We report a 58 year old Caucasian male who presented with abdominal pain, fever and intractable vomiting. Past history was significant for laparoscopic cholecystectomy three weeks earlier complicated by post-operative bile leak that was managed conservatively. Physical examination was remarkable for diffuse abdominal tenderness most prominent in the right upper quadrant. Preliminary laboratory work up showed serum bicarbonate of 74 mmol/L in addition to elevated creatinine, hyponatremia and hypokalemia. Arterial blood gas analysis was consistent with severe combined metabolic and respiratory alkalosis (pH 7.93, pCO2 35.2). CT abdomen confirmed presence of a large perihepatic biliary leak. In consultation with the nephrology service, the patient was started on aggressive fluid resuscitation with normal saline. Additionally he was treated with acetazolamide to promote bicarbonate excretion. Pain control was achieved with intravenous morphine. With these measures the serum bicarbonate was lowered to 23 mmol/L by day 4 of hospital stay and pH corrected to 7.49 by day 3 of hospital stay. The biliary leak was managed with IR guided drainage. The final diagnosis with regard to alkalosis was combined respiratory and metabolic alkalosis resulting from a combination of contraction alkalosis, acid loss from intractable vomiting and inability to achieve respiratory compensation due to impeding effect of abdominal pain on effective respiration.
Discussion:
Metabolic alkalosis is a commonly encountered condition accounting for up to half of all acid-base disturbances. In contrast to acidosis, alkalosis is poorly tolerated with mortality approaching 45% at a pH of 7.55 and exceeding 80% at pH greater than 7.65. Needless to say, the pH seen in this case report was the highest encountered by both primary and nephrology teams and thus afforded unique insight into this deadly disorder. The intrinsic danger to basic cellular physiology posed by unmitigated metabolic alkalosis necessitates the presence of an effective compensatory mechanism to counteract this condition, namely depression of the respiratory drive to promote carbon dioxide retention. Conversely the development of extreme elevations in blood pH typically requires multiple derangements in normal physiology acting synergistically to overwhelm respiratory compensation as was seen in this instance. Therefore, by the very nature of its etiopathogenesis, severe metabolic alkalosis demands a multi-pronged therapeutic approach involving appropriate and aggressive correction of underlying factors. The effectiveness of such an approach is amply demonstrated in our patient who showed a satisfactory recovery with no evidence of organ-system impairment despite his potentially lethal alkalosis.
Conclusions:
Severe alkalosis is a potentially lethal condition that often arises from a combination of multiple pathological mechanisms acting in conjunction. Timely and aggressive correction of these factors can effectively reverse this disorder as was demonstrated in this case report.