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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty patients with spondylitis were treated by decompression of the cord (31 operations). The spondylitis was tuberculous in 28 of septic unspecific aetioloty in two cases. The results with respect to the neurological symptoms were complete recovery in 24 cases, imcomplete recovery in four cases, and failure in three cases, or in ten per cent. Transthoracic anterior decompression was found to be the safest and quickest way to obtain restitution. Out of the ten patients treated by this method, nine recovered completely. One post-operative death from pulmonary embolism occurred. One patient died because of adrenal insufficiency due to adrenal tuberculosis which could not be diagnosed during life. There were no other serious complications attributable to the operative interventions.
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PMID:Paraplegia in spondylitis: results of operative treatment. 117 13

A woman aged 62 developed a septic shock and pulmonary embolism after skin grafting for extensive burns. She was put on anticoagulants. A second shock led to renal insufficiency. Hypercalcaemia developed. A CT scan of the upper abdomen disclosed enlarged adrenal glands. An acute adrenal haemorrhage was suspected. The levels of cortisol were low in the plasma and urine and did not respond to ACTH stimulation. Cortisone replacement therapy improved the condition of the patient and normalized plasma calcium levels. The mechanisms of hypercalcaemia in acute adrenal insufficiency are discussed. Multiple factors have been proposed: haemoconcentration, an increased affinity of plasma proteins for calcium, an increase in the filtrable calcium complexes, and an enhanced calcium mobilization of skeletal origin.
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PMID:Hypercalcaemia in acute adrenal insufficiency. A case report. 216 7

Antiphospholipid syndrome has received considerable attention from the medical community because of its association with a number of serious clinical disorders, including arterial and venous thromboembolism, acute ischemic encephalopathy, recurrent pregnancy loss, thrombocytopenia, and livido reticularis. It can occur within the context of several diseases, mainly autoimmune disorders, and is then called secondary antiphospholipid syndrome. However, it may be also be present without any recognizable disease, or so-called primary antiphospholipid syndrome. There is no defined racial predominance for primary antiphospholipid syndrome, although a higher prevalence of systemic lupus erythematosus (SLE) occurs in African Americans and the Hispanic population. Multiple terms exist for this syndrome, some of which can be confusing. Lupus anticoagulant syndrome, for example, is a misleading term, because patients may not necessarily have SLE, and it is associated with thrombotic rather than hemorrhagic complications. To avoid further confusion, antiphospholipid syndrome is currently the preferred term for this clinical syndrome. Antiphospholipid antibodies are found in 1% to 5% of young healthy control subjects; however, the incidence increases with age and coexistent chronic disease. The syndrome occurs most commonly in young to middle-aged adults; however, it also can occur in children and the elderly. Among patients with SLE, the prevalence of antiphospholipid antibodies is high, ranging from 12% to 30% for anticardiolipin antibodies, and 15% to 34% for lupus anticoagulant antibodies. In general, anticardiolipin antibodies occur approximately five times more often then lupus anticoagulant in patients with antiphospholipid syndrome. This syndrome is the most common cause of acquired thrombophilia, associated with either venous or arterial thrombosis or both. It is characterized by the presence of antiphospholipid antibodies, recurrent arterial and venous thrombosis, and spontaneous abortion. Rarely, patients with antiphospholipid syndrome may have fulminate multiple organ failure, or catastrophic antiphospholipid syndrome. This is caused by widespread microthrombi in multiple vascular beds, and can be devastating. Patients with catastrophic antiphospholipid syndrome may have massive venous thromboembolism, along with respiratory failure, stroke, abnormal liver enzyme concentrations, renal impairment, adrenal insufficiency, and areas of cutaneous infarction. According to the international consensus statement, at least one clinical criterion (vascular thrombosis, pregnancy complications) and one laboratory criterion (lupus anticoagulant, antipcardiolipin antibodies) should be present for a diagnosis of antiphospholipid syndrome. The hallmark result from laboratory tests that defines antiphospholipid syndrome is the presence of antibodies or abnormalities in phospholipid-dependent tests of coagulation, such as dilute Russell viper venom time. There is no consensus for treatment among physicians. Overall, there is general agreement that patients with recurrent thrombotic episodes require life-long anticoagulation therapy and that those with recurrent spontaneous abortion require anticoagulation therapy and low- dose aspirin therapy during most of gestation. Prophylactic anticoagulation therapy is not justified in patients with high titer anticardiolipin antibodies with no history of thrombosis. However, if a history of recurrent deep vein thrombosis or pulmonary embolism is established, long-term anticoagulant therapy with international normalized ratio (INR) of approximately 3 is needed.
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PMID:Antiphospholipid syndrome. 1467 58

There are many noninfectious disorders in the critical care unit (CCU) that mimic sepsis. Pseudosepsis is the term applied to noninfectious disorders that mimic sepsis. Fever/leukocytosis is not diagnostic of infection but frequently accompanies a wide variety of noninfectious disorders. When fever/leukocytosis and hypotension are present, sepsis is the presumptive diagnosis until proven otherwise. After empiric therapy for sepsis is initiated, the clinician should rule out the noninfectious causes of pseudosepsis. The most common causes of pseudosepsis in the CCU setting are pulmonary embolism, myocardial infarction, gastrointestinal hemorrhage, overzealous diuretic therapy, acute pancreatitis, relative adrenal insufficiency, and (rarely) rectus sheath hematoma. Rectus sheath hematoma may occur secondary to trauma/anticoagulation therapy and may present as an acute surgical abdomen mimicking sepsis. Rectus sheath hematoma should be considered when other causes of pseudosepsis or sepsis fail to explain persistent hypotension unresponsive to fluids/pressors. The diagnosis of rectus sheath hematoma is by abdominal ultrasound or computed tomography scan. If the abdominal computed tomography scan is negative for other intra-abdominal pathology and other causes of pseudosepsis are eliminated, then the diagnosis of pseudosepsis caused by rectus sheath hematoma is confirmed by demonstrating a hematoma in the rectus sheath. Treatment of rectus sheath hematoma is surgical drainage and ligation of any bleeding vessels. Evacuation of the rectus sheath hematoma rapidly reverses the patient's hypotension and is curative. We describe a case of pseudosepsis caused by rectus sheath hematoma in an elderly man with hypotension unresponsive to fluids/pressors and mimicking septic shock. Clinicians should be aware that rectus sheath hematoma is a rare but important cause of pseudosepsis in patients in the CCU.
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PMID:Pseudosepsis: rectus sheath hematoma mimicking septic shock. 1713 47

Trauma patients are twice as likely to have adverse reactions to medication as nontrauma patients. The need for medication in trauma patients is high. Surgery is often necessary, and immunosuppression and hypercoagulability may be present. Adverse drug events can be caused in part by altered pharmacokinetics, drug interactions, and polypharmacy. Medications may also have serious long-term adverse effects, which must be considered. It is not the purpose of this review article to discuss all adverse effects of all medications. This article will discuss the more common adverse effects of medications for trauma patients in the acute care setting, in the following categories: pain control, sedation, antibiotics, seizure prophylaxis in head trauma, atrial fibrillation, deep vein thrombosis and pulmonary embolism prophylaxis, hemodynamic support, adrenal insufficiency, factor VIIa.
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PMID:Medication-related complications in the trauma patient. 1837 49

A 76-year-old woman presented to a clinic with fever and loss of body weight. Abdominal echogram showed bilateral adrenal swelling (left adrenal 90x80 mm, right adrenal 50x20 mm) and she was admitted to the hospital for further examination. A tumor was also found inside nasal cavity by enhanced computed tomography (CT), and abnormal uptake in the nasal cavity and adrenal gland was shown in gallium scintigraphy. Laboratory tests revealed the elevation of lactate dehydrogenase (LDH) and sIL-2R. Biopsy of the nasal tumor revealed nasal natural killer or thymus-derived (NK/T) cell lymphoma. No Epstein-Barr virus (EBV) -encoded RNA was detected in tissue. After THP-COP chemotherapy regimen, both the nasal and adrenal tumors decreased in size. However, a CT scan taken on admission revealed a pulmonary embolism. After treatment with heparin and warfarin, emboli disappeared. Chemotherapy was continued, but perforation of the small intestine occurred. Since the prognosis was poor, no operation was performed. Her condition slowly, and she died 60 days after admission. Since she had a high level of plasma ACTH (158.0 pg/ml) and normal serum cortisol (14.6 microg/dl), partial adrenal insufficiency was suspected. In addition, since her cortisol circadian rhythm was lost and cortisol levels were not completely suppressed by the 1 mg and 8 mg dexamethasone test, she met the criteria of the diagnosis of preclinical Cushing syndrome. NK/T cell lymphoma with giant adrenal tumor is extremely rare, but should be considered as one of the differential diagnoses of bilateral adrenal tumor.
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PMID:[A case of nasal NK/T cell lymphoma presenting with bilateral giant adrenal tumors]. 1917

OBJECTIVEPituitary adenomas (PAs) are benign neoplasms that are frequently encountered during workup for endocrinopathy, headache, or visual loss. Transsphenoidal surgery remains the first-line approach for PA resection. The authors retrospectively assessed complication rates associated with transsphenoidal PA resection from an institutional database.METHODSA retrospective analysis of 1153 consecutive transsphenoidal pituitary adenoma resections performed at the Keck Hospital of USC between November 1992 and March 2017 was conducted. Microscopic transsphenoidal resection was performed in 85.3% of cases, and endoscopic transsphenoidal resection was performed in 14.7%. Analysis of perioperative complications and patient and tumor risk factors was conducted.RESULTSThe overall median hospital stay was 3 days. There was 1 perioperative death (0.1%). Surgical complications included postoperative cerebrospinal fluid leak (2.6%), epistaxis (1.1%), postoperative hematoma (1.1%), meningitis (1.0%), cranial nerve paresis (0.8%), hydrocephalus (0.8%), vision loss (0.6%), stroke (0.3%), abdominal hematoma or infection (0.2%), carotid artery injury (0.1%), and vegetative state (0.2%). Perioperative medical complications included bacteremia/sepsis (0.5%), pneumonia (0.3%), myocardial infarction (0.3%), and deep venous thrombosis/pulmonary embolism (0.1%). Endocrine complications were the most frequent, including transient diabetes insipidus (4.3%), symptomatic hyponatremia (4.2%), new hypopituitarism (any axis) (3.6%), permanent diabetes insipidus (0.3%), and adrenal insufficiency (0.2%). There were no significant differences between microscopic and endoscopic approaches with regard to surgical complications (6.4% vs 8.8%, p = 0.247) or endocrine complications (11.4 vs 11.8%, p = 0.888). Risk factors for surgical complications included prior transsphenoidal surgery (11.4% vs 6.8%, p = 0.025), preoperative vision loss (10.3% vs 6.8%, p = 0.002), and presence of PA invasion on MRI (8.5% vs 4.4%, p = 0.007).CONCLUSIONSIn this single tertiary center study assessing complications associated with transsphenoidal PA resection, the rate of death or major disability was 0.26%. Risk factors for complications included prior surgical treatment and PA invasion. No differences in complication rates between endoscopic and microscopic surgery were observed. When performed at experienced pituitary centers, transsphenoidal surgery for PAs may be performed with a high degree of safety.
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PMID:Complications associated with microscopic and endoscopic transsphenoidal pituitary surgery: experience of 1153 consecutive cases treated at a single tertiary care pituitary center. 2999 59

We present a case of isolated adrenocorticotropic hormone (ACTH) deficiency complicated by acute adrenal crisis and severe myocardial dysfunction. A 54-year-old woman developed consciousness disturbance, hypoglycemia, hyponatremia, and rhabdomyolysis. Initial echocardiographic examinations on the sixth hospital day revealed marked right-sided atrial and ventricular dilatation and severe tricuspid regurgitation. A computed tomography scan for pulmonary embolism was negative. On the 14th hospital day, she became dyspneic and hypotensive. Repeated echocardiographic examinations demonstrated diffuse and severe hypokinesis of the left ventricle. The previous right-sided chamber dilatation became less apparent. Congestive heart failure and severe hypotension were refractory to catecholamines, while she was eventually diagnosed as having acute adrenal crisis due to isolated ACTH deficiency. Hydrocortisone replacement therapy was started, and echocardiographic examinations revealed that the left ventricular dysfunction completely returned to normal in the following eight days. Severe myocardial dysfunction is an uncommon but serious complication of acute adrenal insufficiency. The present case was unique in that diffuse left ventricular dysfunction was preceded by right ventricular dysfunction.
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PMID:Isolated ACTH deficiency presenting with severe myocardial dysfunction. 3054 10

A 46-year-old man with antiphospholipid syndrome (APS) and previous pulmonary embolism on anticoagulation with rivaroxaban was brought in to the hospital after a syncopal episode. He was found to be hypotensive and tachycardic and later admitted to the intensive care unit. Clinical presentation and laboratory findings were consistent with adrenal insufficiency. MRI revealed bilateral adrenal haemorrhage and he received appropriate steroid replacement therapy. Symptoms slowly subsided and anticoagulation regimen was changed to warfarin. Adrenal haemorrhage was likely caused by APS and rivaroxaban, which brings into question whether novel oral anticoagulants are safe in this patient population.
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PMID:Bilateral adrenal haemorrhage secondary to rivaroxaban in a patient with antiphospholipid syndrome. 3261 55