# Lab case 371 interpretation

Question 1:

PH = 7.035, that is sever acidaemia

We have high pCO2 and low HCO3, this patient’s acidosis is most likely due to combination of metabolic and respiratory acidosis.

It easier to calculate the compensation using the metabolic process as the respiratory process for this patient is unclear (We can’t tell if it is acute or chronic).

To calculate the compensation for metabolic acidosis we use Winter’s formula, that is expected pCO2 = 1.5 x HCO3 + 8 (+/- 2).

1.5 x 13 + 8 = 27.5 (25.5 – 29.5). This patient’s pCO2 is 52, this patient has additional respiratory acidosis.

Anion gap = Na – (Cl+HCO3) = 18, So we have HAGMA.

Because we have HAGMA, next we will calculate the Delta Ratio. That is calculated as (AG – 12)/(24-HCO3) = 0.54. Ratio between 0.4 and 0.8 means that this patient has combined HAGMA and NAGMA.

Other abnormal findings

Na = 123 mmol/L, However, patients with high blood sugar levels develop pseudohyponatraemia. To calculate the corrected Na level, we use the following formula: Corrected Na = Measured Na + (Glucose – 5)/3. According to that the corrected Na level will be 140 mmol/L.

K = 6.1 mmol/L, that is mild hyperkalaemia. However, in the presence of acidaemia, serum K level will increase by 0.6 for every 0.1 PH higher than 7.35. Accordingly, corrected K level should be 6.1 – (0.6 x 3) = 4.7 mmol/L.

Cl = 92 mmol/L, that is mild hypochloraemia, dilutional similar to hyponatraemia. To calculate correct Cl level, we use the following formula:

Correct Cl = (Normal Na level/measured Na level) x measured Cl = 104.7 mmol/L

Glucose = 55 mmol/L, extremely high.

Lactate = 12.8, that is extremely high, unusual for patients with DKA or HHS to develop a level that high (The average lactate level is 3.05 +/- 1.6). We need to consider other causes of hyperlactataemia.

Ketones = 1.2, that is mildly elevated.

For the diagnosis of DKA, we need the following criteria

• Serum Glucose > 11 mmol/L
• PH < 7.3
• HCO3 < 15 mmol/L
• Presence of ketonaemia/ketonuria

This patient fits these criteria, so we should treat her as DKA.

Creatinine = 211 umol/L, for a 53 year old woman, that will give her eGFR of 22, stage 4 CKD.

This patient had mesenteric ischemia, that explains the excessively high lactate in this case. Patient has DKA and she was a CO2 retainer.

On presentation, patients with DKA, have 7-10 mmol/Kg Na deficiency while the Cl deficiency is 3-5 mmol/L. Some argue that we should use the corrected Na level for diagnostic purposes. (The Metabolic alkalosis associated with the chronic respiratory acidosis in this patient can’t be diagnosed when we use the measured Na level). However, for the management of these patients it is preferred to use the measured Na as ultimately, all patients with DKA will develop NAGMA when the management starts. ( When large amount of N/S is administered). ****

Question 2:

Potential causes of seizures in patients with DKA ***

Neurological

• Cerebral oedema
• Cerebral venous sinus thrombosis
• Pre-existing or first presentation of epilepsy
• Lowered seizure threshold

Electrolyte imbalance

• Hypoglycaemia
• Hypocalcaemia
• Hypophosphataemia
• Hypocapnia

Metabolic disorder

• Mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS)

Special Thanks to Dr Irene Pelletier for providing the details of this case

Reference:

• CMAJ. 2003 Apr 1; 168(7): 859–866.
Diagnosis and treatment of diabetic ketoacidosis and the hyperglycemic hyperosmolar state
• Endocrinol Diabetes Metab Case Rep. 2017; 2017: 17-0048.
Published online 2017 Jul 7. doi: 10.1530/EDM-17-0048
Severe diabetic ketoacidosis complicated by hypocapnic seizure
A Majid and B J Wheeler