Week 4- neuro Flashcards
(50 cards)
Increased intracranial pressure (ICP)
Under normal conditions the balance between the three components maintains a relatively constant intracranial volume and thus a relatively constant intracranial pressure (between 0 and 15mmHg). When required to, the brain can compensate for small and brief increases by:
○ pushing blood into the venous sinuses in the brain
○ increasing the CSF resorption or
○ moving CSF into the spinal column
Monro-Kellie hypothesis
theorises if the volume of one of the components within the skull increases, another must decrease to maintain normal ICP.
Skull contains
brain tissue (intracellular and extracellular fluids, 80%), cerebrospinal fluid (CSF, 10%) and blood (arterial, venous and capillary, 10%).
Cerebral perfusion pressure (CPP)
Cerebral perfusion pressure (CPP) is the pressure needed to maintain blood flow to the brain. Adequate perfusion is critical as it determines whether neurons receive blood (oxygen and glucose) or not. Normal CPP is 60-100 mmHg; less than 50 mmHg is associated with ischaemia and death of neurons.
CPP is determined by the mean arterial pressure (MAP) and intracranial pressure (ICP):
CPP = *MAP minus ICP
*(MAP = Diastolic BP + 1/3 (Systolic BP minus Diastolic BP)
Causes of increased ICP include:
Brain
○ Tumour
○ Infection/ inflammation (meningitis, encephalitis)
○ Cerebral oedema (trauma, hypoxia, stroke)
○ Haemorrhage/ haematoma
Causes of increased ICP include: CSF
○ Increased production
○ Decreased absorption-following meningitis
○ Impaired circulation (obstructive hydrocephalus)
Causes of increased ICP include: Blood
○ Vasodilation (respiratory depression, ↑ CO2, cerebral hypoxia)
○ Obstruction of venous outflow-neck surgery, jugular vein compression
○ Heart failure
Clinical Manifestations- ICP
- Altered level of consciousness
- Changes in speech pattern
- Pupillary changes: unequal/ dilated/ non-reactive (compression of oculomotor nerve)
- Neurological symptoms-weakness, numbness
- Nausea, vomiting
- Seizures: neuronal damage
- Cranial nerve palsy, particularly involving the abducens (VI) nerve
Cushing’s triad is a late response to increasing ICP (possibly brainstem herniation) and results in:
- Hypertension with widening pulse pressure (↑ systolic pressure with ↓ diastolic pressure)
- Bradycardia
- Respiratory depression/ agonal breathing
Assessment and management- ICP: Airway
Is the patient conscious enough to maintain and protect their own airway?
- Airway support as required
- Consider airway adjuncts, head tilt/ chin lift, jaw thrust
- Intubate if GCS < 9
Assessment and management- ICP: breathing
Trends/ changes, ↓ O2 saturation, ↓ rate, agonal breathing
- Apply O2 , ongoing monitoring
- Avoid hypoxaemia: vasodilation, ↑ ICP
Assessment and management- ICP:
circulation
- Normotensive/ hypotensive (sepsis)
- Hypertensive, bradycardia (Cushing’s triad)
- Skin hot to cool, clammy
- Vital signs,
- IVC,
- monitor fluid status (avoid hypovolaemia),
- IVT (Normal saline/ Hartmanns, not Dextrose)
- Avoid hypotension CPP = MAP – ICP, vasopressors
Assessment and management- ICP: disability
- Irritable/ confused/ somnolence/ changes in behaviour
- Slowed speech/ comprehension
- Headache
- Febrile
- Blurred vision/ unequal pupils/ sluggish
- Limb weakness
- Seizures (focal/ generalised)
- Maintain safety, BGL, monitor GCS, pain management, ↓ fever, anticonvulsants
- All patients with an altered conscious state should have a blood glucose performed
Reducing ICP
Minimising further elevations
* Sedate/ paralyse
↓metabolic demand
* ↓ noxious stimuli (noise, procedures)
* Position 30o – 40o angle (↓ ICP)
* Avoid neck flexion
* Coughing/ straining (↑ ICP)
Treatments for ICP
The treatment involves antibiotics, compression, ICP monitoring, hypertonic solutions, loop diuretics, dexamethasone, barbiturates, mechanical ventilation, vasodilation, cerebral blood flow, and cooling for brain metabolism and neuroprotection.
Meningitis
acute inflammation of the meningeal tissues surrounding the brain and the spinal cord.
meningitis Pathophysiology
Bacterial or viral meningitis occurs when an infectious agent invades the central nervous system, leading to a blood brain barrier breach. This inflammatory response causes brain damage, oedema, and ischaemia, resulting in increased intracranial pressure (ICP), cytotoxic damage, and further inflammation.
Clinical manifestations
- Severe headache
- Nausea and vomiting
- Nuchal rigidity (neck stiffness)
- Fever
Meningitis Complications
cerebral oedema, seizures, septic shock, and nerve irritation, leading to altered mental status, seizures, and potential brain damage if untreated.
Meningitis- Viral
- Most commonly affects children and young adults
- Slow onset (days), lasts 7-10 day, self-limiting
- Common viral agents include: enterovirus-coxsackievirus, Epstein-Barr virus
- Often causative agent unknown
- Expect full recovery
Meningitis- Bacterial
- Medical emergency (fatal if not treated quickly)
- Rapid onset (hours), slow recovery
- Causative agents: Streptococcus pneumonia (pneumococcal meningitis) Neisseria meningitides (meningococcal meningitis) Haemophilus influenzae (Hib)
- Death rate ~ 5-10%
- Permanent disabilities include cerebral palsy & deafness
Diagnosis meningitis
- History: helps differentiate
- Physical examination
- Lumbar puncture for CSF specimen:
- Bacterial: cloudy, purulent, under increased pressure ↑ WBC, ↑ Protein, ↓Glucose
- Viral: ↑ lymphocytes, moderate ↑ protein, normal glucose * Relative contraindications: coagulopathy, ↑ ICP
- +/- CT/ neuroimaging
- Blood cultures
- Pathology (CRP etc distinguish between bacterial & non-bacterial)
Key signs of meningitis:
- Severe headache
- Nausea, vomiting
- Change in mental status *
- Nuchal rigidity (neck stiffness) *
- Fever (mostly present) *
Meningitis Assessment & Management: Danger
Organism spread through close contact/ coughing/ sneezing,
- Droplet precautions x 24 hours
- Report incidence to Office of Health Protection (communicable diseases)
- Seizures: minimise injury
