anesthetic considerations in hellp syndrome.pdf

Anesthetic considerations in HELLP syndromeM. del-Rio-Vellosillo1 and J. J. Garcia-Medina2,3

1Department of Anesthesia, University Hospital Virgen de la Arrixaca, El Palmar, Murcia, Spain2Department of Ophthalmology, University Hospital Reina Sofia, Murcia, Spain3Department of Ophthalmology and Optometry, University School of Medicine, University of Murcia, Murcia, Spain

Correspondence

M. del-Rio-Vellosillo, Department of

Anaesthesia, University Hospital Virgen de la

Arrixaca, Ctra. Madrid-Cartagena, s/n, 30120 El

Palmar, Murcia, Spain

E-mail: [email protected]

Conflicts of interest

None for either author.

Funding

None.

Submitted 25 May 2015; accepted 3

September 2015; submission 18 February

2015.

Citation

del-Rio-Vellosillo M, Garcia-Medina JJ.

Anesthetic considerations in HELLP syndrome.

Acta Anaesthesiologica Scandinavica 2015

doi: 10.1111/aas.12639

Background: HELLP syndrome (hemolysis, elevated liverenzymes, low platelets) is an obstetric complication with hetero-

gonous presentation and multisystemic involvement. It is charac-

terized by microangiopathic hemolytic anemia, elevated liver

enzymes by intravascular breakdown of fibrin in hepatic sinusoids

and reduction of platelet circulation by its increased consumption.

Methods: In terms of these patients anesthetic management, itis essential to consider some details: (1) effective, safe periopera-

tive management by a multidisciplinary approach, and quick,

good communication among clinical specialists to achieve correct

patient management; (2) neuroaxial block, particularly spinal

anesthesia, is the first choice to do the cesarean if there is only

moderate, but not progressive thrombocytopenia; (3) if a general

anesthesia is required, it is necessary to control the response to

stress produced by intubation, especially in patients with either

severe high blood pressure or neurological signs, or to prevent

major cerebral complications; (4) invasive techniques, e.g., as tra-

cheostomy, arterial, and deep-vein canalization, should be consid-

ered; (5) if contraindication for neuroaxial anesthesia exists, rapid

sequence intubation with general anesthesia should be regarded

as an emergency in patients with full stomach; (6) increased risk

of difficult airways should be taken into account.

Results: Optimal patient management can be chosen after con-sidering the risks and benefits of each anesthetic technique, and

based on good knowledge of these patients pathophysiological

conditions.

Conclusion: Later, close patient monitoring is recommended forpotential development of hemorrhagic complications, dissemi-

nated intravascular coagulation (DIC), or eclampsia.

Editorial comment: what this article tells us

Hemolysis, elevated liver enzymes, and low platelets HELLP syndrome continues to be a threatto the well-being of some obstetric patients. This article provides an updated review of periopera-

tive approaches for safest care for obstetric patients with HELLP syndrome who need urgent oper-

ative delivery.

Pregnancy-induced hypertension is a broad-

spectrum entity which occurs in approximately

5% of pregnancies whose physiopathology

abnormalities are found in vasoconstrictor and

vasodilator agent production as a response to

diffuse endothelial injury, where placental

Acta Anaesthesiologica Scandinavica (2015)

2015 The Acta Anaesthesiologica Scandinavica Foundation. Published by John Wiley & Sons Ltd 1

REVIEW ARTICLE

vasculitis plays a major role. The clinical trans-

lation is high blood pressure, kidney failure by

fibrin renal deposits, and multiorgan failure by

fibrin extrarenal deposits and consumption

coagulopathy.1

HELLP syndrome (SH), described in 1982 by

Weinstein,2 is a severe manifestation of preg-

nancy-induced hypertension, defined by some

authors as a variation of pre-eclampsia.

Nonetheless, SH may appear alone or in associa-

tion with it.3,4

Despite the improvements made in recent

years in managing this syndrome, many details

of SH remain unknown in terms of its etiology,

diagnosis, management, and treatment.

Incidence

Its incidence is between 212% of all pregnan-cies, and in 1020% of cases of pre-eclampsia.5

It occurs during 70% of antepartum periods and

during 30% of postpartum periods, and emerges

mostly in the first 48 h.6,7

Classification

Several classification systems are used to catego-

rize SH. The first is based on the number of pre-

sent abnormalities (hemolysis, elevated liver

enzymes, and low platelets), in such a way that

patients are classified as partial SH (they present

one or two abnormalities) or complete SH (three

abnormalities are present).4,6

Alternatively, SH may be classified based on

the number of platelets: class I, < 50 9 109/l;class II, 50100 9 109/l; and class III, 100150 9 109/l.8 Morbidity and mortality are high

in class I.8

Clinical manifestations

This syndrome is characterized by hemolysis,

elevated liver enzymes, and thrombocytopenia

(lactate dehydrogenase (LDH) 600 IU/l, AST 70 IU/l, platelets 100 9 109/l).9

Hemolysis is caused by microangiopathic

hemolytic anemia produced by vascular damage

and fibrin deposits. This destruction of red

blood cells causes fragmented red blood cells

and schistocytes on a blood film and increased

LDH.10 Elevated liver enzymes may reflect both

liver damage and a hemolytic process.5 A drop

in platelets is due to increased platelet con-

sumption by adhesion to endothelium damage

with a short half-life.11

Women with partial SH have few symptoms

and develop less complications than those with

complete SH.6 However, partial or incomplete

SH patients may develop complete SH.12

Typical clinical symptoms include abdominal

pain in the right upper quadrant or epigastral-

gia, nausea, and vomiting; therefore, the diagno-

sis of the illness can be delayed for a long

time.1315 Up to 3060% of women complain ofheadaches and up to 20% suffer visual distur-

bances.9 However, women with SH can also

present non-specific symptoms and signs.9

Another common feature of SH is a severe, evo-

lutionary coagulopathy before, during, and after

childbirth or cesarean section, which requires a

close, continuous clinical evaluation.1 This syn-

drome is also characterized by becoming exacer-

bated at night and recovering during the day.16

Diagnosis

The diagnostic criteria to define this syndrome

vary vastly.9

The first thing one should do is to assess the

patients clinical situation, gestational age,

blood pressure control, and the fetus.

A suspected diagnosis is based on clinical

grounds, but is confirmed by laboratory data.

Complimentary laboratory tests should include

a complete blood cell count, in particular a

platelet count, coagulation parameters, AST,

LDH, and haptoglobin and urine examination.

Thrombocytopenia is primary and an early

cause of bleeding disorders in SH. Fibrinogen

degradation products are non-specific unless

they are > 40 mg/l, but 15% of patients withDIC present concentrations of < 40 mg/l.Fibrinogen degradation products also have a

half-life of 572 h and do not always reflect thecurrent coagulation state.17,18

Thromboelastography can be useful for know-

ing the etiology of bleeding in these patients

with SH, but it has not been demonstrated as

being useful for predicting risk of bleeding.17,18

A differential diagnosis in SH patients should

include a wide variety of processes. Neverthe-

less, the most important diagnosis to distinguish


2 2015 The Acta Anaesthesiologica Scandinavica Foundation. Published by John Wiley & Sons Ltd

M. DEL-RIO-VELLOSILLO AND J. J. GARCIA-MEDINA

it are those with thrombocytopenia (gestational

thrombocytopenia, autoimmune thrombocy-

topenic purpura), or those associated with

microangiopathic hemolytic anemia (pre-eclamp-

sia, hemolytic uremic syndrome, thrombotic

thrombocytopenic purpura, acute fatty liver dis-

ease of pregnancy).

Treatment

Based on this literature review, one can see that

the management of these patients is quite

diverse, with the final treatment being delivery

of the fetus and the placenta.19

Following the SH classification, delivering

women with complete SH are at more risk of

complications than those with partial SH, so

they should be scheduled for delivery within

48 h. However, women with partial SH could

be candidates for conservative treatment.20

Nonetheless, most cases are usually indicated

for cesarean section because of deteriorating

maternal conditions.13,21

Other guidelines to follow are weeks of preg-

nancies, for which there are generally three main

options1,22: (1) immediate delivery at 34 weeks

or later; (2) delivery in 48 h after evaluating or

stabilizing the maternal clinical conditions and

treating with corticoids. The most advisable

option appears to be between 27 and 34 weeks;

(3) a wait-and-see attitude in pregnancy earlier

than 27 weeks, and treatment with corticoids.

During treatment, it is important to monitor

the patient by assessing vital signs and balanced

fluid.23

Some of the drugs used in this syndrome are:

corticoids, antihypertensive drugs (e.g., labeta-

lol) and magnesium sulfate.9,23 Another therapy

discussed in SH is plasmapheresis.

Obstetric anesthetists should be cautious with

administrating fluids, and should also consider

transfusing blood products whenever needed.

Corticoids

Although the use of corticoids in these patients

is still controversial, two guidelines for corti-

coids can be used in SH management19,24,25: (1)

For fetal lung maturation (standard regime treat-

ment), and (2) for maternity benefits (high doses

of corticoids) for extremely low levels of plate-

lets, extremely high liver enzymes, or dimin-

ished urine output.

When high doses of corticoids are used in

mothers, treatment duration is variable (there

are studies that have used them from 24 h to

2 weeks) in terms of following up protocols in

their hospital or observing improvements in lab-

oratory parameters.19 An increased platelet

count has been found in observational studies

with this treatment.25 Based on available evi-

dence, it is not clear whether administration of

corticoids increases the number of platelets so

that locoregional anesthesia can be performed.26

Even so, a systematic review has concluded

that there was not enough evidence to accept or

reject the use of corticoids, such as adjuvants, to

treat these patients.25 There is no scientific sup-

port for the use of either corticoids in postpar-

tums as no changes have been observed in

maternal morbidity and mortality, or blood

products in such patients.27

When administering corticoids in the fetus,

the Task Force on Hypertension in Pregnancy

recommends, be it with low-quality evidence,

administering corticoids for fetal benefits to

mothers before gestation week 34 if the mother

and the fetus are stable.28

Antihypertensive drugs

Given the risk of cerebral hemorrhaging and

abruptio placentae due to high blood pressure,

most guidelines recommend lowering systolic

blood pressure to 140150 mmHg and diastolicblood pressure to 90100 mmHg using labetalolas the drug of choice and monitoring the patient

for the first 24 h.5,7,29

Other safe drugs to control high blood pres-

sure in pregnancy are hydralazine, methyldopa,

nifedipine or isradipine, some b-adrenoceptorblockers (metoprolol, pindolol, propranolol),

and low-dose diazoxide.30

Anticonvulsants drugs

Magnesium sulfate (MgSO4) is the drug of

choice for prophylaxis, treatment, and recur-

rences of seizures (eclampsia).31,32 SH patients

must be treated prophylactically with magne-

sium sulfate to prevent seizures, regardless of

them having hypertension or not.33



HELLP SYNDROME AND ANESTHESIA

The guideline recommended by the Collabora-

tive Eclampsia Trial is 45 g of MgSO4 adminis-tered in 5 min, and subsequently 1 g/h for 24 h.

If a recurring seizure appears, 2 g of MgSO4should be administered.34

MgSO4 monitoring is taken by clinical param-

eters of urine output, breathing rate, oxygen sat-

uration, and patellar reflexes. The normal

plasma concentration lies between 1.58 and

2.55 mg/dl. The recommended therapeutic con-

centrations lie between 4 and 7 mg/dl.35

Toxicity is often presented as kidney failure.

Treatment of its toxicity must be given with

10% calcium gluconate, 1 g administered in

10 min.36

Blood products transfusion

In cases with continuing hemolysis and persis-

tent postpartum thrombocytopenia, blood and

platelet transfusion, as well as treatment with

albumin, are standard treatments.23,37

When the platelet count falls below 50 9 109/l,

it can be considered a DIC with a worse progno-

sis. For this reason, it is advisable to keep platelet

levels above 50 9 109/l to avoid the risk of bleed-

ing.38 If DIC occurs, it can be treated with fresh

frozen plasma to replace clotting proteins.33

Plasmapheresis

Plasmapheresis is one of the support therapies

that offers more favorable results in patients

who are refractory to conventional treatment.39

41 The exact mechanism is unknown but, in

general, plasmapheresis removes plasma factors

and replaces new elements by encouraging

plasma from patients. However, more research

work needs to be done into this technique for it

to be recommended.42

Some SH patients, whose bilirubin or crea-

tinine has progressively increased for more than

72 h after delivery, could benefit from plasma-

pheresis with fresh frozen plasma.39,43

Fluid therapy

In line with this, a restrictive therapy in these

patients could exacerbate intravascular vasocon-

strictors and lead to kidney failure.44,45 Never-

theless, a non-restrictive fluid therapy is not

recommended because a positive fluid balance

entails a possible risk of producing a pulmonary

edema.

Evidence suggests that the use of intravenous

fluids to increase plasma volume or to treat olig-

uria in women with normal renal function and

stable creatinine levels is not advisable, nor is

treating oliguria with furosemide and low doses

of dopamine recommended in women with nor-

mal renal function.46,47

Complications

Maternal and fetal morbidity in SH is higher

than normal, which poses a challenge: coopera-

tion for the pediatric, anesthetic, and obstetric

team to optimize maternal-fetal care and to

reduce morbidity and mortality for both the

mother and fetus.

Maternal complications

Since 1982, SH has been associated with a range

of mortalities of between 124%,48 where aver-age mortality is 5%.48

The laboratory values that indicate over 75%

of maternal morbidity and mortality are: LDH

concentration > 1400 U/l, AST > 150 U/l, ALT> 100 U/l, and uric acid concentration > 7.8 mg/100 ml (> 460 lmol/l).44 Nonetheless clinicalsymptoms, such as headaches, visual distur-

bance, epigastric pain, and nauseas or vomiting,

have been suggested to be better predictors of

adverse maternal outcomes than laboratory

parameters.49

The high maternal morbidity and mortality

associated with this syndrome is due to multi-

ple organs being affected: liver, kidney, brain,

and vascular system.50 Therefore, it often

implies having to terminate pregnancy early.51

The maternal complications that can occur

with this syndrome are: eclampsia, placental

abruptio, DIC, acute renal failure, severe ascites,

cerebral edema, pulmonary edema, hematoma

infection, subcapsular liver hematoma, liver

rupture, hepatic infarction, recurrent thrombosis,

retinal detachment, cerebral infarction, cerebral

hemorrhaging, and maternal death.5 Indeed, 1538% of SH patients have complications associ-

ated with kidney failure, pulmonary edema, and

DIC.5154




The risk of renal failure and pulmonary edema

increases in patients with postpartum SH when

compared to patients with prepartum SH.5

A recent study by Habli et al., considered

long-term maternal morbidities in women with

SH, where new-onset essential hypertension

(33%), depression (32%) and anxiety (26%)

appeared more frequently. Other less frequent

morbidities in these women were respiratory dis-

ease (4.8%), renal disease requiring hemodialy-

sis (2.4%) and retinal disease (1.6%).55

Isler et al. detected that cerebral hemorrhaging

or stroke was the primary cause of maternal

death in 26% of cases and a main contributor in

45% of women.48

The incidence of liver rupture in SH is

between 12% of cases and is the cause ofmaternal mortality, estimated to be between 1886% of cases.56 It is due to liver ischemia by

reduced liver flow with the appearance of

infarct, subcapsular hematoma and intra-

parenchimal hemorrhaging, which leads to liver

rupture.5759 Liver bleeding can occur early dur-

ing HELLP syndrome development in patients

with advanced class I.60 In these patients, close

hemodynamic monitoring and assessment of

clotting parameters are necessary, along with

serial imaging test evaluations and manipula-

tion of the liver should be avoided. The clinical

picture includes pain in the upper right quad-

rant, or epigastric or shoulder pain with anemia

and hypotension. Liver rupture is confirmed by

a computed tomography (CT) scan, ultrasonog-

raphy, or magnetic resonance imaging (MRI).5 If

hemodynamic decompensation occurs, surgery

may be necessary. Cases of liver transplantation

with acute liver failure or uncontrolled bleeding

have been documented,61 and other cases with

conservative treatment in hemodynamically

stable patients have been reported.62

Fetal complications

Perinatal mortality in SH, with an incidence of

7.434.0%, depends on gestational age at deliv-ery.9,63 Fetal complications with this syndrome

include: placental abruption, cerebral hemor-

rhaging, perinatal death, preterm delivery,

neonatal thrombocytopenia, respiratory distress

syndrome, and intrauterine growth restriction.5,33

Anesthetic recommendations

Premature delivery in these patients is normal

and deliveries are often complicated by

intrauterine growth retardation or placental

abruption. Therefore, cesarean section is quite a

common practice in such cases.

Given the high incidence in delayed or missed

diagnoses among these patients, the anesthesiol-

ogist should have a high index of suspicion and

should recognize that a delivering woman with

abdominal pain, nausea and vomiting could

have SH.

The key to safe management of such patients

is to treat hypertension and eclampsia, consider-

ing the presence of liver or kidney dysfunction,

and reduce the tendency of bleeding. The deter-

mination of appropriate anesthetic management

is based on the conditions of both the delivering

woman and the fetus, and also on urgent sur-

gery.64,65 So anesthetic treatment in these

patients is complex, and the risks and benefits

of each anesthetic technique must be contem-

plated, based on sound knowledge of these

patients pathophysiological conditions.

First a preoperative examination should be

performed, which should include an electrocar-

diogram (ECG) and a complete blood count

with a platelet count, liver function tests, serum

creatinine concentrations, urea and uric acid,

fibrin degradation products, and prothrombin

and partial thromboplastin times.14 Blood com-

ponents, including cross-matched red cells, pla-

telet concentrates, and plasma, should be

available.21

Moreover, a blood transfusion should be eval-

uated depending on hemoglobin levels.66 In

patients with thrombocytopenia, platelet trans-

fusion should be considered at the time of sur-

gery, and not before, because platelets can be

rapidly consumed.67 Urinary catheterization is

also advisable to control dieresis hourly.

An intravascular volume assessment, proper

blood pressure control, and invasive hemody-

namic monitoring should be performed.

Intravascular volume depletion in SH is usually

related with hypertension severity.21 It is impor-

tant to remember that excessive crystalloid

administration in patients with widespread

vasospasm, drop in colloid oncotic pressure and




increased capillary membrane permeability may

easily produce an pulmonary edema.

Central venous pressure monitoring is not

usually necessary in these patients, unless it is

complicated by oliguria, pulmonary edema, or

some form of heart disease. Although the results

of the control studies are not available, the use

of a catheter in a pulmonary artery has been rec-

ommended in patients with: (1) refractory

hypertension; (2) oliguria with resistance to

fluid therapy; (3) signs or symptoms of pul-

monary edema.33,68,69

Blood sugar monitoring is recommended

because of some case reports of severe hypo-

glycemia in SH with assumed liver dysfunc-

tion.20,29,70

To manage uterine contractions in pregnant

women with hypertension, oxytocin is consid-

ered the treatment of choice. Cases of hyperten-

sive crisis have been attributed to ergometrine,

so it should not be used in these patients.7173

Misoprostol is associated with rising blood

pressure, but to a lesser extent than ergome-

trine.36

In most patients, blood pressure, platelet

count, and levels of liver enzymes normalize

within 4896 h postpartum, so a follow-up ofthese patients in an intensive care unit is con-

sidered necessary.21,74 Moreover, these patients

may develop complications during the postpar-

tum period, such as postpartum bleeding, DIC,

or eclampsia. Abnormal bleeding is often seen

and there is a higher incidence of perioperative

bleeding complications, such as blood loss,

wound hematoma, and postpartum blood trans-

fusions.13,21

Avoiding non-steroidal anti-inflammatory

agents for postoperative pain is recommended

because hypertensive crises have been described

in these patients. Hence, we should use alterna-

tive drugs such as paracetamol and opioids.75

Types of anesthesia

The anesthetic management of these SH patients

poses a challenge to anesthesiologists because

both general and regional anesthetic techniques

are potentially associated with complications in

SH.

Administration of regional anesthesia not only

prevents the complications of general anesthe-

sia, such as difficult intubations, a vasopressor

response to tracheal intubation but also

improves uteroplacental blood flow and neona-

tal results.76 It has been proven that the sympa-

thetic blockade that produces neuroaxial

anesthesia improves intervillous blood flow in

hypertensive delivering women by lowering

uteroplacental resistance.77

Administration of neuraxial anesthesia mini-

mizes the potential risk of fetal exposure to

depressant anesthetic drugs, reduces the risk of

maternal pulmonary aspiration, promotes rapid

wandering and lowers the incidence of maternal

thromboembolism.76 Nevertheless, it is advis-

able to closely monitor the neurological status of

these patients.78

Thus, deciding about the anesthetic technique

to be adopted must be done on an individual

basis in each case, based on maternal and fetal

factors as coagulation and maternal cardiovascu-

lar stability are decisive (Fig. 1).52 Even so, we

must explain to patients the risks and benefits

of the anesthetic technique to be used in each

case.

Regional anesthesia

Regional anesthesia offers benefits to women

and fetuses in SH, but it also involves coagu-

lopathy-related risks.

Epidural venous plexus engorgement in deliv-

ering woman and a smaller number of platelets

predispose them to a higher risk of hematoma

after regional anesthesia.75.

The very few published reports there are on

an epidural hematoma in obstetric patients with

epidural anesthesia have always been associated

with other etiological factors, such as spinal

tumors or arteriovenous malformations.79 The

incidence of epidural hematoma in obstetric

epidural anesthesia is estimated to be about

1:50,0000 cases of anesthesia.80 More than 100

spontaneous epidural hematoma without spinal

puncture have also been published.81

Hemodynamic stability should be ensured

prior to performing locoregional anesthesia, as

should checking the absence of altered blood

coagulation and assessing the number of plate-

lets.

Coagulation in these patients is usually due to

a drop in the number of platelets and is less




frequently attributed to DIC.76 This alteration

prevents having to give regional anesthesia for

cesarean sections in most cases.

From the anesthesiologists point of view, no

consensus on the minimum number of platelets

that confers safety to neuroaxial anesthesia in

these patients has been reached. In the absence

of risks factors (anticoagulants, antiplatelet

agents, acquired or congenital abnormalities of

coagulation or platelet function, a fast drop in

platelets), a platelet count higher than 80,000/

mm3 indicates that it is safe to undertake spinal

and epidural anesthesia. It is likely that lower

counts confer safety, but existing publications

have not yet provided enough evidence to rec-

ommend it.82

There are other published studies where neu-

roaxial anesthesia has been administered safely

in these patients with platelet counts below

10,0000/mm3, but a timely coagulation evalua-

tion is recommended.8385 Studies that have also

investigated coagulation in these patients using

thromboelastography have not described coagu-

lopathies with platelet counts over 10,0000/mm3.

- High-caliber intravenous access - Complete blood count - Blood sugar monitoring - ECG - Urinary catheterization- Cross-matched red cells and possible blood and platelet transfusion should be evaluated - Intravascular volume assessment, and proper blood pressure and invasive hemodynamic monitoring should be performed

PREOPERATIVE

CLINICAL SITUATION AND TYPE OF ANESTHESIA

-Raised increased intracranial pressure (ICP)-Clinical evidence of bleeding -Coagulopathy-Drop in platelet count < 80,000/mm3

-Hemodynamic instability -Maternal or fetal compromise

Yes No

GENERAL ANESTHESIA (GA) REGIONAL ANESTHESIA(RA)

ADVANTAGES

-Rapid onset of anesthesia-Control of airway-Potential for less hypotension than RA

ADVANTAGES

-Reduces serum catecholamine level-Improves uteroplacental blood flow-Precludes the risk of aspiration, failed intubation or laryngoscopic intubation-Minimizes the risk of neonatal exposure to depressant anesthetic drugs- Promotes early ambulation- Lowers the incidence of maternal thromboembolism- Better analgesia and minimizes the consumption of systemic opioids

DISADVANTAGES

- Difficult endotracheal intubation and risk of aspiration-Magnesium sulfate: empowered effect of neuromuscular blocking agents- Slow metabolic degradation of choline-ester drugs can occur- Increases systemic and pulmonary vascular resistance - Hypoproteinemia, low plasma volume, increased interstitial fluid and altered liver function could alter requirements and effects of drugs.

DISADVANTAGES

- A higher risk of epidural hematoma

Fig. 1. Optimal anesthetic management of

delivery in patients with HELLP syndrome.




However, SH-related coagulopathy should not

be assessed only before making the decision

about the anesthetic technique to be adopted

because, as it is evolutionary, it could become

more severe with time after spinal punctures

have been done.1

In addition to thrombocytopenia in SH, this

syndrome causes hepatic alterations, which may

worse in the following hours and add quick

time alterations to platelet problems.51,52 That

is, after performing spinal puncture in these

patients who previously presented acceptable

coagulation tests, closely monitor them because

unfavorable postoperative coagulopathy devel-

opment could imply a significant bleeding risk

in previously traumatized epidural vessels.

Disturbances in hepatic flow during anesthesia

and cesarean section may exacerbate liver func-

tion which, together with fibrinolysis of uterine

and placental manipulation, may act synergisti-

cally to make the coagulopathy worse.1

Even though a spinal hematoma is a potential

risk in these patients,78 neuroaxial anesthesia is

recommended to perform cesarean sections in

patients with moderate, but non-progressive,

thrombocytopenia,74 but is contraindicated in

cases with a severe coagulopathy or preoperative

bleeding.1

Some published studies have observed an

incidence of insignificant spinal hematoma in

patients with SH who have undergone regional

anesthesia.

Vigil-De-Gracia et al. studied 36 SH cases

with levels of platelets below 10,0000/mm3 in

whom locoregional anesthesia was used. Their

study did not mention any epidural hematoma;

in fact the platelet count in 12 patients was

below 50,000/mm3. No patient had either DIC

or disturbances in prothrombine time (PT)/par-

tial thromboplastin time (PPT).86

Ankichetty et al. carried out a retrospective

review of spinal hematoma incidence in deliver-

ing women with SH. It clearly demonstrates that

administration of neuroaxial anesthesia can be

safely performed with a platelet count that

equals or is higher than 90,000/mm3.76

The study by Sibai et al. documented 16

patients with SH who had epidural analgesia;

there was only one case of bleeding in the

epidural space, and the number of platelets in

this patient was 93,000/mm3.13

SH diagnosis is a relative, but not an absolute,

contraindication of using epidural analgesia. If

there is no evidence for abnormal bleeding in

the patients medical history or assessment, and

the platelet count and hemostasis are normal,

epidural analgesia can be performed.21

Prior to undertaking epidural analgesia in

these patients, the evolving nature of the coagu-

lopathy must be taken into account, which not

only affects the initial indication of the tech-

nique but also the appropriate time to remove

the epidural catheter and the need to monitor

coagulation and the appearance of neurological

signs, as they are indicative of epidural hema-

toma. For patients at risk of bleeding, and if

coagulation tests raise doubts, intradural anes-

thesia conducted with a pencil-tip small caliber

needle still offers more advantages than general

anesthesia, provided that maternal hemody-

namic stability is ensured, although there is

very little evidence that it is a frequent prob-

lem.1,87 In this way, we also reduce potential

traumas as no epidural catheter is introduced

into the epidural space.88

As the platelet count often continues to fall

during the postpartum period and bleeding com-

plications are common in SH patients, it is advis-

able to remove the epidural catheter as soon as

possible after delivery.21,44 Sprung et al.89 estab-

lished the following recommendations to remove

the epidural catheter in cases with CID: (1) if

there are no signs of intraspinal bleeding, the

catheter must be removed as soon as possible

given the risk of intravascular catheter migration

and bleeding could begin; (2) if bleeding is

observed around the insertion point, it could also

occur in the intraspinal or the epidural space, so

the catheter must be left without moving it; (3)

in any case, neurological assessments must be

frequently made until the coagulopathy is

solved; (4) in those cases showing neurological

alarm signs, consult a neurologist immediately

and explore the patient by CT. However, an MRI

offers the safest diagnosis, and decompressive

laminectomy may be proposed.

The use of local anesthetics with adrenaline

for bolus in epidural anesthesia seems a safe

procedure in such patients, and it is widely

used to minimize the risks of systemic absorp-

tion of local anesthetics. There is one published

case of a hypertensive crisis with adrenaline




absorption which involved the introduction of

30 ml 2% lidocaine with 1:200,000 adrenaline.90

So frequent observation after its administration

is indicated in these patients.90

General anesthesia

General anesthesia, in comparison with regional

anesthesia, for SH patients involves a higher

materno-fetal anesthetic risk.20,91 A higher risk

of respiratory depression may occur given the

increased incidence of premature fetuses, delete-

rious effects of sympathetic stimulations of the

laryngoscopy, drug interactions, and access to

difficult airways, these being the main causes of

maternal anesthetic mortality.92

Indications of general anesthesia in these

patients are: if there is an immediate threat for

the mother and the fetus, as occurs with eclamp-

sia; pulmonary edema; and if the level of con-

sciousness has altered. Another indication is

when regional anesthesia is contraindicated

(e.g., coagulopathy).

Difficulty in airways is one of the main con-

cerns for such patients in general anesthesia and

there are several reasons for this: pregnancy may

induce an edema in airways and severe bleed-

ing; limited movement of the cervical spine; and

breast enlargement because of obesity in preg-

nancy, which can hinder laryngoscopies and

intubation.69,70 These factors may raise Mallam-

pati category 3 to category 4.93 In fact, a fault in

endotracheal intubation after inducing general

anesthesia is eightfold higher in a delivering

woman that in the general population, and is

one of the causes that leads to maternal morbid-

ity and mortality.94

There are risks related to pulmonary ventila-

tion or gastric aspiration as these patients are

considered to have a full stomach, even though

they have been fasting, because their stomach

takes longer to empty.73 So in such situations,

one should perform general anesthesia with

rapid sequence induction and intubation.76

Prior to anesthetic induction, it is useful to

place the patient in the supine position with a

left uterine displacement, and denitrogenation,

to help ensure optimal maternal oxygenation.

General anesthesia in these patients is at high

cardiovascular risk and may cause a cardiovas-

cular response disproportionately with intuba-

tion by producing cerebral hemorrhaging and

an edema, or cardiovascular decompensation by

causing a pulmonary edema and, therefore,

increases materno-fetal morbidity and mortal-

ity.86,95,96 In addition, a disproportionate pressor

response to intubation may increase the concen-

tration of circulating plasmatic catecholamines

in the mother, which could be harmful for

uteroplacental blood flow.9799

The drugs used to mitigate the hemodynamic

response to intubation, as well as the surgical

procedure, include esmolol, fentanyl, remifen-

tanil, alfentanil, and lidocaine. In such situa-

tions, it is important to consider those drugs

that have minimal effects on the fetus. One of

the drugs used in obstetrical anesthesia is

remifentanil because of its rapid metabolization

and short duration. This opioid is not metabo-

lized by the kidney or liver, so there is no risk

of accumulation. It also involves a low risk of

respiratory depression and sedation in the neo-

nate given its short duration, although some

cases of mild rigidity and respiratory depression

in neonates have been published. Hence more

studies are required to confirm its security in

obstetrical anesthesia.100102

SH patients often have hypoproteinemia, low

plasma volume, increased interstitial fluid, and

altered liver function. Thus, the requirements

and effects of drugs administration may be

altered.103

As a result of kidney and liver involvement in

these patients, it is advisable to choose those

drugs with less liver and kidney metabolism.

Propofol is a good choice for anesthetic induction

because it has no active metabolites, a short half-

life and rapid recovery. Suxamethonium is useful

for ensuring rapid sequence intubation, but its

half-life may be prolonged because of falling

serum cholinesterase concentrations as a result of

liver dysfunction and pregnancy. A neuromuscu-

lar blockade may be performed with atracurium

or cisatracurium, which is independent of liver

and kidney metabolism. Nonetheless, neuromus-

cular monitoring, along with neuromuscular

blocking agents, is advisable in these patients.

The choice of volatile agents depends on each

anesthesiologist as those hepatotoxic drugs must

be avoided. Isoflurane seems a good choice given

its low biotransformation and vasodilator

action.66,104 Drugs such as ketamine should be




avoided in these patients because of their sympa-

thetic and epileptic activity.

It is also important to remember that treatment

with magnesium sulfate has been associated with

an empowered effect of neuromuscular blocking

agents.103,105 Uterine atony and coagulopathy

produced by therapy with magnesium sulfate

may cause considerable intrapartum blood loss.

So intravenous access of high-caliber and blood

products should be made available prior to anes-

thesia.106

Measuring invasive blood pressure in these

patients also enables us to continuously monitor

blood pressure and to remove blood to value the

respiratory function, electrolytes, acidbase bal-ance, and hematological and liver abnormalities,

as well as to monitor the heart rate.36

In conclusion, decisions to administer general

or regional anesthesia to patients with SH must

involve consideration of the evolving nature of

coagulopathy or the existence of thrombocytope-

nia. Whenever regional anesthesia is not

contraindicated and ensures the mothers hemo-

dynamic stability, it should be considered

instead of general anesthesia in these patients.

Early detection and the interdisciplinary treat-

ment of these patients by obstetricians, pediatri-

cians, and anesthesiologists of severe

complications associated with SH are important

to lower maternal-fetal morbidity and mortality.

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