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Respiratory problems are common in pregnancy and it is worth noting that in the most recent Confidential Enquiry into Maternal Deaths (1994–96), 53.7% of direct deaths were as a result of respiratory problems excluding seven other deaths from indirect causes (see table 1).
Some women will have pre-existing conditions such as asthma, tuberculosis, cystic fibrosis, and less commonly restrictive lung diseases or lung transplant. Others may have an acute illness like pneumonia, pneumothorax, or more serious conditions such as pulmonary embolism or adult respiratory distress syndrome (ARDS) complicating pregnancy. Although a team approach is essential, a well informed obstetrician can make a major contribution to the wellbeing and safety of both mother and fetus.
This article intends to provide an overall review of various respiratory conditions which obstetricians may encounter and help in their management.
Pulmonary status in pregnancy1-5
Apart from a decrease in functional residual capacity (FRC) secondary to a decrease in the expiratory reserve volume, pregnancy does not effect the lung volumes.3 5 This fall in FRC begins from the fifth month of pregnancy and by term the FRC is reduced by 10%–20%. Large airway function is not usually impaired by pregnancy, and forced expiratory volumes and their ratios are unaffected.5 The total pulmonary resistance may be decreased due to relaxation of the smooth muscle in the tracheobronchial tree under hormonal influence. Diffusing capacity of the lungs for carbon monoxide remains normal or decreases during the second half of pregnancy.
Progesterone increases ventilation by increasing respiratory centre sensitivity to carbon dioxide as a result the tidal volume and minute ventilation is increased.2 The respiratory rate is unaffected. This results in a decrease in arterial and alveolar carbon dioxide pressure.3 The respiratory alkalosis is compensated by an increase in excretion of bicarbonates by the kidneys resulting in a normal pH.1 There may be an increase in interstitial water in the lungs during pregnancy because there is a general increase in connective tissue water during pregnancy, moreover the plasma oncotic pressure falls during pregnancy, the lung lymphatics may be affected by the smooth muscle relaxation seen in pregnancy. In addition even if the water volume in the lung was normal, it would be contained in a smaller interstitial space because the lungs are at a smaller volume. This can only be confirmed once an accurate and sensitive method for measuring interstitial water is developed.5
The enlarging uterus results in a maximum of 2.1 cm increase in transverse chest diameter on chest radiography and a maximum elevation of 4 cm in the level of the diaphragm. The function of the diaphragm and the chest wall musculature is not impaired.1 5
PULMONARY COMPLICATIONS OF PREGNANCY
Most pregnancies are unaccompanied by pulmonary complications, however pulmonary oedema, pulmonary thromboembolism, pulmonary hypertension, and acute respiratory failure can occur during pregnancy. These conditions can lead to mortality and hence they should be sought and treated appropriately.5
Pulmonary oedema during pregnancy may be cardiogenic or non-cardiogenic.
CARDIOGENIC PULMONARY OEDEMA
Pulmonary oedema occurs when fluid is filtered into the lungs faster than it can be removed. Accumulation of fluid in the alveoli interferes with gas exchange.
Pregnant women are vulnerable to volume overload as their blood volume is already increased. Moreover sodium and water retention can occur secondary to oxytocin administered during delivery. Iatrogenic fluid overload is the commonest cause of oedema near term. In the past, when hypertonic saline was used to induce abortion, volume overload due to its escape into maternal circulation was another iatrogenic cause of pulmonary oedema. Women with pre-existing congenital or rheumatic cardiac disorders may not tolerate the haemodynamic burden of pregnancy and may end up with pulmonary oedema. Peripartum cardiomyopathy is an idiopathic dilated cardiomyopathy seen in pregnancy.5 9It is more commonly seen in underdeveloped countries where the incidence may be 10% of all pregnancies. Patients present during the last trimester or in the early months after delivery with symptoms of biventricular congestive heart failure. The mortality rate can be as high as 30%–50%. In survivors it recurs with subsequent pregnancies. Pulmonary oedema may occur in patients with hypertrophic obstructive cardiomyopathy and in obese hypertensive patients.
Another cause of pulmonary oedema during pregnancy is the use of tocolytic therapy.5 7 Fewer than 5% of the patients receiving this therapy develop pulmonary oedema. The β-adrenergic agents used (ritodrine, salbutamol, terbutaline, and isoxsuprine) result in an increase in intracellular cyclic adenosine monophosphate, which inhibits the myosin light chain kinase activity as well as the uterine contractions. Pulmonary oedema due to the use of these agents is multifactorial. These agents cause vasodilatation and tachycardia and this is treated with fluid loading, tipping the already fluid overloaded patient into pulmonary oedema. By their action on the β-receptors in the proximal tubules, they stimulate renin and antidiuretic hormone synthesis resulting in an increase in sodium and fluid resorption. Most patients receiving tocolytic treatment are also given steroids to accelerate fetal lung maturation in case labour cannot be halted and their mineralocorticoid activity adds to sodium and water retention. Moreover these β-sympathomimetic agents may have direct cardiac effects including myocardial stiffness, ischaemia due to tachycardia, and arrhythmias due to an increase in the excitability of the heart and accelerated conduction in the atrioventricular node. The subtle compromise in cardiac function can result in pulmonary oedema.
In pregnancies complicated by pre-eclampsia and eclampsia, there is generalised arterial vasospasm and this results in proteinuria, hypertension, peripheral oedema, and convulsions. The arterial vasospasm results in contraction of the intravascular volume and fluid loading in this condition tips the balance towards pulmonary oedema.
In addition to pulmonary oedema due to fluid imbalance, acute lung injuries of different aetiologies can result in adult respiratory distress syndrome and pulmonary oedema secondary to increased permeability of the pulmonary vasculature. Pre-eclampsia, septic shock,14 abruptio placentae, major obstetric haemorrhage from any cause, and trophoblastic disease can all induce permeability oedema during pregnancy. Out of a total of 20 maternal deaths from pre-eclampsia, nine died from pulmonary causes: six from ARDS, two from pulmonary oedema, and one from pneumonia. Deaths from ARDS continue to be a significant cause of maternal death.15 Mendelson's syndrome is another well recognised cause of lung injury and pulmonary oedema secondary to aspiration of gastric contents into the tracheobronchial tree.
Non-cardiogenic pulmonary oedema is uncommon during pregnancy and occurs almost always in the last trimester.5
Pulmonary embolism remains the single major cause of direct maternal death in the UK, with a total of 46 deaths in the most recent Confidential Enquiry into Maternal Deaths (1994–96), equating to 2.1/100 000 maternities compared with 1.3 in the previous report.15
Pregnancy is associated with a fivefold increase in thromboembolism16 and this is due to the hypercoagulable state as well as the low grade chronic disseminated intravascular coagulation within the placental bed.5 This risk is greatest in the postpartum rather than the antepartum period.2 16 Bed rest for complications of pregnancy, traumatic instrumental deliveries, and caesarean sections, especially in high risk patients, further increase the risk of thromboembolism.5 Thrombophilic conditions such as deficiency of antithrombin III, protein C and S, factor V Leiden mutation, and the antiphospholipid syndrome need to be excluded as well, especially in those with significant past or family history.
Electrocardiography, arterial blood gas analysis, and chest radiography may help reach to the diagnosis as symptoms such as dyspnoea and leg discomfort may be seen in normal pregnancy. During the third trimester, arterial blood gases should be obtained in an upright position16 since arterial oxygen tension may be 2.0 kPa lower in the supine position. The combination of chest radiography, ventilation-perfusion scanning, and pulmonary angiography exposes the fetus to less than 0.5 rad. Exposure to radiation of less than 5 rad has not been associated with a significant risk of fetal injury.17 The Prospective Investigation of Pulmonary Embolism Diagnosis study supports the use of ventilation-perfusion scanning as sufficient basis for clinical decisions when the results are normal or indicating a high probability of pulmonary embolism. Otherwise pulmonary angiography may be needed to come to a diagnosis.18
Unfractionated heparin and low molecular heparin do not cross the placenta and there is no risk of teratogenesis or fetal haemorrhage. They are not secreted in breast milk and hence can be used during lactation. They may however cause osteoporosis, thrombocytopenia, and allergy.19 Warfarin on the other hand crosses the placenta and has been associated with warfarin embryopathy in 4%–5% (nasal hypoplasia, stippled epiphysis, and limb hypoplasia) of the fetuses. It may also lead to bleeding in the fetus. Warfarin is not secreted in breast milk and hence can be used during lactation.16 20A safe regimen would be to treat pulmonary embolism with low molecular heparin during the first trimester. Thromboembolism occurring during the second and third trimester can also be treated with low molecular heparin, which can be replaced by warfarin after delivery. The dose of unfractionated and low molecular weight heparin may be reduced during delivery to prophylactic dose even though the risk of maternal haemorrhage during vaginal delivery is minimal. The use of low molecular heparin during pregnancy is attractive as it need be given only once daily. Treatment should be continued for at least three months unless there is history of previous thromboembolism, when life long treatment may be necessary.
Inferior vena caval filters have been used during pregnancy. They are indicated when anticoagulants are contraindicated, serious thrombocytopenia develops, or there are recurrences despite adequate anticoagulation.16
Thrombolytics have been used during pregnancy in life threatening situations. There is risk of maternal bleeding specially at the time of delivery or immediately postpartum.
AMNIOTIC FLUID EMBOLISM
Amniotic fluid embolism is fortunately not commonly seen but a total of 17 direct maternal deaths were reported in the latest confidential enquiry.15 It occurs in about 1:40 000 to 1:60 000 deliveries and has a mortality rate over 85%. It usually occurs during delivery but may occur as early as the 20th week of gestation and as late as 32 hours postpartum. Predisposing factors are tumultuous labour, use of uterine stimulants, presence of meconium in the amniotic fluid, advanced maternal age, multiparity, and intrauterine fetal death.2
Patients present mainly as sudden collapse associated with dyspnoea, cyanosis, and hypotension. Those patients surviving the initial phase develop pulmonary oedema (75%), haemorrhage (50%), and seizures (10%–20%). Laboratory studies have also shown the occurrence of disseminated intravascular coagulation in most patients.5
In 10%–15% of the patients a seizure will occur before the cardiorespiratory collapse10; 50% of the patients die in the first hour. Of the remaining patients half will develop significant bleeding. Definitive diagnosis is made at necropsy with the demonstration of fetal squamous cells, mucin, hair, or vernix in the pulmonary vasculature.
Treatment consists of adequate oxygenation with positive pressure ventilation and perfusion with fluid management and ionotropes. Once the patient has been resuscitated from the cardiorespiratory collapse, the coagulopathy will require treatment.10
Air embolism can occur with normal labour, delivery of patients with placenta praevia, criminal abortions, abortions using suction, insufflation of the vagina during gynaecological procedures, and douching.5 Large amounts of air collected in the right ventricle can lead to sudden death by blocking the outflow tract. If air enters into the pulmonary vasculature the patient can develop pulmonary hypertension and right heart failure. It may also lead to permeability pulmonary oedema. Because air is resorbed from the vascular space into the alveoli, air embolism is usually transient and self limited unless the right ventricular outflow tract is obstructed.5
Pulmonary hypertension, irrespective of aetiology, carries a grave prognosis during pregnancy (50% mortality).5 21 In such patients the increase in cardiac output and blood volume during pregnancy is poorly tolerated and precipitates right heart failure with severely decreased cardiac output and sudden death.
Pregnancy is best avoided and abortion is advised in women with even mild pulmonary hypertension of any cause who do get pregnant. If the patient chooses to continue with the pregnancy then bed rest, anticoagulants, and joint management by obstetricians, cardiologists, and anaesthesiologists is recommended.
Acute respiratory failure
Respiratory failure during pregnancy can occur from a variety of causes. These are10:
(1) Obstructive lung disease: asthma, chronic bronchitis, cystic fibrosis10
(3) Infection: pneumonia (bacterial, viral, fungal, AIDS (Pneumocystis carinii pneumonia), pyelonephritis, cystitis, chorioamnionitis, sepsis
(4) Pulmonary oedema: cardiogenic, non-cardiogenic
(5) Miscellaneous: Mendelson's syndrome, pulmonary embolism
In addition to the features of the underlying cause, patients present with tachypnoea and dsypnoea. The onset may be acute (over minutes to hours) as seen in pulmonary embolism and pulmonary oedema or subacute (over days) as seen in asthma or pneumonia. As the patient attempts to increase ventilation and oxygenation, respiratory rates of 40–50/min may be seen. Although dyspnoea may be physiological during pregnancy, tachypnoea is always abnormal and hence should be sought in any pregnant patient complaining of breathlessness.
As the patient gets tired the respiratory rate begins to fall and hence portends respiratory arrest. The ability of a patient to complete sentences is a useful bedside indicator of the severity of the respiratory insufficiency. The hypoxaemia results in impairment of the mental status.10 The most useful test, however, is the analysis of the arterial blood gases. Patients with respiratory failure should be categorised into type I or type II failure and treated accordingly. Type I failure should be corrected with high concentration oxygen while type II failure may require temporary ventilation, either endotracheal or non-invasive, while the underlying aetiology is corrected.
Asthma has been reported to occur in 0.4%–1.3% of pregnant women and it is the most common obstructive pulmonary disorder during pregnancy. The aim of managing asthma during pregnancy is to prevent death, respiratory failure, and status asthmaticus and to achieve good control.1 The effect of pregnancy on asthma is variable and unpredictable. Turner et al reviewed nine studies involving 1059 pregnancies from 1953 to 1976 and concluded that 49% of the patients had no substantial change in their asthma during pregnancy, 29% improved, and 22% were worse.22Some earlier studies suggested that prematurity, low birth weight, and perinatal and maternal death were more likely to occur in pregnancies in asthmatic women. In contrast some later studies showed that adequate control of equally severe asthma eliminated maternal and perinatal mortality; however findings from a 1998 database study show that pregnancies in asthmatic women are still associated with an increased risk of preterm birth, low birth weight, pre-eclampsia, and congenital malformations.23 Allergic bronchopulmonary aspergillosis may occur during pregnancy and it may cause lung damage leading to hypoxia.
The care of an asthmatic woman when pregnant differs little from that when she is not pregnant. Control of asthma should be adequate and the patient should be educated regarding the disorder. Precipitating factors should be identified and avoided if possible. The inhaler technique should be checked and a chart recording peak expiratory flow rate should be maintained. A self management plan should be agreed upon. Most of the drugs commonly used in asthma are safe for the fetus and any new drug should be avoided unless it has been shown to be non-teratogenic. Oral steroids in high doses may be associated with intrauterine growth retardation, diabetes, toxaemia, and neonatal adrenal suppression. Oral corticosteroid use in the first trimester has been associated with risk of oral clefts. Patients requiring 10 mg or more of prednisolone daily will need hydrocortisone cover during labour to prevent addisonian crisis.10 Hence patients with severe asthma on regular oral steroids should be assessed by a respiratory physician before conception. With optimum treatment of asthma during pregnancy, maternal and fetal risks can be minimised.
Most cases of bronchiectasis undergo successful pregnancy, however bronchiectasis can have an adverse effect on both the pregnant woman her fetus.24 A respiratory physician should assess a bronchiectatic patient planning pregnancy. A lung function test should be done and any obstructive defect corrected with bronchodilators. At the first sign of respiratory infection, appropriate antibiotics should be prescribed. The nutritional status of the mother should be maintained and any hypoxaemia corrected as it can lead to intrauterine growth retardation.25 26 Postural drainage should be continued aggressively to prevent retention of the secretions and their subsequent infection.
This is the most common abnormality of the thoracic cage affecting pregnancy. Kyphoscoliosis is known to result in ventilatory failure by interfering with the respiratory mechanics. Severe kyphoscoliosis is associated with increased perinatal and maternal mortality. Pregnant patients with kyphoscoliosis should have regular lung function tests, have arterial blood gases measured, and be given oxygen if hypoxaemic. Patients with ventilatory failure developing acutely may need ventilatory support temporarily. Hypercapnia poses a serious threat to the fetus because the fetal carbon dioxide pressure is 1.3 kPa higher than the maternal pressure and fetal acidosis and respiratory distress may be seen at levels not harmful to the mother.10
Patients suffering from kyphoscoliosis wishing to become pregnant should be assessed thoroughly by a respiratory physician.
Cystic fibrosis is an autosomal recessive disorder. Among white people one in 20 are carriers and about one in 2000 births are affected. With the improvement in medical care, the life expectancy of cystic fibrosis patients has increased. Whereas men with the disorder are usually infertile, women can conceive. Patients with good antenatal pulmonary function and nutritional status have a high likelihood of a favourable maternal and fetal outcome.27 The best predictor of bad maternal outcome is considered to be a forced expiratory volume in one second <60% and termination of pregnancy should be recommended to those with poor functional status. The increasing nutritional demands of pregnancy in cystic fibrosis with associated malabsorption and the extra 50 ml/min of oxygen consumption of pregnancy can be critical in patients with severely limited ventilation.
Bronchodilators and chest physiotherapy should be recommended, and chest infections should be treated aggressively. Haemoptysis is usually self limiting. Pneumothorax tends to recur and may need thoracoscopy and pleurodesis with non-toxic agents. Patients with cystic fibrosis should be managed jointly by experienced obstetricians and respiratory physicians with experience in cystic fibrosis. The anaesthetist should be informed well in advance, as these patients may need humidified gases and more aggressive suction.10 28
Sarcoidosis is the most common interstitial lung disease complicating pregnancy.6 It is a multisystem granulomatous disorder and frequently affects the lungs. Patients may have asymptomatic hilar lymphadenopathy, but extensive disease can result in pulmonary fibrosis and hypoxaemia. Pulmonary functions reveal reduced lung volumes and reduced diffusing capacity. Patients suffering from sarcoidosis and planning pregnancy should be assessed for disease activity by high resolution computed tomography and treated with prednisolone. The lung function tests should be monitored and dose of the steroids adjusted accordingly. Usually the symptoms of sarcoidosis improve during pregnancy; however they may worsen during pregnancy. This improvement in symptoms has been attributed to an increase in circulating corticosteroids and to suppressed immune responses during pregnancy.5 Patients on steroids are at an increased risk of developing lung infections and hence should be instructed to seek medical aid if signs and symptoms of infection develop.10These patients should be followed up regularly by a chest physician even after delivery as they may have an exacerbation after delivery.
In their retrospective study of antepartum pneumonia, Benedettiet al reported a perinatal mortality rate of 40/1000.29 Hence the need of aggressive treatment of pneumonia during pregnancy.
The organisms causing bacterial pneumonia during pregnancy are the same as those found in the non-pregnant state. Pneumococcal pneumonia followed by mycoplasma pneumonia are the usual community acquired pneumonias. However other organisms such as legionella,Haemophilus influenzae,Staphylococcus aureus, chlamydia, etc should be suspected in the appropriate setting. In hospital, nosocomial infection with a Gram negative organism must be considered.10
The clinical features are fever, cough, dyspnoea, tachycardia, and pleuritic chest pain. All patients suspected to be suffering from pneumonia should have their leucocyte count measured, blood cultures, sputum cultures, and chest radiography with fetal protection. These patients should be treated aggressively with intravenous antibiotics, hydration, oxygen, and chest physiotherapy.
Atelectasis is common during the third trimester secondary to the already decreased functional residual capacity.10
Patients with persistent pyrexia may have underlying empyema and this should be treated with a chest drain. While choosing antibiotics, the fetal adverse effects should be borne in mind (effects of tetracycline on the fetal bone). Pneumonia may lead to type I or type II respiratory failure and this should be treated accordingly.
Varicella pneumonia requires special mention since it is associated with high mortality of 45% during pregnancy compared with 20% in non-pregnant patients.5 Contact with chickenpox during pregnancy is common, but infection occurs in only one in 2000 pregnancies.30 31
Varicella zoster is a DNA virus of the herpes family and is highly contagious. The incubation period is 10–20 days and the disease is infectious 48 hours before the rash appears and remains so until the vesicle crust. Chickenpox is a common disease of childhood and 85% of adults are seropositive for varicella zoster IgG antibody and hence are immune to varicella. Although complications do not occur in the majority of pregnant women, seronegative contacts should be given varicella zoster immune globulin32 since primary varicella zoster infection can be more severe and may progress to pneumonia in pregnant women.5 Early treatment with intravenous acyclovir can improve survival in established varicella pneumonia.33 It may be necessary to ventilate in severe cases and in the third trimester of the pregnancy this may be facilitated by delivery, but elective delivery at this time will be associated with a high risk of neonatal varicella.34
Varicella infection occurring before 20 weeks' gestation is associated with the congenital varicella syndrome (limb hypoplasia, microcephaly, skin scarring, cortical atrophy, cataracts, chorioretinitis microphthalmia, mental retardation, and dysfunction of bowel and bladder sphincters). It can be diagnosed during the prenatal period by ultrasound examination. The risk of developing this syndrome can be between 1.2%–2%.35
Maternal varicella infection during the last few weeks of pregnancy may result in transplacental passage of the virus and babies may develop clinical varicella despite high titres of maternal antibody. This should be treated with acyclovir, as it can be lethal in up to 20%–30% of the infants. Varicella vaccine is available but is not yet licensed for use in UK.
Influenza immunisation is recommended for pregnant women with heart disease, diabetes mellitus, chronic lung disorders, and altered immune response. The vaccine is made up of inactivated viruses, however it should be given in the second or third trimester to minimise fetal risks.10 In patients with severe infection or patients with pre-existing lung disorders, amantadine hydrochloride has been used.
Among the fungal diseases, Coccidioides immitis, usually a benign organism affects as many as one in 1000 pregnancies in the USA.10 It can enter the lungs after inhalation of its spores. Patients may remain asymptomatic or develop a transient pneumonitis. It has been shown that the raised 17β-oestradiol in pregnant women stimulates the growth of this fungus10 and women who are infested by it during pregnancy may have fetal loss rates of 90%. The signs of disseminated disease are non-specific and are fever, cough, and dyspnoea. It may also cause meningeal irritation, acute polyarthiritis, and erythema nodosum.36 Skin testing, serological testing, sputum examination, and chest radiography should be performed. Direct examination of fresh sputum may reveal the characteristic spherules, which are diagnostic. More than 75% of patients have abnormal chest radiography. The commonest abnormality is a single or multiple area of patchy pneumonitis. Hilar lymphadenopathy may also be seen. Occasionally the patchy infiltrates evolve into spherical lesions and when uncalcified they resemble metastatic disease. These lesions are also known to cavitate. It may lead to massive haemoptysis, which can be life threatening. The cavities may become infected and rupture into the pleural cavity leading to the development of a pyopneumothorax.36
Amphotericin B is the drug of choice for treating disseminated infection.
It was once believed that pregnancy represented a period of risk to women infected with tuberculosis. However there is no evidence that tuberculosis is more common or serious in pregnant women. Pregnancy does not increase the risk of relapse in patients who have been adequately treated. Active untreated tuberculosis represents a deadly risk to the fetus and the newborn baby if it is not treated properly in the mother.
Carter and Mates reported that pregnant women with tuberculosis are more often symptom free.38 They suggested that all pregnant women should be screened for tuberculosis.
The tuberculin skin test and chest radiography has been used for screening. The skin test identifies persons infected byMycobacterium tuberculosis but does not define disease activity. In a patient with a positive skin test and symptoms chest radiography should be performed with fetal protection after the 12th week of gestation.37 If the chest radiograph is compatible with tuberculosis, sputum should be examined and if this confirms tuberculosis, treatment started. In the presence of a positive skin test and normal radiography further evaluation to exclude extrapulmonary tuberculosis is needed if the symptoms suggest its presence. In an asymptomatic patient with a positive skin test and normal radiography, isoniazid preventive therapy is recommended for 6–12 months.40 Since isoniazid during pregnancy is associated with a high risk of developing hepatitis, it can be delayed until after delivery.37
The treatment of tuberculosis during pregnancy differs little from that in the non-pregnant state. A six month regimen with isoniazid, rifampicin, and pyrazinamide for the first two months followed by isoniazid and rifampicin for the remaining four is the most commonly used regimen. Ethambutol may be included in the first two months if there is a chance of isoniazid resistance. Streptomycin is associated with fetal ototoxicity and hence should not be used during any stage of the pregnancy.
In a nursing mother small amounts of the drugs are secreted in the milk and since the risk of toxic reactions in breast fed infants is minimal, breast feeding should not be discouraged.39
Lung transplant patients41
There have been few reported pregnancies in patients with lung transplant. These patients should be carefully assessed before the pregnancy and should be advised to wait for two years after transplant, before getting pregnant. At this time their risk for developing obliterative bronchiolitis can be assessed, as this is a serious long term complication of lung transplantation. There is little information whether pregnancy increases the risk of developing obliterative bronchiolitis.41 Such patients should have regular lung function tests and flow volume loop recorded, a reduction in expiratory flow at low lung volumes being a sensitive marker of obliterative bronchiolitis. Obliterative bronchiolitis, once diagnosed, should be treated with aggressive immunosuppression or total lymphoid irradiation.
The immunosuppressive drugs do not have any significant effect on fetal immunity and the risk of teratogenicity is low. However in high doses, they predispose the mother to life threatening infections. Since the five year survival rate after single lung transplantation is 40%42 there is a risk that the mother will not live to see her child reach maturity.
As described previously, during pregnancy there is an increase in the tidal volume as well as the minute ventilation. The overall increase in alveolar ventilation can lead to rupture of the subpleural apical bullae and lead to a pneumothorax. This is a potentially serious condition for both the patient and her fetus. A pregnant patient has a 20% increased oxygen demand and a 50% increased oxygen requirement during labour. Hence any impairment in ventilation may lead to life threatening hypoxia.43
Initial management depends on the size and effects of the pneumothorax on arterial oxygenation. In an asymptomatic patient with a pneumothorax less than 15%–20% of the hemithorax inpatient observation is warranted. In patients with a large pneumothorax (more than 20% of the hemithorax) or symptomatic patients, aspiration is recommended.43 Failure of aspiration or recurrence of pneumothorax should be managed by tube thoracostomy. In those cases that resolve spontaneously, after aspiration or drainage, careful monitoring during labour is essential as the recurrence rate is high. Chemical pleurodesis is contraindicated as the chemical can be absorbed systemically and result in maternal liver toxicity or placental transfer and fetal toxicity.
Patients with persistent pneumothorax need thoracotomy or thoracoscopy. The optimal time for surgery is during the second trimester after the period of organogenesis and before pregnancy is advanced, as surgery during the third trimester may lead to preterm labour and preterm delivery.43
Pregnancy alters lung function and the natural history of common pulmonary disorders. Pregnant women with respiratory problems pose a challenge, as the wellbeing of the fetus has to be kept in mind. The fetus depends on the mother's lungs for oxygenation and any impairment in the mother may result in fetal distress. Hence pregnant women with pre-existing lung disorders should be advised to have planned pregnancies. They should also be assessed before pregnancy by a chest physician and should be followed up by the chest physicians during the pregnancy. The paediatricians and anaesthetists should also be involved in the care of such high risk patients.