The Journal of Emergency Medicine, Vol. -, No. -, pp. 1–5, 2014 Copyright Ó 2014 Elsevier Inc. Printed in the USA. All rights reserved 0736-4679/$ - see front matter
Case Presentations of the Harvard Emergency Medicine Residencies
NEAR DROWNING AND ADULT RESPIRATORY DISTRESS SYNDROME Micheal Buggia, MD, Louisa Canham, MD, Carrie Tibbles, MD, and Alden Landry, MD, MPH Department of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Corresponding Address: Micheal Buggia, MD, Department of Emergency Medicine, Beth Israel Deaconess Medical Center, One Deaconess Road, WCC-2, Boston, MA 02215
Dr. Micheal Buggia: Today’s case is that of a 19-year-old man presenting to the Emergency Department (ED) as a trauma activation. The patient was water tubing behind a boat, and as the boat stopped suddenly, he ran into it head first. The patient was wearing a life preserver vest. Witnesses reported that the patient had loss of consciousness and was pulled into the boat shortly after the accident. It took approximately 2 min for the patient to return to his baseline level of consciousness. On arrival to the ED, the patient was awake and his only complaint was mild headache. He denied any shortness of breath, chest pain, abdominal pain, or extremity injury. Dr. Alden Landry: Did the patient have any significant past medical history? Dr. Buggia: No, this was an otherwise healthy 19-year-old man. Dr. Carrie Tibbles: What did you find on your primary survey of this patient? Dr. Louisa Canham: On presentation, his initial vital signs were: temperature 36.8 C (98.2 F), heart rate 87 beats/min, blood pressure 130/70 mm Hg, respiratory rate 24 breaths/min, and oxygen saturation 94% on room air. On primary survey, the patient’s airway was intact, he had equal and clear breath sounds bilaterally, and palpable radial pulses. His score on the Glasgow Coma Scale was 15. Dr. Tibbles: What findings were discovered on secondary survey? Dr. Canham: On secondary survey, the only significant finding was a 4-cm laceration to the chin. The patient had a nonfocal neurologic examination and did
not seem to be in any acute distress. Our bedside FAST (focused assessment with sonography for trauma) was also negative. Dr. Landry: After the primary and secondary survey, what was your differential diagnosis and work-up plan? Dr. Buggia: Although his examination was reassuring, this patient had a significant mechanism of injury to his head, and our primary concerns were ruling out intracranial hemorrhage and cervical spine injury. As such, we ordered a STAT computed tomography (CT) scan of the head and cervical spine without contrast and a portable chest x-ray study. Dr. Landry: What were the findings? Dr. Buggia: The portable chest x-ray study was reassuring (Figure 1). There was no evidence of bony injury, pneumothorax, or pulmonary edema. Our radiologists quickly read his CT scans reporting no intracranial hemorrhage or cervical spine injury. Dr. Tibbles: What were the results of the basic laboratory studies? Dr. Canham: Laboratory tests showed: sodium 139 mEq/L, potassium 3.9 mEq/L, chloride 98 mEq/L, bicarbonate 28 mEq/L, blood urea nitrogen 17 mg/dL, creatinine 0.9 mg/dL, and glucose of 106 mg/dL; white blood cells 9 K/uL, hematocrit 40%, platelets K/uL. A serum toxicology screen including ethanol level was negative. Dr. Landry: So essentially, the patient’s initial workup was reassuring, without any significant injuries identified. What was your plan with this patient?
1
2
Figure 1. Initial portable anteroposterior chest x-ray study without any acute process.
Dr. Buggia: Although the patient seemed quite stable, we planned to observe him in the ED. This patient likely had a component of freshwater aspiration secondary to his loss of consciousness while still in the water. Based on multiple studies on near-drowning events, there are recommendations that patients be observed for approximately 6 h, paying close attention to vital signs, utilizing continuous pulse oximetry and cardiac rhythm monitoring, and paying close attention to mental status (1–3). We know that initial chest radiographs can and often do underestimate the severity of pulmonary injury, and that the development of clinical signs of pulmonary compromise can be insidious. If there is evidence of respiratory distress, repeat chest radiograph, as well as arterial blood gas analysis, is indicated. Dr. Landry: What was the patient’s course while in observation? Dr. Canham: About 90 min after our initial evaluation, the patient’s respiratory rate increased and oxygen saturation decreased, as noted by the nursing staff. Repeat vital signs at that time revealed a heart rate of 82 beats/min, blood pressure of 124/80 mm Hg, respiratory rate of 28 breaths/min, and 88% oxygen saturation on 4 L oxygen via nasal cannula. Over the next 30 min, the patient’s respiratory rate and oxygen requirement continued to climb. On examination, he had preserved mental status but significantly increased work of breathing. Auscultating his lungs revealed diffuse coarse crackles. At that time, a repeat anteroposterior chest x-ray study was obtained. Dr. Tibbles: What was the result of the chest x-ray study?
M. Buggia et al.
Dr. Canham: Significant bilateral pulmonary edema, most likely noncardiogenic (Figure 2). Dr. Tibbles: What was your plan for the patient at that time? Dr. Buggia: As the patient’s respiratory status continued to decline, we held a discussion with the patient and his family regarding the likely need for mechanical ventilation. At that time we prepared to perform endotracheal intubation. Three hours after initial presentation, rapid sequence intubation was performed using etomidate and succinylcholine. The patient was successfully intubated with a 7.5 mm endotracheal tube via direct laryngoscopy. Dr. Tibbles: Did you initially feel that this patient was at risk for pulmonary decline? Dr. Canham: Yes, as it was a near drowning, water aspiration and subsequent pulmonary compromise was a concern. Aspiration of 1–3 mL/kg body weight of either salt or fresh water compromises the integrity of pulmonary surfactant, leading to alveolar collapse, atelectasis, intrapulmonary shunting, and ventilationperfusion mismatching and noncardiogenic pulmonary edema, resulting in acute respiratory distress syndrome (ARDS) (4–6). Pulmonary compromise can develop insidiously or rapidly. Signs and symptoms usually include tachypnea, shortness of breath, hypoxia, crackles, and wheezing, none of which were present in this patient initially. Dr. Tibbles: What is the pathophysiology of drowning?
Figure 2. Repeat anteroposterior chest x-ray study when patient became hypoxic showing pulmonary edema likely representing acute respiratory distress syndrome.
Near Drowning and Adult Respiratory Distress Syndrome
Dr. Canham: Drowning and near drowning typically begin with a period of panic, loss of the normal breathing pattern, breath holding, air hunger, and a struggle by the victim to stay above the water. Reflex inspiratory efforts eventually occur, leading to hypoxemia by either aspiration or laryngospasm when water hits the lower respiratory tract (7). Dr. Landry: Besides pulmonary compromise, what are other common complications of drowning? Dr. Canham: Neurologic damage is also a concern. Hypoxemia and ischemia are known to cause neuronal damage and can lead to elevations in intracranial pressure. Approximately 20% of near-drowning victims sustain neurologic damage, limiting functional recovery despite successful cardiopulmonary resuscitation (8). Cardiac dysrhythmias are also a concern, and can incite a submersion injury or develop as a consequence. However, our patient did not have any concerning findings for significant neurologic injury and had a reassuring electrocardiogram. Dr. Tibbles: Did this patient have any special circumstances that put him at risk for drowning? Dr. Buggia: We know there are many risk factors associated with drowning and near drowning, including substance abuse, specifically alcohol consumption, inadequate adult supervision, hypothermia, seizure disorder, risk-taking behavior, concomitant trauma, stroke, or myocardial infarction. However, the only major risk factor was concomitant trauma. The patient did not endorse any substance abuse prior to his accident that day, including alcohol. However, we did obtain a serum toxicology screen. We know that 30–50%of drownings can be attributed to alcohol intoxication (9,10). Smith et al., in their study of drownings, were able to show an odds ratio for death of 37.4 for a blood ethanol concentration of 150 mg/dL or greater, compared to sober case controls (11). Dr. Landry: Did you consider the use of empiric antibiotics? Dr. Buggia: Initially we did not give the patient antibiotics. We know that empirical antibiotics do not increase survival and should only be administered to the rare patient who was submerged in grossly contaminated water or who shows signs of infection or sepsis (10). However, later in the patient’s course he did become febrile and hypotensive, requiring fluid resuscitation. At that time we did give the patient a dose of cefepime. After the initial fever he remained afebrile, and his blood cultures remained negative during his hospital course. Dr. Tibbles: Although the chemistry panel was normal in this patient, should you be worried about possible electrolyte abnormalities in the setting of near drowning? Dr. Canham: No. It is unlikely this patient aspirated a significant enough volume to cause electrolyte changes.
3
Aspiration of more than 11 mL/kg of body weight must occur before blood volume changes occur, and more than 22 mL/kg before electrolyte changes take place, and autopsy studies show that most drowning victims aspirate < 4 mL/kg (12–14). Dr. Landry: Why do you think that the patient deteriorated so rapidly? Dr. Canham: This patient had suffered a trauma and near-drowning event. Given his presentation and the findings on his repeat chest x-ray study, the most likely etiology for his decompensation was ARDS, which is a severe form of noncardiogenic pulmonary edema. ARDS can occur in many disease states, the most common of which is infection. Pneumonia is the leading cause of ARDS, followed by sepsis from any infectious source. Other triggers for ARDS include noninfectious injury such as pancreatitis, trauma, transfusion reactions, and drug reactions. Despite recent advances in our understanding of the pathophysiology of ARDS, the mortality rate remains approximately 40% (15). Dr. Tibbles: How do you determine if a patient has developed ARDS? Dr. Buggia: ARDS exists on a spectrum with acute lung injury (ALI). Patients must meet the following conditions to be diagnosed with ARDS: acute onset, evidence of bilateral infiltrates on chest x-ray study, normal left atrial pressure, and PaO2/FiO2 ratio < 200. If the PaO2/ FiO2 ratio is < 300, then the patient is said to have ALI, where the lung injury is considered less severe. The condition of having a normal left atrial pressure is meant to distinguish patients with a cardiac etiology for their pulmonary edema from patients with ARDS (15). Dr. Tibbles: What is the mechanism behind ARDS? Dr. Buggia: ARDS generally develops in patients who have an underlying inflammatory condition, such as those mentioned above. The capillary-alveolar barrier is damaged by the inflammatory response, leading to fluid overload in the lungs. The molecules that cause this damage include neutrophils, inflammatory cytokines, and free radicals. The accumulation of fluid in the alveoli inhibits gas exchange (both oxygen and carbon dioxide), leading to hypoxemia, tachypnea, and respiratory distress. Intubation is often necessary due to rapid clinical deterioration, and in fact, positive pressure ventilation can help reduce fluid accumulation in the lungs (15,16). Dr. Landry: Did you consider alternative treatments prior to intubation in this patient? Dr. Canham: The use of noninvasive positive pressure ventilation such as continuous positive airway pressure (CPAP)/bilevel positive airway pressure (BiPAP) in ARDS is controversial. In a 2010 meta-analysis, Agarwal et al. looked at the pooled results of 13 studies from 1995–2009 in an attempt to determine whether noninvasive ventilation would be beneficial in patients with
4
ARDS/ALI and possibly prevent the need for intubation (17). Their results were limited by paucity of randomized control trials, as well as by the diverse clinical and statistical outcomes of patients in these studies. Within these limits, they did find a significant reduction in the need for intubation when CPAP or BiPAP was utilized. They caution, however, that these beneficial results are likely limited to a select group of patients, primarily those who are awake and relatively stable, with no major organ dysfunction or hypoxic injury. In general, the optimal use of noninvasive ventilation in ARDS/ALI remains unclear, and for the time being should be used judiciously, without delaying intubation of patients who are unstable. Nonventilatory adjunctive treatments for ARDS have also been studied. Given that inflammation is the primary process driving early ARDS, it has been thought that treatments that reduce inflammation might help to lessen the severity of the disease. Corticosteroids in particular have been studied; however, results have been mixed, and in fact, often contradictory (18,19). Similarly, inhaled vasodilators such as prostacyclin and nitric oxide would theoretically improve perfusion and oxygenation, but have not been shown clinically to improve outcomes in patients with ARDS (18). One adjunctive strategy that may prove useful in patients with ALI/ARDS is fluid restriction. A study published in the New England Journal of Medicine demonstrated that fluid restriction in patients with ARDS resulted in decreased need for ventilator support, decreased intensive care unit length of stay, and improved lung function in patients treated with fluid-restrictive approach vs. those who got liberal fluid replacement (20). Of note, there was no improvement in 60-day mortality in the study group. Obviously, fluid replacement strategies depend on the overall clinical status of the patient; however, this study suggests that in patients who do not have evidence of poor perfusion, fluid restriction may be helpful in improving ARDS-related morbidity (18,20). Dr. Tibbles: How did you determine your ventilator settings once the patient was intubated? Dr. Canham: The ARDS network is a National Institutes of Health-funded research group that conducts studies on prevention and treatment of acute respiratory distress syndrome. In 2000, this group published the results of a multisite clinical trial that compared ventilation strategies for patients with ARDS. Patients were given either a standard tidal volume of 12 cc/kg or a ‘‘lung protective’’ tidal volume of 6 cc/kg. These volumes were based on ideal body weight. Study enrollment was terminated early due to the finding of a 22% mortality reduction for the study group treated with smaller tidal volumes (21). It is thought that high tidal volumes may contribute to the cycle of inflammation and alveolar/ capillary damage, as well as cause direct barotrauma.
M. Buggia et al.
Therefore, low-volume ventilation has now become the standard strategy for patients with ARDS. The respiratory rate should be adjusted to maintain a PCO2 in the normal range, with a goal pH of 7.30–7.45. In terms of oxygenation, the goal is to adjust the FiO2 and positive endexpiratory pressure to keep the PaO2 between 55 and 80, or maintain oxygen saturation of 88–95% (16). Dr. Landry: What was the ultimate disposition of this patient? Dr. Buggia: The patient was admitted to the trauma surgery intensive care unit. He was successfully extubated on hospital day 1 and discharged home on hospital day 4. Unintentional drowning events cause over 3500 deaths per year in the United States, and one to four admissions occur per fatal event (10). It is very important for the emergency physician to quickly recognize and treat those at risk for near drowning and be familiar with complications, including cardiac dysrhythmias, neurologic injuries, concomitant trauma, and, as in this case, pulmonary compromise. Noncardiogenic pulmonary edema is a well-known complication of near drowning, and this case outlines the need for close observation in the ED. Patients who are asymptomatic on presentation, maintain normal room-air oxygen saturation, and have no chest radiograph or arterial blood gas abnormalities can be discharged safely after an observation period of 6 h (1–3). If there is any evidence of pulmonary compromise, the patient should be admitted to the hospital for long-term monitoring. If advanced airway management is required secondary to pulmonary compromise, ARDS network protocol should be followed to decrease the rate of ventilatorassociated lung injury.
REFERENCES 1. Pratt FD, Haynes BE. Incidence of ‘‘secondary drowning’’ after saltwater submersion. Ann Emerg Med 1986;15:1084–7. 2. Causey AL, Tilelli JA, Swanson ME. Predicting discharge in uncomplicated near-drowning. Am J Emerg Med 2000;18:9–11. 3. Ibsen LM, Koch T. Submersion and asphyxial injury. Crit Care Med 2002;11:S402–8. 4. Bierens JJ, Knape JT, Gelissen HP. Drowning. Curr Opin Crit Care 2002;8:578–86. 5. DeNicola LK, Falk JL, Swanson ME, Gayle MO, Kissoon N. Submersion injuries in children and adults. Crit Care Clin 1997;13:477–502. 6. Orlowski JP, Szpilman D. Drowning: rescue, resuscitation, and reanimation. Pediatr Clin North Am 2001;48:627–46. 7. Salomez F, Vincent JL. Drowning: a review of epidemiology, pathophysiology, treatment and prevention. Resuscitation 2004;63:261–8. 8. Gonzalez-Rothi RJ. Near drowning: consensus and controversies in pulmonary and cerebral resuscitation. Heart Lung 1987;16:474–82. 9. Cummings P. Trends in unintentional drowning: the role of alcohol and medical care. JAMA 1999;281:2198–202. 10. Brenner RA. Committee on Injury, Violence, and Poison Prevention: prevention of drowning in infants, children, and adolescents. Pediatrics 2003;112:440–5. 11. Smith GS, Keyl PM, Hadley JA, et al. Drinking and recreational boating fatalities: a population-based case-control study. JAMA 2001;286:2974–80.
Near Drowning and Adult Respiratory Distress Syndrome 12. Modell JH, Davis JH. Electrolyte changes in human drowning victims. Anesthesiology 1969;30:414–20. 13. Modell JH, Moya F. Effects of volume of aspirated fluid during chlorinated fresh water drowning. Anesthesiology 1966;27:662–72. 14. Modell JH, Moya F, Newby EJ, Ruiz BC, Showers AV. The effects of fluid volume in seawater drowning. Ann Intern Med 1967;(1):68–80. 15. Matthay MA, Zemans RL. The Acute Respiratory Distress Syndrome: pathogenesis and treatment. Annu Rev Pathol 2011;6: 147–63. 16. Girard TD, Bernard GR. Mechanical ventilation in ARDS: a state of the art review. Chest 2007;131:921–9. 17. Agarwal R, Aggarwal AN, Gupta D. Role of noninvasive ventilation in acute lung injury/acute respiratory distress syndrome: a proportion meta-analsysis. Respir Care 2010;55:1653–60.
5 18. Walkey AJ, Summer R, Ho V, Alkana P. Acute respiratory distress syndrome: epidemiology and management approaches. Clin Epidemiol 2012;4:159–69. 19. Peter JV, John P, Graham PL, Moran JL, George IA, Bersten A. Corticosteroids in the prevention and treatment of acute respiratory distress syndrome (ARDS) in adults: meta-analysis. BMJ 2008; 336:1006–9. 20. Wiedemann HP, Wheeler AP, Bernard GR, et al. Comparison of two fluid-management strategies in acute lung injury. N Engl J Med 2006;354:2564–75. 21. The Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 2000;342:1301–8.
Case Presentations of the Harvard Emergency Medicine Residencies
NEAR DROWNING AND ADULT RESPIRATORY DISTRESS SYNDROME Micheal Buggia, MD, Louisa Canham, MD, Carrie Tibbles, MD, and Alden Landry, MD, MPH Department of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Corresponding Address: Micheal Buggia, MD, Department of Emergency Medicine, Beth Israel Deaconess Medical Center, One Deaconess Road, WCC-2, Boston, MA 02215
Dr. Micheal Buggia: Today’s case is that of a 19-year-old man presenting to the Emergency Department (ED) as a trauma activation. The patient was water tubing behind a boat, and as the boat stopped suddenly, he ran into it head first. The patient was wearing a life preserver vest. Witnesses reported that the patient had loss of consciousness and was pulled into the boat shortly after the accident. It took approximately 2 min for the patient to return to his baseline level of consciousness. On arrival to the ED, the patient was awake and his only complaint was mild headache. He denied any shortness of breath, chest pain, abdominal pain, or extremity injury. Dr. Alden Landry: Did the patient have any significant past medical history? Dr. Buggia: No, this was an otherwise healthy 19-year-old man. Dr. Carrie Tibbles: What did you find on your primary survey of this patient? Dr. Louisa Canham: On presentation, his initial vital signs were: temperature 36.8 C (98.2 F), heart rate 87 beats/min, blood pressure 130/70 mm Hg, respiratory rate 24 breaths/min, and oxygen saturation 94% on room air. On primary survey, the patient’s airway was intact, he had equal and clear breath sounds bilaterally, and palpable radial pulses. His score on the Glasgow Coma Scale was 15. Dr. Tibbles: What findings were discovered on secondary survey? Dr. Canham: On secondary survey, the only significant finding was a 4-cm laceration to the chin. The patient had a nonfocal neurologic examination and did
not seem to be in any acute distress. Our bedside FAST (focused assessment with sonography for trauma) was also negative. Dr. Landry: After the primary and secondary survey, what was your differential diagnosis and work-up plan? Dr. Buggia: Although his examination was reassuring, this patient had a significant mechanism of injury to his head, and our primary concerns were ruling out intracranial hemorrhage and cervical spine injury. As such, we ordered a STAT computed tomography (CT) scan of the head and cervical spine without contrast and a portable chest x-ray study. Dr. Landry: What were the findings? Dr. Buggia: The portable chest x-ray study was reassuring (Figure 1). There was no evidence of bony injury, pneumothorax, or pulmonary edema. Our radiologists quickly read his CT scans reporting no intracranial hemorrhage or cervical spine injury. Dr. Tibbles: What were the results of the basic laboratory studies? Dr. Canham: Laboratory tests showed: sodium 139 mEq/L, potassium 3.9 mEq/L, chloride 98 mEq/L, bicarbonate 28 mEq/L, blood urea nitrogen 17 mg/dL, creatinine 0.9 mg/dL, and glucose of 106 mg/dL; white blood cells 9 K/uL, hematocrit 40%, platelets K/uL. A serum toxicology screen including ethanol level was negative. Dr. Landry: So essentially, the patient’s initial workup was reassuring, without any significant injuries identified. What was your plan with this patient?
1
2
Figure 1. Initial portable anteroposterior chest x-ray study without any acute process.
Dr. Buggia: Although the patient seemed quite stable, we planned to observe him in the ED. This patient likely had a component of freshwater aspiration secondary to his loss of consciousness while still in the water. Based on multiple studies on near-drowning events, there are recommendations that patients be observed for approximately 6 h, paying close attention to vital signs, utilizing continuous pulse oximetry and cardiac rhythm monitoring, and paying close attention to mental status (1–3). We know that initial chest radiographs can and often do underestimate the severity of pulmonary injury, and that the development of clinical signs of pulmonary compromise can be insidious. If there is evidence of respiratory distress, repeat chest radiograph, as well as arterial blood gas analysis, is indicated. Dr. Landry: What was the patient’s course while in observation? Dr. Canham: About 90 min after our initial evaluation, the patient’s respiratory rate increased and oxygen saturation decreased, as noted by the nursing staff. Repeat vital signs at that time revealed a heart rate of 82 beats/min, blood pressure of 124/80 mm Hg, respiratory rate of 28 breaths/min, and 88% oxygen saturation on 4 L oxygen via nasal cannula. Over the next 30 min, the patient’s respiratory rate and oxygen requirement continued to climb. On examination, he had preserved mental status but significantly increased work of breathing. Auscultating his lungs revealed diffuse coarse crackles. At that time, a repeat anteroposterior chest x-ray study was obtained. Dr. Tibbles: What was the result of the chest x-ray study?
M. Buggia et al.
Dr. Canham: Significant bilateral pulmonary edema, most likely noncardiogenic (Figure 2). Dr. Tibbles: What was your plan for the patient at that time? Dr. Buggia: As the patient’s respiratory status continued to decline, we held a discussion with the patient and his family regarding the likely need for mechanical ventilation. At that time we prepared to perform endotracheal intubation. Three hours after initial presentation, rapid sequence intubation was performed using etomidate and succinylcholine. The patient was successfully intubated with a 7.5 mm endotracheal tube via direct laryngoscopy. Dr. Tibbles: Did you initially feel that this patient was at risk for pulmonary decline? Dr. Canham: Yes, as it was a near drowning, water aspiration and subsequent pulmonary compromise was a concern. Aspiration of 1–3 mL/kg body weight of either salt or fresh water compromises the integrity of pulmonary surfactant, leading to alveolar collapse, atelectasis, intrapulmonary shunting, and ventilationperfusion mismatching and noncardiogenic pulmonary edema, resulting in acute respiratory distress syndrome (ARDS) (4–6). Pulmonary compromise can develop insidiously or rapidly. Signs and symptoms usually include tachypnea, shortness of breath, hypoxia, crackles, and wheezing, none of which were present in this patient initially. Dr. Tibbles: What is the pathophysiology of drowning?
Figure 2. Repeat anteroposterior chest x-ray study when patient became hypoxic showing pulmonary edema likely representing acute respiratory distress syndrome.
Near Drowning and Adult Respiratory Distress Syndrome
Dr. Canham: Drowning and near drowning typically begin with a period of panic, loss of the normal breathing pattern, breath holding, air hunger, and a struggle by the victim to stay above the water. Reflex inspiratory efforts eventually occur, leading to hypoxemia by either aspiration or laryngospasm when water hits the lower respiratory tract (7). Dr. Landry: Besides pulmonary compromise, what are other common complications of drowning? Dr. Canham: Neurologic damage is also a concern. Hypoxemia and ischemia are known to cause neuronal damage and can lead to elevations in intracranial pressure. Approximately 20% of near-drowning victims sustain neurologic damage, limiting functional recovery despite successful cardiopulmonary resuscitation (8). Cardiac dysrhythmias are also a concern, and can incite a submersion injury or develop as a consequence. However, our patient did not have any concerning findings for significant neurologic injury and had a reassuring electrocardiogram. Dr. Tibbles: Did this patient have any special circumstances that put him at risk for drowning? Dr. Buggia: We know there are many risk factors associated with drowning and near drowning, including substance abuse, specifically alcohol consumption, inadequate adult supervision, hypothermia, seizure disorder, risk-taking behavior, concomitant trauma, stroke, or myocardial infarction. However, the only major risk factor was concomitant trauma. The patient did not endorse any substance abuse prior to his accident that day, including alcohol. However, we did obtain a serum toxicology screen. We know that 30–50%of drownings can be attributed to alcohol intoxication (9,10). Smith et al., in their study of drownings, were able to show an odds ratio for death of 37.4 for a blood ethanol concentration of 150 mg/dL or greater, compared to sober case controls (11). Dr. Landry: Did you consider the use of empiric antibiotics? Dr. Buggia: Initially we did not give the patient antibiotics. We know that empirical antibiotics do not increase survival and should only be administered to the rare patient who was submerged in grossly contaminated water or who shows signs of infection or sepsis (10). However, later in the patient’s course he did become febrile and hypotensive, requiring fluid resuscitation. At that time we did give the patient a dose of cefepime. After the initial fever he remained afebrile, and his blood cultures remained negative during his hospital course. Dr. Tibbles: Although the chemistry panel was normal in this patient, should you be worried about possible electrolyte abnormalities in the setting of near drowning? Dr. Canham: No. It is unlikely this patient aspirated a significant enough volume to cause electrolyte changes.
3
Aspiration of more than 11 mL/kg of body weight must occur before blood volume changes occur, and more than 22 mL/kg before electrolyte changes take place, and autopsy studies show that most drowning victims aspirate < 4 mL/kg (12–14). Dr. Landry: Why do you think that the patient deteriorated so rapidly? Dr. Canham: This patient had suffered a trauma and near-drowning event. Given his presentation and the findings on his repeat chest x-ray study, the most likely etiology for his decompensation was ARDS, which is a severe form of noncardiogenic pulmonary edema. ARDS can occur in many disease states, the most common of which is infection. Pneumonia is the leading cause of ARDS, followed by sepsis from any infectious source. Other triggers for ARDS include noninfectious injury such as pancreatitis, trauma, transfusion reactions, and drug reactions. Despite recent advances in our understanding of the pathophysiology of ARDS, the mortality rate remains approximately 40% (15). Dr. Tibbles: How do you determine if a patient has developed ARDS? Dr. Buggia: ARDS exists on a spectrum with acute lung injury (ALI). Patients must meet the following conditions to be diagnosed with ARDS: acute onset, evidence of bilateral infiltrates on chest x-ray study, normal left atrial pressure, and PaO2/FiO2 ratio < 200. If the PaO2/ FiO2 ratio is < 300, then the patient is said to have ALI, where the lung injury is considered less severe. The condition of having a normal left atrial pressure is meant to distinguish patients with a cardiac etiology for their pulmonary edema from patients with ARDS (15). Dr. Tibbles: What is the mechanism behind ARDS? Dr. Buggia: ARDS generally develops in patients who have an underlying inflammatory condition, such as those mentioned above. The capillary-alveolar barrier is damaged by the inflammatory response, leading to fluid overload in the lungs. The molecules that cause this damage include neutrophils, inflammatory cytokines, and free radicals. The accumulation of fluid in the alveoli inhibits gas exchange (both oxygen and carbon dioxide), leading to hypoxemia, tachypnea, and respiratory distress. Intubation is often necessary due to rapid clinical deterioration, and in fact, positive pressure ventilation can help reduce fluid accumulation in the lungs (15,16). Dr. Landry: Did you consider alternative treatments prior to intubation in this patient? Dr. Canham: The use of noninvasive positive pressure ventilation such as continuous positive airway pressure (CPAP)/bilevel positive airway pressure (BiPAP) in ARDS is controversial. In a 2010 meta-analysis, Agarwal et al. looked at the pooled results of 13 studies from 1995–2009 in an attempt to determine whether noninvasive ventilation would be beneficial in patients with
4
ARDS/ALI and possibly prevent the need for intubation (17). Their results were limited by paucity of randomized control trials, as well as by the diverse clinical and statistical outcomes of patients in these studies. Within these limits, they did find a significant reduction in the need for intubation when CPAP or BiPAP was utilized. They caution, however, that these beneficial results are likely limited to a select group of patients, primarily those who are awake and relatively stable, with no major organ dysfunction or hypoxic injury. In general, the optimal use of noninvasive ventilation in ARDS/ALI remains unclear, and for the time being should be used judiciously, without delaying intubation of patients who are unstable. Nonventilatory adjunctive treatments for ARDS have also been studied. Given that inflammation is the primary process driving early ARDS, it has been thought that treatments that reduce inflammation might help to lessen the severity of the disease. Corticosteroids in particular have been studied; however, results have been mixed, and in fact, often contradictory (18,19). Similarly, inhaled vasodilators such as prostacyclin and nitric oxide would theoretically improve perfusion and oxygenation, but have not been shown clinically to improve outcomes in patients with ARDS (18). One adjunctive strategy that may prove useful in patients with ALI/ARDS is fluid restriction. A study published in the New England Journal of Medicine demonstrated that fluid restriction in patients with ARDS resulted in decreased need for ventilator support, decreased intensive care unit length of stay, and improved lung function in patients treated with fluid-restrictive approach vs. those who got liberal fluid replacement (20). Of note, there was no improvement in 60-day mortality in the study group. Obviously, fluid replacement strategies depend on the overall clinical status of the patient; however, this study suggests that in patients who do not have evidence of poor perfusion, fluid restriction may be helpful in improving ARDS-related morbidity (18,20). Dr. Tibbles: How did you determine your ventilator settings once the patient was intubated? Dr. Canham: The ARDS network is a National Institutes of Health-funded research group that conducts studies on prevention and treatment of acute respiratory distress syndrome. In 2000, this group published the results of a multisite clinical trial that compared ventilation strategies for patients with ARDS. Patients were given either a standard tidal volume of 12 cc/kg or a ‘‘lung protective’’ tidal volume of 6 cc/kg. These volumes were based on ideal body weight. Study enrollment was terminated early due to the finding of a 22% mortality reduction for the study group treated with smaller tidal volumes (21). It is thought that high tidal volumes may contribute to the cycle of inflammation and alveolar/ capillary damage, as well as cause direct barotrauma.
M. Buggia et al.
Therefore, low-volume ventilation has now become the standard strategy for patients with ARDS. The respiratory rate should be adjusted to maintain a PCO2 in the normal range, with a goal pH of 7.30–7.45. In terms of oxygenation, the goal is to adjust the FiO2 and positive endexpiratory pressure to keep the PaO2 between 55 and 80, or maintain oxygen saturation of 88–95% (16). Dr. Landry: What was the ultimate disposition of this patient? Dr. Buggia: The patient was admitted to the trauma surgery intensive care unit. He was successfully extubated on hospital day 1 and discharged home on hospital day 4. Unintentional drowning events cause over 3500 deaths per year in the United States, and one to four admissions occur per fatal event (10). It is very important for the emergency physician to quickly recognize and treat those at risk for near drowning and be familiar with complications, including cardiac dysrhythmias, neurologic injuries, concomitant trauma, and, as in this case, pulmonary compromise. Noncardiogenic pulmonary edema is a well-known complication of near drowning, and this case outlines the need for close observation in the ED. Patients who are asymptomatic on presentation, maintain normal room-air oxygen saturation, and have no chest radiograph or arterial blood gas abnormalities can be discharged safely after an observation period of 6 h (1–3). If there is any evidence of pulmonary compromise, the patient should be admitted to the hospital for long-term monitoring. If advanced airway management is required secondary to pulmonary compromise, ARDS network protocol should be followed to decrease the rate of ventilatorassociated lung injury.
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