Diabetes mellitus and its acute complications

1. Acute Complications
OF
Diabetes Mellitus
By
Dr. Sayan Chakraborty
2nd Year JR- MD Tropical Medicine
School of Tropical Medicine, Kolkata
E-mail: dr.sayan@gmail.com

2. The Ticking Time Bomb

4. Classification of Acute
Complications of DM
 Diabetic Ketoacidosis
 Hyperglycemic Hyperosmolar state
 Lactic acidosis
 Hypoglycemic coma

5. Case History
• 32 yr old woman, T1 DM, 30 weeks pregnant. Had been
unwell with dysuria and vague abdominal pain and felt
nauseous.
• Presented to the obstetric day unit where she was found to be
slightly breathless and mildly febrile (37.9 ° C), and urinalysis
showed 3+ ketones, trace proteinuria and glycosuria 55
mmol/L (990 mg/dL). Her CBG was 11.9 mmol/L (214 mg/dL).
• A diagnosis of UTI was made, commenced on oral cefalexin
and discharged.
• 12 hrs later, brought to the ER, severely breathless & vomiting
with severe abdominal pain. O/E: pulse 120/min, regular,
hypotensive (BP 90/50 mmHg lying, 70/40 mmHg sitting),
dehydrated and unwell. Laboratory plasma glucose was 35.6
mmol/L (641 mg/dL), blood 3 - hydroxybutyrate was 8.1
mmol/L. Arterial pH was 7.0.

6. DIABETIC
KETOACIDOSIS

7. Basic Pathophysiology of DKA

8. Ketone body synthesis

9. Clinical Manifestations of DKA

11. Bedside Investigations

13. What to expect !!

14. Goals of Therapy
1. Reduction of
hyperglycemia
2. Rehydration
3. Correction of electrolyte
imbalance
4. Correction of acid-base
imbalance
5. Investigation of
precipitating factors,
treatment of
complications.

16. AmericanDiabetesAssociationDiaCare2004;27:s94-s102
Protocol of Management of DKA in adults

17. Protocol for management in patients <20 yrs
AmericanDiabetesAssociationDiaCare2004;27:s94-s102

18. Case History
• 60 year old male T2 DM on Sitagliptin and
Metformin
• 3 week history of polyuria, weight loss and
diminished oral intake; H/o CVA 2 months back
• No history of nausea, vomiting, tachypnea
• Presented with mental confusion and lethargy
• O/E: Pulse 120/min; BP 90/50 mm Hg; Tongue
dry
• CBG >600 mg/dL; Arterial pH 7.32

19. HYPERGLYCEMIC
HYPEROSMOLAR STATE

20. Pathophysiology
• Relative insulin deficiency and inadequate fluid
intake
• Increased hepatic glucose production and
impaired glucose utilization in skeletal muscle
• Lower levels of counter-regulatory hormones
and free fatty acids
• Insulin/glucagon ratio does not favor ketogenesis

21. Predisposing Factors
1. Spontaneous occurrence in 5 – 7 % of patients.
2. Infection: pneumonia, UTI, Gm -ve sepsis
3. Drugs: steroids increase glucogenesis;
• potassium-wasting diuretics (hypokalemia
decreases insulin secretion), e.g., thiazides,
furosemide;
• other drugs, e.g., propranolol, azathioprine,
diazoxide.
5. Misc: CVA, SDH, acute pancreatitis, severe
burns
6. Use of conc. glucose solutions, such as used in
peripheral hyperalimentation or renal dialysis
7. Peritoneal or hemodialysis, tube feeding.

22. Clinical Manifestations
• Mental confusion, lethargy or coma
• Profound dehydration
• Hypotension, tachycardia
• Notably absent are symptoms of nausea,
vomiting, abdominal pain and the
Kussmaul respirations (characteristic of
DKA)

23. Lab Work-up

24. Protocol for the management of HHS
AmericanDiabetesAssociationDiaCare2004;27:s94-s102

25. DKA/HHS flowsheet
AmericanDiabetesAssociationDiaCare2004;27:s94-s102

26. LACTIC
ACIDOSIS

27. Causes
TYPE A
Poor tissue perfusion
• Shock, Cardiac failure
• Severe anemia
• Mitochondrial enzyme
defects
• Inhibitors (Cyanide, CO)
TYPE B
Aerobic disorders
• DM
• Malignancies
• NRTIs
• Renal or hepatic failure
• Thiamine deficiency
• Severe infections:
cholera, malaria
• Drugs/toxins:
Biguanides, ethanol,
isoniazid, methanol

28. Clinical Manifestations
1. Tachycardia & Hypotension.
2. Poor skin turgor and dry skin
3. Hypothermia
4. Hyperpnea or Kussmaul breathing
5. Findings associated with coexisting
medical problems (e.g., renal disease,
cardiovascular disease)

29. Laboratory Diagnosis
 Arterial blood gas analysis: Metabolic
acidosis with usually high anion gap.
Normal anion gap lactic acidosis has also
been reported.
 Blood lactate levels:
• >2 mEq/L : abnormal
• >4 mEq/L: more prognostic value in sepsis

30. Management
• Correct the underlying metabolic abnormality.
• Alkali therapy is of questionable value.
• HCO3 generates CO2 & lowers the intracellular &
CSF pH
• blood lactate levels
• If pH < 7.1 & the patient deteriorating rapidly, a
trial of bicarbonate therapy by administering 1/2
of the estimated bicarbonate deficit
[= 0.6 x wt in kg (15- measured HCO3 )]
• Final aim: to maintain HCO3 level at 15 mEq/L by
bicarbonate therapy

31. HYPOGLYCEMIA

33. Introduction
• Whipple’s triad:
(1) symptoms consistent with hypoglycemia
(2) a low plasma glucose concentration measured with a
precise method (not a glucose monitor)
(3) relief of symptoms after the plasma glucose level is raised

42. Management

43. Management
(Somatostatin analogue can be used)
[T1 DM]
[25% D]

45. References
• Harrison’s Principles of Internal Medicine 19th edition
• Williams Textbook of Endocrinology 13th ed. - S. Melmed, et.
al., (Saunders, 2011)
• Handbook of Diabetes 4th ed - R. Bilous, R. Donnelly (Wiley-
Blackwell, 2010)
• Paul Marino, The ICU book 3rd edition
• Guidelines of American Diabetic Association
• Gosmanov et al Diabetes, Metabolic Syndrome and Obesity:
Targets and Therapy 2014:7 255-264
• Wittlesey, Case study: Diabetes Ketoacidosis complications in
Type 2 Diabetes: Clinical Diabetes Vol. 18 No.2 Spring 2000
• Diabetes Care Volume 27 Supplement 1, January 2004