The proposed steroid dose is too low.

Idiopathic thrombocytopenic purpura, but with very low platelets, so replenishment is necessary. The proposed steroid dose is too low.

A 19-year-old girl with no medical history of interest, except for a self-limited case of influenza 3 weeks earlier, who comes to the emergency department with petechiae and ecchymosis of spontaneous onset. On physical examination the patient was in good general condition, afebrile, normotensive and oriented in time and space. There were petechiae scattered throughout the lower extremities and abdomen and small ecchymoses in decubitus areas. No lymphadenopathy or splenomegaly were palpated. Laboratory tests showed the following findings: Hb 12.6 g/dL, leukocytes 5,500/mm3, platelets 7000/mm3. The peripheral blood smear showed normal erythrocyte morphology, normal differential leukocyte count and the planetary count was concordant with the autoanalyzer figure without platelet aggregates. Biochemistry and proteinogram, beta 2 microglobulin and LDH are normal. Which of the following do you think is the most appropriate initial treatment?

Cyclophosphamide in 4-day pulses every 21 days.

[Thrombotic thrombocytopenic pupura (TTP)--remission following treatment with high-dose immunoglobulin].

A 60-year-old man was admitted to our hospital because of fever, hemorrhagic tendency, anemia and neurological abnormality. A blood count revealed that the hemoglobin was 6.8 g/dl, the reticulocyte was 17.3 percent with 2 erythroblasts per 100 white cells, the white cell count was 7,100/microliters and the platelet count was 0.8 x 10(4)/microliters. Peripheral blood smear demonstrated marked fragmentation of red cells. Bone marrow examination disclosed the marked erythroid hyperplasia. Although the bleeding time was prolonged (14 minutes 30 seconds), the other hemostatic data were within normal limits. The serum bilirubin level was 1.57 mg/dl; LDH level, 1,437 U/l; creatinine level, 0.92 mg/dl; BUN level 14.7 mg/dl. Haptoglobin was below 10 mg/dl. Results of immunological tests were all negative except the result of PAIgG (576.6 ng/10(7) cells). The urinalysis showed proteinuria, microhematuria and trace granular and hyaline casts. A diagnosis of thrombotic thrombocytopenic purpura was made. The patient was initially treated with prednisolone (60 mg), aspirin (1,000 mg), dipyridamole (150 mg), gabexate mesilate (1.5 g), sodium oxagrel (80 mg) daily with little response. The thirty days after admission, infusion of gamma globulin (20 g, daily) was given for 3 days. The clinical state and laboratory findings became dramatically improved shortly after the administration of gamma globulin and the laboratory data came to be normalized after 1 month. After ten months of this treatment, the patient is remained asymptomatic and the hematological data are within normal range without using any drug. A trial seems justified to confirm the value of this mode of therapy.

[Chronic lymphocytic leukemia].

Chronic lymphocytic leukemia (CLL) is a lymphoproliferative disorder that accounts for approximately 30 % of adult leukemias and 25 % of Non-Hodgkin lymphomas (NHL). It is the most common form of leukemia in the western world (incidence 3-5/100 000). Elderly people are mainly affected, median age at diagnosis is around 70 years and there is a slight predominance in men. The etiology of the disease is unknown. The initial symptoms are nonspecific. Cervical lymphadenopathy and splenomegaly followed by general fatigue are seen most commonly. Other possible symptoms include night sweats, fever, loss of weight (so-called B symptoms) and frequent infections. Several patients develop autoimmune complications as autoimmune hemolytic anemia (AIHA) or immune thrombocytopenia (ITP). To confirm the diagnosis more than 5000 B-lymphocytes/µl need to be present. The expression of the typical surface markers CD5, CD19, and CD23 has to be confirmed by flow cytometry. Imaging studies as X-ray of the chest, ultrasound of the abdomen, or CT scan are used to assess the degree of lymphadenopathy or organomegaly. A bone marrow biopsy is not mandatory for the diagnosis. According to the European Binet staging system, CLL is divided into 3 stages (A, B and C). Patients in Binet stage A have 0 to 2 areas of node or organ enlargement with normal levels of hemoglobin and platelets. Binet stage B patients have 3 to 5 areas of node or organ enlargement and normal or slightly decreased levels of hemoglobin and platelets. Binet stage C patients have anemia (hemoglobin < 10 g/dl) and/or thrombocytopenia (platelet counts < 100 000/µl), with or without lymphadenopathy or organomegaly. As there is no survival benefit associated with early intervention, asymptomatic patients with early stage CLL (Binet stage A and B) are usually not treated but are followed on a "watch and wait" principle. Treatment indications include stage Binet C or signs of an active disease as rapidly progressive lymphadenopathy or organomegaly together with physical limitation, B symptoms that cannot be tolerated, rapidly deteriorating blood values, or rapidly increasing leukocyte counts. The patient's physical condition has major impact on the treatment decision. Currently immunochemotherapy with fludarabine, cyclophosphamide and the CD20-antibody rituximab (FCR) is the standard of care in previously untreated and physically fit CLL-patients. An alternative regimen is the combination of bendamustine and rituximab (BR). Physically compromised patients can be treated with the oral drug chlorambucil or with bendamustine with or without rituximab. Due to high morbidity and mortality, allogeneic stem cell transplantation is limited to a small group of patients and should be discussed in a high-risk situation, such as 17p deletion, lack of response to standard therapy or early relapse.

Cases from the Osler Medical Service at Johns Hopkins University.

PRESENTING FEATURES: An 18-year-old white man was admitted to the Osler Medical Service with the chief complaint of back pain. Two weeks prior to admission, the patient developed diffuse and aching upper back pain. Over the next couple of days, he also developed severe anterior chest pain that was somewhat pleuritic in nature but diffuse and extending bilaterally into the shoulders. One week prior to admission, he developed intermittent fevers and night sweats. The patient denied any lymphadenopathy, pharyngitis, sick contacts, shortness of breath, rash, or bleeding. He was seen by a physician and told that he had thrombocytopenia. There was no history of recent or remote unusual bleeding episodes. His medical history was unremarkable except for a childhood diagnosis of attention deficit/hyperactivity disorder. He was not taking any medications and had no history of tobacco, alcohol, or illicit drug use. He had no risk factors for human immunodeficiency virus infection. Physical examination showed that he was afebrile and had normal vital signs. He was a well-appearing man who was lying still because of pain. HEENT examination was unremarkable. There was no pharyngeal erythema or exudates. His lungs were clear. His neck was supple and without lymphadenopathy. Examination of his back and chest revealed no focal tenderness. There was no hepatosplenomegaly, and his skin was without petechiae or rashes. Examination of the patient's joints showed pain on passive and active movement of his shoulders bilaterally, but no frank arthritis. There was no rash, petechiae, or echymoses. Chest radiograph and electrocardiogram were unremarkable. On admission, the laboratory examination was notable for a hematocrit level of 32.5%, with a mean corpuscular volume of 79 fL, and white blood cell count of 2.8 x 10(3)/microL. Platelet count was 75 x 10(3)/microL. A white blood cell differential revealed 7% bands, 53% polys, 34% lymphs, 5% atypical lymphocytes, 2% nucleated red cells, and a few young unidentified cells. His chemistry studies were unremarkable. What is the diagnosis?

[A case of autoimmune lymphoproliferactive syndrome and literature review].

To summarize the clinical characteristics, diagnosis and treatment of a case with autoimmune lymphoproliferative syndrome (ALPS) . The patient was diagnosed as autoimmune lymphoproliferactive syndrome (ALPS) after being admitted to the Department of Rheumatism and Immunology of Tianjin Children's Hospital in February 20, 2014. The clinical characteristics, physical examination, laboratory tests, gene tests, and treatment process were analyzed and related literature was reviewed. The patient was a 16-month- old boy.Since the first month of life, he started to have repeatedly fever, diarrhea, shortness of breath, lymphadenopathy, hepatosplenomegaly, anemia (HGBmin 50 g/L) and thrombocytopenia (min 35 × 10⁹/L) . But multiple exams showed a normal peripheral blood leukocyte count, hypergammaglobulinemia (IgG 19 800 mg/L, IgA 1 710 mg/L, IgM 2 590 mg/L) and significantly increased serum vitamin B12. Flow cytometric measures showed that CD3⁺ CD4⁻ CD8⁻ T lymphocytes significantly increased ( > 10%) at four times. The count of CD3⁺ TCRαβ⁺ CD4⁻ CD8⁻T lymphocytes (double negative T cells; DNTs) >3% twice. The genetic test showed that 309th FAS gene area showed heterozygous mutations, the boy was diagnosed as ALPS. Added examinations of lymphocytes apoptosis induced by FAS was positive. He was treated with prednisone 15 mg once daily and immunomodulator 150 mg three times a day, while in maintaining period with normal levels of hemoglobin and platelet, the dose of prednisone was reduced gradually. Till now, the patient has been treated and observed for 8 months. We retrieved the reports of ALPS in the databases at home and abroad published in recent 10 years, more than 400 cases reported from foreign countries, but there were only 5 domestic cases. Among those, 4 had onset in infancy and 1 at 6-years of age. All the cases presented servere lymphadenopathy and hepatosplenomegaly with anemia (4 of them with hemolytic anemia) and thrombocytopenia. Three cases had a history of frequent infection, one of them had glomerulonephritis. All patient with significant high level of serum immunoglobulin ( > 1.5 times upper limit of normal range), in 3 of them serum vitamin B12 was > 1.5 pg/L (the other 2 cases missed the exam). In 5 cases CD3⁺ CD4⁻ CD8⁻T cells > 10%, and in 2 case DNTs were 8.9% and 15.7% respectively (the other 3 cases missed the exam). Three cases were clearly detected with FAS mutations. All patients were treated with corticosteroid, 2 of them were added with mycophenolate mofetil. The therapy presented effective result in early 1-3 months, but no long-term follow-up reports were available. ALPS is a disorder of disrupted lymphocyte homeostasis caused by defective Fas-mediated apoptosis, and it is one of the primary immunodeficiency diseases. The onset of the disease occurs during infancy mainly. Clinical lymphoid hyperplasia and autoimmune phenomena are outstanding signs, which can be associated with frequent infections and allergies. The level of serum vitamin B12 > 1.5 pg/L and the count of CD3⁺ CD4⁻ CD8⁻ T cell show important significance. Exact diagnosis should depend on detecting DNTs and FAS gene.

Idiopathic thrombocytopenic purpura associated with splenic tuberculosis: case report.

Tuberculosis is still one of the most prevalent and fatal infectious diseases in spite of considerable improvements in medical science. Splenic tuberculosis is a rare form of extrapulmonary tuberculosis. There are limited numbers of cases in which immune thrombocytopenia is associated with splenic tuberculosis. We report a case of immune thrombocytopenic purpura due to splenic tuberculosis. Our case was a 58-year-old female with headache, gum bleeding, redness in legs, and ecchymoses on the arms for 10 days. On admission to hospital, laboratory tests were as follows: platelet count 6.000/mmc (150 000-450 000), haemoglobin: 12 g/dl, WBC: 8000/mm3, erythrocyte sedimentation rate: 58 mm/h and C-reactive protein was in normal ranges. After standard laboratory tests, the patient was diagnosed with idiopathic thrombocytopenic purpura. The patient presented abdominal lymphadenopathies and spleen in normal size in radiological examinations. Diagnostic laparotomy and splenectomy and lymph node excision was performed and splenic tuberculosis was detected in pathologic and microbiologic examination. The patient was successfully treated with apheresis platelets suspension, intravenous immunoglobulin and antituberculous therapy. In conclusion, splenic tuberculosis should be suspected in patients who have fever, abdominal lymphadenopathies and immune thrombocytopenic purpura. Histopathological examination is still an ideal method to confirm the diagnosis, suitably aided by microbiological examination.

Immune Thrombocytopenia Purpura Secondary to COVID-19.

A 73-year-old female with past medical history of essential hypertension, hyperlipidemia, seasonal allergies, and chronic back pain presented to the hospital with complaints of headaches, fevers, fatigue, generalized body aches, shortness of breath, and diarrhea. Initial complete blood count was remarkable for leukopenia with an absolute lymph count of 0.60 K/µL and severe thrombocytopenia (platelet count < 3 K/µL). She was tested for COVID-19 via nasopharyngeal swab polymerase chain reaction (PCR) testing and found positive. Additional labs showed an elevated D-dimer, C-reactive protein, fibrinogen, and lactate dehydrogenase. Vitamin B12 and folate levels were obtained and found to be normal. Peripheral smear showed no schistocytes or additional hematologic abnormalities apart from thrombocytopenia. The patient was transfused one unit of platelets with no improvement in platelet count. Fibrinogen count was obtained and found in normal range at 458 mg/dL. Prothrombin time (PT), activated partial thromboplastin time (aPTT), and international normalized ratio (INR) were all found to be normal. Immune thrombocytopenia purpura (ITP) was suspected and intravenous immunoglobulin (IVIG) was administered at a dose of 1 g/kg/day for two doses. By day 4, the patient had marked response to treatment with platelet recovery to 105 K/µL and subsequently discharged by day 5 with complete resolution of symptoms and platelet count of 146 K/µL. Twenty-eight days after discharge, she presented to hematology clinic with platelet count of 8 K/µL. Repeat nasopharyngeal swab PCR COVID testing was negative and she was treated with IVIG and pulse dexamethasone with prompt response, confirming suspicion of underlying, undiagnosed ITP prior to COVID infection.

InternalMed_Harrison

Fever ˜38.3° C (101° F) and illness lasting ˜3 weeks and no known immunocompromised state History and physical examination Stop antibiotic treatment and glucocorticoids Obligatory investigations: ESR and CRP, hemoglobin, platelet count, leukocyte count and differential, electrolytes, creatinine, total protein, protein electrophoresis, alkaline phosphatase, AST, ALT, LDH, creatine kinase, antinuclear antibodies, rheumatoid factor, urinalysis, blood cultures (n=3), urine culture, chest x-ray, abdominal ultrasonography, and tuberculin skin test

Waldenström macroglobulinemia

Chemistry tests include lactate dehydrogenase (LDH) levels, uric acid levels, erythrocyte sedimentation rate (ESR), kidney and liver function, total protein levels, and an albumin-to-globulin ratio. The ESR and uric acid level may be elevated. Creatinine is occasionally elevated and electrolytes are occasionally abnormal. A high blood calcium level is noted in approximately 4% of patients. The LDH level is frequently elevated, indicating the extent of Waldenström macroglobulinemia–related tissue involvement. Rheumatoid factor, cryoglobulins, direct antiglobulin test and cold agglutinin titre results can be positive. Beta-2 microglobulin and C-reactive protein test results are not specific for Waldenström macroglobulinemia. Beta-2 microglobulin is elevated in proportion to tumor mass. Coagulation abnormalities may be present. Prothrombin time, activated partial thromboplastin time, thrombin time, and fibrinogen tests should be performed. Platelet aggregation studies are optional. Serum

InternalMed_Harrison

Fever >38.3°C (101°F) on at least two occasions 2. Illness duration of ≥3 weeks 3. 4. Diagnosis that remains uncertain after a thorough history-taking, physical examination, and the following obligatory investigations: determination of erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) level; platelet count; leukocyte count and differential; measurement of levels of hemoglobin, electrolytes, creatinine, total protein, alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, creatine kinase, ferritin, antinuclear antibodies, and rheumatoid factor; protein electrophoresis; urinalysis; blood cultures (n = 3); urine culture; chest x-ray; abdominal ultrasonography; and tuberculin skin test (TST). The range of FUO etiologies has evolved over time as a result of changes in the spectrum of diseases causing FUO, the widespread Percentage of Cases Due to Indicated Cause

Megadose Methylprednisolone for Immune Thrombocytopenia in an Infant Positive for SARS-CoV-2: A Case Report.

BACKGROUND Immune thrombocytopenia (ITP) is rare in infants under 1 year old. Bleeding often occurs when the platelet count is <20 000/uL. The disease can progress because of accompanying COVID-19 disease. CASE REPORT A 9-month-old boy, weighing 8.5 kg, came to the hospital with petechiae on the forehead, cheeks, mouth, and extremities. The patient had rhinorrhea for 3 days previously and was febrile, pale, weak, and could not drink. He had the measles-rubella vaccination 19 days prior. Physical examination showed no abnormalities of the eyes, ears, nose, throat, and mouth. Heart and lungs were within normal limits, with no organomegaly, lymphadenopathy, or congenital anomaly of the abdomen. Laboratory examination showed hemoglobin, 12.7 g/dL; leukocytes, 7420/uL; platelet count, 16 000/uL; and hematocrit, 37.9%. Erythrocyte sedimentation rate was 14 mm at 1 h and 21 mm at 2 h. Peripheral blood smear showed normal RBC morphology, normal leukocytes, and few platelets. IgG was reactive and IgM was nonreactive on rapid antibody test. RT-PCR was positive for SARS-COV-2. Chest-X-ray showed pneumonia. The diagnosis was newly diagnosed ITP with COVID-19. Patient was treated with 30 mg/kg body weight/day of IV methylprednisolone for 3 days (250 mg); then 20 mg/kg body weight/day (175 mg) orally for 4 days in 3 divided doses. Azithromycin 100 mg/day, zinc 20 mg/day, and vitamin C 50 mg/day orally were also given. CONCLUSIONS COVID-19 screening is highly recommended during this pandemic to identify it as a potential cause of childhood ITP. Megadose methylprednisolone had an excellent response in alleviating ITP with confirmed COVID-19 in an infant.

Teetering on a liver's edge: a case report highlighting clinical decision-making in thrombocytopenia.

This report illustrates the importance of a detailed history and physical exam and careful analysis of hematologic parameters when diagnosing ITP. This case demonstrates that even with subtle deviations from typical ITP findings one must promptly reevaluate the diagnosis. This case also highlights the importance of peripheral smear review by an expert in pediatric hematopathology. A previously healthy 10 year-old Asian boy presented with 2 months of easy bruising. Review of systems was negative for any constitutional symptoms. On examination, he appeared well but had numerous large ecchymoses. He had no appreciable lymphadenopathy or splenomegaly. The liver was palpable 1.5 cm below the costal margin. A complete blood count (CBC) showed: platelets = 17 × 109/L, hemoglobin = 128 g/L, white blood cell count = 5.43 × 109/L, and neutrophils = 1.63 × 109/L. A blood smear was reported as normal. Urate was 370 umol/L and lactate dehydrogenase (LDH) was 803 U/L. The child was admitted with a presumptive diagnosis of immune thrombocytopenic purpura (ITP) and treated with intravenous immunoglobulin. The following day, the blood smear was reviewed by a hematopathologist who identified blasts. A bone marrow aspiration (BMA) confirmed the diagnosis of precursor B-cell acute lymphoblastic leukemia. In children presenting with suspected ITP, leukemia should always be considered. A BMA was historically performed on all patients with presumed ITP to rule out leukemia. In 2011, the American Society of Hematology (ASH) stopped recommending routine BMA in patients suspected of having ITP. ASH advises in cases with unusual findings on history, physical examination or CBC, it is reasonable to perform a BMA. Our patient had mild hepatomegaly, which may have qualified him for a BMA. He also had an elevated LDH and urate, which are not listed as criteria for BMA by ASH but were considered atypical for ITP by the clinical team. A literature search did not reveal any primary data assessing these markers. While corticosteroids are a first line treatment in ITP, they must be reserved for when clinicians are confident that the patient does not have leukemia. Steroid administration prior to diagnosing leukemia results in delayed diagnosis and may increase the risk of complications and decrease survival.

Thrombocytopenia

Signs and symptoms Thrombocytopenia usually has no symptoms and is picked up on a routine complete blood count. Some individuals with thrombocytopenia may experience external bleeding such as nosebleeds, or bleeding gums. Some women may have heavier or longer periods or breakthrough bleeding. Bruising, particularly purpura in the forearms and petechiae in the feet, legs, and mucous membranes, may be caused by spontaneous bleeding under the skin. Eliciting a full medical history is vital to ensure the low platelet count is not secondary to another disorder. Ensuring that the other blood cell types, such as red blood cells and white blood cells are not also suppressed, is also important. Painless, round, and pinpoint (1 to 3 mm in diameter) petechiae usually appear and fade, and sometimes group to form ecchymoses. Larger than petechiae, ecchymoses are purple, blue, or yellow-green areas of skin that vary in size and shape. They can occur anywhere on the body.

Severe thrombocytopenia possibly associated with TMP/SMX therapy.

To report a case of possible severe, life-threatening thrombocytopenia associated with trimethoprim/sulfamethoxazole (TMP/SMX) therapy. A 54-year-old white woman received a 10-day course of TMP/SMX for treatment of chronic sinusitis. One day after finishing the course of TMP/SMX therapy, the presented to the emergency department because of the development of scattered petechiae on both hands and blood blisters in her mouth. On admission, her complete blood cell count results revealed a severely low platelet count of 2 x 10(3)/mm3. Other laboratory test results were normal, except for elevated blood glucose (nonfasting blood glucose). TMP/SMX was believed to be the most likely cause of thrombocytopenia. She was treated successfully with a transfusion of 2 units of platelets and oral prednisone. Her platelet count increased to 110 x 10(3)/mm3 4 days after discontinuation of TMP/SMX. She was discharged on hospital day 5. On follow-up (2 wk after hospital discharge), her platelet count was normal (351 x 10(3)/mm3). TMP/SMX has been implicated as a cause of thrombocytopenia, which is defined as platelet count < 150 x 10(3)/mm3. Although it is uncommon, spontaneous severe bleeding may occur when platelet count decreases to < or = 10 x 10(3)/mm3. Thrombocytopenia associated with TMP/SMX appears to be an immune-mediated process resulting in platelet destruction by drug-dependent platelet antibodies. Treatment of thrombocytopenia associated with TMP/SMX therapy includes discontinuation of the offending drug and the use of corticosteroids. Platelet transfusion and intravenous immunoglobulin may be required in some patients. Thrombocytopenia associated with TMP/SMX therapy can be serious or life threatening because it may result in significant bleeding complications. This hematologic adverse effect of TMP/SMX may occur even with the usual recommended dosage and duration of therapy. Careful monitoring of complete blood cell count, including platelet count, before and during TMP/SMX therapy is suggested.

[Castleman disease].

A 66 years female, who was since last year under astenia, arthralgias, pimply lesions in spread plates and tests showing eritrosedimentation over 100 mm, anemi, leucocitosis with neutrofilia, policlonal hypergammaglobulinemia, slight proteinuria and IgE on 900. This patient was sporadically treated with corticoids. When made the medical consult had lost 34lb., was under anorexy, as well as dyspepsia. Hemoglobyn 6.9 gr/dl, leucocytes 20000/mm3, neutrofils at 90%, proteinogram the same as former, with hypoalbuminemia. She was taking prednisona, 16 mg/day. When examined showed depress of conscience, astenia, and dermic lesions already quoted. 4 cm nonpainful right axillary adenopaty adhered to deep planes. Medulogram with increased iron, hyperegenerative. Ganglionar biopsia: linfoid hyperplasic process linked to inmune response. Toracoabdominal tomography with adenomegalia in torax and retroperitoneo. Skin biopsia: neutrofilic vasculitis. The patient suspends the 16 mg of prednisona and fever as well as generalized adenopatias come up. After laying aside other ethiologies, and understanding as Castleman Multicentric disease, it is started to supply prednisona 1 mg/kg of weight with a clinical and biochemical fast and outstanding response. After 7 months it was progressively suspended the esteroids and 60 days later, the process fall back; for that, corticoids are restarted, with a good evolution. The illness of Castleman although it is not very frequent, it should be considered as differential diagnosis in those clinical cases that are accompanied with important general commitment, linphadenopaties and respons to steroid therapy.

Waldenström macroglobulinemia

The International Prognostic Scoring System for Waldenström's Macroglobulinemia is a predictive model to characterise long-term outcomes. According to the model, factors predicting reduced survival are: Age > 65 years Hemoglobin ≤ 11.5 g/dL Platelet count ≤ 100×109/L B2-microglobulin > 3 mg/L Serum monoclonal protein concentration > 70 g/L The risk categories are: Low: ≤ 1 adverse variable except age Intermediate: 2 adverse characteristics or age > 65 years High: > 2 adverse characteristics Five-year survival rates for these categories are 87%, 68% and 36%, respectively. The corresponding median survival rates are 12, 8, and 3.5 years. The International Prognostic Scoring System for Waldenström's Macroglobulinemia has been shown to be reliable. It is also applicable to patients on a rituximab-based treatment regimen. An additional predictive factor is elevated serum lactate dehydrogenase (LDH).

Extreme thrombocytosis as a sign of coeliac disease in the elderly: case report.

Increase in the number of blood platelets to over 1,000,000/mm3 in elderly patients is generally considered secondary to a myeloproliferative or neoplastic disease. To report the case of an elderly woman hospitalized for extreme thrombocytosis associated with severe anaemia, who was found to be suffering from coeliac disease. The patient, aged 83 years, was hospitalized presenting with fatigue. Laboratory tests showed microcytic hypochromic anaemia (haemoglobin 4 g/dl) and extreme thrombocytosis (platelet count 1,400,000/mm3). Physical examination was normal, with the exception of marked thinness. There was no evidence of macroscopic bleeding from the gastrointestinal or genitourinary tracts. She had never suffered from gastrointestinal problems and had no family history of gastroenterological diseases. Oesophagogastroduodenoscopy and histology of the gastric and duodenal mucosa evidenced atrophic gastritis and an adenomatous polyp. The duodenal mucosa showed total villous atrophy, suggesting the diagnosis of coeliac disease. Antiendomysial IgA and anti-transglutaminase IgA antibodies were also positive. Colonoscopy was negative. An ultrasound examination of the abdomen was normal, and the spleen was within the normal range. A peripheral blood smear showed no alterations in erythrocyte morphology typical of hyposplenism due to coeliac disease. The platelet count decreased rapidly after blood transfusions, when both serum iron and ferritin levels were still below normal limits. Furthermore, we observed a significant inverse correlation between the platelet count and haemoglobin concentration (r = -0.94, P < 0.003). Platelet count and red blood cell count normalized after 2 months of a gluten-free diet; the haemoglobin concentration was also normal at this time. After 1 year of following a gluten-free diet, the patient remained well and had no complaints. There were no gastrointestinal disturbances. All haematological parameters were within normal limits. Intestinal biopsies showed normal villi and crypts without inflammatory infiltration of the lamina propria. This case shows that the association of haematological signs--extreme thrombocytosis and severe anaemia--considered in an elderly patient to be typical of myeloproliferative disorders or neoplastic conditions can be due to coeliac disease; thus, coeliac disease must also be considered among the possible diagnoses.

Clinical features of Waldenstrom macroglobulinemia in Korea.

Waldenstrom macroglobulinemia (WM) is a lymphoproliferative disorder characterized by monoclonal IgM. Its rarity makes it difficult to know the clinical manifestations and outcomes of patients with WM. The clinical records of 13 patients diagnosed with WM between 1983 and 2003 were reviewed, and 12 patients were eligible. The median age was 57 years (range, 40 to 85), and the male to female ratio was 2. B symptoms and hyperviscosity requiring plasmapheresis existed in 5 and 4 patients, respectively, at the time of diagnosis. Hepatomegaly and splenomegaly were detected in 5 and 3 patients, respectively. Sites of extranodal involvement were bone (3) and lung (1) in 3 patients. The peripheral neuropathy was complicated in 3 patients. (Ed note: check this sentence.) Cryoglobulin was checked in 6 patients and it was detected in 3 of them. The median concentration of serum IgM was 4.2 g/dL (0.7-6.2). The median albumin, hemoglobin, WBC, and platelet levels were 2.8 g/dL, 8 g/dL, 5,400/microL, and 138,000/microL, respectively. One patient had transitional cell carcinoma concomitantly, and one patient developed small cell lung cancer. Of the 11 patients receiving chemotherapy (7-chlorambucil, 2-melphalan, 1-cyclophosphamide, 1-CHOP), 4 patients showed the objective responses including 2 complete remissions, but they all ultimately relapsed. The response rate of second-line therapy was 14% (1/7). After a median follow-up of 20 months, 3 patients were still alive with disease. The median overall and progression-free survival were 24 months (95% confidence interval (CI): 5-43) and 24 months (95% CI: 8-40), respectively. The initial high levels of serum IgM and severe anemia reflect a lack of suspicion of WM at the early stage. Careful suspicion and proper diagnostic approaches will allow more patients to show an improved outcome.

[Malignant peritoneal mesothelioma].

The peritoneal mesothelioma is a rare pathology with unspecific symptoms reason to be a difficult diagnosis. We report a case of a 58 year old man with diabetes mellitus type 2, arterial hypertension and smoking; without precedent of asbestos exposure. The patient presented a one month history characterized by progressive increase of the abdominal volume and sensation of fullness; three weeks later they added breathlessness and hyporexia. The patient was in regular general condition; he was not presenting hepatic stigmas, edema or adenomegalies. The examination of thorax and cardiovascular it was normal. The abdomen distended by ascites, not painful, liver and spleen not examined. Laboratory: Hemoglobin 11,9 gr/dl, WBC 6840/mm3 Bands 1 %, lymphocytes 10 %, platelets 620000/mm3, PT 12 seconds, PTT 34 seconds, glucose 158 mg/dl, BUN 20,5 mg/ dl, creatinine 1,2 mg/dl, proteins 6,1 gr/dl, albumin 2,6 gr/dl. LDH 316 U/l, beta2microglobulin 2,2 mg/l (0.83-1.15 mg/l). HBV and HCV negative. Ca 19.9, CEA, AFP and PSA negative. Hemocultive negative. Ascitic fluid: ADA 20,3 U/l, serum-ascitic albumin gradient (SAAG) 1,1. Leukocytes 2237 cells/mm3, PMN 6 %, lymphocytes 90 %, mesothelial cells 4 %, proteins 4,6 gr/dl, albumin 2,34 gr/dl, glucose 44 mg/dl, LDH 1918 U/l. Gram and cultive: negatives. BAAR and cultive: negative . Cytology: mesothelial cells with changes of type reagent, Block cell for tumour cells: negative. Abdominal US: increased peritoneum and abundant ascitic fluid. Thoracic-abdominal CT: left side pleural effusion, severe ascites with thick epyplon. Upper GI endoscopy: moderate gastritis. Colonoscopy: two small sessile polyps in sigmoid colon. The finds of the laparoscopy were interpreted like carcinomatosis or peritoneal tuberculosis. The report of the peritoneal biopsy was informed as suggestive of undifferentiated carcinoma; the reappraisal with inmunohystochemic (calretinin +,cytokeratin +, vimentin +) indicated malignant peritoneal mesothelioma, type epithelial. The evolution was torpid. The patient was transferred to the Service of Oncology where they initiated chemotherapy with Cysplatin (CDDP) and died 20 days later. The malignant mesothelioma peritoneal is a unfrequent entity, with limited therapeutic options; generally detected late, with a palliative treatment.

Case 294.

History A 50-year-old woman presented to the emergency department of our hospital with a 2-day history of lower limb pain associated with unusual asthenia and diffuse arthralgia over the past 3 weeks. She was a native of Guinea and had lived in France for most of her life, working as a personal care assistant. Her only medical history of note was an occurrence of fetal death at 12 weeks gestation when she was 35 years old. She had bilateral lower limb swelling, without changes in skin temperature or color. All proximal and distal arterial pulses were felt. General physical examination findings were otherwise unremarkable. Her laboratory tests showed a decreased hemoglobin concentration of 8.9 g/dL (normal range, 12-16 g/dL), a decreased platelet count of 45 × 10<sup9</sup/L (normal range, 150-400 × 10<sup9</sup/L), a C-reactive protein level of 158 mg/L (normal range, <5 mg/L) and a d-dimer level of 2000 mg/L (normal range, <500 mg/L). Compression US of the lower limbs revealed bilateral calf vein thrombosis involving the fibular and posterior tibial veins. Curative anticoagulation using low-molecular-weight heparin (enoxaparin, subcutaneous injection of 100 units per kilogram of body weight twice a day) was started. The day after the start of anticoagulation therapy, the patient reported dyspnea and acute chest and abdominal pain. Her vital signs were assessed, and she had elevated blood pressure and increased heart rate and respiratory rate, but she remained afebrile. Her cardiac auscultation was unremarkable, besides tachycardia. Skin examination revealed small areas of necrosis on the fingertips of her right hand. Laboratory studies were repeated and showed an increase in serum creatinine level from a baseline value of 0.49 mg/dL to a new value of 1.01 mg/dL (normal range, 0.6-1.1 mg/dL), an apparition of low-grade proteinuria of 0.43 g per day (normal range, <0.3 g/day), and a high serum troponin level of 1066 ng/L (normal range, <14 ng/L), whereas electrocardiography showed no ST segment modification and echocardiography revealed a moderately altered left ventricular ejection fraction (45%). There was no coronary occlusion seen at emergency coronarography. Contrast-enhanced CT of the chest, abdomen, and pelvis was performed (Figs 1, 2) together with cardiac MRI (Figs 3, 4).

InternalMed_Harrison

During the prodrome, the differential diagnosis of HPS is difficult, but by the time of presentation or within 24 h thereafter, a number of diagnostically helpful clinical features become apparent. Cough usually is not present at the outset. Interstitial edema is evident on a chest x-ray. Later, bilateral alveolar edema with a central distribution develops in the setting of a normal-sized heart; occasionally, the edema is initially unilateral. Pleural effusions are often seen. Thrombocytopenia, circulating atypical lymphocytes, and a left shift (often with leukocytosis) are almost always evident; thrombocytopenia is a particularly important early clue. Hemoconcentration, hypoalbuminemia, and proteinuria should also be sought for diagnosis. Although thrombocytopenia virtually always develops and prolongation of the partial thromboplastin time is the rule, clinical evidence for coagulopathy or laboratory indications of disseminated intravascular coagulation (DIC) are found in only a

Case 294: Catastrophic Antiphospholipid Syndrome.

History A 50-year-old woman presented to the emergency department of our hospital with a 2-day history of lower limb pain associated with unusual asthenia and diffuse arthralgia over the past 3 weeks. She was a native of Guinea and had lived in France for most of her life, working as a personal care assistant. Her only medical history of note was an occurrence of fetal death at 12 weeks gestation when she was 35 years old. She had bilateral lower limb swelling, without changes in skin temperature or color. All proximal and distal arterial pulses were felt. General physical examination findings were otherwise unremarkable. Her laboratory tests showed a decreased hemoglobin concentration of 8.9 g/dL (normal range, 12-16 g/dL), a decreased platelet count of 45 × 10<sup9</sup/L (normal range, [150-400] × 10<sup9</sup/L), a C-reactive protein level of 158 mg/L (normal range, <5 mg/L), and a d-dimer level of 2000 mg/L (normal range, <500 mg/L]). Compression US of the lower limbs revealed bilateral calf vein thrombosis involving the fibular and posterior tibial veins. Curative anticoagulation using low-molecular-weight heparin (enoxaparin, subcutaneous injection of 100 units per kilogram of body weight twice a day) was started. The day after the start of anticoagulation therapy, the patient reported dyspnea and acute chest and abdominal pain. Her vital signs were assessed, and she had elevated blood pressure and increased heart rate and respiratory rate, but she remained afebrile. Her cardiac auscultation was unremarkable, besides tachycardia. Skin examination revealed small areas of necrosis on the fingertips of her right hand. Laboratory studies were repeated and showed an increase in serum creatinine level from a baseline value of 0.49 mg/dL to a new value of 1.01 mg/dL (normal range, 0.6-1.1 mg/dL), an apparition of low-grade proteinuria of 0.43 g per day (normal range, <0.3 g/ day), and a high serum troponin level of 1066 ng/L (normal range, <14 ng/L), whereas electrocardiography showed no ST segment modification and echocardiography revealed a moderately altered left ventricular ejection fraction (45%). There was no coronary occlusion seen at emergency coronarography. Contrast-enhanced CT of the chest, abdomen, and pelvis was performed (Figs 1, 2) together with cardiac MRI (Figs 3, 4).

Cutaneous manifestations of Strongyloides stercoralis hyperinfection in an HIV-seropositive patient.

A 41-year-old human immunodeficiency virus (HIV)-positive man was hospitalized with complaints of a 4-week history of nausea and vomiting, associated with decreased oral intake, and a 4-day history of frontal headache and fever. His medical history was significant for a gunshot wound to the head 3 years prior, with a residual seizure disorder. He also had two previous hospitalizations, both for culture-negative bacterial meningitis; the first episode occurred 12 months before admission and the second episode occurred 5 months later. At that time, he was found to be positive for serum antibodies against HIV and a CD4+ T-lymphocyte count of 126/mm3. He had no known drug allergies and was not receiving any medication. On admission, the patient was febrile (104.0 degrees F) and hypotensive (blood pressure, 92/40 mm Hg). Pertinent physical examination findings included cachexia with bitemporal wasting, dry mucus membranes, adherent white patches on the oral mucosa, and negative Kernig's and Brudzinski's signs. His laboratory results revealed macrocytic anemia, a decreased serum sodium of 125 mEq/L, and a normal total leukocyte count with a CD4+ T-lymphocyte count < 50/mm3. Lumbar puncture opening pressure was elevated at 160 mm Hg, and cerebrospinal fluid analysis showed an increased white cell count of 97/microL (84% lymphocytes), a decreased glucose level of 26 mg/dL, and a decreased protein level of 42 mg/dL. The patient was started on empiric therapy that included intravenous ampicillin and cefotaxime, oral Bactrim, and clotrimazole lozenges for thrush. Cerebrospinal fluid culture was positive for Escherichia coli, sensitive to cefotaxime. Two days later, the patient developed fine, erythematous, nonblanchable macules primarily on his abdomen, with minimal involvement of his thorax and back. His skin lesions remained unchanged for the next 2 weeks. Repeat lumbar puncture was performed after 14 days of cefotaxime. The cerebrospinal fluid analysis showed an elevated white cell count of 7/microL (100% lymphocytes), a decreased glucose level of 53 mg/dL, and a decreased protein level of 33 mg/dL. The cerebrospinal fluid culture was now positive for Pseudomonas aeruginosa resistant to cefotaxime. The patient was started on imipenem. On day 34 of his admission, the patient became tachypneic with complaints of dyspnea. A chest roentgenogram revealed bilateral patchy infiltrates. He was transferred to the intensive care unit and intubated for hypoxemic respiratory failure (arterial blood gas values on 6 L of oxygen: pH, 7.46; bicarbonate, 23; and oxygen saturation, 37). That evening, the patient was also noted to have diffuse petechiae and purpura in a reticulated pattern over his abdomen (Figure 1A and 1B), most heavily concentrated in the periumbilical region, extending to the axillae and upper thighs. A 3x3-mm punch biopsy from abdominal skin demonstrated Strongyloides stercoralis larvae in the dermis (Figure 2A and 2B). His sputum specimen was teeming with adult S stercoralis worms (Figure 3) and, subsequently, numerous S stercoralis larvae were observed not only from the bronchoalveolar lavage but also from the nasogastric fluid specimen. These findings confirmed the diagnosis of disseminated strongyloidiasis. On hospital day 35, the patient was doing poorly and was started on thiabendazole (1250 mg twice daily for 28 days). Nine days later, ivermectin (4.5 mg once daily for 3 days for 2 courses) was also added. He continued to clinically deteriorate. The patient died 31 days after systemic antihelminthic treatment was initiated.

Severe hemolysis with negative direct antiglobulin test: A case report.

A 49-year-old woman with type 2 diabetes mellitus (T2DM) presented to the emergency department. Her examination showed marked pallor, exhaustion, lethargy, yellowish eyes, anorexia, nausea and vomiting. Hematuria; negative standard direct antiglobulin test (DAT); normal glucose 6 phosphate dehydrogenase (G6PD); hemoglobin (Hb), 4.8 g/dl; Mean cell volume (MCV), 91fl; platelet count, 233 × 10<sup6</sup/L; Total bilirubin, 7.0 mg/dl; Glucose, 316 mg/dl; lactate dehydrogenase (LDH), 1750U/L. Undoubtedly, therapeutic panel should have been used for hemolytic anemia. Intravenous (IV) fluids and 2 units of packed cell were transfused. Methylprednisolone with rituximab were started for the patient. After 3 weeks of the patient admission, she was discharged home with stable vital signs and Hb, 10 g/dl. We concluded in the cases that presented along with a severe drop in Hb and evidence of hemolysis which non immune hemolytic anemia is excluded in spite of negative standard DAT limited transfusion besides corticosteroids combined with rituximab, could be helpful in saving the patient.

Hairy cell leukemia

Diagnosis The diagnosis of HCL may be suggested by abnormal results on a complete blood count (CBC), but additional testing is necessary to confirm the diagnosis. A CBC normally shows low counts for white blood cells, red blood cells, and platelets in HCL patients. However, if large numbers of hairy cells are in the blood stream, then normal or even high lymphocyte counts may be found. On physical examination, 80–90% of patients have an enlarged spleen, which can be massive. This is less likely among patients who are diagnosed at an early stage. Peripheral lymphadenopathy (enlarged lymph nodes) is uncommon (less than 5% of patients), but abdominal lymphadenopathy is a relatively common finding on computed tomography scans.

Possible green tea-induced thrombotic thrombocytopenic purpura.

A case of a patient who developed thrombotic thrombocytopenic purpura (TTP) after consuming a weight-loss product containing green tea is reported. A 38-year-old, 68-kg Caucasian woman arrived at the emergency department with a one-week history of malaise, fatigue, and petechiae of the skin. She had no symptoms of infection and denied illegal drug use. Her medical history included hypothyroidism, for which she was treated with levothyroxine 150 microg daily for the past four years. She reported that she had been using a green tea preparation for the two months before admission to lose body weight. The daily preparation contained 200 mg of green tea extract 5:1, equivalent to 1 g of natural green tea. On clinical examination, the patient appeared acutely ill and was afebrile, with pallor, petechiae, and purpura of the extremities. Laboratory test results at the time of admission revealed that the patient had anemia and marked thrombocytopenia. A peripheral blood smear demonstrated a feature of microangiopathic hemolytic anemia. Immunoglobulin G autoantibodies against ADAM metallopeptidase with thrombospondin type 1 motif, 13 were detected. On hospital day 3, the patient appeared confused and exhibited aphasia that was initially transient but then recurrent. Brain computerized tomography did not exhibit focal pathology. Over the next few days, her neurologic symptoms subsided and her platelet count and hematocrit value gradually increased. Plasmapheresis was performed (12 procedures). Corticosteroid treatment was also initiated. After 20 days of hospitalization, the patient was discharged. A 38-year-old woman developed TTP after consuming a weight-loss product containing green tea extract for two months.

[Laboratory findings in patients with hemorrhagic fever with renal syndrome].

To examine the frequency and distribution of hematologic and biochemical laboratory findings in 94 patients with hemorrhagic fever with renal syndrome (HFRS) in the epidemic year 2002. The following laboratory findings were retrospectively analyzed: erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), hemoglobin, hematocrit, leukocyte count and differential percentage (segmented neutrophils, band neutrophils, atypical lymphocytes), platelet count, coagulation tests, blood urea nitrogen (BUN), creatinine, urine, potassium, bilirubin (BIL), aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyltransferase (GT), alkaline phosphatase (ALP), and serum protein electrophoresis. The study included 94 HFRS patients treated at the Dr Fran Mihaljević University Hospital for Infectious Diseases in Zagreb during 2002. ESR increase, mostly mild to moderate, was found in 86.2% of study patients. Increased CRP was recorded in 98.9% of study patients, however, one-fourth had CRP higher than 100 mg/L. Leukocytosis was recorded in 38.3% (10.1 +/- 4.2 x 10(9)/L), thrombocytopenia in 89.4% patients (68.2 +/- 48.3 x 10(9)/L), and severe thrombocytopenia (x 10(9)/L) in six patients. Three patients had abnormal coagulation tests. Increased values of BUN and creatinine were recorded in more than a half of patients, while only four patients had mild hyperkalemia. Only three patinets required hemodialysis. Mildly to moderately increased values of aminotransferases (AST, ALT, GT) were observed in more than 2/3; hypoalbuminaemia in nearly 1/3, and elevated alpha-2 fraction in more than 2/3 of patients. The majority of patients had pathologic urine findings. First laboratory abnormalities were usually found between day 5 and 7 of the disease (increased CRP level, thrombocytopenia, leukocytosis, and elevation of hemoglobin and hematocrit). Biochemical abnormalities(elevation of cratinine and urea, increased levels of aminotransferases) usually occurred at the beginning of the second week, and ESR increase in the second week of disease. The majority of our patients had laboratory findings characteristic of HFRS. Thrombocytopenia and increased level of CRP were the most common laboratory findings during the first week of the disease. Renal and liver impairment occurred at the beginning of the second week of the disease.

A 47-year-old white woman with a history of stage III squamous cell carcinoma of the anus was transferred to Johns Hopkins Hospital for further evaluation of renal failure, hemolytic anemia, and thrombocytopenia. The patient was first diagnosed with squamous cell carcinoma of the anus 1 year before admission. She was treated with external beam radiation of the pelvis and two cycles of mitomycin C-based chemotherapy (a cumulative dose, 34 mg/m(2)). Her clinical course was complicated by Clostridium difficile colitis and myositis successfully treated with prednisone. Three months before admission, the patient developed dysuria. Her creatinine increased from normal to 1.7 mg/dL, and microscopic hematuria was present. A renal ultrasound and an abdominal computed tomographic scan showed no abnormalities or obstruction. One month before admission, she underwent a cystoscopy, which showed only radiation-induced changes in the bladder. Two weeks before admission, the patient became delirious and was taken to a hospital, where she was found to be anemic, with a hematocrit level of 23.7%, and thrombocytopenic with a platelet count of 110,000/mm(3). Her creatinine level was 5.9 mg/dL. Previous values of hematocrit, platelet count, and serum creatinine were normal. On admission at Johns Hopkins Hospital the patient had no complaints. She was afebrile on physical examination and had normal vital signs. Head, neck, chest, cardiovascular, and abdominal examinations were normal. There was skin pallor, but no echymoses or petechiae. She was alert and oriented with normal mental status. Her neurologic examination was normal. Laboratory data showed a white blood cell count of 6390/mm(3), a hematocrit level of 26.5%, and a platelet count of 26,000/mm(3). Her blood urea nitrogen level was 57 mg/dL, creatinine level was 4.0 mg/dL, and lactate dehydrogenase was 550 U/L (reference, 115 to 275 U/L). Urinalysis showed innumerable red blood cells and large protein. A peripheral blood smear showed fragmented red blood cells, schistocytes, no abnormal white blood cells, and few platelets. There was no radiographic or clinical evidence of relapse of her squamous cell carcinoma. What is the diagnosis?

An improbable and unusual case of thrombotic thrombocytopenia purpura.

Thrombotic thrombocytopenic purpura (TTP) is a life-threatening medical emergency which may be difficult to recognize given the wide spectrum in which it presents. A delay in treatment may be catastrophic as untreated cases of TTP have a mortality rate exceeding 90%. Given the high fatality rate of untreated TTP and its range of presenting symptoms, we present our unusual case of TTP in a post-splenectomy patient with early treatment and positive outcome. This case describes a 54-year-old female who presented with hematuria and gingival bleeding, followed by the development of a bilateral lower extremity petechial rash. Her past medical history was significant for multiple episodes of TTP, the last of which resulted in a splenectomy and a 20-year history of remission thereafter. On exam, she was alert, well appearing, and neurologically intact. Her only significant finding was a bilateral lower extremity petechial rash. Laboratory studies revealed mild anemia and thrombocytopenia, an elevated lactate dehydrogenase, and a decreased haptoglobin. Peripheral smear showed poikilocytosis, helmet cells, and schistocytes. Corticosteroid therapy was promptly initiated, her platelets were monitored closely, and she underwent urgent therapeutic plasma exchange. Due to the risk of significant morbidity and mortality that may result from delayed treatment of TTP as well as the significant variations of presentation, TTP requires a consistently high index of suspicion. Our patient suffered multiple relapses of TTP within a 30-year span, underwent splenectomy in early adulthood, and presented with atypical symptoms during her most recent relapse illustrating how persistent TTP can be as well as how unusually it may present. Providers should be aware of the vast spectrum of presentation and remember that TTP may recur following splenectomy despite prolonged remission.

A Case of Evans Syndrome and Unstable Angina.

Evans syndrome (ES) is characterized by autoimmune hemolytic anemia (AIHA) and immune-mediated thrombocytopenia. It is more common in the pediatric population than in adults. ES has been reported to be associated with thrombotic events and rarely can lead to acute coronary syndrome (ACS). There have been only a few reported cases of ACS secondary to ES. We present an interesting case of ES with unstable angina (UA) which had a limited response to oral and intravenous (IV) steroids requiring rituximab. A 64-year-old male with past medical history significant for hypertension, hyperlipidemia, diabetes mellitus and coronary artery disease, presented to the emergency room complaining of a 2-week history of chest pain, shortness of breath and hematuria. Physical examination indicated splenomegaly but was otherwise unremarkable with no petechiae or rash. Labs showed hemoglobin of 9.6 g/dL, platelet count 58 × 10<sup3</sup/µL, troponin < 0.03 ng/mL, lactic acid 2.5 mmol/L and with parameters indicative of hemolysis, evidenced by elevated lactate dehydrogenase, low haptoglobin and elevated bilirubin levels. Electrocardiography (EKG) demonstrated ST depression in leads I, aVL, V5 - V6 and T wave inversions in lead III and aVL, which were new compared to previous EKG. Peripheral blood smear indicated spherocytes. Direct antiglobulin test was positive for immunoglobulin G (IgG). Patient was admitted for ES and initially treated with oral prednisone 80 mg daily. He was also diagnosed with UA thought to be possibly secondary to ES. He then underwent cardiac stress test which showed mild reversible inferior apical ischemia. Cardiac catheterization revealed 95% stenosis of proximal left circumflex artery requiring single drug eluding stent placement and dual antiplatelet therapy. Patient continued to have anemia despite blood transfusions, although platelet count improved. Prednisone was transitioned to high-dose IV dexamethasone, and patient was also started on rituximab which resulted in stabilization of anemia. The presentation of ES with ACS is a rare occurrence. ACS can be challenging to manage as stent placement may be required followed by dual antiplatelet therapy. Treatment of ES involves steroids followed by rituximab, IV immunoglobulin (IVIG) or splenectomy for non-responsive cases. Early intervention and management can prevent mortality and morbidity.

Efficient diagnosis of thrombocytopenia.

Thrombocytopenia may be a benign, incidental finding in an asymptomatic patient or the sign of a potentially life-threatening disorder. The history, physical examination and peripheral blood smear can assist the physician in determining the diagnosis and treatment. After the initial blood count is repeated to help eliminate the possibility of laboratory error, a thorough history, complete physical examination, complete blood cell count and appropriate laboratory tests are required. The history may reveal related illnesses, risk factors such as infection or drug use, or a family history suggestive of congenital thrombocytopenia. The physical examination should concentrate on the lymphatic and hepatosplenic systems, with the physician looking for jaundice, fever or petechiae. With the review of a complete blood cell count and a peripheral smear examination, the initial work-up is completed and may prevent additional, unnecessary testing. Etiology-specific tests follow if needed. Serious spontaneous bleeding is usually a risk only in patients with platelet levels under 20,000 per mm3.

Amegakaryocytic thrombocytopenia with a positive direct Coombs' test.

A 50-year-old previously well woman developed a sudden onset of ecchymoses and petechiae over the trunk and extremities and gum bleeding. There was no history of alcohol use or drug ingestion. Physical examination was normal except for the ecchymoses, purpuric rash, and gum bleeding. Complete blood count showed Hb 8.0 g/dl, leucocytes 10.9 x 10(9)/L with a normal differential, platelets 8 x 10(9)/L and reticulocytes, 4%. The bone marrow was normocellular and showed absence of megakaryocytes; there was normoblastic erythroid hyperplasia and the myelopoiesis was normal. The direct Coombs test result was positive. There was poor response to treatment with prednisone and bolus doses of vincristine. Therapy with danazol resulted in the complete normalization of the blood counts, and the patient remains well 32 months after diagnosis and is currently taking 100 mg danazol daily.

[Adult-onset Still-disease: survey of 18 cases].

Adult onset Still's disease (juvenile rheumatoid arthritis with septic appearance) is rare, leading to clinical signs similar to those seen in bacterial sepsis, lymphomas, rheumatological, or systemic autoimmune diseases. The disease can present with a fever of unknown origin, and can cause difficulties in the diagnosis. It is based upon, partly, the exclusion of other diseases and on diagnostic criteria. Its characteristic feature is the rise of acute phase proteins. Exanthemata are temporary. The basis of treatment is immunosuppression, however relapses can occur. The aim of the authors was to evaluate on the most characteristic clinical signs and laboratorical data of their patients, and to examine the revealing parameters of the course of the disease. Retrospective epidemiological survey of the data obtained from 18 patients. The characteristic signs of the disease were, fever, sore throat, arthritis, joint pain, exanthemata, hepato-splenomegaly, lymphadenomegaly, pleurisy. The typical laboratorical data were: elevated CRP, low PCT, negative Waaler-Rose and ANA test, low serum iron level, leukocytosis, thrombocytosis, elevated alkalic phosphatase activity, high LDH, positive bone scintigraphy. The fever was steroid dependent. Generally, the illness was recognised after 2-3 months, and relapses were frequent. Still's disease has an important role in the differential diagnosis of fever of unknown origin. The diagnosis is based upon the evaluation of clinical signs and laboratorical data together. Prolonged immunosuppressive therapy is required.


The trick to this question is that there are 8 cervical roots for 7 vertebrae, therefore the C1 root exits ABOVE the atlas, and so on up to C8 which exits BETWEEN C7 and T1. The thoracic roots come out respectively below the vertebra with their same numbering (nerve T1 under T1, T2 under T2, etc.). Therefore, between C4 and C5 the 5th cervical nerve exits, and between T4 and T5 the 4th thoracic nerve exits. The correct answer is 4.

The trick to this question is that there are 8 cervical roots for 7 vertebrae, therefore the C1 root exits ABOVE the atlas, and so on up to C8 which exits BETWEEN C7 and T1. The thoracic roots come out respectively below the vertebra with their same numbering (nerve T1 under T1, T2 under T2, etc.). Therefore, between C4 and C5 the 5th cervical nerve exits, and between T4 and T5 the 4th thoracic nerve exits. [HIDDEN]

A 42-year-old woman with breast cancer has metastases at the level of the intervertebral foramina between the 4th and 5th cervical vertebrae and between the 4th and 5th thoracic vertebrae. Which spinal nerves will be injured?

Fourth cervical and fourth thoracic nerves.

Fifth cervical and fifth thoracic nerves.

Fourth cervical and fifth thoracic nerves.

Fifth cervical and fourth thoracic nerve.

Third cervical and fourth thoracic nerve.

Thoracic vertebrae

Third thoracic vertebra (T3) The thoracic spinal nerve 3 (T3) passes out underneath it. Fourth thoracic vertebra (T4) The fourth thoracic vertebra, together with the fifth, is at the same level as the sternal angle. The thoracic spinal nerve 4 (T4) passes out underneath it. Fifth thoracic vertebra (T5) The fifth thoracic vertebra, together with the fourth, is at the same level as the sternal angle. The human trachea divides into two main bronchi at the level of the 5th thoracic vertebra, but may also end higher or lower, depending on breathing. The thoracic spinal nerve 5 (T5) passes out underneath it. Sixth thoracic vertebra (T6) The thoracic spinal nerve 6 (T6) passes out underneath it. Seventh thoracic vertebra (T7) The thoracic spinal nerve 7 (T7) passes out underneath it. Eighth thoracic vertebra (T8) The eighth thoracic vertebra is, together with the ninth thoracic vertebra, at the same level as the xiphisternum.

Cervical spinal nerve 5

The cervical spinal nerve 5 (C5) is a spinal nerve of the cervical segment. It originates from the spinal column from above the cervical vertebra 5 (C5). It contributes to the phrenic nerve, long thoracic nerve, and dorsal scapular nerve before joining cervical spinal nerve 6 to form the upper trunk, a trunk of the brachial plexus, which then forms the lateral cord, and finally the musculocutaneous nerve. Additional Images References Spinal nerves

Variations of the ventral rami of the brachial plexus.

We studied the variations in the ventral rami of 152 brachial plexuses in 77 Korean adults. Brachial plexus were composed mostly of the fifth, sixth, seventh and eighth cervical nerves and the first thoracic nerve (77.0%). In 21.7% of the cases examined, the fourth, fifth, sixth, seventh and eighth cervical and the first thoracic nerves contributed to the plexus. A plexus composed of the fourth, fifth, sixth, seventh and eighth cervical and the first and second thoracic nerves, and a plexus composed of the fifth, sixth, seventh eighth cervical nerves were also observed. The plexuses were classified into three groups according to cephalic limitation, and the plexus of group 2 in which the whole fifth cervical nerve enters the plexus, were observed the most frequent. The average diameter of the sixth and the seventh cervical ventral rami of the plexus was greatest and that of the fifth cervical was smallest. The largest nerve entering the plexus was the sixth or the seventh cervical nerve in about 79% of cases. The dorsal scapular nerve originated from the fifth cervical ventral ramus in 110 cases (75.8%). The long thoracic nerve was formed by joining of roots from the fifth, sixth, and seventh cervical nerves in 76.0% of cases. Also, a branch to the phrenic nerve, the suprascapular nerve, a nerve to the pectoralis major muscle and a nerve to the subscapular muscle arising from the ventral rami of the plexus were observed.

Spinal nerve

The cervical nerves innervate the sternohyoid, sternothyroid and omohyoid muscles. A loop of nerves called ansa cervicalis is part of the cervical plexus. Thoracic nerves The thoracic nerves are the twelve spinal nerves emerging from the thoracic vertebrae. Each thoracic nerve T1 -T12 originates from below each corresponding thoracic vertebra. Branches also exit the spine and go directly to the paravertebral ganglia of the autonomic nervous system where they are involved in the functions of organs and glands in the head, neck, thorax and abdomen. Anterior divisions: The intercostal nerves come from thoracic nerves T1-T11, and run between the ribs. At T2 and T3, further branches form the intercostobrachial nerve. The subcostal nerve comes from nerve T12, and runs below the twelfth rib.

Inferior cervical ganglion

The inferior cervical ganglion is situated between the base of the transverse process of the last cervical vertebra and the neck of the first rib, on the medial side of the costocervical artery. Its form is irregular; it is larger in size than the middle cervical ganglion, and is frequently fused with the first thoracic ganglion, under which circumstances it is then called the "stellate ganglion." Structure It is connected to the middle cervical ganglion by two or more cords, one of which forms a loop around the subclavian artery and supplies offsets to it. This loop is named the ansa subclavia (Vieussenii). The ganglion sends gray rami communicantes to the seventh and eighth cervical nerves.

The communicating branch of the 4th cervical nerve to the brachial plexus: the double constitution, anterior and posterior, of its fibers.

Twenty-four adult cadavers (48 sides) were used to investigate the incidence of a branch arising from the ventral ramus of the fourth cervical nerve (C4) with the phrenic nerve and subsequently joining the brachial plexus. Six brachial plexuses with spinal cords and phrenic nerves were dissected under a surgical microscope to investigate localization of fibers contained in the C4 branch to the brachial plexus. The incidence of the C4 branch was 23% (11/48 sides). Branches from C4 to the brachial plexus divided into anterior and posterior divisions on four sides (4/6 sides). On two sides, the branch did not divide but consisted entirely of an anterior division (2/6 sides). In the brachial plexus, anterior division fibers of the C4 branch were intertwined with fibers from the anterior divisions of the ventral rami of the fifth and sixth cervical nerves. They then passed to the suprascapular nerve and the anterior division of the superior trunk (6/6 sides). On the other hand, posterior division fibers of the C4 branch were intertwined with fibers from the posterior divisions of the ventral rami of the fifth and sixth cervical nerves. They then passed to the suprascapular nerve (2/6 sides) and the posterior division of the superior trunk (4/6 sides). The anterior division of the C4 branch received fibers from the ventral rootlets of the entire fourth cervical segment, whereas the posterior division received fibers from the ventral rootlets of the caudal half of the fourth cervical segment only. The fact that the suprascapular nerve received fibers from both the anterior and posterior divisions of the C4 branch was considered to support our claim that the human suprascapular nerve belongs to both the anterior and posterior divisions of the brachial plexus.

Cervicoaxillary canal

The cervicoaxillary canal is the passageway that extends between the neck and the upper extremities through which the long thoracic nerve and other structures pass. Its structure is defined by being posteriorly bordered by the scapula, anteriorly by the clavicle, and medially by the first rib. The long thoracic nerve traverses this passageway in addition to axillary blood vessels and the brachial plexus. This complex nerve network arises in the neck from the fifth, sixth, seventh and eighth cervical roots, C5, C6, C7 and C8, together with the first thoracic root, T1. It then enters the canal in the axilla. References Skeletal system Upper limb anatomy Shoulder Nerves

Cervical enlargement

The cervical enlargement corresponds with the attachments of the large nerves which supply the upper limbs. Located just above the brachial plexus, it extends from about the fifth cervical to the first thoracic vertebra, its maximum circumference (about 38 mm.) being on a level with the attachment of the sixth pair of cervical nerves. The reason behind the enlargement of the cervical region is because of the increased neural input and output to the upper limbs. An analogous region in the lower limbs occurs at the lumbar enlargement. References External links - "Vertebral Canal and Spinal Cord: Regions of the Spinal Cord" - "Spinal Cord, Fetus, Posterior View" Nerves of the upper limb

Outline of the human nervous system

Intermediate nerve Greater petrosal nerve Chorda tympani (also in trigeminal? redundancy?) Vestibulocochlear nerve Vestibular nerve Cochlear nerve Glossopharyngeal nerve Tympanic nerve Tympanic plexus Lesser petrosal nerve Vagus nerve Superior laryngeal nerve Recurrent laryngeal nerve Accessory nerve Hypoglossal nerve Spinal nerves Cervical nerves Suboccipital nerve Greater occipital nerve Third occipital nerve Cervical plexus Ansa cervicalis Lesser occipital nerve Great auricular nerve Transverse cervical nerve Supraclavicular nerves Phrenic nerve Brachial plexus Supraclavicular part Dorsal scapular nerve Long thoracic nerve Subclavian nerve Suprascapular nerve Subscapular nerves Lower subscapular nerve Upper subscapular nerve Thoracodorsal nerve Medial pectoral nerve Lateral pectoral nerve Infraclavicular part Musculocutaneous nerve Medial cutaneous nerve of arm Medial cutaneous nerve of forearm Median nerve Ulnar nerve Radial nerve Axillary nerve Thoracic nerves Lumbar nerves

The vertebral level of origin of spinal nerves in the rat.

Several dissections were performed to determine the level of spinal cord termination and the vertebral level at which the dorsal and ventral roots of spinal nerves C1-S4 emerged from the spinal cord in the rat. These levels of emergence were then compared to the level of exit from the vertebral canal. The dissections demonstrated that the effect of differential growth between spinal cord and vertebral column begins in the lower cervical region and becomes progressively more pronounced throughout thoracic and lumbar levels. The disparity between the vertebral level of emergence of spinal roots from the spinal cord and their level of exit via intervertebral foramina was found to be considerably larger than was previously reported by Greene ('68). It was further noted that the spinal cord terminated at the level of the intervertebral disc between the third and fourth lumbar vertebrae, not between the fourth and fifth lumbar vertebrae as reported by Greene ('68).

Posterior thoracic nucleus

The posterior thoracic nucleus, (Clarke's column, column of Clarke, dorsal nucleus, nucleus dorsalis of Clarke) is a group of interneurons found in the medial part of lamina VII, also known as the intermediate zone, of the spinal cord. It is mainly located from the cervical vertebra C7 to lumbar L3-L4 levels and is an important structure for proprioception of the lower limb. Anatomy It occupies the medial part of the base of the posterior grey column and appears on the transverse section as a well-defined oval area. It begins caudally at the level of the second or third lumbar nerve, and reaches its maximum size opposite the twelfth thoracic nerve. Above the level of the eight thoracic nerve its size diminishes, and the column ends opposite the last cervical or first thoracic nerve.

Intertransversarii

There are seven pairs of these muscles, the first pair being between the atlas and axis, and the last pair between the seventh cervical and first thoracic vertebræ. Thoracic In the thoracic region they are present between the transverse processes of the lower three thoracic vertebrae, and between the transverse processes of the last thoracic and the first lumbar. These are called the thoracic intertransversarii and are supplied by the posterior rami of the spinal nerves. Lumbar In the lumbar region they are arranged in pairs, on either side of the vertebral column, one set occupying the entire interspace between the transverse processes of the lumbar vertebrae, are the lateral lumbar intertransversarii. the other set, the medial lumbar intertransversarii, passing from the accessory process of one vertebra to the mammillary of the vertebra below.

Anatomy_Gray

Nomenclature of spinal nerves There are approximately 31 pairs of spinal nerves (Fig. 2.62), named according to their position with respect to associated vertebrae: eight cervical nerves—C1 to C8, twelve thoracic nerves—T1 to T12, five lumbar nerves—L1 to L5, five sacral nerves—S1 to S5, one coccygeal nerve—Co. The first cervical nerve (C1) emerges from the vertebral canal between the skull and vertebra CI (Fig. 2.63). Therefore cervical nerves C2 to C7 also emerge from the vertebral canal above their respective vertebrae. Because there are only seven cervical vertebrae, C8 emerges between vertebrae CVII and TI. As a consequence, all remaining spinal nerves, beginning with T1, emerge from the vertebral canal below their respective vertebrae.

Anatomical variations of the spinal accessory nerve and its relevance to level IIb lymph nodes.

This study was conducted to identify anatomical variations of the spinal accessory nerve (SAN) in the upper neck, the landmark of the anterior and inferior border of level IIb, and to evaluate the nerve's effect on the border and the number of lymph nodes (LNs) in level IIb. Case series with planned data collection. A total of 181 neck dissections (NDs) were prospectively enrolled in this study. The relation between the SAN and adjacent structures (internal jugular vein [IJV], sternocleidomastoid muscle [SCM], cervical plexus) and the number of LNs in level IIb was investigated. The SAN crossed the IJV ventrally in 72 cases (39.8%) and dorsally in 104 cases (57.4%), and passed through the IJV in five cases (2.8%). The SAN ran along the inner surface of the SCM and sent branches to the SCM without penetration of the muscle in 83 cases (45.9%), whereas in 98 cases (54.1%) the nerve sent branches to the SCM by penetration. Cervical plexus contribution to the SAN was seen from C2 in 96 cases (53.1%), C2 and C3 in 69 cases (38.1%), and C3 in 16 cases (8.8%). The mean number of LNs of level IIa and level IIb was 6.5 and 8.2 in cases in which the SAN crossed the IJV ventrally, and 6.8 and 5.4 in dorsally crossing cases. LNs included in the neck level IIb in ventrally crossing SAN cases were significantly larger than the dorsally crossing cases (P < 0.05). Our results may help to minimize the incidence of injuring the SAN in the upper neck during ND. Neck level IIb would contain more LNs if the course of the nerve leans toward the ventral side.

Longus colli muscle

It is broad in the middle, narrow and pointed at either end, and consists of three portions, a superior oblique, an inferior oblique, and a vertical. The superior oblique portion arises from the anterior tubercles of the transverse processes of the third, fourth, and fifth cervical vertebrae and, ascending obliquely with a medial inclination, is inserted by a narrow tendon into the tubercle on the anterior arch of the atlas. The inferior oblique portion, the smallest part of the muscle, arises from the front of the bodies of the first two or three thoracic vertebrae; and, ascending obliquely in a lateral direction, is inserted into the anterior tubercles of the transverse processes of the fifth and sixth cervical vertebrae. The vertical portion arises, below, from the front of the bodies of the upper three thoracic and lower three cervical vertebrae, and is inserted into the front of the bodies of the second, third, and fourth cervical vertebrae.

Four cases of spinal accessory nerve passing through the fenestrated internal jugular vein.

Neck dissection (ND) is an important technique for the treatment of cervical lymph node metastasis in patients with head and neck cancer. Since the introduction of functional ND (FND), various modifications have been made to reduce the adverse effects of radical ND. Recently, many investigators have documented cases of FND with preservation of the spinal accessory nerve (SAN) and/or the sternocleidomastoid muscle, which have contributed to improve the quality of life following ND. For this type of ND, special attention must be paid to identify the SAN and the internal jugular vein (IJV). We performed 123 NDs over 2 years at the Department of Otolaryngology, Head and Neck Surgery, Kobe University Hospital. We collected data of all patients who underwent NDs by retrospectively reviewing the relevant hospital medical records and operative notes. In 4 out of 123 NDs (3.3%), an anomaly of the SAN passing through the fenestrated IJV was observed. Although this anomaly is rare, head and neck surgeons should be aware of this anomalous relationship between the SAN and the IJV in order to avoid accidental injury to these structures during ND.

Vertebral artery

The vertebral artery may be divided into four parts: The first (preforaminal) part runs upward and backward between the Longus colli and the Scalenus anterior. In front of it are the internal jugular and vertebral veins, and it is crossed by the inferior thyroid artery; the left vertebral is crossed by the thoracic duct also. Behind it are the transverse process of the seventh cervical vertebra, the sympathetic trunk and its inferior cervical ganglion The second (foraminal) part runs upward through the transverse foramina of the C6 to C2 vertebrae, and is surrounded by branches from the inferior cervical sympathetic ganglion and by a plexus of veins which unite to form the vertebral vein at the lower part of the neck. It is situated in front of the trunks of the cervical nerves, and pursues an almost vertical course as far as the transverse process of the axis.

Vertebral column

Lateral surfaces The sides of the vertebral column are separated from the posterior surface by the articular processes in the cervical and thoracic regions and by the transverse processes in the lumbar region. In the thoracic region, the sides of the bodies of the vertebrae are marked in the back by the facets for articulation with the heads of the ribs. More posteriorly are the intervertebral foramina, formed by the juxtaposition of the vertebral notches, oval in shape, smallest in the cervical and upper part of the thoracic regions and gradually increasing in size to the last lumbar. They transmit the special spinal nerves and are situated between the transverse processes in the cervical region and in front of them, in the thoracic and lumbar regions.

Anatomy, Head and Neck, Posterior Cervical Region -- Nerves

The phrenic nerve can be found deep to the posterior triangle within the prevertebral fascia as it runs along the anterior surface of the anterior scalene muscle. The spinal nerves of the fifth cervical vertebra through the first thoracic vertebra form the roots and trunks of the brachial plexus, which can also appear within the prevertebral fascia between the anterior and middle scale muscles. [11]

Semispinalis muscles

The semispinalis cervicis (or semispinalis colli), arises by a series of tendinous and fleshy fibers from the transverse processes of the upper five or six thoracic vertebrae, and is inserted into the cervical spinous processes, from the axis to the fifth cervical vertebrae inclusive. The semispinalis cervicis is thicker than the semispinalis thoracis. The fasciculus connected with the axis is the largest, and is chiefly muscular in structure. The semispinalis thoracis (or semispinalis dorsi) muscle consists of thin, narrow, fleshy fasciculi, interposed between tendons of considerable length. It arises by a series of small tendons from the transverse processes of the sixth to the tenth thoracic vertebrae, and is inserted, by tendons, into the spinous processes of the upper four thoracic and lower two cervical vertebrae. The semispinalis muscles are innervated by the dorsal rami of the cervical spinal nerves. See also List of muscles of the human body Additional images

The superficial branches of the cervical plexus that supply cutaneous sensation to the skin overlying the cervical region emerge from the posterior aspect of the sternocleidomastoid muscle near its midpoint, at a site known as the nerve point of the neck. The anterior rami of the spinal nerves pierce the investing fascia and split to form four cutaneous nerves that run deep to the platysma. The lesser occipital nerve forms from the second cervical spinal nerve and ascends posterior to the sternocleidomastoid to innervate the skin of the scalp and neck posterior to the ear. The greater auricular nerve forms from the second and third cervical spinal nerves and ascends on the anterior surface of the sternocleidomastoid to innervate the skin over the mastoid and parotid region inferior to the ear. The transverse cervical nerve forms from the second and third cervical spinal nerves and crosses horizontally over the sternocleidomastoid to innervate the anterior aspect of the neck. The supraclavicular nerve forms from the third and fourth cervical spinal nerves and descends across the surface of the investing fascia over the posterior triangle as it branches widely to innervate the skin over the clavicle and first two ribs. [10]

Anatomy_Gray

Middle cervical ganglion. A second ganglion inferior to the superior cervical ganglion along the course of the sympathetic trunk (the middle cervical ganglion) is encountered at about the level of cervical vertebra CVI (Figs. 8.193 and 8.194). Branches from this ganglion pass to: cervical spinal nerves C5 and C6 through gray rami communicantes, and the heart as middle cardiac nerves. Inferior cervical ganglion. At the lower end of the cervical part of the sympathetic trunk is another ganglion (the inferior cervical ganglion), which becomes very large when it combines with the first thoracic ganglion and forms the cervicothoracic ganglion (stellate ganglion). The inferior cervical ganglion (Figs. 8.193 and 8.194) is anterior to the neck of rib I and the transverse process of cervical vertebra CVII, and posterior to the first part of the subclavian artery and the origin of the vertebral artery.

Cervical vertebrae

Vertebra prominens The vertebra prominens, or C7, has a distinctive long and prominent spinous process, which is palpable from the skin surface. Sometimes, the seventh cervical vertebra is associated with an abnormal extra rib, known as a cervical rib, which develops from the anterior root of the transverse process. These ribs are usually small, but may occasionally compress blood vessels (such as the subclavian artery or subclavian vein) or nerves in the brachial plexus, causing pain, numbness, tingling, and weakness in the upper limb, a condition known as thoracic outlet syndrome. Very rarely, this rib occurs in a pair. The long spinous process of C7 is thick and nearly horizontal in direction. It is not bifurcated, and ends in a tubercle that the ligamentum nuchae attaches to. This process is not always the most prominent of the spinous processes, being found only about 70% of the time, C6 or T1 can sometimes be the most prominent.

Interspinales muscles

The interspinales are short muscle fascicles, found in pairs between the spinous processes of the contiguous vertebrae, one on either side of the interspinal ligament. In the cervical region the cervical interspinales are most distinct, and consist of six pairs, the first being situated between the axis and third vertebra, and the last between the seventh cervical and the first thoracic. They are small narrow bundles, attached, above and below, to the apices of the spinous processes. In the thoracic region the thoracic interspinales are found between the first and second vertebrae, and sometimes between the second and third, and between the eleventh and twelfth. In the lumbar region there are four pairs of lumbar interspinales in the intervals between the five lumbar vertebrae. There is also occasionally one between the last thoracic and first lumbar, and one between the fifth lumbar and the sacrum.

Neurology_Adams

the neck, third cervical; the epaulet area, fourth cervical; the deltoid area, fifth cervical; the radial forearm and thumb, sixth cervical; the index and middle fingers, seventh cervical; the little finger and ulnar border of hand and forearm, eighth cervical–first thoracic; the nipple, fourth to fifth thoracic; the umbilicus, tenth thoracic; the groin, first lumbar; the medial side of the knee, third lumbar; the medial malleolus, the fourth lumbar; the great toe, fifth lumbar; the little toe, first sacral; the back of the thigh and lateral foot, second sacral; and the genitoanal zones, third, fourth, and fifth sacral segments.

Cervical ganglia

The cervical ganglia are paravertebral ganglia of the sympathetic nervous system. Preganglionic nerves from the thoracic spinal cord enter into the cervical ganglions and synapse with its postganglionic fibers or nerves. The cervical ganglion has three paravertebral ganglia: superior cervical ganglion (largest) - adjacent to C2 & C3; postganglionic axon projects to target: (heart, head, neck) via "hitchhiking" on the carotid arteries middle cervical ganglion (smallest) - adjacent to C6; target: heart, neck inferior cervical ganglion. The inferior ganglion may be fused with the first thoracic ganglion to form a single structure, the stellate ganglion. - adjacent to C7; target: heart, lower neck, arm, posterior cranial arteries Nerves emerging from cervical sympathetic ganglia contribute to the cardiac plexus, among other things. Unlike all other ganglia, the medial branches of the cervical ganglia are 95% postganglionic axons. Additional images References

Vertebra

The spinous process on C7 is distinctively long and gives the name vertebra prominens to this vertebra. Also a cervical rib can develop from C7 as an anatomical variation. The term cervicothoracic is often used to refer to the cervical and thoracic vertebrae together, and sometimes also their surrounding areas. Thoracic vertebrae The twelve thoracic vertebrae and their transverse processes have surfaces that articulate with the ribs. Some rotation can occur between the thoracic vertebrae, but their connection with the rib cage prevents much flexion or other movement. They may also be known as "dorsal vertebrae" in the human context. The vertebral bodies are roughly heart-shaped and are about as wide anterio-posteriorly as they are in the transverse dimension. Vertebral foramina are roughly circular in shape. The top surface of the first thoracic vertebra has a hook-shaped uncinate process, just like the cervical vertebrae.

Cervical spinal nerve 3

The cervical spinal nerve 3 (C3) is a spinal nerve of the cervical segment. It originates from the spinal column from above the cervical vertebra 3 (C3). References Spinal nerves

Spinal cord

Within the Central Nervous System (CNS), nerve cell bodies are generally organized into functional clusters, called nuclei. Axons within the CNS are grouped into tracts. There are 31 spinal cord nerve segments in a human spinal cord: 8 cervical segments forming 8 pairs of cervical nerves (C1 spinal nerves exit the spinal column between the foramen magnum and the C1 vertebra; C2 nerves exit between the posterior arch of the C1 vertebra and the lamina of C2; C3–C8 spinal nerves pass through the IVF above their corresponding cervical vertebrae, with the exception of the C8 pair which exit between the C7 and T1 vertebrae) 12 thoracic segments forming 12 pairs of thoracic nerves 5 lumbar segments forming 5 pairs of lumbar nerves 5 sacral segments forming 5 pairs of sacral nerves 1 coccygeal segment

Neuromere

Spinal Cord Anatomy Spinal segments are the part of the spinal cord, from which ventral and dorsal roots exit to form a specific pair of spinal nerves. The spinal chord is not segmented itself, it is only made into segments by the spinal nerves as they leave. 31 deferent segments exists in a human spinal cord: 8 cervical segments Cervical nerves exit above C1 segment and below C1-C7. Note that this creates 8 nerves and segments corresponding to only 7 cervical vertebra. 12 thoracic segments Nerves exit below T1-T12. 5 lumbar segments Nerves exit below L1-L5. 5 sacral segments Nerves exit below S1-S5. 1 coccygeal segment Originally, during development there are two segments S1 and S2 which fuse. The nerves in this case exit at the coccyx. In more detail

Thoracic vertebrae

Individual thoracic vertebrae First thoracic vertebra (T1) The first thoracic vertebra has, on either side of the body, an entire articular facet for the head of the first rib, and a demi-facet for the upper half of the head of the second rib. The body is like that of a cervical vertebra, being broad, concave, and lipped on either side. The superior articular surfaces are directed upward and backward; the spinous process is thick, long, and almost horizontal. The transverse processes are long, and the upper vertebral notches are deeper than those of the other thoracic vertebrae. The thoracic spinal nerve 1 (T1) passes out underneath it. Second thoracic vertebra (T2) The thoracic spinal nerve 2 (T2) passes out underneath it. The second thoracic vertebra is larger than the first thoracic vertebra Third thoracic vertebra (T3) The thoracic spinal nerve 3 (T3) passes out underneath it.

The eleventh nerve in radical neck surgery.

The greatest morbidity associated with the radical neck dissection has been the "shoulder syndrome" due to the sacrifice of the spinal accessory nerve. Despite the fact that the XIth nerve can be spared by a careful dissection of the postcervical triangle, to do so remains a controversial issue. The 125 radical neck dissections performed at the University of Wisconsin Clinical Science Center from 1970 through 1975 were carefully evaluated to determine the incidence of recurrent tumor in the operated-on neck. In 60 cases the spinal accessory nerve was resected with the neck specimen, and in 65 cases the nerve was preserved. A second study was then undertaken involving 245 neck dissections performed from 1975-1978 in the Wisconsin Head and neck Cancer Control Network Hospitals. In 69 instances the spinal accessory nerve was spared. The total number of neck dissections (370 cases) from both studies were analyzed. The overall rate for recurrent tumor in the neck with the classical neck dissection was 12%. When the spinal accessory nerve was spared, the recurrent rate was 6%. On the basis of these observations we propose that the classical neck dissection can be modified to preserve the spinal accessory nerve without jeopardizing the chances for a cure in elective neck dissections and selected therapeutic neck dissections.