Nontraumatic intracerebral hemorrhage (ICH) is bleeding into the parenchyma of the brain that may extend into the ventricles and subarachnoid space. The consequences of ICH can be devastating. Although current practices vary, there are several concrete considerations when it comes to treating ICH. What are some risk factors for ICH? What kind of clinical presentation would one expect for ICH? How would you work up and manage ICH in the Emergency Department?
–Hypertension is the most prevalent and modifiable risk factor for spontaneous ICH. Noncompliance with antihypertensive meds, being older than 55, and smoking further increase this risk. Areas of the brain supplied by small perforating arteries and arterioles (putamen, globus pallidus, external capsule, subcortical white matter, thalamus, cerebellum and brain stem) are most sensitive to rupture secondary to chronic degenerative changes induced by HTN.
–Alcohol: Excessive EtOH use directly affects the integrity of cerebral vessels. It also induces increases in BP during ingestion and withdrawal, has deleterious effects on coagulation pathways, and affects platelet function directly.
–HYPOcholesterolemia: HYPERcholersterolemia is associated with cardiac disease, but hypocholesterolemia has been found to be associated with increased risk for ICH in multiple trials. Low serum cholesterol might weaken the endothelium of intracerebral arteries, resulting in ICH (esp in the presence of HTN).
–ASA: Risk is low: approximately 0.15% (as per the International Stroke Trial)
–Coumadin: In population-based studies, absolute risk for ICH from warfarin therapy ranges from 0.3% to 1.7%, depending on the underlying disease and degree of anticoagulation. Several other studies have found higher numbers.
–Vascular abnormalities: AVMs, venous angiomas, intracranial aneurysms, and moyamoya disease may also result in ICH (the typical patient for this type of ICH is the young, normotensive woman).
–Drug abuse: Cocaine, amphetamines, heroin and methylphenidate all cause elevate BP (except heroin), which is of course implicated in the pathogenesis of ICH.
–Other (skipping the obscure diseases): Bleeding into a tumor, bleeding diatheses, intracranial trauma or surgery, carotid endarterectomy, and underlying vasculitis.
–ICH can present with signs of increased intracranial pressure (vomiting or diminished consciousness) suddenly or over the course of minutes to days. Smooth/gradual onset of stroke is more common in ICH (63%) when compared to other causes (34%–specifically: 5-20% of ischemic strokes and 14% of SAHs). ICHs have been demonstrated to worsen slowly when imaged by CT at presentation, 1 hour, and 24 hour intervals. This growth is well-correlated with clinical deterioration as measured by serial GCS and NIHSS scores.
–Global features of ICH include headache (40%), nausea/vomiting (49% with supratentorial ICH), decreased consciousness, and elevated BP. A typical course would be sudden onset of symptoms, followed by gradual worsening of the above features.
–Differentiating between etiologies of neurological symptoms generally requires imaging of the brain. Noncontrast CT remains the most rapid, reliable, and readily available method for diagnosing ICH. Cerebral angiography (or MRI or magnetic-resonance angiography—sensitivity not well studied for either) is generally needed to diagnose secondary causes of ICH (aneurysms, AVMs, dural venous thromboses, and vasculitis).
–Differential: Victims are often “found down,” forcing a comprehensive (but rapid) MD assessment looking for evidence of trauma, dehydration, compartment syndrome, and rhabdomyolysis. GCS or NIHSS both provide simple, objective measurements of the levels of consciousness and neurologic impairment.
–RNs work simultaneously while MDs are performing cursory exam: Cardiac monitoring, IV access, and phlebotomy should be started. Prompt blood sugar evaluation is necessary. EKG is helpful for looking for arrhythmias and/or acute MI.
–Be cautious in allowing the above interventions from taking away time to CT, however.
–Airway Management: Bulbar deficits, decreased levels of consciousness, and/or vomiting (all of which are common in ICH) may necessitate intubation. Objective measurements include GCS cutoffs and/or respiratory insufficiency (PCO2 > 50 mm Hg or PO2 < 60 mm Hg) may be helpful. Keep in mind that inadequate sedation and paralysis during any procedure is likely to cause agitation leading to an elevation in BP. This may require the use of longer-acting sedatives, decreasing the ability to perform serial neuro exams.
–The next phase of management is directed at preventing secondary injury caused by perihematomal edema growth, seizures, hydrocephalus, or increased ICP. Frequent re-examination is critical if possible.
–BP Management: The AHA recommends BP levels be maintained at a mean pressure of < 130 mm Hg in persons with a history of HTN. Cerebral perfusion pressure should be maintained at > 70 mm Hg. Therapy for the generally normotensive patient is less well defined, but it is recommended that mean BP be kept at < 110. If systolic is < 90, fluid resuscitation with non-dextrose-containing crystalloids (e.g., normal saline) should be started. Start pressors if fluid does not help. See table 3 in source #1 if interested for specific meds recommended by the AHA.
–ICP management: Elevated ICP is > 20 mm Hg for > 5 minutes. Therapeutic goals include ICP < 20 mm Hg and CPP > 70 mm Hg. Patients with mass effect or rapid deterioration require placement of ICP monitor and immediate management: Osmotherapy (1st line) e.g., mannitol (< 5 days only due to rebound) with or without furosemide; check serum osmolality twice daily), hyperventilation (failure to respond indicates poor prognosis), and elevation of head of bed. Steroids are generally avoided as per AHA (multiple side effects and no proven clinical benefit).
–Fluid/electrolyte management: Goal is euvolemia (CVP 5-12 mm Hg). Monitor serum electrolytes (e.g., sodium, potassium, Mg, and Ca) in addition to acid/base status very closely.
–Prevention of seizures (usu with Dilantin): most common within 24 hours of onset of ICH symptoms and occur in up to 15% of patients.
–Appropriate reversal of anticoagulation.
–Surgical intervention: Goal may be rapid evacuation of hematoma to decrease mass effect. AHA Stroke Council and EUSI guidelines do NOT recommend routine evacuation of supratentorial hemorrhage by standard open craniotomy within 96 hours of ictus (increases risk of neural damage and recurrent bleeding; STICH trial of 1033 patients demonstrated no change in long-term outcome with early surgical vs conservative management)—no recommendations on less invasive sterotactic and endoscopic evacuation with the use of thrombolytic drugs have been made yet (although several trials have shown improved outcomes). Both guidelines recommend surgery for patients presenting with lobar hemorrhage within 1 cm of the surface, particularly those with good neurological status who are deteriorating clinically.
1) Panagos PD, Jauch EC, and Broderick JP. Intracerebral hemorrhage. Emergency Medicine Clinics of North America. 2002: 20 (631-655)
2) Qureshi A, Mendelow D, and Hanley D. Intracerebral Hemorrhage. Lancet. 2009: 373.