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Introduction

Sepsis is defined as a life-threatening organ dysfunction caused by a dysregulated host response to infection and is characterized by a dramatic increase in inducible nitric oxide synthase (NOS) expression and activity with excessive production of nitric oxide (NO) [,]. As a result, sepsis leads to endothelial dysfunction and profound systemic vasodilation with associated hypotension which can have deleterious effects [,]. Therefore, a careful, sustained reduction in NO burden represents a potential therapeutic target. Hydroxocobalamin (HCB), which has traditionally been used in the treatment of cyanide toxicity, affects NO-mediated vasoplegia by (1) directly inhibiting NOS, decreasing NO production, and (2) by binding directly to NO and acting as a scavenger [-]. HCB has been successfully used in the treatment of refractory vasoplegia, particularly in cardiac surgery and liver transplant patients [-], but has not been extensively explored in septic shock. Shapeton et al. comprehensively summarized the pharmacology, toxicology, and clinical evidence surrounding the use of HCB in vasoplegic patients []. In this case report, we describe how a single extended duration infusion of high-dose HCB facilitates the resolution of catecholamine-refractory septic shock.

Case presentation

A 73-year-old male with a 30-pack-year tobacco smoking history and poorly differentiated T4N0M0 right upper lobe lung adenocarcinoma status post-neoadjuvant chemotherapy underwent a right upper lobectomy. His comorbidities included type 2 diabetes mellitus, hyperlipidemia, and prostate cancer status post-radiation therapy and radical prostatectomy. He was discharged on postoperative day (POD) 12 but was re-admitted on POD 16 in the setting of a right-sided empyema and septic shock. After administration of empiric antibiotics, the patient was taken to the operating room for right thoracotomy with decortication. His intraoperative course was complicated by poor gas exchange with profound hypoxemia (arterial pO2/fraction inspired O2 or P/F ratio = 50; ref >300) and hypercarbia (partial pressure of carbon dioxide = 100 mmHg). In the context of this new-onset acute respiratory distress syndrome (ARDS) with poor compliance and associated elevated driving pressures (plateau pressure = 37 cmH20, positive end-expiratory pressure = 12 cmH20), the patient suffered an intraoperative, contralateral tension pneumothorax that required emergent needle decompression and subsequent left-sided chest tube placement. Intraoperatively, the patient required escalating doses of epinephrine, norepinephrine, and vasopressin to support hemodynamics. An intraoperative transthoracic echocardiogram (TTE) was performed, which revealed right ventricular (RV) dysfunction with an underfilled and hyperdynamic left ventricle (LV). These compounding factors resulted in a severe respiratory and metabolic acidosis with a pH of 7.1 at the time of arrival to the intensive care unit (ICU).

Case presentation

Despite normalization of his cardiac function (by bedside TTE and calculated CI), the patient continued to require high-dose infusions of norepinephrine (up to 0.09 mcg/kg/min), vasopressin (up to 0.04 units/min), and epinephrine (up to 0.1 mcg/kg/min), suggestive of vasodilatory shock. His vasopressor requirement did not improve after administration of stress dose steroids. Indeed, 23 hours after admission to the ICU, repeat central venous SatO2 was 73.9% for a calculated CI of 6 L/min/m2 by Fick. To address the refractory shock, he was given a one-time sustained infusion of HCB (5 g) administered over four hours. This resulted in a rapid, complete, and definitive weaning from all vasoactive agents over the ensuing 14 hours (Figure ).