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The management of the patient with major trauma requires a multidisciplinary team effort.

Trauma management is based on ATLS protocols.

Rapid primary survey Resuscitation of vital functions Detailed secondary survey Definitive care

Rapid primary survey


Recognition & treatment of any immediately

life-threatening complications (ABCDE)

Resuscitation of vital functions


Haemorrhage control, intravenous access &

volume resuscitation.

Detailed secondary survey


Recognition of potentially life-threatening

injuries

Airway obstruction Breathing difficulty Circulatory status Disability Exposure

The first priority for the anaesthetist when confronted by a unconscious multitrauma victim is to establish patency of the airway whilst assuming immobilisation of the cervical spine ("manual in-line stabilization" or MILS).
Although unstable cervical spine injury are

relatively uncommon, all patients should be assumed to be at risk until proven otherwise.

If upper airway obstruction is present the pharynx is cleared of any debris and the jaw displaced forward (jaw thrust).
Neck tilt & chin lift are avoided as these

manoeuvres could displace an unstable cervical spine.

Unconscious patients with major trauma are always considered to be at increased risk for aspiration, and the airway must be secured as soon as possible with an endotracheal tube or tracheostomy. Neck hyperextension and excessive axial traction must be avoided, and manual immobilization of the head and neck by an assistant should be used to stabilize the cervical spine during laryngoscopy ("manual in-line stabilization" or MILS).

If the patient is apnoeic ventilation by mask is started with 100% O2


Good oxygenation & correction of hypercapnia should be ensured before tracheal intubation is undertaken.

The possibility of cervical spine injury does not contraindicate the orotracheal intubation provided it is performed with care & in-line immobilisation of the cervical spine is maintained throughout the procedure.

If there are clinical signs suggesting a pneumothorax or surgical emphysema and/or flail chest apparent then a chest drain should be inserted simultaneously or before mechanical ventilation is commenced.

Persistence of hypoxemia after institution of mechanical ventilation suggests unrecognised


pneumothorax, haemothorax, pulmonary contusion, or poor cardiac output due to hypovolaemia, tamponade, etc.

When the airway is under control, ventilation deemed adequate and any other external bleeding has been arrested, the next priority is evaluation of the cardiovascular system

Assessment of
Blood volume status Pump function

Patients with major trauma often require urgent restoration of circulating blood volume.
Two large-gauge (14 gauge) IV cannulae

(preferably attached to warming coils)

Isotonic electrolyte solutions are used for resuscitation initially


1-2 L of hartmanns solution is given as

rapidly as possible & patients response assessed.

If this does not significantly improve perfusion or arterial blood pressure and cross-matched blood is not yet available, either plasma or a plasma substitute should be considered. (Hetastarch, Gelatin)
Up to 1500ml may be given initially; in most

circumstances this is adequate to restore circulating blood volume until crossmatched blood is available.

Warm, stored blood is administered subsequently to maintain Urine Output, Arterial Pressure & CVP. As soon as possible a reliable CVP catheter is inserted.

The right internal jugular is the preferred sight. Fluid infused through the peripheral IV

cannulae to produce a CVP of approximately 5-10 mmHg

Whilst whole blood is the ideal fluid for restoration of blood volume in haemorrhagic shock, If the patient is exsanguinating (>40% blood loss), a synthetic colloid should be given immediately while cross-matching is undertaken.
Type specific blood may be given, as the

chance of a reaction is less than 1% in males (over 2% is parous females).

If the breach in the circulation is large then the prime objective of resuscitation is to maintain cerebral and coronary perfusion whilst control of the source of bleeding is accomplished, not to restore a normal blood pressure.

The commonest cause of pump failure in major trauma is the presence of a pneumothorax, but other possibilities include Severe myocardial contusion Traumatic pericardial tamponade Tension pneumothorax causes compression of the mediastinum (heart & great vessels) and presents with extreme respiratory distress, shock, unilateral air entry, a shift in the trachea towards the normal side, & distension of the veins in the neck. The last sign may not be seen in hypovolaemic shock .

It may be relieved immediately by insertion of a 14gauge cannula through the second intercostal space in the midclavicular line.
This should be followed by a standard chest drainage.

If there is any suspicion of tension pneumothorax, IPPV should not be instituted until decompression has been achieved, otherwise mediastinal compression is increased. Patients with blunt chest trauma and fractured ribs may develop a tension pneumothorax rapidly when positive pressure ventilation is commenced.

consideration should be given toward the prophylactic

insertion of chest drains in such patients.

Whenever possible hypovolaemia should be corrected before anaesthesia is induced, but if the rate of haemorrhage is likely to exceed the rate of transfusion & continued transfusion results only in further bleeding, it is necessary to induce anaesthesia in a hypovolaemic patient.

On arrival in the OT, the patient is placed on the operating table which is covered by a warming blanket at 370C. 100% O2 is given. Standard monitoring which is necessary for the management of major trauma patients should be commenced.

In the unconscious patient, the trachea may be intubated after administration of a paralysing dose of succinylcholine. After intubation, the lungs are ventilated at the lowest peak airway pressure consistent with an acceptable tidal volume. Pancuronium or rocuronium is given in small incremental doses of 1 or 5 mg, respectively, to maintain relaxation.

When the haemodynamic situation has stabilised & systolic arterial pressure exceeds 90 mmHg, consideration may be given to deepening the anaesthesia.
This should be undertaken cautiously and, in

principle, agents which are rapidly reversible or rapidly excreted should be used.

In the shock state, there is very rapid uptake of inhalation agents.


As a result of chemoreceptor stimulation, the patient hyperventilates, thus accelerating the rate of increase of alveolar concentration of anaesthetic gas. Similarly, reduced cardiac output & pulmonary blood flow decrease the rate of removal of anaesthetic gas from the alveoli, producing a rapid increase in alveolar concentration.

Thus the MAC value is approached more rapidly than normovolaemic patients.

Monitoring
Blood may be sampled from the arterial line to

monitor changes in the acid-base state, haemoglobin concentration, coagulation, & electrolyte concentrations. Requirement for further colloid replacement may be assessed from CVP measurement and urine output.

When surgical bleeding has been controlled, the patients cardiovascular status should improve, but if hypotension persists despite adequate fluid administration, other causes of haemorrhage should be sought.

It is important that the anaesthetist monitors the patient regularly during prolonged anaesthesia to exclude these latent complications of trauma.

If an amount greater than 50% of the patients blood volume is replaced rapidly, the transfusion is deemed massive. E.g. 5 units of blood in a 70 kg adult. Features of stored blood pH: 6.6 7.2 Serum [K+] : 5-25 mmol/L Temperature: 4 60C. Citrate as anticoagulant > 5 days storage time insignificant amounts of 2,3 DPG. >24 hours storage time no functional platelets, Factors V & VIII 10% of normal & factor IX 20% of normal. Debris; effete cells clumped together with platelets

Citrate is removed by metabolic conversion in the liver forming mostly HCO3Transfused cells act as K+ sink; mopping up excess K+ quickly. The post transfusion alkalosis (resulting from citrate metabolism) may contribute to hypokalaemia in the post transfusion period. If the transfused blood is warmed to body temperature before transfusion & a 20 micron filter used to remove unwanted cellular debris, the commonest problem is acute haemostatic failure.

Transfusion of bank blood in quantities approaching the patients blood volume causes a dilutional thrombocytopenia & some degree of clotting factor deficiency, both of which affect haemostasis adversely. These abnormality may be detected by a platelet count, PT, aPTT, reflecting disorders of extrinsic & intrinsic systems as a result of dilutional loss of factor V & VIII.

Treatment should be directed at correcting the dilutional coagulation change and consists of
Fresh frozen plasma (at least 1 unit for every

4 units of blood) Platelet concentrate for severe thrombocytopenia (Plt count < 30 X 109/L ) or milder in patients with intracranial injury.

Request

of these expensive blood products should be made early as there is often delay in obtaining them & it is better, if possible, to prevent the development of coagulation failure and the resulting bleeding tendency.

Although diffuse pathological bleeding may be secondary to dilutional effects, it is also a manifestation of tissue hypoperfusion due to shock & inadequate or delayed resuscitation.
Clinically, this microvascular bleeding produces oozing from the mucosae, raw surfaces and puncture sites & may increase the extent of soft tissue & pulmonary contusions. It is difficult to treat and this underscores the importance of rapid and adequate resuscitation

The rapid and effective restoration of an adequate circulating blood volume is crucial in the management of major haemorrhage, as mortality increases with increasing duration & severity of shock. Inadequate volume replacement is the most common complication of haemorrhagic shock The importance of prevention of hypothermia during massive transfusion cannot be overstated.

Hypothermia causes
Platelet dysfunction Reduced metabolism of citrate & lactate Increased tendency to cardiac arrhythmias

Which may result in


A bleeding diathesis Hypocalcaemia Metabolic acidaemia Cardiac arrest

Core temperature should be measured continuously during massive transfusion and every effort must be made to prevent heat loss. Thermally insulating plastic drapes can be used to cover the patient, who should be placed on a heated ripple mattress Efficient systems for heating stored blood & allowing rapid infusion should be available
However all fluids should be warmed to body temperature if possible.

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