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HOUSE OFFICER Dr. Soe Myat Thwe
(Medical Unit 1, Yangon General Hospital)
DIABETIC EMERGENCY
DIABETIC EMERGENCY
DIABETIC KETOACIDOSIS
HYPEROSMOLAR HYPERGYLCAEMIC STATE
HYPOGLYCAEMIA
DIABETIC
KETOACIDOSIS
DEFINITION
A **MEDICAL EMERGENCY** in which
hyperglycemia is associated with metabolic
acidosis due to greatly raised(>5mmol/l)
ketone levels
• Hallmark of type 1 diabetes
DIABETIC KETOACIDOSIS
PRECIPITATING FACTORS
DIABETIC KETOACIDOSIS
PATHOGENESIS
PATHOGENESIS
CARDINAL BIOCHEMICAL FEATURES
• Hyperketonaemia(> 3.0 mmol/l) or ketonuria(>2+ on standard
urine sticks)
• Hyperglycaemia(blood glucose >11 mmol/l(approx:
200mg/dl))
• Metabolic acidosis(venous bicarbonate <15 mmol/l and/or
venous pH <7.3(H+ > 50 nmoll))
20.13 Average loss of fluid and electrolytes in adult diabetic
ketoacidosis of moderate severity
• Water 6L
• Sodium 500 mmol
• Chloride 400 mmol
• Potassium 350 mmol
3 L extracellular
-replace with saline
3L intracellular
-replace with dextrose
DIAGNOSIS
CLINICAL FEATURES
SYMPTOMS (History Taking)
 Polyuria, Polydipsia*
 Weight loss
 Weakness
 Nausea, vomiting
 Leg cramps
 Blurred vision
 Abdominal pain
SIGNS(PHYSICAL EXAMINATION)
 Ill appearance
 Signs of dehydration
 Air hunger(Kussmal breathing)
 Decreased reflexes
 Characteristic smell of acetone
 Delirium, drowsiness
 Coma(10%)
 Hypotension(postural or
supine)
 Cold extremities(peripheral
cyanosis)
 Tachycardia
 Hypothermia
 Abdominal tenderness
DIAGNOSIS
• ***No time should be lost and treatment
is started as soon as the first blood
sample has been taken
Clinical observation
• Pulse > 100 b.p.m or <60 b.p.m
• Systolic blood pressure <90mmHg
• Glasgow coma scale score of <12 or abnormal ‘alert,
voice, pain, unresponsive’(AVPU) scale
• O2 saturation <92% on air (if normal respiratory
function)
Investigation
• Blood ketones > 6 mmol/L
• Bicarbonate <12 mmol/L
• Venous/arterial pH <7.1 (H+ > 80nmol/L)
• Hypokalaemia on admission <3.5 mmol/L
• Electrocardiogram
• Infection screen
MANAGEMENT
EMERGENCY MANAGEMENT OF DIABETIC
KETOACIDOSIS
TIME 0-60 MINS
• Establish IV access, assess patient and perform initial
investigations
• Commence 0.9% sodium chloride:
If systolic BP > 90mmHg, give 1 L over 60 mins
If systolic BP <90 mmHg, give 500ml over 10-15 mins, then re
assess: if BP remains <90mmHg, repeat an seek senior review
• Commence insulin treatment;
50 U human soluble insulin in 50 ml 0.9 % sodium chloride
infused intravenously at 0.1 U/kg body weight/hr
Continue with SC basal insulin analogue if usually taken by
patient
• Perform further investigations
• Establish monitoring schedule:
Hourly capillary blood glucose and ketone testing
Venous bicarbonate and potassium after 1 and 2 hrs., then
every 2hrs for first 6 hrs.
Plasma electrolytes every 4 hrs.
Clinical monitoring of O2 saturation, pulse, BP, respiratory
rate and urine output every hour
• Treat any precipitating cause
TIME: 60 MINS TO 6 HRS
• Iv infusion of 0.9 % sodium chloride with potassium chloride
added as indicated below
1L over 2hrs
1L over 2hrs
1L over 4hrs
1L over 4hrs
1L over 6hrs
• Add 10% glucose 125 mL/hr IV when glucose ,14mmol/L
• Be more cautious with fluid replacement in older or young
people , pregnant patients and those with renal or heart
failure; if plasma sodium is >155mmol/L, 0.45% sodium
chloride may be used
• Adjust potassium chloride infusion:
Plasma potassium(mmol/L)
>5.5
3.5 – 5.5
<3.5
Potassium replacement
(mmol/L of infusion)
Nil
40
Senior review – additional
potassium required
TIME : 6-12hrs
• Clinical status, glucose, ketonaemia, and acidosis should be
improving request senior review if not
• Continue IV fluid replacement
• Continue insulin administration
• Assess for complications of treatment(fluid overload, cerebral
edema)
• Avoid hypoglycemia
TIME : 12 -24 HRS
• By 24 hrs, ketonaemia and acidosis should have
resolved(blood ketones<0.3mmol/L, venous bicarbonate > 18
mmol/L)
• If patients is not eating and drinking
Continue IV insulin infusion at lower rate of 2-3 U/hr
Continue IV fluid replacement and biochemical monitoring
• If ketoacidosis has resolved and patient is able to eat and
drink;
Reinitiate SC insulin with advice from diabetes team, do not
discontinue IV insulin until 30 mins after SC short acting
insulin injection
ADDITIONAL PROCEDURES
• Consider urinary catheterization if anuric after 3hrs or
incontinent
• Insert nasogastric tube if obtunded or there is persistent
vomiting
• Insert central venous line if cardiovascular system is
compromised, to allow fluid replacement to be adjusted
accurately; also consider in older patients, pregnant woman ,
renal or cardiac failure other serious comorbidities and severe
DKA
• Measure arterial blood gases; repeat chest X-ray if O2
saturation<92%
• Institute ECG monitoring in sever cases
• Give thromboprophylaxis with low molecular weight heparin
PROBLEMS OF MANAGEMENT
 Hypotension
 Coma
 Cerebral edema
 Hypothermia
 Late complications – pneumonia, DVT
 Complication of therapy – hypoglycemia, pulmonary
edema
MEIDCAL UNIT 1 DKA TREATMENT CHART
ONGOING MANAGEMENT
When possible, refer patient to diabetes specialist team
within 24 hrs of admission.
HYPERGLYCAEMIC
HYPEROSMOLAR STATE
DEFINITION
Hyperglycemic hyperosmolar state
• A metabolic emergency in which uncontrolled
hyperglycemia induce a hyperosmolar state in
the absence of significant ketosis
Characterized by
• Hypovolemia
• severe hyperglycemia(>30mmol/l (600mg/dl))
• Hyper osmolality (serum osmolality >320
mOsom/kg)
• Without significant ketonaemia (<3mmol/l) or
• Acidosis (pH .7.3 (H+ <50 nmol/l)
• Bicarbonate > 15 mmol/l
PRECIPITATING FACTORS
What is the difference between
DKA and HHS??
DKA HHS
Common Uncommon
Diagnostic criteria Serum HCO3 low
pH <7.3
BG <800 can be close to
normal
Serum ketone > 5 mmol/L
Urine ketone : large
Serum Osom <320
Serum HCO3 normal
pH >7.3
BG often >800
Serum ketones < 5mmol/L
Urine ketone : small
Serum osm oftern >320
Type of diabetes(most
common form)
DM1 DM2
Pathophysiology Absolute insulin deficiency 
hyperglycaemia and lipolysis.
Lipolysis very sensitive to
insulin so more likely to occur
with absolute deficiency of
insulin  leads to ketone
formation. Dehydration from
hyperglycaemia  osmotic
diuresis
Relative insulin deficiency 
hyperglycaemia
No lipolysis = no ketones!!
Dehydration from
hyperglycaemia  osmotic
diuresis
Presentation onset Short prodromal sympts Longer prodromal sympts
Mortality Less More
Age (most common form) Young Older
Signs and Symptoms Acidemia  kusmaul
respiration, fruity breath *
acetone, abdominal
pain(correlation with degree
of acidemia)
Hyperglycemia(polyuria,
polydipsia, blurry vision)
Dehydration
Hyperglycemia(same as DKA)
Dehydration(more than DKA)
More mental status changes
due to more hyperosmolarity
Laboratory diagnostic criteria of DKA
and HHS
Parameter Normal range DKA HHS
Plasma glucose,
mg/dl
76-115 > 250 >600
Arterial pH 7.35-7.45 <7.30 >7.30
Serum bicarbonate,
mmol/L
22-28 <15 >15
Effective serum
osmolality mmol/kg
275-295 <320 >320
Anion gap mmol/L <12 >12 Variable
Serum ketones Negative Moderate to high None or trace
Urine ketones Negative Moderate to high None or trace
if venous pH is used, a correction of 00.3 must be made
Calculation: Na – (Cl + HCO3)
Plasma osmolarity = 2(Na+) + glucose + urea
• Normal value = 280-296mOsmol/l
HYPOGLYCAEMIA
DEFINITION
Hypoglycemia
 Diabetic people - blood glucose <3.9mmol/l (70
mg/dl)
• Severe hypoglycemia – the need for external
assistance to provide glucose, glucagon or other
corrective action actively
 Non-diabetic people(spontaneous hypoglycemia)
PATHOGENESIS
CLINICAL FEATURES
CIRCUMSTANCES OF HYPOGLYCAEMIA
Dead-in-bed syndrome
• Hypoglycemia induced cardiac arrhythmia
• Young patient with type 1 DM
Exercise-induced hypoglycemia
• Well controlled insulin treated diabetes due to
hyperinsulinaemia
• But high intensity exercise(due to increased
adrenaline) cause rise in blood glucose
Nocturnal hypoglycemia
MANAGEMENT
REFERENCES
• Davidson’s Principles and Practice of medicine 23rd edition
• Kumar & Clark’s clinical medicine 9th edition
• Diabetic emergencies : diagnosis and clinical management
2011 by John Wiley & Sons, Ltd.
• Photos from Internet
Diabetic emergency

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Diabetic emergency

  • 1. HOUSE OFFICER Dr. Soe Myat Thwe (Medical Unit 1, Yangon General Hospital) DIABETIC EMERGENCY
  • 2. DIABETIC EMERGENCY DIABETIC KETOACIDOSIS HYPEROSMOLAR HYPERGYLCAEMIC STATE HYPOGLYCAEMIA
  • 5. A **MEDICAL EMERGENCY** in which hyperglycemia is associated with metabolic acidosis due to greatly raised(>5mmol/l) ketone levels • Hallmark of type 1 diabetes DIABETIC KETOACIDOSIS
  • 9. PATHOGENESIS CARDINAL BIOCHEMICAL FEATURES • Hyperketonaemia(> 3.0 mmol/l) or ketonuria(>2+ on standard urine sticks) • Hyperglycaemia(blood glucose >11 mmol/l(approx: 200mg/dl)) • Metabolic acidosis(venous bicarbonate <15 mmol/l and/or venous pH <7.3(H+ > 50 nmoll))
  • 10.
  • 11. 20.13 Average loss of fluid and electrolytes in adult diabetic ketoacidosis of moderate severity • Water 6L • Sodium 500 mmol • Chloride 400 mmol • Potassium 350 mmol 3 L extracellular -replace with saline 3L intracellular -replace with dextrose
  • 14. SYMPTOMS (History Taking)  Polyuria, Polydipsia*  Weight loss  Weakness  Nausea, vomiting  Leg cramps  Blurred vision  Abdominal pain
  • 15. SIGNS(PHYSICAL EXAMINATION)  Ill appearance  Signs of dehydration  Air hunger(Kussmal breathing)  Decreased reflexes  Characteristic smell of acetone  Delirium, drowsiness  Coma(10%)  Hypotension(postural or supine)  Cold extremities(peripheral cyanosis)  Tachycardia  Hypothermia  Abdominal tenderness
  • 16. DIAGNOSIS • ***No time should be lost and treatment is started as soon as the first blood sample has been taken
  • 17. Clinical observation • Pulse > 100 b.p.m or <60 b.p.m • Systolic blood pressure <90mmHg • Glasgow coma scale score of <12 or abnormal ‘alert, voice, pain, unresponsive’(AVPU) scale • O2 saturation <92% on air (if normal respiratory function) Investigation • Blood ketones > 6 mmol/L • Bicarbonate <12 mmol/L • Venous/arterial pH <7.1 (H+ > 80nmol/L) • Hypokalaemia on admission <3.5 mmol/L • Electrocardiogram • Infection screen
  • 19. EMERGENCY MANAGEMENT OF DIABETIC KETOACIDOSIS TIME 0-60 MINS • Establish IV access, assess patient and perform initial investigations • Commence 0.9% sodium chloride: If systolic BP > 90mmHg, give 1 L over 60 mins If systolic BP <90 mmHg, give 500ml over 10-15 mins, then re assess: if BP remains <90mmHg, repeat an seek senior review • Commence insulin treatment; 50 U human soluble insulin in 50 ml 0.9 % sodium chloride infused intravenously at 0.1 U/kg body weight/hr Continue with SC basal insulin analogue if usually taken by patient
  • 20. • Perform further investigations • Establish monitoring schedule: Hourly capillary blood glucose and ketone testing Venous bicarbonate and potassium after 1 and 2 hrs., then every 2hrs for first 6 hrs. Plasma electrolytes every 4 hrs. Clinical monitoring of O2 saturation, pulse, BP, respiratory rate and urine output every hour • Treat any precipitating cause
  • 21. TIME: 60 MINS TO 6 HRS • Iv infusion of 0.9 % sodium chloride with potassium chloride added as indicated below 1L over 2hrs 1L over 2hrs 1L over 4hrs 1L over 4hrs 1L over 6hrs • Add 10% glucose 125 mL/hr IV when glucose ,14mmol/L • Be more cautious with fluid replacement in older or young people , pregnant patients and those with renal or heart failure; if plasma sodium is >155mmol/L, 0.45% sodium chloride may be used
  • 22. • Adjust potassium chloride infusion: Plasma potassium(mmol/L) >5.5 3.5 – 5.5 <3.5 Potassium replacement (mmol/L of infusion) Nil 40 Senior review – additional potassium required
  • 23. TIME : 6-12hrs • Clinical status, glucose, ketonaemia, and acidosis should be improving request senior review if not • Continue IV fluid replacement • Continue insulin administration • Assess for complications of treatment(fluid overload, cerebral edema) • Avoid hypoglycemia
  • 24. TIME : 12 -24 HRS • By 24 hrs, ketonaemia and acidosis should have resolved(blood ketones<0.3mmol/L, venous bicarbonate > 18 mmol/L) • If patients is not eating and drinking Continue IV insulin infusion at lower rate of 2-3 U/hr Continue IV fluid replacement and biochemical monitoring • If ketoacidosis has resolved and patient is able to eat and drink; Reinitiate SC insulin with advice from diabetes team, do not discontinue IV insulin until 30 mins after SC short acting insulin injection
  • 25. ADDITIONAL PROCEDURES • Consider urinary catheterization if anuric after 3hrs or incontinent • Insert nasogastric tube if obtunded or there is persistent vomiting • Insert central venous line if cardiovascular system is compromised, to allow fluid replacement to be adjusted accurately; also consider in older patients, pregnant woman , renal or cardiac failure other serious comorbidities and severe DKA • Measure arterial blood gases; repeat chest X-ray if O2 saturation<92% • Institute ECG monitoring in sever cases • Give thromboprophylaxis with low molecular weight heparin
  • 26. PROBLEMS OF MANAGEMENT  Hypotension  Coma  Cerebral edema  Hypothermia  Late complications – pneumonia, DVT  Complication of therapy – hypoglycemia, pulmonary edema
  • 27.
  • 28. MEIDCAL UNIT 1 DKA TREATMENT CHART
  • 29. ONGOING MANAGEMENT When possible, refer patient to diabetes specialist team within 24 hrs of admission.
  • 32. Hyperglycemic hyperosmolar state • A metabolic emergency in which uncontrolled hyperglycemia induce a hyperosmolar state in the absence of significant ketosis
  • 33. Characterized by • Hypovolemia • severe hyperglycemia(>30mmol/l (600mg/dl)) • Hyper osmolality (serum osmolality >320 mOsom/kg) • Without significant ketonaemia (<3mmol/l) or • Acidosis (pH .7.3 (H+ <50 nmol/l) • Bicarbonate > 15 mmol/l
  • 35.
  • 36. What is the difference between DKA and HHS??
  • 37. DKA HHS Common Uncommon Diagnostic criteria Serum HCO3 low pH <7.3 BG <800 can be close to normal Serum ketone > 5 mmol/L Urine ketone : large Serum Osom <320 Serum HCO3 normal pH >7.3 BG often >800 Serum ketones < 5mmol/L Urine ketone : small Serum osm oftern >320 Type of diabetes(most common form) DM1 DM2 Pathophysiology Absolute insulin deficiency  hyperglycaemia and lipolysis. Lipolysis very sensitive to insulin so more likely to occur with absolute deficiency of insulin  leads to ketone formation. Dehydration from hyperglycaemia  osmotic diuresis Relative insulin deficiency  hyperglycaemia No lipolysis = no ketones!! Dehydration from hyperglycaemia  osmotic diuresis
  • 38. Presentation onset Short prodromal sympts Longer prodromal sympts Mortality Less More Age (most common form) Young Older Signs and Symptoms Acidemia  kusmaul respiration, fruity breath * acetone, abdominal pain(correlation with degree of acidemia) Hyperglycemia(polyuria, polydipsia, blurry vision) Dehydration Hyperglycemia(same as DKA) Dehydration(more than DKA) More mental status changes due to more hyperosmolarity
  • 39. Laboratory diagnostic criteria of DKA and HHS Parameter Normal range DKA HHS Plasma glucose, mg/dl 76-115 > 250 >600 Arterial pH 7.35-7.45 <7.30 >7.30 Serum bicarbonate, mmol/L 22-28 <15 >15 Effective serum osmolality mmol/kg 275-295 <320 >320 Anion gap mmol/L <12 >12 Variable Serum ketones Negative Moderate to high None or trace Urine ketones Negative Moderate to high None or trace if venous pH is used, a correction of 00.3 must be made Calculation: Na – (Cl + HCO3)
  • 40. Plasma osmolarity = 2(Na+) + glucose + urea • Normal value = 280-296mOsmol/l
  • 41.
  • 44. Hypoglycemia  Diabetic people - blood glucose <3.9mmol/l (70 mg/dl) • Severe hypoglycemia – the need for external assistance to provide glucose, glucagon or other corrective action actively  Non-diabetic people(spontaneous hypoglycemia)
  • 46.
  • 48.
  • 50.
  • 51. Dead-in-bed syndrome • Hypoglycemia induced cardiac arrhythmia • Young patient with type 1 DM
  • 52. Exercise-induced hypoglycemia • Well controlled insulin treated diabetes due to hyperinsulinaemia • But high intensity exercise(due to increased adrenaline) cause rise in blood glucose
  • 55.
  • 56.
  • 57.
  • 58. REFERENCES • Davidson’s Principles and Practice of medicine 23rd edition • Kumar & Clark’s clinical medicine 9th edition • Diabetic emergencies : diagnosis and clinical management 2011 by John Wiley & Sons, Ltd. • Photos from Internet