Severe Head Injury Flashcards
Describe the causes of a severe head injury
-Penetrating injury causing focal damage to one area of the brain
-Blunt force injury causing a depressed skull fracture = focal brain injury
-Rapid acceleration/deceleration injury causing a diffuse brain injury (-Coup injury: head is stopped suddenly, brain continues to moves forwards and hits the anterior wall of skull. -Contrecoup: brain bounces off primary surface and impacts against the opposite side of the skull)
All causes axonal injury - grey matter of brain (outer layer) moves faster than the white matter which causes stretching and tearing of neuronal axons
What are the types of head injuries?
Skull fractures:
-open, closed, base of skull, linear, depressed
Brain bleeds:
-Epidural: arterial bleed often secondary to skull fracture
-Subdural: rupture of bridge veins usually secondary to falls, slow venous bleed with slow onset of symptoms
-Subarachnoid: arterial bleed secondary to trauma or aneurysms, results in bloody CSF and signs of meningeal irritaton
-Intracerebral: bleeding within brain tissue, secondary to penetrating or rapid deceleration often
Diffuse brain injury:
-Mild (concussion), moderate and severe secondary to axonal injury
Explain the difference between primary and secondary injury
- Primary injury is damage to the brain that is caused directly to that area that was impacted
- Secondary injury is the damage to cells that werent initially injured, caused by the ‘after effects’ of the initial damage - eg. increasing ICP, cerebral oedema, hypoxia and ischaemia or infection. Secondary injury can occur up to days after the initial impact.
Explain the pathophysiology of a head injury in relation to the Monroe-Kellie doctorate.
Monroe-Kellie Doctorate:
-Describes the pressure-volume relationship in the closed compartment of the skull
-3 things make up the volume inside the cranium: blood, CSF and tissue. These maintain an equilibrium, so when one increases, the other decreases
Spiral of death:
-Trauma leads to a brain bleed or release of cell contents from axonal tearing and cell rupture leading to cerebral oedema and therefore increasing ICP.
-Increasing contents of the cranium (M-KD) leads to increased ICP and therefore decreased cerebral perfusion pressure and hypoxia of neurons
-Hypoxia leads to anareobic metabolism, failure of Na/K pump, accumulation of Na+ and swelling of cells = further cerebral oedema and increasing ICP = positive feedback cycle
-BBB integrity begins to fail = fluid leak into interstitial space = further swelling
-Ctyotoxic effect of release of cellular contents = fluid drawn into interstitium
-Some ability to compensate by decreased CSF production, increased reabsorption and CSF pushed into spinal cord
Explain CPP = MAP - ICP. What are the normal values and how is this effected in a head injury?
-CPP: pressure of the blood that is perfusing the brain (needs to be sufficient to maintain CBF). Normal is 60-80mmHg
-MAP: average BP (Systolic minus diastolic, divided by 3, plus diastolic). Normal is 70-100mmHg
-ICP: pressure inside of cranium. Normal is 5-10mmHg.
In TBI, ICP increases. In order to maintain adequate CPP, MAP needs to be maintained to overcome ICP.
Explain cerebral autoregulation and how it changes in a severe head injury.
Normally:
-Autoregulation is the intrinsic changing of blood vessel diameter in response to changes in BP to maintain adequate cerebral blood flow
-Autoregulation is effective between a MAP of 50-150mmHg to maintain a constant cerebral blood flow.
-Below MAP 50, blood vessels collapse = ischaemia
-Above MAP 150, there is forced dilation causing increased flow = risk of BBB interruption leading to
oedemia, risk of stroke etc.
-Graph can shift R-wards with chronic HT
TBI:
-Autoregulation may be absent or impaired with a TBI
-This causes a high risk of ischaemia and secondary injury if hypotension occurs
-With autoregulation loss, CBF relies on maintanence of adequate MAP as the graph becomes linear and a small decrease in MAP can cause a large change to CBF.
What are the signs and symptoms of a severe head injury?
- obvious trauma to the head - boggy masses, depressed fractures, obvious deformities
- CSF leak from nose, ears
- Battle’s sign or raccoon eyes
- Pupil abnormalities - unequal or unreactive/sluggish
- seizure activity
- posturing (decorticate, decerebrate)
- GCS - Mild: 15-13, Moderate: 12-9, Severe: 8 or less
- Cushing’s triad: hypertension, bradycardia, irregular/irratic breathing patterns (cheyne stokes)
Treatment priorities?
- Clinical support (ICP, MedSTAR)
- High flow 02 - prevent hypoxia and further secondary injury to brain tissue
- IV Access
- Fluid administration for MAP >90mmhg (consult for paeds)
- Posture with head raised 30 degrees
- Transport ASAP
- Hyperventilation as a last resort with signs of herniation
When is fluid administered in severe head injury and why?
Fluid is given to achieve a MAP of above 90 or systolic above 120.
-Map of 90 prevents blood vessels from collapsing or become over-dilated while also maintaining an adequate CBF (according to the linear graph)
What is the aim of 02 therapy?
02 should be administered as high-flow in order to prevent hypoxia as much as possible.
If patient becomes hypoxic it can cause further secondary injury to the brain tissue - failure of Na/K pump causes build up of Na leading to water retention and neuron swelling = increasing ICP.
Also receiving less blood flow = less 02 delivery.
What is Cushing’s triad and what does it indicate?
Cushing’s triad is a set of clinical signs that indicate increased ICP and imminent coning (herniation of brain out the foramen magnum).
-Stage 1: increased ICP activates SNS = activation of a1 and b1 receptors = increased HR and increased systolic BP - widening pulse pressure
-Stage 2: baroreceptor reflex detects increasing BP and causes bradycardia, also compression of vagal nerve leads to bradycardia.
-Stage 3: brainstem dysfunction from compression leads to irregular respirations, shallow breathing and periods of apnoea.
Indicates the brain beginning to herniate and the patient may die.
When would you hyperventilate a patient and what is the rationale?
- Hyperventilation is a final attempt to prevent the brain from herniating.
- It should only be considered in extreme circumstances where evidence of herniation is present.
- Hypoventilation = increased alveolar ventilation and therefore increased expulsion of C02. This causes hypocapnia which induces vasoconstriction. This in turn reduces cerebral blood flow and is an attempt to then decrease ICP and prevent the brain from herniating.
- Hyperventilation rates should double the patient’s respiratory rate or aim for 24-26 R/min.
- Lots of evidence against it due to hypoxic effects causing a worsening secondary injury to the brain and insufficient evidence to indicate it has better long-term patient outcomes.
