Drowning patient resuscitation and monitoring

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By Kelly Grayson

Drowning is a significant public health issue in the United States and worldwide, and represents a frequent need for resuscitation from EMS and emergency department providers. While the frequency of unintentional drowning has decreased over the last generation, roughly 10 people still die of drowning every day in the United States, 20 percent of which are ages 14 and under [1].

Drowning is the leading cause of unintentional traumatic death in children ages 1-4, the second-ranked cause of unintentional trauma death in children ages 5-9 years old, and the 5th ranked cause of death in children ages 10-14. Drowning ranks 10th among causes of accidental trauma deaths for all ages in the United States [2].

For every child that dies from accidental drowning, another five are treated in the ED for non-fatal injuries. Roughly one-third of survivors suffer moderate to severe neurologic sequelae.

Terminology
The root cause of death by drowning is fatal asphyxia, but due to a historically wide variance in terminology and definitions, environment (water temperature, cleanliness of the water, salt versus fresh water, submersion interval, and other comorbidities), the pathophysiology of the drowning process has been somewhat muddled.

At the 2002 World Congress on Drowning, a consensus definition was reached, defining drowning as "primary respiratory impairment from submersion in a liquid medium [3]." It was further resolved that other terminology adhere to Utstein reporting criteria to ensure conformity in pooled data. Outcomes reporting for drowning was classified as death, morbidity or no morbidity; other non-standard terminology such as dry drowning, wet drowning, near drowning, active or passive drowning or delayed drowning are discarded. The World Congress on Drowning met again in November 2015, but findings from that meeting have yet to be promulgated.

Drowning can further be classified as warm-water (>20 C) or cold-water (<20 C). While sequelae and the management of each may vary somewhat depending on the salinity of the drowning medium, salt versus fresh water makes little difference in the prehospital management of the drowning patient.

Drowning pathophysiology
The drowning process begins with the victim's airway submerged beneath the surface of the water. While victims initially attempt to hold their breath and may reflexively swallow substantial quantities of water, relatively little aspiration of water occurs in the initial phase of a drowning.

The body's natural response is, "OK, if I can drink the lake first, then I'll be able to breathe." When that unobstructed breath does not occur, the first water to enter the oropharynx or larynx during an attempted breath may trigger a brief laryngospasm.

It was long believed that a significant percentage of drowning victims suffered prolonged laryngospasm, resulting in the proverbial "dry drowning," but a number of studies have disproven that notion [3, 4]. In one study of 598 autopsied drowning victims, 98.6 percent had water in their lungs [3]. The study authors noted that active ventilation is required to aspirate water into the lungs; water does not flow passively into the lungs of drowning victims. Those few victims found without significant amounts of water in their lungs were believed to be dead, and thus without respiratory effort, when they went into the water.

As time submerged increases, hypoxia and hypercarbia set in, the brainstem triggers involuntary breathing, and water enters the lungs whether there was a brief interval of laryngospasm or not.

Water — regardless of type — entering the lungs disrupts surfactant, resulting in atelectasis, pulmonary shunting and significant ventilation/perfusion (V/Q) mismatch. Water is also toxic to pneumocytes, the cells that make up alveoli. Contact with fresh water, relatively hypotonic to plasma, results in disruption of alveolar surfactant, while hypertonic salt water creates an osmotic gradient that draws fluid into alveoli, diluting and washing out surfactant.

The end result is disruption of alveolar capillary membranes, damage to the alveolar basement membrane and inflammation of pneumocytes. In addition, aspirated fluid produces vagally-mediated vasoconstriction and pulmonary hypertension. Bronchoconstriction, edema and varying degrees of atelectasis and pulmonary shunting usually follow.

In the past, it was common to differentiate salt versus fresh water drownings based upon the premise that aspiration of hypertonic sea water could cause fluid shifts, electrolyte imbalances, and lysis of red blood cells. However, this premise was based upon canine studies in which the test animals typically aspirated a great deal of water, roughly 20 mL/kg. Human drowning subjects typically aspirate far less (2-4 mL/kg), and this amount is not believed to significantly alter body chemistry, at least in the resuscitation phase of management [5].

Drowning patient with adequate perfusion management and resuscitation
The primary goal in the management and resuscitation of the drowning victim is to reverse the hypoxic insult. In the patient with respiratory compromise or arrest, but with adequate perfusion, oxygenation should be provided with 100 percent oxygen, and artificial ventilation should be performed if necessary.

Advanced airway management, if it can be performed quickly by expert rescuers, should be performed if indicated. Keep in mind that supraglottic airways, while convenient and effective short-term alternatives to endotracheal intubation, offer limited protection against further aspiration. The victim will likely have swallowed a good deal of water in addition to whatever amount may have entered the lungs.

Use waveform capnography to guide patient ventilation. The goal is a physiologically normal ETCO2 of 35-45 mm Hg, with normal waveform morphology.

Because of the amount of water aspirated by most drowning patients, pulmonary secretions may be a concern, and frequent suctioning may be required. These pulmonary secretions also necessitate vigilant monitoring of capnograph waveforms, and frequent replacement of sidestream capnograph adapter and tubing if it becomes occluded.

Remember that the inflammatory cascade triggered by aspirated water contacting pneumocytes may require positive-end expiratory pressure to recruit and retain patent alveoli. Most BVM devices include a PEEP adapter that attaches to the exhalation valve, and a PEEP setting of 7.5 – 10.0 cm H20 may be beneficial.

For the adequately perfusing drowning patient with spontaneous breathing, CPAP may accomplish the same thing.

Be alert for the characteristic shark fin waveform of acute bronchospasm and administer bronchodilators and corticosteroids as appropriate. While some sources note that analyzing the slope of the alveolar plateau (Phase III) can be useful for detecting significant ventilation/perfusion (VQ) mismatch from increased dead space ventilation or intrapulmonary shunt — both of which may be present in drowning patients — this is only true of volumetric capnography, a technology not commonly found in prehospital monitor/defibrillators [6].

Drowning patient in low perfusion states management and resuscitation
Waveform capnography is also an excellent indirect measure of perfusion. In drowning victims in cardiac arrest, waveform capnography can reliably confirm tube placement, gauge effectiveness of chest compressions, detect migration or displacement of advanced airway devices and detect return of spontaneous circulation [7].

Diminishing ETCO2 during cardiopulmonary resuscitation can indicate compressor fatigue, or if there is a significant disparity in ETCO2 readings between rescuers, a flaw in one rescuer's compression technique. A sudden increase in ETCO2 during cardiopulmonary resuscitation is a strong indicator of ROSC and may precede a palpable pulse [8, 9, 10].

Remember that the root cause of the arrest is hypoxia. As such, conventional CPR techniques with artificial ventilation should be performed, rather than cardiocerebral resuscitation techniques utilizing passive oxygenation.

One caveat applies in using capnography in drowning patients. While ETCO2 readings consistently below 10 mm Hg despite effective chest compressions and artificial ventilation have been considered a criterion for terminating resuscitation efforts, ETCO2 readings may be significantly decreased in hypothermic states. Do not terminate resuscitation prematurely.

However, although the mantra has long been, "You don't have a dead body until you have a warm dead body," it should be noted that even with hypothermic arrest patients, the prognosis for patients who have undergone resuscitation longer than 30 minutes is dismal [11]. The majority of patients are not resuscitated and those who survive usually suffer profound neurological impairment.

Conclusion
Since the common pathophysiology in all types of drowning death is profound hypoxic insult, oxygenation and ventilation are the most effective tools in managing the drowning patient. Knowing the benefits and limitations of waveform capnography in these patients and how to troubleshoot equipment will help guide the provision of oxygenation and ventilation.

References

1. Laosee OC, Gilchrist J, Rudd R. Drowning 2005-2009. Morbidity and Mortality Weekly Report 2012; 61(19):344-347. 
2. Centers for Disease Control and Prevention. (2013). 10 Leading Causes of Injury Death by Age Group Highlight Unintentional Injury Deaths, United States 2009. In Centers for Disease Control and Prevention. Retrieved February 16, 2016, from http://ift.tt/1VEHEE1
3. Lunetta P, Modell JH, Sajantila A. What is the Incidence and Significance of "Dry-Lungs" in Bodies Found in Water? American Journal of Forensic Medical Pathology. 2004 Dec. 25(4):291-301.
4. Orlowski JP, Szpilman D. Drowning, Rescue, Resuscitation, and Reanimation. Pediatric Clinics of North America. 2001;48(3):627–646.
5. Oehmichen M, Hennig R, Meissner C. Near-Drowning and Clinical Laboratory Changes. Legal Medicine (Tokyo). 2008;10(1):1–5.
6. Blanch L, Romero PV, Lucangelo U. Volumetric Capnography in the Mechanically Ventilated Patient. Minerva Anestesiologica. 2006 Jun;72(6):577-85.
7. Morisaki H, Takino Y, Kobayashi H, Ando Y, Ichikizaki K. End-tidal Carbon Dioxide Concentration During Cardiopulmonary Resuscitation in Patients with Pre-hospital Cardiac Arrest. Masui. 1991 Jul;40(7):1048-51.
8. Berg RA, Henry C, Otto CW, Sanders AB, Kern KB, Hilwig RW, Ewy GA. Initial End-tidal CO2 Is Markedly Elevated During Cardiopulmonary Resuscitation After Asphyxial Cardiac Arrest. Pediatric Emergency Care. 1996 Aug;12(4):245-8.
9. Steedman DJ, Robertson CE. Measurement of End-tidal Carbon Dioxide Concentration During Cardiopulmonary Resuscitation. Archives of Emergency Medicine. 1990 Sep;7(3):129-34.
10. Falk JL, Rackow EC, Weil MH. End-tidal carbon dioxide concentration during cardiopulmonary resuscitation. New England Journal of Medicine. 1988 Mar 10;318(10):607-11.
11. Kieboom JK, Verkade HJ, Burgerhof JG, Bierens JJ, van Rheenen PF, Kneyber MC, Albers MJ. Outcome After Resuscitation Beyond 30 Minutes in Drowned Children with Cardiac Arrest and Hypothermia: Dutch Nationwide Retrospective Cohort Study. British Medical Journal. 2015;350:h418.

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