Neurological Emergencies Flashcards
1
Q
Whats the first thing we should do when they patient gets to the ER?
A
- Assess neurological status
- glascow coma scale
2
Q
If patient has deteriorated during transport what do they need?
2
A
- needs immediate non-contrast CT scan and
2. possible neurosurgery consult
3
Q
What can allow us to proceed more slowly with ER head trauma?
4
A
If patient is
- stable and
- not comatose with
- stable VS and
- no focal neurologic findings
4
Q
What is our goal in the ER setting for head trauma?
2
A
Goal is to
- prevent brainstem or uncal herniation and
- brain edema with elevated ICP that causes further brain injury
5
Q
What should be on the physical exam for an ER pt with head trauma?
5
A
- Vital signs
- Glasgow coma scale
- Examining head for signs of outward trauma (i.e. penetrating trauma, lacerations, swelling, bruises, abrasions etc.)
- Patient should be in cervical spine collar
- Neurological exam
6
Q
What is the Neurological exam consist of?
3
A
- Pupils
- Level of alertness
- Look for focal deficits
7
Q
TBI: head injury due to contact and/or acceleration/deceleration forces
- Whats a mild GCS?
- Moderate?
- Severe?
A
- Mild: GCS score 13-15 measured 30 min after injury
- Moderate: GCS 9-12
- Severe: GCS
8
Q
Clinical Features of TBI
1. 1 central feature?
- Associated symtpoms? 4
A
- (+) or (-) LOC, confusion and amnesia—important to know the presence and length of any of these symptoms
- Associated Symptoms:
- Headache
- Dizziness, vertigo or imbalance
- Lack of awareness of surroundings (disorientation)
- Nausea and vomiting
9
Q
Signs of TBI?
7
A
- Vacant stare
- Delayed verbal expression
- Inability to focus
- Slurred or incoherent speech
- Gross incoordination
- Memory deficits
- Emotionality out of proportion to events
10
Q
What is a cortical contusion and what ar the two kinds?
A
Cortical contusion: (direct trauma)
- Coup-Direct blow to brain
- Contrecoup-injury to brain on opposite side of blow
11
Q
- What is a diffuse axonal injury?
- Happens because of what kind of trauma?
- What happens at the cellular level?
A
- disruption of axonal neurofilament organization… impairs axonal transport leads to axonal swelling
- Indirect trauma
- Greatly stretches and damages nerve cells causing significant damage and even death and in adults may cause permanent brain damage
12
Q
Examples of trauma that cause diffuse axonal injury?
2
A
As in
- Shaken Baby Syndrome or
- severe whiplash that shakes or rotates the brain
13
Q
Guidelines for CT Scan in the ER?
11
A
- GCS less than 15
- Suspected open or depressed skull fracture
- Any sign of basilar skull fracture….. (hemotympanum, raccoon eyes, Battle’s sign, cerebrospinal fluid leak)
- Two or more episodes of vomiting
- 65 years of age or older
- Amnesia before impact of 3 or more minutes
- Dangerous mechanism of injury (ejected from vehicle)
- Bleeding diathesis or oral anticoagulant use
- Seizure
- Focal neurologic sign
- Intoxication
14
Q
Reading the CT Scan in ED
7 Steps?
A
- Look at cranial contours
- Cisterns- open vs. closed?
- Midline shift?
- Lesions? Type and location
- Acute blood is white
- Old blood is darker
- Ventricles and cisterns are black
15
Q
CT scan abnormalities that require consult? 4
A
- Subdural hematoma
- Intracranial bleeding
- Cerebral edema
- Significant skull trauma
16
Q
Hospitalization or transfer for those at risk:
4
A
- GCS less than 15 or deteriorating
- Abnormal CT
- Seizures
- Abnormal bleeding parameters
17
Q
Outpatient observation for GCS = 15, normal CT scan— observer to awaken patient from sleep every 2 hours check for the following warning signs:
8
A
- Inability to awaken patient
- Severe or worsening HAs
- Somnolence or confusion
- Unsteadiness or seizures
- Difficulties with vision
- Vomiting, fever or stiff neck
- Urinary or bowel incontinence
- Weakness or numbness involving any part of the body
18
Q
How should we proceed with scalp lacerations and repair?
5
A
- When repairing a scalp wound palpate the skull for depression or “step off”…..fracture
- Anesthetize wound edges with
lidocaine 1-2% with epinephrine - Epinephrine helps with hemostasis
- Thoroughly debride and irrigate
- If deep may use horizontal mattress sutures, otherwise interrupted sutures or staples
19
Q
Clinically significant skull fractures:
4
A
- pass through an air-filled space (sinus)
- associated with an overlying scalp laceration
- depressed below the level of the skull’s inner table
- overlie a major dural venous sinus or the middle meningeal artery
20
Q
What is the major sign that a skull fracture is clinically significant?
A
Clinically important if they cross the middle meningeal artery or a major venous sinus
Most other linear fractures are not clinically significant
21
Q
How can we tell between fractures and the natural sutures on the brain?
2
A
Fractures are more lucent on xray than sutures and usually wider (3mm vs 2mm for sutures)
22
Q
Skull fractures heal in children in how long?
In adults?
A
Skull fx in children heal in 3-6 months
In adults it can take 3 years
23
Q
What are depressed fractrues dangerous?
A
They are important because they predispose to significant underlying brain injury and to complications of head trauma (infection & seizures)
24
Q
- What are basilar fractures?
- Usually occur through what bone?
- Often the fracture causes a dural tear producing a communication between the what three areas?
- Can lead to infection of the what?
- Can produce a CSF leak through the?
- How can we see basilar fractures the best?
A
- Linear fractures at the base of the skull
- Usually occurs through the temporal bone
- subarachnoid space
- the paranasal sinuses
- the middle ear
- Cranial cavity
- nose
- Radiographs do not detect basilar fracture well
Usually need CT if suspected
25
1. Raccoon eyes show?
2. Battle's sign?
3. Hemotympanum?
1. Intraorbital bruising
2. Retroauricular bruising
3. Blood behind the TM
26
What is the definition of a open skull fracture?
| 2
1. Defined as open if there is an overlying scalp laceration and the dura is disrupted
2. A fracture that disrupts the paranasal sinuses or middle ear structures is also considered open
27
1. What do open skull fractures require for treatment?
| 2. What should we avoid and why (2)?
1. Open skull fractures require careful debridement and irrigation
2. Blind probing of the wound should be avoided as
- contaminants can be introduced into the wound and
- can further depress comminuted fracture pieces
28
Migraine characteristics?
| 4
1. Unilateral
2. throbbing
3. Aura
4. Do they have a hx of migraine?
29
1. First line treatment of Migraines?
| 2. Second line? 2
1. Treatment—1st line: Tryptans
| 2. Treatment—2nd line: Ketorolac + antiemetic (metoclopramide or prochlorperazine)
30
Cluster HA chracteristics?
| 5
1. men
2. excrititaing pain behind the eye
3. Hx of these
4. red, profuse tearing, running nose
5. poker in eye pain
31
Cluster HA treatments?
1. First line?
2. Second line?
1. Treatment—1st line: 100% oxygen
| 2. Treatment—2nd line: Sumatriptan
32
Worst headache ever:
1. What do we have to rule out? 5
2. Thunderclap HA?
3. Associated with what symptoms? 2
1.
- Subarachnoid Hematoma
- Bacterial Meningitis
- Cerebral Ischemia
- Subdural Hematoma
- Brain Tumor
2. Something severe
3.
- Associated with nausea +/- vomiting
- +/- focal neurologic findings
33
Seizures-Etiologies
| 8
1. Alcohol associated
2. Metabolic
3. Infectious
4. Trauma
5. CVA
6. Sleep deprivation
7. Noncompliance with anticonvulsant
8. First time idiopathic seizures
34
Alcohol associated causes of seizures?
| 3
1. Withdrawal
2. Exacerbation of idiopathic seizures
3. Acute intoxication
35
Status Epilepticus Etiologies?
| 13
1. Hyponatremia
2. Hypocalcemia
3. Hypoglycemia
4. CNS abscess
5. Meningitis or encephalitis
6. Neoplasm
7. AV malformations
8. Acute hydrocephalus
9. Intracerebral hematomas
10. CVA
11. Cyclic antidepressants (amitriptyline…Elavil)
12. Migraines
13. Failure to take anticonvulsants
36
A patient presenting with generalized seizures or status epilepticus: Management?
6
1. Airway management
2. Consider thiamine as 20-40% of seizure patients are alcoholics
3. IV established
4. Benzodiazepines 1st choice—will effectively terminate ictal activity in 75-90% patients
5. dextrose bolus,
6. Narcan
37
2nd line drugs for seizures?
| 2
Phenytoin and Phenobarbital
38
1. Why isnt phenytoin first line?
2. Phenytoin IV can cause what? 2
3. Phenobarbital causes what? 3
Phenytoin
1.
- does not suppress the electrical activity of ictogenic focus and
- takes 20 min to onset of action—benzodiazepine support should be continued
2. hypotension and bradycardia
3.
- sedation,
- depression of respiratory drive
- depression of BP so patient must be monitored closely
39
What is a post-ictal state?
| 3
1. Usually sleepy and may be confused
2. Often incontinent
3. Tongue bitten
40
Decorticate posturing can progress to decerebrate posturing. What does this indicate?
uncal herniation/brain stem injury
41
Vertigo etiologies:
1. Central? 4
2. Somatic? 2
3. Peripheral? 9
Central
1. Migrainous
2. Brainstem ischemia
3. Cerebellar infarction and hemorrhage
4. MS
Somatic
1. Panic attack
2. The “weak, dizzy, nearly fainting” patient
Peripheral
1. Benign paroxysmal positional vertigo
2. Vestibular neuritis
3. Herpes zoster oticus
4. Meniere's disease
5. Labyrinthitis
6. Perilymphatic fistula
7. Acoustic neuroma
8. Aminoglycoside toxicity (gentamicin,etc)
9. Otitis media
42
If there is nausea and vomiting with the vertigo what does this indicate?
N & V often more severe with peripheral causes
43
When would you see gait distrubances with vertigo?
central etiologies
44
Generally central etiologies last for _________, while peripheral are recurrent and last how long?
1. hours to days
| 2. for a few minutes to 2-3 hours
45
What are we looking for on the PE with vertigo?
| 2
1. nystagmus
| 2. focal neurologic signs
46
Describe nystagmus in peripheral caused vertigo and central:
1. Direction?
2. Type?
3. Effect of visual fixation?
Peripheral:
1. Unidirectional, fast phase toward the normal ear. Never reverses direction.
2. Horizontal with a torsional component, never purely torsional or vertical
3. Suppressed
Central:
1. Sometimes reverses direction when patient looks in the direction of the slow phase
2. Can be any direction
3. Not suppressed
47
Describe the following signs of peripheral caused vertigo and central caused:
1. Other neurological signs?
2. Postural signs?
3. Deafness or tinnitus?
Peripheral:
1. Absent
2. Unidirectional instability, walking preserved
3. May be present
Central:
1. Often present
2. Sevre instability, patient often falls when walking
3. Absent
48
1. What are TIAs?
2. How long?
3. Without evidence of?
1. brief stroke-like attack…
2. most symptoms last 5-20 minute, rarely longer than an hour,
3. without evidence of acute infarction
49
If neurological defects last 4 hours or longer patients often have what?
infarcts on MRI
50
Symptoms of TIAs include:
5
1. Hemiparesis, hemiparesthesia
2. Dysarthria, dysphasia, diplopia
3. Circumoral numbness
4. Imbalance
5. Monocular blindness
51
What is crucial in determining the proper therapy to prevent a second, more disabling event?
Urgently identifying the cause of a patient's first stroke or TIA
52
TIA workup:
| 1. What are the types of low flow TIAs?
1. Internal carotid:
2. MCA:
3. Vertebrobasilar:
53
What should we order for the following for low flow TIAs?
1. Internal carotid: 2
2. MCA: 2
3. Vertebrobasilar: 1
1. duplex US or transcranial doppler
2. MRA or CT angiography
3. CT angiography
54
TIA workup: What would we order?
| 2
1. EKG….. looking for atrial fibrillation
| 2. Echocardiography- embolic stroke caused by AFIB
55
What is a lacunar stroke and what is it a diagnosis of?
1.
| diagnosis of exclusion
56
Cerebrovascular Accident (CVA) is what?
Whats on our differential?
9
Sudden loss of focal brain function
Differential:
1. Seizures
2. Atypical migraines
3. Syncope
4. Transient global amnesia
5. Hypoglycemia
6. Multiple sclerosis
7. Brain tumors
8. Subdural hematoma
9. Infection
57
HOw do we distinguish what kind of CVA a pt is having?
| 4
1. Focal or nonfocal nature of the episode
2. Nature of symptoms and their progression
3. Duration and timing of symptoms
4. Associated symptoms during and after the episode if it is more like a TIA
58
Describe what positive symptoms and negative symtpoms of a CVA mean?
1. Positive sx—indicate active discharge from CNS neurons (e.g. visual, auditory, somato-sensory, motor)
2. Negative sx—indicate absence or loss of function (e.g. loss of vision, feeling or ability to move a part of the body)
59
CVA management: Goals of initial assessment?
| 4
1. Ensuring medical stability (ABCs)
2. Quickly reversing any conditions that are contributing to the patients problem
3. Moving toward uncovering the pathophysiologic basis of the patient’s neurologic symptoms
4. Screening for potential contraindications to thrombolysis in acute ischemic stroke patients
60
What should we ask about the history of a CVA? 3
PE? 5
History:
1. Find out if pt diabetic, hx of seizure disorders
2. Hx of alcohol or drug abuse
3. Meds and any recent trauma
PE
1. Thorough CV exam—for murmurs, pulses to check if irregular, listen for bruits
2. Skin—signs of endocarditis, cholesterol emboli, ecchymosis, tongue laceration
3. Fundoscopic
4. Neck immobilized if evidence of serious trauma or question of fall
5. Examine extremities for DVT, signs of systemic arterial emboli
61
Immediate studies to order for a CVA?
| 9
1. Noncontrast CT* or MRI of the brain
2. EKG
3. CBC w/ platelets
4. CMP
5. Serum glucose (do quick fingerstick glucose on admission)
6. PTT, PT and INR
7. Oxygen saturation
8. Pregnancy test if woman of child bearing age
9. Blood cultures x2 if fever
62
1. CVA treatment for all strokes? 2
2. Treatment for ischemic CVA? 2
3. Treatment for Hemorrhagic CVA? 2
1.
- Patient should be kept flat or elevate head of bed no more than 15 degrees
- BP
2.
- BP often elevated—need that perfusion pressure
- Do not treat BP unless SBP > 220 or DBP > 120
3.
- Balance between increased BP worsening bleeding and decreased BP decreasing perfusion
- Titrate BP to SBP 140-160
63
Hemorrhagic stroke on warfarin
treatment?
4
1. Need to reverse effects of warfarin
2. IV vitamin K,
3. prothrombin-complex concentrates,
4. fresh frozen plasma
64
1. When do we need to give thrombolytic therapy?
2. R/O what?
2
3. When should we give antithrombotic therapy?
1. Should be within 3-4.5 hr “window”
- -New studies allow for longer window
2.
- R/O hemorrhage
- Meet eligibility criteria (no contraindications)
3. Initiate antiplatelet agent within 48 hours of stroke onset
65
Myasthenia gravis is what?
a disorder of neuromuscular transmission affecting the ocular, bulbar, limb and respiratory muscles
66
Myasthenic crisis occurs when ?
there is severe enough weakness to necessitate intubation
67
1. Severe bulbar weakness produces what in Myasthenia gravis?
2. What do they experience as a warning?
dysphagia and aspiration that often complicates respiratory failure
Often the patient experiences generalized weakness as a warning
68
1. If the patient presents with weakness and not acute respiratory failure hw should we manage?
2. Elective intubation should be considered if what?
3. At times because of the weakness of oropharyngeal muscles, secretions cannot be handled and the patient is at risk for what? What is done in this setting?
4. Other treatment? 2
1. the forced vital capacity (FVC) can be monitored every 1-2 hours
2. serial measurements of the FVC consistently decline approaching 15 mL/kg body weight
3. aspiration so elective intubation is done in this setting
4. Plasmapharesis or IV Immune globulin are done for treatment
69
1. Acute exercerbations of MS result in what?
2. Treatment?
Sometimes MS causes seizures
Treat the seizure
1. in functionally disabling symptoms with objective neurologic impairment (e.g. loss of vision, motor and/or cerebellar symptoms)
1. Treated w/ high dose IV glucocorticoids
- --such as methylprednisolone 1000 mg IV a day for 5 days
70
1. What is neuropathic pain syndromes?
| 2. What should we ask about first?
1. Generally patients with chronic pain…. may be on prophylactic medications to control pain… but are having breakthrough pain
2. First elicit if anything new or different about pain to r/o a new injury or illness
71
Neuropathic Pain Syndrome:
If its a chronic pain exacerbation discuss with patient level of pain and options for treatment?
4
1. 1 time IM dose of dilaudid or morphine
2. 1 time dose of PO opioid
3. Start or increase prophylactic med…Neurontin (gabapentin)
4. Importance of regular follow up with primary medical provider and/or pain specialist
72
Neuropathic Pain Syndromes:
1. What can we not do?
2. What else do we need to access for?
1. DO NOT give prescriptions for narcotics
| 2. Assess for associated depression and/or anxiety that may be making pain worse and make appropriate referral
73
Presentation of Guillian-Barre Syndrome:
1. What kind of weakness?
2. Weakness starts where?
3. What can it progress to thats serious?
4. 80% will have what?
5. What kind of severe pain?
6.
1. Symmetric ascending*** muscle weakness
2. Weakness usually starts proximal legs
3. Progresses to severe respiratory muscle weakness
30% of patients will need ventilatory support
4. 80% will have paresthesias in hands/feet but sensory abnormalities on exam often mild
5. Often severe back pain
Dysautonia-70%
Tachycardia, urinary retention, HTN-hypotension
Bradycardia, ileus, loss of ability to sweat
