15y F, near drowning experience 1/7 prior rescued by lifeguards and sent to hospital. No LOC, no interventions given. X-ray at hospital and sent home that afternoon. Pt out with friends and felt SOB with aching in her joints. Mother collected her and bought home. Use of own inhalers with nil effect and persistent cough. Ambulance called.
O/A: GCS 15, HR 160, RR 56, WPB 3, SpO2 86%, T 38.3°C. LUNGS – L) & R) crackles all fields wet, tripod positioning and retractions, mild stridor at front of throat. Peak flow normally 400, today 100.
Rx: Nebulisers – ICP insisted on continuing with nebulisers and treating as asthma.
ED arrival: GCS 15, HR 164, RR 44, WPB 4, SpO2 97%, LUNGS – L) & R) crackles all fields wet, tripod positioning, mild stridor at front of throat. Bp 126/70,
Respiratory impairment from submersion/immersion in a liquid medium.
Submersion – the airway goes below the level of the surface of the liquid
Immersion – a liquid is splashed across the persons face
- Neurological event – epilepsy, stroke
- Cardiac event – MI, HOCM, dysrhythmia, SYNCOPE
- Impaired judgement – alcohol or drug ingestion
- Overdose, suicide
- Diabetes, hypoglycaemia
During the drowning process a spasmodic breath drags water into the mouth and windpipe and then one of 2 things occur. In about 10% of cases water that touches the vocal cords can trigger an immediate contraction in the muscles around the larynx, known as laryngospasm. This is so powerful that it overcomes the breathing reflex and eventually suffocates the person. A person with laryngospasm dies without water in the lungs (this can occur in people who choke on other fluids including drunk or intoxicated people and their vomitus).
In the other 90% of people, water floods the lungs during a breath and ends any warning transfer of O2 to the blood. (This is not passively done and does not occur once the person is dead). Half conscious and enfeebled by O2 depletion, the drowning person is in no condition to fight. After suffering for 2 minutes only the brain is alive, but as electricity activity gets weaker, after 15-20mins it ceases all together.
Fluid in the lungs acts as an irritant
Extrusion of liquid (pulmonary oedema) over hour’s ↓ gas exchange
Can take up to 72hrs after initial event
As little as 1-3ml/kg of fluid can lead to impaired gas exchange. The period of hypoxia/hypoxaemia is limited to the time frame of apnoea or hypopnoea may resolve with adequate initial rescue efforts.
Patients with prolonged hypoxic episodes are prone to alveolar fluid aspiration resulting in vagally mediated pulmonary vasoconstriction, hypertension, and fluid-induced bronchospasm.
Hypoxia serves as the primary insult and, with alveolar aspiration, culminates in surfactant disruption, alveolar collapse and decruitment, intrapulmonary shunting, increased pulmonary vascular resistance, and ventilation-mismatch. These processes result in acute lung injury (ALI) and acute respiratory distress syndrome (ARDS).
Pulmonary hypertension may be exacerbated by inflammatory mediator release. In a minor percentage of patients, aspiration of vomitus, sand, silt, stagnant water, and sewage may result in occlusion of bronchi, bronchospasm, pneumonia, abscess formation, and inflammatory damage to alveolar capillary membranes.
- moves rapidly across the alveolar – capillary membrane into the microcirculation.
- considered hypotonic relative to plasma and cause disruption of surfactant.
- disruption of alveolar surfactant produces instability, atelectasis, and & ↓ compliance, with marked V/Q mismatching.
- as much as 75% of blood may circulate through hypoventilated lungs.
- hyperosmolar, ↑ osmotic gradient, & therefore draws fluid into the alveoli, diluting surfactant (surfactant washout).
- protein-rich fluid then exudates rapidly into the alveoli and pulmonary interstitium.
- compliance is reduced, the alveolar-capillary basement membrane is damaged directly, & shunting occurs.
- this results in rapid induction of serious hypoxia.
Continued aspiration → Hypoxaemia → LOC & Apnoea
Tachycardia → Bradycardia → PEA → Asystole
Prompt correction of hypoxaemia and acidosis as a result of poor lung compliance from pulmonary oedema.
– Provides distending pressure to improve volume of gas at end of exhalation (↑ functional residual capacity.
– Minimises atelectasis or alveolar collapse by maintain pressure above which the lungs collapse (closing pressure).
– ↑ intrathoracic pressure, which transmits the applied PEEP to transmural capillary pressure (results in minimising interstitial lung water).
– ↑ the diameter of both small and large airways to improve distribution of ventilation.
Letitia Friend I BN I RN I BHSc I Paramedic
St John I South Island
M 027 3186280
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