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Traumatic shock

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Pathophysiology

  • initially predominantly hypovolaemic shock although may be a contribution from:
    • cardiogenic shock due to cardiac contusion or tamponade, valve rupture, coronary damage
    • obstructive shock due to tension pneumothorax
  • subsequently patient may develop distributive shock due to systemic inflammation resulting from tissue trauma and reperfusion injury
  • tissue hypoperfusion occurs as a result of microvascular obstruction and thrombosis
  • circulating humoral factors and metabolic acidosis this may result in impaired cardiac function (late stage).

If resuscitation is inadequate or excessively delayed death occurs, even if it is possible to restore normal blood pressure and intravascular volume, as a result of multiorgan failure (subacute irreversible shock). This is, in part, due to cellular swelling which results in obstruction of capillaries and a failure to restore microvascular blood flow even in the presence of normal macrovascular flow. If the delayed is even longer acute irreversible shock occurs: this is a spiral of on-going haemorrhage, acidosis and coagulopathy.

Assessment

Clinical

  • history
    • volume of overt blood loss
    • injuries
      • unilateral haemothorax ~3L
      • haemoperitoneum causing abdominal distension ~2-5L
      • pelvic fracture ~1.5-2L
      • femur fracture ~0.8-1.2L
      • tibia fracture ~0.5 L
      • full thickness soft tissue defect 5 cm3 ~0.5L
  • physical examination
    • heart rate
    • blood pressure (hypotension is a late sign)
    • tissue perfusion
      • capillary refill
      • end-organ function: mental status, urine output

Investigations

  • Tissue perfusion
    • base deficit
    • lactate
  • FAST (focused abdominal sonography in trauma)
    • to detect free fluid in patients with suspected torso trauma
    • sensitivity 97-100% but specificity only 56-71%
      • positive FAST highly suggestive of intra-abdominal bleeding and patients who cannot be stabilized should undergo early surgery without further abdominal imaging
      • negative FAST does NOT exclude intra-abdominal bleeding
  • CT
    • haemodynamically stable patients with suspected head, chest and/or abdominal bleeding following high-energy injuries
    • if CT is not available in emergency department decision to proceed to CT needs to take into account the risks of transport

Fluid therapy

Targets

  • moderate hypotension may be preferable in patients, who have not suffered significant brain injury, prior to definitive control of haemorrhage
    • aim for systolic pressure 80-100 mmHg
    • resuscitation to higher pressure may disrupt clot and exacerbate both dilutional coagulopathy and hypothermia
    • benefit from this approach not demonstrated in all studies
  • mental status
  • urine output
    • may overestimate adequacy of resuscitation due to a tubular defect
  • base deficit, lactate
    • after initial 12 hours base deficit not an accurate reflection of lactate
  • mixed venous saturation
  • Hb 7-9 g/dl
    • experimental evidence suggests that red cells contribute to platelet function
    • appropriate haemoglobin concentration has never been studied in a RCT

What fluid?

  • no evidence to support any particular type of fluid, except use of albumin (as opposed to crystalloid) is associated with a worse outcome in head injured patients. (Click here to view paper)
  • data from a large randomized controlled trial do not support use of hypertonic saline in head injured patients

Blood products

  • FFP for patients with PT or APTT >1.5 times control
    • initial dose 10-15 ml/kg
  • Platelets to keep platelet count >50 x109/l
  • Fibrinogen concentrate (3-4 g) or cryoprecipitate (15-20 U) for:
    • significant bleeding PLUS
    • plasma fibrinogen <1g/l

Definitive treatment

  • all patients presenting with haemorrhagic shock and an identified source of bleeding should undergo an immediate bleeding control procedure unless initial resuscitation measures are successful

Pelvic ring disruption

  • patients with pelvic ring disruption and haemorrhagic shock should undergo immediate pelvic ring closure and stabilization
  • if haemodynamic instability continues proceed to early angiographic embolization or surgical bleeding control, including packing

Damage control surgery

Click here

Other supportive management

Anti-fibrinolytics

  • consider anti-fibrinolytics in bleeding trauma patient (based on data from elective and cardiac surgery):
    • tranexamic acid 10-15 mg/kg followed by 1-5 mg/kg/h
    • ε-aminocaproic acid 100-150 mg/kg followed by 15 mg/kg/h
    • aprotonin 2 million KIU followed by 0.5 million KIU/h

Activated factor VII

  • Indications unclear
  • Consider giving 200μg/kg followed by 100μg/kg at 1 and 3 hours after initial dose for patients with on-going bleeding (with transfusion >8 units blood) despite:
    • surgical haemostasis
    • transfusion of blood and blood products
      • unclear at what point factor VIIa should be given but the following indicators of adequate transfusion of blood products have been suggested:
        • Platelets >50 x 109/l
        • Fibrinogen >0.5-1 g/l
        • Hct >24%
    • correction of severe acidosis, severe hypothermia and hypocalcaemia such that:
      • pH>7.2
      • core temperature >32ºC
      • ionized calcium >0.8 mmol/l
  • a small randomized controlled trial showed no benefit from factor VIIa in patients with penetrating trauma but a reduction in blood transfusion requirements in patients with blunt trauma who survived >48 h. There was no mortality benefit. (View abstract)

Mechanical ventilation

 

Further reading

Spahn DR et al. Management of bleeding following major trauma: a European guideline. Crit Care, 2007; 11:R17 


©Charles Gomersall, April, 2014 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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