Acute complication of diabetes Flashcards
Consider diabetic keto-acidosis (DKA)
What are the effects of inuslin deficiency?
Lipolysis and reduced esterification of fatty acids
- NEFA –> (Acetyl CoA) –>Ketones
- Glycerol –> gluconeogenesis
Proteolysis and reduced uptake of AA’s
- Alanine –> gluconeogenesis
Increased heaptic glucose output and hyperglycaemia
Consider diabetic keto-acidosis (DKA)
What is the pathophysiology of it?
Unchecked gluconogenesis –> hyperglycaemia
Osmotic diuresis –> dehydration
Unchecked ketogenesis –> ketosis
Dissociation of ketone bodies into H+ and anions –> aniongap metabolic acidosis
Often a precipitating event is identified (infection, lack of insulin administeration)
Consider diabetic keto-acidosis (DKA)
Outline how insulin deficiency is responsible for the pathophysiology of DKA
Insulin deficiency –> hyperglycaemia –> hyperosmolality and glycosuria
Glycosuria –> electrolyte losses and dehydration
Renal failure can be caused by or cause dehydration. This leads to shock and eventually CV collapse
Alternatively insulin deficiency can cause lipolysis –> increased FFA’s –> ketones –> acidosis (causing CV collapse or electrolyte losses)
Consider diabetic keto-acidosis (DKA)
Describe the physiological effects of insulin deficiency in adipose tissue
- Increased lipolysis and decreased esterification of fat (by insulin deficiency/ glucagon/ adrenaline excess) –> excess FFA and glycerol from breakdown TG’s
- –> FFA is a substrate for hepatic synthesis of ketone bodies
- –> Rate of ketogenesis is linked to rate of gluconeogenesis
- Muscle and brain can use ketone bodies as main energy substrate, however ketoacidosis results when ketogenesis> utilisation rate in periphery (+renal clearance)
Consider diabetic keto-acidosis (DKA)
What symptoms may accompany acidosis?
- Nausea
- Abdominal pain
- K+ depletion –> osmotic diuresis –> dehydration
Consider diabetic keto-acidosis (DKA)
Why is there metabolic derangement?
In order to manage the acidosis:
- Intracellular buffering (H+/ K+ exchange pump)
- Potassium to kidney and H+ result from metabolic acidosis (low pH) - Respiratory compensation - hyperventilation
- H+ stimulates respiratory centres, breathe off CO2
H+ + HCO3- H2O + CO2 - Renal excretion of K+ (slow)
Consider diabetic keto-acidosis (DKA)
What electrolyte disturbances are there?
Potassium depletion
Sodium depletion
Dehydration (osmotic diuresis)
Caused by renal losses
Consider diabetic keto-acidosis (DKA)
What are the differences/similarities in cations and anions in ECF and ICF?
PLASMA- Na+, K+, HCO3-
Interstitual fluid- Na+, K+, HCO3-
ICF (muscle)- Na+, K+, PO43-, Plasma proteins (-)
Consider diabetic keto-acidosis (DKA)
What are the clinical features?
Subsequent course
- Usually young patients with T1DM
- Precipitating causes: relative or absolute insulin deficiency
Serum sodium: normal [b/g] < 40mmol/L serum bicarbonate <14mmol/L Mortality- 5% Ketones presence pH <7.3
Subsequent course: insulin dependent
Consider diabetic keto-acidosis (DKA)
What factors could possibly precipitate DKA?
Infections (pneumonia, UTI, virus, gastro-enteritis)
Error/missed insulin administeration
MI
Previously undiagnosed T1DM
Drugs: steroids
Idiopathic
Consider diabetic keto-acidosis (DKA)
For the following cause, outline the symptoms signs:
- Hyperglycaemia (+dehydration)
- Acidosis
- Symptoms: thirst and polyuria, weakness and malaise, drowsiness and confusion
Signs: dry mouth, sunken eye, postural/supine hypotension, hyperthermia and coma - Symptoms: nausea and vomiting, abdominal pain, breathlessness
Signs: facial flush, hyperventilation,ketone breathe and ketonuria
Consider diabetic keto-acidosis (DKA)
How would you go about managing it?
What factors would affect your course of management?
- Confirm diagnosis and check precipitating factors
- Rehydrate and monitor fluid balance (IV fluids- saline + K+, consider urinary catheter)
- Lower glucose –> IV insulin fixed rate 0.1 unit/kg/hour
- Monitor electrolytes - K (and Na)
- Prevent clots- prophylactic lowmolecular weight heparin
Is the management conscious? (Assess GCS, ITU?)
Risk of aspiration (consider NG tube)
Monitor recovery (glucose, ketones, pH, K+ hourly)
- AIM: normal pH, Ketones <2 (urine), vomitting settled
- resume normal diet and switch from IV to normal sc insulin
Consider Hyperosmolar hyperglycaemic state (HHS)
What are the clinical features?
Subsequent course?
Age >40
Precipitating causes: previously undiagnosed, steroids, diuretics, sugar
Serum Na: high [b/g]> 40mmol/L Serum HCO3-: normal pH : 7.4 NO KETONES Mortality - 30% (thromboses)
Subsequent course: diet/tablet controlled
Consider Hyperosmolar hyperglycaemic state (HHS)
How is it managed?
CORRECT PROFOUND DEHYDRATION
Management as for ketoacidosis but IV insulin fixed rate lower (0.05 unit/kg/hour)
Things to consider: Patients are often elderly and and severely ill
Consider Hypoglycaemia
State 5 neuroglycopenic symptoms
- Nausea
- Dizziness, lightheadedness
- Hunger
- Headache
- Inability to concentrate, confusion, difficulty speakingm poor coordination, behavioural change (irritability), automatism
- Coma and convulsions, hemiplegia
Consider Hypoglycaemia
State 5 autonomic (sympathomedullary activation) symptoms
- Shakiness
- Tachycardia
- Sweating, hot sensation
- Anxiety
- Palpitations
Consider Hypoglycaemia
How is the onset of symptoms like? How does the clinical syndrome relate to the biochemistry?
Sudden, may pass out if untreated
The clinical syndrome associated with hypoglycaemia develops as the NS becomes glucose deficient (neuroglycopaenic)
- Asymptomatic (awake, sleeping)
- Mild (patient can treat themselves)
- Severe (help needed)
- Coma and convulsions
Consider Hypoglycaemia
What causes hypoglycaemia?
- Insulin (inappropraitely high doses, starvation and low/no carbs)
- Sulfonylureas
Consider Hypoglycaemia
Describe the role of counter regulation
Glucagon stimulates glycogenolysis and gluconeogenesis, primary response
Adrenaline increases glycogenolysis
GH and cortisol limit glucose disposal in peripheral tissues bu this effect takes several hours (little acute benefit)
! Sympathetic nerves may also directly activate hepatic glycogenolysis and stimulate glucagon secretion
** ALL HAVE ANTI-INSULIN EFFECTS
Consider Hypoglycaemia
How does treatment of a minor episode differ to that of a hypoglycaemic coma?
MINOR EPISODE
- 20g carbohydrate as sugary drink, juice, glucose tablet/gels followed by ‘starch’
HYPEOGLYCAEMIC COMA
- IM/IV glucagon 1mg
- IV Dextrose 25g (150ml 10% glucose)
CLINICAL APPLICATION
Suppose you have a conscious patient with mild/moderate hypoglycaemia, how would you proceed in treating them?
Why should you be wary about administering glucagon?
Give 5 level teaspoons glucose powder in water/ 120ml lucozade/ 5 glucose tablets
Test b/g after 15 minutes, if <4mmol/L repeat up to 3x
- Next: 10% glucose IV
Then give a long acting carb (e.g. 2 biscuits/ slice of bread)
Dont omit subsequent doses of insulin
Glucagon can only be given 1/day (it will not reverse hypoglycaemia in patients with recurrent hypos, anorexia, severe liver disease)
CLINICAL APPLICATION
Suppose you have an unconscious patient with severe hypoglycaemia, how would you proceed in treating them?
How would it differ if the patient was NBM?
(Patient unconscious/ fitting/ aggressiveness/ NBM)
Check ABC, stop any IV insulin (if suitable IM glucagon/mg, otherwise 10% IV glucose 150ml, repeat up to three times)
Recheck glucose after 15 minutes (Aim <4mmol/L)
Give long acting carbohydrate or next meal if due
(if NBM give 10% glucose infusion at 100ml/hr until no longer NBM)
