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

avoid hyperventilation, unless specifically indicated for head injury, as this may reduced cardiac output and is associated with increased mortality
likewise avoid excessively high levels of PEEP