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

Authors report 49 patients bacteriologicallyly diagnosed of acute meningococcal infection collected during a 12 months period out of a series of 76 cases diagnosed on clinical grounds. "N. meningitidis" was found in 18 blood and 43 CSF cultures. 31 cases were of the B-group, one was A-group and 17 were not typed. All of them were sulphamide resistant. Hyperthermia with vomiting, cephalea, arthralgia and seizures were the initial symptoms. All patients showed pettechiae, purpura and/or ecchymoses. Endotoxic shock was diagnosed in 26,5% of the cases. In them systolic blood pressures were under p-5. Overall mortality was 14%, and that of endotoxic patients 53%. Therapeutic routines and chemoprophylaxis are reviewed.
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PMID:[Acute meningococcal infection (author's transl)]. 11 89

79 patients with meningococcal disease were evaluated retrospectively between 1972-1986. All the neisseria isolated were sensitive to penicillin but resistant to sulphonamides. Most of the infections (54%) were caused by serogroup B strains. Clinical features included fever (98%), vomiting (65%), and headache (60%). Purpura appeared in 95% and severe neurological features in 25%. Most patients (83%) were children less than 10 years old. The incidence was 1.4/100,000 in the non-Jewish population and 2.3/100,000 in the Jewish population. The overall mortality was 23%, but about 50% in the Jewish population (10 deaths in 18 cases). In kibbutzim the incidence (7.5/100,000) and mortality were especially high. The need for awareness of the disease and the importance of early diagnosis and aggressive treatment are emphasized.
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PMID:[Meningococcal disease in western Galilee]. 156 81

A 70-year-old previously healthy woman was admitted with a 1-day history of malaise, sore throat, nausea, vomiting, rigors, and confusion. She was found to be in septic shock with purpura fulminans and disseminated intravascular coagulation. She died within 36 hours of admission. Blood cultures grew Neisseria meningitidis group Y. Necropsy revealed evidence of shock and bilateral adrenal hemorrhage.
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PMID:Purpura fulminans and adrenal hemorrhage due to group Y meningococcemia in an elderly woman. 190 68

A 44-year old woman had pain in the epigastric region under the thorax aperture on the left side 6 weeks prior to admission. Her doctor had prescribed Rewodina and Myocuran without success. Then she suffered circulatory collapse twice. Upon hospitalization, she experienced colicky upper abdominal pain and vomiting. She had been taking oral contraceptives (OCs) for 13 years. Spontaneous liver rupture attributable to adenoma was suspected, based on computer tumograms, and laparotomy bore out the suspicion. However, the cause was peliosis hepatis: the left half of the liver was more altered than the right, and a 10cm parenchyma defect was located under the left lateral liver lobe to which a large intrahepatic cavity filled with coagulum was attached. There was a copious amount of blood in the upper abdomen and another hole was filled with old blood. Partial liver resection was performed. The patient returned 3 weeks after recuperation because of fluctuating inflamed swelling developed on the right side. An incision was made to remove the abscess, but instead of finding pus, massive bleeding ensued whose source could not be located; it was squelched by tampons. Removal of the tampons 7 days later started another rupture with signs of liver insufficiency, and the patient died. Although the role of OCs in inducing liver changes has not been conclusively proven, the fact that she had taken OCs for years without any medical supervision seems to implicate this contraceptive method.
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PMID:[Liver rupture in peliosis hepatis]. 190 60

In late 1984, 10 children in a small, rural town in Brazil had high fever associated with vomiting and abdominal pain. Within 12-48 h of the onset of fever, purpura developed associated with vascular collapse and peripheral necrosis. All 10 children died. Cerebrospinal fluid examinations did not suggest meningitis and, when done, tests were negative for Neisseria meningitidis. Other culture, serological, and necropsy examinations did not reveal a cause. Case-finding uncovered another cluster of similar illness in children in a second town and sporadic cases in five other cities. Two case-control studies demonstrated that children who became ill were significantly more likely than control children to have had conjunctivitis during the month before illness. This conjunctivitis was purulent, preceded the onset of more severe disease by 3-15 days, and had resolved before fever began. Although no conjunctival cultures were obtained from case-children, Haemophilus aegyptius was the most common pathogen isolated from other conjunctival cultures during the epidemic. This organism was also isolated from a non-aseptic skin scraping from 1 case child. A 25-megadalton plasmid distinguished the H aegyptius isolates epidemiologically associated with illness from other Brazilian conjunctival isolates. Brazilian purpuric fever is a newly recognized syndrome of epidemic purpura fulminans associated with antecedent purulent conjunctivitis, possibly caused by H aegyptius.
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PMID:Brazilian purpuric fever: epidemic purpura fulminans associated with antecedent purulent conjunctivitis. Brazilian Purpuric Fever Study Group. 288 85

Blood pressure, which ist the product of cardiac output and peripheral vascular resistance is regulated by a complex feedback mechanism involving the sympathetic and parasympathetic systems and hormones. An acute disturbance of regulation may lead to a life-threatening increase in blood pressure. Diagnosis is based upon a careful measurement of blood pressure, which must be performed under internationally standardized conditions. Hypertensive crisis refers to a rapid blood pressure increase greater than 30 mmHg above the age-related 95th percentile. The main causes of hypertension in childhood are renal diseases, which may be aggravated by additional conditions either by the clinician himself (e.g. cyclosporin, steroids) or by the patient (lack of compliance). Crisis affects the brain (hypertensive encephalopathy), the heart (left ventricular insufficiency), the retina (visual disturbances) and the mucous membranes (epistaxis). Hypertensive encephalopathy is induced by a break-through of the autoregulation of brain flow, leading to hyperperfusion and, thus to cerebral oedema. The clinical manifestations are characterized by restlessness, severe and diffuse headache, vomiting, nystagmus, impaired vision, dizziness, paraesthesia, seizures and palsies, which may lead - if untreated - to coma and death. The course is usually prolonged and reversible by adequate treatment. The morphological consequences are purpura cerebri, fresh retinal haemorrhages and papillary oedema, apart from left ventricular dilatation and hypertrophy. The diagnostic procedure rests on the quick realization of essential anamnestic (blood pressure, renal disease, drugs), clinical (oedema, cardiac action, central nervous system, fundus) and laboratory parameters (serum creatinine, electrolytes, glucose, blood count, urine). Treatment should start before the manifestation of clinical signs (hypertensive emergency) with rapidly acting antihypertensive drugs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The hypertensive crisis in childhood]. 305 87

The currently recognized toxic effects of quinine in humans are identified and the problems of management of overdosage of quinine are discussed. Quinine, available therapeutically as sulphate or hydrochloride salts, also is widely used in tonic water, and there are several case reports of allergic reactions to the drug when a patient has consumed the drug in this way. Another unintentional source of poisoning is its use as an adulterant in heroin for "street" use. This appears to be a problem in the US. Quinine, termed a "general protoplasmic poison" is toxic to many bacteria, yeasts, and trypanosomes, as well as to malarial plasmodia. Quinine has local anesthetic action but also is an irritant. The irritant effects may be responsible in part for the nausea associated with its clinical use. In addition it has a mild antipyretic effect. Several features are common to both an acute single overdose in self-poisoning and accumulation of quinine during therapy for malaria: together they are termed cinchonism. Auditory symptoms, gastrointestinal disturbances, vasodilatation, sweating, and headache occur with moderately elevated plasma quinine concentration. As these rise, increasingly severe visual disturbances and then cardiac and neurologic features occur. Mild nausea may be the only symptom, but with large overdoses profuse vomiting, abdominal pain, and diarrhea may occur. These result from a combination of the local irritant effect of quinine on the gut and the central effects of quinine on the chemoreceptor trigger zone. Vasodilatation and sweating are well recognized, and tinnitus is common. Visual symptoms usually are delayed, and blindness may not be discovered for a day or more. Aspirin-sensitive patients, and others, may develop angioedema by nonimmunological mechanisms in response to drugs, and quinine has been reported to produce pseudo-allergic reactions in aspirin-sensitive patients. Quinine also can cause drug-induced thrombocytopenia and purpura. In patients suffering with malaria due to "Plasmodium falciparum," anemia and acute intravascular hemolysis with renal failure are recognized complications. There appears to be little evidence in the literature in support of the folk tradition of quinine as an inducer of abortion. Quinine is known to cause deterioration in patients with myasthenia gravis and erythema multiforme, to stimulate insulin release in patients receiving treatment for falicparum malaria, and to be responsible at times for ataxia following moderate overdosage. Clinically, quinine poisoning is observed in 3 situations: self-poisoning; accidentally; and following use of quinine in excessive doses in the hope of achieving abortion. Treatment courses are reviewed.
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PMID:Quinine toxicity. 354 70

A bizarre form of purpura seen on the face and neck after vigorous vomiting is described. Physicians should be familiar with this form of purpura since patients are very concerned about the mask that appears suddenly. Recovery is spontaneous, and no treatment is needed.
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PMID:Mask phenomenon: postemesis facial purpura. 373 65

The aim of this work was to describe the endoscopic features and clinical outcome of the duodenal complications in anaphylactoid purpura. Over a 3-year period, 20 patients were hospitalized in our unit because of purpura rheumatica. Duodenal complications occurred in 5 cases warranting endoscopic assessment. All patients had bilious vomiting and epigastric pain, constantly associated with low-grade purpuric rash. Plasma factor XIII concentrations were always decreased. The duodenal complication was suspected radiologically in 2 cases when "thumbprint" impressions were seen. Petechiae, oedema and intramural hematoma with superficial erosions were present endoscopically in 3 cases. The lesions were severe and extensive, involving the entire duodenum in 3 cases and the jejunum in one case. In one patient, there was a stricture of the upper part of the second duodenum. Treatment consisted of parenteral nutrition (using a central catheter: 3 cases, or a peripheral vein: 2 cases) and cimetidine (30 mg/kg.bw). The clinical outcome was favorable in 4 patients; the symptoms vanished and the endoscopic lesions were reversible (including the stricture) with restitutio ad integrum after 10 days. The last patient died the 8th day of treatment, 3 days after digestive improvement; the cause of death was probably iatrogenic and related to accidental migration of the central catheter. These results suggest that endoscopic examination should be performed in all patients with anaphylactoid purpura presenting with bilious vomiting. Endoscopy seems to be of great value in deciding if parenteral nutrition is indicated--or not--and perhaps in order to contraindicate the use of steroid therapy in the case of ulcerated hematomas.
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PMID:[Duodenal complications of rheumatoid purpura. Endoscopic aspects]. 643 33

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


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