International Journal of Obstetric Anesthesia (2015) xxx, xxx–xxx 0959-289X/$ - see front matter c 2015 Elsevier Ltd. All rights reserved. http://dx.doi.org/10.1016/j.ijoa.2015.01.004
REVIEW ARTICLE
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Anesthetic management of labor and delivery in patients with elevated intracranial pressure J.A. Anson, S. Vaida, D.M. Giampetro, P.M. McQuillan Department of Anesthesiology, Penn State Milton S. Hershey Medical Center, Hershey, PA, USA ABSTRACT The anesthetic management of labor and delivery in patients with elevated intracranial pressure is complex. This review discusses the etiologies of diffuse and focal pathologies which lead to elevated intracranial pressure in pregnancy. The role of neuraxial and general anesthesia in the management of labor and delivery is also examined. Finally, a comprehensive review of strategies to minimize increases in intracranial pressure during general anesthesia for cesarean delivery is presented. c 2015 Elsevier Ltd. All rights reserved.
Keywords: Intracranial pressure; Anesthesia; Analgesia; Pregnancy
Introduction The anesthetic management of labor and delivery parturients with elevated intracranial pressure (ICP) is complex and controversial. Studies of obstetric patients with intracranial hypertension are rare, thus many principles that guide management are extrapolated from neurosurgical literature. Of necessity, clinical decisions are often made based on known principles of neurologic and obstetric physiology and case reports, rather than randomized clinical studies. Hemodynamic management of these patients is critical. Cerebral perfusion pressure (CPP) is defined as mean arterial pressure (MAP) minus ICP. To maintain adequate CPP and brain tissue oxygenation, acute increases in ICP or decreases in MAP must be avoided. While the primary anesthetic goal is prevention of further elevation of ICP, anesthetic management of labor and delivery can vary widely based on the etiology of increased ICP. This review discusses physiologic changes in pregnancy that may impact ICP as well as the etiology of focal and diffuse lesions that increase ICP (Fig. 1). The role of neuraxial and general anesthesia for labor and delivery in the presence of neurologic diseases that may alter ICP is also reviewed.
in ICP that occur with intracranial lesions. The Monro-Kellie doctrine summarizes the dynamics of ICP in the setting of pathologic intracranial processes and explains how ICP increases occur in a relatively predictable fashion, based on the volume of intracranial contents. Normal structures within the cranium can be divided into the brain, blood, and cerebrospinal fluid (CSF). Because the intracranial compartment and vertebral canal form a relatively fixed volume structure, any increase in the volume of one component or addition of a new pathologic structure requires a compensatory decrease in the volume of other components. Of the three normal structures, the brain is the least compressible, so the blood and CSF compartments offer the greatest degree of compliance. This intracranial compliance allows for ICP to increase marginally with small increases in the volume of intracranial components. Additional compliance is afforded as the brain shifts and eventually herniates across dural compartments. Once these compensatory mechanisms fail, ICP rises exponentially and may eventually compromise CPP, leading to further neuronal injury.
Physiological changes during pregnancy and relationship to intracranial pressure
Dynamics of intracranial pressure The physiologic principles described by the MonroKellie doctrine are critical to understanding elevations Accepted January 2015 Correspondence to: J. A. Anson MD, Department of Anesthesiology, Penn State Milton S. Hershey Medical Center, 500 University Drive, mail code H187, P.O. Box 850, Hershey, PA 17033-0850, USA. E-mail address: [email protected]
The physiologic changes of pregnancy have the potential to alter ICP. Plasma osmolality and albumin concentration decrease, while blood volume and cardiac output increase (35% and 40–50%, respectively). These changes, in conjunction with sodium and free water retention, make the pregnant patient susceptible to cerebral edema.1 The increase in cardiac output, combined with
Please cite this article in press as: Anson JA et al. Anesthetic management of labor and delivery in patients with elevated intracranial pressure. Int J Obstet Anesth (2015), http://dx.doi.org/10.1016/j.ijoa.2015.01.004
2 estrogen-mediated vasodilatation, results in a progressive increase in cerebral blood flow (CBF) which reaches a peak of 20% above non-pregnant values in the third trimester.2 Other changes which might have an impact are the fluctuation in brain volume, which decreases intrapartum and increases postpartum, and the increase in size of the pituitary gland.3,4 Despite the increased susceptibility to cerebral edema, CSF pressure is unaltered in normal pregnancy (normal ICP 7–15 cmH2O; upper normal limit 20–25 cmH2O).5 However, CSF pressure can increase during the first and second stages of labor to 39 cmH2O and 71 cmH2O, respectively.5 Epidural blood vessels become engorged during the third trimester of pregnancy, resulting in a reduction in both CSF volume and dural sac surface area.6 This may explain the increased sensory level achieved by neuraxial anesthesia in pregnancy.6
Focal etiologies of increased intracranial pressure Intracranial masses Tumors Although intracranial neoplasms are very rare during pregnancy, space-occupying lesions can cause pathologic elevations in ICP. Tumors increase ICP by occupying that part of the intracranial compartment that would normally accommodate non-pathologic structures. Tumor progression eventually overcomes intracranial compliance mechanisms, leading to pathologic increases in ICP. The incidence of intracranial neoplasms in pregnancy is not known; however, the incidence in women of child-bearing age is estimated at 3.4–13.2 per 100 000.7 The frequency of intracranial neoplasms is not affected by pregnancy, with the possible exception of choriocarcinoma.7 Although the incidence may not increase during pregnancy, physiologic changes can lead to significant tumor growth and symptomatology. Intraparenchymal hemorrhage/cerebral infarction Intracranial hemorrhage (ICH) is uncommon during pregnancy. It can, however, be a devastating complication, accounting for 7.1% of total pregnancy related mortality with an in-hospital mortality rate of 20.3%.8 A USA nationwide database of pregnancy-related admissions found that subarachnoid hemorrhage (SAH) occurred in 5.8 per 100 000 deliveries over a 13-year period and accounted for 4.1% of maternity-related deaths.9 Like intracranial tumors, SAH increases ICP by occupying that part of the intracranial compartment that would normally accommodate non-pathologic structures. The risk of rupture of an aneurysm or arterial-venous malformation (AVM) may be increased during pregnancy secondary to increased cardiac output, increased blood volume, and hormonally-mediated vascular connective tissue changes.10 The risk of ICH
Raised intracranial pressure during pregnancy is highest in the postpartum period. Known risk factors include, advanced maternal age, African-American race, Hispanic ethnicity, intracranial venous thrombosis, drug and alcohol abuse, pre-existing hypertension (especially if superimposed with preeclampsia), coagulopathy, and tobacco use.8,9 Subdural/epidural hematoma Most reported subdural hematomas in obstetrics occur postpartum with trauma.11 However, antepartum atraumatic subdural hematoma has been reported in patients with preeclampsia.11 A case of subdural hematoma as the initial presenting symptom of metastatic choriocarcinoma has been reported.12 Choriocarcinoma should be ruled out in any woman of reproductive age presenting with intracranial hemorrhage of unknown origin.12 Radiographic imaging often fails to demonstrate choriocarcinoma lesions. Diagnosis is made through CSF b-human chorionic gonadotropin levels and histologic examination. Brain abscess Though rarely associated with pregnancy, brain abscesses are a potentially life threatening condition. The abscess occupies intracranial space normally filled by non-pathologic tissue, and ICP rises when intracranial compliance limits are exceeded. Risk factors include pre-existing infection such as sinusitis, otitis media, mastoiditis, dental and scalp infections, foreign body and immunosuppression. A small review of pregnancies complicated by brain abscess demonstrated that up to 30% of patients had no risk factors.13 Presenting symptoms are often non-specific indicators of increased ICP such as headache, mental status changes, and seizures. Diagnosis is made via radiologic imaging combined with surgical aspiration and culture. Treatment varies with the size, etiology and severity of the lesion, but typically includes antibiotic therapy and, potentially, surgical intervention. Term vaginal delivery appears safe in the absence of other maternal or fetal indications for cesarean delivery.13
Non-communicating hydrocephalus Hydrocephalus is a condition characterized by excess CSF in the cerebral ventricles leading to elevated ICP. Non-communicating hydrocephalus (NCH) is caused by physical obstruction of CSF from the choroid plexus to the subarachnoid space. Non-communicating hydrocephalus (NCH) increases ICP via expansion of the CSF compartments upstream from the CSF flow obstruction. As these compartments accumulate CSF and expand in size, the additional volume of CSF in the fixed space increases ICP. Obstruction can be caused by external compression or intraventricular masses, and can occur at multiple anatomic areas. Obstruction at the foramen of Monro can be unilateral or bilateral and leads to
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J.A. Anson et al.
3
FOCAL ETIOLOGIES
DIFFUSE ETIOLOGIES
Intracranial Masses
Generalized Brain Edema
•
Tumor
•
Anoxia
•
Intraparenchymal hemorrhage
•
Hepatic failure
•
Subdural/epidural hematoma
•
Hypertensive encephalopathy
•
Brain abscess
Increased Venous Pressure
Non-Communicating Hydrocephalus
•
Cerebral venous sinus thrombosis
•
Arterial-venous malformation
•
Heart failure
Communicating Hydrocephalus
Fig. 1
Etiologies of elevated intracranial pressure in pregnancy.
dilation of a single lateral ventricle or both, respectively. Occlusion at the aqueduct of Sylvius leads to dilation of both lateral ventricles and the third ventricle. Obstruction at the fourth ventricle leads to dilation of all upstream ventricles and the aqueduct of Sylvius. Finally, obstruction can also occur at the foramina of Luschka, Magendie and the subarachnoid space around the brainstem, leading to expansion of the entire ventricular system. Congenital causes of NCH include, neural tube defects, congenital syndromes, X-linked hydrocephalus, congenital malformations (Chiari and Dandy-Walker malformations), vein of Galen malformation, or intrauterine infection.14–16 Acquired hydrocephalus in adults is most commonly caused by trauma (SAH), meningitis, intraventricular hemorrhage or brain tumor (posterior fossa medulloblastoma, astrocytoma, ependymoma).14 Subarachnoid hemorrhage induces an inflammatory response followed by fibrosis which can impair CSF flow. Symptoms and signs of NCH are similar to those associated with elevated ICP.
Generalized etiologies of increased intracranial pressure Generalized brain swelling Hypertensive encephalopathy Increased ICP leading to hypertensive encephalopathy occurs via several mechanisms, including vasogenic edema due to dysfunction of cerebral autoregulation, vasodilatation, and break down of the blood brain barrier.17 Hypertensive heart disease occurs in 12–22% of all pregnancies and is responsible for 17.6% of maternal deaths in the USA.18 Severe preeclampsia is defined as a systolic blood pressure P160 mmHg and/or a diastolic blood pressure P110 mmHg at two measurements at least four hours apart.18–20 Women with a hypertensive crisis, defined as a blood pressure of P160/ 110 mmHg for 15 min, are treated with antihypertensive
medications to reduce the risk of adverse cerebrovascular events.20 The threshold for antihypertensive therapy varies based on institutional protocols, as there are no large clinical trials with defined outcomes to guide management.21 Many practitioners initiate antihypertensive therapy only for preeclampsia with severe features or symptomatic hypertension.21 In 423 patients with intracerebral hemorrhage, a significant risk factor was hypertension either pre-existing or pregnancy related.8 Eclampsia Eclamptic seizures are a major cause of increased ICP. The mechanism of eclamptic seizures has not been elucidated fully, however, there are two possible hypotheses involving development of vasogenic and cytotoxic brain edema.22 Vasogenic edema, consistent with posterior reversible encephalopathy syndrome (PRES), can be explained by loss of autoregulation after an abrupt increase in blood pressure, leading to endothelial dysfunction, capillary leak and interstitial fluid extravasation.23 Untreated, this may progress to diffuse cerebral edema. Brewer et al. reported classical findings of PRES affecting cortical or subcortical edema of the parietal or occipital lobes, in all patients with eclampsia undergoing neuroimaging.24 Alternatively, cytotoxic brain edema occurring in eclampsia, can be explained by cerebral over-regulation and multifocal cerebral arterial vasoconstriction leading to brain tissue hypoperfusion, ischemia and possible infarction.23 Uncontrolled hypertension may lead to intracerebral hemorrhage: thrombocytopenia, a common finding in severe preeclampsia, further increases the risk of bleeding. Anoxia Oxidative stress and inflammation, secondary to hypoxemia, result in transvascular leakage and cerebral edema.25 Anoxia causes hypoxic-ischemic encephalopathy secondary to diffuse neuronal injury predominantly
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4 in the gray matter of the cerebellum and cortex. Subsequent cytotoxic and interstitial edema leads to an increase in ICP. Risk factors for anoxic brain injury in pregnancy are similar to those in non-pregnant patients of similar age, with trauma being the most common cause. In the USA, 6–8% of pregnancies are complicated by trauma, with 30 000 women per year seeking medical care.26 The most common causes include motor vehicle accidents, assaults, and falls.26 Hepatic failure Increased ICP in hepatic failure is evident in 70% of patients with fulminant liver failure of any cause.27 The mechanism of ICP elevation is attributed to rapid changes in serum ammonia levels. Brain astrocytes metabolize ammonia into glutamine, and excessive accumulation of glutamine leads to intracellular edema.27 Hepatic encephalopathy, a spectrum of mental status change ranging from confusion to coma, often is present. Anesthetic management of patients with hepatic failure may be complicated by coagulation abnormalities such as elevated international normalized ratio or thrombocytopenia, which preclude the use of neuraxial techniques. Acute fatty liver of pregnancy is a rare disease occurring in the third trimester of 1:13 000 pregnancies.28 Untreated, it can progress to encephalopathy, cerebral edema with coma, and elevations in ICP with an overall mortality rate of 12%.29,30 Viral hepatitis can also occur in pregnancy, leading to fulminant hepatic failure.31 Anesthetic management of these patients is complex, as they often have coagulation defects.
Increased venous pressure Pathologic states causing increased venous pressure limit the outflow of venous blood from the intracranial compartment. Accumulation of blood in the fixed intracranial vault eventually exceeds the compliance of the space, resulting in increased ICP. Cerebral venous sinus thrombosis Cerebral venous sinus thrombosis (CVST) is an uncommon cause of stroke accounting for 0.5–1% of all cerebral infarctions.32 The etiology is multifactorial, with over 100 causes described.33 Thrombosis of the sagittal sinus, jugular vein and lateral sinus pose a higher risk of increased ICP. Approximately 25% of patients presenting with CVST exhibit signs of intracranial hypertension.32 Inherited prothrombotic disorders such as Factor V Leiden, Protein C and S deficiencies and antithrombin III deficiency account for 10–15% of all cases.34 The incidence of CVST increases significantly during the third trimester and immediately postpartum. It accounts for 2% of all strokes during pregnancy, and the frequency is estimated at 12 per 100 000 deliveries.32 Management often includes antiplatelet therapy or full anticoagulation.32 These patients are predisposed to
Raised intracranial pressure developing seizures and may require anticonvulsant therapy.34,35 Large cerebral arterial-venous malformation The mechanism by which cerebral AVM increases ICP is unclear, but is likely due to high shunt volumes exhausting venous drainage capacity or a direct mass effect.36 Intracranial hypertension associated with AVM is thought to be rare, and the incidence is currently the focus of investigation.36 The incidence of cerebral AVM is estimated to be 0.01–0.5% in the general population, and it presents most commonly between the ages of 20–40.37 While the exact incidence of AVM in pregnancy is unknown, one retrospective study found just four cases of hemorrhagic stroke attributable to AVM in 58 429 deliveries.38 A retrospective study found an 8.1% rate of hemorrhage per pregnancy in patients with a known AVM.39 The frequency of AVM re-bleeding during the same pregnancy is 27% (four times greater than the general population) and AVM rupture during pregnancy carries a mortality rate of 28%.37
Communicating hydrocephalus Communicating (non-obstructive) hydrocephalus is caused by impaired CSF reabsorption into the systemic venous circulation in the absence of physical obstruction. Interruption of normal CSF resorption pathways leads to accumulation and subsequent ICP elevation when compensatory mechanisms are exceeded. Multiple neurologic conditions can result in communicating hydrocephalus, including congenital absence of arachnoid villi, SAH and meningitis. Hemorrhage and infection can lead to fibrosis and impaired CSF outflow.
Subarachnoid hemorrhage During pregnancy SAH is less likely to be caused by a cerebral aneurysm than SAH in a non-pregnant patient. This is represented by the fact that fewer aneurysms are coiled during pregnancy than in non-pregnant controls.9 The clipping/coiling rate in the postpartum period is even lower (6.2%).9 Additionally, SAH in pregnancy has a lower mortality rate compared to non-pregnant women.9 Collectively, these data further suggest that SAH in pregnancy is often non-aneurysmal in origin.
Idiopathic intracranial hypertension Idiopathic intracranial hypertension (IIH), also known as also known as pseudotumor cerebri, is an increase in intracranial pressure (>20 mmHg) of unknown origin with normal sensorium.40 It occurs in pregnant patients at approximately the same rate as in the general population (0.9 per 100 000).41 The most common symptoms and signs are headache, papilledema, and visual
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J.A. Anson et al. changes.40 Diagnostic criteria include papilledema, documented elevation in ICP measured in the lateral decubitus position, normal CSF composition, negative computed tomography (CT) or magnetic resonance imaging (MRI) for intracranial mass, structural or vascular lesions.40 Magnetic resonance imaging can reveal subtle findings suggestive but not specific of IIH. These include flattening of the posterior sclera, empty sella, dilation and tortuosity of the optic nerve sheath and distension of the perioptic subarachnoid space.42 If any of these features are present and no secondary causes of intracranial hypertension (such as CVST or mass lesion) are identified, a diagnostic lumbar puncture can be performed. An opening pressure of greater than 250 mmH2O is suggestive of IIH.40,43 A diagnosis of IIH is not a contraindication to neuraxial anesthesia, and there are multiple reports of the safe use of neuraxial techniques in these patients.44,45
Anesthetic management labor and delivery The choice of anesthetic technique in parturients with increased ICP is dependent on balancing their risks and benefits. Neuraxial analgesia and anesthesia are preferred in the healthy parturient; however, they may be contraindicated in those with intracranial lesions or increased bleeding risk. Furthermore, elevated ICP leading to altered mental status may complicate the anesthesiologist’s ability to safely administer neuraxial blocks. Many anesthesiologists avoid neuraxial techniques due to possible medicolegal implications.46 General anesthesia in pregnancy entails the risk of difficult airway, aspiration, and awareness in addition to potentially masking neurologic changes. Regardless of the planned anesthetic technique, obtaining informed consent can be difficult in patients with altered mental status. Preoperative multidisciplinary planning, involving neurology, neurosurgery, anesthesia, and obstetrics, is essential before selecting an anesthesia technique. The patient and family should be included in preoperative discussions, if feasible. While surgery of any kind during pregnancy entails possible risk to the fetus, the family should be counselled that appropriate care of the mother maximizes the chance of a good fetal outcome.
Neuraxial anesthesia Even though non-complicated spinal anesthesia for cesarean delivery has been reported in a patient with focal increased ICP from a glioblastoma, increased ICP generally is considered a contraindication for spinal anesthesia.47 Loss of CSF secondary to dural puncture may increase the pressure gradient between the supratentorial and infratentorial compartments, resulting in rapid brain stem herniation or intracranial hemorrhage.48 The use of narrow gauge needles (25-
5 gauge or smaller) significantly decreases, but does not eliminate, the risk of complications from dural puncture.49 Epidural anesthesia potentially may be hazardous in patients with increased ICP. Epidural injection can elevate ICP transiently, as an increase in epidural volume may transmit pressure to the intrathecal space. In a porcine model, epidural injection has been shown to be associated with an increase in ICP, with more pronounced changes occurring when ICP was increased at baseline.50 Also, continuous epidural infusion may lead to increased ICP due to compression of the thecal sac.51 Patients may be at increased risk for developing a subdural hematoma due to acute CSF changes.48 If epidural anesthesia is utilized, slow injection of incremental volumes is strongly recommended. The greatest risk with epidural insertion is accidental dural puncture. Based on their findings in patients with traumatic head injuries, Hilt et al. recommended against the use of epidural anesthesia in patients with spaceoccupying lesions, not only due to the risk of decreased cerebral perfusion but also that of herniation.51 The larger size of an epidural needle, compared to a spinal needle, causes greater CSF loss and increases the risk of brain stem herniation in patients with increased ICP.52 Experimental models show that narrower gauge needles are associated with shorter duration of CSF leak after dural puncture and that 20-gauge needles produce a slower rate of fluid loss than 17-gauge needles.53,54 Epidural analgesia has, however, been safely used in labor in patients with intracranial neoplasms.7,55 An epidural anesthetic also can be used to attenuate the expected rise in ICP associated with instrumental vaginal delivery: ICP can rise to 70 cmH2O with instrumentation.5 An MRI of the brain should be obtained preoperatively in patients with intracranial neoplasms where neuraxial anesthesia is being considered. Magnetic resonance imaging evidence of mass effect or hydrocephalus can help predict the risk of herniation with dural puncture.52 Conversely, if a small brain lesion is located in a region remote from CSF pathways it may have little effect on ventricular compression or CSF flow. In this circumstance, ICP may not rise due to caudal displacement of CSF over time. Therefore, dural puncture, and likewise the transient increase in ICP with epidural injection, should be well tolerated and should not result in herniation of brain tissue.52 The use of neuraxial anesthesia in parturients with intracranial pathology requires a comprehensive assessment of the patient’s history, physical examination and radiographic imaging. In patients with space-occupying lesions and MRI evidence of significant mass effect, the risk of herniation is high and dural puncture is contraindicated.52 If there is subtle evidence of mass effect in these patients, the risk of herniation is considered mild to moderate and further neurologic assessment is
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6 warranted before proceeding with neuraxial anesthesia.52 In patients with hydrocephalus, it is critical to determine the location of the obstruction and look for any clinical findings suggestive of elevated ICP. If there is obstruction to CSF flow at or above the level of the foramen magnum, the patient has a mild to moderate risk of herniation with dural puncture. Alternatively, if there is no obstruction to CSF flow at the foramen magnum and there are no clinical findings suggestive of elevated ICP, the patient has minimal to no risk of herniation and it may be reasonable to proceed with neuraxial anesthesia.52 Patients with IIH may experience symptomatic relief if a combined spinal-epidural technique, with small volume CSF withdrawal, is used.45,56 Intrathecal catheters have been used to manage labor analgesia in parturients with IIH.56
Neuraxial anesthesia and severe preeclampsia Historically, it was believed that spinal anesthesia in the setting of severe preeclampsia could result in severe hypotension and subsequent uteroplacental perfusion impairment. However, modern studies show that patients with severe preeclampsia experience less frequent and less severe hypotension than healthy parturients.57 A small prospective study utilizing a non-invasive beat-to-beat cardiac output monitor in patients with severe preeclampsia, demonstrated clinically insignificant changes in cardiac output with spinal anesthesia.58 A randomized, multicenter study similarly concluded spinal anesthesia can safely be used in this patient population and, if hypotension does occur, it is easily treated.59 The decision to utilize neuraxial anesthesia in patients with eclampsia is based on multiple factors. First, coagulation must not be impaired. The mental status of the patient should be evaluated as seizures may depress the level of consciousness. Patients with lower Glasgow Coma Scale (GCS) scores are unlikely to cooperate with neuraxial procedures, and may require tracheal intubation, regardless of the planned obstetric procedure. The potential for a difficult airway should also be considered. If difficulty is anticipated, and the GCS and coagulation are normal, neuraxial anesthesia should be offered.
Neuraxial anesthesia in the presence of lumboperitoneal shunts Some authors have suggested that the presence of an lumboperitoneal shunt (LP) shunt is a contraindication to neuraxial anesthesia due to theoretical concerns of shunt trauma or loss of local anesthetic into the peritoneal cavity.60 However, more recently, epidural anesthesia has been used successfully in patients with LP shunts in IIH.61,62 To minimize the risk for shunt trauma, epidural catheters should be inserted away from the level of the LP shunt: radiographic imaging should be considered before catheter insertion.62 A midline
Raised intracranial pressure approach should be used during epidural catheter insertion, as LP shunt tubing is frequently tunneled subcutaneously in a lateral direction.61,62 In the absence of radiographic imaging, an epidural catheter should be inserted below the LP shunt insertion scar.63 An epidurogram can be considered to confirm the locations of the LP shunt and the epidural catheter.62 The anesthetic principles for shunt insertion or revision during pregnancy are similar to those for cesarean delivery.
General anesthesia Basic anesthetic considerations The presence of symptoms and signs of increased ICP or focal neurological deficits may favor general anesthesia for cesarean delivery.7 However, general anesthesia in the parturient presents the inherent risks of difficult airway, aspiration, and awareness.64,65 In addition, it is not possible to detect alterations of mental status under general anesthesia which may be of concern in patients with intracranial lesions.
Hemodynamic considerations Induction of general anesthesia requires careful planning to avoid potentially devastating hemodynamic changes in a pregnant patient with increased ICP. The use of lidocaine in patients with increased ICP has been well studied. A meta-analysis of 37 randomized trials including 1429 non-obstetric patients, concluded intravenous lidocaine reduces the cardiovascular response to laryngoscopy across all age groups as compared to placebo.66 The authors stated that further studies are necessary to determine the optimal lidocaine dose and timing of administration. Pharmacologic ablation of the response to laryngoscopy and intubation can be achieved with opioids. However, many avoid this practice in the parturient due to placental transfer of opioids and the potential for neonatal respiratory depression. In a randomized, double-blinded, placebo-controlled study in non-parturients, a remifentanil bolus of 1 lg/kg effectively attenuated the heart rate and blood pressure response to laryngoscopy. Lower doses were ineffective, while higher doses resulted in decreased arterial blood pressure which may negatively impact CPP.67 Similar results have been shown in obstetric patients, where compared to a saline placebo, remifentanil 1 lg/kg consistently improved the hemodynamic response to laryngoscopy, although neonatal depression was observed in 10%.68 Remifentanil infusions in healthy volunteers decrease CBF.69 The successful use of remifentanil as an adjunct to general anesthesia has been reported in patients with preeclampsia and HELLP (hemolysis, elevated liver enzymes, low platelet count) syndrome.70,71 Due to the unpredictable neonatal effects of remifentanil, physicians trained in neonatal resuscitation should be present at delivery.72
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J.A. Anson et al. The ability of other opioids to attenuate the hemodynamic response of laryngoscopy has been studied. Fentanyl and alfentanil minimize changes in heart rate and blood pressure during intubation of trauma patients.73 In a prospective, randomized non-obstetric study of patients with baseline hypertension, fentanyl (with and without lidocaine) decreased but did not eliminate the hemodynamic response to laryngoscopy.74 In a randomized trial of obstetric patients, fentanyl 1 lg/kg administered three minutes before induction of general anesthesia resulted in a stable hemodynamic profile during laryngoscopy, without affecting Apgar scores or blood gas analysis.75 Another alternative to blunt the response to laryngoscopy is magnesium. An early study in healthy nonobstetric patients demonstrated pre-intubation administration of magnesium 60 mg/kg resulted in lower plasma catecholamine levels and attenuated heart rate and blood pressure responses post-intubation as compared to saline placebo.76 A subsequent study in patients undergoing general anesthesia for cesarean delivery found magnesium was superior to lidocaine at blunting the hemodynamic response to tracheal intubation.77 One review found Grade B evidence (moderate level of certainty) supporting the use of magnesium to attenuate the hypertensive response to tracheal intubation.78 Esmolol is used frequently to rapidly treat transient hemodynamic changes caused by tracheal intubation. However, in animal models esmolol crosses the placenta and causes fetal bradycardia. As such, it should be avoided in pregnant patients.79 Labetalol, on the other hand, has been used safely in parturients.19
Induction of anesthesia When selecting an intravenous induction agent, the effects on ICP, CBF and cerebral metabolic rate of oxygen (CMRO2) must be considered. Propofol, etomidate, and thiopental all decrease ICP, CBF and CMRO2 and are used routinely in neurosurgical patients. In animal models, propofol causes a dose-dependent decrease in CBF.80 The administration of a 2 mg/kg propofol bolus decreases ICP, without altering CPP, in non-obstetric head trauma patients with normal and compromised intracranial compliance.81 Propofol effectively blunts the response to laryngoscopy in healthy volunteers.82 It has also been shown in a non-obstetric study to be effective in treating seizures; a potential benefit in patients with increased ICP.83 In conjunction with its antiemetic effect, propofol is an attractive choice for patients with elevated ICP. In a study of non-obstetric patients with intracranial lesions, etomidate 0.2 mg/kg significantly decreased ICP without changing CPP or hemodynamics.84 Similarly, in pediatric patients with severe brain trauma there were significant reductions in ICP following an etomidate bolus of 0.3 mg/kg, and improvement in CPP.85
7 However, etomidate also possesses pro-convulsant properties; the exact mechanism of which is unclear.86 Etomidate has pro-emetic tendencies, making it less ideal for neurosurgical patients. Therefore, despite the ICP lowering effects of etomidate, it should not be considered a first-line agent in patients with elevated ICP. It may be, however, an appropriate choice in hemodynamically unstable parturients. There are few comparative studies of various induction agents regarding their effects on ICP. A computer model was developed to predict ICP responses to various induction agents in simulated patients. This demonstrated induction of anesthesia with intravenous agents reduces ICP by up to 30%, with propofol having the greatest impact (propofol > thiopental > etomidate).87 In a study of 40 patients presenting for elective cesarean delivery, propofol was significantly better than thiopental in reducing the systolic blood pressure response to laryngoscopy (propofol 17.4 mmHg vs. thiopental 32.1 mmHg).88 Thiopental is now unavailable to many obstetric anesthesiologists. The choice of neuromuscular blocking drugs in parturients with elevated ICP is controversial. Succinylcholine is used frequently for rapid-sequence induction but has the potential to elevate ICP which may already be increased. Rocuronium 1.2 mg/kg may be a better alternative in terms of ICP to succinylcholine.48 Both succinylcholine and rocuronium provide excellent intubating conditions during a rapid-sequence induction. A 2008 Cochrane review of 37 studies comparing the intubating conditions achieved with succinylcholine using at least 1 mg/kg and rocuronium 1.2 mg/ kg during rapid-sequence induction and intubation found no significant difference between the two drugs.89 As demonstrated in a swine model, pre-treatment with a non-depolarizing muscle relaxant does not prevent the rise in ICP associated with succinylcholine.90 While these studies suggest there is a role for rocuronium in patients with increased ICP, to date, there are no studies directly addressing its use in an obstetric patient population. Concurrent use of anticonvulsant therapy can impact the expected duration of action of non-depolarizing drugs. Acute administration of antiepileptic drugs can potentiate the effect of non-depolarizing muscle relaxants, while chronic antiepileptic therapy confers resistance to these drugs. This resistance is thought to be multifactorial, with induction of hepatic drug metabolism, increased protein binding and up-regulation of acetylcholine receptors all playing a role.91 A summary of strategies to minimize elevations of ICP during induction of anesthesia is presented in Table 1.
Maintenance of anesthesia General anesthesia for cesarean delivery confers an increased risk of intraoperative awareness, particularly in the interval before delivery.92 As such, attention must
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8 Table 1
Raised intracranial pressure Induction of general anesthesia in patients with increased intracranial pressure Strategies
Induction agent
1st line: propofol (flICP, flCBF, flCMRO2, flSeizures, Antiemetic) 2st line: etomidate (flICP, flCBF, flCMRO2, ›Seizures, pro-emetic)*
Neuromuscular blockade
1st line: rocuronium 1.2 mg/kg Anticonvulsant therapy may affect duration
Hemodynamic considerations
Remifentanil bolus (1 lg/kg) before intubation Magnesium bolus (40–60 mg/kg) before intubation Labetalol can be safely administered Avoid esmolol as it crosses placenta and may cause fetal bradycardia
ICP: intracranial pressure; CBF: cerebral blood flow; CMRO2: cerebral metabolic rate of oxygen.*Thiopental may be used if available.
Table 2
Intraoperative intracranial pressure management considerations Strategies
Depth of anesthesia
Bispectral index monitor (BIS) Titrate agent to BIS
REVIEW ARTICLE
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Anesthetic management of labor and delivery in patients with elevated intracranial pressure J.A. Anson, S. Vaida, D.M. Giampetro, P.M. McQuillan Department of Anesthesiology, Penn State Milton S. Hershey Medical Center, Hershey, PA, USA ABSTRACT The anesthetic management of labor and delivery in patients with elevated intracranial pressure is complex. This review discusses the etiologies of diffuse and focal pathologies which lead to elevated intracranial pressure in pregnancy. The role of neuraxial and general anesthesia in the management of labor and delivery is also examined. Finally, a comprehensive review of strategies to minimize increases in intracranial pressure during general anesthesia for cesarean delivery is presented. c 2015 Elsevier Ltd. All rights reserved.
Keywords: Intracranial pressure; Anesthesia; Analgesia; Pregnancy
Introduction The anesthetic management of labor and delivery parturients with elevated intracranial pressure (ICP) is complex and controversial. Studies of obstetric patients with intracranial hypertension are rare, thus many principles that guide management are extrapolated from neurosurgical literature. Of necessity, clinical decisions are often made based on known principles of neurologic and obstetric physiology and case reports, rather than randomized clinical studies. Hemodynamic management of these patients is critical. Cerebral perfusion pressure (CPP) is defined as mean arterial pressure (MAP) minus ICP. To maintain adequate CPP and brain tissue oxygenation, acute increases in ICP or decreases in MAP must be avoided. While the primary anesthetic goal is prevention of further elevation of ICP, anesthetic management of labor and delivery can vary widely based on the etiology of increased ICP. This review discusses physiologic changes in pregnancy that may impact ICP as well as the etiology of focal and diffuse lesions that increase ICP (Fig. 1). The role of neuraxial and general anesthesia for labor and delivery in the presence of neurologic diseases that may alter ICP is also reviewed.
in ICP that occur with intracranial lesions. The Monro-Kellie doctrine summarizes the dynamics of ICP in the setting of pathologic intracranial processes and explains how ICP increases occur in a relatively predictable fashion, based on the volume of intracranial contents. Normal structures within the cranium can be divided into the brain, blood, and cerebrospinal fluid (CSF). Because the intracranial compartment and vertebral canal form a relatively fixed volume structure, any increase in the volume of one component or addition of a new pathologic structure requires a compensatory decrease in the volume of other components. Of the three normal structures, the brain is the least compressible, so the blood and CSF compartments offer the greatest degree of compliance. This intracranial compliance allows for ICP to increase marginally with small increases in the volume of intracranial components. Additional compliance is afforded as the brain shifts and eventually herniates across dural compartments. Once these compensatory mechanisms fail, ICP rises exponentially and may eventually compromise CPP, leading to further neuronal injury.
Physiological changes during pregnancy and relationship to intracranial pressure
Dynamics of intracranial pressure The physiologic principles described by the MonroKellie doctrine are critical to understanding elevations Accepted January 2015 Correspondence to: J. A. Anson MD, Department of Anesthesiology, Penn State Milton S. Hershey Medical Center, 500 University Drive, mail code H187, P.O. Box 850, Hershey, PA 17033-0850, USA. E-mail address: [email protected]
The physiologic changes of pregnancy have the potential to alter ICP. Plasma osmolality and albumin concentration decrease, while blood volume and cardiac output increase (35% and 40–50%, respectively). These changes, in conjunction with sodium and free water retention, make the pregnant patient susceptible to cerebral edema.1 The increase in cardiac output, combined with
Please cite this article in press as: Anson JA et al. Anesthetic management of labor and delivery in patients with elevated intracranial pressure. Int J Obstet Anesth (2015), http://dx.doi.org/10.1016/j.ijoa.2015.01.004
2 estrogen-mediated vasodilatation, results in a progressive increase in cerebral blood flow (CBF) which reaches a peak of 20% above non-pregnant values in the third trimester.2 Other changes which might have an impact are the fluctuation in brain volume, which decreases intrapartum and increases postpartum, and the increase in size of the pituitary gland.3,4 Despite the increased susceptibility to cerebral edema, CSF pressure is unaltered in normal pregnancy (normal ICP 7–15 cmH2O; upper normal limit 20–25 cmH2O).5 However, CSF pressure can increase during the first and second stages of labor to 39 cmH2O and 71 cmH2O, respectively.5 Epidural blood vessels become engorged during the third trimester of pregnancy, resulting in a reduction in both CSF volume and dural sac surface area.6 This may explain the increased sensory level achieved by neuraxial anesthesia in pregnancy.6
Focal etiologies of increased intracranial pressure Intracranial masses Tumors Although intracranial neoplasms are very rare during pregnancy, space-occupying lesions can cause pathologic elevations in ICP. Tumors increase ICP by occupying that part of the intracranial compartment that would normally accommodate non-pathologic structures. Tumor progression eventually overcomes intracranial compliance mechanisms, leading to pathologic increases in ICP. The incidence of intracranial neoplasms in pregnancy is not known; however, the incidence in women of child-bearing age is estimated at 3.4–13.2 per 100 000.7 The frequency of intracranial neoplasms is not affected by pregnancy, with the possible exception of choriocarcinoma.7 Although the incidence may not increase during pregnancy, physiologic changes can lead to significant tumor growth and symptomatology. Intraparenchymal hemorrhage/cerebral infarction Intracranial hemorrhage (ICH) is uncommon during pregnancy. It can, however, be a devastating complication, accounting for 7.1% of total pregnancy related mortality with an in-hospital mortality rate of 20.3%.8 A USA nationwide database of pregnancy-related admissions found that subarachnoid hemorrhage (SAH) occurred in 5.8 per 100 000 deliveries over a 13-year period and accounted for 4.1% of maternity-related deaths.9 Like intracranial tumors, SAH increases ICP by occupying that part of the intracranial compartment that would normally accommodate non-pathologic structures. The risk of rupture of an aneurysm or arterial-venous malformation (AVM) may be increased during pregnancy secondary to increased cardiac output, increased blood volume, and hormonally-mediated vascular connective tissue changes.10 The risk of ICH
Raised intracranial pressure during pregnancy is highest in the postpartum period. Known risk factors include, advanced maternal age, African-American race, Hispanic ethnicity, intracranial venous thrombosis, drug and alcohol abuse, pre-existing hypertension (especially if superimposed with preeclampsia), coagulopathy, and tobacco use.8,9 Subdural/epidural hematoma Most reported subdural hematomas in obstetrics occur postpartum with trauma.11 However, antepartum atraumatic subdural hematoma has been reported in patients with preeclampsia.11 A case of subdural hematoma as the initial presenting symptom of metastatic choriocarcinoma has been reported.12 Choriocarcinoma should be ruled out in any woman of reproductive age presenting with intracranial hemorrhage of unknown origin.12 Radiographic imaging often fails to demonstrate choriocarcinoma lesions. Diagnosis is made through CSF b-human chorionic gonadotropin levels and histologic examination. Brain abscess Though rarely associated with pregnancy, brain abscesses are a potentially life threatening condition. The abscess occupies intracranial space normally filled by non-pathologic tissue, and ICP rises when intracranial compliance limits are exceeded. Risk factors include pre-existing infection such as sinusitis, otitis media, mastoiditis, dental and scalp infections, foreign body and immunosuppression. A small review of pregnancies complicated by brain abscess demonstrated that up to 30% of patients had no risk factors.13 Presenting symptoms are often non-specific indicators of increased ICP such as headache, mental status changes, and seizures. Diagnosis is made via radiologic imaging combined with surgical aspiration and culture. Treatment varies with the size, etiology and severity of the lesion, but typically includes antibiotic therapy and, potentially, surgical intervention. Term vaginal delivery appears safe in the absence of other maternal or fetal indications for cesarean delivery.13
Non-communicating hydrocephalus Hydrocephalus is a condition characterized by excess CSF in the cerebral ventricles leading to elevated ICP. Non-communicating hydrocephalus (NCH) is caused by physical obstruction of CSF from the choroid plexus to the subarachnoid space. Non-communicating hydrocephalus (NCH) increases ICP via expansion of the CSF compartments upstream from the CSF flow obstruction. As these compartments accumulate CSF and expand in size, the additional volume of CSF in the fixed space increases ICP. Obstruction can be caused by external compression or intraventricular masses, and can occur at multiple anatomic areas. Obstruction at the foramen of Monro can be unilateral or bilateral and leads to
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J.A. Anson et al.
3
FOCAL ETIOLOGIES
DIFFUSE ETIOLOGIES
Intracranial Masses
Generalized Brain Edema
•
Tumor
•
Anoxia
•
Intraparenchymal hemorrhage
•
Hepatic failure
•
Subdural/epidural hematoma
•
Hypertensive encephalopathy
•
Brain abscess
Increased Venous Pressure
Non-Communicating Hydrocephalus
•
Cerebral venous sinus thrombosis
•
Arterial-venous malformation
•
Heart failure
Communicating Hydrocephalus
Fig. 1
Etiologies of elevated intracranial pressure in pregnancy.
dilation of a single lateral ventricle or both, respectively. Occlusion at the aqueduct of Sylvius leads to dilation of both lateral ventricles and the third ventricle. Obstruction at the fourth ventricle leads to dilation of all upstream ventricles and the aqueduct of Sylvius. Finally, obstruction can also occur at the foramina of Luschka, Magendie and the subarachnoid space around the brainstem, leading to expansion of the entire ventricular system. Congenital causes of NCH include, neural tube defects, congenital syndromes, X-linked hydrocephalus, congenital malformations (Chiari and Dandy-Walker malformations), vein of Galen malformation, or intrauterine infection.14–16 Acquired hydrocephalus in adults is most commonly caused by trauma (SAH), meningitis, intraventricular hemorrhage or brain tumor (posterior fossa medulloblastoma, astrocytoma, ependymoma).14 Subarachnoid hemorrhage induces an inflammatory response followed by fibrosis which can impair CSF flow. Symptoms and signs of NCH are similar to those associated with elevated ICP.
Generalized etiologies of increased intracranial pressure Generalized brain swelling Hypertensive encephalopathy Increased ICP leading to hypertensive encephalopathy occurs via several mechanisms, including vasogenic edema due to dysfunction of cerebral autoregulation, vasodilatation, and break down of the blood brain barrier.17 Hypertensive heart disease occurs in 12–22% of all pregnancies and is responsible for 17.6% of maternal deaths in the USA.18 Severe preeclampsia is defined as a systolic blood pressure P160 mmHg and/or a diastolic blood pressure P110 mmHg at two measurements at least four hours apart.18–20 Women with a hypertensive crisis, defined as a blood pressure of P160/ 110 mmHg for 15 min, are treated with antihypertensive
medications to reduce the risk of adverse cerebrovascular events.20 The threshold for antihypertensive therapy varies based on institutional protocols, as there are no large clinical trials with defined outcomes to guide management.21 Many practitioners initiate antihypertensive therapy only for preeclampsia with severe features or symptomatic hypertension.21 In 423 patients with intracerebral hemorrhage, a significant risk factor was hypertension either pre-existing or pregnancy related.8 Eclampsia Eclamptic seizures are a major cause of increased ICP. The mechanism of eclamptic seizures has not been elucidated fully, however, there are two possible hypotheses involving development of vasogenic and cytotoxic brain edema.22 Vasogenic edema, consistent with posterior reversible encephalopathy syndrome (PRES), can be explained by loss of autoregulation after an abrupt increase in blood pressure, leading to endothelial dysfunction, capillary leak and interstitial fluid extravasation.23 Untreated, this may progress to diffuse cerebral edema. Brewer et al. reported classical findings of PRES affecting cortical or subcortical edema of the parietal or occipital lobes, in all patients with eclampsia undergoing neuroimaging.24 Alternatively, cytotoxic brain edema occurring in eclampsia, can be explained by cerebral over-regulation and multifocal cerebral arterial vasoconstriction leading to brain tissue hypoperfusion, ischemia and possible infarction.23 Uncontrolled hypertension may lead to intracerebral hemorrhage: thrombocytopenia, a common finding in severe preeclampsia, further increases the risk of bleeding. Anoxia Oxidative stress and inflammation, secondary to hypoxemia, result in transvascular leakage and cerebral edema.25 Anoxia causes hypoxic-ischemic encephalopathy secondary to diffuse neuronal injury predominantly
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4 in the gray matter of the cerebellum and cortex. Subsequent cytotoxic and interstitial edema leads to an increase in ICP. Risk factors for anoxic brain injury in pregnancy are similar to those in non-pregnant patients of similar age, with trauma being the most common cause. In the USA, 6–8% of pregnancies are complicated by trauma, with 30 000 women per year seeking medical care.26 The most common causes include motor vehicle accidents, assaults, and falls.26 Hepatic failure Increased ICP in hepatic failure is evident in 70% of patients with fulminant liver failure of any cause.27 The mechanism of ICP elevation is attributed to rapid changes in serum ammonia levels. Brain astrocytes metabolize ammonia into glutamine, and excessive accumulation of glutamine leads to intracellular edema.27 Hepatic encephalopathy, a spectrum of mental status change ranging from confusion to coma, often is present. Anesthetic management of patients with hepatic failure may be complicated by coagulation abnormalities such as elevated international normalized ratio or thrombocytopenia, which preclude the use of neuraxial techniques. Acute fatty liver of pregnancy is a rare disease occurring in the third trimester of 1:13 000 pregnancies.28 Untreated, it can progress to encephalopathy, cerebral edema with coma, and elevations in ICP with an overall mortality rate of 12%.29,30 Viral hepatitis can also occur in pregnancy, leading to fulminant hepatic failure.31 Anesthetic management of these patients is complex, as they often have coagulation defects.
Increased venous pressure Pathologic states causing increased venous pressure limit the outflow of venous blood from the intracranial compartment. Accumulation of blood in the fixed intracranial vault eventually exceeds the compliance of the space, resulting in increased ICP. Cerebral venous sinus thrombosis Cerebral venous sinus thrombosis (CVST) is an uncommon cause of stroke accounting for 0.5–1% of all cerebral infarctions.32 The etiology is multifactorial, with over 100 causes described.33 Thrombosis of the sagittal sinus, jugular vein and lateral sinus pose a higher risk of increased ICP. Approximately 25% of patients presenting with CVST exhibit signs of intracranial hypertension.32 Inherited prothrombotic disorders such as Factor V Leiden, Protein C and S deficiencies and antithrombin III deficiency account for 10–15% of all cases.34 The incidence of CVST increases significantly during the third trimester and immediately postpartum. It accounts for 2% of all strokes during pregnancy, and the frequency is estimated at 12 per 100 000 deliveries.32 Management often includes antiplatelet therapy or full anticoagulation.32 These patients are predisposed to
Raised intracranial pressure developing seizures and may require anticonvulsant therapy.34,35 Large cerebral arterial-venous malformation The mechanism by which cerebral AVM increases ICP is unclear, but is likely due to high shunt volumes exhausting venous drainage capacity or a direct mass effect.36 Intracranial hypertension associated with AVM is thought to be rare, and the incidence is currently the focus of investigation.36 The incidence of cerebral AVM is estimated to be 0.01–0.5% in the general population, and it presents most commonly between the ages of 20–40.37 While the exact incidence of AVM in pregnancy is unknown, one retrospective study found just four cases of hemorrhagic stroke attributable to AVM in 58 429 deliveries.38 A retrospective study found an 8.1% rate of hemorrhage per pregnancy in patients with a known AVM.39 The frequency of AVM re-bleeding during the same pregnancy is 27% (four times greater than the general population) and AVM rupture during pregnancy carries a mortality rate of 28%.37
Communicating hydrocephalus Communicating (non-obstructive) hydrocephalus is caused by impaired CSF reabsorption into the systemic venous circulation in the absence of physical obstruction. Interruption of normal CSF resorption pathways leads to accumulation and subsequent ICP elevation when compensatory mechanisms are exceeded. Multiple neurologic conditions can result in communicating hydrocephalus, including congenital absence of arachnoid villi, SAH and meningitis. Hemorrhage and infection can lead to fibrosis and impaired CSF outflow.
Subarachnoid hemorrhage During pregnancy SAH is less likely to be caused by a cerebral aneurysm than SAH in a non-pregnant patient. This is represented by the fact that fewer aneurysms are coiled during pregnancy than in non-pregnant controls.9 The clipping/coiling rate in the postpartum period is even lower (6.2%).9 Additionally, SAH in pregnancy has a lower mortality rate compared to non-pregnant women.9 Collectively, these data further suggest that SAH in pregnancy is often non-aneurysmal in origin.
Idiopathic intracranial hypertension Idiopathic intracranial hypertension (IIH), also known as also known as pseudotumor cerebri, is an increase in intracranial pressure (>20 mmHg) of unknown origin with normal sensorium.40 It occurs in pregnant patients at approximately the same rate as in the general population (0.9 per 100 000).41 The most common symptoms and signs are headache, papilledema, and visual
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J.A. Anson et al. changes.40 Diagnostic criteria include papilledema, documented elevation in ICP measured in the lateral decubitus position, normal CSF composition, negative computed tomography (CT) or magnetic resonance imaging (MRI) for intracranial mass, structural or vascular lesions.40 Magnetic resonance imaging can reveal subtle findings suggestive but not specific of IIH. These include flattening of the posterior sclera, empty sella, dilation and tortuosity of the optic nerve sheath and distension of the perioptic subarachnoid space.42 If any of these features are present and no secondary causes of intracranial hypertension (such as CVST or mass lesion) are identified, a diagnostic lumbar puncture can be performed. An opening pressure of greater than 250 mmH2O is suggestive of IIH.40,43 A diagnosis of IIH is not a contraindication to neuraxial anesthesia, and there are multiple reports of the safe use of neuraxial techniques in these patients.44,45
Anesthetic management labor and delivery The choice of anesthetic technique in parturients with increased ICP is dependent on balancing their risks and benefits. Neuraxial analgesia and anesthesia are preferred in the healthy parturient; however, they may be contraindicated in those with intracranial lesions or increased bleeding risk. Furthermore, elevated ICP leading to altered mental status may complicate the anesthesiologist’s ability to safely administer neuraxial blocks. Many anesthesiologists avoid neuraxial techniques due to possible medicolegal implications.46 General anesthesia in pregnancy entails the risk of difficult airway, aspiration, and awareness in addition to potentially masking neurologic changes. Regardless of the planned anesthetic technique, obtaining informed consent can be difficult in patients with altered mental status. Preoperative multidisciplinary planning, involving neurology, neurosurgery, anesthesia, and obstetrics, is essential before selecting an anesthesia technique. The patient and family should be included in preoperative discussions, if feasible. While surgery of any kind during pregnancy entails possible risk to the fetus, the family should be counselled that appropriate care of the mother maximizes the chance of a good fetal outcome.
Neuraxial anesthesia Even though non-complicated spinal anesthesia for cesarean delivery has been reported in a patient with focal increased ICP from a glioblastoma, increased ICP generally is considered a contraindication for spinal anesthesia.47 Loss of CSF secondary to dural puncture may increase the pressure gradient between the supratentorial and infratentorial compartments, resulting in rapid brain stem herniation or intracranial hemorrhage.48 The use of narrow gauge needles (25-
5 gauge or smaller) significantly decreases, but does not eliminate, the risk of complications from dural puncture.49 Epidural anesthesia potentially may be hazardous in patients with increased ICP. Epidural injection can elevate ICP transiently, as an increase in epidural volume may transmit pressure to the intrathecal space. In a porcine model, epidural injection has been shown to be associated with an increase in ICP, with more pronounced changes occurring when ICP was increased at baseline.50 Also, continuous epidural infusion may lead to increased ICP due to compression of the thecal sac.51 Patients may be at increased risk for developing a subdural hematoma due to acute CSF changes.48 If epidural anesthesia is utilized, slow injection of incremental volumes is strongly recommended. The greatest risk with epidural insertion is accidental dural puncture. Based on their findings in patients with traumatic head injuries, Hilt et al. recommended against the use of epidural anesthesia in patients with spaceoccupying lesions, not only due to the risk of decreased cerebral perfusion but also that of herniation.51 The larger size of an epidural needle, compared to a spinal needle, causes greater CSF loss and increases the risk of brain stem herniation in patients with increased ICP.52 Experimental models show that narrower gauge needles are associated with shorter duration of CSF leak after dural puncture and that 20-gauge needles produce a slower rate of fluid loss than 17-gauge needles.53,54 Epidural analgesia has, however, been safely used in labor in patients with intracranial neoplasms.7,55 An epidural anesthetic also can be used to attenuate the expected rise in ICP associated with instrumental vaginal delivery: ICP can rise to 70 cmH2O with instrumentation.5 An MRI of the brain should be obtained preoperatively in patients with intracranial neoplasms where neuraxial anesthesia is being considered. Magnetic resonance imaging evidence of mass effect or hydrocephalus can help predict the risk of herniation with dural puncture.52 Conversely, if a small brain lesion is located in a region remote from CSF pathways it may have little effect on ventricular compression or CSF flow. In this circumstance, ICP may not rise due to caudal displacement of CSF over time. Therefore, dural puncture, and likewise the transient increase in ICP with epidural injection, should be well tolerated and should not result in herniation of brain tissue.52 The use of neuraxial anesthesia in parturients with intracranial pathology requires a comprehensive assessment of the patient’s history, physical examination and radiographic imaging. In patients with space-occupying lesions and MRI evidence of significant mass effect, the risk of herniation is high and dural puncture is contraindicated.52 If there is subtle evidence of mass effect in these patients, the risk of herniation is considered mild to moderate and further neurologic assessment is
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6 warranted before proceeding with neuraxial anesthesia.52 In patients with hydrocephalus, it is critical to determine the location of the obstruction and look for any clinical findings suggestive of elevated ICP. If there is obstruction to CSF flow at or above the level of the foramen magnum, the patient has a mild to moderate risk of herniation with dural puncture. Alternatively, if there is no obstruction to CSF flow at the foramen magnum and there are no clinical findings suggestive of elevated ICP, the patient has minimal to no risk of herniation and it may be reasonable to proceed with neuraxial anesthesia.52 Patients with IIH may experience symptomatic relief if a combined spinal-epidural technique, with small volume CSF withdrawal, is used.45,56 Intrathecal catheters have been used to manage labor analgesia in parturients with IIH.56
Neuraxial anesthesia and severe preeclampsia Historically, it was believed that spinal anesthesia in the setting of severe preeclampsia could result in severe hypotension and subsequent uteroplacental perfusion impairment. However, modern studies show that patients with severe preeclampsia experience less frequent and less severe hypotension than healthy parturients.57 A small prospective study utilizing a non-invasive beat-to-beat cardiac output monitor in patients with severe preeclampsia, demonstrated clinically insignificant changes in cardiac output with spinal anesthesia.58 A randomized, multicenter study similarly concluded spinal anesthesia can safely be used in this patient population and, if hypotension does occur, it is easily treated.59 The decision to utilize neuraxial anesthesia in patients with eclampsia is based on multiple factors. First, coagulation must not be impaired. The mental status of the patient should be evaluated as seizures may depress the level of consciousness. Patients with lower Glasgow Coma Scale (GCS) scores are unlikely to cooperate with neuraxial procedures, and may require tracheal intubation, regardless of the planned obstetric procedure. The potential for a difficult airway should also be considered. If difficulty is anticipated, and the GCS and coagulation are normal, neuraxial anesthesia should be offered.
Neuraxial anesthesia in the presence of lumboperitoneal shunts Some authors have suggested that the presence of an lumboperitoneal shunt (LP) shunt is a contraindication to neuraxial anesthesia due to theoretical concerns of shunt trauma or loss of local anesthetic into the peritoneal cavity.60 However, more recently, epidural anesthesia has been used successfully in patients with LP shunts in IIH.61,62 To minimize the risk for shunt trauma, epidural catheters should be inserted away from the level of the LP shunt: radiographic imaging should be considered before catheter insertion.62 A midline
Raised intracranial pressure approach should be used during epidural catheter insertion, as LP shunt tubing is frequently tunneled subcutaneously in a lateral direction.61,62 In the absence of radiographic imaging, an epidural catheter should be inserted below the LP shunt insertion scar.63 An epidurogram can be considered to confirm the locations of the LP shunt and the epidural catheter.62 The anesthetic principles for shunt insertion or revision during pregnancy are similar to those for cesarean delivery.
General anesthesia Basic anesthetic considerations The presence of symptoms and signs of increased ICP or focal neurological deficits may favor general anesthesia for cesarean delivery.7 However, general anesthesia in the parturient presents the inherent risks of difficult airway, aspiration, and awareness.64,65 In addition, it is not possible to detect alterations of mental status under general anesthesia which may be of concern in patients with intracranial lesions.
Hemodynamic considerations Induction of general anesthesia requires careful planning to avoid potentially devastating hemodynamic changes in a pregnant patient with increased ICP. The use of lidocaine in patients with increased ICP has been well studied. A meta-analysis of 37 randomized trials including 1429 non-obstetric patients, concluded intravenous lidocaine reduces the cardiovascular response to laryngoscopy across all age groups as compared to placebo.66 The authors stated that further studies are necessary to determine the optimal lidocaine dose and timing of administration. Pharmacologic ablation of the response to laryngoscopy and intubation can be achieved with opioids. However, many avoid this practice in the parturient due to placental transfer of opioids and the potential for neonatal respiratory depression. In a randomized, double-blinded, placebo-controlled study in non-parturients, a remifentanil bolus of 1 lg/kg effectively attenuated the heart rate and blood pressure response to laryngoscopy. Lower doses were ineffective, while higher doses resulted in decreased arterial blood pressure which may negatively impact CPP.67 Similar results have been shown in obstetric patients, where compared to a saline placebo, remifentanil 1 lg/kg consistently improved the hemodynamic response to laryngoscopy, although neonatal depression was observed in 10%.68 Remifentanil infusions in healthy volunteers decrease CBF.69 The successful use of remifentanil as an adjunct to general anesthesia has been reported in patients with preeclampsia and HELLP (hemolysis, elevated liver enzymes, low platelet count) syndrome.70,71 Due to the unpredictable neonatal effects of remifentanil, physicians trained in neonatal resuscitation should be present at delivery.72
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J.A. Anson et al. The ability of other opioids to attenuate the hemodynamic response of laryngoscopy has been studied. Fentanyl and alfentanil minimize changes in heart rate and blood pressure during intubation of trauma patients.73 In a prospective, randomized non-obstetric study of patients with baseline hypertension, fentanyl (with and without lidocaine) decreased but did not eliminate the hemodynamic response to laryngoscopy.74 In a randomized trial of obstetric patients, fentanyl 1 lg/kg administered three minutes before induction of general anesthesia resulted in a stable hemodynamic profile during laryngoscopy, without affecting Apgar scores or blood gas analysis.75 Another alternative to blunt the response to laryngoscopy is magnesium. An early study in healthy nonobstetric patients demonstrated pre-intubation administration of magnesium 60 mg/kg resulted in lower plasma catecholamine levels and attenuated heart rate and blood pressure responses post-intubation as compared to saline placebo.76 A subsequent study in patients undergoing general anesthesia for cesarean delivery found magnesium was superior to lidocaine at blunting the hemodynamic response to tracheal intubation.77 One review found Grade B evidence (moderate level of certainty) supporting the use of magnesium to attenuate the hypertensive response to tracheal intubation.78 Esmolol is used frequently to rapidly treat transient hemodynamic changes caused by tracheal intubation. However, in animal models esmolol crosses the placenta and causes fetal bradycardia. As such, it should be avoided in pregnant patients.79 Labetalol, on the other hand, has been used safely in parturients.19
Induction of anesthesia When selecting an intravenous induction agent, the effects on ICP, CBF and cerebral metabolic rate of oxygen (CMRO2) must be considered. Propofol, etomidate, and thiopental all decrease ICP, CBF and CMRO2 and are used routinely in neurosurgical patients. In animal models, propofol causes a dose-dependent decrease in CBF.80 The administration of a 2 mg/kg propofol bolus decreases ICP, without altering CPP, in non-obstetric head trauma patients with normal and compromised intracranial compliance.81 Propofol effectively blunts the response to laryngoscopy in healthy volunteers.82 It has also been shown in a non-obstetric study to be effective in treating seizures; a potential benefit in patients with increased ICP.83 In conjunction with its antiemetic effect, propofol is an attractive choice for patients with elevated ICP. In a study of non-obstetric patients with intracranial lesions, etomidate 0.2 mg/kg significantly decreased ICP without changing CPP or hemodynamics.84 Similarly, in pediatric patients with severe brain trauma there were significant reductions in ICP following an etomidate bolus of 0.3 mg/kg, and improvement in CPP.85
7 However, etomidate also possesses pro-convulsant properties; the exact mechanism of which is unclear.86 Etomidate has pro-emetic tendencies, making it less ideal for neurosurgical patients. Therefore, despite the ICP lowering effects of etomidate, it should not be considered a first-line agent in patients with elevated ICP. It may be, however, an appropriate choice in hemodynamically unstable parturients. There are few comparative studies of various induction agents regarding their effects on ICP. A computer model was developed to predict ICP responses to various induction agents in simulated patients. This demonstrated induction of anesthesia with intravenous agents reduces ICP by up to 30%, with propofol having the greatest impact (propofol > thiopental > etomidate).87 In a study of 40 patients presenting for elective cesarean delivery, propofol was significantly better than thiopental in reducing the systolic blood pressure response to laryngoscopy (propofol 17.4 mmHg vs. thiopental 32.1 mmHg).88 Thiopental is now unavailable to many obstetric anesthesiologists. The choice of neuromuscular blocking drugs in parturients with elevated ICP is controversial. Succinylcholine is used frequently for rapid-sequence induction but has the potential to elevate ICP which may already be increased. Rocuronium 1.2 mg/kg may be a better alternative in terms of ICP to succinylcholine.48 Both succinylcholine and rocuronium provide excellent intubating conditions during a rapid-sequence induction. A 2008 Cochrane review of 37 studies comparing the intubating conditions achieved with succinylcholine using at least 1 mg/kg and rocuronium 1.2 mg/ kg during rapid-sequence induction and intubation found no significant difference between the two drugs.89 As demonstrated in a swine model, pre-treatment with a non-depolarizing muscle relaxant does not prevent the rise in ICP associated with succinylcholine.90 While these studies suggest there is a role for rocuronium in patients with increased ICP, to date, there are no studies directly addressing its use in an obstetric patient population. Concurrent use of anticonvulsant therapy can impact the expected duration of action of non-depolarizing drugs. Acute administration of antiepileptic drugs can potentiate the effect of non-depolarizing muscle relaxants, while chronic antiepileptic therapy confers resistance to these drugs. This resistance is thought to be multifactorial, with induction of hepatic drug metabolism, increased protein binding and up-regulation of acetylcholine receptors all playing a role.91 A summary of strategies to minimize elevations of ICP during induction of anesthesia is presented in Table 1.
Maintenance of anesthesia General anesthesia for cesarean delivery confers an increased risk of intraoperative awareness, particularly in the interval before delivery.92 As such, attention must
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8 Table 1
Raised intracranial pressure Induction of general anesthesia in patients with increased intracranial pressure Strategies
Induction agent
1st line: propofol (flICP, flCBF, flCMRO2, flSeizures, Antiemetic) 2st line: etomidate (flICP, flCBF, flCMRO2, ›Seizures, pro-emetic)*
Neuromuscular blockade
1st line: rocuronium 1.2 mg/kg Anticonvulsant therapy may affect duration
Hemodynamic considerations
Remifentanil bolus (1 lg/kg) before intubation Magnesium bolus (40–60 mg/kg) before intubation Labetalol can be safely administered Avoid esmolol as it crosses placenta and may cause fetal bradycardia
ICP: intracranial pressure; CBF: cerebral blood flow; CMRO2: cerebral metabolic rate of oxygen.*Thiopental may be used if available.
Table 2
Intraoperative intracranial pressure management considerations Strategies
Depth of anesthesia
Bispectral index monitor (BIS) Titrate agent to BIS
