Diabetes Emergencies - Slides

Diabetic Emergencies
Department of Diabetes & Endocrinology

Nelson R Mandela School of Medicine
University of KwaZulu-Natal
Acute metabolic emergencies
1. Hyperglycaemia
 Ketoacidosis
 Hyperosmolar hyperglycaemic state
2. Hypoglycaemia
Diabetic ketoacidosis (DKA)
Setting:
1. Acute presentation of type 1 diabetes

2. Acute decompensation in both type 1 & type 2
diabetes
Precipitants:
1. Omission of insulin
2. Underlying illness, especially infections
Pathogenesis of DKA
Two major metabolic abnormalities:
1. Insulin deficiency
2. Glucagon excess
DKA : Insulin deficiency
Consequences:
 Decreased peripheral glucose uptake

 Increased hepatic gluconeogenesis & glycogenolysis
 Hyperglycaemia
 Osmotic diuresis
 Dehydration
 Activation of lipolysis
 Lipaemic serum (increased free fatty acids)
 Increase in hepatic fatty acid content
DKA : Glucagon excess
Consequences:
 Further increases hepatic gluconeogenesis

 Increases hepatic carnitine content
 Decreases hepatic malonyl CoA content
 Activates fatty acid oxidation
 Fatty acids are the prime substrates in ketogenesis
 Glucagon activates and drives mitochondrial
ketogenesis in the liver
DKA: Pathogenesis -CELL FAILURE
Insulin Deficiency
Glucagon Excess  Lipolysis  Glucose  Glucose

production uptake
 Free fatty acids

 Blood glucose
- Fatty acid oxidation
 Fatty acyl coA
- Mitochondrial ketogenesis
OSMOTIC
DIURESIS
Ketoacidosis
KETONE
Ketonuria BODIES Dehydration
Pathogenesis of HHS
Differs from DKA:
 Typical of type 2 diabetes

 Hyperglycaemia is present to a greater extent
 Volume depletion is worse
 No ketogenesis
 ? Due to sufficient insulin to suppress lipolysis

 Not clearly understood why no ketosis
DKA & HHS: Clinical features
Symptoms:
 Abdominal pain
 Nausea, vomiting, polyuria, polydipsia
 “Dyspnoea”
 Confusion, disorientation, stupor, coma
 Symptoms of precipitating illnesses
Signs:
 Dehydration
 Kussmaul breathing
 Tender abdomen
 Confusion, coma
 Focal neurologic signs indicate complications
Table 2 Diagnostic criteria for diabetic ketoacidosis and hyperglycaemic hyperosmolar state
Umpierrez, G. & Korytkowski, M. (2015) Diabetic emergencies — ketoacidosis, hyperglycaemic hyperosmolar state and hypoglycaemia
Nat. Rev. Endocrinol. doi:10.1038/nrendo.2016.15
DKA & HHS: Management
Principles:
• Hospitalise - ALL PATIENTS

• Rehydrate
• Provide insulin – preferably by intravenous
infusion
• Correct electrolytes
• Treat any associated illnesses
All patients:
• IV line (18 G or larger)

• CVP if hypotensive
• Nasogastric tube if conscious level abnormal
• Bladder catheter if conscious level abnormal
• Chest X-ray, ECG, blood culture, urine culture
Fluids
 Average deficit: 6 litre

 15 – 20 ml per kg in 1st hour, then 5 – 15 ml/hour
 Take account of co-morbidities
 Normal saline or plasmalyte initially
 ½ normal saline if serum [Na+] > 140 mmol/L
Requirements must be constantly re-assessed

DKA : Management
Insulin: Soluble insulin - Actrapid®, Humulin R® or

Rapid-acting analogue insulin – Novorapid®,
Humalog®, Apidra®
 Bolus injection of 0.15 units per kg ivi
 Then infuse 0.1 U/kg/hour in normal saline

 60 Kg patient = 6 U/hr
 Use infusion pump, if available

DKA : Management
Insulin (soluble insulin or rapid-acting analogue)
 Aim to lower glucose by 3-4 mmol/L per hour
 When glucose < 15 mmol/L, reduce insulin infusion

and change fluids to glucose infusion
(eg. 5-10% dextrose )
NB: DO NOT STOP THE INSULIN INFUSION

Potassium
 Serum K+ < 3.0 mmol/L: add 40 mmol K+ to each litre fluid *

 Serum K+ 3.5-5.5 mmol/L: add 20 mmol K+ to each litre
 Serum K+ > 5.5 mmol/L: no supplemental K+ needed
* Note: insulin must be withheld until K+ > 3.3 mmol/L
Requirements must be constantly re-assessed

Adjunctive management
• Bicarbonate:
 Contentious issue
 Give 100 mmol ivi over 2 hours, if pH < 6.9
• Antibiotics:
 All female patients, empirically, after cultures sent
 Used for conventional clinical indications
Figure 1 Protocol for management of adult patients with diabetic ketoacidosis and hyperglycaemic
hyperosmolar state recommended by the ADA
© 2009 American Diabetes Association. From Diabetes Care®, Vol. 32, 2009; 1335–1343. Modified by permission of The
American Diabetes Association
Umpierrez, G. & Korytkowski, M. (2015) Diabetic emergencies — ketoacidosis, hyperglycaemic hyperosmolar state and hypoglycaemia
Nat. Rev. Endocrinol. doi:10.1038/nrendo.2016.15
DKA & HHS: Resolution
Criteria for resolution

 Plasma glucose < 11.1 mmol/L
 Serum bicarbonate ≥ 18.0 mmol/L
 Venous blood pH > 7.30 (0.03 units lower than arterial pH)
Change to maintenance insulin or introduce insulin
Overlap infusion with first dose of maintenance insulin

DKA & HHS: Pitfalls
Common errors
• Delay in diagnosis
• Inadequate fluids
• Stopping insulin therapy when glycaemia controlled
• Inadequate monitoring and adjustment in therapy
• Failure to recognise underlying illnesses timeously
DKA & HHS: Complications
1. Cerebral oedema:
 Associated with rapid glucose flux

 Occurs in severe DKA
 Treated with mannitol infusion
2. ARDS
 May be related to precipitant or DKA/ HHS per se
3. Thromboembolism
 Due to dehydration and hyperosmolality

Summary of DKA management: SEMDSA 2017
Hypoglycaemia
in
Diabetes
Hypoglycaemia in Diabetes
Definition & classification
Level 1: venous plasma glucose < 3.9 mmol/L
Level 2: venous plasma glucose < 3.0 mmol/L
Level 3: no specific threshold; neuroglycopaenia,

requires 3rd party assistance
Defence against hypoglycaemia:
• Cessation of insulin secretion

• Secretion of counter-regulatory hormones:
 Glucagon Gluconeogenesis
 Adrenaline Glycogenolysis
 Growth hormone Lipolysis
 Cortisol
Hypoglycaemia: Counter-regulation
Glucose level (mmol/l)
4.0 Insulin secretion ceases
3.0 Glucagon, catecholamines
2.0 Cortisol, growth hormone
1.0 Neuroglycopaenia
Hypoglycaemia: clinical features
Symptoms & Signs:
 Tremor
 Pallor
 Sweating Adrenergic
 Palpitations, tachycardia
 Feeling of hunger
 Confusion, disorientation
 Aggression, irritability Neuroglycopaenia
 Seizures, headache
 Coma
Hypoglycaemia: common causes
• Therapy errors
 Too much insulin / sulphonylurea / glinide
 Profile of agent inappropriate
• Inadequate nutrition
• Exercise
 Unplanned exercise
• Alcohol and drugs

 Beta blockers (decrease adrenergic symptoms)
• Miscellaneous situations
 Onset of renal insufficiency
 Sleeping late
Hypoglycaemia: therapy
Mild reactions:
 Identify the cause

 Give 10-15 g carbohydrate
 100 ml fruit juice
 1 tablespoon of honey
 4 teaspoons of granular sugar
 6 sugar cubes
 If overnight, or > 2 hours to next meal:

 give milk (100 ml) – protein content provides
gluconeogenic substrate
Chocolate and ice cream have too much fat and retard
glucose absorption
Hypoglycaemia: therapy
Moderate & severe reactions:
 Give oral carbohydrate first, if possible

 Repeated doses may be required
 If conscious level impaired, iv glucose is therapy of
choice:
 20 ml of 50% dextrose solution, followed by:

 5% dextrose infusion (40-80 ml per hour) until
able to eat
 Constant monitoring is required

Glucagon
Moderate & severe reactions:
 1 mg imi or subcutaneous injection

 Mobilises liver glycogen
 Stimulates gluconeogenesis
 Clinical response in 10 – 15 minutes
BUT
 Induces insulin release

 May worsen SU-induced hypoglycaemia
Hypoglycaemia: Anticipate & Prevent
• Unplanned exercise: ingest 10-20 g CHO

• Avoid excess alcohol
• Monitor 2-3 am glucose with basal night-time insulin
initiation or dose change
• Frequent use of home glucose readings
• Do not sleep too late
• Avoid skipping meals
• Take snacks and meals timeously according to the
therapeutic plan

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Diabetic Emergencies

Department of Diabetes & Endocrinology

1. Acute presentation of type 1 diabetes

Two major metabolic abnormalities:

 Decreased peripheral glucose uptake

 Further increases hepatic gluconeogenesis

Glucagon Excess  Lipolysis  Glucose  Glucose

 Free fatty acids

Differs from DKA:

 Typical of type 2 diabetes

 ? Due to sufficient insulin to suppress lipolysis

• Hospitalise - ALL PATIENTS

• IV line (18 G or larger)

 Average deficit: 6 litre

Requirements must be constantly re-assessed

Insulin: Soluble insulin - Actrapid®, Humulin R® or

 Bolus injection of 0.15 units per kg ivi

 Then infuse 0.1 U/kg/hour in normal saline

 Use infusion pump, if available

Insulin (soluble insulin or rapid-acting analogue)

 Aim to lower glucose by 3-4 mmol/L per hour

 When glucose < 15 mmol/L, reduce insulin infusion

NB: DO NOT STOP THE INSULIN INFUSION

 Serum K+ < 3.0 mmol/L: add 40 mmol K+ to each litre fluid *

* Note: insulin must be withheld until K+ > 3.3 mmol/L

Requirements must be constantly re-assessed

Criteria for resolution

Change to maintenance insulin or introduce insulin

Overlap infusion with first dose of maintenance insulin

 Associated with rapid glucose flux

 May be related to precipitant or DKA/ HHS per se

 Due to dehydration and hyperosmolality

Definition & classification

Level 1: venous plasma glucose < 3.9 mmol/L

Level 2: venous plasma glucose < 3.0 mmol/L

Level 3: no specific threshold; neuroglycopaenia,

• Cessation of insulin secretion

Glucose level (mmol/l)

4.0 Insulin secretion ceases

3.0 Glucagon, catecholamines

2.0 Cortisol, growth hormone

Symptoms & Signs:

• Alcohol and drugs

 Identify the cause

 If overnight, or > 2 hours to next meal:

Moderate & severe reactions:

 Give oral carbohydrate first, if possible

 20 ml of 50% dextrose solution, followed by:

 Constant monitoring is required

Moderate & severe reactions:

 1 mg imi or subcutaneous injection

 Induces insulin release

• Unplanned exercise: ingest 10-20 g CHO

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