A 45 year old previously healthy man was admitted to your ICU five (5) days ago after a motor vehicle accident with chest and abdominal injuries. He is currently intubated and ventilated, is on 100% oxygen and PEEP of 10cm water. He is deeply sedated and on noradrenaline and adrenaline infusions at 10mcg/min each. He has become oliguric.

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

Venous biochemistry

Test

Value

Normal Range

Sodium

138 mmol/L

135 -145

Potassium*

7.1 mmol/L

3.5 - 4.5

Chloride

104 mmol/L

95 -105

Urea*

27 mmol/L

2.9 - 8.2

Creatinine*

260   mol/L

70 -120

Haematology

Test

Value

Normal Range

Hb*

120 G/L

135 -180

WBC*

12.8 x 109/L

4.0 -11.0

Platelets*

42 x 109/L

140 - 400

Arterial blood gases

Test

Value

Normal Range

pH*

7.01

7.35 – 7.45

PCO2*

45 mm Hg (6 kPa)

40 - 44

PO2*

70 mm Hg (9.3 kPa)

80 - 100

Bicarbonate*

11 mmol/L

22 - 26

Base Excess*

-19 mmol/L

-2.0 to +2.0

Glucose*

7.5 mmol/L

4 - 6

Lactate*

13 mmol/L

<2.0

13.1     Summarise the findings of the blood tests.

13.2     What are the likely underlying causes of the lactic acidosis?

13.3     What are your management priorities at this point?

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College Answer

13.1     Summarise the findings of the blood tests.

•    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

13.2     What are the likely underlying causes of the lactic acidosis?

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

13.3     What are your management priorities at this point?

•    Optimise cardiovascular function. Urgent echocardiogram. Volume replacement if possible. Measure continuous cardiac output (PiCCO or PAC). Measure SvO2 or ScvO2. Exclude abdominal compartment syndrome.


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


•    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

Analysis of the biochemistry:

  • Life-threatening hyperkalemia
  • Acute renal failure

Analysis of the haematology:

  • Thrombocytopenia

Analysis of the ABG:

  • Severe hypoxia
  • High anion gap metabolic acidosis with failure of respiratory compensation (pCOshould be about 25mmHg) - thus, a respiratory acidosis is also present.
  • The anion gap is (138) - (104 + 11) = 23, or 30.1 when calculated with potassium. It is not clear where the college got their value of 33 from.
  • 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, giving you the impression that there is some non-anion gap acidosis mixed in with the HAGMA. 
     
  • The lactate is 13.  Notably, the college forcefully points out that the lactate of 13 is insufficient to explain the entire rise in the anion gap. This could be argued. It must be remembered that the lactate does not need to account for all of the calculated 23 mmol/L of the anion gap.  Depending on the laboratory and the anion gap equation which you decided to use (sans or avec potassium), your acceptable standard anion gap could be 12 or 16, and this scenario's anion gap could be 23 or 30 (...or 33?). Ergo, the anion gap has risen by some value in the low teens (let's say 10 to 14). Therefore, the lactate accounts for almost all of the anion gap increase, with only maybe 1 mmol/L remaining unaccounted for. Given that the college do not follow on with any additional suggestions as to the origin of these mysterious anions, it is unclear where they were going with their "NOT adequately explained" statement, or how it factored into their marking rubric.

Causes of the lactic acidosis in this case:

  • Increased production:
    • Hypovolemia and poor tissue perfusion
    • Cardiac injury and cardiogenic shock
    • Sepsis
    • Hypoxia
    • Use of adrenaline
    • Massive rhabdomyolysis
    • Gut ischaemia and abdominal compartment syndrome
    • Toxicity due to mitochondrial toxins
  • Decreased clearance
    • Hepatic injury, ischaemic hepatitis or pre-existing hepatic disease
    • Failure of renal clearance (with lactate above 10mmol/L, renal clearance begins to play a role)

Management priorities:

Something like this benefits from a structured approach.

Airway:

  • Exclude acute airway obstruction
  • Ensure the ETT is well positioned (not in the right main bronchus)
  • Ensure ETT is not kinked and not semiobstructed with secretions or blood, and that it is of an appropriate diameter for this patient (CO2 clearance could be impaired)

Breathing:

  • Exclude tension pneumothorax by clinical examination
  • Exclude more minor pneumothorax with CXR or bedside ultrasonography
  • Increase PEEP to 12
  • Increase I:E ratio to 1:1.5 or 1:1 if the EtCO2 trace does not demonstrate an obstructive pattern (otherwise, hypercapnea could be exacerbated)

Circulation:

  • Exclude cardiac tamponade with bedside TTE
  • Assess fluid responsiveness by static or dynamic manoeuvres; administer volume
  • Assess cardiac output by combination of physical examination, measured variables (PAC or PiCCO) and surrogate measures (ScvO2, A-V CO2 difference)
  • Wean β-2 agonist medications to minimise pharmacological causes of lactate excess. Move on to pure α-1 agonists in pursuit of a normal MAP.

Disability/neurology is not a matter of priority at present.

Electrolyte derangement however is.

  • Administer sodium bicarbonate to replenish buffer systems, correct pH to improve catecholamine efficacy and at the same time shift potassium into the intracellular compartment
  • Administer calcium gluconate to stabilise excitable tissues and prevent arrhythmia
  • Consider insulin and dextrose
  • CVVHDF is indicated:
    • Without renal clearance, dialysis may be the only option to remove the potassium from this organism. One may consider calcium resonium resin if the GI tract is working.
    • In any case, given the history, there is likely massive rhabodomyolysis, and CVVHDF is indicated for this alone.
  • The college also recommends broad spectrum antibiotics. Sepsis is not excluded, so a broad spectrum beta lactam like piperacillin/tazobactam would be a sensible choice.