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DIABETIC PARTURIENTDr.CHANDRA PRAKASH
Prof. &HOD DEPARTMENT OF ANAESTHESIOLOGY
Dr.PARVEEN SKP. G IIYr
MNR MEDICAL COLLEGE
ClassificationClassification
Pregestational diabetesPregestational diabetes
Type 1 DMType 1 DM
Type 2 DMType 2 DM
Secondary DMSecondary DM Gestational diabetes Gestational diabetes
DefinitionDefinition
Gestational diabetes (GDM) is defined as glucose Gestational diabetes (GDM) is defined as glucose intolerance of variable degree with onset or first intolerance of variable degree with onset or first recognition during the present pregnancy. recognition during the present pregnancy.
Pregestational diabetes precedes the diagnosis of pregnancy.
Gestational diabetes and impaired glucose tolerance (IGT) in pregnancy affects
between of all pregnancies and both have been associated with pregnancy
complications.
2-3%
EPIDEMIOLOGY
The prevalence of gestational diabetes { GDM} in india varied from 3.8 to 21% in different parts of the country,depending on the geographical locations and diagnostic methods used.
GDM is found to be more prevalent in urban areas than in rural areas.
Normal hepatic glucose metabolism represents a balance between insulin and counter-regulatory hormones
Counterregulatory hormones are glucagon, cortisol, epinephrine and growth hormone
Insulin also an important anabolic regulator of lipids and amino acids
Progressive resistance to insulin at receptor and postreceptor level due to increase in counterregulatory hormones (placental lactogen and growth hormone, cortisol and progesterone) in third trimester
Placental lactogen most plausible cause Placental lactogen has growth hormone like activity Gestational diabetes results when a patient can’t mount
a sufficient compensatory insulin response during pregnancy
In patients with pregestational diabetes, the therapeutic dose of insulin increases progressively during pregnancy
At term, the requirement is 1 U/kg compared to 0.7 U/kg before pregnancy
Type I diabetes: insulin requirements decrease with onset of first stage of labor
Insulin requirements increase during second stage of labor
After delivery, insulin requirements decrease markedly and return to normal within several weeks of delivery
Before discovery of insulin (1921), pregnancies were rare in diabetic patients
Despite improved obstetric and medical care, maternal mortality remains ten times higher in diabetic than non diabetic patients
Major complications of DM
ACUTE : Diabetic ketoacidosis Hyperosmolar hyperglycaemic nonketotic coma Hypoglycaemia
CHRONIC : Macrovascular(atherosclerosis) coronary cerebrovascular peripheral vascular Microscopic retinopathy nephropathy Neuropathy Autonomic Somatic
DKA: 8%-9% of diabetic pregnancies One case report of DKA with gestational diabetes Perinatal mortality as high as 30%-70% with DKA Occurs most commonly during second and third trimester Associated with ᵦ-adrenergic therapy, emesis, decreased caloric
intake, poor medical management, patient non-compliance and infection (3.2 higher in type I than non-diabetic)
ᵦ -adrenergic agents used to treat preterm labor and corticosteroids for fetal lung maturity can precipitate DKA during pregnancy
Fetal heart rate patterns consistent with fetal distress during DKA Probably related to decreased placental perfusion secondary to
acidosis HHNC: Rare during pregnancy, one case report
Hypoglycemia: Significant risk during pregnancy for patients with
pregestational type I diabetes. Occurs in approx 33%-71% of patients. (or 3-15 times greater than for non pregnant type I
diabetics) 73% of episodes of hypoglycemia occur before 16 weeks
gestation. Risk increases with tight glucose control. Counter regulatory responses to hypoglycemia impaired
after intensive insulin therapy in both pregnant and non-pregnant patients.
Relationship between pregnancy and development of macrovascular complications unknown.
Patients with pregestational type I diabetes have higher systolic and diastolic pressures during pregnancy.
PIH three times more common. MI occurs during diabetic pregnancies but is a rare
complication. Pregnancy may accelerate the progression of proliferative
retinopathy. In contrast, pregnancy doesn’t accelerate the development of
diabetic nephropathy. It is unclear whether pregnancy accelerate progression of
somatic or autonomic neuropathy.
Both pregestational and gestational diabetes associated with increased incidence of PIH, polyhdramnios and cesarean delivery
CS rate increased 3-10 fold in patients with pregestational diabetes
1.5 times with gestational diabetes Pregestational diabetes associated with 2-3
fold increase in incidence of preterm labor and delivery
FETAL COMPLICATIONS OF MATERNAL DM DURING PREGNANCY AND PUERPERIUM
Macrosomial/large for gestational age -shoulder dystocia -birth injury/trauma Structural malformatins CNS: anencephaly,encephalocele meningomyelocele,spina bifida,holoprosencephaly CARDIAC : Transposition of great vessels,VSD, situs inversus,single ventricle, hypoplastic ventricle SKELETAL : caudal regression RENAL : agenesis, multicystic dysplasia GASTROINTESTINAL : anal/rectal atresia,small left colon PULMONARY : hypoplasia AFTER BIRTH IUD/Neonatal death Neonatal respiratory distress syndrome Neonatal hypoglycaemia Neonatal hyperbilirubinaemia Glucose intolerance Possible impairment of cognitive development
Fetal macrosomia well known complication of both pregestational and gestational diabetes
Fetal macrosomia (4000 gms vs. 4500 gms depending on definition)
9%-25% incidence with pregestational diabetes 4-6 fold increase when compared to non-diabetic Macrosomia results in increased incidence of shoulder
dystocia and birth trauma Mechanism probably anabolic response in fetus
secondary to hyperinsulinemia from hyperglycemia
Increased risk of fetal anomalies with pregestational diabetes
Incidence 6% to 18% which is 7-10 times higher than non-diabetics
Cardiovascular anomalies most common followed by CNS anomalies.
3%-8% with gestational diabetes Ten fold decreased incidence of malformations with
strict glycemic control
Higher perinatal mortality rate with pregestational > gestational diabetes
Intrauterine fetal death accounts for 40% of perinatal fetal deaths
68% of stillbirths occur between 36-40 weeks gestation
Risk factors: fetal macrosomia and recurrent episodes of hypoxia from reduced placental perfusion
Now congenital anomalies have emerged as leading cause of perinatal mortality
Cardiac: transposition, VSD, situs inversus, single ventricle, hypoplastic left ventricle
CNS: anencephaly, encephalocele, meningomyelocele, spina bifida
Skeletal: Caudal regression syndrome Renal: Agenesis, multicystic kidney GI: anal/rectal atresia Pulmonary hypoplasia
Caudal regression syndrome
Caudal regression syndrome
Intrauterine/neonatal death Respiratory distress syndrome Neonatal hypoglycemia: occurs in 5%-12%
cases of pregestational and gestational diabetics
(6-16 fold increase in incidence when compared to nondiabetics)
Neonatal hyperbilirubinemia: 2-5 fold increase
Gestational Diabetes associated with advanced maternal age, obesity, family history of diabetes, prior stillbirth, neonatal death, fetal malformation or macrosomia.
1 hr glucose tolerance test with cut off of 140 mg/dl.
Patients with +ve screen undergo a 100 g 3-hr glucose tolerance test.
Glycosylated hemoglobin: 4.1% to 5.9% in pregnant nondiabetic.
1. Symptoms of DM plus casual plasma glucose concentration ≥ 200 mg/dL. Casual is defined as any time of day without regard to time since last meal. The classic symptoms of DM include polyuria polydipsia, and unexplained weight loss.
or
2. Fasting plasma glucose (FPG) ≥ 126 mg/dL. Fasting is defined as no caloric intake for at least 8 hours.
or
3. Two-hour postload plasma glucose (2hPG) ≥ 200 mg/dL during an oral glucose tolerance test (OGTT). This test should be performed as described by the World Health Organization, using a glucose load containing the equivalent of 75 g of anhydrous glucose dissolved in water.
• In the absence of unequivocal hyperglycemia with acute metabolic decompensation, these criteria should be confirmed by repeat testing on a different day.
• The Third measurement (OGTT) is not recommended for routine clinical use.• Normal fasting glucose = FPG < 110 mg/dL.• Normal glucose tolerance = 2hPG < 140 mg/dL.• Impaired fasting glucose = FPG ≥ 110 and < 126 mg/dL.• Impaired glucose tolerance = 2hPG ≥ 140 and < 200 mg/dL.
_________________________________________________________________________________
From American Diabetes Association Expert Committee on the Diagnosis and Classification of Diabetes Mellitus.Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. Diabetes Care 1997; 20:1183-97.
Whom to screen ?Whom to screen ?
Risk stratification based on certain variablesRisk stratification based on certain variables
Low risk : no screeningLow risk : no screening
Average risk: at 24-28 weeksAverage risk: at 24-28 weeks
High risk : as soon as possibleHigh risk : as soon as possible
Essentially all Indian women have to be Essentially all Indian women have to be screened for gestational diabetes mellitusscreened for gestational diabetes mellitus
as they belong to a high risk ethnicityas they belong to a high risk ethnicity
How to screen?How to screen?
Oral glucose tolerance Oral glucose tolerance
test ( OGTT) with 100 gm test ( OGTT) with 100 gm glucoseglucose
FastingFasting 95 mg/dl95 mg/dl
1-h1-h 180 mg/dl180 mg/dl
2-h2-h 155 mg/dl155 mg/dl
3-h3-h 140 mg/dl140 mg/dl
• Overnight fast of at least 8 hours
• At least 3 days of unrestricted diet and unlimited physical activity
• > 2 values must be abnormal
CLARITY IN CATEGORIZING ABNORMAL CLARITY IN CATEGORIZING ABNORMAL GLUCOSE TOLERENCE IN PREGNANCYGLUCOSE TOLERENCE IN PREGNANCY 2h plasma glucose in2h plasma glucose in pregnancy outside pregnancypregnancy outside pregnancy
>200mg/dl Diabetes Diabetes
>140-199mg/dl GDM IGT
120-139mg/dl Gestational glucose intolerance
-
<120mg/dl Normal Normal
Urine glucose monitoring is not useful in gestational Urine glucose monitoring is not useful in gestational diabetes mellitusdiabetes mellitus
Urine ketone monitoring may be useful in detecting Urine ketone monitoring may be useful in detecting insufficient caloric or carbohydrate intake in women insufficient caloric or carbohydrate intake in women treated with calorie restrictiontreated with calorie restriction
Urine monitoring
Daily self-monitoring of blood glucose (SMBG) appears to be superior to intermittent office
monitoring of plasma glucose.
Monitoring
For women treated with insulin, preprandial monitoring is postprandial monitoring. However, the success of
either approach depends on the glycemic targets that are set and achieved.
Monitoring
superior superior toto
Glycosylated haemoglobin (Hb A1(
It is normally accounts for 5-6% of the total haemoglobin mass. A value over 10% indicates poor diabetes control in the previous 4-8 weeks.
If this is detected early in pregnancy, there is a high risk of congenital anomalies .
If this is detected in late pregnancy it indicates increased incidence of macrosomia and neonatal morbidity and mortality.
Monitoring
Assessment for asymmetric fetal growth by ultrasonography,
particularly in early third trimester, may aid in identifying fetuses that can benefit from maternal insulin therapy
Monitoring
Maternal surveillance should include blood pressure and urine protein monitoring to detect hypertensive
disorders.
Monitoring
ManagementManagement
Clinical parameters: checked at each visitClinical parameters: checked at each visit
medicationsmedications pre-pregnancy weight pre-pregnancy weight weight gainweight gain edemaedema pallorpallor blood pressure blood pressure Fundal height Fundal height
Patient educationPatient education
Cornerstone in GDM managementCornerstone in GDM management
1) Preconceptional counselling 2) Medical nutrional therapy 3) Drugs- Oral hypoglycaemics, Insulin therapy 4) Fetal monitering 5) Timing of delivery 6) managemant during labour & delivery 7) glycaemic management during labour 8)Post-partum followup 9) Longterm risk-followup 10) Immediate management of neonate 11) Anaesthetic implications
Preconception counsellingPreconception counselling
Diabetic mother : glycemic control with insulin/SMBGDiabetic mother : glycemic control with insulin/SMBG Target: HbA1c < 7% Target: HbA1c < 7%
Folic acid supplementation: 5 mg/day Folic acid supplementation: 5 mg/day
Ensure no transmissible diseases: HBsAg, HIV, rubellaEnsure no transmissible diseases: HBsAg, HIV, rubella
Try and achieve normal body weight: diet/exerciseTry and achieve normal body weight: diet/exercise
Stop drugs : ?oral hypoglycemic drugs, ACE inhibitors, Stop drugs : ?oral hypoglycemic drugs, ACE inhibitors, beta blockersbeta blockers
Medical nutrition therapyMedical nutrition therapy
Promote nutrition necessary for maternal and fetal healthPromote nutrition necessary for maternal and fetal health
Adequate energy levels for appropriate gestational weight Adequate energy levels for appropriate gestational weight
gain,gain,
Achievement and maintenance of normoglycemiaAchievement and maintenance of normoglycemia
Absence of ketones Absence of ketones
Regular aerobic exercisesRegular aerobic exercises
Medical nutrition therapyMedical nutrition therapy
Approximately 30 kcal/kg of ideal body weightApproximately 30 kcal/kg of ideal body weight
> 40-45% should be carbohydrates> 40-45% should be carbohydrates
6-7 meals daily( 3 meals , 3-4 snacks). Bed time snack to prevent 6-7 meals daily( 3 meals , 3-4 snacks). Bed time snack to prevent ketosis ketosis
Calories guided by fetal well being/maternal weight gain/blood Calories guided by fetal well being/maternal weight gain/blood sugars/ ketonessugars/ ketones
Energy requirements during the first 6 months of lactation Energy requirements during the first 6 months of lactation require an additional 200 calories above the pregnancy meal require an additional 200 calories above the pregnancy meal plan.plan.
Self monitored blood glucoseSelf monitored blood glucose
4 times/day minimum, fasting and 1 to 2 4 times/day minimum, fasting and 1 to 2 hours after start of mealshours after start of meals
Maintain log bookMaintain log book
Use a memory meterUse a memory meter
Calibrate the glucometer frequentlyCalibrate the glucometer frequently
GDM
Failure to maintain glycemic targets
INSULIN THERAPY
Medical nutrition therapy
insulin therapy is recommended when medical nutrition therapy fails to maintain self-monitored glucose at the
following levels:Fasting whole blood glucose <95 mg/dL Fasting plasma glucose <105 mg/dL or1-hour postprandial whole blood glucose <140 mg/dL 1-hour postprandial plasma glucose <155 mg/dL or2-hour postprandial whole blood glucose <120 mg/dL 2-hour postprandial plasma glucose <135 mg/dL
insulin therapy
GOAL Self-blood glucose monitoring combined
with aggressive insulin therapy has made the maintenance of maternal
normoglycemia (fasting and premeal glucose between
50-80mg/dl and 1 hour postprandial glucose <140mg/dl)
Insulin therapy …..cont.
Insulin
Preparations Onset (hr) Peak (hr) Duration (hr)
Short-Acting Class•Regular 0.5-1 2-4 4-8•Lispro* 0.25 1 2-4•Aspart* 0.25 1 2-4
Intermediate Class•NPH 1-4 6-10 12-20•Lente 2-4 6-12 12-20
Long-Acting Class•Ultralente 3-5 10-16 18-24•Glargine* 2 None 24
*Insulin analogs
Insulin therapy …..cont.
Twice daily ( before breakfast and before dinner) injections of a combination of short
and intermediate acting insulins are usually sufficient to control most patients
otherwise a subcutaneous insulin pump is used.
The total first dose of insulin is calculated according to the patient’s weight as follow:
Insulin therapy …..cont.
In the first trimester .......... weight x In the first trimester .......... weight x
0.70.7
In the second trimester........ weight x In the second trimester........ weight x
0.80.8
In the third trimester........... weight x In the third trimester........... weight x
0.90.9
If the total dose of insulin is less than 50 units/ day, it is given in a single morning dose with the ratio: Short acting (regular or Actrapid)/Intermediate (NPH or Monotard) = 1 : 2
In higher doses, As a general rule, the amount of intermediate-acting insulin will exceed the short-acting component by a 2:1 ratio. Patients usually receive two thirds their total dose with breakfast and the remaining third in the evening as a combined dose with dinner
Suggested Flow Chart Suggested Flow Chart For GD TreatmentFor GD Treatment
In patients who are not well controlled, a brief period of hospitalization is often necessary for the initiation of therapy. Individual adjustments to the regimens
implemented can then be made.
3-Hospitalisation
Fetal monitoringFetal monitoring
Baseline ultrasound : fetal sizeBaseline ultrasound : fetal size At 18-22 weeks: major malformationsAt 18-22 weeks: major malformations
fetal echocardiogramfetal echocardiogram 26 weeks onwards: growth and liquor volume26 weeks onwards: growth and liquor volume III trimester: frequent USG for accelerated growthIII trimester: frequent USG for accelerated growth
( abdominal: head circumference) ( abdominal: head circumference)
Timing of deliveryTiming of delivery
Small risk of late IUD even with good controlSmall risk of late IUD even with good control Delivery at 38 weeksDelivery at 38 weeks Beyond 38 weeks, increased risk of IUD without an Beyond 38 weeks, increased risk of IUD without an
increase in RDSincrease in RDS Vaginal delivery: preferredVaginal delivery: preferred Caesarian section only for routine obstetric indicationCaesarian section only for routine obstetric indication just GDM is not an indication !just GDM is not an indication ! Unfavorable condition of the cervix is a problemUnfavorable condition of the cervix is a problem 4500 grams, cesarean delivery may reduce the likelihood of 4500 grams, cesarean delivery may reduce the likelihood of
brachial plexus injury in the infant (ACOG)brachial plexus injury in the infant (ACOG)
Management of labor and deliveryManagement of labor and delivery
Maternal hyperglycemia in labor: fetal hyperinsulinemia, Maternal hyperglycemia in labor: fetal hyperinsulinemia,
worsen fetal acidosisworsen fetal acidosis Maintain sugars: 80-120 mg/dl (capillary: 70-110mg/dl )Maintain sugars: 80-120 mg/dl (capillary: 70-110mg/dl ) Feed patient the routine GDM diet Feed patient the routine GDM diet Maintain basal glucose requirementsMaintain basal glucose requirements Monitor sugars 1-4 hrly intervals during labourMonitor sugars 1-4 hrly intervals during labour Give insulin only if sugars more than 120 mg/dlGive insulin only if sugars more than 120 mg/dl
Glycemic management during labourGlycemic management during labour
Later stages of labour: start dextrose to maintain basal Later stages of labour: start dextrose to maintain basal nutritional requirements: 150-200 ml/hr of 5% dextrose nutritional requirements: 150-200 ml/hr of 5% dextrose
Elective LSCS: check FBS, if in target no insulin, start Elective LSCS: check FBS, if in target no insulin, start dextrose dripdextrose drip
Continue hourly SMBGContinue hourly SMBG Post delivery keep patients on dextrose-normal saline till Post delivery keep patients on dextrose-normal saline till
fedfed No insulin unless sugars more than normal ( No insulin unless sugars more than normal ( not GDM not GDM
targets ! )targets ! )
Glycemic targetsGlycemic targets
Fasting venous plasma < 95 mg/dlFasting venous plasma < 95 mg/dl 2 hour postprandial <120 mg/dl2 hour postprandial <120 mg/dl 1 hour postprandial <130 mg/dl (140)1 hour postprandial <130 mg/dl (140)
Pre-meal and bedtime: 60 to 95 mg/dlPre-meal and bedtime: 60 to 95 mg/dl
If diet therapy fails to maintain these targets > 2 times/week, start insulin
These are venous plasma targets, not glucometer targets
Why these tight glycemic targets?Why these tight glycemic targets?
Prospective study in type1 patients with pregnancyProspective study in type1 patients with pregnancy
FBSFBS MacrosomiaMacrosomia
>105 mg/dl>105 mg/dl 28.6 %28.6 %
95-105 95-105 10%10%
<95 mg/dl <95 mg/dl 3%3%
Post partum follow upPost partum follow up : :
Check blood sugars before dischargeCheck blood sugars before discharge
Breast feeding: helps in weight lossBreast feeding: helps in weight loss
Lifestyle modification: exercise, weight reductionLifestyle modification: exercise, weight reduction
OGTT at 6-12 weeks postpartum: classify patients into OGTT at 6-12 weeks postpartum: classify patients into normal/impaired glucose tolerance and diabetesnormal/impaired glucose tolerance and diabetes
Preconception counseling for next pregnancyPreconception counseling for next pregnancy
Increased risk of cardiovascular disease,future diabetes and dyslipidemia
Immediate management of neonateImmediate management of neonate
Hypoglycemia : 50 % of macrosomic infants Hypoglycemia : 50 % of macrosomic infants 5–15 % optimally controlled GDM5–15 % optimally controlled GDM
Starts when the cord is clamped Starts when the cord is clamped
Exaggerated insulin release secondary to pancreatic ß-cell Exaggerated insulin release secondary to pancreatic ß-cell hyperplasiahyperplasia
Increased risk : blood glucose during labor and delivery Increased risk : blood glucose during labor and delivery exceeds 90 mg/dlexceeds 90 mg/dl
Anticipate and treat hypoglycemia in the infant
Management of neonateManagement of neonate
Hypoglycemia <40 mg/dl Hypoglycemia <40 mg/dl
Encourage early breast feeding Encourage early breast feeding
If symptomatic give a bolus of 2- 4 cc/kg, IV, 10% dextroseIf symptomatic give a bolus of 2- 4 cc/kg, IV, 10% dextrose
Check after 30 minutes, start feedsCheck after 30 minutes, start feeds
IV dextrose : 6-8 mg/kg/min infusionIV dextrose : 6-8 mg/kg/min infusion
Check for calcium, if seizure/irritability/RDSCheck for calcium, if seizure/irritability/RDS
Examine infant for other congenital abnormalitiesExamine infant for other congenital abnormalities
Long term risk: offspringLong term risk: offspring
Increased risk of obesity and abnormalIncreased risk of obesity and abnormal
glucose toleranceglucose tolerance
Due to changes in fetal islet cell function Due to changes in fetal islet cell function
Encourage breast feeding: less chance of obesity in later Encourage breast feeding: less chance of obesity in later lifelife
Lifestyle modificationLifestyle modification
Anaesthetic implicationsAnaesthetic implications AIMS:AIMS:Avoid hypoglycaemiaAvoid hypoglycaemiaAvoid hyperglycaemiaAvoid hyperglycaemiaMinimise electrolyte dysfunctionMinimise electrolyte dysfunctionPrevention of lipolysis and proteolysisPrevention of lipolysis and proteolysis
?Tight glycaemic control??Tight glycaemic control?
Effects of AnaesthesiaEffects of Anaesthesia
There is no evidence that anaesthetic There is no evidence that anaesthetic technique affects mortality or morbiditytechnique affects mortality or morbidity
Regional techniques have some Regional techniques have some advantage in obtunding the stress advantage in obtunding the stress response, decreasing blood loss, and response, decreasing blood loss, and decreasing thrombo-embolic complicationsdecreasing thrombo-embolic complications
Hence they are the prefered over general Hence they are the prefered over general anaesthesia.anaesthesia.
Potential for hypotension during regional;:noninvasive testing for autonomic dysfunction may be useful.
In nonpregnant diabetic patients, corrected QT interval correlates with severity of autonomic neuropathy.
Autonomic dysfunction: more frequent blood pressure monitoring and more vigorous IV hydration before and during regional.
Gastroparesis is a manifestation of autonomic neuropathy in diabetic patients.
Consider preanesthetic administration of metoclopramide. Autonomic neuropathy also associated with decreased cough
reflex threshold and increased incidence of obstructive sleep apnea.
Neonatal acidosis not a problem during spinal or epidural anesthesia provided maternal glycemic control satisfactory.
Aggressive volume expansion with non dextrose containing solution.
Treat hypotension aggressively with ephedrine Some diabetic parturients have chronic uteroplacental
insufficiency; epidural may be preferable in these patients compared to spinal due to slower onset of sympathetic blockade.
Perioperative peripheral nerve injuries reported after administration of anesthesia in nonpregnant diabetic patients .
These nerve injuries may represent either unrecognized preanesthetic neurologic deficits or a propensity of nerve injury because of latent peripheral nerve disease
Proper perioperative positioning and padding of extremities important
Preanesthetic neuro exam may be helpful Diabetic stiff joint syndrome in type I diabetics has been described
as a cause of difficult direct laryngoscopy and intubation Associated with nonfamilial short stature, joint contractures and
tight skin Limited movement of atlantooccipital joint Screening for stiff joint syndrome by looking for prayer sign Some have suggested phalangeal visualization on an ink print of
palm
Inability to approximate the palmer surfaces of the phalangeal joints (prayer sign) despite maximal effort, secondary to diabetic stiff-joint syndrome. (From Hogan K, Rusy D, Springman SR. Difficult laryngoscopy and diabetes mellitus. Anesth Analg 1988; 67:1162-5.)
Besides difficult laryngoscopy and intubation, these patients can have noncompliant epidural space.
One case report in a pregnant patient with pregestational diabetes and diabetic scleroderma of anterior spinal artery syndrome after administration of epidural anesthesia for cesarean section
Cause of vascular compression could have resulted from preexisting microvascular disease, stiff epidural space because of connective tissue disease or administration of large volume (35 ml) of local anesthetic
ConclusionConclusion
Gestational diabetes is a common problem in India.Gestational diabetes is a common problem in India.
Risk stratification and screening is essential in all Indian Risk stratification and screening is essential in all Indian pregnant women.pregnant women.
Tight glycemic targets are required for optimal maternal Tight glycemic targets are required for optimal maternal and fetal outcome.and fetal outcome.
Patient education is essential to meet these targets.Patient education is essential to meet these targets.
Long term follow up of the mother and baby is essential .Long term follow up of the mother and baby is essential .
17 pound baby born to Brazilian diabetic mother Courtesy: MSNBC News ServicesJan. 24, 2005
Wissler RN. Endocrine Disorders in Principles and Practice of Anesthesia, Editor David Chestnut, Elsevier Mosby, PA.
Indian Journal of Anaesthesia vol54/issue5/sep-oct2010.
PLASMA GLUCOSE AND INSULIN iv FLUID
Drip rate : 16 to 20 drops per minute. Maternal capillary blood glucose to be checked by glucometer every 1hr and drip rate adjusted.
Plasma glucose at time of onset of labour
Insulin IV fluid
<70mg/dl 5% DNS-100ml/hr
90-120mg/dl NS-100ml/hr
120-140mg/dl NS-100ml/hr plus
4 units of Reg.insulin
140-180mg/dl NS-100ml/hr plus
6 units of Reg.insulin
>180mg/dl NS-100ml/hr plus
8 units of Reg.insulin
INTRAOPERATIVE INSULIN REGIMEN
Blood glucose level (mMol/L) Rate/hour (units)
Fluid infusion: 10% dextrose(1L) with 20 mmol potassium.insulin infusion: 50U of actropid in 50 ml of 0.9% sodium chloride in a syringe driver.
0-3 0U, call docter immediately
3.1-6 1U
6.1-9 2U
9.1-12 3U
12.1-15 4U repeat after 30 min,call docter if rising
>15 6U, call docter immediately