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decreases CSF leakage. e volume of blood also exerts
pressure against the dura, subsequently increasing CSF
pressure in the subarachnoid space. is pressure increase
transmits to the cranium, reversing the intracranial hypotensive eects, and relaxing stretched meningeal struc-
EBP if deemed necessary. However, if not substantially
responsive to these therapies, clinicians must not rule out
less common etiologies of HA that can develop in patients
post– neuraxial anesthesia, as unfortunately, they are associ-
ated with signicantly increased morbidity and mortality.
tures.1 eoretically any injectate could yield this same
eect, however crystalloid solutions such as normal saline
lack viscosity as well as clotting factors, and any benet
CASE- BASED LEARNING DISCUSSION
in restoring pressure gradients is time- limited due to its
resorption from the epidural space.
Injection of blood, however, introduces autologous
clotting factors into the epidural space, hastening clot formation at the dural puncture to block further CSF leakage
from the intrathecal space.6 Apatient’s in- situ clotting factors will eventually self- repair the puncture, but this process
may take weeks. To improve success, the patient should lie
1. e clinical case represents a UDP. Do you retract the
Tuohy needle and start over, and if so, at what level
should you next attempt epidural placement? Or do
you thread the catheter intrathecally, using it as a spinal
catheter for labor analgesia?
2. What should you explain to the patient about the
circumstances? When is an appropriate time todoso?
supine for 20– 30 minutes immediately following the EBP,
with continuous vital sign monitoring. is allows time
for clot formation at the site of the dural injury, with minimized risk of dislodgement due to CSF leakage, as CSF
pressures are equalized throughout the spinal canal in the
supine position.
Over the next 20– 30 min, the head of the bed can be
3. How do you ensure that this patient has appropriate
follow- up to evaluate for PDPH in the immediate
postpartum period, and for how long should you follow
the patient?
4. e patient develops an HA 12 hours aer delivery.
Would you treat the patient at this time, and if so, how?
incrementally elevated to gradually bring the patient to a
semiupright position as symptoms allow. Within the rst
hour post- EBP, the vast majority of patients should begin to
appreciate an improvement in symptoms, and many experience nearly instant relief. If the patient had been readmitted
5. e patient is diagnosed with PDPH and received
an EBP on postpartum day 2.Her HA returns with
the same intensity the next day. How do you further
manage herHA?
from home for the EBP, he/ she may be discharged at this
point, with instructions to avoid heavy liing, straining, and
any other maneuvers that may promote clot dislodgement.
REFERENCES
e ecacy of one EBP is greater than 70% in completely
resolving PDPH indenitely.1 Unfortunately for some,
either the HA returns, never fully dissipates at all, or symptoms continue to be incapacitating, not amenable to conservative management. Such patients may opt for a repeat EBP
(usually performed at least 24 hours aer last EBP), since the
long- term ecacy increases with successive procedures.
If an HA persists aer repeated EBP, or if a new array of
neurological symptoms develops, it is imperative to review
the dierential diagnosis of PDPH to evaluate whether a
more serious complication should be evaluated. If alternative diagnoses are suspected, it is incumbent on the clinician
or to consult a neurologist to help guide in the continued
management of the patient’s condition.
Headache in the postpartum period is especially common, and if the presentation is consistent with PDPH,
it can be safely managed either conservatively, or with an
1. Sachs A, Smiley R. Post- dural puncture headache:the worst common complication in obstetric anesthesia. Seminars in Perinatology.
2014;38(6):386– 94.
2. Monserrate AE, etal. Factors associated with the onset and persistence of post– lumbar puncture headache. Journal of the American
Medical Association:Neurology. 2015;72(3):325– 32.
3. Choi P, etal. PDPH is a common complication of neuraxial blockade in parturients:a meta- analysis of obstetrical studies. Canadian
Journal Anaesthesia. 2003;50:460– 9.
4. Bardon J, etal. Risk factors of post- dural puncture headache receiving a blood- patch in the obstetric patient. Minerva Anestesiologica.
2016;82:641– 8.
5. Peralta F. e relationship of body mass index with the incidence
of postdural puncture headache in parturients. Anesthesia and
Analgesia. 2015;121(2):451– 6.
6. Turnbull D, Sheperd D. Post- dural puncture headache: pathogenesis, prevention and treatment. British Journal of Anaesthesia.
2013;91(5):718– 29.
7. Loures V, et al. Atypical headache following dural puncture
in obstetrics. International Journal of Obstetric Anesthesia
2014;23(3):246– 52.
416 SECTION D.NEUROLOGICCRISES
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417
8. Malhotra S. All patients with a postdural puncture headache should
receive an epidural blood patch. International Journal of Obstetric
Anesthesia. 2014;23(2):168– 70.
9. Verstraete S, etal. Lower incidence of post- dural puncture headache with spinal catheterization aer accidental dural puncture in obstetric patients. Acta Anaesthesiologica Scandanavia.
2014;58(10):1233– 9.
10. Russel IF. A prospective controlled study of continuous spinal analgesia
versus repeat epidural analgesia aer accidental dural puncture in labour.
International Journal of Obstetric Anesthesia. 2012;21(1):7– 16.
11. Mahoori A, et al. Comparing the eect of pregabalin, gabapentin, and acetaminophen on post- dural puncture headache. Saudi J
Anaesth. 2014;8(3):374– 7.
12. Stein MH, etal. Prophylactic vs therapeutic blood patch for obstetric patients with accidental dural puncture:a randomised controlled
trial. Anaesthesia. 2014;69(4):320– 6.
13. Kokki M, et al. e inuence of timing on the eectiveness of
epidural blood patches in parturients. International Journal of
Obstetric Anesthesia. 2013;22(4):303– 9.
14. Scavone BM, etal. Ecacy of a prophylactic epidural blood patch in
preventing post dural puncture headache in parturients aer inadvertent dural puncture. Anesthesiology. 2004;101(6):1422– 7.
15. Paech MJ, etal. e volume of blood for epidural blood patch in
obstetrics: a randomized, blinded clinical trial. Anesthesia and
Analgesia. 2011:113(1):126– 33.
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SECTIONE
METABOLIC/ ENDOCRINECRISES
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58.
DIABETIC EMERGENCIES INPREGNANCY
Maribeth Guletz and Rebecca Minehart
CLINICALCASE
its incidence is growing.
of pregnancies are complicated byGDM.
An obese, Hispanic, G3P2, female with a history of type I
diabetes mellitus presents at 37 weeks with a 2- day history
of persistent emesis and labor contractions. On examination, she is tachycardic and tachypneic and appears dehydrated with poor capillary rell. Labs are drawn, which
reveal plasma glucose 430 mmol/ L, sodium 142 mmol/ L,
potassium 3.2 mmol/ L, bicarbonate 10 mmol/ L, chloride
100 mmol/ L, urea 8 mmol/ L, and a creatinine of 1.36.
e chest radiograph is normal. A urine dipstick shows
3+ glycosuria and 4+ ketones. Fetal heart rate monitoring is performed, revealing minimal variability with
recurrent late decelerations. e obstetrician determines
this patient should have an urgent cesarean section.
Gestational diabetes mellitus is usually diagnosed aer
20 weeks of gestation, when maternal metabolic adaptations direct glucose and amino acids to the growing fetus.
During a healthy pregnancy, increases in placental hormones, including prolactin and human placental lactogen,
stimulate pancreatic beta cell proliferation, leading to a subsequent increase in insulin secretion. e increased insulin
secretion is accompanied by decreased maternal insulin
sensitivity in the second half of pregnancy, creating what
has been termed the “diabetogenic state” of pregnancy. In
comparison with healthy parturients, women with GDM
have relatively reduced levels of insulin secretion, which,
when combined with impaired insulin sensitivity, results in
higher intrapartum maternal glucose levels.
PATHOPHYSIOLOGY OFDIABETES MELLITUS
Diabetes mellitus is a group of diseases characterized by
chronic hyperglycemia due to insucient insulin action
on target tissues. Glucose metabolism disorders are classied by etiology, and include staging of pathophysiology
based on the degree of insulin activity deciency. ese
e medical literature contains fewer than 100 reports
of pregnancies in diabetic women prior to the advent of
insulin in 1921. ese few untreated diabetic mothers
had >90% infant mortality rate and a 30% maternal mortality rate. Until 1980, diabetic women were counseled to
avoid pregnancy. Advancements in insulin therapy have
greatly enhanced both the management and the safety of
all forms of diabetes in pregnancy.
2– 3
In the United States, up to 14%
4
5– 7
8
disorders are classied into four groups: (I) type 1 diabetes mellitus, (II) type 2 diabetes mellitus, (III) diabetes mellitus due to other specic mechanisms or disease
states, and (IV) gestational diabetes mellitus. As a brief
overview, type 1 diabetes is thought to be precipitated by
an immune- associated destruction of insulin- producing
pancreatic beta cells. Type 2 is characterized by combinations of decreased insulin secretion and decreased insulin
sensitivity.1 Gestational diabetes is the fourth group and is
the primary focus of this chapter.
Gestational diabetes mellitus (GDM) is dened as glucose intolerance rst discovered in pregnancy. It is currently
the most common medical complication of pregnancy and
RISK FACTORS FORGESTATIONAL DIABETES
MELLITUS
Risk factors for the development of GDM include obesity, a
family history of GDM or type II diabetes, polycystic ovarian syndrome, multiple gestation, hypertension, chronic
systemic steroid use, previous macrosomia with shoulder
dystocia, unexplained perinatal loss or malformation, or a
personal history of abnormal glucose tolerance or GDM.
Certain ethnicities are also at increased risk for the development of gestational diabetes, including Hispanic, Native
American, African American, Asian, or Pacic Islander.
9
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DIAGNOSIS OFGESTATIONAL DIABETES
MELLITUS
e following tests can be used to diagnose gestational
diabetes
10– 11
:
• Afasting plasma glucose (FPG) test measures blood
glucose in a person who has not eaten anything for at
least 8 hours. is test is used to detect diabetic and
prediabetic states.
• An oral glucose tolerance test (OGTT) measures
blood glucose aer a person fasts at least 8 hours and
2 hours aer the person drinks a glucose- containing
beverage. is test can be used to diagnose diabetic and
prediabetic states.
• Arandom plasma glucose test, also called a casual
plasma glucose test, measures blood glucose without
regard to when the person being tested last ate. is
test, along with an assessment of symptoms, is used to
diagnose diabetes, but not prediabetic states.
• Test results indicating that a person has diabetes should
TABLE58.2 WHITE CLASSIFICATION SYSTEM OFDIABETES
MELLITUS INPREGNANCY
Type A Abnormal glucose tolerance test at any age or
of any duration treated only by diet therapy
Type B Onset at age 20years or older, and duration
of less than 10years
Type C Onset at age 10- 19years, or duration of
10- 19years
Type D Onset before 10years of age, duration over
20years, benign retinopathy, or hypertension
(not preeclampsia)
Type D1 Onset before age 10years
Type D2 Duration over 20years
Type D3 Calcication of vessels of the leg (macrovascular
disease)
Type D4 Benign retinopathy (microvascular disease)
Type D4 Hyper tension (not preeclampsia)
Type R Proliferative retinopathy or vitreous hemorrhage
Type F Renal nephropathy with over 500 mg/ day
proteinuria
be conrmed with a second test on a dierentday.
Type RF Meets criteria for both types R and F
Pregnant women at low risk for GDM are screened with
a 1- hour OGTT at approximately 26– 28 weeks gestational
Type G Many pregnancy failures
Type H Evidence of arteriosclerotic heart disease
age. Gestational diabetes is diagnosed based on elevated
plasma glucose value approximately 1 hour aer consumption of liquid glucose. If the 1- hour test reveals elevated
blood glucose, the patient must return for a 3- hour OGTT,
during which blood glucose levels are checked four times. If
blood glucose levels are above normal at least twice during
Type T Prior renal transplant
GDM type A1 Controlled by diet and exercise
GDM type A2 Requires insulin
SOURCE: Adapted from Gilmartin ABH, Ural SH, Repke JT. Gestational diabetes mellitus.
Rev Obstet Gynecol. 2008;1(3):129– 34.
the test, the woman has gestational diabetes. Screening is
oen done earlier in patients with known GDM risk factors. Table 58.1 shows the blood glucose levels for diagnos-
TREATMENT OFGESTATIONAL DIABETES
MELLITUS
ing gestational diabetes during a 3- hourOGTT.
e White Classication is used to classify gestational
diabetes (see Table58.2).
Aer the diagnosis of GDM has been established, glucose
monitoring, dietary modications, and a regular moderate
exercise program should be initiated.
Glucose monitoring, both fasting and 2- hour postpran-
TABLE58.1 GESTATIONAL DIABETES DIAGNOSIS:ABOVE-
NORMAL RESULTS FORTHE ORAL GLUCOSE TOLERANCE
TEST OFA 100- G LOAD OVERTHREEHOURS.
Time Plasma Glucose Result (mg/ dL)
Fasting 95 or higher
dial, should be done four times daily with goals < 95 mg/ dL
and < 120 mg/ dL for fasting and 2- hour postprandial levels
respectively. A1- hour postprandial blood glucose level may
also be performed, with a goal of < 140mg/ dL.
Dietary modications should focus on low- fat and high
ber content. e patient should avoid sugar and concen-
1 hour 180 or higher
2 hours 155 or higher
3 hours 140 or higher
trated sweets and eat small, frequent meals. Carbohydrates
should be restricted to 35%– 45% of daily calories.
If a trial of diet control and exercise is insucient and glu-
cose levels remain >20% above fasting or postprandial glucose
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423
goals, then pharmacologic treatment should be initiated.
Options for pharmacologic treatment include oral hypoglycemics, such as metformin or glyburide, or insulin therapy.
resistance, which in turn decreases adipocyte storage of free
fatty acids and leads to production of ketones.
16
Late pregnancy is characterized by a state of insulin
resistance, accelerated starvation, and respiratory alkalosis.
TIMING AND ROUTE OFDELIVERY
e American College of Obstetricians and Gynecologists
(ACOG) states that no evidence- based recommendation
can be made regarding timing of delivery in women with
GDM. Decisions should be guided by local standards
of care. Women with well- controlled GDM should not
be induced before 39 weeks. However, if estimated fetal
weight is above 4,500 grams, counseling regarding elective
cesarean section should be performed. Also, if the patient’s
glucose is poorly controlled or there is evidence of growth
restriction or preeclampsia, delivery earlier than 39 weeks
may be considered.
12
Insulin sensitivity is known to decrease by as much as 56% by
36 weeks of gestation. e production of insulin antagonistic
hormones such as human placental lactogen, prolactin, and
cortisol contributes to insulin resistance.17 Other hormones,
such as human chorionic gonadotropin and progesterone
also play a role. Diabetic pregnant women at more than 20
weeks of gestation are more prone to develop more severe
and rapidly progressive episodes of DKA and at lower glycemic levels (<300 mg/ dL) compared with nonpregnant diabetic women.18 us, DKA remains a critical problem during
pregnancy, as signicant danger may be present at blood glucose levels that usually do not portend severe pathology.
19
Important risk factors for the development of DKA
include starvation resulting from poor nutritional status or
DIABETIC OBSTETRICAL EMERGENCIES
Diabetic ketoacidosis (DKA) is one of the most serious
metabolic complications of diabetes mellitus. During pregnancy, DKA is associated with both maternal and fetal
mortality, and is therefore considered a medical emergency
requiring immediate medical attention. Formerly considered a hallmark of type 1 diabetes mellitus, DKA is now
increasingly reported in individuals with poorly controlled
type 2 diabetes mellitus or GDM.13 e true incidence of
DKA in pregnancy is dicult to ascertain. Data mainly
based on case reports, retrospective studies, and review articles suggest an incidence ranging from 6% to 7% overall,
with 90% of these cases reported in women with GDM.
15
However, this incidence may rise given the increased
frequency of type 2 diabetes mellitus and GDM related to
obesity and advanced maternal age in pregnancy.
persistent vomiting (e.g., hyperemesis gravidarum) leading
to reduced carbohydrate intake and development of DKA
in euglycemic women.
20– 21
Eating disorders may also play
a role in the development of DKA. Other major risk factors in the pregnant population include infections, use of
beta- sympathomimetic agents for tocolysis, steroid use for
fetal lung maturation, and diabetic gastroparesis. In addition, the increased minute alveolar ventilation places the
pregnant women in a state of respiratory alkalosis, resulting
in a compensatory increased renal excretion of bicarbonate.
is excretion results in a lowered buering capacity, which
also contributes to the development of DKA at lower glycemic levels than those seen in nonpregnant patients.22
Finally, fulminant type 1 diabetes mellitus is also a well-
14–
known cause of pregnancy- related DKA.23 ese patients
experience very rapid onset of hyperglycemia followed by
rapid development of DKA with a normalHbA1C.
e majority of patients with DKA in pregnancy
recover with no complications. However, delayed diagnosis
PATHOPHYSIOLOGY
or inappropriate management can result in serious maternal
and perinatal complications. In recent years, the reported
e etiology of DKA is the result of an exaggerated counterregulatory response to a perceived lack of glucose supply
at the cellular level. Without adequate insulin, cells enter
a state of starvation. is state leads to rapid depletion of
glycogen stores, and gluconeogenesis becomes the primary
metabolic pathway. ere are abundant sources of glucose
precursors. During this process of energy substrate creation,
lipolysis results in excess amounts of glycerol released to the
circulation and muscle breakdown results in the release of
amino acids, both of which are readily available as sources
of energy. Lipolysis further increases in the state of insulin
maternal mortality in DKA was less than 1%, while the
reported fetal mortality rate was higher at 9%– 36%.
24– 26
Maternal complications of DKA include acute renal failure,
adult respiratory distress syndrome, myocardial ischemia,
cerebral edema, hyperkalemia resulting in arrhythmia, and
death. Cerebral edema is a rare but potentially fatal complication mostly seen in the pediatric population as a result
of aggressive uid resuscitation, in particular with normal
saline, resulting in a hyperchloremic acidosis.
Perinatal complications include preterm delivery,
hypoxia, acidosis, and fetal loss. e mechanism of fetal loss
DIABETIC EMERGENCIES IN PREGNANCY 423
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during episodes of DKA remains unclear. Massive osmotic
TABLE58.3
diuresis and consequent volume depletion results in reduced
uteroplacental perfusion. Maternal acidemia may also contribute to decreased uteroplacental perfusion and fetal
hypoxia. Hypophosphatemia may cause a decrease in 2,3diphosphoglycerate, resulting in decreased oxygen release
from maternal red blood cells to the fetal circulation.27
Fetal hyperinsulinemia resulting from maternal hyperglycemia increases fetal oxygen requirements by stimulating
the oxidative metabolic pathway,
27,28
impacting fetal oxygen
demand– supply balance. Maternal hypokalemia could also
result in fetal hypokalemia, leading to fatal arrhythmias.
29– 31
Due to these mechanisms, fetal heart rate (FHR) monitoring is recommended in a pregnant patient with DKA and
a fetal gestational age of 24 weeks or more.22 Monitoring
FHR may reveal minimal or absent variability, absent accelerations, repetitive variable, and late decelerations. e fetal
Signs and Symptoms of DKA Management of DKA
Intractable nausea/ vomiting
Abdominal pain, including
uterine contractions
Kussmaul respirations
Lethargy, CNS symptoms
Lab ndings:
• Hyperglycemia
• Arterial pH<7.30
• Anion gap > 12mEq/ L
• Elevated base decit
• Positive urine or serum
ketones
1. Establish large bore IV access,
initiate aggressive uid
resuscitation (1- 2 L/ hr for rst 1- 2
hours)
2. Correction of hyperglycemia with
an IV bolus of regular insulin (8- 10
units) followed by an insulin gtt
(start ~0.1 units/ kg/ hr). Continue
infusion until anion gap has
normalized and serum ketones are
negative.
3. Closely monitor for hypokalemia
and hyperchloremia. Replete K to a
goal of 4- 5MEq/ L.
4. OB population:monitor fetal heart
rate tracing, biophysical prole, and
fetal Doppler studies.
5. Search for underlying etiology.
biophysical prole can be abnormal, and Doppler studies
may reveal redistribution of blood ow. Aer uid resuscitation and correction of maternal metabolic abnormalities,
the fetal tracing should improve within 4– 8 hours.
32
ere has also been a reported association between
elevated ketoacids during pregnancy and lower IQ scores,
as well as decreased mental development during the second
year of life.33 e fetal brain is susceptible to increased levels
of [beta]- hydroxybutyrate and lactate concentrations, which
decrease glucose uptake by the fetal brain. ese substances
2 diabetes mellitus, it is not well described in pregnancy.
Hyperosmolar hyperglycemic state is distinguished from
DKA primarily by the absence of serum ketones, in the
presence of a glucose level of >600 mg/ dL and increased
plasma osmolality >320 mOsm/ kg.37 Since it confers a
higher mortality than DKA, obstetric care team providers
should remain vigilant for any metabolic derangements in
their pregnant diabetic patients.
may accumulate in the basal ganglia of children during DKA,
leading to poor myelination and cortical connectivity.
34
MANAGEMENT OFDIABETIC KETOACIDOSIS
ASSESSMENT OFTHE PATIENT AND DIAGNOSIS
e assessment and management of DKA is outlined in
Table 58.3. Signs and symptoms of DKA tend to develop
faster during pregnancy than in the nonpregnant state,
and providers should maintain a high level of suspicion
for diagnosis. Concerning physical symptoms include
intractable nausea and vomiting, abdominal pain including uterine contractions, Kussmaul respirations with
a fruity odor, or lethargy and central nervous system
manifestations including disorientation, obtundation,
and even coma from cerebral edema. Laboratory ndings include hyperglycemia, arterial pH less than 7.30, an
anion gap greater than 12 mEq/ L, elevated base decit,
and positive serum/ urine ketones. In the setting of DKA
in a patient with type 1 diabetes mellitus, point- of- care
[beta]- hydroxybutyrate capillary ketone testing is routinely used.
35,36
While hyperosmolar hyperglycemic state (HHS) is
a serious complication occurring in patients with type
424 SECTION E. METABOLIC/ENDOCRINE CRISES
Upon diagnosis of DKA, prompt and aggressive treatment
with a low threshold for admission to the intensive care unit
is mandatory. Management should be provided by physi-
cians with expertise in this condition, including consultants
where appropriate. e treatment of DKA in a pregnant
patient is the same as the nonpregnant state, with the addi-
tion of fetal monitoring depending on gestational age.
Treatment includes aggressive volume replacement, intra-
venous insulin therapy, correction of acidosis and electro-
lyte disturbances, correction of underlying pathology, and
intensive monitoring of both maternal and fetal response to
treatment. Precipitating factors such as infection and beta-
agonist agents should be ruledout.
Initial goals should include establishing large bore IV
access to initiate aggressive uid resuscitation with normal saline. e uid decit is typically 100 mL/ kg of body
weight. Seventy- ve percent of this uid decit should
be replaced within the rst 24 hours. Much literature
in non- diabetic- ketoacidotic patients has demonstrated
that large volumes of normal saline administered can lead
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425
to hyperchloremic metabolic acidosis.38 However, a study
evaluating resuscitation of patients who present with
DKA in whom isotonic normal saline is administered,
compared with lactated Ringer’s solution, found that
there was actually increased time to normalization of glucose levels as well as pH, with no other perceived clinical
benet to using lactated Ringer’s.39 Without additional
high- quality evidence to the contrary, isotonic saline
remains the preferred crystalloid in DKA, and should
be administered at a rate of 1– 2 L/ hr for 1– 2 hours,
then 250– 500 mL/ hr to obtain glucose levels less than
250 mg/ dL. Aer therapy has achieved a blood glucose
level of 250 mg/ dL or less, it is advised to switch to an
intravenous solution with 5% dextrose to avoid overcorrection and hypoglycemia. Aggressive uid resuscitation
should be accompanied by correction of hyperglycemia
with an intravenous bolus of regular insulin (8– 10 units)
followed by an insulin infusion starting at 0.1 units/ kg/
hr. e insulin drip should be continued until the serum
bicarbonate and anion gap have normalized and serum
ketones are negative. Prior to discontinuing the insulin
infusion, an additional subcutaneous dose of regular
insulin should be administered.
40
While treating DKA, a patient should be closely monitored for electrolyte disturbances, specically for hypokalemia and hyperchloremia. Serum levels may appear normal
or elevated, but the total potassium decit is typically 5– 10
mEq/ L. With the administration of insulin, uid resuscitation, and correction of acidosis, potassium shis from
the extracellular to the intracellular space. Prevention of
hypokalemia is vital to prevent arrhythmias; thus, potassium should be repleted to 4– 5 mEq/ L with IV potassium chloride. Phosphorus may also need to be repleted.
Administration of bicarbonate is associated with alkalosis
or worsening academia secondary to increased partial pressure of carbon dioxide, leading to impaired fetal oxygen
transfer.
16
Based on the severity and duration of DKA, the fetal
heart rate tracing, biophysical prole, and fetal Doppler
studies, a decision must be made to continue the pregnancy
ADDITIONAL COMPLICATIONS OFDIABETES
INPREGNANCY
Besides the acute metabolic derangements of DKA, parturients with all forms of diabetes are at risk for additional
maternal and fetal or neonatal complications.
Maternal gestational diabetes is associated with a
higher rate of fetal macrosomia,41 which predisposes both
the mother and child to additional complications. Amacrosomic fetus confers a greater risk of shoulder dystocia,
maternal genital tract lacerations, uterine atony, and uterine rupture. A few possible fetal complications include
intrauterine demise, premature birth, brachial plexus injury
during delivery, neonatal hypoglycemia, neonatal jaundice,
and congenital cardiac and neural tube defects.
41,42
Any
fetal concerns during labor and delivery may necessitate
an emergent cesarean delivery, a mode of delivery that is
higher in diabetic mothers when compared with nondiabetic mothers.
42
In addition, the altered immune state of pregnancy
combined with diabetes may predispose these women to
higher rates of infection, which in turn may lead to worsened sepsis, a noted complication that is on the rise.43
While a recent study did not nd an increased risk of
uncomplicated sepsis in diabetic pregnant women versus the nondiabetic pregnant population, the authors
found an increase in progression to septic shock in pregnant women with diabetes (adjusted odds ratio 1.47,
p=0.014).
44
Polyhydramnios may result from poorly controlled
diabetes during pregnancy and is a risk factor for uterine
atony, which itself is the most common precursor for postpartum hemorrhage.45 Postpartum hemorrhage itself is an
obstetric emergency (see the chapter “Severe Peripartum
Hemorrhage”) needing specic interventions, and remains
a leading cause of maternal mortality.
3
Finally, diabetes in pregnancy and preeclampsia appear
to occur together at a more frequent rate, and women who
develop hypertension and renal dysfunction during pregnancy have increased cardiovascular morbidity and mortality in later life.
46
or proceed with delivery. Diabetic ketoacidosis itself is not
an indication for emergent delivery, as it may lead to unnecessary delivery of a hypoxic and acidotic neonate. It is most
CONCLUSION
important to stabilize the maternal condition rst, which
allows intrauterine fetal resuscitation. However, if fetal
status does not improve or the maternal condition continues to deteriorate despite therapy, delivery is warranted. If
maternal condition improves with treatment, it may be safe
to continue the pregnancy.
40
Diabetic ketoacidosis is a recognized diabetic emergency, and treatment can be additionally complicated
in the pregnant patient due to associated maternal and
fetal comorbidities. While uid resuscitation, glucose
management, and resolution of acidosis and electrolyte
DIABETIC EMERGENCIES IN PREGNANCY 425
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