DIABETIC EMERGENCIESDr. Mohammad HobEldien Sulieman

Military hospital – OmdurmanMarch 23 2015

DIABETES MELLITUS

•Acute complications:•DKA

•Hypoglycemic coma.

•Hyperosmolar Non-Ketotic Coma

DIABETIC KETOACIDOSIS

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

Hyperglycemia

Ketosis

Acidosis

*

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,…)

Insulindeficiency

Increased• glucagon• GH• cortisol• catecholamines

Pathophysiology of DKA

Relative or absolute insulin deficiency

Gluconeogenesis

glycogenolysis

liver

glucose uptake

muscle

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

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.

"HAVE YOU EATEN TODAY?"

Someone who has eaten, but has not taken prescribed medication may be in a diabetic coma.

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.

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

• 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.

MANAGEMENT

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.

MANAGEMENT (CONT.)

• Fluids:• with 0.9% saline. Average loss of water is 5–7 litres with

a sodium loss of 500 mmol.

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.

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.

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.

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.

HYPOGLYCEMIC COMA

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.

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

CLINICAL FEATURES

• Autonomic symptoms are generated by the activation of the sympathoadrenal system and neuroglycopenicsymptoms 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.

INVESTIGATIONS

• Blood : glucose is markedly decreased.

• Urine: No glucose in urine.

TREATMENT

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

• In early hypoglycemia oral glucose.

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

HYPEROSMOLAR NON-KETOTIC COMA

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.

PATHOGENISIS

• insulin deficiency: This is less severe in the hyperosmolar hyperglycaemic state.

• Low endogenous insulin Hyperglycema osmotic diuresisdehydration.

• Endogenous insulin levels are sufficient to inhibit hepatic ketogenesis, no acidosis.

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.

INVESTIGATIONS

• 1. Blood: glucose is markedly increased, Na increased due to dehydration.

• 2. Urine: Glucose appears in urine BUT NO ACETON.

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.

LACTIC ACIDOSIS

• Lactic acidosis may occur in diabetic patients on biguanidetherapy.

• 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%.

REFERENCES

• Joint British Diabetes Societies.

• Kumar clinical medicine.

THANK YOU