Tag Archives: protocol

Blood Pressure Augmentation in DCI

HIMALAIA Study – Netherlands. The only RCT looking at efficacy of BP augmentation in DCI in increasing cerebral blood flow (via CT perfusion).  Small n, negative study.

Tey article – XeCt to measure regional CBF, at onset of DCI suspicion, 5 days of induced HTN, hypervolemia, hemodilution. Compared XeCT before and after treatment and showed increase in regional CBF in worst vascular territories from 19 to 227ml/100g/min, significant reduction of regions with CBF <20ml/100g/min from 26 to 10%.

Indications:

  1. decrease in GCS >=1
  2. new focal deficits
  3. other etiologies excluded:
    1. worsening HCP
    2. recurrent bleeding
    3. epilepsy
    4. infectious disease
    5. hypoglycemia
    6. hyponatremia
    7. metabolic enceph from renal or liver failure

 

Baseline echo:  cardiomyopathy is a contraindication

Drug of choice:  Induce HTN with norepinephrine? based on reference below (we usually use phenylephrine)

End points:

  1. improvement of neurologic deficits
  2. occurrence of complication
  3. MAP 130 mm Hg
  4. SBP 230 mm Hg

 

Risks of Induced HTN:

  1.  line placement risks
  2. vasopressor risks
  3. can induce PRES, neurologic deterioration

 

Literature does not support the use of induced HTN, but how can we ignore bedside observations of patients who clinically improve with induced HTN?

Critique:

  1. Uses surrogate physiologic endpoints (CBF / cerebral o2 delivery). Are we looking at the right endpoint?  CBF correlates with cerebral O2 delivery assuming that other factors are constant (cerebral metabolism, arterial O2 content, partial pressure of O2 and CO2).
  2. Different patients have varied responses to induced HTN.  Induced HTN increases CBF only if cerebral autoregulation is distupted.

 

Dr. Diringer’s Advice: use induced HTN in a thoughtful and individualized manner.  Trial of induced HTN at onset of DCI.  If patient improves, continue.  If no change, back off and explore alternative treatments. If patient exam is poor (no followable exam), answer less clear but prolonged extreme elevations should be avoided.

References:

Gathier, C., Dankbaar, J., van der Jagt, M., Verweij, B., Oldenbeuving, A., Rinkel, G., van den Bergh, W. and Slooter, A. (2015). Effects of Induced Hypertension on Cerebral Perfusion in Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage. Stroke, 46(11), pp.3277-3281.

Diringer, M.  Editorial. Hemodynamic Therapy for Delayed Cerebral Ischemia in SAH.  Neurocritical Care Journal.  Pre-print.

 

 

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Classification and Severity of Diabetes Insipidus

Interesting classification of DI, taken from Neurology India, groups DI into mild and severe based on some clinical and lab findings.

 

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This was their protocol for diagnosis and management of DI in patients who underwent craniopharyngioma surgery.

 

Protocol for diabetes insipidus

  • Diagnosis:  UO > 4ml/kg/h over 6 h perior OR Na >145 mEq/L with USG <1.005
  • Monitoring
    • if drowsy, unable to drink – measure Is and Os hourly, sum every 6 hours
    • Foley until UO reasonably controlled
    • intraop Na if surgery >6h determines type of IV fluids and if pitressin required in OR
    • measure Na q6h day 1
    • measure Na q12h day 2 until stable x 3 days
    • measure Na daily x 1 week
  • Treatment
    • Fluids until patient is awake and demonstrates intact thirst mechanism
      • 0.45% saline when UO 4-6 ml/Kg/h
      • D5W when UO >6ml/kg/h
    • DDAVP
      • day 1 – 5 unit IV boluses of pitressin
      • started as early as possible, usually on 2nd day, oral DDAVP 100 ug tablets of fractions of tablets
  • Adequacy of control
    • based on serum Na rather than Is and Os
      • check frequency >150 or <130 or inc/dec by >10mEg/L in 1 day

 

Other pearls:

  • Adipsia may be complication of hypothalamic damage
    • diminished thirst sensation
    • higher risk of developing hpyernatremia
    • require round the clock DDAVP
    • need to be trained to drink 2-3L water per day
    • gradually resolves with partial or complete thirst recovery by 9 months
  • Polydipsic with high UO
    • patient compensating with increased PO intake, normal or low Na
    • at risk for water intoxication or hyponatremia
    • use oral rehydration solution rather than plain water

 

Reference:

Chacko, AriG et al. “Evaluation Of A Protocol-Based Treatment Strategy For Postoperative Diabetes Insipidus In Craniopharyngioma”. Neurology India 63.5 (2015): 712.

Dexmedetomidine for Nonventilated Patients with Delirium

IV Haloperidol 2.5-5mg every 10-30minutes until RASS 0 to -2 or max dose of 30mg

 

Haloperidol responders:

  • haldol infusion 0.5-1mg/hr titrate to RASS of 0

 

Haloperidol nonresponders:

  • continue Haldol infusion (0.5-1mg/hr)
  • start dexmedetomidine without loading dose at 0.2 ug/kg/hr and titrate to RASS of 0 to max of 0.7 ug/kg/min
  • once RASS = 0 on both drips, gradually taper and discontinue haldol

 

 

Reference:

Carrasco, Genís et al. “Dexmedetomidine For The Treatment Of Hyperactive Delirium Refractory To Haloperidol In Nonintubated ICU Patients”. Critical Care Medicine 44.7 (2016): 1295-1306.

 

EVD Weaning Protocols

10cm H20 prior to weaning

Initiation of weaning left to discretion of attending neurosurgeon.

GRADUAL WEANING

  1. raise drain height by 5 cm q24h to final level of 25 cm H20
  2. on Day 4, close the drain
  3. reopen if:
    1. ICP>20mm H20 x >5 minutes
    2. neurologic deterioration
    3. CT next day shows hydrocephalus

RAPID WEANING (within 24 hours)

  1. close drain immediately
  2. reopen if:
    1. ICP>20mm H20 x >5 minutes
    2. neurologic deterioration
    3. CT next day shows hydrocephalus

Failure of weaning = VP shunt insertion

**No differnece in incidence of HCP / need for VP shunting (62.5 vs 63.4% p=0.932)

**gradual weaning group spent 2.8 more days in the ICU (p=0.0002)

Neurocritical Care Society Guideline:

EVD weaning should be accomplished as quickly as is clinically feasible so as to minimize the total duration of EVD monitoring and VRI risk.

Two main methods to select those who will need permanent CSF diversion: clamping trial vs progressive wean.1. Clamping Trial: clamp EVD and monitor ICP, clinical status, ventricle size – determine whether VPS is required2. Progressive wean – progressively increase level of ventricular drainage (usually 5mm Hg/d) while monitoring ICP, clinical status, ventricular size, drainage volume Only 1 RCT (Klopfenstein, see reference listed) comparing the two methods. Clamping trial associated with shorter duration of EVD and ICU and hospital LOS with similar clinical outcomes.Currently decision to shunt is based on clinical deterioration. There is little information about the effects of subclinical hydrocephalus on cognitive function, chronic headache and fatigue. Studies have shown decrease in CBF in NPH, correlating with cognitive dysfunction.

References:

Fried, Herbert I. et al. “The Insertion And Management Of External Ventricular Drains: An Evidence-Based Consensus Statement”. Neurocritical Care 24.1 (2016): 61-81. Web.

Klopfenstein, Jeffrey D. et al. “Comparison Of Rapid And Gradual Weaning From External Ventricular Drainage In Patients With Aneurysmal Subarachnoid Hemorrhage: A Prospective Randomized Trial”. Journal of Neurosurgery 100.2 (2004): 225-229. Web.

Rabinstein, A. and Lanzino, G. (2018). Aneurysmal Subarachnoid Hemorrhage. Neurosurgery Clinics of North America, 29(2), pp.255-262.

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”