Diabetic emergencies are acute and potentially life threatening complications of Diabetes mellitus : Diabetic Keto-Acidosis ( DKA ). Hypoglycemic coma. Hyperosmolar Non-Ketotic Coma.

1. DIABETIC EMERGENCIES
Dr. Mohammad HobEldien Sulieman
Militaryhospital–Omdurman
March232015

2. DIABETES MELLITUS
•Acute complications:
• DKA
• Hypoglycemic coma.
• Hyperosmolar Non-Ketotic Coma

3. DIABETIC KETOACIDOSIS

4. DIABETIC KETOACIDOSIS
• A metabolic emergency in which hyperglycaemia is
associated with a metabolic acidosis due to greatly raised
(>5 mmol/L) ketone levels .
• It’s a hallmark of type 1 DM

5. Hyperglycemia
Ketosis
Acidosis
*

6. ETIOLOGY
• It is usually seen in the following circumstances:
• Previously undiagnosed diabetes (10%)
• Interruption of insulin therapy (15%)
• The stress of intercurrent illness (30%).
• (psychological stress, stroke, surgery, infection,…)

7. Insulin
deficiency
Increased
• glucagon
• GH
• cortisol
• catecholamines
Pathophysiology of DKA

8. Relative or absolute insulin deficiency
Gluconeogenesis
glycogenolysis
liver
glucose uptake
muscle

9. 1. Insulin:
very low Hyperglycemia Osmotic durisis Dehydration.
2. Fats:
lipolysis to produce energy increased keton bodies
which will cause:
Ketonemia Metabolic acidosis.
Ketonurea Aceton in urine
3. Hyperkalemia
• insulin defficincy
• acidosis
Pathophysiology of DKA

10. CLINICAL FEATURES
• nausea, vomiting and, occasionally, abdominal pain.
• hyperventilation (Kussmaul respiration).
• confusion and stupor are present in more severe cases.
• Evidence of marked dehydration is present and the eyeball is lax to pressure
in severe cases.

11. "HAVE YOU EATEN TODAY?"
Someone who has eaten, but has not
taken prescribed medication may be in a
diabetic coma.

12. DIAGNOSIS
• Clinical:
• Pulse >100 b.p.m. or <60 b.p.m.
• Systolic BP <90 mmHg.
• Glasgow Coma Score of <12 or abnormal ‘Alert, Voice, Pain.
• O2 saturation <92% on air (if normal respiratory function)
• Bloods:
• Blood ketones >6 mmol/L.
• Bicarbonate <12 mmol/L .
• Venous/arterial pH <7.1.
• Hypokalaemia on admission <3.5 mmol/L
• Urine: Glucose and acetone appear in urine.

13. INITIAL CLINICAL EVALUATION
• History and physical examination
• Secure patient’s ABC
• Mental status
• Cardiovascular-renal status
• Source of infection
• Evaluation of volume and hydration status
• Laboratory studies

14. • Physical examination may reveal a source of infection (e.g.
a perianal abscess). Two common markers of infection are
misleading: fever is unusual even when infection is present,
and polymorpholeucocytosis is present even in the absence
of infection. Relevant investigations include a chest X-ray,
urine and blood cultures and an ECG (to exclude
myocardial infarction). The serum amylase may be elevated
in the absence of pancreatitis. If infection is suspected,
broad-spectrum antibiotics are started once the
appropriate cultures have been taken.

15. MANAGEMENT

16. MANAGEMENT
• Admission and IV lines.
• Insulin:
• Short-acting insulin is given as an intravenous infusion
where facilities for adequate supervision exist or as
hourly intramuscular injections. The subcutaneous
route is avoided because subcutaneous blood flow is
reduced in shocked patients.

17. MANAGEMENT (CONT.)
• Fluids:
• with 0.9% saline. Average loss of water is 5–7 litres with
a sodium loss of 500 mmol.

18. MANAGEMENT
• Electrolyte:
• Patients have a total body potassium deficit of 350
mmol, although initial plasma levels may not be low.
Insulin therapy leads to uptake of potassium by the
cells with a consequent fall in plasma K+ levels.
Potassium is therefore given as soon as insulin is
started.

19. MANAGEMANT (CONT.)
• Restore the acid–base balance: A patient with
healthy kidneys will rapidly compensate for the
metabolic acidosis once the circulating volume is
restored. Bicarbonate is seldom necessary and is
only used if the pH is below 7.0 ([H+] >100 nmol/L),
and is best given as an isotonic (1.26%) solution.
• Monitor blood glucose closely.
• Seek the underlying cause.

20. COMPLICATIONS OF DKA AND ITS TREATMENT
• Coma
• Hypotension
• hyperkalaemia
• Cerebral oedema
• Complications of therapy.:
• These include hypoglycaemia and hypokalaemia, due to
loss of K+ in the urine from osmotic diuresis.

21. SUBSEQUENT MANAGEMENT
• Intravenous glucose and insulin are continued until the
patient feels able to eat and keep food down. The drip is
then taken down and a similar amount of insulin is given as
four injections of soluble insulin subcutaneously at meal
times and a dose of intermediate-acting insulin at night.
Sliding-scale regimens are unnecessary and may even
delay the establishment of stable blood glucose levels. The
mortality of diabetic ketoacidosis is around 5%, and is
increased in older patients. Its treatment is incomplete
without a careful enquiry into the causes of the episode and
advice as to how to avoid its recurrence.

23. HYPOGLYCEMIC COMA

24. HYPOGLYCEMIC COMA
• blood glucose <3.0 mmol/L.
• For the purposes of people with diabetes requiring hospital
admission, any blood glucose less than 4.0mmol/L should be
treated.

25. "HAVE YOU TAKEN YOUR
MEDICATION TODAY?"
Someone who has not eaten, but did take their medication,
may be having HYPOGLYCEMIA.

26. CLINICAL FEATURES
• Autonomic symptoms are generated by the activation of
the sympathoadrenal system and neuroglycopenic
symptoms are the result of cerebral glucose deprivation.
The brain is dependent on a continuous supply of circulating
glucose as the substrate to fuel cerebral metabolism and
support cognitive performance.
• If blood glucose levels fall sufficiently, cognitive dysfunction
is inevitable.

30. INVESTIGATIONS
• Blood : glucose is markedly decreased.
• Urine: No glucose in urine.

31. TREATMENT
• In severe hypoglycemia: Iv glucose & IV glucagon (in resistant
cases).
• In early hypoglycemia oral glucose.

32. DKA Hypoglycemia
1. History Missed insulin Missed meal
2. Onset Slow Rapid
3. Coma Silent Irretable
4. Skin Dry Moist
5. Tounge Dry Moist
6. Eyes Sunken Normal
7. Pupils Normal Dialated
8. Respiration Kausmal’s Normal
9. Breath Aceton oudor Normal
10. Pulse Weak and rapid Strong
11. Bp Low High
12. Urine Glucose and aceton Normal
13. Blood glucose Very high Low
14. Response to glucose No effect Rapid improvement

33. HYPEROSMOLAR NON-KETOTIC COMA

34. HYPEROSMOLAR NON-KETOTIC COMA
• This condition, in which severe hyperglycaemia develops
without significant ketosis, is the metabolic emergency
characteristic of uncontrolled type 2 diabetes.
• . Patients present in middle or later life, often with previously
undiagnosed diabetes.
• Common precipitating factors include consumption of
glucose-rich fluids, concurrent medication such as thiazide
diuretics or steroids, and intercurrent illness.

35. PATHOGENISIS
• insulin deficiency: This is less severe in the hyperosmolar
hyperglycaemic state.
• Low endogenous insulin Hyperglycema osmotic diuresis
dehydration.
• Endogenous insulin levels are sufficient to inhibit hepatic
ketogenesis, no acidosis.

36. CLINICAL FEATURES
• The characteristic clinical features on presentation are
dehydration and stupor or coma.
• Impairment of consciousness is directly related to the
degree of hyperosmolality.
• Evidence of underlying illness such as pneumonia or
pyelonephritis may be present, and the hyperosmolar state
may predispose to stroke, myocardial infarction or arterial
insufficiency in the lower limbs.

37. INVESTIGATIONS
• 1. Blood: glucose is markedly increased, Na increased due to
dehydration.
• 2. Urine: Glucose appears in urine BUT NO ACETON.

38. TREATMENT
• Admission
• It is sometimes useful to infuse insulin at a rate of 3 U/hour for
the first 2–3 hours, increasing to 6 U/ hour if glucose is falling
too slowly.
• The standard fluid for replacement is 0.9% saline. Avoid
0.45% saline, since rapid dilution of the blood may cause
more cerebral damage than a few hours of exposure to
hypernatraemia. Low-molecularweight heparin should be
given to counter the increased risk of thromboembolic
complications associated with this condition.
• Treatment of precipitating factors.

39. LACTIC ACIDOSIS
• Lactic acidosis may occur in diabetic patients on biguanide
therapy.
• The risk in patients taking metformin is extremely low provided
that the therapeutic dose is not exceeded and the drug is
withheld in patients with advanced hepatic or renal dysfunction.
• Patients present in severe metabolic acidosis with a large anion
gap (normally <17 mmol/L), usually without significant
hyperglycaemia or ketosis.
• Treatment is by rehydration and infusion of isotonic 1.26%
bicarbonate.
• The mortality is in excess of 50%.

40. REFERENCES
• Joint British Diabetes Societies.
• Kumar clinical medicine.

41. THANK YOU