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A Man in His 20s With Diffuse Lung Opacities and Acute Respiratory Failure After Hookah Smoking FREE TO VIEW

Mohleen Kang, MD; Vishal Raj, MD; Andrew R. Berman, MD
Author and Funding Information

aDepartment of Medicine, Rutgers New Jersey Medical School, Newark, NJ

bDivision of Pulmonary and Critical Care Medicine/Allergy and Immunologic Diseases, Department of Medicine, Rutgers New Jersey Medical School, Newark, NJ

cDepartment of Pulmonary Medicine, Norton Community Hospital, Norton, VA

CORRESPONDENCE TO: Andrew Berman, MD, Division of Pulmonary and Critical Care Medicine/Allergy and Immunologic Diseases, Department of Medicine, Rutgers New Jersey Medical School, 150 Bergen St, Room I 354, Newark, NJ 07101


Copyright 2016, American College of Chest Physicians. All Rights Reserved.


Chest. 2016;150(6):e175-e178. doi:10.1016/j.chest.2016.10.009
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A man in his 20s with no medical history presented with 2 days of progressively worsening shortness of breath accompanied by subjective fevers, chills, body aches, decreased appetite, night sweats, and cough producing nonbloody sputum. He denied childhood lung diseases, allergies, or a family history of lung disease. He did not smoke cigarettes but had smoked hookah in Saudi Arabia before moving to the United States 1 month before presentation and had restarted 2 days before the start of symptoms. He denied travel outside of the northeastern United States. He did not take medications, use illicit drugs, or engage in high-risk behavior.

Figures in this Article

The patient was febrile with a temperature of 102.3°F and had tachycardia (110 beats/min) and tachypnea (26 breaths/min), with oxygen saturation measured at 98% on ambient air. He had dyspnea at rest without the use of accessory muscles. Auscultation of the lungs revealed bilateral diffuse bronchial sounds with scattered coarse crackles. The cardiac examination was pertinent for no jugular venous distention and a regular rhythm without S3 gallop or murmurs. No lower-extremity edema or clubbing was noted. The remainder of the examination was unrevealing.

Laboratory diagnosis was notable for a WBC count of 25.1 × 103/μL, with a normal differential count with the exception of 92% neutrophils. Serum chemistry results were normal. A urine drug screen was negative.

Chest radiography showed mixed interstitial and airspace opacities throughout both lung fields, with the left side being greater than the right side (Fig 1). A CT scan of the chest with IV contrast medium revealed extensive thoracic adenopathy along with diffuse consolidation that was primarily central (Fig 2). The workup for infection, including HIV antibodies, blood cultures, sputum cultures, a smear for acid-fast bacilli, a respiratory panel for common respiratory viruses and subtypes, a urine Legionella antigen test, a urine streptococcal antigen test, Chlamydia antibodies, and Mycoplasma antibodies, was negative.

Figure 1
Figure Jump LinkFigure 1 Chest radiograph showing mixed interstitial and airspace opacities that were greater on the left side than the right side.Grahic Jump Location
Figure 2
Figure Jump LinkFigure 2 CT scan of the chest with IV contrast medium showing diffuse patchy consolidation.Grahic Jump Location

On day 2, a repeated chest radiograph revealed progression of airspace opacities throughout the lungs. On day 4, the patient was intubated for hypoxic respiratory failure, with further progression of airspace opacities (Fig 3). Bronchoscopy on day 4 showed diffusely inflamed bronchial mucosa. BAL fluid was normal with the exception of 78% eosinophils.

Figure 3
Figure Jump LinkFigure 3 Chest radiograph on the fourth day after admission showing diffuse airspace opacities in both lungs.Grahic Jump Location

What is the diagnosis?

Diagnosis: Acute eosinophilic pneumonia

Acute eosinophilic pneumonia (AEP) is a rare and acute febrile illness characterized by rapid accumulation of eosinophils into the lungs. Laboratory test results are usually characterized by leukocytosis with a left shift, but peripheral eosinophilia is often absent. Chest radiographic findings of AEP include bilateral interstitial opacities, which can progress to diffuse airspace opacities, and are in contrast to the often described peripheral airspace consolidation of chronic eosinophilic pneumonia. BAL is essential to the diagnosis of AEP and also provides an opportunity to investigate for infectious causes. An eosinophilic count of > 25% in BAL fluid in the absence of peripheral eosinophilia is often diagnostic and obviates the need for a lung biopsy. AEP has an excellent response to corticosteroids and, unlike chronic eosinophilic pneumonia, does not relapse. Commonly, however, the diagnosis is delayed, and patients may progress to hypoxic respiratory failure.

Water pipe or hookah smoking is becoming increasingly popular outside of the Middle East, especially among the younger generation, and is often touted as a harmless way to smoke tobacco. A hookah, also commonly known as “shisha,” “narghile,” or “hubble bubble,” is a water pipe used for smoking a preparation of tobacco, glycerol, and other additives and flavors using charcoal separated by thin aluminum foil to heat the mixture. Air is drawn in over the charcoal and then passes through the tobacco mixture through the water pipe and then into a water bowl before the vapors cool and are released as a dense aerosol, which is inhaled by the user. Hookah smoking, compared with cigarette smoking, produces a greater content of tobacco smoke, tar, carbon monoxide, polyaromatic hydrocarbons, and carbonylic compounds. The tobacco-free versions of hookahs contain less nicotine but produce a similar exposure to toxins and particulates when compared with tobacco-containing hookahs.

In animal models, hookah smoking causes inflammatory and physiological changes. In mice, exposure to 1 month of nose-only tobacco water pipe smoke led to pulmonary infiltration of neutrophils and lymphocytes and increased levels of proinflammatory markers such as tumor necrosis factor-α, interleukin-6, granulocyte macrophage colony-stimulating factor in BAL fluid. An increase in oxidative stress was demonstrated by a decrease in glutathione concentration and glutathione S- transferase and superoxide dismutase activity. In the same model, a forced oscillation technique demonstrated increased airway resistance to methacholine.

Hookah smoking leads to acute and long-term biochemical and physiological changes in humans. In the acute setting, hookah smoking leads to increased heart rate, blood pressure, and asthma exacerbations. Hookah smoking leads to increased levels of carboxyhemoglobin, and these levels are significantly higher than those seen in cigarette smoking. Acute carbon monoxide poisoning due to hookah smoking necessitated hospitalization and hyperbaric oxygen therapy in one patient.

Chronic hookah smoking can lead to changes that occur in chronic cigarette smokers, such as a decline in lung function, especially FEV1. The amount of tobacco smoked and the frequency of hookah smoking correlates with increased functional residual capacity and residual volume measurements. Increased prevalence of COPD is seen in hookah-smoking individuals, even when adjusted for cigarette smoking. Young hookah smokers with a water-pipe-smoking history of less than four sessions per week for < 5 years have an increase in cough frequency and sputum production and a reduction in diffusing capacity. These findings among cigarette smokers indicate a risk for the development of COPD.

Although the underlying mechanisms of hookah smoking leading to AEP are not well understood, case reports and case series suggest a strong correlation between recent cigarette smoking or alteration in smoking habits and development of AEP. There are no published data regarding the cessation of hookah smoking. There is only one other reported case of an association between AEP and hookah smoking. Whether hookah smoking directly causes lung inflammation with recruitment of eosinophils or makes the lung more susceptible to other exposures is unknown.

AEP should be considered early in cases of unexplained acute febrile respiratory failure, especially in patients who report recent hookah smoking. Early diagnosis and treatment with corticosteroids produces an excellent prognosis.

Clinical Course

The patient presented with fever, chills, a productive cough, and radiographic opacities, and antibiotic therapy was started for community-acquired pneumonia. The following day, he remained febrile and became hypoxic. Broad-spectrum antibiotic therapy was started. On day 4, the patient required intubation for hypoxic respiratory failure. Empirical treatment for Pneumocystis pneumonia with trimethoprim/sulfamethoxazole and methylprednisolone 60 mg daily was initiated.

Bronchoscopy performed after intubation revealed diffusely inflamed bronchial mucosa. BAL fluid showed rare reactive bronchial cells and 78% eosinophils, which led to the diagnosis of AEP. The patient had worsening hypoxia and was transferred to an outside hospital for extracorporeal membrane oxygenation, and methylprednisolone 125 mg every 6 hours was started. He was discharged home 1 week after the transfer.

  • 1.

    AEP should be suspected and treated early in noninfectious rapidly progressive respiratory failure and can be diagnosed by a eosinophil count > 25% in the absence of peripheral eosinophilia in BAL fluid.

  • 2.

    Hookah smoking, similar to cigarette smoking, has been reported to cause AEP, which can progress to respiratory failure.

  • 3.

    Chronic hookah smoking, similar to cigarette smoking, can lead to a decline in FEV1and is associated with an increased prevalence of COPD.

Financial/nonfinancial disclosures: None declared.

Other contributions:CHEST worked with the authors to ensure that the Journal policies on patient consent to report information were met.


Figures

Figure Jump LinkFigure 1 Chest radiograph showing mixed interstitial and airspace opacities that were greater on the left side than the right side.Grahic Jump Location
Figure Jump LinkFigure 2 CT scan of the chest with IV contrast medium showing diffuse patchy consolidation.Grahic Jump Location
Figure Jump LinkFigure 3 Chest radiograph on the fourth day after admission showing diffuse airspace opacities in both lungs.Grahic Jump Location

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