Hemorrhagic stroke natural history

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Natural history

In intracerebral hemorrhage (ICH), underlying small vessel disease may result in acute vessel rupture. This acute vessel rupture can progress can result in brain injury by folllowing mechanisms:

All of these mechnisems can lead to perihematomal edema formation and secondary brain injury. Additionally, continued bleeding, or hematoma expansion, occurs in many patients—either continued bleeding from the primary source or secondary bleeding at the periphery of the hemorrhage.

Intracerebral hemorrhage also can result in dysphagia and aspiration. These two are the major risk factors for the development of pneumonia in patients with stroke.[1] Heart failure can occur as the result of myocardial ischemia, infarction, stress-induced cardiomyopathy, or uncontrolled hypertension in the setting of acute Intracerebral hemorrhage (ICH).[2][3]

Complications

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

The most common complications following intracerebral hemorrhage (ICH) include:[4][5][6]

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

Wide range of factors associated with outcome after acute hemorrhagic stroke. Identification of these factors result in the development of models to predict mortality and functional outcome. These prediction models include individual patient characteristics such as:[7][8][9][10]

Prognostic factors

Intracranial hemorrhage

  • 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.[11]
  • Case-fatality at 1 month is over 40 % and has not improved in last few decades.[12]

Prognsostic factors in Intracerebral hemorrhage include:[9]

Poor prognostic factors Associations
Fever[13]
  • Associated with early neurologic deterioration
Higher initial blood pressure[14]
  • Associated with early neurologic deterioration and increased mortality
Higher creatinine[15]
Higher serum glucose[14]
  • Associated with hematoma expansion and worse outcome
Warfarin-related hemorrhages[16][17]
  • Associated with an increased hematoma volume, greater risk of expansion, and increased morbidity and mortality
Warfarin therapy with an INR >3[18]
  • Associated with larger initial hemorrhage volume as well as poorer outcomes
Intraventricular hemorrhage[19][20]
  • IVH occurs in approximately 45% of patients with spontaneous ICH and is an independent factor associated with poor outcome

Subarachnoid hemorrhage

The Hunt and Hess scale describes the severity of subarachnoid hemorrhage, and is used as a predictor of survival.[21]

Grading Associations Survival
Grade 1
  • Asymptomatic
  • Minimal headache and slight neck stiffness
  • 70% survival
Grade 2
  • 60% survival
Grade 3
  • Drowsy
  • Minimal neurologic deficit
  • 50% survival
Grade 4
  • 20% survival
Grade 5
  • 10% survival

2015 AHA/ASA Guidelines for the Management of Spontaneous Intracerebral Hemorrhage[22]

Outcome Prediction and Withdrawal of Technological Support: Recommendation

Class III (Harm)
"1. Current prognostic models for individual patients early after ICH are biased by failure to account for the influence of withdrawal of support and early DNAR orders. DNAR status should not limit appropriate medical and surgical interventions unless otherwise explicitly indicated (Level of Evidence: C)"
Class IIa
"1. Aggressive care early after ICH onset and postponement of new DNAR orders until at least the second full day of hospitalization is probably recommended. Patients with preexisting DNAR orders are not included in this recommendation (Level of Evidence: B)"

References

  1. ↑ Lyden PD, Shuaib A, Lees KR, Davalos A, Davis SM, Diener HC, Grotta JC, Ashwood TJ, Hardemark HG, Svensson HH, Rodichok L, Wasiewski WW, Ahlberg G; CHANT Trial Investigators. Safety and tolerability of NXY-059 for acute intracerebral hemorrhage: the CHANT Trial. Stroke. 2007;38:2262–2269. doi: 10.1161/STROKEAHA.106.472746.
  2. ↑ Gattringer T, Niederkorn K, Seyfang L, Seifert-Held T, Simmet N, Ferrari J; et al. (2014). "Myocardial infarction as a complication in acute stroke: results from the austrian stroke unit registry". Cerebrovasc Dis. 37 (2): 147–52. doi:10.1159/000357799. PMID 24481543.
  3. ↑ Maramattom BV, Manno EM, Fulgham JR, Jaffe AS, Wijdicks EF (2006). "Clinical importance of cardiac troponin release and cardiac abnormalities in patients with supratentorial cerebral hemorrhages". Mayo Clin Proc. 81 (2): 192–6. doi:10.4065/81.2.192. PMID 16471073.
  4. ↑ 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.
  5. ↑ 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.
  6. ↑ 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.
  7. ↑ Bernstein RA, Hemphill JC. Critical care of acute ischemic stroke. Curr Neurol Neurosci Rep. 2001;1:587–592.
  8. ↑ Rost NS, Smith EE, Chang Y, Snider RW, Chanderraj R, Schwab K, FitzMaurice E, Wendell L, Goldstein JN, Greenberg SM, Rosand J. Prediction of functional outcome in patients with primary intracerebral hemorrhage: the FUNC score. Stroke. 2008;39:2304–2309. doi: 10.1161/ STROKEAHA.107.512202
  9. ↑ 9.0 9.1 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.
  10. ↑ Broderick JP, Brott TG, Duldner JE, Tomsick T, Huster G. Volume of intracerebral hemorrhage: a powerful and easy-to-use predictor of 30-day mortality. Stroke. 1993;24:987–993.
  11. ↑ 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.
  12. ↑ 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.
  13. ↑ 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.
  14. ↑ 14.0 14.1 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.
  15. ↑ 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.
  16. ↑ 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.
  17. ↑ 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.
  18. ↑ 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.
  19. ↑ 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.
  20. ↑ 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.
  21. ↑ Hunt WE, Hess RM (1968). "Surgical risk as related to time of intervention in the repair of intracranial aneurysms". J Neurosurg. 28 (1): 14–20. doi:10.3171/jns.1968.28.1.0014. PMID 5635959.
  22. ↑ 2015 AHA/ASA Guidelines for the Management of Spontaneous Intracerebral Hemorrhage http://stroke.ahajournals.org/content/early/2015/05/28/STR.0000000000000069 Accessed on November 10, 2016


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