Neurological Emergencies Flashcards
Viral meningitis
Commonly affects children and you adults
Symptoms less severe than bacterial meningitis and last for 7-10 days
Self limiting and slower onset
Management is symptomatic relief and may include antivirals depending on pathogen
Bacterial meningitis
Acute inflammation of the meningies- mainly the Pia and arachnoid matter
Neurological and infectious emergency
Most common causative organism: N.meningitidis and streptococcus pneumoniae
Can trigger a systemic inflammatory response; increased capillary permeability contributes to fluid shifts resulting in hypovolaemia
Blood vessels are damaged, blood leaks from capillaries as seen in the petechial rash of meningococcal meningitis
Thrombolysis
For pts with potentially disabling ischaemic stroke due to large vessel occlusion with in 4.5 hours who meet specific criteria after the time patient was last seen well with Intravenous tenectaplase or altaplase
Subarachnoid haemorrhage
Is the presence of extravasated blood within the subarachnoid space.
Most common cause is head trauma.
Non traumatic or spontaneous SAH results from rupture of a cerebral aneurysm in approx 85% of cases.
Blood leaks into the subarachnoid space from a cerebral vessel inducing acute global ischaemia
Signs and symptoms of spontaneous SAH
Sudden severe headache is the hallmark presentation in up to 95% of cases
Typically described as being occipital and the worst headache experienced
Nausea and vomiting are common
Pts can also experience a brief LOC and neck stiffness
33% of pts will experience a warning week or days prior -niggling headache
Encephalitis clinical features
Headache, fever, and altered conscious state are hallmarks as well as seizures, behavioural changes and speech and movement disorders.
Management of encephalitis
Acyclovir +- AB’s while waiting specific results, supportive care.
ICP management, respiratory, circulation and seizure management
Guillian-Barre syndrome key diagnostic findings
Recent onset - days or at most 4 weeks of symmetrical weakness, usually starting in the legs
Abnormal sensation such as pain, numbness and tingling in the feet
Absent or diminished deep tendon reflexes
Sometimes pts will have had a recent viral infection
Meninges
Three connective tissue membranes that cover and protect the brain and spinal cord
Made up of: dura mater (outer most layer and has two layers),
arachnoid mater: web like
Pia mater (lines the surface of the brain and spinal cord follows every fold)
Functions of the meninges
Cover and protect the CNS
Protect blood vessels and enclose venous sinuses
Contain CSF
Form partitions in the skull
Subdural haematoma
Bleeding in the space between the dura mater and arachnoid mater
Sluggish pupil response
Increased ICP
Fixed dilated pupils
Compression on the occipital nerve through foramen magnum
Cerebral perfusion pressure (CCP)
The pressure required to adequately perfuse the brain. CCP is determined by the mean arterial pressure (MAP) and intracranial pressure (ICP). CCP = MAP - ICP
Normal CCP
60-100mmHg
A change in either the ICP or the MAP can result in an inadequate CCP - resulting in inadequate cerebral perfusion.
Monro-Kellie hypothesis
Blood, CSF brain tissue exist in a dynamic equilibrium.
If the volume of any of the 3 increases the volume of the others must decrease to maintain normal pressures
Compensatory mechanisms to preserve the integrity of the brain
Displacing or shifting CSF, increasing absorption of CSF or decreasing cerebral blood flow. Without these changes ICP will increase
Early signs and symptoms of Increased ICP
Changes in mental status, such as disorientation, restlessness and mental confusion
Purposeless movements
Pupillary changes
Constant headache that increases in intensity and is aggravated by movement
Nausea and vomiting
Seizures
Late signs and symptoms of raised ICP
Deterioration in level of consciousness until the pt become comatose
The cushings response
Decrease in respiratory and pulse rates
Increased BP and temp
Altered respiratory patterns
Severe TBI <8 gcs
Prolonged LOC at time of injury
Increasingly severe headache with or with out vomiting
Decreased conscious state - responding only to pain or unresponsive
Abnormal/change in behaviour
Bleeding/csf leak from nose or ears
Unequal pupils
Laterlising motor weakness
Signs of increased ICP
The Cushings response
Changes in pupillary size or reactiveness
Seizures
Out of hospital arrest
Penetrating head injuries
Management of severe TBI
Adequate ventilation and oxygenation- PO2 80mmHg and PCO2 35-40 mmHg
Elevate head 30 degrees
Midline head position
Correct hypovolaemia
Sedation and analgesia to prevent movement, coughing and pain that can increase ICP
Normoglycaemia
Seizure management
Management of seizures
A- protect and prevent aspiration (lateral position, suction)
B- supplemental O2
C- usually maintained
D- duration of seizure and type
E- injury prevention (pillows, blankets)
Identify and treat complications and precipitating factors
The Penumbra (ischaemic CVA)
Is the area surrounding the ischaemic area - some of this may be salvageable depending on time to Reperfusion and the severity and duration of occlusion
Subarachnoid haemorrhage signs and symptoms
Sudden severe headache and may be the only symptom
Typically described as occipital and the worst headache ever experienced
Nausea and vomiting common
Patient can also experience a brief LOV and neck stiffness
Some patients experience a warning days or weeks prior of a niggling headache or NQR
SAH
Blood leaks in to the subarachnoid space from a cerebral vessel inducing acute global ischaemia. 85% due to rupture of a cerebral aneurysm
Acute global ischaemia (SAH)
Acute rise in ICP
The bleed increases intracranial volume and impairs circulation of CSF
CBF also decreased reducing blood supply to the brain
Haemotoma compresses and displaces brain tissue
Interferes with adequate CPP delivery of O2 and glucose to brain tissue
Typical presentation of a CVA
Sudden onset of neurological deficit with headache- often severe
Vomiting
Collapse and or transient LOC
HTN
CVA symptoms
FAST
Facial asymmetry
Arm weakness/drift
Motor and sensory deficits (uni or bilateral)
Time/onset
Slurred speech
Difficulty writing and calculating numbers
Unilateral neglect (usually Left side)
Difficulty dressing
Ataxia
Causes of ischaemic strokes
Thromboembolism
Vascular stenosis
Arterial dissection
Vasoconstriction- pre eclampsia, drug induced, SAH
Causes of haemorrhagic stroke
HTN
Aneurysm
Trauma
Tumours
Coagulation disorders
Anterior circulation of the brain
Supplies the optic nerve, retina, frontoparietal and temporal lobes
S&S : visual disturbances, dysphagia, difficulty writing and calculating numbers, difficulty dressing, unilateral neglect, facial disturbances (motor and sensory)
Posterior circulation of the brain
Supplies the cerebellum, brain stem, thalamus, temporal and occipital lobes
S&S: uni or bilateral sensory and motor alternatives
Visual disturbances
Ataxia, acute vertigo, or nystagmus
Diplopia or dysarthria
Altered LOC
Reperfusion - CVA
For pts with potentially disabling ischaemic stroke within 4.5 hrs of onset who meet specific criteria
Endovascular thrombectomy
Ischaemic stroke caused by large vessel occlusion - endovascular thrombectomy should be undertaken within 6 hrs of CVA onset
Acute antithrombotic therapy
Pts with ischaemic stroke not receiving Reperfusion should have antiplatelet therapy as soon as CT has excluded haemorrhage
Minor ischaemic CVA or high risk TIA
Aspirin + clopidogrel to be commenced with in 24hrs and used in the short term (first 3 weeks)
Management of cerebral oedema in ischaemic CVA
Osomtherapy and hyperventilation can be trialled
Glycaemic therapy post CVA
BGL monitoring for first 72hrs. Treat hyperglycaemia >10mmol/L regardless of diabetic status
Infections of the CNS
Meningitis- involves the meninges
Encephalitis- confined to the brain parenchyma
Cerebral oedema
Is excess accumulation of fluid in the intercellular or extracellular spaces of the brain - occurs in response to brain insult - trauma, CVA, haemorrhage, contusion or inflammation
Signs and symptoms of bacterial meningitis
Fever, neck stiffness, headache and altered mental status
Encephalitis
Inflammation of the brain
Meningitis
Inflammation of the leptomeningies
(Arachnoid + Pia mater) between these layers is the subarachnoid space which houses the CSF
Diagnosis of meningitis
LP- to measure pressure of CSF and to analyse it for WBC’s, protein and glucose
Kernigs sign
Brudinski sign
Encephalitis - clinical features
Headache, fever, alter LOC. abnormalities of brain function are the differentiating feature from meningitis. Includes altered mental status, motor and sensory deficits, altered behaviour, personality changes and speech and movement disorder
Management of encephalitis
Aciclovir, +- AB’s while awaiting results.
ICP management, respiratory, circulatory and seizure management
Steroids not recommended
Gillian Barre syndrome
Rare neurological disorder where the body’s immune system mistakenly attacks part of the peripheral nervous system
GBS (Gillian- Barre)
Usually occurs following a respiratory or gastrointestinal viral illness
GBS
Immune system attacks the PNS
Antibodies or white cells attack the myelin sheath of nerves
Causes nerves to inflame, slowing communication to and from the brain
Eventually the brain is not able to communicate effectively with the PNS causing a state of paralysis
Diagnosis of GBS
LP- csf will have high protein or albumin with or without an increase in WBC
Nerve conduction tests and electomyographic studies
Raised ICP management
Treat underlying cause
ABCD- hypoxia and hypotension worsen secondary brain injuries
Maintain adequate CPP - raise Map
Lower ICP
Raised ICP management (medications)
Analgesia + sedation (opioid infusion)
Osmotic diuretics: Mannitol 0.25-1g/kg
Hypertonic saline solution 3% (bolus or continuous infusion)
Fever control
Seizure management
Desmopressin
Stoke management
A- consider LOC, nil orally, swallow assessment with in 4hrs
B- monitor hypo ventilation (rise in CO2 = vasodilation)
C- manage hypotension, monitor BP 48hrs reduce BP by no more 20% if >220/120 in first 24hrs
Reduce BP <185/110 sus before and after thrombolysis
ECG, 2 x lge bore cannulas
D- neurological assessment (pupils, GCS)
BGL for 72hrs
Elevate head 30 degrees
Monitor for signs of ICP
NBM
?NGT
E- manage hyperthermia and attend to wounds
Absolute Contraindications for Reperfusion
Acute intracranial haemorrhage
Onset of sx outside time window
Bleeding risk (active bleeding, suspected SAH in normal CT, coagulopathies, low platelet count)
Pt is anti- cougulated
Refractory HTN >185/110
Stroke or head trauma last 3 months
Major surgery/trauma last 2 weeks
Severe liver disease
Bacterial meningitis- medication management
IVAB’s with in 39-60 minutes of management : ceftriaxone or cefotaxime, +- penicillin with pts >50yrs
Corticosteroids before or with first dose of IVABs
Seizure management
Fever management
Bacterial meningitis investigations
LP - CSF analysis
CT - pre LP if signs of ICP
Blood cultures
Routine bloods
PCR
AB’s should not be delayed for investigations
Subarachnoid haemorrhage investigations and management
Non contrast CT: if neg LP (6-12hrs) looking for RBC
CTS - once confirmed
ECG
Baseline bloods and coags
Management:
Stabilise ABCD
Fever, seizure and no control <160
BGL monitoring
Analgesia
Nimidipine starting with 48hrs
Elevation of head in increased ICP
30 degrees to facilitate venous drainage; cluster care; low stimulation (turn down the lights, don’t shout)
CPP
CPP = map - ICP. As ICP increases CPP is compromised if Map is not maintained. Maintain MAP >80 however aim BP <160
CCP =
MAP-ICP
MAP: SBP + 2 (DBP) / 3. - ICP
Normal CCP is 60-100
Clinical manifestations of raised ICP
Headache
N & V
Double vision (Diplopia)
Pupillary dilation
Cushings triad - severe HTN, bradycardia, irregular respiration
