Case Presentation:
53 year old male with a history of alcohol abuse presented to the ED with hyponatremia and elevated LFTs after a week of nausea, vomiting, and diarrhea. The patient had a previous drinking history of a 12-pack of beer per day, denied IV drug use and any recent travel outside of Texas. Determined to be hyponatremic in clinic and sent to the emergency room where he had transaminitis, severe thrombocytopenia (37), a maculopapular rash on his abdomen and a creatinine of 1.77. Patient was admitted and started on cefepime, vancomycin, and doxycycline. He was transferred overnight to the MICU for septic shock unresponsive to 4L of IVF, hyponatremia (115) and new episodes of melena. Initial RUQ ultrasound demonstrated no liver cirrhosis or cholecystitis. Peripheral MICU course was complicated by pancreatitis, stroke and severe acute renal injury (Cr 5.55). Head CT and MRI demonstrated no acute findings and facial weakness and slurred speech resolved after a two week hospital stay. Rickettsia panel was sent and the patient’s serum was positive for IgM and IgG, suggesting Rocky mountain spotted fever. After MICU course, the patient was transferred back to the general medicine floor. Upon discharge, he had complete resolution of hyponatremia, transaminitis, and AKI.
Discussion:
Murine Typhus initially suspected due to maculopapular rash on abdomen, leading to initial treatment with doxycycline. Without rash, he was likely to have had a delay in treatment with appropriate antibiotics. Initial presentation with AST, ALTs, and Tbili elevations and a past history of alcoholism masqueraded his RMSF as a toxic presentation of a patient with alcoholic liver disease. Despite initiation of treatment with doxycycline, patient continued to worsen with pancreatitis, focal neurological findings, severe acute renal injury (Cr 6.14), and persistent thrombocytopenia. AKI was thought initially to be prerenal due to hypovolemia and sepsis. Despite severe AKI, produced adequate urine with furosemide over hospital stay and did not require hemodialysis.
R. Rickettsia infects endothelial cells and can cause systemic symptoms such as noncardiogenic pulmonary edema, interstitial pneumonia, meningoencephalitis, acute renal failure, GI vasculitis, hypovolemic hypotension. R. Rickettsia may infect portal vasculature, liver sinusoids and cause renal failure via hypotension-induced acute tubular necrosis, intravascular thrombosis, or direct infection of endothelial cells. We hypothesize that melena, pancreatitis and AMS was due to vasculitis in the GI tract and cerebral vessels.
Conclusions:
A high index of clinical suspicion is needed in suspicion of RMSF, given that standard broad spectrum antibiotics are ineffective for treatment and confirmatory tests may take several days. Advanced cases of RMSF may present with hyponatremia, transaminitis, hyperbilirubinemia, azotemia, thrombocytopenia that may be confused with other pathologies requiring a broad differential.