Diabetic Emergencies Flashcards
Who is effected by Diabetic ketoacidosis?
Type 1 diabetics
Describe the pathophysiology of Diabetic ketoacidosis
Caused by hyperglycaemia causing Hyperglycaemia resulting in osmotic diuresis and electrolyte abnormalities.
Lack of insulin = glucose accumulates in blood
Glucose is not being used, body thinks it needs more energy. Increases in glycogenolysis and gluconeogenesis
]This is coupled with an increase in counter-regulatory hormone release (e.g. cortisol, glucagon, growth hormone), which exacerbates the hyperglycaemia and drives the production of alternative energy sources.
The lack of utility of glucose leads to the break down of fats (lipolysis) that increases serum free fatty acids. Fatty acids can be used as an alternative energy source through ketogenesis.
This increases the levels of ketone bodies
What is the biochemical abnormality triad which characterises Diabetic ketoacidosis
Hyperglycaemia: > 14.0 mmol/L or known DM
Ketonaemia: ≥ 3 mmol/L or significant ketonuria (> 2+ on dipstick)
Acidosis: bicarbonate < 15.0 mmol/L and/or venous pH < 7.3
What are the main ketone bodys within DKA?
3-beta-hydroxybutyrate
acetoacetic acid
List 5 main precipitants of DKA
Infection: 30-40% Non-compliance: 25% Inappropriate dose alteration: 13% New diagnosis of diabetes: 10-20% Intoxication / drugs Myocardial infarction: 1%
What are the signs and symptoms of DKA?
Symptoms
- Polyuria
- Polydipsia
- Nausea
- Vomiting
- Abdominal pain
- Leg cramps
- Headache
Signs
- Kussmaul breathing
- Ketotic breath
- Dehydration
- Hypotension
- Abdominal tenderness
- Reduced consciousness
- Coma
How is DKA diagnosed?
based on identification of the biochemical triad of hyperglycaemia, acidaemia and ketonaemia/ketonuria.
Laboratory glucose: > 14.0 mmol/L
Venous/arterial blood gas: pH < 7.3 or bicarbonate < 15 mmol/L
Ketone testing: capillary blood ketone ≥ 3 mmol/L or urinary ketones +++ or above
Frequently raised Urea and Creatinine
Which type 2 diabetic patients are at risk of DKA?
Some patients with T2DM are at risk of diabetic ketoacidosis. These patients are referred to as ketosis-prone. African Caribbean patients are particularly at risk.
What is Euglycaemic DKA?
DKA with normal or near-normal blood glucose levels
may occur in the presence of exhausted glycogen stores in the liver (e.g. protracted vomiting, alcohol use, malnutrition).
Which drug is known to cause Euglycaemic DKA?
sodium-glucose co-transporter-2 inhibitors (SGLT-2 inhibitors).
How is DKA treated?
ABCDE assessment
Investigations-
Intravenous access (x2 large bore cannula)
Blood / urinary ketones
Capillary & plasma blood glucose
HbAIc
FBC, U&Es, venous blood gas (VBG)
Blood cultures
Urinalysis +/- MSU,
Pregnancy test (as indicated) ECG
Cardiac monitoring
Establish usual diabetic pharmacotherapy
- Fluid assessment (catheter)
- 0.9% normal saline
- Especially in hypotension- Systolic BP < 90 mmHg
- If BP does not improve seek help
- Potassium replacement
- fixed rate intravenous short acting insulin- actropid infusion (FRIII) immediately, which is based on the patients weight - 0.1 units/kg/hr
If the patient is usually on a long-acting insulin therapy then this should be continued during the fixed rate intravenous insulin infusion
How are patients being treated with DKA monitored?
Patients should be monitored regularly to assess for an adequate fall in ketones, glucose and rise in bicarbonate with normalisation of acid-base balance.
Each hour, blood ketones and blood glucose should be checked.
A venous blood gas should be used for the pH and bicarbonate at 1 hour and 2 hours, and then 2 hours thereafter.
Potassium should be checked as a minimum of every 4 hours within the first 24 hours, but sooner if abnormal.
In those with severe DKA, they should have continual cardiac and saturation monitoring.
accurate fluid balance should be kept. Use catheter if required
Level 2 bed (High Dependency Unit)
Cardiac monitor
Nasogastric tube if impaired conscious level
Consider Central Venous Pressure line – especially in elderly
Oxygen if PaO2 < 10.5 kPa on air
Urinary catheter
Prophylactic LMW heparin
iv antibiotics as appropriate if suspected infection
Frequent monitoring of conscious level, BP, Pulse, Temp, Glucose, Urine
output, Potassium, Acidosis
What are the Metabolic treatment targets in DKA?
Blood ketones: falling by at least 0.5 mmol/L/h
Bicarbonate: rising by at least 3.0 mmol/L/h
Blood glucose: falling by at least 3.0 mmol/L/h
insulin should continue until - ketone measurement is less than 0.6 mmol/L,
venous pH over 7.3 and/or
venous bicarbonate over 18 mmol/L.
How is a low blood glucose treated while treating DKA?
If the blood glucose level falls below 14.0 mmol/L then 10% dextrose should be given at approximately 125ml/hr (8 hour bag)
How does potassium status change during DKA presentation and treatment?
Severe dehydration can lead to pre-renal acute kidney injury and transmembrane shifts in potassium due to the ketoacidosis. These collectively lead to hyperkalaemia. However, on initiation of insulin therapy plasma potassium concentrations dramatically fall leading to dangerous hypokalaemia.
What are the complications of DKA?
hypokalaemia adult-respiratory distress syndrome (ARDS) sepsis myocardial infarction cerebral oedema hypoglycaemia
What is Hyperglycaemic hyperosmolar state? Who does it occur in?
acute diabetic emergency that occurs in patients with type 2 diabetes mellitus.
Describe what Hyperglycaemic hyperosmolar state is characterised by
HHS occurs insidiously over several days with dehydration and metabolic disturbances
It is characterised by:
Hypovolaemia
Hyperglycaemia (> 30 mmol/L)
Mild or absent ketonaemia (blood ketones < 3 mmol/L)
High osmolality (> 320 mOsm/kg)
Which type of individuals usually develop Hyperglycaemic hyperosmolar state?
Patients are usually elderly with multiple co-morbidities, and as a result may be very unwell.
Can occur in younger patients
What are the counter regulatory hormones released when here is a lack of insulin?
cortisol, growth hormone, glucagon
Describe the pathophysiology of Hyperglycaemic hyperosmolar state
retain a certain level of insulin, which prevents the development of ketosis that epitomises DKA. However, the level of insulin is inadequate to prevent profound hyperglycaemia.
excessive glucose leads to massive osmotic diuresis within the kidneys with the loss of essential electrolytes such as sodium and potassium
proximal tubules in kidneys have a limited capacity for reabsorption of glucose. Once this is reached, the remaining glucose is passed through the renal nephrons causing diuresis.
As water is lost, there is profound dehydration and reduced circulating volume, resulting in hyperosmolarity and marked hyperglycaemia
increase in osmolality increases compensatory mechanisms such as release of anti-diuretic hormone (ADH) and stimulation of thirst. However, if this cannot compensate for the renal water loss (e.g. elderly patients with co-morbidities) then hypovolaemia develops with progression to acute kidney injury, electrolyte disturbances, hypotension and coma.
How does Hyperglycaemic hyperosmolar state increase the risk of DVT and stroke?
hyperosmolar state of the condition leads to hyperviscosity that increases the risk of arterial and venous thrombosis
State 6 precipitants of HHS
Infection High-dose steroids Myocardial infarction Vomiting Stroke Poor treatment concordance
What are the signs and symptoms of Hyperglycaemic hyperosmolar state?
Symptoms - Polydipsia Polyuria Nausea Vomiting Muscle cramps Weakness Altered mental status Seizures Coma
Signs Dehydration Hypotension Decreased urine output Decreased conscious level Coma
How is Hyperglycaemic hyperosmolar state diagnosed?
Laboratory glucose: > 30 mmol/L
Serum osmolality: > 320 mOsm/kg
Ketones:
Urine: 1+, trace, negative OR
Blood: < 3 mmol/L
How is Hyperglycaemic hyperosmolar state treated?
ABCDE
Same investigations as DKA
- fluid resuscitation to restore circulating volume
0. 9% sodium chloride
Insulin therapy
- Insulin use in such patients should be handled by a specialist or senior
Insulin should only be commenced if there is evidence of significant ketonaemia (> 1 mmol/L) or ketonuria (2+ or more). Or when blood glucose levels are falling less than 5 mmol/L per hour.
If so, insulin should be commenced as a fixed rate intravenous insulin infusion (FRIII) at 0.05 units/kg/hr
Electrolyte replacement
- sodium, potassium, phosphate and magnesium should be monitored regularly (4 hourly minimum) and replaced as necessary.
What are the Metabolic treatment targets in HHS?
Plasma osmolality: falling by 3-8 mOsm/kg/hr
Blood glucose/l falling by at least 5 mmol/L/hr
What are the complications of HHS?
Myocardial infarction:
Thrombotic complications:
Cerebral oedema:
At what blood glucose concentration do symptoms of hypoglycaemia present?
Symptoms typically occur at glucose ~3.6mmol/L
What is false hypoglycaemia?
Patients with consistently
high glucose levels may experience symptoms of hypoglycaemia at a higher level than someone with good glycaemic control
Which non medical conditions can cause hypoglycaemia?
Imbalance between
carbohydrate and insulin or sulfonylurea therapy
Exercise with too much insulin or not enough carbs
Alcohol – can cause hypoglycaemia even in non-diabetic people
Vomiting
Breastfeeding
Which medical conditions can cause hypoglycaemia?
Liver disease Progressive renal impairment Hypoadrenalism (is associated with Type 1 diabetes) Hypothyroidism Hypopituitarism (rare) Insulinoma (rare)
In patients with type 1 diabetes, new onset of hypoglycaemia can occur with new diagnosis of
which 2 conditions?
hypoadrenalism or adult coeliac disease
which are commoner in patients with T1D
What are the Autonomic symptoms of hypoglycaemia? At which blood glucose do these symptoms present?
Sweating Shaking or tremor Anxiety Palpitations Hunger Nausea
Present at -
Glucose ~ 3.6 mmol/L
What are the Neuroglycopenic symptoms of hypoglycaemia? At which blood glucose do these symptoms present?
Confusion Slurred speech Visual disturbances Drowsiness Aggression
present at
Glucose ~ 2.7 mmol/L
List 3 potential causes of hypoglycaemia unawareness? How can these be reversed?
Increased duration of diabetes
Very tight glycaemic control
Autonomic neuropathy
Reversal
May be improved by “hypo holiday”
- Strict hypoglycaemia avoidance by relaxing glycaemic control
- Use of analogue insulin
- Continuous Subcutaneous Insulin Infusion (insulin pump therapy)
How is mild hypoglycaemia treated?
Mild (conscious can self treat)
- Sugary drink, e.g. lucozade, ordinary coke, orange juice
- 5-7 glucose tablets, or 3-4 heaped teaspoons of sugar in water
How is Moderate hypoglycaemia treated?
Moderate - conscious but needs help with medication
Glucogel® – 1-2 tubes buccally, or jam, honey, treacle massaged into the cheek.
Intramuscular glucagon
How is sever hypoglycaemia treated?
Sever = unconscious
Place the person in the recovery position
Administer 0.5-1mg glucagon IM
In the hospital
Ideally 75mls of 20% glucose or 150mls 10% glucose over 15 mins
50mls 50% glucose can be given, but take care with veins – extravasation can cause chemical burns
How to treat hypoglycaemia when the patient is out of hypoes?
glucose above 4.0 mmol/L, must have some longer acting carbs, eg:
Two biscuits
One slice of bread/toast
200-300ml glass of milk (not soya)
Normal meal with carbs if due
While driving, how often should a diver on insulin check there blood glucose?
Check blood glucose before driving
Check blood glucose every 2 hours
Divers on insulin should inform who about there condition?
All drivers on insulin must inform DVLA and insurance company (if
they fail to do so, they will not be covered)
What is nocturnal hypoglycaemia? How is it treated?
Consider in patients with diabetes who wake up with:
- High blood glucose levels (rebound hyperglycaemia)
Headaches – feels “hungover” despite no alcohol! - Confirm by advising testing blood glucose levels during the night (3.00am), or
using continuous glucose monitoring sensor (CGMS), which monitors glucose over 5 days subcutaneously
How is nocturnal hypoglycaemia treated?
Analogue insulins
Pre bed snack
Change timing of insulin
Insulin pump therapy
What causes acidosis in DKA?
Acidosis is caused by ketone body accumulation
What are the features which indicate greater severity of DKA
Blood ketones > 6 mmol/L
Bicarbonate < 5 mmol/L
pH < 7.1
Potassium < 3.5 mmol/L
GCS <12
O2 sats < 92%
Systolic BP < 90 mmHg
Pulse >100 or < 60 bpm
Which fluid therapy is used in those with DKA?
Sodium chloride 0.9%
1 Litre stat
1 Litre in 1 hour
1 Litre over 2 hours (+20 mmol potassium chloride)
1 Litre over 4 hours (+potassium chloride)
1 Litre over 4 hours (+potassium chloride)
5% or 10% Glucose
Start when the CBG is <12 mmol/L and continue at 125ml/hr
10 % glucose may be necessary to increase insulin infusion
Increase infusion rate if glucose falls below 6.0 mmol/L
How is potassium administered in DKA?
- For the first 1-2 bags fluid, give no potassium as fluid is given
too rapidly - For every subsequent bag of NaCl 0.9% or glucose 5% use a bag
of fluid containing KCl as follows according to serum K
< 3.5 - May need additional K+ and delay insulin
3.5-5.5 - 20-40 mmol/l
> 5.5 - none
How is insulin used in treating DKA?
If patient known to be diabetic, continue their normal long acting
insulin on admission
Commence insulin infusion by intravenous syringe pump (containing
50 units Actrapid® made up to 50ml in Sodium Chloride 0.9%)
Fixed rate IV insulin infusion
0.1 u /kg – around 6-8 u / hr for most patients
Aiming for bicarb rise of 3 mmol/hr and glucose fall by 3 mmol/hour
If not achieved – increase rate by 1 u / hr
How is cerebral oedema treated in DKA?
dexamethasone or mannitol
What can be used to indicate lack of adequate glucose and
insulin administration?
Persisting ketonuria usually reflects lack of adequate glucose and
insulin administration
