Question 23

A 37-year-old previously healthy man was admitted to your ICU five days ago after a motor vehicle crash with chest and abdominal injuries. He is currently intubated and ventilated, with FIO2 1.0 and PEEP 10 cmH2O. 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 Adult 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 μmol/L*	70 – 120

Haematology

Test	Value	Normal Adult Range
Haemoglobin	120 G/L*	135 -180
White Blood Cells	12.8 x 109/L*	4.0 -11.0
Platelets	42 x 109/L*	140 - 400

Arterial Blood Gases

Test	Value	Normal Adult Range
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 – 6
Lactate	13 mmol/L*	< 2.0

a) Summarise the findings of the blood tests.

b) List the likely causes of the raised lactate.

c) Briefly outline your management priorities for this man.

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College Answer

High anion gap metabolic acidosis Note AG 33 - NOT adequately explained just by a lactate of 13 mmol. Delta ratio approx. 2
Inadequate or inappropriate respiratory compensation
Hypoxaemia (P/F ratio 70)
Acute renal failure
Hyperkalaemia,
Thrombocytopenia
Anaemia
Leukocytosis
Mild hyperglycaemia (? Stress-induced)

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

Management Priorities should encompass both immediate resuscitation and investigation for the cause of the abnormalities.

Respiratory:

Clinical examination and CXR looking for cause of hypoxia – consider lung contusion, haemothorax/pneumothorax with shock, ARDS secondary to other process. Institute ARDS ventilation strategy if appropriate.

Cardiovascular:

Clinical examination and further investigations to determine cause of inotrope and vasopressor requirement. Consider ECHO. Fluid resuscitation if hypovolaemia suggested by examination /ECHO findings.

Cease adrenaline if possible.

Renal

Emergency management of hyperkalaemia – calcium, bicarbonate, dextrose, insulin, followed by institution of renal replacement therapy.

Examination and investigation for cause of deterioration:

Abdominal examination and measurement of intrabadominal pressures Examination for potential sources of infection, including GI, lines, ventilator acquired

pneumonia, wounds, urine. Consider empirical antibiotic treatment if thought to be septic aetiology.

Serum lipase, troponin, CK, blood cultures.
Examination to exclude limb compartments, rhabdomyolysis.

Imaging as suggested by results of examination – may require abdominal/thoracic CT scan, renal USS if anuric, angiography/endoscopy if evidence of ongoing bleeding.

Discussion

Let us dissect these results systematically.

The A-a gradient is very high; 194 or 337.6mmHg depending on what FiO₂ you are delivering.
PAO₂ = (1.0 × 713) - (45 × 1.25) = 656.75
Thus, A-a = (656.75 - 70) = 586.75mmHg.
There is acidaemia
The PaCO₂ is not compensatory, suggesting there is respiratory acidosis
The SBE is -19, suggesting there is also a severe metabolic acidosis
The respiratory compensation is totally lacking - the expected PaCO₂(11 × 1.5) + 8 = 24.5mmHg, and thus there is also a significant respiratory acidosis
The anion gap is raised:
(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
This suggests that there is mainly a high anion gap metabolic acidosis here, with some minor contribution from a normal anion gap acidosis. It is not completely accounted for by the lactate (13mmol/L), according to the college. However, you'd have to agree that it's pretty close.
Urinary pH and electolytes are not reported, and are irrelevant.

Thus, in summary there is both a respiratory acidosis and a HAGMA, which is only partially related to lactate.

On top of that, the patient is severy hypoxic, thrombocytopenic, hyperkalemic, and in renal failure with uremia.

The likely causes of raised lactate are

Shock
Hypoxia
Gut ischaemia
Microvascular shunting due to sepsis
The use of adrenaline

In general, the causes of lactic acidosis are discussed at great length elsewhere.

The management priorities - if one were going to approach this with some sort of system - would resemble the following list:

Airway

Investigate ETT malfunction as a cause of hypoxia and hypercapnea (i.e. is it kinked, or leaking?)

Ventilation

Hypoxia needs to be investigated; potential causes include
- ARDS
- Lung contusion
- Pneumothorax / haemothorax
These can be excluded with a quick bedside ultrasound and mobile CXR
Thereafter, one may adjust the ventilator accoridngly (eg. increase resp rate, go to 1:1 I:E ratio, increase the PEEP, decrease the tidal volume, practicing lung protective ventilation)

Circulation

Shock state needs to be investigated; potential causes include

Hypovolemia
Cardiogenic "pump failure" (eg. due to contusions or cardiac tamponade)
Vasoplegia (due to sepsis)

A TTE can rule out many of these causes.

Thereafter, it would be helpful to wean off adrenaline, and if need be change over to a non-catecholamine inotrope (eg. milrinone).

Sedation and paralysis

Neuromuscular blockade may improve ventilation

Electrolytes

Hyperkalemia needs immediate attention. Calcium gluconate and an insulin/dextrose bolus need to be administered, and bicarbonate should be considered (but it may impair the metabolism of lactate)

Fluid balance

CVVHDF should commence to correct the uremia and manage the hyperkalemia
Depending on dynamic assessment of fluid responsiveness, further fluids may be necessary

Abdominal injuries

Abdominal compartment pressure should be measured
A surgical opinion should be sought regarding mesentric ischaemia as the cause of the lactic acidosis
A serum lipase and LFTs should be sent to rule out pancreatitis and hepatic dysfunction as causes of the hyperlactataemic shock state.

Haematological disturbances

Hb should be checked at regular intervals to screen for non-obvious internal blood loss (eg. a retroperitoneal hematoma or aortic dissection)
A PR should be performed to look for melaena
The coagulation parameters should be measured
CoAgulopathy should be corrected if invasive procedures are planned or if bleeding is suspected

Infectious complications

A septic screen should be sent
Line sites and wounds should be inspected
If no evidence of infection is discovered, empirical antibiotics are not indicated.

References

Luft FC. Lactic acidosis update for critical care clinicians. J Am Soc Nephrol 2001 Feb; 12 Suppl 17 S15-9.

Ohs manual – Chapter 15 by D J (Jamie) Cooper and Alistair D Nichol, titled “Lactic acidosis” (pp. 145)

Cohen RD, Woods HF. Lactic acidosis revisited. Diabetes 1983; 32: 181–91.

Lange, H., and R. Jäckel. "Usefulness of plasma lactate concentration in the diagnosis of acute abdominal disease." The European journal of surgery= Acta chirurgica 160.6-7 (1994): 381.

WEIL, MAX HARRY, and ABDELMONEN A. AFIFI. "Experimental and clinical studies on lactate and pyruvate as indicators of the severity of acute circulatory failure (shock)." Circulation 41.6 (1970): 989-1001.

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