Diabetes emergencies Flashcards
How can we categorize diabetic emergencies
- ) Hyperglycaemic emergencies
2. )Severe hypoglycaemia
Outline hyperglycaemic emergencies
- ) DKA= diabetic ketoacidosis
2. ) HHS= hyperosmolar hyperglycaemic state ( previously known as HONK hyperosmolar non ketotic state)
What is DKA
- Complex disordered metabolic state due to absolute or relative insulin deficiency
- Mainly occurs in people with T1DM
- DKA defined by biochemical triad of
1. )hyperglycaemia
2. )Hyperketonaemia
3. )Metabolic acidosis
Diagnostic criteria:
- Blood glucose>11mmol/l or known diabetes
- Blood ketones>/= 3mmol/l or ketonuria>2+
- Bicarbonate<15mmol/l and/ or venous pH<7.3
How do our ketone levels increase?
- Lipolysis of our adipose tissue& triglycerides results in FAs which a processed by the liver to form ketones, so the as the amount of lipolysis occurs, so does the concentration of blood ketones
- Catecholamines, cortisol, glucagon & GH promote the production of FAs
What are some osmotic consequences of DKA
-dehydration
-Disordered potassium
This is due to osmotic diuresis
This can cause the release of stress hormones
What role can physiological stress have in the precipitation of DKA?
- Physiological stress results in stress hormones being released which leads to production of NEFAs which are partially oxidised by the liver and thus increases the concentration of ketones
- Stress hormones can also cause production of glucose by the liver
- Physiological stress can precipitate DKA in someone who’s still producing insulin or in someone who’s taking insulin
Explain the disordered potassium that occurs as an osmotic consequence of DKA
- Insulin causes K+ to move into cells usually
- In insulin deficiency K+ leaks out of cells leading to high EXTRAcellular K+ called hyperkalaemia
- Hyperkalaemia leads to renal k+ loss which leads to WHOLE BODY K+ depletion
- Acidosis has similar effects ( H+ & K+ compete)
What is ketonaemia?
Uncontrolled lipolysis and production of ketone bodies by the liver
- In the liver FA is partially oxidised to ketone bodies
- These ketone bodies are acetoacetate and 3-hydroxybutyrate and leads to acidosis
What happens to the K+ levels when DKA is treated?
-K+ moves rapidly into cells & because whole body k+ is deplete, extracellular k+ ( reflected in serum k+) falls very quickly
What could be the cause of DKA?
- Infection
- Acute illness
- Poor compliance
- Newly diagnosed
- Failure of care
- Unknown
What type of Diabetes is DKA classically associated with?
- To develop DKA you have to have absolute/relative insulin deficiency therefore its classically associated with people who have T1DM, so you would treat the patient as having T1DM until it’s proven otherwise
- Sometimes people with T2DM can still develop DKA
What are the complications of DKA?
- death
- cerebral oedema (decline conscious level)
- Adult respiratory distress syndrome/acute lung injury(due to fluid shifts)
- Pulmonary embolus (due to severe dehydration)
- Arrhythmias( due to K+ changes)
- Multi-organ failure (because your body has evolved to operate within quite a narrow pH & if you become acidotic everything starts to fail)
- Co-morbid states
What are the symptoms of DKA?
- Polyuria, polydipsia, thirst
- Weight loss
- Blurred vision( not from retinopathy, from fluid shifts in the lens in the eye)
- Vomiting
- Abdominal pain( due to ketones)
- Weakness
- Leg cramps (related to the hyperglycaemia; at this state there’s reduced glucose intake by muscle/fat and glucose is needed for the muscle to contract & relax properly. There is also a reduced amount of electrolytes due to increased excretion of glucose?)
Outline the signs of DKA
- Kussmaul respiration
- Ketotic factor
- Dehydration
- Tachycardia
- Hypotension
- Mild hypothermia
- Confusion, drowsiness, coma
What bedside tests can be performed when investigating DKA?
- CBG
- Blood ketones( portable ketone meters) or urine ketones
- Venous blood gases
What other investigations can be performed when investigating ketones
- Glucose/ U&Es( in testing for the electrolytes we are particularly looking for k+ & levels of dehydration
- FBC
- ECG
- CXR
- Blood culture
- MSU
What are the principles of DKA treatment?
- Fluid replacement (i.v 0.9% saline -normal saline)
- Insulin replacement ( Fixed rate i.v insulin infusion-0.1units/kg/hour)
- Potassium replacement (serum high but total body k+ low. once fluid & k+ is started, serum K falls rapidly; close monitoring of k+ is needed because a rapid drop will occur due to low total body k+)
- Identify and treat the cause ( may be an infection as the cause)
- Venous thromboembolism prophylaxis ( Low molecular weight heparin to reduce risk of getting a PE)
- Monitor in a high dependency unit( k+ may fall too rapidly; cerebral oedema may worsen due to i.v fluids; could put them in pulmonary oedema
what is the time frame of immediate management of DKA
Up to an hour
How should the patient be assessed after fluids and insulin infusions
check RR; temp, BP, pulse, oxygen sat
- Use the Glasgow coma scale
- Undergo a full clinical examination
What is important to do after all the clinical tests being performed and give an example
Establish your monitoring regimen
- Hourly CPG
- hourly ketone measurement
- Venous bicarbonate at 60mins, 2 hours & 2 hourly thereafter
- 4 hourly plasma electrolytes
- Continue cardiac monitoring if required
- Continuous pulse oximetry( a test used to measure the oxygen saturation of the blood) if required
What is HHS?
Hyperosmolar hyperglycaemic state
- State of severe uncontrolled diabetes
- Enough insulin to suppress ketogenesis
- T2DM
- No precise definition but characterized by:
1. ) Hypovolaemia & severe dehydration
2. )Marked hyperglycaemia (>/=30mmol/l)
3. ) Hyperosmolarity (serum osmolarity>/=320mosmol/kg) - calculated osmolality= (2xNa) +glucose+urea
4. ) No significant ketonaemia ( serum ketones< 3mmol/l) or acidosis (pH>7.3, bicarbonate >15mmol/l)
What is responsible for increased glucose, leading to osmotic diuresis & volume depletion?
-Insufficient fluid intake and/or drinking sugary drinks
What are the complications of HHS?
- life threatening
- develops over days(more slowly than DKA) & the metabolic disturbance is more severe than DKA (more profoundly dehydrated)
- higher mortality than DKA
- Cerebral oedema
- osmotic demyelination syndrome (pontine myelinolysis) ( due to profound changes in osmolarity and can occur during treatment as well as during the development of HHS)
- seizures
- arterial thrombolsis MI, CVA, peripheral arterial
- Venous thrombosis (PE)
- Multiorgan failure
- Foot ulceration (due to being bed bound with poor perfusion
- Co-morbid condition
What are the clinical features of HHS
- Thirst, polyuria
- Blurred vision
- weakness
- dehydration
- tachycardia
- hypotension
- confusion & drowsiness
- coma
What bedside investigations for HHS can we perform?
- CPG
- Blood ketones ( portable ketone meters)
- urine ketones
- venous blood gases
What other investiagtions can we perform for HHS?
- Glucose/ U&Es/FBC
- ECG,CXR,Blood culture,MSU
How can we manage HHS?
- Aim to gradually and safely normalised osmolality, fluid status & glucose
- Avoid complications of HHS & its treatment
- Fluid replacement (normal saline) (to start with at same rate at DKA then be careful not to replace the fluids too quickly)
- Insulin replacement ( Fixed rate i.v insulin infusion; lower than for DKA 0.05units/kg/hour)
- Identify and treat the cause
- PE thrombolaxis
- monitor (HDU)
Compare and contrast DKA with HHS
- ) DKA=n T1DM (&T2DM) ; HHS=T2DM
- ) HHS= older age
- ) DKA = rapid onset (<24hr); HHS= days-weeks
- ) DKA mortality<5%; HHS up to 15-20%
- ) DKA ph<7.3 ; HHS= normal
- )DKA bicarbonate= low ; HHS=normal
- ) DKA= high ketones ; HHS=normal/ 1+
- ) DKA= glucose>11mmol/L ; HHS Glucose= >30mmol/l
Outline the sick day rules for someone with T1DM
- Never stop background insulin (long-acting) even if vomiting
- Check CBG frequently, 2-4hourly
- Check for ketones
- Extra short acting insulin ( to reduce the blood glucose and ketones even if you’re not eating) if…
1. ) CPG>13mmol/l
2. )Blood ketones>1.5mmol/l - Keep drinking fluid (eg 100ml/hour)
- Bolus for carbs
On a sick day for a T1DM patient, when is medical help required?
If…
- Vomiting/diarrhoea
- CBG not improving/ ketones persist
- Troublesome hypos
What is hypoglycaemia
-Can be, but isnt usually a medical emergency
-Low blood glucose
-In diabetes defined as< 3.5mmol/L ( <4mmol/L in hospital inpatients)
Classification of hypoglycaemia
-Mild symptomatic- person recognises the hypo and is able to treat themselves
-asymptomatic
-severe-diabetes emergency (because of cognitive capacity induced by hypoglycaemia)
Why does hypoglycaemia occur in diabetes
- side effect of treatment to lower BG by increasing insulin levels eg insulin or sulphonyureas
- Mismatch between insulin levels & insulin requirements
Why is hypoglycaemia a problem?
- The brain needs BG/ketones as a fuel source cos it has not energy stores and can’t use alternate energy sources
- In diabetes hypoglycaemia is due to excess insulin: suppressed glucose& ketone production by the liver; glucose diverted to muscle&fat
Outline the progression of the consequecnes of hypoglycaemia
- ) Hunger
- ) Start of brain dysfunction
- ) Neuroglycopenic symptoms, confusion, poor concentration etc
- ) Coma/seizure
Why do T1DM patients struggle with hypoglycaemia counterregulation?
- They have no endogenous insulin
- Glucagon response is impaired
What physiological methods of hypoglycaemic counteregulation exist
- Suppression of insulin secretion
- Glucagon release
- Adrenaline release & Sympathetic NS
- GH & cortisol
Explain hypoglycaemia unawareness
- You’re unware youre developing hypoglycaemia& you don’t get the autonomic symptoms
- The first thing that happens is your brain stops working so you become confused & muddled & don’t behave sensibly so don’t get treatment
- These people are more at risk of having severe hypos where they need intervention
What are the autonomic symptoms of hypoglycaemia
- activation of ANS
- swetaing/tremor/palpitations
What are the neuroglycopaenic symptoms of hypoglycameia
- Brain dependent on glucose due to brain glucose deprivation
- Confusiion
- Drowsines
- Affected speech &behaviour
- Visual disturbance
- Incoordination
- Circumoral paraesthesiae
What other symptoms may a hypoglycaemic patient present with?
- Hunger
- Headache & nausea
How can you treat mild hypoglycaemia?
-Check CBG (<3.5mmol/l)
Conscious & able to swallow safely..
eg take one of the following
150-200ml lucozade; 5 dextrose tablets ; 150-200ml fruit juice; 150-200ml lemonade/coke; 4-5 jelly babies
- Wait 10mins and recheck
- If still hypoglycemic repeat, and recheck in 5-10mins
How can we treat severe hypoglycaemia if the patient is unconscious & unable to swallow safely
- Call for help
- ABCDE
- Check CPG
- If possible IV glucose
- If no IV access/out of hospital, administer glucagon 1mg sc/im
- wait 10mins, if still hypoglycaemic repeat (not glucagon) and recheck in 5-10mins
How can we treat severe hypoglycaemia if the patient is =conscious & able to swallow safely
- Check CPG if possible, if not assume hypoglycaemic
- Treat as for mild hypoglycaemia if possible
- Otherwise try glucogel 2 tubes ( squeeze between teeth & inner cheek if possible)
- Otherwise treat as for unconscious
- wait 10mins, if still hypoglycaemic repeat (not glucagon) and recheck in 5-10mins
What is important to ensure after treatment of hypoglycaemia
-Once recovered (>/= 3.5mmol/l (or 4mmol/l)) eat 15-20g long-acting/complex carbs eg
2 biscuits or 1 slice of bread
-Do not omit insulin injection if due (may need to reduce dose)
-Establish the cause to ensure it doesn’t happen again
