Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 56-year-old woman with aortic regurgitation (AR) developd a high fever on April 25th, 2003, followed by the sudden onset of left hemiparesis and dysarthria on May 10th, 2003. MRI and MRA showed cerebral infarction due to occlusion of the right proximal portion of the middle cerebral artery. Streptococcus was isolated from arterial blood culture at the time of admission and cardiac examination such as echocardiography revealed active infective endocarditis. Cerebral angiography on the 31st day after the onset of symptoms demonstrated a fusiform-shaped aneurysm at the occluded M2 portion of the middle cerebral artery. Despite administration of antibiotics, a small subcortical hematoma was observed in the right temporal lobe surrounding the aneurysm on the 35th day. The direct surgery of aneurysmal trapping and resection was subsequently performed to prevent rebleeding. The sylvian fissure and perianeurysmal area were strongly adherent to granulation tissue and blood clot. After exposing the aneurysm, the dilated portion of the vessel was successfully trapped and resected. Other than residual left hemiparesis, the postoperative course was uneventful. Histological examination confirmed bacterial aneurysm due to bacterial embolization originating from infective endocarditis (IE). We report a rare case having a ruptured bacterial aneurysm of the middle cerebral arterial bifurcation requiring surgery following occlusion due to bacterial embolization after sepsis and meningitis due to infective endocarditis.
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PMID:[A surgically treated case with a ruptured bacterial aneurysm of the middle cerebral arterial bifurcation following occlusion]. 1528 88

Cerebral edema is a life-threatening condition that develops as a result of an inflammatory reaction. Most frequently, this is the consequence of cerebral trauma, massive cerebral infarction, hemorrhages, abscess, tumor, allergy, sepsis, hypoxia, and other toxic or metabolic factors. At present, the following types of cerebral edema are differentiated: the vasogenic cerebral edema resulting from an increased permeability of the endothelium of cerebral capillaries to albumin and other plasma proteins; the cytotoxic cerebral edema resulting from the exhaustion of the energy potential of cell membranes without damage to the barrier; the hydrostatic cerebral edema resulting from disturbance of the autoregulation of cerebral blood circulation; the osmotic cerebral edema resulting from dilution of blood; and the interstitial cerebral edema resulting from acute hydrocephaly. Some authors also differentiate ischemic cerebral edema. At present, when various traumas and traumatic cerebral injuries are frequent causes of death in young people, treatment strategy for cerebral edema is of utmost importance. Monitoring of the patient's condition in the intensive care unit is a necessity. It is important to ensure proper positioning of the patient--the head should be tilted at 30 degrees in order to optimize the cerebral perfusion pressure and control of the increase in intracranial pressure. Hyperventilation should be applied. Controlled hypothermia decreases the rate of metabolism in the brain. Slightly positive fluid balance should be maintained using crystalloid or colloid (hypertonic-hyperoncotic) solutions, at the same time maintaining cerebral perfusion pressure exceeding 70 mmHg. The treatment includes administration of antihypertensive medications, nonsteroidal antiinflammatory drugs, and barbiturates. Steroids decrease the permeability of capillaries and the hemato-encephalic barrier, promoting the movement of Na(+)/K(+) ions and water through the main endothelial membrane, and therefore they are used in the treatment of vasogenic cerebral edema as well as edema caused by a cerebral tumor. Glutamate and N-methyl-D-aspartate receptor antagonists improve cerebral microcirculation and metabolism. Trometamol corrects cerebral acidosis. Extended cerebral edema is treated surgically via a bilateral decompressive craniotomy, sometimes including craniotomy of lateral and posterior fossae. The treatment of cerebral edema is complex, and positive results may be expected only if the diagnosis and the provision of assistance are timely.
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PMID:[Cerebral edema and its treatment]. 1732 53

We reported a Japanese first case of thrombotic thrombocytopenic purpura (TTP) induced by clopidogrel, a newly developed antithrombotic drug, marketed in May 2006 in Japan. This 80 years old woman developed cerebral infarction and suffered from Broca's aphasia and right hemiparesis. Clopidogrel was started on Day 6 after the onset. On Day 10, four days after the administration of clopidogrel, two egg-sized purpura with marked decrease in platelet count was found. The purpura extended over the entire body in next few days. Despite total seven times of plasma exchange, platelet count did not normalize. Twenty four days after the onset of TTP, the patient developed central catheter infection and died of sepsis. TTP will become a lethal side effect of clopidogrel, when diagnosis and treatment are late. Because it is assumed that the mechanism of clopidogrel induced TTP differs from that of ticlopidine, we should establish firm treatment urgently.
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PMID:[Case of thrombotic thrombocytopenic purpura associated with clopidogrel]. 1893 79

Brain dysfunction is a severe complication of sepsis with an incidence ranging from 9% to 71% that is associated with increased morbidity and mortality. Its diagnosis relies mainly on neurologic examination with clinical manifestations ranging from confusion to coma. An electroencephalogram, somatosensory evoked potentials, and measurement of plasma S-100b protein and neuron-specific enolase can be useful for the detection of brain dysfunction. Brain MRI can identify brain lesions such as cerebral infarction, posterior reversible encephalopathy syndrome, and leukoencephalopathy. The mechanism of sepsis-associated encephalopathy involves inflammatory and non-inflammatory processes that affect endothelial cells, glial cells, and neurons and induce blood-brain barrier breakdown, derangements of intracellular metabolism, and cell death. Specific treatments for sepsis-associated encephalopathy need to be developed. Currently, treatment is mainly the management of sepsis.
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PMID:The encephalopathy in sepsis. 1824 79

A 13-month-old Japanese female with Haemophilus influenzae type b meningitis presented with unusually severe septic shock and cerebral infarction in half a day of fever. The initial therapy of plasma-derived activated protein C (Anact C) led to an impressive effect on the aggressive condition. However, purpura fulminans and the consistent decline of plasma protein C activity (<20%) required prolonged activated protein C therapy and gene analysis. The patient carried a novel heterozygous mutation of PROC (exon 4; 335 GAC>TAC, Asp46Tyr). This is the first report of infectious purpura fulminans in a protein C-deficient heterozygote. The clinical onset and treatment course adequately corroborated the aggravated immune/hemostatic reactions and the cytoprotective effects of activated protein C replacement in human heterozygous protein C deficiency. The monitoring of plasma protein C activity and sufficient administration of activated protein C product could improve the outcome of severe sepsis in children.
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PMID:Fulminant sepsis/meningitis due to Haemophilus influenzae in a protein C-deficient heterozygote treated with activated protein C therapy. 1875 23

We report 2 patients showing invasion of aspergillosis into the central nerve system (CNS). Patient 1, an 81-year-old woman, underwent surgery for sphenoidal sinusitis. She developed cerebral infarction with unconsciousness on 12th postoperative day. CSF examination demonstrated pleocytosis with increased protein and aspergillus antigen. She was diagnosed as having invasion of aspergillosis into the CNS, and was treated with voriconazole. Her clinical manifestations and CSF findings markedly improved. However, the effects of voriconazole gradually attenuated and she demonstrated recurrence of the cerebral infarction. After 2 months, she died of systemic aspergillosis and sepsis. Autopsy studies. Severe atherosclerotic changes with calcification were demonstrated in the bilateral carotid and basilar arteries, and many aspergillus were clustered in the vessel walls. Granulomatous inflammatory lesions with aspergillus were also demonstrated in the area surrounding the chiasm. There were no massive infarcts or bleeding in the brain, but multiple small infarcts were present. Patinet 2, a 64-year-old man, showing bilateral visual loss, was receiving treatment with corticosteroids under a diagnosis of optic neuritis. Two weeks later, he developed cerebral infarction. CSF examination showed pleocytosis with increased protein and aspergillus antigen. He was diagnosed as having invasive aspergillosis from the sphenoidal sinusitis into the CNS. He was treated with voriconazole, and unconsciousness and CSF findings improved transiently. However, he developed a recurrence of the brain infarction and pneumonia and finally died 6 months later. Treatment by voriconazole was definitely effective in both patients, but both patients died of recurrent cerebral infarction, possibly due to resistance for voriconazole, or developing multicellular filamentous biofilms. Voriconazole is recommended as the first choice of antifungal agents for aspergillosis. Aspergillus infection is strongly invasive into arterial vessels. It is important to consider the possible occurrence of cerebrovascular disease when treating invasion of aspergillosis into the CNS.
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PMID:[Effects of voriconazole and vascular lesions in invasion of aspergillosis into the central nerve system]. 1982 95

We report a rare case of infected left atrial myxoma. A 69-year-old male was admitted to our hospital due to cerebral infarction accompanied by lower limb ischemia. Transesophageal echocardiography showed a mobile left atrial tumor. On the 16th hospital day, he sufferd from high fever and Klebsiella pneumoniae was positive by blood culture. We excised the left atrial tumor, preventing systemic embolism and progression of sepsis. Histological examination showed a typical myxoma and organized thrombus with Gram-positive bacterial colonies, which disagreed with those in blood culture. After he recovered from sepsis, the 3rd toe of the right foot was amputated and then right femoro-popliteal bypass was done because of failure of wound healing. He was discharged from the hospital on the 74th postoperative day in good condition.
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PMID:[Infected left atrial myxoma; report of a case]. 2095 60

The incidence of the diabetic foot is increasing worldwide. Because evidence has shown that transmetatarsal amputation is associated with fewer failures in amputations of the diabetic foot with or without peripheral arterial disease, improving its management and surgical technique is a mission for the surgeon. Conventional transmetatarsal amputation has held firm, however, for more than 150 years. With a new concept for the transmetatarsal amputation method aimed at a better outcome, we propose a modified procedure for preserving the soft tissue between the metatarsal bones (the vasculature complex with the muscles, periostea, and vessels) and applying it to the distal bone stumps. The purpose of this method is to secure a functional foot by preserving the longitudinal arch. The new method was applied to 11 patients with diabetes mellitus or peripheral arterial disease, or both. All wounds closed successfully. Of the 11 patients, 8 were still alive with no complications. Of these 8 patients, 6 were able to ambulate with a custom-made shoe and 2 used a wheelchair, just as preoperatively. Of the 3 patients who died, 1 died a natural death, 1 died of sepsis, and 1 of cerebral infarction. We believe that the modified transmetatarsal amputation that we have described in this report is a potential breakthrough in the care of patients with forefoot gangrene and may gain acceptance over time.
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PMID:A modified transmetatarsal amputation. 2157 52

A 65-year-old man with diabetes mellitus (DM) presented with an indwelling urethral catheter placed for urinary retention by his previous doctor. Thereafter, he had fever, vomiting and general fatigue. His blood examination showed severe inflammatory findings. He was diagnosed with acute prostatitis and immediately admitted to our hospital. Pelvic computerized tomography (CT) showed a prostate abscess. We performed transrectal ultrasonographic-guided puncture of the prostate abscess for drainage and blood culture was tested. Methicillin-sensitive Staphylococcus aureus (MSSA) was cultured from the puncture fluid and blood. We administered antibiotics with strict control of DM. After the prostate abscess improved and the urethral catheter was removed, the patient was systematically examined for potential sepsis-related disease caused by MSSA septic infection. Magnetic resonance imaging (MRI) of the head indicated multiple cerebral infarction, abdominal CT indicated splenetic infarction, ultrasonography of the heart indicated vegetation on the mitral valve and aortic valve, and chest X-ray indicated pulmonary congestion. Furthermore, MRI of the lumbar spine showed a high intensity lesion at the 4th and 5th lumbar spine, indicating pyogenic spondylitis. We diagnosed prostate abscess with sepsis, infectious endocarditis, congestive heart failure and pyogenic spondylitis. Aortic valve replacement, mitral annuloplasty, tricuspid valvuloplasty and ovale hole closure surgeries were performed to treat these conditions.
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PMID:[A case of prostate abscess with sepsis, infectious endocarditis and pyogenic spondylitis]. 2323 81

Since it was proposed in 2007, molecular hydrogen therapy has been widely concerned and researched. Many animal experiments were carried out in a variety of disease fields, such as cerebral infarction, ischemia reperfusion injury, Parkinson syndrome, type 2 diabetes mellitus, metabolic syndrome, chronic kidney disease, radiation injury, chronic hepatitis, rheumatoid arthritis, stress ulcer, acute sports injuries, mitochondrial and inflammatory disease, and acute erythema skin disease and other pathological processes or diseases. Molecular hydrogen therapy is pointed out as there is protective effect for sepsis patients, too. The impact of molecular hydrogen therapy against sepsis is shown from the aspects of basic vital signs, organ functions (brain, lung, liver, kidney, small intestine, etc.), survival rate, and so forth. Molecular hydrogen therapy is able to significantly reduce the release of inflammatory factors and oxidative stress injury. Thereby it can reduce damage of various organ functions from sepsis and improve survival rate. Molecular hydrogen therapy is a prospective method against sepsis.
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PMID:Molecular Hydrogen Therapy Ameliorates Organ Damage Induced by Sepsis. 2741 21


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