Assessment

Victims of heat stroke have a profoundly elevated body temperature (above 104° F [40° C]). Although the patient’s skin is hot and dry, the presence of sweating does not rule out heat stroke—people with heat stroke may continue to perspire.

Mental status changes occur as a result of thermal injury to the brain. Manifestations can include confusion, bizarre behavior, seizures, or even coma (Chart 11-2). Vital sign abnormalities may include hypotension, tachycardia, and tachypnea. Recent research demonstrates that cardiac troponin I (cTnI) is frequently elevated during non-exertional heat-related illnesses. A severe increase (>1.5 ng/mL) indicates severe myocardial damage and decreases the chance of patient survival 1 year after the event (Hausfater et al., 2010a).

Complications of classic heat stroke include multiple organ dysfunction syndrome (MODS), renal impairment, electrolyte and acid-base disturbances, coagulopathy (abnormal clotting), pulmonary edema, and cerebral edema (Johnson et al., 2008). Any of these problems can lead to death and are described in detail elsewhere in this book.

Interventions

Coordinate care with the health care team to recognize and treat immediately and aggressively to achieve optimal patient outcomes. Chart 11-3 lists evidence-based emergency care of patients with heat stroke.

First Aid/Prehospital Care

Do not give food or liquid by mouth because vomiting and aspiration are risks in patients with neurologic impairment, especially those older than 65 years. Immediate medical care using advanced life support is essential.

Hospital Care

The first priority for collaborative care is to monitor and support the patient’s airway, breathing, and circulatory status. Provide high-concentration oxygen therapy, start several IV lines with 0.9% saline solution, and insert a urinary catheter. Continue aggressive interventions to cool the patient until the rectal temperature is 100° F (37.8° C) (Auerbach, 2009). External continuous cooling methods include using cooling blankets and applying ice packs in the axilla and groin and on the neck and head. Internal cooling methods may include iced gastric and bladder lavage. Use a continuous core temperature–monitoring device (e.g., rectal or esophageal probe) or a temperature-monitoring urinary bladder catheter to prevent hypothermia.

If shivering occurs during the cooling process, give a parenteral benzodiazepine such as diazepam (Valium). Chlorpromazine (Thorazine) is an alternative agent. Because seizure activity can further elevate body temperature, be sure to have an IV benzodiazepine immediately available. Once the patient is stabilized, admission to a critical care unit is usually needed to monitor for complications such as multi-system organ dysfunction syndrome and severe electrolyte imbalances; these problems can lead to death.

Assessment

The clinical manifestations of venom release are based on the type and amount of venom injected; the bite location; and the age, size, and health status of the victim. Puncture wounds in the skin are a key local sign of pit viper envenomation. One or more puncture wounds may be present, depending on how many fangs the snake has and how many times the snake struck the patient. Severe pain, swelling, and redness or ecchymosis (bruising) in the area around the bite are common. Hours later, vesicles or hemorrhagic bullae may form. Systemic responses to venom must be distinguished from the effects of anxiety and panic related to being bitten by a snake. Commonly reported complaints include a minty, rubbery, or metallic taste in the mouth and tingling or paresthesias of the scalp, face, and lips. Other effects include muscle fasciculations (twitching) and weakness, nausea, vomiting, hypotension, seizures, and coagulopathy (clotting abnormalities) or DIC. If the bite site does not show evidence of local tissue swelling or redness within 8 hours, systemic effects are less likely to develop.

First Aid/Prehospital Care

First aid interventions for snakebite should begin in the field and can improve the victim’s outcome.

Immobilizing the affected extremity in a position of function with a splint helps limit the spread of the venom. Maintain the extremity at the level of the heart (Auerbach et al., 2008). Keep the person warm, and provide calm reassurance. Do not offer any alcohol because it can cause the venom to spread through vasodilation (Bledsoe et al., 2009). Do not incise or suck the wound, apply ice to it, or use a tourniquet!

Hospital Care

Acute care in a hospital is required as soon as possible because envenomation is a medical emergency. Supportive care includes supplemental oxygen, two large-bore IV lines, and infusion of crystalloid fluids such as normal saline solution or Ringer’s lactate solution. Apply continuous cardiac and blood pressure monitoring equipment to quickly detect clinical deterioration. Because venom can cause severe pain at the bite site, opioids are indicated. Provide tetanus prophylaxis and wound care as part of the collaborative plan of care.

Severe pit viper bites cause coagulopathy and promote hemorrhage and tissue destruction. Along with typical baseline laboratory studies, anticipate obtaining specimens for a coagulation profile, complete blood count (CBC), creatine kinase (CK), type and crossmatch for possible blood transfusion, and urinalysis. An electrocardiogram (ECG) is necessary to detect evidence of myocardial ischemia or other cardiac abnormalities.

Obtain pertinent patient history related to the event, including a full description of the snake’s appearance, the time the bite occurred, prehospital interventions, and any past incidence of snakebite or antivenom use. To accurately assess the development of tissue edema at the bite site, measure and record the circumference of the bitten extremity every 15 to 30 minutes.

Venom potency varies. Not all snakebite victims need antivenom administration. The decision whether or not to give antivenom is based on the severity of the snakebite. Table 11-1 classifies envenomation severity. Contact the regional poison control center so that toxicologists can provide specific advice for antivenom dosing and medical management.

TABLE 11-1 GRADES OF PIT VIPER ENVENOMATION

The newest and safest antivenom for pit viper bites is Crotalidae Polyvalent Immune Fab (CroFab), which is derived from sheep (ovine). This drug consists of specific antibody fragments of immunoglobulin G (IgG) that bind, neutralize, and redistribute toxins in pit viper venom so that they may be removed from the patient’s body (Schaeffer & Badillo, 2009). Unlike the older antivenoms that were derived from horse serum, serum sickness rarely occurs after IV CroFab administration. Serum sickness is a type III hypersensitivity reaction that develops within 3 to 21 days, first as a skin rash with progression to fever, joint pain, and pruritus (itching). Although mild to moderate allergic reactions such as pruritus and urticaria (hives) can occur, anaphylaxis is rare. If the patient has a known hypersensitivity to papain or papaya, which is used during the manufacturing process, CroFab is contraindicated unless the benefits are believed to outweigh the risks (Protherics, Inc., 2008). Give CroFab cautiously to patients who have:

CroFab should be given to patients as soon as possible, with the optimal timing within 6 hours of the bite (Protherics, Inc., 2008). The recommended initial IV dose is 4 to 6 vials infused over 60 minutes. During the first 10 minutes, the infusion should be slow (25-50 mL/hr). Monitor the patient closely for an allergic reaction (e.g., hives, rash, difficulty breathing). If symptoms are not effectively controlled with the first dose, an additional 4 to 6 vials are recommended. Once the symptoms are under control, 2 more vials of CroFab are administered every 6 hours for a total of 18 hours of administration (Protherics, Inc., 2008).

Assessment

Manifestations of coral snake envenomation are the result of its neurotoxic properties. The physiologic effect is to block neurotransmission, which produces ascending paralysis, reduced perception of pain, and, ultimately, respiratory paralysis (Wozniak et al., 2006). Unlike the pain from pit viper bites, pain at the coral snakebite site may be only mild and transient. The venom is spread via the lymphatic system, but swelling is unlikely. Fang marks may be difficult to find because of the coral snake’s small teeth. The toxic effects of coral snake venom also may be delayed up to 12 to 18 hours after a bite but then produce rapid clinical deterioration. Early signs and symptoms are nausea, vomiting, headache, pallor, and abdominal pain. Assess for neurologic manifestations, such as paresthesias (painful tingling), numbness, and mental status changes, as well as cranial nerve and peripheral nerve deficits. Total flaccid paralysis may occur later, and the patient may have difficulty speaking, swallowing, and breathing. Clotting changes do not occur.

Respiratory problems and cardiovascular collapse can occur in severe cases (Norris, 2008). Arterial blood gas analysis reveals respiratory insufficiency. The muscle toxin in the venom can cause an elevation in creatine kinase (CK) levels from muscle breakdown and produce myoglobinuria (release of muscle myoglobulin into the urine). Despite these clinical effects, death is rare if the patient receives timely management.

First Aid/Prehospital Care

Because several varieties of harmless snakes resemble the coral snake, the first priority, if possible, is to identify the snake as a coral snake. However, if the snake cannot be positively identified, the victim should be treated as if venom has been injected. Because coral snake venom does not destroy tissue, the field treatment to limit the spread of venom includes the use of pressure immobilization techniques (Auerbach et al., 2008). The affected extremity is encircled snugly with an elastic bandage or roller gauze dressing to impede lymphatic flow and then splinted (Wozniak et al., 2006). This compression bandage must not be so tight that it impairs arterial flow. It should not be removed until the victim is managed at an acute care facility (Norris, 2008).

Hospital Care

Once in an acute care setting, patients who have had an actual or potential coral snake envenomation will have continuous cardiac, blood pressure, and pulse oximetry monitoring and are admitted to a critical care unit. Prepare to provide aggressive airway management via endotracheal intubation if respiratory insufficiency or severe neurologic impairment occurs. Aspiration of secretions is a significant risk for this patient.

Early antivenom administration is recommended (Auerbach et al., 2008). The onset of symptoms after coral snake bites can be delayed but can persist for a week in spite of treatment (Norris, 2008). The antivenom for the North American coral snake is Antivenin Micrurus fulvius (Wyeth). However, this drug is no longer in active production by any drug manufacturer; only very limited supplies are available. Contact the regional poison control center immediately for specific advice on antivenom administration and patient management. The same precautions are applied when administering coral snake antivenom as with Crotalidae (pit viper) antivenom.