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ASTHMA IN
PREGNANCY
PREPARED BY:DERIC
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.
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.
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
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
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.
CLINICAL PRESENTATION.
• Shortness of breath
• Wheezing(on expiration)
• Rhonchi(inspiration and or expiration)
• Cough
• Chest tightness
• Nocturnal awakenings
• Tachypnea
• Agitation(due to hypoxia)
Investigaions
• CBC or FBC{looking for eosinophilia}
• CXR(concurrent illnesses eg pneumonia)
• Spirometry[lung function test]
• Peak respiratory flow rate
• Serum IgE
Management
Goal
• Control symptoms
• Prevent acute exacerbations
• Maintain normal pulmonary function
• Minimize use of drugs/medications
• Protect mother and fetus
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
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
Maternal monitoring
• Symptoms
• Spirometry
• Peak flows
Fetal monitoring
• Uss; early in pregnancy, regularly after 32 weeks and after every
exacerbation
• NST
Delivery in case of caesarean section;
• Lumbar epidural anesthesia preferred
• Ketamine as general anesthesia
Asthma control
• No/minimal daytime symptoms
• No limitations to activity
• Nonocturnal symptoms
• No/minimal need for rescue medications
• Normal lung fucntion
• No exacerbations
• No effect of lactation on asthma
• Medications used for asthma are not contraindicated
during lactation.
Pregnancy outcomes
• Uterine hemorrhage (uterine fatigue causes uterine atony)
• Premature birth
• Gestational diabetes
• Fetal growth restriction
• Low birth weight
PATHOPHYSIOLOGY
DIAGRAM OF ASTHMA.
PATHOPHYSIOLOGY
CONT..
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 .
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.
RELLEVER MEDICINES IN
ASTHMA.
• Short acting beta 2 agonist( SABA) e.g. salbutamol
• Short acting muscarinic antagonist e.g. salmetorl
THANK YOU

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ASTHMA IN PRG.pptx

  • 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
  • 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