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Diabetic emergencies –update and controversies Diabetic emergencies –update and controversies

Diabetic emergencies –update and controversies - PowerPoint Presentation

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Diabetic emergencies –update and controversies - PPT Presentation

Dr S Parthasarathy MD DA DNB MD Acu Dip Diab DCA Dip Software statistics PhD physio Mahatma Gandhi Medical college and research institute puducherry India ID: 916175

dka insulin serum glucose insulin dka glucose serum blood ketones patient 250 coma positive meq units severe replacement saline

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Slide1

Diabetic emergencies –update and controversies

Dr. S.

Parthasarathy

MD., DA., DNB, MD (

Acu

), Dip.

Diab

. DCA, Dip. Software

statistics

PhD

(

physio

)

Mahatma Gandhi Medical college and research institute ,

puducherry

India

Slide2

When ever there are updates , there will be controversies

Slide3

Diabetic emergencies

Diabetic

keto

acidosis

Hyper

osmolar

hyperglycemic non

ketotic

coma

Hypoglycemia

Lactic acidosis - ?? nonexistent

Slide4

Definition – clinical and biochemical

DKA is defined clinically as an acute state of severe

uncontrolled diabetes

associated with

ketoacidosis

that requires emergency treatment with

insulin and intravenous fluids

RBS = > 250 mg %

Ketones

> 5

meq

/l

pH < 7.3

bicarb

< 18

meq

/ l

Slide5

Insulin Deficiency

(Absolute or Relative)

Protein catabolism

Amino

acids

Nitrogen

loss

Glycerol

Free

Fatty acids

Glucose uptake

Hepatic glucose

Production

Hyperglycemia

Gluconeogenesis

Ketogenesis

Ketonemia

Osmotic diuresis

ELECTROLYTE

DEPLETION

Ketonuria

Hypotonic losses

DEHYDRATION

ACIDOSIS

Lipolysis

Pathophysiology

of DKA

Slide6

Mind boggling slide !!

Looks like

As simple as this

Uncontrolled DM

Trigger factor

Severe hyperglycemia

Glycosuria

, loss of water, electrolytes

Protein breakdown

Lipid breakdown and

Ketogenesis

Slide7

What happens in DKA ??

Hyperglycemia

Glycosuria

Water ( 6

litres

)

Electrolytes ( K+ 300,

Cl

- 400 Na 500

meq

)Beta oxidation of fatty acids – Keto acids -acetone, beta-hydroxy

butyrate, aceto acetate.Fruity odour, nausea

Slide8

The “I” problem

I am the professor !!

I am rich !!

I am well qualified !!

I am the best doctor !!

I am the best husband !!

Slide9

The precipitating factors

Infection.

Infarction (heart or cerebrum)

Insulin lack.

Indiscrete drugs.

Infant (pregnancy)

Injuries

And as usual unidentified ??

Slide10

Update

avoid DKA

self-testing for urinary

ketones

and adjusting their insulin regimens on sick days.

Slide11

Symptoms

Anorexia, Nausea, vomiting, Acute abdomen

Lethargy,

Myalgia

,

Dyspnea

Hypothermia,

Hyporeflexia

,

Hypotonia

,

Seizures

, Stupor, coma

Headache, chest pain,

pleurisy

Slide12

Signs

Air hunger –

acidotic

(

kussmaul

) respiration

Dehydration,Confusion

, drowsiness, coma (= 10%).

Hypotension,Tachycardia

Acetone

odour

on breath

Any system

Slide13

We know medicine !!

symptom spectrum is a clinical collection but a patient may present with uncontrolled diabetes, an UTI and vomiting.

Beware don’t treat as gastritis.

It may be DKA

Uncontrolled diabetes ,

Discomfort,vomiting

ECG – MI ,

Ketones

+

ve

Slide14

Diagnostic Criteria For DKA

Features

Mild

Moderate

Severe

Plasma glucose (mg/dl)

Arterial pH

Serum bicarbonate (

mEq

/L)

Urine

ketones

Serum

ketones

Effective serum

osmolality

(

mOsm

/kg)

Anion gap

Alteration in

sensoria

> 250

7.25-7.30

15-18

Positive

Positive

Variable

> 10

Alert

> 250

7.00-7.24

10 to <15

Positive

Positive

Variable

> 12

Alert/drowsy

> 250

<7.00

< 10

Positive

Positive

Variable

> 12

Stupor/coma

Slide15

Take history !!

Slide16

Investigate

Blood

– sugar , urea ,

creatinine

, electrolytes

ABG, (venous BG)

ketones

, TC, DC, blood cultures ,amylase, Serum lipase

CVP , X ray,

CT , MRI

sos

ECG every 6 hours if doubted Urine

ketones, deposits and culture

Slide17

Plasma osmolarity

2 (Na + K) + BUN/3 + glucose/18

2( 135 +5) + 15/3 + 300/18

280 + 5 + 16.6 = 301.6

Around 290 in DKA

Around 310 in HHS

Slide18

Don’t believe lab fully

Test

false

High glucose

hyponatremia

High triglycerides low glucose

Ketones

high

creatinine

Slide19

Treat patients – not labs

Urine tests

acetoacetate

But

betahydroxy

butyrate is predominant

Next day urine positive but patient better

Slide20

Treatment of DKA in Adults

Fluid replacement

Insulin replacement

Potassium replacement

Phosphate replacement

Bicarbonate replacement

Management of precipitating factor

General Medical Care (ICU).

Slide21

The average fluid deficit is 3–5

liters

In young, otherwise healthy patients

begin with bolus of

1

liter

of normal saline

followed by an infusion of normal saline at

500 ml/hour for several hours.

Slide22

1 +1

2 in medicine

IV fluids - Vary in infarct patients ,

Appropriate monitoring and infusion

mild DKA should be given normal saline at 250 ml/hour;

those with elevated corrected serum sodium should be given half-normal saline at 250 ml/hour

. (150

meq

0r

osm

330 )

Glucose NS at 250 mg or 180 mg

If sure of the electrolytes, Ringer lactate infusion is acceptable

Slide23

Insulin

loading dose of regular insulin at 0.1 units/kg

60 kg means 6 units regular insulin IV

Followed by 6 units / hour

RBS comes down by 50 – 75 mg/ hour

RBS does not fall – double the dose

Mild cases no loading dose

Slide24

Actre

Actress

jayamala

sabarimala

controversy

Insulin 0.14 units / kg start – no loading dose

IM regular insulin

(0.3 units/kg),

– some centers

Oral intake - SC insulin 6 hours prior to stopping IV

Extended insulin- better results

Slide25

Electrolyte replacement:

Serum potassium (

mEq

/L) Action

> 5.3 No additional potassium; recheck in 1 hr

 

4.0–5.3 Add

KCl

10

 

3.5 to < 4.0 Add

KCl

20

 

< 3.5 Hold insulin Add

KCl

20–60

Continuous cardiac monitoring

Slide26

Critically ill patients with DKA manifest

hypophosphatemia

during resuscitation

avoid potential cardiac and skeletal muscle weakness and respiratory depression from

hypophosphatemia

,

a serum phosphate of < 1.5 mg/dl

should be

repleted

with K2PO4 at 0.5 ml/hour.

Usually rare

Slide27

NO ROUTINE bicarbonate

SIX’ indications

of sodium bicarbonate after ABG

Arterial pH ≤

7.0

Serum HCO3

≤ 5

mmol

/L

Imminent cardiovascular collapse /shock

Coma

Life threatening

hyperkalemia

Severe lactic acidosis complicating DKA

Slide28

Laboratory tests follow up

Blood tests for glucose every 1-2 h until patient is stable, then every 6 h

Serum electrolyte determinations every 1-2 h until patient is stable, then every 4-6 h

Initial blood urea nitrogen (BUN)

Initial arterial blood gas (ABG) measurements, followed with bicarbonate as necessary

Slide29

Complications of DKA

The recovery pattern may be slow to come but complications like

cerebral oedema, arrhythmias stroke, infarction, aspiration, infection and sepsis

may hinder the recovery to cause death in some patients.

Mortality (5-10%)

Slide30

Remember clinical clues

Monitor blood pressure,

pulse, respirations,

mental status,

fluid intake and output every 1–4 h.

Slide31

Update

DKA is a thrombotic state

DKA can precipitate stroke

Stroke can precipitate DKA

Slide32

DKA in pregnancy- points to note

with

pregestational

, insulin dependent diabetes

Foetal loss – 50 %

Maternal loss - 1 %

Proper antibiotic choice

Labour may precipitate DKA

Slide33

Paediatric DKA

0.05 units /kg insulin

ideal to rehydrate in

36 hours than 24 fours

initial resuscitation with 20 ml/kg of 0.9 % NS

0.45% saline avoids cerebral

edema

SC

lispro

suggested

Slide34

Hyperglycemic hyperosmolar

syndrome

Some insulin – no ketosis, no acidosis

Less common

Coma

Hyper

osmolarity

,

RBS 500- 600

10

liters

or more

Its is ideal to switch to half normal saline if either the

osmolality or sodium is high.No urgent insulin

Slide35

Hypoglycemia:

In practice,

hypoglycemia

is generally defined as a blood glucose level < 60 mg/dl. A definitive diagnosis

Whipple’s triad:

1. Symptoms compatible with hypoglycaemia

2. A low plasma glucose concentration

3. Relief of symptoms after plasma glucose is raised

.

Slide36

Why important

Brain needs glucose

It cant synthesize glucose

We cant let it starved of

glucose for even a few minutes

Slide37

40 or 50 or 60 or 70???

Arterial plasma 10 % higher than venous.

Fasting ok but pp no good.

Whole blood (finger pricks) 10% lower!!

High

hematocrit

– venous-arterial gap is more.

Slide38

Incidence of hypo

Type 2 without insulin :

4-10 /patient/year

Type 2 on insulin : 16 /patient/year

Type 1 : 40 episodes /patient/year

Slide39

What happens if sugar decreases ??

approx 80 mg

Decreased insulin secretion

Approx 70 mg

Increased glucagon

Approx 65 mg

Increased epinephrine

Approx 55-65 –

Cortisol

& growth hormone (Noncritical)

Less than 55 - cognition affecte

d

Slide40

Symptoms

Autonomic

neuroglycopenic

Palpitation headache

Sweats fatigue

Anxiety mental dullness

Tremors vision blurring

Tachycardia confusion

Hypertension amnesia

Nausea ,hunger

seizure,coma

Slide41

Risk factors

Use of insulin

secretagogues

(

sulphonyl

ureas

)

insulin therapy

Missed or irregular meals

Advanced age

Duration of diabetes, strict control

Impaired awareness of

hypoglycemia

Autonomic failure, beta blockers

DPP 4 inhibitors – less incidence

Slide42

In insulin patients !!

The depth of needle

Exercising limb

Hot bath after injection

Bigger size needle

Type of insulin

Glargine

and

detemir

- less hypoglycemia

Slide43

Potentially hypoglycemic combines

Aspirin

-

dec

. insulin resistance

Quinine

– inc. insulin secretion.

Tetracyclics

- inc. insulin secretion

Gatifloxacin

- inc. insulin secretion

Beta blockers- interact hepatic

gluconeoFibrates – sensitivity to insulin

Fluoxetine -stimulate beta cells And a few others.

Slide44

Other diseases – prone for hypos

Adrenal

Gastrointestinal

Hepatic

Renal

Dementia

sepsis

Slide45

Categories of hypoglyemia

Mild

:

55-70 mg

pallor,sweats,palpitation

Moderate :

45-55 mg-

headache,vertigo,mood

changes

Severe

:

< 45 mg. Conscious status?

Slide46

Treatment

Mild :

15 grams glucose =

increase 18 mg- 18 min

4 cubes sugar

2 spoons honey

150 ml fruit juice

Slide47

Chocolate ,milk ,cereal bars – some sweets are not good

Moderate: 20 -25 grams

Sulphonyl

ureas

induced

hypos – prolonged ,

Observe and give snacks

Slide48

Severe – what is it??

Patient needs someone’s help

50 ml of 25 % dextrose IV –--------

2cc/kg-10% - infants

2cc/kg – 25% - adolescents

2cc/kg - 50% - adults

See that the vein is free flowing –

other wise risk of necrosis

Slide49

Some antidiabetics

Acarbose

- alpha

glucosidase

inhibitor

So only glucose should be given

Miglitol

-- sometimes even glucose may be refractory

Slide50

Treatment continuum

Measure blood sugar ,Assess conscious status

Maintain vitals, Start 10 % dextrose solution

1 mg glucagon IM or SC

Look for precipitating factors

-alcohol

Assess for

liver

status,renal

status

,

Serum insulin, c peptide, epinephrine, cortisol

TSH, growth hormones etc,etc…..

Slide51

Sulfonyl urea overdose

Inj.

Octretide

50 µgm SC can be repeated 8

hrly

Refractory unconscious state

can be cerebral edema

IV

mannitol

and dexa 10 mg to be considered

Slide52

Summary

I hope

the lecture

was pushed into your brains

Diabetic emergencies –update and controversies

Or

atleast

the picture

Slide53

Thank you all