In various forms of vasodilatory shock such as septic shock ADH levels are inappropriately low. Some authors have attributed the hypotension of refractory septic shock to relative vasopressin deficiency and clinical trials have used vasopressin successfully in the treatment of vasodilatory shock. End stage liver disease with hypotension has a pathophysiology similar to other forms of vasodilatory shock and vasopressin administration has been shown to improve renal function in hepatorenal syndrome. We thus speculated that vasopressin levels may be low in hepatic failure with hypotension or concurrent renal failure.
100% chart review of patients admitted to our institution with hepatic failure between November 2002 and April 2003. Hemodynamic, hematologic and serum chemistry data were recorded at the time of measurement of the ADH level. Vital signs, demographics and outcome were also recorded.
Of the 11 patients admitted, 3 survived and 8 died. The patients were 7 male, 4 female aged 57 ± 34 years. Length of stay was 4 to 40 days. Two of the patients had positive blood cultures at the time of ADH measurement, and were excluded. Of the remaining 9 patients, 4 (44%) had mean arterial pressures (MAP) of < 65 mmHg. Three (33%) had systolic blood pressures of <90 mmHg. Calculated osmolarity ranged from 269 to 310 with average of 290.96 mOsm/L. Azotemia with BUN > 30 mg/dL was present in 4 (44%) of the patients. ADH levels ranged from 1.6 to 4.4 pg/ml (normal range 1-13.3 pg/ml). These levels bore no relationship to blood pressure, osmolarity or azotemia.
ADH levels were low in hepatic failure despite hypotension, hyperosmolar stimuli and renal failure, which would ordinarily be expected to make them rise.
ADH levels in hepatic failure were low despite stress and may contribute to vasomotor instability in this setting. Studies are needed to evaluate the possible utility of vasopressin administration as treatment for hypotension in hepatic failure.
W.D. Marino, None.