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Year : 2016  |  Volume : 17  |  Issue : 1  |  Page : 25-28

Anesthetic concern during cesarean delivery in patient with ruptured cerebral arteriovenous malformation

Department of Anaesthesiology, Dr. S N Medical College, Jodhpur, Rajasthan, India

Date of Submission05-Apr-2016
Date of Acceptance22-Apr-2016
Date of Web Publication17-Jun-2016

Correspondence Address:
Rakesh Karnawat
Near Mohammedi Masjid, Hanuman Ji Ki Bhakhari, Nai Sarak, Jodhpur - 342 001, Rajasthan
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0973-0311.183571

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Vascular malformations of the brain are a rare cause of intracranial hemorrhage during pregnancy. The presentation of arteriovenous malformations during pregnancy is usually a result of hemorrhage following rupture. Once hemorrhage occurs, it accounts for 5–12% of all the maternal deaths and remains the third most common nonobstetric cause of maternal morbidity. Successful anesthetic management during cesarean delivery requires close monitoring to address both the varying maternal and fetal needs. The fundamental aims are to maintain oxygenation and stable systemic, cerebral, and placental hemodynamics and to avoid increase in intracranial pressure.

Keywords: Arteriovenous malformation, intracranial hemorrhage, pregnancy

How to cite this article:
Karnawat R, Mohammed S, Gupta S, Paliwal N, Agarwal M. Anesthetic concern during cesarean delivery in patient with ruptured cerebral arteriovenous malformation. Indian Anaesth Forum 2016;17:25-8

How to cite this URL:
Karnawat R, Mohammed S, Gupta S, Paliwal N, Agarwal M. Anesthetic concern during cesarean delivery in patient with ruptured cerebral arteriovenous malformation. Indian Anaesth Forum [serial online] 2016 [cited 2023 Jun 1];17:25-8. Available from: http://www.theiaforum.org/text.asp?2016/17/1/25/183571

  Introduction Top

Cerebral arteriovenous malformations (AVMs) are present in approximately 1:10,000 of the general population and more than 50% of them present with intracranial hemorrhage (ICH).[1] Intracerebral hemorrhage occurs more commonly although subarachnoid hemorrhage (SAH) and intraventricular hemorrhage can also occur.[2] It typically appears between the age of 25 and 45 years, with a peak incidence in the 4th decade.[3] Other manifestations of AVMs include seizures, focal neurological deficits, headache, hydrocephalus, and rarely congestive heart failure.[4]

Incidence of ICH during pregnancy and puerperium varies from 6 to 31 per 100,000 deliveries.[5],[6] Vascular malformations of the brain are a rare cause of ICH including both spontaneous intracerebral hemorrhage and SAH, during pregnancy and puerperium and estimated at 1–10 per 100,000 pregnant women.[7] Other causes are eclampsia, coagulopathy, arterial dissection, intracranial venous thrombosis, pituitary apoplexy, and bleeding into metastases from choriocarcinoma.[8] When ICH occurs, both the mother and the fetal well-being is affected and accounts for 5–12% of all the maternal deaths and remains the third most common nonobstetric cause of maternal morbidity.[9]

Due to the rarity of this condition, no definitive guidelines exist regarding the choice of anesthetic technique for cesarean section (CS) in such patients, but maternal cardiovascular stability should be considered during selection of anesthetic technique. With this case report, we described anesthetic management of a pregnant patient with ruptured AVM posted for CS.

  Case Report Top

A 32-year-old primipara with 5′2″ height and 60 kg weight presented to the emergency department at 38 weeks of gestation with sudden onset of headache along with severe vomiting and left hemiparesis since morning. It was not associated with loss of consciousness or seizures. Medical history was significant for such migrainous headaches on and off in the parietal area since the 7th month of pregnancy. Her prenatal course was uneventful except for a few episodes of vomiting throughout pregnancy.

On examination, the patient was conscious and cooperative with blood pressure (BP) of 170/110 mmHg, pulse rate (PR) of 120/min, and oxygen saturation of 99%. On neurological examination, power in the left upper and lower limb was Grade II. Neurosurgery consultation was sought and the patient was advised for magnetic resonance imaging of the brain with cerebral angiogram and fundus examination. Magnetic resonance angiogram revealed a bunch of dilated and tortuous vessels suggestive of AVM in the right parietal lobe with hemorrhagic component [Figure 1]. Venous drainage appeared to be in superior sagittal sinus through prominent cortical veins. Fundus examination revealed bilateral papilledema. Obstetrician planned to terminate the pregnancy by CS after medical stabilization of the patient. Measures to reduce intracranial pressure (ICP) with intravenous (IV) mannitol (60 g followed by 20 g every 8 h) and IV steroid (dexamethasone 8 mg every 6 h) and seizure prophylaxis with IV phenytoin (900 mg over 30 min followed by 100 mg every 8 h) were started. Definitive treatment of AVM was postponed till the termination of pregnancy.
Figure 1: Magnetic resonance angiogram showing bunch of dilated and tortuous vessels in right parietal lobe

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All the routine investigations were performed and reports were unremarkable. The sample was also sent for blood grouping and crossmatching. Aspiration prophylaxis with IV ranitidine (50 mg) and sodium citrate suspension (30 ml) was given.

After medical stabilization, the patient was taken to the operation room (OR). General anesthesia (GA) was planned considering raised ICP. In OR, continuous monitoring such as electrocardiography, pulse oximetry, and capnography was applied and baseline vitals were recorded. Arterial line was secured under local anesthesia (LA) in the right radial artery with 20 gauge IV cannula for invasive BP monitoring. The patient was premedicated with IV fentanyl 60 mcg, magnesium sulfate 2 g, and midazolam 1 mg, 15 min before induction. Preoxygenation with 100% oxygen (O2) was done for 3 min. Induction was done with IV propofol 120 mg with continuous cricoid pressure. Muscle relaxation was provided with IV rocuronium 60 mg. Hemodynamic stress response to laryngoscopy was prevented using IV nitroglycerine (NTG) (30 mcg/min) and IV lignocaine (60 mg) before intubation. The trachea was intubated with a 7.0 mm inner diameter cuffed endotracheal tube in the first attempt without any difficulty. A left lateral tilt (to decrease pressure on the inferior vena cava) and 15° reverse Trendelenburg tilt (to decrease ICP) was applied to the operation table. The patient was mechanically ventilated with a tidal volume of 8 ml/kg and a respiratory rate sufficient to maintain end-tidal CO2 around 30 mmHg. Anesthesia was maintained with nitrous oxide and O2 (60:40) mixture and continuous infusion of propofol (100 mcg/min). After delivery of the baby, IV oxytocin 5 unit bolus and 5 units in 500 ml 0.9% NaCl infusion were started. IV fentanyl 60 mcg was repeated following the delivery. Apgar scores were 8 and 10 at the 1st and the 5th min, respectively. NTG infusion continued and titrated accordingly to maintain mean arterial pressure (MAP) around 70 mm Hg so as to maintain adequate ICP and uteroplacental perfusion.

At closure, the LA agent was infiltrated along the suture line for postoperative analgesia. Following completion of the surgical procedure, muscle relaxation was reversed with IV neostigmine 2.5 mg and IV glycopyrrolate 0.5 mg. The trachea was extubated when the patient responded to verbal stimulation. There was neither any significant hemodynamic change nor any further neurological deterioration in the OR and postanesthesia care unit. Postoperative analgesia was maintained with 1 g of IV paracetamol every 6 h and IV tramadol 50 mg sos. Patient was discharged on day 6 postpartum, clinically stable and referred for the interventional neuroradiology consultation for definitive management of AVM.

  Discussion Top

AVMs are defects of the circulatory system comprising snarled tangles of arteries and veins. The absence of capillaries creates a shortcut for blood to pass directly from arteries to veins. Although their cause is not known, they are generally believed to arise during embryonic development or soon after birth.[10] Brain AVMs are of special concern because of the damage they cause when they bleed. AVM damages the brain through three basic mechanisms: By reducing the amount of O2 reaching neurological tissues, by causing bleeding (hemorrhage) into surrounding tissues, and by compressing or displacing parts of the brain.[10]

Previously, it was thought that pregnancy increases the risk of hemorrhage from an AVM due to the increased blood circulation that occurs during pregnancy. Robinson et al.[11] evaluated 24 cases of AVM and concluded that a woman who has had AVM would have 87% chances of developing ICH during pregnancy. While recently Horton et al.[9] studied 451 women with AVM and concluded that pregnancy does not increase the risk of bleeding of an AVM, estimating it at 3.5% in pregnant versus 3.1% in nonpregnant female. Commonly, hemorrhage due to AVM in pregnant women occurs at 15–20th weeks, but it may occur at any stage including during labor or in the puerperium.[12] Although not all AVMs bleed during pregnancy, it is recommended to delay pregnancy until after the AVM has been completely treated.[13]

Although the best strategy for management of symptomatic AVM during pregnancy is not yet defined, the risk–benefit analysis seems not to support the elective treatment of AVM during pregnancy.[2] It is believed that uterine contractions of labor and the Valsalva effect of vaginal delivery are accompanied by dramatic and transient increases in venous pressure, cardiac output, and ICP, so most clinicians advocate delivery by CS.

Osmotic diuresis with mannitol was used for decreasing ICP. Animal and human studies have proposed that mannitol causes fetal hypovolemia and electrolyte imbalance. However, there is no evidence of mannitol 0.5–1 g/kg having any significant effect on fetal fluid balance.[14] Dexamethasone was used to decrease cerebral edema. Its acute use may be safe for fetus, but chronic use may result in fetal adrenal suppression and fetal hypoadrenalism, particularly during the third trimester.[15]

There are very few published reports of anesthetic management for pregnant women with symptomatic AVM.[1], 7, [16],[17],[18],[19] Successful anesthetic management requires close monitoring to address both the varying maternal and fetal needs. The fundamental aims are to maintain oxygenation and stable systemic, cerebral, and placental hemodynamics and to avoid increase in ICP.[20] The regional anesthetic technique could be preferred because it avoids the hemodynamic stress associated with laryngoscopy, intubation, and extubation during GA.[16],[17] In our case, because of the raised ICP, we preferred GA and hemodynamic stress was prevented using NTG, fentanyl, lidocaine, and magnesium sulfate. During the maintenance of anesthesia, invasive BP monitoring was used to prevent exaggerated hemodynamic perturbation. We maintained both the cerebral perfusion and the uteroplacental perfusion by keeping MAP within normal limits (65–90 mmHg). Oxytocin has been used in patients with intracranial tumors without any adverse effect.[15] On the other hand, ergotamine has been associated with hypertensive responses, which may increase ICP more.

  Conclusion Top

In a pregnant patient with symptomatic AVM, GA can be used satisfactorily for cesarean delivery keeping in mind hemodynamic stability to maintain adequate cerebral and uteroplacental perfusion and to avoid further increase in ICP. Measures to reduce ICP should be started during preoperative period and should be continued during intra- and post-operative periods.


We would like to acknowledge the support of Dr. Ranjana Desai, Professor and Head, Department of Obstetrics and Gynaecology, Dr. S. N. Medical College, Jodhpur, Rajasthan, India.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Viscomi CM, Wilson J, Bernstein I. Anesthetic management of a parturient with an incompletely resected cerebral arteriovenous malformation. Reg Anesth 1997;22:192-7.  Back to cited text no. 1
Ogilvy CS, Stieg PE, Awad I, Brown RD Jr., Kondziolka D, Rosenwasser R, et al. AHA Scientific Statement: Recommendations for the management of intracranial arteriovenous malformations: A statement for healthcare professionals from a special writing group of the Stroke Council, American Stroke Association. Stroke 2001;32:1458-71.  Back to cited text no. 2
Söderman M, Andersson T, Karlsson B, Wallace MC, Edner G. Management of patients with brain arteriovenous malformations. Eur J Radiol 2003;46:195-205.  Back to cited text no. 3
Black S, Sulek CA, Day AL. Cerebral aneurysm and arteriovenous malformation. In: Cucchiara RF, Black S, Michenfelder JD, editors. Clinical Neuroanesthesia. 2nd ed. New York: Churchill Livingstone; 2000. p. 265-318.  Back to cited text no. 4
Jaigobin C, Silver FL. Stroke and pregnancy. Stroke 2000;31:2948-51.  Back to cited text no. 5
Kittner SJ, Stern BJ, Feeser BR, Hebel R, Nagey DA, Buchholz DW, et al. Pregnancy and the risk of stroke. N Engl J Med 1996;335:768-74.  Back to cited text no. 6
Lanzino G, Jensen ME, Cappelletto B, Kassell NF. Arteriovenous malformations that rupture during pregnancy: A management dilemma. Acta Neurochir (Wien) 1994;126:102-6.  Back to cited text no. 7
Breen DP, Klijn CJM, Al-Shahi Salman R. “Vascular malformations of the brain in pregnancy”. In: Marsh MS, Nashef LAM, Brex PA. editors. Neurology and Pregnancy Clinical Management. London (UK): Informa Healthcare; 2012.  Back to cited text no. 8
Horton JC, Chambers WA, Lyons SL, Adams RD, Kjellberg RN. Pregnancy and the risk of hemorrhage from cerebral arteriovenous malformations. Neurosurgery 1990;27:867-71.  Back to cited text no. 9
Millar C, Bissonnette B, Humphreys RP. Cerebral arteriovenous malformations in children. Can J Anaesth 1994;41:321-31.  Back to cited text no. 10
Robinson JL, Hall CS, Sedzimir CB. Arteriovenous malformations, aneurysms, and pregnancy. J Neurosurg 1974;41:63-70.  Back to cited text no. 11
Wilkins RH. Natural history of intracranial vascular malformations: A review. Neurosurgery 1985;16:421-30.  Back to cited text no. 12
Brown RD Jr., Wiebers DO, Torner JC, O'Fallon WM. Incidence and prevalence of intracranial vascular malformations in Olmsted County, Minnesota, 1965 to 1992. Neurology 1996;46:949-52.  Back to cited text no. 13
Wlody DJ. Neurosurgery in the pregnant patient. In: Newfield P, Cottrell JE, editors. Handbook of Neuroanesthesia. Philadelphia: WW Lippincott; 1999. p. 285-98.  Back to cited text no. 14
Todd MM, Warner DS, Sokoll MD, Maktabi MA, Hindman BJ, Scamman FL, et al. A prospective, comparative trial of three anesthetics for elective supratentorial craniotomy. Propofol/fentanyl, isoflurane/nitrous oxide, and fentanyl/nitrous oxide. Anesthesiology 1993;78:1005-20.  Back to cited text no. 15
Laidler JA, Jackson IJ, Redfern N. The management of caesarean section in a patient with an intracranial arteriovenous malformation. Anaesthesia 1989;44:490-1.  Back to cited text no. 16
Yih PS, Cheong KF. Anaesthesia for caesarean section in a patient with an intracranial arteriovenous malformation. Anaesth Intensive Care 1999;27:66-8.  Back to cited text no. 17
Coskun D, Mahli A, Yilmaz Z, Cizmeci P. Anesthetic management of caesarean section of a pregnant woman with cerebral arteriovenous malformation: A case report. Cases J 2008;1:327.  Back to cited text no. 18
Le LT, Wendling A. Anesthetic management for cesarean section in a patient with rupture of a cerebellar arteriovenous malformation. J Clin Anesth 2009;21:143-8.  Back to cited text no. 19
Jaeger K, Ruschulte H, Mühlhaus K, Tatagiba M. Combined emergency Caesarean section and intracerebral aneurysm clipping. Anaesthesia 2000;55:1138-40.  Back to cited text no. 20


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