1.
ASTHMA IN
PREGNANCY
PREPARED BY:DERIC

2.
LEARNINIG OBJECTIVES
• Define asthma
• Describe risk factors for asthma in pregnancy
• Explain clinical features and complications of asthma
in pregnancy
• Establish diagnoses of asthma in pregnancy
• Treat conduct follow up services and refer as
appropriate in a patient with asthma in pregnancy
according to guidline.

3.
Introduction
• Definition;
-is a result of chronic inflammation of airways that result in airway
obstruction and can be triggered by various stimuli.
OR
It is a chronic reseversible obstractive inflammatory disease in which
many cells and cellular elements play a role by constriction of bronchial
smooth muscles causing bronchospasm,oedema of bronchial mucous
membrane and blockage of the smaller bronchi with plug of mucus.
• >50% of asthmatics are prone to exacerbations during pregnancy
• Women with severe asthma tend to have worsening of their asthma.
• Asthma exacerbations can occur at anytime during pregnancy but tend
to occur more between 17th and 34th weeks of GA.

4.
CHANGES …
Respiratory physiological changes during pregnancy;
• Tidal volume increases due to increased ventilatory
drive(from the effect of progesterone which is a direct
respiratory stimulant)
• Increased minute ventilation which causes
hyperventilation picture.
• No change in RR and vital capacity
• In general, airway conductance is increased and
pulmonary resistance is reduced hence more effective
gaseous exchange

5.
Risk/triggering factors
• Allergens; pollen, house-dust mites, cockroach, molds
• Irritants; cigarette smoke, air pollution, odors, chemicals,
drugs such as NSAIDs
• Medical conditions; Respiratory viral infections, allergic
rhinitis, sinusitis, GERD, ascariasis
• Cessation of medications
• Psychological stress
• exercise

6.
Pathophysiology
• Inflammation of the airways in response to trigger
• Abnormal accumulation of eosinophils, lymphocytes,
mast cells, macrophages, dendritic cells and
myofibroblasts
• Reduction in airway diameter resulted from smooth
muscle contraction.
• Vascular congestion, bronchial wall edema and thick
secretions.

7.
CLINICAL PRESENTATION.
• Shortness of breath
• Wheezing(on expiration)
• Rhonchi(inspiration and or expiration)
• Cough
• Chest tightness
• Nocturnal awakenings
• Tachypnea
• Agitation(due to hypoxia)

8.
Investigaions
• CBC or FBC{looking for eosinophilia}
• CXR(concurrent illnesses eg pneumonia)
• Spirometry[lung function test]
• Peak respiratory flow rate
• Serum IgE

9.
Management
Goal
• Control symptoms
• Prevent acute exacerbations
• Maintain normal pulmonary function
• Minimize use of drugs/medications
• Protect mother and fetus

10.
III. Pharmacologic therapy
 treatment same as in non-pregnant women
 beta adrenergic agonists are the mainstay treatment option
includes SABA(salbutamol) & LABA(salmeterol)
 Other meds; leukotriene antagonists such as montelukast, theophylline
 Cortcosteroids such as beclomethasone
 Tranquilizers and sedatives should be avoided due to their respiratory
depressant effect.
 Anti histamines not useful
 Mucolytic agents increase bronchospasm

11.
Management of acute asthma in pregnant women
• Oxygen supplementation
• Iv fluid hydration
• Salbutamol inhalation; every 20 minutes up to 3 doses in
the 1st hour
• Systemic corticosteroid IV/oral
NB; aminophylline generally not recommended

12.
Maternal monitoring
• Symptoms
• Spirometry
• Peak flows
Fetal monitoring
• Uss; early in pregnancy, regularly after 32 weeks and after every
exacerbation
• NST

13.
Delivery in case of caesarean section;
• Lumbar epidural anesthesia preferred
• Ketamine as general anesthesia

14.
Asthma control
• No/minimal daytime symptoms
• No limitations to activity
• Nonocturnal symptoms
• No/minimal need for rescue medications
• Normal lung fucntion
• No exacerbations

15.
• No effect of lactation on asthma
• Medications used for asthma are not contraindicated
during lactation.

16.
Pregnancy outcomes
• Uterine hemorrhage (uterine fatigue causes uterine atony)
• Premature birth
• Gestational diabetes
• Fetal growth restriction
• Low birth weight

17.
PATHOPHYSIOLOGY
DIAGRAM OF ASTHMA.

18.
PATHOPHYSIOLOGY
CONT..

19.
DIFFERENCE BETWEEN
WHEEZING AND STRIDOR.
• Wheezing is a sound produced primarily during
expiration by air ways of any size .
WHILE
• Stridor is a single pitch , inspiratory sound that is
produced by large airways with severe narrowing .
• It may be caused by severe obstruction of any
proximal airway .

20.
TREATMENT : CONTROLLER
MEDICINES IN ASTHMA.
• Inhaled corticosteroids (ICS) e.g.
Blecomethasone,fluticasone.
• Leukotriene modifiers e.g. Montelukast.
• Long acting muscarinic antagonist (LAMA)
e.g.tiotropium
• Long acting beta 2 e.g. formoterol, salmeterol.

21.
RELLEVER MEDICINES IN
ASTHMA.
• Short acting beta 2 agonist( SABA) e.g. salbutamol
• Short acting muscarinic antagonist e.g. salmetorl

22.
THANK YOU