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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