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Diabetes Mellitus Fifth Stage-Medicine. Dr. Sarbast Fakhradin MBChB, MSc Diabetes Care & Management. Acute complications of diabetes. 1. Diabetic ketoacidosis 2. Non-ketotic hyperosmolar hyperglycemic coma 3. Hypoglycemia 3. Lactic acidosis. Diabetic ketoacidosis.

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diabetes mellitus fifth stage medicine

Diabetes MellitusFifth Stage-Medicine

Dr. Sarbast Fakhradin

MBChB, MSc Diabetes Care & Management

acute complications of diabetes
Acute complications of diabetes
  • 1. Diabetic ketoacidosis
  • 2. Non-ketotic hyperosmolar hyperglycemic coma
  • 3. Hypoglycemia
  • 3. Lactic acidosis
diabetic ketoacidosis
Diabetic ketoacidosis
  • Principally in people with type 1 diabetes
  • Might be the first presentation
  • The average mortality in developed countries is 5-10%
  • In established diabetes a common course of events is that patients develop an intercurrent infection, lose their appetite, and either stop or reduce their dose of insulin in the mistaken belief that under these circumstances less insulin is required.
ada criteria for diagnosis of dka
ADA criteria for diagnosis of DKA
  • 1. hyperglycaemia: blood glucose >250mg/dl
  • 2. hyperketonaemia
  • 3. metabolic acidosis: PH<7.3
  • 4. S.Bicarbonate < 18mmol/l
  • 5. anion gap >10
precipitating cause of dka
Precipitating cause of DKA:
  • 1. Infection
  • 2. Erratic insulin supply.
  • 3. In type2 DM who have failure of treatment by oral hypoglycemic agents & need insulin, so when they refuse to take it, might lead to DKA
  • 4. Acute MI (uncommon)
  • 5. C.V.A.
  • 6. Pancreatitis
  • 7. Massive trauma or other serious illness.

Average loss of fluid and electrolytes in adult (moderate severity)

  • Water: 6 L (extracellular fluid3 L replace with saline+ intracellular fluid 3L replace with dextrose)
  • Sodium: 500 mmol
  • Chloride: 400 mmol
  • Potassium: 350 mmol

Every patient in diabetic ketoacidosis is potassium-depleted, but the plasma concentration of potassium gives very little indication of the total body deficit. Plasma potassium may even be raised initially due to disproportionate loss of water, catabolism of protein and glycogen, and displacement of potassium from the intracellular compartment by H+ ions.

• The magnitude of the hyperglycaemia does not correlate with the severity of the metabolic acidosis

→Pyrexia may not be present initially because of vasodilatation secondary to acidosis.

  • The following are important but should not delay the institution of intravenous fluid and insulin replacement:
  • 1. Venous blood: for urea and electrolytes, glucose, bicarbonate.
  • 2. Arterial blood gases to assess the severity of acidosis.
  • 3.Urinalysis for ketones
  • 4. ECG.
  • 5. Infection screen: full blood count, blood and urine culture, C-reactive protein, chest X-ray. Although leucocytosis invariably occurs, this represents a stress response and does not necessarily indicate infection.
  • 6. Serum amylase may be elevated but rarely indicates coexisting pancreatitis.
  • It is a medical emergency
  • Regular clinical and biochemical review is essential, particularly during the first 24 hours of treatment including: Glucose, urea, electrolyte, creatinine, bicarbonate, blood gases.
  • The principal components of treatment are:
  • 1. Fluid replacement
  • 2. Short-acting insulin
  • 3. Potassium replacement
  • 4. Antibiotics if infection is present.
fluid replacement
Fluid replacement
  • Early and rapid rehydration is essential (2 lines); otherwise the administered insulin will not reach the poorly perfused tissues
  • fluids given by mouth may be poorly absorbed
  • 0.9% saline (NaCl) i.v. (extracellular fluid replacement)
    • 1 L over 30 mins
    • 1 L over 1 hr
    • 1 L over 2 hrs
    • 1 L over next 2-4 hrs
fluid replacement cont
Fluid replacement (Cont)
  • When blood glucose < 270 mg/dl (intracellular fluid replacement)
    • Switch to 5% dextrose, 1 L 8-hourly
    • If still dehydrated, continue 0.9% saline and add 5% dextrose, 1 L per 12 hrs
  • Typical requirement is 6 L in first 24 hrs but avoid fluid overload in elderly patients
  • Subsequent fluid requirement should be based on clinical response including urine output
  • 50 U soluble insulin in 50 ml 0.9% saline i.v. via infusion pump
    • 6 U/hr initially
    • 3 U/hr when blood glucose < 270 mg/dL
    • 2 U/hr if blood glucose <180 mg/dL
  • Check blood glucose hourly initially; if no reduction in first hour, rate of insulin infusion should be increased
  • Aim for fall in blood glucose of approximately 55-110 mg/dl/hour
  • A more rapid fall in blood glucose should be avoided, as hypoglycaemia & cerebral oedema may develop.
insulin cont
Insulin (Cont)
  • If an intravenous infusion of insulin is not possible, soluble insulin can be given by intramuscular injection (loading dose of 10-20 U followed by 5 U hourly) or, alternatively, a fast-acting insulin analogue can be given hourly by subcutaneous injection (initially 0.3 U/kg body weight, then 0.1 U/kg hourly).
  • When the blood glucose concentration has fallen to180-270 mg/dl the dose of insulin should be reduced to 1-4 U hourly.
  • Restoration of the usual insulin regimen, by subcutaneous injection, should not be instituted until the patient is able to eat and drink normally.
potassium replacement
Potassium Replacement
  • None in first L of i.v fluid unless plasma potassium < 3.0 mmol/L
  • When < 3.5 mmol/L, give 20-40 mmol/hr
  • When plasma potassium is 3.5-5.0 mmol/l, give 10 mmol/hr
  • Cardiac rhythm should be monitored in severe cases because of the risk of electrolyte-induced cardiac arrhythmia.
  • In patients who are severely acidotic (pH < 7.0), hypotensive, arrhythmia, & in coma; the infusion of sodium bicarbonate (300 mL 1.26% over 30 mins into a large vein) should be considered, with the simultaneous administration of potassium.
  • otherwise correction of the total bicarbonate deficit should not be attempted because rapid correction
  • 1. Aggravate tissue hypoxia
  • 2. Reduce consciousness by paradoxical acidosis of CSF
  • 3. HCO3 & insulin increase risk of hypokalemia
additional procedures
Additional procedures
  • 1. Catheterisation if no urine passed after 3 hrs
  • 2. NG tube to keep stomach empty in unconscious or semiconscious patients, or if vomiting is protracted
  • 3. CV line if cardiovascular system compromised, to allow fluid replacement to be adjusted accurately
  • 4. Plasma expander if systolic BP is < 90 mmHg or does not rise with i.v. saline
  • 5. Antibiotic if infection demonstrated or suspected
  • ECG monitoring in severe cases

Poor prognostic sign in DKA at Admission include:

  • Hypotension
  • ARF
  • Deep coma
complications of diabetic ketoacidosis
Complications of diabetic ketoacidosis
  • 1. Cerebral oedema
    • May be caused by very rapid reduction of blood glucose, use of hypotonic fluids and/or bicarbonate
    • High mortality
    • Treat with mannitol, oxygen
  • 2. Acute respiratory distress syndrome
  • 3. Thromboembolism
  • 4. Disseminated intravascular coagulation (rare)
  • 5. Acute circulatory failure/ARF
  • 6. Gastric stasis & upper GIT bleeding
  • 7. Mucormycosis.
non ketotic hyperosmolar diabetic coma
Non-ketotic hyperosmolar diabetic coma
  • Severe hyperglycaemia (> 900 mg/dL) without significant hyperketonaemia or acidosis.
  • Severe dehydration and pre-renal uraemia are common
  • Mortality is high (40%).
  • Treatment differs from DKA in two main respects:
  • 1.Half the dose of insulin is required because they are relatively sensitive to insulin (3 U/hr).
  • 2. The plasma osmolarity should be measured,based on plasma values in mmol/L:
non ketotic hyperosmolar diabetic coma1
Non-ketotic hyperosmolar diabetic coma

Plasma osmolarity= 2(Na+) + 2(K+) + (Glucose) + (Urea)

The normal value is 280-290 mmol/kg, the conscious level is depressed when it is high (> 340 mmol/kg).

→Start with 0.45% saline until the osmolality approaches normal, then replace by isotonic (0.9%) saline.

• Monitor CVP & plasma sodium frequently.

• Thromboembolic complications are common, prophylactic subcutaneous LMWH is recommended

lactic acidosis
Lactic acidosis
  • The patient is likely to be on metformin for type 2 diabetes.
  • Very ill & overbreathing but not as profoundly dehydrated as is usual in coma of DKA.
  • The patient's breath does not smell of acetone, and ketonuria is mild or absent.
  • Plasma bicarbonate is reduced & the anion gap and H+ are increased.
  • Diagnosis: lactic acid in the blood is high (usually > 5.0 mmol/L)
  • Treatment:intravenous sodium bicarbonate +insulin + glucose.
  • Mortality is over 50%
  • Diabetic: blood glucose < 63 mg/dL
  • Non-diabetic (spontaneous hypoglycaemia): <54mg/dl
  • Clinical features:
  • 1. Autonomic:
  • Sweating , Trembling, Pounding heart, Hunger , & Anxiety
  • 2. Neuroglycopenic:
  • Confusion, Drowsiness, Speech difficulty, Inability to concentrate
  • Incoordination, Irritability, & anger
  • 3. Non-specific:
  • Nausea, Tiredness, Headache

Nocturnal hypoglycaemia:

  • Especially in type 1 diabetes
  • does not usually waken a person, it is often undetected.
  • patients may have poor quality of sleep, morning headaches, 'hangover', chronic fatigue and vivid dreams or nightmares.
  • Sometimes a partner may observe profuse sweating, restlessness, twitching or even seizures.
  • measure the blood glucose during the night.

Exercise-induced hypoglycaemia:

causes of hypoglycemia in non diabetics
Causes of hypoglycemia in non-diabetics


1.Exogenous drugs (Insulin, SU) & alcohol.

2. Pituitary insufficiency

3. Liver failure & inherited enzyme defect

4. Addison’s disease

5. Islet cell tumors (Insulinoma) & Anti-insulin receptor antibody in hodgkin’s disease)

6. Non-pancreatic neoplasm eg hemangiopericytoma.


Causes of hypoglycaemia in diabetic patients

  • 1. Missed, delayed or inadequate meal
  • 2. Unexpected or unusual exercise
  • 3. Alcohol
  • 4. Errors in oral anti-diabetic agent(s) or insulin
  • 5. Poorly designed insulin regimen
  • 6. Lipohypertrophy at injection sites causing variable insulin absorption
  • 7. Gastroparesis due to autonomic neuropathy
  • 8. Malabsorption, e.g. coeliac disease
  • 9. Unrecognised other endocrine disorder, e.g. Addison's disease
  • 10. Factitious (deliberately induced)
  • 11. Breastfeeding by diabetic mother

Unawareness of hypoglycaemia

Risk Factors:

  • 1. Strict glycaemic control
  • 2. Gastroparesis due to autonomic neuropathy
  • 3. Increasing duration of diabetes
  • 4. Frequent hypoglycaemia (impaired central activation of counter-regulation)
  • → Frequent blood glucose monitoring
  • → Frequent small meals
  • →higher glycemic target

Morbidity of severe hypoglycaemia

  • 1. CNS:
  • Impaired cognitive function, Coma, Convulsions,
  • Intellectual decline, Transient ischaemic attack, stroke, Brain damage (rare) , Focal neurological lesions .
  • 2. Heart:
  • Cardiac arrhythmias, Myocardial ischaemia
  • 3. Eye:
  • Vitreous haemorrhage, Worsening of retinopathy
  • 4. Other :
  • Accidents, Hypothermia
  • → Severe hypoglycaemia has a recognised mortality of up to 4% in insulin-treated patients
  • Mild (self-treated)
  • Oral fast-acting carbohydrate (10-15 g) is taken as glucose drink or tablets, followed by a snack containing complex carbohydrate
  • Severe (external help required)
  • A. If patient is semiconscious or unconscious:
    • I.v. 75 ml 20% dextrose
    • I.m. glucagon (1 mg) (ineffective if hepatic glycogen store are depleted as in prolonged starvation)
  • B. If patient is conscious and able to swallow:
    • Give oral refined glucose as drink or sweets (=25 g) or
    • Apply glucose gel or jam or honey to buccal mucosa
    • →continuous I.V infusion of dextrose (5%or 10%)may be necessary to prevent recurrence
    • →Use of 50% dextrose is no longer recommended (Thrombophlebitis).
    • →Recurrence may occur (long- or intermediate-acting insulin or sulphonylurea).

If the patient fails to regain consciousness after blood glucose is restored to normal consider:

  • 1. cerebral oedema (Mannitol & O2)
  • 2. alcohol intoxication
  • 3. post-ictal state
  • 4. cerebral haemorrhage
  • Search for the underline cause & educate the patient