A 27-year-old male presented to the emergency department after exposure to phosgene gas while burning refrigerator lines at work. He was exposed for several hours without wearing appropriate respiratory protection. His symptoms during the exposure included:
Throat and mouth irritation
Shortness of breath
Wheezing (which has since been resolved)
Vomiting
He reports no significant past medical history and denies any prior lung issues, such as asthma or chronic bronchitis. He has no known allergies, is a non-smoker, and does not use alcohol or recreational drugs. His workplace does not regularly handle hazardous chemicals, and this incident was considered accidental.
Physical Presentation:
Vital signs:
Blood pressure: 136/83 mmHg
Heart rate: 91 beats per minute
Respiratory rate: 18 breaths per minute
Oxygen saturation (SpO2): 98% on 3 liters of oxygen via nasal cannula
Temperature: 98.2°F
Physical examination:
The patient is alert and in mild discomfort.
Lung auscultation: Fine crackles were noted bilaterally, consistent with early lung irritation.
There were no signs of cyanosis or accessory muscle use, and his breathing pattern appeared stable.
Initial tests:
A chest X-ray (CXR) and laboratory tests, including a complete blood count (CBC), complete metabolic panel (CMP), and venous blood gas (VBG), were ordered, but results were still pending at the time of initial evaluation.
What is the most concerning delayed complication this patient is at risk for developing? A) Pneumonia B) Acute respiratory distress syndrome (ARDS) C) Bronchospasm D) Pleural effusion E) Pulmonary embolism
Diagnostic Journey and Discussion:
Phosgene is a highly toxic pulmonary irritant used historically in chemical warfare. It is also found in industrial settings, where the thermal decomposition of chlorinated hydrocarbons, such as refrigerants, can produce it. Phosgene is an insidious poison—its initial symptoms are often mild and nonspecific, but it can lead to severe delayed lung injury.
Upon initial presentation, the patient’s symptoms included throat and mouth irritation, shortness of breath, and vomiting, typical of acute upper airway irritation from inhaling a toxic substance. The crackles on auscultation suggest early pulmonary involvement, which is expected after phosgene exposure.
Rationale for the Correct Answer:
The most critical complication of phosgene inhalation is delayed-onset acute respiratory distress syndrome (ARDS), which can develop hours to days after exposure. Phosgene gas interacts with the alveolar-capillary membrane, leading to:
Increased capillary permeability
Pulmonary edema
Acute lung inflammation
This sequence results in compromised gas exchange, hypoxemia, and the hallmark clinical findings of ARDS. Even if initial symptoms resolve, admitting the patient for observation is crucial, as pulmonary edema may develop 12 to 24 hours post-exposure. The current fine crackles on the lung exam may represent early signs of phosgene-induced lung injury, highlighting the need for careful respiratory monitoring.
Why Other Options Are Less Likely:
A) Pneumonia: While chemical inhalation can predispose a patient to infection, phosgene's acute and delayed effects are more likely due to direct lung injury rather than secondary infection. Pneumonia may occur if the patient becomes immunocompromised or if aspiration occurs, but it is not the primary concern immediately post-exposure. While pneumonia may concern immunocompromised patients, phosgene-induced lung damage is primarily inflammatory rather than infectious.
C) Bronchospasm: This patient's wheezing resolved, suggesting bronchospasm was a transient reaction to upper airway irritation. Phosgene’s primary damage occurs in the alveoli, not the bronchi, making bronchospasm less of a concern.
D) Pleural effusion: Phosgene does not typically cause pleural effusions. It primarily affects the alveoli and capillary membranes, leading to pulmonary edema rather than fluid accumulation in the pleural space.
E) Pulmonary embolism: There is no indication that this patient is at high risk for a pulmonary embolism. Phosgene exposure does not predispose individuals to thromboembolism but rather to lung injury due to its caustic effects on the lung tissue.
Takeaways:
Phosgene gas exposure can lead to delayed and severe pulmonary complications, including ARDS. Even if initial symptoms are mild or resolved, patients must be monitored for at least 24–48 hours due to the risk of delayed pulmonary edema.
Supplemental oxygen should be used cautiously in phosgene inhalation patients to avoid further oxidative injury to compromised lung tissue. The target oxygen saturation should be around 94%, as excessive oxygenation may exacerbate lung injury.
The role of steroids in phosgene exposure remains controversial. While they may reduce inflammation, evidence is inconclusive, and decisions should be made on a case-by-case basis.
Immediate and delayed diagnostic evaluations (such as chest X-rays and arterial or venous blood gases) are essential to assess the severity of the lung injury and guide treatment.
Observation and early supportive care are critical in preventing complications, particularly ARDS, which is the most serious delayed outcome of phosgene inhalation.
Non-invasive ventilation and careful oxygen titration are crucial components of supportive therapy, as excessive oxygenation can exacerbate the oxidative stress initiated by phosgene.
This case reminds us of the importance of workplace safety, particularly when dealing with toxic industrial gases. Proper respiratory protection is crucial to prevent life-threatening inhalation injuries.
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Authors:
Dr. Omid Mehrpour is a distinguished medical toxicologist known for his extensive clinical and research expertise. He focuses on understanding and treating toxic exposures. Renowned for his ability to diagnose and manage poisoning cases, Dr. Mehrpour has authored numerous impactful publications and is dedicated to educating future medical toxicologists. His innovative approach and commitment to patient care make him a leading figure in medical toxicology.
References:
Asgari A, Parak M, Nourian YH, Ghanei M. Phosgene Toxicity Clinical Manifestations and Treatment: A Systematic Review. Cell J. 2024 Feb 1;26(2):91-97. doi: 10.22074/cellj.2024.2011864.1405