GROUP MEMBERS 1. Dholu Ekta 2. Katara Miteshkumar 3. Bhammar Atubhai

A.4. Herma Bhavendra5. Amrutiya Himendra6. Patel Rahul7. Ahad Sabahat8. Ezemonye Benson9. Erhire Aboloje10. Oisamokhai

Kenneth11. Mehta Punit

DIABETIC KETOACIDOSIS

CASE PRESENTATION

HISTORY AND PHYSICAL EXAMINATION 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 accordingly had been brought to the emergency department.

CLINICAL FINDINGS

HISTORY AND PHYSICAL EXAMINATION

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.

PLASMA OR SERUM RESULTS (NORMAL LEVELS IN PARENTHESES, SI UNITS):

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 mOsm/kg serum water)

Hematocrit, 0.500 (0.354–0.444)

DIFFERENTIAL DIAGNOSIS

TREATMENT 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.

Continual monitoring of K+ levels is extremely important in the management of diabetic ketoacidosis because inadequate management of K+ balance is the main cause of death.

Bicarbonate is not needed routinely, but may be required if acidosis is very severe.

DISCUSSION 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 type I diabetes mellitus.

Perhaps the sore throat this patient had several weeks before admission reflected the initiating viral infection.

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 lacticacidosis and intoxication by methanol, ethylene glycol, and salicylates.

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 thorough familiarity with the actions of insulin.

CONCLUSION 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.

REFERENCES 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

SALAMAT PO!