Post on 08-Apr-2019
Case Review: Subarachnoid
Hemorrhages Franklin Marquez, CCPA
Department of Neurosurgery
Kingston Health Science Center
Atlantic Vice President
1. DISCRIMINATE THE DIFFERENCES
BETWEEN INTRACRANIAL HEMORRHAGES
(COGNITIVE LEVEL 4)
2. DISTINGUISH THE PREDICTIVE VALUE OF
THE GCS WHEN MANAGING A SAH
(COGNITIVE LEVEL 4)
3. DIFFERENTIATE THE BEST DIAGNOSTIC
TOOLS AND TREATMENT MODELS FOR
SAH (COGNITIVE LEVEL 4)
Here’s Today’s Discussion
LET’S START THE CASE
Mechanism of Injury
• 35yo female presents three days after a concert
• Acute severe headache with nausea and vomiting – waking from sleep
• Left facial droop, dysarthria and left sided weakness
• Presented to the emergency department for imaging
CT Head
Aneurysm
Subarachnoid
Hemorrhage A. comm ACA
MCA
PCA
P. comm
Intraparacheymal
Hemorrhage
Ruptured
Aneurysm
L
MCA
R
MCA
ANATOMY REVIEW
It’s all mater of fact!
HOW TO TELL THE DIFFERENCE
BETWEEN BRAIN BLEEDS
Epidural Hematomas
• Tear of the outer most
internal lining of the
brain
• Trauma related due to
a shear effect
• MVC/collision,
damage during fall,
physical abuse
• LOC, headache,
nausea, vomiting, one
sided eye blindness,
seizures, hemiparesis
Epidural Hematoma
Not
here!
Epidural
Hematoma
Epidural Hematoma
Epidural Hematoma
Epidural Hematoma
Epidural Hematoma
The
classic
concave
view
Epidural Hematoma
Epidural Hematoma
Epidural Hematoma
Epidural Hematoma
Epidural Hematoma
Epidural Hematoma
Epidural Hematoma
Epidural Hematoma
Epidural Hematoma
Epidural Hematoma
Epidural Hematoma
Subdural Hematomas
• Acute (young) vs
Chronic (old)
• Acute are from trauma,
fall or blow to the head
• Chronic are from mild
head injuries or
repetitive falls +/-
anticoagulation
• Possibility of an acute
on chronic!
• LOC, dysarthia,
seizures, headaches,
hemiparalysis,
weakness, parathesia
Subdural Hematoma
Out with
the old
aka
chronic!
Subdural Hematoma
In with the
new aka
acute
Subdural Hematoma
Subdural Hematoma
Subdural Hematoma
Subfalcine
herniation
Significant
midline shift
and mass
effect
Subdural Hematoma
Subdural Hematoma
Double down and venture a guess
what this is??
Tension
pneumocephalus
Intracerebral Hemorrhage
• Sudden burst of blood vessel in brain tissue
• Associated with HTN, AVM, recreational drug use, tumours, anticoagulants, hematology disorder
• Acute symptoms – H/A, hemiparalysis, LOC, dysarthia, LOV, dysphagia, aphasia, ataxia, seizure
• Long-term complications depending on ischemia and severity
Intracerebral Hematoma
Subarachnoid
Hemorrhage
Intracerebral
Hematoma
Intracerebral Hematoma
Intracerebral Hematoma
Intracerebral Hematoma
Intracerebral Hematoma
Intracerebral Hematoma
Intracerebral Hematoma
Intracerebral Hematoma
Just a gorgeous view of the ICH
and SAH working together as one
• Blood in the
arachnoid space –
between the pia
mater and arachnoid
membrane
• Post traumatic or
spontaneous
• Aneurysmal ruptures
most common
spontaneous
Subarachnoid Hemorrhage
Outcome by the Numbers for
Aneurysmal SAH
• 10-15% mortality before reaching medical care
• 10% mortality within first few days
• 25% mortality from medical complication
• 8% mortality from progressive deterioration
• 15-20% mortality in first weeks from re-bleeding
• ~66% successful clipping not returning to normal QOL – 8-20% require living assistance
– ~30% moderate-severe morbidity
– 7% mortality from vasospasm
– 7% severe morbidity from vasospasm
Incidence and Eitology
• Female > Male (1.24)
• African Amercians
and Hispanics >
Caucasians
• Avg age >50y/o
• Japan and Finland >
North America >
South and Central
America
Incidence and Eitology
• Trauma is public enemy number one!
• “Spontaneous” SAH – Rupture at 75-80%
– AVM 4-5%
– Vasculitis
– Cerebral artery dissection
– Superficial vessel
– Rupture infundibulum
– Coagulation disorder
– Rarely by tumour
Risk Factors Associated with
SAH
• Behavioural
• Certain gender and
race
• History of cerebral
aneurysm
• Family history of
aneurysm
• Genetic disorder
Clinical Features
• Headache with emesis
• Syncope (apoplexy)
• Neck pain (meningismus)
• Photophobia
• LOC with subsequent regain or coma
• CN III palsy – ptosis and diplopia
• Lower back pain
• Hypertension
• Ocular Hemorrhage
What’s in a headache??
• “Worst H/A of my life”
• Paroxysmal
• Blood on CT and LP
• Warning H/A
– May represent a small
hemorrhage
– May be aneurysmal
enlargement
– Sudden onset, milder
and lasts a few days
What could a severe, acute and
paroxysmal headache be??
• The obvious – SAH
• Benign Thunderclap
Headache or Crash
Migraine
• Reversible Cerebral
Vasoconstrictive
Syndrome
• Benign Orgasmic
Cephalgia
The Work-Up
• Start with a non-
contrast CT Head
• If negative, head on
to the Lumbar
Puncture
• Consider a CTA for
aneurysm location
• Of course don’t forget
your standard
bloodwork
Lumbar Puncture
• Although a bit difficult,
can be a great
adjunct
• Measure opening
pressure
• Appearance
• Cell Count
• Protein
• Glucose
Management
• Assess the CABCDE of the patient!!
• Call neurosurgery!
• Seriously? What is this guy talking about?? Just call neurosurgery! We all think we can MacGyver ourselves out of situations, but this one may be a little dicey to wing it – who wants to just toss a tube in a brain or decompress with a craniotomy? Yes, neurosurgery does!
• The Triple H’s! – Hypertension, hypervolemia and hemodilution
Admission Orders!
• Admit to the ICU
• Neurovitals q1h for 4h then q4h
• Elevate head to 30deg and bathroom privileges only
• Foley catheter
• Strict I&O’s
• NPO
• IV Fluids – N/S in 20mEq KCL at 2ml/h/kg (~150cc/h)
• TED’s stockings
I can tolerate that one that sounds
like di la la… otherwise I’m allergic
• Prophylactic anti-epileptic drugs
• Avoid sedation
• Analgesics – fentanyl over morphine (ICP depressant); studies showing NO bleeding risk with Toradol!
• Dexamethasone
• Ondansetron – doesn’t lower seizure threshold
• Nimodipine (CCB)
• Labetolol, hydralazine, captopril
Importance of Hyponatremia and
Hypovolemia
• Natriuresis and diuresis common cause at 10-30% post SAH
• Transient raise in ADH
• Rise in ANP (28-amino acid polypeptide; atrial natriuretic factor)
• Cerebral salt wasting is another cause
Cerebral Salt
Wasting
SIADH Diabetes
Insipidus
Volume Status Hypovolemia Euvolemia/Hypervolemia Hypovolemia
Serum Sodium
Con.
Decreased Decreased Increased
Urine Sodium
Con.
Increased Increased Decreased
Urine Output Increased Normal Increased
Mechanism Excessive secretion
of sodium and
water
Water retention from
increased ADH secretion
Free water loss
from decreased
ADH
Post-operative SAH Aneurysm
Size matters for…vasospasm!
Size
matters… Smaller
diameter
Post-operative SAH Aneurysm
Evidence of
vasospasm
Post-operative SAH Aneurysm
Post-operative SAH Aneurysm
Post-operative SAH Aneurysm
Post-operative SAH Aneurysm
Post-operative SAH Aneurysm
Narrow R
MCA -
vasospasm
Post-operative SAH Aneurysm
Post-operative SAH Aneurysm
HOW DOES GCS DETERMINE
MORBIDITY AND MORTALITY?
Prediction Outcomes
• Many different
prediction scales
• GCS, GOS, WFNS
and Hunt and Hess
Scale
• Timing of
assessment, age,
ICP, CT, clinical
presentation and
motor function highest
predictions
Prediction Outcomes
• Multiple studies suggest age of 50 to be a critical determinant
• Better outcome < 50y/o > Worse outcome
• CT data were codependent factors that independently did not predict outcome
Prediction Outcomes - GCS
• The motor function plays the biggest determinant
• Pupillary response – bilateral, unilateral, abnormal bilateral helps yield prognostic accuracy
• All of which contribute to the Hunt and Hess and WFNS scales
The Prediction Tree
Pupillary Response
Age
Motor Response
G/MD/S
3
G/MD
1
Age
Intracerebral Lesion
G/MD
2
S/V/D
5
D
7
Motor Response
S/V/D
8 Age
G/MD/S
4
D
6
Bilaterally Normal Unilaterally or Bilaterally Absent
<26 >26
<3 >3
>3 <3
>33 <33
<61 >61
Absent Present
G = good recovery
MD = moderately
disabled
S = severely disabled
V = vegetative
D = dead
Clinical Grading Scales Grade Botterell Hunt and Hess WFNS
1 Conscious with or without signs
of blood in the subarachnoid
space
Asymptomatic or minimal
H/A and slight nuchal
rigidity
GCS 15, no
motor deficit
2 Drowsy without significant neuro
deficit
Moderate-to-severe H/A
nuchal rigidity, no neuro
deficit other than cranial
nerve palsy
GCS 13-14,
no motor
deficit
3 Drowsy with neuro deficit and
probably intracerebral clot
Drowsy, confusion, or mild
focal deficit
GCS 13-14,
motor deficit
4 Major neuro deficit, deteriorating
because of large intracerebral
clots or older patients with less
severe neuro deficit but pre-
existing CVD
Stupor, moderate to severe
hemiparesis, possibly early
decerebrate rigidity and
vegetative disturbances
GCS 7-12,
+/- motor
deficit
5 Moribund or near moribund with
failing vital centers and extensor
rigidity
Deep coma, decerebrate
rigidity, moribund
appearance
GCS 3-6,
+/- motor
deficit
THE OTTAWA SAH GUIDELINE
Ottawa SAH Guidelines
MANY THANKS FOR YOUR
PARTICIPATION!
QUESTIONS?