DIABETIC KETOACIDOSIS (DKA)
&
HYPERGLYCEMIC HYPEROSMOLAR STATE (HHS)
ACUTE DIABETIC EMERGENCIES
DKA
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
by
 Hyperglycemia, usually above 250 mg/dl
(>14mmol/l)
 Ketones-ketonemia or ketonuria
 Metabolic Acidosis
• In addition to the classic diabetic symptoms, most
patients will have varying levels of reduced level
of consciousness and varying levels of dyspnea
(Kaussmall breathing)
DKA cont’d
• 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.
Insulin deficiency
Glucose uptake Lipolysis
Hyperglycaemia Gluconeogenesis
Glycerol Free fatty
acids
Ketogenesis
Ketonemia
Ketonuria
Osmotic diuresis
Urinary water losses
Electrolyte
depletion
Dehydration
Acidosis
Diabetic ketoacidosis pathogenesis
Glucosuria
Electrolyte
Losses
Renal Failure
Shock CV
Collapse
Insulin Deficiency
7
Hyperglycemia
Hyper-
osmolality
Lipolysis
FFAs
Acidosis
Ketones
CV
Collapse
Glycosuria
Dehydration
Unchecked
gluconeogenesis
 Hyperglycemia
Osmotic diuresis  Dehydration
Unchecked ketogenesis  Ketosis
Dissociation of ketone
bodies into hydrogen
ion and anions
 Anion-gap
metabolic acidosis
• Often a precipitating event is identified (infection,
lack of insulin administration)
COMMON TRIGGERS of DKA
• Infections like UTI, pneumonia, malaria, viral infections
• Stress
• Withdrawal of insulin therapy.
• Surgery, pregnancy, myocardial infarction,
• Skin and soft tissue infections
• Meningitis,stroke
RECOGNITION OF DKA
• A quick history to find 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 trigger
should be established.
symptoms
• Nausea/ vomiting
• Lethargy
• Acetone(fruity) breath
• Tachypnea (Kussmaul)
• Tachycardia
• Dizziness
• Abdominal pain esp epigastric
• Altered mental state/coma
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 Specimens e.g
blood or urine culture, pus swab etc
• RFTs, LFTs
• Serum ketone tests, urine ketone tests, serum
electrolytes
NON ROUTINE LABS
Done as case by case basis
• Cardiac enzymes in case myocardial infarction is
suspected
• Relevant X-rays, CT scans
• Lumbar punctures, blood cultures
• Sputum tests
• Abdominal ultrasound.
management
• Confirm 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 fluids: fluid deficit 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 first 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. if
infusion pump not available use IM route
• The aim is to lower glucose at a rate of about 50-100 mg/dl per
hour (3-5mmol/l 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.
Electrolyte replacement
• Check initial potassium
• If less than 3.5 mmol/l, don’t give insulin but first give IV
KCL.
• During treatment give IV KCl 20 Meq in each litre of
Normal saline from 2nd
hour of treatment
• Maintain serum potassium between 3.5-5 mmol/l
• In ideal setting check electrolytes 4 hrly
• Monitor Vitals-BP, pulse, RR, Mental status, Fluid
intake/output 4 hourly
• GLUCOSE GOAL :150-250mg/dl, when it reaches here give
SC NPH(Isophane ) insulin and switch patient to GIK
infusion (5 or 10 % Dextrose, soluble insulin and KCl) until
patient is awake, able to eat and Ketones are normal(blood
ketones < 1mmol/l, urine ketones-nil)
• Insulin and fluid regimens should be switched to a 6 hourly
using soluble insulin
AFTER CARE
• After 24- 48 hours add 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 deficit 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 fluid therapy.
Hyperglycemic hyperosmolar state
• Formerly known as hyperosmolar hyperglycaemic non-ketotic
syndrome (HONK)
• Primarily in elderly with T2DM
• Develops over weeks
• Always associated with severe dehydration and hyperosmolar state
• Precipitated by concurrent illness MI,STROKE, SEPSIS,
PNEUMONIA
• NO symptoms of abdominal pain, nausea/vomiting or Kussmaul
breathing
Pathophysiology of HHS
• Relative insulin deficiency and inadequate fluid 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 fluid
intake
• Hyperglycemia + dehydration =thicker blood=high serum osmolality
• Absence of ketosis: caused by the relative insulin deficiency
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
Differences between DKA and HHS
Diabetic Ketoacidosis (DKA)
Hyperglycemic Hyperosmolar 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 osmolarity <320 mosm/l Serum osmolality >320 mosm/L
Diabetic Ketoacidosis (DKA)
Hyperglycemic Hyperosmolar State
(HHS)
Absolute (or near-absolute) insulin
deficiency, resulting in
• Severe hyperglycemia
• Ketone body production
• Systemic acidosis
Severe relative insulin deficiency,
resulting in
• Profound hyperglycemia and
hyperosmolality (from urinary 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 diabetes, but
increasingly seen in type 2 diabetes
Typically presents in type 2 or
previously unrecognized diabetes
Higher mortality rate
Treatment of HHS
• Aggressive fluid resuscitation; fluid
requirement 8-10 litres
• Small doses of soluble insulin
• Rest of care same as in DKA

ACUTE DIABETIC EMERGENCIES.pptx management

  • 1.
    DIABETIC KETOACIDOSIS (DKA) & HYPERGLYCEMICHYPEROSMOLAR STATE (HHS) ACUTE DIABETIC EMERGENCIES
  • 2.
    DKA INTRODUCTION • Diabetic Ketoacidosisis 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
  • 3.
    MAIN OBJECTIVES • Earlyand prompt recognition of Diabetic Ketoacidosis • Appropriate management of Diabetic Ketoacidosis • Prevention of Diabetic Ketoacidosis
  • 4.
    DEFINITION • DKA isan acute metabolic disorder characterized by  Hyperglycemia, usually above 250 mg/dl (>14mmol/l)  Ketones-ketonemia or ketonuria  Metabolic Acidosis • In addition to the classic diabetic symptoms, most patients will have varying levels of reduced level of consciousness and varying levels of dyspnea (Kaussmall breathing)
  • 5.
    DKA cont’d • Symptomsdevelop within 24hours • Typically present with • Dehydration following the osmotic diuresis, • An anion gap metabolic acidosis • Ketonuria, • Hyperkalemia with low total body potassium • Acetone breath.
  • 6.
    Insulin deficiency Glucose uptakeLipolysis Hyperglycaemia Gluconeogenesis Glycerol Free fatty acids Ketogenesis Ketonemia Ketonuria Osmotic diuresis Urinary water losses Electrolyte depletion Dehydration Acidosis Diabetic ketoacidosis pathogenesis Glucosuria
  • 7.
    Electrolyte Losses Renal Failure Shock CV Collapse InsulinDeficiency 7 Hyperglycemia Hyper- osmolality Lipolysis FFAs Acidosis Ketones CV Collapse Glycosuria Dehydration
  • 8.
    Unchecked gluconeogenesis  Hyperglycemia Osmotic diuresis Dehydration Unchecked ketogenesis  Ketosis Dissociation of ketone bodies into hydrogen ion and anions  Anion-gap metabolic acidosis • Often a precipitating event is identified (infection, lack of insulin administration)
  • 9.
    COMMON TRIGGERS ofDKA • Infections like UTI, pneumonia, malaria, viral infections • Stress • Withdrawal of insulin therapy. • Surgery, pregnancy, myocardial infarction, • Skin and soft tissue infections • Meningitis,stroke
  • 10.
    RECOGNITION OF DKA •A quick history to find 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 trigger should be established.
  • 11.
    symptoms • Nausea/ vomiting •Lethargy • Acetone(fruity) breath • Tachypnea (Kussmaul) • Tachycardia • Dizziness • Abdominal pain esp epigastric • Altered mental state/coma
  • 12.
    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
  • 13.
    ROUTINE LABORATORY PROCEDURES •Full blood count, ESR, hourly blood glucose monitoring • Culture and sensitivity of relevant Specimens e.g blood or urine culture, pus swab etc • RFTs, LFTs • Serum ketone tests, urine ketone tests, serum electrolytes
  • 14.
    NON ROUTINE LABS Doneas case by case basis • Cardiac enzymes in case myocardial infarction is suspected • Relevant X-rays, CT scans • Lumbar punctures, blood cultures • Sputum tests • Abdominal ultrasound.
  • 15.
    management • Confirm 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 fluids: fluid deficit is usually 3-5litres • Rapid infusion of saline at an approx rate of 1 Liter/hour but less in those with heart failure
  • 16.
    Fluid resuscitation • Administer1 liter over the first 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.
  • 17.
    Insulin therapy • Solubleinsulin 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. if infusion pump not available use IM route • The aim is to lower glucose at a rate of about 50-100 mg/dl per hour (3-5mmol/l 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.
  • 18.
    Electrolyte replacement • Checkinitial potassium • If less than 3.5 mmol/l, don’t give insulin but first give IV KCL. • During treatment give IV KCl 20 Meq in each litre of Normal saline from 2nd hour of treatment • Maintain serum potassium between 3.5-5 mmol/l • In ideal setting check electrolytes 4 hrly
  • 19.
    • Monitor Vitals-BP,pulse, RR, Mental status, Fluid intake/output 4 hourly • GLUCOSE GOAL :150-250mg/dl, when it reaches here give SC NPH(Isophane ) insulin and switch patient to GIK infusion (5 or 10 % Dextrose, soluble insulin and KCl) until patient is awake, able to eat and Ketones are normal(blood ketones < 1mmol/l, urine ketones-nil) • Insulin and fluid regimens should be switched to a 6 hourly using soluble insulin
  • 20.
    AFTER CARE • After24- 48 hours add 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
  • 21.
    complications • The leadingcause of DKA mortality in children is cerebral edema • Hypokalemia is a complication that is precipitated by failing to rapidly address the total body potassium deficit 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 fluid therapy.
  • 22.
    Hyperglycemic hyperosmolar state •Formerly known as hyperosmolar hyperglycaemic non-ketotic syndrome (HONK) • Primarily in elderly with T2DM • Develops over weeks • Always associated with severe dehydration and hyperosmolar state • Precipitated by concurrent illness MI,STROKE, SEPSIS, PNEUMONIA • NO symptoms of abdominal pain, nausea/vomiting or Kussmaul breathing
  • 23.
    Pathophysiology of HHS •Relative insulin deficiency and inadequate fluid 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 fluid intake • Hyperglycemia + dehydration =thicker blood=high serum osmolality • Absence of ketosis: caused by the relative insulin deficiency
  • 24.
    HHS – causesor triggers Incidence Infection 40-60% New-onset diabetes 33% Acute illness 10-15% Medicines, steroids <10% Insulin omission 5-15%
  • 25.
    Signs and symptomsof 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
  • 26.
    HHS – biochemicalfindings 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
  • 27.
    Differences between DKAand HHS Diabetic Ketoacidosis (DKA) Hyperglycemic Hyperosmolar 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 osmolarity <320 mosm/l Serum osmolality >320 mosm/L
  • 28.
    Diabetic Ketoacidosis (DKA) HyperglycemicHyperosmolar State (HHS) Absolute (or near-absolute) insulin deficiency, resulting in • Severe hyperglycemia • Ketone body production • Systemic acidosis Severe relative insulin deficiency, resulting in • Profound hyperglycemia and hyperosmolality (from urinary 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 diabetes, but increasingly seen in type 2 diabetes Typically presents in type 2 or previously unrecognized diabetes Higher mortality rate
  • 29.
    Treatment of HHS •Aggressive fluid resuscitation; fluid requirement 8-10 litres • Small doses of soluble insulin • Rest of care same as in DKA

Editor's Notes

  • #6 This diagram shows the pathways in the development of DKA. The influence of counterregulatory hormones on gluconeogenesis and ketogenesis is not shown but is important. Note the osmotic diuresis that promotes the severe degree of electrolyte depletion and dehydration. DKA is the combination of dehydration and acidosis, both of which require treatment.
  • #17 Subcut absorption of insulin is reduced in DKA because of dehydration; therefore, using IV or IM routes is always preferable
  • #23 Urine ketones are usually negative or only mildly positive. Severely raised osmolality dehydrates the brain markedly and causes major changes in mental function. It is these changes and the treatment with fluids that make this ‘syndrome’ so dangerous.
  • #24 HHS is most often associated with an infection – sometimes seen in people who are newly diagnosed – especially type 2 diabetes. This happens more frequently in older people who have been increasingly tired and confused; it is frequently mistaken for signs of the aging process. Other illnesses and the use of medicines, such as steroids, diuretics, and anti-psychotics, have all been associated with cases of HHS. In some communities, insulin omission in type 2 diabetes has precipitated HHS as progressive hyperglycaemia has occurred without adequate hydration.
  • #25 This can make it difficult to obtain the person’s history. Family and friends may be important in supplying information about the person’s history over the previous few weeks. It is important to recognize mental deterioration and dehydration in older people with type 2 diabetes. There may be precipitating factors which require treatment, such as: Infection Heart attack Stroke Pancreatitis.
  • #26 These are the serious biochemical results one would expect in a person with HHS. Although acidosis is not a typical feature, it does sometimes occur.