NOVEMBER 2023 | VOLUME 20 | ISSUE 11

PEDIATRIC

Emergency Medicine Practice Evidence-Based Education • Practical Application

CLINICAL CHALLENGES
• Which patients are at the highest risk
for complications from diabetes?

• Which diagnostic studies should be

obtained? How often should they be
repeated?

• Should IV fluids or insulin be

administered first?

• When should insulin infusion be

discontinued?

Authors
Amani Sanchez, DO, FAAP
Fellow Physician, Department of Pediatrics,
University of Texas at Austin Dell Medical School;
Division of Pediatric Emergency Medicine, Dell
Children’s Medical Center, Austin, TX

Timothy Ruttan, MD, FACEP, FAAP Pediatric Diabetes:

Associate Professor of Pediatrics, Department of
Pediatrics, University of Texas at Austin Dell Medical Management of Acute
Complications in the
School, Austin, TX; US Acute Care Solutions,
Canton, OH

Peer Reviewers
Jay D. Fisher, MD, FACEP, FAAP
Associate Professor, Pediatric Emergency Medicine,
University of California San Diego, Rady Children’s
Hospital, San Diego, CA
Joseph Wolfsdorf, MB, BCh
Attending Physician, Division of Endocrinology,
Boston Children’s Hospital; Professor of Pediatrics,
Harvard Medical School, Boston, MA
Prior to beginning this activity, see the
“CME Information” on page 2.
Emergency Department
n Abstract
Children with diabetes mellitus are at high risk for acute life-
threatening complications of their chronic disease. Identification
and management of these emergencies can be complex and
challenging. This issue provides guidance for recognizing pedi-
atric patients with new-onset diabetes as well as diabetic crises
in established patients. The most recent literature is reviewed
and an approach to managing emergent diabetic complica-
tions in the pediatric patient is provided, with a focus on initial
stabilization and management. Key features in treating pediatric
patients with hyperglycemic emergencies are discussed, includ-
ing rapid fluid resuscitation when indicated, initiation of insulin,
and addressing complicating comorbidities.

For online For mobile

access: app access:

This issue is eligible for 4 CME credits. See page 2. EBMEDICINE.NET

 CME Information
Date of Original Release: November 1, 2023. Date of most recent review: October 1, 2023. Termination date: November 1, 2026.
Accreditation: EB Medicine is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing
medical education for physicians.
Credit Designation: EB Medicine designates this enduring material for a maximum of 4 AMA PRA Category 1 CreditsTM. Physicians should
claim only the credit commensurate with the extent of their participation in the activity.
Specialty CME: Included as part of the 4 credits, this CME activity is eligible for 2 Pharmacology CME credits, subject to your state and institutional ap-
proval.
ACEP Accreditation: Pediatric Emergency Medicine Practice is approved by the American College of Emergency Physicians for 48 hours of ACEP Category
I credit per annual subscription.
AAP Accreditation: This continuing medical education activity has been reviewed by the American Academy of Pediatrics and is acceptable for a maximum
of 48 AAP credits. These credits can be applied toward the AAP CME/CPD Award available to Fellows and Candidate Members of the American Academy
of Pediatrics.
AOA Accreditation: Pediatric Emergency Medicine Practice is eligible for up to 4 American Osteopathic Association Category 2-B credit hours per issue.
Needs Assessment: The need for this educational activity was determined by a practice gap analysis; a survey of medical staff, including the editorial board of
this publication; review of morbidity and mortality data from the CDC, AHA, NCHS, and ACEP; and evaluation responses from prior educational activities for
emergency physicians.
Target Audience: This enduring material is designed for emergency medicine physicians, physician assistants, nurse practitioners, and residents.
Goals: Upon completion of this activity, you should be able to: (1) identify areas in practice that require modification to be consistent with current evidence
in order to improve competence and performance; (2) develop strategies to accurately diagnose and treat both common and critical ED presentations; and
(3) demonstrate informed medical decision-making based on the strongest clinical evidence.
CME Objectives: Upon completion of this activity, you should be able to: (1) recognize pediatric patients with a diabetic crisis and identify those who are
at high risk for complications; (2) discuss the differences in resuscitation of pediatric patients with diabetic ketoacidosis and hyperglycemic hyperosmolar
crises; (3) provide weight-based management of fluids and dosing of insulin, mannitol, dextrose, and hypertonic saline; (4) discuss the options available
for managing pediatric diabetic crises, including the 2-bag system; and (5) avoid actions that may worsen a pediatric patient’s diabetic crisis or even cause
death.
Discussion of Investigational Information: As part of the activity, faculty may be presenting investigational information about pharmaceutical products that
is outside Food and Drug Administration-approved labeling. Information presented as part of this activity is intended solely as continuing medical educa-
tion and is not intended to promote off-label use of any pharmaceutical product.
Disclosure: It is the policy of EB Medicine to ensure objectivity, balance, independence, transparency, and scientific rigor in all CME activities. All indi-
viduals in a position to control content have disclosed all financial relationships with ACCME-defined ineligible companies. EB Medicine has assessed all
relationships with ineligible companies disclosed, identified those financial relationships deemed relevant, and appropriately mitigated all relevant financial
relationships based on each individual’s role(s). Please find disclosure information for this activity below:
EVIDENCE-BASED
Planners Faculty
• Ilene Claudius, MD (Editor-in-Chief): Nothing to Disclose • Amani Sanchez, DO (Author): Nothing to Disclose
• Tim Horeczko, MD (Editor-in-Chief): Nothing to Disclose • Timothy Ruttan, MD (Author): Nothing to Disclose
PEER-REVIEWED
• Jay D. Fisher, MD (Peer Reviewer): Nothing to Disclose
• Joseph Wolfsdorf, MB, BCh (Peer Reviewer): Nothing to Disclose
• Aimee Mishler, PharmD (Pharmacology Editor): Nothing to Disclose
• Brian Skrainka, MD (CME Question Editor): Nothing to Disclose
• Cheryl Belton, PhD (Content Editor): Nothing to Disclose
• Dorothy Whisenhunt, MS (Content Editor): Nothing to Disclose
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will be emailed to you.
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 Case Presentations
A 3-year-old previously healthy girl presents to the ED with fatigue and vomiting…
• The girl’s parents tell you she has had increased thirst and appetite over the last 6 weeks but has lost 2
kg since her last check-up.
• She developed a runny nose and cough yesterday and a fever of 101°F, which has resolved. Today, she
began vomiting and became fatigued.
CASE 1

• Upon arrival to the ED, the girl is alert, but given her pale and fatigued appearance in triage, she was
immediately taken to a room. Her vital signs are: temperature, 37°C; heart rate, 132 beats/min; blood
pressure, 70/40 mm Hg; respiratory rate, 31 breaths/min; and oxygen saturation, 100% on room air. Her
examination is notable for pallor and ill appearance. She has dry and cracked lips and is breathing fast,
with clear lungs. She has epigastric tenderness, but otherwise her abdominal examination is normal.
• You can tell this patient is ill, and her history is concerning. What treatment will you initiate to immedi-
ately address her shock?

A 13-year-old boy with known type 2 diabetes mellitus and cough for the past 3 days presents to the
ED with a glucose level of >600 mg/dL at his pediatrician’s office during his well-adolescent check…
• The boy was diagnosed 1 year ago and has been using diet and exercise to manage his diabetes. He
has felt a little more tired this week and also says he thinks his vision is a little blurry, but he has not had
a recent eye examination.
CASE 2

• Upon arrival to the ED, he is well-appearing and in no distress. He is eating a bag of spicy chips in the
room. His examination is notable for obesity and acanthosis nigricans circumferentially on his neck. His
vital signs are normal for his age except for a heart rate of 110 beats/min and blood pressure of 131/87
mm Hg.
• As you assess this patient, you think about his elevated glucose at the pediatrician’s office. You are
surprised he is so well-appearing, but you are worried about progression of his illness. How should you
manage this patient?

A 17-year-old girl with type 1 diabetes mellitus presents to the ED for altered mental status…
• She is here with her mother who found her daughter on the floor in her room after hearing a “thud.”
The girl was not responsive to voice, but woke up in a drowsy state when her mother shook her vigor-
ously. She continued to fall asleep and had to be repeatedly stimulated. The mother called 911 and
CASE 3

then brought her daughter by private vehicle to the ED, which is only 5 minutes from their house.
• Upon arrival, the patient is minimally responsive, with a Glasgow Coma Scale score of 8. She has no
signs of visible trauma, but on rapid examination, you notice that she has an insulin pump. You check a
point-of-care glucose level, which is 29 mg/dL. You rapidly administer the adult dose of dextrose.
• How does the presence of an insulin pump change your initial differential diagnosis prior to obtaining
laboratory information? In addition to treating her low glucose, what additional steps are necessary to
keep this patient safe?

n Introduction (DKA) had a medical visit in the prior week.1 This

Diabetes and its complications can present sig-
nificant diagnostic and management challenges in
pediatric patients. Delay in identifying new-onset
diabetes can be life-threatening, and the sever-
ity of illness in pediatric patients often necessitates
rapid intervention to prevent both short-term and
long-term morbidity or mortality. In one study, 34%
of children with a new diagnosis of diabetes in the
emergency department (ED) had a medical visit in
the prior week. Similarly, approximately 39% of chil-
dren presenting to the ED with diabetic ketoacidosis
demonstrates how critical it is to consider new-onset
diabetes, DKA, and hyperglycemic hyperosmolar
state (HHS) in pediatric patients presenting to the
ED, even for seemingly unrelated complaints.
Patients often have comorbidities that can impact
both their clinical presentation and mortality. Children
with obesity and type 2 diabetes are especially at risk
for having complicating hypertension, dyslipidemia,
and nonalcoholic fatty liver disease. Depending on
the etiology of their diabetes and related conditions,
patients may also have other types of liver disease,

NOVEMBER 2023 • www.ebmedicine.net 3 © 2023 EB MEDICINE

hemochromatosis, chronic or acute pancreatitis, and
even cystic fibrosis. Patients with new-onset diabe-
tes should be screened for coinciding autoimmune
disorders such as celiac disease and thyroid disease.2
When necessary, transfer to an appropriate level of
pediatric specialty care with services such as critical
care and endocrinology should be arranged early in
the care of a sick patient with diabetic complications
for timely management and disposition. Engaging the
closest children’s ED on the phone for early guidance,
consultation, and follow-up care is recommended,
when possible. This issue of Pediatric Emergency
Medicine Practice provides an evidence-based guide
to identifying and managing the most common pedi-
atric diabetic complications and emergencies.
n Critical Appraisal of the Literature
A literature search was performed using PubMed and
the search terms diabetes, pediatrics, children, DKA,
diabetic ketoacidosis, cerebral edema, HHS, hyper-
glycemic hyperosmolar, hypoglycemia, autoimmune,
cerebral edema, fluids, insulin, two-bag system, intu-
bation, hypophosphatemia, phosphate, and preva-
lence diabetes children.
Though HHS has been thoroughly described in the
adult literature, the pediatric literature is focused pri-
marily on DKA and hypoglycemic events. The majority
of studies and articles related to pediatric diabetes
and diabetic emergencies are retrospective reviews
and case reports, with very few randomized controlled
trials. The PECARN DKA Fluid Study Group performed
a 13-center randomized controlled trial that analyzed
1389 episodes of DKA to determine whether infusion
rates and/or NaCl content of fluids (half-normal [0.45%]
vs normal [0.9%] saline) impacted long-term out-
comes.3 This study guides current fluid therapy prac-
tice in pediatric DKA and is one of the few randomized
controlled trials of pediatric patients with diabetes.
n Etiology and Pathophysiology
According to the International Diabetes Founda-
tion, there are currently over 1 million people aged
<20 years with diabetes. Over 130,000 children and
adolescents are diagnosed with diabetes each year.
The estimated prevalence of type 1 diabetes mellitus
in children is approximately 2.15 children per 1000.4
New-onset pediatric type 1 diabetes mellitus occurs
most commonly in children aged 4 to 6 years and 10
to 14 years.5 Nearly half of all patients are diagnosed
before 10 years of age and almost all patients diag-
nosed with diabetes before 10 years of age have type
1 diabetes mellitus. The incidence of new-onset type
1 diabetes is estimated to be increasing at an annual
percentage change (measured from 2002-2015) of up
to 1.9% annually.4,5 The estimated prevalence of type
2 diabetes mellitus is estimated to be 0.67 per 1000
NOVEMBER 2023 • www.ebmedicine.net
children aged ≤19 years.6 DKA is present at initial di-
agnosis of type 1 diabetes in at least 30% of children
in the United States and Canada and occurs at a rate
of 6% to 8% per year in children with known type 1 di-
abetes.7,8 Contrary to what is often assumed, children
with type 2 diabetes can also have DKA; one study
showed that 13% of children with DKA had type 2 dia-
betes.9 In addition, some children have HHS or mixed
DKA-HHS. Children with HHS or mixed DKA-HHS are
at significant risk for complications and are more often
severely dehydrated compared to those with DKA,
though they may appear more stable initially.10
n Differential Diagnosis
Preschool-age patients are often unable to describe
their symptoms, and it is difficult to obtain an accu-
rate history, especially if they have vague complaints.
Patients with hyperglycemic emergencies may appear
relatively well but can have significant electrolyte
abnormalities and dehydration. Children can become
ill quickly, and it is therefore critical to have a high
suspicion for metabolic abnormalities in a child or
adolescent presenting in an atypical manner. The
only significant symptom may be fatigue, vomiting, or
abdominal pain. Infants pose an even greater diag-
nostic challenge, as they are at higher risk for rapid
decompensation, and the effects of vomiting and
fatigue are amplified in younger patients. In addition
to hyperglycemia, hypoglycemia and toxic or inten-
tional ingestion should be considered for all pediatric
patients presenting with vomiting or unusual/incon-
sistent symptoms. For a list of high-yield differential
diagnoses for the pediatric patient presenting with
fatigue and vomiting, see Table 1, page 5.
n Prehospital Care
Parents and caregivers often call emergency medical
services (EMS) for transport of their children to the
ED. Any concerning symptoms or history may be
a clue to an insidious illness that should prompt
treatment and evaluation. The caretaker may mention
vomiting, lethargy, fussiness, decreased wet diapers,
or simply that the child is “more tired than usual.”
A point-of-care glucose measurement should be
obtained and antiemetics should be administered if
the child is vomiting, as persistent emesis can worsen
the child’s condition. One key finding may be isolated
tachypnea without increased work of breathing or
desaturation, which should prompt consideration
of a metabolic crisis as the etiology for distress. If
the glucose level is high, it is appropriate to give a
weight-based 10-mL/kg isotonic crystalloid fluid IV
bolus, preferably with 0.9% NaCl (normal saline).
If there is concern for shock, 20 mL/kg of 0.9%
isotonic crystalloid fluid should be administered for
rapid resuscitation. If glucose is low (<70 mg/dL)
4 © 2023 EB MEDICINE
and the patient is symptomatic, intravenous (IV) or should consider transporting the patient directly to
intraosseous (IO) dextrose should be given. Dextrose a pediatric center to avoid the need for a second
concentration multiplied by dose in mL/kg should transport between hospitals.
equal 50; for example, a child should receive 5 mL/kg
of 10% dextrose (D10) up to the maximum adult dose
of 25 g/dose (250 mL/dose for D10). Another option n Emergency Department Evaluation
for a second-line agent is glucagon at 0.03 mg/kg History
intramuscular (IM), IV, or subcutaneous; alternatively, It is important to ask very specific and focused ques-
children estimated to weigh <25 kg may receive 0.5 tions, since parents and family members may not real-
mg, and children aged ≥6 years with unknown weight ize the importance of seemingly unrelated symptoms.
and those weighing ≥25 kg may receive 1 mg. The Prior sick visits to the pediatrician and urgent care or
child should remain nothing by mouth (NPO) en ED visits are important to note. A seemingly minor
route. If there is concern for new-onset diabetes or illness can trigger a diabetic emergency in pediatric
a diabetic crisis, intubation (discussed further in the patients. A detailed account of recent hours and days
“Complications During Treatment” section, page leading up to the illness plus any concerning symp-
11) should be avoided, if possible. Intubation should toms over the past few months should be obtained.
be reserved for severely obtunded or unconscious Questions that should be asked include: When did the
patients with abnormal airway protective reflexes.11,12 child last eat or drink? Has the child had regular urine
It is important for EMS to relay any medical history output today? Has the child had upper respiratory in-
available, including possible exposures or ingestions, fection symptoms? Has anyone else that spends time
to the receiving emergency physician, in addition to with the child been ill? For a female patient, has she
interventions that have been taken en route. EMS had menarche? Has the child been growing well and
maintaining their growth trajectory? Does the child
have any known or suspected medical problems?
In addition to a detailed review of systems,
Table 1. Differential Diagnosis of Children weight changes (which often can be determined by
With Fatigue and Vomiting in the asking how the child’s clothes are fitting or asking
Emergency Department what their weight was at their last well check), fatigue,
Metabolic fever, episodes of dizziness, thirst, hunger and eating
• Adrenal insufficiency habits, enuresis, and night-time awakenings should
• Diabetic ketoacidosis
be discussed. Some young children will have a history
• Inborn error of metabolism
• Hyperglycemic hyperosmolar state of recurrent diaper rash or thrush.
• Hypercalcemia/hypocalcemia In addition to focused questions about the
• Renal failure patient, family history can help determine the cause
• Dehydration of a child’s illness. History of familial autoimmunity
• Hypoglycemia
such as diabetes, thyroid disorders, gastroenterologic
Infectious problems (eg, celiac disease, inflammatory bowel
• Myocarditis disease), lupus, and rheumatoid arthritis increases the
• Appendicitis likelihood that a child may have diabetes. Are there
• Pneumonia medications in the home such as insulin, metformin,
• Pelvic inflammatory disease
beta blockers, or other medications? What about
• Urinary tract infection
• Gastroenteritis supplements or vitamins? Has the child been unsu-
• Cholecystitis pervised at all or is there a possibility that they could
have ingested something from the home or garage?
Abdominal/Genitourinary If the child has known diabetes, what is the medi-
• Intussusception
cation dosing and how many times in the past week
• Pyloric stenosis
• Malrotation has the medication been taken? Does the patient
• Pregnancy (ectopic pregnancy) have an insulin pump? Does the patient have a log
• Testicular/ovarian torsion with glucose values recorded? Finding out whether
• Pancreatitis the child is responsible for their own medication man-
agement is also critical, as children often omit insulin
Other
• Head injury/trauma doses. Obtaining insulin dosing with basal, correction
• Ingestion (drugs/medications, household) factors, and sliding scale doses can be important for
• Neoplasm (intracranial, intra-abdominal) management. In addition, older patients often strug-
• Heart failure (especially infants) gle with many aspects of disease management, given
• Migraine
social and other pressures. Asking specific questions
• Cannabis hyperemesis syndrome
of the patient with their parents out of the room can
www.ebmedicine.net help reveal details in a judgment-free manner and

NOVEMBER 2023 • www.ebmedicine.net 5 © 2023 EB MEDICINE

help guide both initial management and long-term
counseling for disease management. Consideration of
psychiatric comorbidities should also be considered,
as intentional ingestions (or omissions of medications)
are causes of repeated DKA.13
Physical Examination
Experienced clinicians can often make a diagnosis
of DKA in adults and children on arrival by patient
appearance alone. A tool such as the Pediatric As-
sessment Triangle may also be helpful in the rapid
assessment of the stability of the child. The Pediatric
Assessment Triangle is a brief view from the door that
includes determining the child’s general mental state
and appearance, seeing their work of breathing, and
assessing their skin/circulation. Is the child calm or
irritable? Is the child lethargic? Does the child display
an abnormal work of breathing? Is the child pale or
mottled? This takes just seconds and can be done
without touching the child.
If a pediatric patient appears lethargic or ill,
immediate action should be taken to stabilize them
and begin treatment. This includes rapid placement
of 2 peripheral IV lines and obtaining a point-of-care
glucose level. Although this issue is focused on hyper-
glycemic emergencies, hypoglycemia is common in
children with type 1 diabetes and must be recognized
and treated promptly. Consider oxygen supplementa-
tion for the patient who appears to be in shock, unless
the patient has known high-risk cardiac history or is an
infant with unknown medical history that could have
a cardiac abnormality worsened by oxygen. Mental
status changes can be due to hypoglycemia or cere-
bral edema, which must be recognized and treated
early. Signs of cerebral edema include altered mental
status, abnormally slow heart rate, elevate blood
pressure, and severe headache. (See the “Cerebral
Edema” section on page 11 for more details.)
Once the initial assessment has occurred, per-
form a thorough head-to-toe examination, looking
for other complicating factors and signs/symptoms
of differential diagnoses. Listen closely for gallops or
murmurs and for crackles that could be evidence of
an underlying cardiac abnormality or secondary ill-
ness/precipitating event that can be life-threatening.
Identifying abnormal breathing (Kussmaul breathing)
may be an indicator that the child is severely acide-
mic. Rashes, bruises, or abnormal skin pigmentation,
including acanthosis nigricans (which can be on the
neck, axilla, or groin), should be documented. Skin
turgor, hydration status, and evidence of edema
should be evaluated. All patients should have an
abdominal examination, and a genitourinary examina-
tion (with parental permission) should be performed.
Additional underlying pathology must be con-
sidered, because illness often triggers DKA, HHS,
or hypoglycemic emergency,14,15 and needs to be
treated. The examination should include additional
NOVEMBER 2023 • www.ebmedicine.net
assessment of areas that may be precipitating the
child’s illness, such as evaluating the ears for otitis
media and palpating the abdomen for focal pain that
could indicate urinary tract infection, pancreatitis, ap-
pendicitis, or other pathology.
n Diagnostic Studies
Diabetic crises may be related to prolonged hypergly-
cemia. Insulin omission is the most common etiology,
and it can be intentional or due to pump malfunction.
Hyperglycemic crises can be due to triggered new-
onset diabetes, ischemia (especially intestinal/mes-
enteric ischemia), or infection. Consider triggers for
the patient’s crisis early to help guide diagnosis and
treatment decisions. All children arriving to the ED
should have a complete set of vital signs obtained, in-
cluding weight in kilograms and height. Patients who
present with recurrent vomiting, fatigue, or who ap-
pear ill should have a point-of-care glucose checked
immediately upon arrival. Hypoglycemia or hypergly-
cemia should be addressed promptly, without wait-
ing for confirmation or secondary laboratory studies
to result. A peripheral IV should be placed; 2 IVs are
better than 1 in the ill-appearing child. While this oc-
curs, additional laboratory studies should be drawn,
which should initially include a venous blood gas with
electrolytes and lactate, a complete blood cell count,
and a comprehensive metabolic panel. An electrocar-
diogram (ECG) should be obtained, especially if there
is a delay in obtaining serum electrolyte levels.
For patients with hyperglycemia, the following
studies should be performed: serum magnesium and
phosphate levels, hemoglobin A1C, serum osmolality,
lipid levels, and urinalysis with urine dipstick to look
for ketones. Serum beta-hydroxybutyrate should be
obtained if the urinalysis demonstrates ketones, but
it also may be obtained with the initial blood draw.
DKA is diagnosed via blood gas and laboratory test-
ing. Biochemical criteria include the presence of all of
the following:16
• Venous pH <7.3 or bicarbonate <18 mEq/L
• Hyperglycemia >200 mg/dL (11.1 mmol/L)
• Ketosis >3 mmol/L beta-hydroxybutyrate in se-
rum or moderate or large urine ketones
HHS is differentiated from DKA by the following:16
• Less severe acidosis with venous pH >7.3
• Plasma glucose concentration >600 mg/dL (33.3
mmol/L)
• Ketosis mild to absent
• Serum bicarbonate >15 mEq/L
• Marked elevation in serum osmolality, typically
>320 mOsm/kg
Low sodium levels are present in most patients
with DKA or HHS, though patients who are very
dehydrated from osmotic diuresis may have normal
6 © 2023 EB MEDICINE
or elevated levels.17 Measured serum sodium levels
will fall by approximately 1.6 to 2 mEq/L for every
100 mg/dL increase in glucose.18 Elevated lipid levels
may result in a pseudohyponatremia. It is common for
children with DKA or HHS to have acute kidney injury
due to dehydration, and this should be identified and
monitored throughout treatment. For patients with
abnormal glucose levels, studies to further evaluate
the presenting complaint or precipitating illness, such
as lipase, respiratory panel, and chest radiograph
should be ordered. Consider urine and serum drug
tests; cocaine specifically has been associated with
recurrent DKA.19,20
Though rare, a near-normal serum glucose level
during ED evaluation does not rule out DKA. Patients
with especially poor oral intake or those who have
recently received insulin at home prior to ED arrival
may have near-normal glucose levels, referred to as
euglycemic DKA, and evaluation of all the laboratory
tests is crucial.
If there is clinical concern for a bacterial infection,
diagnostic studies such as a chest x-ray and blood
and urine cultures should be collected, especially
because patients with uncontrolled diabetes are at
higher risk for complications from infection.
Imaging Studies
Imaging such as computed tomography (CT), testicu-
lar or ovarian ultrasound, or abdominal ultrasound to
rule out appendicitis and/or intussusception should
be obtained on a case-by-case basis. A head CT scan
should be obtained for patients with altered mental
status; however, fluid resuscitation and treatment of
altered mental status should not be delayed pending
diagnostic studies (see the “Complications During
Treatment” section, page 11).
n Treatment
All pediatric patients with diabetic complications
should undergo initial stabilization in the ED. Patients
should remain NPO until their acidosis is resolved.
Treatment of DKA or HHS and subsequent complica-
tions varies on a case-by-case basis, but the mainstay
is fluid resuscitation and management of metabolic
acidosis and hyperglycemia, usually with continuous
insulin infusion; however, the use of insulin, especially
via continuous infusion, comes with a high risk for hy-
poglycemia. Hypoglycemia is associated with worse
patient outcomes and can cause significant complica-
tions and even death. Indeed, the risk for iatrogenic
harm is significant during the treatment of DKA, and
careful monitoring and titration of treatment is critical
to avoid harm. To mitigate this risk, a “2-bag system”
to treat pediatric DKA is becoming common practice
rather than using 1 bag of fluids; however, either
method of fluid management is appropriate.
NOVEMBER 2023 • www.ebmedicine.net
2-Bag System
The 2-bag system allows for a fine-tuned approach to
rehydration, repletion of electrolytes, and co-admin-
istration of glucose as needed. Two bags of fluids can
be titrated independently, but run through the same
IV line. If the patient has a normal potassium level
(3.5-5.4 mEq/L) and does not show signs of cere-
bral edema, the 2-bag system may be initiated. The
2-bag system is typically initiated with the use of 1.5
times the maintenance IV rate, based on the patient’s
weight. Bag 1 contains either 0.45% or 0.9% NaCl
plus potassium (usually 20-30 mEq/L of potassium
phosphate plus 20-30 mEq/L of potassium acetate).
Bag 2 contains D10 with either 0.45% or 0.9% NaCl
plus potassium at a total of 40 to 60 mEq/L (the same
composition as bag 1).21 The rate of fluid administra-
tion is based on serum glucose levels.
Protocols for the 2-bag system will vary, but an ex-
ample is provided in Table 2. Using both bags simulta-
neously at variable rates for dextrose and fluid deliv-
ery (based on patient weight or body surface area)
can help lower glucose levels with less likelihood of
hypoglycemia. Using a 2-bag system has been shown
to be cost-effective by reducing both the number of
fluid bags used and reducing the time of continuous
IV fluid administration by decreasing serum glucose
levels more rapidly.21-26 Currently, there is no evidence
of increased risk for adverse neurological outcomes
based on use of a 1-bag versus a 2-bag system.27
If persistent hypoglycemia develops while meta-
bolic acidosis persists, increase the dextrose in bag
2 to 12.5%. If hypoglycemia with acidosis persists,
decrease or pause the continuous insulin infusion.
For any symptomatic hypoglycemia, pause the insulin
infusion for at least 10 minutes and then recheck glu-
cose prior to restarting insulin. Conceptually, the key
point is to reverse the metabolic abnormalities and
eliminate the acidosis and not just resolve the hypo-
glycemia. Stopping insulin for hypoglycemia without
resolution of the acidosis can lead to rebound of DKA.
Table 2. Sample 2-Bag System28
Blood Bag 1 (NS + K) Bag 2 (D10 + Total Dextrose
Glucose (% of Total NS + K) Concentration
(mg/dL) Fluid Rate) (% of Total (% When Using
Fluid Rate) D10)
>300 100 0 0
251-300 75 25 2.5
201-250 50 50 5
151-200 25 75 7.5
<151 0 100 10
Abbreviations: D10, 10% dextrose; K, potassium; NS, normal saline
(0.9% NaCl).
7 © 2023 EB MEDICINE
Diabetic Ketoacidosis
Mild Diabetic Ketoacidosis
Patients with mild DKA (pH 7.2-7.29) should receive
an initial 10- to 20-mL/kg normal saline IV bolus.
Verify the patient’s potassium level (normal range
3.5-5.4 mEq/L; see the “Potassium and Phosphate
Supplementation” section, following). Regular insulin
is started at 0.05 to 0.1 unit/kg/hr IV. Hourly point-of-
care glucose and ketone checks should be obtained,
ideally obtaining a second check after initial fluids
and before insulin initiation. Patients in mild DKA are
estimated to have an extracellular volume deficit of
3% to 5% of body weight and should be receiving
maintenance IV fluids using the 2-bag system (see the
“2-Bag System” section, page 7) or 0.45% saline or
0.9% saline (with added potassium), Plasma-Lyte, or
lactated Ringer’s solution after initial fluid resuscita-
tion. True body weight rather than ideal body weight
should be used for fluid replacement, which typically
occurs over 24 to 48 hours.16 Mild and moderate DKA
may resolve in <24 hours.
The use of subcutaneous insulin is recommended
only if IV insulin is unavailable and should ideally be
used with the help of a pediatric endocrinologist via
telehealth consult or with existing institutional proto-
cols. Subcutaneous rapid-acting insulin (insulin lispro or
insulin aspart) may be used; however, absorption may
be less reliable in dehydrated patients. One hour after
initial fluid resuscitation begins, subcutaneous rapid-
acting insulin may be given. The types of insulin that are
approved for pediatric patients are listed in Table 3.
The patient should remain on maintenance IV
fluids, with addition of dextrose once serum glucose
is <250 mg/dL (or sooner if the rate of decrease in
glucose is substantial), until DKA is resolved, they are
tolerating oral intake, and they are in preparation for
discharge. Hourly glucose and ketone checks should
be obtained.
Moderate to Severe Diabetic Ketoacidosis
Children with moderate to severe DKA (pH <7.2)
should be managed initially with fluid resuscitation of
10 to 20 mL/kg of IV isotonic crystalloid, preferably
Table 3. Types of Insulin Approved for Pediatric Patients29
Category Insulin Type Onset
Ultra-rapid • Fast-acting aspart • ~12-16 min
Rapid • Lispro • ~30 min
• Aspart • ~18 min
• Glulisine • 12-30 min
Short • 30- 60 min
• Regular human
Intermediate • NPH (neutral protamine • 1-2 hr
Hagedorn) human
Long • Glargine • 3-4 hr
• Detemir • 3-4 hr
• Degludec • ~60 min
• Glargine-U300 • 6 hr
NOVEMBER 2023 • www.ebmedicine.net
0.9% NaCl. Those with shock should initially receive
20 mL/kg IV and further fluids as indicated. Some
patients with DKA may have hypertension. Do not
assume that they are euvolemic, and the presence of
hypertension should not impact fluid resuscitation,
especially if the patient is dehydrated. Additional IV
fluid boluses of similar volume should be given until
adequate perfusion is restored. Children with moder-
ate DKA are assumed to have an extracellular fluid
deficit of 7% of body weight and those with severe
DKA are assumed to have a 10% deficit. Once the pa-
tient is hemodynamically improved, additional IV fluid
administration should continue with maintenance and
replacement of fluid deficit. In addition to correcting
hypovolemia, fluid replacement improves hypergly-
cemia and other electrolyte imbalances. For children
who do not show evidence of cerebral edema, the
following maintenance fluid types may be utilized:
0.45% NaCl or 0.9% NaCl with potassium, Plasma-
Lyte, or lactated Ringer’s solution.3,16 Cerebral edema
should be treated immediately, and patients with
cerebral edema should not receive hypotonic fluids.
At least 1 hour after initial IV fluid resuscitation
has begun, hyperglycemia should be addressed with
initiation of continuous IV regular insulin at a rate of
0.1 unit/kg/hr. Patients who show marked sensitivity
to insulin may have their continuous insulin infusion
rate reduced to 0.05 unit/kg/hr. An initial “loading
dose” or “bolus” of insulin should not be admin-
istered.16 Using an IV insulin bolus can precipitate
shock, rapidly change osmotic pressure, increase risk
for cerebral edema, and exacerbate hypokalemia, and
it has not been shown to significantly change time to
resolution of DKA.30-32 Treatment with an insulin infu-
sion should continue until pH >7.3, serum bicarbon-
ate is at least 18 mmol/L, and beta-hydroxybutyrate
is <1 mmol/L, or when the anion gap has closed.16,33
Fluid management may occur via traditional 1-bag
system or 2-bag system. Potassium supplementation
should begin after initial fluid bolus and be given with
insulin therapy as long as the potassium level is ≥3.5
mEq/L. If the potassium level is <3.5 mEq/L, it should
be replaced prior to initiation of insulin therapy (see
the following section).
Potassium and Phosphate
Peak Duration Supplementation
• 1.5-2.5 hr • 5-7 hr
Children in DKA have a total
body potassium deficit from
• ~2.5 hr • 6 hr
• 1-3 hr • 3-7 hr
both vomiting and loss of potas-
• 1.5-3 hr • 3-4 hr sium through osmotic diure-
• 1.5-3.5 hr • 8 hr sis. Serum potassium may be
normal, high, or low at the time
• 4-12 hr • 12-24 hr
of initial laboratory draw but can
rapidly decline with initiation of
• ~12 hr • 24-30 hr
• 3-9 hr • 22-23 hr
treatment of DKA. For this rea-
• 9 hr • >42 hr son, potassium supplementation
• 12-16 hr • >24 hr based on initial laboratory values
8 © 2023 EB MEDICINE
should occur after the initial IV fluid bolus. Children
with initial serum potassium of <3.5 mEq/L (mmol/L)
should receive IV potassium replacement of no more
than 0.5 mEq/kg/hr prior to initiation of treatment
with insulin. Repeat potassium supplementation
should occur until serum potassium levels, checked
hourly, are within normal range (3.5-5.4 mEq/L).16 Po-
tassium replacement via potassium-containing main-
tenance IV fluids for children with normal potassium
levels should occur concomitantly with insulin initia-
tion. Patients with hyperkalemia should not receive
potassium supplementation until their potassium level
falls to normal (<5.5 mEq/L) and they are having urine
output. Once normalized, potassium levels should
be checked every 2 to 4 hours during treatment with
an insulin infusion (and potassium-containing fluids).
Due to the impact of insulin on serum potassium
levels, the use of insulin can cause dramatic changes
in serum potassium even to the extent of causing
cardiac arrest.34 If a patient is hypokalemic prior to
initial fluid expansion, insulin administration should
be delayed until a normal serum potassium level has
been achieved with potassium supplementation.
Similarly, patients often develop hypophospha-
temia with DKA treatment. Usually, the degree of
hypophosphatemia is related to the severity of meta-
bolic acidosis.16 Though hypophosphatemia is usu-
ally asymptomatic, it may have adverse effects and
should be avoided. Therefore, potassium phosphate
added to maintenance IV fluids is a good choice for
both potassium and phosphorus replacement. Serum
phosphate levels should be obtained at least every 2
to 3 hours until phosphate levels normalize. Patients
with severe hypophosphatemia (<1 mg/dL or with un-
explained weakness or other manifestations of severe
hypophosphatemia) should be treated aggressively
with phosphate infusion, as they have a high risk for
cardiac arrest. Phosphate can be replenished with use
of sodium phosphate or potassium phosphate. Data
are lacking regarding dosing for pediatric DKA and
phosphate repletion; however, some investigators
recommend 0.25 to 0.5 mmol/kg over 8 to 12 hours,
while others recommend up to 1 mmol/kg for critical-
ly ill adult patients.35 In the case of severe hypophos-
phatemia, insulin should be paused until phosphate is
replenished, and phosphate levels should be checked
every 1 to 2 hours during treatment.16
Magnesium and Calcium Supplementation
Magnesium and calcium deficiency can secondarily oc-
cur during phosphate infusion, and these levels should
be monitored throughout treatment of DKA.16 Hypo-
magnesemia and hypocalcemia often occur and are
usually mild and asymptomatic. Symptomatic patients
or those with severely low levels should be treated
quickly with magnesium and calcium supplementation
and have continuous ECG monitoring.
NOVEMBER 2023 • www.ebmedicine.net
Sodium Bicarbonate
Do not give sodium bicarbonate to patients with DKA
or HHS unless the patient is in cardiac arrest, has
severe life-threatening hyperkalemia, or has severe
acidosis (pH< 6.9) with evidence of impaired cardiac
function.16 Infusion of IV sodium bicarbonate has
been shown to worsen morbidity. It can decrease
respiratory drive, causing an increase in total carbon
dioxide and subsequent fall in cerebral pH, worsen-
ing cerebral edema.16,36 A multicenter study of 61
children demonstrated that treatment with sodium
bicarbonate was associated with cerebral edema.37
Rapid use of IV sodium bicarbonate may also cause
hypokalemia.
General Fluid and Electrolyte Management
Recommendations
A concise overview of fluid and electrolyte manage-
ment to assist with rapid initiation of treatment during
DKA is outlined in Table 4, page 10.
Hypoglycemia
Hypoglycemia (glucose <70 mg/dL), even if mild,
should be addressed. The first preference is for oral
replacement if the patient is able to take fluids and
food. If the patient has a glucose level <50 mg/dL and
is stable, with normal mental status, critical labora-
tory studies should be obtained in the absence of a
clear explanation (discussed in the following section).
Symptomatic hypoglycemia should be treated quickly,
ideally with use of IV D10 if the patient cannot take
oral therapy. When treating pediatric hypoglycemia,
dextrose concentration multiplied by dose in mL/kg
should equal 50. For example, a 10 kg child should
receive 5 mL/kg (50 mL) of D10. Similarly, a 10 kg
child should receive 2 mL/kg (25 mL) of D25. Though
D50 is often used in adult patients, multiple studies
have demonstrated that D10 may be a better solution,
given ease of administration through a small periph-
eral IV and less severe posttreatment hyperglycemia
(which has been shown to worsen mortality), when
compared to D50.38-40 One large systematic review of
adults with hypoglycemia noted similar time to resolu-
tion of hypoglycemia and no difference in episodes
of subsequent hypoglycemia with both D10 and D50.
No adverse events were observed in the D10 group
(1057 patients) compared with 13 adverse events in
the D50 group (310 patients).38 Although D10 is typi-
cally used to treat hypoglycemia in pediatric patients,
the most rapidly available concentration of dextrose-
containing fluids should be used.
Hypoglycemia of Unknown Etiology
While beyond the scope of this review, in patients
with hypoglycemia of unknown etiology (eg, unrelated
to known insulin overdose) with glucose level <50 mg/
dL, consider obtaining “critical laboratory studies”
for future evaluation for inborn errors of metabolism.
9 © 2023 EB MEDICINE
These laboratory studies include serum comprehen-
sive metabolic panel, cortisol, insulin, beta-hydroxybu-
tyrate, C-peptide, free fatty acids, lactate, ammonia,
growth hormone, acylcarnitine panel, and free and
total carnitine levels. This blood sample should be ob-
tained prior to dextrose administration with D10 at 5
mL/kg. If the patient is unstable, do not delay admin-
istration of dextrose to obtain laboratory studies.
Hyperglycemic Hyperosmolar State
The management of HHS has some key differences
compared to DKA, as patients are likely more se-
verely dehydrated, often with a fluid deficit of 12% to
15% of body weight.16,41 Initial IV fluid boluses should
be 20 mL/kg of 0.9% NaCl until intravascular volume
is adequate to support perfusion, followed by 0.45%
NaCl at twice the maintenance rate. Fluids should be
adjusted to decrease total sodium slowly, approxi-
mately 0.5 mmol/L/hr, to avoid complications from a
rapid change in serum sodium concentration.41 Fluids
are the mainstay of initial management.
In contradistinction to DKA, insulin should not
be initiated for patients with HHS until glucose levels
are decreasing at a rate of <50 mg/dL/hr. Insulin may
be initiated at a lower rate of 0.025 to 0.05 unit/kg/
hr. If blood glucose is decreasing at a rate faster than
100 mg/dL/hr, consider decreasing the insulin infusion
rate. In adults, HHS is considered resolved when the
patient is alert and effective plasma osmolality is <315
mOsm/kg. Though there are fewer guidelines on use
of insulin and resolution of pediatric HHS, consider
transitioning to subcutaneous insulin once serum
glucose drops to 250 to 300 mg/dL.30,42 A 2-bag sys-
tem may still be used, especially if ketosis is present,
indicating mixed DKA-HHS. Additionally, the treat-
ment team should consider replacing urine output at
0.5-1:1 if urine output is profound (>5 mL/kg/hr).
Hyperkalemia is more likely to occur in patients
with HHS than DKA. In addition, rhabdomyolysis and
kidney injury are more common.43 Once diagnosed,

Table 4. Fluid and Electrolyte Management for Patients With Diabetic Ketoacidosis
Management
Fluids:
Give 10 to 20 mL/kg of 0.9% NaCl (normal saline), or other isotonic solution, administered as an IV bolus over 20 to 30 minutes:
• Mild DKA – 10 mL/kg bolus.
• Moderate or severe DKA – 20 mL/kg bolus.
Give additional boluses if necessary, based on cardiovascular status. Larger fluid volumes are usually needed for patients presenting with mixed
features of DKA and HHS (hyperosmolar DKA), regardless of the level of acidosis.
Hypovolemic shock is a rare occurrence in DKA; continued shock after initial fluid resuscitation should prompt evaluation for other causes, such as
sepsis.
Following initial fluid resuscitation, replace the estimated fluid deficit over 24 to 48 hours, in addition to maintenance fluids. IV fluids with sodium
content between 0.45 and 0.9% NaCl should be used as the replacement fluid.
Electrolytes
Sodium: Serum sodium levels are generally low (due to dilutional effect of hyperglycemia) but may be normal or even high (due to water loss). If
serum sodium is low, it should rise as hyperglycemia is corrected.
Potassium: The timing of potassium replacement depends on the initial serum potassium concentrationa:
• Low potassium (<3.5 mEq/L) – Add 40 mEq/L of potassium to IV fluids as soon as possible, and delay insulin therapy until serum potassium is in
the normal range.
• Normal potassium (3.5 to 4.5 mEq/L) – Add 40 mEq/L of potassium to IV fluids when insulin therapy is started.
• High potassium (>4.5 mEq/L) – Monitor every hour and begin potassium replacement when serum potassium decreases to the normal range and
when urine production or adequate renal function is documented.
• Provide potassium as a 1:1 mixture of potassium phosphate plus either potassium chloride or potassium acetate.
Insulin: After the initial fluid bolus is complete, begin a continuous insulin infusion at 0.1 units/kg per hourb. Mix 50 units of regular insulin in 50 mL of
saline (0.45 or 0.9% NaCl), such that 1 mL of the infusion provides 1 unit of insulin.
Glucose: Add dextrose to the IV fluids when the blood glucose falls below approximately 300 mg/dL (17 mmol/L) to prevent hypoglycemia during
treatmentc.

a
Regardless of the initial measured serum potassium concentration, patients with DKA have a total body potassium deficit and therapy with insulin and
fluids will lower serum potassium concentration. Use of a mixture of potassium salts (potassium phosphate plus either potassium chloride or potassium
acetate) is recommended to decrease chloride administration and replace phosphorus losses.
b
For mild DKA treated in the emergency department or in unusual circumstances where facilities to administer IV insulin are not readily available,
subcutaneous insulin can be used.
c
A "2-bag system" is a method to maintain the patient's blood glucose in an acceptable range. In this technique, 2 bags of the selected IV fluid solution
are infused concurrently, one containing 10% dextrose and the other containing no dextrose. By adjusting the relative rates of fluid administration from
each bag, the rate of fluid and electrolyte administration can be maintained constant, while varying the rate of dextrose infusion to respond to changes
in the patient's blood glucose concentrations.

Reproduced with permission from: Glaser N. Diabetic ketoacidosis in children: treatment and complications. In: UpToDate, Post TW (Ed), UpToDate,
Waltham, MA. (Accessed on October 1, 2023.) Copyright © 2023 UpToDate, Inc. and its affiliates and/or licensors. All rights reserved.

NOVEMBER 2023 • www.ebmedicine.net 10 © 2023 EB MEDICINE

treatment should be initiated as with any patient who
has rhabdomyolysis or kidney injury. Patients with
HHS are also at higher risk for thrombosis due to the
hyperosmolar state and severe dehydration.41,44 Con-
sideration should be given to preventive strategies—
either pharmacological or mechanical—as well as
avoiding central line placement, especially in higher
risk locations (such as the femoral access sites) due to
risk for venous thromboembolism.45
Monitoring During Treatment
The patient’s hydration (via examination and urine
output), neurological status, clinical condition, and
metabolic state should be monitored closely through-
out treatment. Patients should be on full monitors
continuously and should have hourly neurological
checks in the early treatment phase and if there is
concern for cerebral edema. Serum glucose levels
(measured by point-of-care or by blood draw) should
be checked every hour while the patient is receiving
continuous insulin infusion. Basic metabolic panel
and venous blood gas should be obtained every 2
to 4 hours and additional laboratory studies includ-
ing magnesium, phosphorus, and calcium should be
obtained every 4 to 6 hours unless significant de-
rangements are present, in which case, they should
be checked more frequently.16 Depending on the
clinical setting, this will often necessitate admission to
a critical care unit.
Complications During Treatment
Children with DKA or HHS are at high risk for compli-
cations throughout their episode of illness.
Cerebral Edema
The most worrisome complication is cerebral edema,
which is more common in children than adults. Chil-
dren at the greatest risk for cerebral edema include
those aged <5 years, those with new-onset diabetes,
children with elevated urea nitrogen levels (>20 mg/
dL), and those with arterial partial pressure of car-
bon dioxide (pCO2) <21 mm Hg (severe DKA).26,45
Symptoms of clinically significant cerebral injury most
commonly occur within 12 hours of presentation, but
they can occur prior to therapy initiation and up to
48 hours later.16 These symptoms can vary, but often
include severe headache, persistent vomiting, leth-
argy, irritability, and elevated blood pressure. More
severe symptoms include decrease in heart rate when
not asleep (usually >20 beats/minute), altered mental
status (slurred speech, agitation), and urinary inconti-
nence. Though there are suggested diagnostic criteria
for cerebral edema, it is critical to intervene should
there be any suspicion of cerebral injury. Do not delay
treatment to obtain imaging.46 Children who are at
high risk and those with cerebral edema should be
monitored in a pediatric intensive care unit (ICU).
The most recent guidelines from the International
NOVEMBER 2023 • www.ebmedicine.net
Society for Pediatric and Adolescent Diabetes recom-
mend either mannitol or hypertonic saline for treat-
ment of cerebral edema.16 The authors of this issue
recommend use of whichever agent is most readily
available. Treatment with mannitol is 0.5 to 1 g/kg
given IV over 10 to 15 minutes.16 Improvement should
be apparent within approximately 15 minutes of treat-
ment. Continue fluids at a standard maintenance rate
to maintain normal blood pressure and avoid hypoten-
sion. Mannitol use has been shown to demonstrate
benefits to cerebral blood flow in pediatric pa-
tients.29,47 If mannitol does not result in improvement,
2.5 to 5 mL/kg of hypertonic saline (3% NaCl) should
be given IV over 15 to 20 minutes.16 Theoretically, use
of hypertonic saline alone will be effective for treat-
ing cerebral edema; however, there has been some
concern that it may increase mortality.48 Some experts
use hypertonic saline if the patient has cerebral edema
early in the course, when they are still dehydrated.16,37
Therefore, early in the course of treatment or for a pa-
tient with HHS, hypertonic saline should be considered
as initial treatment of cerebral edema.
Fluid therapy has not been demonstrated as the
primary etiology for pediatric cerebral edema.47-52 This
was initially shown in the PECARN DKA Fluid Trial,
which studied nearly 1300 children in a randomized
controlled trial.3 Further studies demonstrated similar
results; therefore, fluids should be given liberally dur-
ing management of hyperglycemic emergencies.11,16,53
Intubation
Supplemental oxygen should be used when needed.
Intubation should be reserved for patients with severe
obtundation when there is concern for airway protec-
tion.16,37 Most patients with cerebral edema due to
DKA or HHS will not need mechanical ventilation,
and especially not prior to treatment with mannitol or
hypertonic saline. Even patients with markedly abnor-
mal respiratory patterns should be managed without
intubation, when possible. Mechanical ventilation is
associated with increased mortality, as the ventilator
parameters rarely approximate the sick child’s innate
physiologic compensation, and the severe metabolic
acidosis leads to morbidity and mortality.12,54
Additional Complications
Additional complications of DKA and HHS to be
aware of include venous thromboembolism (espe-
cially associated with young children with central
lines, particularly femoral), pancreatitis, kidney injury,
fungal infections, and long-term cognitive impair-
ment.16,44 Avoid placing a central venous catheter un-
less absolutely necessary and peripheral IV access is
not sufficient. Malignant hyperthermia has occurred in
several pediatric patients with HHS.41 Those with a fe-
ver and elevated creatine kinase should be managed
with dantrolene.41 Patients with HHS and malignant
hyperthermia rarely survive.16
11 © 2023 EB MEDICINE
n Special Circumstances
Managing Patients With Diabetes in the
Emergency Department
Patients with diabetes mellitus may present to the ED
for other reasons and subsequently have hypergly-
cemia or even DKA or HHS while in the ED. Patients
with known diabetes who present for any illness, those
who have been NPO or had minimal intake, or those
with expected long stays should have regular glu-
cose checks. It is imperative to ensure these patients
receive their usual insulin doses as they would at
home and that they have appropriate food available.
It is also critical to continue to treat underlying thyroid
disease or consider additional comorbidities, espe-
cially in patients who are not following the expected
clinical course. Mental health patients are at high risk
for poor insulin management and need special atten-
tion to their glycemic control while in the ED, espe-
cially in settings in which patients may be boarding for
a prolonged time period in the ED.13,55 Additionally,
patients who are attempting to lose weight may use
insulin omission to assist this. It is critical to involve so-
cial work and pediatric endocrinology early for mental
health patients, ill patients, and those who are NPO.
Insulin Pumps
Many patients with known diabetes mellitus will pres-
ent with insulin pumps. Insulin is stored in a reser-
voir (that requires refills) and is delivered via a small
subcutaneous catheter that should be changed by
the patient every 2 to 3 days.56 Some patients may be
using a pump that does not have tubing. The majority
of patients with an insulin pump also use a continuous
glucose monitor. Insulin pumps use only rapid-acting
insulin (or less commonly, short-acting insulin) and
have both a basal rate and a bolus insulin dose that is
Figure 1. Sample Insulin Pumps
A B
A. Traditional insulin pump, B. Insulin pump patch
Reproduced from Brooke H McAdams, Ali A Rizvi. An overview of insulin pumps and glucose sensors for the generalist. Journal of Clinical Medicine.
2016 Jan 4;5(1):5. © 2016 Brooke H McAdams and Ali A Rizvi. DOI: 10.3390/jcm5010005. Used under the Creative Commons by Attribution (CC-BY)
license http://creativecommons.org/licenses/by/4.0/
C. Implantable insulin pump
Reprinted from Advanced Healthcare Materials, Volume 10, Issue 17. Chi Hwan Lee, Hyowon Lee, James K. Nolan, et al. Wearable glucose monitoring
and implantable drug delivery systems for diabetes management. Pages 1-23, © 2021 Wiley-VCH GmbH. https://onlinelibrary.wiley.com/doi/10.1002/
adhm.202100194
NOVEMBER 2023 • www.ebmedicine.net
used when eating. Pumps are programmed with basal
rates, insulin:carbohydrate ratios, and correction or
sensitivity factors. Newer pumps receive glucose val-
ues from a continuous glucose monitor and have the
ability to modulate insulin delivery to achieve preset
blood glucose targets (automated insulin delivery or
“artificial pancreas”).57,58 The pump itself is able to be
“interrogated” to determine the current basal rate,
bolus insulin settings, and recent delivery of insulin.
Parents and the majority of adolescent patients (even
some younger, adept patients) should be able to in-
terrogate the pump. Technology is constantly chang-
ing and improving, so emergency clinicians should be
aware of local practices and devices commonly used
in their region.
Patients with pump malfunctions or incorrectly
placed or kinked subcutaneous catheters will have
hyperglycemia and may present with DKA. Patients
with DKA should have the catheter removed from
their body and the pump turned off. If there is no
one available with personal knowledge of the pump,
the emergency clinician may have to turn it off. This
can easily be done by following prompts and using
the touch-screen on the hand-held pump or case.
It is recommended to remove the catheter that is
directly attached to the patient prior to manipulating
the pump. For tubeless insulin pumps, the cannula
is underneath the device. To remove the catheter,
simply remove the adhesive and material from the
patient’s body. A very small plastic catheter attached
to the delivery unit should be seen. For patients using
a pump with an infusion set, the catheter is similarly
attached to the patient, but may have prongs that
snap onto the delivery unit. This may be unsnapped
and the adhesive unit removed. Examples of insulin
pumps are shown in Figure 1.
C
12 © 2023 EB MEDICINE
 For patients who are in the ED for a reason
unrelated to their diabetes, the insulin pump may be
used to deliver insulin, provided the patient’s blood
glucose levels are in an acceptable range and they
are not ketotic. Critically ill patients should have their
pump disconnected and/or removed, and insulin
should be delivered via an alternative method, either
via subcutaneous delivery or IV infusion.
If it is unclear whether an insulin pump is working,
remove the pump and the infusion catheter from
the patient and transition to subcutaneous insulin
dosing. If the patient is in DKA or HHS, they should
not be treated with subcutaneous insulin and should
instead be treated with IV insulin and fluids as
discussed in prior sections. Most patients have an
insulin:carbohydrate ratio and a glucose correction
or insulin sensitivity factor, which should be used
similarly for subcutaneous insulin. All pediatric
patients with type 1 diabetes, including those with
insulin pumps should have “sick day” regimens.
Usually, parents have this with them, and they should
be asked directly for this information. If the sick day
regimen cannot be determined, disconnect and
remove the pump from the patient. Consulting a
pediatric endocrinologist, pediatric ED, or intensive
care unit (ICU) for guidance is prudent until the
patient can be transferred.
If there are any concerns about a patient inten-
tionally omitting insulin or overdosing on insulin, their
insulin pump should be disconnected and both the
pump and infusion set should be removed from the
patient and stored in a secure location.
n Controversies and Cutting Edge
The current prevalent debates in pediatric diabetic
emergencies include the etiology and management
of cerebral edema and the use of a 1-bag versus a
2-bag system.
Cerebral Edema
Cerebral edema is the cause of 60% to 90% of DKA-
related deaths. Survivors have shown long-term
cognitive deficits, which range from mild to severe.
Historically, it was thought that fluid resuscitation was
the etiology of cerebral edema in pediatric patients;
however, that has been refuted. Instead, cerebral
edema is thought to occur due to a number of fac-
tors that appear to be intrinsic to DKA and HHS,
specifically cerebral hypoperfusion and dehydration.
The degree of dehydration and hyperventilation at
presentation correlates to development of cerebral
edema.11,12,54 Furthermore, there have been patients
who presented with cerebral edema prior to fluid
resuscitation.53,59 It is imperative to treat patients with
hyperglycemic crises with IV fluids as indicated, even
if they have alterations in mental status.
NOVEMBER 2023 • www.ebmedicine.net
1-Bag Versus 2-Bag Systems
Use of both the 1-bag and 2-bag systems has been
studied and discussed. Ideally, a 2-bag system can be
used to avoid hypoglycemia and decrease cost. Fluid
administration should be given in the manner that is
most quickly available and with the system that the
treating clinician and nursing team is most comfort-
able with.
n Disposition
All patients with new-onset DKA, high-risk patients,
or those with moderate to severe DKA or HHS should
be admitted to the hospital after initial resuscitation in
the ED. If an inpatient unit suitable for management
of pediatric diabetic complications is not available,
those patients should be transferred to the nearest
capable facility. If this is not possible, we recommend
admission to the ICU or an inpatient floor where the
patient will have close monitoring. Once admitted,
insulin infusion may be discontinued when all of the
following conditions are met:16,33
• Venous pH >7.3 or serum bicarbonate ≥18 mEq/L
• Blood glucose <200 mg/dL (11.1 mmol/L)
• Serum anion gap is normal or serum beta-
hydroxybutyrate is ≤1 mmol/L
• The patient is tolerating oral intake
Patients may continue to have a mild hyperchlore-
mic acidosis after the criteria are met; this should not
prevent transition to subcutaneous insulin. Patients
should be transitioned to subcutaneous insulin at the
time of a meal; they should receive a dose of rapid-act-
ing subcutaneous insulin according to their pre-meal
blood glucose concentration and the carbohydrate
content of the meal. The continuous insulin infusion
should be stopped 15 to 30 minutes after injection of
rapid-acting insulin. Basal (long-acting) insulin should
be given either before (prior evening) or at the same
time as the injection of the first dose of rapid-acting
insulin.16,33 Before a patient is discharged from hos-
pital, the caregivers and, when age-appropriate, the
patient should demonstrate excellent understanding
of home diabetes management, including checking
glucose, checking blood and/or urine ketones, how to
determine the dose of insulin to be administered for
meals and use of a correction factor, management of
hypoglycemia, and dietary requirements. They must
have available supplies, have reliable contact with their
diabetes team, and have a follow-up appointment
within 24 hours before they are discharged.
It is uncommon for a pediatric patient with an
emergency due to diabetes to be discharged home;
however, established patients with mild DKA may
be considered for discharge after DKA has resolved.
These patients must have excellent follow-up and un-
derstanding of home diabetes management and have
all supplies; however, it is preferred to admit them or
13 © 2023 EB MEDICINE
transfer them to a pediatric hospital. If a patient is to
be discharged home, it is strongly recommended to
consult with a pediatric endocrinologist, pediatric ED,
or pediatric ICU prior to discharge.
n Summary
The patients at highest risk for complications from
diabetes (most notably cerebral edema) are children
aged <5 years, those with new-onset diabetes, and
those with prolonged symptoms before presenta-
tion. Any pediatric patient, including infants, with
unexplained vomiting, lethargy, or altered mental
status should have a glucose check as part of their
initial evaluation. All patients with DKA or HHS should
receive an isotonic crystalloid fluid bolus IV as soon
as their illness is identified. DKA requires vigorous
administration of IV fluids and IV insulin, while the
mainstay of treatment in HHS is IV fluids. During re-
suscitation of patients with DKA or HHS, the following
laboratory values should be measured: glucose every
hour; basic metabolic panel, venous blood gas, se-
rum beta-hydroxybutyrate or urine ketones every 2 to
4 hours; calcium, magnesium, and phosphorus every
4 to 6 hours if normal, and more often if abnormal; an
ECG on initial assessment; continuous cardiopulmo-
nary monitoring if there are potassium, phosphorus,
magnesium, or calcium derangements or if the pa-
tient is very dehydrated
5 or altered. Other secondary
Recommendations
To Apply in Practice
5 Things
5 That Will
Recommendations
Change To
Your Practice
Apply in Practice
1. Appropriate fluid resuscitation for the pa-
tient’s clinical condition does not increase
5
the risk for Recommendations
cerebral edema and is the most
important initialTo Apply infor
treatment Practice
DKA and HHS.
2. Administering sodium bicarbonate may lead
to worse cerebral outcomes; it should not be
given unless the patient is in cardiac arrest,
has life-threatening hyperkalemia, or has a
pH <6.9 with evidence of cardiac dysfunction.
3. A 2-bag system should be used, when possi-
ble, to decrease fluid change time, decrease
risk for hypoglycemia, decrease cost of care,
and decrease time in the hospital.
4. Any change in mental status should be taken
seriously and cerebral edema should be man-
aged early, prior to obtaining a CT scan.
5. Prevention of DKA and HHS with excellent
education, regular follow-up, and psycho-
social intervention is the best way to keep
patients from having long-term and life-
threatening consequences.
NOVEMBER 2023 • www.ebmedicine.net
illnesses should be searched for and treated. Central
lines, sodium bicarbonate, and intubation should be
avoided. A high index of suspicion should be main-
tained for pancreatitis, venous thrombosis, kidney
injury, rhabdomyolysis, and malignant hyperthermia
(specifically in HHS patients). Patients who have agita-
tion, alteration in mental status, or any concerning
neurological symptoms should be treated immedi-
ately with 0.5 to 1 g/kg of IV mannitol. Hypertonic
saline at 5 mL/kg IV may be used, especially if man-
nitol is unavailable or if the patient is severely dehy-
drated. All high-risk patients and those with cerebral
edema should be admitted to the pediatric ICU. Early
involvement of social work, child life (if available), and
endocrinology is critical.
n Time- and Cost-Effective Strategies
• Consult pediatric ICU and endocrinology as soon
as DKA, HHS, or new-onset diabetes is recog-
nized. Initiate the transfer process early if your
institution does not have an inpatient pediatric
unit that is equipped to manage the patient.
• Consider use of a 2-bag system to facilitate easy
and quick transitions based on glucose levels and
to save money in fluid bag changes.
• Anticipate that the pediatric patient with diabetic
complications will need supplies, medications, and
follow-up appointments; involve social work early
if the patient may be discharged from the ED.
• Consult a pharmacist as soon as it is suspected
that special fluids or an insulin infusion will be
needed. The pharmacist can help determine what
fluids and electrolyte replacement are most ap-
propriate and can help ensure timely administra-
tion and monitoring.
n References
Evidence-based medicine requires a critical appraisal
of the literature based upon study methodology and
number of subjects. Not all references are equally
robust. The findings of a large, prospective, random-
ized, and blinded trial should carry more weight than
a case report.
To help the reader judge the strength of each refer-
ence, pertinent information about the study, such as the
type of study and the number of patients in the study is
included in bold type following the references, where
available. The most informative references cited in this
paper, as determined by the authors, are noted by an
asterisk (*) next to the number of the reference.
1. Bui H, To T, Stein R, et al. Is diabetic ketoacidosis at disease
onset a result of missed diagnosis? J Pediatr. 2010;156(3):472-
477. (Retrospective cohort; 3947 children)
2. American Diabetes Association. Standards of medical care in
diabetes-2021 abridged for primary care providers. Clin Diabe-
14 © 2023 EB MEDICINE
 Case Conclusions
For the 3-year-old girl with vomiting and fatigue after having fever for 1 day…
You were worried about dehydration, shock, and electrolyte abnormalities in addition to new-onset diabe-
tes and possible DKA. Immediate IV access and laboratory studies were obtained, including a point-of-care
glucose and venous blood gas with lactate and electrolytes, which were most notable for a glucose of 385
mg/dL, pH of 7.0, bicarbonate of 8 mEq/L, and lactate of 2.2 mmol/L. The girl was diagnosed with new-
onset DKA triggered by a viral illness. While her IV lines were obtained, you were able to obtain additional
blood to send to the laboratory for testing, including a complete blood count; hemoglobin A1C; beta-hy-
droxybutyrate; comprehensive metabolic panel that included calcium, magnesium, and phosphorus levels;
CASE 1

lipase; C-reactive protein; serum osmolality; and diabetes diagnostic panel. The patient also gave a sample
for a urinalysis. Prior to receiving the results, you initiated a 20-mL/kg 0.9% NaCl IV bolus to reverse her
shock and then a 2-bag system with a continuous 0.05 unit/kg/hr insulin infusion (because you were wor-
ried she would be sensitive to insulin), while the front desk clerk paged the endocrinologist on call. You also
remembered to evaluate the etiology of her fever and vomiting and were reassured that she did not have
pneumonia, appendicitis, intussusception, or pancreatitis, based on your examination and workup. Though
she was alert and improved, she was admitted to the pediatric ICU, given her young age and new-onset di-
agnosis of diabetes mellitus with DKA. While in the pediatric ICU, she developed some change in behavior
and thus received 0.5 g/kg of IV mannitol. A subsequent head CT was normal, but her treatment team was
glad they had given her the mannitol. She returned to her clinical baseline and was discharged home with
insulin and close endocrinology follow-up.

For the 13-year-old boy with type 2 diabetes mellitus and cough with a glucose of >600 mg/dL…
You obtained a point-of-care glucose and venous blood gas with lactate and electrolytes. The results were:
glucose, 620 mg/dL; pH, 7.3; bicarbonate, 16 mEq/L; and sodium, 130 mEq/L. The boy was diagnosed with
HHS. A peripheral IV line was placed when obtaining the blood gas, and additional laboratory studies were
drawn, including a complete blood cell count, comprehensive metabolic panel, serum osmolality, beta-
CASE 2

hydroxybutyrate, lipid panel, lipase, and hemoglobin A1C. You knew the patient was at high risk for throm-
bosis and that expanding his intravascular volume was important, so you initiated rapid fluid resuscitation
with a 1-L normal saline IV bolus. You calculated his corrected sodium, which was 138 mEq/L, so you started
him on maintenance 0.45% NaCl at a rate of 300 mL/hr because he was only mildly dehydrated. Compared
to patients with DKA, this patient needed more aggressive fluid resuscitation, which you communicated to
the intensive care team, who also initiated insulin. He was admitted for 5 days and discharged home with
close follow-up.

For the 17-year-old girl with type 1 diabetes mellitus with altered mental status…
The patient improved with the dextrose bolus and maintenance fluids containing dextrose, but you realized
that her insulin pump may still be on, so you turned it off and removed the pump and infusion set from the
patient. It was unclear whether she had also ingested another substance, so in addition to basic laboratory
CASE 3

studies, you obtained serum and urine drug screens, a urine pregnancy test, and an ECG. You also wor-
ried about intentional insulin overdose, so you completed a detailed HEADSS (Home, Education, Activities,
Drugs/alcohol, Suicide/safety, Sexuality) examination and had a social worker visit the patient. During the
discussion with the patient, she admitted to intentionally giving herself too much insulin after a fight with
her boyfriend. You were able to have psychiatry meet the patient in the ED, and they continued to see her
while she was admitted to the hospital. She was discharged to the care of her mother after 4 days, with
plans to start a partial-hospitalization program for her suicide attempt.

tes. 2021;39(1):14-43. (Consensus guideline) multicenter study; 3,470,000 children)

3.* Kuppermann N, Ghetti S, Schunk JE, et al. Clinical trial of fluid
infusion rates for pediatric diabetic ketoacidosis. N Engl J Med.
2018;378(24):2275-2287. (Randomized controlled trial; 1255
children) DOI: 10.1056/NEJMoa1716816
4. Lawrence JM, Divers J, Isom S, et al. Trends in prevalence of
type 1 and type 2 diabetes in children and adolescents in the
US, 2001-2017. JAMA. 2021;326(8):717-727. (Cross-sectional,
5. Divers J, Mayer-Davis EJ, Lawrence JM, et al. Trends in inci-
dence of type 1 and type 2 diabetes among youths - selected
counties and Indian reservations, United States, 2002-2015.
MMWR Morb Mortal Wkly Rep. 2020;69(6):161-165. (Retro-
spective review; 69,400,000 children)
6. Pierce JS, Kozikowski C, Lee JM, et al. Type 1 diabetes in very
young children: a model of parent and child influences on man-

NOVEMBER 2023 • www.ebmedicine.net 15 © 2023 EB MEDICINE

 Risk Management Pitfalls for Pediatric Patients
With Diabetic Complications and Emergencies
1. “A 4-year-old patient presented with vomiting
and altered mental status after a recent upper
respiratory infection. I was focused on the
infection and missed diagnosing DKA.” Do not
fail to recognize the signs and symptoms of a pa-
tient with new-onset DKA or HHS; consider these
diagnoses in all ill or lethargic pediatric patients,
including infants.
2. “A 16-year-old girl presented in DKA with po-
tassium of 3.9 mEq/L. I wanted to address the
DKA quickly, so I gave her insulin.” An initial IV
bolus of isotonic crystalloid is critical; do not give
insulin for at least 1 hour after initiation of fluids.
3. “A 7-year-old girl presented with new-
onset DKA. Her laboratory results were
notable for sodium, 134 mEq/L; potassium,
5.3 mEq/L; and bicarbonate, 8 mEq/L. I
gave sodium bicarbonate to help with the
acidosis.” Avoid overcorrection of acidosis and
electrolyte abnormalities. Sodium may be falsely
abnormal due to hyperglycemia. Giving sodium
bicarbonate can worsen outcomes and should be
avoided, except in the most critical of patients (ie,
those in cardiac arrest).
4. “A 3-year-old with a pH of 7.1 and glucose of
283 mg/dL presented with slurred speech and
ataxia. I wanted to correctly address his neu-
rologic issues, so I ordered a CT before admin-
istering medications.” Mannitol or hypertonic
saline should be initiated immediately upon sus-
picion for cerebral edema. Waiting for CT results
should not delay treatment of cerebral edema.
5. “The 9-year-old girl with DKA received a 20-
mL/kg normal saline IV bolus over 30 minutes
but was still hyperglycemic and acidemic. I
wasn’t sure whether I should initiate subcu-
taneous insulin aspart or continuous insulin
infusion.” Subcutaneous insulin or IV boluses of
insulin are not recommended; continuous insulin
infusion is preferred to prevent hypoglycemia and
to achieve rapid glucose control, due to the risk
for precipitating shock, hypokalemia, and cerebral
edema with insulin boluses. Insulin should not be
started until at least 1 hour after fluids have be-
gun, so there should be time to time to prepare a
continuous insulin infusion.
NOVEMBER 2023 • www.ebmedicine.net
6. “The patient who was on an insulin infusion
was feeling weak and shaky. I wasn’t sure
whether I should check any additional labs.”
Do not forget to monitor and address hypogly-
cemia; stop insulin temporarily if the patient is
symptomatic. Patients may have rebound hyper-
glycemia, so continue glucose checks even if the
patient is hypoglycemic.
7. “A 6-year-old boy presented in DKA after 2
days of abdominal pain, vomiting, and diar-
rhea. He was febrile. I thought his symptoms
were likely related to his DKA, so I did not
look into other causes.” After initiating treat-
ment for DKA or HHS, do not forget to search
for and address the primary trigger (eg, acute
appendicitis).
8. “The patient with known type 1 diabetes
had DKA. I wanted to wait to receive the lab
results before obtaining an ECG.” Electrolyte
abnormalities can be severe and cause
complications such as cardiac arrhythmia; obtain
an ECG early.
9. “The 11-year-old patient with a pH of 7.03 and
glucose of 311 mg/dL was just moved from
triage to the resuscitation bay. She was lethar-
gic but responsive to stimulation. She had a
heart rate of 100 beats/min, blood pressure of
105/60 mm Hg, respiratory rate of 20 breaths/
min, and oxygen saturation of 96% on room
air. I decided to prepare for rapid sequence
intubation.” Avoid intubation unless the patient
is obtunded with poor respiratory effort. Con-
sultation with the pediatric ICU and transfer to a
pediatric hospital should be considered prior to
intubation. This patient likely will improve with ini-
tiation of treatment for cerebral edema and DKA.
10. “The 17-year-old patient with HHS was here
with his mom, and they wanted to leave. Since
they were in a hurry, I discharged them and
told them to follow up with their pediatri-
cian to get lancets and a glucometer.” Do not
discharge the patient before adequate under-
standing of diagnosis and management has been
achieved and the patient has all of their supplies
and medications in hand.
16 © 2023 EB MEDICINE
 agement and outcomes. Pediatr Diabetes. 2017;18(1):17-25.
(Review)
7. Cengiz E, Xing D, Wong JC, et al. Severe hypoglycemia and
diabetic ketoacidosis among youth with type 1 diabetes in the
T1D Exchange clinic registry. Pediatr Diabetes. 2013;14(6):447-
454. (Retrospective review; 13,487 patients)
8. Rewers A, Chase HP, Mackenzie T, et al. Predictors of acute
complications in children with type 1 diabetes. JAMA.
2002;287(19):2511-2518. (Prospective cohort; 1234 children)
9. Sapru A, Gitelman SE, Bhatia S, et al. Prevalence and characteris-
tics of type 2 diabetes mellitus in 9-18 year-old children with dia-
betic ketoacidosis. J Pediatr Endocrinol Metab. 2005;18(9):865-
872. (Retrospective case-control; 98 patients with 133
episodes of DKA, 69 with 1-year complete follow-up)
10. Laffel L, Svoren B. Epidemiology, presentation, and diagnosis
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Date. 2023. Accessed October 1, 2023. Available at: https://
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diagnosis-of-type-2-diabetes-mellitus-in-children-and-adoles-
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adverse outcomes in children with diabetic ketoacidosis-related
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12.* Marcin JP, Glaser N, Kuppermann N. Ventilation in pediatric
diabetic ketoacidosis--not too much, but not too little. Pediatr
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diabetes. J Pediatr (Rio J). 2020;96 Suppl 1(Suppl 1):39-46.
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15. Casqueiro J, Casqueiro J, Alves C. Infections in patients with
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16.* Glaser N, Fritsch M, Priyambada L, et al. ISPAD Clinical Practice
Consensus Guidelines 2022: diabetic ketoacidosis and hyper-
glycemic hyperosmolar state. Pediatr Diabetes. 2022;23(7):835-
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18. Magee MF, Bhatt BA. Management of decompensated dia-
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1998;158(16):1799-1802. (Retrospective cohort; 112 adults)
20. Nyenwe EA, Loganathan RS, Blum S, et al. Active use of
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ketoacidosis in a city hospital. Endocr Pract. 2007;13(1):22-29.
(Retrospective cohort; 168 adults)
21. Grimberg A, Cerri RW, Satin-Smith M, et al. The “two bag
system” for variable intravenous dextrose and fluid administra-
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22. Velasco JP, Fogel J, Levine RL, et al. Potential clinical benefits
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(Consensus guideline)
29. Cengiz E, Danne T, Ahmad T, et al. ISPAD Clinical Practice
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39. Weant KA, Deloney L, Elsey G, et al. A comparison of 10%
17 © 2023 EB MEDICINE
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(Retrospective case-control; 311 adults)
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44. Gutierrez JA, Bagatell R, Samson MP, et al. Femoral central
venous catheter-associated deep venous thrombosis in children
with diabetic ketoacidosis. Crit Care Med. 2003;31(1):80-83.
(Retrospective case-control; 24 children)
45. Rosenbloom AL. Hyperglycemic crises and their complica-
tions in children. J Pediatr Endocrinol Metab. 2007;20(1):5-18.
(Review)
46. Soto-Rivera CL, Asaro LA, Agus MS, et al. Suspected cerebral
edema in diabetic ketoacidosis: is there still a role for head CT
in treatment decisions? Pediatr Crit Care Med. 2017;18(3):207-
212. (Retrospective analysis; 96 children)
47. Soriano SG, McManus ML, Sullivan LJ, et al. Cerebral blood
flow velocity after mannitol infusion in children. Can J Anaesth.
1996;43(5 Pt 1):461-466. (Case-control; 10 children)
48. Decourcey DD, Steil GM, Wypij D, et al. Increasing use of
hypertonic saline over mannitol in the treatment of symp-
tomatic cerebral edema in pediatric diabetic ketoacidosis: an
11-year retrospective analysis of mortality*. Pediatr Crit Care
Med. 2013;14(7):694-700. (Retrospective case-control; 43,107
children)
Class of Evidence Definitions
Each action in the clinical pathways section of Pediatric Emergency Medicine Practice receives a score based on the following definitions.
Class I Class II
• Always acceptable, safe • Safe, acceptable
• Definitely useful • Probably useful
• Proven in both efficacy and effectiveness
Level of Evidence:
Level of Evidence: • Generally higher levels of evidence
• One or more large prospective studies • Nonrandomized or retrospective stud-
are present (with rare exceptions) ies: historic, cohort, or case control
• High-quality meta-analyses studies
• Study results consistently positive and • Less robust randomized controlled trials
compelling • Results consistently positive
This clinical pathway is intended to supplement, rather than substitute for, professional judgment and may be changed depending upon a patient’s individual
needs. Failure to comply with this pathway does not represent a breach of the standard of care.
Copyright © 2023 EB Medicine. www.ebmedicine.net. No part of this publication may be reproduced in any format without written consent of EB Medicine.
NOVEMBER 2023 • www.ebmedicine.net
49. Glaser NS, Wootton-Gorges SL, Marcin JP, et al. Mechanism of
cerebral edema in children with diabetic ketoacidosis. J Pediatr.
2004;145(2):164-171. (Case-control; 14 children)
50. Dhochak N, Jayashree M, Singhi S. A randomized controlled
trial of one bag vs. two bag system of fluid delivery in children
with diabetic ketoacidosis: experience from a developing
country. J Crit Care. 2018;43:340-345. (Randomized controlled
trial; 30 children)
51. Long B, Koyfman A. Emergency medicine myths: cerebral
edema in pediatric diabetic ketoacidosis and intravenous fluids.
J Emerg Med. 2017;53(2):212-221. (Review)
52. Brown TB. Cerebral oedema in childhood diabetic ketoacido-
sis: is treatment a factor? Emerg Med J. 2004;21(2):141-144.
(Review)
53. Lawrence SE, Cummings EA, Gaboury I, et al. Population-
based study of incidence and risk factors for cerebral edema in
pediatric diabetic ketoacidosis. J Pediatr. 2005;146(5):688-692.
(Case-control; 13 patients)
54. Tasker RC, Lutman D, Peters MJ. Hyperventilation in severe dia-
betic ketoacidosis. Pediatr Crit Care Med. 2005;6(4):405-411.
(Review)
55. Hu TY, Price J, Pierce JS, et al. The association between
pediatric mental health disorders and type 1 diabetes-related
outcomes. Pediatr Diabetes. 2022;23(4):507-515. (Retrospec-
tive cohort; 237 adults)
56. Levitsky L, Misra M. Insulin therapy for children and adolescents
with type 1 diabetes mellitus. UpToDate. 2023. Accessed Octo-
ber 1, 2023. Available at: https://www.uptodate.com/contents/
insulin-therapy-for-children-and-adolescents-with-type-1-diabe-
tes-mellitus (Review)
57. Beck RW, Bergenstal RM, Laffel LM, et al. Advances in
technology for management of type 1 diabetes. Lancet.
2019;394(10205):1265-1273. (Review)
58. Nimri R, Nir J, Phillip M. Insulin pump therapy. Am J Ther.
2020;27(1):e30-e41. (Review)
59.* Azova S, Rapaport R, Wolfsdorf J. Brain injury in children with
diabetic ketoacidosis: review of the literature and a proposed
pathophysiologic pathway for the development of cerebral
edema. Pediatr Diabetes. 2021;22(2):148-160. (Review)
DOI: 10.1111/pedi.13152
Class III Indeterminate
• May be acceptable • Continuing area of research
• Possibly useful • No recommendations until further
• Considered optional or alternative research
treatments
Level of Evidence:
Level of Evidence: • Evidence not available
• Generally lower or intermediate levels • Higher studies in progress
of evidence • Results inconsistent, contradictory
• Case series, animal studies, • Results not compelling
consensus panels
• Occasionally positive results
18 © 2023 EB MEDICINE
 Clinical Pathway for Management of Pediatric Diabetic
Ketoacidosis in the Emergency Department16

Patient presents with signs and symptoms of DKA (polyuria, polydipsia, weight loss, vomiting, abdominal pain, difficulty breathing,
confusion, dehydration, ketones odor, ill appearance, drowsiness, abnormal breathing [Kussmaul])

• Stabilize the patient as needed: obtain 2 peripheral IV lines and point-of-care glucose level, initiate fluid resuscitation with 10-20 mL/kg 0.9%
normal saline bolus IV (repeat until circulation is restored), consider oxygen supplementation
• Perform head-to-toe examination
• Obtain electrocardiogram and initial laboratory studies: point-of-care glucose, venous blood gas with electrolytes and lactate, complete blood cell
count, comprehensive metabolic panel, beta-hydroxybutyrate
• Obtain additional studies: serum magnesium and phosphate levels, hemoglobin A1C, serum osmolality, lipid levels, and urinalysis with urine
dipstick to look for ketones

DKA confirmed Signs or symptoms concerning for cerebral edema (severe headache,
Criteria: persistent vomiting, lethargy, irritability, elevated blood pressure,
• Metabolic acidosis (venous pH <7.3) decrease in heart rate when not appropriate, altered mental status,
• Hyperglycemia (blood glucose >200 mg/dL or 11.1 mmol/L) urinary incontinence)?
• Ketosis (>3 mmol/L beta-hydroxybutyrate in serum or moderate or
large urine ketones
(Mild DKA, pH 7.2-7.29; moderate to severe DKA, pH <7.2) NO YES

• Administer 10-20 mL/kg 0.9% normal saline bolus IV, can repeat if • Rule out hypoglycemia
necessary (Class II) • Administer mannitol 0.5-1 g/kg or 3% saline 5 mL/kg
• Correct fluid deficit over 24-48 hours with maintenance fluids (with (Class II)
potassium if indicated) or using a 2-bag system • Administer fluids to maintain normal blood pressure
• Order imaging once the patient is stable
• Avoid intubation unless the patient is unable to protect their
airway or severely obtunded (Class III)
After at least 1 hr of initial fluid administration, start continuous insulin
infusion at 0.05-0.1 units/kg/hr (do not administer as a bolus)
(Class II); continue until pH >7.3 serum bicarbonate ≥18 mmol/L,
and beta-hydroxybutyrate <1 mmol/L
• Continue to treat diabetic ketoacidosis
• Admit to pediatric intensive care unit

During treatment, observe/monitor:

Hourly: blood glucose, neurologic check, fluid in/out
Every 2-4 hr: basic metabolic panel and venous blood gas
Every 4-6 hr: Magnesium, phosphorus, calcium

Patient improving? YES Admit to hospital or pediatric intensive care unit

NO

• Reassess IV fluid calculations

• Check insulin delivery system and dose
• Check for additional fluid resuscitation
• Consider sepsis or other conditions
• Seek consultation with pediatric specialist and attempt transfer to a
pediatric center

Abbreviations: DKA, diabetic ketoacidosis; IV, intravenous.

For Class of Evidence definitions, see page 18

NOVEMBER 2023 • www.ebmedicine.net 19 © 2023 EB MEDICINE

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1. A 3-year-old unvaccinated boy presents with 2
days of vomiting and diarrhea, a temperature
of 38°C, and decreased appetite. On your
initial assessment from the door, you see an
ill-appearing child who is hunched over. On
examination, the child’s abdomen is tender,
and he has very dry mucous membranes. His
initial metabolic panel is notable for pH, 7.2;
sodium, 145 mEq/L; potassium, 3.9 mEq/L;
bicarbonate, 9 mEq/L; and glucose, 270 mg/
dL. You suspect this is new-onset diabetes
with DKA, so you obtain further laboratory
studies and initiate fluid resuscitation. In
addition to preparing a 2-bag system and IV
insulin, what next step will you take?
a. Order an abdominal ultrasound
b. Call his pediatrician to find out what medica-
tions he is taking
c. Order a head computed tomography (CT)
without contrast
d. Update his Haemophilus influenzae type B
vaccine
2. A 15-year-old obese boy presents to the
hospital with abdominal pain and dysuria. He
is alert and talkative. His initial laboratory
workup is notable for a glucose of 635 mg/
dL. Which of the following is most likely to be
found in this patient?
a. Venous pH of 7.21
b. Urine dipstick with large ketones
c. Serum bicarbonate of 13 mEq/L
d. Potassium of 5.1 mEq/L
3. Which of the following components is not typi-
cally part of a 2-bag system?
a. 10% dextrose
b. Magnesium
c. 0.45% NaCl
d. Phosphate
NOVEMBER 2023 • www.ebmedicine.net
4. A 6-year-old boy with type 1 diabetes presents
with 3 days of vomiting and fatigue. He is alert
and oriented. You obtain initial laboratory stud-
ies, including a venous blood gas, which are no-
table for the following values: pH, 7.22; partial
pressure of carbon dioxide (pCO2), 24 mm Hg;
bicarbonate, 12 mEq/L; sodium, 131 mEq/L;
potassium, 2.8 mEq/L; phosphate, 1.5 mg/dL:
glucose, 350 mg/dL; and lactate, 3.2 mmol/L.
You give him a 20-mL/kg 0.9% NaCl IV bolus.
Which of the following is your next course of
action?
a. Give 50 mg/kg of ceftriaxone IV
b. Give 5 mL/kg of 3% NaCl IV
c. Start a 2-bag system and IV insulin
d. Give 40 mEq/L of potassium phosphate IV
5. A 6-year-old 20-kg girl with type 1 diabetes
mellitus presents with 1 day of vomiting, de-
creased oral intake, and 2 hours of abnormal
mentation. Her initial blood gas results are:
pH, 7.33; pCO2, 44 mm Hg; bicarbonate, 17
mEq/L; sodium, 144 mEq/L; potassium, 3.2
mEq/L; glucose, 39 mg/dL; and lactate 1.6
mmol/L. Which of the following is the most
appropriate initial fluid resuscitation?
a. 100 mL of D10 IV
b. 25 mL of D25 IV
c. 20 mL/kg of 0.9% NaCl IV
d. 5 mL/kg of 3% NaCl IV
6. Which of the following patients is at highest
risk for long-term diabetes-related complica-
tions?
a. A 17-year-old girl with an insulin pump
b. A 4-year-old boy presenting with vomiting
and weight loss
c. A 6-year-old girl with known type 1 diabetes
mellitus
d. A 15-year-old boy with home glucose of 240
mg/dL
7. A 16-year-old girl with known type 1 diabetes
presents with vomiting and altered mental sta-
tus. She is combative in the room and appears
moderately dehydrated. Her laboratory stud-
ies are notable for a pH of 7.2, pCO2 of 30 mm
Hg, bicarbonate of 12 mmol/L, glucose of 396
mg/dL, and sodium of 134 mg/dL. After giving
an initial fluid bolus, what is the next step in
management?
a. Give a repeat 20-mL/kg lactated Ringer’s
solution IV bolus
b. Obtain a CT scan of the head
c. Give 5 mL/kg of 3% NaCl IV
d. Perform rapid sequence intubation
20 © 2023 EB MEDICINE
8. A 14-year-old girl with type 1 diabetes melli-
tus presents from home. The night before, her
mother heard her talking to her friend about
feeling depressed. You see tubing coming
out from her under her pants and discover an
insulin pump. The girl currently has a Glasgow
Coma Scale score of 8. In addition to check-
ing a point-of-care glucose, which is 32 mg/dL,
what is your next course of action?
a. Try to interrogate the pump
b. Review her continuous glucose monitor
c. Remove the pump and tubing from the pa-
tient
d. Give the patient a 20-mL/kg 0.9% NaCl
bolus IV
9. A 4-year-old girl with no known medical prob-
lems presents with coughing, runny nose, and
vomiting for 2 days. She is ill-appearing and
dehydrated. Your initial workup includes a
blood gas with venous pH of 7.2, which makes
you suspicious that she is in DKA. Where is the
ideal place for her to be managed?
a. Endocrinology unit at the closest available
hospital
b. Pediatric intensive care unit
c. Emergency department until transitioned to
subcutaneous insulin
d. Pediatric hospital medicine floor
…Make it five minutes well spent.
Points & Pearls
QUICK READ
JANUARY 2022 | VOLUME 19 | ISSUE 1
Points
• Using age in hours and a TSB level, the AAP
recommends using the hour-specific nomogram
(see Figure 3, page 5) to determine appropriate
management and follow-up to reduce the risk of
severe hyperbilirubinemia.
• The presence of hyperbilirubinemia risk factors is
used to help interpret the results of the hour-spe-
cific nomogram. Hyperbilirubinemia risk factors
include:
l A newborn nursery predischarge TSB in the
high-risk zone
l Jaundice observed in the first 24 hours
l ABO incompatibility or other known hemo-
lytic disease
l Gestational age 35 to 36 weeks
l Previous sibling who received phototherapy
l Cephalohematoma or significant bruising
l Exclusive breastfeeding with excessive
weight loss
l Asian race
• The plotted results of the hour-specific nomo-
gram will classify neonates into a low-, low inter-
mediate-, high intermediate-, or high-risk zone
for the development of severe hyperbilirubine-
mia. Neonates in the low- or low intermediate-
risk zones can be safely discharged home, while
neonates in the high intermediate- or high-risk
zones should have the TSB plotted on the pho-
totherapy and exchange transfusion nomograms.
(See Figures 4 and 5, page 6.)
• The AAP recommends using the TSB plotted
on the phototherapy and exchange transfusion
nomograms (with neurotoxicity risk factors) to
determine treatment with phototherapy and/or
exchange transfusion, respectively.
• Neurotoxicity risk factors include:
l Isoimmune hemolytic disease
l G6PD deficiency
l Asphyxia
l Significant lethargy
l Temperature instability
l Sepsis
l Acidosis
l Albumin <3.0 g/dL
JANUARY 2022 • www.ebmedicine.net
NOVEMBER 2023 • www.ebmedicine.net
10. Which of the following is not a part of the
criteria for discontinuing a continuous insulin
infusion?
a. Venous pH >7.3
b. Blood glucose <200 mg/dL (11.1 mmol/L)
c. Beta-hydroxybutyrate ≤1 mmol/L
d. Serum bicarbonate >14 mEq/L
When five minutes
can mean a world of
difference in the ED…
With Points & Pearls, you get the key takeaways from each
Pediatric Emergency Medicine Practice issue. They’re great when
Neonatal Hyperbilirubinemia:
Recommendations for
Diagnosis and Management in
the Emergency Department
Pearls
l Jaundice can be recognized by examination
of the skin, sclera, and mucous membranes.
you don’t have time to read the full issue or you need a refresher
on a topic.
The examination of the skin is best achieved
by blanching the skin to reveal the color of the
underlying skin. Jaundice is first observed in
the face and progresses in a cephalocaudal
direction. Visual estimation of jaundice is not
recommended for estimation of TSB levels.
l Physiologic jaundice usually begins on day 2 to
3 of life, peaks around day 4 to 5, and usually
resolves within 2 weeks. Breastfeeding jaundice
overlaps with physiologic jaundice in the first few
days of life. Breast milk jaundice appears after
the first week of life, peaks in the second week,
and can take up to 12 weeks to resolve. Visible
The best part: Points & Pearls is included with your subscription
jaundice that lasts longer than 2 to 3 weeks
should raise concern for a pathologic etiology.
l There are no current recommendations for
diagnostic testing for ABE except for the clinical
examination. ABE is characterized by lethargy
and abnormal behavior, progressing to neonatal
encephalopathy, opisthotonus, and seizures.
at no charge! Go to the back page of this issue to view this
• When initiating phototherapy, double conven-
tional phototherapy may be more effective than
single conventional phototherapy at reducing the
mean TSB and duration of treatment. Conventional
month’s Points & Pearls. You can also access all past editions at
phototherapy plus fiberoptic phototherapy may
be more effective than either alone at reducing
bilirubin levels. There does not appear to be any
additional benefit of triple therapy compared to
double therapy.
• If the exchange transfusion nomogram recommends
exchange transfusion or if TSB is >25 mg/dL at
www.ebmedicine.net/pearls or on our mobile app.
any time, it is a medical emergency, and the infant
should be admitted. Immediate exchange transfu-
sion is recommended for any infant who is jaun-
diced and manifests the signs of ABE. Exchange
transfusion is associated with significant complica-
tions, so this procedure is reserved for neonates in a
neonatal intensive care unit.
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The Pediatric Emergency Medicine Practice Editorial Board
EDITORS-IN-CHIEF
Ilene Claudius, MD
Professor; Director, Process &
Quality Improvement Program,
Harbor-UCLA Medical Center,
Torrance, CA
Tim Horeczko, MD, MSCR,
FACEP, FAAP
Associate Professor of Clinical
Emergency Medicine, David
Geffen School of Medicine,
UCLA; Core Faculty and Senior
Physician, Los Angeles County-
Harbor-UCLA Medical Center,
Torrance, CA
EDITORIAL BOARD
Jeffrey R. Avner, MD, FAAP
Chairman, Department of
Pediatrics, Professor of Clinical
Pediatrics, Maimonides
Children's Hospital of
Brooklyn, Brooklyn, NY
Steven Bin, MD
Associate Clinical Professor,
UCSF School of Medicine;
Medical Director, Pediatric
Emergency Medicine, UCSF
Benioff Children's Hospital, San
Francisco, CA
Richard M. Cantor, MD, FAAP,
FACEP
Professor of Emergency
Medicine and Pediatrics; Section
Chief, Pediatric Emergency
Medicine; Medical Director,
Upstate Poison Control Center,
Golisano Children's Hospital,
Syracuse, NY
Steven Choi, MD, FAAP
Chief Quality Officer and
Associate Dean for Clinical
Quality, Yale Medicine/Yale
School of Medicine; Vice
President, Chief Quality Officer,
Yale New Haven Health System,
New Haven, CT
Ari Cohen, MD, FAAP
Chief of Pediatric Emergency
Medicine, Massachusetts
General Hospital; Instructor
in Pediatrics, Harvard Medical
School, Boston, MA
NOVEMBER 2023 • www.ebmedicine.net
Jay D. Fisher, MD, FAAP, FACEP
Associate Professor of Emergency
Medicine; Program Director,
Pediatric Emergency Medicine
Fellowship, Kirk Kerkorian School
of Medicine at UNLV; Medical
Director, Pediatric Emergency
Services, UMC Children's
Hospital, Las Vegas, NV
Marianne Gausche-Hill, MD,
FACEP, FAAP, FAEMS
Medical Director, Los Angeles
County EMS Agency; Professor
of Clinical Emergency Medicine
and Pediatrics, David Geffen
School of Medicine at UCLA;
Clinical Faculty, Harbor-UCLA
Medical Center, Departments
of Emergency Medicine and
Pediatrics, Los Angeles, CA
Michael J. Gerardi, MD, FAAP,
FACEP, President
Associate Professor of
Emergency Medicine, Icahn
School of Medicine at Mount
Sinai; Director, Pediatric
Emergency Medicine, Goryeb
Children's Hospital, Morristown
Medical Center, Morristown, NJ
Sandip Godambe, MD, PhD,
MBA
Chief Medical Officer, SVP
Medical Affairs, Attending
Physician, Pediatric Emergency
Medicine, Children’s Health of
California (CHOC) Children’s
Hospital, Orange, CA
Ran D. Goldman, MD
Professor, University of British
Columbia, Pediatric Emergency
Physician, BC Children’s
Hospital, Vancouver, BC, Canada
Alson S. Inaba, MD, FAAP
Pediatric Emergency Medicine
Specialist, Kapiolani Medical
Center for Women & Children;
Associate Professor of Pediatrics,
University of Hawaii John A.
Burns School of Medicine,
Honolulu, HI
Madeline Matar Joseph, MD,
FACEP, FAAP
Professor of Emergency
Medicine and Pediatrics,
Associate Dean for Inclusion and
Equity, Emergency Medicine
Department, University of
Florida College of Medicine-
Jacksonville, Jacksonville, FL
23
Anupam Kharbanda, MD, MSc
Chief, Critical Care Services,
Children's Hospital Minnesota,
Minneapolis, MN
Tommy Y. Kim, MD
Health Sciences Clinical
Professor of Pediatric Emergency
Medicine, University of California
Riverside School of Medicine,
Riverside Community Hospital,
Department of Emergency
Medicine, Riverside, CA
Melissa Langhan, MD, MHS
Associate Professor, Departments
of Pediatrics and Emergency
Medicine, Section of Emergency
Medicine, Yale University School
of Medicine, New Haven, CT
Robert Luten, MD
Professor, Pediatrics and
Emergency Medicine, University
of Florida, Jacksonville, FL
Garth Meckler, MD, MSHS
Associate Professor of Pediatrics,
University of British Columbia;
Division Head, Pediatric
Emergency Medicine, BC
Children's Hospital, Vancouver,
BC, Canada
Joshua Nagler, MD, MHPEd
Associate Division Chief and
Fellowship Director, Division of
Emergency Medicine, Boston
Children's Hospital; Associate
Professor of Pediatrics and
Emergency Medicine, Harvard
Medical School, Boston MA
James Naprawa, MD
Attending Physician, Emergency
Department USCF Benioff
Children's Hospital, Oakland, CA
Joshua Rocker, MD, FAAP,
FACEP
Chief, Division of Pediatric
Emergency Medicine, Associate
Professor of Pediatrics and
Emergency Medicine, Cohen
Children's Medical Center of
New York, New Hyde Park, NY
Steven Rogers, MD
Associate Professor, University of
Connecticut School of Medicine,
Attending Emergency Medicine
Physician, Connecticut Children's
Medical Center, Hartford, CT
Jennifer E. Sanders, MD, FAAP,
FACEP
Assistant Professor, Departments
of Pediatrics, Emergency
Medicine, and Education, Icahn
School of Medicine at Mount
Sinai, New York, NY
Christopher Strother, MD
Associate Professor, Emergency
Medicine, Pediatrics, and
Medical Education; Director,
Pediatric Emergency Medicine;
Director, Simulation; Icahn
School of Medicine at Mount
Sinai, New York, NY
Adam E. Vella, MD, FAAP
Associate Professor of
Emergency Medicine and
Pediatrics, Associate Chief
Quality Officer, New York-
Presbyterian/Weill Cornell
Medicine, New York, NY
David M. Walker, MD, FACEP,
FAAP
Chief, Pediatric Emergency
Medicine, Joseph M. Sanzari
Children's Hospital, Hackensack
University Medical Center;
Associate Professor of Pediatrics,
Hackensack Meridian School of
Medicine, Hackensack, NJ
Vincent J. Wang, MD, MHA
Professor of Pediatrics and
Emergency Medicine; Division
Chief, Pediatric Emergency
Medicine, UT Southwestern
Medical Center; Director of
Emergency Services, Children's
Health, Dallas, TX
INTERNATIONAL EDITOR
Lara Zibners, MD, FAAP, FACEP,
MMEd
Honorary Consultant, Paediatric
Emergency Medicine, St. Mary's
Hospital Imperial College
Trust, London, UK; Nonclinical
Instructor of Emergency
Medicine, Icahn School of
Medicine at Mount Sinai, New
York, NY
PHARMACOLOGY EDITOR
Aimee Mishler, PharmD, BCPS
Emergency Medicine Pharmacist,
St. Luke's Health System, Boise, ID
© 2023 EB MEDICINE
 Points & Pearls
QUICK READ
NOVEMBER 2023 | VOLUME 20 | ISSUE 11
Points
• When evaluating ill children with suspicion for
glucose abnormalities in the ED, history over the
prior few months is critical. Questions may need
to be tailored towards children, for example, ask-
ing about clothing fitting rather than “Have they
lost weight?”
• Ill children decompensate quickly and need
expedient and aggressive fluid resuscitation. Chil-
dren with HHS are usually moderately to severely
dehydrated. They may be hypertensive despite
being very dehydrated.
• Children presenting with hyperglycemic crises may
have an unknown primary trigger that may compli-
cate the clinical picture. It is critical to consider an
additional pathology, such as appendicitis, ovar-
ian/testicular torsion, thyroid disease, or myocardi-
tis, among others. (See Table 1, page 5.)
• Continuous IV insulin is preferred to subcutaneous
insulin for initial treatment of DKA. Continuous
insulin should be infused at a rate of 0.05 to 0.1
unit/kg/hr. Continue maintenance IV fluids during
insulin initiation. (See Table 3, page 8 and Table
4, page 10.)
• Insulin should not be initiated in HHS patients
until glucose levels are dropping at a rate of <50
mg/dL/hr and should be initiated at a rate of
0.025 to 0.05 unit/kg/hr. Fluids are the mainstay
of treatment of HHS.
• Patients with hypokalemia <3.5 mEq/L, severe or
symptomatic hypomagnesemia or hypocalcemia,
or phosphate levels <1 mg/dL should have reple-
tion of their electrolytes prior to insulin initiation.
Electrocardiogram should be obtained in these
patients.
• Upon suspicion for cerebral edema, immediately
initiate treatment with rapid administration of
either 0.5 to 1 g/kg of IV mannitol or 2.5 to 5 mL/
kg of hypertonic saline (3% NaCl).16 Do not delay
treatment to obtain imaging.
• Avoid intubating DKA patients if possible, even if
patients have alterations in mental status or have
a markedly abnormal breathing pattern. Intuba-
tion should be reserved for those with severe ob-
tundation and inability to protect their airway.16,37
NOVEMBER 2023 • www.ebmedicine.net
Pediatric Diabetes:
Management of Acute
Complications in the
Emergency Department
Pearls
l Insulin should not be initiated until at least 1
hour after fluid resuscitation has begun. Nu-
merous normal saline boluses may be needed
to restore circulatory volume prior to insulin
administration.
l Sodium bicarbonate should be given only in
the most dire of circumstances, such as cardiac
arrest, life-threatening hyperkalemia, or severe
acidosis (pH <6.9) with evidence of impaired
cardiac function.16
l Fluid resuscitation should be administered
to restore intravascular volume and improve
electrolyte derangements. Fluids should
not be restricted for fear of causing cerebral
edema.11,16,53
l Insulin boluses should not be given, even for
patients with severe acidosis.16 Insulin bo-
luses can precipitate shock, worsen electrolyte
derangements, and increase risk for cerebral
edema.30,32
• Pediatric patients with DKA or HHS are at risk for
venous thromboembolism, renal failure, and sepsis.
Avoid central line placement unless absolutely
necessary.16,44
• Patients with an insulin pump should have the
pump removed when undergoing treatment for
a hyperglycemic or hypoglycemic crisis. Consider
pump malfunction or intentional misuse in patients
presenting with abnormal glucose levels.
• Patients presenting for reasons unrelated to their
known diabetes should have their insulin regi-
men continued in the ED. They may need regular
point-of-care glucose checks while in the ED for
unrelated issues. It is important to ensure that pa-
tients have appropriate supplies, medications, and
follow-up prior to discharge.
• Ideally, any pediatric patient with a diabetic crisis
should be transferred to a pediatric hospital, if
feasible.
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