Effect of upright and supine posture on hypoxemia during air transport.

BACKGROUND: Change in body position can cause hypoxemia at sea level in patients with lung diseases. Because of concern for the added risk of hypoxemia during air transport, we investigated the effect of body position on arterial oxygen partial pressure (PaO2) in individuals with lung disease under conditions of hypobaric hypoxia. METHOD: The study groups consisted of 8 patients with chronic obstructive lung disease, 4 patients with interstitial lung disease, and 6 healthy subjects. We obtained samples from radial artery catheters at sea level (SL) and altitude (ALT) simulation of 8000 ft (2438 m) in a hypobaric chamber in supine and upright postures. RESULTS: Altitude exposure did not result in a significant change in mean supine minus mean upright PaO2 (dPaO2); however, some individuals had large changes at SL. Moreover, the variance for dPaO2 was significantly smaller at ALT compared to SL with all groups combined (F test, p < 0.05). We found no correlation between dPaO2 at SL vs. ALT (p = 0.293; r = 0.262; n = 18). At both SL and ALT, dPaCO2 correlated negatively with dpH. At SL, dPaO2 did not correlate with either dPaCO2 or dpH; at ALT dPaO2 correlated with dpH (p < 0.05) and correlated negatively with dPaCO2 (p < 0.01). CONCLUSION: We conclude that significantly less postural variation in PaO2 occurs at moderate ALT compared to SL. In our patients with diffuse bilateral pulmonary disease, postural change did not contribute significantly to hypoxemia experienced at ALT. We infer that greater ventilatory response to hypoxemia at ALT in either posture may explain this finding.

Opportunistic pulmonary infections with fludarabine in previously treated patients with low-grade lymphoid malignancies: a role for Pneumocystis carinii pneumonia prophylaxis.

The high incidence of opportunistic pulmonary infections in fludarabine-treated patients at Walter Reed Army Medical Center (WRAMC) and in the literature are described. A CancerLit search of fludarabine from June 1983-April 1994 with subsequent cross referencing and a retrospective review of all patients receiving fludarabine at WRAMC was performed. A total of 2,269 patients with low-grade lymphoid malignancies who received 7,547 + cycles of fludarabine were identified from the literature. Seventy-three (3.2%) of these patients developed opportunistic infections. Seventy-one (97%) of these infections occurred in patients who were pretreated with alkylator regimens or corticosteroids. Forty-five (2%) of these were of respiratory origin and associated with a 56% mortality rate. In contrast, 6 of the 21 patients (29%) treated with fludarabine at WRAMC developed opportunistic pulmonary infections which included three Pneumocystis carinii (PCP), one PCP/disseminated Candidiasis, one Mycobacterium avium intracellulare, and one Aspergillus niger pneumonia. These infections developed during and after treatment with fludarabine in alkylator-resistant patients who had received corticosteroids before (n = 6), during (n = 1), or after (n = 4) fludarabine therapy. Lack of PCP prophylaxis was the only significant (P = .018) variable that differentiated patients who developed opportunistic pulmonary infections. Corticosteroid treatment before, during, or after fludarabine treatment in patients with alkylator-resistant, low-grade lymphoid malignancies who have not received PCP prophylaxis is associated with an increased risk of opportunistic pulmonary infections. Aggressive work-up of pulmonary syndromes and PCP prophylaxis in these patients should be considered during and after treatment with fludarabine.

Epinephrine-induced lactic acidosis in the setting of status asthmaticus.

A relationship between intravenous epinephrine infusion and the development of lactic acidosis has been well described. We report a temporal association between the administration of subcutaneous epinephrine and the development of lactic acidosis in the setting of status asthmaticus. A 20-year-old woman with a history of asthma came to the emergency service in acute respiratory distress and was treated with subcutaneous epinephrine. Six hours later, serial arterial blood gas studies revealed the onset of a primary metabolic acidosis. Additional diagnostic studies revealed a serum lactate level of 9.5 mumol/L. The lactic acidosis resolved within 15 hours. The patient never exhibited signs of hypotension, hypoxemia, or sepsis, and other potential etiologies for lactic acidosis were excluded. We believe the events of this case constitute a new observation and theorize a mechanism of peripheral vasoconstriction and transient tissue hypoperfusion mediated by the subcutaneous epinephrine.