Chapter 59: Environmental Injuries and Toxic Exposures

Man's interactions with the environment may result in an untoward affliction of injury for both. From the patient's standpoint, the common theme in prevention of environmental injury is preparedness and sound awareness of environmental factors. From the practitioner's standpoint, a sound grasp of the diagnosis and management of these relatively rare presentations may aid the patient in these sometimes-critical settings. This chapter will focus on heat stroke, accidental hypothermia, drowning, envenomation, electrical injury and injury due to ionizing radiation. Emphasis will be on basic understanding of the epidemiology, pathophysiology and management of the individual disorders, with some added focus on problems the practitioner might encounter in the critical care setting. For detailed discussions of the individual disorders the reader is advised to consult the references.

One common theme among all disorders included in this chapter is the need for their early recognition and speedy initiation of appropriate therapy in the prehospital environment and emergency department, with critical care continuing such care and management of any associated organ failures in the in-hospital setting. Any deviation from such timely response is likely to result in significant additional injury and increased risk of poor outcome.

Essentials of diagnosis are as follows:

• Temperature > 40°C (104°F)^1,2,3,4,5

• Central nervous dysfunction

General Considerations

The body's basal rate of metabolism is responsible for heat generation. Almost all energy released in the body will end in heat production. The body's core temperature is maintained in the vicinity of 36°C to 37.5°C to ensure optimal functioning of the enzymatic and molecular machinery. The principal responses to an elevated core temperature are vasodilatation and sweating. Vasodilatation intensifies the rate of heat transfer to the skin, and the evaporation of sweat from the skin surface dissipates this heat. Heat loss via electromagnetic radiation is a negligible form of energy loss, while conduction, that is, heat loss via direct contact with substances of lower temperatures (such as swimming in cool water on a hot day), can play a significant role in maintaining adequate body heat in the right circumstances. Excessive environmental heat and humidity, or increased core heat production (exercise), and interference with sweating (dehydration, hyponatremia, medications), skin perfusion (cardiovascular disorders, medications) or dissipation of heat from the surface of the skin (excessive clothing, such as in firefighters or soldiers) will result in an imbalance of heat production and heat dissipation, exposing the individual to a risk of hyperthermia, and the resulting molecular and subsequent cellular malfunction. This malfunction can manifest itself in a spectrum of presentations, ranging from transient dehydration, hypotension, tachycardia, electrolyte disturbances, heat exhaustion, lower extremity edema and heat cramps, all the way to heat stroke and the associated organ dysfunctions, and death. Pathophysiologically, temperatures above 42°C are generally thought to result in cessation of adequate function of many enzymes and will be associated with uncoupling of oxidative phosphorylation, with neural tissue, hepatocytes and vascular endothelium being the most sensitive cell types. This will be accompanied by findings that are consistent with systemic inflammatory response syndrome (SIRS) with varying degrees of multiple-organ dysfunction.

Although the critical care practitioner will usually not encounter either heat exhaustion or heat cramps as sole presentations, it is worthwhile expanding on the presentations of these milder disorders.

Heat Exhaustion results from the depletion of water and salt (sweat production and dehydration) in the setting of vasodilated integument and muscles (decreased effective plasma volume). The depletion of salt occurs as the patient consumes fluids without sufficient salt quantities. The patient's presentation will vary, but may include weakness, fatigue, headache, nausea, and vomiting. Laboratory data will demonstrate hyponatremia and hypochloremia. Fluid therapy targeted toward the basic metabolic panel and clinical scenario should correct this syndrome.

Heat Cramps manifest as muscle cramps after strenuous exertion; the patient may endorse a history of copious sweating and consumption of hypotonic fluids. The hyponatremia and hypochloremia will correct with crystalloid infusion, as will the patient's symptoms.

Heat stroke is defined by a body temperature above 40°C (or 104°F) with evidence of central nervous system dysfunction, and is classified as exertional or nonexertional.

The exertional form of heatstroke afflicts the unacclimatized individual performing strenuous activity in hot or excessively humid conditions, such as military recruits, athletes during training or competition and other persons who overexert themselves in conditions of high temperature. In these individuals, the heat loss mechanisms (through the skin and lungs) are overwhelmed by the endogenous heat production (which can rise up to 20 times the baseline of ~100 kcal/h). The reduced effects of vasodilatation and sweating in an excessively hot and humid climate result in a decreased transition of thermal energy to the environment, compounding the situation.

The nonexertional form of heat afflicts typically the elderly, economically disadvantaged and chronically debilitated, and reflects an inability to either liberate oneself from or hydrate oneself in an excessively hot environment. Prescribed therapeutics (diuretics, anticholinergics, psychotropic medications), alcohol and illicit drugs increase one's susceptibility. As opposed to the rapid development of exertional heatstroke, nonexertional heat stroke develops over a longer period.

Clinical Features of Heat Stroke

Symptoms and Signs

Fever above 40°C and central nervous dysfunction must be present to satisfy the definition of heat stroke. The presentation may range from mild confusion in the earliest stages of the illness in an elderly individual to multiorgan failure in the severe extreme. Lethargy, delirium, stupor, obtundation, and seizures, may be seen. Myocardial depression may result in jugular venous distention. The patient may be hypotensive or in a state of high-output cardiac failure, tachycardic and tachypneic, with presence of acute respiratory distress syndrome (ARDS), disseminated intravascular coagulation (DIC), acute kidney injury, hypoglycemia, rhabdomyolysis, and hepatic dysfunction.

Laboratory Findings

Basic metabolic panel, magnesium, and phosphorus, may reveal hyponatremia, hyperkalemia, hypophosphatemia, hypomagnesemia, and acute kidney injury. Complete blood count may initially reveal hemoconcentration. Coagulation panel, fibrin degradation products, and D-dimer may reveal DIC. Elevated creatinine phosphokinase, LDH, urine myoglobin may point toward increased muscle breakdown and rhabdomyolysis. ABG and lactic acid may reveal a metabolic acidosis.

Differential Diagnosis

Hyperthyroidism should be evaluated for on presentation. Drug ingestion and therapeutic prescriptions should be evaluated for by corroborative history and toxicology screen. Malignant hyperthermia, neuroleptic malignant syndrome, and serotonin syndrome can be included or excluded from the differential after evaluation of drug history. Infection (meningitis, encephalitis, sepsis) should be excluded based on clinical, biochemical, microbiologic, and hematologic evaluation. The exclusion of a cerebral insult (eg, hemorrhage, infarct) may require imaging.

Treatment of Heat Stroke

Following initial assessment and stabilization of vital cardiopulmonary function, it is essential to immediately begin the cooling process. This should take precedence over all additional investigations. The principle of the “golden hour” should guide initial management choices. Cooling should commence as soon as the victim is encountered and should essentially be nearly completed before the patient reaches the critical care environment.

Continual temperature monitoring via rectal or esophageal thermistor is indicated. Although previous recommendations stressed that a target of 38°C should not be exceeded, recent case reports suggest that there may be a role for induction of controlled hypothermia in patients who fail to respond to the initial temperature reduction.^6,7

Suggested cooling methods include the placement of the naked patient on a net followed by spraying with water in addition to the application of a cooling fan. One can place the naked patient in sheets, which have been submerged in ice-cold water, with the application of a cooling fan. One can also place the patient in ice-cold water, though this may hamper further resuscitative efforts. The recent use of therapeutic hypothermia for patients with cardiac arrest led to the development of protocols for strict temperature control and maintenance in many institutions, and it appears intuitive that the same protocols could be used for rapid temperature reduction from excessively high to normal or near-normal levels in patients who did not suffer from cardiac arrest.^6,7 However, this specific approach will need to be tested before it is adopted as a standard in patients with heat stroke. Additional measures include administration of crystalloid infusions; however, one should avoid overzealous resuscitation, and instead utilize goal-oriented approaches (eg, CVP monitoring, ultrasound evaluation of the inferior vena cava with specific attention to respirophasic variation or urine output). As the vasodilation is addressed with the above stated methods, the intravascular volume status will change accordingly. Other measures may include lavage of various spaces with ice-cold saline (GI tract, pleural space, bladder) and use of cold humidified oxygen. Neither antipyretics (acetaminophen and salicylate) nor dantrolene are indicated, as neither of these drugs' targeted pathways will ameliorate the pathophysiology of heatstroke. Under favorable circumstances failure to respond to simpler measures to cool the patient can be addressed with cardiopulmonary bypass (CPB) or extracorporeal membrane oxygenation (ECMO), although these options are available only in specialized centers. Subsequent standard care for individual organ dysfunctions should not be any different than for other disorders encountered in the critical care setting. Some sources advocate the avoidance of vasopressive agents, with concern that they could diminish skin perfusion and further impede efficient heat removal.⁵ However, these recommendations may be difficult to follow in the setting of refractory hypotension that threatens organ perfusion and survival while the patient fails to respond to resuscitative crystalloid infusion.

Essentials of diagnosis are as follows:

• Mild (35°C to 32°C): shivering, impaired judgment, “cold diuresis”^8,9,10

• Moderate (less than 32°C to 28°C): CNS depression, loss of shivering, atrial arrhythmias

• Severe (less than 28°C to 24°C): coma, ventricular arrhythmias, hypotension, oliguria

• Profound (less than 24°C): absence of vital signs

General Considerations

The definition of accidental hypothermia is an unintentional drop of core body temperature to less than 35°C.

Risk factors for accidental hypothermia include extremes of age, alcohol or drug use, homelessness, psychiatric illness, endocrine disorders, and low temperatures during the winter season (in addition to wind-chill). A professional, lifestyle or recreational activity that is based in remote environments (eg, boating, mountain climbing, backcountry skiing, military missions in remote areas) runs the risk of exposure to a frigid environment without easy access to either warm shelter or medical facilities.

Heat loss occurs via 5 mechanisms: convection, conduction, radiation, respiration, and evaporation. The initial response to cold is shivering, a process that serves to generate heat, so long as the energy and glycogen stores permit. Hypothermia results when the environmental cold temperature overwhelms this internal heat generation mechanism.

Clinical Features

Symptoms and Signs

The patient will initially exhibit shivering, tachycardia, and peripheral vasoconstriction. The mental status will be changed to a degree that is roughly correlating with the temperature drop (see above); altered sensorium may be the first subtle feature of hypothermia. Cold-induced diuresis may occur even in the setting of dehydration; it may not be “productive urine” in the sense that the urination does not reflect adequate excretion of nitrogenous waste products. The stiff chest wall will cause increased work of breathing and ultimately contribute to hypoventilation. The hypothermic heart shows a predisposition to develop arrhythmias, and is extremely sensitive to mechanical irritation; any unnecessary movement of the patient may precipitate fatal ventricular fibrillation. The altered level of consciousness favors aspiration. At the most extreme form (< 28°C), “paradoxical undressing” may occur.¹¹

Electrocardiography Findings

The bradycardia of hypothermia is caused by decreased pacemaker cell depolarization, and may be refractory to cardiovascular drugs. The characteristic EKG finding in bradycardia is the Osborn (J) wave, which appear at temperatures less than 32°C. As the temperature lowers, the irritable myocardium is predisposed to atrial and ventricular dysrhythmias.

Laboratory Findings

It is essential to monitor serial ABGs (results are typically reported as if the patient has a normal temperature and may be different if corrected for actual body temperature), Basic metabolic panel, Magnesium, Phosphorus, calcium, creatinine phosphokinase, coagulation panel, amylase, and lipase. Endocrine markers such as TSH and Cortisol should be evaluated, as should a toxicology screen. If trauma is suspected, the appropriate imaging should be evaluated.

Temperature Monitoring

The patient should be monitored via a thermistor probe in the esophagus that has been placed 24 cm below the larynx (or in the lower third of the esophagus). The temperature recorded via devices in the bladder or rectum may be markedly different from core temperatures in the proximity of the heart (as measured by a distal esophageal probe). The esophageal probe is the device of choice.

Management

Survival after prolonged CPR, and downtime of up to several hours, in the setting of hypothermia has been described. It is essential that resuscitative efforts be continued until the patient is rewarmed, unless other findings, such as severe injuries incompatible with life, a frozen and nondeformable chest wall, or changes present in prolonged death suggest that such efforts will be futile. Available data suggests that serum potassium can serve as a guide and that levels more than 12 mmol/L are not compatible with survival.⁸ While cardiovascular interventions (medications, defibrillation) used in ACLS may show decreased response in the hypothermic patient, current lack of other evidence suggests that it is reasonable to apply the standard ACLS protocol while actively rewarming the patient.⁹

Airway

Orotracheal intubation should be performed unless the patient demonstrates mastery of the airway. As ileus is common in hypothermia, an orogastric tube should be inserted at the time of intubation.

Breathing

Mechanical ventilation with warm humidified air should be delivered.

Circulation

Crystalloids should be warmed and infused with a general assumption that the patient is hypovolemic, while the volume status should be serially assessed. One should ensure that central venous catheters, or guidewires used during their placement, are not inserted into the ventricle, as this may precipitate fatal dysrhythmias.

Rewarming

As wet clothing will strikingly increase heat loss via conduction, these items should be removed. Passive Rewarming consists of simply insulating the patient (eg, with a blanket) with the intent of preventing further heat loss. However, in the typical patient admitted to the ICU with hypothermia, this alone will not be an adequate intervention. In general, the patient should be rewarmed at a rate of 0.5°C to 2°C/h in mild hypothermia cases without significant hemodynamic instability.

Indications for a more expedient rewarming rate (active rewarming) include cardiovascular instability, temperature below 32°C, examination suggestive of peripheral vasodilatation, and endocrine insufficiency. If the patient fails to rewarm in appropriate fashion with “passive rewarming,” then “active rewarming” should be performed. Faster rates of rewarming (> 2°C/h) can be achieved with active rewarming.

Active rewarming falls under following 2 categories:

Active external rewarming—involves application of heat to the body surface, and is the method of choice used in Operating rooms (the “Bair Hugger”).

Active core rewarming—includes the use of warm humidified oxygen (40°C-45°C), warm intravenous crystalloids (42°C), irrigation of the peritoneal or pleural surfaces with warmed isotonic fluid, hemodialysis, venovenous rewarming circuits, or suitable devices used for therapeutic hypothermia that are capable of active rewarming (eg, endovascular devices commercially available for that purpose). Additional techniques to be considered when core temperature is less than 28°C, or if there is cardiac instability, are extracorporeal membranous oxygenation (ECMO) or cardiopulmonary bypass (CBP).

Essentials of diagnosis are as follows:

• Numbness/paresthesias^12,13

• Peripheral vasoconstriction

• Clumsiness of extremity (“chunk of wood”) sensation

Frostbite describes local tissue injury incurred during exposure to cold or freezing temperatures. It occurs when the tissue temperature drops below 0°C. Ice crystal formation will result in disruption of cell structure. Damage to the vascular endothelium promotes stasis and thrombosis. At the macroscopic level, edema, thrombosis, ischemia, and superficial necrosis will result.

Clinical Features

Symptoms and signs always include sensory deficit affecting light touch, pain, and temperature perception, particularly in the acral areas and distal extremities. The hands, feet, nose, ears, and face are especially susceptible. Patients may complain of a clumsy or “chunk of wood” sensation in the extremity. Deep frostbitten tissue may appear waxy, mottled, yellow, or violaceous-white. In advanced cases and delayed presentation there may be bullous formation (the bullae may be filled with clear or hemorrhagic fluid), or changes progressing to eschar formation and tissue necrosis. Superficial frostbite does not entail subsequent tissue loss unless subjected to additional trauma or subsequent infection.

Treatment

Before Thawing

The best field management essentially involves protecting the frozen part, and avoiding attempts at thawing, especially if there is risk of refreezing present, as this will markedly exacerbate any tissue injury. If thawing is inevitable, then it is essential to prevent refreezing of the injured part. The current literature is quite insistent on forbidding the practitioner from rubbing or massaging the affected part, as this action may exacerbate injury.

During Thawing

Immerse the body part in circulating water 37°C to 39°C (water containing antiseptic flush) for 10 to 45 minutes. Encourage patient to move the body part. If pain is refractory, reduce the temperature to 33°C to 37°C. Parenteral analgesia may be required. Hyperemia is to be expected during the thawing process. In general, these patients may be hypovolemic, and crystalloid infusion should be administered accordingly.

After Thawing

Skin care should be directed by plastic surgery or burn care specialists. The decision about viability of deeper tissue structures, and the need and timing of amputation will also require specialized surgical input. Vascular thrombosis is characteristically present in the affected tissue. Anticoagulation and administration of thrombolytic therapy are options that should be discussed with appropriate surgical consultants.^10,14 Other possible therapies such as pentoxifylline, acetylsalicylic acid (ASA), surgical or chemical sympathectomy to the affected tissue, or use of prostacyclin analogues, are supported by limited data and are not recommended for routine use.

Essentials of diagnosis are as follows:

• Obtundation^{9,15,16,17,18}

• Asystole

• Hypoxemia

• Hypotension

General Considerations

The WHO defines drowning as: “the process of experiencing respiratory impairment from submersion/immersion in liquid.” Immersion syndrome refers to syncope resulting from arrhythmias/vagally mediated asystole induced upon the patient's exposure to cold water.

Risk factors include alcohol, lapses in supervision of children, aquatic sports, boating, seizures, and central nervous system depressants.

In contrast to the general image of the victim waving and shouting for help, the “instinct drowning response” takes over. The individual, in an attempt to increase buoyancy, spreads the arms horizontally under the water surface and breath holds. After this mechanism is overcome by involuntary gasping for air, water is aspirated. The irritation induced by the water induces laryngospasm that results in hypoxemia and hypercapnia. The contents of the water may inactivate the surfactant, promoting alveolar collapse and atelectasis. The actual contents of the water may obstruct the terminal airways. The fluid-filled alveolar sacs are rendered incapable of providing adequate gas exchange. This series of events culminates in cardiac arrest. It is emphasized that it is the hypoxemia that initiates the cascade of events, and is responsible for the cardiac arrest.

Clinical Features

The victim will be cold to touch, and appear mottled and discolored. Water or “foam” may be coming out of the mouth. The respiratory manifestations will be those of distress and will include tachypnea, rhonchi, rales, and cyanosis. The hypoxemia, to an extent, will dictate neurologic sequelae (from altered sensorium to coma). The metabolic state will dictate the arrhythmias.

Management

Taking into account the primary respiratory nature of the event, the current C-A-B approach in resuscitation should be modified to the more traditional A-B-C.⁹

Airway—The act of “mouth-to-mouth” resuscitation should not wait for arrival to the shore, and should instead be initiated immediately upon meeting the victim in the water. The Heimlich maneuver is contraindicated unless there is evidence of a foreign object obstructing the airway. The possibility of cervical injury must be considered in cases of drowning in shallow water after a fall or a dive, and this should prompt appropriate precautions during transport, resuscitation, and airway management. The gastric distention caused by manually ventilating the patient may promote aspiration, and further exacerbate the situation. Chin-lift and rapid orotracheal intubation can prevent gastric inflation. In the same spirit, bag-mask ventilation should be performed by only those experienced in the technique.

Breathing—if Mechanical ventilation is instituted, one generally avoids liberation trials for the first 24 hours. Complications may include the Acute Respiratory Distress Syndrome, hemothorax, and pneumothorax. One should demonstrate findings of pneumonia (infiltrate upon resolution of pulmonary edema, sustained leukocytosis and fever) prior to initiation of antibiotics.

Circulation—CPR must be initiated promptly. Following initial resuscitation or stabilization in the field and the emergency department, the patient will frequently require admission to a critical care area for close monitoring and subsequent management of the expected complications.

Specific manifestations of drowning are as follows:

• Cardiac: arrhythmias may result due to prolonged hypoxia or cardiac arrest may develop

• Pulmonary: mechanical ventilation is frequently necessary for development of pulmonary edema and ARDS. Pulmonary infections may be present and this will be dependent on the characteristics of the aspirated water. Case reports describe the use of ECMO in drowning victims.¹⁹

• Neurologic: various degrees of anoxic injury with subsequent seizures, and cerebral edema can be expected in prolonged submersion or with associated cardiac arrest

• Hypothermia: can be a complication of prolonged immersion in cold water. This may be associated with additional complications as described above in the separate section of this chapter, but may also contribute to a better outcomes after prolonged immersion due to some degree of associated cerebral protection. However, therapeutic hypothermia has not been associated with improvements in outcome in drowning, and is currently not recommended for routine clinical use.¹⁷

SNAKEBITES

Essentials of diagnosis are as follows:

Crotalidae

• Potential for limb-threatening local reactions^20,21,22,23

• Coagulopathy, bleeding

• Compartment syndrome

• Rhabdomyolysis

• Capillary leak with intravascular volume depletion and shock

• Metallic taste, nerve paralysis and respiratory failure

Elapidae

• Minor local reactions

• Neurotoxicity

• Respiratory depression

General Considerations

In North America, venomous snakes include:

• Crotalidae (pit viper): Crotalus (rattlesnakes), Agkistrodon (copperheads), and cottonmouths. Crotalidae are present in most states of the US and are the cause of most snakebites.

• Elapidae (coral snakes). Elapidae are present in Gulf Coast states.

Clinical Features: Crotalidae (pit vipers)

Pit viper venom contains numerous proteins with complex and variable effects. Digestive enzymes, myotoxins, metalloproteinases, fibrinolytic and thrombin-like molecules, amongst others, induce extensive local tissue damage, edema, and rhabdomyolysis with a cascade of events that may incorporate acute kidney injury, compartment syndrome, coagulopathy, thrombocytopenia, hemorrhage, diffuse capillary leak, and shock. The rattlesnake may deliver an anticholinergic neurotoxin imparting weakness, cranial nerve palsies, and in some cases respiratory failure. The severity of pit viper envenomation can range from very minimal local reactions with no systemic reactions, to very severe limb-threatening local reactions and vital organ failure-inducing systemic reactions. Generally rattlesnakes cause more systemic symptoms, sometimes associated with minimal local reactions, while the other Crotalid snakes cause more local reactions.

Treatment in the in-hospital setting and ICU consists of administration of polyvalent Crotalide antivenom for more serious reactions, and additional supportive care and management of the usual complications (hypovolemia, shock, bleeding, compartment syndromes, respiratory failure, acute kidney injury, and others). Initiation and dosing of antivenom is dependent on the severity of reaction observed and should be made with expert toxicologic consultation through the toxicology center network at 1-800-222-1222. Antivenom administration can be associated with immediate life-threatening anaphylaxis and delayed hypersensitivity reactions; preparations should be made for the possibility of severe immediate systemic reactions as the antivenom is prepared for administration. Anaphylaxis and other severe immune reactions associated with antivenom administration are treated in the standard fashion, and may preclude repeat administration of such treatment. Close communications with expert toxicology support is essential for determining the optimal course of action in the individual patient. Some of the above complications of Crotalide envenomation, such as severe local reactions, hemorrhages and compartment syndrome, will require surgical consultation and subsequent management.

Clinical Feature of Elapidae (coral snakes)

The venom of these snakes contains phospholipase and a neurotoxin, respectively causing local wound reactions and neurotoxic effects. Systemic reactions can occur in the absence of local reactions and be delayed in onset up to 12 hours. Envenomation from the Eastern coral snake results in predominant systemic reactions consisting of nausea, vomiting, headache, paresthesias or numbness, and may progress to paralysis with respiratory failure. The Texas coral snake causes mostly minor local reactions resulting in local pain, swelling, erythema and paresthesia, requiring mostly management of local pain. Given the delayed systemic reaction that could be associated with respiratory failure and significant paralysis following Elapidae envenomation, close observation in a monitored setting is indicated for the first 12 to 24 hours. Treatment of patients is complicated by limited availability of the antivenom whose production has ceased in 2006. If residual stock of FDA-approved antivenom is available, it should be administered in the presence of any systemic signs of envenomation and this should be done with expert consultative support from the poison control center (1-800-222-1222). The serum used in this antivenom is derived from horse serum and can cause similar hypersensitivity reactions as the Crotalide antivenom; similar degrees of precaution are advised before its use.

SPIDER BITES AND SCORPION STINGS

Essentials of Lactrodecism (Black Widow Spider Bite) are as follows:^{23,24,25,26,27,28,29}

• Throughout United States

• Intense pain

• Muscle spasms

• Hyperadrenergic response

• Neuromuscular manifestations (fasciculations, ptosis, facial spasm)

• Abdominal pain may mimic surgical abdomen

Essentials of Loxoscelism are as follows:

• Southeastern United States

• Intense local pain and reaction that may result in necrotic eschar formation

• Systemic manifestations (hemolysis, acute kidney injury, rhabdomyolysis)

Essentials of Scorpion Stings are as follows:

• Southern United States

• Intense pain

• Neuromuscular manifestations (muscle jerking, opsoclonus, tongue fasciculations, paralysis, and respiratory failure)

Spider bite

General Considerations

In North America, the clinically important insults incurred by spider bites are Lacrodectism (bite from Black Widow Spider—Lacrodectus species) and Loxoscelism (bite from the Loxosceles species).

Clinical Features—Lactrodecism (Black Widow Spider Bite)

Present throughout the US, this spider resides mostly in dark places, such as woodpiles or garages. The venom contains a toxin that causes catecholamine and acetylcholine release from presynaptic terminals. The ensuing muscle spasms and severe pain are generally accompanied by a hyperadrenergic response. The resulting presentation may suggest an acute abdomen, a primary cardiovascular condition such as an acute coronary syndrome, as well as rabies or tetanus. Treatment of severe reactions requiring admission to an ICU includes management of symptoms with opiates for pain and benzodiazepines for muscle spasms. Expert toxicology consultation via the regional poison control center (1-800-222-1222) should be sought before administration of the available black widow spider antivenom for severe reactions. As in all animal-derived serums, this antivenom can cause serious immediate and delayed hypersensitivity reactions that have resulted in patient fatalities.

Clinical Features—Loxoscelism (Recluse or Brown Spider Bite)

Loxoscelism is the term used to describe the syndrome caused by the Loxosceles species (the recluse or brown spider) that is present in the Southeastern US. Envenomation is most likely to be incurred by the female upon unintended provocation; sphingomyelinase D and hyaluronidase are the active enzymatic components of the venom. As the initial bites are often painless, the victim will often be unaware of the insult and thus unable to identify the spider. Cutaneous insult is manifested as pain and erythema (within 12-24 hours). Painful edema, irregular areas of ecchymosis and hemorrhagic blisters may form. Within 72 hours, there is a possibility of ulcer and necrosis formation. This may eventually culminate in dry necrotic eschar formation within 5 to 7 days. This progression of events, if it is to occur, will culminate in a fairly well defined ulcer with granulation formation in 2 to 3 weeks. In about 50% of cases, the cutaneous form will be accompanied by nonspecific symptoms such as headache, nausea, and vomiting. The systemic variant of loxoscelism may occur in approximately 10%, and includes renal failure, rhabdomyolysis, and intravascular hemolysis. Systemic loxoscelism occurs 24 to 72 hours after the bite, and this presentation may require ICU admission.

Management of the rare systemic loxoscelism is supportive, and may include mechanical ventilation and hemodialysis. In other cases, expertise from a wound specialist should be sought. Loxosceles antivenom is not available in the United States, but is used in South America.

Scorpion Envenomation

Scorpions, located in the Southern USA, are nocturnal and favor dry environments. Accidental transport of scorpions as stowaways may result in envenomation outside of their endemic area. Only the Centruroides sculpturatus (also known as Centruroides exilcauda or the “bark scorpion”) causes clinically relevant presentations in the USA. The intent of the scorpion venom, which acts as a neurotoxin via its action on sodium channels, is to immobilize the victim. Envenomation may result in vomiting, adrenergic effects (tachycardia, hypertension), localized pain, paresthesias, muscle jerking, opsoclonus, tongue fasciculations, rhabdomyolysis, and respiratory failure (loss of airway muscle tone in combination with increased salivation resulting in the inability to handle secretions). In the absence of antivenom administration, 24% may end up requiring mechanical ventilation. Symptom onset will begin 15 minutes after envenomation. Severity of envenomation ranges from self-limited local discomfort and paresthesia, to a more generalized pain with associated skeletal and cranial nerve paralysis, and autonomic nervous dysfunction. Supportive management will include analgesia (opioid analgesia is indicated), benzodiazepines, and intravenous fluid administration. Severe systemic symptoms warrant the administration of the antivenom, immune F(ab')2 (equine) injection, with readministration at 30 minute serial evaluations if symptoms persist. This equine preparation has been successfully demonstrated to resolve Centruroides scorpion envenomation mediated neurotoxicity in children if administered within 4 hours of insult. Expedient administration in the emergency room may altogether obviate the need for ICU admission. For patients admitted to the intensive care unit with persistent symptoms or significant organ dysfunction expert consultation with toxicology specialists at a regional poison control center (1-800-222-1222) is advised.

Marine Life Envenomations

Essentials of diagnosis are as follows:

• Local pain and edema^30,31

• Erythema

• Systemic symptoms including cardiovascular collapse are possible

Stingrays (Class Chondrichthyes)

Stingrays are found worldwide, and account for around 2000 emergency room visits per year in the United States. The insult inflicted on the human will be the result of an unintended encounter, as opposed to an attack. The stingray is often buried in the sand; the victim may unknowingly step on it, causing the stingray to unleash its tail (decorated with up to 6 barbs) on the extremity. The laceration induced by this may cause hemorrhage if an artery is struck. The embedded spines then release their venom. The venom of the Stingray consists of amino acids, serotonin, 5'-nucleotidase, and phosphodiesterase. The net effect of the venom is potent vasoconstriction and wound necrosis, with the victim experiencing considerable pain and edema. Clinical examination reveals swelling, erythema, and cyanosis. The symptoms peak at 30 to 90 minutes, and last up to 48 hours. The embedded spines, if not removed, remain an active source of venom. The affliction of the heart or secondary trauma accounts for mortality. Systemic symptoms may include excessive salivation, muscle cramps, nausea, and vomiting.

The hallmarks of therapy include hemostasis, hot-water immersion, analgesia, and wound-exploration. Hemostasis should the first priority. The treatment of hot water immersion (43.3°C-45.6°C) takes advantage of the heat-labile nature of the venom. Imaging and exploration should be directed at removing embedded spines.

Spiny Fish

The Scorpaenidae Family (spiny fish) consists of Stonefish and Lionfish. In the United States, the afflicted victims will usually be aquarium owners. The affected extremity will be edematous and painful, with the possibility of wound necrosis development. Systemic effects, though rare, may include myotoxicity, neurotoxicity, and cardiotoxicity. It is suggested that the systemic effects of nausea and syncope may actually be due to the pain inflicted by envenomation from the embedded spines.

As with the envenomation induced by the Stingray, the hallmarks of therapy include hemostasis, hot-water immersion (45°C), analgesia, and wound exploration. In the case of the Stonefish, antivenom may be administered intramuscularly. All spines must be removed (and confirmation should be sought with plain radiographs). The affected extremity must be elevated and washed with water. The wounds may take months to heal, and expert consultation from a Wound specialist should be sought.

Portuguese-man-of-war (Physalia physalis)

The Portuguese-man-of-war is found in the Atlantic Ocean, in shallow water and along the shore. Its nematocysts may remain active for months. The victim experiences pain upon exposure; the erythematous skin irritation that accompanies it may eventually progress to wound necrosis. Some may develop a delayed hypersensitivity reaction. Systemic reactions in the form of nausea, vomiting, dyspnea, headache, abdominal pain, and cardiovascular compromise are infrequent but have resulted in death.

The victim should be removed from the water to prevent further envenomation. The tentacles can be removed manually (preferably with forceps or the gloved hand) or by pouring salt water over the affected area. Hot-water immersion will serve to inactivate the heat-labile venom. As of yet, there is no definitive antivenom targeting Physalia physalis.

Essentials of diagnosis are as follows:

• Arrhythmias^{32,33,34,35,36}

• Skin lesions or burns

• Deep tissue injury and rhabdomyolysis

Lightning Injury

General Considerations

Although lightning strikes the earth more than 8 million times per day, its infliction on the human remains relatively rare. Lightning strike occurs when a potential energy gradient (between the clouds and the earth) exceeds the resistance of the air.

Lightning strike can afflict the patient via following 1 of 5 manners:

1. Direct Contact—this is the rarest and deadliest form of injury. Either the person is the direct recipient of the lightning strike. The entire energy of the lightning strike is discharged into the patient (possibly via an open orifice such as the ears).

2. Contact injury—the victim is touching the object (eg, car), which is the strike point of the lightning path.

3. Side Flash or “Side Splash”—Part of the energy from the strike is diverted to the victim, who happens to be within proximity (~6 feet) of the lightning strike's recipient (object or living creature).

4. Ground current or Step Voltage—the lightning strike hits the ground and travels along the ground to the victim, who is within close proximity (usually up one leg and down the other). This is the mechanism that afflicts farm animals.

5. Blunt trauma—the current imposes an opisthotonic contraction on the victim; in addition to the explosive/implosive force that the recipient suffers from the blast effect.

Clinical Features

Cardiac manifestations include Asystole predominantly, Ventricular fibrillation, and myocardial contusion (in those who have suffered blunt injury). Absence of peripheral pulses in the aftermath of a Lightning injury should raise suspicion for significant vasospasm. The Clinician should assess for skin lesions or burns, muscle injury, and compartment syndrome in extreme cases. Neurologic sequelae include loss of consciousness, headache, amnesia, paresthesias, injuries sustained during blunt trauma (eg, traumatic subdural hematoma), and transient paralysis associated with the hyperadrenergic state (keraunoparalysis). Ophthalmologic evaluation should assess for “lightning cataract” and corneal burns. Tympanic membrane rupture is fairly common and should be evaluated on admission.

Management

1. General Measures—Duration of the lightning strike is measured in milliseconds; the first responder will not be at any risk in approaching the victim. Standard evaluation should address the Airway, Breathing, and Circulatory status, with interventions as indicated. The patient should be evaluated in the same manner as a trauma victim with particular attention paid to the cervical spine.

2. Specific Considerations—Hypotension should prompt an investigation into a possible source of bleeding, resulting from blunt trauma.

   If there is concern for rhabdomyolysis or clinical signs of dehydration, adequate tissue perfusion needs to be ensured with intravenous crystalloids. Any resulting kidney injury may require dialysis.

   If there is altered sensorium or other neurologic complaints, then evaluate for cerebral edema or traumatic intracranial bleed with CT-brain. Peripheral nerve injury is a common occurrence.

   Otolaryngology should be engaged to evaluate for tympanic membrane rupture, as this is fairly common.

   In the same spirit, an Ophthalmology opinion should be sought early in the patient's course with the intent of evaluating for cataracts, vitreous hemorrhage, and optic nerve injury.

   Standard wound care should be applied to burns. Patients who suffer burns as the result of lightning strike may require referral to a Burn Center.

Electrical Injury

General Considerations

Electrical injury will afflict injury on the patient via 1 of 3 mechanisms:

1. The direct effect of the electrical current on cells and tissues

2. The conversion of electrical energy to heat injury, with its resultant tissue damage

3. The electrical current mediated muscle contractions and its subsequent traumatic sequelae.

Clinical Features

Electricity is delivered as direct current (DC) or alternating current (AC). DC induces a single muscle contraction, and its duration of delivery is brief (it will propel the patient away from the source, thus lessening the exposure time). The repetitive delivery of AC, on the other hand, when encountered with the hand will lead to a progressively tighter grip around the source of delivery (the hand flexors are stronger than the extensors). In effect, AC induces sustained contraction or tetany, thus increasing the exposure time and tissue damage.

The physical examination may be misleading, and these patients should be managed as if they are victims of crush injury, as opposed to burn injury.

Well-demarcated partial-thickness and full-thickness burns may be seen, with an evolution toward the latter.

Management

In the field, as opposed to the site of lightning strike, the first responder must be particular about disengaging active hazards such as live wires.

Cardiac arrhythmia and arrest can occur, and respiratory failure is possible, requiring advanced cardiac and mechanical respiratory support.

Deep tissue injury with development of compartment syndrome, bone fracture, osteonecrosis, and spinal injury, and injury to blood vessels may require surgical consultation and management.

Rhabdomyolysis may result in acute kidney injury and should be addressed with adequate volume infusions.

The skin may show significant burn injury at sites of entry and exit of the electrical charge and require expert burn center management.

Essentials of diagnosis are as follows:

• Nausea, vomiting, diarrhea^37,38,39

• Hypovolemia

• Dermatitis, erythema, blister formation, ulceration

• Pancytopenia, agranulocytosis

• Infections

• SIRS, progression to multiorgan failure

General Considerations

Our clinical knowledge of ionizing radiation injury is largely derived from the occurrences in Hiroshima and Nagasaki (1945), Three Mile Island (1979), Chernobyl (1986), and Fukushima (2011).

Unlike nonionizing radiation, electromagnetic radiation not capable of displacing electrons and thereby generating ions, but with potential for injury via heat production, ionizing radiation (subsequently referred to as “radiation”) generates ions via displacement of electrons thereby creating unstable atoms that interact with other molecules. The larger alpha particles are incapable of penetrating clothing or the skin and exert their damaging effects via ingestion or inhalation. The smaller beta particles are capable of limited penetration through skin and can reach the subcutaneous tissue, and will also be harmful when ingested or inhaled. Photons in the form of X-rays or gamma rays are capable of penetration through all tissues. At the biochemical and molecular level, the mechanism of injury is via damage to deoxyribonucleic acid (DNA).

Radiation is measured in units of Gray (Gy) or radiation absorbed dose (rad). (1 Gray = 1 joule of radiation absorbed per kilogram of tissue, with 1 Gray = 100 rads). The exposure of the human body to 1 Gray of radiation may result in acute radiation syndrome (ARS).

Clinical Features

The critical care practitioner may be primarily involved with ARS, a syndrome that involves 3 organ systems: the hematopoietic system, the gastrointestinal tract, and the skin. Exposures of less than 1 Gy are unlikely to result in ARS, doses more than 10 Gy are usually fatal in 5 to 12 days. Massive exposure to more than 20 Gy may result in acute neurovascular compromise, but such exposures may be infrequent in the absence of a nuclear explosion; for comparison, the highest absorbed dose at Chernobyl was 16 Gy.

The hematopoietic system will manifest varying degrees of bone marrow suppression and this will result in the expected complications related to leukopenia, anemia, and thrombocytopenia. Changes in the gastrointestinal tract will result in abdominal pain, nausea, vomiting, diarrhea, ileus, and result in disruptions of the mucosal barrier. The skin will show varying degrees of erythema, edema, blistering, desquamation, ulceration, and necrosis. Changes in all these systems will predispose to infections. The combined effects of injury experienced by these organ systems may be presenting as SIRS or sepsis, and in severe cases as multiorgan failure and lead to death.

The acute radiation syndrome is divided into 3 phases:

• Prodromal phase—nausea, vomiting, diarrhea, erythema, hypotension, hypovolemia, and headache.

• Latent phase—the symptoms will lessen and even disappear. Lymphocyte depletion kinetics may help determine the possible length of this phase.

• Manifestation phase—depending on the intensity and nature of the radiation exposure, this phase will show changes involving the hematopoietic system, the gastrointestinal tract, the skin, and the neurovascular system. This phase may occur after several weeks in case of a mild exposure (1-2 Gy) or may occur immediately following the initial exposure in severe lethal exposures (> 10-20 Gy).

The Combined Injury Syndrome incorporates the generalized trauma, burns, and wounds, inflicted upon the victim, in addition to the radiation exposure.

Management

The culprit radioisotope(s) must be identified, as this will dictate decontamination techniques, helping to maximize the safety of the involved first responders and the victims.

The provider is referred to specific guidance from governmental agencies; latter should direct all aspects of the decontamination process.

Poison Control should be engaged regarding the early administration of blocking agents (eg, Potassium iodide for I¹³¹ exposure) and chelating agents (eg, Penicillamine for radioactive lead poisoning).

The extreme result of hematopoietic insult is pancytopenia. Transfusion support and colony stimulating factors are used as needed to correct anemia, reduce the risk of or control bleeding, and increase the leukocyte count. Hematopoietic cell transplantation may be considered, with the appropriate triaging and consultations. The immunosuppressed radiation victim is at risk for graft-versus-host disease following transfusions, and all cellular products must be leukoreduced and irradiated.

The cutaneous damage may require specialized care by burn specialists and plastic surgeons in a specialized center.

The management of gastrointestinal symptoms is supportive, and should include prophylaxis against gastric ulceration and avoidance of invasive instrumentation due to the friability of the mucosa that is very prone to bleeding.

The patients are at very high risk of development of infections due to combined effects of damage to the integument and mucosal surfaces, and the immune suppression. Current guidelines advise the use of prophylactic broad-spectrum antimicrobials targeted at bacterial, viral, and fungal organisms. Because control of infections is of critical importance in patients who, otherwise, do not have a lethal exposure to ionizing radiation, specialist input by infectious disease experts may be of critical benefit.

Patients who have been exposed to radiation doses that are more than 10 Gy have a universally fatal outcome and appropriate focus on comfort should be the mainstay of management.