Neuro ICU Book Flashcards
Most important step for a patient with high-grade acute SAH with poor mental status and IVH?
EVD
SAH with IVH cause of vertical eye movement impairment and depressed level of arousal
Acute obstructive hydrocephalus from mass effect on thalamus and midbrain
Independent risk factor for development of symptomatic vasospasm after SAH
IVH
Hunt and Hess SAH grade: asymptomatic or mild headache and slight nucal ridigity
Grade I
Hunt and Hess grade for SAH: moderate to severe headache, nucal rigidity, no neurologic deficit other than cranial nerve palsy
Grade II
Hunt and Hess grade for SAH: drowsiness, confusion or mild focal deficit
Grade III
Hunt and Hess Grade for SAH: stupor, moderate to severe hemiparesis, possibly early decerebrate rigidity and vegetative disturbances
Grade IV
Hunt and Hess Grade for SAH: deep coma, decerebrate rigidity, moribund appearance
Grade V
In patients with aneurysmal SAH, does initial GCS correlate with long-term outcome?
Yes
Fischer Scale of SAH: no detectable SAH on CT scan
1
Fisher Scale of SAH: diffuse SAH, no localized clot >3 mm thick or vertical layers >1 mm thick on CT scan.
2
Fisher Scale of SAH: localized clot >5 x 3 mm in subarachnoid space or >1 mm in vertical thickness.
3
Fisher Scale of SAH: Intraparenchymal or intraventicular hemorrhage with either absent or minimal SAH on CT scan.
4
Which Fisher group has the highest incidence of vasospasm?
3
Modified Fisher Scale with thick diffuse or localized thick SAH and IVH
4
Modified Fisher Scale with diffuse thick or localized thick SAH and absent IVH
3
Modified Fisher Scale with diffuse thin or localized thin SAH and IVH
2
Modified Fisher Scale with diffuse or localized thin SAH and absent IVH
1
Modified Fischer Scale with no SAH and IVH
2
Modified Fisher Scale with no SAH and no IVH
0
The quantitative blood volume in contact with the cisternal space (directly in cisternal subarachnoid or intraventricular space) acts as what type of burden? And what is the risk of DCI?
Cumulative blood burden
Increased risk of DCI
What is the most consistent predictor of vasospasm after SAH?
Amount of SAH on the post ictal CT scan (IVH also a risk but not as strong)
What is the step-wise progression for treating intracranial hypertension after SAH?
Surgical Decompression (EVD, decompressive craniotomy or craniotomy)
1. Sedation with short-acting agents (IV propofol, versed or fentanyl)
2. Hyperventilation and osmotic agents (hyperventilation, mannitol 1 - 1.5 g/kg, hypertonic saline 30 mL 23.4%/5 mins q4-6h PRN, avoid Na >155)
3. Barbiturate Coma (pentobarbital: 10 mg/kg over 1 hr then 1-3 mg/kg/hr to 1-2 burst per 10 sec suppression - causes cardiac suppression, t 1/2 = 15=50 hrs)
4. Therapeutic hypothermia (32-34 deg C)
What are antishivering methods for therapeutic hypothermia?
- Skin counterwarming (warm, forced-air blankets)
- IV magnesium (60-80 mg/kg then 2g/hr)
- Buspirone (20-30 mg TID)
- IV dexmetomidine (0.4 - 1.5 microgram/kg/hr)
- IV meperidine (0.4 mg/kg q4-6 h 0 usual dose: 25-50)
- IV propofol (50-100 mg rapid IV push, 0.3-3 mg/kg/hr maintenance)
- IV Clonidine (1-3 micro gm/kg prn)
Caution with labetalol after ICH
Bradycardia
CHF
Bronchospasm
Caution with esmolol after ICH
Bradycardia
CHF
Bronchospasm
Caution with nicardipine after ICH
Severe aortic stenosis
Myocardial Ischemia
Caution with Fenoldopam after ICH
Tachycardia
Headache
Nausea
Flushing
Glaucoma
Portal Hypertension
Caution with Nitroprusside after ICH
Increased ICP
Variable response
Myocardial Ischemia
Thiocyanate and cyanide toxicity
Agents for RSI that don’t affect ICP
Propofol
Etomidate
Cis-atricurium
Vecuronium
Mannitol dosing (initial and bolus) with goal mOsm/kg
Initial dose: 1.0 - 1.5 g/kg 20% solution
Bolus dose: 0.25 - 1.0 g/kg
Goal: 300 - 320 mOsm/kg
Admission hyperglycemia in ICH is a predictor of what?
30 day mortality (diabetics and non-diabetics)
Goal Na and mOsm with hyperosmolar therapy?
Na: 150 - 155
mOsm/L: 300 - 320
Treatment of seizures in ICH
Lorazepam 0.05 - 0.1 mg/kg -> loading phenytoin or fosphenytoin (20 mg/kg)
May benefit from seizure prophylaxis
Predictors of seizures in ICH
Lobar location
Small hematomas
Risk factors for ICH
Age
Male
African Americans
Japanese
HTN
CAA
Cocaine
Low cholesterol levels
Oral anticoagulants
Excessive Etoh abuse
First AED for seizures IV and if IV access can’t be established?
IV: Lorazepam
No IV access: midazolam (10 mg IM, buccal or intranasal) or diazepam (20 mg rectal)
What should all patients with GCSE get after benzo and why?
Second-line antieplileptic
Benzodiazepines are not long term therapy that prevent recurrence of SE - instead of first and second line in sequence, give second-line with benzo (do not delay second-line AED to see if patient responds to initial benzo) - the benzo is the first line therapy
Phenytoin/fosphenytoin, valproate, levetiracetam, lacosamide and phenobarbital
Treatment for RSE
Add third line AED
Rapid and aggressive escalation with continuous IV anethestics with intubation: midazolam, propofol, pentobarbitol
If unable to intubate: valproic acid if not already used as second line
Traditionally: phenobarbital load with escalation to cIV pentobarbital (however, with caveats of barbiturates, preference for versed/midazolam and propofol have emerged)
Status epilepticus titration goal for cIV propofol and barbiturates and midazolam
Propofol and barbiturates: burst suppression
Midazolam: seizure supression
Maintain for 24 hours while conventional AED levels are optimized
Definition of super refractory status epilepticus
SE that continues for 24 hours or more after initiation of anesthetic agents
What is the potential problem of using valproic acid and phenytoin at the same time?
Valproate produces inhibition of CYP2C9 that leads to inhibition of clearance of phenytoin
Valproate also displaces the drug from it’s protein binding sites -> increasing the free fraction and total amount of phenytoin present
Closely monitor and follow total levels and free levels of phenytoin
What drug can be used in RSE if a patient doesn’t have an ileum for prevention of breakthrough and withdrawal siezures during tapering cIV infections?
Enteric topic image
Dosage: 300 - 1600 mg/d to abort RSE
Meds that can be used in SE when weaning from cIV meds?
Lacosamide
Enteric topiramate
Oxcarbazepine
Fella ate
Pregabalin
Carbamazepine
Ketamine
Issues with using inhaled anesthetics (isoflurane, halothane and desflurane) in terminating refractor SE?
Hypotension
Logistic issues in ICU
Frequent seizure recurrence upon withdrawal
When do you see generalized periodic discharges and what should be done about them?
Range of periodic or rhythmic patterns that don’t meet formal seizure criteria and aer seen after convulsive or Nonconvulsive SE, can be lateralized, generalized, bilateral independent and multifocal locals with varying secondary terms (periodic discharge, rhythmic delta and spike and wave)
Consider treating if 2 or more per second or on the ictal-interictal continuum
Investigate the cause (imaging, etc…), give conventional AEDs, consider benzo trial to determine ictal nature, continue cEEG monitoring to ID definitive seizure or SE later during hospitalization
Long term management: if they resolve without seizures - taper AEDs after 1 month, if PDs with seizure: continue AED for 3-12 months
NCSE Treatment Protocol cIV and non continuous IV
Continuous infusion (respiratory depression): midazolam, propofol or pentobarbital, ketamine (only if failure of or contraindication to midazolam, propofol and barbiturates), hypothermia
Non continuous infusion (no respiratory depression): fosphenytoin/phenytoin or valproate, levetiracetam, lacosamide (only if failure or contraindications to the above agents), phenobarbital
NCSE Treatment Protocol cIV and non continuous IV
Continuous infusion (respiratory depression): midazolam, propofol or pentobarbital, ketamine (only if failure of or contraindication to midazolam, propofol and barbiturates), hypothermia
Non continuous infusion (no respiratory depression): fosphenytoin/phenytoin or valproate, levetiracetam, lacosamide (only if failure or contraindications to the above agents), phenobarbital
What do you need to know about myoclonus status epilepticus
Most frequently seen after cardiac arrest
Has epileptiform nature (versus status myoclonus EEG has slow waves or burst suppression patters without epileptiform discharges)
Subcortical white matter injury - corticospinal tract
Tx: symptomatic, benzos, valproic acid, levetiracetam
EEG: generalized poly-spike and wave complexes on a nearly flat background
Treat like other RSE (keep poor prognosis in mind)
What do you need to know about epilepsia partialis continua (subtype of focal motor SE)
Can be very persistent
Epilepticus focal jerking activity can last days, weeks or decades
Focal structural brain lesion: heterotopias, infectious lesions, vascular abnormalities, subdural hematomas, or neoplasms
Prognosis: depends on the underlying lesion
Can have long term morbidity from weakness, sensory deficits, language dysfunction or cognitive deficits
Tx: benzos can prevent secondary generalization but usually do not stop seizure activity, occasionally can resolve without reverent or surgical treatment may be needed for intractable cases
Note: Nonketotic hyperglycemia can be associated with EPC in patients with concomitant focal cerebral lesion and respond best to conventional AEDs in concert with correction of metabolic disorder)
What factors increase risk of seizure in neuotrauma and duration of prophylactic AED in neurotrauma
Risks: GCS <10, cortical contusions, depressed skull fractures, wounds with dural penetration, prolonged (>24 hr) coma post traumatic amnesia
Phenytoin x 7 days, some keppra (levetiracetam)
CRASH trial
Corticosteroids after TBI - no benefit, increased mortality
Brain tissue oxygen tension monitoring after neurotrauma
Provides insight into cerebral metabolism
Pbto2 <15 mmHg associated with poor outcome
Which neurotrauma patients get hypothermia?
Refractory to osmotic therapy or unable to receive osmotic therapy
Correct ABG for temp to assure accurate readings (solubility of gas in liquid increases with lowering temp) - lower temp means increased CO2 in blood -> can lead to hypercapnea, cerebral vasodilatation and increased ICP)
Mannitol Side effects
Significant diuresis
Acute renal failure
Hyperkalemia
Hypotension
Rebound increased ICP
Mannitol dosing
0.25 - 1.0 gm / kg
Why is sodium chloride a better osmotic agent than mannitol?
NaCl has a better reflection coefficient (1.0 vs 0.9)
Normalizes resting membrane potential and cell volume by restoring normal intracellular electrolyte balance in injured cells
Can also raise MAP
Medications for sympathetic storming?
Bromocriptine
Beta-blockers (propranolol)
Morphine
Dantrolene
Clonidine
Steroids in spinal cord injury level of recommendation?
Controversial, not standard of care
Can be considered if you can minimize the risk of high-dose steroids (option, not recommendation)
STASCIS trial
Surgical Timing in Acute Spinal Cord Injury Study: early decompression within 24 hours of injury has a higher odds of improving neurologic outcome by a 2-grade improvement on ASIA impairment scale at 6 month follow-up
Early signs of infarct on CT scan
- Loss of insular ribbon
- Sulcal effacement
- Loss of grey-white junction
Diagnosis
Dense middle cerebral artery sign - intravascular dense clot material
ASPECTS grading score
The Alberta Stroke Program Early CT Score (ASPECTS) is a scoring system used to evaluate the severity of acute ischemic stroke:
Scoring
A score of 10 indicates a normal CT scan, while 1 point is subtracted for each region that shows early signs of ischemia. A score of 0 indicates diffuse involvement throughout the MCA territory.
Interpretation
An ASPECTS score of 8–10 indicates greater benefit from IV thrombolysis, while a score of ≤7 predicts a worse functional outcome at three months and symptomatic intracerebral hemorrhage.
Variations
There are variations of the ASPECT scoring system for the posterior circulation, known as pc-ASPECTS.
Diabetic patients
Diabetic patients have lower ASPECTS scores than non-diabetic patients, indicating more extensive strokes.
Mechanical thrombectomy
According to current American and European guidelines, mechanical thrombectomy is recommended for patients with an ASPECTS score of 6 or higher.
Indications and Contraindications to rTPA for ischemic stroke
Dose of TPA
0.9 mg/kg with a 10% bolus over 1-2 minutes then rest over 60 minutes
Should GP IIb-IIIa inhibitors be used in ischemic stroke patients
No secondary to significant safety concerns
What can be used after acute CVA?
ASA mild benefit
Heparin mild benefit offset by hemorrhage risk but can consider in setting of post cardiac surgery stroke, in select patients with carotid dissection and those with mechanical valve
Short course DAPT
What has a clear benefit in secondary stroke prevention after ischemic stroke?
Statins (independent of serum lipid panel)
What can the BP be in ischemic stroke patients if they haven’t received thrombolysis?
220/120 mmHg
When should carotid revascularization be done after ischemic stroke?
Stenosis >70%
CEA vs CAS
Similar for CVA, MI, death
CAS higher periop stroke
CEA higher periop MI
<2 weeks (unless larger cerebral infarction to minimize risk of hemorrhagic conversion)
Treatment to prevent malignant cerebral edema after complete MCA infarct
In patients that are difficult to arouse with symmetric or dilated but reactive pupil:
Neuro checks q2-4 hrs
Hypertonic saline or mannitol
Hemicraniectomy within 72 hours
Myesthenia Gravis target and symptoms
Target: T-cell dependent response targeted to postsynaptic acetylcholine receptor or receptor associated proteins
Symptoms: voluntary muscles (spares smooth and cardiac muscles), respiratory insufficiency
Treat trigger, plasmapheresis, IVIg
Symptom tx: Pyridostigmine
CHronic: prednisone, azathioprine, mycophenolate, cyclosporoine, some tacrolimus
Surgery: thymectomy with thymoma or <50 years old, not for MUSK+ patients or isolated ocular myathenia
Cholinergic crisis target and symptoms, what should be avoided
Excess acetylcholine esterase inhibitor
Symptoms: SLUDGE (salivation, lacrimation, urination, diarrhea, GI upset and emesis), mioisis, bronchospasm, flaccid weakness
Avoid tensilon challenge (can be dangerous, can distinguish from MG)
Lambert-Eaton myesthenic syndrome target, association, symptoms, uncommon?
Target: presynaptic autoimmune attack of voltage-ated calcium channels
Association: cancer (typically SCLC)
Symptoms: limb symptoms more prominant than occular/bulbar symptoms, faciculation with exercuse, autonomic dysfunction, reduced reflexes
Respiratory failure is uncomon
Botulism etiology, target, symptoms, treatment
Etiology: clostridium botulinum neurotoxin
Target: permanent blockage of presynaptic acetylcholne release at neuromuscular junction
Symptoms: symmetric descending paralysis and DIALTED PUPILS, dysautonomia, no sensory deficit
Treatment: equine antitoxin
Tick paralysis location, tick, symptoms, cure
Target: presynaptic neuromuscular blockage
Ticks: Rocky mountain wood tick, american dog tick, lone star tick, black-legged tick, western black-legged tick, gulf coast tick, austrialian Ixodes holocyclus tick
Symptoms: ascending paralysis, opthalmoparesis, bulbar dysfunciton, ataxia, reduced reflexes, can be rapid, no sensory symptoms,
Cure: tick removal
Snake venom snakes, target, symptoms
Snakes: tiger snake taipan, brazilian rattle snake target presynaptic blockage
Snakes: krait, cobras, mambas, coral snake sea snakes target postsynaptic blockage from alpha-bungarotoxin
Snakes: copperheads, cottonmouths, moccasins, rattlesnakes, vipers, adders, boomslang, twig snake block neuromuscular junction
Initially affects cranial nerves -> ptosis, opthalmoplagia, dysarthria and dysphagia to progressive limb weakness
Organophosphate toxicity sources, target, symptoms, what can happen 2-3 weeks later, treatment, avoidance?
Source: malathion, parathion, sarin, soman
Target: inactivates acetylchoilnesterase
Symptoms: SLUDGE, miosis, bronchospasm, blurred vision, bradycardia, confusion, optic neuropathy, extrapyramidal effects, dysautonomia, fasciculatios, seizures, cranial nerve palsy, weakness from continued depolarization of the neuromusclar junction
Delayed polynuropathy 2-3 weeks after exposure
Treatment: atropine, pralidoxime (2-PAM), benzodiazepine
Avoid: succinylcholine
Miller-Fischer Variant of GBS
Peripheral nervous system
Symptoms:
- Ophthalmoplegia (weakness or paralysis of the eye muscles),
- Ataxia (lack of muscle coordination),
- Areflexia (absence of reflexes).
Unlike typical GBS, which often presents with progressive weakness, the Miller-Fisher variant tends to have a more distinct presentation. It is often associated with antibodies against GQ1b gangliosides, and the symptoms can develop relatively quickly.
Treatment: supportive, IVIg, plasmapheresis
Diphtheria cause, symptoms
Cause: corynebacterium diphtheriae
Symptoms: thick gray pharyngeal pseudomembrane, AV block, endocarditis, myocarditis, lymphadenopathy, neuropathy, craniopharyngeal involvement, proximal-to-distal weakness and decreased reflexes
GBS
Immune- mediated poly neuropathyies with motor, sensory and dysautonimic features, early loss of F waves on MEG
Molecular mimicry from recent infection produces an autoimmune humeral and cell-mediated response to the ganglioside surface molecules of peripheral nerves,
Acute ascending weakness (often begins in proximal legs)
Paretehsia of hands and feet, low back pain,, displopia, dysautonomia (tachycardia/bradycardia, wide swings in blood pressure, orthostasis, tonic pupils, urinary retention, ileus/constipation, hypersalvation, anhidrosis), respiratory fialure
LP - elevated protein levels without elevation in leukocytes
Arsenic, lead poisoning and porphyrias lead to what?
Acute motor polyneuropathies
What do n-haxane (glue sniffing), peripheral nerve vasculitis (PAN, Churg-Strauss, RA, lupus), lyme disease, sarcoidosis, paraneoplastic disease and critical illness polyneuropathy all cause?
Polyneuropathy
Ciguatera toxin from red snapper, grouper, barracuda
Targets: voltage-gated sodium channels of muscles and nerves
Symptoms: metallic taste, hot-cold reversal,
Where do MG, Lambert-Eaton mysathenic syndrome, botulisum, organophosphate toxicity, neurotoxic fish poisoning all affect and what do they NOT cause?
Neuromuscular junction
Do NOT cause sensory involvement
EMG: when is insertional activity increased?
Denervated muscle
EMG: when is insertional activity decreased?
Muscle replaced by fat
What does spontaneous fibrillation potentials and sharp waves suggest on EMG?
Recent denervation or muscle necrosis
When is recruitment decreased on EMG?
When rapid firing results in damage to axon, neuro or nerve conduction or as a result of the loss of large number of motor units
When does poor activation/recruitment on EMG occur?
Central disorders with a decreased number of motor units recruited and firing is slow rather than rapid
What does early recruitment on EMG mean?
Myopathies
What does long motor unit potential duration indicate?
Lower motor neuro disorders
What does short-duration motor units indicate?
Myopathies
Can be seen in neuromuscular disorders and in early phases of reinnervation after neuropathy
What does long-duration, high-amplitude motor units indicate?
chronic neurogenic disorders