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Welcome to
Morning session
By: Dr. Abdullah Al Noman
Intern doctor
Medicine dept.
TMMC&H
Diabetic
Ketoacidosis
CONTENTS
Introduction
Definition
Epidemiology
Pathophysiology
Etiology
Clinical Presentation
Laboratory Evaluation
Management
Complications
Strategies to Prevent Diabetic Ketoacidosis
Patient Counseling
References
INTRODUCTION
*Diabetic Ketoacidosis is an acute, major,
life-threatening complication of Diabetes.
*It mainly occurs in patients with Type 1
Diabetes but it is not uncommon in some
patients with type 2 diabetes.
DEFINITION
High anion gap metabolic acidosis due
to excessive blood concentration of ketone
bodies is Ketoacidosis.
Diabetic Ketoacidosis is a state of
absolute or relative insulin deficiency
aggravated by ensuing hyperglycaemia,
dehydration & acidosis producing
derangements in intermediary metabolism.
EPIDEMIOLOGY
A cross-sectional study was conducted at BIRDEM General
Hospital from January 2008 to December 2011. Total
patients were 200 with:
~Female predominence - 56%
~Mean age of study population was - 37.6years
~Incidence was more in known diabetic patients
- 71%
~Low income group -76.5%
~RBS during admission was -27.1mmol/L
~In hospital mortality was -6.5%
PATHOPHYSIOLOGY
A- The basic underlying mechanisms are:
-Absolute deficiency of circulating insulin.
-Secretion of insulin counterregulatory
hormones: glucagon, adrenaline, cortisol and
growth hormone.
PATHOPHYSIOLOGY
B-This leads to disturbances in the following
physiological processes:
-glucose utilization (hyperglycemia).
- proteolysis ( amino acids, glutamine and
alanine).
- lipolysis ( glycerol and FFAs).
- glycogenolysis (breakdown of muscle glycogen
 lactate).
- gluconeogensis (glutamine & alanine & glycerol
& lactate are the precursors).
PATHOPHYSIOLOGY
C- This results in the following abnormalities:
1-Hyperglycemia.
2-Hyperketonemia
3-Metabolic acidosis
4-Dehydration
5-Electrolyte Imbalance
PATHOPHYSIOLOGY
C- This results in the following abnormalities:
1-Hyperglycemia.
2-Hyperketonemia
3-Metabolic acidosis
4-Dehydration
5-Electrolyte Imbalance
ETIOLOGY
Precipitating Factors:
Infections – pneumonia, UTI, sepsis, gastroenteritis
Inadequate insulin treatment or non-compliance
Infarction - Myocardial infarction, cerebral, mesenteric.
Stress
New onset diabetes
Surgery
Hyperthyroidism
Drugs – cocaine, atypical antipsychotics, corticosteroids,
glucagon, interferon
Pregnancy
Symptoms of DKA:
1-Classic symptoms of hyperglycemia:
Polyuria, polydipsia, wt loss and thirst.
2-Other symptoms:
- General weakness, malaise and lethargy.
-Nausea, vomiting and abdominal pain.
- Perspiration.
- Disturbed consciousness and confusion.
3-Symptoms of underlying infections or other
conditions;
-fever, abdominal pain, dysuria, chest pain.
Physical signs of DKA:
General signs: Ill appearance and disturbed consciousness.
Signs of dehydration:
-Skin: Dry, hot, flushed, and loss of skin turgor.
-Tongue: Dry (sometimes woody tongue).
-Eyes: Sunken eyes and dark circles under the eyes.
Vital signs:
-Tachycardia, hypotension and tachypnea.
Specific signs:
-Ketotic breath: A strong, fruity breath odour (similar to nail
polish remover or acetone).
-Acidotic breath (Kussmaul's respiration): deep and rapid.
-Abdominal tenderness.
Investigations
Venous blood:
Urea
Na+/ K+
Glucose
Bicarbonate
Ketones
Urine:
Ketones
Leucocyte esterase
Investigations
ECG
Infection screen
Full blood count
Blood and urine culture
C-reactive protein
Chest X-ray
Amylase/ lipase
Rule out Pancreatitis
*Hyperketonaemia (≥ 3 mmol/L) and ketonuria
(>2+ on standard urine sticks)
*Hyperglycaemia (blood glucose ≥ 11 mmol/L
(~200 mg/dL))
*Metabolic acidosis (venous bicarbonate <15
mmol/L and/or venous pH < 7.3)
Cardinal biochemical
features
ER Evaluation
ABC
V/S
Cardiac monitoring
Physical examination
IV access : 2 large bore lines (16-18gauge )
CVP may be needed
Blood sugar
Foley catheter
Diabetic Ketoacidosis
MANAGEMENT
Diabetic Ketoacidosis
The main lines of management include:
1. Correction of fluid loss with intravenous
fluids.
2. Correction of hyperglycemia with insulin.
3. Correction of electrolyte disturbances
particularly potassium.
4. Correction of acid-base balance.
5. Treatment of concurrent infection, if present.
Fluid replacement
•0.9% NaCl solution (Normal saline) i.v.
.aIf systolic BP < 90 mmHg
Give 500 mL over 10–15 mins
Repeat if SBP< 90mmHg
.bIf systolic BP ≥ 90 mmHg (for a previously well
70kg adult)
1L over 1st hour
1L over next 2 hours
1L over next 2 hours
1L over next 4 hours
1L over next 4 hours
1L over next 6 hours
Fluid replacement
•When blood glucose < 15 mmol/L (270
mg/dL)
• Switch to 5% dextrose, 1 L 8-hourly
• If still dehydrated, continue 0.9% saline
and add 5% dextrose, 1 L per 12 hrs
•Typical requirement is 6 L in first 24 hrs but
avoid fluid overload in elderly patients
Insulin Therapy
Type of insulin : Regular : Rapid or short acting insulin U-40 &
U-100.
Regimen:
Initial bolus: 0.1 U/kg body wt given IV.
Maintenance: 0.1 U/kg/body wt /hour:
IV Infusion set: Add 100 units of regular insulin +500 ml
saline i.e. every 5 cc fluid contains 1 unit of insulin
Targets:
↓ blood ketone by 0.5 mmol/L/hour
↑ bicarbonate by 3 mmol/L/hour
↓ glucose by 3 mmol/L/hour
Potassium Therapy
Careful monitoring of potassium is essential in Mx of DKA
because both hypo & huperkalamia may occur and potentially
life threatening.
Potassium replacement
Plasma K+> 5.5 mmol/LNil
3.5–4.5 mmol/L20 mmol/L
< 3.5 mmol/L40 mmol/L
Correction of Acidosis
~Bicarbonate therapy is a bone of contention among
physicians and still remains a controversial subject, as
clear evidence of benefit is lacking.
~Bicarbonate therapy is only administered if the
arterial pH is less than 6.9.
~100 mEq of sodium bicarbonate in 400 mL sterile
water is administered over two hours. Repeat doses
until pH rises above 7.0.
~Bicarbonate therapy has several potential harmful
effects.
Additional procedures:
•Catheterisation if no urine passed after 3 hrs((do it from the
start))
•Nasogastric tube to keep stomach empty in unconscious or
semiconscious patients, or if vomiting is protracted
•Central venous line if cardiovascular system compromised, to
allow fluid replacement to be adjusted accurately
•Plasma expander if systolic BP is < 90 mmHg or does not rise
with i.v. saline
•Antibiotic if infection demonstrated or suspected
•ECG monitoring in severe cases
Diabetic ketoacidosis by dr. noman
Complications of DKA
1-Complications of associated illnesses e.g.
sepsis or MI.
2-Adult respiratory distress syndrome.
3-Thromboembolism (elderly).
4-Complications of treatment:
a-Hypokalemia: Which may lead to:
-Cardiac arrhythmias.
-Cardiac arrest.
-Respiratory muscle weakness.
Complications
b-Hypoglycemia.
c-Overhydration and acute pulmonary edema:
particularly in:
-Treating children with DKA.
-Adults with compromised renal or cardiac
function.
-Elderly with incipient CHF.
Complications
d-Neurological complications: Cerebral Edema.
-It occurs only in children with DKA.
-Very dangerous and increases mortality.
-The risk is related to the severity, duration and rapid
correction of DKA.
Mechanism: The brain adapts by producing intracellular osmoles
(idiogenic osmoles) which stabilize the brain cells from
shrinking while the DKA was developing. When the
hyperosmolarity is rapidly corrected, the brain becomes
hypertonic towards the extracellular fluids  water flows into
the cells  cerebral edema
Strategies to Prevent Diabetic
Ketoacidosis
Diabetic education
Blood glucose monitoring
Sick-day management
Home monitoring of ketones or beta-hydroxybutyrate
Supplemental short-acting insulin regimens
Easily digestible liquid diets when sick
Reducing, rather than eliminating, insulin when
patients are not eating
Guidelines for when patients should seek medical
attention
Case monitoring of high-risk patients
Special education for patients on pump management
Patient Counseling
Importance of medication adherence.
Proper injection technique.
Re-teach self-glucose monitoring.
Educate patient and family about
complications.
Importance of regular MD appointments.
Ways to prevent UTIs.
Q&A with patient and family.
References
Davidsons Principles and Practice of Medicine 22nd Edition
WWW.resarchgate.net
En.m.wikipedia.org
Joint British Diabetes Societies Inpatient Care Group guidelines
for The Management of Diabetic Ketoacidosis in Adults
British Society for Paediatric Endocrinology and Diabetes
guidelines for the management of DKA
American diabetic association guidelines
Diabetic Ketoacidosis

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Diabetic ketoacidosis by dr. noman

  • 1. Welcome to Morning session By: Dr. Abdullah Al Noman Intern doctor Medicine dept. TMMC&H
  • 4. INTRODUCTION *Diabetic Ketoacidosis is an acute, major, life-threatening complication of Diabetes. *It mainly occurs in patients with Type 1 Diabetes but it is not uncommon in some patients with type 2 diabetes.
  • 5. DEFINITION High anion gap metabolic acidosis due to excessive blood concentration of ketone bodies is Ketoacidosis. Diabetic Ketoacidosis is a state of absolute or relative insulin deficiency aggravated by ensuing hyperglycaemia, dehydration & acidosis producing derangements in intermediary metabolism.
  • 6. EPIDEMIOLOGY A cross-sectional study was conducted at BIRDEM General Hospital from January 2008 to December 2011. Total patients were 200 with: ~Female predominence - 56% ~Mean age of study population was - 37.6years ~Incidence was more in known diabetic patients - 71% ~Low income group -76.5% ~RBS during admission was -27.1mmol/L ~In hospital mortality was -6.5%
  • 7. PATHOPHYSIOLOGY A- The basic underlying mechanisms are: -Absolute deficiency of circulating insulin. -Secretion of insulin counterregulatory hormones: glucagon, adrenaline, cortisol and growth hormone.
  • 8. PATHOPHYSIOLOGY B-This leads to disturbances in the following physiological processes: -glucose utilization (hyperglycemia). - proteolysis ( amino acids, glutamine and alanine). - lipolysis ( glycerol and FFAs). - glycogenolysis (breakdown of muscle glycogen  lactate). - gluconeogensis (glutamine & alanine & glycerol & lactate are the precursors).
  • 9. PATHOPHYSIOLOGY C- This results in the following abnormalities: 1-Hyperglycemia. 2-Hyperketonemia 3-Metabolic acidosis 4-Dehydration 5-Electrolyte Imbalance
  • 10. PATHOPHYSIOLOGY C- This results in the following abnormalities: 1-Hyperglycemia. 2-Hyperketonemia 3-Metabolic acidosis 4-Dehydration 5-Electrolyte Imbalance
  • 11. ETIOLOGY Precipitating Factors: Infections – pneumonia, UTI, sepsis, gastroenteritis Inadequate insulin treatment or non-compliance Infarction - Myocardial infarction, cerebral, mesenteric. Stress New onset diabetes Surgery Hyperthyroidism Drugs – cocaine, atypical antipsychotics, corticosteroids, glucagon, interferon Pregnancy
  • 12. Symptoms of DKA: 1-Classic symptoms of hyperglycemia: Polyuria, polydipsia, wt loss and thirst. 2-Other symptoms: - General weakness, malaise and lethargy. -Nausea, vomiting and abdominal pain. - Perspiration. - Disturbed consciousness and confusion. 3-Symptoms of underlying infections or other conditions; -fever, abdominal pain, dysuria, chest pain.
  • 13. Physical signs of DKA: General signs: Ill appearance and disturbed consciousness. Signs of dehydration: -Skin: Dry, hot, flushed, and loss of skin turgor. -Tongue: Dry (sometimes woody tongue). -Eyes: Sunken eyes and dark circles under the eyes. Vital signs: -Tachycardia, hypotension and tachypnea. Specific signs: -Ketotic breath: A strong, fruity breath odour (similar to nail polish remover or acetone). -Acidotic breath (Kussmaul's respiration): deep and rapid. -Abdominal tenderness.
  • 15. Investigations ECG Infection screen Full blood count Blood and urine culture C-reactive protein Chest X-ray Amylase/ lipase Rule out Pancreatitis
  • 16. *Hyperketonaemia (≥ 3 mmol/L) and ketonuria (>2+ on standard urine sticks) *Hyperglycaemia (blood glucose ≥ 11 mmol/L (~200 mg/dL)) *Metabolic acidosis (venous bicarbonate <15 mmol/L and/or venous pH < 7.3) Cardinal biochemical features
  • 17. ER Evaluation ABC V/S Cardiac monitoring Physical examination IV access : 2 large bore lines (16-18gauge ) CVP may be needed Blood sugar Foley catheter
  • 19. Diabetic Ketoacidosis The main lines of management include: 1. Correction of fluid loss with intravenous fluids. 2. Correction of hyperglycemia with insulin. 3. Correction of electrolyte disturbances particularly potassium. 4. Correction of acid-base balance. 5. Treatment of concurrent infection, if present.
  • 20. Fluid replacement •0.9% NaCl solution (Normal saline) i.v. .aIf systolic BP < 90 mmHg Give 500 mL over 10–15 mins Repeat if SBP< 90mmHg .bIf systolic BP ≥ 90 mmHg (for a previously well 70kg adult) 1L over 1st hour 1L over next 2 hours 1L over next 2 hours 1L over next 4 hours 1L over next 4 hours 1L over next 6 hours
  • 21. Fluid replacement •When blood glucose < 15 mmol/L (270 mg/dL) • Switch to 5% dextrose, 1 L 8-hourly • If still dehydrated, continue 0.9% saline and add 5% dextrose, 1 L per 12 hrs •Typical requirement is 6 L in first 24 hrs but avoid fluid overload in elderly patients
  • 22. Insulin Therapy Type of insulin : Regular : Rapid or short acting insulin U-40 & U-100. Regimen: Initial bolus: 0.1 U/kg body wt given IV. Maintenance: 0.1 U/kg/body wt /hour: IV Infusion set: Add 100 units of regular insulin +500 ml saline i.e. every 5 cc fluid contains 1 unit of insulin Targets: ↓ blood ketone by 0.5 mmol/L/hour ↑ bicarbonate by 3 mmol/L/hour ↓ glucose by 3 mmol/L/hour
  • 23. Potassium Therapy Careful monitoring of potassium is essential in Mx of DKA because both hypo & huperkalamia may occur and potentially life threatening. Potassium replacement Plasma K+> 5.5 mmol/LNil 3.5–4.5 mmol/L20 mmol/L < 3.5 mmol/L40 mmol/L
  • 24. Correction of Acidosis ~Bicarbonate therapy is a bone of contention among physicians and still remains a controversial subject, as clear evidence of benefit is lacking. ~Bicarbonate therapy is only administered if the arterial pH is less than 6.9. ~100 mEq of sodium bicarbonate in 400 mL sterile water is administered over two hours. Repeat doses until pH rises above 7.0. ~Bicarbonate therapy has several potential harmful effects.
  • 25. Additional procedures: •Catheterisation if no urine passed after 3 hrs((do it from the start)) •Nasogastric tube to keep stomach empty in unconscious or semiconscious patients, or if vomiting is protracted •Central venous line if cardiovascular system compromised, to allow fluid replacement to be adjusted accurately •Plasma expander if systolic BP is < 90 mmHg or does not rise with i.v. saline •Antibiotic if infection demonstrated or suspected •ECG monitoring in severe cases
  • 27. Complications of DKA 1-Complications of associated illnesses e.g. sepsis or MI. 2-Adult respiratory distress syndrome. 3-Thromboembolism (elderly). 4-Complications of treatment: a-Hypokalemia: Which may lead to: -Cardiac arrhythmias. -Cardiac arrest. -Respiratory muscle weakness.
  • 28. Complications b-Hypoglycemia. c-Overhydration and acute pulmonary edema: particularly in: -Treating children with DKA. -Adults with compromised renal or cardiac function. -Elderly with incipient CHF.
  • 29. Complications d-Neurological complications: Cerebral Edema. -It occurs only in children with DKA. -Very dangerous and increases mortality. -The risk is related to the severity, duration and rapid correction of DKA. Mechanism: The brain adapts by producing intracellular osmoles (idiogenic osmoles) which stabilize the brain cells from shrinking while the DKA was developing. When the hyperosmolarity is rapidly corrected, the brain becomes hypertonic towards the extracellular fluids  water flows into the cells  cerebral edema
  • 30. Strategies to Prevent Diabetic Ketoacidosis Diabetic education Blood glucose monitoring Sick-day management Home monitoring of ketones or beta-hydroxybutyrate Supplemental short-acting insulin regimens Easily digestible liquid diets when sick Reducing, rather than eliminating, insulin when patients are not eating Guidelines for when patients should seek medical attention Case monitoring of high-risk patients Special education for patients on pump management
  • 31. Patient Counseling Importance of medication adherence. Proper injection technique. Re-teach self-glucose monitoring. Educate patient and family about complications. Importance of regular MD appointments. Ways to prevent UTIs. Q&A with patient and family.
  • 32. References Davidsons Principles and Practice of Medicine 22nd Edition WWW.resarchgate.net En.m.wikipedia.org Joint British Diabetes Societies Inpatient Care Group guidelines for The Management of Diabetic Ketoacidosis in Adults British Society for Paediatric Endocrinology and Diabetes guidelines for the management of DKA American diabetic association guidelines