Abnormalities in tissue perfusion leading to an imbalance between oxygen delivery and oxygen demand (ie, shock) are common in patients being treated on an emergency basis. Shock is defined clinically as the presence of hypotension, oliguria, and poor peripheral perfusion.1 In cats, physical examination findings considered to be consistent with hypoperfusion include pale mucous membranes, prolonged capillary refill time, tachycardia or bradycardia, hypothermia, and poor or absent peripheral pulses.2,3 Intermittent or prolonged hypotension, defined as SAP < 90 mm Hg in cats, can lead to inadequate tissue perfusion and oxygen delivery.4 Therefore, the ability to identify and treat hypoperfusion is fundamental in an emergency setting, and initial therapeutic interventions are aimed to reverse or prevent the development of shock.
In the early stages of shock, termed occult or compensated shock, many patients may have relatively normal vital signs and blood pressure; however, tissue oxygen delivery may be compromised. In a study5 of healthy cats, heart rate, respiratory rate, and blood pressure were found to increase significantly in a hospital environment, which suggests the accuracy of these vital signs in detecting early shock may be limited. In addition, pain may also contribute to increases in sympathetic tone influencing these vital signs and potentially rendering them insensitive for monitoring the adequacy of tissue perfusion. Because of this, potential biomarkers for shock such as circulating lactate concentration have been investigated. In conditions of poor tissue perfusion where there is inadequate oxygen delivery, cells switch from aerobic to anaerobic metabolism for cellular energy production, leading to increased production of lactate. Lactate is metabolized back to pyruvate through the Cori cycle in the liver and to a lesser extent by the kidneys.6 In conditions of circulatory dysfunction, prolonged hyperlactatemia may occur because the liver becomes a net producer of lactate and clearance of lactate is impaired as well.7 There are other conditions associated with high circulating lactate concentration, such as liver failure, neoplasia, seizures, and sepsis; however, in patients seen on an emergency basis that have altered physical examination perfusion variables and hypotension, hyperlactatemia is most commonly secondary to hypoperfusion. In people, circulating lactate concentration has been extensively studied and it is generally considered to be a better predictor of shock, compared with traditional vital signs alone.8
Blood lactate concentration reference values in healthy dogs and cats are < 2.5 mmol/L, although results of a recent study9 in healthy cats suggest that a blood lactate concentration up to 2.8 mmol/L can be present. Investigators found that lactate concentration was not affected by struggling, venipuncture site, age, sex, or time after admission to the hospital.9 Several studies10–15 in dogs have indicated that those with higher blood lactate concentrations at admission or persistent hyperlactatemia may have a worse outcome than those with lower lactate concentrations or in which lactate concentration becomes normalized. It has been suggested that clinical signs of mild systemic hypoperfusion lead to minor increases in blood lactate concentration (3 to 5 mmol/L), whereas signs of severe systemic hypoperfusion are associated with values > 7 mmol/L.16 In a recent study17 evaluating the use of shock index (where shock index = heart rate divided by SAP), dogs with hemorrhage were assigned to shock categories according to severity (level 1 [no shock] to 4 [severe shock]). In that study,17 dogs in shock had a lower body temperature and SAP as well as higher heart rate and plasma lactate concentration, compared with healthy control dogs. However, the category of shock, whether shock was mild or severe, and the degree of increase in blood lactate concentration were not reported. To the authors' knowledge, no other clinical studies have been performed to evaluate the severity of shock and degree of blood lactate increase in dogs or cats seen on an emergency basis. In addition, a literature search revealed no veterinary clinical studies evaluating the relationships between blood lactate concentration and perfusion variables assessed by physical examination or SAP in cats.
The goal of the study reported here was to assess potential associations of lactate concentration with physically assessed perfusion variables, SAP, and outcome in ill cats evaluated at an emergency service. Our hypothesis was that blood lactate concentration would be higher in cats with abnormalities in tissue perfusion variables and hypotension, compared with cats that had values within the expected ranges. We also hypothesized that hyperlactatemia would be associated with a worse outcome, compared with cats without this finding.
Materials and Methods
Cats evaluated at the University of Pennsylvania School of Veterinary Medicine emergency service that underwent physical examination, with or without SAP measurement, and had blood lactate concentration measured during initial evaluation (prior to any interventions) were eligible for inclusion in the study, which was performed between February 3, 2011, and December 9, 2013. Cats were enrolled in the study only once. Emergency room faculty and house officers (interns and emergency and critical care residents) completed a data collection sheet to record the cat's initial physical examination perfusion variables, SAP, and venous blood lactate concentration. Perfusion variables included subjectively (mucous membrane color, capillary refill time, and femoral and metatarsal pulse quality) and objectively (heart rate and rectal temperature) assessed data. On the data collection sheet, mucous membranes were characterized as white, pale pink, or pink. Capillary refill time was recorded as < 2 seconds, 2 seconds, or > 2 seconds. Femoral and metatarsal pulse quality as assessed via digital palpation was recorded as absent, poor, moderate, or strong. Heart rate was determined by thoracic auscultation. Bradycardia and tachycardia were defined as a heart rate < 160 or > 225 beats/min, respectively.3,4 Hypothermia and hyperthermia were defined as a rectal temperature < 37.8°C (100°F) or > 39.4°C (103°F), respectively.3,5 Veterinarians were asked to classify the cats as having either normal perfusion or hypoperfusion on the basis of their clinical evaluation. The SAP was measured by trained veterinary technicians through use of a Doppler flow detectora with a 9.5-MHz probe following standard technique.18 This measurement was repeated, and if the same reading was obtained, this number was recorded. If readings differed, a third or fourth measurement was obtained and the average of all the measurements was recorded. If one reading differed substantially from the other readings, it was considered erroneous and additional readings were performed.
A measurement that was too low for detection was recorded as 30 mm Hg (chosen on the basis of clinical experience, where this was the lowest value recorded with the equipment) for purposes of statistical analysis. Cats were considered to be hypotensive if the SAP was < 90 mm Hg.
Cats having complete physical perfusion variable assessment and SAP measurement were retrospectively assigned to 1 of 3 shock categories: no shock, mild to moderate shock, or severe shock (Appendix). For purposes of analysis, pink and pale pink mucous membranes, capillary refill time ≤ 2 seconds, strong or moderate femoral and metatarsal pulses, absence of bradycardia or tachycardia, and rectal temperature 37.8°C were considered normal results for perfusion variables.
Blood samples used for lactate concentration measurement were collected during IV catheter placement (from a cephalic or saphenous vein) or via direct venipuncture and were immediately analyzed with a laboratory analyzer.b The site used for blood sample collection was not recorded. Lactate concentration < 2.5 mmol/L was considered normal19 (analyzer measurement range, 0.3 to 20 mmol/L). Additional lactate concentration measurements (after the initial determination at hospital intake) were performed during hospitalization at the discretion of the attending clinician. Time following the first measurement and whether there was a change in lactate concentration (ie, no change, increase, or decrease) were recorded. The underlying disease and outcome were recorded. Possible outcomes were survival to hospital discharge and euthanasia or death.
The study protocol was reviewed by the privately owned animal protocol committee. As this observational study involved recording information that was already being obtained as part of the cat's medical treatment directed by the primary veterinarian, institutional animal care and use review and client consent for study inclusion was waived.
Statistical analysis—Continuous variables were assessed for normality by means of the Shapiro-Wilk test. Median (range) data were reported for non-normally distributed variables, and mean ± SD data were reported for normally distributed variables. The Kruskal-Wallis test was used to compare continuous variables when there were > 2 categories; if findings were significant (P < 0.05), the Wilcoxon rank sum test was used for pairwise comparisons to determine which groups were significantly different. For the purpose of analysis, femoral and metatarsal pulse quality data were combined and cats were grouped as having either normal (moderate or strong pulses) or abnormal (poor or absent) peripheral pulses. The Spearman rank correlation was used to assess the association between 2 continuous variables. Values of P < 0.05 were considered significant for all comparisons. All statistical tests were performed with the aid of statistical software.c
Results
One hundred eleven cats were enrolled in the study. Median age was 9.5 years (range, 0.4 to 20.3 years), and mean weight was 4.68 ± 1.54 kg (10.3 ± 3.4 lb). Breeds included domestic shorthair (n = 96), domestic longhair (8), Persian (2), and 1 each of British Shorthair, Siamese, and Devon Rex. Two cats were described as purebred, but breed was not specified. The study cats had a variety of underlying diseases; primary conditions included renal disease (n = 23), gastrointestinal disease (15), endocrine disorders (14), neoplasia (11), trauma (11), sepsis or systemic inflammatory response syndrome (7), cardiovascular disease (7), neurologic disease (4), hepatic disease (2), and respiratory disease (2). Fifteen cats were categorized as having other conditions (including anemia, toxicosis, anaphylaxis, or unknown illness). Median initial blood lactate concentration for all cats was 2.7 mmol/L (range, 0.5 to 19.3 mmol/L). Fifty of 111 (45%) cats had a lactate concentration < 2.5 mmol/L and 61 cats had hyperlactatemia. Of the 61 hyperlactatemic cats, 40 (66%) had a lactate concentration from 2.5 to 5.0 mmol/L, 12 (20%) from > 5.0 to 9.9 mmol/L, and 9 (15%) > 10.0 mmol/L.
The relationships between initial blood lactate concentration and perfusion variables assessed by physical examination as well as SAP were summarized (Table 1). Cats classified as having white mucous membranes, abnormal femoral or metatarsal pulses, or hypothermia (rectal temperature < 37.8°C) had a higher median lactate concentration, compared with cats in the alternative groups for each category (P < 0.05). Neither bradycardia nor tachycardia was significantly associated with an increased lactate concentration. Of the 35 bradycardic cats, 27 (77%) were concurrently hypothermic, 5 (14%) were normothermic, and 1 (3%) was hyperthermic. Two of the 35 cats did not have rectal temperature measured. Seventeen (48%) of the bradycardic cats were concurrently hypothermic and hypotensive; these cats had a median lactate concentration of 3.2 mmol/L (range, 0.9 to 17.5 mmol/L).
The SAP was measured for 102 of 111 (92%) cats. Median SAP was 92.5 mm Hg (range, 30 to 240 mm Hg). Of the 102 cats, 43 (42%) had hypotension (ie, SAP < 90 mm Hg) and 59 (58%) had an SAP ≥ 90 mm Hg. Median initial blood lactate concentration for hypotensive cats was significantly (P < 0.01) higher than that for cats with SAP ≥ 90 mm Hg (Table 1). Seventeen of 43 (40%) cats with hypotension had an SAP of 30 mm Hg assigned because no blood flow was detected via Doppler flow detector. All of these cats were considered to be hypoperfused by the attending clinician and had femoral and metatarsal pulses classified as absent or poor. Several hypotensive cats (15/43 [35%]) had a lactate concentration < 2.5 mmol/L (range, 0.8 to 2.4 mmol/L). Conversely, 27 of 59 (46%) cats with an SAP > 90 mm Hg had a lactate concentration > 2.5 mmol/L. Despite the normal SAP measurement, 17 of these 27 (63%) cats were classified as having hypoperfusion by the attending clinician; the remaining 10 were considered to have normal perfusion. The median lactate concentrations of cats with subjectively abnormal femoral (3.85 mmol/L) or metatarsal pulses (3.4 mmol/L) were significantly (P < 0.05) greater than that of cats with normal results for the same variable (2.3 mmol/L and 2.45 mmol/L, respectively; Figures 1 and 2). Initial lactate concentration was significantly (P = 0.006) inversely correlated (Spearman ρ = −0.299) with SAP (Figure 3).
Physically assessed perfusion variables with median (range) SAP and initial blood lactate concentration in 111 cats evaluated by an emergency service.
Variable | Lactate (mmol/L) | P value |
---|---|---|
Mucous membrane color | ||
Pale pink or pink (n = 98) | 2.6 (0.5–19.3) | 0.013 |
White (n = 6) | 4.65 (3.1–16.5) | |
Capillary refill time (s) | ||
≤ 2 (n = 58) | 2.3 (0.5–11) | 0.062 |
> 2 (n = 39) | 3.3 (0.8–17.5) | |
Femoral pulses | ||
Strong or moderate (n = 63) | 2.3 (0.5–14.4) | 0.022 |
Weak or absent (n = 48) | 3.85 (0.7–19.3) | |
Metatarsal pulses | ||
Strong or moderate (n = 62) | 2.45 (0.5–14.4) | 0.024 |
Weak or absent (n = 49) | 3.4 (0.7–19.3) | |
Heart rate (beats/min) | ||
> 160 (n = 76) | 2.95 (0.5–19.3) | 0.181 |
≤ 160 (n = 35) | 2.3 (0.7–17.5) | |
< 225 (n = 101) | 2.9 (0.5–19.3) | 0.119 |
≥ 225 (n = 10) | 1.65 (0.7–13.3) | |
160–225 (n = 66) | 3.15 (0.5–19.3) | 0.03 |
< 160 or > 225 (n = 45) | 2.1 (0.7–17.3) | |
Temperature (°C) | ||
≥ 37.8 (n = 52) | 2.3 (0.8–19.3) | 0.037 |
< 37.8 (n = 59) | 3.3 (0.5–17.5) | |
SAP (mm Hg) | ||
≥ 90 (n = 59) | 2.35 (0.5–9.9) | 0.010 |
< 90 (n = 43) | 3.3 (0.8–19.3) |
Initial lactate concentration was assessed in a sample collected (from a cephalic or saphenous vein) during IV catheter placement or via direct venipuncture, prior to any therapeutic interventions. Lactate concentration < 2.5 mmol/L was considered normal. For purposes of analysis, pink or pale pink mucous membranes, capillary refill time ≤ 2 seconds, strong or moderate femoral and metatarsal pulses, absence of bradycardia (< 160 beats/min) or tachycardia (> 225 beats/min), rectal temperature ≥ 37.8°C, and SAP ≥ 90 mm Hg were categorized as normal results. Median lactate concentrations were compared between normal and abnormal categories for each variable; heart rate was additionally compared between cats with and without bradycardia and between cats with and without tachycardia. Not all cats had every variable assessed.
Evaluation of retrospectively assigned shock categories revealed that 35 cats had no signs of shock (ie, these were considered to have normal perfusion), 42 cats had mild to moderate shock, and 23 cats had severe shock. Eleven cats were not assigned to a shock category because of missing data (either physical perfusion variables or SAP measurement). Median initial blood lactate concentration of cats with severe shock (4.3 mmol/L [range, 0.9 to 19.3 mmol/L]) was significantly higher than that of cats with either mild to moderate shock (2.25 mmol/L [range, 0.7 to 10 mmol/L]; P = 0.002) or no shock (2.3 mmol/L [range, 0.5 to 9.9 mmol/L]; P = 0.002; Figure 4).
Of the 111 cats, 60 (54%) survived to hospital discharge and 51 (46%) were euthanized in the hospital. There were no naturally occurring deaths among study cats. The median initial blood lactate concentration was not significantly (P = 0.386) different between cats that survived to hospital discharge (2.45 mmol/L; range, 0.5 to 14.4 mmol/L) and those that were euthanized (3.2 mmol/L; range, 0.7 to 19.3 mmol/L). Most of the nonsurviving cats (33/51 [65%]) were euthanized ≤ 12 hours after initial evaluation. Forty-seven cats had lactate concentration measurement repeated during hospitalization, with a median time after initial measurement of 8.75 hours (range, 1 to 34 hours). Compared with the initial (admission) value, lactate concentration measured during hospitalization either did not change or was increased in 6 of 47 (13%) cats and was decreased in the remaining 41 (87%) cats. Neither an increase nor a decrease in lactate concentration from the first measurement was associated with patient outcome (P = 0.91). Similarly, among 27 cats that were initially hyperlactatemic and underwent repeated lactate concentration measurement while hospitalized, there was no significant (P = 0.32) difference in median lactate concentration change for cats that survived (–3.62 mmol/L) versus those that were euthanized (–2.3 mmol/L).
Discussion
In the present study, cats with abnormal findings for peripheral perfusion variables (white mucous membranes, abnormal peripheral pulses, and hypothermia) and hypotension had significantly increased pretreatment blood lactate concentration, indicating altered tissue oxygen delivery, compared with cats that did not have these abnormalities detected. However, bradycardia, a common finding in critically ill cats,3,4 was not associated with an increased lactate concentration in our study population. Many clinicians with various amounts of experience were involved in making the subjective and objective perfusion assessments, and the fact that lactate concentration was significantly increased in cats that had these abnormalities reflects the strength of the study findings. Therefore, physical examination and SAP measurements to assess peripheral perfusion variables remain valuable tools for assessing circulatory status of critically ill cats.
When perfusion variables were combined with SAP to retrospectively assign cats to shock categories, the median initial blood lactate concentration of cats with severe shock (4.3 mmol/L) was significantly higher than that of cats in other categories (≤ 2.3 mmol/L for each). It should be noted that there was overlap in lactate concentrations among cats in the no shock, mild to moderate shock, and severe shock categories. This may in part be attributable to the fact that 15 cats with initial lactate concentration < 2.5 mmol/L were categorized as having mild to moderate or severe shock. The normal lactate concentration in these cats suggests that tissue oxygen delivery and use remained normal despite the presence of hypotension and abnormalities in physically assessed perfusion variables. To our knowledge, there is no gold standard for identifying circulatory shock in small animal patients. We elected to classify these cats into shock categories on the basis of findings for perfusion variables together with SAP, which is consistent with the human and veterinary literature, where shock tends to be a clinical diagnosis. However, some definitions of shock also include an evaluation of metabolic markers of abnormal tissue oxygen delivery such as hyperlactatemia, metabolic acidosis, and decreased base excess, tissue oxygen saturation, and central venous oxygen saturation.16,17
Additionally, there were 10 hyperlactatemic cats in the study that were included in the no shock category because they were classified as having normal perfusion and had SAP > 90 mm Hg. It is important to note that we did not evaluate for causes of hyperlactatemia other than shock, such as hepatic dysfunction, hypoxia, or neoplasia in these patients. There is also a possibility that, for these 10 cats, struggling or phlebotomy technique contributed to the high lactate concentration. Two studies9,20 in which investigators evaluated whether struggling during phlebotomy affects blood lactate concentration in cats had conflicting results. In 1 study,20 healthy cats that struggled during a 5-minute water-spray bath had significant increases in plasma lactate concentration (mean of 3.56 mmol/L, at the end of the bath, compared with 0.33 mmol/L at baseline [before the bath]). However, in a more recent study9 of healthy cats, neither struggling during venipuncture nor the site of sample collection affected the blood lactate concentration. Although struggling or duration of blood vessel occlusion during phlebotomy was not recorded in the present study, anecdotally, the authors believe that these factors may contribute to increased lactate concentration in some cats, and because of this possibility, lactate concentration should not be used as a sole indicator of tissue perfusion. Concurrent evaluation of physical perfusion variables and a blood pressure measurement should be completed to determine the presence of shock. A cat with high blood lactate concentration without any other additional supporting physical examination evidence for hypoperfusion should be evaluated for other disease processes that could cause hyperlactatemia.
In the present study, the median initial blood lactate concentration of cats that were euthanized (3.2 mmol/L) did not differ significantly from that of cats that survived to discharge (2.45 mmol/L). In addition, for cats that had the measurement repeated during hospitalization, there was no association between an increase or decrease in lactate concentration and outcome. These findings are in contrast to findings in dogs, in which a high blood lactate concentration at hospital admission and persistent lactate concentration increases have been associated with increased morbidity and mortality rates.10–15,21 The small numbers of cats in our study likely decreased our ability to detect a significant association between initial lactate concentration or lactate concentration change during hospitalization and outcome. Also, the heterogeneous disease processes (eg, liver disease) in the cats of this study may have influenced lactate concentrations in addition to perfusion, resulting in greater variability in measured values and further decreasing statistical power. Finally, all cats that died were euthanized, with no naturally occurring deaths, which may have also precluded the ability to detect a difference in outcome.
Results of the present study suggested that hyperlactatemia can be present in cats with and cats without abnormalities in physical perfusion variables and hypotension. Ultimately, no single variable can provide an accurate and consistent estimate of the adequacy of global tissue perfusion. Blood lactate concentration should always be evaluated in the clinical context of the patient. In animals with physical perfusion abnormalities and hypotension, therapeutic interventions should be aimed at restoring global tissue perfusion, regardless of the blood lactate concentration. Conversely, in a hyperlactatemic patient, if there is no other clinical evidence of hypoperfusion, other reasons for the blood lactate concentration elevation should be investigated. Future studies are needed targeting specific disease populations in cats, such as sepsis, to determine whether hyperlactatemia or lactate clearance is associated with outcome.
ABBREVIATION
SAP | Systolic arterial blood pressure |
Parks Medical Electronics Inc, Aloha, Ore.
Nova Stat Profile pHOx Ultra, Nova Biomedical Corp, Waltham, Mass.
Stata, version 12.0 for MAC, Stata Corp, College Station, Tex.
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Appendix
Physically assessed perfusion variables and SAP categories used to retrospectively assign cats evaluated by an emergency service to 1 of 3 shock categories.
Category | Physical perfusion assessment | SAP |
---|---|---|
No shock | ≥ 3 variables normal | ≥ 90 mm Hg |
Mild-moderate shock | ≥ 3 variables abnormal | > 60 to < 90 mm Hg |
Severe shock | ≥ 3 variables abnormal | ≤ 60 mm Hg |
Perfusion variables included subjective (mucous membrane color, capillary refill time, and peripheral pulse quality) and objective (heart rate and rectal temperature) assessments. Pink or pale pink mucous membranes, capillary refill time ≤ 2 seconds, strong or moderate femoral and metatarsal pulses, normal heart rate (absence of bradycardia or tachycardia), and rectal temperature > 37.8°C (100°F) were considered normal results for perfusion variables.