Answers:
Question 1 answer:
PH = 7.315, that is mild acidaemia.
pCO2 = 48 mmHg. For venous blood, pCO2 level up to 48 mmHg is considered normal (40 for arterial blood).
HCO3 = 24 mmol/L, that is also normal.
As these 2 values don’t explain the patient acidosis, we will calculate the anion gap
Anion Gap = Na – (Cl + HCO3), for this patient it will be: 158 – (118 + 24) = 16, so we have HAGMA.
We usually calculate the Delta Ratio in the presence of HAGMA. Delta Ratio is calculated as: (AG – 12) / (24 – HCO3). Since this patient’s HCO3 is 24 then this calculation is not appropriate.
We are going to calculate the Delta Gap as alternative. Delta gap is calculates as:
Delta gap = Na+ – Cl– – 36
Delta gap = (change in anion gap) – (change in bicarbonate). The normal anion gap is assumed to be 12, and the normal HCO3 is assumed to be 24. This is a simplified equation as 36 is the sum of 24 + 12.
Interpretation of the Delta Gap:
- -6 = Mixed HAGMA and NAGMA
- -6 to 6 = Only a HAGMA
- over 6 = Mixed HAGMA and metabolic alkalosis.
For this patient, Delta Gap = 158 – 118 – 36 = 4. So we have pure HAGMA.
Other abnormal findings:
Na = 158 mmol/L, that is moderate hypernatraemia.
Cl = 118 mmol/L, that is hyperchloraemia
Glucose = 19.5 mmol/L, that is hyperglycemia. In the presence of hyperglycemia we get pseudohyponatraemia. To correct Na level, we use the following equasion:
Corrected Na = Measured Na + (Glucose – 5)/3 = 163 mmol/L. That is reflection of the degree of dehydration.
This patient has high sodium and glucose levels. Both these values affect serum osmolality level.
Serum osmolality is calculated as Na x2 + Glucose + urea. Usual value is 285 to 295 mmol/L. For this patient the value is 335.5 + Urea level. Serum osmolality for this patient is high and since it is higher than 320 mmol/L, then this patient has HHS.
Lactate = 2.4 mmol/L, that is mildly elevated
Ketones = 1.9 mmol/L, that is also mildly elevated.
Both Lactate and ketones levels are unlikely to cause acidosis.
Next we look at the cause of HAGMA for this patient. For the differential diagnosis of HAGMA we use the mnemonic CAT MUDPILES.
- C = cyanide, carbon monoxide
- A = alcoholic ketoacidosis and starvation Ketoacidosis.
- T = toluene
- M = methanol, metformin
- U = uraemia
- D = diabetic ketoacidosis
- P = phenformin, pyroglutamic acid, paraldehyde, propylene glycol, paracetamol
- I = iron, isoniazid
- L = lactate
- E = ethanol, ethylene glycol
- S = salicylates
From the list above, uraemia is the only possible cause. ( For DKA to be considered in this patient, Ketones level should be at least 3 mmo/L).
Urea level is usually elevated in patients presenting with HHS. For this patient urea level was 20 mmol/L. This level gave this patient a Urea: Creatinine ratio of 327. This means that the cause of renal impairment for this patient is pre-renal.
Urea: Creatinine ratio is calculated as: (Urea x 1000) / Creatinine
- Ratio > 100:1 means the cause of renal impairment is Pre-renal.
- Ratio 40 – 100 means Normal or Post-renal.
- Ratio < 40 means Renal.
Urea level of 20 mmol/L gave this patient serum osmolality level of 355.5 mmol/L
Question 2:
HHS is different from DKA. HHS is usually characterised by high glucose level without ketoacidosis. Patient’s with HHS usually have enough insulin to prevent Ketoacidosis. However, the hyperglycemia is usually more severe and the dehydration level is also more severe.
Those patient’s are managed with more fluids and less insulin compared to DKA. Average free fluid loss in HHS is 9 L (100 – 200 ml/Kg). While in DKA, average free fluid loss is 6L (100 ml/Kg).
The insulin requirement in HHS is half that needed for DKA, that is 0.05 Unit/Kg.
Always, think about the precipitating cause. In general, any illness that predisposes to dehydration or to reduced insulin activity may lead to HHS. Acute febrile illnesses, including infections, account for the largest proportion of HHS cases. Consider starting patients on broad spectrum antibiotics while investigating for the cause.
Mortality of HHS is higher than DKA, about 20%.