neurologic emergencies
Post on 02-Jan-2016
39 Views
Preview:
DESCRIPTION
TRANSCRIPT
Case 1 A 71 year old male presents for progressive difficulty
walking Developed back pain several weeks ago Reports numbness in his legs Has been having increasing difficulty walking
Physical Examination Vitals stable Normal cranial nerve findings Increased tone of the LE bilaterally with moderate LE
weakness; UE’s normal LE reflexes are brisk with upgoing toes; UE reflexes
normal Reduced sensation to all modalities to mid-abdomen Gait slow with a spastic quality & requiring assistance
Case 1Can you localize the lesion?
LocalizationCentral nervous
systemBrain
Spinal cord
Peripheral nervous system
Nerve root
Plexus
Peripheral nerve
Neuromuscular junction
Muscle
4
The most important step in neurologic localization is
differentiating a central nervous system lesion from a peripheral
nervous system lesion
LocalizationUpper motor neuron
Mildly reduced bulk
Increased tone
Mild/moderate weakness
Hyper-reflexia & pathologic responses
Lower motor neuron
Severely reduced bulk with fasciculations
Reduced tone
Severe weakness
Hypotonia
5
Grading muscle power5: Full strength4: Movement against some resistance3: Movement against gravity only2: Movement with gravity eliminated1: Flicker or trace contraction0: No contraction
Grading reflexes4: Hyper with pathologic responses 3: Hyperactive2: Normal1: Diminished0: Absent
LocalizationSpinal levels
S1/2S1/2
L3/4L3/4
C5/6C5/6
C7/8C7/8Its easy to Its easy to
remember…1/2, remember…1/2, 3/4, 5/6, 7/83/4, 5/6, 7/8 ALWAYS ABNORMAL:
Asymmetric reflexes
Pathologic responses (Babinski, clonus = CNS)
Absent reflexes (PNS)6
Case 11. What studies do you want to order and why?
Where does the spinal cord end?
Spinal Cord CompressionManagement
Dexamethasone (100 mg IV followed by 16 mg PO daily in divided doses)
Surgical evaluation
Radiotherapy
Differential
Metastatic disease
Epidural hematoma
Epidural abscess
Vertebral collapse (2’ malignancy)
Aortic dissection
Case 2 28 year old male presents for progressive difficulty
walking “Stomach flu” 2 weeks ago Recently developed low back pain and paresthesias in
his feet Has been having difficulty standing, climbing stairs, and
has been tripping frequently
Physical Examination Vitals stable Cranial nerves normal Tone is relatively reduced; There is mild weakness of
bilateral ankle dorsiflexion with normal muscle bulk Distal sensation is reduced to all modalities but normal
in the trunk Reflexes are reduced throughout There is a mild bilateral foot drop
Case 2Can you localize the lesion?
LocalizationCentral nervous
systemBrain
Spinal cord
Peripheral nervous system
Nerve root
Plexus
Peripheral nerve
Neuromuscular junction
Muscle
13
The most important step in neurologic localization is
differentiating a central nervous system lesion from a peripheral
nervous system lesion
Localization
REFLEX ARC
Case 21. What studies do you want to order and why?
What else do you need to get the above done?
Test ResultsCSF Analysis
WBC 2
RBC 0
Protein 103 (15-45)
Glucose 50
Coags and platelets WNL
EMG/NCV
Conduction block
Guillain-Barre Syndrome
Clinical FeaturesTypically follows an
infectious process (2/3rds of pts) C. jejuni, CMV, EBV, M.
pneumoniaePresents with
numbness & tingling in the feet that ascends Pain the back & limbs
is commonWeakness follows
sensory disturbances
Areflexia Bowel & bladder are
usually spared Autonomic dysfunctionSymptoms should not
proceed >8 weeks 98% of pts achieve
“plateau phase” by 4 weeks
Duration of “plateau” 12 days
17
Ancillary studiesAlbuminocytological dissociation with elevated
CSF protein with no or a few mononuclear cellsMay be normal in the first week If WBC count >10 think about Lyme, HIV, sarcoidosis
Antiganglioside antibodiesGM1 Abs (correlate with C. jejuni infection)GQ1b associated with C. Miller Fisher variant (ataxia,
areflexia & ophthalmoparesis)
Electrophysiologic data (EMG/NCV)Temporal dispersion, prolonged F-wave latencies,
conduction block & demyelinating range slowing18
Guillain-Barré syndromeGuillain-Barré syndrome
Guillain-Barré syndrome: Subtypes
AIDP Most common type
AMAN 10%-20% of
caseprogressive weakness often with respiratory s
Rapidly failure DTRs can be preserved or
exaggerated! 75% positive for C. jejuni
(vs. 42% in AIDP) GM1, GD1a, GD1b Abs
AMSAN Possibly the most severe
form with slow and/or incomplete recovery
Miller-Fisher variant Ataxia, areflexia,
ophthalmoplegia GQ1b Abs in almost all
patients
Pure sensory
Pure dysautonomic CV involvement is the
most common
Pharyngeal-brachial-cervical GT1a Abs May mimic MG
Paraparetic
19
IVIG (0.4g/kg/day for 5 days) is at least effective as plasma exchange without some side effectsShould be started within 2 weeks Inconclusive data that IVIg has a higher relapse
rate
Corticosteroids have not been shown to be beneficial
Intubation criteria:VC <15-20 mL/kg (oe <30% baseline)PO2<70 mmHgOropharyngeal weakness20
TreatmentTreatment
GBS vs ATM
Case 1A 27 year old female presents to the ER by her
husband for “sudden onset of confusion” The patient is not following commands and is not
talking
Physical Examination She was unable to answer any questions, follow
commands, repeat, or produce spontaneous language
She had right lower facial weakness She had right arm weakness She had decreased sensation over her right arm
and face
Case 3Can you localize the
lesion? Central nervous
system, left hemisphere
The patient has right sided weakness and aphasia, which is highly suggestive of a left hemispheric stroke.
QuestionsWhat helps differentiate cortical from subcortical?
Cortical lesions can be associated with multimodal motor and sensory deficits, such as aphasia and apraxia
White matter lesions (subcortical lesions) usually cause weakness, spasticity, pure motor syndromes…but not aphasia, apraxia, etc.
Stroke: Subcortical strokes
Caused by occlusion of small (0.5-15.0 mm) penetrating branches of cerebral arteries
Chronic HTN>DM>emboli
25
Syndrome Presentation LocalizationPure Motor Face, arm, leg Internal capsule
Pure Sensory Face, arm, leg Thalamus
Sensorimotor Face, arm, leg Thalamocapsular
Ataxic-hemiparesis
Hemi-ataxia & hemiparesis
Basis pontis
Clumsy hand dysarthria
Dysathria, incoordination
Genu of the IC
Acute stroke syndrome
A-B-C’s NPO, intubate for
inadequate airway, ventilate if needed
Correct hypotension, rule out acute MI or arrhythmia (a-fib)
Rule out hypoglycemia Blood glucose is between 50 Blood glucose is between 50
and 400 mg/dland 400 mg/dl
Minimize hyperglycemia by running an IV of 0.9% normal saline initially at a TKO rate
Use parenteral antihypertensive Tx only for sustained, very high BP (>220/120; or >185/110 for IV tPA) BP maintained under 185/110BP maintained under 185/110
IV tPA must be/may be given within 4.5 hrs of stroke onset
Neuro deficit (NIHSS score 5 Neuro deficit (NIHSS score 5 to 22) must not be rapidly to 22) must not be rapidly improving (TIA) or post-ictalimproving (TIA) or post-ictal
Normal PTT, PTNormal PTT, PT<<15 sec, 15 sec, platelets platelets >>100,000100,000
No bleeding, recent surgery, No bleeding, recent surgery, MI, arterial puncture or LPMI, arterial puncture or LP
No blood, or edema/infarct > No blood, or edema/infarct > 1/3 of MCA territory on CT1/3 of MCA territory on CT
TIME IS BRAIN!!!
Clinical HistoryWhat imaging test do you want to order?
CT scanCT scan in deteriorating patient, quickly rules out hemorrhage, in deteriorating patient, quickly rules out hemorrhage,
mass (tumor, abscess) or early infarct edemamass (tumor, abscess) or early infarct edema shows cortical infarcts by 1-2 days, may miss lacunar shows cortical infarcts by 1-2 days, may miss lacunar
infarctsinfarcts
MRI scanMRI scan highest resolution scan, but longer scanning timehighest resolution scan, but longer scanning time DWI (diffusion weighted imaging) detects impaired DWI (diffusion weighted imaging) detects impaired
movement of water in infarct immediatelymovement of water in infarct immediately non-invasively view arterial supply (MRA)non-invasively view arterial supply (MRA) contraindications: pacemakercontraindications: pacemaker
Non Infused Head CT
Non Infused Head CTWhat is your impression of the head CT?
The CT shows loss of gray-white junction and effacement of the sulci throughout the left hemisphere, suggestive of a stroke
EvaluationBased on the patient’s history, physical exam
findings, and CT scan, she was taken to Interventional Radiology for a cerebral angiogram…
Cerebral Angiogram
Angiogram
MCA MCA occlusionocclusion
Clinical HistoryThe patient received intra-arterial t-PA.
Following the procedure, she was transferred to the Neuro-ICU for observation and management. A follow-up MRI was obtained later…
MRI (Diffusion Weighted Image)
QuestionsWhat do you think this patient’s long-term
outcome was? The patient presented within 3 hours of the onset
of symptoms. She received intra-arterial t-PA which was effective in breaking the clot and re-establishing flow to the left hemisphere. She was speaking English by the end of the day…and French (her second language) the next day. Because her symptoms were recognized quickly and action was taken, her injury was limited.
Cerebral Angiogram Post t-PA
Pre tPAPre tPA Post tPAPost tPA
QuestionBy the time everything was done, it was 4:15 in
the afternoon on a Friday. You have time to order one test that might change your management that night….what would you order (ie, what would you be looking for that would have caused her stroke?)
QuestionAnswer….
Lower extremity venous doppler to look for the presence of a deep vein thrombosis (some people would argue for an echo…)
The patient was found to have a DVT and received an IVC filter.
How did a blood clot in her leg get into her left middle cerebral artery? She had a patent foramen ovale (upwards of 30%
of the population do)
Case 4 A 34 year old female presents to the ER with
complaint of eyelid drooping Started about one weak ago following an ER; she was
given steroids for an asthma exacerbation and ciprofloxacin for an asymptomatic UTI
Has felt “weak all over” and has been getting progressively short of breath
Physical Examination Speech is soft with a nasal quality There is fluctuating bilateral ptosis, pupils are equal
and reactive, she has a “snarl” smile Normal bulk/tone; strength can be overcome after
<60s of effort Normal reflexes, normal sensory examination Gait normal, but cannot stand up 10 times
consecutively
Case 4Can you localize the lesion
Peripheral NS
The PNS generally includes The nerve cell bodies The peripheral nerves
RootsPlexusNerve
The neuromuscular junctions (NMJs)
The muscles
43
LocalizationNMJ
Fluctuating weakness (pre- and post-synaptic)
Normal bulk and tone
Normal sensory exam
Normal reflexes (usually)
Case 2How do you want to evaluate the patient?
Studies to Order/Perform Diagnostic
Ice Pack Test Improves ptosis 2° MG in 80% Local cooling slows kinetics of AChRs
Sleep TestTensilon Test
Respiratory Studies!!! BMP w/ Mg/Phos, PT/PTT, ionized calcium May need Quinton catheter placed by IR
Case 2Studies
EMG/NCS with repetitive stimulation or single fiber EMG
Chest CTThose who undergo
thymectomy are more likely to have clinical improvement, become asymptomatic or attain remission
May be less effective in those >60
Labs AChRAb
85% of pts w/ gMG and 50-60% w/ oMG test positive
MuSK antibody Striational muscle
Ab Screen for TSH, RA,
Pernicious anemia, SLE, Sarcoid, Sjogren’s, polymyositis
Case 2 Admit to ICU
Any pt w/ MG w/ questionable respiratory status should be admitted to the ICU for close monitoring
14% of pts in myasthenic crisis have some degree of arrhythmias
Respiratory 30% of pts develop respiratory muscle weakness and
crisis occurs in 15-20% Intubation Criteria/Management:
VC < 15 mL/kg Stop anti-cholinesterase medication (causes excessive
bronchial secretions and diarrhea) If needed, give pyridostigmine IV at 1/30th the oral dose
Case 2 Acute Treatment
TPE Produces impvt in 75% of pts
Long term medication Pyridostigmine 15-60 mg Q3-6
Long acting 180mg Pts w/ primarily ocular symptoms respond poorly
Corticosteroids 10-20 mg/daily initially Increase by 5-10 per week until satisfactory clinical
response or dose of 50-60/day Azathioprine
2-3 mg/kg initially (most start w/ 50 mg/d for 1 week)
Case 5A 32 year-old woman is found on the floor at
work, unconscious, but spontaneously breathing.
Physical Examination BP is 146/75, pulse 80, afebrile. There is complete left lid ptosis. Her left pupil is
5 mm and sluggishly reacts to light; the right pupil is 2 mm and briskly reacts to light.
She does not grimace or move to painful stimuli, nor attempt to speak.
Case 5Can you localize the lesion?
Evaluating the Altered Patient
1. What does the patient look like?Old?How many lines?Noisy neighbor? Jerry Springer is
blasting away and they are tangled in their call light?
Like you need to call the unit?
Evaluating the Patient2. Talk to the patient
Can they stay awake and pay attention to you? Can the patient talk to you?
How do they sound (abnormal rate, dysarthric…)Are they making any sense?
Can they tell you where they are?Patients are first disoriented to time of day, then other
aspects of time, and then to placeDisorientation to self is rare…like raise the red flag
rare
Evaluating the Patient3. Ask them to read and write
Decreased reading comprehension is characteristic of delirium
Writing disturbance is the most sensitive language abnormality in deliriumThe most salient characteristics are abnormalities in
the mechanics of writing…the formation of letters and words is indistinct, and words and sentences sprawl in different directions
Evaluating the Patient4. How does his/her breathing look?
Does it look like he/she is breathing comfortably and can protect the airway?
What does the breathing pattern look like?Rule of thumb: if breath sounds can be
heard at both lung bases and if the RR is >8/min, ventilation is probably adequateQuick FVC: How high can they count with one
breath (counting to 20 is roughly equal to 2 L)ABG is the only certain method of determining
adequate ventilation
Evaluating the Patient5. What do the eyes look like?
The eyes are your biggest friend in an emergency When examining pupils, make sure the lights are
off and the room is as dark as possible Use a bright light If there are abnormalities, ask to look at a drivers
license or other photo or ask family members (is it old or new?)
Evaluating the Patient: The Eyes
1. Observe for blinking at rest, to light, to threat, or loud sound
2. Observe the position of the eyelids Lift and release the lids, noting the tone In unconscious pts the eyelids close gradually after they
are released, a mvt that can not be duplicated voluntarily by a hysterical patient
3. Observe the position of the eyes A light held 50 cm from the face should reflect from the
same point on each pupil if the eyes lie on conjugate axes
4. Test for corneal reflex (if the patient is not easily arousable) Should cause bilateral response of eyelid closure and
upward deviation of the eye (Bell’s phenomenon)
Evaluating the Patient6. Observe the size of the pupils and
reactivity to lightThe presence or absence of the light reflex is
the single most important physical sign potentially distinguishing structural from metabolic coma
Pupillary pathways are relatively resistant to metabolic insult; midbrain lesion destroy it
Both anatomic innervations (sym and parasymp) are tonically active, and the resting pupil represents a balanceUnopposed parasymp pupil: 1.5-2 mmUnopposed symp pupil: 8-9 mm
Coma: pupil size and reactivity
Smaller, reactive pupils persist in metabolic coma
Larger, unreactive pupil(s) reflect third cranial nerve or midbrain lesion
Pinpoint, reactive pupils from pontine lesion (or narcotic overdose)
Medicinal eyedrops may impair light reflex
Evaluating the Patient7. Examine for the Oculocephalic reflex (“Doll’s
Head Eye Phenomenon”) Hold the eyelids open and briskly rotate the head
from one side to the other, at least briefly holding the endpointsPositive response: contraversive conjugate eye
deviation (head to the right, eyes to the left) Briskly flexed and then extended
Positive response: deviation of the eyes opposite; the eyelids may open reflexly (dolls head phenomenon)
Evaluating the Patient8. Cold calorics (oculovestibular reflex)
Can be very helpful in evaluating for brain death Not useful in an acute setting as it is time
consuming and somewhat cumbersome
Evaluating the Patient 9. Examine the motor
function What is the tone
(normal, flaccid rigid) What is the strength (if
the patient can cooperate) or response to pain Apply nailbed
pressure or other noxious stimuli
Normal response: pushing the stimulus away, quick and non-stereotyped withdrawal of the limb, or mvt of the body and limb away from the stimulus
Evaluating the Patient10. Check the Reflexes
Have a reflex hammer (even skilled examiners cannot elicit reflexes with a stethescope)
Reflexes should be symmetric Upgoing toes/pathologic reflexes always indicate
some CNS dysfunction
Case 5What test do you want to order for this patient?
Subarachnoid hemorrhage
Berry aneurysm Berry aneurysm commonest if no commonest if no traumatrauma
Verify blood by CT, Verify blood by CT, or LP if CT normalor LP if CT normal
Emergent angio and Emergent angio and surgical or surgical or interventional interventional managementmanagement
Intubate if GCS <8 or hypoxemia
IV Fluids (2L 0.9% NS)
MAP ≤120 mm Hg and systolic <180 mg Hg
Nimodipine 60 mg 6xs/daily
Phenytoin (if seizures occur)
EVD for acute hydrocephalus
top related