Intracerebral Hemorrhage

Intracerebral Hemorrhage (ICH) 

1️⃣ Introduction

It accounts for:

  • 10–15% of all strokes
  • But causes disproportionately high mortality (35–50%)

2️⃣ Classification

A. By Etiology

Type

Cause

Primary ICH

Hypertension, cerebral amyloid angiopathy

Secondary ICH

AVM, aneurysm, tumor, anticoagulation, trauma

B. By Location

 Deep ICH (Hypertensive)- Pathophysiology- presence of small penetrating arteries in deeper lobe with no collaterals.

  • Basal ganglia (putamen) – most common (60-65%)
  • Thalamus
  • Pons
  • Cerebellum

 Lobar ICH (Amyloid / tumor related)

  • Frontal
  • Parietal
  • Temporal
  • Occipital

3️⃣ Etiology 

 1. Chronic Hypertension

  • Lipohyalinosis
  • Charcot-Bouchard microaneurysms
  • Deep hemorrhage

2. Cerebral Amyloid Angiopathy (CAA)

  • Deposition of beta-amyloid 
  • Recurrent lobar bleeds therefore should not be restarted on anticoagulation 
  • Most common cause of lobar hemorrhage in normotensive elderly patients.

 3. Anticoagulation

  • Warfarin
  • DOACs
  • Thrombolysis(Alteplase)

 4. Vascular Malformations

  • AVM
  • Cavernoma

 5. Others

  • Brain tumor (glioblastoma, metastasis)
  • Cocaine
  • Coagulopathy
  • Vasculitis
  • Cerebral venous thrombosis (CVT) with secondary hemorrhage(CT venography )

4️⃣ Pathophysiology 

Primary Injury

  • Mass effect
  • Hematoma expansion (first 6–24 hrs)-therefore follow-up CT scans at ~6 hours and at 24 hours(2022 AHA)

Secondary Injury

  • Perihematomal edema
  • Thrombin toxicity
  • Excitotoxicity
  • Blood–brain barrier disruption
  • toxic effects of parenchymal blood

Hematoma expansion occurs in ~30–40% patients within 24 hrs.best predictor of edema volume is the size of the hematoma


5️⃣ Clinical Presentation/History

  • The clinical presentation of ICH is often indistinguishable from that of ischemic stroke.
  • Known hypertension?Compliance with medications?Home BP records?Previous hypertensive crises?
  • On Antiplatelets/anticoagulation ? Drug Abuse History?
  • Exact time last known well?
  • Bleeding Disorder History
  • Trauma History,Cancer history
  • Previous Stroke History
  • Cerebral Venous Sinus Thrombosis(Pregnancy/postpartum,Oral contraceptives)
  • Baseline functional status
  • Signs and symptoms usually correspond to the location of ICH.

Location

Features

Basal ganglia

Contralateral hemiplegia

Thalamus

Sensory deficit, altered sensorium

Lobar

Seizures common

Cerebellar

Ataxia, vomiting, brainstem compression

Pontine

Coma, pinpoint pupils

Classic features:

  • Sudden headache
  • Vomiting
  • Decreased GCS
  • Focal deficit
  • Seizures(15% cases)

6️⃣ Diagnosis

 1. Non-Contrast CT Brain – GOLD STANDARD (Initial)

  • Hyperdense area(due to clot) surrounded by a rim of hypodensity.(hematoma become isodense with adjacent brain parenchyma by 2–6 weeks.)
  • Isodense or hypodense blood on a CT scan may be an indicator of coagulopathy.
  • Midline shift
  • Intraventricular extension(Intraventricular hemorrhage occurs in >40% of patients with ICH. )
  • Swirl sign(fresh unclotted blood )
  • Blend sign: Hemorrhage contains hyperdense and hypodense regions.
  • Island sign: At least three small hemorrhages that are separated from the main hemorrhage.
  • Fluid-fluid level: This suggests coagulopathy 
  • Black hole sign: Relatively dark area within a hematoma that is not connected with adjacent brain tissue. 


  • Edema takes several hours to develop, so it is usually not seen initially.
  • An unusually extensive or irregular amount of edema raises the possibility of: 
    • CVT (cerebral venous thrombosis) with subsequent hemorrhage. 
    • Ischemic stroke followed by hemorrhagic transformation. 
    • Tumor followed by intratumoral hemorrhage.

 2. CTA

  • test to evaluate for an underlying cause of ICH
  • Detects spot sign (active extravasation of contrast into the hematoma)- analogous to swirl sign

Indications(AHA 2022)

  • Lobar ICH in a patient <70 years old.
  • Deep/posterior fossa ICH in a patient <45 years old.
  • Deep/posterior fossa ICH in a patient 45-70 years old without a history of hypertension.

 3. MRI

  • Better for CAA(non-Gadolinium-enhanced MRI)
  • Underlying tumor

If you wish to administer gadolinium Do MRI within 2 days of ictus. -Reason after 2 days, the blood becomes hyperintense on T1, and you may not be able to see beneath the hemorrhage when the gadolinium is administered. 

7️⃣ ICH Score 

Parameter

Points

GCS 3–4

2

GCS 5–12

1

Age ≥80

1

Volume ≥30 ml

1

IVH present

1

Infratentorial origin

1

  • Hematoma volume may be estimated as the product of the diameters divided by two (ABC/2). 

Parameter

How to Measure

A

Largest diameter of hematoma on the CT slice showing the largest hemorrhage area (cm)

B

Diameter perpendicular (90°) to A on the same slice (cm)

C

Approximate craniocaudal depth = Number of CT slices containing hemorrhage × slice thickness (cm)(which may vary from 3-10 mm depending on the scanner).

  • All measurements should be made in centimeters. This will yield a volume measured in milliliters (mL).
  • However, the location of the ICH is often more important than absolute blood volume (e.g., 20 ml of blood in the pons is more dangerous than 40 ml in the frontal lobe).

Modified ABC/2 Method

Hemorrhage Area on Slice

Count as

>75% of largest slice area

1 slice

25–75%

0.5 slice

<25%

Ignore

The FUNC score -provides an estimate of the likelihood of functional independence at 90 days.


Routine Investigations 

Investigation

Reason

Complete Blood Count (CBC)

Detect anemia, leukocytosis, thrombocytopenia

Platelet Count

Assess bleeding risk and need for platelet transfusion

PT/INR

Identify warfarin-associated coagulopathy and guide reversal

aPTT

Detect heparin effect or coagulation abnormalities

Fibrinogen Level

Evaluate coagulopathy; guide cryoprecipitate replacement

Blood Group and Crossmatch

Prepare for possible transfusion or surgery

Random Blood Glucose

Hyperglycemia is associated with worse outcomes; detect hypoglycemia mimic

HbA1c

Assess underlying diabetes control

Serum Electrolytes (Na, K, Cl, HCO₃)

Detect electrolyte abnormalities affecting neurological status

Serum Calcium

Hypocalcemia may contribute to coagulopathy and seizures

Serum Magnesium

Detect abnormalities associated with arrhythmias and seizures

Blood Urea Nitrogen (BUN)

Assess renal function before contrast studies and medication dosing

Serum Creatinine

Assess renal function and contrast eligibility

Liver Function Tests (LFTs)

Detect hepatic dysfunction causing coagulopathy

Arterial Blood Gas (ABG)

Assess oxygenation, ventilation, acid-base status

Cardiac Troponin

Detect neurogenic myocardial injury or concurrent ACS

12-Lead ECG

Detect arrhythmias, ischemia, QT abnormalities

Chest X-ray

Evaluate aspiration, pulmonary edema, pneumonia, cardiomegaly

Urinalysis

Baseline assessment and infection screening

Toxicology Screen (selected patients)

Detect cocaine, amphetamine, or drug-induced ICH

Pregnancy Test (women of childbearing age)

Important before imaging and medication decisions

Blood Cultures (if febrile)

Suspected infective endocarditis or septic embolic source

ESR/CRP (selected patients)

Evaluate inflammatory or vasculitic causes

Autoimmune/Vasculitis Workup (selected patients)

Young patients with unexplained ICH

Echocardiography (selected patients)

Suspected endocarditis or cardiac embolic source


CRITICAL CARE MANAGEMENT

1️⃣ Initial Stabilization (ABC)

  • Airway protection (GCS ≤8)-

-Premedication should be given to ensure adequate sedation, good jaw relaxation, and to prevent any rise in intracranial pressure (ICP) during the procedure. Short-acting intravenous anesthetic agents such as etomidate or thiopental are used because they help blunt this ICP response and also reduce the brain’s metabolic demand. 

-Among these, etomidate is generally preferred since it is less likely to cause a drop in blood pressure compared to thiopental. -Intravenous lidocaine in a dose of 1–1.5 mg/kg has traditionally been used to further attenuate the rise in ICP, 

-Muscle relaxants are usually not required, but if needed, short-acting agents should be chosen.

  • Maintain SpO₂ >94%
  • Avoid hypercapnia
  • Maintain normoglycemia
  • Control temperature
  • Always make sure that pain and anxiety have been treated before starting antihypertensives. Especially among intubated patients, hypertension can be a manifestation of pain. 

2️⃣ Blood Pressure Management 

According to 2022 AHA/ASA Guidelines

  • If SBP 150–220 mmHg
    Target SBP 140 mmHg(130-150 mmhg)
  • If SBP >220 mmHg then target SBP 140-160 mmhg

Avoid:SBP <130 mmHg

Related trials-INTERACT,ATTACH

Preferred IV agents:

Drug

Dose

Nicardipine

5 mg/h IV infusion; increase by 2.5 mg/h every 5–15 min (max 15 mg/h)

Clevidipine

1–2 mg/h IV infusion; double every 2–5 min

Labetalol

10–20 mg IV over 1–2 min; may repeat

Esmolol

Alternative when β-blockade desired

Avoid nitroprusside ( ICP) AND NTG

  • Oral drugs are typically started once the patient is clinically stable, able to receive enteral medications, and BP is controlled on IV therapy—usually within the first 24–48 hours—with overlap before discontinuing the IV infusion.(overlapping oral agents with IV infusion reduces BP variability, which is important because BP fluctuations are associated with worse outcomes after ICH.)

Time After ICH

BP Management

First 24 hours

IV agents preferred (nicardipine, clevidipine, labetalol infusion/intermittent bolus).

24–48 hours

If hematoma is stable, no neurological deterioration, and swallowing is safe (or enteral access available), start oral antihypertensives while tapering IV drugs.

>48–72 hours

Most patients should be on an oral regimen unless ongoing BP instability requires IV therapy.

3️⃣ Reversal of Anticoagulation

  • Don’t delay reversal of warfarin/DOACs while awaiting labs – empiric reversal should be given immediately. (2022 AHA)

Drug

Reversal

Warfarin

PCC + Vitamin K

Dabigatran

Idarucizumab

Apixaban/Rivaroxaban

Andexanet alfa

Heparin

Protamine

  • Target INR <1.4
  • Routine use of factor VIIa is not recommended
  • Avoid platelet transfusion in antiplatelet-related ICH-(unless surgery planned)(PATCH trial -2016)
  • DDAVP  may be considered (RCT-level evidence is minimal, limited to the DASH pilot trial).
  • Target platelet count >100K if possible.
  • In patients with spontaneous ICH, the effectiveness of TXA to improve functional outcome is uncertain(Class 2b = May be considered,Key Trial: TICH-2)

4️⃣ ICP Management

Indications:

  • GCS <8
  • Large hematoma
  • Hydrocephalus

Measures:

  • Head elevation 30°
  • Sedation (propofol)
  • Hypertonic saline preferred over mannitol
  • Target Na 145–155 in refractory ICP
  • Avoid prophylactic hyperventilation

5️⃣ Surgical Management

According to 2022 AHA/ASA Guidelines

1. Supratentorial ICH

Routine Craniotomy

Situation

Recommendation

Moderate or large supratentorial ICH (>10 cc with neurological deficit)

Craniotomy to improve mortality or functional outcome is of uncertain usefulness (Class 2b)

Deteriorating patient

Craniotomy may be considered as a life-saving measure (Class 2b)

Key Point

The STICH and STICH-II trials failed to show a clear overall functional benefit of routine early craniotomy for most supratentorial ICH.


2. Decompressive Craniectomy

Large Hematoma With Mass Effect

Indication

Comatose patient

Large hematoma with significant midline shift

Refractory intracranial hypertension

Clinical deterioration despite medical therapy

Decompressive craniectomy ± hematoma evacuation may be considered to reduce mortality (Class 2b).

Effect on long-term functional outcome remains uncertain.


3. Cerebellar Hemorrhage (Most Important Surgical Indication)

  • Cerebellar hemorrhage >3 cm/Larger volume (>15 ml)
  •  Brainstem compression
  •  Obstructive hydrocephalus

Deep basal ganglia bleeds Usually medical management.

EVD indicated if IVH with hydrocephalus.


4. Minimally Invasive Surgery (MIS)

Catheter-Based Hematoma Evacuation

Examples:

  • MISTIE technique
  • Endoscopic evacuation
  • Stereotactic aspiration

Criteria

Supratentorial ICH volume >20–30 mL

GCS 5–12

MIS ± thrombolysis can be useful for reducing mortality (Class 2a).

Improvement in functional outcome remains uncertain (Class 2b).


6️⃣ Seizure Management

  • Treat clinical seizures(The use of phenytoin is discouraged)
  • No routine prophylaxis(2015 American Heart Association/American Society of Anesthesiologists)

Indications for continuous EEG:

  • Impaired consciousness that is out of proportion to what would be expected based on the CT scan.
  • Unexplained fluctuations in mental status.
  • Any history or clinical signs of seizure.

7️⃣ DVT Prophylaxis

  • Intermittent Pneumatic Compression  from day 1
  • LMWH after 24–48 hrs if stable CT

8️⃣ Glycemic & Temperature Control

  • Target glucose 140–180
  • Treat fever aggressively,neurogenic fever(diagnosis of exclusion) can be treated with bromocriptine. 
  • Similar to patients with ischemic stroke, ICH patients should not be fed orally until swallowing is evaluated. Dysphagia is a common complication after ICH and a cause for aspiration pneumonia


REFERENCES

  1. Benjamin R, Karsonovich T. Intracerebral Hemorrhagic Stroke. [Updated 2026 Mar 23]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2026 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK553103/
  2. 2022 Guideline for the Management of Patients With Spontaneous Intracerebral Hemorrhage: A Guideline From the American Heart Association/American Stroke Association
  3. Irwin Rippe 9th edition 
  4. https://emcrit.org/ibcc/ICH/#top

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