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Journal of Medical Cases

Case Report

Volume 9, Number 6, June 2018, pages 157-159

Rare Presentation of Ceftriaxone-Induced Hypersensitivity Pneumonitis

Drug-induced hypersensitivity pneumonitis is an immune response, normally associated with inhaled agents that can present with varying degrees of respiratory distress. It is important to recognize the effect of drug reaction on the body and differentiate from primary lung pathology. We present a case of hypersensitivity pneumonitis induced by a commonly administered medication, ceftriaxone [1]. This patient originally presented asymptomatic, with a rapid progression and then resolution of symptoms.

This is a 60-year-old male, receiving treatment for right hallux osteomyelitis with ceftriaxone and vancomycin as an outpatient. On a routine follow-up visit, he was sent to the hospital after presenting with a fever, as well as an incidental finding of elevated creatinine. Upon admission, only vancomycin was discontinued, and admission chest X-ray (CXR) was within normal limits (Fig. 1). On admission day two, he developed acute respiratory failure requiring mechanical ventilation with CXR findings of right-sided infiltrate and non-specific left-sided changes (Fig. 2). No skin rash was noted and the labs did not show eosinophilia at the time. Bronchoalveolar lavage was negative for microorganisms, ruling out the differential of Acinetobacter pneumonia. Ceftriaxone was empirically stopped, given the rare possibility of hypersensitivity pneumonitis. After cessation of ceftriaxone, the patient’s condition improved significantly and was extubated, CXR demonstrated improvement (Fig. 3).

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Figure 1. Chest X-ray at admission was “within normal limits”.

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Figure 2. Chest X-ray on admission day two, for evaluation of respiratory distress showing right-sided infiltrate and non-specific left sided changes.

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Figure 3. Chest X-ray post ceftriaxone cessation showing resolving right-sided infiltrate.

The original differential diagnosis for this case was broad, ranging from health-care-associated pneumonia to pulmonary embolism to drug-induced lung injury. The acute presentation, however, helped limit the differential, with interstitial pneumonitis being high on the list. Possible etiologies were ruled out by negative extremities ultrasound and bronchoalveolar lavage negative for microorganisms. In this case, lack of rash and eosinophilia lessened the possibility of a hypersensitivity reaction, though rapid improvement after cessation of the causative agent was supportive of this diagnosis.

Interstitial pneumonitis is defined as an inflammation change of the lung interstitium, including the alveolar septa, due to a broad range of etiologies. The etiology of interstitial pneumonitis can either be idiopathic or from known causes, such as drug-induced [2, 3]. In immunocompromised populations, interstitial pneumonitis is more commonly caused by fungal, atypical bacterial, and viral [4] infections [5]. In healthy populations, the cause of interstitial pneumonitis is more commonly an extrinsic particulate; fungal or plant antigens in farmer’s lung [6], aerosolized metallic or organic chemicals [7], or even possibly radiation [8].

The presentation of drug-induced pneumonitis commonly includes dyspnea, fever, cough, and rash. Investigation will often reveal inflammatory changes on CXR or CT [9], and eosinophilia on lab analysis. If a drug hypersensitivity reaction is suspected as the cause of pneumonitis, the medication can be restarted after cessation to confirm the reappearance of symptoms; this however may cause the patient to require intubation and supportive treatment. As with other hypersensitivity reactions, the first step in treatment of drug-induced pneumonitis, after life supporting measures, is cessation of the drug or inhalation agent [10]. Patients with severe disease may require treatment with corticosteroids [10], however, this has been shown to have no effect on long-term outcomes [11].

While hypersensitivity reactions are a known adverse effect of the use of cephalosporins, there are few reported cases of pneumonitis associated with ceftriaxone [1]. This case is suggestive that clinicians should continue to be aware of the possibility of drug-induced pneumonitis, even in the absence of rash or eosinophilia. At this time, more investigation is required to establish the exact mechanism behind ceftriaxone-induced pneumonitis, and to determine if there is population with an elevated risk of this complication. We believe that the addition of hypersensitivity pneumonitis to the differentials of patients with similar presentations, and early recognition of this complication can reduce or even prevent significant morbidity and mortality.

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Journal of Medical Cases is published by Elmer Press Inc.