ENVIRONMENTAL EMERGENCIES

0733-8627/97 $0.00

PEARLS, PITFALLS, AND UPDATES

+ .20

ENVIRONMENTAL EMERGENCIES Russ Braun, MD, MPH, FACEP, and Scott Krishel, MD, MPH

Environmental exposures and emergencies are - occurring more frequently owing to a greater interest in outdoor activities, and especially because of the public’s interest in more extreme and challenging endeavors. The emergency physician should have current information relevant to potential environmental emergencies and how to handle them and should know where to obtain additional information on these areas. For a complete review of environmental topics relevant to emergency medicine, the following text is recommended: ”Management of Wilderness and Environmental Emergencies, ed 2.” edited by colleagues in our specialty; Paul S. Auerbach and Edward C. Geehr. This article focuses on pearls and pitfalls of high-altitude sickness, decompression sickness, and barotrauma; new findings relevant to the near-drowning patient; continued controversies on hyperbaric oxygen for carbon monoxide poisoning; pitfalls in hypothermia management; and updates on the management of venomous snakebites.

High-Altitude Sickness* More than 40 million people a year travel above 8000 feet in the United States. As these numbers increase, more physicians will be called on to diagnose and manage high-altitude illnesses. This article reviews the presentation and management of acute mountain sickness, high-altitude pulmonary edema, and high-altitude cerebral edema. At altitudes above 1500 m (4900 ft), the partial pressure of oxygen decreases, *This section prepared by Scott Krishel, MD, MPH.

From the Department of Emergency Medicine, Highland General Hospital, Oakland (RB); and the Department of Emergency Medicine, UCSD Medical Center, San Diego (SK), California

EMERGENCY MEDICINE CLINiCS OF NORTH AMERICA

-

VOLUME 15 NUMBER 2 MAY 1997

451

452

BRAUN &I KRISHEL

and the higher the altitude, the lower the partial pressure. This decreased ambient pressure of oxygen diminishes the gradient along which the oxygen travels from the alveolus to cell, resulting in hypoxia. The arterial blood gas Paoz at 5000 ft is approximately 80 mm Hg, at 7500 feet it is 70 mm Hg, and at 15,000 feet it is 50 mm H g 4 Hypoxia is a stimulus to the body that drives changes in the pulmonary, circulatory, and central nervous systems. Climbers begin to hyperventilate as they ascend a mountain, and the degree of hyperventilation is proportional to the degree of hypoxia. The hyperventilation leads to a respiratory alkalosis. There is an increase in tidal volume, an elevation of the alveolar and arterial partial pressure of oxygen, and a greater diffusion gradient between the blood and tissues.2, The pulmonary circulation constricts in response to the hypoxia, resulting in an increase in the pulmonary pressure. The hematocrit increases, initially owing to a decrease in plasma volume from a bicarbonate diuresis, and fluid shifts from the intravascular space. Within 4 to 5 days, red blood cell production is stimulated, resulting in an increase in the oxygen-carrying capacity and viscosity of the blood, The number of capillaries to carry oxygen increases, as well as an increase in the density of mitochondria and the concentration of cyto~hrome.~ The illnesses of high altitude are primarily caused by hypoxia and the pulmonary and circulatory changes that occur in response to the hypoxia. ACUTE MOUNTAIN SICKNESS Pathophysiology

Acute mountain sickness (AMS) is a constellation of symptoms that usually develop within the first 24 hours of a rapid ascent to 2000 m (6600 ft) or higher. Up to one third of people with an abrupt ascent to a height of 2500 m (8200 ft) will develop AMS9 Forty percent to 70% of those who reach an altitude of 4500 m (15,000 ft) or more will also develop the syndrome. Headaches are the most prominent complaint and can be severe. Other symptoms include shortness of breath, extreme fatigue and lassitude, insomnia, irritability, vertigo, memory deficits, tinnitus, and anorexia, nausea, or vomiting. The physical findings are nonspecific, and vital signs are usually normal. The most common finding is fluid retention, resulting in edema of the extremities and the face. Many people will develop peripheral edema, yet show no other signs or symptoms of AMS. Additionally, up to 20% will have rales on pulmonary examination. The duration of the symptoms of AMS is related to the sleeping level altitude. At levels below 10,000 ft, most people will be symptom-free in 4 days; at levels above 10,000 to 15,000 ft, the syndrome may last for a few weeks. Climbers of the higher altitudes who develop AMS and go untreated are also more likely to develop cerebral edema or pulmonary edema. Although hypobaric hypoxia is the underlying cause of AMS, the exact causes of the symptoms are unclear. The aldosterone and antidiuretic hormone feedback loops appear to be inhibited, resulting in fluid overload. The fluid overload can cause peripheral edema and can contribute to pulmonary and cerebral edema. Mild cerebral edema is probably the most important cause of the symptoms of AMS.Z,4, Prevention and Treatment

Prevention of the syndrome can be accomplished by acclimatization, by a slow ascent of no more than 350 m/d, or by taking acetazolamide. Acetazolam-

ENVIRONMENTAL EMERGENCIES

453

ide is a carbonic anhydrase inhibitor and causes a metabolic acidosis by enhancing the kidney excretion of bicarbonate ions. The metabolic acidosis stimulates ventilation with a resultant increase in the rate and depth of breathing. This medication-induced hyperventilation leads to an increase in the person's oxygen tension. It also causes a diuresis, which helps to alleviate the general fluid overload that occurs with AMS. Acetazolamide administration of 500 mg daily begun in the 24 hours before ascent, has been shown to significantly reduce the incidence and severity of AMS.6, Side effects of acetazolamide include parasthesias of the hands and feet, nausea, vomiting, and urinary frequency. The mainstay of treatment is to descend once symptoms have developed, because the syndrome may progress in severity despite only minimal initial complaints. Descending as little as 500 meters can provide relief. Oxygen will also alleviate the symptoms and should be used if available. Acetazolamide can be given after symptoms have begun, and should be continued until the individual is completely well.3 Dexamethasone also has been shown to decrease the incidence and severity of symptoms of AMS, but has more side effects than acetazolamide and is associated with a rebound of symptoms?, 5, Because acetazolamide is a sulfa compound, dexamethasone can be given for prophylaxis or treatment, if the person is allergic to sulfa drugs. If the climber does not respond to descent, oxygen, and medical management, then hyperbaric oxygen (HBO) may be required. HBO can also be used in place of descent, if descent is not possible because of weather or other factors prohibiting a timely descent. HIGH-ALTITUDE PULMONARY EDEMA Pathophysiology

High-altitude pulmonary edema (HAPE) is much less common than AMS, occurring in approximately 1% to 2% of those who rapidly ascent to 3000 m? The decrease in partial pressure of oxygen with increasing altitude leads to a pulmonary overperfusion hydrostatic leakage of exudative fluid into the alveoli. High pulmonary flow and pressure, in addition to altered membrane integrity, are believed to contribute to the pulmonary edema. It is a noncardiogenic pulmonary edema with normal left ventricular filling pressures, elevated pulmonary artery pressure, normal to low pulmonary capillary wedge pressure, and arterial desaturation.2,lo Symptoms of HAPE include shortness of breath, cough, hemoptysis, fatigue, and confusion, and begin anywhere from 6 hours to 4 days after arrival at altitude. Because of arterial desaturation during sleep, people may initially feel ill during the night. Physical findings include tachypnea and respiratory distress, tachycardia, hypotension, cyanosis, frothy sputum, decreased urine output, decreased mental status, and pulmonary rales. HAPE may be unilateral or bilateral, and thus chest radiograph findings include unilateral or bilateral pulmonary edema, with a normal heart size. Acute right-side heart strain may be evident on an electrocardiogram. Most people who develop HAPE have no history of AMS and have no pre-existing cardiac or pulmonary disease. It occurs in men and women and is more common in adolescents and those that reascend after climbing down to a lower elevation. Treatment

The single most important aspect of management is early recognition of the syndrome and immediate descent. Any decrease in exercise tolerance, dyspnea

454

BRAUN & KRISHEL

at rest, or new cough should be considered a possible sign of early HAPE. Failure to appreciate the onset of pulmonary edema with subsequent descent leads to increased mortality. One large retrospective study on HAPE found an overall mortality rate of 11%in those that descended and 44% in those that did not.* If the edema is diagnosed early, oxygen alone is sufficient to increase oxygen saturation and lower pulmonary artery pressure, and can completely resolve mild cases in 2 to 3 days. Oxygen should be given if available, and may be life-saving if immediate descent is not possible. Acetazolamide does not significantly reduce the incidence or severity of HAPE. Digoxin does not help, and morphine should be used with caution because it is a respiratory depressant. Although some authors have found that lasix may be helpful to decrease symptoms of AMS, others have found that it may exacerbate circulatory abnormalities and may predispose to pulmonary embolism.z, Administering nifedipine to patients with HAPE has been shown to reduce pulmonary artery pressure and enhance the clearing of alveolar edema, and should be considered.', 8, It is unclear if prophylactic nifedipine decreases the severity and incidence of HAPE. HBO may be considered for those who do not respond to descent and oxygen. The treatment of HAPE should otherwise be the same as with other causes of noncardiogenic pulmonary edema.

HIGH-ALTITUDE CEREBRAL EDEMA High altitude cerebral edema (HACE) develops in those with AMS or HAPE. Hypoxia-induced alterations in the blood-brain barrier and increased cerebral blood flow are believed to be responsible for the cerebral edema. The increased cerebral blood flow is primarily a reflex response to the reduced oxygen saturation. Symptoms include headache, insomnia, nausea, vomiting, irritability, ataxia, mental status changes, cranial nerve palsies, paralysis, and seizures. Papilledema can be found in approximately 50% of patients. As with HAPE, early recognition, descent, and oxygen are the mainstays of management. Dexamethasone may decrease the cerebral edema and should be considered. HBO can be considered if the person does not improve with descent. Treatment should otherwise be supportive and approached in a similar manner to other causes of cerebral edema. In addition to HACE, it is also important to consider other causes of altered mental status, focal neurological deficits, or seizures. The high altitude may unmask or exacerbate previously existing neurologic problems. There are also individuals who develop transient ischemic attacks and hemorrhagic and nonhemorrhagic strokes without significant cerebral edema. A CAT-scan of the head should be considered on anyone whose altered mental status or neurologic findings do not resolve with oxygen and descent.

References 1. Bartsch P, Maggiorini M, Ritter M, et al: Prevention of high-altitude pulmonary edema. N Engl J Med 3251284-1289, 1991 2. Coote JH: Medicine and mechanisms in altitude sickness: Recommendations. Sports Med 20:148-159, 1995 3. Grissom CK: Acetazolamide in the treatment of acute mountain sickness: Clinical efficacy and effect on gas exchange. Ann Intern Med 116:461, 1992 4. Hackett PH. High altitude medical problems. In Tintinalli J, Krome R, Ruiz E (eds):

ENVIRONMENTAL EMERGENCIES

4%

Emergency Medicine: A Comprehensive Study Guide, ed 4. New York, McGraw-Hill, 1996, pp 670-678 5. Hackett P H Dexamethasone for prevention and treatment of acute mountain sickness. Aviat Space Environ 59:950, 1988 6. Hackett PH, Rennie D Acute mountain sickness. Semin Respir Med 5:132-140, 1983 7. Hackett PH, Roach RC: High altitude medicine. In Aueurbach PS (ed): Wilderness Medicine: Management of Wilderness and Environmental Emergencies, ed 3. St. Louis, Mosby, 1995, pp 1-37 8. Oelz 0, Maggiorini M, Ritter M, et al: Nifedipine for high altitude pulmonary edema. Lancet 21241-1244,1989 9. Rom WN: High altitude environments. In Rom WN (ed): Environmental and Occupational Medicine, ed 2. Boston, Little, Brown and Co., 1992, pp 1143-1151 10. Tso E High altitude illnesses. Emerg Med Clin North Am 10:251-247, 1992 11. Yaron M, Honigman B High altitude illness. In Rosen P, Arkin RM (eds): Emergency Medicine: Concepts and Clinical Practice, ed 3. St. Louis, Mosby, 1992, pp 994-012

Decompression Sickness and Barotrauma* There are more than 3.5 million trained divers in the United States, many of whom will suffer from a variety of illnesses specific to divers. Most of these illnesses are related to the changes in absolute pressure that divers experience while diving. This article reviews the clinical presentations and management of decompression sickness and barotrauma. As one descends under water, the weight of the water increases the absolute pressure. The greater the depth, the greater the pressure. At 33 ft, the absolute pressure is 2 atmospheres, at 66 ft it is 3 atmospheres, and at 99 ft it is 4 atmospheres. Most people dive between 33 and 99 ft.3As pressure increases and decreases, as occurs during diving descent and ascent, respectively, the gases in body spaces and gas-filled organs change. It is the pressure-related changes of gases and gas spaces in the body that cause decompression sickness and barotra~ma.~, * DECOMPRESSION SICKNESS Pathophysiology

Decompression sickness (DCS) or the ”bends,” results from the evolution of gas bubbles within the body. Henry’s law states that under pressure, more gas will be dissolved in a liquid. As the ambient pressure increases with descent, more nitrogen gas becomes dissolved in tissues. As the ambient pressure decreases with ascent, the previously dissolved nitrogen needs to be eliminated. If there is a rapid reduction of pressure, there may be inadequate time for the elimination of the nitrogen from the tissues. The nitrogen will then come out of the tissues in the form of intravascular and tissue bubbles. 5, * The first is a The nitrogen bubbles lead to three types of pr~blerns.~, mechanical obstruction of the lymphatic and vascular systems. The second is an activation of the compliment and inflammatory mediators, and platelet and white blood cell aggregation. The final problem caused by the bubbles is tissue ‘This section prepared by Scott Krishel, MD, MPH.

456

BRAUN & KRISHEL

distention. These three mechanisms work together to cause increased blood viscosity, microvascular hypoperfusion, transcapillary fluid loss, and ischemic tissue damage. Clinical Presentations

Most people with DCS will begin to feel ill within 1 hour of surfacing from a dive. Only approximately 2% will have onset of their symptoms more than 6 hours after surfacing. The clinical effects of the bubbles are classically divided into two main categories. Type I DCS is a mild form affecting mainly the skin, lymphatics, and musculoskeletal areas. Type I1 DCS includes more seriously ill patients, and those with primarily neurologic changes. Another way to categorize the DCS a person is experiencing is by describing the organ systems affected.', 3, Joint DCS results in periarticular joint pain most frequently affecting the shoulders, elbows, hips, and knees. Approximately 70% of people with DCS will have joint pain with or without other symptoms. The pain is classically described as deep and dull and increases with movement. Inflating a blood pressure cuff around the joint may decrease the pain. Some patients will have numbness or dysesthesias around the affected joint, but these changes do not follow anatomic distributions and should not be considered a sign of neurologic decompression sickness. Cutaneous DCS can cause subcutaneous emphysema, pruritus, and scarlatiniform, erysipeloid, or mottled rashes called cutaneous marmarata. Lymphatic obstruction can cause a peau d'orange appearance of localized swelling. Pulmonary DCS, or the "chokes," develops in approximately 2% to 8% of patients and can be fatal.*,4, These patients experience paroxysmal cough, shortness of breath, and chest pain in response to massive venous air embolization. They may present with pulmonary edema, be in mild to severe respiratory distress, appear cyanotic, and be hypotensive or in shock. Recompression will usually result in complete reversal of symptoms, and patients with pulmonary DCS may do very poorly if they are not recompressed as soon as possible. Neurologic DCS is a serious form of DCS primarily affecting the spinal cord, although any part of the nervous system can be affected causing virtually any type of neurologic deficit. It occurs in approximately 20% of the patients. The lower thoracic, lumbar, and sacral spinal cord is most frequently affected. Patients will classically have transient back pain that radiates to the abdomen or chest shortly after a rapid decompression. Without treatment, paresthesisias develop in the legs, followed by paresis, bladder dysfunction, and paralysis. Treatment

The mainstay of management for all types of DCS is HBO, with treatment beginning as soon as possible. The time to instituting HBO is one of the main predictors of outcome, and DCS should be considered a true medical ernergenc~.~,If you do not know where to send a patient for HBO, you can call the Divers Alert Network (DAN) 24-hour medical emergency hotline at (919) 684-8111. All patients should be given high-flow oxygen and have an intravenous line established while waiting for transfer to the hyperbaric chamber. Owing to the impairment of microvascular blood flow and loss of intravascular fluids, many patients will require isotonic fluid resuscitation. Other treat-

ENVIRONMENTAL EMERGENCIES

457

ment modalities should be supportive and based on the person’s clinical presentation. Besides hemoconcentration, there are no other classic laboratory abnormalities associated with DCS. Controversy still exists surrounding the use of aspirin and steroids in the treatment of DCS. BAROTRAUMA

Boyle’s law states that as the pressure of a gas is increased, its volume is decreased. The expansion and contraction of gas in the natural air cavities of the body, as one descends and ascends in the water, can cause distortion and damage to the surrounding structures and is known as barotrauma. The middle ear, sinuses, and lungs are the most commonly affected areas. Divers suffer barotrauma much more frequently then decompression sickness. BAROTRAUMA OF DESCENT Middle Ear Squeeze

During descent, the surrounding pressure increases, which leads to a decrease in volume in any air cavity in the body. If the pressure inside the cavity is not equalized to the pressure outside the cavity, tissue damage will occur, resulting in a squeeze. The middle ear is the most common site of squeeze. The increase in external water pressure across the compressible tympanic membrane displaces it inwards. If the pressure is not equalized by forcing air into the middle ear by a Valsalva maneuver, then the tympanic membrane will be damaged or will rupture. The mucosa surrounding the middle ear cavity will swell, leading to hemorrhage within the middle ear. Patients complain of pain, vertigo, and variable amounts of hearing loss. If the membrane ruptures, the pain should resolve, but the patient may have increased vertigo with vomiting caused by caloric stimulation. The changes found on examination of the tympanic membrane range from retraction of the membrane, to hemorrhage within the membrane, to hemorrhage within the middle ear, to perforation of the membrane. If the membrane is intact, most will recover in approximately 2 weeks, and decongestants is the only treatment required. If the membrane is ruptured, the patient should be started on oral antibiotics and referred for follow-up audiometric testing? The patient should not dive or fly until he or she is completely recovered. Inner Ear Barotrauma

Inner ear barotrauma can also occur, resulting in perforation of the round or oval windows. These patients present with vertigo, tinnitus, nystagmus, ataxia, and hearing loss. The hearing loss is sensorineural, occurring immediately or developing over several days, and can be a partial or complete loss of hearing. The diagnoses should be suspected in a diver with hearing loss or vestibular symptoms. The initial management is bed rest with the head of the bed elevated, avoidance of loud noises, and no diving or All patients should be given otolaryngology follow-up as operative intervention will be considered if the patient does not improve within 1 to 2 days. Additionally, some advocate immediate surgical intervention if the symptoms are particularly severe.

458

BRAUN & KRISHEL

External Ear Barotrauma

External ear barotrauma occurs if the external auditory canal is blocked by cerumen, ear plugs, or other foreign bodies, and the occlusion prevents water from entering the canal as the diver descends. Hemorrhage, tissue collapse, or an outward bulging of the tympanic membrane will occur to compensate for the decreased volume of the air trapped in the auditory canal. The patients will complain of difficulty with valsalva, ear pain, or bloody otorhea. Physical findings include petechial hemorrhages in the canal, blood-filled blebs that may extend onto the tympanic membrane, or rupture of the tympanic membrane. The occluding object should be removed from the ear, the canal should be cleaned and then kept dry, and antibiotics should be given if there are any signs of infection. Sinus Squeeze

Sinus squeeze occurs if the sinus ostia, which are normally used to passively equalize the pressure in the sinus, are blocked during descent. Mucosal congestion and hemorrhage occur to compensate for the increased pressure and contraction of air within the sinus cavity. Sinusitis and rhinitis can have associated mucosal hypertrophy and congestion and block sinus ostia. The frontal sinuses are most commonly affected, followed by the maxillary sinuses, and the patients complain of severe pain over the sinus or adjacent teeth and may have bloody nasal discharge. Treatment includes topical and systemic decongestants to help drain the sinus. Antibiotics should be given to people with signs of secondary infection, and occasionally, submucosal hemorrhage and hematoma formation blocking ostia may require surgery. BAROTRAUMA OF ASCENT Reverse Squeeze

During ascent, the pressure surrounding the air cavities decreases, and the volume increases, resulting in a distention of the surrounding tissues. If the excess volume of gas in the air cavity is not allowed to be vented, the tissue distention will continue and cause injury, known as a "reverse squeeze." Barotrauma of ascent of the ear and sinuses occur much less frequently than barotrauma of descent, and present in a similar fashion. Treatment includes decongestants, no diving until all symptoms have resolved, and antibiotics for signs of infectiomR If the right and left middle ear pressure gradients are not the same during ascent, then there will be unequal stimulation of the vestibular apparatus, and the diver will experience ear pain and vertigo. This condition is called alternobaric vertigo and although it is usually transient, its acute onset during ascent can cause a diver to panic. Pulmonary Barotrauma

Pulmonary barotrauma is second only to drowning as a cause of death in SCUBA divingz, As with other air-filled cavities, the gas in the lungs will

ENVIRONMENTAL EMERGENCIES

459

expand as a diver ascends. Normally, the extra volume of gas is exhaled. If the gas is not allowed to escape, the lungs can become overinflated to the point of rupture. Failure of the expanding gases to escape can be caused by voluntary or inadvertent breath holding, or from local pulmonary obstruction owing to underlying lung disease, such as bronchospasm, bronchiolitis, and pulmonary secretions. The mildest form of pulmonary barotrauma is overdistention without rupture. These patients will complain hemoptysis, with or without chest pain. The injury is localized to the small area that was overinflated, and only symptomatic treatment is required. Chest radiographs will be normal or may reveal a small pleural effusion. Rupture of the overdistended alveoli into the interstitial space results in more serious injuries. Pneumomediastinum is produced if the air dissects to the root of the lung and into the mediastinum. These patients will present with chest pain, which is often exacerbated by breathing or coughing. A crunching sound synchronous with cardiac activity (Hammon’s sign) may be appreciated during physical examination. The chest radiograph reveals mediastinal air, but this finding can subtle and easily missed.* Subcutaneous emphysema can also be produced if the air dissects superiorly into the neck and supraclavicular fossae. These patients can present with swelling, crepitus, dysphagia, hoarseness, and sore throat. These conditions will begin immediately on surfacing or develop within a few hours of surfacing, and are usually benign. Treatment consists of observation, rest, and occasionally supplemental oxygen. HBO is only indicated for severe cases. Pneumothorax occurs infrequently and is caused by the alveoli rupturing into the pleural space. The patients will complain of chest pain and may have diminished breath sounds. Treatment is similar to other causes of uncomplicated pneumothorax and will depend on the size of the pneumothorax. Since intrapleural gas cannot be released into the environment, a simple pneumothorax can convert into a tension pneumothorax, resulting in syncope or shock. Arterial Gas Embolism

Arterial gas embolism (AGE) is the most dangerous clinical syndrome associated with gas expansion during ascent and accounts for approximately one third of fatal diving accidents.s,6Pulmonary veins around the alveoli can be injured owing to the overstretching of the lung during ascent. Alveolar gas can then enter the pulmonary venous circulation traveling to the heart and embolize throughout the systemic circulation. The brain is the most frequent organ affected, and people will become symptomatic immediately or within minutes of surfacing. The victims can be divided into two groups. The first group accounts for less than 5% of the cases, and these people will suffer immediate apnea and cardiac arrest. This presentation is believed to result from a lethal arrhythmia or from complete filling of the central vascular bed with air. The second group will present with varying neurologic and systemic signs and symptoms including altered mental status, loss of consciousness, hemiparesis, seizures, vertigo, visual disturbances and other sensory changes, and headaches. Any diver with a sudden loss of consciousness on surfacing should be assumed to have an arterial gas embolism, even though severe neurologic DCS may present in a similar fashion3 The physical findings vary, but asymmetric multiplegias frequently occur. A detailed mental status examination should be performed and

460

BRAUN & KRISHEL

include fluency of speech, comprehension, reading, writing, memory, calculation, tests for agnosia, apraxia, and right-left disorientation! Other pulmonary barotrauma is associated with arterial gas embolism, and a chest radiograph should be considered on all patients. Serum creatine kinase (CK) levels are elevated, and a level should be obtained. Smith and Neuman9 found a significant correlation between peak serum CK levels and clinical neurologic outcomes. It is hypothesized that the gas emboli distribute widely throughout the body to skeletal muscles, the heart, and other organs. Elevated CK levels may be marker for arterial gas embolism, as well as a predictor of outcome. Liver function tests are also elevated as a result of the systemic embolization of gas. Significant hemoconcentration in these patients has also been reported and is believed to be caused by diffuse endothelial injury from gas emboli allowing fluid to leak out of the vascular space.'O The amount of hemoconcentration may also be a predictor of outcome. Patients should be kept flat, 100% oxygen should be administered, hydration should be maintained with intravenous fluid, and other supportive care should be provided as needed. As with DCS, arterial gas embolism should be considered a medical emergency, and arrangements for HBO should be made immediately. Approximately two thirds of the patients will be completely cured with HB0.5 Some patients will recover spontaneously for unclear reasons, but should still be referred for HBO because subtle but permanent neurologic damage may result if not treated. References 1. Clenney TL, Lassen LF: Recreational scuba diving injuries. Am Fam Physician 53:17611774,1996 2. Dickey LS Barotrauma. In Rosen P, Barkin RM (eds): Emergency Medicine: Concepts and Clinical Practice, ed 3. St. Louis, Mosby, 1992, pp 985-993 3. Kizer KW: Dysbarism. In Tintinalli J, Krome R, Ruiz E (eds): Emergency Medicine: A Comprehensive Study Guide, ed 4. New York, McGraw-Hill, 1996 4. Kizer KW, Neuman TS: Meeting the challenge of scuba diving emergencies: Recognition, resuscitation, and recompression. Emergency Medicine Reports 12151-160, 1991 5. Lee TC, Neville K Barometric medicine. In Rom WN (ed): Environmental and Occupational Medicine, ed 2. Boston, Little, Brown and Co., 1992, pp 1133-1142 6. Leitch DR, Green R D Pulmonary barotrauma in divers and the treatment of cerebral arterial gas embolism. Aviat Space Environ Med 57931-938, 1986 7. Madsen J, Hink J, Hyledgaard 0:Diving physiology and pathophysiology. Clin Physiol 14597-626, 1994 8. Moon RE, Vann RD, Bennett PB: The physiology of decompression illness. Sci Am 273:70-77, 1995 9. Smith RM, Neuman TS: Elevation of serum creatine kinase in divers with arterial gas embolization. N Engl J Med 33019-24, 1994 10. Smith RM, Van Hoesen KB, Neuman TS Arterial gas embolism and hemoconcentration. J Emerg Med 12:147-153, 1994 11. Van Hoesen KB: Diving medicine. Emergency Medicine Symposium, Postgraduate Institute for Emergency and Primary Care Physicians, San Diego, CA, 1996, pp 259-257

ENVIRONMENTAL EMERGENCIES

461

Near Drowning* Drowning continues to be a problematic issue for the pediatric population, the leading cause of death in children under 5 years of age in California, Arizona, and Florida.* The focus of this section is to highlight epidemiologic trends, management issues, and prognostic factors for the near-drowning victim. EPIDEMIOLOGY LEADING TO PREVENTION In a retrospective incidence and cost analysis in California, the highest rates per 100,000 for near drowning (alive or dead) were found among males (3.6), Blacks (3.6), and children 1 through 5 years old (18.4).In this series, swimming pools accounted for 62% of events, other recreational sites 21%, and bathtubs 10%. Although there was an overall male predominance, females had twice the rate of bathtub near drownings (15% versus 8%). In addition, infants under 1 year of age had a 59% rate of bathtub submersions? There was a seasonal association with all near drownings (52% summer), yet no seasonal pattern in bathtub incidents. There was an overall mortality rate of 9%. Other identifiable risk factors for near drowning from national data include males (15 through 24 years old) and low socioeconomic status. Most studies suggest an association between bathtub submersions and inflicted intent as opposed to accidental cause? A retrospective review in Kings County (Washington), using reestablished criteria, determined that 8% (16 of 205) submersions in children 18 years old or younger likely to have been inflicted. Inflicted patients were younger (2.1 years old, median age), the youngest sibling in a large (3 or more children) household, most commonly occurring in bathtubs (56%), less likely to be revived by bystanders, and more likely to die. Pertinent physical findings consistent with abuse (old or multiple bruises, lacerations, burns, scars) were found in 69% of the inflicted submersion victims. Of interest, the authors report that only one of the submersions was classified as a homicide by the medical examiner, consistent with previous reports of the under-recording of infant homicide in the United States.15 The importance of public education, especially for parents, siblings, and caretakers of children, is highlighted by the work of Kyriacou and associates,8 reviewed below in the section on prognostic indicators. Their major finding was that immediate resuscitation before paramedic arrival is associated with better neurologic outcome, which supports the need for community education in cardiopulmonary resuscitation (CPR). A recent review was able to support and quantify an increased risk of near drowning in children with epilepsy, both in the pool and the b a t h t ~ b . ~ TREATMENT GUIDELINES REVISITED Advanced Cardiac Life Support (ACLS) Guidelines The most recent 1992 American Heart Association (AHA) Guidelines included an expanded section on special resuscitation situations, including near drowning. Specific recommendations included the following7: “This section prepared by Russ Braun, MD, MPH, FACEP

462

BRAUN & KRISHEL

1. Rescue breathing, with mouth-to-mouth technique, should be initiated as soon as possible, as long as the rescuer’s safety can be ensured. 2. Neck injury should always be suspected, the neck should be supported in a neutral position, and the jaw thrust or chin lift should be used without head tilt. 3. There is no need to clear the airway of aspirated water, aspiration of freshwater or saltwater is believed to be minimal. 4. Chest compressions should not be attempted in the water. 5. Near-drowning victims undergoing ACLS for cardiac arrest should be transported to the hospital, and ACLS continued especially for victims of cold water submersion. 6. The Heimlich maneuver is of no proven value, and in fact will only delay the initiation of rescue breathing. A full discussion regarding this controversy was undertaken by Rosen and co-w~rkers’~ commissioned by the Institute of Medicine in 1993, with conclusions consistent with the current AHA recommendation^.'^ Surfactant Treatment

Over the last few years, there have been a number of articles and case reports regarding the possible use.of surfactant therapy for the near-drowning victim. This includes a case report of a 3-year-old near-drowning victim successfully treated with bovine surfactant. It is believed that fresh water near drownings lead to depletion of endogenous surfactant by the aspirated water, causing reduced compliance, atelectasis, and potentially leading to adult respiratory distress syndrome. However, recent clinical and animal studies have not demonstrated improved pulmonary function with surfactant therapy.’, l 3 Outpatient Management

Most near-drowning victims are admitted to the hospital because of concern for clinical deterioration. A recent review has examined this issue and suggested that most submersion victims can be observed and managed as outpatients. This review of hospitalized near-drowning victims found that 98% of patients developed symptoms during the first 4.5 hours after the immersion, the longest duration of symptom development was 7 hours in one victim. Their findings led to the following recommendations: 1. Ill, symptomatic: Admit for observation and treatment 2. All others: Medical evaluation/observation 6 to 8 hours 3. Asymptomatic after observation: Discharge and follow-up call or evaluation 4. Symptomatic/deterioration after observation: Admit

In addition, they found that initial chest radiographs, normal or abnormal, were not helpful predictors for prognosis or disposition.12 Another study, a 1991 California retrospective review, found that 84% of near-drowning victims had a disposition of a routine discharge home, most occurring on the admission day or after 1 night’s stay.4 The preceding findings are not meant to minimize the importance of initial medical assessment of all submersion victims, even in the event that minimal resuscitation was r e q ~ i r e d . ~

ENVIRONMENTAL EMERGENCIES

463

Prognostic Factors for Survival

A retrospective review comparing favorable versus unfavorable outcomes (vegetative state and death) after near drowning was conducted on a study population of 194 children, median age 2.6 years (5 months to 18 years old) in Kings County. A predictor combination of absent pupillary light reflex, increased blood glucose concentration, and male sex among comatose children had a 65% sensitivity for unfavorable outcome (thus 35% overly optimistic for patients with unfavorable outcomes), yet was 100% specific for a favorable outcome. The authors caution the use of prediction rules in clinical practice, yet believe this combination rule was acceptable in this application because current medical practice is to provide full supportive care to comatose near-drowning victims.6 As expected, duration of hypoxemia and subsequent anoxic brain injury is the most critical sequela of submersion injury. Kyriacou and colleaguesRfound that a good outcome (neurologically normal or mild anoxic encephalopathy), using logistic regression, and controlling for age, gender, duration of submersion, and hypothermia, were 4.75 (adjusted operating room) times more likely to have a history of immediate resuscitation. In addition, as expected, longer submersion periods were associated with poor clinical outcome. Hypothermia was significantly associated with poor outcome as well, but probably confounded with duration of submersion. This case-controlled study, consisting of a study population of 166 children based in Los Angeles County, probably does not reproduce the protective effect of hypothermia demonstrated in other studies, because hypothermia in this population is more likely a manifestation of long submersion times as opposed to cold water exposures.8 Serologic neurologic examinations after near drowning have been found to be predictive and helpful for determination of outcome. Bratton and associates2 retrospectively reviewed 44 critical pediatric near drownings (71% with a Glasgow Coma Scale [GCS] of 5 or less on admission, 40 of 44 patients intubated) and applied a 14-point coma scale to evaluate both cortical and brainstem function on admission and on subsequent days. Predictors for satisfactory (none to very mild deficits) versus unsatisfactory (custodial care or death) outcome were evaluated. At 24 hours after presentation, survivors with normal or mild deficits were awake and initiated spontaneous purposeful movement (6 points out of 6 on the motor component of the GCS). Whereas, patients with poor prognosis, including severe deficits or death, remained comatose on reexamination at 24 hours.Z Other prognostic factors previously reported include age < 3 years old, prolonged submersion time (>5 minutes), delay in initiation of CPR (>lo minutes), persistent apnea after CPR, and requirement of CPR in the emergency department (ED), arterial pH < 7.1° When To WithholdMlithdraw Treatment

The previous section on prognostic factors provides data to support that we are getting closer to predicting when a resuscitation attempt will not only be futile, but worse, may result in resuscitation of a child to a persistent vegetative state. Both authors of this review had experience with this phenomenon on a number of cases of vegetative resuscitations on near-drowning victims in 1990, while rotating through the Phoenix Children’s Hospital intensive care unit (ICU), a period during which there was a record number of near drownings. A number of pediatric intensivists now question the role of aggressive cerebral

464

BRAUN & KRISHEL

resuscitation and whether or not cardiopulmonary resuscitation is even necessary on patients that present, not meeting cold water drowning criteria, without vital signs. Lavelle and Shaw,'" in a retrospective review of 41 near-drowning victims admitted to the Children's Hospital of Philadelphia ICU, 44% survived in a vegetative state or died. Multivariate analysis for predictors of poor outcome were unreactive pupils in the ED or a GCS of 5 or less in the ICU. However, 3 patients requiring CPR survived neurologically intact. In addition, others have documented full recovery in other patients presenting with unreactive pupils. Thus, these authors believe it is premature to withhold ED resuscitation on near-drowning victims, because of inconclusive data on predictor variables on ED presentation at this time. Yet, they do agree with Batton and co-workers2 and others, that serial neurologic examinations may be the best predictors of outcome to date. The Philadelphia series found that a GCS improvement of 2 or more points was associated with an 83% chance of good outcome, and a 3-point or greater increase in GCS on arrival to the ICU had a 100% chance of full recovery.'" The decision to treat or not treat the critical near-drowning child with a poor prognosis is addressed in a 1993 editorial in Critical Care Medicine by Modell" from the University of Florida. His point is that the answer to this question becomes more of an ethical than medical issue, and that in the absence of absolute predictors we may have a legal imperative to treat the near-drowning victim. However, each individual patient presents with its own circumstances, and the ultimate decision rests with the physician in attendance." References 1. Anker AL, Santora T, Spivey W: Artificial surfactant administration in an animal model of near drowning. Academic Emergency Medicine 2204-210, 1995 2. Bratton SL, Jardine DS, Morray JP: Serial neurologic examinations after near drowning and outcome. Archives of Pediatrics and Adolescent Medicine 148:167-170, 1994 3. Diekema DS, Quan L, Holt VL: Epilepsy as a risk factor for submersion injury in children. Pediatrics 91:612-616, 1993 4. Ellis AA, Trent RB: Hospitalizations for near drowning in California: Incidence and costs. Am J Public Health 85(8 pt 1):1115-1118, 1995 5. Gillenwater JM, Quan L, Feldman KW: Inflicted submersion in childhood. Archives of Pediatrics and Adolescent Medicine 150:298-303, 1996 6. Graf WD, Cummings P, Quan L, et al: Predicting outcome in pediatric submersion victims. Ann Emerg Med 26:312-319, 1995 7. Guidelines for cardiopulmonary resuscitation and emergency cardiac care: Emergency Cardiac Care Committee and Subcommittees. American Heart Association: IV. Special resuscitation situations [see comments]. JAMA 268:2242-2250, 1992 8. Kyriacou DN, Arcinue EL, Peek C, et al: Effect of immediate resuscitation on children with submersion injury. Pediatrics 94:137-142, 1994 9. Lavelle JM, Shaw KN, Seldi T, et al: Ten-year review of pediatric bathtub neardrownings: Evaluation for child abuse and neglect. AM Emerg Med 25:344-348, 1995 10. Lavelle JM, Shaw KN: Near drowning: Is emergency department cardiopulmonary resuscitation or intensive care unit cerebral resuscitation indicated [see comments]? Crit Care Med 21:368-373, 1993 11. Modell JH: Drowning: To treat or not to treat-An unanswerable question [editorial]? Crit Care Med 21:313-315, 1993 12. Noonan L, Howrey R, Ginsburg C M Freshwater submersion injuries in children: A retrospective review of seventy-five hospitalized patients. Pediatrics 98:36&371, 1996 13. Perez-Benavides F, Riff E, Franks C: Adult respiratory distress syndrome and artificial surfactant replacement in the pediatric patient. Pediatr Emerg Care 11:153-155, 1995

ENVIRONMENTAL EMERGENCIES

465

14. Rosen P, Stoto M, Harley J: The use of the Heimlich maneuver in near drowning: Institute of Medicine report. J Emerg Med 13:397405, 1995

Carbon Monoxide* This update provides the emergency physician with epidemiologic data to remind the demographic groups at higher risk for carbon monoxide (CO) exposure, the utility of prevention and education to minimize CO exposure in highrisk areas, and the current guidelines and controversies regarding HBO therapy. In addition, newer findings regarding CO measurements and reliability in young children, arterial versus venous blood samples, and issues regarding organ transplantation, treatment concerns regarding CO and cyanide exposure, and newer diagnostic studies for prediction of central nervous system injury is presented.

EPIDEMIOLOGY Accidental CO remains the number one cause of poisoning deaths, approximately 500 to 600 per year in the United States3 Attributable causes vary according to location in the United States, yet consistently a high percentage were associated with alcohol intake. In New Mexico, an almost equal percentage of deaths were associated with a home heating mechanism (42%) and motor vehicle exhaust (46y0).~ Other demographic trends include higher incidence of unintentional CO poisonings during the colder months of the year, higher mortality among men, and in areas with cold winters or high altitude. There have been a number of poisonings recently reported after large snowfall, when individuals spend time in idling automobiles with exhaust pipes blocked by snow? In addition, there is an association between CO poisonings and indoor use of charcoal briquets and minority race in one series.6

PREVENTION Prevention begins at the home, including inspection of home heating appliances (especially older systems), space heaters, chimneys, and education to avoid alcohol and driving especially before and during the colder seasons. Public health agencies need to promote the use of low cost CO detectors for home and apartment dwellers. Such information is available from the US Consumer Product Safety Commission hotline (800) 638-2772. Mandatory prevention mechanisms may not be universally accepted. For example, the nations first CO detector ordinance was passed and implemented by the Chicago City Council in 1994. In the first 3 months after implementation, the Chicago Fire Department responded to over 12,000 CO detector alarming, most (85%) with minimal CO levels (<9 parts per million). A revised protocol for fire department response to CO detector alarms followed, and the ordinance became more politically acceptable.8 *This section prepared by Ross Braun, MD, MPH, FACEP.

466

BRAUN & KRISHEL

MANAGEMENT UPDATE Does HBO Therapy for CO Poisonine Work?

Clinical practice and substantiating scientific evidence about the use of HBO for CO poisoning continues to be controversial since its implementation more than 30 years ago. In addition, guidelines for HBO (100% oxygen at 2 atmospheres, HBO) compared with 100% oxygen at ambient pressure vary among clinicians, as discussed in the next section. A recent prospective randomized study in patients with mild to moderate poisonings, presenting within 6 hours of exposure, addresses the question of HBO efficacy by Thorn and a~sociates,'~ yet falls short in design for conclusive recommendations to clinical practice. Olson and Seger'" also address this controversy, the study by Thorn, and call for the scientific community to undertake a double-blinded investigation, including "sham" HBO treatment, and thorough pre-post neuropsychologic testing to better understand the use of HBO therapy. We have referenced responses to the Olson and Seger editorial that worth reading to better understand the challenges one faces when developing a design to test HBO treatment effica~y.'~ Guidelines for HBO

Criteria for use of HBO therapy in the setting of CO poisonings vary. Most would agree to use HBO for coma, transient loss of consciousness (LOC, including syncope, seizures), acute cardiac ischemia or pulmonary edema, severe metabolic acidosis, focal neurologic deficits, abnormal psychometric testing, and pregnant patients regardless of CO level. Similarly, most would also use HBO for COHb of 40% in the setting of headache and nausea. However, in a questionnaire administered to medical directors of US and Canadian HBO facilities, only 62% use a specific CO level as the sole criterion for HBO in an asymptomatic patient? The same survey found that when a specific level was used as indication for treatment, 25% was the most common level cited but chosen as such by only half the respondents that apply COHb as sole criteria. The Hyperbaric Oxygen Committee of the Undersea and Hyperbaric Medical Society (UHMS) supports functional testing as the best criteria for HBO management among patients with minimal symptoms. Time to treatment with HBO remains variable. It is unknown after which time after exposure, that HBO would not be beneficial. Mortality does increase with duration after CO exposure, 13.5% mortality if HBO treatment is begun within 6 hours, and 30.1% if HBO is administered after 6 hours of treatment. Clearly, randomized clinical studies need to be undertaken to better understand the parameters for effective HBO management in the setting of CO poi~onings.'~, l6 NEWER CNS PROGNOSTIC MODALITIES

Newer, higher tech modalities are being investigated to determine acute and prolonged neuro and neuropsychiatric abnormalities among CO poisoning patients. European researchers are evaluating the use of computerized EEG mapping (topographical EEG analysis) and brain single-photon emission computed tomography (SPECT). Up to now, standard EEG studies and head CT studies have been ineffective in predicting permanent neuropsychiatric sequelae

ENVIRONMENTAL EMERGENCIES

467

(occurring in 10% to 40% CO poisoning survivor^).^ Others are evaluating cerebral blood flow with xenon-enhanced CT in CO poisoning.'2

.

SPECIAL CONSIDERATIONS Pulse Oximetry

Pulse oximetry is unreliable in CO poisonings, specifically it is falsely elevated. This pulse oximetry, or saturation "gap," the difference between the accurately measured oxygen saturation, and the falsely elevated oximetry reading approximates the COHb level. A small clinical study by Buckley and associates2 confirmed these findings, noting that oximetry did not go below 96% despite CO levels as high as 44%. They remind us that pulse oximetry may be falsely elevated in smokers, who commonly have CO levels between 5% and 9%. Post-CO Poisoning Organ Transplantation

Recommendations and data on organ transplantation following poisoning cases are limited. End-organ damage from CO exposure versus rejection mechanisms may be hard to distinguish. One author states, based on limited clinical experience, that in the CO-poisoned patient, the liver and kidneys may be donated yet heart donation is probably more risky because this organ is less resistant to h y p ~ x i a . ~ Falsely Elevated COHb Levels Owing to Fetal Hemoglobin

Infants have various degrees of fetal hemoglobin (Hb), ranging from newborn (70% fetal and 30% adult Hb) to 3 months of age (30% fetal and 70% adult Hb), which has clinical implications when measuring CO. The clinician must be aware that the COHb level measured by co-oximetry can be falsely elevated in direct proportion to the fetal Hb content. If the clinician is unaware of this interference by the fetal Hb, children less than 3 months of age may be subjected to unnecessary HBO treatment based on a falsely elevated COHb in this setting." Combined CO and Cyanide Poisonings

Victims of home and industrial fires are at risk for both CO and hydrogen cyanide (CN) toxicity. Some researchers have suggested that lower concentrations of each gas are more toxic when combined. The diagnosis of CN toxicity and decision to treat is almost more difficult than that involving CO, yet becomes even more relevant in the setting of CO toxicity because the treatment options for CN may compound the toxicity of CO. CN toxicity should be suspected in possible exposure to CO, persistent lactic acidosis, and hemodynamic compromise. CN toxicity is managed by two specific antidotes: (1)sodium thiosulfate to increase conversion of CN to thiocyanate and (2) sodium nitrite to induce methemoglobin (metHb), which binds CN. Unfortunately, metHb contributes to decreasing oxygen-carrying capacity which has already been reduced by COHb." A canine model has been used to address this scenario of dual gas exposure providing guidelines for treatment.'

468

BRAUN & KRISHEL

CO Measurements: Arterial Versus Venous?

Recommendations on whether arterial or venous blood samples should be used for CO determination vary in the literature. A recent comparison of arterial and venous CO measurements among 61 victims of CO poisonings found excellent and reliable correlation between these measurements and demonstrated differences le'ss than 2% when CO venous levels were below 25%.15

PEARLS

1. The emergency physician must have a high index of suspicion for CO poisonings because the early signs and symptoms are nonspecific, including headache, dizziness, fatigue, gastrointestinal upset, and lethargy. Up to 30% of symptomatic CO poisonings will be missed and given an alternative diagnosis! 2. Public education and home CO detectors could be extremely helpful to reduce the high morbidity and mortality associated with CO poisonings, especially in areas with colder seasons. 3. Carboxyhemoglobin levels and symptoms are dependent on (1) concentration of CO exposure, (2) duration of exposure, and (3) time to evaluation and treatment. Normal carboxyhemoglobin concentrations are <2% for nonsmokers and 5% to 9% for smokers. 4. Initial treatment of CO poisoning should include termination of exposure and administration of 100% oxygen. 5. There is recent literature to support normobaric oxygen therapy for 4 to 6 hours or until symptoms resolve as being as effective as HBO for mild to moderate toxicity. 6. Indications for HBO therapy include patients with neurologic or cardiac symptoms, severe acidosis, gastrointestinal symptoms, pregnant women, and children who cannot give a reliable examination or history. 7. Although there is no correlation with carboxyhemoglobin level and severity of CO poisoning, when regional poison directors were surveyed about absolute level in the asymptomatic patient as an indication for HBO treatment, those responding most often selected a COHb level of 25% or greater. 8. In pregnancy, because the fetus is at a relatively increased risk from CO exposure, the referral level for HBO is lowered to 15% to 20% COHb by some researchers. 9. The clinician must be aware that fetal Hb can contribute to falsely elevated COHb in infants less than 3 months of age. 10. Patients presenting to the ED with unstable angina should be asked about indoor heating. Although a small percentage, it is known that CO can precipitate cardiac ischemia, and individuals may benefit from HBO treatment. 11. Both immediate and delayed treatment with HBO may be recommended and beneficial for minimizing neuropsychological sequela. 12. The clinician should suspect dual toxic gas (CO and CN) exposure among indoor fire victims and consider CN antidote therapy for victims with persistent metabolic acidosis and hemodynamic compromise. 13. Venous CO levels are reliable among patients with CO levels less than 25%.

ENVIRONMENTAL EMERGENCIES

469

References 1. Breen PH, Isseries SA, Westley J, et al: Effect of oxygen and sodium thiosulfate during combined carbon monoxide and cyanide poisoning. Toxicol Appl Pharmacol 134:229234, 1995 2. Buckley RG, Aks SE, Eshom JL, et al: The pulse oximetry gap in carbon monoxide intoxication [see comments]. Ann Emerg Med 24:252-255, 1994 3. Carbon monoxide poisonings associated with snow-obstructed vehicle exhaust systems-Philadelphia and New York City, January 1996. MMWR Morb Mortal Wkly Rep 45:l-3,1996 4. Denays R, Makhoul E, Dachy B, et al: Electroencephalographic mapping and 99mTc HMPAO single-photon emission tomography in carbon monoxide poisoning. Ann Emerg Med 24947-952, 1994 5. Hampson NB, Dunford RG, Kramer CC, et al: Selection criteria utilized for hyperbaric oxygen treatment of carbon monoxide poisoning. J Emerg Med 13:227-231, 1995 6. Hampson NB, Kramer CC, Dunford RG, et al: Carbon monoxide poisoning from indoor burning of charcoal briquets. JAMA 271:52-53, 1994 7. Hantson P, Vekemans MC, Squifflet JP, et al: Organ transplantation from victims of carbon monoxide poisoning [letter]. Ann Emerg Med 27673-674, 1996 8. Leikin JB: Carbon monoxide detectors and emergency physicians [editorial]. Am J Emerg Med 1490-94,1996 9. Moolenaar RL, Etzel RA, Parrish RG: Unintentional deaths from carbon monoxide poisoning in New Mexico, 1980 to 1988. A comparison of medical examiner and national mortality data. West J Med 163:431434, 1995 10. Olson KR, Seger D Hyperbaric oxygen for carbon monoxide poisoning: Does it really work [editorial]? Ann Emerg Med 25:535-537, 1995 11. Perrone J, Hoffman RS: Falsely elevated carboxyhemoglobin levels secondary to fetal hemoglobin [letter]. Academic Emergency Medicine 3287-289, 1996 12. Sesay M, Bidabe AM, Guyot M, et a1 Regional cerebral blood flow measurements with Xenon-CT in the prediction of delayed encephalopathy after carbon monoxide intoxication. Acta Neurol Scand Suppl 166:22-27, 1996 13. Thom SR, Taber RL, Mendlguren 11, et al: Delayed neuropsychologic sequelae after carbon monoxide poisoning: Prevention by treatment with hyperbaric oxygen [see comments]. Ann Emerg Med 25:474480, 1995 14. Tibbles PM, Edelsberg JS: Hyperbaric-oxygen therapy. N Engl J Med 334:1642-1648, 1996 15. Touger M, Gallagher EJ, Tyrell J: Relationship between venous and arterial carboxyhemoglobin levels in patients with suspected carbon monoxide poisoning. AM Emerg Med 25:481483, 1995 16. Weaver LK Randomized clinical trial in carbon monoxide poisoning needed [letter]. Am J Emerg Med 12:685487, 1994 17. Weaver LK, Hopkins RO, Larson-Lohr V Hyperbaric oxygen and carbon monoxide poisoning. Ann Emerg Med 26390-392,1995

Hypothermia* The American Heart Association has included Hypothermia as a Special Resuscitation Situation in the most recent 1992 JAMA guideline review on cardiopulmonary resuscitation and emergency cardiac care. This section reviews their recommendations, provides an update on rewarming techniques, and discusses presentation and management of hypothermia among special populations.* “This section prepared by Ross Braun, MD, MPH, FACEP.

470

BRAUN & KIUSHEL

RESUSCITATION GUIDELINE UPDATE Hypothermia is distinguished and managed differently depending on severity, defined as core temperature above (mild to moderate) or below (severe) 30°C. However, actions for all patients should include removal of wet clothing, protection against continued heat loss, monitoring of cardiac status, and minimization of instrumentation and manipulation for fear of precipitation of ventricular fibrillation (VF). Standard ACLS protocols should be initiated, including cervical spine precautions, if trauma is suspected (i.e., near-drowning). This includes CPR if patient is not breathing or pulse is absent, followed by standard defibrillation for a total of three shocks if indicated. If the patient is severely hypothermic (<3OoC), intravenous resuscitation medications and subsequent defibrillation should be withheld until active external and internal rewarming is successful in raising the core temperature to 30°C or greater. Many texts provide an algorithm for rewarming, and the one provided by the American Heart Association in the 1992 JAMA issue on resuscitation is excellent and should be referred to for management guidelines? REWARMING TECHNIQUES Management algorithms vary in the distinction between mild and moderate hypothermia. Most would agree that one could use a combination of both passive and active external rewarming modalities for management for either.8 Passive Rewarming This includes removal of the patient from the environmental exposure, protection against wind chill, removal of wet clothing, and insulation of patient in a warm environment. Active External Rewarming This involves direct exposure of the patient to exogenous heat sources, such as radiant heat, forced warmed air, heating blankets, and hot water bottles/ warmed saline bags (microwave works well)? The concern here is peripheral warming, leading to peripheral vasodilatation with subsequent core-temperature "afterdrop." Thus, to minimize this concern, most recommend active external rewarming of the truncal (i.e., armpits, groin) areas only.2 Active Core Rewarming There are several different modalities for active core rewarming; a synopsis of different active core rewarming techniques follows with recent findings and advances found in the literature. Active core rewarming techniques are indicated for any patient with severe hypothermia (<3OoC), whereas the modality of choice should depend on the patient's hemodynamic compromise and local experience at your facility.

ENVIRONMENTAL EMERGENCIES

471

Airway Rewarming

Heated humidified air or oxygen, up to 45"C, via endotracheal tube, will provide core temperature elevation from 1°C to 2°C per hour.2 Although less efficient as a core rewarming technique than heat exchange via the peritoneum or pleura, it is a simple technique that should be considered. GastridBladder Irrigation

This is often considered, but of minimal benefit owing to the small surface areas available for heat exchange. In addition, another source of manipulation placing the patient at risk for VF with minimal core rewarming advantage to the patient. Peritoneal Lavage

The usual parameters for this modality include liquid heated up to 45"C, administered from 10 to 20 mL/kg at a rate up to 6 L/h via two exchange catheters, with core rewarming rates from 2 to 4°C per hour. Pleural Irrigation

This technique usually involves two large-bore thoracostomy tubes, infusing sterile saline up to 42"C, preferably to the right chest to minimize cardiac irritability. Hemodialysis An effective alternative, when cardiopulmonary bypass is not available. In addition, heparin-free hemodialysis is available thus potentially useful for polytraumatized individuals and those with moderate to severe hypothermia.

Extracorporeal Rewarming

Normally reserved for the critical hypothermic patient, it is indicated for patients without perfusion or completely frozen extremities. Techniques include cardiopulmonary bypass with mechanical pump, oxygenator, and heat exchanger. Core rewarming rates via the femoral vein, with flow rates at 3 L/min can be as high as 2°C every 3 to 5 minutes. European experience, indications for, and a schematic of an extracorporeal circulation circuit (ECC) is provided in the review by Antretter and associates.' A collective literature review on 68 hypothermic patients resuscitated with cardiopulmonary bypass was undertaken by Vretenar and co-worker~.~ This patient population was described by age range of 2 to 72 years old, mean of 32 years old, with an initial mean core temperature of 21°C. Most (90%) of the patients presented in cardiac arrest, yet the overall survival was 60%. Although initial core temperature was not a predictive prognostic factor, no patient with a core temperature less than 15°C survived. Very Hot (65°C)Intravenous Fluids

Centrally administered very hot (65°C) versus standard (40°C) intravenous fluids were compared in a hypothermic beagle model by researchers at Cook

472

BRAUN & KRISHEL

County Hospital? Rewarming rates were significantly different (3.7”C versus 1.75”C),and all animals survived without significant, including vascular, pathologic examinations after 7 days of observation. The authors suggest that rapid hypothermic management with 65°C fluid be considered even for iatrogenic (operative) conditions. HYPOTHERMIA AND SPECIAL POPULATIONS

Hypothermia may be a manifestation of other disease processes or situations besides environmental exposure that we must be aware of, recognize, and be prepared to manage. This includes a variety of medical diseases, a result of drug or alcohol use, manifestation of psychiatric illness, subsequent to traumatic/ burn injury or toxicologic exposure, or neurologic disease. In fact, one reference cited that in some rural areas, 90% of hypothermic deaths were found to have detectable blood alcohol level^.^ Another source approximates that 50% of trauma patients are hypothermic, which contributes to m ~ r b i d i t y . ~ Both the young and the elderly are at higher risk for development of and morbidity from hypothermia. Children are at increased risk primarily from a relative increased body surface area and the elderly population because of reduced muscle mass, subcutaneous tissue, and underlying metabolic, primarily endocrine diseases.’ PEARLS AND PITFALL SUMMARY

1. Unrecognized severe hypothermia because core thermometer does not record lower than 30°C. 2. Precipitation of VF with patient manipulation/instrumentation-this author witnessed such an event when transferring patient from ED gurney to ICU bed. 3. Administration of ACLS medications (epinephrine, lidocaine, procainamide) when used repeatedly in the hypothermic patient, may accumulate to toxic levels. 4. Bradycardia, in the severely hypothermic, may be physiologic and should not be managed with a pacer unless persisting with rewarming. 5. “Urban hypothermia,” associated with substance abuse and trauma, should be suspected and evaluated for underlying conditions and predisposing factors. 6. Central venous catheters should be preferentially placed in the femoral vein to minimize cardiac irritability via the internal jugular or subclavian route. 7. Cardiopulmonary bypass is contraindicated in hypothermic patients with concomitant trauma because of the need for anticoagulation for the procedure. 8. Fixed and dilated pupils in severe hypothermia are not indicative of brain death. 9. Resuscitation of severely hypothermic patients is more likely if the cardiac arrest is a consequence oiihypothermia, and not anoxia and acidosis. 10. Death cannot be pronounced “until warm and dead” and inability to wean off cardiopulmonary bypass. 11. Emergency physicians should always consider adrenal insufficiency as

ENVIRONMENTAL EMERGENCIES

473

a cause for hypothermia, especially if there is a history suggesting steroid dependence or failure to respond to rewarming, and it should be treated appropriately. 12. Consider antibiotic administration in high-risk patients, including hypothermic neonates, elderly, and immunocompromised. References 1. Antretter H, Bonatti J, Dapunt OE: Accidental hypothermia [letter]. N Engl J Med 332:1033, 1995 2. Dam1 DF, Pozos RS: Accidental hypothermia [see comments]. N Engl J Med 331:17561760, 1994 3. Freedland ES, McMicken DB, DOnofrio G: Alcohol and trauma. Emerg Med Clin North Am 11:225-239, 1993 4. Guidelines for cardiopulmonary resuscitation and emergency cardiac care: Emergency Cardiac Care Committee and Subcommittees, American Heart Association, Part IV, Special resuscitation situations [see comments]. JAMA 268:2242-2250, 1992 5. Sheaff CM, Fildes JJ, Keogh P, et al: Safety of 65 degrees C intravenous fluid for the treatment of hypothermia. Am J Surg 172:52-55, 1996 6. Steele MT, Nelson MJ, Sessler DI, et a1 Forced air speeds rewarming in accidental hypothermia. Ann Emerg Med 27479484, 1996 7. Vretenar DF, Urschel JD, Parrott JC, et al: Cardiopulmonary bypass resuscitation for accidental hypothermia. Ann Thorac Surg 585395498, 1994 8. Weinberg A D Hypothermia. Ann Emerg Med 22:370-377, 1993

Venomous Snakebites in the United States* Ninety-eight percent of venomous snakebites in this country are from the Crotalidae family, also known as pit vipers. Pit vipers include rattlesnakes, copperheads, water moccasins, and bushmasters. The mainstay of treatment for moderate to severe envenomations is antivenin. This section reviews the clinical presentation and management of crotalid envenomations. INTRODUCT10 N

Of the approximate 45,000 snakebites in the United States each year, only 7000 to 8000 are from venomous snakes. Death in the United States from a venomous snakebite is rare, accounting for less than 10 to 15 fatalities a year. Although there are five venomous families of snakes, most venomous snakebites in the United States are inflicted by members of the Crotalidae Crotalids, also known as pit vipers, include rattlesnakes (Crotatus), massasauguas rattlesnakes (Sistrurus), and copperheads and cottonmouths (Akistrodon). The most severe envenomations tend to be from rattlesnakes, who will strike out when threatened. Pit vipers can be differentiated from harmless snakes by several characteristic features. They have a facial ”pit” located below each nostril, their heads are triangular, and they have elliptical pupils. The pit is an organ that can sense *This section prepared by Scott Krishel, MD, MPH.

474

BRAUN & KRISHEL

temperature and allows the snake to locate warm-blooded prey, or the hands and feet of a potentially threatening human. They have fangs that may be up to 2 cm in length and can penetrate muscular compartments to introduce venom. Most pit vipers also have terminal horny scales that have evolved into a rattle. A frightened snake may or may not use this warning before striking. Because even a dead snake can envenomate a handler, the best way to identify a pit viper is from a distance. PATHOPHYSIOLOGY

Snake venom mainly consists of enzymes and polypeptides that are cytotoxic, hemotoxic, and neurotoxic, and can injure vascular endothelium.2, Envenomation can cause local and systemic damage. Twenty-five percent to 50% of snakebites do not result in envenomation, and the only clinical findings are puncture wounds.2, The clinical presentation of those who are envenomated varies and depends on the amount of venom introduced, the anatomic location of the bite, the size and age of the victim, and the patient's overall state of health. The seriousness of the envenomation can only be determined by observing the patient's clinical course. The first symptom of envenomation is an immediate burning pain at the site. Within the next 6 to 8 hours, there will be increasing pain and swelling in proximity to the puncture wound. The edema can progress rapidly and involve the entire extremity. Circulatory compromise of the extremity is rare, even with massive swelling of the affected extremity, and compartment syndrome does not usually develop?, Hemorrhagic blisters can form around the punctures, enlarging over several days. Third-degree tissue destruction can occur from these blisters, and there can be significant soft-tissue defects. Many systemic symptoms can also occur. Victims frequently complain of a metallic taste soon after being envenomated. The patients may complain of fasciculations, weakness, dizziness, nausea and vomiting, fever, and numbness and tingling around the mouth. The person may be hypotensive, but this is less common than the other signs and symptoms. There can also be significant hematologic toxicity from crotalid enven~mation.~ The venom can disrupt the coagulation cycle by a thrombinlike effect, resulting in decreased fibrinogen levels. The patients may develop a coagulopathy with elevated prothrombin (PT) and partial thromboplastin (PTT) levels. Massive envenomation can lead to a clinical state similar to disseminated intravascular coagulation. Thrombocytopenia can also occur, with and without alterations in the coagulation system. The systemic toxicity of the venom can lead to increased membrane permeability, hypotension, and pulmonary edema.2, Cardiac and kidney failure can occur as secondary problems. TREATMENT What Not to Do: Suction, Tourniquet, Ice, and Fasciotomy

There are no data that have shown any suction device, or the use of one's mouth to remove the venom, to affect patient outcome.', Additionally, bacterial inoculation leading to infection may occur during such attempts. There is also no evidence that placing a tourniquet proximal to the wound site will affect outcome.', 2, Although animals studies have shown that a tourniquet can de-

ENVIRONMENTAL EMERGENCIES

475

crease lymphatic flow of venom in a swine model, the risk of venous or arterial obstruction with subsequent tissue ischemia and injury is too great to warrant this practice. A sling or splint can be applied, as limiting movement may decrease pain. Extended exposure to ice in these patients can lead to thermal injury, circulatory compromise, and tissue damage. Ice should be used sparingly, if at all, for prehospital analgesia. Some institutions have advocated prophylactic fasciotomy on arrival of patients with crotalid envenomations who have massive extremity edema, even when there are no signs or symptoms of compartment syndrome. In addition to compartment syndrome being uncommon in these patients, this surgical approach has not been shown to be superior to aggressive medical management. A fasciotomy is not indicated on a victim of crotalid envenomation unless there is a severe envenomation with increased compartment pressures and signs and symptoms of impaired circulation.z, What to Do: Antivenin

The victim should be transported to a health care facility as rapidly as possible. Because the signs of toxicity may not develop immediately, all patients should be observed for 6 to 12 hours. If there are no signs or symptoms of envenomation or toxicity after the period of observation, then the patient may be sent home with follow-up care. If there is evidence of envenomation, such as swelling or pain, or early systemic effects, such as nausea or dizziness, the patient should be placed on cardiac monitor and have intravenous access established. Large amounts of fluid can be lost owing to third-spacing, and fluid resuscitation may be necessary. Blood work should be sent for a complete blood count with platelets, fibrinogen level, fibrin split products, and coagulation studies. A CK level should also be obtained, as rhabdomyolysis can result from severe swelling of muscle compartments and from direct muscle toxicity of the venom. The mainstay of treatment for moderate to severe crotalid envenomations is antivenin.’,z7,* A minimal envenomation will have localized pain and swelling and normal laboratory tests and does not require antivenin. Moderate envenomation consists of increasing pain and swelling, mild systemic symptoms, such as dizziness, nausea, or vomiting, and mild to moderately abnormal coagulation studies or thrombocytopenia. A severe envenomation will produce rapidly spreading and extensive pain and edema, hypotension, severe gastroenteritis, hypotension, or an altered level of consciousness. There will be a marked coagulopathy, thrombocytopenia, or disseminated intravascular coagulation. Pit viper antivenin is a horse serum derived from the venoms of four crotalids, and can produce immediate and delayed hypersensitivity reactions. Patients with allergies to horses or horse serum, and severe asthmatics, should not receive the antivenin unless a severe envenomation has occurred. All patients should be skin tested with a subcutaneous dose of horse serum that comes with the antivenin. A positive reaction identifies people who are allergic, but a negative test does not rule out the possibility of an anaphylactic reaction developing, and all patients who receive antivenin should be observed closely for this complication. If an allergic reaction occurs, stop the antivenin and treat the reaction aggressively with epinephrine and histamine receptor blockers. Antivenin should be administered in 5- to 10-vial increments, with the contents of the vials infused over 30 to 60 minutes.2 After the infusion is completed, the person should be re-evaluated for ongoing toxicity. Blood tests should be repeated approximately 1 to 3 hours after the end of the infusion,

476

BRAUN & KRISHEL

m d if there are laboratory or clinical signs of continued toxicity, more antivenin should be given. It is not uncommon to administer 20 to 30 vials before seeing a resolution of signs and symptoms. One of the biggest mistakes made in the management of snakebites is not giving enough antivenin, with tissue necrosis as a r e ~ u l t Even .~ though antivenin will slow the progression of edema, it is important to elevate the effected extremity to further decrease swelling. Although some authors recommend prophylactic antibiotics, there are data that suggest that this practice may not decrease wound infection rates or improve outcome, and therefore routine prophylactic antibiotics may not be warranted?, 3, Tetanus toxoid booster should be given as indicated. A delayed hypersensitivity reaction will occur in most who receive more than 10 vials of antivenin. The symptoms begin within the first week and resemble a viral syndrome. These symptoms can be reduced with antihistamines and corticosteroids. It is important to inform patients about this delayed serum sickness when consenting them for treatment with antivenin.

References 1. Blackman JR, Dillion S Venomous snakebite: Past, present, and future treatment options. J Am Board Fam Pract 5:399405, 1992 2. Clark RF: Venomous snakebite. In Rake1 RE (ed): Conn’s Current Therapy. Philadelphia, WB Saunders, 1995, pp 1080-1082 3. Clark RF, Selden BS, Furbee 8:The incidence of wound infection following crotalid envenomation. J Emerg Med 11:58%586,1993 4. Forks TP: Evaluation and treatment of snakebites. Am Fam Phys 50123-130, 1994 5. Hutton RA, Warrell DA: Action of snake venom components of the haemostatic system. Blood Rev 7176-189, 1993 6. Otten EJ: Venomous animal injuries. In Rosen P, Arkin RM (eds): Emergency Medicine: Concepts and Clinical Practice, ed 3. St. Louis, Mosby, 1992, pp 875-893 7. Podgorny G: Reptile ites and scorpion stings. In Tintinalli J, Krome R, Ruiz E (eds): Emergency Medicine: A Comprehensive Study Guide, ed 4. New York, McGraw-Hill, 1996, pp 660-665 8. Rudolph R, Neal GE, Williams JS, et al: Snakebite treatment at a Southeastern regional referral center. Am Surg 61:767-772, 1995 9. Weed HG: Nonvenomous snakebite in Massachusetts: Prophylactic antibiotics are unnecessary. Ann Emerg Med 22220-224, 1993

Address reprint requests to Russ Braun, MD, MPH, FACEP Department of Emergency Medicine Highland General Hospital 1411 East 31st Street Oakland, CA 94602