Acute cyanide toxicity caused by apricot kernel ingestion

A 41-year-old woman ingested apricot kernels purchased at a health food store and became weak and dyspneic within 20 minutes. The patient was comatose and hypothermic on presentation but responded promptly to antidotal therapy for cyanide poisoning. She was later treated with a continuous thiosulfate infusion for persistent metabolic acidosis. This is the first reported case of cyanide toxicity from apricot kernel ingestion in the United States since 1979.     

Reexpansion pulmonary edema

Reexpansion pulmonary edema is a rare complication attending the rapid reexpansion of a chronically collapsed lung, such as occurs after evacuation of a large amount of air or fluid from the pleural space. The condition usually appears unexpectedly and dramatically-immediately or within 1 h in 64% of patients and within 24 h in the remainder. The clinical manifestations are varied; they range from roentgenographic findings alone in asymptomatic patients to severe cardiorespiratory insufficiency. The radiographic evidence of reexpansion pulmonary edema is a unilateral alveolar filling pattern, seen within a few hours of reexpansion of the lung. The edema may progress for 24-48 h and persist for 4-5 days. Human data on the pathophysiology of reexpansion pulmonary edema derive from small series of patients, case reports, and reviews of the literature. On the other hand, a larger body of data exists on experimental reexpansion pulmonary edema in cats, monkeys, rabbits, sheep, and goats. This review examines the clinical and experimental evidence for reexpansion pulmonary edema. In addition, we detail the historical background, clinical setting, treatment, and outcome of reexpansion pulmonary edema.     

Salicylate-induced pulmonary edema

A case of pulmonary edema secondary to salicylate intoxication is described. The pulmonary wedge pressure was normal, excluding cardiogenic pulmonary edema. Thus salicylate intoxication should be considered as a rare cause in the differential diagnosis of pulmonary edema with a normal heart size. The pulmonary edema resolved gradually over 8 days. Literature relative to salicylate-induced pulmonary edema is reviewed.     

Massive verapamil overdose complicated by noncardiogenic pulmonary edema

We describe two cases of pulmonary edema, bradycardia, and hypotension associated with massive verapamil overdose. A noncardiogenic etiology of the pulmonary edema was indicated in one patient by normal thermodilution cardiac output and pulmonary artery occlusion pressure, and in the other patient by a normal echocardiogram. We hypothesize that calcium channel blocker overdose predisposes patients to develop pulmonary edema.     

Acromegaly caused by pulmonary carcinoid tumours

Vascular input impedance and associated hydraulic power was measured in rabbit isolated lungs. The study was focused on changes in impedance and in pulsatile hydraulic power during relaxation and contraction of vascular smooth muscle. Pulsatile power was found to be at a minimum when smooth muscle tone was such that the pulmonary arterial pressure was in the physiological range, and increased both when the vessels were relaxed and further constricted. Input impedance was found to be determined mainly by the large, proximal ('extra-alveolar') arteries.     

Regional measurements of pulmonary edema by using magnetic resonance imaging

A three-dimensional magnetic resonance imaging (MRI) method to measure pulmonary edema and lung microvascular barrier permeability was developed and compared with conventional methods in nine mongrel dogs. MRIs were obtained covering the entire lungs. Injury was induced by injection of oleic acid (0.021-0.048 ml/kg) into a jugular catheter. Imaging followed for 0.75-2 h. Extravascular lung water and permeability-related parameters were measured from multiple-indicator dilution curves. Edema was measured as magnetic resonance signal-to-noise ratio (SNR). Postinjury wet-to-dry lung weight ratio was 5.30 +/- 0.38 (n = 9). Extravascular lung water increased from 2.03 +/- 1.11 to 3.00 +/- 1.45 ml/g (n = 9, P < 0.01). Indicator dilution studies yielded parameters characterizing capillary exchange of urea and butanediol: the product of the square root of equivalent diffusivity of escape from the capillary and capillary surface area (D1/2S) and the capillary permeability-surface area product (PS). The ratio of D1/2S for urea to D1/2S for butanediol increased from 0.583 +/- 0.027 to 0.852 +/- 0.154 (n = 9, P < 0.05). Whole lung SNR at baseline, before injury, correlated with D1/2S and PS ratios (both P < 0.02). By using rate of SNR change, the mismatch of transcapillary filtration flow and lymph clearance was estimated to be 0.2-1.8 ml/min. The filtration coefficient was estimated from these values. Results indicate that pulmonary edema formation during oleic acid injury can be imaged regionally and quantified globally, and the results suggest possible regional quantification by using three-dimensional MRI.