Sepsis in the immunosuppressed patient is associated with very high mortality and morbidity. Treatment of sepsis in immunocompromised patients is especially challenging due to an unbalanced systemic inflammatory reaction with subsequent development of profound vasoplegia. Methylene blue (MB) has been successfully used for the treatment of refractory hypotension, but its use has not previously been reported for treatment of sepsis in immunosuppressed patients. The mechanism of MB's action is thought to be due to its inhibitory effect on cGMP-mediated vasodilatation. This case report describes the successful use of MB for treatment of severe septic shock in an immunosuppressed patient after liver transplantation. Hypotension in this patient was refractory to volume repletion and a combination of vasopressors. After MB administration, hemodynamic stability was rapidly reestablished. In the setting of severe sepsis in an immunosuppressed patient, MB should be considered early as a therapeutic option for treatment of refractory vasoplegia. 1. Introduction Sepsis in the immunosuppressed patient is often resistant or unresponsive to conventional pharmacologic therapy and is associated with mortality significantly higher than in the immunocompetent patient. The fulminant course of sepsis in immunosuppressed patients is related to an unbalanced systemic inflammatory response with subsequent development of pharmacologically resistant hemodynamic depression. Severe septic shock with vasoplegia is a devastating complication of sepsis in the immunocompromised patient. Therapy resistant hypotension is thought to be the result of dysregulation of nitric oxide (NO) synthesis. A number of investigations performed in critically ill, although not pharmacologically immunosuppressed patients, have demonstrated the efficacy of methylene blue (MB) administration in reducing plasma NO and restoring hemodynamic stability [1–4]. 2. Case Description Before the preparation of this paper, written informed consent was obtained from the patient. A 64-year-old male patient presented for a routine liver biopsy after orthotopic deceased donor liver transplantation (OLT). The original cause of the patient's liver failure was nonalcoholic steatohepatitis complicated by hepatocellular carcinoma. The patient’s past medical history was otherwise not significant. Postoperative immunosuppressive medications included both mycophenolate and tacrolimus. Two years after transplantation, the patient underwent a scheduled liver biopsy. A few hours after the procedure, he developed severe right upper
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