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Neurocritical Care
| @NeuroFOD | @NeuroFOD |
|---|---|
| Neurocritical Care | Neurocritical Care |
| GCS | Eyes = 4, Verbal = 5, Motor = 6 |
| FOUR Score | Eyes, Motor, Brainstem, Respiration. All from 0-4 |
| Decorticate posturing anatomy | Lesion in corticospinal tract above red nucleus |
| Decerebrate posturing anatomy | Lesion in corticospinal tract between red nucleus and vestibular nuclei |
| Triple flexion anatomy | Lesion in corticospinal tract below vestibular nuclei (ie. below medulla) |
| Cheyne-Stokes breathing | Looks like torsades with fluctuating high-low amplitudes |
| Apneustic breathing | Pauses at full inspiration. Pontine lesions |
| Ataxic breathing | Random pattern. Low pontine or medullary lesions |
| Three types of edema | Vasogenic (blood-brain barrier), Cytotoxic (cell damg), Interstitial (CSF) |
| TTM Criteria | Must be: >18yo, altered mental status, not pregnant, no coagulopathy |
| TTM Goal | Temp goal 36. References: HACA, Bernard, TTM Trials 1 & 2 |
| TTM Shivering treatment | Tylenol, surface warming (baer hugger), Buspirone 30q8, Magnesium |
| TTM Complications | Coagulopathy, hypokalemia, hyperglycemia, hypotension |
| Apnea test basics | Pre-oxygenate 100% O2, stop vent, ABG in 10 mins showing PCO2 >60 |
| Brain death tests | Clinical exam, apnea test, EEG, Angiogram, Tech99 scan, CT perfusion |
| Battle sign | Posterior auricular brusing. Seen with skull fractures |
| Monroe Kelli doctrine | Skull is closed cavity containing only brain + CSF + blood |
| Cerebral perfusion pressure | CPP = MAP - ICP |
| Cerebral blood flow | CBF (flow) = CPP (pressure) / CVR (resistance) |
| Cushing's response | /\BP \/HR \/RR. Sign of baroreceptor dysfunction |
| Uncal herniation sign | Ipsilateral CN3 = ipsilateral pupillary dilation |
| Central herniation sign | Bilateral CN3 + CN4, PCA stroke |
| Subfalxine herniation sign | ACA stroke |
| Lundberg A waves | A = high plateau of intracranial pressure for >5 mins. Poor compliance |
| ICP monitor: P1, P2, P3 | P1 = systole, P2 = dural compliance, P3 = dicrotic notch |
| ICP 1st line interventions | Raise head, stop fever, hypervent (pCO2 30-35), 3%, 23%, mannitol |
| ICP 2nd line interventions | Propofol, Pentobarbitol, EVD/drain, craniotomy |
| Durett hemorrahges | Brainstem hemorrage due to shear injury |
| Status epilepticus pathophysiology | Seizure = /\Glut \/GABA --> over time --> \/GABA-receptors = resistant status epilepticus |
| ESES | Electrographic Status in Sleep. Presents with aphasia and regression |
| Status epilepticus treatment protocol | Benzos q5mins x3 -> Pheny/VPA/Keppra load -> rpt load x2 -> propofol/pentobarb |
| Ketamine mechanism of action | NMDA antagonist. Better in late stage status when GABA-receptors are non-functional |
| Status epilepticus mortality | 10-30% mortality. Note: 20% have ongoing subclinical status even after clinical seizures end |
| Man-in-a-barrel | Watershed infarcts (MCA-ACA territory). Inability to move arms/legs, but intact thorax/midline |
| Neurons most susceptible to hypoxia | CA1 hippocampal neurons. Also cerebellar purkingee fibers, basal ganglia, thalamus |
| Hypoxic ischemic encephalopathy histopathology | Red eiosinophilic cytoplasm, laminar necrosis, pyknotic nuclei |
| Post cardiac arrest / hypoxia care | TTM to 36, sedation, MAP>80, continuous EEG. Rewarm after 24-48hrs |
| Post cardiac arrest / hypoxia prognosis | Worse prognosis if arrest >10mins, no reflexes at day 3, absent N20s on SSEP, myoclonic status |
| Concussion vs contusion | Concussion = transient, can have loss of conciousness, n/v, dizziness. Contusion = ICH on CT |
| Test to assess CSF leak | Send fluid for b2-transferrin. If positive = fluid is CSF |
| Steroid use in TBI | Used to be given, but now there is no indication for empiric steroids |
| Seizure prophylaxis in TBI | YES, must do seizure prophylaxis. Literature says phenytoin x7 days, but clinically Keppra |
| When ok to rejoin sports after head trauma | Must: no symptoms + normal exam + no pain meds. NO duration guideline, just restart gradually |
| Post-TBI fatigue medications | Methylphenidate, modafanil, amantadine |
| Post-TBI agitation medications | Try propanolol first. Then go for antipsychotics |
| Acute SCI symptoms | Early LMN is still flaccid and areflexic. Atonic bladder, constipation |
| Most important intervention in acute SCI | Foley! { atonic bladder = sympathetic collapse (\/HR, \/BP, code blue) }. Also DVT prophylaxis |
| Chronic SCI symptoms | Late LMN is spastic and hyperreflexic. Bladder retention, \/rectal tone (fecal incontinence) |
| SCI level with high risk of autonomic dysreflexia | Injury must be higher than T6. Sympathetic plexus runs from T1 to L2 |
| Conus medularis | Only end part of cord (not roots) = perineal anestheia and \/ ankle reflex, minimal pain/retention |
| Cauda Equina | Roots = perineal+saddle anesthesia, \/ ankle reflex, sciatica (radiculopathy), urine retention |
| Best MRI sequence for spinal cord pathology | Sagital STIR and axial T2 |
| Most sensitive test for spinal cord injury | ESR. Random fact, but clinically useless because it's very non-specific |
| SCI level with high risk of respiratory failure | Above T5. Diagpharm is innervated by peroneal nerve T4 |
| Steroid use in SCI | Steroids if cancer or disc herniation. Generally avoided in trauma and spinal stroke |
| How to clear C-collar? | Must: (1) CT: no injury + (2) full motion with no pain. Altered pt = MRI to r/o ligamentous injury |
| AED with reflex bradycardia | Phenytoin |
| DAI pathophysiology | Sudden acceleration/deceleration/rotation that causes angular or shear injury to white matter |
| DAI MRI findings | Microhemorrhages, corpus callosum hyperintensities, diffuse white matter hyperintensities |
| DAI histopathology | Axon spheroids (swollen bulbs/balloons), disconnected axons. Use H&E or silver stain |
| Coup-contracoup injury most common location | Coup = primary = orbitofrontal, contracoup = secondary = occipital |
| 1st sign of AIDP on EMG | Absent F-wave |
| Antibody in Miller Fisher syndrome | Anti-GQ1b |
| Acute AIDP crisis treatment | (1) airway, (2) evaluate for dysautonomia. Then IVIG or PLEX. Never steroids |
| Drugs that exacerbate myasthenia gravis | Aminoglycosides, quinine, IV-magnesium, beta-blockers, calcium-channel blockers, pencillamine |
| Acute MG crisis treatment | (1) airway (stop ACEi pyridostigmine b/c /\secretions), (2) IVIG/PLEX. Then consider steroids |
| FVC and NIF numbers in respiratory failure | FVC <20% of normal, NIF < -30 |
| Botox mechanism | Block SNARE and SNAP proteins = block vesicle fusion with membrane = \/ Ach release |
| Critical Illness Neuropathy vs Myopathy histopathology | CIN = microvascular axonal injury. CIM = absent myosin filaments |
| Central Core Myopathy gene | RYR1 on chromosome 19q13 (same as for malignant hyperthermia) |
| Seretonin syndrome presentation | /\ sympathetic activity, /\ GI motility, /\ reflexes, /\ tremors. {""Seretonin=move, NMS=rigid""} |
| Neuroleptic malignant syndrome presentation | /\ parasymp (sweat, saliva), \/ reflexes, rigidity/bradykinesia. {""Seretonin=move, NMS=rigid""} |
| Seretonin syndrome treatment | Stop SSRI/SNRI/MAO/TCA/etc. Cyproheptadine (5HT antagonist), benzos |
| Neuroleptic malignant syndrome treatment | Bromocriptine (DA agonist), dantrolene, amantadine, benzos |
| Sympathetic storming treatment | Propanolol, gabapentin, clonidine |
| Paroxysmal intermittent /\BP /\RR /\Temp | Sympathetic storming. Rule out infections |
Created by:
amitchaudharimd
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