The size of the hematoma grows due to rebleeding in the next few hours after the onset in up to 40% of cases which results in early neurological deterioration, poor functional outcome and increased mortality.

3. ◘ S-ICH is defined as rapidly developing
neurological signs attributable to a focal
collection of blood within the brain
parenchyma and/or the ventricular system that
is not caused by trauma.
◘ S-ICH is the 2nd most common stroke subtype
accounting for 15% of all cases.
◘ S-ICH is the most lethal stroke subtype with
nearly 40% of patients die within 1-month, and
75% of survivors are left with severe disabilities.

4. ◘ Structural vascular lesions.
◘ Medication induced S-ICH.
◘ Cerebral Amyloid angiopathy.
◘ Systemic disease related S-ICH.
◘ Hypertension related S-ICH.
◘ S-ICH of Undetermined etiology.
◘ S-ICH is classified to:
(1) Primary: HTN, CAA.
(2) Secondary: SVL, MI, SD related S-
ICH.

7. ◘ AME is a 49 year old HTN male, presented by
sudden onset of right sided weakness with
baseline NCCT showed left thalamo-ganglionic
hematoma.
◘ The patient received medical treatment and early
neurosurgical consultation was answered “the
patient’s neurological state is good and no need for
early hematoma evacuation”.
◘ The patients deteriorated within 2-days, rescan
showed huge HE and neurosurgical re-
consultation stated that “the patient’s is comatose
and can’t withstand evacuation surgery”.
◘ The patient died few days later.

8. ◘ The shocking fact is that current management of
S-ICH is predominantly supportive, including
airway protection, optimization of
hemodynamic parameters, and management of
increased ICP.
◘ Active anti-expansion medical treatments
resulted in thromboembolic complications
while neurosurgical evacuation is associated
with increased risk of hematoma recollection
and postoperative complications.
◘ To date, non of both revealed any superiority.

9. 1. Patients with cerebellar hemorrhage who are deteriorating neurologically or who have brainstem
compression and/or hydrocephalus from ventricular obstruction should undergo surgical removal of the
hemorrhage as soon as possible (Class I; Level of Evidence B).
2. For supratentorial S-ICH, the usefulness of surgery is not well established (Class IIb; Level of Evidence A).
3. A policy of early hematoma evacuation is not clearly beneficial compared with hematoma evacuation
when patients deteriorate (Class IIb; Level of Evidence A).
4. Supratentorial hematoma evacuation in deteriorating patients might be considered as a life-saving measure
(Class IIb; Level of Evidence C).
5. Decompressive craniectomy with or without hematoma evacuation might reduce mortality for patients
with supratentorial S-ICH who are in a coma, have large hematomas with significant midline shift, or
have elevated ICP refractory to medical management (Class IIb; Level of Evidence C).
6. The effectiveness of minimally invasive clot evacuation with stereotactic or endoscopic aspiration with or
without thrombolytic usage is uncertain (Class IIb; Level of Evidence B).

10. ◘ There is an observable slowdown of the research pace after this era.
◘ In 2016, the median citation of the top 100 most cited S-ICH papers was 15.

11. ◘ The NINDS stated that, increasing researches is crucial as there is a noticeable
deficiency in studies related to S-ICH, HE and IVH management.

13. ◘ The size of the hematoma grows due to
rebleeding in the next few hours after the
onset in up to 40% of cases which results in
early neurological deterioration, poor
functional outcome and increased mortality.
◘ Early prediction of the upcoming HE is a
crucial inlet to improve S-ICH prognosis as it
allows early intervention for high risk
patients before brain herniation and
irreversible neuronal damage take place.

14. ◘ No fixed definitions of HE.
◘ In retrospective studies, HE was defined as an
increase HV > 12.5 ml or 50% from baseline
assessment.
◘ However, these levels were considered too
high in prospective studies where HE is
defined as increased baseline HV > 6 ml or
30% in follow-up images associated with
worsening of the patient's neurological state.

15. ◘ Two predominant models currently exist:
(1) Persistent bleeding model, which proposes
that the vessel that initially rupture may re-
bleed leading to enlargement of the hematoma.
(2) Secondary expansion model, postulates
that the mass effect caused by the initial
hematoma results in mechanical disruption of
neighboring vasculature and secondary re-
hemorrhage.

16. ◘ Ultra-early hemostatic therapy with (within 4-
hours of S-ICH onset) was used to reduce the
likelihood of HE.
◘ Recombinant factor VIIa was the most
commonly investigated and despite its success
in prevention of hematoma growth, the value
of its use was limited by the increased
thromboembolic complications.
◘ AHA/ASA, 2015 stated that rFVIIa is not
routinely recommended for S-ICH
patients.

17. ◘ Stereotactic hematoma aspiration following its lysis by locally administrated
r-tPA had been used instead of open hematoma evacuation and
decompressive hemicraniectomy. This is followed by catheter insertion for
hematoma drainage.

18. ◘ Endoscopic evacuation through minimally invasive surgeries is under trial.
◘ These strategies permit reliable visualization and cauterization of active
arterial bleeding than blind stereotactic aspiration.

21. ◘ The NCCT biomarkers may have the potential
to become an easy-to-use and readily
available tool to stratify the risk of HE in
patients with S-ICH.
◘ These NCCT predictors of impending HE are
valuable when present during baseline
assessment within few hours post-stroke.

22. ◘ The baseline hematoma volume is one of
the most important prognostic factors and
a major determinants of increased
mortality and poor functional outcome in
S-ICH.
◘ Large volume is a reflection of large tear in
the arterial wall with higher risk of re-
hemorrhage,.
◘ The risky volume varies regarding to the
hematoma location; > 30 ml for lobar
hematomas and >20 ml for deep ones.

23. ◘ Perihematomal edema formation results from
inflammation, neurotoxicity and disruption
of the BBB in the perihematomal tissue.
◘ The impact of perihematomal edema volume
on subsequent HE is controversial
◘ Some studies revealed that, early
disproportionate rapid rate of edema growth
contribute to higher risk of HE and poor
functional outcome.

25. ◘ Hematoma border irregularity and
multiple hematomas in baseline CT are
considered as independent risks of HE
as they indicate bleeding from multiple
foci or underlying CAA with high risks
of re-hemorrhage.

26. ◘ First described by Shimoda et al. 2017 as
a predictor HE and poor outcome.
◘ Has 60% sensitivity and 69% specificity for HE.
◘ Criteria of Satellite Sign:
(1) A small hematoma separate from main
hematoma on at least one slice.
(2) The largest transverse diameter of small
hematoma <10 mm.
(3) The minimal distance between the small and
main hematomas is 1 – 20 mm.
(4) SAH and IVH are excluded

27. ◘ First described by Li Qi et al., in 2017 as a
predictor of impending HE, poor functional
outcome and increased mortality.
◘ Has 40% sensitivity and 90% specificity for HE.
◘ Criteria of Island Sign:
(1) ≥ 3 small scattered rounded or oval separate
hematomas around the main one.
(2) ≥ 4 small hematomas separate from or
connected to the main one.
(3) The connected hematomas should be bubble- or
sprout-like but not lobulated.

29. ◘ Hematoma heterogenicity represents blood of different age which is an
indicator of active bleeding from multiple sites prone to re-bleeding and
HE.

30. ◘ Hypodensities within the hematoma and
not reaching the margin:
(1) Type-1: brain like density and distinct margin.
(2) Type-2: brain like density and indistinct
margin.
(3) Type-3: CSF like density.
(2) Black hole sign.
◘ Hypodensities reaching the margin:
(1) Type-4 (niveau formation): mixed density
with a fluid level.
(2) Swirl sign.
(3) Blend sign

32. ◘ Barras et al., 2009 created a novel 5-point
categorical scales reflecting the spectrum of
hematoma shape irregularity and
heterogenicity.
◘ Hematomas with categories 1 and 2 are
considered regular and homogenous while
categories 3 – 5 have irregular shapes and
heterogenous densities.
◘ Presence of IVE was not included in the ratings.

33. ◘ Barras scale category IV and V assumed
lobulated hematomas with broad base
projections.
◘ The island sign consisted of separate as well
as bubble- or sprout-like small
hematomas.
◘ Note that the large lobule (big arrow) in
the bottom of the main hematoma was not
considered islands.
BarrasShapeLiQi’sIslandSign

34. ◘ Described by Li Qi et al., in 2016.
◘ Has 55% sensitivity and 70% specificity for HE
prediction.
◘ Black Hole Criteria:
(1) Relatively hypo-attenuated area encapsulated
within the hyper-attenuated hematoma.
(2) Could be round, oval, or rod-like but is not
connected with the adjacent brain tissue.
(3) Should have an identifiable border.
(4) The black hole / hematoma heterogenicity
difference should be ≥ 28 HU.

35. (A, D) Absence of a clearly identifiable border, (B) The CT HU difference was <
28, (c) The 3 rod-like hypointense regions are connected with the adjacent
brain tissue and were not fully wrapped within the hematoma.

36. ◘ First defined by Selariu et al., 2012 as a
hypo- or iso-attenuation region (relative to the
brain parenchyma) within the hyper-
attenuated hematoma.
◘ The shape of this area may be rounded, streak-
like, or irregular.
◘ Swirl sign has 46.5% sensitivity and 71.3%
specificity for subsequent HE and is an
independent predictor of increased mortality
and poor functional outcome following S-ICH.

37. ◘ Described by Li Qi et al., in 2015.
◘ Blend Sign Criteria:
(1) Blending of relatively hypoattenuating area
with adjacent hyperattenuating region within
a hematoma.
(2) A well-defined margin between both regions
easily recognized by the naked eye.
(3) A difference of >18 HU between the two
density regions.
(4) The relatively hypoattenuating area was not
encapsulated by the hyperattenuating region.

38. ◘ Blend sign occurs as a result of active
bleeding followed by clot retraction and
serum sequestration out of the hematoma
resulting in 2 density areas.
◘ Blend Sign Mimics:
(1) Heterogeneous hematoma with no well-
defined margin between the 2 density
regions.
(2) Hypointense region within a
hyperattenuating hematoma which is
consistent with a swirl sign.
(1)
(2)

40. ◘ Most NCCT predictors have high
specificities but their study separately
resulted in low / moderate sensitivities.
◘ The development of a collective multi-
modality scores may overcome this
limitation.
◘ The HEAVN, BAT, Barras and NAG
scores have been emerged but their use
still limited.

42. ◘ Intra-hematoma contrast leakage as a predictor of HE has been studied since
the work of Murai et al., 1999.
◘ The Leakage Sign is defined as >10% HU increase in the hematoma density in
delayed 3-min. post-contrast injection phase.

43. ◘ First described by Wada et al., in 2007.
◘ Spot Sign Criteria:
(1) ≥ 1 focus of contrast pooling within the
hematoma.
(2) Attenuation ≥120 HU.
(3) Discontinuous from normal or abnormal
vasculature adjacent to the hematoma.
(4) Any size and morphology.
◘ Positive spot sign is associated with increased
risk of intraoperative bleeding and
postoperative hematoma recollection.

44. ◘ The underlying pathophysiology of SS still
unclear with a series of possible explanations,
including Charcot-Bouchard micro-
aneurysms (of penetrating arteries),
pseudoaneurysms, fibrin globes, and
breakdown of BBB.
◘ Correct recognition of SS is important as
several mimics are described including
micro-AVM, aneurysm or lesion calcification
which necessitate evaluation of NCCT
together with CTA source images.

45. ◘ Overcomes the false negative first pass CTA due to delayed contrast
extravasation (40 sec. to 3 min. after contrast injection).
◘ Needs high slices multi-detector scanners (128 – 320) which allow repeated
rapid whole head acquisition with reconstruction of CTA and CT perfusion
data.

51. ◘ Malfunctioning perforators in cerebral
small vessel diseases spectrum is
considered as an independent risk of
upcoming HE.
◘ Both lobar CMBs (CAA) as well as non-
lobar ones carry high risks of HE.
◘ There are controversial results between the
presence of WMHs or occult LBIs and
risks of HE.

52. ◘ B-mode TCD can be used as a bedside tool to
follow up the hematoma size through the
contralateral trans-temporal approach.
◘ The hematoma appears hyperechogenic relative to
the surrounding brain-parenchyma where the
size could be calculated by measuring the
sagittal, transverse and coronal diameters.
◘ TCD could be also used as a bedside maneuver
that optimizes catheter placement after
stereotactic insertion.

54. ◘ This work is adapted from the Master’s
Degree thesis submitted by Dr. Hany
Helal, to the Faculty of Medicine,
Tanta University.
◘ The aim was to study the predictors of
early HE after S-ICH and its effect on
patient’s survival and functional
outcome.

55. Inclusion Criteria Exclusion Criteria
◘ Traumatic ICH.
◘ Subarachnoid hemorrhages.
◘ Hemorrhagic transformation of
a recent ischemic stroke.
◘ Hemorrhage inside a space
occupying lesion.
◘ Vitally unstable patients.
◘ Patients had contraindications
to iodinated IV contrasts
◘ The work was a prospective
cohort study conducted on 72
patients with S-ICH admitted
to the neurovascular units
and/or the ICUs of the
Neurology Unit,
Neuropsychiatry Department,
Tanta University Hospitals in
the period from December
2016 till September 2018.

56. (1) Baseline clinical assessment, GCS, NIHSS and
non-contrast CT (hematomas sites, volumes,
heterogenicity and blend sign).
(2) 6-hours post-admission CTA for detection of
spot sign and estimation of SSS.
(3) 48-hour clinical reassessment and NCCT for
estimation of HE.
(4) Modified Rankin Scale was done 3-months post-
stroke to assess functional outcome (≤ 3 means
good outcome and ≥ 4 means bad outcome)

59. 55.6%
19.4%
19.4%
5.6%
HTN related Systemic Diseases
Antithrombotics Structural Vascular Lesion

60. 56.9%
29.2%
6.95%
6.95%
Thalamo-ganglionic Lohar Hemorrhage
Cerebellar Hemorrhage Brainstem Hemorrhage

61. 38.9%
61.1%
Hematoma Expansion Non-Hematoma Expansion

62. 0
20
40
60
80
100
HTN Medication Systemic Structural

63. 0
20
40
60
80
100
Lobar Deep Cerebellar Brainstem

64. 0
20
40
60
80
100
120
140
160
Age Mean ABP Random Sugar
HE non-HE

65. 0
5
10
15
20
25
30
35
Smoking Index NIHSS Hematoma Volume
HE non-HE

66. 0
10
20
30
40
50
60
% IVE % Hematoma Irregularity
HE non-HE

67. 0
10
20
30
40
50
60
70
Blend Sign Spot Sign
HE non-HE

69. 0
20
40
60
80
100
% Good Outcome % Bad Outcome % Mortality
HE non-HE

70. ◘ This figure shows positive correlations between the spot sign score and each
of; (a) the hematoma expansion volume, (b) the mRS 3-months post-
stroke.

73. Clinical HE Predictors Imaging HE Predictors
(1) NCCT predictors include large
hematoma volume, heterogenous
density, shape irregularity and IVE.
(2) The blend sign has lower sensitivity
but high specificity as a biomarker of
rebleeding.
(3) The CTA spot sign has moderate
sensitivity and high specificity for
impending HE prediction.
(1) History of warfarin use.
(2) High smoking index.
(3) High admission mean ABP.
(4) Admission GCS ≤ 8.
(5) Baseline NIHSS > 10.

74. ◘ From now and then, keep your eyes
familiar for NCCT / HE signs.
◘ Development of a NCCT multi-modality
collective score to increase the sensitivity of
HE prediction is needed as the CTA is not
24/7 readily available in emergency settings.
◘ Clinically and radiologically based scores that
predict impending HE are needed to be
applied practically.

75. ◘ Patients with signs of upcoming HE should be
managed in a different way from those
lacking these signs to ensure early
intervention before irreversible brain damage
takes place
◘ Funding is needed for the researches directed
to improve S-ICH outcome.

76. ◘ Decreasing first-month case-fatality rates to < 25% and increasing
the rate of good functional outcomes to > 50%.

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