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

A 57-year-old woman presented in severe respiratory distress 30 minutes after ingesting hydrochlorothiazide. Pulmonary edema was evident clinically and radiographically. A noncardiogenic etiology was suggested by the lack of jugular venous distention, S3 gallop, or pedal edema, and the presence of a normal cardiac silhouette on chest radiograph. The patient's pulmonary edema remitted with supportive therapy.
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PMID:Noncardiogenic pulmonary edema following hydrochlorothiazide ingestion. 361 70

These experiments characterize the effects of hemoglobin and erythrocyte membrane lipids on the dynamic surface activity and adsorption facility of whole lung surfactant (LS) and a calf lung surfactant extract (CLSE) used clinically in surfactant replacement therapy for the neonatal respiratory distress syndrome (RDS). The results show that, at concentrations from 25 to 200 mg/ml, hemoglobin (Hb) increased the minimum dynamic surface tension of LS or CLSE mixtures (0.5 and 1.0 mumol/ml) from less than 1 to 25 dyn/cm on an oscillating bubble apparatus at 37 degrees C. Similarly, erythrocyte membrane lipids (0.5-3 mumol/ml) also prevented LS and CLSE suspensions (0.5-2.0 mumol/ml) from lowering surface tension below 19 dyn/cm under dynamic compression on the bubble. Surface pressure-time adsorption isotherms for LS suspensions (0.084 and 0.168 mumol phospholipid/ml) were also adversely affected by Hb (0.3-2.5 mg/ml), having a slower adsorption rate and magnitude. Significantly, these inhibitory effects of Hb and membrane lipids could be abolished if LS and CLSE concentrations were raised to high levels. In complementary physiological experiments, instillation of Hb, membrane lipids, or albumin into excised rat lungs was shown to cause a decrease in pressure-volume compliance. This decreased compliance was most prominent in lungs made partially surfactant deficient before inhibitor delivery and could be reversed by supplementation with active exogenous surfactant. Taken together, these data show that molecular components in hemorrhagic pulmonary edema can biophysically inactivate endogenous LS and adversely affect lung mechanics. Moreover, exogenous surfactant replacement can reverse this process even in the continued presence of inhibitor molecules and thus has potential utility in therapy for adult as well as neonatal RDS.
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PMID:Effects of hemoglobin and cell membrane lipids on pulmonary surfactant activity. 369 77

The respiratory manifestations of leptospirosis are usually benign. A case is reported of anicteric leptospirosis with serious pulmonary affection. The clinical symptoms, the radiological manifestations and haemodynamic investigation were suggestive of an acute respiratory distress by non-haemodynamic pulmonary oedema. In accordance with other authors, one would be justified in including this acute respiratory failure as part of the acute respiratory distress syndrome of the adult (ARDS).
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PMID:[Acute respiratory distress disclosing leptospirosis]. 382 92

To determine if vascular abnormalities in preterm neonates might be related to vasoactive prostaglandins, stable prostacyclin (6-KPGF1 alpha) and thromboxane A2 (T X B2) metabolites in arterial blood were measured at less than or equal to 6 hours after birth and at 24, 48, and 72 hours using a radioimmunoassay. Neonates of less than 32 weeks gestation (N = 26) were diagnosed as having either the idiopathic respiratory distress syndrome (IRDS, N = 15) or pulmonary edema (PE, N = 11), and were also grouped according to the presence or absence of intracranial hemorrhage (ICH, N = 11) or patent ductus arteriosus (PDA, N = 10). Initial plasma 6-KPGF1 alpha was greater in neonates with ICH (0.23 +/- 0.04 ng/ml, mean +/- SE) than without ICH (0.11 +/- 0.04, p less than 0.05). Neonates with both ICH and IRDS (N = 8) had significantly elevated T X B2 at all sampling times compared to neonates with IRDS and no ICH (N = 7). Both T X B2 and 6-KPGF1 alpha increased with time in those with major ICH. Among neonates without ICH, 7 with IRDS had higher initial 6-KPGF1 alpha (0.19 +/- 0.07 ng/ml) and lower T X B2 (0.15 +/- 0.04 ng/ml) than 8 with PE (0.04 +/- 0.01 and 0.37 +/- 0.09 ng/ml, respectively). The initial 6-KPGF1 alpha (0.024 + 0.003 ng/ml), measured in neonates with PE and without PDA or ICH (N = 6), was significantly less than the corresponding value in the other neonates (0.201 +/- 0.036 ng/ml) (N = 20).
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PMID:Plasma 6-keto prostaglandin F1 alpha and thromboxane B2 in sick preterm neonates. 385 77

Severe head trauma patients frequently develop pulmonary failure. The aetiology of this respiratory distress may be central (neurogenic pulmonary oedema, delayed neurogenic pulmonary dysfunction, abnormal respiratory patterns) or peripheral, due to chest trauma, multiple trauma or lung infection. Hypoxia and hypercarbia alter cerebral haemodynamics, increase intracranial pressure and cause secondary deterioration of neurological function. Ventilatory support is of utmost importance in supportive care of head trauma patients. Continuous mechanical ventilation and intermittent mandatory ventilation are most frequently employed. Hyperventilation is used to lower intracranial pressure and positive end-expiratory pressure (PEEP) is applied in lung disorders characterized by interstitial oedema and alveolar collapse. The effects of PEEP on cerebral perfusion pressure and on intracranial pressure depend on the interaction of pulmonary compliance, cerebral pressure/volume relationship and cerebral vascular autoregulation. High levels of PEEP may be deleterious in patients with altered cerebral autoregulation. High frequency ventilation theoretically has less influence on intrathoracic pressures and on cerebral haemodynamics but has not been shown superior in the respiratory support of severe head trauma patients.
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PMID:Ventilatory support for pulmonary failure of the head trauma patient. 389 Sep 90

1. With improvements in treatment of burn shock and wound sepsis, inhalation injury has emerged as the number one cause of fatality in the burn patient; it accounts for 20 to 84 per cent of burn mortality. 2. Only steam is capable of inflicting direct thermal damage; most injury is caused by incomplete products of combustion, the most important being aldehydes. 3. More accurate diagnostic techniques, including fiberoptic bronchoscopy and 133Xe scanning, have been added to the traditional clinical signs of inhalation injury, such as facial burns, singed nasal vibrissae, and closed space injury, and have led to a new estimation of a 30 per cent incidence among patients with major burns. 4. Patients with inhalation injury typically pass through three stages, those of acute pulmonary insufficiency, pulmonary edema, and bronchopneumonia. 5. The major early pathophysiologic changes seen in the lungs of burned patients related to edema. With inhalation injury this is probably mediated by the products of activated neutrophils. Later changes are the result of the reduction of surfactant and thus lung compliance. 6. Treatment consists of intubation at the first hint of respiratory distress; the issue of tracheostomy versus endotracheal intubation has not been scientifically resolved, but most centers employ prolonged nasotracheal intubation. Prophylactic antibiotics or steroids are not of benefit. Further care is only supportive and includes CPAP, PEEP, vigorous pulmonary toilet, humidification of inspired air, and antibiotics for documented infection. 7. Further advances await the development of pharmacologic methods of affecting the lung's response to injury, which includes altered capillary permeability and decreased immune function.
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PMID:Pulmonary injury in burned patients. 391 76

Pneumocystis carinii (P.c.) pneumonia was induced in 40 rats by a prolonged corticosteroid treatment (group 1); 40 healthy rats of equal weight constituted the control group (group 2); 9 rats received the same corticosteroid treatment as group 1, together with trimethoprim-sulfamethoxazole (TMP-SFZ) in order to prevent P.c. multiplication (group 3). We could distinguish the respiratory effects induced by corticosteroids from those caused by P.c. pneumonia (group 3 vs group 1). For six weeks the blood leukocyte count, the weight of the spleen and the thymus and the pulmonary status were monitored. Blood gases and acid-base status were measured in conscious rats. There was no pulmonary oedema. The infected P.c. rats had a low PaCO2 and a slight disturbance of blood oxygenation, exemplified by A-aDO2 of 30 mmHg, compared with 17.5 mmHg in control rats and 17 mmHg in TMP-SFZ treated rats. P.c. infected rats had a lymphocyte depletion induced by corticosteroids. They did not exhibit respiratory distress. P.c. pneumonia alone in rats did not cause frank hypoxemia.
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PMID:Respiratory and pulmonary alterations in experimental Pneumocystis carinii pneumonia in rats. 391 91

Five cases of coagulopathy caused by consumption of indanedione (diphacinone)-based rodenticides are reported. In each case, acute onset of lethargy and respiratory distress were the predominant initial clinical signs. Thoracic radiography revealed pulmonary edema, pleural effusion, and/or pericardial effusion as consistent findings. Laboratory evaluations confirmed coagulopathies that responded to vitamin K1 therapy.
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PMID:Diphacinone-induced coagulopathy in the dog. 394 17

In patients with subacute toxic reactions from paraquat poisoning (death within 11 to 41 days), the extent of lipid peroxidation, expressed as serum malondialdehyde level, was 2.7-fold higher (12.33 +/- 4.42 nmole/mL) before pulmonary fibrosis than that in normal controls (4.55 +/- 1.23 nmole/mL). The extent of lipid peroxidation in patients with acute toxic reactions (death within one to three days) was not elevated; these patients died of pulmonary edema and hemorrhage (acute respiratory distress), liver failure, renal failure, and adrenal necrosis. Remarkable high levels of paraquat (greater than 5 mg/L) were found in the urine, serum, and tissues of patients with acute toxic reactions; a small amount of paraquat was found in the serum or urine of patients with subacute toxic reactions five to 11 days after ingestion. Patients who survived had no elevation in lipid peroxidation. Administration of vitamin E (100 to 4,000 mg/day from the first hospital day) had no effect on survival.
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PMID:Further studies of lipid peroxidation in human paraquat poisoning. 396 49

Two children, aged 3 1/2 and 5 1/2 years, are described. Both developed pulmonary oedema (PE) following a short episode of choking on a sweet and an orange, respectively. On admission diagnosis was made by chest X-ray. One child was asymptomatic despite PE while the other showed only mild respiratory distress. Both children recovered spontaneously and chest X-rays showed a return to normal within 24 h. The mechanism of PE production is discussed. It is suggested that oedema formation occurs during the obstruction and that it is due to hypoxia and the severe negative pleural pressure resulting from attempts to inspire against the obstructed airway. both hypoxia and severe negative pleural pressure cause an increase in pulmonary capillary pressure and transduration of fluid across the capillary membrane.
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PMID:Pulmonary oedema following choking: report of two cases. 398 29


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