PICU Q+A: airway injuries due to burns

Cite this article as:
Davis, T. PICU Q+A: airway injuries due to burns, Don't Forget the Bubbles, 2013. Available at:
https://dontforgetthebubbles.com/picu-qa-airway-injuries-due-burns/

PICU Q+A: Discuss the mechanism, clinical symptoms and management of upper respiratory tract injuries due to burns.

This is based on teaching from Sydney Children’s Hospital PICU.

Mechanism of injury

Primary/local reaction

—Within moments the capillaries of the injured tissue become leaky.

—Plasma is lost, drawing water with it. This continues for between 3 and 36 hours and results in oedema of the tissues involved.

—Local airway swelling may lead to loss of the airway by both internal and external oedema.

—Chest wall oedema may make ventilation difficult and oedema of the limbs may cause ischaemia leading to limb loss (especially if the burn is circumferential).

Systemic reaction

  • —Damaged tissue will release inflammatory cytokines (leukotrienes, prostaglandins, oxygen free radicals and histamine) into the circulation leading to a systemic increase of capillary permeability & pulmonary oedema/ARDS.
  • —At the peak of oedema formation, essentially all whole blood elements up to the size of RBCs are able to transmigrate through the vessel wall in burned tissue.

Secondary reaction

  • —Reduced mucociliary defence and clearance mechanism.
  • —Surfactant deficiency secondary to insult.
  • —CO – carboxyhaemoglobin levels raised – oxygen-dissociation curve shifts to the left.

Clinical symptoms of airway burns

  • —Facial burns: soot in mouth, nares; carbonaceous sputum; swelling, ulceration of oral mucosa or tongue
  • —Dyspnoea
  • —Hoarseness
  • —Drooling
  • —Stridor, wheeze, crepitations
  • —Increased work of breathing

Management of upper respiratory tract injuries due to burns

—MDT input: anaesthesia, ICU, ENT, allied support.

—Investigations: —lactate, gases, Hb, electrolytes, albumin, CXR.

—Resuscitation: O2 + intubate early + airway personnel support; prevention of further injury; modified Parklands formula + albumin + crossmatch.

—Monitoring: —pCO2, CVP, lactate, urine output (>0.5ml/kg/hr); —ICU setting.

—Ventilation: lung protective strategies – PEEP 10-12, PIP<30. HFOV, NO, higher CO2.

—Bronchial toilet: regular physiotherapy, prone position, nebulised NAC + salbutamol, bronchoscopy + BAL, consider nebulised heparin.

—Other adjunct therapies

—Steroids: No indication for routine use. Limit to bronchospasm, and peri-extubation. Consider use in ARDS.

—Bronchial alveolar lavage with NaHCO3 (3-5 ml) until return solution is clear of soot is practiced in some units. This may also neutralise acid toxins. There is no evidence to support this anecdotal practice.

—Naso-gastric tube and commence feeds at outset to optimise nutrition. If not tolerated, early passage of naso–jejunal tube.

—Consider peritoneal drain if ascites is compromising ventilation

If all else fails – ECMO.

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About Tessa Davis

AvatarTessa Davis is a Consultant in Paediatric Emergency Medicine at the Royal London Hospital and a Senior Lecturer at Queen Mary University of London.

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Author: Tessa Davis Tessa Davis is a Consultant in Paediatric Emergency Medicine at the Royal London Hospital and a Senior Lecturer at Queen Mary University of London.

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