90% of the brain metabolism requires blood-borned glucose.
During normal circumstances, the cerebral autoregulation mechanism maintains the cerebral blood flow above 70mmHg, even though the Mean Arterial Pressure (MAP), varies as much as between 50mmHg - 150 mmHg.
*Cerebral perfusion pressure (CPP) = MAP - ICP
However, when there's head injury, this autoregulatory mechanism is disordered. Hence, the CPP fluctuates with MAP, and hence, brain is more vulnerable towards ischaemia.
According to Monro-Kellie's hypothesis, our skull is a rigid structure, and hence will not expand. Intracranial pressure is directly proportionate to the increase in volume of the intracranial structures, including vascular components (blood in vessels), Cerebrospinal fluid (CSF), or the brain tissue itself.
Initially, when there's formation of a space-occupying lesion, the rise in ICP is prevented by transient displacement of venous blood and CSF away from the brain. This decrease in volume compensates for the rise in volume due to formation of space occupying lesion.
But, further rise in the volume of a brain compartment -> even a slightest increase in volume is going to cause a surge in ICP.
Note : ICP can be measured by passing a catheter through the frontal horn of lateral ventricle. In head injuries, ICP is monitored in btw 5-15 mmHg. Bear in mind that normal ICP is <10mmHg
One should never forget that intracranial hypertension is the dreadliest consequence of head injury. The end-stage of raised ICP will be cerebral herniation, which can be :
a) Herniation through the Tentorial hiatus
Tentorial hiatus is an opening at the tentorium cerebelli
As with central herniation, involving the midbrain, features are :
-> Altered consciousness due to midbrain ischaemia
-> Increased muscle tone, and eventually decorticate rigidity
-> Bilateral +ve babinski's sign
-> pupillary constriction, which followed by dilatation, and lastly, becomes static
As for Lateral herniation, involving the temporal lobe (uncus) :
-> Altered consciousness
-> Contralateral hemiparesis, hemiplegia
-> Compression on the 3rd nerve, initially causing ipsilateral pupillary constriction, followed by dilatation, then becomes fixed to light response. Continued rise in ICP results in involvement of the contralateral side of pupil. The sequence of changes in pupillary response is known as Hutchingson's pupil.
-> Others : ptosis, eye deviated inferolaterally
b) Herniation into foramen magnum
If ICP continues to rise, the cerebellar tonsils will herniates into the foramen of magnum, thereby compressing the brainstem and medulla.
This results in Cardiorespiratory collapse, bilateral pinpoint pupil, and flaccid quadriplegia due to lateral corticospinal tract compression.
Note : Signs of Raised intracranial pressure
Papilloedema (swollen optic disc)
Altered level of consciousness
Widened pulse pressure*
Decreased systolic BP*
Abnormal breathing pattern (Cheyne's-Stokes/Hyperventilation)
DO NOT PERFORM LUMBAR PUNCTURE IN A PATIENT WITH RAISED ICP!!
Classification of Head injuries
Classification can be made via :
a) Glasgow Coma scale
Minor head injury = No lost of consciousness and GCS is full 15/15
Mild head injury = GCS 14-15 with lost of consciousness
Moderate head injury = GCS 9-13
Severe head injury = GCS 3-8
b) Mechanism of head injury
i) Blunt trauma
Direct injury (Croup injury)
The brain substance collide against a fixed skull.
Usually caused by sudden deceleration/acceleration forces
Resulting in contusion, laceration and intra-cranial bleeding
Indirect injury (Counter-croup)
Injury to the side opposite to the side of trauma.
Hence, subdural/extradural hematoma may be seen opposite to the side blunt trauma
This occurs in acceleration/deceleration injury.
Such forces creates rotational injury at the junction btw white/grey matter of brain.
ii) Penetrating injury
High velocity - gunshot injuries
Low velocity - stab injuries
In penetrating injury, there's risk of intracranial infection, due to introduction of foreign bodies
i) Scalp injuries
More commonly seen in infants and children.
Due to collection of blood under the periosteum, resulting in formation of a tense swelling, confined to the margins of underlying bones.
It takes weeks to resolve
Blood collection in between aponeurosis and pericranium
Formation of a fluctuant swelling involving the whole scalp
Take weeks to resolve as well
Others : Scalp laceration, Scalding (avulsion)
ii) Skull fractures
It can involve the vault or base, and can be open or closed.
In closed fractures, there's no communication with the exterior, so do not expect a nose, ear bleed or leakage of CSF.
For open vault fractures, expect visible brain substance.
For open base fractures :
If it's an anterior cranial fossa fracture -> Raccoon's Sign (periorbital hematoma) + subconjunctival haemorrhage with no posterior limits + CSF rhinnorhoea and nose bleeding
If it's a middle cranial fossa fracture -> Battle's sign (Bruises seen over mastoid and post-auricular region, which forms within 48 hrs) CSF otorrhoea and ear bleeding
Posterior cranial fossa fracture is not easily identified clinically. Most of the time, when there's occipital bone fracture, there'll be a dural venous sinus tear. Usually, there'll be hypertension, bradycardia, changes in respiration and consciousness.
A closed fracutre can be depressed, communited, or linear.
Primary head injury occurs during time of impact, it's irreversible, and not treatable, and recovery will largely depends on the type and extent of injury. Remember that neurons once damaged, will not regenerate.
Hence, most of the our treatment will be focusing on secondary head injury.
Causes of Secondary head injury :
1) Hypoxia, with PaO2 <8Kpa
2) Hypotension, with SBP <90mmHg
3) Cerebral perfusion pressure <65mmHg
4) Intracranial pressure >20 mmHg
7) Metabolic disturbances
e) Intracranial hematomas
More common in children as their dura strips easily to accomodate blood clot
Here, blood collects between the skull and dura mater
Common at the frontal and temporal region, usually associated with local fractures
Middle meningeal artery or dural venous sinuses are teared
Classical presentation : Lucid interval
Others : Headache, vomiting, lost of consciousness, hemiparesis, seizures, signs of raised ICP
Diagnosis is confirmed by CT brain, which reveals a biconvex, lense-shaped hyperdense hematoma.
If the hematoma is stable, conservative treatment suffice.
However, if there's evidence that it's enlarging, perform blurr hole and craniotomy
More common than extradural hematoma
Here, blood collects between the dura mater and arachnoid mater
Clinical features are similar to extradural hematoma
CT brain reveals a cresent shaped hematoma, which concavity directing towards the brain.
Treatment - same
HISTORY TAKING IN HEAD INJURY
1) How did you injure your head?
Basically, you're asking what's the mechanism of injury.
For dangerous mechanisms, such as falling from a height, or high-speed motor vehicle accident, it may be a multisystem injury, including the spine.
For head injury with lost of consciousness, but without any accidental mechanism, consider hypoglycemia, syncope, aneurysmal subarachnoid haemorrhage
2) Ask about the neurological state of patient during and after injury
Is there lost of consciousness?
Is there seizures?
Is the patient able to respond, move, or talk properly after the injury?
Is there antegrade (can't recall what happened after injury) or retrograde (can't recall what happened before injury) amnesia?
3) Then, What's the GCS of the patient during the scene, prior to intubation, and on arrival in hospital?
4) Is there any evidence suggestive of hypoxia, or any cardiovascular instability?
5) Any co-morbid medical illness?
6) Is the patient taking any drugs? (esp antiplatelets or anticoagulants)
7) Any ilicit drung intake or alcohol consumption
TO BE CONTINUED.....