A 40-year-old patient with a background of alcohol abuse presents with a history of 8 days of diarrhoea and vomiting.


The following results are obtained: 

Parameter

Patient Value

Adult Normal Range

Sodium

116 mmol/L*

137 – 146

Potassium

2.9 mmol/L*

3.5 – 5.0

Chloride

67 mmol/L*

95 – 110

Bicarbonate

14 mmol/L*

24 – 31

Urea

2.9 mmol/L*

3.0 – 8.5

Creatinine

46 µmol/L*

60 – 120

Glucose

6.8 mmol/L

3.0 – 7.8

Osmolality

254 mOsm/kg*

274 – 295

Phosphate

0.6 mmol/L*

0.7 – 1.4

Magnesium

0.7 mmol/L

0.7 – 1.05

Calcium corrected

2.3 mmol/L

2.1 – 2.6

Albumin

44 g/L

36 – 52

Bilirubin

13 µmol/L

0 – 18

Aspartate transferase

80 U/L*

0 – 30

Alanine transferase

67 U/L*

0 – 30

Alkaline phosphatase

148 U/L*

30 – 100

g-Glutamyl transferase

480 U/L*

0 – 35

a)    What is the acid-base disturbance in this patient? (20% marks)

b)    What are the likely causes in this context? (30% marks)
 

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College answer

a)
Metabolic acidosis- Anion gap= 116-(67+14) = 35 Delta ratio= 23/10=2.3
HAGMA with metabolic alkalosis OR Increased SID

b)
Metabolic alkalosis – due to vomiting- Acid loss and contraction alkalosis. HAGMA-
Lactic acidosis from hypovolaemia or bowel obstruction/sepsis, Ketoacidosis from starvation/alcohol.
 

Discussion

In some sort of a structured fashion:

  • The bicarbonate is low, suggesting a metabolic acidosis
  • The anion gap is (116-67-15) = 34
  • The delta ratio is therefore (34-12)/(24-15) =  2.44; 
    in other words, this is a mixed HAGMA and metabolic alkalosis.
  • The calculated osmolality is (116 × 2) + 2.9 + 6.8 = 241.7, and so the osmolar gap is minimal (254-241.7 = 12.3)

Causes of HAGMA appropriate to this scenario include:

  • Toxic alcohol ingestion (classically, methanol) - though the low osmolar gap makes this less likely
  • Alcohol-induced or starvation-associated ketoacidosis (more likely)
  • Lactic acidosis due to the hypovolemic state, and the failure of the liver to metabolise it 

The metabolic alkalosis can be attributed to the vomiting and diarrhoea, and more directly to the aldosterone excess which develops in states of volume depletion.

References