• The prompt recognition and management of shock is essential in the management of trauma patients. These patients are often elderly with comorbidities or may be polytraumatised patients.
• Correction of this presurgical condition will ensure that surgical intervention is safe, effective and will reduce morbidity/mortality in these patients.

• Clinical condition resulting from insufficient blood flow to tissues to meet metabolic demands of tissues.
• Cellular dysoxia occurs with rising lactate levels.

• Shock can occur in isolation or as a combination of these four main types:

• Hypovolaemia -
  Decreased venous return secondary to reduced circulating intravascular volume.
  Common causes include: blood loss; third space fluid sequestration; gastrointestinal losses; renal losses.

• Cardiogenic -
  Due to impairment/failure of cardiac pump function.
  Commonest cause is myocardial infarction but others include dysrhythmias, cardiomyopathy, myocarditis, myocardial contusions (trauma).

• Obstructive -
  Characterised by triad of low cardiac output, tachycardia, raised jugular venous pressure (JVP) with peripheral vasoconstriction.
  Causes include cardiac tamponade, tension pneumothorax and pulmonary embolism.

• Distributive -
  Peripheral vasodilatation leads to a fall in peripheral vascular resistance and maldistribution of blood.
  As mean arterial pressure (MAP) = cardiac output (CO) ´systemic vascular resistance (SVR), this leads to a drop in blood pressure.
  Causes include sepsis, anaphylaxis and neurogenic shock.

Table 1. Change in physiology with progressive hypovolaemia

• Clinical

• Peripheral shutdown – cold,* pale, cyanotic, increased capillary refill time (CRT)
• Renal – decreased urine output <0.5 ml/kg/hour
• Mental – disorientation, confusion, obtunded

• Haemodynamic

• Abnormal heart rate**
• Hypotension
• Tachypnoea
• Increased JVP in obstructive shock

• Biochemical

• Increased urea and creatinine
• Decreased haemoglobin (haemorrhagic causes)
• Deranged coagulation factors
• Increased venous lactate levels (>2 mmol/L), metabolic acidosis
• Decreased central venous oxygen saturations

• Identifying the type of shock is essential for underlying treatment. History and clinical examination help to direct towards a diagnosis.
• Monitoring:

• Blood pressure (BP), pulse oximetry, heart rate
• Temp, continuous ECG
• Urinary catheter
• Central line may be inserted for central venous pressure (CVP) measurements

• Fluid challenge with 250 ml of crystalloid. Response based on type of shock but patients categorised:

• Responder
• Transient responder
• Non-responder

• Hypovolaemic – dependent on volume lost but produces a transient increase in BP (CVP), which is only sustained when lost fluid is replaced. Massive haemorrhage is replaced with blood components as per local massive blood loss protocols.
• Cardiogenic – initial BP (CVP) may be normal, low or high. If underlying cause is myocardial infarction, then fluid challenges may lead to decompensation (sustained rise in pressure and pulmonary oedema). Inotropes are needed to assist ventricular contractility to maintain cardiac output.
• Distributive – due to reduced peripheral vascular resistance (PVR) there may not be any response from fluid challenge (transient or non-responder). Vasopressor agents or inotropes are often needed; however, it should be ensured that the patient is adequately filled prior to these adjuncts. Target a MAP of 65 mmHg with noradrenaline and adrenaline adjunct used if required.
• Obstructive – initial BP (CVP) may be high in tamponade or tension pneumothorax and little detectable response to fluid challenge. Underlying cause must be treated first.

• Therapeutic interventions to improve perfusion:

• Haemodynamic stabilisation (with fluid resuscitation and vasopressor treatment if needed) and treatment of the shock aetiology.
• Inotropic agents (e.g. dobutamine) should be added when the altered cardiac function is accompanied by a low or inadequate cardiac output and signs of tissue hypoperfusion persist after preload optimisation.
• Do not to give inotropes for isolated impaired cardiac function.

• Evaluation of response to therapy

• Routine measurement of cardiac output is not recommended for patients with shock responding to the initial therapy.
• Cardiac output and stroke volume measurement for those not responding to initial resuscitation.
• Recommendation for sequential evaluation of haemodynamic status during shock.