Question 12

College answer

Causes:

Pre- operative drug therapy: - metformin, linezolid, anti-retroviral therapy

Prolonged bypass time

Lactate containing priming solution

Inadequate bypass flow rates

Prolonged hypothermia

Low cardiac output post-surgery – 

Tamponade, 

Myocardial ischaemia/infarction, 

Inadequate replacement valve function

Splanchic ischaemia

Hepatic insufficiency

High dose inotrope therapy

Measurement error

Ischaemic muscle/rhabdomyolysis

Thiamine deficiency

Determining cause

History:

          Review patients comorbidities, and drug history

          History of liver disease or alcohol/malnutrition

          Review course of procedure including bypass time and any complications

Examination

          Current infusions, including beta agonists

          Evidence of poor cardiac output

          Temperature

          Evidence of bleeding – drain losses

Evidence of tamponade – CVP, urine output, drains

          Abdominal examination for gut ischaemia

          Signs of liver failure

          Compartments for signs of muscle ischemia

Investigations

Confirm measurement with repeat

Standard haematology, coagulation and biochemistry tests including creatinine kinase – specifically for evidence of bleeding or liver failure

CXR – evidence of bleeding

ECHO if suspicion of tamponade/valve failure

CT /USS abdomen if suspicion of gut ischaemia/hepatic failure Red cell transketolase if thiamine deficiency suspected

Examiner Comments:

Many candidates provided a general list of causes of hyperlactataemia without being specific to immediately following an aortic valve replacement. When outlining an approach to diagnosing the cause of the elevated lactate, some candidates instead outlined an approach to managing the patient

Discussion

Among the questions which demand a mindless regurgitation of the Cohen-Woods classification of lactic acidosis, this CICM SAQ shines brightest because it then goes on to stress the higher cognitive functions of the candidates with some analysis and interpretation. The aortic valve replacement patient could have a raised lactate for a thousand reasons.

The examiner comments warn against producing a "general list of causes of hyperlactataemia",  but if they then go on to include things like thiamine deficiency and lactated priming solution in their model answer, then surely anything is permitted and no stretch of the imagination is too tenuous. Maybe this patient has HIV, was getting the valve replaced because of syphilitic aortitis, and the lactate is raised because of the effect of antiretroviral drugs. In view of this, a general list of causes is offered here, of which some are more related to a recent AVR than others. (In the colleges' defence, the bypass circuit does cause depletion of thiamine levels).

Increased rate of glycolysis due to lack of ATP

• Shock: circulatory collapse or regional ischaemia
  • embolic phenomena
  • low cardiac output state for any cause
• Lactic acidosis due to severe hypoxia (post-operative atelectasis, pneumothorax)
• Lactic acidosis due to severe anaemia (post-operative bleeding)
• Regional hypoxia and microvascular shunting in sepsis (vasoplegia; preoperative sepsis, eg. AVR for infective endocarditis)

Increased rate of glycolysis due to exogenous pro-glycolytic stimulus

• Beta-2 adrenoceptor agonists: salbutamol, adrenaline, isoprenaline (post-operative inotrope choice of the anaesthetist) 
• Catecholamine excess in hypovolemic shock (post-operative blood loss)

Pyruvate dehydrogenase inactivity

• Thiamine deficiency as a cause of lactic acidosis (major surgery)
• Inhibition of pyruvate dehydrogenase in sepsis ( vasoplegia ; preoperative sepsis, eg. AVR for infective endocarditis)
• Lactic acidosis due to inborn errors of metabolism (if NRTIs are on the table, this is too)

Defects of oxidative phosphorylation

• Cyanide (and by extension nitroprusside) toxicity (sodium nitroprusside use for hypertension post bypass is not completely unreasonable)
• Paracetamol toxicity
• Salicylate toxicity
• Lactic acidosis due to inborn errors of metabolism
• Metformin
• Propofol
• Isoniazid
• NRTIs (nucleoside reverse transcriptase inhibitors)

Decreased lactate clearance

• Lactic acidosis due to impaired hepatic or renal function (low flow state)
• Decreased gluconeogenesis due to ketoacidosis (a fasted Type 1 diabetic, a forgotten insulin/dextrose infusion prescription)

With regards to the investigations for this problem, the college answer is actually quite good, and little can be done to improve on it. One may merely reorganise it into some different shape. Thus:

Urgent ABCs:

• A) Confirm that the airway is well-placed and hypoxia is not being caused by tube kinking or dislodgement
• B) Ensure oxygenation is satisfactory and ventilation is unaffected:
  • Check the patient (pneumothorax, haemothorax)
  • Check the ventilator (make sure it is connected to gas, and that the waveforms suggest correct ventilation)
  • CXR to confirm auscultation findings
• C) Assess circulation:
  • Infusions: excessive catecholamines? Catastrophic shock?
  • Adequacy of perfusion of the extremities (palpation, inspection)
  • Adequacy of preload: CVP, PAOP, any evidence of tamponade on TTE
  • Signs of fluid responsiveness (eg. arterial line reverse pulsus paradoxus)
  • Adequacy of cardiac contractility (TTE, cardiac index measurement)
  • Adequacy of valve function (TTE, auscultation - looking for torrential paravalvular leak)
  • Adequacy of graft perfusion (ECG)
• D) Neurological causes:
  • Assess toxic effects of sedation
    • Propofol dose
    • Paracetamol dose 
  • Exclude seizures through history and examination
• E) Repeat electrolytes
  • Confirm lactic acidosis is not a measurement error
  • Send red cell transketolase to exclude thiamine deficiency
  • Ensure ionised hypocalcemia is not contributing to shock state
• F) Assess renal function
  • Exclude rhabdomyolysis - examine muscle compartments and check CK level
  • Ensure there is urine output (aortic dissection or embolic phenomena?)
• G) Assess hepatic function
  • Exclude pre-exisitng liver disease through history and examination
  • Exclude new onset of liver dysfunction by LFTs and ultrasound
• H) Exclude anaemia/ blood loss 
  • Coags, FBC, fibrinogen level
• I) Consider infectious causes
  • Explore infection history and examine for features of infective endocarditis
  • Investigate history for HIV (NRTIs) tuberculosis (isoniazid) or malignancy.
  • Culture blood, urine, sputum