Introduction

Substance abuse in pregnancy poses serious health risks to mothers and the developing baby, as well as potentially hindering parents’ ability to care adequately for their children. Babies can suffer from consequences of congenital malformations and the adverse effects of drugs on pregnancy, or develop acute drug withdrawal after birth.

Drug abuse is common in women of childbearing age: the European Monitoring Centre for Drugs and Drug Addiction annual report for 2008 ( ) states that, in the 16–34-year age group in England and Wales, 13.8% of individuals have used cannabis, 4.5% cocaine, 3.1% ecstasy and 1.8% amphetamines during the preceding year. Rates are slightly higher for all drugs in Scotland and lower in Northern Ireland. Drug use is even higher in the 16–24-year age group and 0.2% of all adults surveyed in England and Wales admitted to opiate use in the preceding year. Accurate figures for fetal exposure to substance abuse are difficult to obtain because of the illegal status of most drugs of abuse. In pregnancy rates of abuse of 0.4–31% have been reported ( ). Although drug abuse occurs in all races and social classes, there is an increased risk in women who are younger, unmarried or who have lower educational achievements. In the USA, the National Survey on Drug Use and Health of 2008 revealed 5.2% of pregnant women admitted using illicit drugs in the previous month; however underreporting is very likely ( ).

A study of 3000 babies born in a high-risk obstetric population in the USA revealed 44% were positive for morphine, cocaine or cannabis using meconium immunoassay, although only 11% of mothers admitted using illegal drugs ( ). A study of 30 000 maternal urine samples at delivery in 1992 in California showed 5% of samples contained one or more illicit drugs ( ). Meconium analysis from 400 infants in a study in Glasgow in 2001 revealed that approximately 13% of samples were positive for cannabinoids, 2.75% for cocaine and 1.75% for amphetamines ( ). Testing of 807 consecutive positive pregnancy tests in an urban UK population revealed approximately 17% (one in six women) were positive for illegal substances: 14.5% for cannabinoids, 1.4% for opiates, 0.5% for benzodiazepines, 0.4%, ethanol 0.2% for cocaine, 0.1% for amphetamines and 0.1% for methadone ( ).

General effects of substance abuse in pregnancy

Substance abuse during pregnancy can have adverse effects on the health of the mother, the pregnancy itself, the fetus and the newborn infant after birth. Poverty, poor nutrition and lack of antenatal care also independently have a detrimental effect on pregnancy outcome. There is also a high risk of acquiring human immunodeficiency virus (HIV), hepatitis B and hepatitis C infection with intravenous drug use. Intrauterine growth restriction and preterm birth are more common ( ).

The effects of substance abuse on the fetus can be divided into drugs that have a direct teratogenic effect during the first trimester of pregnancy (e.g. cocaine; see Table 26.1 ), those which influence ongoing fetal growth or development through continued exposure (e.g. alcohol and barbiturates) and those which can have an adverse effect in the neonatal period by causing sedation, fits or withdrawal (e.g. benzodiazepines or opioids).

Providing appropriate care to this group is often challenging. Flexible care from experienced multidisciplinary teams is required, with child safeguarding a priority.

Approach to management of substance abuse in pregnancy

If a mother is suspected of abusing drugs a careful history should be taken regarding the quantity, duration, frequency and route of drug use, and counselling and support should be offered, along with multidisciplinary antenatal care. A careful search should be made for comorbid conditions such as psychiatric disorders, domestic violence, sexual or emotional abuse, the presence of sexually transmitted diseases and blood-borne virus infection (hepatitis B, hepatitis C and HIV infection). Frequent antenatal visits with serial ultrasound scans should be offered to confirm gestation and monitor fetal growth and well-being. If there has been high-risk behaviour such as sex-working or intravenous drug abuse continuing during the pregnancy, repeated virology testing is indicated (see Ch. 39.2 ).

The precise model of care will vary depending on local circumstances, but an example of a care pathway is given in Figure 26.1 . A multidisciplinary open-access service may improve engagement by reducing the burden of appointments and improve continuity and consistency of care. Such a service might involve a specialist midwife, obstetrician, liaison heath visitor, neonatologist, neonatal nurse and social worker. In general, the initial approach should be to deal with the elements of substance abuse that contribute the greatest risk to the mother and fetus, such as injecting or regular alcohol abuse. The aim is then to reduce chaotic drug use, eventually achieving a stable period without use of illegal drugs before considering detoxification. Moving to detoxification too quickly can increase the chances of relapse.

Model care plan.

General management of infants of substance-abusing mothers

Assessment following birth should include careful physical examination for evidence of malformation ( Tables 26.1 and 26.2 ). Further investigations may be indicated, such as cranial ultrasound and eye examination. Toxicology screening (see Methods of testing , below) should be considered, particularly if there was no toxicology monitoring in pregnancy. Assessment for signs of neonatal withdrawal – also called neonatal abstinence syndrome – should be made (see Assessment of withdrawal , below). The most common drugs likely to result in withdrawal are opioids, benzodiazepines, antidepressants and alcohol. The timing of onset of symptoms depends on the drug(s) taken ( Table 26.3 ), and there may be more than one phase in polydrug abuse. The signs and symptoms of withdrawal from different drugs are broadly similar and largely non-specific with central nervous system irritability and autonomic system dysfunction. Opioids are more likely to cause significant autonomic dysfunction ( Table 26.4 ) than substances such as cocaine, amphetamines or benzodiazepines that cause predominantly central nervous system symptoms (see Table 26.2 ) ( ). Differential diagnoses include hypoglycaemia, hypocalcaemia, hypomagnesaemia, hyperthyroidism and causes of neonatal encephalopathy, such as central nervous system haemorrhage, sepsis and hypoxia. Drugs that are associated with neonatal seizures include opioids, shorter acting barbiturates, tricyclic antidepressants, alcohol, selective serotonin reuptake inhibitors (SSRIs) and serotonin noradrenaline reuptake inhibitors (SNRIs).

Supportive therapy should be offered with minimal stimulation and with swaddling or skin-to-skin care, the use of a dummy and frequent feeding. If pharmacological therapy is required a drug from the same class as that which is causing withdrawal may be preferable where possible. There are few comparative studies of different drugs used in the treatment of withdrawal. The most commonly used treatments, their main components and their mechanism of action are outlined in Table 26.5 . A survey of the management of withdrawal in the UK and Ireland ( ) showed morphine sulphate was the most commonly used first-line agent for opiate withdrawal by 92% of units, and in polysubstance withdrawal by 69% of units. Phenobarbital was the first choice for treatment of seizures from opiate withdrawal and polydrug withdrawal in 73% and 81% of units respectively. A similar survey in the USA revealed that 63% of neonatal units used opioids (either tincture of opium or morphine sulphate) to treat opioid withdrawal and 52% used opioids to treat polydrug withdrawal. In the USA, 70% of units used phenobarbital and 25% used morphine to control opioid seizures; 81% used phenobarbital to control seizures secondary to polydrug withdrawal ( ).

Table 26.5

Agents used for treating neonatal withdrawal

DRUG	MAIN COMPONENTS/MECHANISM OF ACTION/INDICATIONS FOR USE	DOSE
Opiates
Morphine	Opiate replacement Opiate/opioid withdrawal Treatment of withdrawal seizures	50–100 µg/kg 6-hourly increasing by 25–50% every 24–48 hours until symptoms are controlled. Can be increased to 4-hourly ( ) Methadone 100 µg/kg 6-hourly increased by 50 µg/kg until symptoms controlled ( )
Methadone	Opiate replacement Opiate/opioid withdrawal Treatment of withdrawal seizures
Tincture of opium * Paregoric †	Opiate replacement Opiate/opioid withdrawal Treatment of withdrawal seizures
Chlorpromazine	A phenothiazine antipsychotic which can cause sedation, reduce seizure threshold and cause cerebellar dysfunction Controls CNS and gastrointestinal signs of opiate/opioid withdrawal ( ). High risk of seizures if used as sole agent in opioid withdrawal May be useful in the treatment of SSRI withdrawal ( ) and in benzodiazepine withdrawal	0.5–1 mg/kg every 6 hours intramuscularly or orally (maximum 6 mg/kg daily). When stable wean dose by maximum 2 mg/kg daily every third day
Phenobarbital	A barbiturate anticonvulsant. Sedative Long half-life: monitor blood levels Most commonly used treatment for opiate/opioid withdrawal seizures May be a useful second-line treatment of opioid withdrawal but does not alleviate gastrointestinal symptoms; however reduces duration of care needed ( ) Reported to be effective in withdrawal from volatile inhalant substance abuse ( )	Loading dose 20 mg/kg intravenously then maintenance 2.5–5 mg/kg once daily intravenously or orally. (Check trough levels: aim for 20–40 mcg/ml)
Diazepam	A benzodiazepine Widely used in adults to control symptoms of alcohol withdrawal Replacement in benzodiazepine withdrawal As an anticonvulsant	For seizures 1.25–2.5 mg per rectum 300–400 µg/kg intravenously
Clonidine	A non-narcotic alpha 2 stimulant which decreases symptoms of withdrawal in opiate-addicted adults and children ( ; ) May be useful adjunct therapy to decrease hypertension and tachycardia in alcohol withdrawal Reduces duration of drug treatment in opioid withdrawal when used with opiate replacement ( ) 6 out of 7 infants with opiate withdrawal treated successfully with clonidine ( )	3–5 µg/kg/day, divided into 4–8-hourly doses (test dose–1mcg/kg watch for hypotension)

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