Hyperglycemia Emergencies Patho-physiology Diabetes educators basics to remember

1. DKA & HHS
PATHOGENESIS
DR MOHAMMAD DAOUD
CONSULTANT ENDOCRINOLOGIST
KAMC -JEDDAH

2. OBJECTIVES
Introduction
Definitions
Pathogenesis
S & S
Management

3. ACUTE DIABETIC COMPLICATIONS
1-Hyperglycemia : High
-Diabetic Ketoacidosis (DKA)..Type 1 DM
-Hyperosmolar Hyperglycemia Syndrome
(HHS) ..Old Type 2 DM
2-Hypoglycemia : Low

4. WHAT CONTROLS YOUR BLOOD SUGAR?
When we eat …blood sugar (Glucose)
increases
This stimulates insulin secretion
Insulin moves the glucose out of the
Blood Cells

5. GLUCOSE :FACTS
 Carbohydrates (Glucose) are the main
calorie source for our body
 Extra CHO are stored as:
Glycogen (liver and muscles)
OR
Fat (Adipose tissue)

6. GLUCOSE :FACTS
The brain relies almost exclusively on
glucose as a fuel, but cannot synthesize or
store it
Adequate uptake of glucose from the
plasma is essential for normal brain function
and survival

7. GLUCOSE PHYSIOLOGY
Glycogen
Breakdown -Liver
Increased
Glucagon
Energy
Fat Synthesis
Glycogen
Synthesis
Glucose release
to blood
(+) Pancreas secretion
of Glucagon
Blood
Glucose
Pool(+) Pancreas
secretion of
Insulin
(+) Circulating
Insulin
Uptake of glucose
by cells
Decrease blood
glucose

8. GLUCOSE :FACTS
In case of CHO shortage ( ex: Starvation)
OR
Unable to use CHO ( ex: No insulin as in
DKA)
Body shifts gear to other sources of energy

9. GLUCOSE :FACTS
Other sources of energy …
Protein breakdown to amino acids
and glucose synthesis
Fat breakdown into FFA and
ketones formation (with acidosis)..
Minimal amount of Insulin can prevent Ketogenesis

10. WHAT CONTROLS YOUR BLOOD SUGAR?
-Insulin …Lowers
-Glucagon…Increases
-Other hormones
Amount of CHO load
Physical activity
Stress factors
Counter Regulatory Hormones

11. HYPERGLYCEMIA
Hyperglycemia basic processes are :
1-Impaired/decreased glucose use
2-Increased gluconeogenesis
(Make up of glucose from other sources)
3-Increased glycogenolysis
(breakdown of Glycogen to Glucose )

12. HYPERGLYCEMIA
Due to variable reasons…
Insulin deficiency (Absolute / Relative)
Insulin Resistance
Excess counter regulatory hormones
(Glucagon, Cortisol…)
Defected secretion of GLP-1…

13. Electrolyte
LossesRenal Failure
Shock CV
Collapse
INSULIN DEFICIENCY
13
Hyperglycemia
Hyper-
osmolality
Δ MS
Lipolysis
FFAs
Acidosis
Ketones
CV
Collapse
Glycosuria
Dehydration

14. VS
Type 1DM
Immune system stops
insulin from being made
All ages :
More in younger
age groups
Type 2 DM
-Not enough insulin
-Insulin resistance)
Combination of the two
Alpha cell defect
Others: GLP-1 , SGLT2
Affects older age group
Can affect children

15. VS
Treatment ?
Type 1 DM
The insulin must be replaced
By injection or continuous infusion
Type 2 DM
Lifestyle changes (TLC)
Medications : tablets and/or Insulin

16. DIABETIC HYPERGLYCEMIC CRISES
Diabetic Ketoacidosis
(DKA)
Hyperglycemic
Hyperosmolar State (HHS)
Younger, type 1 diabetes Older, type 2 diabetes
No hyperosmolality Hyperosmolality
Volume depletion Volume depletion
Electrolyte disturbances Electrolyte disturbances
Acidosis No acidosis

17. DIABETIC KETOACIDOSIS (DKA)
PATHOPHYSIOLOGY
Unchecked gluconeogenesis  Hyperglycemia
Osmotic diuresis  Dehydration
Unchecked ketogenesis  Ketosis
Dissociation of ketone bodies
into hydrogen ion and anions

Acidosis
Anion-gap metabolic
17
Often a precipitating event is identified
(infection, lack of insulin administration)

18. HYPEROSMOLAR HYPERGLYCEMIC STATE
(HHS) PATHOPHYSIOLOGY
Unchecked gluconeogenesis  Hyperglycemia
Osmotic diuresis  Dehydration
• Presents commonly with renal failure
• Insufficient insulin for prevention of hyperglycemia but
sufficient insulin for suppression of lipolysis and ketogenesis
• Absence of significant acidosis
• Often identifiable precipitating event (infection, MI)
Major body water loss
DKA 5-7 L
HHS 8- 10 L

20. HYPERGLYCEMIA
PRECIPITATING FACTORS
Stress: through excess counter regulatory hormones:
-Glucagon
-Catecholamines (Adrenaline and Nor-Adrenaline)
-Cortisol
Medications: Steroids, Thiazides ,Beta blockers,…
Stopping DM medications
Acute illness: Infections (ex;UTI, Pneumonia) ,MI (ACS),
Stroke , Acute Pancreatitis, Burn
Others: Trauma ,Alcohol, Drug abuse (cocaine )
Feeding (NGT/ PEG/ TPN)

21. DKA -PRECIPITATING FACTORS
Inadequate insulin treatment
Noncompliance
Insulin error or insulin pump malfunction
Poor “sick-day” management
New onset diabetes (20 -25%)
 Acute illness
Infection ,CVA, MI ,Acute pancreatitis
 Drugs:
Steroids ,Clozapine or olanzapine
Cocaine Lithium ,Terbutaline

22. HHS -PRECIPITATING FACTORS
Acute illness :
Infection : Pneumonia UTI, Sepsis
CVA, MI, Pancreatitis , PE, Severe burns…
Endocrine
Acromegaly ,Thyrotoxicosis,
Cushing's syndrome
Drugs
Ex ;Steroids Thiazides,TPN
Previously undiagnosed DM

23. HYPERGLYCEMIA
WHAT IS DKA?
Severe hyperglycemia ; 250-300 mg/dl
Ketonemia : ketone bodies in the blood
(β-OH-butyric acid, Acetoacetic acid and Acetone)
Acidosis: PH <7.3
= Lack of insulin

24. Hyperglycemia
Ketosis
Acidosis
Adapted from Kitabchi AE, Fisher JN. Diabetes Mellitus. In: Glew RA, Peters SP, ed. Clinical
Studies in Medical Biochemistry. New York, NY: Oxford University Press; 1987:105.
DKA : DEFINITION

25. HYPERGLYCEMIA
DKA
Inadequate insulin &
excess glucagon,catecholamines…
Body cannot burn glucose properly
Glucose builds up in the bloodstream

26. HYPERGLYCEMIA
DKA
Symptoms of DKA include:
Nausea, vomiting Abdomen/Stomach pain
Frequent urination Excessive thirst
Weakness, fatigue Speech problems
Confusion /Unconsciousness

27. HYPERGLYCEMIA
DKA
Signs of DKA include:
Kussmaul respirations : Heavy, deep breathing
Fruity breath – the smell of ketoacid
Tachycardia
Supine hypotension,
Orthostatic drop of BP (feel dizzy when standing)
Dry mucous membranes Poor skin turgor
Confusion /Unconsciousness

28. HYPERGLYCEMIA
DKA
Inadequate insulin …
Fat comes out of fat cells (Free Fatty Acids)….
Free Fatty Acids >> Liver (Mitochondria/ Glucagon)
Used as an alternative energy source
Makes ketoacids ( ketones) out of the fat

29. HYPERGLYCEMIA
HHS
1- Severe hyperglycemia
2- S. Osmolality > 320 msom/kg
3- Severe dehydration
4- No ketonemia
5- No acidosis

30. HHS
There is just enough insulin
to keep fat in fat cells and
prevent ketone /acids formation
ketone levels are usually normal in HHS.

31. Hyperglycemi
a
Hyperosmolarit
y
Ketoacidosis
HHS
DKA

32. Take Home
Messages

33. HYPERGLYCEMIC CRISIS
DKA & HHS
• LIFE THREATENING EMERGENCIES
• DKA …MOSTLY TYPE 1 –YOUNG
INSULIN DEFICIENCY -ACIDOSIS
• HHS….TYPE 2 DM –OLDER
WORSE DEGREE OF DEHYDRATION
• BOTH: SIMILAR PRECIPITATING FACTORS
ELECTROLYTES DISTURBANCES

34. DKA VS HHS
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

35. DKA & HHS
• EARLY AGGRESSIVE MANAGEMENT
• HYDRATION
• INSULIN
• ELECTROLYTES DISTURBANCES RX
• LOOK FOR PRECIPITATING FACTORS :
TREAT AND TEACH TO AVOID ..IF POSSIBLE
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36. PREDISCHARGE CHECKLIST
• EDUCATION
• DIET INFORMATION
• TREATMENT GOALS
• “SURVIVAL SKILLS” TRAINING
• “MEDIC-ALERT” BRACELET
• PROVIDE :
GLUCOSE MONITOR AND STRIPS
MEDICATIONS, INSULIN, NEEDLES
• CONTACT PHONE NUMBERS

37. Thank You
Any Questions ?