NSS SGD Ontok.Rodriguez.Salongcay.Samson.Bautista Case Presentation

NSS SGDOntok.Rodriguez.Salongcay.Samson.Bau

tista

Case Presentation

General DataT.A. 43 year old femaleLagunaRight-handedMarriedRoman CatholicBeautician in BruneiDate of admission: October 6, 2009On her 8th hospital day

Source of HistoryInformant: patientReliability: good

Chief Complaint

Headache

History of Present IllnessPatient is apparently well, with no known co-

morbidity.

2 months PTA, while cleaning the toilet(+) Headache – VAS 10/10, sudden onset, fronto-

parietal area, throbbing, non-radiating(+) Weakness and numbness – both lower

extremities(+) Loss of consciousness – lasted for 3 days

allegedly(+) Diaphoresis(-) Nausea / Vomiting

History of Present Illnessadmitted at local hospital in BruneiBlood pressure was 160 / 100 mmHgCT scan - subarachnoid hemorrhage

- Right PCOM aneurysm, infundibular type

Nimodipine 60 mg x 21 days, other meds unrecalled

History of Present Illnessadvised surgery for clipping of aneurysm -

deferredPreferred to be further treated in the

PhilippinesPatient allegedly discharged with normal

neurologic findingsPatient admitted at PGH for further

management

Review of Systems(-) fever, weight loss, anorexia(-) dyspnea, cough, colds(-) palpitations, chest pain, easy fatigability(-) abdominal pain, mass, tenderness,

bowel movement changes(-) dysuria, hematuria, tea-colored urine(-) muscle or joint pain, tenderness,

swelling

Past Medical History(-) Diabetes mellitus(-) Tuberculosis(-) Cardiovascular disease(-) Bronchial asthma(-) Allergy to food or medication(-) Connective tissue disease(-) Substance abuse(-) Previous surgical operations or

hospitalizations

Family History(-) similar illness(+) Hypertension – mother(+) Stroke – uncle, maternal side(-) Diabetes mellitus(-) Tuberculosis(-) Cardiovascular disease(-) Bronchial asthma(-) Allergy to food or medication(-) Connective tissue disease(-) Substance abuse

Personal and Social History Vocational course graduateWorks as a beautician in BruneiMarried with 2 childrenDenies use of cigarette, alcoholic beverage,

or illicit drugsEats fatty, salty, and sweet foods regularlyNo regular physical exercise

Physical Examination General Survey: Patient is awake, coherent, ambulatory

and not in cardiorespiratory distressVital Signs: BP 130/90 mmHg HR 90 beats/min RR 20

breaths/min T 37.3˚C Head, Eyes, Ears, Nose, Throat: Pink palpebral

conjunctivae, anicteric sclerae, (-) anterior neck mass, (-) cervical lymphadenopathy, (-) neck vein engorgement, (-) bruits

Chest/Lungs: Equal chest expansion, clear breath sounds, (-) rales, (-) crackles, (-) wheezes

Cardiovascular: Adynamic precordium, distinct heart sounds, normal rate, regular rhythm, (-) murmurs

Abdomen: Flat, normoactive bowel sounds, soft, (-) masses or tenderness

Genitourinary: Deferred Skin/Extremities: Pink nail beds, full and equal pulses, (-)

cyanosis, (-) edema, (-) clubbing, (-) skin lesion

Physical Examination Neurologic:

GCS 15 (E4 V5 M6)

Patient presently awake, conversant, oriented to time, place and person

Physical Examination Neurologic:

Cranial NervesI – can smellII – can read fine printIII – pupils 3 mm, equally briskly reactive to light; EOM’s

full and equalIV – EOM’s full and equalV – can clench jaw, intact light touch sensation on face,

brisk corneal reflexVI – EOM’s full and equalVII – can raise eyebrow, smile, frown, (-) facial asymmetryVIII – can hear grosslyIX – symmetrical uvula and soft palate, (+) gag reflex X – can taste, (+) gag reflexXI – good shoulder shrug XII – tongue midline

Physical Examination Neurologic: Sensory – intact light touch, temperature, vibration, pain sensationMotor - Muscle strength 5/5 in all extremitiesDeep tendon reflex ++ (triceps, biceps, brachioradialis, patella, Achilles’)Cerebellar – (-) dysdiadochokenisia, dysmetria, nystagmus, tandem walk, heel-to-shin test(-) Brudzinski sign, Kernig’s sign, nuchal rigidity

Summary of hx and PEThis is a case of a 43 year old female with no known co-morbidity presenting with acute onset of severe headache, bilateral lower extremity weakness and numbness, loss of consciousness for three days, allegedly resolving after several days. Physical examination upon admission revealed essentially normal systemic and neurologic findings.

CT scan

Differentials

DifferentialsIntracranial Hemorrhage (Subarachnoid

Hemorrhage)- Rule In

- Acute onset- Severe headache- Focal neurologic deficits- Loss of consciousness- Patient’s age- Patient is hypertensive- Family history of stroke- Patient’s diet preferences (increased cholesterol)- Patient was doing household chores during onset

- Rule Out- Cannot be ruled out

DifferentialsIschemic Stroke

Rule InAcute onsetFocal neurologic deficitsPatient’s ageFamily history of stroke- Patient’s diet preferences – fatty, salty and sweet

foodsRule Out

Cannot be completely ruled out (without CT Scan)

DifferentialsBrain Tumor

Rule InHeadacheFocal neurologic deficits

Rule OutOnset of symptoms is acute

DifferentialsBrain Abscess

Rule InHeadacheFocal neurologic deficits

Rule OutOnset of symptoms is acuteNo evidence of infection (afebrile, no cough/colds,

no previous head surgery, etc.)

DifferentialsMigraine

Rule InHeadachePatient’s sex

Rule OutFirst episodeNo perceived “aura” prior to onsetFocal neurologic deficits rarely occurs with migraine

AssessmentSubarachnoid Hemorrhage

Course in the Wards

Course in the Wards10/6/09

S> Patient admitted at ACU ER. Patient seen by the treatment officer,(+) HA, VAS 2/10 fronto-temporal.(-) fever, coughs, dyspnea, chest pains, epigastric pain, urinary or bowel changes

O> BP: 120/70 HR: 80 RR: 20E/N systemic PE findingsNeuro Exam : intact cranial nerves, (-) sensory and motor deficits, (-) cerebellar/ meningeal signsCT scan:

A> SAH

P>Dx: Blood typing, CBC, Blood Chem, CT scan (plain and with contrast) TX:Tramadol 50mg/cap q8 prn for HA, Captopril 2mg TID, Lactulose 30cc HS

Patient was referred to Neurology


S> Seen by the Neurology service.No new symptoms/ complaints, no neurological deficits. (-) headache, (-) dizziness, (-) nausea, (-) vomiting, (-) nape pain (-) blurring of vision

O> BP: 120/80 HR: 80 RR: 20E/N systemic PE findingsNeuro Exam : intact cranial nerves, (-) sensory and motor deficits, (-) cerabellar/ meningeal sigins

A> SAH secondary to cerebral aneurysm

P> For repeat 4V angiography Patient transferred to NSS WOF: decrease in sensorium, severe headache,seizures, new onset neurological deficits


S> Patient admitted at W6B17. (-) headache, (-) dizziness, (-) nausea, (-) vomiting, (-) nape pain. No other neurologic complaint.

O> BP: 120/70 HR: 80 RR: 20E/N systemic PE findingsNeuro Exam : intact cranial nerves, (-) sensory and motor deficits, (-) cerebellar/ meningeal signs

A> SAH

P> Tx: Tramadol 50mg/cap was shifted to Etorocoxib 120mg/tab For 4V angiography For possible craniotomy, clipping of the aneurysm


S> Patient had headache, VAS 5/10 (fronto-temporal), (+) nape pain, (+) dipahoresis, (+) vomiting (3x, non-bloody, non bilous, non-mucoid, about 3 tablespoons per episode), (+) chest pain, non radiating, ‘described as mabigat’ , (point tenderness)

O> BP: 140/90 HR: 105 RR: 20

Neuro Exam : intact cranial nerves, (-) sensory and motor deficits, (-) cerabellar/ meningeal signs

A> t/c costohondritis r/o ACE

P> for stat ECG for Na, K, Cl Encourage deep breathings Captopril 20mg/tab BID Etoricoxib 120mg/tab for headache Referred to Gen MeD


S> Patient seen by Gen Med. At that time (-) chest pain, (-) headache,(-) blurring of vision, (-)nape pain, (-) nausea, (-)vomiting, (-)fever, (+) palpitations

0> BP 90/60 HR 100 RR 20 E/N systemic PE findingsNeuro Exam : intact cranial nerves, (-) sensory and motor deficits, (-) cerabellar/ meningeal signs

ECG: ST, NA, NSSTTWC

A> SAH Hypertension most probably secondary (reactive) Chest pain not anginal

P> Suggest decrease Captopril to ½ tab for BP >160/100


S> Patient seen by SAPOD for clearance for 4v angiography and possible clipping of the aneurysm. (-) chest pain, (-) headache, (-)nape pain, (-) nause, (-)vomiting, (-)fever, (+) palpitations, (-) orthopnea, (-) PND, (-) exertional dyspnea

O> > BP: 120/70 HR: 80 RR: 20E/N systemic PE findingsNeuro Exam : intact cranial nerves, (-) sensory and motor deficits, (-) cerabellar/ meningeal signs

A> SAH Hypertension St. II

P> Shift Captopril to Metoprolol 50mg/tab, ½ tab BID

LABSECG: ST, NA, NSSTTWCPT 11.8/11.6/>1.0/ 1.10 APTT/ 35.5/30.9Blood Chemis try : FBS: 5.81 Na: 141 BUN 3.34 K: 3.6 Crea: 6.4 Hemoglobin: 123 Hematocrit: 0.38 WBC:5.7 Platelet : 302

Discussion

Subarachnoid hemorrhage

RELEVANT ANATOMYsaccular aneurysms - bifurcations of vessels

of circle of Willis. Circle of Willis• close proximity to ventral surface of

diencephalon • adjacent to optic nerves and tracts. • important anastomosis for the 4 arteries

that supply the brain - 2 vertebral and the 2 internal carotid arteries

• divided into anterior and posterior sections

Anterior portion of the circle of Willis

• Consists of:1.internal carotid

arteries2.anterior cerebral

artery3.anterior

communicating artery

Posterior portion of the circle of Willis

• consists of:1. posterior cerebral

arteries 2. posterior

communicating arteries, paired

Location of aneurysm ruptureanterior circulation - 85% of saccular aneurysmsmost common sites of rupture are as follows:1. internal carotid artery,

including posterior communicating junction (41%)

2. anterior communicating artery/ anterior cerebral artery (34%) 3. middle cerebral artery (20%) 4. vertebral-basilar arteries (4%) 5. other arteries (1%)

Subarachnoid hemorrhage DISCUSSION

DEFINITION:extravasation of blood into the

subarachnoid space between the pial and arachnoid membranes

detrimental effect on both local and global brain function and leads to high morbidity and mortality rates.



Subarachnoid hemorrhage:1.Traumatic: head trauma2.Non-traumatic (spontaneous):

a. ruptured cerebral aneurysm b. arteriovenous malformation (AVM)


FREQUENCYAge• Incidence increases with age• peaks at age 50 years • 80% of SAH cases: 40-65 years

Sex• women to men ratio (3:2)• risk of SAH from aneurysmal rupture - maternal

deaths in pregnancy• AVM rupture during pregnancy.

Race• different ethnic groups develop intracranial

aneurysms


ETIOLOGYNontraumatic subarachnoid hemorrhage

(SAH)- caused by extravasation of blood from

abnormal blood vessels onto the surface of brain

- result of:1. aneurysmal ("berry," or saccular)2. AVM leakage or rupture – 10 %


Less common causes of SAH:• Fusiform and mycotic aneurysms • Fibromuscular dysplasia • Blood dyscrasias • Moyamoya disease • Infection • Neoplasm • Trauma (fracture at the base of the skull

leading to internal carotid aneurysm) • Amyloid angiopathy (especially in elderly

people) • Vasculitis • Idiopathic SAH


Etiology Of Cerebral Aneurysms - unknown

Congenital defects in the muscle and elastic tissue of the arterial media in the

vessels of the circle of Willis

• familial cerebral aneurysm - 10% • multiple aneurysms in patients with SAH 15% • congenital diseases

coarctation of the aortaMarfan syndromeEhlers-Danlos syndromefibromuscular dysplasiapolycystic kidney disease


Aneurysmal formation - Acquired factors

Atherosclerosis Hypertension Hemodynamic stress


RISK FACTORSSmoking heavy alcohol consumptionhypertension and SAH – conflicting

evidence

hypertension has been identified as a risk factor for aneurysm formation, the data with respect to rupture are conflicting

hypertensive states (stimulants e.g. cocaine) - promote aneurysm growth and earlier rupture


The following do not appear to be significant risk factors for SAH:

• Use of oral contraceptives • Hormone replacement therapy • Hypercholesterolemia • Vigorous physical activity• The risk of AVM rupture is greater during

pregnancy


PATHOPHYSIOLOGY• Aneurysms - occur at branching sites on large cerebral arteries of circle of

Willis.

defects in media of arteriessmall outpouchings

↓

expand due to hydrostatic pressure 1. pulsatile blood flow

2. blood turbulence

(greatest at the arterial bifurcations)↓

mature aneurysmpaucity of media

replaced by connective tissue

diminished or absent elastic lamina


Law of La Place:‘tension is determined by the radius of the aneurysm and the pressure gradient across the wall of the aneurysm’

probability of rupture ~ aneurysm wall tension


rate of rupture is directly related to the size of the aneurysm

< 5 mm diameter - 2% risk of rupture6-10 mm diameter - 40% risk of rupture


aneurysm ruptures↓

blood extravasation(under high arterial pressure)

↓1. local tissue damage

2. global increase in intracranial pressure (ICP)

3. meningeal irritation


PRESENTATIONsigns and symptoms:

subtle prodromal events toclassic presentation of catastrophic headache

clinical history physical examination

- neurologic examination


Cause of prodromal signs and symptoms:1. sentinel leaks2. mass effect of aneurysm expansion3. emboli


1. Sentinel (‘warning’) leaks• produce minor blood leakage• symptoms:

head pain - sudden focal or generalized, severenausea, vomitingphotophobiamalaiseneck pain

• not elevated ICP• not in setting of AVM


2. Mass effect• characteristic features based upon aneurysm location.

a. Posterior communicating artery/internal carotid artery Focal, progressive retro-orbital headaches

oculomotor nerve palsy (Just posterior and superior to the cavernous sinus, the oculomotor nerve crosses

the terminal portion of the internal carotid artery at its junction with the posterior communicating artery.)

b. Middle cerebral arteryContralateral face or hand paresisaphasia (left side)contralateral visual neglect (right side) c. Anterior communicating arteryBilateral leg paresisbilateral Babinski sign d. Basilar artery apex Vertical gaze, paresis, and coma e. Intracranial vertebral artery/posterior inferior

cerebellar artery Vertigo, components of lateral medullary syndrome


3. Emboli: transient ischemic attacks from intra-aneurysmal

thrombus formation.

classic symptoms and signs of aneurysmal rupture:Headache - sudden onset, severe, ‘worst headache of

my life’Nausea, vomiting meningeal irritation

nuchal rigidity and painback painbilateral leg pain

Photophobia and visual changes sudden loss of consciousness (LOC)

Transient or comatose for several daysSeizures


Physical Examination Findings normal or consistent with the following: a. Focal neurologic abnormalities -

hemiparesis, aphasia, hemineglect, cranial nerve palsies, and memory loss

b. Motor neurologic deficits - middle cerebral artery aneurysms

c. Ophthalmologic examination - subhyaloid retinal hemorrhages, papilledema

d. Blood pressure elevatione. Temperature elevation - chemical

meningitis from subarachnoid blood productsf. Tachycardia


CLINICAL GRADING SCALES• Clinical scales:

1. Hunt and Hess grading system2. World Federation of Neurological Surgeons (WFNS) grading system

• Imaging scale:Fischer scale

CT scan appearancesubarachnoid blood quantification


HUNT AND HESS GRADING SYSTEM

Grade 1 Asymptomatic or mild headache

Grade 2 Moderate-to-severe headache, nuchal rigidity, and no neurological deficit other than possible cranial nerve palsy

Grade 3 Mild alteration in mental status (confusion, lethargy), mild focal neurological deficit

Grade 4 Stupor and/or hemiparesis

Grade 5 Comatose and/or decerebrate rigidity


WFNS SCALE

Grade 1 Glasgow Coma Score (GCS) of 15, motor deficit absent

Grade 2 GCS of 13-14, motor deficit absent

Grade 3 GCS of 13-14, motor deficit present

Grade 4 GCS of 7-12, motor deficit absent or present

Grade 5 GCS of 3-6, motor deficit absent or present


FISCHER SCALE (CT SCAN APPEARANCE)

Grade 1 No blood detected

Grade 2 Diffuse deposition of subarachnoid blood, no clots, and no layers of blood greater than 1 mm

Grade 3 Localized clots and/or vertical layers of blood 1 mm or greater in thickness

Grade 4 Diffuse or no subarachnoid blood, but intracerebral or intraventricular clots are present


Hunt and Hess and WFNS grading systems

- correlation with patient outcome.Fischer classification - predict likelihood of symptomatic cerebral

vasospasm,

All 3 grading systems are useful in determining the indications for and timing of surgical management.


‘For an accurate assessment of SAH severity, these grading systems must be used in concert with the patient's overall general medical condition and the location and size of the ruptured aneurysm.’

Management

Work-up

Work-upCBC count - For evaluation of possible infection or

hematologic abnormalityProthrombin time (PT) and activated partial

thromboplastin time (aPTT) - For evaluation of possible coagulopathy

Serum electrolytes - To establish a baseline for detection of future complications

Blood type and screen - In case intraoperative transfusion is required or in the setting of massive hemorrhage

Cardiac enzymes - For evaluation of possible myocardial ischemia

Arterial blood gas (ABG) - Assessment is necessary in cases with pulmonary compromise

ImagingCT scan: The diagnosis of SAH usually

depends on a high index of clinical suspicion combined with radiographic confirmation via CT scan without contrast.

CT scan has a sensitivity of 98% within the first 12 hours of the ictus and 93% within 24 hours;

sensitivity decreases to approximately 80% at 72 hours and 50% at 1 week.

CT scan findings are positive in 92% of patients who have SAH.

Lumbar PunctureLP should be performed when strong clinical

suspicion of SAH exists with a negative finding on CT scan or when a CT scan is not available. If possible, a CT scan should be performed

before LP to exclude significant intracranial mass effect, elevated ICP, obstructive hydrocephalus, or obvious intracranial bleed.

LP findings often are negative within 2 hours of the ictus, and LP is most sensitive 12 hours after the bleed.

Lumbar PunctureLP should not be performed if the CT scan demonstrates

an SAH because of the (small) risk of further intracranial bleeding associated with a drop in ICP.

SAH often can be distinguished from traumatic LP by comparing the red blood cell count of the first and last tubes of CSF. The RBC count usually will not decrease between the first and last tubes in the setting of SAH; however, case reports of this phenomenon do exist.

The most reliable method of differentiating SAH from a traumatic tap is to spin down the CSF and examine the supernatant fluid for the presence of xanthochromia, a pink or yellow coloration of the CSF supernatant caused by the breakdown of RBCs and subsequent release of heme pigments.

Cerebral angiographyCerebral angiography is particularly useful in

cases of diagnostic uncertaintyCerebral angiography can provide the following

important surgical information in the setting of SAH:Cerebrovascular anatomyAneurysm location and source of bleedingAneurysm size and shape, as well as orientation

of the aneurysm dome and neckRelation of the aneurysm to the parent artery

and perforating arteriesPresence of multiple or mirror aneurysms

(identically placed aneurysms in both the left and right circulations)

Medical Therapy

Medical therapyThe initial management of patients with

SAH is directed at patient stabilization. Assess the level of consciousness and

airway, as well as breathing and circulation (ABCs).

Endotracheal intubation should be performed for patients presenting with coma, depressed level of consciousness, inability to protect their airway, or increased ICP.

Medical therapyTherapeutic goals of subarachnoid

hemorrhage:1.blood pressure control2.prevention of seizures3.treatment of nausea4.management of ICP5.prevention of vasospasm6.control of pain7.maintenance of cerebral perfusion

Medical therapyThe traditional treatment of ruptured

cerebral aneurysms included strict blood pressure control, with fluid restriction and antihypertensive therapy.

This approach was associated with a high rate of morbidity and mortality from the ischemic complications of hypovolemia and hypotension.

Medical therapyThe current recommendations advocate

the use of antihypertensive agents when the mean arterial pressure (MAP) exceeds 130 mm Hg.

Intravenous beta-blockers, which have a relatively short half-life, can be titrated easily and do not increase ICP.

Beta-blockers are the agents of choice in patients without contraindications.

Medical therapyCalcium channel blockercalcium - involved in the generation of the action

potential. calcium channel blockers - inhibit movement of calcium ions across the cell membrane, depressing both impulse formation (automaticity) and conduction velocity.

Nimodipine (Nimotop) - 60 mg PO q4h x 21 dFor improvement of neurological impairments

resulting from spasms following SAH caused by ruptured congenital intracranial aneurysm in patients who are in good postictal neurological condition.

Medical therapytherapeutic interventions for increased ICP

include the following:• Osmotic agents (eg, mannitol), which can

decrease ICP dramatically (50% after 30 min postadministration)

• Loop diuretics (eg, furosemide) also can decrease ICP

• The use of IV steroids (eg, Decadron) is controversial but is recommended by some authors.

Prophylaxis and treatment of complicationsCommon complications of SAH:RebleedingVasospasmHydrocephalusHyponatremiaSeizuresPulmonary complicationsCardiac complications

RebleedingRebleeding is the most dreaded early

complication of SAH.

The greatest risk of rebleeding occurs within the first 24 hours of rupture (4.1%).

The cumulative risk of rebleeding is 19% at 14 days. The overall mortality rate from rebleeding is reported to be as high as 78%.

Measures to prevent rebleeding Bedrest Analgesia. Pain is associated with a

transient elevation in blood pressure and increased risk of rebleeding.

SedationStool softenersAntifibrinolytics have been shown to

reduce the occurrence of rebleeding. However, outcome likely does not improve because of a concurrent increase in the incidence of cerebral ischemia.

VasospasmCerebral vasospasm, the delayed narrowing of the

large capacitance vessels at the base of the brain

leading cause of morbidity and mortality in survivors of nontraumatic SAH.

Vasospasm is reported to occur in as many as 70% of patients with SAH and is clinically symptomatic in as many as 30% of patients.

Most commonly, this occurs 4-14 days after the hemorrhage.

Risk factors for vasospasm Larger volumes of blood in the

subarachnoid spaceClinically severe SAHFemale sexYoung ageSmoking

Measures used for prevention of vasospasm

Maintenance of normovolemia, normothermia, and normal oxygenation are paramount to vasospasm prophylaxis.

Volume status should be monitored closely

Prophylaxis with oral nimodipine: Calcium channel blockers have been shown to reduce the incidence of ischemic neurological deficits

nimodipine has been shown to improve overall outcome within 3 months of aneurysmal SAH

Measures used for prevention of vasospasmSome evidence indicates that subarachnoid

clot removal achieved via intracisternal injections of recombinant tissue plasminogen activator (rTPA) may dramatically reduce the risk of vasospasm.

Aspiration and irrigation of the subarachnoid clot at the time of aneurysmal clipping associated with a significant risk of iatrogenic trauma to pial surfaces and small vessels.

Surgical therapy

Surgical Clippingintroduced by Walter Dandy of the Johns

Hopshins Hospital in 1937.

It consists of performing a craniotomy, exposing the aneurysm, and closing the base of the aneurysm with a clip.

The aneurysmal neck is obliterated via application of a clip that occludes blood flow to the aneurysmal dome without compromising flow to the parent artery.

Surgical ClippingSurgical clipping has a lower rate of aneurysm recurrence after treatment.

Direct aneurysmal clipping is still

considered first-line treatment in the United States.

Clips are available in various sizes and shapes.

Endovascular coilingEndovascular coiling was introduced by Guido

Guglielmi at UCLA in 1991. It consists of passing a catheter into the

femoral artery in the groin, through the aorta, into the brain arteries, and finally into the aneurysm itself.

Once the catheter is in the aneurysm, platinum coils are pushed into the aneurysm and released.

These coils initiate a clotting or thrombotic reaction within the aneurysm that, if successful, will eliminate the aneurysm.

Endovascular coilingGuglielmi detachable coil system (GDC) is

the first-line therapy in Europe.

They are soft, flexible, and can be contoured to the configuration of the aneurysm. Sizes range from 2-20 mm in diameter and 2-30 cm in length.

In limited clinical trials, GDCs have been reported to achieve excellent rates of aneurysmal occlusion combined with a low complication rate in appropriate patients.

.

Surgical clipping vs. Endovascular coilingthe risks associated with surgical clipping and

endovascular coiling, in terms of stroke or death from the procedure, are the same .

The major problem associated with endovascular coiling is a higher aneurysm recurrence rate.

Although endovascular coiling is associated with a shorter recovery period as compared to surgical clipping, it is also associated with a significantly higher recurrence rate after treatment.

Other surgical optionsProximal ligation of the parent artery or

trapping of aneurysms with or without bypass.

Proximal ligation is effective for giant aneurysms.

Wrapping or coating of aneurysms may be the only option in rare cases of dissecting or fusiform aneurysms

Timing of surgical intervention

Advantages of early surgery (0-3 d) :

Prevention of rebleeding, which is associated with a high mortality rate

Possible prophylaxis against vasospasm by removal of subarachnoid clot

Prevention and treatment of ischemic complications

Prevention of medical complicationsDecreased duration of hospitalization

Timing of surgical interventionDisadvantages of early surgery for SAH :

Technical problems associated with edematous brain tissue

High risk of intraoperative rupture of fragile aneurysm

Higher surgical morbidity and mortality rates

Timing of surgical interventionAdvantages of delayed surgery for SAH (>10 d

posthemorrhage)Brain tissue is less edematous.Lower risk of intraoperative aneurysm ruptureLower surgical morbidity and mortality ratesFlexibility of scheduling

The disadvantages of delayed surgery: Increased rate of morbidity and mortality due to

rebleedingTechnical difficulties due to adhesions around

the aneurysm

Complications of surgical clippingHemorrhagic complicationsIschemic complicationsDamage to parent artery or perforating

arteriesAcute or delayed neurological deficits

from iatrogenic traumaMeningitisCellulitis and wound infectionNonspecific postsurgical syndrome

similar to postconcussive syndrome

Common complications of endovascular therapy

Aneurysm rupture (GDCs, balloons)Thromboembolism (GDCs) with acute or

delayed neurologic deficitBalloon rupture or deflation

PrognosisDespite advances in medical and surgical therapy,

the mortality rate for aneurysmal SAH remains 50% at 1 year.

Survival is inversely proportional to SAH grade upon presentation.

Hunt and Hess Grading and Survival RateGrade 1 – 70%

Grade 2 – 60%

Grade 3 – 50%

Grade 4 – 20%

Grade 5 – 10%

PrognosisApproximately 25% of survivors have

persistent neurologic deficits.

Most survivors have either a transient or a permanent cognitive deficit.

Mortality and morbidity are influenced by:magnitude of the bleedage of the patientco-morbid conditionsmedical complications.

Stroke, Journal of the American Heart Association

(Sep 28, 2008)

Sentinel Headache and the Risk of Rebleeding After

Aneurysmal Subarachnoid Hemorrhage

INTRODUCTIONThe presence of a severe, sudden headache,

often referred to as a warning leak, minor leak, or sentinel headache (SH), during the days or weeks before subarachnoid hemorrhage (SAH) has been reported in 15% to 60% of all patients eventually admitted with an SAH

Pathophysiology of an SH: changes in the wall of the aneurysm without rupture or rupture of an intracranial aneurysm causing minor SAH

INTRODUCTIONThe current mainstay of treatment of acute

SAH consists of prevention of another bleed, because the rebleeding rate and associated mortality are exceedingly high

Most protocols favor early treatment in 48 to 72 hours after the ictus

INTRODUCTIONBecause the rebleeding rate may be

highest immediately after SAH, some investigators have suggested a general policy of “ultraearly” surgery, which is unlikely to gain wide acceptance, because it does not provide treatment with the best team under the optimum circumstances for many patients

INTRODUCTIONIt would be of important clinical value

to identify a subgroup of patients that is more likely than others to experience rebleeding

The hypothesis of this study was that there is a causal relation between the aneurysm or SAH and the clinical sign of an SH; ie, patients with an SH may have more fragile aneurysms

INTRODUCTIONThis hypothesis was prospectively tested

by investigating whether patients who presented with an SH before the index SAH indeed had a higher rate of rebleeding compared with those without an SH

SUBJECTS AND METHODSPatient Population237 consecutive patients with SAH proven

by computed tomography (CT) or lumbar puncture

Patient characteristics, treatment, radiological features, the presence of an SH, and rebleeding, was prospectively entered in an SPSS database

SUBJECTS AND METHODSGeneral Patient ManagementEarly surgery strategy (24 to 48 hours) was

done in patients of all clinical grades unless the patients were hemodynamically unstable or moribund

Routine surveillance included daily transcranial Doppler measurements and, in selected cases, multimodal monitoring of brain tissue O2, regional cerebral blood flow, and interstitial metabolites

SUBJECTS AND METHODSGeneral Patient ManagementAll patients received Nimodipine from the

day of admissionFludrocortisone was administered as an

adjunct in case of hyponatremiaDesmopressin was used to control

excessive diuresisOutcome was assessed according to a

modified Rankin Scale (mRS) after 6 months

SUBJECTS AND METHODSSentinel HeadacheThorough history was taken of patients,

relatives, accompanying persons, general practitioners, and emergency or admitting doctors

Inquired about a sudden, severe headache of unknown character and intensity lasting at least 1 hour in the last 4 weeks before the index SAH that had never been experienced before

There had to have been an improvement before the index SAH or another deterioration that led to a diagnosis of SAH

SUBJECTS AND METHODSRebleeding Only included CT-proven episodes of

rebleeding (neuroradiologist was blinded to a history of SH)

Cases with a high clinical suspicion of rebleeding but without confirmation by at least 2 subsequent CT scans were not included

SUBJECTS AND METHODSRebleeding All patients underwent CT scanning after

clipping/intervention within 48 hours as well as at day 14 or at discharge

Rebleeding after aneurysm obliteration was not included

SUBJECTS AND METHODSData Analysis To test for an association with rebleeding,

categorical variables were tested with Fisher exact test or x2 test

Continuous variables were subjected to the Mann-Whitney U test or a t-test

Binary logistic-regression model for the prediction of rebleeding was used to find the most important baseline predictors

Results with P<0.05 were considered statistically significant

RESULTSPatient Population

RESULTSRebleedingOverall rebleeding rate - 9.7% (23 of 237)SH before the index SAH - 17.3% (41 of

237)Univariate analysis revealed that the

presence of an SH, maximum aneurysm size, and the number of aneurysms an individual patient presented with were significantly associated with rebleeding

RESULTSRebleedingTrend for an association with less

rebleeding for aneurysms of the anterior circulation

No association between the frequency of rebleeding and patient age, sex, smoking habits, or findings on the initial CT scan

RESULTSRebleeding

The odds of eventually experiencing a rebleeding episode for a patient with an SH compared with a patient without an SH was 13.6 (P<0.0001) in the univariate model

RESULTSRebleedingRelative risk was 9.0Sensitivity was 65.2% Specificity 87.9%Positive predictive value was 36.6%Negative predictive value was 95.9%

RESULTSRebleedingIn a binary logistic-regression model,the

presence of an SH remained a very statistically significant and independent predictor of rebleeding after controlling for age, aneurysm size, number of aneurysms, and the time at risk

RESULTSOutcomeOverall outcome at 6 months was available

for 212 patientsRebleeding significantly increased the odds

of death, reduced the odds of survival with good outcome, and reduced the odds of survival with functional independence

RESULTSOutcome

CONCLUSIONThe presence of an SH is strongly related to

an increased frequency of rebleeding before aneurysm obliteration

Therefore, a history of SH might be used to identify a subgroup of patients with a high risk for rebleeding and who could benefit from ultraearly aneurysm obliteration or immediate clot-stabilizing drug treatment

Thank you vey much!!!!!Block_U_lala

Documents

NSS SGD Ontok.Rodriguez.Salongcay.Samson.Bautista Case Presentation