Case History

Ms. S, a 36-year-old white female, presented to her local emergency department with a complaint of abdominal pain of one week's duration. She described the pain as sharp in character but somewhat diffuse. She had nausea and had vomited at least four or five times daily over the past week. She denied hematemesis. There was no change in her bowel habit. She described subjective fever and chills for the duration of this illness.

Her past medical history was significant for Hepatitis C, diagnosed one year previously, and alcohol abuse. She admitted to drinking at least a fifth of vodka a day and had done so for many years. She last drank about five days previously. She smokes 30 cigarettes a day, and had done so for 20 years. Her surgical history included an appendectomy in the distant past and a tubal ligation four years earlier. Her last menstrual period had just finished.

The patient's medication included the use of over-the-counter multivitamins and antacids. She was allergic to penicillin.

She had no other positive history on systematic review.

Physical Findings

On examination, Ms. S was a thin white female, who looked to be in some discomfort. She had a temperature of 99°F, pulse rate of 110, respiration rate of 18 and a blood pressure of 92/65. There was evidence of abdominal distension but no evidence of jaundice or anemia clinically. She scored 30 out of 30 on a mini mental status examination and there were no stigmata of chronic liver disease. Positive findings on examination were confined to the abdomen, where there was evidence of epigastric tenderness. Bowel sounds were diminished. Rectal examination was unremarkable and stool tested guaiac negative.

Q. What investigations would you consider at this point and what would be your most likely diagnosis?

A. This patient has a history of liver disease but this appears to be relatively stable at present. However, an exacerbation of an alcohol or hepatitis C related liver disorder cannot be completely excluded. Given the long history of alcohol abuse and the nature of the abdominal pain, it is more likely that this patient has developed pancreatitis.

Investigations at this stage should aim to assess any degree of electrolyte dysfunction as a consequence of her vomiting, assess her liver enzymes and liver function and check for evidence of hematological disturbance, secondary to a bleed, poor diet or long-term alcohol abuse. Coagulation studies are required. Renal function should be recorded. A urine specimen should be analyzed for ketones and, despite the previous tubal ligation, a urine pregnancy test should be performed.

Q. What are the component questions of the mini mental status examination and how is it scored?

A. The components of the Folstein mini mental status examination include:

Further Information

Investigations were significant for the following results:

Q. Given these blood gas results, what is the acid-base abnormality?

A. This patient has the picture of a metabolic alkalosis. There is an elevation in the extracellular pH and an elevated serum bicarbonate level. Alkalosis is often associated with a compensatory increase in the pCO₂ due to alveolar hypoventilation.

Q. Given that the patient has a metabolic alkalosis, in general what are the causes of this acid-base abnormality and how are the causes of metabolic alkalosis grouped? What do you think is the most likely explanation in this case?

A. The classic causes of metabolic alkalosis are usually divided into so-called 'chloride responsive' and 'chloride unresponsive' types. Recently, there has been debate about this terminology. The concern is that this focus on the chloride anion ignores the required associated deficiency in the cation. The cation may be hydrogen, sodium or potassium. However, for the purposes of our list, we will maintain the accepted terminology:

If there is a question as to the underlying type of metabolic alkalosis, measurement of the urinary chloride will help to provide the answer. Chloride responsive alkalosis reveals a urinary chloride of less than 10mEq/L, while chloride resistant alkalosis reveals a urinary chloride of greater than 20mEq/L.

It is most likely that in this case the cause of the metabolic alkalosis is prolonged severe vomiting. Another factor that may be involved included her use of antacid medications. This should be discussed in more detail with her and the use of sodium bicarbonate specifically should be explored.

Q. What are the major adverse effects observed in patients with a severe alkalosis?

A. Complications may be characterized as cardiovascular, pulmonary, metabolic or cerebral. Cardiovascular complications include arteriolar constriction, a reduction in coronary blood flow, a reduction in the anginal threshold and a predisposition to refractory supraventricular and ventricular arrhythmias. Ventilatory complications, such as hypoventilation, hypercapnia and hypoxia, may occur. Metabolically, we may find stimulation of anaerobic glycolysis and organic acid production, hypokalemia, decreased plasma ionized calcium concentration, hypomagnesemia and hypophosphatemia. Cerebral complications include a reduction in cerebral blood flow, tetany, seizures, lethargy, delirium and coma.(1)

Q. How may this patient be managed in the Emergency Department?

A. Once the basics of the resuscitation have been performed, attention is turned to the correction of the acid base disturbance. The aim should not necessarily involve complete correction of the alkalosis but rather a moderation of the alkalosis.

As we surmise that the cause of the alkalosis is our patient's prolonged vomiting, it is likely that she has an alkalosis of the 'chloride responsive' type. However, from her results, we also note that she is hypokalemic and thus correction of the serum potassium and the presumed total body potassium deficit will also be required. If the patient is still actively vomiting, she should be given antiemetics. She should be discouraged from the further use of antacid medications. If it is felt that the patient requires nasogastric suction, then she should have concomitant administration of an H2 receptor blocker or a proton pump inhibitor to reduce further loss of gastric acid.

Once these measures are in place, the patient should be rehydrated using 0.9% saline, with potassium supplements. In the majority of cases, this treatment alone will be sufficient to correct the alkalosis. Only rarely are other measures required. Other measures may include the use of hydrochloric acid as a 0.1 or 0.2N solution (i.e., containing 100 to 200 mmol of hydrogen per liter). The acid is sclerosing to veins and so needs to be given through a central line at a rate not to exceed 0.2 mmol/Kg/hour. If the hydrochloric acid is mixed with an amino acid solution and added to a fat emulsion, it may be given through a peripheral line. The amount of hydrochloric acid required can be estimated if the space of distribution of bicarbonate is assumed to be 50% of the body weight. Thus, if the bicarbonate concentration needs to be lowered by 10mmol/L, the amount of hydrochloric acid required in a 70Kg patient will be: 10x70x0.5, or 350mmol (1750mls of a 0.2N solution).

However, it must again be stressed that many authorities feel that correction of the fluid deficit and the associated electrolyte deficits will usually be all that is required. Administration of hydrochloric acid (or the other agents used occasionally, such as ammonium chloride and arginine monohydrochloride) should be reserved for all but the direst of situations.

Management in the case discussed included the use of 0.9% saline and intravenous potassium, after the vomiting had been controlled with antiemetics. Hydrochloric acid was not used. Note that management of this problem can be very complex if the patient has underlying renal or cardiovascular disease. In these cases, hydrochloric acid may be required (though the fluid load may be a concern). Dialysis may also be required.

Management of chloride resistant metabolic alkalosis focuses on identifying and correcting the underlying disease process. Correction of the associated potassium depletion should be aggressive.

Hospital Course

This patient had a stormy hospital course. Her vomiting and abdominal pain was the result of pancreatitis secondary to her alcohol abuse. She developed a pancreatic pseudocyst, sepsis, significant ascites, pleural effusions and spontaneous bacterial peritonitis. She required placement of a pancreatic stent and, eventually, after a six week hospitalization, was discharged home.