College Answer

a)

• 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)

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)

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.

1. 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.
2. There is acidaemia
3. The PaCO₂ is not compensatory, suggesting there is respiratory acidosis
4. The SBE is -19, suggesting there is also a severe metabolic acidosis
5. The respiratory compensation is totally lacking - the expected PaCO₂(11 × 1.5) + 8 = 24.5mmHg, and thus there is also a significant respiratory acidosis
6. 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.
7. 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.