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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seventeen patients had spontaneous orbital hemorrhages. The usual symptoms were acute onset of pain, proptosis, and vomiting with decreased vision, limitation of motility, and ecchymosis of the eyelids occurring in some patients. The children often developed a progressive space occupying lesion that simulated a neoplasm. Most patients had underlying venous anomalies, although several elderly patients with atherosclerosis developed arterial hemorrhages with more abrupt and dramatic symptoms. Other associated conditions included hypertension, anemia, labor, and von Willebrand's disease. The visual outcome was good except in the elderly patients, half of whom had severe and permanent visual loss.
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PMID:Orbital hemorrhage. 47 97

The clinical and pathological features of 28 fatal cases of acute uncomplicated massive cerebellar infarction are reviewed. Although infarcts may involve any portion of the cerebellum, they predominantly involve the posteroinferior half of one cerebellar hemisphere. The frequency of acute uncomplicated fatal cerebellar infarction is much greater than previously appreciated, approximating that of acute fatal cerebellar hemorrhage. All patients were past middle age. Atherosclerosis and acute vertebral artery occlusion were the most common etiological factors. The onset was sudden in most cases, with vomiting, dizziness, vertigo, and cerebellar dysfunction. All patients died with progressive brain stem dysfunction and medullary respiratory failure secondary to compression by a swollen cerebellum. Death usually occurred between the third and sixth days following the onset of symptoms, but only six to 30 hours after the onset of obtundation; therefore, decompressive therapy must be instituted promptly.
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PMID:Cerebellar infarction. A clinicopathological study. 113 Oct 69

A 41-year-old male with a 25-year history of diabetes mellitus requiring 25 to 30 units of neutral protamine hagedorn (NPH) insulin daily was found dead at home. Recent history revealed that he was well until the last four days of life when he had the onset of nausea, vomiting, and anorexia coinciding with procurement of a new bottle of insulin from his pharmacist. Pertinent autopsy findings included coronary and aortic atherosclerosis, a peptic ulcer, and diabetic glomerulopathy. Chemical analysis of the vitreous humor, including glucose (813 mg/dL) and acetone (40 mg/dL), revealed that he died of diabetic ketoacidosis. Further investigation revealed that the pharmacist had accidentally substituted regular insulin, with a duration of action of up to 6 h as opposed to 24 to 28 h, for NPH. Cultures of blood and of the regular insulin yielded no growth. Analysis of this case emphasizes the importance of obtaining a careful medical and medication history and the usefulness of vitreous electrolytes when investigating a sudden death in a diabetic.
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PMID:Pharmaceutical error resulting in fatal diabetic ketoacidosis. 308 89

Atherosclerosis was diagnosed on necropsy in 21 dogs in a 14-year period. Nine dogs died and 12 were euthanatized because of complications associated with the disease. The mean age was 8.5 +/- 0.5 years; 18 dogs were male. Three breeds (Miniature Schnauzer, Doberman Pinscher, and Labrador Retriever) had a higher prevalence of the disease than other breeds in the canine necropsy population of The Animal Medical Center. Most common clinical signs were lethargy, anorexia, weakness, dyspnea, collapse, and vomiting. Hypercholesterolemia, lipidemia, and hypothyroidism were common in affected dogs tested, and protein electrophoresis revealed high values for alpha 2 and beta fractions in all dogs tested. Electrocardiography indicated conduction abnormalities and myocardial infarction in 3 of 7 dogs. Necropsy revealed that affected arteries (including coronary, myocardial, renal, carotid, thyroidal, intestinal, pancreatic, splenic, gastric, prostatic, cerebral, and mesenteric) were yellow-white, thick and nodular, and had narrow lumens. Myocardial fibrosis and infarction also were observed in the myocardium. Histologically, affected arterial walls contained foamy cells or vacuoles, cystic spaces, mineralized material, debris with or without eroded intima, and degenerated muscle cells.
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PMID:Clinical and pathologic findings in dogs with atherosclerosis: 21 cases (1970-1983). 374 84

A series of 12 patients with cerebellar infarcts diagnosed by computerized tomography are reviewed. The clinical features of cerebellar infarctions cover a wide spectrum, mimicking symptoms and signs from an acute labyrinthitis to a rapidly expanding posterior fossa mass lesion with brain stem and cerebral dysfunction. Two patients were asymptomatic and three showed signs of cerebellar dysfunction only. Three patients had evidence of brain stem dysfunction with cranial nerve palsies accompanying the cerebellar deficit. Two presented a pseudovestibular form with sudden onset of nausea, vomiting, rotary dizziness and ataxia. A pseudotumoral form with intracranial hypertension was found in two cases, in which softening tissue acts as a rapidly expanding posterior foss mass lesion. It is difficult to identify the exact artery involved in a cerebellar infarct because of the collateral circulation and connections between the three major arteries. Atherosclerosis and general decrease in blood flow can be regarded as the most likely factors precipitating focal cerebellar infarction. Surveillance is necessary during the first days with anti-edematous therapy. Rapid deterioration of consciousness should be considered a sign of increasing intracranial pressure progressing with the development of hydrocephalus. If necessary, surgical decompression by external drainage or by direct access to the posterior fossa can be carried out.
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PMID:[Cerebellar infarct. Clinical presentation and x-ray computed tomography of the brain]. 394 88

A possible relation between parenteral Depo-Provera and the subsequent development of medullary infarction in a heavy smoker is reported. The patient, a 40-year old Chinese woman had smoked 30 cigarettes daily for many years. She received injections of 150 mg Depo-Provera in April and July 1979. 2 days after the 2nd injection she was admitted to the hospital for vomiting and vertigo of 2 days duration. Clinical examination showed a 12th nerve palsy with the tongue deviated to the right but no other neurological abnormalities. She was treated symptomatically with intravenous fluids and stemetil and improved. On the 5th day her vertigo and vomiting progressed and she developed more lower brain stem signs. The same day she had a grand mal fit and went into a coma. She died on the 7th hospital day. A partial autopsy limited to the skull revealed minimal atherosclerosis of the vertebral artery but no thrombosis or occlusion. Cut sections after perfusion revealed an area of softening associated with some hemorrhage involving the whole length of the right half of the medulla oblongata dorsal to the olivary nucleus. Histological examination revealed an infarct undergoing liquefaction necrosis. The possibility of a causative relationship is suggested by the development of tinnitis about 12 hours after injection of Depo-Provera.
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PMID:Medullary infarction--was it depo-provera? 645 93

Forty patients with mesenteric vascular occlusion were observed over a ten-year period. The main clinical findings were abdominal tenderness (in 80% of the patients), abdominal pain (in 83%), guarding and rigidity (in 60%) and vomiting. At operation, twelve patients (30%) had massive gangrene of the small and large bowel, 10 (25%) of the small bowel alone, and six (15%) had subsequent gangrene of the small bowel. Atherosclerosis with thrombosis of the superior mesenteric artery was found in 70% of cases, and embolism in 17.5%. Mortality was 77.5%. Nine patients (22.5%) who underwent resection survived.
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PMID:Acute mesenteric vascular occlusion: a review of 40 cases. 722 44

This study included 125 cases of cerebellar infarction followed during an average period of 4.3 years. The diagnosis was made by CT or MRI. Infarctions localized to the territory of the superior cerebellar artery (SCA) and the territory of the posterior inferior cerebellar artery (PICA) occurred with the same frequency. Transient ischemic attacks preceded infarction in 26% of cases. Symptoms and signs were usual with sudden association of headache, dizziness, unsteadiness and vomiting. Vestibular signs were more important in infarctions of the PICA territory; cerebellar signs and dysarthria were more frequent in infarction of the SCA territory. A decreased level of consciousness developed in only 21% of cases. Surgical operation was required in 9 cases. Investigations have showed the large responsibility of cardiac embolisms and atherosclerosis. Short term outcome was more often favourable: 116 patients were alive at the end of the first month; 80% of survivors were independent one year later. At 5 years, 73% of patients were alive. After the acute period, mortality was mainly due to cerebro-vascular and cardiac events.
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PMID:[Clinical and evolutive aspects of cerebellar infarction]. 786 66

A 40-year-old HIV-infected woman developed nausea, vomiting, and epigastric pain and died following her third dose (per study protocol) of interleukin (IL)-2. Her HIV infection was diagnosed in 1996. Her last CD4 cell count was 390/microL, and her viral load was negligible (as of November 28, 1998). She had no known general risk factors for thrombosis other than HIV infection, injection drug abuse, and antiretroviral therapy with indinavir. Abdominal films showed no sign of mechanical obstruction but a generalized gas distention of the bowel, which was suggestive of paralytic ileus. Autopsy revealed dilation of the small bowel with extensive necrosis and hemorrhage involving all the segments. The superior and inferior mesenteric arteries revealed severe atherosclerosis. The stenotic celiac artery was occluded by a recent thrombus at the aortic ostium. Clinicians need to be aware of the potential for thrombosis and accelerated atherosclerosis in HIV-infected patients. Both injection drug abuse and protease inhibitors, such as indinavir, have been shown to be risk factors for thrombosis. However, it is likely IL-2 contributed to the severe thrombosis in this patient, although definitive proof is lacking. An acute awareness of intestinal infarction in HIV-infected patients is warranted.
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PMID:Case report. Intestinal infarction due to vascular catastrophe in an HIV-infected patient. 1118 43

One of the keys to achieving glycemic control in animals with diabetes mellitus is the appropriate selection and interpretation of analytic monitoring tests. Diabetic animals are subject to many of the same problems described in human diabetics. Diabetics are more susceptible to infection, and wound healing is often impaired. Decreased insulin promotes lipolysis and moderate hyperlipidemia, which can lead to falsely lowered fructosamine levels, impaired renal circulation, and atherosclerosis. Hyperglycemic, hypoinsulinemic animals continue to lose weight despite an increased appetite and an increased intake because they are not able to use glucose. Many unregulated diabetic animals will present with vomiting and diarrhea that can exacerbate electrolyte abnormalities seen with the osmotic diuresis present in an uncontrolled state. Canine diabetics are prone to cataract formation secondary to sorbitol accumulation in the lens. Cats, on the other hand, can present with diabetic distal neuropathy, which may be reversible with appropriate treatment. With all of these potential complications, it is important to monitor these animals regularly; this is the only way that glycemic control can be properly maintained over time. This article reviews the monitoring parameters available to the modern practitioner and outlines the benefits of each test, as well as caveats, in their interpretation.
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PMID:Monitoring techniques for diabetes mellitus in the dog and the cat. 1221 18


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