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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Their frequency is estimated with difficulty, although on autopsy pulmonary edema is found almost routinely. It is a major complication of overdoses (48 p. 100 of severe intoxications). Their formation can be suspected, when after the first phase of respiratory depressions, with coma, myosis, and a variable latent period, a second attack of respiratory insufficiency occurs with tachypnea, and cyanosis. The chest X-ray shows diffuse alveolar infiltration, sparing the apices. The heart being generally of normal size. Rapid disappearance of this infiltrate (24 to 48 hours) enables the elimination of two diagnoses: pneumonia due to inhalation of gastric fluid, an infectious pneumonia. Their pathogenesis remains very debatable: - in the majority of cases abrupt L.V.F. can be eliminated: -on the other hand it could be an allergic accident of the anaphylactic type, or local liberation of histamine, or a local toxic action on the pulmonary capillaries; - hypoxia, secondary to respiratory depression, could lead to pulmonary edema, by the same mechanism as at altitude; - finally, owing to the central neurological disorders a neurogenic theory can be put forward. Their treatment is essentially a combination of Nalorphine with oxygen therapy (by mask, or if necessary by assisted, controlled ventilation) with prevention of inhalation of gastric fluid (gastric emptying) or curative treatment of possible aspiration by antibiotics, and cortico-steroids. Diuretics can be useful, as well as cardiotonics.
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PMID:[Pulmonary edemas due to acute heroin poisoning]. 0 75

Two cases of acute pulmonary distress following very shortly after irradiation of the upper half of the body are described. The first occurred one hour and forty minutes after irradiation and led to the patient's death three hours after irradiation. The second occurred 15 minutes after irradiation and was successfully treated with hydrocortisone and Frusemide. The features are the sudden onset of dyspnoea and cyanosis associated with pyrexia. Auscultatory evidence of pulmonary oedema was not apparent initially. The response to steroid alone is transitory. High single-dose pulmonary irradiation causes transudation of extracellular fluid and diapedesis of red cells from the alveolar capillaries. The supervention of these effects on severly compromised pulmonary function can well prove dangerous.
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PMID:Acute pulmonary distress following high-dose irradiation of the upper half of the body. 11 68

A primigravida was induced for PET, the liquor was meconium stained; she was put on oxytocin in-fussion and developed hypertonic uterine action. She then had an amniotic fluid embolism which presented clinically as profound shock, dyspnoea, tachycardia, cyanosis, hypotension and pyrexia. The patient was delivered by vacuum extraction. The picture was further complicated by pulmonary oedema intravascular microcoagulation and anuria. She deteriorated rapidly and died despite treatment with double strength plasma (in the absence of fibrinogen), massive hydrocortiosone therapy, blood transfusion amd sub-total hysterectomy. Post mortem findings in the lungs confirmed amniotic fluid embolism.
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PMID:Case report: a fatal case of amniotic fluid embolism. 12 35

Of 22 patients with the classical clinical signs of pulmonary oedema (orthopnoe, cyanosis, sweating and rales heard at a distance) 15 (Group A) were observed clinically, while seven (Group B) underwent haemodynamic studies. Those in Group A were given 0.8-2.4 mg nitroglycerin sublingually one to six times at 5--10 minute intervals. Within five minutes of nitroglycerin administration 7 of the 15 had their first signs of clinical improvement. In 11 patients the rales had disappeared after 15--20 minutes or had regressed. In the remainder the dyspnoea had decreased so that at this point in 14 of the 15 patients various degrees of improvement had occurred. Four patients were completely without clinical signs after 30 minutes. The increased arterial blood pressure and heart rate had fallen markedly. In the seven patients of Group B mean left ventricular filling pressure fell within ten minutes of nitroglycerin administration (1.6 mg) from 33 +/- 10 to 24 +/- 8 mmHg, cardiac output rising sifnificantly from 3.3 +/- 0.8 to 3.7 +/- 0.8 1/min. Such favourable results with nitroglycerin are to be expected only if the pulmonary oedema is of cardiac origin.
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PMID:[Effect of nitroglycerin sublingually in the emergency management of "classical" pulmonary oedema (author's transl)]. 40 57

The study comprised seven children between 6-12 years admitted to Hospital Infantil "Lorencita Villegas de Santos" with progressive respiratory distress attended with cyanosis consistent with pulmonary edema. In all patients there was a previous history of a sudden change in altitude from sea level to 2,600 m. Changes consistent with pulmonary edema were made evident at the X-rays studies. The electrocardiogram showed right ventricular overload. No significant changes were found at the blood picture. All patients were treated with oxygen and rest; relief was attained within 72 hours.
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PMID:[Pulmonary edema of high altitude in childhood. Study of 7 cases]. 87 27

From June 1969 to April 1973, B.A.S. was carried out in 2-day to 6-month-old 65 infants at the Institute of Paediatrics of the Academy of Medicine in Warsaw. There were 16 infants up to one week old, 39 infants--up to one month, and 10 infants more than one month old. There were 43 boys and 22 girls among them. Cardiac catheterization and B.A.S. were carried out in most children up to 24 hours following hospitalization under local anaesthesia and premedication with robenzperidol and dolantin. In 11 of the 65 infants after B.A.S. the saturation with oxygen in the right atrium under-went no significant changes; in 54 cases it increased by 10 to 49 per cent. Of the 65 infants in whom B.A.S. was performed, 37 are alive, 28 had died. In 20 children under constant outpatient cardiological follow up the observation period has amounted from 6 months to 3 years. Their motoric development and growth is retarded, there is moderate cyanosis, but no symptoms of congestive failure were found. All these children are administered digitalis in chronic maintenance doses. Respiratory infections occured frequently in these patients. As mentioned above, 28 infants died at the age of 2 days to 6 months. Post mortem examination revealed that the B.A.S. was unsufficient in 14 cases. However, 14 infants died in spite of the satisfactority performed atrioseptostomy. Pulmonary oedema or haemorrhagic-and-inflammatory changes in the lungs as well as generalized thrombosis were the most frequent causes of death. On the basis of their own experience the authors elaborated indications and instructions for B.A.S. in neonates and infants with congenital heart diseases. These directives are based on the Team Work of cardiologists, anaesthesiologists, cardiac surgeons and paediatric radiologists. Because ever greater numbers of neonates are being sent to the Institute of Paediatric of the Academy of Medicine from all over Poland, the authors organized continuous cardiological emergency service to carry out B.A.S. procedures as soon as possible, without delay.
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PMID:[Balloon atrioseptostomy (B.A.S.) in the management of neonates and infants with transposition of great vessels (author's transl)]. 124 41

Five patients with neurogenic pulmonary edema (NPE) were reported. The edemas were caused by head injuries in four patients and by a craniotomy in the fifth. The onset of NPE was either acute (3 hours after injury) or was slow to develop (4 days later). Clinical symptoms included the sudden onset of coughing, tachypnea, tachycardia, and pink bubbly sputum. Moreover, the patients also suffered cyanosis, confusion, or respiratory failure. The distribution of the resulting pulmonary edema was diffuse in 4 cases and localized within a single lobe of the lung in 1 case. Treatment of the NPE included reducing intracranial pressure (glycerol), diuresis (furosemide and mannitol), narcotics (morphine, phenobarbital), and blocking the peripheral effect of sympathetic reflex activity (hydralazine, sodium nitroprusside). Mechanical ventilation support (CPU-1) in combination with controlled hyperventilation may also be necessary. The inability to correct hypoxemia without toxic levels of oxygen necessitates the use of PEEP (positive end-expiratory pressure, +5-10 cmH2O). Resolution of symptoms was noted 24 to 48 hours after treatment in 4 patients. Early diagnosis and intensive care of the pulmonary edema may have a significant bearing on the recovery of lung functions. Unfortunately, 4 of the patients failed to survive because of central nervous system failure. We therefore want to emphasize that NPE can cause secondary deterioration of neurological functions. In conclusion, when dealing with respiratory distress patients with CNS injuries, the possibility of additional damage from a NPE must be taken into consideration.
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PMID:[Neurogenic pulmonary edema: five cases report]. 129 67

A case of re-expansion pulmonary oedema is reported. A 7-year-old girl, after having been operated on for a lung tumour, had a postoperative haemothorax combined with atelectasis of the left upper lobe. After she had recovered from the first dose of chemotherapy, the thoracotomy wound was reopened to remove the partially organised and lysed haemothorax, as well as the very thickened pleura. The patient developed clinical signs of pulmonary oedema very shortly after the end of the anaesthetic (tachypnoea, cyanosis, a decrease in oxygen saturation when FIO2 < 1, pink frothy secretions in the endotracheal tube). End-inspiratory crepitations became audible in the left lung field only. The chest film showed left-sided diffuse nodular alveolar opacities. The girl was again ventilated, with + 5 cmH2O positive end-expiratory pressure. She was extubated 36 h later, and discharged a few days later without any sequela. This case was the first to be described in a child after pleural surgery. The death rate, estimated from a literature survey, is about 20%.
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PMID:[Postoperative re-expansion causing unilateral pulmonary edema]. 141 82

Eighty-two patients were hospitalized following an accidental exposure to chlorine. All patients presented with dyspnoea and cough. The other symptoms included irritation of throat (53.6%), irritation of eyes (42.3%), headache (29.2%), abdominal pain (26.8%), vomiting (24.3%) and giddiness (9.7%). All of them had bronchospasm and 5 (6%) had cyanosis at the onset. An x-ray of the chest revealed patchy infiltrates in 3 (3.85%) and hilar congestion in 2 (2.44%). Pulmonary function tests showed an obstructive pattern in 27.4%, restrictive in 3.25% and mixed in 53.2%. Pulmonary functions were normal in 16.1% of the patients. Bronchoscopy revealed tracheobronchial mucosal congestion in all cases, hemorrhagic spots in 35.7%, erosions and ulcers in 12.5%. All patients were treated with oxygen, aminophylline, hydrocortisone and antibiotics. Haematemesis (n = 1) and pulmonary oedema (n = 2) developed 12 hours after the admission. Two other patients developed pneumonia 48 hours later. All patients recovered satisfactorily. On follow-up 16 patients had no sequelae after one year. Pulmonary functions were normal in 5 patients after 3 years of follow-up.
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PMID:Acute accidental exposure to chlorine fumes--a study of 82 cases. 145 67

Aluminum phosphide (ALP) is highly toxic to the lungs, heart and blood vessels causing pulmonary edema, shock and arrhythmias. There is massive focal myocardial damage resulting in raised cardiac enzymes. This study included 92 patients of proven ALP poisoning. The age varied between 20-50 years and the majority (74) were females. Clinical manifestations were nausea and vomiting (92), dyspnea and palpitation (72 each), cyanosis (54), hypotension (32) and shock (46) etc. Cardiac arrhythmias were present in 80 cases and hypermagnesemia in 78 patients. Mean serum magnesium level (1.95 +/- 0.18 mE/l) was significantly (p less than 0.01) raised compared to mean magnesium level in control subjects (1.62 +/- 0.26 mEq/l). Hypermagnesemia results from myocardial and liver damage and to our knowledge has not been described in the literature. Of 92 cases studied, 66 died, 60 of whom died within 24 hours of ALP ingestion. Treatment is supportive.
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PMID:Hypermagnesemia following aluminum phosphide poisoning. 202 69


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