Transcript
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
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