PATHOLOGIC OBSTETRICS
Topic: Pulmonary Disorders
Lecturer: Dr. Brillantes (RCB)
ASTHMA
Asthma:
 A chronic inflammatory airway syndrome with a major hereditary
component
 Pathology: Increased airway responsiveness and persistent subacute
inflammation
Lecture Discussion: Bronchiole of Asthmatic Patients
Asthmatic Patients  even without the triggers, the airways are persistently
inflamed therefore there will be narrowing of the airways.
 When there is trigger, there will be narrowing of the already
narrowed airway so the airflow will be more difficult during an
attack
 There are 3 mechanisms by which an asthmatic patient can have
narrowing or obstructed gas exchange:
1. Further narrowing of the already inflamed airways
2. Excessive mucus production
3. Contraction of the bronchiolar muscle
 To improve the condition of the patient, you should be able to
control the abovementioned mechanisms
Pathophysiology of Asthma
Lecture Discussion: Pathophysiology of Asthma
The pathology in asthma is that the lining of the airways are riddled with cells
such as eosinophils, mast cells, etc.  all these cells in the bronchiolar lining
are going to secrete substances like histamine, proteases, cytokines,
leukotrienes, prostaglandins which are actually inflammatory mediators. Due
to the presence of these, the mucosa will be hyperresponsive. When there is
presence of trigger  cascade of events happen causing inflammation of the
mucous lining, mucus production, contraction of bronchiolar muscles. IgE is
thought to have a role in the pathophysiology of asthma
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Asthma Triggers:
 Outdoor substances: pollen, smoke, pollution, cold weather
 Indoor substances: mold, pet dander, dust mites, cockroach droppings
 Food allergens: fish, shellfish, eggs, peanuts, soy
 Conditions: respiratory infections, stress, strong emotions, exercise
Symptoms:
 Coughing
 Wheezing
 Shortness of breath
 Tightness in the chest
Effect of Pregnancy on Asthma:
 No evidence that pregnancy has a predictable effect on underlying
asthma
 Some have exacerbations during labor and delivery
Since labor and delivery is a form stress  may trigger an asthmatic
attack
 Perinatal outcomes are generally good
 Incidence of spontaneous abortion may be slightly increased
 Incidence of fetal-growth restriction increases with asthma severity
 No evidence that commonly used anti-asthmatic drugs are harmful
Diagnosis:
Clinical Evaluation
 Clinical Signs
o Labored breathing
o Tachycardia
o Pulsus paradoxus
o Prolonged expiration
o Use of accessory muscles
o Central cyanosis
o Altered consciousness
Lecture Discussion: Diagnosing Asthma
To diagnose asthma, we go by the clinical manifestations but
unfortunately, none of them are going to be specific for asthma
(even the characteristic wheezing is not specific for asthma since
they are also seen in other lung pathologies like COPD). The clinical
signs will just tell us the degree of hypoxemia
 Use of accessory muscles  may tell us that there is
severe hypoxemia
 Central cyanosis, Altered consciousness  signs of a
potentially fatal attack (impending respiratory arrest)
 Subjective severity does not correlate well with objective measures
Unfortunately, even the laboratory tests will not tell you the
diagnosis because there is no chest x-ray finding that it is asthma.
Whatever we find on CXR, it would non-specific. More so, the
severity of hypoxemia (found on objective measures) may not even
correlate with actual subjective severity. But nevertheless, we
would want to request for: Arterial blood gas analysis and
Pulmonary function test
 Arterial blood gas analysis – objective assessment of maternal
oxygenation, ventilation, and acid base status
 Pulmonary Function testing – should be routine
o FEV, PEFR – best measures of severity
(Forced expiratory volume, Peak expiratory flow rate)
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 PATHOLOGIC OBSTETRICS
Topic: Pulmonary Disorders
Lecturer: Dr. Brillantes (RCB)

Management of Chronic Asthma______________________________________ Cromones

 Patient who is not in an acute attack is called chronic asthma  what  Examples:
we would want to do with them is provide baseline control so there o Cromolyn
would be no attacks (giving maintenance) o Nedocromil
 Treatment depends on disease severity  Inhibit mast cell degranulation
 β-agonists- to abate bronchospasm; inhaled for mild asthma Inhibiting mast cell degranulation  reduces the hypersensitivity of
o First line treatment the bronchiolar mucosa
o If this does not work, then you add corticosteroids
 Corticosteroids- to treat the inflammatory component; inhaled- every  Ineffective for acute asthma
3 to 4 hours for persistent asthma  Taken chronically for prevention
 The goal is to reduce the use of β-agonists for symptomatic relief  Not as effective as inhaled corticosteroids
o We would want to use the smallest possible dose that give
symptomatic relief Management of Acute Asthma_______________________________________
 Treatment of acute asthma during pregnancy is similar to that for the
nonpregnant asthmatic
 Antibiotics are not given unless with pneumonitis
Since the pathology is not infectious  no need to give antibiotics
UNLESS there is presence of pneumonitis

 IV hydration - to clear (dilute) the pulmonary secretions

 Supplemental oxygen
o Maintain the PO2 >60 mmHg, and preferably normal, along
with 95% oxygen saturation
 Baseline pulmonary testing- FEV1 or PEFR
This is done because we would want to monitor the patient later on
for the response of medications

 Continuous pulse oximetry

Lecture Discussion: Convenient but not as accurate as ABG. Reduces the need for having
As the asthma severity progresses  treatment from inhaled form goes up the patient pricked for ABG
to using oral or IV form.
If the patient already needs oral or systemic antiasthma medications   Electronic fetal monitoring
already on severe condition To check if there is any fetal compromise going on secondary to
maternal hypoxemia caused by asthma
Theophylline
 This maybe added if the corticosteroid and β-agonist do not give an  β-adrenergic agonist- first line
optimal response o terbutaline
 Methylxanthine o albuterol
 Bronchodilator, anti-inflammatory o isotharine modulate bronchial smooth muscle relaxation
 Minimal benefits – when compared to the 2 main drugs o epinephrine
 Useful for maintenance therapy if the initial response to inhaled o isoproterenol
corticosteroids and B agonists is not optimal o metaproterenol
 Maintenance: inhaled corticosteroids + intense β-agonist therapy
Antileukotrienes o Oral or parenteral corticosteroids
 Another option if the first-line drugs do not work  Severe Exacerbation: magnesium sulfate – relaxes the bronchiolar muscles
 Inhibit leukotriene synthesis  Intensive therapy:
Hypersensitivity to the triggers are due to the presence of o Inhaled β-agonists
leukotrienes in the bronchialar mucosa o Intravenous corticosteroids
o Close observation for worsening respiratory distress or fatigue
 Given orally or by inhalation for prevention in breathing
 Are not effective for acute disease o Delivery unit or intermediate or intensive care unit
It will only be useful for maintenance because you will be taking this
drug for long-term to get the benefit of inhibiting leukotriene Status Asthmaticus
synthesis  Severe asthma if any type not responding after 30-60 minutes of
intensive therapy
 For maintenance, they are used in conjunction with inhaled  If patient already has Fatigue, CO2 retention, Hypoxemia  Early
corticosteroids to allow minimal dosing intubation, Mechanical ventilation
 Not as effective as inhaled corticosteroids  Life threatening complications:
 Little experience with their use in pregnancy o Muscle fatigue with respiratory arrest
o Pneumothorax
o Pneumomediastinum
o Acute cor pulmonale
o Cardiac arrhythmias

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 PATHOLOGIC OBSTETRICS
Topic: Pulmonary Disorders
Lecturer: Dr. Brillantes (RCB)
Labor and Delivery:
 Labor and delivery is a form of stress  asthmatic attack possible
 Maintenance medications are continued through delivery
 Stress-dose corticosteroids are administered to any woman given
systemic corticosteroid therapy within the preceding 4 weeks
o Severe asthmatic patient  1 month before she sets into
labor, she should have IV or Oral corticosteroid
o Hydrocortisone 100mg IV q8 (during labor and for 24 hours
after delivery)
 PEFR or FEV1 – determined on admission; serial measurements taken if
symptoms develop
For Labor:
 Nonhistamine-releasing narcotic ie. Fentanyl may be preferable to
meperidine; epidural analgesia
 Meperidine is usually given for non-asthmatic patient. You shy away
from this drug is the patient is asthmatic. Use fentanyl instead or if you
can do epidural analgesia, then better
For Surgical Delivery:
 Conduction analgesia (general anesthesia) is preferred because
tracheal intubation can trigger severe bronchospasm
For Postpartum Hemorrhage:
 After the delivery of the placenta, our main goal is to keep the uterus
contracted  prevent postpartum hemorrhage
 Preferred uterotonic postpartum  Methergine (methylergonovine
maleate)  preferred for non-asthmatic patient because it gives very
strong and sustained uterine contractions
 Oxytocin or Prostaglandin E2  Preferred for asthmatic patients
Prostaglandin F2a or ergotamine derivatives are contraindicated because
they may cause significant bronchospasm
ACUTE BRONCHITIS
 -itis  means there is inflammation
 Infection of the large airways
 Manifested by cough without pneumonitis
 Caused by viruses:
o Influenza A and B
o Parainfluenza
o Respiratory syncytial
o Coronavirus
o Adenovirus
o Rhinovirus
 Bacterial agents causing community-acquired pneumonia are rarely
implicated
 Cough persists for 10-20 days (mean 18 days) and occasionally lasts for
a month or longer
 Routine antibiotic treatment is not justified
Not given because the etiologic agent is NOT bacterial in origin
 However, be wary of worsening or persistence of symptoms of viral
upper RTI may represent developing pneumonia
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PNEUMONIA
 Pathology is on the alveolar sac
 Etiologic agents have already reached the alveolar sacs  triggers an
immune response causing:
o Inflammation of the alveolar sac walls and endothelial lining of
capillaries
o Production of fluid in the alveolar sac
 There will be poor oxygenation because alveolar sacs are blocked
 During pregnancy, severe pneumonitis with appreciable loss of
ventilator capacity is not as well tolerated
Classification of Pneumonia: this is according to where you get the infection
 Community-acquired pneumonia (CAP)
 Healthcare associated pneumonia (HCAP)
o Develops in patients in outpatient care facilities
 Hospital-acquired pneumonia (HAP)
 Nursing home acquired pneumonia (NHAP)
 Ventilator associated pneumonia (VAP)
Classification of Pneumonia: based on etiologic agent
 Bacterial pneumonia
 Influenza pneumonia
 Varicella pneumonia
 Fungal & Parasitic pneumonia
Bacterial Pneumonia_______________________________________________
 Follow viral upper respiratory illness
 Risk factors:
o Smoking
o Asthma
o Binge drinking
o HIV infection
 Any pregnant women suspected of having pneumonia should undergo
chest radiography
Although we know that pregnant patients are contraindicated to do
CXR, if we are highly suspicious of pneumonia  justified to do CXR
Diagnosis
 Cough
 Dyspnea
 Sputum production
 Pleuritic chest pain
 Mild upper respiratory symptoms
 Malaise
 Mild leukocytosis
 Chest radiography – shows a characteristic finding
 Test to identify pathogen is optional
It may not be important for us to gram stain and culture the sputum
because our antibiotic of choice is empirical anyway
Management
 Hospitalize – all pregnant women with radiographically proven
pneumonia
 ICU or intermediate care unit – with severe disease
 Antimicrobial – empirical
o Monotherapy initially with a macrolide
 Azirthromycin
 Clarithromycin
 Erythromycin
o 3 most common etiologic agent: pneumococci, mycoplasma,
chlamydophila  reason why macrolides are given
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 PATHOLOGIC OBSTETRICS
Topic: Pulmonary Disorders
Lecturer: Dr. Brillantes (RCB)

Bacterial Pneumonia continued….. Influenza Pneumonia_______________________________________________

Indications to Hospitalize a Pregnant Patient with Pneumonia  Caused by RNA viruses- Influenza A and B viruses
 Spread by aerosolized droplets
 Quickly infects ciliated columnar epithelium, alveolar cells, mucus
gland cells, and macrophages
 Disease onset 1-4 days following exposure
 Self-limited
 Sparse spectrum sputum production
 Radiographic infiltrates

Secondary pneumonia develops from bacterial superinfection by streptococci

or staphylococci after 2-3 days of initial clinical improvement from influenza
pneumonia

Management
 Supportive – since it is viral; self-limiting
Lecture Discussion: Indications for Hospitalization of Pregnant with Pneumonia  Antipyretics – for fever
Confusion/disorientation  indicates that there is already severe  Bed rest
hypoxemia (less oxygenation on the brain)  Early antiviral treatment
Leukopenia  although we expect that the WBC to be very high (indicative o Neuraminidase inhibitors – given within 2 days of symptom
of sepsis) but leukopenia could also tell us that there is sepsis onset
Hypothermia  in the same manner, we expect a high fever in infection  Vaccination for influenza A – affords protection for infants up to 6
(indicative of sepsis) but hypothermia may also be indicative of ongoing months
sepsis
Varicella Pneumonia_______________________________________________
For Severe Disease
 Infection with varicella zoster virus- chickenpox results to pneumonitis
 A respiratory fluoroquinolone
o Levofloxacin, moxifloxacin, gemifloxacin Fungal & Parasitic Pneumonia________________________________________
 Or a macrolide plus a B-lactam  Pneumocystis Pneumonia
o High dose amoxicillin or amoxicillin-clavulanate (preferred B-
 Pneumocystis jiroveci, formerly called Pneumocystis carinii
lactams)
 Common complication in women with AIDS – immunocompromised
 B-lactam alternatives include:
 Most frequent HIV-related disorder in pregnant women
o Ceftriaxone, cefpodoxime
 Opportunistic
 If Community Acquired methicillin-resistant S. aureus is suspected:
o Vancomycin, Linezolid
Characterized by
 Pneumonia treatment is recommended for a minimum of 5 days
 Dry cough
 If fever persists >2-4 days  follow-up radiography is recommended
 Tachypnea
 Treatment failure:
 Dyspnea
o Warrants wider antimicrobial regimen
 Diffuse radiographic infiltrates
o More extensive diagnostic testing
 Organism on sputum culture, bronchoscopy with lavage or biopsy
Pregnancy Outcome with Pneumonia
Treatment
 Prematurely ruptured membranes
 Trimethoprim-sulfamethoxazole – may be given prophylactically as
 Preterm delivery
double strength in HIV pregnant
 Low-birth weight infants
 Pentamidine
 Growth restriction
 Dapsone
 Atovaquone
Prevention
 Tracheal intubation
 Pneumococcal vaccine
 Mechanical ventilation
o Decrease emergence of drug-resistant pneumococci
o Not recommended for otherwise healthy pregnant women
Other Fungal Pneumonia
o Recommended for:
 Histoplasmosis
 Immunocompromised
 With HIV infection  Blastomycosis
 Significant smoking history  Coccidiomycosis
 Diabetes  Cryptococcosis
 Cardiac, pulmonary, or renal disease
 Asplenia ie. sickle cell disease Treatment
 Itraconazole - preferred therapy for disseminated fungal infections
 Amphotericin B - no embryofetal effects (give for 1st trimester pneumonia)
 Ketoconazole
 Fluconazole
Itra-,Keto-,Fluco-nazole  embryotoxic

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 PATHOLOGIC OBSTETRICS
Topic: Pulmonary Disorders
Lecturer: Dr. Brillantes (RCB)

SARS (Severe Acute Respiratory Syndrome)  PPD (Purified Protein Derivative) Skin test
 SARS-CoV-1 o PPD is injected intradermally (within the skin) in the inner
 Corona viral infection surface of the forearm
 Causes atypical pneumonitis o If the site becomes indurated (Hard) after 48-72 hours, then
the reaction may be positive
TUBERCULOSIS o If negative, no further evaluation is needed
 Infection is via inhalation of Mycobacterium tuberculosis
 Incites granulomatous reaction Classification of the Tuberculin Skin Test (PPD) Reaction:
 If your immune system is good  infection of TB will go dormant  >5 mm
 However, if your immune system goes down  dormant infection will o HIV positive
o Recent contact with an active TB patient
get reactivated
o Nodular or fibrotic changes on chest X-ray
 Manifestations:
o Organ transplant
o Cough with minimal sputum If the patient is (+) and has the abovementioned risk factors
o Low-grade fever  You may initiate treatment or do further testing
o Hemoptysis
o Weight loss  >10 mm
 Infiltrative patterns on chest radiograph: o Recent arrivals (<5yrs) from high-prevalence countries
o Cavitation o IV drug users
o Resident/employee of high-risk congregate settings
o Mediastinal lymphadenopathy
o Mycobateriology lab personnel
 Acid-fast bacilli on stained smears of sputum
o Comorbid conditions
o Children <4yrs old
Extrapulmonary TB: o Infants, children, & adolescent exposed to high risk
Forms categories
 Lymphadenitis If the patient is (+) and has the abovementioned risk factors
 Pleural  you may need a bigger induration in order to justify
 Genitourinary initiation of treatment. Can do further work-ups
 Skeletal
 Meningeal  >15 mm
 Gastrointestinal o Persons with no known risk factors for TB
If the patient is (+) and has no risk factors  you may need
 Military or disseminated Intraperitoneal TB
a bigger induration in order to justify initiation of treatment.
Do further work-ups
TB & Pregnancy:
 Early diagnosis  is important because we want to institute therapy
Laboratory Methods for detection or verification of infection:
early such that the patient should have completed the regimen prior to
 Microscopy
delivery for good perinatal outcome
 Culture
 Without antiTB therapy, active tuberculosis has adverse effects on
 Nucleic acid amplification assay
pregnancy
 Drug-susceptibility testing
 Active pulmonary TB was associated with increased incidences of:
o Preterm delivery
Treatment: Active TB in pregnant
o Low birth weight
 Will need 6 months of treatment
o Growth restriction
 Bactericidal phase- first 2 months
o Perinatal mortality
o Isoniazid
 Outcomes are dependent on the site of infection and timing of
o Rifampin
diagnosis in relation to delivery
o Ethambutol
 Adverse outcomes correlate with late diagnosis, incomplete or irregular
o Pyrazinamide
treatment, and advanced pulmonary lesions
o Pyridoxine
 Continuation phase- next 4 months
Diagnosis:
o Isoniazid + rifampin
 Types of tests to detect latent or active tuberculosis:
 Breastfeeding is not prohibited during antituberculous therapy
o Tuberculin skin test (TST)
o Interferon-gamma release assays (IGRAs) - preferred; for
Second-line regimen
those who received BCG vaccination
 Aminoglycosides
o Streptomycin
o Kanamycin only used in non-pregnant
o Amikacin patients because it is ototoxic
o Capreomycin

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 PATHOLOGIC OBSTETRICS
Topic: Pulmonary Disorders
Lecturer: Dr. Brillantes (RCB)

Neonatal TB: Carbon Monoxide Poising & Pregnancy:

 Neonatal infection is unlikely if the mother with active disease has been
treated before delivery or if her sputum culture is negative
 Isolation from the mother recommended – because neonates are
susceptible
 Because carbon monoxide is bound so tightly to hemoglobin F, the
fetus may be hypoxic even before maternal carbon monoxide levels are
appreciably elevated
Clinical Significance: carbon monoxide will seek out first the fetal
hemoglobin so the baby will get toxic before the mother gets toxic

 The half-life of carboxyhemoglobin is 2 hours in the mother but 7 hours

in the fetus
The mother after 2 hours of inhalation of carbon monoxide 
carbon monoxide will be expelled
Baby will still hold on for the carbon monoxide for 7 hours

 Anomalies - associated with embryonic exposure to carbon monoxide

 Anoxic encephalopathy – later fetal exposure to carbon moxide

Treatment:
 Immediate administration of 100% inspired oxygen
 Hyperbaric oxygen treatment- controversial
Lecture Discussion: Pathophysiology of Congenital TB
Maternal TB, vertical transfer to fetus:
 Hematogenous spread from placenta via the umbilical vein
 In-utero aspiration or ingestion of amniotic fluid infected from the
placenta
 Ingestion of the infected secretions from maternal genital tract
during delivery

CARBON MONOXIDE POISONING

 Most frequent cause of poisoning
 Toxic levels in inadequately ventilated areas

 The silent killer

 Can’t be seen, can’t be smelled, can’t be heard
 Hemoglobin carries oxygen and carbon monoxide  Carbon monoxide
binds very tightly to hemoglobin (carbon monoxide will displace oxygen
& CO2)  Oxygen and carbon dioxide can no longer be carried

Symptoms:
 Headaches
 Nausea
 Dizziness
 Breathlessness
 Collapse
 Loss of consciousness
 Weakness, palpitations, visual impairment
 Anoxic encephalopathy
 Cognitive defects
 Death

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