Unexpected refractory intra-operative hypotension during non-cardiac surgery: Diagnosis and management guided by trans-oesophageal echocardiography
A 48-year-old, dialysis dependent male (ASA physical status III, body weight 82 kg) with polycystic kidney and liver disease and post bilateral nephrectomies status presented with persistent massive ascites, mild pericardial and bilateral pleural effusions. His ascites and effusions were secondary to a combination of obstruction of hepatic venous outflow and compression of the right heart by cysts in the liver and chronic renal failure. He was scheduled for a debulking liver resection and deroofing of cysts to relieve compression. Other pertinent medical history included diabetes and hypertension. He was also on the waiting list for a combined liver and kidney transplant. His pre-transplant cardiac workup included a trans-thoracic echocardiography (TTE) that showed mild left ventricular dysfunction (EF 45-50%), normal right ventricular function, mild pericardial effusion, no LVOT gradient and no valvular or wall motion abnormalities. Nuclear myocardial perfusion scan demonstrated a small reversible septal defect consistent with myocardial ischemia and a follow-up coronary angiography showed normal coronary circulation.\nGeneral anaesthesia was induced after establishing standard ASA monitors and central venous pressure (CVP) was monitored from a pre-existing right internal jugular dialysis catheter. At baseline his blood pressure (BP) was 107/56 mmHg, heart rate (HR) 102 bpm, CVP 16. Intravenous bolus induction drugs include fentanyl 150 mcg, midazolam 2 mg, propofol 150 mg, and rocuronium 40 mg. Anaesthesia was maintained on O2/N2O (50:50), sevoflurane at 0.5-1 MAC and fentanyl boluses as required. His ventilation parameters included a tidal volume of 8 ml/kg, respiratory rate of 10/min and PEEP of 8 cm H2O. A 20-gauge radial arterial line and a 14-gauge intravenous cannula were inserted in the left arm post induction. He became progressively hypotensive, prompting volume replacement, several bolus doses of phenylephrine (100-200 μg aliquots) and initiation of IV norepinephrine infusion. Hypotension and tachycardia worsened following drainage of a large ascites, despite aggressive volume replacement with colloid and crystalloid guided by trends in CVP (range 9-14 cm H2O), systolic pressure variation (SPV) on the arterial line tracing (7-14 mmHg) and increasing norepinephrine infusion (0.02-0.15 mcg/kg/min). Given his continued hypotension, IV epinephrine infusion (0.02-0.07 mcg/kg/min) was initiated, which resulted in further deterioration of haemodynamics. (Please see for haemodynamic trends).\nEmergent TOE demonstrated an under filled and hyper dynamic LV with SAM of the AML leading to functional LVOT obstruction and moderate mitral regurgitation (MR) [Figures and ]. Hypotension resolved after cessation of epinephrine, further volume replacement, increasing norepinephrine infusion (0.3 mcg/kg/min), addition of IV vasopressin infusion (0.04 units/min) and reduction in heart rate with beta blocker (10 mg of IV metoprolol in increments).\nThe procedure lasted 4.5 hours and was remarkable for a large blood loss of 1500 cc requiring blood and blood product transfusion. He was transferred to ICU postoperatively, extubated on day 3 and weaned off pressors on day 5. He was discharged from ICU on day 6 and from hospital on day 17. He returned back after 6 months to receive a combined liver and kidney transplantation successfully without any complications.