Hyperemesis gravidarum

From Wikipedia, the free encyclopedia

Jump to: navigation, search
Hyperemesis gravidarum, with
metabolic derangement
Classification and external resources
ICD-10 O21.1.
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)

Pregnancy Pregnancy
Ectopic pregnancy (Abdominal pregnancy, Cervical pregnancy,
with
Ovarian pregnancy, Interstitial pregnancy) · Hydatidiform
abortive
mole · Miscarriage
outcome

Oedema,
proteinuria
Gestational hypertension (Pre-eclampsia, Eclampsia, HELLP
and
syndrome) · Gestational diabetes
hypertensive
disorders

Hyperemesis gravidarum · Intrahepatic

Digestive
cholestasis of pregnancy · Acute fatty liver of
system
pregnancy · Hepatitis E

PUPPP · Gestational pemphigoid

Integumentary
Impetigo herpetiformis · Intrahepatic cholestasis
Other, system/
of pregnancy · Linea nigra · Prurigo gestationis ·
predominantlydermatoses of
Pruritic folliculitis of pregnancy · Striae
related to pregnancy
gravidarum
pregnancy
Nervous
Chorea gravidarum
system

Gestational thrombocytopenia · Pregnancy-

Blood
induced hypercoagulability

Maternal care amniotic fluid (Polyhydramnios, Oligohydramnios) ·

 chorion/amnion (Chorioamnionitis, Chorionic hematoma,
related to the Premature rupture of membranes, Amniotic band syndrome,
fetus and Monoamniotic twins) · placenta (Placenta praevia, Placental
amniotic abruption, Monochorionic twins, Twin-to-twin transfusion
cavity syndrome, Circumvallate placenta) · Braxton Hicks
contractions · Hemorrhage (Antepartum)

Preterm birth · Postmature birth · Cephalopelvic disproportion · Dystocia

(Shoulder dystocia) · Fetal distress · Vasa praevia · Uterine rupture ·
Labor
Hemorrhage (Postpartum) · placenta (Placenta accreta) · Umbilical cord
prolapse · Amniotic fluid embolism

Puerperal fever · Peripartum cardiomyopathy · Postpartum thyroiditis ·

Puerperal 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 Gravidarum
Nausea 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

Background
Gestational 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.6
There 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.14
Figure 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 process
An 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 GDM
For 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 population
o 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.