Proceeding of the NAVC North American Veterinary Conference Jan. 8-12, 2005, Orlando, Florida

Transcription

1 Proceeding of the NAVC North American Veterinary Conference Jan. 8-12, 2005, Orlando, Florida Reprinted in the IVIS website with the permission of the NAVC

2 The North American Veterinary Conference 2005 Proceedings NURSING MANAGEMENT OF HEATSTROKE PATIENTS stimulates the release and consumption of coagulation factors and platelets. Harold Davis, BA, RVT, VTS (ECC) Veterinary Medical Teaching Hospital University of California, Davis, Davis, CA Heatstroke is defined as a state of extreme non-pyrogenic hyperthermia or a temperature of F ( C). The extreme elevation in temperature results in direct thermal injury to body tissues ultimately causing a multiorgan failure. Heatstroke is a result of thermoregulatory failure. THERMOREGULATION Body temperature is the balance between heat production and heat dissipation. When the rate of heat production exceeds heat dissipation, body temperature increases. Hyperthermia occurs when the thermoregulatory system is overwhelmed by metabolic production of heat, excessive environmental heat or impaired heat dissipation. Heat dissipation occurs through radiation, convection, conduction, and evaporation. Heat loss through radiation and convection is enhanced by cutaneous vasodilation. The continuous movement of cooler air adjacent to the skin allows conduction of heat to the air and convection. Conductive heat loss occurs through contact with cool surfaces. Evaporative heat loss when liquid water becomes a vapor. This occurs from the normal skin surface and is enhanced by sweating. Evaporation also occurs when inhaled air is humidified on its way to the alveoli and is the primary mechanism by which panting cools an animal. CLINICAL PRESENTATION The most common clinical sign reported by owners is excessive panting. Other commonly reported clinical signs include vomiting, ataxia, hypersalivation, diarrhea, loss of consciousness, seizures, listlessness and muscle tremors. PATIENT ASSESSMENT When a patient presents with a core temperature greater than 106 F (41.1 C) and a history consistent with environmental exposure or other risk factors, heat stroke should be considered. The mucus membranes may be hyperemic and capillary refill faster than normal due to systemic vasodilation, or slower than normal due to cardiovascular failure. The mucous membranes may also reveal petechia or ecchymosis indicating disseminated intravascular coagulation (DIC). Tachycardia with weak pulses is suggestive of hypovolemia. The patient may display signs consistent with central nervous system dysfunction. The CBC may reflect hemoconcentration and elevated white cell count. Serum alanine transaminase (ALT), aspartate transaminase (AST) and alkaline phosphatase may be elevated due to hepatocellular damage. Blood glucose concentration may be decreased due to hepatic dysfunction, increased metabolic demands, or sepsis. Acute tubular necrosis results in increased creatinine and blood urea nitrogen levels. Elevation in renal parameters may also be due to renal hypoperfusion. Thrombocytopenia, decreased fibrinogen and elevations in activated prothrombin time, activated partial thromboplastin time, and fibrin split products are indicative of a coagulation disorder. Arterial blood gases can be variable and dependent on the stage of heatstroke. The patient may have respiratory alkalosis, metabolic acidosis or a mixed acid base disturbance. Hypernatremia and hyperkalemia may be seen as a result of pure water loss and tissue damage, respectively. PATHOPHYSIOLOGY The extreme increase in body temperature causes direct cellular injury and destruction of enzymes. The body systems commonly affected include the cardiovascular, hepatic, renal, central nervous system, gastrointestinal, and the hemostatic system. TREATMENT Hyperthemia leads to increased cardiac output, peripheral The primary goal of therapy is to rapidly normalize the body vasodilation, and decreased peripheral vascular resistance. temperature to prevent further organ damage. Care should As it progresses, splanchnic blood pooling occurs, resulting in be taken not to over-cool the animal so as to cause a decreased circulating blood volume or hypovolemia. hypothermia. In addition to cooling the patient, oxygen Myocardial ischemia may occur and lead to the development should be provided. Pretreatment blood samples are taken of arrhythmias. for laboratory analysis. Fluid resuscitation to correct Excessive heat interferes with hepatic metabolism and hypovolemia and or support cardiac function is initiated; protein synthesis. hypoglycemia is treated if present; and acid base or Heat stroke may result in acute renal failure due to tubular electrolyte abnormalities are corrected. GI-protective therapy damage. Dehydration, hypoperfusion and muscle necrosis should also be considered. leading to rhabdomyolysis can also aggravate the tubular damage. Cooling Heat stress can cause neuronal damage and cerebral The owner can begin therapy for heatstroke prior to their edema. The end result may be altered levels of arrival at the hospital. The owners should be told to consciousness or seizures. Damage to the thermoregulatory thoroughly wet the animal with cool water. To enhance centers may predispose the patient to subsequent radiant and convection cooling the owners can lower the car hyperthermic episodes. windows or turn on the air conditioner during transport. One The effects of excessive heat can compromise study reported that the mortality rate of dogs cooled by their gastrointestinal wall integrity resulting in translocation of owners was 19% as compared to a rate of 46% for those not bacteria and bacterial toxins. Hematochezia and melena cooled by their owners. may be seen secondary to gut epithelial damage. Upon arrival to the hospital the cooling process should be Disseminated intravascular coagulation (DIC) is a common continued (or started) thoroughly wetting the animal with cool consequence of heat stroke. Thermal injury to the water or immersing it in cool water. The use of a fan will help endothelium and widespread cell activation or damage promote convective heat loss. Massage may help with cooling by increasing cutaneous blood flow and enhancing 18

3 Veterinary Technician cutaneous vasodilation. Ice water baths are dangerous in that they can easily cause over-cooling. In addition, it may cause vasoconstriction and actually decrease cutaneous blood flow, decreasing heat loss. Cold-water enemas and iced gastric and peritoneal lavage have all been suggested as a method of reducing core temperature in extreme situations. Enemas, of course, impair the ability to monitor the patient s temperature. One study suggests that evaporative cooling techniques appears to be the most rapid and effective technique for cooling when compared to iced gastric lavage. Active cooling should be discontinued when the core temperature reaches103 F (39.4 C). The temperature will continue to fall after cooling measures have been discontinued. The goal is to not allow the patient to become hypothermic and begin shivering. Fluid Therapy Fluid therapy can aid in cooling the patient. The use of room temperature fluids has been suggested. Crystalloids are usually the initial fluid of choice. Synthetic colloids should be considered if total proteins are below 3.5 g/dl or colloid oncotic pressure is less than 15 mmhg or if crystalloids don t seem to meeting the needs of the patient. Blood products are used if anemia or decreased clotting factors are of concern. The volume and rate of fluids will be dictated by the patent s presenting condition and response to therapy. Cardiovascular / perfusion parameters are re-evaluated frequently to determine fluid therapy endpoints. GI Protectant & Antibiotics A potential complication of heatstroke is the ulceration and disruption of the GI mucosal barrier. This can lead to bacterial translocation, bacteremia, SIRS and sepsis. Histamine-two receptor blockers such as Cimetidine, Famotidine, or Ranitidine along with sucralfate have been used to provide some protection to the GI tract. The use of antibiotics prophylactically is controversial because of the concern of contributing to bacterial resistance. If they are used, the antibiotics should cover especially gram negative and anaerobic bacteria, but also gram positive. Acid Base & Electrolytes Because acid base and electrolytes can vary, they should be monitored and the appropriate therapy rendered as needed. In the case of metabolic acidosis, fluid therapy alone may improve the acidosis. In severe cases therapy with sodium bicarbonate may be required. GI losses, and fluid therapy can contribute to decreased potassium levels while acute renal failure could lead to hyperkalemia. Potassium supplementation will be needed in the event of hypokalemia. NURSING MANAGEMENT Following the initial management of the heatstroke patient, thought must be given to the nursing management of the patient. When planning nursing care, consideration must be given to the potential complications associated with this multisystemic syndrome. Once we are aware of the potential complications we can then be on the look out for the complications and have a plan of action in mind should we encounter the problem. The proactive veterinary technician will try to anticipate what action the veterinarian will want to pursue. Thermoregulatory System Following the initial cooling process the temperature should be monitored continuously or at frequent intervals until stable. The goal is to maintain normothermia. Cardiovascular System Cardiovascular complications may include hypovolemia and arrhythmias. Physical parameters such as mm color, capillary refill time, pulse rate and quality, extremity temperature and mentation should be observed. Other monitoring modalities include blood pressure, central venous pressure, and ECG. Fluid therapy will be the primary treatment in the event of hypovolemia. If, after vigorous fluid resuscitation, the patient s cardiovascular parameters do not improve, consider sympathomimetics such as dopamine and dobutamine. Antiarrhythmics may be necessary if the patient has tachyarrhythmias. Renal System Because of the risk of acute renal failure, urinary output should be monitored. This will necessitate the placement of a urinary catheter attached to a closed collection system. Normal urine production is 1 2 ml/kg/hr. Input and output (urine, diarrhea, vomitus, third space losses) should be documented at regular intervals. Ideally ins and outs should balance. If ins exceeds outs the patient is at risk for fluid overload. Likewise, if outs exceed ins the patient is at risk for dehydration. Another helpful tool to assess fluid balance is daily weighing of the patient. Acute gains or losses in body weight are a result of fluid gains or losses. Urine sediment and specific gravity, creatinine and BUN, and electrolytes should be rechecked daily. If the patient becomes oliguric and it is well hydrated, diuretic therapy should be considered. Central Nervous System Neurological deterioration is commonly seen in the heatstroke patient. The deterioration may be due to cerebral edema, hemorrhage and / or infarction. The patient s neurological status (level of consciousness, pupillary size and light response, breathing pattern, and posture) should be observed frequently. Steps should be taken to minimize increased intracranial pressure, which may result from cerebral edema or hemorrhage. Avoid drugs or events that increase intracranial blood flow. Avoid drugs or events that decrease intracranial outflow. Avoid hyperthermia and or control seizures. Should the patients neurological statues deteriorate mannitol is considered. If seizures occur, hypoglycemia is ruled out and the seizures controlled. Gastrointestinal System As mentioned previously, the effects of excessive heat can compromise gastrointestinal wall integrity leading to translocation of bacteria. As a result of the bacterial translocation, many inflammatory mediators may be produced and a high index of suspicion must be maintained with regard to the development of SIRS, sepsis or septic shock. Sepsis or septic shock should be suspected in any 19

4 The North American Veterinary Conference 2005 Proceedings patient with hypovolemia, hypotension, tachycardia, hypothermia or fever, low or high white blood cell count and signs of multiple organ involvement. Therapy is directed at treating the underlining cause and supportive care. Therapy will include fluid support, correction of acid base and electrolyte abnormalities, oxygen delivery support, antibiotics, nutritional support, pain management, wound care, and patient comfort needs. 20

5 Veterinary Technician Hemostatic Thermal injury activates the coagulation cascade, which may result in DIC. Patients should be observed for signs that are consistent with DIC such as hypercoagulability, bleeding from venipuncture sites, petechia, and ecchymosis. Platelet estimation and activated clotting time can be monitored in the clinic setting. Complete coagulation profile, fibrin degradation products, and anti-thrombin III are sent to a reference laboratory. Therapy for DIC includes heparinization, the administration of blood products, treatment of underlying cause and supportive care. 21