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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

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Michael mansfield diabetes consultant leeds teaching hospitals

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


Michael mansfield diabetes consultant leeds teaching hospitals

type 1 diabetes

type 2 diabetes

gestational diabetes

diabetes secondary to pancreatic disease

unknown / unclear

genetic diabetes

other


Michael mansfield diabetes consultant leeds teaching hospitals

MODY 3

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


Michael mansfield diabetes consultant leeds teaching hospitals

New units for glycated haemoglobin


Michael mansfield diabetes consultant leeds teaching hospitals

Umpierrez et al JCEM 2002, Memphis, Tennessee and Atlanta Georgia


Michael mansfield diabetes consultant leeds teaching hospitals

Baker et al Thorax 2006 St George’s Hospital London


Michael mansfield diabetes consultant leeds teaching hospitals

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.


Michael mansfield diabetes consultant leeds teaching hospitals

Training of staff

Links to and alerting of diabetes team

New and NHS-wide documentation

Importance of careful medicines reconciliation

IV insulin infusion safety

cannula

IV fluid

Insulin storage and insulin syringes


Michael mansfield diabetes consultant leeds teaching hospitals

National or local guidelines for:

DKA, HHS hypoglycaemia

surgery, endoscopy

hyperkalaemia

end of life

tube feeding

labour

steroids for fetal lung maturation

Capillary glucose monitoring and recording

Patient self-management/admin of insulin

“Sliding scales” and other insulin prescribing


Michael mansfield diabetes consultant leeds teaching hospitals

www.diabetes.nhs.uk


Michael mansfield diabetes consultant leeds teaching hospitals

withdrawn

(USA)

withdrawn

withdrawn

SGLT-2 inhibitors

oral

2012


Michael mansfield diabetes consultant leeds teaching hospitals

The incretin effect

oral glucose

IV glucose

oral glucose

IV glucose


Michael mansfield diabetes consultant leeds teaching hospitals

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


Michael mansfield diabetes consultant leeds teaching hospitals

DPP4 inhibitors


Michael mansfield diabetes consultant leeds teaching hospitals

NICE 2009


Michael mansfield diabetes consultant leeds teaching hospitals

The problem with…..

Metforminis bowel side effects, risk of lactic acidosis when eGFR decreased

Sulphonylureasweight gain and risk of hypoglycaemia

Insulinis weight gain, risk of hypoglycaemia, some driving restrictions

injections

Glitazonestake 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

Exenatideexpensive, nausea and vomiting in first months

injected, no long-term safety record, pancreatitis signal

Liraglutideeven more expensive, nausea and vomiting in first months

injected, no long-term safety record

pancreatitis signal, v weak thyroid malignancy signal

Dapaglifozinexpensive, genital thrush, no long-term safety record


Michael mansfield diabetes consultant leeds teaching hospitals

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

steroids

psychological stress

mental illness


Michael mansfield diabetes consultant leeds teaching hospitals

July 2012


Michael mansfield diabetes consultant leeds teaching hospitals

Key principles


Michael mansfield diabetes consultant leeds teaching hospitals

  • 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


Michael mansfield diabetes consultant leeds teaching hospitals

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


Michael mansfield diabetes consultant leeds teaching hospitals

Low circulating volume (NB intact thirst)

acute medical emergency including sepsis

surgical abdomen

hypoadrenalism (Addisons or suppressed HPA axis)

diuretics

ascites

nephrosis

congestive cardiac failure

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

sick cell syndrome

Redistribution of body water

hyperglycaemia


Michael mansfield diabetes consultant leeds teaching hospitals

Management

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


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