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Heatstroke in a military working dog.

CLINICAL VIGNETTE

Max II F241, an 11-year-old castrated male Dutch shepherd, presented to the Fort Bragg Veterinary Medical Center at approximately 1030 on June 7, 2012 for possible bloat. Max II F241 had episode history of bloat while deployed to Afghanistan in May 2011, and had a gastropexy performed at that time. In July 2011 he developed acute hindlimb lameness, which was attributed to severe lumbosacral spondylosis and progressive degenerative joint disease (DJD). At that time he was prohibited from further bite work and work on the obstacle course. Max II F241 had a history of extreme aggression, with several serious bites to handlers. Prior to presentation, he had been receiving Rimadyl (carprofen, an nonsteroidal anti-inflammatory drug) (75 mg orally twice a day) and tramadol (50 mg to 100 mg orally 3 times a day) to control pain associated with DJD. He was undergoing disposition due to his inability to function as a military working dog (MWD). To evaluate his suitability for adoption, a behavioral assessment termed a bite muzzle video (BMV) was required.

The Military Police MWD handlers were filming the BMV for Max II F241's disposition packet. He had successfully completed the first section of the video and was rested in a shaded area. He was observed to have an increased respiratory rate and effort that resolved during the rest period. After completing the second portion of the BMV, Max II F241 developed marked respiratory distress, a distended abdomen, and an episode of diarrhea. The handlers immediately brought him to the Veterinary Medical Center, which is located close to the Military Police kennels and training yard, for treatment.

On presentation, Max II F241 was distressed, with a temperature of 108.8[degrees]F (99.5[degrees]F-102.5[degrees]F), pulse of 140 beats per minute (bpm) (70 bpm-120 bpm), markedly increased respiratory rate (>100 respirations per minute (rpm) (8 rpm-40 rpm)) with severe distress, and cyanotic, injected mucous membranes. Thoracic auscultation revealed moderate crackles in all lung fields, normal cardiac sounds, and weak femoral pulses. No gastric distension was noted on abdominal palpation, and other organs appeared normal. No ping was heard during simultaneous percussion and auscultation of the abdomen, and a slight ping was heard in the caudal thorax. The presumptive diagnosis for Max II F241 was heatstroke with possible gastric distension due to aerophagia.

Flow-by oxygen was provided on presentation, an 18 gauge intravenous catheter was immediately placed in the left cephalic vein, and a 1 liter bolus of lactated ringer's solution was given rapidly. Active cooling measures were initiated immediately following assessment of his temperature: soaking with room-temperature water, applying isopropyl alcohol to the pads of his feet, and using fans to provide evaporative cooling. Due to marked distress of the patient, Max II F241 was sedated with 1 mg acepromazine and 2 mg hydromorphone injections. Max II F241 remained distressed and cyanotic, and was given an intravenous (IV) bolus of propofol and then intubated, whereupon his color and pulse oximetry improved. A second 18 gauge IV catheter was placed in the right cephalic vein. Vital signs were continuously monitored and reassessed. Initial complete blood cell (CBC)/ chemistry panel showed hemoconcentration (packed cell volume, total protein, etc.). His blood glucose (BG) on presentation was 67 mg/dL, and 30 ml 50% dextrose diluted with 30 ml 0.9% NaCl was given IV. After administration of dextrose, his BG increased to 255 mg/ dL. After over an hour of active cooling measures, Max II F241's rectal temperature was 102.7[degrees]F. Active cooling measures were stopped, and he was dried off.

Radiographs of the thorax and abdomen were obtained after he was cardiovascularly stabilized and his temperature had decreased. There was no evidence of bloat on abdominal radiographs, and thoracic radiographs showed diffuse pulmonary disease, which could have been caused by acute respiratory distress syndrome/ acute lung injury, pneumonia, or noncardiogenic pulmonary edema, none of which could be ruled out.

The CBC/chemistry panels were repeated approximately 90 minutes postpresentation. Hemodilution was characterized by a panhypoproteinemia and decreased hematocrit. Ninety minutes after presentation, his BG was 86 mg/dL. Nasal catheters were placed in both nares for oxygen administration. One hundred five minutes after presentation, Max II F241's BG had dropped to 70 mg/ dL, so a 5% dextrose constant rate infusion (75 mL/hr) was initiated. Despite additional dextrose support, his BG continued to fall, with a maximum value of 69 mg/ dL. Two and a half hours postpresentation, Max II F241 was extubated and placed on 10 L/min oxygen via nasal catheter, maintaining his PA[O.sub.2] at 92%. Petechiae developed on mucus membranes, his abdomen, and areas of shaved skin, and hemorrhage was noted from IV catheter and nasal catheter sites, as well as venipuncture sites. Coagulation testing was performed. Both a PTT and PT were within normal limits, although his platelet levels dropped markedly from 349 K/[micro]L to 213 K/[micro]L (175 K/ [micro]L-500 K/[micro]L). He developed hypothermia (T=98.2[degrees]F) 3 hours postpresentation.

Due to worsening prognosis for recovery from heatstroke and poor prognosis for adoption, euthanasia was elected and performed immediately. A complete necropsy was performed with tissue samples submitted to the Joint Pathology Center. Notable gross lesions on necropsy were hemorrhagic streaks throughout duodenum, jejunum, and ileum, enlarged gastric blood vessels, and atelectasis in approximately 25% of lung tissue.

HEATSTROKE IN VETERINARY PATIENTS

Pathophysiology

The development of heat injury is a multifaceted physiological process that encompasses varied cellular and systemic responses to heat stress. (1-5) Thermoregulatory processes initially attempt to control the internal body temperature. If the body's ability to control internal temperature via evaporative (panting, sweating), conductive (laying on a cool tile floor), or convective (sitting by a fan) methods is exceeded, heat illness occurs. (2,3) Over time, the body can acclimate to environmental temperatures above those found in the dog's habitual location. This acclimatization occurs through the enhancement of cardiovascular performance, alterations in kidney salt and water processing, plasma volume expansion, and mechanisms to resist exertional rhabdomyolysis. This process takes several weeks to occur in humans. (4)

When an animal is rapidly exposed to prolonged, increased body temperatures due to environmental or exertional causes without the ability to acclimate properly, heat stress occurs. (4,5) The physiologic response to this heat stress has 2 components: the acute-phase response and the heat-shock response. The acute-phase response occurs at the cellular level, primarily involving the leukocytes, while the heat-shock response occurs at the gene transcription level in cells throughout the body. (1-5)

During the acute-phase response, interleukin-1 (IL-1), interleukin-6 (IL-6), and various other cytokines are produced. (4) These cytokines act to stimulate hepatic acute-phase protein synthesis, endothelial cell adhesion, and angiogenesis, along with a myriad of other responses. (4) The sequence of leukocyte activation and amplitude of the acute-phase response in heat injury is known to be similar to that seen in septic patients. (4,6) This acute-phase response is initially protective, although it becomes detrimental when auto-regulation is lost and the response is exaggerated. (2)

Working in conjunction with a controlled acute-phase response, the heat-shock response acts to protect individual cells. (4) When exposed to extreme heat, almost all cells in the body have the capability to activate heat-shock transcription factors. These bind to the genome and upregulate the production of heat-shock proteins. (4) These heat-shock proteins then act as chaperones, preserving the conformation and function of enzymes throughout the body. (2,4,7) Decreases in the levels of heat-shock proteins are associated with an increased risk of heat injury, and may contribute to the increased risk of heat injury in elderly patients. (2,4)

When the acute-phase and heat-shock responses fail to protect the animal from heat stress, heat injury develops. Heat injury is a continuum of disease severity, ranging from slight physiologic stress (heat cramps) up to severe physiologic derangement (heatstroke) and potentially death. (1-4,8,9) Multiorgan dysfunction in the presence of prolonged elevated body temperature is the hallmark of heatstroke. Typically, patients suffering from heatstroke present in shock secondary to decreased effective circulating volume. They are typically dehydrated, and the heat injury compromises vasoconstriction, leading to decreased systemic vascular resistance and pooling of blood in the splancnic vasculature. (2,3) Altered cardiovascular function combined with direct cytotoxicity and increased metabolic demand leads to multiorgan failure which, if progressive, can quickly result in patient death. Compounding these problems are coagulation abnormalities brought on by the heat injury. (2-4) Ultimately, if not controlled by appropriate medical treatment, these systemic disruptions lead to multiorgan dysfunction, disseminated intravascular coagulation, and potentially death. (2-4)

Risk Factors

There are numerous risk factors for the development of heat-related illness in veterinary patients. Exogenous factors include lack of acclimation to a new environment, elevated humidity (prevents evaporative cooling), lack of access to potable water, confinement in a poorly ventilated space, and some medications. (1-3) Endogenous factors include laryngeal paralysis or brachycephalic syndrome (unable to pant effectively), cardiovascular or neurologic disease, advanced age, obesity, and hair coat thickness and color. (1-3) The risk for development of a heat injury can be reduced by controlling some of the predisposing factors, such as obesity and acclimation. There is some thought that a previous heat injury may predispose veterinary patients to successive heat injuries. (1-3) However, this belief is extrapolated from human medicine (4) and has yet to be documented in the veterinary literature through a peer-reviewed study.

Diagnosis and Treatment

The diagnosis of a heat-related injury is based largely upon the history of the patient, clinical signs on presentation, and potentially the patient's rectal temperature. It is important to remember that during the heat injury process, the patient's ability to thermoregulate is compromised. This may lead to heat injury patients presenting persistently hyperthermic, normothermic, and even hypothermic if excessively cooled prior to arrival at the treatment facility. (1-4) In human medicine, a diagnosis of heatstroke requires the presence of central nervous system dysfunction accompanied by hyperthermia. (4) There is not a single diagnostic test that can confirm the presence of heat injury. Thus initial therapy should never be delayed while awaiting diagnostic testing results for any patient presenting with a potential heat injury.

Current therapy for heat injury in military working dogs is initiated by their handlers in the field. (8,9) If the rectal temperature is above 106[degrees]F, handlers are trained to begin active cooling measures: removing any muzzle, moving the dog to shade, rubbing alcohol to pads of feet and ears, soaking the dog in tepid water (no ice or chilled water), and placing the dog in a vehicle with the air conditioning on full and directed at the MWD. If an air conditioned vehicle is not available, the MWD will be transported in a vehicle with windows down. If the MWD is showing clinical signs of heat injury, such as uncontrollable panting, dyspnea, increased upper airway noise, tachycardia, dark mucous membranes, collapse, altered mentation, vomiting, or diarrhea, the handlers are trained to place an intravenous catheter and adminster room temperature fluids. All MWDs suffering heat-related injury are then immediately transported to a veterinarian. (8-9).

Two IV catheters are placed to allow for rapid fluid therapy. The shock dose of IV fluids in dogs is 80 mL/kg, given at 1/4 dose increments with reassessment between doses. (10) Blood products, such as plasma, are given if indicated. Diazepam or midazolam are used to control seizures if present. Mannitol is administered if increased intracranial pressure is suspected. Dextrose is given if hypoglycemia is present. Lidocaine is used as a free radical scavenger and for control of arrhythmias, if present. Broad spectrum antibiotics are used only if indicated (hemorrhagic diarrhea, evidence of infection). (1-4) Gastroprotectants, such as famotidine or omeprazole, may also be indicated.

The initial minimum database includes CBC, chemistry, electrolytes, and bedside blood glucose assessment, and is repeated as often as necessary. (1-4) Care should be taken in smaller patients to ensure repeated monitoring does not exsanguinate the patient. Coagulation tests and lactate monitoring can also be useful in these cases, and should be performed if available. Electrocardiogram, blood pressure, vitals, and blood glucose are continually monitored.

Cooling measures are maintained until the MWD's rectal temperature falls to 103[degrees]F, at which point all active cooling measures are ceased, and the dog is dried completely. (1-4) The rectal temperature must be continually monitored for persistent hyperthermia or the development of hypothermia. Once cooled, it is beneficial to maintain the patient in a normal, physiologic temperature range.

Complete blood cell abnormalities associated with heatstroke often include (1-4) thrombocytopenia, neutrophilia with a left shift, toxic changes in neutrophils, and nucleated red blood cells. Abnormalties in the chemistry panel can include alterations in total protein or electrolytes, increases in creatinine kinase, lactate dehydrogenase, alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase, azotemia, hypoglycemia, and elevated lactate. Coagulation abnormalities can include prolonged clotting times, which may progress to disseminated intravascular coagulation.

Respiratory alkalosis can develop as a result of increased panting. Metabolic acidosis often develops secondary to increased lactate, hypoperfusion, and electrolyte abnormalities. Additionally, the development of confounding disease processes, such as acute renal failure, can compound acid-base disturbances. As such, the patient's acid-base status should be closely monitored. (3)

Negative prognostic indicators include semicoma/ coma, seizures, coagulopathy on presentation (PT>18s, PTT>30s), hypoglycemia unresponsive to treatment, elevated creatinine after 24 hours of therapy, hypothermia, and greater than 18 nucleated red blood cells per 100 white blood cells. (11)

SUMMARY

Heatstroke is an environmental emergency that threatens our MWDs throughout the world. Proper education of the handlers, veterinary technicians, and Veterinary Corps officers is essential to minimize the risk of losing an MWD to this condition. Understanding the risk factors, initial therapy, and pathophysiology is key to prevention and treatment of heat illnesses regardless of location.

Max II F241 had many of the predisposing factors for a heat injury. He was an elderly dog (11 years old), was obese (body condition score 7/9), had not been worked for a few months, so he was not acclimated to the level of exercise required for the BMV, and the temperature and humidity were both elevated. The personnel involved worked to minimize his risk by completing the video in the early morning, prior to the day becoming extremely hot. Ultimately, Max II F241 died as he lived, happily biting anyone who offered an available limb.

REFERENCES

(1.) Drobatz KJ. Heatstroke. In: Silverstein DC, Hopper K. Small Animal Critical Care Medicine. St. Louis, MO: Saunders Elsevier; 2009:723.

(2.) Johnson SI, McMichael M, White G. Heatstroke in small animal medicine: a clinical practice review. J Vet Emerg Crit Care. 2006;16(2):112-119.

(3.) Flournoy WS, Macintire DK, Wohl JS. Heatstroke in dogs: clinical signs, treatment, prognosis, and prevention. Compend Contin Educ Vet. 2003;25(6):422-431.

(4.) Bouchama A, Knochel JP. Heatstroke. New Engl J Med. 2002;346(25):1978-1988.

(5.) Epstein Y, Druyan A, Heled Y. Heat injury prevention-a military perspective. J Strength CondRes. 2012;26(suppl 2):S82-S86.

(6.) Kurahashi K, Kajikawa O, Sawa T, et al. Pathogenesis of septic shock in pseudomonas aeruginosa pneumonia. J Clin Invest. 1999;104(6):743-750

(7.) Fields PA. Review: protein function at thermal extremes: balancing stability and flexibility. Comp Biochem Physiol A Mol Integr Physiol. 2001;129(2-3):417-431.

(8.) Army Tactics, Techniques, and Procedures No. 3-39.34 (FM 3-19.17). Military Working Dogs. Washington, DC: US Dept of the Army; May 10, 2011. Available at: https://armypubs.us.army. mil/doctrine/DR_pubs/dr_d/pdf/attp3_39x34. pdf. Accessed July 9, 2012.

(9.) Vogelsang RL. Care of the military working dog by medical providers. J Spec Oper Med. 2007;7(2):33-47.

(10.) Aldrich J. Shock Fluids and Fluid Challenge. In: Silverstein D, Hopper K. Small Animal Critical Care Medicine. St. Louis, MO: Saunders Elsevier; 2009:276.

(11.) Bruchim Y, Klement E, Saragusty J, Finkeilstein E, Kass P, Aroch I. Heat stroke in dogs: a retrospective study of 54 cases (1999-2004) and analysis of risk factors for death. J Vet Intern Med. 2006;20(1):38-46

CPT Miranda Andress, VC, USA

MAJ Michelle E. Goodnight, VC, USA

CPT Andress is Officer-in-Charge, Fort Bragg Veterinary Center, Fort Bragg, North Carolina.

MAJ Goodnight is the Chief of Clinical Services, Fort Bragg Veterinary Center, Fort Bragg, North Carolina. She is also the Veterinary Clinical Specialist, US Army Public Health Command District, Fort Eustis, Virginia.
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Author:Andress, Miranda; Goodnight, Michelle E.
Publication:U.S. Army Medical Department Journal
Article Type:Clinical report
Geographic Code:1USA
Date:Jan 1, 2013
Words:2740
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