CLINICAL OBSTETRICS AND GYNECOLOGY
Volume 00, Number 00, 000–000
Endocrine
Emergencies
in Obstetrics
CHRISTOPHER G. GOODIER, MD
Department of Obstetrics and Gynecology, Division of Maternal
Fetal Medicine, Medical University of South Carolina,
Charleston, South Carolina
Abstract: Endocrine emergencies in pregnancy can be
life threatening and are associated with increased
morbidity for both the mother and fetus. Thyroid
storm, diabetic ketoacidosis, and hypercalcemic crisis
require a high clinical suspicion, rapid treatment, and
multidisciplinary care to ensure best outcomes. Crit-
ical care consultation and intensive care unit admis-
sion are often warranted. Fetal testing may initially be
concerning; however often improves with correction
of the underlying metabolic derangement(s) and de-
livery is generally avoided until maternal status
improves.
Key words: pregnancy, diabetic ketoacidosis, thyroid
storm, hypercalcemia
Thyroid Storm
Occurring in 1% to 2% of pregnant women
with hyperthyroidism, thyroid storm is a
rare but life-threatening endocrine emer-
gency characterized by a severe hyperme-
tabolic state precipitated by an excess of
endogenous thyroid hormones. It typically
has an acute onset and is diagnosed based
Correspondence: Christopher G. Goodier, MD,
Department of Obstetrics and Gynecology, Division
of Maternal Fetal Medicine, Medical University of
South Carolina, 96 Jonathan Lucas St. Suite 634,
Charleston, SC 29425. E-mail: goodier@musc.edu
The author declares that there is nothing to disclose.
CLINICAL OBSTETRICS AND GYNECOLOGY
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Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved.
on a constellation of symptoms, including
fever, tachycardia, and central nervous sys-
tem dysfunction (restlessness, altered men-
tal status, and seizures). If not treated, it
can ultimately lead to cardiac dysrhythmia,
multiorgan failure and even death. Case
fatality rates range from 10% to 30% in the
literature.1 Given the severity of the disease
process, a high clinical suspicion, rapid
recognition, intervention, and supportive
care are needed to maximize the maternal
and fetal outcome.
Although the exact triggering mecha-
nism is unknown, most cases are due
to poorly controlled disease. Preceding
events include such as preeclampsia,
trauma, surgery, infection, stress, and
ketoacidosis have been associated with
storm.2,3 A careful search for underlying
associated etiologies should be per-
formed.
A high clinical suspicion is needed as the
presenting signs and symptoms may be non-
specific enough to be confused with any
number of other conditions.4 Elevated blood
pressure, headaches, abdominal pain and
even pulmonary edema or heart failure are
features compatible with preeclampsia that
/ VOLUME 00 / NUMBER 00 / ’’ 2019
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2 Goodier
may make the diagnosis of thyroid storm
more difficult.5
Overt signs of hyperthyroidism such as
a goiter, thyroid bruit, or exopthalmos
may be discriminating physical signs that
are more specific to thyroid dysfunction.
Interpretation of maternal acid-base sta-
tus must take into consideration the mod-
erate compensated respiratory alkalosis
that occurs in pregnancy. These metabolic
changes can lead to fetal heart rate tracing
abnormalities, including tachycardia, loss
of variability, and late decelerations ulti-
mately resulting in increased fetal mor-
bidity and mortality.6
Laboratory analysis includes thyroid-
stimulating hormone, free tri-iodothyronine
(FT3) and free thyroxine (FT4), complete
blood count, and complete metabolic panel.
Thyroid-stimulating hormone is usually low/
undetectable in thyroid storm, although cau-
tious interpretation is required in the first
trimester due to the human chorionic gona-
dotropin effect on the thyroid gland. FT4 and
FT3 are often well above the upper limits
of normal in pregnancy. Total hormone
levels are also usually elevated. There are
no generally accepted levels at which the
diagnosis of thyroid storm is assured, and
there may be significant laboratory overlap
with simple hyperthyroidism. There is typi-
cally an associated leukocytosis as well as
evidence of hyperglycemia, hypercalcemia,
elevated liver enzymes, and electrolyte dis-
turbances on metabolic panel screening.
Given a high incidence of case fatality
rates and the need for early recognition,
Burch and Wartofsky7 have outlined a
commonly cited clinical scoring system for
the probability of thyroid storm. Points are
allocated for elevation in temperature, ma-
ternal pulse, and a number of organ system
dysfunctions indicating a high, medium, or
low probability of the diagnosis. Thyroid
imaging is of limited benefit; although a
chest x-rays and/or computed tomographic
scan can be useful when looking for asso-
ciated precipitating factors such as infections
or pulmonary embolus.
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A diagnosis of thyroid storm requires
prompt intervention for both mother and
fetus. Thyroid storm is considered a med-
ical emergency and multidisciplinary care
is required, including maternal fetal med-
icine, endocrinology, neonatology, and
critical care specialists. In addition, prep-
aration should be made for admission to
an intensive care unit, with the availabil-
ity of continuous fetal monitoring if the
fetus has reached viability. Efforts to
correct the underlying maternal metabolic
derangement(s) are key in order to im-
prove the underlying fetal status. It is
important to exhaust all attempts to
correct the underlying maternal abnor-
malities before intervening for the fetus,
as often correction of the underlying
metabolic abnormality will improve fetal
status.8 The presence of a persistent fetal
bradycardia or the development of cat-
egory III heart rate tracing that is unre-
sponsive to resuscitative measures may
require expedited delivery.
Intravenous access should be obtained and
cooling measures performed. Fluid balance
and vital signs, including continuous pulse
oximetry need to be carefully monitored. An
initial echocardiography (EKG) and contin-
uous telemetry is recommended, as arrhyth-
mias, such as atrial fibrillation can occur. In
addition some patients can have thyrotoxic
heart failure due to the myocardial effects of
excess free T4. Any cardiorespiratory com-
plaints should be thoroughly evaluated in-
cluding EKG. Treatment is generally the
same for thyroid storm and thyrotoxic heart
failure. Respiratory failure is generally not
associated with thyroid storm; however can
occur and intubation and mechanical venti-
lation is sometimes necessary.
In addition to supportive care, treatment
of thyroid storm involves the use of several
medications to decrease the level of thyroid
hormone. Propylthiouracil (PTU) and me-
thimazole (MMI) are thionamides and act
within the thyroid gland to inhibit follicular
growth and development, as well as the
packaging of iodothyronines into T4 and

T3.9 PTU has the advantage of antithyroid
effects within the thyroid gland as well as
inhibiting the peripheral conversion at the
tissue level, limiting the active form of
thyroid hormone. However, there is a sig-
nificant disadvantage of the use of PTU in
that there have been rare cases of fulminate
liver failure and death associated with its
use, including instances in pregnancy.
There is a Food and Drug Administration
“black box” warning for PTU concerning
this link to hepatotoxicity. It is unclear how
thyroid storm specifically affects this risk.
MMI use in pregnancy has been linked to
some teratogenic effects, specifically aplasia
cutis and choanal atresia.10 In addition,
rarely a life-threatening agranulocytosis
may develop after MMI use. Given these
conflicting risks there is no clear recom-
mendation for which thionamide to initiate
in thyroid storm.
The use of an iodide-containing medica-
tion inhibits the further release of active
thyroid hormone from the thyroid gland.
Oral potassium iodide, 5 drops every 8 hours,
or IV sodium iodide 500 to 1000 mg every 8
to 12 hours may be used. One of the side
effects of iodine agents is the paradoxical
release of thyroid hormone from the thyroid
gland, thus it is important to start iodine
administration ~1 hour after the use of
thionamides.9 Corticosteroids are also impor-
tant in the treatment of thyroid storm due to
the effect of decreasing systemic inflamma-
tion as well as peripheral effects of decreasing
T4 to T3 conversion. Beta-blockers such as
propranolol will reduce peripheral conversion
of T4 to T3, and lessen the complications of
tachycardia including high output cardiac
failure. Long-term use of beta-blockers has
been associated with fetal growth restriction,
but is generally considered safe in a risk/
benefit consideration. Other supportive med-
ications include antipyretics such as acetami-
nophen (Table 1).
Conventional treatments may fail after
trials of medical management in the most
severe cases. There also may be adverse
reactions to the thionamides which may
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Endocrine Emergencies in Obstetrics 3
require discontinuation. Emergency thyroi-
dectomy, with or without plasmaphoresis has
been described successfully in thyroid storm,
but must be considered high risk and last line
treatment.11
In summary, thyroid storm is a rare,
life-threatening condition which requires
early recognition, multidisciplinary care,
and aggressive therapy.
Diabetic Ketoacidosis (DKA)
DKA is a medical emergency, which can
result in both maternal and fetal morbid-
ity and mortality. Before the discovery of
insulin it was uniformly fatal. With early
recognition and aggressive multidiscipli-
nary management, the overall incidence
has decreased from ~10% to 20% in the
late 1970s to ~1% to 2% in most recent
reports,3,12,13 resulting in improved ma-
ternal and fetal mortality. Preterm birth,
both from premature labor and from
medical intervention, is a common occur-
rence after DKA.
The pathophysiology of DKA occurs due
to the lack of insulin resulting in a perceived
hypoglycemia at target cells such as those in
the liver, adipose, and muscle tissues. As
a result, stores of glucagon are released,
worsening the hyperglycemia and causing
osmotic diuresis, hypovolemia, and elec-
trolyte depletion.
Counter regulatory hormones in the adi-
pose tissue cause the release of free fatty acids
into the circulation which are then oxidized to
ketone bodies. Ultimately a metabolic acido-
sis ensues which manifests as an anion gap on
blood chemistry. Ketoacids bind sodium and
potassium, which are excreted in the urine,
further worsening the electrolyte balance. If
untreated, patients can experience cardiac
dysfunction, decreased tissue perfusion, and
worsened real function leading to shock,
coma, and death.3,14
The normal physiological changes of
pregnancy increase the susceptibility to
DKA. Insulin resistance primarily attribut-
able to human placental lactogen causes
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4 Goodier

TABLE 1. Thyroid Storm Treatment

Treatment Dose
Maternal Supportive care
IV access LR bolus then IVF at 150-250 mL/h
Continuous pulse oximetry, serial BP
Consultation ICU admission, critical care, endocrine, maternal fetal
medicine
Cooling measures Acetaminophen 500 mg q6 h
Cooling blankets
Testing
Laboratory TSH, FT3/4, CBC diff, ABG, CMP
Ancillary EKG/telemetry, CXRAY, echocardiogram
Additional testing as needed (cultures, CT scan, etc.)
Medications
First line PTU 300 mg PO or NG q6 h
Initial dose given was 30-60 Potassium iodide (SSKI) 5 drops PO/NG q8 h
min after PTU
Block T4- > T3 conversion Dexamethasone 2 mg IV q6 h×4 doses
Heart rate control (goal <120 Propranolol 40-60 mg PO/NG q 6 h (IV
bpm)* alternative = propranolol prn or esmolol gtt)
Fetal
Monitoring Consult maternal fetal medicine
Initiate fetal monitoring if viability achieved
Fetal optimization Maternal left lateral decubitus
Maternal O2 supplementation
Stabilize maternal condition before delivery

*Ensure no evidence of heart failure or medical contraindication (eg, Asthma).

ABG indicates arterial blood gas; BP, blood pressure; CBC, complete blood count; CMP, comprehensive metabolic panel;
CT, computed tomography; EKG, echocardiography; FT3, free tri-iodothyronine; FT4, free thyroxine; ICU, intensive care unit;
IV, intravenous; IVF, in vitro fertilization; LR, lactated ringers; NG, nasogastric; PTU, propylthiouracil; TSH, thyroid-
stimulating hormone.

insulin requirements to increase with ad-
vancing gestation. Respiratory adaptations
during pregnancy result in a compensated
maternal respiratory alkalosis. The com-
pensatory decrease in serum bicarbonate
reduces the body’s normal buffering
capacity, thus predisposing the patient to
DKA.3,12,14
Patients generally present with abdominal
pain, malaise, persistent vomiting, increased
thirst, hyperventilation, tachycardia, dehy-
dration, and polyuria. As the level of acidosis
worsens altered mental status can occur. The
diagnosis is confirmed with documentation
of hyperglycemia, acidosis, and ketonuria.
Other laboratory findings include anion gap,
ketonemia, renal dysfunction, and possible
electrolyte abnormalities.12,14 Typically pa-
tients present with severely elevated serum
glucose levels; however DKA can occur with
levels <200 mg/dL in pregnancy.13
Common precipitating factors in
pregnancy include emesis, infection, beta-
sympathomimetic tocolytic agents, corti-
costeroids, poor compliance, and medical
errors.15,16 Although beta-sympathomi-
metics (eg, terbutaline) are not routinely
used for prolonged ( > 48 h) tocolysis due
to the Food and Drug Administration
safety communication in 2011, it is impor-
tant to remember that they should be used
very cautiously, if ever, for patients with
diabetes.3
Although the mechanism is not clearly
understood, DKA presents a significant
risk to overall fetal well-being. The likely
mechanism is related to maternal ketoacids
which cross the placenta leading to decreased

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fetal tissue perfusion and oxygenation.14 The
fetus has a limited ability to buffer significant
acidemia, and therefore is quite sensitive to
maternal acidosis.
This often results in alterations of the
fetal heart rate tracing, including decreased
variability and/or late decelerations. It is
important to exhaust all attempts to correct
the underlying maternal abnormalities be-
fore intervening for the fetus.13,14
Like thyroid storm, DKA is considered a
medical emergency and a multidisciplinary
team, including maternal fetal medicine,
endocrinology neonatology and critical care,
should be assembled. In addition, strong
consideration should be made for admission
to an intensive care unit.
Treatment includes adequate IV access
and placement of an indwelling urinary
catheter. Significant fluid deficits should
be anticipated and corrected, insulin
should be started and electrolyte abnor-
malities corrected. Fluid balance and vital
signs need to be carefully monitored and
documented.
Basic laboratory analyses, including a
complete metabolic panel with magnesium
and phosphorous, complete blood count
with differential, urinalysis, fingerstick blood
glucose, arterial blood gas, and serum ke-
tones should be collected. Additional testing
(urine culture, blood culture, chest x-ray,
etc.) should be performed based on clinical
suspicion and any potential underlying proc-
esses. Initially, serum ketones, electrolytes,
and maternal acid/base status should be
monitored every 2 hours until ketosis and
acidosis are resolved. Blood sugars should be
collected hourly during this time to titrate
insulin.3,12,14,17,18
Once viability is confirmed, fetal mon-
itoring should be initiated. As noted, the
fetal heart tracing will likely appear concern-
ing during the initial phase of metabolic
compromise. Maternal oxygen supplementa-
tion and left lateral decubitus positioning
should be used to increase blood flow to
fetus and improve oxygenation. Adequate
hydration and correction of acid/base
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Endocrine Emergencies in Obstetrics 5
derangements must be started. Delivery is
generally postponed until after maternal
metabolic condition is stabilized, as this will
usually correct the fetal heart tracing abnor-
mality. There are exceptions, including se-
verely prolonged bradycardia or a persistent
category III tracing.
Table 2 illustrates a general algorithm for
treatment of DKA in pregnancy, including
rehydration, reduction of hyperglycemia,
correction of acid-base and electrolyte im-
balance while searching for and treating the
underlying etiology.3,12,14,17,18
The hypovolemia associated with
DKA is estimated at 100 mL/kg of total
body weight and is typically 4 to 10 L.19
Initially, aggressive intravenous replace-
ment with isotonic normal saline should
be started with the goal to replace ~75%
of the overall deficit within the first
24 hours. Hypotonic fluids (eg, lactated
ringers and 0.45% saline) should be
avoided initially as they can cause a rapid
decline in plasma osmolarity leading to
cerebral edema. Blood glucose values
should be monitored hourly and once
the serum glucose reaches <250 mg/dL,
IV fluids should be switched to D5-0.45%
normal saline.
Intravenous insulin administration should
be undertaken immediately to aid in low-
ering of the blood glucose levels. Subcuta-
neous and intramuscular are typically
avoided due to the slower onset of action,
which is worsened in DKA.3 The initial
blood glucose target is 150 to 200 mg/dL in
order to avoid rapid correction and resulting
complications. It is important to remember
that insulin requirements can be significant
and most protocols suggest an initial bolus
dose of 10 to 20 units of regular insulin,
followed by an infusion rate of 5 to 10 units/
h. This amount should be increased if the
blood glucose values do not fall 20% to 25%
over 2 hours.
It is important to continue the insulin
infusion until the anion gap is closed
and acidosis resolved. This can take
significantly longer than correcting the
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6 Goodier
TABLE 2. Treatment of DKA
Treatment Modality
Maternal Identify cause
Fluid replacement (estimated
~100 mL/kg)
Insulin administration
Goal FSBG 150-200 in DKA
Laboratory evaluation
Fetal
Monitoring
Fetal optimization
CMP indicates comprehensive metabolic panel; DKA, diabetic ketoacidosis; FSBG, fingerstick blood glucose; ICU, intensive
care unit; IV, intravenous; Phos, phosphorous; SQ, subcutaneous.
hypoglycemia and typically takes 12 to
24 hours. Once it is deemed safe to
transition to subcutaneous insulin, the first
dose should be given before the discontin-
uation of the intravenous infusion to de-
crease the risk of recurrent ketoacidosis.
Potassium is the most common electro-
lyte abnormality in DKA, although levels
are often normal initially. The actual
deficit is estimated at 5 to 10 meq/kg.
Once the serum potassium level falls
below 5 mmol/L, IV replacement should
begin with the goal to maintain potassium
levels between 4 and 5 mmol/L. Adequate
renal function should be documented
before replacing potassium. Serum potas-
sium levels should be checked every 2 to
4 hours as significant hypokalemia can
precipitate a cardiac arrhythmia.
Replacement of low serum bicarbonate
levels remain a source of controversy and
replacement is generally agreed upon if the
patients pH is <7.0. Some studies have shown
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Plan
H&P, rule out infection, place foley catheter, serial vital signs,
I/0’s
Consider ICU admission
Consult critical care, endocrinology, maternal fetal medicine
Correct 75% total deficit in first 24 h
Begin with 0.9% normal saline
Convert to D5-0.45% normal saline when FSBG < 250
Regular insulin via IV
IV bolus 0.1units/kg followed by 0.1 u/kg/h continuous
infusion
Goal reduction 20%-25% over 2 h (if not increase IV infusion
1.5-2×)
Continue IV insulin until acidosis and ketosis resolves
Start SQ insulin therapy 1-2 h before stopping IV insulin
CMP/Mg and Phos, pH, serum ketones every 2-4 h initially
Replete K+ once <5 mmol/L (goal 4-5)
Replete HCo3 if pH < 6.9 with NaHCo3 until pH > 7.0
Consult maternal fetal medicine
Initiate fetal monitoring if viability achieved
Maternal left lateral decubitus, maternal O2 supplementation,
stabilize maternal condition before delivery
that routine replacement of low serum levels
of bicarbonate have not proven beneficial in
DKA and may cause unnecessary maternal
and fetal complications. Replacement can
delay the correction of ketoacidosis in the
maternal bloodstream and, if corrected to
rapidly, elevate fetal PC02 impairing fetal
ability to maintain adequate O2 transfer.3,18
Hyperparathyroidism
Primary hyperparathyroidism (pHPT) is
the third most common endocrine disor-
der (prevalence: 0.1% to 0.4% in the
general population) and rare in preg-
nancy. In a review by Ruda et al20 solid
parathyroid disorders account for 80% of
cases in the general population, with the
remaining cases a result of diffuse hyper-
plasia and adenomas.
The diagnosis requires an elevated total
calcium level adjusted for serum albumin
[serum calcium+0.8×(4−serum albumin)]

or elevated serum ionized calcium level
with an elevated parathyroid hormone
level. Patients with hyperparathyroidism
caused by a parathyroid adenoma or hyper-
plasia typically have inappropriately high
PTH secretion in relation to the serum
calcium concentration.
Symptoms typically include nausea, vom-
iting, anorexia, constipation, depression, and
mental confusion. Kidney stones, pancreati-
tis, abdominal pain as well as EKG changes
including short QT interval and arrhythmia
can be seen.
In pregnancy most patients are asympto-
matic and undiagnosed, as routine calcium
levels are not checked. In addition, nausea
and vomiting is common in pregnancy and is
more commonly associated with pregnancy
associated physiological changes.21
Once the diagnosis of hyperparathyr-
oidism is ascertained, careful search for
the underlying etiology should begin.
Although less sensitive, imaging via ultra-
sound is the first line modality to screen
for determination of mass as it offers less
radiation compared with computed
tomographic scan.
As noted above, there are many cases of
asymptomatic pHPT that go undiagnosed
in pregnancy. In pregnancy the most
common presenting symptom is renal colic
secondary to nephrolithiasis.22 pHPT is
more often associated with pancreatitis in
the pregnant population (7% to 13%) than
in the nonpregnant state. This is thought to
be secondary to elevated serum calcium
levels resulting in damaged pancreatic
ducts.23 Other clinical findings that can
be seen in pregnancy include hypertension
and preeclampsia.
pHPT does not seem to be associated with
increased risk of miscarriage; however with-
out treatment fetal complications can be seen
in up to 80% of pregnancies; specifically
neonatal hypocalcemia, preterm birth, intra-
uterine growth restriction, stillbirth, and neo-
natal tetany. These complications can be
significantly reduced with maternal treatment
and neonatal evaluation.24,25 Neonatal
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Endocrine Emergencies in Obstetrics 7
calcium levels should be checked after
delivery to screen for hypocalcemia.
Treatment of pHPT includes conservative
therapy such as increased fluids and de-
creased calcium intake with vitamin D sup-
plementation. Calcitonin does not cross the
placenta and thus is likely safe; however, is
not generally effective. Bisphosphonates
should be avoided unless absolutely necessary
due to the effect on fetal bones. Surgical
removal of the parathyroid glands is generally
reserved for symptomatic hypercalcemia and
preferred in the second trimester due to
decreased maternal and fetal risks. It is the
only definitive treatment.26
Pregnancy tends to offer protection
from maternal hypercalcemia, due to
transplacental transport to meet fetal
needs, especially during the third trimes-
ter. This protection is eliminated after
delivery and thus there is an increased
risk of maternal hypercalcemia in the
puerperal period.
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