# Lab case 363 interpretation

Question 1:

PH = 7.52, that is moderate alkalaemia

pCO2 = 34, so we have respiratory alkalosis.

Next we calculate the compensation.

• For acute respiratory alkalosis we expect HCO3 to drop by 2 for every 10 pCO2 below 40. According to that, the expected HCO3 should be 23 mmol/L if this patient was suffering from acute respiratory alkalosis only.
• For chronic respiratory alkalosis we expect HCO3 to drop by 5 for every 10 pCO2 below 40. For that the expected HCO3 would be 21.5 mmol/L if that case was chronic respiratory alkalosis only.

This patient had elevated HCO3, 28. o, this patient has additional metabolic alkalosis.

Always try to calculate the anion gap to exclude associated HAGMA. for this patient, the anion gap is: 130 – (95 + 28) = 7. However, in the presence of high glucose level we get pseudohyponatraemia. (That might affect the calculation of the AG).

Corrected Na level = calculated Na + (glucose-5)/3. For this patient, corrected Na level will be 130 + (17 – 5)/3 = 134, that is normal.

The corrected AG will be 11, still within normal range.

Lactate = 2 mmol/L, that is slightly elevated, which reflects reduced tissue prefusion.

The final conclusion is combined metabolic and respiratory alkalosis

Next we will look at the potential causes of both respiratory and metabolic alkalosis for this patient,

For the causes of  respiratory alkalosis, we use the mnemonic CHAMPS

• C = CNS diseases
• H = Hypoxia
• A = Anxiety/Pain
• M = Mechanical ventilation/ over ventilation
• P = Progesterone
• S = Salicylates / sepsis

From the causes listed above, the patient had abdominal pain and was anxious.

For the causes of  Metabolic alkalosis, we use the mnemonic CLEVER PD

• C – contraction (dehydration)
•  L – liquorice (diuretic), laxative abuse
•  E – endocrine (Conn’s, Cushing’s)
•  V – vomiting, GI loss (villous adenoma)
•  E – excess alkali (antacids)
•  R – renal (Bartter’s), severe K depletion
•  P – post hypercapnia
•  D – diuretics

From the list above, the patient was vomiting and most probably he was dehydrated (Lactate =2).

That presentation is typical for patients presenting with THC hyperemesis.

Question 2:

• IV fluids to correct dehydration and electrolytes imbalance
• Anti-emetics to suppress the vomiting
• Consider medication to treat associated anxiety (Benzodiazepines)
• Pain medication.

Due to the similarities between cannabinoid hyperemesis and cyclical vomiting, anti-dopamine was tried and it was successful.

HAVOC trial compared ondansetron to haloperidol for the treatment of cannabinoid hyperemesis. The results showed that haloperidol was superior to ondansetron (both in small and high doses).

Hot showers temporarily relieve the symptoms. Prolonged exposure to THC leads to inactivation of Transient Receptor Potential Channels (TRPV), these are group of membrane proteins. This inactivation leads to nausea and emesis, both by central effect and vagal afferent. (TRPV1 inactivation alters gastric motility).

Cutaneous heat normalises gastric motility via activation of TRPV1 (nociceptors). Topical capsaicin has a similar effect. Now, some centres use topical capsaicin (rub on the gastric area) for the the management to cannabinoid hyperemesis.

Some people use inhaled isopropyl alcohol wipes to help the symptom of nausea and vomiting. **

** Beadle et al. (Ann Emerg Med 2016) Nasal inhalation of isopropyl alcohol provides clinically important relief from acute nausea, of at least a short duration, in community ambulatory patient.