Approach to metabolic alkalosis: Clinical sciences

Metabolic alkalosis refers to an increase in serum bicarbonate concentration, either due to the loss of hydrogen ions from the body or the gain of bicarbonate itself. This can cause the arterial pH to rise above 7.45, and the serum bicarbonate above 27 milliequivalents per liter. As a reference bicarbonates normally range from 22 to 27 miliequivalents per liter. Common causes include prolonged vomiting, hypovolemia, diuretic use, and hypokalemia.

If a patient presents with a chief concern suggesting metabolic alkalosis, first perform an ABCDE assessment to determine if they are stable or unstable. If your patient is unstable, stabilize their airway, breathing, and circulation; obtain IV access and put them on continuous vital sign monitoring. Also, provide supplemental oxygen, if needed.

Here’s a clinical pearl! Patients with severe metabolic alkalosis, meaning pH over 7.6 sometimes require urgent correction of blood pH with hemodialysis, especially if there is volume overload or renal dysfunction.

Let’s move on to stable patients. After the ABCDE assessment, obtain a focused history and physical examination; and order labs, including an arterial blood gas analysis or ABG, and CMP. The history may reveal vomiting or use of loop or thiazide diuretics. Alkalosis increases the protein binding of ionized calcium, so you might find headaches, lethargy, neuromuscular excitability, delirium, tetany, and seizures. Additionally, alkalemia lowers the threshold for anginal symptoms and arrhythmias. Lastly, if there is hypokalemia, the patient might report weakness.

The physical exam might show signs of dehydration, like dry mucous membranes, and decreased skin turgor. As for the labs, ABG typically shows an arterial pH above 7.45, while CMP reveals elevated serum bicarbonate, often above 27 milliequivalents per liter. If you see these findings in history, physical exams and labs, that’s metabolic alkalosis.

Here’s a clinical pearl! Metabolic alkalosis can sometimes coexist with un acid-base disorders, making it hard to identify. To figure this out, you need to check the partial pressure of carbon dioxide or pCO2 on the ABG. If the pCO2 is above the reference range, it might be due to respiratory compensation, or it could mean that metabolic alkalosis and respiratory acidosis are occurring at the same time.

Keep in mind that in chronic metabolic acidosis, pCO2 should increase by about 5 millimeters of mercury for every 10 milliequivalents per liter increase in bicarbonates. On the other hand, if the pCO2 is below the reference range, metabolic alkalosis might be associated with a coexisting respiratory alkalosis.

Now that you’ve diagnosed metabolic alkalosis, let’s assess for exogenous causes. First up is milk-alkali syndrome. Milk-akali is characterized by hypercalcemia, renal insufficiency, and metabolic alkalosis. Hypercalcemia often results from ingestion of excessive amounts of calcium, either as supplements or calcium-based antacids. If it’s not addressed, hypercalcemia can cause renal insufficiency, where the kidney’s ability to excrete bicarbonate is impaired. Consequently, serum bicarbonate levels increase, leading to metabolic alkalosis.

Patients usually have a history of excessive calcium supplementation, or the use of absorbable antacids, like calcium carbonate or sodium bicarbonate. The CMP often shows elevated serum calcium, BUN, and creatinine levels. If you see these findings, diagnose milk-alkali syndrome.

Next, there’s bicarbonate administration. These patients present with a recent history of large-volume alkaline fluid infusion, such as IV sodium bicarbonate, usually to treat acidosis. In this case, bicarbonate administration is the cause of metabolic alkalosis.

Here’s another clinical pearl! In individuals with normal kidney function, the ingestion or administration of alkali results in only transient metabolic alkalosis. Normally functioning kidneys will quickly increase bicarbonate excretion to restore the pH balance. However, in individuals with kidney dysfunction, the effective elimination of excess bicarbonate is compromised, which leads to sustained alkalosis.

Now for endogenous causes… Alright, if there are no exogenous causes of metabolic alkalosis, consider endogenous causes, and obtain a spot urine chloride test. If the urine chloride is 20 milliequivalents per liter or less, it means there is significant renal chloride reabsorption so your patient has chloride-responsive metabolic alkalosis. This is often found in conditions such as gastric alkalosis, cystic fibrosis, and laxative abuse.

Let’s go over chloride-responsive metabolic alkalosis. Let’s start with gastric alkalosis also known as contraction alkalosis. During vomiting or nasogastric suction, hydrogen chloride is lost in the form of gastric acid, so less acid reaches the duodenum where hydrogen chloride is necessary to counterbalance the pancreatic and duodenal secretions of bicarbonates. With insufficient acid, an excess of bicarbonate gets absorbed into the bloodstream, contributing to metabolic alkalosis.

Patients with gastric alkalosis typically present with a history of vomiting or prolonged nasogastric suction. The physical exam might reveal signs of hypovolemia, such as increased heart rate, decreased blood pressure, and dry mucous membranes. With these findings, diagnose gastric alkalosis.

Next up is cystic fibrosis, in which excessive amounts of sodium chloride and water are lost through sweat, leading to extracellular volume contraction. This activates the renin-angiotensin-aldosterone system, or RAAS, which is followed by a rise in angiotensin II and aldosterone levels. Increased aldosterone levels cause the kidneys to secrete more potassium and hydrogen ions while reabsorbing more bicarbonate, which eventually results in metabolic alkalosis.

The patient typically reports a history of recurrent respiratory infections, poor weight gain, and fatty stool, called steatorrhea. The physical exam usually reveals digital clubbing, and lung crackles or wheezing. With these findings, consider cystic fibrosis. Next, order a sweat chloride test and if it’s elevated, diagnose cystic fibrosis.

Okay, time to talk about laxative abuse. History might reveal the use of laxative medications and possibly an eating disorder like bulimia nervosa. Since some patients might not be comfortable reporting this in their history, during physical exam look for signs of self-induced vomiting, such as tooth decay and abrasions on the dorsum of the hands or fingers. CMP usually reveals decreased serum potassium levels. If you see these findings, think laxative abuse.