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Deep venous thrombosis and splenic infarction — What diagnosis?
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Abstracts
f.e.). Paraneoplastic RS3PE usually presents a worse respond to corticoids, although improvement was observed in our case. Finally, it is necessary to remember that, especially in older patients with pain and edema in hands and/or feet, this syndrome should be considered.
doi:10.1016/j.ejim.2013.08.322
ID: 474 Destructive arthropathy of the shoulder in siringomielia. Report of a case G. Lopez-Barros, P. Quiroga, A. Cadavid, A. Bravo, L. Alvarez Internal Medicine Division, Complejo Hospitalario Universitario de Ourense, Ourense, Spain A 44-year-old-man was seen in an outpatient internal medicine clinic because of severe pain and functional impotence in his right shoulder and arm in the last 3 months. On examination there was mild terdeness at the right shoulder and massive swelling of the shoulder, arm, and right chest area. The patient had previously been diagnosed of syringomyelia at the age of 20 years due to type I Arnold–Chiari malformation, which caused a suspended hypoesthesia, loss of strength and areflexia of his arms. A cysto-subdural shunt was performed when he was 23 years old. At 37 years of age, decompressive craniectomy suboccipital and occipital-cervical duraplasty was performed. The patient was treated with tramadol, clonazepam and duloxetine. An elemental analytical study of blood and urine showed no significant alterations. ESR and tumoral markers were within normal limits. A thoracic and abdominal CT scan revealed no anatomic abnormalities. Radiological examination of the affected shoulder showed massive soft tissue swelling and absence of the head and humeral metaphysis, reabsorption of the glenoid, and scattered areas of ectopic ossification. Magnetic resonance imaging revealed the presence of a mantle of polilobulated tissue at the shoulder area, and absence of the humeral head. The final diagnosis was neuropathic arthropathy secondary to syringomyelia. We highlight this rare and agressive arthropathy as a possibility during the evolution of this neurological disease, which can present a difficult differential diagnosis with neoplastic or infectious diseases.
doi:10.1016/j.ejim.2013.08.323
ID: 476 Inappropriate secretion of antidiuretic hormone syndrome in a patient with systemic lupus erythematosus: What are the causes? N. Essid, O. Harzallah, R. Klii, D. Braham, M. Kechida, S. Mahjoub Internal Medicine Department, Fattouma Bourguiba Hospital, Monastir, Tunisia
Introduction: The syndrome of inappropriate antidiuretic hormone (ADH) secretion (SIADH) is defined by the hyponatremia and hypo-osmolality resulting from inappropriate, continued secretion or action of the hormone despite normal or increased plasma volume, which results in impaired water excretion. Causes of SIADH are numerous and variable. Reports of SIADH in patients with systemic lupus erythematosus (SLE) are scarce. We report here a case of SIADH in a young female lupic patient and try to analyze its possible causes. Observation: A 23 year old female patient with a 1 year
pernicious anemia history was admitted in our department for fever, repeated convulsions and an agitation state. Clinical exam and biological tests allowed retaining SLE diagnosis according to ACR criteria: mouth ulcers, convulsion, leuco-lymphopenia, positive, antinuclear, anti-DNA, and anticardiolipin antibodies. Brain magnetic resonance imaging showed vasculitis lesions with multiple left middle cerebral artery strokes. The association of cerebral strokes to anticardiolipin antibodies in a lupic patient led to an associated antiphospholipid antibody syndrome diagnosis. The patient was treated by high doses of steroids, intravenous cyclophosphamide, anticoagulant and anticonvulsive agents (sodium valproate and phenobarbital). The evolution was initially favorable but 3 days later, fever and convulsions relapsed. Blood cultures were positive to Salmonella. Biochemical tests showed severe hyponatremia (118 mmol/l), a plasmatic hypo-osmolality and a natriuresis increase. The patient was treated by intravenous antibiotherapy and a fluid restriction with syndrome hypertonic saline serum perfusion. However, the evolution was rapidly unfavorable and the patient deceased. Discussion: SLE doesn't seem to be the cause of SIADH. Our patient had multiple possible causes that could explain this SIADH complicated of severe hyponatremia: treatment with cyclophosphamide and/or phenobarbital, neurological lesions and infection.
doi:10.1016/j.ejim.2013.08.324
ID: 486 Deep venous thrombosis and splenic infarction — What diagnosis? M.J. Ferreira da Silva, A. Lages, R. Pinto Alves, I. Trindade, C. Rodrigues, F. Nunes Gonçalves Internal Medicine, Hospital de Braga, Braga, Portugal
Background: Hypercoagulative status is defined by a tendency to venous or arterial thrombus formation. In 1845 Virchow claimed 3 responsible facts that appear to be relevant: hypercoagulability, vascular lesion and stasis. Secondary hypercoagulability can lead to thrombotic events due to multifactorial pathophisiological mechanisms in which etiology is frequently not clear. Methods: The authors present a clinical case of a 43 year-old male, with smoking habits and history of epilepsy and thrombophlebitis, that presented in the emergency room with right gastrocnemius pain, redness and swelling, related to diminished ability to walk. The analysis showed anemia, thrombocytopenia and altered coagulation, which lead to the patient admission in the medical ward to be studied. Results: After evaluation, it was stated that a deep venous thrombosis of right femoral-popliteal vein and a 2.5 cm splenic infarction showed in the angio-CT. The analytical study revealed: microcytic and normochromic anemia (11.9 mg/dL); thrombocytopenia (75 000 platlets/μL); aPTT 53.2 s; anti-cardiolipin antibodies IgG 39 U/mL; lupus antibody 2.3 and anti-beta(2)-glycoprotein IgM 25 and IgG 47.60 UA. The patient initiated hypocoagulation with favorable clinical evolution. Conclusion: Six weeks after hospital discharge antibody dosages were repeated with results that allowed assuming anti-phospholipidic syndrome diagnosis. Months later and under hypocoagulation therapeutic values, the patient presented a new deep venous thrombosis event urging the need to raise INR to 3–4. It becomes decisive to emphasize the importance of the closest evaluation of these patients that sometimes end up in a catastrophic clinical event, in which an effective treatment won't be possible. doi:10.1016/j.ejim.2013.08.325
Abstracts
f.e.). Paraneoplastic RS3PE usually presents a worse respond to corticoids, although improvement was observed in our case. Finally, it is necessary to remember that, especially in older patients with pain and edema in hands and/or feet, this syndrome should be considered.
doi:10.1016/j.ejim.2013.08.322
ID: 474 Destructive arthropathy of the shoulder in siringomielia. Report of a case G. Lopez-Barros, P. Quiroga, A. Cadavid, A. Bravo, L. Alvarez Internal Medicine Division, Complejo Hospitalario Universitario de Ourense, Ourense, Spain A 44-year-old-man was seen in an outpatient internal medicine clinic because of severe pain and functional impotence in his right shoulder and arm in the last 3 months. On examination there was mild terdeness at the right shoulder and massive swelling of the shoulder, arm, and right chest area. The patient had previously been diagnosed of syringomyelia at the age of 20 years due to type I Arnold–Chiari malformation, which caused a suspended hypoesthesia, loss of strength and areflexia of his arms. A cysto-subdural shunt was performed when he was 23 years old. At 37 years of age, decompressive craniectomy suboccipital and occipital-cervical duraplasty was performed. The patient was treated with tramadol, clonazepam and duloxetine. An elemental analytical study of blood and urine showed no significant alterations. ESR and tumoral markers were within normal limits. A thoracic and abdominal CT scan revealed no anatomic abnormalities. Radiological examination of the affected shoulder showed massive soft tissue swelling and absence of the head and humeral metaphysis, reabsorption of the glenoid, and scattered areas of ectopic ossification. Magnetic resonance imaging revealed the presence of a mantle of polilobulated tissue at the shoulder area, and absence of the humeral head. The final diagnosis was neuropathic arthropathy secondary to syringomyelia. We highlight this rare and agressive arthropathy as a possibility during the evolution of this neurological disease, which can present a difficult differential diagnosis with neoplastic or infectious diseases.
doi:10.1016/j.ejim.2013.08.323
ID: 476 Inappropriate secretion of antidiuretic hormone syndrome in a patient with systemic lupus erythematosus: What are the causes? N. Essid, O. Harzallah, R. Klii, D. Braham, M. Kechida, S. Mahjoub Internal Medicine Department, Fattouma Bourguiba Hospital, Monastir, Tunisia
Introduction: The syndrome of inappropriate antidiuretic hormone (ADH) secretion (SIADH) is defined by the hyponatremia and hypo-osmolality resulting from inappropriate, continued secretion or action of the hormone despite normal or increased plasma volume, which results in impaired water excretion. Causes of SIADH are numerous and variable. Reports of SIADH in patients with systemic lupus erythematosus (SLE) are scarce. We report here a case of SIADH in a young female lupic patient and try to analyze its possible causes. Observation: A 23 year old female patient with a 1 year
pernicious anemia history was admitted in our department for fever, repeated convulsions and an agitation state. Clinical exam and biological tests allowed retaining SLE diagnosis according to ACR criteria: mouth ulcers, convulsion, leuco-lymphopenia, positive, antinuclear, anti-DNA, and anticardiolipin antibodies. Brain magnetic resonance imaging showed vasculitis lesions with multiple left middle cerebral artery strokes. The association of cerebral strokes to anticardiolipin antibodies in a lupic patient led to an associated antiphospholipid antibody syndrome diagnosis. The patient was treated by high doses of steroids, intravenous cyclophosphamide, anticoagulant and anticonvulsive agents (sodium valproate and phenobarbital). The evolution was initially favorable but 3 days later, fever and convulsions relapsed. Blood cultures were positive to Salmonella. Biochemical tests showed severe hyponatremia (118 mmol/l), a plasmatic hypo-osmolality and a natriuresis increase. The patient was treated by intravenous antibiotherapy and a fluid restriction with syndrome hypertonic saline serum perfusion. However, the evolution was rapidly unfavorable and the patient deceased. Discussion: SLE doesn't seem to be the cause of SIADH. Our patient had multiple possible causes that could explain this SIADH complicated of severe hyponatremia: treatment with cyclophosphamide and/or phenobarbital, neurological lesions and infection.
doi:10.1016/j.ejim.2013.08.324
ID: 486 Deep venous thrombosis and splenic infarction — What diagnosis? M.J. Ferreira da Silva, A. Lages, R. Pinto Alves, I. Trindade, C. Rodrigues, F. Nunes Gonçalves Internal Medicine, Hospital de Braga, Braga, Portugal
Background: Hypercoagulative status is defined by a tendency to venous or arterial thrombus formation. In 1845 Virchow claimed 3 responsible facts that appear to be relevant: hypercoagulability, vascular lesion and stasis. Secondary hypercoagulability can lead to thrombotic events due to multifactorial pathophisiological mechanisms in which etiology is frequently not clear. Methods: The authors present a clinical case of a 43 year-old male, with smoking habits and history of epilepsy and thrombophlebitis, that presented in the emergency room with right gastrocnemius pain, redness and swelling, related to diminished ability to walk. The analysis showed anemia, thrombocytopenia and altered coagulation, which lead to the patient admission in the medical ward to be studied. Results: After evaluation, it was stated that a deep venous thrombosis of right femoral-popliteal vein and a 2.5 cm splenic infarction showed in the angio-CT. The analytical study revealed: microcytic and normochromic anemia (11.9 mg/dL); thrombocytopenia (75 000 platlets/μL); aPTT 53.2 s; anti-cardiolipin antibodies IgG 39 U/mL; lupus antibody 2.3 and anti-beta(2)-glycoprotein IgM 25 and IgG 47.60 UA. The patient initiated hypocoagulation with favorable clinical evolution. Conclusion: Six weeks after hospital discharge antibody dosages were repeated with results that allowed assuming anti-phospholipidic syndrome diagnosis. Months later and under hypocoagulation therapeutic values, the patient presented a new deep venous thrombosis event urging the need to raise INR to 3–4. It becomes decisive to emphasize the importance of the closest evaluation of these patients that sometimes end up in a catastrophic clinical event, in which an effective treatment won't be possible. doi:10.1016/j.ejim.2013.08.325