Drowning & Near Drowning

Drowning is...
Death secondary to asphyxia while immersed in a liquid, usually water, or within 24 hours of submersion

 In 2004 an estimated 388 000 people died world wide as a result of drowning. This total, taken from Global Burden of Disease figures, makes drowning the third leading cause of death from unintentional injury (after road traffic accidents and falls).

 It is a significant underestimate, as it includes only deaths from accidental drowning and submersion, excluding drowning due to cataclysms (floods), assaults, suicides ,and transport accidents. Drowning is a global public health concern which results in significant morbidity and mortality.

 Drowning is the process of experiencing respiratory impairment from submersion/ immersion in liquid. Drowning outcomes classified as: death morbidity or no morbidity.

Factors increasing the risk of drowning

Toddler and adolescent age groups Pools / dams / drains etc in children Water with currents / rips / waves Colder water Alcohol and drugs (esp. in men) Associated head and neck injury Fatigue

Predisposing Factors
Coma, seizures Alcohol/Drugs Exhaustion Hyperventilation Rapidly moving water

Predisposing Factors
Poor swimming ability Exhaustion Panic Hypothermia Trauma

PATHOPHYSIOLOGY
The primary physiological consequences of drowning are prolonged hypoxemia and the resultant metabolic acidosis. When a drowning victims airway lies below a liquid surface, initial breath-holding is inevitably followed by a gasp which draws water into the hypo pharynx and triggers laryngospasm. After a period of hypoxemia, the laryngospasm breaks and there is a further gasp, followed by hyperventilation and aspiration of variable amounts of water.

 The aspiration of 1-3ml.kg-1 of water results in significantly impaired gas exchange. Injury to other organs arises from the subsequent hypoxia and acidosis. In 10 to 20 per cent of patients laryngospasm is maintained until cardiac arrest occurs and, in this situation, no aspiration occurs (previously referred to as dry drowning).

Salt vs Fresh
There are REAL differences

 When fresh water is aspirated, the hypotonic solution moves rapidly across the alveolar-capillary membrane. This destroys the surfactant layer and results in alveolar collapse and decreased compliance, with marked ventilation/perfusion (V/Q) mismatching. As much as 75% of blood flow may circulate through hypo ventilated lung segments.

 Aspiration of salt water causes washout of surfactant and exudation of protein rich fluid into the alveoli and pulmonary interstitium. The result is a reduction in compliance, damage to the alveolar-capillary membrane and intrapulmonary shunting.

 Bronchospasm may occur in both fresh and salt water drowning. There is no difference in outcome between fresh water and salt water drowning; both may result insignificant submersion injuries and management is identical.

 The release of inflammatory mediators may result in pulmonary hypertension, whilst pulmonary oedema occurs as a result of both negative pressure (following obstruction and laryngospasm) and hypoxic neuronal injury. The destruction of surfactant commonly results in acute respiratory distress syndrome (ARDS). Another frequent complication is ventilator associated lung injury (VALI). In a small number of patients, aspiration of stagnant water, silt, sand, sewage or vomitus may cause bronchial occlusion, pneumonia, abscess formation and inflammatory damage to the alveolar membranes.

 Neurological injury is a major determinant of outcome and subsequent quality of life in drowning victims. As well as direct trauma, primary neurological injury occurs due to brain hypoxia and ischemia. Secondary injury may result from multiple factors including sustained hypoxia, hypotension, acidosis, hyperglycaemia, release of excitatory neurotransmitters, seizures and cerebral oedema.

 Autonomic instability is common in both severe hypoxic and severe traumatic brain injury,3 and may result in tachycardia, hypertension ,diaphoresis, agitation and muscle rigidity. This encephalic hypothalamic storm may present as a syndrome of transient left ventricular hypo kinesis, dyskinesis or akinesis, manifesting as ECG changes and raised troponin levels, in the absence of obstructive coronary artery disease or myocarditis. This is also known as Takosubo cardiomyopathy.

 Rhabdomyolysis may occur, since there is extensive hypoxic muscle injury and the subsequent myoglobinaemia may precipitate acute kidney injury. Electrolyte disturbances may also occur, for example hyponatraemia is seen in children who have ingested large quantities of fresh water.

COLD WATER
and

WARM WATER
drownings are different

 In warm water death from drowning, slow onset hypothermia In cold water stress response may cause early death, so too can drowning, hypothermia may be protective in total immersion, hypothermia is a late (>30 mins ) cause of death

In cold water...
Cold stress leads to:

Respiratory and cardio-vascular responses

Gasp reflex Mammalian dive reflex (total immersion or face-only) esp. in young children, very cold water, excessive stress

Cold vs icy water immersion

Usually hypothermia is an unfavorable sign Several case reports of dramatic neurologic recovery after prolonged (10-150 min) icy water submersions
Freezing-temperature water (<5C) Core body temperature less than 28-30C, or much lower

For hypothermia to be protective, core body temperature must fall rapidly, decreasing cellular metabolic rate, before significant hypoxemia begins

Warm Water Submersion Poor Prognosis

In warm water submersion
Submersion > 5 minutes Fixed and dilated pupils (in the ED) No CPR for 10 minutes or more pH less than 7.1 on arrival at hospital Need for in hospital resuscitation or ventilation

Severe neurologic impairment or mortality is likely

Hot Water
Body temperature and above Hot tubs, bath tubs, hot springs

Wet Drowning
Approximately 90% of drowning victims
aspirate water vomit cough gasp flood lungs with water

Asphyxia
Laryngospasm maintained
Respiratory arrest Cardiac arrest Dry drowning Wet drowning
*mechanism in fresh and salt water slightly different

Relaxation of the airway

Water enters lungs Surfactant washout V / Q mismatch*

Initial Assessment and Resuscitation

Restating the obvious

Initial Assessment and Resuscitation

Specialized issues
No Heimlich maneuver: thought to clear airways of liquid obstruction
Amount of fluid is usually small and nonobstructive May increase risk of aspiration of gastric contents Do not waste time, correcting hypoxia is paramount

Initial Assessment and Resuscitation

Threshold for intubation should be very low Indications for intubation
Arrest Loss of airway protective reflexes Deteriorating neurologic exam Severe respiratory distress or hypoxia despite supplemental oxygen Hypothermia (core temperature < 30oC)

Cold water (<10C) immersion is different from that in warmer water

Hypothermia
Cerebral blood flow decreases 6-7% per 1oC drop Negative effects include dysrhythmias, increased blood viscosity Must be cold before hypoxic

In cold water...
Cold stress leads to:

Respiratory and cardio-vascular responses

Gasp reflex

Initial Assessment and Resuscitation

Hypovolemia Marked vasoconstriction IV fluids

Labs & tests

Very mild electrolyte changes Moderate leukocytosis Hct and Hgb usually normal initally
Fresh water aspiration, the Hct may fall slightly in the first 24 hrs due to hemolysis Increase in free Hgb without a change in Hct is common

EKG
Sinus tachycardia & nonspecific ST-segment and T-wave changes Reverts to normal within hours Ominous - ventricular arrhythmias, complete heart block

CXR
May be normal initially despite severe respiratory disturbances Patchy infiltrates Pulmonary edema

DIC occasionally ABG metabolic acidosis & hypoxemia

Laboratory
Arterial blood gases Electrolytes BUN/ Creatinine Platelets/ PT & PTT/ CBC Serum & Urine Hemoglobin

Findings at autopsy
Wet, heavy lungs Varying amounts of hemorrhage and edema Disruption of alveolar walls ~70% of victims had aspirated vomitus, Cerebral edema and diffuse neuronal injury Acute tubular necrosis

Therapy for the lungs

CPAP or PEEP Aerosolized -agonists for bronchospasm Bronchoscopy Prophylactic antibiotics have not been shown to be beneficial Steroids:
No controlled human studies to support use Animal models and retrospective studies in humans have failed to demonstrate benefit

Brain therapy
ICP monitoring - not indicated, typically irreversible hypoxic cellular injury Brain CT not indicated, unless TBI suspected Mild hyperventilation? Osmotherapy not indicated Corticosteroids (dexamethasone) - no proven benefit Seizures - treat aggressively Shivering or random, purposeless movements can increase ICP Hypothermia and barbiturate coma - highly controversial & unlikely to benefit the patient (31 comatose kids, J Modell, NEJM 1993)

Bad prognostic indicators

Submerged >10 min Time till BLS >10 min CPR >25 min Initial GCS <5 Age <3 years CPR in ER Initial ABG pH <7.1 Initial core temp <33o

Recommendations
Pre-hospital resuscitation, including early intubation, ventilation, vascular access, and administration of advanced life support medications Continued resuscitation and stabilization in the ED Full supportive care in the ICU for a minimum of 48 hrs Consider withdrawal of support if no neurologic improvement is detected after 48 hours
Testing such as brainstem evoked responses, EEG, and MRI (not CT) may prove helpful for neurologic examination

Pediatrics, 1997 Christenson, Jansen, Perkins

Near Drowning Pulmonary Injury

Aspiration as little as 1-3 cc/kg can cause significant effect on gas exchange
Increased permeability Exudation of proteinaceous material in alveoli Pulmonary edema decreased compliance

ICU Management Strategies

Intubation/Ventilation
Indications
SpO2 < 90% on FIO2 > 0.6 PaCO2 > 50 with pH < 7.3 Increased work of breathing Abnormal CNS exam

Treatment of near drowning victims, some important points:

Immediate on site CPR is the key to increase the chance of survival. DO NOT DO any specific maneuvers (Heimlich) to expel water from the lungs. ED observation for 8 hours to screen for those requiring hospital admission. Arterial blood gas analysis and chest x-rays are the most reliable parameters. Warning of any pyrexial illness after discharge (secondary pulmonary infection).

Resuscitation Fluids
Current practice
Normal Saline 5% Albumin 25% Albumin Lactated Ringers Solution Hypertonic Saline

Choice dependent on provider, cost, habit

Albumin Infusion During Injury

Proposed Mechanisms for Protection

Anti-inflammatory agent Reduction of platelet aggregation

Reduction of microvascular thrombosis

Improved local blood flow

Albumin Infusion During Injury

Proposed Mechanisms for Protection

Regulates pyruvate dehydrogenase

Improved cellular bioenergetics
Tabernero et al. Glia 1999

Binds free calcium

Directly decreases cellular injury
Wortsman et al. Am J Physiol 1980

Oxygen radical scavenger

Loban et al. Clin Sci 1997 Kooy et al. Crit Care Med 1995

Outcomes
Long Term Prognosis
Overall, >15% survivors with significant neurologic deficits Children with spontaneous, purposeful movements and had a normal brainstem examination at 24 hours progressed to full recovery Those without these findings by 24 hours suffered severe neurologic deficits or death

Outcome Measures
Death Cardiovascular function as measured by:
Blood pressure, heart rate, and initial arterial blood gas measurements Echocardiogram Need and duration of inotropic support

Need and duration of mechanical ventilation Modified Multi-organ Failure Score on Days 1, 2, 3, and 7
Serum Creatine Cardiac Troponin I Total Bilirubin

Outcome Measures
Lengths of stay in pediatric intensive care unit Length of stay in hospital. Admission neurologic examination as measured by the:
Glasgow Coma Scale score pupillary reactivity other brain stem reflexes presence of apnea

Magnetic resonance imaging and spectroscopy abnormalities at post-arrest day 7. Pediatric Cerebral Performance Category Scale Score (PCPCS) at 6 to 12 months post injury. Glasgow Outcome Score (GOS) on discharge from PICU GOS on discharge from hospital

The problem with looking well...

Aspiration of water can cause late complications:
Neurogenic pulmonary oedema, Pneumonia, SIRS, DIC, Haemolysis, Hepatic & renal failure, bowel necrosis Plus complications of hypothermia

Assessing aspiration:
Historical factors Prolonged head immersion Period of apnoea CPR required Symptoms / signs Cough, breathlessness, Retrosternal discomfort Cyanosis, tachycardia Tachypnoea, wheeze or Crackles in chest Pink frothy sputum