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Diabetes Complication

(DKA and HHS)


by Armando HF
Diabetic Ketoacidosis and hyperosmolar hyperglycemic state
are two acute serious metabolic complications of diabetes
mellitus.

Diabetic Ketoacidosis
Definition
Ketoacidosis: A condition resulting from deficient insulin
availability, leading to lipid oxidation and metabolism rather than
glucose metabolism. The insulin absence results in free fatty acid
(FFA) released from adipose tissue and in unregulated hepatic FFA
oxidation and ketogenesis.
Type I Diabetes: Autoimmune disease where there is attack of
beta cells of the pancreas leading to insulin deficiency and a
requirement for exogenous insulin to prevent ketoacidosis.
Type II Diabetes: It usually consists of tissue-level insulin
resistance (although exogenous insulin is often required) and
rarely leads to ketoacidosis.
Kussmaul breathing: Deep, rapid respirations associated with
acidosis.
Diabetic Ketoacidosis may be the presenting feature in a
patient not previously recognised as having diabetes. In a
patient with known diabetes, it may be precipitated by omitting
insulin doses, or by the insulin
Summary
Clinical Presentation
& Signs of dehydration
& GI symptoms
& Hyperventilation (Respiratory Rate Kussmaul breathing)
& True coma
Side Note Kussmaul breathing is air hunger, rapid deep
breathing a sign of metabolic acidosis. This is different to
Kusmauls sign looks at JVP relationship with breathing.
Aetiology (5Is)
& Infection
& Infarction
& Insufficient insulin
& Intercurrent illness
& Inappropriate withdrawal of Insulin
Remember Precipitating factors of DKA 5 Is: Infection Ischemia
Infarction Intoxication Insulin missed
Investigations
& Bloods EUC, Glucose, bicarbonate (HCO3 < 12 mmol/L
indicates severe acidosis)
& ABG Assess severity of acidosis
& Urine Ketones, Glucose
& ECG Hypokalaemia arrythmias
& Infection screen FBC, Blood and urine culture, CRP,
CXR. Although leukocytosis invariably occurs, this represents a
stress response and does not necessarily indicate infection
Think Check ABG, EUC and glucose every 4hours. Monitor ECG
for hypokalaemia/hyperkalaemia. Monitor IV fluid, insulin, glucose
and K+ should all be run in separate lines.
Diagnosis of DKA
& Hyperglycemia
& Metabolic acidosis
& Hyperketonemia
& Ketonuria
Management The main aim in treating DKA is to progressively
improve blood pH and clear the body of excessive ketones by
aggressive fluid replacement and insulin therapy.
& Assess Airway, Breathing, Circulation
& IV Fluids Normal Saline 0.9% NaCL (switch to 5%
dextrose with 0.45% NaCl when serum glucose reaches ~15)
& Insulin Insulin infusion until pH stabilizes
& Potassium Administration of Insulin can cause
hypokalemia, potassium levels should be checked prior to
insulin administration
& ABG assessment assess pH and need for bicarbonate
& Monitoring
& Check ABG, EUC every 4hours.
& Check Urine Glucose and Ketone 4hourly
& Check Blood glucose hourly.
& Monitor ECG for hypokalaemia/hyperkalaemia
& Monitor GCS regularly
Remember Hypokalaemia ECG changes include flat/inverted T-
wave, ST Depression and widened QRS

Glasgow Coma Scale

Behaviours Response Scor


e

Eye response (score 1-4) Spontaneously 4


To Speech 3
To Pain 2
No response 1

Verbal response (score 1- Orientated good 5


5) Confused 4
Inappropriate words 3
Incomprehensible sounds 2
No response 1

Motor response (score 1- Obeys command 6


6) Moves to localised pain 5
Withdrawal from pain 4
Decorticate 3
Decerebrate 2
No response 1

Score Best response 15


Coma <8
Unresponsive (Lowest 3
possible)
Complications of DKA
& 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 Acute respiratory distress
syndrome
& Thromboembolism
& Disseminated intravascular coagulation (rare)
& Acute circulatory failure
&

Hyperosmolar
Hyperglycaemia
Definition
Hyperosmolar Hyperglyaecmic State is a complication of
type 2 diabetes. It involves extremely high blood sugar (glucose)
levels without the presence of ketones.
Type I Diabetes: Is caused by a severe endogenous insulin
deficiency and a requirement for exogenous insulin to prevent
ketoacidosis.
Type II Diabetes: It usually consists of tissue-level insulin
resistance (although exogenous insulin is often required) and can
lead to HHS, rarely leads to ketoacidosis.
Pathophysiology of Diabetes Type II and Hyperosmolar state
Hyperosmolar Hyperglycaemia state occurring primarily in type
2 diabetes and is characterised by marked hyperglycaemia and
dehydration without ketoacidosis. The disturbance in
consciousness in patients varies from drowsy to comatose.
Management
& IV Fluids Normal Saline 0.45% NaCL (switch to 5%
dextrose with 0.45% NaCl when serum glucose reaches ~15)
& Insulin Slow Insulin infusion until pH stabilizes
& Potassium Administration of Insulin can cause
hypokalemia, potassium levels should be checked.
& ABG assessment assess pH and need for bicarbonate
Complication
Venous thromboembolism