Adult Pelvic Injury

Question 1

SAM Splint Indications

Answer 1

• Suspected pelvic fracture.
• An awake patient complaining of pain to pelvic area including lower back (sacroiliac joint), groin or hips.
• An unconscious or altered conscious state patient with significant mechanism of injury.
• In the case of traumatic cardiac arrest, a pelvic splint should be applied as a matter of clinical priority if
  mechanism of injury is suggestive of a pelvic fracture.

Question 2

SAM Splint Contraindications

Answer 2

Impaled object preventing application.

Question 3

SAM Splint Precautions

Answer 3

The pelvic splint should be appropriately sized for the patient. Smaller paediatrics may require a
sheet/towel/pillow-case as a pelvic wrap.
* The following sizes should be considered for the SAM splint:
SAM splint size Hip circumference
Large 91 – 152 cm
Small 69 – 112 cm
* A traction splint to limbs should not be applied until after the pelvis has been stabilised.

Question 4

Location for SAM Splint

Answer 4

the greater trochanters

Question 5

Explain why an open book pelvic fracture is potentially life threatening?

Answer 5

Haemorrhage from pelvic fracture is essentially bleeding into a free space
 The pelvis potentially capable of accommodating the patient’s entire blood volume
 This may occur without sufficient pressure-dependent tamponade

Question 6

Why do we administer prophylactic anti-emetics to the spinally immobilised patient?

Answer 6

Spinally immobilised patients are at a greater risk of aspiration if they vomit due to being supine.
 This risk is further heightened with the movement in the back of the ambulance.
 Prophylactic administration of an anti-emetic assists to decrease this risk

Question 7

5 H’t for TBI

Answer 7

Hypovolemia
Hypoxia
Hypokalemia
Hypoglycaemia
Hypothermia

Question 8

Pathophysiology of hypovolaemic shock

Answer 8

□ A continuous process of intravascular blood/fluid loss externally or internally leading to inadequate circulating blood volume causing inadequate tissue and organ perfusion causing profound multi-organ damage and death.

Initial stage
□ Absolute fluid loss – external or internal

Compensated stage
□ Sympathetic nervous system stimulation by catecholamine release
□ Fluid conservation by kidneys by renin-angiotensin-aldosterone system
□ Widespread vasoconstriction leading to increased peripheral vascular resistance
□ Increased ADH leading to fluid retention and decreased GFR

Progressive stage
□ Adrenal gland releases adrenaline
□ Increased HR and myocardial contractility
□ Noradrenaline released leading to innervation of arteriolar and venous smooth muscle contraction = increased PVR

Decompensation stage
□ Decreased CO and VR =decreased BP and MAP
□ Decreased cerebral perfusion = altered conscious state
□ Widespread tissue and organ hypoxia secondary to hypoperfusion
□ Anaerobic glycolysis = metabolic acidosis
□ Cell injury and cell death
□ DIC
□ MODS
□ Death