Diabetes mellitus

DiabetesMellitus
 Chronic metabolic disorder
 Body cannot metabolise fats, carbohydrates,
and proteins because of a lack of, or
ineffective use of the hormone insulin
 classified into three primary types that are
different disease entities but share the
symptoms and complications of
hyperglycemia (high blood glucose)

DiabetesMellitus
 Type I Diabetes Mellitus:
 Previously “Insulin Dependent Diabetes Mellitus” (IDDM)
 Or Juvenile-Onset Diabetes
 Type II Diabetes Mellitus:
 Previously “Non-Insulin Dependent Diabetes Mellitus”
(NIDDM)
 Or Adult-Onset Diabetes
 Gestational Diabetes Mellitus:
 Or GDM

NormalCarbohydrateMetabolism
andInsulinAction
 Following the consumption of food,
carbohydrates are broken down into glucose
molecules in the gut
 Glucose is absorbed into the bloodstream
elevating blood glucose levels
 This rise in glycaemia stimulates the
secretion of insulin from the beta cells of the
pancreas
 Insulin is needed by most cells to allow
glucose entry

andInsulinAction
 Insulin binds to specific cellular receptors and
facilitates entry of glucose into the cell, which
uses the glucose for energy
 The increased insulin secretion from the
pancreas and the subsequent cellular
utilization of glucose results in lowered of
blood glucose levels
 Lower glucose levels then result in decreased
insulin secretion

andInsulinAction
 Following meals, the amount of glucose
available from carbohydrate breakdown
often exceeds the cellular need for glucose
 Excess glucose is stored in the liver in the
form of glycogen, which serves as a ready
reservoir for future use
 When energy is required, glycogen stores in
the liver are converted into glucose via
glycogenolysis, elevating blood glucose levels
and providing the needed cellular energy
source

andInsulinAction
 The liver also produces glucose from fat (fatty
acids) and proteins (amino acids) through the
process of gluconeogenesis
 Glycogenolysis and gluconeogenesis both
serve to increase blood glucose levels
Thus, glycaemia is controlled by a complex
interaction between the gastrointestinal
tract, the pancreas, and the liver

TheRoleof Insulinin
hyperglycaemiaandhypoglycaemia
 If insulin production and secretion are altered by
disease, blood glucose dynamics will also change
 If insulin production is decreased, glucose entry
into cells will be inhibited, resulting in
hyperglycaemia
 The same effect will be seen if insulin is secreted
from the pancreas but is not used properly by
target cells
 If insulin secretion is increased, blood glucose
levels may become very low (hypoglycaemia) as
large amounts of glucose enter tissue cells and
little remains in the bloodstream.

TypeI DiabetesMellitus
 Beta cells of pancreas are destroyed or
suppressed
 Subdivided into idiopathic and immune-
mediated types

 Onset is usually abrupt, before 30 years of
age but may be diagnosed at any age
 Type I Diabetics are usually of normal weight,
or may be thin in stature
 Since the pancreas produces absolutely no
insulin, the patient must rely on exogenous
insulin, administered for survival
 Patients are highly susceptible to diabetic
ketoacidosis

PathophysiologyofIdiopathicDiabetesMellitus
 With idiopathic type, patients have a
permanent insulin deficiency with no
evidence of autoimmunity
 Often lack antibodies found in immune-
mediated type 1 diabetes
 May be able to go without insulin therapy for
some periods of time

PathophysiologyofImmune-MediatedDiabetes
 Occurs when there is autoimmune
destruction in which the body secretes
substances that attack and destroy the beta
cells in the islets of Langerhans within the
pancreas
 This attack causes an inflammatory response
in the pancreas called insulitis, ceasing insulin
production
 One or more key antibodies are found in 85-
90% of people with this form of type 1
diabetes

DiabeticKetoacidosis(DKA)
 Inadequate insulin hinders glucose uptake by
fat and muscle cells
 Glucose accumulates in blood
 Liver responds to demands of energy starved
cells by converting glycogen to glucose,
further increasing blood glucose levels
 When glucose levels exceed renal threshold,
excess excreted in urine
 Insulin-deprived cells respond by rapid
metabolism of proteins

 Results in loss of intracellular potassium and
phosphorus and excessive liberation of amino
acids
 Liver converts these acids into urea and
glucose
 Blood glucose levels grossly elevated
 Results in increased serum osmolarity and
glucosuria, leading to massive fluid loss from
osmotic diuresis causing fluid and electrolyte
imbalances

 Water loss excedes glucose and electrolyte
loss, contributing to hyperosmolarity
 This perpetuates dehydration, decreasing the
glomerular filtration rate and reducing
amount of glucose excreted in urine
DEADLY CYCLE:
Diminished glucose excretion  raises blood
glucose levels  hyperosmolarity and
dehydration  SHOCK  COMA  DEATH

 SIMULTANEOUSLY – Absolute insulin
deficiency causes cells to convert fats into
glycerol and fatty acids for energy
 Fatty acids can’t be metabolised as quickly as
released, so accumulate in liver
 Converted to ketones (ketoacids)
 Ketones accumulate in blood and urine
(acidosis)
 Acidosis leads to more tissue breakdown 
More ketosis  More acidosis  Eventually
SHOCK  COMA  DEATH

TypeII DiabetesMellitus
 Caused by:
 Resistance to insulin action in target tissues
 Abnormal insulin secretion
 Inappropriate hepatic gluconeogenesis (over
production of glucose)
 Consequence of obesity and sedentary lifestyle

TypeII DiabetesMellitus
Pathophysiology
 Problems arise when insufficient insulin
produced or body (fat, muscle or liver) cells
resist insulin
 When body cells develop a resistance to
insulin, there is a difficulty with glucose
entering cells
 As a result, cells don’t get enough energy
 Lack of energy causes glucose to build up in
the blood vessels
 Can result in damage to body organs
especially if poorly managed

GestationalDiabetesMellitus
 Gestational diabetes mellitus (GDM) is
defined as glucose intolerance of variable
degree with onset or first recognition during
pregnancy
 The placental hormones – oestrogen,
placental lactogen , glucagon and cortisol
interfere with insulin receptors making the
woman temporarily diabetic
 Usually develops in the second or third
trimester

 Risk factors for gestational diabetes include:
 Advanced maternal age (>30 years)
 Ethnicity (Maori, Pacific Islander, Indian, Chinese)
 Obesity (Prepregnancy BMI >30
– dependent on ethnicity)
 Obstetrical history of diabetes , unexplained still birth
or neonatal death or macrosomia
 Strong family history of diabetes
 Glucosuria on two separate occassions in current
pregnancy
 Multiple pregnancy

DiabetesinPregnancy
 Pregnancy characterised by several factors that
produce a diabetogenic state
 Insulin and carbohydrate metabolism is altered
in order to make glucose more readily available
to the fetus
 Women with DM do not have the capacity to
increase insulin secretion in response to the
altered carbohydrate metabolism in pregnancy
 Glucose therefore accumulates in the maternal
and fetal system, leading to significant morbidity
and mortality

SignsandSymptoms
 Polyuria and polydipsia: Polyuria is due to
osmotic diuresis secondary to hyperglycemia.
Thirst is due to the hyperosmolar state and
dehydration
 Polyphagia with weight loss or muscle
wasting:The weight loss with a normal or
increased appetite is due to depletion of
water and a catabolic state with reduced
glycogen, proteins, and triglycerides

SignsandSymptoms
 Fatigue and weakness:This may be due to
muscle wasting from the catabolic state of
insulin deficiency, hypovolemia, and
hypokalemia
 Nocturnal enuresis (bed-wetting): Severe
enuresis secondary to polyuria can be an
indication of onset of diabetes in young
children

SignsandSymptoms
 Blurred vision:This also is due to the effect of
the hyperosmolar state on the lens and
vitreous humor. Glucose and its metabolites
cause dilation of the lens, altering its normal
focal length
 Muscle cramps:This is due to electrolyte
imbalance

SignsandSymptoms
 Gastrointestinal symptoms: Nausea,
abdominal discomfort or pain, and change in
bowel movements may accompany acute
DKA. Acute fatty liver may lead to distention
of the hepatic capsule, causing right upper
quadrant pain. Persistent abdominal pain
may indicate another serious abdominal
cause of DKA, eg, pancreatitis. Chronic
gastrointestinal symptoms in the later stage
of diabetes are due to visceral autonomic
neuropathy

SignsandSymptoms
 Peripheral neuropathy:This presents as
numbness and tingling in both hands and
feet, in a glove and stocking pattern. It is
bilateral, symmetric, and ascending
neuropathy, which results from many factors,
including the accumulation of sorbitol in
peripheral sensory nerves due to sustained
hyperglycemia

SignsandSymptoms
Symptoms at the time of the first clinical
presentation can usually be traced back several
days to several weeks; however, beta cell
destruction may have started months, or even
years, before the onset of clinical symptoms

FetalComplications
 Miscarriage
 In women with pre-existing diabetes, there is a 9-
14% risk of miscarriage
 Supoptimal glycaemic control and advanced
diabetes also posses a significant risk

FetalComplications
 Birth Defects
 With DM the risk of structural abnormality is increased
to 5-10% (normally 1-2%)with poor glycaemic control
prior to conception
 Two-thirds of anomalies affect the cardiovascular and
nervous systems
 Neural tube defects occur 13-20 times more frequently
in diabetic women
 Genitourinary, gastrointestinal, and skeletal anomalies
are also more common
 Because birth defects occur during the critical 3-6 weeks
after conception, nutritional and metabolic intervention
must be initiated well before pregnancy begins

FetalComplications
 Fetal Growth Restriction
 IUGR occurs significantly in pregnancy where
women have pre-existingType 1 DM
 The most important predictor of fetal growth
restriction is underlying maternal vascular disease
 Specifically, pregnant patients with diabetes-
associated retinal or renal vasculopathies and/or
chronic hypertension are most at risk for growth
restriction

FetalComplications
 Fetal Growth Acceleration
 Caused by excessive body fat stores, stimulated by
excessive glucose delivery during diabetic
pregnancy
 Approximately 30% of fetuses of women with
diabetes mellitus in pregnancy are large for
gestational age (LGA). In pre-existing diabetes
mellitus this incidence appears slightly higher, 38%
 Maternal obesity, common in type 2 diabetes,
appears to significantly accelerate the risk of infants
being LGA

FetalComplications
 Fetal Obesity
 The macrosomic fetus in diabetic pregnancy
develops a unique pattern of overgrowth, involving
central deposition of subcutaneous fat in the
abdominal and interscapular areas. Skeletal growth
is largely unaffected
 Macrosomia is typically defined as a birthweight
above the 90th percentile for gestational age or
greater than 4000 grams
 Birth injury, including shoulder dystocia and brachial
plexus trauma, are more common among infants of
diabetic mothers, and macrosomic fetuses are at the
highest risk

FetalComplications
 Metabolic Syndrome
 Glucose intolerance and higher serum insulin levels
are more frequent in children of diabetic mothers as
compared to normal controls
 The childhood metabolic syndrome includes
childhood obesity, hypertension, dyslipidemia, and
glucose intolerance
 Fetuses of diabetic women that are born large for
gestational age appear to be at the greatest risk

FetalComplications
 BirthTrauma
 Injuries of birth, including shoulder dystocia and
brachial plexus trauma, are more common among
infants of diabetic mothers
 Common birth injuries associated with diabetes are
brachial plexus, facial nerve injury, and
cephalohematoma

FetalComplications
 Polycythaemia
 Hyperglycemia is a powerful stimulus to fetal
erythropoietin production mediated by decreased
fetal oxygen tension
 Hypoglycaemia
 Aproximately 15-25% of neonates delivered from
women with diabetes during gestation develop
hypoglycemia during the immediate newborn
period
 Unrecognized postnatal hypoglycemia may lead to
neonatal seizures, coma, and brain damage

FetalComplications
 Hyperbilirubinaemia
 Causes of hyperbilirubinemia in infants of diabetic
mothers are multiple, but prematurity and
polycythemia are the primary contributing factors
 Increased destruction of red blood cells contributes
to the risk of jaundice and kernicterus

FetalComplications
 Respiratory Problems
 The majority of the literature indicates a signiﬁcant
biochemical and physiological delay in infants of
diabetic mothers
 Fetal lung maturity is thought to occur later in
pregnancies with poor glycaemic control regardless
of class of diabetes

MaternalComplications
 Diabetic Retinopathy
 Leading cause of blindness in women aged 24-64 years
 Some form of retinopathy is present in virtually 100% of
women who have had type 1 diabetes for 25 years or
more
 Studies show that while half the women with pre-
existing retinopathy experienced deterioration during
pregnancy, all the patients had partial regression
following delivery and returned to their prepregnant
state by 6 months postpartum
 Rapid induction of glycaemic control in early pregnancy
stimulates retinal vascular proliferation

 Renal Function
 In general, patients with underlying nephropathy can
expect varying degrees of deterioration of renal
function during a pregnancy
 As renal blood flow and glomerular filtration rate
increase 30-50% during pregnancy, the degree of
proteinuria will also increase
 Perinatal complications are greatly increased in
patients with diabetic nephropathy. Preterm birth,
intrauterine growth restriction, and preeclampsia are
all significantly more common in women with diabetic
nephropathy during pregnancy

 Chronic Hypertension
 Complicates approximately 1 in 10 diabetic
pregnancies overall
 Patients with underlying renal or retinal vascular
disease are at a substantially higher risk
 Patients with chronic hypertension and diabetes are
at increased risk of intrauterine growth restriction,
superimposed preeclampsia, abruptio placentae,
and maternal stroke

 Pre-Eclampsia
 Preeclampsia is more frequent among women with
diabetes, occurring in approximately 12% as compared
to 8% of the nondiabetic population
 The risk of preeclampsia is also related to maternal age
and the duration of preexisting diabetes
 In patients who have chronic hypertension coexisting
with diabetes, preeclampsia may be difficult to
distinguish from near-term blood pressure elevations
 The rate of preeclampsia has been found to be related
to the level of glycemic control and pregravid body
mass index

TestsandInvestigations
HbA1c
 HbA1c is a test that measures the amount of
glycosylated hemoglobin in blood
 Glycosylated hemoglobin is a molecule in red
blood cells that attaches to glucose (blood sugar)
 Elevated levels of glycosylated hemoglobin if
there more glucose in the blood
 The test gives a good estimate of how well
diabetes is being managed over the last 2 or 3
months (life of erythrocyte)
 No preparation or fasting required prior

HbA1c
 Results
 An elevated HbA1c increases the risk of
complications such as retinopathy, nephropathy,
neuropathy, heart disease, and stroke
 Especially true if HbA1c remains high for a long
period of time
 HbA1c normally 3-6%
 Abnormal results mean that blood glucose levels
have not been well-regulated over a period of weeks
to months
 If HbA1c is above 7%, it means diabetes is poorly
controlled

Polycose
 Woman without known diabetes should be
offered routine screening for GDM
 Test is a non fasting 1 hour 50g glucose challenge
test, preferably in morning
 One hour later, blood is taken
 Performed at 24-28 weeks of pregnancy
 Women need written and full information about
this so they can make an informed choice

Polycose
 Results
 If result is >7.8 mmol/L
 GTT
 If result is 7.2 – 7.7 mmol/L
 Rescreen 2 weeks later if known risk
factors for GDM
 If result is <7.8 mmol/L but known risk factors are
present
 Offer rescreening or GTT to assess whether
glucose tolerance deteriorating

GlucoseToleranceTest
 Test is a fasting 75g glucose tolerance test
 Blood is taken:
- Prior to test
- 1 hour after glucose load
- 2 hours after glucose load
 Usual diet in days prior to the test
 Fast for 12 hours prior to the test
 Repeat if clinically indicated, even though first
GTT has been normal

GlucoseToleranceTest
 Results
 Gestational Diabetes Mellitus confirmed if:
 Fasting glucose: 5.5 mmol/L or greater
 2 hour glucose: 9.0 mmol/L or greater

Section88 MaternityNotice
ReferralGuidelines
 LEVEL 3 (Code 1019)
- Pre-existing DM Insulin Dependent or Non Insulin
Dependent
- GDM well controlled on diet
- GDM requiring Insulin
Consideration of ‘Shared Care’ or intrapartum
midwifery care may be an option for women
with GDM

Section88 MaternityNotice
ReferralGuidelines
- Infant of a Diabetic Mother with any abnormal
findings e.g.
 Hypoglycaemia
 Poor feeding
 Macrosomia

Management
Pre-PregnancyCareforType1or2DM
 Assessment is made of current diabetic control,
aiming for pre-meal glucose of <6 mmol/L and
HbA1c of ≤7%
 Insulin dosage reviewed
 Women withType 2 DM on oral hypoglycaemics
will need to transfer to insulin to prevent
possibility of teratogenesis
 Higher-dose folic acid supplementation
 Smoking cessation support is arranged
 Assessment and management is provided for
diabetes complications

Management
Pre-ExistingDiabetesMellitus
 Booking visit – care recommendations and options
 Ideally should be seen in a combined clinic by a team
that includes a physician, obstetrician, specialist
diabetes nurse, specialist midwife and dietician
 Seen as often as required in order to maintain good
diabetic control and undertake relevant screening
 Blood glucose levels should be monitored frequently
(4-8x per day using reflective meter) and insulin levels
adjusted accordingly
 Additional estimations of blood glucose control, such as
monthly HbA1c measurements recommended
 Diet high in fibre beneficial as carbohydrates released
slowly and therefore more constant BSL can be
achieved

Management
Pre-ExistingDiabetesMellitus
 Advise women on early recognition of the signs and
symptoms of urinary and vaginal infections
 Anomaly ultrasound should be offered at 20 weeks
gestation, and consider fetal echocardiography at
20-22 weeks to detect cardiac abnormalities
 Serum screening for Down Syndrome is altered with
maternal diabetes and care should be taken when
interpreting results
 A baseline measurement of the fetal AC should be taken
at 20 weeks gestation, followed by serial measurements
every 2-4 weeks commencing at 24 weeks to detect
IUGR, macrosomia and polyhydramnios
 See in daily assessment unit if problems or on wards if
inpatient

Management
 After screening and confirmation, referral according to
Section 88 Guidelines
 Educate women regarding complications of
uncontrolled blood glucose levels on her health and her
baby’s
 Partake in 3-way discussion as MultidisciplinaryTeam
member
 Good communication with women regarding scope
and with other professionals regarding care
 Refer if Blood glucose levels high/unstable
 Be aware of local protocols
 Continue to support, educate, offer continuity of care
eg. for postnatal care, etc

Medications
Insulin
 NovoRapid
 Insulin aspart, whereby its molecules enable the
uptake of glucose into cells by binding onto
receptor sites and concurrently preventing the
release of glucose from the liver
 Dosage is based on the needs of the patient when
reviewed by the physician and facilitates a quick
onset of action when comparing it to human
insulin, and a shorter duration of action after
subcutaneous injection
 Unlike glucose however, insulin does not cross the
placental barrier

Medications
Insulin
 Protaphane
 Similar to NovoRapid
 Is an isophane insulin suspension and its actions
are equal to that of human insulin
 One significant difference is that its time of onset
is 1.5 hours, longer than NovoRapid and long
acting, lasting for up to 24 hours
 Again, the dose is patient-dependent, and
determined by the physician in accordance with
the needs of the patient

Medications
Metformin
 Metformin is a biguanide by-product, which produces an
antihyperglycaemic effect where there is insulin secretion
from the pancreas, although the action of the drug is not fully
understood
 It is suggested that it may mimic or improve the effects of
insulin on peripheral receptor sites, and that this increased
sensitivity appears to be a result of an increase in the amount
of insulin receptor sites on the cell surface
 Other proposed mechanisms of action include glucogenesis
inhibition within the liver or a delay in the absorption of
glucose from the gastrointestinal tract
 In pregnancy metformin does cross the placenta, however
there is no research to indicate that metformin is teratogenic

Diabetes mellitus

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