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��ࡱ�>��	�����������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������[�	���Sbjbj����	4lΐΐhK+���������������������8+Do$�t&f���������%�%�%�%�%�%�%$�'�|*N&������&�����.&\"\"\"��	�����%\"��%\"\"?$�$��������r��  �W$�%D&0t&_$,�*� ��*�$�*��$T��\"�����&&\"���t&�������������������������������������������������������������������������*����������	�:	INTRACEREBRAL HAEMORRHAGE IN A PREGNANT WOMAN WITH SUDDEN ONSET AND RAPIDLY DETERIORATED PREECLAMPSIA; A CASE REPORT 
*Mbamara S.U, *Ogbuagu L.C, **Mbah I.C
*Department of Obstetrics & Gynaecology Abuja Clinics Limited Maitama
**Department of Radiology, Abuja Clinics Limited Maitaima

Abstract 
Stroke is major contributor to morbidity and mortality during pregnancy and the puerperium. Intracerebaral haemorrhage, which is bleeding within the cerebral parenchyma as a result of rupture of a blood vessel, is the second most common type of stroke after ischaemic stroke 1. (Feigin VL, Lawes CM,). We report a case of intracerebral haemorrhage that was suspected to have occurred shortly before Caesarean section due to severe pre-eclampsia and imminent eclampsia in a woman with normal prenatal care. She recovered completely without any neurological deficit.

Key words: preeclampsia, intracerebral haemorrhage, full recovery, stroke

CASE REPORT 
A 30-year-old primigravid black woman in her 38th week of gestation presented to the accident and emergency department of Abuja Clinics Limited on the 27/02/2013 at 8pm with complaints of diffuse headache, dizziness and epigastric pain, all of about 12 hours duration. She also reported a slight reduction in her urine output. There was no history of visual disturbances, loss of consciousness or convulsion. 
The positive findings on physical examination in the emergency room were generalized anasarca, severely elevated blood pressure of 220/110mmHg and epigastric tenderness. She was fully conscious and alert with no neurologic deficit. Obstetric examination revealed a symphysio-fundal height of 36cm, longitudinal lie, cephalic presentation and the fetal heart rate was 148 beats per minute. Other aspects of the systemic examination were unremarkable. Urine dipstick analysis showed significant proteinuria (4+). 
Her pregnancy had been relatively uneventful until 48 hours prior to her presentation at the accident and emergency when she was noticed to have had mildly elevated blood pressure (140/90mmHg) during a routine prenatal visit but her urinalysis dipstick test was normal. 
 She booked for prenatal care at 13weeks gestation and had made regular prenatal care visits. At booking, her pulse rate was 70 beats per minute, blood pressure was 120/80mmHg and her weight was 56.3kg. Obstetric ultrasound scans and urine analysis using dipstick done throughout the prenatal period were normal.
Her clinical history revealed repeated complaints of palpitation which was extensively evaluated on several occasions by different Cardiologists but no cardiovascular abnormality was detected. The initial laboratory work-up at the ER showed thrombocytopenia (platelet count of 72,000/ul), haematocrit of 37%; hemoglobin of 12.2g/dl, Clotting time of 5.54min and INR of 1.19. There was slightly elevated total serum bilirubin (2.2mg/dl) but normal level of liver enzymes. The serum electrolyte, urea and creatinine values were essentially normal. 
A diagnosis of severe preeclampsia with imminent eclampsia was made. The patient, her husband and relatives were all counseled extensively on the diagnosis and management options. Stabilization of the patient was commenced immediately. 
Parenteral antihypertensive therapy with parenteral hydrallazine and Seizure prophylaxis also with magnesium sulfate using the regimen as proposed by Pricharad was instituted.  Approximately one hour after admission, and while being stabilized for delivery, she developed sudden alteration in her level of consciousness and mental status. She became disorientated and confused and could recognize neither her husband nor mother. 
Emergency lower segment Caesarean section was performed under spinal anesthesia leading to the delivery of a healthy 2.5kg male infant with Apgar scores of 8 and 10 in the 1st and 5th minute respectively. 
She was admitted into the intensive care unit (ICU). In the immediate post-operative period, she remained drowsy and confused with persistent inappropriate speech and altered consciousness. There was a continuous drop in her Glasgow Coma Score. However, there was no obvious lateralizing sign, visible cranial nerve deficit or seizure. Fundoscopy showed evidence of papilloedema. CT scan of the brain was done due to lack of improvement in her mental status within the first few hours after surgery because of suspected brain injury. 
The non-contrast brain CT scan revealed intracerebral and intraventricular haemorrhage within the left parieto-temporo-occipital region with extension into the subarachnoid space. (FIGURE 1)
Emergency neurosurgical consultation was sorted. The neurosurgical unit opted for conservative management instead of emergency craniotomy because of worsening thrombocytopenia, uncontrolled hypertension and the high risk of damage to adjacent normal brain tissue from an anticipated possible reactionary bleed.
She received supplemental oxygen via nasal prongs and carefully titrated intravenous hydrallazine. Magnesium sulfate was continued for the next 24 hours post operatively with careful monitoring of her urine output, respiratory rate and patellar reflex/knee jerk. She was also treated with analgesics, intravenous fluids and antibiotics.
Cerebral decompression was immediately initiated with intravenous mannitol infusion for 24 hours. The patient was also commenced on amlodipine via a nasogastric tube because of worsening blood pressure control despite IV hydrallazine. She was nursed at 30 degrees head-up position and was later given antioxidants (vitamins C & E). Her Glasgow Coma Score improved to 14 by the first 24 hours after delivery.
Forty fives (45) hours after surgery, the patient became very restless and aggressive with incoherent speech. She was then given parenteral phenobarbitone for 48 hours at 60mg IV q8hours. 
Serial post-operative hematological profiles revealed a persistent decline in her haematocrit (to 22%) as well as a further drop in her platelet count (to 39,000/ul). She was subsequently transfused with packed cells which elevated her hematocrit to 31%. Thrombocytopenia was treated by administering platelet concentrates. Repeat brain CT imaging done on the third day showed some resolution of the intraventricular hematoma, organization of the left intracerebral hematoma, effacement of the sulci and gyri and persistence of the subarachnoid hemorrhage. CT angiography did not suggest any intracranial aneurysm or arteriovenous malformations (AVM).
At this point, the option of surgical intervention (craniotomy and evacuation of accessible intracerebral hematoma) was offered by the neurosurgeon but was declined by the patient�s relations.
Four days after the Caesarean section, the patient developed high grade fever and was empirically treated for malaria with a full course of oral artemisinin-based combination therapy antipyretic. Physiotherapy was done throughout the period. There was persistent papilloedema, restlessness, headache and vomiting till the 8th day. 
Repeat hematological profiles done on the 6th post-operative day showed resolution of the anemia and thrombocytopenia with hematocrit and platelet count of 31% and 185,000/ul respectively. Serum potassium also normalized (3.7meq/L) by the 7th post-operative day. The dose of oral amlodipine was increased to 10mg PO daily because of persistent high blood pressure spikes.
There was severe constant headache and vomiting. A third brain CT imaging showed resolution of the intraventricular hematoma but persistence of the intracerebral hematoma with surrounding edema which was creating a pressure effect. The patient had another 24-hour course of cerebral decompression with mannitol infusion and was commenced on oral phenobarbitone. Surgical intervention was again declined by the patient�s relations. Intermittent bolus doses of diazepam and chlorpromazine were administered to control aggressive episodes. She was continued on conservative management until the twenty second day when she was discharged in a stable condition to continue further management as an outpatient. 




Fig1




DISCUSSION
Stroke is not only a leading cause of disability worldwide but also the second leading cause of death in the general population 1, 2. The overall incidence of ischaemic stroke during pregnancy is low (3.5 � 5 per 100,000 pregnancies) in developed world with the majority of these events occurring late in pregnancy and the post partum period3.  However when considering stroke in the young people, it has been estimated that stroke related to pregnancy accounts for 12 to 35% of stroke events in this otherwise low risk populate3 (Feske S).  The overall incidence of stroke in pregnancy is low and occurs primarily in late pregnancy and peuperium. The incidence of haemorrhagic stroke is similar to ischaemic stroke but intracerebral haemorrhage has a higher maternal mortality rate and has been estimated to account for 5% - 12% of the overall maternal mortality 4.
The aetiology of stroke in pregnancy is generally similar to that of stroke in the general population with the exception of conditions which occur only in pregnancy. Stroke aetiology includes age above 35years, cerebral aneurysm, arteriovenous malformation (AVM), cerebral amyloid, angiopathy and vasculaopathies. Other  aetiological factors are antiplatelet(s), anticoagulant medications, exertion, tobacco use, cocaine use, family history of SAH, female sex, African origin and connective tissue disorder It can also follow trauma and hypertension. Hypertension which is the commonest risk factor for stroke in the general population is also a component of pre-eclampsia/eclampsia that is the most common cause of stroke in pregnancy. 4. It has been noted that preeclampsia is associated with a fourfold increase in stroke during pregnancy5. Researchers have noted an increased risk of stroke both in subsequent pregnancy and later in life with diagnosis of preeclampsia during pregnancy, 6,  7. Stroke associated with pregnancy however are also associated with conditions which occur only in pregnancy. These include preeclampsia, eclampsia, amniotic fluid embolism, peripartum cardiomyopathy and post partum angiopathy. The risk of intracerebral haemorrhage (ICH) has been postulated to be highest in the post partum period 7, 8, 9. 
 The clinical features in our patient that lead to the suspicion of stroke include persistent headache, altered consciousness, vomiting, incoherent speech, worsening Glasgow coma score. The diagnosis of stroke is usually considered in patients who presented with acute onset of focal neurological changes in the absence of an alternative etiology. Rarely some patients may present with non focal symptoms like headache and altered consciousness as did Mrs. A. S.  
The investigations necessary to establish the diagnosis of intracerebral haemorrage include CT scan, CT angiography and MRI.  The C T scan and CT angiography were used both in the diagnosis, assessment of the severity of the neurological injury, evaluation for causes and progression of the disease condition � bleeding and rebreeding. The safety of neuroimaging in pregnancy has been a subject of great controversy among many obstetricians.   However obtaining an early non contrast computerized tomography (with appropriate shielding or magnetic resonance imaging of the brain will greatly facilitate diagnosis with minimal risk to the fetus during pregnancy. 
The definitive management of pre-eclampsia is aimed at the delivery of the fetus and placenta, antihypertensive and seizure prophylaxis and treatment.  Magnesium sulphate was used for seizure prophylaxis. It has also been confirmed to be effective in the treatment of eclampsia and reduction of the rate of eclampsia and its complications in pre-eclamptic patients. 
Caesarean section under spinal anaesthesia was our preferred mode of delivered as general anaesthesia has been reported to be associated with increased risk of stroke when compared with neuraxial anaesthesia in pre-eclamptic women15.  
Early emergency neurosurgical consultation is necessary to assess the nature, severity and location of injury, management options, need to establish devices to monitor intracranial pressure (ICP), brain temperature and brain oxygen, and patient suitability for decompression. Elevated intracranial pressure (ICP >20mmHg) may lead to herniation and death.  Interventions that were done to reduce ICP include sedation to a calm motionless state, optimizing cerebral perfusion by giving intranasal oxygen, and mannitol infusion. Other interventions that could be done are infusion of hypertonic saline, hyperventilation, hpothermia, paralysis and induction of coma with medications.  Mannitol is also effective in the management of cereal oedema which may result from cerebral ischaemic infarction or contusion. 

Continuous assessment of the degree of consciousness using the Glasgow coma scale (GCS) is essential in the management of stroke.  Other assessment methods that can be used include the NHN stroke scale and Disease specific scale score using the Haunt and HUSS scale. 

Fever as noted in our patient is a common complication of intracranial haemorrhage. The risk factors for fever include intraventricular blood, blood in pituitary, damage to anterior hypothalamus and ventricular drainage catheter. Most often infectious sources are not detected. It has been noted that the greater the burden of fever the worse the outcome (51). Other complications that should be anticipated include myocardial stunning, pulmonary oedema and functional and cognitive disorders.
Antihypertensive agents are necessary to lower the blood pressure, reduce blood extravasation into the cerebral tissue as sustained severe hypertension is associated with haematoma growth and worsen clinical outcome. However caution must be applied in the use of antihypertensive agents as blood pressure reduction may lead to reduced cerebral perfusion, cerebral ischaemia and infarction.  
Where the patient is on anticaogulant this should be stopped and reversed. She received platelet and red cell transfusion. Red cell transfusion is shown to be associated with reduced mortality. Where seizure is present or where there is unexplained worsening level of consciousness monitoring with continuous electroencephalogram is necessary.  
She made a routine antenatal visit  with blood pressure of 140/90mmHg and urinalysis showing protein one plus and within 28 hours presented in the accident and emergency department with severe blood pressure of 240/190mmHg and clinical signs of imminent eclampsia. The sudden, rapid and dramatic deterioration of the hypertensive state of the patient may suggest the need for obstetrician(s) to consider an early commencement of antihypertensive(s) and a more aggressive treatment of hypertension in women with mild hypertension in pregnancy to prevent/ guild against intracerebral heamorhage/stroke.    This may suggest that any level of rise in blood pressure during pregnancy can lead to hypertensive encephalopathy in a pregnant woman without any previous history of hypertension. Similar assertion has also been also been collaborated in another case report11. 
The prognosis of intracerebral haemorrhage has been noted to be poor with a case fatality at 1 month being over 40%. In the same vein only a small percentage of those who survive reach independent life after 1 year. However our patient recovered completely probably due to early diagnosis and immediate institution of critical care.  The pregnant woman is vulnerable to delayed diagnosis and complications in that many diagnostic evaluations are avoided during pregnancy due to the concern of causing harm to the fetus.  
 There is therefore the need for increased vigilance in hypertensive management in preeclamptic patients.  Intracerebral haemorrhage occurring in the background of preeclampsia/eclampsia should be managed closely with antihypertensives, antiseizure medications preferably magnesium sulphate12, 13, 14. 
Routine cardiovascular risk reduction counseling should be provided for ante natal women in general but more specifically women with the risk and or history of pre-eclampsia.  

Conclusion
Pregnancy associated stroke although a rare /uncommon phenomenon is an important cause of morbidity and mortality among pregnant women.  There should be a high index of suspicion among the obstetricians for early diagnosis. Multidisplinary management   should be the bedrock of care. Adequate follow up and rehabilitation should be an important component of the care. Obstetricians should increase their use of radiological investigations in the management of neurological conditions in pregnancy. 

References
Feigin VL, Lawes CM, Benneth DM , Barker-Collo SL, Parag V. Worldwide stroke incidence and early case fatality reported in 56 population based studies; a systematic review. Lancet Neurol 2009;   8(4):355 � 369. 
Feigin VL. Stroke in developing countries: can epidemic be stopped and outcome improved? Lancet Neurol 2007;6(2): 94 � 7
O�Donnell M, Yusuf S. Tackling the global burden of stroke: the need for large � scale international studies. Lancet Neurol 2009; 8(4):306 � 7 
Feske S, Stroke in pregnancy. Semin Neurol 2007; 27(5):442 � 452. 
James AH, Bushnell CD, Jamison MG, Meyers ER. Incidence and risk factors for stroke in pregnancy and puerperium. Obst Gynecol. 2005; 106(3):509 � 516.  

Josephson CB, Frantzias J, Samarasekera N, Al-Shahi Salman R.(2010). The persisting burden of the intracerebral haemorrhage: can effective treatment be found? PloSMed ;7:e1000353 . doi:10.1371/journal.pmed.1000353
Brown DW, Ducker N, Jamieson J D, Cole JW, Wozniak MA, Stern JB, Giles WH, Kittner JS. Preeclampsia and the risk of Ischaemic stroke among young women: results from the stroke prevention in young women study. Stroke 2006; 37(4): 1055 � 1059.
Bellamy L, Cesas JP, Hiagorani AD, Williams DJ. Pre eclampsia and risk of cardiovascular disease and cancer in later life; systematic review and meta-analysis. BMJ.2007; 335(7627): 974 
Kittner SJ, Stern BJ, Feeser BR, Hebel R, Nagey DA, Buchlolz DW, Earleu CJ, Johnson CJ, Macko RF, Sloan MA, Wityk RJ, Wozniak MA. Pregnancy and the risk of sroke. N Engl J Med. 1996; 335: 768 � 774. 
Bateman BT, Sihumacher HC, Bushnell CD, Pile-Spellman J, Simpson L, Sacco RL, Berman MF. Intrcranial haemorrhage in pregnancy; frequency, risk factors and outcome. Neurol 2006 August8; 67(3):424 � 9.
Ransis F Ghaly,  Kenneth D Candido, Ruben aner, Nebojsa Nick Knezenic.  Complete recovery after antepartum massive intracerebral heamorrhage in an atypical case of sudden eclampsia. Neurol Int 2012; 3: 65 
Treadwell S, Thanri B, Robinson T. Stroke in pregnancy and the peurperium. Postgrad Med J. 2008; 84(991):238 � 245.
Duley L, Hendersen, Smart DJ, Chou D, Magnesium Sulphate verses Phenytoin for eclampsia. Cochrane data base Syst 2010; 10:CD00128
Deshaies EM, Boulos AB, Drazin D, Popp AJ. Evidence � based Pharmatherapy for cerebral spasm. Neurol Res 2009; 31(6):1274 � 1282
Huang CT, Fan YC, Tsain FS. Differantial impacts of modes of anaesthesia on th e risk of stroke among preeclamptic women who undergo caesarean delivery a prospective study. Br J Anaesth 2010 Dec 105(67)818 - 26













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