Intracerebral hemorrhage overview

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Classification

Pathophysiology

Causes

Differentiating Stroke from other Diseases

Epidemiology and Demographics

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Natural History, Complications and Prognosis

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Emergency Diagnosis and Assessment

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

CT

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Early Assessment

Management

Surgery

Primary Prevention

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Mehrsefat, M.D. [2]

Overview

Intracerebral hemorrhage (ICH) is bleeding directly into the brain tissue and based on the location and size of the bleeding, it may be classified into intraparenchymal hemorrhage, Intraventricular hemorrhage, and cerebral microbleeds.[1][2][3] Intracerebral hemorrhage (ICH) usually results from the rupture of small penetrating arteries in the brain near the bifurcation of affected arterioles.[4][5] It is thought that ICH may result in brain injury by decreasing blood flow into the area surrounding the clot and causing neuronal ischemia or by overexertion of matrix metalloproteinases (MMPs), which may result in the breakdown of the blood brain barrier and edema.[6][7] The two major causes of intracerebral hemorrhage include long-standing hypertension and cerebral amyloid angiopathy.[8][9][10]

Intracerebral hemorrhage is a medical emergency requiring urgent diagnosis and treatment. If left untreated, it may result in irreversible brain tissue damage. causing permanent neurological deficit and death.[11][12] Hematoma expansion and early deterioration are common within the first few hours after onset. CT and magnetic resonance imaging (MRI) are both reasonable for initial evaluation.[13] Spontaneous intracerebral hemorrhage (ICH) remains a significant cause of morbidity and mortality throughout the world. However, the excellent medical care has a potent, direct impact on spontaneous intracerebral hemorrhage (ICH) morbidity and mortality.[14] Prevention of intracerebral hemorrhage is mainly aimed at treatment and modifcation of risk factors which are directly associated with increased occurrence of intracerebral hemorrhage.[15]

Classification

Intracerebral hemorrhage is bleeding within the brain itself. This category includes:[1][2][3]

 
 
 
 
 
 
 
 
Intracerebral bleeding
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Intraparenchymal hemorrhage
 
 
 
 
Intraventricular hemorrhage
 
 
 
 
Cerebral microbleeds


Pathophysiology

Intracerebral hemorrhage (ICH) is bleeding directly into the brain tissue and usually results from rupture of small penetrating arteries in the brain. Degenerative changes in the vessel wall may be associated with advancing age, chronic HTN, diabetes, and other vascular risk factor and It usually occurs at or near the bifurcation of affected arterioles.[4][5] The exact cause of brain damage following intracerebral hemorrhage is unknown. It is thought that ICH may result in brain injury by decreasing blood flow into the area surrounding the clot and causing neuronal ischemia or by overexertion of matrix metalloproteinases (MMPs), which may result in the breakdown of the blood brain barrier and edema.[6][7]

Causes

The two major causes of intracerebral hemorrhage include long-standing hypertension and cerebral amyloid angiopathy.[8][9][10][16][17][18] Other causes of intracerebral hemorrhage include vascular malformations (arteriovenous malformations (AVMs)) aneurysms, drugs (cocaineamphetamines), and vasculitis.[8][9]

Differential diagnosis

Differential diagnosis of intracerebral hemorrhage may include ischemic stroke, SAH, TIA, acute hypertensive crisis, sentinel headache, sinusitis, hypoglycemia, cerebral venous thrombosis, spontaneous intracranial hypotension, and reversible cerebral vasoconstriction syndrome.[19][20][21][22][23] It is clinically difficult to distinguish ICH or subarchnoid hemorrhage (SAH) from an ischemic stroke. However, the symptoms like headache, nausea, vomiting, and depressed level of consciousness should raise the suspicion for a hemorrhagic event compared to ischemic stroke.[24][25]

Epidemiology

The overall incidence of intracerebral hemorrhage (ICH) ranges from 12 to 31 per 100,000 population.[26] The incidence of intracerebral hemorrhage gets doubled every 10 years after age 35 every, but the prevalence and incidence does not vary by gender.[27][28] The incidence of intracerebral hemorrhage is the highest in Asians.[29]

Risk factors

Common risk factors in the development of intracerebral hemorrhage (ICH) include hypertension, anticoagulation medication(warfarin), acquired or congenital coagulation factor disorder (such as vitamin K deficiency, liver disease, disseminated Intravascular Coagulation (DIC), and hemophilias), platelet abnormalities, embolic strokes, and Sickle Cell Anemia.[30][31][32][33]

Natural history, Complications, and Prognosis

Intracerebral hemorrhage is a medical emergency requiring urgent diagnosis and treatment. If left untreated, it may result in irreversible brain tissue damage. causing permanent neurological deficit and death.[11][12] The most common complications following intracerebral hemorrhage (ICH) include hematoma expansion, venous thromboembolism (VTE), pneumonia, apiration, respiratory failure/distress pulmonary embolism, sepsis, neurogenic pulmonary edema, acute respiratory distress syndrome, and acute kidney injury.[34][35][36]

Despite aggressive and newer management strategies, the prognosis of patients with intracerebral hemorrhage is very poor. The main powerful predictor of 30-day mortality and morbidity in patients with spontaneous intracerebral hemorrhage is a volume of hemorrhage in combination with the initial Glasgow Coma Scale score (GCS).[37][38]

Diagnosis

Emergency diagnosis and assessment

Intracerebral hemorrhage is a medical emergency, characterized by high morbidity and mortality, which should be promptly diagnosed and aggressively managed. Hematoma expansion and early deterioration are common within the first few hours after onset. CT and magnetic resonance imaging (MRI) are both reasonable for initial evaluation.[13]

History and Symptoms

It is critical to obtain a detailed and focused history in patient with intracerebral hemorrhage. History of gradual onset of symptoms,Vomiting, hypertension, lipid disorders, smoking, antiplatlete/anticoagulation medication, or illicit drug use, dementia, liver, and chronic kidney disease may suggest intracerebral hemorrhage as one of the initial differential diagnosis..[1][2][3][4][5][6]

Physical examination

Physical examination of patients with Intracerebral hemorrhage usually varies based on the location of the bleeding.[39] Physical examination of patients with intracerebral hemorrhage should include vital signs check and assessment of level of consciousness (GCS) and the severity of the neurological defect (NIHSS).[40][41]

Laboratory findings

Routine laboratory studies in patient with intracerebral hemorrhage should include complete blood count (CBC) with platelets,electrolytes, renal function, coagulation studies (prothrombin time (PT), partial thromboplastin time (PTT), and INR), toxicology screen, blood glucose level, and pregnancy test in women of childbearing age.[1][2][3][4][5][6]

Electrocardiogram

Following intracerebral hemorrhage and secondary to catecholamines release following posterior hypothalamus hypoperfusion, the EKG changes may show changes which is a reflection of left ventricular ischemia. Additionally, brainstem compression may result in ventricular arrhythmias.[42][43]

CT

CT is very sensitive for identifying acute hemorrhage and is considered the gold standard.[44][45]

MRI

MRI is better than CT for detection of acute and chronic hemorrhage. Therefore it should be the preferred test for accurate diagnosis of patients with suspected intracerebral hemorrhage.[46]

Other imaging findings

Other imaging findings in diagnosis of intracerebral hemorrhage may include CT angiography (CTA), CT venography (CTV), MR angiography (MRA), MR venography (MRV), and ctheter angiogram.[47][48]

Treatment

Early assessment

Intracerebral hemorrhage (ICH) is a medical emergency. Rapid diagnosis and management is crucial because early deterioration is common in the first few hours after ICH onset.[49]

Management

Spontaneous intracerebral hemorrhage (ICH) remains a significant cause of morbidity and mortality throughout the world. However, the excellent medical care has a potent, direct impact on spontaneous intracerebral hemorrhage (ICH) morbidity and mortality.[14] The non-surgical management of intracerebral hemorrhage is mainly directed to hemostasis/coagulopathy management, blood pressure (BP) management, glucose/temperature/seizure management, and other medical complications and procedures, including management of intracranial pressure (ICP) and intraventricular hemorrhage.[50]

For AHA/ASA guidelines for the management of ICH, please click here

Surgery

The indications for surgery in patients with Intracerebral hemorrhage vary with the site of the bleed. Open craniotomy is the most widely studied surgical techniques in patients with supratentorial ICH.[51][52] Recently, several studies have shown minimally invasive aspiration associated with better outcomes with less invasive approaches compared to standard craniotomies.[53][54][55]

Primary prevention

Primary prevention of intracerebral hemorrhage is mainly aimed at treatment and modifcation of risk factors which are directly associated with increased occurrence of intracerebral hemorrhage.[15]

Secondary prevention

Effective measures for the secondary prevention of intracerebral hemorrhage include life style modification, treatment of modifiable risk factors such as blood pressure control and anticoagulation medication avoidance, and enforcing the measures to prevent the complications.[56][15][57][58][59][60][61]

References

  1. ↑ 1.0 1.1 Caplan LR (1992). "Intracerebral hemorrhage". Lancet. 339 (8794): 656–8. PMID 1347346.
  2. ↑ 2.0 2.1 van Asch CJ, Velthuis BK, Greving JP, van Laar PJ, Rinkel GJ, Algra A; et al. (2013). "External validation of the secondary intracerebral hemorrhage score in The Netherlands". Stroke. 44 (10): 2904–6. doi:10.1161/STROKEAHA.113.002386. PMID 23920015.
  3. ↑ 3.0 3.1 Liu W, Liu R, Sun W, Peng Q, Zhang W, Xu E; et al. (2012). "Different impacts of blood pressure variability on the progression of cerebral microbleeds and white matter lesions". Stroke. 43 (11): 2916–22. doi:10.1161/STROKEAHA.112.658369. PMID 22949472.
  4. ↑ 4.0 4.1 Qureshi AI, Tuhrim S, Broderick JP, Batjer HH, Hondo H, Hanley DF (2001). "Spontaneous intracerebral hemorrhage". N Engl J Med. 344 (19): 1450–60. doi:10.1056/NEJM200105103441907. PMID 11346811.
  5. ↑ 5.0 5.1 Fisher CM (1971). "Pathological observations in hypertensive cerebral hemorrhage". J Neuropathol Exp Neurol. 30 (3): 536–50. PMID 4105427.
  6. ↑ 6.0 6.1 Lee KR, Kawai N, Kim S, Sagher O, Hoff JT (1997). "Mechanisms of edema formation after intracerebral hemorrhage: effects of thrombin on cerebral blood flow, blood-brain barrier permeability, and cell survival in a rat model". J Neurosurg. 86 (2): 272–8. doi:10.3171/jns.1997.86.2.0272. PMID 9010429.
  7. ↑ 7.0 7.1 Mendelow AD (1993). "Mechanisms of ischemic brain damage with intracerebral hemorrhage". Stroke. 24 (12 Suppl): I115–7, discussion I118-9. PMID 8249006.
  8. ↑ 8.0 8.1 8.2 Meretoja A, Strbian D, Putaala J, Curtze S, Haapaniemi E, Mustanoja S; et al. (2012). "SMASH-U: a proposal for etiologic classification of intracerebral hemorrhage". Stroke. 43 (10): 2592–7. doi:10.1161/STROKEAHA.112.661603. PMID 22858729.
  9. ↑ 9.0 9.1 9.2 Hart, Robert G., Bradley S. Boop, and David C. Anderson. "Oral anticoagulants and intracranial hemorrhage facts and hypotheses." Stroke 26.8 (1995): 1471-1477.
  10. ↑ 10.0 10.1 Knudsen, Katherine A., et al. "Clinical diagnosis of cerebral amyloid angiopathy: validation of the Boston criteria." Neurology 56.4 (2001): 537-539.
  11. ↑ 11.0 11.1 Caplan LR (1992). "Intracerebral hemorrhage". Lancet. 339 (8794): 656–8. PMID 1347346.
  12. ↑ 12.0 12.1 van Asch CJ, Velthuis BK, Greving JP, van Laar PJ, Rinkel GJ, Algra A; et al. (2013). "External validation of the secondary intracerebral hemorrhage score in The Netherlands". Stroke. 44 (10): 2904–6. doi:10.1161/STROKEAHA.113.002386. PMID 23920015.
  13. ↑ 13.0 13.1 Chalela JA, Kidwell CS, Nentwich LM, Luby M, Butman JA, Demchuk AM; et al. (2007). "Magnetic resonance imaging and computed tomography in emergency assessment of patients with suspected acute stroke: a prospective comparison". Lancet. 369 (9558): 293–8. doi:10.1016/S0140-6736(07)60151-2. PMC 1859855. PMID 17258669.
  14. ↑ 14.0 14.1 Schmoldt A, Benthe HF, Haberland G (1975). "Digitoxin metabolism by rat liver microsomes". Biochem Pharmacol. 24 (17): 1639–41. PMID 10.1136/jnnp.2005.077164.  10.1136/jnnp.2005.077164. Check |pmid= value (help).
  15. ↑ 15.0 15.1 15.2
  16. ↑ Lovelock, C. E., A. J. Molyneux, and P. M. Rothwell. "Change in incidence and aetiology of intracerebral haemorrhage in Oxfordshire, UK, between 1981 and 2006: a population-based study." The Lancet Neurology 6.6 (2007): 487-493.
  17. ↑ Rümke CL (1975). "Letter: Implications of the statement: No side effects were observed". N Engl J Med. 292 (7): 372–3. PMID 1117973.
  18. ↑ van Asch CJ, Velthuis BK, Greving JP, van Laar PJ, Rinkel GJ, Algra A; et al. (2013). "External validation of the secondary intracerebral hemorrhage score in The Netherlands". Stroke. 44 (10): 2904–6. doi:10.1161/STROKEAHA.113.002386. PMID 23920015.
  19. ↑ Polmear A (2003). "Sentinel headaches in aneurysmal subarachnoid haemorrhage: what is the true incidence? A systematic review". Cephalalgia. 23 (10): 935–41. PMID 14984225.
  20. ↑ Dodick DW, Wijdicks EF (1998). "Pituitary apoplexy presenting as a thunderclap headache". Neurology. 50 (5): 1510–1. PMID 9596029.
  21. ↑ Mitsias P, Ramadan NM (1992). "Headache in ischemic cerebrovascular disease. Part I: Clinical features". Cephalalgia. 12 (5): 269–74. PMID 1423556.
  22. ↑ Touzé E, Gauvrit JY, Moulin T, Meder JF, Bracard S, Mas JL; et al. (2003). "Risk of stroke and recurrent dissection after a cervical artery dissection: a multicenter study". Neurology. 61 (10): 1347–51. PMID 14638953.
  23. ↑ Schievink WI, Wijdicks EF, Meyer FB, Sonntag VK (2001). "Spontaneous intracranial hypotension mimicking aneurysmal subarachnoid hemorrhage". Neurosurgery. 48 (3): 513–6, discussion 516-7. PMID 11270540.
  24. ↑ Linn FH, Rinkel GJ, Algra A, van Gijn J (1998). "Headache characteristics in subarachnoid haemorrhage and benign thunderclap headache". J Neurol Neurosurg Psychiatry. 65 (5): 791–3. PMC 2170334. PMID 9810961.
  25. ↑ Markus HS (1991). "A prospective follow up of thunderclap headache mimicking subarachnoid haemorrhage". J Neurol Neurosurg Psychiatry. 54 (12): 1117–8. PMC 1014694. PMID 1783930.
  26. ↑ Gebel JM, Broderick JP (2000). "Intracerebral hemorrhage". Neurol Clin. 18 (2): 419–38. PMID 10757834.
  27. ↑ van Asch CJ, Luitse MJ, Rinkel GJ, van der Tweel I, Algra A, Klijn CJ (2010). "Incidence, case fatality, and functional outcome of intracerebral haemorrhage over time, according to age, sex, and ethnic origin: a systematic review and meta-analysis". Lancet Neurol. 9 (2): 167–76. doi:10.1016/S1474-4422(09)70340-0. PMID 20056489.
  28. ↑ Stein M, Misselwitz B, Hamann GF, Scharbrodt W, Schummer DI, Oertel MF (2012). "Intracerebral hemorrhage in the very old: future demographic trends of an aging population". Stroke. 43 (4): 1126–8. doi:10.1161/STROKEAHA.111.644716. PMID 22282880.
  29. ↑ Inagawa T, Ohbayashi N, Takechi A, Shibukawa M, Yahara K. Primary intracerebral hemorrhage in Izumo City, Japan: incidence rates and outcome in relation to the site of hemorrhage. Neurosurgery. 2003; 53: 1283–1298
  30. ↑ Huhtakangas J, Tetri S, Juvela S, Saloheimo P, Bode MK, Hillbom M. Effect of increased warfarin use on warfarin-related cerebral hemor- rhage: a longitudinal population-based study. Stroke. 2011;42:2431– 2435. doi: 10.1161/STROKEAHA.111.615260.
  31. ↑ Rådberg JA, Olsson JE, Rådberg CT. Prognostic parameters in sponta- neous intracerebral hematomas with special reference to anticoagulant treatment. Stroke. 1991;22:571–576. doi: 10.1161/01.STR.22.5.571.
  32. ↑ Flaherty ML, Kissela B, Woo D, Kleindorfer D, Alwell K, Sekar P, Moomaw CJ, Haverbusch M, Broderick JP. The increasing incidence of anticoagulant-associated intracerebral hemorrhage. Neurology. 2007;68:116–121. doi: 10.1212/01.wnl.0000250340.05202.8b.
  33. ↑ Ariesen MJ, Claus SP, Rinkel GJ, Algra A (2003). "Risk factors for intracerebral hemorrhage in the general population: a systematic review". Stroke. 34 (8): 2060–5. doi:10.1161/01.STR.0000080678.09344.8D. PMID 12843354.
  34. ↑ Elmer J, Hou P, Wilcox SR, Chang Y, Schreiber H, Okechukwu I; et al. (2013). "Acute respiratory distress syndrome after spontaneous intracerebral hemorrhage*". Crit Care Med. 41 (8): 1992–2001. doi:10.1097/CCM.0b013e31828a3f4d. PMC 3752686. PMID 23760151.
  35. ↑ Oleinik A, Romero JM, Schwab K, Lev MH, Jhawar N, Delgado Almandoz JE; et al. (2009). "CT angiography for intracerebral hemorrhage does not increase risk of acute nephropathy". Stroke. 40 (7): 2393–7. doi:10.1161/STROKEAHA.108.546127. PMC 2726774. PMID 19461032.
  36. ↑ Malhotra A (2007). "Low-tidal-volume ventilation in the acute respiratory distress syndrome". N Engl J Med. 357 (11): 1113–20. doi:10.1056/NEJMct074213. PMC 2287190. PMID 17855672.
  37. ↑ Franke CL, van Swieten JC, Algra A, van Gijn J (1992). "Prognostic factors in patients with intracerebral haematoma". J Neurol Neurosurg Psychiatry. 55 (8): 653–7. PMC 489199. PMID 1527534.
  38. ↑ Broderick JP, Brott TG, Duldner JE, Tomsick T, Huster G (1993). "Volume of intracerebral hemorrhage. A powerful and easy-to-use predictor of 30-day mortality". Stroke. 24 (7): 987–93. PMID 8322400.
  39. ↑ Fisher CM (1971). "Pathological observations in hypertensive cerebral hemorrhage". J Neuropathol Exp Neurol. 30 (3): 536–50. PMID 4105427.
  40. ↑ Bos MJ, Koudstaal PJ, Hofman A, Breteler MM (2007). "Decreased glomerular filtration rate is a risk factor for hemorrhagic but not for ischemic stroke: the Rotterdam Study". Stroke. 38 (12): 3127–32. doi:10.1161/STROKEAHA.107.489807. PMID 17962600.
  41. ↑ Hackam DG, Mrkobrada M (2012). "Selective serotonin reuptake inhibitors and brain hemorrhage: a meta-analysis". Neurology. 79 (18): 1862–5. doi:10.1212/WNL.0b013e318271f848. PMID 23077009. Review in: Evid Based Ment Health. 2013 May;16(2):54
  42. ↑ Davis AM, Natelson BH (1993). "Brain-heart interactions. The neurocardiology of arrhythmia and sudden cardiac death". Tex Heart Inst J. 20 (3): 158–69. PMC 325088. PMID 8219819.
  43. ↑ Hasegawa K, Fix ML, Wendell L, Schwab K, Ay H, Smith EE; et al. (2012). "Ischemic-appearing electrocardiographic changes predict myocardial injury in patients with intracerebral hemorrhage". Am J Emerg Med. 30 (4): 545–52. doi:10.1016/j.ajem.2011.02.007. PMC 3684165. PMID 21450435.
  44. ↑ Fiebach JB, Schellinger PD, Gass A, Kucinski T, Siebler M, Villringer A, Olkers P, Hirsch JG, Heiland S, Wilde P, Jansen O, Röther J, Hacke W, Sartor K; Kompetenznetzwerk Schlaganfall B5. Stroke magnetic resonance imaging is accurate in hyperacute intracerebral hemorrhage: a multicenter study on the validity of stroke imaging. Stroke. 2004;35:502– 506. doi: 10.1161/01.STR.0000114203.75678.8
  45. ↑ Chalela JA, Kidwell CS, Nentwich LM, Luby M, Butman JA, Demchuk AM, Hill MD, Patronas N, Latour L, Warach S. Magnetic resonance imaging and computed tomography in emergency assessment of patients with suspected acute stroke: a prospective comparison. Lancet. 2007;369:293–298. doi: 10.1016/S0140-6736(07)60151-2.
  46. ↑ Chalela JA, Kidwell CS, Nentwich LM, Luby M, Butman JA, Demchuk AM; et al. (2007). "Magnetic resonance imaging and computed tomography in emergency assessment of patients with suspected acute stroke: a prospective comparison". Lancet. 369 (9558): 293–8. doi:10.1016/S0140-6736(07)60151-2. PMC 1859855. PMID 17258669.
  47. ↑ Bartlett ST, Kuo PC, Johnson LB, Lim JW, Schweitzer EJ (1996). "Pancreas transplantation at the University of Maryland". Clin Transpl: 271–80. PMID 9286577.
  48. ↑ Yoon HK, Shin HJ, Lee M, Byun HS, Na DG, Han BK (2000). "MR angiography of moyamoya disease before and after encephaloduroarteriosynangiosis". AJR Am J Roentgenol. 174 (1): 195–200. doi:10.2214/ajr.174.1.1740195. PMID 10628478.
  49. ↑ Moon JS, Janjua N, Ahmed S, Kirmani JF, Harris-Lane P, Jacob M; et al. (2008). "Prehospital neurologic deterioration in patients with intracerebral hemorrhage". Crit Care Med. 36 (1): 172–5. doi:10.1097/01.CCM.0000297876.62464.6B. PMID 18007267.
  50. ↑
  51. ↑
  52. ↑
  53. ↑
  54. ↑ Wang WZ, Jiang B, Liu HM, Li D, Lu CZ, Zhao YD, Sander JW. Minimally invasive craniopuncture therapy vs. conservative treat- ment for spontaneous intracerebral hemorrhage: results from a ran- domized clinical trial in China. Int J Stroke. 2009;4:11–16. doi: 10.1111/j.1747-4949.2009.00239.x.
  55. ↑ Mould WA, Carhuapoma JR, Muschelli J, Lane K, Morgan TC, McBee NA, Bistran-Hall AJ, Ullman NL, Vespa P, Martin NA, Awad I, Zuccarello M, Hanley DF; MISTIE Investigators. Minimally invasive surgery plus recombinant tissue-type plasminogen activator for intrace- rebral hemorrhage evacuation decreases perihematomal edema. Stroke. 2013;44:627–634. doi: 10.1161/STROKEAHA.111.000411.
  56. ↑
  57. ↑
  58. ↑
  59. ↑
  60. ↑
  61. ↑


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