Komplikasi Akut DM
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Transcript of Komplikasi Akut DM
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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
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●Endogenous insulin secretion suppressed
Release of glucagon, epinephrine, cortisol, growth hormone
Autonomic response
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Hypoglycaemia stimulates release
It acts in the liver to increase glucose production
– releasing stored glycogen
– activating production of new glucose
– stimulating production of ketones
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Releases stored glycogen
Activates production of glucose from protein
Reduces uptake of glucose
Reduces production of insulin
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• Reduce cellular uptake of glucose
• Stimulate breakdown of proteins to make glucose
• Stimulate breakdown of body fats
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Symptoms Low blood glucose Relief of symptoms when blood
glucose raised
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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
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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
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Increased risk:
• Recent severe hypoglycaemia
• Gastroparesis
• Liver disease or kidney failure
• Pregnancy
• Injection-related
• Over-correction of high BGL
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Mild or moderate• Test if possible• 15 g glucose; re-test• Glucose tablets• Fruit juice • Soft drink• Sugar• Re-treat if level remains low
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Severe• 20 g glucose• glucagon • intravenous dextrose• Manage seizure – place
person on their side if not too agitated
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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
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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
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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
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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
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Incidence
New-onset diabetes 5-40%
Acute illness 10-20%
Insulin omission/non-adherence 33%
Infection 20-38%
Heart attack, stroke, pancreatitis <10%
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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
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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
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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
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Earlier clinical symptoms and signs of DKA
• Polyuria
• Polydipsia
• Polyphagia
• Tiredness
• Muscle cramps
• Flushed facial appearance
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Later clinical symptoms and signs of DKA
• Weight loss• Nausea and vomiting• Abdominal pain• Dehydration • Acidotic breath• Hypotension • Shock• Altered consciousness • Coma
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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)
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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
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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
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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
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Marked hyperglycaemia Hyperosmolarity Absence of severe ketosis Altered mental awareness
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Incidence
Infection 40-60%
New-onset diabetes 33%
Acute illness 10-15%
Medicines, steroids <10%
Insulin omission 5-15%
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Initially polyuria and polydipsia
Altered mental status
Profound dehydration
Precipitating factors
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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
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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
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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
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