Assessment and Care of the

Patient with Submersion Injury

Case
17 year old previously healthy boy was on a raft in a
homemade pond at his home partying with friends,
dove in and did not come up.

Friends jumped into the water and pulled him onto

the shore, then called 911
Scene/Initial Survey
Pond is approximately 100 meters from any paved
road/path. There is a narrow path cut through grass.

Ambient temperature is 76 degrees F.

Patient is now on the shore, lying on the ground,

covered with towels.
Scene/Initial Survey
Primary Survey
Airway – intact, pt talking, occasional gasping breaths.
Breathing – diaphragmatic breathing with use of accessory
muscles of neck, coarse breath sounds. Diminished
posteriorly.
Circulation – heart tones S1S2, rate 50s, weak central pulses.
Disability – alert and oriented, unable to move arms and
legs, no sensation below the clavicles.
Exposure – gaping laceration of scalp, priapism, no
deformity or other apparent trauma. Pts breath smells of
alcohol.
Initial Actions?
Secondary Survey/Interventions
ABCs unchanged, pt placed in full spine immobilization.
BP 82/40, HR 54, regular, RR16, O2 sat 96% on ambient
air
Oxygen applied via NRB
IV started, NS bolus administered without change in BP.
Dressing applied to scalp laceration. No other signs of
visible trauma.
Pt carried to ambulance on board by paramedics and
firefighters.
Problem list
What is wrong here?
Problem list
Slightly labored respirations – Does not have hypoxia
at this point and is talking. Is there a need to
administer positive pressure ventilation? What will
positive pressure ventilation do to his hemodynamics?
Hypotension – possibly multifactorial
Neurogenic shock
Hemorrhagic shock – scalp wound
Initial treatment
Problem list
Paralysis and total sensory deficit?

What is the cause?

Does this affect his disposition?

How can you optimize chances for a better outcome?

Transport
Pts blood pressure falls to 60/30 despite initial IV NS
bolus, HR remains in the 50s
O2 saturation begins to fall to low 90s/upper 80s on
NRB mask, pt breathing becomes more labored.
Pt remains lucid, but is becoming anxious
What next (you are 15 minutes out from your receiving
hospital)?
Near Drowning/Submersion Injury
Occurs when a person is submerged in water, attempts
to breathe (wet drowning) or has largyngospasm (dry
drowning), and sustains neurologic deficit secondary
to impaired oxygen delivery.
Drowning is defined as death from asphyxia within 24
hours from a submersion episode.
Near drowning refers to survival (even with eventual
death) greater than 24 hours from the submersion
episode.
Epidemiology
3rd most common accidental death (2nd in children 1-14
yrs)
Children under 4, teenagers (15-19 yrs), elderly
Swimming pools 15 times more likely involved than
auto accident in children under age 5
Males, particularly adolescents, higher risk (4:1 M:F).
Males 12 times more likely to be involved in boat –
related drowning.
Risk factors include water sports and boating,
particularly when mixed with alcohol.
Mechanism of Injury
Death from respiratory failure and anoxic brain injury

Electrolyte abnormalities, hemolysis and disseminated

intravascular coagulation are rare
Mechanism of Injury
CNS effects:
Cerebral hypoxemia, cerebral edema, reperfusion injury.
Injury may be limited by hypothermia at the time of the
submersion event.
Autonomic instability (diencephalic/hypothalamic
storm) may result as demonstrated by tachycardia,
hypertension, tachypnea, diaphoresis, muscle rigidity.
May have delayed CNS infection with atypical soil and
water borne pathogens.
Mechanism of Injury
Pulmonary effects:
Fluid aspiration as little as 1-3 ml/kg can result in
significantly impaired gas exchange, often due to altered
alveolar surfactant (hypotonic fresh water caused disruption
and hypertonic salt water causes osmotic washout).
Injury to the alveolar – capillary unit results in lower FRC
and pulmonary edema, and may progress to ARDS. This may
also occur with anoxic brain injury due to neurogenic
pulmonary edema.
Pneumonia is a rare, delayed consequence of submersion
injury.
Mechanism of Injury
Cardiovascular impairment may be caused by:
Direct coronary ischemia secondary to hypoxemia from
lack of ventilation and subsequent decreased cardiac
output (decreased EF or arrhythmia)
Hypotension of rewarming secondary to vasodilatation
These effects are usually transient unless there is
sustained hypoxic stress
Dry vs Wet
Dry drowning may account for as much as 15% of near
drowning
Caused by largyngospasm and glottic closure causing
asphyxiation
Some recent literature questions the incidence and
pathophysiology however
Wet drowning
Flooded alveoli impairing oxygenation and ventilation

Pulmonary edema caused by flooding, fluid shifts,

neurogenic edema, altered capillary permeability
Diving reflex
Occurs when face submerged in cold water
Produces bradycardia, breath holding, central
redistribution of blood flow (may mimic death in
profound cases even after the pt is removed from the
water)
May improve cerebral outcome, particularly when the
water is colder and the body temperature is rapidly
lowered or hypothermia present at the time of
submersion.
Important HPI
Witnessed/unwitnessed, time of event or time person
last seen
Known trauma
PMH (seizures, cardiac problems, DM)
Drug or alcohol use
Environmental (air and water temp)
Clinical Exam
Respiratory distress, tachypnea, use of accessory
muscles. This can progress to failure, even hours out
from the submersion
May hear wheezing, rales, rhonchi
Neurologic impairment
Hypothermia, even in warm weather
Pre-hospital care
Airway: All should receive O2
Rescue breathing/assisted ventilation ASAP (even in water)
ETT for hypoxia, airway protection
CPAP if airway and neurological exam intact
C-spine immobilization as indicated
Breathing: May use PEEP valve or higher vent pressure settings to
overcome poor compliance due to pulmonary edema and
atelectasis
Circulation: IV, monitor. No chest compressions while in water
Exposure: Keep warm. Hypothermia is only protective during the
exposure. Extricate the patient from the water as quickly as
possible.
Additional Concerns
Don’t forget c-spine immobilization
May see paralysis, weakness, hypotension, bradycardia
with associated low cervical spine injuries (may mimic
diving reflex)
Always protect c-spine if submersion unwitnessed
Evaluate for associated injuries
Evaluate for causative illnesses (cardiac event, stroke,
hyper/hypoglycemia, seizure, suicide attempt,
ingestion)
Be Aggressive
While cardiac and respiratory arrest present a worse
outcome, as may as 20% of these patients will survive
neurologically intact

Poor outcomes are associated with requirement of

sustained CPR on arrival at the hospital, particularly
with warm water drowning
Special Considerations
Resuscitation of the pulseless and apneic patient
C-spine immobilization
Heimlich Maneuver
Tracheal intubation
Treatment in the ED
Pulseless and apneic drowning pt
RESUSCITATE! – Begin ventilations and compressions
as soon as practicable
Bystander estimates of immersion time often
inaccurate
Case reports document functional recovery after an
hour of submersion
No prognostic scale or clinical findings accurately
predict long-term neurologic outcome
C-Spine immobilization?
A 2001 Journal of Trauma review of 2244 cases from
Washington state identified only 11 (.5%) with a
cervical spine injury
Each case had either clinical signs of trauma, or
history of MVA, fall from height, or diving accident
Thus, routine immobilization absent such factors may
be unnecessary
Heimlich: Yes or No?
This maneuver has been suggested as a way to remove
fluid from the lungs
Ineffective and dangerous, as it may delay ventilation
and precipitate vomiting and aspiration
No Heimlich
Aspiration Risk
Submersion victims swallow much more water than
they aspirate
If you use BVM or CPAP, remember the increased risk
of gastric distention and subsequent vomiting and
aspiration
Submersion in sewage or water with high particulate
content increases risk of infection from subsequent
aspiration
Aspiration Risk – cont’d
Inability to maintain O2 sats greater than 90% on high
flow
Capnometry of 50 or greater
These findings would normally indicate CPAP
Because of increased risk of aspiration in the
drowning victim, RSI may be preferred
Emergency Department Care
For normal exam on arrival, pts may be discharged after 6
hour observation period if no deterioration
Admit any patient with respiratory symptoms or dysfunction
Airway, oxygen, management of arrhythmias (which are often
due to hypoxia)
Volume repletion in patients with severe respiratory
involvement due to fluid shifts
Rewarm aggressively (unless VT/VF – may wish to follow
hypothermia protocol)
Identify other injuries/medical issues
Steroids and prophylactic antibiotics not helpful
In Hospital Care
Hospital care is directed toward optimizing CNS
oxygenation and perfusion
Aggressive ventilatory support
Correct arrhythmias and use dopamine/dobutamine for
hemodynamic support as needed
Monitor and manage serum glucose
Appropriate consultation (surgery, neurosurgery,
orthopedic surgery) for management of traumatic
injuries
Prevention Efforts
EMS can play a major role in prevention
Inadequate supervision of children playing in or
around water is chief cause of pediatric submersion
death
Mortality rate from drowning has declined in the US
since 1990, probably in part due to increased public
awareness of prevention, ETOH risks, and CPR
Back to our case
Transport (part 2)
Pt is started on CPAP
Dopamine is started through his large-bore peripheral
IV and BP and HR improve
Pt has some recurrent bleeding through the dressing
on his scalp wound after his hemodynamics improve –
controlled with direct pressure for the remainder of
transport
ED Course
Pt switched to BiPAP ventilation and hypoxia further
improves
Trauma line placed for vasopressor support.
Phenelephrine added
Pt started on methylprednisolone protocol
Raney clips used to temporize scalp bleeding
Trauma evaluation significant for unilateral facet
dislocation at C5-6
SICU Course
Pt placed in Wells’ tongs and traction with eventual
reduction of his facet dislocation
Scalp wound debrided and repaired at bedside
Neurological exam does not improve
MRI shows cord disruption with extension of
hematoma and edema to the C3 level
Eventually weaned from pressors and positive pressure
ventilation
Transferred to rehabilitation with persistent
quadriplegia
After discharge
Pt eventually able to manage powered wheelchair
independently. Continues to need total assistance for
ADLs.
Commits suicide by driving his wheelchair off a dock
within months of moving back home
Questions?