Environmental emergencies encompass all issues that people can encounter as a result of the environment they are in. This includes heat- and cold-related emergencies, such as heat exhaustion and frostbite. It also includes animal bites and stings, such as spiders, snakes, and scorpions. The bee sting is covered in the immunologic section about allergic reactions. Injuries related to height or depth also will be addressed in this section, such as diving injuries, near drowning, and altitude sicknesses.
The body always works to maintain an internal environment within a narrow range for all electrolytes, pH, and glucose, and it also regulates internal temperature to stay within a narrow band of 98.6°F (37°C). The hypothalamus in the brain is central to thermoregulation. When the core body temperature (CBT) declines, the hypothalamus will send signals to initiate thermogenesis, the process by which the body generates its own heat internally. Similarly, if the CBT increases too much, the hypothalamus initiates thermolysis, or the intentional liberation of excess body heat. The hypothalamus receives input from the body from warm and cold receptors located peripherally and centrally. Peripheral heat sensors are located in the skin and in muscles located near the surface of the skin and respond to environmental changes in temperature, whereas central heat sensors constantly measure the temperature of the circulating blood and are believed to be located within the hypothalamus itself. Central temperature receptor mechanisms are not yet well understood.
Thermogenesis is the production of heat and energy for the body. Increasing thermogenesis is the primary way the body will attempt to maintain CBT. The hypothalamus will signal for an overall increase in the systemic basal metabolic rate, which will generate heat through chemical bond breaking. This body also will increase the basal metabolic rate by stimulating increased muscle activity, which is experienced as shivering. Increasing the metabolism also is combined with shunting blood away from the cold periphery and toward the core. Starting with the most distal areas first, the body will shunt away from feet and hands, then as heat loss continues, it will shunt away from the lower legs and forearms, and so on, until there is no way to shunt away from the cold areas of the body. Once the ability of the body to prevent heat loss and internally generate heat is exceeded, the CBT begins to fall and hypothermia sets in.
Thermolysis is the body’s ability to dissipate excess heat. This is an ongoing process as the body tends to, under normal circumstances, generate more heat than is necessary to maintain CBT and ongoing body functions. Heat will always move from the area where heat is concentrated to the area where it is less concentrated. Put another way, heat will always move from the hotter object or area to the cooler object or area. When you grab a metal object in the winter, it is common to say it feels cold. But a shift in thinking about this process leads to a realization of how this happens: It obeys the rule that heat moved from the hotter area to the colder area. The reason the object feels cold is because the cold object is stripping heat from your body! Thinking about this further, what happens if the hand is kept there longer? Eventually, assuming the body’s thermogenic mechanisms are not overwhelmed, both the metal object and your hand will be the same temperature.
There are 4 ways the body, or any object for that matter, can dissipate heat.
Thermolysis is always happening and always dependent on the ambient (surrounding) temperature gradient. Remember the main concept here: Heat will always move from the hotter area to the colder area. This means that even if a person is in a pool in the summer, and the temperature of that pool is, say, 88°F, the person will lose heat by all 4 mechanisms listed above to the pool water. Therefore, the person’s CBT could drop, and thermogeneration mechanisms within the body—shivering, keeping arms close to the core, etc.—will begin. The temperature of the pool is by no means cold, but relative to the CBT, it is.
A similar process takes place in a sauna or a hot tub. Here the ambient temperature generally exceeds the CBT by a few degrees or more, causing the body to be the cooler area into which heat will move. After an extended period in such heat, thermolysis of the internal body heat will be initiated. Sweating begins, and peripheral vasodilation happens (seen as flushing of the body, particularly in the face) to enhance conductive cooling and radiation. In this situation of a warmer ambient temperature, vasodilation will actually enhance the absorption of heat from the environment, further increasing the CBT. In addition, the basal metabolic rate decreases to slow internal generation of heat. These factors can combine to cause the patient to pass out as peripheral vasodilation becomes so profound that the patient becomes hypotensive, and the basal metabolic rate drops to the point that the brain shuts down. This is why it is recommended to stay in these places for <15 minutes at a time.
Heat emergencies occur whenever a patient is not able to regulate his or her internal body temperature by getting rid of excess heat. There are many situations where a person cannot decrease body temperature, resulting in any of 3 heat illnesses. The temperature of the patient’s surroundings is perhaps the most obvious risk factor for heat-related illnesses; however, it is by no means the only thing that will affect a person’s likelihood of getting sick from heat. The following is a list of factors to consider in a patient who presents with any of the heat-related illnesses.
In addition to these, the very old and the very young are at increased risk from heat-related problems. The elderly often are on medications that interfere with the body’s ability to regulate heat dissipation. The chronic disease processes themselves also may impact their ability to feel temperature changes, initiating peripheral vasodilation or sweat to begin with. Also, in some cases, impaired mobility may reduce how often a patient rehydrates. Limited resources may prevent the patient from having access to air conditioning and fans to keep him or her cool.
Children have primitive thermoregulatory centers that prevent them from responding as older children do. Ever seen a sweaty infant? Probably not. An infant’s primary thermoregulatory mechanism is radiation of heat so you may see a flushed infant. Otherwise, infants rely on external factors to assist in thermoregulation, especially convection. Under most circumstances, an infant’s high surface-area-to-volume ratio is usually enough to keep him or her cool in warmer areas and present a heat maintenance issue in colder environments.
Heat cramps are involuntary, painful muscle contractions, most commonly in the muscles of support and posture in the legs, abdomen, and back. The following 3 factors contribute to a person getting heat cramps:
Heat cramps usually begin during exercise, and the pain can be so bad as to be incapacitating. Patients may be nauseous but usually will not vomit. Hypotension is rare because the patient is still able to accelerate the heart rate to compensate for the fluid loss.
Treatment for heat cramps involves getting the patient out of the hot environment and into a cooler one, preferably one where there are air currents. Encourage the patient to drink a commercial sports drink or add a half teaspoon of salt to at least 8 ounces of juice or water, as long as the patient is not nauseous. If the patient is nauseous, avoid a salt solution or ice cold drinks because this can worsen nausea and possibly cause the patient to vomit. Consider intravenous NSS run wide and expect to deliver about a liter of fluid. This will help correct the fluid and the salt issue at one time.
Heat exhaustion is more severe in the progression of heat-related illnesses. Heat exhaustion may stem from being sodium depleted, fluid depleted, or both. Sodium-depleted heat exhaustion can be caused by the loss of sodium through sweat and urine or by replacing water and not sodium, as seen with heat cramps. In heat exhaustion, the patient is not hypovolemic to the point where tachycardia is not enough to fully maintain blood pressure. Patients with heat exhaustion usually exhibit orthostatic hypotension, which is characterized by a change in SBP of 20 mmHg even with a compensatory increase in heart rate as the patient goes from lying down to standing up. Initial symptoms are similar to heat cramps: nausea, occasionally with vomiting and headache. As the exhaustion worsens, neurological changes are noted, including dizziness, confusion, mental status changes, and possibly seizures and syncope.
The patient is usually still capable of sweating, although it is diminished in volume. If available, measure the person's temperature and correlate it to CBT. It will likely be elevated though not higher than 106°F (41.1°C). The heart rate will be elevated, and blood pressure may be normal or low, and the patient may have positive orthostatic changes in blood pressure.
To treat the patient with heat exhaustion, remove the person from the heat and cool him or her off, taking care to not cool the person off so quickly that he or she begins to shiver. Initiate cardiac monitoring and have the patient drink sports drinks or lightly salted water or juice if he or she can tolerate it without worsening nausea or inducing vomiting. Initiate an intravenous line and administer at least 1 L of fluid over the first half hour. Administering 4 mg ondansetron can help with the nausea and prevent further fluid loss through vomiting.
Heat stroke is the ultimate form of heat illness. It is fortunately the least common because it is the most deadly. Heat stroke’s hallmark signs are a CBT >106°F (41.1°C) and neurological dysfunction, most notably, altered mental status. There are 2 forms of heat stroke: exertional and nonexertional. Exertional heat stroke is generally associated with younger people who are active in a hot environment for a prolonged period, and nonexertional heat stroke more often affects elderly and people who are more sedentary and have a greater amount of comorbidities, such as obesity, a cardiovascular history, a psychiatric history (because of their medications), and peripheral neurovascular changes such as that seen in diabetes.
Excessive heat for prolonged periods can be devastating to the body. Temperatures in excess of 106°F (41.1°C) can begin to denature proteins, change the cellular membrane structure, cause breakdown of skeletal muscle, and prevent normal enzyme functioning at a cellular level, leading to altered cellular metabolism.
Patients with heat stroke will present with altered mental status and will be very hot to the touch. Patients with nonexertional heat stroke are likely to be red, hot, and dry, whereas patients with exertional heat stroke will be pale and diaphoretic. If this has set in over time, the urine may be very concentrated, foul smelling, and possibly even tea colored, indicating skeletal muscle breakdown (rhabdomyolysis).
Treatment for heat stroke should include aggressive fluid resuscitation with NSS after getting the patient to a cool environment. Infuse cold saline if available but stop if the patient begins to shiver. In heat stroke, cool the patient actively with cold packs to the groin, axillae, and neck. Monitor the ECG and treat any cardiac dysrhythmia as usual.
Local cold injuries, such as frostbite, often affect the extremities or exposed areas, including the fingers and toes, ears, cheeks, and the tip of the nose. Frostnip is a mild or early warning sign of possible frostbite if warmer areas are not sought out soon. In frostnip, the aforementioned areas begin to dull sensation and are sometimes described as numb and may appear red. Body parts with frostnip can be warmed by placing fingers or hands in warmer areas of the body such as the armpits or groin; other areas, such as the nose or ears, can be warmed by covering them with a warm hand.
Frostbite generally involves actual freezing of a body part. As part of the body’s routine process of conserving heat, blood flow to the distal extremities is minimized and even completely shut down to shunt it back to the core. This allows the extremity to cool even faster. Ice crystals can form in the tissues, and eventually the entire area will be completely frozen. Frostbite can be accelerated if the area is wet because that accelerates cooling.
Superficial frostbite involves only the outermost layers of the skin. The superficial layers are frozen, but the deeper tissues are not frozen. Symptoms usually include numbness and tingling or a burning sensation to the affected areas. Deep frostbite can be thought of as full thickness frostbite and includes the muscles, nerves, vessels, and possibly even the bone. On light-skinned people, the frozen areas will be darker or even black, whereas in dark-skinned people, the same areas will have a more waxy, gray-white appearance.
Move the patient indoors or to a warmer area and remove any wet or constricting clothing. Avoid the temptation to rub or massage the affected area. Rubbing the area will cause the ice crystals in the tissue to move around, essentially becoming like little knives that lacerate the tissue and possibly cause extensive cellular level damage. If the transport time will be extensive, wrap the area with warm, dry sterile dressing, placing gauze between the fingers and toes to help prevent rubbing of the areas together. Consider rewarming on the way to the hospital if there is no danger of refreezing by using water that is about body temperature to a few degrees warmer and is easily tolerable to a person with normal sensation in his or her fingers. Remember, the patient will not be able to feel heat or pain, so it is possible, if the water is too hot, to actually cause burns to the affected, numb area. As the area defrosts, it will become extremely painful, so intravenous analgesics can be given as needed for pain.
Trench foot is a condition that was first seen on men who served in trenches during World War I. The cold water at the bottom of the trenches would cause essentially localized hypothermia of the feet. This can occur in temperatures as warm at 65°F. The affected area will lose circulation because of the local vasoconstriction, and the affected foot would be painful and appear blotchy. If allowed to be in the cold water for a long enough period of time, some areas of the foot can die and possibly require amputation. Treatment involves removal of the wet and constricting clothing and active rewarming of the area; once again, avoid rubbing it or walking on it.
Chilblains are similar to trench foot and usually occur after exposure to nonfreezing temperatures and are not associated with that area being wet. They can occur anywhere on the body, usually the fingers, toes, face, and ears. Chilblains appear as reddish-purple spots after the patient has come in out of the cold and rewarmed. The spots can become blisters or open sores, putting the patient at risk for infection. They will generally heal and disappear within about a week or so, although the area may remain sensitive to cold for life.
Hypothermia is defined as a drop in CBT to <95°F (35°C) resulting from exposure to cold environments. In hypothermia, the body’s ability to prevent heat loss and generate internal heat is ultimately overwhelmed, and body temperature begins to drop and will continue to drop until the patient can get to warmer environments.
The risk factors for hypothermia are as follows:
Hypothermia can be classified as mild, moderate, or severe. Many outlets warn to be aware of the “umbles.” This should remind us that as the cognitive state of the patient declines, he or she will start to fumble, tumble, and stumble as coordination declines, which also includes beginning to mumble and grumble as the patient begins to become confused and develop an altered mental status. This can begin after the CBT drops just a few degrees below physiologic normal.
Drowning is a process resulting in respiratory impairment from submersion in a liquid medium, which ultimately prevents the patient from taking in O2. Other terms related to drowning (near, wet, dry, active, and passive drowning, among others) should not be used because it can create confusion. Drowning can, however, be classified based on the temperature of the water the person was in. Temperatures higher than 20°C are considered warm water drowning, and temperatures less than that are considered cold water drowning. It is believed that cold water drowning can have a protective effect on the body similar to hypothermia, although hypoxic time can eliminate the effect of the temperature.
Drowning can be further classified by the type of water in which the patient was submerged. Fresh water, such as ponds and lakes; saltwater in oceans, or man-made, such as pools or bathtubs, are types of water in which a person can drown. The type of water has no impact on initial treatments and resuscitative efforts; however, once the patient is resuscitated, the type of water can have widely varying effects on the electrolyte balance in the body, particularly if a lot of water was inhaled or swallowed.
The drowning sequence usually begins with a person becoming tired in a body of water. The thrashing and splashing of a person trying to remain above water does not happen as often as Hollywood would have us believe. The patient starts by holding his or her breath as he or she becomes submerged. When water enters the mouth and nose, the patient initially chokes on the water, invariably swallowing a considerable amount. Water hitting the larynx triggers laryngospasm. Known as the diver’s reflex, this is an attempt by the body to keep water out of the lungs and is the reason why bodies will float initially after a drowning. As part of the standard progression of death, the muscles of the body relax, including those responsible for laryngospasm. Water then is allowed to rush into the lungs, resulting in the body sinking. Resuscitation of the patient after the laryngospasm has released often is difficult because the water has washed away surfactant produced by the lungs. This will make them exceedingly difficult to inflate, resulting in an even worsened outcome.
Assessment of the drowning patient is really no different from assessing any other patient in cardiac or respiratory arrest. Treatment for the patient in cardiac arrest should follow the same protocol as any “dry” cardiac arrest, including antidysrhythmic and pressor administration, the delivery of defibrillations, and CPR. If the patient is hypothermic as a result of the drowning, continue resuscitation efforts until the patient has reached a physiologic temperature.
In the patient who regains consciousness and spontaneous breathing, aggressive treatment must be continued. The patient is at risk for severe lung complications, including adult respiratory distress syndrome (ARDS) and pulmonary edema. The patient may have prolonged difficulty breathing because of a lack of surfactant in addition to the ARDS and pulmonary edema, which could cause the patient to stop breathing again. Monitor the ECG, EtCO2, and pulse oximetry throughout treatment. Administer albuterol for wheezing. Even if the patient is breathing, be prepared to intubate.
At sea level, a person—every person—is subjected to 1 atmosphere (atm) of pressure, which also can be denoted as 14.7 pounds per square inch (psi) or 760 mmHg. One atmosphere is the pressure exerted by the weight of the gaseous atmosphere above. This does not change appreciably at most inhabitable altitudes. Divers experience an increase of pressure on their bodies equal to 1 atm for every 33 feet of seawater (fsw) above them. Gases, unlike liquids, are compressible and therefore behave according to the following laws:
Paramedics will need to get information regarding the dive from the patient or those who accompanied the patient on the dive. These questions can be made into a questionnaire for services that are near common diving locations, such as shore points and lakes or quarries.
Nitrogen narcosis is a problem with dives of depths >100 ft, particularly those that used regular compressed air, not nitrogen. Excessive nitrogen in the bloodstream can cause a person to pass out while underwater, and it can be worsened if the patient is brought up to the surface too quickly. Divers afflicted with nitrogen narcosis at depth often engage in risky behavior and may even spit out the regulator and surface too quickly. Patients will present confused and also may complain of pain in their joints. Patients will likely need to be transported to a facility that has a hyperbaric chamber. They will need to be artificially taken back down to the approximate depth they were at when the problem started and then brought back up to the “surface” in a more controlled manner.
Barotrauma occurs when there is a pressure difference between the air-filled areas in the body and the external atmosphere. These spaces include the middle ear, the lungs, the joints, and the sinuses. During descent, the pressure outside increases, causing the gas-filled areas to be compressed. As long as these areas are given time to equilibrate with the surroundings during both descent and ascent, there should not be any issue. Problems arise when there are blockages, such as a sinus or middle ear infection that prevents or hinders equilibration. Rupture of the membranes or structures in the ear can lead to dizziness or disorientation in the water. This can further progress to panic and rapid ascent, leading to other injuries. In addition, nausea and vomiting can ensue after the onset of dizziness and further add to complications and panic underwater.
Perhaps the most aptly named of barotrauma syndromes because that is exactly what happens to the lung: it POPS! In pulmonary overpressurization syndrome (POPS), a person holds his or her breath during ascent as described in the Boyle’s Law example above. This causes 1 or multiple ruptures in the lung from the decrease in pressure and a commensurate increase in volume that happens to gas held within the lungs. This can lead to a pneumothorax, pneumomediastinum, and profound subcutaneous emphysema—a feeling of bubbles popping under the skin.
Patients present with signs of a pneumothorax, including dyspnea, tracheal deviation, absent or diminished breath sounds on 1 side, and JVD. If air escaped the lungs and entered the mediastinum, the patient may complain of difficulty swallowing, fullness in the throat, and chest pain. Occasionally, the patient will have a crunching sound with each heartbeat, indicating air surrounding the heart. The physical examination findings, in addition to those above, may include muffled heart sounds, an increasing heart rate and respiratory rate, and a decreasing pulse oximetry reading.
Treatment should include high-flow O2. Perform a needle decompression of the affected side. If sounds from both sides of the lung are diminished or the pulse oximetry does not improve significantly after the first needle decompression, decompress the other side of the chest as well. Pneumomediastinum cannot be treated in the prehospital environment and warrants immediate and rapid transport to the hospital. Initiate an intravenous line and continuous cardiac monitoring.
An arterial gas embolism is one of the most lethal complications of POPS. When the alveoli rupture in POPS, bubbles can enter the bloodstream and lodge anywhere in the circulatory system. If they find their way into the coronary arteries, they will cause the patient to suffer all the same symptoms as an MI. The more likely place for them to travel is the brain and head because this is generally the highest place in the body. Here, the bubbles can cause cerebral ischemia and symptoms similar to a head injury or stroke. In either of these cases, be prepared to treat cardiac arrest or any dysrhythmias if there are cardiac complications. Also be prepared to treat altered mental status, combativity, and seizures should the bubbles travel to the brain. Treatment for this patient will ultimately be to undergo hyperbaric pressure treatment, which will cause the bubbles to go back into solution. The patient will then be brought back to sea level in a controlled fashion. If the patient needs to be intubated, fill the cuff with saline rather than air so that when the patient is receiving hyperbaric therapy, the cuff does not deflate.
Decompression sickness is any of a range of conditions that the patient may experience as a result of nitrogen bubbles in the bloodstream caused by ascending too rapidly. Decompression sickness often mimics arterial gas embolism in symptoms but not in pathology. Treatment is the same and will involve recompression in a hyperbaric chamber.
Shallow water blackout is a condition often seen in boys who compete to see who can hold their breath the longest underwater. Holding their breath for a long period could lead to cerebral hypoxia toward the end of the period of time underwater, leading to syncope. This is generally a diagnosis of exclusion; in other words, after all other possibilities for the loss of consciousness have been ruled out, this is the only plausible explanation left.
A paramedic should be familiar with 3 common altitude sicknesses: acute mountain sickness (AMS), high-altitude cerebral edema (HACE), and high-altitude pulmonary edema (HAPE). People are at risk for these illnesses based not only on how high they go but how quickly they got there. High altitude illnesses can be seen at altitudes as low as 6,500 feet above sea level but become much more common at altitudes >8,000 feet. The primary issue in any high altitude illness is the decline in O2 concentration. The body is capable of acclimatizing to the drop in O2; however, it will take a day or so of rest for this to happen. Patients will often take acetazolamide to counteract the effects of high altitude sickness and help the body acclimatize faster. Acetazolamide forces the kidneys to excrete bicarbonate, establishing metabolic acidosis in the body. This allows the climber to hyperventilate to bring in more O2 without causing respiratory alkalosis.
In AMS, patients will present with a headache and at least 1 of the following: fatigue or weakness, nausea, vomiting or loss of appetite, dizziness, or insomnia. This often can be completely cured by descending until the symptoms resolve and allowing time for the body to acclimatize to that altitude before continuing.
In HAPE, the symptoms include shortness of breath at rest and with exertion, a cough, a frothy sputum, chest tightness, and at least 2 of the following: tachycardia, tachypnea, rales/crackles, and/or central cyanosis. Descent and high-flow O2 are the most important treatments for HAPE. Most patients will improve with rest and O2; nifedipine and acetazolamide are recommended as first-line medications. Dexamethasone prophylaxis and administration upon descent also can help the patient improve from HAPE.
HACE is characterized by any of the symptoms listed with AMS, in addition to the presence of altered mental status and ataxia or clumsiness, which indicate that AMS has worsened to HACE. HACE can appear in a person who continues to ascend despite symptoms of AMS or in people who ascend so rapidly that symptoms of AMS do not actually have time to appear. HAPE also occurs concurrently with HACE.
As members of the family Viperidae, pit vipers include the rattlesnake, cottonmouths, diamondbacks, and copperhead snakes. They have distinctive pits located between the eye and the nostril on each side and vertical pupils. This group is responsible for the greatest number of snake bites in the United States, primarily in the southeastern portion of the country. Pit viper venom is a toxic mixture of hemolytic and proteolytic enzymes. Hemolytic enzymes break down red blood cells and stimulate clot formation, and proteolytic enzymes break down proteins of all kinds. These work together to cause local tissue damage, swelling, necrosis, systemic bleeding, and clotting.
Pit viper bite symptoms are largely localized to the bite site and include swelling and bleeding from the fang marks. No bleeding from the bite site may indicate that a “dry,” or venomless, bite has occurred. In mild envenomations, swelling will start at the site of the bite and slowly progress up the extremity, but the patient will lack systemic symptoms. In severe envenomations, extensive soft-tissue damage occurs locally, and extensive systemic effects, including spontaneous bleeding and coagulopathies, develop, usually followed by shock, cardiovascular collapse, and death. Moderate envenomations fall somewhere in between with little systemic bleeding noted.
Treatment for a pit viper bite involves immobilization of the extremity and rapid transport for antivenin. Remove any constricting clothing and jewelry because swelling can be dramatic. Constricting bands and tourniquets are not recommended in pit viper bites, as they are in elapid bites, below.
As members of the Elapidae family, the coral snake is primarily found across the southern United States from southern California to Florida. The venom of coral snakes contains a neurotoxin that will lead to respiratory failure and death. Fortunately, coral snakes have comparatively small fangs, making it difficult for them to inject their venom. For an elapid bite to be of serious threat to the patient, the snake would have to remain attached for a reasonable amount of time to inject enough venom to be deadly.
Treatment for the elapid bite begins by applying a constriction dressing to slow the spread of the neurotoxin. The constriction dressing should be applied just proximal to the bite over the next major joint and back down to where it was started. Immobilize the extremity. All patients who have been bitten by a coral snake should be taken to the hospital, even if there is no evidence that the snake was able to inject the toxin. During transport, be prepared to aggressively manage the airway and provide ventilatory support.
In the United States, 3 spiders pose a threat to humans when bitten: the black widow (female), the brown recluse, and the hobo spider.
The black widow lives primarily in the southeastern United States but can be found throughout the country. It prefers damp and dark areas, such as sheds, woodpiles, and outhouses. It is one of the most venomous spiders. Its venom is a neurotoxin that triggers the release of neurotransmitters. In less than an hour after the bite, it causes local pain and swelling, followed by muscle spasms and paralysis, both locally to the bite and systemically. Nausea and vomiting can occur. As the diaphragm becomes paralyzed from the venom, respiratory arrest can develop.
Treatment for a black widow spider bite is aimed at preventing paralysis and pain relief. Benzodiazepines can be used to calm the patient as well as relieve any spasms and paralysis from the venom. Narcotic pain medications should be used for pain. An antivenin is available but is generally reserved for the extremes in age. Most symptoms can be managed symptomatically until the venom wears off.
The brown recluse spider is known as the fiddleback spider, owing to the dark pattern on its thorax that resembles a violin. It makes its home primarily in the southeastern United States, extending into the Midwest and Texas. Brown recluse spider bites are typically painless and rarely cause any major problems of any kind for the patient. In a rare subset of patients, however, the patient will develop what is known as loxoscelism. This begins within hours of the bite and starts off as a fluid-filled vesicle at the location of the bite. This progresses to gangrene and a larger necrotic area after about a week or so that often will require skin grafting. The area will then take months to heal fully. Any systemic symptoms are far rarer. When a systemic reaction does occur, it is generally caused by coagulopathies and hemolysis that often lead to death.
The hobo spider is very similar in all aspects to the brown recluse except that it calls the Pacific Northwest home. The bite and sequelae of the hobo spider resemble that of the brown recluse.
There is no known treatment for bites from the brown recluse spider or the hobo spider.
Scorpions of the genus Centruroides are the only ones whose sting poses a genuine threat to humans. Fortunately, it is the least common scorpion sting in the United States. Other scorpion stings cause only a local painful reaction. Scorpions of this species, called the bark scorpion, live primarily in the southwestern United States and northern Mexico. It is not aggressive and is active only at night.
A vast majority of scorpions produce only localized reactions similar to that of bee stings. The area around the scorpion sting will be red and itchy, and a burning pain similar to a strong electrical shock has been described. Local effects tend to subside within a few hours of the bite, and local tissue necrosis has not been reported.
Bark scorpion sting symptoms, on the other hand, rarely include local symptoms. The toxin in this scorpion’s sting causes sodium channels in the nerves of both the parasympathetic and sympathetic autonomic nervous system to remain open. This leads to continued stimulation of these nerves. The symptoms depend entirely on which side of the autonomic nervous system is dominating—sympathetic or parasympathetic. If the sympathetic nervous system dominates, then the patient will have tachycardia, hypertension, dry mouth, and elevated temperature. Conversely, if the parasympathetic nervous system is running the show, symptoms are similar to that of organophosphate poisoning and include everything in the SLUDGE mnemonic.
Treatment for the bark scorpion sting involves maintaining the ABCs and is otherwise supportive. Intubate if necessary and treat any cardiac dysrhythmias. Applying a constricting band to slow lymph return to the heart is recommended. Rapid transport to the hospital is essential for careful management of the autonomic symptoms. There is an antivenin available in the Southwest, but it is rather hard to come by outside that region.