Traumatic intracerebral hemorrhage

Background

It is the pathological accumulation of blood within the cranium. This may occur within the brain parenchyma or the surrounding meningeal spaces.

Adult GCS

Eye Opening Verbal Motor
6: Obeys commands
5: Oriented 5: Localizes to pain
4: Spontaneously opens 4: Confused speech 4: Withdraws from pain (normal flexion)
3: Opens to command 3:Inappropriate words 3: Decorticate posturing (abnormal flexion)
2: Opens to pain 2: Incomprehensible sounds 2: Decerebrate posturing (extension)
1: Does not open 1: No response 1: No response
  • 14-15: Mild
  • 9-13: Moderate
  • 3-8: Severe

Clinical Features

Differential Diagnosis

Intracranial Hemorrhage Types

Concussion

Maxillofacial Trauma

Evaluation

Workup

Management

Prevent further brain injury

Elevating head of bed

  • 30 degree elevation will help decrease ICP by increasing venous outflow[2]

Seizure Prophylaxis and Treatment

  • Prophylactic antiepileptics not recommended[3]
  • Continuous EEG monitoring probably indicated in ICH patients with depressed mental status that is out of proportion fo degree of brain injury[4]
  • Antiepileptics indicated for clinical seizures or seizures on EEG in patients with altered mental status[5]

Blood Pressure

  • Rapid SBP lowering <140 has been advocated with early research showing improved functional outcome[6], but more recent work has found no difference between SBP <140 and <180[7]
  • SBP >200 or MAP >150
    • Consider aggressive reduction w/ continuous IV infusion
  • SBP >180 or MAP >130 and evidence or suspicion of elevated ICP
    • Consider reducing BP using intermittent or continuous IV meds to keep CPP >60-80
  • SBP >180 or MAP >130 and NO evidence or suspicion of elevated ICP
    • Consider modest reduction of BP (e.g. MAP of 110 or target BP of 160/90)


  • Nicardipine in ICH: Start at 5mg/hr, increase 2.5mg q5min until the target blood pressure is achieved and then immediately titrate down to maintenance infusion of 3mg/hr.
  • Labetalol in ICH: 20mg bolus over 1-2 minutes, repeat q3-5 mins until target blood pressure is achieved and then start an infusion of 1-8mg/min.

Reverse coagulopathy

Antiplatelet Reversal

Includes aspirin, prasugrel, clopidogrel

  • Consider desmopressin (0.3mcg/kg)
  • Platelet transfusion
    • No known thrombocytopenia: increases mortality; do NOT give[9]
    • Known or diagnosed thrombocytopenia: consider if platelets <50,000
      • Some hematologists and neurosurgeons recommend for <100,000, despite lack of evidence for improved outcomes

Increased ICP Treatment[10]

Head of Bed elevation

  • 30 degrees or reverse Trendelenburg will lower ICP[11]
  • 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[12]
  • Provide fluids and vasopressors if needed for goal cerebral perfusion pressure (CPP) of 70-80 mmHg[13][14][15]
    • 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[16]
  • Vasopressors
    • Phenylephrine increases CPP without increasing ICP in animal models[17][18]
    • 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[19]
  • IV fluids[20]
    • 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[21]
    • 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[22]
    • Obtain baseline serum osmolarity and sodium
    • Most studies used 250 mL bolus of 7.5% saline with dextran[23]
    • 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[24]
  • Hyperventilation to PaCO2 < 30 mmHg not indicated, and decreases cerebral blood flow to ischemic levels[25][26]

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[27]
  • 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[29]
      • 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[30]
      • 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[31]

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[32]

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[33]
  • Steroids, methylprednisolone contraindicated in severe TBI (risk of death increased in CRASH 2004 trial)[34]
  • Routine paralysis not indicated[35]
    • Increased risk of pneumonia and ICU length of stay
    • However, may be used for refractory ICP elevation
Barbiturate Coma[36]
  • 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

Repeat Imaging in Traumatic Subarachnoid Hemorrhage[37][38]

  • Patients with normal neurologic exam NOT on anticoagulation do not need a repeat head CT
    • Recommend 6 hour observation
  • Patients with GCS 13 or higher may not need a NSGY consult, regardless of antiplatelet or anticoagulation, as long as agent properly reversed

See Also

References

  1. ↑ Choosing wisely ACEP
  2. ↑ http://stroke.ahajournals.org/content/38/6/2001.full
  3. ↑ AHA/ASA Guidelines for the Management of Spontaneous Intracerebral Hemorrhage 2015
  4. ↑ AHA/ASA Guidelines for the Management of Spontaneous Intracerebral Hemorrhage 2015
  5. ↑ AHA/ASA Guidelines for the Management of Spontaneous Intracerebral Hemorrhage 2015
  6. ↑ Anderson CS, Heeley E, Huang Y, et al. Rapid blood-pressure lowering in patients with acute intracerebral hemorrhage. N Engl J Med. 2013; 368:2355-2365.
  7. ↑ Qureshi AI, Palesch YY, Barsan WG, et al. Intensive Blood-Pressure Lowering in Patients with Acute Cerebral Hemorrhage. N Engl J Med. 2016; 1-11. [Epub ahead of print].
  8. ↑ Crash-3 Trial
  9. ↑ (PATCH trial)
  10. ↑ 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
  11. ↑ 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
  12. ↑ 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.
  13. ↑ 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
  14. ↑ Rosner MJ et al. Cerebral perfusion pressure management in head injury. J Trauma 30:933-941, 1990
  15. ↑ 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.
  16. ↑ Vespa P. What is the Optimal Threshold for Cerebral Perfusion Pressure Following Traumatic Brain Injury? Neurosurg Focus. 2003;15(6).
  17. ↑ 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.
  18. ↑ 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.
  19. ↑ 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.
  20. ↑ Haddad SH and Arabi YM. Critical care management of severe traumatic brain injury in adults. Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine201220:12.
  21. ↑ 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.
  22. ↑ 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.
  23. ↑ Holmes, J. Therapeutic uses of Hypertonic Saline in the Critically Ill Emergency Department Patient. EB Medicine 2013
  24. ↑ 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.
  25. ↑ Stocchetti N et al. Hyperventilation in head injury: a review. Chest. 2005 May;127(5):1812-27.
  26. ↑ Bullock R, et al: Guidelines for the Management of Severe Traumatic Brain Injury. J Neurotrauma. 2007, 24 (Suppl 1): S1-S106.
  27. ↑ 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.
  28. ↑ 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.
  29. ↑ 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.
  30. ↑ Szaflarski JP et al. Prospective, randomized, single blinded comparative trial of intravenous levetiracetam versus phenytoin for seizure prophylaxis. Neurocrit Care 2010;12:165-172.
  31. ↑ Schulz-Stübner S: Sedation in traumatic brain injury: avoid etomidate. Crit Care Med. 2005, 33 (11): 2723.
  32. ↑ Marion DW, Penrod LE, Kelsey SF, et al: Treatment of traumatic brain injury with moderate hypothermia. New Engl J Med. 1997, 336: 540-546.
  33. ↑ Marion DW: Optimum serum glucose levels for patients with severe traumatic brain injury. F 1000 Med Rep. 2009, 1: 42.
  34. ↑ 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.
  35. ↑ 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.
  36. ↑ 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.
  37. ↑ Borczuk, et al. Patients with traumatic subarachnoid hemorrhage are at low risk for deterioration or neurosurgical intervention. J Am Coll Surg. 2014; 219.
  38. ↑ Nahmias JT, et al. Mild Traumatic Brain Injuries Can Be Safely Managed Without Neurosurgical Consultation: The End of a Neurosurgical "Nonsult"? American Association for the Surgery of Trauma. Annual Meeting. 2016
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