Obesity hypoventilation syndrome: hypoxemia during continuous positive airway pressure.

BACKGROUND: Polysomnography findings between matched groups with obstructive sleep apnea (OSA) and OSA plus obesity-hypoventilation syndrome (OHS) before and after continuous positive airway pressure (CPAP), particularly in the extremely severe obese (body mass index [BMI] >or= 50 kg/m2), are unclear. DESIGN: Prospective study of subjects (BMI >or= 50 kg/m2) undergoing diagnostic polysomnography. Subjects with an apnea-hypopnea index (AHI) >or= 15/h underwent a second polysomnography with CPAP. The effect of 1 night of CPAP on sleep architecture, AHI, arousal indexes, and nocturnal oxygenation was assessed. OHS was defined as those subjects with obesity, PaCo2 > 45 mm Hg, and PaO2 < 70 mm Hg in the absence of lung disease. RESULTS: Twenty-three subjects with moderate-to-severe OSA and 23 subjects with moderate-to-severe OSA plus OHS underwent a 1-night trial of CPAP. Both groups were matched for spirometry, BMI, and AHI, but oxygen desaturation was worse in the OSA-plus-OHS group. CPAP significantly improved rapid eye movement (REM) duration (p < 0.005), AHI (p < 0.005), arousal indexes (p < 0.005), and percentage of total sleep time (TST) with oxygen saturation (SpO2) < 90% (p < 0.005) in both groups. In subjects with OSA plus OHS, 43% continued to spend > 20% of TST with SpO2 < 90%, compared to 9% of the OSA group, despite the adequate relief of upper airway obstruction. CONCLUSIONS: Extremely severe obese subjects (BMI >or= 50 kg/m2) with moderate-to-severe OSA plus OHS exhibit severe oxygen desaturation but similar severities of AHI, arousal indexes, and sleep architecture abnormalities when compared to matched subjects without OHS. CPAP significantly improves AHI, REM duration, arousal indexes, and nocturnal oxygen desaturation. Some subjects with OHS continued to have nocturnal desaturation despite the control of upper airway obstruction; other mechanisms may contribute. Further long-term studies assessing the comparative role of CPAP and bilevel ventilatory support in such subjects with OHS is warranted.

Obesity-associated hypoventilation in hospitalized patients: prevalence, effects, and outcome.

BACKGROUND: Severe obesity is associated with hypoventilation, a disorder that may adversely affect morbidity and mortality. We sought to determine the prevalence and effects of obesity-associated hypoventilation in hospitalized patients. METHODS: Consecutive admissions to internal medicine services were screened over a 6-month period. In all eligible subjects with severe obesity (body mass index > or =35 kg/m2), we administered a sleep questionnaire, and performed neuropsychological, arterial blood gas, and pulmonary function testing. Hospital course and mortality at 18 months was also determined. RESULTS: Of 4,332 admissions, 6% (n = 277) of patients were severely obese, of whom 150 were enrolled, 75 refused to participate, and 52 met the exclusion criteria. Hypoventilation (mean [+/- SD] arterial partial pressure of carbon dioxide [PaCO2], 52 +/- 7 mm Hg) was present in 31% (n = 47) of subjects who did not have other reasons for hypercapnia. Decreased objective attention/concentration and increased subjective sleepiness were present in patients with obesity-associated hypoventilation compared with in severely obese hospitalized patients without hypoventilation (simple obesity group; mean PaCO2, 37 +/- 6 mm Hg). There were higher rates of intensive care (P = 0.08), long-term care at discharge (P = 0.01), and mechanical ventilation (P = 0.01) among subjects with obesity-associated hypoventilation. Therapy for hypoventilation at discharge was initiated in only 6 (13%) of the patients with obesity-associated hypoventilation. At 18 months following hospital discharge, mortality was 23% in the obesity-associated hypoventilation group as compared with 9% in the simple obesity group (hazard ratio = 4.0; 95% confidence interval: 1.5 to 10.4]. CONCLUSION: Hypoventilation frequently complicates severe obesity among hospitalized adults and is associated with excess morbidity and mortality.

Hyperkalemia with concomitant watery diarrhea: an unusual association.

Four patients presented to the emergency room with life-threatening hyperkalemia and concomitant watery diarrhea. Hypovolemia, acidosis, and renal insufficiency were present in all 4 cases. In 2 patients, hyperkalemia followed initiation of angiotensin-converting enzyme (ACE) inhibitor therapy, whereas 1 patient experienced hyperkalemia after a dose increase of an ACE inhibitor, and the fourth patient was on continuous ACE-inhibitor therapy at the time of the hyperkalemia episode. Two of the 3 patients with functioning kidneys required hemodialysis to correct the hyperkalemia, whereas the other patient was on long-term hemodialysis therapy. In the 2 patients in whom transtubular potassium (K+) gradients were available, their values ranged far below normal, indicating tubular failure to secrete K+. This abnormality was attributed to decreased distal delivery of sodium and water and to renin/angiotensin II/aldosterone blockade. It has been proposed that aldosterone blockade impairs the capacity of the colonic epithelial cells to secrete K+. In all 4 patients the watery diarrhea ceased in parallel with the correction of serum K+ to normal values. It is suggested that hyperkalemia, most likely by stimulating intestinal motility, induced the watery diarrhea in all 4 patients. The watery diarrhea, however, failed to compensate for the renal tubular failure to secrete K+.