of pulmonary edema secondary to drowning (Courtesy of Soroosh Mahboubi, MD, The Children’s Hospital of Philadelphia.) FIGURE 90.2 Algorithm for pulmonary assessment for drowning Other initial laboratory evaluation should include complete blood cell count (CBC), electrolytes, and urinalysis Patients with abnormalities of gas exchange with normal chest radiographs can usually be managed with supplemental oxygen and pulmonary physiotherapy Noninvasive ventilatory support, such as high-flow humidified nasal cannula oxygen or CPAP, may be beneficial Any change in mental status or increase in respiratory distress may reflect arterial hypoxemia and should also prompt a repeat ABG determination Continuous SaO2 or serial PaO2 measurements will guide the physician to continue conservative treatment or to intensify ventilatory support Patients with obvious respiratory distress, hypoxemia (SaO2 less than 90% or PaO2 less than 60 on 60% inspired oxygen), and extensive pulmonary edema or infiltration generally require more vigorous treatment All should be monitored for heart rate, cardiac rhythm, respiratory rate, and BP Most will require frequent blood gas analysis and may be more easily monitored through arterial cannulation Intubation, supplemental oxygen, and mechanical ventilation with positive end-expiratory pressure (PEEP; to 15 cm H2 O) may be needed Once BP is stabilized, fluid restriction (to approximately one-half the maintenance rate) and diuretic therapy (e.g., furosemide 0.5 to mg/kg intravenously, usual maximum 20 mg/dose) may improve gas exchange In the setting of extensive pulmonary damage, pulmonary and cardiovascular components of the disease are intimately entwined Optimum management requires monitoring of blood gases and systemic arterial pressure Patients who have experienced significant hypoxemia are often not able to be aroused Again, reversal of hypoxemia and acidosis is critical, as well as fluid resuscitation and avoidance of hyperglycemia Avoiding hypercapnia and resultant cerebral hyperemia is generally accepted, but hyperventilation, barbiturate coma, and other measures initially believed to provide cerebral protection and prevent or treat elevated intracranial pressure have not been helpful in these patients Hypothermia does appear to have some protective effect Extreme hypothermia should be corrected to at least 32°C (89.6°F) to achieve hemodynamic stability and to minimize the risk of infection The child should then be allowed to rewarm passively Although data in humans are limited, animal studies suggest that maintenance of mild brain hypothermia may minimize reperfusion injury Hyperthermia, a common result of active rewarming, should be avoided Recent studies suggest that early initiation of extracorporeal membrane oxygenation (ECMO) in hypothermic patients with cardiorespiratory insufficiency may prevent cardiopulmonary failure and improve survival in post-drowning cardiac arrest There is no benefit to prophylactic antibiotics, which should be reserved for strongly suspected or proven bacterial infection Exceptions are when grossly contaminated water is aspirated or when maximal ventilatory support is required to provide any margin for survival Bronchoalveolar lavage and steroids have no demonstrated benefit However, there is anecdotal evidence supporting the use of surfactant therapy, which is consistent with the pathophysiology of the disease process Renal function, normal electrolytes, and an adequate hemoglobin level (more than 10 g/100 mL) should be maintained If significant hemoglobinuria exists, diuresis is recommended Indications for Discharge or Admission The patient’s clinical condition in the ED dictates further management and may provide prognostic clues It is advisable that patients should be observed for to 12 hours after presentation Most studies have demonstrated no delayed symptoms in patients with normal initial oxygen saturations on room air at hours after submersion Patients who develop symptoms usually so by 4.5 hours after submersion Even if initially symptomatic, in most cases symptoms resolve by hours after submersion Patients may be assigned to one of three groups: alert, blunted, or comatose Patients in the first group should be observed in the ED (as above) If they maintain normal oxygenation and normal work of breathing they can be discharged to home Patients in the second group should be admitted for careful monitoring Patients in the third group have experienced severe CNS asphyxia The prognosis for this group includes a much greater risk of death or severe anoxic/ischemic encephalopathy Risk increases with depth of coma on presentation Comatose patients who present flaccid with fixed, dilated pupils rarely survive intact regardless of treatment, although coexistent hypothermia has provided some remarkable exceptions Upon discharge from the ED all caretakers should be educated on drowning prevention The American Academy of Pediatrics recommends the installation of a 4-sided fence that prevents direct access to a swimming pool The fence should be at least ft high, climb-resistant, and the distance between the bottom of the fence and the ground should be less than in The gate should be self-latching and self-closing Parents and caregivers should be advised that small children should always be under the direct supervision of an adult while around bathtubs, pools, or other bodies of water SMOKE INHALATION Goals of Treatment The goals of emergency care include early intubation (if there are signs of airway compromise), stabilization of respiratory and cardiovascular status, and maintenance of fluid and electrolyte balance One must recognize concomitant carbon monoxide or cyanide poisoning or other inhalants that contribute to morbidity CLINICAL PEARLS AND PITFALLS Early intubation should be accomplished if there is any evidence of airway burns or edema Severe smoke inhalation can occur without cutaneous burns Current Evidence Respiratory complications of smoke inhalation rank with carbon monoxide poisoning as a major cause of early death from fire Although serious cutaneous injury may occur in the absence of pulmonary involvement, inhalation injury is present in up to one-third of all burn injuries and accounts for up to 90% of all burn-related mortality The severity of carbon monoxide inhalation and respiratory problems is related to the duration of exposure, the occurrence in a closed space (more likely in very young or elderly victims), the nature of materials involved, and the presence of products of incomplete combustion Severe hypovolemic shock, massive tissue destruction, extensive fluid resuscitation, and infection further complicate direct inhalational trauma The mechanism of destruction can be categorized in the following categories: upper airway injury, lower airway injury, pulmonary parenchymal injury, and systemic toxicity (carbon monoxide and cyanide) The relatively low heat capacity of dry air and the excellent heat exchange properties of the nasopharynx usually limit direct thermal injury to the upper airway Dry air above 160°C (320°F) has little effect on the lower airway The greater heat capacity of steam increases the risk of lower airway damage In addition, continuing combustion of soot particles carried deeply into the lung may exacerbate thermal injury to the lower airways and pulmonary parenchyma Chemical injury may occur at any level of the respiratory tract Oxides of sulfur and nitrogen combine with lung water to form corrosive acids Incomplete combustion of any carbon-containing material, such as wood, may produce carbon monoxide Combustion of cotton or plastic generates aldehydes that cause protein denaturation and cellular damage Burning polyurethane may produce cyanide gas Fire retardants that contain phosphorus may produce phosgene gas The upper airway filters most soot particles, but those carried into the lung may adsorb various substances and cause reflex bronchospasm to further extend chemical damage Immediate effects of smoke inhalation on the lower airway and alveoli include loss of ciliary action, mucosal edema, bronchiolitis, alveolar epithelial damage, and impaired gas exchange, particularly oxygenation Areas of atelectasis or air trapping, and loss of surfactant activity, worsen ventilation–perfusion mismatch and hypoxemia Hours later, sloughing of tracheobronchial mucosa and mucopurulent membrane formation increases the degree of obstruction, poor gas exchange, and likelihood of infection Beyond the first 24 hours, pulmonary pathology that results from smoke inhalation is largely indistinguishable from adult respiratory distress syndrome, which arises from other insults Patient with inhalation injury are at increased risk for pneumonia and multisystem organ failure Children who die from smoke inhalation may sustain serious respiratory damage in the absence of cutaneous injury ... discharge from the ED all caretakers should be educated on drowning prevention The American Academy of Pediatrics recommends the installation of a 4-sided fence that prevents direct access to a swimming... around bathtubs, pools, or other bodies of water SMOKE INHALATION Goals of Treatment The goals of emergency care include early intubation (if there are signs of airway compromise), stabilization