A 45-year-old previously healthy male was admitted to your ICU 5 days ago after a motor vehicle crash with chest and abdominal injuries. He is currently intubated and ventilated, is on FiO2 1.0 and positive end-expiratory pressure (PEEP) of 10 cmH2O. He is deeply sedated and on nor-adrenaline and adrenaline infusions at 10 μg/min each. He has become oliguric.

His blood biochemistry, haematology and arterial blood gases are as follows:

Venous Sample
Parameter Patient Value Normal Adult Range
Sodium  138 mmol/L 134 – 146
Potassium  7.1 mmol/L 3.4 – 5.0
Chloride  104 mmol/L 95 – 105
Urea  27 mmol/L* 3.0 – 8.0
Creatinine 260 µmol/L* 45 – 90
Haematology
Parameter Patient Value Normal Adult Range
Haemoglobin 120 g/L* 135 – 180
White blood cell 12.8 x 109 /L* 4.0 – 11.0
Platelets 42 x 109 /L* 140 – 400
Arterial Blood Gas
Parameter Patient Value Normal Adult Range
FiO2 1.0  
pH 7.01* 7.35 – 7.45
PCO2 45 mmHg (6 kPa) 35 – 45 (4.6 – 6.0)
PO2 70 mm Hg (9.3 kPa)  
Bicarbonate 11 mmol/L* 22 – 26
Base Excess -19 mmol/L* -2.0 – +2.0
Glucose  7.5 mmol/L* 4.0 – 6.0
Lactate 13 mmol/L* < 2.0

a) Summarise the findings of the blood tests.

b) What ae the likely underlying causes of the lactic acidosis?

c) Outline your immediate management priorities at this point.

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College Answer

a)
High anion gap metabolic acidosis (with apparent normal SID). Note AG 33 which is NOT adequately
explained just by a lactate of 13 mmol
Inadequate or inappropriate respiratory compensation
Hypoxaemia (P/F ratio 70)
Acute renal failure (note urea:creatinine ratio).
Hyperkalaemia

b)
Sepsis with shock
Ongoing hypovolaemia
Hypoperfusion eg septic cardiomyopathy; abdominal compartment syndrome
Possible gut ischemia
Perhaps adrenaline (also seen with other catecholamines – unpredictable)

c)
Optimise ventilation.
Exclude pneumothorax.
Probably needs more PEEP after some volume.
Minimise airway pressures, limit tidal volume, tolerate hypercarbia (though concerned about pH < 7!!!)

Optimise cardiovascular function.
Urgent echocardiogram.
Volume replacement if possible.
Measure continuous cardiac output (PiCCO or PAC).
Measure SvO2 or ScvO2.
Exclude abdominal compartment syndrome
Rationalise inotropes. Stop adrenaline, use noradrenaline as required

Emergency management of hyperkalaemia with calcium, bicarbonate, insulin, dextrose and then haemodialysis!
Urgent CRRT – for both potassium and acidosis use of hemosol buffer

Broad-spectrum IV antibiotics (rational answer required)

Discussion

a)

Let us dissect these results systematically.

  1. The A-a gradient is high; ~586.8mmHg. The P/F ratio is 70.
  2. There is acidaemia
  3. The PaCO2 is not compensating for the acidaemia
  4. The SBE is -19, suggesting a severe metabolic acidosis
  5. The respiratory compensation is essentially non-existent - the expected PaCO2 (11 × 1.5) + 8 = 21mmHg, according to the Boston rules. Thus, there is also a respiratory acidosis.
  6. The anion gap is (138) - (104 + 11) = 23, or 30.1 when calculated with potassium
    The delta ratio, assuming a normal anion gap is 12 and a normal bicarbonate is 24, would therefore be (23 - 12) / (24 - 11) = 0.84 Thus, this is an almost pure HAGMA, with some minor contribution from the normal anion gap acidosis.

The college seem to have used some sort of weird anion gap formula. Usually they omit potassium from the calculations, but if you did not include potassium, the anion gap would be 23. What mysterious cation did the college include? Who can say. There must have been either 2.9 or 10mmol/L of it, whatever it was. Anyway, it does not change the interpretation in this case, but it does demonstrate some of the shortcomings of the anion gap as a diagnostic tool.

b) The causes of lactic acidosis are discussed at great length elsewhere.

In brief, here is the familiar table of Cohen-Woods aetiologies, with the causes most relevant to this case highlighted in bold script:

Causes of Lactic Acidosis

Type A lactic acidosis: impaired tissue oxygenation 

  • Shock: circulatory collapse
  • Regional ischaemia (eg. the gut)
  • Severe hypoxia
  • Severe anaemia
  • Carbon monoxide poisoning

Type B1 lactic acidosis, due to a disease state

  • Malignancy
  • Thiamine deficiency
  • Ketoacidosis /HONK
  • Septic shock
  • Impaired hepatic or renal clearance

Type B2 drug-induced lactic acidosis

  • Beta-2 adrenoceptor agonists
  • Metformin
  • Isoniazid
  • Cyanide (and by extension nitroprusside)
  • Xylitol, sorbitol, fructose
  • Propofol
  • The toxic alcohols eg. methanol
  • Paracetamol
  • Salicylates
  • NRTIs (nucleoside reverse transcriptase inhibitors)

Type B3 : inborn errors of metabolism

  • Numerous possible defects:
    • Pyruvate dehydrogenase deficiency
    • Electron transport chain enzyme defects
    • G6PD

c)

The management priorities presented by the college are difficult to improve upon, short of pruning away some of the excess exclamation marks. It does not vary greatly from the many other "manage your way out of this multiorgan system failure" questions. The specific feature which the college wanted us to focus on seems to have been the hyperkalemia; any management strategy which failed to address it would probably have been viewed as irresponsible.