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)

We describe a 22-month-old boy with iron deficiency anemia and reactive thrombocytosis who developed vomiting, headache, mental status changes, and seizures. Computed tomography showed infarction of the basal ganglia and thalami. Magnetic resonance imaging revealed cerebral venous thrombosis, delineated the extent of the vascular and associated parenchymal involvement, showed the infarcts to be hemorrhagic (a finding not imaged by computed tomography due to our patient's depressed hemoglobin level), and obviated the need for invasive angiography.
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PMID:Cerebral venous thrombosis in a child with iron deficiency anemia and thrombocytosis. 230 75

A five-year-old male was admitted to the hospital with generalized seizures. Enlarged lymph nodes raised the suspicion of cat-scratch disease. The diagnosis was confirmed by a positive history of a cat bite, typical histopathologic findings in the biopsy of the lymph nodes, and a positive skin test. Brain CT scan and LP were repeatedly normal. The clinical course was remarkable for recurrent episodes of status epilepticus refractory to usual anticonvulsant therapy and prolonged encephalopathy consisting of mental confusion, hemiparesis, tremor, chorea, and vomiting. All neurologic symptoms gradually resolved within nine months, without sequelae. Cat-scratch encephalopathy should be suspected in a child presenting with status epilepticus and enlarged lymph nodes. Aggressive and prolonged anticonvulsant therapy is strongly recommended.
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PMID:Cat-scratch encephalopathy presenting as status epilepticus and lymphadenitis. 232 Apr 87

To evaluate the safety and possible efficacy of high-dose naloxone for the treatment of acute cerebral ischemia, 38 patients received a loading dose of 160 mg/m2 over 15 minutes followed by a 24-hour infusion at the rate of 80 mg/m2/hr. Nausea and/or vomiting were common side effects. Naloxone was discontinued in seven patients (because of hypotension in one, bradycardia and hypotension in two, myoclonus in one, focal seizures in two, and hypertension in one); all seven patients responded to treatment and no permanent sequelae to naloxone were noted. Twelve of the 38 patients showed early neurologic improvement (by completion of the naloxone loading dose). However, there was no correlation between such a loading dose response and clinical outcome at 3 months. Our experience suggests that naloxone is safe at the dose used, but data for efficacy are inconclusive.
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PMID:High-dose intravenous naloxone for the treatment of acute ischemic stroke. 233 51

We performed a retrospective review to investigate the safety of prehospital naloxone administration by paramedics as part of a protocol for all patients presenting with an acutely depressed level of consciousness (LOC). The prevalence of naloxone-induced vomiting, seizures, hypotension, hypertension, and cardiac arrest was sought from the prehospital records of 813 patients treated during a 12-month period. The mean age of the treated patients was 42.4 +/- 9.7 years. The initial dose of naloxone was 0.4 to 0.8 mg, and the mean total dose was 0.9 +/- 0.6 mg. No patients lost a pulse within ten minutes of receiving naloxone. Two patients (0.2%) experienced a significant drop in systolic blood pressure, and one patient (0.1%) demonstrated a significant rise in systolic blood pressure within five minutes of naloxone administration. Vomiting occurred in two patients (0.2%), and one patient (0.1%) suffered a tonic-clonic seizure within five minutes of naloxone administration. Of the 813 patients treated, 60 patients (7.4%: mean age, 32.3 +/- 6.7 years) were judged to have an improved LOC after naloxone, with 27 (3.3%) regaining a normal LOC. We conclude that in the above doses, naloxone is safe as part of prehospital protocols for paramedics treating patients with an acutely depressed LOC. However, the vast majority of patients treated empirically with naloxone in the field demonstrated no benefit.
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PMID:The safety of prehospital naloxone administration by paramedics. 237 73

The pathophysiology and treatment of acute subarachnoid hemorrhage (SAH) are reviewed. SAH occurs when blood is released into the subarachnoid space, which surrounds the brain and spinal cord. Symptoms of SAH include severe headache, nausea, vomiting, neck pain, nuchal rigidity, and photophobia. The initial hemorrhage is fatal in 20-30% of patients. Complications of SAH include rebleeding, hydrocephalus, delayed cerebral ischemia associated with cerebral vasospasm, and seizures. The likelihood of rebleeding is increased by measures that rapidly lower intracranial pressure. The risk of developing hydrocephalus is associated with the volume of blood within the subarachnoid space and ventricular system. Cerebral vasospasm develops in 20-40% of patients, and up to 50% of affected patients die or suffer permanent neurological damage. Seizures occur in 5-15% of patients with SAH. Radiologic procedures form the foundation for the diagnosis of SAH. The most commonly used rating scale classifies the severity of SAH based on the clinical presentation of the patient. Surgery is the definitive treatment for the prevention of rebleeding. Hydrocephalus can only be treated surgically, most commonly by insertion of a drain. The only measures proved to be effective for treatment of delayed cerebral ischemia are volume expansion and the induction of hypertension. The calcium-channel blocker nimodipine was recently approved for treatment of arterial spasm in SAH. Intravenous nicardipine is also being studied for the same indication. These agents may improve clinical outcome substantially by limiting fixed neurological deficits. To prevent seizures, prophylactic antiepileptic therapy with phenytoin sodium is generally accepted. The SAH complications of rebleeding, hydrocephalus, delayed cerebral ischemia, and seizures are managed by surgical, drug, and fluid therapy.
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PMID:Pathophysiology and treatment of subarachnoid hemorrhage. 240 1

An epidemic of group A meningococcal disease began in Auckland in May 1985. There were 122 paediatric cases of meningococcal disease in the next 25 months including 98 cases due to group A. The commonest clinical symptoms were vomiting, headache and photophobia, while frequent signs included fever, seizures, petechial rash and meningism or a bulging fontanelle. Complications were uncommon and included sterile arthritis and prolonged fever. The majority had disease confirmed by positive blood or cerebrospinal fluid culture. Significantly fewer positive cultures were seen in those treated with antibiotics prior to admission. The overall mortality was 7%. If the acute illness was survived, the only detected long term sequela was sensorineural hearing loss seen in 6%. A vaccine programme has been undertaken to control this epidemic.
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PMID:The clinical features of paediatric meningococcal disease Auckland, 1985-87. 249 88

An 81-year-old woman had chills, fever, nausea, vomiting, and epigastric pain. On day 3 she had hematuria and was treated with trimethoprim-sulfamethoxazole. On day 5 she had a cough, hypotension, anemia, azotemia, and elevated hepatic enzyme levels. Her condition deteriorated with thrombocytopenia, anuria requiring dialysis, edema, and hypoalbuminemia. Treatment with chloramphenicol and doxycycline was started on day 10. By day 11, she was in hypotensive shock; on day 12 she had seizures and died. Murine typhus was diagnosed by demonstration of antibodies to Rickettsia typhi by indirect immunofluorescence. Necropsy revealed interstitial pneumonia, pulmonary edema, hyaline membranes, alveolar hemorrhages, petechiae and vasculitis in the central nervous system, interstitial myocarditis, multifocal interstitial nephritis and hemorrhages, splenomegaly, portal triaditis, and mucosal hemorrhages in urinary tract. Immunofluorescent R. typhi were demonstrated in the lungs, brain, kidneys, liver, and heart. This unusual death occurred in an elderly patient without rash who was treated too late with antirickettsial drugs.
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PMID:Histopathology and immunohistologic demonstration of the distribution of Rickettsia typhi in fatal murine typhus. 249 81

To evaluate the value of the nonsedative anticonvulsants carbamazepine and valproic acid a controlled study including drug monitoring was carried out. Intoxicated alcoholics (n = 138) were admitted for inpatient detoxication and randomly assigned to either carbamazepine (n = 43), sodium valproate (n = 46) or placebo (n = 49) in a double-blind fashion. Drug treatment lasted for four days and the daily doses of both drugs amounted to 1200 mg in the beginning of the study. Sodium valproate induced gastric distress, nausea and vomiting more frequently than placebo. About half of the subjects had to stop carbamazepine because of intolerable side-effects including vertigo, nausea, vomiting, diplopia and rash. Serum carbamazepine levels (18-89 mumol/l) were found to be high (greater than 40 mumol/l) in many but not all of these subjects. Seizures occurred in 3 subjects on placebo, 2 on carbamazepine and 1 on sodium valproate. Delirium tremens developed in 2 on sodium valproate and 1 on placebo. The study demonstrates that drug side-effects may seriously hamper the utility of carbamazepine and sodium valproate as routine treatment for the prevention of alcohol withdrawal symptoms.
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PMID:Prevention of alcohol withdrawal seizures with carbamazepine and valproic acid. 250 Jan 38

Desmopressin (DDAVP), a synthetic vasopressin, temporarily corrects bleeding abnormalities associated with mild hemophilia A, von Willebrand disease, and disorders of platelet function. The side effects of DDAVP are considered benign although most of its use has been in adults and older children. We report four children under the age of 2 years who became hyponatremic after intravenous DDAVP administration (0.3 microgram/kg). Three of them developed grand mal seizures. A review of the literature and these cases indicate that associated risk factors for hyponatremia after DDAVP administration include stress, surgery, anesthesia and narcotics (endogenous release of antidiuretic hormone), vomiting (loss of Na+), liver disease (hindered metabolism of DDAVP), renal tubular acidosis (chronically low serum Na+), multiple doses of DDAVP, and overhydration with hyponatremic fluids. DDAVP is not a benign drug in this age group and shows a serious potential for hyponatremia and seizures. Fluid restriction, avoidance of hyponatremic solutions, and close monitoring of serum electrolytes and urine output for at least 15-20 hr after the administration of DDAVP, when used in children under the age of 2 years, is warranted.
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PMID:Hyponatremia and seizures in young children given DDAVP. 250 Aug 51

The emetic agent ipecac is widely used for the initial treatment of acute oral drug overdose. Its emetic and gastric evacuative efficacies have been studied extensively but its potential for pharmacologic interactions with various drugs and other possible poisons has not been explored. The purpose of this investigation was to determine if ipecac can alter the acute toxicity of two widely used drugs that act on the central nervous system, phenobarbital and theophylline. Ipecac syrup, 5 ml/kg, was administered by gavage to male Lewis rats either 1 hr before or 15 or 30 min after the start of an iv infusion of phenobarbital or theophylline. Control animals received the syrup vehicle only. Ipecac elicited vomiting-like behavior (frequent, wide opening of the mouth) for more than 1 hr. The drug infusion was stopped immediately after onset of the loss of righting reflex (phenobarbital) or maximal seizures (theophylline). Samples of cerebrospinal fluid, blood (for serum), and the brain were obtained at that time for analysis of drug concentrations. There were no significant differences between control and ipecac-treated animals with respect to the dose requirements and drug concentrations in cerebrospinal fluid, serum, and brain at the respective pharmacologic endpoint. It is concluded that ipecac has no apparent effect on the acute toxicity of phenobarbital and theophylline in rats.
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PMID:Systemic effect of ipecac on acute toxicity of phenobarbital and theophylline in rats. 257 54


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