SETScore for Early Tracheostomy in Stroke

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**APS acute physiology score, LIS lung injury score

 

  • initially an in-house screening tool for tracheostomy prediction
  • performed within 1st 24 hours after admission – use worst value in the first 24 hours
  • Dysphagia either
    • reported from a transferring neurological department or
    • observed by clinical signs on admission
      • non-successful swallowing test
      • impaired saliva handling
      • loss/reduction of gag reflex
    • if already intubated on admission, scored with “0”
  • (Neuro)surgical intervention
    • decompressive surgery, hematoma removal, non-cranial major surgery
    • NOTE EVD or probe placement, thrombectomy, angioplasty for vasospasm or coiling
  • Diffuse lesion = a multilocular or widespread affection of brain (i.e. SAH, brain edema, multiple infarcts, hematomas)
  • hydrocephalus = distension of ventricles requiring EVD
  • total sum ranges between 3 and 37

Previously used (with score of >10) to screen for eligibility to be included in pilot trial of SETPOINT study for early tracheostomy (within 3 days) to standard regimen (late tracheostomy between day7 and day14).

 

 

Reference

Schönenberger, Silvia et al. “The Setscore To Predict Tracheostomy Need In Cerebrovascular Neurocritical Care Patients”. Neurocritical Care 25.1 (2016): 94-104.

 

Organ Donor Protocol

VS parameters:

  • SBP >100mm Hg and/or MAP >70mm Hg
  • HR 60-140 bpm
  • Temp 36-38 Celcius

Electrolytes parameters:

  • pH 7.35-7.45    PCO2 35-45    PO2 >100
  • Bicarb 24-30    BE 00 +/- 2
  • Na+ 135-145 mg/dL
  • K+ 3.5-4.5 mg/dL
  • Ca++ >8.7 mg/dL
  • Mg++ >1.5 mg/dL
  • Phosphate >2.5 mg/dL
  • Glucose <200 mg/dL

Corrections:

  • POTASSIUM
    • >5.0 (or if UO <1 ml/kg/hr) eliminate KCl from IV fluids
    • 3.7-3.9 mg/dL – 1 run of KCl 10 mEq (premixed)
    • 3.5-3.7 mg/dL – 2 runs of KCl 10 mEq (premixed)
    • 3.3-3.5 mg/dL  – 3 runs of KCl 10 mEq (premixed)
    • 3.1-3.3 mg/dL  – 4 runs of KCl 10 mEq (premixed)
    • <3.1mg/dL         –  contact coordinator
  • GLUCOSE – check serum glucose q4h
    • >500 mg/dL 20 units Regular insulin IV
    • >400 mg/dL 15 units Regular insulin IV
    • >300 mg/dL 10 units Regular insulin IV
    • >200 mg/dL 5 units Regular insulin IV
    • >100 mg/dL 3 units Regular insulin IV
  • SODIUM
    • >160 Run D5W for primary IV
    • >150 Run D5W/0.2NS for primary IV
    • 135-150 Run 0.45NS for primary IV
    • <135 Run NS for primary IV
  • CALCIUM
    • <8.7 (if ionized Ca <4.2) Calcium chloride 1 Gm IV over 10 minutes
  • MAGNESIUM
    • <1.5 Magnesium sulfate 10% 1.5 ml/min infusion
  • PHOSPHORUS
    • <2.5 Potassium phosphate replacement (no specific dose indicated)

Infusions:

  • BLOOD PRESSURE
    • Dopamine infusion:  400mg in D5W 250ml premixed, titrate to SBP >100
    • Dobutamine infusion (if hypotensive from cardiac dysfunction):  250mg in D5W 250ml premixed, titrate to SBP >100
    • Norepinephrine infusion:  8mg in D5W 500ml, titrate to SBP >100
  • LEVOTHYROXINE protocol (if prescribed by transplant coordinator)
    • Monitor glucose and potassium levels q2h.
    • administer IV bolus of in rapid succession:
      • dextrose 50% x 1 amp (50 ml)
      • solumedrol 1 gram
      • regular insulin 20 units
      • levothyroxine 20 mcg
    • Begin Levothyroxine infusion (200 mcg in 500 ml NS) at 25 ml/hr
    • Reduce pressors as much as possible and adjust levothyroxine infusion to maintain SBP >100
  • DIABETES INSIPIDUS
    • if UO >400cc/hr x 2 hours – 5 units aqueous vasopressin (Pitressin) ffd by infusion: Vasopressin 50 units in D5W 500mL at 20 ml/hr
    • titrate to urine output 100-150cc/hr
    • bolus 5 units vasopressin q2h PRN if IV pump not available

 

Reference:

New York Organ Donor Network’s “ICU Donor Guidelines and Routine Orders”

Antibiotic-Associated Encephalopathy

What are the clinical, radiologic, and electrophysiologic features of antibiotic-associated encephalopathy (AAE)?

3 types of AAE

  1. Type 1 AAE
    • onset within days of antibiotic initiation
    • common occurrence of myoclonus or seizures, abnormal EEG, normal MRI, and resolution within days
    • seen with penicillin and cephalosporins
    • most common in setting of renal insufficiency.
  2. Type 2 AAE
    • onset within days of antibiotic initiation
    • frequent occurrence of psychosis, rare seizures, infrequently abnormal EEG (nonspecific rather than epileptic), normal MRI, and resolution within days
    • seen with procaine penicillin, sulfonamides, fluoroquinolones, and macrolides
  3. Type 3 AAE
    • seen only with metronidazole
    • onset weeks after initiation
    • frequent occurrence of cerebellar dysfunction, rare seizures, rare and nonspecific EEG abnormalities, and omnipresence of abnormal MRI
  4. Isoniazid did not fit into any of these categories
    • time to onset is weeks to months
    • psychosis is common, seizures are rare, EEG is frequently abnormal but nonspecifically

 

F2.medium

*INH does not fit into any of the subtypes.

 

Features:

  • Time of onset after antibiotic initiation – 5 days (except INH and MNZ – 3 weeks)
  • Time to resolution of encephalopathy after ABx discontinuation – 5 days (except MNZ – 13 days)
  • MRI findings
    • abnormal in all MNZ-associated encephalopathy but normal in all others
      • T2 hyperintensities in dentate nuclei of cerebellum (also ?involvement of brainstem, corpus callosum, etc)
    • Bilateral frontal subcortical T2 MRI hyperintensities in isolated case of cefditoren pivoxil toxicity
  • CT findings
    • normal in all cases except 1 case of cerebellar hypodensity with MNZ toxicity and 1 report of L thalamic hypodensity with imipenem toxicity
  • EEG findings:
    • abnormal in 70%
    • abnormal in nearly all cases of cephalosporin-associated encephalopathy
    • common with PCN (83%), cipro (83%) and INH (69%)
    • most common abnormalities: nonspecific signs of encephalopathy (slowing, generalized periodic discharges with triphasic morphology
    • epileptiform discharges / seizures seen in 28% (55% in cephalosporins, 44% in quinolones and 40% of PCN, but not in macrolides, MNZ or sulfonamides)
  • check serum and CSF trough levels of antibiotics?
    • cefepime trough 0.2 to 1.1 mg/L
    • 50% probability of neurologic toxicity at trough of 22mg/L
    • CSF level during toxicity in 2 cases with values of 2.4 mg/L and 18 mg/L

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A – FLAIR hyperintensities bilatearl deep cerebellar nuclei
B – DWI showing restricted diffusion in splenium with MNZ toxicity
C – ADC sequences

 

 

 

 

Reference

Bhattacharyya, Shamik et al. “Antibiotic-Associated Encephalopathy”. Neurology 86.10 (2016): 963-971.

AEDs in Renal Failure / Hemodialysis

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How does renal disease affect AED levels?

  • Renal insufficiency alters the pharmacokinetics of seizure medications that are metabolized by the kidneyes, leading to increased half-lives and accumulation of the drug.
  • Albuminuria and acidosis that frequently occur in renal failure also decreases drug binding, increasing the free levels of AEDs and volume of distribution.
  • Gastroparesis delays maximum serum levels of AEDs, intestinal edema diminishes absorption of AEDs.

Take home message:  It is difficult to predict drug levels based on the creatinine clearance.

AEDs that are extensively eliminated by kidneys:

  • hydrosoluble
  • low molecular weight
  • low Vd
  • little protein-bound
  • Examples:  gapabentin, topiramate, ethosuxamide, vigabatrin, levetiracetam
  • accumulate in renal disease
  • easily removed by hemodialysis and requires post-HD administration

AEDs that are not extensively eliminated by kidneys:

  • lipophylic
  • high protein-bound
  • Examples:  carbamazepine, phenytoin, lamotrigine, benzodiazepines, valproate
  • little affected by renal disease
  • HD has little impact on carbamazepine, phenytoin and valproate levels
  • HD has unpredictable effects on benzodiazepines or oxcarbazepine monohidroxi derivative
  • 4-hour HD decreases lamotrigine levels by ~20%

Peritoneal dialysis has variable effects on AED serum levels, check free levels for drug adjustment

LEVETIRACETAM:

  • CrCl >80 mL/minute/1.73 m2: 500 to 1,500 mg every 12 hours
  • CrCl 50 to 80 mL/minute/1.73 m2: 500 to 1,000 mg every 12 hours
  • CrCl 30 to 50 mL/minute/1.73 m2: 250 to 750 mg every 12 hours
  • CrCl <30 mL/minute/1.73 m2: 250 to 500 mg every 12 hours
  • End-stage renal disease (ESRD) requiring hemodialysis: Dialyzable (50%); 500 to 1,000 mg every 24 hours; supplemental dose of 250 to 500 mg is recommended posthemodialysis
  • Peritoneal dialysis (PD): 500 to 1,000 mg every 24 hours (Aronoff 2007)
  • Continuous renal replacement therapy (CRRT): 250 to 750 mg every 12 hours (Aronoff 2007)

PHENYTOIN:

  • There are no dosage adjustments provided in the manufacturer’s labeling; <5% excreted as unchanged drug. Serum concentration may be difficult to interpret in renal failure. Monitoring of free (unbound) concentrations or adjustment to allow interpretation is recommended.
  • Fosphenytoin:  There are no dosage adjustments provided in the manufacturer’s labeling. Free (unbound) phenytoin levels should be monitored closely in patients with renal disease or in those with hypoalbuminemia; furthermore, fosphenytoin clearance to phenytoin may be increased without a similar increase in phenytoin clearance in these patients leading to increase frequency and severity of adverse events.

CARBAMAZEPINE:

  • Dosage adjustments are not required or recommended in the manufacturer’s labeling; however, the following guidelines have been used by some clinicians:
  • Children and Adults:
    • GFR <10 mL/minute: Administer 75% of dose
    • Hemodialysis, peritoneal dialysis: Administer 75% of dose (postdialysis)
  • Continuous renal replacement therapy (CRRT):
    • Adults: No dosage adjustment recommended
    • Children: Administer 75% of dose

PHENOBARBITAL

  • There are no specific dosage adjustments provided in the manufacturer’s labeling; reduced doses are recommended.
  • The following guidelines have been used by some clinicians:
    • CrCl ≥10 mL/minute: No dosage adjustment necessary.
    • CrCl <10 mL/minute: Administer every 12 to 16 hours.
    • HD (moderately dialyzable [20% to 50%]): Administer dose before dialysis and 50% of dose after dialysis.
    • PD:  Administer 50% of normal dose.
    • CRRT: Administer normal dose and monitor levels.

VALPROIC ACID:

  • Mild to severe impairment: No dosage adjustment necessary (including patients on hemodialysis); however, due to decreased protein binding in renal impairment, monitoring only total valproate concentrations may be misleading.

 

LORAZEPAM:

  • Dosing: Renal Impairment
  • Oral: No dosage adjustment necessary
  • IM, IV: Risk of propylene glycol toxicity. Monitor closely if using for prolonged periods of time or at high doses.
    • Mild-to-moderate disease: Use with caution.
    • Severe disease or failure: Use is not recommended.

MIDAZOLAM:

  • Dosing: Renal Impairment
    • There are no dosage adjustments provided in manufacturer’s labeling; however, patients with renal failure receiving a continuous infusion cannot adequately eliminate the active hydroxylated metabolites (eg, 1-hydroxymidazolam) contributing to prolonged sedation sometimes for days after discontinuation
  • Intermittent HD:  Supplemental dose not necessary
  • CVVH: Unconjugated 1-hydroxymidazolam not effectively removed; 1-hydroxymidazolamglucuronide effectively removed; sieving coefficient = 0.45
  • PD: Significant drug removal unlikely

LAMOTRIGINE:

  • There are no dosage adjustments provided in the manufacturer’s labeling. Decreased maintenance dosage may be effective in patients with significant renal impairment; has not been adequately studied; use with caution.

PROPOFOL:

  • No dosage adjustment necessary.

 

Reference:

Lacerda, Glenda Corrêa Borges de. “Treating Seizures In Renal And Hepatic Failure”. J. epilepsy clin. neurophysiol. 14 (2008): 46-50.

Uptodate.  Accessed 07/12/2016.

 

Watershed Infarcts

Patients presenting with severe hypertension are at risk for watershed infarcts if blood pressure is rapidly and dramatically reduced, even without frank hypotension.  Blood pressure should be lowered by no more than 25% to reduce the chance of cerebral, coronary or renal ischemia.

Watershed infarcts comprise ~10% of all ischemic strokes.  These infarcts are localized to borderzones between major vascular territories in the brain, and are classified as internal borderzone (IBZ) or cortical borderzone (CBZ) infarcts.

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*CBZ in red, IBZ in blue.

The CBZ are located at the junctions of the distal branches of the ACA, MCA and PCA territories.  CBZ infarcts are associated with small cortical infarcts that are more likely due to thromoembolism.

The IBZ are located at the junctions of the distal branches of the ACA/MCA/PCA with the deep perforating arteries (lenticulostriate, artery of Heubner, anterior choroidal artery).  IBZ infarcts are more often associated with severe stenosis or occlusion in the ICA or MCA.  The IBZ is more vulnerable to decreased perfusion due to the anatomic characteristics of cerebral arterioles within this area – being the most distal branches of the ICA, perfusion pressure is likely to be the lowest.  Also the lenticulostriate arteries have limited collateral blood supply.

Examples:

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Patient admitted for hypertensive emergency, started on nicardipine drip and blood pressure lowered from 200+ to 100 systolic.  Relative hypotension maintained for 2 hours.  Patient became comatose thereafter.  MRI showed IBZ infarcts.

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Patient with aortic dissection, BP lowered from 200s with nicardipine drip.  Patient became unarousable at SBP 114 where it remained for ~3 hours.   MRI showed IBZ and corpus callosum infarctions.  Patient never regained consciousness.

 

 

Reference:

Kurowski, Donna, Michael T. Mullen, and Steven R. Messé. “Pearls & Oy-Sters: Iatrogenic Relative Hypotension Leading To Diffuse Internal Borderzone Infarctions And Coma”. Neurology 86.24 (2016): e245-e247.

Classification of Hemorrhagic Transformation

Hemorrhagic infarction (HI) describes a heterogeneous hyperdensity in in an ischemic infarct zone.  Parenchymatous hematoma (PH) refers to a more homogenous, dense hematoma with mass effect.  Fiorelli, et al in 1999 refined these definitions to include two subtypes of HI and two subtypes of PH.

Definitions as per Fiorelli (1999):

  • HI is a petechial infarction without space-occupying effect.
  • PH is a hemorrhage (coagulum) with mass effect.
  • 2 subtypes of HI:
    • HI1 (small petechiae)
    • HI2 (more confluent petechiae)
  • 2 subtypes of PH:
    • PH1 (≤30% of the infarcted area with some mild space-occupying effect)
    • PH2 (>30% of the infarcted area with significant space-occupying effect, or clot remote from infarcted area)

fneur-04-00069-t001

Hemorrhages that occur within the first week after stroke were more likely to be PH2-type, whereas hemorrhages that occur later tend to be HI1, HI2 or PH1.  PH2-type was found to be a significant predictor of neurologic deterioration (OR32.3) and of 3 month mortality (OR 18.0) whereas HI1, HI2 and PH1 were not associated with either increased morbidity or mortality.

 

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Subtypes of hemorrhagic transformation: HI1 (top left), HI2 (top right), PH1 (bottom left), and PH2 (bottom right).

 

References

Fiorelli, M. et al. “Hemorrhagic Transformation Within 36 Hours Of A Cerebral Infarct : Relationships With Early Clinical Deterioration And 3-Month Outcome In The European Cooperative Acute Stroke Study I (ECASS I) Cohort”. Stroke 30.11 (1999): 2280-2284.

Sussman, Eric S. and E. Sander Connolly. “Hemorrhagic Transformation: A Review Of The Rate Of Hemorrhage In The Major Clinical Trials Of Acute Ischemic Stroke”. Frontiers in Neurology 4 (2013): n. pag.

Neuroendoscopic Ventricular Irrigation for Ventriculitis

Ventriculitis carries a high  mortality and morbidity, even with prompt diagnosis and treatment with antibiotics.  A retrospective study from Kyoto Univeristy Graduate School of Medicine concluded that neuroendoscopic irrigation effectively treats ventriculitis, with lower mortality and duration of drainage catheter compared to historical control.  The study population was small and the design was retrospective.  Larger, prospective studies are needed to confirm these promising initial results.

Since 2011, this institution has adopted neuroendoscopic irrigation as standard treatment for ventriculitis.  After diagnosis on MRI (high intensity on DWI and gad enhancement of ventricular lining), antibiotics was started and neuroendoscopic irrigation was performed, followed by drainage catheter insertion.  Intraparenchymal abscess </=3cm in diameter was treated by placement of drainage catheter (without irrigation).  Abscesses >3cm was surgically evacuated.

Method of Neuroendoscopic Irrigation:

An oval-shaped Burr hole was created in the left frontal bone for insertion of 2 drainage tubes.  One tube was advanced into the abscess and the other was placed in the lateral ventricle under neuronavigator guidance.  Pus was aspirated from the intraparenchymal abscess.  A sheath was introduced to the lateral ventricle along with the ventricular drainage.  Artificial CSF was flushed through the drainage tube.  Ventricle was inspected with a rigid neuroendoscope, and white material suspended in the CSF was irrigated out.  After sufficient irrigation, structures around foramen of Monro (initially covered by white material) were visualized.  Under endoscopic guidance, the tip of drainage tube was placed at the posterior part of the lateral ventricle.

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(a) Lateral ventricle filled with white, sticky material;  (b) ventricular wall and choroid plexus (arrow) covered with grayish infectious material; (c) normal structures, choroid plexus (arrow), visualized after irrigation

 

Reference

Terada, Yukie et al. “Effectiveness Of Neuroendoscopic Ventricular Irrigation For Ventriculitis”.Clinical Neurology and Neurosurgery 146 (2016): 147-151.

tPA Dosing for Acute Ischemic Stroke

Acute ischemic stroke:

  • Within 3 hours of the onset of symptom onset (labeled use)
  • Within 3 to 4.5 hours of symptom onset (off-label use)
  • Recommended total dose: 0.9 mg/Kg (max 90mg)
    • ≤100 kg:
      • Load 10% as IV bolus over 1 minute, then
      • 90% as continuous infusion over 1 hour
    • >100 kg:
      • Load 9 mg as IV bolus over 1 minute, then
      • 81 mg as continuous infusion over 1 hour
  • No heparin or aspirin within 24 hours after tPA, start 24-48 hours after stroke onset.
  • SQH (<10,000 units) or LMWH for DVT prophylaxis within 24 hours did not increase ICH

Low dose alteplase (0.6mg/kg) recently shown to be “not noninferior” in a recent trial published in NEJM (06/2017) by ENCHANTED group. Whether this lower dose (which resulted in less ICH) may benefit patients who are at higher risk of post-tPA hemorrhage remains to be investigated.  [2]

 

References

[1] Uptodate: “Alteplase: Drug information.” Accessed 07/08/2016.

[2] Anderson, Craig S. et al. “Low-Dose Versus Standard-Dose Intravenous Alteplase In Acute Ischemic Stroke”. New England Journal of Medicine 374.24 (2016): 2313-2323. Web.

 

Blood Pressure Goals in Neurocritical Care

Subarachnoid Hemorrhage (Take home:  target SBP <140mm Hg)

Optimal blood pressure target unknown.  2012 American Stroke Association guidelines suggests that a systolic BP goal <160mm Hg is reasonable.  Avoid nitroprusside or NTG (increases cerebral blood volume / ICP). Use labetalol, nicardipine, enalapril.

Lowering BP decreases risk of rebleeding in unsecured aneurysm, but may increase risk of infarction.  CPP = MAP – ICP.  Increased ICP necessitates an elevated MAP to keep CPP.  CPP threshold may be 70mm Hg.

In the absence of ICP measurement, clinical findings (i.e. alertness) may guide therapy, Uptodate recommends keep SBP <140mm Hg in these instances.

Traumatic Brain Injury (Take home:  target CPP 50-70mm Hg)

Cerebral autoregulation is disrupted in about a third of patients with severe TBI, these patients are described as “pressure-passive.”  In these patients, rise in MAP leads to elevated ICP due to increased cerebral blood volume, while drops in MAP may be associated with hypoperfusion and ischemia.

Bedside measurement of cerebral blood flow is not easily obtained.  CPP = MAP – ICP, is a surrogate measure.  Low MAP, high ICP or low CPP are associated with secondary brain injury and worse outcomes.

Old strategy to induce hypertension to CPP >70mm Hg (using saline boluses or vasopressors) does not improve outcome, and increases risks of other complications s.a. ARDS.  2007 Guidelines from BTF recommend CPP target of 60 mm Hg, avoid <50 and >70 mm Hg.  In children, lower thresholds are recommended (40-65 mm Hg).  Target ICP first before MAP.

Post-neurosurgical Procedure

[coming soon]  Our practice is to keep SBP within 100-150mm Hg during the immediate post-operative period.

Cerebrovascular Accident (Take home:  tPA <185/110 then <180/105; no tPA treat if >220/120)

After stroke, CPP distal to obstructed vessel is low and distal vessels are dilated.  Blood flow depends on systemic blood pressure.  Elevated BP is necessary to maintain perfusion in ischemic penumbra.  BP rises spontaneously after stroke, this is transient and BP falls by as much as 20/10 within 10 days.

Analysis from International Stroke Trial showed a U-shaped relationship between SBP and outcomes.  SBP >200mm Hg is associated with risk of recurrent stroke while SBP <120mm Hg was associated with excess number of deaths from coronary heart disease.

Lowering BP within 24 hours of acute stroke has been associated with clinical deterioration.  Some may even benefit from pharmacologic increases in BP (studies show improvement in aphasia or perfusion imaging). [Induced HTN currently not recommended except in the setting of a clinical trial.]  Severe increase in BP can also cause hypertensive encephalopathy.

No good RCTs to guide BP management in hyperacute phase (<12hours) of stroke.

Ultra-acute treatment: ongoing RIGHT-2 Trial is assessing safety and efficacy of transdermal NTG [8]

For patients eligible for tPA:  Blood pressure goal  ≤185/110 mmHg is recommended prior to starting lytic therapy.  Maintain BP ≤180/105 mmHg x 24 hours after tPA.

*Ongoing ENCHANTED trial is assessing effects of early intensive BP lowering post-tPA.  Results expected in early 2019.[8]

For patients not treated with tPA:  most guidelines recommend no treatment for BP unless hypertension is extreme (SBP >220mm Hg or diastolic >120m Hg) or patient has active ischemic coronary disease, heart failure, aortic dissection, hypertensive encephalopathy, acute renal failure, or pre-eclampsia / eclampsia.  If so, lower BP by ~15% during first 24 hours.

Restart antihypertensive medications ~24 hours after stroke in patients with pre-existing HTN who are neurologically stable.  Patients with large artery stenosis may require a slower reduction in BP (over 7-10 days after stroke)

Guidelines suggest IV labetalol and nicardipine as first-line antihypertensives.

*UK National Clinical Guidelines for stroke advocate only restarting preexisting antihypertensive therapy when patients are medically stable and can swallow their medication safely. [8]

Blood Pressure s/p thrombectomy:  optimal BP range not well defined; keep SBP 150-180mm Hg prior to reperfusion (to maintain adequate collateral flow while occluded);  keep SBP <140mm Hg once recanalized.

Blood Pressure s/p thrombectomy and s/p tPA:  keep SBP <=180/105 x 24h

BEST TRIAL (2019) – BP after Endovacular Therapy for Ischemic Stroke [9]; study validates that a peak SBP of 158 mm Hg during 1st 24h post-EVT best dichotomies good versus bad outcomes in EVT-treated patients.

Malignant MCA Infarction:  IV antihypertensive therapy recommended if SBP >220mm Hg or DBP >120mm Hg in trials demonstrating benefit with DHC (DECIMAL / HAMLET) [8]

 

Intracerebral Hemorrhage

Elevations in BP may cause hemorrhage to expand, but increased MAP may be necessary to maintain cerebral perfusion.  INTERACT2 trial compared intensive BP lowering (<140mm Hg within 1 hour) vs traditional management (<180mm Hg) in patients with acute ICH (within 6 hours).  Intensive BP lowering improved modified Rankin scores, with similar adverse events.  INTERACT study suggested that more aggressive BP lowering is associated iwth reduced hematoma growth.  ATACH II is in progress.

  • SBP >200 or MAP >150aggressively reduce BP   [aggressive lowering is safe based on INTERACT2]
  • SBP >180 or MAP >130 + high ICP – insert ICP bolt, keep CPP 61-80 mm Hg
  • SBP >180 or MAP >130 + no ICP issues – reduce BP modestly (MAP 110 or BP 160/90)

Useful IV antihypertensives include: labetalol, nicardipine, esmolol, enalapril, hydralazine, nitroprusside, and nitroglycerin.

The results of INTERACT2 trial was published in NEJM (June, 2013).  In this trial, early intensive lowering of BP compared with a more conservative BP control did not result in reduced rates of death or major disability.  However, there were significantly better functional outcomes among patients assigned to intensive treatment, as well as better physical and psychological well-being. [5]

(ENLS 2017) AHA/ASA Guidelines and European Stroke Organization recommend target BP of <140mm Hg

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INTERACT studies equivocal, but recent ATACH2 shows more definitely negative results. Aggressive control of BP does not result in improved functional outcome or decreased hematoma expansion. Consider SBP control to 140-160mm Hg instead of 120-140mm Hg. [7]

Spinal Surgery

[coming soon]  Some neurosurgeons routinely keep MAP goals >85 mm Hg in spinal surgeries where perfusion of the spinal cord is critical.  Evidence for this practice is lacking, whereas the harms from induced hypertension and prolonged ICU stay is real.

References

[1] Uptodate.  “Treatment of Aneurysmal Subarachnoid Hemorrhage.”  Accessed 07/07/2016.

[2] Uptodate.  “Initial assessment and management of acute stroke.”  Accessed 07/07/2016.

[3] Uptodate.  “Management of acute severe traumatic brain injury.”  Accessed 07/07/2016.

[4] Uptodate.  “Spontaneous intracerebral hemorrhage: Treatment and prognosis.”  Accessed 07/07/2016.

[5] Anderson, Craig S. et al. “Rapid Blood-Pressure Lowering In Patients With Acute Intracerebral Hemorrhage”. New England Journal of Medicine 368.25 (2013): 2355-2365.

[6] ENLS 2017 (ICH)

[7] Burns, J., Fisher, J. and Cervantes-Arslanian, A. (2018). Recent Advances in the Acute Management of Intracerebral Hemorrhage. Neurosurgery Clinics of North America, 29(2), pp.263-272.

[8] Appiah, K., Minhas, J. and Robinson, T. (2017). Managing high blood pressure during acute ischemic stroke and intracerebral hemorrhage. Current Opinion in Neurology, p.1.

[9] Mistry EA et al, Stroke. 2019 Oct 7:STROKEAHA119026889. doi: 10.1161/STROKEAHA.119.026889. [Epub ahead of print] Blood Pressure after Endovascular Therapy for Ischemic Stroke (BEST): A Multicenter Prospective Cohort Study.