10/21/13 @ 0800 AM
Rx Consult: acute management of DKA in T1DM
Subjective
CC: “I felt weak and nauseated during softball practice. I checked by blood glucose and it read ‘HI.’”
HPI: MM is a 21 yo F with hx of T1DM, dx 3 years ago. She started using an insulin pump ~ 6 mo. ago. She
noticed she was unusually tired and SOB at the beginning of her practice and then began feeling weak and
nauseated. She was very thirsty during softball practice. Her coach said she seemed “a little confused” and
advised her to check her blood glucose and it read HI. She checked her insulin pump and noticed it had
become disconnected. She is unsure how long she has been without insulin. She vomited x 2 since shortly
thereafter and was transported via emergency medical services to the ED.
PMH: T1DM dx 3 years ago
FH: Twin sister with T1DM
SH: College student; no tobacco, alcohol, or illicit drug use
Meds: NovoLog 100 units/mL, per insulin pump
Basal rates: 0.6 units/h: 0000-0300
0.9 units/h: 0300-0700
0.8 units/h: 0700-1100
0.7 units/h: 1100-1730
0.8 units/h: 1730-0000
correction factor 1 unit: 40 mg/dL >120 mg/dL
insulin: carbohydrate ratios: 1:10 insulin: carbohydrate before breakfast
1:15 insulin: carbohydrate before lunch and dinner
Glucagon injection kit, as needed
Allergies: NKDA
ROS: c/o blurry vision, lethargy, SOB, nausea, polyuria, and polydipsia. Denies constipation, diarrhea, and HA.
Objective
Gen: WDWN Caucasian F appearing her stated age, with deep respirations, ketones on her breath, and slurred
speech; slightly confused, but responds appropriately to questions
VS: BP 101/72, P 123, RR 32, T 37.0°C; Wt 56 kg, Ht 5’6’’
HEENT: mucous membranes are dry
Lungs: CTA, Kussmaul respirations
MS/EXT: no edema, pulses 2+ throughout, mild calluses
Neuro: A & O x3; DTRs 2+ throughout; feet with normal sensation and vibration
Labs: 136 101 23
479
4.8 10 1.4
Anion gap: 136 – (101 +10) = 25
ABG: pH 7.26; pCO2 21 mm Hg; pO2 128 mm Hg; HCO3 7.1 mEq/L; oxygen sat 97%
UA: (+) Ketones; (+) glucose
ECG: sinus tachycardia
CrCl: 56.2 mL/min
Assessment: MM presents with s/sx consistent with diabetic ketoacidosis (DKA), likely secondary to insulin
pump disconnection causing inadequate insulin therapy and resultant hyperglycemia. MM c/o blurred vision,
nausea, weakness, vomiting, and her coach mentioned she seemed disoriented, despite being A & O x 3 upon
admission. She presents with tachypnea; Kussmaul respirations (often associated with DKA) were noted. EKG
reveals sinus tachycardia. MM has polyuria, polydipsia, and is hypotensive. Ketones are noted on her breath
and both her serum and her urine are (+) for ketones. Her electrolytes reveal an anion gap of 25, indicating
anion gap metabolic acidosis. MM’s mucous membranes are dry, indicative of dehydration, occurring because
hyperglycemia results in glucosuria and loss of H2O and electrolytes.
MM’s dx of DKA is supported by the ADA’s “Hyperglycemia Crises in Adult Patients with Diabetes” (2009),
which includes hx, PE, and lab findings, including (+) ketones, sx of DKA, and BG levels >250 mg/dL. Goals of
acute therapy for MM are to achieve rehydration and subsequently normalize electrolytes and to correct DKA
and hyperglycemia. Fluid replacement to correct dehydration should occur over the first 24 hours. MM’s
serum K+ is WNL; however insulin therapy will result in hypokalemia. Serum sodium appears normal; however
this does not account for her hyperglycemia. MM’s corrected Na+ level is 142 mEq/L. DKA should be corrected
through subcutaneous insulin administration to normalize ketones and reduce hyperglycemia. Normoglycemia
is the ultimate goal for MM, but this can be achieved post-discharge. A secondary, long-term goal for MM is to
prevent future episodes of DKA and prevent recurrence of insulin pump disconnection.
Per ADA 2009 recommendations (mentioned above), mild dehydration with high serum Na+ can be corrected
through the administration of 0.45% NaCl at a rate of 200-500 mL/h depending on dehydration state. Upon
achieving a serum glucose level of 200 mg/dL, change to 5% dextrose with 0.45% NaCl infused at a rate of 150250 mL/h.
DKA and hyperglycemia can be corrected through regular insulin IV administration. The ADA protocol dictates
two options: 1) administer regular insulin as IV bolus of 0.1 units/kg body weight followed by continuous
infusion of 0.1 units/kg/h, or 2) administer regular insulin as continuous IV infusion without bolus at rate of
0.14 units/kg body weight/h. If serum glucose does not reduce by at least 10% in the first hour, 0.14 units/kg
regular insulin should be given as IV bolus and previously prescribed insulin therapy should be continued.
When serum glucose reaches 200 mg/dL, reduce regular insulin infusion to 0.02-0.05 units/kg/h IV or give
rapid-acting insulin at 0.1 units/kg SC every 2 hours. After resolution of DKA, transfer from IV to SC insulin.
Serum sodium levels should only be corrected with bicarbonate administration if the pH < 6.9. Bicarbonate is
not beneficial in these patients and can result in harm. Serum potassium is WNL, but proposed DKA treatment
regimen may result in hypokalemia. This can be prevented through potassium replacement in patients with
sufficient renal function (urine output ~ 50 mL/h). If serum K+ is between 3.3 and 5.2 mEq/L give 20-30 mEq
K+ in each liter of IV fluid to keep serum K+ between 4-5 mEq/L. If K+ falls < 3.3 mEq/L, hold insulin and give
20-30 mEq/L K+ until K+ > 3.3 mEq/L.
Plan: 1) Administer 0.45% NaCl at rate of 250-500 mL/h until serum Na+ normalizes.
2) When serum glucose reaches 200 mg/dL or 300 mg/dL, change to 5% dextrose with 0.45% NaCl
administered at a rate of 150-250 mL/h.
3) Administer IV bolus of 6 units of regular insulin.
4) Continue regular insulin infusion of 6 units/h.
5) If glucose does not reduce by at least 10% (~50 mg/dL) in first hour, give 8 units (0.14 units/kg) regular
insulin as IV bolus. Continue previous insulin therapy.
6) When serum glucose reaches 200 mg/dL reduce regular insulin infusion to 1-3 units/h, or give 6 units rapidacting insulin SC every 2 hours. Keep serum glucose between 150-200 mg/dL until resolution of DKA.
7) Check electrolytes, BUN, venous pH, creatinine, and glucose every 2-4 hous until stable. DKA is resolved
when BG < 200 mg/dL and two of the following are present: serum bicarbonate ≥ 15 mEq/L, venous pH > 7.3,
and calculated anion gap ≤ 12 mEq/L. Resolved DKA warrants the switch from IV to SC insulin administration,
permitting patient is not fasting or NPO. Continue IV insulin infusion for 1-2 h after SC insulin begun to ensure
adequate plasma insulin levels.
8) Monitor BP, pulse, and RR.
9) To maintain serum K+ of 4-5 mEq/L, administer 20-30 mEq K+ in each liter of IV fluid.
10) MM was able to tolerate insulin, so insulin pump dose prior to DKA onset can be resumed.
11) Encourage MM to check connection of insulin pump periodically. With MM’s permission, educate MM,
softball coach, and team about s/sx of DKA (i.e., polyuria, polydipsia, fatigue, etc.) to ensure MM receives
treatment if she experiences another episode of DKA. Have MM carry backup insulin pens, pen needles, and
glucagon emergency kit.
12) Recommend MM make an appointment for diabetes educator for diabetes management.
Briana Santaniello, PharmD Candidate, x12345