Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Well known complications related to cocaine use are myocardial insufficiency, myocardial infarction, myocarditis, aortic dissection, neurologic damages, ischemic colitis, thrombotic phenomenons, renal infarction and acute liver failure. Cases of splenic infarctions related to cocaine use are extremely rare. A 17-year-old drug addict was found by her boy-friend liveless in her bed. She was well known using cocaine since years. Autopsy revealed multiple splenic infarctions with secondary mixed bacterial infection and abscesses. Petechial bleedings were found and microabscesses in the myocardium, the meninges and the kidneys. The absolutely rare bacterial infection of the cocaine-associated splenic infarction leads to sepsis with lethal course.
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PMID:Cocaine-associated abscesses with lethal sepsis after splenic infarction in an 17-year-old woman. 1501 62

This paper describes four cases of visceral artery aneurysms (VAAs) successfully treated with endovascular stent-grafts and discusses the endovascular approach to VAAs and the long-term results. Four balloon expandable stent-grafts were used to treat three splenic artery aneurysms and one bleeding common hepatic artery pseudoaneurysm. The percutaneous access site and the materials were chosen on the basis of CT angiography findings. In all cases the aneurysms were successfully excluded. In one case a splenic infarction occurred, with nonrelevant clinical findings. At 16- to 24-month follow-up three patients had patent stents and complete exclusion and shrinkage of the aneurysms. One patient died due to pancreatitis and sepsis, 16 days after successful stenting and exclusion of a bleeding pseudoaneurysm. We conclude that endovascular treatment using covered stent-grafts is a valid therapeutic option for VAAs. Multislice CT preoperative study helps in planning stent-graft positioning.
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PMID:Endovascular exclusion of visceral artery aneurysms with stent-grafts: technique and long-term follow-up. 1792 63

Splenic infarction occurs when occlusion of splenic vasculature leads to ischemia, and subsequent tissue necrosis. It is a rare condition. Most patients have an underlying haematological or malignant process or a potential source of embolism. This article describes a patient who presented with unexplained sepsis to the acute medical unit; investigation revealed a splenic abscess and primary hyperparathyroidism, but no evidence of an underlying cause.
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PMID:An unusual cause of septicaemia. 2157 61

Splenic infarction is most commonly caused by cardiovascular thromboembolism; however, splenic infarction can also occur in hematologic diseases, including sickle cell disease, hereditary spherocytosis, chronic myeloproliferative disease, leukemia, and lymphoma. Although 10% of splenic infarction is caused by hematologic diseases, it seldom accompanies autoimmune hemolytic anemia (AIHA). We report a case of a 47-year-old woman with iron deficiency anemia who presented with pain in the left upper abdominal quadrant, and was diagnosed with AIHA and splenic infarction. Protein C activity and antigen decreased to 44.0% (60-140%) and 42.0% (65-140%), respectively. Laboratory testing confirmed no clinical cause for protein C deficiency, such as disseminated intravascular coagulation, sepsis, hepatic dysfunction, or acute respiratory distress syndrome. Protein C deficiency with splenic infarction has been reported in patients with viral infection, hereditary spherocytosis, and leukemia. This is a rare case of splenic infarction and transient protein C deficiency in a patient with AIHA.
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PMID:Splenic infarction in a patient with autoimmune hemolytic anemia and protein C deficiency. 2225 34

Clarkson's syndrome, also known as idiopathic systemic capillary leak syndrome, is characterised by vascular hyperpermeability resulting in intravascular hypovolaemia and shock. A clinician should consider the diagnosis if other causes of shock, for example, sepsis and anaphylaxis, are ruled out and concomitant hyperviscosity is not caused by a myeloproliferative disease. Here, we describe a patient presenting with severe plasma leakage and assumable blood hyperviscosity leading to splenic infarction, gastrointestinal ischaemia-reperfusion syndrome and transient dysarthria. Our patient was first suspected of polycythaemia vera and phlebotomies were performed. Awareness of this syndrome and subsequent correct treatment is essential to prevent complications and to reduce mortality. As in our patient, most patients with Clarkson's syndrome have a monoclonal gammopathy, light-chain-type kappa. Prophylactic treatment with intravenous immunoglobulin (IVIg) is advised to prevent recurrence of capillary leak. Our patient did not suffer from another symptomatic episode after starting IVIg.
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PMID:Hyperviscosity-related splenic infarction, gastrointestinal ischaemia-reperfusion injury and transient dysarthria in a patient with distributive shock due to idiopathic systemic capillary leak syndrome (Clarkson's syndrome). 3198 Apr 75


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