CASE REPORT/CASE SERIES

Ipsilateral Parenchymal Hemorrhage After
Hemicraniectomy in a Patient Suffering From Malignant
Middle Cerebral Artery Infarction
Claudia Disqué, MD, and Georg Gahn, MD

Introduction: Early hemicraniectomy reduces mortality in malignant middle cerebral artery (MCA) infarctions to 16%, although the
benefit on functional outcome is still unclear. We treat patients with
malignant MCA infarction younger than 60 years. Epidural or
subgaleal hemorrhages are relatively common complications. Only 1
trial described parenchymal hemorrhage as a complication of hemicraniectomy.
Case Report: A 55-year-old man was admitted to our stroke unit
with right-sided hemiparesis and aphasia. NIHSS was 18; GCS, 3.
The initial CT showed hypoattenuation in the basal ganglia and the
insular ribbon on the left side. CT-angiography showed M1 occlusion. Despite thrombolysis with rtPA in the 3-hour time window, no
recanalization was achieved. We performed early hemicraniectomy.
Additionally, we started mild hypothermia and deep sedation to
prevent increasing cerebral edema. Control CT on day 2 showed
intracerebral hemorrhage and an obstructive hydrocephalus because
of intraventricular blood. To avoid herniation, the patient received
an extraventricular drainage (EVD). Thereafter, the intracerebral
pressure remained stable. The patient was discharged, with a NIHSS
of 18 and GCS of 10.
Conclusion: The reported patient is the first in the literature that
suffered from deep hemorrhage after hemicraniectomy. Hemorrhagic transformation might be a risk factor for clinically relevant
hemorrhage after hemicraniectomy.
Key Words: stroke, hemicraniectomy, hemorrhage, malignant
middle cerebral artery infarction
(The Neurologist 2007;13: 95–97)

A

bout 10% of ischemic strokes are classified as malignant
middle cerebral artery (MCA) infarctions.1 Without interventional therapy, 80% of these patients die secondary to
transtentorial herniation.2 Surgery is able to reduce the mortality to 16% in early hemicraniectomy and 34% in delayed

From the Technical University Dresden, Neurology Department, Dresden,
Germany.
Reprints: Claudia Disqué, Technical University Dresden, Neurology Department, Fetscherstr. 74, 01307 Dresden, Germany. E-mail: claudiadisque@
web.de.
Copyright © 2007 by Lippincott Williams & Wilkins
ISSN: 1074-7931/07/1302-0095
DOI: 10.1097/01.nrl.0000254662.41344.73

The Neurologist • Volume 13, Number 2, March 2007

hemicraniectomy.3 Although the benefit on functional outcome is still unclear, hemicraniectomy is performed in many
centers because of the desperate prognosis of malignant
infarction. In our institution, we treat patients with malignant
MCA infarction younger than 60 years with early hemicraniectomy. Ipsilateral to the side of infarction, the frontotemporoparietal bone flap is removed and a duraplasty performed
to allow the brain to swell. Epidural or subgaleal hemorrhages are relatively common complications.4 Only 1 trial
described parenchymal hemorrhage as a complication of
hemicraniectomy. Those parenchymal hemorrhages were
mostly located in the cortex close to the bone edge.4 To our
knowledge, this patient is the first one with a parenchymal
hemorrhage after hemicraniectomy reported in the literature.

Hemicraniectomy is performed in many centers
because of the desperate prognosis of
malignant infarction.

CASE REPORT
A 55-year-old man was admitted to our stroke unit with
right-sided hemiparesis and aphasia. The initial CT showed a
hyperdense MCA sign and hypoattenuation in the basal
ganglia and the insular ribbon on the left side (Figs. 1, 2). The
CT-angiography showed M1 occlusion of the left MCA (Fig.
3). NIHSS was 18; GCS, 3. The patient received thrombolysis with rtPA in the 3-hour time window. Despite recanalization of the MCA after 2 hours shown by duplex ultrasound,
the patient did not improve. Control CT revealed a malignant
infarction of the left MCA territory, with a hemorrhagic
transformation of the lentiform nucleus and a slight spaceoccupying effect (Fig. 4). We performed hemicraniectomy 20
hours after onset of ischemic symptoms. For intracranial
pressure (ICP) measurements, the patient received a Codman
probe. According to our local protocol for malignant MCA
infarction, we also treated the patient with mild hypothermia
and deep sedation to prevent increasing cerebral edema.
Subsequently, ICP rose continuously up to 30 mm H2O.
Therefore, a second CT on day 2 was performed, showing

95

Disqué and Gahn

The Neurologist • Volume 13, Number 2, March 2007

FIGURE 3. CT angiography on day 0: occlusion of the MCA.

FIGURE 1. CT on day 0: hyperdense middle cerebral artery
sign on the left side.

FIGURE 4. CT on day 1: malignant infarction in the left MCA
territory; hemorrhagic transformation in the lentiform nucleus.

intracerebral hemorrhage of 5 ⫻ 4 cm in the left basal
ganglia, extending in the left lateral, the third and fourth
ventricle, as well as ballonation of the right lateral ventricle
(Fig. 5). To avoid herniation, the patient received an extraventricular drainage (EVD). Thereafter, the ICP remained
stable. After 10 days, we were able to remove the EVD. The
patient was discharged with a NIHSS of 18 and GCS of 10.
Except borderline INR of 1.6 on day 2, extensive blood
coagulation tests showed no evidence for coagulation disorder. At time of surgery, INR was normal. Routine stroke
workup revealed a cardiac source of embolism.

DISCUSSION
FIGURE 2. CT on day 0: hypoattenuation of the basal ganglia and the insular ribbon.

96

Epidural or subgaleal hematoma is a common complication after hemicraniectomy in patients with malignant
© 2007 Lippincott Williams & Wilkins

The Neurologist • Volume 13, Number 2, March 2007

Ipsilateral Parenchymal Hemorrhage After Hemicraniectomy

occurred in the basal ganglia rather than cortically. CT
demonstrated hemorrhagic transformation in the lentiform
nucleus already before hemicraniectomy. The damaged vessels in this area probably became further stretched after
hemicraniectomy and may have facilitated hemorrhage.
Another, in our opinion, rather implausible reason for
hemorrhage might be the vessel was damage by the Codeman
probe because of the local relationship (Fig. 5). Borderline
coagulation parameters might have contributed to the hemorrhage. rtPA might have caused hemorrhagic transformation
in the lentiform nucleus but, because of its short half-life, is
unlike to cause hemorrhage 2 days later.

The reported case is the first one in the
literature suffering from deep hemorrhage
after hemicraniectomy.

CONCLUSION
FIGURE 5. CT on day 2 after hemicraniectomy: hemorrhage
in the basal ganglia of 4.5 ⫻ 3 cm, blood in the ventricular
system, and obstructive hydrocephalus of the right lateral
ventricle.

MCA infarction. We did not find a single case of deep
intracerebral hemorrhage after hemicraniectomy in the literature. Wagner et al4 observed patients who developed intracerebral hemorrhage, but all of them were localized in the
cortex. They explained hemorrhage mostly with shearing.
After hemicraniectomy, there is a sudden loss of counterpressure, and shear forces may develop. Shear forces seem to be
highest in the cortex.4 The reported 55-year-old male is the
first case in whom we observed intraparenchymal hemorrhage after hemicraniectomy. In our patient, shear forces also
might have caused hemorrhage, even if the hemorrhage

© 2007 Lippincott Williams & Wilkins

The reported case is the first one in the literature
suffering from deep hemorrhage after hemicraniectomy.
Hemorrhagic transformation might be a risk factor for clinical
relevant hemorrhage after hemicraniectomy.
REFERENCES
1. Moulin DE, Lo R, Chiang J, et al. Prognosis in middle cerebral artery
occlusion. Stroke. 1985;16:282–284.
2. Hacke W, Schwab S, Horn M, et al. “Malignant” middle cerebral artery
territory infarction: clinical course and prognostic signs. Arch Neurol.
1996;53:309 –315.
3. Schwab S, Steiner T, Aschoff A, et al. Early hemicraniectomy in patients
with complete middle cerebral artery infarction. Stroke. 1998;29:1888 –
1893.
4. Wagner S, Schnippering H, Aschoff A, et al. Suboptimum hemicraniectomy as a cause of additional cerebral lesions in patients with malignant
infarction of the middle cerebral artery. J Neurosurg. 2001;94:693–
696.

97