- Ghaly Neurosurgical Associates, Aurora, IL, USA
- Department of Anesthesiology, Advocate Illinois Masonic Medical Center, Chicago, IL, USA
- Department of Anesthesiology, John Stroger Cook County Hospital, Chicago, IL, USA
- Department of Anesthesiology, University of Illinois, Chicago, IL, USA
Ramsis F. Ghaly
Department of Anesthesiology, Advocate Illinois Masonic Medical Center, Chicago, IL, USA
Department of Anesthesiology, University of Illinois, Chicago, IL, USA
DOI:10.4103/2152-7806.97167Copyright: © 2012 Ghaly RF. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
How to cite this article: Ghaly RF, Candido KD, Sauer R, Knezevic NN. Complete recovery after antepartum massive intracerebral hemorrhage in an atypical case of sudden eclampsia. Surg Neurol Int 19-Jun-2012;3:65
How to cite this URL: Ghaly RF, Candido KD, Sauer R, Knezevic NN. Complete recovery after antepartum massive intracerebral hemorrhage in an atypical case of sudden eclampsia. Surg Neurol Int 19-Jun-2012;3:65. Available from: http://sni.wpengine.com/surgicalint_articles/complete-recovery-after-antepartum-massive-intracerebral-hemorrhage-in-an-atypical-case-of-sudden-eclampsia/
Background:Intracerebral hemorrhage is an infrequent but severe complication in pregnant women with hypertension.
Case Description:We describe an atypical case of a patient with no risk factors who developed sudden eclampsia and spontaneous intracerebral hemorrhage during the 34th week of pregnancy. She underwent successful emergent Cesarean section followed by craniotomy. Both intraoperative surveillance and postoperative magnetic resonance angiographic examination of the cerebral vessels failed to identify an aneurysm, arteriovenous malformation, tumor, or leptomeningeal disease.
Conclusion:We discuss the management of this case and review the literature regarding the threshold for which initiation of antihypertensive treatment is indicated in pregnant patients.
Keywords: Eclampsia, intracerebral hemorrhage, pregnancy
The incidence of preeclampsia–eclampsia in the USA is 7–10%.[
We present a unique case of sudden eclampsia and intracerebral hemorrhage (ICH) during an otherwise normal pregnancy.
A-32-year-old female, G2P1 at 34 weeks of gestational age, with regular prenatal care, and with no history of headache, proteinuria, or hypertension on previous visits presented to the OB clinic for a routine follow-up visit. On the day of the visit, her BP was 150/90 mmHg, thought to be due to anxiety, and she was admitted to the OB ward for observation. Hypertension was considered borderline and was intermittently treated by IV labetalol, but without resolution. Approximately 10 h after admission, she started to complain of diffuse headache, nausea, vomiting, and epigastric pain. The work-up was negative for other findings of preeclampsia (liver function test, proteinuria, uric acid). During the course of the admission, the BP ranged between 150/90 and 180/110 mmHg, and her headache symptoms increased. The patient's condition progressed to a sudden onset of a focal seizure on the left side, which progressed to generalized tonic–clonic seizures, and she suddenly became unresponsive. At that point, magnesium sulfate was administered (4 g loading dose over 20–30 minutes) with a maintenance dose of 1 g/h. One gram of phenytoin was administered to control the seizure. Immediate blood analysis showed the following: a drop in platelets to 116,000/μl; elevated liver function tests alanine transaminase (ALT; 866 units/L) and aspartate transaminase (AST; 971 units/L); uric acid of 6.2 mg/dl; and alkaline phosphatase of 169 mg/dl. Arterial blood gases showed a metabolic acidosis (pH = 7.1, base deficit= -14). The diagnosis of eclampsia was made and the decision to deliver the fetus by an emergency Cesarean section was determined. The airway was secured using a rapid sequence technique, and a healthy infant was delivered under general anesthesia with Apgar scores of 8 and 10 at 1 and 5 minutes, respectively. Postoperatively, the patient remained comatose, and the Glasgow Coma Scale (GCS) revealed a score of 4 (1 + 2 + 1), 1 h after the Cesarean section. Ninety minutes later, she demonstrated a decerebrate posture with non-reactive pupils (3 mm diameter). At this point, the OB team considered it to be a structural brain injury. A non-contrast computed tomography (CT) scan revealed an intracerebral hematoma [
Pre-operative CT scans of the head (a) axial view showing dissecting intraparenhymal right frontal hematoma and absence of brain sulci indicating extensive brain swelling (b) axial view showing extensive intraventricular hemorrhage, 1 cm midline shift, subarachnoid hemorrhage and brain swelling (c) axial view showing 4th ventricular hemorrhage and prominence of temporal ventricular horns indicating obstruction
Post-operative CT scans of the head (a) axial view showing resolution of ventricular and cerebral hemorrhage, placement of right intraventricular drain and resolution of midline shift (b) axial view represents successful resolution of dissecting evacuation of right frontal intracerebral hemorrhage
In the ICU, the intracranial pressure (ICP) was normalized to less than 10 mmHg, and supported hemodynamic and ventilatory measures were weaned off over the next couple of days. The patient opened her eyes and started responding to commands by the third postoperative day. Liver function tests and the coagulopathy normalized by postoperative day 5. Postoperatively, the pupils were increasingly reactive over the next 7 days. The GCS was 9 (1 + 3 + 5), and platelet transfusions were required to maintain the platelet count to ≥100,000/μl. The trachea was extubated on postoperative day 7. In less than 3 weeks, the patient was transferred to rehabilitation services where physical, occupational, and speech therapies were conducted for 4 weeks. In the outpatient clinic, all antihypertensive medications (angiotensin-converting-enzyme [ACE] inhibitor, calcium channel blocker, and vasodilator) were weaned off within 2 months. The patient regained all her intellectual functions, personality, and various social activities within 6 months. She was also weaned off all seizure medication, and 3 years later she was deemed to have regained a full cognitive recovery.
This case illustrates an atypical presentation of a patient with uneventful prenatal care for the first 34 weeks, who developed a sudden onset of hypertension and rapid progression within hours to seizure and ICH. Ideally, CT scan should have been ordered and concomitant Cesarean section and craniotomy performed. However, the differential diagnosis of ICH was not in the armamentarium of the OB team at that time. The elevation of BP was considered borderline by the OB team and the seizure was underplayed early, until the patient did not awaken from anesthesia and the anesthesia team examined the pupils and decided to get a CT scan. This case is unique because the patient had a complete recovery by employing aggressive medical and surgical intervention for the ICH, despite a poor preoperative neurological status (GCS 4) and a 7-h delay of definitive diagnosis and decompression.
Eclampsia is the most common cause of ICH associated with pregnancy,[
Cerebrovascular malformations are evident in 20–67% of patients with pregnancy-related ICH.[
To the best of our knowledge, ICH in this case was due to the escalation in the BP, with no other preeclampsia findings and normal prenatal care. The brief BP rise led the OB team to believe that the rise of BP was related to anxiety. The sequence of events began with hypertension, followed shortly thereafter by development of severe preeclampsia, eclampsia, and ICH. A sudden increase in BP can lead to hypertensive encephalopathy in pregnant women without a history of hypertension, even with a diastolic BP around 100 mmHg. Clinical manifestations of severe headache, visual disturbances, seizure, and coma may rapidly follow.[
Additional studies in patients with preeclampsia/eclampsia found a moderate decrease in cerebrovascular resistance together with increased cerebral blood flow velocities, causing cerebral hyperperfusion,[
Even though there are reports of simultaneous Cesarean section and craniotomy,[
This case emphasizes that even short time hypertension should be treated aggressively to prevent ICH. Even though eclampsia can cause seizures with no ICH, OB and family practitioners should be suspicious about ICH. The prompt intervention of a multidisciplinary team (obstetric, neurosurgery, and anesthesiology) is required to ameliorate the devastating effects of eclampsia and ICH.
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