Reexpansion pulmonary edema occurring after thoracoscopic drainage of a pleural effusion

Video assisted thoracoscopic drainage and tale pleurodesis was used to treat a recurrent pleural effusion in a 60 year-old woman undergoing major gynecologic surgery. She developed reexpansion pulmonary edema immediately following surgery. Several important risk factors that were present in this patient are discussed. In addition to almost, complete collapse of the underlying lung for several weeks, thoracoscopy resulted in manipulations and rapid re-inflation of the underlying lung, which further increased the risk to the patient.     

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.     

Post-obstructive pulmonary edema after adenoid-amygdalectomy

A two-years-old boy with Down's Syndrome and a small interauricular communication was given priority scheduling for adenoidectomy and tonsillectomy to correct subacute obstruction of the upper airway. The only noteworthy event during surgery was an SpO2 of 92% during mechanical ventilation with FiO2 of 0.5 from no apparent cause. The patient suffered acute respiratory insufficiency due to the post-obstructive pulmonary edema in the hours immediately following surgery. The incidence of post-obstructive pulmonary edema is higher than might be expected, as symptoms can be interpreted as aspiration pneumonitis or left ventricular failure. Given the high prevalence of adenoiditis and tonsillitis with varying degrees of airway obstruction in children, we consider it useful to report this case. Such patients should be monitored carefully in the early postoperative period.     

High-altitude pulmonary edema: a clinical crisis

High-altitude pulmonary edema is a serious clinical condition observed in individuals participating in mountain climbing and skiing at high altitudes. High-altitude pulmonary edema is an oncardiogenic form of pulmonary edema. Atrial natriuretic factor and endothelin are implicated and ventilatory support is important in preventing fatalities.     

Care of postoperative patients with pulmonary edema

The quality of life of dialysis-dependent patients in any centre reflects the standards of its vascular access service. Poor access invariably causes inadequate dialysis while fistula failure disrupts the patient's life style, results in the need for further surgical intervention, frequently leads to hospitalization and has adverse financial implications for the patient as well as the provider. The authors review the fundamental principles and recent advances in the establishment and preservation of vascular access for chronic haemodialysis.     

Arterial blood gases in acute pulmonary edema

Arterial blood gas and pH measurements in 82 patients with acute pulmonary edema of cardiogenic origin entering the emergency department varied widely and were unpredictable using clinical examination. The mean arterial oxygen tension (PaO2) measured in 71 patients breathing room air was 59 mm Hg. Fourteen of the 82 patients were acidemic; 35, alkalemic and 33 had a pH in the normal range. The acidemic group had markedly lower PaO2, all under 60 mm Hg. Oxygen and furosemide were used in all cases and effectively corrected the hypoxia and reduced pulmonary congestion. Other drugs used included aminophylline (14 patients), morphine sulfate (9 patients) and digoxin (3 patients). Five of the nine patients who received morphine were hypercarbic initially but the CO2 retention did not worsen. No patient died during the initial 48 hours. This study reiterates the importance of directing therapy at ventilatory and cardiac abnormalities and points out the value of arterial blood gas monitoring to assess the initial status, monitor the patient's course, and to select drug therapy.     

High-altitude pulmonary edema at a ski resort

MRI can accurately define the extension of cervical carcinoma to the parametria. However, in patients with cervical carcinoma clinical stage IB, the definition of the dimensions of the tumour, prior to surgery, and may also modify the treatment procedure. Recently pre-operative neoadjuvant chemotherapy has been proposed for patients with bulky tumours. Multiple factors may influence the prognosis of clinical stage IB and survival varies greatly among these patients. In particular the maximum dimensions of the tumour seem to have a prognostic relevance. The aim of this paper is to evaluate the potential of MRI to measure tumour size, in order to discriminate between patients needing surgery alone or pre-operative therapy followed by surgery. In 20 patients with clinical stage IB cervical carcinoma we performed MRI to measure the radius of the cervix, the radius of the tumour and their ratios. The measurements obtained have been compared with the corresponding data from histopathology of the operative specimens. The close correspondence between these linear measurements allows us to propose MRI as a reliable method to define tumour size in clinical stage IB patients before surgery.     

Role of nitric oxide in sepsis-associated pulmonary edema

Transient pulmonary hypertension after inhibition of nitric oxide synthase (NOS) does not alter pulmonary reflection coefficients or lymph flows in endotoxemic sheep. To test the effects of persistent pulmonary hypertension induced by N omega-nitro-L-arginine methylester (L-NAME) and of inhaled NO on pulmonary edema, 18 sheep (three groups) were chronically instrumented with pulmonary artery catheters, femoral arterial fiberoptic thermistor catheters, and tracheostomy. The awake, spontaneously breathing animals received Salmonella typhi endotoxin (lipopolysaccharide; LPS) (10 ng/kg/ min) for 28 h. After 24 h, an airflow of 6 L/min was delivered through the tracheostomy. One group of animals (L-NAME/air) received L-NAME intravenously (25 mg/kg + 5 mg/kg/h) and breathed air. The second group (L-NAME/NO) was given L-NAME and NO (40 ppm) was added to the airflow. The third group was given NaCl 0.9% and breathed air (NaCl/air). Extravascular lung water was measured through the double-indicator dilution technique. Endotoxemia caused pulmonary edema, which was aggravated by L-NAME. Breathing of NO normalized pulmonary artery pressure (Ppa) and ameliorated pulmonary edema. Inhalation of NO may therefore be a therapeutic option for pulmonary edema associated with pulmonary hypertension.     

Monocrotaline model of noncardiogenic pulmonary edema in dogs

Monocrotaline, a plant alkaloid shown histologically to produce pulmonary endothelial damage and edema, was used in dogs to produce an acute model of noncardiogenic pulmonary edema. Following intravenous injection there was no change in pulmonary vascular pressures or heart rate; cardiac output fell and pulmonary vascular resistance increased. After 2 h measurement of lung water demonstrated modest pulmonary edema in all animals. The degree of edema produced was more consistent and reproducible than that following alloxan or alpha-naphthylthiourea.