NSS SGD Ontok.Rodriguez.Salongcay.Samson.Bautista Case Presentation.
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Transcript of 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
Course in the Wards10/07/09
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
Course in the Wards10/09/09
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
Course in the Wards10/10/09
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
Course in the Wards10/11/09
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
Course in the Wards10/12/09
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 DISCUSSION
Subarachnoid hemorrhage DISCUSSION
Subarachnoid hemorrhage:1.Traumatic: head trauma2.Non-traumatic (spontaneous):
a. ruptured cerebral aneurysm b. arteriovenous malformation (AVM)
Subarachnoid hemorrhage DISCUSSION
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
Subarachnoid hemorrhage DISCUSSION
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 %
Subarachnoid hemorrhage DISCUSSION
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
Subarachnoid hemorrhage DISCUSSION
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
Subarachnoid hemorrhage DISCUSSION
Aneurysmal formation - Acquired factors
Atherosclerosis Hypertension Hemodynamic stress
Subarachnoid hemorrhage DISCUSSION
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
Subarachnoid hemorrhage DISCUSSION
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
Subarachnoid hemorrhage DISCUSSION
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
Subarachnoid hemorrhage DISCUSSION
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
Subarachnoid hemorrhage DISCUSSION
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
Subarachnoid hemorrhage DISCUSSION
aneurysm ruptures↓
blood extravasation(under high arterial pressure)
↓1. local tissue damage
2. global increase in intracranial pressure (ICP)
3. meningeal irritation
Subarachnoid hemorrhage DISCUSSION
PRESENTATIONsigns and symptoms:
subtle prodromal events toclassic presentation of catastrophic headache
clinical history physical examination
- neurologic examination
Subarachnoid hemorrhage DISCUSSION
Cause of prodromal signs and symptoms:1. sentinel leaks2. mass effect of aneurysm expansion3. emboli
Subarachnoid hemorrhage DISCUSSION
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
Subarachnoid hemorrhage DISCUSSION
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
Subarachnoid hemorrhage DISCUSSION
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
Subarachnoid hemorrhage DISCUSSION
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
Subarachnoid hemorrhage DISCUSSION
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
Subarachnoid hemorrhage DISCUSSION
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
Subarachnoid hemorrhage DISCUSSION
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
Subarachnoid hemorrhage DISCUSSION
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
Subarachnoid hemorrhage DISCUSSION
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.
Subarachnoid hemorrhage DISCUSSION
‘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