DIABETIC THOMAS

KIGGUNDU
EMERGENCIES
 INTRODUCTION

• Diabetic Ketoacidosis is one of the commonest

metabolic emergencies

• When adequately managed, it has very good

recovery rates and is one of the conditions
clinicians feel proud of treating.

• It is a common initial presentation for T1DM in

association with cessation of insulin

• Frequently precipitated by an underlying

stressful condition commonly an infection e.g.
G.E, pancreatitis
 MAIN OBJECTIVES

Early and prompt recognition of

Diabetic Ketoacidosis

Appropriate management of
Diabetic Ketoacidosis

Prevention of Diabetic
Ketoacidosis
 DEFINITION

• DKA is an acute metabolic disorder

characterized
• Hyperglycemia, usually above 350
mg/dl (20mmol/l)
• Ketones
• Acidosis

• In addition to the classic diabetic

symptoms, most patients will have
varying levels of L.O.C and varying
levels of dyspnea (Kaussmall type)
• Symptoms develop within 24hours

• Typically present with

• Dehydration following the osmotic
diuresis,
• An anion gap metabolic acidosis
• Ketonuria,
• Hyperkalemia with low total body
potassium
• Acetone breath.
Diabetic ketoacidosis
Insulin deficiency

Glucose uptake Lipolysis

Glycerol Free fatty

acids

Hyperglycaemia Gluconeogenesis
Ketogenesis
Glucosuria Ketonemia

Osmotic diuresis Electrolyte Ketonuria

depletion

Urinary water losses Dehydration

Acidosis
 INSULIN DEFICIENCY

Hyperglycemia Lipolysis

Hyper-
osmolality FFAs
Glycosuria

Ketones
Dehydration
Acidosis
Electrolyte
Renal Failure Losses

Shock CV
Collapse 7
Unchecked  Hyperglycemia
gluconeogenesis

Osmotic diuresis  Dehydration

Unchecked ketogenesis  Ketosis

Dissociation of ketone
 Anion-gap
bodies into hydrogen
metabolic acidosis
ion and anions

• Often a precipitating event is identified (infection,

lack of insulin administration)
 ELECTROLYTE DERANGEMENTS

 Metabolic acidosis and osmotic diuresis lead

to total body hypokalemia (extracellular
shift may lead to falsely elevated values)

 Hypophosphatemia also results with osmotic

diuresis

 Pseudohyponatremia (hyperglycemia and

hyperlipidemia result in falsely lowered
plasma sodium

 (Na actual = Na measured + 1.6[(glucose –

100)/100]
Hyperosmolality as a result of progressive
hyperglycemia contributes to cerebral
hypoperfusion in DKA

Serum osmolality:
 COMMON TRIGGERS

Infections like UTI, pneumonia, malaria, viral

infections

Stress

Withdrawal of insulin therapy.

Surgery, pregnancy, myocardial infarction

Skin and soft tissue infections

 RECOGNITION OF DKA

• A quick history to fi nd out whether patient

is known diabetic

• The classic symptoms of diabetes shall be

sought.

• Presence of air hunger, loss of

consciousness, dehydration, convulsions
an hypotension

• Symptoms and signs of a possible cause or

 SYMPTOMS

Nausea/ vomiting

Lethargy

Acetone(fruity) breath

Tachypnea (Kussmaul)

Tachycardia

Dizziness

Abdominal pain esp epigastric

 PHYSICAL EXAM

• Gen:Dehydration, skin and soft tissue infections

• Resp: Rate, Kaussmall pattern and acetone breath.

Chest exam for pneumonia signs.

• CNS: Level of consciousness

• Abd: Tenderness, distension and loss of bowel sounds

due to low potassium

• CVS:BP, pulse rate, heart failure and arrhythmias

• The clinician should be guided on case by case basis

ROUTINE LABORATORY PROCEDURES

Full blood count, ESR, hourly blood

glucose monitoring

Culture and sensitivity of relevant pus

swab specimens

RFTs, LFTs

Serum ketone tests, urine ketone tests,

serum electrolytes
 NON ROUTINE LABS

Done as case by case basis

Cardiac enzymes

Relevant X-rays, CT scans

Lumbar punctures, blood cultures

Sputum tests

Abdominal ultrasound.
 MANAGEMENT

 Confi rm diagnosis(Hyperglycemia, ketones, metabolic

acidosis)

 Admit to hospital (HDU)

 Assess serum electrolytes, Arterial blood gases, CBC

 IV line access established with large bore cannula

 Replace fl uids: fl uid defi cit is usually 3-5litres

 Rapid infusion of saline at an approx rate of 1 Liter/hour

but less in those with heart failure
 FLUID
RESUSCITATION
Administer 1 liter over the fi rst 30 mins

Administer 1 liter over the second hour

Administer 1 liter over the following 2

hours

Administer 1 liter every 4 hours,

depending on the degree of
dehydration .
 INSULIN THERAPY

• Soluble insulin at 10IU/hr irrespective of body

weight or age given I.V/I.M with hourly blood
glucose monitoring

• The initial insulin dose is a continuous IV

insulin infusion using an infusion pump, if
available, at a rate of 0.1 IU/kg/h.

• The aim is to lower glucose at a rate of about 50-100

mg/dl per hour

• When blood glucose lowering is noted to be poor

after at least three hourly administrations, the
hourly dose of insulin should be doubled to 20 units.
 Assess patient
 Precipitating factors- CBC, Chest x-ray, ECG, cultures, Trauma,
toxin/drug screen
 NG tube
 Urethral catheter

 Monitor Vitals-BP, pulse, RR, Mental status, Fluid

intake/output 4 hourly

 GLUCOSE GOAL :150-250mg/dl

 Insulin and fl uid regimens should be switched to a 6

hourly using soluble insulin
Replace potassium (greatly reduced in DKA
due to urinary losses)

Potassium needs to be checked every 1-2

hours during initial treatment.

If less than 3.3mmol/l : NO INSULIN, Give

40mmol/l KCL in 500mls of saline over 2- 4
hours

If >3.3 but < 5.0mmol/l: Give 10-40mmol/l

KCL
 AFTER CARE

• If blood glucose rises to more than 22 mmol/L or 400

mg/dl, revert back to the hourly regimen with saline
infusion

• After 24- 48 hours and the total daily dose used to

calculate the insulin requirements for subsequent days.

• Fixing of insulin regimen should be done in such a way

that 2/3 of the dose is given in the morning and 1/3 in
evening.

• Also 2/3 should be intermediate acting while 1/3

should be short or rapid acting.

• Premixed insulin like Mixtard may be used

 COMPLICATIONS
The leading cause of DKA mortality in children is
cerebral edema

Hypokalemia is a complication that is precipitated

by failing to rapidly address the total body
potassium defi cit brought out by rehydration

Hypoglycemia may result from inadequate

monitoring of glucose levels during insulin therapy.

Acute pulmonary edema potentially is related to

aggressive or excessive fl uid therapy.
 DKA MANAGEMENT PITFALLS

 Not assessing for and/or treating underlying cause of

the DKA

 Not watching K + closely enough and/or not replacing K +

aggressively enough

 Following serial serum ketone concentrations

 Interrupting IV insulin too soon (eg, patient not yet

eating) closed)

 Occurrence of rebound ketosis consequent to

inadequate insulin dosing

 Inadequate patient education, training and follow up

 EDUCATION IN TYPE 1 DIABETES
TO PREVENT DKA
Recognize symptoms and fi ndings that
require contact with a healthcare
provider

Prevent ketoacidosis through self-

management skills:
 Glucose testing
 Appropriate maintenance of insulin
 Use of supplemental insulin during
illness
 HYPERGLYCEMIC HYPEROSMOLAR
STATE
Formerly known as hyperosmolar hyperglycaemic
non-ketotic syndrome (HONK)

Because
 Ketosis may be present
 Its more of a state of altered consciousness
Coma not always present

Primarily in elderly with T2DM

Develops over weeks

Always associated with severe dehydration and
hyperosmolar state

Precipitated by concurrent illness MI,STROKE,

SEPSIS, PNEUMONIA, DEMENTIA

NO symptoms of abdominal pain,

nausea/vomiting or Kussmaul breathing
 PATHOPHYSIOLOGY

Relative insulin defi ciency and inadequate fl uid intake

Hepatic glucose production and impaired glucose

utilization by skeletal muscles

Hyperglycemia induces osmotic diuresis which leads to

intravascular volume depletion often worsened by
inadequate fl uid intake

Hyperglycemia + dehydration =thicker blood=high

serum osmolality

Absence of ketosis: caused by the relative insulin

defi ciency
 HHS – CAUSES OR TRIGGERS
Incidence

Infection 40-60%

New-onset diabetes 33%

Acute illness 10-15%

Medicines, steroids <10%

Insulin omission 5-15%

 SIGNS AND SYMPTOMS OF HHS

Several history of polyuria , polydipsia ,

weight loss and diminished oral intake
which leads to;
Altered mental status or coma
Lethargy
Reduced urine output
Tachycardia
Hypotension
 HHS – BIOCHEMICAL
FINDINGS
Blood glucose >33mmol/L (600mg/dl)

Ketones Urine: negative – small

Blood: <0.6 mmol/L

Osmolality >320mOsm/kg - (raised Na, BG, urea)

Electrolytes Raised Na, BG, urea creatinine

Anion gap <12

Blood gases pH >7.30

normal or raised HCO3
 DKA AND HHS ARE LIFE-
THREATENING EMERGENCIES

Hyperglycemic Hyperosmolar
Diabetic Ketoacidosis (DKA)
State (HHS)

Plasma glucose >250 mg/dL Plasma glucose >600 mg/dL

Arterial pH <7.3 Arterial pH >7.3

Bicarbonate <15 mEq/L Bicarbonate >15 mEq/L

Moderate ketonuria or ketonemia(+ Minimal ketonuria and

+++) ketonemia(+)

Anion gap >12 mEq/L Anion Gap near normal

Serum osmolality >320

Serum osmolarity <320 mosm/l
mosm/L
 Hyperglycemic Hyperosmolar
Diabetic Ketoacidosis (DKA)
State (HHS)

Absolute (or near-absolute) Severe relative insulin

insulin deficiency, resulting in deficiency, resulting in
• Severe hyperglycemia • Profound hyperglycemia and
• Ketone body production hyperosmolality (from urinary
• Systemic acidosis free water losses)
• No significant ketone
production or acidosis

Develops over hours to 1-2 days Develops over days to weeks

Most common in type 1 Typically presents in type 2 or

diabetes, but increasingly seen previously unrecognized
in type 2 diabetes diabetes

Higher mortality rate