Hookah smoking, at one time confined to North Africa, the eastern Mediterranean region, the Arabian peninsula, and Southeast Asia, has begun to spread throughout the world. As some practices of eastern and Arab cultures reach the United States, the number of people using hookah on an experimental or regular basis has increased. Carbon monoxide poisoning can be a common adverse effect, possibly undetected by physicians, in hookah smokers. The authors report a case of carbon monoxide poisoning secondary to smoking tobacco through a hookah.

Hookah—also known as argileh, goza, narghile, hubble-bubble, and shisha—is a water pipe for smoking tobacco. Hookahs have been used in social activity from Africa to Southeast Asia for more than 400 years.It has spread worldwide and has become a recreational practice among adolescents and young adults in the United States, Europe, and Brazil.Smoke generated through a water pipe has increased levels of carcinogens, carbon monoxide, nicotine, and tar.Research has shown that hookah smokers have substantially higher levels of carboxyhemoglobin (COHb), an accurate marker of carbon monoxide in the blood, compared with individuals who smoke cigarettes.The authors report a case of carbon monoxide poisoning secondary to hookah smoke inhalation that manifested as syncope. A basic explanation of hookah smoking, its health effects, and treatments for carbon monoxide poisoning are provided.

Report of Case

A 21-year-old man presented to the emergency department with an episode of syncope. His family was at bed-side and noted that the patient had lost consciousness after an episode of emesis. The patient's vomit was nonbloody and nonbilious, and the family reported that the patient was unconscious for only several seconds. The patient denied any chest pain, dizziness, or weakness prior to the event. The family noted that the patient had been outdoors all day at a family function, where the temperature was high. On arrival to the emergency department, the patient complained of headache and nausea.

The patient's medical history was significant for a recent diagnosis of gallstones. Family history was negative for any cardiac or neurologic diseases. He stated that he drank alcohol and smoked only socially and occasionally. The patient did report, however, that he drank alcohol earlier in the day and smoked tobacco from a hookah.

Physical examination revealed that the patient was intoxicated but alert, oriented, and in no acute distress. His vital signs included a body temperature of 97.5°F, a blood pressure of 138/80 mm Hg, a pulse of 97 beats per minute, a respiratory rate of 22 breaths per minute, and an oxygen saturation of 98%. Mucous membranes were dry, but the patient had good skin turgor. Skin was warm and dry with no obvious discoloration or rash. Results of cardiovascular, pulmonary, and neurologic examinations were unremarkable. An electrocardiogram revealed a normal sinus rhythm with a rate of 95 beats per minute and a normal axis deviation with no evidence of ischemia. Laboratory test results showed an unremarkable complete blood cell count and comprehensive metabolic blood panel. Blood tests were negative for the presence of cardiac enzymes, aspirin, and acetaminophen. The patient's ethanol level was 169 mg/dL (normal-negative). The COHb level was substantially elevated at 15.3% (normal: 1-2 packs per day, 4%-5%; elevated: >2 packs per day, 8%-9%). A computed tomographic image of the head revealed no acute abnormalities.