Hypertensive intracerebral hemorrhage

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Hypertensive intracerebral hemorrhage

High blood pressure is one of the Spontaneous Intracerebral Hemorrhage Risk Factors.

Elevated blood pressure (BP), which presents in approximately 80 % of patients with acute intracerebral hemorrhage (ICH), is associated with an increased risk of poor outcomes. Edit

Clinical features

Patients will present depending on the region and size of the hemorrhage:

Basal ganglia hemorrhage clinical features.

Thalamic hemorrhage clinical features.

Pontine hemorrhage clinical features

Cerebellar hemorrhage clinical features Edit

Pathology

The pathology of hypertensive ICH involves several steps:

Hypertension: The sustained high blood pressure causes damage to small blood vessels in the brain, leading to weakening and thickening of their walls. This makes them more susceptible to rupture.

Rupture: When the blood vessel ruptures, blood leaks into the surrounding brain tissue, causing inflammation and damage to brain cells.

Hematoma formation: The leaked blood accumulates and forms a hematoma, which can put pressure on surrounding brain tissue, causing further damage.

Edema: The inflammation caused by the presence of blood in the brain tissue can lead to swelling, called edema, which can worsen the pressure on the brain tissue.

Secondary injury: The pressure and inflammation caused by the hematoma and edema can lead to secondary injury to the brain tissue, which can cause further neurological deficits.

Microaneurysms of perforating arteries (Charcot-Bouchard aneurysms)

small (0.3-0.9 mm) diameter

occur on small (0.1-0.3 mm) diameter arteries

distribution matches the incidence of hypertensive hemorrhages

80% lenticulostriate

10% pons

10% cerebellum

found in hypertensive patients

may thrombose, leak (cerebral microhemorrhages), or rupture

accelerated atherosclerosis: affects larger vessels

hyaline arteriosclerosis

hyperplastic arteriosclerosis: seen in very elevated and protracted cases

Lenticulostriate artery are particularly susceptible to damage from hypertension. They may either rupture, producing an intracerebral hemorrhage that is initially centered in the region they supply, or become occluded producing a lacunar infarct in the tissue they supply. Edit

Guidelines

Chinese multidisciplinary guideline for the management of hypertensive intracerebral hemorrhage 1). Edit

Treatment

Hypertensive intracerebral hemorrhage treatment Edit

Outcome

Characteristics of hypertensive hemorrhages that lead to poorer prognosis include :

bleed in the posterior fossa

a large amount of mass effect

extension into the ventricular system —-

Optimal recovery from intracerebral hemorrhage was observed in hypertensive patients who achieved the greatest SBP reductions (≥20 mm Hg) in the first hour and maintained for 7 days 2).

Hematomas within the basal ganglia comprise 60% of all cases with hypertensive intracerebral hemorrhage, and these cases have a particularly high morbidity and mortality despite optimized treatments 3).

Dennis MS et al. have reported that the one-year survival rate of patients with these hematomas is only 38% 4) and that most survivors are disabled 5).

see putaminal hemorrhage Edit

Case series

Clinical data of 184 patients with HICH in the hospital from January 2019 to May 2021 were analyzed retrospectively. The patients were divided into mini-open craniotomy group and neuroendoscopic-assisted group. The operation time, hematoma clearance rate, intraoperative blood loss, neurological function recovery, and postoperative mortality of the two groups were compared by retrospective analysis.

Results: The operation time and intraoperative blood loss in the mini-open craniotomy group were more than those in the neuroendoscopic-assisted group, but there was no significant difference between the two groups. There was no significant difference in hematoma clearance rate between the two groups, but for the rugby hematoma, the hematoma clearance rate in the neuroendoscopic-assisted group was higher than in the mini-open craniotomy group, the difference was statistically significant. Within 1 month after the operation, there was no significant difference in mortality between the two groups. 6 months after the operation, there was no significant difference in the recovery of neurological function between the two groups.

Conclusion: Neuroendoscopic-assisted and mini-open craniotomy for the treatment of HICH has the advantages of minimal trauma with good effects, and its main reason for short operation time, reduced bleeding, and high hematoma clearance rate. Although the two surgical methods can improve the survival rate of patients, they do not change the prognosis of patients. Therefore, the choice of surgical methods should be adopted based on the patient’s clinical manifestations, hematoma volume, hematoma type, and the experience of the surgeon 6).

From February 2013 to November 2018, 60 patients diagnosed as basal ganglia ICH were divided into the filled type hematoma expansion group (FTE group) and the expanded type hematoma expansion group (ETE group). we performed follow-up CT and three-dimensional reconstruction for the patients and compared the hematoma before and after the expansion of size and extent.

The regression analysis showed that the irregular sign (odds ratio, 3.64; 95 % CI, 1.46-9.12), black hole sign (odds ratio, 3.85; 95 % CI, 1.40-10.60), blend sign (odds ratio, 2.86; 95 % CI, 1.03-7.95), and early use of dehydration (odds ratio, 4.59; 95 % CI, 1.59-13.19) were possible risk factors for the ETE group, while the high systolic blood pressure (odds ratio, 1.51; 95 % CI, 1.04-2.30), early use of dehydration (odds ratio, 3.27; 95 % CI, 1.10-9.69) and low density low-density band (odds ratio, 4.52; 95 % CI, 1.54-13.28) were possible risk factors for the FTE group.

The irregular sign, black hole sign, blend sign and early use of dehydration may be the main risk factors for hematoma expansion group, whereas early use of dehydration, high systolic blood pressure, and low-density band may be the main risk factors for hematoma expansion 7).

96 HIH patients were performed the craniotomic hematoma dissection (CHD) and the hematoma-cavity drilling drainage (HCDD), respectively. Meanwhile, the intracranial pressure and mean arterial pressure of each patient were continuously monitored for 7 days, the postoperative 1st, 3rd, 7th and 14th-day average flow velocities and pulsatility indexes of the bilateral middle cerebral arteries were monitored. CHD exhibited the significant difference in the long-term quality of life (ADL classification 6 months later) of patients with hematoma >50 ml than HCDD; furthermore, the postoperative 1st, 3rd, 7th and 14th-day TCD parameter analysis revealed that CHD exhibited better results in relieving the intracranial pressure and improving the cerebral blood flow than HCDD, and the postoperative ICP and MAP monitoring towards all patients could effectively control the blood pressure and prevent the further bleeding. The patients with hematoma >50 ml should choose CHD, and all HIH patients should be routinely performed the ICP and MAP monitoring 8). Edit

1) 

Yu Z, Tao C, Xiao A, Wu C, Fu M, Dong W, Liu M, Yu X, You C. Chinese multidisciplinary guideline for management of hypertensive intracerebral hemorrhage. Chin Med J (Engl). 2022 Oct 31. doi: 10.1097/CM9.0000000000001976. Epub ahead of print. PMID: 36315009.

2) 

Wang X, Arima H, Heeley E, Delcourt C, Huang Y, Wang J, Stapf C, Robinson T, Woodward M, Chalmers J, Anderson CS. Magnitude of Blood Pressure Reduction and Clinical Outcomes in Acute Intracerebral Hemorrhage: Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trial Study. Hypertension. 2015 Mar 23. pii: HYPERTENSIONAHA.114.05044. [Epub ahead of print] PubMed PMID: 25801872.

3) 

Waga S, Miyazaki M, Okada M, Tochio H, Matsushima, Tanaka Y. Hypertensive putaminal hemorrhage: analysis of 182 patients. SurgNeurol. 1986;14:159–166.

4) 

Dennis MS, Burn JP, Sandercock PA, Bamford JM, Wade DT, Warlow CP. Long-term survival after first-ever stroke: the Oxfordshire Community Stroke Project. Stroke. 1993;14:796–800. doi: 10.1161/01.STR.24.6.796.

5) 

Houguang Z, Yu Z, Ling L, Xu H, Yinghong T, Yuping T, Wei H, Jianzhong X, Qiang D. A prospective controlled study: minimally invasive stereotactic puncture therapy versus conventional craniotomy in the treatment of acute intracerebral hemorrhage. BMC Neurol. 2011;14:76. doi: 10.1186/1471-2377-11-76.

6) 

Lu W, Wang H, Feng K, He B, Jia D. Neuroendoscopic-assisted versus mini-open craniotomy for hypertensive intracerebral hemorrhage: a retrospective analysis. BMC Surg. 2022 May 14;22(1):188. doi: 10.1186/s12893-022-01642-8. PMID: 35568858.

7) 

Wei L, Lin C, Zhou Z, Zhang J, Tan Q, Zhang Y, Zhang B, Ye D, Wu L, Liu Q, Xian J, Chen Z, Feng H, Zhu G. Analysis of different hematoma expansion shapes caused by different risk factors in patients with hypertensive intracerebral hemorrhage. Clin Neurol Neurosurg. 2020 Apr 12;194:105820. doi: 10.1016/j.clineuro.2020.105820. [Epub ahead of print] PubMed PMID: 32315941.

8) 

Liu Z, Chen Q, Tian D, Wang L, Liu B, Zhang S. Clinical significance of dynamic monitoring by transcranial doppler ultrasound and intracranial pressure monitor after surgery of hypertensive intracerebral hemorrhage. Int J Clin Exp Med. 2015 Jul 15;8(7):11456-11462. eCollection 2015. PubMed PMID: 26379963.