Intracranial hemorrhage

Type	Location
Subarachnoid hemorrhage	Bleeding into the potential space between the arachnoid and pia mater
Subdural hematoma	Bleeding into the potential space between dura and arachnoid membrane
Epidural hematoma	Bleeding into the space between skull and the dura
Intracerebral hemorrhage	Bleeding into the space within the brain parenchyma

Presentation

Classic and critical presentation

Patient presentation varies widely depending on location and extent of the hemorrhage and can include:
- Altered mental status
- Headache
- Nausea/vomiting
- Focal neurological deficits
- Coma
- Seizure
- Brief loss of consciousness followed by lucid interval.
The classic presentation of SAH is the sudden onset of ‘the worst headache of one’s life.’ SAH accounts for 1% of all patients presenting to the ED with the complaint of “the worst headache of my life.”
The most common features of SAH include headache (74%), nausea or vomiting (77%), loss of consciousness (53%), nuchal rigidity (35%), and focal neurological deficits.

Diagnosis and evaluation

Radiology
- Emergent noncontrast head CT is the cornerstone for detection of intracranial hemorrhage. MRI is equally effective in identifying intracranial hemorrhage and better at detecting predisposing underlying parenchymal or vascular anomalies. However, for many emergent clinical scenarios, MRI is not practical.
- For SAH, the most current AHA guidelines recommend lumbar puncture for detection of potential SAH if noncontrast head CT is negative; more recent literature suggests that the newer, multidetector CT scanners can safely rule out SAH if obtained within 6 hours of headache onset, thereby eliminating the need for LP.
- The presence of red blood cells or xanthochromia in the CSF sample suggests possible SAH and warrants further evaluation and neurosurgical consultation. Current evidence suggests that it takes approximately 12 hours for xanthochromia to develop.
- In patients with confirmed SAH, immediate CTA of the head and neck should be obtained to evaluate for cerebral aneurysm as prompt intervention via clipping or coiling may improve patient outcomes.
- If trauma suspected, consider CT cervical spine as well.
Laboratory tests
- Check serum electrolytes as derangements can worsen brain function.
- Check serum glucose as hypoglycemia can mimic the signs and symptoms of intracranial hemorrhage.
- Check coagulation studies (PT/PTT) to identify coagulopathy.
- Type and screen/cross-match blood products.
- Consider toxicology screens.
- Pregnancy test as needed.

Critical management

Emergency department management focuses on protecting cerebral perfusion by balancing the forces of MAP and ICP.
Patients should be positioned with the head of the bed elevated to 30 degrees to support cerebral venous drainage to reduce ICP.
Securing the airway
- Laryngeal manipulation transiently increases ICP. If anticipating endotracheal intubation, premedication with lidocaine 3–5 minutes prior to laryngoscopy may blunt this effect on ICP.
- Induction agents for rapid sequence intubation should support MAP. Etomidate is an effective, fast-acting induction agent, which is hemodynamically neutral. Other potential induction agents include benzodiazepines, ketamine and propofol.
- Depolarizing neuromuscular blockers such as succinylcholine produce diffuse muscle fasciculations that can raise ICP. Nondepolarizing neuromuscular blockers do not cause muscle contraction and have no effect on ICP. Consider one of the nondepolarizing neuromuscular blockers such as rocuronium.
- Adequate sedation prevents agitation and subsequent elevations in ICP. Propofol is a rapid-onset sedative, which is cleared quickly once discontinued, thereby facilitating frequent monitoring of the neurological examination. Propofol can precipitate hypotension and should be used with caution as secondary insults to the brain are known to produce worse outcomes.
- Respiratory rates should be titrated to a goal PaCO₂ of 35–40 mmHg to prevent cerebral vasodilation.
Blood pressure control
- Hypertension
  - Extremely elevated blood pressures in patients with intracranial hemorrhage may be associated with hematoma expansion and poor clinical outcomes.
  - Current 2010 AHA guidelines recommend aggressive blood pressure reduction in hypertensive patients with intracranial hemorrhage. While current evidence is limited, a target of 160/90 is probably reasonable as long as CPP is preserved, but further study is warranted. This target may be lowered in patients with unsecured cerebral aneurysms, and discussion with a neurosurgeon for these patients is critical.
    - The INTERACT trial (published in Lancet in 2008) suggested that tight blood pressure control SBP <140 mmHg is safe and decreases hematoma expansion.
    - The ATACH trial (published in Neuro Critical Care in 2007) suggested that aggressive blood pressure reduction with nicardipine is not associated with neurological deterioration.
  - Consider nicardipine, labetalol, and nitroprusside. Do not use hydralazine, as it causes cerebral vasodilatation and increased ICP.
- Hypotension
  - Injured brains depend on the balance between MAP and ICP for perfusion. MAP should be maintained >60 mmHg by vasoactive agents if necessary to protect cerebral perfusion pressure.
  - Consider arterial line insertion to help monitor all patients requiring antihypertensive drips or pressors for MAP management.
Anticoagulation reversal (Table 17.2)
- Immediate review of the patient’s medications is crucial to identify potential underlying medication-induced coagulopathy. Rapid, aggressive reversal of anticoagulation can prevent hematoma expansion and improve clinical outcomes (see Table 17.2).
ICP management
- Elevate the head of the bed to 30 degrees to promote venous drainage from the head to reduce ICP. Be sure to maintain the head in a midline position to ensure drainage of the neck veins.
- Empiric treatment for presumed herniation includes use of osmotic agents to reduce cerebral edema. These are purely temporizing measures until invasive ICP monitoring is established to guide therapy, or until surgical interventions become available.
  - Mannitol is a sugar alcohol used as an osmotic diuretic to draw hypotonic fluid (edema) into the hypertonic intravascular space. Mannitol can precipitate hypotension and should be used with caution in patients with low MAP and renal failure.
  - Hypertonic saline is an alternative osmotic agent that is effective in lowering ICP and improving CPP. It is generally not associated with hypotension unless infused rapidly. There are various concentrations of hypertonic saline with various dosing regimens that may be chosen based on the clinical scenario. Ultimately, close monitoring of serum sodium levels and serum osmolarity dictates infusion volume.

Invasive ICP monitoring is crucial for aggressive management of patients with presumed ICP elevations.
- Extraventricular drains allow real-time ICP monitoring while allowing drainage of CSF to help lower ICP.
- Other devices including Camino bolts and intraparenchymal pressure catheters can also be used for ICP monitoring but do not offer the option of draining CSF to lower ICP.
Surgical intervention
- The majority of these patients will require a neurosurgical consultation.
- Timely consultation or transfer to a tertiary care center for neurosurgical evaluation is an essential component of emergency medicine management. Continued management should be in a critical care setting as soon as feasible.
- Various surgical procedures including craniotomy, craniectomy, stereotactic aspiration, and hematoma drainage may be used by neurosurgery to further lower ICP.
- Various interventional and surgical techniques including clipping and coiling are crucial for management of spontaneous SAH from aneurysmal rupture.