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Intracerebral Hemorrhage (ICH) - What to know

Etiology

As far as the non-traumatic ICH there are several etiologies:

  • hypertension
  • cerebral amyloid angiopathy (most important cause of ICH in elderly)
  • vascular malformations (most important cause of ICH in children)
  • hemorrhagic infarction (also venous sinus thrombosis)
  • ruptured saccular aneurysm

Other etiologies

Other causes: brain tumors, bleeding disorders, CNS infections, vasculitis and drugs

 

Risk Factors

  • hypertension
  • older age
  • alcoholism
  • black ethnicity (interact with the age)
  • lower cholesterol and lower LDL cholesterol
  • lower triglycerides
  • street drugs (cocaine, amphetamine) 

 

Pathogenesis

The hypertension has effects on penetrating vessels because they branch off from the intracerebral vessels with a 90° angle: so the high pressure is transmitted rapidly distally without a gradual increase. If this situation is perpetuated for very long time (chronic hypertension), the arteries could be predisposed to the rupture of their wall: this situation is called “pseudoaneurysm” and account for a small quantitative of blood in the hemorrhage (so it causes a subclinical leaks of blood).

If the patient suffers for a bleeding disorder the hemorrhage doesn’t’ stop and a severe ICH occurs. The site of the microscopic bleed is different according to the etiology: hypertensive microbleeds arise from the deep subcortical and infratentorial regions, amyloid microbleeds arise in superficial lobar regions. 

Histology

The arteries involved in chronic hypertension develop intimal hyperplasia and hyalinosis that predispose to their rupture.

Prevalence of microbleeds

Note that the prevalence of pseudoaneurysm (or microbleeds) is 5% in healthy adults, 34% in patients with ischemic stroke and 60% in patients with non-traumatic ICH. The prevalence is higher in male and in the elderly.

Common sites

The vessels where the micro bleeding occur, supply the pons and midbrain (branch of the basilar artery) but also the thalamus (thalamostriate branches of P1 and P2), putamen and caudate (lenticulostriate branches of M1). Putamenal hemorrhage occurs in 35% of cases, subcortical hemorrhage in 30%, cerebellar hemorrhage in 16%, thalamic hemorrhage in 15% and pontine hemorrhage in 5-12% of cases.

 

Pathophysiology

After a ICH occurs, there is the formation and expansion of a blood clot and the brain is damaged firstly because of the mechanical injury.

In the area surrounding the lesion there is a perilesional edema that is rich of cytotoxic molecules.

Both the edema and the blood clot contribute to generate mass effect and to increase the intracranial pressure (ICP). As a consequence, the cerebral perfusion was reduced causing an ischemic injury. If the ICP raise to higher levels a cerebral herniation develops.  

Enlargement of ICH

Note that in the first six hours the ICH could enlarge:

  • the blood clot stretches the vessels around the lesion leading to the rupture. Several molecules (metalloproteinase, il-6 etc.) are involved in this process.
  • the hemorrhage grows until the pressure generated on the artery equals the systolic blood pressure

 

Clinical Presentation

Note that the symptoms don’t begin abruptly (like in SAH) but they increase during minutes or in a few hours.

Most of the ICH occurs during the normal people activity.

Most frequent symptoms and signs

  • headache: due to meningeal retraction, blood in CSF or increase in ICP
  • vomiting
  • decrease of the level of consciousness

Note that in small ICH these symptoms are less common.

Less frequent symptoms and signs

  • stiff neck and meningismus if there is blood in ventricles
  • stupor or coma: inauspicious signs with the exception of the thalamic hemorrhage
  • seizures: in 4-29% of the cases
  • ECG abnormalities: prolonged QT, depressed ST, flat or inverted or tall and peaked T waves, U waves

Symptoms and signs according to the site

  • Putaminal hemorrhage. Spread of the hemorrhage occurs along the white matter fier tracts causing:
    • Hemiplegia
    • Hemisensory loss
    • Homonymus hemianopsia
    • Gaze palsy
    • Stupor and coma
  • Lobar hemorrhage. The neurological signs depend upon the location. More frequently the hemorrhage occurs in the parietal and occipital lobes.
    • Contralateral homonymous hemianopsia if the occipital lobe is involved
    • Seizures
    • Controlateral plegia or paresis of the leg; relative sparing of the arm if the frontal lobe is involved
  • Cerebellar hemorrhage. Usually they origin in the dentate nucleus then they extend in the hemisphere and involved the fourth ventricle. Note that there isn’t hemiparesis.
    • Imbalance and inability to walk
    • Vomiting
    • Headache (referreto to the shoulder, neck or occipital region)
    • Neck stiffness
    • Gaze palsy
    • Facial weakness
    • Stupor for brainstem compression
  • Thalamic hemorrhage. This type of hemorrhage could expand in the posterior limb of the internal capsule, downward pressing the tectum of the midbrain or it could expand in the third ventricle.
    • Hemiparesis
    • Hemisensory loss
    • Transient homonimus hemianopsia (occasionally)
    • Upgaze palsy with miotic and unreactive pupils
    • Pupils peering at the nose, distorted
    • “wrog way eyes” directed to the weak side
    • aphasia if the dominant hemisphere is involved
    • neglect if the non-dominant hemisphere is involved
  • Pontine hemorrhage. Hemorrhage at the base of the pons
    • coma due to a disruption of the reticular activating system
    • total paralysis
    • “pinpoint” pupils
    • horizontal eye
    • movements absent

 

Diagnosis

If there is a suspect of intracerebral hemorrhage, there are two different strumental tests:

Head CT

  • Hyeracute hemorrhage: hyperdense (unless the patient is anemic, in this case is isodense)
  • Subacute: isodense with ring enhancement
  • Chronic hemorrhage: hypodense

Head MRI

The appearance on MRI depends upon both the paramagnetic properties of the haemoglobin and the mode of the acquisition.

  • Hyperacute hemorrhage: within the first six hours. The radiological finding are created by the deoxyhemoglobin.
    • Center: isointense or hyperintese on T2. After two hours the center could disappear because of the compression of the periphery
    • Pheriphery: hypointense or dark on T2
    • Rim: hypointense on T1 and hyperintense on T2. It represent the vasogenic edema.
  • Subacute: hyperintense in the periphery on T1 because of methemoglobin, dark and only later hyperintense on T2
  • Chronic: the macrophages produce hemosiderin. Hypointense on both T1 and T2

 

References

Meretoja A, Strbian D, Putaala J, et al. SMASH-U: a proposal for etiologic classification of intracerebral hemorrhage. Stroke 2012; 43:2592.

Balami JS, Buchan AM. Complications of intracerebral haemorrhage. Lancet Neurol 2012; 11:101.

Mendelow AD. Mechanisms of ischemic brain damage with intracerebral hemorrhage. Stroke 1993; 24:I115.

Prabhakaran S, Naidech AM. Ischemic brain injury after intracerebral hemorrhage: a critical review. Stroke 2012; 43:2258.

Gebel JM, Broderick JP. Intracerebral hemorrhage. Neurol Clin 2000; 18:419.

Ariesen MJ, Claus SP, Rinkel GJ, Algra A. Risk factors for intracerebral hemorrhage in the general population: a systematic review. Stroke 2003; 34:2060.

Faught E, Peters D, Bartolucci A, et al. Seizures after primary intracerebral hemorrhage. Neurology 1989; 39:1089.

Kidwell CS, Wintermark M. Imaging of intracranial haemorrhage. Lancet Neurol 2008; 7:256.

Kidwell CS, Chalela JA, Saver JL, et al. Comparison of MRI and CT for detection of acute intracerebral hemorrhage. JAMA 2004; 292:1823.

Schlunk F, Greenberg SM. The Pathophysiology of Intracerebral Hemorrhage Formation and Expansion. Transl Stroke Res. 2015 Aug;6(4)

Mark S. Greenberg, Handbook of Neurosurgery, Thieme.

 

Authors

 

Giorgio Saraceno, MS

University of Brescia (Italy) 
Scientific Team UpSurgeOn

 

Giannantonio Spena, MD

University of Brescia
"Spedali Civili" Hospital Brescia (Italy)
Scientific Team UpSurgeOn