Diabetes emergencies Flashcards
1
Q
How can we categorize diabetic emergencies
A
- ) Hyperglycaemic emergencies
2. )Severe hypoglycaemia
2
Q
Outline hyperglycaemic emergencies
A
- ) DKA= diabetic ketoacidosis
2. ) HHS= hyperosmolar hyperglycaemic state ( previously known as HONK hyperosmolar non ketotic state)
3
Q
What is DKA
A
- 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
4
Q
How do our ketone levels increase?
A
- 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
5
Q
What are some osmotic consequences of DKA
A
-dehydration
-Disordered potassium
This is due to osmotic diuresis
This can cause the release of stress hormones
6
Q
What role can physiological stress have in the precipitation of DKA?
A
- 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
7
Q
Explain the disordered potassium that occurs as an osmotic consequence of DKA
A
- 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)
8
Q
What is ketonaemia?
A
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
9
Q
What happens to the K+ levels when DKA is treated?
A
-K+ moves rapidly into cells & because whole body k+ is deplete, extracellular k+ ( reflected in serum k+) falls very quickly
10
Q
What could be the cause of DKA?
A
- Infection
- Acute illness
- Poor compliance
- Newly diagnosed
- Failure of care
- Unknown
11
Q
What type of Diabetes is DKA classically associated with?
A
- 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
12
Q
What are the complications of DKA?
A
- 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
13
Q
What are the symptoms of DKA?
A
- 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?)
14
Q
Outline the signs of DKA
A
- Kussmaul respiration
- Ketotic factor
- Dehydration
- Tachycardia
- Hypotension
- Mild hypothermia
- Confusion, drowsiness, coma
15
Q
What bedside tests can be performed when investigating DKA?
A
- CBG
- Blood ketones( portable ketone meters) or urine ketones
- Venous blood gases
16
Q
What other investigations can be performed when investigating ketones
A
- Glucose/ U&Es( in testing for the electrolytes we are particularly looking for k+ & levels of dehydration
- FBC
- ECG
- CXR
- Blood culture
- MSU
17
Q
What are the principles of DKA treatment?
A
- 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
18
Q
what is the time frame of immediate management of DKA
A
Up to an hour
19
Q
How should the patient be assessed after fluids and insulin infusions
A
check RR; temp, BP, pulse, oxygen sat
- Use the Glasgow coma scale
- Undergo a full clinical examination
20
Q
What is important to do after all the clinical tests being performed and give an example
A
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
21
Q
What is HHS?
A
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)
22
Q
What is responsible for increased glucose, leading to osmotic diuresis & volume depletion?
A
-Insufficient fluid intake and/or drinking sugary drinks
23
Q
What are the complications of HHS?
A
- 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
24
Q
What are the clinical features of HHS
A
- Thirst, polyuria
- Blurred vision
- weakness
- dehydration
- tachycardia
- hypotension
- confusion & drowsiness
- coma
25
What bedside investigations for HHS can we perform?
- CPG
- Blood ketones ( portable ketone meters)
- urine ketones
- venous blood gases
26
What other investiagtions can we perform for HHS?
- Glucose/ U&Es/FBC
| - ECG,CXR,Blood culture,MSU
27
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)
28
Compare and contrast DKA with HHS
1. ) DKA=n T1DM (&T2DM) ; HHS=T2DM
2. ) HHS= older age
3. ) DKA = rapid onset (<24hr); HHS= days-weeks
4. ) DKA mortality<5%; HHS up to 15-20%
5. ) DKA ph<7.3 ; HHS= normal
6. )DKA bicarbonate= low ; HHS=normal
7. ) DKA= high ketones ; HHS=normal/ 1+
8. ) DKA= glucose>11mmol/L ; HHS Glucose= >30mmol/l
29
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
30
On a sick day for a T1DM patient, when is medical help required?
If...
- Vomiting/diarrhoea
- CBG not improving/ ketones persist
- Troublesome hypos
31
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)
32
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
33
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
34
Outline the progression of the consequecnes of hypoglycaemia
1. ) Hunger
2. ) Start of brain dysfunction
3. ) Neuroglycopenic symptoms, confusion, poor concentration etc
4. ) Coma/seizure
35
Why do T1DM patients struggle with hypoglycaemia counterregulation?
- They have no endogenous insulin
| - Glucagon response is impaired
36
What physiological methods of hypoglycaemic counteregulation exist
- Suppression of insulin secretion
- Glucagon release
- Adrenaline release & Sympathetic NS
- GH & cortisol
37
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
38
What are the autonomic symptoms of hypoglycaemia
- activation of ANS
| - swetaing/tremor/palpitations
39
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
40
What other symptoms may a hypoglycaemic patient present with?
- Hunger
| - Headache & nausea
41
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
42
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
43
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
44
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
