Cerebral anuerysm account for 75-80% spontaneous subarachnoid hemorrhage (SAH), cerebral arteriovenous malformation(AVM) for 4-5%,and in 15-20% of patients no source of hemorrhage can be found. Other cause of SAH include trauma,dural and spinal AVM,mycotic aneurysm
sickle cell disease,cocaine abuse and coagulation disorders.
Ruptured aneurysm usually present acutely as SAH and less common into epidural space or brain.Aneurysm often occur at branch point of vessels around the circle of Wills and the bifurcation of the middle cerebral artery.
Most are supratentorial and aproximately 30% of patients will have multiple aneurysm.The incidence of aneurysmal SAH is 12-15 per 100.000 population per year with a peak incidence between 55 and 60 years of age.
Females to male ratio of approximately 3:2 and genetic factors may contribute. Most aneurysm are 6 to 15mm in diameter and aneurysm >25 mm are referred to as a giant
aneurysm. Aneurysms that have ruptured carry a much greater chance of future hemorrhage. About 50% ruptured aneurysm will rebleed within 6 months after the initial hemorrhage, after this period this risk of repeat hemorrha-
ge decreases to 3% per year.
One third of patients will die before reaching hospital and the remaining patients will have a 30-50% mortality.
The major risk facing patients who reach hospital are recurrent hemorrhage; the development of delayed ischaemic neurological deficits (vasospam) and hydrocepha-
lus.Conservative non surgical treatment of SAH is associa-
ted with much higher mortality than surgical treatment (40% vs <10%)respectively within six months of the bleed.
However conservative medical treatment has been recently
recomended in elderly patients (>64 years) with unruptured aneurysms less than 1 cm diameter as in the risk of surgery outweigh the benefit.
PATHOLOGY:(4)
More than 90% of cerebral aneurysm occur at the following location :
1.The origin of posterior communicating artery.
2.The region of the anterior communicated artery.
3.The middle cerebral artery bifurcation.
4.The apex of basillar artery.
5.The internal carotid artery bifurcation.
Wiebers,Whisant and O'Fallon suggested that there was little likelihood of bleeding from asymptomatic aneurysm greater less than 1 cm in diameter.
Other studies also suggest that aneurysm greater than 0,5 cm should be considered at risk for rupture but that those less than 0,5 cm carry little risk of hemorrhage.Smaller aneurysm have been documented to enlarge with time
so predicting fully the future risk in these case is difficult.
Evidence of hypertension has been found in as many as 80% of individuals with cerebral aneurysm and hypertension may be etiologic factor in the development of aneurysm. The coarctation of the aorta is often associated with cerebral aneurysm and SAH is responsible for the death of about 10% of these patients. Approximately 16% of patients with polycystic kidney disease are found at autopsy to have cerebral aneurysm and SAH is the cause of death in 15%
of patients.In addition fibromuscular dysplasia is associated with cerebral aneurysm and the aneurysm have been found more than 20% of those patients with disease involving
the head and neck.
The authors report an elevenfold increase in the change of aneurysmal hemorrhgae in smookers and developing delayed ischemic events after SAH also appears to be increased in smookers.
GRADING OF ANEURYSM:(3,4)
A system for the grading of patients after SAH was introduced by Botterell in 1956 to facilitate the assessment of surgical risk the prediction of outcome and the evaluation of the patient's condition as it evolved from the post hemorrhage period to that immediately preceeding operation.
The five grades describe the patient level of conciousness and degree of neulogic impairment as 1 to 5,each grade representing increased severity.
BOTTERELL CLINICAL GRADE :
Grade Criteria
I. Conciousness with or without meningeal signs.
II.Drowsy without significant neurologic deficits.
III.Drowsy with neurologic deficit and probable cerebral
clot.
IV.Major neurologic deficit present.
V.Moribund with failing vital centers and extensor rigidity.
Botterell's system was modified by Hunt and Hess to include description of the accompanying headache and neurologic deficit and a provision for the affect of serious systemic illness(e.g.hypertension,diabetes,chronic pulmonary
disease,vasospasm) that would move the patient into the next less favorable category.
HUNTS and HESS MODIFICATION GRADE:
Grade Criteria
0 Unruptured aneurysm
I Asymptomatic or minimal headache
and slight nuchal rigidity.
II. Moderate to severe headache,nuchal
rigidity no neurologic deficit other
than cranial nerve palsy.
III. Drowsiness,confusion or mild local
deficit.
IV. Stupor,moderate to severe decebra-
te rigidity,hemiparesis,possibly ear-
ly vegetative disturbances.
V. Deep coma,decerebrate rigidity,mo-
ribund appearance
The World Federation of Neurologic Surgeons(WFNS) subsequently developed a grading scale based on the Glasgow Coma Scale(GCS) in which preoperative
of conciousness was found to correlate most directly with outcome.
WFNS grade GCS Motor deficit
I. i5 absent
II. 14-13 absent
III. 14-13 present
IV 12-7 present or absent
V. 6-3 present or absent.
Grade I and II before surgery are likely to do well whereas patients who are moribund preoperatively have a high morbidity or mortality. Poor grade patients are more likely to have impairment of cerebral autoregulation and the cerebrovascular response to hypocapnia, intracranial hypertension and vasospasm as well as fluid and electrolyte imbalance, myocardial dysfunction,cardiac arrhythmias and respiratory impairment.
Predictors of mortality after SAH :
Decreased level of conciousness
Increased age
Thickness of subarachnoid clot on CT scan
Elevated blood pressure
Pre existing medical illness
Basilar aneurysm
CLINICAL PRESENTATION :
Signs and Symptoms of SAH from intracranial aneurysmal rupture:(1,3,5)
Meningeal irritation:
Sudden severe headache
Meningismus
Photophobia
Confusion,dysphasia
Focal neulogic signs
Depressed level of conciousness
Coma
Cranial nerve palsies
Seizure
Nausea and vomiting
Elevated temperature
Increased sympathetic activity,hypertension
ECG abnormalities
Hypovolemia
Hyponatremia,electrolyte imbalance
Clotting abnormalities
Leukocytosis
Proteinuria,glycosuria
SAH classically present with sudden onset severe headaches radiating to occipital or cervical region with or without loss of conciousness asociated with nausea/vomiting is typically pasien complain.
Photophobia,lethargy and signs of meningism are all common. Hypertension,hyperpyrexia,seizures,motor or sensory deficits,cranial nerve palsies(third and six)and visual field defects may also occur. Transient loss of conciousness may occur from sudden rise in ICP and precipitous drop in cerebral perfusion pressure(CPP),if ICP does not decrease rapidly after the initial sudden increase,death usually follows.
Large blood clots can cause focal neurologic sign in some patients. A sudden rise in ICP in conjunction with normal coagulation is thought to prevent continuing bleeding from the aneurysm site.
PREOPERATIVE ASSESSMENT :
Cardiovascular assessment:(1,2,3)
Volume status :
More than half of patients with a ruptured aneurysm have a significant (>10%)decrease in plasma volume. The patient with recent SAH may be vasoconstricted because of high
cathecolamine levels and may be hypovolemic because of the influence of atrial natriuretic factor.
Now however investigators believe that distension of the ventricel,as with post SAH hydrocephalus cause the release of atrial natriuretic factor from hypothalamus.
In keeping with this association patients who have evidence of intracranial hypertension on CT scan are morelikely to be hypovolemic.Such hypovolemic may inturn increase the degree vasospasm and lead to cerebral ischemia and infarction.
Maroon and Nelson have identified bedrest,negative nitrogen balance,supine diuresis decreases erythropoesis and iatrogenic blood loss are factors contributing to the hypovolemia.
The hyponatremia that accompanies the hypovolemia noted in 30% of patients who have vasospasm was originally thought to be due to the either the cerebral salt wasting syndrome or the inappropriate secretion of ADH(SIADH),in both groups the plasma sodium concentration is low(<134 mmol/L). Patient with salt wasting syndrome are hypovolemia and require fluid to prevent intravascular volume contraction.
In contrast patient with SIADH secretion required fluid retrisction. Hyponatremia may be iatrogenic because of the administration of hypotonic maintenance fluids instead of 0,9% sodium chloride.
Hyponatremia can be associated with impaired level of conciousness,cerebral edema,seizures and vasospasm.
Half to three quarters of patients also developes hypokalemia commonly in association with the use of diuretics and hypocalcemia after SAH and require appropri-
ate replacement.
Hyperkalemia and hypernatremia occurs as well but less frquently. Therefore the volume status of each patient should be carefully reviewed by the usual clinical means before anesthesia is induced.
A CVP line or pulmonary artery flottation catheter may be required to guide fluid management.
Normoglycaemia should be maintained as hyperglycaemia is associated with worse neurologic outcome after brain injury. Dextrose containing solutions are best avoided and an insulin infusion may be needed to control stress-induced hyperglycaemia when present.
The Ringers lactate solution is hypoosmolar to plasma this may contribute to the formation of cerebral oedema when the blood brain barrier disruptured.The use of blood or blood products is indicated to maintain the Ht the low normal range of 30 to 35% as hemodilution enhances cerebral perfusion in humans.
Five percent albumin may confer some rheologic advantages by making red blood cells more slippery.
HYPERTENSION
Many patients with aneurysmal disease are basically healthy adults who may or may not have essential hypertension.
But evidence of hypertension has been found in as many as 80% of individuals with cerebral aneurysm and may be an
etiologic factor in the development of aneurysm.
Hypertension may represent a proper physiologic response, an attempt to maintain cerebral perfusion in the face of increased ICP resulting from blood,edema and hydrocepha-
lus.In this case it is essential to ensure the clinician's reflex treatment of blood pressure does not result in the ischemia that the organism is (wisely)trying to avoid.Clearly it is important to avoid severe spikes of hypertension especially in the patient with a freshly ruptured aneurysm.
If vasospasm is also present the treatment becomes complicated between to maintain adequate perfusion by hypervolemia and hypertension and rerupture of the aneurysm.
The choice drugs used are considered by availability ,familiarity,and concurent medical problems.For example nitroprusside,nitroglycerine,calcium channel blockers,and even hydralazine shoul be used with caution in the patient with increased ICP on the other hand NTG might be the
drug of choice in the patient with clinically significant coronary artery disease.Intravenous channel blockers such as nicardipine when available may be prefered if hypertension is to be treated in the presence of vasospasm.
Drugs that are alpha receptor agonists such a clonidine the theoretic advantage of providing some element of brain protection but are not currently available in a parenteral form that allows for intra operative supplementation.
The current favorite is labetalol, a combined alpha and beta receptor antagonist. In the hypertensive adult patient a dose of 10 to 20 mg given intravenously before the induction of anesthesia often helps minimized the blood pressure spike of laryngoscvopy and intubation without producing severe hypotension during the subsequent long period of neurosurgical preparation.
In the anesthetized patient it's prudent to administer a small labetalol dose such as 2,5 to 5mg and to wait about 5 minutes before a double dose is administered (unless the blood pressure requires a very quick and extensive reduction).
Other clinicians favor esmolol (0,5 to 1,0 mg/kg bolus) which has the advantage of an extremely short half life and can be used continuously as an infusion.
Preoperative administration of angiotensin converting enxyme(ACE) inhibitor such as captopril can also be used but with clonidine it may be a strugle to keep bloodpressure acceptably high after induction and before significant surgical stimulation. ACE inhibitors can now be used intravenously (enalapril 1,25 to 5,0 mg).
The over all goal is to avoid blood pressure elevation that thought cause or contribute to rupture of the aneurysm.
To be continued
0 comments:
Post a Comment