A Rare Cause of a Common Presentation: Hyperammonemic Encephalopathy Secondary to Mycoplasma Hominis Pneumonia (P3.220)

Objective: We aimed to characterize the presentation of hyperammonemic encephalopathy, and discuss common neuroimaging features which may aid in its recognition. We further aimed to highlight the broad differential diagnosis one must consider, including rare entities that must be invoked when common etiologies are ruled out. Background: Hyperammonemia is a metabolic derangement which can present with a wide array of clinical signs, with severity ranging from mild encephalopathy to coma, depending on the degree of ammonia accumulation. Etiology can be classified by physiologic mechanism, be it increased protein catabolism, decreased nitrogen clearance, or genetic/acquired defects of nitrogen processing. Less commonly, one may consider large exogenous nitrogen loads, or infection with ammonia-producing organisms. Methods: We described a clinical case and performed a PubMed review of pertinent literature for this case report. Results: A 34 year old immunocompromised male was seen for acutely decreased level of consciousness in the context of recent lung transplantation. On examination he was ventilated and unresponsive. While corneal, gag, and pupillary reflexes were intact, the patient demonstrated decerebrate posturing with light stimulation. CT scan showed diffuse cerebral edema, with MRI showing FLAIR hyperintensity and restricted diffusion in much of the cortex, including symmetric cingulate and insular involvement. Laboratory investigations were pertinent for moderate-severe renal dysfunction but normal hepatic function, and ammonia level of 200. The patient was also found to have Mycoplasma hominis pneumonia, a commensal organism which is ammonia-producing. The patient was aggressively dialysed and treated with ciprofloxacin, neurologically improving to the point of verbalizing coherently, obeying commands, and subsequent extubation. Metabolic/genetic profile, completed in follow-up, did not reveal an underlying urea cycle defect. Conclusions: We demonstrate a case of reversible hyperammonemic encephalopathy, with well-described neuroimaging findings, caused in part by Mycoplasma hominis, an ammonia-producing organism and rare treatable cause of hyperammonemia if recognized acutely.

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