DKA 31-05-11

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DIABETIC KETOACIDOSIS

BY

DR.WAQAS HUSSAIN

PG

MEDICAL UNIT-4

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45 yrs old male patient known diabetic for

last 5 years and was on oral hypoglycemicagents had history of wound in the left foot

for which he was taking medications. He

was presented to the accident andemergency department because of extreme

shortness of breath for 6hrs after which he

became unconscious.

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On examination there was markedhyperventilation 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.

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How will you proceed and what differentials

come in your mind

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Urine D/R show:

Sp gravity 1.015

Proteins nil

Glucose +

Ketones +WBCs 4-5

RBCS 3-4

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ABGs

pH = 7.15

PCO2 = 20 mmHg

PO2 = 80 mm Hg

HCO3 = 07

SO2 = 93%

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OBJECTIVES

INTRODUCTION

DIAGNOSIS

CAUSES

PHYSIOLOGY OF INSULIN AND DK

CLINICAL FEATURES

DIFFERENTIATION FROM OTHER CAUSESMANAGEMENT

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INTRODUCTION

A metabolic emergency in which hyperglycemiais associated with metabolic acidosis due togreatly raised ketone levels.

Dabetic ketoasidosis is usually coupled with anincrease in glucagon concentration with twometabolic consequences:

Maximal gluconeogenesis with impairedperipheral utilization of glucose

Activation of the ketogenic process anddevelopment of metabolic acidosis.

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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.

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CAUSES:

Un diagnosed type I.

Insulin defeciency. Known diabetic

Insulin missed

Insulin stopped deliberately.

Infection Pneumonia

UTI most commonly

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Un treated newly diagnosed patient.

Medical, surgical or emotional stress

Use of insulin pump with leakage Drugs

Corticosterioids Thiazide diuretics

Pancreatitis

Myocardial Infarction

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14

CARBOHYDRATESFATS

GLUCOSE UPTAKE

GLYCOGEN SYNTHESISGLUCONEOGENEIS(LIVER)

GLYCOLYSIS (MUSCLE)

CONVERSION OF CARBOHYDRATETO FAT (LIPOGENESIS)

LIPOLYSIS

PROTEIN

AMINO ACID UPTAKE(PROTEIN SYTHESIS)

K+ UPTAKEINTO CELLS

POTASSIUM

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GLUCOSE UPTAKE

HYPERGLYCEMIA

GLYCOSURIA

DEHYDRATION

AAmobilization

PLASMA AA

LIPOLYSIS

PLASMA FFA

KETOSIS

ACIDOSIS

GLUCOSE

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Hyperglycemia results from

Increased gluconeogenesisConversion of glycogen to glucose

Inadequate use of glucose by peripheraltissues

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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 thehormone sensitive lipase.

Beta oxidation of FFA.

Decreased concentrations of malonyl coA (an

inhibitor of ketogenesis)

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Hyperglycemia leads to

1. Glycosuria

2. Polyuria (osmotic diuresis)

3. Polydipsia4. Polyphagia

5. Weight loss

6. Dehyrdation

Ketone bodies lead to

1. Metabolic acidosis

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PATHOGENESIS

LACK OF INSULIN

OsmoticDiuresis

Renal Hypoperfusion

Impaired Excretion of

Ketones & Hydrogen ions

Fluid & ElectrolyteDepletion

Vomiting

AcidosisHyperglycaemia

Glycosuria

Glucose Ketones

Ketoacidosis

is a state of

uncontrolled catabolismassociated with

insulin deficiency.

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FLUID AND ELECTROLYTE DEPLETION

Average water depletion is about 5 litres

Sodium depletion is 300-500 mmol

Ptassium depletion is 270400 mmol Chloride depletion is 100400 mmol

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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

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LAB FINDINGS

Glycosuria 4+

Strong ketonuria

Hyperglycemia

Ketonemia

Low arterial pH

Low Bicarbonatelevels

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Elevated serum amylase levels

Azotemia show renal status

Leukocytosis

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MANAGEMENT

Therapeutic goals

Improving circulatory volume and tissue perfusion

Reducing blood glucose and serum osmolalitytoward normal levels

Clearing ketones from serum and urine at a steadyrate

Correcting electrolyte imbalances and identifyingprecipitating factors.

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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

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Send labsGlucose.

U & E.

HCO3.

Osmolality.

Blood gases.FBC.

Blood culture.

Urinary ketons.

Urine DR.

CXR.

ECG.

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INDWELLING URINARY CATHETER

In comatose pt.

To monitor output.

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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

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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.

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INSULIN REPLACEMENT contd

Start continuous infusion by adding1ml(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.

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Rarely a pt. with immune insulin resistance

is encountered, and this requires doubling

the dose every 2-4 hrly if the hyperglycemiadoes not improve after the first two doses of

insulin.

Reduce the insulin infusion to 0.05 units/kgif the blood glucose falls below 200mg/dl

AND OF COURSE NOT TO STOP IT!!!!

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Change to s/c insulin when the pt regainsconsciousness 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.

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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 requirementImmune insulin resistance

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FLUID REPLACEMENT

The total body deficit

is about 5 litres

Total fluidreplacement should be

about 6 litres.

Failure to give

adequate fluid

adversely affects the

outcome.

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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 eachat a rate of 300 - 400 ml/hr

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If the serum sodium is greater than

150mEq/L use 0.45% saline.

Excessive fluid replacement of more than5litres in 8 hours leads to ARDS or cerebral

edema.

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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 thelikelihood of cerebral edema, which could

result from too rapid decline in blood

glucose.

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POTASSIUM REPLACEMENT

Dont add Potassium to the first bag.

Give potassium according to serum level.

< 3.0 40 mmol.

34 30 mmol.

45 20 mmol.

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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

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Calculate the base deficit by following

formula:

Base Deficit = 0.4 x Wt. in kg (24HCO3)

Give half of the calculated deficit in first 8 hrs and

the rest in next 12 hours if necessary.

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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

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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

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PHOSPHATE THERAPY

As potassium salts

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TREATMENT OF ASSOCIATED INFECTIONS

ANTIBIOTICS

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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.

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Hyperkalemia cardiac arrest

Hypokalemia cardiac arrythmias.

Sepsis is known by fever

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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.

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ARDS: Hypoxemia in absence of Pneumonia

COPD

HF

Vascular thrombosis:

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

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COUNCELLING:

We have to make sure that each patient

receives intensive detailed instructions

about how to avoid this potentiallydisastrous complication of diabetes mellitus.

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SICK DAY RULES:

Monitor blood glucose 46 times a day.

Test for Ketone daily.

Never stop insulin.

Determine insulin need and adjust it.

Keep up carbohydrate intake.

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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.

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DKA 31-05-11