References

Ghorani E, Evans MI, Simmons D HHS in type 1 diabetes associated with medication overdose: can counter-regulatory hormone suppression prevent diabetic ketoacidosis?. Practical Diabetes. 2016; 33:(2)54-6

Hamblin PS, Topliss DJ, Chosich N, Lording DW, Stockigt JR Deaths associated with diabetic ketoacidosis and hyperosmolar coma. 1973-1988. Med J Aust. 1989; 151:(8)441-2

Hermes F, Valencia WM How to prevent the microvascular complications of type 2 diabetes beyond glucose control. British Medical Journal. 2017; 356

Pinhas-Hamiel O, Zeitler P Acute and chronic complications of type 2 diabetes mellitus in children and adolescents. The Lancet. 2007; 369:(9575)1823-9

Savage MW, Dhatariya KK, Kilvert A, Rayman G, Rees JAE, Courtney CH, Hilton L, Dyer PH, Hamersley MS Joint British Diabetes Societies, Joint British Diabetes Societies guideline for the management of diabetic ketoacidosis. Diabetic Medicine. 2011; 28:(5)508-15

Continuing Professional Development: Diabetes in pre-hospital care

02 March 2017
Volume 9 · Issue 3

Abstract

Overview

This CPD module aims to outline some of the complications a diabetic patient may present with in a pre-hospital setting. Diabetes Mellitus (DM) is a long term condition of high blood sugar. It is a condition of hormones, a condition of metabolism and a condition of inflammation. These multiple aspects give rise to various long term complications that the paramedic should be aware of. This module highlights the complexities that could present to paramedics when attending to a diabetic patient in pre-hospital settings.

LEARNING OUTCOMES

After completing this module the paramedic will be able to:

  • develop an awareness of the various complications linked to diabetes.
  • identify the key signs of diagnosis for diabetes.
  • know the tests to diagnose diabetic ketoacidosis in an out-of-hospital setting.
  • recognise the difference between diabetic ketoacidosis and hyperglycaemic hyperosmolar state.
  • If you would like to send feedback, please email jpp@markallengroup.com

    If ever there was a disease which could win an award for being complex, diabetes would definitely be up there. Diabetes Mellitus (DM) is a long term condition of high blood sugar. It is a condition of hormones, a condition of metabolism and a condition of inflammation. These multiple aspects give rise to various long term complications that the paramedic should be aware of.

    Insulin is required for uptake of glucose from the blood into the cells. There are a number of classifications of diabetes including type 1 diabetes mellitus (T1DM) where there is a lack of insulin production. There is a classification of Type 2 diabetes mellitus (T2DM) which was classically of mature onset, although with western diets, sedentary lifestyle and increased adiposity the mature aspect is seen as occurring much younger at diagnosis. T2DM is more linked to resistance of a cell to recognise and use the produced insulin.

    Gestational diabetes (GDM) is linked with pregnancy and is more common in the third trimester of pregnancy. Diabetes in pregnancy is associated with risks to the woman and to the developing foetus. Miscarriage, pre-eclampsia and pre-term labour is more common in women with pre-existing diabetes. In addition, diabetic retinopathy can worsen rapidly during pregnancy. Stillbirth, congenital malformations, macrosomia, birth injury, perinatal mortality and postnatal adaptation problems can occur. An unwell female who is pregnant should have diabetic ketoacidosis considered as a possibility.

    Cystic fibrosis (abnormality of chloride cells) which leads to thickened mucus, recurring infections, gut problems and a dysfunctional pancreas has its own associated form of diabetes called Cystic Fibrosis Related Diabetes (CFRD). This is of particular challenge as the malabsorption element of CF requires high calorie intake, where the diabetic patient needs to limit this. This tends to occur in the CF patient in the 30+ age range and is associated with increased earlier mortality. There are a number of other categorisation models and diabetes can occur secondary to a disease or process, such as surgical removal of the pancreas. The term pre-diabetes is a patient that is likely to become diabetic and their serum blood tests show a raised glucose level, but not enough to meet the threshold for full diagnosis (via a blood test called a HbA1c or fasting plasma glucose). These pre-diabetic patients have the opportunity to reverse modifiable risk factors and potentially prevent the onset of full diabetes.

    What are the cardinal signs of diagnosis for diabetes?

    There are four ‘Ts’ associated with diagnosis of diabetes which are toileting (polyuria), excessive thirst (polydipsia) – caused by dehydration, excessive tiredness and being thin (mostly in T1DM). Blurred vision is often an early sign due to lens dehydration, secondary to the polyuria.

    Long-term complications of diabetes

    There are a number of areas which put you at risk of developing diabetes. Having diabetes is a risk factor for diabetes-related complications and comorbid conditions. The research shows that diabetes that is poorly controlled increases the risk of developing blood vessel disease (macrovascular and microvascular), metabolic issues, end organ damage, problems with feet (peripheral neuropathy), eye disease (retinopathy), central nerve disease (neuropathy) and kidney disease (nephropathy) (Pinhas-Hamiel and Zeitler, 2007; Hermes and Valencia, 2017).

    Metabolic disturbances include diabetic ketoacidosis and hyperosmolar hyperglycaemic state (HHS) (Ghorani et al, 2016). Complications of taking diabetic tablets and insulin include hypoglycaemia (low blood sugar). We will discuss diabetic ketoacidosis and hyperglycaemic hyperosmolar state (HHS) in more depth later given its prevalence in the pre-hospital environment. Low blood sugar levels are rapidly fatal, whereas acidosis is eventually toxic.

    What other conditions are likely to be linked with diabetes?

    Linked co-morbidities

    There are a number of other diseases that are closely linked to, or a consequence of, diabetes. These include coeliac disease (gluten intolerance), thyroid disease, polycystic ovarian syndrome, mastopathy, musculoskeletal conditions (frozen shoulders, trigger fingers, carpel tunnel syndromes), dental issues as well as a skin condition called Necrobiosis Lipoidica Diabeticorum (NLD). Non-alcoholic fatty liver disease is common in the diabetic patient, as are fatty deposits elsewhere (increased visceral adiposity – ‘the spare tyre effect’). Cardiovascular disease associated with inflammatory processes and accelerated atherosclerosis puts patients with diabetes at massively heightened risk of myocardial infarction, stroke, claudication and other venothromboembolism disease. It is not clear whether tight sugar control can prevent this inflammatory response. Other cardiac related processes include diabetic cardiomyopathy as well as ‘silent MI’ derived from nerve damage (neuropathy). Cardiac risk is heightened by accelerated chronic kidney disease, where kidneys are responsible for blood pressure levels through hormonal regulation.

    Sugar levels to worry about

    Diabetic Ketoacidosis

    If we consider how our body gets energy, we can start to think about when this process goes wrong. We ingest carbohydrates (complex sugars) which are broken down to simple sugars, such as glucose. Glucose needs to get into the cells by the hormone insulin. Glucose is broken down through a process called glycolysis. It is metabolised into pyruvate and then into acetyl-Co-A. The acetyl-Co-A is entered into the Kreb cycle where through different metabolism processes and with the help of various enzymes various by-products are made, including an ATP-like usable energy source, as well as some lesser metabolites which can be used later. Where the body cannot enter glucose into the cells, this kreb process cannot happen and diabetic ketoacidosis (DKA) will occur. DKA is a complex disordered metabolic state characterised by hyperglycaemia, acidosis, and ketonaemia. DKA usually occurs as a consequence of absolute or relative insulin deficiency that is accompanied by an increase in counter regulatory hormones (i.e., glucagon, cortisol, growth hormone, catecholamines). This type of hormonal imbalance enhances hepatic gluconeogenesis (generation of sugar from non-carbohydrates) and glycogenolysis (breakdown of glycogen to glucose) resulting in severe hyperglycaemia but an alternative source of available fuel, albeit short lived. Enhanced lipolysis (fat breakdown) increases serum free fatty acids that are then metabolised as an alternative energy source in the process known as ketogenesis.

    As described energy is required for cellular processes and to not have these would lead to toxicity because of the alternative, but less friendly pathways that replace the Kreb cycle. An alternative source is sought and this is in the form of breaking down fatty acids and finding non-carbohydrate energy. The by-product ketones are acidic and lower the blood pH causing a metabolic acidosis. This toxic poison process will then cause a number of other symptoms such as abdominal pains (from the breakdown of fats), vomiting, drowsiness (acidotic poisoning) and eventual cerebral oedema and coma. Kussmaul respirations are deep sighs in a homeostatic attempt to balance the acidity, by breathing off more acidic CO2. Note the brain does not require insulin to use glucose, so there are fewer brain related symptoms in the early stages of diabetic ketoacidosis until the poisoning effect of acidosis takes place. The main causes of mortality in the adult population include severe hypokalaemia, adult respiratory distress syndrome, and co-morbid states such as pneumonia, acute myocardial infarction and sepsis (Hamblin et al, 1989).

    What assessment towards DKA can be made in the home?

    There are three diagnostic points to confirm a DKA which are a raised sugar above 11mmol/l, which can be obtained using a capillary blood glucose measurement (CBGM) in the pre-hospital environment. Raised ketones (>2+) on urine dipstick showing ketosis is the second criteria to be met. Some ambulance services carry urine dipsticks and some patients have ketone urine sticks at home. The third diagnostic feature is a blood pH level of <7.30 (normal range pH7.35-7.45). It is likely in the pre-hospital environment that you will be unable to assess blood pH. So the paramedic must suspect DKA in any patient who is unwell and their CBGM level is greater than 11 mmol/l. If you are unable to perform ketone testing to exclude DKA, then this patient must be admitted for exclusionary tests. Also keep in mind that the first presentation of the young diabetic (often teenage) is often a DKA, so a formal diagnosis of diabetes may not be known when the patient first presents to you. Many DKA's are missed in urgent care when they are the first presented, put down to impressions such as gastroenteritis or viral presentations. Paramedics who often see CBGM in the 20–30mmol/l range may be falsely reassured with a CBGM of 12mmol/l or similar and may just put it down to be ‘a little raised’. Do not be falsely reassured as this could still be a DKA. The triad of diagnostic features must be present for DKA diagnosis.

    Management of DKA

    There is universal agreement that the most important initial therapeutic intervention in DKA is appropriate fluid replacement followed by insulin administration. The main aims for fluid replacement are:

  • Restoration of circulatory volume
  • Clearance of ketones
  • Correction of electrolyte imbalance
  • Dehydration can be severe. For example, an adult weighing 70kg presenting with DKA may be up to 7 litres in deficit. This should be replaced as crystalloid, and consideration for starting this in the pre-hospital environment should be made. In patients with kidney failure or heart failure, as well as in the elderly and adolescents, the rate and volume of fluid replacement may need to be modified. The aim of the first few litres of fluid is to correct any hypotension, replenish the intravascular deficit, and counteract the effects of the osmotic diuresis with correction of the electrolyte disturbance. As well as water deficit, there is often a deficit of sodium, chloride and potassium.

    A fixed rate intravenous insulin infusion (FRIII) calculated on 0.1 units/kilogram body weight is recommended. Insulin has several effects, but the following are the most important when treating DKA:

  • Suppression of ketogenesis
  • Reduction of blood glucose
  • Correction of electrolyte disturbance
  • Hyperglycaemic hyperosmolar state (HHS)

    The hyperglycaemic hyperosmolar state (HHS) is a medical emergency. HHS is different from diabetic ketoacidosis (DKA) and treatment requires a different hospital based approach. HHS is associated with a significant morbidity and higher mortality than DKA and must be diagnosed promptly and managed intensively; with a suspicion from the paramedic greatly raising the chances of this being found (Savage 2011). Although typically occurring in the elderly, HHS is presenting in ever younger adults and teenagers, often as the initial presentation of type 2 diabetes mellitus (T2DM). It is linked with vascular complications such as MI or stroke as well as brain presentations such as seizure, cerebral oedema and central pontine myelinolysis (CPM).

    How does DKA and HHS differ in diagnosis?

    A precise definition of HHS does not exist. There are characteristic features that differentiate it from other hyperglycaemic states, such as DKA, and these are;

  • Hypovolaemia
  • Marked hyperglycaemia (30 mmol/l or more) without significant ketones or acidosis.
  • Osmolality usually 320mosmol/kg or more (hospital-based test)
  • To complicate things further, a mixed picture of DKA and HHS may occur. The goals of the treatment in HHS are to normalise the osmolality, replace the fluid and electrolytes lost, and normalise glucose levels. Prevention of complication such as thrombus, oedema or CPM is also important. The rate of rehydration will be determined by assessing the combination of initial severity and any pre-existing co-morbidities, but IV fluid replacement aims to achieve a positive balance of 3–6 litres by 12 hours, so could be started pre-hospital. Caution is needed, particularly in the elderly, where very rapid rehydration may precipitate heart failure, but insufficient rehydration may fail to reverse acute kidney injury.

    Pre-hospital assessment of this is difficult. To measure osmolality, you will need sodium levels, serum glucose levels and urea levels. Sodium Chloride 0.9% is the principle fluid used for correction, but a careful and timely reassessment of blood levels is important as well as monitoring oral fluid intake and urine output.

    Summary

    Diabetes mellitus is a long-term condition of high sugar. It is a condition of hormones, a condition of metabolism and a condition of inflammation. The complexities of complications extend to every organ of the body and have key effects on end organs, such as the brain, heart, liver and kidneys. There are two main complications of untreated high blood sugars which will lead to the patient becoming eventually toxic and developing reduced consciousness prior to death. DKA is a hyperglycaemic state which may have mild hyperglycaemia up to marked raised hyperglycaemia, but also has raised ketones and lowered blood pH. HHS is a condition more closely associated with T2DM and is characterised by very high sugar levels and hypovolaemia. The paramedic should be cautious not to miss a DKA or HHS diagnosis, and must remember that a formal diagnosis of diabetes may not have been made previously; you may encounter the patient at first ever presentation of these symptoms.