komplikasi akut dm

When the level of glucose falls in the

blood so that the cells in the periphery,

and eventually the brain cells, do not

get adequate glucose to function

HYPOGLYCAEMIA

●Endogenous insulin secretion suppressed

Release of glucagon, epinephrine, cortisol, growth hormone

Autonomic response

Hypoglycaemia stimulates release

It acts in the liver to increase glucose production

– releasing stored glycogen

– activating production of new glucose

– stimulating production of ketones

Releases stored glycogen

Activates production of glucose from protein

Reduces uptake of glucose

Reduces production of insulin

• Reduce cellular uptake of glucose

• Stimulate breakdown of proteins to make glucose

• Stimulate breakdown of body fats

Symptoms Low blood glucose Relief of symptoms when blood

glucose raised

Mild Moderate Severe

Capable of self-treating

May require prompting

Not capable of self-treatment

Tremors, palpitation, sweating,

hunger, fatigue

Headache, mood changes, low attentiveness

Conscious or unconscious

Adrenergic Neuroglycopenic Neuroglycopenic

Only those taking glucose-lowering medicines or insulin

Increased risk:◦ too little or wrong type of

carbohydrate◦ late or missed meal ◦ fasting or malnourishment◦ too much insulin or insulin

secretagogues◦ prolonged or unplanned activity

Increased risk:

• Recent severe hypoglycaemia

• Gastroparesis

• Liver disease or kidney failure

• Pregnancy

• Injection-related

• Over-correction of high BGL

Mild or moderate• Test if possible• 15 g glucose; re-test• Glucose tablets• Fruit juice • Soft drink• Sugar• Re-treat if level remains low

Severe• 20 g glucose• glucagon • intravenous dextrose• Manage seizure – place

person on their side if not too agitated

If unable to treat orally: Glucagon subcutaneously or

intramuscular◦1 ml for adult (0.5ml for child)◦blood glucose 3.0 to 11.8 in 45 min◦vomiting◦severe headache

IV dextrose:◦25-50 ml IV over 2-3 minutes◦immediate response

Risk of injury from falls

May be missed or mistaken for dementia

Malnutrition may increase risk of hypoglycaemia

Avoid long-acting sulphonylureas in older people

Hypoglycaemia • Common• Frightening for person with diabetes

and family• Can usually be prevented• Reduced through education, self-

monitoring and self-care• Must be addressed at every visit to

healthcare professional• Treatment must be revised if recurrent

Absolute or relative insulin deficiency

Increase in counter-regulatory hormones

Breakdown of fat and muscle Biochemical triad

◦hyperglycaemia◦ketoacids◦metabolic acidosis

High blood glucose, ketones, acidosis and dehydration

Incidence

New-onset diabetes 5-40%

Acute illness 10-20%

Insulin omission/non-adherence 33%

Infection 20-38%

Heart attack, stroke, pancreatitis <10%

Insulin deficiency

Glucose uptake Lipolysis

Hyperglycaemia Gluconeogenesis

Glycerol Free fatty acids

Ketogenesis

Ketonemia

KetonuriaOsmotic diuresis

Urinary water losses

Electrolyte depletion

Dehydration

Acidosis

Diabetic ketoacidosis

Glucosuria

Used as fuel when calories are restricted

Physiological ketosis when fasting or with prolonged exercise

Insulin deficiency lypolysis and ketone production acidosis◦beta-hydroxybutyrate◦acetoacetate◦acetone

Beta-hydroxybutyrate predominant – not detected by test strips or acetone tablets

Ketoacidosis may be present without detectable urinary ketones

Blood ketone testing may enable early identification of DKA

Earlier clinical symptoms and signs of DKA

• Polyuria

• Polydipsia

• Polyphagia

• Tiredness

• Muscle cramps

• Flushed facial appearance

Later clinical symptoms and signs of DKA

• Weight loss• Nausea and vomiting• Abdominal pain• Dehydration • Acidotic breath• Hypotension • Shock• Altered consciousness • Coma

Blood glucose >14mmol/L (252mg/dL)

Ketones Urine: moderate to large

Blood: >3mmol/L

Osmolality Increased – high blood glucose and urea/creatinine, dehydration

Electrolytes Low/normal Na+ and Cl-

Low/normal/high K+ (often misleading)

Low HCO3 (normal 23-31)

Anion gap >10 mild

>12 moderate to severe

Blood gases pH <7.30, HCO3 <15 (mild)

pH <7.00, HCO3 <10 (severe)

Rehydration 1. Correct shock with bolus saline

2. Rehydration rate depends on clinical status, age and kidney function

Normal saline (0.9%) for resuscitation and rehydration initially

Glucose/saline solution when glucose around 14 mmol/L (252mg/dL)

Rehydrate steadily over 48 hours

3. Consider NG tube

Potassium Essential after resuscitation and when urine output confirmed

Insulin Infusion: 0.1 units/kg/hour after resuscitation, saline established and BG falling

Rate should be increased by 10-20% if glucose not fallen by 2-3 mmol/L (45-54mg/dL) over first hour

Monitoring BG, BP, urine output and hourly neurological status

Blood gases and electrolytes 2-hourly initially

Ketosis may be present

Coma not always present

Primarily in older people with/without history of type 2 diabetes

Always associated with severe dehydration and hyperosmolar state

Develops over weeks

Marked hyperglycaemia Hyperosmolarity Absence of severe ketosis Altered mental awareness

Incidence

Infection 40-60%

New-onset diabetes 33%

Acute illness 10-15%

Medicines, steroids <10%

Insulin omission 5-15%

Initially polyuria and polydipsia

Altered mental status

Profound dehydration

Precipitating factors

Blood glucose >33mmol/L (600mg/dl)

Ketones Urine: negative – small

Blood: <0.6 mmol/L

Osmolality >320mOsm/kg - (raised Na, BG, urea)

Electrolytes Raised Na, BG, urea creatinine

Anion gap <12

Blood gases pH >7.30

normal or raised HCO3

Rehydration Caution!

Normal saline 1 l per hour initially

Consider ½ strength normal saline

Potassium Only if hypokalaemic and renal function adequate – give before insulin

Insulin May be needed as slow infusion0.1 unit/kg/hour to be increased with care if BG is slow to fall

Monitoring BG, BP, neurological function hourly until stableElectrolytes 2-hourlyCardiac or CVP monitoring

Identify and treat underlying cause

Can be prevented by ◦better public awareness◦improved access to medical

care ◦improved education in treating

hyperglycaemia during illness ◦emergency communication

with healthcare provider