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Michael Mansfield Diabetes Consultant Leeds Teaching Hospitals. New units for HbA1c Diabetes is relevant to in-patient care NHS diabetes resource Gliptins & GLP-1 analogs & SGLT-2 inhibitors End of life Sodium. type 1 diabetes type 2 diabetes gestational diabetes

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Michael Mansfield

Diabetes Consultant

Leeds Teaching Hospitals

New units for HbA1c

Diabetes is relevant to in-patient care

NHS diabetes resource

Gliptins & GLP-1 analogs & SGLT-2 inhibitors

End of life



type 1 diabetes

type 2 diabetes

gestational diabetes

diabetes secondary to pancreatic disease

unknown / unclear

genetic diabetes




Mutations of the hepatocyte nuclear factor 1α gene

Disordered insulin release

Autosomal dominant pedigree over 2, ideally 3 generations

Age of onset < 25 years in at least one family member

No need for insulin (or detectable C-peptide) in first 2-5 years after diagnosis

Progressive rise in glucose levels through life

Low renal threshold for glucose

Often very sensitive to sulphonylurea therapy

Permanent neonatal diabetes mellitus

Activating mutations of the KCNJ11 gene, which codes for the Kir6.2 subunit of the beta cell K-ATP channel.

Congenital impairment of insulin release

Mostly new mutations

Onset in first 3 (- 6) months of life but no immune markers of type 1 diabetes

Often responds well to sulphonylurea therapy


The Think Glucose programme provides a package of tried and tested products, learning and support to improve awareness and remove the obstacles to the treatment of patients with diabetes as a secondary diagnosis.

Implementing a clinical pathway will improve the patient experience and the quality of their care.


Training of staff

Links to and alerting of diabetes team

New and NHS-wide documentation

Importance of careful medicines reconciliation

IV insulin infusion safety


IV fluid

Insulin storage and insulin syringes


National or local guidelines for:

DKA, HHS hypoglycaemia

surgery, endoscopy


end of life

tube feeding


steroids for fetal lung maturation

Capillary glucose monitoring and recording

Patient self-management/admin of insulin

“Sliding scales” and other insulin prescribing






SGLT-2 inhibitors




The incretin effect

oral glucose

IV glucose

oral glucose

IV glucose


Satiety effect

reduced food intake

Increased glucose uptake

& glycogenesis

Slowed gastric emptying

Increased insulin release

Reduced glucagon release

Site of GLP-1 synthesis

Secretion increased after meals

Overview of GLP-1 physiology


The problem with…..

Metformin is bowel side effects, risk of lactic acidosis when eGFR decreased

Sulphonylureas weight gain and risk of hypoglycaemia

Insulin is weight gain, risk of hypoglycaemia, some driving restrictions


Glitazones take weeks to start working, expensive, very marked weight gain,

fluid retention and heart failure, distal bone fracture risk

Gliptins (DPP4 inhibitors) expensive, no long-term safety record

weak pancreatitis signal

Exenatide expensive, nausea and vomiting in first months

injected, no long-term safety record, pancreatitis signal

Liraglutide even more expensive, nausea and vomiting in first months

injected, no long-term safety record

pancreatitis signal, v weak thyroid malignancy signal

Dapaglifozin expensive, genital thrush, no long-term safety record


glucose control in diabetes at the end of life

altered nutrition

negative energy balance

weight reduction

reduction in physical activity

systemic humoral stress response

pancreatic destruction

renal impairment

liver destruction

loss of fat and muscle


psychological stress

mental illness


Aims for glucose levels:

  • No glucose level less than 6 mmol/L
  • No glucose level higher than about 15 mmol/L
  • Breaks down care in to 4 scenarios:
  • End of life but prognosis of more than 1 year
  • Prognosis in months
  • Prognosis in weeks
  • Prognosis in days

A few words on hyponatraemia

Always check for hyperglycaemia:

For every 3.5 mmol/L the glucose is high, sodium falls by 1 mmol/L

It’s all about the brain

Always look for timescale of sodium fall

Brain tolerates slow changes (up or down) remarkably well

SIADH is not the only cause, dehydration is common too

Assessment of patient’s circulating volume status is key

A cause for appropriate ADH release/activity excludes SIADH

If patient has been on steroids then suppressed HPA axis possible


Low circulating volume (NB intact thirst)

acute medical emergency including sepsis

surgical abdomen

hypoadrenalism (Addisons or suppressed HPA axis)




congestive cardiac failure

Normal or increased circulating volume syndromes of inappropriate ADH activity (secretion or receptor)

sick cell syndrome

Redistribution of body water




Usually not urgent unless the cause itself is emergency

Treatment obviously depends on the cause

In practice it often seems to self correct

May need treatment anyway if brain function impaired by sudden and/or severe fall:

ie neurological signs / seizures / reduced GCS

IV saline and in some exceptional circumstances hypertonic saline appropriate.

Aim for slow improvement in Na 5mmol/L in 12 hours.

Not much improvement needed to reverse brain dysfunction

Read this article:

Adrogue 2000 NEJM 342: 1851