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NUR3120 PPNP3 Patho - Coggle Diagram

- - - - IV adrenaline 1mg every 3-5mins + IV amiodarone 300mg (repeat 150mg if necessary)
        OR
        IV lignocaine 1-1.5mg/kg, repeat if necessary
  - - - Nurse role
        Place patient supine, and nurse begin CPR (Compression)
        Resus trolley arrive, Nurse (Airway) to fix air viva and start BVM --> Nurse RN
        Nurse (Circulation) to apply 3 lead ECG, check ECG rhythm and prepare emergency drug --> Nurse in charge
    - - When ROSC restored, doctor 2 to liase and arrange transfer to ICU
        Condition for transfer: stabilise SBP at/above 90mmHg for continuous 15 mins
        Speak to/update family members
      - Transferring to ICU
        
        Patient connecteed to portable defibri
        Maintain airwawy
        Bring alot E-kit
    - - Staff prep
      - Readiness of resuscitation trolley
    - - Revieww events leading to patient collapse
        Evaluate resuss
        Team members can ventilate eand letgo
        Lessons learnt
      - Resupp resus trolley
  - - - VT/pulseless VT:
        Adrenaline
        Amiodarone
        Lignocaine
        Magnesium
        Others
      - Pulseless electrical activity
        Adrenaline
        Others: e.g. potassium, calcium, antidotes
      - Asystole:
        Adrenaline
- - - - Focal- coup: localised on side of impact of skull
      - Diffuse: wide neural injury
      - Polar: brain shifting between skull and meninges during course of acceleration and deceleration, resulting in local injury in two opposite poles of brain
      - Intracranial hematomas: epidural, subdural, subarachnoid
    - - Causes
        
        Rotation of cerebral hemisphere on relatively fixeed brain stem
        Electro-physiological dysfunction of reticular activating system
        However, no structural lesion and residual sequelae
      - Manifestations
        
        Amnesia may occur after injury
        
        Retrograde amnesia: cannot recall series of events before injury (indicate severity of lesions)
        
        Antegrade amnesia: forget events after, very brief
    - - Causes
        
        Due to deceleration of brain against skull rupturing the blood vessels on the surface of the brain
        Usually frontal and occipital lobes affected
        
        Coup injury: directly under point of immpact
        Contrecoup injury: at a point opposite to the point of impact
      - Manifestations
        
        Hemiparesis/gazee paralysis (occur with frontal injuries)
        Visual defect in occipital injuries
        Cranial nerve dysfunction: commonly olfactory
        More severe injury: cerebral edema, decorticate/decerebrate rigidity
        Cerebral lesions are bilateral: coma
    - - Causes
        
        Direct trauma, causing temporal bone and damage to middle meningeal artery
        Bleeding arterial: rapid worsening of patient's condition
      - Manifestations
        
        Brief LOC (due to concussion) followed by short LUCID interval then coma again (progressive neurological deterioration due to herniation)
        Carries bad prognosis
        Usually requires surgical evacuation
        Untreated: decerebrate rigidity, coma, death
    - - Causes
        
        Follows severe head injury: change in velocity
        Due to rupture of surface cerebral veins that join the dural venous sinuses
        TWICE as common as extradural hematoma
      - Manifestation
        
        Brief LOC, then relatively longer lucid interval, then coma again (progressive neurological deterioration due to herniation)
        
        Bleeding is via the VEINS, so bleeding very slow
        
        Carries bad prognosis if associated with cerebral injury due to high velocity
        Usually requires surgical evacuation
        Untreated: decerebrate rigidity, coma, death
    - - Causes
        
        Follows minor injuries which may not be remembered
        Due to shrinking of brain coupled with fragility of blood vessels
      - Manifestation
        
        Signs and symptoms appear months to years after trivial injury due to slow accumulation of venous blood around atrophied brain
        
        Minor headaches over a period of time due to slow bleeding
        
        Other symptoms: personality changes, fluctuating drowsiness, confusion, weakness, seizures
        
        Can be confused with stroke, dementia
  - - - Pupil reflex: brainstem, CN II, III.
        Indicator of brain herniation
        Increasing ICP may impair eye movements controlled by CN III, IV and VI
      - Oculovestibular reflex: brainstem dysfunction, doll's eye test
        Caloric Ice Water Test: normal response: conjugate eye movements
      - Corneal reflex: absence of blink response, indicator of severely impaired brain function
  - - - Eggshell: child abuse
      - Open fractures associated with infections
      - Stellate: impact by blunt object
    - - Soft tissue injuries may give clues
        Hemotympanum (blood in middle ear)
        CSF rhinorrhea (nose) and otorrhea (ear)
        Postauricular ecchymoses (Battle's sign)
        Periorbital ecchymoses (Raccoon's eyes)
        REFER TO PIC
      - Basal skull fractures often associated with cranial nerve injuries
  - - - Blood pressure usual level (MAP 90)
        Maintain CPP between 50-70mmHg
- - - - Haemorrhagic stroke
        
        Causes:
        Intracerebral (hypertension + thrombolytic drugs) --> dependent on which artery
        Subarachnoid (Aneurysm rupture Severe headache) --> usually in the center (brain scan)
        
        Intracerebral haemorrhage
        
        Form a clot, space occupying lesion increasing intracranial pressure. Affects cerebral perfusion, may cause displace structures and cause herniatiion. Brain stem compression cause death
        
        Subarachnoid haemorrhage
        
        Saccular/Berry aneurysm (congenital pouch like dilation of arterial wall)= mostly circle of Willis (occurs usually in adolescents)
        
        Causes
        Accident, trauma --> venous in nature
        Rupture of aneurysm --> arterial bleed
        
        Manifestations
        
        Sudden onset of worst headache
        Vomiting
        May/may not lose consciousness
        No focal neurological deficits
        
        Small vs Major rupture
        Small: leak of blood into subarachnoid space
        Major: result in loss of consciousness, preceded by severe headache and severe exertion
        
        Major rupture complication
        Vasospasm:blood is irritant, irritate neighbouring arteries, vasospasm and ischemia
        Hydrocephalus: blockage of reabsorption of CSF can result in hydrocephalus and increase in ICP
        Rerupture: chances of rupture higher
        
        Treatment
        
        Stop antiplatelet and anticoagulation
        Reverse antithrombotic effect and correct coagulation
        
        ICH systolic blood pressure: <160mmHg, >120mmHg
        SAH: Maintain MAP <130mmHg or >80mmHg
        
        Monitor neurological condition, control Intercranial pressure
        Keep blood sugar level 6-10mmol/L
        
        Surgical and interventional managemment
        
        External ventricle drainage (EVD)
        
        Clipping of aneurysm
        
        Coiling of aneurysm
        
        Post surgery
        
        Reduce risk of re-bleeding
        Prevent vasopasm
        Prevent seizure
        Control ICP/BSL/fever
        
        Craniactemy
      - Transient Ischemic Attacks (TIA)
        
        No permanent damage to the brain BUT, warning sign that there might be another stroke
        
        Depending on which arteries involved
        
        Carotid
        
        Loss of vision on one eye
        
        Hemiparesis
        
        Inability to speak
        
        Vertebrobasilar
        
        Tinnitus
        
        Vertigo and blurring vision
        
        Hemiparesis
        
        Neurological dysfunction that lasts for a few seconds to a few minutes.
        
        Low flow states in vascular obstruction
        Small emboli which get dissolved later
      - Ischemic stroke
        
        Causes:
        Thrombotic
        Embolic
        
        Penumbra region can help to reduce damage as it will provide oxygen due to collateral arteries
        
        Thrombosis: slow, during rest time
        Embolism: sudden, during exertion
        
        Embolism causes
        
        Heart disease/surgery
        
        Atrial fibrilation
        
        Thrombosis causes
        
        Blood disorders
        
        Arterial disease
        
        Infarction of brain tissue occurs due to lack of blood. Deficit permanent
        Increasing obstruction may involve proximal branch of artery and increase deficit: Stroke in evolution
        Edema occurs in surrounding area
        
        Signs and symptoms
        
        Dependent on site of obstruction, state of circulation, onset
        
        Middle cerebral artery
        
        Superficial
        Paralysis of face and hand, conjugate gaze paralysis, motor aphasia
        Conduction/sensory aphasia
        
        Deep
        Paralysis of opposite side
        
        Posterior cerebral
        
        Visual defects, central/color blindness, memory impairment
        
        Anterior Cerebral Artery
        
        Deep
        Obstruction well tolerated because of collateral flow
        
        Superficial
        Confusion, disorientation, paralysis and sensory loss in opposite leg, urinary incontinence
        
        Basilar and vertebral
        
        Sensory loss, mild hemiparesis, disturbance of gait, speecl, swallowing and vision
        
        Right brain damage
        
        Paralysed left side
        Spatial-perceptual deficits
        Behaviour: quick impulsive
        Memory deficits
        Indifference to disability
        
        Left brain damage
        
        Pralayzed right side
        Speech-language deficits
        Behaviour: slow, cautious
        Memory dedficits: language
        Distress and depression in relation to disability
        
        Cerebellar syndrome
        
        Treatment
        
        IV tissue plasminogen activator (TPA)
        
        MoA: Bind to fibrin, convert plasminogen to plasmin, stimulate fibrinolysis
        
        Inclusion criteria
        
        18 years old and more
        Last seen well less than 4.5hrs
        Ischemmic stroke with significant neurological deficit, NIHSS>4
        
        Exclusion criteria
        
        Evidence of ICH/SAH
        Active internal bleeding
        Stroke within 3 months
        Platelet <100 000 On anticoagulation Received heparin within 48hr/aPTT elevated Intracranial/intraspinal surgery within last 3 mths Persistent blood pressure elevation Blood sugar level <2.7 or >22.2mmol/l
        
        mixed with swirling not shaking
        
        blood pressure, neurological status checked within 15 minutes prior to administration
        
        Antiplatelet/anticoagulant therapy (if cannot give IV TPA)
        
        Aspirin
        
        Clopidogrel
        
        Warfarin anticoagulation (3mths) followed by antiplatelet agent
        
        Heparin anticoagulation
        
        Warfarin counselling
        
        Modify diet,
        
        Need monitor INR and mmake sure within therapeutic range
        
        Monitor side effect
        
        Special precautions (peptic ulcer, blood disorder, pregnancy, alcohol --> more risk of bleeding)
        
        Endovascular treatment: Stent
    - - Rupture (Hemorrhagic stroke)
      - Blockage
        
        Less than 24hrs --> Transient Ischemic Attack
        
        More than 24hrs --> Stroke
    - - Facial weakness
        Arm weakness
        Speech problems
        Time orientated
      - Sudden severe headache --> More likely haemorrhagic stroke
      - Other symmptoms: sudden weakness/numbness on one side, difficulty finding words/speaking clear sentences
        Sudden memory loss or confusion
      - Assess airway, breathing, circulation (ABC) + vital signs
        Provide oxygen if hypoxemic
        Obtain IV access
        Blood samples
        Determine last known well time
      - Perform neurologic screening assessmment
        
        Glasgow Coma Scale (GCS)
        
        Eye opening (E4), Verbal response (V5), Motor response (M6)
        
        Lower the score, the worse it is
        
        NIH Stroke Scale (NIHSS)
        
        13 areas, 42 points
        
        More points, the worse it is
        
        Afterwards, go for CT scan
        
        White patch = high density, haemorrhages
        Dark patch = low density = infarct
      - Neurologic assessment -> CT scan -> CT angiogram -> MRI scan
      - Time is brain, within 60 minutes of emergency arrival
        
        If not haemorrhage, consider thrombolysis therapy
        
        Targeted temperature management (TTM) is often used in neurocritical care to minimize secondary neurologic injury and improve outcomes.
    - - Non-modifiable
        
        Gender
        
        Age
        
        Race
        
        Heredity
      - Modifiable
        
        Lifestyle habits
        
        Hypertension
        
        Diabetes
        
        Hyperlipidaemia
        
        Obesity
    - - Extra cranial factors
        
        Systemic blood pressure, cardiac output, viscosity of blood
      - Intracranial
        
        Intracranial pressure, atherosclerosis, blood vessels
  - - - Idiopathic partial epilepsy
        
        Begin in childhood (fammily history) but outgrown in puberty
        
        Seizure tend to occur during sleep, partial motor seizure that involve the face
        
        Types (small area of brain surface affected during seizure):
        
        Simple (awareness is retained)
        Simple motor: jerking, muscle rigidity, spasms
        Simple sensory: unusual sensations affecting either the vision, hearing, smell, taste or touch
        Simple psychological: memory or emotional disturbances
        
        Complex (impaired awareness) Automatisms such as lip smacking, chewing, fidgeting, walking and other repetitive, involuntary but coorrdinated movement
        
        3.Partial seizure with secondary generalization = preservation of consciousness that evolves into loss of consciousness and convulsions
      - Idiopathic generalised epilepsy
        
        Appears during childhood/adolescence though not diagnosed until adulthood
        
        Types (entire brain surface affeected during seizure):
        1.Myoclonic seizures (sporadic jerks, both side of the body jerking. Described as electrical shocks)
        
        Absence seizures (brief loss of consciousness, activity interrupted, blankly staring. May occur several times a day)
        
        Generalized tonic-clonic seizures (3 phases: unconsciouss, body stiffening (tonic), violent jerking (clonic), goes into deep sleep due to exhaustion (postictal)
        
        Clonic (rhythmic jerks of both side of body)
        
        Tonic (muscle stiff, rigidity)
        
        Atonic (loss of muscle tone in all 4 limbs)
        
        EEG identified seizure, but no nervous system abnormalities and normal intelligence
      - Status epilepticus
        
        Serious form, continuously in seizure, 5 or more, then recover, then have seizure again
    - - EEG: sleep deprivation, hyperventilation to illicit pathological mechanism
      - Not idiopathic: lumbar puncture, labs, CT scan, MRI to find out the ethiology of pathological epilepsy
  - - - Affects all ages and races
        More frequent in males
        Viral infections precede GBS (2/3 of cases)
        Immunisation for influenza
        Systemic illnesses like Hodgkin's disease, SLE, cancer
    - - Muscle weakness, paralysis, respiratory failure
        Reduced/absent deep tendon reflees
        Sensory symptoms- paresthesias of hands
        Cranial nerve involvement affected
        Dysautonommia (occurs when there's a malfunction in the autonomic nervous system (ANS).) Cardiac arrythmias, bowel/bladder involvement and pupillary changes
        
        Experience proximal lower extremity weakness with ascending paralysis within hours to days
        -> may worsen rapidly with possibility of respiratory failure
        
        Significant autonomic instability can accompany GBS symptoms and require extensive care monitoring
    - - Can progress to Chronic inflammatory demyeliinating polyneuropathy (CIDP) 3-10% of GBS patients with progression of more than 2 months
      - Miller-Fisher syndrome (5%): ophthalmoplegia, also called extraocular muscle palsy, paralysis of the extraocular muscles that control the movements of the eye.
        Ataxia: term for a group of disorders that affect co-ordination, balance and speech
        Areflexia: Areflexia means the absence of deep tendon reflexes
    - - History taking + physical examination (no single test can detect)
      - Electrodiagnostic test: demyelination (slow nerve conduction)
      - CSF analysis
      - Anti-GQ1B antibodies
    - - ICU (respiratory + cardiovascular function closely monitored)
      - Plasmapharesis: plasma exchange to remove damaging antibodies
      - IV IG: once a day for 5 consecutive days
        
        IgA need to be checked. Why?
        High doses of immunoglobulin may block harmful antibodies that contribute to GBS. Contains traces of IgA which may provoke anaphylaxis in patients with IgA antibodies
      - Neuropathic pain: gabapentin/carbamazepine
    - - tachypnea
        Accessory muscle use
        Tachycardia
        Weak cough
        Dyspnea
    - - Physical and psychosocial well-being
      - Assist in recovery of function during rehab stages
      - Patient education: illness and disease process and anticipated course
  - - - Axons degenerate --> permanent and irreversible damage
    - - Genetic
        Immune mediated disorder, auto-reactive lymphocytes
        Infectious agents
    - - No unique manifestations but some characteristics:
        Relapses between 15-50
        Optic neuritis
        Fatigue
        Lhermitte's sign (escribes a transient sensation of an electric shock extending down the spine and/or extremities upon flexion of the neck, often a sequela of neurologic disease)
        Inter nuclear ophthalmoplegia (paralysis of the extraocular muscles that control the movements of the eye)
        Heat sensitivity (Uhthoff phenomenon)
      - Sensory loss in limbs
        Visual loss
        Motor (subacute)
        Diplopia ( double vision or seeing double.)
        Gait disturbance
        Balance problems
        Bladder problems
      - 80-85% remit but residual side effects remain and accumulate leading to functional decline
      - Earlier age of disease onset = associated with benign/relapsing remitting forms of MS
      - Presenting symptoms: visual compromise, stiffness, weakness
        
        May have brain lesions
      - Symptoms of MS worsen with elevation of temperature or fever
    - - No test. 2 more attacks, 2 lesions with significant history
      - MRI test of choice for scanning of brain and spine
      - Evoked potentials (EP) and CSF studies
      - Neurologic findings
        
        Cranial nerves- optic atrophy
        
        Motor - paraparesis
        
        Reflexes- hyperreflexia
        
        Sensory- hemihyperaesthesia
        
        Coordination- intention tremor
    - - Interferon beta 1b
        
        MoA: modulates immune responsiveness
        
        Side effects:
        Flu like symptoms (paracetamol)
        Potential liver damage
        Depression
      - Acute attacks of MS = glucocorticoids
      - Transplant of autologous stem cell transplant
    - - Psychosocial, discharge planning
      - Patient education
        
        Self-care
        Avoid hot temperatures
        Balance of rest and activities
        Nutrition
        Healthy lifestyle: avoid alcohol/cigarette smoking
        Rehab
  - - - (Diagnosis requires 2 out of 3)
        Bradykinesia (slowness of movement)
        Rigidity
        Tremor (primarily at rest)
      - Other signs: masked face, decreased arm swing, hypovolemic speech, swallowing difficulty, micrographia, stooped posture, shuffling gait
      - Non motor features
        
        Loss of sense oof smell
        Aches/pains
        Cognitive impairment- executive functions, memory and visuospatial functions
        Mood disorders
        Feeling of anxiety/depression
        Autonomic symptoms- excessive and uncontrolled sweating, paroxysmmal flushing, orthostatic hypotension, gastric and urinary retention
      - Cardinal features: resting tremor, rigidity, bradykinesia and postural instability
        
        Failure to respond to large doses of levodopa is storng evidence that patient does not have idiopathic parkinson disease
    - - Imbalance of excitatory (acetylcholine) and inihbiting (dopamine) neurotransmitters in corpus striatum (decreased amount of dopamine) --> extrapyramidal tract impairment --> parkinsonism
        
        Striatal dopamine deficiency syndrome
        Severity of dopamine loss best correlates with bradykinesia in PD
    - - Stage 0: No sign
        Stage 3: Postural instability but independent
        Stage 4: Severe disability but still able to walk
        Stage 5: Wheelchair/bed bound
    - - Genetic + environmental
        
        Envi.: exposure to herbicides/pesticides, heavy metals, proximity to industry, rural residence, repeated head trauma etc.
      - Age definite risk factor but substantia nigra not a proper part of aging
    - - No definite diagnostic test
      - History taking and neurological examination
        MRI brain/spine
      - Positron emission tomography (PET) still uncertain
        Singple photon emission computed tomography (SPECT) disease and syndrome cannot determine from one another
    - - No cure, control symptoms
        
        Major drugs available for treatment of PD motor SYMPTOMS:
        Levodopa
        Dopamine agonists
        Monoamine oxidise B inhibitors
        
        Early
        
        Amantadine: anti viral agent that relieve symptoms in 2/3 of patients
        
        Selegiline
        
        Benzhexol: anti-cholinergics useful in treating tremors (side effects present!)
        
        Main (PD more significant, must replace dopamine deficiency)
        
        Dopamine agonist: act like dopamine in brain and stimulate brain cells to function normally
        
        Start low dose, then gradually increase to reduce side effects
        
        Levodopa- most potent drug for treating PD
        
        Converted to dopamine in brain hence restoring dopamine levels
        
        Wearing off effect
        
        2 more items...
        
        Amantadine- reduce severity of dyskinesia
        
        COMT inhibitors prolong duration of levodopa (may worsen dyskinesia)
        
        CAN LEAD TO DYSKINESIA
        
        Selegiline- Monoamine Oxidise enzyme inhibitors
        
        reduce rate of progression of PD in laboratory settings + improve symptoms of disease
        
        Coenzyme Q-10: powerful antioxidant
        
        Reduce rate of progression
      - Complementary/supportive therapy
      - Deep brain surgery
      - Deep Brain stimulation
        
        Idiopathic PD
        Good levodopa response
        Presence of disabling symptoms despite optimal medical management
        Good general health
        Normal brain immaging
        No dementia, no psychiatric problems
    - - Emotional well-being
        Medication compliance
        Physiotherapy
        Occupational Therapy: ADL and home safety
        Patient education
      - Family/friends community resources
- - - - Migraine: neurally induced dilatation and inflammation of intracranial and extra cranial vessels
      - Tension type: unknown; may be increased sensitivity of pain-mediating systems in brain
      - Cluster headache: neurally induced inflammation and edema of internal carotid artery
    - - Meningitis, fasting, nose/sinus, non-vascular intracranial disease including tumours
        
        Low intracranial pressure state (post-lumbar puncture): Traction through brain sagging on dural attachments; intracranial vasodilation
        
        Meningitis, subarachnoid haemorrhage: inflammation of vessels in meniges and of perivascular dura
        
        Intracranial mass lesion (brain tumour, hydrocephalus): displacement (traction) of pain-senitive vessels
        
        Temporal arteritis, intracranial vasculitis: inflammation of scalp and intracranial vessels
  - - - Presence of papilledema --> Increased ICP warrants diagnostic imaging to rule out mass lesion/benign intracranial hypertension
      - Nuchal rigidity (neck stiffness) --> meningeal irritation associated with meningitis/subarachnoid or intraparenchymal hemorrhage
    - - Migraine with Aura
        
        About 15% experience aura (visual disturbances)
        Aura precedes headache, lasting 20-60 min and then clears before headache (may trespass into first few min of headache)
        Same as 'migraine without aura' + neurological dysfunction before/during attack
        
        Visual: crescents of light that drift across visual field. Glistening points of light, shimmering heat-wave like obscurations
        Sensory: tingling and/or numbness. Originate in mouth and/or hand
        Others: monoparesis (partial loss of voluntary motor function), dysphasia, cognitive changes
      - Migraine without aura
        
        At least 5 attacks
        Each attack, unsuccessfully treated lasts 4-72hrs
        Attack characteristic: unilateral location, pulsating quality, moderate or severe intensity, pain aggravated by exertion/routine physical activity
        During attack symptoms present: nausea, vomiting, photophobia, phonophobia
        NO OTHER EVIDENCE THAT POINTS TO OTHER CAUSES
  - - - When to start?
        2 or more attacks each month with significalt disability that lasts 3 or more days
        Contraindication/ineffectiveness of symptomatic medications
        Use of abortive medication for more than 2 times a week
        Migraine variants/rare headache attacks ---> profound disruption/risk of permanent neurological injury
      - B-blocker
        
        Tricyclic antidepressant
        
        Calcium antagonists
        
        NSAIDs
        
        Anticonvulsant
    - - Comfort measures
        Patient education
        
        Patient education
        
        Type of headache
        
        Headache diary
        
        Identify triggers of migraine headache
        
        Lifestyle modification
        
        Stress reduction and relaxation
        
        Medication
    - - NSAID
        
        Mixed barbiturate analgesics
        
        Triptans
        
        Anti-emetics
    - - 80% patients with chronic daily headache
        Female: Male = 3.5: 1
      - General considerations
        Simple analgesics: >5days/week
        Triptans/combination analgesics: >3days/week
        Opoids/erogtamine: >2days/week
- - - - Inflammation of parenchyma of brain by viruses
        
        Can occur in cortex, white matter, basal ganglia, brain stem, depending on type of virus
      - Causes (viruses)
        
        herpes simplex
        VZ
        CMV
        JE virus
      - Types
        
        Herpes simplex encephalitis
        
        Caused by herpes simplex virus
        
        Pathology: edema, haemorrhage, necrosis of temporal lobes
        
        Manifestations
        
        Fever
        Chills
        Increased ICP
        
        Behavioural and peersonality changes
        Focal neurological signs (aphasia, hemiplegia)
        Seizures
        Drowsiness and coma
        
        Sign of meenigism: neck stiffness, photophobia and headache
        
        Japanese eencephalitis
        
        Leading cause of viral encephalitis in Asia
        
        Cause
        
        JE virus
        Vector: culex mosquito
        
        Risk factors
        
        Rural residents in padi fields
        Expatriates working in rural areas during transmission period
        
        Vaccinee available
      - Diagnosis
        
        Lumbar puncture
        
        Increased lymphocytes
        Protein elevated
        Glucose normal
        
        EEG
        
        Slow waves in temporal lobes in herpes simplex encephalitis
        
        CT scan
        
        Localise site of lesion: temporal lobes in herpes simplex encephalitis
      - Treatment
        
        Anticonvulsants
        
        Dexamethasone, mannitol --> reduced raised ICP
        
        Antivirals: IV acyclovir for herpes simplex encephalitis
        
        Poor prognosis:
        10-30% mortality
        Residual epilepsy/cognitive impairment
    - - Localized collection of pus within the brain parenchyma
      - Treatment
        
        Drainage
        
        Excision of abscess
        
        IV antibiotic therapy
      - Cause: pus forming bacteria (pyogenic)
    - - Inflammation of meninges surrounding brain and spinal cord --> results in irritation of nerves that pass through the meninges
      - Early meningitis: red in colour
        Late meningitis: white colour (fibrosis)
      - Manifestations
        
        Fever
        headache
        irritability
        delirium
        loss of consciousness (extreme)
        
        Signs
        
        Kernig sign: trying to extend flexed knee while hip is flexed- causes spasm of hamstring muscles
        
        Brudzinski sign: Severe neck stiffness causes a patient’s hips and knees to flex when neck is flexed
        
        Neck stiffness: chin does not touch sternum
        
        Purpura and meningoccal meningitis
      - Types
        
        Bacterial meningitis
        
        Causes (Bacteria)
        
        Strep pneumoniae
        Hemophilus influenzae
        Meningococcus
        
        Associated with Waterhouse-Friderichsen syndrome: adrenal hemorrhagic necrosis
        
        Manifestations
        
        Neutrophils in subarachnoid space
        Hemorrhagic infraction of penetrating vessels
        Purulent exudate and thrombosed veins on surface and base of brain
        Sepsis
        Haemorrhages over body
        
        Tubercolous meningitis
        
        Causes
        
        Blood to CNS (primary site lungs)
        
        Manifestations
        
        Small yellow nodulees (tubers) on brain surface
        Histology:
        Langhan's giant clls
        lymphocytes
        Vasculitis
        
        Lymphocytic/viral meningitis
        
        Causes (viruses)
        
        Mumps
        Measles
        Echoviruses
        
        Manifestations
        
        Dense lymphocytic infiltration on microscopy
        CSF shows lymphocytes
      - Diagnosis
        
        Lumbar puncture
        
        Neutrophils > 5000cells/mm3, glucose reduced --> bacterial
        
        Lymphocytes --> viral and tuberculous
        
        Protein elevated
        Glucose reduced
        Gram stain may show organism
        
        Blood culture
        
        CT scan (exclude mass lesion in drowsy or unconscious patient)
      - Treatment
        
        IV antibiotics: depending on organism
        
        Those with close contact need rifampicin prophylaxis
        
        Vaccinations
      - Complications
        
        Cranial nerve palsies: fibrosis
        
        Cortical atrophy: vessel thrombosis -> increased ICP
        lead to mental retardation, blindness, deafness, paralysis
        
        Hydrocephalus: blockage of aqueduct
  - - - Diagnostic
        
        Rule out meningitis
        
        Rule out subarachnoid hemorrhage when CT/MRI is normal/beyond 3 days
      - Therapeutic
        
        To evaluate for normal pressure hydrocephalus (with walk test)
      - Contraindications
        
        Presence of infection in tissue near puncture site
        Presence of space occupying lesion
        Bleeding tendencies INR>1.4
      - Procedure
        
        Check level of iliac crest, L3/L4 level
        
        lignocaine (5-10mls)
        3 mins
        Measure opening pressure
        Collect 15 drops (1ml per bottle)
        Number each bottle in sequence
        Measure closing pressure
        
        Opening pressure
        
        Normal: 10-18
        
        Elevated:
        Infective - TB/bacterial/fungal
        Hydrocephalus - communicative type
        Benign intracranial hypertension
        
        Low
        Blockage- spinal block but ICP is high
        Intracranial hypotension
    - - NEVER send 1st bottle for cell count and microscopy. Why?
        Contain high RBC
      - Compare blood and CSF glucose level
        
        Low glucose in CSF indicates bacterial infection
      - Colour of CSFs + type of findings (Refer to word)
- - - - Allergies
        Viral and bacterial infections (Syphillis)
        Head trauma
        Metabolic derangements
        Chronic stress
    - - Tinnitus
        Fluctuating hearing loss (sensorineural)
        Severe vertigo + progressive sensorineural hearing loss
        Vertigo may improve as hearing impairment worsens
    - - Disease of internal ear
  - - - Others: premature birth
        male gender
        Family history of recurrent OM
        orofacial abnormalities
      - Dysfunction of Eustachian tube --> most important factor that contributes to OM
      - More frequent in pre-school age children (3mths-3years old, peak 6-11mths) --> Eustachian tube more horizontal, very easy for viruses to travel from nasopharynx to middle ear. Age become more inclined, viruses need go against gravity
    - - 1.Perforation of tympanic membrane
        2.Calcification of the ossicles (small bones of the ear: 3, malleus, incas and steppes)
        3.Formation of cholesteatomas (hardening of bones and tympanic membrane, formation of masses)
        4.Purulent drainage from ear
        5.Hearing loss(conductive hearing loss: Rinne test positive)
    - - OME: fluid in the middle ear without signs and symptoms of acute infection; can be due to poor Eustachain tube function (nasal pharynx to middle ear)
      - AOM: abrupt onset, related to middle ear inflammation and effusion (most common)
        
        Common viruses
        
        Rhinovirus
        
        Respiratory synctial virus (RSV)
        
        Common bacteria
        
        Streptococcus pneumoniae
        
        Haemmophilus influenzae
        
        Moraxella catarrhalis
        
        Follow an uncomplicated URTI
    - - Otalgia (pain in the ear)
        Fever
        (Conductive)Hearing loss
        (Younger children may have non-specific signs and symptoms)
        (Otitis media with effusion: usually asymptomatic)
        Sensory hearing loss usually because of inner ear
    - - Otoscopic examination: look into tympanic membrane
        Presence of middle ear effusion/inflammation
        (MEI: fullness or bulging of tympanic membrane, may/may not be red. Limited mobility of tympanic membrane, purulent effusion, pain
        Blow through the ears: tympanic membrane should move
      - Pneumatic otoscopy: middle ear effusion and immobility of tympanic membrane
        Push air into ear to look into mobility of tympanic membrane
      - Others: tympanogram, acoustic reflectometry
    - - Pain management
        
        Myringotomy: make a cut, to release pressure & effusion (Tympanocentesis: poke through tympanic membrane and suck effusion out)
        
        Observation: uncomplicayed AOM
        
        Antibiotics (bacterial origin!)
  - - - History taking: single/recurrent episodes?
        -Aggravating factors: head movement, coughing, sneezing, loud noises, head trauma, hyperextension of neck, viral infection
        -Past medical history: history of migraine attacks, stroke risk factors (BP, initial symptoms may be vertigo), family history, medications associated with vestibular (aminoglycosides) and cerebellar (phenytoin) toxicity
      - 2.Physical examination
        Distinguish central from peripheral (nystagmus suggest originates from vestibular system)
        Look for abnormalities in balance and gait
        Neurologic examination: look for cranial nerve abnormalities, sensory and motor changes/abnormal reflexes
        Hearing tests: Rinne and Weber tests
        Caloric test: differentiate abnormalities in vestibular system
        
        Peripheral vs Central
        Direction of nystagmus: Unidirectional vs sometimes reverses direction
        Type of nystagmus: Horizontal vs any direction
        Effects of visual fixation: supressed vs not supressed
        Other neurologic signs? Absent vs Often present
        Postural instability: Unidirectional instability, walking preserved vs Severe instability, patient falls while walking
        Deafness/tinnitus: Present vs Absent
      - Diagnostic tests
        
        MRI: suspect CENTRAL cause of vertigo (CT scan is less sensitive)
        Electronystagmography: electrodes used to record eye movements
        Video nystagmography: video cameras used to record eye movements
        Audiometry: to detect hearing loss (rule out peripheral cause of vertigo)
    - - Benign paroxysmal positional vertigo (not continuous, related to patient's position)
        -MOST COMMONLY cause
        -Spinning sensation when tilting head upward/turning in bed: briefly in seconds
        -calcium deposits in posterior semicircular canal (canalithiasis) --> send wrong signals to brain
      - Vestibular neuritis: viral fever, affect vestibular portion of cranial nerve VIII, severe with rapid onset of vertigo
      - Meniere's Disease: excess endolymphatic fluid pressure
        Severe vertigo, sensorineural hearing loss
        Often associated with nausea and vomiting and disabling imbalance
        Remission spontaneously/can recur
      - Herpes zoster: activation of latent herpes zoster infection of geniculate ganglion
        hearing loss, ipsilateral facial paralysis, ear pain, vesicles in auditory canal annd auricle
        Acute unilateral dermatological rash and neuritis with vesicular lesions
      - Labryinthitis: inflammation of inner ear labrinyth
        Due to infection, drug toxicity, trauma, tumour, viral infection (most common)
        Head movement: causes severe vertigo and sensorineural hearing loss
    - - Nausea and vomitng (Severe, can cause electrolyte imbalance)
        Postural and gait instability (central origin>peripheral origin)
        Pallor and sweating
        Tinnitus, deafness, headache, photophobia
        Nystagmus: oscillation of the eyes
    - - Not a disease but could be a symptom of vestibular disorder
        Some perceive self motion (subjective), whereas others perceive motion of the environment (objective)
      - CNS receives signals from both right and left labrynths via vestibular portion of CN VIII to brain stem vestibular nuclei, then cerebellum--> ocular motor nuclei and spinal cord, compares these signals
        
        Still: tonic discharges in both vestibular afferents =balanced
        During motion: right and left labryinths are alternatively excited and inhibited --> left-right difference in 8th nerve activity, recognized as motion
        Acute unilateral peripheral vestibular disorder: interpreted by CNS as motion/vertigo due to left-right differences
        
        Vestibuloocular connections: responsible for coordinated eye movements during head motion
        Vestibulospinal pathways: maintain upright posture
        Cerebellar connections: modulate activites by the vestiboocular and vestibulospinal connections
      - Semicircular canals: sense angular motion
        Otolith organs: sense linear motion
        Presence of vertigo --> suggest abnornality in SEMICIRCULAR CANALS or the CENTRAL NERVOUS SYSTEM structures that process signals from semicircular canals
    - - Multiple sclerosis: demyelination of brain
        MS with plaques near vestibular nuclei and root entry zone of CN VIII
      - Epileptic vertigo
        -ictal manifestation of focal epilepsy
        motor and sensory changes accompany vertigo as well as consciousness level changes
      - Cerebellar infarction and haemorrhage: sudden and intense vertigo
        Nausea and vomiting also present
        Likely to occur on patients > 60 years old
      - Vestibular migraine
        -recurrent vertigo usually due to migraine attacks
        variability of vertigo severity
        mechanism poorly understood
      - Brainstem ischaemia: TIA, occlusions of vertebrobasilar arterial system
        Vertigo not sole clinical presentation
    - - Disease specific treatment
        Symptom specific treatment
        
        Antihistamines
        -Anti-emetics
        -Benzodiazepines
        
        Vestibular rehab
        Exercise based program designed by specialty trained vestibular physical therapist to immprove balanve and reduce problems related to dizziness
        -encourages patients to perform challenging balance exercises with several potential benefits
      - Nursing considerations
        
        Assist patient make sure comfortable position
        Monitor vitals and LOC
        Fall precaution
        Keep patient calm, and room darkened to ensure comfort
        Administer medication to reduce patient's signs and symptoms