Sara Jackson

Hey,

Based on my ECC exam question VHS could be used once the patient is stabilised to provide further info?

S

Annette challenge is always good 🙂

Here’s another pneumonic I’ve come across recently in the human literature plus seen it on VIN

MUD PILERS

Increased AG: metabolic AG acidosis (methanol, uraemia, diabetes/diabetic ketoacidosis (DKA), paraldehyde, isopropyl alcohol, lactate, ethylene glycol, rhabdomyolysis, salicilate (aspirin) MUD PILERS).

All of these can cause an increased AG as they’re increases in unmeasured anions.

A metabolic acidosis due to bicarbonate loss e.g. diarrhoea usually results in a normal AG

We can’t differentiate between these groups without an AG.

In this question we’re assuming it’s the hyperlacteraemia causing the acidosis which is fair but vomiting is so non-specific without hx I was thinking to be aware of a DKA/ureamic patient too.

Re lactate and hypovol. I agree we don’t know the cause of the hyperlacteraimia until fluid resuscitation is complete. I guess what I was disagreeing with is the concept of high lactate is lactic acidosis or poor tissue perfusion. Poor tissue perfusion is a cause of lactic acidosis.

S

My understanding is that bicarb buffers acids to compensate for a metabolic acidosis hence the decrease in bicarb, and hyperventilation is also a buffer by blowing off CO2, therefore this also decreases

Here I would say:
pH = acidosis
Co2 is the wrong direction for it to be respiratory acidosis therefore likely metabolic metabolic acidosis with correct respiratory compensation.
Bicarb will decrease because it’s buffering the metabolic acid.
The hyperlacteraemia would indicate a cause of the acidosis.

Where I would disagree with Annette (sorry Annette!) is that the lacteraemia is due to lactic acidosis OR poor tissue perfusion. We know we have an acidosis here, wholly or partly due to hyperlacteraemia. Poor tissue perfusion is one cause of hyperlacteraemia.

Lactate production may be higher than this indicates if severely dehydrated and may only be noted as such on our bloods once fluids are given and the lactate leaves the capillary beds to enter the venous circulation. Many vomiting patients are alkalaemic, due to acid loss, until hypoperfused/hypovolaemic secondary to severe dehydration or third spacing.

What underlying disease could cause an acidosis in a vomiting patient which is not related to lactate?

We transfused feline blood 24-48hr later if I remember correctly – the patient deteriorated again with the flea anaemia