PHYSIOLOGIC CHANGES OF OBESITY

Obesitas adalah penyakit yang kompleks dengan keterlibatan komponen neural, hormonal,

neuroendokrin, genetik dan psikososial. Komponen ini menghasilkan perubahan fisiologis pada wanita

gemuk yang hamil, yang mengakibatkan peningkatan resiko pada ibu, janin, tindakan operasi dan

pembiusan.

Pulmonary Changes

Obesitas meningkatkan kebutuhan sistem respirasi.

As energy expenditure increases proportionate to the

increase in body mass, oxygen consumption and carbon

dioxide (CO2) production also increase proportionate to the

increase in work performed. Minute ventilation then

increases owing to the elevated respiratory demand,

except in the 5% to 10% of patients with pickwickian syndrome,

who display a reduced sensitivity to CO2. Obesity

affects the body’s ability to meet these demands by changing

pulmonary mechanics, altering lung volumes, and

impairing oxygen consumption.

Cardiovascular Changes

Kegemukan meningkatkan jumlah volume darah dan cardiac output.

Penambahan berat badan dari 70-170 kg menghasilkan penambahan sebanyak dua kali lipat cardiac

output dan volume darah pada wanita tidak hamil.

Kardiak indeks relatif normal. Peningkatan cardiac

output terjadi karena peningkatan stroke volume.

The systemic arteriovenous oxygen difference remains

normal.

Pulmonary blood volume increases in proportion to

increases in cardiac output and total blood volume.

Pulmonary hypertension can occur and may be position

dependent. Paul et al. observed an 11% increase in oxygen

consumption and a 44% increase in pulmonary capillary

wedge pressure when morbidly obese patients were

placed in a supine position. Hypoxemia, if present, increases

pulmonary vascular resistance. Airway obstruction may

also increase pulmonary artery pressure. Teeple and

Ghia, in their examination of an obese patient, noted a

decline in pulmonary capillary wedge pressure from 38 to

5 mm Hg after endotracheal intubation and relief of airway

obstruction.

Perubahan Endokrin

Diabetes gestasional dan diabetes mellitus lebih sering terjadi pada pasien gemuk.

Farmer dkk mengidentifikasi kekurangan insulin relatif dan penurunan sensitifitas insulin pada sejumlah

wanita gemuk selama kehamilan. Diperkirakan sebanyak 92% wanita dengan diabetes gestasional

berkembang menjadi diabetes mellitus tipe 2, tergantung etnis, kriteria diagnosis yang digunakan dan

lamanya penelitian.

Perubahan Koagulasi

Pasien gemuk memiliki resiko yang lebih tinggi terkena thrombosis vena dalam. Ini karena

kegemukan meningkatkan resiko penyakit tromboembolik yang berhubungan dengan kehamilan,

terutama pada pasien yang kurang aktif, walaupun hal ini masih menjadi perdebatan.

INTERACTION WITH PREGNANCY

Obesity is associated with higher risks for chronic hypertension,

gestational hypertension, and diabetes mellitus

during pregnancy.

Morbidly obese women have a two- to eight-fold higher

risk of acquiring diabetes mellitus during pregnancy than

nonobese women. Obesity also is associated with an

increased risk for development of type 2 diabetes mellitus

after pregnancy.

Most importantly, obesity increases the risk of death

during pregnancy. Kaunitz et al. suggested that

advanced age and a higher incidence of hypertension, diabetes,

thromboembolic disease, and infection are factors

that increase the risk of maternal death in obese pregnant

women.

ANESTHETIC MANAGEMENT

Preanesthetic Assessment

The high incidence of comorbid conditions among obese

pregnant women necessitates early, careful preanesthetic

assessment (as discussed earlier).

Unless the length of the sphygmomanometer cuff

exceeds the circumference of the arm by 20%, systolic

and diastolic blood pressure measurements may overestimate

true maternal blood pressure. Use of an appropriately

sized blood pressure cuff and an automated blood pressure

measurement device often obviate the need for intraarterial

monitoring in the obese parturient. However, an

intra-arterial catheter may be beneficial in patients with

chronic hypertension or preeclampsia and in those requiring

frequent arterial blood gas measurements during and

after cesarean delivery.

Pulse oximetry may be used to assess the adequacy of

maternal oxygenation; however, arterial blood gas measurements

are invaluable in assessing maternal ventilation when

there is cause for concern. The presence of preeclampsia

makes platelet count assessment necessary. Unless there is

clinical evidence of coagulopathy or rapid patient deterioration,

other coagulation tests are not indicated.

When administering neuraxial anesthesia in obese

patients, the anesthesia provider should anticipate the

need for a longer spinal needle.69 In the majority of obese

parturients, the epidural space can be identified with a

standard-length epidural needle. In contrast, for spinal

anesthesia in morbidly obese patients, longer-than-normal

needles are more frequently required.

Appropriately sized labor beds, transportation gurneys,

and operating tables, and sufficient personnel to assist with

patient transport, are imperative. Although standard operating

tables are generally rated for persons weighing up to

500 lb (227.3 kg), this rating may be insufficient for morbidly

obese patients, especially when the table is articulated.

Regardless of the weight rating of the table, it is critical that

the obese patient be centered over the operating table pedestal

at all times.

Preeclampsia is defined as the new onset of hypertension

and proteinuria after 20 weeks’ gestation (Table 45-1).

The NHBPEP has recommended that clinicians consider

the diagnosis of preeclampsia in the absence of proteinuria

when any of the following findings are present: (1) persistent

epigastric or right upper quadrant pain, (2) persistent

cerebral symptoms, (3) fetal growth restriction, (4) thrombocytopenia,

and (5) elevated serum liver enzyme concentrations.

7 The term eclampsia is used when central nervous

system (CNS) involvement results in the new onset of seizures

in a woman with preeclampsia. The term HELLP

syndrome refers to the development of hemolysis, elevated

liver enzymes, and low platelets in a woman with preeclampsia.

This condition is considered a variant of severe

preeclampsia.

PREECLAMPSIA

Preeclampsia is a multisystem disease unique to human

pregnancy. Although advances have been made in the

understanding of the pathophysiology of the disease, the

specific proximal etiology remains unknown. Management

is supportive; delivery of the infant and placenta remains

the only definitive cure.

The clinical syndrome of preeclampsia is defined as

the new onset of hypertension and proteinuria after

20 weeks’ gestation. Previous definitions included edema,

but edema is no longer part of the diagnostic criteria

because it lacks specificity and occurs in many healthy pregnant

women.9 The severity of preeclampsia is categorized

as either mild or severe according to clinical criteria.

TABLE 45-1 Diagnostic Criteria for Mild and SeverePreeclampsiaMild Preeclampsia BP _140/90 mm Hgafter 20 weeks’gestationProteinuria (300 mg/24 hr or 1+ result ondipstick specimen

Severe Preeclampsia

BP _160/110 mm HgProteinuria >5 g/24 hrElevated serum creatininePulmonary edemaOliguriaIntrauterine growth restrictionHeadacheVisual disturbancesEpigastric or right upperquadrant painSigns of HELLP syndrome

TABLE 45-2 Hypertensive Disorders of PregnancyClinical Feature Chronic Hypertension Gestational Hypertension PreeclampsiaTime of onset ofhypertension

<20 weeks’ gestation Typically in third trimester _20 weeks’ gestation

Severity of hypertension Mild or severe Mild Mild or severeProteinuria* Absent Absent Typically presentSerum urate>5.5 mg/dL(0.33 mmol/L)

Rare Absent Present in almost all cases

Hemoconcentration Absent Absent Present in severe diseaseThrombocytopenia Absent Absent Present in severe diseaseHepatic dysfunction Absent Absent Present in severe

disease

Complications of Preeclampsia

Severe preeclampsia is associated with an increased risk of

maternal morbidity and mortality, including HELLP syndrome,

cerebrovascular accident, pulmonary edema, renal

failure, placental abruption, and eclampsia. In general, these

complications are more common in women with earlyonset

preeclampsia and in women with prepregnancy medical

conditions such as diabetes mellitus, chronic renal disease,

and thrombophilia.1

CEREBROVASCULAR ACCIDENT

Although the absolute risk of cerebrovascular accident is

low, stroke remains the leading cause of death in women

with preeclampsia. In the 2003-2005 Confidential Enquiry

into Maternal and Child Health (CEMACH) report,

18 deaths were attributed to eclampsia and preeclampsia;

67% resulted from a cerebrovascular accident (10 intracranial

hemorrhages and 2 cerebral infarctions).188 The endothelial

dysfunction of preeclampsia can promote edema,

vascular tone instability, platelet activation, and local

thrombosis. Reversible cerebral edema is the most

common CNS feature of preeclampsia or eclampsia. The

leading hypothesis regarding the loss of endothelial

integrity is that cerebral lesions are caused by a loss of

cerebral autoregulation, which results in hyperperfusion

that leads to interstitial or vasogenic edema.189,190 The presence

of HELLP syndrome or DIC increases the risk for a

hemorrhagic event.

There is growing recognition that mean arterial blood

pressure and diastolic blood pressure may not reflect the

true risk for stroke. A review of 28 case histories of severely

preeclamptic women who suffered a stroke revealed that

(1) systolic blood pressure in excess of 160 mm Hg was a

far superior predictor of stroke than diastolic hypertension

or mean arterial pressure, (2) the majority of strokes were

hemorrhagic (93%) as opposed to thrombotic (7%), and

(3) the majority of strokes (57%) occurred in the postpartum

period.191 Close attention to blood pressure control

throughout the peripartum period is the mainstay of

stroke prevention.

PULMONARY EDEMA

Pulmonary edema is a severe complication of preeclampsia

that occurs in approximately 3% of affected women.110 It is

relatively infrequent in younger (previously healthy)

women; the risk is higher in older multigravid women

and in women with preeclampsia superimposed on chronic

hypertension or renal disease. The clinical presentation is

characterized by worsening dyspnea and orthopnea with

concomitant signs of respiratory compromise, such as

tachypnea, rales, and hypoxemia. Causes of pulmonary

edema include low colloid osmotic pressure, increased

intravascular hydrostatic pressure, and greater pulmonary

capillary permeability.192 All of these factors may coexist in

a single patient. A large proportion of cases of pulmonary

edema occur postpartum, usually within 2 to 3 days of

delivery, and management is directed toward the underlying

cause (e.g., fluid overload, sepsis, cardiac failure).193

Echocardiography can be helpful in the diagnosis of cardiogenic

causes of pulmonary edema.194,195 Initial treatment

includes administration of supplemental oxygen, fluid

restriction, and diuretic therapy (e.g., furosemide). A retrospective

study of more than 16,000 deliveries found that

although peripartum pulmonary edema was associated

with extensive radiographic infiltrates and severe hypoxemia,

resolution was typically rapid, with a limited need for

intensive care unit admission.196 Placement of a pulmonary

artery catheter can facilitate management of patients with

severe refractory pulmonary edema; these women should

be managed in an intensive care unit. Notably, in the

2003-2005 CEMACH report, there were no deaths attributed

solely to pulmonary causes.188 Presumably, this trend

reflects improvements in the fluid management of women

with severe preeclampsia.

RENAL FAILURE

Acute renal failure is a rare but serious complication of

severe preeclampsia and HELLP syndrome.197 The true

incidence remains unknown. Acute renal failure is divided

into three categories: (1) prerenal, which refers to renal

hypoperfusion; (2) intrarenal, which suggests intrinsic

renal parenchymal damage; and (3) postrenal, which

implies obstructive uropathy.198 The majority of cases

(83% to 90%) of acute renal failure in preeclampsia result

from prerenal and intrarenal disease (most commonly

acute tubular necrosis) and resolve completely after

delivery.199-201 In contrast, bilateral renal cortical necrosis

is a rare and serious condition associated with considerable

maternal and perinatal morbidity and mortality. It occurs

most commonly in association with known renal parenchymal

disease, chronic hypertension with superimposed

preeclampsia, placental abruption, or DIC.202

PLACENTAL ABRUPTION

Placental abruption occurs in approximately 2% of women

with preeclampsia and increases perinatal morbidity

and mortality. A retrospective case-control study of

161 women with placental abruption and 2000 women

without abruption found a threefold higher risk of placental

abruption in women with preeclampsia.203 The incidence

is also increased in women with underlying chronic hypertension.

193 Management depends on the extent of abruption

and associated hypotension, coagulopathy, or fetal

compromise (see Chapter 37). Placental abruption is also

associated with the development of DIC.

HELLP Syndrome

HELLP syndrome is a variant of severe preeclampsia characterized

by rapid clinical deterioration. It is associated with

a higher risk of maternal death (1%) and increased rates of

maternal morbidities, including DIC, placental abruption,

pulmonary edema, acute renal failure, liver hemorrhage or

failure, acute respiratory distress syndrome, sepsis, and

stroke (Table 45-7).204 Additionally, the syndrome is associated

with a 70% rate of preterm delivery204; prematurityrelated

neonatal complications increase the risk of perinatal

morbidity and mortality. The onset of HELLP syndrome

occurs antepartum in 70% of cases, and postpartum in

30%.204