Many patients presented for treatment in emergency practices are in shock of various etiologies. Shock is present when there is an imbalance between oxygen delivery to tissues and oxygen demand by tissues, and is characterized by hypotension (systolic arterial blood pressure [SAP] <90 mm Hg in cats), oliguria, and poor peripheral perfusion. Cats with hypoperfusion tend to have pale mucous membranes, prolonged capillary refill times, tachycardia or bradycardia, hypothermia, and weak to absent peripheral pulses. Signs of shock in cats may be masked by increases in heart rate, respiratory rate, and blood pressure just due to the influence of the hospital environment. Increases in sympathetic tone secondary to pain may also influence these vital signs and confound the diagnosis of shock. For these reasons, evaluation of other biomarkers for shock such as blood lactate concentration may be useful in emergency settings.

Lactate is produced by cells in situations of poor tissue perfusion where there is inadequate oxygen delivery. Cells receiving insufficient oxygen will switch from aerobic to anaerobic metabolism, producing significantly more lactate.  Although there are a number of conditions associated with hyperlactatemia, including liver failure, sepsis, neoplasia, and seizures, most patients presented to an emergency service will have high lactate levels secondary to hypoperfusion. In humans, blood lactate concentration is considered a better predictor of the presence of shock than vital signs alone. Dogs with higher blood lactate concentrations upon admission to a hospital or persistent hyperlactatemia have a poorer outcome than those dogs with lower blood lactate concentrations or in which hyperlactatemia is corrected. In healthy cats, an earlier study demonstrated that blood lactate concentration is not altered by struggling, venipuncture, age, sex, or time after hospital admission.

In this prospective, observational study of 111 cats admitted to a university emergency service, blood lactate concentrations were measured during initial evaluation. Median age of the cats was 9.5 years (range 0.4 to 20.3 years) and represented a variety of breeds; 104 of the cats were mixed breed. The patients had a variety of underlying diseases and conditions: renal disease (n=23), gastrointestinal disease (n=15), endocrine disease (n=14), neoplasia (n=11), trauma (n=11), sepsis or systemic inflammatory response syndrome (n=7), and cardiovascular disease (n=7), among others. Vital signs referable to perfusion (mucous membrane color, capillary refill time, peripheral pulse quality, heart rate, and rectal temperature) as well as SAP were also measured. Based on these parameters, the cats were assigned to one of three categories: no shock (n=35), mild to moderate shock (n=42), or severe shock (n=23); 11 cats were not categorized due to missing data. While the cats were hospitalized, additional blood lactate concentrations beyond the initial measurement were performed at the discretion of the attending clinician.

Median initial blood lactate concentration for all of the cats was 2.7 mmol/L (range, 0.5-19.3 mmol/L). Fifty of the cats had a blood lactate concentration that was considered normal (<2.5 mmol/L), and 61/111 cats had hyperlactatemia. Of the cats with hyperlactatemia, 40 (66%) had a blood lactate concentration of 2.5-5.0 mmol/L; 12 (20%) had a lactate level of >5.0 to 9.9 mmol/L, and 9 (15%) had a lactate level exceeding 10.0 mmol/L.  Those cats with white mucous membranes, hypothermia (rectal temperature <37.8 degrees C), or weak or absent femoral or metatarsal pulses had a higher median blood lactate concentration than those in the alternative groups for each of these categories. Neither bradycardia, commonly observed in critically ill cats, nor tachycardia was significantly associated with hyperlactatemia. Almost all (102/111) cats had SAP measured. Of these 102 cats, 42 were considered hypotensive (SAP<90 mm Hg) and 59 had SAP > 90 mm Hg. In the hypotensive cats median initial blood lactate concentration was higher than for those with SAP > 90 mm Hg.

Cats considered to be in severe shock had a median initial blood lactate concentration of 4.3 mmol/L (range, 0.9-19.3 mmol/L), higher than those with mild to moderate shock (median blood lactate concentration 2.25 mmol/L) or no shock (median blood lactate concentration 2.3 mmol/L). None of the study cats died naturally; they either survived to discharge (n=60; 54%) or were euthanized (n=51; 46%). The median initial blood lactate concentration was not significantly different among cats who survived to hospital discharge (2.45 mmol/L) and those who were euthanized (3.2 mmol/L). The majority of the cats who did not survive to discharge (33/51; 65%) were euthanized early on in their hospitalization (< 12 hours after initial evaluation).

Blood lactate levels measured in 47 of the cats anywhere from 1-34 hours subsequent to initial evaluation did not change or was increased in 6/47, and decreased in 41/47. Neither an increase or decrease in blood lactate concentration during hospitalization was associated with patient outcome.

Hyperlactatemia can be present in cats with and without abnormalities in vital signs referable to tissue perfusion and hypotension. Blood lactate measurements, in conjunction with the clinical context of the patient as evaluated through physical examination, SAP, and historical information regarding disease states that may cause hyperlactatemia outside of shock, may be useful in identifying abnormalities in oxygen delivery to tissues in cats. Future studies utilizing a larger number of cats, including hospitalized cats with naturally occurring deaths rather than euthanasia, and cats with specific disease states often associated with shock, such as sepsis, could further elucidate whether, as in dogs, hyperlactatemia or lactate clearance during hospitalization is associated with outcome. [PJS]