Case Studies

Case 11

You see two patients in casualty. Jill is a 40-year-old office worker with diabetes who is away from home but forgot to bring her insulin; she is now hyperglycaemic, and her breathing is heavy and laborious. Sheila is a 20–year–old student who attempted suicide by taking an aspirin overdose last night. Their ABG and blood analyses are shown below.

• 1. What is your diagnosis of the acid–base status of these two patients, and what is the cause their acid–base disorders?

  Show Answer

  Correct answer:
  

  Jill: As she has hyperglycaemia, your immediate thought should be that she has ketoacidosis. Her acidaemia indicates the presence of an acidosis (Step 2), and as both pH and P_aCO₂ are reduced, a metabolic acidosis is likely to be the primary cause (Step 3). Her predicted P_aCO₂ (Step 4) is 3.0 kPa, very close to her actual P_aCO₂, suggesting normal respiratory compensation (reflected by her Kussmaul breathing), and no other acid–base disorder. Her anion gap is 30 mmol/L, significantly above normal (Step 5) and consistent with ketoacidosis; ΔAG/Δ[^HCO₃–] is ~0.2, signifying a simple high anion gap metabolic acidosis. Diabetic ketoacidosis is caused by metabolism of fatty acids when glucose in not available to the cells due to the lack of insulin. This leads to generation of keto–acids (e.g. acetoacetate, β–hydroxybutyrate).
  Diagnosis: Simple anion gap metabolic acidosis due to diabetic ketoacidosis.

  Sheila: Sheila is more complicated. Her alkalaemia indicates that an alkalosis is present (Step 2), and as her PCO₂ is reduced we can infer this is a respiratory alkalosis (Step 3). However, her predicted [^HCO₃–] (Step 4) is 9 mmol/L (even assuming full renal compensation, which is unlikely in this time course), well below her actual [^HCO₃–] of 17 mmol/L, indicating the presence of an additional metabolic acidosis. She has a high anion gap (26 mmol/L), suggesting she has a high anion gap metabolic acidosis as well as a respiratory alkalosis.
  Diagnosis: Respiratory alkalosis coupled with high anion gap metabolic acidosis due to aspirin poisoning.

• 2. How might Sheila’s acid–base status have differed if you had seen her shortly after she ingested the aspirin?

  Show Answer

  Correct answer:
  Salicylate (aspirin) poisoning is quite complicated, as it has at least two independent effects with different time courses. In the first stage, which lasts a few hours, salicylate causes direct stimulation of respiratory centres in the brain, and consequent hyperventilation and respiratory alkalosis. But salicylate also affects cellular metabolism, and after a few hours can cause increased production of metabolic (fixed) acids, and thus a metabolic acidosis (the stage Sheila has reached now). In the third stage, starting after ~24 hours in adults, the metabolic acidosis may become predominant causing an acidaemia, coupled with dehydration and hypokalaemia due to renal fluid loss. So if you had seen Sheila within an hour or so of her ingesting the aspirin, you would have most likely seen just a simple respiratory alkalosis.

Cases 10 & 11: An example of a step approach to diagnosing acid–base disorders

The history and preliminary evaluation of the patient may provide important clues as to the disorder and underlying problem, for example, respiratory dysfunction, vomiting, diarrhoea, diabetes.

Step 1	Are ABG values consistent and thus valid?
Step 2	Is there an acidaemia or alkalaemia? Acidaemia means an acidosis MUST be present Alkalaemia means an alkalosis MUST be present If pH normal, then EITHER no acid–base disorder (PCO2 and [HCO3–] normal),OR mixed (acidosis + alkalosis) OR fully compensated disorder (unusual)
Step 3	Is the (primary) disorder respiratory or metabolic?
Step 4	Is compensation appropriate for primary disorder? These empirical rules (based on experience) give an estimate of what [HCO3–] or PCO2 would be if there was only the one disorder and there was normal compensation (N.B. PCO2 in kPa). Respiratory compensation is very rapid; renal compensation may take days to reach full effectiveness. Greater or lesser changes (outside the +/− range) suggest a mixed disorder. For use as a guide only, and confirm diagnosis from the history and further tests as appropriate. Acute respiratory acidosis [HCO3–] = 24 + (ΔPCO2 × 0.75)                          +/− 3 Chronic respiratory acidosis [HCO3–] = 24 + (3.5 × (ΔPCO2 × 0.75))              +/− 3 Acute respiratory alkalosis [HCO3–] = 24 - (2 × (ΔPCO2 × 0.75))                  +/− 3 Chronic respiratory alkalosis [HCO3–] = 24 - (5 × (ΔPCO2 × 0.75))                  +/− 3 Metabolic acidosis [HCO3–] = (0.2 × [HCO3–]) + 1                               +/− 3 Metabolic alkalosis [HCO3–] = (0.2 × [HCO3–]) + 2.7                          +/− 0.7
Step 5	If metabolic acidosis suggested, calculate anion gap (AG) Normally ~12 mmol/L (Chapter 11, and see Fig. 11c and 11d) Note that hypoalbuminaemia reduces AG by ~2.5 mmol/L per 10g/L reduction in plasma albumin

3. Normal AG suggests simple loss of (hyperchloraemic acidosis, Fig. 11c and 11d).

4. High AG (>20) suggests production of metabolic acids or renal failure.