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
Normal Adult Range
135 – 145
3.5 – 4.5
95 – 105
2.9 – 8.2
70 – 120
Normal Adult Range
White Blood Cells
12.8 x 109/L*
42 x 109/L*
140 - 400
Arterial Blood Gases
Normal Adult Range
7.35 – 7.45
45 mmHg (6 kPa)
35 – 45 (4.6 – 6.0)
70 mm Hg (9.3 kPa)*
22 - 26
-2.0 – + 2.0
4 – 6
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.
- 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
- 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.
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.
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.
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.
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 + 7.1) - (104 + 11) = 30.1
The delta ratio suggests that there is a pure high anion gap metabolic acidosis here. It is not accounter for by the lactate (13mmol/L)
(30.1 - 12) / (24 - 11) = 1.39
- 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
- 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:
- Investigate ETT malfunction as a cause of hypoxia and hypercapnea (i.e. is it kinked, or leaking?)
- Hypoxia needs to be investigated; potential causes include
- 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)
Shock state needs to be investigated; potential causes include
- 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
- 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)
- CVVHDF should commence to correct the uremia and manage the hyperkalemia
- Depending on dynamic assessment of fluid responsiveness, further fluids may be necessary
- 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.
- 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
- 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.
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.