Elsevier

Critical Care Clinics

Volume 24, Issue 3, July 2008, Pages 533-549
Critical Care Clinics

Diagnosis and Management of Obesity Hypoventilation Syndrome in the ICU

https://doi.org/10.1016/j.ccc.2008.02.003Get rights and content

Obesity hypoventilation syndrome (OHS) is characterized by obesity, daytime hypercapnia, and sleep-disordered breathing in the absence of other known causes of hypercapnia. Because of the global obesity epidemic and the high prevalence of obstructive sleep apnea in the general population, critical care physicians are likely to encounter patients who have acute-on-chronic respiratory failure attributable to OHS in their clinical practice. In this review we define the clinical characteristics of OHS, review its pathophysiology, and discuss the morbidity and mortality associated with OHS. Finally, we offer treatment strategies during ICU management using noninvasive positive pressure ventilation that may guide the physician in the care of these challenging patients.

Section snippets

Historical perspective and definition

In 1955, Auchincloss and colleagues [1] described in detail the first case of a patient who had obesity hypoventilation syndrome (OHS). The following year, Burwell and colleagues [2] compared patients who had OHS to an obese, somnolent Charles Dickens' character and popularized the description “Pickwickian syndrome.” The central features of OHS include obesity (body mass index [BMI] ≥ 30 kg/m2), chronic alveolar hypoventilation leading to daytime hypercapnia (Paco2 ≥ 45 mm Hg), and

Morbidity and mortality

OHS is often unrecognized and treatment is frequently delayed, and can cause secondary erythrocytosis, pulmonary hypertension, and cor pulmonale. The delay in recognizing and treating this condition increases health care resource use and the likelihood of requiring hospitalization compared with patients who have similar degrees of obesity [7]. The most common reasons for hospitalizations are dyspnea and acute-on-chronic hypercapnic respiratory failure. Once hospitalized, patients who have OHS

Pathophysiology

The mechanism by which morbid obesity leads to hypoventilation is complex and not fully understood. Proposed mechanisms include abnormal respiratory system mechanics because of obesity, impaired central responses to hypercapnia and hypoxia, sleep-disordered breathing, and neurohormonal abnormalities, such as leptin resistance (Box 3) [4], [15].

Obesity imposes a significant mechanical load leading to a reduction in total respiratory system compliance, increased lung resistance, and a relative

Epidemiology

Because of the global obesity epidemic and the high prevalence of OSA in the general population, critical care physicians are likely to encounter patients who have acute-on-chronic respiratory failure attributable to OHS in their clinical practice. The prevalence of OHS amongst patients who have OSA has been estimated between 10% and 20% and is higher in the subgroup of patients who have extreme obesity (Fig. 1) [20], [21]. The prevalence of OHS is even higher (31%) in obese patients admitted

Clinical presentation

OHS is slightly more prevalent in men and most patients are diagnosed in their fifth or sixth decade of life. The vast majority of patients have the classic symptoms of OSA, including loud snoring, nocturnal choking episodes with witnessed apneas, excessive daytime sleepiness, and morning headaches. In contrast to eucapnic OSA, patients who have stable OHS frequently complain of dyspnea and may have signs of cor pulmonale. With acute-on-chronic hypercapnic respiratory failure, patients who have

Therapeutic options

In an ICU setting there are several therapeutic modalities that can improve ventilation and oxygenation in patients who have OHS who are experiencing an acute-on-chronic hypercapnic respiratory failure: NPPV, endotracheal intubation with invasive mechanical ventilation, and tracheostomy with or without mechanical ventilation. Although most of these patients need supplemental oxygen therapy in addition to positive airway pressure therapy, supplemental oxygen alone is inadequate and does not

Noninvasive positive pressure ventilation

Contrary to eucapnic OSA, effective treatment strategies for OHS must relieve upper airway obstruction and increase alveolar ventilation. The therapy of choice for the acutely decompensated patient who has OHS with hypercapnic respiratory failure is NPPV. NPPV can be applied with volume-limited, or more commonly, pressure-limited devices (eg, bilevel positive airway pressure [bilevel PAP] or pressure support ventilation). Although these two modes of NPPV have not been compared in patients who

Tracheostomy

Tracheostomy should be reserved for patients who have refractory OHS who have failed other modes of ventilatory support, are intolerant of NPPV, have severe cor pulmonale, or have a longstanding history of nonadherence with outpatient NPPV therapy. Tracheostomy may also become necessary in a subset of patients who cannot be successfully extubated and liberated from invasive mechanical ventilation. Tracheostomy bypasses the crowded upper airway and can substantially decrease apneas and hypopneas

Discusssion

Because of the global obesity epidemic and the high prevalence of OSA in the general population, critical care physicians are likely to encounter patients who have acute-on-chronic hypercapnic respiratory failure attributable to OHS in their clinical practice. We believe that early recognition of OHS leads to effective treatment and likely results in a decrease in morbidity and mortality. In the ICU setting, implementation of NPPV has marked beneficial effects leading to improvement in alveolar

Summary

  • OHS is characterized by obesity (BMI ≥ 30 kg/m2), daytime hypercapnia (Paco2 ≥ 45 mm Hg), and sleep-disordered breathing in the absence of other known causes of hypercapnia.

  • Patients who have OHS have increased health care resources use and require more frequent hospitalization because of dyspnea or acute-on-chronic hypercapnic respiratory failure compared with patients who have similar degrees of obesity.

  • The pathophysiology of OHS is multifactorial and includes abnormal respiratory system

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