Neuro‎ > ‎

Neuro Notes

Strom 2010 - analgesia without sedation did better: less fluid administered, increased urine output, less renal dysfunction; no difference in delirium or VAP
Dex vs diazepam - more bradycardia, decreased LOS, better neuro exam, extubations 2d earlier, fewer infections, benefit in sepsis. 
Dexmedetomidine is a cost-effective treatment (Dasta JF CCM 2010 497-503)
SEDCOM - dex vs midaz or loraz; less delirium and fewer ventilator days but did not reduce LOS in ICU or hospital (JAMA 2007, 2009, 2012)
Propofol equivalent to precedex in sedation efficacy, LOS, and ventilator days (JAMA 2012)

Methylnatrexone resolved constipation in 45% of patients within 4 hours compared to 15% in placebo.
Stimulating BMs decreased ICU LOS. 

Propofol vs benzos decreases LOS and potentially mortality (Wunsch CCM 2009; 3031)
PRIS: rhabdo, renal failure, AGMA, TG, RBBB with convex and curved STseg in R precordial leads.

Ely studied SBT in NEJM and found that it reduced mechanical ventilation by 2d
Kress studied SAT in NEJM 2000 and found that it reduced mechanical ventilation by 2d
Lancet 2008 showed SBT and SAT together reduced ICU LOS by 4d and reduced mortality with ARR of 14%.

    4 : 0-75% blockage of nACH-R
    3 : 75%
    2 : 80%
    1 : 90%
    0 : 100%

    lasting > 7min has a 0% chance of spontaneously stopping
    neuronal damage occurs at about 30min in animals
    status is 30min of continuous seizure but operationally is 7-10min
    early phase (first 30min) there is usually significant motor activity and adrenergic tone leading to metabolic derangements but progressives to electromechanical dissociation - nonconvulsive status with normalization of vital signs and metabolic derangements. nonconvulsive status still causes brain damage but slower. 

Neuro monitoring
    Arterial line zeroed at tragus, Normal CPP 70-100 with normal ICP 5
    HTN without ICP monitoring can reflect elevated ICP; treat with 3% bolus and if HTN resolves then suggests ICP
        treat pain and agitation
        HOB up
        hyperventilation (peak effect 30min)
            however, randomization to PCO2 of 25-30 results in worse outcomes
            there is rebound vasodilation after renal compensation
            air trapping can increase ICP
        mannitol 1g/kg for Sosm < 320 but OG > 10
            can aggravate vasogenic edema in areas of injury
        3% HTS
            rule of thumb 1mg/kg HTS increases SNA by 1meq/L
        Treat fever (1deg C increases cerebral metabolic rate by 7%), reduce shivering
        Hypothermia unhelpful overall but can decrease ICP in refractory patients
        Pentobarb coma 20mg/kg for refractory cases
    Trial demonstrated titrating to jugular venous oximetry fluid overloaded patients without change in outcomes.
    Trials titrating to PbtO2 are mixed: mortality benefit, no change, higher mortality
BP in Neuro
    INTERACT trial showed rapidly lowering BP reduced hematoma growth over 72h in ICH (n=404)
    ATACH trial rapidly reduced and normalized BP - no harm no benefit (n=60)
    INTERACT 2 (NEJM 2013) trial showed rapid reduction of BP to 140 had same mortality but slightly less severe disability. No changes in hematoma growth as was found in INTERACT. 

    seizure prophylaxis x 1 week
    cerebellar bleed > 3cm in diameter require NSGY

    nothing within 24h of tPA or within 48h of demonstrated stable head bleed
        - ASA or ASA + dipyridamole or plavix for strokes from intracranial small vessel strokes
        - heparin for extracranial large vessel or cardioembolic
    BP (no TPA ) treat by 15% if over 220/120
    BP (tPA) < 180
    glucose 140-185 x24h
    unknown if treating hyperthermia helps
    steroids not helpful in cytotoxic edema
        young patients had fewer ventilator days and shorter ICU stay but no difference in LOS
        DECRA trial showed patients had less time with ICP > 20 BUT more chronically debilitated pts
        DESTINY II trial (NEJM 2014) increased survival without severe disability in pts > 61yo from MCA

    surgery within 72h or coils beyond that
    unsecured aneurysms have 4% rebleed risk on d0 then 1.5%/d x 13d or about 25% in first 2w
    ?anti-fibrinolytic therapy in delays to surgery
    BP < 140
    Vasospasm occurs in 20-30% starting d3-d7 (uncommon before d3) 
        hypertension (in secured), hypervolemia, hemodilution is traditionally taught
        do not fluid restrict as it is associated with increased vasospasm
        3% HTS

    Vital capacity is important in prognosis
    normal is >45ml/kg, one loses cough at <30mL/kg, one loses sigh at 25ml/kg with excessive atelectasis and shunting, hypoventilation and hypercapnea occurs at 5-10ml/kg range
    20-70% of chronic SCI develop autonomic dysreflexia and 5% of acute SCI if above T6
        triggers include fecal impaction, medical procedures, sexual stimulation, childbirth, abdominal distension/gas, somatic pain
    Acute SCI
        MAP 85-90
        NACIS I controversial
        NACIS II small slight improvement with methylpred within 8 h of injury
        50-100% of SCI develop DVT/PE 3-14d if untreated
        IV lidocaine can blunt ICP rise
        avoid succhinylcholine as denervated muscle expresses fetal ACH-R which results in excessive depolarization and hyperkalemia
        no etomidate in ruptured globe due to myoclonus

Abnormal Respiratory Patterns
    Cheyne Stokes occurs in bihemispheric lesions
    central neurogenic hyperventilation is typically midbrain
    apneustic breathing is typically pontine (insp, long pause, exp)
    cluster breathing is typically medulla and resembles Biots
    ataxic breathing (totally random) is lowest

    plasma exchange decreases time on MV and improves ambulation by 50%
        5 exchanges over 10d (4 better than 2 but 6 not better than 4 in bedbound pts)
    IVIG versus exchange is not clear. Sequential dose not add much. 
    can cause severe autonomic dysreflexia

    40% responds to steroids
    needs chronic IVIG vs plasmapheresis

    axonal degeneration of motor and sensory fibers or mostly motor
    manifests after 7-14d in ICU, can involve phrenic nerve
    50% have full recovery

    MG crisis happens to 20% of patients typically within the first 2y of diagnosis
        infection, aspiration, surgery, trauma, childbirth, change in medications
        FQ, aminoglycosides, Bb, CCB
    ACh-R antibodies are only 90% sensitive; even less so (70%) for those with just ocular sx due to other antibodies (MuSK, NaK channels, tintin).
    plasma exchange or IVIG
    steroids not used in acute because of temporary worsening

    symmetrical CN dysfunction, no fever
    very similar to Miller Fischer GBS, MG crisis, paralytic fish poisoning
    skin-poppers high risk of wound botulism and starts where the infection begins 4-14d after
    tx is antitoxin. Ingestion or inhalation does not need abx. Skin needs debridement and abx

    thick filament - from steroids and NMJ blockers - absense of thick myosin filaments
    acute necrotizing myopathy - widespread muscle necrosis
    critical illness myopathy - flaccid weakness, myoglobinuria, ophthalmoplegia

ICU weakness
    MGC - proximal, nl reflexes, nl sensation, improves with edrophonium
    GBS - distal, CN ultimately involved, absent reflexes
    CIPN - distal and no CN, 2/3 with absent reflexes