Asthma is a complex disorder, involving biochemical, autonomic nervous system, immunological, endocrine and psychological factors which differ from person to person. Airway inflammation is present even when the person is symptom-free. There is a familial incidence and environmental factors such as dust, pollens, moulds, animal dandruff and foods interact with inherited factors to cause bronchospasm. About half of sufferers develop asthma in childhood and another third before age 40. Complete remission is quite common in children but less so in adults, in whom symptomatic episodes tend to occur more frequently (Liu et al 2001).

Respiratory rate is not changed by pregnancy; progesterone increases hyperventilation by term. The effects of the gravid uterus on the diaphragm cause a decrease in expiratory and residual volumes and this may cause some problems for the woman who is pregnant and asthmatic (Blackburn 2007). Bronchoconstriction occurs after exposure to an allergen and causes immunoglobulin E (IgE) antigen to bind to mast cell surface receptors. These release inflammatory substances such as histamine, bradykinin, prostaglandins and thromboxane A₂ and chemotactic factors which attract eosinophils, neutrophils, T lymphocytes and platelets. Eosinophils produce a protein that stops epithelial cell cilia from beating, disrupts mucosal integrity and causes damage and sloughing of epithelial cells.

During pregnancy some asthmatic women improve, some deteriorate and some experience no change in lung function. It is difficult to predict events, so close monitoring and ensuring compliance with treatment is essential. Pregnancy is a state of slight immunosuppression so the asthmatic may be slightly more prone to chest infections, depending on the season; it is less likely in the summer months (Ie et al 2002). Women with asthma may have more complications in pregnancy such as preterm birth and small-for-gestational-age babies particularly if asthma attacks increase, typically in the second trimester, and if there is non-compliance with medication (Murphy et al 2006). Other researchers suggest there are few complications but more caesarean sections in the moderate to severe asthmatic (Dombrowski et al 2004).

Asthma requires long-term administration of bronchodilators and anti-inflammatory agents and the effect of these on early fetal development must be considered. Women sometimes decrease their medication for fear of harming their babies to the detriment of treating their asthma. They must be encouraged to recognise the early symptoms of an attack to avoid hypoxia. Up to 15% of pregnant asthmatic women require hospitalisation for status asthmaticus or recurrent asthmatic episodes (Blackburn 2007). Anxiety exacerbates asthma attacks but sedative drugs are contraindicated, as these may cause respiratory depression.

Normal inhalation medications may continue, with regular examination of peak flow levels (Beckmann 2006). Aminophylline is safe in pregnancy and may be used in acute-to-severe asthma attacks to aid breathing, and oral steroids may be used to treat repeated asthma attacks. Medications in labour that cause vasoconstriction such as prostaglandin F _2α and ergometrine should not be used. Syntocinon (oxytocin) should be used for the third stage of labour (de Swiet 1995).

The disease is caused by the bacillus Mycobacterium tuberculosis, a soil-living organism pathogenic to some animals such as cattle. It infects far more people than it causes to be ill and infected people have a 10% lifetime risk of developing TB. It may manifest as pulmonary or extrapulmonary TB. Pulmonary TB with infected sputum is more contagious. The causative organism is a slow-growing bacterium with a waxy outer coat that protects it from immune system attack. The body responds by forming fibrinous tubercles to contain the microbe. The bacillus can lie dormant for years (latent TB) inside macrophages; 10% of these people will develop active TB (Bothamley 2006).

TB exploits the vulnerable, with poverty, overcrowding, institutionalisation, the presence of other disease and immune suppression leading to an increase in active disease. It is highly contagious and all contacts with tuberculosis should be followed up and vaccinated (Joint Tuberculosis Committee of the British Thoracic Society 2000).

Pregnancy increases the demands on the body systems, but general tiredness of pregnancy may be overlooked as a normal occurrence until other factors accumulate such as country of origin, length of time in the UK, co-existing infection such as HIV (Bothamley 2006). There is a rare possibility of transplacental fetal infection (Ormerod 2001). The woman’s poor health may affect fetal growth adversely.

Symptoms of active TB can include: (Bothamley 2006):

A chest physician should be involved in the woman’s care. If there are clinical signs of TB or the woman has been in contact with active TB, a chest X-ray is performed with adequate protection of the fetus. Sputum specimens and pleural effusions may be cultured to confirm the presence of the bacillus. If the sputum contains the organism, the woman may need to be admitted to hospital but drug therapy is usually carried out at home. After 2 weeks of therapy there is no risk of infection to others (BNF 2007a).

Tuberculin skin tests are performed in the USA on those who have been at risk of TB and the family is investigated. The sole manufacturer of tuberculin in the UK has recently put in its data sheet that tuberculin testing should not be carried out in pregnancy but does not supply any data to support this recommendation. This has not been backed up by the Vaccination and Immunisation Committee (Ormerod 2001). However, BCG vaccination should not be performed in pregnancy as it is a live vaccine.

If the mother is on effective treatment and has negative sputum, there is no reason for the baby to be isolated from her. Staff will be protected by vaccination, which is a prerequisite before employment. If treatment commenced late in pregnancy and sputum is still positive, the baby will need prophylactic isoniazid and a tuberculin test should be performed at 6 weeks. If the mother has a multiple drug-resistant strain of TB, the infant will need to be separated from her. The mother would also need to be isolated and staff should use dust/mist/fume masks. TB drugs cross into breast milk but there is no contraindication to breastfeeding, except where the neonate is separated from its mother (Ormerod 2001).

The bacillus Calmette-Guérin (BCG), a live attenuated strain developed from cattle TB, is given by injection into the skin to stimulate an immune response. In babies, care must be taken to inject intradermally to prevent abscess formation. The vaccine is effective in the prevention of tuberculosis in children but of variable value when given to adults. It can reduce the incidence of pulmonary tuberculosis by up to 80% and minimises the risk of complications.

The effectiveness of BCG programmes remains controversial. In the USA, vaccination is thought to create difficulties in interpreting the results of any future use of the tuberculin test performed to establish whether a person is infected with TB. In the UK, BCG vaccination has been discontinued in children aged 10–14 years. Adults who have contact with someone suffering from active pulmonary tuberculosis should be tuberculin tested and given BCG if the test is negative. Babies in contact with active TB should be vaccinated without having a tuberculin test as their immune systems may be too immature to show a response. In the UK it is recommended that all immigrants from countries with a high incidence of TB are tested and BCG vaccination given to those with a negative result and that all babies born to recent immigrants are vaccinated (BNF 2007a). All neonates born in an area of high TB incidence and neonates of health care workers are offered BCG soon after birth (Joint Tuberculosis Committee 2000, Bothamley 2006).

Women who have had previous episodes of asymptomatic bacteriuria or urinary tract infection should have a midstream specimen of urine cultured. If the presence of a specific bacterium exceeds 10 ⁵ organisms/ml of urine (100 000 organisms/ml) asymptomatic bacteriuria is diagnosed. Appropriate antibiotics should be successful in treating the condition (Lindsay 2000).

Acute pyelonephritis occurs in 1–2% of pregnancies, usually in the second and third trimesters. It begins with the onset of malaise, fatigue, chills and back pain located in the upper lumbar region, accompanied by muscle guarding. The pain follows the path of the ureters and may radiate round to the suprapubic area. Some women complain of nausea, vomiting and uterine contractions. Affected women may have a temperature as high as 40°C with a corresponding increase in pulse rate. There may be dehydration and frequency of micturition with scalding on voiding. The urine appears cloudy and even bloodstained and on urinalysis red blood cells, leucocytes and casts may be present as well as bacteria (Bewley 2004).

It is essential to treat acute pyelonephritis immediately to avoid serious side-effects. The woman may need to be admitted to hospital and the following treatment instigated:

Most women will respond to the combination of rehydration and antibiotics. In cases of persistent problems, there may be an abnormality of the renal tract and such women should be referred appropriately (Bewley 2004).

The onset of acute renal failure (ARF) has occurred if the urine output falls below 400 ml in 24 h or to less than 20 ml/h. There is a reduced glomerular filtration rate (GFR) and a rise in blood urea and creatinine. Acute renal failure usually results from a severe deficit in cortical renal blood flow that results in ischaemia to the kidneys. Pregnancy conditions associated with ARF are shown in Table 34.1 (Thorsen & Poole 2002).

If cortical hypoperfusion is allowed to persist, acute tubular necrosis or cortical necrosis may follow. Renal cortical necrosis is a severe form of ARF that usually results from large, sudden blood loss or vascular collapse such as in severe pre-eclampsia or haemorrhage. There is sudden onset of oliguria (less than 400 ml in 24 h) or anuria and a rise in serum creatinine (Thorsen & Poole 2002). Immediate treatment of ARF prevents necrosis occurring.

In a study of 72 pre-eclamptic women with renal failure, median gestation was 32 weeks and perinatal mortality was 38%. Twelve women had previous renal disease and only seven women required short-term dialysis. In the long term there was no need for dialysis or transplantation (Drakeley et al 2002). Those women with renal impairment had HELLP syndrome or abruptio placenta.

The aims are to re-establish urinary output and treat the underlying condition. Blood is taken for estimation of urea, electrolytes and plasma proteins. Haematocrit and blood osmolality findings indicate the degree of dehydration. Blood culture and liver function tests help to identify a cause. Urine is tested for culture and sensitivity of organisms, protein estimation, specific gravity and osmolality. Maternal and fetal condition is monitored closely with assessment of fetal growth and delivery gauged to both maternal and fetal condition (Gammill & Jeyabalan 2005, Thorsen & Poole 2002).