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.
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)
a)
Let us dissect these results systematically.
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:
|
Type A lactic acidosis: impaired tissue oxygenation
Type B1 lactic acidosis, due to a disease state
|
Type B2 drug-induced lactic acidosis
Type B3 : inborn errors of metabolism
|
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.