Case Review: Subarachnoid Hemorrhages · Epidural Hematoma Not here! Epidural Hematoma . Epidural...

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

The

classic

concave

view

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

Subfalcine

herniation

Significant

midline shift

and mass

effect

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

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


Evidence of

vasospasm


Narrow R

MCA -

vasospasm

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?

Case Review: Subarachnoid Hemorrhages · Epidural Hematoma Not here! Epidural Hematoma . Epidural...

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