CHAPTER 17 Conni Wehausen Animal Emergency and Referral Center of Minnesota, St Paul, Minnesota Alterations of body temperature are common in the critical small animal patient, providing insight into systemic and environmental conditions affecting the animal. In general, heat will increase and cold will decrease the metabolic rate. When all parts of the heat‐regulating mechanism operate smoothly, body temperature stays near the normal temperature or “set‐point” temperature of the body. However, there are times when body temperature can go awry. Significant changes in the body temperature can be a consequence of one or more problems, such as: Measuring body temperature is a vital component of every physical examination, with temperature reported in either degrees Fahrenheit (°F) or degrees Celsius (°C). The formulae to convert between °F and °C are given in Box 17.1. Homeostatic mechanisms maintain a normal temperature range rather than a fixed value, with the body temperature oscillating around the desired normal set‐point temperature of the body. Normal rectal body temperature in the dog and cat varies throughout the day between 99.5 °F and 102.5 °F (37.5–39.2 °C) in the dog and 100–103.1 °F (37.8–39.5 °C) in the cat [1]. The set‐point may vary with changing environments or differing activity levels and is controlled by thermoregulation. Thermoregulation is the process of maintaining body temperature by balancing heat production and heat loss. Body heat is a product of heat‐generating metabolism as well as absorption of environmental heat. The basal metabolism of the truncal organs, brain, and skeletal muscle produces body heat, with accelerated metabolism resulting in accelerated heat production [1,2]. Increased muscle (shivering), hormone (thyroxine, growth hormone), catecholamine (epinephrine, norepinephrine), and sympathetic activity can all contribute to increased metabolism and heat production [2]. The skin and subcutaneous fat act to insulate the body and retain heat. To maintain normothermia, heat loss must match heat input and production (Figure 17.1). Heat is transferred from the body core to the skin through a dynamic vasculature system, allowing the skin temperature to fluctuate [2]. Four mechanisms allow heat loss from the skin to the surroundings. Conduction is the transfer of heat from the body directly to an object it comes into contact with (such as a metal table or kennel surface). Convection is the transfer of heat from the body to the air that surrounds it. Radiation is the transfer of heat through electromagnetic waves to surrounding objects that do not come into direct contact with the body. Evaporation is heat loss that occurs when water is turned into vapor (seen with panting and sweating) [1–3]. Figure 17.1 Maintenance of normothermia. The process of thermoregulation is controlled by the hypothalamus (Figure 17.2). The anterior hypothalamus contains warm‐sensitive, cool‐sensitive, and temperature‐insensitive neurons that determine the desired set‐point of the body. The preoptic nuclei in the anterior hypothalamus act as central temperature sensors, sensing both heat and cold in the blood circulating through the hypothalamus. Temperature receptors in the skin sense peripheral temperatures while core receptors sense the temperature in the abdominal viscera, spinal cord, and great vessels. Information is then transferred to the posterior hypothalamus where the signals are integrated to control thermoregulation [1,2] through stimulation of the autonomic nervous system. During hyperthermia (temperatures above the set‐point), the hypothalamus initiates mechanisms to decrease temperature by causing vasodilation of blood vessels in the skin, inhibiting chemical thermogenesis (decrease heat production), and causing the animal to pant and, in some species, to sweat. During hypothermia (temperatures below the set‐point), the hypothalamus initiates mechanisms to increase temperature by causing vasocontriction of the skin vasculature to minimize heat loss, stimulating piloerection to trap insulating air close to the body, and increasing heat production through shivering, sympathetic excitation, and increased thyroxine secretion. Hypothermia can stimulate behavioral changes causing the animal to seek warmth and curl up to conserve heat [2]. Figure 17.2 Hypothalamic regulation of normothermia. Following the trends of change in body temprature can provided insight into the metabolic demands on the ICU patient. While measuring the body temperature can be a simple procedure, determining the underlying cause of a temperature change and the possible consequences provides a stimulating challenge. Careful assessment of the results of diagnostic and monitoring procedures is necessary to identify a potential source of a critical temperature change. Important information can be derived from the history, physical examination, clinicopathological testing, diagnostic imaging, and monitoring procedures. The history begins with the signalment (age, sex, breed) and can reveal variables potentially contributing to changes in body temperature, such as a breed predisposition to altered heat regulatory mechanisms (such as brachycephalic breeds), dysregulation of temperature in geriatric dogs and cats, poor heat generation in toy breeds or very young animals or a genetic predisposition to malignant hyperthermia. Exposure to elevated or cold environmental temperatures, vigorous exercise, inadequate access to water or shelter, and important past medical problems (such as collapsing trachea, laryngeal paralysis, hypothyroidism) are factors that could affect thermoregulation identified through history. A list of prescribed drugs (human and veterinary), exposure to possible toxins or recreational stimulants and any over‐the‐counter medications administered could reveal a potential source of temperature change. Table 17.1 lists drugs known to affect thermoregulation. Table 17.1 Drugs which affect body temperature. ADHD, attention deficit hyperactivity disorder. Physical examination begins with temperature, pulse rate and intensity, and respiratory rate and effort. Core body temperature will provide a true reflection of the internal body temperature and can be measured using a pulmonary artery catheter, esophageal probe or urinary bladder thermistor. These techniques are invasive, require heavy sedation or anesthesia for placement and precise positioning to obtain reliable measurements [4,5]. More commonly, minimally to noninvasive methods are utilized to measure temperature in veterinary patients and include rectal, auricular, and axillary thermometry. The methods available to measure body temperature are listed in Table 17.2 with recognized advantages and disadvantages of each technique [4,6–8]. The rectal temperature remains the “gold standard” for the noninvasive estimation of the core temperature by a peripheral method. Table 17.2 Methods of temperature measurement. Heart rate, pulse intensity, capillary refill time, and mucous membrane color constitute the physical peripheral perfusion parameters used to assess tissue perfusion. Both high and low extremes in body temperature can cause hypovolemia and inadequate perfusion. Hydration is often affected, with dehydration reflected by dry mucous membranes, dull corneas, poor skin turgor, and sunken eye position. Other clinical signs resulting from a body temperature change can be either focal and specific to the temperature change (such as burns with heat or frostbite with cold) or signs that are nonspecific to body temperature (such as shock, dehydration, panting). Any area of pain, heat or swelling is investigated as a site of infection or inflammation. A careful examination of the joints and deep palpation of bones may reveal a hidden site of inflammation. A list of organ systems and the clinical signs commonly associated with hyper‐ and hypothermia is provided in Table 17.3. Point of care (POC) testing (minimum database), clinicopathological testing, and diagnostic imaging are used to further define the cause and expose the consequences of a temperature abnormality. Table 17.3 Common clinical signs associated with altered body temperature. Afib, atrial fibrillation; CNS, central nervous system; CRT, capillary refill time; RR, respiratory rate; Vfib, ventricular fibrillation; Vtach, ventricular tachycardia. The POC minimum database should consist of packed cell volume (PCV), total proteins (TP), glucose, blood urea nitrogen (BUN), electrolytes, blood gas analysis, and coagulation profile (including platelet number estimate and buccal mucosal bleeding time). The PCV can reveal hemoconcentration due to dehydration or anemia due to blood loss or red blood cell lysis with either temperature extreme. Thrombocytopenia is common with both temperature disorders. Azotemia can also occur due to dehydration, hypovolemia or direct cytotoxic injury to the cells of the kidney. Hyperglycemia can be seen associated with an initial stress response, followed by hypoglycemia associated with glucose consumption with either hyper‐ or hypothermia. Electrolyte results are assessed to identify hypernatremia since temperature alterations can stimulate the loss of free water. Potassium concentrations can be elevated with muscle necrosis or lowered through diuresis, each a potential serious consequence of an extreme alteration in body temperature. Blood gases often show metabolic acidosis with high blood lactate in patients with hyperthermia. Hypothermic patients often have respiratory acidosis. Coagulopathies are common, with the prothrombin time (PT) and activated partial thromboplastin time (aPTT) frequently prolonged as a result of coagulation factor consumption surpassing production. Alterations in coagulation parameters (PT, aPTT) should be interpreted cautiously in hypothermic patients since the tests are run at a controlled (normal body) temperature and do not necessarily reflect in vivo coagulation [24]. Platelet function can be abnormal, demonstrated by a prolongation of the buccal mucosal bleeding time. A thorough evaluation of a patient for the consequences or causes of an unexplained change in temperature can be quite extensive. A complete blood count (CBC), serum biochemical profile, and urinalysis will provide an initial screen for problems associated with alterations in body temperature. The white blood count may be high with active inflammation or infection or low due to consumption and margination seen during sepsis. Nucleated red blood cells are seen in up to 90% of dogs with heat stroke [25]. Animals with a fever may show evidence of anemia with spherocytosis, nucleated red cells and reticulocytosis from immune‐mediated diseases or nonregenerative anemia associated with chronic infectious or inflammatory diseases. There are many chemistry abnormalities seen in patients with abnormal body temperature, with specific changes dependent upon the cause and the organs impacted by disease. Heat stroke often results in elevated liver enzymes and total bilirubin due to hepatocellular hypoxia. Urinalysis may reveal pigmenturia (myoglobin or hemoglobin), hematuria, proteinuria, renal tubular casts or isosthenuria due to urinary tract injury from temperature extremes. Urinary tract infections may be the primary indicator of systemic infection that is causing fever. Special testing may be requested, such as fluid analysis, culture and susceptibility testing, serology for infectious diseases, aspiration and cytology of mass lesions, immune panels, toxicology screening, and drug levels. Diagnostic imaging begins with plain thoracic and abdominal radiographs. Thoracic radiographs are evaluated for pulmonary, cardiac or pleural space abnormalities. Pulmonary infiltrates can be found with pneumonia, cardiogenic, and noncardiogenic causes of edema, pulmonary hemorrhage, neoplasia, and acute lung injury or acute respiratory distress syndrome. Abdominal radiographs provide an initial assessment of bone density and structure, peritoneal fluid or air and organ size, shape, and position. Ultrasound may provide a more detailed evaluation of organs for evidence of cysts, fluid, infiltrates, hemorrhage, cardiac disease or anatomical abnormalities. Free abdominal or pleural fluid or mass lesions can be aspirated and evaluated by culture, cytology, and biochemistry as indicated. Advanced imaging with computed tomography or nuclear magnetic resonance may be used to better define the extent and nature of a suspected or confirmed abnormality. Physical patient parameters provide the basis for continuous monitoring of the ICU patient with an abnormal body temperature. Frequent assessment of the physical peripheral perfusion parameters, hydration status, mentation, and respiratory rate and rhythm will aid in the early detection of consequences of extreme alterations in temperature (such as poor perfusion, dehydration, depressed mentation, seizures, labored breathing, panting). Indirect blood pressure monitoring provides additional information regarding peripheral perfusion, with trends of change monitored during and after resuscitation. The body temperature can be continuously monitored by inserting an indwelling rectal thermistor that provides data to a digital monitor, often found as part of the electrocardiogram (ECG) or other multiparameter monitoring equipment. The ECG can detect cardiac rate and rhythm abnormalities frequently noted with temperature abnormalities and allow timely intervention. Pulse oximetry and end‐tidal CO2 monitoring may be indicated for patients with respiratory changes. Investigation of the physiological responses to hyperthermia and hypothermia provides insight into possible causes and potential complications. Fever, heat stroke, and malignant hyperthermia represent common hyperthermia syndromes encountered in the ICU patient. The systemic inflammatory response syndrome (SIRS) is anticipated in these patients. Hypothermia can be a consequence of critical problems in the ICU patient such as excessive heat loss (sedation, anesthesia or surgery), impaired circulation, and severe metabolic disease. Regardless of the cause, the effects of hyperthermia and hypothermia on patient perfusion and metabolism can be significant. Hyperthermia is defined as an elevation in body temperature; this occurs when internal heat production or external heat input is greater than heat loss. It has been characterized as either pyrogenic (due to endogenous or exogenous pyrogens) or nonpyrogenic (due to environmental or metabolism‐related heat sources) [25]. Pyrogenic hyperthermia is referred to as “fever.” A pyrogen is a heat‐inducing substance that causes the thermoregulatory set‐point in the anterior hypothalamus to rise or “reset” [26]. This higher temperature is now the new “normal” temperature for the animal. Exogenous pyrogens come from an external source and include substances such as bacterial endotoxins and other microbial products, viruses, incompatible blood products, and drugs. These exogenous pyrogens stimulate the body to produce additional pyrogens. These are called endogenous pyrogens and are low molecular weight proteins produced by phagocytic leukocytes and released into the circulation. Factors causing pyrogenic hyperthermia (fever) in small animals are listed in Table 17.4. Table 17.4 Common causes of fever. ARDS, acute respiratory distress syndrome; IMHA, immune‐mediated hemolytic anemia; IMTP, immune‐mediated thrombocytopenia; SIRS, systemic inflammatory response syndrome; UTI, urinary tract infection. Nonpyrogenic hyperthermia occurs when heat from the environment or heat generated from exercise and metabolism exceeds heat dissipation mechanisms. This causes the body temperature to rise above the thermoregulatory set‐point of the hypothalamus [25]. Factors causing nonpyrogenic hyperthermia in small animals are listed in Table 17.5. Table 17.5 Common factors predisposing to nonpyrogenic hyperthermia. Elevated body temperature can have severe deleterious effects on patients and cause prominent clinical signs (see Table 17.3). When body temperature rises, heat receptors stimulate the thermoregulatory center, immediately triggering cooling mechanisms (vasodilation, decreased metabolic rate, panting). Over time, the body begins to acclimate to a warmer body temperature by enhancing cardiovascular performance, stimulating the renin‐angiotensin‐aldosterone axis resulting in salt conservation by the kidneys, increasing glomerular filtration rate, expanding plasma volume, and increasing the ability to resist exertional rhabdomyolysis [27]. Heat stress activates the acute‐phase response, resulting in production of both proinflammatory and antiinflammatory cytokines. Finally, heat shock proteins are formed to protect cells from injury by decreasing denaturation of protein and regulating the baroreceptor response to prevent hypotension [28]. The ICU patient may present with an elevated body temperature or develop the problem during hospitalization. The causes of fever or pyrogenic hyperthermia (infection, inflammation, immune disorder, neoplasia) are vastly different from the causes of nonpyrogenic hyperthermia (heat stroke, malignant hyperthermia, drug reaction), with temperature extremes (>106 °F (41.1 °C)) more likely with the nonpyrogenic causes. The onset of fever in an ICU patient triggers an investigation for both infectious and noninfectious etiologies. The source of the inciting exogenous pyrogens can include infection (bacterial, viral, rickettsial, protozoal, parasitic, fungal), inflammation (ischemia, internal hemorrhage, necrosis), neoplasia or immune‐mediated disease [26]. In humans, fevers have noninfectious origins in 25–50% of cases and the incidence in veterinary patients is thought to be similar [29–31]. Treatments commonly administered in the ICU can also act as exogenous pyrogens and cause fever. Blood transfusion, drug administration, and invasive medical procedures (such as indwelling catheter placement) can result in transfusion reaction, drug reaction, and catheter‐related phlebitis respectively. Drugs have been found to cause increased body temperature in at least five ways: altered thermoregulatory mechanisms, drug administration‐related fever, fever from the pharmacological action of the drug, idiosyncratic reactions, and hypersensitivity reactions [32]. The more common causes of infectious and noninfectious fever are listed in Table 17.4. The body response to exogenous pyrogens is initiated by production of endogenous pyrogens that reset the hypothalamic thermoregulatory set‐point [26]. Studies on the peripheral and central action of cytokines demonstrated that peripheral cytokines can communicate with the brain in several ways, including stimulation of afferent neuronal pathways and induction of the synthesis of a noncytokine pyrogen (prostaglandin E2) in endothelial cells in the periphery and in the brain. Cytokines synthesized in the periphery may cross the blood–brain barrier and act directly through neuronal cytokine receptors [33]. Following a rise in the set‐point, the animal will increase heat production and decrease heat loss. Patients with true fever (reset set‐point) are not likely to show signs of heat dissipation (such as panting) and may be curling up or shivering to generate heat and reduce heat loss. Fever rarely leads to body temperatures high enough to result in host tissue damage. In fact, fever is thought to be an adaptation that has evolved to protect the body from invading pathogens. Fever has been shown to strengthen immune function by enhancing neutrophil and lymphocyte function, improving the antimicrobial activity of antibiotics and decreasing the availability of iron needed by bacteria to replicate [29,30]. Increased survival has been seen in both humans and animals with elevated body temperature in the face of infection [34,35].
Temperature
Introduction
Initial diagnostics and monitoring methods
Initial history and physical examination
Temperature elevation
Temperature reduction
Methylxanthine derivatives
Caffeine, theobromine, chocolate
Illicit/recreational drugs
Marijuana, cocaine, amphetamines, cocaine
Belladonna alkaloids
Atropine, scopolamine
Antibioitics
Tetracyclines, beta‐lactams, sulfonamides
Sympathomimetics (allergy/ADHD/diet drugs)
Amphetamines, ephedrine, pseudoephedrine, phenylpropanolamine
Inhaled anesthetics (malignant hyperthermia)
Allergy drugs
Loratadine, promethazine
Mental illness drugs
Thioridazine, chlorpromazine, prochlorperazine
Major tranquilizers
Phenothiazines, butyrophenones, thioxanthenes
Blood pressure drugs
Mecamylamine, beta‐blockers
Migraine drugs (triptanes)
Opioids
Muscle relaxants
Sedatives
Narcotics
Anesthetics
Nonsteroidal antiinflammatory drugs
Glucocorticosteroids
Antipsychotic drugs
Thermometry site
Advantages
Disadvantages
Comment
Rectal
Mercury in glass
Digital
Easy, inexpensive, widely available
Requires 3 minutes contact time
Equilibration type requires 1 minute contact time; predictive requires 10–15 seconds, calculates final result
Fecal material can affect contact with rectal mucosa. Patient discomfort, increased stress response [7]. Could spread infectious disease [9,10]. Avoid if anal area trauma, wounds or masses
Potential for leakage of mercury – not recommended.
Rectal thermometry is the “gold standard” for peripheral estimate of core temperature [4,6,11]. Requires contact with rectal mucosa. Two types of rectal thermometers, which have similar reported results [12,13]
Pulmonary artery
Accurate core body temperature
Invasive and costly. Requires placement of pulmonary artery catheter
The ideal method for measuring core body temperature
Esophageal
Highly accurate reflection of core temperature
Considered invasive, used primarily during anesthesia. Requires specialized equipment
Placement of sensor is in the lower 1/3 of esophagus close to heart and aorta [14]
Urinary bladder
Highly accurate reflection of core temperature
Considered invasive, used during anesthesia or ICUs. Requires specialized equipment. Results affected by urine flow and volume.
Urine temperature is a reflection of temperature of renal blood flow (20% of cardiac output) [15]
Auricular
Reasonably priced. Veterinary brands available. Generally nonstressful to patient. Can use device in axillary region, as well
Temperatures reported as variable, poorly correlating with rectal and pulmonary arterial temperatures. Under estimates core temperature, especially if hyperthermia.6,8,16–18 Affected by ceruminous debris or fluid behind tympanic membrane.
Uses infrared thermometry to measure heat from tympanic membrane and ear canal [8,12]. Tympanic membranes share blood supply with hypothalamus for good indication of core temperature [4,19,20]
Axillary
Found to be less stressful in dogs [7]
Wide variation in correlation with rectal temperatures.18,21–23 Found less accurate if higher body condition scores.21
Can use digital rectal or auricular thermometer. Place at the midpoint of the axilla as far anterior as possible against the thorax [21]
Toe web
Large difference with rectal temperature suggests poor peripheral perfusion. Can use to assess response to treatment for perfusion abnormalities
Not an accurate method without comparison to rectal temperature.
Can use rectal thermometer or thermistor probe. Place between toes of rear paw and compare to rectal temperature. Toe web normally 2–9 °F (1–4 °C) lower than rectal temperature
Body system
Hypothermia
Hyperthermia
Cardiovascular
Hypotension, dysrhythmias: pulse deficit (bradyarrhythmias), decreased cardiac output (shock); ECG: prolonged PR interval, wide QRS, J waves, Afib, Vtach, Vfib
Early (dogs: tachycardia, hyperemia, CRT <1 sec, bounding pulses
Later (dogs,cats): bradycardia, weak pulses, CRT >2 sec, pale membranes, dysrhythmias: pulse deficit
Respiratory
Initially increased RR, then decreased respiratory depth and rate; finally apnea
Rapid RR (panting), loud upper airway noises, cyanosis if airway obstruction; increased respiratory rate and effort with crackles if lung edema or hemorrhage
CNS/neuromuscular
Altered mentation, shivering (dogs), stiff movements and hyporeflexia
Altered mentation, obtunded stupor, comatose, seizures, tremors
Renal
Polyuria (cold diuresis)
Dehydration, oliguria, anuria, hematuria, pigmenturia
Gastrointestinal
Decreased bowel sounds, ileus
Vomiting, diarrhea, blood, and mucosa from rectum, decreased bowel sounds, ileus
Coagulation
Bleeding from venipuncture sites, petechiation, ecchymosis
Bleeding from venipuncture sites, petechiation, ecchymosis
Skin/subcutaneous tissues
Cold to touch, vasoconstriction, piloerection, necrosis if frostbite
Vasodilation, hyperemia, skin tenting with dehydration, blistering, burns
Point of care testing
Clinicopathological testing
Diagnostic imaging
Monitoring techniques
Disorders of body temperature
Hyperthermia
Body system
Infectious etiology
Noninfectious etiology
Cardiovascular
Catheter infection
Vasculitis
Endocarditis
Thrombophlebitis
Thromboemboli
Endocrine
Hypoadrenocorticism
Gastrointestinal
Infectious diarrhea
Pancreatitis
Cholangiohepatitis
Hepatitis
Peritonitis
Bowel infarct
Immune
IMHA
IMTP
Integument/muscle
Wound infection
Surgical wounds
Abscess
Trauma
Burns
Nervous
Meningitis
Steroid‐responsive meningitis
Intracranial hemorrhage
Reproductive
Pyometra
Prostatitis
Respiratory
Pneumonia
Aspiration pneumonitis
Pyothorax
Atelectasis
Upper respiratory infection
ARDS
Bacterial Viral
Pulmonary thromboembolism
Systemic
Rickettsial
Neoplasia
Fungal
Paraneoplastic syndrome
Protozoal
SIRS
Parasitic
Transfusion reaction
Urinary
UTI
Pyelonephritis
Other
Hemorrhage into confined spaces
Drugs
Decreased heat dissipation
Abnormal upper airway
Tracheal collapse
Brachycephalic airway syndrome
Laryngeal paralysis
Obesity
Exposure to high environmental temperatures
Lack of water and shade
Enclosed environment
Inadequate ventilation
Heat cramps
Heat exhaustion
Heat stroke
Increased muscle activity
Exercise (exertional)
Seizures
Tremors, twitching
Hypothalamic disorders
Drugs (see Table 17.1)
Malignant hyperthermia
Vasoconstrictive drugs
Increased metabolic rate
Hyperthyroidism
Pheochromocytoma
Fever
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