Intracranial Hemorrhage

Written By: Zoe Oliver
University of Manitoba, Winnipeg, Canada

Edited By: Emily Senecal, MD
Harvard Medical School, Boston Massachusetts

Intracranial Hemorrhage Objectives

Upon completion of this self-study module, you should be able to:

  • Cite classic history and physical exam findings in intracranial hemorrhage.
  • Categorizing the types of hemorrhage seen on computed tomography (CT) images of the brain
  • Interpreting lumbar puncture results
  • Describe the role of CT angiography
  • Outline the first steps in managing a patient with a deteriorating level of consciousness
  • Outline the steps in managing a patient with an intracerebral hemorrhage.

Hemorrhage within the fixed vault of the cranium is a life-threatening emergency. The accumulated blood volume causes increased intracranial pressure, which in turn damages the brain and can lead to permanent neurologic deficit or death. Timely diagnosis and intervention by the emergency physician can be a major determinant of patient outcome.

Intracranial hemorrhages (ICH) fall into four broad categories:

  1. Epidural hematoma
  2. Subdural hematoma
  3. Subarachnoid hemorrhage
  4. Intracerebral hemorrhage

Be sure to understand the difference between the terms intracranial hemorrhage and intracerebral hemorrhage. The former refers to all bleeding occurring within the skull, while the latter indicates bleeding within the brain parenchyma.

Classic Presentation

All intracranial hemorrhages (ICH) share some classic clinical features. Common presenting symptoms include headache, nausea, vomiting, confusion, somnolence, or seizure. There is a wide clinical spectrum: patients can be alert and conversant, or moribund. In elderly, alcoholic, and anticoagulated patients, even minor head trauma can result in devastating intracranial bleeding. Trauma can precede any type of ICH, but it is most commonly associated with epidural and subdural hematomas.

Despite these commonalities, there can be differences in the presentation of the four types of ICH:

Subarachnoid Hemorrhage

The classic presenting symptom of SAH is acute onset �thunderclap� headache that may be accompanied by loss of consciousness, vomiting, neck stiffness, or seizure. Thunderclap headaches reach maximum intensity within seconds. The headache is typically occipital or unilateral. A significant proportion of patients will also have a warning (sentinel) headache. Of note, not all patients with SAH present with this classic symptom and a gradual onset headache does not preclude the diagnosis of SAH. The Hunt and Hess Grading System is one method used to describe patients with SAH.

Hunt & Hess Scale (Non-Traumatic SAH)
Description Grade
Asymptomatic, mild headache, slight nuchal rigidity 1
Moderate to severe headache, nuchal rigidity , no neurologic deficit other than cranial nerve palsy 2
Drowsiness / confusion, mild focal neurologic deficit 3
Stupor, moderate-severe hemiparesis 4
Coma, decerebrate posturing 5

Recent exertion, hypertension, excessive alcohol consumption, sympathomimetic use, and cigarette smoking are risk factors as well for both SAH and intracerebral bleeds. However, the strongest risk factor for SAH is family history, which carries a 3 - 5 fold risk. Epidural Hematoma (EDH)

Epidural Hematomas

Epidural hematomas are accumulations of blood between the skull and the dura, and typically occur after significant blunt head trauma. Fractures of the temporal bone can disrupt the middle meningeal artery, leading to high-pressure bleeding within the cranial vault. Herniation can occur within hours if the hematoma is not evacuated, so early recognition is key.

Classically, patients with epidural hematomas have a brief loss of consciousness after their injury, followed by a lucid period. Then, they lose consciousness again and deteriorate into herniation and death. You might hear this described as the 'talk and die' phenomenon. In reality, most EDH patients either do not lose consciousness, or do not regain it.

Subdural Hematomas (SDH)

Subdural hematomas are extra axial blood collections between the dura and the arachnoid mater. While epidural hematomas are usually ipsilateral to the trauma, subdural bleeds are typically on the contre-coup side. Subdural hematomas form when bridging veins are sheared during acceleration-deceleration of the head.

As the bleeding is venous and low-pressure in nature, the hematoma can grow fairly slowly and the presentation can be delayed by days to weeks. This is particularly true in patients with brain atrophy, whose bridging vessels are more susceptible to shear and who can more readily accommodate the additional intracranial blood volume.

Subdural hematomas have a wide clinical spectrum. Acute SDH is more common in younger patients with a history of trauma. Rapid accumulation of extra-axial blood, the absence of pre-existing atrophy, and the presence of other traumatic brain injuries correspond to a worse neurologic status at presentation. As the younger brain is less atrophic, even small volumes of extra-axial blood can increase ICP and result in severe deficits.

In the pediatric population, presence of acute or chronic SDH should raise suspicion of for child abuse, although SDH can also occur as a result of birth trauma. The physician should search for other signs of 'Shaken Baby Syndrome', including retinal hemorrhages and long bone fractures. Infants with increased ICP might present with a bulging fontanel, enlarged head circumference, emesis, failure to thrive, and seizure.

Chronic SDH is a grand imitator. It occurs more often in elderly and alcoholic patients as they are most prone to atrophy and/or coagulopathy. The most common presentation is altered mental state. Hemiparesis, headache, and falls are other common features. As the symptoms can be subtle, the differential diagnosis broadly encompasses any potential cause of weakness or confusion in the elderly. This highlights the need to perform a CT scan in any elderly patient with a change in mentation that is not convincingly explained by other pathologies.

Computed tomography (CT) is the mainstay of diagnosis, and the CT appearance varies depending on the age of the lesion. In the acute phase (days 0-3), the lesion appears hyperdense relative to the parenchyma. The clot is fresh and jelly-like. Subacutely, between 3 and 14 days, the lesion is isodense or hypodense as a result of fibrinolysis occurring within the clot. An injection of contrast may be helpful in illuminating isodense lesions. Chronic subdural hematomas, older than 2 weeks, are usually hypodense. Unlike epidural hematomas, SDH's can extend past the suture lines. Acute bleeds are typically concave in shape.

As an SDH grows, mass effect becomes evident; midline shift, sulci effacement, obliteration of the basal cisterns, and ventricular compression might be seen. Bilateral hematomas are fairly common, leading to medial compression of both ventricles, making them slit like. This is called �squeezed ventricle� or �rabbit's ears� sign. Small isodense hematomas at the vertex, the base of the skull, and in the posterior fossa can be particularly difficult to visualize. In these cases, MRI can be of assistance in making the diagnosis.

Initial Actions and Primary Survey

A patient with any type of intracranial hemorrhage may present with coma, rapidly declining level of consciousness, or seizure. In such cases, the priority is the ABCD's.

Cushing's triad describes the physiologic response to rapidly increasing intracranial pressure and imminent brain herniation. Its features are:

  1. Hypertension
  2. Bradycardia
  3. Abnormal respiratory patterns

Other signs of imminent herniation are lack of pupillary reaction and/or pupillary asymmetry. Signs of imminent herniation necessitate emergent intervention (see 'Treatment').

Diagnostic Testing

CT scan

Head CT is the mainstay of diagnosis in ICH. On CT, acute bleeding appears hyperdense (whiter) relative to the surrounding tissues. The subacute phase occurs between days 3 and 14, when blood becomes isodense to the brain parenchyma. It is particularly easy to miss intracranial bleeding during this phase as the blood and the brain may appear the same shade of grey. After about two weeks, blood appears hypodense (darker) relative to the brain.

Larger volumes of blood can cause radiologic signs of increased intracranial pressure. These include:

CT scans of various Intracranial Hemorrhages
CT scan (click to see) Description

Epidural hematomas appear convex, or lens-shaped, and do not cross suture lines.

Subdural hematomas appear convex, or crescent-shaped, and may cross suture lines.

Subarachnoid hemorrhage appears as blood in the ventricles, sulci, and cisterns. The overall sensitivity of CT is best within the first 12 hours. Sensitivity declines with time and for more minor bleeds.

Cerebral (Intra-parenchymal) bleeds appear as patches of bright white in the acute phase.

While CT is the initial investigation at most centers, MRI is gaining recognition as a more sensitive test. For more neuroradiology examples, see the links below.

Lumbar puncture

Approximately 7% of acute SAH will not be visualized on initial head CT, typically because there is a small volume of bleeding. In cases of suspected SAH with a negative CT, lumbar puncture is the second diagnostic step. An excellent (but password protected) tutorial video on lumbar puncture is available through the New England Journal of Medicine website (try accessing through your university library).

Two CSF features are most important:

  1. Absence or clearing of blood.
  2. Xanthochromia

Normal CSF does not contain red blood cells. Blood in the CSF may be a result of SAH, infection, or traumatic tap. Many sources state that if the number of red blood cells decreases by 50% from tube 1 to tube 4, the blood can be attributed to tap trauma. However, this decrease can occur in SAH as well, so the tap should only be labeled 'traumatic' if the fourth tube is almost completely free of blood (less than 5 rbc's per high powered field).

Xanthocrhomia refers to a yellow or pink discoloration of the supernatant once the CSF is centrifuged. It results from the breakdown of blood cells within the CSF. Xanthochromia is determined with either visual inspection or spectrophotometry; the latter being less commonly available. The presence of xanthochromia is highly sensitive for SAH.

If the CT or LP results are consistent with SAH, some form of angiography is necessary. While conventional digital subtraction angiography (DSA) is the gold standard, it may be less readily available than CT or MR angiography. Since CT angiography is rapid and non-invasive, it is commonly used to identify saccular aneurysms once the diagnosis of SAH is confirmed.

If the patient's CT and LP are normal, no further investigations are required. 1

How do I make the diagnosis?

  1. Suspect the illness. Complete a good history and physical exam.
  2. Order a CT head when appropriate. For trauma cases, you might consider using the Canadian CT Head Rules.
  3. Know the limitations of CT: small SAH's or those with delayed presentation might be hard to spot on CT. Isodense subdurals and epidurals can also be subtle.
Canadian Head CT Rules
High Risk (for Neurological Intervention)
  • GCS score < 15 at 2 hrs after injury
  • Suspected open or depressed skull fracture
  • Any sign of basal skull fracture*
  • Vomiting (more than 2 episodes)
  • Age greater than 65 years
Medium Risk (for Brain Injury on CT)
  • Amnesia before impact > 30 min
  • Dangerous mechanism ** (pedestrian,occupant ejected, fall from elevation)
  • * Signs of Basal Skull Fracture: hemotympanum, ?racoon? eyes, CSF otorrhea/ rhinorrhea, Battle's sign
  • ** Dangerous Mechanism: pedestrian struck by vehicle, occupant ejected from motor vehicle, fall from elevation more than 3 feet or 5 stairs
  • Rule Not Applicable If: Non-trauma cases, GCS < 13, Age < 16 years, Coumadin or bleeding disorder, Obvious open skull fracture

Treatment

Medical Treatment

Some tenets of medical treatment apply to all patients with intracranial hemorrhage:

  1. Assess and reassess the ABCD's
  2. Discontinue or reverse anticoagulation
  3. Prevent hypotension and hypoxemia
  4. Control ICP
  5. Prevent seizure: prophylaxis may be necessary depending on the type and extent of bleeding
  6. Treat fever and infection aggressively
  7. Control blood glucose (target 140-185 mg/dL)

ICP control can be managed by:

Surgical Treatment

In 2006, a comprehensive set of guidelines for the surgical management of intracranial emergencies was published in Neurosurgery.4,5 As a medical student, your focus should be on facilitating timely consultation with Neurosurgery for all patients with intracranial hemorrhage, unless it is clear that surgical or intensive care management would be against the patient's wishes.

Disposition

The vast majority of patients with intracranial hemorrhage require close observation in either an intensive care unit or neurosurgical ward. Most will require intensive physiotherapy and occupational therapy before hospital discharge is possible.

Pearls and Pitfalls

References

Selected Publications

  1. Edlow JA, Panagos PD, Godwin SA, Thomas TL, Decker WW. Clinical policy: critical issues in the evaluation and management of adult patients presenting to the emergency department with acute headache. Ann Emerg Med. 2008;52:407-436.
  2. Rincon F, Mayer SA. Clinical review: Critical care management of spontaneous intracerebral hemorrhage. Crit Care. 2008;12:237.
  3. Diringer MN. Management of aneurysmal subarachnoid hemorrhage. Crit Care Med. 2009;37:432-440.
  4. Bullock MR, Chesnut R, Ghajar J et al. Surgical management of acute epidural hematomas. Neurosurgery. 2006;58:S2.
  5. Bullock MR. Surgical Management of Acute Subdural Hematomas. Neurosurgery. 2006;58:S2-16-S2-24

Selected Online Resources