Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of cryptococcosis simulating brain tumor was reviewed. A 66-year-old female was admitted to our hospital with chief complaint of vertigo, gait disturbance and dysarthria. These symptoms started about one year before admission and worsened. Vomiting and urinary incontinence appeared. Neurological examination revealed left cerebellar ataxia and dysarthria. In plain CT (computerized tomography) irregular ill-defined low density area was noted in the cerebellar vermis and bilateral cerebellar hemispheres. And slight ventricular dilatation was found. Irregular shape of ring-like enhancement corresponding to capsule and patchy or mottled enhancement inside the tumor were seen. Suboccipital craniectomy was performed and yellowish necrotic tumor with hard capsule was removed. Histological diagnosis was not neoplasm or tuberculoma. Postoperatively liver function progressively worsened. She died due to disseminated intravascular coagulation. Autopsy revealed typical liver cirrhosis without malignant change. 3.0 X 2.5 cm sized, slightly hard, yellowish lesion was found on upper part of cerebellar hemispheres. This had extremely necrotic tissue and a great number of cryptococcus neoformans were found. And other intracranial lesion was not confirmed. Finding of pulmonary cryptococcosis was not gained. Our case is very rare because of solitary cerebellar abscess and absence of meningitic episode or pulmonary cryptococcosis. There are three types of inflammation in cerebral cryptococcosis. The commonest manifestation is the meningitic type, the second mode is granulomatous lesion and the third and the least presentation is intracranial abscess formation. CT reveals various findings according to clinical stage. CT findings are those of meningitis, meningoencephalitis, granuloma and abscess. Cryptococcal granuloma or abscess often simulates brain abscess, glioma and metastatic brain tumor.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of cerebral cryptococcosis, with special reference to computerized tomography findings]. 646 65

Cerebellar infarcts have been neglected for a long time and are now shown well by CT and especially MRI. Some infarcts involve the full territory supplied by a cerebellar artery. They are frequently complicated by edema with brain stem compression and supratentorial hydrocephalus, requiring at times emergency surgery, and are often accompanied by other medullary, medial pontine, mesencephalic, thalamic and occipital infarcts. On the other hand, partial territory infarcts are usually confined to the cerebellum and have a benign outcome with total recovery or minimal disability. They are more common than full territory infarcts. However, clinical presentations are similar to those full territory infarcts, differing mainly by the lack of drowsiness or unconsciousness. The main symptoms are vertigo, headache, vomiting, unsteadiness of gait and dysarthria. Signs include ipsilateral limb dysmetria, ipsilateral axial lateropulsion, ataxia and dysarthria. Vertigo is more severe and rotary in posterior inferior cerebellar artery territory infarcts, whereas dysarthria and ataxia are prominent in superior cerebellar artery territory infarcts. A few brain stem signs are sometimes added. In these territorial cerebellar infarcts, cardioembolism is the most common cause. Atherosclerotic occlusion comes next, involving the intracranial part of the vertebral artery and, less frequently, the lower basilar artery, both locations inaccessible to surgery. Other causes are artery to artery embolism from a vertebral artery origin stenosis, or the aortic arch, in situ intracranial branch atherosclerotic occlusion, and vertebral artery dissection. Border zone cerebellar infarcts occur in one third of the cases. They are small cortical or deep infarcts. They have the same symptoms and signs as territorial infarcts except for more frequent postural symptoms occurring over days, weeks or months after the ischemic event. The infarcts mainly have a thromboembolic mechanism, and sometimes have a hemodynamic mechanism: 1) focal cerebellar hypoperfusion due to large artery occlusive disease in more than half the cases, 2) small or end (pial) artery disease due to hypercoagulable state (thrombocythemia, polycythemia, hypereosinophilia, disseminated intravascular coagulation), arteritis or intracranial atheroma, and 3) rarely systemic hypotension due to cardiac arrest.
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PMID:[Cerebellar infarctions and their mechanisms]. 809 Oct 85

A case of severe lithium carbonate self-poisoning is described, presenting with sustained vasodilatory shock, DIC and neurologic manifestations. Lengthy and repeated haemodialysis was required to lower lithemia to non-toxic levels in accordance with which the haemodynamic instability and multi organ dysfunction ceased. The patient survived with marked loss of hearing, tinnitus and vertigo as the only sequelae. We discuss the mechanism of lithium's inhibitory effect on the phosphoinositide cascade as the possible explanation for the vasodilatory shock as well as the hearing deficiency.
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PMID:[Development of sustained vasodilatory shock and permanent loss of hearing after severe lithium carbonate poisoning]. 1825 69

Spinning is a popular indoor stationary cycling program that uses group classes as a motivational tool. Exertional rhabdomyolysis (ER) is frequently reported in athletes and military recruits; however, infrequently it has been reported after spinning class. ER is diagnosed by clinical history, physical exam, and laboratory values. Hydration, electrolyte management, and pain control are key components to treatment of this condition. Severe cases can be complicated by acute renal failure, compartment syndrome, arrhythmia, and disseminated intravascular coagulation. We describe three cases of admission due to rhabdomyolysis after spinning. The diagnosis, admission criteria, and medical treatment of ER are presented in the context of a literature review. A retrospective review of three cases with review of the current literature. The medical and laboratory records of three patient cases were reviewed. A search of the PubMed database was used to perform a comprehensive review of exertional rhabdomyolysis. Our institution's IRB reviewed this study. We report three cases of exertional rhabdomyolysis after spinning and describe the diagnostic workup and medical management of these patients. The diagnosis of ER is made by clinical history, physical exam, and laboratory values. The disease spectrum ranges from mild to severe with the potential of serious complications in some patients. We demonstrate three cases of ER in deconditioned individuals who presented to the emergency department for evaluation. Careful medical management and patient monitoring resulted in improved patient symptomatology and eventual return to physical activity.
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PMID:Exertional rhabdomyolysis after spinning: case series and review of the literature. 2566 50