Spontaneous Intracerebral Hemorrhage (ICH)

You’ve been diagnosed with an intracerebral hemorrhage — what does this mean?

“Intracerebral hemorrhage” means that a blood vessel has ruptured within the brain and blood has collected as a hematoma inside the brain tissue. This is not bleeding around the brain (e.g., subarachnoid hemorrhage) but bleeding within the parenchyma itself.

For you or your loved one, this typically involves:

• an acute neurologic deficit (weakness, speech disturbance, imbalance, etc.),
• risk of hemorrhage expansion in the first hours,
• risk of swelling (edema) and raised intracranial pressure,
• the need for immediate, closely monitored inpatient care in a hospital with neurosurgical coverage.

The care team’s goal is to stabilize the patient, reduce the risk of ongoing bleeding or secondary injury, and—when appropriate—remove the hematoma to maximize the chance of meaningful recovery.

What exactly is spontaneous supratentorial intracerebral hemorrhage?

“Spontaneous” refers to hemorrhage that is not caused by trauma, and is not clearly due to a tumor, aneurysm rupture, venous thrombosis, or another obvious structural cause. Most commonly, it reflects:

• rupture of small perforating arterioles,
• chronically damaged by hypertension-related lipohyalinosis and microatheroma formation,
• or fragile vessels due to cerebral amyloid angiopathy in older adults (often lobar hemorrhages).

“Supratentorial” means the hematoma is located above the tentorium—within the cerebral hemispheres (lobes, basal ganglia, thalamus).

Causes & risk factors

Important contributors include:

• Age — the strongest non-modifiable risk factor.
• Chronic uncontrolled hypertension — the most important modifiable factor. Markedly elevated pressures (e.g., systolic > 160 mmHg or diastolic > 110 mmHg) are strongly associated with ICH risk.
• Anticoagulants (e.g., warfarin, DOACs) — increase both the risk of ICH and the likelihood of hematoma expansion.
• Antiplatelet agents (aspirin, clopidogrel, dual antiplatelet therapy) — associated with higher ICH risk, larger hematoma volumes, and worse outcomes.
• Heavy alcohol use or stimulant exposure (cocaine, amphetamines).
• Low cholesterol levels in some observational studies.
• Vascular conditions such as cerebral amyloid angiopathy (especially in older adults).

Consistent, long-term blood pressure control and appropriate use of anticoagulants/antiplatelets in coordination with your treating physician are cornerstone prevention measures.

Symptoms & clinical course

The classic presentation is sudden onset of symptoms over seconds to minutes. Common features include:

• acute weakness or paralysis on one side of the body,
• speech or language disturbance,
• visual or sensory changes,
• sudden severe headache, nausea, vomiting,
• confusion, drowsiness, and sometimes loss of consciousness.

The hematoma may:

• remain stable, or
• expand within the first hours, leading to clinical deterioration.

In a significant proportion of patients, blood extends into the ventricular system (intraventricular hemorrhage – IVH), which is associated with a more severe prognosis.

How is it diagnosed, and what is the ICH score?

Diagnosis is made urgently with:

• Non-contrast head CT — rapidly confirms the hemorrhage, its location and size, and identifies IVH and/or hydrocephalus.
• MRI — useful in selected settings (e.g., suspected underlying vasculopathy or prior microbleeds/hemorrhages).
• Angiography / CTA / MRA — when there is concern for an aneurysm, vascular malformation, or another secondary cause.

Severity is often summarized using the ICH score, which typically incorporates:

• age (> 80 years),
• hemorrhage location (supratentorial vs infratentorial),
• presence of intraventricular hemorrhage,
• hematoma volume (> 30 mL),
• Glasgow Coma Scale (GCS) at presentation.

In general, higher ICH scores are associated with higher 30-day mortality. The score is a prognostic tool; it does not replace individualized clinical judgment or a detailed discussion with the patient’s family.

What does neurocritical / conservative management involve?

All patients with spontaneous ICH require:

• Immediate hospital admission, often to an ICU, stroke unit, or dedicated neurocritical setting,
• airway, breathing, and circulation stabilization,
• close neurologic monitoring,
• management of raised intracranial pressure when present (osmotherapy, etc.),
• blood pressure control — prompt but carefully titrated reduction to lower the risk of hematoma expansion while preserving cerebral perfusion.
• optimization of glucose, electrolytes, and temperature.

Large international protocols (INTERACT, ATACH, etc.) have refined how aggressively blood pressure should be targeted; clinically, the priority is avoiding sustained severe hypertension that can promote ongoing bleeding.

Anticoagulants, antiplatelets & reversal — why it matters

If the hemorrhage occurs in the setting of anticoagulant therapy (e.g., warfarin or a DOAC), management typically includes:

• immediate cessation of the medication,
• rapid reversal of anticoagulant effect using protocol-based agents (e.g., vitamin K, PCC, or medication-specific reversal agents when available),
• fresh frozen plasma (FFP) was used historically but requires large volumes and may reverse anticoagulation more slowly.

If the patient is taking antiplatelet agents (aspirin, clopidogrel, etc.), the situation is more nuanced. What we know:

• dual antiplatelet therapy increases risk and is associated with larger hematoma volumes and worse outcomes,
• the benefit of platelet transfusion remains context-dependent and is still debated in specific clinical scenarios,
• decisions are individualized based on hematoma characteristics and bleeding-versus-thrombosis risk.

These decisions are made collaboratively with neurointensivists, neurologists, and hematology teams, guided by contemporary protocols and best available evidence.

When is surgery needed?

The objectives of surgical management are to:

• reduce mass effect (pressure from the hematoma and surrounding edema),
• lower intracranial pressure,
• stabilize and, when possible, improve neurologic function.

Large randomized trials (STICH, STICH II) did not demonstrate a uniform benefit for all patients, but:

• selected subgroups—such as patients with superficial (lobar) hematomas close to the cortex—may benefit from surgical evacuation,
• massive deep hematomas with poor neurologic status at presentation often have a very poor prognosis regardless of strategy, making decisions complex and highly individualized,
• cerebellar hematomas with fourth ventricle compression frequently require urgent evacuation.

Surgical decision-making typically integrates:

• hematoma size, location, and evolution over time,
• age and comorbidities,
• neurologic examination (GCS, focal deficits),
• patient values and previously expressed wishes, when known.

Surgical options & minimally invasive techniques

The main options include:

Traditional craniotomy with hematoma evacuation

• A bone window is created over the hematoma.
• Blood is removed using microsurgical technique while minimizing injury to surrounding brain tissue.
• Most suitable for superficial, surgically accessible hematomas.

Minimally invasive evacuation

• Stereotactic catheter placement into the hematoma with staged aspiration.
• Local thrombolytic administration (e.g., rtPA or urokinase) via the catheter to facilitate gradual clot liquefaction and evacuation (e.g., MISTIE-style approaches).
• Endoscopic evacuation through a small burr hole under endoscopic visualization.

Minimally invasive strategies continue to evolve in international studies and can be particularly attractive for deep hematomas, where open craniotomy may be more disruptive.

There is no single “best” technique for every patient—selection is made by an experienced team based on location, size, physiology, and overall clinical context.

Prognosis, mortality & neurorehabilitation

Even with maximal treatment, spontaneous intracerebral hemorrhage is associated with:

• approximately 40% 30-day mortality in large series,
• only ~20% of patients achieving full functional independence at 3 months.

Prognosis depends mainly on:

• ICH score (higher scores typically correlate with worse outcomes),
• hematoma volume and location,
• presence of intraventricular hemorrhage,
• age and comorbidities,
• the quality and timeliness of neurocritical and surgical care.

For survivors, the next major phase is neurorehabilitation:

• intensive physical and occupational therapy,
• speech therapy when aphasia or dysarthria is present,
• neuropsychological support,
• practical home and lifestyle adaptations.

The goal is maximal attainable independence based on the individual’s recovery potential—even if full return to baseline is not possible.

When is it an emergency, and what should I do now?

Intracerebral hemorrhage is always an emergency. Call your local emergency number immediately if you notice:

• sudden weakness or numbness on one side of the body,
• sudden difficulty speaking or understanding speech,
• sudden vision or balance disturbance,
• a sudden severe headache that is different from usual,
• loss of consciousness, seizures, or severe confusion.