DIABETES AND REHYDRATION
Educational Objectives
| The goal of this program is improve patient care through appropriate management of the complications of diabetes
and pediatric dehydration in emergency care settings. After hearing and assimilating this program, the clinician
will be better able to:
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 | 1. Describe the management of diabetic ketoacidosis in adults and children in emergency settings.
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| 2. Identify and treat hyperglycemia hyperosmolar syndrome and hypoglycemia.
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| 3. Initiate long-term care for patients diagnosed with diabetes in emergency settings.
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| 4. Implement pediatric oral rehydration therapy in emergency settings.
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| 5. List the risks and benefits of antiemetic therapy for children with acute gastroenteritis.
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Faculty Disclosure
In adherence to ACCME guidelines, the Audio-Digest Foundation requests all faculty and members of the planning committee
to disclose relevant financial relationships within the past 12 months that might create any personal conflicts of interest.
Any identified conflicts were resolved to ensure that this educational activity promotes quality in health care and not a proprietary
business or commercial interest. For this program, the faculty and planning committee reported nothing to disclose.
Acknowledgments
Dr. Lundberg was recorded at 20th Annual National Conference on Advances in Emergency Medicine and Primary Care,
held April 18-20, 2007, in Las Vegas, NV, and sponsored by Olive View-UCLA Department of Emergency Medicine
and the American College of Emergency Physicians, State Chapter of California, Inc. Dr. Scherzer was recorded at
the 2007 Emergency Medicine Conference, held November 30 to December 2, 2007, in Columbus, OH, and sponsored
by Nationwide Children’s Hospital. The Audio-Digest Foundation thanks the speakers and the sponsors for their cooperation
in the production of this program.
| MANAGEMENT OF DIABETES COMPLICATIONS IN THE ED —Scott Lundberg, MD, Assistant Professor of Medicine,
the David Geffen School of Medicine at the University of California, Los Angeles; Associate Program Director,
UCLA Combined IM/EM Residency, and Assistant Medical Director, Olive View-UCLA Medical Center, Sylmar, CA
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| Screening for diabetic ketoacidosis (DKA): assess mental status and hydration; urine dipstick for ketones shows
nearly 100% sensitivity and 100% negative predictive value for excluding DKA; urine dipstick poorly specific test, since
ketones also caused by, eg, vomiting, lack of food; serum chemistries required to confirm DKA; new fingerstick whole-
blood ketone test done simultaneously with glucose measurement; fingerstick ketone test 94% specific and 100% sensitive;
potentially minimizes laboratory testing when excluding diabetes; definition of DKA—hyperglycemia, positive ketones,
and anion gap acidosis; if only 2 of these present, possibly DKA
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| Pitfalls in diagnosis: DKA with normal bicarbonate (HCO3 -)—may be due to vomiting; use anion gap to confirm acidosis;
potassium (K) levels main treatment focus, since wide swings of K potentially lethal; American Diabetes Association
(ADA) 2006 guidelines— check K before starting insulin therapy; if K <3.3 mEq/L, withhold insulin because insulin
causes decrease in K, potentially leading to arrhythmia; electrocardiography (ECG) and blood gas analysis also used to
screen for K; K supplementation—be aggressive in all patients, ie, ≥10 to 20 mEq/hr while on insulin therapy, unless K
>5.3 mEq/L; most patients K depleted, so K given with insulin
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| Insulin therapy: regular insulin intravenous (IV) starting dose 0.1 U/kg per hour; bolus insulin of 0.1 U/kg optional depending
on patient’s condition; bolus insulin does not affect long-term outcome
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| Follow-up testing: check glucose q1h; check chemistry panels, including K, magnesium (Mg), and phosphorus (P) every
2 to 4 hr; follow-up testing assesses whether K supplementation and insulin adequate and values not too far out of
range
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| Follow-up treatment: continue normal saline; usually physicians initiate correct therapy for DKA, but neglect some
follow-up measures; if patient’s glucose <250 mg/dL while on insulin drip and anion gap not decreased yet, add dextrose
to allow for continued insulin to break acidosis and recover normal acid-base status
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| Saline therapy: when using D5, change from normal saline to half-normal saline; D5 normal saline slightly hypertonic
and may cause problems due to increased tonicity; if anion gap closed but HCO3 - concentration too low, ie, chloride
(Cl- ) increasing but HCO3 - <20 mEq/L, switch to half-normal saline; common for patient who has received 2 to 3 L of
saline to have blood chemistry showing increasing Cl-
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| Anion gap: common pitfall anion gap not decreasing; if glucose decreasing (150 or 200 mg/dL) but anion gap still
present, increase insulin drip and amount of dextrose; use D5 or even D10 saline to decrease anion gap, because sometimes
glucose corrects faster than acidosis; keep insulin at high dose until anion gap closed; consider 10 to 12 U/hr, depending
on severity of acidosis
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| Transitioning patients: IV drip stopped when—anion gap closed; HCO3 - 18 to 20 mEq/L; patient eating; subcutaneous
(SC) insulin therapy—initiated 1 hr before discontinuing IV insulin; total dose two-thirds U/kg consisting of one-third regular
insulin and two-thirds NPH insulin, delivered one-third in evening and two-thirds in morning; when stopping IV insulin,
give ≥10 U of regular, preferably 15 or 20 U of 70/30 or mixture of NPH and regular, to prevent DKA; 10 U absolute
minimum before stopping insulin drip, since 1 hr for onset of action of regular insulin; insulin lispro—absorbed in 10 to 15
min; use as transitional agent, allows quicker discontinuation of insulin drip; ADA guidelines for treating DKA recommend
initial dose of 0.3 U/kg, followed by 0.1 U/kg per hour; can space out dosing to q2h and give 0.2 U/kg; intensive monitoring
and fluid management still required, but treatment outside intensive care unit (ICU)
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| Hyperosmolar hyperglycemic state (HHS): characterized by altered mental status, severe hyperglycemia (>600
mg/dL), more severe dehydration and renal insufficiency, hyperosmolarity (osmolarity >320 mOsm/L), and minimal
or absent ketosis and acidosis; commonly seen in older patients with type 2 diabetes; renal impairment due to dehydration;
HHS now seen in adolescents with type 2 diabetetes
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| Treating HHS: fluid management main priority, with patients deficient by 8 to 12 L; water pulled into urine by glucose,
and very low effective circulation present; large dose of insulin worsens circulatory collapse, with potential neurologic,
renal, and cardiac impairment; correct patient’s sodium levels for glucose; if patient’s corrected sodium level high or
normal, and glucose >600 to 700 mg/dL, minimize use of normal saline and use half-normal saline; patients often in renal
failure; underlying heart failure can complicate fluid management; consider monitoring of central pressure, and initiate
aggressive fluid therapy; infection most common trigger for HHS (consider sepsis)
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| DKA in children: 25% of new-onset diabetes in children presents as DKA; fingerstick glucose and urine dipstick both
excellent screens for DKA in children (use liberally); older children or adolescents diagnosed with diabetes commonly
noncompliant with therapy; cerebral edema most common cause of death or serious morbidity with DKA
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| 2006 ADA guidelines on management of DKA in children: recommend assessment of patient for severity of illness,
including vital signs, dehydration, mental status, and venous pH
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| Fluids: recommend less aggressive approach with fluids than in adult patients; initial bolus 10 mL/kg, about half of what
physicians normally give for pediatric dehydration; after initial bolus, start normal saline infusion; calculate maintenance
rate, then double that; maintenance rate 40 mL/hr for first 10 kg, 20 mL for next 10 kg, and 1 mL/kg per hour after
that; after 6 hr, switch to half-normal saline for next 2 days
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| Potassium: supplementation as in adults; deliver at tolerable rate and monitor frequently; if phosphate <1 mg/dL, give
some K as phosphate rather than chloride; respiratory and muscle weakness with low phosphorous more common in
children than adults
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| Monitoring: same as for adults; neurologic checks by nursing; glucose levels q1h; chemistries and blood gases repeated
every 2 to 4 hr; recommend monitoring urine ketones q4h
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| Insulin therapy: no bolus; start IV insulin drip; dosing same as adults (0.1 U/kg per hour or SC insulin lispro given at 0.1
U/kg per hour); once glucose <300 mg/dL or if glucose decreases by >90 mg/dL in 1 hr, add glucose; glucose dropping
faster than recommended guidelines increases risk for cerebral edema; continue drip till acidosis cleared and glucose
controlled
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| Cerebral edema: develops in ≈1% of pediatric patients with DKA; related mortality ≥40%; risk factors
(uncontrollable)—initial PCO2 <10 mm Hg on blood gas increases risk to 3% to 4%; serum urea nitrogen (BUN) >30 mg/
dL increases risk 2-fold; risk factors (controllable)—use of bicarbonate increases risk for cerebral edema 4-fold; cerebral
edema ischemic in origin, and giving bicarbonate not only increases cerebral vasoconstriction, but worsens acidosis, since
CO2 crosses blood-brain barrier and bicarbonate does not; diagnosis—headache not present initially or worsens with therapy,
vomiting, and neurologic changes; head computed tomography (CT) necessary, but results negative in 40% of cases;
treatment—use hypertonic agent (mannitol preferred); guidelines list hypertonic saline as option; intubation—
hyperventilation increases mortality in children with DKA and cerebral edema; if intubating and ventilating pediatric patient,
keep CO2 at 35 to 40 mEq/L (normal range) or monitor pH; disposition—pediatric ICU default treatment setting; if
risk factors present, DKA severe, or early signs that neurologic status changing, send child to pediatric ICU
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| Hypoglycemia: initial manifestations include shakiness, sweatiness, and nausea, which progress, if not treated, to neuroglycopenic
symptoms, eg, seizures, coma, altered mental status; diagnosis straightforward with fingerstick test; if untreated
or not properly treated, hypoglycemia can cause permanent neurologic deficit; causes—exogenous insulin
(most common cause in adults); oral medications, eg, sulfonylureas, meglitinides (eg, repaglinide [Prandin]); metformin
and thiazolidinediones do not cause hypoglycemia
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| Treatment: IV dextrose 55 mL (1 ampule) standard treatment; if alcoholism or malnourishment suspected, thiamine given
concurrently; monitor patients q1h; use dextrose drip if patients taking long-acting insulin or oral agent; if IV access
not possible, or if patient in prehospital setting, glucagon 1 mg alternative to dextrose; consider octreotide in patients
with sulfonylurea ingestion, since sulfonylureas stimulate insulin secretion and octreotide suppresses insulin secretion;
use 1 µg/kg q8h SC or as drip in refractory cases
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| Disposition: look for recurrent hypoglycemia or serious infection or sepsis; only patients with known insulin overdose
should be sent home immediately; recurrence of hypoglycemia likely in patients taking oral agents or very long-acting
insulin until appropriate adjustments made
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| Managing out-of-control diabetes: goals—prevent DKA, HHS, or serious infection, eg, malignant otitis, and start
preventing long-term complications; short-term treatment indicated for most inpatients, particularly critical care patients;
treatment goal glucose <200 mg/dL
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| Pregnant patients: first-trimester patients require tight glycemic control; if admitting patients, use sliding scale for insulin;
if glucose high, give SC dose; have patients check blood glucose (BG) again in 4 to 6 hr; consider insulin drip in
pregnant patients with very high BG; in early pregnancy, consider admission and work closely with gynecology service
or patient’s obstetrician; regular insulin consumed in 6 hr; give IV fluids; if starting patient on oral agent, normalizing BG
at start improves efficacy of oral agent; BG >200 to 300 mg/dL toxic to pancreatic islet cells, and impairs insulin production
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| Maximizing long-term outcomes: blood pressure biggest concern, not BG; lipid lowering with statins next most effective
intervention, then smoking cessation, and aspirin use; normalizing BG in patients with diabetes helps long-term
outcomes, but not as important as other risk factors
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| Clinical approach: rule out DKA, HHS, sepsis, or infection; check blood chemistry; if symptoms present, or other reason
to suspect renal insufficiency, leave IV in and give patients fluid while waiting for results; perfuse kidneys; identify
reasons for poor control, eg, newly diagnosed, knowledge deficit, lack of access to care, out of medication, or inadequate
treatment; treatment—metformin first choice since inexpensive and given bid; generally well tolerated, with some gastrointestinal
side effects; contraindicated when creatinine >1.4 mg/dL, significant CHF, or other ketosis-prone states
present; can use glipizide or glimepiride instead (inexpensive and given qd or bid); if glucose control inadequate, start insulin;
when starting insulin in clinic, use 10 U of insulin NPH at night or glargine; consider inhaled insulin
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| REHYDRATION THERAPIES AND ANTIEMETICS IN THE ED—Daniel J. Scherzer, MD, Clinical Assistant Professor,
Section of Emergency Medicine, Nationwide Children’s Hospital, Department of Pediatrics, Ohio State University College of
Medicine, Columbus
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| Dehydration: pathophysiology—children similar to metabolic furnaces; evaporative and insensible losses about twice
that of adults; when fever present, their insensible water losses easily double; children autonomically reactive; behaviorally,
children expert at oral-fecal route (impossible to avoid gastroenteritis); oral rehydration solution (ORS)—common
homemade recipe 1 L water, 1 tsp salt, and 8 tsp sugar; sophisticated recipe 6 tsp sugar, 1 tsp baking soda, and 1 tsp potassium
salt or one banana; mechanism—even in ileus, peristalsis still relatively effective; with excessive secretory activity,
cotransport mechanisms of sodium and glucose remain relatively intact and remove water; challenge to provide
enough substrate for that cotransport mechanism to remain on absorptive side and outpace secretory activity
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| American Academy of Pediatrics (AAP) guidelines: oral rehydration endorsed since 1985; in 1996, revision
eliminated restrictions on milk and milk products; guidelines target children aged 1 mo to 5 yr with acute gastroenteritis;
oral rehydration therapy (ORT)—preferred treatment for fluid and electrolyte losses caused by diarrhea in children with
mild-to-moderate dehydration; ORT inexpensive and administered in many settings by most people; electronic measurements
unnecessary; vomiting not contraindication for ORT; give in small amounts for success; child who refuses ORT
probably not dehydrated; breast-feeding—ideal form of oral rehydration for infants; begin refeeding as soon as possible;
lactose restriction usually unnecessary; IV fluids recommended for severe dehydration; oral rehydration—perform rapidly
(in 3-4 hr) in mildly to moderately dehydrated patients; initiate unrestricted diet as soon as acute phase ends; for
breast-fed infants, continue nursing; if formula-fed, do not dilute formula; ORS administered for ongoing losses due to
diarrhea
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| United States practice: most pediatric emergency physicians prefer to use IV fluids (IVF) for dehydraton; about one-
third use IVF for mild dehydration, due to familiarity; barriers to ORT—lack of familiarity and misguided information
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| Degree of dehydration: categorized as mild, moderate, or severe; infants more autonomically active; while more susceptible
to dehydration, infants more refractory to hemodynamic effects; percentage dehydration defined in terms of
body weight; older persons develop more dry weight, and percentage dehydration less reflective of percentage fluid loss;
adipose tissue dry weight; to determine dehydration, subtract current weight from immediate pre-illness weight; difference
reflects acute weight loss (mostly water)
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| Managing moderate dehydration: AAP and Centers for Disease Control and Prevention (CDC) suggest IVF unnecessary
for moderate dehydration; common practice to provide IVF, although probably not essential; avoid bland diet
and gut rest; oral rehydration followed by diet of fruits, vegetables, and meats; retrospective descriptive-type studies
indicate similar treatment times for rehydration with IVF or ORT in ED; IVF rehydration more frequently reimbursed
than ORT
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| IV rehydration: rehydrate with solution containing 75 to 90 mEq/L of sodium; using pulse rate, once circulation adequate,
switch to maintenance solution; regimen recommended for patients with cholera in less-developed countries; in
United States, use maintenance solution initially; dose at 50 mL/kg within 4 hr (equivalent to 1 mL/kg every 5 min);
when pediatric patient very hypo- or hypernatremic, volume repletion needed, so do not change sodium too quickly;
use bolus, reassess, and repeat bolus if needed; prepare for usual dehydration patient using 0.9% normal saline at 20
mL/kg; continue boluses until mental status improved and other indicators of good perfusion seen; begin ORT as soon
as possible; if parents or clinician choose to continue hydration via IVF, add substrate because calorie depletion occurs
with water depletion
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| Severe dehydration: ORT works when no other resources available, but usually not appropriate in United States
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| Antiemetics: AAP and CDC do not recommend use of antiemetics; promethazine—FDA recommends against use in pediatric
patients <6 yr of age; long history of promethazine shows neither harm (generally) nor clinical benefit; given severity
of associated risks, use not worthwhile; affects patient’s mental status, and lessens physician’s ability to assess
patient’s progress; ondansetron (Zofran)—found very safe, and used effectively in sickest children with greatest vulnerabilities;
effective in children undergoing chemotherapy and does show clinical value in emesis from gastroenteritis; in
study, children given 3 doses over 2 days had increased visits with diarrhea; in another study, one dose of ondansetron
given in ED reduced vomiting, need for IV rehydration, and ED length of stay; overall ondansetron beneficial, with less
nausea and vomiting but at risk of increased diarrhea
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Suggested Reading
Practice Parameter: The management of acute gastroenteritis in young children. Pediatrics. 97:424, 1996; Alhashimi D
et al: Antiemetics for reducing vomiting related to acute gastroenteritis in children and adolescents. Cochrane Database
Syst Rev. 19:CD005506, 2006; Glaser N et al: Risk factors for cerebral edema in children with diabetic ketoacidosis. N
Engl J Med. 344:264, 2001; Kitabchi AE et al: Hyperglycemic crises in adult patients with diabetes: a consensus statement
from the American Diabetes Association. Diabetes Care. 29:2739, 2006; Stoner MJ et al: Rapid fluid resuscitation
in pediatrics: testing the American College of Critical Care Medicine guideline. Ann Emerg Med. 50:601, 2007; Umpierrez
GE et al: Efficacy of subcutaneous insulin lispro versus continuous intravenous regular insulin for the treatment of
patients with diabetic ketoacidosis. Am J Med. 117:291, 2004; Van den Berghe G et al: Intensive insulin therapy in
critically ill patients. N Engl J Med. 345:1359, 2001; Wolfsdorf J et al: Diabetic ketoacidosis in infants, children, and
adolescents. Diabetes Care. 29:1150, 2006.
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