Diabetic emergencies Flashcards
(85 cards)
1
Q
What is diabetic ketoacidosis?
A
Metabolic acidosis due to accummulation of ketone bodies in the serum of patients with (usually Type 1 diabetes).
2
Q
What causes DKA?
A
- Although there is excessive glucose in the bloodstream, a lack of insulin to prevents glucose up-take into cells
- The body is put in a starvation-like state where ketones are produced as an energy source
- Ketones are relatively strong organic acids and when present in high concentrations in the plasma, they cause a metabolic acidosis
3
Q
Why do patients with DKA have a fruity smelling breath?
A
- Acetone is volatile and can be excreted via the lungs - it has a fruity smell
- Acetone is one of the ketones produced in the body (the other 2 are acetoacetate and beta-hydroxybutyrate)
- Ketones are produced in response to the low insulin levels in the bloodstream in diabetes
4
Q
How does low insulin levels in the bloodstream result in ketone production?
A
- Low plasma/glucagon ratio activates lyase and inhibits reductase
- AcetylcoA is diverted to the pathway that produces ketones rather than cholesterol
5
Q
Where in the body are ketones produced?
A
Liver
6
Q
What is the typical presentation of DKA?
A
Gradual drowsiness, vomiting and dehydration in a Type 1 diabetic
7
Q
List 5 symptoms of DKA.
A
- unexplained vomiting
- abdominal pain
- polyuria
- polydipsia
- lethargy
8
Q
List 5 signs of DKA.
A
- Fruity smelling breath
- Weight loss
- Signs of dehydration - dry mucous membranes, reduced skin turgor
- Tachypnoea and deep breathing - Kussmaul hyperventilation
- Confused - deteriorating GCS (can result in coma)
9
Q
What is the diagnostic triad for DKA?
A
- Ketonaemia [>3mmol/L or significant ketonuria on dispstick (2+ on urine dipstick)]
- Hyperglycaemia [Blood glucose >11mmol/L or known diabetes mellitus]
- Acidaemia [venous pH<7.3 or bicarbonate<15mmol/L)
10
Q
What immediate bedsite test should you do in anyone presenting with unexplained vomiting, abdominal pain and drowsiness?
A
CAPILLARY BLOOD GLUCOSE
11
Q
How should you assess someone with suspected DKA?
A
A-E assessment
12
Q
What tests should you do in a patient suspected to have DKA?
A
- B - CXR
- C
- ECG
- Bloods - capillary and venous blood glucose, ketones, pH, FBC, U&Es, osmolality, blood culture
- E - dipstick and MSU for MC&S
13
Q
ABG or VBG in DKA?
A
VBG usually, only use ABG if reduced GCS or hypoxia
14
Q
Name 4 common triggers for DKA.
A
- Infection e.g. UTI, pneumonia
- Inadequate insulin treatment - non-compliance, insulin pump failure
- Surgery
- MI
15
Q
A patient fulfils the diagnostic criteria for DKA. They have a GCS<12 and hypokalaemia on admission. What are your next steps.
A
- GCS<12 and hypokalaemia are features of severe DKA
- This may require admission to HDU/ITU and insertion of a venous central line
- Therefore, GET SENIOR HELP IMMEDIATELY
16
Q
Name 3 features of DKA that would prompt immediate senior review.
A
- Blood ketones greater than 6mmol/L
- Bicarbonate less than 5mmol/L
- Venous/arterial pH less than7.0
- Hypokalaemia( lessthan3.5mmol/L) on admission
- GCS less than 12 or abnormal AVPU or NEWS* >6
- Oxygen saturation less than 92% (assuming normal respiratory baseline)
- Systolic BP less than 90mmHg
- Pulse greater than 100 or less than 60 bpm
- Anion gap greater than 16 N.B. Anion gap = (Na + K) – (Cl + HCO3)
(The above are all features of severe DKA)
17
Q
What are the fundamental principles in the management of DKA?
A
- replacement of fluid deficit
- insulin treatment
- monitoring and maintaining electrolyte/potassium balance in a safe environment
- avoiding complications of treatment
18
Q
What are the commonest causes of death associated with DKA?
A
- cerebral oedema - especially in children and adolescents
- hypokalaemia
- ARDS
- co-morbid conditions e.g. pneumonia
- acute MI
- sepsis
19
Q
What serious complications can arise during the management of DKA as a result of treatment?
A
- insulin
- hypokalaemia
- hypoglycaemia
- fluid replacement
- cerebral oedema
- pulmonary oedema
- potassium replacement
- hyperkalaemia
20
Q
Which groups of patients with DKA require extra caution in their care and management to avoid complications?
A
- young perople 16-25 years
- elderly >70 years
- pregnant
- cardiac or renal failure
- other serious comorbidities
21
Q
You are the junior doctor in A&E. You have clerked a patient with suspected DKA. Their NEWS score is stable. What are your next steps?
A
Initiate treatment and immediate senior review
(If NEWS indicated senior review sooner, then senior review immediately before initiating treatment)
22
Q
You have clerked a patient in A&E with DKA. You have completed your A-E assessment and requested the relavent tests. What are your initial steps in managing this patient?
A
- Use the correct prescription chart e.g. Adult diabetic ketoacidosis prescription chart
- STEP 1 - insert large bore IV cannula and commence IV 0.9% sodium chloride 1000ml/hr (circle 1000 on prescription chart and sign name)
- STEP 2 - 10 units ActRapid if likely to be delay of longer than 15mins from diagnosis of starting IV insulin (sign name next 10 units of soluble insulin SC)
- STEP 3 - Potassium is often high on admission but falls rapidly with insulin, check VBG and add 20mmol/500ml potassium to infusion as necessary
- STEP 4 - Commence IV fixed rate insulin - 0.1units/kg/hr (if 70kg then put 7 in the initial rate box and sign name)
23
Q
You have commenced initial management of DKA with 1 litre of 0.9% sodium chloride over an hour and IV fixed rate insulin infusion. What are the next steps?
A
- Senior review
- Monitor patient closely
- Review the IV fluid regimen based on the patient’s clinical and biochemical assessment
- Consider precipitating causes and treat appropriately
- VTE prophylaxis
- Refer to Diabetes team
24
Q
Describe how you would monitor a patient with DKA.
A
- Biochemistry
- Capillary blood glucose and ketones hourly
- VBG for potassium and pH hourly then 2 hourly
- Clinical assessment
- Regular assessment of GCS and vital signs
- Regular assessment of fluid status, monitor input/output
- Cardiac monitoring if severe DKA
25
What is resolution of DKA defined as?
* Blood ketones \<0.6mmol/L
* Venous pH \>7.3
26
You are managing a patient with DKA. The patient is vomiting and drowsy despite initial management. What will you do next?
* Senior review
* Consider NG tube
27
When prescribing fluids in DKA, what should you tailor the fluid prescription to?
* Hypoglycaemia - when blood glucose \<14mmol/L prescribe 10% glucose 500ml alongside sodium chloride
* Hypokalaemia - when potassium 3.5-5.5 add 20mmol/500ml K+ to sodium chloride
* Fluid status - monitor for fluid overload and cerebral oedema (any sudden deterioration in GCS is likely to be cerebral oedema)
28
What would you expect to see for WCC and Na+ blood results in DKA?
High wcc may be seen in the absence of infection.
Hyponatraemia is common, due to osmolar compensation for the hyperglycaemia. ↑ or ↔ [Na+] indicates severe water loss. As treatment commences Na+ rises as water enters cells.
29
Does ketonuria always indivate ketoacidosis?
Ketonuria does not equate with ketoacidosis. Anyone may have up to ++ketonuria after an overnight fast. Not all ketones are due to diabetes—consider alcohol if glucose normal. Always check venous blood ketones.
30
How should you investigate for infection as a cause of DKA?
Often there is no fever. Do msu, blood cultures, and cxr. Start broad-spectrum antibiotics (eg co-amoxiclav, p[link]) early if infection is suspected.
31
Why do we continue to treat DKA when glucose is \<14mmol/L?
Blood glucose may return to normal long before ketones are removed from the blood, and premature termination of insulin infusion may lead to lack of clearance and return to dka. This may be avoided by maintaining a constant rate of insulin infusion (with co-infusion of glucose 10% to maintain plasma glucose at 6–10mmol/L) until blood ketones \<0.6mmol/L and pH \>7.3.
32
Pancreatitis can trigger DKA. Is amylase helpful in determining whether pancreatitis is the trigger?
In DKA, serum amylase is often raised (up to ×10) and non-specific abdominal pain is common, even in the absence of pancreatitis.
33
Once DKA is resolved according to biochemical parameters and patient is feeling better. The patient is due her lunch. How do you stop the fixed rate insulin infusion?
Ensure she takes her subcutaneous rapid-acting insulin before her meal. Then stop the FRII 30-60 mins after S/C insulin.
(This is because the half-life of IV insulin is only 3-4 mins and subcutaneous insulin may take considerably longer to be absorbed)
34
When treating DKA, what should you with regards to the patients usual insulin regime?
* **CONTINUE** long acting or intermediate acting insulin with FRII
* Stop the fast-acting meal-time insulin until FRII is stopped
35
In a newly diagnosed diabetic patient, what should you ensure before stopping the FRII in DKA?
They should be established on some form of background/long acting insulin - the diabetes team will start this
36
capillary blood ketones
VBG - pH, bicarbonates
37
A patient is diagnosed with DKA.
## Footnote
The patient is now able to tell you that she has type 1 diabetes and her usual treatment is:
• Tresiba 18 units at bedtime (Flextouch device) and Novorapid 6 units at mealtimes (Flexpen device)
Which of these insulins will you continue whilst treating the DKA? Why?
Tresiba 18 units at bedtime (Flextouch device)
Continuation of subcutaneous analogues during the initial management of DKA provides background insulin when the IV insulin is discontinued. This avoids rebound hyperglycaemia when IV insulin is stopped 49 and should avoid extending the length of stay.
38
How does hypoglycaemia typically present?
Usually rapid onset; may be accompanied by odd behaviour (eg aggression), sweating, ↑pulse, seizures.
39
How is hypoglycaemia diagnosed?
diagnosis only if Whipple’s criteria are met:
Plasma glucose \<3mmol/L
Symptoms or signs of hypoglycaemia
Resolution of symptoms or signs post glucose rise
40
What are the common causes of hypoglycaemia in diabetic patients?
Increased their physical activity
Missed a meal
Insulin overdose – accidental/non-accidental
Sulphonylurea treatment
41
What are the main causes of hypoglycaemia in non-diabetics?
**ExPLAIN**
Exogenous drugs e.g. insulin, oral hypoglycaemics, alcohol binge with no food
Pituitary insufficiency
Liver failure
Addison’s disease
Islet cell tumours (insulinoma) and immune hypoglycaemia
Non-pancreatic neoplasms e.g. fibrosarcoma
42
How can the symptoms of hypoglycaemia be divided?
Autonomic – Sweating, Anxiety, Hunger, Tremor, Palpitations, Dizziness
Neuroglycopenic – Confusion, Drowsiness, Visual trouble, Seizures, Coma, Personality change, Restlessness, Incoherence (can lead to misdiagnosis of alcohol intoxication or psychosis
43
Which patients have an increased risk of hypoglycaemia and may not exhibit the typical autonomic features of hypoglycaemia?
Patients taking beta blocker therapy may not exhibit the sign of symptoms hypoglycaemia predominantly mediated by the sympathetic nervous system. Beta blockers also inhibit hepatic gluconeogenesis and will increase the risk of hypoglycaemia
44
A patient presents with hypoglycaemia and treatment is initiated. Do any further investigations need to be carried out?
Investigations are not usually required if the patient is taking hypoglycaemic agents
Check drug history and rule out liver disease
If the patient is seen at the time of hypoglycaemia, it is essential to take a laboratory sample for glucose to confirm the diagnosis as BMs can be inaccurate (grey bottle)
Baseline bloods - FBC, U&Es, LFTs, Calcium, TFTs, 9am cortisol
45
How should hypoglycaemia be managed if the patient is conscious.
1. Give patient 15-20g quick acting carbohydrate e.g. 150-200ml orange juice
2. Test blood sugar after 10-15mins. If 4mmol/L or above and better move on to third step. If not, repeat first step up to 3 times.
3. Eat main meal containing carbohydrate
46
How should hypoglycaemia be managed if the patient is unconscious?
ABCDE approach
1mg IM glucagon injection
If unresponsive in 10mins, IV 10% glucose infusion 200ml over 15 mins
47
How should a patient with hypoglycaemia be managed if they are conscious but confused and unable to swallow?
1.5-2 tubes of glucogel squeezed into the mouth between teeth and gums
48
If blood glucose remains \<4mmol/L after 3 cyles of oral glucose, what are the next steps?
Ask for senior support
1mg IM glucagon injection
If hypoglycaemia unresponsive to glucagon after 10 mins, give Glucose IV infusion. If conscious - 10% at 200ml/hour
49
What should be given once hypoglycaemia resolves?
Long-acting carbohydrate
* 2 biscuits
* a slice of bread/toast
50
How can hypoglycaemia be avoided?
If episodes are often, advise many small high-starch meals
In diabetics, rationalise insulin therapy - refer to diabetic team
51
* Work out serum osmolality (2Na + Gluc + Ur) = 354.2
52
What is the diagnosis
Hyperosmolar hyperglycaemic state (HHS)
53
What is hyperosmolar hyperglycaemic state?
no precise definition, but characteristic features that differentiate it from other hyperglycaemic states like DKA are:
* Hypovolaemia
* Marked hyperglycaemia (\>30mmol/L) without significant hyperketonaemia (\<3mmol/L) or acidosis
* Osmolality usually 320mosmol/kg or more
54
Describe the typical presentation of HHS.
Seen in unwell patients with type 2 DM. The history is longer (eg 1wk), with marked dehydration and glucose \>30mmol/L
55
What triggers HHS in patients with type 2 DM?
* Intercurrent or co-existing illness
* Infection - UTI, pneumonia, cellulitis
* Stroke
* PE
56
Name 5 symptoms of HHS.
* Frequent urination
* Thirst
* Nausea or vomiting
* Confusion
* Fatigue
57
Name 3 signs of HHS.
* Dry mouth and skin
* Tachypnoea
* Hyperglycaemia
58
What are the complications of HHS?
Vascular occlusive complications are most common- MI, stroke, peripheral arterial thrombosis (give lmwh prophylaxis to all unless contraindication)
Neurological complications are less common - seizures, cerebral oedeam, central pontine myelinolysis
59
What are the goals of treatment of HHS?
treat the underlying cause and to gradually and safely:
Normalise the osmolality
Replace fluid and electrolyte losses
Normalise blood glucose
Other goals include prevention of:
Arterial or venous thrombosis - **LMWH**
Other potential complications e.g. cerebral oedema/central pontine myelinolysis
Foot ulceration
60
What serious complications may arise during the management of HHS as a result of treatment?
a) Hypo or hyperkalaemia
b) Hypoglycaemia
c) Cerebral oedema
d) Pulmonary Oedema
e) Central pontine myelinolysis
61
A patient has been diagnosed with HHS. How would you initiate management?
A-E assessment
Insert large bore IV cannula
Prescribe in **adult HHS prescripton chart**
Commence **IV 0.9% sodium chloride – 1 litre over 1 hour** (circle 1000ml and sign name in first box)
Caution in the elderly where too rapid rehydration may precipitate heart failure but insufficient may fail to reverse acute kidney injury
62
Should insulin be routinely prescribed in patients with HHS?
**NO**
Only commence insulin infusion (0.05 units/kg/hr) IF there is significant ketonaemia (3β- hydroxybutyrate (blood ketone level) greater than 1 mmol/L) or ketonuria 2+ or more (i.e., mixed DKA and HHS picture)
63
You have completed an A-E assessment in a patient with HHS and have initiated treatment with fluid replacement. What else should you include in your clinical assessment?
Examine for source of sepsis (e.g. foot ulcer/cellulitis) or evidence of vascular event (as a result of increased osmolality)
64
What initial investigations should be requested in a patient with HHS?
* B - CXR
* C - ECG, VBG, Bloods (blood glucose, U&Es, osmolality), blood cultures if indicated
* D - capillary blood glucose
* E - capillary blood ketones, urine dip and MSU for culture
65
How quickly do you want Na+ to fall after initiating treatment in a patient with HHS?
The rate of fall of plasma Na+ should not exceed 10mmol in 24 hours
66
What is the risk of correcting plasma osmolality too quickly in a patient with HHS?
Cerebral oedema
67
When prescribing fluids in HHS, what should you base your prescription on?
* Clinical assessment - examine patient for fluid overload, check fluid balance
* Biochemistry
* If osmolality not falling, then increase rate of sodium chloride
* If osmolality falling too wuckly, then reduce rate of IV fluds
68
What should you do if blood glucose is falling at a rate \<5mmol/L/hr after initial management of HHS?
* Increase rate of infusion of 0.9% sodium chloride in inadequate
* Commence low dose IV soluble insulin (0.05units/kg/hr)
69
What are the similiarities and differences in management of DKA and HHS?
* Both treated with 1 litre of 0.9% saline initially
* Fluids tailored to fluid balance, blood glucose (add glucose 10% if \<14mmol/L) and potassium (add 20mmol/500ml if 3.5-5.5)
* FRII is started immediately in DKA, FRII is only indicated if ketonaemia at presentation or blood glucose falling at rate \<5mmol/L/hr despite fluids
* Long-acting insulin is continued while on FRII in DKA. Long-acting insulin is discontinued while on FRII in HHS (other diabetic treatments can be continued)
70
A patient is diagnosed with HHS.
## Footnote
This patient has an eGFR of 28 and takes both metformin and empagliflozin
What are the main recognised risks of continuing both of these?
* Metformin - lactic acidosis
* Empagliflozin - risk of DKA with dehydration and increased insulin requirements
71
How does HHS affect the long-term management of the patient's DM?
Most patients require regular insulin treatment on discharge
72
Wjat are the 6 Rs of a safe insulin prescription?
73
What should you do everytime you prescribe insulin or a sulphonylurea?
pre- prescribe anticipatory treatment for hypoglycaemia and a bedtime snack to help prevent hypos at night (50% of hospital hypos happen at night)
74
How should an insulin regime be revised if a patient is having recurrent hypos?
Review CBG daily and reduce doses of insulin (by 20%) or SU (by 50% or stop) if concerned re: hypo risk – be pro-active rather than reactive
Night-time is high risk and so often the insulin/SU at tea-time needs reducing
75
Who is at an increased risk of hypos in hospital?
Elderly patients with an HbA1c \<7.0% who take insulin/SU are at increased risk of hypos in hospital – review/reduce their meds to prevent hypos
76
On day 10 (whilst awaiting placement in a care home) Mr AB develops signs and symptoms of sepsis (? HAP). He has Type 2 diabetes.
He is unable to eat and drink and his CBGs have risen to between 12.3 – 24.6 over past 24 hrs.
You have excluded DKA and HHS by checking pH, bicarb, ketones and osmolality.
How will you manage his hyperglycaemia?
VRIII
77
What fluid needs to be prescribed alongside a VRII?
**VRII should NEVER be administered without IV dextrose**
This prevents hypoglycaemia
78
Should long-acting insulin be continued whilst on VRIII?
YES (remember that for patients undergoing surgery or fasting procedures, background insulin is reduced by 20% while on VRIII
79
How should a patient be monitored while on VRIII?
* Check CBG hourly (only reduce to 2 hourly if the patient is stable after 12 hours)
* Review infusion rate hourly
* Aim for CBG range 6-10mmol/L
80
What do you do if a patient on a VRIII becomes hypoglycaemic?
* Stop VRIII
* Treat hypoglycaemia according to Trust guidelines
* Re-start VRIII when CBG \>4MMOL/l
* If recurrent hypos then reduce insulin doses in infusion scale or use 10% dextrose as substrate fluid
81
If not managed appropriately, stopping VRIII is high risk of DKA in Type 1 diabetes. How can you prevent this?
* VRIII discontinuation should be well planned and switch over should be at meal time
* Ensure usual treatment has been prescribed and administered
* Ensure 30-60 min overlap between adminstration of usual diabetes medication and stopping VRIII
* Monitor CBG regularly minimum 4 hourly if patient is still in hospital
82
Who is at high risk of euglycaemic DKA?
people with diabetes with covid-19, on SGLT2i or if pregnant
83
What increases the risk of the rare but serious complication, lactic acidosis?
A rare but serious complication of dm with metformin use or septicaemia. Blood lactate: \>5mmol/L. Seek expert help. Treat sepsis vigorously, maintain blood pressure and hence tissue perfusion. Stop metformin.
84
What substrate is most commonly used with VRIII?
National guidance recommends (depending on the potassium requirement):
0.45% NaCl with 5% glucose and 0.15%KCl (20 mmol/L)
or 0.45% NaCl with 5% glucose with 0.3% KCl (40 mmol/L)
85
What are the indications for VRIII?
Vomiting (exclude DKA and HHS)
Nil by mouth and will miss more than one meal
Severe or acute illness with need to achieve good glycaemic control e.g. sepsis
When indicated following Hyperglycaemia Decision support tool
