Intracerebral hemorrhage demands several decisions at once: identify the vessel disease, determine whether bleeding continues, prevent secondary injury, and eventually weigh the risks of recurrent hemorrhage and ischemic stroke. A deep hemorrhage associated with longstanding hypertension and a recurrent lobar hemorrhage associated with cerebral amyloid angiopathy may share an emergency pathway, but their implications for investigation and anticoagulation differ. My starting point is to treat ICH as an active emergency and use the imaging to understand the disease behind it. This review draws on Sebastian Koch’s medical management lecture and evidence available through October 4, 2026 (University of Miami, 2026).

ICH has historically had fewer effective treatments than ischemic stroke. Incidence varies geographically, with particularly high rates reported in East Asia. The lecture’s estimate of approximately 100,000 annual U.S. cases indicates scale; exact counts depend on year and ascertainment. U.S. hospitalization data show higher incidence among Black and Hispanic populations than among White populations, including premature stroke. These disparities cannot simply be extrapolated worldwide or treated as a biological explanation for an individual hemorrhage. Hypertension, access to preventive care, and social conditions matter when interpreting them (Baig et al., 2023).

An aging population also changes the patients we see. Older adults accumulate small vessel disease and CAA, while antithrombotic exposure becomes more common. Anticoagulation and dual antiplatelet therapy can contribute to bleeding risk, although they often have important indications. A shift toward older presentations must still be interpreted within the population and time period studied. Hypertension remains the most important modifiable risk factor. Advancing age, previous ischemic stroke or TIA, antithrombotic use, heavy alcohol consumption, and familial or genetic susceptibility also contribute. Associations with lower educational attainment and low cholesterol do not establish a direct mechanism. Observational associations with low cholesterol, including in patients not taking statins, are not a reason to raise cholesterol deliberately or automatically discontinue an indicated statin.

Hypertensive arteriopathy primarily injures small penetrating vessels. Chronic vascular remodeling, lipohyalinosis, smooth muscle degeneration, and sometimes fibrinoid necrosis weaken the wall until rupture occurs. The precise trigger for that final event is often unknown. The usual locations are the putamen, caudate, thalamus, pons, and cerebellum. A relatively compact, rounded, homogeneous hematoma in one of these territories supports a perforator-related mechanism. Shape and location are useful clues, but neither proves the cause. A deep hemorrhage in a young patient, or one with atypical imaging, still deserves an etiologic investigation.

CAA affects a different vascular compartment. Amyloid-beta accumulates in the walls of cortical and leptomeningeal vessels, particularly within the media and adventitia, compromising their structure and function. Congo red staining produces the characteristic apple-green birefringence under polarized light. Clinically, the familiar presentation is a lobar hemorrhage in an older adult, sometimes recurrent and sometimes accompanied by cortical microbleeds or superficial siderosis. The hematoma may be irregular or multilobulated, with subarachnoid or subdural extension. Bleeding across several compartments can make the source and surgical target less obvious, although morphology alone does not establish CAA or determine whether evacuation is appropriate.

The MRI surrounding the hematoma often tells us more than the hematoma itself. FLAIR shows white matter injury, including leukoaraiosis. GRE or susceptibility-weighted imaging reveals microbleeds and chronic blood products. Lacunes and deep microbleeds favor arteriolosclerosis; strictly lobar microbleeds and cortical superficial siderosis support CAA. Enlarged perivascular spaces also have a distribution: basal ganglia predominance is associated with deep perforator disease, whereas marked centrum semiovale involvement supports an amyloid-related pattern. On T2, these spaces follow small vessels and have CSF-like signal. None of these findings is perfectly specific, and mixed vascular disease is common. The task is to interpret their distribution together.

CAA can present without a large lobar hematoma. Transient focal neurological episodes may resemble TIAs, particularly when symptoms recur or spread across a limb. Convexity subarachnoid blood or superficial siderosis can provide the explanation. Calling every such episode a TIA risks prescribing antithrombotic treatment for a hemorrhagic process. Cognitive impairment and dementia are other presentations. CAA-related inflammation is a less common, potentially treatable syndrome involving subacute cognitive or behavioral change, seizures, and asymmetric vasogenic edema that can resemble a mass. Immunosuppressive treatment, usually corticosteroids, may help appropriately diagnosed CAA-related inflammation. That indication is separate from using steroids for ordinary ICH-associated edema, where they offer no benefit and can cause harm (Regenhardt et al., 2020).

Boston criteria version 2.0 applies to an appropriate presentation at age 50 or older after competing causes are excluded. Probable CAA requires at least two strictly lobar hemorrhagic lesions, including lobar ICH, microbleeds, or qualifying superficial siderosis/convexity subarachnoid hemorrhage foci; alternatively, one strictly lobar hemorrhagic lesion plus a specified white matter marker can qualify. Those markers are severe centrum semiovale perivascular spaces or a multispot white matter hyperintensity pattern. Deep hemorrhagic lesions preclude these MRI pathways. Formal counting rules matter. Lobar ICH with additional lobar microbleeds and superficial siderosis may satisfy the hemorrhagic pathway without counting perivascular spaces. Possible CAA is a lower-confidence category; definite CAA requires appropriate pathology (Charidimou et al., 2022).

The broader diagnostic question is whether a macrovascular lesion or another secondary cause has been missed. Rapid noncontrast CT establishes the hemorrhage, while CTA can identify vascular abnormalities and characterize expansion risk. The 2022 AHA/ASA guideline recommends acute CTA, with consideration of venography, for lobar ICH below age 70; deep or posterior fossa ICH below age 45; and deep or posterior fossa ICH at ages 45–70 without a history of hypertension. Venous imaging is particularly relevant when the presentation suggests cerebral venous thrombosis. Catheter angiography has a separate role when imaging suggests a vascular lesion, suspicion persists despite noninvasive studies, or spontaneous intraventricular hemorrhage occurs without an identifiable parenchymal hemorrhage (Greenberg et al., 2022).

Lobar hemorrhage in a younger patient broadens the differential to vascular malformations, tumors, venous disease, and conditions such as reversible cerebral vasoconstriction syndrome. MRI can reveal a cavernous malformation, an underlying mass, hemorrhagic transformation of an infarct, or a small vessel disease pattern. Disproportionate edema should prompt a closer look, although it is not specific for any one diagnosis. Blood can obscure a lesion during the acute admission, so an initially unrevealing study may need repeat imaging after the hematoma evolves. Brain biopsy and autopsy provide pathological information in selected circumstances; routine CAA diagnosis generally relies on clinical and MRI findings rather than tissue sampling.

Once a vessel ruptures, the first CT is a snapshot of a moving process. Blood pressure and coagulation influence early hematoma formation, but mechanical propagation may also matter. C. Miller Fisher’s pathological observations described multiple small vessel ruptures around a pontine hemorrhage, including vessels without the same chronic pathological changes. The proposed mechanism is that the original hematoma stretches or shears neighboring vessels, producing further bleeding until local tamponade and hemostasis develop. This is a mechanistic model, not proof that every hematoma expands in this fashion. Early University of Miami CT reports from Kelley, Berger, Scheinberg, and Stokes documented active bleeding and interval enlargement. Recognizing a hematoma does not establish that hemostasis has occurred (Fisher, 1971; Kelley et al., 1982).

Approximately one-third of patients in early-imaged cohorts experience hematoma expansion, with the observed proportion changing according to scan timing and definition. Common research definitions use an increase exceeding 6 mL or 33%, rather than a universal 30% threshold. Earlier presentation, baseline volume, and anticoagulant exposure provide useful risk information, but bedside findings cannot reliably exclude continued bleeding. Expansion is concentrated in the first hours and becomes less frequent with time. Six hours is not a guarantee of stability, particularly with coagulopathy or delayed deterioration. As the acute bleeding phase subsides, perihematomal edema, inflammation, mass effect, and blood product toxicity become increasingly important. Attempts to modify those cellular processes have not yet produced a broadly established pharmacological treatment.

The CTA spot sign is contrast enhancement within the hematoma that indicates leakage and identifies a higher risk of expansion. A negative scan does not rule out subsequent growth (Demchuk et al., 2012). On noncontrast CT, the blend sign describes adjacent areas of different attenuation with a recognizable interface. The black hole sign describes a relatively hypodense area enclosed within a denser hematoma. Both are associated with expansion, although sensitivity is limited and definitions should be applied consistently (Li et al., 2015, 2016). These are risk markers, not proof that every dark region represents ongoing bleeding. A local comparison described in Koch’s lecture found no predictive difference between peripheral and central spot signs. Whether position adds useful information beyond established markers remains unresolved without a full published analysis.

Blood pressure control is the most immediately scalable intervention. For mild to moderate spontaneous ICH presenting with systolic pressure of 150–220 mm Hg, the 2022 AHA/ASA guidance supports targeting approximately 140 and maintaining a range of 130–150. The recommendation does not apply with equal certainty to massive hemorrhage, severe intracranial hypertension, or patients requiring decompression. Above 220, treatment still requires urgency, but the magnitude and rate of reduction need individualized assessment. Cerebral perfusion, mass effect, chronic hypertension, and renal vulnerability all influence the plan. Driving systolic pressure below 130 in the population addressed by the guideline can be harmful (Greenberg et al., 2022).

The major trials answer related but different questions. INTERACT2 compared a target below 140 with a target below 180. Its primary dichotomous outcome narrowly missed statistical significance, while the secondary ordinal analysis favored intensive treatment (Anderson et al., 2013). ATACH-2 tested a more intensive range of 110–139 against 140–179; it did not improve the primary outcome and produced more renal adverse events (Qureshi et al., 2016). Describing both trials as identical comparisons loses the distinction that matters clinically. Together, they support prompt, controlled reduction without assuming that progressively lower pressure produces progressively better outcomes.

Timing and variability deserve as much attention as the prescribed target. The goal is smooth, sustained control, with frequent reassessment and minimal overshoot. Post hoc analyses suggest that treatment initiated within two hours may reduce expansion and improve outcomes, but they are less definitive than a randomized timing comparison (Li et al., 2020). An emergency pathway should begin treatment immediately after ICH confirmation and aim to achieve the appropriate target within an hour of treatment initiation. An IV beta blocker such as labetalol may serve as a bridge to a titratable nicardipine infusion. Rapid access to controlled treatment and monitoring matters more than a particular sequence of drugs.

INTERACT4 illustrates why the diagnosis matters before this strategy is generalized to all suspected strokes. Ambulance treatment before imaging targeted systolic pressure of 130–140, and the trial’s overall functional outcome was neutral. The hemorrhagic stroke subgroup did better, while the ischemic stroke subgroup did worse (Li et al., 2024). These results strengthen the rationale for early ICH treatment but do not justify routine pre-imaging blood pressure reduction in undifferentiated stroke. Permissive hypertension in ischemic stroke is also conditional: thrombolysis, thrombectomy, and other urgent medical indications have their own blood pressure requirements.

Small diffusion-restricted lesions introduce another layer of complexity. The lecture estimates that about one-fifth of patients show such lesions, although prevalence varies with MRI timing and patient selection. Proposed mechanisms include underlying small vessel disease, adrenergic stress, microthrombosis or vasoconstriction, and impaired perfusion during large pressure swings. The occipital hemorrhage with a remote DWI lesion and the thalamic hemorrhage with a reported 125-mm Hg systolic swing illustrate why fluctuations deserve attention. Internal border-zone lesions after marked reduction raise concern for hypoperfusion. They do not establish that every remote DWI lesion is treatment-induced, or that ischemic injury explains every neutral blood pressure trial. In ICHADAPT-2, randomized lowering to below 140 did not significantly increase DWI lesions compared with below 180, although the MRI sample was limited and the findings should not be extrapolated to every severe presentation (Butcher et al., 2025).

The other hyperacute target is hemostasis. Routine recombinant factor VIIa or tranexamic acid has not established functional benefit in unselected spontaneous ICH. TICH-2 did not significantly improve 90-day functional outcome with tranexamic acid, despite reducing some bleeding-related measures (Sprigg et al., 2018). FASTEST tested factor VIIa within two hours and stopped for futility: hematoma growth decreased, the primary functional outcome did not improve, and life-threatening thromboembolic complications increased (Broderick et al., 2026). Reducing blood volume does not necessarily improve recovery. FASTEST Part 2 tests treatment within 90 minutes with or without a spot sign, or within two hours with a positive spot sign. Rapid imaging and delivery remain challenges; this is investigational treatment (University of California, Davis, 2026).

PATCH demonstrated worse outcomes with platelet transfusion in antiplatelet-associated spontaneous ICH without emergency surgery (Baharoglu et al., 2016). Aspirin exposure alone is therefore insufficient reason for routine platelets. Emergency neurosurgery may create a specific indication in an aspirin-treated patient; severe thrombocytopenia and genuine coagulation factor deficiencies require their own treatment. Platelets are not automatically appropriate before every operation. The clinical distinction is between correcting a defined hemostatic defect and giving a procoagulant empirically to every patient with ICH.

Clinically relevant anticoagulant-associated hemorrhage needs immediate reversal. Warfarin-associated ICH often has worse outcomes, and higher INR correlates with bleeding severity. Four-factor PCC provides rapid reversal; IV vitamin K sustains correction. Dabigatran has a specific reversal agent, idarucizumab. Factor Xa inhibitor-associated hemorrhage requires an agent-appropriate pathway, commonly four-factor PCC in current U.S. practice. Medication timing, renal function, and coagulation testing help establish activity without unnecessarily delaying treatment. DOACs cause less intracranial bleeding than warfarin in AF trials, but that advantage does not guarantee a smaller or less dangerous presenting hematoma.

Andexanet alfa needs a dated, geographically specific discussion. ANNEXA-I showed better hemostatic efficacy than usual care, which largely involved PCC, but more thrombotic events and no demonstrated improvement in 30-day functional outcome or mortality (Connolly et al., 2024). On December 18, 2025, the FDA stated that the serious thromboembolic risks outweighed the benefits; AstraZeneca ended U.S. manufacture and sales after December 22, 2025 (U.S. Food and Drug Administration, 2025). Availability and regulatory decisions in other countries should be checked locally. Reversal protocols need to reflect the current setting and include surveillance for both continued bleeding and thrombosis.

Hemorrhage after IV thrombolysis is a related emergency with a different coagulation problem. Symptomatic intracranial hemorrhage rates are often quoted in the approximate 2–6% range, depending on the definition and treated population. Older age, greater stroke severity, higher blood pressure, and hyperglycemia are recognized risk factors. Many events occur early, including within the first 12 hours, but monitoring cannot end there. Blood may appear within the infarct or remotely, sometimes in the opposite hemisphere. A remote hemorrhage can reflect an underlying vascular vulnerability, including small vessel disease, rather than simply local transformation of the presenting infarct.

The Heidelberg classification helps describe these patterns accurately. Class 1a is scattered petechial hemorrhage without mass effect; 1b is confluent petechial hemorrhage without mass effect; and 1c is a parenchymal hematoma occupying less than 30% of the infarcted tissue without substantive mass effect. Class 2 is a hematoma occupying at least 30% of the infarcted tissue with obvious mass effect. Class 3a is remote parenchymal hemorrhage, 3b intraventricular hemorrhage, 3c subarachnoid hemorrhage, and 3d subdural hemorrhage. The reference is the infarcted tissue, not one-third of a cerebral hemisphere. Radiographic classification and symptomatic deterioration must both be assessed; not every petechial hemorrhage has the same treatment implications (von Kummer et al., 2015).

For suspected symptomatic bleeding after alteplase or tenecteplase, stop any ongoing thrombolytic administration, obtain urgent CT and coagulation studies including fibrinogen, and activate the hemorrhage pathway. Fibrinogen depletion is a key reason cryoprecipitate is used. The 2026 AHA/ASA ischemic stroke guideline describes an initial 10-unit dose with further replacement to maintain fibrinogen at least 150 mg/dL; repeat measurement and the local blood bank protocol guide additional treatment (Prabhakaran et al., 2026). Antifibrinolytics may be considered in appropriate circumstances, including when cryoprecipitate cannot be given promptly. That rescue indication should not be confused with routine tranexamic acid treatment of primary spontaneous ICH.

A code ICH pathway coordinates rapid CT and appropriate CTA, immediate controlled blood pressure reduction, indicated anticoagulant reversal, and early neurosurgical and neurocritical care assessment. Prompt transfer to a monitored inpatient setting enables frequent examinations and titrated treatment. A local repeat-CT schedule at approximately six and 24 hours helps detect expansion, ventricular extension, hydrocephalus, and mass effect; deterioration requires immediate reassessment and imaging. Glucose, temperature, oxygenation, swallowing safety, nutrition, and prevention of inpatient complications require the same consistency as the initial emergency interventions.

INTERACT3 tested a bundle of blood pressure treatment, glucose and temperature management, and rapid warfarin reversal, largely in low- and middle-income settings. Functional outcomes improved in this stepped-wedge cluster trial. A lower six-month mortality signal became statistically nonsignificant after fuller adjustment, so survival benefit should not be stated categorically (Ma et al., 2023). The result cannot be attributed to one component, but organized delivery of available care clearly matters. A code ICH should define responsibilities, treatment availability, monitoring, and escalation across emergency medicine, stroke neurology, neurocritical care, pharmacy, and neurosurgery.

Supportive care requires knowing which interventions to withhold. Corticosteroids should not treat ordinary ICH-related intracranial pressure elevation. Automatic continuous hyperosmolar therapy has no established outcome benefit; a bolus for an acute pressure crisis has a different purpose. Routine antiseizure prophylaxis is discouraged, while clinical or electrographic seizures require treatment. An unexplained or fluctuating examination can warrant continuous EEG. Neurocritical Care Society guidance favors avoiding prophylaxis; if used, it favors levetiracetam over phenytoin and a short course, with weak recommendations based on limited evidence (Frontera et al., 2025).

Venous thromboembolism prevention starts early. Intermittent pneumatic compression should begin on the day of diagnosis in nonambulatory patients. Compression stockings alone are inadequate. Low-dose unfractionated heparin or LMWH may be reasonable after 24–48 hours, taking hematoma stability, coagulopathy, and procedural plans into account. Prophylactic dosing should be distinguished from therapeutic anticoagulation for an established clot. The decision is a planned reassessment of hemorrhage and thrombosis risk, not an automatic timer-based prescription (Greenberg et al., 2022).

Neurosurgical involvement belongs within the same pathway. Hydrocephalus, declining consciousness, posterior fossa mass effect, and selected hematomas requiring evacuation are time-sensitive problems. The historical statement that ICH has no effective stroke-specific treatment now needs qualification. ENRICH demonstrated functional benefit from early minimally invasive evacuation in a selected population, with the benefit attributable to the lobar subgroup rather than the anterior basal ganglia subgroup (Pradilla et al., 2024). MIND did not demonstrate a significant improvement in its primary functional outcome with a different minimally invasive approach and population (Arthur et al., 2025). Selection, timing, technique, and expertise matter. Neither a purely nihilistic approach nor routine evacuation of all hemorrhages fits the evidence.

After the acute admission, hemorrhage location becomes central to recurrence assessment. Lobar hemorrhage raises particular concern for CAA, but the prior bleeding history and MRI phenotype refine that risk. Multiple previous lobar hemorrhages and disseminated cortical superficial siderosis carry more concern than an isolated finding of a few microbleeds. APOE epsilon-2 and epsilon-4 have associations with CAA-related hemorrhage and recurrence, but routine APOE testing is not generally recommended for ordinary clinical risk prediction. The most actionable prevention measure remains sustained blood pressure control, with a long-term target around 130/80 when tolerated. Appropriate activity, reduced heavy alcohol consumption, smoking cessation, and medication adherence support vascular health even where ICH-specific lifestyle trial evidence is less complete.

Anticoagulation after ICH is where the acute diagnosis becomes a long-term treatment decision. AF is increasingly common in older ICH survivors, and these patients remain vulnerable to ischemic stroke, cardiovascular events, and death. Historical estimates cited in the lecture describe AF prevalence around 11%, subsequent increases, and high first-year event rates. Those figures are cohort-specific rather than a universal forecast. Observational reports associating resumed anticoagulation with roughly halved stroke risk are also vulnerable to selection bias: patients chosen for treatment may differ substantially from patients in whom treatment is withheld. Such observations cannot establish that anticoagulation has a favorable net benefit for every survivor, whether the hemorrhage was lobar or deep.

For nonvalvular AF, the first question is whether anticoagulation should be resumed at all. The 2022 AHA/ASA guideline recommends weighing individual benefit and risk; if anticoagulation is chosen, initiation around seven to eight weeks after ICH may be considered. It does not prescribe a universal four-week restart or an absolute prohibition for every lobar hemorrhage (Greenberg et al., 2022). The 2025 International CAA Association/World Stroke Organization statement is cautious after CAA-related ICH or convexity SAH: net benefit remains unclear, and anticoagulation may be avoided. If selected for nonvalvular AF, a DOAC is generally preferred to a vitamin K antagonist. Mechanical heart valves are a separate situation requiring VKA therapy, not substitution of a DOAC (Cordonnier et al., 2025).

MRI adds information that conventional embolic-risk scores miss. CROMIS-2 followed anticoagulated AF patients after ischemic stroke or TIA. Cerebral microbleeds were associated with an adjusted hazard ratio of 3.67 for symptomatic intracranial hemorrhage, with a wide confidence interval. The absolute rates were approximately 9.8 versus 2.6 per 1,000 patient-years in patients with and without microbleeds (Wilson et al., 2018). This identifies a higher-risk group; it is not an automatic contraindication, and the cohort was not a trial of anticoagulation in survivors of a recent major ICH. Burden, distribution, superficial siderosis, prior symptomatic hemorrhage, and blood pressure control all contribute to the individual decision.

PRESTIGE-AF randomized 319 ICH survivors with AF to a DOAC or no anticoagulation. Ischemic stroke rates were approximately 0.83 versus 8.60 per 100 patient-years; recurrent ICH rates were approximately 5.00 versus 0.82 (Veltkamp et al., 2025). Anticoagulation prevented ischemic strokes, but hemorrhage increased and the prespecified hemorrhage noninferiority criterion was not met. Limited sample size, few events, and uncertainty about imaging subgroups prevent a declaration of net benefit for all survivors. The severity and consequences of competing events matter alongside their frequency.

In 2023, ENRICH-AF’s monitoring board recommended stopping study anticoagulation and further enrollment after qualifying lobar ICH or convexity subarachnoid hemorrhage because of excess recurrent hemorrhagic stroke. The sponsor still lists the trial as ongoing for its remaining population (Shoamanesh & ENRICH-AF Steering Committee, 2023; Population Health Research Institute, n.d.). ASPIRE is a separate, double-blind phase III trial comparing apixaban with aspirin after ICH in nonvalvular AF. Planned enrollment is 700, with a primary outcome of stroke or death. Definitive results were unavailable in the sources checked (NYU Langone Health, n.d.). Aspirin is the comparator, not established equivalent protection against AF-related embolism.

Mechanical valves and LVADs can create a more urgent need to resume anticoagulation. The 2022 guideline considers early resumption reasonable in selected patients at high thromboembolic risk, but it does not impose a universal 10–14-day schedule. Hematoma stability, hemorrhage severity, the device or valve, evidence of thrombosis, and procedural plans need joint review with cardiology, cardiac surgery, and the neurological team. Deep location may reduce concern for CAA-related recurrence, but it does not by itself make early therapeutic anticoagulation safe. Conversely, a lobar location does not erase the potentially catastrophic thrombotic risk of a mechanical valve.

Left atrial appendage closure may be considered when long-term anticoagulation presents an unfavorable balance. Prior-ICH patients have been studied in observational cohorts (Abramovitz Fouks et al., 2025), but ICH- and CAA-specific randomized evidence remains insufficient. CLOSURE-AF, conducted in a broader population at high stroke and bleeding risk, failed to establish noninferiority to medical therapy; it does not resolve the ICH-specific question (Landmesser et al., 2026). Immediate procedural risks and temporary antithrombotic exposure need comparison with lifelong anticoagulation and with withholding embolic prevention. The follow-up plan should record the presumed hemorrhage mechanism, relevant MRI findings, blood pressure strategy, indication for antithrombotic treatment, and the date and conditions for revisiting the decision.

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