PH = 7.82 that is life threatening alkalemia
PaCO2 is 28.7, that is low (<40), so we have respiratory alkalosis. this can be acute or chronic (not clear from the history).
With Respiratory alkalosis we expect HCO3 to be less than 24. However, in this case HCO3 is 49.4. That is high. So we have additional metabolic alkalosis.
Other abnormal findings
Hb = 181 g/L. that is to the high range
Na = 111 mmol/L. that is severe hyponatraemia and from the history it is of unknown duration (possibly more than 48 hours). Patients with severe hyponatraemia are at risk of neurological complications and seizures. (especially if it is acute).
K = 2.5 mmol/L, that is moderate hypokalaemia.
Cl = 64 mmol/L. Here we have severe hypochloraemia.
Lactate = 3 mmol/L. That is moderate lactataemia.
Creatinine = 554umol/L, This patient is in stage IV (Moderate to severe AKI).
Final conclusion, this patient has combined respiratory alkalosis and hypokalaemic hypochloraemic metabolic alkalosis with severe acute hyponatraemia and acute renal failure.
Using the mnemonic CLEVER PD for the differential diagnosis (Causes) of Metabolic acidosis:
- C – contraction (dehydration) – This patient is dehydrated, this can be supported by the presence of Hb of 181 (high) and AKI
- L – liquorice (diuretic), laxative abuse. Cleared by history taking
- E – endocrine (Conn’s, Cushing’s), usually associated with hypernatraemia
- V – vomiting, GI loss (villous adenoma). This patient was vomiting for 5 days.
- E – excess alkali (antacids), cleared by history taking
- R – renal (Bartter’s), severe K depletion. We have moderate hypokalaemia.
- P – post hypercapnia, this is in ventilated patients
- D – diuretics, cleared by history taking.
According to that, metabolic alkalosis happened due to loss of acid and chloride through vomiting and the associated dehydration.
This patient was also hyperventilating, and this caused the metabolic alkalosis.
Most severe metabolic alkalosis is of the chloride-responsive, usually these responds to simple replacements measures. However, the presence of AKI makes the management of this case more challenging.
Patients with severe hyponatraemia with neurological symptoms require ICU admission where close biochemical and clinical monitoring can be provided.
Replacement of NaCl will improve both hyponatraemia and improve alkalosis by replacing Cl. We need to limit the increase in serum sodium to 10 mmol/L in the first 24 hour and 8 mmol/during every 24 h thereafter until the serum sodium concentration reaches 130 mmol/L.
If the patient develops seizures or neurological symptoms then promptly infuse 150 ml of 3% hypertonic saline IV over 20 min.
In cannabinoid hyperemesis syndrome (CHS), the effectiveness of the traditional anti-emetics is limited, which is also a clue for the diagnosis of CHS. If traditional agents fail in controlling the symptoms, droperidol or haloperidol can be tried, but it has been used with limited success.
Consider PPI, this will reduce acid production, hence reduces Cl and H+ loss with vomiting.
K+ replacement can be challenging in the presence of renal failure. It will be safer to be performed in ICU. (Hypokalaemia might be causes by severe alkalosis, then correction of alkalosis might fix K level).
Hypomagnesemia may contribute to alkalosis and make it difficult to successfully treat the hypokalemia. Therefore, hypomagnesemia should also be corrected.
Acetozolamide, can be used for the treatment of metabolic acidosis, however the presence of renal failure and dehydration makes this therapy contraindicated.
Dialysis is a potential treatment of metabolic alkalosis among patients with renal failure.
Intravenous hydrochloric acid is a potential treatment of severe metabolic alkalosis if the patient fails to respond to the above treatment measures or if urgent correction of alkalosis is needed (delirium, seizure, or arrhythmia). Hydrochloric acid is usually given through central line.
For severe metabolic alkalosis, don’t depend on a single treatment (e.g. normal saline). Instead, a multimodal strategy may be most effective, with attention to all factors that may led to the metabolic alkalosis