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Diabetic Ketoacidosis
Lynne Resendes
Nursing, College of Health and Human Services
DEMN Cohort 12
MEDICATIONS
SITUATION
• 49 year old female came to the emergency department complaining
of weakness and confusion.
• Patient presents with a blood glucose of 878mg/dl, an anion gap of
28mEq/L, and a troponin of 5.7mg/mL.
BACKGROUND
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Patient is a dialysis dependent, type two diabetic.
Pancreatic transplant and s/p kidney transplant failure in 2006.
End stage renal disease secondary to type two diabetes.
Patient has history of hematuria, diabetic retinopathy, and pleural
effusion.
Social drinker
Patient has an internal defibrillator after undergoing a coronary
artery bypass graft.
Has a history of hyperlipidemia, hypertension, anxiety, and coronary
artery disease.
Lives at home with son who is primary caretaker.
Amlodipine Besylate
Atorvastatin Calcium
Aspirin
Enteric Coated
LABS
Route
Freq.
Class
Adverse
Effects
PO
Q 24 hrs.
Antihypertensive/Ca+
Channel Blocker
Headache, Edema,
Palpitations
Antilipemics/HMG CoA
reductase inhibitors
Headache, UTI,
bronchitis, infection
PO
PO
Beclomethasone Dipropionate Inhalation
Q 24 hrs.
Q 24 hrs.
Q 12 hrs.
NSAIDs, Salicylates
Corticosteroids
Cerebral edema, GI
bleeding,
hyperkalemia
Nausea, rhinorrhea,
light headedness
Clonidine HCl
PO
Q 12 hrs.
Antihypertensive/Centrally
acting alpha agonists
Agitation,
bradycardia, pruritus
Fentanyl
Transdermal
Q 72 hrs.
Opioid analgesics/
Opioid agonists
Euphoria,
arrhythmias, PE, DVT
Isosorbide Mononitrate
PO
Q 24 hrs.
Antianginals/
Nitrates
Tachycardia,
palpitations, fainting,
rash
Metoprolol Tartrate
PO
Q 12 hrs.
Antihypertensive/Selective
beta adrenergic blockers
Bradycardia, heart
failure, AV block,
dyspnea, edema
Pantoprazole Na
PO
Q 24 hrs.
Antiulcer, Proton pump
inhibitor
Chest pain, dyspnea,
pharyngitis
Tacrolimus
PO
Q 24 hrs.
Immunosuppressant/Macrol Delirium,
ides
hyperkalemia,
hypomagnesia
Ticagrelor
PO
Q 12 hrs.
Antiplatelet drugs/ P2Y12
platelet inhibitor
Bleeding, atrial
fibrillation,
bradyarrhythmia
Acetaminophen
PO
PRN
Analgesics/paraaminophenol derivatives
Leukopenia,
hypoglycemia,
hypokalemia
Glucagon
PO
PRN
Glucagon supplement
Anaphylaxis, urticaria,
hypotension,
hyperglycemia
NaCl 0.9% & Regular Insulin
IV Infusion
CONT.
Antidiabetics/human insulin
analogues
Hypoglycemia,
hypomagnesaemia,
urticaria
Nitroglycerin Paste
Transdermal
PRN
Vasodilators/Nitrates
Headache,
tachycardia,
palpitations
Atropine Sulfate
IV Push
PRN
Antiarrhythmic/Anticholinerg Bradycardia,
ic-belladonna alkaloids
anaphylaxis, ataxia,
photophobia
ASSESSMENT
Neuro: Alert and oriented to person
and place.
Resp: Lungs clear bilateral
throughout.
Cardio: Rhythm regular and
palpable peripheral pulses.
GI: Bowel sounds present;
hypoactive.
4/20/15 11:57
GU: Anuria
BP: 144/46
HR: 96 bpm
RR: 18
O2 Saturation: 97% on room air
Temp: 99○F
Pain: 10/10 “everywhere”
Allergies: Dilaudid, Morphine, Plavix, OxyContin
Aschenbrenner, D. S., & Venable, S. J. (2012). Drugs affecting blood glucose levels. In Drug therapy in nursing (4th ed., pp. 1036-1039). New York, NY: Wolters Kluwer Health/Lippincott Williams & Wilkins.
Koul, P. B. (2009). Diabetic ketoacidosis: A current appraisal of pathophysiology and management. Clinical Pediatrics, 48(2), 135-144. doi:10.1177/0009922808323907
Linfoot, P., Bergstrom, C., & Ipp, E. (2005). Pathophysiology of ketoacidosis in type 2 diabetes mellitus. Diabetic Medicine, 22, 1414-1419. doi:10.1111/j.1464-5491.2005.01660.x
Nursing 2015 drug handbook. (2014). Philadelphia, PA: Wolters Kluwer.
Glucose
211
4/20/15
07:35
96
4/19.15
21:45
878
Sodium
141
142
130
Potassium
4.2
4.4
5.5
Chloride
102
105
89
CO2
22
24
13
BUN
93
91
80
Calcium
9.4
10
9.9
Creatinine
10.0
9.77
8.99
Creatinine/ BUN Ratio
9.3
9.3
8.9
Troponin
6.1
5.7
5.7
Cap. Glucose
185
73
>500
Anion Gap
17.0
13.0
28
HIGH
LOW
PATHOPHYSIOLOGY
Diabetic ketoacidosis is commonly a complication associated with
Type 1 diabetes; however, it is now recognized in individuals with
Type 2 diabetes (Koul135). This condition is typically characterized
by hyperglycemia, hyperketonemia, and metabolic acidosis. “Ketone
production by the liver outpaces ketone loss by the kidneys.”
(Aschenbrenner & Venable 1039). There is a reduction of circulating
insulin, elevated levels of glucagon, catecholamine, cortisol, and
growth hormone. Lipolysis occurs to free fatty acids from peripheral
tissues which occurs in the liver. This then results in excess ketones
circulating in the blood causing ketonemia and metabolic acidosis
(Linfoot, Bergstrom, & Ipp 1418).
RECOMMENDATIONS
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Educate patient on proper diabetic management
Advise patient to avoid alcohol due to diabetic involvement
Consult with social work to organize VNA services for patient
Meet with nutritional services to organize heart healthy diet
Physical therapy consult to address concerns for weakness
Occupational therapy consult to address diminished vision due to
diabetic retinopathy.
Special thanks to Deb Simonton, Deb Irish, and the nursing staff of 5 North at Concord Hospital