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MBBS 4: Accidents and Emergency > Neurological Emergencies > Flashcards

Neurological Emergencies Flashcards

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Royal College: Emergency Medicine flashcards
1
Q

Common neurological emergency presentations?

A
  1. Coma
  2. seizures
  3. Status Epilepticus
  4. Headache
  5. Acute neuromuscular weakness
  6. Intra cranial infections
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2
Q

What is a seizure?

A

excessive abnormal neuron activity associated with alterations in sensory,
motor, autonomic, and/or cognitive function.

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3
Q

What is a convulsion?

A

refers specifically to the motor manifestations of a seizure

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4
Q

What is the ictal period?

A

is the time during which a seizure or seizure-like activity occurs

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5
Q

What is the postictal period?

A

is an interval of altered mental status immediately following a seizure,
generally lasting less than 1 hour.

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6
Q

What is status epilepticus?

A

is a single seizure lasting more than 5 minutes in length or two or more
seizures without recovery of consciousness (return to baseline)
between seizures
- SE has long term consequences.

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7
Q

Causes of status epilepticus?

A
  1. metabolic disturbances
    - hepatic encephalopathy, hypocalcemia, hypo/hyperglycemia, hyponatremia, uremia
  2. infectious
    - CNS abscess, encephalitis, meningitis
  3. withdrawal symptoms
    - alcohol, antiepileptics, barbiturates
  4. CNS lesions
    - acute hydrocephalus, CVA, anoxic/hypoxic insult, brain metastases
  5. Intoxication
    - lead, isoniazid, lidocaine, metronidazole, MDMA
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8
Q

Goal of management in status epilepticus?

A
  1. Resuscitation
  2. Terminate seizure
  3. Decrease cerebral metabolic rate
  4. Diagnose and treat cause
  5. Treat complications
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9
Q

Resuscitation of status epilepticus?

A
  1. Airway
    - Risk of aspiration
    - Recovery position
    - may need suction, adjuncts ±intubation
  2. Breathing
    - Give supplemental O2
  3. Circulation
    - Initial tachycardia giving way to hypotension (especially when Benzos or Barbiturates are given)
    - IV infusion important
  4. Dextrose
    - Symptomatic hypoglycemia is causing irreversible brain injury until corrected
  5. Thiamine can be considered for alcoholics, and he malnourished
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10
Q

Pharmacological management of status epilepticus?

A
  1. Diazepam10mg iv stat, can be repeated in 15minutes if no response
  2. Lorazepam 1-2mg/midazolam 10mg can be considered if available
  3. If no response give phenobarbitone 20mg/kg IV over 20min.
    OR
    sodium valproate 15mg/kg IV over 5min or phenytoin 15mg/kg
    over 30min
  4. Consider ICU admission if no response to 2nd line anticonvulsants (phenobarbitone/sodium valproate/ phenytoin)
    - Midazolam, propofol and thiopentone infusions can be given in this setting
  5. Watch for respiratory depression and hypotension when using these drugs
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11
Q

History in status epilepticus?

A

A thorough history is the most valuable part of the workup:
1. Witness accounts
2. History of prior seizures
3. Presence of acute illness
4. Past medical problems
5. History of substance use

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12
Q

Physical exam in status epilepticus?

A
  1. Aim at finding possible cause
  2. Signs of trauma, nuchal rigidity, end organ injury
  3. Signs of pregnancy
  4. Subtle signs of seizures (tachycardia, pupil dilation and hippus, nystagmus, irregular respirations)
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13
Q

New onset seizure workup in status epilepticus?

A
  1. Urea and Electrolytes including calcium, phosphorus
  2. CT of brain
  3. Toxicology screen
  4. Pregnancy test if woman is of childbearing age
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14
Q

When to do a lumbar puncture in status epilepticus?

A
  1. New-onset seizure with fever
  2. Severe headache
  3. Immunocompromised state
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15
Q

Workup in chronic seizure disorder?

A

may need to have only serum glucose and anticonvulsant levels checked if new cause of seizure is not suspected

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16
Q

Short stay disposition for SE?

A
  1. Known epileptic with stabilization within 2hrs and identified reversible cause that can be treated within 12hrs.
  2. Patient remains seizure free for more than 12hrs after stabilization
  3. Good social support
  4. Good follow up care system
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17
Q

Long stay disposition for SE?

A
  1. New onset seizure
  2. Known epileptic with defined severe cause of SE
  3. Persistently unconscious for more than 2hrs
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18
Q

What is a headache?

A

Headache is a pain related to irritation and/or inflammation of intracranial or extracranial structures with pain receptors (e.g., meninges, cranial nerves, blood vessels)

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19
Q

Types of headaches?

A
  1. Primary headache: a headache that is not caused by another underlying condition
    - Includes migraine headache, tension headache, trigeminal autonomic cephalalgias (e.g., cluster headache)
  2. Secondary headache: a headache that is caused by another underlying condition (e.g., trauma, space-occupying lesion)
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20
Q

Associated symptoms of headaches?

A

altered mental status
seizure
fever
neurologic symptoms
visual changes

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21
Q

Medication history in headaches?

A
  1. anticoagulants/antiplatelets
  2. recent antibiotic use
  3. immunosuppressants
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22
Q

Past history in headaches?

A
  1. no prior headache
  2. change in headache quality or progressive headache worsening over weeks/months
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23
Q

Associated conditions with headaches?

A
  1. pregnancy/postpregnancy status
  2. SLE
  3. Behcets disease
  4. vasculitis
  5. sarcoidosis
  6. cancer
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24
Q

Physical exam in headaches?

A
  1. altered mental status
  2. fever
  3. neck stiffness
  4. papilledema
  5. focal neurologic signs
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25
Q

Management of headaches?

A
  • Full neurological/cardiac and relevant system examination
  • Fundoscopy
  • Analgesia
  • LP and broad spectrum antibiotics ASAP if meningitis suspected
  • CT/MRI if raised ICP/SOL or stroke suspected
  • Discuss with senior if not sure
  • Admit if serious cause suspected
26
Q

What is non-traumatic subarachnoid hemorrhage?

A

Refers to extravasated blood in the subarachnoid space.
* Presence of the blood activates meningeal nociceptors, leading to
diffuse occipital pain along with signs of meningismus

27
Q

Causes of subarachnoid hemorrhage?

A
  1. Aneurysmal rupture accounts for 80% of cases
  2. arteriovenous malformations
  3. cavernous angiomas
  4. mycotic aneurysms
  5. neoplasms
  6. blood dyscrasias.
28
Q

Risk factors for SAH?

A
  1. Age, smoking
  2. Hypertension
  3. Cocaine use
  4. Heavy alcohol use,
  5. Connective tissue disorders
  6. Sickle cell disease
  7. First degree relatives with aneurysms
29
Q

Symptoms of SAH?

A
  1. Cataclysmic thunderclap headache, “the worst headache of my life.”
  2. The onset of headache may be associated with exertion, the Valsalva maneuver
  3. The headache peaks in intensity within seconds to minutes.
  4. Associated signs/symptoms include syncope, nausea and vomiting, neck stiffness, photophobia, and seizures.
30
Q

Physical examination

A
31
Q

Physical exam in SAH?

A
  1. Findings depend on the extent of the SAH.
  2. Meningism is present in more than 50% of patients
  3. Funduscopic examination may reveal retinal or subhyaloid hemorrhages
  4. Up to 20% have focal neurologic abnormalities.
  5. Patients also may have isolated third or sixth nerve palsy.
  6. Approximately 50% of patients with a ruptured aneurysm are restless or have an altered level of consciousness.
  7. Up to one-third of patients recall a sentinel headache days to weeks before diagnosis of subarachnoid hemorrhage.
  8. Outcome largely dependent on clinical presentation and CT findings
32
Q

Diagnosis of SAH?

A
  1. CT brain
    * Blood will be noted in the subarachnoid space, and angiogram may be indicated to diagnose an aneurysm
  2. LP
    * Blood that does not clot in CSF
    * Xanthochromia may be seen
33
Q

Treatment of SAH?

A
  1. Aimed at treating acute medical and neurologic complications, preventing recurrent hemorrhage,
    and forestalling the ischemic complications of vasospasm
  2. Nimodipine 60mg every 4 hours
  3. Blood pressure monitoring, analgesia
  4. Anticonvulsants if seizures present
  5. Referral to neurosurgery depending cause
34
Q

What is acute muscle weakness?

A
  • Fatigue describes the inability to continue performing a task after
    multiple repetitions
  • Primary weakness is inability to perform the task, the first time
35
Q

Causes of muscle weakness?

A
  1. electrolyte
    - hypercalcemia, hyper/hypokalemia, hyper/hypomagnesia
  2. endocrine
    - acromegaly, primary hyperparathyroidism, vit D deficiency
  3. rheumatologic
    - polymyalgia rheumatica, systemic sclerosis/scleroderma
36
Q

Medications that can cause muscle weakness?

A
  1. amiodarone
  2. ARVs: zidovudine, lamivudine
  3. chemotherapy
  4. cocaine
  5. corticosteroids
  6. statins
  7. NSAIDs
  8. penicillin
37
Q

Infectious causes of muscle weakness?

A
  1. EBC
  2. HIV
  3. influenza
  4. lyme disease
  5. meningitis
  6. polio
  7. rabies
  8. syphilis
  9. toxoplasmosis
38
Q

Neurological causes of muscle weakness?

A
  1. CVA
  2. subdural/epidural hematoses
  3. Guilian Barre syndrome
  4. Multiple sclerosis
  5. neoplasm
  6. botulism
  7. myasthenia gravis
  8. organophosphate intoxication
  9. spinal cord injury
  10. spinal muscle atrophy
39
Q

History of muscle weakness?

A
  • R te of onset and progression – acute vs chronic with slow
    progression
  • Fatigable weakness
  • Trauma
  • Associated symptoms
  • Travel history, toxin exposure, drug history, family history
40
Q

Examination of muscle weakness?

A
  • Full neurological examination:
  • Grade and define area of weakness
  • Muscle tenderness
  • Tendon reflexes
  • Associated sensory loss
  • General examination
  • Identify causes that other causes of muscle weakness
41
Q

Investigating muscle weakness?

A
  • Dependent on suspected cause
  • Bloods
  • U&E,
  • liver function test
  • thyroid function may assist where cause unclear
  • CSF - cells, protein, blood, culture if meningitis of GBS suspected
  • Nerve conduction tests
  • Creatine kinase
  • Viral studies
42
Q

Treatment of muscle weakness?

A
  • Watch for respiratory failure
  • Treatment of electrolyte imbalance, vitamin deficiencies, toxins and
    drug withdraw or Correction of organ failure/treatment of systemic
    illness may reverse weakness
  • Myasthenia – pyridostigmine 60mg, some require thymectomy
  • Acute polymyositis- Corticosteroids
43
Q

What is Guillain Baree syndrome?

A

Acute polyneuropathy characterized by immune-mediated peripheral nerve myelin sheath or axon destruction
* Progressive weakness of limb muscles and ventilation
* Typically follows an infectious process (2/3)

44
Q

Causes of Guillain Barre syndrome?

A
  1. C. jejuni
  2. CMV
  3. EBV
  4. M. pneumoniae
45
Q

Features of Guillain Barre syndrome?

A
  1. Presents with ascending numbness/tingling, can be painful
  2. Weakness typically follows sensory disturbances
  3. Areflexia/hyporeflexia
  4. Autonomic dysfunction
    - Labile BP, arrhythmia
  5. Bowel and bladder function typically spared
  6. Symptoms should not proceed >8 weeks
46
Q

Investigations in Guillan Barre syndrome?

A

The diagnosis is mostly historical
1. lumbar puncture
2. CSF analysis shows high protein levels (>45 milligrams/dL)
3. WBC counts typically 100 cells/mm3
4. Electrodiagnostic testing demonstrates demyelination.
5. Nerve biopsy reveals a mononuclear inflammatory infiltrate.

47
Q

Treatment of Guillan Barre syndrome?

A
  1. Assessment of respiratory function.
  2. Monitor vital capacity, with normal values ranging from 60 to 70 mL/kg.
  3. IV immunoglobulin and plasmapheresis shorten the time to recovery (Should be started within 2
    weeks )
  4. Corticosteroids have not been shown to be beneficial
48
Q

Intubation criteria in Guillan Barre syndrome?

A
  1. VC <15-20 mL/kg (<30% baseline), PO2<70 mmHg, Oropharyngeal weakness, weak cough, suspected
    aspiration
  2. Intubation before development of airway compromise decreases the incidence of aspiration and other
    complications.
  3. Avoid depolarizing neuromuscular blockers like succinylcholine for intubation in Guillain Barré syndrome due to the risk of a hyperkalemic response.
49
Q

Disposition in Guillan Barre syndrome?

A
  1. Admit patients to a unit where cardiac, respiratory, and neurologic functions can be monitored.
  2. Even if a patient does not initially meet the criteria for intubation, intensive care unit admission may still be indicated in order to avoid sudden, unmonitored respiratory failure
50
Q

What is acute spinal cord compression?

A

Presents with signs of impending or established paraparesis
May present with back or neck pain, incontinence

51
Q

Signs of acute spinal cord compression?

A
  • Fever (abscess), gait trouble, weakness or sensory deficit below lesion
  • Imaging
  • MRI
52
Q

Treatment of acute spinal cord compression?

A
  • IV corticosteroids
  • Surgical decompression
  • Chemotherapy/steroid for malignant lesions
53
Q

CNS infections

A
  • Infectious prodrome usually present
  • Neurologic symptoms can evolve rapidly
  • May produce global (encephalitis) or focal (abscess) signs
54
Q

Diagnosis of CNS infections?

A
  • Meningeal irritation (meningitis)
  • Systemic signs (e.g. rash in meningococcus)
  • Imaging (CT) if focal signs
  • Blood cultures
  • CSF exam
55
Q

Treatment of CNS infections?

A

Specific to cause

56
Q

ABCs in acute stroke syndrome?

A
  1. NPO, intubate for inadequate airway, ventilate if needed
  2. Correct hypotension, rule out acute
    MI or arrhythmia (a-fib)
  3. Rule out hypoglycemia
  4. Blood glucose is between 50 and 400 mg/d
57
Q

Treatment of acute stroke syndrome?

A
  1. Use parenteral antihypertensive Tx
    only for sustained, very high BP
    (>220/120; or >185/110 for IV tPA)
    maintained under 185/110
  2. IV tPA must be/may be given
    within 4.5 hrs of stroke onset
    <5 sec,
  3. Normal PTT, PT>100,000
    platelets
  4. No bleeding, recent surgery, MI,
    arterial puncture or LP
  5. No blood, or edema/infarct >
    1/3 of MCA territory on CT
58
Q

Localization of stroke?

A
  • Central nervous system
  • Left hemisphere
  • Dominant in 99% of R handers, 60-70% L
    handers
  • Cortex: perisylvian language area
  • Expressive, nonfluent aphasia (frontal lobe)
  • Receptive aphasia (temporal lobe)
59
Q

Acute stroke symptoms?

A
  1. Hemiparesis or isolated limb weakness
  2. Hemisensory deficit
  3. Monocular or binocular (typically
    homonymous) vision loss
  4. Brainstem deficits (diplopia, dysphagia,
    deafness, crossed sensory or motor signs)
  5. Ataxia of limbs or gait
  6. Cortical signs (aphasia, neglect, apraxia…)
60
Q

Subcortical/lacuna strokes?

A
  1. Caused by occlusion of small
    penetrating branches of cerebral
    arteries
  2. Chronic HTN>DM>emboli
61
Q

Diagnostic tests?

A
  1. CT scan
    - in deteriorating patient, quickly rules out hemorrhage, mass (tumor, abscess) or early infarct
    edema
    - shows cortical infarcts by 1
    2 days, may miss lacunar infarcts
  2. MRI
    - highest resolution scan, but longer scanning time
    - DWI (diffusion weighted imaging) detects impaired movement of water in infarct immediately
    - non-invasively view arterial supply (MRA)
    - contraindications: pacemaker
62
Q

Acute stroke in younger patients?

A
  • Arterial
  • HIV infection
  • Dissection (spontaneous, traumatic)
  • Fibromuscular dysplasia, Marfan’s, vasculitis
  • Vasoactive drugs: cocaine, Migraine, amphetamines
  • Paradoxical cardiac embolus (PFO)
  • Hypercoagulable states : HIV

MBBS 4: Accidents and Emergency (34 decks)

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