Case 13 Head Injury

Lecture:
o Cellular response to brain injury
o Learning outcomes:
o Describe the arterial blood supply to the brain
o Identify the mechanisms of nerve cell damage and the response to injury
Blood supply to the brain:
Artery in the Circle of Which part of the brain does it supply What happens when
Willis it is blocked?
Anterior cerebral artery Lower limb Contralateral loss of
sensation and motor
control of the lower
limb
Anterior Accounts for 40% of
communicating artery berry aneurysm
Middle cerebral artery Upper limb, face Contralateral loss of
sensation and motor
control of upper limb
and face, Broca’s area
Accounts for 34% of
Barry aneurysm
Internal carotid artery Middle cerebral artery is a straight continuation of the internal
carotid, clots from the carotid are most likely to travel to the
middle cerebral
Posterior cerebral artery Vision Homonymous
hemianopia (loss of
nasal and temporal
visual field)
Basilar artery Locked in syndrome
*Strokes involving the (complete paralysis of
vertebral and basilar the body, except eye
arteries and their movements, can
branches have 85% blink)
mortality rate as the Affect the cortical
brainstem controls spinal tracts
many life support Patient is alert and
functions e.g. breathing, conscious
chewing and
swallowing via the
cranial nerves
Brainstem stroke can
also result in coma due
to the damage to the
Ascending Reticular
Activating System
which sends signals to
the thalamus to cortex
to maintain
consciousness. If this is
damaged, then coma
results
AICA Lateral pontine
syndrome (affect CN7
facial nerve palsy),
can damage the
vestibular nuclei
(vertigo, deafness)
ipsilateral, can
damage the middle
cerebellar peduncles
(poor coordination of
muscle tone and
balance)
IPSILATERAL,
Contralateral loss of
pain and temperature
of the body
Spinal artery Medial medullary
syndrome (affect the
hypoglossal nerve),
Ipsilateral CN XII
palsy (tongue,
swallow movement),
contralateral loss of
pressure, vibration
and proprioception
PICA Lateral Medullary
Syndrome –
Contralateral pain and
temperature on the
body, spinothalamic
tract is damaged

Ipsilateral loss of pain

and temperature on
the face, trigeminal
tract is damaged
Vagus nerve palsy
(dysphagia) trouble in
swallowing, loss of
gag reflex, vulva
deviated, nucleus
ambiguous and CN9
and 10 damaged
Ipsilateral Horner’s

2
 syndrome (ptosis, loss
of sweating, pupil
constricted)
Dizziness, vertigo,
double vision
(diplopia) , due to
damage of the
vestibular nuclei
Tendency to fall to
ipsilateral side
Ipsilateral ataxia –
spinocerebellar tract
affected

Basics:
 Most neuronal cell division stops a few weeks after birth
 Glial cells, however, will still continue to divide throughout life
 This means that when there are brain tumors, they do not contain neuronal tissues,
only glial cells exit (gliomas) or cells of the meningeal coverings of the brain
(meningiomas)
 Oligodendrocytes form the myelin sheath in the CNS, Schwann cells are the one in
PNS
 Astrocytes control the extracellular ion concentration (K+) and remove and
deactivate some neurotransmitters (glutamate)
 Microglia: They are the WBC in the cell, WBC can’t enter due to BBB. They attack
disease organisms and phagocytoses damaged cells

3
Cell death:
 There are 2 types of cell death: Necrosis and Apoptosis
 Necrosis: Cell ruptures and contents of the cell spill out, leading to an inflammatory
reaction in the tissue which can lead to further damage. MESSY DEATH
 Apoptosis: Cell breaks up into membrane mound bodies containing intact
organelles, does not spill contents into tissues. TIDY DEATH. No inflammatory
response
o This occurs due to the loss of trophic factors needed for cell to survive, e.g.
brain derived neurotrophic factor BDNF, nerve growth factor NGF or
triggered by extracellular ligands e.g. tumor necrosis factor TNF
o Break down is mediated by proteolytic enzymes that trigger cell death –
Caspases and DNAses
o Resulting apoptotic bodies are phagocytosed

Axonal regeneration – Peripheral Nervous System

 After peripheral nerve injury, axons readily regenerate. This is different to that in
CNS, because axons do not spontaneously regenerate after injury
 Initially, an axonal injury occurs. The distal portion of the axon, which is
disconnected from the cell body undergoes Wallerian degeneration (in 24 hours)
 The degeneration is triggered by extra and intracellular Ca2+ entering the cytosol
activating calpain which breaks down the cytoskeleton
 Macrophages are recruited to clear the debris (within a week)
 Schwann cells phagocytose the debris but also secrete trophic factors promoting
axonal growth but only for 1-2 months
 Schwann cells differentiate, starts dividing but stay within the basal lamina tube in
the same neuron and axons grow down the tube
 Invading macrophages secrete factors e.g. galectin 1 also promote Schwann cell
migration and axon growth
 Speed of growth 1mm/day

Central Nervous System Response to injury

 Formation of glial scars - involve astrocytes, oligodendrocytes, precursors, microglia,
meningeal and vascular endothelial cells and form over the weeks following injury

4
  Blood borne monocytes and macrophages invade injury site as BBB is breached
 Microglia (WBC in CNS) multiply and activate to remove cellular debris
 From about 24 hours, oligodendrocytes precursors divide and hypertrophy,
astrocytes will carry out the same action but after a further 24 hours
 Astrocytes will then link together and form a barrier surrounding the lesion
 Meningeal cells may invade the lesion cavity forming a plug
 Glial scar formation is controlled by molecules such as cytokines. There are small
proteins involved in cell signalling e.g. IL6

Lack of axonal regeneration in the CNS

 Initial axonal injury, but no macrophage to clear the debris
 Regeneration of the axonal is blocked physically by glial scar formation and
chemically by the release of the inhibitory molecule by glial cells and macrophages
 These inhibitory molecules include NogoA, MAG, Ogmp
 Astrocytes also produce inhibitors of axonal regrowth, e.g. CSPGs (proteoglycans)
 Macrophages also produce toxic molecules to neurons

Diffuse axonal injury

 This is due to impact on the skull, shaking the brain up
 This is very common in racing car injuries
 Axons ae being twisted and ruptured, involve the torsion of the forebrain
 Skull impact – coup and contracoup (coup = blow)
o Head being thrown back (brain moves back within the skull, causing a bruise
to the back of the brain// and then the brain bounces back to the front,
leading to a contusion (bruising) on the opposite side)

Whiplash
coup and

 Rupture of bridging veins between the brain surface and the dural sinuses can lead
to slow subdural hemorrhage as well
 Severer DAI results in immediate unconsciousness
 Patient may either remain in coma or go into PVS
 Cerebral concussion is probably a mild form of DAI with limited pathology
 Unconsciousness in concussion is probably due to a functional disturbance of the
ascending reticular activating system of the brainstem – this region is subjected to
the highest twisting force during sagittal rotation of the hemispheres
 DAI are often associated with petechial hemorrhages (small sources of blood
leakage) at the interface of grey and white matter.

5
\

Excitotoxicity – glutamate recycling

 Glutamate is the main excitatory neurotransmitters in the CNS
 Extracellular concentration is normally 0.6umol/L, it becomes excitotoxicity when it
reaches 2-5 umol/L
 Traumatic brain injuries can raise the level to 10 umol/L if neurones are ruptured
 The main Glutamate receptor is NMDA receptor
 In excitotoxicity:
o There is an abnormally high amount of glutamate in the synapse when it
should be normally removed by pumps
o NMDA receptor is permeable to Na+ and Ca2+ and these ions can flow
through the channels causing depolarization.
o But with very high amount of Ca2+, this can induce mitochondrial ATP
synthesis (less energy for the cells) causing a fall in ionic transmembrane
gradients (less energy for the pump to maintain the gradient) and outward

6
 glutamate leakage due to transporter reversal (cell becomes more
depolarized than it should be)
o High level of Na+ and Ca2+ also cause osmotic swelling and cell rupture

7
Oxidative stress, caused by the imbalance between the generation and detoxification of
reactive oxygen species in cells and tissues .

How to Assess an unconscious patient

 Learning outcomes:
 Describe the physiology of ICP and how this relates to GCS
 Describe how to assess a patient with altered consciousness, including the use of
GCS
GCS – max: 15, min: 3
 Eyes 4
o Open spontaneously 4
o Open to sound/speech 3
o Open to pain 2
o No respond 1
 Voice 5
o Orientated 5
 Patients can tell you the date, time, where they are, their name
o Confused 4
 Wrong date
o Inappropriate words 3
 Complete words but not related to what you ask
o Incomprehensible sounds 2
 Groans, moans…
o No verbal response 1
 Motor 6
o Obeys command 6

8
 o Localized to pain 5
 This means if someone hurts your right arm, your left arm will move
to the right arm to get rid of the pain away from you
o Withdrawal to pain 4
 Move your right arm away from the pain (same arm from the stimuli)
o Abnormal flexion to pain 3 = Decorticate flexion = towards the body
o Abnormal extension to pain 2 = Decerebrate extension = away from body
o No motor response 1
By convention GCS 3-8 coma and requires intubation as airway is not protected, GCS 9-13
Moderate, GCS 14-15 Mild
Examples:

AVPU scale – This scale is used when there is no time for GCS, but rare
A: Patient is awake
V: Patient responds to verbal stimulation
P: Patient responds to painful stimulation
U: Patient is completely unresponsive

Basics:
 Consciousness: State of being alert, aware, orientated and responsive to the
environment
 This is mainly controlled by the reticular activating system
 Unconsciousness: When the ability to maintain an awareness of self and
environment is lost
 Causes of coma:
o Coma without primary neurological cause: drugs, alcohol, hyponatremia,
hypoglycaemia
o Coma with a primary neurological cause (often structural): tumors, infarction,
hemorrhage

9
Brain is about 1.5L, CSF 10%, blood 10%
Monro-Kellie hypothesis:
 Basically, they are saying that the brain is like a fix box, with fixed volume of mass,
CSF and blood
 If either one of them increase e.g., intracranial mass, then the rest must decrease in
order to reach an equilibrium and move into the spinal canal (CSF) and extracranial
vasculature (blood)

10
Buffer originally but beyond the critical point, no longer to push the CSF or blood out, a tiny
increase in volume will cause ICP to rise dramatically
First thing you lose: CSF >venous blood> arterial blood > pushing the brain out
Intracranial hypertension
 Brain herniation is the displacement of part of the brain through an opening into a
region that it does not normally occupy
 The most common: cingulate herniation
 Cerebellar tonsilar herniation > coning, the brain is being pushed down into the
foramen magnum, the herniated tissue blocks the normal flow of CSF

11
  Cushing’s triad: hypertension, bradycardia and irregular respirations – this is a
physiological nervous system response to acute elevations of the ICP
o Cushing’s triad occurs before coning starts to take place
 Other signs: Papillodema (blurring of the optic disc, no clear margin), pupillary
changes (dilation or respond to light), headache
 In children, there are other signs as well: sunset eye sign, increase the size of the
head, cotton spot in papillodema


12
ICP waveform – 3 pulses and each of the pulse gets lower than the previous one normally.
When there is raised ICP, there will be a peak in the middle

13
Management of coma
 ABCDE approach, call for help, investigations

1. Airway
 If the patient is able to talk to you, their airway is protected
 If the patient is snoring, gargling with secretions, then you need to be worried
o To open the airway, you can do a chin lift or a jaw thrust
o Make sure the trachea is straight
o Chin lift when it is not a C-spine injury

14
 o SpO2 should increase if the airway is opened
 Oral pharyngeal airways (Guedel), can be used to open the airway

2. Breathing
 SpO2: above 95%, with COPD: 92%-84%
 RR: 12-20 normal
 Can try to move the patient to lay on their left hand side
 Trachea is central or not ? Pneumothorax can cause deviation of Trachea
 15L oxygen non-rebreather mask

3. Circulation
 Capillary refill (2s or less)
 HR 60-100bpm
 BP
 JVP
 FBC, U&E, glucose

4. Disability assessment – GCS / AVPU

 Pupil fixed and dilated? Shine light should normally constrict
 Blood monitoring

5. Exposure
 Fluid leaking out of ear?

Medical management
 Increased ICP is a medical emergency and should be treated immediately
 Inserting ICP monitor catheter in the patient’s head to measure pressure over time

15
 o NEUROSURGICAL emergencies
o Learning outcomes:
o Identify the basic structures of the cranial cavity and their blood supply
o Outline how the mechanism of neuronal injury relates to its functional consequences
o Relate the main cranial and spinal neurosurgical emergencies, their specific radiology
and management
Basics:
 Neurosurgical emergencies: Either a threat to life or a neurological deficit
 These emergencies can be split into:
o Cranial – Head injuries (extra/subdural hematoma, contusions, depressed
skull fracture), hydrocephalus, infections in the brain (e.g. subdural
empyema, intracerebral abscess). Intercranial hemorrhages (e.g.
subarachnoid, intracerebral, intraventricular)

16
 o Spinal – Cauda equina syndrome, acute spinal cord compression (e.g. bleed,
infection, disc, trauma)
 Pathophysiology of the raised intracranial pressure is based on the Monroe-Kellie
Principle
o Intracranial volume (constant) = volume of the brain + volume of CSF +
volume of blood
o Normally: brain 80%, CSF 10%, Blood 10%
o The brain is a fixed box and if any of the constant increases, there will be a
compensatory mechanism in which the other two will decrease
o However, once we run out of CSF and venous volume (i.e., hit the threshold),
we can no longer compensate and every increase in volume of the brain will
lead to a mass increase in pressure as there is only a fixed volume in our skull
 Symptoms and signs of raised intracranial pressure:
o Headache, nausea, vomiting
o Altered consciousness if untreated
o Cranial nerve palsies: 3rd 6th
o Vital sign changes due to the compression of the brainstem – leading to
Cushing’s response (hypertension, bradycardia, abnormal breathing)
o Papilloedema (more chronic)
 Primary brain injury: This is when the injury occurs to the brain at the time of injury
e.g. you fall off from the motorbike and bang your head (can’t prevent this from
happening)
 Secondary brain injury: This is when a bleed in you skull compress the brain leading
to a loss of function xs

Epidural/Extradural Hemorrhage
 Presentations: Physical trauma (e.g. hit with a
baseball bat), then brief LOC for few seconds then
woke up and was alert (lucid interval); 2 hours
later, felt horrible and had a headache, vomiting
and with fluctuating level of consciousness
 Fixed dilated pupil when it is sluggish reaction to
light (normally it should constrict when shine with
light), most likely on the RHS (bad bad sign of ICP
and compression of the 3rd nerve)
 CT scan: Lemon shaped / biconvex / lentiform
 Usually related to the fracture of temporal
squamous bone and leading to the rupture of the
middle meningeal artery, resulting in rapidly expanding acute hematoma
 Brain in this case is intact, so we should prevent secondary brain injury by taking
patient to surgery immediately

Initial management:
 Use the ABCDE guidelines (airway, breathing, circulation, disability, exposure)

17
  Admit the patient and send off bloods
 Prescribe mannitol (osmotic diuretic, reduce swelling from the brain to reduce ICP)
 If the GCS is below 8/15, call the anaesthetist and intubate (as patient is unconscious
so airway can collapse)
 Prevent hypotension/hypoxia as they have been shown to worsen prognosis by
causing ischaemic stroke
 Contact neurosurgeon – for urgent craniotomy for evacuation of hematoma

Subdural hematoma
 On a CT scan: Banana shaped/ concave collection on the surface of the brain
 Usually caused by ruptured bridging veins due to high
impact mechanisms (crashing cars, falling off ladders)
 Primary brain injury
 Tears on the brain, acute clot, swelling of the
hemispheres, midline shift
 Worse outcome

Contusion
 Bruise
 Managed conservatively initially
 Observe for signs of raised ICP
 Surgery for persistent raised ICP
o Craniotomy (temporary removal of bone and which the bone is replaced
before the surgery is complete with screws)
o Craniectomy (removal of bone, and the bone is not immediately replaced, if
patient has a diffuse axonal injury (this is when there is multiple scattered
lesions over a widespread area)
 For example, this can occur when someone collapses and falls backwards, they
would get an occipital fracture and the brain will smash forward in the skull, hitting
the frontal lobes against the frontal bones (coup and contrecoup injury)
 Contusions tend to swell and mature over 72 hours, so someone can develop a lower
GCS score due to swelling in the brain

18
Depressed skull fracture
 Majority managed conservatively
 Clean and suture overlying lacerations
 +/- antibiotics esp with leaking of CSF for a week
 Increase risk of epilepsy
 Hit by a hammer – clean wound // hit by a brick –
messy can contaminate the wound
 Scalp is highly vascularized as we should
immediately clean and suture any underlying
lacerations to prevent bleed to dead

Spontaneous intracranial hemorrhages

 e.g. Subarachnoid, Intracerebral, Intraventricular hemorrhages
 Causes: Cerebral aneurysms, arteriovenous malformation, hypertension,
anticoagulants, drug abuse

Subarachnoid hemorrhage
 Presentations: Sudden onset occipital headache (worse
headache of my life), nausea and vomiting,
photophobia (eyes are very sensitive to light)
 On examination: patient is conscious and has neck
stiffness
 The arrow shows the subarachnoid space is full of blood
 Causes: Barry aneurysm (surgical clipping and coiling)
Management
 Keep the patient flat in bed (bed rest)
 Give them IV fluids
 Analgesics for the pain
 Give patient nimodipine (Ca2+ channel blocker, protects
the cells from becoming ischaemic from toxicity due to
vasospasm)
 Refer to neurosurgeon

Intracerebral hemorrhage
 Often in elderly with untreated and undiagnosed hypertension and diabetes
 Management: stop aspirin/ warfarin, control hypertension, surgery for large
superficial hematoma causing mass effect
Intraventricular hemorrhage
 Often in elderly with untreated and undiagnosed hypertension
 Blood normally collects in the ventricles, for this reason, the patient is normally
intact mentally as the hemorrhage hasn’t damaged the brain

19
  We put an extraventricular drain in the brain to drain out any blood and treat any
hydrocephalus (CSF not flowing out)

Hydrocephalus
 Quick recap of CSF: Ependymal cells in the choroid plexus in the lateral ventricles >
Third ventricle via the intraventricular foramen/ foramen of Monroe then to the
fourth ventricle via the cerebral aqueduct. Then leaves laterally via the foramen of
Luschka into the subarachnoid space. Round the surface and then reabsorbed into
the intravenous sinuses
 This is a buildup of water pressure in the brain due to increase in CSF in ventricles
and this can be obstructive or non-obstructive (leading to enlarged ventricles)
 Obstructive: Mechanical obstruction to the flow of CSF, e.g. tumors, abscess, cysts,
congenital aqueduct stenosis, Chiari malformations ( this is when the tonsils of the
cerebellum hang down from the foramen magnum and cause an out-flowing
problem)
 Non-obstructive/ communicating: Post-hemorrhage, post infective (meningitis), post
traumatic

Left: normal ventricles

Right: Enlarged ventricles and CSF
is being pushed out into the brain

 Management:
 Insertion of ventriculo-peritoneal shunt, this shunt works by taking the fluid out of
your brain and moving it into your abdomen where it is absorbed by your body, this
helps to lower the pressure and swelling in your brain
 The amount of fluid to be drained by VP shunt depends on the settings of the shunt/
valves. The valves can be with fixed pressure, only opens when the CSF hits the
threshold or variable valves where Dr. can change the pressure
 Endoscopic third ventriculostomy – this is for non-obstructive hydrocephalus. A
small hole is made in the skull and the brain and uses an endoscope to look inside
the ventricles of the brain and drain the fluid. After the procedure, the camera is
removed and the wound is closed using stitches
 There is less risk of infection after ETV than shunt surgery

Intracranial infections
 Intracerebral
 Subdural/extradural empyema – collection of pus in the subdural or extradural space
 More common in young children or young adults

20
  Causes: direct spread from the paranasal sinus infections, dental abscess, middle ear
and mastoid infections, hematogenous spread, penetrating head trauma, post-op
 Common organisms: Aerobic/ anaerobic streptococci (around sinuses) and staph.
Aureus (around your skin, penetrating skin, post-op and trauma)
 Inflammatory markers (WCC<, CRP), blood cultures
 Fever and headache past few days
 Acute presentation following seizure with weakness (when seizure and headache
think intracranial infections)
 Was treated for middle ear infection for last 4 weeks

Surgical emergency and evacuation

Long term antibiotics 6-12 weeks
Treat primary source of infection

Cerebral abscess
 Often presents with seizure or vocal deficit

Spinal emergencies
Cauda Equina Syndrome

21
  Acute loss of neurological function of the nerve roots below the conus medullaris
(L1/L2)
 Mainly affecting the lower limbs, bowel and bladder
 Cause: Acute disc prolapse/ herniated disc usually L4/L5, L5/S1
 Big central prolapse, can lead to bilateral sciatica
 Surgical emergency
 S2 S3 S4 sacral nerve
 Presentations: Sudden onset back pain with bilateral leg pain, numbness in perianal
region, episodes of urinary incontinence and difficulty passing urine
 On exam: loss of anal tone and reduced perianal sensation, absent tendon reflexes
 Urgent MRI scan / urgent referral to neurosurgeon or orthopaedic spinal surgeon

Acute spinal cord compression

 Causes: disc herniation/ spondylosis, subdural/extradural haematoma, subdural/
extradural empyema, tumor, vertebral body fractures
 Disease of the spinal cord – myelopathy
 Disease of the spinal nerve root – radiculopathy
 Disease of the peripheral nerve – neuropathy

 Most common is cord compression in the neck

22
 

 Management:
o Urgent decompression
o Stabilize the spine
o Steroids- good for metastases, tumors NOT trauma

o Introduction to Stroke
o Stroke and TIA are focal neurological deficits
o Stroke: With CT changes due to blockage of blood supply or bleed within the
brain
o TIA: This is when there is a sudden onset of focal neurological deficit
attributed to a vascular cause but there is no infarction of brain tissues. There
is only a temporary blockage of blood vessels, normally resolves in 24 hours
o Most strokes occur as a complication of cardiac and other vascular disease, e.g. AF
causing stroke as the clot breaks off and enters the anterior cerebra artery causing
ischaemic stroke
o There are 2 type of strokes: Ischaemic and Haemorrhagic
o Ischaemic: Embolus/ thrombus prevents blood getting into the brain tissue,
leading to cell death and tissue infarction

23
 o Hemorrhagic: Bleed within the brain resulting in a reduced blood supply to
the brain tissues, compression of the structure within the brain

24
  Large artery occlusions
Clot to MCA reduced cortex function
 Lacunes
Clot to small arteries supplying the internal capsule, but the cortex is spared
 Leukokraurosis
Clot to arteries supplying white matter connections, resulting in loss of function as we loose
the connections between cortices

o Infections of the CNS

o Learning outcomes:

25
  Describe the different kinds of CNS infections, including post-surgical
 Describe the initial diagnosis and treatments of CNS infections

Basics:
 Meningitis, encephalitis and brain abscesses are medical emergencies which require
rapid diagnosis and management
 Blood vessels and nerves that surround the skull and vertebral column are the main
routes of invasion for infectious agents (direct trauma, breakage of the skull)
 Meninges: They are the 3 layers coverings of the brain and the spinal cord (PAD)
o From inside to outside:
o Pia meter: Innermost layer, lines every sulci and gyri of the hemispheres and
all the fold of the cerebellum
o Subarachnoid space: Contains CSF
o Arachnoid mater: Filled with collagen
o Subdural space
o Dura mater: Toughest and outermost layer, meningeal layer (only present in
the vertebral column) and periosteal layer (lines the inner surface of the
bones of the cranium)
 Function of meninges: Protect brain and spinal cord from mechanical injury, provide
blood supply to the skull and hemispheres, provide space for the flow of CSF

Routes of infection
 Blood borne invasion – takes place across the blood brain barrier to cause
encephalitis or blood CSF barrier to cause meningitis
 Invasion via peripheral nerves – This is a feature of herpes simplex, varicella-zoster
and rabies virus infections. HSV and VZV travel from mucosal and skin lesions up
axons at a rate of 200mm/day to reach dorsal root ganglion. Rabies virus introduced
into muscle via bite from infected animal, then enter peripheral nerves and travel to
CNS to reach glial cells and neurons, where virus multiplies (8cm/ day)
 Local invasion from ears, sinus
 Local injury from face, skull, face
 Congenital defects
Microbes can grow and multiply, then infect the cells and infect from cell to cell ///
transported across in intracellular vacuoles/// being carried by infected WBC

Meningitis
 Inflammation and infection of the meninges
 Aetiology:
o Bacterial (most serious because often associated with sepsis)
 Streptococcus pneumonia (gram +ve)
 Neisseria Meningitidis (gram -ve)

26
  Listeria monocytogenes (gram +ve)
o Viral (more common but less severe)
 Enterovirus
 HSV
 CMV
 EBV
o Fungal
 Cryptococcus neoformans
o Septic
 Drug reactions

 Babies are at an increased risk compared to other age groups, but people of any age
can develop bacterial meningitis
 Infectious diseases tend to spread where large group of people gather together, like
uni halls, army barracks have reported outbreaks of meningococcal disease, caused
by N. Meningitidis
 Working with meningitis-causing pathogens
 Travelers may be at an increased risk for meningococcal disease if they travel to
certain places such as sub-Saharan Africa, particularly during the dry season
How is infection spread from one person to another?
 Mothers can pass group B streptococcus and E. Coli to their babies during labor and
birth
 Streptococcus pneumoniae and Hib can be spread by coughing or sneezing

27
  Neisseria meningitidis can be spread by respiratory or throat secretions (saliva or
spit). This typically occurs during close contact (coughing or kissing) or live in the
same household contact
 E. Coli and Listeria monocytogenes, people usually get sick from food poisoning from
eating contaminated food

Symptoms and Signs in young children

Symptoms and signs in adults

28
General management – ABCDE approach
Airway – may be compromised if reduced consciousness
Breathing
Circulation – may be in septic shock
Disability – consciousness, neurological deficit
Exposure – rash present and other infection site
 Do a CT head scan if there is a reduced GCS score, new focal neurology, other signs
of raised ICP (e.g. papillodema), immunocompromised
 Perform lumbar puncture ASAP if no contraindication
Lumbar puncture contraindications
 Signs suggesting a raised ICP / reduced GCS
 Shock
 Extensive purpura (rash)
 Convulsions – experience rigidity and uncontrolled muscle spasms (jerky motions
that generally last a minute or two) along with altered consciousness
 Coagulation abnormalities
 Superficial infection at the lumbar puncture site
 Respiratory insufficiency

29
CSF findings in Meningitis

Explain:
 Bacteria: increased in neutrophils (polymorphs)!
 Virus: increased in lymphocytes
 TB: increased in lymphocytes
 Fungal: increased in lymphocytes

Treatment
 Meningitis is a notifiable disease and cases must be reported to the consultant in the
communicable disease control. Close contacts will need to be traced and started on
chemoprophylaxis such as rifampicin or ciprofloxacin
 For bacterial:
o Antibiotics and steroids – Cefotaxime/ Ceftriaxone (do not use with calcium
containing infusions), (+/- Vancomycin if there is any drug resistance),
newborn and elderly may require Ampicillin/ Amoxicillin ( to cover listeria
monocytogenes)

Prevention
 Vaccinations against S. Pneumoniae, N. Meningitidis, H. influenza

Viral Meningitis
 Most common form of meningitis
 Milder disease characterized by headache, fever, photophobia and less neck stiffness
 Usually benign course and complete recovery expected
 Causative agents:

30
 o HSV, Mumps (paramyxovirus), Enteroviruses (coxsackievirus, echovirus and
poliovirus), HIV

Encephalitis
 Acute inflammation and swelling of the brain
 Caused by infection or immune response (can be post infection/ vaccination RARE)
 Most common viral aetiology in UK – HSV1
 Presentations: Headache, fever, change in cognitive state (e.g. confusion, personality
change), reduced GCS, seizures…
 Causative agents: HSV, VZV, CMV, Mumps, Poliovirus, Rabies, HIV
 Diagnosis:
o CSF for viral PCR and microscopy, culture and sensitivities, blood culture
o CT head, MRI brain or EEG to confirm
 Treatment:
o Anti-viral – Acyclovir
o The earlier you treat, the better because this can reduce the development of
haemorrhagic necrosis
 Mortality: HSV encephalitis has a high mortality rate up to 30% in treated individuals
and up to 80% if left untreated
 Long- term effects bc of the damage to the brain include:
o Memory problems, personality and behavioral changes, speech and language
problems, problems with swallowing, seizures
 Complications:
o Emotional and psychological problems, anxiety, depression and mood swings
o Problems with attention, concentrating, planning and problem solving
o Problems with balance, co-ordination and movement
o Persistent tiredness

Cerebral abscess
 From an infection in or around the skull , e.g. sinuses, otitis media, dental abscess
 From severe head injury – fracturing skull and providing entry point for bacteria,
fungi
 From an infection elsewhere in the body (commonly lungs)
 Symptoms associated with expanding intracranial mass septic signs (Fever, fits, focal,
fetal)

Danger triangle of the face

 Danger triangle: Area from the corners of the mouth to the bridge of the nose,
including the nose and maxilla
 The skin in this region is thin and in intimate relation with underlying muscles
 Facial veins are valveless and communicate directly with cavernous sinus through
pterygoid plexus, angular and ophthalmic veins (direct super highway of blood
vessels straight to the brain)

31
  Infection of this area can spread intracranially and cause septic cavernous sinus
thrombosis
Diagnosis:
 Contrast enhanced CT
 Lumbar puncture is contraindicated in here
 Locate original source of infection
 Blood cultures likely also requested
Cerebral abscess Treatment
 Antibiotics based on most likely causative organism
 Surgical debridement of the abscess
 Surgical removal/debridement of any distal infected area such as tooth extraction or
skin lesion

Postoperative CNS infections

 Mechanical shunts may be a source of
infection – these are important devices
which regulate ICP by diverting CSF and
preventing accumulation
 The causative agents involved tend to be
those commonly those on the skin or in
the environment

Polio
 Caused by poliovirus
 Close to eradication, vaccine available
 <1% cases include CNS involvement, but severe complications of the disease

Rabies encephalitis
 Caused by rabies virus
 Predominantly in Africa and Asia
 99% associated with dog bites
 40% of cases in children under 15 yo
 Infection spreads from the bite site to the CNS, virus is then spread from cell to cell
(8cm/day), 3-12 weeks to see any symptoms
 The striking symptoms of furious rabies (80% of cases) are due to dysfunction and
invasion of the limbic system – removing inhibition and initiating aggression
 The virus is shed in saliva

32
  Following a bite, rapid post bite wound washing with warm soapy water and rapid
assessment can have a big impact on whether or not you develop disease
 Post exposure vaccines are also available

CNS infection in the immunocompromised patient

 They are much more susceptible to unusual infections

All of the red infections are listed as AIDS defining illness

33