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THORACIC TRAUMA
TRAUMA RESUSCITATION

 

 

Emergency Department Thoracotomy
Resuscitation

What does and does not happen before and during the emergency thoracotomy is as important as the operative procedure itself.

Many patients die because of inappropriate interventions in the prehospital or early in-hospital phase, because of delay in performing thoracotomy and due to poor peri-operative management.

Emergency Thoracotomy

Introduction
Indications
Rationale

Resuscitation
Operative technique
References

ACLS algorithms DO NOT APPLY to traumatic arrest.

The primary causes of traumatic arrest are hypoxia, hypovolaemia due to haemorrhage, tension pneumothorax, and cardiac tamponade. Hypoxic arrests respond rapidly to intubation and ventilation.

Hypovolaemia, tension pneumothorax and cardiac tamponade are all characterised by loss of venous return to the heart. External chest compressions can provide a maximum of 30% of cardiac output in the medical arrest situations and are dependent on venous return to the heart. Chest compressions in the trauma patient are wholly ineffective, may increase cardiac trauma by causing blunt myocardial injury and obstruct access for performing definitive manoeuvers.

The administration of inotropes and vasopressors such as adrenaline to the hypovolaemic patient (who is already maximally vasoconstricted) causes profound myocardial hypoxia and dysfunction.

Management of Traumatic Arrest

Immediate treatment of traumatic arrest is directed at treating the cause of the traumatic arrest.

Hypoxic arrest.

Tracheal intubation is mandatory and should be secured immediately. Ventilation with 100% oxygen should rapidly reverse hypoxic traumatic arrest without the need for further interventions. This is especially true of paediatric head injuries.

Tension pneumothorax.

Relief of tension pneumothorax should be accomplised rapidly either by needle chest decompression or preferably bilateral thoracostomies (as per chest tube insertion). Bilateral tension pneumothoraces may exist and the classic signs of a tension (tracheal deviation, unilateral hyperresonance) may not be present. Tension pneumothoraces should therefore be presumed and bilateral decompression undertaken in all cases of traumatic arrest.

Massive haemorrhage

Performing bilateral thoracostomies has the advantage of identifying major haemorrhage and which side of the chest the major injury is on. This will determine the initial incision for the thoracotomy.

The treatment of massive thoracic haemorrhage is control of haemorrhage, not intravenous fluid therapy. Fluid therapy prior to haemorrhage control worsens outcome in penetrating thoracic trauma (and perhaps all penetrating trauma patients). If there is no response to a small (500ml) fluid challenge, fluid administration should be halted until haemorrhage control is achieved.

Cardiac tamponade

The classic signs of distended neck veins and muffled heart sounds are almost universally absent in traumatic cardiac tamponade. Needle pericardiocentesis may also fail as a diagnostic measure due to blood in the pericardial sac being clotted. FAST ultrasound scan, if available, will indicate the presence of pericaridal fluid. The pericardium may be felt through the left thoracostomy to assess for the presence of tamponade.

Anaesthesia

Patients in traumatic arrest will not require induction of anaesthesia prior to intubation and thoracotomy. Patients who are hypotensive but awake will require a modified rapid sequence intubation. Induction of anaesthesia may lead to a dramatic loss of blood pressure and care should be taken with the choice of induction agent. Ketamine and/or an opiate (such as fentanyl or alfentanil) may be preferable to the standard intravenous induction agents. Even etomidate may cause a large fall in cardiac output in the hypovolaemic patient. Anaesthesia may be maintained with an infusion or bolus doses of intravenous anaesthetic. Muscle relaxation is maintained throughout.

Fluid Therapy

Large-volume fluid therapy should be avoided prior to haemorrhage control. Once haemorrhage is controlled patients will need rapid correction of hypovolaemia to refill the heart and restore perfusion to non-vital organ systems. Patients will be cold and profoundly coagulopathic. Blood and component therapy should be warmed and administered rapidly AFTER haemorrhage is controlled. See 'Transfusion for Massive Blood Loss'. Administration of colloid solutions is not indicated.

Inotropic support

As mentioned above, the use of adrenaline (or other inotropes) is contra-indicated in the presence of hypovolaemia.

Inotropes may be required after control of haemorrhage and cardiac repair. Direct myocardial injury, ischaemic myocardial injury, acute cardiac dilatation, pulmonary hypertension and mediator release due to global tissue ischaemia can all lead to cardiogenic shock which may require inotropic support.

Operative technique
Karim Brohi, trauma.org 6:6, June 2001