Hemorrhagic Stroke: Clinical Guidelines

List of Abbreviations

CMA – cerebral aneurysm

AVM – arteriovenous malformation

BP – blood pressure

CoW – circle of Willis

aPTT – activated partial thromboplastin time

CCB – calcium channel blockers

aSAH – aneurysmal SAH

ICH – intracerebral hematoma

IVH – intraventricular hemorrhage

ICA – internal carotid artery

ICH – intracranial hypertension

ICP – intracranial pressure

HS – hemorrhagic stroke

DC – decompressive craniectomy

PICA – posterior inferior cerebellar artery

IMV – invasive mechanical ventilation

IIPMR – individualized medical rehabilitation program

CT – computed tomography

КТА – computed tomography angiography

PSV – peak systolic velocity

IU – international units

INR – international normalized ratio

МРА – magnetic resonance angiography

MRI – magnetic resonance imaging

EVD – external ventricular drain

nICH – nontraumatic intracranial hemorrhage

LMWH – low molecular weight heparin (ATC B01AB Heparin group)

UFH – unfractionated heparin (sodium heparin**)

CVA – cerebrovascular accident

ICU – intensive care unit

ICU – intensive care unit

PICS – post-intensive care syndrome

ПМА – anterior cerebral artery

ACoA – anterior communicating artery

SAH – subarachnoid hemorrhage

SBP – systolic blood pressure

СМА – middle cerebral artery

SRS – stereotactic radiosurgery

SDH – subdural hematoma

TCD – transcranial color-coded duplex sonography with monitoring

Dura – dura mater

DSA – digital subtraction angiography

CVS – cerebral vasospasm

CPP – cerebral perfusion pressure

CN – cranial nerves

HR – heart rate

GCS – Glasgow Coma Scale

ECG – electrocardiography

CBF – cerebral blood flow

CBV – cerebral blood volume

MTT – mean transit time

S-M – Spetzler-Martin scale

Terms and Definitions

Hemorrhagic stroke is a multi-etiological disease characterized by nontraumatic intracranial hemorrhage.

Brain aneurysm is a localized out-pouching of an intracranial artery wall [1].

Arteriovenous malformation is a congenital pathological vascular lesion of the brain consisting of a tangle of vessels in which feeder arteries and draining veins are connected directly without an intervening capillary bed (arteriovenous fistulas) [2, 3].

Intraventricular hemorrhage is bleeding into the cerebral ventricles (including secondary rupture of blood into the ventricles during the formation of an intracerebral hematoma) [4].

Intracerebral hemorrhage (parenchymal, intracerebral hematoma) is localized bleeding from blood vessels into the brain parenchyma [5].

Subarachnoid hemorrhage is an accumulation of blood under the arachnoid mater of the brain [6].

Subdural hemorrhage (subdural hematoma) is an accumulation of extravasated blood or blood clots between the arachnoid mater and the inner surface of the dura mater [7].

Working group consists of two or more individuals of the same or different professions working collaboratively and in coordination to develop clinical practice guidelines and sharing joint responsibility for the outcomes of this work.

Level of evidence – reflects the degree of confidence that the observed effect of a medical intervention is true.

Level of recommendation confidence reflects not only the degree of certainty regarding the reliability of the intervention's effect, but also the degree of certainty that adherence to the recommendations will yield more benefit than harm in a specific clinical situation.

1. Brief information on the disease or condition

1.1 Definition of the disease or condition

Hemorrhagic stroke is a multi-etiological disease characterized by nontraumatic intracranial hemorrhage (NTICH).

Depending on the pattern of blood spread within the cranial cavity, the following forms of NTICH are distinguished:

subdural hemorrhage (subdural hematoma),

subarachnoid hemorrhage (SAH),

intracerebral hemorrhage (parenchymal, intracerebral hematoma (ICH)),

intraventricular hemorrhage (IVH).

In some cases, NTICH can be mixed (subarachnoid-parenchymal, parenchymal-ventricular, etc.) [8].

1.2 Etiology and pathogenesis of the disease or condition (group of diseases or conditions)

Causes of NTICH include various diseases and pathological conditions of the cerebral vascular system that can lead to arterial wall rupture.

The most frequent cause of so-called "spontaneous" NTICH is arterial hypertension (hypertensive NTICH), which leads to hypertensive angiopathy—vascular wall changes manifested by over-stretching, thinning, fibrinoid necrosis, miliary aneurysm formation, and dissection [9]. The arteries supplying the deep structures of the cerebral hemispheres are most commonly affected, and hemorrhages result in deep ICH formation. The second most common cause of cerebral artery rupture is amyloid angiopathy, which predominantly affects cortical arteries, with ICH localizing in the subcortical and cortical regions of the hemispheres.

NTICH may develop in various cerebrovascular diseases:

brain aneurysms (BA),

arteriovenous malformations (AVMs),

cavernous malformations (CMs),

dural arteriovenous fistulas (DAVFs),

moyamoya disease.

BAs are circumscribed dilations of cerebral arteries. They are classified as multifactorial diseases. Etiological factors include genetic factors leading to vascular wall alterations, as well as external triggers such as arterial hypertension, atherosclerosis, smoking, infection (mycotic aneurysms), etc. [10–18]. The role of genetic factors is most clearly evident in familial forms of the disease (7–20%) and the association of BAs with genetically determined connective tissue disorders (autosomal dominant polycystic kidney disease; Ehlers-Danlos syndrome type IV, etc.). BAs most typically manifest as SAH—aneurysmal SAH (aSAH) (90%), but ICH (up to 40%) and IVH (up to 20%) can also occur. The mechanism of hemorrhage is the rupture of the pathologically altered aneurysm wall.

AVMs are congenital vascular lesions consisting of a tangle of vessels in which feeder arteries and draining veins are connected directly without an intervening capillary bed (arteriovenous fistulas). AVMs result from impaired angiogenesis. In extremely rare cases, AVMs may form postnatally in the presence of pre-existing arteriovenous fistulas or venous thrombosis [2, 3]. In recent years, AVM development has been linked to mutations in various genes, though these are non-specific [19, 20]. AVMs are associated with hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu disease), in which they are detected 10 times more frequently than in the general population [21, 22]. AVMs typically present with hemorrhage forming an ICH, which is combined with SAH in 50% of cases and with IVH in 50% (mixed hemorrhages). The primary mechanism of hemorrhage is the rupture of arteries subjected to high pressure within the malformation's arteriovenous shunts.

Causes of NTICH can also include dural sinus and cerebral vein thrombosis, thrombophilia, coagulopathies, vasculitis, and vasculopathies. Hemorrhage may occur during anticoagulant therapy (ATC code B01A Antithrombotic agents), thrombolytic therapy, or eclampsia. Special forms of ICH include hemorrhage into a tumor and hemorrhagic transformation of an ischemic stroke via diapedesis.

1.3 Epidemiology of the Disease or Condition

Hypertensive intracerebral hemorrhage (hypertensive ICH) accounts for 10–15% of all stroke cases. In the Russian Federation (RF), approximately 40,000 hypertensive ICH cases are diagnosed annually. The mean patient age is 60–65 years, with a male-to-female ratio of 1.6:1. The risk of occurrence increases significantly after age 55 and doubles with each subsequent decade. Mortality reaches 40–50%, and disability develops in 70–75% of survivors. Risk factors include high blood pressure, alcohol abuse, a history of prior cerebrovascular events, and liver dysfunction accompanied by thrombocytopenia, hyperfibrinolysis, and reduced coagulation factors [8, 23, 24].

Aneurysmal subarachnoid hemorrhage (aSAH) accounts for 2–5% of all strokes, which corresponds to 10,000–15,000 patients per year in the RF. This figure should be distinguished from the significantly higher prevalence of BAs in the general population, which averages 2.8%. aSAH occurs most frequently between the ages of 30 and 50 years. Children account for about 3%, and elderly and senile patients for 8%. BAs are 1.5 times more common in women. aSAH carries a high risk of mortality (up to 60% if untreated) and disability (up to 30% of survivors) [25–27].

Hemorrhages from AVMs account for 1–2% of all strokes, with an estimated population prevalence of AVMs of 0.015%–0.14% [28, 29]. The disease typically manifests between 20 and 40 years of age [30]. The annual hemorrhage risk is 2–4% [31]. In patients who have suffered a hemorrhage, this risk accumulates over time, reaching 45% at 20 years. The risk of bleeding increases with deep AVM location, venous drainage into deep cerebral veins, and a history of prior hemorrhage. In the absence of these factors, the annual risk of malformation rupture is 0.9%, rising to up to 34% when they are combined [32]. The mortality rate following AVM hemorrhage averages approximately 20%. Aneurysms associated with AVMs—intranidal and on feeder vessels (proximal and distal)—are detected in 14% of AVM patients [33, 34]. Such aneurysms are the established cause of hemorrhage in 16% of AVM cases [35]. The risk of hemorrhage increases as the size of the associated aneurysms grows [36].

1.4 Features of Coding the Disease or Condition

I60 – Subarachnoid hemorrhage

I60.0 – Subarachnoid hemorrhage from carotid siphon and bifurcation

I60.1 – Subarachnoid hemorrhage from middle cerebral artery

I60.2 – Subarachnoid hemorrhage from anterior communicating artery

I60.3 – Subarachnoid hemorrhage from posterior communicating artery

I60.4 – Subarachnoid hemorrhage from basilar artery

I60.5 – Subarachnoid hemorrhage from vertebral artery

I60.6 – Subarachnoid hemorrhage from other intracranial arteries

I60.7 – Subarachnoid hemorrhage from intracranial artery, unspecified

I60.8 – Other subarachnoid hemorrhage

I60.9 – Subarachnoid hemorrhage, unspecified

I61 – Intracerebral hemorrhage

I61.0 – Intracerebral hemorrhage in hemisphere, subcortical

I61.1 – Intracerebral hemorrhage in hemisphere, cortical

I61.2 – Intracerebral hemorrhage in hemisphere, unspecified

I61.3 – Intracerebral hemorrhage in brain stem

I61.4 – Intracerebral hemorrhage in cerebellum

I61.5 – Intraventricular intracerebral hemorrhage

I61.6 – Intracerebral hemorrhage of multiple localizations

I61.8 – Other intracerebral hemorrhage

I61.9 – Intracerebral hemorrhage, unspecified

I62 – Other nontraumatic intracranial hemorrhage

I62.0 – Subdural hemorrhage (acute) (nontraumatic)

I62.1 – Nontraumatic extradural hemorrhage

Nontraumatic epidural hemorrhage

I62.9 – Intracranial hemorrhage (nontraumatic), unspecified

Q28.2 – Arteriovenous malformation of cerebral vessels

1.5 Classification of the disease or condition

Classification of hypertensive ICH

- by localization (5 variants) [37]:

1. Lobar – localized in a single brain lobe.

2. Lateral, or putaminal – hemorrhages into the subcortical structures of the cerebral hemisphere, lateral to the internal capsule. This is the most frequent type of hemorrhage.

3. Medial, or thalamic – the hematoma is located medial to the internal capsule.

4. Mixed – as a rule, massive hemorrhages in which the hematoma extends to multiple anatomical structures.

5. Hemorrhages in the posterior cranial fossa. ICH can form in the cerebellar hemispheres and in the brain stem, where localization at the pontine level is most typical.

Up to 90% of hemorrhages are localized in the cerebral hemispheres, with an approximately equal distribution of frequency among variants 1–4. In the posterior cranial fossa, ICH most frequently forms in the cerebellar hemispheres.

- by volume [38, 39]:

small – up to 20–30 ml,

moderate – from 30 to 50–60 ml,

large – over 60 ml.

The volume of ICH is of crucial importance for determining management strategy and predicting outcomes.

Classification of SAH

- by periods (three main ones) [40]:

1. Acute period – 14 days from the last SAH (the period during which patient deterioration most commonly occurs due to brain edema, vasospasm, and ischemia). This period includes the ultra-acute period (0–72 hours), when the patient's clinical manifestations are directly caused by the hemorrhage itself (prior to the onset of vasospasm).

2. Subacute period – 15–31 days from the last SAH (the period during which the main complications of SAH regress).

3. Cold period – 1 month or more from the SAH (the period when residual deficits related to the prior SAH may persist).

Classification of aneurysms [41–43]:

- by location: bifurcation and trunk cerebral aneurysms.

- by shape: saccular (about 90% of cerebral aneurysms, single- or multi-chambered) and fusiform.

- by number of cerebral aneurysms: single (80%) and multiple (20%).

- by size: miliary aneurysms (up to 2 mm inclusive), medium-sized (3–14 mm), large (15–24 mm), and giant cerebral aneurysms (25 mm and more).

90% of cerebral aneurysms are located in the anterior circulation of the brain, and 10% in the posterior circulation (vertebrobasilar system).

Classifications of arteriovenous malformations

About two dozen classifications have been proposed for evaluating AVMs. The most popular is the Spetzler-Martin (S-M) scale, named after the authors who proposed it in 1986 [44]. The scale is based on the evaluation of three AVM characteristics determined by angiography and head CT/MRI: 1) size, 2) location relative to eloquent cortex (sensorimotor, speech, and visual cortex, thalamus and hypothalamus, brainstem, and cerebellar nuclei), and 3) the pattern of venous drainage of the brain (Appendix G10). Based on the point score, five grades of surgical risk are distinguished.

Grade I–II (1–2 points) – low risk of neurological deficit, surgery is recommended;

Grade III (3 points) – moderate risk, surgery based on individual indications;

Grade IV–V (4–5 points) – high risk, conservative management is advisable.

Two modifications of this scale have also been proposed: the Spetzler-Ponce scale (Appendix G11), which divides patients into three risk categories [45], and the Lawton-Young scale, which M. Lawton developed based on the original S-M scale by adding three additional factors influencing treatment outcomes: age, history of hemorrhage from the AVM, and compactness of the AVM structure [46, 47] (Appendix G13). This scale has the highest prognostic accuracy. At a score of 6 points and above, the risk of disabling deficit or death from surgery is 39–63% [48].

For radiosurgical treatment of AVMs, the Radiosurgery Based AVM Score [49,50] (Appendix G15) and the Virginia Radiosurgery AVM Scale [51] (Appendix G14) are used.

1.6 Clinical presentation of the disease or condition

1.6.1 Clinical manifestations of hypertensive intracerebral hematoma

Clinical manifestations and the course of hypertensive ICH vary depending on its location, size, and rate of development [52]. Symptoms typically develop suddenly, usually during the day, amid physical exertion or emotional stress, but most commonly during routine daily activities. Neurological symptoms generally worsen over the course of several minutes or hours before and during hospitalization, reflecting early hematoma expansion or increasing brain edema [53]. A more frequent presentation is the gradual, smooth progression of symptoms over minutes and occasionally hours; a less frequent presentation is the abrupt onset of symptoms with a depressed level of consciousness within a few seconds. General cerebral symptoms are predominant; however, in elderly patients and/or with small hematomas confined to the cerebral white matter, general cerebral and meningeal symptoms may be mild or absent.

Decreased level of consciousness (about 50% of cases)

In extensive hemorrhages, the level of consciousness frequently decreases due to elevated intracranial pressure and compression of the thalamus and brainstem. As the hematoma volume increases, the level of consciousness drops to coma and death due to elevated intracranial pressure (ICP) and compression of brainstem centers.

Nausea and vomiting (40–50%)

Vomiting is a typical sign of ICH caused by increased intracranial pressure and distortion of brain structures. Vomiting is observed in approximately 50% of patients with lobar ICH and occurs even more frequently in patients with cerebellar hemorrhages. In patients with cerebellar hematomas, vomiting almost always occurs in the early stages of the clinical course.

Headache (about 40%)

Hemorrhage directly into the brain parenchyma, without involving the cerebrospinal fluid (CSF) space, is painless. Therefore, headache is not a mandatory symptom of ICH. Headache is more common in patients with large hematomas and is associated with meningeal traction, elevated intracranial pressure, and the presence of blood in the cerebrospinal fluid. Patients with small deep hematomas often experience no headache throughout the entire course of the disease. Headache may be the sole manifestation of hemorrhage in the region of the caudate nucleus, which is typically accompanied by intraventricular hemorrhage.

Seizures (up to 10%)

Seizures are observed in approximately 10% of patients with ICH and in about 50% of patients with lobar hematomas. Seizures typically occur at the onset of ICH or within the first 24 hours [54].

Focal neurological symptoms

About 40% of hypertensive ICHs occur in the basal ganglia, 30% in the thalamus, 20% are lobar, and about 10% occur in the cerebellum and pons [55]. The corpus striatum (caudate nucleus and putamen) is the most common site of origin for hypertensive ICH. With this location, hematoma formation causes deep contralateral hemiparesis and hemisensory disturbance, whereas thalamic hemorrhage is accompanied by more pronounced sensory deficits than motor deficits. Lobar hemorrhages may be accompanied by cortical dysfunction such as aphasia, neglect, body schema disorders, anosognosia, and hemianopia. As the hematoma increases in size, conjugate eye deviation toward the ICH may join (gaze palsy in the direction opposite to the hematoma). Oculomotor disorders, such as upward gaze palsy, convergence paralysis, unreactive constricted pupils, other cranial nerve palsies, and alternating syndromes, suggest a brainstem localization. In some cases, brainstem ICH immediately leads to coma and vital function disorders. Cerebellar hemorrhages are characterized by severe dizziness, nystagmus, sharp occipital pain, and ataxia. When a cerebellar ICH is of significant volume, direct compression of the brainstem occurs with involvement of brainstem nerves and pathways, impaired respiration and hemodynamics, or obstructive hydrocephalus with the development of tentorial herniation syndrome.

Meningeal signs in the first hours are predominantly represented by photophobia and Bekhterev's zygomatic sign. Later, nuchal rigidity, Kernig's, and Brudzinski's signs appear. In elderly patients, meningeal irritation is absent in 1/3 of cases.

Blood breakthrough into the ventricular system (isolated IVH or ICH breakthrough) occurs in half of the patients. IVH is characterized by hyperthermia and hypersalivation. Occlusion of the cerebrospinal fluid pathways is accompanied by the development of occlusive-hypertensive syndrome; massive IVH leads to impaired wakefulness, hormotonia, muscle hypotonia, respiratory and hemodynamic disorders.

Herniation syndrome develops with a significant volume of ICH, most often of temporal localization, and is accompanied by impaired wakefulness, anisocoria with mydriasis on the affected side, transition from hemispheric gaze palsy to brainstem palsy, respiratory and cardiovascular disorders [56].

1.6.2 Clinical manifestations of subarachnoid hemorrhage

Typical (70%) and atypical (30%) manifestations of SAH are distinguished.

In a typical onset of the disease, the main clinical symptom of SAH is a sudden, severe headache ("thunderclap headache"), which patients describe as "the worst headache of my life." Often, the headache is accompanied by vomiting, photophobia, short-term or prolonged loss of consciousness. Blood pressure is usually elevated. Initially, meningeal signs are associated with the spread of blood into the ventricular system. As the spilled blood spreads to the spinal cord level, neck pain and nuchal rigidity occur.

General cerebral and/or focal neurological deficits are found in more than 25% of patients. Depression of consciousness and confusion may be noted; patients with severe subarachnoid hemorrhage often present in a coma. Motor neurological deficits occur in 10-15% of patients, usually due to middle cerebral artery aneurysms. A characteristic sign of a supraclinoid ICA aneurysm is cranial nerve III palsy (ptosis, mydriasis). Increased intracranial pressure after rupture can cause abducens nerve palsy due to its compression. In some patients, the onset of SAH is accompanied by a seizure [57].

In 30% of patients with cerebral aneurysm ruptures, a masked or atypical clinical picture of SAH is observed (pseudomigraine, pseudohypertensive, pseudoinflammatory, pseudopsychotic, pseudotoxic, and pseudoradicular forms). In 40% of patients, no neurological symptoms are observed upon examination.

Approximately half of the patients show a mild or moderate increase in blood pressure.

1.6.3 Clinical manifestations of AVM rupture

AVM rupture in 97% of patients is accompanied by the development of general cerebral syndrome. Meningeal syndrome is observed in 88%: in 60% it is moderately pronounced, in 28% – severe. In 42% of patients with AVM rupture, consciousness is clear, in 44% there is a disturbance in the level of wakefulness to lethargy, in 14% – to stupor and coma. Limb muscle paresis is observed in 53%, plegia – in 21% [58].

Focal neurological deficits and depression of consciousness in hemorrhage from an AVM occur less frequently than in hemorrhage from aneurysms or ICH. This is due to the fact that ICH upon malformation rupture usually does not extend to the internal capsule, does not always have a large size, the course of the disease is rarely complicated by the development of vasospasm, and rupture of deep efferents often leads to isolated ventricular hemorrhages. In addition, the hematoma near the AVM core often pushes the brain parenchyma apart and does not damage its pathways. Patients with AVM rupture are younger, which contributes to their recovery [31, 59].

Focal neurological deficits develop more frequently in the presence of ICH (52%), less frequently – with isolated SAH (41%), and even less frequently – with isolated IVH (28%) [31].

In 28%, hemorrhage from an AVM clinically manifests only as general cerebral and meningeal syndromes without focal neurological deficits. Such a clinical picture requires differentiation from a cerebral aneurysm rupture. Evidence in favor of malformation rupture in such patients is the lesser severity of the meningeal syndrome (moderately pronounced in 65%), and in 20% of patients, changes in muscle tone, anisoreflexia, and the presence of pathological reflexes can be detected [58].

2. Diagnostics, medical indications and contraindications for diagnostic methods

The criteria for diagnosing hemorrhagic stroke are:

1) clinical data (acute development of general cerebral/focal symptoms),

2) CT/MRI data (detection of blood).

Based on the examination results, decisions on further management tactics are made [60].

The main diagnostic tasks in patients with hemorrhagic stroke are: establishing the cause of the hemorrhage, determining the localization and volume of the hemorrhage and the accompanying state of the brain (edema, herniation, secondary damage foci), and determining the severity of the patient's condition.

The diagnostic algorithm includes:

1) collection of complaints and anamnesis,

2) physical examination,

3) laboratory tests,

4) instrumental examinations.

Comment: the consultation is carried out no later than 60 minutes¹ from the moment of receiving the computed tomography results in a patient whose computed tomography or magnetic resonance imaging findings establish signs of hemorrhagic stroke.

¹ Order of the Ministry of Health of the Russian Federation No. 203n dated April 14, 2025 "On approval of criteria for assessing the quality of medical care"; (Registered with the Ministry of Justice of Russia on May 28, 2025, No. 82382); (http://publication.pravo.gov.ru/document/0001202505290045); entered into force on 01.09.2025

2.1 Complaints and Anamnesis

Complaints and medical history are described in the section "Clinical Presentation".

Patients with hemorrhagic stroke, if capable of verbal contact, usually complain of headache, nausea, vomiting, dizziness, as well as impaired functions corresponding to the brain lesion site (limb weakness, speech impairment, sensory disturbances, double vision, visual impairment, etc.). Anamnestically, it is established that the disease developed acutely against the background of elevated blood pressure. In the majority of patients, hemorrhage is preceded by long-standing, untreated arterial hypertension, urolithiasis, obesity, and diabetes mellitus.

Comments: when taking the anamnesis and complaints, it is necessary to pay attention to the timing and acuteness of symptom onset;

in a patient with an unclear history and impaired consciousness, traumatic brain injury and polytrauma should be ruled out [60].

2.2 Physical Examination

Physical examination findings are described in the "Clinical Presentation" section.

During a general examination, the level of consciousness, severity of the condition, and functions of vital organs and systems are assessed.

During a neurological examination, the presence of meningeal and focal symptoms (cranial nerve, cerebral hemisphere, and brainstem lesions) is assessed.

Comments: Glasgow Coma Scale (GCS) – see Appendix G4,

National Institutes of Health Stroke Scale (NIHSS) – see Appendix G17,

Canadian Neurological Scale – see Appendix G18,

Hunt-Hess scale – see Appendix G1,

WFNS scale – see Appendix G5,

modified Rankin scale – see Appendix G9.

Comments: Dysphagia is a frequent manifestation of stroke, which is a risk factor for aspiration pneumonia and is associated with higher mortality [69, 70]. Early screening for dysphagia in adult patients presenting with acute stroke reduces the risks of pneumonia, death, dependency on assistance, and prolonged hospital stay [68, 70].

Dysphagia assessment should be performed before the patient is given food or oral medications in the ICU.

Swallowing screening test (see Appendix G20).

If swallowing function testing is impossible or dysphagia is identified, placement of a nasogastric tube is indicated for nutritional support.

2.3 Laboratory Diagnostics

A patient with hemorrhagic stroke must undergo a number of laboratory tests, including a complete (clinical) blood count [71, 72], a general (clinical) urinalysis [73], a general general-medical blood biochemistry test [74], a coagulogram (exploratory study of the hemostatic system) [75], and a platelet aggregation study (if there is a history of antiplatelet drug use, except for heparin) [76, 77].

Comments: assessment of platelet count and mean platelet volume has prognostic value.

Comments: changes in the blood coagulation system towards hypocoagulation can be caused both by the disease (blood pathology, liver pathology, etc.) and by medications.

2.4 Instrumental Diagnostics

Comments:

The study must be performed within the first 40 minutes from the moment of hospitalization².

The volume of hemorrhage is determined either using the software supplied by the CT scanner manufacturer or by the ABC/2 formula, where A is the largest diameter, B is the perpendicular diameter to A, and C is the number of slices multiplied by the slice thickness. Patients in whom neuronavigation is planned to be used during surgery also undergo scanning in the mode required for subsequent image transfer to a specific navigation station [82, 83].

When performing CT (MRI), the following should be determined:

presence and topographic location of the pathological lesion(s);

volume of each type of lesion (hypo- and hyperdense parts);

position of the midline brain structures and the degree of their displacement in mm;

state of the cerebrospinal fluid-containing system of the brain (size, shape, position, deformation of the ventricles) with determination of ventriculocranial coefficients;

state of the brain cisterns;

state of the cerebral sulci and fissures.

The severity of subarachnoid hemorrhage (SAH) is assessed according to the Fisher scale (see Appendix G2) and/or the Hijdra scale (see Appendix G6). If concomitant intraventricular hemorrhage (IVH) is present, the Graeb scale is used (see Appendix G3).

Comments: subdural hematoma may be due to head trauma for which there is no information

Comments: if there are clinical and/or instrumental signs of brain herniation, lumbar puncture is contraindicated.

Comments: one of the listed types of angiography is performed. CTA for suspected non-traumatic hemorrhage should be performed from the aortic arch, including the main arteries of the head and neck, in the arterial and venous phases to rule out all types of vascular malformations and assess access to them. The sensitivity of CTA in detecting AVMs and aneurysms in the setting of hemorrhage is 84–100% with a specificity of 77–100% [90]. When performing CTA in patients with hemorrhagic stroke, the "spot sign" is often observed, caused by contrast medium extravasation. When CTA is performed within the first 3 hours from disease onset, the probability of this sign is 66%, decreasing to 13% after 6 hours [23]. The "spot sign" is a sign of increasing intracerebral hemorrhage volume and worsens disease outcome [91].

Comments: one of the listed types of angiography is performed.

Comments: in the case of the "spot sign", its configuration and density change due to the mixing of the contrast medium with the hematoma during the follow-up scan. In AVMs and aneurysms, this does not happen; their density corresponds to the density of adjacent normal arteries on both scans.

Comments:

The hemorrhage assessment using the SICH (secondary intracerebral hemorrhage score) was proposed by Almandoz J.E.D. et al. in 2010 (see Appendix G12) [93].

Risk factors for identifying vascular pathology in patients with intracerebral hemorrhage include: anatomical shape of the hemorrhage according to native CT data, young patient age, female sex, absence of arterial hypertension and coagulation disorders (see Appendix G12). When assessed using the SICH score at 0–2 points, the probability of vascular pathology is 3%, and at 3 points or more, it is 34%.

Malformations may not be detected on angiography due to their small size and compression by the hematoma [94, 95].

If no AVM is found on initial CTA or DSA, it is advisable to perform repeat CTA or DSA after resorption of the ICH to detect the malformation.

Angiographic risk factors for AVM rupture include stenosis and varicosity of efferent veins, exclusively deep venous drainage, a single efferent vein, venous reflux, and extra- and intranidal aneurysms [32, 96–98].

² Order of the Ministry of Health of the Russian Federation No. 203n dated April 14, 2025 "On Approval of Criteria for Assessing the Quality of Medical Care" (Registered with the Russian Ministry of Justice on May 28, 2025, No. 82382); (http://publication.pravo.gov.ru/document/0001202505290045); entered into force on September 1, 2025

2.5 Other Procedures

Comments:

The advantages of TCD include its non-invasive nature, speed and ease of performance, and the ability to perform serial examinations tracking blood flow velocity dynamics in the presence of cerebral vasospasm (CVS). If a decision is made regarding invasive treatment of CVS, DSA is required.

The Lindegaard index is the ratio of the mean blood flow velocity in the M1 segment of the MCA to the mean blood flow velocity in the extracranial portion of the ipsilateral ICA.

To characterize the presence and severity of CVS according to TCD data, it is advisable to calculate the mean blood flow velocity (MBFV) in the M1 segment of the MCA [27, 101]. At the same time, in the domestic neurosurgical school, calculating the Lindegaard index using systolic velocities is acceptable. The grades of CVS severity according to the Lindegaard index and systolic (mean) blood flow velocities are presented in Table 1.

Table 1. Grades of severity of cerebral vasospasm based on TCD data [27, 101]

Comments: for the Fisher scale, see Appendix G2.

Comments: in CT perfusion, a critical decrease in cerebral blood flow (CBF) in the territory of the spastic artery below 10–15 mL/100 g/min, cerebral blood volume (CBV) below 1–1.5 mL/100 g, and an increase in mean transit time (MTT) above 6 seconds are considered significant [27, 108].

3. Treatment, including drug and non-drug therapies, diet therapy, and pain management

3.1 Treatment of patients with hypertensive intracerebral hematoma

The management of hemorrhagic stroke is complex and not fully resolved. Existing published clinical trial results do not allow for definitive conclusions regarding the superiority of conservative versus neurosurgical treatment in terms of functional recovery during inpatient treatment or subsequent outpatient care. Clinical trial results for neurosurgical treatment indicate that it can prevent mortality in some patients, but its positive impact on the degree of subsequent disability has not been definitively established. The results of clinical trials of conservative treatments are also not entirely conclusive, which often hinders their practical application. What remains certain is that the patient must undergo treatment and rehabilitation in a medical institution that includes departments of neurosurgery, critical care and intensive care, and early rehabilitation.

3.1.1 Intensive care for patients with hypertensive intracerebral hematoma

Blood pressure management in hypertensive intracerebral hematoma

The safety and efficacy of lowering systolic blood pressure (SBP) within 7 days of symptom onset were evaluated in the ATACH [110], INTERACT [111], INTERACT2 [112], ATACH-II, and INTERACT3 [113] randomized clinical trials, as well as in a pooled analysis of patient data from the INTERACT2 and ATACH-II trials [114].

Comments: Blood pressure reduction within 6 hours of symptom onset in patients with intracerebral hemorrhage is associated with a lower risk of hematoma expansion. A meta-analysis of four randomized controlled trials involving 2,919 participants showed an odds ratio of 0.76 (95% CI 0.60–0.95) regarding hematoma growth. This indicates that early blood pressure lowering is an effective strategy for preventing hematoma expansion in intracerebral hemorrhage [115]. The results of the combined INTERACT2 and ATACH-II analysis showed that blood pressure reduction was linearly associated with an increased probability of a more favorable 90-day outcome (modified Rankin scale score of 0–2). In patients with SBP values exceeding 220 mm Hg, more aggressive blood pressure lowering may be justified [37, 114, 115]. According to INTERACT3, it is advisable to achieve a target SBP below 140 mm Hg within 1 hour of treatment initiation [113], but no faster than 60 mm Hg per hour [115]. Lowering SBP below 130 mm Hg is not recommended [113].

Body temperature control

Comments: it is advisable to reach a target body temperature of ≤37.5°C within 1 hour of treatment initiation and maintain it for 7 days [113].

Glycemic control

Comments: it is advisable to achieve target glycemic levels within 7 days [113].

Correction of hemostatic disorders in hypertensive intracerebral hematoma

Currently, due to the increasingly active use of anticoagulant therapy, particularly for the prevention of ischemic stroke, the number of hemorrhagic strokes occurring against the background of these drugs is increasing. In addition, hypertensive ICH may also occur against the background of antiplatelet therapy, as well as in patients with pre-existing hemostatic disorders. The regimen for reversing antithrombotic agents in patients with newly developed hypertensive ICH is presented in Appendix B2.

Comments: it is advisable to achieve the target INR level of <1.5 within 1 hour of treatment initiation and maintain it for 7 days [113].

In 2024, a parenteral form of vitamin K1 (phytomenadione; B02BA01) registered for use in patients became available in Russia as an emulsion for intravenous administration. Unlike the oral form, intravenous administration of phytomenadione (vitamin K1) increases clotting factor production within 1–2 hours and achieves maximum effect as early as 12 hours. In case of persistent INR elevation, administration of phytomenadione (vitamin K) can be repeated every 12 hours. In most patients with bleeding associated with VKAs, administration of phytomenadione (vitamin K1) is recommended to be started without waiting for laboratory tests and imaging data, as the risks associated with vitamin K1 administration are low [37].

Compared to fresh frozen plasma (FFP), blood coagulation factors II, VII, IX and X in combination [Prothrombin complex]** (B02BD01) may cause fewer complications, and their administration allows for a more rapid correction of INR [37, 116].

Administration of FFP requires not only time for blood transfusion preparation (thawing, cross-matching, etc.), but also the administration of a significantly larger volume (20 mL/kg), which often delays the normalization of INR and can take an average of up to 30 hours. In addition, the large volume of administered FFP increases the risks of fluid overload (especially against the background of concomitant cardiac pathology that originally required vitamin K antagonist therapy) and the development of transfusion reactions. The incidence of thrombotic complications is similar both with prothrombin complex concentrate therapy and FFP administration [117].

Comments: administration of recombinant coagulation factor VIIa** is not recommended, as it may lead to a decrease in INR but does not replace all necessary coagulation factors. In addition, it is characterized by a rapid half-life (2–3 hours), after which a repeat dose or another drug will be required [117].

Comments: The frequency and doses of administration are calculated individually based on the patient's body weight and INR value. It is advisable to consider administering 25–50 IU/kg depending on the INR value with subsequent re-evaluation [37, 119, 120]. At the same time, the maximum single dose should not exceed the recommended dose for each individual drug within the group of coagulation factors II, VII, IX and X in combination [Prothrombin complex]** (B02BD01).

Comments: against the background of therapeutic doses of heparin sodium** (B01AB01), intravenous administration of protamine sulfate** (V03AB14) is indicated, which is injected as a bolus at a rate of 1 mL (10 mg) of solution over 2 minutes. If necessary, injections are repeated at intervals of 15–30 minutes; the total dose is usually 5 mL (50 mg) of solution, administered over 10 minutes. No more than 150 mg should be administered within 1 hour. An alternative method for calculating the required dose is the administration of 1 mg of protamine sulfate** per 100 units of UFH, taking into account the half-life of heparin sodium** (from 1 to 2 hours). Protamine sulfate** should be administered by slow intravenous infusion not exceeding 20 mg/min (due to the risk of anaphylactic reactions). Neutralization of intravenously administered heparin sodium** (UFH) occurs on average 5 minutes after administration and persists for 2 hours. Subcutaneously administered heparin sodium** (UFH) is characterized by a more prolonged effect due to slow absorption from the subcutaneous adipose tissue [119]. Reversal of a prophylactic dose of subcutaneous heparin sodium** (UFH) is not indicated [116].

Comments: Unlike UFH (heparin sodium**), protamine sulfate** is less effective in reversing the effect of LMWHs because it does not bind to short carbohydrate chains of LMWHs, but it can neutralize higher molecular weight fractions, which are believed to be more frequently associated with bleeding [104]. Thus, protamine sulfate** (V03AB14) effectively inhibits the effect of LMWHs on FII, but only partially inhibits their effect on FX. The following dosing regimen for #protamine sulfate** is recommended: for enoxaparin sodium** (B01AB05) administered within the previous 8 hours – 1 mg of #protamine sulfate** per 1 mg of enoxaparin sodium**; administered more than 8 hours ago – 0.5 mg of #protamine sulfate** per 1 mg of enoxaparin sodium**. For dalteparin sodium** (B01AB04) and nadroparin calcium (B01AB06) – 1 mg of #protamine sulfate** per 100 anti-Xa IU [116].

Reversal is indicated only for therapeutic, but not prophylactic doses of LMWHs [116]. However, in a number of clinical situations associated with impaired LMWH elimination and drug accumulation, a therapeutic effect has been identified with prophylactic dosages [117]. Therefore, a personalized approach to LMWH dosing, based inter alia on laboratory monitoring, is increasingly taking a prominent place.

The presence and severity of the anticoagulant effect against the background of LMWHs can be determined by anti-Xa levels. Reversal of LMWHs in ICH is indicated at anti-Xa ≥0.3 and/or the occurrence of ICH less than 12 hours from the last LMWH administration.

Comments: The potential positive effect of platelet transfusion in hypertensive ICH has not been established. An important issue in reversing the effect of antiplatelet agents, other than heparin, is the laboratory assessment of their efficacy, since, according to various data, some patients have resistance to acetylsalicylic acid** and clopidogrel**. Irreversible inactivation of cyclooxygenase by acetylsalicylic acid** means that it exerts a prolonged pharmacodynamic effect and inhibits platelets for the remainder of their lifespan (up to 10 days). However, acetylsalicylic acid** has a very short pharmacokinetic half-life, so the drug remains in the circulation for only a few minutes. Consequently, platelet transfusion may be advisable in the management of bleeding associated with acetylsalicylic acid**, since new platelets will not be exposed to acetylsalicylic acid**. The 2016 guidelines suggest performing platelet transfusion in patients with ICH on acetylsalicylic acid** who are scheduled for neurosurgery. Following the discontinuation of irreversible P2Y12 inhibitors (clopidogrel** (B01AC Platelet aggregation inhibitors excluding heparin), prasugrel (B01AC Platelet aggregation inhibitors excluding heparin)), the recovery of normal platelet function will occur only with the synthesis and release of new platelets into the bloodstream. When platelets are transfused less than 3–5 half-lives of P2Y12 inhibitor drugs (clopidogrel** (B01AC Platelet aggregation inhibitors excluding heparin), prasugrel (B01AC Platelet aggregation inhibitors excluding heparin)), pharmacological inhibition of the transfused platelets will be observed, and the presence of active metabolites of the drug may lead to even more prolonged platelet inhibition. Thus, in ICH on the background of P2Y12 inhibitors (clopidogrel** (B01AC Platelet aggregation inhibitors excluding heparin), prasugrel (B01AC Platelet aggregation inhibitors excluding heparin)), it is recommended to refrain from platelet transfusion even in the context of impending neurosurgical intervention [117].

Comments:

The administration of #tranexamic acid** (B02AA02) (1 g IV bolus + 1 g IV infusion over 8 h) may be considered in patients with hypertensive ICH within 4.5 hours of symptom onset and at high risk of hematoma expansion in order to reduce the final ICH volume [121]. A high risk of hematoma expansion in addition to the time window of up to 4.5 hours from symptom onset is associated with the following CT/CTA neuroimaging signs:

1. Lobar hemorrhages (especially those associated with amyloid angiopathy)

2. Hematoma volume >30 ml or with rapid enlargement (>33% or >6 ml within 24 hours)

3. Specific features:

   - "Spot sign" – punctate foci of contrast extravasation within the hematoma on CTA.

   - "Black hole sign" – a hypodense area within a hyperdense hematoma on unenhanced CT.

   - "Blend sign" – a combination of areas of varying density within the hematoma.

   - "Island sign" – small, separate foci of hemorrhage surrounding the main hematoma.

Tranexamic acid** (B02AA02) in spontaneous intracerebral hemorrhage compared with placebo or open-label control had no statistically significant effect on mortality or dependence at 90 days, nor on 90-day mortality; however, tranexamic acid** (B02AA02) to some extent prevented hematoma growth at 24 hours compared with placebo or open-label control [121].

Management of cerebral edema and elevated intracranial pressure in patients with hypertensive intracerebral hematoma

The course of hypertensive ICH is significantly affected by the development of cerebral edema, which may also be accompanied by an increase in ICP. This requires measures for their management.

Comments: The effect of #mannitol** (B05BC) was studied in a subanalysis of the INTERACT2 patient cohort, which included 2,839 patients [124]. Its administration was safe, and the incidence of adverse events in the subgroup of patients receiving #mannitol** (B05BC) did not exceed that in patients not receiving #mannitol** (B05BC).

Prevention of lower extremity venous thrombosis and thromboembolic complications

One of the important factors influencing the course of the acute period of hypertensive ICH is the risk of deep vein thrombosis of the lower extremities and thromboembolic complications (VTE), which is particularly high in patients with severe motor impairments or those who are immobile due to other reasons. VTE prevention in hypertensive ICH presents a particular challenge, requiring an assessment not only of the VTE risk itself, but also of the risk of re-bleeding [128].

Comments: The use of lower extremity elastic compression alone does not reduce the risk of deep vein thrombosis or improve disease outcomes [129]. A prospective randomized trial comparing intermittent pneumatic compression combined with medical compression stockings versus the use of stockings alone showed a significant reduction in the risk of deep vein thrombosis [130]. However, the use of medical compression stockings may cause skin damage [131].

Before initiating intermittent pneumatic compression, it is justified to perform duplex scanning of the lower extremity veins to rule out pre-existing deep vein thrombosis.

Comments: The recommended dose of #enoxaparin sodium** (B01AB05) is 40 mg once daily subcutaneously. Doses are calculated individually based on the patient's body weight. According to a meta-analysis including 1,000 ICH patients from 4 studies, 2 of which were randomized [133], early administration of #enoxaparin sodium** (B01AB05) or #heparin sodium** (B01AB01) preparations (1–6 days after admission) was associated with a statistically significant reduction in the incidence of pulmonary embolism and a slight increase in hematoma volume. An individualized approach is required, taking into account the surgical intervention and the patient's clinical status, with mandatory monitoring of hemostasis and neurological dynamics.

Resumption of antithrombotic therapy in patients who have developed a hypertensive intracerebral hematoma

Patients who have suffered a hypertensive ICH and have been receiving antiplatelet/anticoagulant therapy for other conditions or for the prevention of cardiovascular and cerebrovascular disease, and who have indications for the resumption of such therapy, should be considered as candidates to resume the appropriate treatment [134].

Comments: the timing of resumption should be determined individually in each case [134]. Existing data are insufficient to definitively determine the optimal timing for resuming antiplatelet therapy. When administered, the risk of recurrent hemorrhage was significantly lower than the positive effect of secondary prevention of acute cerebrovascular accidents.

Comments: the optimal timing for resuming antithrombotic therapy is unknown. Clinical studies are currently underway to identify patient groups in whom resumption of antithrombotic therapy will be feasible.

3.1.2 Surgical treatment of patients with hypertensive intracerebral hematoma

Surgical treatment is aimed at removing the ICH, eliminating brain compression and displacement, and resolving obstructive hydrocephalus [139,141–145].

Conditions for surgical treatment of hemorrhagic stroke

To perform surgical interventions, the operating room must be equipped in accordance with current regulations. Minimally invasive surgeries, such as:

puncture aspiration (A16.23.015 Puncture of brain hematoma, A16.23.017 Removal of brain hematoma),

local fibrinolysis (A16.23.017.001 Closed drainage of brain hematoma using fibrinolytic agents),

endoscopic aspiration (A16.23.015 Puncture of brain hematoma, A16.23.017 Removal of brain hematoma)

can be performed under locoregional anesthesia (B01.003.004.002 Regional block anesthesia).

Risk factors for an unfavorable outcome in surgical treatment include [8, 142, 143]:

- decrease in wakefulness to stupor and below;

- intracerebral hematoma volume greater than 50 cm³;

- massive ventricular hemorrhage;

- midline shift of 10 mm or more;

- deformation of the brainstem cisterns;

- rebleeding.

Indications and contraindications for surgical treatment

Comments: The advisability of surgical removal of hypertensive thalamic hematomas with a volume greater than 10 cm³ and brainstem hematomas accompanied by severe neurological deficit is under discussion, and neurosurgeons have not yet reached a consensus on this matter [141].

Comments: In comatose patients, outcomes do not depend on the treatment method (intensive care or surgical intervention) [146].

Comments: A relative contraindication to surgery is the presence of severe somatic pathology (diabetes mellitus, sub- and decompensated renal, hepatic, cardiovascular, and pulmonary pathology, coagulopathies, sepsis) [8].

Selection of surgical timing

Comments: If the patient's condition is compensated, wakefulness is normal or depressed no deeper than lethargy, there are no signs of progressive brain compression, but blood pressure values are high (systolic above 200 mm Hg), it is advisable to postpone surgery until blood pressure is lowered and stabilized to avoid difficulties with intraoperative hemostasis and postoperative hematoma recurrence. In some cases, the hematoma may continue to form during the first 24 hours and is prone to recurrence, therefore surgical removal of hematomas in the first 24 hours is associated with an increased risk of rebleeding [144, 151, 152].

Surgical treatment methods

Some procedures can be supplemented with local fibrinolysis (A16.23.017.001 Closed drainage of brain hematoma using fibrinolytic agents). If it is used, taking into account the use of off-label drugs, a medical committee meeting is required, indicating the necessity of this type of treatment for life-saving indications. The most studied drug for local fibrinolysis in the Russian Federation is recombinant #prourokinase**. The average single dose is 50,000 IU, and the exposure time is 6-12 hours [160,161].

Comments:

For basal ganglia ICH with a volume greater than 25-30 cm³, surgical intervention reduces mortality and improves functional outcomes [143, 155, 156].

Surgery may be supplemented with local fibrinolysis (A16.23.017.001 Closed drainage of brain hematoma using fibrinolytic agents) [8,147,161].

Comments: In subcortical hemorrhages, microsurgical exploration of the hematoma cavity is necessary to remove a potential angiographically occult malformation, the incidence of which can reach 30% [157, 158].

Comments: A mandatory condition in this case is total selective cerebral angiography to rule out vascular malformation.

In subcortical ICH with a volume of more than 25–30 cm³, surgical intervention helps reduce mortality and improve functional outcomes [142, 153, 159].

The surgery may be supplemented by local fibrinolysis (A16.23.017.001 Closed drainage of cerebral hematoma using fibrinolytic agents).

Comments: In complete tamponade of both lateral ventricles, it is recommended to place two external ventricular drains into the frontal horns and administer a dose of 50,000 IU of recombinant #prourokinase** into each ventricle.

3.1.3 Postoperative management of patients with hypertensive intracerebral hematoma

After surgery, the patient is admitted to the neuro-ICU/step-down unit (see section 3.1.1. Intensive care of patients with hypertensive intracerebral hematoma).

3.2 Treatment of patients with aneurysmal subarachnoid hemorrhage

3.2.1 Intensive care for patients with aneurysmal subarachnoid hemorrhage

Preoperative management and treatment of patients with subarachnoid hemorrhage

The goals of conservative treatment in preoperative SAH patients are stabilizing their condition, preventing SAH recurrence, and preventing and treating cerebral vasospasm and ischemia.

General recommendations

Comments: In case of persistent fever, an infectious origin must be ruled out. Fever should be managed pharmacologically or using external cooling systems.

Comments: duration of use should not exceed 7 days.

Comments: Dosage regimen:

low-intensity therapy: monotherapy: levetiracetam** at a dose <2000 mg/day (<1000 mg/day in renal impairment), valproic acid** at a dose ≤15 mg/kg/day or average level <75 µg/mL;

high-intensity therapy: for more than 48 hours, levetiracetam** at a dose ≥2000 mg/day (≥1000 mg/day in renal impairment), valproic acid** at a dose >15 mg/kg/day or average level ≥75 µg/mL;

duration of use should not exceed 7 days.

Prevention of rebleeding

Prevention of respiratory disorders

Normalization and stabilization of systemic hemodynamic parameters.

Prevention of cerebral vasospasm and brain ischemia

Comments: If the patient develops arterial hypotension, consider discontinuing the drug.

The use of other calcium channel blockers, as well as alternative routes of administration (intravenous), is not recommended [27, 177].

3.2.2 Surgical treatment of patients with aneurysmal subarachnoid hemorrhage

Indications for surgery (impact of patient status)

Comments: in isolated cases, the decision to perform surgery in severe patients is made by a medical board.

Timing of surgery

Comments: in patients with complex aneurysms (giant, fusiform, vertebrobasilar, and paraclinoid localization), preoperative preparation may take longer. If surgical care cannot be provided at the site of diagnosis verification, the patient should be transferred to tertiary medical centers with neurosurgical and endovascular capabilities for emergency indications.

Choice of Surgical Treatment Method

There are 2 alternative treatment methods for cerebral aneurysms – microsurgical and endovascular. The choice of treatment method depends on the technical equipment of the center and the level of development of each technique within it [27,186,192–200].

Comments: if for any reason microsurgical intervention cannot be performed, the possibility of endovascular intervention should be considered.

Comments: if for any reason endovascular intervention cannot be performed, the possibility of microsurgical intervention should be considered.

Surgeries in Patients with Multiple Aneurysms

Comments: The feasibility of excluding all aneurysms from the bloodstream in a single surgical procedure or in multiple stages, including a combination of microsurgical and endovascular interventions, is decided individually in each specific case.

Direct Microsurgical Interventions for Aneurysms in the Acute Period

Comments: if the parent artery is sacrificed along with the aneurysm, the decision regarding the need for an additional revascularization surgery or mandatory decompressive craniectomy is made by the operating surgeon depending on the specific situation.

Comments: the feasibility of simultaneous microsurgical exclusion of aneurysms in the acute period of hemorrhage is determined by the surgeon during the operation, taking into account the state of the brain, the severity of hemorrhage, etc.

Control of Microsurgical Efficacy

Comments: The absence of bleeding will indicate the complete exclusion of the aneurysm sac.

Comments: in the postoperative period following microsurgical clipping of an aneurysm, control angiographic examinations (CTA or DSA) are performed to assess the state of the neck and confirm the radicality of clipping [16, 181, 201]. CTA is a minimally invasive method with a lower radiation dose; it requires a 64-slice or higher CT scanner. DSA is a more invasive method and is indicated when CT angiography cannot be performed [209]. If technically feasible, it is recommended to perform CTA with metal artifact reduction software to minimize artifacts from the clip for precise visualization of arteries in the clip zone [210].

Intraoperative sanation of the basal cisterns

Comments:

modified Fisher scale – see Appendix G2;

Hijdra scale – see Appendix G6;

when using off-label drugs, a medical panel (consilium) must be convened, indicating the necessity of this treatment type for life-saving reasons!

Comments: when administering a fibrinolytic intraoperatively (ATC: B01AD Enzymes), the procedure should be performed after the ruptured aneurysm has been excluded from the circulation. Visual control of hemostasis efficacy should be performed at the end of the microsurgical stage.

Comments: for intraoperative irrigation of the basal cisterns, the fibrinolytic agent (ATC: B01AD Enzymes) should be diluted in 10 ml of sodium chloride** physiological solution. For postoperative administration of the fibrinolytic (ATC: B01AD Enzymes) into the cisternal drain, it should be diluted in 5 ml of sodium chloride** physiological solution.

Comments: cisternal drainage should be discontinued when the erythrocyte count in the clinical CSF analysis drops below 10,000 cells/µl

Endovascular procedure

Comments:

The evaluation is performed according to the Raymond Roy classification (see Appendix 19) [221].

Incomplete aneurysm occlusion (Raymond Roy class II–III) is considered sufficient in the absence of contrast opacification of the suspected aneurysm rupture site (aneurysm dome, diverticula) and acceptable if the medical facility where the patient was hospitalized lacks the necessary consumables. Repeat more complete embolization is performed in the delayed period. If the high risk of rerupture persists, the patient is indicated for transfer to a specialized federal center.

Comments: Balloon assistance (or supportive endovascular vessel occlusion using a balloon – A16.12.041.003 according to the Ministry of Health nomenclature) should be used when it is impossible to achieve a stable position of the vascular microcatheter in the aneurysm, when forming a tight complex of endovascular microcoils in the aneurysm is difficult, when cerebral vessel angioplasty is required, or when there is a high risk of intraoperative aneurysm rupture. Alternative techniques allowing the formation of a stable endovascular microcoil complex in the aneurysm may be used: the double-catheter technique and temporary remodeling devices. Parent artery deconstruction is possible provided there is adequate collateral blood flow [194, 222–224].

Comments: the use of an assisting uncovered metal intracranial vascular stent*** in the acute period of aneurysm rupture in tertiary care medical centers is permitted, provided all potential sources of intracranial hemorrhage are completely eliminated and open surgery is not required. Implantation should be performed against the background of intravenous administration of glycoprotein IIb/IIIa receptor inhibitors (ATC B01AC Platelet aggregation inhibitors excluding heparin), followed by a switch to oral antiplatelet agents excluding heparin after surgery. Discontinuation of IIb/IIIa blockers (ATC B01AC Platelet aggregation inhibitors excluding heparin) is allowed no earlier than 2–4 hours after starting dual antiplatelet therapy [225–227].

Monitoring the efficacy of endovascular surgery

Comments: if there are prerequisites for early life-threatening recanalization of the treated aneurysm, a follow-up examination may be performed promptly.

MRA of intracranial arteries is a non-invasive imaging method that does not require contrast administration; it requires a facility equipped with a magnetic resonance imager of at least 1.5 Tesla.

CAG is a more invasive method indicated when MRA cannot be performed [228].

Other surgical interventions in the acute period of subarachnoid hemorrhage

External ventricular drainage placement

Comments: An external ventricular drain (EVD) (Neurosurgical system for external drainage, CSF drainage and monitoring) is placed from the standard Kocher's point into the hemisphere contralateral to the main surgical approach. It is advisable to place the EVD (Neurosurgical system for external drainage, CSF drainage and monitoring) in a single operation, as a first stage prior to craniotomy and aneurysm clipping.

In the case of an endovascular intervention, an EVD (neurosurgical system for external drainage, CSF drainage and monitoring) is placed in the operating room immediately after aneurysm occlusion, prior to the patient's emergence from general anesthesia.

If endovascular surgery involves planned stenting and administration of antiplatelet agents in addition to heparin, the EVD (neurosurgical system for external drainage, CSF drainage and monitoring) should be placed before the procedure following induction of anesthesia.

Comments: the systemic antibacterial drug and its dose are determined by internal protocols approved at the hospital.

Decompressive craniectomy

Primary (performed during aneurysm clipping surgery) and secondary (performed in a delayed manner) decompressive craniectomy (DC) are distinguished.

Comments: when performing decompressive craniectomy, adhere to the following surgical parameters [15,242–244]:

DC is performed on the side of the hemisphere with the most prominent edema;

frontotemporoparietal craniectomy is optimal;

the dimensions of the DC should be 12–15 cm in the anteroposterior direction;

resection of the temporal bone squama down to the middle cranial fossa base is mandatory;

an important condition for DC is duraplasty to expand the subarachnoid space for the edematous brain, which is achieved by suturing in a periosteal graft or artificial dura mater substitutes;

watertight closure of the dura mater during plasty reduces the risk of postoperative CSF leakage;

during the surgery, it is advisable to avoid opening the frontal sinus and air cells of the temporal bone and to ensure reliable stepwise and definitive hemostasis.

Intracranial pressure monitor placement

Anesthetic management for surgeries in the acute period of aneurysmal subarachnoid hemorrhage

Goals of anesthesia during surgeries for cerebral aneurysms in the acute period:

A. patient anesthesia and analgesia during surgery;

B. prevention of re-rupture of the aneurysm at all stages of surgery until the aneurysm is obliterated;

C. provision of brain relaxation to facilitate the surgical procedure and reduce retraction injury to the brain parenchyma;

D. maintenance of adequate cerebral perfusion for the prevention of cerebral ischemia;

E. prevention of postoperative pain, nausea, and vomiting.

General recommendations

Comments: Intravenous general anesthetic agents, in particular propofol** (N01AX10), provide a lower ICP level, which may translate into less brain tissue tension and more favorable working conditions for the neurosurgeon. In addition, propofol** (N01AX10) exhibits antiepileptic and antiemetic activity [246–248].

Comments: it is preferable to administer the drugs into a central vein at a high rate (over 10–15 min). Infusion should be initiated at the moment of the skin incision.

Comments: a stable $ ext{PaCO}_₂$ level ensures stable cerebral blood volume and stable ICP; normoventilation leaves a reserve for potential ICP reduction via hyperventilation. It is important to consider that in the presence of impaired cerebral autoregulation under conditions of vasospasm in patients with severe SAH, even a minor increase in $ ext{PaCO}_₃$ leads to a spike in ICP. For this reason, periods without ventilation (during intubation or emergence) should be as short as possible.

Comments: Comments: if thromboelastography (TEG, ROTEM) is not available, the hemostatic system can be assessed by determining the activated partial thromboplastin time (aPTT), prothrombin time, and blood fibrinogen level

Systemic Hemodynamic Management

Comments: Given the high incidence of hypovolemia, forced infusion therapy may be required as early as the beginning of surgery.

Comments: initiating an infusion of cardiotonic drugs (ATC C01CA Adrenergic and dopaminergic agents) (e.g., norepinephrine** (C01CA03)) when mean arterial pressure persistently drops below 60–65 mm Hg helps reduce the risk of damage to ischemia-sensitive organs (brain, heart, kidneys). It is especially important to prevent hypotension during temporary arterial clipping. When performing intraoperative ICP monitoring, target a cerebral perfusion pressure (CPP) of at least 60 mm Hg.

Comments: it is advisable to avoid a sustained increase in systolic blood pressure above 160–180 mm Hg intraoperatively, correcting hypertension with calcium channel blockers (e.g., nimodipine**) (C08CA), alpha-adrenoceptor blockers (e.g., urapidil**) (C02CA), organic nitrates (C01DA), etc., taking into account the need to maintain CPP sufficient for brain perfusion.

3.2.3 Postoperative management of patients with aneurysmal subarachnoid hemorrhage after aneurysm clipping/coiling

The main goals of intensive care in patients after aneurysm occlusion are the correction of postoperative complications (cerebral and somatic). The most frequent cerebral causes of a severe postoperative course are progressive cerebral vasospasm, delayed cerebral ischemia and cerebral edema, and the development of resorptive hydrocephalus. Patient management and treatment after surgery follow the same principles as before surgery, but with certain specific features.

Basic Principles of Intensive Care

Prevention of Lower Extremity Vein Thrombosis and Venous Thromboembolism

Comments: The decision on the exact timing of starting anticoagulant prophylaxis and the choice of dose is determined individually, taking into account the specific features of the neurosurgical intervention.

Management of Systemic Hemodynamic Parameters and Volemia after Aneurysm Occlusion

Correction of Anemia

Respiratory Support

Control of Blood Sodium Concentration

Comments: Hyponatremia can develop both as a result of the syndrome of inappropriate antidiuretic hormone secretion (SIADH) and cerebral salt-wasting syndrome (CSW) [279]. Patients with SIADH are euvolemic, and hyponatremia develops against the background of water retention. Fluid restriction is undesirable in patients with aneurysmal SAH. In CSW, hyponatremia is caused by Na losses against the background of excessive secretion of natriuretic peptides. CSW is characterized by an increased rate of diuresis. The main difference between SIADH and CSW is the increased diuresis rate in CSW.

Execution of External Ventricular Drainage

Comments: EVD insertion (Neurosurgical system for external drainage, CSF drainage and monitoring) is performed under sterile operating room conditions, a burr hole is made at standard points (Kocher's point, Dandy's point), puncture of the anterior or posterior horn of the lateral ventricle is performed, the ventricular end of the catheter is inserted to a depth of 5–7 cm, the outer end of the catheter is brought out through a stab incision, secured to the skin with sutures, and connected to a sterile CSF collector (lumbar reservoir) [283]. See section "Insertion of External Ventricular Drainage".

Prevention and Treatment of Cerebral Vasospasm and Cerebral Ischemia

Tactics for conscious patients with a stable neurological status

Management of neurological deterioration in conscious patients

Comments: Differential diagnosis between cerebral vasospasm and delayed cerebral ischemia is based on:

a. Clinical presentation: delayed cerebral ischemia is defined as the onset of new focal neurological deficits or a decrease of at least 2 points on the Glasgow Coma Scale (either in the total score or in any of its individual components, such as eye opening, verbal response, or motor response on either side). This must last for at least 1 hour, not be apparent immediately after aneurysm occlusion, and not be explained by other causes [273, 274].

b. Neuroimaging methods: brain CT, CTA, brain CT perfusion, DSA. Manifestations of cerebral vasospasm and ischemia will be confirmed by areas of decreased density corresponding to specific vascular territories on CT, hypoperfusion zones on brain CT perfusion (cerebral blood flow <25 mL/100 g/min, cerebral blood volume <1.5 mL/100 g, and/or mean transit time >6.5 seconds), and visualization of cerebral vasospasm on CTA or DSA. Severe angiospasm is defined as narrowing of at least 70% compared to the baseline level on DSA or CTA angiograms [106, 274, 275]. Other causes of deterioration are also excluded: intracranial hematoma, hydrocephalus, etc.

c. Emergency TCD: an increase in mean blood flow velocity in the MCA by more than 50 cm/s within 24 hours, mean LBFV exceeding 200 cm/s in the MCA, or a Lindegaard index >6 [287].

Management in unconscious patients and/or during sedation

Comments: indirect signs of worsening cerebral vasospasm and delayed cerebral ischemia in an unconscious (sedated) patient include: a decrease in the neurological status score on the GCS by 1 or more points, the appearance of pupillary asymmetry, any additional focal neurological deficit, Cushing's triad, and elevated ICP if monitoring is in place.

Cerebral vasospasm and the development of delayed cerebral ischemia are confirmed by:

A. TCD

B. Neuroimaging methods: brain CT, SCT angiography, SCT perfusion, DSA.

Hyperdynamic therapy for cerebral vasospasm and delayed cerebral ischemia

Considered as the first-line treatment for cerebral vasospasm and delayed cerebral ischemia [288]. It involves increasing mean arterial pressure (MAP) to improve cerebral perfusion. Therapy includes the use of vasopressors (ATC C01CA Adrenergic and dopaminergic agents) (norepinephrine** (C01CA)), while maintaining euvolemia with a combination of crystalloid (B05BB Solutions affecting the electrolyte balance) or colloid (B05AA Blood substitutes and plasma protein fractions) solutions (human #albumin** solution (B05AA)) [17, 184].

If cardiac output decreases, it is recommended to use inotropic agents (dobutamine** (C01CA)), in the absence of an effect from isolated vasopressor use (ATC C01CA Adrenergic and dopaminergic agents) or decreased cardiac output. Hyperdynamic therapy may lead to pulmonary hypertension, pulmonary edema, patient hypervolemia, myocardial contractility impairment, and cardiac arrhythmias. Echocardiography is necessary when cardiac complications are suspected. An elevated troponin level, as well as electrocardiographic signs of ischemic injury, are grounds for immediate correction of target MAP parameters and consultation with a cardiologist.

Recommended hyperdynamic therapy algorithm:

Comment: recommended doses for 25% human #albumin**: 0.625 g/kg/day for 7 days; 1.25 g/kg/day for 7 days; 1.875 g/kg/day for 7 days; 2.5 g/kg/day for 7 days

Endovascular treatment of cerebral vasospasm via intra-arterial administration of calcium channel blockers after aneurysm clipping/coiling

Comments: Signs of severe cerebral vasospasm: mean linear LBFV in the M1 segment of the MCA according to TCD data greater than 200 cm/s or a Lindegaard index >6; appearance of focal neurological deficit and decreased level of consciousness.

Comments: Considering the use of off-label drugs a medical board (consilium) must be held indicating the necessity of this type of treatment for life-saving indications!

Comments: The following are used for therapy: #verapamil** (C08DA01) 0.25 mg/mL (5 mg per 25 mL of 0.9% sodium chloride** (B05BB01)) at an average rate of 10 mL/min or #nimodipine** (C08CA06) 0.01 mg/mL (after dilution in 0.9% sodium chloride** (B05BB01)). Infusion into the ICA is performed slowly. The infusion rate depends on hemodynamic parameters and ICP.

The procedure of intra-arterial administration of calcium channel blockers may be repeated multiple times, according to indications and depending on the patient's condition, with an interval of at least 8 hours.

Comments: Intraarterial administration of CCBs is accompanied by a temporary (10–30 min) increase in ICP, which normalizes spontaneously. In patients with ICP exceeding 18 mm Hg, the procedure carries a risk of axial shift (herniation). If the patient is undergoing medicinal sedation at the time of the procedure, intraoperative ICP monitoring is indicated. If ICP rises above 18–20 mm Hg, osmotherapy and/or placement/opening of an external ventricular drain (Neurosurgical system for external drainage, CSF drainage and monitoring) may be required. If high ICP cannot be controlled, the intraarterial calcium channel blocker administration procedure is terminated.

Comments: The criteria for terminating intraarterial CCB administration are the presence of at least two of the following factors:

A. Improvement in the patient's neurological status.

B. Decrease in mean flow velocity (MFV) according to transcranial Doppler sonography (TCD) (below 200 cm/s).

C. Absence of cerebral vasospasm progression noted upon comparison of at least two consecutive angiographic studies.

Intracranial hypertension in patients with aneurysmal subarachnoid hemorrhage

Intracranial pressure monitoring

The causes of intracranial hypertension in patients with aneurysmal SAH include: mass effect exerted by the extravasated blood, hydrocephalus, and delayed cerebral ischemia [296].

Immediate EVD placement and cerebrospinal fluid drainage (A16.23.001 Ventricular puncture of the brain, A16.23.047 External drainage of lateral ventricles of the brain) (Neurosurgical system for external drainage, CSF drainage and monitoring) is necessary in patients with aneurysmal SAH who exhibit a decreased level of alertness or impaired consciousness and signs of hydrocephalus and/or ICH on CT imaging [297].

General principles of intracranial hypertension management in patients with aneurysmal subarachnoid hemorrhage

Comments: Intracranial hypertension is considered refractory when it does not respond to conservative therapy and ICP remains above 18–20 mm Hg [122,123,243,299].

Evaluation of patient treatment outcomes

Comments: earlier evaluation (at patient discharge or at other selected time points) is possible as an intermediate stage.

3.3 Treatment of patients with arteriovenous malformation

3.3.1 General recommendations

There are three treatment methods for AVMs: microsurgical resection, endovascular embolization, and radiosurgery. Each has its own advantages and disadvantages. At the same time, all of them aim to prevent hemorrhages, which requires the complete exclusion of the malformation from the bloodstream [95].

In the acute period of AVM rupture, surgical treatment of the malformation itself is often not required due to the low risk of re-rupture; the strategy is mainly based on the volume of intracranial hemorrhage, the degree of brain displacement, and the compression of CSF pathways [31, 288].

3.3.2 Surgical treatment of patients with arteriovenous malformation

Comments: Emergency surgical treatment is possible for an ICH volume of less than 30 ml in the presence of massive perifocal edema with the development of lateral shift greater than 5 mm or axial shift.

In patients over 80 years of age, in the presence of severe comorbid pathology, or in case of impaired consciousness down to coma (3–8 points on the GCS), the decision to perform emergency neurosurgery should be made by a medical board taking into account the risks of the natural disease course and perioperative complications [305].

Comments: In patients over 80 years of age, in the presence of severe comorbid pathology, or in case of impaired consciousness down to coma (3–8 points on the GCS), the decision to perform emergency neurosurgery should be made by a medical board taking into account the risks of the natural disease course and perioperative complications [306].

Comments: In specialized neurosurgical centers with extensive experience in emergency vascular neurosurgery, early AVM removal in the acute period of hemorrhage is possible [307].

Embolization of arteriovenous malformations

Comments: It is necessary to examine both carotid territories (separately ICA and ECA), as well as the vertebrobasilar system from both vertebral arteries. Special attention should be paid to visualizing potential sources of hemorrhage: flow-related and intranidal aneurysms, arteriovenous fistulas within the AVM structure, and varicose-altered draining veins.

Comment: if a direct high-flow fistula is present within the AVM structure, treatment can be divided into multiple stages.

Comments: Embolization of more than 60% of large AVMs in a single stage should be avoided.

Radiosurgical treatment of arteriovenous malformations

Comments: If MRI is not feasible for dynamic assessment of the radicality of malformation closure, CT angiography is acceptable.

3.3.3 Postoperative patient management

Comments: The duration of therapy is determined individually.

4. Medical Rehabilitation and Sanatorium-Resort Treatment

Comments: rehabilitation begins no later than 48 hours of stay in the intensive care unit (ICU) or intensive care and reanimation unit and continues in the inpatient neurology or neurosurgery department until discharge from the medical facility [326–329]. Afterward, the patient is routed to subsequent stages of rehabilitation treatment depending on the degree of functional recovery and independence in daily life, established in accordance with the gradations of the rehabilitation routing scale models.

In the early recovery period (up to 6 months), the patient is provided with 1–3 courses of rehabilitation treatment in medical rehabilitation departments for patients with CNS diseases in inpatient, day-care, or outpatient settings, including the use of telemedicine technologies.

In the late recovery period (after 6 months), the decision to continue the rehabilitation program is made within the framework of regional standards for developing an individualized medical rehabilitation program [329].

4.1 Rehabilitation of patients in the acute period of hemorrhagic stroke (days 3–28)

In addition to the primary neurological deficit resulting from primary brain injury due to hemorrhagic stroke, patients are at high risk of developing post-intensive care syndrome (PICS) as a side effect of specific intensive care, particularly prolonged immobilization, sedation, and mechanical ventilation [326, 327].

The main syndromes forming the clinical picture of PICS are:

✓ critical illness polymyoneuropathy: diffuse reduction of limb strength;

✓ respiratory polymyoneuropathy leading to prolonged mechanical ventilation due to weakness of the respiratory muscles and diaphragm;

✓ reduced exercise tolerance (fatigue);

✓ complications of forced positioning (bedrest and prone positioning): brachial plexus injury, foot drop and early plantar flexion contractures, pressure ulcers;

✓ orthostatic intolerance when sitting up;

✓ impaired urinary passage and predisposition to urolithiasis;

✓ bowel dysfunction (constipation);

✓ complications of learned non-use: dysphagia due to tracheoesophageal dissociation;

✓ delirium;

✓ chronic pain syndrome (musculoskeletal, neuropathic);

✓ emotional and cognitive impairment (depression, memory impairment);

✓ dyssomnia.

This necessitates the prevention of PICS as a basic primary technology of early rehabilitation. To this end, the "ReabIT" technology [332] is used, implemented by the multidisciplinary rehabilitation team (MDRT) of the early medical rehabilitation department and the primary vascular center (ICU of the PVC). Within the framework of these guidelines, we present the main points and comments on the specifics of their application in patients with SAH and ICH.

Comments: A complete list of clinimetric scales, reference values, and specialties of MDRT members responsible for monitoring and interpreting data using the respective scale are presented in the relevant clinical guidelines [332]. The PICS index is calculated by summing the ranked symptoms established by MDRT members according to their profile (Appendix G16). A total score ranging from 0 to 10 reflects both the presence of PICS and its severity, as well as the effectiveness of rehabilitation measures. When interpreting PICS manifestations, it should be taken into account that such PICS modalities as motor deficit, swallowing disorders, cognitive impairment, and decreased gravitational gradient are manifestations of the primary brain and spinal cord lesion. In this case, they should not be included in the calculation. In the differential diagnosis of movement disorders, significant symptoms on the unaffected side are recorded; for example, the presence of critical illness polymyoneuropathy is confirmed if the sum of strength scores on the healthy side did not exceed 8 points. The advantages of other methods for assessing PICS severity have not been proven [335–338].

Comments: current guidelines for the management of HS are evasive [5, 27] regarding the timing and types of rehabilitation initiation, but insist on early initiation. From the perspective of general pathophysiology of acute cerebral insufficiency, the prevention of learned non-use syndrome is justified for both PICS and acute focal deficit [332].

Comments: depending on the patient's ability to participate in rehabilitation measures (severity of condition, level of consciousness), rehabilitation is carried out in active, passive, and active-passive modes. The rehabilitation program should include a combination of kinesiologic maneuver techniques (positioning, verticalization and mobility, cycle ergometer loads, and electroneuromyostimulation), as well as practices by medical psychologists, occupational therapists, and medical speech therapists [326, 327].

Comments: when contraindications (STOP signals) appear (Appendix B3) at the moment of verticalization, mobilization, or any other rehabilitation procedure, this procedure should be stopped immediately. If stop signals developed at the moment of verticalization, it should be discontinued and the patient returned to the previous position (lowered by 20°) or lowered to 0° without stopping at elevation angles. Contact patients should be thoroughly explained the essence and expected sensations of the planned procedure so as not to provoke undesirable autonomic reactions caused by fear and uncertainty, especially in children. The level of evidence of these signs does not exceed level C, but obtaining higher-quality arguments in this context is difficult due to ethical considerations regarding the formation of a control group in such studies.

Comments: on the one hand, a positive passive leg raising test indicates hypovolemia, which during the verticalization maneuver will lead to orthostatic intolerance, which is highly undesirable in any emergency condition. On the other hand, this situation should not be considered an absolute contraindication to mobilization. The causes and a plan for restoring euvolemia should be evaluated, after which, upon obtaining a negative result on retesting, the implementation of the rehabilitation plan should be resumed.

Comments: unlike mobilization, non-verticalizing [332] positioning has no absolute contraindications and should be used from the 1st day regardless of the scope of other early rehabilitation modalities by the on-duty medical staff. Positioning is used for gravitational stimulation when raising the head of the bed, so the head of the bed should always be elevated no lower than 30°. Patients are assisted in successively assuming lying positions (on the right and/or left side or on the back), with an elevated head of the bed, or sitting. Positioning must necessarily include turns onto paralyzed limbs for proprioceptive stimulation and prevention of the "learned non-use" syndrome.

Comments: Standing is the best body position for effective patient breathing and maintaining lung volume [334, 336]. The higher the gravitational gradient and the duration of the patient's stay in it, the lower the risk of aspiration, pressure ulcers, polyneuromyopathy, contractures, pathological (painful) sensitization, and other factors of PICS. Patients on spontaneous breathing and mechanical ventilation in any mode should aim to maintain the longest possible anti-gravity vertical positioning at the level of the gravitational gradient achieved during passive verticalization. In communicative patients, the gravitational gradient is determined by the patient's individual request. Such patients should be taught to lean forward—in this position, gravity improves the drainage of secretions from the posteroinferior segments of the lungs. Verticalization procedures should be performed 3 times a day for 30 minutes. The duration of the procedure depends on tolerance, but should be at least 15 minutes. In any position, the head should be in the midline position to prevent impaired venous outflow, secondary increases in intracranial and intraocular pressure, and an increase in pathological muscle tone in paretic limbs [351].

Comments: early mobilization is an element of the rehabilitation process for stroke patients in the ICU [343]. A meta-analysis of data from sixteen studies involving 1,757 patients with SAH showed that early mobilization improved the mRS score at discharge (mean difference -1.39, 95% CI from -2.51 to -0.28, I2 = 86%) and at 3 months (mean difference -1.10, 95% CI from -1.54 to -0.66, I2 = 7%). Early mobilization was associated with a reduction in the incidence of cerebral vasospasm, both radiologic (OR 0.66, 95% CI from 0.45 to 0.96, I2 = 7%) and clinical (OR 0.44, 95% CI from 0.27 to 0.72, I2 = 8%); 6% of mobilization sessions included adverse events, mainly hemodynamic changes. The duration of mobilization is recommended to be from 15 to 45 minutes, divided into one, two, or three sessions per day. The main focus of early mobilization should be on sitting, standing, and walking activities.

Comments: Mobilization is a type of rehabilitation intervention that facilitates patient movement and increases energy expenditure to improve outcomes [353].

Passive mobilization [349] for non-communicative patients consists of a series of 10 repeated passive movements (passive joint gymnastics) in each of the main joints with very light stretching at the extremes of the physiological range of motion at least 2 times a day. Passive kinesiotherapy can also be performed using cyclotherapy with a bedside cycle ergometer (9140790) for the lower/upper extremities with reverse motion capability and other mechanical exercise devices (140790) that provide cyclic training for individual joints and have sensors to determine the patient's contribution in active-passive mode. Active mobilization involves training the patient and monitoring the execution of available independent movements in all joints (active joint gymnastics) at a frequency of 10 repetitions 3–6 times a day [325, 340].

Comments: unlike other nosological forms of acute cerebral insufficiency, hemorrhagic stroke carries a higher risk of cortical ischemia and herniation syndrome provoked by verticalization and physical activity. An analysis of observations of 148 patients with SAH before and during mobilization revealed a critical rSO2 value of 57%, at which there is a risk of complications; meanwhile, changes in rSO₂ during mobilization were not associated with changes in vital signs, suggesting that rSO₂ is an independent stop signal.

Comments: procedures aimed at reducing dyspnea, improving tracheobronchial clearance, training skeletal muscles, and maintaining the level of self-care are indicated during the period of weaning the patient from mechanical ventilation or immediately after it; expiration using positive pressure can be used. For this purpose, it is advisable to use incentive spirometry devices, devices with high-frequency intra-/extrapulmonary oscillations, and electrical stimulation of the diaphragm and intercostal muscles. The use of respiratory rehabilitation practices in neurointensive care patients does not adversely affect intracranial pressure [357]. To restore vocal cord function and the possibility of verbal communication, the use of a speaking valve for a tracheostomy tube is effective [358], as it creates useful expiratory resistance and helps improve the patient's emotional status [345, 346].

Comments: the inclusion of resistance exercises, provided there is adequate protein intake of at least 1.3 g/kg/day [364], helps preserve muscle mass under conditions of forced immobilization of a critically ill patient. Without muscle activity, the prevention of ICU-acquired weakness is less effective even with an adequate protein-energy balance. Early initiation of enteral nutrition reduces the risk of further nutritional deficiency and supports anabolic processes. At the same time, early mobilization and physical rehabilitation must be planned. A progressive exercise regimen, ranging from passive mobilization to active strength training, should be tailored to the patient's current functional capacity. This rehabilitation strategy aims to preserve skeletal muscle integrity, improve neuromuscular function, and accelerate functional recovery.

Comments: electrical muscle stimulation has been investigated as a treatment for the prevention of critical illness myopolyneuropathy. The treatment involves minimal joint movement and does not require patient interaction. Electrical muscle stimulation treatment administered in studies lasted 30–60 minutes daily for at least 4 days. A meta-analysis [368] including 11 randomized controlled trials involving 576 patients showed that early use of electrical muscle stimulation in intensive care unit patients reduced the duration of mechanical ventilation, length of intensive care unit stay, and overall hospital length of stay.

Comments: the incidence of post-extubation dysphagia in intensive care unit patients is 18.3% prior to intensive care unit discharge, of which up to 80% retain signs of dysphagia at hospital discharge [356, 357]. Furthermore, "silent" aspiration was noted in 36%. In the presence of post-extubation dysphagia, swallowing rehabilitation measures should be performed under the supervision of a multidisciplinary rehabilitation team speech-language pathologist [358, 359]. The essence of early medical speech therapy sessions is to maintain the swallowing reflex in conditions where it is impossible due to endotracheal intubation [375].

Comments: multicomponent interventions carried out by the intensive care unit multidisciplinary rehabilitation team can minimize the risks of cognitive impairment and delirium [361, 364].

The basis for the prevention of delirium and other emotional and cognitive disorders is the implementation of the core requirements of analgosedation recommendation protocols as a primary priority in the prevention of post-intensive care syndrome [380][381][382,383].

The multicomponent rehabilitation prevention program includes simple limb movement complexes, spontaneous breathing cycles, maintaining the patient's current level of orientation in place and time, measures to ensure nighttime sleep, performing elementary self-care activities [384], and using individually selected pieces of music for no more than 45 minutes per day [367, 370].

Comments: the intensive care unit environment, constant lighting, staff conversations, monitor alarms, respirator sounds—all these stimuli inevitably affect sleep quality. Meanwhile, ensuring sleep during the intensive care unit stay is a method of reducing the risk of cognitive impairment, including psychomotor agitation and delirium. In addition, preserving sleep architecture helps maintain the patient's positive emotional state and motivation to participate in the treatment and rehabilitation program, and also increases tolerance to muscle activity. A pooled analysis of studies demonstrated an overall reduction in the prevalence of delirium with a sleep-promoting protocol [389]. A mandatory component of the protocols is the creation of an optimal patient environment to ensure normal sleep (natural sleep markers such as a window or light/dark adjustment, avoidance of nighttime procedures, regular care breaks of 60–90 minutes). Pharmacological sleep modulation is not excluded [387]

Comments: occupational therapy is a separate section of emotional and cognitive rehabilitation. In the ICU setting, an occupational therapy specialist [392] trains the patient in simple everyday activities that ensure personal self-care (personal hygiene, dressing, eating, using a bedpan, alternative and augmentative communication). The significance of occupational therapy in the structure of rehabilitation is that it helps accelerate the restoration of the patient's premorbid performance patterns, i.e., return to habitual routines, lifestyle, and social status. The inclusion of occupational therapy in the rehabilitation complex makes it possible to shorten the ICU stay, and in patients with chronic critical illness, the time of adaptation to spontaneous breathing, and prevents the development of delirium.

4.2 Rehabilitation of patients in the early convalescence period of hemorrhagic stroke (up to 180 days)

Comments: the basis of the individualized multidisciplinary rehabilitation program (IMRP) for patients with hemorrhagic stroke should consist of basic procedures, including sessions with physical therapy specialists (kinesitherapists) [380, 384, 385], medical speech therapists [401], occupational therapy specialists [402], and medical psychologists. The program structure depends on the predominant domain of activity limitations that determines the cause of decreased independence in daily life [403]. At the initial stage, rehabilitation training lasts at least 45 minutes per day, and a corresponding increase in training intensity helps improve the patient's functional capabilities [404]. Sessions in accordance with the patient's personal needs and goals should be conducted 2–5 times a week, at least 45 minutes a day, and for at least 8 weeks. The intensity of rehabilitation training should be selected individually, fully taking into account the patient's physical strength, endurance, and cardiopulmonary function. It is recommended to personalize the parameters of exercise intensity based on the heart rate reserve percentage, the percentage of maximum heart rate, and perceived exertion.

Comments: post-stroke patients should have the opportunity to receive regular and continuous medical supervision, as well as the opportunity to continue rehabilitation treatment if transport limitations prevent regular visits to rehabilitation departments. Home-based training creates a sense of comfort for the patient and increases patient adherence to the procedures [407]. In addition, telerehabilitation helps reinforce the skills acquired by patients during their stay in inpatient departments.

Comments: more than 75% of patients discharged from the ICU exhibit symptoms of post-intensive care syndrome (PICS) as a barrier within the rehabilitation cycle. This necessitates mandatory diagnosis of this condition and the inclusion of a specific module of basic and auxiliary rehabilitation practices in the individual patient rehabilitation program (IPRP), aimed at its elimination and the prevention of further progression.

Comments: dosage regimen is 10.0 mL intravenously drip once daily for 10 days.

Comments: few studies on the pharmacotherapy of ICH consequences have not revealed significant results. The use of fluoxetine** for the prevention of depression and the improvement of motor function has been studied for a long time, but its benefit has not been proven [397, 398]. Meanwhile, a series of studies investigating pharmacotherapy for PICS during various rehabilitation periods after acute cerebrovascular accident (ACVA) without subpopulation separation for ICH has shown that supplementing the rehabilitation program with medications targeted at motor disorders (#Inosine + Nicotinamide + Riboflavin + Succinic acid** (N07N6E)) [411] and mild/moderate cognitive impairments (Ethylmethylhydroxypyridine succinate** (N002161/01)) [394, 396] caused by the learned non-use phenomenon in PICS accelerates their recovery.

Comments: there is a gap in specialists' knowledge regarding sexual life after a stroke, which leads to this topic rarely being brought up in conversations with patients. Many people are afraid to return to sexual activity after a stroke. However, during sexual intercourse, blood pressure appears to increase only slightly (up to ≈140 mm Hg) for a short time, and then returns to baseline shortly after the onset of sexual activity in healthy adults. There is a lack of knowledge regarding physical conditioning after ICH. For example, it is unclear how to guide individuals post-ICH regarding weight lifting (lifts using large muscle groups vs. small ones, heavy lifting vs. repetitive lifting) and how much and for how long blood pressure should be allowed to rise. Furthermore, it is unclear what advice should be given regarding the potential bleeding risk associated with physical exertion when blood pressure reaches >300 mm Hg.

5. Prevention and Dispensary Observation

5.1 Prevention of hemorrhagic stroke

Comments: If complete obliteration is absent, the issue of repeated radiosurgery or microsurgical removal of the AVM is addressed.

The examination is a key element of standard follow-up because it:

1. Reliably confirms or excludes complete obliteration (the goal of treatment).

2. Determines further tactics (observation or re-intervention).

3. Allows for retreatment to be carried out as effectively and safely as possible.

4. Complies with international clinical guidelines.

Treatment of arterial hypertension

Comments: In a study by Biffi A. et al. [421] with a mean follow-up period of 36.8 months, it was determined that recurrent hemorrhages occur more frequently with lobar hematoma location (102 out of 505 cases) than with non-lobar location (44 out of 640 cases). The frequency of hematomas in patients with inadequate blood pressure control was 84 cases per 1,000 patient-years, while with successful blood pressure control it was 49 cases per 1,000 patient-years. The risk of intracerebral hemorrhage recurrence was 3.53 (95% CI 1.65–7.54), and for non-intracerebral hemorrhage, it was 4.23 (95% CI 1.02–17.52). Systolic blood pressure was associated with an increased risk of recurrence of both lobar hemorrhage (RR 1.21, 95% CI 1.02–1.76 per 10 mm Hg increase in blood pressure) and non-lobar hemorrhage (RR 1.54, 95% CI 1.03–2.30).

Comments: In a large prospective cohort study involving 1,145 patients with intracranial hematoma, the risk of hemorrhage recurrence was significantly higher in patients with SBP ≥120 mm Hg and DBP ≥80 mm Hg compared to patients with SBP <120 mm Hg and DBP <80 mm Hg [420]. In the PRoFESS study (Prevention Regimen for Effectively Avoiding Second Strokes), the risk of ICH during follow-up was higher in patients with SBP ≥160 mm Hg compared to those with SBP of 130 to 139 mm Hg (RR 2.07 [95% CI 1.22–3.51]), while a statistically non-significant trend toward a lower incidence of intracranial hematoma was found at SBP <130 mm Hg [422].

Anticoagulant therapy

Comments: To date, there is no clear consensus on the timing of prescribing oral anticoagulants (B01AA Vitamin K antagonists) in patients with hypertensive ICH and atrial fibrillation [424]. Studies in which patients were prescribed #warfarin** focused on therapy initiation 4–8 weeks after intracerebral hematoma development [139]; in the APACHE-AF trial, the mean time to therapy initiation was 46 days, the mean follow-up period was 1.9 years (IQR 1.0–3.1; 222 patient-years), and non-fatal stroke or vascular death occurred in 13 (26%) participants receiving #apixaban** (annual event rate 12.6% [95% CI 6.7–21.5]) and in 12 (24%) in the no-anticoagulant group (11.9% [95% CI 6.2–20.8]; adjusted RR 1.05 [95% CI 0.48–2.31]; p=0.90) [425]. In the open-label randomized pilot SoSTART trial, oral anticoagulants (B01AA Vitamin K antagonists) were prescribed at a median of 115 days (IQR 49–265). Recurrent intracranial hemorrhage was observed in 8% of 101 individuals in the oral anticoagulant initiation group (B01AA Vitamin K antagonists) and in 4% of 102 individuals in the oral anticoagulant avoidance group (B01AA Vitamin K antagonists) (adjusted RR 2.42 [95% CI 0.72–8.09]; p=0.152) [423].

Comments: Patients with AF and non-traumatic ICH who are unsuited for anticoagulant therapy (e.g., an unsecure aneurysm in subarachnoid hemorrhage) require consideration of surgical prevention of vascular events.

Two meta-analyses of the PROTECT-AF (WATCHMAN) and PREVAIL (WATCHMAN) trials reported that the rates of ischemic stroke, as well as hemorrhagic stroke and bleeding, were lower in the left atrial appendage closure group (A16.12.041.007 Endovascular occlusion of the left atrial appendage), while cardiovascular mortality was similar across all treatment groups [304, 426]. In patients with a history of non-traumatic intracerebral hemorrhage (ntICH) and atrial fibrillation, data from a small, non-randomized, retrospective cohort also showed lower cardiovascular mortality, all-cause mortality, risk of hemorrhagic stroke, and major bleeding events with left atrial appendage closure (A16.12.041.007 Endovascular occlusion of the left atrial appendage) compared to standard medical therapy [428].

Other small retrospective studies have reported low event rates—similar to those in patients without ntICH and without ischemic stroke or ntICH within 30 days after left atrial appendage closure (A16.12.041.007 Endovascular occlusion of the left atrial appendage)—among patients diagnosed with cerebral amyloid angiopathy [429].

Comments: One study [430] in patients with mechanical heart valves reported that although the number of hemorrhagic complications significantly increased when anticoagulation was resumed at therapeutic doses prior to day 14 following hypertensive intracerebral hemorrhage, the calculated cumulative risk of bleeding and thromboembolism suggested that therapeutic anticoagulation may be considered in patients with mechanical heart valves as early as day 6 post-intracerebral hematoma. Another study [431] demonstrated that in patients with left ventricular assist devices, resuming anticoagulation with #warfarin** on average 14 days after cerebral hemorrhage was associated with fewer fatal and non-fatal thrombotic complications compared to resuming antiplatelet therapy alone, with a similar rate of recurrent cerebral hemorrhage.

Lipid-lowering therapy

Comments: In patients with ntICH and established indications for HMG-CoA reductase inhibitor pharmacotherapy, the risks and benefits of HMG-CoA reductase inhibitor therapy regarding ntICH outcomes and recurrence versus general cardiovascular risk reduction remain unclear. There is currently no consensus on the optimal lipid management strategy following ntICH. The association of HMG-CoA reductase inhibitor use with both acute outcomes and the reduction of recurrent vascular events in patients with a history of ntICH has not been established.

The SPARCL trial revealed an increased risk of ICH with high-dose atorvastatin** in the setting of very-low-density lipoproteins. Additional non-randomized observational studies found no association with HMG-CoA reductase inhibitor use in patients with intracerebral hemorrhage [432, 433].

Other retrospective analyses suggest potential for improved outcomes following ntICH with the use of HMG-CoA reductase inhibitors and a reduction in short- and long-term mortality. However, these results should be interpreted with caution due to selection bias and confounding by indication in these non-randomized studies. Given this uncertainty, the decision to use HMG-CoA reductase inhibitors in patients with ntICH depends on balancing the risk of ischemic cardiovascular and cerebrovascular events against recurrent ntICH. Clinical trials of these agents (C10AX Other lipid-modifying agents) have not thus far suggested an increased risk of first ntICH, but have not yet studied the risk of recurrence in patients with prior intracerebral hemorrhage [434–436].

Comments: NSAID use is associated with an increased bleeding risk. The overall incidence of ntICH is low in the general population, but a large meta-analysis of observational studies identified an increased risk of hemorrhagic stroke with the use of diclofenac** and meloxicam [432]. A subsequent large meta-analysis identified an increased risk of ntICH with the use of any NSAID.610 One small short-term study of patients with ntICH found no association between NSAID use and outcomes or recurrent ntICH, but follow-up was limited to 90 days [433].

5.2 Dispensary monitoring of patients

All patients with hemorrhagic stroke undergo outpatient follow-up after hospital discharge. In accordance with Order No. 168n of the Russian Ministry of Health dated March 15, 2022, "On approval of the procedure for dispensary observation of adults," dispensary observation of patients who have suffered a hemorrhagic stroke is carried out by a general practitioner (therapist) for 24 months after inpatient medical care in medical organizations: at least once every 3 months during the first year of dispensary observation, and at least once every 6 months thereafter. Monitored health indicators include peripheral blood pressure measurement, heart rate measurement, low-density lipoprotein cholesterol level testing (A09.05.028), ECG recording (A05.10.006), and—when treated with HMG-CoA reductase inhibitors—transaminases (A09.05.041 Determination of aspartate aminotransferase activity in blood, A09.05.04 Determination of alanine aminotransferase activity in blood) and CK (A09.05.043 Determination of creatine kinase activity in blood) (at 4 weeks after therapy initiation or in case of muscular symptoms). Additional preventive, diagnostic, therapeutic, and rehabilitation measures may be prescribed according to medical indications. It is advisable to assess the presence/risk of spasticity in patients who have suffered a hemorrhagic stroke as part of dispensary observation and to refer them for medical rehabilitation using botulinum toxin therapy to increase the effectiveness of rehabilitation measures and improve functional recovery. Referral for a consultation (examination, consultation) with a neurologist, neurosurgeon, cardiovascular surgeon, or cardiologist is also recommended when medically indicated in cases of ineffective drug therapy (refractory symptoms, failure to reach target blood pressure, heart rate, or LDL-C levels).

Comment: Patients at high risk of cerebral aneurysm recurrence include those with incomplete aneurysm exclusion from the circulation, presence of an aneurysm neck remnant, positive family history, infundibular dilations of intracranial artery ostia, and a number of aneurysm-associated conditions (genetic connective tissue disorders—autosomal dominant polycystic kidney disease; Ehlers-Danlos syndrome type IV, Marfan syndrome, etc.). The schedule for follow-up angiographic examinations is determined on an individual basis.

Comments: the purpose of follow-up is to detect disease progression, recurrence, and to correct epileptic syndrome. Patients who underwent surgery for AVMs are at risk of developing recurrent intracranial hemorrhage in the postoperative period. The most frequent causes of these complications are: malformation recanalization, residual malformation, and concomitant aneurysm. Duration of dispensary follow-up: after AVM eradication and in the absence of clinical manifestations—at least 5 years; in all other cases—lifelong.

Follow-up groups:

1) patients with inoperable AVMs;

2) patients with residual AVMs after interventions;

3) patients after AVM eradication (removal, total obliteration);

4) patients after radiosurgical treatment of AVMs.

In most cases, the scope of dispensary follow-up is limited to the correction of epileptiform syndrome and monitoring the status of the AVM.

5.3 Palliative care

Comments: For the mRS scale, see Appendix G21.

Comments: The best assessment method currently is the mRS. Compartmentalization of stroke care stages (stroke unit, rehabilitation unit, nursing home) can improve the quality of care in a specific location, but complicate the global perspective if communication is fragmented between various specialists (neurologists, anesthesiologists-resuscitators, neurosurgeons, physical therapists, palliative care staff, geriatricians) and institutions. Most specialists receive limited training in communication skills for patient-centered care. However, patient-centeredness as a communication strategy with stroke survivors and their families can increase satisfaction, safety, and treatment outcomes [440]. Knowledge and use of effective communication techniques is a vital core competency for improving the quality of stroke decision-making, patient and family satisfaction, and treatment outcomes (see Appendix A3).

Comments: Establishing treatment goals requires predicting the probability of survival and quality of life. Depending on the stage of the disease, the patient's health status, and stroke severity, preference-sensitive decisions may span the full spectrum of available treatments, from various forms of aggressive resuscitation to time-limited trials of therapy that are not usually considered burdensome [420, 422].

6. Organization of Medical Care

Indications for hospitalization in a medical organization

All patients with ICH must be hospitalized.

In case of suspected ICH, emergency medical care is accessed through the emergency medical services system.

The EMS service treats calls regarding ICH as high priority and ensures the fastest possible arrival of medical personnel to the patient.

The EMS service performing medical evacuation of a patient with ICH shall notify the receiving medical facility in advance that a patient with suspected ICH is expected to arrive, indicating the estimated travel time.

All patients with a suspected diagnosis of ICH undergo emergency hospitalization to a medical facility featuring a neurology department for patients with acute cerebrovascular accidents.

Organization of neurosurgical consultative care

Once a diagnosis of hemorrhagic stroke is established, all patients must be provided with a neurosurgical consultation, including via telemedicine technologies, within 60 minutes of receiving CT/MRI results to decide on the need for transferring the patient to a neurosurgical hospital.

If round-the-clock interpretation of CT results and teleradiology systems are unavailable for timely CT reporting, it is advisable to use artificial intelligence-based medical imaging software as a clinical decision support system for suspected ICH.

Telemedicine consultations are conducted with the participation of specialists (neurosurgeon, endovascular diagnostic and treatment surgeon, anesthesiologist-resuscitator, etc.).

During a telemedicine consultation, it is possible to discuss the examination plan and patient management tactics, as well as to coordinate the terms of patient transfer to another hospital.

Patients with stroke (including SAH) are provided with round-the-clock consultative care by mobile neurosurgical consultation teams based in departments providing surgical care to patients with acute cerebrovascular pathology (typically at a multidisciplinary hospital).

Patients with hemorrhagic stroke are subject to hospitalization/transfer to a medical facility equipped with:

A. Neurosurgery department;

B. Specialists experienced in direct microsurgical operations for cerebral aneurysms, AVMs, and hypertensive ICH;

C. Specialists experienced in endovascular occlusion of cerebral aneurysms and AVMs;

D. Specialists experienced in minimally invasive surgery for hypertensive ICH;

E. Radiology department equipped with devices for CT or MRI, CTA, MRA;

F. Angiographic operating room for cerebral angiography (DSA) and endovascular procedures;

G. Operating room equipped in accordance with the current Procedure for Providing Medical Care to Patients with Acute Cerebrovascular Accidents;

H. Neuro-ICU / intensive care unit for patients with acute cerebrovascular accidents;

I. Neurology department for patients with acute cerebrovascular accidents.

Transfer of a patient with hemorrhagic stroke from a neurosurgical hospital to a neurological hospital for further rehabilitation treatment is indicated upon satisfactory healing of the postoperative wound and absence of surgical complications.

Indications for patient discharge from a medical organization

Patient discharge is carried out depending on their status according to the Medical Rehabilitation Routing Scale (MRRS).

MRRS score 0–1—the patient does not need continued medical rehabilitation.

MRRS score 2–3—the patient is referred to the third stage of medical rehabilitation in a medical facility of the first, second, third, and fourth groups, determined in accordance with the Procedure for Organizing Medical Rehabilitation for Adults, approved by Order of the Ministry of Health of the Russian Federation No. 788n dated July 31, 2020.

MRRS score 4–5—the patient is referred to the second stage of medical rehabilitation in a medical facility of the second, third, and fourth groups.

MRRS score 4–6—the patient is referred to the second stage of medical rehabilitation in a medical facility of the third and fourth groups.

Medical rehabilitation at the second and third stages is carried out in the medical rehabilitation department for patients with central nervous system disorders.

Educational activities for the public and medical professionals

Public health and healthcare organization specialists must ensure regular educational events on specialized medical care for acute cerebrovascular accidents for physicians, hospital staff, and EMS personnel to improve the quality of care.

Public health and healthcare organization specialists must develop and implement public educational activities aimed at informing the population about the stroke care system and the need for prompt seeking of emergency medical care at disease onset to improve disease outcomes.

Regional healthcare organizers must develop triage algorithms and routing protocols for patients with acute cerebrovascular accidents aimed at ensuring rapid delivery to a medical facility providing the appropriate level of care, in order to improve disease outcomes.

7. Additional Information

Large medical inpatient facilities (national and federal neurosurgical centers, regional, territorial, and republican clinical hospitals) providing specialized care to patients with hemorrhagic stroke (HS) (including subarachnoid hemorrhage [SAH]), based on their own scientific research and practical experience, may develop and approve their own ("internal") protocols for the management of patients with HS at a meeting of the medical commission (signed by the head physician) or at a meeting of departments accredited to teach the specialties of "neurosurgery" and/or "neurology" (signed by the head of the department).

An "internal" protocol for managing patients with HS within a specific inpatient facility may introduce additions but must not contradict the main provisions of these clinical guidelines.

Criteria for Evaluating the Quality of Medical Care

References

Appendix A1. Working Group Composition

1. Neurosurgeons and endovascular surgeons

Krylov Vladimir Viktorovich – Academician of the RAS, Doctor of Medical Sciences, Professor, Chief freelance specialist neurosurgeon of the Russian Ministry of Health, Director of the Institute of Functional Neurosurgery of the Federal State Budgetary Scientific Institution "Federal Center of Brain Research and Neurotechnologies", Head of the Department of Fundamental Neurosurgery of the Institute of Neurosciences and Neurotechnologies of the Federal State Autonomous Educational Institution of Higher Education "Pirogov Russian National Research Medical University" of the Russian Ministry of Health, Chief Researcher of the Department of Emergency Neurosurgery of the State Budgetary Healthcare Institution "Sklifosovsky Research Institute of Emergency Care of the Moscow Healthcare Department"

Usachev Dmitry Yuryevich – Academician of the RAS, Doctor of Medical Sciences, Professor, Director of the Federal State Autonomous Institution "National Medical Research Center for Neurosurgery named after Academician N.N. Burdenko" of the Ministry of Health of the Russian Federation, Head of the Department of Neurosurgery of the Federal State Budgetary Educational Institution of Additional Professional Education "Russian Medical Academy of Continuous Professional Education" of the Ministry of Health of the Russian Federation, President of the Association of Neurosurgeons of Russia

Arustamyan Sergey Razmikovich – D.Sc. in Medicine, Leading Researcher at the 4th Department, National Medical Research Center for Neurosurgery named after Academician N.N. Burdenko of the Ministry of Health of the Russian Federation, Professor at the Department of Neurosurgery with Neuroscience Courses, National Medical Research Center for Neurosurgery named after Academician N.N. Burdenko of the Ministry of Health of the Russian Federation

Bakharev Evgeny Yuryevich – Ph.D. in Medicine, Senior Researcher at the Department of Emergency Neurosurgery, Sklifosovsky Research Institute for Emergency Medicine of the Moscow Healthcare Department

Berestov Vadim Vyacheslavovich – Ph.D. in Medicine, Researcher at the Research Center for Endovascular Neurosurgery, Federal Center of Brain Research and Neurotechnologies of the Federal Medical-Biological Agency of Russia, Neurosurgeon at the Morozov City Children's Clinical Hospital of the Moscow Healthcare Department

Godkov Ivan Mikhailovich – D.Sc. in Medicine, Head of the Neurosurgery and Neurotrauma Service, Kommunarka Moscow Multidisciplinary Clinical Center of the Moscow Healthcare Department, Associate Professor at the Department of Fundamental Neurosurgery, Institute of Neurosciences and Neurotechnologies, Pirogov Russian National Research Medical University of the Ministry of Health of the Russian Federation

Dmitriev Alexander Yuryevich – Ph.D. in Medicine, Associate Professor at the Department of Neurosurgery, Russian University of Medicine of the Ministry of Health of the Russian Federation, Neurosurgeon at the Department of Emergency Neurosurgery, Sklifosovsky Research Institute for Emergency Medicine of the Moscow Healthcare Department

Orlov Kirill Yuryevich – D.Sc. in Medicine, Professor at the Department of Neurology and Neurosurgery with a Course in Complex Rehabilitation, Faculty of Continuing Medical Education, Medical Institute, Peoples' Friendship University of Russia named after Patrice Lumumba, Head of the Research Center for Endovascular Neurosurgery, Federal Center of Brain Research and Neurotechnologies of the Federal Medical-Biological Agency of Russia, Neurosurgeon at the Neurosurgical Department, Morozov City Children's Clinical Hospital of the Moscow Healthcare Department, Director of the Academician F.A. Serbinenko Association of Endovascular Neurosurgeons

Pilipenko Yury Viktorovich – D.Sc. in Medicine, Leading Researcher at the 3rd Department, National Medical Research Center for Neurosurgery named after Academician N.N. Burdenko of the Ministry of Health of the Russian Federation, Associate Professor at the Department of Neurosurgery with Neuroscience Courses, National Medical Research Center for Neurosurgery named after Academician N.N. Burdenko of the Ministry of Health of the Russian Federation

Polunina Natalya Alekseevna – D.Sc. in Medicine, Associate Professor at the Department of Fundamental Neurosurgery, Institute of Neurosciences and Neurotechnologies, Pirogov Russian National Research Medical University of the Ministry of Health of the Russian Federation, Senior Researcher at the Department of Emergency Neurosurgery, Sklifosovsky Research Institute for Emergency Medicine of the Moscow Healthcare Department, Neurosurgeon at the Kommunarka Moscow Multidisciplinary Clinical Center of the Moscow Healthcare Department

Prirodov Alexander Vladislavovich – D.Sc. in Medicine, Professor at the Department of Fundamental Neurosurgery, Institute of Neurosciences and Neurotechnologies, Pirogov Russian National Research Medical University of the Ministry of Health of the Russian Federation, Head of the Neurosurgical Department, Leading Researcher, Sklifosovsky Research Institute for Emergency Medicine of the Moscow Healthcare Department

Rak Vyacheslav Avgustovich – Ph.D. in Medicine, Associate Professor at the Department of Fundamental Neurosurgery, Institute of Neurosciences and Neurotechnologies, Pirogov Russian National Research Medical University of the Ministry of Health of the Russian Federation

Khamurzov Valery Albertovich – Neurosurgeon at the Department of Emergency Neurosurgery, Sklifosovsky Research Institute for Emergency Medicine of the Moscow Healthcare Department

Kheyreddin Ali Sadek – D.Sc. in Medicine, Leading Researcher, National Medical Research Center for Neurosurgery named after Academician N.N. Burdenko of the Ministry of Health of the Russian Federation

Eliava Shalva Shalvovich – Corresponding Member of the Russian Academy of Sciences, D.Sc. in Medicine, Professor, Head of the 3rd Department, National Medical Research Center for Neurosurgery named after Academician N.N. Burdenko of the Ministry of Health of the Russian Federation

Yakovlev Sergey Borisovich – D.Sc. in Medicine, Head of the 4th Department, National Medical Research Center for Neurosurgery named after Academician N.N. Burdenko of the Ministry of Health of the Russian Federation, Professor at the Department of Pediatric Neurosurgery, Russian Medical Academy of Continuous Professional Education of the Ministry of Health of the Russian Federation

2. Neurologists

Shamalov Nikolay Anatolyevich – D.Sc. in Medicine, Professor, Chief freelance Specialist Neurologist of the Ministry of Health of the Russian Federation, Chief freelance Specialist Neurologist of the Moscow Healthcare Department, Director of the Institute of Cerebrovascular Pathology and Stroke, Federal Center of Brain Research and Neurotechnologies of the Federal Medical-Biological Agency of Russia, Executive Secretary of the National Stroke Association.

Alasheev Andrey Marisovich – D.Sc. in Medicine, Chief freelance Specialist Neurologist of the Ministry of Health of the Russian Federation in the Ural Federal District, Head of the Neurological Department for Patients with Acute Cerebrovascular Accidents, Sverdlovsk Regional Clinical Hospital No. 1, WSO member and ESO fellow.

Belousova Olga Bennuanovna – D.Sc. in Medicine, Chief Researcher at the 3rd Department, National Medical Research Center for Neurosurgery named after Academician N.N. Burdenko of the Ministry of Health of the Russian Federation, Professor at the Department of Neurosurgery with Neuroscience Courses, National Medical Research Center for Neurosurgery named after Academician N.N. Burdenko of the Ministry of Health of the Russian Federation

Voznyuk Igor Alekseevich – D.Sc. in Medicine, Professor, Chief freelance Specialist Neurologist of the Health Committee of Saint Petersburg, Chief freelance Specialist Neurologist of the Ministry of Health of the Russian Federation in the Northwestern Federal District, Professor at the Department of Neurology, Deputy Chief Physician for Neurology, Pavlov First Saint Petersburg State Medical University.

Gekht Alla Borisovna – D.Sc. in Medicine, Professor, Corresponding Member of the Russian Academy of Sciences, Director of the Solovyov Research and Practical Center for Mental Health of the Moscow Healthcare Department, Professor at the Department of Neurology, Neurosurgery and Medical Genetics, Pirogov Russian National Research Medical University of the Ministry of Health of the Russian Federation, Member of the Presidium of the National Stroke Association, Scientific Secretary of the All-Russian Society of Neurologists

Gusev Evgeny Ivanovich – D.Sc. in Medicine, Academician of the Russian Academy of Sciences, Professor at the Department of Neurology, Neurosurgery and Medical Genetics, Pirogov Russian National Research Medical University of the Ministry of Health of the Russian Federation, President of the National Stroke Association, Chairman of the All-Russian Society of Neurologists.

Zavaliy Lesya Bogdanovna – Ph.D. in Medicine, Senior Researcher at the Scientific Department of Emergency Neurology and Restorative Treatment, Neurologist, Sklifosovsky Research Institute for Emergency Medicine of the Moscow Healthcare Department.

Koltsov Ivan Alekseevich – Ph.D. in Medicine, Senior Researcher at the Research Laboratory of Cerebral Vascular Diseases, Pirogov Russian National Research Medical University of the Ministry of Health of the Russian Federation, Senior Researcher at the Department of Neuroimmunology, Federal Center of Brain Research and Neurotechnologies of the Federal Medical-Biological Agency of Russia.

Marskaya Nataliya Andreevna – Researcher at the Department of Vascular Diseases of the Nervous System Federal Center of Brain Research and Neurotechnologies of the Federal Medical-Biological Agency of Russia.

Martynov Mikhail Yuryevich – D.Sc. in Medicine, Professor, Corresponding Member of the Russian Academy of Sciences, First Deputy General Director of the Federal Center of Brain Research and Neurotechnologies of the Federal Medical-Biological Agency of Russia, Head of the Department of Neurology, Neurosurgery and Medical Genetics, Pirogov Russian National Research Medical University of the Ministry of Health of the Russian Federation, Scientific Secretary of the All-Russian Society of Neurologists, Board Member of the National Stroke Association.

Fidler Mikhail Sergeevich – Expert Analyst at the Department of Analytical Work, Directorate for the Implementation of National Medical Research Center Functions in Neurology, Assistant Professor at the Department of Neurology, Neurosurgery and Medical Genetics, Faculty of General Medicine, Pirogov Russian National Research Medical University of the Ministry of Health of the Russian Federation.

Kharitonova Tatyana Vitalievna – Ph.D. in Medicine, Senior Researcher, Saint Petersburg I.I. Janelidze Research Institute of Emergency Medicine.

Khasanova Dina Rustemovna – D.Sc. in Medicine, Professor, Professor at the Department of Neurology, Kazan State Medical University of the Ministry of Health of the Russian Federation, Chief freelance Neurologist of the Ministry of Health of the Russian Federation in the Volga Federal District, Board Member of the National Stroke Association, Board Member of the All-Russian Society of Neurologists.

Shchukin Ivan Alexandrovich – Ph.D. in Medicine, Associate Professor at the Department of Neurology, Neurosurgery and Medical Genetics, Faculty of General Medicine, Pirogov Russian National Research Medical University of the Ministry of Health of the Russian Federation, Senior Researcher at the Department of Neuroimmunology, Federal Center of Brain Research and Neurotechnologies of the Federal Medical-Biological Agency of Russia

Yanishevsky Stanislav Nikolaevich – D.Sc. in Medicine, Professor, Head of the Research Laboratory of Neurology and Neurorehabilitation, Professor at the Department of Neurology with Clinic, Almazov National Medical Research Centre, President of the Association "Society of Neurologists of Saint Petersburg and Leningrad Region"

3. Radiologists

Grigorieva Elena Vladimirovna – D.Sc. in Medicine, Head of the Department of Radiology, Russian University of Medicine of the Ministry of Health of the Russian Federation, N.A. Semashko Research Institute of Clinical Medicine, Head of the Department of Radiation Diagnostics, University Clinic of the N.A. Semashko Research Institute of Clinical Medicine

Igor N. Pronin – Academician of the RAS, Dr. Sc. (Med.), Professor, Head of the Department of X-ray and Radioisotope Diagnostic Methods, Deputy Director of the Academician N.N. Burdenko National Medical Research Center of Neurosurgery of the Russian Ministry of Health

4. Radiation therapists

Golanov A.V. – Corresponding Member of the RAS, Dr. Sc. (Med.), Professor, Head of the Department of Radiotherapy, Academician N.N. Burdenko National Medical Research Center of Neurosurgery of the Russian Ministry of Health

Lestrovaya Arina Igorevna – Cand. Sc. (Med.), Junior Researcher, Department of Radiotherapy, Academician N.N. Burdenko National Medical Research Center of Neurosurgery of the Russian Ministry of Health

5. Anesthesiologists and intensive care physicians

Baranich Anastasia Ivanovna – Cand. Sc. (Med.), Anesthesiologist-Intensivist, Clinical Pharmacologist, Department of Anesthesiology and Intensive Care, Academician N.N. Burdenko National Medical Research Center of Neurosurgery of the Russian Ministry of Health

Karpunin Andrey Yuryevich – Cand. Sc. (Med.), First Deputy Minister of Health of the Republic of Altai, Deputy Director for Organizational and Methodological Work, Sklifosovsky Research Institute of Emergency Medicine

Kulikov Alexander Sergeevich – Dr. Sc. (Med.), Head of the Department of Anesthesiology and Intensive Care, Academician N.N. Burdenko National Medical Research Center of Neurosurgery of the Russian Ministry of Health

Kurdyumova Nataliya Vyacheslavovna - Dr. Sc. (Med.), Anesthesiologist-Intensivist, Department of Anesthesiology and Intensive Care, Academician N.N. Burdenko National Medical Research Center of Neurosurgery of the Russian Ministry of Health

Lubnin Andrey Yuryevich – Dr. Sc. (Med.), Professor, Leading Researcher, Department of Anesthesiology and Intensive Care, Academician N.N. Burdenko National Medical Research Center of Neurosurgery of the Russian Ministry of Health

Petриkov Sergey Sergeevich – Academician of the RAS, Professor of the RAS, Dr. Sc. (Med.), Director of the Sklifosovsky Research Institute of Emergency Medicine, Head of the Department of Anesthesiology, Intensive Care and Emergency Medicine, Russian University of Medicine of the Russian Ministry of Health, President of the Interregional Public Organization "Association of Neuroanesthesiologists and Neurointensivists"

Savin Ivan Anatolyevich – Dr. Sc. (Med.), Head of the Reanimation and Intensive Care Unit, Department of Anesthesiology and Intensive Care, Academician N.N. Burdenko National Medical Research Center of Neurosurgery of the Russian Ministry of Health

6. Rehabilitation specialists

Ivanova Galina Evgenyevna – Dr. Sc. (Med.), Professor, Head of the Research Center for Medical Rehabilitation, Federal Center of Brain Research and Neurotechnologies of the FMBA of Russia, Head of the Department of Medicosocial Stroke Rehabilitation, Research Institute of Cerebrovascular Pathology and Stroke, Head of the Department of Medical Rehabilitation, Institute of Professional Education, Pirogov Russian National Research Medical University of the Russian Ministry of Health, Chairman of the Dissertation Council at Pirogov Russian National Research Medical University of the Russian Ministry of Health, Chief freelance specialist in medical rehabilitation of the Russian Ministry of Health, Chairman of the Presidium of the All-Russian Public Organization for the Promotion of Medical Rehabilitology "Union of Rehabilitologists of Russia", Secretary General of the Russian Association for Sports Medicine and Rehabilitation of Patients and Persons with Disabilities.

Belkin Andrey Avgustovich – Dr. Sc. (Med.), Professor of the Departments of Anesthesiology and Intensive Care, Physical and Rehabilitation Medicine and Nervous Diseases, Ural State Medical University, Director of the Clinical Institute of Brain, Chief freelance rehabilitation specialist of the Russian Ministry of Health in the Ural Federal District.

Conflict of interest: none.

Appendix A2. Methodology for Developing Clinical Guidelines

Target audience for these clinical guidelines:

1. neurologists

2. neurosurgeons

3. anesthesiologists-resuscitators

4. physicians in medical rehabilitation

5. radiologists

Table 1. Levels of Evidence (LoE) grading scale for diagnostic methods (diagnostic interventions)

Table 2. Scale for grading levels of evidence certainty (LEC) for prevention, treatment, and rehabilitation methods (preventive, therapeutic, and rehabilitative interventions)

Table 3. Scale for grading grades of recommendation (GR) for prevention, diagnostic, treatment, and rehabilitation methods (preventive, diagnostic, therapeutic, and rehabilitative interventions)

Procedure for updating clinical guidelines.

The mechanism for updating clinical guidelines provides for their systematic revision at least once every three years, as well as upon the emergence of new evidence-based medicine data on the diagnosis, treatment, prevention, and rehabilitation of specific diseases, or in the presence of justified additions/comments to previously approved clinical guidelines, but no more frequently than once every 6 months.

Appendix A3. Reference Materials

1. Federal Law No. 323-FZ of November 21, 2011 (as amended on July 2, 2021) "On the Fundamentals of Protecting Public Health in the Russian Federation" (Collected Legislation of the Russian Federation, 2011, No. 48, Art. 6724) (with amendments and additions, effective from October 1, 2021) (https://roszdravnadzor.gov.ru/documents/100)

2. Order of the Russian Ministry of Health No. 203n dated May 10, 2017, "On Approval of Criteria for Assessing the Quality of Medical Care" (Registered with the Ministry of Justice of Russia on May 17, 2017, No. 46740); (http://publication.pravo.gov.ru/Document/View/0001201705170016?rangeSize=1) valid until August 31, 2025;

3. Order of the Ministry of Health of the Russian Federation No. 203n dated April 14, 2025, "On Approval of Criteria for Assessing the Quality of Medical Care" (Registered with the Ministry of Justice of Russia on May 28, 2025, No. 82382); (http://publication.pravo.gov.ru/document/0001202505290045); entered into force on September 1, 2025;

4. Order of the Ministry of Health of the Russian Federation No. 103n dated February 28, 2019, "On Approval of the Procedure and Deadlines for the Development of Clinical Practice Guidelines, Their Revision, Standard Template of Clinical Practice Guidelines and Requirements for Their Structure, Composition and Scientific Validity of Information Included in Clinical Practice Guidelines."

5. International Statistical Classification of Diseases and Related Health Problems (ICD-10) (https://mkb-10.com/);

6. State Register of Medicines (http://www.grls.rosminzdrav.ru/grls.aspx);

7. Order of the Russian Ministry of Health No. 804n dated October 13, 2017, "On Approval of the Nomenclature of Medical Services", registered with the Ministry of Justice on November 7, 2017, registration No. 48808 (as amended on March 24, 2020)

Table 1. Methods of communication with post-stroke patients used in palliative care  [439]

Appendix B. Physician Action Algorithms

Appendix B1. Algorithm for the management of a patient with hemorrhagic stroke of the hypertensive intracerebral hematoma type (diagnosis and choice of surgical treatment method)

Appendix B2. Algorithm for the inactivation of antithrombotic agents (B01) in hypertensive intracerebral hematoma [5, 37, 116, 117].

Appendix B3. STOP signals for initiating and continuing rehabilitation procedures [330, 331].

Absolute contraindications to the initiation of mobilization:

• Acute myocardial infarction at the time of mobilization initiation

• Subarachnoid hemorrhage with an unclipped aneurysm

• Shock

• Pulmonary embolism, progressive deep vein thrombosis according to ultrasound data, or the presence of a floating thrombus (in the absence of a vena cava filter, temporary or permanent***)

• Unstable fracture of the spine, pelvis, or lower extremities

• Patient refusal

• Need for neuromuscular blockade

• Active bleeding

• External cardiac pacing

Relative contraindications to the initiation of mobilization:

• Absence of a trained anesthesiologist-reanimatologist and a medical rehabilitation specialist in the multidisciplinary rehabilitation team (MDRT), as well as the lack of adequate instrumental monitoring capabilities at the rehabilitation stages

Dynamic STOP signals

Appendix C. Patient Information

Information for the patient, patient's relatives, and caregivers

Stroke is an acute cerebrovascular event caused by the rupture or occlusion of a blood vessel supplying the brain. Signs of a stroke include the sudden onset of weakness in the facial muscles or limbs, especially on one side of the body, sensory disturbances, also most commonly on one side, and difficulty speaking or understanding speech. In severe cases, loss of consciousness occurs.

The condition can be recognized on the spot immediately. The "FAST" test is used for this purpose. Ask the person to:

"F" (Face) – Smile. The smile may be uneven, the corner of the mouth on one side may point downward instead of upward, and the face may be drooping.

"A" (Arms) – Raise both arms. The arms may not rise equally, or one may not rise at all.

"S" (Speech) – Speak a simple sentence. Speech may be slurred, or the instruction may not be understood.

It is very important to note that all these symptoms occur SUDDENLY (ACUTELY)! If the person has difficulty performing any of these tasks, you must immediately call an ambulance, describe the symptoms, and inform the arriving paramedics of the time of symptom onset. Before the ambulance arrives, make the patient comfortable, with the head and shoulders elevated to prevent flexion, loosen restrictive clothing, and ensure a sufficient supply of fresh air. Do not give anything by mouth; treatment for a stroke patient is carried out exclusively in a hospital in a specialized department.

Following the inpatient treatment course upon discharge, the patient is advised to continue treatment, which includes medications to prevent a recurrent stroke. The patient must strictly follow all recommendations of the physician supervising them for the required period. If any new symptoms appear, seek medical attention immediately.

A patient who has suffered a hemorrhagic stroke requires follow-up by a neurologist at their place of residence, blood pressure monitoring (a blood pressure log must be maintained), increased physical activity, body weight control, proper nutrition, and smoking cessation.

Blood pressure and heart rate monitoring log for a patient with hemorrhagic stroke

Appendix G. Assessment Scales, Questionnaires, and Other Evaluation Tools

Appendix G1. Hunt-Hess scale

Russian title: Hunt-Hess Classification

Original title: Classification of patients with intracranial aneurysms according to surgical risk

Source: [18]

Type: rating scale

Purpose: assessment of surgical risk depending on the timing of intervention in intracranial aneurysm repair

Content (template) and key (interpretation):

* Serious systemic diseases and/or vasospasm downgrade the patient to a lower grade

Appendix G2. Severity of hemorrhage on CT based on the original and modified Fisher scales

Russian title: Fisher scale (original and modified)

Original title: Fisher scale, modified Fisher scale

Source: [11,12]

Type: rating scale

Purpose: assessment of hemorrhage severity on CT

Content (template) and key (interpretation):

Appendix G3. Severity of intraventricular hemorrhage according to D.A. Graeb

Russian title: Severity of intraventricular hemorrhage according to D.A. Graeb

Original title: none

Source: [13]

Type: rating scale

Purpose: assessment of intraventricular hemorrhage severity

Content (template) and key (interpretation):

Appendix G4. Glasgow Coma Scale

Russian title: Glasgow Coma Scale

Original name: Glasgow Coma Scale

Source: [442]

Type: rating scale

Purpose: assessment of surgical risk depending on the timing of intervention in intracranial aneurysm repair

Content (template):

Key (interpretation):

Appendix G5. Assessment of the severity of patients with SAH using the WFNS scale

Russian title: World Federation of Neurological Surgeons (WFNS) Subarachnoid Hemorrhage (SAH) Grading

Original title: World Federation of Neurological Surgeons (WFNS) Subarachnoid Hemorrhage (SAH) Grading

Source: [443]

Type: rating scale

Purpose: Assessment of the severity of patients with subarachnoid hemorrhage

Content (template) and key (interpretation):

WFNS Grade 0 SAH: unruptured aneurysm.

WFNS Grade I SAH: Glasgow Coma Scale score of 15, no major neurological deficit (aphasia, hemiparesis/hemiplegia).

WFNS Grade II SAH: Glasgow Coma Scale score of 13-14, no major neurological deficit.

WFNS Grade III SAH: Glasgow Coma Scale score of 13-14, major neurological deficit present.

WFNS Grade IV SAH: Glasgow Coma Scale score of 7-12, major neurological deficit present/absent.

WFNS Grade V SAH: Glasgow Coma Scale score of 3-6, major neurological deficit present/absent.

Appendix G6. Hijdra scale for assessing the intensity of aneurysmal SAH

Russian name: Hijdra scale

Original name: Hunt-Hess classification

Source: [18]

Type: rating scale

Purpose: evaluation of aneurysmal subarachnoid hemorrhage severity

Content (template) and key (interpretation):

Assessment of each of the 10 basal cisterns and fissures separately on a scale according to the amount of blood:

no blood = 0,

small amount = 1,

moderate amount = 2,

completely filled with blood = 3.

*blood clots that exceed the true dimensions of the cistern or fissure are scored as 3 points

Calculation of the amount of blood in the subarachnoid space [sum of scores]; range = 0-30.

The average score is used for an inadequately visualized cistern or fissure.

Assessment of blood in the four cerebral ventricles:

no blood = 0,

sedimentation in the lower part of the ventricle = 1,

partially filled = 2,

completely filled = 3.

Calculation of the amount of blood in the cerebral ventricles [sum of scores]; range = 0-12

Appendix G7. Raymond classification of aneurysm occlusion grades

Russian name: Raymond classification

Original title: none

Source: [444]

Type: other (classification)

Purpose: evaluation of aneurysm occlusion grades

Content (template):

angiographic scheme used to assess the degree of occlusion of intracranial aneurysms following endovascular treatment.

Key (interpretation):

Raymond I – complete aneurysm occlusion

Raymond II – filling of the aneurysm neck

Raymond III – residual aneurysm filling

Appendix G8. Intracerebral hemorrhage outcome prediction scale

Russian name: Intracerebral Hemorrhage Outcome Score

Original name: The ICH score

Source: [38]

Type: rating scale

Purpose: prediction of intracerebral hemorrhage outcomes

Content (template):

Key (interpretation): mortality depends on the score and is as follows: 0 points – 0%, 1 point – 13%, 2 points – 26%, 3 points – 72%, 4 points – 97%, 5-6 points – 100%.

Appendix G9. Modified Rankin Scale

Russian name: Modified Rankin Scale

Original name: The Modified Rankin Scale (mRS)

Source: [445]

Type: rating scale

Purpose: degree of functional limitation in stroke survivors (to assess overall disability and approximate patient dependency on the assistance of others)

Content (template) and key (interpretation):

Key (interpretation): 0 points correspond to no functional limitations in the patient, including minor ones; 1 point corresponds to no significant limitations despite the presence of some symptoms. The patient is able to carry out all normal activities and duties; 2 points correspond to slight disability. The patient is unable to carry out previous activities, but can manage daily affairs without outside help; 3 points correspond to moderate disability. The patient requires some outside assistance, but is able to walk independently (including using walking aids or a walker); 4 points correspond to moderately severe disability. The patient is unable to walk and attend to personal needs without outside help; 5 points correspond to severe disability. The patient is bedridden and incontinent of urine and feces. Constant care is required.

Notes: the evaluator should not attempt to separate disability due to stroke from disability due to other causes.

Appendix G10. Spetzler-Martin Scale (1986)

Russian name: Spetzler-Martin Scale

Original name: Spetzler-Martin Scale

Source: [44]

Type: other (classification)

Purpose: grading system for arteriovenous malformations

Content (template) and key (interpretation):

AVMs with 1-2 points have a low surgical risk, 3 points – intermediate, 4-5 points – high.

Comment: * AVM drainage is considered deep if blood outflow through at least one of the veins occurs into the great vein of Galen, internal cerebral veins, basal veins of Rosenthal, and precentral cerebellar veins.

** Eloquent areas: sensorimotor, speech, and visual cortex, hypothalamus, thalamus, internal capsule, brainstem, cerebellar peduncles, and deep cerebellar nuclei.

Appendix G11. Spetzler-Ponce Scale (2011)

Russian name: Spetzler-Ponce scale

Original name: Spetzler-Ponce scale

Source: [45]

Type: rating scale

Purpose: stratification of patients with cerebral arteriovenous malformations into surgical treatment risk classes

Content (template):

Comment:

* exceptions include patients with recurrent hemorrhages, progressive neurological deficit, AVMs with the steal syndrome, and hemodynamic aneurysms

Appendix G12. Simplified SICH scale (2010)

Russian name: SICH scale

Original name: Secondary Intracerebral Hemorrhage Score

Source: [93]

Type: rating scale

Purpose: identification of patients with intracerebral hemorrhage at the highest risk of underlying vascular etiology

Content (template):

Key (interpretation):

Recommendations for clinics that do not perform CTA in all patients with non-traumatic intracerebral hemorrhage:

SICH 0 – CTA and DSA are not indicated;

SICH 1-2 – CTA is performed, and DSA is performed only if vascular pathology is present or suspected;

SICH 3-6 – DSA is performed without CTA.

Recommendation for clinics where all patients with ICH undergo CTA:

SICH 0-2 – DSA is performed if vascular pathology is present or suspected on CTA;

SICH 3-6 – all patients undergo DSA regardless of pathology findings on CTA.

*High probability of vascular anomaly on non-contrast CT includes:

1) dilated vessels or calcifications along the edges of the ICH;

2) hyperdense foci in the venous sinuses or cortical veins along the suspected venous drainage pathway of the ICH;

Low risk of vascular anomaly on non-contrast CT includes:

1) absence of high-risk criteria for vascular anomaly (see above);

2) location of the ICH in the basal ganglia, thalamus, or brainstem.

Moderate risk of vascular anomaly on non-contrast CT is considered when high- and low-probability criteria for vascular anomaly are absent (in lobar and cerebellar ICH).

**Coagulation disorder criteria according to the SICH scale:

1) daily intake of acetylsalicylic acid** or clopidogrel**;

2) thrombocytopenia less than 50,000 per µL;

3) INR greater than 3.0;

4) activated partial thromboplastin time greater than 80 seconds.

Appendix G13. Lawton-Young Scale (2010)

Russian name: Lawton-Young scale

Original name: Grading Scale for Selecting Patients with Brain Arteriovenous Malformations for Surgery

Source: [47]

Type: rating scale

Purpose: selection of patients with cerebral arteriovenous malformations for surgical intervention

Content (template):

Key (interpretation): in combination with the Spetzler-Martin classification, AVMs scored 2–6 points carry a low surgical risk, while 7–10 points indicate a high risk.

Combination of the Spetzler-Martin and Lawton-Young scales

Comment: * AVM drainage is considered deep if blood outflow through at least one of the veins occurs into the great vein of Galen, internal cerebral veins, basal veins of Rosenthal, and precentral cerebellar veins.

** Eloquent areas: sensorimotor, speech, and visual cortex, hypothalamus, thalamus, internal capsule, brainstem, cerebellar peduncles, and deep cerebellar nuclei.

Appendix G14. Virginia Radiosurgery AVM Scale (VRAS, 2013)

Russian title: VRAS Classification

Original title: Virginia radiosurgery AVM scale

Source: [51]

Type: rating scale

Purpose: prediction of outcomes following radiosurgical treatment of arteriovenous malformations

Content (template):

Key (interpretation): For AVM radiosurgery scored 0 points, an excellent outcome (complete AVM obliteration without neurological worsening) is predicted in 83%, 1 point — in 79%, 2 points — in 70%, 3 points — in 48%, 4 points — in 39%.

Appendix G15. Radiosurgery-Based AVM Score (RBAS), modified version (2008)

Russian title: RBAS scale, modified version (2008)

Original title: Radiosurgery-based AVM score

Source: [446]

Type: index

Purpose: prediction of radiosurgical treatment outcomes in patients with AVM

Content (template):

AVM score = (0.1) × (AVM volume in ml) + (0.02) × (patient age in years) + (0.5) × (malformation location *).

Comments:

* AVM location:

0 points — frontal and temporal lobes

1 point — parietal and occipital lobes, intraventricular location, corpus callosum, and cerebellum

2 points — basal ganglia, thalamus, brainstem.

Key (interpretation): for an AVM grading of 1 point or less, an excellent outcome (complete AVM obliteration without neurological worsening) is predicted in 95%, 1.25 points — in 80%, 1.5 points — in 70%, 1.75 points — in 60%, 2 points — in 50%, more than 2 points — in less than 40%.

Appendix G16. Scale for assessing the severity of PICS

Russian title: Scale for assessing the severity of post-intensive care syndrome

Original title: -

Source: [447]

Type: rating scale

Purpose: assessment of PICS severity

Content (template):

Note: severity grading of PICS is defined as:

1–3 points — mild

4–6 points — moderate

6–10 points — severe

Appendix G17. National Institutes of Health Stroke Scale for assessing the severity of neurological deficit in stroke patients

Russian title: National Institutes of Health Stroke Scale

Original title: National Institutes of Health Stroke Scale (NIHSS)

Source: [448]

Type: rating scale

Purpose: for assessing the severity of neurological deficit in stroke patients

Contents:

1a. Level of consciousness. The examiner must assign the appropriate score even if assessment is difficult due to endotracheal intubation, language barrier, orotracheal trauma, or bandages. Three points are assigned only if the patient has no motor response to a painful stimulus (except for reflex posturing). Ask the patient two or three general questions regarding the circumstances of their hospital admission. Based on the responses obtained, evaluate the results. Remember that the patient should not be assisted.

0 = alert, responsive immediately to examination.

1 = drowsy, responsive to minor stimulation.

2 = stuporous, requires repeated stimulation to respond, or unresponsive requiring more intense stimulation to elicit a non-stereotypic motor response.

3 = comatose, response only via reflex motor acts, spontaneous movements, or complete unresponsiveness, atonia, areflexia.

1b. Level of consciousness. Questions. Ask the patient: "What month is it? How old are you?" Close but incorrect answers are not scored. Patients with aphasia and/or decreased level of alertness who cannot answer the two questions correctly will receive 2 points. Patients who cannot speak due to endotracheal intubation, orotracheal trauma, severe dysarthria, language barrier, or other reasons (excluding aphasia) will receive 1 point. Only the first attempt is scored; verbal and non-verbal assistance from the physician is not permitted.

0 = correct answer to both questions.

1 = correct answer to one question.

2 = incorrect answer to both questions.

1c. Level of consciousness. Commands. The patient must be asked to close and open their eyes, make a fist with the non-paretic hand, and then release it. If the patient's hand cannot be used for this item, another command may be substituted. If the patient cannot understand the command, the task may be demonstrated to them. Patients with trauma, amputation, or other physical defects should be assessed using a single-step command. Only the first attempt is scored. Questions are also asked only once.

0 = both commands performed correctly.

1 = one command performed correctly.

2 = neither command performed correctly.

1. Eye movements. Only horizontal eye movements are evaluated. Spontaneous or reflexive (oculocephalic reflex) eye movements are assessed. Caloric testing is not permitted. If the patient has conjugate gaze deviation that the patient can overcome spontaneously or by eliciting the oculocephalic reflex, 1 point is assigned. If the patient has an isolated extraocular muscle paresis innervated by the III, IV, or VI cranial nerves, 1 point is assigned. Eye movements should be examined in all patients, including those with aphasia. Patients with ocular trauma, a bandage, prior blindness, or other visual acuity or visual field disorders must be examined by eliciting the oculocephalic reflex. To detect partial gaze paresis, it is recommended to establish eye contact with the patient and move from side to side relative to the patient.

0 = normal.

1 = partial gaze palsy, overcome voluntarily or by eliciting the oculocephalic reflex.

2 = forced deviation of the eyes not overcome by eliciting the oculocephalic reflex.

2. Visual fields. Visual fields (upper and lower quadrants) are tested separately. Finger counting or a sudden appearance of a visual stimulus (the examiner's finger) in the patient's visual field may be used if necessary. During testing, the patient should look into the examiner's face; however, if they track the movement of the fingers, this can be assessed as a normal positive reaction. In the presence of unilateral blindness or enucleation, visual fields are assessed in the healthy eye. If there is a clearly demarcated visual field defect in the form of upper or lower quadrantanopia, a score of 1 is given. If the patient is blind for any other reasons, a score of 3 is given. Simultaneous bilateral stimulation must also be performed. If this reveals a difference (visual field constriction towards the affected eye), a score of 1 is given, and the test results are used to answer question No. 11. Two points correspond to cases of complete hemianopia, and the presence of any partial visual field disturbance, including quadrantanopia, corresponds to 1 point.

0 = normal.

1 = partial hemianopia.

2 = complete hemianopia.

3 = bilateral hemianopia (blindness, including cortical blindness).

3. Facial palsy. Using verbal and non-verbal techniques, ask the patient to show their teeth, raise their eyebrows, close their eyes, and squeeze their eyes shut. Demonstration of these commands by the physician is permitted. Assess the symmetry of the pain grimace in response to a noxious stimulus in patients who cannot understand you. If there is a facial bandage, orotracheal intubation, or other barriers, they should be removed (as far as possible) for the duration of the assessment.

0 = normal.

1 = minor paralysis, facial asymmetry in the form of flattening of the nasolabial fold, asymmetry when smiling.

2 = partial paralysis (partial or complete paralysis of the lower facial muscles).

3 = complete paralysis of the lower and upper facial muscles on one or both sides (complete absence of movement in the upper and lower facial muscles).

5a. Upper limb movements (left arm). The patient's limbs must be positioned as follows: arms outstretched (palms down) at an angle of 90° (if the patient is sitting) or 45° (if the patient is supine). Each limb is assessed in turn, starting with the non-paretic arm. Demonstration of the maneuver by the physician is permitted in patients with aphasia. Administration of noxious stimuli is not permitted. In the event of limb amputation or shoulder joint pathology, the examiner must enter UN (untestable) in the appropriate box. Clearly count aloud to ten and demonstrate the count on your fingers so that the patient can see it. Start counting as soon as you let go of the patient's limb.

0 = limb holds the 90° or 45° position for 10 seconds without downward drift.

1 = limb drifts down before the full 10 seconds, but does not hit the bed or other support.

2 = limb cannot sustain the raised position (drifts down to the bed or other support within 10 seconds), but has some effort against gravity.

3 = limb falls to the bed with no effort against gravity, minimal movement is present.

4 = no active movement.

UN = limb amputation or shoulder joint injury.

5b. Upper limb movements (right arm).

6a. Lower limb movements (left leg). The limbs are placed in the appropriate position: at an angle of 30° in the supine position. Demonstration of the maneuver by the physician is permitted in patients with aphasia. Administration of noxious stimuli is not permitted. Each limb is assessed in turn, starting with the non-paretic leg. Only in the event of limb amputation or hip joint pathology, the examiner must enter UN (untestable) in the appropriate box. Clearly count aloud to five and demonstrate the count on your fingers so that the patient can see it. Start counting as soon as you let go of the patient's limb.

0 = leg holds the 30° position for 5 seconds without downward drift.

1 = leg drifts down before the full 5 seconds, but does not hit the bed or other support.

2 = leg cannot sustain the raised position (drifts down to the bed or other support within 5 seconds), but has some effort against gravity.

3 = leg falls to the bed with no effort against gravity, minimal movement is present.

4 = no active movement.

UN = limb amputation or hip joint injury.

6b. Lower limb movements (right leg).

4. Limb ataxia. Unilateral cerebellar signs are assessed. The test is performed with eyes open. If there is any visual defect, test in the unaffected visual field. Ataxia will be absent in a patient who does not understand what is required or is paralyzed. In the event of joint pathology or limb amputation, UN (untestable) is scored. Ask the patient to perform the finger-nose-finger, finger-finger, and heel-knee tests with both limbs. In case of blindness, the finger-finger test must be omitted. A patient with aphasia will often be able to perform the test normally if the examiner moves the limb beforehand.

0 = absent.

1 = present in one limb.

2 = present in two limbs.

5. Sensory loss. Only sensory loss due to the current illness is considered. The examiner should test as many areas of the patient's body as possible (face; arms, excluding hands; legs, excluding feet; trunk). Patients in a stupor and/or with aphasia are scored 1, and patients with brainstem stroke and bilateral sensory loss are scored 2. If the patient does not respond to external stimuli and has tetraplegia, a score of 2 is given, as well as for a level of consciousness reduced to coma.

0 = normal; no sensory loss.

1 = moderate sensory loss; the patient feels pinprick as less sharp or as dull on the affected side.

2 = severe to total sensory loss; the patient feels nothing (is not aware of being touched) in the face, arm, and leg.

6. Aphasia. The patient is asked to describe the attached picture, list the objects depicted on a sheet of paper, and read sentences from the attached list. If the patient is blind, they must name objects by taking them in their hand, repeat something after the examiner, or say something independently. An intubated patient should be asked to answer in writing. Three points should only be scored if the patient does not respond to any commands and does not answer questions. Mild aphasia is scored 1 point. To correctly choose between 1 and 2 points, use the provided materials; it is assumed that a patient who misses more than 2/3 of the items offered for this purpose or performs a small number of simple commands will receive 2 points. In a comatose state, a score of 3 is given.

0 = no aphasia; normal.

1 = mild to moderate aphasia.

2 = severe aphasia.

3 = mute, global aphasia.

7. Dysarthria. If the patient's condition is assessed as normal, they must be able to speak adequately in response to the examiner's request to read something or repeat words from the attached list. If the patient shows signs of severe aphasia, the clarity of articulation is assessed during spontaneous speech. Only if the patient is intubated or there is some other physical barrier to speech, the patient's condition is scored 9, and the examiner must provide a clear written explanation for the inability to assess the patient's condition. Do not tell the patient the reason for testing them.

Use the provided word list for all patients and do not inform them that you are performing a speech clarity test. As a rule, unclear pronunciation of one or more words is considered normal. Zero points are given to patients who read all words distinctly. Patients with aphasia or those who cannot read are evaluated based on the quality of their spontaneous speech or their repetition of words spoken aloud by the examiner. Two points are given when the patient is completely incomprehensible or remains mute.

0 = normal.

1 = mild to moderate dysarthria; the patient slurs at least some words and, at worst, can be understood with some difficulty.

2 = severe dysarthria; the patient's speech is so slurred as to be unintelligible in the absence of or out of proportion to any dysphasia, or is mute/anarthric.

UN = patient intubated or has other physical barrier to speech.

8. Extinction and inattention (formerly termed "neglect"). Information obtained during the previous tests is sufficient to detect neglect (inattention). If, due to a severe visual impairment, simultaneous bilateral visual stimulation cannot be performed in the patient, but the reaction to cutaneous stimuli is normal, their condition is assessed as normal. If the patient has aphasia, but by all indications attentively tracks the voice from both sides, their condition is assessed as normal. The presence of visuospatial neglect, or anosognosia, is regarded as pathological. Since pathology is scored only if present, this item is always tested.

It can be assumed that significant variation in examiner opinion is possible when assessing this item, as all neurologists use somewhat different methods for testing neglect. Therefore, to increase the reliability of the study, perform only bilateral simultaneous stimulation for visual and tactile stimuli. With unilateral neglect of stimuli in both modalities, assess inattention as 2, and with unilateral neglect of a stimulus in one modality, as 1. If the patient is conscious but demonstrates any other pronounced type of neglect, assess the level of inattention as 1.

0 = no abnormalities.

1 = depressed response (extinction, inattention) to simultaneous bilateral stimulation in one of the listed modalities (visual, tactile, auditory, spatial).

2 = marked unilateral extinction or extinction of stimuli in more than one modality; the patient does not recognize (fails to distinguish) their own hand or other landmarks on one side only.

Key (interpretation): maximum score is 42. Absence of neurological deficit corresponds to 0 points.

Notes: scale items are scored in order. It is unacceptable to instruct the patient, even if this contradicts routine clinical practice. The patient's first reaction is recorded. Only the patient's actual reaction is assessed, not their (in your opinion) possible actions. All symptoms present in the patient must be noted, including those that may have arisen as a result of previous strokes.

To examine speech output, the patient is asked to describe events in a picture, name objects, and read sentences and words presented by the evaluating physician.

Appendix G18. Canadian Neurological Scale

Russian title: Canadian Neurological Scale

Original title: Canadian Neurological Scale (CNS)

Source: [64]

Type: rating scale

Purpose: for assessing the severity of neurological deficit in stroke patients

Contents:

Appendix G19. Raymond-Roy classification

Russian name: Raymond-Roy Classification

Original name: Raymond–Roy Occlusion Classification

Source: [221,449]

Type: rating scale

Purpose: to assess the degree of aneurysm occlusion

Contents:

3 degrees of aneurysm occlusion:

Grade I – complete obliteration, Grade II – residual neck,

Grade III – aneurysm fills with contrast between the coil loops or contrast freely fills part of the aneurysm dome along the wall.

Notes:

Grade I is considered a good result,

Grade II – satisfactory,

Grade III – unsatisfactory.

Appendix G20. Swallowing screening test

Russian name: Screening swallowing test

Original name: -

Source: -

Type: -

Purpose: to assess swallowing function

Contents:

"___" ____________ 20___ Time _________ Patient's Full Name ____________ Medical Record No. _____________

SWALLOWING FUNCTION ASSESSMENT

Symptoms alarming for dysphagia

PREPARATION FOR SWALLOWING ASSESSMENT

1. The patient is fully alert and actively responds when addressed □

   The patient is in a sitting position (help sit up if necessary) □

   The patient can independently control head position □

2. The patient can cough □

   The patient can manage saliva (swallows on time, no drooling) □

   The patient can breathe freely □

3. The voice is not wet or hoarse □

Appendix G21. Rehabilitation routing scale

Russian title: Rehabilitation Routing Scale (RRS)

Original title: - Rehabilitation Routing Scale 2025 [329]

Source: Union of Rehabilitologists of Russia

Type: rating scale

Purpose: to assess functional impairments and determine rehabilitation potential