Environmental emergencies (Proceedings)

Environmental emergencies tend to be regional and dependent on the local climate and geographic locations. Environmental emergencies may include heat and cold related injury, smoke inhalation, water accidents, reptile and insect bites, and an endless list of toxins. Here we will focus on heat stroke, hypothermia, smoke inhalation, and near drowning.

Definitions

Heat stroke: a core body temperature that rises above 104.0°F and that is accompanied by hot, dry skin and central nervous system abnormalities such as delirium, convulsions, or coma.

• Hyperthermia: a pryogenic or nonpyrogenic elevation in body temperature.

• Heat cramps: dehydration, hyponatremia, and muscle cramps.

• Heat exhaustion: lethargy brought on by extreme heat conditions.

• Heat prostration: more severe than heat exhaustion with headache, vomiting, tachycardia, and hypotension

Heat Stroke

Heat stroke is a common emergency that is seen in most ER clinics through out the country, but is localized mostly in the southern states and hot climates. As acclimation is somewhat protective, cases are often seen earlier in the summer months. This is a life threatening injury that results in thermal injury to the organs, tissues, cells, and proteins. The thermal injury can result in severe cellular necrosis. Heat stroke, if severe can lead to multiple organ dysfunction and subsequent death if not treated immediately and aggressively upon presentation. Even with prompt therapy, death is common among severely affected individuals. The diagnosis is made based on a core body temperature above 104°F, central nervous system dysfunction (e.g., delirium, convulsions, or coma), and varying degrees of organ dysfunction..

Mechanisms for heat loss

Heat is normally dissipated by 4 mechanisms: conduction, convection, radiation, and evaporation. Conduction is when body is in contact with a cooler surface (allowing heat transferred to surface). Convection is the transfer of heat from the body as air passes over it (Fan). Radiation is the process of the body releasing heat into environment. Evaporation is the process of a fluid changing into to a vapor (panting). As the environmental temperature increases above 89.6°F, evaporation becomes the most important mechanism for dissipating body heat.

Acclimatization is the process that allows the body to adapt to environmental changes. In animals this process is partially completed over 10 to 20 days, but 60 days are usually required for full acclimatization. During acclimatization, water is conserved through the action of aldosterone and ADH (antidiuretic hormone). Other mechanisms include tachycardia and increased cardiac output , salt conservation, increased glomerular filtration rate, plasma volume expansion, and an increase in the ability to resist exertional rhabdomyolysis.

Conditions that predispose to heat stroke include, but are not limited to laryngeal paralysis, cardiovascular disease, obesity, CNS disease, increasing age, and long hair coat. Exogenous factors include lack of acclimatization, confinement/poor ventilation, increased humidity, water deprivation, furosemide, negative inotropic drugs, prior heat stoke, and phenothiazines.

Pathophysiology

Direct cytotoxicity occurs in tissues and is dependent on the critical thermal maximum (level and duration of heat) required to initiate tissue injury. Temperatures as low as 102.2–104.0°F have been reported to damage the gut wall and allow bacterial translocation to occur. In experimental animal models, apoptosis in the liver, spleen, thymus, lymph nodes, and the small intestinal mucosa has been observed within a few minutes after exposure to temperatures ranging from 106.7–107.6°F. At temperatures greater than or equal to 109.4°F, oxidative phosphorylation is uncoupled and critical enzymes are denatured. Cardiovascular effects, initially show increased cardiac output and decreased systemic vascular resistance. This response is mainly protective initially, but with progression of heat stroke, the splanchnic vasculature dilates, and there is cutaneous vasodilation, which then leads to venous pooling and decreased cardiac output (loss of heat dissipation). Coagulation abnormalities are common in heatstroke and leads to thrombocytopenia due to direct heat injury to platelets and endothelium, with elevated PT, and aPTT as coagulation factors are consumed. With in the CNS, temperatures as low as 105.8°F can cause permanent brain damage. This can lead to cerebral edema, hemorrhage, and infarction. With in the lungs fibrin deposition and microthrombi can lead to noncardiogenic pulmonary edema, and direct thermal injury and increased pulmonary vascular resistance can even lead to ARDS (acute respiratory distress syndrome). Rhabdomyolysis can also occur due to direct thermal injury and muscle necrosis. With in the kidneys, tubular necrosis can occur as the result of thermal injury, microthrombi, and hypoperfusion. Myoglobin released from muscle necrosis can lead to damage to the kidneys.

Treatment

The main aim of therapy for treating heat stroke include cooling the patient through use of fans and spaying small amount of water on the patient and IV fluid (room temperature crystalloids) administration. The use of ice water baths or soaking the animal in water should be avoided, because this can cause rebound hypothermia and vasoconstriction in the periphery (decreasing the dissipation of heat from the periphery). Some have advocated the use of peritoneal dialysis or gastric lavage to aid in the cooling of patients, but this should be reserved for highly staffed and referral centers, as it requires specific equipment and lots of labor to be performed correctly and safely, and may be unnecessary. Stop cooling the patient once they have reached a temperature of 103.5-104.0°F, or the patient maybe at the risk of rebound hypothermia. Correct and maintain normal blood glucose concentrations. The use of steroids is not indicated and has many deleterious effects (hyperglycemia, vasoconstriction, gastric ulceration, immune suppression, and can be nephrotoxic). Correction of any coagulation abnormalities with the use of fresh frozen plasma, frozen platelet concentrates or whole blood should be considered if available. NSAIDS are not recommended, as hyperthermia is not due to the hypothalamus, but NSAIDS have been shown to up regulate HSP (heat shock proteins), which have been shown to be protective during heat stroke. . Broad spectrum antibiotics should be advocated, since heat stroke has been shown to induce bacterial translocation. Collect baseline laboratory samples to establish degree of organ compromise. Include CBC, chem., UA (free catch/cath) and coagulation panels (PT, aPTT, platelets). Heatstroke changes can include thrombocytopenia, coagulopathy, azotemia, hypoglycemia, elevation I liver enzymes, and pigmenturia.

In a recent retrospective of heat stroke in dogs, risk factors for death were identified. Hypoglycemia (<47 mg/dL), prolonged PT (>18 seconds), and aPTT (>30 sec, at admission were associated with death. Also, serum creatinine >1.5 mg/dL after 24 hours, delayed admission (>90 minutes), seizures, and obesity were also found to be risk factors for death.

Hypothermia

Hypothermia can be classified as mild (90-99°F), moderate (82-90°F), and severe (<82°F). Effects of hypothermia may include coagulopathy (prolonged platelet aggregation, platelet sequestration in liver and spleen, and decreased thromboxane), acid base disturbances, electrolyte abnormalities, CNS disturbances, cardiovascular and respiratory depression. When temperature falls below 93°F, vasodilation occurs with an overall decrease in metabolic rate. At body temperatures below 88 °F, thermoregulation ceases completely. Hypothermia can be primary or secondary, where primary would be from exposure to the elements and secondary results from preexisting or concurrent underlying disease, trauma, toxins, immobility, or anesthesia from surgery.

With hypothermia there is a left shift in the oxyhemoglobin dissociation curve, causing a decrease in the off loading of oxygen at the tissue beds. Also, the partial pressures of both oxygen and carbon dioxide decrease with a decrease in temperature. The pH will also increase (more alkaloid) as temperatures decrease, also shifting the curve to the left. Severe hypothermia decreases the response to catecholamines, which can result in bradycardia, hypotension, and decreased cardiac output. Hypothermia has been shown to decrease heart rates by 50% with temperatures of 82°F or less. Hypothermia also decreases hepatic metabolism, which can be of considerable importance when administering drugs that have significant liver metabolism. Mild to moderate hypothermia can cause cold diuresis, due to an increases in GFR, vasoconstriction, and decreased sensitivity to ADH. Although, severe hypothermia may result in decreased renal blood flow, decreased GFR, ischemia, and ultimately in acute renal tubular necrosis. Severe hypothermia has been shown to decrease respiratory rate and tidal volume. Mild to moderate hypothermia can cause a reduction in cerebral blood flow and may lead to derangements in mentation. Cerebral blood flow decreases by 6–7% for each 1°C drop in body temperature.

Treatment consists of two goals, one is stop any further heat loss and two is to actively rewarm the patient. Placing blankets on and under the patient will help to reduce conduction and convection losses. Active surface rewarming would include warm water bottles, circulating warm-water heating blankets, and forced air warming blankets (Bair hugger). Active core rewarming includes warm IV fluids, warm peritoneal lavage with saline, warm pleural lavage with saline, warm water enemas, and instillation of warm saline to the urinary bladder. Complications of rewarming include burn injury, rebound hyperthermia, increased metabolic rate, and increased oxygen demand and consumption.

Smoke Inhalation

Most patients with smoke inhalation present with respiratory signs and ocular irritation (hint - check for corneal ulcers). The majority of the cases occur during the colder months due to heater malfunctions. Patients are most commonly affected by house fires, although chemical fires or wildfires may also result in injury.

Pathogenesis

The insults to the patients of main concern are hypoxia, thermal damage, and pulmonary irritation. Cardiovascular effects are mild and limited to occasional ventricular arrhythmias. The initial loss of consciousness is likely due to decreased inspired O2 due to the production of CO2 by combustion. Combustion can lower the FiO2 (inspired oxygen, normal is 21%) to 15%. Tissue hypoxia also results from the inhalation of carbon monoxide and cyanide, and the production of methemoglobinemia. Carbon monoxide has 200 -250 times the affinity for hemoglobin as oxygen. It also shifts the oxyhemoglobin curve to the left, preventing release of oxygen to the tissues. Carbon monoxide may have cardiotoxic effects by binding myoglobin, and it also poisons the mitochondria cytochrome oxidase system. Combustion of wool, plastics, polyurethane, silk, nylon, rubber, paper products, can produce cyanide. Cyanide binds to the Ferric ion on Cytochrome A3, and arrests the Tricarboxylic acid cycle. This leads to anaerobic metabolism and lactate production. Finally, heat denaturation of hemoglobin, oxidation of nitrogen, and combustion of nitrates can cause methemoglobinemia.

Direct thermal injury can occur, but is limited to the upper airways due to efficient heat exchange. If steam is inhaled it can cause damage to the lower airways and alveoli. Swelling, inflammation, and edema of the supraglottic area can occur in the first several hours and can be worsened by aggressive fluid therapy. Chemical irritants in smoke include sulfur dioxide, chlorine gas, and acroleins. Irritants cause direct injury to the respiratory mucosa by producing acids and alkali burns, and by free radical formation and protein denaturation (acroleins). This can cause reflex bronchoconstriction and pulmonary inflammation. High water soluable irritants tend to cause damage to the upper airways, while low water soluable irritants tend to penetrate the lower airways/alveoli and cause damage there. Irritants may also inactivate surfactants and lead to atelectasis and decreased pulmonary compliance.

Clinical signs

According to a recent articles dealing with smoke inhalation in dogs, the more severely effected had a higher PCV. Dogs presented in stupor or coma (47%), coughing/gagging (35%), respiratory difficulty (35%). While cats presented with difficulty breathing (44%), open mouth breathing (44%), vocalizing (44%), coughing (22%), loss of consciousness (22%), and lethargy (22%). The majority (62%) of cats that were stable on presentation or improved by the day after admission had an uncomplicated clinical course while hospitalized. The cats that were worse on the day after admission tended to have a complicated clinical course. Alveolar and interstitial patterns on radiographs were the most commonly reported radiographic changes in both dogs and cats.

Treatment

Oxygen therapy will decrease the half life of carboxyhemoglobin. Administering 100% oxygen decreases the half life of carboxyhemoglobin from 4hrs to 30 minutes. Steriods and antibiotics are not indicated. Bronchodilators such as beta 2 agonists or phosphodiesterase inhibitors may help with bronchoconstriction. Nebulization and coupage may aid in moistening the airways and clearing of particles from the airways. Overall survival for oets that are admitted are 90%. Delayed neurologic sequelae may occur in dogs after smoke inhalation (presumably carbon monoxide). The most common pathological lesion noted in humans is a myelinopathy and is seen predominately in the deep white matter and periventricular areas of the brain. Neurologic recovery can be complete and sustained, even when severe.

Near Drowning

Drowning is defined as death from asphyxia while submerged or with in 24 hrs of being submerged. Near drowning is suffocation by submersion in a liquid with temporary survival. Death from near drowning occurs after the first 24 hours. Wet drowning is when fluid is aspirated into the lungs. With dry drowning fluid is not aspirated into lungs and death is thought to be due to larygospasm and glottic closure. Immersion syndrome causes sudden death after being submersed into extremely cold water. Death is thought to be due to cardiac arrest or ventricular fibrillation.

Pathophysiology

Hypoxia occurs due to laryngeal spasm with no aspiration or due to aspiration with loss of surfactant and atelectasis and intrapulmonary shunting. Hypoxemia can occur with as little as 2.2 ml/kg of fluid. Hypertonicity of fluid water (sea water) may contribute to pulmonary edema seconadary to its osmotic effect, while fresh water causes disruption of alveolar surfactant and leads to atelectasis.

Other factors that are important include temperature and contaminates (chlorine in pools). Lakes contain bacteria and protozoa, the sea contains bacteria, algae, sand, and other particles. These can obstruct airways and can cause pneumonia. Submersion in ice cold water (<5°C), may increase the chance of survival due to diving reflex, which is when submersion takes place in cold water and before unconsciousness occurs, the trigeminal nerve send signals to the CNS causing bradycardia, hypertension, and preferred shunting of blood to the cerebral and coronary arteries. This is thought to protect the brain and heart from hypoxemia. Cold also decreases the metabolic need of the brain. Although, hypothermia in submersion victims in warm water is a negative prognostic sign.

Treatment

The aim of therapy is to improve tissue oxygenation and perfusion, and prevent further pulmonary edema. Supplemental oxygen therapy should be provided, either via flow by with a mask or hood, oxygen cage if available, or via intubation and ventilation if the patient is not able to adequately ventilate. The maintenance and restoration of perfusion is accomplished with judicious use of IV crystalloid therapy, and some advocate the use of colloids when fluid therapy is required in the face of non-cardiogenic pulmonary edema.

Three factors have been associated with 100% mortality in people < 20 years of age, and those are submersion greater than 25 minutes, resuscitation greater than 25 minutes, and pulseless cardiac arrest upon arrival at the ER.

References

Drobatz KJ, Walker LM, Hendricks JC. Smoke Exposure in Dogs: 27 Cases (1988-1997). J Am Vet Med Assoc 215(9) 1999, pp 1306-1311.

Drobatz KJ, Walker LM, Hendricks JC. Smoke Exposure in Cats: 22 Cases (1986-1997). J Am Vet Med Assoc 215(9) 1999, pp 1312-1316.

Heffner GG, Rozanski EA, Beal MW, et al. Evaluation of fresh water submersison in small animals: 28 cases (1996-2006). J Am Vet Med Assoc 232(2) 2008, pp 244-248.

Johnson SJ, McMichael M, White G. Heatstroke in Small Animal Medicine: a clinical practice review. JVECC 16(2) 2006, pp 112-119.

Mariani CL. Full recover following delayed neurologic signs after smoke inhalation in a dog. JVECC 13(4) 2003, pp 235-239.

Powell LL. Accidental Drowning and Submersion Injury. In: Respiratory Diseases of Dogs and Cats. King LG, editor. WB Saunders Company, Phil Pa, 2004, pp 484-486.