Elevated intracranial pressure: Difference between revisions

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**CN 6 palsy (false localizing sign)
**CN 6 palsy (false localizing sign)
*Papilloedema (bilaterally blurred optic disc margins)
*Papilloedema (bilaterally blurred optic disc margins)
*EKG with [[QT prolongation]] and [[T-wave inversions]]
*EKG with [[QT prolongation]] and T-wave inversions


==Differential Diagnosis==
==Differential Diagnosis==

Revision as of 22:46, 18 April 2016

Background

  • Monroe-Kellie hypothesis: The total volume of the intracranial space is constant, and comprises 3 main complements, namely the brain tissue (80%), blood (10% or 150mL) and CSF (10% or 150mL). An increase in the volume of any one of the components must necessarily be accompanied by a reduction in that of the other two in order to maintain the fixed total intracranial volume.
  • CSF is created at a rate of 20mL/hr or 500mL/day.
  • Neuronal injury occurs secondary to vascular compromise to brain cells either by a reduction in cerebral blood flow or direct ischemia. This is an emergency and requires emergent intervention if sustained > 5-10 minutes

Clinical Features

  • Headache (from increased pressure on heavily innervated meninges)
  • Characteristically worse in the morning
  • Nausea/vomiting
    • Vomiting due to increased ICP typically occurs in the morning
  • CN palsies
    • CN 6 palsy (false localizing sign)
  • Papilloedema (bilaterally blurred optic disc margins)
  • EKG with QT prolongation and T-wave inversions

Differential Diagnosis

Increased ICP is due to an increase in any one of the 3 components of the intracranial space

  1. Increased brain tissue
    • Neoplasms
    • Cerebral abscess
  2. Increased CSF volume
  3. Increased blood volume
    • Intracranial haemorrhage
    • Cerebral venous sinus thrombosis
    • Failed cerebral autoregulation (causing increases CBF or CBV)

ED Management

Increased ICP Treatment[1]

Head of Bed elevation

  • 30 degrees or reverse Trendelenburg will lower ICP[2]
  • Keep head and neck in neutral position, improving cerebral venous drainage
  • Avoid compressing IVJ or EVJ with tight C-collars or fixation of ETT

Maintain cerebral perfusion

  • CPP = MAP-ICP
    • If MAP <80, then CPP<60
    • Ultimately no Class 1 evidence for optimal CPP
  • Transfuse PRBCs with goal Hb > 10 mg/dL in severe TBI[3]
  • Provide fluids and vasopressors if needed for goal cerebral perfusion pressure (CPP) of 70-80 mmHg[4][5][6]
    • Mortality increases 20% for each 10 mmHg loss of CPP
    • Avoid dips in CPP < 70 mmHg, which is associated with cerebral ischemia and glutamate increase[7]
  • Vasopressors
    • Phenylephrine increases CPP without increasing ICP in animal models[8][9]
    • May be beneficial when patient is tachycardic (reflex bradycardia), but avoid phenylephrine if patient is already bradycardic (Cushing's reflex)
    • Phenylephrine may be associated with less cell injury as compared to norepinephrine in TBI[10]
  • IV fluids[11]
    • Maintain euvolemia, initially resuscitate with Normal Saline
    • Then consider hypertonic saline and/or mannitol
    • Do not use free water, low osmolal, dextrose-alone solutions, and colloids
    • Do not use Ringer's lactate as it is slightly hypotonic
    • Prefer NS over D5-NS if possible, but D5-NS may be necessary to avoid hypoglycemia, especially in younger pediatric patients
    • Correction of severe hypernatremia > 160 mmol/L (hypothalamic-pituitary injury, diabetes insipidus) should be gradual to not worsen cerebral edema

Osmotherapies

Therapies include either mannitol or hypertonic saline. In choosing the appropriate agent, coordinate with neurosurgery and take into account the patient's blood pressure. Mannitol may cause hypotension due to the osmotic diuresis.

  1. Mannitol[12]
    • If SBP > 90 mmHg
    • Bolus 20% at 0.25-1 gm/kg as rapid infusion over 15-20 min
    • Target Osm 300-320 mOsm/kg
    • Reduces ICP within 30min, duration of action of 6-8hr
    • Monitor I/O to maintain euvolemia during expected diuresis and use normal saline to volume replace
    • Do not use continuous infusions, as mannitol crosses the BBB after prolonged administration and contributes to cerebral edema
      • Consider hypertonic saline for further boluses
      • Hypertonic saline has higher osmotic gradient and is less permeable across BBB than mannitol
  2. Hypertonic saline may be more effective than mannitol, current standard of care[13]
    • Obtain baseline serum osmolarity and sodium
    • Most studies used 250 mL bolus of 7.5% saline with dextran[14]
    • Initial 250 cc bolus of 3% will reduce ICP and can be delivered through a peripheral line
    • Target sodium 145-155 mmol/dL

Prevent Cerebral Vasoconstriction

  • Hyperventilation does not improve mortality, used only as temporizing measure
  • Should only be used if reduction in ICP necessary without any other means or ICP elevation refractory to all other treatments:
    • Sedation
    • Paralytics
    • CSF drainage
    • Hypertonic saline, osmotic diuretics
  • Maintain PaCO2 35-40 mmHg for only up to 30 minutes, no longer if it can be avoided[15]
  • Hyperventilation to PaCO2 < 30 mmHg not indicated, and decreases cerebral blood flow to ischemic levels[16][17]

Seizure Control

  • Treat immediately with benzodiazepines and antiepileptic drugs (AEDs)
  • Consider propofol for post-intubation sedation
  • Seizure prophylaxis reduces seizures but does not improve long-term outcomes[18]
  • Treat any clinically apparent and EEG confirmed seizures
    • Consider prophylaxis in patients with any risk factors as above
    • Phenytoin or fosphenytoin first line agent by BTF guidelines[20]
      • Load 20 PE/kg IV, then 100 PE IV q8hrs for 7 days
      • Measure serum levels to titrate to therapeutic levels
    • Levetiracetam may be used as alternative[21]
      • 20 mg/kg load IV, followed by 1000 mg IV q12h for 7 days
      • Levetiracetam may have less frequent and severe adverse drug side effects events as compared to phenytoin
      • In many EDs, levetiracetam is current first line therapy

Intubation Pretreatment

Goal cerebral perfusion pressure (CPP) ~70mmHg

  • If need for RSI, consider pretreatment with lidocaine and/or fentanyl
    • May contribute to peri-intubation hypotension
  • Also ensure adequate sedation (prevent gag reflex)
  • Etomidate may cause adrenal insufficiency especially in head injured patients, so consider hydrocortisone if refractory hypotension post-intubation[22]

Decrease metabolic rate

  • Provide adequate sedation and analgesia
  • Avoid HYPERthermia and treat fever aggressively
    • However, hypothermia is not a necessary goal
    • Moderate hypothermia 32°C to 34°C controversial, large RCT showed no effect[23]

Other Critical Care Measures

  • DVT prophylaxis with SCDs, no anticoagulation
  • Stress ulcer prophylaxis with H2 blocker/PPI and sucralfate to avoid Cushing's ulcers
  • Good glycemic control, but tight maintenance not supported[24]
  • Steroids, methylprednisolone contraindicated in severe TBI (risk of death increased in CRASH 2004 trial)[25]
  • Routine paralysis not indicated[26]
    • Increased risk of pneumonia and ICU length of stay
    • However, may be used for refractory ICP elevation
Barbiturate Coma[27]
  • For ICP refractory to maximal medical and surgical therapy
  • Only for hemodynamically stable patients
  • Induce with the following:
    • Pentobarbital 10 mg/kg over 30 min
    • Then 5 mg/kg/hr for 3 hrs
    • Followed by 1 mg/kg/hr

Neuro ICU Management

  • Ensure data accurate
    • Observe for accurate waveforms in arterial and ICP monitors
      • EVD zeroed at ear, changes with coughing/positioning
      • Arterial line zeroed at ear (for accurate CPP measurement; although typically level at heart reasonably accurate
  • Assess ABC (as increased ICP often causes decline in mental status)
    • If need to intubate - ensure measures to avoid coughing/bucking (increases ICP)
      • Lidocaine 1% 1ml/kg 1x IV bolus as premedication

Goals

  • Keep CPP 60-110mmHg
    • If <110 utilize pressors (levophed [preferred] or neosynephrine)
    • Levophed: start at 4 mcg/min; maximum 20 mcg/min.
    • Phenylephrine: start at 0.4 mcg/kg/min; maximum 9 mcg/kg/min.
  • Keep ICP < 20mmHg (nonsustained temporary elevations <5 minutes ok)

Take Stepwise approach to treatment

1st (conservative)

  • Elevate Head of bed to 30-45 deg and keep head midline
    • May "sandbag" head of those in c-collar to promote venous drainage(c-collar can restrict venous outlfow)
  • Control agitation/pain
    • Narcotics, benzodiazepines, sedative hypnotics
      • Favor short acting medications to allow neuro exam checks
      • Versed, Fentanyl and propofol are often appropriate.
  • Maintain normocapnia (pCO2 35-40)
  • Maintain normothermia
    • Treat shivering
      • Bair hugger (warms skin temperature)
      • APAP 650 q6prn for temp >38.5°F
  • Maintain euvolemia
  • Maintain euglycemia

2nd (Intervention-short term)

  • Hyperventilate to pCO2 30-35mmHg
    • This is short term as patient will equilibrate; is only meant as a temporizing measure. Attempt to wean to normocapnia as soon as able. Further do not overventilate past 25mmHg as may exacerbate damage via cerbral hypoxia (CO2 is primarily involved in autoregulation of cerebral vasculature).
  • Hypertonic fluids
    • Mannitol 20% 1-1.5g/kg rapid IV bolus (no need for central line) OR
    • 23% Na 30mL over 15 minutes (Needs central line)
  • Consult Neurosurgery (urgent) for possible evacuation or ventricular drainage
    • This is especially relevant for mass lesions causing mass effect, hydrocephalus and intracranial bleeds

3rd (Intervention- long term)

  • Hypertonic fluid maintenance
    • Iatrogenic hypernatremia. Use 3% NaCl to maintain na >145 with q6hr serum Na cks.
      • 3%NS at 1mL/kg/hr appropriate (typically start at 50mL/hr).
      • May continue to push Na > 145, then >150 then >155 prn to manage ICP
        • Eventually osmotic pressures will equilibrate over days. requiring higher Na values (rationale behind pushing Na slowly upward as needed rather than pushing hypernatremia to maximum).
    • Iatrogenic hyperosmolar maintenance
      • Mannitol 20% 0.5g/kg q4hrs with seurm Osm checks q6hrs. (Target osm of 300-320 mOsm/L)

4th (Intervention - Refractory elevation)

  • Pentobarbital coma
    • loading dose: 5-20mg/kg bolus then 4mg;kg/hr titrated to burst supression on EEG.
  • Induced hypothermia (32-34°F)
    • Cooling System (ie. Arctic Sunt, Stryker Medi-Therm)
      • Must perform surveillance cultures (routine blood culture, UA, CXR) every 48 hours since artificially supressing fever.
    • Shivering protocol
      • Vecuronium or Pancuronium [28]
  • Paralytics
    • Risk of ICU myopathy/neuropathy with long term use.

See Also

References

  1. ↑ Brain Trauma Foundation, American Association of Neurological Surgeons, Congress of Neurological Surgeons. Guidelines for the management of severe traumatic brain injury. J Neurotrauma. 2007;24 Suppl 1(supplement 1):S1-S106.fulltext
  2. ↑ Schwarz S et al. Effects of body position on intracranial pressure and cerebral perfusion in patients with large hemispheric stroke. Stroke. 2002; 33: 497-501
  3. ↑ Schöchl H, Solomon C, Traintinger S, Nienaber U, Tacacs-Tolnai A, Windhofer C, Bahrami S, Voelckel W: Thromboelastometric (ROTEM) findings in patients suffering from isolated severe traumatic brain injury. J Neurotrauma. 2011, 28 (10): 2033-2041.
  4. ↑ Bouma GJ et al. Blood pressure and intracranial pressure-volume dynamics in severe head injury: relationship with cerebral blood flow. J Neurosurg 77:15-19, 1992
  5. ↑ Rosner MJ et al. Cerebral perfusion pressure management in head injury. J Trauma 30:933-941, 1990
  6. ↑ Kirkman MA, Smith M. Intracranial pressure monitoring, cerebral perfusion pressure estimation, and ICP/CPP-guided therapy: a standard of care or optional extra after brain injury? Br J Anaesth. 2014 Jan;112(1):35-46.
  7. ↑ Vespa P. What is the Optimal Threshold for Cerebral Perfusion Pressure Following Traumatic Brain Injury? Neurosurg Focus. 2003;15(6).
  8. ↑ Friess SH et al. Early cerebral perfusion pressure augmentation with phenylephrine after traumatic brain injury may be neuroprotective in a pediatric swine model. Crit Care Med. 2012 Aug;40(8):2400-6.
  9. ↑ Watts AD et al. Phenylephrine increases cerebral perfusion pressure without increasing intracranial pressure in rabbits with balloon-elevated intracranial pressure. J Neurosurg Anesthesiol. 2002 Jan;14(1):31-4.
  10. ↑ Friess SH et al. Differing Effects when Using Phenylephrine and Norepinephrine To Augment Cerebral Blood Flow after Traumatic Brain Injury in the Immature Brain. J Neurotrauma. 2015 Feb 15; 32(4): 237–243.
  11. ↑ Haddad SH and Arabi YM. Critical care management of severe traumatic brain injury in adults. Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine201220:12.
  12. ↑ Muizelaar JP, Lutz HA, Becker DP: Effect of mannitol on ICP and CBF and correlation with pressure autoregulation in severely head-injured patients. J Neurosurg. 1984, 61: 700-706.
  13. ↑ Kamel H, Navi BB, Nakagawa K, Hemphill JC, Ko NU: Hypertonic saline versus mannitol for the treatment of elevated intracranial pressure: a meta-analysis of randomized clinical trials. Crit Care Med. 2011, 39 (3): 554-559.
  14. ↑ Holmes, J. Therapeutic uses of Hypertonic Saline in the Critically Ill Emergency Department Patient. EB Medicine 2013
  15. ↑ Coles JP, Minhas PS, Fryer TD, Smielewski P, Aigbirihio F, Donovan T, Downey SP, Williams G, Chatfield D, Matthews JC, Gupta AK, Carpenter TA, Clark JC, Pickard JD, Menon DK: Effect of hyperventilation on cerebral blood flow in traumatic head injury: clinical relevance and monitoring correlates. Crit Care Med. 2002, 30 (9): 1950-1959.
  16. ↑ Stocchetti N et al. Hyperventilation in head injury: a review. Chest. 2005 May;127(5):1812-27.
  17. ↑ Bullock R, et al: Guidelines for the Management of Severe Traumatic Brain Injury. J Neurotrauma. 2007, 24 (Suppl 1): S1-S106.
  18. ↑ Khan AA, Banerjee A. The role of prophylactic anticonvulsants in moderate to severe head injury. Int J Emerg Med. 2010 Jul 22;3(3):187-91.
  19. ↑ Thompson K, Pohlmann-Eden B, Campbell LA. Pharmacological treatments for preventing epilepsy following traumatic head injury (Protocol). Cochrane Database of Systematic Reviews 2012, Issue 6. Art. No.: CD009900.
  20. ↑ Khan AA, Banerjee A. The role of prophylactic anticonvulsants in moderate to severe head injury. Int J Emerg Med. 2010 Jul 22;3(3):187-91.
  21. ↑ Szaflarski JP et al. Prospective, randomized, single blinded comparative trial of intravenous levetiracetam versus phenytoin for seizure prophylaxis. Neurocrit Care 2010;12:165-172.
  22. ↑ Schulz-Stübner S: Sedation in traumatic brain injury: avoid etomidate. Crit Care Med. 2005, 33 (11): 2723.
  23. ↑ Marion DW, Penrod LE, Kelsey SF, et al: Treatment of traumatic brain injury with moderate hypothermia. New Engl J Med. 1997, 336: 540-546.
  24. ↑ Marion DW: Optimum serum glucose levels for patients with severe traumatic brain injury. F 1000 Med Rep. 2009, 1: 42.
  25. ↑ Roberts I, Yates D, Sandercock P, Farrell B, Wasserberg J, Lomas G, Cottingham R, Svoboda P, Brayley N, Mazairac G, Laloë V, Muñoz-Sánchez A, Arango M, Hartzenberg B, Khamis H, Yutthakasemsunt S, Komolafe E, Olldashi F, Yadav Y, Murillo-Cabezas F, Shakur H, Edwards P, CRASH trial collaborators: Effect of intravenous corticosteroids on death within 14 days in 10008 adults with clinically significant head injury (MRC CRASH trial): randomised placebo-controlled trial. Lancet. 2004, 364: 1321-1328.
  26. ↑ Haddad SH and Arabi YM. Critical care management of severe traumatic brain injury in adults. Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine 2012. 20:12.
  27. ↑ Kassell NF, Hitchon PW, Gerk MK, Sokoll MD, Hill TR: Alterations in cerebral blood flow, oxygen metabolism, and electrical activity produced by high dose sodium thiopental. Neurosurgery. 1980, 7: 598-603.
  28. ↑ Angela Logan et al Optimal Management of Shivering During Therapeutic Hypothermia After Cardiac Arrest Crit Care Nurse 2011;31:e18-e30 http://ccn.aacnjournals.org/content/31/6/e18.full.pdf
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