Diabetic Ketoacidosis is a disease secondary to Uncontrolled hyperglycemia. It can occur in Type I as well as advancement of Type II DM (Diabetes Mellitus). Biochemistry case presentation from harper's biochemistry case 6 - diabetic ketoacidosis.

1. 1. Dholu Ekta
2. Katara Miteshkumar
3. Bhammar Atubhai A.
4. Herma Bhavendra
5. Amrutiya Himendra
6. Patel Rahul
7. Ahad Sabahat
8. Ezemonye Benson
9. Erhire Aboloje
10. Oisamokhai Kenneth
11. Mehta Punit

5. 14y/F admitted to a hospital in coma. Her mother stated
that the girl had been in good health until approximately
2 weeks previously, when she developed a sore throat
and moderate fever. She subsequently lost her appetite
and generally did not feel well. Several days before
admission she began to complain of undue thirst and
also started to get up several times during the night to
urinate.
However, on the day of admission the girl had started to
vomit, had become drowsy and difficult to arouse, and

7. On examination :
• She was dehydrated
• Her skin was cold
• She was breathing in a deep sighing manner (Kussmaul
respiration/Air hunger) and
• Her breath had a fruity odour(acetone breath)
• BP 90/60 mmHg
• HR 115/min. (Tachycardia)
• She could not be aroused.
• A diagnosis of type 1 diabetes mellitus (formerly called
insulindependent diabetes mallitus-IDDM) with resulting
ketoacidosis and coma (DKA) was made by the intern on duty.

8.  Glucose, 50 mmol/L (4.2–6.1 mmol/L)
 Ketoacids ++++ (trace)
 Bicarbonate, 6 mmol/L (22–30 mmol/L)
 Urea nitrogen, 15 mmol(2.5–7.1 mmol/L)
 Arterial blood pH, 7.07 (7.35–7.45)
 Na+ , 136 (136–146 mmol/L)
 Cl– , 100 (102–109 mmol/L)
 PCO2 2.7 (4.3–6.0 kPa [or 32–45 mm Hg])
 Anion gap, 31 (7–16 mmol/L)
 Potassium, 5.5 mmol/L (3.5–
5.0 mmol/L)
 Creatinine, 200 mol/L (44–80
mol/L)
 Albumin 50 g/L (41–53 g/L)
 Osmolality, 325 (275–295

10. The most important initial measures in treatment of diabetes
ketoacidosis are intravenous administration of insulin and saline
solution.
This patient was given intravenous insulin (10 units/h) added to
0.9%NaCl.
Glucose was withheld until the level of plasma glucose fell below
15 mM.
Insulin and glucose facilitate entry of K+ into cells.
 KCl was also administered cautiously, with plasma K+ levels
monitored every hour initially.

11. The precise cause of type 1 (insulin-dependent) diabetes mellitus has not
been elucidated, and is under intense investigation.
Genetic, environmental and immunologic factors have all been implicated.
A very tentative scheme of the chains of events is the following.
 Patients with this type of diabetes have a genetic susceptibility (a large
number of genes, including histocompatibility genes located on
chromosome 6, have been implicated), which may predispose to a viral
infection (eg, by coxsackie or rubella viruses).
The infection and consequent inflammatory reaction may alter the
antigenicity of the surface of the pancreatic B cells and set up an
autoimmune reaction involving both cytotoxic antibodies and T
lymphocytes.
 This leads eventually to widespread destruction of beta cells, resulting in

12.  The marked hyperglycemia, glucosuria, ketonemia and ketonuria confirmed the
diagnosis of DKA.
 The low pH indicated a severe acidosis due to the greatly increased production
of acetoacetic acid and -hydroxybutyric acid.
 The low levels of bicarbonate and PCO2 confirmed the presence of a metabolic
acidosis with partial respiratory compensation (the hyperventilation).
 Calculation of the anion gap is useful in a number of metabolic situations.
 In this case it is elevated because of the presence of excess ketoacids in the
blood.
 There are a number of other causes of elevation of the anion gap, including

13.  The elevated values of urea and creatinine indicated some renal impairment (due to
diminished renal perfusion because of low blood volume secondary to dehydration),
dehydration, and increased degradation of protein.
 A high plasma level of potassium is often found in DKA owing to a lowered uptake of
potassium by cells in the absence of insulin.
 Thus, the clinical picture in DKA reflects the abnormalities in the metabolism of
carbohydrate, lipid, and protein that occur when plasma levels of insulin are sharply
reduced.
 The increased osmolality of plasma due to hyperglycemia also contributes to the
development of coma in diabetic ketoacidosis.
 It should be apparent that the rational treatment of a patient with DKA depends on

15. In this case, the patient was admitted to the intensive care
unit and administered IV regular insulin, 8 units/hour. Given
fluids and bicarbonate concurrently with the insulin, he was
alert, comfortable, and eating within 24 hours. Because this
patient had issues with long-term glycemic control, a follow-
up was scheduled with an endocrinologist on discharge. The
patient also received diabetic education while in the unit.

17.  Harper’s Biochemistry 28th Edition
 https://www.youtube.com/watch?v=xvsukGKRhx4
 https://www.youtube.com/watch?v=aJpC3W1_4I0
 http://accounts.smccd.edu/felixf/nurs232/dka.pdf

18. SALAMAT
PO!