Unformatted text preview: Grand Rounds
Avi Schiowitz, D.O.
4/24/07 Case Presentation
Pt is a 37 y/o female who
presented to the ED on 2/17/07
with a complaint of a constant
pressure like headache which had
lasted for the last 2 weeks. The
headaches awoke her from sleep.
headaches History of Present Illness
Onset was 2/4/2007. At first got better with OTC medication,
now is constant.
now Pt describes headaches as a tight feeling
bifrontal, extending posterior, left side
hurts more than right.
hurts Exacerbated by light and in the sitting,
standing Relieved somewhat by lying flat. HPI cont.
Complains of new onset nausea and vomiting.
vomiting. Patient felt lightheaded for last few days,
“nearly walking into walls”.
“nearly Unable to perform daily activities or go to
work. Pt was seen in OSH – SWGH twice during
last 2 weeks for same condition. Allergies: Latex PMHx: denies PSHx: C/S twice under spinal.
PSHx: Social Hx: Non-smoker, social drinker,
denies drug use Takes no medications. In the ED
Physical exam: BP 144/81, HR 77, T 96.8, RR 14, 99% RA
Gen: Pt lying on cot, cloth covering her face.
Slow to move but is A & O x 3. Winced to light
being turned on, but no photophobia to
Neuro: CN’s normal and intact. 5/5 strength and
motor in UE/LE. Movement is slightly slow but
not Rest of physical exam normal. Hospital Course
IV started. 1 liter NS bolus given, second
liter CBC, BMP and urine Hcg ordered. CT Head without contrast and CT angio of
head Pt given pain meds with slight
Pt admitted to 9C Diagnosis of Headache, Pain control and
dehydration. Neurology consult requested. Differential diagnosis of Acute
Headache. Migraine Tension HA Cluster HA Stroke Subarachnoid
Hemorrhage Cerebral Infarction Arterial
Arterial Dissection –
Carotid or Vertebral
Carotid Acute Hydrocephalus Meningitis Encephalitis Giant Cell Arteritis Tumor Trauma Neurology consult
Neurology Pt seen by neurologist next day. History consistent with that given in ED. No visual disturbances No tinnitus or diplopia. No history of trauma. Neurology Exam
Neurology ROS negative Physical Exam WNL Neurologic Exam:
A & O x 3 , CN intact
Motor, sensation, coordination – WNL
Reflexes 2+ & symmetric
Gait normal, no romberg. Imaging
CT of head – slit like ventricles and low
lying cerebellar tonsils. Findings could be
either due to pseudotumor cerebri with
coexistent Chiari I malformation or CSF
CT Angio of brain – Negative except for
somewhat prominent venous structures
supplying the transverse sinuses
bilaterally. Findings could be manifestation
of CSF hypotension syndrome. Although
given the plain CT results pseudotumor
cerbri also warrants consideration. Most
significantly, no evidence of dural sinus
thrombosis. Pseudotumor cerebri
Pseudotumor AKA Benign Intracranial hypertension Defined as a syndrome of elevated ICP without
evidence of hydrocephalus, focal lesions or frank
brain Usually occurs in obese women between ages
15-45. Symptoms include HA, visual disturbances, or
diplopia secondary to abducens nerve palsies.
diplopia Fundoscopic exam shows papilledema. Pseudotumor cerebri
Pseudotumor Usually a benign and self limiting disorder. Condition associated with drugs such as
Vit A intoxication, Danazol, Accutane,
Tetracyclines, oral contraceptives and
corticosteroid Systemic disorders include
hypoparathyroidism, CT of head can show small ventricles Treatment includes carbonic anhydrase
inhibitors – reduce CSF production.
Corticosteroids, Weight loss. Correct underlying systemic disorder. In the most severe cases
Ventriculoperitoneal shunt can be done.
Radiology Impression: Orthostatic HA
suspect spontaneous low CSF pressure
HA. Neurology Recommendation: Trial of
caffeine 500mg IV. If no relief in 1 hour
give 2nd dose. If no relief in AM will do MRI
MRI of head done – Results show inferior
displacement of the brainstem and
cerebellum towards the foramen magnum
with diffuse dural venous enhancement.
Findings most consistant with intracranial
hypotension. Neurology recommends epidural blood
patch and Anesthesia was consulted.
Acute pain service saw the patient and
recommended conservative treatment at
this Abdominal binder, caffeine, fluids and
percocet for pain.
percocet Patient was referred to Chronic pain for
followup. Patient was discharged on 2/20/07. Instructed to follow with chronic pain and
neurology as outpatient.
neurology Told to come to ED if symptoms do not
improve. What is Intracranial Hypotension?
Escape of fluid that normally surrounds
the brain and spinal cord.
the Usually characterized by an orthostatic
headache – one that worsens with sitting
or Headache can be chronic or patient can
present without headache.
present Location of headache varies between
patients. Headaches in intracranial
hypotension Orthostatic Acute
onset of orthostatic Cervical or
interscapular pain that Second half of day
HA Lingering non Paradoxic orthostatic
HA Exertional HA wihout No HA
orthostatic Cause of Headache
Cause CSF supports the brain. Brain weight of 1500gr in air weighs only 48gr in
the Remaining weight supported by pain sensitive
structures. Meninges, cerebral and cerebellar
veins, CN V, VII, IX and X, upper 3 cervical
nerves. CSF decreases – decrease in buoyancy causing
traction on these structures.
traction In the upright position the downward
displacement is exagerated.
Evidence of this theory is supported first by
study data documenting downward displacement
of cranial structures.
of Evidence in support of this theory comes from
data collected by Kunkle, et al who induced
postural HA in healthy volunteers by draining
CSF. One of his subject had undergone a
section of the roots of CN V and IX and upper 4
cervical roots on L side with analgesia in the
regions to which these nerves project. This pt
experienced HA only on right side.
Another theory proposes the dilitation of
the intracranial vascular structures causes
the headaches. This is based on the
Monroe-Kellie hypothesis which states
that the sum of the volumes of intracranial
blood, CSF and brain tissue must remain
constant in an intact cranium. According to
this hypothesis a loss of CSF will cause an
increase in intracranial blood volume.
Most compensation occurs via venous
dilitation due to greater compliance and
capacitance. Venous sinus engorgement,
pachymeningeal enhancement, subdural
effusions and enlargement of pituitary
gland may represent compensatory
changes to maintain intracranial volume.
changes Pain is exacerbated by:
Jugular Venous Compression
Analgesics have minimal effect and pain is
usually relieved with lying flat. Other Symptoms:
Other Nausea Vomiting Anorexia Neck pain Dizzyness Diplopia Photophobia Changes in hearing Unsteadiness
staggering gait Facial numbness or
weakness Transient visual
obscuration Upper limb radicular
symptoms Rare symptoms
Rare Galactorrhea Stupor Ataxia Parkinsonism Coma Result
Result of compression of pituitary stalk,
diencephalon, posterior fossa, and midline
structures. Etiology of CSF volume depletion
Etiology True Hypovolemic state – reduced total body water
CSF shunt overdrainage
After definite trauma
Spinal tap or epidural
Spinal or cranial surgery
Unknown cause – most common
weakness of the dural sac – ex. Meningeal
diverticula or connective tissue abnormalities
This patient was diagnosed with
spontaneous CSF hypotension. Syndrome recognized for more than 55
years First proposed by Schaltenbrand in 1938
and described as a headache syndrome
virtually identical to one following an LP.
virtually Proposed the following mechanisms:
1. Decreased CSF production
2. Increased CSF absorption
3. CSF Leakage through small tears
Today the accepted etiology is of CSF
Most occur at the cervicothoracic junction
and thoracic levels.
Can be attributed to minor trauma such as
fall, sneezing, sudden twist or stretch.
fall, Can cause rupture of preexisting spinal
epidural cysts or tarlov cysts or tear in
dural nerve sheath.
CSF analysis – opening pressure can be low –
around Dry taps are encountered Rare instances the was negative pressure –
sucking noise as stylet is removed.
sucking CSF is typically clear. Protein concentration
normal or high. WBC count can be normal or
high. Cytology and microbiology are always normal Glucose concentration is never low. CT
CT of head is of limited value. It might
show subdural fluid collections. Used more
to rule out other causes.
to MRI will show diffuse pachymeningeal
enhancement following the administration
of gondolinium. This is the most
characteristic feature of this syndrome.
characteristic MRI findings in SIH
MRI Diffuse pachymeningeal enhancement. Descent of brain – Cerebellar tonsils, obliteration
of some subarachnoid cisterns, crowding of
post. Enlargement of pituitary Flattening or tenting of optic chiasm Subdural fluid collections Engorged cerebral venous sinuses Decreased size of ventricles In
In the spine – extra arachnoid fluid
collections Meningeal diverticula ID of level of leak ID of actual leak site – rare Engorgement of epidural veins Spinal pachymeningeal enhancement CT Myelogram – used to demonstrate CSF leaks and is
the study of choice to find its location.
Radioisotope cisternography – Uses indium-111.
introduced intrathecally and its movement is followed by
sequential scanning at certain time intervals.
Normally by 24 hours radioactivity can be detected over
the cerebral convexities.
If there is a CSF leak there will be minimal activity.
Early accumulation will be detected in the kidneys and
bladder Treatment of CSF leaks
Treatment HA usually resolve with conservative treatment within 212 days.
Bed rest – supine position reduces CSF pressure at leak
site and promote meningeal healing.
Fluids – increases CSF volume by fluid restoration.
Caffeine – Thought to produce arterial vasoconstriction
through blockade of adenosine receptors. Intracranial
blood flow venous engorgement are decreased.
Steroids – effort to restore CSF volume. No evidence
indicates that steroids have any effect on CSF
Production or absorption.
Abdominal binder Treatment
Treatment Other treatment options include: Epidural Blood Patch Continuous epidural saline infusion Epidural infusion of dextran Epidural injection of fibrin glue Intrathecal fluid injection Surgical correction Epidural blood patch
According to Mokri, epidural blood patch
is the treatment of choice in individuals
who have failed conservative therapy. Technique introduced by Gormley who
observed that the incidence of ICH
following a lumbar puncture is less in
individuals when the LP is traumatic and
Study by Mokri, Sencakova, and
McClelland identified 54 patients with SIH. 29 patients received EBP 4 Patients were eliminated. Followup was obtained via review of
records, correspondence and phone calls.
records, Ages ranged for 18 to 62. 20 women 5
All patients received EBP using 10 -20ml
of First EBP 9 out of 25 improved. 15 who failed first EBP underwent 2nd. 5 reponded well. Of the 10 remaining, 2 were treated
surgically. Remainder underwent a 3rd
EBP 4 responded well. 4 other underwent
This technique involves injecting blood into the
epidural Pt experiences immediate relief due to volume
replacement. In spontaneous CSF leaks patients usually
require more than one blood patch.
require Procedure is most effective is done at level of
leak. If level unknown – blood can be injected into
lumbar space and pt head can be lowered to
allow the blood to ascend. Data indicates that
this might be effective over 9 spinal segments
Most common complication is back
discomfort at injection site – 30%
discomfort Paresthesia Radiculopathy Chemical meningitis Pt
Pt arrives back in ED on 2/28/07 with
worsening of HA.
worsening Pt is actively vomiting. HA is continuous
and getting worse.
and Pt was compliant with abdominal binder,
caffeine, fluids. Pain meds give mild relief. Pt admitted to 9C. Neurology and
Anesthesia Acute Pain Service went to
evaluate pt. on 9C.
evaluate Risks and Benefits of epidural blood patch
discussed at length. All question were
asked and answered.
asked Pt wanted to try a trial of steroids prior to
epidural blood patch.
On 3/2/07 pt was brought to OR for epidural
blood patch under fluoroscopy.
blood Epidural space was identified and 3cc of blood
was injected. Pt states that she has immediate resolution of
symptoms. Post op – pt sitting in bed. Denies HA, denies
N/V. Pt discharged home. Follow with neurology and
chronic pain as needed.
chronic 3/9/07 pt calls MHMC complaining of HA. Pain no longer occipital. Only bifrontal
L>R. Has nausea and vomiting. Sees neurology and a 2nd epidural blood
patch is recommended. Pt started on
steroids – 8mg Decadron for 5 days.
Repeat CT of head shows cerebellar
tonsils inferiorly displaced within the
foramen magnum. 4th ventricle appears
small. Findings consistent with intracranial
hypotension. Chronic pain was consulted by neurology. Recommendations by chronic pain were to start
cafergot TID, abdominal binder, phenergan for
nausea. Will do epidural blood patch – 15ml of blood. If no response, CT myelogram to evaluate were
CSF leakage is. Rupture of Tarlov cyst.
CSF F/U one week after procedure. Epidural
Epidural blood patch done on 3/19/07. 15ml blood injected in epidural space. Resolution of symptoms. Pt followed up on April 3 with chronic pain. Pts symptoms have improved. Still has a mild
HA but is functional.
HA No further treatment needed at this time. If HA returns – pt to undergo CT myelogram. ...
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- Fall '11
- Anatomy, Intracranial pressure, Cerebrospinal fluid, Headaches, CSF, Cerebral venous sinus thrombosis, epidural blood patch