Diabetes management

Detailed management

Existing palliative care guidance for diabetes management at the end of life defines the approach depending on the prognosis of the patient. See the guidance below which gives specific guidance with prognoses of months, weeks to days, and last days of life

Within the hospice in patient unit setting, these forms can be held in the drug chart folder, to act as a prompt on managing the changing needs of a palliative diabetic patient. In this situation they can be used in conjunction with Diabetes monitoring chart for inpatients (Diabetes Downloads) on the reverse of the form, to act as both guidance and a place to record the CBG regimen and readings.

However, for hospital and community teams, these forms can simply act as a reference for some steps to consider when caring for these patients.

If it is felt that the patient has years to live, treatment would usually remain within national guidelines (See reference 1) and glycaemic targets should be individualised and potentially relaxed. Diabetes care should be provided by the primary or secondary care team, depending on patient need.

Type 1 Diabetes

Type 1 diabetes accounts for 5-10% of diabetes.

It is a disease of absolute insulin deficiency; therefore insulin withdrawal is likely to lead to death. Unless a patient is imminently dying, we would recommend the continuation of insulin, with the regimen simplified wherever possible, unless the patient specifies otherwise. CBG monitoring can also be reduced according to prognosis.

If a mentally competent patient requests withdrawal of their insulin, this should be respected but clinicians should first ensure that the patient is aware of the full implications. If such a request is because of undesirable symptoms such as pain and sickness, we should treat these and involve the palliative care team if not done so already.

Once the clinician has stopped the insulin either during the terminal phase of life or at the request of a mentally competent patient, CBG monitoring should cease as well.

The types of commonly used insulin are listed in the Diabetes Medication section.

Type 1 diabetes

Aim to be symptom free, CBG range 6 – 15. If CBG<4 treat as per hypoglycaemia guidance.

  • Follow patient’s normal glucose monitoring and insulin regimen.
      • If CBG <6 consider 20% reduction in basal insulin every three days until within target range
      • If CBG >15 consider 20% increase in basal insulin every three days until within target range
  • Check CBG if condition changes or unwell
      • Treat diabetic emergencies as per guideline (see DKA)
  • If oral intake reducing, reduce insulin regimen by 20% initially and then by 20% every 3 days until CBG within target range, to avoid hypoglycaemia
  • Aim to avoid hypoglycaemia, limit symptoms of hyperglycaemia (polyuria, thirst, nausea, vomiting, blurred vision) and avoid unnecessary monitoring
  • Consider switching insulin to OD regimen if not already done so (See Simplifying an insulin regime)
  • Check CBG pre-dinner
      • If <6 reduce insulin by 50%. If remains <6 reduce insulin by 20% daily until within range
      • If >15 increase insulin by 20% initially and then every three days until CBG within range
  • Consider reducing insulin levels in presence of reduced PO intake, weight loss, N+V and renal impairment.
  • Stop all rapid acting and pre-mixed insulin and change to long acting insulin at 50% of the preexisting basal insulin dose (See Simplifying an insulin regime)
  • If already on LA insulin reduce by 50%
  • Check CBG once daily
      • If 6-15 – continue at current dose and continue to monitor
      • If <6 reduce long acting insulin by 50% and continue to monitor
      • If >15 increase long acting insulin by 20% ad continue to monitor
  • If imminently dying and burden of injections and monitoring outweighs benefits, insulin can be stopped after discussion with patient (if possible) and/or family

REMEMBER: when commencing steroids, hyperglycaemia more likely. Consider increasing frequency of CBG monitoring and be aware of likely need to adjust insulin doses. For more information on management of steroid induced hyperglycaemia, see full Steroid induced diabetes guidance below.

Type 2 Diabetes

Type 2 diabetes accounts for 90% of diabetes.

It occurs when there is resistance to the insulin being produced by the pancreas. It can initially be managed with dietary modification and/or oral antidiabetic drugs. However, overtime the beta cells of the pancreas struggle to produce enough insulin and 20% of type 2 diabetics go on to develop insulin deficiency. Patients with type 2 diabetes can develop HHS or DKA.

The mechanism of action, dose range, efficacy and elimination route of non-insulin antidiabetic drugs for T2DM are listed in the Diabetes Medication section.

The types of commonly used insulin are listed in the Diabetes Medication section.

Refer to the details on this page on how to manage patients with T2DM in the last stages of life. Given the various ways in which T2DM can be treated, the detailed guidance is divided into:

T2DM: diet or taking non-insulin anti diabetic drugsSee Type 2 diabetes – diet or non-insulin anti diabetic drugs below (and references 1,3,6)

Gliclazide can be commenced at 40mg OD and be increased by 40mg every 3 days until the target CBG is achieved. Initially up titrate to 240mg in the morning and, if CBG still not in range, add 80mg in the evening (See reference 1).

Remember to check renal function before commencing/up titrating gliclazide to avoid prolonged hypoglycaemic episodes.

Metformin should be withdrawn if the creatinine is >150.
Additionally metformin can cause unpleasant side effects and a low threshold for withdrawal should be considered if there is any concern regarding side effects (nausea, heartburn, diarrhoea, flatulence) (See reference 1)

AND

T2DM: on insulinsee Type 2 diabetes – on insulin below (References 1,3,6)

Insulin provides rapid, effective and more predictable control, is easier to titrate, and has less risk of hypoglycaemia compared with some oral hypoglycaemics (10). It is a better choice in patients with: (see reference 11)

  • A short prognosis (<3 months)
  • Poor or erratic oral nutritional intake
  • Contra-indications to the use of oral hypoglycaemics
  • Severe symptoms from hyperglycaemia

Where the guidance refers to once daily insulin, the choice would be a long acting (LA) insulin, eg lantus/levemir.

See Simplifying an insulin regime for guidance on how to switch to a LA insulin from a pre-mixed or basal bolus regimen.

Type 2 diabetes – diet or non-insulin anti diabetic drugs

Aim to be symptom free, CBG range 6 – 15. If CBG<4 treat as per hypoglycaemia guidance.

  • Only check CBG if unwell or symptoms of hypo/hyperglycaemia. However, if on existing CBG monitoring regimen, can continue.
  • If oral intake reducing or variable consider reducing or stopping oral treatment
  • Commence treatment for confirmed persistent hyperglycaemia with symptoms
      • Gliclazide 40mg OD, increasing by 40mg increments to a max dose of 360mg/24hr ( be split depending on when hyperglycaemia is most problematic) until within range. Monitor predinner CBGs
      • OR Long acting insulin OM 0.2units per kg (or approx. 10 units) and increase by 20% every three days until within range. Monitor pre-dinner CBGs
  • Avoid metformin due to SE profile
  • If deteriorating renal function, review doses of oral diabetic medications (See Diabetes Medications)

Diet/Metformin

If admission CBG <15 don’t recheck unless symptoms of hyperglycaemia. If symptomatic hyperglycaemia identified, treat as above.

Consider stopping metformin

On oral hypoglycaemic medication:

  • Check CBG on admission, looking for hypoglycaemia if rapid decline
      • <6 consider stopping oral hypoglycaemics, or reduce by 50% and continue to monitor predinner CBG, checking more frequently if concern regarding persistent hypoglycaemia.
      • 6-15 monitor pre-dinner CBG
      • >15
          • increase gliclazide by 40mg increments to a max of 320mg/24hrs which can be split to 240mg OM and 80mg ON.
          • OR consider commencing long acting insulin OM at 0.2units per kg (or approx. 10 units) and increase by 20% every 3 days until within range. Monitor pre-dinner CBGs
  • No indication to treat high CBGs with rapid acting insulin. Instead either recommence or uptitrate hypoglycaemics/insulin. If concern regarding Hyperglycaemic Hyperosmolar State, refer to full HHS guidelines.
  • Stop all oral diabetic medication if not already done so
  • Stop all CBG monitoring

REMEMBER: if commencing steroids, hyperglycaemia is more likely to occur and uptitration of oral hyperglycaemics or switching to insulin may be necessary to maintain symptom control. Consider increasing CBG monitoring until CBGs are more stable. See full Steroid induced diabetes guidance below for more information and the management options.

Type 2 diabetes – on-insulin

Aim to be symptom free, CBG range 6 – 15. If CBG <4 treat as per hypoglycaemia guidance.

  • Follow patients usual blood monitoring regime
      • If CBG <6 consider withholding basal insulin for next 24-48 hours and reassess, or consider 50% reduction in basal insulin every three days until within target range
      • If CBG >15 consider 20% increase in basal insulin every three days until within target range
  • If oral intake reducing/variable consider adjusting regimen
  • Consider switching insulin to once daily regimen for simplicity (See Simplifying an insulin regime)
  • If acutely unwell check CBG and treat diabetic emergencies as per guideline.
  • Aim to avoid hypoglycaemia, limit symptoms of hyperglycaemia (polyuria, thirst, nausea, vomiting, blurred vision), and avoid unnecessary monitoring
  • Consider switching insulin to OD regimen if not already done so, especially if CBGs running low (See Simplifying an insulin regime)
  • Check CBG on admission, looking for hypoglycaemia if rapid decline
      • If <6 consider withholding basal insulin for next 24-48 hours and reassess, or reduce by 50%, until CBG in target range. Monitor pre dinner CBGs
      • If 6-15 monitor pre dinner CBGs
      • If >15 increase basal insulin by 20% every 3 days until within target range. Monitor pre dinner CBGs
  • Consider reducing insulin levels in presence of reduced PO intake, weight loss, N+V and renal impairment.
  • Stop insulin after discussion with patient (if possible) and/or family
  • Stop all CBG monitoring

REMEMBER: if commencing steroids, hyperglycaemia is more likely to occur and uptitration of insulin may be necessary to maintain symptom control.

When using long acting insulin in presence of steroids, consider increasing CBG monitoring to BD until CBGs more stable, as there is a small risk of early morning hypoglycaemia. See full Steroid induced diabetes guidance below for more information and the management options.

Steroid induced diabetes

Identifying steroid induced diabetes

The existing guidance for how best to screen for steroid induced diabetes is variable (See references 1,2,3,6,14). Pragmatically, the method used will depend on the care setting.

Guidance from Joint British Diabetes Societies (Reference 2) produced guidance for hospital inpatients which suggests first identifying those who are at high risk of developing steroid induced diabetes based on patient characteristics and venous blood sampling. The results inform risk stratification with various monitoring arms using CBGs. The guidance is for use for hospital in patients, encouraging tight glycaemic control and is logistically difficult to apply to a hospice or community setting.

A further guideline from Joint British Diabetes Societies and the UK Chemotherapy Board offers guidance for commencement of steroid therapy in the outpatient setting (See reference 14). This focuses on CBG monitoring at each appointment and offers advice of treatment arms dependent on results obtained.

This guideline recommends a pragmatic approach in the hospice and community settings, informed by the existing guidance and applied to a palliative population.

The aim is to capture those who are at risk of developing diabetes, and those who are previously undiagnosed. Commence treatment only in those who have a CBGs of >15 or are symptomatic.

See Diabetes Downloads: Steroid initiation/monitoring form, for the flow chart intended for the hospice setting. The flow chart is used whenever steroids are commenced or the steroid dose is increased.

The community setting can be particularly challenging when monitoring for steroid induced diabetes, predominantly due to the resources available and the logistics of who is responsible for testing and responding to results. If a CBG machine is available Diabetes Downloads: Steroid initiation/monitoring form, can be followed. The logistics of who would hold responsibility for the ongoing monitoring would depend on the local service framework and would need to be considered on an individual basis. If CBG testing is not possible for all those on steroids in the community, it may feel appropriate for the patient to have once weekly urine testing, looking for evidence of raised blood sugar. Urinary glucose sticks demonstrate high specificity (99.3) for ruling in patients with diabetes (See reference 15) , making it a useful test in this population. There exists no information to make a direct comparison of glucose stick results (ie trace, 1+ etc) to CBG values.

However, a pragmatic approach supports using a value of 1-2+ as a prompt to consider the development of steroid induced diabetes. In this situation, initiation of blood sugar monitoring with a home CBG machine and monitoring regimen should be considered.

As per (Diabetes Downloads) Steroid initiation/monitoring form, this would ideally be OD pre dinner, to establish whether anti diabetic medication may be required if readings >15 persist.

Steroid induced diabetes and hyperglycaemia is dose dependent (See references 11, 13, 14). It is therefore important to keep the steroid dose at the minimum effective.

When steroid levels are reduced, there may be a risk of hypoglycaemia. Insulin requirements are likely to decline in parallel (See references 11). Remember to review diabetic regimens when titrating steroids up or down.

Steroid Induced Diabetes/Hyperglycaemia

The use of steroids in high doses is common in advanced cancer.
These agents have a direct hyperglycaemic effect which starts 11 very early after ingestion, and can also increase appetite.

Steroids can cause ‘steroid induced hyperglycaemia’ in known diabetic patients. One in ten non-diabetics on steroids develop ‘steroid induced diabetes (See references 12,14). The hyperglycaemia in both conditions is dose dependent (See references 13,14)

Steroids cause an increase in blood sugar levels 4-8 hours after ingestion. This leads to peak blood glucose levels between lunch and dinner (See references 2,14). In the hospice setting we recommend testing CBGs pre-dinner to look for the resultant high CBGs, but they can be checked any time between lunch and evening meal.

if a patient takes steroids twice daily, the resulting hyperglycaemia is more likely to persist and be more consistent throughout the day and night (See references 2,14), although this can be hard to predict. In this situation, increasing CBG monitoring to TDS or QDS may be advisable.

However, given that there is no pharmacological benefit to splitting the dose of steroid (unless there is adrenal insufficiency) the recommendation is to give the full dose of steroid between once daily in the morning between 6am and 10am. This will minimise side effects, not only prolonged hyperglycaemia, but also HPA-axis suppression and insomnia.

In the type 1 and type 2 diabetes sections there are foot notes to encourage clinicians to consider the effect of steroids on diabetes control.

When faced with steroid induced hyperglycaemia in a known diabetic, uptitrating the existing regimen is a good place to start, taking into consideration when the hyperglycaemia is likely to be most problematic.

When faced with a new diagnosis of steroid induced diabetes, the options are gliclazide or insulin (See references 1,2,3,6,14) . Once the choice of drug is made, refer to Type 2 diabetes – diet or non-insulin anti diabetic drugs and Type 2 diabetes – on insulin for suggested uptitration regimens.

Initiating treatment for steroid induced diabetes (References 1,2)

Once Daily Steroid

Gliclazide: Once daily dose Uptitrate as per Type 2 diabetes – diet or non-insulin anti diabetic drugs above.

Insulin: Once daily intermediate insulin (See Diabetes Medications)

Twice Daily Steroid

Gliclazide: Not advisable.
OD regimen unlikely to be effective BD regimen leads to an increased risk of night time hypoglycaemia

Insulin: Once daily long acting insulin given in the morning BD intermediate insulin leads to an increased risk of night time hypoglycaemia

It is recognised that patients often move between OD and BD steroid regimens throughout an admission. Switching between various insulins based on the frequency of the steroid prescription could lead to confusion and complexity. It is advisable to respond to the pattern of hyperglycaemia observed rather than preemptively changing diabetic regimens based on the frequency of steroids. This illustrates the importance of increasing the frequency of CBG monitoring when on steroids. Contact the DSN for more support and guidance if needed.

Considerations if the patient is already on a more complex regimen

If the patient is on a twice daily insulin regimen, an increase the morning dose (10-20%) will be required to treat any pre-dinner hyperglycaemia. However, if on twice daily steroids, there may be some benefit in increasing the evening dose additionally (although caution may be required regarding night time hypoglycaemia) (See reference 1) . Aim to increase every 2-3 days until the CBG is within target range and increase CBG monitoring up to a maximum of QDS until more stable(See reference 2,3) . Contact DSN for more support and guidance in this complex scenario.

If the patient is on a basal bolus regimen, an increase (10- 20%) in the rapid acting insulin dose at breakfast and lunch may be required to treat the pre-dinner hyperglycaemia. The basal insulin may also need to be increased due to any persistent hyperglycaemia (See reference 2) . Aim to increase every 2-3 days until the CBG is within the target range and increase CBG monitoring up to a maximum of QDS until more stable (See reference 2,3) . Contact the DSN for more support and guidance in this complex scenario.

Optimisation of insulin delivery – move to steroid induced

Insulin delivery pens may need to be reassessed if the physical capabilities of patient alters or carers/family becomes involved in insulin delivery.

Similarly, any change to the insulin regimen should be implemented near the beginning of the week if at all possible.

If there is isolated hyperglycaemia avoid stat doses of short acting insulins such as Novorapid (see Target Setting in Background section). Instead, explore reasons for hyperglycaemia (consider DDDISH)

  • Have the Drugs of diabetes been modified (ie insulin reduced or metformin stopped)
  • Have Drugs causing diabetes been introduced (steroids, immunosuppressives, check point inhibitors)
  • Has the Diet been altered (nutritional supplements)?
  • Infection
  • Stress hyperglycaemia
  • HbA1c

If there is a persistent trend, maintenance therapy should be reviewed. The information above gives further detail on how to up titrate medications depending on the type of diabetes and estimated prognosis of the patient. A DSN can be involved if required.

Disclaimer (SPAGG - Rewrite)

This Guide is intended for use by healthcare professionals and the expectation is that they will use clinical judgement, medical, and nursing knowledge in applying the general principles and recommendations contained within. They are not meant to replace the many available texts on the subject of palliative care.

Some of the management strategies describe the use of drugs outside their licensed indications. They are, however, established and accepted good practice. Please refer to the current BNF for further guidance.

While WMPCPS takes every care to compile accurate information , we cannot guarantee its correctness and completeness and it is subject to change. We do not accept responsibility for any loss, damage or expense resulting from the use of this information.