Biomedical subjects

I A Fein

Publications and source records attributed to I A Fein.

22 records · Page 2Linked to original sources

PubMed1978

Acute pulmonary edema in Plasmodium falciparum malaria.

This report describes a patient who developed acute pulmonary edema as a complication of Plasmodium falciparum malaria. Hemodynamic evaluation revealed a pulmonary artery wedge pressure of 3 mm Hg and a cardiac index of 4.6 liter per min per m2. The patient exhibited an acute decrease in serum colloid osmotic pressure from 25.1 mm Hg to 16.8 mm Hg. These findings suggest that pulmonary edema in this patient was the result of altered capillary membrane permeability.

Acute Disease↗

PubMed1978

Hyperchloremic acidosis during the recovery phase of diabetic ketosis.

We have studied 35 patients to find the occurrence of hyperchloremic acidosis during the recovery phase of diabetic ketoacidosis. At admission the patients had typical normochloremic acidosis, with increased anion gap exactly balancing decreased serum bicarbonate. In contrast, in 18 patients with phenformin-induced lactic acidosis, the increase in anion gap at admission was much greater than the decrease in bicarbonate. The difference between lactic acidosis and ketoacidosis may be explained by a slower rate of excretion of lactate than of ketone anions. After the patients with ketoacidosis were treated, the acidosis became predominantly hyperchloremic with normal anion gap. Failure to normalize serum bicarbonate is attributed to excretion of ketone anions in the urine.

Adolescent↗

PubMed1977

Colloid osmotic pressure as a prognostic indicator of pulmonary edema and mortality in the critically ill.

The relationship of colloid osmotic pressure (COP) to pulmonary edema and mortality in 128 critically ill patients was investigated in our critical care unit, and confirms previously reported observations. The COP in the 86 survivors was 22.0 (+/- 0.4 SEM) mm Hg versus 17.2 (+/- 0.6 SEM) mm Hg in the 42 who died (P less than 0.001). The patients were divided into three groups: 71 with no pulmonary edema, COP of 21.5 (+/- 0.5 SEM) mm Hg; 40 with cardiogenic pulmonary edema, COP of 21.4 (+/- 0.4 SEM) mm Hg; and 17 with noncardiogenic pulmonary edema, COP OF 13.6 (+/- 0.8 SEM) mm Hg. Colloid osmotic pressure was significantly lower in patients with noncardiogenic pulmonary edema (P less than 0.001). In 36 patients in whom pulmonary artery wedge pressures (PWP) were available, a COP-PWP gradient of 4.0 mm Hg or less was always associated with pulmonary edema, while a COP-PWP gradient greater than 4.0 mm Hg was never associated with pulmonary edema. Colloid osmotic pressure is a useful prognostic indicator of pulmonary edema and mortality in the critically ill.

Adolescent↗

PubMedDate not supplied

Fulminant noncardiogenic pulmonary edema in the critically ill.

The relationship between the serum colloid osmotic pressure (COPs), pulmonary artery wedge pressure (PWP), and pulmonary edema fluid colloid osmotic pressure was studied in six critically ill patients with fulminant noncardiogenic pulmonary edema. The relationship between COPs and PWP was also studied in 36 critically ill patients without pulmonary edema. The COPs-PWP gradient was normal in those patients without pulmonary edema. Three patients with noncardiogenic pulmonary edema had markedly reduced COPs-PWP gradients secondary to decreases in COPs. Their pulmonary edema fluid colloid osmotic pressure averaged 61% that of their serum colloid osmotic pressure. Three patients with noncardiogenic pulmonary edema had normal COPs-PWP gradients. Their pulmonary edema fluid colloid osmotic pressure averaged 92% that of their COPs. Noncardiogenic pulmonary edema in the critically ill patient may be caused by either a decrease of COPs-PWP gradient or an increase in capillary membrane permeability.

Adult↗