Pickwickian Syndrome

Affects 5–10% of morbidly obese pts

Usually associated with long-standing obesity

Markedly greater risk among the morbidly obese vs. pts with normal BMI.

With intraabdominal or intrathoracic procedures lasting more than 2 h, there is approximately 40% of serious morbidity.

Hypoventilation

Hypercarbia

Hypoxemia

Polycythemia, thrombophlebitis, and subsequent pulm embolism

Pulm Htn

Hypersomnolence

Biventricular cardiac failure

Pickwickian syndrome, or OHS, is defined as the combination of obesity (BMI above 30 kg/m ² ), hypoxia during sleep, and hypercapnia.

Morbidly obese pts who hypoventilate due to sleep apnea and severe restrictive ventilatory disorder have permanent pulm Htn, acidosis, and polycythemia because of their chronic hypoxemia and CO ₂ retention.

OHS is usually associated with systemic Htn and acompensatory increase in circulating blood volume, leading to right and left ventricular failure.

Two subtypes are recognized, depending on the nature of the disordered breathing detected on further investigation. The first is OHS in the context of obstructive sleep apnea; this is confirmed by the occurrence of five or more episodes of apnea, hypopnea, or respiration-related arousals per h (high apnea-hypopnea index) during sleep. The second is OHS primarily due to “sleep hypoventilation syndrome;” this requires a rise of CO ₂ levels by 10 mm Hg (1.3 kPa) after sleep compared to awake measurements and overnight drops in O ₂ levels without simultaneous apnea or hypopnea. Overall, 90% of all people with OHS fall into the first category and 10% in the second.

On physical exam, characteristic findings are the presence of a raised jugular venous pressure, a palpable parasternal heave, a heart murmur due to tricuspid regurgitation, hepatomegaly, ascites, and leg edema.

Work of breathing is increased as adipose tissue restricts the normal movement of the chest muscles and makes the chest wall less compliant, causing the diaphragm to move less effectively. Respiratory muscles are fatigued more easily, and airflow is impaired by excessive tissue in the head and neck area.

Under normal circumstances, central chemoreceptors in the brain stem detect decreased pH and respond by increasing the respiratory rate; in OHS, the ventilatory response is blunted.

Episodes of nighttime acidosis due to sleep apnea lead to renal compensation with retention of bicarbonate.

Nighttime apnea leads to hypoxia, causing hypoxic pulm vasoconstriction. This vasoconstriction, in turn, leads to pulm Htn as well as right ventricular failure and remodeling.

The chronically low O ₂ levels in the blood also lead to increased release of erythropoietin, causing polycythemia.