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Reliable, easy-to-read patient information on common medical conditions — written in plain language, free of jargon, and grounded in current evidence. Browse the most frequent diagnoses, understand what they mean for everyday life, and learn which steps and questions help you have a focused conversation with your doctor.

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Intracerebral hemorrhage natural history

Introduction

Overview

Overview

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.[1][2] 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.[3][4][5]

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).[6][7]

Natural history

Natural history

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. ICH has a mortality rate of 44 percent after 30 days, higher than ischemic stroke or even the very deadly subarachnoid hemorrhage.[1][2] Massive hemorrhage may occur when the patients have a bleeding disorder and clotting system is unable to control the bleeding.[8] The hematoma enlarges until pressure from surrounding tissue limits its growth, or until it decompresses by emptying into the ventricular system, CSF or the pial surface. [9][10]

The frequency of medical complications after intracerebral hemorrhage is high, although there is substantially more information reported for ischemic stroke than intracerebral hemorrhage (ICH).[11]

Complications

Complications

The most common complications following intracerebral hemorrhage (ICH) include:[3][4][5][11]

Approximately 50% of deaths after stroke are attributed to medical complications, usually after 7 days of hospitalization. Stroke patients who experience medical complications while in the hospital have increased mortality up to 4 years after the initial event.

Prognosis

Prognosis

Prognostic factors

  • Despite aggressive and newer management strategies, the prognosis of patients with intracerebral hemorrhage is very poor. However, some studies suggested that excellent medical care has a direct impact on intracerebral hemorrhage (ICH) morbidity and mortality.[12]
  • 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).[6][7]
  • Case-fatality at 1 month is over 40 % and has not improved in last few decades.[13]

Prognsostic factors in Intracerebral hemorrhage may include:[14]

Poor prognostic factors Associations
Fever[15]
  • Associated with early neurologic deterioration
Higher initial blood pressure[16]
  • Associated with early neurologic deterioration and increased mortality
Higher creatinine[17]
Higher serum glucose[16]
  • Associated with hematoma expansion and worse outcome
Warfarin-related hemorrhages[18][19]
  • Associated with an increased hematoma volume, greater risk of expansion, and increased morbidity and mortality
Warfarin therapy with an INR >3[20]
  • Associated with larger initial hemorrhage volume as well as poorer outcomes
Intraventricular hemorrhage[21][22]
  • IVH occurs in approximately 45% of patients with spontaneous ICH and is an independent factor associated with poor outcome
  • Following conditions are associated with a higher risk of death in patient with IVH[23][24]
References

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 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.
  4. ↑ 4.0 4.1 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.
  5. ↑ 5.0 5.1 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.
  6. ↑ 6.0 6.1 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.
  7. ↑ 7.0 7.1 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.
  8. ↑ Garcia JH, Ho KL (1992). “Pathology of hypertensive arteriopathy”. Neurosurg Clin N Am. 3 (3): 497–507. PMID 1633473.
  9. ↑ Brott T, Broderick J, Kothari R, Barsan W, Tomsick T, Sauerbeck L; et al. (1997). “Early hemorrhage growth in patients with intracerebral hemorrhage”. Stroke. 28 (1): 1–5. PMID 8996478.
  10. ↑ Chen ST, Chen SD, Hsu CY, Hogan EL (1989). “Progression of hypertensive intracerebral hemorrhage”. Neurology. 39 (11): 1509–14. PMID 2812332.
  11. ↑ 11.0 11.1 Balami JS, Buchan AM (2012). “Complications of intracerebral haemorrhage”. Lancet Neurol. 11 (1): 101–18. doi:10.1016/S1474-4422(11)70264-2. PMID 22172625.
  12. ↑ Hemphill JC, Newman J, Zhao S, Johnston SC (2004). “Hospital usage of early do-not-resuscitate orders and outcome after intracerebral hemorrhage”. Stroke. 35 (5): 1130–4. doi:10.1161/01.STR.0000125858.71051.ca. PMID 15044768.
  13. ↑ Apanasenko BG, Kunitsyn AI, Isaev GA, Khodyrev LP (1976). “[Determination of the weight of disemulsified lipid circulating in the blood as a method of diagnosis of fat embolism]”. Lab Delo (1): 41–3. PMID 0056489.
  14. ↑ Tuhrim S, Horowitz DR, Sacher M, Godbold JH. Volume of ventricular blood is an important determinant of outcome in supratentorial intracere- bral hemorrhage. Crit Care Med. 1999;27:617–621.
  15. ↑ Leira R, Dávalos A, Silva Y, Gil-Peralta A, Tejada J, Garcia M; et al. (2004). “Early neurologic deterioration in intracerebral hemorrhage: predictors and associated factors”. Neurology. 63 (3): 461–7. PMID 15304576.
  16. ↑ 16.0 16.1 Sawyer GJ, Fabre JW (1997). “Indirect T-cell allorecognition and the mechanisms of immunosuppression by allogeneic blood transfusions”. Transpl Int. 10 (4): 276–83. PMID 9249937.
  17. ↑ Miller CM, Vespa PM, McArthur DL, Hirt D, Etchepare M (2007). “Frameless stereotactic aspiration and thrombolysis of deep intracerebral hemorrhage is associated with reduced levels of extracellular cerebral glutamate and unchanged lactate pyruvate ratios”. Neurocrit Care. 6 (1): 22–9. doi:10.1385/NCC:6:1:22. PMID 17356187.
  18. ↑ Cucchiara B, Messe S, Sansing L, Kasner S, Lyden P, CHANT Investigators (2008). “Hematoma growth in oral anticoagulant related intracerebral hemorrhage”. Stroke. 39 (11): 2993–6. doi:10.1161/STROKEAHA.108.520668. PMID 18703803.
  19. ↑ Broderick JP, Diringer MN, Hill MD, Brun NC, Mayer SA, Steiner T; et al. (2007). “Determinants of intracerebral hemorrhage growth: an exploratory analysis”. Stroke. 38 (3): 1072–5. doi:10.1161/01.STR.0000258078.35316.30. PMID 17290026.
  20. ↑ Flaherty ML, Tao H, Haverbusch M, Sekar P, Kleindorfer D, Kissela B; et al. (2008). “Warfarin use leads to larger intracerebral hematomas”. Neurology. 71 (14): 1084–9. doi:10.1212/01.wnl.0000326895.58992.27. PMC 2668872. PMID 18824672.
  21. ↑ Bhattathiri PS, Gregson B, Prasad KS, Mendelow AD; STICH Investigators. Intraventricular hemorrhage and hydrocephalus after spon- taneous intracerebral hemorrhage: results from the STICH trial. Acta Neurochir Suppl. 2006;96:65–68.
  22. ↑ Hallevi H, Albright KC, Aronowski J, Barreto AD, Martin-Schild S, Khaja AM, Gonzales NR, Illoh K, Noser EA, Grotta JC. Intraventricular hemorrhage: anatomic relationships and clinical implications. Neurology. 2008;70:848–852. doi: 10.1212/01.wnl.0000304930.47751.75.
  23. ↑ Flint AC, Roebken A, Singh V (2008). “Primary intraventricular hemorrhage: yield of diagnostic angiography and clinical outcome”. Neurocrit Care. 8 (3): 330–6. doi:10.1007/s12028-008-9070-2. PMID 18320145.
  24. ↑ Engelhard HH, Andrews CO, Slavin KV, Charbel FT (2003). “Current management of intraventricular hemorrhage”. Surg Neurol. 60 (1): 15–21, discussion 21-2. PMID 12865003.

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