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Received: 9 February 2001
Accepted: 17 October 2001
Published online: 29 November 2001
© Springer-Verlag 2001
Abstract Objectives: To review
clinical and radiological findings in
patients with Duret hemorrhages and
to discuss the pathophysiology and
differential diagnosis of these le-
sions. Patients and methods: We re-
viewed the case records of four pa-
tients with Duret hemorrhages who
had been admitted to the neurologi-
cal intensive care unit with supraten-
torial mass lesions. Results: Descend-
ing transtentorial and subfalcine her-
niations were present in all cases.
Three patients were admitted with
acute subdural hematoma and one
with intraparenchymal hemorrhage.
Computed tomography revealed the
presence of blood in the mesenceph-
alon and upper pons. Three patients
died; one survived with severe dis-
abilities. Discussion: Duret hemor-
rhages are typically located in the
ventral and paramedian aspects of
the upper brainstem (mesencephalon
and pons). The pathophysiology of
Duret hemorrhage remains under
debate: arterial origin (stretching
and laceration of pontine perforat-
ing branches of the basilar artery),
versus venous origin (thrombosis
and venous infarction). Multifac-
torial causation seems likely.
Conclusion: Duret hemorrhages are
delayed, secondary brainstem hem-
orrhages. They occur in craniocere-
bral trauma victims with rapidly
evolving descending transtentorial
herniation. Diagnosis is made on
computed tomography of the brain.
In most cases the outcome is fatal.
On the basis of our observations we
believe that arterial hypertension and
advanced age are risk factors for the
development of Duret hemorrhage.
Keywords Brain, computed
tomography · Brain, hemorrhage ·
Brain, injuries · Brain, herniation ·
Duret hemorrhage
Intensive Care Med (2002) 28:85–88
DOI 10.1007/s00134-001-1160-y
BRIEF REPORT
Paul M. Parizel
Smitha Makkat
Philippe G. Jorens
Özkan Özsarlak
Patrick Cras
Johan W. Van Goethem
Luc van den Hauwe
Jan Verlooy
Arthur M. De Schepper
Brainstem hemorrhage in descending
transtentorial herniation (Duret hemorrhage)
Introduction
Brainstem hemorrhages are commonly reported in autop-
sy series of severely head-injured patients [1, 2]. They
can be classified as primary or secondary [2, 3]. Causes
of primary brainstem hemorrhage include: direct lacera-
tion or contusion, penetrating injury, shearing injuries,
petechial hemorrhages, disruption of the pontomedullary
junction [3]. Secondary hemorrhages of the brainstem in
craniocerebral trauma victims occur at a later stage as a
result of descending transtentorial herniation [4]. These
are known as Duret hemorrhages.
The neuropathological features of Duret hemorrhages
are well known. However, the frequency of brainstem
hemorrhages observed with computed tomography (CT)
or magnetic resonance imaging (MRI) is much lower
than that observed in autopsy series of head trauma vic-
tims [3]. Descriptions of Duret hemorrhages documented
in vivo are rare. Most have been published as case re-
ports [5] or included in articles reporting primary and
secondary brainstem injuries [3, 6].
We present a series of four patients with Duret hemor-
rhages, review the pertinent clinical and radiological
findings, and discuss the pathophysiology and differen-
P.M. Parizel (
✉
) · S. Makkat · Ö. Özsarlak
J.W. Van Goethem · L. van den Hauwe
A.M. De Schepper
Department of Radiology,
University of Antwerp, Wilrijkstraat 10,
2650 Edegem, Belgium
e-mail: parizelp@uia.ua.ac.be
Tel.: +32-3-8213732
Fax: +32-3-8252026
P.G. Jorens
Department of Intensive Care,
University of Antwerp, Wilrijkstraat 10,
2650 Edegem, Belgium
P. Cras
Department of Neuropathology,
University of Antwerp, Wilrijkstraat 10,
2650 Edegem, Belgium
J. Verlooy
Department of Neurosurgery,
University of Antwerp, Wilrijkstraat 10,
2650 Edegem, Belgium
tial diagnosis. Finally, we conclude that a previous medi-
cal history of systemic hypertension and advanced age
constitute risk factors for the development of this condi-
tion.
Case reports
Patient A
A 55-year-old comatose woman was admitted to the emergency
room. Glasgow coma scale (GCS) was 4/15. Clinical neurological
examination showed dilated pupils, with brisk light reflexes. The
patient had a previous medical history of arterial hypertension.
Noncontrast CT of the brain revealed a massive hemorrhage in the
left cerebral hemisphere. Midline structures were shifted to the
right, and perimesencephalic cisterns were flattened. There was no
brainstem hemorrhage at this time. Cerebral arteriography showed
a small aneurysm at the M1 segment of the left middle cerebral ar-
tery. The patient’s neurological condition continued to deteriorate.
Repeat CT after 24 h showed subfalcine and descending transten-
torial brain herniations. Moreover, a hematoma in the brainstem
was seen (Fig. 1a). The aneurysm was successfully clipped on day
4 after admission. After 2 months the patient was discharged to a
nursing home.
Patient B
A 76-year-old man was brought to the emergency ward in coma-
tose state. GCS upon admission was 4/15. Blood pressure was
228/96 mmHg. Clinical neurological examination revealed aniso-
coria with nonreactive pupils and Kussmaul’s breathing. The pa-
tient had suffered a head trauma 48 h before admission. Emergen-
cy CT revealed a large and recent left subdural hematoma (SDH),
resulting in a subfalcine herniation (Fig. 1b). Additionally, there
was a downward transtentorial herniation as evidenced by the in-
ferior displacement of the pineal calcification. In the brainstem
multifocal slitlike hemorrhagic foci were observed. The patient
died during the evening of the same day due to hemodynamic in-
stability.
Patient C
A 69-year-old man was found at home. He was unconscious with
a GCS of 11/15. On arrival at the hospital GCS was 3/15. Pupils
were asymmetric and nonreactive. The patient was known to have
essential hypertension. Once previously he had suffered an acute
myocardial infarction and a cerebrovascular accident with left
hemiparesis. He was treated with oral anticoagulants and pro-
thrombin time was within therapeutic range. Emergency CT upon
admission disclosed a large left SDH with layering effect in the
frontoparietal region. A midline shift with compression of the left
lateral ventricle was also observed. Moreover, there was extensive
bleeding in the mesencephalon and pons with extension into the
left cerebellar hemisphere and fourth ventricle. Under the protec-
tion of intravenously administered vitamin K dependent clotting
factors the SDH was evacuated neurosurgically. The patient was
transferred to the neurointensive care unit and given maximal anti-
edematous treatment. However, he remained comatose; electroen-
cephalography showed markedly decreased electrical activity over
the left hemisphere suggestive of irreversible brain damage. The
patient died on the fourth day.
Patient D
A 56-year-old comatose woman was brought to the emergency
ward. GCS was 3/15 with unequal and nonreactive pupils. Previ-
ous medical history showed that the patient was known with se-
vere hypertension. She had undergone coronary artery bypass
86
Fig. 1a, b Secondary brain-
stem hemorrhages (Duret
hemorrhages) in two patients
with descending transtentorial
herniation due to a rapidly ex-
panding supratentorial mass le-
sion. a Noncontrast axial CT in
a 55-year-old woman (patient
A) with a massive left cerebral
hemisphere hemorrhage, ex-
tending into the temporal lobe
(black arrowheads) 29 h after
admission. There is a descend-
ing transtentorial herniation.
There is a midline hemorrhagic
focus in the upper brainstem,
consistent with a Duret hemor-
rhage (white arrow). b Noncon-
trast axial CT in a 76-year-old
man (patient B) after a fall on
his head 2 days prior to admis-
sion. A left subdural hematoma
is present (black arrowheads).
Duret hemorrhage is observed
in the upper pons (white arrows).
Note the dilatation of the right
temporal horn
grafting 4 years previously. Noncontrast CT of the brain disclosed
an extensive left SDH with a mixed density pattern. There was a
marked subfalcine shift of the midline structures to the right. The
perimesencephalic cisterns were obliterated due to a downward
transtentorial herniation. Infratentorially there was a large pontine
hematoma, which had ruptured into the fourth ventricle. Emergen-
cy surgery was performed and the SDH was drained. The patient
remained comatose during the postoperative period and finally
died on the eighth postoperative day due to septic shock.
Discussion
Historical perspective and definitions
The Duret hemorrhage is named after Henri Duret, a
nineteenth century French surgeon who worked in
Charcot’s laboratory in the Salpêtrière Hospital in Paris.
Duret experimented on dogs to investigate the mecha-
nisms of concussion. When he injected either gelatin or
water inside the animal’s skull, he observed that the
swift increase in intracranial pressure caused multiple,
minute hemorrhages in the brainstem near the floor of
the fourth ventricle [5]. Discussion continues as to
whether the hemorrhages observed by Duret in laborato-
ry animals are the same as those that occur in the human
brainstem with transtentorial herniation. Despite this un-
certainty, the eponymous term “Duret hemorrhage” is
now widely accepted to describe secondary brainstem
hemorrhages due to descending transtentorial herniation
of any cause.
Pathogenesis and risk factors
The pathogenesis of Duret hemorrhages remains contro-
versial. Most authors support an arterial origin, but
others consider venous congestion as a possible cause
[7]. It is likely that more than one mechanism may be in-
volved [2, 7]. A rapidly expanding supratentorial mass
lesion causes severe increase in intracranial pressure and
results in a descending transtentorial herniation. The
most common causes include hematomas (epidural, sub-
dural, intraparenchymal), and acute cerebral edema. The
brainstem is pushed inferiorly, foreshortened and buck-
led. This leads to stretching, spasm, infarction, and hem-
orrhage of the central perforating arteries, which arise
from the relatively immobile basilar artery [7]. Thus Du-
ret hemorrhages usually commence in the midline of the
mesencephalon and upper pons. Moreover, as a result of
side-to-side compression there occurs an anterior-poste-
rior elongation of the brainstem, which further stretches
perforating arterial branches.
It is noteworthy that three of four of our patients had
a previous medical history of arterial hypertension; the
one patient without hypertension was 76 years old (rele-
vant patient data are summarized in Table 1). The associ-
ation of Duret hemorrhage and arterial hypertension has
not been reported before. Our hypothesis is that, with ar-
terial hypertension and advancing age, the elasticity of
the blood vessel walls decreases, and the propensity to
develop Duret hemorrhages increases. Venous conges-
tion has also been reported as a possible cause of these
hemorrhages [8]. Prolonged elevation in intracranial
pressure could cause vascular thrombosis within the
brainstem, which then can evolve to hemorrhage. The
venous thrombosis and venous infarction theory is sup-
ported by the finding that small, thin-walled veins are
more easily compressed and can undergo anoxic degen-
eration with subsequent vessel rupture and extravasation
of blood.
Incidence
The reported incidence of secondary brainstem hemor-
rhages is significantly higher in neuropathological
(30–60%) than in radiological studies (5–10%). Second-
ary brainstem damage was found in 51% of an autopsy
87
Table 1 Summary of relevant patient data
Patient A Patient B Patient C Patient D
Patient data Woman aged Man aged Man aged Woman aged
55 years 76 years 69 years 56 years
Previous medical history Hypertension Bronchogenic Essential Hypertension
carcinoma hypertension,
myocardial infarction
Cause of supratentorial mass effect Intracerebral Left SDH Left SDH Left SDH
hemorrhage
Subfalcine herniation + + + +
Descending transtentorial herniation + + + +
Downward bowing of tentorium + + + +
Dilatation of contralateral lateral ventricle + + + +
Hemorrhage in mesencephalon + + + –
Hemorrhage in pons – + + +
Obliteration of 4th ventricle – + + +
series of 434 patients with nonmissile head injury [4].
Brainstem hemorrhage was observed in 37% of cases in
a postmortem study of 132 fatal head injuries [9]. How-
ever, in CT studies the frequency of brainstem lesions
was remarkably low. Secondary brainstem hemorrhages
are found only in a small percentage of cerebral trauma
patients with fatal prognosis. This discrepancy can be
partially explained by the fact that up to 20% of second-
ary brainstem lesions are seen only microscopically [4].
Another factor may be the delayed development of sec-
ondary brainstem hemorrhages, occurring after the initial
emergency CT. Finally, it could be possible that many of
these severely injured patients do not survive long
enough for a subsequent CT to confirm the diagnosis.
Differential diagnosis
Not all hemorrhagic lesions in the brainstem are
Duret hemorrhages. Differential diagnosis includes pri-
mary traumatic brainstem hemorrhages (e.g., direct im-
pact and penetrating injury, shearing injuries, disruption
of the pontomedullary junction), as well as hypertensive
bleeds and ruptured arteriovenous malformations. Direct
impact hemorrhagic contusions of the brainstem occur
with a lateral blow to the head, which causes a sudden
acceleration-deceleration displacement of the brainstem
relative to the tentorium. Patients with a narrow tentorial
incisura are more vulnerable to this type of injury. Pete-
chial shearing hemorrhages can be found in the posterior
lateral quadrant of the brainstem [3, 10]; these are
caused by a severe rotational force applied to the brain-
stem. Hypertensive brainstem hemorrhages usually arise
in the dorsal region of the basis pontis. The pons is prone
to hypertensive bleeds because it is supplied by direct
perforating branches. This vascularization pattern is sim-
ilar to that of the basal ganglia and thalamus, which are
also sites of predilection. Hemorrhagic necrosis of the
pons is a rare cause of brainstem hemorrhage and should
be differentiated from pontine infarct, central pontine
myelinolysis, and Duret hemorrhage. Brainstem hemor-
rhages can also occur due to rupture of an arteriovenous
malformation. These instances are rare because clearcut
arteriovenous malformations are infrequent in the poste-
rior fossa, with the exception of cavernous malforma-
tions.
Conclusion
Duret hemorrhages are secondary brainstem hemorrhag-
es that are caused by descending transtentorial hernia-
tion. They are typically found in the lower mesencepha-
lon and ventral portion of the pons. The pathophysiology
remains controversial; although most authors favor an
arterial origin (stretching and laceration of perforating
branches of the basilar artery), there are equally strong
arguments for a venous origin (thrombosis and venous
infarction). Intensive care physicians should understand
the pathophysiology of descending transtentorial herniat-
ions. The delayed appearance of brainstem hemorrhage
in a comatose patient with severe supratentorial hyper-
tension is an ominous sign. Outcome is almost always
fatal.
Acknowledgements This work was supported by a Clinical Re-
search Associate Grant (number G.3C06.96) of the Fund for Sci-
entific Research – Flanders (F.W.O.), Belgium. We are grateful to
Geert Van Hoorde for photographic assistance.
88
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