NEUROSURGERY FOR MEDICAL STUDENTS
Katherine E. Wagner, MD∗
Tamar R. Binyamin, MD‡
Patrick Colley, MD§
Amrit K. Chiluwal, MD∗
James S. Harrop, MD¶
Gregory W. Hawryluk, MD,
PhD||
Zachary L. Hickman, MD#
Konstantinos Margetis, MD#
George N. Rymarczuk, MD¶ ∗∗
Martina Stippler, MD‡‡
Jamie S. Ullman, MD∗
∗
Department of Neurosurgery, North-
well Health, Manhasset, New York; ‡ Dep-
artment of Neurosurgery, University of
California Davis Medical Center, Sacram-
ento, California; § Department of Otola-
ryngology, Icahn School of Medicine at
Mount Sinai, New York, New York; ¶ De-
partment of Neurosurgery, Thomas Jeffer-
son University Hospital, Philadelphia,
Pennsylvania; || Department of Neuro-
surgery, University of Utah, Salt Lake City,
Utah; # Department of Neurosurgery,
Icahn School of Medicine at Mount Sinai,
New York, New York; ∗∗ Division of Neuro-
surgery, Walter Reed Medical Center,
Bethesda, Maryland; ‡‡ Department of
Neurosurgery, Beth Israel Deaconess
Medical Center, Harvard Medical School,
Boston, Massachusetts
Given constraints of this publication
modality (ie, a book rather than journal
articles), the citations and bibliography
are not to the level of detail of a journal
article. Readers are directed to the
suggested reading lists, which contain
references to subsequent references and
derivatives of the article content.
Correspondence:
Jamie S. Ullman, MD,
Department of Neurosurgery,
Northwell Health,
300 Community Drive,
9 Tower,
Manhasset, NY 11030.
Email: jullman1@northwell.edu
Trauma
T
his section outlines the management
of common neurological injuries,
including closed head injury and
spinal trauma. Many closed head injuries
require hospitalization, management in the
intensive care unit (ICU), and occasionally
placement of intracranial pressure (ICP)
monitors. The guidelines for the critical
care management of such patients along
with the technique for placing monitoring
devices are discussed. This section also
reviews the surgical and medical management
of acute (aSDH) and chronic subdural
hematomas (cSDH), acute epidural hematomas
(EDH), and temporal lobe contusions.
Diagnosis and management of skull base
fractures and associated cerebrospinal fluid
(CSF) leakage are also discussed. Additionally,
acute spinal cord injury management and guide-
lines are also reviewed, with an emphasis on
the American Spinal Injury Association grading
scale and its utility. Video representation of these
conditions and their treatment accompany the
text.
CHAPTER 1: CLOSED HEAD INJURY
ICU/ICP MANAGEMENT
For the following cases, please note that
that institutional review board approval was not
required or sought, as no identifying information
has been included.
ABBREVIATIONS: AED, anti-epileptic drug;
AOD, atlanto-occipital dislocation; aSDH, acute
subdural hematoma; ASIA, American Spinal
Injury Association; BTF, Brain Trauma Foundation;
CPP, cerebral perfusion pressure; cSDH, chronic
subdural hematoma; CSF, cerebrospinal fluid;
CT, computed tomography; DAI, diffuse axonal
injury; ED, emergency department; EDH, epidural
hematoma; EVD, external ventricular drain; GCS,
Glasgow Coma Scale; GOS, Glasgow Outcome
Score; ICP, intracranial pressure; ICU, intensive care
unit; IMPACT, International Mission for Prognosis
and Analysis of Clinical Trials; MAP, mean arterial
blood pressure; MRI, magnetic resonance imaging;
NPI, Neurological Pupil Index; TBI, traumatic brain
injury; tSAH, traumatic subarachnoid hemorrhage
Case Presentation
An 18-year old woman presents to the
trauma bay following an all-terrain vehicle (ATV)
accident. She is intubated, pupils are 5 mm and
reactive. Corneal reflex, cough, and gag reflex
are present. She does not open her eyes to pain.
She has extensor posturing. Her vital signs are as
follows: blood pressure 139/83, pulse 101, O2
saturation 98%, respiratory rate 8. Hemoglobin
is 9.7 g/dL and glucose 107 mg/dL (6 mmol/L).
Her head computed tomography (CT) scan is
shown below (Figure 1).
Questions
1. The next step in this patient’s care should be:
a. Repeat CT in 12 h to follow the aSDH.
b. Admit to ICU with hourly neuro checks
and repeat head CT if patient exam
changes.
c. Place an ICP monitor.
d. Take the patient to the operating room for
hemicraniectomy.
2. An ICP monitor is placed and the ICP is 30.
What is your next step?
a. Take the patient for a hemicraniectomy
now.
b. Start barbiturate coma and cool the patient.
c. Make sure the patient’s head of bed (HOB)
is elevated, she is sedated, and her pain is
controlled.
d. Hyperventilate the patient for the first 24 h
only.
3. What is the patient’s Glasgow Coma Scale
(GCS) score?
a. 8
b. 4
c. 3
d. 10
4. Which of the following Brain Trauma
Foundation (BTF) guidelines is a level 1
recommendation?
a. Anti-epileptic drugs (AED) after traumatic
brain injury (TBI) to prevent post-
traumatic epilepsy
b. Prophylactic hyperventilation should be
avoided
c. GCS ≤ 10 warrants an ICP monitor
d. The use of steroids is not recommended for
improving outcome or reducing ICP
WAGNER ET AL

TABLE 1. Glasgow Coma Scale

Eye opening Verbal response Motor response

4 spontaneous 5 oriented 6 obeys

3 to speech/sound 4 confused 5 localizes
2 to pain 3 inappropriate 4 withdraws from pain
1 no response 2 incomprehensible 3 abnormal flexion
1 none 2 abnormal extension
1 no response

r About 2.5 million people experience some form of TBI in the

FIGURE 1. CT scan of an 18-yr-old female with traumatic brain
injury.
United States each year.
r TBI contributed to the deaths of more than 50 000 people.
r Over the past decade TBI-related emergency department (ED)
visits increased by 70%.
r Over the same time death rates decreased by 7%.
r In one year, about 250 000 children (age 19 or younger) were
treated for sports and recreation-related TBIs or concussions.
r During the past decade, the diagnosis of concussion or TBI rose
57% among children. This is probably due to more awareness
of concussions and their consequences.

Natural History
About one-third of patients who present with a severe TBI will
not survive the injury and one third will have severe disability. The
remaining third of patients may survive with a minor disability.
Some live independently, even if they are not able to return to
gainful employment (CDC, 2017 and Langlois et al, 2006).

FIGURE 2. Leading causes of traumatic brain injury.
Clinical Presentation
There are different methods to stratify TBI. One is by severity.
The GCS, which was first published by Teasdale and Jennett out
of Glasgow in 1974, assesses level of consciousness by scoring the
patient in 3 categories (Table 1). The minimum score is 3; the
maximum score is 15. A score ≤ 8 is considered unconscious and
in the setting of TBI is considered a severe TBI.
Every patient with a TBI will be assigned a GCS score, but the
scale is not designed to detect focal neurological deficits and does
not replace a formal neurological examination.
Patients with a severe closed head injury present with a
GCS ≤ 8 and do not follow commands. Some patients have
multiple trauma besides the head injury, yet some have no other
injuries, which is referred to as isolated head injury. The trauma
surgeon and the neurosurgeon need to triage when TBI is accom-
panied by injuries that are more life-threatening, and treat the
patient accordingly.

Morphology
Epidemiology Patients with closed severe TBI often present with diffuse
Figure 2 shows the leading cases of TBI. The Centers for intracranial injury. The diffuse injury can come in the form of
Disease Control and Prevention reported the following statistics traumatic subarachnoid hemorrhage (tSAH), contusion(s), small
in 2017. SDHs, or diffuse axonal injury (DAI).

As described in Eijick et al. (2018), DAI is characterized clini-
cally by a poor neurological examination in the absence of a
focal, operative lesion. It is a result of stretching and shearing of
axons and small vessels, which leads to damage of axonal transport
and axonal dysfunction. Clinical DAI is not visible on a CT
scan. Some evidence of blood production might be seen only in
the areas of the most severe DAI. To diagnose DAI, a magnetic
resonance imaging (MRI) of the brain needs to be performed. The
diagnosis is made when microhemorrhages are seen in the gray
matter-white matter junction of the frontal and temporal areas,
corpus callosum, deep gray matter, internal capsule, and upper
brainstem.
Decision-Making
Management of nonoperative severe TBI is directed by the
evidence-based Guidelines for the Management of Severe Traumatic
Brain Injury. The most recent (Fourth) edition was published in
2016 by the Brain Trauma Foundation.
ICP-guided therapy is the fundamental principle for all
treatment. Patients with a GCS score ≤8 with signs of high ICP
on their CT scan need ICP monitoring. This can be an external
ventricular drain (EVD) that is placed in the frontal horn of the
lateral ventricle, or fiber-optic or microstrain gauge devices, which
are placed in the brain parenchyma.
An escalating protocol should be followed to control ICP
(Table 2) using sedation and hyperosmolar therapy in the form
of mannitol and hypertonic saline. Serum sodium should not be
elevated beyond 155 mEq/L and serum osmolality should not
rise above 320 mOsm/kg. The cerebral perfusion pressure (CPP)
should be kept above 60 mm Hg. Hyperventilation should be
used cautiously or not at all; hyperventilation has the potential
to decrease ICP and cerebral blood flow and cause ischemia.
Pharmacological paralysis is less frequently used because of a
higher incidence of ventilator-associated pneumonia and longer
hospital stays.
If the ICP remains elevated despite maximal medical therapy,
a unilateral or bilateral frontal decompressive craniectomy should
be performed to allow more space for brain swelling.
Hypothermia has not been shown beneficial in several
randomized clinical trials. However, advanced cooling methods to
maintain normothermia (36.5-37.5◦ C) are recommended. High-
dose barbiturates to control elevated ICP should only be used after
maximum standard medical and surgical treatment has failed.
Hemodynamic management can be quite challenging after a
severe TBI. Hypo-osmolar solutions should be avoided because
they lead to an increase in ICP, and hyperosmolar treatments of
elevated ICP such as mannitol can actually lower CPP. Normal
saline is commonly used to achieve euvolemia. A hypertonic saline
bolus with a 3% sodium solution is optimal for patients who are
volume depleted, need to be resuscitated, or have elevated ICP.
The advantage of hypertonic saline is that it remains intravas-
cular longer than normal saline and has an osmolar mechanism
of action similar to that of mannitol, without the diuretic effects.
Other theoretical benefits of hypertonic saline include improve-
TRAUMA
ments in vasoregulation, cardiac output, immune modulation,
and plasma volume expansion.
Currently, most severe TBI patients have other monitors
in addition to the ICP monitor. Other parameters that can
be measured are: brain-tissue oxygen tension (PbtO2 ), cerebral
blood flow, microdialysis variables, bispectral index, and cerebral
oximetry. These additional parameters help to guide ICP and CPP
treatment.
Table 2 outlines an escalating ICP treatment protocol. In the
case of medical refractory high ICP the entire protocol can be
exhausted in 2 to 4 h. Further details can be found in Krausz et
al (2013).
Surgical Techniques
Video 1 accompanying this chapter describes the techniques
below in detail.
External Ventricular Drain Placement
1. Draw a line on the scalp along the midline from the nasion
backward to the vertex of the skull.
2. Draw a perpendicular line 11 cm from the nasion.
3. At 11 cm behind the nasion, mark the Kocher point, a point
3 cm from the midline laterally just anterior to the coronal
suture, roughly in the mid-pupillary line.
4. Mark the proposed trajectory of the catheter. Draw a line from
the Kocher point to the ipsilateral medial canthus. Draw a
second line from the Kocher point to a point 1 cm in front
of the ipsilateral tragus.
5. Make an incision over the Kocher point with a scalpel (approx-
imately 2 cm long).
6. After a small retractor is placed, a manual twist drill is used to
make a hole. Once the inner table of the skull is breached the
dura needs to be opened.
7. The ventricular catheter is placed aiming toward the foramen
of Monro following the plane toward the medial canthus of
the ipsilateral side in the sagittal plane and toward a point 1
cm anterior to the tragus in the coronal plane. It should not
be advanced beyond 6 cm below the skull surface. This will
place the tip of the catheter just above the ipsilateral foramen
of Monro.
8. Immediate egress of clear or bloody (depending on the
pathology) CSF is seen. Care must be taken not to lose too
much CSF at this point, as the brain might not tolerate sudden
decompression of the ventricles.
9. The catheter is tunneled 5 to 7 cm posteriorly and laterally
under the scalp and secured with sutures.
An ICP monitor is placed at the same location using slightly
different hardware, as shown in Video 1.
Discussion of Case
This patient presented above arrives to the ED after a high
velocity injury with a GCS of 4. She does not open her eyes = 1;
she is intubated = 1; and she is extensor posturing = 2. Her
head CT shows diffuse brain swelling with a 3-mm right-sided
WAGNER ET AL

TABLE 2. ICP Treatment Protocol

ICP module for ICP > 20 for 10 min

1. Verify ICP
r Check if EVD is still patent
r Check if wave form EVD is present and adequate
r Check if EVD ICP correlates with intraparenchymal monitor, if present
2. Check for 30-degree head elevation
3. Loosen cervical collar if in place
4. Open EVD for ICP > 20 for 10 min and then close and transduce ICP
r Repeat once
r If ICP > 20 keep open at 15 above midbrain, and proceed with ICP module
5. Treat temperature > 37.5◦ C with 650 mg Tylenol once
6. Sedation
r Titrate Propofol to a Ramsay score of 4
r Do not exceed 5 mg/kg/h for more than 24 h
r Monitor potassium, triglycerides, and creatinine kinase (CK), and monitor urine for myoglobinuria every 8 hours for 24 h
r If maximum dose of Propofol is reached and ICP > 20
∼ Start Fentanyl drip to 0.8 mcg/kg/h
∼ Apply BIS monitor
∼ Titrate Fentanyl drip to a BIS of 30 or maximum of 5 mcg/kg/h
∼ Start Propofol with a loading infusion of 1 mg/kg over 10 min
∼ Continue maintenance infusion of 0.2 to 0.7 mcg/kg/h
7. Hyperosmolar therapy
r 3% Hypertonic saline bolus of 250 cc
∼Before administering 3% hypertonic saline bolus, check if Na < 130 mEq/L
r Mannitol 0.5 to 1 mg/kg bolus once in emergency
∼Check sodium and serum osmolality Q4 h × 2 after every bolus
r Start 3% hypertonic saline drip at 0.5 cc/h if ≥ three 3% hypertonic saline boluses within 6 hours
∼ Check sodium and serum osmolality Q 2 h while on drip
∼ If sodium > 160 mEq/L or serum osmolality > 320 sOsm/L, call MD
∼ If serum sodium increased > 10 mEq/L within the last 24 h, call MD
∼ If CBF > 35 mL/min/100 g white matter or > 80 m/min/100 g gray matter, refer to CBF module
8. Core body temperature > 37.5◦ C, start normothermia protocol
9. Hyperventilation
r Do not hyperventilate in the first 24 h (goal of PaCO2 of 35-40 mm Hg)
r If PbtO2 is < 20 mm Hg, go on hypoxia module
r If CBF is < 18 mL/min/100 g white matter, or < 67 mL/min/100 g gray matter, go to CBF module
∼ If PbtO2 and CBF is optimized hyperventilate to PaCO2 to 33 to 35 mm Hg
10. Radiology
r If refractory, ICP > 20 despite above intervention, obtain portable head CT without contrast STAT if no head CT since ICP is elevated despite
maximum therapy
11. Consider surgery
12. Induce pentobarbital coma
! Only for diffuse, nonoperative injuries
! Only with attending approval
r Order continuous EEG if not already in place. Order continuous electroencephalography (ie, EEG), if not already in place, to confirm burst
suppression
r Have norepinephrine drip ready at the bedside for MAP < 80 mm Hg/CPP < 60 mm Hg
r Pentobarbital bolus/loading: 10 mg/kg, then 5 mg/kg Q 1 h until burst suppression
r Pentobarbital maintenance dose: 1 mg/kg/h titrate to burst suppression
CBF, cerebral blood flow; CPP, cerebral perfusion pressure; CT, computed tomography; EVD, external ventricular drain; ICP, intracranial pressure; MAP, mean arterial blood pressure

aSDH. The SDH does not warrant evacuation because of the
size. Because of the diffuse nature of this injury, the patient is
diagnosed with a closed head injury. Because the GCS < 8, the
correct step in this patient’s care should be the placement of an
ICP monitor. A repeat head CT will probably be ordered within
the next 12 to 24 h, but the ICP needs to be measured immedi-
ately. Primary or early decompressive hemicraniectomy—taking
the patient immediately to the operating room—without placing
an ICP monitor and trying to manage the ICP medically—
should only be considered if there is a focal surgical lesion in
addition to the diffuse head injury. Hemicraniectomies have a
30 to 40% complication risk. Once the ICP is measured and

VIDEO 1. Closed head injury and ICU/ICP management.
found to be > 22 mm Hg, the first step should be head elevation,
and adequate sedation and pain control. After that, medical
and surgical treatment options are employed as outlined in
Table 2.
TRAUMA
Pearls
√
ICP monitoring is required in a patient with a head CT positive
for TBI and high ICP and a GCS < 8 who is not following
√ commands.
√ Steroids should not be given in TBI management.
Hyperventilation should be used sparingly, if at all, because it
can lead to further brain hypoxia.
SUGGESTED READING
1. Brain Trauma Foundation. Guidelines for the Management of Severe TBI, 4th
Ed. https://braintrauma.org/guidelines/guidelines-for-the-management-of-severe-
tbi-4th-ed#/. Accessed March 30, 2018.
2. Langlois JA, Rutland-Brown W, Wald MM. The Epidemiology and impact of
traumatic brain injury a brief overview. J Head Trauma Rehabil. 2006;21(5):375-
378.
3. Eijck MMV, Schoonman GG, Naalt JVD, Vries JD, Roks G. Diffuse axonal
injury after traumatic brain injury is a prognostic factor for functional outcome: a
systematic review and meta-analysis. Brain Inj. 2018;32(4):395-402.
4. Carney N, Totten AM, O’Reilly C, et al. Guidelines for the management of severe
traumatic brain injury, 4th ed. Neurosurgery. 2016;80(1):6-15.
5. Krausz MM, Ashkenazi I, Soustiel JF. Acute traumatic brain injuries and their
management. In: DiSaverio S, Tugnoli G, Catena F, Ansaloni L, Naidoo N, eds.
Trauma Surgery. New York: Springer; 2013:165-181.
CHAPTER 2: ACUTE SUBDURAL HEMATOMA
Case Presentation
A 64-yr-old man with unknown medical history was found
down on the side of a street, with multiple facial and scalp lacera-
tions. On presentation to the ED, he was lethargic, not following
commands, and weak on his left side. Due to his poor mental
status, he was intubated. CT of the head revealed a right sided
aSDH with 7 mm of midline shift (Figure 3).
After confirming his coagulation panel and platelet levels were
within normal levels, the patient was taken emergently to the
operating room. A right-sided craniotomy was performed, and the
hematoma was evacuated. On postoperative day 1, the patient was
awake, able to follow commands, and his hemiparesis had signif-
icantly improved. His postoperative CT showed resolution of the
aSDH (Figure 4).
Questions
1. Which are the most frequent sources of bleeding in case
of SDH?
2. Which are the indications for conservative treatment of
a patient with acute SDH?
3. Which are the indications for surgical treatment of a
patient with acute SDH?
4. Which other additional injuries may be associated with
an acute SDH?
5. Which are the mortality rates for acute SDH? Which are
the poor outcome prognosis factors?
WAGNER ET AL

FIGURE 3. CT scan showing an acute subdural hematoma with mass effect and midline shift.

Epidemiology
An aSDH is usually seen over the lateral cerebral convexity
in a patient suffering blunt head trauma (Krausz et al, 2013).
These patients may have a relatively limited head trauma or signif-
icant polytrauma depending on their mechanism of injury. Motor
vehicle accidents are common causes of aSDH in children and
young adults; older adults, especially those on anticoagulants and
antiplatelet agents, may present after a minor fall.

FIGURE 4. Postoperative CT scan showing resolution of the acute
subdural hematoma.
Anatomical Causes
The typical culprit in aSDH is a bridging cortical vein traveling
between the dura and arachnoid. These veins can be stretched
and torn in acceleration–deceleration injuries (Timmons, 2008).

Blood usually does not track into the underlying sulci, unless
there is an associated tSAH. aSDHs can also result directly
from an underlying brain laceration as a result of trauma. These
patients are generally unconscious and have a significant under-
lying brain injury, resulting in higher mortality. Brain lacerations
can directly injure cortical arteries and result in aSDH, and are
also associated with cerebral contusions, which can “blossom” and
cause significant mass effect. These patients may need immediate
surgery. Those who do not must be monitored carefully for signs
of increased ICP and possible need for operative intervention
(Timmons, 2008, and Leitgeb et al, 2012).
A less common cause of an aSDH is a ruptured intracranial
aneurysm, usually arising from the posterior communicating
artery. These patients will usually have significant subarachnoid
hemorrhage on their scans, and they may require an urgent
decompression in addition to treatment of their aneurysm.
Iatrogenic Causes
Removal of an aSDH or cSDH can also result in a life-
threatening contralateral or recurrent ipsilateral aSDH. In cases
of a contralateral skull fracture, the patient may develop an acute
EDH under the fracture site. Patients can develop an aSDH
after a craniotomy for another pathology, or after placement of
a ventriculoperitoneal shunt or EVD secondary to venous injury
or over drainage. Excessive anticoagulation can also cause sponta-
neous bleeds.
Additional Injuries
Evaluate the patient for concomitant intraparenchymal and/or
subarachnoid hemorrhage, skull fractures, and EDH, and work
with the surgical trauma team to rule out limb fractures, vascular
injuries, and trauma to the thorax and abdomen (Timmons,
2008). Keep in mind that even minor traumas can cause large
bleeds in patients who take anticoagulants/antiplatelet medica-
tions or who have an underlying bleeding disorder. Attention to
airway, breathing, and circulation is the hallmark of resuscitation
of all trauma patients regardless of intracranial pathology.
Imaging Findings
CT scan will often show an extra-axial, hyperdense mass that
is crescent-shaped. Midline shift may be present, and may be out
of proportion to the size of the hematoma, which may indicate
significant underlying brain injury (Leitgeb et al, 2012 and Bartels
et al, 2015).
Pathophysiology
It is difficult to separate the pathophysiology of an aSDH from
that of TBI, since the 2 often go hand in hand. High-speed
acceleration–deceleration events can also result in diffuse-axonal
injury and significant polytrauma. Yokobori et al and Karibe et
al present concise reviews on aSDH pathophysiology. Briefly, the
initial impact initiating the aSDH causes a primary brain injury.
Treatment is geared towards minimizing the “secondary injury”
that results from decreased cerebral blood flow in the vicinity
of the SDH. Surgery can rapidly reduce the ICP and minimize
TRAUMA
VIDEO 2. Craniotomy for acute subdural hematoma. T
the risk of stroke. Postoperatively, though, the brain is subject
to reperfusion injury, hyperperfusion, and hyperemia. Damage is
thought to be initiated by oxygen free radicals. This topic is the
subject of ongoing research.
Conservative Management
Patients with small aSDHs can be monitored carefully if the
hematoma is not causing significant mass effect and there is little
or no cerebral edema. This is especially true in elderly patients
who have varying degrees of brain atrophy. Close follow-up
imaging, usually at 4 to 6 h and again 24 h is suggested, especially
if the patient was on an anticoagulant/antiplatelet agent(s) with
high risk of expansion. Administration of platelets, desmopressin,
coagulation factors, and antiepileptics should be considered. In
comatose patients with small aSDHs, ICP monitoring is recom-
mended (see the Closed Head Injury part of this chapter). Surgery
should be considered for persistent elevations >20 mm Hg
(Timmons, 2008, and Hayashi et al, 2014).
Operative Treatment
Surgery is appropriate for patients with a hematoma >1 cm
in thickness and/or a hematoma causing >5 mm of midline
shift, regardless of initial examination, or a unilateral fixed and
dilated pupil. Generally, mortality is lower if surgery is performed
within 4 h of injury (Timmons, 2008, Hayashi et al, 2014, and
Timmons, 2015). That said, functional recovery may not be
improved despite rapid decompression. Factors, platelets, and/or
AEDs should be given when appropriate. Surgery usually consists
of a large craniotomy or craniectomy (Timmons 2008 and 2015).
The dura may be left open with an on lay or sutured dural graft.
If a sutured duraplasty is performed, it must be large enough to
accommodate some swelling, the so-called expansile duraplasty, to
avoid kinking of cortical vessels at the edge of the defect. Video 2
for this chapter, shows a craniotomy and evacuation of a sizeable
acute hematoma in a patient who sustained a fall.
WAGNER ET AL
SUGGESTED READING
1. Krausz MM, Ashkenazi I, Soustiel JF. Acute traumatic brain injuries and their
management. In: DiSaverio S, Tugnoli G, Catena F, Ansaloni L, Naidoo N, eds.
Trauma Surgery. New York: Springer; 2013:165-181.
Postoperative Care 2. Timmons SD. Extra-Axial Hematomas. In: Ullman JS, Raksin PB, eds. Atlas of
Emergency Neurosurgery. New York, NY: Thieme; 2008:52-67.
Patients should be monitored in an ICU after surgery. A 3. Leitgeb J, Mauritz W, Brazinova A, et al. Outcome after severe brain
postoperative CT of the head should be obtained, either shortly trauma due to acute subdural hematoma. J Neurosurg. 2012;117(2):324-333.
after surgery or the next morning if the patient remains stable. A https://thejns.org/view/journals/j-neurosurg/117/2/article-p324.xml. Accessed
subdural and/or subgaleal drain may be placed at the discretion of May 2, 2019.
4. Bartels RH, Meijer FJ, Hoeven HVD, Edwards M, Prokop M. Midline shift
the surgeon (Timmons 2008 and 2015). A decline in mentation, in relation to thickness of traumatic acute subdural hematoma predicts mortality.
worsening motor exam, or seizure will usually prompt an BMC Neurol. 2015;15:220-225. doi:10.1186/s12883-015-0479-x.
emergency CT. Prophylactic antiepileptic medications are usually 5. Karibe H, Hayashi T, Hirano T, Kameyama M, Nakagawa A, Tominaga T.
Surgical management of traumatic acute subdural hematoma in adults: a review.
maintained for 7 d. Neurol Med Chir (Tokyo). 2014;54(11):887-894.
6. Yokobori S, Nakae R, Yokota H, et al. Subdural hematoma decompression model:
Outcomes a model of traumatic brain injury with ischemic-reperfusional pathophysiology: a
Even relatively small aSDHs can be fatal. Mass effect on the review of the literature. Behav Brain Res. 2018;340:23-28.
7. Timmons SD. Surgery for epidural and subdural hematomas. In: Ullman JS, Raksin
underlying brain from the hemorrhage and swelling from the PB, eds. Atlas of Emergency Neurosurgery. New York, NY: Thieme; 2015:2-15.
TBI can result in subfalcine and/or transtentorial herniation.
Untreated, the mass can also reduce cerebral blood flow, resulting
in cerebral ischemia and infarction (Timmons 2008 and 2015).
Mortality rates for aSDH vary significantly depending on the
size of the hematoma, severity of associated TBI, and patients’
age. Patients presenting with poor neurological status at the time
of surgery have worse outcomes. Leitgeb et al found a mortality
rate of 47% when reviewing data from 17 Austrian Centers. The
outcomes in elderly patients are especially poor, with some sources
citing >80% mortality.
At one institution Bartels et al found that adult patients who
had midline shift that was 3 or more mm larger than the under-
lying hematoma all died. The additional shift in these patients
is presumably from brain swelling secondary to the traumatic
injury. Given these data, the family members of comatose patients
with significant TBI and a sizeable aSDH should be counseled on
outcome early in the patient’s course.

Pearls
√
Patients with aSDH should be evaluated immediately. Many of
these lesions, including the one in the case presentation and the
one in the video accompanying the text (Craniotomy for Acute
√ Subdural Hematoma), represent neurosurgical emergencies.
Most aSDHs result from blunt force trauma, and patients
should be evaluated for other intracranial and extracranial
CHAPTER 3: EPIDURAL HEMATOMA
√ injuries.
Despite research efforts, the outcomes in older patients with Case Presentation
significant TBI and aSDH remain poor.
A 38-yr-old man presents after a fall from a 10-ft high scaffold
onto a concert floor. In the ED, he has a GCS of 7 and is
Discussion of Case intubated. He only moves his left side, his pupils are equal
The patient presented at the beginning of this chapter and reactive, and his brainstem reflexes are intact. His CT scan
presented with altered mental status and a focal neurological (Figure 5) was obtained within 2 h of the injury and showed a left-
deficit. An emergency CT of the head revealed a large right SDH sided skull fracture and convex extra-axial hematoma consistent
with midline shift. He was taken to the operating room shortly with an EDH with midline shift.
after arrival with improvement in his neurological condition.
Early recognition and treatment of aSDHs can favorably impact Questions
outcome, especially in younger patients. 1. The best next step in the care of this patient is:
a. Place ICP monitor because of GCS < 8
b. Admission to the ICU for serial neurological exams
S52 | VOLUME 17 | NUMBER 2 | AUGUST 2019 SUPPLEMENT c. Emergency left-sided craniotomy for EDH evacuation
d. Repeat head CT
 TRAUMA

FIGURE 5. CT scan showing an acute left-sided subdural hematoma on the brain window (left) and an associated skull
fracture on the bone window (right).

2. Which parameter is associated with delayed progression to
surgery?
a. Temporal location
b. 1 cm midline shift
c. Clot thickness greater than 5 mm on the initial CT scan
d. First CT less than 6 h from injury
3. What is the indication of evacuation of an EDH following the
BTF guidelines?
a. EDH with a volume greater than 10 cm3
b. 15 mm thickness
c. EDH associated with a skull fracture
d. All arterial EDHs should be evacuated regardless of size
4. What bleeding source can result in venous EDH?
a. Lacerated meningeal artery
b. Bone bleeding
c. Brain contusion
d. Lacerated transverse sinus
5. Compared with other traumatic brain injuries, the mortality of
EDH is:
a. Lower than SDH
b. Higher than closed severe head injury
c. Lower than tSAH in awake patients
d. Similar to depressed skull base fractures
Epidemiology
The reported incidence of surgical and nonsurgical EDH
among TBI patients ranges from 2.7 to 11% (Bullock et al,
2006, and Stippler, 2016). A patient in a coma has a higher
likelihood (about 9%) of harboring an EDH. In most patients
that present in a coma, the EDH requires surgical evacuation. The
peak incidence of EDH is from 20 to 30 yr of age. EDHs are also
seen in children from 6 to 10 yr old. Traffic-related accidents, falls,
and assaults account for over half of all EDHs (Bullock et al 2006,
Stippler 2016, and Knuckey et al 1989).
Natural History
Mortality
The mortality in patients in all age groups and GCS scores
undergoing surgery for evacuation of EDH is approximately 10%
(Carney et al, 2016, and Krausz et al, 2013). The mortality
in comparable pediatric case series is approximately 5%. By
comparison, the mortality for SDH is 30 to 50% and about 30%
in severe TBI. The mortality for isolated tSAH and linear skull
fracture is very low (Stippler, 2016 and Knuckey et al, 1989).
Factors determining outcome from EDH are:
r GCS
r Age
r Pupillary abnormalities
r Associated intracranial lesions
r Time between neurological deterioration and surgery
r ICP (Bullock et al, 2006, Stippler, 2016, and Knuckey et al,
1989)
Clinical Presentation
About 20 to 50% of patients with an EDH are comatose
when they arrive in the ED or directly before surgery (Bullock
et al, 2006). Patients with an EDH often wake up after
WAGNER ET AL

initial unconsciousness and then deteriorate again. This is called

the “lucid interval” and has been reported in about half of
patients. It is important not to miss this in a patient who
presents to the ED during the awake period. Delayed deteri-
oration is also seen in patients in which the first CT was
obtained less than 6 h following injury. That is also why
many patients with a history of TBI are observed before
being discharged. Many patients have pupillary abnormalities
as the only neurological sign. Other presenting symptoms
include focal deficits, such as hemiparesis, decerebration, and
seizures. Early seizures are more often noted in pediatric patients
with an EDH low (Stippler, 2016 and Knuckey et al, 1989).

Anatomy and Distribution

EDH can result from injury to the middle meningeal artery
and its accompanying veins, the diploic veins, or the venous
sinuses (Stippler, 2016, and Knuckey et al, 1989). Bleeding
from the middle meningeal artery has been considered the main
source for EDH. Most of the time, EDHs are associated with
skull fractures that lead to bone bleeding or injury to the
middle meningeal artery. The middle meningeal artery runs in
the temporal bone, which is thinner than the rest of the skull
and hence easily broken. Therefore, EDHs more frequently are
located in the temporoparietal and temporal regions compared
with other locations (Bullock et al, 2006, Stippler, 2016, and FIGURE 6. A standard question-mark shaped incision for trauma
Knuckey et al, 1989). craniotomy.
However, venous EDHs from lacerated venous sinuses are also
seen and often present in a delayed fashion (Knuckey et al, 1989).
Venous EDHs are no less dangerous and are more difficult to us what might predict the need for surgery (Kang et al, 2015,
treat because the underlying venous sinus injury can lead to life- Stippler, 2016, and Knuckey et al, 1989). Table 3 lists CT and
threatening blood loss during surgery. patient characteristics that can guide the decision to proceed with
surgery or manage a patient nonoperatively.
Decision-Making
Indications for Operative and Nonoperative Management Surgical Techniques
The decision to operate on an acute EDH is based on Once the decision is made that a patient will undergo a
the patient’s level of consciousness assessed by the GCS score, craniotomy for EDH evacuation, a standard question mark
pupillary abnormalities, CT scan findings, and neurological (Figure 6) or linear incision is made (Timmons, 2015). It is
deterioration in delayed surgeries. Prospective, randomized trials important to choose an incision that allows adequate exposure
comparing surgical treatment with nonoperative management are of the EDH (Figure 7) and fracture site to allow adequate
not available. By looking at patient series in which patients were hemostasis. If the EDH is thought to be venous, the neurosurgeon
initially treated nonsurgically but deteriorated and then needed should consider the venous sinus anatomy and how to control
surgery, the factors associated with delayed surgery can teach bleeding of the sinus once the bone is elevated.

TABLE 3. Summary of the Criteria of Surgical and Nonsurgical Management of EDH According to the Guidelines of Surgical Management

Criteria for surgical treatment Criteria for nonsurgical treatment

GCS 3-15 r Volume > 30 cc No focal neurological r EDH volume < 30 cc

deficits and GCS > 8 r Midline shift < 5 mm
r Thickness < 15 mm
GCS 14-15 r Midline shift > 5 mm
r Thickness > 15 mm
EDH, epidural hematoma; GCS, Glasgow Coma Scale.

FIGURE 7. Intraoperative picture of an EDH in situ after the bone flap has
been removed.
VIDEO 3. Epidural hematoma.
If there is no SDH, the dura is not opened. If the dura looks
or feels tight after removing the EDH and there is concern for a
new SDH, a small opening is made in the dura and the subdural
space is inspected and irrigated. If no blood is encountered, the
dura is closed. The bone bleeding can be stopped with bone wax
or tack-up sutures. At the end of the case, it is important to place
a central tack-up suture to prevent re-accumulation of the EDH.
Video 3 outlines the indications for surgery and shows a
craniotomy for evacuation of an acute EDH.
Discussion of Case
The patient described has a history that is consistent with
an EDH. A fall from height onto a hard surface can lead to
a skull fracture and hence EDH. The CT scan demonstrates
TRAUMA
an extra-axial convex fluid collection along the convexity. This
appearance is consistent with an EDH. The bone window of the
CT scan also demonstrates an underlying skull fracture cementing
the diagnosis and the etiology of the bleeding: lacerated middle
meningeal artery. This leads to the conclusion that this is an
arterial EDH and will expand rapidly. These facts, together with
the EDH size and the patient’s poor neurological examination
(he is comatose, has clear localized findings), make the decision,
according to the guidelines, clear that this patient needs an
emergency craniotomy for EDH evacuation.
Pearls
√
An EDH greater than 30 cm3 should be surgically evacuated
regardless of the patient’s clinical examination or level or
√ consciousness as measured3 by the GCS score.
An EDH less than 30 cm , with less than a 15-mm thickness
and less than a 5-mm midline shift in patients with a GCS score
greater than 8 without focal deficit, can be managed nonoper-
atively with serial CT scanning and close neurological obser-
vation in a neurosurgical center.
√
It is strongly recommended that patients with a skull fracture
and a negative CT scan less than 6 h from the injury should
be monitored for a delayed EDH with serial neurological
and/or a follow-up head CT within 6 to 12 h from the last
head CT.
SUGGESTED READING
1. Bullock MR, Chesnut R, Ghajar J, et al. Surgical management of acute epidural
hematomas. Neurosurgery. 2006;58(Supplement):S7-15.
2. Stippler M. Craniocerebral trauma. In: Jankovic J, Mazziotta J, Pomeroy S eds.
Bradley’s Neurology in Clinical Practice. 7th ed. New York, NY: Elsevier; 2016:867-
880.
3. Knuckey NW, Gelbard S, Epstein MH. The management of “asymptomatic”
epidural hematomas. J Neurosurg. 1989;70(3):392-396.
4. Carney N, Totten AM, O’Reilly C, et al. Guidelines for the management of severe
traumatic brain injury, 4th ed. Neurosurgery. 2016;80(1):6-15.
5. Krausz MM, Ashkenazi I, Soustiel JF. Acute traumatic brain injuries and their
management. In: DiSaverio S, Tugnoli G, Catena F, Ansaloni L, Naidoo N, eds.
Trauma Surgery. New York: Springer; 2013:165-181.
6. Kang J, Hong S, Hu C, et al. Clinical analysis of delayed surgical epidural
hematoma. Korean J Neurotrauma. 2015;11(2):112-117.
7. Timmons SD. Surgery for epidural and subdural hematomas. In: Ullman JS, Raksin
PB, eds. Atlas of Emergency Neurosurgery. New York, NY: Thieme; 2015:2-15.
WAGNER ET AL
FIGURE 8. CT scan demonstrating right temporal contusions and traumatic subarachnoid hemorrhage.
CHAPTER 4: CLOSED HEAD INJURY WITH
TEMPORAL CONTUSION AND SUBARACHNOID
HEMORRHAGE
Case Presentation
A 23-yr-old man is brought in by ambulance after car
surfing and falling onto his left side with an associated loss of
consciousness. On emergency medical services arrival, he was not
eye opening and was withdrawing his extremities when stimu-
lated. He was intubated in the field and brought to the emergency
room. A CT of the head showed right temporal contusions with
4 mm of midline shift as well as tSAH over the brain convexity
(Figure 8).
Questions
1. Which is the GCS of this patient?
2. Which is the most appropriate management for this
patient? Explain the reasons.
3. In case you choose the conservative treatment, which are
your next steps?
4. Which are the indications for surgical treatment?
5. Which are the medical treatment options for high ICP?
from 3.2 to 1.4. Which of the following would not be an appro-
priate management strategy?
a. Decrease sedation
b. Give hyperosmolar/rescue therapy
c. Repeat a CT head
Anatomy and Natural History
Areas of post-traumatic hemorrhage within or on the surface of
the brain often correspond to bony prominences of the skull base
which the brain can strike when it moves within the skull. Coup
lesions tend to occur near the site of an externally applied force
and can be suggested by the presence of a scalp hematoma as seen
in the CT head above. Contrecoup injuries occur at contralateral
sites or those otherwise remote from the externally applied force
as a result of brain movement within the skull after impact. These
lesions are seen when the brain strikes the anterior skull base
causing frontal contusions, the sphenoid wing causing temporal
contusions, or the occipital bone causing occipital contusions
(Khoshyomn and Tranmer, 2004). In the case discussed here,
the temporal contusion would be considered a contrecoup lesion.
Contusions can be seen on CT as an area of high attenuation
representing blood and low attenuation which represents the
edema around the area of injury. Some sources classify a lesion
which is at least two-third high-attenuating blood as a traumatic
intraparenchymal hematoma as opposed to a contusion (Bullock
et al, 2006).
Contusions may be seen on the patient’s initial cranial imaging,
may expand with time (“blossoming”) or may be delayed,
appearing only on delayed imaging (Khoshyomn and Tranmer,
2004). This delayed appearance on imaging has been correlated
 TRAUMA

TABLE 4. The Rotterdam Scorea

Cisternal effacement 0 Normal
1 Partially effaced
2 Completely effaced
Midline shift 0 <5 mm
1 >5 mm
Epidural hematoma 0 Present
1 Absent
Intraventricular or 0 Neither present
subarachnoid 1 Either present
hemorrhage
a
The Rotterdam Score is the sum of each component listed below. 0 to 2 points for
cisternal effacement, and 0 to 1 points each for midline shift, epidural hematoma, and
intraventricular/subarachnoid hemorrhage. The minimum score is 1 (regardless of the
subcomponent scores), and the maximum is 6. VIDEO 4. Closed head injury with temporal lobe contusions and subarachnoid
hemorrhage.
with a poor outcome. Edema associated with these lesions can be
targeted by medical therapies to prevent clinical decline. Multiple
variables must be taken into account when determining if surgical
management is appropriate for these hematomas including the
First, the patient should be positioned head up with care to ensure
volume, neurological status of the patient, ICP burden, degree of
the jugular veins are not compressed. Additional treatments
midline shift, and brain compression (Khoshyomn and Tranmer,
include sedation, hyperosmolar therapy, paralysis, hypothermia,
2004, Mrozek et al, 2015, and Burgess et al, 2016).
and preventing hypercarbia (Khoshyomn and Tranmer, 2004,
tSAH is also frequently seen in more diffuse injuries. Indeed,
Mrozek et al, 2012, and Burgess et al, 2016). The earlier part
trauma is a more common cause of subarachnoid hemorrhage
of this chapter outlines an algorithm for the escalating medical
than aneurysmal rupture (Randhawa and Rabb, 2015, and
management of a patient’s ICP.
Lin et al, 2012). tSAH is less defined than its aneurysmal
Of note, prolonged hyperventilation to pCO2 values below
counterpart, which is characterized by Fisher Grade and a
30 mm Hg has been associated with harm and this historical
well-understood risk of vasospasm. tSAH has, however, been
practice is now avoided (Carney et al, 2016). There is insufficient
associated with worse outcomes as reflected by the Rotterdam
evidence to recommend prophylactic cooling; however, hyper-
Score (Table 4) referenced later in this chapter (Randhawa and
thermia has been shown to be a poor predictor of outcome. On
Rabb, 2015, and Mrozek et al, 2012). Isolated SAH can also
this basis, fever is avoided while hypothermia is reserved as a
occur in mild TBI and may be a risk factor for injury progression
treatment option for refractory ICP elevation (Carney et al, 2016,
and adverse outcomes. When assessing post-tSAH, the possibility
and Jennett et al, 1976).
of an aneurysm rupture preceding the trauma must always be
There is some controversy in the selection of hyperosmolar
considered, especially when the subarachnoid hemorrhage lies at
therapies. Literature from 1992 demonstrated in an animal model
the base of the brain—screening with CT angiography should be
that mannitol—which has historically been the most frequently
undertaken liberally.
used treatment for ICP elevation—can accumulate in areas of
Decision Making disrupted blood–brain barrier such as contusions and ultimately
exacerbate ICP elevation. The study demonstrated that mannitol
Indications for surgical evacuation per the published Surgical
failed to reduce water content in a single dose, and that multiple
Guidelines include:
doses cause a local increase in water content in these areas.
r Refractory intracranial hypertension (sustained ICP > 20) Multiple studies have sought to elucidate the differences between
r Volume > 50cc (relative criteria) hypertonic saline and mannitol, but evidence to date has not
r GCS 3-8 with frontal or temporal volume > 20 cc and midline suggested any difference in mortality, neurological outcomes, or
shift > 5 mm and/or compressed cisterns (Brain Trauma ICP reduction (Steyerberg et al, 2008).
Foundation, 2016, and Bullock et al, 2006)
Outcomes
There have been numerous efforts to develop prognostic
Medical Management models of TBI based on severity of the initial injury, as summa-
There are many medical options for treating the elevated ICP rized in Mass et al, and Chakraborty et al. The mainstay of
that commonly results from cerebral contusions and associated assessment on arrival are GCS which look at eye opening, motor
edema. The earlier discussion of closed head injury also outlines movement, and verbalization. The GCS has strong prognostic
some of these, and Video 4 also discusses these in some detail. abilities, particularly the motor score. However, there are multiple
WAGNER ET AL
TABLE 5. Mortality Predictions Based on the
Rotterdam Score
Score Mortality
1 0%
2 7%
3 16%
4 26%
5 53%
6 61%
other important variables for which the GCS cannot account.
There have been multiple attempts to create models to weight
these variables and determine how to specifically integrate them
into a clinically significant tool that can be used at the bedside to
predict outcome at 6 mo.
The Rotterdam Score (Table 4), discussed in Video 4, is an
important prognostic model in TBI. It is a modification of the
Marshall CT Head score, which had been developed previously.
Both models use CT features to predict mortality. The Rotterdam
score adds the presence or absence of tSAH and EDH to variables
assessed by the Marshall score (cisternal effacement, presence of
midline shift > 5 mm, and presence of an evacuated or nonevac-
uated mass lesion). The summed score (Table 5) can be used to
directly predict mortality (Chen et al, 2011).
Scientists have worked extensively to develop a medication that
reduces brain injury or improves brain repair leading to improved
outcomes for TBI patients. To date, no therapeutic has been
successfully translated. The calcium channel blocker, nimodipine,
was studied in a series of multicenter trials. Subgroup analysis in
these studies suggested that nimodipine may benefit men with
tSAH; however, this has not been further validated. Progesterone
was recently studied in complementary high-profile studies and
both failed to find evidence for benefit despite a large body of
supportive preclinical data (Chakraborty et al, 2016).
The IMPACT (International Mission for Prognosis and
Analysis of Clinical Trials in TBI) model is another validated
prognostic calculator which was developed by pooling patient
data from completed TBI studies from the United States and
Europe (Steyerberg et al, 2008). The model uses both patient
characteristics and radiographic features to determine outcome.
There is a core model that used age, motor value of the GCS,
and pupil reactivity. The accuracy of the model is improved
with the addition of additional information pertaining to the
secondary brain insults hypoxia and hypotension. Radiographic
characteristics also refine the prediction: the Marshall CT classi-
fication, the presence of subarachnoid hemorrhage, and EDH
are of prognostic significance. Laboratory values including blood
glucose levels and hemoglobin are also included in the most
complex IMPACT model. These values are weighted in the
IMPACT model and are ultimately used to predict outcome at 6
mo with approximately 80% accuracy.25 A web-based calculator
is available to aid in the calculations (http://www.tbi-impact.org).
Other Clinical Considerations
Automated pupillometry has gained popularity as a sensitive
pupillary assessment which can provide early warning of
uncal herniation. Commercially available pupillometers assess
multiple facets of the pupillary response to light including
minimum and maximum pupillary size, percent change, time
latency, constriction velocity, and dilation velocity. The NPITM
(NeurOptics, Laguna Hills, California) is the result of a propri-
etary formula which accounts for each of these measures. Pupil-
lometers have substantially better intra-rater and inter-rater
reliability than human pupillary examinations, as discussed in
Chen et al, Couret et al, and Marshall et al. Pupillometers are
believed to be particularly helpful in detecting decline related
to temporal lesions; Marshall et al. reported that herniation can
occur with temporal lesions due to focal edema at the level of the
midbrain without elevation of ICP as detected by traditional ICP
monitors.
Surgical Management
Parenchymal contusions causing mass effect with progressive
neurological decline directly attributable to the lesion and
medically refractory intracranial hypertension meet criteria for
surgery based on the consensus guidelines published in the 2006
Guidelines for Surgical Management of Severe TBI by Bullock et
al. The specific criteria suggesting surgery in this guideline include
frontal or temporal lesions greater than 20 cm3 or any lesion over
50 cm3 if the patient’s GCS is <9. The surgical goal in these cases
is to evacuate a mass lesion, when possible, or to perform a decom-
pression.
Discussion of Case
Using the online TBI-IMPACT calculator, the patient had a
6 mo 11% predicted probability of mortality, and 25% predicted
probability of unfavorable outcome. He required admission to the
ICU with placement of an EVD and directed therapy to control
ICP. This included sedation, use of hyperosmolar therapy, and
ventilator-directed therapy. Ultimately, after a week of treatment,
ICPs were well controlled and sedation was able to be weaned.
The patient was successfully extubated and transferred to an acute
rehabilitation facility successfully. On transfer to acute rehabili-
tation he scored a Glasgow Outcome Score (GOS) of 3, following
commands but unable to live independently. On discharge from
acute rehabilitation, he was a GOS 5 and eventually able to return
to school with some mild attention difficulty.
 TRAUMA

Pearls
√
Cerebral contusions are lesions that often evolve with time
√ requiring management that evolves in turn.
Monitoring of ICPs and follow-up imaging can aid in identi-
√ fying blossoming contusions.
Treatment varies by amount of hemorrhage, neurological
√ examination, and ICP.
Pupillometer may detect early increases in temporal lobe edema
or blossoming contusion.

SUGGESTED READING
1. Khoshyomn S, Tranmer BI. Diagnosis and management of pediatric closed head
injury. Semin Pediatr Surg. 2004;13(2):80-86.
2. Bullock MR, Chesnut R, Ghajar J, et al. Surgical management of traumatic
parenchymal lesions. Neurosurgery. 2006;58(Supplement):S25-S46.
3. Mrozek S, Vardon F, Geeraerts T. Brain Temperature: physiology and pathophys-
iology after brain injury. Anesthesiol Res Pract. 2012. doi:10.1155/2012/989487.
4. Burgess S, Abu-Laban RB, Slavik RS, Vu EN, Zed PJ. A systematic review of
randomized controlled trials comparing hypertonic sodium solutions and mannitol
for traumatic brain injury. Ann Pharmacother. 2016;50(4):291-300.
5. Randhawa PS, Rabb C. Surgery for cerebral contusions of the frontal and temporal
lobes, including lobar resections. In: Ullman JS, Raksin PB, eds. Atlas of Emergency
Neurosurgery. New York, NY: Thieme; 2015:33-52.
6. Lin TK, Tsai HC, Hsieh TC. The impact of traumatic subarachnoid hemorrhage
on outcome: a study with grouping of traumatic subarachnoid hemorrhage and
transcranial Doppler sonography. J Trauma Acute Care Surg. 2012;73(1):131-136.
7. Brain Trauma Foundation. Guidelines for the Management of Severe TBI, 4th Ed.
https://braintrauma.org/guidelines/guidelines-for-the-management-of-severe-tbi-
4th-ed#/. Accessed March 30, 2018.
8. Carney N, Totten AM, O’Reilly C, et al. Guidelines for the management of severe
traumatic brain injury, 4th ed. Neurosurgery. 2016;80(1):6-15.
9. Jennett B, Teasdale G, Braakman R, Minderhoud J, Knill-Jones R.
Predicting outcome in individual patients after severe head injury. Lancet.
1976;307(7968):1031-1034.
10. Steyerberg EW, Mushkudiani N, Perel P, et al. Predicting outcome after traumatic
brain injury: development and international validation of prognostic scores based
on admission characteristics. PLoS Med. 2008;5(8).
11. Maas AI, Hukkelhoven CW, Marshall LF, Steyerberg EW. Prediction of outcome
in traumatic brain injury with computed tomographic characteristics: a comparison
between the computed tomographic classification and combinations of computed
tomographic predictors. Neurosurgery. 2005;57(6):1173-1182.
12. Chakraborty S, Skolnick B, Narayan RK. Neuroprotection trials in traumatic
brain injury. Curr Neurol Neurosci Rep. 2016;16(4).
13. Chen JW, Gombart ZJ, Rogers S, Gardiner SK, Cecil S, Bullock RM. Pupillary
reactivity as an early indicator of increased intracranial pressure: the introduction
of the neurological pupil index. Surg Neurol Int. 2011;2(1):82.
14. Couret D, Boumaza D, Grisotto C, et al. Reliability of standard pupillometry
practice in neurocritical care: an observational, double-blinded study. Crit Care.
2016;20(1).
15. Marshall LF, Barba D, Toole BM, Bowers SA. The oval pupil: clinical significance
and relationship to intracranial hypertension. J Neurosurg. 1983;58(4):566-568.
WAGNER ET AL

NEUROSURGERY FOR MEDICAL STUDENTS

CHAPTER 5: CHRONIC SUBDURAL HEMATOMA

Case Presentation
A 66-yr-old man was previously treated for acute pedestrian
trauma with mild intracranial hemorrhage after being struck
by a motor vehicle. He had been followed as an outpatient
and developed a left cSDH which was managed, initially, with
observation. He was subsequently treated with a steroid taper
after the cSDH began to enlarge over serial images. Later, he
presented to the office during one visit with increased lethargy
and new right sided weakness. He was not taking any anticoag-
ulant or antiplatelet agents. A repeat CT scan showed a larger,
subacute/chronic left-sided SDH with approximately 7 mm of
midline shift (Figure 12).
On initial examination, the patient opened his eyes to voice,
was fully oriented, followed commands, and was 5/5 on the
left side. His right upper extremity and right lower extremity
were 4-4 + /5 and he had a right-sided pronator drift. He was
admitted for observation and possible surgery the following day,
but he deteriorated in the emergency room. Immediately preop-
eratively, he required noxious stimuli to open his eyes and was
not answering orientation questions or following commands.
Laboratory values revealed that the patient had a coagulopathy
and elevated white blood cell count. The coagulopathy resolved
quickly after administration of 4-factor prothrombin complex
concentrate and vitamin K. The patient was brought to the
operating room that evening for a left-sided burr hole drainage
of his SDH. He was ultimately treated for urosepsis and was
 TRAUMA

FIGURE 12. CT scan demonstrating a chronic left-sided subdural hematoma with a subacute component.

2. A 65-yr-old man presents with a small, thin, cSDH found on

CT scan performed after he had a witnessed fall down the
stairs. His neurological examination is normal and he does not
have headaches, nausea, or vomiting. His wife recalls that he
bumped his head on the kitchen cabinet about a month ago,
but he did not seek care. Which of the following medications
should he avoid?
a. Acetaminophen (Tylenol) for occasional headaches
b. Aspirin for headaches
c. Odansetron (Zofran) for occasional nausea
d. Finasteride (Proscar) for his benign prostatic hyperplasia
3. Which structure(s) is/are considered the culprit in most SDH?
a. The middle meningeal artery
b. The middle meningeal vein
VIDEO 6. Chronic subdural hematoma. c. Bridging veins
d. The superior sagittal sinus

Chronic Subdural Hematoma

Epidemiology
discharged with intact neurological and mental status exami- cSDHs are more common than many other neurosurgical
nation. Video 6 shows placement of 2 burr holes for cSDH. pathologies, with an incidence of approximately 1.7/100 000/yr.
As reported in Adhiyaman, these hematomas are more common
Questions in elderly patients, with the incidence increasing to over 7/100
1. What are the indications for operating on a patient with a 000/yr in patients over the age of 70. Infants may present with
cSDH? benign subdural collections, which can resolve spontaneously at
a. Midline shift greater than or equal to 5 mm 8 to 9 mo after diagnosis (Greenberg, 2016).
b. Focal neurological deficit Risk factors for cSDH include advanced age, cerebral atrophy,
c. Decrease in mental status use of anticoagulant or antiplatelet drugs, other coagulopathic
d. All of the above states, hemodialysis, epilepsy, and frequent falls/head traumas
WAGNER ET AL
(Timmons, 2015). Older patients who abuse alcohol are suscep-
tible to cSDH, as they are often malnourished, may be coagulo-
pathic, and have frequent trips/falls and occasionally seizures that
result in head trauma. Another risk factor that may be unrelated to
age is decreased ICP, which can be seen in patients with CSF leaks.
As described earlier, these leaks may be spontaneous or occur after
a lumbar puncture, epidural anesthesia, or trauma (Lemole et al,
2001).
Anatomical Causes
In contrast to acute EDHs, which often result from injury and
rupture of the middle meningeal artery, cSDHs are usually caused
by ruptured bridging veins. Sometimes oozing from these veins is
visible intraoperatively. Rarely a cSDH can be seen accompany
dural tumors or metastases. Subdural effusions/hygromas may
evolve into a cSDH. aSDHs can be caused from significant
injury to these veins or venous sinuses, rupture of cortical veins
(usually following trauma), or rupture of certain intracranial
aneurysms or dural arteriovenous fistulas. If managed conserva-
tively, a small acute subdural may evolve into a cSDH. These
SDHs can also develop multiple, complex membranes, which
occasionally allow the formation of loculations. The pathogenesis
of membrane formation is somewhat complex, with multiple
inflammatory proteins implicated. Yadav et al provide a concise,
updated summary of membrane pathogenesis.
Iatrogenic Causes
cSDHs may be suspected in patients with a persistent headache
one or more weeks following a lumbar puncture, spine surgery
with a CSF leak, or epidural anesthesia. Patients can also develop
cSDH following intracranial surgery. Overdrainage from an
EVD, lumbar drain, or shunt can also cause a subdural effusion
and/or hematoma.
Presentation
A cSDH can present with symptoms ranging from mild
forgetfulness and cognitive impairment to lethargy to mild
or severe motor weakness. Patients may also have seizures,
and these can present with aphasia, decreased mental status,
motor weakness, paresthesias, etc. Less common presentations
include an isolated third nerve palsy and abnormal parkinsonian
movements. Symptoms can progress slowly as the cSDH enlarges
and causes more mass effect on the underlying brain. In some
patients there is no reported history of a head trauma, even minor.
The astute physician should rule out a CSF leak, tumor, and/or
hematological disorder in a young and otherwise healthy patient
presenting with an atraumatic cSDH (Skovrlj et al, 2015).
Treatment
There are multiple ways to handle cSDHs, and significant
debate among neurosurgeons about the pros and cons of each.
Neurologically intact, otherwise asymptomatic patients can be
monitored with serial CT scans and followed on an outpa-
tient basis. Steroids, especially dexamethasone, can help reduce
patients’ headaches and nausea and can reduce hematoma volume
over time in some patients. Tranexamic acid, an antithrobolytic
agent, has also been used in selected patients. Patients who
are at very high risk for surgery due to their medical comor-
bidities may also be monitored with serial scans, especially if their
symptoms are minor. Surgical procedures for cSDH include twist-
drill craniostomy, including placement of a Subdural Evacuating
Port System (Medtronic), burr hole evacuation, craniotomy, or
craniectomy. A demonstration of SEPS placement (Medtronic)
can be viewed on YouTube (https://www.youtube.com/watch?v=
8Ykg2Mu7Mzg).
Twist-drill craniostomy procedures can be performed at the
bedside and do not require general anesthesia in most cases.
They are well suited for patients who are high-risk surgical candi-
dates and who have obvious fluid collections without many
membranes. These procedures cannot evacuate acute blood. A
ventricular catheter can be threaded into the subdural space for
drainage to a canister by gravity over several days. In the case of
the subdural portal system, the drain is entirely extracranial to a
small suction bulb (Yadav et al, 2016, and Skovrlj et al, 2015).
Burr-hole evacuation usually takes place in the operating room,
under general anesthesia or sedation. As shown in Video 6, more
than one burr hole can be placed to maximize drainage and allow
passage of a red rubber catheter under the dura to irrigate out
the hematoma. If visible, membranes can be addressed. Most
surgeons leave a subdural drain after burr hole drainage, to allow
the remaining hematoma and irrigation fluid to drain slowly and
give the underlying brain a chance to re-expand. Options include
leaving a ventricular drainage catheter in the subdural space or
using a small flat or round silicon drain hooked up to a small bulb,
as shown in Video 6. Patients must stay in a monitored setting
with the subdural drains in place (Yadav et al, 2016, and Skovrlj
et al, 2015).
A craniotomy may be more appropriate in patients with large
collections, especially those with significant loculations. Patients
with a significant amount of acute blood may benefit more from
this procedure. It allows for better visualization, and occasionally
a bleeding vein can be found and hemostasis obtained. Coagu-
lating large cortical veins can cause a postoperative venous
infarction. This surgery also requires the patient to be under
general anesthesia and takes longer than a burr hole. Craniectomy
is rare and usually reserved for patients with significant rebleeding
in the perioperative period. Regardless of the procedure used to
address a patient’s cSDH, drains should only be connected to light
bulb suction or to a canister for gravity drainage.
Anesthetic Considerations
Twist-drill craniostomy, subdural portal placement, and burr
hole drainage can be performed under conscious sedation with
local anesthetic in appropriate patients. Patients with obstructive
sleep apnea or lung disease may require intubation and general
anesthesia. Craniotomies are performed under general anesthesia.
 TRAUMA

Postoperative Considerations SUGGESTED READING

All patients undergoing a procedure for cSDH should be
monitored in an ICU for at least 24 to 48 h, or until the subdural
portal system or subdural drains have been removed. A CT scan
is usually performed postoperatively. Some surgeons will also
want a “post-pull” scan following the removal of the drains to
evaluate for acute hemorrhage. Patients should be monitored
carefully until discharge. Seizures, altered mental status, or new or
worsening neurological deficits warrant a stat CT of the head to
rule out re-accumulation, re-expansion hemorrhage into the brain
parenchyma, or development of a contralateral aSDH. Upwards
of 20% of patients may experience a recurrence of the SDH, and
some need a second procedure to address reaccumulation (Han et
al, 2017). There is nearly always residual hematoma after drainage
that can persist for many weeks due to slow re-expansion of the
brain. Serial outpatient imaging is recommended to follow the
residual collection to resolution.
Many elderly patients with cSDHs are on antiplatelet or antico-
agulant medications because of their medical comorbidities,
including coronary artery disease, peripheral vascular disease,
and/or history of ischemic stroke. The input of other physicians
is important, and a thoughtful, individualized, risk/benefit evalu-
ation is required for these patients.
1. Adhiyaman V, Asghar M, Ganeshram KN, Bhowmick BK. Chronic subdural
haematoma in the elderly. Postgrad Med J. 2002;78(916):71-75.
2. Greenberg MS. Handbook of Neurosurgery. 8th ed. New York, NY: Thieme; 2016.
3. Timmons SD. Surgery for epidural and subdural hematomas. In: Ullman JS,
Raksin PB, eds. Atlas of Emergency Neurosurgery. New York, NY: Thieme; 2015:2-
15.
4. Lemole GM, Henn JS, Zabramski JM, Sonntag VKH. The Management
of cranial and spinal CSF leaks. Barrow Quarterly. 2001;17(4). https://www.
barrowneuro.org/education/grand-rounds-publications-and-media/barrow-
quarterly/volume-17-no-4-2001/the-management-of-cranial-and-spinal-csf-leaks/.
Accessed May 2, 2019.
5. Yadav Y, Parihar V, Chourasia I, Bajaj J, Namdev H. The role of subgaleal suction
drain placement in chronic subdural hematoma evacuation. Asian J Neurosurg.
2016;11(3):214-218.
6. Skovrlj B, Rasouli J, Levy AS, Raskin PB, Ullman JS. Chronic subdural
hematomas. In: Ullman JS, Raksin PB, eds. Atlas of Emergency Neurosurgery. New
York, NY: Thieme; 2015:16-25.
7. Han MH, Ryu JI, Kim CH, Kim JM, Cheong JH, Yi H-J. Predictive factors
for recurrence and clinical outcomes in patients with chronic subdural hematoma.
J Neurosurg. 2017;127(5): 1117-1125.

Pearls
√
There are many ways to manage cSDH. Treatment depends
on the patient’s symptoms, medical comorbidities, and overall
√ health.
Patients with atraumatic subdurals, especially if they are not
taking anticoagulant or antiplatelet medications, should be
evaluated for an underlying CSF leak or other source of
√ intracranial hypotension.
Immediately obtain a CT scan on patients with new or
worsening deficits, seizures, or altered mentation.

Discussion of Case
The case represents an example of a patient who initially
presented with acute trauma with mild intracranial hemorrhage
that ultimately developed into a chronic collection which became
symptomatic over a course of observation and medical treatment.
This case highlights the need for continued monitoring of
patients after head injury. Patients who undergo surgery for cSDH
will require follow-up monitoring until the residual subdural
collection has appropriately resolved.