Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Six children who remained in deep coma after immersion accidents in fresh water received therapy to maintain normal intracranial pressure (ICP). This involved controlled ventilation to ensure hypocapnia and hyperoxaemia, maintenance of low normothermia, fluid restriction, dexamethasone (1-1.5 mg/kg initially, 1-1.5 mg/kg/day as maintenance) and barbiturates (phenobarbitone and thiopentone). The latter were given in a wide range of dosage. Increased ICP was common to all patients, but could always be kept at acceptable levels. All patients suffered from pulmonary oedema; three developed broncho-pneumonia and two developed adult respiratory distress syndrome. All children survived with good recovery, two needed active rehabilitation for several months.
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PMID:Intensive care after fresh water immersion accidents in children. 718 Oct 62

Disease secondary to heroin abuse constitutes a rarity in Spain. While there had been no previous cases in earlier years four young heroin addicts were admitted to the Hospital "1st de Octubre" for severe medical complications of their addiction within the last twelve months. Two patients were admitted in deep coma due to drug overdose, being cardiac arrhythmias and pulmonary edema the main associated complications. Cardiac rhythm disturbances are due to a heightened vagal tone, either secondary to inhibition of acetylcholine hydrolysis or to hypoxia, hypercapnia, and acidosis, factors that diminish cholinesterase activity and act synergistically to increase vagal tone. Pulmonary edema secondary to heroin overdose is non-cardiogenic and probably due to hypoxia added to the local action of heroin on the alveolocapillary membrane. The goal of therapy in such cases is to obtain an appropriate alveolar ventilation, the use of continuous positive pressure ventilation being required when there is pulmonary edema. The third patient had staphylococcal pneumonia with multiple abscess formation secondary to venous septic embolization originated peripherally where the drug was injected. Finally, the fourth patient was admitted because of a clinical and biochemical picture of HBsAg negative acute viral hepatitis, having suffered a similar clinical picture three years previously.
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PMID:[Severe medical sequelae in heroin addicts]. 720 89

This report describes a patient who presented with coma and acute pulmonary edema after severe carbon monoxide poisoning. Hemodynamic evaluation revealed elevated systemic and pulmonary arterial, pulmonary wedge and right atrial pressures, together with an increased cardiac output. These findings are compatible with the hypothesis that a neurogenic mechanism plays a role in the pulmonary edema of carbon monoxide poisoning.
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PMID:Acute pulmonary edema following carbon monoxide poisoning. 739 47

22 patients with severe preeclampsia-eclampsia were treated in our Intensive Care Unit from 1972 to 1978. Control of convulsions was achieved by diazepam, diphenylhydantoin and phenobarbital. In 11 comatose patients brain monitoring was carried out by frequent neurological examination and use of computerized x-ray tomography; aspiration of gastric contents was prevented by nasotracheal intubation. Brain oedema therapy included controlled hyperventilation, steroids and mannitol (7 patients). 10 patients with respiratory failure (due to pulmonary oedema, "shock lung" or aspiration pneumonitis) were treated by mechanical ventilation. Diastolic blood pressure above 100 mm Hg was reduced by hydralazine. Diuresis was induced by normalization of hypovolaemia with albumin and plasma expanders. Six patients died (27%); main causes of death included intracerebral haemorrhage, brain oedema, heart failure, acute pulmonary thromboembolism and bleeding from DIC.
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PMID:[Intensive care of severe preeclampsia-eclampsia. A report on 22 cases (author's transl)]. 742 60

A 14-year-old girl with sickle cell disease and nephrotic syndrome developed bone pain, followed by pulmonary edema, seizures, coma, and bilateral flaccid paralysis. Fat embolism syndrome was diagnosed by cranial magnetic resonance imaging and an exchange transfusion was performed. Within 3 months, all symptoms had resolved. It is concluded that fat embolism syndrome must be considered as a possible cause of acute neurologic deterioration in patients with sickle cell anemia.
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PMID:Nontraumatic fat embolism syndrome in sickle cell anemia. 774 67

Our aim was to assess clinically whether there was any benefit in adding a single dose of sublingual nifedipine (a slow calcium channel blocker) to prazosin in the management of the cardiovascular manifestations of envenoming by the Indian red scorpion (Mesobuthus tamulus). A total of 163 patients stung by this species was admitted to hospital at Mahad between January 1991 and October 1993. Cardiovascular abnormalities were hypertension (59), of whom 42 had bradycardia and 17 had tachycardia; pulmonary oedema (14), of whom eight had hypertension and six hypotension; supraventricular tachycardia (eight), of whom three had hypotension and one died. Of the remaining patients, 78 demonstrated severe excruciating local pain at the site of sting but had no systemic involvement. Nineteen patients with hypertension and tachycardia were given a single dose of sublingual nifedipine plus prazosin on admission, then prazosin alone repeated 6 hourly. Five patients with massive life-threatening pulmonary oedema recovered after being given intravenous sodium nitroprusside. Prazosin alone helped to alleviate cardiovascular manifestations in the remaining 52 victims. One patient was admitted in a deep coma, 12 hr after the sting, and died. Eight victims whose blood pressure had been controlled in hospital by nifedipine plus prazosin developed acute pulmonary oedema necessitating additional doses of prazosin for recovery. Fifty-two victims treated with prazosin alone did not develop pulmonary oedema and the drug appeared to hasten the recovery. In the presence of high blood pressure, tachycardia, a murmur and impending myocardial failure, nifedipine appeared to contribute to cardiopulmonary instability and to augment myocardial oxygen consumption. In this situation calcium channel blockers should probably be avoided.
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PMID:Vasodilators: scorpion envenoming and the heart (an Indian experience). 780 38

Adult respiratory distress syndrome (ARDS) after tricyclic antidepressant (TCA) overdose has been reported, but has not received as much attention in the literature as hemodynamic instability, cardiac arrhythmias or seizures. This report concerns a 33-year-old female who ingested a large amount of imipramine in an attempted suicide. She developed deep coma, hypotension, cardiac dysrhythmias and seizures. Although she survived initially, ARDS developed and she died of severe hypoxia nine days later. Her lung injury may have been the result of a variety of factors including prolonged hypotension, aspiration pneumonia, sepsis or a direct action on the lung parenchyma by imipramine. The literature pertaining to etiology, epidemiology, pathophysiology and management of TCA-induced lung injury has been reviewed. In one series of severe TCA overdose, an ARDS rate of 9% was reported. The risk of developing pulmonary edema and ARDS should be considered in severe TCA-poisoned patients. To try to prevent this complication, early intubation should be considered to avoid aspiration, and cautious volume loading, plus judicious use of alpha-adrenergic agonists, is indicated to prevent protracted hypotension.
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PMID:Adult respiratory distress syndrome and late death following imipramine overdose: a case report. 785 Jun 87

The unusual case of a 65-year-old woman with intermittent hypotension, fever, pulmonary edema and coma as initial presentation of pheochromocytoma is reported. The patient developed respiratory, cardiac and renal failure, disseminated intravascular coagulation and liver dysfunction. She had to be defibrillated on multiple occasions, occurring in periods of severe hypertension. After successful surgical removal of a pheochromocytoma a thyroid medullary carcinoma was detected. Several members of the patients family had presented with multiple endocrine neoplasia (MEN II).
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PMID:Multiple organ failure and coma as initial presentation of pheochromocytoma in a patient with multiple endocrine neoplasia (MEN) type II A. 810 32

Plasmodium falciparum malaria is endemic in the northern KwaZulu areas of South Africa. The clinical morbidity produced by this parasite has not been studied since the institution of the present malaria control programme. Fifty-nine patients were prospectively studied at a peripheral clinic during the peak malaria season; symptoms and signs of the infection, parasite loads, haemoglobin values and leucocyte counts were recorded in all patients. Haemoglobin and leucocyte counts were also measured in 37 control subjects without malaria. The commonest symptoms were persistent headache (100%), rigors (98%) and myalgia (93%). None of the patients presented with coma, pulmonary oedema, hypoglycaemia or algid malaria. Splenomegaly was found in 49%, hepatomegaly in 20% and mental confusion in 5% of patients. Mean parasite load was 1.71% and 57% of patients had parasite loads of < 1%. Anaemia of < 10 g/dl was significantly more frequent (P < 0.0001) in the patient group than in the control group. Leucopenia (white cell count < 4.0 x 10(9)/l) was present in 12 of 50 patients in whom it was measured compared with 2 controls (P = 0.0175). The results show a wide range of morbidity, without severe complications as presenting manifestations. Symptomatic infection in the presence of low parasite loads suggests that there may be little or no immunity in this population.
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PMID:Morbidity from falciparum malaria in Natal/KwaZulu. 845 85

A case of acute renal failure due to rhabdomyolysis in a patient who used cocaine on a daily basis is presented. In contrast to many prior reports of renal failure occurring with cocaine-associated rhabdomyolysis, our patient did not use intravenous cocaine and did not have any evidence of trauma, seizure, hypotension, hyperthermia, hyperactivity, or coma. His creatine phosphokinase peaked at 448,000 U/liter. He was treated initially with forced diuresis and i.v. furosemide, but he became oliguric, developed pulmonary edema, and required hemodialysis. He recovered fully after 3 weeks of dialysis. The literature is reviewed in an attempt to delineate a rational approach to evaluating cocaine users at risk for rhabdomyolysis.
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PMID:Severe rhabdomyolysis with renal failure after intranasal cocaine use. 940 1


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