Acute Stroke Management — Part 4: Intracerebral Hemorrhage
ICH pathophysiology, ICH Score, hematoma expansion, blood pressure management (INTERACT2, ATACH-2), anticoagulant reversal protocols, surgical intervention criteria (STICH, MISTIE III, ENRICH), and ICP management.
1. Intracerebral Hemorrhage — Overview
Spontaneous (non-traumatic) intracerebral hemorrhage (ICH) accounts for approximately 10-15% of all strokes and carries the highest acute mortality rate of any stroke subtype. Approximately 30-50% of patients die within 30 days, and only 20% of survivors are functionally independent at 6 months. ICH represents a true medical emergency, with early hematoma expansion occurring in up to 30% of patients within the first few hours, a process that is strongly associated with clinical deterioration and death.1 2
2. Etiology and Risk Factors
2.1 Primary Etiologies
| Etiology | Proportion | Typical Location | Risk Factors |
|---|---|---|---|
| Hypertensive arteriopathy | ~55-65% | Deep structures: basal ganglia, thalamus, pons, cerebellum | Chronic hypertension; lipohyalinosis and microaneurysms of small perforating arteries |
| Cerebral amyloid angiopathy (CAA) | ~15-20% | Lobar (cortical/subcortical); may be multifocal or recurrent | Age > 65; APOE ε2 and ε4 alleles; associated with lobar microbleeds on MRI |
| Anticoagulant-related | ~10-15% | Any location | Warfarin (risk increases sharply with INR > 3.0); DOACs (lower risk than warfarin); heparin |
| Structural lesions | ~5-10% | Variable | Arteriovenous malformations, cavernous malformations, dural AV fistulas, aneurysms, tumors |
| Other | ~5% | Variable | Coagulopathy, vasculitis, moyamoya, sympathomimetic drugs (cocaine, amphetamines), hemorrhagic transformation of ischemic stroke |
2.2 Key Risk Factors
| Risk Factor | Relative Risk |
|---|---|
| Hypertension (uncontrolled) | 3-5× |
| Anticoagulant therapy | 7-10× (warfarin); 2-3× (DOACs) |
| Heavy alcohol use (> 2 drinks/day) | 2-4× |
| Cerebral amyloid angiopathy | 5-10× for lobar ICH |
| Prior stroke (ischemic or hemorrhagic) | 2-3× |
| Dual antiplatelet therapy | 1.5-2× |
| Cocaine/amphetamine use | 5-6× |
| Liver disease / coagulopathy | Variable |
| Cerebral microbleeds (≥ 5 on MRI) | 2-5× |
3. ICH Score — Prognostic Grading
The ICH Score is the most widely used and validated grading scale for predicting 30-day mortality after spontaneous ICH. It was developed by Hemphill and colleagues and validated in multiple cohorts.3
3.1 Complete ICH Score Table
| Component | Criteria | Points |
|---|---|---|
| Glasgow Coma Scale (GCS) | 13-15 | 0 |
| 5-12 | 1 | |
| 3-4 | 2 | |
| ICH volume | < 30 mL | 0 |
| ≥ 30 mL | 1 | |
| Intraventricular hemorrhage (IVH) | No | 0 |
| Yes | 1 | |
| Infratentorial origin | No | 0 |
| Yes | 1 | |
| Age | < 80 years | 0 |
| ≥ 80 years | 1 |
Total score range: 0-6
3.2 ICH Score and 30-Day Mortality
| ICH Score | 30-Day Mortality |
|---|---|
| 0 | 0% |
| 1 | 13% |
| 2 | 26% |
| 3 | 72% |
| 4 | 97% |
| 5 | 100% |
| 6 | 100% |
3.3 ICH Volume Estimation — ABC/2 Method
ICH volume can be rapidly estimated on CT using the ABC/2 formula:4
Volume (mL) = (A × B × C) / 2
Where:
- A = greatest diameter of hemorrhage on the axial CT slice with the largest hemorrhage (cm)
- B = diameter perpendicular to A on the same slice (cm)
- C = number of CT slices with hemorrhage × slice thickness (cm) — or approximate craniocaudal extent
This simplified formula approximates the hemorrhage as an ellipsoid and provides a clinically useful estimate within minutes.
3.4 Important Caveats About the ICH Score
- The ICH Score was developed as a prognostic tool, NOT a treatment-decision tool
- Self-fulfilling prophecy risk: If clinicians use the ICH Score to justify withdrawal of care, the high mortality rates become self-reinforcing. The 2022 guidelines from the major cardiovascular and stroke professional societies explicitly warn against early limitation of aggressive care based solely on prognostic scores.1
- Recommendation: Full aggressive medical and surgical management should be provided for at least 24-72 hours before any discussion of care limitation, unless the patient has a valid advance directive or the clinical situation is clearly non-survivable
- No prognostic score should be used in isolation to limit treatment
4. Blood Pressure Management in ICH
Acute blood pressure management is one of the most important early interventions in ICH. The rationale is to reduce the rate of hematoma expansion, which occurs in up to 30% of patients within 6 hours and is a major driver of mortality and poor outcomes.1 5 6
4.1 Key Trials
INTERACT2 (Intensive Blood Pressure Reduction in Acute Cerebral Haemorrhage Trial 2)
| Parameter | Details |
|---|---|
| Design | International RCT; n = 2,839 |
| Population | Spontaneous ICH within 6 hours; SBP 150-220 mmHg |
| Intervention | Intensive SBP target < 140 mmHg (within 1 hour) vs standard target < 180 mmHg |
| Primary outcome | Death or major disability at 90 days: 52.0% (intensive) vs 55.6% (standard); OR 0.87 (95% CI 0.75-1.01; p = 0.06) — did not reach significance for primary endpoint |
| Ordinal analysis | Significant shift toward better outcomes across the entire mRS distribution (OR 0.87, p = 0.04) |
| Safety | No significant increase in adverse events with intensive lowering |
| Conclusion | Intensive BP lowering to SBP < 140 mmHg is safe and may improve functional outcomes; adopted as standard of care5 |
ATACH-2 (Antihypertensive Treatment of Acute Cerebral Hemorrhage 2)
| Parameter | Details |
|---|---|
| Design | International RCT; n = 1,000 |
| Population | Spontaneous ICH within 4.5 hours; SBP ≥ 180 mmHg; ICH volume < 60 mL |
| Intervention | Intensive SBP target 110-139 mmHg vs standard SBP target 140-179 mmHg |
| Antihypertensive | IV nicardipine in both groups |
| Primary outcome | Death or disability (mRS 4-6) at 90 days: 38.7% (intensive) vs 37.7% (standard); RR 1.04 (95% CI 0.85-1.27; p = 0.72) — no difference |
| Hematoma expansion | No significant difference between groups |
| Safety | Renal adverse events significantly higher in intensive group (9.0% vs 4.0%; p = 0.002) |
| Conclusion | Achieving SBP < 140 is safe and reasonable (consistent with INTERACT2), but targeting SBP < 120-130 provides no additional benefit and may cause harm (renal injury)6 |
4.2 Current Blood Pressure Recommendations
| Presenting SBP | Target | Timing | Agent |
|---|---|---|---|
| 150-220 mmHg | < 140 mmHg | Within 1 hour of presentation; maintain for at least 24 hours | Nicardipine infusion (preferred) or labetalol or clevidipine |
| > 220 mmHg | Reduce cautiously; avoid sustained SBP < 130 mmHg | Gradual reduction; avoid precipitous drops | Nicardipine infusion or clevidipine; may require multiple agents |
| < 150 mmHg | Monitor; generally no acute intervention | — | — |
4.3 Practical BP Management Protocol for ICH
| Step | Action |
|---|---|
| 1 | Obtain baseline SBP; if > 150 mmHg, initiate treatment immediately |
| 2 | First-line: Nicardipine 5 mg/h IV infusion; titrate by 2.5 mg/h every 5-15 minutes; max 15 mg/h |
| 3 | Alternative: Labetalol 10-20 mg IV push every 10-20 minutes (max 300 mg); then infusion 2-8 mg/min |
| 4 | Alternative: Clevidipine 1-2 mg/h IV infusion; titrate by doubling every 90 seconds; max 32 mg/h |
| 5 | Target SBP 130-140 mmHg; avoid SBP < 130 (risk of renal injury) or > 160 (risk of hematoma expansion) |
| 6 | Maintain target for at least 24-72 hours |
| 7 | Transition to oral antihypertensives when patient is neurologically stable and tolerating PO |
5. Hematoma Expansion
5.1 Definition and Significance
Hematoma expansion is defined as an increase in hemorrhage volume of > 33% or > 6 mL from the initial CT scan to follow-up imaging (typically at 24 hours). It occurs in approximately 20-30% of patients, primarily within the first 3-6 hours.1 7
5.2 Predictors of Hematoma Expansion
| Predictor | Clinical Significance |
|---|---|
| CT angiography spot sign | Active contrast extravasation within the hematoma on CTA; sensitivity ~60%, specificity ~90% for expansion; strongest imaging predictor |
| Time from onset | Earlier presentation = higher risk of ongoing expansion |
| Initial hematoma volume | Larger initial volume associated with greater expansion |
| Anticoagulant use | Warfarin-related ICH has a prolonged expansion phase (up to 24-48 hours unless INR is reversed) |
| Dual antiplatelet therapy | Modest increase in expansion risk |
| Shape irregularity | Irregular or heterogeneous hematoma morphology |
| Blend sign | Hyper-dense region adjacent to hypo-dense region within the hematoma; suggests active bleeding |
| Black hole sign | Encapsulated low-density area within the hematoma on NCCT |
5.3 Strategies to Limit Hematoma Expansion
| Strategy | Evidence |
|---|---|
| Aggressive BP lowering (SBP < 140) | INTERACT2 evidence; standard of care |
| Anticoagulant reversal | Critical for warfarin/DOAC-related ICH; see Section 6 |
| Tranexamic acid | TICH-2 trial: no significant reduction in mortality or functional outcome at 90 days, but modest reduction in hematoma expansion; not routinely recommended8 |
| Platelet transfusion (for antiplatelet-related ICH) | PATCH trial: platelet transfusion was associated with WORSE outcomes; NOT recommended9 |
| Recombinant Factor VIIa | FAST trial: reduced hematoma expansion but no improvement in outcomes; increased thromboembolic events; NOT recommended for routine use10 |
6. Anticoagulant Reversal in ICH
Reversal of anticoagulation is a critical and time-sensitive intervention in patients with anticoagulant-related ICH. The goal is to normalize hemostasis as rapidly as possible to limit hematoma expansion.1 2
6.1 Warfarin (Vitamin K Antagonist) Reversal
| Agent | Dose | Onset | Additional Notes |
|---|---|---|---|
| 4-Factor Prothrombin Complex Concentrate (4F-PCC) | 25-50 units/kg IV (dose based on INR — see dosing table below) | 15-30 minutes | First-line treatment; contains Factors II, VII, IX, X, and Proteins C and S; preferred over FFP due to faster onset, smaller volume, and more reliable INR correction11 |
| Vitamin K (phytonadione) | 10 mg IV infused slowly over 10-20 minutes | 2-4 hours (partial); 12-24 hours (full) | Always administer WITH 4F-PCC; vitamin K provides sustained factor production once the PCC effect wanes (~12-24 hours); IV route preferred over PO for speed |
| Fresh Frozen Plasma (FFP) | 10-15 mL/kg IV | 30-60 minutes (after thawing, which adds 30-45 min) | Second-line if 4F-PCC unavailable; slower onset; larger volume (risk of volume overload); requires ABO compatibility; less reliable INR correction |
4F-PCC Dosing by INR
| INR | 4F-PCC Dose (units/kg) | Maximum Dose |
|---|---|---|
| 2.0-3.9 | 25 units/kg | 2,500 units |
| 4.0-5.9 | 35 units/kg | 3,500 units |
| ≥ 6.0 | 50 units/kg | 5,000 units |
Recheck INR 15-30 minutes after 4F-PCC administration. If INR remains > 1.5, administer an additional dose of 4F-PCC.
Target INR: < 1.5 (ideally < 1.3).
6.2 Direct Oral Anticoagulant (DOAC) Reversal
Dabigatran (Direct Thrombin Inhibitor)
| Agent | Dose | Notes |
|---|---|---|
| Idarucizumab | 5 g IV (two 2.5 g vials given as two consecutive infusions or boluses) | Specific reversal agent for dabigatran; humanized monoclonal antibody fragment that binds dabigatran with high affinity; complete reversal within minutes; FDA approved for this indication; RE-VERSE AD trial12 |
| 4F-PCC (if idarucizumab unavailable) | 50 units/kg IV | Non-specific; may partially restore hemostasis but does not directly reverse dabigatran; second-line option |
| Activated charcoal | 50 g PO/NG | Only useful if dabigatran was ingested within the last 2 hours |
| Hemodialysis | — | Dabigatran is ~35% dialyzable; consider if idarucizumab unavailable and renal failure present; not practical in the acute setting |
Factor Xa Inhibitors (Rivaroxaban, Apixaban, Edoxaban)
| Agent | Dose | Notes |
|---|---|---|
| Andexanet alfa | Low-dose bolus: 400 mg IV at 30 mg/min, then 4 mg/min infusion × 120 min (total ~480 mg) OR High-dose bolus: 800 mg IV at 30 mg/min, then 8 mg/min infusion × 120 min (total ~960 mg) | Specific reversal agent for Factor Xa inhibitors; recombinant modified Factor Xa decoy; ANNEXA-4 trial; FDA approved13 |
| 4F-PCC (if andexanet unavailable) | 50 units/kg IV | Non-specific; may partially restore hemostasis; widely available and significantly less expensive than andexanet; many institutions use 4F-PCC as first-line given availability and cost considerations14 |
| Activated charcoal | 50 g PO/NG | Only useful if Xa inhibitor was ingested within the last 2 hours (rivaroxaban, edoxaban) or 6 hours (apixaban) |
Andexanet Alfa Dosing by Agent and Timing
| Factor Xa Inhibitor | Last Dose < 8 hours (or unknown) | Last Dose ≥ 8 hours |
|---|---|---|
| Rivaroxaban (≤ 10 mg) | Low dose | Low dose |
| Rivaroxaban (> 10 mg) | High dose | Low dose |
| Apixaban (≤ 5 mg) | Low dose | Low dose |
| Apixaban (> 5 mg) | High dose | Low dose |
| Edoxaban | High dose | Low dose |
| Enoxaparin | High dose | Low dose |
6.3 Heparin Reversal
| Agent | Dose | Notes |
|---|---|---|
| Protamine sulfate (for unfractionated heparin) | 1 mg protamine per 100 units of heparin given in the preceding 2-3 hours; max single dose 50 mg; give IV slowly over 10 minutes | Rapidly neutralizes UFH; recheck aPTT 15 minutes after administration; risk of hypotension, bradycardia, anaphylaxis (especially in patients with fish allergy or prior protamine exposure) |
| Protamine sulfate (for enoxaparin/LMWH) | 1 mg protamine per 1 mg of enoxaparin given in the preceding 8 hours; give IV slowly over 10 minutes; a second dose of 0.5 mg per 1 mg enoxaparin may be given if bleeding continues | Only partially reverses LMWH (~60% of anti-Xa activity neutralized); if last dose > 8 hours ago, may not be needed |
6.4 Reversal Summary Table
| Anticoagulant | First-Line Reversal | Second-Line | Target |
|---|---|---|---|
| Warfarin | 4F-PCC + Vitamin K 10 mg IV | FFP + Vitamin K | INR < 1.5 |
| Dabigatran | Idarucizumab 5 g IV | 4F-PCC 50 U/kg; hemodialysis | Clinical hemostasis; normalized TT/aPTT |
| Rivaroxaban/Apixaban/Edoxaban | Andexanet alfa OR 4F-PCC 50 U/kg | Activated charcoal (if recent ingestion) | Clinical hemostasis; normalized anti-Xa |
| Unfractionated heparin | Protamine sulfate | — | Normalized aPTT |
| Enoxaparin (LMWH) | Protamine sulfate (partial reversal) | — | Clinical hemostasis |
7. Surgical Intervention in ICH
7.1 Key Trials
| Trial | Year | Design | Key Finding |
|---|---|---|---|
| STICH (Surgical Trial in Intracerebral Haemorrhage) | 2005 | RCT; n = 1,033; early surgery vs initial conservative management | No overall benefit of early surgery; subgroup analysis suggested possible benefit in lobar hemorrhages within 1 cm of the cortical surface15 |
| STICH II | 2013 | RCT; n = 601; lobar ICH without IVH; 10-100 mL; within 1 cm of cortical surface | No significant benefit of early surgery (mRS 0-3: 59% surgery vs 62% conservative; p = 0.37); post-hoc analysis suggested benefit when GCS declining16 |
| MISTIE III (Minimally Invasive Surgery plus Alteplase for ICH Evacuation) | 2019 | RCT; n = 506; minimally invasive catheter-based clot evacuation with alteplase irrigation vs standard medical care | No significant benefit on primary endpoint (mRS 0-3: 45% vs 41%; p = 0.33); however, achieving clot reduction to < 15 mL was associated with significantly better outcomes17 |
| ENRICH (Early Minimally-Invasive Removal of ICH) | 2024 | RCT; n = 300; early minimally invasive parafascicular surgery (using BrainPath approach) vs standard medical management; lobar or anterior ICH ≥ 30 mL | Significant benefit of early minimally invasive surgery (utility-weighted mRS favoring surgery; p = 0.02); first positive surgical trial for ICH18 |
7.2 Surgical Indications — Current Recommendations
| Scenario | Recommendation | Evidence Level |
|---|---|---|
| Cerebellar hemorrhage > 3 cm or with brainstem compression or hydrocephalus | Surgical evacuation recommended (neurosurgical emergency) | Strong; consistent across all guidelines |
| Cerebellar hemorrhage with neurological deterioration | Urgent surgical evacuation | Strong |
| Supratentorial lobar ICH with neurological deterioration | Consider surgical evacuation, especially if clot is superficial (within 1 cm of cortex) | Moderate; supported by STICH subgroup and ENRICH |
| Supratentorial lobar ICH ≥ 30 mL, stable | Early minimally invasive surgery may be considered based on ENRICH | Moderate; emerging evidence |
| Deep (basal ganglia/thalamic) ICH | Surgical evacuation generally NOT recommended | Strong; STICH/STICH II showed no benefit for deep hemorrhages |
| IVH with hydrocephalus | External ventricular drain (EVD) placement | Strong; addresses hydrocephalus; see Section 7.3 |
| Comatose with large hematoma and brainstem herniation | Surgery unlikely to benefit; goals-of-care discussion | Weak; most patients with GCS 3-4 and large ICH have very poor prognosis |
7.3 Intraventricular Hemorrhage (IVH) Management
IVH is present in approximately 45% of ICH patients and is an independent predictor of poor outcome. Treatment focuses on CSF diversion and clot clearance:1
| Intervention | Indication | Details |
|---|---|---|
| External ventricular drain (EVD) | IVH with hydrocephalus (ventriculomegaly) or declining consciousness | Standard neurosurgical procedure; allows CSF drainage and ICP monitoring |
| Intraventricular tPA (alteplase) | IVH causing obstructive hydrocephalus with blood in 3rd or 4th ventricle | 1 mg alteplase through EVD every 8 hours (max 12 doses or until 3rd/4th ventricle clear); CLEAR III trial showed reduced mortality but not improved functional outcome (mRS 0-3)19 |
8. Intracranial Pressure (ICP) Management in ICH
8.1 ICP Monitoring
| Indication | Method |
|---|---|
| GCS ≤ 8 with large ICH or IVH | EVD (allows both monitoring and therapeutic CSF drainage) |
| Clinical signs of elevated ICP (declining consciousness, pupil asymmetry, Cushing triad) | EVD or intraparenchymal ICP monitor |
ICP targets: < 20 mmHg; cerebral perfusion pressure (CPP) > 60 mmHg.1
8.2 Stepwise ICP Management Protocol
| Step | Intervention | Details |
|---|---|---|
| 1 | General measures | Head of bed elevated 30°; head midline; avoid neck flexion/rotation (impedes venous drainage); avoid hyperthermia; adequate sedation/analgesia |
| 2 | CSF drainage | If EVD in place, open to drainage at 10-15 cmH2O |
| 3 | Osmotic therapy — Mannitol | 0.25-1.0 g/kg IV bolus (20% solution); may repeat every 4-6 hours; hold if serum osmolality > 320 mOsm/kg or osmolar gap > 10 |
| 4 | Osmotic therapy — Hypertonic saline | 23.4% NaCl: 30 mL IV via central line over 10-20 min; OR 3% NaCl: 150-250 mL bolus or continuous infusion at 0.5-2 mL/kg/h; target Na 145-155 mEq/L |
| 5 | Hyperventilation (short-term rescue) | Target PaCO2 30-34 mmHg; short-term bridge to definitive treatment; rebound ICP elevation occurs with prolonged hyperventilation |
| 6 | Barbiturate coma | Pentobarbital 5-20 mg/kg loading dose, then 1-4 mg/kg/h; continuous EEG monitoring to target burst suppression; significant risk of hypotension |
| 7 | Decompressive craniectomy | Rescue therapy for refractory ICP elevation; more commonly performed for malignant MCA infarction than primary ICH; limited evidence for ICH |
9. General ICH Management
9.1 Initial ED Management Checklist
| Domain | Action |
|---|---|
| ABCs | Secure airway if GCS ≤ 8; avoid hypoxia (SpO2 > 94%); IV access |
| Blood pressure | Initiate IV antihypertensive immediately if SBP > 150 (target < 140) |
| Anticoagulant reversal | Identify agent; administer reversal immediately; do not wait for coagulation results if agent is known |
| Labs | CBC, CMP, PT/INR, aPTT, fibrinogen, type and screen; anti-Xa level if on Factor Xa inhibitor; thrombin time if on dabigatran |
| Imaging | NCCT head (hemorrhage confirmed); CTA head to evaluate for spot sign and underlying structural lesion (AVM, aneurysm) |
| Neurosurgery consultation | For all ICH patients; urgent for cerebellar hemorrhage, large supratentorial hemorrhage with declining exam, or IVH with hydrocephalus |
| Neurology/stroke team | Activate stroke code; ICH is a stroke |
| Seizure management | Treat clinical seizures with IV lorazepam, then levetiracetam or fosphenytoin loading; prophylactic antiepileptics are NOT routinely recommended1 |
| DVT prophylaxis | Intermittent pneumatic compression devices immediately; pharmacologic prophylaxis (LMWH or UFH) may begin 24-48 hours after onset if hemorrhage is stable on repeat imaging |
| Temperature | Target normothermia (< 38°C); treat fever with acetaminophen, cooling blankets |
| Glucose | Target 140-180 mg/dL; avoid hypoglycemia |
| Disposition | ICU or dedicated stroke unit with neuro-monitoring capability |
9.2 Secondary ICH Prevention
| Factor | Recommendation |
|---|---|
| Blood pressure | Long-term target < 130/80 mmHg; single most important modifiable risk factor |
| Anticoagulation restart | Risk-benefit analysis; generally restart after 4-8 weeks if strong indication (mechanical heart valve, high CHA2DS2-VASc); consider PFO closure or left atrial appendage occlusion if recurrent lobar ICH |
| Antiplatelet therapy | Can generally be restarted after 2-4 weeks if indicated; RESTART trial showed no significant increase in recurrent ICH20 |
| Statin therapy | Continue or initiate; despite theoretical concerns about ICH risk, statin benefits for cardiovascular risk reduction generally outweigh hemorrhagic risk |
| Alcohol cessation | Counsel all patients with alcohol-related risk |
| Imaging follow-up | MRI with GRE/SWI to evaluate for cerebral amyloid angiopathy (lobar microbleeds) or other structural lesions |
10. Prognostication and Goals of Care
10.1 Timing of Prognostication
The 2022 guideline from the major cardiovascular and stroke professional societies explicitly recommends:1
Recommendation: It is reasonable to postpone new DNR orders for at least the first 24 hours after ICH onset, and to provide aggressive full care during that time, to allow for initial clinical stabilization and to avoid the self-fulfilling prophecy of early withdrawal of care.
10.2 Factors Associated with Poor Prognosis
| Factor | Impact |
|---|---|
| ICH Score ≥ 3 | 30-day mortality > 70% |
| GCS ≤ 4 at presentation | Very high mortality |
| Hematoma volume > 60 mL | Poor functional outcomes in nearly all patients |
| IVH with hydrocephalus | Independent predictor of poor outcome |
| Brainstem hemorrhage | Very high mortality |
| Infratentorial location | Worse prognosis than supratentorial for same volume |
| Ongoing hematoma expansion | Poor prognosis if not controlled |
| Anticoagulant-related and reversal delayed | Higher mortality if reversal not achieved promptly |
10.3 Principles of Goals-of-Care Discussions
- Avoid premature prognostication in the first 24-72 hours
- Communicate uncertainty honestly — prediction models have limited accuracy for individual patients
- Consider the patient’s values and previously expressed wishes
- Engage palliative care for complex discussions, not just end-of-life care
- Document goals-of-care discussions and decisions clearly
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