CLINICAL STUDIES

DELAYED POSTTRAUMATIC ACUTE SUBDURAL HEMATOMA
IN ELDERLY PATIENTS ON ANTICOAGULATION
Eyal Itshayek, M.D.
Department of Neurosurgery,
Hadassah-Hebrew University
Medical Center,
Jerusalem, Israel

Guy Rosenthal, M.D.
Department of Neurosurgery,
Hadassah-Hebrew University
Medical Center,
Jerusalem, Israel

Shifra Fraifeld, M.B.A.
Department of Neurosurgery,
Hadassah-Hebrew University
Medical Center,
Jerusalem, Israel

Xicotencatl Perez-Sanchez, M.D.
Department of Neurosurgery,
Hadassah-Hebrew University
Medical Center,
Jerusalem, Israel

Jose E. Cohen, M.D.
Department of Neurosurgery,
Hadassah-Hebrew University
Medical Center,
Jerusalem, Israel

Sergey Spektor, M.D., Ph.D.
Department of Neurosurgery,
Hadassah-Hebrew University
Medical Center,
Jerusalem, Israel
Reprint requests:
Eyal Itshayek, M.D.,
Department of Neurosurgery,
Hadassah-Hebrew University
Medical Center,
Kiryat Hadassah,
PO Box 12000,
Jerusalem, Israel 91120.
Email: eyalit@md.huji.ac.il
Received, July 5, 2005.
Accepted, December 2, 2005.

NEUROSURGERY

OBJECTIVE: To discuss delayed acute subdural hematoma (DASH), a relatively neglected entity, and to emphasize the potentially elevated risk for DASH among elderly,
anticoagulated mild traumatic brain injury (TBI) patients.
METHODS: The authors reviewed clinical and radiological data for four patients who
had normal neurological examinations and normal computed tomographic scans after
mild TBI, and who subsequently developed DASH and deteriorated rapidly.
RESULTS: The patients included two men and two women, aged 65 to 86 years, who
presented to the emergency department after mild TBI between January 2002 and June
2004. All were treated with chronic anticoagulation or anti-aggregation therapy. They
deteriorated owing to DASH from 9 hours to 3 days after TBI. Three of the four patients
underwent craniotomy for evacuation of their hematomas. One patient, who suffered
only focal neurological deficit, was treated conservatively, and her hematoma gradually resolved. Two patients died and two reached Glasgow Outcome Scores of 3 and
4 after extended inpatient rehabilitation.
CONCLUSION: A suspicion of DASH should be raised in elderly, anticoagulated, mild
TBI patients, including those who present to the emergency department with Glasgow
Coma Scores of 15 and normal computed tomographic scans after injury. Based on our
experience, we recommend that elderly, anticoagulated mild TBI patients should be
admitted for 24 to 48 hours of observation after injury.
KEY WORDS: Anticoagulation, Delayed subdural hematoma, Elderly patients, Intracranial injury, Glasgow
coma scale, Mild traumatic brain injury, Subdural hematoma
Neurosurgery 58:851-856, 2006

M

DOI: 10.1227/01.NEU.0000209653.82936.96

ore than one million patients experience blunt traumatic brain injury
(TBI) in the United States and Canada each year, with 66 to 75% of the injuries
classified as minor (15, 19, 35). Mild TBI frequently occurs in elderly patients, many of
whom are treated with anticoagulants, which
are known to increase the risk of bleeding
events (14, 22, 32, 38, 45, 46, 49).
Most mild TBI patients do not develop significant neurosurgical complications. Retrospective studies report incidence of intracranial lesions on computed tomographic (CT)
scans in 16 to 28% of patients (7, 21). More
recently, prospective studies have found that
3 to 13% of mild TBI patients with Glasgow
Coma Scores (GCS) of 15 had intracranial lesions on CT scans (7, 12, 19, 21, 27, 34, 44).
Posttraumatic intracranial hemorrhages, including epidural hematoma (EDH), subdural

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hematoma (SDH), subarachnoid hemorrhage,
intracerebral hemorrhage (ICH), and intraventricular hemorrhage, are usually seen in the
initial CT scan. But, a small subset of head
trauma patients experience delayed intracranial bleeding. Delayed ICH, delayed EDH,
and delayed chronic SDH are discussed in the
literature (2, 3, 8, 10, 31, 37, 39, 40, 43, 45, 46),
and may occur after a normal CT scan at admission. However, delayed acute SDH
(DASH) is rarely reported. Cohen and Gudeman (6) define DASH as acute SDH that is not
apparent on the initial CT scan, but appears
on a follow-up CT scan during the patient’s
post-injury course. They report DASH incidence of approximately 0.5% among operatively treated acute SDH patients at their institution.
We present here a group of elderly patients
on anticoagulation who experienced DASH

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ITSHAYEK ET AL.

after mild TBI. On admission, all patients had GCS of 15, no
history of loss of consciousness (LOC) or post-traumatic amnesia, no cranial fracture, no focal neurological deficit, and
normal CT scans. All deteriorated owing to DASH within
hours or days after their mild trauma.
The entity of DASH has experienced a lack of critical focus
in the literature (6). Reports of DASH appear only in relation
to patients with severe head trauma and/or multiple traumatic injuries (6, 45, 46). The purpose of this article is to add
focus to DASH as a distinct entity, to describe the occurrence
of DASH in a much more lightly injured subset of patients in
whom it has not been reported previously, and to raise the
degree of awareness among emergency department physicians towards elderly, anticoagulated mild TBI patients.

MATERIALS AND METHODS
Hadassah Ein Kerem is the sole Level I Trauma Center in
the Jerusalem region, serving a population of 800,000 people.
All patients who arrive at the emergency department after
experiencing head trauma are evaluated and managed according to accepted neurosurgical standards of care by the neurosurgical resident on call, under the supervision of the attending neurosurgeon. High resolution, contiguous, 3 mm, axial
CT head studies, without contrast, with brain and bone windows, are performed on spiral or multidetector systems (Philips, Best, The Netherlands) in all patients on anticoagulation,
even following minor head injury. The authors describe their
experience treating four mild TBI patients who later deteriorated as a result of DASH.

RESULTS
Four patients, two men and two women aged 65 to 86 years
(mean, 73 yr), who presented to the emergency department
after minor head trauma between January 2002 and June 2004,
are included in this study. All were treated with chronic
anticoagulation medication, and one patient was also on antiplatlet therapy. All patients had a GCS of 15, no history of
LOC, no focal neurological deficit, no evidence of cranial
fracture, and normal head CT scans on arrival at the emergency department. All subsequently developed DASH, with
rapid neurological deterioration.
Three of the four patients underwent craniotomy for evacuation of their hematomas. The two male patients died after
complicated postoperative courses. One female patient underwent surgical evacuation and rehabilitation, eventually
achieving a Glasgow Outcome Score (GOS) of 3. In the second
female patient, the hematoma was treated conservatively. She
achieved a GOS of 4.

Patient 1
An 86-year-old man was hospitalized for treatment of pneumonia. He was receiving 100 mg of aspirin and 40 mg of
subcutaneous low molecular weight heparin (enoxaparin)

A852 | VOLUME 58 | NUMBER 5 | MAY 2006

daily owing to ischemic heart disease. On admission, the
patient’s neurological examination was normal and blood
tests, including a clotting screen, were unremarkable. Two
days after admission, the patient fainted and hit his head. He
was awake and oriented immediately after the fall, with a GCS
of 15. Physical examination revealed slight scalp bruising. He
had no LOC or amnesia. A head CT scan performed 6.5 hours
after the fall revealed moderate brain atrophy with no evidence of intracranial hemorrhage (Fig. 1A). During the next 2
days, the patient did well.
On Day 3, the patient was found comatose in his bed, with
bilateral, dilated, nonreactive pupils and a decerebrate response to pain (GCS 4). An emergency CT scan revealed a
large acute SDH on the right with midline shift (Fig. 1B). The
patient underwent an emergency craniotomy with evacuation
of a large subdural clot. He expired on postoperative Day 6.

Patient 2
A 69-year-old man presented to the emergency department
after a fall from his bed. There was no LOC or amnesia, and no
sign of cranial fracture. The patient was on anticoagulation
with Coumadin (DuPont Pharmaceuticals, Wilmington, DE)
owing to a prosthetic aortic valve, and on hemodialysis owing
to end-stage renal disease. His initial international normalized
ratio (INR) was 2.99. A CT scan obtained 3 hours after the fall
revealed an old infarction in the right occipital region and
generalized atrophy (Fig. 1C), without evidence of intracranial
hemorrhage. He was discharged from the emergency department alert and without focal neurological deficit.
Approximately 12 hours after the fall, the patient’s level of
consciousness abruptly deteriorated. Upon return to the emergency department, he opened his eyes to voice stimulation
and localized to painful stimuli with no verbal response (GCS
9). His pupils were equal and reactive to light bilaterally.
There was obvious left-sided weakness. Emergent head CT
scanning demonstrated a large right side acute SDH with
mass effect (Fig. 1D). Fresh frozen plasma and vitamin K were
given concomitantly, before craniotomy and evacuation of the
hematoma. After surgery, the patient was conscious with leftside weakness. Postoperative CT scanning revealed fair hematoma evacuation, but the patient experienced a series of infections and died after 3 months.

Patient 3
A 65-year-old woman on Coumadin because of mitral valve
replacement presented to the emergency department after she
fell and experienced minor TBI. She had no history of LOC or
amnesia and no sign of cranial fracture. Her neurological
exam was normal. Initial head CT scan was without sign of
intracranial hemorrhage (Fig. 1E). Her INR was 3.03. After 6
hours of observation, she was discharged home.
The following day, she was found unconscious and was
transferred immediately to the emergency department. On
neurological examination, she did not open her eyes, and
responded to pain stimulus with left side pain localization and

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DELAYED ACUTE SUBDURAL HEMATOMA

FIGURE 1. A, head CT scan in an 86-year-old man (Patient 1) obtained
6.5 hours after mild TBI revealing moderate brain atrophy. B, head CT
scan in the same patient, performed after abrupt neurological deterioration
3 days after trauma, revealing a large right acute subdural hematoma with
mass effect. C, head CT scan in a 69-year-old man (Patient 2), obtained in
the emergency department approximately 3 hours after a fall in the nursing home where the patient resided, revealing an old infarction in the right
occipital region and generalized atrophy. D, repeat head CT scan, performed 12 hours after the initial fall owing to a sudden deterioration in
the patient’s consciousness, with obvious left-sided weakness, revealed a
large right side acute subdural hematoma with mass effect and consequent
subfalcial herniation. E, initial posttrauma head CT scan in a 65-year-old
woman (Patient 3). F, 1 day after her mild TBI, the patient was found
unconscious at her home. At readmission, she had right hemiplegia and
her left pupil was fixed and dilated. Head CT scanning revealed a large
acute subdural hematoma. G, normal head CT scan upon admission in a
72-year-old woman (Patient 4) who was assaulted when her home was
burglarized. H, a second CT scan, obtained 1 day later, after the patient
developed left leg plegia, revealing acute interhemispheric subdural hematoma.

uation of the hematoma were performed. Postoperatively, the
left pupil became small and reactive, and a CT scan demonstrated absence of SDH. Eventually the patient improved neurologically, and, 26 months later, she has a GOS of 3.

Patient 4
A 72-year-old woman on Coumadin because of a history of
paroxysmal atrial fibrillation was assaulted and suffered minor head trauma. She arrived at the emergency department of
a community hospital alert and lucid, with no neurological
deficit (GCS 15), no history of LOC, and no sign of cranial
fracture. Her INR at presentation was 3.2. Her initial head CT
scan was normal (Fig. 1G). Her Coumadin was changed to
enoxaparin and she was admitted for observation.
The next day, she developed severe progressive headache
and weakness in her left leg. Repeat head CT scanning revealed an acute interhemispheric SDH (Fig. 1H). She was
transferred to our hospital conscious, lucid, and responsive,
but with full plegia of the left leg. During the hospitalization,
she was treated conservatively owing to clinical and radiological improvement. One year later, she has a GOS of 4.

DISCUSSION

right side extension (GCS 7). Her left pupil was fixed and
dilated. An emergent head CT scan revealed large acute SDH
with midline shift (Fig. 1F). She received fresh frozen plasma
and vitamin K, and an emergency left craniotomy and evac-

NEUROSURGERY

Many studies address risk factors in patients with mild TBI
(1, 3–5, 12, 13, 19, 23, 27, 29, 40, 47, 48). Although the great
majority of these patients make uneventful recoveries, misdiagnosis often results in death, a prolonged vegetative state, or
significant disability (3, 7, 16, 24, 25, 27, 28, 40, 41). Thus
accurate evaluation and treatment of patients who initially
seem to be at low risk is one of the most important factors in
the reduction of mortality in head-injured patients (19, 28, 47,
48).
Guidelines to determine which mild TBI patients should
undergo CT scanning, remain for observation, or be discharged home continue to evolve. It is generally accepted that

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ITSHAYEK ET AL.

elderly TBI patients are at greater risk for clinically important
brain injury (1, 5, 12, 16, 19, 23, 27, 40, 47, 48). Increasing age
is associated with a higher risk of intracranial lesions on CT
scans in head-injured patients (5, 18, 19, 22, 27, 47, 48, 51), and
elderly patients with ICH tend to have worse outcomes (16, 21,
36). Oral anticoagulation is associated with a significant risk of
intracranial bleeding, even after minor head trauma (13, 14, 16,
20, 29, 30, 46). As a result, TBI patients with coagulopathy are
often included in a high-risk group regardless of clinical presentation (1, 3, 5, 16, 23, 40, 48).
We reviewed several recently proposed guidelines for the
management of mild TBI patients, with a special focus on
discussion of patients who are older and anticoagulated (13,
19, 23, 40, 46–48). The European Federation of Neurological
Societies (48) recommends that patients with a GCS of 15 after
mild TBI, who are over 60 years of age or who are on anticoagulation, be admitted to the hospital for 24-hour observation.
In a prospective study of 1101 mild TBI patients, Ibanez et al.
(23) found positive CT findings to be very significantly related
to both coagulation disorder and patients older than 65 years
of age. The authors included older and anticoagulated patients
in a high risk group. In a prospective study of 520 mild TBI
patients, Haydel et al. (19) found that patients over the age of
60 years were three times more likely to have a positive CT
scan than younger patients and found age to be one of seven
risk factors predicting positive CT findings.
Both delayed posttraumatic ICH and EDH have been well
described in the neurosurgical literature (2, 6, 17, 33, 37, 39, 45,
50). DASH, however, is rarely mentioned. Cohen and Gudeman (6) described their experience with DASH in patients
with severe TBI. The occurrence of DASH is mentioned in
several large series of head trauma patients, but without discussion or analysis (1, 7, 12, 31, 46).
One commonly discussed mechanism for development of
acute SDH is rupture of bridging veins. Cerebral veins empty
into the dural sinuses, which are adherent to the inner table of
the skull. As the veins cross the subdural space, they have
little supporting structure, and are therefore most vulnerable
to injury at this point. In the presence of cerebral atrophy,
which is common in elderly patients, bridging veins are
stretched and transverse a greater distance in the subdural
space. Cohen and Gudeman (6) and others (9, 26, 42) suggest
that rupture of these veins is the mechanism for DASH in
patients with trauma-induced hypotension and/or cerebral
edema. In 1961, before the CT era, Drake (11) noted that small,
perisylvian cerebral arteries were the origin of bleeding in 11
of 100 operated acute SDH patients. These arteries protrude
through the arachnoid and are adherent to the dura mater. He
reported that six patients with bleeding of arterial origin experienced delayed deterioration, some owing to subacute
SDH, and suggested that this phenomena occurs because of a
tiny opening in the ruptured artery.
In patients with hypotension, delayed bleeding may develop as blood pressure returns to normal after resuscitation.
Suggested mechanisms for the formation of DASH in the
presence of cerebral edema and elevated ICP include intense

A854 | VOLUME 58 | NUMBER 5 | MAY 2006

treatment to reduce ICP by CSF drainage, administration of
mannitol, or evacuation of an accompanying mass lesion.
These mechanisms may promote formation of DASH in severely injured trauma patients, and the injuries may well be
aggravated by coagulopathy, but they do not explain the
occurrence of DASH in the subpopulation of elderly, anticoagulated, mild TBI patients described here. The pathogenesis
of DASH in these patients remains obscure.
In this series, we report our experience with four mild TBI
patients aged 65 to 89 years, with no history of LOC, posttraumatic amnesia, or epileptic seizure, no evidence of cranial
fracture or cranial soft-tissue injury, and no evidence of drug use
or intoxication. At the first evaluation after trauma, they had
normal neurological examinations and normal CT scans. All
were on anticoagulation therapy. Three patients deteriorated
within 24 hours after TBI. The fourth patient deteriorated during
the night, and was found deeply unconscious 72 hours after TBI.
Three patients underwent operation. One was treated conservatively, and her hematoma gradually resolved. The two male
patients were sicker and eventually died. One of them arrived
after deterioration with a GCS of 4, and the second man experienced several unrelated complex medical problems. The two
female patients survived with GOS 3 and 4. One of these women,
at an age of 65 years, was the youngest patient in the series. The
second had an interhemispheric subdural hematoma, and experienced only a focal neurological deficit.
This series suggests that DASH occurs in some older mild TBI
patients who receive anticoagulation. This is only a small series
showing our recent experience, the common denominator in
these patients is not fully established, and the pathogenesis for
DASH is not understood. However, we wish to raise the degree
of awareness among emergency department physicians who
treat trauma patients on a daily basis that elderly, anticoagulated
patients may face higher risk for acute ICH and delayed deterioration after mild TBI. We define this population as high risk
minor head injury. Previously we managed these patients with
full neurological examination and head CT scans. Patients who
had normal examination and normal CT scans were usually
discharged home with a responsible observer. We have since
changed this policy. Elderly, anticoagulated, mild TBI patients,
including those with normal neurological examination and normal CT scans, are hospitalized for 48-hour observation in the
Department of Neurosurgery.
In conclusion, we emphasize the need to maintain a high level
of vigilance in mild TBI patients with risk factors including
anticoagulation therapy, advanced age, and cerebral atrophy. In
these patients even a normal neurological exam and normal CT
scan does not preclude subsequent rapid deterioration. We recommend that such patients be admitted for neurosurgical observation. Follow-up CT scans should be obtained immediately
upon any change in neurological condition.

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I

tshayek et al. describe four elderly patients on anticoagulation therapy who experienced delayed acute subdural hematomas after minor head trauma. The authors correctly point out that delayed intracranial hematomas are more commonly described in the brain
parenchyma or in the epidural space. They are also correct that most
of the delayed subdural hematomas described in the recent literature
follow more severe head trauma. They thus apprise the neurosurgical
community that a delayed acute subdural hematoma may occur in
elderly patients on anticoagulation. Because we do not have a denomination, the incidence is unknown.
I was surprised that the authors found these hematomas to be
venous in origin. In the older literature, delayed arterial hematomas
have been reported to occur (1). It is known that traumatic intracranial
aneurysms commonly rupture after a delay. Similarly, I would speculate that the subdural hematomas arose from a damaged vessel that
bled in a delayed fashion. I can only assume that, in the cases presented, it was a damaged vein that bled.
Patients who “talk and die” have always troubled neurosurgeons.
The authors propose that elderly patients on anticoagulants who
experience minor head trauma should be observed for 48 hours. It is
unsettling that their first patient experienced a fatal subdural hemorrhage 72 hours after his trauma while under observation in the hospital. Monitoring patients for the rare hemorrhage after head trauma
poses a challenge to the neurosurgical community.
Allan H. Friedman
Durham, North Carolina

1. Drake CG: Subdural haematoma from arterial rupture. J Neurosurg 18:597–
601, 1961.

tshayek et al. have summarized four cases of elderly patients on
anticoagulation or antiplatlet therapy who developed acute subdural hematomas well after presenting with a non-focal neurological
exam and unremarkable head computed tomographic scans. Although delayed deterioration is typically encountered with small
asymptomatic epidural hematomas that rapidly enlarge several hours
after the initial injury, this report emphasizes the importance of close
observation for at least 24 to 48 hours in all patients with head trauma,

A856 | VOLUME 58 | NUMBER 5 | MAY 2006

Ricardo J. Komotar
E. Sander Connolly, Jr.
New York, New York

T

COMMENTS

I

particularly those with additional risk factors such as antiplatelet
therapy or anticoagulation.

he authors describe a theoretically well known complication of
anticoagulation therapy: hemorrhage after trauma. Their point
that actual cases have not been described in the literature is, however,
valid. I think this basic clinical observation in four patients merits
publication to show that this is not just a theoretical threat, but can be
observed in patients. I reviewed the literature and could, to my
surprise, not find any comprehensive description of this category of
patients. Given economic pressures, these patients may be sent home
too early and are then exposed to comparatively high risks of delayed
deterioration. We cannot usually heal primary injuries, but we should
not fail to prevent fatal deterioration if at all possible.
Tiit Mathiesen
Stockholm, Sweden

T

his article on delayed post-traumatic subdural hematomas in the
elderly who are anticoagulated should be seen as one part of a
greater problem, i.e., the increasing frequency of anticoagulation and
the development of intraparenchymal hemorrhages after trivial falls.
Many years ago, the Traumatic Brain Injury research group from
Hong Kong presented a study on the need to observe the elderly for
48 hours if the head was struck. This provided recognition that the
softened, often atrophied, brain is more vulnerable to bleeding. Itshayek et al. focus on subdural hematomas, but this is a relatively
limited part of the difficulty. We need to educate Trauma and Emergency Room physicians that patients on anticoagulation must be
admitted for at least 24 hours of observation, even with trivial head
injuries. Ongoing trials with Factor VIIA may provide evidence that
this agent may have utility in these patients.
Lawrence F. Marshall
San Diego, California

T

he message of this paper is important for emergency room physicians, neurosurgeons, hospital administrators, and insurance companies. Neurosurgeons who hospitalize patients who are being
treated with anticoagulation, who sustain what initially seems to be a
minor head injury, are often faced with denial of the admission by
insurance companies. In appealing such denials, it is helpful to have a
recent article with the message of the devastating outcomes of missed
subdurals in the elderly.
Robert G. Grossman
Houston, Texas

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