The consequences of ND are primarily those of asphyxia. When effective gas exchange ceases, the individual presents the consequences of hypoxia and hypercapnia. Excellent summaries of the demographics and emergency response to ND are available and are not covered here.38–40 This section summarizes the pathogenesis of ND injury of the frequently injured systems supported in the intensive care unit (ICU): lungs, brain, heart, and kidneys.
The pathogenesis of lung injury in ND is initiated by upper airway obstruction when fresh water (FW) or sea water (SW) contacts the respiratory tract mucosa and provokes laryngospasm. Laryngospasm is a protective response provided the duration of hypoxemia is limited by a brief immersion time. Approximately 10% to 15% of individuals with ND aspirate trivial amounts of water, but some of these individuals develop sufficient O2 deprivation to produce hypoxic encephalopathy or ventricular arrhythmia due directly to laryngospasm.41 Aspiration of SW and FW also induces mechanical airway obstruction with a small airway component. Small airway obstruction is aggravated by bronchoconstriction, mucosal edema, and plugging by water and suspended debris such as algae, diatoms, sand, mud or by teeth and gastric contents.42
Aspiration of even small quantities of water immediately decreases lung compliance and creates persistent areas of low ventilation-perfusion ratio and shunt.42,43 Therefore, aspiration of water may produce a longer lasting hypoxemia than laryngospasm alone. Some of the mechanisms of the early changes in pulmonary gas exchange have been elucidated in animals and are attributable, in general, to loss of surfactant or its activity, damage to the alveolar epithelium and capillary endothelium, and alveolar flooding. In human beings, vomiting and aspiration of stomach contents during ND is common and aggravates mucosal and alveolar epithelial injury.
The combination of alveolar flooding, loss of surfactant or its function, atelectasis, and alveolar damage may give rise to progressive hypoxemia from intrapulmonary shunting, which in severe cases may reach 70% of the cardiac output.42,44 In about 40% of individuals with ND, the injury culminates in ARDS hours to days after the episode.45,46 Hypoxemia usually necessitates treatment with supplemental oxygen at high inspired O2 fraction, which may superimpose pulmonary oxygen toxicity on ARDS. Fortunately, ARDS, which develops after ND, is more likely to be reversible than ARDS from other causes.46
ND is the second leading cause of brain death, after trauma, in children admitted to a pediatric ICU.47 Brain injury pathogenesis in ND is that of global anoxia or severe hypoxia. Prolonged anoxia or hypoxia produces diffuse neuronal damage that, if severe, compromises the function of the blood-brain barrier, leading to cerebral edema. As edema develops, intracranial pressure (ICP) may increase, further decreasing brain perfusion, exacerbating intracellular hypoxia, and, in severe cases, causing uncal herniation. Profound increases in ICP are infrequent after ND but tend to appear more than 24 hours after resuscitation of patients who already show evidence of neurologic dysfunction.46 There is some evidence that the increase in ICP indicates severity of neuronal injury rather than being a major contributor to the insult.46,48
The difference between ND and anoxic brain injury of other etiologies involves the potential mitigating effects of the diving reflex and hypothermia.49 In human beings, the diving reflex is not well developed and most apparent in young children exposed to cold water.49,50 ND in cold water leading to rapid hypothermia slows cerebral metabolism, thereby postponing the deleterious effects of anoxia.51 These factors are associated with a better prognosis after an apparently severe ND episode.50–52
The most important cardiac effects of ND are atrial and ventricular arrhythmias, in particular ventricular fibrillation.53 Studies of drowning in animals have demonstrated hemolysis and rapid shifts in blood electrolyte composition after instillation of FW and SW into the lungs. These responses correlated with the occurrence of ventricular arrhythmias. However, human studies have not confirmed significant electrolyte changes even in patients with ventricular fibrillation,54 except for drowning in Dead Sea waters, which have a much higher mineral content than other SW. Individuals with ND in the Dead Sea develop hypernatremia, hyperchloremia, hypermagnesemia, and hypercalcemia more than 24 hours after exposure because electrolytes are absorbed from the gastrointestinal tract after swallowing large amounts of water during the episode.52
ND in human beings differs from that in animal studies primarily because humans rarely aspirate enough water to produce significant electrolyte changes.54 Human pathologic studies after SW or FW drowning have demonstrated cardiac myocyte hypercontraction and hypereosinophilic sarcomeres. These pathologic changes are characteristic of catecholamine excess and suggest that intense adrenergic stimulation contributes to the arrhythmias after ND.55 Thus, the etiology of ventricular fibrillation in human beings is most likely related to hypoxia, respiratory and metabolic acidosis, and catecholamine excess. A review of cases of children with brain death has demonstrated myocardial infarction to be commonly associated with ND.56
The incidence of renal insufficiency after ND is unknown but is reported far less frequently than lung, brain, or cardiac injury. The renal complication cited most often is oliguria attributable to acute tubular necrosis,57 probably caused by hypoxemia and hypotension. Infrequently, ND may be complicated by rhabdomyolysis and hemolysis with disseminated intravascular coagulation.58,59 Hemolysis and disseminated intravascular coagulation also may contribute to acute tubular necrosis. Although patients with acute renal failure after ND may require transient dialysis, recovery of adequate renal function can be expected in most patients.
ND in adults and adolescents is associated with several predisposing factors and complicating injuries, which are easily overlooked in the unconscious, critically ill ND patient. They must be considered in each case because they may affect the treatment and prognosis of the patient.
Alcohol and other drugs that alter the central nervous system are commonly implicated in adult ND.60 Sedatives and alcohol in particular may complicate the patient's initial ICU course by exacerbating hypothermia and hypotension and impairing mental status and respiratory drive. Levels of toxic drugs and blood alcohol should be measured in complicated patients admitted to the ICU.
Other predispositions to ND include unrelated pathologic events in otherwise unimpaired adult swimmers. Myocardial infarction, cardiac arrhythmias, seizures, subarachnoid hemorrhage, and AGE in the SCUBA diver have been implicated in many ND episodes.60 These events may require extraordinary diagnostic efforts in the immediate postresuscitation environment of the ICU. Electrocardiography should be obtained routinely because the heart is a target organ for hypoxemia in patients with ND. Serial measurements of cardiac enzymes in ND are useful for confirming the diagnosis of myocardial infarction when electrocardiographic changes are nondiagnostic. Acute intracranial hemorrhage or status epilepticus may need to be ruled out in patients whose course is complicated by neurologic dysfunction. Recompression and HBO therapy should be considered for ND in SCUBA divers with unexplained obtundation, coma, or other neurologic deficit (see section on VGE and AGE).
Injuries to the spine and skull are common in patients with ND. These occur most often when a swimmer dives into shallow water and strikes the head on the bottom or on a submerged object.60 A common scenario involves a motor vehicle accident that leaves the passenger submerged in a body of water. Burst fractures of the cervical vertebrae resulting in tetraplegia have been reported in these settings. In addition, skin, middle ear, or sinus trauma sustained during ND may serve as portals of entry for infection.61
The ND patient should be placed in an ICU for respiratory insufficiency, after cardiac arrest or arrhythmia, and for altered mental status. Clinically, the patient may exhibit cyanosis, tachycardia, hypo- or hypertension, hypothermia, respiratory distress with frothy, blood-tinged sputum, diffuse crackles, and wheezing on examination. Initial laboratory evaluation often shows a metabolic acidosis (caused by lactic acid) and hypoxemia on arterial blood-gas analysis. Serum electrolytes, with the exception of a decreased bicarbonate concentration, are rarely perturbed significantly.62 However, ND in industrial fluids or the Dead Sea can perturb serum electrolytes. As an example, a 28-year-old male developed severe hypercalcemia after a ND incident in an industrial vessel with oil-well drilling fluid that contained calcium salts.63 Hypoglycemia is common.64 Hemolysis and rhabdomyolysis, if seen, tend to occur early in the clinical course unless they are the result of late sepsis. Electrocardiographic abnormalities include evidence of ischemia or injury and ventricular and atrial arrhythmias. Initial chest radiographic findings range from patchy infiltrates to diffuse airspace disease (Fig. 112-2). Progressive increase in parenchymal infiltrates over hours to days is not unusual.
Chest radiograph 2 hours after an episode of near drowing shows typical patchy infiltrates.
Mechanical ventilation can be a challenge in the severely injured ND patient. Atelectasis and pulmonary edema with intrapulmonary shunting are encountered in all types of ND. ARDS can develop with poor lung compliance that should be treated, like all cases of ARDS, with normal tidal volume ventilation (6mL/kg ideal body weight; see Chap. 38). These conditions can be further complicated by the presence of foreign bodies in the airways. Heavy sedation or muscle relaxants are best avoided in ND patients because the drugs impair the clinician's ability to follow the neurologic examination. However, careful use of these agents may improve mechanical ventilation by synchronizing the patient with the ventilator or decreasing airway pressures and the risk of barotrauma. The advantages of positive end-expiratory pressure in decreasing intrapulmonary shunt can be dramatic in severe hypoxemia after ND. Treatment of children with ARDS after ND with artificial surfactant did not improve outcome but did improve pulmonary function modestly.65
Respiratory insufficiency in ND may be complicated by factors other than atelectasis and intrapulmonary shunt. Airway obstruction may occur as bronchospasm or from a foreign body. Bronchodilator therapy may benefit the patient with diffuse wheezing. Patients with localized atelectasis that fails to improve with effective ventilation or those who exhibit localized wheezing should undergo fiberoptic bronchoscopy to exclude or remove a foreign body.
Many ND accidents occur in water contaminated with human or animal waste or naturally containing pathogenic bacteria or fungi. The lung is the most common portal of entry for a wide variety of these organisms. Infection is heralded by fever 2 to 7 days after the event and should prompt sputum and blood cultures before initiation of antibiotic therapy.66 Prophylactic antibiotic coverage has not improved outcome after ND, and routine use of antibiotics is not indicated. Reported infections are presented in Table 112-3. Awareness of infection by more unusual organisms is crucial because they may have specific culture requirements not offered routinely in many hospital microbiology laboratories.61
Table 112–3. Microbial Isolates Associated with Infection in Individuals after Near Drowninga ||Download (.pdf)
Table 112–3. Microbial Isolates Associated with Infection in Individuals after Near Drowninga
|Type of Water||Reference|
| Klebsiella oxytoca||FW||64, 58|
| Herellea spp.||FW||55|
| Neiserria meningitidis||FW||55|
| Pseudomonas aeruginosa||FW||64|
| Listeria monocytogenes||FW||64|
| Plesiomonas shigelloides||FW||64|
| Edwardsiella tarda||FW||64|
| Chromobacterium violaceum||FW|
| Aeromonas hydrophila||SW, FW||64, 58|
| Escherichia coli||SW, FW||64, 58|
| Proteus mirabilis||SW, FW||58, 64|
| Staphylococcus aureus||SW, FW||64, 65|
| Neiserria mucosus||Brackish||66|
| Pseudomonas putrefaciens||SW||58, 65|
| Francisella philomiragia||SW||63|
| Vibrio parahemolyticus||SW||58|
| Pseudoallescheria boydii||FW||64|
| Aspergillus fumigatus||FW||67, 64|
Brain resuscitation measurements after ND are controversial. The debate is complicated by the diverse parameters that influence brain injury and recovery, including age, water temperature and submersion time (or period of asphyxia), coexisting injuries, and preexisting disease.67 The matter is complicated further by anecdotes of complete or nearly complete neurologic recovery in association with specific therapeutic modes after prolonged immersion. The initial prognostic uncertainties about brain recovery after ND mandate a full effort at cardiopulmonary resuscitation, including correction of hypothermia.68
Classification of neurologic status 1 to 2 hours after resuscitation allows assessment of prognosis. A system with reasonable discrimination for outcome in humans classifies patients after resuscitation into three categories, as listed in Table 112-4.50,51
Table 112–4. Classification of Individuals after Near Drowning and Initial Resuscitation ||Download (.pdf)
Table 112–4. Classification of Individuals after Near Drowning and Initial Resuscitation
|Category A||Awake, fully conscious|
|Category B||Blunted consciousness, stuporous but arousable|
| C.1||Decorticate posturing|
| C.2||Decerebrate posturing|
The best discrimination for outcome using this system has been found in children in whom all category A and B patients (n = 57) recovered completely. Level C patients (n = 39) had 33.3% and 23.9% cerebral morbidity rates (mortality rate + morbidity rate = 56.2%), with the lowest survival rate in the C.3 group.51 In another series of patients that included 52 adults, the category A patients recovered completely, and two adults and one child in level B eventually succumbed to barotrauma or other complications.50 Eight of 11 (73%) adult and 8 of 18 (44%) child category C patients recovered completely in that series.
Use of a brain resuscitation regimen known as HYPER (hyperhydration, hyperpyrexia, hyperexcitability, and hyper-rigidity) suggested that a larger fraction of seriously injured ND children had complete recovery.51 The acronym addressed the overhydration, fever, excitability, and muscular rigidity noted in some patients. These findings were thought to affect outcome adversely, and aggressive therapy was recommended to minimize them.
HYPER therapy consists of systemic corticosteroids, osmotic diuretics, hyperventilation, barbiturate coma, and muscle relaxants administered to minimize cerebral edema and decrease ICP. Controlled hypothermia (32°C, 89.6°F) to decrease neuronal metabolism also was advocated.52 ICP monitoring is necessary to guide such aggressive therapy. The rationale for HYPER therapy was based on the idea that control of ICP would minimize neuronal damage after diffuse anoxia. However, the increase in ICP that develops 24 to 48 hours after ND may be a result of severe neuronal injury rather than its cause.
Critical reviews and subsequent experience with HYPER therapy failed to confirm its efficacy and highlighted its potentially detrimental effects.41,46,68 A retrospective review of 40 ND patients from the same institution that reported the original experience with HYPER found increased incidences of sepsis and multiple organ failure in patients treated with hypothermia.67 This may result from cold-induced immune suppression (including neutropenia) complicated by cold-induced bronchorrhea and decreased mucociliary clearance.67
Corticosteroids have no proved benefit in decreasing brain edema associated with trauma, intracerebral hemorrhage, or stroke. In the absence of convincing evidence that corticosteroids increase edema and, hence, ICP and that decreased ICP improves neurologic outcome after ND, these agents should be avoided because they are immunosuppressive and predispose to infection and gastric ulceration.69 Although hypothermia and barbiturates can decrease ICP in some circumstances, their use has not been demonstrated to improve neurologic outcome. Attempts to decrease ICP by use of osmotic agents also have not been shown to improve neurologic outcome after ND and may induce hyperosmolarity and renal insufficiency. Mild hyperventilation is a comparably benign intervention to decrease ICP temporarily, and ICP monitoring may help direct therapy in the subset of ND patients with increased ICP and poor prognosis. More recent experience with aggressive cerebral monitoring and resuscitation of the ND patient has shown no benefit.70
Overall, about 80% of child and adult ND victims recover completely, 8% to 10% survive but with brain damage, and 10% to 12% die. About 90% of category A and B and approximately 50% of category C patients survive with full recovery, whereas 10% to 23% of the later group survive but have permanent neurologic sequelae.45,46,50,54 Thus, respiratory insufficiency in the absence of sepsis or infection is seldom the cause of death in ND patients in hospitals with modern intensive care capabilities.
Many parameters such as serum electrolytes, arterial blood-gas and pH values, electroencephalographic findings or clinical features (body temperature, absence of pupillary response, cardiac arrest, duration of submersion, and resuscitative efforts), and cross-brain oxygen content differences71 have been examined for use as indicators of prognosis. None is sufficiently discriminating to guide early therapy. Conversely, the presence of cardiac arrest and absence of spontaneous respirations after resuscitation are ominous signs associated with permanent neurologic impairment or death.68 In a retrospective review of 44 ND children, all survivors who regained good neurologic function, were awake with purposeful motion 24 hours after the incident.72