Hormone changes in pregnancy affect the upper respiratory tract and airway mucosa. Estrogen probably responsible for producing tissue edema, capillary congestion and hyperplasia of mucus glands. No difference in Pulmonary Function between singleton and twin pregnancies.
Hormone changes in pregnancy affect the upper respiratory tract and airway mucosa. Estrogen probably responsible for producing tissue edema, capillary congestion and hyperplasia of mucus glands. No difference in Pulmonary Function between singleton and twin pregnancies.
Hormone changes in pregnancy affect the upper respiratory tract and airway mucosa. Estrogen probably responsible for producing tissue edema, capillary congestion and hyperplasia of mucus glands. No difference in Pulmonary Function between singleton and twin pregnancies.
Respiratory Physiology Hormonal changes in pregnancy affect the upper respiratory tract and airway mucosa o Hyperemia, mucosal edema, hypersecretion and increased mucosal friability Estrogen is probably responsible for producing tissue edema, capillary congestion and hyperplasia of mucus glands
Anatomic changes in pregnancy The diaphragm is displaced cephalad by as much as 4 cm The A-P and transverse diameter of the thorax increases chest wall circumference enlarges Diaphragm excursion greater than in non-pregnant
Pulmonary Function in pregnancy Decreased o Functional residual capacity, 10-20% by term o Residual volume o Expiratory reserve volume o Peak expiratory flow rate o Total lung capacity Unchanged o RR o Vital capacity o Lung compliance Increased o Tidal volume o Airway conductance o Total pulmonary resistance **No difference in pulmonary function between singleton and twin pregnancies
Ventilation Minute ventilation increases significantly reaching 20-40% above baseline at term Alveolar ventilation increases by 50-70% Because of o Enhanced respiratory drive due to high serum progesterone level o Compensated respiratory alkalosis o Low expiratory reserve volume
Oxygen Delivery Maternal arteriovenous oxygen difference is decreased o Increased tidal volume delivers more oxygen than required o Increased total hemoglobin and oxygen carrying capacity (Bohr effect) during normal pregnancy
Arterial Blood Gases Physiological hyperventilation results in respiratory alkalosis Compensatory renal excretion of bicarbonate Reduced pC02 from maternal hyperventilation aids CO2 (waste) transfer from the fetus to the mother while facilitating oxygen release to the fetus
Physiologic Dyspnea Increased awareness of desire to breathe Can occur early in pregnancy Does not interfere with daily activities Actual exercise tolerance not greatly affected Increase progesterone levels probably is the most important mechanism Mechanical impediment of the gravid uterus often blamed
It is important to distinguish the physiologic dyspnea from disorders complicating pregnancy
The presence of other symptoms and signs of cardiopulmonary disease indicates a possible pathologic nature of dyspnea and the patient should further be evaluated
ASTHMA in pregnancy Chronic inflammatory airway disorder with major hereditary component Environmental stimulant can trigger reversible airway obstruction Airway obstruction are due to bronchial smooth muscle contraction, vascular congestion, mucosal edema and tenacious mucus
Pregnancy outcome in Asthma Clinical features of asthma during pregnancy are the same as those in non-pregnant women Unless there is severe disease, pregnancy outcomes are generally excellent According to a study by Gluck et al: 1/3 improved, 1/3 unchanged, 1/3 clearly worsened Increased morbidity linked with progressively more severe disease, poor control or both o Preterm delivery, preeclampsia, abruptio placenta, LBW, miscarriages, CS delivery
Status Asthmaticus Life threatening complication o Muscle fatigue, respiratory arrest o Pneumothorax, pneumomediastinum o Acute cor pulmonale o Arrhythmias Maternal and perinatal mortality significantly increased when mechanical ventilation is required
Fetal Effects of Asthma Response to maternal hypoxemia o Decreased umbilical blood flow o Increased systemic and pulmonary vascular resistance o Decreased CO fetal growth restriction Fetal response is an indicator of maternal status
Fetal outcome Physician and patients should not inappropriately avoid the use of effective pharmacotherapy because of concerns for fetal effects of drugs
Clinical Course Mild wheezing to severe bronchoconstriction Can be intermittent to persistent (mild, moderate, severe) Symptoms o Nocturnal awakening o Interference with normal activity Short acting beta-agonist for symptoms Assess lung function
Clinical Evaluation Subjective severity of asthma does not frequently correlate with objective measures of airway function or evaluation PE is also an inaccurate predictor of severity
Useful clinical signs Labored breathing Tachycardia Pulsus paradoxus Prolonged expiration Use of accessory muscle Central cyanosis and altered consciousness are sign of potentially fatal attack
Pulmonary function testing Should be routine in management of acute and chronic asthma Best measure of severity o FEV1 less than 1 L or <20% of predicted value o Peak expiratory flow rate Woman determines her own baseline when asymptomatic (personal best), to compare with values when symptomatic
Ideally FEV1 >80% of predicted PEFR predicted values 380-550 L/min Therapeutic adjustments based on womans personal best
Therapy 1. Avoidance and control of asthma triggers a. Including allergy, URTI, sinusitis, exercise, aspirin, NSAIDs b. Irritants (tobacco smoke , chemical fumes, humidity, emotional upset) c. F-series prostaglandins , ergonovine d. GERD i. Due to relaxation of LES 2. Medications during pregnancy a. Poorly controlled asthma is potentially more dangerous for the fetus than medication i. Teratogenic period at 4-10 weeks after LMP b. Medications are added in a sequential fashion with few differences from the non-pregnant patient
Guidelines for Chronic Asthma 1. Patient education effect on pregnancy and general management 2. Avoidance or control of environmental precipitating factors 3. Objective assessment of pulmonary function and fetal well being 4. Pharmacologic therapy to provide baseline control and treat exacerbations
Step Therapy Medical Management of Asthma during Pregnancy Mild Intermittent Asthma o No daily medications, inhaled beta agonist as needed Mild Persistent Asthma o Preferred: low dose inhaled CS o Alternative: Cromolyn, leukotriene receptor antagonist, or theophylline (serum level: 5-12 mcg/mL) Moderate Persistent Asthma o Preferred: low dose inhaled CS and long acting beta agonist or medium dose inhaled CS or medium dose inhaled CS and long acting beta agonist o Alternative: low dose or (if needed) medium dose inhaled CS and either leukotriene receptor antagonist or theophylline (serum level 5-12 mcg/mL) Severe persistent asthma o Preferred: High dose inhaled CS and long acting beta agonist and (if needed) oral CS o Alternative: High dose inhaled CS and theophylline and oral CS if needed
Leukotriene receptor antagonists Not effective for acute disease Used with inhaled steroids to minimize dosing No widespread experience with use in pregnant women
Theophylline Might be used as a third line agent after beta agonist therapy and inhaled steroids Extensive experience Does not appear to cause developmental risk Has limited use in acute exacerbation
Acute Asthma Exacerbation Beta agonist with or without ipratropium via a metered dose inhaler with a spacer or in nebulized form Systemic CS Oxygen to maintain pO2 >60 mmHg and preferably normal, the O2 saturation at or above 95% to ensure fetal well being IV hydration FEV1 or PEFR o Continuous pulse oximetry and EFM Lowered threshold for hospitalization in pregnant Aggressive management of asthma exacerbation is recommended because of greater risk to the fetus from untreated asthma
Non-responders EARLY INTUBATION for worsening respiratory status despite aggressive treatment Indications for MECHANICAL VENTILATION o Fatigue o CO2 retention o Hypoxemia
PNEUMONIA in Pregnancy Infrequent, yet, serious complication o Most frequent cause of non-obstetric infection o 3 rd most frequent cause of indirect obstetric death Can occur at any time during gestation o In the 3 rd trimester it is associated with preterm labor Causes significant fetal complications o Hypoxia and acidosis poorly tolerated by fetus
Bacteriology Virtually any infectious agent can cause pneumonia in a pregnant patient S. pneumonia is the most common Other etiologic agents o M. pneumonia o H. influenzae o Influenza and other viruses
Clinical features Preceding URTI Cough, fever, dyspnea and chills Delay in recognition might lead to development of complications such as respiratory failure or empyema
Diagnosis CXR is essential for diagnosis Tests to identify specific pathogen are optional
Management Hospitalize pregnant women with radiologically proven pneumonia MONOTHERAPY with macrolide: azithromycin, clarithromycin, erythromycin Severe disease admit to ICU o ARDS common o Mechanical ventilation may be needed o Respiratory fluoroquinolones: Levofloxacin o Or Beta Lactam + Macrolide: Amoxicillin or Co- amoxiclav, Cefuroxime or Ceftriaxone Clinical improvement in 48-72 hours: o Fever lyses o Pleural effusion develops in 20% Radiographic abnormalities may take 6 weeks to resolve Persistent fever requires follow up radiograph
Criteria for severe CAP RR >30/min PaO/FiO 250 below Confusion or disorientation Uremia Leukopenia 4,000 below Thrombocytopenia 100,000 below Hypothermia Hypotension requiring aggressive fluid resuscitation
Pregnancy outcome 0.8% maternal mortality rate 7% required intubation and mechanical ventilation 1/3 of cases PROM, preterm delivery, LBW
Prevention Pneumococcal vaccine recommended for: o Immunocompromised o Significant smoking history o Diabetes, cardiac, pulmonary or renal disease o Asplenia
Severe pneumonitis Life threatening o Influenza pneumonia o Varicella pneumonia
TUBERCULOSIS in pregnancy Mycobacterium tuberculosis granulomatous pulmonary reaction 90% disease contained, dormant for lung In immunocompromised or with other disease, reactivated to clinical disease
Clinical features Cough with minimal sputum production Low grade fever Hemoptysis Weight loss Extrapulmonary TB in immunocompromised Infiltrative patterns on chest radiograph AFB bacilli in sputum of 2/3 of culture positive patients
High risk TB 1. Healthcare workers 2. Contact with infectious patient 3. Working or living in homeless shelters 4. Alcoholics 5. Illicit drug users 6. Detainees and prisoners 7. HIV infected
Skin Testing A 5 tuberculin units of purified protein derivative P No further evaluation if negative Positive skin test of 5 mm or more requires CXR
Skin Testing B Very high risk 5 mm o HIV positive, abnormal CXR, recent contact with active case High risk 10 mm o Foreign-born, drug users, HIV negative, low income population, with medical conditions that increase risk for TB No risk factors 15 mm
Treatment DOTS Quadruple regimen for active infection o HRZE o + pyridoxine 25 mg daily to reduce hepatic toxicity Monotherapy with INH for latent infection Breastfeeding not prohibited during therapy
Neonatal TB Transplacental Aspiration of infected secretions at delivery Congenital TB: hepatosplenomegaly, respiratory distress, fever and lymphadenopathy Unlikely if mother treated before delivery or sputum negative Newborn is susceptible (50%) so isolate from mother with active disease