DIABETIC COMA_Clinical Features and Management

7/28/2019 DIABETIC COMA_Clinical Features and Management

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DIABETIC COMA

clinical features and management


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HYPOGLYCEMIA


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DEFINITION

Hypoglycemia or low blood glucose is aclinical state associated with < 50mg/dl or

low plasma glucose with typicalsymptoms.

Whipples triad =

venous plasma glucose


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DCCT Definition

Event resulting in seizure,coma ,confusion orsymptoms like sweating,palpitation,hungerwith finger stick glucose < 50 mg/dl andamelioration of symptom by elevation of bloodglucose.

Prodromal symptoms occuring before the eventare well remembered.

Severe hypoglycemic symptoms requiringhospital admission and treatment with IVglucose or glucagon.


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Mechanisms for fasting hypoglycemia

Under production

hormonedeficiencies

enzyme defects

substrate deficiency

chronic infections.

drugs

Over utilization

hyper insulinism

insulinomaexogeneous insulin

overdose.

auto immunity

Normal insulin levelextra pancreatic tumour

carnitine def, cachexia.


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Fed state hypoglycemia

Early(alimentary)within 2-3 hours after meals

Alimentary

hyperinsulinism Postgastrectomy

Functional(increasedvagal tone)

Hereditary fructoseintolerance

Galactosemia

Leucine sensitivity

Late(occult diabetic) 3-5hours after meals

Delayed insulin release

due to beta celldysfunction

Counter regulatorydeficiency of growthhormone,glucagon,cortisone,autonomicresponse,epinephrine.


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Factors that precipitate hypoglycaemia

Excessive insulin or SU administration-

- Error by patient or doctor.

- Poor matching to patients lifestyle.Increased insulin bioavailability-

-Exercise.

-Injecting into abdomen.-Change to human insulin/analogs

-Insulin antibodies.

-Mismatch of syringes


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Risk factors for severe hypo

Intensive insulin therapy & tight glycemic control.

Hypoglycemia unawarenessacute & chronic.

Long duration of diabetes. Increasing age.

Sleep.

Excessive alcohol.

Renal failure/ Hepatic failure

Hypothyroidism/ Hypopituitarism/Hypoadrenalism


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Hypoglycemia in non diabetic scenario

ZE syndrome -Whipples triad, diarrhea ,muscle

wasting,tiredness. May be associated with

neurofibroma. 5 hour OGGT shows < 50mg/dl.Serum insulin level-20micro units /ml, increased

proinsulin level.

Hereditary fructose intoleranceenlarged

liver,jaundice,cirrhosis,albuminurIa,aminoaciduria,mental retardation. Ingestion of

fruit leading to vomiting and hypoglycemia.


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Common symptoms

Autonomic Neuroglycopenic General

Adrenergic

Sweating confusion nausea

Palpitation drowsiness headache

Tremor speech problems

Hunger incoordinationatypical behaviour

diplopia


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Grading of Hypoglycaemia

Grade 1 or mild: patient can recognizehypo and able to self treat

Grade 2 or moderate: severe hypo preventspatient from self treating but with assistanceoral treatment is possible.

Grade 3 or severe

: severe degreeofneuroglycopenia requiring parenteralglucagon/dextrose.


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Sequence of responses to decrements in

plasma glucose mg/dl70 Counter regulation

60 Adrenergic symptoms

50 Neuroglycopenic symptoms40 Lethargy

30 Coma

20 Convulsions

10 Permanent Damage Death

0


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Hierarchy of Glucoregulation

Insulin (83 + 9 mg)

Glucagon (68 + 2 mg)

Epinephrine (68 + 2 mg)

Growth hormone (66 + 2 mg)

Cortisol (58 + 6 mg)

Symptoms of hypoglycemia (53 + 2)Cognitive dysfunction (49 + 2)


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Nocturnal Hypoglycemia

Is common (biochem hypos occur frequently).

Asymptomatic/morning headache/hangover.

Often identified by partner: sweating, fretting.May lead to sudden death.

Unsatisfactory time action profile of certaininsulins; physio defences against hypo reduced in

flat position; sympathetic responses to hyporeduced in slow wave sleep

Dawn phenomenon vs Somogyi effect.


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Morbidity of Hypoglycemia

CNS Coma/convulsions/transientdeficits/ataxia/brain damage/ intellectualimpairment.

PsychoCognitive disorders/personalitychanges/ behavioural disorders/ automatism/

psychosis.

CVSArrhythmia/MI/TIA/stroke.

EyeVitreous haemorrhage

MusculoskeletalFracture/accidental injury.


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Hypoglycaemic mortality

Causes Severe brain damage

Hypostatic pneumonia

Acute vascular events

Dead in Bed Cardiac

arrhythmia


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Hypoglycaemic Unawareness

Absence of classical adrenergic warning

symptom,

More vulnerable to develop severe hypoglycaemiaCounter-regulatory failure :

Glucagon failure - 5 yr.to20 yr.

Adrenaline failure - follows then

25 times higher risk for severe hypoglycaemia


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Hypoglycemia unawareness

Perception of early warning symptoms impaired.

Is not an all-or-none phenomenon.

Affects one quarter of Type 1 diabetic patients.

Correlates with glycemic control ? Duration of

diabetes ?

May be Acute or Chronic (Central autonomicfailure).


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Hypoglycaemia in Diabetes

HypothyroidismInsulin degradation is

less

Insulin sensitivity ismore

Decreased appetite

Decreased GH

Decreased

glycogenolysis


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HypocortisolismDecreased

gluconeogenesis

By decreasing substrate

By decreasing PEPCK

By decreasing Glu-6-

phosphatase.

Decreased permissive

effect on glucagon and

epinephrine

Decreased appetite


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Diabetic NephropathyDecreased catabolism

of insulin

ProteinuriaDecreased appetite

Nausea and vomiting

Impaired absorptionImpaired

gluconeogenesis


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Alcohol and hypoglycemia

Reduced

gluconeogenesis

Reduced hypoawareness

Reduced tremors


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DD of hypoglycemic and hyperglycemic coma

Symptoms,signs and hypoglycemic coma hyperglycemic coma

laboratory findings

Physical findings

pulse rate increased increased

pulse volume full weak

temperature may be decreased may be decreasedrespiration shallow or normal rapid and deep

blood pressure normal,may be increased decreased

skin clammy,sweating dry

Tongue moist dry

tissue turgor normal reducedeyeball tension normal reduced

breath no acetone acetone may be

present

reflex brisk reflexes diminishedreflexes


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Symptoms,signs and hypoglycemic coma hyperglycemiccoma

laboratory findings

Laboratory tests

urine glucose -ve to +ve depending +veon time of last voiding

plasma glucose -ve to +ve +ve greater

than200mg/dl

plasma acetone -ve usually presentplasma bicarbonate normal low less than

20mg/litre

plasma CO2 normal diminished

blood pH normal less than 7.35


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MANAGEMENT ALGORITHM

Patient consciousOral glucose/sucrose

Patient unconscious

IV glucose (50%)IM/SC glucagon

Recovery No recoveryI.V glucose (5%)

Follow up

-Identify cause

-Re-educate


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CAUTION

Glucagon may lose effect with repeated use.

Glucagon is contraindicated in SU induced

hypos.SU induced hypoglycemia may be very

prolonged.It can be more fatal than insulininduced hypoglycemia.

Duration of treatment depends on cause ofhypo


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Measures to avoid hypoglycemia in patients

on insulin and/or sulfonylureas

Do not delay,skip or reduce food intake.

Take a snack before physical exercise.

Avoid insulin injections in the limb which is actively involved inthe exercise.

Avoid exercise during the peak time period of insulin action. When on human insulins,the time gap between insulin and food

should be 15 minutes.

When on analogs, keep the time gap less than 5 minutes

Do not use sulfonylureas in patients with hepatic/ renal

insufficiency. Ask the patient to avoid alcohol.

In older diabetics do not insist on very tight control of bloodglucose;prefer short acting sulfonylureas

Regularly monitor blood glucose.


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Drugs causing hypo

Increase in SU effect

Salicylates, probenecid, sulfonamides,

nicoumalone, fluconazole [inhibits CYP2C9 which

metabolizes glimepiride], ketoconazole,

ciprofloxacin [inhibits CYP3A4 which metabolizes

glibenclamide], gatifloxacin

Direct hypoglycemic effect

ACE(I), disopyramide, SSRIs, quinine,

sulfamethoxazole, mefloquine, pentamidine,

doxycycline, ethanol


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Neonatal hypoglycemia

Hypoglycemia in the immediate

postpartum period needs recognition,as this

phenomenon is transient. Every newborn ofdiabetic mothers must be given a 5%

glucose infusion for the first six hours and

subsequently blood glucose monitored toprevent potentially fatal hypoglycemic

convulsions.


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Take home message

Single most important limiting factor in

maintaining strict glycemic control.

Can be life threatening

Delicate balance needs to be kept between

tight control & hypoglycemia.

BE ON THE LOOK OUT FOR HYPO

ALL THE TIME


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ETIOLOGY

GLYCEMIA-

RELATED

Hypoglycemia Ketoacidosis

HHNKC

NON-GLYCEMIA

RELATED

Meningitis Stroke

SDH

Associatedencephalopathy


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BHARTI HOSPITAL EXPERIENCE

10 April to 16 May 2004 20 patients; 7 aged less than 18 yrs

10 with BG Hi; 14 with large UK; 7 with clinical

acidosis; 4 with altered sensorium [ 1 notresponding to pain]; 2/2 with BK Hi

OPD management for 3 [successful in 2 with 30 U

insulin each, unsuccessful in 1]

ADA recommends admission for moderate

ketosis

Green: male


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Age/gender distribution

0

1

2

3

4

5

6

40 y

Blue: female


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Precipitating factors

[Bharti Hospital, 10 Apr to 16 May, 2004]

0

0.5

1

1.5

2

2.5

3

3.5

4

4.5

5

omit inad ins alc TB preg new AGE uncer

ppt factor


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Ketosis: Symptoms

Polyuria, nocturia, thirst

Rapid weight loss

Muscular weakness Visual disturbance

Air hunger

Abdominal pain, nausea, vomiting

Leg cramps

Altered sensorium


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Ketosis: Signs

Acetone breath

Air hunger

Impaired consciousness Hyperglycemia, osmolarity

Cerebral edema if sensorium worsens during treatment

Hypotension: due to peripheral vasodilatation due to acidosis

Hypothermia Succussion splash

May mimic surgical emergency


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D/D

Hyperosmolar non-ketotic coma

Hypoglycemia

Lactic acidosis

Associated CNS pathology

Other metabolic encephalopathies

Acute pancreatitis


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Cardinal principles

Replace insulin

Replace fluids

Correct electrolytes Treat the cause

Supportive treatment

Prevent complications


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Insulin

Begin IV infusion of NS

and regular insulin

Monitor BG hourly

Shift to 5D + insulin when

BG = 200250 mg%

Try 0.10.2 U insulin/ kg

body wt/ hour initially;

reduce gradually

Check BG after every

2nd to 3rd bottle of IV

fluid Give first few vacs

fast until patient

regains consciousness/

BG comes down fromHi/BK come down

from Hi


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Who saved


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SC insulin

Begin as soon as

patient is fit to eat

Inject at least 30 minbefore stopping IV

insulin

Always begin with

regular or short-actinganalogue

me: the

insulin or the

nurse ?


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Electrolyte balance

Focus on K

Total body K is loweven if plasma reportis high

Insulin and rising pHboth stimulate entry ofextracellular K intocells

Aim for K > 3.5 mEq/l

Average req = 20mmol of K per 1000ml of NS

Do not give K in firsthour unless K < 3.5

Reduce if anuria/renalfailure

ECG monitoring canhelp


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Fluids

1000 ml/hour x first 2-3hrs, thereafter adjust accto need, hydration status

NS, N/2 saline, 5D Consider NaHCO3 if

pH < 7.0

Avoid N/2S as it ishypotonic, and promotesrapid movement of waterinto cells; may pptcerebral edema

Remember to

adjust for

polyuria


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Bicarbonate

Beneficial ONLY ifpatient is severely acidoticor nearing

cardiorespiratory collapse HCO3 + H = carbonic acid

= H2O + CO2 in ECF

CO2 readily enters cells,where reverse reaction

occurs, i.e., H is producedintracellularly, leading tointracellular acidosis

Hypokalemia

Paradoxical acidosis ofCSF

Adverse effects on oxyHbdissociation curve: tissuehypoxia

Overshoot alkalosis

Acceleration ofketogenesis by raising pH

Cerebral edema

Local necrosis


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Management

Always count

insulin, fluid, KCl

requirement tomake your patient

is conscious/

ketone-free

Correlate with pptfactor, other

variates

Average requirement

is 100 U insulin in 4 l

fluid over 24 hours Keep BG 150200

mg%

Requirement varies

acc to ppt factor,duration of ketosis


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Management

Avoid recurrent

ketosis: stopping IV

infusion for few

minutes can revert

patient to ketotic state

Maintain IV infusion

(5D + insulin) until atleast 2 urine samples

are ketone-negative

Keep separate IV line

for IV antibiotic

infusions

Give SC NPH insulin

b.d.; give first dose as

soon as patient is

reasonably hydrated


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Management

Check BG hourly

initially, then 24

hourly

If patient is on 5D

infusion, stop the drip

1530 mins prior to

test; take blood fromcontralateral arm

Keep a glass bottle of

NS + 2 units insulin;

give 100 ml after

completing 5D

infusion; check BG

after that


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Our experience

Insulin req: 14 to 410 U [mean 115.53 U]

minimum: 14, 32, 38 U

maximum: 260, 410 U all others: 48 to 146 U

Per kg body wt: 0.71 to 14.6 U [mean 3.6 U/kg]

minimum: 0.53, 0.71

maximum: 5.91, 8.5, 14.6

all others: 1.2 to 3.8


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Our experience

Fluid req: 1500 ml to 17 000 ml

minimum 1500 ml in 4 patients

maximum 9500, 17000 ml Per kg body wt: 25 to 607 ml/kg [mean 128]

minimum 25, 25, 30

maximum 607 ml/kg till ketone-free


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Complications

Cerebral edema

Incr intracellular osmolarity

in CNS neurone [glucose,

ketones, idiogenic osmoles] Sudden fall in ECF

osmolarity [insulin

hypotonic fluids]

Increased gradient

Increased entry of waterinto CNS

CEREBRAL EDEMA

ARDS

Thromboembolism

DIC Rhinocerebral

mucormycosis


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Prevention/treatment of c. edema

Slow rate of IV

infusion

Avoid hypotonicfluids

Slow insulin

replacement

IV mannitol dose

0.2 to 1 g/kg


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Reading lab tests

First capillary BG may be low because ofdehydration; next value can be higher

inspite of insulin Initial TLC/DLC, bl urea may be high due

to hemoconcentration; OT/PT, se amylasehigh

Initial Na is low, K may be high

If in doubt, repeat the next day


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Thank you for your attention

Thank you for

saving me

from coma

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DIABETIC COMA_Clinical Features and Management