Critical care of the near-drowned patient

Critical care of the near-drowned patient

Critical Care of the Near-Drowned P a t i e n t Andrea Gabrielli and A. Joseph Layon HE RATE of unintentional or accidental death decreased in 1997 af...

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Critical Care of the Near-Drowned P a t i e n t Andrea Gabrielli and A. Joseph Layon HE RATE of unintentional or accidental death decreased in 1997 after 4 consecutive years of increases. 1 Nonetheless, unintentional injuries are the fifth leading cause of overall death--outpaced only by heart disease, cancer, stroke, and chronic obstructive pulmonary disease--and the leading cause of death for individuals between 1 and 38 years old. 1 Drowning is the fifth leading cause of death from unintentional injury among persons of all ages in the United States and the second leading cause of death for persons 10 to 20 years old. 2 Approximately 4,000 persons died in 1997 as a result of drowning in the United States, a 2% decrease from 1996, 3 but the death rate decreased by approximately 50% over the last 30 to 35 years. However, the death rate for children 0 to 4 years old remains quite high--3.1 deaths per 105 popul a t i o n - c o m p a r e d to the next highest group, adults 75 years or older--l.9 deaths per 105 population. 3 Although drowning rates across age and ethnic groups have decreased, rates for toddlers and youngsters have changed little in the United States. In fact, according to the National Safety Council, approximately 1,000 children (0 to 14 years old) drown each year in the United States. 3 Worldwide, approximately 150,000 deaths per year are thought to occur from drowning. 4 Given the incidence of 1 death per 13 near-drownings in the United States each year, there are approximately 2 million neardrowning events annually throughout the world. More than one third (35%) of drowning victims are accomplished swimmers. 5 States with warm climates, an abundance of water, or both that attract vacationers have had a drowning rate almost twice the national average for each of the past 10 years. In fact, drowning has

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Assistant Professor of Anesthesiology, College of Medicine, University of Florida, Gainesville, FL Professor of Anesthesiology, Surgery, and Medicine, College of Medicine, University of Florida, Gainesville, FL Address reprint requests to Andrea Gabrielli, MD, University of Florida, College of Medicine, 1600 SW Archer Rd, Box 100254, Gainesville, FL 32610-0254. Copyright 9 1999 by W.B. Saunders Company 90277-0326/99/1803-0004510.00/0

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become the leading cause of injury and death among children younger than 5 years old in California, Arizona, and Florida. 6 Although no national data on emergency department (ED) visits for immersion injuries are available, the two largest studies published to date report that ED visits for near-drowning result in hospital admission approximately once in every four visits6'7; the criteria for making this decision are not commented on. Although most drownings and near-drownings occur in private swimming pools (50%), lakes, rivers, streams, and storm drains (20%), or bathtubs (15%), 8 accidents occur at other unusual sites. For example, the suction generated in some hot tubs has been known to be of sufficient force to trap children underwater. 9 Also, because of the difference between torso and lower body size, toddlers can become trapped in a bucket or toilet when they lean over to play in the water contained in these vessels. 4'8'1~ Bross and Clark suggested that child abuse may be the cause in up to 50% of the cases involving infant or toddler drowning. 11 In 25% and 50% of cases, alcohol and other drug abuse, limited swimming ability, exacerbation of existing medical problems--such as seizure disorder and coronary artery disease--and attempted suicide are contributing factors. 12-15 In a subset of accomplished swimmers who drowned, approximately half of the cases involved alcohol u s e . 6'8 Gender-related differences in aquatic skills and behavior have been noted, and the drowning rate is t w i c e as high for men as for women. 2 In early adolescence and adulthood, the ratio of male-tofemale drowning victims is approximately 10:I. Male drowning rates peak between the ages of 1 to 3 years, decrease thereafter until 10 years, then increase sharply during the late teens. In contrast, the overall human drowning rate peaks by 1 year of age and decreases over the years to a relative low and consistent level. Data from the 1991 national household survey on aquatic activities (3,042 cases) were used to examine this interesting phenomenon. 16 Despite better overall swimming training and ability, teenaged and young adult men probably overestimate their swimming ability and

Seminars in Anesthesia, PerioperativeMedicine and Pain, Vol 18, No 3 (September),1999: pp 216-230

CRITICAL CARE OF IMMERSION INJURIES engage in aquatic risk-taking behavior more readily. Furthermore, men consume more alcohol on or near the water than do women. 16 Thus, the higher rate of drowning and near-drowning for men reflects, in part, differences in alcohol consumption and the interaction between alcohol and overconfidence or both. Young men also may take risks to "show off" to their women friends.

DEFINITIONS Historicaly, there has been confusion regarding the terminology used to describe persons who have "drowned." Dorland's medical dictionary offers the following definition of drowning: "suffocation and death resulting from filling of the lungs with water or other substance or fluid so that gas exchange becomes impossible". 17 It is well known, however, that victims of drowning frequently aspirate only relatively small quantities of water and the lungs are seldom "filled with water." Furthermore, drowning implies death, yet many individuals are resuscitated and eventually recover. The following subdefinitions are now part of the dictionary definition of the verb "to drown." Neardrowning is "survival for any length of time after submersion in water and temporary suffocation.''17 Modell 5 further delineated drowning and neardrowning events in an attempt to foster greater accuracy: to drown without aspiration is to die secondary to respiratory obstruction and asphyxiate while submerged in water. To drown with aspiration is to die secondary to asphyxia resulting from aspiration of water while submerged. To near-drown without aspiration is to survive, at least initially, after an asphyxic event resulting from submersion in water. To near-drown with aspiration is to survive, at least initially, after submersion in and aspiration of water or other liquid material. Delayed death subsequent to neardrowning is death resulting from complications such as adult respiratory distress syndrome, sepsis, and irreversible brain damage after the initial asphyxic event. Because several factors impact the individual who drowns or near-drowns, no two cases are identical. For example, the type, temperature, and quantity of water aspirated may differ, and the person's state of health before drowning may be important, is One individual might have died secondary to complete physical exhaustion, whereas a second may have dived into the water and suffered

217 a concussion after traumatizing his or her head. Yet another individual might suffer from diabetes mellitus and coronary artery disease and have an episode of severe myocardial ischemia while swimming, with resultant loss of consciousness, aspiration of water, and drowning. The temperature of the water in which the individual was submerged is another factor of some significance and may, in fact, be either protective or increase the risk of death. Water cold enough to result in rapid hypothermia may decrease the person's requirement for oxygen, thereby prolonging the period of time he or she may stay submerged and still completely recover. 19.20Additionally, several groups 21-23 have shown that exposure to or immersion in cold (0~ to 15~ water increases minute ventilation and decreases maximal duration of breath-holding. This might result in a degradation of the dive response, resulting in increased likelihood of drowning or near-drowning. Finally, severe hypothermia may cause cardiac arrest. Each of the bystanders must be queried about these factors by the prehospital care providers, and the responses should be presented to the ED physicians on arrival at the hospital.

WHY DO DROWNINGS OCCUR? In most cases of drowning, the individual does not, apparently, "fight" for survival. Witnesses of drowning describe the person as suddenly becoming immobilized in the water, diving into the water and never resurfacing, or floating motionless on the surface. In some cases, head or neck trauma may be sustained during a dive. 24 When the person is submerged, breath-holding is frequently followed by glottic spasm of variable duration. 25 With the onset of severe hypoxia, the glottis eventually relaxes, and the individual breathes, taking variable amounts of water into the lungs. Until recently, it was believed that between 12% and 15% of drowned individuals maintained tight laryngeal spasm until death and did not aspirate at all; this appears to have been based on a mistranslation of one of the classics in the drowning literature. 26 This sequence of events--breath holding, loss of consciousness, and tight laryngeal spasm followed by death without aspiration of water--is somewhat different from that observed in animal models of drowning in which, after initial breathholding, the animal will breathe and aspirate water,

218 perhaps vomit, and eventually proceed to asystole and death from hypoxia. 26'27 There is no reason not to think that what occurs in the animal model also occurs in humans (Jerome H. Modell, personal communication). Indeed, it appears that all of the animals in Cot's 26 original work aspirated water after consciousness was lost with the exception of two that were removed from the water before to this event (J. H. Modell, personal communication, March 1999). Swimming under water essentially is an exercise in breath-holding. In humans, hyperventilation may play a role in the onset of cerebral hypoxia. Hyperventilation before breath-holding acutely decreases the arterial partial pressure of carbon dioxide (Paco2), which results in the swimmer becoming hypoxic before Paco 2 increases to the threshold at which the urge to breathe again becomes overwhelming. 2s Pao 2 in the range of 30 mm Hg was documented in 30% of healthy underwater swimmers after breath-holding in the laboratory. 28 At this Pao 2, the breath-holding swimmer loses consciousness, breathes water, and dies from hypoxemia. Alternatively, a cardiac dysrhythmia, a sudden seizure, drug use, invertebrate stings (in ocean drownings), chemical intoxication (such as carbon monoxide contamination of a scuba diver's air supply or rust formation in a tank of air, which consumes oxygen and leavs behind nitrogen) may be responsible for loss of consciousness while submerged. TM When the individual is awake in cold water, it is possible that a temporary increase in oxygen consumption may accelerate the process of complete physical exhaustion. However, the predominant cardiovascular response in healthy volunteers under these circumstances has been severe peripheral vasoconstriction and bradycardia, ie, the Cushing reflex. 29 Furthermore, a long-term protective effect on central nervous system function may be seen in patients submerged in cold water, secondary to a rapid decrease in the metabolic rate, because oxygen consumption (V02) decreases 10% for each ~ below 37~ 19"3~ Interestingly, at least in endothermic animals, hypoxia results in both a lowered set point of the thermoneutral zone and vasodilation32; the result is hypothermia without shivering and, thus, a decrease in Vo 2 of approximately 11%/~ Whether this phenomenon is of any significance in humans is unclear.

GABRIELLI AND LAYON PATHOPHYSIOLOGY Drowning and near-drowning can be viewed as an acute multiorgan system dysfunction syndrome secondary to hypoxemia. Although the ultimate outcome in near-drowning is related primarily to the severity of CNS hypoxia, other organ systems are involved and affected as well. The challenge to the intensivist is to identify organ dysfunction and prevent failure, allowing the patient, if CNS damage is not irreversible, to recover neurologically. The authors will first discuss some of the lesser alterations seen in near drowning, and then they will focus on the pathophysiology of the pulmonary and central nervous systems, the two organ systems of central importance in drowning and near-drowning. Where they exist, treatment options will be discussed separately.

Cardiovascular System In both freshwater and sea-water drowning and near-drowning, electrocardiographic changes may be seen. These are most frequently related to hypoxemia, and they resolve with reoxygenation; therapy other than this is uncommonly required. Ventricular fibrillation after freshwater aspiration resulting in death is rare. If very large amounts of fluid are aspirated, 33'34 although initially thought to result from profound hyponatremia, with relative elevation in the serum potassium 35 hypoxemia no doubt plays an important, if not the dominant, role. Modell et al36 studied canines in whom 22 mL/kg of saline or distilled water were instilled intratracheally. Bigeminy occurred in 9 of 15 dogs, and T-wave elevation was noted in 6 of 15 dogs. However, in another animal study, Karch 37 reported significant cardiac pathological changes 29 minutes after either a freshwater or saltwater (6 mL/kg intratracheal instillation) drowning episode. Light microscopy showed focal areas of disruption of the normal striation pattern and. on occaslon, of the intercalated discs as well as hypereosinophilia of myocytes. Electron microscopic evaluation of the damaged myocytes showed hypercontraction with swelling and an increased lucency of the mitochondria: also seen in the myocyte nuclei was chromatin clumping and crenation. Alterations of this type were not noted in the one control animal. Although the clinical relevance of these findings is uncertain, they are of interest to the further study of cardiac abnormalities after near-drowning. In humans, bradycardia is the most common nonmalignant ar-

CRITICAL CARE OF IMMERSION INJURIES rhythmia described in near-drowned victims. It most likely results from profound hypoxia, from decreased myocardial metabolic rate resulting from hypothermia in those cases in which the near-drowning event occurs in cold water, or from the physiological diving reflex seen with the acute increase in systemic vascular resistance, which is seen when the near-drowning involves cold water immersion. 38'39 The role of the diving reflex in humans is unclear. However, in marine animals, this reflex results in an increase in systemic vascular resistance, bradycardia, and the redistribution of blood flow to the heart and brain, thus decreasing overall Vo 2.

Renal System Although renal dysfunction is uncommon, albuminutia, hemoglobinuria, oliguria, acute renal failure, and anuria have all been noted in neardrowned patients. 4~ Although the causes of renal dysfunction include myoglobinuria resulting from muscle trauma, hypoxemia, hypoperfusion, and hemolysis with secondary hemoglobinuria, 5 a few cases of rhabdomyolysis and acute renal failure have been described after near-drowning in cold saltwater. 46 Hypothermia leads to reduced blood flow to the skin and muscle, preserving core temperature and central organ perfusion. The pathophysiology of rhabdomyolysis is likely secondary to acute vasoconstriction of muscle vasculature as a result of the need for heat conservation, with consequent myocyte injury.46 Acute myoglobinuria and hemodynamic instability result in acute renal failure. Metabolic, Electrolytes, and Blood Volume The most common metabolic abnormality detected in the near-drowned patient is an anion-gap metabolic acidosis secondary to hypoxemia with a resultant increase in lactic acid. 47'48 The severity of the metabolic acidosis and acidemia depends on the duration of hypoxia and the metabolic rate. Cold-water near-drowning may be associated with less acidosis than expected because the metabolic rate is decreased 10% for each ~ below 37~ 19'30'31 The rate of cooling is a function of the absolute water temperature, amount of water aspirated, and the extent to which the victim is insulated from the water. In adults, near-ice water may be associated with a core temperature decrease as much as 3~ within 10 minutes of immersion. When the victim

219 aspirates cold water, the rate of onset of hypothermia is accelerated. Surface cooling occurs more rapidly in infants because of their large body surface area-to-weight ratio. The diving reflex-again, there is some question as to its relevance in humans--and/or hypothermia, with resulting systemic vasoconstriction, redistributes blood flow from the spleen and intestine to the myocardium and brain. 29 Near-drowned humans generally do not show significant serum electrolyte changes after aspiration of either freshwater or sea water. However, serum electrolyte concentrations can change after drowning and near-drowning and are dependent on the amount and type of fluid aspirated. Modell et al, in a canine model, showed that with aspiration of -<22 mL/kg of either freshwater49 or sea water,5~ significant long-term changes in serum electrolyte concentrations did not occur. Aspiration of water in excess of this amount is highly unlikely in near-drowned humans and is found in only 15% of humans who die in the water from drowning. 5~ This likely explains why life-threatening changes in serum electrolyte concentrations are not reported in individuals who have suffered freshwater or sea-water near-drowning. Thus, at the scene or in the ED, intravenous (IV) fluid therapy should be 0.9% saline solution, and serum electrolyte concentrations should be evaluated before any specific corrective electrolyte therapy is started. The need for emergent treatment secondary to electrolyte abnormalities should be rare unless the neardrowning event occurs in an extremely concentrated liquid media, such as the Dead Sea, with concentrations of Na +, K +, CI-, Ca ++, and Mg ++, which are 3 to 36 times as concentrated in this body of water as in the Mediterranean Sea. 52 Although of much historical concern, 33 significant blood volume changes are not usually seen in patients after near-drowning in either freshwater or sea water. Aspiration of freshwater in an amount > 11 mL/kg body weight is associated with an increase of blood volume in direct proportion to the volume aspirated. 49 This occurs within 1 minute of aspiration and is followed by the rapid distribution of water throughout the intracellular and extracellular compartments if resuscitation is successful. Hypovolemia has occurred within 60 minutes of aspiration of this quantity of freshwater: 3 The hematocrit may or may not be altered slightly by the presence of hemolysis secondary to hypox-

220 emia. Freshwater aspiration does not result in any significant hemolysis in the absence of hypoxemia. 54 Modell et al showed, in a canine model, that rapid central venous injection of up to 44 mL/kg distilled water would result in hemolysis only if there were concomitant hypoxemia. 54 In another canine-based near-drowning model, Modell et a136 instilled chlorinated or unchlorinated distilled water or saline, 22 mL/kg, into the animal's trachea. Gross hemolysis was observed in 9 of 10 animals that aspirated distilled water but in none of those that aspirated saline, thus demonstrating that both a hypotonic environment and hypoxemia are necessary for hemolysis to occur in this situation. Significant changes in hemoglobin and hematocrit values are rarely found in humans, 55 supporting the theory that near-drowned humans do not suffer large fluid aspirations. When significant hemolysis does occur, it may be confirmed by the pink color of the plasma when blood is spun to determine a hematocrit or by finding high serum lactic dehydrogenase and low serum haptoglobin levels. In the subacute period, an elevation of indirect bilirubin will be seen. Of note, intravascular hemolysis may be associated with disseminated intravascular coagulation secondary to intravascular release of erythrocyte thromboplastin. 56 Only 1 of 91 consecutive near-drowning patients reported by Modell et a155 had a plasma hemoglobin level of 500 mg/100 mL. This individual later died of massive lung consolidation.

Pulmonary System Between 85% and 90% of human near-drowning incidents are associated with significant aqueous media aspirated into the lungs. 55 Victims may aspirate fresh, brackish, or salt water along with various foreign material, either from the water itself or from the stomach. 55 Sea water is hypertonic--with saline concentrations ranging from 530 mmole/L in the Mediterranean Sea to 1,500 mmole/L in the Dead Sea--and includes high concentrations of potassium, calcium, and magnesium. 52 When sea water is aspirated, fluid is drawn from the plasma into the alveoli and down an osmotic gradient, most often resulting in a significant decrease in Pao 2. Although there may be some differences in the degree of hypoxemia, depending on the volume of fluid aspirated a significant deterio-

GABRIELLIAND LAYON ration in arterial oxygenation may occur when as little as 1 to 2.2 mL/kg water is aspirated into the lungs. 49'5~ In an animal model, hypoxemia resulted when volumes as small as 2.2 mL/kg were instilled intratracheally and when treatment was limited to restoring spontaneous ventilation and circulation. 49 In another study, when 11 mL/kg of freshwater or sea water were instilled into the trachea, Pao 2 decreased for at least 72 hours after aspiration. 47 Finally, Modell et al36 showed that, after instillation of 22 mL/kg freshwater or normal saline solution into the tracheas of anesthetized dogs, arterial hypoxemia of a significant degree persisted even though the animals were breathing spontaneously and hyperventilating at the time (60 minutes postaspiration) that blood samples were drawn. The pathophysiology of intrapulmonary shunting varies with the type of water aspirated. For example, the hypoxia and intrapulmonary shunting seen immediately after near-drowning with freshwater aspiration result largely from alteration of the surface-tension properties of pulmonary surfactant. 59 Conversely, aspiration of seawater does not alter surfactant surface-tension properties; however, fluid-filled perfused alveoli result in intrapulmonary shunt and hypoxemia after sea water is aspirated. 59 Thus, aspiration of either type of water leads to intrapulmonary shunting in the terminal gas-exchanging airways. In a study of 91 patients, Modell et al55 analyzed arterial blood gas (ABG) values (Pao 2, Pac%, and pHa) at various times after a near-drowning event in either sea water, freshwater, or brackish water. Profound arterial hypoxemia was noted in almost all. Pao2:Fi % (Pao2-to-inspired oxygen fraction ratio), an indicator of intrapulmonary shunt, ranged from 30 to 585 mm Hg. Only one patient with a Pao2:Fio 2 ratio >150 mm Hg died; this individual was judged as neurologically unsalvageable, and therapy was withdrawn. Ten patients had Pao 2 >80 mm Hg while breathing room air; these individuals were thought to be victims of near-drowning without aspiration. Although in some patients Pao 2 returns to normal within 48 hours, others show persistent hypoxia for days and even weeks after an episode of near-drowning. 55'6~ In addition to the gas exchange abnormalities, drowning and near-drowning have been associated with other pulmonary pathological findings. Hyperexpansion of the lungs is a frequent finding on

CRITICALCAREOF IMMERSION INJURIES autopsy40'62'63 and is attributed63 to an increase in airway pressure with alveolar rupture secondary to violent ventilatory efforts against a closed glottis, although the mechanism is not precisely clear. Furthermore, various materials may be aspirated with water, including gastric contents, mud, sand, and fragments of aquatic vegetation. 4~ These materials have been found in up to 70% of drowned victims and may be associated in near-drowned patients with late-onset ( > 12 h) miliary pneumonitis secondary to acute inflammatory reactions of the lower airways. 64 Bacterial infection may occur when the near-drowning event occurs in grossly contaminated water, such as sewage, stagnant ponds, or public hot tubs. 65-69 However, in the majority of cases bacterial infection does not seem to play an early role in the respiratory failure secondary to near drowning. In a retrospective review of 91 near-drowned persons, the prophylactic use of antibiotics resulted in no clinical improvement. 55 Indeed, prophylactic antibiotic use may predispose to the development of resistant organisms. The authors recommend the early use of antibiotics only in individuals who suffered a near-drowning event in contaminated water in which pathogenic organisms may likely exist. If possible, a sample of the contaminated water should be sent to the nearest microbiology laboratory for bacteriological analysis.

Central Nervous System Because one is usually able to reverse the abnormal physiology seen in the pulmonary system but not that of the CNS, the presenting state of the CNS is of great significance when attempting to influence the morbidity and mortality of neardrowned patients. A near-drowned patient with ARDS will, if able to recover, have little or no residual disability. 61 The permanent neurological impairment seen secondary to cerebral hypoxia is, by definition, irreversible. A variety of neurological abnormalities, not all permanent or fatal, have been described after neardrowning. A period of unconsciousness, thought to be secondary to cerebral hypoxia, is seen in most patients. 34 The status of the patient's CNS is a central issue with regard to the evaluation and care of the near-drowned patient. Thus, frequent neurological assessment, using the Glasgow Coma Scale (GCS), should be performed. This issue has been studied by both Conn et al 7~ and Modell et al. 71

221 The investigators found that patients awake and oriented on arrival to the ED survive without neurological sequelae if any pulmonary dysfunction present is treated successfully. Ninety percent 71 to 100% 70 of patients arriving in the ED with blunted mentation (stuporous but capable of being aroused; purposeful movements to pain) survived without neurological residua. Patients presenting to the ED comatose had much worse outcomes: although 44% 70 to 55% 71 recovered completely, 10% 71 to 23% 70 had severe persistent neurological dysfunction; the highest incidence of this was seen in pediatric near-drowning cases. Approximately 34% 7~ of patients presenting comatose to the ED died after presentation: In Modell et al, 71 91% of adults survived normally overall, and 9% died; none survived with severe persistent neurological dysfunction. When the comatose adults in the series by Modell et a171 were evaluated separately, 73% survived normally, and 27% died. Again, there were no survivors with severe persistent neurological dysfunction. In comatose children, on the other hand, survival with normal brain function approximated 44% in the studies of both Conn et al and Modell et al, whereas 33% to 39% died, and 17% to 23% survived with incapacitating brain damage. 7~ These data may be interpreted as follows: The overall normal survival of children is worse than that of adults. Children's hearts are more likely to be resuscitated after a prolonged hypoxic insult than are those of adults, but the child's brain is not resuscitable after prolonged hypoxia. For this reason, more children than adults exist with severe persistent neurological dysfunction. Conn et a170'72 used hypothermia, barbiturate coma, neuromuscular blockers, hyperventilation, and dehydration in an attempt to enhance neurological outcome; this treatment regimen was termed HYPER therapy. Although initial results led the authors to believe that there was significant improvement in the number of normal outcomes in some subgroups of near-drowned patients, a comparable series presented by Modell et a171 found similar results without using HYPER therapy. Other attempts to "resuscitate" the brain in pediatric near-drowning cases have been largely unsuccessful. Three small studies 73-75 involving 75 severe pediatric near-drowned patients found that, in spite of aggressive cerebral resuscitation, only 12 (16%) survived neurologically intact; the remain-

222 der either died, remained in a persistent vegetative state, or, in one case, was mildly to moderately retarded. Extensive neuropsychological testing in a portion of the apparently intact survivors showed nearly average cognitive function with mild gross motor and coordination defects.75 Further work 19'76 suggests that aggressive attempts at brain "resuscitation" result in more surviving, severely braindamaged children. Recent findings by other groups have suggested that the use of multimodality therapy for brain protection is of little u s e . 77-79 HOWever, a study by Kemp et al suggested that those children who show significant neurological improvement within hours after successful cardiopulmonary resuscitation (CPR) usually recover; those who do not are more likely to have a poor outcome. so Despite these rather dismal data, in a study of 121 near-drowned children, of whom 51 were in the C 3 stage of coma (no response to pain, fixed and/or dilated pupils, absence of spontaneous respiration, hypotension, and poor perfusion as described by Conn et al and Modell et al,70,71 Nussbaum 81 found that with aggressive resuscitation as described above, 19 of 51 patients (37%) had complete recovery, 14 of 51 (27%) had significant brain damage, and 18 of 51 (35%) died. The outcome correlates in the C 3 group were submersion time, mean intracranial pressure (ICP), and mean cerebral perfusion pressure. Although this report is encouraging, the fact that aggressive therapy is so often unsuccessful suggests that the cerebral insult is not related to ICP per se but rather to the duration of the ischemic injury and/or to reperfusion injury. Further work in this area is needed to sort out the inconsistencies. Because there are no absolute predictors of outcome, Model182 suggested, and the authors agree, that all near-drowned victims should be treated. The decision to cease treatment, if there is no improvement after 24 to 48 hours, should be made by the attending physician and the family. One must " . . . respect the opinion of others on this subject, since there is no medical indicator that will predict certain success or failure. ''82 On the patient' s arrival of the ED, careful review of the emergency medical service run report and a comprehensive debriefing of the paramedic and witnesses are more illuminating and helpful than a history and physical examination done in a hurry by the admitting physician. A full clinical assess-

GABRIELLIAND LAYON ment of neurological status at the time of ED admission may be difficult if sedatives or neuromuscular blocking agents were used during cardiopulmonary resuscitation and, especially, in the presence of hypothermia. Furthermore, the literature occasionally reports patients who survived and fully recovered neurologically after prolonged submersion, severe hypothermia, low GCS score, and prolonged asystole, s3 Occasionally, withdrawal of care for a deeply comatose patient becomes an ethical dilemma when, despite the fact that the patient is rewarmed and has full recovery from neuromuscular blockade by peripheral nerve twitch monitor, there is discordance between family members and physician consultants. If there is still doubt that sedative or hypnotic agents are present (eg, the patient received a large dose of thiopental or benzodiazepine or has evidence of low hepatic or renal drug clearance) in the system after 24 hours, a cerebral blood flow scan is performed. The apnea test is simple to perform and costs less than cerebral blood flow scanning, but it can be misleading in the presence of residual sedatives. Goodwin et al s4 used multimodality evoked potentials (MEPs) to predict outcome in 41 children who were comatose from a variety of causes, and they identified another 982 patients in 19 studies in whom evoked potentials were recorded. In the 1,023 cases, there was only 1 valid case of false pessimism. The authors suggest that the use of MEPs, in conjunction with clinical information, may help in identifying patients who should receive aggressive therapy. Very rarely, a patient with anoxic coma will recover nearly complete intellectual and neurological function only to suffer a relapse and progress to coma and death. The time interval between the initial anoxic insult and onset of the relapse is usually between 1 and 2 weeks and has been associated with pathological findings of diffuse demyelination involving the lower lobes of the cerebral hemispheres, including the brain stem and the cerebellum, s5 This rare and etiologically unknown clinical course has not been described in neardrowning; the case series of Plum et a185 included gas (illuminating, cooking, and gasoline) intoxication, intraoperative hypotension, and postoperative cardiac arrest. The significance of this phenomenon for near-drowned patients is unclear at this time,

CRITICAL CARE OF IMMERSION INJURIES TREATMENT OF THE NEAR-DROWNED VICTIM Scene

The treatment of the near-drowned victim begins with rescue and removal from the water. Despite major technological advances in the field of emergency and critical care medicine, the initiation of effective CPR at the scene, normally performed by a lifeguard, paramedic, or bystander, is the first and probably most important factor to influence the rate of survival and recovery of normal cerebral function. Specially trained lifeguards and other equipped rescuers may be able to initiate rescue breathing in deep water using a snorkel-to-mouth technique. A high index of suspicion for cervical spine injury should be maintained. Care should be taken by the rescuer to stabilize and protect the victim's cervical spine, minimize movement and, as rapidly as possible, place a rigid cervical collar and initiate lateral immobilization with a cervical immobilization device and/or tape across the forehead attached to the backboard (Table 1). The rescuer, if needed, should provide mouth-to-mouth ventilation with the head in a neutral position (without extension). If there is particulate matter in the upper airway, it should be removed manually or suctioned, again while minimizing head movement. Even though previous work has shown that water exiting the mouth after drowning comes from the stomach, 86 the subdiaphragmatic thrust (Heimlich) maneuver has been recommended for use in the near-drowned victim. 87"88Furthermore, studies by Werner et a189 did not show increased benefit from an abdominal thrust over gravity drainage on the outcome of experimental animals who aspirated sea water. A thorough review of publications and testimony by the Institute of Medicine in 1994 concluded that use of this maneuver is inappropriate for treatment of a drowned or near-drowned

Table I. Immobilization of the Cervical Spine

9 Requires lateral and A-P stabilization 9 Rigid collar 9 Cervical immobilization device or sandbags lying bilaterally from crown of head past auricular lobule and abutting on the supraclavicular fossae plus 3-inch tape across forehead and fixed to backboard or side of stretcher Abbreviation: A-P, anteroposterior.

223 victim unless a foreign object is obstructing the airway. 9~ Furthermore, use of this technique may result in delay of effective CPR or in regurgitation and aspiration of gastric contents, resulting in consequences as serious as aspiration pneumonitis, respiratory failure, and death. 89~92 Finally, no matter how well the patient appears, he or she must be taken to a hospital for evaluation because the initial appearance of the near-drowned patient may be misleading. It is the authors' opinion that transport to the hospital should be carried out with basic monitoring, including electrocardiography and pulse oximetry. Oxygen (100%) should be administered en route until analysis of oxygenation by pulse oximetry (Sp02) or Pao 2 shows that it can be reduced safely; the lowest Fio 2 yielding an Sp02 of 93% to 95% is acceptable. Once the patient arrives in the ED, pulmonary supportive measures, such as continuous positive airway pressure (CPAP) and positive end-expiratory pressure (PEEP), should be added to improve oxygenation and allow Fio 2 to be decreased.

In the Emergency Department If the patient survives initial CPR at the scene, it is essential for the ED physician to evaluate the adequacy of the prehospital CPR with an immediate ABG measurement, neurological examination, and review of the resuscitation record. Other factors requiring immediate evaluation on the patient's arrival at the ED are past medical history, conditions leading up to the near-drowning event, estimated submersion and CPR times (although these are notoriously unreliable), evaluation for the presence of ongoing malignant arrhythmias or severe bradycardia, oxygen saturation, core temperature, and evidence of concomitant trauma. If the patient is unconscious in the ED, the cervical spine remains immobilized, and the patient is evaluated for cervical spine injury with a full neck radiograph series or computed tomographic scan of the spine; the films are then evaluated by the ED attending and radiology physicians. When radiographic studies are performed, they must be done without discontinuing or compromising the patient's Supportive therapy. The initial clinical evaluation in the ED is not: different from any other trauma resuscitation; airway, breathing, and circulation (ABCs) have priority. Patients who arrive awake and alert at the hospital may have received CPR on the scene. 71

224

GABRIELLI A N D L A Y O N

These patients thus require observation and treatment for deterioration in cardiopulmonary or neurological status; nonetheless, survival of this population is reported as 100% (class A according to the classification systems of the Conn et al7~ and Modell et al. 71 Class B patients (lethargic), if hemodynamically stable, may require airway protection, mechanical ventilation, and intensive care unit observation for a several days. Modell et a171 pointed out that one of the three deaths they observed in this group occurred before the importance of intensive care therapy was appreciated. Approximately 90% of these patients survive the initial insult without severe neurological deficits.71 Patients who are comatose on arrival, like all near-drowned individuals, require immediate evaluation, again emphasizing the ABCs. Severe bradycardia resulting from hypoxia, hypothermia, or vasoconstriction may make the arterial pulse difficult to palpate, even at the carotid level. If there is any question about the existence of a pulse, closedchest cardiac compression and artificial ventilation should be initiated. In any stuporous or comatose patient, the authors protect the airway with an endotracheal tube because the near-drowned victim may have swallowed large amounts of water, particulate matter, or both, and is prone to regurgitate and suffer the consequences of pulmonary aspiration of gastric contents. Rapid sequence intubation (Table 2) is performed using an in-line cervical stabilization technique (stabilization of the head in neutral position by an assistant); temporary removal of the cervical collar may be necessary to perform adequate cricoid pressure. Fiberoptic bronchoscopy may be used to facilitate intubation Table 2. Rapid Sequence Intubation

9 9 9 9

Monitors Preoxygenation Cricoid pressure Induction of sodium thiopental, 0.5 to 4 mg/kg, or etomidate, 0.25 to 0.5 mg/kg 9 Succinylcholine, 1 mg/kg IV, without defasiculation* or a nondepolarizing rapid-onset IV NMB agent Abbreviations: IV, intravenous; NMB, neuromuscular blocking. *Because there is a small risk of significant neuromuscular blockade even with a "defasciculating" dose of a nondepolarizing NMB agent, 115 and given the conflicting data, it is the authors' practice not to defasciculate for the prevention of myalgias.

or to remove particulate material from the tracheobronchial tree. The authors do not recommend any brain preservation technique at this time because survival with or without the use of brain preservation techniquest is identical in the largest series in the literature. 19'76'93 Hypothermia occurring at the time of immersion, however, does appear to be protective and on occasion has been on occasion associated with a few cases of "miraculous" recovery of cerebral function from a deep coma. 94'95 In children, bradycardia may be an expression of hypoxemia, hypothermia, the diving reflex, and/or a physiological protective clinical feature. 96 Interestingly, Yanagawa et al, 96a using an active mild hypothermia (33~ to 36~ protocol after return of spontaneous circulation in patients who suffered out-of-hospital cardiac arrest, found that outcome was improved in the mild hypothermia group compared with historical controls. Although not a definitive study and of uncertain relevance to near drowning, it is nonetheless quite intriguing and deserves further evaluation. Interestingly, a recent study in patients undergoing cardiopulmonary bypass showed that rapid rewarming may be associated with increased lactic acid in jugular venous bulb blood and increased brain A-Vo2 .97 For this reason, if there is no evidence of severe bradycardia and the patient is hemodynamically stable, the authors favor slow external rewarming (removal of clothing and covering with dry blankets) to achieve core rewarming. Others have reported success with invasive active core rewarming techniques such as cardiopulmonary bypass. 98 In the Intensive Care Unit

Once again, re-evaluation of the ABCs is appropriate, ensuring that the patient has a viable airway, that adequate gas exchange is occurring, and that circulatory status is acceptable. The circulation is usually manageable without the use of a pulmonary artery catheter; however, if there is concern as to the adequacy of intravascular volume, invasive monitoring with a pulmonary artery catheter, central venous pressure catheter, or transesophageal echocardiography is appropriate. Blood pressure is usually monitored invasively. Advanced age, signs, or history of congestive heart failure and the need for pharmacological cardiovascular support usually are indications for an echocardiographic evaluation of left ventricular function. The presence of severe dysfunction (ejection fraction

CRITICAL CARE OF IMMERSION INJURIES <30%) is an indication of replacement of a pulmonary artery catheter to optimize intravascular volume and oxygen delivery. Although cardiac output may decrease when mechanical ventilation, PEEP, and CPAP are used as pulmonary supportive measures, fluid loading is most often all that is required to improve it, and prolonged inotropic support is rarely required. 53 The authors' initial resuscitation goal is euvolemia and a mean arterial blood pressure of 60 to 70 mmHg; although rarely necessary, vasopressors are used when needed. When hemodynamically stable, the intubated comatose patient is transported to the radiology department, where a computed tomography scan of the head and neck is performed. It is critical that such transport does not compromise the supportive intensive therapy in progress. In the series by Allman et al,78 patients with intracranial pressure (ICP) monitoring and aggressive therapy to achieve and maintain control of ICP had outcomes that were no better than those who did not receive this type of monitoring. Despite the controversy that surrounds the use of ICP monitoring and treatment, it is reasonable to consider placing an ICP monitoring device in comatose, neardrowned victims as soon as possible after arrival in the intensive care unit. Even without an ICP monitor, mild hyperventilation (Paco 2 - 30 mm Hg) may be used to empirically decrease ICP without significant risk. If the ICP is elevated (->15 to 20 mm Hg), hyperventilation to achieve Paco 2 of 25 to 30 mm Hg is carried out in an attempt to decrease cerebral blood flow, and thereby the ICP, while simultaneously keeping CPP (defined as the mean arterial pressure [MAP]-ICP) ->70 mm Hg. Although this number is higher than the lower end of acceptable CPP (50 mm Hg) for normal brain, in head-injured patients one wishes to avoid the possibility of cerebral ischemia resulting from inadequate perfusion; this topic recently has been reviewed by Sulek. 99 A mannitol bolus, 0.5 g/kg ideal body weight, may be used to decrease ICP if hyperventilation alone does not produce the desired result. However, the damage to the brain in near-drowning likely results from anoxia at the time of the injury as opposed to late elevated ICP; elevated ICP in these patients may well be nothing more than a marker of damage already done. The patient's head and chest are elevated to between 15 ~ and 30 ~ to enhance cerebral venous drainage, and the head is kept in a neutral position. ~~176176

225 There are no data to support the use of barbiturates or steroids to lower ICP that is refractory to the above-mentioned techniques in the near-drowned patient. On the contrary, the use of corticosteroids has been associated with decreased host response to infections5'~~ and worsened outcome. Seizure prophylaxis (usually phenytoin) is initiated in the ED, and enteral feeding is most often begun within 24 hours, usually via a nasoduodenal (ie, Dobhoff) feeding tube. Severe metabolic acidosis (pH <7.20) secondary to lactic acidosis is corrected pharmacologically. Empirically, the authors recommend correction of the base deficit with bicarbonate to achieve a pH between 7.20 and 7.30. Lactic acid levels may be checked every 4 to 6 hours during resuscitation. Patients who previously were poorly perfused and then resuscitated may exhibit a rewarming "wash-out" effect, with a temporary lactic acid surge in the blood; thereafter, lactic acid will decrease as resuscitation is completed. Once the patient is rewarmed, persistently elevated lactic acid levels usually result from oxygen debt and may require pharmacological augmentation of oxygen delivery with the pulmonary artery catheter employed for guidance of volume status and stroke volume. Critically ill patients who have progressively increasing levels of lactic acid despite aggressive resuscitation usually have a poor outcome.l~ Severe electrolyte abnormalities are rarely observed in the near-drowned victim. In general, the authors' preferred IV resuscitation fluid is 0.9% NaC1 for near-drowned victims; isotonic solutions do not aggravate the cerebral edema that may be present. In select cases, the use of intermittent small bolus doses (100 to 150 mL) of 3% saline solution to maintain intravascular volume might be considered; however, this has not been studied in near-drowned victims. The serum sodium usually is maintained between 140 and 155 mEq/L, although serum sodium as high as 160 mEq/L generally will cause no difficulties. 1~ This usually results in 750 to 1,000 mL of a 3% NaCI solution infused over 24 hours in a 70-kg patient with normal initial plasma sodium. In the patient with severe metabolic acidosis (acidemia with pH < 7.2) a hypertonic solution of sodium acetate and NaCI may be considered. This solution is prepared by adding 154 mEq sodium acetate to 1 L 0.9% saline solution; this "balanced" hypertonic solution prevents the development of metabolic alkalosis.

226 The authors have successfully used this technique extensively on patients with closed head injury in whom control of ICP and maintenance of CPP are considered of critical importance. The authors do not administer blood as long as the hematocrit is at least 25% unless there is a documented need for additional oxygen delivery that cannot be met by augmenting stroke volume with either nonheme fluids or inotropes. Supplemental oxygen administration is continued while obtaining data from ABG measurements or a pulse oximeter to evaluate for the presence of hypoxemia. Awake, alert, and cooperative patients do not require endotracheal intubation unless their pulmonary pathology does not respond favorably to enriching inhaled gas with oxygen, a CPAP mask, or both. 34 All comatose patients require endotracheal intubation, and those with blunted mental status must be evaluated individually. Both for patient comfort and to optimize V/Q relationships, spontaneous breathing is preferred if the patient can tolerate it; intermittent mandatory ventilation and pressure support ventilation are often used to achieve this. The patient may be fully supported with controlled mechanical ventilation if this does not provide adequate ventilation. The work imposed on the spontaneously breathing patient by the endotracheal tube and breathing apparatus may be eliminated by pressure support ventilation (PSV) starting at 10 c m H20.106'107 Very small endotracheal tubes (<6.5 mm internal diameter) may require higher levels of PSV. 1~ Additional levels of PSV (5 to 15 cm H20 ) may be required to unload the respiratory muscles and offset the increased elastic work load secondary to pulmonary edema. When the pulmonary damage is massive and compliance is extremely low (high plateau inspiratory pressure), the pressure control mode of ventilation may be useful. In general, a plateau pressure >40 cm H20 is usually an indication to alter the ventilator mode. In selective cases, equalizing or reversing the inspiratory-to-expiratory (I:E) ratio may allow adequate oxygenation and ventilation at lower PEEP and peak inspiratory pressure, lO9 This mode of ventilation is difficult for the patient to tolerate without sedation and, sometimes, neuromuscular blockade, which decreases the ability to perform frequent neurological examinations. Bronchodilators such as albuterol and ipratropium are administered via a one-way in-line valve as needed so as to not break the ventilator

GABRIELLIAND LAYON circuit with each use; pulmonary edema often is associated with mild bronchospasm. Expiratory wheezes and a wide gap between peak and plateau pulmonary pressure (eg, >5 cm H20) are indications for bronchodilator therapy. Although the degree of intrapulmonary shunting after near-drowning is variable, the single most important therapeutic intervention to reverse hypoxemia is the application of CPAP/PEEP. CPAP/ PEEP is tit-rated to maintain oxygen saturation ---92% to 93% using the lowest possible FIoz; FIo 2 < 0.5 indicates minimal risk for oxygen toxicity. 11~ The titration of CPAP/PEEP may be limited by its effect on cardiovascular function, such as decreasing venous return to the right ventricle and left shift of the intraventricular septum with reduced left ventricular end-diastolic volume. When high levels of CPAP/PEEP compromise cardiovascular function, and fluid administration does not ameliorate the problem, the authors recommend the insertion of a pulmonary artery catheter to optimize intravascular volume status and monitor oxygen delivery and consumption. If analysis of the patient's hemodynamic status is complicated by high mean airway pressure (eg, high level of CPAP or reverse I:E ratio), the early use of transesophageal echocardiography may be useful for assessment of left ventricular end-diastolic volume. In the authors experience in general intensive care unit patients, this relatively simple diagnostic procedure allows correlation between the echocardiographic images and the hemodynamic data, thus providing data for the adjustment of IV fluid therapy to maintain euvolemia. Sedatives and/or muscle relaxants should only be used if necessary to keep a patient from "fighting" the ventilator, thus compromising V/Q ratios. When necessary, the authors' choice of sedative is Propofol (Zeneca, Wilmington, DE); the drug's potency and short redistribution half-life make it very useful when frequent neurological evaluations are required.111 Steroids and prophylactic antibiotics are not recommended. In fact, experience with animal models indicates that steroids do not increase survival rates after submersion, 1~ and, in a non-near-drowning model, they actually interfere with normal pulmonary healingll2; however, the use of broad-spectrum antibiotics may enhance the emergence of resistant organisms. Broad-spectrum antibiotic coverage is appropriate in patients who have un-

CRITICAL CARE OF IMMERSION INJURIES dergone near-drowning in contaminated bodies of water. 64,69 Prevention

By identifying age-related drowning risks, communities can reduce drowning rates (Table 3). This is particularly true regarding infants, children, and adolescents. The most successful preventative strategy so far--the installation of four-sided (bartier) fencing that isolates the pool from the house and yard--has reduced drowning rates in children 1 to 4 years old. 113 Pool alarms and covers have not been shown to significantly reduce drowning and near-drowning of children. Infants should never be left unattended in bathtubs, whirlpools, swimming pools, irrigation ditches, or any open standing water; even toilets and partially filled cleaning buckets may represent household hazards. Furthermore, children who can swim should never do so alone or without adult supervision. Effective CPR and water safety skills should be encouraged in the community, particularly for parents who own home swimming pools and who have small children. Everyone participating in water sports should wear a personal floatation device. Adolescents must be taught to swim and informed about the dangers of alcohol and other drug use during water sport activities. In adolescents 13 and 19 years between old, risk-taking behavior increases significantly in boys; therefore, extra counseling is warranted. Swimming with a partner or "buddy" is particularly important for individuals with medical conditions that may abruptly alter their level of consciousness, such as seizure disorders, cardiac disease, and diabetes mellitus. In summary, an awareness of the hidden dangers of recreational activities in and around water, and close supervision of infants, children, and adolescents, is the secret to preventing drowning and Table 3. Methods of Prevention

9 Barrier (perimeter) fencing around pools 9 Careful, compulsivesupervisionof children 9 "Buddy" swimming 9 Limit use of licit/illicit drugs; "just say no" is inadequate

9 Community CPReducation 9 Personal flotation deviceswhen engaging in water sports 9 Legal sanction of those who transgresssafety rules

Abbreviation: CPR, cardiopulmonary resuscitation.

227 near-drowning events. The community expects the government to enforce safety rules, to promote health education through medical and nonmedical personnel, and to punish individuals who transgress basic safety rules or who engage in water sports while intoxicated. T M At the time of this article's publication, prevention is still the most fundamental way to limit neurological disasters resulting from near-drowning. The role of the critical care physician is to maximize and accelerate without causing irreversible cerebral hypoxic damage, the recovery of the patient who survives drowning.

ACKNOWLEDGMENT The authors especially thank Jerome H. Modell, MD, for his review of this manuscript as well as his continued support and counsel.

REFERENCES 1. National Safety Council: Accident Facts, 1997. Itasca, IL, 1997 2. National Safety Council: Accident Facts, 1997. Itasca, IL, 1997, pp 15-16 3. National Safety Council: Web site data. http://www. nsc.org/lrs/statinfo/af8.htm. 4. Orlowski JP: Drowning, near-drowning, and ice-water submersions. Pediatr Clin North Am 34:75-92, 1987 5. Modell JH: The Pathophysiology and Treatment of Drowning and Near-Drowning. Springfield, IL, Thomas, 1971 6. Wintemute GJ: Childhood drowning and near-drowning in the United States. Am J Dis Child, 1990;144:663-669. 7. Spyker DA: Submersion injury: Epidemiology, prevention, and management. Pediatr Clin North Am 32:113-125, 1985 8. Wintemute G J, Kraus JF, Teret SP, et al: Drowning in childhood and adolescence--A population based study. Am J Public Health 77:830-832, 1987 9. Monroe B: Immersion accidents in hot tubs and whirlpool spas. Pediatrics 69:805-807, 1982 10. Cardiner SD, Smeeton WMI, Koelmeyer TD, et al: Accidental drownings in Auckland children. N Z Med J 98:579582, 1985 11. Bross MH, Clark JL: Near-drowning. Am Faro Physician 51:1545-1551, 1995 12. Olshaker JS: Near drowning. Emerg Med Clin North Am 10:339-350, 1992 13. Gulaid JA, Sattin RW: Drownings in the United States, 1978-1984. Division of Injury Epidemiology and Control, Center for Environmental Health and Injury Control, 37(SS-1): 27-33 14. Smith JD, Marcus RA, Sikes RK, et al: Perspectives in disease prevention and health promotion: Drownings--Georgia, 1981-1983. MMWR, 1985;34:281-283

228 15. Abel E, Zeidenberg P, Regan S, et al: Perspectives in disease prevention and health promotion: Alcohol and violent death--Erie County, New York, 1973-1983. MMWR, 1984;33: 226-227. 16. Howland J, Hingson R, Mangione TW, et al: Why are most drowning victims men? Sex differences in aquatic skills and behaviors. Am J Public Health 86:93-96, 1996 17. Dorland's Illustrated Medical Dictionary (ed 28th). Philadelphia: Saunders, 1994, p 507 18. Davis JH: Autopsy findings in victims of drowning, in Modell JH: The Pathophysiology and Treatment of Drowning and Near-Drowning. Springfield, IL: Thomas, 1971, pp 74-82 19. Biggart MJ, Bohn DJ: Effect of hypothermia and cardiac arrest on outcome of near-drowning accidents in children. J Pediatr 117:1"/9-183, 1990 20. Kemp AM, Sibert JR: Outcome in children who nearly drown--A British Isles study. Br J Med 302:931-933, 1991 21. Hayward JS, Hay C, Matthews BR, et al: Temperature effect on the human dive response in relation to cold water near-drowning. J Appl Physiol 56:202-206, 1984 22. Keatinge WR, Nadel JA: Immediate respiratory response to sudden cooling of the skin. J Appl Physiol 20:65-69, 1965 23. Cooper KE, Martin S, Riben P: Respiratory and other responses in subjects immersed in cold water. J Appl Physiol 40:903-910, 1976 24. Redding JS: Drowning and near drowning---Can the victim be saved? Postgrad Med 74:85-97, 1983 25. Rivers JF, Orr G, Lee HA: Drowning--Its clinical sequelae and management. Br Med J 2:157-161, 1970 26. Cot C: Les asphyxies accidentecelles (submersion, electrocution, intoxication oxycarbonique) Paris, France, Etude Clinique, Therapeutique, et Preventive, Editions Medicales, Maloine, 1931 27. Kurpovich PV: Water in the lungs of drowned animals. Arch Pathol 15:828-833, 1993 28. Craig AB Jr: Causes of loss of consciousness during underwater swimming. J Appl Physiol 16:583-586, 1961 29. Gooden BA: Drowning and the diving reflex in man. Med J Aust 2:583-587, 1972 30. Kemp AM, Silbert JR: Outcome in children who nearly drown--A British Isles study. Br Med J 302:931-933, 1991 31. Martin TG: Near drowning and cold water immersion. Ann Emerg Med 13:263-273, 1984 32. Wood SC: Interactions between hypoxia and hypothermia. Ann Rev Physiol 53:71-85, 1991 33. Swarm HG, Brucer M: The cardiorespiratory and biochemical events during rapid anoxic death VI--Freshwater and seawater drowning. Tex Rep Biol Med 7:604-618, 1949 34. Layon AJ, Modell JH: Drowning and near-drowning. Tinker J, Zapol WM (eds): Care of the Critically Ill Patient. London, England: Springer Verlag, 1992, pp 909-918 35. Swann HG, Spafford NR: Body salt and water changes during fresh water and sea water drowning. Tex Rep Biol Med 9:356-382, 1951 36. Modell JH, Gaub M, Moya F, et al: Physiologic effects of near drowning with chlorinated fresh water, distilled water and isotonic saline. Anesthesiology 27:33-41, 1966 37. Karch SB: Pathology of the heart in drowning. Arch Pathol Lab Med 109:176-178, 1985

GABRIELLIAND LAYON 38. Hayward JS, Hay C, Matthews BR, et al: Temperature effect on the human dive response in relation to cold water near-drowning. J Appl Physiol 56:202-206, 1984 39. Gooden BA: Why some people do not drown: Hypothermia versus the diving response. Med J Aust 157:629-630, 1992 40. Fuller RH: The 1962 Wellcome prize essay: Drowning and the postimmersion syndrome. Mil Med 128:22-36, 1963 41. Kvittingen TD, Naess A: Recovery from drowning in freshwater. Br Med J 5341:1315-1317, 1963 42. Rath CE: Drowning hemoglobinuria. Blood 8:1099-1104, 1953 43. Munroe WD: Hemoglobinuria from near-drowning. J Pediatr 64:57-62, 1964 44. King RB, Webster IW: A case of recovery from drowning and prolonged anoxia. Med J Aust 1:919-920, 1964 45. Redding JS, Pearson JW: Management of drowning victims. Gen Pract 29:100-104, 1964 46. Agar JWM: Rhabdomyolysis and acute renal failure after near-drowning in cold saltwater. Med J Aust 161:685-687, 1994 47. Modell JH, Moya F, Williams HD, et al: Changes in blood gases and A-aDOz during near-drowning. Anesthesiology 29:456-465, 1968 48. Modell JH, Davis JH, Giammona ST, et al: Blood gas and electrolyte changes in human near-drowning victims. JAMA 203:99-105, 1968 49. Modell JH, Moya F: Effects of volume of aspirated fluid during chlorinated fresh water drowning. Anesthesiology 27: 662-672, 1966 50. Modell JH, Moya F, Newby EJ, et al: The effects of fluid volume in seawater drowning. Ann Intern Med 67:68-80, 1967 51. Modell JH, Davis JH: Electrolyte changes in human drowning victims. Anesthesiology 30:414-420, 1969 52. Yagil Y, Stalnikowicz EL, Michaeli J, et al: Near drowning in the Dead Sea: Electrolyte imbalances and therapeutic implications. Arch Intern Med 145:50-53, 1985 53. Tabeling BB, Modell JH: Fluid administration increases oxygen delivery during continuous positive pressure ventilation after freshwater near-drowning. Crit Care Med 11:693-696, 1983 54. Modell JH, Kuck EJ, Ruiz BC, et al: Effect of intravenous vs aspirated distilled water on serum electrolytes and blood gas tensions. J Appl Physiol 32:579-584, 1972 55. Modell JH, Graves SA, Ketover A: Clinical course of 91 cumulative near-drowning victims. Chest 70:231-238, 1976 56. Culpepper RM: Bleeding diathesis in fresh water drowning. Ann Intern Med 83:675, 1975 57. Halmagyi DFJ: Lung changes and incidence of respiratory arrest in rats after aspiration of sea and freshwater. J Appl Physiol 16:41-44, 1961 58. Colebatch HJH, Halmagyi DFJ: Lung mechanics and resuscitation after fluid aspiration. J Appl Physiol 16:684-696, 1961 59. Giammona ST, Modell JH: Drowning by total immersion: Effects on pulmonary surfactant of distilled water, isotonic saline, and seawater. Am J Dis Child 114:612-616, 1967 60. Modell JH, Davis JH, Giammona ST, et al: Blood gas and electrolyte changes in human near-drowning victims. JAMA 203:337-343, 1968 61. Butt MP, Jalowayski A, Modell JH, et al: Pulmonary function after resuscitation from near-drowning. Anesthesiology 32:275-277, 1970

CRITICAL CARE OF IMMERSION INJURIES 62. Imburg J, Hartney TC: Drowning and the treatment of non-fatal submersion--l: Drowning and non-fatal submersion laboratory studies and human data. Pediatrics 37:684-698, 1966 63. Miloslavich EL: Pathological anatomy of death by drowning. Am J Clin Pathol 4:42-49, 1934 64. Mangge H, Plecko B, Grubbauer HM, et al: Late-onset miliary pneumonitis after near drowning. Pediatr Pulmonol 15:122-124 65. Tron VA, Baldwin VJ, Pirie GE: Hot tub drownings. Pediatrics 75:789, 1985 66. Vernon DD, Banner W Jr, Cantwell GP, et al: Streptococcus pneumoniae bacteremia associated with near-drowning. Crit Care Med 18:1175, 1990 67. Washburn J, Jacobson JA, Marston E, et al: Pseudomonas aeruginosa rash associated with a whirlpool. JAMA 235:22052207, 1976 68. Sausker WF, Aeling JL, Fitzpatrick JE, et al: Pseudomonas folliculitis acquired from a health spa whirlpool. JAMA 239:2362-2365, 1978 69. Reines HD, Cook FV: Pneumonia and bacteremia due to Aeromonas hydrophila. Chest 80:264, 1981 70. Conn AW, Montes JE, Barker GA, et al: Cerebral salvage in near-drowning following neurological classification by triage. Can Anaesth Soc J 27:201-210, 1980 71. Modell JH, Graves SA, Kuck EJ: Near-drowning---Correlation of level of consciousness and survival. Can Anaesth Soc J 27:211-215, 1980 72. Conn AW, Edmonds JF, Barker GA: Near-drowning in cold fresh water: Current treatment regimen. Can Anaesth Soc J 25:259-265 73. Sarnaik AP, Preston G, Lieh-Lai M, et al: Intracranial pressure and cerebral perfusion pressure in near-drowning. Crit Care Med 13:224-227, 1985 74. Frewen TC, Sumabat WO, Han VK, et al: Cerebral resuscitation therapy in pediatric near-drowning. J Pediatr 106: 615-617, 1985 75. Bell TS, Ellenberg L, McComb JG: Neuropsychological outcome after severe pediatric near-drowning. Neurosurgery 17:604-608, 1985 76. Bohn DJ, Biggar WD, Smith CR, et al: Influence of hypothermia, barbiturate therapy, and intracranial pressure monitoring on morbidity and mortality after near-drowning. Crit Care Med 14:529-534, 1986 77. Nichter MA, Everett PB: Childhood near-drowning. Is cardiopulmonary resuscitation indicated? Crit Care Med 17: 993-995, 1989 78. Allman FD, Nelson WB, Pacentine GA, et al: Outcome following cardiopulmonary resuscitation in severe pediatric near-drowning. Am J Dis Child 140:571-575, 1986 79. Biggart MJ, Bohn DJ: Effect of hypothermia and cardiac arrest on outcome of near-drowning accidents in children. J Pediatr 117:179-183, 1990 80. Kemp AM, Sibert JR: Outcome in children who nearly drown--A British Isles study. Br J Med 302:931-933, 1991 81. Nussbaum E: Prognostic variables in nearly drowned comatose children. Am J Dis Child 139:1058-1059, 1985 82. Modell JH: Drowning--To treat or not to treat--An unanswerable question? Crit Care Med 21:313-315, 1993 83. Lavelle JM, Shaw KN: Near drowning--Is emergency department resuscitation or intensive care unit cerebral resuscitation indicated? Crit Care Med 21:368-373, 1993

229 84. Goodwin SR, Friedman WA, Bellefleur M: Is it time to use evoked potentials to predict outcome in comatose children and adults? Crit Care Med 19:518-524, 1991 85. Plum F, Posner J, Hain R: Delayed neurological deterioration after anoxia. Arch Intern Med 110:56-63, 1962 86. Ruben A, Ruben H: Artificial respiration--Flow of water from the lung and the stomach. Lancet 1:780-781, 1962 87. Heimlich HJ: Subdiaphragmatic pressure to expel water from the lungs of drowning persons. Ann Emerg Med 10:476480, 1981 88. Heimlich HJ, Patrick EA: Using the Heimlich maneuver to save near-drowning victims. Postgrad Med 84:62-73, 1988 89. Werner JZ, Safar P, Bircher NG, et al: No improvement in pulmonary status by gravity drainage or abdominal thrusts after seawater near-drowning in dogs (abstr) Anesthesiology 57:A81, 1982 90. Rosen P, Stoto M, Harley J (eds): The use of the Heimlich maneuver in near-drowning. Washington, DC, Institute of Medicine, 1994, pp 1-27 91. Ornato JP: Special resuscitation situations--Near-drowning, traumatic injury, electric shock, and hypothermia. Circulation 74:IV-23-IV-25 (Suppl IV) 92. Orlowski JP: Vomiting as a complication of the Heimlich maneuver. JAMA 258:512-513, 1987 93. Dean JM, Kaufman ND: Prognostic indicators in pediatric near drowning--The Glasgow Coma Scale. Crit Care Med 9:536-539, 1981 94. Harold S, Harold B, Rod T, et al: Survival after 40 minutes of submersion without cerebral sequelae. Lancet 1:1275-1277, 1975 95. Edward ND, Timmins AC, Randalls B, et al: Survival in adult after cardiac arrest due to drowning. Intensive Care Med 16:336-337, 1990 96. Ramey CA, Ramey DH, Hayword JS: Dive response of children in relation to cold water drowning. J Appl Physiol 63:665-668, 1987 96a.Yanagawa Y, Ishihara S, Norio H, et al: Preliminary clinical outcome study of mild resuscitative hypothermia after out-of-hospital cardiopulmonary arrest. Ruscitation 39:61-66, 1998 97. Sapire, KJ, Gopinath SP, Farhat G, et al: Cerebral oxygenation during warming after cardiopulmonary bypass. Crit Care Med 25:1655-1662, 1997 98. Leesou GV, Kopf GS, Elefteriades JA, et al: Is cardiopulmonary bypass effective for treatment of hypothermic arrest due to drowning or exposure? Arch Surg 127:525-528, 1992 99. Sulek SA: Intracranial pressure, in Cucchiara RF, Black S, Michenfelder JD (eds): Clinical Neuroanesthesia (ed 2). New York, Churchill Livingstone, 1998, pp 73-123 100. Durward QJ, Amacher AL, Del Maestro RF, et al: Cerebral and cardiovascular responses to changes in head elevation in patients with intracranial hypertension. J Neurosurg 59:938-944, 1983 101. Rosner MJ, Coley IB: Cerebral perfusion pressure, intracranial pressure and head elevation. J Neurosurg 65:636641, 1986 102. Feldman Z, Kanter MJ, Robertson CS: Effect of head elevation and intracranial presure, cerebral perfusion pressure, and cerebral blood flow in head injured patients. J Neurosurg 76:207-211, 1992

230 103. Calderwood HW, Modell JH, Ruiz BC: The ineffectiveness of steroid therapy for treatment of fresh-water near-drowning. Anesthesiology 43:642-650, 1975 104. Iberti TJ, Leibowitz AB, Papadokos PJ: Low sensitivity of the anion gap as a screen to detect hyperlactemia in critically ill adults. Crit Care Med 18:275-277, 1990 105. Vassar MJ, Fischer RP, O'Brien PE: A multicenter trial for resuscitation of injured patients with 7.5% sodium chloride: The effect of added Dextran 70--The Multicenter Group for the study of hypertonic saline in trauma patients. Arch Surg 128:1003-1011, 1993 106. Banner MJ, Kirby RR, Blanch PB: Site of pressure measurement during spontaneous breathing with continuous positive airway pressure--Effect on calculating imposed work of breathing. Crit Care Med 20:528-533, 1992 107. Banner MJ, Kirby RR, Blanch PB, et al: Decreasing imposed work of the breathing apparatus to zero using pressure-support ventilation. Crit Care Med 21:1333-1338, 1993 108. Banner MJ, Kirby RR, Gabrielli A, et al: Partially and totally unloading respiratory muscles based on real-time mea-

GABRIELLIAND LAYON surements of work of breathing: A clinical approach. Chest 106:1835-1842, 1994 109. Tharrat RS; Allen RP, Albertson TE: Pressure controlled reverse ratio ventilation in severe adult respiratory failure. Chest 94:755-762, 1988 110. Winter PM, Smith G: The toxicity of oxygen. Anesthesiology 37:210-241, 1972 111. Failing PA, Johnson JR, Coppel DL: Propofol infusion for sedation of patients with head injury in intensive care. Anaesthesia 44:222-226, 1989 112. Wynn JW, Reynolds JC, Hod CL, et al: Steroid therapy for pneumonitis induced in rabbits by aspiration of foodstuff. Anesthesiology 51:11-19, 1979 113. Orlowski JP: It's time for pediatricians to "rally" round the pool fence. Pediatrics 83:1065-1066, 1989 114. Carey VF: Childhood drownings: Who is responsible? Governments should act. Br Med J 307:1086-1087, 1993 115. Engba~k J, Viby-Mogensen J: Precurarization--A hazard to the patient? Acta Anaesthesiol Scand 28:61-62, 1984