Professor Rounds
LSU Neurology
Jonathan Guterman, M.D.
HPI
81 y/o AAM p/w the Chief Complaint
of sudden onset of confusion and noted
to have bilateral flickering of his eyes
while at home per his daughter. He
was not talkative but responded
appropriately without any complaints
of pain.
HPI Continued
His daughter put him in her car and drove
to Ochsner North Shore ED. CT Head was
done and subsequently was directly
transferred to Ochsner Main Hosp. Pt. was
intubated and sedated in the ED for airway
protection. No reports of LOC, head
trauma, headaches, chest pain, N/V, or SOB.
Past Medical History/Past Surgical
History
GERD
BPH
Hypothyroidism
Insomnia
Hernia Repaired 30 years ago
Hemorrhoids Removed 25 years ago
No known drug allergies/No known food allergies
Family History/Social History
Sister: Hx of Ischemic Stroke in her 60’s
Mother: Hx of DM2 in 50’s
Lives with his wife in an apartment
Quit Smoking approximately 30 years ago; used to
be a 25 pack year Smoker
Drinks 6 pack of Beer daily x 30 years
No history of elicit drug use
Home Medications
Synthroid 50 mcg po daily
Nexium 20 mg po daily
Ambien 10 mg po qhs
Patient was not on any Anti-platelet or Anticoagulant medications at home
Initial Presentation
T 98.3, BP 182/89, P 115, R 18, SpO2 100% on vent
Intubated/Sedated/PERRLA
Corneal reflexes were present bilaterally
Gag reflex present
Cough reflex present
No teeth were present
Moves all extremities to painful stimuli
Right arm and Right hand were contracted
Initial Presentation
Reflexes: Symmetric 2+ Biceps, 2+ Brachioradialis,
2+ Triceps/ 3+ Symmetric Patellars/ 1+ Achilles
Bilateral Toes were Upgoing
Heart: S1/S2 were appreciated, No murmurs noted
Lungs: Clear to auscultation bilaterally
Abdomen: Soft, non-tender, Bowel sounds present
Extremities: No peripheral edema bilaterally
GU: Foley was in place and making urine
Labs
Sodium=135
Potassium=3.6
Chloride=99
CO2=27
BUN=8
Creatinine=0.8
Glucose=100
Calcium=9.4
Magnesium=1.9
Phosphorus=3.1
Labs Continued
WBC=4.3
Hemoglobin=13.4
Hematocrit=41.8
Platelets=160
LFT’s=WNL
PT/PTT/INR=WNL
Diagnostic Studies
EKG: NSR at 73 BPM with no ST-T changes
TT-Echo: Normal LV function with EF=65%,
Concentric remodeling, normal diastolic function,
moderate left atrial enlargement, mildly enlarged
aortic root, trivial to mild Aortic Regurgitation,
trivial Mitral Regurgitation
CXR: No acute disease with ET tube in good
position
CT Head: Done at Ochsner North Shore prior to
transfer
Diagnostic Studies
CT Head Report
Large Left Subdural hematoma with 1.4 cm
Left to Right Midline shift that measures
approximately 2.8 cm in greatest dimension.
Acute and Subacute with no fractures.
Hospital Course
Patient was admitted to the Neuro-Critical
Care Service and Neurosurgery was
consulted immediately.
A Cardene Gtt was started with goal to keep
SBP<160
A-line was placed
Patient was kept NPO and Neuro checks Q1H
Hospital Course
Lopressor 10 mg IV Q4H was started
Keppra 1500 mg IV Q12H was given for seizure
prophylaxis
Banana Bag hung
All Anti-platelets and Anti-Coagulants were held and
patient was put on SCD’s and a PPI
Within a few hours, the Patient was sent to the OR
for a Craniotomy with Clot removal
Hospital Course
The Surgery was tolerated well and he was
extubated 2 days later and noted to be
Awake, Alert and Oriented to Person, Place,
and Time and moving all extremities
symmetrically and following all commands.
Discussion of Subdural hematoma
A SDH is a type of hematoma, a form of traumatic
brain injury in which blood gathers within the
outermost meningeal layer, between the Dura
mater, which adheres to the skull, and the
Arachnoid mater enveloping the brain.
Discussion of SDH
Usually resulting from tears in bridging veins that
cross the subdural space, subdural hemorrhages
may cause an increase in intracranial pressure,
which can cause compression of and damage to
delicate brain tissue.
Discussion of SDH
Subdural hematomas are often life threatening when
acute, but chronic subdural hematomas are usually
not deadly if treated.
Discussion of SDH
Subdural hematomas are divided into acute,
subacute, and chronic, depending on their speed of
onset. Acute SDH’s that are due to trauma are the
most lethal of all head injuries and have a high
mortality rate if they are not rapidly treated with
surgical decompression.
Discussion of SDH
Acute bleeds develop after high speed acceleration
or deceleration injuries and are increasingly severe
with larger hematomas.
Discussion of SDH
Acute Subdural bleeds have a high mortality rate,
higher even than epidural hematomas and diffuse
brain injuries. The mortality rate associated with
acute SDH is around 60-80%.
Discussion of SDH
Chronic subdural bleeds develop over a period of
days to weeks, often after minor head trauma,
though such a cause is not identifiable in 50% of
patients.
They may not be discovered until they present
clinically months or years after a head injury.
Discussion of SDH
The bleeding from a chronic bleed is slow, probably
from repeated minor bleeds, and usually stops by
itself.
Discussion of SDH
Small chronic subdural hematomas, (less than a
centimeter wide) have much better outcomes than
acute subdural bleeds. Chronic subdural
hematomas are common in the elderly.
Discussion of SDH
Symptoms of subdural hemorrhage have a slower
onset than those of epidural hemorrhages because
the lower pressure veins bleed more slowly than
arteries.
Discussion of SDH
Signs and symptoms may show up in minutes, if not
immediately but can be delayed 2 weeks.
If the bleeds are large enough to put pressure on the
brain, signs of increased ICP or damage to part of
the brain will be present.
Discussion of SDH
Other signs and symptoms of subdural hematoma
can include any combination of the following:
History of recent head injury
Loss of consciousness or fluctuating levels of
consciousness
Irritability
Seizures
Discussion of SDH
Pain
Numbness
Headache (either constant or fluctuating)
Dizziness
Disorientation
Amnesia
Weakness or lethargy
Discussion of SDH
Nausea or vomiting/Loss of appetite
Personality changes
Inability to speak or slurred speech
Ataxic Gait
Altered breathing patterns
Hearing loss or ringing
Blurred vision
Deviated gaze or Abnormal eye movements
Discussion of SDH
Subdural hematomas are most often caused by head
injury, when rapidly changing velocities within the
skull may stretch and tear small bridging veins.
Discussion of SDH
SDH’s due to head injury are described as traumatic.
They generally result from shearing injuries due to
various rotational or linear forces.
Discussion of SDH
SDH is a classic finding in shaken baby syndrome,
in which similar shearing forces classically cause
intra- and pre-retinal hemorrhages.
Discussion of SDH
SDH is also commonly seen in the elderly and in
alcoholics, who have evidence of cerebral atrophy.
Cerebral atrophy increases the length the bridging
veins have to traverse between the two meningeal
layers, increasing the likelihood of shearing forces
causing a tear.
Discussion of SDH
It is also more common in patients on Aspirin and
Coumadin. Patients on these medications can
have a SDH with a minor injury.
A further cause can be a reduction in CSF pressure
which can create a low pressure in the Dura and so
cause rupture of the blood vessels.
Discussion of SDH
Factors increasing the risk of a subdural hematoma
include very young or very old age.
As the brain shrinks with age, the subdural space
enlarges and the veins that traverse the space must
travel over a wider distance, making them more
vulnerable to tears.
Discussion of SDH
Infants have larger subdural spaces and are more
predisposed to subdural bleeds than are young
adults.
SDH is a common finding in shaken baby syndrome.
In Juveniles, an Arachnoid Cyst is a risk factor for
a subdural hematoma.
Discussion of SDH
Collected blood from the subdural bleed may draw
in water due to osmosis, causing it to expand,
which may compress brain tissue and cause new
bleeds by tearing other blood vessels.
Discussion of SDH
In some subdural bleeds, the Arachnoid Layer of the
meninges is torn, and CSF and blood both expand
in the intracranial space, increasing pressure.
Discussion of SDH
Substances that cause vasoconstriction may be
released from the collected material in a subdural
hematoma, causing further ischemia under the site
by restricting blood flow to the brain leading to
brain cell death.
Diagnosis of SDH
SDH’s occur most often around the tops and sides of
the frontal and parietal lobes. They also occur in
the posterior cranial fossa, and near the falx
cerebri and tentorium cerebelli.
Diagnosis of SDH
Unlike Epidural hematomas, which cannot expand
past the sutures of the skull, SDH’s can expand
along the inside of the skull, creating a concave
shape that follows the curve of the brain, stopping
only at the Dural reflections like the Tentorium
Cerebelli and Falx Cerebri.
Diagnosis of SDH
On a CT scan, SDH’s are classically crescentshaped, with a concave surface away from the
skull. However, they can have a convex
appearance, especially in the early stage of
bleeding.
Diagnosis of SDH
A more reliable indicator of a subdural bleed
is its involvement of a larger portion of the
cerebral hemisphere since it can cross
suture lines, unlike an Epidural bleed.
Diagnosis of SDH
Subdural blood can also be seen as a layering
density along the Tentorium Cerebelli.
This can be a chronic, stable process, since
the feeding system is low-pressure.
Diagnosis of SDH
In such cases, subtle signs of bleeding such as
effacement of sulci or medial displacement
of the gray matter and white matter junction
may be apparent.
Diagnosis of SDH
A chronic bleed can be the same density as brain
tissue (isodense to brain), potentially obscuring
the finding.
Treatment of SDH
A CT scan or MRI scan will usually detect
significant SDH’s.
Treatment of a SDH depends on its size and
rate of growth.
Treatment of SDH
Some small SDH’s can be managed by careful
monitoring until the body heals itself.
Other small SDH’s can be managed by inserting a
temporary small catheter through a hole drilled
through the skull and sucking out the hematoma.
This procedure can be done at the bedside.
Treatment of SDH
Large or symptomatic hematomas require a
craniotomy, the surgical opening of the skull.
A surgeon then opens the Dura, removes the blood
clot with suction or irrigation, and identifies and
controls sites of bleeding.
Treatment of SDH
Postoperative complications include increased
ICP, brain edema, new or recurrent
bleeding, infection, and seizure.
The injured vessels must be repaired.
Treatment of SDH
Dependent on the size and deterioration, age
of the patient and anaesthetic risk posed,
some Subdurals will be inoperable and
palliative management is the best treatment
option.