Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The diagnosis of traumatic injury of the gallbladder may only be discovered at the time of celiotomy. The patient initially may be asymptomatic; later, he may develop nausea, vomiting, or paralytic ileus. Hemoconcentration, leukocytosis, and biliurea all have been observed, but are inconstant findings. However, increasing abdominal distention without a change in hematocrit value, jaundice, dark urine, or acholic stools accompanied by a rising bilirubin level should aid in diagnosis. Although the treatment of traumatic rupture of the gallbladder may be altered to fit the clinical situation and degree of anatomic disruption, most authors agree that cholecystectomy is the method of choice.
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PMID:Rupture of the gallbladder after blunt abdominal trauma. 112 32

A retrospective study was done during 1984-1988 in the pediatric ward of Dr. Pirngadi Hospital revealing 41 cases of acute hepatitis, consisted of 61.0% boys and 39.0% girls. The majority of patients were below five years of age (68.3%). There were 37.1% cases with malnutrition. The common symptoms were fever, jaundice, vomiting and dark urine. On laboratory examination there were 10 cases with positive HBs Ag. Accompanying diseases were malnutrition, bronchopneumonia, anemia, bronchitis and pulmonary tuberculosis. A total of 63.4% of patients were healed, 29.3% discharged against medical advice and 7.3% died because of bronchopneumonia and hepatic coma.
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PMID:Acute hepatitis at the Department of Pediatrics, School of Medicine, University of North Sumatra/Dr. Pirngadi Hospital Medan. 189 96

A computer system for probabilistic diagnosis of jaundice was tested on a patient sample from a geographical area different from that for which it was first constructed. 144 consecutive patients with jaundice seen in two Stockholm hospitals were interviewed and examined to record a total of 82 indicants from history, demographic details, physical findings and laboratory tests. Data were compared with those of 319 jaundiced patients previously interviewed and examined at different London hospitals. It was found that disease incidences were different in the two patient samples. There were more patients with acute viral hepatitis, chronic active hepatitis and primary biliary cirrhosis in the London data base whereas the Stockholm data base included significantly more patients with Gilbert's syndrome and alcoholic cirrhosis. Indicant frequencies, standardised for disease incidence, differed with respect to age (Stockholm patients were on average six years older), time from onset of first symptom to hospital admission (Stockholm patients had on average a two-week shorter history of disease) and a number of symptoms such as nausea, vomiting, anorexia, weight loss, itching, pale stools and dark urine which were more frequent among the London patients. Differences in hospital admission policy was regarded as an important reason for the differences in indicant frequency. The results of probabilistic diagnosis were poor. Only 49% of the cases were correctly classified into twelve diagnostic groups. In particular the computer model was poor at separating different causes of malignant bile duct obstruction and at differentiating between malignant and benign bile duct obstruction. However, all cases of acute viral hepatitis were correctly classified and the computer model was 87% accurate in differentiating between medical and surgical jaundice. Reclassification of the 144 patients on their own data showed the computer system to be well calibrated and 97% of the cases were correctly classified according to this procedure. In conclusion, the computer system could not be directly transferred for use in a Swedish hospital but the results of reclassification were sufficiently encouraging to warrant prospective studies.
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PMID:Computer aided diagnosis of jaundice. A comparison of two data bases. 330 98

This report describes five cases of hepatocellular injury following halothane anesthesia. Four patients had multiple exposures to the anesthetic. Three of the five died from submassive to massive liver cell necrosis. The two survivors developed jaundice and/or dark urine following each exposure to halothane; liver biopsy in one showed centrilobular and linear areas of necrosis. Fever, anorexia, nausea, vomiting, abdominal pain and jaundice were present in all cases. In the two survivors the prothrombin time was less than 20 seconds throughout the course of the disease, whereas in the three who died the prothrombin time was more than 20 seconds from the onset. The English literature to the end of 1971 is reviewed. Approximately 600 cases of halothane-related hepatitis have been reported
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PMID:Halothane hepatitis. 468 24

Ninety-one children with chronic schistosomiasis mansoni were selected for this double blind trial. 48 (Group 1) were treated with a single oral dose of oxamniquine (20mg/kg body-weight) and 43 (Group 2) received the placebo. Clinical, laboratory and radiological examinations were performed before and after treatment. Dark urine and vomiting were observed only in the oxamniquine group. Pulmonary condensations with or without air bronchogram were observed in the chest X-ray of 15% of Group 1 patients, between days 3 and 5 after treatment. In the urinalysis made on the first day after treatment, a false positive reaction was reported for urobilinogen and bilirubin in up to 50% of the patients treated with oxamniquine. In Group 1, 69.6% of the patients were cured. No patient was cured in Group 2. There was a 4.4% incidence of infection in the control group. There was a 77.9% egg excretion reduction in the 14 Group 1 patients not cured by oxamniquine. The authors conclude that oral oxamniquine in the prescribed dosage, has low toxicity and good therapeutic efficacy in children with chronic schistosomiasis mansoni.
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PMID:A double blind trial with oxamniquine in chronic schistosomiasis mansoni. 676 5

A case is described wherein a 29 year old woman was admitted to the hospital because of the possibility of a hepatic tumor; symptoms included abdominal pain, diffuse hepatic enlargement and absence of uptake in an area of the right hepatic lobe. After a normal pregnancy and delivery 11 years earlier the patient used oral contraceptives (OCs) composed of norethindrone with mestranol until 8 years before entry; 5 years before admission she resumed use of an OC containing norethindrone and ethinyl estradiol. She smoked 1.5 packages of cigarettes and drank 1 glass of wine daily, and there was no history of nausea, vomiting, melena, jaundice, dark urine, light stools, hepatitis, or blood transfusions. Benign lesions which are known to be caused by OCs fall into 2 groups: designated focal nodular hyperplasia and liver-cell adenoma. The evidence linking the latter with OCs is more convincing since in case-controlled studies the risk of development of adenomas has been shown to increase with the estrogen strength of the OCs and duration of use; in women who have been taking OCs over 7 years the relative risk is 500 times that for matched control nonusers. The vascular complications of OC therapy include Budd-Chiari syndrome, peliosis hepatis, and periportal sinusoidal dilatation. The patient in this case was diagnosed to have periportal and midzonal hepatic sinusoidal dilatation association with OC medication. She underwent an operation on her liver which proved to be successful combined with cessation of OC use. The mechanism by which OCs cause these lesions is not known. In 5 of 13 cases similar to the one described here clinical and biochemical abnormalities resolved and 1 patient had a follow-up liver biopsy that revealed normal findings 10 months after cessation of OC therapy; there is no evidence to suggest that sinusoidal dilatation is irreversible.
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PMID:Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 40-1982. Tender hepatomegaly in a 29-year-old woman. 711 Feb 74

We describe two siblings affected by chronic relapsing thrombotic thrombocytopenic purpura from infancy. The elder brother, a 12-year-old boy had 50 such episodes characterized by acute onset of fever, headache, drowsiness, vomiting, dark urine, thrombocytopenia and anemia. The younger sister, a 6-year-old girl, had 8 episodes with the same clinical manifestations. Petechiae and ecchymoses on the extremities were present throughout their lives. Furthermore, anemia with evidence of red blood cell fragmentation and thrombocytopenia were present chronically. Periodical transfusion of frozen fresh plasma prevented recurrent episodes. These cases suggest that there is a congenital variant of thrombotic thrombocytopenic purpura.
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PMID:A congenital variant of thrombotic thrombocytopenic purpura in two siblings. 771 55

A case of fulminant hepatitis with microvesicular steatosis resembling Labrea's fever, diagnosed in Vitoria (ES) is reported. The 16 year old boy presented with severe epistaxis, agitation, jaundice and hemorrhagic vomiting and died two days after admission to the emergency unit of the University Hospital. The disease started five days before with fever, myalgias, dark urine and jaundice and progressed with psychic agitation, torpor and coma. The liver and spleen were not palpable. HBsAg was negative in the serum. The autopsy showed acute hepatitis with lytic necrosis confluent in the midzonal and periportal areas with massive microvesicular steatosis in the remaining hepatocytes. Mononuclear cells predominated in the exudate. The reticulum showed condensation in the necrotic areas without typical bands of collapse. The portal tracts were edematous with mononuclear infiltration and mild bile duct proliferation. Absence of cholestasis. Except for the confluent midzonal and periportal necrosis this case showed several clinical and morphological aspects of the Labrea fever described from the East Amazon, demonstrating that the anatomical picture of this disease probably is not in related to a factor peculiar to the Amazon region.
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PMID:Labrea-like hepatitis in Vitoria, Espirito Santo State, Brazil: report of a case. 815 25

The report concerns a two-month-old suckling, affected on the 20th day of life with occurrence of icterus, dark urine and acholic stool, and on the 34th day--fever, vomiting and enlargement of the abdomen. Bile ascites is demonstrated by abdominal puncture, and perforation of the extrahepatic biliary ducts--by hepatobiliary scintigraphy. In the course of emergency laparotomy, diffuse bile peritonitis is established against the background of punctiform perforation at the site of d. cysticus and d. hepaticus communis union. Following sanation of the abdominal cavity, a draining catheter is inserted into the perforation area. The serious postoperative course, characterized by progressive hepatic failure, results in a fatal outcome on the third postoperative day. The etiopathogenesis, clinical symptomatology, timely diagnosis and effective operative management of this exceptionally rare surgical disease in children are discussed against the background of pertinent literature data survey.
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PMID:[Idiopathic perforation of the extrahepatic bile ducts in a nursing infant]. 901 73

The authors report a case of post-traumatic rhabdomyolysis in a victim of a car accident who, after having being initially examined at an emergency ward, was sent home having been requested to return for a control visit a few days later. The patient did not attend the control visit on the appointed day but returned to the same emergency ward eight days after the accident suffering from vomiting, general malaise and violent pain in the left forearm that appeared swollen. Anamnesis revealed a severe condition of rhabdomyolysis with dehydration, pale red urine and general signs of marked renal insufficiency. Tests showed marked myoglobinemia and myoglobinuria, very high CPK, azotemia, creatinemia, transaminase and high diastasemia. Given the disappearance of peripheral pulse and the severe neurovascular impairment of the left forearm caused by edematous compression, it was decided to proceed to surgical decompression using extensive longitudinal fasciotomy under supraclavicular anesthesia. After surgery peripheral pulse returned to normal, as was confirmed by Doppler. After adequate hydration while renal insufficiency lasted, hemodialysis was commenced immediately and repeated during the following days. Given that all the tests had improved and results were virtually within the norm, the patient was transferred to the medical ward after eight days for continuation of therapy. It is important to underline the importance of possible signs, such as oleguria, dark urine, swelling and edemas of the limbs, in injured patients. If renal insufficiency occurs, it is important to commence early hemodialysis. On day 23 the patient was again transferred to the intensive care ward because he presented epigastric pain and vomiting. CAT showed acute pancreatitis which resolved leading to full recovery after 20 days.
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PMID:[Traumatic rhabdomyolysis. A clinical case]. 901 71


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