Intracranial hemorrhage(ICH) cause catastrophic complica
tions during pregnancy and is considered an important non
obstetric of maternal morbidity and mortality.
Generally SAH resuls from cerebral aneurysmal rupture or bleeding from arteriomalformation(AVM).
SAH has been reported to be the third leading the cause of non obstetric maternal morbidity.
About 50% of the patients who present with SAH during pregnancy have a ruptured AVM,as compared with 10%
in the non pregnant group.
In non pregnant patient,SAH is more commonly caused by the rupture of an intracerebral aneurysm than by AVM.
In pregnancy these occur with equal frequency.
SAH from an aneurysm during pregnancy usually occurs in multiparous women between 25 to35 years of age,where
as bleeding from AVM occurs in patients between 18 to 25 years of age and parity is not a factor.
The risk of rebleeding after a hemorrhage during the same pregnancy is 27%.
AVMs tend to rupture at any stage of pregnancy but most commonly between 20 weeks of gestationn and 6 weeks
postpartum.
The relationship of aneurysmal hemorrhage to stage of pregnancy has been reported as follows :
First trimester 6%,second trimester 31%,third trimester 55% and postpartum 86%.
The tendency to rupture may be related to hemodynamic,
hormonal and coagulation changes that occur during
the third trimester including the increase of blood volume.
PATHOPHYSIOLOGIC CEREBROVASULAR ACCIDENT(CVA)
during pregnancy :
Arterial aneurysm are the most common cause of non traumatic SAH and the spontaneous of an aneurysm has been temporally related to the use of cocaine,booth
cocaine and alcohol abuse have been linked to intracereb
ral hemorrhage. Studies indicate that 2 to 9% of pregnant women are heavy drinkers and about 8 to 17% of pregnant women abuse cocaine.
Robinson reported a ruptured aneurysm in ascociation with severe preeclampsy and Amios reported a relation
ship between pregnancy associated hypertension and ruptured cerebral aneurysm.
An aggressive treatment regiment of antihypertensive is indicated when blood pressure rise above 160/110 mmHg as chronic hypertension are at increased risk of ruptures of intracranial aneurysm.
The onset of aneurysmal bleeding has also occured during an elective caesarean section. Vasospasm is frequent complication of SAH.
Vascular compression and/or vasospasm may produce ischemic and infarction in 5 to 7 days after the initial SAH and cause delayed neurologic deficit.
NEUROLOGIC ASSESSMENT :
The clinical feature of CVA in pregnant women are not any different than in the general population.
The initial investigation needs to be prompt and thorough in order to differentiate CVA from other disorders pre
senting with severe headaches associated with neurologic signs.
The differential diagnosis includes pre eclampsy,chronic hypertensi,seizure disorder,intracranial tumors,abscess and other space ocupying lesions,saggital sinus thrombo
sis,meningitis,encephalitis,demyelinating disease,cerebral arterial occlussive disease and moya moya disease all of which may worsen during pregnancy and are associated with intracerebral hemorrhage.
Pituitary apoplexy,abuse of cocaine and alcohol,dissemi
nated intravascular coagulation,ectopic endometriosis,
subacute bacterial endocarditis,and choriocarcinoma
may also produce symptom complexes that are indis
tinguisable from ICH and should be included in the differential diagnosis.
The clinical examination after SAH may reveal fever,
nuchal rigidity,and high blood pressure(BP).
There may be focal neurologic deficits caused by hemato
ma hydrocephalus,ischemia and recurrent bleeding,inclu
ding aphasia,hemiparesis and hemianopsia.
Seizures may be the presenting symptom in some cases of SAH from AVM,
Hypothalamus irritation from SAH may cause a variety of systemic abnormalities.
Contraction of intravascular volume or secretion of atrial natriuretic hormone lead to electrolyte imbalances.
SAH may also mimic eclampsy especially as severe hypertension and protenuria may develop after SAH.
PHYSIOLOGIC CHANGES DURING PREGNANCY :
Pregnancy has a stimulating effect on aneurysmal growth especially during the third trimester.
There is an increased incidence of rupture during this period. The hemodynamic stress of increased blood volume ,heart rate,cardiac output and stroke volume,
pregnancy induced hypertension in the third trimester and hormonal alteration in pregnancy which cause changes in the wall of the arteries and vein may all contribute to the increased risk of of intracerebral lesions during pregnancy
The hemodynamic alteration of pregnancy do not,howe
ver,alter CBF or the CMR for O2. As such any factore that reduce perfusion pressure or increasevascular resistance will adversely affect placental perfusion with concequent ill effect on the fetus.
Maternal hypotension should be avoided during operation.
Pregnancy itself causes a progressive increase in minute ventilation and decrease in functional residual capacity (FRC).Changes in minute ventilation,the mechanical
effect of possitive pressure ventilation and decrease in the PaCO2 may reduce placental blood flow to the fetus.
Respiratory alkalosis shift the oxygen Hb dissociation curve to the left and increases the affinity of maternal Hb for oxygen thereby fetal oxygen supply.
Hypocapnia also reduces uterine blood flow with
attendant fetal hypoxia and acidosis.
Maternal PaCO2 should therefore be maintained at about 30 mmHg.
to be continued
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