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Slides current until 2008

Diabetic ketoacidosis and

hyperosmolar hyperglycaemic state

Section 4 | Part 2 of 2

Curriculum Module III6 | Short-term complications

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DKA and HHSCurriculum Module III-6

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What is DKA?

Absolute or relative insulindeficiency

Increase in counter-regulatoryhormones

Breakdown of fat and muscle

Biochemical triadhyperglycaemiaketoacids

metabolic acidosis

High blood glucose, ketones, acidosisand dehydration

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Incidence of DKA

Varies

Death mainly from cerebral oedema

Most common at onset in type 1diabetes

Recurrent episodes Can occur in type 2 diabetes

Kitabchi et al 2001, Joslin 2005

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DKA cause or trigger

Incidence

New-onset diabetes 5-40%

Acute illness 10-20%

Insulin omission/non-adherence 33%

Infection 20-38%

Heart attack, stroke,pancreatitis

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Insulin deficiency

Glucose uptake Lipolysis

Hyperglycaemia Gluconeogenesis

Glycerol Free fattyacids

Ketogenesis

Ketonemia

KetonuriaOsmotic diuresis

Urinary water losses

Electrolyte

depletion

Dehydration

Acidosis

Diabetic ketoacidosis

Adapted from Davidson 2001

Glucosuria

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Ketones

Used as fuel when calories arerestricted

Physiological ketosis when fastingor with prolonged exercise

Insulin deficiency lypolysis andketone production acidosis

beta-hydroxybutyrateacetoacetate

acetone

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Ketones

Beta-hydroxybutyratepredominant not detected by

test strips or acetone tablets

Ketoacidosis may be presentwithout detectable urinary ketones

Blood ketone testing may enableearly identification of DKA

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Earlier clinical symptoms andsigns of DKA

Polyuria

Polydipsia

Polyphagia

Tiredness

Muscle cramps

Flushed facial appearance

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Later clinical symptoms and signsof DKA

Weight loss

Nausea and vomiting

Abdominal pain

Dehydration

Acidotic breath

Hypotension Shock

Altered consciousness

Coma

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DKA investigations

Immediate for diagnosis Capillary blood glucose, urinary

glucose and ketones

Urgent for assessment and treatment Blood glucose Blood gases Electrolytes, urea, creatinine WBC

Consider Cardiac monitor Blood culture, urine culture Chest X-ray

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DKA laboratory findings

Blood glucose >14mmol/L (252mg/dL)

Ketones Urine: moderate to large

Blood: >3mmol/L

Osmolality Increased high blood glucose andurea/creatinine, dehydration

Electrolytes Low/normal Na+ and Cl-

Low/normal/high K+(often misleading)

Low HCO3 (normal 23-31)

Anion gap >10 mild

>12 moderate to severe

Blood gases pH

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DKA treatment

Rehydration 1. Correct shock with bolus saline

2. Rehydration rate depends on clinicalstatus, age and kidney function

Normal saline (0.9%) for resuscitationand rehydration initially

Glucose/saline solution when glucosearound 14 mmol/L (252mg/dL)

Rehydrate steadily over 48 hours

3. Consider NG tube

Potassium Essential after resuscitation and whenurine output confirmed

Kitabchi et al 1976

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DKA treatment

Insulin Infusion: 0.1 units/kg/hour afterresuscitation, saline established and BGfalling

Rate should be increased by 10-20% if

glucose not fallen by 2-3 mmol/L (45-54mg/dL) over first hour

Monitoring BG, BP, urine output and hourlyneurological status

Blood gases and electrolytes 2-hourlyinitially

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DKA complications

Hypoglycaemia +/- hypokalaemia

Acidosis not improving consider

continuing dehydration orinfection

Aspiration pneumonia

Headache +/- falling level ofawareness consider cerebraloedema and urgent treatmentwith Mannitol

Joslin 2005

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DKA recovery

Rapid improvement

Continue IV insulin while ketosis

present Oral intake when possible

Rapid-acting insulin 30-60 minutesbefore discontinuing IV insulin

Usual insulin regimen

Consider drinks and food containingpotassium

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What is HHS?

Ketosis may be present

Coma not always present

Primarily in older peoplewith/without history of type 2diabetes

Always associated with severedehydration and hyperosmolarstate

Develops over weeksKitabchi et al 2001

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HHS incidence and features

0.5% of primary diabetes hospitaladmissions

~15% mortality rate

Can occur in type 1 diabetes and

younger people

Kitabchi et al 2001

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HHS key features

Marked hyperglycaemia

Hyperosmolarity

Absence of severe ketosis

Altered mental awareness

Joslin 2005

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HHS causes or triggers

Booth 2001

Incidence

Infection 40-60%

New-onset diabetes 33%

Acute illness 10-15%

Medicines, steroids

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Signs and symptoms of HHS

Initially polyuria andpolydipsia

Altered mental status

Profound dehydration

Precipitating factors

d

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HHS biochemical findings

Jones 2001

Blood glucose >33mmol/L (600mg/dl)

Ketones Urine: negative small

Blood: 320mOsm/kg - (raised Na,

BG, urea)

Electrolytes Raised Na, BG, urea creatinine

Anion gap 7.30

normal or raised HCO3

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Treatment

Rehydration Caution!

Normal saline 1 l per hour initially

Consider strength normal saline

Potassium Only if hypokalaemic and renal functionadequate give before insulin

Insulin May be needed as slow infusion0.1 unit/kg/hour to be increased withcare if BG is slow to fall

Monitoring BG, BP, neurological function hourly untilstableElectrolytes 2-hourlyCardiac or CVP monitoring

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HHS complicationsComplication PreventionHypoglycaemia Prevent by adding glucose infusion

when glucose

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DKA and HHS prevention iskey

Identify and treat underlyingcause

Can be prevented bybetter public awareness

improved access to medicalcare

improved education in treatinghyperglycaemia during illness

emergency communicationwith healthcare provider

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Managing diabetes during illness

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Diabetes and illnesses

People with adequate glycaemiccontrol not at increased risk ofinfection

Poor metabolic control increasesrisk

- decreases immunity

- leads to persistent glycosuria anddehydration

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Impact of illness

Infective illness increased stress hormones

gluconeogenesis + insulin insensitivity hyperglycaemia + ketones

Nausea, vomiting, diarrhoea

poor gastric emptying + rapid intestinaltransit + poor food absorption

hypoglycaemia

Milder illnesses

little or no effect

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Illnesses and hyperglycaemiaGeneral management

Identify and treat cause of illness

Treat symptoms such as fever with

paracetamol Adequate fluids frequent diet

drinks

More frequent blood glucose tests Check urine for ketones

Blood ketone tests if available

Laffel et al 2005

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Insulin management

Never stop insulin (fever andstress increase insulin needs)

Continue intermediate- or long-

acting insulin

Shorter-acting insulin (soluble orrapid acting) should be adjusted

according to blood glucose values People with type 2 diabetes may

need short-term insulin treatmentif illness severe

Hanas 2004

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Algorithm for guidance

Breakfast Lunch Supper Bedtime

Usual dose (example) Soluble 10 Soluble 8 Soluble 12 NPH 24

If blood glucose is... Units of insulin reduced (-) or added (+) to usual dose

18.1 (325) + 10 units + 8 units + 12 units

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Insulin correction doses

Blood glucose >15mmol/L(270 mg/dL), ketones present

Usual insulin

PLUS

Short- or rapid-acting insulin10-20% of total daily doseevery 2-4 hours(short-actinginsulin) or every 1-2 hours(rapid-acting insulin)

Glucose tests every 1-2 hours

Eg: blood glucose 20 mmol(360 mg/dL)

normal doses insulin

Rapid acting =10 + 8 +

12 NPH = 22

Total = 52 units/day

Give 20% ~10 units of rapidacting

Give additional doses every 1 to 4 hours untilblood glucose

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Sick days and pump therapy

Rapid-acting insulin; no long-acting

If pump problem, no insulin after 3hours

Become sick very quickly

Need to carry or able to access a

new infusion set and insulin pen atall times

Need to be able to test ketones

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Insulin pump therapy

basal (25% to 100%)

Know effect of a unit of insulin onblood glucose

Correction dose for ketones up todouble usual correction

Test in 1 hour and 12 hourly

thereafter If no change suspect site problem

Use pen

Re-site cannula

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Food tolerance

Insulin must be given but may bereduced

Eg: blood glucose 10-12mmol/L

(180-216mg/dL)

About 150 ml sweetened fluidseach hour to hydrate and avoid

hypoglycaemia

If feverish, additional 150 ml low-calorie fluid each hour may be

needed for re-hydration

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If unable to tolerate food

Eg: blood glucose >15mmol/L

(270mg/dL)(additional insulin needed as above)

Give 150 ml to 300 ml of low-caloriefluid each hour for hydration and tohelp blood glucose to fall

Monitor blood glucose every 1-2hours

Food tolerance

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Slide 37 of 55ACTIVITY


Provide a list of drinks easily

available in your community that

are suitable for an ill person with

diabetes who is nauseated and

unable to eat food.

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When to seek professional help

Advise to call the physician or nurse if...

Uncertain of diagnosis

Persistent vomiting or diarrhoea

(3 episodes or more within 6 hours)

Unwell for 2 days and not getting better

Blood glucose remains above 15 mmol/L(270 mg/dL) despite extra fluid andinsulin

Moderate to large ketones persist,despite extra fluid and insulin

DKA and HHS
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Hospital transfer

Transfer to hospital if...

Abdominal pain worsening

Breathing difficulty orhyperventilation

Co-existing serious diseases

Person looking increasinglyunwell/exhausted

Care-givers exhausted oruncertain of diagnosis

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Slide 40 of 55ACTIVITY


Type 2 diabetes

Mr M: 20 years, type 2 diabetes

maximal sulphonylureas and metformin

twice a day intermediate acting insulin

Presented with 12 hours diarrhoea,

nausea, no appetite

What do you do?

Stop tablets, remain on insulin, or stop

insulin and remain on tablets?

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Type 2 diabetes

Metformin can aggravate gutproblems

Often easier to cease medication andcontinue insulin

Easier to control glucose levels withinsulin; may need reduced dose

Re-introduce oral medication whenfood intake normal and symptomssubside

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Type 2 diabetes

Metformin

Cease 24 hours before

surgery

Restart!

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a d SCurriculum Module III-6

Slide 43 of 55


Develop clear plans for sick days

Make written guideline availableand review plans with all peoplewith diabetes regularly

Determine when healthcareprovider should be contacted oralerted

Establish blood glucose goals forsick days

Adapted from: Diab Care 2004; 27 Suppl 1

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Curriculum Module III-6Slide 44 of 55


Develop clear plans for sick days

Define how to use supplementalshort-acting insulin

Explain how to use a fluid dietwhen unable to eat

Explain what equipment is

required

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Education tips

Under-treated sick days are acommon cause of diabetic

ketoacidosis and hospitalization At each annual complication

assessment, ask your patient tosolve a sick-day scenario

Access a 24-hour hotline

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Summary diabetes and illness

Never stop insulin

Do more blood glucose tests

high blood glucose levels meansmore insulin

In case of loss of appetite, eatfoods that are easy to digest and

drink more sugar-free fluids In case of vomiting, drink frequent

small volumes of carb-containing

fluids

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Summary diabetes and illness

Call for help in case of

persistent or severe vomiting

exhaustion or confusion

rapid breathing

worsening abdominal painuncertainty

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Review question

1. Which of the following is the mostimportant ketone body in DKA?

a. Acetone

b. Acetoacetate

c. Beta-hydroxybutyrate

d. None of the above

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Review question

2. Which feature is more indicative ofHHS than DKA?

a. Extreme hyperglycaemia

b. Extreme insulin deficiency

c. Large anion gap

d. Acetone breath

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Review question

3. Which of the following strategies shouldalways be a part of the treatment plan fora person with DKA?

a. Insulin therapy and magnesiumreplacement

b. Possible insulin therapy and re-

hydration

c. Insulin therapy and re-hydration

d. Possible insulin therapy and sodiumbicarbonate replacement

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Review question

4. Which of the following strategies shouldalways be a part of the treatment plan fora person with HHS?

a. Insulin therapy and magnesiumreplacement

b. Insulin therapy and re-hydration

c. Possible insulin therapy and sodiumbicarbonate replacement

d. Possible insulin therapy and re-hydration

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Review question

5. Which electrolyte is critical to monitorduring DKA as correction of themetabolic acidosis can possibly result in

cardiac arrythmias and muscleweakness?

a. Sodium

b. Potassium

c. Acetoacetate

d. Beta-hydroxybutyrate

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Answers

1. c

2. a

3. c

4. d

5. b

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References DKA and HHS

1. Booth GL. Short-Term Clinical Consequences of diabetes. In H. Gerstein & RB Haynes(EDs.), Hamilton: BC Decker. Evidence-Based Diabetes Care 2001; 75-90.

2. Jones H, Cleave B, Fredericks C, Hamilton C, Opsteen C. Building Competency inDiabetes education: the essentials. Canadian Diabetes Association, Canada, 2001.

3. Kitabchi AE, Umpierrez GE, Murphy MB, et al. Management of hyperglycemic crises inpatients with diabetes. Diabetes Care 2001; 24(1): 131-53.

4. Kitabchi AE, Ayyagari V, Guerra SMO. The efficacy of low dose versus conventionaltherapy of insulin for treament of DKA. Ann Int Med 1976; 84: 633-8.

5. American Diabetes Association. Hyperglycemic crisis in patients with diabetes.Diabetes Care 2001; 26(S1): S109-17.

6. Meltzer S, Yale JF, Belton AB, Clement M. Eds. Practical Diabetes Management;Clinical support for primary care physicians 5th ed.Canadian Diabetes Association,Canada, 2004.

7. Davidson MB. Hyperglycemia. In: Franz MJ, ed. A Core Curriculum for DiabetesEducation: Diabetes and Complications. 4th ed. Chicago: American Association of

Diabetes Educators 2001; 23.

8. Joslins Diabetes Mellitus. Eds Kahn CR,Weir GC et al. Publ Lippincott Williams &Wilkins, Philadelphia, 2005; 53.

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References managing illness

1. Hyperglycemic crises in diabetes. ADA position statement. Diab Care 2004; 27(Suppl 1).

2. Hanas R. Type 1 diabetes in children, adolescents and young adults. 2nd edition2004. Publ Class Publishing, London

3. Laffel L, Pasquarello C, Lawlor M. Treatment of the child and adolescent withdiabetes. Chap 35 in Joslins Textbook Diabetes. Publ Lippincott Williams &Wilkins, Philadelphia, 2005.

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