Hyperlactatemia

pattismith

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Approach to Lactic Acidosis of Uncertain Cause


Clinicians occasionally encounter patients with lactic acidosis
in whom the cause is not obvious.

Transient lactic acidosis
may result from a period of occult hypoglycemia or an
unrecognized seizure.

Tables 67.1 and 67.2 provide an outline
of the mechanisms, associated clinical manifestations, and
diagnostic considerations of other less common, yet important
mechanisms of lactic acidosis in the critically ill patient.


Within that framework, and in patients with persistent lactic
acidosis, the following approach is suggested:


• Consider the possibility of thiamine deficiency.

Empiric administration of thiamine carries little risk, and a prompt
response strongly supports the diagnosis.

• Discontinue potentially causative drugs
(i.e., antiretroviral agents, β2 agonists, nitroprusside, propofol, parenteral
lorazepam, metformin).

 Consider the possibility of poisoning (i.e.,toxic alcohol,
cyanide) and evaluate the need for empiric therapy.

• Congenital mitochondrial dysfunction occasionally may
manifest in adults and should be considered in patients
with unexplained weakness or difficulty weaning from
mechanical ventilation.
(PDF) Hyperlactatemia and Lactic Acidosis (researchgate.net)
 

pattismith

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The normal blood lactate concentration in unstressed patients is 0.5-1 mmol/L.

Patients with critical illness can be considered to have normal lactate concentrations of less than 2 mmol/L.

Hyperlactatemia is defined as a persistent, mild to moderate (2-4 mmol/L) increase in blood lactate concentration without metabolic acidosis,

whereas lactic acidosis is characterized by persistently increased blood lactate levels (usually >5 mmol/L) in association with metabolic acidosis.
Lactic Acidosis: Background, Etiology, Epidemiology (medscape.com)