“Mr. A,” a 56-year-old, gay-identified Caucasian man, was hospitalized on our adult psychiatry unit 15 times over a 10-year span and hospitalized multiple times at other hospitals in the area. Several hospitalizations were protracted, lasting several weeks. Mr. A had a distant history of at least one suicide attempt, an overdose of clonazepam. Often, he presented with severe depressive symptoms, suicidal ideation, and auditory hallucinations criticizing him and/or commanding him to commit suicide. He did not exhibit grossly psychotic behavior. He at times tested positive for stimulants, but made inconsistent statements about his history of stimulant use and attempts at drug abuse treatment. He was variously diagnosed with schizoaffective disorder, major depression with or without psychotic features, posttraumatic stress disorder, and polysubstance or stimulant dependence. Usually he self-presented through the emergency department; on the last admission, he came in complaining of a broken tooth. During his last hospitalization, he reported severe depression, anxiety, insomnia, and irritability. He described his health as fair and ascribed several limitations due to multiple physical and mental health problems. He struggled with extreme pain despite daily prescribed opiate and sedative use. He held a college degree but was fully disabled and received a pension for psychiatric disability.

Mr. A was found by a friend, unresponsive, within his unsecured single residency hotel room in San Francisco, Calif. He was lying in a prone position near his bed. Emergency services arrived and pronounced him dead. According to the friend, Mr. A had called earlier that day saying he was “not feeling good,” although this was characterized as typical. At the scene, there was a styrofoam cup on the bedside table with empty medication vials containing the labels hydrocodone/apap and trazodone. There was no evidence of foul play or involvement by another person noted about the cluttered room or evidence of alcohol or illicit drug use. There was evidence of cigarette smoking. An initial physical examination noted an abrasion on Mr. A’s left forehead. No other obvious signs of trauma were documented.

The friend and a neighbor both told police that Mr. A suffered from depression and had a history of abusing his medications. The neighbor added that Mr. A was frequently “too stoned” to remember to lock his door. Paperwork found at the scene indicated outpatient treatment for major depression, rule out bipolar II disorder and posttraumatic stress syndrome. Mr. A’s psychiatrist, who was contacted, confirmed this clinical information and reported an additional history of anxiety and insomnia along with medication abuse. The psychiatrist further commented that Mr. A frequently voiced suicidal ideation, although he did not recall any past suicide attempts.

The medical examiner’s report described Mr. A as obese (body mass index=34 kg/m²) with multiple pierce marks in each earlobe and several superficial abrasions. There were no acute fatal traumatic injuries. No pill fragments or foreign bodies were identified in the gastrointestinal system. The toxicology report detected oxycodone, 0.1 mg/liter, dextromethorphan, and doxylamine, all within therapeutic levels.

Contrary to initial assumptions by the neighbor, friend, and consulting psychiatrist, the medical examiner’s report showed no evidence of suicide or accidental drug overdose. The actual cause of death, however, was just as preventable. According to the medical examiner, this 56-year-old man died from complications of pulmonary emphysema due to tobacco use. External examination showed an increased anterior-posterior thoracic diameter characteristic of patients with chronic obstructive pulmonary disease. The presumptive diagnosis was confirmed on autopsy with evidence of emphysematous pulmonary parenchyma and apical bullae along the pleural surfaces. The lung tissue overall was grossly edematous and had signs of diffuse vascular congestion with marked amounts of blood and frothy fluid, concerning for pulmonary edema. A cardiac examination further indicated signs of right heart failure with dilatation of the right ventricle. Anthracotic pigmentation of subpleural lymphatics also was noted on autopsy, a finding often consistent with chronic tobacco use.

Although there are a number of ways in which physicians can diagnose pulmonary emphysema, including spirometry and radiographic imaging, pulmonary emphysema is definitively recognized as a pathologic diagnosis. The disease process, moreover, carries with it systemic manifestations, such as pulmonary hypertension, right heart failure, global muscle atrophy, and wasting. In the case of Mr. A, cardiac complications included right ventricular dilatation and pulmonary edema. These features are concerning for advanced disease; over time, patients are at greater risk for hypoxic events that can cause tissue damage, including cardiac ischemia and eventual death. Proof of Mr. A’s disease is seen in the pathology; the anthracotic pigmentation noted on autopsy is evidence of the causal agent: chronic tobacco use. In the United States and abroad, tobacco remains the most significant risk factor for emphysema (1).

Atherosclerotic cardiovascular disease also was noted on the medical examiner’s report with moderate (up to 30%) multifocal calcifications of the right and distal left anterior coronary arteries. Although we have no proof of an acute coronary event, the presence of pulmonary emphysema and right ventricular dilatation may raise the issue of cardiac arrhythmia in a patient with underlying atherosclerosis as a potential mechanism to explain his sudden death.

Mr. A’s medical record at our hospital was notably absent of detected pulmonary or cardiovascular disease. Over the 10 years of admissions, sporadic reference was made to hypercholesterolemia, use of a beta-blocker, and a heart murmur. His oxygen saturation was checked in the emergency department and was normal at the time (97% on room air). There also was one visit recorded in which the patient presented with chest pain and ultimately was admitted to the medical center. The evaluation was notable for negative cardiac enzymes, a normal ECG, and an echocardiogram demonstrating good cardiac function. Mr. A had a portable chest X-ray that was read by the radiologist as low lung volumes. Examination of the films by one of the authors (R.S.), a pulmonary/critical care physician, indicated that the study was poor in quality because Mr. A did not give a good inspiratory effort, which makes confirmation of any lung pathology difficult. Mr. A’s chronic use of tobacco, however, was noted in the chart.

In our interviews with Mr. A during his last hospitalization, he reported smoking two packs of cigarettes per day for 25 years. It was estimated that he spent $289 per month on cigarettes, 10% of his income. He described 10 attempts to quit using tobacco in his lifetime, including two trials in the previous year. Each quit attempt was unassisted, that is, without clinical support or use of any of the cessation medications approved by the Food and Drug Administration. The longest period he reported being tobacco-free in any single attempt was 7 days. He stated he had not received any advice to quit smoking in the past year by a mental health or general medical provider. While hospitalized on our smoke-free unit, Mr. A expressed a craving for cigarettes but a desire to quit smoking with the eventual goal of complete abstinence. We spoke with Mr. A about his use of tobacco and thoughts about quitting and provided him with a self-help guide on smoking cessation. Despite these efforts, we learned that soon after hospital discharge, he resumed smoking two packs of cigarettes per day. It is this addiction to nicotine which ultimately killed him—not his depression, suicidal thoughts, or use of opiates, which traditionally are perceived as more acute and pressing psychiatric issues.