For drowning victims in cardiac arrest, it is important that cardiopulmonary resuscitation be performed in the traditional airway-breathing-circulation rather than circulation-airway-breathing sequence.
Drowning is a process causing respiratory insufficiency from submersion or immersion in a liquid medium, which may or may not result in the victim’s death.
The outcome of drowning victims depends largely on the success of resuscitative measures at the scene of injury and the duration of submersion.
Intensive care management of multisystem organ dysfunction following drowning is similar to that of other disease entities. It centers around early hemodynamic support, open-lung strategies for acute respiratory distress syndrome, and cerebral resuscitation strategies to prevent secondary brain injury.
Of all of the clinical entities encountered in a pediatric intensive care unit (PICU), drowning is among the most tragic. Within minutes, previously healthy children with hopeful futures die or may be left severely incapacitated with no chance of meaningful cognition. The parents, once full of dreams for their children, are suddenly beset with tremendous grief and guilt because, in most instances, the accident could have been prevented by simple measures.
The definition of drowning events continues to be a source of confusion. While there has been some improvement in the use of appropriate terms, review of literature shows that terms such as near drowning and suffocation by submersion in water remain in use. The use of terms other than drowning makes it difficult to analyze and compare studies and outcomes. Similar issues involving terminology and definitions existed in the resuscitation literature. These problems were addressed in 1990 by a group of investigators who met at the Utstein Abbey in Stavanger, Norway, by coming up with a standardized format for reporting of research involving out-of-hospital cardiac arrest. In June 2002, the World Congress on Drowning was convened to develop a more standard definition of drowning using the Utstein style for uniform reporting of data and to make recommendations regarding preventive measures and care. The Congress was initiated by the Maatschappij tot Redding van Drenkelingen (Dutch Organization to Rescue People from Drowning) , an organization established in Amsterdam in 1767 to promote drowning awareness in the Netherlands. The final recommendation of the Congress was to define drowning as “… a process resulting in primary respiratory impairment from submersion/immersion in a liquid medium. Implicit in this definition is that a liquid/air interface is present at the entrance of the victim’s airway, preventing the victim from breathing air. The victim may live or die after this process, but whatever the outcome, he or she has been involved in a drowning incident.” Immersion is defined as having face and airway covered in water. Submersion is defined as the entire body, including the airway, being under water. The definition implies that a drowning victim develops an air-liquid interface that prevents the victim from breathing air. A recommendation was made to abandon all other terms such as near drowning and secondary drowning . Outcome is described according to death or survival, and survivors can be further categorized according to neurologic function. Papa and colleagues performed a systematic review of definitions for drowning accidents in 2005, identifying at least 43 publications in which various definitions of drowning were used ( Table 115.1 ). They concluded that there is a need to use a single, uniform definition of drowning and supported the one recommended by the Utstein Focus World Congress on Drowning. The Second International Utstein-Style Consensus on drowning, which convened in Potsdam, Germany, in 2013, recommended updates on data that should be used in reporting of resuscitation events in drowning.
|Primary vs. secondary||Secondary drowning is delayed death from drowning due to complications or death occurring in minutes to days after initial recovery.|
|Wet vs. dry/with aspiration versus without aspiration||Dry drowning or without aspiration is defined as laryngeal spasm with no or little aspiration of water or from respiratory obstruction and asphyxia from a liquid medium. |
Wet drowning or with aspiration indicates that aspiration of fluids has occurred.
|Warm vs. cold water||Cold-water drowning is defined as drowning in an outside body of water during the autumn, winter, and early spring months with a patient core temperature of ≤32°C on arrival to the emergency department. Some use water temperature <20°C.|
|Saltwater vs. freshwater||Describes kind of water in which incident occurred.|
|Active vs. passive (or silent)||Active refers to a witnessed drowning event in which the victim makes some motion. In passive , the victim is found motionless.|
|Intentional vs. nonintentional||Describes cause.|
|Fatal vs. nonfatal||Describes outcome.|
|With and without hospitalization||Describes whether the victim was admitted to hospital.|
|Iceberg phenomenon||Iceberg phenomenon is described as people who have been submerged but have subsequently not died from drowning.|
|Immersion frigida||Immersion frigida is defined as death from cooling in water.|
|Immersion syndrome/immediate disappearance syndrome||Occurs when syncope is provoked by sudden contact with water at least <5°C presumably from bradycardia, tachycardia, or arrhythmia.|
|Save||Rescue of victim from water by someone who perceived individual to be a potential victim of submersion injury.|
Childhood drowning deaths have decreased from 2.68 per 100,000 in 1985 to 1.11 per 100,000 in 2017 in the United States, perhaps because of greater emphasis on water safety. , Australia has reported a similar decline in deaths due to drowning in recent years. The greatest decline (46%) occurred in infants under the age of 1 year, followed by persons aged 5 to 19 years (30%). Despite these encouraging data, drowning remains a major cause of death from unintentional injury in young children worldwide. According to the World Health Organization (WHO), there are an estimated 372,000 drowning deaths per year, accounting for the third leading cause of worldwide unintentional injury death. In the United States, drowning is the leading cause of death in children ages 1 to 14 years. Further stratifying this age group, in 2013, drowning was also reported as the number one cause of death from unintentional injuries (393 of 1316) in children aged 1 to 4 years. Of these, 52.2% occurred in a swimming pool. Drowning is the second most common cause of death from unintentional injuries in children aged 5 to 9 years (15.5%) and, in children aged 10 to 14 years (12%), second to motor vehicle accidents. While the majority of drowning deaths in children aged 1 to 9 years occurred in a swimming pool, drowning deaths in older children aged 10 to 14 years occurred in natural bodies of water. Sociodemographic factors also impact drowning rates in children. There are disparities in participation in swimming among different racial, religious, and ethnic groups. Among children in the United States, African Americans have the highest population-based drowning mortality rate, followed by Native American/Alaskan Native, white, Asian/Pacific Islander, and Hispanic groups. Drowning is also an important cause of morbidity in children. In 2017, almost 9000 children younger than 20 years were treated in an emergency department for drowning, and 25% were admitted to a hospital or transferred for further care.
In 2011, Shields and colleagues reported on drowning events in portable aboveground pools. Data were obtained from the US Consumer Product Safety Commission. There were 209 fatal and 35 nonfatal drowning cases in children younger than 12 years. Of the victims, 94% were less than 5 years of age, and 56% were boys. Portable aboveground pools pose a special risk because they are small, inexpensive, installed by the consumer, and do not generate the same feeling of risks associated with in-ground pools. In some instances, water depth was as low as 2 inches (wading pools). In addition, it is uncommon to provide barriers for portable aboveground pools. Ladders cannot be moved to block access, and wading pools do not come with safety covers.
Children younger than 1 year most often drown in bathtubs, buckets, or toilets. While child abuse should be suspected in these situations, as many as 35% of children between the ages of 10 to 18 months were shown to be able to climb into a bathtub. , Drowning in a bathtub should therefore not be considered as prima facie evidence of child abuse. Others at risk for bathtub drowning are those with seizure disorders. Drowning is highest during the summer months and on weekends. Most children who drown were last seen inside the home, in the care of one or both parents, but left unsupervised for less than 5 minutes.
Other important risk factors in drowning deaths include failure to wear a life jacket and alcohol use. In 2006, the US Coast Guard reviewed reports of boating incidents. Of the 500 people who drowned, 9 out of 10 were not wearing life jackets. Alcohol use is involved in up to half of adolescent and adult deaths associated with water recreation. Ethanol and other neurotropic agents can diminish manual dexterity, impair judgment, and increase risk-taking behavior. Recent alcohol consumption by supervising adults may also contribute to drowning accidents involving children. Expert swimmers have also been known to drown during underwater swimming. The practice of hyperventilation to prolong the duration of underwater swimming is particularly hazardous in this regard because significant hypoxemia may result in loss of consciousness before hypercarbia stimulates respiration. Although an uncommon cause of drowning, arrhythmia from long QT syndrome (LQTS) should be suspected and investigated after syncope, seizure, or cardiac arrest during or after swimming.
The key to prevention includes careful supervision of children and education of the public regarding drowning prevention and the hazards of drowning. Children playing near or in water should always be supervised by a responsible adult who is not distracted by any other activity. Alcohol should be avoided before or during swimming, boating, and while supervising children. A four-sided, self-closing, self-latching fence at least 4 feet high that completely separates the house and play area of the yard should be installed around household pools. Those who are in or around natural bodies of water should wear US Coast Guard–approved life jackets irrespective of distance to be travelled, size of boat, or swimming ability.
The sequence of events after submersion has been described by Karpovich in animal studies. The drowning process has been described by the World Congress on Drowning as a continuum that begins when the victim’s airway lies below the surface of the liquid ( Fig. 115.1 ). After an initial period of voluntary breath holding, reflex laryngospasm is initiated by the penetration of liquid in the oropharynx or larynx. Hypoxia, hypercarbia, and acidosis ensue and, when sufficiently severe, result in lessening of laryngospasm, and breathing of liquid into the lungs. The amount of liquid aspirated varies considerably among the victims. Once the liquid reaches the alveoli, a pernicious sequence develops characterized by marked disruption in pulmonary architecture and pathophysiologic alterations. These include surfactant washout, atelectasis, pulmonary edema, pulmonary hypertension, and continuing intrapulmonary shunting. The victim may be rescued at any time during the drowning process thus aborting or minimizing lung injury. Although the term dry drowning had previously been used in the pathology literature to describe autopsy cases without evidence of water in the airways and alveoli, this terminology has been abandoned by the Utstein-style definition of drowning.
The single most important and prognostically significant consequence of drowning is decreased oxygen (O 2 ) delivery to the tissues. A number of clinical variables determine the magnitude of hypoxia and the subject’s ability to withstand it. Thus, the pathophysiology of drowning is closely integrated with the genesis of hypoxemia and its effects on various organ functions. A working knowledge of these pathophysiologic principles and multiorgan involvement is extremely helpful in directing therapeutic strategies for optimum survival.
Type of aspirated fluid
There are several reports in the literature regarding physiologic differences in electrolytes and blood volume after seawater and freshwater drowning. Aspiration of more than 11 mL of fluid per kg of body weight is required for blood volume to be altered, and aspiration of more than 22 mL/kg is necessary before significant electrolyte changes occur. , Drowning victims are often hypovolemic regardless of the type of aspiration because of increased capillary permeability resulting from asphyxia and the loss of protein-rich fluid into the alveoli. In a canine model of drowning, aspiration of cold fresh water led to a 16% increase in body weight, compared with 6% for saltwater aspiration. Reported outcomes in freshwater drowning are worse than in saltwater drowning. In a meta-analysis of seven studies with 2163 drowning victims, saltwater drowning compared to freshwater drowning was associated with a favorable outcome, with a relative risk of 1.16 (95% confidence interval, 1.08–1.24). Also, hypoxia, as assessed by partial pressure of arterial O 2 /fraction of inspired O 2 (Pa o 2 /F io 2 ) ratios, was worse in a matched cohort of freshwater versus saltwater adult drowning victims upon ICU admission. This is consistent with the known effect of the aspirated fluid on pulmonary surfactant, which is destroyed by fresh water but only diluted by salt water.
Functional residual capacity (FRC) is the only source of gas exchange at the pulmonary capillary level in the submerged state. Increased metabolic demands from struggling, breath holding, a depletion of FRC from breathing efforts, and aspiration of fluid into the lungs all result in seriously compromised O 2 uptake and carbon dioxide (CO 2 ) elimination, with consequent hypoxia and hypercarbia. Between 10% and 15% of drowning victims have severe laryngospasm after submersion, resulting in fatal asphyxiation without aspiration of significant water into their lungs (see Fig. 115.1 ). There is often a combined respiratory and metabolic acidosis caused by hypercapnia and anaerobic metabolism. Patients without significant fluid aspiration recover from asphyxia rapidly if they are successfully resuscitated before cardiac arrest or irreversible brain damage occurs. Aspiration of fluid, however, results in persistently abnormal gas exchange. Aspiration of as little as 1 to 3 mL per kg body weight results in profound impairment of gas exchange. , Soon after the aspiration of fluid, there is an elevation of partial pressure of arterial carbon dioxide (Pa co 2 ) and a fall in Pa o 2 as a result of airway obstruction, hypoventilation, and impaired gas exchange between alveoli and pulmonary capillary blood. With adequate resuscitation, normocapnia or even hypocapnia is usually achieved while hypoxemia persists, indicating a significant ventilation/perfusion mismatch and diffusion defect leading to intrapulmonary shunting and venous admixture.
The surfactant system of the lung is affected differently in freshwater versus seawater aspiration. Freshwater aspiration results in marked disruption of the surfactant system of the lung, leading to alveolar instability and atelectasis. Sea water, because of its hypertonicity, draws water into the alveoli. Although surfactant may be diluted by the presence of sea water in the alveoli, its surface tension properties are not significantly altered. Zhu and colleagues examined serum levels of pulmonary surfactant-associated protein (SP-A) and lung weights in 53 victims of fatal drowning. They showed significantly heavier lungs in those who drowned in sea water versus fresh water, suggesting an osmolar effect. Although they found no difference in serum SP-A, intraalveolar aggregates of pulmonary surfactant-associated protein were noted more frequently in those who drowned in fresh water. This is likely related to the disruption of surfactant noted in freshwater drowning. Karch demonstrated marked changes in the pulmonary vasculature in rabbits within 30 minutes of aspiration of both fresh water and salt water. Mitochondrial swelling and disruption of pulmonary vascular endothelial cells were consistently observed in these experiments. Clinically, pulmonary abnormalities are encountered in both freshwater and seawater aspiration. These are consistent with pronounced injury to alveoli and pulmonary capillaries resulting in increased membrane permeability, exudation of proteinaceous material in alveoli, pulmonary edema, decreased lung compliance, and increased airway resistance. The extent of these abnormalities may not be manifested fully for several hours after the submersion episode and may be progressive in nature. Acute respiratory distress syndrome (ARDS) is the hallmark of delayed pulmonary insufficiency resulting from aspiration in drowning . This is characterized by progression of ventilation/perfusion mismatch, alveolar-capillary block, increased capillary permeability, and pulmonary edema. Reduced FRC and diffusion barrier resulting from accumulation of fluid and inflammatory cells in the alveoli and interstitium further accentuate hypoxemia. Aspiration of stomach contents and other debris such as sand, mud, and algae may also impair gas exchange. Bacterial pneumonia resulting from aspiration of contaminated water may further contribute to pulmonary insufficiency. Factors that contribute to drowning-associated pneumonia include aspiration of vomitus or aspiration of contaminated material from water that may contain sewage. Water temperature plays a role, with warmer temperatures predisposing to a higher number of organisms. The chemical composition of the water—such as pH, salt content, and presence of organic and inorganic substances—influences bacterial growth as well. Implicated organisms include aerobic gram-negative bacteria, such as Enterobacter spp., Klebsiella spp., and Pseudomonas spp., as well as gram-positive bacteria, including Streptococcus pneumoniae and Staphylococcus aureus . Oropharyngeal flora, as well as pathogens present in the body of water that the child drowned in, have been implicated in drowning-associated pneumonia. , There have been reports of multidrug-resistant bacteria and fungal pneumonia as well. The diagnosis of pneumonia is based on clinical parameters such as fever, leukocytosis, and new infiltrates on chest radiographs. When pneumonia is suspected, respiratory cultures are a valuable tool to guide antimicrobial therapy.
Understanding the alterations in pulmonary mechanics is important in order to provide the necessary support in the least injurious fashion. Predominant manifestations are those of ARDS complicating the drowning event. Although pulmonary involvement is often bilateral and diffuse, there is considerable inhomogeneity, with some areas more affected than others. Overall, lung compliance is reduced, necessitating higher inflation pressures to maintain adequate tidal volume (V t ). Low V t at low FRC leads to a vicious cycle of atelectasis, decreased compliance, and further reduction in V t . Critical opening pressure necessary to begin alveolar inflation is increased. Appropriate positive end-expiratory pressure (PEEP) needs to be administered to maintain the necessary FRC for adequate oxygenation and ventilation above the critical opening pressure. Airway resistance is relatively less affected or only minimally elevated unless there is airway obstruction from aspirated debris. Time constant, a product of compliance and resistance, reflects the time needed for pressure equilibration between the proximal airway and alveoli to occur. In ARDS, time constant is decreased, allowing for quicker approximation of pressures at these sites during the inspiratory and expiratory phases of the mechanical ventilation. Relatively large V t (10–12 mL/kg) is associated with greater ventilator-associated lung injury in ARDS, whereas smaller V t (6 mL/kg) is associated with less volutrauma. Because of the short time constant, prolongation of inspiratory time to improve oxygenation and increasing the respiratory rate for CO 2 elimination often are effective options during mechanical ventilation. A more detailed description of management of ARDS in drowning appears later in this chapter.
Profound cardiovascular instability is often encountered after a severe drowning event, which poses an immediate threat to survival after the initial rescue. The hypoxemia that occurs due to ventilation-perfusion mismatch can cause life-threatening dysrhythmias, such as ventricular tachycardia, ventricular fibrillation, and asystole. The two determinants of O 2 delivery—namely, cardiac output and arterial O 2 content—can be adversely affected by the drowning event. A decrease in Pa o 2 , if sufficiently severe, decreases O 2 saturation and therefore arterial O 2 content. This decrease in arterial O 2 content can cause a decrease in myocardial O 2 delivery, which contributes to worsening cardiac output and decreased myocardial perfusion pressure. Smooth muscle contraction banding in the media of major coronary arteries and local ventricular myocytes with focal myocardial necrosis have been described after a drowning episode. , Cytosolic calcium overload and O 2 -derived free radicals have also been implicated in the mechanism of myocardial injury after resuscitation following cardiac arrest. Cardiogenic shock may result from hypoxic damage to the myocardium. Metabolic acidosis may further impair myocardial performance. Additionally, therapeutic application of PEEP decreases venous return and right and left ventricular preload. Right ventricular afterload is also increased by structural pulmonary microvascular damage and humoral inflammatory mediators involved in ARDS. The right ventricle is anatomically designed to tolerate increased preload, but it is not as tolerant of high pressures and afterload as the left ventricle. If pulmonary hypertension is severe enough, left ventricular preload further decreases owing to right ventricular failure. These factors, as well as the excessive permeability of pulmonary and systemic capillaries, result in hypovolemia and decreased left ventricular filling pressures. The end result is that of inadequate supply of O 2 to tissues to meet their metabolic demands.
Central nervous system effects
Owing to a lack of metabolic substrate reserves, the brain depends on continuous O 2 delivery. Metabolic failure can begin within seconds after an immediate disruption in circulation. Hypoxia, if sufficiently prolonged, causes profound disturbances of central nervous system (CNS) function. The severity of brain injury depends on the magnitude and duration of hypoxemia and cerebral hypoperfusion, as well as on mechanisms of secondary brain injury. The most important components of brain-specific management include prompt rescue, early and successful resuscitation, and mitigation of secondary injuries.
Following restoration of adequate cerebral O 2 delivery after the initial hypoxemia and/or hypoperfusion after drowning, there are several mechanisms of secondary brain injury at the tissue, synaptic, and cellular level. At the tissue level, increased intracranial pressure (ICP) and alterations in cerebral blood flow (CBF) can adversely impact local tissue O 2 delivery. At the synaptic level, the excitotoxic neurotransmitter glutamate can cause an imbalance in the neuronal supply and demand. Delayed neuronal death occurs owing to cellular responses to hypoxia and subsequent reperfusion, leading to complex pathways of pro-survival and pro-death signals. Intracellularly, accumulation of cytosolic calcium, neuronal energy failure associated with DNA damage and repair, and generation of O 2 -free radicals can all contribute to secondary neuronal death.
There are several developmental factors that render the neurologic effects of pediatric cardiac arrest different from that of adults. Brain injury from sudden cardiac arrest, which more commonly occurs in adults, results when CBF suddenly stops. In contrast, brain injury from drowning, along with most causes of pediatric cardiac arrest, is caused by asphyxia. Cerebral O 2 delivery continues for some time and progressively decreases because of hypoxemia and decreased CBF. Cardiac arrest may occur but is usually preceded by this period of decreased O 2 delivery. Neurologic injury is similar to that of other causes of pediatric asphyxia, including foreign body airway obstruction, apnea, asthma, and suffocation. Approximately 46% of all children with cardiopulmonary arrest survive to hospital discharge and only 38% if the arrest occurred outside the hospital. Studies in humans and animals indicate that there are several developmental differences in excitotoxic pathways. In the neonatal period, there is increased vulnerability to N -methyl- d -aspartate receptor activation and glutamate toxicity, as well as heightened capability for apoptosis, which, albeit an important process of normal brain development, may render the immature brain vulnerable to neuronal loss after an insult. In addition, a developmental difference exists in CBF after cardiac arrest. In adult models of cardiac arrest, global hyperemia is present for 15 to 30 minutes after return of spontaneous circulation (ROSC) followed by delayed hypoperfusion that persists for several hours. In an immature animal model of a brief asphyxial cardiac arrest, hyperemia was observed for 10 minutes after ROSC followed by restoration of baseline CBF, whereas prolonged cardiac arrest was followed by hypoperfusion and blood pressure–dependent CBF.
Effects on other organ systems
Drowning victims are at significant risk for the development of hypoxemia and/or ischemia, particularly in the face of cardiac or respiratory arrest. These factors increase the risk for multiple-organ dysfunction syndrome (MODS). In addition to neurologic injury and acute lung injury, hepatic and renal injuries have been observed. Typpo and colleagues reported on the incidence of MODS on day 1 in children admitted to the PICU. Of the 18% of children who developed MODS on the first day, 30% to 35% had an unfavorable neurologic outcome. In 2015, Mtaweh et al. reported on the patterns of MODS in children after drowning. Pediatric Logistic Organ Dysfunction Score-1 (PELOD-1) and Pediatric Multiple Organ Dysfunction Score (P-MODS) were calculated for the first 24 hours of admission. Of the 60 children, 39 (65%) were in respiratory arrest and 21 (35%) were in cardiac arrest at the scene. Seventeen of 60 patients had severe neurologic injury. Of the children who developed MODS, approximately half had been in respiratory or cardiac arrest. Children who had been in cardiac arrest had much more significant organ dysfunction, which included neurologic, respiratory, hepatic, and renal systems. Of those children who developed acute kidney injury (3 in 60), one child required continuous renal replacement therapy and hemodialysis.
Mammalian diving reflex
A certain degree of protection against hypoxia in drowning may occur in the form of a response similar to the diving reflex observed in seals and other air-breathing diving mammals. While the heart, brain, and lungs remain adequately perfused, blood flow to tissues resistant to hypoxia (i.e., gastrointestinal tract, skin, and muscle) is markedly reduced. Significant bradycardia occurs with a reduction in cardiac output. The mammalian diving reflex acts as an O 2 -conserving adaptation in response to submersion. It has been proposed that this reflex is most active in infancy and is potentiated by fear and low water temperature. A combination of marked bradycardia and impalpable pulses resulting from vasoconstriction may make the victim appear dead at a time when mouth-to-mouth resuscitation could be life-saving. Clinical studies involving children and adults have failed to demonstrate an efficient diving reflex in response to cold-water submersion. ,
Preexisting associated conditions
An underlying etiologic mechanism should be explored depending on a given clinical scenario involving unexplained drowning. Children with seizure disorders are at greater risk for submersion accidents. Similarly, an occurrence of vasovagal syncope or a hypoglycemic episode during swimming may be the underlying factor responsible for drowning. Occult cardiomyopathy or a cardiac arrhythmia should also be considered in an unexplained drowning event. An episode of drowning might be the first manifestation of LQTS. Ackerman et al. studied blood samples or archived autopsy tissue samples in 35 cases of autosomal-dominant LQTS. Six of these patients had a personal history or extended family history of near-drowning. All of these patients were found to have LQTS causing mutations in KVLQT1 , whereas such an abnormality was found in only 3 of the remaining 29 patients who did not have a personal history of submersion episode. Thus, swimming appears to be a gene-specific ( KVLQT1 ) arrhythmogenic trigger for LQTS. Diagnosis of inherited LQTS allows for identification of other family members with similar affliction. Yoshinaga et al. showed that face immersion in cold water results in abnormal lengthening of the QT interval in children identified with nonfamilial LQTS and that such children could potentially be at risk of a life-threatening arrhythmia during swimming. More recently, Albertella et al. described the presentation of outcome of water-related events in children with LQTS. Of the 10 children identified with LQTS and who had a documented history of water-related syncope, nine had LQTS type 1. Seven were swimming at the time of the syncopal event. Factors leading to arrhythmias during swimming in patients with LQTS are thought to include facial immersion in cold water and the dive reflex, which causes a fall in heart rate, competing with epinephrine release from exercise. Patients with LQTS should avoid swimming and diving and any medications that can prolong the QT interval. It has been shown that β-blockers reduce the risk of sudden death in LQTS by 75%.
A significant risk factor for drowning is epilepsy. Accidental drowning causes 8% of all deaths in children and young adults with epilepsy. These patients have a four-fold higher prevalence of drowning than those without the condition. Unwitnessed bathtub drownings occur in roughly 30% of these cases and are more common in children age 5 years and older. , In older children and adolescents with epilepsy who are able to bathe independently, showers are advised over baths to reduce this risk.
Children with intellectual delays may be at reduced risk of drowning because they are more likely to be supervised in pools and tubs. However, there remains the risk of ambulatory children wandering off. One study of children with autism spectrum disorder who drowned found that 74% of these deaths occurred in natural bodies of water (pond, river, lakes) in close proximity to home.
Cold water drowning
Proposed protective mechanisms of hypothermia for the injured brain include a decrease in cerebral metabolic rate, ICP, excitotoxic neurotransmission, cytotoxic edema, generation of deleterious O 2 -derived free radicals, and cerebral hyperemia, which can cause ischemia/reperfusion injury and further increase ICP. The effects of hypothermia may apply to drowning injury, as good outcomes have been reported in children submerged in ice water (<5°C) for prolonged periods. , It appears that if hypothermia is protective in drowning, rapid cooling in ice water is necessary, as a lesser degree of hypothermia in warmer water does not offer cerebral protection. It is also possible that a publication bias exists in reporting of cold water drowning, as cases with good outcome are more likely to be published than cases with poor outcome. Indeed, more recent studies call into question the protective effects of hypothermia in drowning. Quan et al. studied more than 1000 child and adult open-water drowning victims and did not find a protective effect of cold water but rather estimated that submersion duration was the most powerful predictor of outcome. In this study, young age was also a predictor of good outcome, which may reflect the capacity of children to become hypothermic faster and possibly benefit from its neuroprotective effects. A meta-analysis of 24 cohort studies by the same author again reported no change in outcome based on water temperature. Children who were submerged for less than 5 minutes generally had good outcome, and those submerged for more than 25 minutes invariably died. Shorter emergency medical services arrival time was also associated with favorable outcome. This meta-analysis, however, found no correlation between age and outcome.
Because the full extent of CNS injury cannot be adequately determined immediately after the rescue, all drowning victims should receive aggressive basic and advanced life support at the site of the accident and in the emergency department. It cannot be overemphasized that the major determinant of survival and maximal brain salvage is prompt and effective management of hypoxemia and acidosis. In this context, the management in the immediate post-drowning period is of paramount importance. The success or failure of cardiopulmonary resuscitation (CPR) at the site of the accident often determines the outcome. , In a study of more than 900 drowning victims, neurologically favorable survival was associated with bystander-administered CPR as well as witnessed drowning. The issue of the duration of submersion in relation to the success of resuscitation is often raised. Although asphyxia for longer than 5 minutes frequently results in significant brain injury, this should not be a consideration in deciding whether or not to initiate on-site resuscitation. The emotional excitement surrounding the accident makes it difficult to accurately estimate the duration of hypoxia.
Management at the scene
Ensuring the adequacy of the airway, breathing, and circulation is the goal of basic life support after the initial rescue. In cases of inadequate airway and cardiopulmonary status, CPR must be instituted immediately. The fundamentals of basic life support are the same after drowning as for any other situation requiring CPR; however, some practical aspects are worth considering. Unlike the out-of-hospital cardiac arrests in adults, cardiac arrests from drowning in children are initiated by hypoxia due to disconnection of atmosphere from the airways and lungs. Therefore, it is important that CPR is performed in the traditional airway-breathing-circulation (ABC) rather than circulation-airway-breathing (CAB) sequence. Although in recent years there has been a push for chest compression–only CPR for out-of-hospital cardiac arrests, rescue breathing as well as chest compressions is essential for successful resuscitation. The aim of resuscitation at the scene is to prevent irreversible tissue injury from prolonged hypoxia and ischemia. After ensuring a safe environment for a rescue attempt and calling for help, the victim should be removed from the water as soon as possible. Wet clothing should be removed to prevent heat loss. Less than 0.5% of drowning victims sustain cervical spine injuries; thus, application of cervical spine precautions is not routinely indicated. Cervical spine immobilization in the water is indicated when head and neck injury is strongly suspected, such as in accidents involving diving, water-skiing, and surfing. In such situations, the preferred airway opening maneuver is anterior displacement of the jaw, rather than extension of the neck. If breathing is either absent or agonal, rescue breathing should be performed even while the victim is in the water if possible, either via bag-valve-mask if available or by mouth-to-mouth. Chest compressions should not be attempted in water because they are ineffective and waste valuable time. After the victim is removed from the water and placed on a hard board, chest compressions should be given at a rate of 100 per minute with a ratio of 15:2. If available, an automatic defibrillator should be applied to detect a shockable rhythm and defibrillate if necessary. Prolonged attempts to remove water from the lungs are futile and may hinder ongoing ventilatory support. Heimlich and Patrick have recommended the use of subdiaphragmatic pressure in drowning victims to remove water from the airway, but this practice is ill advised. In addition to the fact that most drowning victims aspirate relatively small amounts of water, there is no evidence to suggest that the Heimlich maneuver can remove aspirated fresh water or pulmonary edema fluid. On the other hand, such patients frequently swallow large amounts of water. Consequently, increased abdominal pressure may result in regurgitation of gastric contents into the oropharynx and aspiration into the tracheobronchial tree. Any debris observed in the oropharynx should be removed before initiation of mouth-to-mouth breathing. Presence of airway obstruction caused by a foreign body should be suspected if effective chest expansion cannot be accomplished with appropriate ventilatory technique. A subdiaphragmatic thrust in such a situation would be indicated. As soon as the equipment becomes available, ventilation with 100% oxygen via bag-valve mask device should be initiated for patients who are not breathing adequately. Pressure used during resuscitation to inflate the lungs of drowning victims may have to be higher than anticipated because of reduced compliance of the edematous lungs. A PEEP valve should be used if available. Overinflation should be avoided, however, because this can lead to pulmonary barotrauma and overdistention of the stomach with regurgitation and aspiration of gastric contents. In patients who are too obtunded to maintain airway protection, exhibit hypoxia, or otherwise unable to maintain oxygenation despite bag-valve mask ventilation, endotracheal intubation should be performed.
Emergency department evaluation and stabilization
As with any form of accidental injury, other forms of associated trauma must be considered. Children who slip and fall into the pool may sustain external head injury, such as abrasions, lacerations, and contusions. Occasionally, profuse bleeding from scalp lacerations may be sufficient to aggravate hypovolemic shock. In bathtub drowning, or in instances in which child abuse is suspected, fractures and other evidence of previous injury should be looked for. In adolescent victims, drowning is frequently associated with illicit drug or alcohol use. When appropriate, urine and blood toxicology tests should be performed. Spinal injuries should be suspected in diving, water-skiing, and surfing accidents involving young adults.
The need for hospitalization should be determined by the severity of the drowning episode and clinical evaluation. All patients with a history of drowning should be observed in the emergency department for at least 4 to 6 hours in case they were to develop respiratory distress. Those with insignificant history and normal physical examination may be safely released. Patients with respiratory symptoms, decreased O 2 saturation indicated by pulse oximetry or blood gas determination, and altered sensorium should be hospitalized. Although the Glasgow Coma Scale was originally designed for use in head trauma, it has been routinely used to assess hypoxic encephalopathy in drowning.
Maintaining adequate airway, respirations, and peripheral perfusion with continued attention to oxygenation, ventilation, and cardiac performance should take priority. Electrocardiographic monitoring and arterial blood gas determination should be performed as soon as possible. Ventricular dysrhythmias, asystole, and hypotension may be encountered during the early resuscitation phase. The standard CPR techniques also apply to the drowned child. Patients with respiratory acidosis and hypoxemia, and those who are unconscious with significant respiratory distress or poor respiratory efforts, require intubation and mechanical ventilation. Early use of PEEP is effective in reversing hypoxemia. Because pulmonary edema is not caused by hypervolemia in drowning, diuretics are not helpful. In addition, they may exacerbate the prevalent hypovolemia. Therefore, pulmonary edema after near-drowning is best treated mechanically with positive-pressure breathing and PEEP rather than diuretics. Hypovolemia is commonly encountered in the early resuscitation phase. Isotonic crystalloids (20 mL/kg) or colloids (10 mL/kg) infused over 15 to 20 minutes should be used for intravascular volume expansion. Additional volume expansion can be carried out based on clinical and hemodynamic status. Administration of large amounts of hypotonic fluid is contraindicated because such solutions are ineffective for intravascular volume expansion. Furthermore, the resultant decrease in serum osmolality may exacerbate cerebral edema. In the face of continued hypotension and/or impaired peripheral perfusion after appropriate intravascular volume expansion, inotropic/vasopressor support may be necessary. Central venous pressure monitoring is extremely helpful for ongoing assessment and management of intravascular volume. Metabolic acidosis resolves with improvement of oxygenation and tissue perfusion. Radiologic studies should include a chest radiograph to determine the presence or absence of pneumothorax or pneumomediastinum. Unless head injury is suspected, a computed tomography scan of the head is usually not necessary because early findings are often normal even in the face of severe hypoxic damage.
Prevention and treatment of hypoglycemia is extremely important. It is reasonable to maintain blood sugar between 80 and 160 mg/dL. The issue of controlling body core temperature also deserves mention. Therapeutic hypothermia after pediatric cardiac arrest has been proven to be of no benefit. However, there may be special considerations in drowning victims since most are relatively hypothermic at the time of rescue. After return of spontaneous circulation, a reasonable approach is to not rewarm the victim aggressively as long as the core temperature is between 32°C and 34°C. Rewarming should occur at a rate no greater than 0.5°C per hour. Hyperthermia (>37°C), on the other hand, must be prevented or treated aggressively if present. , Severe bradycardia and intense vasoconstriction associated with marked hypothermia (<32°C) may make drowning victims appear dead. However, resuscitative efforts should be continued while normalizing body temperature.
Management in the intensive care unit
The drowning victim can sustain insults to many organ systems, including the brain, lungs, cardiovascular system, liver, and kidneys. Since the major contributor to mortality and long-term morbidity is cerebral hypoxic-ischemic injury, management in the ICU should focus on supporting these organ systems as they relate to the brain. Continued attention to oxygenation and ventilation status and cardiac performance is essential. ARDS can occur as a result of aspiration injury, pneumonia, and surfactant deficiency or dysfunction. Both hypoxemia and hyperoxemia have been associated with poor outcome after cardiac arrest. Maintenance of O 2 saturation between 94% and 98% and Pa o 2 between 70 and 100 are reasonable goals. The cerebral vasculature of the injured brain is reactive to changes in Pa co 2 . Hypercapnia increases cerebral blood volume and can raise ICP. Conversely, arterial hypocapnia decreases CBF and therefore cerebral O 2 delivery. Thus, ventilation should be titrated to achieve Pa co 2 around 40 torr. To monitor these effects, arterial and central venous pressure monitoring are necessary in most patients who require intensive care. A useful parameter to monitor is mixed venous O 2 saturation (Sv o 2 ). Provided that arterial O 2 content and O 2 consumption remain constant, Sv o 2 is a useful indicator of changes in cardiac output.
The need for endotracheal intubation and different ventilatory strategies should be determined on an individual basis and by clinical judgment. Respiratory acidosis, PaO 2 less than 60 torr in F io 2 greater than 0.5, clinical signs of impending respiratory fatigue, and depressed level of consciousness are the most common indications for mechanical ventilation. Lung injury may not peak until at least 24 hours; thus, weaning from mechanical ventilation should not occur before then. Early use of PEEP and supplemental O 2 are extremely effective in reversing hypoxemia.
The goal of mechanical ventilation is to provide adequate gas exchange to ensure tissue viability while minimizing the inevitable ventilator-associated injury from oxytrauma, barotrauma, volutrauma, and ineffective tracheobronchial toilet. Ventilatory strategy should take into account the major alterations in pulmonary mechanics. As noted earlier, most children who drown have decreased FRC, compliance and time constant and increased critical opening pressure. Salutary effects of PEEP are from maintaining alveolar stability, alveolar recruitment, and increasing FRC. It stabilizes the relatively softer chest wall of a child, thus minimizing chest wall recoil and further decrease in FRC. PEEP also displaces intraalveolar water into interstitial and perilymphatic spaces, resulting in decreased venous admixture and improved compliance. Excessive PEEP can result in decreased venous return and cardiac output, pulmonary overdistension and decreased compliance, and barotrauma. Maintenance of normovolemia is an important consideration in patients receiving PEEP. Furthermore, excessive PEEP can decrease cerebral venous drainage and increase cerebral blood volume and ICP. Overdistention can also impair ventilation, and the subsequent increase in partial pressure of carbon dioxide (P co 2 ) can increase ICP. Thus, PEEP should be titrated to maintain lung recruitment, ventilation, and oxygenation while maintaining hemodynamics.
The pulmonary management of pediatric drowning victims should follow the same standard approach as in other children with acute lung injury and ARDS: low V t (6–7 mL/kg), lung recruitment with PEEP, and titration of F io 2 to achieve adequate O 2 delivery. We recommend pressure-controlled ventilation with a relatively low peak airway pressure and prolonged inspiration while still allowing adequate time for complete exhalation. Alternatively, pressure-regulated volume control mode can also be used to deliver a preset V t with minimum possible inflation pressure. The level of PEEP can be optimized by gradual increments depending on its effects on increasing Pa o 2 /F io 2 ratio. Optimal PEEP as evidenced by improvement in dynamic compliance can be determined by measuring exhaled V t at varying levels of PEEP. When PEEP exceeds critical opening pressure or the lower inflection point on the pressure/volume curve, dynamic compliance improves. Ventilatory rate, inspiratory/expiratory times, and peak airway pressures can also be adjusted according to their effects on dynamic compliance and by ascertaining the return of expiratory flow to baseline. In patients without CNS injury and intracranial hypertension, the technique of permissive hypercapnia can be used to minimize barotrauma in a patient with ARDS. This involves using lower inflation pressures or V t and accepting higher levels of P co 2 as long as pH remains near normal.
High-frequency ventilation is another strategy that can be used in the management of hypoxic respiratory failure. This mode of ventilation uses a relatively high mean airway pressure while minimizing excessive fluctuations in pressures during the respiratory cycle. High-frequency ventilation is a safe and effective modality in the treatment of severe acute respiratory failure that is unresponsive to conventional mechanical ventilation. ,
While extracorporeal life support (ECLS) has been used for rewarming in patients with severe hypothermia following drowning in cold water, the routine use of ECLS for the treatment of ARDS associated with drowning is less clear. The presumed benefit of ECLS is the provision of lung rest to mitigate barotrauma and O 2 toxicity in patients who do not improve despite maximum ventilatory support. Criteria for ECLS in drowning with refractory cardiovascular or respiratory dysfunction should be similar to other disease states.
There is no evidence to suggest that “prophylactic” antibiotics help prevent drowning-associated pneumonia; in addition, they may lead to the selection of resistant organisms. Furthermore, drowning in swimming pools rarely results in pneumonia. However, fulminant S. pneumoniae bacterial sepsis and pneumonia have been described shortly after a severe drowning injury. Therefore, it is reasonable to institute broad-spectrum antibiotic therapy in patients with positive sputum cultures, fever, sepsis, or severe cardiopulmonary deterioration, especially when this occurs after a period of stability.
CNS injury is by far the most important cause of death and long-term functional impairment among the immediate survivors of drowning accidents. Studies have failed to demonstrate beneficial effects in improving outcome of various cerebral protective strategies, such as therapeutic hypothermia, ICP control, corticosteroids, and barbiturate coma. Our experience suggests that significant intracranial hypertension is not commonly encountered in the early postdrowning period, whereas late, uncontrollable intracranial hypertension carries an unfavorable prognosis. Additionally, satisfactory control of intracranial hypertension is not necessarily associated with improved outcome. It appears that the occurrence of cerebral edema and intracranial hypertension 2 to 3 days after drowning is a reflection of the early hypoxic injury rather than a manifestation of a reversible process. Late, persistent intracranial hypertension associated with a comatose state is of ominous significance and is almost always associated with an unfavorable outcome.
The most practical tool of neuromonitoring is the standard neurologic examination. The vast majority of patients who are awake and interactive in the emergency department survive neurologically intact. Admission neurologic examination by itself is not predictive of outcome. However, persistent absence of cognitive function 48 to 72 hours after the drowning episode is of grave prognostic significance. Large and unreactive pupils portend a severe hypoxic ischemic injury and a poor neurologic prognosis. Components of the examination that should be performed serially include pupillary reactivity, level of consciousness, brainstem reflexes, and motor function. The use of ICP monitoring in children with hypoxic-ischemic encephalopathy after drowning is not recommended. The emphasis of management of a comatose child in the immediate post-drowning period should be on maintaining adequate oxygenation/ventilation, O 2 delivery, and avoidance of hypotonic fluid overload. Pathophysiologic changes from asphyxia—as well as various nonindicated therapies aimed at cerebral salvage, such as barbiturates and osmotic diuresis—adversely affect myocardial performance. Cardiovascular support with maintenance of intravascular volume and the use of inotropic agents is often necessary to maintain optimum organ perfusion in patients who have sustained a significant hypoxic-ischemic insult.
The neuroprotective properties of hypothermia that have been extensively demonstrated in laboratory studies suggest potential merits as a therapy in some children, including victims of drowning. A randomized controlled trial of therapeutic hypothermia has shown benefits in neonatal hypoxic-ischemic encephalopathy. Although therapeutic hypothermia has been shown to be effective in neonatal hypoxic-ischemic injury, studies in pediatric drowning showed that not only did hypothermia not improve outcome, it increased infectious complications, and improved survival to merely a vegetative state. , , In cases of cold-water drowning, although the patient should be actively warmed to prevent arrhythmias and secondary infections, once a core body temperature of 30°C is achieved, warming should not exceed 0.5°C per hour to prevent rises in CBF and ICP, ischemia/reperfusion injury, and fever.
The outcome of drowning victims depends largely on the success of resuscitative measures at the scene of injury and the duration of submersion. Survival is extremely poor among drowning victims who have sustained cardiac arrest and is comparable to other causes of out-of-hospital cardiac arrest. Other markers of poor outcome in pediatric drowning victims include generalized edema and respiratory arrest. Patients who are successfully resuscitated and who are conscious on arrival at the hospital have an excellent chance of intact survival. , , Patients who have a witnessed arrest are more likely to survive, presumably due to more rapid resuscitation. A recent observational study of 131 children admitted to an ICU after drowning found an excellent recovery rate of 96% after witnessed drowning versus 69% when unwitnessed. Of children who required CPR, epinephrine, and intubation, 96% had poor outcomes. Other predictive factors were pH less than 7.1 and initial Glasgow Coma Scale score of less than 5.
A secondary analysis of children of the Therapeutic Hypothermia after Pediatric Cardiac Arrest (THAPCA) trial who experienced out-of-hospital cardiac arrest due to drowning found significant decreases in all aspects of behavioral and cognitive testing at 1-year follow-up. In this study, enrolled children were comatose on presentation and had received at least 2 minutes of chest compressions. Patients were randomly assigned to either a normothermia or hypothermia group. There was no difference between groups in mortality or neurobehavioral testing at 1-year follow-up, presenting the strongest evidence to date that therapeutic hypothermia does not improve outcome after drowning. All patients enrolled who required CPR more than 30 minutes either died or had severe disability, consistent with published literature. Our experience suggests that the absence of cognitive function 72 hours after the hypoxic episode is strongly associated with either death or survival in a persistent vegetative state.
Because the majority of children who drown are previously healthy, they may represent a subpopulation of children who have better outcome after cardiac arrest. , Another secondary analysis was done using data from the previously described THAPCA trial, comparing drowning victims to children who had been in cardiac arrest from other respiratory causes. The children who drowned had a significant decrease in neurobehavioral and cognitive function. However, loss of function was less than that experienced by children who had been in hypoxic arrest from other causes. These differences were present in categories of cognition, adaptive behavior composite scores, communication, and motor function. There was a broad range of function and some positive results, with 28% of drowning victims having average or above cognitive scores. Children overall of younger age and who received few doses of epinephrine scored higher on functional and cognitive testing. The children in the “other” group had more premorbid conditions that likely affected their outcome.
A study of long-term follow-up 5 to 14 years after drowning of 21 drowned and resuscitated children admitted to the PICU found that 57% had neurologic dysfunction and 40% had low full-scale intelligence quotient. This study included children who had both prolonged submersion more than 5 minutes and those with briefer submersion times who were revived on the scene. Children who had normal IQ had an average submersion time of 4 minutes versus 7.5 minutes for those with low IQ. The most common motor disturbances were coordination and fine motor skills. Length of submersion, need for ongoing CPR, mechanical ventilation, and longer PICU stay were associated with worse outcome.
Though there have been several case reports of patients receiving ECLS and rewarming who have recovered with good neurologic outcome, , most drowned children with prolonged cardiac arrest and hypothermia have poor chance of functional recovery. The data are scarce, consisting of small retrospective studies of 9 to 13 children, with reports of good long-term neurologic recovery ranging from 11% to 16%. A large retrospective study using the Extracorporeal Life Support Organization (ELSO) registry measured survival of drowned patients who required ECMO. Of the 247 patients, most (198) were children and overall survival was 51%. This encompassed all indications for ECMO, including those patients who had not been in cardiac arrest but required venovenous cannulation for respiratory failure. When looking at the group required that ECLS for refractory cardiac arrest (extracorporeal cardiopulmonary resuscitation [ECPR]), the survival was still an encouraging 23%, much higher than previous reports. However, functional recovery was not evaluated and it is unclear what the neurologic outcome was for survivors. Patients who required ECPR were more likely to be hypothermic and had a higher mortality rate.
ECLS may be a life-saving option for select patients with hypothermia, which in and of itself may cause cardiac arrhythmias and coagulopathy. Shock and disseminated intravascular coagulopathy may further complicate transitioning to extracorporeal support. In centers experienced with extracorporeal cannulation in children, ECLS may be considered as a salvage therapy. However, the risk of bleeding complications and severity of organ dysfunction must be carefully weighed prior to cannulation.