a 1cm lateroaortic adenopathy and a PET-scan revealed hyperfixation in the referred adenopathy and left testicle. At that time a scrotal ultrasonography was done, and a voluminous testicle of 5 x 5 x 3 cm with hypoechogenic and hypervascularized areas were found. This was followed by a left radical inguinal orchiectomy with testicle prosthesis introduction. Histological exam revealed a mixed TGCT (with seminoma, embrionary carcinoma and immature teratoma components) and a pathological stage pT2N1M0S1 – IIA. Chemotherapy was started with BEP protocol (bleomycin, etoposide and cisplatin), administered every 21 days for 3 cycles. Retroperitoneal adenopathy disappeared, HCG normalized and a surveillance program was initiated. The patient was disease-free in the 5 months after having finished his treatment.

Write a detailed clinical case vignette based on the following key phrases: testicular cancer, germ cell tumors, orchidectomy

The patient is a forty-one-year-old man with an unremarkable medical history presented with a two-month history of scrotal swelling and discomfort. He denied a history of mal-descent, and there was no family history of testicular cancer. Physical exam was pertinent for an enlarged, nontender left testicle. An ultrasound revealed well-circumscribed hypo-echoic, heterogeneous lesions in both testicles (). The left testicular mass measured 3.0 × 2.6 × 4.3 cm, while the mass in the right testicle measured 2.1 × 3.1 × 0.5 cm. Doppler was suggestive of normal blood flow. Pertinent labs included (AFP) alpha fetoprotein 6.2 µg/L, (beta HCG) beta human chorionic gonadotropin <3 IU/L, (LDH) lactase dehydrogenase levels 572 U/L, and serum testosterone 375 ng/dL, and all prognostic markers are within normal limits. CT of the chest, abdomen, and pelvis was negative for evidence of metastatic disease or lymphadenopathy.\nHe underwent bilateral inguinal orchiectomy. Final pathology () revealed classical seminoma in both specimens. Both right and left tumors exhibited invasion of the rete testis. There was possible angiolymphatic space invasion noted within the left testicular mass. There was no tumor extension through the tunica albuginea, epididymis, or spermatic cord. Surgical margins were free. Both tumors were pathologically staged IA.\nThe patient did not have concerns regarding fertility and declined to consider an organ preserving approach. Our patient was uncomfortable with surveillance as an option. He declined medical oncology referral for discussion about systemic therapy and was therefore treated with external beam radiotherapy. He received 2550 cGy in 17 fractions at 150 cGy per fraction via 6 MV/18 MV photons with AP/PA fields. Field borders () included superior border at T10/11 interspace, inferior border at L5/S1 interspace, and lateral borders of vertebral transverse processes (field width approximately 10 cm). The patient did not have a history of previous pelvic surgery, and only the paraaortic lymph nodes were targeted. He tolerated treatment well, experiencing grade I nausea (as per Common Terminology Criteria for Adverse Events, version 3.0). He is currently disease-free, 18 months from completion of radiation therapy. His serum testosterone levels fell to 248 ng/dL after treatment, and he uses testosterone gel for hormone replacement.

We present the case of a 41-year-old male with repeated visits to outside emergency\ndepartments over a 3-month period with a waxing and waning pattern of worsening\ncognitive dysfunction as well as intermittent fevers. He also complained of\ngeneralized weakness and fatigue. His initial diagnosis was viral meningitis. He had\na negative workup for infectious etiologies, including negative CSF cultures,\nnegative Lyme titers, normal ACE level. Previous lumbar puncture was notable for\nelevated white blood cells, elevated protein, and glucose below 50g/dL. CT scan of\nthe abdomen at an outside hospital revealed a right pericaval lymph node measuring\n3.8 x 3.7 cm with central necrosis ().\nExternal genitalia were incompletely visualized on this scan. After transfer to our\ninstitution, the condition continued to worsen and after being admitted, the patient\nwas unable to speak and reported weakness in all four extremities that progressed to\nalteration of awareness, disorientation, and difficulty speaking. Labs at this time\nwere significant for phosphorous less than 2 mg/dL, which is known to precipitate\nseizures and altered mental status, however it was felt that the lower extremity\nshaking was not consistent with a seizure. He was placed on Keppra prior to arrival\nat our hospital. Based on this presentation, a CT of the head was obtained to rule\nout a primary central nervous system etiology. This imaging showed no acute process.\nFurther work up with MRI could not be obtained due to a non-compatible internal\npacemaker. Pacemaker analysis showed no abnormalities. Due to the para-aortic\nlocation of the mass, a 24-hour urine metanephrine was also performed to rule out a\nneuroendocrine tumor.\nAfter the negative initial workup, concern for distant metastasis led to the belief\ncurrent symptomatology was due to secondary to a paraneoplastic process.\nSpecifically, the presence of retroperitoneal lymphadenopathy with necrosis raised\nconcern for testicular origin. Sonographic evaluation of the testicles showed a\nright sided, ill-defined, multi-cystic 2.4 x 2.1 x 2.2cm mass (). Further laboratory evaluation revealed an\nelevated B-hCG of 49.9 mIU/mL, alpha fetoprotein level of 1.67 ng/mL and normal LDH\nlevel. A right radical orchiectomy was performed.\nGross pathology obtained from the right radical orchiectomy showed a 2.1 x 1.8 x 1.6\ncm tan-white, ill defined, soft, multicystic lesion in the medial and inferior pole\nof the testis, without hemorrhage or necrosis. Histologic evaluation revealed mixed\nrespiratory epithelium, gastrointestinal glands, and squamous epithelium with\nkeratinization consistent with a post-pubertal testicular teratoma with associated\ngerm cell neoplasia in situ (Figures , ).\nRepeat CT scan of the abdomen and pelvis showed continuous enlargement of the right\nperi-aortic lymph node, now measuring 5.6 cm in greatest dimension, as well as a new\nleft peri-aortic node measuring 2.2 cm in the largest dimension. After\nmultidisciplinary discussion, given the likelihood of a paraneoplastic syndrome that\nwould likely worsen with up front chemotherapy, the decision was made to proceed\nwith a primary retroperitoneal lymph node dissection. The large aortocaval mass was\nadherent to the inferior vena cava (IVC), but no invasion was noted. Measurement of\nthe extirpated mass was noted to be 7 x 6 x 4.5 cm in size cm in the largest\ndiameter. A complete bilateral template retroperitoneal lymph node dissection was\nperformed extending inferiorly from the renal veins to the bifurcation of the common\niliac arteries and to the ureters bilaterally.\nOn gross pathology, the aortocaval mass was well encapsulated with hemorrhagic and\nnecrotic cut surfaces. Microscopic evaluation displayed large anaplastic cells with\nepithelioid features, nuclear pleomorphism and frequent mitoses. Giant cells with\ngranular cytoplasm were also present. One node measuring 1.5 x 1.0 x 1.0 cm was\npositive for malignancy. Immunostaining of the mass and positive lymph node\ndisplayed positive staining for Pan-Keratin and OCT4, and negative staining for\nCD30, S-100, Desmin, pan-melanoma, and SOX2. The microscopic evaluation and\nimmunostaining combination led to the diagnosis of poorly differentiated embryonal\ncarcinoma ().\nThe patient’s neurological symptoms were managed with methylprednisolone, and Keppra\nwas continued for seizure prophylaxis. Following resection of the aortocaval mass,\nthe patient recovered well, and the diplopia and paralysis resolved. He was managed\npost-operatively with Bleomycin-Etoposide-Cisplatin (BEP) therapy. At the time of\npublication, he had received three cycles of BEP and has shown no evidence of tumor\nrecurrence.

Write a detailed clinical case vignette based on the following key phrases: testicular cancer, germ cell tumors, orchidectomy

The patient is a forty-one-year-old man with an unremarkable medical history presented with a two-month history of scrotal swelling and discomfort. He denied a history of mal-descent, and there was no family history of testicular cancer. Physical exam was pertinent for an enlarged, nontender left testicle. An ultrasound revealed well-circumscribed hypo-echoic, heterogeneous lesions in both testicles (). The left testicular mass measured 3.0 × 2.6 × 4.3 cm, while the mass in the right testicle measured 2.1 × 3.1 × 0.5 cm. Doppler was suggestive of normal blood flow. Pertinent labs included (AFP) alpha fetoprotein 6.2 µg/L, (beta HCG) beta human chorionic gonadotropin <3 IU/L, (LDH) lactase dehydrogenase levels 572 U/L, and serum testosterone 375 ng/dL, and all prognostic markers are within normal limits. CT of the chest, abdomen, and pelvis was negative for evidence of metastatic disease or lymphadenopathy.\nHe underwent bilateral inguinal orchiectomy. Final pathology () revealed classical seminoma in both specimens. Both right and left tumors exhibited invasion of the rete testis. There was possible angiolymphatic space invasion noted within the left testicular mass. There was no tumor extension through the tunica albuginea, epididymis, or spermatic cord. Surgical margins were free. Both tumors were pathologically staged IA.\nThe patient did not have concerns regarding fertility and declined to consider an organ preserving approach. Our patient was uncomfortable with surveillance as an option. He declined medical oncology referral for discussion about systemic therapy and was therefore treated with external beam radiotherapy. He received 2550 cGy in 17 fractions at 150 cGy per fraction via 6 MV/18 MV photons with AP/PA fields. Field borders () included superior border at T10/11 interspace, inferior border at L5/S1 interspace, and lateral borders of vertebral transverse processes (field width approximately 10 cm). The patient did not have a history of previous pelvic surgery, and only the paraaortic lymph nodes were targeted. He tolerated treatment well, experiencing grade I nausea (as per Common Terminology Criteria for Adverse Events, version 3.0). He is currently disease-free, 18 months from completion of radiation therapy. His serum testosterone levels fell to 248 ng/dL after treatment, and he uses testosterone gel for hormone replacement.

A 35-year-old man with no known risk factors for testicular malignancy presented at the urology department with a right testicular mass causing painful swelling. He had been experiencing discomfort and heaviness for 10 days. His general practitioner had started antibiotic and anti-inflammatory treatment a week prior to his arrival at our department. The patient had no past medical history of testicular issues.\nPhysical examination revealed a lump, which testicular ultrasound confirmed as an 18 mm × 12 mm × 25 mm heterogeneous hypoechogenic mass localized to the upper pole of the right testis (Fig. ). A computed tomography (CT) scan showed no evidence of abdominopelvic or thoracic metastases. The blood serum tumor marker levels were as follows: human chorionic gonadotropin (HCG) < 1.20 U/ml (normal is < 5.01 U/ml); α-fetoprotein (AFP) = 3.4 ng/ml (normal is < 7 ng/ml); and lactate dehydrogenase (LDH) = 599 IU/l (normal is 313–618 IU/l).\nA right inguinal radical orchiectomy was performed in September of 2009. Histological examination revealed a pure seminoma of 4 cm × 2.5 cm, without lymphatic, vascular, or tunica albuginea infiltration. The tumor node metastasis (TNM) classification was pT1pNxpMx according to the Union for International Cancer Control (UICC) staging system, seventh edition. Two weeks after the surgery, this case was discussed during a multidisciplinary uro-oncology meeting. From October 21 to November 10 of 2009, the patient underwent adjuvant radiotherapy with doses of 25.2 Gy delivered to the paraaortic lymph nodes in 14 fractions.\nThe patient was considered to be disease-free and received follow-up in accordance with our standard protocol, which includes chest and abdominal CT, physical examination, and tumor marker assessment every 4 months for the first 2 years, and testicular ultrasound of the contralateral side once each year. A total-body CT scan at 1 year after radical surgical treatment showed a 16-mm lymph node under the patient’s left collarbone (Fig. ). The lesion was confirmed by positron emission tomography (PET) scan, and surgical node excision was performed. Histological examination revealed a typical seminoma (Fig. ). Chemotherapy was initiated with a bleomycin, etoposide, and cisplatin (BEP) protocol administered every 21 days for 2 cycles from October to December of 2010.\nFour years later, a follow-up ultrasound of the left testis revealed a 15 mm × 6 mm node with microcalcifications (Fig. ). Blood serum tumor markers were normal, and a CT scan showed no evidence of abdominopelvic or thoracic metastasis. The possibility of radical or partial orchiectomy was discussed with the patient. In March of 2014, the patient underwent left inguinal testicular exploration of the lesion with ultrasound image guidance and excisional biopsy. Analysis of frozen biopsy sections revealed a seminomatous tumor with an intense chronic granulomatous inflammatory lesion. Due to the diffuse nature of the tumor, radical left orchiectomy was performed. The final pathological diagnosis was a pure seminoma that presented as isolated and scattered neoplastic cells within an inflammatory and granulomatous reaction and multifocal intratubular germ cell neoplasia (IGGNU).\nThe patient remained under surveillance and received androgen replacement therapy with long-acting testosterone undecanoate every 12 weeks (Nebido®). A bilateral testicular prosthesis was proposed but was refused. Sperm cryopreservation was not performed because the patient had children and did not desire any additional offspring. Follow-up was performed following the standard protocol. At 2 years after left radical orchiectomy, the patient remained disease free. At the most recent visit, the patient reported maintenance of libido, no adverse effects from the androgen replacement therapy, and comfortable sexual activity and quality of life.\nReported TGCT incidence rates from multiple countries between 1991 and 2011 show geographical variations, with the highest rates observed in Denmark. Over recent decades, TGCT prevalence has gradually increased in most populations of European origin and in the USA [, ]. Some studies suggest an increased incidence of bilateral disease in the post-chemotherapy and radiotherapy era [, ]. A retrospective review shows a threefold higher incidence of bilateral testicular cancers in the post-chemotherapy era compared to the pre-chemotherapy era []. The apparent increase in the number of metachronous tumors may reflect the increased life expectancy of the general population as well as the prolonged survival associated with higher cure rates for initial tumors.\nA systematic literature review—including 50,376 men with TGCT between 1991 and 2011 from many countries—reported a BTGCT prevalence of 1.82 % []. Among those with BTGCT, 69.2 % had metachronous tumors and 30.8 % had synchronous tumors. Several studies indicate that metachronous testicular tumors seem to be more frequent than synchronous ones [, ]. Bilateral metachronous TGCT was first described in a case report in 1942. Metachronous testicular cancer is diagnosed when at least 6 months elapse between the appearance of the first tumor and the second tumor and when there is an ultrasound-documented absence of a contralateral mass at diagnosis of the first tumor.\nAmong patients with metachronous tumors, the mean age at diagnosis of the first tumor is 28 years old and the mean age at diagnosis of the second tumor is 35 years old []. Our present patient was 36 years old when the first tumor was diagnosed and 40 years old when the second tumor was diagnosed. In 70 % of cases, the second testicular malignancy arises within 5 years after the first TGCT []. Seminoma is the most common histological type of bilateral testicular cancer, comprising approximately 68 % of such cases [], as well as the most common histological type of metachronous tumor []. When the second tumor is a seminoma, the median interval between tumors seems to be longer (~10 years) []. There have been 25 reported cases of BTGCT in which the contralateral testicular tumor occurred 20 years or more after the original tumor. Within a series of 25 cases, 4 cases involved a second tumor that occurred at least 30 years after the original testicular tumor, with the longest interval being 40 years [, ]. Contralateral testicular seminoma can occur even at an advanced age, underscoring the importance of life-long follow-up for these patients [, ].\nThe incidence of metachronous germ cell tumors in patients diagnosed with a seminoma is influenced by the patient’s age at the time of the initial diagnosis. Evidence suggests that men who develop a seminoma when they are 30 years of age or younger may be at greater risk of developing a second tumor [, ]. Patients diagnosed with a seminomatous tumor at less than 30 years of age show an increased risk of relapse in the following 15 years compared to men who are over 30 years old at diagnosis (3.1 vs 1.2 %) [].\nAlthough the etiology of BTGCT remains unknown, both genetic and environmental causes are implicated. Presently known epidemiological risk factors for TGCT development include a history of cryptorchidism, Klinefelter syndrome, the presence of a contralateral tumor, infertility, and a history of testis cancer in first-degree relatives []. The elevated risk in family members and associations with inherited genotypes suggest genetic causes [, ]. On the other hand, testicular cancer incidence rates nearly doubled in industrialized countries between 1975 and 2007, suggesting an influence of environmental factors [, ]. Our present case involved no known genetic or environmental risk factors.\nIn our present case, serum markers were negative both at the diagnosis of the first tumor and at tumor recurrence. This is in accordance with the typical presentation of a seminoma. Most second tumors are discovered by the physician via scrotal ultrasonography or by the patient via testicular self-examination. Ultrasonography is a safe and simple screening procedure. One major difficulty regarding the diagnosis of second tumors is that patients may be reluctant to seek help due to fear of castration.\nUltrasound detection of microlithiasis in the contralateral testis is associated with a 30-fold increase in the risk of presenting with a second TGCT, and diagnosis of the first tumor is associated with a 5–8 % risk of testicular intraepithelial neoplasm (TIN) in the contralateral testis. These data highlight the need for long-term surveillance to support early detection of the second TGCT. Within 7 years, 70 % of all TINs will progress to invasive neoplasia [, ], although this risk is somewhat lower among patients who undergo chemotherapy for their first tumor. The 5-year survival rates for men with synchronous and metachronous bilateral testicular tumor are 88 and 95 %, respectively [], suggesting that metachronous tumors have a more favorable survival outcome than synchronous tumors. Synchronous tumors are also associated with more advanced disease than metachronous tumors []. Among patients with bilateral testicular cancer, 70 % present with stage I disease upon diagnosis of the second tumor. This is most likely due to close follow-up and increased patient awareness.\nThe optimal management of patients with intratubular germ cell neoplasms remains controversial. The choices include surveillance and irradiation of the contralateral testis. Since radiotherapy can result in infertility and may affect Leydig cell function [], surveillance is an important part of TGCT follow-up. Clear guidelines are also lacking for treatment of bilateral testicular tumors. Treatment of the second tumor is based on the stage and histology []. The incidence of contralateral testicular cancer is not significantly influenced by the use of radiation therapy for the initial testicular cancer [].\nTreatment for advanced germ cell tumors includes combination chemotherapy with bleomycin, cisplatin, and etoposide, followed by surgical salvage for residual disease. Depending of the patient’s risk profile, 3–4 cycles of chemotherapy are needed []. The patient in our present case received adjuvant radiation therapy after the onset of the first tumor as well as chemotherapy. Additionally, a metastatic lymph node was removed at relapse, which occurred long before the diagnosis of the second tumor. Notably, 5 years elapsed between diagnosis of the first and second tumors. A left radical orchidectomy was performed to eliminate the recurrent tumor due to its diffuse character and the history of metastases. Sparing the testis would have carried a risk of recurrence. Taking into account that he did not desire more children, the patient wanted radical surgery despite the need for hormonal replacement.\nIn the present case, the detection of a contralateral supradiaphragmatic lymph node 3 years prior to the contralateral testis diagnosis indicated metastatic relapse. A review by Cooper et al. reported that approximately 75 % of seminomas present as stage 1, with disease limited to the testis []. All tumors of germ cell origin have the propensity to metastasize via lymphatic pathways, which typically occurs in a sequential pattern, beginning with abdominal lymph node involvement, followed by successive involvement of lymph nodes in the chest and neck []. Wood et al. demonstrated that cervical metastasis is almost exclusively left-sided, with 21 of 23 patients showing disease in supraclavicular or scalene lymph nodes []. Metastatic tumors can also appear in locations outside of the direct line of spread from the primary site []. A review by Vledder reported that 4 % of seminoma patients showed cervical metastasis and that only 5 % of these patients had the neck mass as their initial disease sign []. Seminomas can metastasize to the supraclavicular lymph nodes, and tumors from the right testis can spread to the interaortocaval, precaval, and paraaortic regions, with crossover to left-sided lymph nodes. The left testis drains into the paraaortic and preaortic regions. Interaortocaval lymph node involvement occurs in higher-stage disease. From there, the tumors usually grow along the thoracic duct into the left supraclavicular lymph node and the subclavian vein and then show disseminated spread []. This hypothesis may be applicable to our present patient, since metastasis was not found elsewhere.

Write a detailed clinical case vignette based on the following key phrases: testicular cancer, germ cell tumors, orchidectomy

The patient is a forty-one-year-old man with an unremarkable medical history presented with a two-month history of scrotal swelling and discomfort. He denied a history of mal-descent, and there was no family history of testicular cancer. Physical exam was pertinent for an enlarged, nontender left testicle. An ultrasound revealed well-circumscribed hypo-echoic, heterogeneous lesions in both testicles (). The left testicular mass measured 3.0 × 2.6 × 4.3 cm, while the mass in the right testicle measured 2.1 × 3.1 × 0.5 cm. Doppler was suggestive of normal blood flow. Pertinent labs included (AFP) alpha fetoprotein 6.2 µg/L, (beta HCG) beta human chorionic gonadotropin <3 IU/L, (LDH) lactase dehydrogenase levels 572 U/L, and serum testosterone 375 ng/dL, and all prognostic markers are within normal limits. CT of the chest, abdomen, and pelvis was negative for evidence of metastatic disease or lymphadenopathy.\nHe underwent bilateral inguinal orchiectomy. Final pathology () revealed classical seminoma in both specimens. Both right and left tumors exhibited invasion of the rete testis. There was possible angiolymphatic space invasion noted within the left testicular mass. There was no tumor extension through the tunica albuginea, epididymis, or spermatic cord. Surgical margins were free. Both tumors were pathologically staged IA.\nThe patient did not have concerns regarding fertility and declined to consider an organ preserving approach. Our patient was uncomfortable with surveillance as an option. He declined medical oncology referral for discussion about systemic therapy and was therefore treated with external beam radiotherapy. He received 2550 cGy in 17 fractions at 150 cGy per fraction via 6 MV/18 MV photons with AP/PA fields. Field borders () included superior border at T10/11 interspace, inferior border at L5/S1 interspace, and lateral borders of vertebral transverse processes (field width approximately 10 cm). The patient did not have a history of previous pelvic surgery, and only the paraaortic lymph nodes were targeted. He tolerated treatment well, experiencing grade I nausea (as per Common Terminology Criteria for Adverse Events, version 3.0). He is currently disease-free, 18 months from completion of radiation therapy. His serum testosterone levels fell to 248 ng/dL after treatment, and he uses testosterone gel for hormone replacement.

A 27 year old single male presented to our patient department with complaint of one month testicular swelling with left side preference. He has no complaints of pain in the testicles and abdomen. No problem in erectile function. He had no problems during puberty. He had no history of smoking and use of opioid in social habits. There is no family history and no evidence of risk factor for testicular cancer such as cryptorchidism or congenital abnormalities in the patient. Physical examination specified the left side testis with twice the normal volume swelling and without tenderness. The size of right side testis has increased slightly. Laboratory workup revealed azoospermia and an elevated a-FP (258.4IU/mL), and b-hcG (3.12mIU/mL) within normal levels. On ultrasound study the testes have 50mm×30mm in right side and 72mm×50mm in left side dimensions. No hydrocele was seen. Images of the right testis demonstrated 38mm×27mm hypoecho mass that accounting for (occupying) three-quarters of the volume of the parenchyma. Images of the left testis demonstrated approximately 70mm×47mm mixed echogenic mass, comprises almost the entire volume of the testis. Epididymis have normal parenchymal dimensions and echoes.\nThe ultrasound study of abdomen and pelvis showed no abnormality. The abdomen CT scan was not indicative of enlargement of the lymph nodes of retroperitoneum. The chest x-ray did not show evidence of metastasis. The patient underwent bilateral radical orchiectomy. Right testicular mass, excisional biopsy, for frozen section and intra-operative diagnosis, consists of a piece of creamy colored soft tissue specimen, with homogenous appearance, measured 45×35×22 mm in the largest diameters. Cryo and permanent sections of right testis mass, confirmed invasive, classic type seminoma that limited to the testis with intratubular and invasion to lympho-vascular tissues (tumor stage: at-least PT2) ().\nIn the left testis, in cut sections, almost all testicular volume replaced by tumoral tissue with heterogeneous appearance, containing solid and cystic, hemorrhagic and necrotic areas, measured 80×50×40 mm. the left side tumor was a malignant GCT with component of invasive, classic type seminoma (50-60%), yolk sac tumor (40-50%) and embryonal carcinoma (about 10%) (). Tumor extended to rete testis, tunica albuginea and tunica vaginalis. Epididymis was not involved. Intratubular and lympho-vascular invasion was present (tumor stage: PT2). Immunocytochemical study with AE1/AE3, CD30 and CD117 markers demonstrated a positive reaction (). The patient was discharged without problems and complications one day after surgery. The elevated a-FP on the postoperative measurement decreased to lower values (6,05mIU/mL). The patient was advised to go to an oncologist and was submitted to one cycle of adjuvant chemotherapy with bleomycin, etoposide, and cisplatin (BEP). As the follow-up physical examination, serum markers, chest X ray, and CT of the abdomen, were checked. Six months after the orchiectomy there was no residual tumor or recurrence, neither local nor systematic. Finally the patient is under a follow-up by an endocrinologist for the long-term management regarding the testosterone replacement therapy and he has been started on topical testrogel for life.

Write a detailed clinical case vignette based on the following key phrases: testicular cancer, germ cell tumors, orchidectomy

A 40-year-old male presented at our outpatients department complaining about a testicular painless mass on the right testis, which had shown a gradual enlargement over the past two months. The only symptom the patient had was discomfort in the scrotum and a sensation of testicular heaviness. His medical history did not report any known risk factors for testis cancer, such as cryptorchidism, and he did not have any comorbidities. Physical examination revealed a firm and nontender mass both on the right and on the left testis, which were easily separable from the epididymis. No other constitutional signs were present. Laboratory workup revealed a moderately elevated b-hcG (24,7 mIU/mL) and CEA (1,97 ng/mL), a-FP (1,62 ng/mL), and LDH (180 IU/L) within normal levels. Firstly, he was submitted to a scrotal ultrasonography which revealed a testicular mass that measured approximately 2,3 × 3,1 cm on the right testis () and another testicular mass of 2,4 × 1,5 cm in size on the left testis (). The computer tomography (CT) of the abdomen did not demonstrate any enlarged retroperitoneal lymph nodes. The chest X-ray showed no abnormality. The patient was scheduled for operation and he did not want to have frozen storage of sperm, although he was fully informed about the consequences, since he was a father of two children and also was informed about the occurrence of hypogonadism after the operation and that he will have to be under a strict endocrinologist follow-up and hormone replacement. He chose bilateral orchiectomy for oncological reasons. Finally, he underwent bilateral orchiectomy with high ligation of the spermatic cord. The postoperative period was uneventful and the patient exited the hospital the next day. The elevated b-hcG on the postoperative measurement (the 15th day) was within normal values (0,3 mIU/mL). Histopathological evaluation of the specimens revealed the following: (a) an embryonal cell carcinoma of the right testis limited to the testis with lymphovascular invasion of pathological stage pT2 (): staining with antibodies showed CD30(+) and a-FP(−); (b) a seminoma of the left testis, limited to the testis without invasion of the tunica albuginea or vascular invasion of pathological stage pT1 (): staining with antibodies showed CD117(+), CD30(−), and a-FP(−). On both testicles intratubular germ cell neoplasia of unclassified type (IGCNU) was present. The patient was referred to an oncologist and was submitted to two cycles of adjuvant combined chemotherapy with bleomycin, etoposide, and cisplatin (BEP). His follow-up consisted of physical examination, serum markers, chest X-ray, and CT of the abdomen, according to the EAU Guidelines recommended follow-up schedule. Six months after the operation no residual tumor or recurrence was observed, neither local nor systematic. Finally the patient is under a strict endocrinologist follow-up for the management of his hypogonadism state.

An 18-year-old man, without any known risk factor for testicular malignancy, presented to our hospital with a painful right testicular mass with 1 month of evolution. Physical examination detected a small lump, confirmed by testicular ultrasound as a hypoechoic nodule. A CT-scan revealed no metastatic disease. α-fetoprotein (AFP) and lactate dehydrogenase (LDH) were above the normal limit. A right inguinal orchiectomy was performed and the histological exam revealed a mixed germ cell testicular tumor (composed by embrionary carcinoma and mature teratoma). Tumoral markers normalized after surgery, and the tumor was staged as pT1N0M0S0 - IA, according to the American Joint Committee on Cancer guidelines. The patient remained under surveillance. Twelve years later he developed bilateral gynecomastia and a high human chorionic gonadotropin (HCG). CT-scan found a 1cm lateroaortic adenopathy and a PET-scan revealed hyperfixation in the referred adenopathy and left testicle. At that time a scrotal ultrasonography was done, and a voluminous testicle of 5 x 5 x 3 cm with hypoechogenic and hypervascularized areas were found. This was followed by a left radical inguinal orchiectomy with testicle prosthesis introduction. Histological exam revealed a mixed TGCT (with seminoma, embrionary carcinoma and immature teratoma components) and a pathological stage pT2N1M0S1 – IIA. Chemotherapy was started with BEP protocol (bleomycin, etoposide and cisplatin), administered every 21 days for 3 cycles. Retroperitoneal adenopathy disappeared, HCG normalized and a surveillance program was initiated. The patient was disease-free in the 5 months after having finished his treatment.

Write a detailed clinical case vignette based on the following key phrases: testicular cancer, germ cell tumors, orchidectomy

A 40-year-old male presented at our outpatients department complaining about a testicular painless mass on the right testis, which had shown a gradual enlargement over the past two months. The only symptom the patient had was discomfort in the scrotum and a sensation of testicular heaviness. His medical history did not report any known risk factors for testis cancer, such as cryptorchidism, and he did not have any comorbidities. Physical examination revealed a firm and nontender mass both on the right and on the left testis, which were easily separable from the epididymis. No other constitutional signs were present. Laboratory workup revealed a moderately elevated b-hcG (24,7 mIU/mL) and CEA (1,97 ng/mL), a-FP (1,62 ng/mL), and LDH (180 IU/L) within normal levels. Firstly, he was submitted to a scrotal ultrasonography which revealed a testicular mass that measured approximately 2,3 × 3,1 cm on the right testis () and another testicular mass of 2,4 × 1,5 cm in size on the left testis (). The computer tomography (CT) of the abdomen did not demonstrate any enlarged retroperitoneal lymph nodes. The chest X-ray showed no abnormality. The patient was scheduled for operation and he did not want to have frozen storage of sperm, although he was fully informed about the consequences, since he was a father of two children and also was informed about the occurrence of hypogonadism after the operation and that he will have to be under a strict endocrinologist follow-up and hormone replacement. He chose bilateral orchiectomy for oncological reasons. Finally, he underwent bilateral orchiectomy with high ligation of the spermatic cord. The postoperative period was uneventful and the patient exited the hospital the next day. The elevated b-hcG on the postoperative measurement (the 15th day) was within normal values (0,3 mIU/mL). Histopathological evaluation of the specimens revealed the following: (a) an embryonal cell carcinoma of the right testis limited to the testis with lymphovascular invasion of pathological stage pT2 (): staining with antibodies showed CD30(+) and a-FP(−); (b) a seminoma of the left testis, limited to the testis without invasion of the tunica albuginea or vascular invasion of pathological stage pT1 (): staining with antibodies showed CD117(+), CD30(−), and a-FP(−). On both testicles intratubular germ cell neoplasia of unclassified type (IGCNU) was present. The patient was referred to an oncologist and was submitted to two cycles of adjuvant combined chemotherapy with bleomycin, etoposide, and cisplatin (BEP). His follow-up consisted of physical examination, serum markers, chest X-ray, and CT of the abdomen, according to the EAU Guidelines recommended follow-up schedule. Six months after the operation no residual tumor or recurrence was observed, neither local nor systematic. Finally the patient is under a strict endocrinologist follow-up for the management of his hypogonadism state.

We present the case of a 41-year-old male with repeated visits to outside emergency\ndepartments over a 3-month period with a waxing and waning pattern of worsening\ncognitive dysfunction as well as intermittent fevers. He also complained of\ngeneralized weakness and fatigue. His initial diagnosis was viral meningitis. He had\na negative workup for infectious etiologies, including negative CSF cultures,\nnegative Lyme titers, normal ACE level. Previous lumbar puncture was notable for\nelevated white blood cells, elevated protein, and glucose below 50g/dL. CT scan of\nthe abdomen at an outside hospital revealed a right pericaval lymph node measuring\n3.8 x 3.7 cm with central necrosis ().\nExternal genitalia were incompletely visualized on this scan. After transfer to our\ninstitution, the condition continued to worsen and after being admitted, the patient\nwas unable to speak and reported weakness in all four extremities that progressed to\nalteration of awareness, disorientation, and difficulty speaking. Labs at this time\nwere significant for phosphorous less than 2 mg/dL, which is known to precipitate\nseizures and altered mental status, however it was felt that the lower extremity\nshaking was not consistent with a seizure. He was placed on Keppra prior to arrival\nat our hospital. Based on this presentation, a CT of the head was obtained to rule\nout a primary central nervous system etiology. This imaging showed no acute process.\nFurther work up with MRI could not be obtained due to a non-compatible internal\npacemaker. Pacemaker analysis showed no abnormalities. Due to the para-aortic\nlocation of the mass, a 24-hour urine metanephrine was also performed to rule out a\nneuroendocrine tumor.\nAfter the negative initial workup, concern for distant metastasis led to the belief\ncurrent symptomatology was due to secondary to a paraneoplastic process.\nSpecifically, the presence of retroperitoneal lymphadenopathy with necrosis raised\nconcern for testicular origin. Sonographic evaluation of the testicles showed a\nright sided, ill-defined, multi-cystic 2.4 x 2.1 x 2.2cm mass (). Further laboratory evaluation revealed an\nelevated B-hCG of 49.9 mIU/mL, alpha fetoprotein level of 1.67 ng/mL and normal LDH\nlevel. A right radical orchiectomy was performed.\nGross pathology obtained from the right radical orchiectomy showed a 2.1 x 1.8 x 1.6\ncm tan-white, ill defined, soft, multicystic lesion in the medial and inferior pole\nof the testis, without hemorrhage or necrosis. Histologic evaluation revealed mixed\nrespiratory epithelium, gastrointestinal glands, and squamous epithelium with\nkeratinization consistent with a post-pubertal testicular teratoma with associated\ngerm cell neoplasia in situ (Figures , ).\nRepeat CT scan of the abdomen and pelvis showed continuous enlargement of the right\nperi-aortic lymph node, now measuring 5.6 cm in greatest dimension, as well as a new\nleft peri-aortic node measuring 2.2 cm in the largest dimension. After\nmultidisciplinary discussion, given the likelihood of a paraneoplastic syndrome that\nwould likely worsen with up front chemotherapy, the decision was made to proceed\nwith a primary retroperitoneal lymph node dissection. The large aortocaval mass was\nadherent to the inferior vena cava (IVC), but no invasion was noted. Measurement of\nthe extirpated mass was noted to be 7 x 6 x 4.5 cm in size cm in the largest\ndiameter. A complete bilateral template retroperitoneal lymph node dissection was\nperformed extending inferiorly from the renal veins to the bifurcation of the common\niliac arteries and to the ureters bilaterally.\nOn gross pathology, the aortocaval mass was well encapsulated with hemorrhagic and\nnecrotic cut surfaces. Microscopic evaluation displayed large anaplastic cells with\nepithelioid features, nuclear pleomorphism and frequent mitoses. Giant cells with\ngranular cytoplasm were also present. One node measuring 1.5 x 1.0 x 1.0 cm was\npositive for malignancy. Immunostaining of the mass and positive lymph node\ndisplayed positive staining for Pan-Keratin and OCT4, and negative staining for\nCD30, S-100, Desmin, pan-melanoma, and SOX2. The microscopic evaluation and\nimmunostaining combination led to the diagnosis of poorly differentiated embryonal\ncarcinoma ().\nThe patient’s neurological symptoms were managed with methylprednisolone, and Keppra\nwas continued for seizure prophylaxis. Following resection of the aortocaval mass,\nthe patient recovered well, and the diplopia and paralysis resolved. He was managed\npost-operatively with Bleomycin-Etoposide-Cisplatin (BEP) therapy. At the time of\npublication, he had received three cycles of BEP and has shown no evidence of tumor\nrecurrence.

Write a detailed clinical case vignette based on the following key phrases: testicular cancer, germ cell tumors, orchidectomy

A 35-year-old man with no known risk factors for testicular malignancy presented at the urology department with a right testicular mass causing painful swelling. He had been experiencing discomfort and heaviness for 10 days. His general practitioner had started antibiotic and anti-inflammatory treatment a week prior to his arrival at our department. The patient had no past medical history of testicular issues.\nPhysical examination revealed a lump, which testicular ultrasound confirmed as an 18 mm × 12 mm × 25 mm heterogeneous hypoechogenic mass localized to the upper pole of the right testis (Fig. ). A computed tomography (CT) scan showed no evidence of abdominopelvic or thoracic metastases. The blood serum tumor marker levels were as follows: human chorionic gonadotropin (HCG) < 1.20 U/ml (normal is < 5.01 U/ml); α-fetoprotein (AFP) = 3.4 ng/ml (normal is < 7 ng/ml); and lactate dehydrogenase (LDH) = 599 IU/l (normal is 313–618 IU/l).\nA right inguinal radical orchiectomy was performed in September of 2009. Histological examination revealed a pure seminoma of 4 cm × 2.5 cm, without lymphatic, vascular, or tunica albuginea infiltration. The tumor node metastasis (TNM) classification was pT1pNxpMx according to the Union for International Cancer Control (UICC) staging system, seventh edition. Two weeks after the surgery, this case was discussed during a multidisciplinary uro-oncology meeting. From October 21 to November 10 of 2009, the patient underwent adjuvant radiotherapy with doses of 25.2 Gy delivered to the paraaortic lymph nodes in 14 fractions.\nThe patient was considered to be disease-free and received follow-up in accordance with our standard protocol, which includes chest and abdominal CT, physical examination, and tumor marker assessment every 4 months for the first 2 years, and testicular ultrasound of the contralateral side once each year. A total-body CT scan at 1 year after radical surgical treatment showed a 16-mm lymph node under the patient’s left collarbone (Fig. ). The lesion was confirmed by positron emission tomography (PET) scan, and surgical node excision was performed. Histological examination revealed a typical seminoma (Fig. ). Chemotherapy was initiated with a bleomycin, etoposide, and cisplatin (BEP) protocol administered every 21 days for 2 cycles from October to December of 2010.\nFour years later, a follow-up ultrasound of the left testis revealed a 15 mm × 6 mm node with microcalcifications (Fig. ). Blood serum tumor markers were normal, and a CT scan showed no evidence of abdominopelvic or thoracic metastasis. The possibility of radical or partial orchiectomy was discussed with the patient. In March of 2014, the patient underwent left inguinal testicular exploration of the lesion with ultrasound image guidance and excisional biopsy. Analysis of frozen biopsy sections revealed a seminomatous tumor with an intense chronic granulomatous inflammatory lesion. Due to the diffuse nature of the tumor, radical left orchiectomy was performed. The final pathological diagnosis was a pure seminoma that presented as isolated and scattered neoplastic cells within an inflammatory and granulomatous reaction and multifocal intratubular germ cell neoplasia (IGGNU).\nThe patient remained under surveillance and received androgen replacement therapy with long-acting testosterone undecanoate every 12 weeks (Nebido®). A bilateral testicular prosthesis was proposed but was refused. Sperm cryopreservation was not performed because the patient had children and did not desire any additional offspring. Follow-up was performed following the standard protocol. At 2 years after left radical orchiectomy, the patient remained disease free. At the most recent visit, the patient reported maintenance of libido, no adverse effects from the androgen replacement therapy, and comfortable sexual activity and quality of life.\nReported TGCT incidence rates from multiple countries between 1991 and 2011 show geographical variations, with the highest rates observed in Denmark. Over recent decades, TGCT prevalence has gradually increased in most populations of European origin and in the USA [, ]. Some studies suggest an increased incidence of bilateral disease in the post-chemotherapy and radiotherapy era [, ]. A retrospective review shows a threefold higher incidence of bilateral testicular cancers in the post-chemotherapy era compared to the pre-chemotherapy era []. The apparent increase in the number of metachronous tumors may reflect the increased life expectancy of the general population as well as the prolonged survival associated with higher cure rates for initial tumors.\nA systematic literature review—including 50,376 men with TGCT between 1991 and 2011 from many countries—reported a BTGCT prevalence of 1.82 % []. Among those with BTGCT, 69.2 % had metachronous tumors and 30.8 % had synchronous tumors. Several studies indicate that metachronous testicular tumors seem to be more frequent than synchronous ones [, ]. Bilateral metachronous TGCT was first described in a case report in 1942. Metachronous testicular cancer is diagnosed when at least 6 months elapse between the appearance of the first tumor and the second tumor and when there is an ultrasound-documented absence of a contralateral mass at diagnosis of the first tumor.\nAmong patients with metachronous tumors, the mean age at diagnosis of the first tumor is 28 years old and the mean age at diagnosis of the second tumor is 35 years old []. Our present patient was 36 years old when the first tumor was diagnosed and 40 years old when the second tumor was diagnosed. In 70 % of cases, the second testicular malignancy arises within 5 years after the first TGCT []. Seminoma is the most common histological type of bilateral testicular cancer, comprising approximately 68 % of such cases [], as well as the most common histological type of metachronous tumor []. When the second tumor is a seminoma, the median interval between tumors seems to be longer (~10 years) []. There have been 25 reported cases of BTGCT in which the contralateral testicular tumor occurred 20 years or more after the original tumor. Within a series of 25 cases, 4 cases involved a second tumor that occurred at least 30 years after the original testicular tumor, with the longest interval being 40 years [, ]. Contralateral testicular seminoma can occur even at an advanced age, underscoring the importance of life-long follow-up for these patients [, ].\nThe incidence of metachronous germ cell tumors in patients diagnosed with a seminoma is influenced by the patient’s age at the time of the initial diagnosis. Evidence suggests that men who develop a seminoma when they are 30 years of age or younger may be at greater risk of developing a second tumor [, ]. Patients diagnosed with a seminomatous tumor at less than 30 years of age show an increased risk of relapse in the following 15 years compared to men who are over 30 years old at diagnosis (3.1 vs 1.2 %) [].\nAlthough the etiology of BTGCT remains unknown, both genetic and environmental causes are implicated. Presently known epidemiological risk factors for TGCT development include a history of cryptorchidism, Klinefelter syndrome, the presence of a contralateral tumor, infertility, and a history of testis cancer in first-degree relatives []. The elevated risk in family members and associations with inherited genotypes suggest genetic causes [, ]. On the other hand, testicular cancer incidence rates nearly doubled in industrialized countries between 1975 and 2007, suggesting an influence of environmental factors [, ]. Our present case involved no known genetic or environmental risk factors.\nIn our present case, serum markers were negative both at the diagnosis of the first tumor and at tumor recurrence. This is in accordance with the typical presentation of a seminoma. Most second tumors are discovered by the physician via scrotal ultrasonography or by the patient via testicular self-examination. Ultrasonography is a safe and simple screening procedure. One major difficulty regarding the diagnosis of second tumors is that patients may be reluctant to seek help due to fear of castration.\nUltrasound detection of microlithiasis in the contralateral testis is associated with a 30-fold increase in the risk of presenting with a second TGCT, and diagnosis of the first tumor is associated with a 5–8 % risk of testicular intraepithelial neoplasm (TIN) in the contralateral testis. These data highlight the need for long-term surveillance to support early detection of the second TGCT. Within 7 years, 70 % of all TINs will progress to invasive neoplasia [, ], although this risk is somewhat lower among patients who undergo chemotherapy for their first tumor. The 5-year survival rates for men with synchronous and metachronous bilateral testicular tumor are 88 and 95 %, respectively [], suggesting that metachronous tumors have a more favorable survival outcome than synchronous tumors. Synchronous tumors are also associated with more advanced disease than metachronous tumors []. Among patients with bilateral testicular cancer, 70 % present with stage I disease upon diagnosis of the second tumor. This is most likely due to close follow-up and increased patient awareness.\nThe optimal management of patients with intratubular germ cell neoplasms remains controversial. The choices include surveillance and irradiation of the contralateral testis. Since radiotherapy can result in infertility and may affect Leydig cell function [], surveillance is an important part of TGCT follow-up. Clear guidelines are also lacking for treatment of bilateral testicular tumors. Treatment of the second tumor is based on the stage and histology []. The incidence of contralateral testicular cancer is not significantly influenced by the use of radiation therapy for the initial testicular cancer [].\nTreatment for advanced germ cell tumors includes combination chemotherapy with bleomycin, cisplatin, and etoposide, followed by surgical salvage for residual disease. Depending of the patient’s risk profile, 3–4 cycles of chemotherapy are needed []. The patient in our present case received adjuvant radiation therapy after the onset of the first tumor as well as chemotherapy. Additionally, a metastatic lymph node was removed at relapse, which occurred long before the diagnosis of the second tumor. Notably, 5 years elapsed between diagnosis of the first and second tumors. A left radical orchidectomy was performed to eliminate the recurrent tumor due to its diffuse character and the history of metastases. Sparing the testis would have carried a risk of recurrence. Taking into account that he did not desire more children, the patient wanted radical surgery despite the need for hormonal replacement.\nIn the present case, the detection of a contralateral supradiaphragmatic lymph node 3 years prior to the contralateral testis diagnosis indicated metastatic relapse. A review by Cooper et al. reported that approximately 75 % of seminomas present as stage 1, with disease limited to the testis []. All tumors of germ cell origin have the propensity to metastasize via lymphatic pathways, which typically occurs in a sequential pattern, beginning with abdominal lymph node involvement, followed by successive involvement of lymph nodes in the chest and neck []. Wood et al. demonstrated that cervical metastasis is almost exclusively left-sided, with 21 of 23 patients showing disease in supraclavicular or scalene lymph nodes []. Metastatic tumors can also appear in locations outside of the direct line of spread from the primary site []. A review by Vledder reported that 4 % of seminoma patients showed cervical metastasis and that only 5 % of these patients had the neck mass as their initial disease sign []. Seminomas can metastasize to the supraclavicular lymph nodes, and tumors from the right testis can spread to the interaortocaval, precaval, and paraaortic regions, with crossover to left-sided lymph nodes. The left testis drains into the paraaortic and preaortic regions. Interaortocaval lymph node involvement occurs in higher-stage disease. From there, the tumors usually grow along the thoracic duct into the left supraclavicular lymph node and the subclavian vein and then show disseminated spread []. This hypothesis may be applicable to our present patient, since metastasis was not found elsewhere.

A 40-year-old male presented at our outpatients department complaining about a testicular painless mass on the right testis, which had shown a gradual enlargement over the past two months. The only symptom the patient had was discomfort in the scrotum and a sensation of testicular heaviness. His medical history did not report any known risk factors for testis cancer, such as cryptorchidism, and he did not have any comorbidities. Physical examination revealed a firm and nontender mass both on the right and on the left testis, which were easily separable from the epididymis. No other constitutional signs were present. Laboratory workup revealed a moderately elevated b-hcG (24,7 mIU/mL) and CEA (1,97 ng/mL), a-FP (1,62 ng/mL), and LDH (180 IU/L) within normal levels. Firstly, he was submitted to a scrotal ultrasonography which revealed a testicular mass that measured approximately 2,3 × 3,1 cm on the right testis () and another testicular mass of 2,4 × 1,5 cm in size on the left testis (). The computer tomography (CT) of the abdomen did not demonstrate any enlarged retroperitoneal lymph nodes. The chest X-ray showed no abnormality. The patient was scheduled for operation and he did not want to have frozen storage of sperm, although he was fully informed about the consequences, since he was a father of two children and also was informed about the occurrence of hypogonadism after the operation and that he will have to be under a strict endocrinologist follow-up and hormone replacement. He chose bilateral orchiectomy for oncological reasons. Finally, he underwent bilateral orchiectomy with high ligation of the spermatic cord. The postoperative period was uneventful and the patient exited the hospital the next day. The elevated b-hcG on the postoperative measurement (the 15th day) was within normal values (0,3 mIU/mL). Histopathological evaluation of the specimens revealed the following: (a) an embryonal cell carcinoma of the right testis limited to the testis with lymphovascular invasion of pathological stage pT2 (): staining with antibodies showed CD30(+) and a-FP(−); (b) a seminoma of the left testis, limited to the testis without invasion of the tunica albuginea or vascular invasion of pathological stage pT1 (): staining with antibodies showed CD117(+), CD30(−), and a-FP(−). On both testicles intratubular germ cell neoplasia of unclassified type (IGCNU) was present. The patient was referred to an oncologist and was submitted to two cycles of adjuvant combined chemotherapy with bleomycin, etoposide, and cisplatin (BEP). His follow-up consisted of physical examination, serum markers, chest X-ray, and CT of the abdomen, according to the EAU Guidelines recommended follow-up schedule. Six months after the operation no residual tumor or recurrence was observed, neither local nor systematic. Finally the patient is under a strict endocrinologist follow-up for the management of his hypogonadism state.

Write a detailed clinical case vignette based on the following key phrases: testicular cancer, germ cell tumors, orchidectomy

A 40-year-old male presented at our outpatients department complaining about a testicular painless mass on the right testis, which had shown a gradual enlargement over the past two months. The only symptom the patient had was discomfort in the scrotum and a sensation of testicular heaviness. His medical history did not report any known risk factors for testis cancer, such as cryptorchidism, and he did not have any comorbidities. Physical examination revealed a firm and nontender mass both on the right and on the left testis, which were easily separable from the epididymis. No other constitutional signs were present. Laboratory workup revealed a moderately elevated b-hcG (24,7 mIU/mL) and CEA (1,97 ng/mL), a-FP (1,62 ng/mL), and LDH (180 IU/L) within normal levels. Firstly, he was submitted to a scrotal ultrasonography which revealed a testicular mass that measured approximately 2,3 × 3,1 cm on the right testis () and another testicular mass of 2,4 × 1,5 cm in size on the left testis (). The computer tomography (CT) of the abdomen did not demonstrate any enlarged retroperitoneal lymph nodes. The chest X-ray showed no abnormality. The patient was scheduled for operation and he did not want to have frozen storage of sperm, although he was fully informed about the consequences, since he was a father of two children and also was informed about the occurrence of hypogonadism after the operation and that he will have to be under a strict endocrinologist follow-up and hormone replacement. He chose bilateral orchiectomy for oncological reasons. Finally, he underwent bilateral orchiectomy with high ligation of the spermatic cord. The postoperative period was uneventful and the patient exited the hospital the next day. The elevated b-hcG on the postoperative measurement (the 15th day) was within normal values (0,3 mIU/mL). Histopathological evaluation of the specimens revealed the following: (a) an embryonal cell carcinoma of the right testis limited to the testis with lymphovascular invasion of pathological stage pT2 (): staining with antibodies showed CD30(+) and a-FP(−); (b) a seminoma of the left testis, limited to the testis without invasion of the tunica albuginea or vascular invasion of pathological stage pT1 (): staining with antibodies showed CD117(+), CD30(−), and a-FP(−). On both testicles intratubular germ cell neoplasia of unclassified type (IGCNU) was present. The patient was referred to an oncologist and was submitted to two cycles of adjuvant combined chemotherapy with bleomycin, etoposide, and cisplatin (BEP). His follow-up consisted of physical examination, serum markers, chest X-ray, and CT of the abdomen, according to the EAU Guidelines recommended follow-up schedule. Six months after the operation no residual tumor or recurrence was observed, neither local nor systematic. Finally the patient is under a strict endocrinologist follow-up for the management of his hypogonadism state.

A 27 year old single male presented to our patient department with complaint of one month testicular swelling with left side preference. He has no complaints of pain in the testicles and abdomen. No problem in erectile function. He had no problems during puberty. He had no history of smoking and use of opioid in social habits. There is no family history and no evidence of risk factor for testicular cancer such as cryptorchidism or congenital abnormalities in the patient. Physical examination specified the left side testis with twice the normal volume swelling and without tenderness. The size of right side testis has increased slightly. Laboratory workup revealed azoospermia and an elevated a-FP (258.4IU/mL), and b-hcG (3.12mIU/mL) within normal levels. On ultrasound study the testes have 50mm×30mm in right side and 72mm×50mm in left side dimensions. No hydrocele was seen. Images of the right testis demonstrated 38mm×27mm hypoecho mass that accounting for (occupying) three-quarters of the volume of the parenchyma. Images of the left testis demonstrated approximately 70mm×47mm mixed echogenic mass, comprises almost the entire volume of the testis. Epididymis have normal parenchymal dimensions and echoes.\nThe ultrasound study of abdomen and pelvis showed no abnormality. The abdomen CT scan was not indicative of enlargement of the lymph nodes of retroperitoneum. The chest x-ray did not show evidence of metastasis. The patient underwent bilateral radical orchiectomy. Right testicular mass, excisional biopsy, for frozen section and intra-operative diagnosis, consists of a piece of creamy colored soft tissue specimen, with homogenous appearance, measured 45×35×22 mm in the largest diameters. Cryo and permanent sections of right testis mass, confirmed invasive, classic type seminoma that limited to the testis with intratubular and invasion to lympho-vascular tissues (tumor stage: at-least PT2) ().\nIn the left testis, in cut sections, almost all testicular volume replaced by tumoral tissue with heterogeneous appearance, containing solid and cystic, hemorrhagic and necrotic areas, measured 80×50×40 mm. the left side tumor was a malignant GCT with component of invasive, classic type seminoma (50-60%), yolk sac tumor (40-50%) and embryonal carcinoma (about 10%) (). Tumor extended to rete testis, tunica albuginea and tunica vaginalis. Epididymis was not involved. Intratubular and lympho-vascular invasion was present (tumor stage: PT2). Immunocytochemical study with AE1/AE3, CD30 and CD117 markers demonstrated a positive reaction (). The patient was discharged without problems and complications one day after surgery. The elevated a-FP on the postoperative measurement decreased to lower values (6,05mIU/mL). The patient was advised to go to an oncologist and was submitted to one cycle of adjuvant chemotherapy with bleomycin, etoposide, and cisplatin (BEP). As the follow-up physical examination, serum markers, chest X ray, and CT of the abdomen, were checked. Six months after the orchiectomy there was no residual tumor or recurrence, neither local nor systematic. Finally the patient is under a follow-up by an endocrinologist for the long-term management regarding the testosterone replacement therapy and he has been started on topical testrogel for life.

Write a detailed clinical case vignette based on the following key phrases: testicular cancer, germ cell tumors, orchidectomy

An 18-year-old man, without any known risk factor for testicular malignancy, presented to our hospital with a painful right testicular mass with 1 month of evolution. Physical examination detected a small lump, confirmed by testicular ultrasound as a hypoechoic nodule. A CT-scan revealed no metastatic disease. α-fetoprotein (AFP) and lactate dehydrogenase (LDH) were above the normal limit. A right inguinal orchiectomy was performed and the histological exam revealed a mixed germ cell testicular tumor (composed by embrionary carcinoma and mature teratoma). Tumoral markers normalized after surgery, and the tumor was staged as pT1N0M0S0 - IA, according to the American Joint Committee on Cancer guidelines. The patient remained under surveillance. Twelve years later he developed bilateral gynecomastia and a high human chorionic gonadotropin (HCG). CT-scan found a 1cm lateroaortic adenopathy and a PET-scan revealed hyperfixation in the referred adenopathy and left testicle. At that time a scrotal ultrasonography was done, and a voluminous testicle of 5 x 5 x 3 cm with hypoechogenic and hypervascularized areas were found. This was followed by a left radical inguinal orchiectomy with testicle prosthesis introduction. Histological exam revealed a mixed TGCT (with seminoma, embrionary carcinoma and immature teratoma components) and a pathological stage pT2N1M0S1 – IIA. Chemotherapy was started with BEP protocol (bleomycin, etoposide and cisplatin), administered every 21 days for 3 cycles. Retroperitoneal adenopathy disappeared, HCG normalized and a surveillance program was initiated. The patient was disease-free in the 5 months after having finished his treatment.

We present the case of a 41-year-old male with repeated visits to outside emergency\ndepartments over a 3-month period with a waxing and waning pattern of worsening\ncognitive dysfunction as well as intermittent fevers. He also complained of\ngeneralized weakness and fatigue. His initial diagnosis was viral meningitis. He had\na negative workup for infectious etiologies, including negative CSF cultures,\nnegative Lyme titers, normal ACE level. Previous lumbar puncture was notable for\nelevated white blood cells, elevated protein, and glucose below 50g/dL. CT scan of\nthe abdomen at an outside hospital revealed a right pericaval lymph node measuring\n3.8 x 3.7 cm with central necrosis ().\nExternal genitalia were incompletely visualized on this scan. After transfer to our\ninstitution, the condition continued to worsen and after being admitted, the patient\nwas unable to speak and reported weakness in all four extremities that progressed to\nalteration of awareness, disorientation, and difficulty speaking. Labs at this time\nwere significant for phosphorous less than 2 mg/dL, which is known to precipitate\nseizures and altered mental status, however it was felt that the lower extremity\nshaking was not consistent with a seizure. He was placed on Keppra prior to arrival\nat our hospital. Based on this presentation, a CT of the head was obtained to rule\nout a primary central nervous system etiology. This imaging showed no acute process.\nFurther work up with MRI could not be obtained due to a non-compatible internal\npacemaker. Pacemaker analysis showed no abnormalities. Due to the para-aortic\nlocation of the mass, a 24-hour urine metanephrine was also performed to rule out a\nneuroendocrine tumor.\nAfter the negative initial workup, concern for distant metastasis led to the belief\ncurrent symptomatology was due to secondary to a paraneoplastic process.\nSpecifically, the presence of retroperitoneal lymphadenopathy with necrosis raised\nconcern for testicular origin. Sonographic evaluation of the testicles showed a\nright sided, ill-defined, multi-cystic 2.4 x 2.1 x 2.2cm mass (). Further laboratory evaluation revealed an\nelevated B-hCG of 49.9 mIU/mL, alpha fetoprotein level of 1.67 ng/mL and normal LDH\nlevel. A right radical orchiectomy was performed.\nGross pathology obtained from the right radical orchiectomy showed a 2.1 x 1.8 x 1.6\ncm tan-white, ill defined, soft, multicystic lesion in the medial and inferior pole\nof the testis, without hemorrhage or necrosis. Histologic evaluation revealed mixed\nrespiratory epithelium, gastrointestinal glands, and squamous epithelium with\nkeratinization consistent with a post-pubertal testicular teratoma with associated\ngerm cell neoplasia in situ (Figures , ).\nRepeat CT scan of the abdomen and pelvis showed continuous enlargement of the right\nperi-aortic lymph node, now measuring 5.6 cm in greatest dimension, as well as a new\nleft peri-aortic node measuring 2.2 cm in the largest dimension. After\nmultidisciplinary discussion, given the likelihood of a paraneoplastic syndrome that\nwould likely worsen with up front chemotherapy, the decision was made to proceed\nwith a primary retroperitoneal lymph node dissection. The large aortocaval mass was\nadherent to the inferior vena cava (IVC), but no invasion was noted. Measurement of\nthe extirpated mass was noted to be 7 x 6 x 4.5 cm in size cm in the largest\ndiameter. A complete bilateral template retroperitoneal lymph node dissection was\nperformed extending inferiorly from the renal veins to the bifurcation of the common\niliac arteries and to the ureters bilaterally.\nOn gross pathology, the aortocaval mass was well encapsulated with hemorrhagic and\nnecrotic cut surfaces. Microscopic evaluation displayed large anaplastic cells with\nepithelioid features, nuclear pleomorphism and frequent mitoses. Giant cells with\ngranular cytoplasm were also present. One node measuring 1.5 x 1.0 x 1.0 cm was\npositive for malignancy. Immunostaining of the mass and positive lymph node\ndisplayed positive staining for Pan-Keratin and OCT4, and negative staining for\nCD30, S-100, Desmin, pan-melanoma, and SOX2. The microscopic evaluation and\nimmunostaining combination led to the diagnosis of poorly differentiated embryonal\ncarcinoma ().\nThe patient’s neurological symptoms were managed with methylprednisolone, and Keppra\nwas continued for seizure prophylaxis. Following resection of the aortocaval mass,\nthe patient recovered well, and the diplopia and paralysis resolved. He was managed\npost-operatively with Bleomycin-Etoposide-Cisplatin (BEP) therapy. At the time of\npublication, he had received three cycles of BEP and has shown no evidence of tumor\nrecurrence.

Write a detailed clinical case vignette based on the following key phrases: testicular cancer, germ cell tumors, orchidectomy

A 35-year-old man with no known risk factors for testicular malignancy presented at the urology department with a right testicular mass causing painful swelling. He had been experiencing discomfort and heaviness for 10 days. His general practitioner had started antibiotic and anti-inflammatory treatment a week prior to his arrival at our department. The patient had no past medical history of testicular issues.\nPhysical examination revealed a lump, which testicular ultrasound confirmed as an 18 mm × 12 mm × 25 mm heterogeneous hypoechogenic mass localized to the upper pole of the right testis (Fig. ). A computed tomography (CT) scan showed no evidence of abdominopelvic or thoracic metastases. The blood serum tumor marker levels were as follows: human chorionic gonadotropin (HCG) < 1.20 U/ml (normal is < 5.01 U/ml); α-fetoprotein (AFP) = 3.4 ng/ml (normal is < 7 ng/ml); and lactate dehydrogenase (LDH) = 599 IU/l (normal is 313–618 IU/l).\nA right inguinal radical orchiectomy was performed in September of 2009. Histological examination revealed a pure seminoma of 4 cm × 2.5 cm, without lymphatic, vascular, or tunica albuginea infiltration. The tumor node metastasis (TNM) classification was pT1pNxpMx according to the Union for International Cancer Control (UICC) staging system, seventh edition. Two weeks after the surgery, this case was discussed during a multidisciplinary uro-oncology meeting. From October 21 to November 10 of 2009, the patient underwent adjuvant radiotherapy with doses of 25.2 Gy delivered to the paraaortic lymph nodes in 14 fractions.\nThe patient was considered to be disease-free and received follow-up in accordance with our standard protocol, which includes chest and abdominal CT, physical examination, and tumor marker assessment every 4 months for the first 2 years, and testicular ultrasound of the contralateral side once each year. A total-body CT scan at 1 year after radical surgical treatment showed a 16-mm lymph node under the patient’s left collarbone (Fig. ). The lesion was confirmed by positron emission tomography (PET) scan, and surgical node excision was performed. Histological examination revealed a typical seminoma (Fig. ). Chemotherapy was initiated with a bleomycin, etoposide, and cisplatin (BEP) protocol administered every 21 days for 2 cycles from October to December of 2010.\nFour years later, a follow-up ultrasound of the left testis revealed a 15 mm × 6 mm node with microcalcifications (Fig. ). Blood serum tumor markers were normal, and a CT scan showed no evidence of abdominopelvic or thoracic metastasis. The possibility of radical or partial orchiectomy was discussed with the patient. In March of 2014, the patient underwent left inguinal testicular exploration of the lesion with ultrasound image guidance and excisional biopsy. Analysis of frozen biopsy sections revealed a seminomatous tumor with an intense chronic granulomatous inflammatory lesion. Due to the diffuse nature of the tumor, radical left orchiectomy was performed. The final pathological diagnosis was a pure seminoma that presented as isolated and scattered neoplastic cells within an inflammatory and granulomatous reaction and multifocal intratubular germ cell neoplasia (IGGNU).\nThe patient remained under surveillance and received androgen replacement therapy with long-acting testosterone undecanoate every 12 weeks (Nebido®). A bilateral testicular prosthesis was proposed but was refused. Sperm cryopreservation was not performed because the patient had children and did not desire any additional offspring. Follow-up was performed following the standard protocol. At 2 years after left radical orchiectomy, the patient remained disease free. At the most recent visit, the patient reported maintenance of libido, no adverse effects from the androgen replacement therapy, and comfortable sexual activity and quality of life.\nReported TGCT incidence rates from multiple countries between 1991 and 2011 show geographical variations, with the highest rates observed in Denmark. Over recent decades, TGCT prevalence has gradually increased in most populations of European origin and in the USA [, ]. Some studies suggest an increased incidence of bilateral disease in the post-chemotherapy and radiotherapy era [, ]. A retrospective review shows a threefold higher incidence of bilateral testicular cancers in the post-chemotherapy era compared to the pre-chemotherapy era []. The apparent increase in the number of metachronous tumors may reflect the increased life expectancy of the general population as well as the prolonged survival associated with higher cure rates for initial tumors.\nA systematic literature review—including 50,376 men with TGCT between 1991 and 2011 from many countries—reported a BTGCT prevalence of 1.82 % []. Among those with BTGCT, 69.2 % had metachronous tumors and 30.8 % had synchronous tumors. Several studies indicate that metachronous testicular tumors seem to be more frequent than synchronous ones [, ]. Bilateral metachronous TGCT was first described in a case report in 1942. Metachronous testicular cancer is diagnosed when at least 6 months elapse between the appearance of the first tumor and the second tumor and when there is an ultrasound-documented absence of a contralateral mass at diagnosis of the first tumor.\nAmong patients with metachronous tumors, the mean age at diagnosis of the first tumor is 28 years old and the mean age at diagnosis of the second tumor is 35 years old []. Our present patient was 36 years old when the first tumor was diagnosed and 40 years old when the second tumor was diagnosed. In 70 % of cases, the second testicular malignancy arises within 5 years after the first TGCT []. Seminoma is the most common histological type of bilateral testicular cancer, comprising approximately 68 % of such cases [], as well as the most common histological type of metachronous tumor []. When the second tumor is a seminoma, the median interval between tumors seems to be longer (~10 years) []. There have been 25 reported cases of BTGCT in which the contralateral testicular tumor occurred 20 years or more after the original tumor. Within a series of 25 cases, 4 cases involved a second tumor that occurred at least 30 years after the original testicular tumor, with the longest interval being 40 years [, ]. Contralateral testicular seminoma can occur even at an advanced age, underscoring the importance of life-long follow-up for these patients [, ].\nThe incidence of metachronous germ cell tumors in patients diagnosed with a seminoma is influenced by the patient’s age at the time of the initial diagnosis. Evidence suggests that men who develop a seminoma when they are 30 years of age or younger may be at greater risk of developing a second tumor [, ]. Patients diagnosed with a seminomatous tumor at less than 30 years of age show an increased risk of relapse in the following 15 years compared to men who are over 30 years old at diagnosis (3.1 vs 1.2 %) [].\nAlthough the etiology of BTGCT remains unknown, both genetic and environmental causes are implicated. Presently known epidemiological risk factors for TGCT development include a history of cryptorchidism, Klinefelter syndrome, the presence of a contralateral tumor, infertility, and a history of testis cancer in first-degree relatives []. The elevated risk in family members and associations with inherited genotypes suggest genetic causes [, ]. On the other hand, testicular cancer incidence rates nearly doubled in industrialized countries between 1975 and 2007, suggesting an influence of environmental factors [, ]. Our present case involved no known genetic or environmental risk factors.\nIn our present case, serum markers were negative both at the diagnosis of the first tumor and at tumor recurrence. This is in accordance with the typical presentation of a seminoma. Most second tumors are discovered by the physician via scrotal ultrasonography or by the patient via testicular self-examination. Ultrasonography is a safe and simple screening procedure. One major difficulty regarding the diagnosis of second tumors is that patients may be reluctant to seek help due to fear of castration.\nUltrasound detection of microlithiasis in the contralateral testis is associated with a 30-fold increase in the risk of presenting with a second TGCT, and diagnosis of the first tumor is associated with a 5–8 % risk of testicular intraepithelial neoplasm (TIN) in the contralateral testis. These data highlight the need for long-term surveillance to support early detection of the second TGCT. Within 7 years, 70 % of all TINs will progress to invasive neoplasia [, ], although this risk is somewhat lower among patients who undergo chemotherapy for their first tumor. The 5-year survival rates for men with synchronous and metachronous bilateral testicular tumor are 88 and 95 %, respectively [], suggesting that metachronous tumors have a more favorable survival outcome than synchronous tumors. Synchronous tumors are also associated with more advanced disease than metachronous tumors []. Among patients with bilateral testicular cancer, 70 % present with stage I disease upon diagnosis of the second tumor. This is most likely due to close follow-up and increased patient awareness.\nThe optimal management of patients with intratubular germ cell neoplasms remains controversial. The choices include surveillance and irradiation of the contralateral testis. Since radiotherapy can result in infertility and may affect Leydig cell function [], surveillance is an important part of TGCT follow-up. Clear guidelines are also lacking for treatment of bilateral testicular tumors. Treatment of the second tumor is based on the stage and histology []. The incidence of contralateral testicular cancer is not significantly influenced by the use of radiation therapy for the initial testicular cancer [].\nTreatment for advanced germ cell tumors includes combination chemotherapy with bleomycin, cisplatin, and etoposide, followed by surgical salvage for residual disease. Depending of the patient’s risk profile, 3–4 cycles of chemotherapy are needed []. The patient in our present case received adjuvant radiation therapy after the onset of the first tumor as well as chemotherapy. Additionally, a metastatic lymph node was removed at relapse, which occurred long before the diagnosis of the second tumor. Notably, 5 years elapsed between diagnosis of the first and second tumors. A left radical orchidectomy was performed to eliminate the recurrent tumor due to its diffuse character and the history of metastases. Sparing the testis would have carried a risk of recurrence. Taking into account that he did not desire more children, the patient wanted radical surgery despite the need for hormonal replacement.\nIn the present case, the detection of a contralateral supradiaphragmatic lymph node 3 years prior to the contralateral testis diagnosis indicated metastatic relapse. A review by Cooper et al. reported that approximately 75 % of seminomas present as stage 1, with disease limited to the testis []. All tumors of germ cell origin have the propensity to metastasize via lymphatic pathways, which typically occurs in a sequential pattern, beginning with abdominal lymph node involvement, followed by successive involvement of lymph nodes in the chest and neck []. Wood et al. demonstrated that cervical metastasis is almost exclusively left-sided, with 21 of 23 patients showing disease in supraclavicular or scalene lymph nodes []. Metastatic tumors can also appear in locations outside of the direct line of spread from the primary site []. A review by Vledder reported that 4 % of seminoma patients showed cervical metastasis and that only 5 % of these patients had the neck mass as their initial disease sign []. Seminomas can metastasize to the supraclavicular lymph nodes, and tumors from the right testis can spread to the interaortocaval, precaval, and paraaortic regions, with crossover to left-sided lymph nodes. The left testis drains into the paraaortic and preaortic regions. Interaortocaval lymph node involvement occurs in higher-stage disease. From there, the tumors usually grow along the thoracic duct into the left supraclavicular lymph node and the subclavian vein and then show disseminated spread []. This hypothesis may be applicable to our present patient, since metastasis was not found elsewhere.

An 18-year-old man, without any known risk factor for testicular malignancy, presented to our hospital with a painful right testicular mass with 1 month of evolution. Physical examination detected a small lump, confirmed by testicular ultrasound as a hypoechoic nodule. A CT-scan revealed no metastatic disease. α-fetoprotein (AFP) and lactate dehydrogenase (LDH) were above the normal limit. A right inguinal orchiectomy was performed and the histological exam revealed a mixed germ cell testicular tumor (composed by embrionary carcinoma and mature teratoma). Tumoral markers normalized after surgery, and the tumor was staged as pT1N0M0S0 - IA, according to the American Joint Committee on Cancer guidelines. The patient remained under surveillance. Twelve years later he developed bilateral gynecomastia and a high human chorionic gonadotropin (HCG). CT-scan found a 1cm lateroaortic adenopathy and a PET-scan revealed hyperfixation in the referred adenopathy and left testicle. At that time a scrotal ultrasonography was done, and a voluminous testicle of 5 x 5 x 3 cm with hypoechogenic and hypervascularized areas were found. This was followed by a left radical inguinal orchiectomy with testicle prosthesis introduction. Histological exam revealed a mixed TGCT (with seminoma, embrionary carcinoma and immature teratoma components) and a pathological stage pT2N1M0S1 – IIA. Chemotherapy was started with BEP protocol (bleomycin, etoposide and cisplatin), administered every 21 days for 3 cycles. Retroperitoneal adenopathy disappeared, HCG normalized and a surveillance program was initiated. The patient was disease-free in the 5 months after having finished his treatment.

Write a detailed clinical case vignette based on the following key phrases: testicular cancer, germ cell tumors, orchidectomy

An 18-year-old man, without any known risk factor for testicular malignancy, presented to our hospital with a painful right testicular mass with 1 month of evolution. Physical examination detected a small lump, confirmed by testicular ultrasound as a hypoechoic nodule. A CT-scan revealed no metastatic disease. α-fetoprotein (AFP) and lactate dehydrogenase (LDH) were above the normal limit. A right inguinal orchiectomy was performed and the histological exam revealed a mixed germ cell testicular tumor (composed by embrionary carcinoma and mature teratoma). Tumoral markers normalized after surgery, and the tumor was staged as pT1N0M0S0 - IA, according to the American Joint Committee on Cancer guidelines. The patient remained under surveillance. Twelve years later he developed bilateral gynecomastia and a high human chorionic gonadotropin (HCG). CT-scan found a 1cm lateroaortic adenopathy and a PET-scan revealed hyperfixation in the referred adenopathy and left testicle. At that time a scrotal ultrasonography was done, and a voluminous testicle of 5 x 5 x 3 cm with hypoechogenic and hypervascularized areas were found. This was followed by a left radical inguinal orchiectomy with testicle prosthesis introduction. Histological exam revealed a mixed TGCT (with seminoma, embrionary carcinoma and immature teratoma components) and a pathological stage pT2N1M0S1 – IIA. Chemotherapy was started with BEP protocol (bleomycin, etoposide and cisplatin), administered every 21 days for 3 cycles. Retroperitoneal adenopathy disappeared, HCG normalized and a surveillance program was initiated. The patient was disease-free in the 5 months after having finished his treatment.

A 27 year old single male presented to our patient department with complaint of one month testicular swelling with left side preference. He has no complaints of pain in the testicles and abdomen. No problem in erectile function. He had no problems during puberty. He had no history of smoking and use of opioid in social habits. There is no family history and no evidence of risk factor for testicular cancer such as cryptorchidism or congenital abnormalities in the patient. Physical examination specified the left side testis with twice the normal volume swelling and without tenderness. The size of right side testis has increased slightly. Laboratory workup revealed azoospermia and an elevated a-FP (258.4IU/mL), and b-hcG (3.12mIU/mL) within normal levels. On ultrasound study the testes have 50mm×30mm in right side and 72mm×50mm in left side dimensions. No hydrocele was seen. Images of the right testis demonstrated 38mm×27mm hypoecho mass that accounting for (occupying) three-quarters of the volume of the parenchyma. Images of the left testis demonstrated approximately 70mm×47mm mixed echogenic mass, comprises almost the entire volume of the testis. Epididymis have normal parenchymal dimensions and echoes.\nThe ultrasound study of abdomen and pelvis showed no abnormality. The abdomen CT scan was not indicative of enlargement of the lymph nodes of retroperitoneum. The chest x-ray did not show evidence of metastasis. The patient underwent bilateral radical orchiectomy. Right testicular mass, excisional biopsy, for frozen section and intra-operative diagnosis, consists of a piece of creamy colored soft tissue specimen, with homogenous appearance, measured 45×35×22 mm in the largest diameters. Cryo and permanent sections of right testis mass, confirmed invasive, classic type seminoma that limited to the testis with intratubular and invasion to lympho-vascular tissues (tumor stage: at-least PT2) ().\nIn the left testis, in cut sections, almost all testicular volume replaced by tumoral tissue with heterogeneous appearance, containing solid and cystic, hemorrhagic and necrotic areas, measured 80×50×40 mm. the left side tumor was a malignant GCT with component of invasive, classic type seminoma (50-60%), yolk sac tumor (40-50%) and embryonal carcinoma (about 10%) (). Tumor extended to rete testis, tunica albuginea and tunica vaginalis. Epididymis was not involved. Intratubular and lympho-vascular invasion was present (tumor stage: PT2). Immunocytochemical study with AE1/AE3, CD30 and CD117 markers demonstrated a positive reaction (). The patient was discharged without problems and complications one day after surgery. The elevated a-FP on the postoperative measurement decreased to lower values (6,05mIU/mL). The patient was advised to go to an oncologist and was submitted to one cycle of adjuvant chemotherapy with bleomycin, etoposide, and cisplatin (BEP). As the follow-up physical examination, serum markers, chest X ray, and CT of the abdomen, were checked. Six months after the orchiectomy there was no residual tumor or recurrence, neither local nor systematic. Finally the patient is under a follow-up by an endocrinologist for the long-term management regarding the testosterone replacement therapy and he has been started on topical testrogel for life.

Write a detailed clinical case vignette based on the following key phrases: testicular cancer, germ cell tumors, orchidectomy

We present the case of a 41-year-old male with repeated visits to outside emergency\ndepartments over a 3-month period with a waxing and waning pattern of worsening\ncognitive dysfunction as well as intermittent fevers. He also complained of\ngeneralized weakness and fatigue. His initial diagnosis was viral meningitis. He had\na negative workup for infectious etiologies, including negative CSF cultures,\nnegative Lyme titers, normal ACE level. Previous lumbar puncture was notable for\nelevated white blood cells, elevated protein, and glucose below 50g/dL. CT scan of\nthe abdomen at an outside hospital revealed a right pericaval lymph node measuring\n3.8 x 3.7 cm with central necrosis ().\nExternal genitalia were incompletely visualized on this scan. After transfer to our\ninstitution, the condition continued to worsen and after being admitted, the patient\nwas unable to speak and reported weakness in all four extremities that progressed to\nalteration of awareness, disorientation, and difficulty speaking. Labs at this time\nwere significant for phosphorous less than 2 mg/dL, which is known to precipitate\nseizures and altered mental status, however it was felt that the lower extremity\nshaking was not consistent with a seizure. He was placed on Keppra prior to arrival\nat our hospital. Based on this presentation, a CT of the head was obtained to rule\nout a primary central nervous system etiology. This imaging showed no acute process.\nFurther work up with MRI could not be obtained due to a non-compatible internal\npacemaker. Pacemaker analysis showed no abnormalities. Due to the para-aortic\nlocation of the mass, a 24-hour urine metanephrine was also performed to rule out a\nneuroendocrine tumor.\nAfter the negative initial workup, concern for distant metastasis led to the belief\ncurrent symptomatology was due to secondary to a paraneoplastic process.\nSpecifically, the presence of retroperitoneal lymphadenopathy with necrosis raised\nconcern for testicular origin. Sonographic evaluation of the testicles showed a\nright sided, ill-defined, multi-cystic 2.4 x 2.1 x 2.2cm mass (). Further laboratory evaluation revealed an\nelevated B-hCG of 49.9 mIU/mL, alpha fetoprotein level of 1.67 ng/mL and normal LDH\nlevel. A right radical orchiectomy was performed.\nGross pathology obtained from the right radical orchiectomy showed a 2.1 x 1.8 x 1.6\ncm tan-white, ill defined, soft, multicystic lesion in the medial and inferior pole\nof the testis, without hemorrhage or necrosis. Histologic evaluation revealed mixed\nrespiratory epithelium, gastrointestinal glands, and squamous epithelium with\nkeratinization consistent with a post-pubertal testicular teratoma with associated\ngerm cell neoplasia in situ (Figures , ).\nRepeat CT scan of the abdomen and pelvis showed continuous enlargement of the right\nperi-aortic lymph node, now measuring 5.6 cm in greatest dimension, as well as a new\nleft peri-aortic node measuring 2.2 cm in the largest dimension. After\nmultidisciplinary discussion, given the likelihood of a paraneoplastic syndrome that\nwould likely worsen with up front chemotherapy, the decision was made to proceed\nwith a primary retroperitoneal lymph node dissection. The large aortocaval mass was\nadherent to the inferior vena cava (IVC), but no invasion was noted. Measurement of\nthe extirpated mass was noted to be 7 x 6 x 4.5 cm in size cm in the largest\ndiameter. A complete bilateral template retroperitoneal lymph node dissection was\nperformed extending inferiorly from the renal veins to the bifurcation of the common\niliac arteries and to the ureters bilaterally.\nOn gross pathology, the aortocaval mass was well encapsulated with hemorrhagic and\nnecrotic cut surfaces. Microscopic evaluation displayed large anaplastic cells with\nepithelioid features, nuclear pleomorphism and frequent mitoses. Giant cells with\ngranular cytoplasm were also present. One node measuring 1.5 x 1.0 x 1.0 cm was\npositive for malignancy. Immunostaining of the mass and positive lymph node\ndisplayed positive staining for Pan-Keratin and OCT4, and negative staining for\nCD30, S-100, Desmin, pan-melanoma, and SOX2. The microscopic evaluation and\nimmunostaining combination led to the diagnosis of poorly differentiated embryonal\ncarcinoma ().\nThe patient’s neurological symptoms were managed with methylprednisolone, and Keppra\nwas continued for seizure prophylaxis. Following resection of the aortocaval mass,\nthe patient recovered well, and the diplopia and paralysis resolved. He was managed\npost-operatively with Bleomycin-Etoposide-Cisplatin (BEP) therapy. At the time of\npublication, he had received three cycles of BEP and has shown no evidence of tumor\nrecurrence.

A 35-year-old man with no known risk factors for testicular malignancy presented at the urology department with a right testicular mass causing painful swelling. He had been experiencing discomfort and heaviness for 10 days. His general practitioner had started antibiotic and anti-inflammatory treatment a week prior to his arrival at our department. The patient had no past medical history of testicular issues.\nPhysical examination revealed a lump, which testicular ultrasound confirmed as an 18 mm × 12 mm × 25 mm heterogeneous hypoechogenic mass localized to the upper pole of the right testis (Fig. ). A computed tomography (CT) scan showed no evidence of abdominopelvic or thoracic metastases. The blood serum tumor marker levels were as follows: human chorionic gonadotropin (HCG) < 1.20 U/ml (normal is < 5.01 U/ml); α-fetoprotein (AFP) = 3.4 ng/ml (normal is < 7 ng/ml); and lactate dehydrogenase (LDH) = 599 IU/l (normal is 313–618 IU/l).\nA right inguinal radical orchiectomy was performed in September of 2009. Histological examination revealed a pure seminoma of 4 cm × 2.5 cm, without lymphatic, vascular, or tunica albuginea infiltration. The tumor node metastasis (TNM) classification was pT1pNxpMx according to the Union for International Cancer Control (UICC) staging system, seventh edition. Two weeks after the surgery, this case was discussed during a multidisciplinary uro-oncology meeting. From October 21 to November 10 of 2009, the patient underwent adjuvant radiotherapy with doses of 25.2 Gy delivered to the paraaortic lymph nodes in 14 fractions.\nThe patient was considered to be disease-free and received follow-up in accordance with our standard protocol, which includes chest and abdominal CT, physical examination, and tumor marker assessment every 4 months for the first 2 years, and testicular ultrasound of the contralateral side once each year. A total-body CT scan at 1 year after radical surgical treatment showed a 16-mm lymph node under the patient’s left collarbone (Fig. ). The lesion was confirmed by positron emission tomography (PET) scan, and surgical node excision was performed. Histological examination revealed a typical seminoma (Fig. ). Chemotherapy was initiated with a bleomycin, etoposide, and cisplatin (BEP) protocol administered every 21 days for 2 cycles from October to December of 2010.\nFour years later, a follow-up ultrasound of the left testis revealed a 15 mm × 6 mm node with microcalcifications (Fig. ). Blood serum tumor markers were normal, and a CT scan showed no evidence of abdominopelvic or thoracic metastasis. The possibility of radical or partial orchiectomy was discussed with the patient. In March of 2014, the patient underwent left inguinal testicular exploration of the lesion with ultrasound image guidance and excisional biopsy. Analysis of frozen biopsy sections revealed a seminomatous tumor with an intense chronic granulomatous inflammatory lesion. Due to the diffuse nature of the tumor, radical left orchiectomy was performed. The final pathological diagnosis was a pure seminoma that presented as isolated and scattered neoplastic cells within an inflammatory and granulomatous reaction and multifocal intratubular germ cell neoplasia (IGGNU).\nThe patient remained under surveillance and received androgen replacement therapy with long-acting testosterone undecanoate every 12 weeks (Nebido®). A bilateral testicular prosthesis was proposed but was refused. Sperm cryopreservation was not performed because the patient had children and did not desire any additional offspring. Follow-up was performed following the standard protocol. At 2 years after left radical orchiectomy, the patient remained disease free. At the most recent visit, the patient reported maintenance of libido, no adverse effects from the androgen replacement therapy, and comfortable sexual activity and quality of life.\nReported TGCT incidence rates from multiple countries between 1991 and 2011 show geographical variations, with the highest rates observed in Denmark. Over recent decades, TGCT prevalence has gradually increased in most populations of European origin and in the USA [, ]. Some studies suggest an increased incidence of bilateral disease in the post-chemotherapy and radiotherapy era [, ]. A retrospective review shows a threefold higher incidence of bilateral testicular cancers in the post-chemotherapy era compared to the pre-chemotherapy era []. The apparent increase in the number of metachronous tumors may reflect the increased life expectancy of the general population as well as the prolonged survival associated with higher cure rates for initial tumors.\nA systematic literature review—including 50,376 men with TGCT between 1991 and 2011 from many countries—reported a BTGCT prevalence of 1.82 % []. Among those with BTGCT, 69.2 % had metachronous tumors and 30.8 % had synchronous tumors. Several studies indicate that metachronous testicular tumors seem to be more frequent than synchronous ones [, ]. Bilateral metachronous TGCT was first described in a case report in 1942. Metachronous testicular cancer is diagnosed when at least 6 months elapse between the appearance of the first tumor and the second tumor and when there is an ultrasound-documented absence of a contralateral mass at diagnosis of the first tumor.\nAmong patients with metachronous tumors, the mean age at diagnosis of the first tumor is 28 years old and the mean age at diagnosis of the second tumor is 35 years old []. Our present patient was 36 years old when the first tumor was diagnosed and 40 years old when the second tumor was diagnosed. In 70 % of cases, the second testicular malignancy arises within 5 years after the first TGCT []. Seminoma is the most common histological type of bilateral testicular cancer, comprising approximately 68 % of such cases [], as well as the most common histological type of metachronous tumor []. When the second tumor is a seminoma, the median interval between tumors seems to be longer (~10 years) []. There have been 25 reported cases of BTGCT in which the contralateral testicular tumor occurred 20 years or more after the original tumor. Within a series of 25 cases, 4 cases involved a second tumor that occurred at least 30 years after the original testicular tumor, with the longest interval being 40 years [, ]. Contralateral testicular seminoma can occur even at an advanced age, underscoring the importance of life-long follow-up for these patients [, ].\nThe incidence of metachronous germ cell tumors in patients diagnosed with a seminoma is influenced by the patient’s age at the time of the initial diagnosis. Evidence suggests that men who develop a seminoma when they are 30 years of age or younger may be at greater risk of developing a second tumor [, ]. Patients diagnosed with a seminomatous tumor at less than 30 years of age show an increased risk of relapse in the following 15 years compared to men who are over 30 years old at diagnosis (3.1 vs 1.2 %) [].\nAlthough the etiology of BTGCT remains unknown, both genetic and environmental causes are implicated. Presently known epidemiological risk factors for TGCT development include a history of cryptorchidism, Klinefelter syndrome, the presence of a contralateral tumor, infertility, and a history of testis cancer in first-degree relatives []. The elevated risk in family members and associations with inherited genotypes suggest genetic causes [, ]. On the other hand, testicular cancer incidence rates nearly doubled in industrialized countries between 1975 and 2007, suggesting an influence of environmental factors [, ]. Our present case involved no known genetic or environmental risk factors.\nIn our present case, serum markers were negative both at the diagnosis of the first tumor and at tumor recurrence. This is in accordance with the typical presentation of a seminoma. Most second tumors are discovered by the physician via scrotal ultrasonography or by the patient via testicular self-examination. Ultrasonography is a safe and simple screening procedure. One major difficulty regarding the diagnosis of second tumors is that patients may be reluctant to seek help due to fear of castration.\nUltrasound detection of microlithiasis in the contralateral testis is associated with a 30-fold increase in the risk of presenting with a second TGCT, and diagnosis of the first tumor is associated with a 5–8 % risk of testicular intraepithelial neoplasm (TIN) in the contralateral testis. These data highlight the need for long-term surveillance to support early detection of the second TGCT. Within 7 years, 70 % of all TINs will progress to invasive neoplasia [, ], although this risk is somewhat lower among patients who undergo chemotherapy for their first tumor. The 5-year survival rates for men with synchronous and metachronous bilateral testicular tumor are 88 and 95 %, respectively [], suggesting that metachronous tumors have a more favorable survival outcome than synchronous tumors. Synchronous tumors are also associated with more advanced disease than metachronous tumors []. Among patients with bilateral testicular cancer, 70 % present with stage I disease upon diagnosis of the second tumor. This is most likely due to close follow-up and increased patient awareness.\nThe optimal management of patients with intratubular germ cell neoplasms remains controversial. The choices include surveillance and irradiation of the contralateral testis. Since radiotherapy can result in infertility and may affect Leydig cell function [], surveillance is an important part of TGCT follow-up. Clear guidelines are also lacking for treatment of bilateral testicular tumors. Treatment of the second tumor is based on the stage and histology []. The incidence of contralateral testicular cancer is not significantly influenced by the use of radiation therapy for the initial testicular cancer [].\nTreatment for advanced germ cell tumors includes combination chemotherapy with bleomycin, cisplatin, and etoposide, followed by surgical salvage for residual disease. Depending of the patient’s risk profile, 3–4 cycles of chemotherapy are needed []. The patient in our present case received adjuvant radiation therapy after the onset of the first tumor as well as chemotherapy. Additionally, a metastatic lymph node was removed at relapse, which occurred long before the diagnosis of the second tumor. Notably, 5 years elapsed between diagnosis of the first and second tumors. A left radical orchidectomy was performed to eliminate the recurrent tumor due to its diffuse character and the history of metastases. Sparing the testis would have carried a risk of recurrence. Taking into account that he did not desire more children, the patient wanted radical surgery despite the need for hormonal replacement.\nIn the present case, the detection of a contralateral supradiaphragmatic lymph node 3 years prior to the contralateral testis diagnosis indicated metastatic relapse. A review by Cooper et al. reported that approximately 75 % of seminomas present as stage 1, with disease limited to the testis []. All tumors of germ cell origin have the propensity to metastasize via lymphatic pathways, which typically occurs in a sequential pattern, beginning with abdominal lymph node involvement, followed by successive involvement of lymph nodes in the chest and neck []. Wood et al. demonstrated that cervical metastasis is almost exclusively left-sided, with 21 of 23 patients showing disease in supraclavicular or scalene lymph nodes []. Metastatic tumors can also appear in locations outside of the direct line of spread from the primary site []. A review by Vledder reported that 4 % of seminoma patients showed cervical metastasis and that only 5 % of these patients had the neck mass as their initial disease sign []. Seminomas can metastasize to the supraclavicular lymph nodes, and tumors from the right testis can spread to the interaortocaval, precaval, and paraaortic regions, with crossover to left-sided lymph nodes. The left testis drains into the paraaortic and preaortic regions. Interaortocaval lymph node involvement occurs in higher-stage disease. From there, the tumors usually grow along the thoracic duct into the left supraclavicular lymph node and the subclavian vein and then show disseminated spread []. This hypothesis may be applicable to our present patient, since metastasis was not found elsewhere.

Write a detailed clinical case vignette based on the following key phrases: testicular cancer, germ cell tumors, orchidectomy

We present the case of a 41-year-old male with repeated visits to outside emergency\ndepartments over a 3-month period with a waxing and waning pattern of worsening\ncognitive dysfunction as well as intermittent fevers. He also complained of\ngeneralized weakness and fatigue. His initial diagnosis was viral meningitis. He had\na negative workup for infectious etiologies, including negative CSF cultures,\nnegative Lyme titers, normal ACE level. Previous lumbar puncture was notable for\nelevated white blood cells, elevated protein, and glucose below 50g/dL. CT scan of\nthe abdomen at an outside hospital revealed a right pericaval lymph node measuring\n3.8 x 3.7 cm with central necrosis ().\nExternal genitalia were incompletely visualized on this scan. After transfer to our\ninstitution, the condition continued to worsen and after being admitted, the patient\nwas unable to speak and reported weakness in all four extremities that progressed to\nalteration of awareness, disorientation, and difficulty speaking. Labs at this time\nwere significant for phosphorous less than 2 mg/dL, which is known to precipitate\nseizures and altered mental status, however it was felt that the lower extremity\nshaking was not consistent with a seizure. He was placed on Keppra prior to arrival\nat our hospital. Based on this presentation, a CT of the head was obtained to rule\nout a primary central nervous system etiology. This imaging showed no acute process.\nFurther work up with MRI could not be obtained due to a non-compatible internal\npacemaker. Pacemaker analysis showed no abnormalities. Due to the para-aortic\nlocation of the mass, a 24-hour urine metanephrine was also performed to rule out a\nneuroendocrine tumor.\nAfter the negative initial workup, concern for distant metastasis led to the belief\ncurrent symptomatology was due to secondary to a paraneoplastic process.\nSpecifically, the presence of retroperitoneal lymphadenopathy with necrosis raised\nconcern for testicular origin. Sonographic evaluation of the testicles showed a\nright sided, ill-defined, multi-cystic 2.4 x 2.1 x 2.2cm mass (). Further laboratory evaluation revealed an\nelevated B-hCG of 49.9 mIU/mL, alpha fetoprotein level of 1.67 ng/mL and normal LDH\nlevel. A right radical orchiectomy was performed.\nGross pathology obtained from the right radical orchiectomy showed a 2.1 x 1.8 x 1.6\ncm tan-white, ill defined, soft, multicystic lesion in the medial and inferior pole\nof the testis, without hemorrhage or necrosis. Histologic evaluation revealed mixed\nrespiratory epithelium, gastrointestinal glands, and squamous epithelium with\nkeratinization consistent with a post-pubertal testicular teratoma with associated\ngerm cell neoplasia in situ (Figures , ).\nRepeat CT scan of the abdomen and pelvis showed continuous enlargement of the right\nperi-aortic lymph node, now measuring 5.6 cm in greatest dimension, as well as a new\nleft peri-aortic node measuring 2.2 cm in the largest dimension. After\nmultidisciplinary discussion, given the likelihood of a paraneoplastic syndrome that\nwould likely worsen with up front chemotherapy, the decision was made to proceed\nwith a primary retroperitoneal lymph node dissection. The large aortocaval mass was\nadherent to the inferior vena cava (IVC), but no invasion was noted. Measurement of\nthe extirpated mass was noted to be 7 x 6 x 4.5 cm in size cm in the largest\ndiameter. A complete bilateral template retroperitoneal lymph node dissection was\nperformed extending inferiorly from the renal veins to the bifurcation of the common\niliac arteries and to the ureters bilaterally.\nOn gross pathology, the aortocaval mass was well encapsulated with hemorrhagic and\nnecrotic cut surfaces. Microscopic evaluation displayed large anaplastic cells with\nepithelioid features, nuclear pleomorphism and frequent mitoses. Giant cells with\ngranular cytoplasm were also present. One node measuring 1.5 x 1.0 x 1.0 cm was\npositive for malignancy. Immunostaining of the mass and positive lymph node\ndisplayed positive staining for Pan-Keratin and OCT4, and negative staining for\nCD30, S-100, Desmin, pan-melanoma, and SOX2. The microscopic evaluation and\nimmunostaining combination led to the diagnosis of poorly differentiated embryonal\ncarcinoma ().\nThe patient’s neurological symptoms were managed with methylprednisolone, and Keppra\nwas continued for seizure prophylaxis. Following resection of the aortocaval mass,\nthe patient recovered well, and the diplopia and paralysis resolved. He was managed\npost-operatively with Bleomycin-Etoposide-Cisplatin (BEP) therapy. At the time of\npublication, he had received three cycles of BEP and has shown no evidence of tumor\nrecurrence.

A 27 year old single male presented to our patient department with complaint of one month testicular swelling with left side preference. He has no complaints of pain in the testicles and abdomen. No problem in erectile function. He had no problems during puberty. He had no history of smoking and use of opioid in social habits. There is no family history and no evidence of risk factor for testicular cancer such as cryptorchidism or congenital abnormalities in the patient. Physical examination specified the left side testis with twice the normal volume swelling and without tenderness. The size of right side testis has increased slightly. Laboratory workup revealed azoospermia and an elevated a-FP (258.4IU/mL), and b-hcG (3.12mIU/mL) within normal levels. On ultrasound study the testes have 50mm×30mm in right side and 72mm×50mm in left side dimensions. No hydrocele was seen. Images of the right testis demonstrated 38mm×27mm hypoecho mass that accounting for (occupying) three-quarters of the volume of the parenchyma. Images of the left testis demonstrated approximately 70mm×47mm mixed echogenic mass, comprises almost the entire volume of the testis. Epididymis have normal parenchymal dimensions and echoes.\nThe ultrasound study of abdomen and pelvis showed no abnormality. The abdomen CT scan was not indicative of enlargement of the lymph nodes of retroperitoneum. The chest x-ray did not show evidence of metastasis. The patient underwent bilateral radical orchiectomy. Right testicular mass, excisional biopsy, for frozen section and intra-operative diagnosis, consists of a piece of creamy colored soft tissue specimen, with homogenous appearance, measured 45×35×22 mm in the largest diameters. Cryo and permanent sections of right testis mass, confirmed invasive, classic type seminoma that limited to the testis with intratubular and invasion to lympho-vascular tissues (tumor stage: at-least PT2) ().\nIn the left testis, in cut sections, almost all testicular volume replaced by tumoral tissue with heterogeneous appearance, containing solid and cystic, hemorrhagic and necrotic areas, measured 80×50×40 mm. the left side tumor was a malignant GCT with component of invasive, classic type seminoma (50-60%), yolk sac tumor (40-50%) and embryonal carcinoma (about 10%) (). Tumor extended to rete testis, tunica albuginea and tunica vaginalis. Epididymis was not involved. Intratubular and lympho-vascular invasion was present (tumor stage: PT2). Immunocytochemical study with AE1/AE3, CD30 and CD117 markers demonstrated a positive reaction (). The patient was discharged without problems and complications one day after surgery. The elevated a-FP on the postoperative measurement decreased to lower values (6,05mIU/mL). The patient was advised to go to an oncologist and was submitted to one cycle of adjuvant chemotherapy with bleomycin, etoposide, and cisplatin (BEP). As the follow-up physical examination, serum markers, chest X ray, and CT of the abdomen, were checked. Six months after the orchiectomy there was no residual tumor or recurrence, neither local nor systematic. Finally the patient is under a follow-up by an endocrinologist for the long-term management regarding the testosterone replacement therapy and he has been started on topical testrogel for life.

Write a detailed clinical case vignette based on the following key phrases: testicular cancer, germ cell tumors, orchidectomy

A 35-year-old man with no known risk factors for testicular malignancy presented at the urology department with a right testicular mass causing painful swelling. He had been experiencing discomfort and heaviness for 10 days. His general practitioner had started antibiotic and anti-inflammatory treatment a week prior to his arrival at our department. The patient had no past medical history of testicular issues.\nPhysical examination revealed a lump, which testicular ultrasound confirmed as an 18 mm × 12 mm × 25 mm heterogeneous hypoechogenic mass localized to the upper pole of the right testis (Fig. ). A computed tomography (CT) scan showed no evidence of abdominopelvic or thoracic metastases. The blood serum tumor marker levels were as follows: human chorionic gonadotropin (HCG) < 1.20 U/ml (normal is < 5.01 U/ml); α-fetoprotein (AFP) = 3.4 ng/ml (normal is < 7 ng/ml); and lactate dehydrogenase (LDH) = 599 IU/l (normal is 313–618 IU/l).\nA right inguinal radical orchiectomy was performed in September of 2009. Histological examination revealed a pure seminoma of 4 cm × 2.5 cm, without lymphatic, vascular, or tunica albuginea infiltration. The tumor node metastasis (TNM) classification was pT1pNxpMx according to the Union for International Cancer Control (UICC) staging system, seventh edition. Two weeks after the surgery, this case was discussed during a multidisciplinary uro-oncology meeting. From October 21 to November 10 of 2009, the patient underwent adjuvant radiotherapy with doses of 25.2 Gy delivered to the paraaortic lymph nodes in 14 fractions.\nThe patient was considered to be disease-free and received follow-up in accordance with our standard protocol, which includes chest and abdominal CT, physical examination, and tumor marker assessment every 4 months for the first 2 years, and testicular ultrasound of the contralateral side once each year. A total-body CT scan at 1 year after radical surgical treatment showed a 16-mm lymph node under the patient’s left collarbone (Fig. ). The lesion was confirmed by positron emission tomography (PET) scan, and surgical node excision was performed. Histological examination revealed a typical seminoma (Fig. ). Chemotherapy was initiated with a bleomycin, etoposide, and cisplatin (BEP) protocol administered every 21 days for 2 cycles from October to December of 2010.\nFour years later, a follow-up ultrasound of the left testis revealed a 15 mm × 6 mm node with microcalcifications (Fig. ). Blood serum tumor markers were normal, and a CT scan showed no evidence of abdominopelvic or thoracic metastasis. The possibility of radical or partial orchiectomy was discussed with the patient. In March of 2014, the patient underwent left inguinal testicular exploration of the lesion with ultrasound image guidance and excisional biopsy. Analysis of frozen biopsy sections revealed a seminomatous tumor with an intense chronic granulomatous inflammatory lesion. Due to the diffuse nature of the tumor, radical left orchiectomy was performed. The final pathological diagnosis was a pure seminoma that presented as isolated and scattered neoplastic cells within an inflammatory and granulomatous reaction and multifocal intratubular germ cell neoplasia (IGGNU).\nThe patient remained under surveillance and received androgen replacement therapy with long-acting testosterone undecanoate every 12 weeks (Nebido®). A bilateral testicular prosthesis was proposed but was refused. Sperm cryopreservation was not performed because the patient had children and did not desire any additional offspring. Follow-up was performed following the standard protocol. At 2 years after left radical orchiectomy, the patient remained disease free. At the most recent visit, the patient reported maintenance of libido, no adverse effects from the androgen replacement therapy, and comfortable sexual activity and quality of life.\nReported TGCT incidence rates from multiple countries between 1991 and 2011 show geographical variations, with the highest rates observed in Denmark. Over recent decades, TGCT prevalence has gradually increased in most populations of European origin and in the USA [, ]. Some studies suggest an increased incidence of bilateral disease in the post-chemotherapy and radiotherapy era [, ]. A retrospective review shows a threefold higher incidence of bilateral testicular cancers in the post-chemotherapy era compared to the pre-chemotherapy era []. The apparent increase in the number of metachronous tumors may reflect the increased life expectancy of the general population as well as the prolonged survival associated with higher cure rates for initial tumors.\nA systematic literature review—including 50,376 men with TGCT between 1991 and 2011 from many countries—reported a BTGCT prevalence of 1.82 % []. Among those with BTGCT, 69.2 % had metachronous tumors and 30.8 % had synchronous tumors. Several studies indicate that metachronous testicular tumors seem to be more frequent than synchronous ones [, ]. Bilateral metachronous TGCT was first described in a case report in 1942. Metachronous testicular cancer is diagnosed when at least 6 months elapse between the appearance of the first tumor and the second tumor and when there is an ultrasound-documented absence of a contralateral mass at diagnosis of the first tumor.\nAmong patients with metachronous tumors, the mean age at diagnosis of the first tumor is 28 years old and the mean age at diagnosis of the second tumor is 35 years old []. Our present patient was 36 years old when the first tumor was diagnosed and 40 years old when the second tumor was diagnosed. In 70 % of cases, the second testicular malignancy arises within 5 years after the first TGCT []. Seminoma is the most common histological type of bilateral testicular cancer, comprising approximately 68 % of such cases [], as well as the most common histological type of metachronous tumor []. When the second tumor is a seminoma, the median interval between tumors seems to be longer (~10 years) []. There have been 25 reported cases of BTGCT in which the contralateral testicular tumor occurred 20 years or more after the original tumor. Within a series of 25 cases, 4 cases involved a second tumor that occurred at least 30 years after the original testicular tumor, with the longest interval being 40 years [, ]. Contralateral testicular seminoma can occur even at an advanced age, underscoring the importance of life-long follow-up for these patients [, ].\nThe incidence of metachronous germ cell tumors in patients diagnosed with a seminoma is influenced by the patient’s age at the time of the initial diagnosis. Evidence suggests that men who develop a seminoma when they are 30 years of age or younger may be at greater risk of developing a second tumor [, ]. Patients diagnosed with a seminomatous tumor at less than 30 years of age show an increased risk of relapse in the following 15 years compared to men who are over 30 years old at diagnosis (3.1 vs 1.2 %) [].\nAlthough the etiology of BTGCT remains unknown, both genetic and environmental causes are implicated. Presently known epidemiological risk factors for TGCT development include a history of cryptorchidism, Klinefelter syndrome, the presence of a contralateral tumor, infertility, and a history of testis cancer in first-degree relatives []. The elevated risk in family members and associations with inherited genotypes suggest genetic causes [, ]. On the other hand, testicular cancer incidence rates nearly doubled in industrialized countries between 1975 and 2007, suggesting an influence of environmental factors [, ]. Our present case involved no known genetic or environmental risk factors.\nIn our present case, serum markers were negative both at the diagnosis of the first tumor and at tumor recurrence. This is in accordance with the typical presentation of a seminoma. Most second tumors are discovered by the physician via scrotal ultrasonography or by the patient via testicular self-examination. Ultrasonography is a safe and simple screening procedure. One major difficulty regarding the diagnosis of second tumors is that patients may be reluctant to seek help due to fear of castration.\nUltrasound detection of microlithiasis in the contralateral testis is associated with a 30-fold increase in the risk of presenting with a second TGCT, and diagnosis of the first tumor is associated with a 5–8 % risk of testicular intraepithelial neoplasm (TIN) in the contralateral testis. These data highlight the need for long-term surveillance to support early detection of the second TGCT. Within 7 years, 70 % of all TINs will progress to invasive neoplasia [, ], although this risk is somewhat lower among patients who undergo chemotherapy for their first tumor. The 5-year survival rates for men with synchronous and metachronous bilateral testicular tumor are 88 and 95 %, respectively [], suggesting that metachronous tumors have a more favorable survival outcome than synchronous tumors. Synchronous tumors are also associated with more advanced disease than metachronous tumors []. Among patients with bilateral testicular cancer, 70 % present with stage I disease upon diagnosis of the second tumor. This is most likely due to close follow-up and increased patient awareness.\nThe optimal management of patients with intratubular germ cell neoplasms remains controversial. The choices include surveillance and irradiation of the contralateral testis. Since radiotherapy can result in infertility and may affect Leydig cell function [], surveillance is an important part of TGCT follow-up. Clear guidelines are also lacking for treatment of bilateral testicular tumors. Treatment of the second tumor is based on the stage and histology []. The incidence of contralateral testicular cancer is not significantly influenced by the use of radiation therapy for the initial testicular cancer [].\nTreatment for advanced germ cell tumors includes combination chemotherapy with bleomycin, cisplatin, and etoposide, followed by surgical salvage for residual disease. Depending of the patient’s risk profile, 3–4 cycles of chemotherapy are needed []. The patient in our present case received adjuvant radiation therapy after the onset of the first tumor as well as chemotherapy. Additionally, a metastatic lymph node was removed at relapse, which occurred long before the diagnosis of the second tumor. Notably, 5 years elapsed between diagnosis of the first and second tumors. A left radical orchidectomy was performed to eliminate the recurrent tumor due to its diffuse character and the history of metastases. Sparing the testis would have carried a risk of recurrence. Taking into account that he did not desire more children, the patient wanted radical surgery despite the need for hormonal replacement.\nIn the present case, the detection of a contralateral supradiaphragmatic lymph node 3 years prior to the contralateral testis diagnosis indicated metastatic relapse. A review by Cooper et al. reported that approximately 75 % of seminomas present as stage 1, with disease limited to the testis []. All tumors of germ cell origin have the propensity to metastasize via lymphatic pathways, which typically occurs in a sequential pattern, beginning with abdominal lymph node involvement, followed by successive involvement of lymph nodes in the chest and neck []. Wood et al. demonstrated that cervical metastasis is almost exclusively left-sided, with 21 of 23 patients showing disease in supraclavicular or scalene lymph nodes []. Metastatic tumors can also appear in locations outside of the direct line of spread from the primary site []. A review by Vledder reported that 4 % of seminoma patients showed cervical metastasis and that only 5 % of these patients had the neck mass as their initial disease sign []. Seminomas can metastasize to the supraclavicular lymph nodes, and tumors from the right testis can spread to the interaortocaval, precaval, and paraaortic regions, with crossover to left-sided lymph nodes. The left testis drains into the paraaortic and preaortic regions. Interaortocaval lymph node involvement occurs in higher-stage disease. From there, the tumors usually grow along the thoracic duct into the left supraclavicular lymph node and the subclavian vein and then show disseminated spread []. This hypothesis may be applicable to our present patient, since metastasis was not found elsewhere.

A 27 year old single male presented to our patient department with complaint of one month testicular swelling with left side preference. He has no complaints of pain in the testicles and abdomen. No problem in erectile function. He had no problems during puberty. He had no history of smoking and use of opioid in social habits. There is no family history and no evidence of risk factor for testicular cancer such as cryptorchidism or congenital abnormalities in the patient. Physical examination specified the left side testis with twice the normal volume swelling and without tenderness. The size of right side testis has increased slightly. Laboratory workup revealed azoospermia and an elevated a-FP (258.4IU/mL), and b-hcG (3.12mIU/mL) within normal levels. On ultrasound study the testes have 50mm×30mm in right side and 72mm×50mm in left side dimensions. No hydrocele was seen. Images of the right testis demonstrated 38mm×27mm hypoecho mass that accounting for (occupying) three-quarters of the volume of the parenchyma. Images of the left testis demonstrated approximately 70mm×47mm mixed echogenic mass, comprises almost the entire volume of the testis. Epididymis have normal parenchymal dimensions and echoes.\nThe ultrasound study of abdomen and pelvis showed no abnormality. The abdomen CT scan was not indicative of enlargement of the lymph nodes of retroperitoneum. The chest x-ray did not show evidence of metastasis. The patient underwent bilateral radical orchiectomy. Right testicular mass, excisional biopsy, for frozen section and intra-operative diagnosis, consists of a piece of creamy colored soft tissue specimen, with homogenous appearance, measured 45×35×22 mm in the largest diameters. Cryo and permanent sections of right testis mass, confirmed invasive, classic type seminoma that limited to the testis with intratubular and invasion to lympho-vascular tissues (tumor stage: at-least PT2) ().\nIn the left testis, in cut sections, almost all testicular volume replaced by tumoral tissue with heterogeneous appearance, containing solid and cystic, hemorrhagic and necrotic areas, measured 80×50×40 mm. the left side tumor was a malignant GCT with component of invasive, classic type seminoma (50-60%), yolk sac tumor (40-50%) and embryonal carcinoma (about 10%) (). Tumor extended to rete testis, tunica albuginea and tunica vaginalis. Epididymis was not involved. Intratubular and lympho-vascular invasion was present (tumor stage: PT2). Immunocytochemical study with AE1/AE3, CD30 and CD117 markers demonstrated a positive reaction (). The patient was discharged without problems and complications one day after surgery. The elevated a-FP on the postoperative measurement decreased to lower values (6,05mIU/mL). The patient was advised to go to an oncologist and was submitted to one cycle of adjuvant chemotherapy with bleomycin, etoposide, and cisplatin (BEP). As the follow-up physical examination, serum markers, chest X ray, and CT of the abdomen, were checked. Six months after the orchiectomy there was no residual tumor or recurrence, neither local nor systematic. Finally the patient is under a follow-up by an endocrinologist for the long-term management regarding the testosterone replacement therapy and he has been started on topical testrogel for life.

Write a detailed clinical case vignette based on the following key phrases: testicular cancer, germ cell tumors, orchidectomy

A 32-year-old male visited our clinic with a major complaint of severe pain in the right knee that started to occur when he managed to stop running over the second base that he had run toward while playing baseball. The right leg that was planted on the second base at the time of injury produced a crackling sound when the knee was flexed with a valgus force applied and severe swelling of the right knee, range of motion (ROM) restriction due to pain, and approximately 40° of extension lag were present. Simple plain radiography showed patella alta on the lateral view (), but other abnormal findings, such as a fracture, were not observed. Magnetic resonance imaging (MRI) was performed to identify if there is an accompanying injury, which revealed a complete tear of the patellar tendon and complete tears of the ACL and the medial collateral ligament (MCL) at the femoral attachment sites, and increased signal intensity in the lateral meniscus led us to suspect an injury to the meniscus ().\nAt 6 days after injury, primary suture repair of the patellar tendon with ACL reconstruction was carried out. The patellar tendon repair preceded the ACL reconstruction. Initially, a 10cm longitudinal skin incision extending from the middle of the patella through the center of the patellar tendon to the tibial tuberosity was made to expose the ruptured patellar tendon. The patellar tendon was completely torn in the midsubstance, the torn end had a frayed mop-end appearance, and the tear extended to the medial retinaculum (). Taking consideration into the shape of the torn end and the distally narrowing anatomical shape of the patellar tendon, the torn end was longitudinally divided into three equal sections, and three core sutures of the patellar tendon were determined. The center of the distal end was repaired with a Fiberwire (Arthrex, Naples, FL, USA) suture using the Krackow method. Two longitudinal bone tunnels were created in the patella using a 2.0-mm Kirschner wire. A suture was passed through the tunnel and pullout repair with the proximal end was performed on the anterosuperior patella with the knee in 45° flexion. The proximal end was sutured with two Fiberwire sutures at medial 1/3 and lateral 1/3 points using the Krackow method. A bone tunnel parallel to the tibial tuberosity was created, through which the sutures were passed and pullout suture with the distal torn end was done. At the torn ends, end-to-end anastomosis was performed additionally (. Subsequently, an anterolateral portal, an anteromedial portal, and an accessory far medial portal for anatomical ACL reconstruction were created through the skin incision. An arthroscope was introduced into the joint. The presence of a transverse tear in the posterior horn of the lateral meniscus that was not clearly identifiable on MRI was confirmed. It was repaired using an all inside technique with two PDS (polydioxanone monofilament; Ethicon Inc., Somerville, NJ, USA) sutures. A complete tear of the ACL at the femoral attachment site was confirmed, and reconstruction was done using an Achilles tendon allograft to avoid a donor site injury (). For anatomical ACL reconstruction, a femoral tunnel was created at the center of the femoral attachment of the ACL using the transportal technique and a tibial tunnel was made at the center of the tibial attachment site using Pinn-ACL tibial guide (Linvatec, Largo, FL, USA). With the calcaneal fragment of the Achilles tendon allograft placed toward the femur, the graft was fixated to the femur using a metal interference screw and to the tibia using a bioabsorbable interference screw with the knee in 20° flexion, and a metal staple was used for additional fixation. Following ACL reconstruction, a primary suture for the medial retinaculum and the patellar tendon sheath was carried out. The complete tear of the MCL at the femoral attachment site was conservatively treated: after 2 weeks of splint immobilization, rehabilitation therapy was administered so that the range of flexion could be gradually increased.\nFor the 14 postoperative days, the patient was treated with compression dressing, application of ice, and elevation of the leg with a long leg splint applied, to reduce swelling. From day 1 after surgery, quadriceps strengthening exercises were recommended. From the second postoperative week, the long leg splint was replaced with a limited motion knee brace and the patient was encouraged to perform flexion exercises within pain-free ranges. The range of flexion was gradually increased to 30° at the 2nd postoperative week, to 60° at the 4th postoperative week, and to 90° at the 6th postoperative week. Weight bearing ambulation was not allowed until 6 weeks after surgery due to the meniscal repair.\nMRI scan at 6 month after surgery showed well-maintained continuity of the ACL and patellar tendon and no abnormal findings in other soft tissue, such as the meniscus (). At 1-year postoperative follow-up, 0°-140° of flexion was possible, and no changes were detected in the Lachman and pivot shift tests. The Lysholm score was satisfactorily high (94 points). Other than discomfort in the knee after long or knee-straining activities, no complication was reported.

We present the case of a 48-year-old man, complaining of a bilateral knee injury and functional disability. The patient fell about two meters down an embankment one hour before the presentation and was unable to stand up due to pain, so he was brought to our hospital by ambulance.\nClinical examination revealed a marked bilateral swelling of both knees, severe pain at the passive mobilization of the knee joints, pain-limiting active flexion to less than 30°, and an inability to actively extend the knee joints or to perform an active straight leg raise bilaterally. Additionally, weight-bearing had hardly been possible. There was a loss of fullness and a palpable deficit at the inferior poles of his patellae. Testing of the ligamentous knee joint stabilizers was significantly limited by guarding due to the severe sharp pain. The patient's medical history revealed that a couple of years earlier, he had a right knee sprain resulting in an acute rupture of the anterior cruciate ligament (ACL), which was treated conservatively. The patient does not take any drugs regularly, and we note that he is allergic to levofloxacin. The weight and height of the patient were recorded at the physical examination as 107 kilograms and 180 cm, with a body mass index (BMI) of 33.\nPlain radiographs of his knees showed bilateral knee effusions with patella alta (high-riding patellae) on both anteroposterior and lateral views. Insall-Salvati ratios measured 1.6 and 1.47 for right and left knee, respectively () (normal values range from 0.8 to 1.2; patella alta > 1.2 and patella baja < 0.8). Moreover, the irregularity and incongruity of the patellar tendons on the lateral radiographs were additional signs suggestive of the extensor mechanism's rupture and consistent with the tendons' rupture from the lower pole of the patellae bilaterally.\nOur patient was operated under general anesthesia 48 hours after the accident. He was placed in the supine position. The clinical examination under anesthesia of both knees demonstrated a full instability of the MCL with a valgus stress test at both 0 and 30° of knee flexion. No laxity was demonstrated in the remaining ligaments of the knee joint. The lower extremities were prepared and draped together in the usual sterile fashion. The intervention was performed without the use of a tourniquet.\nOur ligamentous reconstruction was approached by an anterior longitudinal midline incision. Dissection was carried down through the skin and subcutaneous tissues to the level of the patellar and quadriceps paratenon, which were carefully preserved. The patellar tendon rupture was identified near the proximal osteotendinous junction bilaterally (). The hemarthrosis was evacuated, and the joint was copiously irrigated. A chronic tear of the right ACL was identified, with the proximal portion of the ligament missing and only scar tissue remaining with the ACL stump adhering to an intact Posterior Cruciate Ligament (PCL). A complete proximal (femoral) MCL tear was identified bilaterally, confirming our clinical suspicion. The medial and lateral retinacula, which were involved as well, were identified for later repair.\nAt first, with the same incision, the MCL tear was approached. Proximal reinsertion at the level of the medial femoral condyle using a DePuy Mitek super QuickAnchor™ Plus DS® was done to ensure the stability of the medial motion plane. Then, after debridement of the tendinous tissue and visualization of the inferior pole of the patella, three DePuy Mitek super QuickAnchor™ Plus DS® were screwed into the medial, middle, and lateral thirds of the patella in the proper coronal plane. The purchase of the anchors was tested as we were able to deliver the patella to the distal extent of the incision by pulling on the anchor sutures. Then, a circumferential 1.2 mm thick stainless steel wire was passed through the center of the thickness of the patella superiorly and the tibial tuberosity inferiorly. Gradual tension was applied on the metallic wire to obtain the optimal patellar height, confirmed by an intraoperative lateral X-ray. One suture in each anchor was used to create a running Krackow stitch distally through the tendon, ensuring that full-thickness bites were obtained.\nThe second limb of each suture was passed in a locked fashion through the proximal free tendon and tied within the substance of the tendon. The additional suture within each anchor was incorporated into the repair for reinforcement in a simple continuous fashion. The reconstruction was further protected by a strip of quadriceps tendon measuring 10 × 1 cm, long enough to cover the patellar tendon, which was harvested and turned down. The edges of the turned down quadriceps tendon were fixed to the underlying patellar tendon using slowly absorbable interrupted sutures (Vicryl 2.0). Next, the medial and lateral retinacula tears were repaired using interrupted No. 2 PDS sutures (Ethicon; Somerville, New Jersey, USA). The strength of the repair was tested bilaterally through a gentle range of motion; a flexion up to 130° was possible.\nPostoperatively, the legs were placed in knee immobilizer braces, with the knees locked in full extension. The postoperative course was uneventful, and radiographic control was satisfactory (). On the second postoperative day, the patient began ambulation with a walker while keeping the extension knee braces. Full weight-bearing was permitted as tolerated, along with isometric quadriceps-strengthening exercises. The rest of the protocol is as follows: knee flexion exercises limited to 45° were started at the second postoperative week. He had no pain and reached 45° of active bilateral knee flexion. He had an active flexion of 80° at the sixth week, and the knee braces were discontinued. In the eighth postoperative week, the patient achieved a bilateral active complete knee extension and could walk without crutches. As part of his daily physiotherapy program, he was allowed full knee flexion along with a focus on muscle strengthening exercises. Twelve weeks after surgery, the patient presented 100° maximum bilateral knee flexion and returned to work.\nUpon examination seven months after surgery, the patient showed an adequate range of motion of both knees (135° flexion, 0° extension) (). Quadriceps muscle, the primary contributor to knee joint stability, had a good strength with no clinical signs of muscular atrophy or extensor lag. The patient denied any sense of instability, and, consequently, he returned to his recreational sports activities. In addition, he reported feeling that his knees were as strong as they were before the accident. At the final follow-up 12 months after the injury, the patient was symptom-free and extremely satisfied as he recovered completely.

Write a detailed clinical case vignette based on the following key phrases: Knee Injury, Patellar Tendon Rupture, ACL Tear

A 32-year-old male visited our clinic with a major complaint of severe pain in the right knee that started to occur when he managed to stop running over the second base that he had run toward while playing baseball. The right leg that was planted on the second base at the time of injury produced a crackling sound when the knee was flexed with a valgus force applied and severe swelling of the right knee, range of motion (ROM) restriction due to pain, and approximately 40° of extension lag were present. Simple plain radiography showed patella alta on the lateral view (), but other abnormal findings, such as a fracture, were not observed. Magnetic resonance imaging (MRI) was performed to identify if there is an accompanying injury, which revealed a complete tear of the patellar tendon and complete tears of the ACL and the medial collateral ligament (MCL) at the femoral attachment sites, and increased signal intensity in the lateral meniscus led us to suspect an injury to the meniscus ().\nAt 6 days after injury, primary suture repair of the patellar tendon with ACL reconstruction was carried out. The patellar tendon repair preceded the ACL reconstruction. Initially, a 10cm longitudinal skin incision extending from the middle of the patella through the center of the patellar tendon to the tibial tuberosity was made to expose the ruptured patellar tendon. The patellar tendon was completely torn in the midsubstance, the torn end had a frayed mop-end appearance, and the tear extended to the medial retinaculum (). Taking consideration into the shape of the torn end and the distally narrowing anatomical shape of the patellar tendon, the torn end was longitudinally divided into three equal sections, and three core sutures of the patellar tendon were determined. The center of the distal end was repaired with a Fiberwire (Arthrex, Naples, FL, USA) suture using the Krackow method. Two longitudinal bone tunnels were created in the patella using a 2.0-mm Kirschner wire. A suture was passed through the tunnel and pullout repair with the proximal end was performed on the anterosuperior patella with the knee in 45° flexion. The proximal end was sutured with two Fiberwire sutures at medial 1/3 and lateral 1/3 points using the Krackow method. A bone tunnel parallel to the tibial tuberosity was created, through which the sutures were passed and pullout suture with the distal torn end was done. At the torn ends, end-to-end anastomosis was performed additionally (. Subsequently, an anterolateral portal, an anteromedial portal, and an accessory far medial portal for anatomical ACL reconstruction were created through the skin incision. An arthroscope was introduced into the joint. The presence of a transverse tear in the posterior horn of the lateral meniscus that was not clearly identifiable on MRI was confirmed. It was repaired using an all inside technique with two PDS (polydioxanone monofilament; Ethicon Inc., Somerville, NJ, USA) sutures. A complete tear of the ACL at the femoral attachment site was confirmed, and reconstruction was done using an Achilles tendon allograft to avoid a donor site injury (). For anatomical ACL reconstruction, a femoral tunnel was created at the center of the femoral attachment of the ACL using the transportal technique and a tibial tunnel was made at the center of the tibial attachment site using Pinn-ACL tibial guide (Linvatec, Largo, FL, USA). With the calcaneal fragment of the Achilles tendon allograft placed toward the femur, the graft was fixated to the femur using a metal interference screw and to the tibia using a bioabsorbable interference screw with the knee in 20° flexion, and a metal staple was used for additional fixation. Following ACL reconstruction, a primary suture for the medial retinaculum and the patellar tendon sheath was carried out. The complete tear of the MCL at the femoral attachment site was conservatively treated: after 2 weeks of splint immobilization, rehabilitation therapy was administered so that the range of flexion could be gradually increased.\nFor the 14 postoperative days, the patient was treated with compression dressing, application of ice, and elevation of the leg with a long leg splint applied, to reduce swelling. From day 1 after surgery, quadriceps strengthening exercises were recommended. From the second postoperative week, the long leg splint was replaced with a limited motion knee brace and the patient was encouraged to perform flexion exercises within pain-free ranges. The range of flexion was gradually increased to 30° at the 2nd postoperative week, to 60° at the 4th postoperative week, and to 90° at the 6th postoperative week. Weight bearing ambulation was not allowed until 6 weeks after surgery due to the meniscal repair.\nMRI scan at 6 month after surgery showed well-maintained continuity of the ACL and patellar tendon and no abnormal findings in other soft tissue, such as the meniscus (). At 1-year postoperative follow-up, 0°-140° of flexion was possible, and no changes were detected in the Lachman and pivot shift tests. The Lysholm score was satisfactorily high (94 points). Other than discomfort in the knee after long or knee-straining activities, no complication was reported.

A 15.5-year-old female teenager presented to the emergency room with acute right knee pain after she jumped from a scooter to brake going downhill at high speed. She reported feeling a “popping” in the knee and collapsed. Her knee became swollen, and she was unable to bear weight. The patient had a moderate knee effusion but was nevertheless able to extend the knee against gravity. No laxity during valgus stress testing was found, and the Lachmann test was negative. The foot was well perfused, and pulses were present. As the clinical vascular examination was entirely normal, we did not perform an arteriogram. Radiographs and MRI revealed a partial distal patellar tendon avulsion injury, a complete tear of the ACL, and associated bone bruises on the lateral femoral condyle, and also on the posterolateral tibial plateau (Figures –). The posterior cruciate ligament and the MCL were undamaged (Figures and ). The patient was taken to the operating room to repair the distal patellar tendon avulsion 14 days after her injury. The clinical exam under general anesthesia demonstrated a positive (grade 1) Lachman test, but no laxity during the valgus stress test. Considering the importance of the patellar tendon lesion, we avoided to perform a pivot shift test during general anesthesia. The surgical treatment focused therefore on stabilizing the patellar tendon/extensor mechanism. Surgical exploration demonstrated a partial distal patellar tendon bone avulsion injury; repair of the lesion was realized by osteosuture using suture anchors. At a 9-month follow-up (), the patient recovered a functional range of motion, with a mild 20° flexion restriction. She did not feel any anterolateral rotatory instability, and she could participate in light sports activities. Radiographs demonstrated a normal patellar height with a Caton-Deschamps index measured at 0.7; however, we noted an anterior static tibial translation of 9 mm.

Write a detailed clinical case vignette based on the following key phrases: Knee Injury, Patellar Tendon Rupture, ACL Tear

A 32-year-old male visited our clinic with a major complaint of severe pain in the right knee that started to occur when he managed to stop running over the second base that he had run toward while playing baseball. The right leg that was planted on the second base at the time of injury produced a crackling sound when the knee was flexed with a valgus force applied and severe swelling of the right knee, range of motion (ROM) restriction due to pain, and approximately 40° of extension lag were present. Simple plain radiography showed patella alta on the lateral view (), but other abnormal findings, such as a fracture, were not observed. Magnetic resonance imaging (MRI) was performed to identify if there is an accompanying injury, which revealed a complete tear of the patellar tendon and complete tears of the ACL and the medial collateral ligament (MCL) at the femoral attachment sites, and increased signal intensity in the lateral meniscus led us to suspect an injury to the meniscus ().\nAt 6 days after injury, primary suture repair of the patellar tendon with ACL reconstruction was carried out. The patellar tendon repair preceded the ACL reconstruction. Initially, a 10cm longitudinal skin incision extending from the middle of the patella through the center of the patellar tendon to the tibial tuberosity was made to expose the ruptured patellar tendon. The patellar tendon was completely torn in the midsubstance, the torn end had a frayed mop-end appearance, and the tear extended to the medial retinaculum (). Taking consideration into the shape of the torn end and the distally narrowing anatomical shape of the patellar tendon, the torn end was longitudinally divided into three equal sections, and three core sutures of the patellar tendon were determined. The center of the distal end was repaired with a Fiberwire (Arthrex, Naples, FL, USA) suture using the Krackow method. Two longitudinal bone tunnels were created in the patella using a 2.0-mm Kirschner wire. A suture was passed through the tunnel and pullout repair with the proximal end was performed on the anterosuperior patella with the knee in 45° flexion. The proximal end was sutured with two Fiberwire sutures at medial 1/3 and lateral 1/3 points using the Krackow method. A bone tunnel parallel to the tibial tuberosity was created, through which the sutures were passed and pullout suture with the distal torn end was done. At the torn ends, end-to-end anastomosis was performed additionally (. Subsequently, an anterolateral portal, an anteromedial portal, and an accessory far medial portal for anatomical ACL reconstruction were created through the skin incision. An arthroscope was introduced into the joint. The presence of a transverse tear in the posterior horn of the lateral meniscus that was not clearly identifiable on MRI was confirmed. It was repaired using an all inside technique with two PDS (polydioxanone monofilament; Ethicon Inc., Somerville, NJ, USA) sutures. A complete tear of the ACL at the femoral attachment site was confirmed, and reconstruction was done using an Achilles tendon allograft to avoid a donor site injury (). For anatomical ACL reconstruction, a femoral tunnel was created at the center of the femoral attachment of the ACL using the transportal technique and a tibial tunnel was made at the center of the tibial attachment site using Pinn-ACL tibial guide (Linvatec, Largo, FL, USA). With the calcaneal fragment of the Achilles tendon allograft placed toward the femur, the graft was fixated to the femur using a metal interference screw and to the tibia using a bioabsorbable interference screw with the knee in 20° flexion, and a metal staple was used for additional fixation. Following ACL reconstruction, a primary suture for the medial retinaculum and the patellar tendon sheath was carried out. The complete tear of the MCL at the femoral attachment site was conservatively treated: after 2 weeks of splint immobilization, rehabilitation therapy was administered so that the range of flexion could be gradually increased.\nFor the 14 postoperative days, the patient was treated with compression dressing, application of ice, and elevation of the leg with a long leg splint applied, to reduce swelling. From day 1 after surgery, quadriceps strengthening exercises were recommended. From the second postoperative week, the long leg splint was replaced with a limited motion knee brace and the patient was encouraged to perform flexion exercises within pain-free ranges. The range of flexion was gradually increased to 30° at the 2nd postoperative week, to 60° at the 4th postoperative week, and to 90° at the 6th postoperative week. Weight bearing ambulation was not allowed until 6 weeks after surgery due to the meniscal repair.\nMRI scan at 6 month after surgery showed well-maintained continuity of the ACL and patellar tendon and no abnormal findings in other soft tissue, such as the meniscus (). At 1-year postoperative follow-up, 0°-140° of flexion was possible, and no changes were detected in the Lachman and pivot shift tests. The Lysholm score was satisfactorily high (94 points). Other than discomfort in the knee after long or knee-straining activities, no complication was reported.

A 45-year-old man presented to our clinic with a left knee injury that had occurred a few days before while skiing. He had been immobilized in a brace at the local medical office.\nClinical examination showed marked swelling of the knee joint, with pain at passive mobilization and restricted active motion: 40° of active flexion and an inability to actively extend the knee. Weight-bearing was hardly possible. There was an obvious gap at the level of the insertion of the patellar tendon on the lower pole of the patella. Testing of the MCL compared to the healthy side showed >10 mm widening of the medial joint line with valgus stress in 30° of flexion as well as in full extension. There was no clinical evidence of instability of the other knee ligaments.\nThe X-ray of the injured knee showed a superior migration of the patella compared to its usual position (). An MRI-scan confirmed the clinical suspicion of a complete tear of the MCL next to its proximal insertion on the medial femoral condyle, as well as a complete rupture of the patellar tendon at the level of its insertion on the lower pole of the patella. There were no lesions of the cruciate ligaments and menisci ().\nThe medical history revealed lower back pain due to a herniated disc, which had been treated conservatively. The patient also reported some pain episodes at the level of the left patellar tendon while jogging in the past. No specific treatment was prescribed for these pains.\nOur patient was operated on under epidural anesthesia 5 days after his accident. Clinical examination under anaesthesia confirmed once again the complete instability of the MCL with valgus stress without laxity in the other plains of motion.\nAt first, we approached the patellar tendon through an anterior longitudinal midline incision. After debridement of the tendinous tissue at the level of the tear, a Krackow-stitch was placed in the patellar tendon distally to its tear. The two loops of this stitch were passed through two bony tunnels in the patella and sutured to each other at the proximal pole of the patella. At the level of the tear, the transosseous reinsertion was reinforced by a running suture of a 3/0 wire. As there was a history of pain at the patellar tendon, we decided to reinforce the reinsertion of the tendon with an allograft of fascia lata, which was sutured directly to the tendinous tissue with absorbable stitches.\nThe tear of the MCL was approached via an oblique medial incision. At first we performed a direct suture which was reinforced with an autograft of the homolateral semitendinosus tendon. The semitendinosus was isolated with an open stripper, taking care to preserve its distal insertion on the tibia. After suturing it to the MCL, the autograft was fixed proximally with a staple at the level of the medial femoral condyle and distally with a direct suture to its original insertion in order to obtain a double-loop reinforcement. The staple fixation was done in a position of 30° knee flexion and slight varus.\nPostoperatively the knee was immobilized in 10° of flexion in a synthetic plaster cast with partial weight-bearing allowed. After 3 weeks the knee was placed in a brace with progressive flexion: 30° the first week, 60° the second week, and 90° the last week. After 6 weeks the brace was removed and complete flexion allowed. A rehabilitation programme with progressive mobilization, proprioceptive training, and muscle strengthening exercises was started.\nClinical control 3 months after the operation showed a limitation of flexion of 20° compared to the other side. There was no swelling of the knee but evident atrophy of the quadriceps muscle without limitation of active extension. Mediolateral stability testing showed no residual valgus instability. A bilateral X-ray of the knee showed normal height of the patella.\nAt 6 months, full motion was recovered and the patient had returned to normal daily life and recreational sports activities (cycling, fitness). Due to discomfort at the level of the medial femoral condyle, the staple fixing the semitendinosus autograft was removed at 9 months. After this removal, no medial instability occurred. At final follow-up 18 months after the injury, the patient was symptom-free and he had returned to skiing, protecting his knee with a brace.

Write a detailed clinical case vignette based on the following key phrases: Knee Injury, Patellar Tendon Rupture, ACL Tear

A 32-year-old male visited our clinic with a major complaint of severe pain in the right knee that started to occur when he managed to stop running over the second base that he had run toward while playing baseball. The right leg that was planted on the second base at the time of injury produced a crackling sound when the knee was flexed with a valgus force applied and severe swelling of the right knee, range of motion (ROM) restriction due to pain, and approximately 40° of extension lag were present. Simple plain radiography showed patella alta on the lateral view (), but other abnormal findings, such as a fracture, were not observed. Magnetic resonance imaging (MRI) was performed to identify if there is an accompanying injury, which revealed a complete tear of the patellar tendon and complete tears of the ACL and the medial collateral ligament (MCL) at the femoral attachment sites, and increased signal intensity in the lateral meniscus led us to suspect an injury to the meniscus ().\nAt 6 days after injury, primary suture repair of the patellar tendon with ACL reconstruction was carried out. The patellar tendon repair preceded the ACL reconstruction. Initially, a 10cm longitudinal skin incision extending from the middle of the patella through the center of the patellar tendon to the tibial tuberosity was made to expose the ruptured patellar tendon. The patellar tendon was completely torn in the midsubstance, the torn end had a frayed mop-end appearance, and the tear extended to the medial retinaculum (). Taking consideration into the shape of the torn end and the distally narrowing anatomical shape of the patellar tendon, the torn end was longitudinally divided into three equal sections, and three core sutures of the patellar tendon were determined. The center of the distal end was repaired with a Fiberwire (Arthrex, Naples, FL, USA) suture using the Krackow method. Two longitudinal bone tunnels were created in the patella using a 2.0-mm Kirschner wire. A suture was passed through the tunnel and pullout repair with the proximal end was performed on the anterosuperior patella with the knee in 45° flexion. The proximal end was sutured with two Fiberwire sutures at medial 1/3 and lateral 1/3 points using the Krackow method. A bone tunnel parallel to the tibial tuberosity was created, through which the sutures were passed and pullout suture with the distal torn end was done. At the torn ends, end-to-end anastomosis was performed additionally (. Subsequently, an anterolateral portal, an anteromedial portal, and an accessory far medial portal for anatomical ACL reconstruction were created through the skin incision. An arthroscope was introduced into the joint. The presence of a transverse tear in the posterior horn of the lateral meniscus that was not clearly identifiable on MRI was confirmed. It was repaired using an all inside technique with two PDS (polydioxanone monofilament; Ethicon Inc., Somerville, NJ, USA) sutures. A complete tear of the ACL at the femoral attachment site was confirmed, and reconstruction was done using an Achilles tendon allograft to avoid a donor site injury (). For anatomical ACL reconstruction, a femoral tunnel was created at the center of the femoral attachment of the ACL using the transportal technique and a tibial tunnel was made at the center of the tibial attachment site using Pinn-ACL tibial guide (Linvatec, Largo, FL, USA). With the calcaneal fragment of the Achilles tendon allograft placed toward the femur, the graft was fixated to the femur using a metal interference screw and to the tibia using a bioabsorbable interference screw with the knee in 20° flexion, and a metal staple was used for additional fixation. Following ACL reconstruction, a primary suture for the medial retinaculum and the patellar tendon sheath was carried out. The complete tear of the MCL at the femoral attachment site was conservatively treated: after 2 weeks of splint immobilization, rehabilitation therapy was administered so that the range of flexion could be gradually increased.\nFor the 14 postoperative days, the patient was treated with compression dressing, application of ice, and elevation of the leg with a long leg splint applied, to reduce swelling. From day 1 after surgery, quadriceps strengthening exercises were recommended. From the second postoperative week, the long leg splint was replaced with a limited motion knee brace and the patient was encouraged to perform flexion exercises within pain-free ranges. The range of flexion was gradually increased to 30° at the 2nd postoperative week, to 60° at the 4th postoperative week, and to 90° at the 6th postoperative week. Weight bearing ambulation was not allowed until 6 weeks after surgery due to the meniscal repair.\nMRI scan at 6 month after surgery showed well-maintained continuity of the ACL and patellar tendon and no abnormal findings in other soft tissue, such as the meniscus (). At 1-year postoperative follow-up, 0°-140° of flexion was possible, and no changes were detected in the Lachman and pivot shift tests. The Lysholm score was satisfactorily high (94 points). Other than discomfort in the knee after long or knee-straining activities, no complication was reported.

A 36-year-old female jumped from a four-foot high deck landing flatly on both feet. She felt a pop in the right knee and experienced extreme pain and inability to bear weight on the limb. She sought emergency medical attention where radiographs revealed a joint effusion, and a wavy appearance to the tendon []. There was no patellar elevation, fracture or malalignment. Clinically the patient was believed to have an ACL tear. The patient was treated with a knee brace and instructed to follow-up with an orthopedic surgeon and obtain an MR examination of the knee.\nThe MR examination of the right knee was obtained 10 days later and demonstrated abnormal increased T2 signal in the midsubstance of the ACL and abnormal orientation of the ligament consistent with a complete ACL disruption []. Bone contusions in the posterior medial and lateral tibial plateaus as well as the lateral femoral condyle were present. The patellar tendon was abnormal in morphology and signal. The tendon had an abnormal wavy contour at the junction of the middle and distal thirds of the tendon and had abnormally increased signal on T2-weighted images. The axial images demonstrated near complete disruption of the patellar tendon with only a few intact fibers.\nOrthopedic follow-up visit was delayed for nearly 2 months. At the time of presentation she had persistent pain, instability, and very limited range of motion. She had a positive Lachman test of the right knee. Although the patient had tenderness over the patellar tendon, there was no palpable tendon defect and she was able to hold a straight leg raise with minimal extensor lag. The patient was diagnosed with a complete ACL tear and high-grade partial patellar tendon tear. Physical therapy was instituted to help prevent postoperative fibrosis. A delayed ACL reconstruction was schedule 8 weeks later.\nA diagnostic arthrogram at the time of surgery confirmed a complete midsubstance ACL tear. The ACL was reconstructed with an ipsilateral hamstring autograft. The patellar tendon was not directly inspected at the time of surgery and was treated clinically as a partial patellar tendon tear. The patient's postoperative course was complicated by complex regional pain syndrome requiring multiple nerve block injections. A year following the initial injury, the patient had continued stiffness, difficulty with walking and had developed quadriceps muscle atrophy.

Write a detailed clinical case vignette based on the following key phrases: Knee Injury, Patellar Tendon Rupture, ACL Tear

A 32-year-old male visited our clinic with a major complaint of severe pain in the right knee that started to occur when he managed to stop running over the second base that he had run toward while playing baseball. The right leg that was planted on the second base at the time of injury produced a crackling sound when the knee was flexed with a valgus force applied and severe swelling of the right knee, range of motion (ROM) restriction due to pain, and approximately 40° of extension lag were present. Simple plain radiography showed patella alta on the lateral view (), but other abnormal findings, such as a fracture, were not observed. Magnetic resonance imaging (MRI) was performed to identify if there is an accompanying injury, which revealed a complete tear of the patellar tendon and complete tears of the ACL and the medial collateral ligament (MCL) at the femoral attachment sites, and increased signal intensity in the lateral meniscus led us to suspect an injury to the meniscus ().\nAt 6 days after injury, primary suture repair of the patellar tendon with ACL reconstruction was carried out. The patellar tendon repair preceded the ACL reconstruction. Initially, a 10cm longitudinal skin incision extending from the middle of the patella through the center of the patellar tendon to the tibial tuberosity was made to expose the ruptured patellar tendon. The patellar tendon was completely torn in the midsubstance, the torn end had a frayed mop-end appearance, and the tear extended to the medial retinaculum (). Taking consideration into the shape of the torn end and the distally narrowing anatomical shape of the patellar tendon, the torn end was longitudinally divided into three equal sections, and three core sutures of the patellar tendon were determined. The center of the distal end was repaired with a Fiberwire (Arthrex, Naples, FL, USA) suture using the Krackow method. Two longitudinal bone tunnels were created in the patella using a 2.0-mm Kirschner wire. A suture was passed through the tunnel and pullout repair with the proximal end was performed on the anterosuperior patella with the knee in 45° flexion. The proximal end was sutured with two Fiberwire sutures at medial 1/3 and lateral 1/3 points using the Krackow method. A bone tunnel parallel to the tibial tuberosity was created, through which the sutures were passed and pullout suture with the distal torn end was done. At the torn ends, end-to-end anastomosis was performed additionally (. Subsequently, an anterolateral portal, an anteromedial portal, and an accessory far medial portal for anatomical ACL reconstruction were created through the skin incision. An arthroscope was introduced into the joint. The presence of a transverse tear in the posterior horn of the lateral meniscus that was not clearly identifiable on MRI was confirmed. It was repaired using an all inside technique with two PDS (polydioxanone monofilament; Ethicon Inc., Somerville, NJ, USA) sutures. A complete tear of the ACL at the femoral attachment site was confirmed, and reconstruction was done using an Achilles tendon allograft to avoid a donor site injury (). For anatomical ACL reconstruction, a femoral tunnel was created at the center of the femoral attachment of the ACL using the transportal technique and a tibial tunnel was made at the center of the tibial attachment site using Pinn-ACL tibial guide (Linvatec, Largo, FL, USA). With the calcaneal fragment of the Achilles tendon allograft placed toward the femur, the graft was fixated to the femur using a metal interference screw and to the tibia using a bioabsorbable interference screw with the knee in 20° flexion, and a metal staple was used for additional fixation. Following ACL reconstruction, a primary suture for the medial retinaculum and the patellar tendon sheath was carried out. The complete tear of the MCL at the femoral attachment site was conservatively treated: after 2 weeks of splint immobilization, rehabilitation therapy was administered so that the range of flexion could be gradually increased.\nFor the 14 postoperative days, the patient was treated with compression dressing, application of ice, and elevation of the leg with a long leg splint applied, to reduce swelling. From day 1 after surgery, quadriceps strengthening exercises were recommended. From the second postoperative week, the long leg splint was replaced with a limited motion knee brace and the patient was encouraged to perform flexion exercises within pain-free ranges. The range of flexion was gradually increased to 30° at the 2nd postoperative week, to 60° at the 4th postoperative week, and to 90° at the 6th postoperative week. Weight bearing ambulation was not allowed until 6 weeks after surgery due to the meniscal repair.\nMRI scan at 6 month after surgery showed well-maintained continuity of the ACL and patellar tendon and no abnormal findings in other soft tissue, such as the meniscus (). At 1-year postoperative follow-up, 0°-140° of flexion was possible, and no changes were detected in the Lachman and pivot shift tests. The Lysholm score was satisfactorily high (94 points). Other than discomfort in the knee after long or knee-straining activities, no complication was reported.

A 30-year-old male presented with severe pain and inability to move his right knee following injury in a RTA. The mechanism of injury was a direct force on his flexed knee while riding pillion on a bike, followed by a twisting valgus knee injury with foot landing on the ground. He was brought to the emergency and evaluated for the injury. On clinical examination, abrasions were noted over the anterior aspect of the knee ( and ). A subtle dip was noted on the patellar tendon region and patient was unable to move his knee. Due to severe pain, further clinical examination was not possible. Radiographs revealed patella Alta ( and ). An urgent MRI was done to evaluate all the injuries of the knee. MRI confirmed the presence of patellar tendon injury along with ACL tear and Grade 1 medial collateral ligament sprain ( and ).\nThe patient was planned for immediate extensor mechanism repair, followed by ACL reconstruction at a later date. Under anesthesia, Lachman’s test and anterior Drawer’s test were found to be positive. A longitudinal incision skirting around the abrasion was made over the right knee. Intraoperatively, the patellar tendon and extensor retinaculum were found torn (). The patellar tendon was torn at its mid portion and was attached end to end using prolene 1-0 (). The extensor retinaculum was repaired using Vicryl 1-0. Following closure, the limb was immobilized in a slab. A cylindrical cast was applied after suture removal and kept for a further period of 3 weeks, during which the patient was taught isometric quadriceps exercises. The cast was removed at 5 weeks post repair and knee were mobilized using continuous passive motion and active assisted exercises. Once active full extension with flexion up to 120° was attained by the patient, arthroscopic ACL reconstruction using hamstring graft was done at 6 weeks. The ipsilateral hamstrings graft was harvested and prepared ( and ). The tunnels were drilled using the transtibial technique. The femoral side was fixed using cross pins and tibial side using bioabsorbable screw. Postoperatively patient underwent routine post ACL reconstruction physiotherapy followed at our institute. In the immediate post-operative period, a hinged brace was provided with flexion permitted up to 90° and closed chain exercises were initiated. This was followed by partial weight bearing at 4 weeks, and open chain exercises were started after 3 months. At 6 months post injury, the patient has regained full function of the knee including complete active extension and flexion up to 120°, with full weight bearing and stability ( and ).

Write a detailed clinical case vignette based on the following key phrases: Knee Injury, Patellar Tendon Rupture, ACL Tear

We present the case of a 48-year-old man, complaining of a bilateral knee injury and functional disability. The patient fell about two meters down an embankment one hour before the presentation and was unable to stand up due to pain, so he was brought to our hospital by ambulance.\nClinical examination revealed a marked bilateral swelling of both knees, severe pain at the passive mobilization of the knee joints, pain-limiting active flexion to less than 30°, and an inability to actively extend the knee joints or to perform an active straight leg raise bilaterally. Additionally, weight-bearing had hardly been possible. There was a loss of fullness and a palpable deficit at the inferior poles of his patellae. Testing of the ligamentous knee joint stabilizers was significantly limited by guarding due to the severe sharp pain. The patient's medical history revealed that a couple of years earlier, he had a right knee sprain resulting in an acute rupture of the anterior cruciate ligament (ACL), which was treated conservatively. The patient does not take any drugs regularly, and we note that he is allergic to levofloxacin. The weight and height of the patient were recorded at the physical examination as 107 kilograms and 180 cm, with a body mass index (BMI) of 33.\nPlain radiographs of his knees showed bilateral knee effusions with patella alta (high-riding patellae) on both anteroposterior and lateral views. Insall-Salvati ratios measured 1.6 and 1.47 for right and left knee, respectively () (normal values range from 0.8 to 1.2; patella alta > 1.2 and patella baja < 0.8). Moreover, the irregularity and incongruity of the patellar tendons on the lateral radiographs were additional signs suggestive of the extensor mechanism's rupture and consistent with the tendons' rupture from the lower pole of the patellae bilaterally.\nOur patient was operated under general anesthesia 48 hours after the accident. He was placed in the supine position. The clinical examination under anesthesia of both knees demonstrated a full instability of the MCL with a valgus stress test at both 0 and 30° of knee flexion. No laxity was demonstrated in the remaining ligaments of the knee joint. The lower extremities were prepared and draped together in the usual sterile fashion. The intervention was performed without the use of a tourniquet.\nOur ligamentous reconstruction was approached by an anterior longitudinal midline incision. Dissection was carried down through the skin and subcutaneous tissues to the level of the patellar and quadriceps paratenon, which were carefully preserved. The patellar tendon rupture was identified near the proximal osteotendinous junction bilaterally (). The hemarthrosis was evacuated, and the joint was copiously irrigated. A chronic tear of the right ACL was identified, with the proximal portion of the ligament missing and only scar tissue remaining with the ACL stump adhering to an intact Posterior Cruciate Ligament (PCL). A complete proximal (femoral) MCL tear was identified bilaterally, confirming our clinical suspicion. The medial and lateral retinacula, which were involved as well, were identified for later repair.\nAt first, with the same incision, the MCL tear was approached. Proximal reinsertion at the level of the medial femoral condyle using a DePuy Mitek super QuickAnchor™ Plus DS® was done to ensure the stability of the medial motion plane. Then, after debridement of the tendinous tissue and visualization of the inferior pole of the patella, three DePuy Mitek super QuickAnchor™ Plus DS® were screwed into the medial, middle, and lateral thirds of the patella in the proper coronal plane. The purchase of the anchors was tested as we were able to deliver the patella to the distal extent of the incision by pulling on the anchor sutures. Then, a circumferential 1.2 mm thick stainless steel wire was passed through the center of the thickness of the patella superiorly and the tibial tuberosity inferiorly. Gradual tension was applied on the metallic wire to obtain the optimal patellar height, confirmed by an intraoperative lateral X-ray. One suture in each anchor was used to create a running Krackow stitch distally through the tendon, ensuring that full-thickness bites were obtained.\nThe second limb of each suture was passed in a locked fashion through the proximal free tendon and tied within the substance of the tendon. The additional suture within each anchor was incorporated into the repair for reinforcement in a simple continuous fashion. The reconstruction was further protected by a strip of quadriceps tendon measuring 10 × 1 cm, long enough to cover the patellar tendon, which was harvested and turned down. The edges of the turned down quadriceps tendon were fixed to the underlying patellar tendon using slowly absorbable interrupted sutures (Vicryl 2.0). Next, the medial and lateral retinacula tears were repaired using interrupted No. 2 PDS sutures (Ethicon; Somerville, New Jersey, USA). The strength of the repair was tested bilaterally through a gentle range of motion; a flexion up to 130° was possible.\nPostoperatively, the legs were placed in knee immobilizer braces, with the knees locked in full extension. The postoperative course was uneventful, and radiographic control was satisfactory (). On the second postoperative day, the patient began ambulation with a walker while keeping the extension knee braces. Full weight-bearing was permitted as tolerated, along with isometric quadriceps-strengthening exercises. The rest of the protocol is as follows: knee flexion exercises limited to 45° were started at the second postoperative week. He had no pain and reached 45° of active bilateral knee flexion. He had an active flexion of 80° at the sixth week, and the knee braces were discontinued. In the eighth postoperative week, the patient achieved a bilateral active complete knee extension and could walk without crutches. As part of his daily physiotherapy program, he was allowed full knee flexion along with a focus on muscle strengthening exercises. Twelve weeks after surgery, the patient presented 100° maximum bilateral knee flexion and returned to work.\nUpon examination seven months after surgery, the patient showed an adequate range of motion of both knees (135° flexion, 0° extension) (). Quadriceps muscle, the primary contributor to knee joint stability, had a good strength with no clinical signs of muscular atrophy or extensor lag. The patient denied any sense of instability, and, consequently, he returned to his recreational sports activities. In addition, he reported feeling that his knees were as strong as they were before the accident. At the final follow-up 12 months after the injury, the patient was symptom-free and extremely satisfied as he recovered completely.

A 15.5-year-old female teenager presented to the emergency room with acute right knee pain after she jumped from a scooter to brake going downhill at high speed. She reported feeling a “popping” in the knee and collapsed. Her knee became swollen, and she was unable to bear weight. The patient had a moderate knee effusion but was nevertheless able to extend the knee against gravity. No laxity during valgus stress testing was found, and the Lachmann test was negative. The foot was well perfused, and pulses were present. As the clinical vascular examination was entirely normal, we did not perform an arteriogram. Radiographs and MRI revealed a partial distal patellar tendon avulsion injury, a complete tear of the ACL, and associated bone bruises on the lateral femoral condyle, and also on the posterolateral tibial plateau (Figures –). The posterior cruciate ligament and the MCL were undamaged (Figures and ). The patient was taken to the operating room to repair the distal patellar tendon avulsion 14 days after her injury. The clinical exam under general anesthesia demonstrated a positive (grade 1) Lachman test, but no laxity during the valgus stress test. Considering the importance of the patellar tendon lesion, we avoided to perform a pivot shift test during general anesthesia. The surgical treatment focused therefore on stabilizing the patellar tendon/extensor mechanism. Surgical exploration demonstrated a partial distal patellar tendon bone avulsion injury; repair of the lesion was realized by osteosuture using suture anchors. At a 9-month follow-up (), the patient recovered a functional range of motion, with a mild 20° flexion restriction. She did not feel any anterolateral rotatory instability, and she could participate in light sports activities. Radiographs demonstrated a normal patellar height with a Caton-Deschamps index measured at 0.7; however, we noted an anterior static tibial translation of 9 mm.

Write a detailed clinical case vignette based on the following key phrases: Knee Injury, Patellar Tendon Rupture, ACL Tear

We present the case of a 48-year-old man, complaining of a bilateral knee injury and functional disability. The patient fell about two meters down an embankment one hour before the presentation and was unable to stand up due to pain, so he was brought to our hospital by ambulance.\nClinical examination revealed a marked bilateral swelling of both knees, severe pain at the passive mobilization of the knee joints, pain-limiting active flexion to less than 30°, and an inability to actively extend the knee joints or to perform an active straight leg raise bilaterally. Additionally, weight-bearing had hardly been possible. There was a loss of fullness and a palpable deficit at the inferior poles of his patellae. Testing of the ligamentous knee joint stabilizers was significantly limited by guarding due to the severe sharp pain. The patient's medical history revealed that a couple of years earlier, he had a right knee sprain resulting in an acute rupture of the anterior cruciate ligament (ACL), which was treated conservatively. The patient does not take any drugs regularly, and we note that he is allergic to levofloxacin. The weight and height of the patient were recorded at the physical examination as 107 kilograms and 180 cm, with a body mass index (BMI) of 33.\nPlain radiographs of his knees showed bilateral knee effusions with patella alta (high-riding patellae) on both anteroposterior and lateral views. Insall-Salvati ratios measured 1.6 and 1.47 for right and left knee, respectively () (normal values range from 0.8 to 1.2; patella alta > 1.2 and patella baja < 0.8). Moreover, the irregularity and incongruity of the patellar tendons on the lateral radiographs were additional signs suggestive of the extensor mechanism's rupture and consistent with the tendons' rupture from the lower pole of the patellae bilaterally.\nOur patient was operated under general anesthesia 48 hours after the accident. He was placed in the supine position. The clinical examination under anesthesia of both knees demonstrated a full instability of the MCL with a valgus stress test at both 0 and 30° of knee flexion. No laxity was demonstrated in the remaining ligaments of the knee joint. The lower extremities were prepared and draped together in the usual sterile fashion. The intervention was performed without the use of a tourniquet.\nOur ligamentous reconstruction was approached by an anterior longitudinal midline incision. Dissection was carried down through the skin and subcutaneous tissues to the level of the patellar and quadriceps paratenon, which were carefully preserved. The patellar tendon rupture was identified near the proximal osteotendinous junction bilaterally (). The hemarthrosis was evacuated, and the joint was copiously irrigated. A chronic tear of the right ACL was identified, with the proximal portion of the ligament missing and only scar tissue remaining with the ACL stump adhering to an intact Posterior Cruciate Ligament (PCL). A complete proximal (femoral) MCL tear was identified bilaterally, confirming our clinical suspicion. The medial and lateral retinacula, which were involved as well, were identified for later repair.\nAt first, with the same incision, the MCL tear was approached. Proximal reinsertion at the level of the medial femoral condyle using a DePuy Mitek super QuickAnchor™ Plus DS® was done to ensure the stability of the medial motion plane. Then, after debridement of the tendinous tissue and visualization of the inferior pole of the patella, three DePuy Mitek super QuickAnchor™ Plus DS® were screwed into the medial, middle, and lateral thirds of the patella in the proper coronal plane. The purchase of the anchors was tested as we were able to deliver the patella to the distal extent of the incision by pulling on the anchor sutures. Then, a circumferential 1.2 mm thick stainless steel wire was passed through the center of the thickness of the patella superiorly and the tibial tuberosity inferiorly. Gradual tension was applied on the metallic wire to obtain the optimal patellar height, confirmed by an intraoperative lateral X-ray. One suture in each anchor was used to create a running Krackow stitch distally through the tendon, ensuring that full-thickness bites were obtained.\nThe second limb of each suture was passed in a locked fashion through the proximal free tendon and tied within the substance of the tendon. The additional suture within each anchor was incorporated into the repair for reinforcement in a simple continuous fashion. The reconstruction was further protected by a strip of quadriceps tendon measuring 10 × 1 cm, long enough to cover the patellar tendon, which was harvested and turned down. The edges of the turned down quadriceps tendon were fixed to the underlying patellar tendon using slowly absorbable interrupted sutures (Vicryl 2.0). Next, the medial and lateral retinacula tears were repaired using interrupted No. 2 PDS sutures (Ethicon; Somerville, New Jersey, USA). The strength of the repair was tested bilaterally through a gentle range of motion; a flexion up to 130° was possible.\nPostoperatively, the legs were placed in knee immobilizer braces, with the knees locked in full extension. The postoperative course was uneventful, and radiographic control was satisfactory (). On the second postoperative day, the patient began ambulation with a walker while keeping the extension knee braces. Full weight-bearing was permitted as tolerated, along with isometric quadriceps-strengthening exercises. The rest of the protocol is as follows: knee flexion exercises limited to 45° were started at the second postoperative week. He had no pain and reached 45° of active bilateral knee flexion. He had an active flexion of 80° at the sixth week, and the knee braces were discontinued. In the eighth postoperative week, the patient achieved a bilateral active complete knee extension and could walk without crutches. As part of his daily physiotherapy program, he was allowed full knee flexion along with a focus on muscle strengthening exercises. Twelve weeks after surgery, the patient presented 100° maximum bilateral knee flexion and returned to work.\nUpon examination seven months after surgery, the patient showed an adequate range of motion of both knees (135° flexion, 0° extension) (). Quadriceps muscle, the primary contributor to knee joint stability, had a good strength with no clinical signs of muscular atrophy or extensor lag. The patient denied any sense of instability, and, consequently, he returned to his recreational sports activities. In addition, he reported feeling that his knees were as strong as they were before the accident. At the final follow-up 12 months after the injury, the patient was symptom-free and extremely satisfied as he recovered completely.

A 45-year-old man presented to our clinic with a left knee injury that had occurred a few days before while skiing. He had been immobilized in a brace at the local medical office.\nClinical examination showed marked swelling of the knee joint, with pain at passive mobilization and restricted active motion: 40° of active flexion and an inability to actively extend the knee. Weight-bearing was hardly possible. There was an obvious gap at the level of the insertion of the patellar tendon on the lower pole of the patella. Testing of the MCL compared to the healthy side showed >10 mm widening of the medial joint line with valgus stress in 30° of flexion as well as in full extension. There was no clinical evidence of instability of the other knee ligaments.\nThe X-ray of the injured knee showed a superior migration of the patella compared to its usual position (). An MRI-scan confirmed the clinical suspicion of a complete tear of the MCL next to its proximal insertion on the medial femoral condyle, as well as a complete rupture of the patellar tendon at the level of its insertion on the lower pole of the patella. There were no lesions of the cruciate ligaments and menisci ().\nThe medical history revealed lower back pain due to a herniated disc, which had been treated conservatively. The patient also reported some pain episodes at the level of the left patellar tendon while jogging in the past. No specific treatment was prescribed for these pains.\nOur patient was operated on under epidural anesthesia 5 days after his accident. Clinical examination under anaesthesia confirmed once again the complete instability of the MCL with valgus stress without laxity in the other plains of motion.\nAt first, we approached the patellar tendon through an anterior longitudinal midline incision. After debridement of the tendinous tissue at the level of the tear, a Krackow-stitch was placed in the patellar tendon distally to its tear. The two loops of this stitch were passed through two bony tunnels in the patella and sutured to each other at the proximal pole of the patella. At the level of the tear, the transosseous reinsertion was reinforced by a running suture of a 3/0 wire. As there was a history of pain at the patellar tendon, we decided to reinforce the reinsertion of the tendon with an allograft of fascia lata, which was sutured directly to the tendinous tissue with absorbable stitches.\nThe tear of the MCL was approached via an oblique medial incision. At first we performed a direct suture which was reinforced with an autograft of the homolateral semitendinosus tendon. The semitendinosus was isolated with an open stripper, taking care to preserve its distal insertion on the tibia. After suturing it to the MCL, the autograft was fixed proximally with a staple at the level of the medial femoral condyle and distally with a direct suture to its original insertion in order to obtain a double-loop reinforcement. The staple fixation was done in a position of 30° knee flexion and slight varus.\nPostoperatively the knee was immobilized in 10° of flexion in a synthetic plaster cast with partial weight-bearing allowed. After 3 weeks the knee was placed in a brace with progressive flexion: 30° the first week, 60° the second week, and 90° the last week. After 6 weeks the brace was removed and complete flexion allowed. A rehabilitation programme with progressive mobilization, proprioceptive training, and muscle strengthening exercises was started.\nClinical control 3 months after the operation showed a limitation of flexion of 20° compared to the other side. There was no swelling of the knee but evident atrophy of the quadriceps muscle without limitation of active extension. Mediolateral stability testing showed no residual valgus instability. A bilateral X-ray of the knee showed normal height of the patella.\nAt 6 months, full motion was recovered and the patient had returned to normal daily life and recreational sports activities (cycling, fitness). Due to discomfort at the level of the medial femoral condyle, the staple fixing the semitendinosus autograft was removed at 9 months. After this removal, no medial instability occurred. At final follow-up 18 months after the injury, the patient was symptom-free and he had returned to skiing, protecting his knee with a brace.

Write a detailed clinical case vignette based on the following key phrases: Knee Injury, Patellar Tendon Rupture, ACL Tear

We present the case of a 48-year-old man, complaining of a bilateral knee injury and functional disability. The patient fell about two meters down an embankment one hour before the presentation and was unable to stand up due to pain, so he was brought to our hospital by ambulance.\nClinical examination revealed a marked bilateral swelling of both knees, severe pain at the passive mobilization of the knee joints, pain-limiting active flexion to less than 30°, and an inability to actively extend the knee joints or to perform an active straight leg raise bilaterally. Additionally, weight-bearing had hardly been possible. There was a loss of fullness and a palpable deficit at the inferior poles of his patellae. Testing of the ligamentous knee joint stabilizers was significantly limited by guarding due to the severe sharp pain. The patient's medical history revealed that a couple of years earlier, he had a right knee sprain resulting in an acute rupture of the anterior cruciate ligament (ACL), which was treated conservatively. The patient does not take any drugs regularly, and we note that he is allergic to levofloxacin. The weight and height of the patient were recorded at the physical examination as 107 kilograms and 180 cm, with a body mass index (BMI) of 33.\nPlain radiographs of his knees showed bilateral knee effusions with patella alta (high-riding patellae) on both anteroposterior and lateral views. Insall-Salvati ratios measured 1.6 and 1.47 for right and left knee, respectively () (normal values range from 0.8 to 1.2; patella alta > 1.2 and patella baja < 0.8). Moreover, the irregularity and incongruity of the patellar tendons on the lateral radiographs were additional signs suggestive of the extensor mechanism's rupture and consistent with the tendons' rupture from the lower pole of the patellae bilaterally.\nOur patient was operated under general anesthesia 48 hours after the accident. He was placed in the supine position. The clinical examination under anesthesia of both knees demonstrated a full instability of the MCL with a valgus stress test at both 0 and 30° of knee flexion. No laxity was demonstrated in the remaining ligaments of the knee joint. The lower extremities were prepared and draped together in the usual sterile fashion. The intervention was performed without the use of a tourniquet.\nOur ligamentous reconstruction was approached by an anterior longitudinal midline incision. Dissection was carried down through the skin and subcutaneous tissues to the level of the patellar and quadriceps paratenon, which were carefully preserved. The patellar tendon rupture was identified near the proximal osteotendinous junction bilaterally (). The hemarthrosis was evacuated, and the joint was copiously irrigated. A chronic tear of the right ACL was identified, with the proximal portion of the ligament missing and only scar tissue remaining with the ACL stump adhering to an intact Posterior Cruciate Ligament (PCL). A complete proximal (femoral) MCL tear was identified bilaterally, confirming our clinical suspicion. The medial and lateral retinacula, which were involved as well, were identified for later repair.\nAt first, with the same incision, the MCL tear was approached. Proximal reinsertion at the level of the medial femoral condyle using a DePuy Mitek super QuickAnchor™ Plus DS® was done to ensure the stability of the medial motion plane. Then, after debridement of the tendinous tissue and visualization of the inferior pole of the patella, three DePuy Mitek super QuickAnchor™ Plus DS® were screwed into the medial, middle, and lateral thirds of the patella in the proper coronal plane. The purchase of the anchors was tested as we were able to deliver the patella to the distal extent of the incision by pulling on the anchor sutures. Then, a circumferential 1.2 mm thick stainless steel wire was passed through the center of the thickness of the patella superiorly and the tibial tuberosity inferiorly. Gradual tension was applied on the metallic wire to obtain the optimal patellar height, confirmed by an intraoperative lateral X-ray. One suture in each anchor was used to create a running Krackow stitch distally through the tendon, ensuring that full-thickness bites were obtained.\nThe second limb of each suture was passed in a locked fashion through the proximal free tendon and tied within the substance of the tendon. The additional suture within each anchor was incorporated into the repair for reinforcement in a simple continuous fashion. The reconstruction was further protected by a strip of quadriceps tendon measuring 10 × 1 cm, long enough to cover the patellar tendon, which was harvested and turned down. The edges of the turned down quadriceps tendon were fixed to the underlying patellar tendon using slowly absorbable interrupted sutures (Vicryl 2.0). Next, the medial and lateral retinacula tears were repaired using interrupted No. 2 PDS sutures (Ethicon; Somerville, New Jersey, USA). The strength of the repair was tested bilaterally through a gentle range of motion; a flexion up to 130° was possible.\nPostoperatively, the legs were placed in knee immobilizer braces, with the knees locked in full extension. The postoperative course was uneventful, and radiographic control was satisfactory (). On the second postoperative day, the patient began ambulation with a walker while keeping the extension knee braces. Full weight-bearing was permitted as tolerated, along with isometric quadriceps-strengthening exercises. The rest of the protocol is as follows: knee flexion exercises limited to 45° were started at the second postoperative week. He had no pain and reached 45° of active bilateral knee flexion. He had an active flexion of 80° at the sixth week, and the knee braces were discontinued. In the eighth postoperative week, the patient achieved a bilateral active complete knee extension and could walk without crutches. As part of his daily physiotherapy program, he was allowed full knee flexion along with a focus on muscle strengthening exercises. Twelve weeks after surgery, the patient presented 100° maximum bilateral knee flexion and returned to work.\nUpon examination seven months after surgery, the patient showed an adequate range of motion of both knees (135° flexion, 0° extension) (). Quadriceps muscle, the primary contributor to knee joint stability, had a good strength with no clinical signs of muscular atrophy or extensor lag. The patient denied any sense of instability, and, consequently, he returned to his recreational sports activities. In addition, he reported feeling that his knees were as strong as they were before the accident. At the final follow-up 12 months after the injury, the patient was symptom-free and extremely satisfied as he recovered completely.

A 36-year-old female jumped from a four-foot high deck landing flatly on both feet. She felt a pop in the right knee and experienced extreme pain and inability to bear weight on the limb. She sought emergency medical attention where radiographs revealed a joint effusion, and a wavy appearance to the tendon []. There was no patellar elevation, fracture or malalignment. Clinically the patient was believed to have an ACL tear. The patient was treated with a knee brace and instructed to follow-up with an orthopedic surgeon and obtain an MR examination of the knee.\nThe MR examination of the right knee was obtained 10 days later and demonstrated abnormal increased T2 signal in the midsubstance of the ACL and abnormal orientation of the ligament consistent with a complete ACL disruption []. Bone contusions in the posterior medial and lateral tibial plateaus as well as the lateral femoral condyle were present. The patellar tendon was abnormal in morphology and signal. The tendon had an abnormal wavy contour at the junction of the middle and distal thirds of the tendon and had abnormally increased signal on T2-weighted images. The axial images demonstrated near complete disruption of the patellar tendon with only a few intact fibers.\nOrthopedic follow-up visit was delayed for nearly 2 months. At the time of presentation she had persistent pain, instability, and very limited range of motion. She had a positive Lachman test of the right knee. Although the patient had tenderness over the patellar tendon, there was no palpable tendon defect and she was able to hold a straight leg raise with minimal extensor lag. The patient was diagnosed with a complete ACL tear and high-grade partial patellar tendon tear. Physical therapy was instituted to help prevent postoperative fibrosis. A delayed ACL reconstruction was schedule 8 weeks later.\nA diagnostic arthrogram at the time of surgery confirmed a complete midsubstance ACL tear. The ACL was reconstructed with an ipsilateral hamstring autograft. The patellar tendon was not directly inspected at the time of surgery and was treated clinically as a partial patellar tendon tear. The patient's postoperative course was complicated by complex regional pain syndrome requiring multiple nerve block injections. A year following the initial injury, the patient had continued stiffness, difficulty with walking and had developed quadriceps muscle atrophy.

Write a detailed clinical case vignette based on the following key phrases: Knee Injury, Patellar Tendon Rupture, ACL Tear

We present the case of a 48-year-old man, complaining of a bilateral knee injury and functional disability. The patient fell about two meters down an embankment one hour before the presentation and was unable to stand up due to pain, so he was brought to our hospital by ambulance.\nClinical examination revealed a marked bilateral swelling of both knees, severe pain at the passive mobilization of the knee joints, pain-limiting active flexion to less than 30°, and an inability to actively extend the knee joints or to perform an active straight leg raise bilaterally. Additionally, weight-bearing had hardly been possible. There was a loss of fullness and a palpable deficit at the inferior poles of his patellae. Testing of the ligamentous knee joint stabilizers was significantly limited by guarding due to the severe sharp pain. The patient's medical history revealed that a couple of years earlier, he had a right knee sprain resulting in an acute rupture of the anterior cruciate ligament (ACL), which was treated conservatively. The patient does not take any drugs regularly, and we note that he is allergic to levofloxacin. The weight and height of the patient were recorded at the physical examination as 107 kilograms and 180 cm, with a body mass index (BMI) of 33.\nPlain radiographs of his knees showed bilateral knee effusions with patella alta (high-riding patellae) on both anteroposterior and lateral views. Insall-Salvati ratios measured 1.6 and 1.47 for right and left knee, respectively () (normal values range from 0.8 to 1.2; patella alta > 1.2 and patella baja < 0.8). Moreover, the irregularity and incongruity of the patellar tendons on the lateral radiographs were additional signs suggestive of the extensor mechanism's rupture and consistent with the tendons' rupture from the lower pole of the patellae bilaterally.\nOur patient was operated under general anesthesia 48 hours after the accident. He was placed in the supine position. The clinical examination under anesthesia of both knees demonstrated a full instability of the MCL with a valgus stress test at both 0 and 30° of knee flexion. No laxity was demonstrated in the remaining ligaments of the knee joint. The lower extremities were prepared and draped together in the usual sterile fashion. The intervention was performed without the use of a tourniquet.\nOur ligamentous reconstruction was approached by an anterior longitudinal midline incision. Dissection was carried down through the skin and subcutaneous tissues to the level of the patellar and quadriceps paratenon, which were carefully preserved. The patellar tendon rupture was identified near the proximal osteotendinous junction bilaterally (). The hemarthrosis was evacuated, and the joint was copiously irrigated. A chronic tear of the right ACL was identified, with the proximal portion of the ligament missing and only scar tissue remaining with the ACL stump adhering to an intact Posterior Cruciate Ligament (PCL). A complete proximal (femoral) MCL tear was identified bilaterally, confirming our clinical suspicion. The medial and lateral retinacula, which were involved as well, were identified for later repair.\nAt first, with the same incision, the MCL tear was approached. Proximal reinsertion at the level of the medial femoral condyle using a DePuy Mitek super QuickAnchor™ Plus DS® was done to ensure the stability of the medial motion plane. Then, after debridement of the tendinous tissue and visualization of the inferior pole of the patella, three DePuy Mitek super QuickAnchor™ Plus DS® were screwed into the medial, middle, and lateral thirds of the patella in the proper coronal plane. The purchase of the anchors was tested as we were able to deliver the patella to the distal extent of the incision by pulling on the anchor sutures. Then, a circumferential 1.2 mm thick stainless steel wire was passed through the center of the thickness of the patella superiorly and the tibial tuberosity inferiorly. Gradual tension was applied on the metallic wire to obtain the optimal patellar height, confirmed by an intraoperative lateral X-ray. One suture in each anchor was used to create a running Krackow stitch distally through the tendon, ensuring that full-thickness bites were obtained.\nThe second limb of each suture was passed in a locked fashion through the proximal free tendon and tied within the substance of the tendon. The additional suture within each anchor was incorporated into the repair for reinforcement in a simple continuous fashion. The reconstruction was further protected by a strip of quadriceps tendon measuring 10 × 1 cm, long enough to cover the patellar tendon, which was harvested and turned down. The edges of the turned down quadriceps tendon were fixed to the underlying patellar tendon using slowly absorbable interrupted sutures (Vicryl 2.0). Next, the medial and lateral retinacula tears were repaired using interrupted No. 2 PDS sutures (Ethicon; Somerville, New Jersey, USA). The strength of the repair was tested bilaterally through a gentle range of motion; a flexion up to 130° was possible.\nPostoperatively, the legs were placed in knee immobilizer braces, with the knees locked in full extension. The postoperative course was uneventful, and radiographic control was satisfactory (). On the second postoperative day, the patient began ambulation with a walker while keeping the extension knee braces. Full weight-bearing was permitted as tolerated, along with isometric quadriceps-strengthening exercises. The rest of the protocol is as follows: knee flexion exercises limited to 45° were started at the second postoperative week. He had no pain and reached 45° of active bilateral knee flexion. He had an active flexion of 80° at the sixth week, and the knee braces were discontinued. In the eighth postoperative week, the patient achieved a bilateral active complete knee extension and could walk without crutches. As part of his daily physiotherapy program, he was allowed full knee flexion along with a focus on muscle strengthening exercises. Twelve weeks after surgery, the patient presented 100° maximum bilateral knee flexion and returned to work.\nUpon examination seven months after surgery, the patient showed an adequate range of motion of both knees (135° flexion, 0° extension) (). Quadriceps muscle, the primary contributor to knee joint stability, had a good strength with no clinical signs of muscular atrophy or extensor lag. The patient denied any sense of instability, and, consequently, he returned to his recreational sports activities. In addition, he reported feeling that his knees were as strong as they were before the accident. At the final follow-up 12 months after the injury, the patient was symptom-free and extremely satisfied as he recovered completely.

A 30-year-old male presented with severe pain and inability to move his right knee following injury in a RTA. The mechanism of injury was a direct force on his flexed knee while riding pillion on a bike, followed by a twisting valgus knee injury with foot landing on the ground. He was brought to the emergency and evaluated for the injury. On clinical examination, abrasions were noted over the anterior aspect of the knee ( and ). A subtle dip was noted on the patellar tendon region and patient was unable to move his knee. Due to severe pain, further clinical examination was not possible. Radiographs revealed patella Alta ( and ). An urgent MRI was done to evaluate all the injuries of the knee. MRI confirmed the presence of patellar tendon injury along with ACL tear and Grade 1 medial collateral ligament sprain ( and ).\nThe patient was planned for immediate extensor mechanism repair, followed by ACL reconstruction at a later date. Under anesthesia, Lachman’s test and anterior Drawer’s test were found to be positive. A longitudinal incision skirting around the abrasion was made over the right knee. Intraoperatively, the patellar tendon and extensor retinaculum were found torn (). The patellar tendon was torn at its mid portion and was attached end to end using prolene 1-0 (). The extensor retinaculum was repaired using Vicryl 1-0. Following closure, the limb was immobilized in a slab. A cylindrical cast was applied after suture removal and kept for a further period of 3 weeks, during which the patient was taught isometric quadriceps exercises. The cast was removed at 5 weeks post repair and knee were mobilized using continuous passive motion and active assisted exercises. Once active full extension with flexion up to 120° was attained by the patient, arthroscopic ACL reconstruction using hamstring graft was done at 6 weeks. The ipsilateral hamstrings graft was harvested and prepared ( and ). The tunnels were drilled using the transtibial technique. The femoral side was fixed using cross pins and tibial side using bioabsorbable screw. Postoperatively patient underwent routine post ACL reconstruction physiotherapy followed at our institute. In the immediate post-operative period, a hinged brace was provided with flexion permitted up to 90° and closed chain exercises were initiated. This was followed by partial weight bearing at 4 weeks, and open chain exercises were started after 3 months. At 6 months post injury, the patient has regained full function of the knee including complete active extension and flexion up to 120°, with full weight bearing and stability ( and ).

Write a detailed clinical case vignette based on the following key phrases: Knee Injury, Patellar Tendon Rupture, ACL Tear

A 45-year-old man presented to our clinic with a left knee injury that had occurred a few days before while skiing. He had been immobilized in a brace at the local medical office.\nClinical examination showed marked swelling of the knee joint, with pain at passive mobilization and restricted active motion: 40° of active flexion and an inability to actively extend the knee. Weight-bearing was hardly possible. There was an obvious gap at the level of the insertion of the patellar tendon on the lower pole of the patella. Testing of the MCL compared to the healthy side showed >10 mm widening of the medial joint line with valgus stress in 30° of flexion as well as in full extension. There was no clinical evidence of instability of the other knee ligaments.\nThe X-ray of the injured knee showed a superior migration of the patella compared to its usual position (). An MRI-scan confirmed the clinical suspicion of a complete tear of the MCL next to its proximal insertion on the medial femoral condyle, as well as a complete rupture of the patellar tendon at the level of its insertion on the lower pole of the patella. There were no lesions of the cruciate ligaments and menisci ().\nThe medical history revealed lower back pain due to a herniated disc, which had been treated conservatively. The patient also reported some pain episodes at the level of the left patellar tendon while jogging in the past. No specific treatment was prescribed for these pains.\nOur patient was operated on under epidural anesthesia 5 days after his accident. Clinical examination under anaesthesia confirmed once again the complete instability of the MCL with valgus stress without laxity in the other plains of motion.\nAt first, we approached the patellar tendon through an anterior longitudinal midline incision. After debridement of the tendinous tissue at the level of the tear, a Krackow-stitch was placed in the patellar tendon distally to its tear. The two loops of this stitch were passed through two bony tunnels in the patella and sutured to each other at the proximal pole of the patella. At the level of the tear, the transosseous reinsertion was reinforced by a running suture of a 3/0 wire. As there was a history of pain at the patellar tendon, we decided to reinforce the reinsertion of the tendon with an allograft of fascia lata, which was sutured directly to the tendinous tissue with absorbable stitches.\nThe tear of the MCL was approached via an oblique medial incision. At first we performed a direct suture which was reinforced with an autograft of the homolateral semitendinosus tendon. The semitendinosus was isolated with an open stripper, taking care to preserve its distal insertion on the tibia. After suturing it to the MCL, the autograft was fixed proximally with a staple at the level of the medial femoral condyle and distally with a direct suture to its original insertion in order to obtain a double-loop reinforcement. The staple fixation was done in a position of 30° knee flexion and slight varus.\nPostoperatively the knee was immobilized in 10° of flexion in a synthetic plaster cast with partial weight-bearing allowed. After 3 weeks the knee was placed in a brace with progressive flexion: 30° the first week, 60° the second week, and 90° the last week. After 6 weeks the brace was removed and complete flexion allowed. A rehabilitation programme with progressive mobilization, proprioceptive training, and muscle strengthening exercises was started.\nClinical control 3 months after the operation showed a limitation of flexion of 20° compared to the other side. There was no swelling of the knee but evident atrophy of the quadriceps muscle without limitation of active extension. Mediolateral stability testing showed no residual valgus instability. A bilateral X-ray of the knee showed normal height of the patella.\nAt 6 months, full motion was recovered and the patient had returned to normal daily life and recreational sports activities (cycling, fitness). Due to discomfort at the level of the medial femoral condyle, the staple fixing the semitendinosus autograft was removed at 9 months. After this removal, no medial instability occurred. At final follow-up 18 months after the injury, the patient was symptom-free and he had returned to skiing, protecting his knee with a brace.

A 15.5-year-old female teenager presented to the emergency room with acute right knee pain after she jumped from a scooter to brake going downhill at high speed. She reported feeling a “popping” in the knee and collapsed. Her knee became swollen, and she was unable to bear weight. The patient had a moderate knee effusion but was nevertheless able to extend the knee against gravity. No laxity during valgus stress testing was found, and the Lachmann test was negative. The foot was well perfused, and pulses were present. As the clinical vascular examination was entirely normal, we did not perform an arteriogram. Radiographs and MRI revealed a partial distal patellar tendon avulsion injury, a complete tear of the ACL, and associated bone bruises on the lateral femoral condyle, and also on the posterolateral tibial plateau (Figures –). The posterior cruciate ligament and the MCL were undamaged (Figures and ). The patient was taken to the operating room to repair the distal patellar tendon avulsion 14 days after her injury. The clinical exam under general anesthesia demonstrated a positive (grade 1) Lachman test, but no laxity during the valgus stress test. Considering the importance of the patellar tendon lesion, we avoided to perform a pivot shift test during general anesthesia. The surgical treatment focused therefore on stabilizing the patellar tendon/extensor mechanism. Surgical exploration demonstrated a partial distal patellar tendon bone avulsion injury; repair of the lesion was realized by osteosuture using suture anchors. At a 9-month follow-up (), the patient recovered a functional range of motion, with a mild 20° flexion restriction. She did not feel any anterolateral rotatory instability, and she could participate in light sports activities. Radiographs demonstrated a normal patellar height with a Caton-Deschamps index measured at 0.7; however, we noted an anterior static tibial translation of 9 mm.

Write a detailed clinical case vignette based on the following key phrases: Knee Injury, Patellar Tendon Rupture, ACL Tear

A 15.5-year-old female teenager presented to the emergency room with acute right knee pain after she jumped from a scooter to brake going downhill at high speed. She reported feeling a “popping” in the knee and collapsed. Her knee became swollen, and she was unable to bear weight. The patient had a moderate knee effusion but was nevertheless able to extend the knee against gravity. No laxity during valgus stress testing was found, and the Lachmann test was negative. The foot was well perfused, and pulses were present. As the clinical vascular examination was entirely normal, we did not perform an arteriogram. Radiographs and MRI revealed a partial distal patellar tendon avulsion injury, a complete tear of the ACL, and associated bone bruises on the lateral femoral condyle, and also on the posterolateral tibial plateau (Figures –). The posterior cruciate ligament and the MCL were undamaged (Figures and ). The patient was taken to the operating room to repair the distal patellar tendon avulsion 14 days after her injury. The clinical exam under general anesthesia demonstrated a positive (grade 1) Lachman test, but no laxity during the valgus stress test. Considering the importance of the patellar tendon lesion, we avoided to perform a pivot shift test during general anesthesia. The surgical treatment focused therefore on stabilizing the patellar tendon/extensor mechanism. Surgical exploration demonstrated a partial distal patellar tendon bone avulsion injury; repair of the lesion was realized by osteosuture using suture anchors. At a 9-month follow-up (), the patient recovered a functional range of motion, with a mild 20° flexion restriction. She did not feel any anterolateral rotatory instability, and she could participate in light sports activities. Radiographs demonstrated a normal patellar height with a Caton-Deschamps index measured at 0.7; however, we noted an anterior static tibial translation of 9 mm.

A 36-year-old female jumped from a four-foot high deck landing flatly on both feet. She felt a pop in the right knee and experienced extreme pain and inability to bear weight on the limb. She sought emergency medical attention where radiographs revealed a joint effusion, and a wavy appearance to the tendon []. There was no patellar elevation, fracture or malalignment. Clinically the patient was believed to have an ACL tear. The patient was treated with a knee brace and instructed to follow-up with an orthopedic surgeon and obtain an MR examination of the knee.\nThe MR examination of the right knee was obtained 10 days later and demonstrated abnormal increased T2 signal in the midsubstance of the ACL and abnormal orientation of the ligament consistent with a complete ACL disruption []. Bone contusions in the posterior medial and lateral tibial plateaus as well as the lateral femoral condyle were present. The patellar tendon was abnormal in morphology and signal. The tendon had an abnormal wavy contour at the junction of the middle and distal thirds of the tendon and had abnormally increased signal on T2-weighted images. The axial images demonstrated near complete disruption of the patellar tendon with only a few intact fibers.\nOrthopedic follow-up visit was delayed for nearly 2 months. At the time of presentation she had persistent pain, instability, and very limited range of motion. She had a positive Lachman test of the right knee. Although the patient had tenderness over the patellar tendon, there was no palpable tendon defect and she was able to hold a straight leg raise with minimal extensor lag. The patient was diagnosed with a complete ACL tear and high-grade partial patellar tendon tear. Physical therapy was instituted to help prevent postoperative fibrosis. A delayed ACL reconstruction was schedule 8 weeks later.\nA diagnostic arthrogram at the time of surgery confirmed a complete midsubstance ACL tear. The ACL was reconstructed with an ipsilateral hamstring autograft. The patellar tendon was not directly inspected at the time of surgery and was treated clinically as a partial patellar tendon tear. The patient's postoperative course was complicated by complex regional pain syndrome requiring multiple nerve block injections. A year following the initial injury, the patient had continued stiffness, difficulty with walking and had developed quadriceps muscle atrophy.

Write a detailed clinical case vignette based on the following key phrases: Knee Injury, Patellar Tendon Rupture, ACL Tear

A 30-year-old male presented with severe pain and inability to move his right knee following injury in a RTA. The mechanism of injury was a direct force on his flexed knee while riding pillion on a bike, followed by a twisting valgus knee injury with foot landing on the ground. He was brought to the emergency and evaluated for the injury. On clinical examination, abrasions were noted over the anterior aspect of the knee ( and ). A subtle dip was noted on the patellar tendon region and patient was unable to move his knee. Due to severe pain, further clinical examination was not possible. Radiographs revealed patella Alta ( and ). An urgent MRI was done to evaluate all the injuries of the knee. MRI confirmed the presence of patellar tendon injury along with ACL tear and Grade 1 medial collateral ligament sprain ( and ).\nThe patient was planned for immediate extensor mechanism repair, followed by ACL reconstruction at a later date. Under anesthesia, Lachman’s test and anterior Drawer’s test were found to be positive. A longitudinal incision skirting around the abrasion was made over the right knee. Intraoperatively, the patellar tendon and extensor retinaculum were found torn (). The patellar tendon was torn at its mid portion and was attached end to end using prolene 1-0 (). The extensor retinaculum was repaired using Vicryl 1-0. Following closure, the limb was immobilized in a slab. A cylindrical cast was applied after suture removal and kept for a further period of 3 weeks, during which the patient was taught isometric quadriceps exercises. The cast was removed at 5 weeks post repair and knee were mobilized using continuous passive motion and active assisted exercises. Once active full extension with flexion up to 120° was attained by the patient, arthroscopic ACL reconstruction using hamstring graft was done at 6 weeks. The ipsilateral hamstrings graft was harvested and prepared ( and ). The tunnels were drilled using the transtibial technique. The femoral side was fixed using cross pins and tibial side using bioabsorbable screw. Postoperatively patient underwent routine post ACL reconstruction physiotherapy followed at our institute. In the immediate post-operative period, a hinged brace was provided with flexion permitted up to 90° and closed chain exercises were initiated. This was followed by partial weight bearing at 4 weeks, and open chain exercises were started after 3 months. At 6 months post injury, the patient has regained full function of the knee including complete active extension and flexion up to 120°, with full weight bearing and stability ( and ).

A 15.5-year-old female teenager presented to the emergency room with acute right knee pain after she jumped from a scooter to brake going downhill at high speed. She reported feeling a “popping” in the knee and collapsed. Her knee became swollen, and she was unable to bear weight. The patient had a moderate knee effusion but was nevertheless able to extend the knee against gravity. No laxity during valgus stress testing was found, and the Lachmann test was negative. The foot was well perfused, and pulses were present. As the clinical vascular examination was entirely normal, we did not perform an arteriogram. Radiographs and MRI revealed a partial distal patellar tendon avulsion injury, a complete tear of the ACL, and associated bone bruises on the lateral femoral condyle, and also on the posterolateral tibial plateau (Figures –). The posterior cruciate ligament and the MCL were undamaged (Figures and ). The patient was taken to the operating room to repair the distal patellar tendon avulsion 14 days after her injury. The clinical exam under general anesthesia demonstrated a positive (grade 1) Lachman test, but no laxity during the valgus stress test. Considering the importance of the patellar tendon lesion, we avoided to perform a pivot shift test during general anesthesia. The surgical treatment focused therefore on stabilizing the patellar tendon/extensor mechanism. Surgical exploration demonstrated a partial distal patellar tendon bone avulsion injury; repair of the lesion was realized by osteosuture using suture anchors. At a 9-month follow-up (), the patient recovered a functional range of motion, with a mild 20° flexion restriction. She did not feel any anterolateral rotatory instability, and she could participate in light sports activities. Radiographs demonstrated a normal patellar height with a Caton-Deschamps index measured at 0.7; however, we noted an anterior static tibial translation of 9 mm.

Write a detailed clinical case vignette based on the following key phrases: Knee Injury, Patellar Tendon Rupture, ACL Tear

A 45-year-old man presented to our clinic with a left knee injury that had occurred a few days before while skiing. He had been immobilized in a brace at the local medical office.\nClinical examination showed marked swelling of the knee joint, with pain at passive mobilization and restricted active motion: 40° of active flexion and an inability to actively extend the knee. Weight-bearing was hardly possible. There was an obvious gap at the level of the insertion of the patellar tendon on the lower pole of the patella. Testing of the MCL compared to the healthy side showed >10 mm widening of the medial joint line with valgus stress in 30° of flexion as well as in full extension. There was no clinical evidence of instability of the other knee ligaments.\nThe X-ray of the injured knee showed a superior migration of the patella compared to its usual position (). An MRI-scan confirmed the clinical suspicion of a complete tear of the MCL next to its proximal insertion on the medial femoral condyle, as well as a complete rupture of the patellar tendon at the level of its insertion on the lower pole of the patella. There were no lesions of the cruciate ligaments and menisci ().\nThe medical history revealed lower back pain due to a herniated disc, which had been treated conservatively. The patient also reported some pain episodes at the level of the left patellar tendon while jogging in the past. No specific treatment was prescribed for these pains.\nOur patient was operated on under epidural anesthesia 5 days after his accident. Clinical examination under anaesthesia confirmed once again the complete instability of the MCL with valgus stress without laxity in the other plains of motion.\nAt first, we approached the patellar tendon through an anterior longitudinal midline incision. After debridement of the tendinous tissue at the level of the tear, a Krackow-stitch was placed in the patellar tendon distally to its tear. The two loops of this stitch were passed through two bony tunnels in the patella and sutured to each other at the proximal pole of the patella. At the level of the tear, the transosseous reinsertion was reinforced by a running suture of a 3/0 wire. As there was a history of pain at the patellar tendon, we decided to reinforce the reinsertion of the tendon with an allograft of fascia lata, which was sutured directly to the tendinous tissue with absorbable stitches.\nThe tear of the MCL was approached via an oblique medial incision. At first we performed a direct suture which was reinforced with an autograft of the homolateral semitendinosus tendon. The semitendinosus was isolated with an open stripper, taking care to preserve its distal insertion on the tibia. After suturing it to the MCL, the autograft was fixed proximally with a staple at the level of the medial femoral condyle and distally with a direct suture to its original insertion in order to obtain a double-loop reinforcement. The staple fixation was done in a position of 30° knee flexion and slight varus.\nPostoperatively the knee was immobilized in 10° of flexion in a synthetic plaster cast with partial weight-bearing allowed. After 3 weeks the knee was placed in a brace with progressive flexion: 30° the first week, 60° the second week, and 90° the last week. After 6 weeks the brace was removed and complete flexion allowed. A rehabilitation programme with progressive mobilization, proprioceptive training, and muscle strengthening exercises was started.\nClinical control 3 months after the operation showed a limitation of flexion of 20° compared to the other side. There was no swelling of the knee but evident atrophy of the quadriceps muscle without limitation of active extension. Mediolateral stability testing showed no residual valgus instability. A bilateral X-ray of the knee showed normal height of the patella.\nAt 6 months, full motion was recovered and the patient had returned to normal daily life and recreational sports activities (cycling, fitness). Due to discomfort at the level of the medial femoral condyle, the staple fixing the semitendinosus autograft was removed at 9 months. After this removal, no medial instability occurred. At final follow-up 18 months after the injury, the patient was symptom-free and he had returned to skiing, protecting his knee with a brace.

A 36-year-old female jumped from a four-foot high deck landing flatly on both feet. She felt a pop in the right knee and experienced extreme pain and inability to bear weight on the limb. She sought emergency medical attention where radiographs revealed a joint effusion, and a wavy appearance to the tendon []. There was no patellar elevation, fracture or malalignment. Clinically the patient was believed to have an ACL tear. The patient was treated with a knee brace and instructed to follow-up with an orthopedic surgeon and obtain an MR examination of the knee.\nThe MR examination of the right knee was obtained 10 days later and demonstrated abnormal increased T2 signal in the midsubstance of the ACL and abnormal orientation of the ligament consistent with a complete ACL disruption []. Bone contusions in the posterior medial and lateral tibial plateaus as well as the lateral femoral condyle were present. The patellar tendon was abnormal in morphology and signal. The tendon had an abnormal wavy contour at the junction of the middle and distal thirds of the tendon and had abnormally increased signal on T2-weighted images. The axial images demonstrated near complete disruption of the patellar tendon with only a few intact fibers.\nOrthopedic follow-up visit was delayed for nearly 2 months. At the time of presentation she had persistent pain, instability, and very limited range of motion. She had a positive Lachman test of the right knee. Although the patient had tenderness over the patellar tendon, there was no palpable tendon defect and she was able to hold a straight leg raise with minimal extensor lag. The patient was diagnosed with a complete ACL tear and high-grade partial patellar tendon tear. Physical therapy was instituted to help prevent postoperative fibrosis. A delayed ACL reconstruction was schedule 8 weeks later.\nA diagnostic arthrogram at the time of surgery confirmed a complete midsubstance ACL tear. The ACL was reconstructed with an ipsilateral hamstring autograft. The patellar tendon was not directly inspected at the time of surgery and was treated clinically as a partial patellar tendon tear. The patient's postoperative course was complicated by complex regional pain syndrome requiring multiple nerve block injections. A year following the initial injury, the patient had continued stiffness, difficulty with walking and had developed quadriceps muscle atrophy.

Write a detailed clinical case vignette based on the following key phrases: Knee Injury, Patellar Tendon Rupture, ACL Tear

A 45-year-old man presented to our clinic with a left knee injury that had occurred a few days before while skiing. He had been immobilized in a brace at the local medical office.\nClinical examination showed marked swelling of the knee joint, with pain at passive mobilization and restricted active motion: 40° of active flexion and an inability to actively extend the knee. Weight-bearing was hardly possible. There was an obvious gap at the level of the insertion of the patellar tendon on the lower pole of the patella. Testing of the MCL compared to the healthy side showed >10 mm widening of the medial joint line with valgus stress in 30° of flexion as well as in full extension. There was no clinical evidence of instability of the other knee ligaments.\nThe X-ray of the injured knee showed a superior migration of the patella compared to its usual position (). An MRI-scan confirmed the clinical suspicion of a complete tear of the MCL next to its proximal insertion on the medial femoral condyle, as well as a complete rupture of the patellar tendon at the level of its insertion on the lower pole of the patella. There were no lesions of the cruciate ligaments and menisci ().\nThe medical history revealed lower back pain due to a herniated disc, which had been treated conservatively. The patient also reported some pain episodes at the level of the left patellar tendon while jogging in the past. No specific treatment was prescribed for these pains.\nOur patient was operated on under epidural anesthesia 5 days after his accident. Clinical examination under anaesthesia confirmed once again the complete instability of the MCL with valgus stress without laxity in the other plains of motion.\nAt first, we approached the patellar tendon through an anterior longitudinal midline incision. After debridement of the tendinous tissue at the level of the tear, a Krackow-stitch was placed in the patellar tendon distally to its tear. The two loops of this stitch were passed through two bony tunnels in the patella and sutured to each other at the proximal pole of the patella. At the level of the tear, the transosseous reinsertion was reinforced by a running suture of a 3/0 wire. As there was a history of pain at the patellar tendon, we decided to reinforce the reinsertion of the tendon with an allograft of fascia lata, which was sutured directly to the tendinous tissue with absorbable stitches.\nThe tear of the MCL was approached via an oblique medial incision. At first we performed a direct suture which was reinforced with an autograft of the homolateral semitendinosus tendon. The semitendinosus was isolated with an open stripper, taking care to preserve its distal insertion on the tibia. After suturing it to the MCL, the autograft was fixed proximally with a staple at the level of the medial femoral condyle and distally with a direct suture to its original insertion in order to obtain a double-loop reinforcement. The staple fixation was done in a position of 30° knee flexion and slight varus.\nPostoperatively the knee was immobilized in 10° of flexion in a synthetic plaster cast with partial weight-bearing allowed. After 3 weeks the knee was placed in a brace with progressive flexion: 30° the first week, 60° the second week, and 90° the last week. After 6 weeks the brace was removed and complete flexion allowed. A rehabilitation programme with progressive mobilization, proprioceptive training, and muscle strengthening exercises was started.\nClinical control 3 months after the operation showed a limitation of flexion of 20° compared to the other side. There was no swelling of the knee but evident atrophy of the quadriceps muscle without limitation of active extension. Mediolateral stability testing showed no residual valgus instability. A bilateral X-ray of the knee showed normal height of the patella.\nAt 6 months, full motion was recovered and the patient had returned to normal daily life and recreational sports activities (cycling, fitness). Due to discomfort at the level of the medial femoral condyle, the staple fixing the semitendinosus autograft was removed at 9 months. After this removal, no medial instability occurred. At final follow-up 18 months after the injury, the patient was symptom-free and he had returned to skiing, protecting his knee with a brace.

A 30-year-old male presented with severe pain and inability to move his right knee following injury in a RTA. The mechanism of injury was a direct force on his flexed knee while riding pillion on a bike, followed by a twisting valgus knee injury with foot landing on the ground. He was brought to the emergency and evaluated for the injury. On clinical examination, abrasions were noted over the anterior aspect of the knee ( and ). A subtle dip was noted on the patellar tendon region and patient was unable to move his knee. Due to severe pain, further clinical examination was not possible. Radiographs revealed patella Alta ( and ). An urgent MRI was done to evaluate all the injuries of the knee. MRI confirmed the presence of patellar tendon injury along with ACL tear and Grade 1 medial collateral ligament sprain ( and ).\nThe patient was planned for immediate extensor mechanism repair, followed by ACL reconstruction at a later date. Under anesthesia, Lachman’s test and anterior Drawer’s test were found to be positive. A longitudinal incision skirting around the abrasion was made over the right knee. Intraoperatively, the patellar tendon and extensor retinaculum were found torn (). The patellar tendon was torn at its mid portion and was attached end to end using prolene 1-0 (). The extensor retinaculum was repaired using Vicryl 1-0. Following closure, the limb was immobilized in a slab. A cylindrical cast was applied after suture removal and kept for a further period of 3 weeks, during which the patient was taught isometric quadriceps exercises. The cast was removed at 5 weeks post repair and knee were mobilized using continuous passive motion and active assisted exercises. Once active full extension with flexion up to 120° was attained by the patient, arthroscopic ACL reconstruction using hamstring graft was done at 6 weeks. The ipsilateral hamstrings graft was harvested and prepared ( and ). The tunnels were drilled using the transtibial technique. The femoral side was fixed using cross pins and tibial side using bioabsorbable screw. Postoperatively patient underwent routine post ACL reconstruction physiotherapy followed at our institute. In the immediate post-operative period, a hinged brace was provided with flexion permitted up to 90° and closed chain exercises were initiated. This was followed by partial weight bearing at 4 weeks, and open chain exercises were started after 3 months. At 6 months post injury, the patient has regained full function of the knee including complete active extension and flexion up to 120°, with full weight bearing and stability ( and ).

Write a detailed clinical case vignette based on the following key phrases: Knee Injury, Patellar Tendon Rupture, ACL Tear

A 30-year-old male presented with severe pain and inability to move his right knee following injury in a RTA. The mechanism of injury was a direct force on his flexed knee while riding pillion on a bike, followed by a twisting valgus knee injury with foot landing on the ground. He was brought to the emergency and evaluated for the injury. On clinical examination, abrasions were noted over the anterior aspect of the knee ( and ). A subtle dip was noted on the patellar tendon region and patient was unable to move his knee. Due to severe pain, further clinical examination was not possible. Radiographs revealed patella Alta ( and ). An urgent MRI was done to evaluate all the injuries of the knee. MRI confirmed the presence of patellar tendon injury along with ACL tear and Grade 1 medial collateral ligament sprain ( and ).\nThe patient was planned for immediate extensor mechanism repair, followed by ACL reconstruction at a later date. Under anesthesia, Lachman’s test and anterior Drawer’s test were found to be positive. A longitudinal incision skirting around the abrasion was made over the right knee. Intraoperatively, the patellar tendon and extensor retinaculum were found torn (). The patellar tendon was torn at its mid portion and was attached end to end using prolene 1-0 (). The extensor retinaculum was repaired using Vicryl 1-0. Following closure, the limb was immobilized in a slab. A cylindrical cast was applied after suture removal and kept for a further period of 3 weeks, during which the patient was taught isometric quadriceps exercises. The cast was removed at 5 weeks post repair and knee were mobilized using continuous passive motion and active assisted exercises. Once active full extension with flexion up to 120° was attained by the patient, arthroscopic ACL reconstruction using hamstring graft was done at 6 weeks. The ipsilateral hamstrings graft was harvested and prepared ( and ). The tunnels were drilled using the transtibial technique. The femoral side was fixed using cross pins and tibial side using bioabsorbable screw. Postoperatively patient underwent routine post ACL reconstruction physiotherapy followed at our institute. In the immediate post-operative period, a hinged brace was provided with flexion permitted up to 90° and closed chain exercises were initiated. This was followed by partial weight bearing at 4 weeks, and open chain exercises were started after 3 months. At 6 months post injury, the patient has regained full function of the knee including complete active extension and flexion up to 120°, with full weight bearing and stability ( and ).

A 36-year-old female jumped from a four-foot high deck landing flatly on both feet. She felt a pop in the right knee and experienced extreme pain and inability to bear weight on the limb. She sought emergency medical attention where radiographs revealed a joint effusion, and a wavy appearance to the tendon []. There was no patellar elevation, fracture or malalignment. Clinically the patient was believed to have an ACL tear. The patient was treated with a knee brace and instructed to follow-up with an orthopedic surgeon and obtain an MR examination of the knee.\nThe MR examination of the right knee was obtained 10 days later and demonstrated abnormal increased T2 signal in the midsubstance of the ACL and abnormal orientation of the ligament consistent with a complete ACL disruption []. Bone contusions in the posterior medial and lateral tibial plateaus as well as the lateral femoral condyle were present. The patellar tendon was abnormal in morphology and signal. The tendon had an abnormal wavy contour at the junction of the middle and distal thirds of the tendon and had abnormally increased signal on T2-weighted images. The axial images demonstrated near complete disruption of the patellar tendon with only a few intact fibers.\nOrthopedic follow-up visit was delayed for nearly 2 months. At the time of presentation she had persistent pain, instability, and very limited range of motion. She had a positive Lachman test of the right knee. Although the patient had tenderness over the patellar tendon, there was no palpable tendon defect and she was able to hold a straight leg raise with minimal extensor lag. The patient was diagnosed with a complete ACL tear and high-grade partial patellar tendon tear. Physical therapy was instituted to help prevent postoperative fibrosis. A delayed ACL reconstruction was schedule 8 weeks later.\nA diagnostic arthrogram at the time of surgery confirmed a complete midsubstance ACL tear. The ACL was reconstructed with an ipsilateral hamstring autograft. The patellar tendon was not directly inspected at the time of surgery and was treated clinically as a partial patellar tendon tear. The patient's postoperative course was complicated by complex regional pain syndrome requiring multiple nerve block injections. A year following the initial injury, the patient had continued stiffness, difficulty with walking and had developed quadriceps muscle atrophy.

Write a detailed clinical case vignette based on the following key phrases: Knee Injury, Patellar Tendon Rupture, ACL Tear