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Acute Hemorrhagic Stroke

  • M. R. Rajani
  • Rajshree Deopujari
  • Shwetal Goraksha
  • Joseph Monteiro
Chapter
  • 86 Downloads

Abstract

65-year-old right-handed, male, known case of hypertension since 10 years (irregular medication) is brought to EMS with chief complaints of:

Key Points

  • ICH is a medical emergency—rapid diagnosis and emergent management of patients is important as early deterioration in the first few hours of onset is common

  • Rapid neuroimaging is essential to differentiate between acute ischemic stroke and hemorrhagic stroke. Both CT and MRI are reasonable for initial evaluation within 6 hours of bleed; CT is faster, more easily accessible, and therefore more commonly used

  • Once the diagnosis is confirmed, the main considerations are ABCs, control of elevated BP, correction of any coagulopathy, and assessing need for urgent surgical intervention

  • Although emergency ICH protocol is mainly concerned with initial evaluation and treatment, the first few days following the event are critical for maintaining a secure airway, BP and ICP control, and identification of seizures to prevent secondary brain injury.

Case Scenario

65-year-old right-handed, male, known case of hypertension since 10 years (irregular medication) is brought to EMS with chief complaints of:
  • Headache since 1 day,

  • Giddiness, inability to move left upper limb and lower limb since 6 am early morning

  • Drowsiness since 6 am

  • two episodes of vomiting

Patient was apparently alright 1 day ago when he developed a holocranial headache not responding to simple pain-killer tablet. However, he ignored it and slept off. Next morning, he woke up early with a persistent headache, giddiness, and inability to move left upper and lower limb. He gradually became drowsy over the next 3 h, and also had two episodes of projectile vomiting on his way to EMS.

No history of chest pain/breathlessness/palpitation

No history suggestive of a seizure

Past history: Known case of hypertension (HTN) 10 years. (Compliance with medicines and follow-up poor)

Personal history: Social alcohol intake; no nicotine/illicit drug abuse

Family history: HTN in father

P—90 bpm, BP—220/110 mmHg, jugular venous pressure—Normal, no carotid bruit

No pallor/icterus/edema

CNS: E2-M4-V3, right gaze preference

Pupils: bilaterally equal and reactive to light, bilateral, papilledema on fundoscopy

Motor: Moves Right upper limb (UL) and lower limb (LL) vigorously, left UL 0/5, left LL 0/5

Plantars: Flexor on right/extensor on Left

No neck stiffness

Sensory and cerebellum could not be assessed

RS – AEBE, no adventitious sound

CVS: S1, S2 normal, no murmur

Patient was taken up for CT brain which showed right gangliocapsular bleed 25 × 14 mm with a midline shift of 12 mm

Patient was admitted to ICU with BP management and underwent craniectomy on the same evening. He was discharged on Day 10 with instruction for BP management, physiotherapy, and good nursing care with a Ryles tube in situ for feeding.

10.1 Introduction

Acute intracerebral hemorrhage (ICH) results from bleeding into the brain parenchyma either spontaneously or due to secondary causes. It accounts for 20–30% [1, 2] of all strokes in India and the rest of Asia. It is the most disabling form and has a high mortality rate (40–50%) [3, 4]. The risk of intracranial hypertension, early neurological deterioration, and poor long-term outcome stress the need for aggressive early management.

Guidelines are available for the management of ICH, though there are certain variations in the degree of evidence on treatment recommendations [5, 6]. The purpose of this protocol is to emphasize initial management with the goal of optimizing recovery.

10.2 Emergency Diagnosis and Assessment

ICH is a medical emergency. Rapid diagnosis and appropriate management of patients is very important as early deterioration in the first few hours of onset is common.

10.2.1 Risk Factors

Eighty-five percent of ICH is primary (spontaneous) due to arterial hypertension (60–70%) or amyloid angiopathy (30%) [1, 3]. Secondary ICH can be related to multiple causes—smoking, drug abuse (cocaine, amphetamines), oral anticoagulants, antiplatelets, coagulopathies, arteriovenous (AVM) or cavernous malformations, intracranial tumors, cerebral vasculitis, Moya-Moya syndrome, cerebral aneurysm rupture, and secondary transformation of an arterial or venous infarct [1]. Non- modifiable risk factors include male gender, older age, and African or Asian ethnicity.

10.2.2 Clinical Presentation

Acute hemorrhagic stroke usually presents as acute onset of focal neurological deficits, headache, and vomiting. It is difficult to differentiate between ischemic stroke and hemorrhagic stroke on the basis of clinical characteristics alone, thus neuroimaging is mandatory [7, 8].

Classic symptoms:
  • Acute onset neurological deficit

  • Vomiting

  • Severe headache

  • Altered or decreased consciousness

  • Hypertension—systolic BP >220 mmHg

  • Seizures

  • Others—hemiparesis, cranial nerve palsies, sensory signs, and speech and gait abnormalities present depending on the location and extent of bleed.

10.2.3 Neuroimaging

Rapid neuroimaging is essential to differentiate acute ischemic stroke from hemorrhagic stroke.

Both CT and MRI are reasonable for initial evaluation within 6 h of bleed, but considering the time, cost, proximity to the emergency department (ED), patient tolerance, clinical status, and MRI availability, CT is commonly used as the primary modality.

CT is very sensitive for identifying acute hemorrhage and is considered as “gold standard.” Gradient echo and T2 susceptibility-weighted MRI is as sensitive for the identification of prior hemorrhage [9].

Initial non-contrast CT will help to assess the size and location of hematoma, which influences outcome and treatment. Hypertensive bleeds are commonly seen in basal ganglia, thalamus, pons (brainstem), and cerebellum. AVM bleeds or cerebral amyloid angiopathy bleeds are usually lobar in location. Another strong predictor of patient outcome is the hematoma volume assessed by ABC/2 formula [7, 10].

(A = maximum length of the hematoma along the falx (cm), B = width perpendicular to A on the same head CT slice, and C = the number of slices, starting from the point at which the temporal lobe tips became visible, multiplied by the slice thickness.)

Hematoma expansion after the initial presentation of ICH is associated with worsening of clinical outcome [5, 7].

CT angiography (CTA) and contrast study may identify patients at risk of ICH expansion based on the presence of contrast within the hematoma called as “spot sign” [7, 11]. A larger number of contrast spots suggest a high risk of expansion [11, 12].

Thus the use of a “Stroke CT” which includes non-contrast CT as well as CTA may help identify patients at risk of hematoma expansion [5, 7].

CTA, CT venography, contrast CT, contrast-enhanced MRI, MRA, MRV, DSA catheter angiography can be used for evaluating underlying structural lesions including vascular malformations and tumors when there is clinical or radiological suspicion [5].

10.3 Medical Management

10.3.1 Initial Evaluation and Primary Intervention

The initial prehospital and ED resuscitation is same across the stroke subtypes till the diagnosis is made by neuroimaging.

10.3.2 Prehospital Management

The primary focus is to manage the ABCs and rapid transport to the closest facility prepared to care for patients with acute stroke [13].

10.3.3 ED Management

As with all emergency medical care, the initial assessment of ABC is critical. Once the diagnosis of ICH is confirmed with neuroimaging, disease-specific treatment can be started (Tables 10.1 and 10.2).
Table 10.1

Intracerebral hemorrhage checklist for the first hour

Checklist

 – Complete blood count with platelets, PT, PTT, INR

 – Head imaging results: hematoma size, location

 – Glasgow Coma Scale (GCS) score

 – Calculate ICH Score

 – Interventions:

   Coagulopathy reversal

   Blood pressure lowering

   Surgical hematoma evacuation (if indicated)

   Airway/ventilation management

Table 10.2

Standardized ICH algorithm

Prehospital care

  ABCs

  Determine time of onset and circumstances

  Perform prehospital stroke screen

  Fingerstick for glucose

  Brief medical history and medication list

  Triage to stroke center

  Perform prehospital notification of pending stroke patient

ED care

  Emergent triage to high acuity area

  Perform primary assessment—ABCs

  Perform focused neurologic exam (GCS, NIHSS)

  Obtain baseline screening labs (CBC and platelet count, electrolytes, PT/INR and PTT, glucose)

  Obtain cerebrovascular imaging as soon as possible (non-con CT, stroke CT/CTA/CTP, or MRI)

  Obtain a brief medical history and medication list

After confirmation of ICH

  Reassess ABCs (consider intubation if comatose)

  Initiate blood pressure intervention (target SBP <140 mmHg)

  Quantify ICH volume (ABC/2 calculation)

  Perform the ICH score (0–6)

  Begin correction of anticoagulation as required

  Correction of antiplatelet agents as required

  Consult neurosurgery for potential hematoma evacuation or ICP monitor placement

  Admit to NeuroICU/ stroke unit (may require transfer to another hospital)

In-hospital setting

  Continue to reassess ABCs

  Continue neurologic reassessment

  ICP monitor and/or ventriculostomy for treatment of elevated ICP or hydrocephalus

  Continue management of blood pressure

  Place arterial blood pressure catheter as needed

  Place central venous catheter as needed

  Urine toxicology screen (if not already done)

  Foley catheter (needed for most ICH patients early)

  Feeding tube (goal to begin feeding within the first day)

  DVT prophylaxis with sequential compression devices (consider heparin/LWMH within the first 3 days) recheck PT/INR and PTT (or specific labs for other oral anticoagulants) if patient was coagulopathic and receiving reversal agents

  No anticonvulsant prophylaxis; treat clinical seizures; continuous EEG if level of consciousness impaired out of proportion to ICH or IVH

  Consider the need for repeat head CT

  Consider need for catheter cerebral angiography

Airway management gets priority. Supplemental oxygen should be given if SpO2 is <95% [14].

Intubation should be done to protect airways:
  • Decreased level of consciousness GCS(<8)

  • Poor airway protection

  • Impending ventilatory failure—PaO2 <60 mmHg or PaCO2 >50 mmHg

  • Signs of raised intracranial pressure (ICP)

Rapid sequence induction is done with a goal of normoventilation.

An initial assessment of patients’ condition and a quick focused neurological examination should be performed as part of the initial evaluation to assess the baseline severity of stroke.

The ICH score (Table 10.3) is the most widely used and externally validated clinical grading scale for patients with acute hemorrhagic stroke [15, 16, 17, 18, 19]. Each point increase in the ICH score is associated with an increased risk of mortality and poor functional outcome [7]. It is used as a communication tool among providers to chart the patients’ condition rather than a prognostic tool.
Table 10.3

ICH score and 30-day mortality risk

Feature

Finding

Points

ICH score

30-day mortality (%)

Glasgow Coma Scale

3–4

2

0

0

5–12

1

13–15

0

Age

≥80 years

1

1

13

<80 years

0

Location

Infratentorial

1

2

26

Supratentorial

0

ICH volume

≥30 mL

1

3

72

<30 mL

0

Intraventricular blood

Yes

1

4

97

No

0

ICH score

0–6

5

100

6

100

10.3.4 Primary Intervention

Once the diagnosis of acute ICH is confirmed, the main considerations:
  • Acute control of elevated blood pressure.

  • Correction of any coagulopathy due to medications or underlying medical conditions.

  • Assess the need for urgent surgical hematoma evacuation.

    Urgent treatment of time-sensitive issues like lowering blood pressure and reversal of coagulopathy should be initiated in ED itself, rather than waiting until transfer to an ICU, stroke unit, or another hospital. These decisions will guide further care such as transport from ED, repeat imaging, and need for ICP or EEG monitoring (Fig. 10.1).

Fig. 10.1

Management of Intracerebral hemmorrhage

10.3.5 Blood Pressure

Hypertension is commonly associated with hemorrhagic strokes because of increased ICP, premorbid hypertension, pain, and stress [16]. It is a common risk factor in older people. The commonest sites of hypertensive bleed are basal ganglia (55%), thalamus (26%), cerebral hemisphere (11%), brainstem (8%), and cerebellum (7%) [1].

Presence of hypertension influences both short-term and long-term outcomes in patients with ICH. High systolic blood pressure is associated with a higher risk of hematoma expansion either due to increased bleeding or due to elevated ICP from worsening edema [20, 21]. Cerebral and perihematomal edema are independent predictors of poor functional outcome [16, 22]. Intensive BP lowering in patients within the first 24 h after the onset of ICH has shown to reduce this edema, leading to better outcomes [23, 24].

There has been concern that acute lowering of BP could lead to ischemic brain injury in the perihematomal region, but this is not supported by recent studies [5, 25].

Blood pressure management has been remained controversial, but current studies favor rapid lowering of moderately elevated blood pressure, with the main concerns being reducing brain perfusion with lower BP, and hematoma expansion and increasing perihematomal edema among patients with increased BP [5, 6, 7].

Two trials “Intensive Blood Pressure Reduction In Acute Cerebral Hemorrhage” (INTERACT) and “Antihypertensive Treatment of Acute Cerebral Hemorrhage” (ATACH) suggested that acute lowering of SBP to <140 mmHg is safe [26, 27, 28], while INTERACT II showed better outcomes in intensive lowering of SBP to <140 mmHg, but showed no difference in hematoma expansion between two groups (standard threshold of <180 mm of Hg vs intensive threshold of <140 mmHg). ATACH 2 did not demonstrate a difference in outcome between treatment groups [21]. According to AHA stroke guidelines for ICH and European stroke guidelines, patients with SBP 150–220 mmHg, without contraindication to acute blood pressure treatment lowering of SBP to 140 mmHg is safe. But with new clinical trial results (ATACH 2), NCS recommends a target of SBP 140–180 mmHg with the specific threshold determined based on patient comorbidities and level of chronic hypertension [5, 6, 7].

Table 10.4 lists some commonly used drugs used to reduce BP in ICH. Basic principle of management of BP is that treatment should be started immediately, the drug should have a quick onset, should be easily titrated, and have minimal potential for overshoot. Beta-blockers and calcium channel blockers are commonly used. Labetalol, α and β antagonists, is given as an intravenous bolus of 5–20 mg. Nicardipine, calcium channel blocker, is given at 5 mg/h continuous infusion, titrated every 5–15 min, up to a maximum of 15 mg/h.
Table 10.4

Drugs to control BP

Drug

Standard dose

Mechanism of action

Cautions

Labetalol

10–20 mg bolus every 10 min, max 300 mg;0.5–2 mg/min infusion

Alpha and beta adrenergic receptor blocker

Bradycardia, bronchospasm, CHF, and hypotension

Enalaprilat

0.625–1.2 mgq 6 hrly IV

ACE inhibitor

Precipitous fall in BP, variable response

Nicardipine

5–15 mg/h infusion

L-type CCB

Severe AS, MI, hypotension

Esmolol

0.5 mg/kg bolus,50–300 μg/kg/min

Beta-1 antagonist

Bradycardia, CHF, bronchospasm

10.3.6 Coagulopathy

Antithrombotic medications are a risk factor (12–20%), for the occurrence of ICH, as well as for hematoma expansion [29, 30]. This incidence has increased with an aging population and the use of anticoagulant drugs for the treatment of IHD, stroke, systemic venous thromboembolism [29, 30, 31]. Vitamin K antagonists such as Warfarin is more commonly prescribed, but newer agents like dabigatran, rivaroxaban, and apixaban are increasingly being used. Coagulopathies can also occur due to underlying medical conditions like liver disease and hematological malignancies.

The second main primary intervention in ICH is to treat coagulopathy. Therefore as a part of the primary assessment, brief medical and drug history should be noted from the patient, relatives, or previous medical records especially for any antithrombotic drugs, and if possible the timing of the last dose should be noted. Urgent blood investigations including complete blood count, PT, INR, and APTT should be sent.

A general principle is that any ICH should be considered life-threatening due to the risk of hematoma expansion. Steps taken to treat coagulopathy should be based on history and lab investigations, more than size, location of hematoma, or clinical scores.

10.3.7 Reversal of Oral Anticoagulants

For patients with ICH taking vitamin K agonists such as Warfarin, rapid correction of INR (<1.4) is recommended [5, 7, 32]. Options include FFP, Vitamin K, PCC and rFVIIa (recombinant factor VIIa), although PCC is now a recommended approach [5].

PCC are highly concentrated source of clotting factors containing 3 or 4 factors of coagulation cascade (II, VII, IX, and X) with nearly 25 times the concentration of coagulation factors than FFP (I, II, V, VII, IX, X, XI, XIII, and antithrombin) that can reverse the INR in minutes, faster than FFP, with fewer cardiopulmonary complications [7, 33]. A recent randomized controlled trial has shown the superiority of PCC over FFP for faster resolution of INR and smaller hematoma expansion [34].

FFP requires thawing after cross-matching by blood bank. It takes more time than PCC, and large volume infusions (10–15 mL/kg) putting the patient at risk of volume overload, pulmonary edema, and at risk of transfusion reaction. The recent guidelines (AHA) recommend weight-based dosing for PCC (or FFP only if PCC is not available) with dose adjusted based on INR [5].

Vitamin K injection can also help resynthesize depleted clotting factors but the peak action is 24 h if liver functions are normal, and longer in compromised patients. Current guidelines recommend the use of Vitamin K 10 mg slow IV in combination with other more rapidly acting agents, but it has a longer duration of action than PCC or FFP [35].

rFVIIa has also shown to decrease hematoma growth in ICH patients without coagulopathy, but studies do not show an improved clinical outcome. It is therefore not recommended, but can be used in patients with liver failure related coagulopathy. Reversal of newer anticoagulants is more complicated. There are no randomized trials for reversal agents for newer oral anticoagulants (NOAC). Immediate drug discontinuation is needed. Activated charcoal (50 gm) can absorb NOACs, if administered within 2 h of exposure [36]. Additional administration of PCC, rFVIIa or aPCC, FEIBA (factor VIII inhibitor bypassing activity) can be considered [37].

Specific agents are available for the reversal of newer anticoagulants (Table 10.5). Hemodialysis can be tried in dabigatran (Direct thrombin inhibitor) overdose, but less for more protein bound agents like rivaroxaban, apixaban (Direct Xa inhibitor). Direct Xa inhibitors do not have specific reversal agents. The currently recommended approach is to use FEIBA or 4 factor PCC with the addition of charcoal if the last dose is within 2 h [7, 35].
Table 10.5

Newer anticoagulants and their reversal agents

Newer agents

Dose

Structure

Comment

Idarucizumab

5 gm IV bolus

Humanized monoclonal antibody

Noncompetitive binding to dabigatran. Effective against dabigatran only

Andexanet alfa

400 mg IV bolus at 30 mg/min bolus continuous infusion at 4 μg/min for 120 min

Modified recombinant derivative of human FXa, catalytically inactive

Competitive binding to direct FXa inhibitor

Aripazine/ciraparantag

25–100 mg IV bolus, single dose

Small,512 Dalton water soluble molecule

Against oral factor Xa inhibitors and DTIs, as well as UFH & LMWH, argatroban, known as universal NOAC antidote. Biomarker of activity whole blood clotting time.

DTIs Direct thrombin inhibitors, UFH unfractionated heparin, LMWH low molecular weight heparin, NOACs newer oral anticoagulants

Protamine sulfate can reverse unfractionated heparin at a dose equivalence of 1 mg for 100 U of UFH with the maximum dose of 50 mg. It is used if heparin was given within the last 2 h [5]. If the last dose of heparin was given >4 h before ICH onset, reversal is unnecessary. Protamine is also given to reverse LMWH given within the prior 8 h, however, the reversal may be incomplete.

10.3.8 Antiplatelets Induced ICH

Up to 30% of patients with symptomatic ICH give a history of antiplatelet intake. There are conflicting results about its use increasing the risk of hematoma expansion and increased risk of mortality [38]. A randomized controlled trial (PATCH study) has shown no improvements in outcome by giving platelet transfusion to patients with ICH on antiplatelet agents. On the contrary, they are associated with significantly increased risk of death and more adverse events. As per AHA guidelines [5], the usefulness of platelet transfusion in ICH patients with a history of antiplatelet use is uncertain and not recommended. However recent guidelines from NCS recommend platelet transfusion for patients on antiplatelet medication who are undergoing neurosurgical procedures [7, 35]. They also recommend a single dose of intravenous DDAVP 0.4μg/kg in these patients. Many studies have suggested that platelet dysfunction measured by platelet function assay may help in directing hemostatic interventions, reducing hematoma expansion, and improving clinical outcomes [39].

10.4 Surgical Treatment of ICH

The role of surgery for most patients with spontaneous ICH remains controversial. Theoretical benefits include prevention of brain herniation, decreasing ICP, decreasing the pathophysiological impact of the hematoma on surrounding tissue by decreasing mass effects or cellular toxicity of blood products.

10.4.1 Surgery in Supratentorial ICH

The role of surgery in the management of supratentorial ICH is a matter of debate. The STICH trial was undertaken to determine whether early surgery reduces mortality and improves neurological outcomes compared with conservative management for patients where there is uncertainty of preferred treatment. They found early surgical evacuation of supratentorial ICH was not harmful, but there was no difference in long-term mortality or functional outcome [40]. But subgroup analysis showed benefit in superficial (1 cm from the cortical surface) lobar hemorrhages with those with GCS score <8 showed poorer outcomes. STICH 2 trial compared the outcomes of early vs conservative treatment in conscious patients with superficial lobar hemorrhages (10–100 mL) with intraventricular extension within 48 h of symptom onset.

Minimally invasive techniques including endoscopic hematoma aspiration or instillation of thrombolytic agents as Urokinase or rTPA into the hematoma with aspiration of contents are also being studied but the effectiveness of these measures is uncertain [41].

According to AHA guidelines [5]:
  • Early hematoma evacuation is not beneficial compared with hematoma evacuation when patient deteriorates.

  • In deteriorating patients, surgical evacuation of hematoma might be a life saving measure.

  • Decompressive craniectomy with or without hematoma evacuation might reduce mortality for patients with supratentorial ICH who are in coma, have large hematoma with significant midline shift, or have elevated ICP refractory to medical management.

  • The effectiveness of minimally invasive clot evacuation with stereotactic or endoscopic aspiration with or without thrombolytic usage is uncertain.

10.4.2 Surgery in Infratentorial ICH

According to studies, emergency surgery is beneficial in patients with cerebellar hemorrhages who are deteriorating neurologically or who have brainstem compression and/or hydrocephalus from ventricular obstruction [5, 42, 43].

Initial treatment of the patients with ventricular drainage alone rather than surgical evacuation is not recommended [5, 6]. However, for brainstem hemorrhages, no clear guidelines exist for surgical management and are best treated conservatively. Correction of coagulopathy is very important in patients undergoing surgical hematoma evacuation.

10.5 Secondary Interventions

Although emergency ICH protocol is mainly concerned with initial evaluation and treatment, the first 24 h is critical for BP and ICP control, maintaining a secured airway, identification of seizures to prevent secondary brain injury.

10.5.1 Hospital Admission

Patients with ICH are usually medically and neurologically unstable especially within the first few days after onset. Admission to a dedicated neurological ICU or Stroke Unit is associated with lower mortality rates [5, 7]. All primary interventions such as control of airway and blood pressure, correction of coagulopathy, treatment of acute seizures should be done without any delay in the initial presenting hospital, before shifting the patient to another hospital for neurological ICU management, neuro intervention or neurosurgical procedures.

10.5.2 ICP Management

Elevated ICP is undoubtedly an important factor in ICH management. Intraventricular hemorrhage in ICH is associated with hydrocephalus and elevated ICP.

Current guidelines for ICP monitoring in ICH is similar to TBI.
  • Patients with GCS < 8 that is presumed related to large hematoma with mass effect.

  • Hydrocephalus

  • Patients with significant IVH.

  • Clinical evidence of transtentorial herniation.

An ICP <20 mmHg, MAP <130 mmHg, and CPP around 70 mmHg should be maintained depending on the status of cerebral autoregulation [39, 44].

Ventricular drainage can be considered in patients with decreased or loss of consciousness. Ventricular catheters can measure both ICP and drain CSF; therefore, they should be used in patients with hydrocephalus.

10.5.3 DVT Prophylaxis

These patients are at an increased risk for the development of DVT; current guidelines recommend use of intermittent pneumatic compression devices and elastic stockings after hospital admission, as well as initiation of LMWH or low dose unfractionated heparin within 1–4 days following onset (after documentation of cessation of bleeding) [5, 45].

10.5.4 Temperature Control

Fever in ICH could be due to infections or central causes. Duration of fever correlates with worse outcome and needs to be treated. Paracetamol in Acute Ischemic Stroke (PAIS) trial randomizing stroke patients to either paracetamol 6 g or placebo group showed improved outcomes in the paracetamol group [46].

10.5.5 Glucose Management

Avoiding both hypoglycemia and hyperglycemia is important, as this will influence the outcome [5, 47].

10.5.6 Seizures

ICH as compared to ischemic stroke can cause a higher proportion of seizures (10.6% vs. 8.6%). The majority of early seizures occur at or near the onset of ICH [48]. Cortical involvement is the most important factor. Incidence and impact of seizures on outcomes vary across different studies—30-day risk is about 8%. In a large single-center study, prophylactic anticonvulsants significantly reduced the seizure occurrence in lobar ICH [49]. However, most of the studies suggest that prophylactic anticonvulsants (esp. phenytoin) are associated with worse functional outcomes [50, 51]. Current guidelines do not recommend prophylactic anticonvulsants, although some practitioners still use a short prophylactic course (1 month) in patients with lobar ICH and those undergoing surgical hematoma evacuations [5, 7]. Acute management is with intravenous benzodiazepines such as lorazepam (0.05–0.1 mg/kg) followed by a loading dose of phenytoin (10–15 mg/kg), fosphenytoin (15–20 mg/kg), or sodium valproate (15–45 mg/kg). Levetiracetam is recommended especially in children, and is thought to be more effective for prophylaxis without suppression of cognitive abilities. (July 2011 neurocrit care) [52] Carbamazepine, lamotrigine, sodium valproate, and topiramate are also recommended first-line anticonvulsants for both focal and secondary generalized seizures. Clinical or EEG seizures in patients with a change in mental status should be treated with anticonvulsant drugs. Continuous EEG should be considered in patients with decreased level of consciousness that is disproportionate to the degree of brain injury [5, 7].

10.6 Pediatric Considerations

ICH occurs less frequently in children but can be as devastating and life-threatening. It could be traumatic or spontaneous. Vascular malformations are the most common cause, AVMs almost 50% with 5–10% mortality and 50% neurological morbidity risk. Cavernous malformations represent 20–25% of spontaneous ICH in children; the hemorrhage is usually smaller with better outcomes [53]. Other causes include bleeding diathesis, thrombocytopenias, intracranial tumors, Moya-Moya disease, cerebral venous thrombosis, and sickle cell disease. Thus during neuroimaging, CT contrast and CTA or MRA should be considered. The pediatric ICH score is slightly different from adults, taking into account the volume of hemorrhage as a percentage of total brain volume, and the presence of hydrocephalus and herniation [54]. Emergent management is similar to adults regarding ABCs. The treatment was based on the child’s presentation, the precipitating cause, and the radiological findings. It is essential to avoid hypotension (calculated as <fifth percentile, i.e. <70 mmHg + Age in years> ×2) and hypertension (maintain SBP <140 mmHg). Drugs to control BP are nicardipine and esmolol. Nicardipine 0.5 mcg/kg/min, titrated by 0.5 mcg/kg/min every 15 min to a maximum of 5 mcg/kg/min. In older children (adult weight) 2.5 mg/h, titrated by 2.5 mg/h every 15 min up to a maximum of 15 mg/h. Surgical evacuation of ICH if there is impending herniation, and same-sitting or staged surgical resection of the offending lesion is done. Coagulopathy should also be evaluated and treated in children with ICH who present with coagulation abnormalities to prevent hematoma expansion and before surgical treatment.

10.6.1 Communication

When handing over, referring or accepting a patient with ICH, following points should be noted:
  • Age

  • Hematoma volume and location

  • GCS

  • ICH Score

  • Hydrocephalus present ±

  • Blood pressure

  • Coagulation parameters and reversal treatment

  • Plan for surgery

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Copyright information

© The Editor(s) (if applicable) and The Author(s)  2020

Authors and Affiliations

  • M. R. Rajani
    • 1
  • Rajshree Deopujari
    • 1
  • Shwetal Goraksha
    • 2
  • Joseph Monteiro
    • 2
  1. 1.Jaslok Hospital and research centreMumbaiIndia
  2. 2.P D Hinduja hospital and medical research centreMumbaiIndia

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