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The medical records of 54 dogs presented to the Hebrew University Veterinary Teaching Hospital and diagnosed with heat
stroke were retrospectively reviewed. Data abstracted included history, clinical and clinicopathological signs at admission,
treatment, disease progression, and outcome. Exertional and environmental heat stroke were present in 63% (34 of 54) and
37% (20 of 54) of the dogs, respectively, and 78% (42 of 54) were examined between June and August. The mean temperature
and heat discomfort index in the particular days of heat stroke were significantly increased (P , .001, P , .001, respectively)
compared with their corresponding average daily values. In 27 dogs the body temperature was $41uC (105.8uF). Belgian
Malinois (15%, odds ratio [OR] 5 24, 95% confidence interval [CI95%] 8.2–64.5), Golden and Labrador Retrievers (21%, OR
5 2.08, CI95% 0.95–4.2), and brachycephalic breeds (25%, OR 5 1.7, CI95% 0.81–3.21) were overrepresented, whereas small
breeds (,8 kg) were underrepresented (2%, OR 5 0.08, CI95% 0.002–0.48). Thrombocytopenia (45 of 54 dogs) and
prolongation of the prothrombin (PT) and activated thromboplastin (aPTT) times (27 of 47 dogs) were recorded during
hospitalization. Disseminated intravascular coagulation (P 5 .013) and acute renal failure (P 5 .008), diagnosed in 28 of 54
and 18 of 54 of the cases, respectively, were risk factors for death. The overall mortality rate was 50%. Hypoglycemia
(,47 mg/dL, P 5 .003), prolonged PT (.18 seconds, P 5 .05), and aPTT (.30 sec, P , .001) at admission were associated
with death. Serum creatinine .1.5 mg/dL (P 5 .003) after 24 hours, delayed admission (.90 minutes, P 5 .032), seizures (P
5 .02), and obesity (P 5 .04) were also risk factors for death. Heat stroke in dogs results in serious complications and high
fatality rate despite appropriate treatment.
Key words: Canine; Discomfort index; Disseminated intravascular coagulation; Heat stress; Rhabdomyolysis.
were divided into 3 groups on the basis of their body temperature electrode electrolyte analyzer.g Coagulation tests (47 dogs) included
on admission and were defined as markedly hyperthermic ($41uC, PT and aPTT and were performed with analyzers calibrated for
[105.8uF]), normothermic to moderately hyperthermic (37.6–40.9uC canine blood.h
[99.7–105.7uF]), and hypothermic (,37.6uC [99.7uF]). Nonsurvi-
vors included dogs that died naturally (19 dogs) or were euthanized Statistical Analysis
(8 dogs) during hospitalization.
Statistical analysis for independence of dichotomous variables
was performed by using Fisher’s exact test. A chi-square test was
Definitions of Environmental Heat Stress and used for statistical significance assessment of the independence
Collection of Meteorological Data between nominal variables that consisted of more than 2 categories.
All of the meteorological data (environmental temperature, The Mantel test was used for the linear trend assessment
humidity, and discomfort index [DI]) in the individual days when association in these variables. Mean, median, and SD were
the heat stroke had occurred, average daily temperature, humidity, calculated for continuous variables. The overall assessment of the
and DI with their respective standard deviation (SD) were collected association of continuous variables with survival and occurrence of
from the Israeli National Meteorological Service (INMS).a The DI DIC was analyzed by the receiver operation characteristics (ROC)
was calculated as [Wet Bulb Globe (uC) + Dry Bulb Globe (uC)]/ procedure, by calculation of the area under the curve (AUC) with
2.12 The wet bulb globe is the temperature measured with its 95% confidence interval (CI95%) by the nonparametric method.
a thermometer bearing a wetted wick. The purpose of this measure The cutoff points that optimized the overall correct predictors of
is to determine the amount of cooling provided to a human subject survival and nonsurvival on the ROC curve were selected for the
through evaporation, which is a function of air speed and humidity. division of continuous variables and their dichotomic transforma-
The dry bulb globe is the temperature measured with a standard air tion. The results of the PT and aPTT of the survivors and
thermometer shielded from radiant heat. It measures the effect of nonsurvivors were logarithmically transformed and compared by
the convection and conduction heating or cooling a human. This using the independent t-test. Temperature, humidity, and DI in the
index combines air temperature, humidity, airflow, and radiant particular days of heat stroke events were compared to the average
heat to measure the risk of heat stress disorders in humans,a The DI daily values of their respective months (1987–2002) by using the
was subdivided to mild (22.1–24) moderate (24.1–28), and severe independent t-test. Total weighted comparison was performed for
(.28) on the basis of the definitions used by the INMSa for the the entire daily values in the study.
purpose of risk factor analysis. Because the data concerning survival within the study group can
be regarded as originating in a cohort study, risk ratios (RRs) were
calculated. Risk factor analysis was performed for all nonsurvivor
Definition of Secondary Complications dogs versus survivors, as well as for nonsurvivors that died
All dogs diagnosed with disseminated intravascular coagulation naturally (euthanized cases excluded) versus survivors. Assessment
(DIC) had thrombocytopenia (,150,000/mL) and at least 2 of the of breed as a risk factor for developing heat stroke was performed
following: prolongation (.25%) of the prothrombin time (PT) or by comparison of breed frequencies in the study group to their
activated partial thromboplastin time (aPTT) and clinical signs frequencies in the general HUVTH population (years 1999–2004).
compatible with DIC (including petechiae, echymoses, hematoche- Odds ratios (OR) were calculated for each breed or group of
zia, hematemesis, or hematuria). Dogs were diagnosed with breeds. For the calculation of the OR of small breeds (,8 kg),
acute renal failure if creatinine concentration was .2 mg/dL mixed breed dogs were excluded from both the study and the
after 24 hours of aggressive continuous IV fluid therapy. The HUVTH population. In this analysis, we relied on the pure breed
dogs were divided into 2 groups on the basis of their mental dogs’ standard weight. Exact CI95%s for the RRs and ORs were
status on admission for the purpose of risk factor analysis. Group 1 calculated. Statistical analysis was performed by using statistical
included dogs with neurological signs of disorientation up to software.i–k P-value #.05 was considered statistically significant for
stupor, and group 2 included dogs presented with semicoma or all analyses.
coma.
Results
Laboratory Tests Environmental Factors
Blood samples for hematological, electrolyte, and dry bio-
Fifty-four dogs with heat stroke admitted to the
chemistry analyses and coagulation tests were collected in
potassium-EDTA, heparin, and trisodium-citrate tubes, respective-
HUVTH between 1999 and 2004 were included in this
ly, and analyzed within 30 minutes from collection. CBC was study. All were presented between March and October;
performed on admission and before treatment in 50 dogs, with an however, most had occurred during the hot summer
automated blood impedance analyzer calibrated for canine months of June (28%), July (31%), and August (19%).
blood.b,c Packed cell volume was measured by centrifugation of The DI was mild, moderate, and severe in 1, 33, and 13
heparinized capillaries (in 52 dogs), and total plasma protein was dogs, respectively. It was ,22.1 (ie, no heat stress) in 4
determined with a standard refractometerd calibrated weekly (50 dogs, of which 3 had exertional heat stroke, and 1 had
dogs). Differential white cell counts (19 dogs) were performed environmental heat stroke because of excessive hair
manually by counting 100 leukocytes in Giemsa-stained blood drying with a fan. The average temperature and DI, but
smears. Nucleated red blood cells (NRBC) counts and a semiquan- not the humidity in the particular days of the heat
titive evaluation of platelet numbers were performed manually.
stroke, were significantly increased (P , .001, P , .001,
Blood for wet serum biochemistry (19 dogs) was collected on
admission in plain tubes, centrifuged within 30 minutes from
and P 5 .53, respectively; Table 1) compared with their
collection, and sera were refrigerated (4uC) pending analysis that corresponding average daily (1987–2002) values. The
was performed within 24 hours from collection with an auto- DI, but not the temperature and humidity in the
analyzer.e Specific dry chemistry analyses (50 dogs, glucose and particular days of the heat stroke events, was positively
creatinine only) were performed with dry chemistry analyzers.f and significantly associated with occurrence of DIC
Electrolyte analysis (39 dogs) was performed with a specific- (AUC 5 0.677, P 5 .03). There was no association
40 Bruchim et al
Table 1. Meteorological variables of the time of heat stroke events compared to average daily data (1987–2002).
Temperature (uC) Relative humidity (%) Discomfort Index (uC)
(Mean 6 SD) (Mean 6 SD) (Mean 6 SD)
between the meteorological data and the heat stroke the dogs with time lag .90 minutes (62% versus 27%;
type (ie, exertional and environmental heat stroke). Table 2). The results were similar when euthanized cases
Exertional heat stroke was observed in 63% (34 of 54) were excluded from the analysis. Late admission (time
of the cases (CI95% 49–75%). The mean exertion time lag .90 minutes) was significantly associated with the
was 58 minutes (29/34 dogs, median 30, range 6–300). occurrence of DIC (P 5 .04).
The mean exposure duration to environmental heat Twenty-six dogs (48%) were cooled by their owners
stress in 8 of 20 dogs diagnosed with environmental heat before admission. There was no significant difference in
stroke of which these data were available, was 191 min- the mortality (Table 2) and prevalence of DIC and acute
utes (SD 75, median 210, range 90–300). There was no renal failure in this group (17 and 10 dogs, respectively)
difference in case fatality rate between dogs with compared with the other dogs (12 and 9 dogs,
environmental heat stroke compared with dogs with respectively); however, survival was 100% in 6 dogs that
exertional heat stroke (10 of 20 and 17 of 34, were cooled by their owners before admission and
respectively; Table 2). The results were similar when admitted within a time lag #90 minutes. The results
euthanized cases were excluded from the analysis. were similar when euthanized cases were excluded from
The median time lag from the collapse due to the the analysis. Cooling was negatively and significantly (P
predisposing event to admission (available for 49 dogs) 5 .005) associated with the rectal temperature on
was 240 minutes (range 12–2880). The dogs were divided admission in dogs admitted to the HUVTH within
into 2 time lag groups (#90 minutes, 15 dogs [31%]; a time lag # 4 hours (39.46uC versus 41.17uC [103.03uF
.90 minutes, 34 dogs [69%]) by means of a ROC curve. versus 106.11uF]), but not in dogs admitted to the
The mortality rate was significantly (P 5 .032) higher in HUVTH within a time lag .4 hours.
No. of No. of
Variable n Deaths (%) n Deaths (%) RR Exact CI95% P
RF, risk factor; RR, relative risk; CI95%, 95% confidence interval, aPTT, activated partial thromboplastin time, DIC, disseminated
intravascular coagulation.
a
Platelet count ,150 3 103/mm3.
Heat Stroke in Dogs 41
Table 3. Prevalence of different breeds and their odds ratio for heat stroke.
Breed n % Odds Ratio CI95% % General Hospital Population
Mixed breed 11 20 0.7 0.3–1.3 28.3
Belgian Malinois 8 15 24 8.2–65 0.7
Golden and Labrador Retrievers 11 20 2.1 0.95–4.2 10.9
Boxer 4 7 1.4 0.35–3.9 5.5
Rottweiler 3 6 2.1 0.4–6.8 2.7
English Bulldog 3 6 2.7 0.5–9 2.1
Brachycephalic breedsa 13 25 1.7 0.8–3.21 16.5
Small pure breeds (,8 kg) 1 2b 0.1b 0.002–0.5b 22.9b
were divided into 2 groups on the basis of their 24-hour range 6.3–188.5) during hospitalization. Other common
serum creatinine concentration, with a cutoff point at medications included mannitoll (26 dogs), H2-receptor
1.5 mg/dL. Dogs with creatinine .1.5 mg/dL had blockers (25), antibiotics (25), furosemidem (19), glucose
a significantly (P 5 .003) higher fatality rate (Table 2) (15), heparinn (11), dexamethasone-sodium-phosphateo
and occurrence of DIC (P 5 .02). The dogs were divided (11), dopaminep (9), and diazepamq (9).
into 2 groups on the basis of their serum glucose
concentration on admission (24 dogs) by means of Complications and Outcome
a ROC curve, with a cutoff point at 47 mg/dL. Dogs
with glucose concentration #47 mg/dL had a significant- The overall mortality rate was 50% (27 of 54), of
ly (P 5 .03) higher mortality (Table 2). The results were which 63% (17 dogs) died (of which 4 were euthanized)
similar when euthanized dogs were excluded from the within 24 hours of admission. DIC and acute renal
analysis. Seizures were observed in 67% of these dogs failure were significant (P 5 .013 and .008, respectively)
and in 25% of the dogs with glucose .47 mg/dL; risk factors for death (Table 2). The fatality rate in dogs
however, this difference was not significant. with concurrent DIC and acute renal failure was
significantly higher (P 5 .001) compared with that of
dogs without either DIC or acute failure (92% versus
Treatment
29%, respectively; Table 2). The results were similar
Treatment in all dogs included IV lactated Ringer’s when euthanized dogs were excluded from the analysis.
solution and whole body cooling when indicated. Fresh There was no difference in the prevalence of DIC and
frozen plasma (FFP) was administered in 37 of 54 dogs acute renal failure between dogs with environmental and
(69%; mean 6 SD 2 6 1 units/dog, median 14.3 mL/kg, exertional heat stroke. Other recorded complications
included acute respiratory distress syndrome (ARDS, 4 41.2uC [103.0 versus 106.1uF]). The lack of statistical
of 54), pancreatitis, and pneumonia (1 of 54 each). significance concerning the effect of whole body cooling
Postmortem examination, performed in 6 dogs, by the owners before admission on survival probably
revealed acute tubular necrosis and renal infarcts (5 of resulted from a high variability in cooling efficacy
6), diffuse hemorrhages in the serosal surfaces and (depending on the method, intensity, and duration), type
skeletal muscles, multiple petechiae and diffuse gastro- of hair coat, and its interaction with other parameters
intestinal bleeding (5 of 6), icterus (2 of 6), cerebral (eg, obesity, time lag to admission). A small sample size
hemorrhage, and pancreatitis (1 of 6 each). might have led to a lack of statistical power to reach
significance.
Discussion All cases in this study had occurred between March
and October, but in contrast to a previous report6 in
There is no clear-cut definition of heat stroke in dogs, which most cases were presented in the early summer, in
but there is general agreement that it should be the present study, 79% of the dogs were presented during
considered when heat-related illness leads to an acute the peak of the hot season and heat stress. This
onset of severe systemic clinical signs in an otherwise dissimilarity may be attributed to the fact that the
healthy animal.2,6 However, it has been reported that winter in central Israel is relatively warm (mean 16uC
delay in rectal temperature measurement in both [60.8uF], range 7.3–28.5uC [39.2–83.3uF]) and humid, so
humans and dogs hinders a prompt diagnosis of heat acclimation from winter to summer in Israel occurs
stroke on admission, and that a presence of lower body gradually and does not play a role in the pathogenesis of
temperatures does not negate a positive diagnosis of heat stroke. As both the average temperature and DI in
heat stroke.6,13,14 The selection criteria for all cases in the particular days of heat stroke were significantly
the present study included presence of systemic clinical increased compared with their corresponding average
signs of an acute onset, along with a history of exposure daily values (Table 1), owners should be advised to
to a warm environment, strenuous activity, or both, in avoid exposure of their dogs to such environmental
otherwise healthy dogs, with no other concurrent conditions, and clinicians should be aware that the
unrelated disease. In the present study, there was a high likelihood of heat stroke is higher. Moreover, this study
variability in the body temperature on admission, as has has found that DI in the particular days of heat stroke
been reported previously in canine heat-induced illness.6 events was positively and significantly associated with
Twenty-six dogs went through whole body cooling by occurrence of DIC.
their owners, before admission, and some were admitted Although in humans environmental (classical) heat
later than 3 hours after the heat insult had occurred. stroke is of major concern, in this study, exertional heat
Thus, hyperthermia on admission should not have been stroke was observed more commonly. However, the
an exclusive selection criterion. In contrast, neurological distinction between environmental and exertional heat
manifestations (ie, muscle tremors, seizures, convul- stroke may not be clear-cut in dogs, and heat stroke
sions, disorientation, stupor, coma) were detected on should be a major concern when dogs are exposed to
admission only in 42 of 54 dogs, whereas in all the stressful physical activities in a particularly hot and
remaining 12 dogs, hyperthermia (.41uC [105.8uF]), humid environment. This is exemplified by the fact that
tachypnea, and acute collapse were all present. Thus, there was no association between the meteorological
presence of neurological abnormalities probably should data and HS type (ie, exertional and environmental). It
also not be an exclusive selection criterion for canine should be noted that delays in diagnosis of human heat
heat stroke, or alternatively, if the human definition of stroke occur most commonly in moderate environments
heat stroke (ie, hyperthermia with presence of neuro- when the suspicion of exertional heat stroke is low.13
logical dysfunction) is accepted, then such cases should The overrepresentation of Belgian Malinios (OR 24,
be classified as a less severe form of heat-induced illness. 14.5%) in this study was due to their exposure to
However, as stated earlier, the canine brain has an strenuous activity as working military or police dogs,
intrinsic thermal resistance,8 and it is reasonable to and 7 of 8 had exertional heat stroke. The fact that these
assume that this definition, derived from human highly trained dogs developed heat stroke after a rela-
medicine, may not be applied without reservations to tively short duration of physical activity exemplifies the
dogs. potential hazardous consequences of the combination of
Although there was no statistically significant differ- strenuous physical activity and a high environmental
ence in case fatality rate between dogs that were cooled heat stress. Dog trainers should probably be educated to
by their owners before admission and dogs that were not restrict strenuous physical exercise, especially when heat
(P 5 .173, Table 2), there was a major difference in the stress conditions are severe. Obesity and an active
proportion of nonsurvivors between these groups (38% playful character might have played a role in the
versus 61%, respectively). Thus, although the results of overrepresentation of Golden and Labrador Retrievers
the present study do not clearly prove that whole body (OR 5 2.1) in this study. Brachycephalic dogs had
cooling is essential for survival, they do suggest that it a trend toward overrepresentation (OR 5 1.7) and are
may be beneficial, as cooling was negatively and probably predisposed to heat stroke because of their
significantly (P 5 .005) associated with the rectal poor ineffective evaporation ability and their tendency
temperature on admission in dogs admitted to the to develop laryngeal edema during heat stress.2,15,16
HUVTH within a time lag #4 hours (39.5uC versus English Bulldogs are particularly predisposed to heat
44 Bruchim et al
stroke because of a combination of a brachycephalic P 5 .004, P , .001, respectively). As DIC may appear
conformation and obesity. hours to days after the initial hyperthermic insult, dogs
Obesity was found to be a significant (P 5 .04) risk with heat stroke should be monitored for coagulation
factor for death in the present study. Obesity and high abnormalities and clinical signs of DIC during the first
body weight were reported to be risk factors for 48 hours after insult.25,26
developing heat-induced illness in both people and The treatment of the hemostatic abnormalities in DIC
dogs.2,19–22 Excess body fat increases thermal insulation is based on stabilization of the coagulation, with
and impairs normal heat dissipation in obese people and concurrent prevention of thrombosis. Indeed, FFP was
animals.2 All dogs, with the exception of one in this part of the treatment in 68% of the dogs in the present
study, were of large breed, suggesting that the body study, and heparin was given in 11 dogs (20%). The
weight/body surface ratio is an important factor in the latter should be initiated only when antithrombin III
heat dissipation mechanism under heat stress. However, concentrations are adequate, because its presence is
the possibility that large dogs are more active compared required for heparin to exhibit its beneficial effects.24,27
with small and toy breed dogs and thus are over- Although not proven effective, preincubation of whole
represented, cannot be excluded. Owners of large breed, blood or plasma with heparin was suggested to activate
obese, and brachycephalic dogs should probably restrict donor antithrombin III.28
the activity and exposure of such dogs to heat stress Thrombocytopenia was present in 45 (83%) of the
conditions. dogs in this study; however, only 28 were diagnosed with
In a retrospective study of human heat stroke, there DIC. Thrombocytopenia was most likely caused by
was no significant correlation between the body secondary platelet consumption due to vasculitis,
temperature on admission and the morbidity or mortal- gastrointestinal bleeding, and hyperthermia-induced
ity,21 whereas in a previous study of canine heat-related platelet aggregation.17,29,30 Delayed onset thrombocyto-
illness, hypothermia on admission was a poor prognostic penia was observed in 14 dogs and probably resulted
indicator.6 In the present study, there was no association from development of DIC and decreased bone marrow
between the body temperature on admission and fatality platelet release due to megakaryocyte susceptibility to
rate. high temperatures.17 Presence of metarubricytosis (68%)
The lesions of heat stroke are related to the primary in the present study was not related to erythroid
thermal insult; however, secondary deterioration occurs hyperplasia, as the ratio of NRBC to polychromatic
because of dehydration, shock, and a poor perfusion. RBC was .1 and thus can be considered as patholog-
Thus, early diagnosis and intervention are crucial to the ical. Similar results (58%) have also been previously
prevention of further cerebral and renal deterioration reported in canine heat-induced illness, and it has been
and exacerbation of coagulation abnormalities.1,2,5 This suggested that direct thermal bone marrow injury might
statement is supported by the finding that delayed have resulted in the premature release of NRBC.6
admission (.90 minutes) was found to be a significant Endothelial cell injury and diffuse microvascular throm-
(P 5 .032) risk factor for death in the present study. bosis that are commonly associated with DIC may also
Normalization of the core body temperature and be implicated as contributing factors in lesions to the
supportive care are important, as they inhibit fibrinoly- blood-bone marrow barrier.1,17,22
sis, but are not enough, as the activation of the The most remarkable biochemical abnormalities ob-
coagulation cascade continues in a pattern that resem- served in the present study were increased serum activities
bles that encountered in sepsis.22,23 Thus, early admis- of muscle enzyme activities (CK, LDH, AST), hepatic
sion to an intensive care facility where additional enzyme activities (ALP, ALT), azotemia, and hypogly-
therapy and monitoring are available is advised, cemia. The increase in serum CK activity on admission
although the latter have not been shown to result in was marked and ranged from 7.5- to 1100-fold in most
a better outcome in the present study. (12 of 14) of the dogs (Table 5). Thus, it is reasonable to
Endothelial cell injury, diffuse microvascular throm- assume that rhabdomyolysis was present in all these dogs
bosis, and formation of DIC are prominent features of and probably resulted from direct thermal muscular
heat stroke.1,17,22 Injured endothelium releases tissue damage, increased muscular activity, and seizures. There
thromboplastin and factor XII, which activate the were not enough data to determine whether dogs with
coagulation and complement cascades, inducing a sys- high serum CK activities were predisposed to acute renal
temic inflammatory response syndrome and widespread failure; however, this possibility should be further
coagulation.17,22 Hepatic injury due to hypoperfusion investigated. Rhabdomyolysis of different causes, in-
and microembolism can exacerbate the hemostatic cluding heat stroke, has been associated with myoglobi-
abnormalities.2,6,10 Concurrently, fibrinolysis is also nuric acute renal failure in people.31
highly activated during heat stroke and is manifested Azotemia is a common finding in heat stroke and
by increased plasmin-antiplasmin complexes and results from prerenal and renal mechanisms, such as
D-dimer, and decreased plasminogen concentra- severe hemoconcentration and direct renal tissue dam-
tions.10,22,25 In contrast to a previous study in which age,32 leading to tubular necrosis, as observed at
no association between coagulation test results and postmortem examination of 5 dogs in this study. This
outcome was detected,6 in the present study, occurrence probably occurs as a result of a direct renal thermal
of DIC and prolonged PT and aPTT on admission were injury, dehydration, hypoxia, endotoxemia, release of
found to be significant risk factors for death (P 5 .013, cytokines and vasoactive mediators, and microthrom-
Heat Stroke in Dogs 45
bosis associated with DIC.1,2,18,32 Aggressive fluid in dogs 24% presented coma.6 In the present study, 35%
therapy over the first 24 hours of hospitalization of the dogs presented seizures, and 47% had semicoma
probably eliminated the prerenal component. Therefore, or coma.
measurement of serum creatinine after 24 hours should The presence of ECG abnormalities detected in 14 of
be a more sensitive marker of renal damage compared 54 dogs might have resulted from a direct thermal
with serum creatinine on admission. In the present myocardial damage, as has been reported previously2;
study, acute renal failure (P 5 .008) and serum however, extracardiac causes, such as hypoperfusion,
creatinine .1.5 mg/dL (P 5 .003) after 24 hours were lactic acidosis, electrolyte imbalance, and microthrom-
both risk factors for death. Supportive treatment should bosis could lead to myocardial ischemia and arrhyth-
protect against further renal deterioration but cannot mias.7,37 Thus, dogs with heat stroke will probably
eliminate the primary renal insult that induces tubular benefit from oxygen supplementation, and an improve-
necrosis. It is for this reason that acute renal failure did ment in cardiac function should be expected once
develop in one third of the dogs in the present study, rehydration and restoration of the metabolic imbalances
despite the early and aggressive IV fluid therapy have occurred. Antiarrhythmic therapy should probably
employed. be considered only if the patient has related clinical
Hypoglycemia can result from increased utilization or signs.
decreased production of glucose. Increased glucose Other complications of heat stroke observed in this
utilization results from increased ATP demand, associ- study included ARDS (4), pancreatitis (1), and pneu-
ated with high body temperatures, seizures, and re- monia (1), and all have been previously reported in
spiratory efforts.6,10,32 Sepsis may also be involved in the human heat stroke and are attributed to systemic
pathogenesis of heat stroke–induced hypoglycemia. inflammatory response syndrome and multiple organ
Patients with heat stroke have an increased risk of dysfunction.1,38 These complications also should be
bacterial translocation or endotoxin leakage, and de- looked for and considered in canine heat stroke when
velop bacteremia, endotoxemia, and sepsis because of compatible clinical signs are present.
gastrointestinal mucosal damage and a decline in host
defenses.6,33 Hepatic failure can lead to decreased
glucose production and consequently to hypoglycemia.6
Severe hypoglycemia (,47 mg/mL) on admission was Footnotes
found to be significantly (P 5 .03) associated with death, a
Israeli National Meteorological Service, Beit Dagan 50250, Israel
as has been previously described in dogs and humans b
Minos, ST-Vet, Montpelier, France
with heat-induced illness.6,34 This result exemplifies the c
Abacus, Diatron, Vienna, Austria
importance of restoring and maintaining normoglyce- d
Atago Co Ltd, Tokyo, Japan
mia in dogs with heat stroke as part of the routine e
Kone Progress Selective Chemistry Analyzer, Kone Corporation
treatment. Hypoglycemia may be a risk factor for the Instrument Group, Helsinki, Finland
f
development of central nervous system abnormalities in Reflotron, Boehringer Mannheim, Germany or Reflovet Plus,
canine heat stroke. Roche, Basel, Switzerland
g
Severe hyperthermia results in cerebral hypoperfu- Nova 8, Nova Biomedical, Waltham, MA
h
sion, neuronal necrosis, direct vascular damage, cerebral KC 1A Micro, Amelung, Germany; ACL 200, Instrumentation
edema, hemorrhage, and multifocal vascular thrombosis Laboratory, Barcelona, Spain
i
SPSS 12.0 for Microsoft Windows, SPSS Inc. Chicago, IL
with tissue infarction that may lead to central nervous j
StatXact, Citel Software Corp, Cambridge, MA
system abnormalities and death.2,8,35 However, in k
PEPI 4.0, Computer Programs for Epidemiologists, 4th ed,
experimentally induced hyperthermia in dogs (42.5uC Sagebrush Press, Salt Lake City, UT
[108.5uF] for 90 minutes), there were no significant l
Osmitrol, Baxter Healthcare Corporation, Deerfield, IL
differences in the morphological and biochemical m
Fusid, Teva, Petach Tikva, Israel
indicators of neuronal injury between the study and n
Heparin sodium, Kamada, Rehovat, Israel
the control groups, indicating that the canine brain is o
Dexacort, Teva, Petach Tikva, Israel
intrinsically resistant to sublethal hyperthermia. Thus, it p
Docard, Dexon Ltd, Or Akiva, Israel
q
has been suggested that central nervous system lesions Assival, Teva, Petach Tikva, Israel
in the dogs occur because of the presence of other
physiological derangements rather than the direct
thermal effect on the neuronal tissue.7 Whatever the
mechanisms leading to central nervous system lesions in References
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