CHEST. Postgraduate Education Corner. A 39-Year-Old Male Slaughterhouse Worker With Recurrent Fever, Cough, and Shortness of Breath

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1 CHEST Postgraduate Education Corner PULMONARY, CRITICAL CARE, AND SLEEP PEARLS A 39-Year-Old Male Slaughterhouse Worker With Recurrent Fever, Cough, and Shortness of Breath Tashfeen Mahmood, MD ; Khaled R. Khasawneh, MD, FCCP ; Ruba A. Halloush, MD ; and Faisal A. Khasawneh, MD CHEST 2013; 144 ( 6 ): year-old Hispanic man was admitted for the third A time with a few days history of fever, shortness of breath, cough, and hemoptysis. The patient s initial presentation was 5 weeks earlier. At that time, he was diagnosed with community-acquired pneumonia and was discharged on oral moxifloxacin. He was admitted again 3 weeks prior to this current admission for the same symptoms. He was diagnosed with health-careassociated pneumonia and treated accordingly. During that admission, TB and HIV infections were ruled out. His medical history was negative, and he had no history of smoking. The patient was born in Mexico and immigrated to the United States 18 years ago. He worked at a local slaughterhouse for 10 years. He had no contact with live cattle; the animals were slaughtered, skinned, and washed with treated water before arriving at his workstation where he cut out parts to be packed. None of his family members had similar symptoms. Every time, his complaints resolved promptly after hospitalization to recur once he went back to work. Some of his coworkers complained of eye irritation and cough but none became as sick. Physical Examination Findings The patient was a healthy-looking man in mild respiratory distress. Vital signs were as follows: temperature, 38.7 C; heart rate, 103/min (regular); BP, 109/61 mm Hg; respiratory rate, 24/min; and oxy gen saturation, 93% while on 2 L/min of oxygen via nasal cannula. Significant physical examination findings included basal fine crackles in the chest without wheezing, regular heart sounds without murmurs or gallop, and no lymphadenopathy or skin rashes. Diagnostic Studies Pertinent laboratory findings included WBC count 7,400/ m L (73% neutrophils, 18% lymphocytes, and 6% eosinophils); absence of eosinophilia in either of his previous admissions; hemoglobin level, 14.6 g/dl; platelet count, 234,000/ m L; procalcitonin level, 0.4 ng/ml; negative airway cultures and blood cultures from all three admissions; and negative serologies for Q fever and Brucella. Renal function, electrolytes, liver enzymes, and coagulation studies were within normal limits. Pulmonary function testing was not done. Manuscript received May 14, 2013 ; revision accepted June 11, Affiliations: From the Department of Internal Medicine (Dr Mahmood), Deaconess Health System, Evansville, IN; Division of Pulmonary and Critical Care Medicine (Dr K. Khasawneh), University of Arkansas for Medical Sciences, Little Rock, AR; Amarillo Pathology Group, LLP (Dr Halloush), Amarillo, TX; and Section of Critical Care, Department of Internal Medicine (Dr F. Khasawneh), Texas Tech University Health Sciences Center, Amarillo, TX. Correspondence to: Faisal A. Khasawneh, MD, Section of Critical Care Medicine, Department of Internal of Medicine, Texas Tech University Health Sciences Center, 1400 S Coulter St, Amarillo, TX 79106; faisal.khasawneh@ttuhsc.edu 2013 American College of Chest Physicians. Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details. DOI: /chest Figure 1. Chest radiograph showing bilateral lower lobes interstitial pulmonary infiltrates. CHEST / 144 / 6 / DECEMBER

2 Figure 2. Chest CT scans demonstrating nonspecific bilateral interstitial pulmonary infiltrates affecting predominately the lower lobes without pleural effusions or lymphadenopathy. The chest radiograph from his third admission is shown in Figure 1. CT scan of the chest was obtained ( Fig 2 ). Given the relapsing nature of his complaints and the absence of a definite infectious etiology, open lung biopsy was performed (Fig 3 ) Postgraduate Education Corner

3 Figure 3. Lung wedge biopsy. A, Low magnification shows patchy peribronchiolar and perivascular chronic inflammatory infiltrate (hematoxylin-eosin, original magnification 3 40). B, Higher magnification of the inflammatory infiltrate composed of lymphocytes and plasma cell. No eosinophils present (hematoxylin-eosin, original magnification 3 200). C, Loose aggregates of histiocytes and multinucleated giant cells without granuloma formation (hematoxylineosin, original magnification 3 400). What is the diagnosis? CHEST / 144 / 6 / DECEMBER

4 Diagnosis: Chemical pneumonitis caused by hydrogen bromide exposure Discussion Chemical pneumonitis is a form of lung toxicity that results from exposure to a variety of irritant substances. These chemicals can be in the form of gases, fumes, vapors, or aerosols. Exposure to these toxic substances can be accidental at work or home or intentional as part of chemical warfare or a terrorist act. Respiratory tract injury is mediated by the deposition or formation of an acid, alkali, or free radicals. The toxic effect could involve upper as well as lower airways, depending on the solubility and concentration of the inhaled substance, its physical properties, and duration of exposure. The signs and symptoms of inhalational lung injury are usually acute, but delayed and chronic symptoms are possible. The clinical manifestations of this injury range from upper airway mucosa irritation with tearing of the eyes, laryngospasm, bronchorrhea, and bronchospasm to lower airway damage with pneumonitis, pulmonary edema, and full-blown ARDS. Chronic manifestations of chemical lung injury include cryptogenicorganizing pneumonia and bronchiectasis. Multiple chemicals have been implicated in causing inhalational lung injury including the halogens chlorine, bromine, and iodine. Inhalational lung injury due to bromine compounds is rarely reported. Bromine is a more potent respiratory irritant than chlorine. Hydrogen bromide, the culprit substance in the presented case, is one-third as toxic as bromine. Hydrogen bromide is a colorless to faint-yellow highly toxic gas with a sharp irritating odor. It is used in the synthesis of industrial chemicals, as a veterinary drug, and in the production of hypobromous acid, which is an antimicrobial added to water used to wash meat and poultry in slaughterhouses. Breathing hydrogen bromide gas is the most common route of accidental exposure. Like in chlorine exposure, patients will complain of nose and throat irritation, watery eyes, bloody nose, chest tightness, cough, and shortness of breath. Repeated exposure or chronic exposure to the gas in low concentration can lead to similar manifestations. The diagnosis of inhalational lung injury hinges on documenting exposure to an irritant substance accompanied by ruling out more common diagnoses, especially bacterial pneumonia. Apart from infections, eosinophilic pneumonitis, hypersensitivity pneumonitis, cryptogenicorganizing pneumonia, and sarcoidosis are important differential diagnoses to consider. Inhalational lung injury neither has a pathognomonic radiologic findings nor a characteristic BAL profile. Collecting a lung tissue sample by transbronchial or thoracoscopic biopsy is important in reaching the diagnosis by showing nonspecific lung tissue inflammation in the absence of features of alternative diagnoses. Choosing between the aforementioned methods of biopsy depends on the distribution of lung involvement and the patient s surgical risk. Management of inhalational lung injury is largely supportive. The victim has to be evacuated to a wellventilated area to avoid further exposure. Oxygen and bronchodilators are administered as necessary. A serious consideration needs to be given to early intubation before airway edema progresses. Animal models and anecdotal reports showed a significant beneficial effect from systemic corticosteroids use. Hence, a steroid therapeutic trial is a reasonable option if inhalational lung injury is felt to be the most likely diagnosis, especially if the patient is a poor surgical candidate. There is no role for antimicrobial prophylaxis, and antibiotic use should be reserved for patients with clinical evidence of secondary infection. Slaughterhouses are high-risk work places. Under the pressure of slim profit margins and large work volume, workers, most of whom are from underprivileged backgrounds, continue to have their safety compromised despite multiple federal regulations and laws. If the clinician determines that working conditions are unhealthy, he/she should inform the employer. The clinician may file a complaint with the Occupational Safety and Health Administration (OSHA) concerning hazardous working conditions if the employer is not responsive to the complaint or the problem recurs. Clinical Course After the patient s third hospitalization and based on his history, occupational toxic lung exposure was suspected. The slaughterhouse was contacted for details, and it was found out that for the last few months hydrogen bromide was used to treat the water used for washing slaughtered animals. Given the patient s low surgical risk and the need to avoid sampling errors and inadequacies, an open lung wedge biopsy was performed. It showed variable and patchy peribronchiolar and perivascular chronic inflammatory infiltrate. Foci of loose collections of histiocytes and multinucleated giant cells were also seen. No eosinophilic infiltrate, acute inflammation in alveolar spaces, viral changes, foreign bodies, vasculitis, or granulomas were identified. The findings were consistent with interstitial pneumonitis. Acid-fast bacilli and Gomori methenamine silver special stains were negative. Empirical antibiotic therapy was stopped, and he was discharged on prednisone taper. After reporting the information to his superiors, hydrogen bromide use at the workplace was abandoned Postgraduate Education Corner

5 He was seen in clinic 4 weeks and 3 months after discharge and was completely asymptomatic. Clinical Pearls 1. Chemical pneumonitis is a form of lung toxicity that results from accidental or intentional exposure to a variety of irritant substances. 2. The clinical manifestations of inhalational lung injury are usually acute and include upper as well as lower airway symptoms. 3. Obtaining occupational history is important because halogens, including chlorine and bromine, are used in the industry and have the potential to cause a serious chemical pneumonitis. 4. Management of inhalational lung injury is supportive. Avoiding further irritant exposure, oxygen administration, preemptive endotracheal intubation, and corticosteroid use are mainstay interventions. The clinician needs to notify the employer about the problem and consider informing the Occupational Safety and Health Administration as well. Acknowledgments Financial/nonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article. Other contributions: CHEST worked with the authors to ensure that the Journal policies on patient consent to report information were met. Suggested Readings van Leeuwen FX, Sangster B. The toxicology of bromide ion. Crit Rev Toxicol ;18(3): Kraut A, Lilis R. Chemical pneumonitis due to exposure to bromine compounds. Chest ;94(1): Blanc PD. Chemical inhalation injury and its sequelae. West J Med ;160(6):563. White CW, Martin JG. Chlorine gas inhalation: human clinical evidence of toxicity and experience in animal models. Proc Am Thorac Soc ;7(4): CHEST / 144 / 6 / DECEMBER