Bronchogenic carcinoma, massive hemoptysis, and systemic air embolus.

A 57-year-old woman with squamous carcinoma of the right lung (hilum) developed acute massive hemoptysis with syncope and hypotension. Resuscitation was complicated by the development of massive systemic air embolus, and the patient died.

The rate of fall of arterial oxyhemoglobin saturation in obstructive sleep apnea.

During breath holding, correlations have been demonstrated between the rate of fall of arterial oxyhemoglobin saturation (dSaO2/dt) and the following: thoracic gas volume at apnea onset, resting oxygen consumption, preapneic arterial oxyhemoglobin saturation (SaO2) and obesity. A key factor influencing dSaO2/dt is mixed venous oxyhemoglobin saturation (SvO2) as recently demonstrated in an animal model of obstructive apnea. The purpose of the present study was to see if dSaO2/dt was related to SvO2 during sleep in a group of subjects with severe obstructive sleep apnea (OSA) and varying levels of SvO2. Eight OSA subjects were studied during sleep with indwelling arterial and central venous catheters. Continuous SaO2 was measured by ear oximetry while continuous SvO2 was measured through the fiberoptic bundle of a Shaw Opticath catheter. Thirty percent or more of all obstructive apneas were scored for duration, preapneic SaO2, SvO2 and dSaO2/dt. Least squares regression was used to examine the relationship between dSaO2/dt and other measured variables. The dSaO2/dt showed a consistent negative correlation with preapneic SvO2 and was not related to duration. Mean dSaO2/dt during sleep correlated to some degree with the degree of gas exchange (Qva/Qt) abnormality prior to sleep. It is concluded that in humans, SvO2 plays a substantial role in determining dSaO2/dt. Potentially, the presence of gas exchange abnormalities (eg, found in intrinsic lung disease) causing hypoxemia and low SvO2 may steepen dSaO2/dt, lowering the nadir level of apneic desaturation for the same duration of apnea found in a patient with more normal gas exchange.

Pulmonary vascular hemodynamics in chronic lung disease patients with and without oxyhemoglobin desaturation during sleep.

Nonapneic, nocturnal oxyhemoglobin desaturation (NOD) during rapid-eye-movement (REM) sleep has been proposed as a predecessor and possible etiologic factor in the development of pulmonary hypertension in patients both with restrictive and obstructive chronic lung disease. The association between abnormal waking cardiopulmonary hemodynamics and NOD has not been established in patients with mild daytime hypoxemia. Gas exchange, pulmonary function, red cell mass, radionuclide gated cardiac ejection fraction, and supine cardiopulmonary hemodynamics were examined in 36 patients with chronic lung disease. All had a daytime PaO2 greater than 60 mm Hg and REM sleep-related NOD for greater than 5 minutes, to 85 percent or lower. These data were compared to those from 13 subjects with similar symptoms and objective measures of pulmonary dysfunction but without evidence of NOD. Patients with NOD showed more end organ evidence of hypoxemia and more abnormal cardiopulmonary hemodynamics than patients with similar degrees of lung disease but without NOD. The relative role of daytime vs nocturnal hypoxemia in inducing hemodynamic differences between groups cannot be determined from this study.

Drug-induced linear immunoglobulin A bullous disease that clinically mimics toxic epidermal necrolysis.

Drug-induced linear immunoglobulin A bullous disease is a subepidermal blistering disorder that most commonly occurs after exposure to vancomycin. It can clinically mimic toxic epidermolytic necrolysis. We describe an 87-year-old white woman in whom linear immunoglobulin A bullous disease developed while she was taking vancomycin and phenytoin. A few days after the linear immunoglobulin A bullous disease developed, both medications were discontinued. No new bullae developed, and the eruption completely resolved within 2 weeks. The patient was treated with only topical therapy.

Hereditary epidermolytic palmoplantar keratoderma (Vörner type) in a family with Ehlers-Danlos syndrome.

We describe a kindred in whom epidermolytic palmoplantar keratoderma occurred in association with Ehlers-Danlos syndrome type III (benign hypermobility syndrome). This kindred consisted of 27 members of four generations, 14 of whom had palmoplantar keratoderma (PPK). Of those who had palmoplantar keratoderma, 6 had Ehlers-Danlos type III (EDS II). The proband presented with diffuse, symmetrical hyperkeratotic plaques that were yellow and sharply demarcated, covering the entire palms and soles, in addition to marked large and small joint flexibility and skin hyperextensibility. A biopsy specimen from the palm revealed features of epidermolytic hyperkeratosis with acanthosis. To our knowledge, this is the first report of PPK in a family with Ehlers-Danlos syndrome. Linkage analysis of these two clinical traits showed that the genes responsible for PPK and EDS III are not closely linked, and therefore are not immediately adjacent. However, linkage at greater genetic distances could not be excluded.