Note to myself: When I review this post again, I need to also review the podcast and show notes of Dr. Weingart‘s EMCrit 326 – NeuroEMCrit – 2022 Spontaneous Intracerebral Hemorrhage Guidelines with Casey & Neha, June 16, 2022.
What’s meant by spontaneous ICH?
- Intracerebral hemorrhage can be thought of in 4 buckets
- Trauma
- Other secondary causes of hemorrhage: Hemorrhagic mets, hemorrhagic conversion of ischemic pathology, venous pathology,
- Macrovascular diseases: AVMs, aneurysms
- Microvascular disease: Historically this has been the pathology that has been defined as “primary ICH,” but we now have a much better understanding that what appears spontaneous is precipitated by pathologic small vessel remodeling and breakdown
- Arteriolosclerosis / lipohyliosis (“HTN-hemorrhage”) vs Cerebral Amyloid Angiopathy (CAA)
- Each has a signature location of occurring in the brain.
In this post, I link to and excerpt from 2022 Guideline for the Management of Patients With Spontaneous Intracerebral Hemorrhage: A Guideline From the American Heart Association/American Stroke Association [Full-Text PDF] Stroke. 2022 May 17.
All that follows is from the above resource.
TOP 10 TAKE-HOME MESSAGES FOR THE MANAGEMENT OF PATIENTS WITH SPONTANEOUS INTRACEREBRAL HEMORRHAGE GUIDELINE
1. The organization of health care systems is increas-ingly recognized as a key component of optimal stroke care. This guideline recommends development of regional systems that provide initial intra-cerebral hemorrhage (ICH) care and the capacity, when appropriate, for rapid transfer to facilities with neurocritical care and neurosurgical capabilities.
2. Hematoma expansion is associated with worse ICH outcome. There is now a range of neuroimag-ing markers that, along with clinical markers such as time since stroke onset and use of antithrombotagents, help to predict the risk of hematoma expansion. These neuroimaging markers include signs detectable by noncontrast computed tomography, the most widely used neuroimaging modality for ICH.
3. ICHs, like other forms of stroke, occur as the con-sequence of a defined set of vascular patholo-gies. This guideline emphasizes the importance of, and approaches to, identifying markers of both microvascular and macrovascular hemorrhage pathogeneses.
4. When implementing acute blood pressure lowering after mild to moderate ICH, treatment regimens that limit blood pressure variability and achieve smooth, sustained blood pressure control appear to reduce hematoma expansion and yield better functional outcome.
5. ICH while anticoagulated has extremely high mortality and morbidity. This guideline provides updated recommendations for acute reversal of anticoagulation after ICH, highlighting use of protein complex concentrate for reversal of vitamin K antagonists such as warfarin, idarucizumab for reversal of the thrombin inhibitor dabigatran, and andexanet alfa for reversal of factor Xa inhibitors such as rivaroxaban, apixaban, and edoxaban.
6. Several in-hospital therapies that have historically been used to treat patients with ICH appear to confer either no benefit or harm. For emergency or critical care treatment of ICH, prophylactic cor-ticosteroids or continuous hyperosmolar therapy appears to have no benefit for outcome, whereas the use of platelet transfusions outside the setting of emergency surgery or severe thrombocytopenia appears to worsen outcome. Similar considerations apply to some prophylactic treatments historically used to prevent medical complications after ICH. Use of graduated knee- or thigh-high compres-sion stockings alone is not an effective prophylactic therapy for prevention of deep vein thrombosis, and prophylactic antiseizure medications in the absence of evidence for seizures do not improve long-term seizure control or functional outcome.
7. Minimally invasive approaches for evacuation of supratentorial ICHs and intraventricular hemorrhages‚ compared with medical management alone‚ have demonstrated reductions in mortality. The clinical trial evidence for improvement of functional out-come with these procedures is neutral, however. For patients with cerebellar hemorrhage, indications for immediate surgical evacuation with or without an external ventricular drain to reduce mortality now include larger volume (>15 mL) in addition to previously recommended indications of neurological dete-rioration, brainstem compression, and hydrocephalus.
8. The decision of when and how to limit life-sustaining treatments after ICH remains complex and highly dependent on individual preference. This guideline emphasizes that the decision to assign do not attempt resuscitation status is entirely distinct from the decision to limit other medical and surgical interventions and should not be used to do so. On the other hand, the decision to implement an intervention should be shared between the physician and patient or surrogate and should reflect the patient’s wishes as best as can be discerned. Baseline severity scales can be useful to provide an overall measure of hemorrhage severity but should not be used as the sole basis for limiting life-sustaining treatments.
9. Rehabilitation and recovery are important determi-nants of ICH outcome and quality of life. This guide-line recommends use of coordinated multidisciplinary inpatient team care with early assessment of dis-charge planning and a goal of early supported dis-charge for mild to moderate ICH. Implementation of rehabilitation activities such as stretching and functional task training may be considered 24 to 48 hours after moderate ICH; however, early aggressive mobilization within the first 24 hours after ICH appears to worsen 14-day mortality. Multiple ran-domized trials did not confirm an earlier suggestion that fluoxetine might improve functional recovery after ICH. Fluoxetine reduced depression in these trials but also increased the incidence of fractures.
10. A key and sometimes overlooked member of the ICH care team is the patient’s home caregiver. This guideline recommends psychosocial education, practical support, and training for the care-giver to improve the patient’s balance, activity level, and overall quality of life
2. GENERAL CONCEPTS
2.1. Small Vessel Disease Types
Despite our use of the term primary ICH to distinguish from ICH with a demonstrated structural cause (Section 1.4, Scope of the Guideline), these seemingly spontaneous hemorrhages are not truly primary but rather represent the consequence of defined underlying (and often co-occurring) vascular pathologies. The 2 common cerebral small vessel pathologies that account for the overwhelming majority of primary ICH are arteriolosclerosis and cerebral amyloid angiopathy (CAA). Each is a common age-related pathol-ogy, appearing at autopsy at moderate to severe extents in 30% to 35% of individuals enrolled in a longitudinal study of aging.21 Arteriolosclerosis (also referred to as lipohyalinosis) is detected as concentric hyalinized vascular wall thicken-ing favoring the penetrating arterioles of the basal ganglia, thalamus, brainstem, and deep cerebellar nuclei (collectively referred to as deep territories). Its major associated risk factors are hypertension, diabetes, and age. CAA is defined by deposition primarily of the β-amyloid peptide in the walls of arterioles and capillaries in the leptomeninges, cerebral cortex, and cerebellar hemispheres (lobar territories). The primary risk factors for CAA are age and apolipoprotein E genotypes containing the ε2 or ε4 alleles.
ICH occurs in a relatively small subset of those brains with advanced arteriolosclerosis or CAA, typically in deep territories for arteriolosclerosis and lobar territories for CAA, the brain locations favored by the underlying pathologies. Small, often asymptomatic cerebral microbleeds in these compartments are substantially more common, occurring in >20% of population-based individuals >60 years of age scanned with sensitive T2*-weighted MRI methods.22,23 The presence of multiple strictly lobar ICHs, microbleeds, or cor-tical superficial siderosis (chronic blood products over the cerebral subpial surface) has been pathologically validated as part of the Boston criteria to detect CAA-related hem-orrhage with reasonably high specificity and sensitivity.24Microbleeds associated with arteriolosclerosis tend to occur in deep territories but can appear in lobar territories as well.
he underlying small vessel types of ICH have several practical implications for the formulation of ICH guide-lines. They establish a hemorrhage-prone environment in which use of antithrombotic agents creates increased risk of ICH.25 It is important to note, however, that the small vessel pathologies that underlie ICH are also associated with increased risk of ischemic stroke,26 highlighting the complexity and importance of balancing the risks versus benefits of antithrombotic treatment. Among the cerebral small vessel diseases, CAA inferred by the Boston criteria* appears to confer substantially greater risk for recur-rent hemorrhage than arteriolosclerosis (recurrent ICH rates in a pooled analysis of 7.39%/y after CAA-related ICH versus 1.11%/y after non–CAA-related ICH).27
*Boston criteria for cerebral amyloid angiopathy
Last revised by Dr Francis Deng on 12 Jul 2021 from Radiopaedia
