Lupine Publishers | Journal of Health Research and Reviews
Intravenous thrombolysis for acute ischemic stroke can be complicated
by intracranial haemorrhage. Early decompressive
craniectomy in such patients can be life saving but is associated with
high risk of peri operative bleeding. We managed such a patient
with decompressive craniectomy within 24hrs of thrombolysis by
correcting coagulation with the help of thromboelastograhpy.
Keywords: Decompressive craniectomy; Intravenous thrombolysis; Symptomatic intracranial haemorrhage; Thromboelastography
Acute ischemic stroke is one of the leading causes of death and
permanent disability in the world. Intravenous thrombolysis (IVT)
with recombinant tissue plasminogen activator (rt-PA) has been
the recommended treatment modality in acute ischemic stroke [1].
but the most dreadful complication of thrombolysis is intracerebral
haemorrhage in about 7% cases. The clinicians are faced with
difficult decision of how to best treat these patients as there are
no evidence based guidelines regarding the management of such
complications. The American Heart Association has suggested
only empirical therapies to replace clotting factors and platelets
to reverse coagulopathy [2]. Decompressive craniectomy (DC) is a
life-saving procedure for malignant middle cerebral artery stroke
associated with cerebral oedema, enough to cause herniation and
death [3]. The decision of decompressive craniectomy following
intracerebral haemorrhage after intravenous thrombolysis is not
without the risk of peri operative haemorrhage. We report the first
case where decompressive surgery was uneventfully performed as
a life-saving procedure within 24hours of developing symptomatic
intracerebral haemorrhage after intravenous thrombolysis.
The timing for decompressive craniectomy was guided by
thromboelastography (TEG).
A 63-year old hypertensive, diabetic man presented with left
hemiplegia within 140 minutes of onset. On examination, he was
alert, GCS 15, left hemiplegia, right gaze palsy and dysarthria, NIHSS
(National Institute of Health Stroke Scale) of 17. Magnetic resonance
imaging of the brain revealed infarct in the superior division of right
middle cerebral artery (MCA) (Figure 1a). His blood biochemistry
was unremarkable (Hb-13.8, Plt-145, PT-12.2, and RBS-174). After
written consent, thrombolysis was started at 22:10hrs on 11.1.2015
with rt-PA, 5.8mg as bolus followed by 52.7mg infusion over one
hour. At 5:30hrs on 12.1.2015, he had upper gastrointestinal bleed
followed by impairment in consciousness and his NIHSS score
increased to 28. Immediate repeat CT scan of the brain revealed
extensive infarction of MCA with haemorrhage in the infarct,
extensive oedema and midline shift with uncal herniation (Figure
1b). As he had been recently thrombolysed, his repeat coagulation
profile was performed (Hb-10.4, Plt-160, PT-15.2, APTT-27.8, FDP-
256mg/dL) including thromboelastography which was classical of
fibrinolysis. Eight units of cryoprecipitate and four units of fresh
frozen plasma were transfused in the next six hours and repeat
thromboelastography was normal. Then the decision was to
proceed with decompressive craniectomy (15:30hr on 12.1.15).
A bone window of 12cm in the antero posterior direction in the
fronto parieto temporal region was created and duroplasty was
performed. The procedure was uneventful. He did not receive any
blood products in the peri operative period. Brain CT scan was
again performed on the following day and it showed resolution of
midline shift with no new hematoma (Figure 1c). He was managed in the intensive care unit with gradual weaning of sedation and
ventilation. He was discharged in the sixth week on tracheotomy
and NIHSS score of 12. Three months later he was admitted for
cranioplasty (Figure 1d) and tracheostomy closure with Mrs Score
of 3 (Figure 2a & 2b).
Figure 1: (a) Magnetic resonance imaging of the brain (diffusion weighted image) done at presentation shows acute infarction
of the right superior middle cerebral artery. (b) Non contrast CT of the brain done 8 hours after thrombolysis showed
haemorrhage in the infarct resulting in mid line shift and mass effect. (c) Non Contrast CT of the brain done on the next
day after decompressive craniectomy and hematoma evacuation revealed no new bleed and resolving mass effect.(d) Non
Contrast CT of the brain following cranioplasty.
Figure 2: (a) Thromboelastograph trace obtained after 8hr of thrombolysis with R-1.7min, α-66.80, MA-19.6mm, LY30-97.4%,
EPL%-100%. These features are characteristic features of fibrinolysis with normal R time, decreased maximum amplitude
(MA), raised LY30 (percentage decrease in maximum amplitude or lysis after 30 minutes) and raised EPL. EPL represents the
computer prediction of 30mins clot lysis based on interrogation of actual rate of diminution of the trace commencing 30sec
post MA with a normal value of <15%. It is the earliest indicator of abnormal lysis. (b) Thromboelastographic trace obtained
after infusion of cryoprecipitate and fresh frozen plasma with R-6min, K-1.5min, α-67.50, MA-49.6mm, LY30-0%, EPL%-0%.
Thrombolysis remains the treatment of choice in acute
ischemic stroke but with increased risk of symptomatic intracranial
haemorrhage (ICH).The mortality in these patients is reported to
be as high as 45% [4]. There are a few case reports in literature that
state DC might be beneficial in the context of post IVT in patients
with refractory cerebral oedema [5]. But the most important
void is the optimal time to perform DC following thrombolysis.
To the best of our knowledge there is only one prior case report
where decompressive craniectomy was performed for intracranial
haemorrhage following unsuccessful IVT after 48 hour of
thrombolysis [6]. Here we report the index case where symptomatic
intracranial haemorrhage followed thrombolysis, and was managed
by DC and hematoma evacuation within 24 hours of IVT. This
early life saving surgery was possible only after rapid correction
of coagulation profile with the help of thromboelastography. As, a
large series is difficult to be conducted in such cases, it is of interest
to report small experiences as ours where the clinical dilemma of
performing a surgery following thrombolysis with rt-PA was guided
by thromboelastography.
Recombinant t-PA is an exogenous stimulator of the fibrinolytic
system that enhances local fibrinolysis by converting plasminogen
to plasmin. Our concern was the increased risk of peri operative
haemorrhage associated with high mortality due to the persistent
effect of TPA. With regard to the pharmacokinetics, half-life of rt-
PA is <5 min, with clearance rate of 380-570mL/min [7]. Hence,
80% of rt-PA is cleared from the plasma within 10 minutes of
administration. Despite short half-life of rt-PA fibrinolytic effects
peak at 4hours and can persist up to 24-48hours [7]. The clinical
dilemma in such a scenario was to wait for the disappearance of
the fibrinolytic effects to avoid peri operative bleeding at the cost of
outweighing the benefits of early DC in reducing the raised ICP. The
other option was to efficiently detect and correct the coagulation
abnormality by transfusing specific blood products to minimize the
risk of bleeding. We had the benefit of thromboelastography at our
institute to guide.com with the correction of the deranged coagulation
profile before proceeding for DC. S Takeuchi et al. retrospectively
reviewed 20 patients who underwent DC for malignant hemispheric
infarction after IV TPA administration, with another 20 patients
undergoing DC without prior IV TPA administration [8]. They
observed intracranial bleeding or worsening of pre existing ICH in
two patients (10%) in each group, but tPA was not thought to be
contributory to the hemorrhagic events because of the long intervals
between the IV tPA and DC(185 and 136h, respectively). However,
fibrinolytic markers, such as fibrinogen or fibrin degradation
products were unfortunately not measured in the above series.
Thrombelastography or TEG measures the physical properties
of the clot via a pin suspended in a cup from a torsion wire
connected with a mechanical-electrical transducer. TEG is different
from other coagulation tests as it provides global information on
the dynamics of clot development, stabilization and dissolution [9].
It assesses both thrombosis and fibrinolysis. Its role is established
in cardiac and liver transplant surgery and is being increasingly
explored to study role of fibrinolysis in early trauma coagulopathy
[10]. Although routinely tested coagulation parameters (BT, CT, PTI,
and APTT) were also normal in our case but TEG was characteristic
of enhanced fibrinolysis. Hence, we transfused cryoprecipitate and
fresh frozen plasma after which the TEG was normal, and we could
proceed with surgery.
Decompressive hemicraniectomy with hematoma evacuation
following thrombolysis represents an aggressive life saving
treatment approach, especially for the patients who develop
hemorrhagic complications of intravenous thrombolysis. TEG is
one modality which can guide the reversal of deranged coagulation
parameter so that major surgery can be undertaken with minimal
risk. The decision to proceed with major surgical intervention
requires a competent multi disciplinary team as well as an open
discussion with relatives as DC may preserve both life and functional
ability in well selected patients. More research is needed in this
field to elucidate the potential for both modalities in appropriate
patients.
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