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every eight hours is a commonly used dosing regimen. The PEFR the maximum O2 concentration, and probably adds little value
or FEV1 should be determined upon admission and serial meas- to the anesthetic technique. Maintain anesthesia with a haloge-
urements taken if symptoms develop. nated inhalation agent at a concentration high enough to avoid
Epidural analgesia markedly reduces the work and physiologi- ˜˜light™™ (i.e. inadequate) anesthesia, since inadequate anesthesia
cal stress of labor59 and is strongly recommended for asthmatic will aggravate bronchospasm. Excessive blood loss due to uterine
parturients. A weak bupivacaine-opioid solution has been used atony is unlikely to be a significant problem when using halothane
successfully to produce minimal motor block, and avoid respira- 0.75%, enflurane 1.7%, or isoflurane 1.2% in O2 after a short period
tory embarrassment.60 A combined spinal“epidural technique of overpressure.64 Sevoflurane is an effective agent in preventing
and managing intraoperative bronchospasm.65
(CSE) may also provide rapid onset of good quality analgesia
with minimal motor block.61 However, aseptic meningitis has Intravenous oxytocin infusion should be used routinely after
been reported following CSE and high-dose steroids may, theor- delivery to provide uterine contraction. Ongoing hemorrhage from
etically, increase the risk of this complication. Paracervical and uterine hypotonia, despite oxytocin administration, is treated with
pudendal blocks may be used for the first and second stages of prostaglandin E2 or methergine (ergonovine). Prostaglandin F2a
labor, respectively, when epidural or spinal analgesia is unsuita- (PGF2a) may cause significant bronchospasm in asthmatic patients
ble. An assisted delivery (forceps or vacuum extraction) mini- (see Table 4.5). Oxygen desaturation following 15-methyl PGF2a
has been reported in women without reactive airway disease.66
mizes maternal stress and effort.
If regional anesthesia is contraindicated, opioids (preferably After GA, intensive care admission is advised as it allows for a
i.v. Æ patient controlled) may be used but provide less effective delayed and controlled extubation with optimization of respiratory
analgesia, particularly for the second stage of labor. Fentanyl is and cardiovascular parameters. In view of the potential to aggra-
the preferred opioid for asthmatic patients since it does not vate bronchospasm, some practitioners avoid nonsteroidal anti-
release histamine. Careful assessment must be made of the inflammatory drugs (NSAID), providing postoperative analgesia
effects of opioid analgesia on respiratory function. with continuous regional techniques or parenteral opioids.


Cesarean section Summary
When C/S is necessary for women with asthma, regional anesthe- The greatest risk to an asthmatic mother and her baby stems from
sia is preferable, since it avoids airway stimulation. However, inadequate treatment of acute asthma. All the drugs commonly
acute bronchospasm has been precipitated by spinal anesthesia used in the treatment of acute asthma are reliable, and safe to use
in pregnancy, although the etiology was unclear.62 It is postulated in pregnancy. They should not be withheld from the mother on
that high sensory blockade causes a fall in adrenal epinephrine the basis of potential, unproven and unlikely toxic effects on the
output,63 but this should not be a reason to avoid regional fetus. A low threshold for hospitalization is important for the
anesthesia. Although spinal anesthesia provides a rapid block, successful treatment of acute asthma in pregnant women.
epidural anesthesia allows slow incremental titration, which Regional anesthesia and analgesia have important advantages in
may minimize the risk of respiratory embarrassment from a high this patient population, not least of which is avoidance of airway
sensory level. However, the sensory level must be high enough to stimulation.
provide good-quality analgesia (above T6 sensory level), since
intraoperative pain and distress can worsen bronchospasm.
Pulmonary embolism
The addition of an epidural opioid (e.g. fentanyl or sufentanil)
improves the quality of the sensory block and is recommended.
Epidural epinephrine use is still controversial in obstetric anesthe-
Introduction
sia and risks a potential additive effect with other beta2-adrenergic
agonists, particularly S/C epinephrine. Many anesthesiologists, Pulmonary embolism is a significant cause of morbidity and
mortality during pregnancy.67,68 Emboli may consist of
however, still use epinephrine in the initial test dose.



80
Chapter 4


thrombus, air, or amniotic fluid, and rarely of fat, tumor, sickle Resistance to activated protein C, which is frequently asso-
cell, or infectious material. Amniotic fluid embolism (AFE) is a ciated with Factor V Leiden mutation, is by far the most com-
rare entity with usually catastrophic outcome. In contrast, venous mon identified genetic predisposition to the development
of thrombosis.77,78 Other thrombophilic states that interact
air embolism (VAE) occurs commonly, but is associated with a
less severe clinical course. with the procoagulant state of pregnancy include: antithrom-
bin deficiency, protein S deficiency, and MTHFR C677 T
homozygotes.78
Thromboembolic disease
Incidence
Pathophysiology
Pulmonary thromboembolism (PTE) is a complication of venous
Pulmonary thromboembolism leads to obstruction of the pul-
thrombosis. The risk of venous thromboembolism has been esti-
monary arterial tree. In turn there is an increase in pulmonary
mated to be fivefold to sixfold higher in women who are pregnant
vascular resistance (PVR) and RV afterload, which can cause
compared to nonpregnant women.68,69 Deep vein thrombosis
RV failure. Massive PTE increases RV afterload acutely and
(DVT) occurs in 1 in 300 to 1 in 5000 of all pregnancies and
enlarges the right ventricle. There may be a shift of the ven-
there is evidence that the incidence is more common in the
tricular septum to the left, which can cause LV failure.
antepartum period.70,71,72 Pulmonary thromboembolism occurs
Consequently, the increase in hydrostatic pressure and disrup-
mostly as a result of DVT, and rarely from superficial, pelvic, or
tion of the normal capillary integrity predispose the patient to
ovarian vein thromboses. Pulmonary thromboembolism compli-
pulmonary edema.
cates 1 in 1000 to 1 in 2000 pregnancies and accounts for approxi-
Pulmonary thromboembolism causes an increase in V/Q mis-
mately 12% to 25% of direct maternal mortality.73,74
matching, especially an increase in the alveolar dead space,
which leads to arterial hypoxemia. A decrease in CO in patients
Etiology with RV failure further enhances the effects of V/Q mismatching.
Hypoxemia and hypocapnia are characteristic of PTE.
The uterus grows as pregnancy progresses and may compress the
inferior vena cava, resulting in venous stasis in the pelvic and lower
extremities. In pregnancy, blood is hypercoagulable in that several Clinical presentation
coagulation factors (e.g. fibrinogen V, VII, VIII, X, XII, and von
Deep vein thrombosis
Willebrand factor) increase, while naturally occurring anticoagu-
Pulmonary emboli occur in 50% of patients with documented
lants (antithrombin III, proteins C and S) decrease.75 Increased
DVT. Half of the patients with documented DVT are asympto-
platelet reactivity, as a result of enhanced thromboxane A2 (TXA2)
matic. Most clinically significant emboli arise from thrombi in the
production, further contributes to the hypercoagulability during
deep veins of the thigh. Calf vein thromboses rarely produce large
the third trimester of normal pregnancy.76
emboli. The most common signs and symptoms of DVT are
Vascular trauma during C/S and vaginal delivery and separa-
swelling of calf muscles (with a 2 cm difference in leg circumfer-
tion of the placenta may initiate a series of physiologic events
ence at the mid-calf between the affected and unaffected legs),
leading to an acceleration of coagulation activity and increased
pain, tenderness, positive Homan sign (painful passive dorsiflex-
risk of thromboembolism. The risks of DVT and PTE are five to
ion of the foot), a change in limb color, and a palpable cord due to
fifteen times higher after C/S than after vaginal delivery.
associated thrombophlebitis. Puerperal ovarian vein and pelvic
Table 4.6 shows some coexisting factors and conditions, which
vein thromboses may present in the postpartum period with a
increase the risk of PTE in pregnancy.
fever lasting more than 72 hours which is unresponsive to anti-
biotic therapy.

Table 4.6 Coexisting factors and conditions that increase the Pulmonary thromboembolism
risk of pulmonary thromboembolism in pregnancy The clinical diagnosis of PTE is difficult because the presenting
signs and symptoms may be nonspecific. Most PTE are asympto-
Smoking
matic and not life-threatening. The common presentations of
Obesity
PTE are listed in Table 4.7. The classic triad of dyspnea, pleuritic
Preeclampsia
pain, and hemoptysis is present in only 25% of patients with PTE.
Multiple gestation
Examination of the cardiovascular system reveals tachycardia,
Previous history of thromboembolism
and signs of RV failure (e.g. split-second heart sound, jugular
Antiphospholipid antibody syndrome
venous distension, a parasternal heave, and hepatic enlarge-
Proteins S and C deficiencies
ment). Low-grade fever, cyanosis, diaphoresis, altered mental
Antithrombin III deficiency
status, wheezing, and clinical signs of DVT may also be present.
Hyperhomocysteinemia
Rarely, patients may present with abdominal pain due to
Prothrombin gene mutation
infarcted lung next to the diaphragm, or disseminated intravas-
Factor V Leiden mutation
cular coagulation (DIC).



81
1 Cardiovascular and respiratory disorders


An ECG may show signs of RV strain, right axis shift, P pulmo-
Table 4.7 Signs and symptoms of pulmonary embolism nale, supraventricular dysrhythmias, and S1, Q3, T3 pattern.
However, the most common abnormal ECG findings seen with
No symptoms
PTE are ST-segment changes.
Tachycardia, tachydysrhythmias
The chest radiograph (CXR) is neither specific nor sensitive in
Chest pain
the diagnosis of PTE because similar findings are observed with
Tachypnea
other conditions. Furthermore, in approximately 25“40% of
Flank pain
patients with pulmonary embolism the CXR may be normal.84
Chest x-ray findings:
However, a CXR helps to diagnose other conditions that can
atelectasis
mimic PTE, such as pneumonia and pneumothorax. A negative
pleural effusion
D-dimer assay can be a reassuring diagnostic test in cases of PTE
elevated hemidiaphragm
that are of low clinical suspicion.84
peripheral segmental or subsegmental infiltration
Invasive hemodynamic monitoring with a central venous
Dyspnea
catheter or pulmonary artery catheter may reveal increased cen-
Hypotension
tral venous pressure (CVP), raised mean pulmonary arterial pres-
Hemoptysis
sure (PAP), and normal or low pulmonary artery occlusion
Jugular vein distension
pressure (PAOP). Monitoring PAOP and CO helps to determine
Low-grade fever
the administration of fluids and inotropic drugs.
Accentuated P2
A definitive diagnosis can be made with a V/Q scan if there is a
Syncope
high clinical suspicion of PTE and a scan shows high probability for
Right-side S3
PTE (for example normal ventilation with segmental perfusion
Unexplained shock
defect).85 The probability of PTE is only 10“40% if the perfusion
Cyanosis
defect on the lung scan is subsegmental with normal perfusion.
Normal perfusion on the lung scan excludes the diagnosis of PTE.
Diagnosis However, multiple perfusion defects and V/Q mismatch on the lung
scan suggest a high probability of a pulmonary embolus. If the lung
Deep vein thrombosis
scan reveals low probability of pulmonary embolus but the clinical
Compression ultrasonography is noninvasive and is the primary
suspicion is high, pulmonary angiography should be considered.
test used currently to detect DVT. It has a sensitivity of 97% and a
Spiral computed tomography (CT) allows rapid imaging from
specificity of 94% for the diagnosis of symptomatic, proximal DVT
the main pulmonary arteries to at least the segmental and poss-
and a negative predictive value of 98%.79,80,81
ibly the subsegmental branches. Fetal radiation exposure with
Impedance plethysmography measures volume changes
standard spiral CT is less than with V/Q lung scanning.86
within the leg. It is only 50% sensitive for detection of a clot in
Echocardiography can be useful in the detection of a pulmon-
the small calf veins.82 Furthermore, thrombotic and nonthrom-
ary embolus after C/S.87 Magnetic resonance angiography with
botic occlusions cannot be differentiated by plethysmography.
i.v. contrast allows high-resolution magnetic resonance angio-
Invasive venography is the most accurate test for diagnosis of
graphy during a single suspended breath.88 Standard pulmon-
DVT, and has a negative predictive value of 98%.83 However, it is
ary angiography is currently the most definitive test for PTE,
not useful for the evaluation of the pelvic vasculature, is time
but it is invasive and requires catheterization of the right side
consuming and cumbersome, and has significant complications
of the heart.
compared to popular noninvasive methods.
Isotope scanning is an effective method of diagnosing DVT.
Management
It involves the use of 125I-labeled fibrinogen and its detection as it
incorporates into the developing thrombus. Since this method
Deep vein thrombosis
involves systemic injection of radioactive isotope of iodine,
The clinician should have a high index of suspicion for DVT, but
which may cross the placenta and affect the fetus, its use is
before therapy is started a definitive diagnosis must be estab-
contraindicated during pregnancy. Computerized axial tomogra-
lished. An algorithm for diagnosis and management of DVT and
phy and magnetic resonance imaging (MRI) have been shown
pulmonary embolism has been proposed (see Figures 4.2 and
to be sensitive in the diagnosis of DVT and to follow the clinical
4.3)89 Heparin therapy should be started immediately after the
resolution of puerperal ovarian vein and septic pelvic vein
diagnosis of DVT to prevent the occurrence of PTE. The loading
thromboses.82,83
dose of unfractionated heparin (UFH) is 100 units/kilogram
(U/kg) followed by an initial infusion rate of 1000 U/h. The ade-
Pulmonary thromboembolism quacy of anticoagulation is monitored with serial activated partial
A decrease in SaO2 and end-tidal CO2 (EtCO2) reflect the abnor- thromboplastin times (aPTT), which should be maintained
between 1.5“2.5 times normal for 7“10 days.89 After therapeutic
mal V/Q relationship and increased physiological dead space that
can result from PTE. Table 4.7 shows signs and symptoms of PTT values have been maintained for two days, S/C administra-
pulmonary embolism. tion can be substituted for i.v. administration. Subcutaneous



82
Chapter 4


Suspected DVT


CUS of proximal veins (day 1)


Clearly abnormal Normal Equivocal


Treat Isolate iliac DVT suspected Venography


Normal Abnormal


No treatment Treat


Yes No


Pulsed Doppler with Venography
direct visualization of or
Serial CUS
iliac vein MRV


Normal Abnormal
Normal Abnormal Normal Abnormal


No treatment Treat
Serial CUS Treat or No treatment Treat
confirm with
venography



Suspected PE


V/Q scan



High probability Nondiagnostic Normal


Diagnose PE CUS PE excluded


DVT present DVT absent


Diagnose PE Serial CUS Pulmonary angiography


Negative Positive Negative


PE excluded PE diagnosed PE excluded
Figures 4.2 and 4.3 An algorithmic approach to diagnosis and management of DVT and pulmonary embolism (from Bates, S. M. & Ginsberg, J. S. How we manage
venous thromboembolism during pregnancy. Blood 2002; 100: 3470“8). CUS: compression ultrasonography.




83
1 Cardiovascular and respiratory disorders



Table 4.8 Heparin dosing regimens Table 4.9 Management of pulmonary thromboembolism


Dose Regimen Cardiopulmonary support
 Anticoagulation therapy
Mini-dose UFH UFH 5000 U subcutaneously every 12 h
 Venous interruption
Adjusted-dose UFH UFH subcutaneously every 12 h in doses
 Fibrinolytic therapy
adjusted to target a midinterval PTT into
 Surgical embolectomy
the therapeutic range
Prophylactic-dose Enoxaparin 40 mg once daily or 30 mg twice
LMWH daily adequate because of severe V/Q mismatching and decrea-
Tinzaparin 4500 U once daily sed mixed-venous O2 tension. Mechanical ventilation will be
Dalteparin 5000 U once daily necessary in patients with hemodynamic instability and severe
Weight-adjusted Enoxaparin 1 mg/kg twice daily or hypoxemia. Improved oxygenation reduces RV afterload and
dose LMWH 1.5 mg/kg once daily improves hemodynamic status. Volume resuscitation with col-
Dalteparin 100 U/kg every 12 h or 200 U/kg loids or crystalloids improves CO and arterial blood pressure. If
every 24 h inotropic support for the RV is required dobutamine is preferable
Tinzararin 175 U/kg once daily to dopamine because of its vasodilatory effects.
Heparin therapy should be started immediately. An i.v. bolus
U ¼ units; UFH ¼ unfractionated heparin; LMWH ¼ low molecular
dose of 100 U/kg UFH should be followed by a continuous infusion
weight heparin; PTT ¼ activated partial thromboplastin time
of 1000 U/h to maintain the aPTT at twice normal values.92,93
Heparin improves oxygenation and hemodynamic status by redu-
cing pulmonary artery obstruction and by preventing further release
regimens typically use 5000 U of UFH S/C every 12 hours. This
of vasoactive and bronchoconstrictive mediators from platelets and
dose only minimally prolongs the PTT and theoretically there
thrombin, thus decreasing pulmonary vascular resistance.
should be no increased risk of hemorrhagic complications.
Vena caval ligation or inferior vena caval filter should be con-
Heparin therapy may be discontinued when the patient begins
sidered in patients on anticoagulation therapy who have recurrent
active labor or 4“6 h prior to C/S. Baseline anticoagulant activity
emboli or those who cannot be anticoagulated.94 Caval ligation has
should be assessed by measuring the PTT immediately after dis-
a higher mortality (10“15%) than insertion of a vena caval filter
continuing the heparin therapy. For surgical hemostasis, the use
(< 1%) in nonpregnant patients. In 11 cases of temporary inferior
of protamine in incremental doses up to a calculated dose of 1 mg
vena caval filters inserted prior to delivery, there were no cases of
protamine per 100 U heparin should be considered. Heparin
PTE during or after delivery in pregnant women with DVT.95
therapy can be reinstituted in the postpartum period if the patient
Patients with a massive PTE and acute cardiac decompensation
is stable. Warfarin can be administered concurrently, monitoring
may respond to thrombolytic therapy.96 Although both urokinase
anticoagulation by the prothrombin time (PT). Anticoagulation is
and streptokinase have been used successfully in pregnancy,97,98
maintained for three months postpartum.
urokinase is considered less antigenic. Recombinant tissue plas-
Low-molecular weight heparin (LMWH) does not cross the
minogen activator (rt-PA), has been used successfully in a preg-
placenta and has been used effectively in pregnant patients for
nant patient with massive pulmonary embolism.99 Use of rt-PA is
the prevention and treatment of DVT.90,91 When compared to
associated with minimal bleeding complications, as it does not
UFH, LMWH use during pregnancy has a lower risk of bleeding
induce systemic fibrinolysis and is active only when it binds to
complications, heparin-induced thrombocytopenia, and osteo-
thrombin and is therefore clot specific.124 Thrombolytic therapy
porosis. Prophylaxis for PTE includes S/C dalteparin 5000 U every
24 hours or enoxaparin 40 mg every 24 hours (see Table 4.8).92 should be monitored by thrombin time, which should not be greater
than five times that of normal. Thrombolytic therapy in a pregnant
The dose of LMWH is adjusted to achieve a peak anti-Xa plasma

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