Salicylate pulmonary edema: the mechanism in sheep and review of the clinical literature.

Several clinical reports of salicylate-induced pulmonary edema led us to investigate the mechanism in a chronic unanesthetized sheep preparation. We infused an aspirin-buffer solution intravenously at rates up to 1,200 mg of aspirin per hour and compared effects on lung lymph flow and lymph protein concentration to those seen after mechanical elevation of pulmonary vascular pressures. Aspirin had little effect on lung vascular pressures but caused lung lymph flow to increase an average of greater than twice baseline. Because lymph protein concentrations were higher for a given lymph flow with aspirin than during mechanical pressure elevation, lymph protein (lymph flow X lymph to plasma protein concentration) increased much more with aspirin. Thus, aspirin appears to cause increased permeability to fluid and protein in the pulmonary vascular bed. Aspirin caused arterial PO2 to decrease from 83 +/- 3 SE mm Hg to 74 +/- 3 mm Hg (P less than 0.05) and caused postmortem extravascular lung water to increase. These findings are supported by a review of the clinical literature, indicating that salicylate pulmonary edema in humans is noncardiac in origin and may occur at doses considered therapeutic for some diseases as well as after overdose.     

Hydrochlorothiazide-induced pulmonary edema. Report of a case and review of the literature.

Immediately following the initial ingestion of hydrochlorothiazide, acute pulmonary edema developed in a patient who previously used bendroflumethiazide. Unlike previously published reports, we studied the patient from immunologic and pulmonary function aspects. Using standard techniques, no significant immunological mechanisms could be demonstrated. The pulmonary function testing disclosed a widened alveolar-arterial oxygen gradient and mildly decreased diffusing capacity that cleared on serial testing. We believe that this demonstrates a rare idiosyncratic reaction that apparently is seen specifically with hydrochlorothiazide and not with other thiazide medications.     

Smoking and postoperative pulmonary complications. An evidence-based review of the recent literature

Postoperative pulmonary complications (PPC) lead to significant morbidity after both thoracic and non-thoracic surgical procedures. The role of smoking as an independent risk factor is controversial, though recent level III and IV studies suggest that it may indeed be significant. In addition, the role and timing of pre-operative smoking cessation is not clear. Although some studies suggest that abstinence too soon prior to operation may actually increase the risk of PPC, it still appears that aggressive counseling for smoking cessation prior to any elective procedure is the best overall course of action.     

Fatal postoperative pulmonary embolism in mild haemophilia

The use of thromboprophylaxis in patients with haemophilia receiving factor replacement is often not considered necessary, but remains an area of debate. In this report we describe a patient with mild haemophilia A, who underwent major pelvic surgery. He had several underlying risk factors associated with the development of thromboembolism, and ultimately died as a direct consequence of multiple pulmonary emboli. The need for thromboprophylaxis and the risk balance ratio should always be considered in patients with bleeding disorders if they fall into what would otherwise be high-risk category for hospital acquired venous thromboembolism.     

Noncardiogenic pulmonary edema following upper airway obstruction. 7 cases and a review of the literature

Pulmonary edema is a relatively common problem facing most physicians. Its separation into cardiogenic and noncardiogenic or high-permeability variants is crucial to its proper early management. Our understanding of the disease processes producing noncardiogenic pulmonary edema has greatly expanded in the last 2 decades. Upper airway obstruction (UAO) is one of many recently recognized mechanisms which can produce noncardiogenic pulmonary edema. The UAO may be subtle in some patients, making its association with the subsequent pulmonary edema difficult especially for the physician unaware of this entity and the potential risk factors contributing to it. A high index of suspicion for this diagnosis is required in the right clinical settings. Our clinical results support a noncardiogenic basis for pulmonary edema occurring after UAO. Five of our 7 patients had at least 1 identifiable risk factor for the development of peri-intubation UAO and pulmonary edema. Additionally, the onset of pulmonary edema following UAO and the duration of the pulmonary edema varied considerably in our patients. Individuals with additional risk factors for the development of noncardiogenic pulmonary edema developed a more severe form of pulmonary edema associated with other organ-system disease. However, in most individuals, UAO-associated pulmonary edema appears to be a self-limited reversible process once it is recognized and properly treated.     

High-altitude pulmonary edema: pathophysiology and clinical review

High-altitude pulmonary edema (HAPE) affects young, healthy climbers in an unpredictable fashion. It is potentially fatal, and its underlying pathophysiology is not thoroughly understood. The history and clinical presentation of HAPE, as well as the known underlying pathophysiology, are reviewed. For instance, in HAPE there is an association with blunted respiratory drives to hypoxia and accentuated hypoxic pulmonary vasoconstriction. Recent data show that HAPE is a high permeability leak of protein into the alveolar space associated with an influx of alveolar macrophages. These data have been obtained recently by fiberoptic bronchoscopy in the field setting of Mt McKinley at 4,400 m. The approach to recognition and treatment that involves primarily descent and/or oxygen is discussed.     

Fatal overdose with trazodone: case report and literature review

A fatal case of suicide with trazodone alone in a 40-year-old patient is reported. Life-threatening arrhythmias, such as torsades de pointes and complete AV block, are recorded. Blood collected at admission contained a trazodone toxic concentration of 25.4 micrograms/mL. The patient developed multiple organ failure and died less than 24 hours after his admission to the emergency department. The authors discuss the effects of overdose of trazodone, a well-known safe antidepressant drug.     

Hereditary angioneurotic edema: review of the literature

Congenital C1-inhibitor deficiency, or hereditary angioneurotic edema (HAE), is a rare autosomal dominant disease due to alterations in the C1 inhibitor gene that results in a deficiency of antigenic and/or functional C1-INH. Affected patients are heterozygous, and their deficiency is incomplete, many of them having up to 20% of the normal amount of the inhibitor. The disease is characterised by recurrent, circumscribed, non-pitting, and non-pruritic subepithelial swellings of sudden onset, which fade during the course of 48-72 hours, but can persist up to 1 week. Lesions can be solitary or multiple and primarily involve the extremities, larynx, face, and bowel wall. Bradykinin is believed to be the main, but certainly not the sole, mediator responsible for the bouts of edema in HAE. The diagnosis is suggested by family history, the lack of accompanying pruritus or urticaria, the presence of recurrent gastrointestinal attacks of colics, and episodes of laryngeal edema. Diminished C4 concentrations during symptomatic periods are highly suggestive for the diagnosis. Further laboratory diagnosis depends on demonstrating a deficiency of C1-INH antigen (type I) in most kindreds, but some kindreds have an antigenically intact but dysfunctional protein (type II) and require a functional assay to establish the diagnosis. Prophylactic administration of either attenuated androgens or protease inhibitors has proved useful in reducing frequency or severity of attacks. Infusions of a vapour-heated C1-INH concentrate are safe and effective means of both preventing and treating attacks. Nevertheless, this treatment is expensive and this extract is not readily available. It is emphasised that administration of angiotensin converting enzyme inhibitors is contraindicated in patients suffering from protease inhibitor deficiency states.     

Re-expansion pulmonary edema. A potential role for free radicals in its pathogenesis

Re-expansion pulmonary edema (RPE) has been attributed to decreased lung interstitial pressures from a variety of mechanisms. Because some recent studies have implicated mechanisms that increase microvascular permeability in RPE, we tested whether the edema were due to free radical generation during re-expansion and reoxygenation of the collapsed lung. We used a rabbit model of RPE to test the effects of intracellular (dimethylthiourea) or extracellular (catalase) oxygen metabolite scavengers. Allopurinol was administered separately to determine whether xanthine oxidase was an important source of superoxide in this model. Edema was quantitated both gravimetrically and histologically, and lung xanthine oxidase activity was measured using a sensitive fluorometric assay with pterin as substrate. The results suggest indirectly that OH. or H2O2 (derived from O2-) contribute to the well-documented increase in lung permeability in RPE because dimethylthiourea, dimethylthiourea plus catalase, or catalase alone inhibited the edema to various degrees. Further, we observed histologically that increased numbers of neutrophils were present in re-expanded lungs and that neutrophil infiltration appeared to be diminished by antioxidant administration. Allopurinol did not decrease the edema, because xanthine oxidase activity in rabbit lung tissue is extremely low. We speculate that free radical generation in lung tissue contributes to the pathogenesis of RPE, although reinitiation of lung perfusion and ventilation requires a rapid change in intrathoracic pressure.