DIABETIS, DIABETICKETOACIDOSIS, METABOLIC EMERGENCIES, HYPOGLYCEMIA

1. Metabolic
Emergencies Of
Diabetes Mellitus
Guide –Dr B Srinivas
Co Guide – Dr Arif Maldar
Presenter – Dr Ch Prudhvi Krishna

2. References
▪ ADA journals
▪ William text book of endocrinology
▪ Monograms

3. What are metabolic emergencies in
a diabetic person?
Diabetic ketoacidosis
Hyperglycemic
Hyperosmolar state
Diabetic Hypoglycemia

4. Introduction
▪ Uncontrolled blood sugar often contributes to the
incidence of metabolic emergencies of diabetes.
▪ Individuals who experience blood sugar levels that
are too high or low may develop conditions that
could lead to a coma.
▪ Hypoglycemia results from excessively low blood
sugar levels caused by either insufficient food
consumption or the presence of too much insulin.

5. Introduction
▪ DKA and HHS are life threatening emergencies
results from excessively high blood sugar levels.
▪ It carries significant risk of death and/or
morbidity especially with delayed treatment.
▪ The prognosis of DKA is worse in the extremes of
age, with a mortality rates of 5-10%.
▪ With the new advances of therapy, DKA mortality
decreases to < 1%.
▪ Before discovery and use of Insulin (1922) the
mortality was 100%.

6. Introduction
▪ HHS and DKA are not mutually exclusive but rather two
conditions that both result from some degree of insulin
deficiency.
▪ They can and often do occur simultaneously. In fact, one
third of patients admitted for hyperglycemia exhibit
characteristics of both HHS and DKA.

7. DKA vs HHS
Common
More common in Type 1
Precipitated by infection
Ketoacidosis
Short prodromal sympts
Mortality 2-10%
Any Age :Common in young
Uncommon
More in Type 2
More severe illness ,infctn,MI
Not ketoacidotic
Longer prodromal sympts
Mortality 15-20%
Age 57-70
DKA HHS

8. Precipitating
events
 Infection(Pneumonia / UTI / Gastroenteritis / Sepsis)
 Inadequate insulin administration
 Infarction(cerebral, coronary, mesenteric, peripheral)
 Drugs (cocaine, that affect carbohydrate metabolism,
such as corticosteroids, thiazides, sympathomimetic
agents, and pentamidine)
 Pregnancy.
Harrison’s Principle of internal medicine 18th edition

9. PATHOPHYSIOLOGY
DKA HHS

10. Diagnostic criteria : ADA
DKA
Hyperglycemia: >250 mg/dL
(>13.9 mmol/L)
Urine or serum ketones + or
more
Metabolic acidosis: pH < 7.3
serum bicarbonate < 15
mmol/l.
HHS
>600 mg/dL (> 33 mmol/L)
Absence of severe ketonaemia or
ketonuria. ( ketones +/- )
Arterial pH > 7.3,
serum bicarbonate > 15 mmol/L
Serum total osmolality>330 mOsm/L

11. Classification
DKA classified on the basis of pH and Serum bicarbonate

12. Symptoms and signs of DKA
Symptoms
Excessive thirst
Frequent urination
Nausea and vomiting
Abdominal pain
Weakness or fatigue
Shortness of breath
Confusion
Signs
Kussmal breathing ( Deep respirations )
Dry mucous membranes
Decreased skin turgor
Characteristic acetone (ketotic) Fruity breath
odor
Tachycardia
Hypotension
Fever,cough,chills if associated with
intercurrent infection

13. Symptoms and signs of HHS
▪ Usually presented dehydrated and stupor or
coma.
▪ Loss of appetite and polyuria (several weeks)
▪ Profound dehydration
▪ Hypotension ,
▪ Tachycardia
▪ Absence of nausea, vomiting, abdominal pain

14. DIAGNOSIS Initial Evaluation
▪ Identify precipitating event leading to elevated glucose
(pregnancy, infection, omission of insulin, myocardial
infarction, central nervous system event)
▪ Assess hemodynamic status
▪ Examine for presence of infection
▪ Assess volume status and degree of dehydration
▪ Assess presence of ketonemia and acid-base disturbance
14th edition of Joslin's Diabetes Mellitus

15. DIAGNOSIS LAB INVESTIGATIONS
▪ Complete blood count
▪ Serum ketones/ Urine ketones and sugar
▪ Calculate serum osmolality and anion gap
▪ Urinalysis and urine culture
▪ Consider blood culture
▪ Consider chest radiograph
14th edition of Joslin's Diabetes Mellitus

16. Laboratory values in DKA and HHS
DKA HHS
Glucose,mg/dl 250-600 600-1200
Sodium meq/L 125-135 135-145
Potassium Normal to↑ Normal
Osmolality mosm/kg 300-320 330-380
Plasma ketones ++++ +/-
Serum bicarbonate <15meq/L Normal to slightly ↓
Arterial pH 6.8-7.3 >7.3
Arterial pCO2 20-30 Normal
Anion gap ↑ Normal to slightly↑
Harrison’s Principle of internal medicine 18th edition

18. 14th edition of Joslin's Diabetes Mellitus
Differential Diagnosis of Ketosis and Anion Gap Acidosis
FEATURES DIABETIC
KETOACIDOSIS
ALCOHOL
KETOACIDOSIS
STARVATION
KETOACIDOSIS
URAEMIC
ACIDOSIS
LACTIC
ACIDOSIS
PH
PLASMA
GLUCOSE
ANION GAP
SERUM
KETONES
SERUM
OSMOLALITY

19. Typical body deficit of water and electrolytes

20. Management

21. Treatment Goals
▪ Restoration of volume deficits
▪ Resolution of hyperglycaemia and
ketosis/acidosis
▪ Correction of electrolyte abnormalities
(potassium level should be >3.3 mEq/L before
initiation of insulin therapy; use of insulin in a
patient with hypokalaemia may lead to
respiratory paralysis, cardiac arrhythmias, and
death)
▪ Treatment of the precipitating events and
prevention of complications.

22. Suggested Fluid Replacement in
DKA/HHS
▪ Administer NS as indicated to maintain
hemodynamic status than follow general
guidelines:
▪ NS for first 4 hours
▪ consider 1/2 NS thereafter after checking serum
sodium ,if its low continue with NS.
▪ Change to D5 & 1/2 NS when BG < 200 mg/dl for DKA
BG < 250- 300 mg/dl for HHS
▪ may need to adjust type and rate of fluid
administration in the elderly and in patients with CHF
and CRF

23. Suggested fluid replacement in DKA
/HHS
▪ 1st hour : 1 l
▪ 2nd hour : 1 l
▪ 3rd hour : 500 ml - 1 l
▪ 4th hour: 500 ml - 1 l
▪ 5th hour : 500 ml - 1 l
▪ Total 1st - 5th hour 3.5 - 5 l
▪ 6th - 12th hour : 250 - 500 ml/hr

24. Insulin management
Regular insulin 10 U i.v. stat (for adults) or 0.15 U/kg i.v. stat.
Start regular insulin infusion 0.1 U/kg per hour or 5 U per hour.
Increase insulin by 1 U per hour every 1–2 hr if less than 10% decrease in glucose or no
improvement in acid-base status.
Decrease insulin by 1–2 U per hour (0.05–0.1 U/kg per hour) when glucose ≤250 mg/dL and/or
progressive improvement in clinical status with decrease in glucose of >75 mg/dL per hour.
Do not decrease insulin infusion to <1 U per hour.
14th edition of Joslin's Diabetes Mellitus

25. Insulin management contd…
Maintain glucose between 140 and 180 mg/dL.
If blood sugar decreases to <80 mg/dL, stop insulin infusion for no more
than 1 hr and restart infusion.
If glucose drops consistently to <100 mg/dL, change i.v. fluids to D10 to
maintain blood glucose between 140 and 180 mg/dL.
Once patient is able to eat, consider change to s.c. insulin:
Overlap short-acting insulin s.c. and continue i.v. infusion for 1–2 hr.
For patients with previous insulin dose: return to prior dose of insulin.
For patients with newly diagnosed diabetes: full-dose s.c. insulin based on
0.6 U/kg per day.
14th edition of Joslin's Diabetes Mellitus

26. Potassium replacement
Serum K (mEq/L)
<3.5 - 4.0 -
3.5–4.5 -
4.5–5.5 -
>5.5 -
Additional K required
40 mEq/L
20 mEq/L.
10 mEq/L
Stop K infusion
14th edition of Joslin's Diabetes Mellitus

27. • Hypophasphatemia may develop during increased glucose
usage.
• If serum level <1mg/dl then phosphate supplementation
considered.
• No benefit demonstrated in RCT .
Phosphate

28. Bicarbonate
▪ Clinical trials do not support the routine use of bicarbonate replacement
• However, In the presence of severe acidosis (arterial pH <6.9), the ADA
advises bicarbonate [50 mmol/L (meq/L) of sodium bicarbonate in 200
mL of sterile water with 10 meq/L KCl per hour for 2 h until the pH is
>7.0].
Williams textbook of endocrinology 10th edition and ADA

29. Monitoring of RX
▪ Blood glucose hourly
▪ Electrolytes every 4 hours
▪ Blood gas analysis after fluid management
▪ Ok to check venous pH if you can’t get arterial
line ( 0.03 unit less than arterial ).
▪ Urine ketone bodies 8th hourly

30. Criteria for resolution
Management and monitoring should continue until
resolution of DKA.
▪ Plasma glucose < 200 mg/dl
▪ Serum bicarbonate >18 mmol/L (>18 meq/L)
▪ ABG pH >7.35
▪ Anion gap < 10.

31. Complications of DKA
▪ Infection
▪ Precipitates DKA
▪ Leukocytosis can be secondary to acidosis
▪ Shock
▪ Vascular thrombosis
▪ Severe dehydration
▪ Cerebral vessels
▪ Occurs hours to days after DKA
▪ Pulmonary Edema
▪ Result of aggressive fluid resuscitation
▪ Cerebral Edema
▪ First 24 hours due to aggressive
correction of hypoglycemia or
administration of hypotonic solution
▪ c/p: Mental status changes
▪ Tx: Mannitol

32. Prevention of DKA
▪ Never omit insulin
▪ Prevent dehydration and hypoglycemia
▪ Monitor blood sugars frequently
▪ Sick day management -Monitor for ketosis, Be on non sugary fluids,
increase insulin if sugars are very high.
▪ Provide supplemental fast acting insulin
▪ Maintain contact with medical team

33. Pitfalls in DKA
▪ Plasma glucose is usually high but not always
▪ DKA can be present with RBS < 300 due to
▪ Impaired gluconeogenesis
▪ Liver disease
▪ Acute alcohol ingestion
▪ Prolonged fasting
▪ Insulin-independent glucose is high (pregnancy)
▪ Chronic poor control but taking insulin
▪ Ketone in urine may be –ve in DKA, but always +ve in blood
▪ Due to measurement of acetoacetic acid in urine not,
betahydroxybuteric acid
▪ Acetone in blood should be done in this case

34. Pitfalls in DKA
▪ High WBC may be present without infection
▪ Infection may be present without fever
▪ Blood urea and creatinine may be elevated with prerenal
azotemia secondary to dehydration.
▪ Serum amylase is often raised even in the absence of
pancreatitis, In DKA its of salivary origin. Serum lipase should
be obtained if pancreatitis is suspected.

35. Diabetic
Hypoglycemia

36. Introduction
▪ Hypoglycemia is defined as blood sugar below 55
milligrams per deciliter (mg/dL) or 3 millimoles per
liter (mmol/L).
▪ An estimated 6-10% of people with Type1DM die as
a result of hypoglycemia each year.
▪ Occurs less frequently in Type2DM (People who are
on insulin ).
Whipple traid:
 Symptoms consistent with hypoglycemia
 Low plasma glucose concentration
 Relief of those symptoms after the plasma glucose level is raised

37. Causes
Common causes of diabetic hypoglycemia include:
▪ Taking too much insulin or diabetes medication
▪ Not eating enough.
▪ Postponing or skipping a meal or snack
▪ Increasing exercise or physical activity without
eating more or adjusting your medications
▪ Drinking binge alcohol.

39. Clinical features
MILD HYPOGLYCEMIA
- Mainly adrenergic or
- cholinergic symptoms
 Pallor
 Diaphoresis
 Tachycardia
 Palpitations
 Anxiety
 Tremors
 Sweating
 Paresthesias
 Hunger
MODERATE HYPOGLYCEMIA (<40
mg/dL)
▪ Mainly neuroglycopenic
symptoms
▪ Inability to concentrate
▪ Confusion
▪ Slurred speech
▪ Irrational behaviour
▪ Slower reaction time
▪ Blurred vision
▪ Somnolence
Adrenergic
Cholinergic

40. Clinical features
SEVERE HYPOGLYCEMIA (<20 mg/dL )
▪ Associated with severe impairment of neurologic
function
▪ Completely disoriented behavior
▪ LOC
▪ Coma
▪ Seizures

41. Treatment
▪ MILD HYPOGLYCEMIA
▪ Oral carbohydrates (at least 15gm)
▪ Sources include
▪ Three glucose tablets (5g each)
▪ 2 ½ cups of fruit juice
▪ 1 cup of milk
▪ If patient is unable to take orally give IV dextrose

42. Treatment – Moderate to severe hypoglycemia.
▪ Dextrose - 50mL of 50% dextrose IV bolus after blood
draw followed by 10% dextrose
▪ Glucagon – 1mg IM or SC can be given
▪ Effective in treating hypoglycemia only if sufficient liver
glycogen present( absent in alcohol induced
hypoglycemia)
▪ Patient is urged to eat as soon as possible

43. Prevention
▪ Patient education
▪ Knowing signs and symptoms of hypoglycemia
▪ Take meals on a regular schedule
▪ Carry a source of carbohydrate
▪ Self monitoring of blood glucose
▪ Take regular insulin at least 30 min before eating

44. Thank you

48. Role of Insulin
▪ Required for transport of glucose into:
▪ Muscle
▪ Adipose
▪ Liver
▪ Inhibits lipolysis
▪ Absence of insulin
▪ Glucose accumulates in the blood.
▪ Uses amino acids for
gluconeogenesis
▪ Converts fatty acids into
ketone bodies :
Acetone, Acetoacetate,
β-hydroxybutyrate.