Hyperemesis gravidarumFrom Wikipedia, the free encyclopediaJump to: navigation, search

Hyperemesis gravidarum, with metabolic derangement

Classification and external resourcesICD-10 O 21.1. ICD-9 643.1

Hyperemesis gravidarum (HG) is a severe form of morning sickness, with "unrelenting, excessive pregnancy-related nausea and/or vomiting that prevents adequate intake of food and fluids."[1] Hyperemesis is considered a rare complication of pregnancy but, because nausea and vomiting during pregnancy exist on a continuum, there is often not a good diagnosis between common morning sickness and hyperemesis. Estimates of the percentage of pregnant women afflicted range from 0.3% to 2.0%.[2]

Contents

[hide] 1 Etymology 2 Cause 3 Symptoms 4 Complications

o 4.1 For the pregnant woman o 4.2 For the fetus

5 Diagnosis 6 Treatment

o 6.1 IV hydration o 6.2 Medications o 6.3 Nutritional support o 6.4 Support

7 References

Etymology

Hyperemesis gravidarum is from the Greek hyper-, meaning excessive, and emesis, meaning vomiting, as well as the Latin gravida, meaning pregnant. Therefore, hyperemesis gravidarum means "excessive vomiting in pregnancy."

Cause

The cause of HG is unknown. The leading theories speculate that it is an adverse reaction to the hormonal changes of pregnancy. In particular Hyperemesis may be due to raised levels of beta HCG (human chorionic gonadotrophin)[3] as it is more common in multiple pregnancies and in gestational trophoblastic disease. This theory would also explain why hyperemesis gravidarum is most frequently encountered in first trimester (often around 8 – 12 weeks of gestation), as HCG levels are highest at that time and decline afterwards. Additional theories point to high levels of estrogen and progesterone[citation needed], which may also be to blame for hypersalivation; decreased gastric motility (slowed emptying of the stomach and intestines); immune response to fragments of chorionic villi that enter the maternal bloodstream; or immune response to the "foreign" fetus.[citation needed] There is also evidence that leptin may play a role in HG.[4] Historically, HG was blamed upon a psychological condition of the pregnant women. Medical professionals believed it was a reaction to an unwanted pregnancy or some other emotional or psychological problem.[citation needed] This theory has been disproved, but unfortunately some medical professionals espouse this view and fail to give patients the care they need.[citation needed] A recent study gives "preliminary evidence" that there may be a genetic component.[5]

Symptoms

When HG is severe and/or inadequately treated, it may result in:

Loss of 5% or more of pre-pregnancy body weight Dehydration , causing ketosis and constipation Nutritional deficiencies Metabolic imbalances Altered sense of taste Sensitivity of the brain to motion Food leaving the stomach more slowly Rapidly changing hormone levels during pregnancy Stomach contents moving back up from the stomach Physical and emotional stress of pregnancy on the body Subconjunctival hemorrhage (broken blood vessels in the eyes) Difficulty with daily activities Hallucinations

Some women with HG lose as much as 20% of their body weight. Many sufferers of HG are extremely sensitive to odors in their environment; certain smells may exacerbate symptoms. This is known as hyperolfaction. Ptyalism, or hypersalivation, is another symptom experienced by some women suffering from HG.

As compared to morning sickness, HG tends to begin somewhat earlier in the pregnancy and last significantly longer. While most women will experience near-complete relief of morning sickness symptoms near the beginning of their second trimester, some sufferers of HG will experience severe symptoms until they give birth to their baby, and sometimes even after giving birth. An overview of the significant differences between morning sickness and HG can be found at Hyperemesis or Morning Sickness: Overview.

Complications

For the pregnant woman

If inadequately treated, HG can cause renal failure, central pontine myelinolysis, coagulopathy, atrophy, Mallory-Weiss syndrome, hypoglycemia, jaundice, malnutrition, Wernicke's encephalopathy, pneumomediastinum, rhabdomyolysis, deconditioning, splenic avulsion, and vasospasms of cerebral arteries. Depression is a common secondary complication of HG. On rare occasions a woman can die from hyperemesis; Charlotte Bronté is a presumed victim of the disease.[6]

For the fetus

Infants of women with severe hyperemesis who gain less than 7 kg (15.4 lb) during pregnancy tend to be of lower birth weight, small for gestational age, and born before 37 weeks gestation, in contrast, infants of women with hyperemesis who have a pregnancy weight gain of more than 7 kg appear similar as infants from uncomplicated pregnancies.[7] No long-term follow-up studies have been conducted on children of hyperemetic women.

Diagnosis

Women who are experiencing hyperemesis gravidarum often are dehydrated and losing weight despite efforts to eat. The nausea and vomiting begins in the first or second month of pregnancy. It is extreme and is not helped by normal measures.[8]

Fever, abdominal pain, or late onset of nausea and vomiting usually indicate another condition, such as appendicitis, gallbladder disorders, gastritis, hepatitis, or infection.[8]

Treatment

Because of the potential for severe dehydration and other complications, HG is generally treated as a medical emergency. Treatment of HG may include antiemetic medications and intravenous rehydration. If medication and IV hydration are insufficient, nutritional support may be required.

Management of HG can be complicated because not all women respond to treatment. Coping strategies for uncomplicated morning sickness, which may include eating a bland diet and eating before rising in the morning, may be of some assistance but are unlikely to resolve the disorder on their own. There is evidence that ginger may be effective in treating pregnancy-related nausea; however, this is generally ineffective in cases of HG.

IV hydration

IV hydration often includes supplementation of electrolytes as persistent vomiting frequently leads to a deficiency. Likewise supplementation for lost thiamine (Vitamin B1) must be considered to reduce the risk of Wernicke's encephalopathy.[9] A and B vitamins are depleted within two weeks, so extended malnutrition indicates a need for evaluation and supplementation. Additionally, mineral levels should be monitored and supplemented; of particular concern are sodium and potassium.

After IV rehydration is completed, patients generally progress to frequent small liquid or bland meals. After rehydration, treatment focuses on managing symptoms to allow normal intake of food. However, cycles of hydration and dehydration can occur, making continuing care necessary. Home care is available in the form of a PICC line for hydration and nutrition (called total parenteral nutrition). Home treatment is often less expensive than long-term and/or repeated hospital stays.

Medications

While no medication is considered completely risk-free for use during pregnancy, there are several which are commonly used to treat HG and are believed to be safe.

The standard treatment in most of the world is Benedictin (also sold under the trademark name Diclectin), a combination of doxylamine succinate and vitamin B6. However, due to a series of birth-defect lawsuits in the United States against its maker, Merrill Dow, Benedictin is not currently on the market in the U.S. (None of the lawsuits were successful, and numerous independent studies and the Food and Drug Administration (FDA) have concluded that Benedictin does not cause birth defects.) Its component ingredients are available over-the-counter (doxylamine succinate is the active ingredient in many sleep medications), and some doctors will recommend this treatment to their patients.

Antiemetic drugs, especially ondansetron (Zofran), are effective in many women. The major drawback of ondansetron has been its cost. In severe cases of HG, the Zofran pump may be more effective than tablets. Zofran is also available in ODT (oral disintegrating tablet) which can be easier for women who have trouble swallowing due to the nausea. Promethazine (Phenergan) has been shown to be safe, at least in rats and may be used during pregnancy with minimal/no side effects. Metoclopramide is sometimes used in conjunction with antiemetic drugs; however, it has a somewhat higher incidence of side effects. Other medications less commonly used to treat HG include Marinol, corticosteroids and antihistamines.

Anecdotal evidence suggests that the use of marijuana, or of the pharamaceutical extract Marinol can relieve the symptoms of HG, in a similar way to treating nausea in people with Cancer and AIDS. However, due to the criminalisation of cannabis, there have been no clinical trials into its effectivess or risks to the foetus.[10]

Nutritional support

Women who do not respond to IV rehydration and medication may require nutritional support. Patients might receive parenteral nutrition (intravenous feeding via a PICC line) or enteral nutrition (via a nasogastric tube or a nasojejunum tube).

Support

It is important that women get early and aggressive care during pregnancy. This can help limit the complications of HG. Also, because depression can be a secondary condition of HG, emotional support, and sometimes even counseling, can be of benefit. It is important, however, that women not be stigmatized by the suggestion that the disease is being caused by psychological issues..

[hide]v · d · ePathology of pregnancy, childbirth and the puerperium (O, 630–679)

PregnancyPregnancy withabortive outcome

Ectopic pregnancy (Abdominal pregnancy, Cervical pregnancy, Ovarian pregnancy, Interstitial pregnancy) · Hydatidiform mole · Miscarriage

Oedema, proteinuria andhypertensive disorders

Gestational hypertension (Pre-eclampsia, Eclampsia, HELLP syndrome) · Gestational diabetes

Other, predominantlyrelated to pregnancy

Digestive system

Hyperemesis gravidarum · Intrahepatic cholestasis of pregnancy · Acute fatty liver of pregnancy · Hepatitis E

Integumentary system/dermatoses of pregnancy

PUPPP · Gestational pemphigoidImpetigo herpetiformis · Intrahepatic cholestasis of pregnancy · Linea nigra · Prurigo gestationis · Pruritic folliculitis of pregnancy · Striae gravidarum

Nervous system

Chorea gravidarum

BloodGestational thrombocytopenia · Pregnancy-induced hypercoagulability

Maternal care related to thefetus and

amniotic fluid (Polyhydramnios, Oligohydramnios) · chorion/amnion (Chorioamnionitis, Chorionic hematoma, Premature rupture of membranes, Amniotic band syndrome,

amniotic cavity

Monoamniotic twins) · placenta (Placenta praevia, Placental abruption, Monochorionic twins, Twin-to-twin transfusion syndrome, Circumvallate placenta) · Braxton Hicks contractions · Hemorrhage (Antepartum)

Labor

Preterm birth · Postmature birth · Cephalopelvic disproportion · Dystocia (Shoulder dystocia) · Fetal distress · Vasa praevia · Uterine rupture · Hemorrhage (Postpartum) · placenta (Placenta accreta) · Umbilical cord prolapse · Amniotic fluid embolism

PuerperalPuerperal fever · Peripartum cardiomyopathy · Postpartum thyroiditis · Puerperal mastitis · Breastfeeding difficulties (Agalactia, Fissure of the nipple, Galactorrhea) · Postpartum depression · Diastasis symphysis pubis

Other Maternal death

M: OBS phys/devp mthr/fetu/infc, epon proc, drug(2A/G2C)

Nausea and Vomiting in Pregnancy - including Hyperemesis GravidarumNausea and vomiting are both common in early pregnancy. There is no evidence of fetal damage as a result of the nausea and vomiting.

Hyperemesis gravidarum occurs when vomiting becomes persistent and severe. Hyperemesis affects 1-2% of pregnancies and causes dehydration, electrolyte disturbance and ketosis. Without treatment hyperemesis may lead to central nervous system complications, liver failure and renal failure, but this is now rare in the developed world.

Nausea and vomiting can occur at any time of the day and may be constant.1

The causes of nausea and vomiting in early pregnancy are unknown. Most women do not require treatment. However persistent vomiting and severe

nausea can progress to hyperemesis gravidarum. Hyperemesis gravidarum refers to intractable vomiting leading to fluid and

electrolyte disturbance, marked ketonuria, nutritional deficiency and weight loss.2

Nausea in later pregnancy may be due to reflux oesophagitis and respond to antacids.

Epidemiology Nausea affects about 70% and vomiting about 60% of pregnant women. Nausea and vomiting in pregnancy is more common in:

o Primigravidae

o Multiple pregnancy o History of previous hyperemesis

It is less common with increasing maternal age. It tends to be a disease of Western society and is less common in developing

countries, especially in rural communities.

Presentation Symptoms usually start between 4 and 7 weeks gestation and resolve by 16 weeks

in about 90% of women. Check for signs of dehydration and any possible underlying cause. Pre-eclampsia can cause vomiting so blood pressure may be raised.

Differential diagnosis

Other causes of nausea and vomiting should be considered:

Hydatidiform mole Pre-eclampsia Gastrointestinal cause, e.g. infection, gastritis, cholecystitis, appendicitis,

obstruction, peptic ulceration, hepatitis, pancreatitis, fatty liver of pregnancy Urinary tract infection Twisted ovarian cyst Ear, nose and throat disease (e.g. labyrinthitis, Meniere's disease, motion

sickness) Drug side effects Raised intracranial pressure Metabolic, e.g. diabetes, hypercalcaemia, Addison's disease, hyperparathyroidism Psychological (e.g. bulimia nervosa)

Investigations Only required if there is a possible alternative diagnosis or in the assessment of

the well-being of mother and fetus. If persistent or severe, exclude a urinary tract infection and an ultrasound scan to

exclude multiple pregnancy or hydatidiform mole. In cases of hyperemesis: renal function and electrolytes, liver function tests, mid-

stream urine and ultrasound (exclude multiple or molar pregnancy).

Management

Most cases are mild and do not require treatment. Nausea and vomiting in pregnancy usually resolves spontaneously within 16 to 20 weeks and is not associated with a poor pregnancy outcome. However persistent vomiting and severe nausea can progress to hyperemesis if the woman is unable to maintain adequate hydration; fluid and electrolyte balance as well as nutritional status are jeopardised.3 The following interventions appear to be effective in reducing symptoms:4

Non-pharmacological: ginger, P6 (wrist) acupressure Pharmacological: antihistamines

Management options

Advice:o There is no research-based evidence on the effectiveness of dietary

treatment.5

o Advise to rest; eat small, frequent meals that are high in carbohydrate and low in fat.

o Avoid any foods or smells that trigger symptoms. Ginger: three RCTs and one randomised crossover trial found that ginger reduced

nausea and vomiting in early pregnancy. One further RCT found that ginger reduced nausea and dry retching, but had no effect on episodes of vomiting.5

Drug treatment should only be given when symptoms are persistent, severe and prevent daily activities. Prochlorperazine, cyclizine and metoclopramide are often used. Due to concerns about fetal safety, there have been relatively few studies on the efficacy and safety of anti-emetics used for nausea and vomiting in pregnancy.6

o Antihistamines (H1 antagonists): two systematic reviews found limited evidence that antihistamines reduced nausea and vomiting with no evidence of teratogenicity.7

o Phenothiazines: one systematic review found limited evidence that phenothiazines reduced the proportion of women with nausea and vomiting. However, the results were not conclusive. The review found no evidence of teratogenicity.5

o Pyridoxine (vitamin B6): two systematic reviews found limited evidence that pyridoxine reduced nausea but found no evidence of an effect on vomiting.5

Acupressure: one systematic review of small RCTs found limited evidence that P6 acupressure reduced self reported morning sickness compared with sham acupressure or no intervention. Three subsequent RCTs and two randomised crossover trials found that P6 acupressure reduced the duration, but not necessarily the intensity, of nausea and vomiting.5

Acupuncture: one RCT found that acupuncture reduced nausea and retching compared with no acupuncture, with no evidence of adverse effects. However, an improvement was also found with sham acupuncture compared with no treatment. A second smaller RCT found no significant difference in nausea between acupuncture and sham acupuncture.5

Admission

Women with severe symptoms should be referred for fluid, electrolyte and vitamin replacement (usually intravenously). Nutritional support (enteral or parenteral) is needed in women who have intractable symptoms and weight loss, despite appropriate therapy.

Admit for monitoring, intravenous fluids and correction of electrolyte disturbances. if the vomiting is severe or prolonged or the woman becomes dehydrated or ketotic.

Complications In severe cases, dehydration, weight loss, electrolyte disturbance (e.g. ketosis) and

nutritional deficiency can occur. Hyperemesis gravidarum is rarely associated with death, but may lead to serious

complications, including Wernicke's encephalopathy, central pontine myelinolysis and spontaneous oesophageal rupture.8

Prognosis Most cases are self-limiting and settle without complication as pregnancy

progresses. Nausea and vomiting of pregnancy is associated with favourable pregnancy

outcomes, such as decreased risk of miscarriage and a lower incidence of perinatal death, low infant birth weight and preterm birth.9

However, in severe cases (hyperemesis gravidarum) there may be an increased risk of low birth weight, congenital malformations, undescended testicles and hip dysplasia.9

Infants born of women who had hyperemesis are more likely to experience decreased gestational age and increased length of hospital stay.10

Time off work is needed by 35% of working women, who spend a mean of 62 hours away from their paid work as a result of the symptoms of nausea and vomiting.1

BackgroundGestational diabetes (GDM) is associated with maternal (pre-eclampsia, caesarean section, and perineal trauma) and perinatal (macrosomia, stillbirth, shoulder dystocia, birth injuries, hypoglycaemia, respiratory distress, stillbirth, and jaundice) complications.1 GDM is also associated with an increased risk of later Type 2 diabetes in both the mother and the offspring.2,3 Pregnancy is the only time to identify women with GDM, and provides the opportunity to implement strategies to improve both pregnancy and long-term outcomes. The diagnosis of GDM in New Zealand (NZ) is generally made using a two-step approach. An initial screening test involves a non-fasting 50 glucose challenge test (GCT) at 24–28 weeks’ gestation.1 Women are subsequently referred for a diagnostic 75g oral glucose tolerance test (OGTT) if the 1-hour glucose concentration is ≥7.8 mmol/L. Currently, GDM is diagnosed if the fasting glucose is ≥5.5 mmol/L and/or the 2-hour glucose concentration is ≥9.0 mmol/L. These diagnostic criteria have been used since 1992 and are unique to NZ.1,4 Many other countries use lower glucose levels to diagnose GDM.5

The current criteria for diagnosing GDM are used throughout NZ,6 but the extent of screening for GDM varies markedly. Figure 1 shows the uptake of the 50g GCT by District Health Boards (DHBs) in 2005, ranging from approximately 20% to 89% of pregnancies. This is not surprising as, until the end of 2006, some organisations promoted screening for all pregnant women,4,7 while others recommended screening women with one or more of seven clinical risk factors.8 Similar discordance is also seen between different global screening recommendations.6There are several reasons for reviewing the current approach to screening for GDM. Firstly, since the most potent nihilistic view of GDM was published in 1993,9 a great deal has changed from both global and knowledge perspectives. The world now faces a pandemic of diabetes and obesity,10,11 which has resulted in growing numbers of young women with risk factors for GDM or undiagnosed Type 2 diabetes.12–14 Type 2 diabetes in pregnancy is associated with high rates of fetal loss, congenital malformations, and other adverse perinatal outcomes.14Figure 1. Proportion of births where the mother had a glucose challenge test for each District Health Board (DHB). Proportions are shown for women aged below and above 25 years.

Polycose (Glucose Challenge) Testing as a % of Live Births by DHB

Secondly, there is good evidence that the development of Type 2 diabetes in high risk populations can be prevented or delayed,15–17 thus providing women with GDM the chance to actively try to delay/reduce their chance of permanent diabetes. Interventions are potentially useful for their children, as the intrauterine and postnatal environment influence later health risks (including obesity) for the child.18–20

Thirdly, two recent studies have made important contributions with respect to the value of treating women with GDM during pregnancy. These are the prospective, randomised Australian Carbohydrate Intolerance Study in Pregnant Women (ACHOIS)21 and a case control study by Langer.22 Both studies showed significant benefit from the treatment of GDM and support other studies showing the benefits of tight glucose control during GDM.23,24 In addition, ACHOIS laid to rest concerns that a diagnosis of GDM could be associated with increased caesarean section rates or maternal psychological trauma. The caesarean section rates were not increased in women treated for GDM and maternal well-being scores were better in women treated for GDM. With the combination of all these reasons it was timely to review the approach to screening, diagnosis and models of care for women with GDM in NZ. The Australasian Diabetes in Pregnancy Society (ADIPS) and the New Zealand College of Midwives (NZCOM) worked with representatives from other relevant organisations (Appendix 1) to develop a Technical Report to contribute to this debate. This paper describes the process undertaken and summarises the recommendations made.

The National GDM Technical Working Party processAn open national workshop hosted by ADIPS and NZCOM was held on 10 March 2006 to discuss screening for, and management of, GDM. Presentations included reviews of the current epidemic of obesity and diabetes in NZ. Presentations focussed on:

Recent evidence confirming benefits of treating women with GDM; The inter-generational effect of exposure of the fetus to maternal diabetes; Interventions that reduce progression to Type 2 diabetes in high-risk populations; Potential long-term health benefits for women and their children by identifying and treating GDM; and The rationale for promoting a general, rather than selective, screening approach for GDM, and the controversies around the criteria for diagnosis of GDM and how these may be solved.

A smaller Technical Working Party was established with representatives from stakeholder organisations to develop a Technical Report. The first meeting was on 1 June 2006 to consider GDM within the unique circumstances of the NZ demography and health services. Four groups were formed to address the main issues that had been identified with respect to screening and diagnosis of GDM (described below). Each group provided a written summary of the evidence and made a number of recommendations. These contributed to the body of the Technical Report, which is available for use to ensure that appropriate care is available for women during pregnancy. The draft report was circulated to the member organisations, which led to minor amendments being made. The final report is available on www.midwife.org.nz. The four main issues are outlined below.

(1) Should all pregnant women without known diabetes be offered screening for GDM? If so, how?There is consensus that screening for GDM should be offered in NZ,6 but a debate exists about whether to offer screening to all women or only those with risk factors. GDM fulfils the criteria for a condition warranting screening in NZ,25 as part of routine clinical care, not as a national screening programme (as occurs with cancers of the cervix and breast). The benefits from screening for GDM are to:

Reduce adverse pregnancy outcomes in women subsequently diagnosed and treated for GDM; Reduce risks in subsequent pregnancies by increasing the likelihood of preconceptual identification and management of undiagnosed diabetes; and to Provide education to women with GDM about their predisposition to Type 2 diabetes in association with advice about how to reduce this risk for themselves and (potentially) their children.

Risk factor-based approaches miss a sizable proportion of women with GDM.26 In NZ, even women with risk factors are not being screened27—possibly due to the complexity of this approach. A routine offer of screening would reduce these issues. When offering any screening test it is important that accurate information is provided so that women can decide whether to be screened or not. This includes information about the performance of the test itself, consistent with the Code of Health and Disability Services Consumers' Rights.28 Recommendations:All women should receive an offer of routine screening for GDMFor this to occur, it is crucial that:

Relevant health professionals understand the rationale behind the screening and diagnostic process, and are provided with resources to maintain currency so they are able to advise women and implement screening in a woman-focussed manner; There is written information available about the implications of screening and diagnosis of GDM that is nationally consistent and easily understood by women; Women are informed about their management options should they be diagnosed with GDM and remain the central focus of the model of care provided; Women are informed about screening in a timely and appropriate way; There is documentation that screening for GDM has been discussed, relevant information provided to the woman and the woman has consented to screening; and There is a system to ensure that screening for and management of GDM are continuously assessed, to allow development of further improvements.

(2) What should the diagnostic criteria be for GDM in New Zealand?

Currently, there is no global consensus on criteria for diagnosing GDM.6 Glucose concentrations are a continuum with intra-individual variability, so there is no clear separation between a normal and an abnormal glucose level. When deciding diagnostic criteria, a balance is needed so that women who would benefit from treatment are not missed but other women are not needlessly labelled/treated. While ACHOIS21 used a 2-hour cutoff of 7.8 mmol/L to diagnose GDM (also now recommended by the International Diabetes Federation29), the study was not large enough to show a “cut point” for benefit. However, in NZ, dropping from 9.0 mmol/L to 7.8 mmol/L (or 8.0 mmol/L as endorsed by the Australian branch of ADIPS) would increase the number of women diagnosed with GDM by an estimated 52%: numbers unable to be managed by existing diabetes in pregnancy services. Any change would need to consider resources and cost-effectiveness. Moreover, a large study of 25,000 women across 15 countries (the Hyperglycemia and Adverse Pregnancy Outcomes study—HAPO) will report on the relationship between pregnancy outcomes and maternal glycaemia in 2007.30 The study is powered to relate the fasting, 1-hour, and 2-hour glucose levels to outcomes by 0.5 mmol/L increments, providing relevant data regarding diagnostic criteria for GDM. Recommendations:

Whilst there is evidence that a lower 2-hour glucose level during the 75 g OGTT is associated with a reduction in adverse pregnancy outcomes, there are no clear data demonstrating an optimal level. The Technical Working Party recommend that the status quo be retained and data reviewed again when the results of HAPO are published. Further NZ information should be collated:

o To see if potentially different recommendations from HAPO are relevant to our populationo To see what the impact of any change would be on the number of women diagnosed with GDM and resource implications.o To ensure that there are robust models of care that could be expanded to deal with the increase in numbers if any change to criteria was decided.o Currently, where NZ criteria for a diagnosis of GDM are not reached, but the 2-hour glucose is 8.0–8.9 mmol/L (the ADIPS-Australia criterion), and the clinician and woman have concerns, it would be reasonable to manage the pregnancy as for GDM.

(3) Should any pregnant women be offered earlier screening for GDM, and if so, who and when?

The issue of early screening (prior to 24–28 weeks’) is complex. Women with Type 2 diabetes have similar pregnancy risks to women with Type 1 diabetes,14 so it is logical to try and identify these women as early as possible during pregnancy. The aim of early screening would be to identify women with hitherto undiagnosed Type 2 diabetes, impaired fasting glucose (IFG), or impaired glucose tolerance (IGT). However, within the pregnancy population, the prevalence of abnormal glucose tolerance is low, so offering early screening to all women is not advocated. Also, the lack of a simple and accurate screening test in early pregnancy remains a difficulty. The HbA1c may be the most practical test, as it can be performed with booking bloods. One difficulty is that a proportion of women with abnormal glucose tolerance will have an HbA1c within the reference range. The optimal way of identifying these women needs to be determined. The OGTT is currently the diagnostic test for Type 2 diabetes/GDM in early pregnancy.While women with past GDM or glycosuria should be offered early pregnancy screening, other groups are harder to define but include:

Polycystic ovarian syndrome (PCOS). Morbid obesity: (Ethnic-specific31: European=BMI≥35 kg/m2, Polynesian=BMI≥37 kg/m2, Indian and Asian=BMI≥32 kg/m2). Two first-degree relatives with diabetes. Previous unexplained stillbirth. Previous shoulder dystocia. Previous macrosomic baby (≥97th percentile based on customised birthweight chart.32 If there is no access to customised birth weight, ≥4700 g Polynesian, ≥4400 g European, ≥4000 g Asians (including South Asians).

Women with several weaker risk factors may also require early screening.Recommendations:

Women with known IGT/IFG or thought to have undiagnosed Type 2 diabetes should have an HbA1c requested at booking and be directly referred to the Diabetes in Pregnancy team for management. Women with a past history of GDM should have an HbA1c requested at booking (even if the postnatal OGTT for this woman was normal). If the result is above the reference range (≥ 6.0%), the woman should be referred immediately to the Diabetes in Pregnancy team. If <6.0%, an OGTT should be undertaken at the earliest opportunity, typically 14-16 weeks. If the OGTT is normal, it should be repeated at 24-28 weeks (or earlier if clinical suspicion occurs). Women who have other high risks of GDM: The current practice of offering a diagnostic OGTT to women considered at sufficient risk of undiagnosed Type 2 diabetes should still continue. Measuring HbA1c as an initial screening test should be formally piloted and assessed to determine its role in this population.

(4) How should care be delivered for women with GDM?

The move to a universal offer of screening for GDM and the possible lowering of diagnostic thresholds for GDM are likely to increase demand for services for women with diabetes in pregnancy. Closer working relationships between the various health professionals involved with the women concerned could mitigate such an increase in demand. An approach to facilitate this is shown in Figure 2.Figure 2. Proposed framework for care pathway for women with GDM in New Zealand

Recommendations for the provision of care for women with GDM: Care needs to maintain the focus on women becoming mothers, and on the birth of healthy babies, only part of which is the management of their GDM. All DHBs require a defined Diabetes in Pregnancy team. The process for screening for GDM should include:

o The development and establishment of a programme to increase awareness of GDM in the population.o A comment on screening for GDM in general pregnancy information sheets.o All Lead Maternity Carers (LMCs) should have access to a Diabetes in Pregnancy team, with an agreed process for referral.o The development of a specific information sheet, written with extensive consumer consultation, containing balanced information, in the appropriate languages and at the appropriate educational level. This should be given to, and discussed with, each woman. Information relating to healthy eating and physical activity must be included. Ideally this should be available for women during early pregnancy, as it may guide their diet and activity and reduce later risk of GDM. It can be formally discussed at the time of the offer for a glucose challenge test. The sheet could include a graph of the optimal gestation to screen.o Screening being offered at the 24 weeks visit [unless earlier—see issue (3) above], and if agreed, to be completed between 26 and 28 weeks but before the 28-week visit. Offers of screening should incorporate use of the information sheet and it should be documented that informed consent to screen was given by the woman.

o If the screening result is positive, the woman should be contacted by the person ordering the test to explain the result and refer for an OGTT. This test should be undertaken within one week and include the fasting and 2-hour glucose as a minimum. o If the test results indicate GDM, the results will be explained by the person ordering the test, initial action should be initiated and the woman should be referred to the Diabetes in Pregnancy team.o An ongoing continuing professional education programme should be provided to support primary care services and facilitate primary care and specialist service integration. Lab staff could be included in this in relation to screening

A national ongoing monitoring system that monitors, at the DHB level, the proportion of women being screened, gestation at screening, gestation at OGTT, gestation at referral and gestation at first visit, linking with outcome data, should be in place. A system to ensure that women that have a homebirth are also included in the audit will need to be developed All DHBs should facilitate the local development and definition of a model of care that best suits their region that address the issues/ principles raised in this report particularly:

o All diabetes in pregnancy, including GDM, is high risk and needs careful monitoring (ultrasound, glucose, clinical).o All LMCs should have access to a Diabetes in Pregnancy Team and ultrasound scanning facilities.o A close relationship, particularly good communication, is needed between the woman’s primary healthcare team, the diabetes educator and LMC.o LMCs, primary healthcare, and the Diabetes in Pregnancy Team in each District should develop agreed standards of care and referral pathways based upon Australasian Guidelines.o The ability of midwives to provide dietary advice, glucose monitoring teaching, and management advice about diabetes in pregnancy is not a core competency for midwifery. This does not preclude that women need midwifery care and that some midwives have an interest in this area and will have additional education to provide care for women with GDM in conjunction with the diabetes in pregnancy service in that region. o The management of diabetes in pregnancy should be integrated with the woman’s primary healthcare team. This is essential to provide follow-up—e.g. annual/biannual OGTTs for women with past GDM and they may be involved in initiation and community-based aspects of management of GDM.o Those caring for women with diabetes in pregnancy need to be alert as the woman’s clinical condition can change rapidly.o Those in primary care will need updating and ongoing education about GDM management including pregnancy-specific dietary, glucose monitoring, and overall information advice.

Each district should consider participating in the ADIPS audit and benchmarking programme.33 All pregnancies complicated by GDM would be part of the audit programme as a result.