Acute Hypertension in Intracerebral Haemorrhage - Pathophysiology and Management

Acute Hypertension in Intracerebral Haemorrhage - Pathophysiology and Management

Adnan I Qureshi, Qaisar A Shah
Published: European Neurological Disease 2006 Issue 2
download article

| More
dots

Incidence

Intra-parenchymal bleeding with or without extension into the ventricles and rarely into the subarachnoid space is recognised as spontaneous intracerebral haemorrhage (ICH). Among all strokes spontaneous ICH accounts for approximately 10–15% cases, either primary or secondary.1 Chronic hypertension is regarded as the leading cause of the primary ICH, followed by amyloid angiopathy.2 Vascular malformation, coagulation abnormalities or intracranial tumours accounts for most cases of secondary ICH. Incidence of ICH ranges from 10–20 cases per 100,000 population.3 The mortality from ICH within the first months ranges from 44% to 51% and at two years post-ictus from 56% to 61%.4-6

There have been many studies showing the elevation of the blood pressure after ICH.7-10 Qureshi et al.,11 in their large cross-sectional study, showed elevated systolic blood pressure (SBP) ≥140mmHg in 63% of stroke patients, and the proportion of the patients with ICH with elevated SBP ≥140mmHg were 75%. Prevalence of various blood pressure in ICH were as follows: SBP between 140 and 184mmHg was 50%; SBP between 185 and 219mmHg was 17%; and SBP >220mmHg was 3%.There have been many studies showing the elevation of the blood pressure after ICH.7-10 Qureshi et al.,11 in their large cross-sectional study, showed elevated systolic blood pressure (SBP) ≥140mmHg in 63% of stroke patients, and the proportion of the patients with ICH with elevated SBP ≥140mmHg were 75%. Prevalence of various blood pressure in ICH were as follows: SBP between 140 and 184mmHg was 50%; SBP between 185 and 219mmHg was 17%; and SBP >220mmHg was 3%.

Blood pressure elevation has been associated with poor clinical outcomes including death and dependency.10 This has been demonstrated in retrospective review by Dandapani et al.,12 in which they reviewed 87 patients with ICH with marked elevation of blood pressure on admission. The group of the patients who had SBP higher than 140mmHg had a higher rate of mortality.

Pathological Process
In order to understand how chronic hypertension influences the dynamics of the cerebral autoregulation we have to first understand the normal autoregulation of the brain. The cerebral autoregulation is maintained at the level of arterioles, which vasoconstrict with increase in blood pressure and vasodilate with decrease in blood pressure. These changes in vessel diameter maintain normal CBF under a wide range of cerebral perfusion pressure (CPP). The range of normal autoregulation is considered to be between 50 and 150mmHg. In chronic hypertensive patients there is a shift in the curve to the right, and thus patients with chronic untreated hypertension are at an increase risk of ischemic injury with sudden decrease in the CPP below the lower limit of autoregulation.

The exact reasoning behind the acute elevation of the blood pressure in stroke patients is not absolutely obvious; many different explanations have been put forward to define the acute elevation: first, it could be the reflection of the untreated hypertension;13 second, Cushing-Kocher response, which is a reaction from the compression of the brain stem;4,14 and third, abnormal sympathetic, parasympathetic activity, raised levels of circulating catecholamines15 and brain natriuretic peptide (BNP).16

12345next ›last »
References:
  1. Dennis MS, et al., "Long-term survival after first-ever stroke: the Oxfordshire Community Stroke Project", Stroke (1993);24(6): pp. 796 800.
  2. Foulkes MA, et al., "The Stroke Data Bank: design, methods, and baseline characteristics", Stroke (1988);19(5): pp. 547 554.
  3. Giroud M, et al., "Cerebral haemorrhage in a French prospective population study", J Neurol Neurosurg Psychiatry (1991);54(7): pp. 595 598.
  4. Qureshi AI, et al., "Spontaneous intracerebral hemorrhage", N Engl J Med (2001);344(19): pp. 1450 1460.
  5. Juvela S, "Risk factors for impaired outcome after spontaneous intracerebral hemorrhage", Arch Neurol (1995);52(12): pp. 1193 200.
  6. Lisk DR, et al., "Early presentation of hemispheric intracerebral hemorrhage: prediction of outcome and guidelines for treatment allocation", Neurology (1994);44(1): pp. 133 139.
  7. Wallace JD, Levy LL, "Blood pressure after stroke", JAMA, (1981);246(19): pp. 2177 2180.
  8. Britton M, Carlsson A, de Faire U, "Blood pressure course in patients with acute stroke and matched controls", Stroke (1986);17(5): pp. 861 864.
  9. Aslanyan S, et al., "Effect of blood pressure during the acute period of ischemic stroke on stroke outcome: a tertiary analysis of the GAIN International Trial", Stroke (2003);34(10): pp. 2420 2425.
  10. Willmot M, Leonardi-Bee J, Bath PM, "High blood pressure in acute stroke and subsequent outcome: a systematic review",Hypertension (2004);43(1): pp. 18 24.
  11. Qureshi AI, Ezzedine MA, Nasar Abu, et al., "Acute Hypertension in 563,704 Adult Patients Presenting to the Emergency Room with Stroke in the United States", American Journal of Emergency Medicine (2007); In Press.
  12. Dandapani BK, et al., "Relation between blood pressure and outcome in intracerebral hemorrhage", Stroke (1995);26(1): pp. 21 24.
  13. Arboix A, et al., "Differences between hypertensive and non-hypertensive ischemic stroke", Eur J Neurol (2004);11(10): pp. 687 692.
  14. Qureshi AI, et al., "Long-term outcome after medical reversal of transtentorial herniation in patients with supratentorial mass lesions", Crit Care Med (2000);28(5): pp. 1556 1564.
  15. Cheung RT, Hachinski V, "Cardiac Effects of Stroke", Curr Treat Options Cardiovasc Med (2004);6(3): pp. 199 207.
  16. Nakagawa K, et al., "Plasma concentrations of brain natriuretic peptide in patients with acute ischemic stroke", Cerebrovasc Dis (2005);19(3): pp. 157 164.
  17. Chen ST, et al., "Progression of hypertensive intracerebral hemorrhage", Neurology (1989);39(11): pp. 1509 1514.
  18. Kazui S, et al., "Enlargement of spontaneous intracerebral hemorrhage. Incidence and time course", Stroke (1996);27(10): pp. 1783 1787.
  19. Kelley RE, et al., "Active bleeding in hypertensive intracerebral hemorrhage: computed tomography", Neurology (1982);32(8): pp. 852 856.
  20. Kazui S, et al., "Predisposing factors to enlargement of spontaneous intracerebral hematoma", Stroke (1997);28(12): pp. 2370 2375.
  21. Nath FP, et al., "Effects of experimental intracerebral hemorrhage on blood flow, capillary permeability, and histochemistry", J Neurosurg (1987);66(4): pp. 555 562.
  22. Bullock R, et al., "Intracerebral hemorrhage in a primate model: effect on regional cerebral blood flow", Surg Neurol (1988);29(2): pp. 101 107.
  23. Mendelow AD, et al., "Intracranial haemorrhage induced at arterial pressure in the rat. Part 2: Short term changes in local cerebral blood flow measured by autoradiography"Neurol Res (1984);6(4): pp. 189 193.
  24. Qureshi AI, et al., "No evidence for an ischemic penumbra in massive experimental intracerebral hemorrhage", Neurology (1999);52(2): pp. 266 272.
  25. Hirano T, et al., "No evidence of hypoxic tissue on 18F-fluoromisonidazole PET after intracerebral hemorrhage", Neurology (1999);53(9): pp. 2179 2182.
  26. Zazulia AR, et al., "Hypoperfusion without ischemia surrounding acute intracerebral hemorrhage", J Cereb Blood Flow Metab (2001);21(7): pp. 804 810.
  27. Carhuapoma JR, et al., "Diffusion-weighted MRI and proton MR spectroscopic imaging in the study of secondary neuronal injury after intracerebral hemorrhage", Stroke (2000);31(3): pp. 726 732.
  28. Yang GY, et al., "Experimental intracerebral hemorrhage: relationship between brain edema, blood flow, and blood-brain barrier permeability in rats", J Neurosurg (1994);81(1): pp. 93 102.
  29. Nath FP, et al., "Early hemodynamic changes in experimental intracerebral hemorrhage", J Neurosurg (1986);65(5): pp. 697 703.
  30. Qureshi AI, et al., "Cerebral blood flow changes associated with intracerebral hemorrhage", Neurosurg Clin N Am (2002);13(3): pp. 355 370.
  31. Broderick JP, et al., "Guidelines for the management of spontaneous intracerebral hemorrhage: A statement for healthcare professionals from a special writing group of the Stroke Council, American Heart Association", Stroke (1999);30(4): pp. 905 915. professionals from a special writing group of the Stroke Council, American Heart Association", Stroke (1999);30(4): pp. 905 915.
  32. Meyer JS, Bauer RB, "Medical treatment of spontaneous intracranial hemorrhage by the use of hypotensive drugs", Neurology (1962);12: pp. 36 47.
  33. Qureshi AI, et al., "Pharmacologic reduction of mean arterial pressure does not adversely affect regional cerebral blood flow and intracranial pressure in experimental intracerebral hemorrhage", Crit Care Med, (1999);7(5): pp. 965 971.
  34. Powers WJ, et al., "Autoregulation of cerebral blood flow surrounding acute (6 to 22 hours) intracerebral hemorrhage", Neurology (2001);57(1): pp. 18 24.
  35. Qureshi AI, et al., "A prospective multicenter study to evaluate the feasibility and safety of aggressive antihypertensive treatment in patients with acute intracerebral hemorrhage", J Intensive Care Med (2005); 20(1): pp. 34 42.
  36. Qureshi AI, et al., "Treatment of acute hypertension in patients with intracerebral hemorrhage using American Heart Association guidelines", Crit Care Med (2006);34(7): pp. 1975 1980.
  37. Qureshi AI, "Antihypertensive Treatment of Acute Cerebral Hemorrhage (ATACH): Rationale and Design", Neurocritical Care (2007);. In Press.
  38. Chobanian AV, et al., "The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report", JAMA", (2003);289(19): pp. 2560 2572.
Copyright® 2012 Touch Group PLC. All rights reserved.
Touch Neurology is for informational purposes and should not be considered medical advice, diagnosis or treatment recommendations.