HELLP syndrome - American Association of Nurse Anesthetists

HELLP syndrome (hemolysis, elevated liverenzymes, and low platelets) pathophysiologyand anesthetic considerationsRITHO PORTIS, CRNA, MSMAUREEN A. JACOBS, CRNA, BSJONATHAN H. SKERMAN, BDSc, MScD, DScELIZABETH B. SKERMAN, RNCShreveport, Louisiana

HELLP syndrome in the parturient(hemolysis, elevated liver enzymes, and lowplatelet count) is associated with poormaternal and fetal outcomes. Maternalmortality has been estimated to be as high as24%. Patients with HELLP syndrome arealso at greater risk of pulmonary edema,adult respiratory distress syndrome,abruptio placentae, disseminatedintravascular coagulation, ruptured liverhematomas, and acute renal failure. Perinatalmortality is equally high, ranging from 79 to367 per 1,000 live births, and neonatalcomplications correlate with the severity ofmaternal disease.

Many clinicians view HELLP syndromeas an entity of preeclampsia, and because ofvaried symptomatology, the initial diagnosismay be obscured. Prodromal signs include:(1) weakness and fatigue, (2) nausea andvomiting, (3) right upper quadrant and/orepigastric pain, (4) headache, (5) changes invision, (6) increased tendency to bleed fromminor trauma, (7) jaundice, (8) diarrhea, and(9) shoulder or neck pain.

Before delivery, aggressive obstetricmanagement is directed toward stabilizationof the affected organ systems, if possible, andtimely interruption of the pregnancy in theearly phase of the accelerated diseaseprogression. Definitive therapy is delivery.

Parturients with HELLP syndrome areoften critically ill; their infants are frequentlypremature and their conditions arecompromised. Management criteria shouldinclude a multidisciplinary approach in atertiary care center. Obstetric anesthesiapersonnel should perform a thoroughpreanesthetic evaluation and be familiar withthe pathophysiologic changes of thissyndrome. Determining the anesthetic ofchoice depends on the patient's condition,fetal well-being, and the urgency of thesituation. In the presence of severecoagulopathy, regional anesthesia iscontraindicated.

Key words: HELLP syndrome, obstetricanesthesia, pathophysiology.

IntroductionIn 1982, Weinstein introduced the acronym HELLPto describe symptomatology consisting of hemoly-sis, elevated liver enzymes, and low platelet countthat affected some women with preeclampsia (Fig-ure 1).1 Many clinical investigators view HELLPsyndrome as a variant of severe preeclampsia (Fig-ure 2). Preeclampsia, which is a variant of preg-nancy-induced hypertension (PIH), is associatedwith at least two of the three classic clinical fea-tures: (1) hypertension, (2) proteinuria, and (3) gen-eralized edema. 2

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Elevated liver enzymes

Figure 2Major hypertensive disorders of pregnancy

HELLP syndromeIn 1954, Pritchard et al first described the triad

of hemolysis, elevated liver enzymes, and lowplatelet count in three patients with eclampsia. 3

Since then, similar cases associated with PIH havebeen reported. It was nearly 30 years later thatWeinstein coined the term "HELLP" to describethis syndrome. 1 Although Weinstein consideredHELLP syndrome a unique variant of PIH, othersquestion its existence. Greer and colleagues pro-pose that HELLP syndrome is, in fact, PIH withmild disseminated intravascular coagulation andfurther suggest that more sensitive laboratory testsshould identify an associated coagulopathy. 4 Mar-

Figure 1HELLP syndrome

tin et al state HELLP is a unique variant of severepreeclampsia or eclampsia, which is recognized asa serious cause of multisystemic disease in themother and increased perinatal morbidity andmortality in the fetus and infant.5

In some reported cases of HELLP syndrome,preeclampsia was absent or mild.5 Many parturi-ents have multiple symptoms, making the initialdiagnosis easy to confuse with other medical disor-ders. The presentation of these multiple symptomsmight not, however, coincide with the classic pre-eclamptic picture. All healthcare professionalsdealing with obstetric patients must be familiarwith the varied signs and symptoms associated withthe onset of HELLP syndrome. Some frequentlyreported prodromal symptoms along with weak-ness and fatigue include: (1) right upper quadrantor epigastric pain, (2) nausea and vomiting, (3)headache, (4) changes in vision, (5) increased ten-dency to bleed from minor trauma, (6) jaundice,(7) diarrhea, and (8) shoulder or neck pain. Manypatients report combinations of these symptoms. 5

Several recent articles in the literature havereviewed maternal and neonatal clinical conditionsassociated with HELLP syndrome, which will bediscussed in a following section.

PathophysiologyInadequate uterine perfusion has an impor-

tant role in the etiology of PIH and HELLPsyndrome. 56 A possible mechanism initiating theprocess may be a developmental defect of the spi-ral arteries of the uterus. Typically, with early tro-phoblastic invasion, the muscular walls of the spi-ral arteries lose their ability to contract. In pa-tients with PIH, however, this process is incom-plete and the spiral arteries retain some of theircontractility. This is thought to result in the isch-emic process that produces placental necrosis withsubsequent release of tissue thromboplastin andrenin into the maternal circulation. 7

An alteration of the renin-angiotensin systemoccurs, producing vasospasm with generalized tis-sue hypoxia and vascular endothelial damage. Al-dosterone secretion is increased, resulting in re-tention of sodium and water. Activation of thematernal coagulation system and enhanced plate-let aggregation, resulting from vascular endothe-lial damage, produce fibrinoid deposits in the base-ment membranes of smaller vessels, especiallythose of the placenta. 8-"

Whereas release of mitogens or factors froman ischemic placenta leads to endothelial cell dam-age, release of a peptide (probably fibronectin)8-12and decreased production of prostacyclin result-ing in an imbalance of thromboxane A2 and

Journal of the American Association of Nurse Anesthetists

prostacyclin 3,4 have been cited as causative fac-tors. More recently, investigations of nitric oxidesynthesis in gravid rats and parturients have pro-duced similar aberrations of this syndrome. 5- 17

Overall, a generalized capillary leak causes afluid shift into the extracellular space. The de-crease in colloid oncotic pressure, hypovolemia,hemoconcentration, and increased blood viscositydevelops secondary to the accompanying loss ofalbumin.18

In HELLP syndrome, striking hepatic changesoccur. 19,20 Hepatic blood flow is obstructed whenfibrin deposits develop in the hepatic sinusoids.The liver becomes swollen and engorged, stretch-ing Glisson's capsule and producing epigastric orright upper quadrant pain and tenderness. Hem-orrhagic periportal necrosis, subcapsular hemor-rhage, and in severe cases, spontaneous hepaticrupture may occur. The liver enzymes become ele-vated and the serum glutamic-oxaloacetic trans-aminase value can be 700 U/mL or more. Infre-quently, acute hepatic failure and jaundiceoccur. 19,20 Maternal hypoglycemia is a particularlygrave laboratory finding; however, the cause of thehypoglycemia is yet obscure, even though it is ob-viously related to liver failure. 19' 20

The hemolysis associated with HELLP syn-drome is consistent with a microangiopathic he-molytic anemia.'1821 Vascular endothelial damagewith fibrin deposition results in fragmentation ofred blood cells. The peripheral blood smear re-veals crenated and distorted red cells with spinyprojections along the borders (Burr cells).21 Alsopresent are schistocytes, which are small, irregu-larly shaped red cell fragments. The low plateletcount associated with HELLP syndrome appears tobe due to increased peripheral vascular destruc-tion. Bone marrow studies reveal an increase inmegakaryocytes that suggests rapid platelet turn-over. In addition, recent studies suggest associatedplatelet activation, as well as platelet dysfunc-tion.5,18,20-22

Many tertiary care centers are using a helpfuladjunct to serial coagulation screens-thrombo-elastography (TEG) for a global assessment ofcoagulation. The TEG in normal pregnancy dem-onstrates the hypercoagulable state but also corre-lates with the platelet count. In parturients exhib-iting clinical signs of HELLP syndrome, the TEGappears to remain normal despite prolongedbleeding times, and it often provides a faster re-sult than do clinical laboratory studies in an emer-gency situation.2324

Review of literatureSibai et al described their experience with 442

parturients with HELLP syndrome who weretreated at their tertiary care center.20 The authorsused the criteria listed in Table I to standardize thediagnosis of HELLP syndrome.

Table IHELLP syndrome was based on the clinical diagnosisof preeclampsia and the following laboratoryabnormalities.a. Characteristic peripheral blood smearb. Serum lactate dehydrogenase > 600 pg/L

(or total bilirubin > 1.2 mg/dLc. Serum aspartate aminotransferase > 70 pg/Ld. Platelet count < 100,000/mm 3

Routine laboratory evaluation includeda. Serial measurements of liver function testsb. Complete blood cell countc. Coagulation profiled. Renal function testsDisseminated intravascular coagulation defined asa. Low platelet count (< 100,000/mm3)b. Low fibrinogen (< 300 mg/dL)c. Positive fibrin split products (> 40 pg/dL)d. Prolonged prothrombin time (> 14 seconds)e. Partial thromboplastin time (> 40 seconds)Acute renal failureOliguria-anuria in association with severe renal dys-

function (creatinine clearance _ 20 mL/min)

Poor maternal and fetal prognosis is associ-ated with this symptom complex. Maternal mor-tality ranged from 3.5% to 24%. Other authors alsoobserved that these patients were at greater risk forcomplications, such as liver rupture, disseminatedintravascular coagulation, abruptio placentae, andacute renal failure. 25-27 Perinatal mortality was sim-ilarly high, variously reported as 79 to 100 or 367per 1,000 live births. Death was due to large pla-cental infarcts, abruptio placentae, intrauterinegrowth retardation, intrauterine asphyxia, andprematurity. 19,28

The neonate was at increased risk for a varietyof complications associated with HELLP syndromethat correlate with the severity of maternaldisease.2 6,29 Thrombocytopenia and leukopeniawere frequently diagnosed in neonates (25% to30%) of mothers with HELLP syndrome. Thestrong correlation with the severity of maternaldisease implies that a humoral mechanism may beinvolved in the etiology of HELLP syndrome.2629

Data, however, were minimal regarding theoutcome of subsequent pregnancies and long-termprognosis after the syndrome of hemolysis, ele-


vated liver enzymes, low platelet count, and acuterenal failure. 32 5 Sibai and Ramadan, in a study of32 parturients with HELLP syndrome, indicatedan increased risk for preeclampsia to develop insubsequent pregnancies.' 8 However, pregnancyoutcome and long-term prognosis were usually fa-vorable in the absence of preexisting chronic hy-pertension. Risks were significantly increased forboth mother and fetus if the parturient had preex-isting chronic hypertension. Sibai and Ramadanrecommended that parturients with preexistingchronic hypertension who have had HELLP syn-drome be counseled regarding the high likeli-hood of severe preeclampsia and poor fetal out-come in subsequent pregnancies. s

Obstetric managementDefinitive therapy for the patient with HELLP

is delivery of the placenta.-3 18-20 °,3° Delivery shouldbe expeditious, as any delay is associated with poorneonatal outcome. Prior to delivery, aggressivecontrol of the manifestations of disease is the goal.Pregnancy is usually allowed to continue as longas no evidence of compromise in the fetal or ma-ternal condition is apparent. Medical managementis directed toward stabilization of the cardiovascu-lar system, improvement of intravascular volume,prevention of intracranial hemorrhage, and con-trol of central nervous system irritability. Obstet-ric management of the patient with HELLP syn-drome is less clearly defined. Prediction ofultimate disease severity is difficult because it de-pends on numerous factors. 5 Timely interruptionof the pregnancy (i.e., delivery) is often necessaryearly in the late phase of the disease to preventaccelerated disease progression. Immediate deliv-ery is therefore indicated in patients with progres-sive thrombocytopenia, neurologic deterioration,hepatic or renal deterioration, or fetal distress. 5

Although uterine irritability is frequentlypresent and the cervix is often "ripe" for induc-tion, a significant portion of these patients undergooperative delivery due to fetal distress. In Wein-stein's later series of 57 patients with HELLP syn-drome, 29% of the multiparas and 79% of the pri-migravidas underwent cesarean section.3"

Use of invasive monitoring must be consid-ered according to the following criteria:

1. Hemodynamic alterations can be more ef-fectively controlled.

2. Patients may be critically ill and should bemanaged as such.

3. The severity of the disease is often not clin-ically apparent.

4. Many of these patients will undergo opera-tive delivery.

40

These indications for invasive monitoring aresimilar to those for patients with severe preeclamp-sia.31 The indicated entities include:

1. Unresponsive or refractory hypertension.2. Pulmonary edema.3. Persistent arterial oxygen desaturation.4. Oliguria that is unresponsive to modest

fluid loading.31

The woman's recovery from HELLP syndromeafter delivery depends on the severity of the dis-ease. Platelet counts and serum lactate dehydroge-nase concentrations may be useful predictors ofseverity and recovery. The more severe the expres-sion of the syndrome, the more protracted therecovery.5,18

Anesthetic considerationsMagnesium sulfate therapy is administered

intravenously to reduce central nervous system ir-ritability and prevent seizures. Other effects ofmagnesium sulfate therapy include reduced hyper-reflexia, reduced acetylcholine transmission at theneuromuscular junction, mild vasodilation, mildsedation, and decreased uterine contractility, all ofwhich enhance uterine blood flow.32-36

The parturient should receive a loading doseof magnesium sulfate, 4-6 g intravenously (IV) in a20% solution, infused over 20 minutes. A thera-peutic plasma concentration of 8-8.5 mEq is main-tained by a continuous infusion of 1-2 g/hr. Aplasma magnesium level in excess of the therapeu-tic range can ultimately lead to severe skeletalweakness, ventilatory failure, and cardiac arrest. 37,38

Therapeutic effects of magnesium sulfate ther-apy are estimated by serial assessment of deep ten-don reflexes. Loss or marked depression of the pa-tellar reflexes is an indication of impending toxiceffects of magnesium. It should be kept in mindthat magnesium increases the sensitivity to nonde-polarizing and depolarizing muscle relaxants andreadily crosses the placenta where it may producerespiratory depression, hypotonia, and apnea inthe neonate. 39

Antihypertensive therapy should be consid-ered when the maternal diastolic blood pressureremains over 110 mmHg after administration ofmagnesium sulfate. This therapy is directed towardminimizing the risk of maternal cerebral hemor-rhage and abruptio placentae, while maintainingor improving uteroplacental perfusion. Vasodila-tor therapy combined with plasma volume expan-sion will achieve these goals. The drugs that havebeen most commonly used include hydralazine hy-drochloride, trimethaphan camsylate, nitroglyc-erin, and sodium nitroprusside. Hydralazine is thedrug most commonly used antenatally;40 it pro-


duces an effect within 10-15 minutes and has a rela-tively short half-life. It can produce tachycardiaand elevate cardiac output while increasing renal,hepatic, coronary, and cerebral blood flow. Theeffect of hydralazine on uterine blood flow dependson the degree of preexisting uterine vasoconstric-tion.41 To prevent excessive reduction of the bloodpressure and to maintain adequate uterine bloodflow, hydralazine should be given in small, incre-mental doses of 2.5-5.0 mg IV, spaced at least 15 to20 minutes apart, until the diastolic blood pressurereaches 90 to 100 mmHg or the mean arterial pres-sure is decreased by 15% to 20%. Continuous infu-sion of hydralazine is not recommended because itincreases the potential for precipitous drops inblood pressure and subsequent compromise ofuteroplacental perfusion. Diligent blood pressuremonitoring is indicated whenever antihypertensivetherapy is used. 42

Trimethaphan, a ganglionic blocking agent,can be particularly useful in hypertensive emer-gencies when cerebral edema and increased intra-cranial pressure are of concern, because it does notcause cerebral vasodilation. Trimethaphan canprolong the action of succinylcholine chloride be-cause of intrinsic cholinesterase inhibition.42

In a hypertensive crisis, a continuous infusionof trimethaphan, nitroglycerin, or sodium nitro-prusside can be effective. Sodium nitroprussideshould be limited to short-term use because of thepotential for decreased uterine perfusion and fetalcyanide ion toxicity. Nitroglycerin may be associ-ated with methemoglobinemia. Aggressive therapyby continuous antihypertensive infusion should beaccompanied by continuous invasive hemody-namic monitoring, preferably with an indwellingradial artery cannula. 42

If severe hypertension persists despite vasodi-lator therapy, small doses of propranolol hydro-chloride can be administered. Propranolol cancause fetal bradycardia, so fetal heart rate monitor-ing should be continuous. Other cardioselectivebeta-1 blockers seem less likely to affect uterineactivity, glucose homeostasis, and respirations thandoes propranolol. Labetalol hydrochloride, whichhas both beta- and alpha-blocking properties, hasbeen given orally for long-term treatment of PIHwith encouraging results.43 The intravenous prep-aration of this agent has been used in the pre-induction setting for short-term control of PIH.4344

In pregnant ewes receiving infusions of norepi-nephrine bitartrate (to stimulate vasoconstrictionof the uterine artery), labetalol administration in-creased uterine blood flow by 25%, lowered mater-nal mean arterial pressure by 19%, and did notsignificantly alter fetal heart rate.45 Thus, labetalol

may be an excellent agent for long-term and acutetreatment of PIH. Esmolol hydrochloride holdspromise for acute PIH therapy but has not beenadequately investigated to recommend its routineuse. 46 Calcium channel blockers exert an antihy-pertensive effect through vascular smooth musclerelaxation, but they may also inhibit uterinecontractions.47

Nifedipine, a calcium channel blocker, inhibitsthe influx of extracellular calcium ions into smoothmuscle cells through slow channels. Its effects pre-dominate in arterial and arteriolar smooth muscle.Of the calcium channel blockers, nifedipine hasthe most selective vasodilator properties and theleast cardiodepressant effects. Common maternalside effects include facial flushing, headache, andtachycardia. 48' 49 Currently available only in cap-sules, nifedipine rapidly lowers blood pressureafter oral or sublingual administration. After aninitial dose of 10 mg sublingually, it may be re-peated in 30 minutes and then given in a mainte-nance dosage of 10 to 20 mg every 3 to 6 hours.Physicians should be aware of an exaggerated re-sponse in patients receiving magnesium sulfate. 50

More recently, labetalol has become widelyused for control of hypertension and for attenua-tion of acute hypertension associated with a rapid-sequence induction of general anesthesia in pa-tients with HELLP whose conditions are severelycompromised. 51 It has more rapid onset of actionand does not produce the tachycardia, nausea,headache, excessive hypotension, and decreaseduterine blood flow that are often associated withhydralazine.52' 53 Caution, however, must be used inthe administration of beta-blocking agents to pa-tients with bronchoconstrictive disorders and com-promised myocardial function, because these drugsmay cause bronchoconstriction and decreased ven-tricular function. 54

The best indicator of adequate uteroplacentalperfusion is a fetal heart rate (FHR) within thenormal range (120 to 160 beats per minute) andevidence of adequate variability and no late onsetFHR decelerations. Inadequate perfusion is re-flected by significant ominous changes in the FHR.The rate may accelerate or decelerate, dependingon the level and duration of fetal distress, and,ultimately, late decelerations of the FHR and lossof variability will occur.

Fluid management and monitoringFurther treatment of a patient with such a

compromised condition involves decisions as tomonitoring, fluid management, and type of anes-thetic to be administered. Monitoring required foranesthetic management will obviously be deter-

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mined by the severity of the disease and the extentof prior medical intervention. All such parturientsreceiving anesthesia for labor must be minimallymonitored with continuous supervision, automatednoninvasive blood pressure monitoring, indwell-ing urinary catheter, and monitors for uterinecontraction and FHR. Severe exacerbations of thedisease may require more aggressive invasive mon-itoring. Noninvasive automated blood pressuremonitors have decreased the need for continuousinvasive arterial cannulation, but arterial cannula-tion may be indicated when controlling the bloodpressure is difficult and, especially, when continu-ous infusions of rapidly acting potent vasodilatorsare used, or when frequent blood gas sampling isneeded, as in cases of pulmonary edema. 42'55

Central venous pressure (CVP) monitoring isuseful in guiding fluid and vasodilator therapyand determining the likelihood of congestive heartfailure. Some authorities proclaim the need forpulmonary artery (PA) catheterization in all pa-tients with severe preeclampsia or HELLP syn-drome, citing low correlation between the para-meters. 6'57 Studies by Cotton et al and others haveshown that when the CVP is less than 4 mmHg,the pulmonary catheter wedge pressure (PCWP)will be less than 18 mmHg.5 60 In general, onlywhen the CVP begins to rise above 7-8 mmHg isthere significant risk of an elevated PCWP in thepresence of normal CVP. The initial CVP valueand subsequent response to fluid infusion can alsohelp determine the potential need for PA catheter-ization. The placement of a PA catheter is not with-out risk, 31'54 especially in a patient predisposed tocoagulopathy and is frequently not feasible inmany hospitals' labor units where neither experi-enced personnel nor proper equipment are avail-able. The PA catheter should probably be reservedfor cases in which severe hypertension refractoryto conventional antihypertensive therapy, conges-tive heart failure or pulmonary edema, refractoryoliguria, critical cardiac lesions, or superimposedcardiomyopathy is evident.31' 6162

Oliguria may be due to any of several mecha-nisms that could require different modes of ther-apy, but will usually respond to modest fluid chal-lenge and delivery of the fetus.63 Relative intravas-cular volume depletion and systemic arteriospasmresponds to fluid challenge with hemodynamic im-provement and decreased systemic vascular resis-tance (SVR). Selective renal arteriospasm may re-quire volume expansion along with a decrease inafterload, while decreased renal perfusion due toprofound vasospasm and reduced cardiac outputmay improve with fluid restriction and afterloadreduction."6 65

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Fluid management and volume expansion areimportant issues in these cases. It is important toremember that aggressive crystalloid administra-tion in the face of generalized arterial vasospasm, adecreased colloid oncotic pressure, and increasedcapillary membrane permeability can easily resultin pulmonary edema. Joyce et al recommendedusing CVP measurements during fluid therapyand volume expansion, after demonstrating thatdiastolic blood pressure had an inverse relation-ship to the volume of fluid needed to raise CVPvalues to normal levels (6-8 cm H20). 66 The mostseverely ill patients with preeclampsia (with dias-tolic pressure >110 mmHg) had pretreatmentCVP measurements of -1 to -4 cm H20. Largeamounts of crystalloid frequently precipitated post-partum pulmonary edema. Large amounts of col-loid could have the same effect. A rational ap-proach to volume expansion might be to followcolloid oncotic pressure (COP) measurements and,when indicated, to give moderate amounts of col-loid with limited volumes of crystalloid. Kirshonet al recommended that correction of COP berestricted to cases in which extremely low COPvalues (<12 mmHg) or an extreme negativeCOP-to-PCWP gradient are identified. 67 They alsoconcluded that the primary benefit of volume ex-pansion appears to be in the prevention of sudden,profound drops in blood pressure with antihyper-tensive therapy (or as might be the case with sym-pathectomy from institution of a major regionalblock), but also in the prevention of fetal distressduring labor.67

The role of volume expansion in therapy forpreeclampsia or HELLP syndrome must not beconfused with the need for volume expansion priorto induction of major regional anesthesia. Recom-mendations by Cheek and Samuels for the man-agement of severe preeclampsia are to restricthourly IV fluids in the early stages of manage-ment and then to base further requirements forfluid therapy on clinical signs of inadequate per-fusion, such as decreased urine output, CVP, orPCWP, or increased SVR and normal cardiacoutput.68 Fluid should be restricted in the presenceof signs of hypervolemia, such as increased CVPor PCWP and normal SVR or in the presence ofdecreased cardiac output or impending pulmonaryedema. It is important to assure adequate volumeprior to vasodilation from drugs or regional blockto prevent abrupt, severe decreases in systemic per-fusion pressure. Cheek and Samuels do not recom-mend attempting to increase CVP to 6-8 cm H 20in all patients with preeclampsia before adminis-tering regional anesthesia, as this may result influid overload.68 The same authors believe it suffi-


cient to raise a negative CVP to a positive value(2-3 cm H 20) to avoid hypotension following insti-tution of a major regional anesthetic.68 When dias-tolic blood pressure is less than 100 mmHg, usu-ally 1-2 L of isotonic balanced salt solution isrequired. For patients with severe symptoms-diastolic blood pressure more than 100 mmHg anda CVP of zero or less-Cheek and Samuels recom-mend using no more than 1 L normal saline solu-tion and 25 to 50 g of 25% salt-poor albumin ad-ministered over 30 to 45 minutes prior to inductionof regional anesthesia, with a goal of achieving aCVP of 2-3 cm H 20. 68 Further fluid administrationis guided by CVP after initiation of the regionalanesthetic. Fresh-frozen plasma can be used inplace of albumin for the occasional patient whohas a coagulopathy and is destined for cesareansection.

Anesthetic management of labor and deliveryThe choice of anesthetic, particularly major

conduction anesthesia, in patients with preeclamp-sia or HELLP syndrome has been a subject ofmuch debate.5 469,70

* Parenteral analgesics. Parenteral drugs for se-dation and pain control can be used in labor anddelivery, but this is certainly not optimal manage-ment. This approach is associated with variouscomplications including inadequate relief from thepain and stress of labor and neonatal depression.In the newborn, inefficient metabolism of drugsmay result in respiratory depression with the po-tential for respiratory acidosis, hypoxia, and in-creased intracranial pressure. Narcotics also pos-sess antidiuretic properties that can contribute to adecreased glomerular filtration rate, ineffectiverenal plasma flow, and decreased urine output.The currently available information generally sup-ports the use of epidural analgesia as the anes-thetic of choice for labor, vaginal delivery, and ce-sarean section for most patients with preeclampsiaand HELLP syndrome. 31 ,42,54,55,71- 77

* Epidural anesthesia. Epidural anesthesia hasbeen proven safe and effective in these patientswhen accompanied by careful correction of intra-vascular volume status, appropriate positioning toavoid aortocaval compression, adequate bloodpressure control prior to epidural blockade (pref-erably a diastolic pressure <110 mmHg), slowlyadvanced blockade, and, if necessary, cautious useof small intermittent doses of ephedrine. Thesepatients generally have a more pronounced re-sponse to ephedrine than usual.

Benefits of epidural anesthesia include opti-mal obstetric conditions for labor and delivery,with relief of pain and good maternal relaxation

without the need for systemic depressant drugs.Studies have not reliably demonstrated fetal or ma-ternal compromise from well-conducted epiduralanesthesia. It leads to decreased levels of circulat-ing catecholamines related to relief from the painand stress of labor and delivery, while decreasingthe incidence of maternal hyperventilation and in-creasing intervillous and renal blood flow. It alsopermits the use of low-outlet forceps for a con-trolled delivery and eliminates sudden severe in-creases in blood pressure and maternal bearingdown impulses, both of which can lead to increasedintracranial pressure, cerebral hemorrhage, andpulmonary hypertension. Epidural anesthesia canhelp to alleviate pulmonary edema if it is present,can minimize the risk of aspiration, can be rapidlyextended for surgical intervention if necessary, andcan be continued for relief of postdelivery or post-operative pain. Maternal acidosis and placentaltransport of hydrogen ions can be decreasedthrough inhibition of the motor activity and stressassociated with labor and delivery, thereby decreas-ing the incidence of fetal acidosis. It has also beenassociated with a decreased incidence of eclampticseizures.

Requirements for epidural anesthesia in thispatient population include adequate results of clot-ting studies and the platelet count, adequate vol-ume status, proper positioning to avoid aortocavalcompression, an alert mother with whom person-nel can communicate, and the availability of con-tinuous electronic fetal monitoring. Any decreasein blood pressure of more than 20% should be rap-idly treated with fluids (e.g., crystalloid and/or col-loid), oxygen, change in position, and small, incre-mental doses of ephedrine.

Contraindications to epidural anesthesia in-clude patient refusal, inability to communicatewith the patient, severe fetal asphyxia with result-ant emergency cesarean section, bacteremia orlocal infection at the site of epidural administra-tion, coagulopathy, and severe spinal deformity.In patients with HELLP syndrome, general anes-thesia should only be considered when regionalanesthesia is contraindicated.

There are differing opinions as to the use ofepinephrine in the epidural anesthesia for thesepatients. Arguments against its use include the po-tential for an exaggerated reduction in SVR com-pared with that seen in the absence of epineph-rine, secondary to a beta-agonist effect of a smallamount of systemically absorbed epinephrine78; de-creased umbilical blood velocity observed inDoppler studies79; and possible exaggerated car-diovascular effects or decreased uterine blood flowafter inadvertent intravascular injection.8081 Argu-


ments in favor of its use advocate the necessity ofepinephrine to help establish the extravascular po-sition of the epidural catheter and that currentlyavailable data do not reliably demonstrate anincreased incidence of adverse reaction to epineph-rine delivered to the epidural space. Some work-ers42,82-4 advocate the use of epinephrine in the testdose to rule out an intravascular catheter position,with subsequent avoidance of its use.

For labor and vaginal delivery, epidural anal-gesia should be instituted early in the course oflabor to alleviate the need for parenteral nar-cotics. A segmental block of T-10 to L-1 should beinstituted with small, incremental doses of low-concentration local anesthetic until the patient'scondition is stable and the level of blockade is es-tablished. A higher and denser block can then bereadily obtained to assure adequate anesthesia ifan urgent cesarean section becomes necessary. Pro-found perineal anesthesia can be provided withcorrect positioning of the patient when vaginal de-livery is imminent. Once the desired level of block-ade is established, it can be maintained by inter-mittent injections or, ideally, by continuousinfusion. Addition of narcotics to the local anes-thetic enhances the analgesic effect of the epiduralagent. 85-87

* Subarachnoid anesthesia/analgesia. Subarach-noid block (saddle block) can be used for immi-nent delivery in these patients, as long as they havebeen adequately hydrated and positioned to avoidaortocaval compression and the block level is keptat or below T-10 when possible. Some recommendthe addition of a low-dose narcotic (10-25 pg fen-tanyl) to a low-dose hyperbaric local anesthetic. 42,88

Disadvantages associated with the subarachnoidblock include the potential for more rapid and un-controlled blood pressure changes and the inabil-ity to extend the block once it has been estab-lished.88

Anesthetic management of cesarean section* Nonemergency. For the patient with HELLP

syndrome who is scheduled for a nonemergencycesarean section, epidural anesthesia is usually themethod of choice. Subarachnoid block might be areasonable second choice in patients with mildsymptoms and can be used safely with meticulousattention to detail, adequate blood pressure con-trol and diligent monitoring, adequate hydration,proper positioning, and the use of small, intermit-tent doses of IV ephedrine as necessary. Intrathe-cal narcotics can also be added to the subarachnoidblock for prolonged postoperative pain relief."88

* Emergency with an existing epidural catheter.For emergency cesarean section when an epidural

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catheter is already in place, the catheter can beused to provide surgical anesthesia for the cesar-ean section in most instances. If the epidural cath-eter is functioning properly at an adequate leveland there is not severe fetal distress, the level ofepidural anesthesia can generally be extendedquickly with a rapid-acting local anesthetic duringsurgical preparation without delaying the surgeryor causing further fetal compromise. For acuteemergencies, such as abruptio placentae, uterinerupture, or severe fetal distress with an inadequateor very low block level, it might be unwise to rap-idly extend the anesthetic level in large incrementsdue to the potential time delay and cardiovascularchanges resulting in further compromise to an al-ready jeopardized fetus. If a general anesthetic isunavoidable, any degree of anesthesia present as aresult of epidural administration could help to at-tenuate the severe hypertensive response often seenin these patients after induction, laryngoscopy, in-tubation, and surgical stimulation.

* Emergency without an existing epidural catheter.For a cesarean section that is truly an emergency,the institution of a major regional anesthetic iscontraindicated and a general anesthetic is indi-cated, although it may be fraught with potentialhazards in patients with acute exacerbations ofHELLP syndrome.89 There is a higher incidenceof complicated airway management, 90'9' adverse car-diovascular responses, and altered requirementsfor and responses to administered drugs.92 There isa greater risk of aspiration secondary to difficultor failed intubation as a result of airway edemathat is often present in patients with severe pre-eclampsia or HELLP syndrome.90'91 Diligent ex-amination of the airway is indicated, and an awakeintubation must be considered in the patient whoappears difficult to intubate or in the presence ofhoarseness or stridor.68 Patients with PIH oftenhave extreme cardiovascular responses with poten-tial hypertensive crisis secondary to induction, lar-yngoscopy, intubation, surgical stimulation, andemergence from anesthesia. Decreased plasma vol-ume, increased interstitial fluid, hypoproteinemia,altered hepatorenal function, and magnesium sul-fate therapy can alter maternal requirements foradministered drugs and their effects and disposi-tion.

Prior to induction, the patient should be posi-tioned with left lateral uterine displacement anddenitrogenated to help assure continued adequatematernal oxygenation. 9°93 This should also help todiminish the effects of decreased intervillous bloodflow, which has been demonstrated by some inves-tigators to occur after induction with thiopentalsodium and succinylcholine followed by endotra-


cheal intubation.94 When feasible, rapid-acting an-tihypertensive agents, such as labetalol, sodium ni-troprusside, nitroglycerine, or trimethaphan,should be used to decrease the diastolic blood pres-sure to the range of 100-105 mmHg prior to induc-tion and to minimize the potentially extreme hy-pertensive responses. 42 If magnesium sulfatetherapy is already in use, it should be continuedintraoperatively. Antihypertensive drugs shouldremain available and IV lidocaine and potentshort-acting narcotics can also be used to minimizethe maternal stress response. Even though it maynecessitate neonatal respiratory support and phar-macologic reversal, the use of narcotics may be pru-dent in an effort to blunt the extreme stressresponses and the potentially devastating conse-quences. 95

Induction can then be accomplished by rapid-sequence technique with cricoid pressure (Sellickmaneuver) using thiopental and succinylcholinefollowed by endotracheal intubation. Thiopentalcan be used in larger doses (4-6 mg/kg) to helpblunt the stress response. If magnesium sulfate isbeing used, no defasciculant is necessary, and sen-sitivity to succinylcholine may be increased. Keta-mine should be avoided because of its sympatho-mimetic and epileptogenic activity. Maintenancecan be accomplished with nitrous oxide and oxy-gen, along with low-dose potent inhalation agentsand muscle relaxants as needed. Narcotics and ben-zodiazepines can be given after the embilical cordhas been clamped.

The inspired nitrous oxide concentrationshould be limited until delivery, after which it canbe increased. The potent inhalation agent of choicemight be isoflurane (up to 0.75% prior to delivery)due to its vasodilating activity. The theoretical con-siderations of halothane usage in the presence ofaltered hepatic function and the epileptogenicproperties and potential for renal toxicity ofethrane in the presence of an altered metabolicstate and impaired renal function raise concernabout the suitability of these agents. Low doses (1/3to 2/3 minimum alveolar concentration (MAC) ofthe potent inhalation agents can help to avoid re-call and blunt the response to surgical stimulationand are not associated with decreased uterine con-tractility, increased uterine bleeding, or neonataldepression. Muscle relaxation can be maintainedwith succinylcholine by continuous infusion. Aneuromuscular blockade monitor should be usedto guide the dose because there may be an exagger-ated response due to the reduced pseudocholines-terase activity seen in pregnancy and the potentia-tion by magnesium sulfate. Nondepolarizing neu-romuscular blockers may also be used, again with

careful monitoring. Antihypertensive drugs shouldbe readily available and used as directed by dili-gent blood pressure monitoring.

SummaryAs has been shown, HELLP syndrome can be

an extremely serious and complex multisystem dis-order involving much more than just hyperten-sion. Special considerations in obstetric and anes-thetic management are necessary. Hopefully,continued investigation and new findings mightlead to a better understanding of the etiology andpathophysiologic changes of the syndrome andallow improved capabilities in prevention, diagno-sis and treatment, thus minimizing the morbidityand mortality currently associated with this syn-drome and its complications.

Women with HELLP syndrome are often crit-ically ill. Their infants are frequently prematurewith compromised conditions. There is no idealanesthetic for these patients; however, certain man-agement criteria should be observed. These in-clude early diagnosis, hospitalization in a tertiarycare center, and a multidisciplinary approach withactive involvement of the obstetric anesthesia careteam. The obstetric anesthesia personnel must ob-tain a thorough preanesthetic evaluation and beknowledgeable about the pathophysiologic changesin the parturtient with HELLP syndrome.

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AUTHORSRitho Portis, CRNA, MS, earned his associate degree in nursing

from the University of Southern Mississippi at Natchez in 1974; hecompleted his nurse anesthesia education and earned the bachelor ofscience at the University of Mississippi Medical Center in 1977. Hethen became faculty for the Charity Hospital Nurse Anesthesia Pro-gram in New Orleans, where he gained his master of science from theCharity Hospital/Xavier University in New Orleans in 1986. He ispresently a locum tenens anesthetist in many southern states and iscurrently practicing at University Hospital, Louisiana State UniversityMedical Center (LSUMC), in Shreveport, Louisiana.

Maureen A. Jacobs, CRNA, BS, earned her bachelor of sciencedegree in nursing from Northwestern University in Natchitoches, Lou-isiana in 1973; she graduated from the University of Mississippi Schoolof Nurse Anesthesia, Jackson, Mississippi, with another bachelor ofscience degree in Nurse Anesthesiology in 1976. She has worked atUniversity Hospital, LSUMC, Department of Anesthesiology, since1978 and has practiced obstetric anesthesia exclusively since 1983.

Jonathan H. Skerman, BDSc, MScD, DSc, graduated from the Uni-versity of Queensland, Australia, with his BDSc in 1963. After living inLondon, England, for 8 years, he came to the United States in 1971. Heearned is MScD from Boston University School of Graduate Dentistryin 1973, and his DSc from Boston University in 1974. He completed hisresidency in Anesthesiology at Boston City Hospital in 1983 and hasbeen in the Department of Anesthesiology at the School of Medicine,LSUMC, since that time. He is currently professor of Anesthesiology,professor of Obstetrics and Gynecology, and vice chairman forAdministration and Research in the Department of Anesthesiology.

Elizabeth B. Skerman RNC, graduated from Northwestern StateUniversity School of Nursing in 1975 with an associate degree in Nurs-ing. She has been certified in Inpatient Obstetric Nursing since 1983and has worked in labor and delivery units since graduation. She iscurrently a clinical specialist in Inpatient Obstetrics at University Hos-pital, LSUMC, where she has been since 1986.


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HELLP syndrome - American Association of Nurse Anesthetists