1. Medical and Surgical Management of Intracranial Bleeding
Wendy L. Wright, MD, FCCM, FNCS
Chief of Neurology and Medical Director of the Neuroscience ICU
Emory University Hospital Midtown
Associate Professor of Neurology and Neurosurgery
Emory University School of Medicine
Atlanta, GA

2. Objectives
Review anatomy, physiology and causes of intracranial bleeding
Review management of “surgical” hemorrhages
Epidural hematoma
Subdural hematoma
Subarachnoid hemorrhage
Intraventricular hemorrhage
Discuss important management principles for intracerebral hemorrhage
Differentiate management points for cerebral venous sinus thrombosis

3. Intracranial Hemorrhage
“Intracranial” hemorrhage could be used to describe many locations of bleeding
Epidural hematoma, subdural hematoma
Subarachnoid hemorrhage
Intraventricular hemorrhage
Intraparenchymal (intracerebral) hemorrhage
Hypertensive (“Spontaneous”)
Hemorrhage from vascular malformation
Hemorrhagic conversion of ischemic stroke
Traumatic contusion
Tumor
Cerebral venous sinus thrombosis

5. Intracranial Hemorrhage
Diagnosis made by head CT
Usually not MRI
May need MRI to look at older, smaller bleeds or to look for the etiology of the bleed, but non-contrasted head CT remains the imaging study of choice for intracranial hemorrhage

6. “Surgical” Hemorrhages
Any intracranial blood should prompt neurosurgical consultation
However, many do not require neurosurgical procedures

7. Epidural Hematoma Blood collects between the dura and the skull
Etiology is trauma, usually arterial
Lucid interval, followed by focal signs, then coma due to increased intracranial pressure
Surgical management
With seizure prophylaxis

8. Subdural Hematoma Bleeding between the dura and arachnoid
Etiology is tearing of bridging veins, usually from minor trauma
Gradually increasing headache and confusion
Management can be surgical or non-intervention
Seizure prophylaxis

9. Subarachnoid Hemorrhage
Etiology
About 50/50 traumatic to vascular
Vascular
Overwhelming majority are due to aneurysmal rupture
Can be caused by other vascular malformations
“Non-aneurysmal” SAH may be due to venous bleeding
Symptoms of aneurysmal rupture
Sudden onset worst headache
Stiff neck, seizure, loss of consciousness, focal signs
Diagnosis CT
LP, MRI if CT is non-diagnostic

10. Van Gijn
Liebenberg

11. Mervyn D. I. Vergouwen • Stefan Wolf • Gregory Zipfel
Critical Care Management of Patients Following Aneurysmal Subarachnoid Hemorrhage
Recommendations from the Neurocritical Care Society’s Multidisciplinary Consensus Conference
Michael N. Diringer • Thomas P. Bleck • J. Claude Hemphill III • David Menon • Lori Shutter •
Paul Vespa • Nicolas Bruder • E. Sander Connolly Jr. • Giuseppe Citerio • Daryl Gress •
Daniel Ha¨nggi • Brian L. Hoh • Giuseppe Lanzino • Peter Le Roux • Alejandro Rabinstein •
Erich Schmutzhard • Nino Stocchetti • Jose I. Suarez • Miriam Treggiari • Ming-Yuan Tseng •
Mervyn D. I. Vergouwen • Stefan Wolf • Gregory Zipfel
Neurocrit Care (2011) 15:211–240

12. Management Rapid referral to centers with appropriate facilities
Prevent re-bleeding
Conservative
Secure aneurysm
Surgical
Endovascular
Provide general neurocritical care
Prevent/treat other complications
Especially vasospasm
Hydrocephalus
Cerebral edema/Increased intracranial pressure
Cerebral salt wasting
Cardiac and pulmonary dysfunction
Seizures

13. One common SAH mimic seen in ICU setting:
A CT can be falsely positive for SAH if diffuse cerebral edema is present (for example, after anoxic brain injury). Blood in congested subarachnoid vessels will be hyperdense.
van Gijn

14. Intraventricular Hemorrhage
Bleeding into the ventricular system
Where CSF is produced
IVH can cause fatal hydrocephalus
Can result from trauma or hemorrhagic stroke
Management is CSF diversion
Ongoing trials with intraventricular thrombolysis

15. Intraventricular Hemorrhage

16. Intracerebral Hemorrhage

17. Signs and Symptoms Sudden onset headache Vomiting
Reduced/lost consciousness
Seizure
Stiff neck
Symptoms identical to ischemic stroke
Weakness, numbness, difficulty walking, visual change, speech difficulties

18. Diagnosis Made by Head CT
Normal
Intracerebral Hemorrhage

19. Possible Causes of ICH
“Spontaneous” ICH is meant to designate “non-traumatic”
About 10% of all strokes
Causes may include
Vascular malformations
Arteriovenous malformation
Telangectasia
Cavernous malformation
Venous malformation
Tumors
Primary brain tumors- pilocytic astrocytoma
Metastatic tumors prone to bleeding- lung, renal cell, melanoma, papillary thyroid, hepatocellular
Infectious lesions
Mycotic aneurysm
Hemorrhagic leukoencephalopathy
Cerebral venous thrombosis

20. Underlying Hemostatic Abnormalities
Patients on oral anticoagulants
12-14% of ICH
Correct the INR as rapidly as possible
Vitamin K, fresh frozen plasma, prothrombin complex concentrate
Recombinant factor VIIa?
Heparin
Reverse with protamine sulfate
Dose depends on rate of administration and how long ago heparin was stopped
NTE 5mg/min or can result in hypotension
Acquired or congenital factor deficiencies
Qualitative or quantitative platelet abnormalities
Including antiplatelet therapy
Utility and safety of platelet transfusion is unknown

21. Other Risk Factors for ICH
Vascular risk factors
Hypertension, diabetes, smoking
Recent trauma or surgery
Carotid endarterectomy, carotid stenting may cause hyperperfusion related hemorrhage
Alcohol or illicit drug use
Stimulants (including diet pills, amphetamines), sympathomimetics
Liver disease, hematologic disorders
Cerebral amyloid angiopathy

23. Cerebral Amyloid Angiopathy
Risk for lobar intracerebral hemorrhage
Usually associated with dementia
Risk of bleeding increases with the use of antiplatelet medication
Microbleeds seen on T2*-weighted gradient echo MRI
Usually associated with beta amyloid deposits

24. Lobar Hemorrhage

26. Initial Management of ICH
Rapid neuroimaging with head CT or brain MRI is recommended to distinguish ICH from ischemic stroke
And to look for any underlying causes
Especially those that may require surgical management
Address any underlying bleeding diathesis, antithrombotic agents
Blood pressure management may be needed acutely to prevent the risk of rebleeding
Highest risk in the first hours

27. Blood Pressure and ICH
Chronic hypertension is a modifiable risk factor of intracerebral hemorrhage
Frequently and often markedly elevated in acute ICH
Guidelines for goal blood pressure are merely suggestions, pending the results of ongoing clinical trials
It is “probably safe” to lower markedly elevated blood pressure in the setting of acute ICH
Maintain cerebral perfusion pressure to ensure adequate blood flow to the brain, considering possible increased intracranial pressure
CPP= mean arterial pressure-intracranial pressure
Goal CPP also controversial (≥60mm Hg probably adequate; some recommend a range of mmHg)

29. 2007 ICH Guidelines, Broderick

30. General Management of ICH
Initial monitoring and management is best accomplished in neurocritical care unit
Optimal glucose management is unclear; hyperglycemia seems deleterious but hypoglycemia should be avoided
Fever should be avoided
Maintain normothermia
The utility of prophylactic anticonvulsant medication remains uncertain
Continuous EEG monitoring should be considered in ICH patients with depressed mental status out of proportion to their degree of hemorrhage

31. Medical Treatment of ICH
1999 ICH guidelines reported 4 randomized trials
Steroid vs. placebo (2)
Hemodilution vs. best medical therapy (1)
Glycerol vs. placebo (1)
All showed no benefit
In one of the steroid trials, patients were more likely to suffer infectious complications

32. Management of Increased Intracranial Pressure
Patients with intracerebral hemorrhage often require intracranial pressure monitoring
CSF diversion via ventriculostomy drain should be considered for patients with hemorrhage extending into the 3rd or 4th ventricles
Intracranial pressure may be increased before (or without) being reflected on the monitoring device, and treatments for increase in pressure may need to be started based on clinical scenario
Surgical options may include evacuation of hematoma, mass lesion that caused the bleeding

33. Surgical Management Surgically amenable lesions include:
Cerebellar hematomas causing clinical deterioration and/or hydrocephalus
Initial treatment with intraventricular hemorrhage alone rather than surgical evacuation is not recommended
Lobar hemorrhage >30mL within 1 cm of the surface of the brain may be considered
Surgical therapy in other situations is usually not considered
Minimally invasive clot evacuation is still experimental
Very early craniectomy may be harmful due the risk of rebleeding

34. Withdrawal of Technological Support
DNR orders are extremely common in ICH
May bias predictive models to make ICH outcomes look worse than it would if full care was provided
Withdrawal of life-sustaining support is the most common cause of immediate death in ICH
Recommendations are implement aggressive full care early after ICH onset and postpone any new DNR orders until at least the second full day of hospitalization

35. Prevention of Recurrent ICH
The most consistently identified risk factor for recurrent ICH is lobar location of the initial ICH
This finding likely represents the association of cerebral amyloid angiography
Hemorrhage indicative of hypertensive vasculopathy tends to occur in the basal ganglia, thalamus or brain stem
Other factors linked to recurrence are older age, post-ICH anticoagulation, carriership of the apolipoprotein E ε2 or ε4 alleles, and the greater number of microbleeds on T2*-weighted gradient-echo MRI

36. Prevention of Recurrent ICH
Hypertension is the most important currently modifiable risk factor
After acute ICH, a goal target of a normal BP <140/90 is probably reasonable (<130/80 if diabetes or chronic kidney disease)
Avoidance of long-term anticoagulation for the treatment of non-valvular afib after ICH is probably recommended after lobar ICH because of the high risk of ICH recurrence
The decision of whether (and when) to restart anticoagulation or antiplatelet medications depends on how strong the indication for these medications is, and the presumed risk of rebleeding

37. Cerebral Venous Thrombosis
CVT accounts for 0.5% to 1% of all strokes
Mostly affects young people, women of childbearing age
Commonly presents with headache
Though some present with a focal neurological deficit, decreased level of consciousness, seizures or intracranial hypertension without focal signs
Insidious onset can create a diagnostic challenge

38. 2011 guideline

39. Cerebral Venous Thrombosis
A prothrombotic factor or direct cause is identified in about 2/3 of patients
Diagnosis is usually made by venographic studies with CT (CTV) or MRI (MRV) to demonstrate obstruction of the venous sinuses

42. Risk Factors Acquired Genetic risks Hematologic disorders
Surgery
Trauma
Pregnancy
Puerperium
Antiphospholipid syndrome
Cancer
Exogenous hormones
Oral contraceptives
Infections
Mainly in parameningeal locations
CVT caused by infection is more common in children
Mechanical precipitants
Epidural blood patch
Spontaneous intracranial hypotension
Lumbar puncture
Genetic risks
Inherited thrombophilia/ hypercoaguability
Antithrombin III deficiency
Protein C deficiency
Protein S deficiency
Factor V Leiden positivity
Hyperhomocysteinemia
Mutation G2020A of factor II
Hematologic disorders
Paroxysmal nocturnal hemoglobinuria
Polycythemia, thrombocythemia
Systemic diseases
Systemic lupus erythematosus
Inflammatory bowel disease

43. Pregnancy and the Puerperium
Common causes of prothrombotic states
Most pregnancy related CVTs occur in the third trimester or 6-8 weeks after birth
During the puerperium, additional risk factors include infection; increasing maternal age; hypertension; vomiting; and instrumental delivery or Cesarean section

44. Treatment Initiate anticoagulation, unless there is a contraindication
In the presence of CVT, intracranial hemorrhage is NOT an contraindication to anticoagulation
Treat any underlying cause, if able
Including antibiotics for infection, or surgical drainage of purulent collections of infectious sources associated with CVT when appropriate
Treat a seizure if one occurs, but routine use of prophylatic antibiotics is not recommended

45. Put the treatment algo.

46. Management of Increased Intracranial Pressure
Monitor for visual field loss
May require cerebrospinal fluid diversion
Guidelines say that acetazolamide is reasonable to decrease CSF production
Patients with neurologic deterioration due to severe mass effect or intracranial hemorrhage causing intractable intracranial hypertension may be eligible for hemicraniectomy
Steroids are not indicated to treat cerebral edema
Unless needed for another underlying disease

47. Conclusion
Intracranial bleeding should prompt neurosurgical evaluation
Intracranial blood is usually evaluated by emergent non-contrasted head CT
Intracerebral hemorrhage (ICH) is a distinct form of stroke
Although there is no specific treatment, there are distinct management expectations
Hypertension is a controllable risk factor
There is a specific treatment for CVST
Anticoagulation, which is counterintuitive!

48. References
Rinkel GJE, Djibouti M, Algra A, van Gijn J. Prevalence and risk of rupture of intracranial aneurysms: a systematic review. Stroke 1998; 29:
van Gijn J, Kerr RS, Rinkel GJ. Subarachnoid haemorrhage. Lancet 2007;369:
Liebenberg WA, Worth R, Firth GB, Olney J, Norris JS. Aneurysmal subarachnoid haemorrhage: guidance in making the correct diagnosis. Postgrad Med J 2005; 81:
Suarez JI, Tarr RW, Selman WR. Aneurysmal Subarachnoid Hemorrhage. N Engl J Med 2006;354:
Bederson JB, Issam AA, Wiebers DO, Piepgras D, Haley EC, Brott T, Hademenos G, Chyatte D, Rosenwasser R, and Caroselli C. Recommendations for the management of patients with unruptured intracranial aneurysms: a statement for healthcare professionals from the stroke council of the American Heart Association. Stroke 2000;31:
Mayberg MR, Batjer HJ, Darcy R, Diringer M, Halry EC, Heros RC, Sternau LL, Torner J, Adams, HP, Feinberg W, Thies W. Guidelines for the management of subarachnoid hemorrhage. Circulation 1994; 90 (5):
Broderick J, Connolly S, et al. Guidelines for the Management of Spontaneous Intracerebral Hemorrhage in Adults: 2007 Update: A Guideline From the American Heart Association/American Stroke Association Stroke Council, High Blood Pressure Research Council, and the Quality of Care and Outcomes in Research Interdisciplinary Working Group: The American Academy of Neurology affirms the value of this guideline as an educational tool for neurologists. Circulation 2007;116:e391-e413.