Drowning - ICU Management

Quick Answer

One-liner: Drowning is a process of respiratory impairment from submersion/immersion in liquid where hypoxia is the primary cause of death; resuscitation prioritises early rescue breathing and ventilation, with ICU management focused on lung-protective ventilation for drowning-associated ARDS, targeted temperature management, and neuroprognostication.

30-second summary: Drowning causes death primarily through hypoxaemia from aspiration and/or laryngospasm. The 2003 Utstein definitions standardised terminology: "drowning" describes the process, with outcomes being death, morbidity, or no morbidity. ICU admission is required for respiratory failure, cardiovascular instability, altered consciousness, or hypothermia. Management centres on lung-protective ventilation (6 mL/kg IBW), appropriate PEEP for surfactant-depleted lungs, and rewarming strategies for hypothermic patients. Cold water immersion may be neuroprotective if cooling occurs before hypoxic arrest. Submersion duration is the most important prognostic factor: <5 minutes predicts excellent outcome, while >25 minutes rarely results in survival except in very cold water. Australian drowning epidemiology shows peaks in children 0-4 years (pools) and young adults 15-24 years (natural waterways), with Indigenous Australians experiencing 2-3x higher drowning rates. [1,2,3]

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CICM Exam Focus

Second Part Written SAQ Relevance

High-yield SAQ topics:

• Utstein drowning terminology and why "near-drowning" and "dry/wet drowning" are obsolete
• Pathophysiology of drowning-associated ARDS (surfactant washout, alveolar-capillary injury)
• Differences between resuscitation from drowning vs standard cardiac arrest (ventilation priority)
• Hypothermia as neuroprotective vs indicator of prolonged submersion
• Lung-protective ventilation strategies for drowning-associated ARDS
• Neurological prognostication challenges in post-drowning coma
• Rewarming strategies: passive, active external, active internal, ECMO

Common SAQ stems:

• "A 4-year-old is retrieved from a backyard pool after estimated 8-minute submersion..."
• "A 22-year-old is brought to ED after rescue from a river. Core temperature 29C..."
• "Day 2 in ICU following drowning. P/F ratio 85 despite FiO2 0.8 and PEEP 14..."

Hot Case Presentations

Typical Hot Case scenarios:

1. Day 1-3 post-drowning with ARDS requiring mechanical ventilation
2. Post-drowning cardiac arrest survivor on day 3-5 for neuroprognostication
3. Hypothermic drowning requiring rewarming strategy discussion
4. Paediatric drowning with family communication focus

Key examination findings to identify:

• Ventilator settings (assess lung-protective approach)
• Temperature management status
• Neurological examination (pupils, brainstem reflexes, motor response)
• Evidence of ARDS (bilateral infiltrates, low compliance, high PEEP requirements)
• Signs of aspiration (secretions, consolidation on CXR)

Viva Topics

Commonly tested viva areas:

• Pathophysiology of hypoxic injury in drowning
• Fresh water vs salt water aspiration (clinically irrelevant distinction)
• Diving reflex and neuroprotection mechanisms
• ANZCOR/ILCOR drowning resuscitation guidelines
• Prognostic indicators and timing of prognostication
• Ethical considerations in withdrawal of care
• Indigenous health disparities in drowning

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Key Points

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Red Flags

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Definition and Terminology

Utstein Drowning Terminology (2003)

The World Congress on Drowning (2002) and subsequent Utstein-style consensus statement (2003) standardised drowning terminology to improve research, epidemiology, and clinical communication. [1]

Obsolete Terminology

Important Note: Terms NO LONGER recommended:

• "Near-drowning" - obsolete; replaced by "drowning with survival" or "drowning with morbidity"
• "Dry drowning" - obsolete; historically described laryngospasm without water aspiration (10-15% at autopsy), but likely represents post-mortem water absorption
• "Wet drowning" - obsolete; the distinction is clinically irrelevant as management is identical
• "Secondary drowning" or "delayed drowning"
• media terms with no medical validity; all symptomatic patients should be observed [19]
• "Passive drowning" and "Active drowning"** - behavioural descriptions with no prognostic value

Szpilman Drowning Classification

The Szpilman classification grades drowning severity based on clinical presentation at rescue, providing prognostic information. [13,20]

Clinical utility: Grades 5-6 require ICU admission; Grade 4 requires HDU/ICU; Grades 1-3 can often be managed in ED with observation.

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Epidemiology

Global Burden

Australian Epidemiology

Drowning Locations (Australia)

Indigenous Drowning Disparities

Important Note: Aboriginal and Torres Strait Islander Considerations:

• Drowning rate 2-3x higher compared to non-Indigenous Australians [24,25]
• Children 0-4 years particularly overrepresented (3.5x higher rate)
• Contributing factors:
  • Geographic isolation - proximity to unattended natural water bodies
  • Socioeconomic disadvantage - reduced access to supervised swimming facilities
  • Swimming lessons - lower participation rates
  • Housing - overcrowding, inadequate pool fencing in some communities
  • Cultural water use - fishing, gathering, ceremonial activities
• Remote communities - delayed access to emergency services, RFDS retrieval challenges

Culturally safe practice:

• Involve Aboriginal Health Workers (AHWs) and Aboriginal Liaison Officers (ALOs)
• Respect cultural protocols around death and dying (sorry business)
• Family and community decision-making - involve Elders
• Consider interpreter services - Aboriginal English may differ from Standard Australian English
• Avoid blame - focus on education and support

Mori Health (New Zealand):

• Drowning rate 2-2.5x higher than non-Mori [26]
• Involve whānau in all decision-making
• Engage Mori Health Workers
• Respect tikanga (customs) and manaakitanga (hospitality/care)

Risk Factors for Drowning

Individual factors:

• Age <5 years or >65 years
• Male sex (4:1 ratio)
• Inability to swim / poor swimming skills
• Seizure disorder (15-19x increased risk) [27]
• Cardiac arrhythmias (Long QT syndrome, CPVT)
• Alcohol and drug intoxication (25-50% of adult drownings) [28]
• Developmental delay, autism spectrum disorder

Environmental factors:

• Inadequate supervision (children)
• Absence of pool fencing / non-compliant fencing
• Rip currents (beach drownings)
• Floods, natural disasters
• Boating without life jackets

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Pathophysiology

The Drowning Process

Drowning follows a predictable pathophysiological sequence regardless of water type: [6,9,29]

Submersion/Immersion
        ↓
Initial breath-holding (30-90 seconds in adults)
        ↓
Rising PaCO2 (>50-55 mmHg) triggers involuntary breathing
        ↓
Aspiration of water AND/OR Laryngospasm
        ↓
    ┌───────────┴───────────┐
    ↓                       ↓
Aspiration (85-90%)     Laryngospasm (10-15%)
    ↓                       ↓
Surfactant washout      Hypoxia without aspiration
Alveolar-capillary      ("Dry drowning"
- obsolete term)
membrane injury              ↓
    ↓                   Laryngospasm relaxes
V/Q mismatch            (as hypoxia worsens)
    ↓                       ↓
Intrapulmonary shunt    Aspiration eventually occurs
    ↓                       ↓
REFRACTORY HYPOXAEMIA ←─────┘
        ↓
Myocardial hypoxia → Arrhythmias → Bradycardia → Asystole
        ↓
    CARDIAC ARREST
        ↓
Cerebral hypoxia → Hypoxic-ischaemic brain injury

Hypoxia as Primary Insult

The fundamental pathophysiology of drowning is hypoxaemia leading to multi-organ hypoxic injury. This distinguishes drowning from other causes of cardiac arrest: [4,30]

Clinical implication: Standard ALS algorithms (CAB - Compressions-Airway-Breathing) are modified to ABC for drowning (Airway-Breathing-Compressions). Rescue breathing should begin immediately, even before pulse check. [4,31]

Surfactant Washout and Alveolar Injury

Aspirated water, whether fresh or salt, causes pulmonary injury through: [6,29]

1. Surfactant destruction:

   • Small volumes (1-3 mL/kg) sufficient to cause significant surfactant loss
   • Fresh water: hypotonic → rapid absorption into alveolar epithelium → surfactant dilution and inactivation
   • Salt water: hypertonic → draws fluid into alveoli → surfactant washout
   • Result: increased surface tension → alveolar collapse → atelectasis

2. Alveolar-capillary membrane injury:

   • Direct chemical injury to type I and II pneumocytes
   • Inflammatory cascade activation (neutrophil recruitment, cytokine release)
   • Increased capillary permeability → non-cardiogenic pulmonary oedema
   • Result: ARDS pattern with bilateral infiltrates

3. Ventilation-perfusion mismatch:

   • Collapsed alveoli + oedema-filled alveoli → true shunt
   • Hypoxaemia refractory to supplemental oxygen
   • Requires PEEP to recruit alveoli

Fresh Water vs Salt Water

ARDS Development

Drowning is a recognised direct pulmonary cause of ARDS and fulfils Berlin criteria: [33]

• Timing: Within hours of drowning event (typically <24 hours)
• Chest imaging: Bilateral opacities not explained by effusions/collapse
• Origin of oedema: Not cardiogenic (though myocardial stunning may coexist)
• Oxygenation: P/F ratio categorises severity

Drowning-associated ARDS features:

• Earlier onset than sepsis-associated ARDS (hours vs days)
• Often higher recruitability due to hydrostatic oedema component
• May respond well to PEEP titration
• Surfactant replacement therapy has been used (limited evidence) [34]

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Cold Water Immersion and Hypothermia

Diving Reflex

The diving reflex is a physiological response to cold water facial immersion that may provide neuroprotection: [8,35]

Components:

1. Bradycardia - vagally mediated, reduces myocardial oxygen demand
2. Peripheral vasoconstriction - shunts blood to heart and brain
3. Apnoea - reduces oxygen consumption
4. Splenic contraction - releases red blood cells, increases O2 carrying capacity

Strongest in:

• Infants and young children (more pronounced response)
• Cold water (<15C, especially <10C)
• Face immersion (trigeminal nerve activation)

Clinical significance:

• May explain "miraculous" survivals after prolonged cold water submersion in children
• Reduces cerebral metabolic rate of oxygen (CMRO2) by 5-7% per 1C fall in brain temperature
• Extends the window for hypoxia tolerance

Neuroprotection vs Indicator of Prolonged Submersion

Classification of Hypothermia Severity

"No One is Dead Until They Are Warm and Dead"

This principle applies to hypothermic cardiac arrest: [7,37]

• Death should not be declared until core temperature reaches at least 32-34C
• Resuscitation should continue during rewarming
• Intact neurological survival has been reported after prolonged CPR (hours) with rewarming
• Record-breaking survival: Anna Bgenholm, core temperature 13.7C, 80 minutes submersion, full neurological recovery [38]

Exceptions (consider futility):

• Serum potassium >12 mmol/L (indicates cellular death before cooling) [14]
• Obvious lethal injuries
• Avalanche burial >60 minutes with obstructed airway and asystole
• Warm water submersion with prolonged arrest (>30 minutes) before cooling

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Clinical Presentation

Prehospital and ED Presentation

History (from bystanders, rescue personnel):

Initial clinical assessment:

ICU Admission Criteria

Patients requiring ICU admission after drowning include: [41,42]

• Respiratory failure requiring intubation and mechanical ventilation
• GCS <8 or deteriorating neurological status
• Haemodynamic instability requiring vasopressor support
• Severe hypothermia (<32C) requiring active rewarming
• Post-cardiac arrest (any ROSC achieved)
• ARDS requiring high FiO2 (>0.6) or high PEEP (>10 cmH2O)
• Significant comorbidities (seizure disorder, cardiac disease)

Differential Diagnosis for Drowning Cause

Consider underlying cause of submersion, especially in adults without obvious explanation:

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Resuscitation

Modified BLS/ALS for Drowning

Drowning resuscitation differs from standard cardiac arrest algorithms due to the primacy of hypoxia: [4,31,43]

In-Water Rescue

Safety first:

• Do not enter water unless trained
• Use reaching/throwing assists where possible
• Spinal immobilisation only if high-risk mechanism (diving, trauma) - routine immobilisation NOT recommended [40]

In-water rescue breathing:

• Trained rescuers may provide rescue breaths while in water
• Chest compressions impossible in water - focus on breathing
• Remove from water as quickly as safely possible

On-Land Resuscitation

Drowning BLS sequence (ANZCOR): [43]

1. D - Danger (ensure scene safety)
2. R - Response (tap shoulders, shout)
3. S - Send for help (if alone: 1 minute CPR first, then call)
4. A - Airway (head tilt-chin lift; jaw thrust if trauma suspected)
5. B - Breathing - 5 initial rescue breaths
6. C - Circulation - check pulse for 10 seconds
7. If no pulse: 30 compressions : 2 breaths (15:2 in children)
8. Continue until ROSC, handover to ALS team, or exhaustion

Advanced Life Support

ALS modifications for drowning: [4,31]

Intubation considerations:

• High aspiration risk - RSI preferred
• Gastric distension common (swallowed water) - consider NGT early
• Non-compliant lungs - may need high pressures initially
• Pre-oxygenation may be impossible if already hypoxaemic

Post-ROSC priorities:

• Target SpO2 94-98% (avoid hyperoxia)
• Target PaCO2 35-45 mmHg (avoid hypo/hypercapnia)
• Mean arterial pressure >65 mmHg
• Initiate targeted temperature management (32-36C)
• Transfer to ICU capable of TTM, ARDS management, and ideally ECMO

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Emergency Department Management

Initial Stabilisation

Primary survey (ABCDE):

Core temperature measurement:

• Oesophageal probe (intubated patients) - most accurate
• Rectal probe - acceptable alternative
• Tympanic/axillary - inaccurate in hypothermia, not recommended

Investigations

Immediate (resuscitation bay):

Standard workup:

Advanced investigations (ICU/tertiary):

Chest Radiograph Findings

Typical CXR features in drowning: [44]

DDx on CXR:

• Cardiogenic pulmonary oedema (perihilar "bat-wing", cardiomegaly)
• Aspiration pneumonitis (dependent distribution)
• Bilateral pneumonia

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ICU Management

Respiratory Management

Lung-Protective Ventilation

Drowning-associated ARDS should be managed with standard lung-protective ventilation per ARDSNet protocol: [45,46]

Ideal Body Weight Calculation:

Males:   IBW (kg) = 50 + 2.3 × (height in inches - 60)
Females: IBW (kg) = 45.5 + 2.3 × (height in inches - 60)

Metric: Height (inches) = Height (cm) ÷ 2.54

Example: 170 cm male
Height = 170 ÷ 2.54 = 66.9 inches
IBW = 50 + 2.3 × (66.9 - 60) = 50 + 15.9 = 65.9 kg
Target Vt = 65.9 × 6 = 395 mL

PEEP Strategy

Drowning-associated ARDS often has good recruitability due to the hydrostatic oedema component: [49]

PEEP titration approach:

1. Start with ARDSNet PEEP/FiO2 table
2. Perform recruitment manoeuvre if refractory hypoxaemia
3. Decremental PEEP trial to identify optimal PEEP
4. Target: lowest driving pressure while maintaining oxygenation

Higher PEEP may be beneficial in drowning ARDS:

• Surfactant washout creates recruitable atelectasis
• Alveolar oedema is often recruitable
• Consider PEEP 12-18 cmH2O in severe cases

Prone Positioning

Prone positioning should be considered for severe drowning-associated ARDS: [50]

Indications (per PROSEVA criteria):

• P/F <150 despite FiO2 ≥0.6 and PEEP ≥5 cmH2O
• Optimal sedation and neuromuscular blockade

Protocol:

• Prone for 16-18 hours daily
• Monitor for pressure injuries, facial oedema
• Continue until P/F >150 for 4 consecutive hours supine

ECMO for Refractory Hypoxaemia

VV-ECMO should be considered for drowning-associated ARDS refractory to optimal conventional ventilation: [11,51]

Indications:

• P/F <80 despite optimal ventilation (Vt 6 mL/kg, PEEP optimised, proning)
• Murray Lung Injury Score ≥3.0
• Refractory respiratory acidosis (pH <7.20)
• Consideration of patient age, comorbidities, reversibility

Contact ECMO centre early - within 6-12 hours if trajectory worsening despite optimal management.

Drowning-specific considerations:

• Young patients often good ECMO candidates
• Potentially reversible lung injury (days to weeks)
• May need VA-ECMO if concurrent cardiogenic shock

Cardiovascular Management

Haemodynamic targets:

• MAP ≥65 mmHg (consider higher targets in chronic hypertension)
• Avoid fluid overload - restrictive fluid strategy after initial resuscitation
• Vasopressors if hypotensive despite euvolaemia:
  • Noradrenaline first-line (0.05-0.5 mcg/kg/min)
  • Add vasopressin (0.01-0.04 units/min) if high-dose noradrenaline required

Myocardial dysfunction:

• Hypoxic myocardial injury may cause cardiogenic shock
• Echocardiography to assess LV function
• Inotrope support (dobutamine 2-20 mcg/kg/min) if poor contractility
• Consider VA-ECMO if refractory cardiogenic shock

Neurological Management

Seizure prevention and treatment:

• Subclinical seizures common (20-30%) in comatose drowning survivors [52]
• Continuous EEG monitoring in comatose patients
• Treat clinical seizures with levetiracetam (40-60 mg/kg loading) or phenytoin (20 mg/kg loading)

Sedation:

• Standard ICU sedation (propofol, midazolam, fentanyl)
• Daily sedation holds when stable for neurological assessment
• Avoid long-acting agents if early prognostication required

Cerebral oedema management:

• Elevate head of bed 30 degrees
• Maintain normocapnia (PaCO2 35-45 mmHg)
• Treat fever aggressively (target normothermia 36-37C after TTM)
• Avoid hyperglycaemia (target glucose 6-10 mmol/L)
• Osmotherapy (mannitol, hypertonic saline) if signs of raised ICP

Infection Prevention and Management

Important Note: Antibiotics are NOT Prophylactic in Drowning

Initial lung injury is chemical and mechanical (surfactant washout, hypoxia), not infectious. Prophylactic antibiotics: [10,53]

• Do NOT prevent pneumonia
• Contribute to antibiotic resistance
• Select for resistant organisms

Start antibiotics ONLY if clinical signs of infection develop:

• Fever >38.5C persisting beyond 48-72 hours
• Purulent tracheal secretions
• New/worsening infiltrates on CXR
• Rising inflammatory markers (procalcitonin, WCC)
• Positive cultures

Empiric antibiotic choice (if infection develops):

• Community-acquired aspiration: Amoxicillin-clavulanate OR Ceftriaxone + Metronidazole
• Hospital-acquired (>48h): Piperacillin-tazobactam OR Meropenem (cover Pseudomonas, anaerobes)
• Contaminated water (sewage, stagnant): Broader spectrum, consider Aeromonas, Pseudomonas
• Salt water: Consider Vibrio species (add doxycycline in tropical waters)

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Hypothermia Management

Rewarming Strategies

Rewarming strategy depends on hypothermia severity and haemodynamic stability: [7,54]

Passive External Rewarming

Method:

• Remove wet clothing
• Dry patient thoroughly
• Cover with insulating blankets
• Increase ambient temperature (warm room)

Rate: 0.5-2C per hour Use: Mild hypothermia in stable patients, or as adjunct to active rewarming

Active External Rewarming

Methods:

• Forced-air warming blankets (Bair Hugger) - most effective external method
• Warm blankets
• Radiant heaters
• Warm water immersion (logistically difficult)

Rate: 1-3C per hour Caution: "Afterdrop" phenomenon - core temperature may fall further when periphery rewarmed due to cold blood returning to core. Monitor closely.

Active Internal (Core) Rewarming

Warmed IV fluids:

• Crystalloid warmed to 40-42C
• Administer via pressure bag/rapid infuser
• Rate: 100-200 mL boluses as tolerated
• Limited effectiveness alone (requires large volumes for small temperature gain)

Warmed humidified oxygen/ventilator circuit:

• Heat and moisture exchanger (HME) at 40-42C
• Limited effectiveness alone

Body cavity lavage:

• Peritoneal lavage: Normal saline at 40-42C, 2L boluses via dialysis catheter
• Thoracic lavage: Warmed saline via chest tubes (rarely used)
• Bladder irrigation: Limited surface area, minimally effective

Haemodialysis/CVVH with warmed circuit:

• Can achieve 2-3C per hour
• Useful if ECMO not available
• Provides some circulatory support

Extracorporeal Rewarming (ECMO/CPB)

ECMO is the gold standard for rewarming hypothermic cardiac arrest: [11,55]

Advantages:

• Fastest rewarming (2-4C per hour)
• Provides full circulatory support
• Oxygenates blood (addresses hypoxia)
• Allows chest compressions to cease (reduces CPR-related trauma)

Indications for ECMO in hypothermic drowning:

• Cardiac arrest with core temperature <32C (ideally <28C)
• Serum potassium <12 mmol/L
• No obvious non-survivable injuries
• Witnessed collapse or estimated submersion time compatible with survival

Contraindications/Futility markers:

• Serum K+ >12 mmol/L (indicates cellular death before cooling) [14]
• Obvious lethal injuries
• Known pre-existing terminal illness
• Warm water submersion with prolonged arrest (hypoxic arrest, not cold-protective)

HOPE Score:

• Hypothermia Outcome Prediction after ECLS score
• Predicts survival probability based on: sex, age, mechanism (asphyxia lowers survival), initial K+, core temperature, serum pH, CPR duration [56]

Targeted Temperature Management Post-ROSC

For patients achieving ROSC after drowning cardiac arrest, targeted temperature management (TTM) is indicated: [57,58]

Current recommendations (ILCOR 2021, TTM2 trial):

• Maintain temperature 32-36C for at least 24 hours
• Avoid fever (≥37.7C) for 72 hours after ROSC
• TTM2 trial showed no difference between 33C and 36C [58]
• Avoid hyperthermia - worse neurological outcomes

Practical approach:

• If patient already hypothermic from drowning, rewarm to 32-36C and maintain
• If normothermic after ROSC, cool to 33-36C
• Avoid rebound hyperthermia after TTM

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Neurological Prognostication

Challenges in Drowning Survivors

Neurological prognostication after drowning is challenging and should be approached with caution: [12,59]

Confounders affecting neurological assessment:

• Residual sedation/paralysis
• Metabolic derangement (acidosis, electrolyte abnormalities)
• Hypothermia (may cause fixed pupils, areflexia)
• Seizures (including non-convulsive status)

Standard post-cardiac arrest prognostication guidelines may not apply:

• Most drowning is non-cardiac aetiology
• Hypothermia adds complexity
• Paediatric patients have greater neuroplasticity
• Some patients recover after prolonged coma

Timing of Prognostication

Prognostic Indicators

Clinical examination (≥72h after ROSC, off sedation, normothermic):

Imaging:

Electrophysiology:

Biomarkers

Serum biomarkers have emerging roles in neuroprognostication: [60]

Limitations:

• Haemolysis falsely elevates NSE
• Not validated specifically in drowning
• Use only as part of multimodal assessment

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Prognosis and Outcomes

Survival Predictors

Most important predictor: Submersion duration [5,61]

Other prognostic factors: [62]

Szpilman Classification Outcomes

Long-term Outcomes in Survivors

Neurological outcomes: [63,64]

• 70-80% of hospital survivors have good neurological outcome (CPC 1-2)
• 10-20% have moderate disability (CPC 3)
• 5-10% have severe disability (CPC 4)
• Persistent vegetative state rare with modern prognostication and withdrawal practices

Pulmonary outcomes:

• Most survivors recover normal pulmonary function within 6-12 months
• Some have persistent bronchial hyperreactivity
• Rare long-term fibrosis if severe ARDS

Psychological outcomes:

• PTSD common in survivors (10-30%)
• Anxiety, depression
• Fear of water (aquaphobia)
• Family trauma, survivor guilt

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Prevention

Primary Prevention Strategies

Pool fencing legislation (Australian success story): [65]

• All Australian states/territories mandate pool fencing
• Four-sided isolation fencing (1.2m height, self-closing/latching gate)
• Reduces toddler drowning by 50-70%
• Must be maintained and inspected regularly

Supervision:

• Active supervision (within arm's reach for children <5)
• Designated water watcher (not distracted by phone, alcohol)
• Never leave children unattended near water

Swimming and water safety education:

• Learn-to-swim programs
• Recognise dangerous conditions (rip currents, floods)
• Buddy system

Life jacket use:

• Mandatory for boating activities
• Age and weight-appropriate
• Correctly fitted and fastened

Alcohol and water don't mix:

• 25-50% of adult drownings involve alcohol [28]
• Impairs judgement, balance, swimming ability
• Public education campaigns

Resuscitation Education

Bystander CPR saves lives:

• Early CPR improves survival 2-3 fold [39]
• Emphasise rescue breathing for drowning
• Community CPR training programs
• CPR signage at pools and beaches

Australian/NZ Organisations

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SAQ Practice

SAQ 1: Drowning Resuscitation and ICU Management (15 marks)

Stem: A 3-year-old boy is retrieved from a backyard swimming pool after an estimated 8-minute submersion. Bystander CPR was commenced immediately. On arrival of paramedics, he was in pulseless electrical activity (PEA). ROSC was achieved after 12 minutes of ALS. He is intubated and brought to your tertiary paediatric ICU. On arrival: GCS 3, pupils 4mm bilaterally sluggish, core temperature 34.5C, SpO2 88% on FiO2 1.0, HR 110, BP 65/40 mmHg.

Questions:

(a) Outline your immediate management priorities on ICU admission. (5 marks)

Model Answer:

Airway & Breathing (2 marks):

• Confirm ETT position (ETCO2, CXR)
• Lung-protective ventilation: Vt 6 mL/kg IBW, PEEP 8-12 cmH2O, titrate to SpO2 92-96%
• Target PaCO2 35-45 mmHg (avoid hypo/hypercapnia)
• Consider increasing PEEP if persistent hypoxaemia (surfactant washout, ARDS)

Circulation (1.5 marks):

• IV access confirmation (may need additional access)
• Fluid bolus 10-20 mL/kg if hypovolaemic
• Initiate vasopressor if MAP <50 mmHg (noradrenaline 0.05-0.3 mcg/kg/min)
• Target MAP appropriate for age (>50-55 mmHg)
• 12-lead ECG, arterial line, central venous access

Disability & Temperature (1.5 marks):

• Continue targeted temperature management 32-36C
• Avoid hyperthermia
• Continuous EEG or early EEG to detect subclinical seizures
• Neurological examination: GCS, pupils, brainstem reflexes
• Avoid premature prognostication

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(b) The CXR shows bilateral alveolar infiltrates. ABG on arrival: pH 7.18, PaCO2 48 mmHg, PaO2 55 mmHg, HCO3 17 mmol/L, lactate 6.5 mmol/L, FiO2 1.0. Describe the pathophysiology of lung injury in drowning and outline your ventilatory management. (5 marks)

Model Answer:

Pathophysiology (2.5 marks):

1. Aspiration of water (occurs in 85-90%):

   • Surfactant washout and inactivation (even 1-3 mL/kg sufficient)
   • Increased alveolar surface tension → alveolar collapse (atelectasis)
   • Decreased lung compliance

2. Alveolar-capillary membrane injury:

   • Direct chemical injury to type I and II pneumocytes
   • Inflammatory cascade activation (neutrophil recruitment, cytokines)
   • Increased capillary permeability → non-cardiogenic pulmonary oedema

3. V/Q mismatch and shunt:

   • Collapsed and oedema-filled alveoli → true shunt
   • Results in refractory hypoxaemia
   • Drowning is a recognised cause of ARDS (meets Berlin criteria)

Ventilatory Management (2.5 marks):

• Lung-protective ventilation (ARDSNet protocol):
  • Vt 6 mL/kg ideal body weight
  • Plateau pressure ≤30 cmH2O
  • Driving pressure <15 cmH2O
• PEEP titration:
  • Start 8-10 cmH2O, titrate up if refractory hypoxaemia
  • Higher PEEP often effective (recruitable atelectasis)
• Oxygenation target:
  • SpO2 88-95% (avoid hyperoxia post-arrest)
• Permissive hypercapnia:
  • Accept PaCO2 up to 55-60 mmHg if pH >7.20
• Consider prone positioning:
  • If P/F <150 despite FiO2 ≥0.6 and PEEP ≥10
• ECMO referral:
  • If P/F <80 despite optimal ventilation, contact ECMO centre

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(c) On day 3, the child remains comatose with GCS 4 (E1, V-intubated, M3). How would you approach neurological prognostication, and what factors make prognostication challenging in drowning? (5 marks)

Model Answer:

Approach to Prognostication (3 marks):

1. Timing:

   • Do NOT prognosticate early
   • Wait at least 72 hours after achieving normothermia
   • In children, even longer observation may be warranted

2. Multimodal assessment:

   • Clinical examination (off sedation ≥72h):
     • Pupillary light reflex
     • Corneal reflexes
     • Motor response (best motor response)
   • Neuroimaging:
     • CT brain at 24-48 h: cerebral oedema, loss of grey-white differentiation
     • MRI brain at 3-7 days: DWI changes, extent of injury
   • Electrophysiology:
     • EEG: reactivity, seizure activity, burst suppression
     • Consider SSEP: bilateral absent N20 is poor prognostic sign

3. Poor prognostic indicators (when present in combination):

   • Bilateral absent pupillary and corneal reflexes at ≥72h
   • Motor response M1-2 at ≥72h
   • Unreactive EEG/burst suppression
   • Extensive DWI restriction on MRI
   • Bilateral absent N20 on SSEP

Challenges in Drowning Prognostication (2 marks):

1. Confounding factors:

   • Residual sedation and neuromuscular blockade
   • Metabolic derangement (acidosis, electrolytes)
   • Hypothermia may cause fixed pupils and areflexia
   • Ongoing seizures (including non-convulsive)

2. Paediatric considerations:

   • Greater neuroplasticity - recovery may occur after prolonged coma
   • Standard adult guidelines may not apply
   • Children cool faster (may have had neuroprotection)

3. Aetiology:

   • Drowning is hypoxic-ischaemic, not primary cardiac
   • Different pathophysiology from VF arrest
   • Post-cardiac arrest prognostication studies may not apply

4. Variable cooling:

   • Difficult to know if hypothermia was protective (rapid cooling before arrest) or merely passive (after arrest)
   • Cold water submersion may allow remarkable recoveries

Bottom line: Use multimodal approach, avoid single-test prognostication, involve multidisciplinary team, allow adequate time, and communicate uncertainty to family.

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SAQ 2: Hypothermic Drowning and Rewarming (15 marks)

Stem: A 28-year-old man is brought to ED after being pulled from a frozen lake in Tasmania. Witnesses estimate submersion time of approximately 15 minutes before retrieval by rescue divers. On arrival, he is in cardiac arrest with CPR ongoing. ECG shows fine VF. Core temperature (oesophageal) is 24C. Serum potassium on point-of-care testing is 6.8 mmol/L.

Questions:

(a) Discuss the factors that influence whether hypothermia is neuroprotective or merely an indicator of prolonged submersion. How do these apply to this case? (5 marks)

Model Answer:

Neuroprotective Hypothermia (2 marks):

• Occurs when cooling happens RAPIDLY, BEFORE hypoxic cardiac arrest
• Cold water (<10C) submerges victim, rapid heat loss
• Brain temperature falls before oxygen depletion
• Reduces cerebral metabolic rate of oxygen (CMRO2) by 5-7% per 1C decrease
• Extends hypoxia tolerance from 4-6 minutes to potentially 30-60 minutes
• More common in children (high surface area:mass ratio)
• Associated with "miraculous" survivals

Non-protective Hypothermia (Passive Cooling) (1.5 marks):

• Occurs when cardiac arrest happens BEFORE significant cooling
• Warm water or slow cooling
• Hypoxic arrest at normothermia, then passive cooling of dead/arrested patient
• Hypothermia is merely a marker of prolonged submersion and death
• Associated with poor outcomes

Application to This Case (1.5 marks):

• Favourable factors:

  • Very cold water (frozen lake, likely <5C)
  • Young adult (reasonable cooling potential)
  • Core temp 24C suggests rapid cooling occurred
  • K+ 6.8 mmol/L (below futility threshold of 12)
  • VF rhythm (suggests some cardiac viability)

• Unfavourable factors:

  • 15-minute submersion is prolonged
  • Adult cools slower than child
  • Unknown sequence - did arrest precede cooling?

• Conclusion: Favourable for attempted resuscitation with ECMO rewarming. The low potassium and VF rhythm support ongoing resuscitation.

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(b) Outline your resuscitation strategy for this patient, including modifications for severe hypothermia. (5 marks)

Model Answer:

Continue CPR with modifications (2 marks):

• Continue high-quality chest compressions
• Ventilate with warmed, humidified oxygen
• Establish vascular access (IV or IO)

Defibrillation strategy:

• Attempt defibrillation for VF at 24C
• If VF persists after 1 shock, may withhold further shocks until temp >30C
• Cold myocardium refractory to defibrillation

Medication modifications:

• Adrenaline: withhold or space to every 6-10 minutes if temp <30C
• Slowed drug metabolism, risk of accumulation
• Once temp >30C, resume standard intervals

Rewarming strategy (3 marks):

1. Prevent further heat loss:

   • Remove wet clothing
   • Insulate patient
   • Warm environment

2. Active rewarming:

   • Warmed IV fluids (40-42C)
   • Forced-air warming blankets (limited access during CPR)
   • Warmed ventilator circuit

3. ECMO/Cardiopulmonary bypass:

   • This patient is an ECMO candidate (K+ <12, VF, young, cold water)
   • ECMO provides:
     • Circulatory support (can cease chest compressions)
     • Oxygenation
     • Controlled rewarming (2-4C/hour)
   • Contact ECMO centre immediately for retrieval/transfer
   • Continue CPR during transport if ECMO not immediately available

4. Target core temperature:

   • Rewarm to 32-34C initially
   • Continue resuscitation until this temperature reached
   • "No one is dead until they are warm and dead"

---

(c) The patient achieves ROSC on ECMO. Core temperature reaches 34C. What ICU management and monitoring will you provide over the next 72 hours? (5 marks)

Model Answer:

Temperature Management (1 mark):

• Maintain targeted temperature 32-36C for 24 hours after ROSC
• Avoid rebound hyperthermia (≥37.7C)
• Gradual rewarming if using TTM (0.25-0.5C/hour)

Respiratory Management (1 mark):

• Lung-protective ventilation (anticipate ARDS from aspiration)
• Vt 6 mL/kg IBW, PEEP titration
• Wean ECMO as lung function recovers
• Target SpO2 94-98%, avoid hyperoxia
• Prone positioning if severe ARDS

Cardiovascular Management (1 mark):

• Wean ECMO flow as myocardial function recovers
• Repeat echocardiography to assess LV function
• Vasopressor support for MAP ≥65 mmHg
• Monitor for post-cardiac arrest myocardial dysfunction

Neurological Monitoring (1.5 marks):

• Continuous EEG or daily EEG (detect subclinical seizures)
• Daily neurological examination (off sedation)
• Treat seizures aggressively (levetiracetam, phenytoin)
• CT brain at 24-48h (assess cerebral oedema)
• MRI brain at day 3-7 if comatose (prognostication)
• Delay prognostication until ≥72h post-normothermia

General ICU Care (0.5 marks):

• Glycaemic control (6-10 mmol/L)
• Avoid electrolyte abnormalities
• Stress ulcer prophylaxis
• VTE prophylaxis (after coagulopathy resolved)
• Family communication, psychological support

---

Hot Case Scenarios

Hot Case 1: Day 3 Post-Drowning with ARDS

Setting: Paediatric ICU, 12-bed unit, tertiary children's hospital

Patient: 4-year-old girl, Day 3 post-drowning in backyard pool. Estimated 6-minute submersion. Bystander CPR commenced, ROSC after 8 minutes of ALS. Intubated at scene.

Candidate Instructions: You have 20 minutes to assess this patient and 10 minutes for discussion with examiners. Focus on current status, management, and prognosis.

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Key Findings on Examination:

General:

• Intubated, sedated (midazolam 0.1 mg/kg/hr, fentanyl 1 mcg/kg/hr)
• Core temperature 36.5C
• Nasogastric tube in situ

Monitoring:

• Ventilator: SIMV PC, FiO2 0.6, PEEP 12, PIP 28, Vt 110 mL (6 mL/kg), RR 24
• SpO2 94%, ETCO2 38 mmHg
• Arterial line: BP 85/50 mmHg, MAP 62 mmHg
• CVL: CVP 8 mmHg
• Noradrenaline 0.05 mcg/kg/min

Respiratory:

• Bilateral coarse crackles
• Chest rise symmetrical
• CXR on bedside: bilateral diffuse infiltrates

Cardiovascular:

• HR 110, regular
• Normal heart sounds
• Warm peripheries, CRT 2 seconds

Neurological (during daily sedation hold 2 hours ago):

• GCS 6 (E2, V-intubated, M4)
• Pupils 3mm, reactive bilaterally
• Corneal reflexes present
• Cough on suctioning

Abdomen:

• Soft, non-distended
• NG draining bilious fluid

Investigations:

• ABG: pH 7.32, PaCO2 42, PaO2 72, HCO3 21, lactate 1.8
• P/F ratio: 120
• Na 138, K 4.2, Cr 45, Urea 5.5
• Hb 105, WCC 14, Plt 180
• CRP 85

---

Expected Candidate One-Minute Summary:

"This is a 4-year-old girl, Day 3 following drowning with cardiac arrest. She had a submersion time of approximately 6 minutes and achieved ROSC after 8 minutes of ALS.

Currently, she is ventilated with moderate ARDS - P/F ratio of 120 on FiO2 0.6 and PEEP 12. She is on lung-protective ventilation with appropriate settings. She requires low-dose noradrenaline for haemodynamic support but has good perfusion.

Neurologically, on sedation hold she has GCS 6 with reactive pupils and present brainstem reflexes. This is a cautiously encouraging neurological picture at Day 3.

My immediate priorities are to continue lung-protective ventilation and monitor for ARDS progression, continue cardiovascular support, and prepare for multimodal neuroprognostication if she remains comatose off sedation.

I would also ensure the family has been updated and involve the Indigenous Health Worker if this family is Aboriginal or Torres Strait Islander."

---

Examiner Questions and Model Answers:

Q1: How would you classify the severity of her lung injury and what is the underlying pathophysiology?

A: This is moderate ARDS by Berlin criteria - P/F ratio 120 with bilateral infiltrates and PEEP ≥5. The pathophysiology is aspiration of pool water causing surfactant washout and alveolar-capillary membrane injury. Even small volumes (1-3 mL/kg) destroy surfactant, leading to alveolar collapse, reduced compliance, and V/Q mismatch. This creates refractory hypoxaemia requiring PEEP to recruit collapsed alveoli. The inflammatory cascade also causes increased capillary permeability and pulmonary oedema, contributing to the ARDS picture.

Q2: Her P/F ratio drops to 85 over the next 6 hours despite increasing PEEP to 16. What are your next steps?

A: This is now severe ARDS. My approach would be:

1. Optimise current ventilation - ensure plateau pressure <30, consider recruitment manoeuvre
2. Initiate prone positioning - for 16-18 hours daily (PROSEVA criteria met)
3. Deepen sedation, consider neuromuscular blockade to improve ventilator synchrony
4. Ensure euvolaemia - avoid fluid overload
5. If P/F remains <80 despite proning - contact ECMO centre for retrieval discussion
6. Rule out complications - pneumothorax, consolidation, equipment malfunction

Q3: The family asks about prognosis. How do you approach this conversation?

A: This requires a sensitive, honest conversation acknowledging uncertainty:

1. Context: The 6-minute submersion with bystander CPR and ROSC at 8 minutes are relatively favourable features. Day 3 neurological examination showing reactive pupils and present brainstem reflexes is cautiously encouraging.

2. What we know: The majority of drowning survivors in similar circumstances recover good neurological function. However, we cannot predict individual outcomes with certainty this early.

3. What we don't know yet: We need to see how she progresses off sedation, and may need further testing (EEG, MRI) if she doesn't wake appropriately.

4. Timeline: We will have a better picture over the next few days. I would involve social work and pastoral care, and for Indigenous families, engage the AHW/ALO.

5. Family involvement: What questions do they have? What is their understanding? Are there cultural or spiritual considerations important to them?

Q4: What specific considerations apply if this is an Aboriginal family?

A: Cultural safety is essential:

• Involve Aboriginal Health Worker (AHW) and Aboriginal Liaison Officer (ALO) early
• Ensure culturally appropriate interpreter if needed (Aboriginal English may differ from Standard Australian English)
• Family and extended family decision-making - involve Elders if the family wishes
• Respect cultural protocols - sorry business, family visiting arrangements
• Consider cultural beliefs about illness and healing
• If the child deteriorates, discuss any cultural protocols around death and dying sensitively
• Avoid blame - focus on support and education
• Provide written information in accessible language
• Connect with Aboriginal community support services

---

Hot Case 2: Adult Hypothermic Drowning - Neuroprognostication

Setting: Adult ICU, regional hospital, Day 5 post-drowning

Patient: 35-year-old man, Day 5 following hypothermic drowning in river. Found face-down, estimated submersion 12-15 minutes. Core temperature on retrieval 28C. Cardiac arrest (asystole), CPR 45 minutes including 20 minutes on ECMO during rewarming. ROSC achieved at core temperature 32C.

Candidate Instructions: Assess this patient. The family is asking whether you will withdraw care. Be prepared to discuss neuroprognostication and end-of-life considerations.

---

Key Findings:

General:

• Intubated, minimal sedation (recently weaned off)
• Core temperature 36.8C
• Day 5 post-ROSC

Ventilator:

• SIMV PS, FiO2 0.35, PEEP 8, PS 10
• SpO2 98%, triggering spontaneous breaths
• Lung function recovering

Cardiovascular:

• HR 75, sinus rhythm
• BP 120/70 mmHg, no vasopressors
• Echo Day 2: EF 45% (mildly reduced)

Neurological (off sedation >48 hours):

• GCS 4 (E1, V-intubated, M3)
• Pupils 4mm, bilaterally reactive (sluggish)
• Corneal reflexes: present bilaterally
• Gag: present
• Cough on suctioning: weak
• Motor response: flexor (M3) to painful stimulus, symmetrical
• No spontaneous eye opening
• No response to verbal commands

Investigations:

• CT Brain Day 2: Global cerebral oedema, loss of grey-white differentiation, no herniation
• MRI Brain Day 4: Extensive DWI restriction in bilateral cortex, basal ganglia, and thalami
• EEG Day 4: Low amplitude, unreactive to stimuli, no seizure activity
• Serum NSE Day 3: 68 mcg/L (elevated)

---

Examiner Questions and Model Answers:

Q1: Summarise your assessment of this patient's neurological prognosis.

A: This is a 35-year-old man, Day 5 post-hypothermic drowning cardiac arrest. He had a prolonged submersion (12-15 minutes) with significant CPR duration (45 minutes).

Prognostic indicators are concerning:

• Clinical: GCS 4 off sedation >48 hours, no eye opening, flexor motor response only
• Pupils reactive - this is the only encouraging sign
• CT: Global cerebral oedema with loss of grey-white differentiation
• MRI: Extensive DWI restriction in cortex, basal ganglia, and thalami - this is a very poor prognostic sign
• EEG: Low amplitude, unreactive
• NSE: 68 mcg/L (above 33 mcg/L threshold)

Interpretation: Multiple modalities suggest severe hypoxic-ischaemic brain injury with poor likelihood of meaningful neurological recovery. The extensive DWI changes on MRI are particularly concerning as they indicate widespread irreversible injury.

However, caveats apply:

• He was hypothermic (potential neuroprotection)
• Reactive pupils suggest some brainstem function preserved
• Day 5 is still relatively early for definitive prognostication in hypothermic arrest

Q2: The family asks: "Is he going to wake up?" How do you respond?

A: This requires honesty with compassion:

"I understand this is an incredibly difficult time for your family. Let me explain what we know.

Your husband's brain was without oxygen for a significant period during the drowning. We have been doing tests over the past few days to understand how much injury his brain has suffered.

Unfortunately, the tests show extensive damage to his brain. The MRI scan shows injury to large areas of the brain responsible for consciousness and movement. The electrical activity test shows the brain is not responding normally.

While his heart is beating and his lungs are improving, the injury to his brain appears very severe. Based on what we are seeing, it is very unlikely that he will wake up or be able to interact with you again.

I am so sorry to have to share this news. We want to give you time to process this and discuss with your family. We should also talk about what he would have wanted in this situation, and what the next steps might be."

Q3: The family says they want "everything done" because "he was in cold water and we read about people surviving." How do you address this?

A: I would acknowledge their hope and provide education:

"I completely understand wanting to hold onto hope, and you are right that we have heard of remarkable survivals in cold water drowning. Let me explain how that applies to your husband's situation.

Cold water can protect the brain, but only if the cooling happens very quickly, before the heart stops. In those miracle cases, the person's brain cooled down rapidly before they ran out of oxygen.

In your husband's case, we think the lack of oxygen happened before he cooled down significantly, which is why we are seeing this brain injury despite the cold water.

We have waited 5 days, given him every treatment available, and used multiple tests to assess his brain. All of them point to very severe injury.

I want to be honest with you because I think that is what he would want, and what you deserve. If you would like, we can involve other doctors for a second opinion. We can also give you more time to process this before making any decisions.

What matters most right now is understanding what he would have wanted. Did he ever discuss what he would want if something like this happened?"

Q4: What are the next steps if the family agrees care is futile?

A:

1. Confirm consensus: Involve senior intensivist, treating team, ideally second ICU consultant opinion
2. Family meeting: Formal meeting with all relevant family members, social worker, pastoral care
3. Goals of care: Document decision for comfort care focus
4. Organ donation discussion: This man may be a candidate for DCD; involve DonateLife coordinator
5. Comfort measures:
   • Extubate in controlled setting with family present
   • Symptom management (morphine for dyspnoea, midazolam for distress)
   • Dignified death in appropriate environment
6. Bereavement support: Connect family with bereavement services
7. Documentation: Comprehensive documentation of prognostication process, family meetings, decision-making
8. Coronial considerations: Drowning death may require coronial notification depending on jurisdiction

---

Viva Scenarios

Viva 1: Pathophysiology and Resuscitation

Stem: A 25-year-old woman is pulled from a swimming pool by lifeguards after an apparent seizure in the water. She is unresponsive. Discuss the pathophysiology and resuscitation approach.

---

Examiner: What is the pathophysiology of death in drowning?

Candidate: Drowning causes death primarily through hypoxaemia. The sequence begins with submersion, leading to breath-holding, then involuntary gasping as CO2 rises. This results in either aspiration of water (85-90%) or laryngospasm (10-15%). Both pathways lead to hypoxaemia.

With aspiration, water washes out pulmonary surfactant and damages the alveolar-capillary membrane. This causes alveolar collapse, V/Q mismatch, and intrapulmonary shunting. The result is refractory hypoxaemia that doesn't respond well to oxygen alone - PEEP is required.

The hypoxaemia leads to myocardial hypoxia, bradycardia, arrhythmias, and eventually asystole. This differs from primary cardiac arrest where the initial rhythm is often VF. In drowning, over 95% present in asystole or PEA.

Cerebral hypoxia then causes hypoxic-ischaemic brain injury, which is the major cause of morbidity in survivors.

---

Examiner: How does resuscitation for drowning differ from standard cardiac arrest?

Candidate: The key difference is that drowning is a hypoxic/asphyxial arrest, so ventilation takes priority:

1. ABC not CAB: Start with rescue breaths before compressions. Give 5 initial rescue breaths rather than 2.

2. Ventilation priority: Oxygenation is more important than early compressions because the patient's O2 stores are depleted.

3. Rhythm: >95% are in asystole/PEA, not VF. Defibrillation is rarely indicated initially.

4. If alone: Provide 1 minute of CPR before going for help (vs immediate call in standard BLS).

5. No Heimlich: Abdominal thrusts don't remove water and waste time while increasing aspiration risk.

---

Examiner: This patient has a seizure disorder. What is the significance?

Candidate: People with epilepsy have a 15-19 times increased risk of drowning. The seizure likely occurred while swimming, causing loss of consciousness and submersion. This highlights that:

1. We need to consider seizure as the precipitant of any unexplained drowning, especially in adults
2. Post-ictal state may confound neurological assessment
3. Anti-epileptic drug levels should be checked
4. Brain imaging is important to rule out structural cause for breakthrough seizure
5. Prevention counselling is essential for survivors - swimming only in supervised settings, shower vs bath, etc.

---

Examiner: After ROSC, she has P/F ratio of 95 on FiO2 1.0. What is your ventilation strategy?

Candidate: This is severe ARDS by Berlin criteria. My approach:

Lung-protective ventilation:

• Tidal volume 6 mL/kg ideal body weight
• Plateau pressure ≤30 cmH2O
• Driving pressure <15 cmH2O
• PEEP titration starting at 10-12 cmH2O, increasing as needed

Oxygenation targets:

• SpO2 88-95% (avoid hyperoxia post-cardiac arrest)
• Accept lower targets if achieving them requires dangerous pressures

Rescue therapies if refractory:

• Prone positioning for 16-18 hours (P/F <150)
• Neuromuscular blockade for dyssynchrony
• ECMO referral if P/F <80 despite optimal management

Specific to drowning:

• Surfactant-depleted lungs may be quite recruitable with PEEP
• Expect improvement over days as inflammation resolves
• No prophylactic antibiotics - watch for secondary infection

---

Viva 2: Hypothermia and Ethical Considerations

Stem: A 6-year-old boy falls through ice on a frozen lake. Retrieval takes 30 minutes. He is in cardiac arrest with asystole. Core temperature 22C. Serum potassium 8.5 mmol/L.

---

Examiner: Is this child salvageable? Justify your answer.

Candidate: Yes, this child is potentially salvageable and resuscitation should be attempted. My reasoning:

Favourable factors:

• Very cold water (<4C under ice) - rapid cooling likely occurred BEFORE cardiac arrest, providing neuroprotection
• Child - high surface area:mass ratio means faster cooling
• Core temperature 22C - consistent with rapid cooling
• Serum potassium 8.5 mmol/L - below the 12 mmol/L futility threshold

The potassium is key. Values above 12 mmol/L indicate extensive cell death occurred before cooling, suggesting hypoxic arrest before neuroprotection. At 8.5, while elevated, this could be from acidosis and cold-induced shift rather than cellular death.

Unfavourable factors:

• 30-minute submersion is prolonged
• Asystole rhythm
• Unknown exact sequence of events

My approach: Continue resuscitation with aim for ECMO rewarming. The aphorism "no one is dead until they are warm and dead" applies.

---

Examiner: ECMO is 2 hours away by air retrieval. What do you do?

Candidate: This is challenging. My approach:

1. Continue high-quality CPR:

   • Rotate compressors to maintain quality
   • Mechanical CPR device if available
   • Bag-mask ventilation or intubate with warmed humidified circuit

2. Active rewarming during CPR:

   • Warmed IV fluids 40-42C
   • Forced air warming blankets where accessible
   • Warmed humidified ventilation

3. Defibrillation:

   • Not indicated for asystole
   • If converts to VF, single shock, then withhold until temp >30C

4. Medications:

   • Consider withholding adrenaline or spacing to every 8-10 minutes until temp >30C

5. Retrieval:

   • Activate ECMO retrieval immediately
   • Continue CPR during transport
   • Mechanical CPR devices facilitate transport

6. If ECMO unavailable:

   • Consider cardiopulmonary bypass at cardiac surgical centre
   • Failing that, haemodialysis with warmed circuit provides some rewarming
   • Continue CPR until rewarmed to 32C

---

Examiner: He survives with ROSC on ECMO but is comatose on Day 7. Parents want to continue "as long as it takes." The MRI shows diffuse injury. How do you manage this?

Candidate: This is an ethically challenging situation requiring careful navigation:

First, ensure robust prognostication:

• Confirm MRI findings with neuroradiology
• Obtain EEG and SSEP
• Daily clinical examination off sedation
• Biomarkers (NSE)
• Multidisciplinary team consensus

If multiple modalities confirm poor prognosis:

1. Family meeting:

   • Private, unhurried setting
   • Both parents, extended family if they wish
   • Social work, pastoral care present
   • Explore their understanding
   • Explain findings clearly and compassionately
   • Acknowledge their love and hope

2. Address their hope:

   • Acknowledge that wanting more time is natural
   • Explain that we have waited a week and used every available test
   • Discuss what "survival" would look like (vegetative state, dependent on machines)
   • Ask what their son would want

3. Shared decision-making:

   • We are not asking them to "give up"
   • We are asking what is in the child's best interests
   • If treatment is futile, continuing may constitute harm

4. If disagreement persists:

   • Offer second opinion
   • Involve ethics committee
   • Child protection/guardianship authorities in extremis
   • In Australia, treatment decisions ultimately rest with treating team if consensus cannot be reached, but this is last resort

5. Throughout:

   • Maintain therapeutic relationship
   • Regular updates
   • Demonstrate ongoing care even if outcome predetermined

---

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Basic Cards

Q: What is the Utstein definition of drowning? A: "The process of experiencing respiratory impairment from submersion or immersion in liquid"

• a PROCESS, not an outcome. Outcomes are death, morbidity, or no morbidity.

Q: Why are "near-drowning", "dry drowning", and "wet drowning" obsolete terms? A: Replaced by Utstein 2003 terminology. 85-90% aspirate water, making dry/wet distinction clinically irrelevant. "Near-drowning" replaced by "drowning with survival/morbidity/no morbidity".

Q: What is the primary cause of death in drowning? A: Hypoxaemia. This is why ventilation takes priority over compressions in drowning resuscitation.

Q: How does drowning BLS differ from standard BLS? A: Start with 5 rescue breaths (not 2), ventilation priority (ABC not CAB), 1 minute CPR before calling for help if alone, no Heimlich manoeuvre.

Q: What is the most important prognostic factor in drowning? A: Submersion duration. <5 min = excellent, 5-10 min = moderate, 10-25 min = poor, >25 min = rare survival unless very cold water.

Q: What percentage of drowning victims aspirate water? A: 85-90%. The remaining 10-15% have laryngospasm (historically "dry drowning" but this is obsolete terminology).

Q: How does aspirated water cause lung injury? A: Surfactant washout and inactivation → alveolar collapse → V/Q mismatch. Also causes alveolar-capillary membrane injury → pulmonary oedema → ARDS.

Q: Is there a clinically significant difference between fresh and salt water drowning? A: No. Management is identical. Theoretical electrolyte differences require aspiration of >11 mL/kg, which is rare. Surfactant destruction and hypoxia are the common pathways.

Q: What is the diving reflex and why is it important? A: Bradycardia, peripheral vasoconstriction, apnoea triggered by cold water facial immersion. Shunts blood to heart and brain, reduces CMRO2 by 5-7% per 1C. May explain "miraculous" survivals in cold water, especially in children.

Q: When is hypothermia neuroprotective vs merely a marker of prolonged submersion? A: Neuroprotective if rapid cooling occurs BEFORE hypoxic cardiac arrest (cold water, rapid cooling). Not protective if arrest occurs at normothermia with subsequent passive cooling.

Q: What is the core temperature below which ECMO rewarming should be considered for hypothermic cardiac arrest? A: <32C (ideally <28C) with cardiac arrest.

Q: What serum potassium level indicates futility in hypothermic drowning arrest? A: K+ >12 mmol/L indicates extensive cellular death before cooling occurred.

Q: Should prophylactic antibiotics be given after drowning? A: No. Initial injury is chemical/mechanical, not infectious. Start antibiotics only if clinical signs of infection develop (fever, purulent sputum, worsening infiltrates).

Q: What ventilator settings should be used for drowning-associated ARDS? A: Lung-protective: Vt 6 mL/kg IBW, Pplat ≤30 cmH2O, driving pressure <15 cmH2O, PEEP titrated (often higher needed due to recruitability), SpO2 88-95%.

Q: When should prone positioning be considered in drowning ARDS? A: When P/F <150 despite FiO2 ≥0.6 and PEEP ≥5 cmH2O. Prone for 16-18 hours daily.

Q: What are indications for ECMO in drowning? A: (1) Rewarming for hypothermic cardiac arrest with K+ <12 mmol/L, (2) Refractory hypoxaemia with P/F <80, (3) Refractory cardiogenic shock.

Q: What is the Szpilman Grade 6 mortality? A: 93%. Grade 6 = cardiorespiratory arrest at presentation.

Q: What are the peak age groups for drowning in Australia? A: 0-4 years (pools) and 15-24 years (natural waterways). Also elevated in >65 years.

Q: What is the drowning rate disparity for Indigenous Australians? A: 2-3x higher drowning rates compared to non-Indigenous, particularly in children 0-4 years.

Q: Complete the sentence: "No one is dead until they are..." A: "...warm and dead." Continue resuscitation in hypothermic drowning until core temp reaches 32-34C.

Intermediate Cards

Q: Why does drowning differ from standard cardiac arrest in resuscitation approach? A: Drowning is hypoxic/asphyxial arrest. At time of arrest, arterial oxygen is depleted and CO2/acidosis are severe. Oxygenation is priority. >95% present in asystole/PEA (not VF), so defibrillation rarely indicated initially.

Q: What ABG abnormalities would you expect in a drowning victim on arrival to ED? A: Hypoxaemia (low PaO2), metabolic acidosis (low pH, low HCO3), elevated lactate (tissue hypoperfusion), possible respiratory acidosis (elevated PaCO2) or mixed picture.

Q: What is the P/F ratio threshold for severe ARDS and when should ECMO be considered? A: Severe ARDS: P/F ≤100. Consider ECMO referral when P/F <80 despite optimal ventilation, proning, and neuromuscular blockade.

Q: What clinical examination findings would be concerning for poor neurological prognosis at 72 hours post-drowning? A: Bilaterally absent pupillary reflex, absent corneal reflexes, motor response M1-2 (absent or extensor), myoclonic status epilepticus. But use multimodal assessment - no single test is definitive.

Q: What investigations are part of multimodal neuroprognostication? A: Clinical examination (pupils, corneal, motor response), EEG (reactivity, seizures, burst suppression), SSEP (N20 responses), CT/MRI brain (oedema, DWI restriction), biomarkers (NSE >33 mcg/L).

Q: What is the HOPE score? A: Hypothermia Outcome Prediction after ECLS score. Predicts survival probability in hypothermic cardiac arrest based on: sex, age, mechanism (asphyxia), initial K+, core temp, serum pH, CPR duration.

Q: What CXR findings would you expect in drowning-associated ARDS? A: Bilateral alveolar infiltrates (worse in dependent zones), air bronchograms, may progress to "white-out". No cardiomegaly (distinguishes from cardiogenic pulmonary oedema).

Q: How long should you wait before prognosticating in post-drowning coma? A: At least 72 hours after rewarming to normothermia. In paediatric or hypothermic cases, may need longer. Avoid premature prognostication.

Q: What medications should be modified in hypothermic cardiac arrest? A: Adrenaline: withhold or space to every 6-8 minutes if temp <30C (slowed metabolism, risk of accumulation). Defibrillation: single shock if VF/VT, withhold further until temp >30C.

Q: What are the rewarming strategies for severe hypothermia (<28C) with cardiac arrest? A: ECMO (gold standard) - provides circulation, oxygenation, and controlled rewarming at 2-4C/hour. Alternatives: warmed IV fluids, peritoneal lavage, thoracic lavage, haemodialysis with warmed circuit.

Advanced/Clinical Reasoning Cards

Q: A 4-year-old is pulled from a pool after 7-minute submersion. Core temp 35C. Why is this hypothermia NOT neuroprotective? A: 35C is mild hypothermia that developed slowly AFTER the hypoxic insult. Neuroprotection requires rapid cooling BEFORE oxygen depletion. At 35C, the child was likely normothermic when the hypoxic arrest occurred. Pool water (typically ~25-28C) doesn't cause rapid cooling. Cold water (<10C) is needed for neuroprotective effect.

Q: A drowning survivor is on FiO2 0.8, PEEP 16, but P/F ratio is 75. What are your next steps? A: 1) Optimise current ventilation (ensure Vt 6 mL/kg, Pplat <30), 2) Initiate prone positioning for 16-18h, 3) Deepen sedation, consider NMB for synchrony, 4) Rule out pneumothorax/equipment issues, 5) If still P/F <80 after proning - urgent ECMO referral.

Q: How do you counsel a family who want "everything done" for their hypothermic drowning child with poor prognostic indicators on Day 7? A: Acknowledge their hope and love. Explain that cold water can sometimes be protective, but all our tests show severe injury. Use empathic statements. Explain what "survival" would look like (vegetative state). Ask what their child would want. Offer second opinion. Give time. Maintain therapeutic relationship. Consider ethics committee if impasse.

Q: A patient achieves ROSC after 25-minute CPR for drowning. Core temp was 36C throughout. Would you continue aggressive care? A: This is a warm water drowning with prolonged arrest. Normothermia means no neuroprotection. 25 minutes of CPR is associated with very poor neurological outcome in normothermic drowning. While initial stabilisation is appropriate, prognosis is poor. Multimodal assessment at 72h will likely show severe injury. Early family discussion about expected poor outcome is appropriate while completing prognostication.

Q: Why might a drowning patient's lungs be more "recruitable" than typical ARDS from sepsis? A: Drowning causes ARDS through surfactant washout and hydrostatic oedema (fluid in alveoli) rather than the inflammatory fibroproliferative process of sepsis. The alveoli are collapsed but often structurally intact and can be recruited with PEEP. Sepsis-ARDS has more heterogeneous injury with fibrotic areas that don't recruit. This is why higher PEEP and recruitment manoeuvres may be particularly effective in drowning.

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## Related Topics

- [Acute Respiratory Distress Syndrome (ARDS)](/intensive-care/clinical/respiratory/ards)
- [Mechanical Ventilation Modes](/intensive-care/clinical/respiratory/mechanical-ventilation-modes)
- [Prone Positioning](/intensive-care/clinical/respiratory/prone-positioning)
- [VV-ECMO](/intensive-care/clinical/respiratory/vv-ecmo)
- [Targeted Temperature Management](/intensive-care/clinical/neurology/targeted-temperature-management)
- [Post-Cardiac Arrest Care](/intensive-care/clinical/cardiovascular/post-cardiac-arrest)
- [Accidental Hypothermia](/intensive-care/clinical/environmental/hypothermia)
- [Hypoxic-Ischaemic Encephalopathy](/intensive-care/clinical/neurology/hypoxic-brain-injury)