Lab case 375 interpretation

Question 1:

PH = 7.659, that is severe alkalaemia.

pCO2 = 12.6 mmHg (<40), so we have respiratory alkalosis.

Next, we will calculate the compensation. For acute respiratory alkalosis, we expect HCO3 to drop by 2 for every 10 pCO2 below 40. Accordingly, expected HCO3 should be: 24 – ((40-12.6) x 0.2) = 18.52. The value that we have is less than that (14.4), so we have additional metabolic acidosis.

Since we have metabolic acidosis, then we need to calculate the anion gap, that is calculated as: Na – (Cl + HCO3) = 138 – (109 – 14.4) = 14.6. So, we have HAGMA.

Because we have HAGMA, then we need to calculate the delta ratio to exclude the presence of additional metabolic process.

Delta ratio is calculated as: AG-12/24-HCO3 = 0.27. That means we have additional NAGMA. (Value less than 0.4).

So, we have triple processes here (Acute respiratory alkalosis, HAGMA and NAGMA).

Other abnormal results

K = 2.8 mmol, usually that is considered as moderate hypokalaemia. However, in the presence of alkalosis we get pseudohypokalaemia due to intracellular shift. Recent research showed that alkalosis (Metabolic or respiratory) causes less changes to serum K level compared to acidosis.

For alkalosis, serum K will drop by 0.3 for every 0.1 PH above 7.45. Accordingly, the corrected K for this patient will be around 3.4 mmol/L.

Cl = 109 mmol/L, that is hyperchloremia. That is an expected finding for respiratory alkalosis. There is increase secretion of HCO3 and increase reabsorption of Cl by the kidneys.

The most striking abnormal result for this patient is the very high lactate level (9.4). We will discuss the causes of elevated lactate in Question 2 answer.

Next, we need to look at the causes of these abnormalities.

For acute respiratory alkalosis we use the mnemonic CHAMPS.

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

That patient was very anxious also central respiratory centers stimulation caused by caffeine overdose.

For the potential causes 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

This patient has elevated lactate levels that caused HAGMA

For the causes of NAGMA, we use the mnemonic USED CARP

  • U = Ureteroenterostomy
  • S = Small bowel fistula
  • E = Extra chloride
  • D = Diarrhea
  • C = Carbonic anhydrase inhibitors
  • A = Adrenal insufficiency/ Addison’s disease
  • R = Renal tubular acidosis
  • P = Pancreatic fistula.

Extra chloride is the only possible cause here.

This patient took an overdose of weight-losing tablets that contain caffeine (caffeine overdose).

Caffeine acts as an adenosine receptor antagonist. Caffeine overdose causes central nervous system stimulation as well as positive ionotropic and chronotropic effects. This will present as anxiety and hyperventilation. This is the cause of respiratory alkalosis in patients with caffeine overdose.

Caffeine (in overdose) leads to catecholamine release, and the activation of Na/K ATPase. This causes lipolysis and glycogenolysis leading to pyruvate over production. If pyruvate is not aerobically metabolised, this will convert to lactate and causes hyperlactataemia and HAGMA.

 Question 2:

High serum lactate develops when the rate of lactate production exceeds the rate elimination by liver and kidneys. Lactic acidosis is divided into two categories:

  • Type A: Due to tissue hypoxia/Failure of circulatory system.
  • Type B: Occur with normal tissue perfusion and adequate tissue oxygenation.

Type A lactic acidosis can be further subdivided into

  • Increase O2 demand (Heavy exercises, Seizures, excessive muscles use)
  • Decrease O2 delivery/Decrease tissue perfusion (Cardiac arrest, shock, hypovolaemia, Acute pulmonary oedema, LVF, sepsis, mesenteric ischemia, acute pancreatitis, gangrene or compartment syndrome)
  • Reduced arterial O2 content (Hpoxaemia, severe anaemia, CO poisoning or methaemoglobinaemia).

Type B lactic acidosis can be further subdivided into

  • Type B1 (DM/DKA, liver failure, neoplasia, thiamine deficiency, renal failure, alcohol or hypoglycemia).
  • Type B2, hyperlactataemia caused by drugs or toxin (Metformin, Salicylate, ethylene glycol, HIV medication, cocaine, cyanide, propofol and beta agonists).
  • Type B3, hereditary defects (mitochondrial myopathies or defects in gluconeogenesis).

We can use the mnemonic of BLACK MIST for the causes of type B lactic acidosis.

  • Beta 2 agonists (salbutamol, adrenaline).
  • Liver failure.
  • Alcohols (ethanol, methanol, ethylene glycol), Anticonvulsant (valproate).
  • Cyanide poisoning.
  • Ketoacidosis.
  • Metformin.
  • Inborn errors of metabolism, Iron, Isoniazid.
  • Sepsis, Salicylates.