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Diagnosis of Subarachnoid Hemorrhage: Avoiding Pitfalls and Expediting Assessment

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Title: Diagnosis of Subarachnoid Hemorrhage: Avoiding Pitfalls and Expediting Assessment


1
Diagnosis of Subarachnoid Hemorrhage Avoiding
Pitfalls and Expediting Assessment
2
Cannot Miss Diagnosis Presenting as a
Headache Bacterial meningitis. Subarachnoid
hemorrhage. Space-occupying lesion. Brain
lesion. Brain abscess. SDH and EDH.
Hypertensive encephalopathy. Acute narrow angle
glaucoma. Cerebral venous and dural sinus
thrombosis. Carbon monoxide poisoning. Stroke. Bac
terial sinusitis.
3
Clinical Anatomy and Epidemiology ---SAH is
defined as extravasation of blood into the
subarachnoid space of the CNS. . ---Excluding
head trauma, ruptured intracerebral aneurysm
accounts for about 80 of cases of SAH. ---Other
causes include mycotic aneurysms,AVM, dissection
of intracranial arteries and idiopathic cases.
4
---Most of these aneurysms arise from arterie at
the base of the brain, located in the circle of
Willis and its branches. ---85 of aneuryms are
derived from the ant. Circulation. Most often at
its sites of vessel bifurcation. Its include the
junction of the ICA and PCoA, the anterior
cerebral-ACoA complex, the bifurcation of the
MCA. ---Aneurysms arising from the posterior
circulation are most likely to occur at the
bifurcation of the basilar artery and the
junction of the basilar artery and
posterio-inferior cerebral vessels. ---25 of
patients will have multiple aneurysms usually
2-3. ---Cerebral aneurysms from in areas that are
deficient in medial layer and where the internal
elastic lamina is thin or absent.
5
---In the US , the annual incidence of SAH is
about 30000, or roughly 10 cases per 100,000
population. ---In Japan, the rate is about three
times that number. ---The SAH can occur at any
age, but it is rare in children and the mean age
about 50 years.. ---FM32. ---Below age 40, men
are more often afflicted than women. ---A number
of underlying disease are associated with an
increased risk of aneurysm formation, including
autosomal dominant polycystic kidney,
neurofiromatosis(type l ),Marfans syndrome,
fibromuscular dysplasia. Users of
cocaine. ---Aneurysm rupture risk factor include
smoking, alcoholic use, hypertension.
6
Natural History of Intracranial Aneurysms In
series landmark study of 111 patients who had 132
unruptured aneurysms, patients were divided into
three groups Group1presented with acute
symptoms---acute headache, seizures and cranial
neuropathy. Group2presented with chronic (gt2
weeks in duration)symptoms---headache, visual
symptoms, long-tract dysfunction and facial
pain. Group3were asymptomatic and had been
diagnosed or during the course of being treated
for an aneurysm that had rupture.
7
Groups 1 and 2 had larger aneurysms(mean diameter
2.1cm)than did the asymptomatic patients in
group3(mean diameter about 1.1cm). As a rule,
aneurysms that present with findings suggestive
of a mass effect are generally larger and carry a
higher risk of rupture(estimated at 6 per
year) Aggressive surgical treatment of unruptured
aneurysm is indicated, especially those that are
greater than 2.5 diameter.
8
Rupture Aneurysm Once an aneurysm ruptures
patients may present with a wide range of signs
and symptoms---Abrupt onset of the worst headache
of life, transient loss of consciousness with or
without nausea and vomiting, and new neurologic
deficits. Physical examination may yield a number
of associated findings such as acute hypertension
and low grade fever, level of consciousness(LOC)
may be diminished. The present of ocular
hemorrhage( sub-hyaloid bleeding) is an important
clue. The two most widely improved classification
systems are the Hunt and Hess(HH) and the World
Federation of Neurologic Surgeons
classifications.(Based on the GCS)
9
Classification Systems for Subarachnoid
Hemorrhage(HH) Grade 0 Unruptured
aneurysm. Grade 1 Asymptomatic or mild
headache. Grade 2 Moderate-severe headache,
nuchal rigidity, cranial
nerve deficits. Grade 3 Confusion. Lethargy,
mild focal symptoms. Grade 4 Stupor,
Hemiparesis. Grade 5 Comatose.
10
World federation of neurologic surgeons Grade
GCS Motor deficits
1 15
absent 2 13-14
absent 3 13-14
absent 4
7-12 present or absent 5
3-6 present or
absent
11
Mayer hypothesis---Retrospectively examined 217
patients with symptomatic cerebral
aneurysms. Conclusion1.25 of patients were
initially misdiagnosed by a physician.
2.Misdiagnosed patient were more likely
to be of lower grade(38 of patients with a
modified H H grade 1 and 2 were
misdiagnosed). Another study showed 41 of
181(23) patient were misdiagnosis( nearly
identical to that in Mayers study)
12
The pitfalls fall into three major categories 1.
Failure to consider the diagnosis of SAH. 2.
Failure to understand the limitations of a CT
scan. 3. Failure to understand the limitations of
Lumbar puncture(LP).
13
Failure to consider diagnosis Warning
bleed----1958 by a Scottish neurosurgeon, F. John
Gillingham. ----Occur in 20-60 0f patients
with SAH a mean of 14 days before the major
bleed.(Retrospective reviews of hospitalized
patients with SAH) Warning leak ----A mere leak
of blood from the sac.
----A neurologic examination performed at the
time is usually normal. Warning
headache---represent bleeding into the wall of
the aneurysm this would not account for the
bloody CSF. Thunderclap headache---abrupt,very
intense headache,new.
---leak of blood from the sac.
---LP have bloody GSF.
14
Pitfalls in the Diagnosis of Subarachnoid
Hemorrhage Failure to consider the diagnosis of
SAH A, Over-reliance on the classic
presentation B, Lack of appreciation of the
warning bleed C, Atypical presentation neck pain,
flu-like illness, menigitis, coma, mild
symptoms D, Focus on head trauma resulting from
the SAH E, Focus on the EKG abnormality or the
hypertension F,Failure to realized that the
headache of SAH can improve spontaneous or with
OTC analgesic G,Lack of knowledge of exception to
the rule of the pupil regarding 3rd nerve palsy.
15
Why is this diagnosis missed 1.Over-reliance on
the classic teaching.---the leak occurs at the
stress or Valsalva(43 of patients), 12 of
patient, the hemorrhage occurred during sleep and
rest.Moreover, some patients did not have abrupt
onset of symptoms. 2, Symptom complexes---One
common presentation is primary neck pain.( the
erroneous diagnosis of neck arthritis or muscle
pain).neck stiffness(the erroneous diagnosis of
menigitis.). 3.Head injury---results from a fall
or injury secondary to the transient syncopal
episode sometimes associated with SAH.
16
4.EKG abnormalities.---SAH range from T-wave
flattening,and inversion to prolonged QT
interval, to brady-and-tachyarrhythmia.
---An EKG pattern
simulating acute MI has also been reported.(These
changes may be related to subendocardial
ischemia)
---The vast majority of patients with SAH have
headache, a symptom that is uncommon in acute MI,
unless it is accompanied by administration of
nitrates. 5.Hypertension, which frequently
accompanies SAH, also can confuse the physicians.
17
Limitation of CT Advantage non-invasive,
relatively inexpensive, readily available, and
high sensitivity in the first 24 hrs.other
important information and identify other
diagnostics such as intraventricular or
intracerebral hemorrhage and SDH. ---The pattern
of blood identified on CT scan can sometimes
predict the bleeding sites(frontal
bleeding---suggests ACA or ACoA. Sylvian
fissure---suggests MCA. ---Sensitivity with CT is
high during the first hours of SAH( Two study
showed 98 and 100 sensitivity in first 12 hours.
18
---If more than first 24 hours the sensitivity
drops to 93-95. ---SAH is detected in about 90
of patients after one day. 58-80 after five
days.roughly 50 after seven days. ---The
important factors affecting sensitivity of CT
for detection of SAH are density and
quantity.(Hgblt10g/dL may not show up on CT
caning, small amount of blood can be
missed.) ---Technical factor(may false negative
if too thick cut 10mm. ---If the pre-test
probability is low, and the CT scan has been done
during the first 12 hours, if it is negative,
them the likelihood of SAH approaches
zero. ---MRI is not as sensitive in diagnosis of
acute SAH.
19
Limitations of the Lumbar Puncture(LP) ---The
major patients with suspected SAH whose CT scans
are negative should undergo LP. ---Failure to do
an LP( if CT is negative) in patients with high
pretest likelihood. ---Failure to realize that
visual inspection for xanthochromia is
insensitive.
20
Xanthochromia can differential trauma blood or
SAH blood in CSF. -----there are two ways of
detecting xanthochromia 1.visual
inspection of the CSF with the naked eye( only
50 of specimens that are positive)
2.Spectrophotometry -----If Xanthochromia is
present visually,SAH is strongly
suggested. -----If it is negative by
spectrophotometry and the fluid was obtained
between 12 hours and two weeks after the onset of
headache , this suggested a traumatic LP rather
than SAH.
21
Emergency Department care of the patient with SAH
should be focused on prevention or treatment of
major complications ---Rebleeding---The risk of
early rebleeding is high(apprpximately 4 during
the first day and 1-2 within the next two
weeks.) ---vasospasm. ---seizure. ---obstructive
hydrocephalus.
22
----Severe hypertension should be treated with
drugs such as labetalol or hydralazine. ----Seizur
es occur in 10-25 of cases, phenytoin 17mg/Kg
should be administered. ----Anxiety and Irritable
patients can be treated with small doses of
short-acting benzodiazepines. ----Acute
obstructive hydrocephalus can be seen within the
frist 24 hrs and is manifested by level of
consciousness, stupor, and comas. Diagnosis is by
C-T and emergency ventriculostomy is indicated
for drainage. ----On N-G tube within the first 12
hrs should be treated with Nimodipine 60mg.( for
prevention of vasospasm)
23
----Vasospasm is a serious and common
complication of SAH ----Treated vasospasm
including 1.calcium channel blockers.
2.homodynamic therapy---increased blood pressure
and intravascular volume. 3.percutaneous
transluminal angioplasty. 4.Tissue
plasminogen activator. (3 and 4 these
therapies province of the neurointensivist)
24
---Patients with SAH should not be run dry
(dehydration), should not be fluid restricted
but should be given isotoni or slightly
hypertonic saline. ---Triple-H therapy 1.hyperten
sion--- 2.hypervolemia--- 3.hemodilution---
25
After the patient is stabilized. Four-vessel
angiography is performed by the meuroradiogist to
ascertain the cause of the bleed and location of
aneurysm. Visualization of all four cerebral
arteries is important, even in those cases where
the CT shows the likely source of bleeding,
because of the frequency of multiple aneurysms.
26
  • Timing of Surgery
  • Early surgery---H H grade 1-3 undergo early
    surgery. ---The benefits of
    early surgery are reduced risk of rebleeding,
    opportunity to clear blood from the subarachnoid
    space, ability to aggressively treat vasospasm
    with triple H and other therapies.
  • ---there was no difference in mortality
    outcome.
  • The timing of surgery for H H grade 4 and 5 is
    less clear and the result in these patients are
    not very encouraging.
  • Some advocate using the endovascularly placed
    coil to obliterated the aneurysm at the time of
    initial angiography and then to consider surgical
    therapy if patient improved.

27
  • Conclusion
  • Early diagnosis--- essential in order to improved
    morbidity and mortality in SAH.
  • ---very detailed the
    history taking and physical examination.
  • 2. Prompt diagnosis---Keep SAH in mind.
  • 3 Precise diagnosis---Avoiding pitfalls.
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