Intraparenchymal hemorrhage

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Template:Intraparenchymal hemorrhage

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

Synonyms and keywords:Intracerebral hemorrhage, intraparencymal hematoma, intracerebral hematoma

Overview

Historical Perspective

[Disease name] was first discovered by [name of scientist], a [nationality + occupation], in [year]/during/following [event].

The association between [important risk factor/cause] and [disease name] was made in/during [year/event].

In [year], [scientist] was the first to discover the association between [risk factor] and the development of [disease name].

In [year], [gene] mutations were first implicated in the pathogenesis of [disease name].

There have been several outbreaks of [disease name], including -----.

In [year], [diagnostic test/therapy] was developed by [scientist] to treat/diagnose [disease name].

Classification

[Intraparenchymal hemorrhage] may be classified according to etiology into primary and secondary intraparenchymal hemorrhage. Intraparenchymal hemorrhage occurring as a consequence of hypertension or cerebral amyloid angiopathy is termed as primary intraparenchymal hemorrhage. If the etiology is other than hypertension or cerebral amyloid angiopathy then intraparenchymal hemorrhage is termed as secondary intraparenchymal hemorrhage. [1]


Pathophysiology

[Intraparenchymal hemorrhages] are caused by small bleeds that occur when parenchymal arterioles rupture. Hypertension is the major risk factor for development of intraparenchymal hemorrhage. Hypertension increases the risk of intraparenchymal hemorrhage by inducing certain degenerative changes in small arterioles. Sometimes aneurysm form as a consequence and eventually rupture. Hypertensive hemorrhages usually occur in deep brain structures like basal ganglia, pons, thalamus and cerebellum. [2][3][4]

Cerebral amyloid angiopathy is another risk factor that contributes to a large number of intraparenchymal hemorrhages. It involves deposition of ẞ-amyloid in cortical blood vessels, which results in weakened blood vessels and hence increased risk of rupture. [5]

Certain vascular malformations are also at increased risk of rupture and causing intraparenchymal hemorrhage. Arteriovenous malformations consist of dysplastic arteries that form a web and drain into veins. These Av malformations may rupture leading to intraparenchymal hemorrhage.[6] Dural arteriovenous fistulae are abnormal connections between arteries and veins inside dura matter. If the drainage occurs into a pressurized vein then there is an increased chance of hemorrhage as a result of venous hypertension. [7]

Cerebral venous thrombosis may lead to intraparenchymal hemorrhage as there is poor cerebral venous drainage causing increased pressure in vein and eventually venous rupture.[8][9]
Saccular aneurysm when ruptures may lead to intraparenchymal hemorrhage, although it mostly results in subarachnoid hemorrhage. Moyamoya disease involves the narrowing of intracranial arteries. Collateral blood vessels form as a consequence. These collaterals have fragile walls and are prone to rupture leading to intraparenchymal hemorrhage.[10]

Causes

The most common cause of [spontaneous intra parenchymal hemorrhage] is [hypertensive angiopathy]. In older adults, most common cause of lobar intra-parenchymal hemorrhage is cerebral amyloid angiopathy. For intra-parenchymal hemorrhages in children vascular malformations are the most common cause.[11][12] Less common causes of [spontaneous intra-parenchymal hemorrhage] include [vasculitis], [CNS infection], [rupture of dural AV fistula], septic embolism, mycotic aneurysm rupture, tumors, Av malformation rupture, cerebral hyperperfusion syndrome, rupture of saccular aneursym, dural sinus thrombosis, moyamoya disease, reversible cerebral vasoconstriction syndromes, transformation of ischemic stroke into hemorrhagic, bleeding disorders, systemic illnesses like cirrhosis of liver and thrombocytopenia, medications for anticoagulation, drugs like amphetamines and cocaine. [13][14][15][16][17][18]

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Differentiating intraparenchymal hemorrhage from other Diseases

[Intraparenchymal hemorrhage] must be differentiated from ischemic stroke. But it is difficult to differentiate between the 2 based on clinical features. Therefore, neuroimaging should always be used to confirm the diagnosis. [19]

Epidemiology and Demographics

The incidence of [intra-parenchymal hemorrhage] is approximately [24.6] per 100,000 person years. Asian and older populations have substantially higher incidence. [20]

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Risk Factors

The most potent risk factor in the development of [intraparenchymal hemorrhage] is [hypertension]. [4] Other risk factors include presence of amyloid angiopathy, old age, use of anti-coagulants, [alcohol intake], [smoking], [low LDL and total cholesterol], increased HDL cholesterol, black race, presence of apolipoprotein E with E2 and E4 alleles. [21][22][23][24][25]

Natural History, Complications, and Prognosis

Common complications of [intraparenchymal hemorrhage] include [raised ICP], [seizures], focal neurologic deficits, [functional decline of patients], post hemorrhage dementia, post hemorrhage depression. [26][27][28]

Prognosis of intraparenchymal hemorrhage is generally poor. 30 day case fatality rate of IPH is reported to be around 40%.[20] IPH has the highest mortality rate among all the causes of stroke with the 1-year and 10-year survival rates of 40% and 24% respectively. [29][22][30]

Diagnosis

Clinical Features

Common clinical features of [intraparenchymal hemorrhage] include [acute onset focal neurological deficit], [altered sensorium], [vomiting], headache, brady or tachycardia and seizures. [31]. A substantial proportion of patients with intraparenchymal hemorrhage have lower than normal GCS. [32] Nausea, vomiting, headache and decreased level of consciousness when present point more towards hemorrhage rather than ischemic stroke. [16] Seizures occur more commonly in IPH secondary to venous sinus thrombosis or cavernous malformation as compared to other causes of IPH. [9] [33] Secondary IPH, specially due to venous sinus thrombosis and vascular malformations usually presents at younger age and patients usually have no history of hypertension. [34]

CT scan

Non-contrast Ct scan is the gold standard for diagnosing intra parenchymal hemorrhage in Emergency, as it is readily available and highly sensitive for intra parenchymal hemorrhage. Moreover, it can provide valuable information regarding location and extension of intra-parenchymal hemorrhage, hydrocephalus and compression of brainstem by hematoma. [35][36]

CT angiography is a very useful technique for identifying vascular abnormalities like Av shunts, aneurysms, and venous sinus thrombosis that could have lead to intraparenchymal hemorrhage. [37] Though Ct angiography is very helpful for diagnosing vascular malformations but digital subtraction angiography is the gold standard for this purpose.[36] The presence of "spot sign" on CTA, i.e, extravasation of contrast within hematoma predicts hematoma expansion and adverse outcome.[38]

MRI

Owing to its high senstivity and specificity, MRI is another suitable modality for diagnosis of intraparenchymal hemorrhage. Secondary causes of intraparenchymal hemorrhage like tumor, ischemic stroke or cavernous malformation can be better identified by MRI. Microbleed patterns indicative of hypertensive angiopathy or cerebral amyloid angiopathy may also be detected in a better fashion through MRI.[39]


Treatment

Medical Therapy

[Intraparenchymal hemorrhage] is a medical emergency and requires prompt treatment. Special attention should be given to airway support as these patients may be unable to protect their airways. Blood pressure control is an important feature of IPH management as raised blood pressure is associated with hematoma expansion and poor outcome.[40] According to American Heart Association/American Stroke Association guidelines, for IPH patients presenting with systolic blood pressure of 150 to 220mmHg, the goal should be to keep the systolic blood pressure below 140mmHg if there is no contraindication. [41] Short acting anti hypertensives like nicardipine and labetalol are recommended while drugs like nitrates and hydralazine should not be used. [42]

Specific coagulation factor therapy or platelet transfusion is recommended for patients with coagulation factor deficiency or thrombocytopenia respectively. Platelet transfusion is not reccomended for patients on antiplatelet drugs.Patients who are taking warfarin or any other Vitamin K antagonist and have high INR should be given Vitamin K and prothrombin complex concentrate[43].[31][44] Idarucizumab should be administered to patients on dabigatran while adexanet alfa should be given to patients taking factor Xa inhibitors. [45][46] . For reversal of heparin induced coagulopathy, protamine sulphate should be administered.[47]

Antiepileptics should be given to patients who present with seizures. Prophylactic use of antiepileptics is not recommended. [31]Intermittent pneumatic compression for Dvt prophylaxis should also be done.[48] 1 day after the bleeding cessation, low molecular weight heparin or subcutaneous heparin can also be used for Dvt prophylaxis. [49]


Surgery

Urgent neurosurgical assessment of IPH patients should be done. IPH patients who are comatose, have substantial intraventricular hemorrhage and hydrocephalus should undergo external ventricular drain placement. [31] Benefit of surgical evacuation of hematomas over conservative management is still unproven. Surgical evacuation of hematomas is recommended in case of cerebellar hematomas with evidence of hydrocephalus or/and brainstem compression. [31]

Prevention

Secondary Prevention

Long term blood pressure control is the most important measure in preventing recurrent intraparenchymal hemorrhage. Target blood pressure of less than 130/80mmHg is recommended. [50] In addition to blood pressure control certain other measures like smoking cessation, avoiding illicit drug use as well as alcohol intake can have beneficial effects in this regard. [51]

References

  1. ↑ Gross BA, Jankowitz BT, Friedlander RM (2019). "Cerebral Intraparenchymal Hemorrhage: A Review". JAMA. 321 (13): 1295–1303. doi:10.1001/jama.2019.2413. PMID 30938800.
  2. ↑ Ziai WC, Carhuapoma JR (2018). "Intracerebral Hemorrhage". Continuum (Minneap Minn). 24 (6): 1603–1622. doi:10.1212/CON.0000000000000672. PMID 30516598.
  3. ↑ Dye JA, Rees G, Yang I, Vespa PM, Martin NA, Vinters HV (2014). "Neuropathologic analysis of hematomas evacuated from patients with spontaneous intracerebral hemorrhage". Neuropathology. 34 (3): 253–60. doi:10.1111/neup.12089. PMID 24354628.
  4. ↑ 4.0 4.1 O'Donnell MJ, Xavier D, Liu L, Zhang H, Chin SL, Rao-Melacini P; et al. (2010). "Risk factors for ischaemic and intracerebral haemorrhagic stroke in 22 countries (the INTERSTROKE study): a case-control study". Lancet. 376 (9735): 112–23. doi:10.1016/S0140-6736(10)60834-3. PMID 20561675.
  5. ↑ Greenberg SM, Charidimou A (2018). "Diagnosis of Cerebral Amyloid Angiopathy: Evolution of the Boston Criteria". Stroke. 49 (2): 491–497. doi:10.1161/STROKEAHA.117.016990. PMC 5892842. PMID 29335334.
  6. ↑ Gross BA, Du R (2013). "Natural history of cerebral arteriovenous malformations: a meta-analysis". J Neurosurg. 118 (2): 437–43. doi:10.3171/2012.10.JNS121280. PMID 23198804.
  7. ↑ Gross BA, Albuquerque FC, McDougall CG, Jankowitz BT, Jadhav AP, Jovin TG; et al. (2018). "A multi-institutional analysis of the untreated course of cerebral dural arteriovenous fistulas". J Neurosurg. 129 (5): 1114–1119. doi:10.3171/2017.6.JNS171090. PMID 29243979.
  8. ↑ Saposnik G, Barinagarrementeria F, Brown RD, Bushnell CD, Cucchiara B, Cushman M; et al. (2011). "Diagnosis and management of cerebral venous thrombosis: a statement for healthcare professionals from the American Heart Association/American Stroke Association". Stroke. 42 (4): 1158–92. doi:10.1161/STR.0b013e31820a8364. PMID 21293023.
  9. ↑ 9.0 9.1 Lee SK, Mokin M, Hetts SW, Fifi JT, Bousser MG, Fraser JF; et al. (2018). "Current endovascular strategies for cerebral venous thrombosis: report of the SNIS Standards and Guidelines Committee". J Neurointerv Surg. 10 (8): 803–810. doi:10.1136/neurintsurg-2018-013973. PMID 29871990.
  10. ↑ Scott RM, Smith ER (2009). "Moyamoya disease and moyamoya syndrome". N Engl J Med. 360 (12): 1226–37. doi:10.1056/NEJMra0804622. PMID 19297575.
  11. ↑ Cordonnier C, Demchuk A, Ziai W, Anderson CS (2018). "Intracerebral haemorrhage: current approaches to acute management". Lancet. 392 (10154): 1257–1268. doi:10.1016/S0140-6736(18)31878-6. PMID 30319113.
  12. ↑ Beslow LA, Licht DJ, Smith SE, Storm PB, Heuer GG, Zimmerman RA; et al. (2010). "Predictors of outcome in childhood intracerebral hemorrhage: a prospective consecutive cohort study". Stroke. 41 (2): 313–8. doi:10.1161/STROKEAHA.109.568071. PMC 2821039. PMID 20019325.
  13. ↑ Cordonnier C, Demchuk A, Ziai W, Anderson CS (2018). "Intracerebral haemorrhage: current approaches to acute management". Lancet. 392 (10154): 1257–1268. doi:10.1016/S0140-6736(18)31878-6. PMID 30319113.
  14. ↑ 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.
  15. ↑ Delgado Almandoz JE, Schaefer PW, Goldstein JN, Rosand J, Lev MH, González RG; et al. (2010). "Practical scoring system for the identification of patients with intracerebral hemorrhage at highest risk of harboring an underlying vascular etiology: the Secondary Intracerebral Hemorrhage Score". AJNR Am J Neuroradiol. 31 (9): 1653–60. doi:10.3174/ajnr.A2156. PMC 3682824. PMID 20581068.
  16. ↑ 16.0 16.1 Gross BA, Jankowitz BT, Friedlander RM (2019). "Cerebral Intraparenchymal Hemorrhage: A Review". JAMA. 321 (13): 1295–1303. doi:10.1001/jama.2019.2413. PMID 30938800.
  17. ↑ Swor DE, Maas MB, Walia SS, Bissig DP, Liotta EM, Naidech AM; et al. (2019). "Clinical characteristics and outcomes of methamphetamine-associated intracerebral hemorrhage". Neurology. 93 (1): e1–e7. doi:10.1212/WNL.0000000000007666. PMC 6659002 Check |pmc= value (help). PMID 31142634.
  18. ↑ Martin-Schild S, Albright KC, Hallevi H, Barreto AD, Philip M, Misra V; et al. (2010). "Intracerebral hemorrhage in cocaine users". Stroke. 41 (4): 680–4. doi:10.1161/STROKEAHA.109.573147. PMC 3412877. PMID 20185779.
  19. ↑ Hemphill JC, Greenberg SM, Anderson CS, Becker K, Bendok BR, Cushman M; et al. (2015). "Guidelines for the Management of Spontaneous Intracerebral Hemorrhage: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association". Stroke. 46 (7): 2032–60. doi:10.1161/STR.0000000000000069. PMID 26022637.
  20. ↑ 20.0 20.1 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.
  21. ↑ O'Donnell HC, Rosand J, Knudsen KA, Furie KL, Segal AZ, Chiu RI; et al. (2000). "Apolipoprotein E genotype and the risk of recurrent lobar intracerebral hemorrhage". N Engl J Med. 342 (4): 240–5. doi:10.1056/NEJM200001273420403. PMID 10648765.
  22. ↑ 22.0 22.1 Sacco S, Marini C, Toni D, Olivieri L, Carolei A (2009). "Incidence and 10-year survival of intracerebral hemorrhage in a population-based registry". Stroke. 40 (2): 394–9. doi:10.1161/STROKEAHA.108.523209. PMID 19038914.
  23. ↑ Costa P, Grassi M, Iacoviello L, Zedde M, Marcheselli S, Silvestrelli G; et al. (2018). "Alcohol intake and the risk of intracerebral hemorrhage in the elderly: The MUCH-Italy". Neurology. 91 (3): e227–e235. doi:10.1212/WNL.0000000000005814. PMID 29898970.
  24. ↑ Suh I, Jee SH, Kim HC, Nam CM, Kim IS, Appel LJ (2001). "Low serum cholesterol and haemorrhagic stroke in men: Korea Medical Insurance Corporation Study". Lancet. 357 (9260): 922–5. doi:10.1016/S0140-6736(00)04213-6. PMID 11289349.
  25. ↑ Sturgeon JD, Folsom AR, Longstreth WT, Shahar E, Rosamond WD, Cushman M (2007). "Risk factors for intracerebral hemorrhage in a pooled prospective study". Stroke. 38 (10): 2718–25. doi:10.1161/STROKEAHA.107.487090. PMID 17761915.
  26. ↑ Moulin S, Cordonnier C (2015). "Prognosis and Outcome of Intracerebral Haemorrhage". Front Neurol Neurosci. 37: 182–92. doi:10.1159/000437122. PMID 26587771.
  27. ↑ Passero S, Rocchi R, Rossi S, Ulivelli M, Vatti G (2002). "Seizures after spontaneous supratentorial intracerebral hemorrhage". Epilepsia. 43 (10): 1175–80. doi:10.1046/j.1528-1157.2002.00302.x. PMID 12366733.
  28. ↑ Pendlebury ST, Rothwell PM (2009). "Prevalence, incidence, and factors associated with pre-stroke and post-stroke dementia: a systematic review and meta-analysis". Lancet Neurol. 8 (11): 1006–18. doi:10.1016/S1474-4422(09)70236-4. PMID 19782001.
  29. ↑ 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.
  30. ↑ Dennis MS, Burn JP, Sandercock PA, Bamford JM, Wade DT, Warlow CP (1993). "Long-term survival after first-ever stroke: the Oxfordshire Community Stroke Project". Stroke. 24 (6): 796–800. doi:10.1161/01.str.24.6.796. PMID 8506550.
  31. ↑ 31.0 31.1 31.2 31.3 31.4 Hemphill JC, Greenberg SM, Anderson CS, Becker K, Bendok BR, Cushman M; et al. (2015). "Guidelines for the Management of Spontaneous Intracerebral Hemorrhage: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association". Stroke. 46 (7): 2032–60. doi:10.1161/STR.0000000000000069. PMID 26022637.
  32. ↑ Hemphill JC, Greenberg SM, Anderson CS, Becker K, Bendok BR, Cushman M; et al. (2015). "Guidelines for the Management of Spontaneous Intracerebral Hemorrhage: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association". Stroke. 46 (7): 2032–60. doi:10.1161/STR.0000000000000069. PMID 26022637.
  33. ↑ Bertalanffy H, Benes L, Miyazawa T, Alberti O, Siegel AM, Sure U (2002). "Cerebral cavernomas in the adult. Review of the literature and analysis of 72 surgically treated patients". Neurosurg Rev. 25 (1–2): 1–53, discussion 54-5. doi:10.1007/s101430100179. PMID 11954761.
  34. ↑ Bertalanffy H, Benes L, Miyazawa T, Alberti O, Siegel AM, Sure U (2002). "Cerebral cavernomas in the adult. Review of the literature and analysis of 72 surgically treated patients". Neurosurg Rev. 25 (1–2): 1–53, discussion 54-5. doi:10.1007/s101430100179. PMID 11954761.
  35. ↑ Hemphill JC, Greenberg SM, Anderson CS, Becker K, Bendok BR, Cushman M; et al. (2015). "Guidelines for the Management of Spontaneous Intracerebral Hemorrhage: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association". Stroke. 46 (7): 2032–60. doi:10.1161/STR.0000000000000069. PMID 26022637.
  36. ↑ 36.0 36.1 Macellari F, Paciaroni M, Agnelli G, Caso V (2014). "Neuroimaging in intracerebral hemorrhage". Stroke. 45 (3): 903–8. doi:10.1161/STROKEAHA.113.003701. PMID 24425128.
  37. ↑ Khosravani H, Mayer SA, Demchuk A, Jahromi BS, Gladstone DJ, Flaherty M; et al. (2013). "Emergency noninvasive angiography for acute intracerebral hemorrhage". AJNR Am J Neuroradiol. 34 (8): 1481–7. doi:10.3174/ajnr.A3296. PMID 23124634.
  38. ↑ Demchuk AM, Dowlatshahi D, Rodriguez-Luna D, Molina CA, Blas YS, Dzialowski I; et al. (2012). "Prediction of haematoma growth and outcome in patients with intracerebral haemorrhage using the CT-angiography spot sign (PREDICT): a prospective observational study". Lancet Neurol. 11 (4): 307–14. doi:10.1016/S1474-4422(12)70038-8. PMID 22405630.
  39. ↑ Macellari F, Paciaroni M, Agnelli G, Caso V (2014). "Neuroimaging in intracerebral hemorrhage". Stroke. 45 (3): 903–8. doi:10.1161/STROKEAHA.113.003701. PMID 24425128.
  40. ↑ Qureshi AI, Mendelow AD, Hanley DF (2009). "Intracerebral haemorrhage". Lancet. 373 (9675): 1632–44. doi:10.1016/S0140-6736(09)60371-8. PMC 3138486. PMID 19427958.
  41. ↑ Hemphill JC, Greenberg SM, Anderson CS, Becker K, Bendok BR, Cushman M; et al. (2015). "Guidelines for the Management of Spontaneous Intracerebral Hemorrhage: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association". Stroke. 46 (7): 2032–60. doi:10.1161/STR.0000000000000069. PMID 26022637.
  42. ↑ Elijovich L, Patel PV, Hemphill JC (2008). "Intracerebral hemorrhage". Semin Neurol. 28 (5): 657–67. doi:10.1055/s-0028-1105974. PMID 19115172.
  43. ↑ Hemphill JC, Greenberg SM, Anderson CS, Becker K, Bendok BR, Cushman M; et al. (2015). "Guidelines for the Management of Spontaneous Intracerebral Hemorrhage: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association". Stroke. 46 (7): 2032–60. doi:10.1161/STR.0000000000000069. PMID 26022637.
  44. ↑ Sarode R, Milling TJ, Refaai MA, Mangione A, Schneider A, Durn BL; et al. (2013). "Efficacy and safety of a 4-factor prothrombin complex concentrate in patients on vitamin K antagonists presenting with major bleeding: a randomized, plasma-controlled, phase IIIb study". Circulation. 128 (11): 1234–43. doi:10.1161/CIRCULATIONAHA.113.002283. PMC 6701181 Check |pmc= value (help). PMID 23935011. Review in: Ann Intern Med. 2014 Apr 15;160(8):JC6
  45. ↑ Pollack CV, Reilly PA, van Ryn J, Eikelboom JW, Glund S, Bernstein RA; et al. (2017). "Idarucizumab for Dabigatran Reversal - Full Cohort Analysis". N Engl J Med. 377 (5): 431–441. doi:10.1056/NEJMoa1707278. PMID 28693366.
  46. ↑ Connolly SJ, Milling TJ, Eikelboom JW, Gibson CM, Curnutte JT, Gold A; et al. (2016). "Andexanet Alfa for Acute Major Bleeding Associated with Factor Xa Inhibitors". N Engl J Med. 375 (12): 1131–41. doi:10.1056/NEJMoa1607887. PMC 5568772. PMID 27573206.
  47. ↑ Hemphill JC, Greenberg SM, Anderson CS, Becker K, Bendok BR, Cushman M; et al. (2015). "Guidelines for the Management of Spontaneous Intracerebral Hemorrhage: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association". Stroke. 46 (7): 2032–60. doi:10.1161/STR.0000000000000069. PMID 26022637.
  48. ↑ Dennis M, Sandercock P, Graham C, Forbes J, CLOTS (Clots in Legs Or sTockings after Stroke) Trials Collaboration. Smith J (2015). "The Clots in Legs Or sTockings after Stroke (CLOTS) 3 trial: a randomised controlled trial to determine whether or not intermittent pneumatic compression reduces the risk of post-stroke deep vein thrombosis and to estimate its cost-effectiveness". Health Technol Assess. 19 (76): 1–90. doi:10.3310/hta19760. PMC 4782814. PMID 26418530. Review in: Evid Based Nurs. 2016 Apr;19(2):47
  49. ↑ Paciaroni M, Agnelli G, Venti M, Alberti A, Acciarresi M, Caso V (2011). "Efficacy and safety of anticoagulants in the prevention of venous thromboembolism in patients with acute cerebral hemorrhage: a meta-analysis of controlled studies". J Thromb Haemost. 9 (5): 893–8. doi:10.1111/j.1538-7836.2011.04241.x. PMID 21324058.
  50. ↑ Hemphill JC, Greenberg SM, Anderson CS, Becker K, Bendok BR, Cushman M; et al. (2015). "Guidelines for the Management of Spontaneous Intracerebral Hemorrhage: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association". Stroke. 46 (7): 2032–60. doi:10.1161/STR.0000000000000069. PMID 26022637.
  51. ↑ Hemphill JC, Greenberg SM, Anderson CS, Becker K, Bendok BR, Cushman M; et al. (2015). "Guidelines for the Management of Spontaneous Intracerebral Hemorrhage: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association". Stroke. 46 (7): 2032–60. doi:10.1161/STR.0000000000000069. PMID 26022637.


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