DIABETIC KETOACIDOSIS

BY DR.WAQAS HUSSAIN PG MEDICAL UNIT-4

45 yrs old male patient known diabetic for last 5 years and was on oral hypoglycemic agents had history of wound in the left foot for which he was taking medications. He was presented to the accident and emergency department because of extreme shortness of breath for 6hrs after which he became unconscious.

On examination there was marked hyperventilation with respiratory rate of 50 breaths /min, blood pressure was 90/40 mm of Hg , febrile and has a pussy discharging wound on the planter surface of his foot.

How will you proceed and what differentials come in your mind

Urine D/R show:

Sp gravity 1.015 Proteins nil Glucose + Ketones + WBCs 4-5 RBCS 3-4

ABGs

pH PCO2 PO2 HCO3 SO2

= 7.15 = 20 mmHg = 80 mm Hg = 07 = 93%

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OBJECTIVES
INTRODUCTION DIAGNOSIS CAUSES PHYSIOLOGY OF INSULIN AND DK CLINICAL FEATURES DIFFERENTIATION FROM OTHER CAUSES MANAGEMENT

INTRODUCTION
A metabolic emergency in which hyperglycemia is associated with metabolic acidosis due to greatly raised ketone levels. Dabetic ketoasidosis is usually coupled with an increase in glucagon concentration with two metabolic consequences:

Maximal gluconeogenesis with impaired peripheral utilization of glucose Activation of the ketogenic process and development of metabolic acidosis.

DIAGNOSIS
The initial step in diagnostic approach is testing urine for glucose and ketones. Diagnostic criteria for DKA:
Hyperglycemia >250 mg/dl
Ketosis (ketonemia or ketonuria) Acidosis

pH < 7.3 HCO3 < 15mEq/L

supporting features are volume depletion and Kussmauls breathing.

CAUSES:

Un diagnosed type I.
Insulin defeciency.
Known diabetic Insulin

missed Insulin stopped deliberately.

Infection
Pneumonia UTI most commonly

Un treated newly diagnosed patient. Medical, surgical or emotional stress Use of insulin pump with leakage Drugs
Corticosterioids Thiazide diuretics

Pancreatitis Myocardial Infarction

CARBOHYDRATES
GLUCOSE UPTAKE GLYCOGEN SYNTHESIS GLUCONEOGENEIS(LIVER) GLYCOLYSIS (MUSCLE)

FATS
LIPOLYSIS

PROTEIN
AMINO ACID UPTAKE (PROTEIN SYTHESIS)

CONVERSION OF CARBOHYDRATE TO FAT (LIPOGENESIS)

POTASSIUM
K+ UPTAKE INTO CELLS
14

GLUCOSE UPTAKE

AA mobilization

LIPOLYSIS

HYPERGLYCEMIA

PLASMA AA

PLASMA FFA

KETOSIS

GLYCOSURIA

GLUCOSE

ACIDOSIS

DEHYDRATION

15

Hyperglycemia results from

Increased gluconeogenesis Conversion of glycogen to glucose Inadequate use of glucose by peripheral tissues

KETOGENESIS
Occurs as a results of high glucagon/insulin ratio: Increased liberation of free fatty acids due to the loss of the inhibitory action of insulin on the hormone sensitive lipase. Beta oxidation of FFA. Decreased concentrations of malonyl coA (an inhibitor of ketogenesis)

Hyperglycemia leads to 1. Glycosuria 2. Polyuria (osmotic diuresis) 3. Polydipsia 4. Polyphagia 5. Weight loss 6. Dehyrdation Ketone bodies lead to 1. Metabolic acidosis

PATHOGENESIS LACK OF INSULIN

Glucose Hyperglycaemia Glycosuria Osmotic Diuresis

Ketones
Acidosis Vomiting

Ketoacidosis is a state of uncontrolled catabolism associated with insulin deficiency.

Fluid & Electrolyte Depletion

Renal Hypoperfusion

Impaired Excretion of Ketones & Hydrogen ions

FLUID AND ELECTROLYTE DEPLETION

Average water depletion is about 5 litres Sodium depletion is 300-500 mmol Ptassium depletion is 270 400 mmol Chloride depletion is 100 400 mmol

CLINICAL FEATURES

Polydepsia Polyuria for about 24 hrs. followed by Fatigue Nausea Anorexia Vomiting Abdominal pain and tenderness. Kussmaul breathing with fruity odor acetone Signs of dehydration ( HR, postural hypotension.) low temperature. Stupor Comma Mild hypothermia

LAB FINDINGS

Glycosuria 4+ Strong ketonuria Hyperglycemia Ketonemia Low arterial pH Low Bicarbonate levels

Elevated serum amylase levels Azotemia show renal status Leukocytosis

MANAGEMENT
Therapeutic goals Improving circulatory volume and tissue perfusion
Reducing blood glucose and serum osmolality toward normal levels Clearing ketones from serum and urine at a steady rate Correcting electrolyte imbalances and identifying precipitating factors.

REMEMBER

Ensure ABC Follow standard care of unconscious patient Maintain I/V line and send samples for CBC, UCE, Blood C/S Send urine for ketones and C/S Arrange CXR and ECG Check ABGs

Send labs
Glucose. U & E. HCO3. Osmolality. Blood gases. FBC. Blood culture. Urinary ketons. Urine DR. CXR. ECG.

INDWELLING URINARY CATHETER

In comatose pt. To monitor output.

THERAPEUTIC FLOW SHEET

Monitor BP,TPR and GCS. Auscultate lung bases hourly till pt stabilizes. Check:
Blood sugar hrly for 8 hrs den 2 to 4 hrly afterwards Electrolytes 4 hrly ABGs daily Urinary ketones 4 hrly

INSULIN REPLACEMENT

USE REGULAR INSULIN Give 0.15 Units / kg as IV bolus. Infuse 0.1 unit / kg / hr infusion or hrly I/M injection Dont use s/c insulin Maintain according to labs.

INSULIN REPLACEMENT contd

Start continuous infusion by adding 1ml(100 units) of regular insulin in 99 ml normal saline in paediatric chamber at a dose of 0.1 unit/kg /hr If the plasma glucose fails to fall by 10%in the first hour a repeat loading dose is recommended.

INSULIN REPLACEMENT contd

Rarely a pt. with immune insulin resistance is encountered, and this requires doubling the dose every 2-4 hrly if the hyperglycemia does not improve after the first two doses of insulin. Reduce the insulin infusion to 0.05 units/kg if the blood glucose falls below 200mg/dl AND OF COURSE NOT TO STOP IT!!!!

INSULIN REPLACEMENT contd

Change to s/c insulin when the pt regains consciousness and takes the meal Then start on 8 hrly sliding scale regimen for 24-48 hrs Calculate the daily requirement and then switch to fixed insulin regimen as estimated from 24 hrs requirements and dose should be adjusted according to blood glucose measurements.

Causes of Inadequate Insulin response

Inadequate dose Insulin stick to the tubings ( do the priming

first) Improper storage of insulin Missed dose (buisy interns!!!!) Increasing requirement Immune insulin resistance

FLUID REPLACEMENT

The total body deficit is about 5 litres Total fluid replacement should be about 6 litres. Failure to give adequate fluid adversely affects the outcome.

FLUID REPLACEMENT contd

Initially normal saline is the solution of choice

Give 1 litre of 0.9 % saline stat. Then 1 litre over next hour.

1 litre over 2 hours.

1 litre over 4 hours. Next three litres should be given in 4 hrs each

at a rate of 300 - 400 ml/hr

FLUID REPLACEMENT contd

If the serum sodium is greater than 150mEq/L use 0.45% saline. Excessive fluid replacement of more than 5litres in 8 hours leads to ARDS or cerebral edema.

FLUID REPLACEMENT contd

Use dextrose saline or 10 % dextrose when blood glucose is < 250 mg/dl and decrease the dose of insulin to 0.05 units / kg/ hr. Never stop insulin. Dextore solution prevents the development of hypoglycemia and will also decrease the likelihood of cerebral edema, which could result from too rapid decline in blood glucose.

POTASSIUM REPLACEMENT
Dont add Potassium to the first bag. Give potassium according to serum level.

< 3.0 34 45

40 mmol. 30 mmol. 20 mmol.

BICARBONATE REPLACEMENT

Bicarb use in DK is questionable Give bicarb if the pH is 7.0 or less Dilute it in 5% D/W or 0.45% saline Once pH is 7.1 dont give further bicarb

BICARBONATE REPLACEMENT

Calculate the base deficit by following formula:

Base Deficit = 0.4 x Wt. in kg (24 HCO3) Give half of the calculated deficit in first 8 hrs and the rest in next 12 hours if necessary.

BICARBONATE REPLACEMENT

E.g:
If the HCO3 is 4mEq/L in 50 kg Base decicit = 0.4 x 50 ( 24- 4)

= 0.4 x 50 x 20 = 400

BICARBONATE REPLACEMENT

Following are the deleterious effects of bicarbonate therapy:

Development of hypokalemia

Tissue anoxia due to left ward shift of O2-Hb

dissociation curve Cerebral acidosis Rebound metabolic alkalosis

PHOSPHATE THERAPY

As potassium salts

TREATMENT OF ASSOCIATED INFECTIONS

ANTIBIOTICS

Complications of DKA
Acute gastric dilatation or erosive gastritis
By vomiting blood or coffee-ground material

Cerebral edema
Obtundation Coma with or without neurological signs especially if occurring with initial improvement.

Complications of DKA
Hyperkalemia
Hypokalemia

cardiac arrest
cardiac arrythmias.

Sepsis is known by fever

Complications of DKA
INSULIN RESISTANCE:
UNREMITTING ACIDOSIS AFTER 4-6 HRS OF RX

MI:
Chest pain Appearance of HF Hypotension despite adequate fluids

Mucormycosis:

Facial pain Bloody nasal discharg Blurred vision Proptosis.

Complications of DKA
ARDS: Hypoxemia in absence of
Pneumonia COPD HF

Vascular thrombosis:
Stroke-like picture or signs of ischemia in non nervous tissue

COUNCELLING:

We have to make sure that each patient receives intensive detailed instructions about how to avoid this potentially disastrous complication of diabetes mellitus.

SICK DAY RULES:

Monitor blood glucose 4 6 times a day. Test for Ketone daily. Never stop insulin. Determine insulin need and adjust it. Keep up carbohydrate intake.

SURVIVAL RULES:
Contact the Diabetic care team if: There is vomiting or diarrhea. Blood glucose stays over 380mg/dl for 3 hrs. Urine shows ketone persistantly. There are troublesome hypos.