Author
Information
Sarita Channawar*, Madhva Prasad**, Neha Jain***, Anahita
R. Chauhan****
(*
Assistant Professor, **Registrar, *** Second Year Resident, **** Additional
Professor Department of Obstetrics and Gynecology, Seth
G.S. Medical
College and K.E.M
Hospital , Mumbai , India
Abstract
Diabetic
ketoacidosis (DKA) is a complication seen in type 1 diabetes mellitus (DM) but
can also occur in pregnancies complicated by type 2 DM or gestational diabetes
mellitus (GDM). DKA is a medical emergency with high maternal and fetal
mortality, and requires treatment in an intensive care setting. Prompt
recognition and resuscitative therapy improves medical and obstetric outcomes.
This report of DKA in a case of GDM provides insight into pathophysiology and
successful management.
Introduction
Normal
pregnancy is characterized by a state of decreased insulin sensitivity,
accelerated lipolysis and ketogenesis.[1, 2, 3, 4] The concentration
of serum ketones is estimated to be two to four times greater than in
nonpregnant state.[1, 5] Despite these changes, the incidence of DKA
in pregnant diabetics is only 1 to 3%.[2, 3] Fetal mortality rates
of 30 to 90% in the past have now decreased to 9% due to improvements in
neonatal and diabetic management.[2, 3]
Case History
A 22 year
old primigravida with 34+6 weeks of gestation was referred to our tertiary care
center with giddiness, polyuria, polydipsia, candidial vagina discharge and
deranged blood sugars (fasting blood glucose 280 mg/dl and post-meal value 410 mg/dl
a few days back). She had stable vital signs, 34 weeks’ sized relaxed gravid
uterus with cephalic presentation and normal fetal heart sounds. She had been
diagnosed by her primary care obstetrician as GDM one month earlier and
referred to us; however she did not report nor was she on any treatment. Recent
sonography revealed oligohydramnios (amniotic fluid index 7 cm) but no fetal
malformations.
A
diagnosis of DKA was made. She was urgently hospitalized. Her hemoglucotest
(HGT) on admission was 590 mg%, urinary sugars were 3+, urinary ketones 2+,
venous blood gas (VBG) analysis showed pH of 7.32, bicarbonate of 17.3
meq/L, sodium of 125 meq/L and potassium of 3.9 meq/L. She was initially
hydrated with normal saline (NS) 1liter over 1 hour, followed by 500 ml NS with
20 ml potassium chloride (KCl) over the next hour, and continued on 500 ml NS
with 10 ml KCl over next 4 hours. Insulin therapy was initiated with bolus dose
of 16 units human insulin subcutaneously followed by insulin drip (50 units in
500 ml NS at 70 ml/h). Monitoring was performed with hourly HGT, 4 hourly
urinary sugars/ketones, and 6 hourly serum electrolytes and VBG. The patient
stabilized on insulin drip: blood sugar value was 314 mg% after 3 hours, which
reduced over 10 hours to 115mg%. Urine ketones also disappeared. Hence insulin
drip was discontinued. Fetal heart rate monitoring was done while on insulin
drip and was normal. She was converted to high doses of subcutaneous regular and
isophane human insulin (20 + 30 units respectively), and maintained on thrice
daily doses which were tapered gradually, along with diabetic diet, so as to
maintain her blood glucose levels within normal range. The patient was managed
jointly with the endocrinologist. She remained hospitalized, blood sugars were
monitored six times a day and insulin was continued with good glycemic control.
Fetal assessment was done clinically with daily fetal movement count, nonstress
test on alternate days and weekly Doppler studies, all of which were normal.
Labor was induced electively at 37 weeks’ gestation; however emergency LSCS was
done for failed induction and she delivered a healthy female weighing 2.6 kg.
Postoperatively her blood sugars were normal; and insulin was not required. She
was managed on diabetic diet and oral hypoglycemic agent Metformin 250 mg twice
daily for 10 days, after which it was omitted and she was discharged.
Discussion
Diabetic
ketoacidosis is a life-threatening, acute metabolic state due to insulin
deficiency. Hence all patients with diabetes in pregnancy including GDM
patients should be monitored for DKA. Low levels of insulin cause increased
gluconeogenesis while decreasing glucose uptake and utilization. Increased
levels of counter-regulatory hormones (glucagon, cortisol, catecholamines and
growth hormone) accelerate the development of ketoacidosis by increasing
gluconeogenesis, glycogenolysis, ketogenesis and insulin resistance. Insulin
deficiency also leads to high anion gap metabolic acidosis. Hyperglycemia and
hyperosmolality in patients with DKA produce the characteristic osmotic diuresis
causing intravascular volume depletion; if not corrected by intravenous fluids
and insulin, DKA can rapidly progress to a state of poor tissue perfusion,
diminished cardiac and renal function, multisystem failure and death. A number
of physiological changes during pregnancy influence carbohydrate and fat
metabolism.[2, 3, 4]
- Placental lactogen and increased cortisol contribute to increased insulin resistance, particularly later in pregnancy.
- Pregnant women have respiratory alkalosis with decreased serum bicarbonate concentrations and reduced capacity to buffer organic acids.
- Pregnancy being an accelerated state of starvation, overnight fast can increase lipolysis and ketone body concentrations 2-4 times greater than in nonpregnant state.[1, 5]
- Predisposing factors for DKA include stress of labor, cessation of insulin therapy, use of β-sympathomimetic agents and emesis with accompanying dehydration.
- Both fetus and placenta utilize large quantities of glucose resulting in lower maternal fasting glucose levels.[2, 3, 4 ]
Hence DKA
in pregnancy can develop more rapidly and at lower serum glucose concentrations
often causing delay in the diagnosis.[2, 3, 4] Several cases of
“normoglycemic” DKA have been reported, although in almost every case glucose
has exceeded 130 mg/dl. Our patient had
levels of 590 mg%, low bicarbonate concentration, positive anion gap and VBG pH
of 7.3 suggestive of acidosis; possibly starvation ketosis contributed to
development of high anion gap metabolic acidosis. Management
principles in DKA include aggressive volume replacement, intravenous insulin
therapy, correction of acidosis and electrolyte abnormalities, and management
of precipitating factors, as well as monitoring of maternal-fetal response to
treatment. Nonreassuring fetal heart rate pattern may be seen due to associated
fetal hypoxemia and acidosis, but correction of maternal metabolic
abnormalities should be a priority and delivery considered only after maternal
stabilization if indicated. Prevention strategies include education of diabetic
pregnant women about the risks of DKA, precipitating factors, and the
importance of timely reporting of signs and symptoms. A multidisciplinary
approach including obstetrician, endocrinologist, intensivist and neonatologist
is necessary for good outcome.
References
1.
Carroll MA, Yeomans ER. Diabetic ketoacidosis in
pregnancy. Crit Care Med 2005;33: S347–S353.
2.
Kamalakannan D,
Baskar V, Barton DM, Abdu TAM. Diabetic ketoacidosis in pregnancy. Postgrad Med
J 2003;79: 454–457.
3.
American College
4.
Kitabchi AE, Umpierrez GE, Murphy MB, Barrett
EJ, Kreisberg RA, Malone JI et al. Management of hyperglycemic crises in
patients with diabetes. Diabetes Care 2001;24:131–153
5.
Sibai BM, Viteri OA. Diabetic ketoacidosis in
pregnancy. Obstet Gynecol 2014;123(1): 167-78.
Citation
Channawar
S, Madhva Prasad M, Jain N, Chauhan AR. An Unusual Case of Hyperemesis
Gravidarum. JPGO 2014 Volume 1 Number 5 Available from: http://www.jpgo.org/2014/05/successful-management-of-diabetic.html