An instructive case study report of electrolyte and acid-base disturbance

As this case study report nicely demonstrates, alcohol abuse can result in a range of blood chemistry abnormalities, including acute electrolyte and acid-base disturbances. Initially, the patient who is the subject of this case study denied alcohol use, so many alternative explanations for the abnormal laboratory results she presented with had to be considered before she finally admitted excessive use of alcohol. This challenging aspect of the case is well conveyed in the report.

The case concerns a 28-year-old women who was brought to the hospital emergency department by relatives – whom she was visiting – after she suddenly felt ill while waiting with them in line for a theme park ride. Her main complaints were sudden onset of stiffness and weakness in her limbs and lack of sensation and loss of mobility in her left leg. Additionally, she felt short of breath on minimal exertion, was sweating excessively and experienced feeling of anxiety. Clinical examination was unremarkable, save signs of dehydration (dry mucous membranes); her vital signs were normal, save a marked increase in heart rate (tachycardia) to 150 bpm.

Apart from a diagnosis of hypothyroidism at age 10, which was being treated with daily thyroxine, she reported being healthy all her life, although she did mention two previous episodes similar to what she was now suffering during the past 7 months. These had resolved without medical intervention after 2 hours of rest and hydration. She denied having headache, muscle pain, or recent episodes of vomiting/diarrhea. She also denied smoking, use of recreational drugs, laxatives or alcohol.

Laboratory testing at the time of admission revealed the following results:

• Sodium (Na⁺) 139 mmol/L (normal)
• Potassium (K⁺) 2.3 mmol/L (reduced, hypokalemia)
• Chloride (Cl^-) 81 mmol/L (reduced, hypochloremia)
• Magnesium (Mg⁺) 1.2 mg/dL, 0.49 mmol/L (reduced, hypomagnesemia)
• Calcium (Ca²⁺) 8.8 mg/dL, 2.2 mmol/L (low normal)

• pH 7.48 (increased alkalemia)
• pCO₂ 36 mmHg, 4.8 kPa (normal)
• Bicarbonate (HCO₃-) 27 mmol/L (high normal)

• Lactate 12.9 mmol/L markedly increased (severe hyperlactatemia)
• Calculated anion gap 31 mmol/L elevated (increased anion gap)

• Creatinine 1.2 mg/dL, 106 µmol/L (raised for patient – her recorded baseline creatinine ~0.5 mg/dL, 45 µmol/L)
• eGFR 68 mL/min (interpreted as sign of acute kidney injury (AKI))

• Alanine aminotransferase (ALT) 53 U/L (normal)
• Aspartate aminotransferase (AST) 113 (increased)
• AST/ALT ratio 2.1 (increased – high ratio)
• Abnormal red cell indices MCV 107 fL; (macrocytosis)
• Ethanol <10 mg/dL (no evidence of recent alcohol intake)

• Urinalysis (dipstick testing) – Positive bacteria (3+) Positive white cells (3+) Urine tract infection

Immediate treatment in ER comprised adenosine injection for possible supraventricular tachycardia, crystalloid boluses (fluid replacement) along with magnesium and potassium supplements. When electrolytes were checked, 4 hours after treatment, magnesium had normalized but potassium had dropped further from 2.3 to 1.8 mmol/L despite K⁺ supplementation.

The severe hypokalemia and suspicion of possible sepsis (raised lactate along with urine tract infection) prompted admission to intensive care. Here, she was treated with iv antibiotics and further electrolyte replacement.

Within 28 hours of ICU admission, electrolytes had all normalized but the underlying cause of lady’s symptoms and electrolyte/acid-base disturbance remained a mystery. The combination of high anion gap and raised lactate indicated metabolic acidosis but since pH was increased, indicating alkalosis, it was clear at this time that she had suffered a mixed acid-base disorder (metabolic acidosis and alkalosis).

The finding of raised AST/ALT ratio suggested alcoholic liver injury. Other test results including macrocytosis (MCV 107 fL), raised bilirubin (3.8 mg/dL, 65 µmol/L), raised gamma-glutamyl transferase (𝛾-GT) (380 U/L), increased prothrombin time (15.8 sec) and reduced albumin (30/g/L) were consistent with liver dysfunction. These results prompted clinicians to ask the patient again about her previous alcohol use/abuse. Once again, the patient vehemently denied alcohol use. But in the absence of her relatives she eventually admitted alcohol intoxication and “hangover” symptoms 2 days prior to emergency room admission. She also disclosed that she had suffered 10 episodes of vomiting the day before admission.

A diagnosis of electrolyte disorders with lactic acidosis secondary to alcohol intake was made. She was discharged in good condition the next day with the advice to refrain from alcohol use. At 1 month follow-up the lady remained symptom-free.

In wide-ranging discussion of their case report, the authors outline first the various diagnoses, other than alcohol intoxication, that were considered, and the rationale for their exclusion. They also explain how all the symptoms and abnormal laboratory results that the lady presented with can be related to the alcohol abuse and associated acute vomiting episodes that she finally disclosed. Topics considered in the discussion include: pathogenesis of lactic (metabolic acidosis) in alcohol abuse and the pathogenesis of metabolic alkalosis and respiratory alkalosis in alcohol abuse. They provide mechanistic explanations for each of the electrolyte disturbances (hypokalemia, hypomagnesemia, hypophosphatemia, hypocalcemia) that the patient presented with, in terms of her alcohol abuse.