Environmental exposures lead to numerous emergency calls throughout the United States and beyond each year and result in potentially devastating conditions. Appropriate prehospital care may make the difference for patients experiencing these serious, and sometimes fatal, exposures. By knowing the risks and recognizing the signs, early detection and proper intervention can be instituted.
Define and differentiate between the terms: drowning and near drowning.
Describe the signs and symptoms that occur during the drowning process and the prognosis of individuals who have undergone this process.
Describe the general management of drowning victims.
Comment on the inherent risks associated with water operations (covered in greater detail in Chapter 72).
Describe the cardiovascular and neurological findings of severe hypothermia.
Detail the initial management of life-threatening hypothermia and list deviations from usual ACLS during cardiac arrest or periarrest scenarios.
Describe the cardiovascular and neurological findings of severe hyperthermia.
Detail the management of life-threatening hyperthermia.
EPIDEMIOLOGY AND DEFINITIONS
Although substantial efforts have been taken by health care advocates and public health providers to develop appropriate prevention strategies, drowning remains a significant cause of morbidity and mortality in not only the United States, but also worldwide. The global statistics vary widely on the annual number of deaths from submersion injuries, but depending on sources cited, annual death rates range from 150,000 to 500,000 deaths per year.1,2,3–5 For each death that occurs, there are two to four other related water-related injuries that require hospitalization.6
In the United States, drowning is the second leading cause of death in children only surpassed by deaths from motor vehicle accidents.2 Of those who survive the drowning episode, one-third will suffer from significant morbidity due to irreversible anoxic brain injuries.7 The populations most at risk for submersion injuries are infants and toddlers aged 1 to 4 years. Children in this age bracket account for approximately 27% of all deaths due to submersion.1 Of those patients, males are more apt to suffer from drowning injuries when compared to their female counterparts.7
Most submersion injuries occur in freshwater, even in states with large areas of coastal access. The sites of drowning also vary with age. In the young infant population (<1 year), 55% of drownings occur in the bathtub.1 In older children, up to 50% occur in local swimming pools, followed by freshwater bodies of water (lakes, rivers, and streams).1,2,6,7 It is important to note in older children and adults that greater than 50% of submersion injuries are associated with the concurrent use of alcohol and drugs.1,6,7
For many years, the specific definitions of the types of submersion injuries have been blurred. In 2002, the First World Congress on Drowning met in Amsterdam to delineate definitions based on the mechanism of injury and subsequent physiologic sequelae.2 At the meeting, members defined drowning as the process of experiencing respiratory impairment from submersion or immersion. Patients who have had a mechanical obstruction due to a liquid medium regardless of outcome are said to have been involved in a drowning incident.
Since 2002, the definition of near drowning is slowly being phased out of use by medical professionals due to fact that it is imprecise and has a high level of interpretation by providers. However, it is worth defining due to fact that it is still common verbiage. Near drowning is defined as surviving, at least initially, after being submerged in a liquid medium. Since the decision in 2002 for a standard definition, further delineations have become increasingly irrelevant and for the sake of simplicity have not been included in the text.
As defined by the World Congress on Drowning in 20022:
Drowning is a process resulting in primary respiratory impairment from submersion/immersion in a liquid medium. Implicit in this definition is that a liquid/air interface is present at the entrance of the victim's airway, preventing the victim from breathing air. The victim may live or die after this process, but whatever the outcome, he or she has been involved in a drowning incident.
The process and subsequent continuum of drowning begins the moment the airway is obstructed by the noted liquid medium. Initially, victims are able to hold their breath briefly. This short period is immediately followed by laryngospasm due to the presence of liquid in the posterior oropharynx. This choking response represents the first anoxic insult that the patient experiences in the drowning process. If uncorrected, the patient will become even more hypoxic and hypercarbic due to the fact that gas exchange is inhibited. Depending on multiple physiologic factors and the mechanism of injury, 90% to 98% of cases, the laryngospasm will resolve resulting both swallowing and aspirating the liquid into the pulmonary tissues.2
In earlier literature, providers would describe those patients who had aspirated water, detritus, and vomitus to have suffered a “wet drowning.” Those who had limited abnormal findings on examination or autopsy were to have suffered from a “dry drowning” due to persistent laryngospasm. However, given the fact that the amount of water that can be found in drowning victim's pulmonary tissues can vary widely with no definable pattern, the differentiation between dry and wet drownings has also been discarded. The reason for this is due to the fact that most victims have a degree of fluid in the pulmonary tissues if the mechanism of death is associated with a submersion injury. It is important to note, however, that if the victim has no fluid in the lungs or respiratory tissues, the cause of death is not due to drowning. Fluid will not infiltrate the lungs or associated tissues without active respiratory effort.2,6
The initial hypoxemia that the victim suffers secondary to the apnea of submersion is then exacerbated by a variety of factors including surfactant washout, pulmonary hypertension, and intrapulmonary shunting. As fluid is aspirated, profound alterations in arterial oxygenation occur. Left uncorrected, alveolar collapse, atelectasis, or mechanical obstruction leads to acute lung injury and acute respiratory distress syndrome (ARDS) or noncardiogenic pulmonary edema.
The debate concerning whether respiratory collapse is exacerbated depending on the fluid in which the patient is submerged, salt versus fresh water, continues. Multiple studies have been completed examining the effects of hyper- and hypotonic fluids on blood volume and electrolyte abnormalities in this population, and it has been found that only a small population of less than 15% of individuals has documented physiologic electrolyte changes from the aspiration of the surrounding liquid medium.2 The end result, however, is the same. Whether it is due to mechanical obstruction, dilution of surfactant, loss of osmotic gradient, a ventilation and perfusion mismatch occurs, leading to profound hypoxemia.
Dysrhythmias and complete cardiovascular collapse can occur at the time of the initial hypoxic insult or several minutes after the noted laryngospasm has abated. If the victim is rescued prior to a prolonged period of submersion, the hypoxemia, acidosis, and subsequent electrolyte abnormalities will resolve with basic resuscitation. It is uncommon for drowning patients to suffer a primary ventricular fibrillation or ventricular tachycardic arrest giving the mechanism of injury. However, isolated events have been described anecdotally in lab models or in those patients who aspirate large volumes of fluid.
In the first several minutes of a drowning injury, cerebral ischemia occurs due to the cardiovascular compromise that occurs with submersion. The degree of injury to the brain and the remainder of the nervous system are dependent on the duration and severity of the initial hypoxic-ischemic injury. If the patient is extracted from the liquid medium and resuscitated appropriately, secondary ischemic injuries, including cerebral edema, can occur further exacerbating the initial insult. More than 10% of drowning survivors suffer permanent effects.1,6
Recovery of victims of drowning events vary widely based on duration of submersion injures, associated trauma, other medical conditions, and surrounding environmental factors. In young healthy patients, periods of submersion between 2 and 5 minutes are moderately well tolerated. However, submersions for greater than 25 minutes for all patients are associated with high morbidity and mortality rates.6,7 Many drowning patients present with associated hypothermia due to the immersion in the surrounding environment. Hypothermia as a whole can be indicative of prolonged duration in the water and is associated generally with a much poorer prognosis. In some cases, the cold temperature can limit end-organ perfusion and is associated with some anecdotal cases of prolonged submersion with little to no long-term deficits.6 Given the variability of factors, overall prognosis in victims of drowning incidents is difficult to predict.7
In patients who still have physiologic signs of spontaneous circulation at the time of rescue, the prognosis of recovery is variable. In those victims who are awake and oriented at the time of arrival in the emergency department, they typically survive without neurologic deficits if there is no respiratory compromise at the time of evaluation.1,6,7 Those patients who arrive with altered mental status, but responsive to pain (ie, a GCS of 6 or greater) also typically survive without neurologic sequelae greater than 90% of the time.6,7 However, those patients who arrived and were noted to be obtunded (with a GCS of 5 or less) tended to have poor outcomes.2,6,7 Between 10% and 23% of those patients were neurologically affected and of those impaired patients, 39% died soon after their arrival and 17% had irreversible and incapacitating brain injuries.2
Drowning emergencies can occur in a variety of environments. Proper initiation of prehospital care can heavily impact the overall morbidity and mortality in many cases. Bystander interventions, especially in children, are not uncommon. The role of the prehospital provider is to begin the initial resuscitation promptly to restore normal ventilation and circulation as quickly as possible. Concurrently, rescuers must not only begin basic cardiopulmonary resuscitative measures, but must also consider simultaneously the mechanism of injury and provide cervical spine precautions if applicable and prevent further heat loss if the patient is affected by the surrounding environment.
The initiation of the resuscitation will begin the assessment and establishment of an airway if indicated. If the patient is spontaneously breathing and there is no evidence of any traumatic injury, the patient should be placed in the left lateral decubitus position with supplemental oxygen. However, in most cases, the patient will be apneic and require clearing of the airway and subsequent positive pressure ventilation. As discussed previously, most patients will swallow large amounts of water during the drowning process, which can lead to significant gastric distention. Rescuers should be prepared for an abundance of vomiting and plan for immediate treatment to minimize further risk of an additional pneumonitis. In this early portion of the resuscitation, abdominal thrusts and the “Heimlich” maneuver are contraindicated. They have not shown to be beneficial and can precipitate further vomiting and are associated with additional complications.1,2,6 If the patient remains hypoxemic or continues to be obtunded, placement of a definitive airway (endotracheal intubation, Combitube, or King Airway) will prevent further aspiration and will continue to facilitate appropriate oxygenation and ventilation.
The resuscitation should continue with appropriate cardiac monitoring. As per advanced cardiac life support (ACLS) protocols, pulses should be routinely assessed, and if are not present, CPR should continue. Bystanders and prehospital providers have a variety of monitoring devices available. Automated external defibrillators are available at a variety of locations and have been used in many resuscitations successfully. Advanced Life Support EMS providers routinely use manual defibrillators and monitoring devices, thus demonstrating further benefits for activating a 9-1-1 response.
Once the patient arrives in an appropriate receiving facility, treatment is focused minimizing further hypoxia. If the patient remains obtunded, and a definitive airway has not been established, rapid sequence intubation is required. Patients who are able to protect their airway can be supported with supplemental oxygen or BiPAP. Positive pressure ventilation can aid in minimizing the respiratory effort of the patient until the respiratory status improves. FiO2 and PEEP should be titrated appropriately to maintain oxygen saturations of greater than 96%.
Additional sequelae following a drowning episode are common. Pulmonary edema and subsequent ARDS is a routine finding due to variety of factors including surfactant washout. These patients benefit from elevated PEEP or BiPAP levels to increase alveolar recruitment and ventilation. Diuretics have been used with some success, but it is important to assess the patient's fluid status prior to their routine administration. Lastly, the use of antibiotics is indicated when there is concern for immersion in grossly contaminated fluids. Their routine use is not indicated unless signs and symptoms occur. Other complications including traumatic injuries, hypothermia, and underlying comorbidities need to be addressed during each individual resuscitation. Overall outcomes are dependent on the quality and efficiency of the initial resuscitation and subsequent restoration of optimal oxygenation and ventilation.
When a water rescue team is activated for deployment, operations must be conducted in a safe and efficient manner. These specialty-trained teams undergo vigorous training and preparation to not only rescue victims, but also to conduct the deployments in a safe and efficient manner. Members adequately prepare for missions by not only perfecting skills as individual members by taking swiftwater rescue technician (SRT) courses and education on prehospital emergency care, but they will continuously train as a team to establish clear pathways and effective methods of recovery to minimize risk to the team and maximize the beneficial outcome.
During the course of rescue operations, standard operating procedures (SOPs) are typically defined prior to deployment to minimize adverse outcomes and mission failure. These protocols follow similar guidelines utilized in other rescue situations and are based on the Incident Command System (ICS). Once the mission is activated, staff must make rapid decisions during the course of the initial scene evaluation:
What is the nature of the call?
Is the activation for a rescue of living individual(s) or recovery of deceased victims?
What are the hazards?
Is there a need for additional resources beyond the scope of the first responders?
Once the initial scene assessment is completed, rescue operations can commence. Despite its simplicity, the standard Talk-Reach-Throw-Row-Go is still the standard in water rescue operations.8 Most scenarios requiring rescue personnel require the active intervention of providers, but all attempts should be made to minimize risk. There are clear examples when the standard operation procedures of water rescue cannot retrieve the victim without harming either the victim or placing the team at extreme risk. Helicopter utilization may be appropriate for patient extrication in these situations.
Once the patient is in a safe environment, trained personnel must complete rapid assessment for injuries and illnesses. In most cases, these patients are likely to have multiple complaints including traumatic injuries, hypothermia, and potentially, respiratory distress from inhalation of water. They will require aggressive management and transport to the nearest appropriate facility for evaluation and treatment.
EPIDEMIOLOGY AND PATHOPHYSIOLOGY
The maintenance of the normal core body temperature is dependent on the body's inherent metabolism as well as the interaction with surrounding environmental conditions promoting heat loss. The human body functions optimally with a core temperature between 36.4°C and 37.5°C. Hypothermia is defined as an unintentional decrease in core temperature to less than 35°C (95°F) with severe hypothermia categorized as a body core temperature less than 28°C (82.4°F). At this temperature, body systems responsible for maintenance of homeostasis begin failing and further insult can occur easily.
Hypothermia occurs primarily due to three factors: decreased heat production, increased heat loss, and impaired thermoregulation. In order to maintain “normothermia,” multiple body systems must be operating optimally to ensure homeostasis. To promote cellular respiration and metabolism, sufficient quantities of fuel (ie, food) must be available for consumption. Hypoglycemia can further exacerbate the inability of body temperature maintenance. Heat production can also be limited due to endocrinologic inadequacies including hypothyroidism and hypopituitarism. Other systemic failures can also further impair thermoregulation, including the inability to shiver, extremes of age, and inactivity.
The most common reason, however, for hypothermia is due to heat loss.9,10 Each year, there are multiple cases of fatalities due to environmental exposure with greater than 50% of these fatalities occurring in elderly patients in urban areas.9 It is important to identify the causative factors associated with primary hypothermia (accidental hypothermia) in order to treat patients effectively. Heat loss occurs as a result of the patient's interaction with surrounding environment through evaporation (cooling by conversion of fluid to vapor), conduction (transfer of heat by direct contact), convection (transmission of heat by moving particles), and radiation (nonparticulate heat emission). Heat loss can be further exacerbated through vasoactive medications, including illicit drugs, as well as damage to the skin seen in large-scale burns.
When treating patients with cold-related injuries, it is important to identify that there is a spectrum of illness seen with a decrease in body temperature. Mild and moderate hypothermia will be discussed in further detail in later chapters. Severe hypothermia is defined as a core temperature of less than 28°C (or 82.4°F). Patients with severe hypothermia have significant alterations in critical body systems. These patients typically will present obtunded and comatose with noted global loss of cerebral reflexes. EEG activity, if measured, will be minimal or completely silent with temperatures less than 26°C.9,10 Ocular reflexes will not be present concurrently.
As with all other body systems in hypothermia, the cardiovascular system will be significantly affected. Cardiac output will be decreased significantly and is readily apparent in noted hypotension that may not be correctable with vasoactive medications. As the temperature continues to drop, the myocardium will also have noted sequelae. Bradycardia occurs initially and is followed by myocardial irritability, as evidenced by cardiac dysrhythmias. These include Osborn waves and prolongation of the PR, QRS, and QT intervals.9–11 (Figure 37-1). The 12-lead tracing shows Osborn waves (J waves) in leads II, V5, and V6. With further decreases in temperature less than 28°C, the myocardium is susceptible to ventricular fibrillation and eventually asystole.
Noted Osborn or J waves in leads II, V5, and V6 in a 88-year-old male with hypothermia.
As patient's temperature decreases significantly, further organ system failures can occur. Similar to the effects categorized previously, patient's respiratory status deteriorates with additional cooling. Depression of the respiratory centers result in blunting of airway reflexes, bradypnea, and eventually, respiratory arrest occurs if the cooling is not corrected.9–11 Pulmonary edema can occur with rewarming and reassessment is vital to maintain appropriate oxygenation and ventilation. Renal failure, hypoglycemia, frozen or poorly perfused extremities, coagulopathy are all additional sequelae seen in severe hypothermia (Table 37-1).
Signs and Symptoms of Severe Hypothermia
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Signs and Symptoms of Severe Hypothermia
|Organ System ||Clinical Manifestations in Severe Hypothermia |
|Nervous system || |
Altered mental status, confusion
Loss of ocular reflexes, and dilated/fixed pupils
Decrease in or loss of EEG activity
|Cardiovascular system || |
Bradycardia, Osborn/J waves
Hypotension, loss of peripheral pulses dysrhythmias
|Respiratory system || |
|Renal system ||Oliguria, loss of renal perfusion |
|Hematologic system ||Thrombocytopenia, anemia, leucopenia, coagulopathy |
|Musculoskeletal system ||Muscular rigidity, frostbite |
Management of the severely hypothermic patient requires an understanding of human pathophysiology combined with a rapid assessment of the insult that the patient has encountered. Initial actions focus on the removal of environmental stimulus, the prevention of further cooling, and evaluation of other associated conditions. Once placed in a safe environment, attention is then focused on aggressive rewarming. Similar to other types of resuscitations, initial assessment and treatment focuses on basic cardiopulmonary stabilization.
If the patient is obtunded at the time of initial patient contact, consideration must be made to ensure that the etiology of the patient's altered mental status is due to hypothermia. During the initial assessment, blood glucose and evaluation of pupils to assess the possibility of narcotic use may be completed while initiating other critical interventions. The determination of the patient's temperature should also occur early in the resuscitation. Esophageal probe placement or rectal temperatures are the most accurate means of assessing core temperature. Continuous temperature monitoring is required in patients with severe hypothermia during the rewarming process.
Immediate attention should be focused on determining whether patients have a patent airway and are oxygenating appropriately. If the patient is breathing on her or his own and is protecting the airway, warm humidified oxygen can be applied. In most cases of severe hypothermia, the patient will require endotracheal intubation for airway protection and establishment of a definitive airway. It is important to note that neuromuscular blockade used in rapid sequence intubation (ie, rocuronium and succinylcholine) will not work in patients with body temperatures less than 86°F and should be avoided.9–11 If the jaw is clenched, nasotracheal intubation or other BLS maneuvers may be necessary to maintain the airway.
After the definitive airway is placed, an orogastric tube can be placed to relieve gastric distention. Lastly, a Foley catheter can be placed to monitor urine output during the course of the rewarming process. There are now several companies that manufacture catheters with temperature sensors to aid in monitoring body temperatures during the resuscitation.
Once the initial stabilization has occurred, aggressive active rewarming must then take place. Fluid resuscitation should immediately begin with intravenous fluids heated to 40°C - 42°C. These fluids will not actively rewarm the patient; rather they will prevent further heat loss.9,10 In many cases, the crystalloid administered will treat associated hypotension. It has been recommended not to use lactated Ringer in these resuscitations due to liver's inability to metabolize lactate effectively when in a hypothermic state.10
Although the treatment for severe hypothermia is rewarming, there is little agreement in how to complete this task effectively without additional injury. In patients with severe hypothermia, there is little role for passive rewarming methods. As noted previously, initial treatment methods focus on arresting further hypothermic insult. Therefore, active rewarming methods are required to treat this subset of patients.
Active external rewarming utilizes a variety of methods to treat severe hypothermia.12 Each method, however, has its controversies and side effects.13–15 Devices used include hot water immersion, heated blankets, forced air rewarming, and heating pads. Immersion in hot water has been long utilized in patients with mild to moderate hypothermia. However, it is not typically used in severely affected patients due to the fact that appropriate monitoring and resuscitation cannot occur easily. Burns and thermal injuries can occur with the use of heating blankets, pads, and radiant heat sources. Forced air rewarming (ie, Bair Huggers) can be used appropriately, will prevent further heat loss, and provide radiant heat transfer. External rewarming techniques, however, can cause peripheral vasodilation, which can exacerbate noted hypotension. Further complications can occur due to the transport of cold blood to the core, resulting in a core temperature decrease (afterdrop) before results of treatment are seen.
Recent development in technology in the last several decades has focused on active core rewarming. These internal rewarming techniques began with the instillation of fluids into truncal cavities. Heated irrigation has been used in peritoneal dialysis as well as closed thoracic lavage.10,11,16 Both methods instill large volumes of fluid into noted cavities; however, these require specialized training and knowledge of surgical techniques.
Additionally, there are other methods used in extracorporeal blood rewarming, including hemodialysis, arteriovenous rewarming, venovenous rewarming, and cardiopulmonary bypass. Dialysis has been used successfully in patients who not only require active core rewarming, but also concurrent treatment for severe renal dysfunction and the removal of certain ingested toxins. Cardiopulmonary bypass is the most efficient core rewarming technique and can raise temperatures 1°C to 2°C every 3 to 5 minutes, but is labor intensive and not available at all facilities.10,11
As the human body core temperature drops in severe hypothermia, the patient's myocardium becomes more irritable and is prone to significant cardiac dysrhythmias, resulting in compromised cardiac output. As with other critical systems, the primary treatment is to rapidly warm the patient. Most dysrhythmias will resolve spontaneously once the core body temperature is increased toward baseline. Initially, circulatory support by health care providers is dependent on identifying whether a pulse is present. Nonlethal rhythms including bradycardia and atrial fibrillation require basic supportive care and careful handling. At temperatures less than 32°C (86°F), the possibility of converting a patient from a nonlethal rhythm to ventricular fibrillation, ventricular tachycardia, or asystole is increased according to the irritability discussed previously.10,11 These patients require gentle handling to minimize risks of spontaneous conversion.
Those hypothermic patients without a pulse require aggressive rewarming in addition to extensive resuscitation measures. If the patient is found to be in ventricular fibrillation or ventricular tachycardia, an initial defibrillation is warranted. Typically, attempts will be unsuccessful at temperatures less than 32°C; however, aggressive rewarming should occur with concurrent CPR and airway management.11 As the temperature is increased 1-2 degree Celcius, additional attempts at defibrillation can occur. Once the body temperature achieves 30°C to 32°C (86°F to 89.6°F), antidysrhythmic and vasoactive medications can be utilized successfully.10,11 Given that the body's metabolism is altered at low temperatures, the lowest indicated dose is indicated in hypothermia patients. Higher levels of these medications can lead to systemic toxicity.
Antidysrhythmic and vasoactive medications are useful adjuncts in patients with severe hypothermia. However, their efficacy remains largely unknown. Treatment should focus on aggressive rewarming rather than standard advanced cardiac life support protocols.
If the patient continues to remain hypotensive during the resuscitation, warm intravenous fluids are indicated for volume replacement. Vasopressor therapy has minimal effect on persistent hypotension and can result in worsening dysrhythmias.
Patients with severe hypothermia require an efficient and multifaceted approach during resuscitation. Aggressive rewarming must occur simultaneously with other resuscitative techniques. With this combination of therapies, effects seen after a significant drop in core body temperature, specifically a core afterdrop, will be minimized. Even though the effects of the initial insult can be mitigated with initial treatment, numerous other complications can occur after the patient is rewarmed including rhabdomyolysis, electrolyte imbalance, ARDS, and disseminated intravascular coagulation. Continued monitoring and reassessments will be required to ensure a successful outcome.
Hyperthermia is the elevation of core body temperature due to an excess of heat production, and inability to decrease heat transfer to the ambient environment. Similar to the continuum of severity of illness seen in hypothermia, heat-related effects occur in a like fashion, based on the degrees above normal body temperature. The key difference, however, is that once the core temperature reaches 105.8°F (41°C), cellular apoptosis occurs and complex proteins begin to break down.11 If uncorrected, significant physical impairment and noted sequelae can occur. There is a significant morbidity and mortality related to thermal illness with heat stroke, resulting in the death of greater than 12% of adult patients with body temperatures in excess of 41°C.11 Thus, aggressive treatment to minimize these effects is essential to ensure appropriate outcomes.
There is a significant difference between heat-related illness and basic fevers. Febrile illness is normal physiologic response by the body that results in an elevation of core body temperature by pyrogenic stimuli (ie, infection). This elevation remains under the control of thermoregulatory centers in the hypothalamus and brainstem and rarely exceeds 41°C.17 In heat-related illness, however, there is no thermoregulation and thus body temperatures increase unchecked, leading to significant physiologic injury. It is also critically important to differentiate between heat-related illness and that of malignant hyperthermia (MH) that occurs secondary to a triggering agent. These include such medications as volatile halogenated anaesthetic agents and depolarizing muscle relaxants. Malignant hyperthermia has also noted sequelae including rigidity, and hypercapnia which is not identified in patients with heat stroke. Lastly, MH can be corrected with the use of dantrolene, whereas heat stroke requires rapid cooling by traditional means.17
Heat-related illness occurs primarily in warm climates and is exacerbated by conditions affecting thermoregulatory control. These include mental illness, chronic medical conditions, occupational hazards, and insufficient acclimatization. Rapid increases in body temperature occur when heat production occurs unchecked, and heat dissipation is inhibited. Signs and symptoms occur at various degrees of severity ranging from the mild discomfort related to heat stress to the emergent sequelae of heat stroke. The mild to moderate conditions of heat-related illness are outlined in Chapter 47. The remainder of this section will focus on the identification and treatment of the emergent heat stroke.
Heat stroke is the third leading cause of death behind cardiac disorders and head/ neck trauma in athletes.11,18 Between 350 and 400 deaths occur annually, of which almost 50% occur due to ambient weather conditions.18 All humans are at risk for heat-related illness; however, the population of the young, elderly, and those with chronic conditions, which inhibit appropriate thermoregulations, can be particularly affected. Heat stroke is defined as an elevation of core body temperature to greater than or equal to 41°C with accompanying alterations in the central nervous system (CNS), including altered mental status, ataxia, and other neurologic sequelae.
Heat stroke has been further delineated into classic and exertional, based on the mechanism of injury. Classic heat stroke occurs primarily in compromised patients over the course of several days, usually during environmental conditions which include elevated temperature and humidity. Typically, patients with classic heat stroke present with anhydrosis, but this is not a firm criterion. This population of patients will also present with CNS dysfunction that is manifested by altered mental status, seizures, or coma. In addition, patients can present with signs and symptoms consistent with systemic volume loss from earlier diaphoresis and other insensible losses. Tachycardia, hypotension, and respiratory alkalosis from hyperventilation can be seen in some of these patients.
Exertional heat stroke occurs primarily in poorly acclimatized young patients including athletes and military personnel who participate in strenuous activities and are not adequately prepared for the conditions. These patients present not only with elevated core body temperatures and CNS alteration, but they also demonstrate sequelae resulting from significant hypovolemia. Common manifestations include severe tachycardia, hypotension, and tachypnea. Gastrointestinal signs and symptoms make occur as well including nausea, vomiting, and diarrhea, thus exacerbating the noted dehydrated state even further.
As a result of these sequelae, patients with exertional heat stroke can develop significant lab abnormalities including acute renal failure (increased BUN and creatinine), rhabdomyolysis (elevated CPK), and in extreme cases disseminated intravascular coagulation (DIC). Alterations in electrolytes also occur as a result of the acute volume loss including hypokalemia, hypocalcemia, and hypoglycemia. Lactic acidosis and liver dysfunction can also occur.
When patients present with CNS dysfunction in a warm environment, it is critical that the provider differentiate between heat-related illness and acute hyponatremia. With serum sodium levels less than 130 mmol/L, alterations in sensorium, seizures, and obtundation can occur.18 Health care providers must assess core temperatures in order to differentiate between the two diagnoses. Exertional hyponatremia can occur in similar environments. However, the hyponatremia is due to an excessive amount of water intake prior to, during, and after physical exercise without attention to simultaneous salt loss. If the sodium is not corrected, persistent seizures, coma, and even death may occur (Table 37-2).
Signs and Symptoms of Heat Stroke
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Signs and Symptoms of Heat Stroke
| ||Clinical Manifestations of Severe Hyperthermia: Heat Stroke |
|Organ System ||Temperature Greater Than 41°C |
|Nervous system || |
Altered mental status: confusion, ataxia, obtundation
Dizziness, vertigo, syncope
|Cardiovascular system ||Tachycardia, hypotension, hypovolemic shock |
|Respiratory system ||Tachypnea |
|Renal system ||Prerenal azotemia, electrolyte abnormalities |
|Hematologic system ||Thrombocytopenia, anemia, coagulopathy |
|Skin ||Anhydrosis, hot and flushed skin, diaphoresis |
Treatment of heat stroke requires prompt assessment of critical systems and prompt cooling. Airway, breathing, and circulation must be addressed immediately. With CNS alteration, airway management must be an initial consideration. Simultaneously, the patient must be removed from further exposure followed by rapid cooling. In cases where there is potential for rapid deterioration of the patient, survival from heat-related illness is significantly increased with cooling that brings core body temperature to within normal limits within 30 to 60 minutes of identification.18,19
There are a variety of techniques that can be used to cool patients rapidly. Each has a level of efficacy and can be applied based on the condition of the patient. As noted, the first interventions required are to remove the patient from the heat source, and to remove any clothing that is impeding heat dissipation. In the prehospital environment, air conditioning, and icepacks to critical areas including the groin, axilla and anterior portions of the neck are reasonable locations to initiate cooling. The most effective method of rapid cooling is to immerse patients in cold water baths.11,17–19 If the patient is critically ill (requiring airway management and other invasive procedures), this may be impractical or impossible depending on the circumstances.
Techniques derived from desert warfare place hyperthermic patients on mesh stretchers and regularly douse them with cold water, while simultaneously operating large fans to drop temperatures through evaporative heat loss.11,18 Although studies comparing the two above methods have not been completed, the two techniques may be useful for different patient populations.
Once cooling has been initiated and addressed, additional treatment of related complications can occur. Patients with CNS dysfunction including persistent seizures will require benzodiazepines. These will include lorazepam at doses between 2 to 4 mg IV with a maximum of 8 mg IV during a 12-hour period. The patient with volume depletion will require extensive rehydration. Intravenous access may be initially difficult to obtain, given patient's fluid status. However, newer options including intraosseous access may be useful. Vasopressor and inotropic support is rarely indicated given the etiology of the hypovolemia and these medications can cause further harm by releasing catecholamines that may further elevate core body temperature. Rhabdomyolysis can occur with severe cases of heat illness. Adequate fluid resuscitation and alkalinization of the urine can minimize the renal effects of muscle breakdown and subsequent myoglobin release. Cardiopulmonary effects including dysrhythmias typically resolve with normalization of core body temperatures.
Severe heat-related illness with body temperatures of greater than 41°C and concurrent CNS dysfunction is considered a life-threatening emergency.17–19 Irreversible damage can occur at these temperatures in as little time as 45 minutes.18 Immediate cooling and supportive care of critical systems are essential in minimizing the sequelae of hyperthermia.
When patients suffer from the effects of hyper- and hypothermia, a spectrum of complications can occur. In severe cases, it is imperative that the provider completing these critical resuscitations have a clear understanding of the underlying pathophysiology in order to best treat these populations of patients successfully. With aggressive and well-directed therapy, outcomes can be successful and adverse effects can be minimized.
Patients who have had a mechanical obstruction due to a liquid medium regardless of outcome are said to have been involved in a drowning incident.
The choking response is the first insult that occurs during the drowning process.
If patients suffer from a “true” drowning, there will be fluid noted within the lungs.
There has been no identifiable difference between overall outcomes of patients who suffer from drowning between fresh and saltwater.
Overall prognosis in drowning incidents can be evaluated at the time of hospital arrival. Those who arrive awake, alert, and in no acute respiratory distress tend to survive without sequelae. However, those who arrive obtunded with a GCS less than 5 have poor survival outcomes.
Resuscitation should focus on restoring baseline oxygenation and ventilation as quickly as possible to limit any anoxic brain injury.
Swiftwater rescue requires proper training and preparation to ensure successful retrieval of victims. Basic ICS principles and protocols are typically used in combination with the “talk, reach, throw, row, go” mantra of swiftwater rescue.
Severe hypothermia is defined as a body core temperature of less than 28°C (82.4°F).
Hypothermia can occur due to heat loss or lack of heat production.
In severe hypothermia, all critical systems are affected including nervous, cardiovascular, respiratory, and hematologic.
Restoration of function is dependent on aggressive active core rewarming. Rewarming techniques include removal from cold environment, radiation heat therapy, warm IV fluids, and if available invasive core rewarming techniques (dialysis or cardiac bypass).
Defibrillation and the use of ACLS and vasopressor medications are considered ineffective until body core temperatures reach 30°C -32°C. They should be avoided until body temperature reaches this temperature to avoid toxicity.
In situations where return of spontaneous circulation is a possibility (ie, exclusion of lethal injuries including frozen chest, decapitation) cardiopulmonary resuscitation and rewarming should occur should continue until 30°C-32°C is achieved.
In patients with severe hypothermic injuries, complications occur routinely and should be expected including rhabdomyolysis, ARDS, DIC, and renal abnormalities.
Heat stroke is defined as an elevation of core body temperature to greater than or equal to 41°C with accompanying alterations in the central nervous system (CNS), including altered mental status ataxia and other neurologic sequelae.
Classic heat stroke occurs primarily in compromised patients over the course of several days, usually during environmental conditions which include elevated temperature and humidity leading to elevated core temperatures and altered sensorium.
Exertional heat stroke presents in patients who have been participating in rigorous physical activity in a hot environment leading to an elevation in body core temperature, CNS dysfunction, and concurrent hypovolemia.
Severe heat-related illness can affect multiple critical organ systems, leading to CNS dysfunction, hypovolemic shock, electrolyte abnormalities, and renal failure.
In severe heat stroke, treatment focuses on decreasing core body temperature as rapidly as possible to minimize the effects of the heat-related illness.
Cooling techniques include cold water immersion, evaporative heat loss (cooling in front of a fan), ice packs to the groin and axilla, cool IV fluids.
Additional treatment for complications includes benzodiazepines for seizures, airway management, IV hydration, and alkalinization of the urine for rhabdomyolysis.
Drowning: a review of epidemiology, pathophysiology, treatment and prevention. Resuscitation. December 2004;63(3):261–268.
Drowning: update 2009. Anesthesiology. June 2009
110(6):1390–1401. PubMed PMID: 19417599.
Cardiac arrest due to drowning—changes over time and factors of importance for survival. Resuscitation
. May 2014;85(5):644–648.
PK. Drowning in children: Utstein style reporting and outcome. Acta Anaesthesiol Scand. May 2014;58(5):604-610. doi: 10.1111/aas.12298. Epub 2014 March 3.
Drowning related out-of-hospital cardiac arrests: characteristics and outcomes. Resuscitation. August 2013;84(8):1114–1118.
Drowning and near-drowning in children and adolescents: a succinct review for emergency physicians and nurses. Pediatr Emerg Care. September 2005;21(9):610–616.
Drowning and near drowning: a pediatric epidemic. Pediatr Ann. June 2000;29(6):360–366.
Swiftwater Rescue: A Manual for the Rescue Professional. Asheville, NC: CFS Press; 1997.
The evaluation and management of accidental hypothermia. Respir Care. February 2004;49(2): 192–205.
Accidental hypothermia. Crit Care Clin. April 1999;15(2):235–249.
Environmental illness in athletes. Clin Sports Med. July 2005;24(3):695–718, x.
Surviving two hours of ventricular fibrillation in accidental hypothermia. Prehosp Emerg Care. July-September 2014;18(3):446–449.
Comparison of heat donation through the head or torso on mild hypothermia rewarming. Wilderness Environ Med. March 2014;25(1):4–13.
Mobile warming: lessons learned in hypothermia prevention under difficult field conditions. JEMS. October 2012; 37(10):46–48.
Field torso-warming modalities: a comparative study using a human model. Prehosp Emerg Care.
Van der Ploeg
Accidental hypothermia: rewarming treatments, complications and outcomes from one university medical centre. Resuscitation. November 2010;81(11):1550–1555.
DS. Heat illness and heat stroke. Pediatr Rev. July 2007;28(7):249-258. Erratum in: Pediatr Rev. December 2007;28(12):469.
Heat-related illness in athletes. Am J Sports Med. August 2007;35(8):1384–1395. Epub 2007 Jul 3.
Heat-related illness. Emerg Med Clin North Am
. May 2004;22(2):315–327, viii.