Answers:
Question 1:
PH = 7.12, that is moderate to severe acidaemia.
HCO3 = 7 mmol/L. So, we have metabolic acidosis.
Since we have metabolic acidosis, then we need to calculate the anion gap to know what type of metabolic acidosis this patient has. That is in addition to calculating the compensation.
To calculate the compensation we use Winter’s formula. That is:
Expected pCO2 = 1.5 x HCO3 + 8 (+/-2) = 1.5 x 7 + 8 = 18.5 with expected range between 16.5 and 20.5.
This patients pCO2 is 23, that is higher than the highest value on the range. So, he has additional respiratory acidosis.
Anion gap is calculated as AG = Na – (Cl + HCO3) = 17. This patient has HAGMA.
Since we have HAGMA, next we need to calculate the delta ratio to exclude the presence of a third metabolic process. This is calculated as:
Delta ratio = (AG-12)/(24-HCO3) = 5/17 = 0.29. This means the patient has hyperchloraemic metabolic acidosis (Can be a sign of seriousness of the condition).
Delta ratio < 0.4 means the patient has hyperchloremic metabolic acidosis (NAGMA).
This patient has triple metabolic conditions. HAGMA, Hyperchloraemic NAGMA and mild respiratory acidosis.
Other abnormal findings:
The most obvious other abnormal finding is lactate level of 11 mmol/L. This is severe hyperlactataemia.
Cl = 112 mmol/L, that is hyperchloraemia.
Glucose = 14.2 mmol/L, that is hyperglycemia.
Creatinine = 130 mmol/L, this is elevated. a reflection of poor kidney function. We don’t know if these changes are acute or chronic.
Question 2:
For the deferential diagnosis 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
From the list above, Hyperlactataemia is surly a cause of this patient’s HAGMA. (Whenever lactate level is more than 5, for sure the patient has lactic acidosis and it should be treated.)
Next we will look at the causes of Lactic acidosis. High lactate is either caused by reduced O2 delivery to the tissue (Type A) or impaired lactate metabolism (Type B).
These causes are further sub-divided into further categories.
Type-A lactic acidosis (Absolute or relative tissue hypoxia) is subdivided into 4 types:
- Increase oxygen demand (Seizures, excessive exercise or excessive use of accessory muscles like during asthma,, etc).
- Systemic hypoperfusion (Due to shock state that can be cardiac, septic, hypovolemic,,etc)
- Local hypoperfusion (arterial embolism, mesenteric ischaemia, torsion, valvulus,, etc)
- Decrease arterial oxygen content. (Hypoxaemia, severe anaemia, CO poisoning).
Type-B lactic acidosis (Without tissue hypoxia, usually due to defect in the metabolism of lactate). This is further subdivided into 3 categories.
- Type B1, that is due to underlying disease process (severe liver disease, malignancy, thiamine deficiency,,etc)
- Type B2, that is due to drugs or toxins (Paracetamol, metformin, ethylene glycol, cyanide,, etc)
- Type B3, that is due to congenital metabolic defect (Mitochondrial disease, hypoglycemia, etc).
Looking at these causes,, that patient has either Type-A2 or Type-A3. He underwent CT scan for his abdomen that showed generalised bowel ischaemia without vascular obstruction.
Question 3:
For the management of this patient we should apply the early goal direct therapy for sepsis. That include:
- Immediate IV hydration
- Early broad spectrum antibiotics
- Consider Inotropic support early
- Monitor Vital sign and blood pressure and maintain MAP more than 70
- Monitor urine output and lactate level
- Early source control