INTRODUCTION

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The Fourth Edition of the Diagnostic and Statistical Manual of the American Psychiatric Association states that "the essential feature of a delirium is a disturbance of consciousness that is accompanied by a change in cognition that cannot be better accounted for by a preexisting or evolving dementia" (1). Delirium is one of the most commonly encountered mental disorders in general hospital practice (2), with a mortality rate oscillating between 10% and 65%, depending on the causal disease and on rapid recognition and correction of the disease (3, 4). We describe a case of obstructive sleep apnea (OSA) presenting with acute delirium, which was reversed with nasal continuous positive airway pressure (nCPAP).

	CASE REPORT

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A 72-yr-old man was admitted to our hospital because of an acute confusional state of 24 h evolution. He had no toxic habits or medical history of interest, and did not habitually take medication. According to his wife, the patient presented suddenly one night with psychomotor agitation and episodes of temporospatial disorientation and evident fabulation, during which he opened his bedroom window (approximately 8 m high) and jumped out, suffering only a comminuted fracture of the calcaneum, requiring a plaster splint. The patient was referred to our hospital because of the persistence of his confusion. On admission, he was agitated and space-oriented, but time-disoriented with fluctuations in consciousness. His temperature was 36.5° C, blood pressure 140/75 mm Hg, and heart rate 110 beats/min. Neurologic examination and the remaining physical examination were normal, except for obesity with a body mass index (BMI) of 34.2 kg/m².

Blood and urine analyses, including assays for triiodothyronine (T₃), levothyroxine (T₄), thyroid stimulating hormone (TSH), B₁₂, folate levels, and Bence-Jones proteinuria all gave results within the normal range. Arterial blood gases at room temperature showed a pH of 7.43, PO₂ of 59 mm Hg and PCO₂ of 39.2 mm Hg. Biochemical and cytologic evaluations of centrifuged fluid specimens were normal. Blood, urine, and spinal fluid cultures, and blood and spinal fluid serologies for human immunodeficiency virus (HIV), cytomegalovirus, Borrelia, Epstein-Barr virus, Mycoplasma, herpes, varicella, Brucella, Cryptococcus, and syphilis were negative. An electrocardiogram, chest X-ray, perfusion lung scan, and brain computed tomography (CT) were normal. A nuclear magnetic resonance scan showed only slight signs of cerebral atrophy, and an electroencephalogram showed mild diffuse slowing and diffuse neuronal dysfunction consistent with metabolic encephalopathy, with no focal anomalies.

During admission, the patient's symptoms remained unchanged, but nursing and medical staff members observed that the patient had numerous sleep apneas, and nocturnal pulse oximetry showed multiple and significant decreases in O₂ saturation. On being requestioned, the patient's relatives informed us that he was a heavy snorer with excessive daytime sleepiness. A polysomnogram performed on the tenth day after admission showed an apnea-hypopnea index (AHI) of 81 events/h, a mean event duration of 31 s, and a minimum O₂ saturation of 78%. On the following day the patient was outfitted with an nCPAP mask. It was determined that a pressure of 8 cm H₂O prevented the patient's apneas, and treatment with nCPAP was initiated on the twelfth day after admission. After two nights of nCPAP, the patient's symptoms improved, his delirium resolved, and his mental status returned to baseline. He was discharged with instructions to use nCPAP every night while sleeping and to follow a diet to lose weight. The patient was seen at 1 mo and 3 mo, and again every 6 mo for 2 yr. His excessive daytime sleepiness resolved; no signs of his initial dementia or further episodes of delirium have since been noted. A new room-air arterial blood gas measurement at 1 mo (BMI 31.2 kg/m²) showed a pH of 7.40, PCO₂ of 40 mm Hg, and PO₂ of 79 mm Hg.

	DISCUSSION

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Delirium may be caused by a range of organic factors grouped into four general classes (5): (1) primary cerebral diseases, such as infection, neoplasm, trauma, epilepsy and stroke; (2) systemic diseases that affect the brain, notably metabolic diseases, infections, and cardiovascular and collagen diseases; (3) intoxication with exogenous substances; and (4) withdrawal from substances of abuse in a person addicted to them. In the elderly, more than one causative factor is often implicated, and risk factors for delirium in these patients include a low serum albumin; multiple, severe, or unstable medical problems; dementia or cognitive impairment; polypharmacy, metabolic disturbances; few social interactions; infection, age > 80 yr; fractures; visual impairment; fever or hypothermia; and psychoactive drug use (2, 4, 5).

Whitney and Gannon (6) recently described a patient with delirium managed successfully after OSA was diagnosed and nCPAP treatment initiated. However, in this case, other factors, such as significant alcohol consumption, hydroelectrolytic disorders, and drugs (7) might have been implicated in the clinical picture. Exhaustive study of our patient, however, failed to show any cause that could account for his confusional state, which persisted until OSA was identified and reversed rapidly and permanently with nCPAP treatment. Although fractures in elderly patients may be a risk factor for their developing delirium, the calcaneum fracture in our patient occurred when the symptoms of delirium were already established. Thus, we believe that the symptomatology presented by our patient was a result of OSA.

Several cognitive and psychiatric alterations associated with OSA have been described (8), together with their correction with the use of nCPAP (12, 13). These alterations have been attributed to hypoxemia during sleep and to damaged sleep structure with few episodes of rapid eye movement (REM) sleep (14). Both factors are associated with a decrease in acetylcholinergic neurotransmitter activity (15, 16), one of the principal mechanisms involved in the physiopathology of delirium (2). We hypothesize that persistence of severe OSA could lead to a progressive reduction in cholinergic activity which, if below the threshold level, might trigger the onset of delirium.

We believe the association described in this case to be of great clinical importance, since it identifies a new, treatable cause of delirium and may avoid the use of sedatives recommended for patients with delirium (17) but are potentially dangerous in patients with OSA. We recommend that a careful sleep history be taken in patients with delirium of uncertain origin, and that polysomnography be performed in cases of clinically suspected OSA.