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Wednesday, July 22, 2020

INTRACRANIAL HEMORRHAGE- causes, medical and surgical treatment



The pathological accumulation of the blood within the cranial vault may occur within brain parenchyma or the surrounding meningeal spaces. Intracerebral haemorrhage accounts for 8-13% of all strokes and results from a wide spectrum of disorders. Intracerebral haemorrhage is more likely to result in death or major disability than ischemic stroke or subarachnoid haemorrhage. Intracerebral haemorrhage and accompanying oedema may disrupt or compress adjacent brain tissues, leading to neurological dysfunction. Substantial displacement of brain parenchyma may cause elevation of intracranial pressure (ICP) potentially fatal herniation syndromes.

  • Hypertension 
  • Arterio-venous malformation
  • Aneurysmal rupture
  • Intracranial neoplasm
  • Coagulopathy
  • Hemorrhagic transformation of ischemic infarct
  • Cerebral venous thrombosis
  • Sympathomimetic drug abuse
  • Sickle cell disease
  • Vasculitis
  • Trauma

History: Onset of symptoms of intracerebral haemorrhage is usually during daytime activity, with the progressive development of the following
  • Alteration in the level of consciousness 
  • Nausea and vomiting 
  • Headache
  • Seizures
  • Focal neurological deficits
Physical: Clinical manifestation of intracranial haemorrhage is determined by the size and the location of haemorrhage but may include the following;
  • Hypertension, fever, or cardiac arrhythmia's
  • Nuchal rigidity
  • Retinal haemorrhage
  • Altered level of consciousness 
  • Focal neurological deficits
    • Putamen: Contra-lateral hemiparesis, contralateral sensory loss, contralateral conjugate gaze paresis, homonymous hemianopia,  aphasia, or apraxia
    • Thalamus: Contralateral sensory loss, contralateral hemiparesis, gaze paresis, homonymous hemianopia, miosis, aphasia, or confusion.
    • Lobur: Contralateral hemiparesis or sensory loss, contralateral conjugate gaze paresis, homonymous hemianopia, abulia, aphasia or apraxia
    • Caudate nucleus: Contralateral hemiparesis, contralateral conjugate gaze paresis, or confusion
    • Brain stem: Quadriparesis, facial weakness, decreased level of consciousness, gaze paresis, ocular bobbing, miosis, or autonomic instability
    • Cerebellum: Ataxia, ipsilateral facial weakness, ipsilateral sensory loss, gaze paresis, skew deviation, miosis, or decreased level of consciousness
  • Complete blood count (CBC): Monitor for infection and assess hematocrit and platelet count to identify hemorrhagic risk and complications.
  • Prothrombin time (PT)/activated partial thromboplastin time (aPTT): identify coagulopathy.
  • Serum chemistries including electrolytes and osmolarity: Asses for metabolic derangements, such as hyponatremia, and monitor osmolarity for the guidance of osmotic diuresis.
  • Toxicology screen and serum alcohol level if illicit drug use or excessive alcohol intake is suspected. Identify exogenous toxins that can cause intracerebral hemorrhage
  • Screening for hematologic, infectious, and vasculitic etiologies in the select patient: Selective testing for more uncommon causes of intracerebral haemorrhage.
  • CT scan: readily demonstrate acute haemorrhage as hyperdense signal intensity. Multifocal haemorrhage at the frontal, temporal, or occipital poles suggests a traumatic etiology.
  • MRI: appearance of haemorrhage on conventional T1 and T2 sequences evolves over time because of chemical and physical changes within and around the hematoma.
  • CT angiography: Permits screening of large and medium-sized vessels of AVMs, vasculitis, and other arteriopathies.
  • MR angiography: permits screening of large and medium-sized vessels for AVMs, vasculitis and other arteriopathies.
  • CONVENTIONAL CATHETER ANGIOGRAPHY: Definitively assesses large, medium-sized, and sizable small vessels for AVMs, vasculitis and other arteriopathies. Consider catheter angiography for young patients, patients with lobar haemorrhage, patients without a history of hypertension, and patient without a clear cause of haemorrhage who are surgical candidates. Angiography may be deferred for older patients with suspected hypertensive intracerebral haemorrhage and patient who do not have any structural abnormalities on CT scan MRI. Timing of angioplasty depends on clinical status and neurological consideration

VENTRICULOSTOMY: allows for external ventricular drainage in patients with the intraventricular extension of blood products Intraventricular administration of thrombolytic may assist clot removal.


Medical therapy of intracranial haemorrhage is principally focused on adjunctive measure to minimize injury and to stabilize individuals in the perioperative phase.
  • Perform endotracheal intubation of patients with decreased level of consciousness and poor airway protection
  • Cautiously lower blood pressure to a mean arterial pressure (MAP) less than 130 mm Ug, but avoid excessive hypotension. Early treatment in patients presenting with spontaneous intracerebral haemorrhage is important as it may decrease hematoma enlargement and lead to better neurologic outcome.
  • Rapidly stabilize vital signs, and simultaneously acquire emergent CT scan.
  • Intubate and hyperventilate if intracranial pressure is increased; initial administration of mannitol for further control.
  • Maintain euvolemia, using normotonic rather than hypertonic fluids, to maintain brain perfusion without exacerbating brain edema.
  • Avoid hyperthermia.
  • Correct any identifiable coagulopathy with fresh frozen plasma, vitamin K, protamine, or platelet transfusion.
  • Initiate fosphenytoin or their anticonvulsant definitely for seizure activity or lobar haemorrhage, and optionally in other patients.

Antihypertensive agents reduce blood pressure to prevent exacerbation of intracranial haemorrhage. Osmotic diuretics, such as mannitol, may be used to decrease intracranial pressure. As hyperthermia may exacerbate neurological injury, paracetamol may be given to reduce fever and to relieve headache. Anticonvulsant phenytoin is used routinely to avoid seizure that may be induced by cortical damage. Vitamin K and protamine may be used to restore normal coagulation parameters. Antacids are used to prevent gastric ulcers associated with intracerebral haemorrhage.

  • Consider nonsurgical management for patient with minimal neurological deficits or with intracerebral haemorrhage volumes less than 10 mL.
  • Consider surgery for patients with cerebellar haemorrhage greater than 2.5 cm, for patients with intracerebral haemorrhage associated with a structural vascular lesion, and for young patients with lobar haemorrhage.
Other surgical considerations include the following.
  • Clinical course and timings
  • Elevation of ICP from hydrocephalus
  • Patients age and comorbid conditions
  • Etiology
  • Location of the hematoma
  • Mass effect and drainage patterns
Surgical approaches include the following
  • Craniotomy and clot evacuation under direct visual guidance
  • Stereotactic aspiration with thrombolytic agents
  • Endoscopic evacuation

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