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Diabetic Ketoacidosis Case Study

History of present illness

The patient is a 36-year-old man who has had type 1 diabetes for 15 years. He presents to the emergency room with hyperglycemia and concern for possible diabetic ketoacidosis after not taking his insulin for 3 days. The patient reports that he is currently homeless and has lost his supply of insulin, syringes, glucose meter, and related glucose testing supplies. 

Diabetes-related comorbidities/complications

Hypertension, hyperlipidemia, retinopathy, and bipolar disorder

Diabetes related history

The patient states that at the time of his initial diagnosis with type 1 diabetes, he was hospitalized, with a glucose value >1000 mg/dL, and he was experiencing polyuria, polydipsia, and polyphagia. He reports that he has been on insulin since the time of his diagnosis, and he has never been prescribed oral agents for diabetes management. He recalls that glutamic acid decarboxylase  (GAD) antibodies and a C-peptide level have been previously evaluated. GAD antibodies were positive, and C-peptide value was low, helping to confirm the diagnosis of type 1 diabetes.

Most recently, he has been using insulin glargine 55 units once daily, and insulin aspart per correction doses 3 times daily. There was an imbalance when comparing his basal and bolus insulin doses. When asked about meal doses of insulin aspart, the patient relates that he is currently homeless and eats when food is available, often snacking on bits of food throughout the day. He was not using a meal dose of insulin aspart, but he would use this insulin to correct for hyperglycemia.

The patient has had previous episodes of diabetic ketoacidosis, for which he was hospitalized. With this episode of hyperglycemia, he is not experiencing any nausea, vomiting, or abdominal discomfort, and he appears well. The patient has no recent concerns for hypoglycemia. He reports that with past episodes of hypoglycemia, he experienced sweatiness and shakiness, for which he treated with juice or food.

Laboratory values on admission

  • A1c: 11.3%
  • Creatinine: 0.9 mg/dL with eGFR >60 mL/min
  • Aspartate aminotransferase (AST): 17 U/L
  • Alanine aminotransferase (ALT): 14 U/L
  • Beta-hydroxybutyrate: 0.1 mmol/L
  • Bicarbonate: 25 mEq/L
  • Anion Gap: 14 mEq/L

Case Study 1

 

 

 

 

 

A 32-year-old male with type 1 diabetes since the age of 14 years was taken to the emergency room because of drowsiness, fever, cough, diffuse abdominal pain, and vomiting.

Fever and cough started 2 days ago and the patient could not eat or drink water. He has been treated with an intensive insulin regimen (insulin glargine 24 IU at bedtime and a rapid-acting insulin analog before each meal). On examination he was tachypneic, his temperature was 39° C (102.2° F), pulse rate 104 beats per minute, respiratory rate 24 breaths per minute, supine blood pressure 100/70 mmHg; he also had dry mucous membranes, poor skin turgor, and rales in the right lower chest. He was slightly confused. Rapid hematology and biochemical tests showed hematocrit 48%, hemoglobin 14.3 g/dl (143 g/L), white blood cell count 18,000/ μ l, glucose 450 mg/dl (25.0 mmol/L), urea 60 mg/dl (10.2 mmol/L), creatinine 1.4 mg/dl (123.7 μ mol/L), Na+ 152 mEq/L, K+ 5.3 mEq/L, PO4 3−2.3 mEq/L (0.74 mmol/L), and Cl− 110 mmol/L. Arterial pH was 6.9, PO 2 95 mmHg, PCO 2 28 mmHg, HCO 3−9 mEq/L, and O 2 sat 98%. The result of the strip for ketone bodies in urine was strongly positive and the concentration of β-OHB in serum was 3.5 mmol/L. Urinalysis showed glucose 800 mg/dl and specific gravity 1030.

What is your diagnosis?

The patient has hyperglycemia, ketosis, and metabolic acidosis. Therefore, he has DKA. In addition, because of the pre-existing fever, cough, localized rales on auscultation and high white blood cell count, a respiratory tract infection should be considered. The patient is also dehydrated and has impaired renal function.

Do you need more tests to confirm the diagnosis?

Determination of the effective serum osmolality and anion gap should be performed in all patients presenting with potential DKA. Serum osmolality can be measured directly in the laboratory or be calculated. Calculated effective serum osmolality in this case was 329 mOsm/kg and the anion gap is 33 mEq/L. Typically DKA is a high anion gap metabolic acidosis while serum osmolality may vary from normal to high. In addition a chest X-ray should be performed and blood cultures be obtained to check for lower respiratory tract infection and isolate the pathogenic bacteria.

How will you manage this patient?

Immediate infusion of normal saline and intravenous insulin should be initiated as described in the text. Because his serum potassium level is in the normal range, 10 mEq of potassium should be added to each liter of normal saline infused. Serum potassium levels should be checked at 2, 6, 10, and 24 hours and appropriate adjustment to the dose must be made. In addition, 100 ml of bicarbonate plus 10 mEq of potassium in 200 ml of water can be administered in 1 hour because pH is 6.9 and plasma bicarbonate levels are low. Arterial pH and bicarbonate should be re-checked in 30 minutes and, if uncorrected, infusion of a similar or lower amount of bicarbonate should be repeated as discussed in the text. If infection is confirmed, intravenous administration of antibiotics should begin while waiting for the results of blood cultures. The patient was treated with fluids and electrolyte replacement and intravenous insulin for 48 hours. Afterwards, his blood glucose was 150 mg/dl (8.3 mmol/L), fever, nausea, vomiting and abdominal pain resolved, and he was able to eat and to drink water.

What is your next step?

The patient can start to eat and drink water. Intravenous insulin can safely be discontinued and subcutaneous insulin begun. A bolus of rapid-acting insulin should be administered subcutaneously based on the results of the fingerstick test 1-2 hours before discontinuation of intravenous insulin, and 24 IU of basal insulin should be started. A careful history should be obtained to determine the cause of DKA and to avoid recurrence. This patient was not aware of the sick-day rules and had never been instructed to check often or how to correct high blood glucose values. Because he was not able to eat and drink water he reduced both the basal and the preprandial insulin to avoid hypoglycemia. The patient was educated about sick-day rules and to check urine and blood for ketones if blood glucose is above 300 mg/dl (16.7 mmol/L).

Case study 2

An 18-year-old female was taken to the emergency room in coma. Her parents noticed that she had polydipsia, polyuria, and rapid weight loss which started approximately 1 month ago and had worsened in the last week. She had not been taking any medications and the clinical history was otherwise unremarkable. On examination, breathing was deep and rapid (Kussmaul respiration), pulse rate was 100 beats per minute, and blood pressure 110/70 mmHg; she also had signs of dehydration. She was drowsy and confused. Rapid hematology and biochemical tests showed hematocrit 44%, hemoglobin 13 g/dl (140 g/L), white blood cell count 12,000/ μl, glucose 520 mg/dl (28.9 mmol/L), urea 50 mg/dl (8.5 mmol/L), creatinine 0.8 mg/dl (70.7 μmol/L), Na+ 148 mEq/L, K+ 4.6 mEq/L, PO4 3-2.0 mEq/L (0.64 mmol/L), and Cl− 112 mmol/L. Arterial pH was 7.0, PO 2 98 mmHg, PCO 2 25 mmHg, HCO 3−12 mEq/L, and O 2 sat 98%.

What is your diagnosis?

The patient has marked hyperglycemia and metabolic acidosis. The diagnosis of newly diagnosed type 1 diabetes presenting with DKA should be considered.

Which additional biochemical tests are required to confirm the diagnosis?

Determination of ketone bodies in blood or urine is necessary to confirm ketosis. In this case the strip for ketones in the urine was strongly positive and determination of β-OHB in serum was 4.0 mmol/L. Thus, the patient has the triad of hyperglycemia, ketosis, and acidosis and the diagnosis of DKA is confirmed.

How will you manage the patient?

Urgent administration of intravenous fluid and insulin should begin together with careful monitoring, replacement of electrolytes, and correction of acidosis. After resolution of DKA and as long as the patient is conscious, feeding can start. Transition from intravenous to subcutaneous insulin administration should begin. A bolus of rapid-acting insulin should be administered subcutaneously based on the results of the fingerstick test 1-2 hours before discontinuation of intravenous insulin. A total daily dose of insulin of 0.5-0.8 IU/kg is required, divided as 30-50% basal insulin and the remainder as rapid-acting insulin before each meal.

Next excerpt:Diabetic ketoacidosis in childhood and adolescence 

 

References

  1. Ioannidis I . Diabetic coma . In: Katsilambros N , Diakoumopoulou E , Ioannidis I , Liatis S , Makrilakis K , Tentolouris N , Tsapogas P (ed), Diabetic ketoacidosis in adults 31 Diabetes in Clinical Practice, Questions and Answers from Case Studies , West Sussex , England: John Wiley & Sons Ltd , 2006 : 81 – 91 .
  2. Umpierrez GE , Smiley D , Kitabchi AE . Narrative review: ketosis – prone type 2 diabetes mellitus . Ann Intern Med 2006 ; 144 : 350 – 7 .
  3. Faich GA , Fishbein HA , Ellis SE . The epidemiology of diabetic acidosis: a population – based study Am J Epidemiol 1983 ; 117 : 551 – 8 .
  4. Katsilambros N . Epidemiology of acute manifestations and complications . In: Williams R , Papoz L , Fuller J (ed), Diabetes in Europe, A Monograph on Diabetes Epidemiology in Europe produced as part of the ‘ Eurodiab ‘ Concerted Action Programme of the European Community , London, UK : John Libbey & Company Ltd , 1994 : 39 – 209 .
  5. Ellemann K , Soerensen JN , Pedersen L , Edsberg B , Andersen O . Epidemiology and treatment of diabetic ketoacidosis in a community population . Diabetes Care 1984 ; 7 : 528 – 32 .
  6. Wyckoff J , Abrahamson MJ . Diabetic ketoacidosis and hyperosmolar hyperglycemic state . In: Kahn R , King GL , Moses AC , Weir GC , Jacobson AM , Smith RJ (ed), Joslin ‘ s Diabetes Mellitus , 14 th edn , Philadelphia, USA : Lippincott Williams & Wilkins , 2005 : 887 – 99 .
  7. Javor KA , Kotsanos JG , McDonald RC , Baron AD , Kesterson JG , Tierney WM . Diabetic ketoacidosis charges relative to medical charges of adult patients with Type I diabetes . Diabetes Care 1997 ; 20 : 349 – 54 .
  8. Kitabchi AE , Umpierrez GE , Murphy MB , Barrett EJ , Kreisberg RA , Malone JI , Wall BM . Management of hyperglycemic crises in patients with diabetes . Diabetes Care 2001 : 24 : 131 – 53 .
  9. Kitabchi AE , Umpierrez GE , Miles JM , et al. Hyperglycemic crises in adult patients with diabetes: a consensus statement from the American Diabetes Association . Diabetes Care 2009 ; 32 : 1335 – 43 .
  10. Krentz AJ , Nattrass M . Acute metabolic complications of diabetes: diabetic ketoacidosis, hyperosmolar non – ketotic hyperglycemia and lactic acidosis . In: Pickup JC , Williams G (ed), Textbook of Diabetes Mellitus , 3 rd edn , Oxford, UK : Blackwell Publishing , 2003 : 32 . 1 – 24 .
  11. Maldonado M , Hampe CS , Gaur LK , et al. Ketosis – prone diabetes: dissection of a heterogeneous syndrome using an immunogenetic and beta – cell functional classifi cation, prospective analysis, and clinical outcomes . J Clin Endocrinol Metab 2003 ; 88 : 5090 – 8 .
  12. Balasubramanyam A , Nalini R , Hampe CS , Maldonado M . Syndromes of ketosis – prone diabetes mellitus . Endocr Rev 2008 ; 29 : 292 – 302 .
  13. Umpierrez , GE . Ketosis – prone type 2 diabetes: time to revise the classify cation of diabetes . Diabetes Care 2006 ; 29 : 2755 – 7 .
  14. Newton CA , Raskin P . Diabetic ketoacidosis in Type 1 and Type 2 diabetes mellitus . Arch Intern Med 2004 ; 164 : 1925 – 31 .
  15. Pinero – Pilona A , Raskin P . Idiopathic Type 1 diabetes . J Diabetes Complications 2001 ; 15 : 328 – 35 .
  16. Voulgari C , Tentolouris N . The performance of a glucose – ketone meter in the diagnosis of diabetic ketoacidosis in patients with Type 2 diabetes in the emergency room . Diabetes Technol Ther 2010 ; 12 : 529 – 35 .
  17. Yadav D , Nair S , Norkus EP , Pitchumoni CS . Nonspecifi c hyperamylasemia and hyperlipasemia in diabetic ketoacidosis: incidence and correlation with biochemical abnormalities . Am J Gastroenterol 2000 ; 95 : 3123 – 8 .
  18. Vinicor F , Lehrner LM , Karn RC , Merritt AD . Hyperamylasemia in diabetic ketoacidosis: sources and signifi cance . Ann Intern Med 1979 ; 91 : 200 – 4 .
  19. Fowler M . Hyperglycemic crisis in adults : Pathophysiology, presentation, pitfalls, and prevention . Clinical Diabetes 2009 ; 27 : 19 – 23 .
  20. Kitabchi AE , Ayyagari V , Guerra SMO , Medical House Staff. The efficacy of low dose versus conventional therapy of insulin for treatment of diabetic ketoacidosis . Ann Intern Med 1976 ; 84 : 633 – 8 .
  21. Heber D , Molitch ME , Sperling MA . Low dose continuous insulin therapy for diabetic ketoacidosis; prospective comparison with " conventional " insulin therapy . Arch Intern Med 1977 ; 137 : 1377 – 80 .
  22. Sacks HS , Shahshahani M , Kitabchi AE , Fisher JN , Young RT . Similar responsiveness of diabetic ketoacidosis to low – dose insulin by intramuscular injection and albumin – free infusion . Ann Intern Med 1979 ; 90 : 36 – 42 .
  23. Fisher JN , Shahshahani MN , Kitabchi AE . Diabetic ketoacidosis: low – dose insulin therapy by various routes . N Engl J Med 1977 ; 297 : 238 – 47 .
  24. Umpierrez GE , Latif K , Stoever J , et al. Effi cacy of subcutaneous insulin lispro versus continuous intravenous regular insulin for the treatment of patients with diabetic ketoacidosis . Am J Med 2004 ; 117 : 291 – 6 .
  25. Umpierrez GE , Cuervo R , Karabell A , et al. Treatment of diabetic ketoacidosis with subcutaneous insulin aspart . Diabetes Care 2004 ; 27 : 1873 – 8 .
  26. Maldonado MR , Otiniano ME , Cheema F , et al. Factors associated with insulin discontinuation in subjects with ketosis – prone diabetes but preserved beta – cell function . Diabet Med 2005 ; 22 : 1744 – 50 .
  27. Assal JP , Aoki TT , Manzano FM , Kozak GP . Metabolic effects of sodium bicarbonate in management of diabetic ketoacidosis . Diabetes 1974 ; 23 : 405 – 11 .
  28. Narins , RG , Cohen JJ . Bicarbonate therapy for organic acidosis: The case for its continued use . Ann Intern Med 1987 ; 106 : 615 .
  29. Arieff AI . Cerebral edema complicating nonketotic hyperosmolar coma Miner Electrolyte Metab 1989 ; 12 : 383 – 9 .

Nikolaos Katsilambros, MD, PhD, FACP
SCOPE Founding Fellow
Professor of Internal Medicine
Athens University Medical School
Evgenideion Hospital and Research Laboratory ‘Christeas Hall’
Athens, Greece

Christina Kanaka-Gantenbein, MD, PhD
Associate Professor of Pediatric Endocrinology and Diabetology
First Department of Pediatrics, University of Athens
Agia Sofia Children’s Hospital
Athens, Greece

Stavros Liatis, MD
Consultant in Internal Medicine and Diabetology
Laiko General Hospital

Konstantinos Makrilakis, MD, MPH, PhD
Assistant Professor of Internal Medicine and Diabetology
Athens University Medical School
Laiko General Hospital
Athens, Greece

Nikolaos Tentolouris, MD, PhD
Assistant Professor of Internal Medicine and Diabetology
University of Athens
Laiko General Hospital
Athens, Greece

A John Wiley & Sons, Ltd., Publication This edition first published 2011 © 2011 by John Wiley & Sons, Ltd.

All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, except as permitted by the UK Copyright, Designs and Patents Act 1988, without the prior permission of the publisher. This publication is designed to provide accurate and authoritative information in regard to the subject matter covered. It is sold on the understanding that the publisher is not engaged in rendering professional services. If professional advice or other expert assistance is required, the services of a competent professional should be sought. The contents of this work are intended to further general scientific research, understanding, and discussion only and are not intended and should not be relied upon as recommending or promoting a specific method, diagnosis, or treatment by physicians for any particular patient.

Diabetic Emergencies: Diagnosis and Clinical Management provides emergency room staff, diabetes specialists and endocrinologists with highly practical, clear-cut clinical guidance on both the presentation of serious diabetic emergencies like ketoacidosis, hyperosmolar coma and severe hyper- and hypoglycemia, and the best methods of both managing the emergencies and administering appropriate follow-up care.

For more information and to purchase this book, just follow this link: Diabetic Emergencies: Diagnosis and Clinical Management 

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