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Intracerebral hemorrhage natural history

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

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

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

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

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

  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.


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