Head Trauma & Intracranial Events, Raised ICP Flashcards
What is the difference, with regard to injury mechanism, between open and closed head trauma?
Open trauma is penetrating and causes direct injury to brain structures
Closed trauma causes a rise in ICP and shearing of intracranial structures
Define the term “cerebral contusion”
“Bruising” of brain whereby blood mixes with cortical tissue due to micro-haemorrhages and small blood vessel leaks
What are the most common sites of cerebral contusion?
Inferior frontal and anterior temporal
Explain the pathophysiology of cerebral contusions and how they can lead to coma/death.
Trauma – Micro-haemorrhages– Cerebral contusions– Cerebral oedema/ intracerebral bleed– raised ICP – Coma/death
Explain what is meant by the terms “coup” and “counter-coup” relating to cerebral contusion.
Coup- contusion at the site of impact
Counter-coup- at the opposite side to the site of impact
Define “concussion”
Describe its pathophysiology.
Head injury with a temporary loss of brain function.
Trauma–stretching/injury of axons–imparied neurotransmission–loss of ion regulation–reduced cerebral blood flow– temporary brain dysfunction
Describe some of the features of post-concussion syndrome.
What is meant by the term “diffuse axonal injury”
Shearing of the interface between grey and white matter following acceleration/decelaration or rotational injury to the brain.
Leading to damage of the intracerebral neurones and dendritic connections.
Describe the pathophysiology of diffuse axonal injury.
Trauma–shearing of grey and white matter interface–axonal death–cerebral oedema–raise ICP–coma/death
What is a basillar skull fracture?
Explain its pathophysiology.
A bony fracture within the base of the skull
Trauma–skull fractures–tear in meninges–CSF leakage
What are the clinical signs of basillar skull fracture?
How is a basillar skull fracture managed?
Traumatic brain injury management (including ICP control)
Seek and treat complications
Elevation of depressed skull fractures
Persistent CSF leak management - surgery
According to NICE guidance, what are the criteria for urgent CT head?
CGS <13 at any point
GCS <14 >2hours after injury
Focal neurological deficit, seizure, LOC WITH any of the following: age >65, coagulopathy, dangerous mechanism of injury , angigrade amnesia >30 minutes
Open/depressed skull fracture or signs of basal skull fracture
2 + discrete episodes of vomiting
What is an extradural haemorrhage?
What is the most common cause of this type of haemorrhage?
A collection of blood between the INNER SURFACE of skull and PERIOSTEAL DURA MATER
Trauma/skull fracture causing severed MMA
How does a patient typically present when they have suffered an extradural haemorrhage?
- Loss of consciousness
- Transient recovery “lucid interval”
- Rapid decline and loss of consciousness
CN palsies may be found on examination
What are the features of extradural haemorrhage on CT head?
Bleed is confined to the suture lines
Lemon-shaped
Pushes the hemisphere inward- midline shift and compression of the lateral ventricles
What is the prognosis for individuals that suffer extradural haemorrhage (both large and small)?
Small: generally good with early intervention, observation and conservative management, neurological follow-up
Large: referral to neurosurgery for craniotomy and clot evacuation
List some of the complications of extradural haemorrhage.
Permanent brain damage
Coma
Seizure
Weakness
Psuedoaneurysm
Arteriovenus fistula
What is a subdural haemorrhage?
A bleed between the meningeal dura matter and the arachnoid matter
Subdural haemorrhage can be acute, subacute or chronic.
Give the time span of these classifications.
Acute < 3 days
Subacute 3-12 days
Chronic >3 weeks
Subdural haemorrhage is caused by what?
What can increase the risk of such?
Trauma - shearing of briding veins
Can be spontaneous
Cerebral atrophy increases the risk
Acute, subacute and chronic subdural haemorrhage are usually each caused by what?
Acute- trauma
Subacute/Chronic-elderly with vague or absent history of head trauma
How do acute and chronic bleeds differ in their apperance on CT?
Acute- hyperdense (brighter than brain tissue)
Chronic- hypodense (darker than brain tissue)
How does a subdural haemorrhage look on a CT scan?
Banana shaped
Not confined by suture lines but stopped by falx cerebri
Describe the management of acute, chronic and subacute subdural haemorrhage.
How does the prognosis compare with extradural haemorrhage?
Acute- neurosurgical intervention to relieve raised ICP
Subacute/ Chronic- if symptomatic, via 1 or more burr holes
Poor prognosis compared to extradural haemorrhage
What is a subarachnoid haemorrhage?
A collection of blood between arachnoid matter and pia matter
In what age group do subarachnoid haemorrhages usually occur?
What is the usually cause of subarachnoid haemorrhage?
Middle aged (<60 years)
Usually ruptured berry aneurysm, can be trauma
How do patients with subarachnoid haemorrhage usually present?
Sudden onset “thunderclap” headache
Meningism
Nausea and vomitting
Fever
Focal neurological deficits
Loss of consciousness
The vast majority of subarachnoid haemorrhage occurs spontaneously secondary to what?
Berry aneurysm rupture
Give some risk factors for subarachnoid haemorrhage
Hypertension
Family history
Heavy alcohol consumption
Abnormal connective tissue
In what areas of the cerebral circulation do the majority of berry aneurysms occur?
Where, specifically, are thest most likely to occur?
Circle of Willis- particularly where two vessels join
Anterior cerebral artery
What can be clinical investigation can be performed to aid the diagnosis of subarachnoid haemorrhage?
Lumbar puncture - presence of RBCs in CSF?
Need the same number in 3 bottles
12 hours after symptom onset, what is the name given to the yellowish colour of CSF?
Xanthochromia
What is the management of subarachnoid haemorrhage?
Stabilise patient
Prevent bleeding
Treat cerebral vasospasm
Correct hyponatraemia
(Neurosurgical intervention if large)
What is the range of “normal” ICP?
In mmHg and cmH20
5-15mmHg
7-20cmH20
In a healthy individual, how is blood flow to the brain regulated?
Autoregulation:
Vasoconstriction
Vasodilation
Chemoregulation
From which compartments of the intracranial space does fluid drainin order to compensate for an expanding mass in the cranium?
Venous volume
CSF
An uncompensated state of intracrainial pressure for expanding mass leads to what?
Elevated ICP- signs and symptoms
Drained off most of the CSF that we can, and cannot drain anymore
Describe the pathophysiology of brain injury.
Compression by intracranial tumour/bleed
Reduction of blood supply to brain cells
Cytotoxic cellular oedema (no ATP to drive K/Na ATPase–> Na+ levels in cell increase—> fluid enters cells—> cells burst)
Further swelling and compression
List some of the signs and symptoms of raised ICP
Headache (worse in the morning, bending down, coughing
Nausea/ Vomiting
Visual disturbances- diplopia on horizontal gaze, papilloedema
Depressed conscious level
What is the most common false-localising sign of raised ICP?
How does this occur?
CN 6 palsy
Stretching or compression of the nerve along its corse
What is the most common type of cerebral herniation?
What are the symptoms of this type of herniation?
Subfalcine herniation
Headache, contralateral leg weakness(if ACA affected)
As uncal herniation progresses what structure is at risk?
What signs will pressure on this area cause?
The midbrain
Ipsilateral dilated pupil
Contralateral leg weakness
(May be false localising)
What is tonsillar herniation?
What can this cause?
When the cerebellar tonsils herniate through the foramen magnum
Cardiac and respiratory dysfunction
What is cushing’s reflex?
A triad of symptoms associated with raised ICP
They are: bradycardia, hypertension, low respiratory rate
(Opposite signs to sepsis)
Explain what causes the unusual triad of symptoms seen in Cushing’s reflex
Ischemia at medulla–> sympathetic activation–>hypertension + tachycardia
Baroreceptors react–> bradycardia
Ischemia at pons/medulla (respiratory centres)–> low respiratory rate
Group causes of raised ICP into 4 broad categories.
- Increased cerebral blood volume
- Cerebral Oedema
- Increased CSF
- Expanding mass / other SOL
For each of the broad categories of causes of raised ICP, give some management options for them.
Increased cerebral blood volume:
Anticoagulation, tenting of venous sinuses (RARE)
Cerebral oedema:
Treat the cause, mannitol, hypertonic saline
Increased CSF:
Shunts, tumour resection, diuretics whilst waiting for intervention (fruosemide, CA inhibitors)
SOL:
Surgical resection- crainiotomy, steroids
Give two mechanisms of increased cerebral blood volume that may lead to raised ICP.
Venous outflow obstruction
Venous sinus thrombosis
List some causes of cerebral oedema that might lead to raised ICP
Meningitis
Encephalitis
Diffuse head injury
Infarction
List the mechanisms of increased CSF which may lead to increased ICP
List some space occupying lesions that may cause raised ICP
Tumour
Haemorrhage/ haematoma
Abscess
What is the most common cause of raised ICP?
List some of the risk factors for raised ICP
Use of anticoagulants
Severe infection
Immunosuppressed patients
TB infection
CV risks
Cancer
What is the normal apperance & protein, Ig and leukocyte content of CSF?
Clear, colourless
Contains very little protein (15-45mg/dL)
Little Ig
1-5 leukocytes per ml
What is hydrocephalus?
An imbalance between production and absorption of CSF leading to accumulation and enlargement of brain ventricles
How is hyrdocephalus classified?
Non-communicating/ Obstructive- CSF is obstructed within or between the ventricles and the subarachnoid space
Communicating- IS communication between the ventricles and the subarachnoid space
The problem lies within the ventricular system (reduced abdorption/drainage or overproduction of CSF)
Give examples of some causes of non-communicating hydrocephalus
Aqueduct stenosis
Tumour e.g. meningioma
Give some examples of causes of communicating hydrocephalus
Post-meningitis
Subarachnoid haemorrhage
Trauma
Neoplastic infiltration of subarachois space
Choroid plexus papilloma (excess CSF production)
At what ages are there peak incidences of brain tumours?
What kind of tumours are usually seen at these ages?
Children
- Astrocytomas
- Medulloblastomas
Middle-age
- Gliomas
- Meningiomas
(Mets from lung, breast, kidney)
What is idiopathic intracrainial hypertension?
What are the treatment options?
