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Surgery Block

SECTION VIII: MEDICAL & SURGICAL COMPLICATIONS


2012

CHAPTER 46
Pulmonary Disorders
Dr.

REVIEW ON MATERNAL PHYSIOLOGY

CARDIOVASCULAR CHANGES IN
Pregnancy

Heart
Changes that occurs as the diaphragm becomes
progressively elevated
 Heart is displaced to the left and upward and rotated
somewhat on its long axis
 Apex is moved somewhat laterally from its usual
position, causing a larger cardiac silhouette on chest
radiograph
⚜ pregnant women normally have some degree of
benign pericardial effusion, which may increase
the cardiac silhouette

Pulmonary Function during Pregancy


RESPIRATORY RATE
 essentially unchanged
INCREASES during Pregnancy
 Vital capacity and inspiratory capacity
⚜  by 20% by late pregnancy
 Tidal volume
⚜  by 40% as a result of the respiratory
stimulant properties of Progesterone
 Minute ventilation
⚜  by 30 to 40% due to  tidal volume
 Arterial pO2
⚜  from 100 to 105 mm Hg
 CARDIAC OUTLINE that occurs in pregnancy.  Carbon dioxide production & diffusion capacity
⚜ BLUE LINES: represent the relations between ⚜  production by 30%
⚜  diffusion capacity
the heart and thorax in the nonpregnant woman
 Ventilation
⚜ BLACK LINES: represent the conditions existing
⚜  d/t deeper but not more frequent breathing
in pregnancy DECREASED during Pregnancy
 Expiratory reserve volume
⚜  from 1300 mL to 1100 mL
RESPIRATORY TRACT CHANGES IN  pCO2
Pregnancy
⚜ w/ alveolar hyperventilation, the pCO2  from
40 to 32 mm Hg
 Residual volume
⚜  by 20% from 1500 mL to 1200 mL
Respiratory Tract Changes
 functional residual capacity
DIAPHRAGM ⚜ sum of expiratory reserve and residual volumes
 rises about 4 cm during pregnancy
⚜  by 10 to 25%
SUBCOSTAL ANGLE
⚜  d/t expanding uterus &  abdominal
 widens appreciably
pressure causing chest wall compliance to  by
 transverse diameter of the thoracic cage  2 cm. rd
1/3
 THORACIC CIRCUMFERENCE
CHANGES presumably are induced by:
  by 6 cm
  basal oxygen consumption
 not sufficiently to prevent a reduction in the residual
lung volume created by the elevated diaphragm. ⚜  incrementally by 20 to 40 mL/min in the
DIAPHRAGMATIC EXCURSION second half of pregnancy.
 greater in pregnant than in nonpregnant women KIDNEYS
  bicarbonate excretion   serum levels to 15 to
20 meq/L
 pH is slightly alkalotic at 7.45
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Surgery Block
SECTION VIII: MEDICAL & SURGICAL COMPLICATIONS
2012

PULMONARY COMPLICATIONS CLINICAL COURSE


 Clinical illness ranging from mild wheezing to severe
bronchoconstriction
PULMONARY DISORDERS IN  functional result of acute bronchospasm
Pregnancy ⚜ airway obstruction
⚜ decreased airflow
⚜ work of breathing progressively increases
 Patient present with
Pulmonary Disorders ⚜ chest tightness
ASTHMA ⚜ wheezing
 most common ⚜ breathlessness
 affects up to 4 percent of women  Distribution of airway narrowing is uneven 
CA-PNA + Asthma alterations in oxygenation  Ventilation–Perfusion
 accounts for 10% of nonobstetrical antepartum Mismatching
 HYPOXIA
hospitalizations in one managed care plan
⚜ MILD
advanced pregnancy may intensify the  Initially compensated by hyperventilation
pathophysiological effects of some lung diseases  normal arterial pO2, decreased pCO2 
 disparate number of maternal deaths during the Respiratory Alkalosis
influenza pandemics of 1918 and 1957 ⚜ PROGRESSION
 poor tolerance for pregnancy of women with severe  As airway narrowing worsens  
ventilation–perfusion defects  arterial
chronic lung disease
hypoxemia ensues
 With severe obstruction
Asthma ⚜ Ventilation  impaired because fatigue causes
common in young women and therefore is seen early CO2 retention
frequently during pregnancy.  Because of hyperventilation, this may only
asthma prevalence during pregnancy: 4 and 8 percent be seen initially as an arterial pCO2
Chronic inflammatory airway disorder returning to the normal range
PATHOPHYSIOLOGY
 Major hereditary component
⚜  airway responsiveness and persistent
subacute inflammation a/w:
 Chromosomes 5, 11, and 12
 Cytokine gene clusters
 β-adrenergic and glucocorticoid receptor
genes
 T-cell antigen receptor gene
 environmental allergic stimulant
⚜ influenza
⚜ cigarette smoke
 Hallmarks of asthma:
⚜ Reversible airway obstruction from
 bronchial smooth muscle contraction
 Vascular congestion
 Tenacious mucus
 Mucosal edema
 Airway inflammation
⚜ d/t  responsiveness to stimuli
 irritants
 viral infections
 aspirin
 cold air
 exercise
⚜ Inflammatory response caused by:
 mast cells
 eosinophils
 lymphocytes
 bronchial epithelium
 Inflammatory Mediators:
⚜ Histamine
 changes are generally reversible and well tolerated
⚜ Leukotrienes
by the healthy nonpregnant individual
⚜ Prostaglandins
 However, even early stages of asthma may be
⚜ Cytokines
dangerous for the pregnant woman and her fetus
⚜ IgE
⚜ Because the smaller functional residual capacity
 F-series prostaglandins and ergonovine
and increased effective shunt render the woman
⚜ Exacerbate asthma
more susceptible to hypoxia and hypoxemia
⚜ commonly used obstetrical drugs
⚜ should be avoided if possible

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 direct relationship with birthweight


 inverse relationship with rates of
gestational hypertension and preterm
delivery
 Life-threatening complications from status
asthmaticus include
 muscle fatigue with respiratory arrest
 pneumothorax
 pneumomediastinum
 acute cor pulmonale
 cardiac arrhythmias
 Maternal and perinatal mortality rates are
substantively increased when mechanical
ventilation is required
⚜ FETAL EFFECTS
 No significant adverse neonatal sequelae
from asthma
 But when respiratory alkalosis develops
EFFECTS OF PREGANCY ON ASTHMA  fetal hypoxemia develops well before
the alkalosis compromises maternal
 no evidence that pregnancy has a predictable effect
oxygenation
on underlying asthma  Fetal Compromise results from
⚜ baseline severity correlated with asthma   uterine blood flow
morbidity during pregnancy  decreased maternal venous return
 MILD disease:  alkaline induced shift to the left of the
 12% w/ exacerbation oxyhemoglobin dissociation curve
 2.3 % require admission  Fetal response to Maternal hypoxemia:
 MODERATE disease:   umbilical blood flow
 26% w/ exacerbation   systemic and pulmonary vascular
 7% require admission resistance
 SEVERE Disease:   cardiac output
 52% w/ exacerbation  incidence of fetal-growth restriction
 27% require admission
increases with asthma severity
⚜ 1/3 each: improved, remained unchanged or
worsened  hence, need for aggressive
⚜ 20% w/ Intrapartum Exacerbation among management
women w/ MILD to MODERATE asthma  CLINICAL EVALUATION
⚜ 18 fold increased risk of exacerbation following ⚜ subjective severity of asthma frequently does
caesarean vs vaginal delivery not correlate with objective measures of airway
function or ventilation
Asthma & Pregnancy
⚜ Clinical examination
ASTHMA Exacerbation (%) Admission (%)
Mild 13-20 2.3
 inaccurate as a predictor of severity
Moderate 26 7  Useful clinical signs include
Severe 50 27  labored breathing
 tachycardia
 PREGNANCY OUTCOMES  pulsus paradoxus
⚜ MATERNAL & PERINATAL OUTCOMES  prolonged expiration
 slightly increased incidence of  use of accessory muscles
 preeclampsia  Signs of a potentially fatal attack
☀  risk in moderate to severe  central cyanosis
asthma, regardless of treatment  altered consciousness.
 preterm labor ⚜ Arterial blood gas analysis
☀ increased about twofold in severe  provides objective assessment of maternal:
asthma  oxygenation
 low-birthweight infants  ventilation
 perinatal mortality  acid–base status.
 placental abruption  severity of an acute attack can be assessed
 preterm rupture of membranes  ROUTINE arterial blood gas analysis
 most obstetrical complications were not  did not help to manage most pregnant
higher in asthmatic women vs women who required admission for
nonasthmatics, except: asthma control.
 depression  If used, the results must be interpreted in
 miscarriages relation to normal values for pregnancy
 cesarean delivery  pCO2 > 35 mm Hg with a pH < 7.35
 significantly increased morbidity is linked to ☀ consistent with hyperventilation
 progressively more severe disease and CO2 retention in a pregnant
 poor control woman.
 combination of both ⚜ Pulmonary function testing
 baseline pregnancy forced expiratory  should be routine in the management of
volume at 1 second (FEV1) chronic and acute asthma.

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 Sequential measurement of the FEV1 or the STEPWISE THERAPY OF CHRONIC ASTHMA DURING PREGNANCY
peak expiratory flow rate—PEFR SEVERITY STEPWISE THERAPY
 best measures of severity MILD INTERMITTENT Inhaled β-agonists (ALBUTEROL) as needed
Low-dose inhaled corticosteroids
 FEV1 (BUDESONIDE)
☀ If < 1 L or < 20% of predicted value MILD PERSISTENT
ALTERNATIVE: Cromolyn, leukotriene
❧ correlates with severe disease antagonists, or theophylline
defined by Low-dose inhaled corticosteroids and long-
acting β-agonists (SALMETEROL) or
☘ hypoxia medium-dose inhaled steroids and long-
☘ poor response to therapy MODERATE PERSISTENT acting β-agonist if needed
☘ high relapse rate Alternative—low-dose (or medium if
needed) inhaled steroids and either
 PEFR theophylline or leukotriene antagonists
☀ correlates well with the FEV1 High-dose inhaled corticosteroids and long-
☀ can be measured reliably with acting β-agonist and oral steroids if needed
SEVERE PERSISTENT ALTERNATIVE: high-dose inhaled
inexpensive portable meters
corticosteroids and theophylline and oral
☀ Each woman determines her own steroids
baseline when asymptomatic—
personal best ⚜ ALTERNATIVE DRUGS
❧ compared with values when  Theophylline
symptomatic  Methylxanthine
☀ PEFR did not change during the  bronchodilators and possibly anti-
course of pregnancy in normal inflammatory agents
women.  used less frequently since inhaled
 MANAGEMENT OF CHRONIC ASTHMA corticosteroids became available
⚜ Management Guidelines on Asthma &  Some theophylline derivatives are
Pregnancy: considered useful for oral maintenance
 Objective assessment of pulmonary therapy if the initial response is not
function & fetal well being optimal to inhaled corticosteroids and
 monitor with PEFR or FEV1 β-agonists
 Environmental precipitating factors  Leukotriene modifiers
 Avoidance or control of triggers  inhibit their synthesis and include
 Pharmacological drugs ☀ zileuton
 to provide baseline control and treat ☀ zafirinkast
exacerbations ☀ montelukast
 Patient education  given orally or by inhalation for
 general asthma management and its
prevention
effect on pregnancy
☀ not effective for acute disease
⚜ women with moderate to severe asthma
 For maintenance
 should measure and record either their
☀ used in conjunction with inhaled
FEV1 or PEFR twice daily
corticosteroids to allow minimal
 FEV1
dosing
☀ Ideally >80 percent of predicted.
 not as effective as inhaled
 PEFR
corticosteroids
☀ predicted values range from 380 to  Cromolyn and nedocromil
550 L/min  inhibit mast cell degranulation
☀ Each woman has her own baseline  ineffective for acute asthma
value, & therapeutic adjustments  taken chronically for prevention
can be made using this  not as effective as inhaled
⚜ Treatment depends on the severity of disease corticosteroids
 β-agonists  been replaced by leukotriene modifiers
 help to abate bronchospasm  omalizumab
 corticosteroids  no experience in pregnant women
 treat the inflammatory component  a recombinant humanized monoclonal
 For mild asthma anti-IgE antibody
 inhaled β-agonists  binds circulating IgE to deactivate it
☀ as needed are usually sufficient  MANAGEMENT OF ACUTE ASTHMA
 For persistent asthma ⚜ Similar to that for the nonpregnant asthmatic
 inhaled corticosteroids  Except for those w/ lowered threshold for
☀ administered every 3 to 4 hours. hospitalization
☀ Goal: ⚜ Intravenous hydration may help clear
❧ to  the use of β-agonists for pulmonary secretions
symptomatic relief ⚜ Supplemental oxygen is given by mask
☀  hospitalizations by 80 percent ⚜ THERAPEUTIC AIM:
 55%  in readmissions for severe  Maintain the pO2 > 60 mm Hg to NORMAL
exacerbations in pregnant asthmatics with 95-% oxygen saturation
given maintenance inhaled ⚜ Baseline pulmonary function testing:
corticosteroids along with β-agonist  Includes FEV1 or PEFR
therapy ⚜ Continuous pulse oximetry and electronic fetal
monitoring

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⚜ First-line therapy ⚜ Maintenance medications are continued


 β-adrenergic agonist through delivery
 given SQ, oral or inhaled ⚜ Give anesthesia preferably EPIDURAL
 EXAMPLES ANESTHESIA
☀ Terbutaline ⚜ Stress-dose corticosteroids
☀ Albuterol  administered with systemic steroid therapy
☀ Isoetharine within the preceding 4 weeks
☀ Epinephrine  Usual dose is 100 mg of HYDROCORTISONE
IV q 8 hours during labor and for 24 hours
☀ Isoproterenol
after delivery
☀ Metaproterenol
⚜ PEFR or FEV1
 bind to specific cell-surface receptors
 determined on admission
 activate adenylyl cyclase 
 serial measurements taken
intracellular cyclic AMP  modulate
⚜ Oxytocin or prostaglandins E1 or E2
bronchial smooth muscle relaxation
 Used for cervical ripening and induction of
 Long-acting preparations are used for
labor
outpatient therapy
⚜ Fentanyl:
 Maintenance drug
 Nonhistamine-releasing narcotic
 Inhaled corticosteroids  intensive β-
 May be preferable to meperidine for labor,
agonist therapy
and epidural analgesia is ideal
 For Severe exacerbations:
⚜ Conduction analgesia
 Inhaled Ipratropium Bromide is given
 For surgical delivery
 Corticosteroids
 preferred because tracheal intubation can
☀ should be given early to all
trigger severe bronchospasm
patients with severe acute asthma
⚜ Postpartum hemorrhage
☀ Given orally or parenteral  Treated with oxytocin or prostaglandin E2.
☀ IV methylprednisolone  Prostaglandin F2α or ergotamine derivatives
❧ 40 to 60 mg, every 6 hours  CONTRAINDICATED
☀ Hydrocortisone by infusion  may cause significant bronchospasm
☀ Prednisone orally.
☀ Give along w/ beta agonists for Acute Bronchitis
acute asthma Infection of the large airways
☀ onset of action is several hours MANIFESTATION
 For acute asthma  cough without pneumonitis
 Corticosteroids β-agonists common in adults, especially in winter months
⚜ If initial therapy with β-agonists is a/w Infections are usually caused by viruses commonly:
improvement of FEV1 or PEFR >70 % of baseline  influenza A and B
 discharge can be considered  parainfluenza
 Some may benefit from observation.
 respiratory syncytial
 coronavirus
⚜ for the woman with obvious respiratory distress,
 adenovirus
or if the FEV1 or PEFR <70% of predicted after  rhinovirus
three doses of β-agonist Bacterial agents causing community-acquired pneumonia
 admission is advisable are rarely implicated.
 Intensive therapy includes cough
 inhaled β-agonists  persists for 10 to 20 days (mean 18 days)
 occasionally lasts for a month or longer
 intravenous corticosteroids
routine antibiotic treatment is not justified
 close observation for worsening
respiratory distress or fatigue in Pneumonia
breathing TYPES OF PNA
 woman is cared for in the delivery unit or an  Community Acquired PNA
intermediate or intensive care unit ⚜ encountered in otherwise healthy young
 STATUS ASTHMATICUS AND RESPIRATORY FAILURE women, including during pregnancy
⚜ Severe asthma of any type NOT responding after ⚜ relatively common in pregnant women
30 to 60 minutes of intensive therapy ⚜ caused by a number of bacterial or viral
⚜ Managed in ICU pathogens
⚜ Management of nonpregnant patients in an  Healthcare-Associated PNA
intensive care setting  good outcome in most ⚜ in patients in outpatient care facilities
cases ⚜ more closely resembles hospital-acquired
⚜ Consider Early intubation when maternal pneumonia (HAP)
respiratory status worsens despite aggressive  nursinghome-acquired pneumonia (NHAO)
treatment  ventilator-associated pneumonia (VAP).
 Indications for mechanical ventilation: accounts for 4.2% of antepartum admissions for
 Fatigue nonobstetrical complications
 Carbon dioxide retention Mortality from pneumonia
 Hypoxemia  infrequent in young women
 LABOR & DELIVERY

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 during pregnancy severe pneumonitis with ⚜ Outpatient or 23-hour observation is reasonable


appreciable loss of ventilatory capacity is not as well if home care & follow up are optimal
tolerated
 Hypoxemia and acidosis
⚜ poorly tolerated by the fetus
⚜ frequently stimulate preterm labor after
midpregnancy. B
⚜ worsening or persistence of symptoms may
represent developing pneumonia.
 Any pregnant woman suspected of having
pneumonia should undergo chest radiography.
BACTERIAL PNEUMONIA
 Many bacteria that cause community-acquired
pneumonia, such as Streptococcus pneumoniae, are
part of the normal resident flora
 Some Factors that perturb the symbiotic relationship
b/w colonizing bacteria and mucosal phagocytic
defenses include
⚜ acquisition of a virulent strain
⚜ bacterial infections following a viral infection
 Cigarette smoking and chronic bronchitis favor
colonization of:
⚜ S. pneumonia CHEST RADIOGRAPHS in a pregnant woman with RIGHT LOWER LOBE
PNEUMONIA. A. Complete opacification of the right lower lobe (arrows)
⚜ Haemophilus influenza is consistent with the clinical suspicion of pneumonia
⚜ Legionella species
 Risk factors include: CRITERIA FOR SEVERE COMMUNITY ACQUIRED PNEUMONIA
⚜ Asthma CRITERIA VALUES
⚜ binge drinking RESPIRATORY RATE ≥30/min
⚜ human immunodeficiency virus (HIV) infection PaO2/FiO2 ratio ≤250
 INCIDENCE AND CAUSES LUNG INFILTRATES MULTILOBULAR infiltrates
⚜ Pregnancy itself DOES NOT predispose to LEVEL OF CONSCIOUSNESS Confusion/disorientation
pneumonia UREMIA UREMIA
⚜ Hospitalization for pneumonia to be 1.5 per Leukopenia—WBC <4000/µL
1000 deliveries CBC Thrombocytopenia—platelets
<100,000/µL
⚜ > 50% of adult PNA are bacterial
TEMPERATURE Hypothermia—core temperature <36°C
⚜ 75% of the Causes of PNA are:
Hypotension requiring aggressive fluid
 S. pneumoniae (37%) BLOOD PRESSURE
resuscitation
 most common bacterial & overall cause
of PNA ⚜ If w/ SEVERE PNA
 AKA: Pneumococci  admission to an intensive care or
 Influenza A (14%) intermediate care unit is advisable
 MC viral cause of PNA  common cause of acute respiratory distress
 Chlamydophila pneumonia (10%) syndrome during pregnancy
 H. Influenza (5%)  mechanical ventilation maybe necessary
 Mycoplasma pneumoniae (2%) ⚜ Antimicrobial treatment is empirical
 Legionella pneumophila (2%)  MOST ADULT PNA are caused by
⚜ CA-MRSA  Pneumococci
 Cause Necrotizing pneumonia  Mycoplasma
 DIAGNOSIS  Chlamydophilia
⚜ Typical Symptoms include:  Monotherapy initially is with a MACROLIDE:
 Cough  Azithromycin
 Dyspnea  Clarithromycin
 Sputum production  Erythromycin
 Pleuritic chest pain ☀ Given intravenously and then
⚜ Mild upper respiratory symptoms and malaise orally, was effective in 99% of
 Precededs above symptoms women w/ uncomplicated PNA
⚜ Diagnostic Tests  If w/ SEVERE disease:
 CBC:  Respiratory Fluoroquinolone
 Mild leukocytosis ☀ DRUGS
 Chest radiography
❧ Levofloxacin
 Essential to establish dx & help monitor
disease ❧ Moxifloxacin
 Does not accurately predict etiology ❧ Gemifloxacin
⚜ Other Recommended Tests ☀ Teratogenicity risk: LOW
 Rapid Serological Testing (RAST) ❧ given if indicated
 Test for Influenza A & B  β-Lactam + Macrolide
 MANAGEMENT ☀ Preferred β-Lactams:
⚜ Hospitalize all pregnant women w/ ❧ high-dose amoxicillin
radiographically proven PNA ❧ amoxicillin-clavulanate

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☀ Alternatives for MACROLIDE


resistant Pneumococci (25%)
❧ Ceftriaxone
❧ Cefpodoxime
❧ Cefuroxime
❧ Levofloxacin
 CA-MRSA
  vancomycin
⚜ RESOLUTION OF PNA
 Clinical improvement is usually evident in
48 to 72 hours
 Resolution of fever in 2 to 4 days
 Resolution of X-ray abnormalities takes up
to 6 weeks
⚜ Worsening disease
 poor prognostic feature
 follow-up radiography is recommended
if fever persists
 20% of women develop a pleural effusion
⚜ FACTOR that increase the risk of death or
complications w/ CA PNA CHEST RADIOGRAPH of a 30-week pregnant woman with INFLUENZA A
PNEUMONIA. Extensive right lower lung field opacification (arrows),
 Coexisting chronic conditions
which represents parenchymal infiltrate and pleural effusion, obscures
 Clinical Findings the right hemidiaphragm
 RR > 30
 Hypotension
 quickly infects ciliated columnar
 Tachycardia: PR > 125 bpm
 Hypothermia epithelium, alveolar cells, mucus gland
 Temp <36ᵒC or > 40ᵒC cells, and macrophages
 ALOC  ONSET
 Extrapulmonary dse ⚜ 1-4 days after exposure
 LABS  FLU shots recommended in pregnancy
 Leukopenia or leukocytosis  Infection is self-limited
 PREGNANCY OUTCOME  PRIMARY INFLUENZA PNEUMONITIS
rd
⚜ Without antibiotics, 1/3 pregnant women with ⚜ Most severe
pneumonia died ⚜ CHARACTERISTICS
⚜ maternal mortality rate was 0.8 percent of 632  sparse sputum production
women.  radiographic interstitial infiltrates
⚜ 7% required intubation and mechanical  SECONDARY PNEUMONIA
ventilation. ⚜ More Common
⚜ COMMON COMPLICATIONS of PNA during ⚜ Develops from bacterial superinfection by
Pregnancy: Streptococci or Staphylococci after 2 to 3 days
 Prematurely ruptured membranes of initial clinical improvement
 Preterm delivery  MANAGEMENT
 low-birthweight infants ⚜ RECOMMENDED for UNCOMPLICATED PNA
 PREVENTION  Supportive treatment
⚜ Pneumococcal vaccine  Antipyretics
 60-70% protective against its 23 serotypes  Bed rest
  Emergence of drug-resistant ⚜ influenza A
pneumococci  H3N2 strains
 Not recommended for otherwise healthy  Has rapid resistance to
pregnant women ☀ AMANTADINE
 Recommended for: ☀ RIMANTADINE
 Immunocompromised  H1N1 strain
 HIV infection  Resistant to OSELTAMIVIR
 Significant smoking history ⚜ DRUGs for CHEMOPROPHYLAXIS & TREATMENT
 Diabetes  Neuraminidase inhibitors
 Cardiac, pulmonary, or renal disease  given within 2 days of symptoms onset
 Asplenia (sickle-cell disease)  for influenza A and B infection
INFLUENZA PNEUMONIA  MOA
 Respiratory infection ☀ interfere with the release of
⚜ PNEUMONITIS progeny virus from infected host
 PNA cells and thus prevent infection of
 MC complication new host cells
 Caused by RNA viruses of which influenza A and B  Effective for early influenza
form one genus  DRUGS
⚜ Influenza A ☀ Oseltamivir
 Serious, epidemic in winter months ❧ oral, 75 mg BID
 MOA ☀ Zanamivir
⚜ aerosolized droplets ❧ inhalation, 10 mg BID

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shorten the course of illness by 1 to 2  Should NOT BE GIVEN to women who may
days become pregnant during the month
 may reduce the risk for pneumonitis following each vaccine dose
 PREVENTION  Attenuated vaccine virus is not secreted in
⚜ Vaccination for influenza A breast milk
⚜ Prenatal vaccination affords protection for a  Postpartum vaccination MUST NOT be
third of infants for at least 6 months delayed
 EFFECTS ON PREGNANCY FUNGAL & PARASITIC PNA
⚜ Severe viral pneumonitis is life-threatening  Greatest consequence in immunocompromised
during pregnancy hosts, especially in women with acquired
 FETAL EFFECTS: immunodeficiency syndrome (AIDS).
⚜ No firm evidence causes congenital  Pneumocystis Pneumonia
malformations ⚜ Lung infection with Pneumocystis jiroveci
⚜ Increased neural-tube defects in neonates  aka Pneumocystis carinii
(possibly associated with early hyperthermia) ⚜ Common complication in women with AIDS
⚜ May predispose to schizophrenia in later life ⚜ Causes INTERSTITIAL PNA characterized by:
VARICELLA PNEUMONIA  Dry cough
 AGENT  Tachypnea
⚜ Varicella Zoster Virus  Dyspnea
 Double-stranded DNA herpesvirus  Diffuse radiographic infiltrates
 Attack rate in seronegative individual is 90% ⚜ Management:
 PRIMARY INFECTION  Trimethoprim-sulfamethoxazole
 Chickenpox or Varicella  Pentamidine
☀ CLINICAL MANIFESTATIONS  Tracheal intubation and mechanical
ventilation
❧ 1- to 2-day flulike prodrome
⚜ Prophylaxis
❧ pruritic maculopapular
 Double-strength TRIMETHOPRIM-
vesicular lesions that crust
SULFAMETHOXAZOLE tablet
over in 3 to 7 days
 daily for some HIV-infected pregnant
☀ MORTALITY d/t Varicella PNA women
❧ More severe in adulthood  Fungal Pneumonia
especially during pregnancy ⚜ Usually seen in women with HIV infection
 10% of Pregnancy PNA ⚜ Who are otherwise immunocompromised
 Risk of developing PNA ⚜ Organisms:
⚜ Smoking  Histoplasmosis & Blastomycosis
⚜ >100 skin lesions  not common
 Clinical Manifestations:  more severe during pregnancy
⚜ Symptoms of pneumonia (appear 3 to 5 days)  (+) erythema nodosum
characterized: ☀ symptomatic infection
 Fever, tachypnea, dry cough, dyspnea, and
☀ better overall prognosis
pleuritic pain
 Cryptococcosis
 Nodular infiltrates are similar to other viral
 manifest as MENINGITIS
pneumonias
⚜ Management:
 Fever and compromised pulmonary
 ITRACONAZOLE
function may persist for weeks
 PREFERRED therapy for disseminated
 Diagnosis:
fungal infections
⚜ Performing a Tzanck smear
 INTRAVENOUS AMPHOTERICIN B OR
 Fetal and Neonatal Varicella Infection:
KETOCONAZOLE
⚜ Fetus may develop Congenital Varicella
 Amphotericin B
Syndrome
☀ used extensively in pregnancy with
 Chorioretinitis
no embryo-fetal effects
 Microphthalmia
 FLUCONAZOLE, ITRACONAZOLE, AND
 Cerebral cortical atrophy
KETOCONAZOLE
 Growth restriction
 embryotoxic in large doses in early
 Hydronephrosis
pregnancy
 Skin or bone defects
 ITRACONAZOLE
 Management
⚜ Supportive care ☀ reasonable later in pregnancy
⚜ Intravenous ACYCLOVIR therapy
 For Invasive candidiasis
2
 500 mg/m or 10 to 15 mg/kg every 8 hours  CASPOFUNGIN, MICAFUNGIN, AND
⚜ Serious maternal infection w/sepsis of varicella
ANIDULAFUNGIN
PNA is a/w PRETERM DELIVERY ☀ Embryotoxic and teratogenic in
 VACCINATION laboratory animals
⚜ Attenuated live-virus vaccine—VARIVAX SEVERE ACUTE RESPIRATORY DISTRESS SYNDROME
 2 doses, given 4 to 8 weeks apart  CORONAVIRUS respiratory infection
 recommended for adolescents and adults  ATYPICAL Pneumonitis
with no history of varicella  case-fatality rate :
 NOT RECOMMENDED for pregnant women ⚜ NONPREGNANT: ~ 5%
⚜ PREGNANT: 25%

8 Williams Obstetrics 23rd Edition


Surgery Block
SECTION VIII: MEDICAL & SURGICAL COMPLICATIONS
2012

 PLACENTAL EFFECT: ⚜ Cycloserine


⚜ abnormal intervillous or subchorionic fibrin ⚜ Para-aminosalicylic acid
deposition TUBERCULOSIS AND PREGNANCY
⚜ extensive fetal thrombotic vasculopathy  OUTCOMES
⚜ dependent on the site of infection and timing of
Tuberculosis diagnosis in relation to delivery
MOT  active pulmonary tuberculosis associated with
 inhalation of Mycobacterium tuberculosis incidences:
⚜ incites a granulomatous pulmonary reaction ⚜ preterm delivery: 2x
In 90% of patients, infection contained and dormant for ⚜ low-birthweight: 2x
long periods ⚜ growth-restricted infants
 reactivated in IMMUNOCOMROMISED patients ⚜ perinatal mortality: 6x
MANIFESTATIONS:
⚜ Preeclampsia: 2x
 Cough with minimal sputum production
 Adverse outcomes correlate with
 Low-grade fever
 Hemoptysis ⚜ Late diagnosis
 Weight loss. ⚜ Incomplete or irregular treatment
 Mediastinal lymphadenopathy ⚜ Advanced pulmonary lesions
LABORATORY FINDINGS  CDC GUIDELINES FOR TB
 Culture ⚜ SKIN TESTING of pregnant women who are in
⚜ Ziehl-Neelsen acid-fast staining any of the high-risk groups
 (+) Acid Fast Bacilli on stained smears of  Purified Protein Derivative (PPD)
sputum  preferred antigen
 Chest radiograph  intermediate strength of 5 tuberculin
⚜ Variety of infiltrative pattern units.
 intracutaneously applied
⚜ Cavitation
 If NEGATIVE
EXTRAPULMONARY TB
 Middle ear ☀ no further evaluation is needed.
 Tonsils  IF POSITIVE
 Lungs ☀ (+) skin test measures > 5 mm in
 Pericardium diameter
 CNS ☀ requires evaluation for active
 Bones, spine, psoas mm disease, including a chest
 Pelvic TB radiograph
⚜ Common ☀ VERY HIGH-RISK patients:
⚜ Amenorrhea, ascites, adhesions ❧ HIV-positive
 Intestine ❧ abnormal chest radiography
 Genitals ❧ recent contact with an active
⚜ especially epididymis case— > 5 mm
 Liver,spleen, peritoneum, ☀ HIGH RISK patients
 Adrenal glands ❧ Foreign-born individuals
 Ureter ❧ intravenous drug users who
 Bladder are HIV-negative
 Adnexa
❧ low-income populations
 Prostate, seminal vesicles
❧ medical conditions that
MILIARY TB
increase the risk for
 40%of affected HIV-positive patients have
tuberculosis— >10 mm
disseminated disease
TREATMENT ☀ For persons with no risk factors but
 Cure rates with 6-month short-course DIRECTLY w/ > 15 mm or greater is defined
OBSERVED THERAPY (DOT) as requiring treatment
 Multidrug-resistant tuberculosis (MDR-TB)
⚜  rapidly as TB incidence fell during the 1990s
FOUR-DRUG REGIMEN for initial empirical treatment:
 Isoniazid
 Rifampin
 Pyrazinamide
 Ethambutol
Extensively Drug-Resistant Tuberculosis—XDR-TB
st
 Resistance in vitro to at least the 1 -line drugs
⚜ Isoniazid
⚜ Rifampin
ND
 Resistance to >3 of the 6 main classes of 2 -LINE
DRUGS
⚜ Aminoglycosides
⚜ Polypeptides
⚜ Fluoroquinolones
⚜ Thioamides

9 Williams Obstetrics 23rd Edition


Surgery Block
SECTION VIII: MEDICAL & SURGICAL COMPLICATIONS
2012

⚜ In Vitro Quantiferon-TB Gold Test NEONATAL TUBERCULOSIS


 same indications as skin testing  Tubercular bacillemia can infect the
 useful in identifying patients with latent ⚜ Placenta
TB and at risk for progression to active ⚜ Fetus
disease.  Congenital Tuberculosis
 distinguish between immune responses  d/t aspiration of infected secretions at
delivery
due to infection and responses resulting
 simulates other congenital infections
from bacille Calmette-Guérin (BCG)  MANIFESTATIONS
vaccination ☀ Hepatosplenomegaly
 TREATMENT
☀ respiratory distress
⚜ Principles are similar in pregnant & nonpregnant
☀ fever
 except STREPTOMYCIN NOT ALLOWED in
pregnancy ☀ lymphadenopathy
 unlikely if the mother with active disease has been
⚜ LATENT INFECTION
treated before delivery or if her sputum culture is
 ISONIAZID:
negative
 For Nonpregnant; (+) Tuberculin; < 35
 recommend isolation from the mother suspected of
Years; (-) Evidence Of Active Disease
having active disease
☀ 300 mg orally daily for 1 year
⚜ contradicts EINT
 Considered safe in pregnancy st
 After delivery, NORMALLY, the 1 thing you
 COMPLIANCE is a major problem
is do place the baby on top on mother’s
 Delayed administration until after
chest w/ baby wrapped & dried,
delivery:
 wait for the cord to stop pulsating (around
☀ For possibly increased isoniazid- 2 minutes) before clamping
induced hepatitis risk in  Allows more blood to flow to baby
postpartum women  After 2 mintues, double clamp & cut
☀ Withholding treatment until 3 to 6 umbilical cord
months after delivery  Wait for the baby to crawl & look for nipple
☀ Exceptions to delayed treatment in & latch naturally
pregnancy:  Occurs ~ 20-30 minutes after delivery
❧ Known recent skin-test ⚜ So if mother is w/ tuberculosis
convertors  Recommend to still follow EINT but
❧ Skin-test-positive women MOTHER MUST WEAR MASK FIRST
exposed to active infection  If untreated, the risk of disease in the infant
❧ HIV-positive women born to a woman with active infection is
⚜ ACTIVE INFECTION 50% in the first year
 Recommended initial treatment:
 Three-drug regimen
☀ ISONIAZID
☀ RIFAMPIN
☀ ETHAMBUTOL
 Prevalence of isoniazid-resistant
tuberculosis
☀  PYRAZINAMIDE
 If organism is susceptible:
☀ Regimen is given for 9 months
 Breast feeding is not prohibited
 To decrease hepatic toxicity:
 ISONIAZID  PYRIDOXINE (25 mg/day
orally)
 HIV-INFECTED WOMEN:
 Rifampin or Rifabutin
☀ CONTRAINDICATED If certain
protease inhibitors or non-
nucleoside reverse transcriptase
inhibitors are being administered
 Resistance to rifabutin or rifampin:
☀ Pyrazinamide therapy is given
 Second-line regimens
 CONTRAINDICATED
 ototoxic to the fetus
 Aminoglycosides
☀ Streptomycin
☀ Kanamycin
☀ Amikacin
☀ Capreomycin

10 Williams Obstetrics 23rd Edition

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