Sequential Change of Brain Edema by Semiquantitative Measurement on MRI in Patients with Hypertensive Intracerebral Hemorrhage

Suga, S.; Sato, Shuzo; Yunoki, Kazuta; Mihara, Ban

doi:10.1007/978-3-7091-9334-1_156

Cited by 13 publications

(19 citation statements)

References 3 publications

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“…Our literature search identified seven studies that exam ined the time course of PHO-early, delayed or bothand its association with patient outcome. 8,[12][13][14]91,96,97 One study of early PHO showed that the increase in abso lute PHO in the first 72 h after the ictus was predictive of inhospital mortality; 96 this finding is consistent with the fact that PHO grows most rapidly during this time period. Five other studies that examined the time course of early PHO found no association between early PHO and outcome.…”

Section: Pho As a Predictor Of Clinical Outcomesupporting

confidence: 74%

“…Five other studies that examined the time course of early PHO found no association between early PHO and outcome. 8,[12][13][14]91 However, evidence suggests that oedema continues to accumulate for 2-3 weeks after ICH, 12,91 and the implications of this delayed oedema are unclear. Of six studies that examined the time course of delayed PHO, [12][13][14]91,96,97 only one 97 documented an association between delayed oedema and clinical outcome.…”

Section: Pho As a Predictor Of Clinical Outcomementioning

confidence: 97%

“…Overall, PHO progresses fastest in the first 2-3 days, peaks after ~2 weeks, and typically resolves by 1 month. [12][13][14] Stage 1: ionic oedema Formation of PHO following ICH initiates with the presence of serum from both primary and secondary haemorrhages in the interstitium of the brain. After Key points ■ Secondary injury following intracerebral haemorrhage (ICH) is caused by perihaemorrhagic inflammation, toxic products of blood breakdown, and perihaematomal oedema (PHO) ■ Secondary injury contributes to neurological deterioration over an extended period of hours to days and, therefore, offers a long therapeutic window ■ PHO forms in three stages in accordance with Starling's principle: stage 1 is characterized by ionic oedema, and stages 2 and 3 by progressive vasogenic oedema ■ PHO is a pathophysiological marker of secondary injury that could provide a useful surrogate end point for testing novel neuroprotective agents ■ PHO might also be clinically relevant, as it augments the mass effect of haemorrhage; further studies could identify subgroups of patients who would benefit from therapies that ameliorate PHO ■ Combination treatment regimens that target different stages of PHO formation might be most effective to reduce swelling the haemorrhagic event, PHO advances rapidly before frank disruption of the BBB occurs.…”

Section: Pathophysiology Of Phomentioning

confidence: 99%

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Targeting secondary injury in intracerebral haemorrhage—perihaematomal oedema

et al. 2015

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Perihaematomal oedema (PHO) is an important pathophysiological marker of secondary injury in intracerebral haemorrhage (ICH). In this Review, we describe a novel method to conceptualize PHO formation within the framework of Starling's principle of movement of fluid across a capillary wall. We consider progression of PHO through three stages, characterized by ionic oedema (stage 1) and progressive vasogenic oedema (stages 2 and 3). In this context, possible modifiers of PHO volume and their value in identifying patients who would benefit from therapies that target secondary injury are discussed; the practicalities of using neuroimaging to measure PHO volume are also considered. We examine whether PHO can be used as a predictor of neurological outcome following ICH, and we provide an overview of emerging therapies. Our discussion emphasizes that PHO has clinical relevance both as a therapeutic target, owing to its augmentation of the mass effect of a haemorrhage, and as a surrogate marker for novel interventions that target secondary injury.

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Section: Pho As a Predictor Of Clinical Outcomesupporting

confidence: 74%

Section: Pho As a Predictor Of Clinical Outcomementioning

confidence: 97%

Section: Pathophysiology Of Phomentioning

confidence: 99%

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Targeting secondary injury in intracerebral haemorrhage—perihaematomal oedema

et al. 2015

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“…It is unclear, however, what criteria were used to define edema and how many patients had similar neuroimaging findings without neurological deterioration. Finally, in a series of 7 patients with ICH, 42 changes in the volume of the high-signalintensity area on T2-weighted MRI scans (increasing relative to initial CT hyperdensity at 1 week, peaking at 2 weeks, and declining at 4 weeks) did not correlate with clinical status.…”

Section: Discussionmentioning

confidence: 99%

Progression of Mass Effect After Intracerebral Hemorrhage

Zazulia

Diringer

Derdeyn

et al. 1999

Stroke

363

241

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Background and Purpose-While the evolution of mass effect after cerebral infarction is well characterized, similar data regarding intracerebral hemorrhage (ICH) are scant. Our goal was to determine the time course and cause for progression of mass effect after ICH. Methods-Patients with spontaneous supratentorial ICH who underwent Ն2 CT scans were identified in our prospectively collected database. CT lesion size and midline shift of the pineal and septum pellucidum were retrospectively measured and correlated with clinical and CT characteristics. Causes for increased midline shift were determined by 2 independent observers. Results-Seventy-six patients underwent 235 scans (3.1Ϯ1.3 per patient). Initial CT was obtained within 24 hours of ICH in 66. Twenty-five scans were repeated on day 1, 80 on days 2 through 7, 31 on days 8 through 14, and 24 Ͼ14 days after ICH. Midline shift was present on 88% of the initial scans. There were 17 instances of midline shift progression: 10 occurred early (0.2 to 1.7 days) and were associated with hematoma enlargement, and 7 occurred late (9 to 21 days) and were associated with edema progression. Progression of mass effect due to edema occurred with larger hemorrhages (PϽ0.05). Of 65 scans repeated for clinical deterioration, only 10 were associated with increased mass effect. Conclusions-Progression of mass effect after ICH occurred at 2 distinct time points: within 2 days, associated with hematoma enlargement, and in the second and third weeks, associated with increase in edema. The clinical significance of later-developing edema is unclear.

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“…11 Perifocal edema was shown for at least 2 to 3 weeks in several studies. 9,12 In ICH early progression is related to hematoma enlargement whereas late progression is associated with the development of extensive edema. 9 To date there is no data to decide whether in the first day of ICH onset mannitol is harmful due to promoting hematoma expansion or beneficial due to decreasing early edema.…”

Section: Responsementioning

confidence: 99%

Response to Letter by Prakash

Bereczki

Liu²,

Prado

et al. 2008

Stroke

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Response to Letter by Prakash Response:In his letter regarding our systematic review on mannitol in acute stroke 1 Dr Prakash expresses his astonishment that hypertonic mannitol is used at all in the treatment of patients with intracerebral hemorrhage (ICH). Despite his surprise, several articles suggest that mannitol has been used to treat this condition all over the world including India, 2 China, 3 Japan, 4 Italy, 5 Romania, Hungary, 6 and the United States. 7 This practice is based on several studies like that of Haass et al 8 over 20 years ago, showing that the pronounced brain edema which develops during several days after an ICH could lead to an increase in intracranial pressure requiring treatment.A bimodal time course of mass effect is typical after ICH: the first peak occurs in the first 48 hours after the onset of ICH representing the growth of the hemorrhage, and the second peak starts a few days later associated with an increase in edema. 9 Hematoma enlargement occurred in 38% of patients in the first day of ICH: in 26% within the first hour, and in a further 12% between 1 to 20 hours. 10 Not only the hematoma itself but the perihematomal edema also grows in the hyperacute phase of ICH-an approximately 75% increase in edema volume was described during the first 24 hours. 11 Perifocal edema was shown for at least 2 to 3 weeks in several studies. 9,12 In ICH early progression is related to hematoma enlargement whereas late progression is associated with the development of extensive edema. 9 To date there is no data to decide whether in the first day of ICH onset mannitol is harmful due to promoting hematoma expansion or beneficial due to decreasing early edema. As the risk of hematoma expansion decreases after the second day, whereas edema progresses thereafter, the lowest risk and largest benefit of mannitol use might be achieved if treatment starts only 1 to 2 days after ICH onset. This, however, remains a hypothesis until well-designed large studies decide whether a very early or a delayed use of mannitol is justified in acute ICH. However, because mannitol is inexpensive, academic trials are extremely difficult to run unless the current regulations change, and the limited evidence does not suggest that mannitol is beneficial in ICH, we do not think that such a large trial will be organized in the near future. According to the current guidelines based on limited evidence, osmotherapy-including mannitol-after ICH has received a Class IIa, Level of Evidence B recommendation, ie, the weight of evidence or opinion is in favor of the procedure or treatment. 13 Despite all the above, based on our earlier observations on over 100 patients 6 and on our systematic review 1 we share the concerns of Dr Prakash that mannitol might do more harm than good in acute ICH. We assume that even if we have more reliable evidence in the future against the use of mannitol, because of the lack of an evidence-based alternative treatment, the practice of osmotherapy will not change in cases when clinical signs of increasi...

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Sequential Change of Brain Edema by Semiquantitative Measurement on MRI in Patients with Hypertensive Intracerebral Hemorrhage

Cited by 13 publications

References 3 publications

Targeting secondary injury in intracerebral haemorrhage—perihaematomal oedema

Targeting secondary injury in intracerebral haemorrhage—perihaematomal oedema

Progression of Mass Effect After Intracerebral Hemorrhage

Response to Letter by Prakash

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