LEARNING OUTCOMES
After completing this module, the paramedic will be able to:
You are called to attend a 19-year-old female known diabetic, who has had episodes of vomiting and retching for the past hour. Her mother explains that she usually becomes unwell during her menstrual cycle, when her blood sugar rises, which is normally well controlled by her insulin. Today she has persistent episodes of nausea and vomiting. Her baseline observations are as follows:
According to the World Health Organization (WHO) (2018a), diabetes is a chronic, metabolic disease characterised by elevated levels of blood glucose, which leads over time to serious damage to the heart, blood vessels, eyes, kidneys, and neurones. The most common is type II diabetes, usually in adults, which occurs when the body becomes resistant to insulin or does not make enough insulin. In the past three decades, the prevalence of type II diabetes has risen dramatically in countries of all income levels (WHO, 2018b).
In 2016, 422 million people were diagnosed as having the condition worldwide, up from 108 million in 1980 (WHO, 2018a). Global occurrences of diabetes in adults over 18 years old rose from 4.7% in 1980 to 8.5% in 2016 (WHO, 2018a).
An estimated 1.6 million deaths in 2016 were directly caused by diabetes. WHO estimates that diabetes was the seventh leading cause of death in 2016 (WHO, 2018a; 2018b).
According to the National Institute for Health and Care Excellence (NICE) (2015), diabetes, type II in particular, increases the risk of health problems like heart disease, stroke and kidney failure. If people know they are at risk, they can often prevent or delay diabetes by making healthy changes to their diet and lifestyle. This is the focus of the NHS Diabetes Prevention Programme. For people from certain ethnic communities (e.g. South Asian), the risk increases at an earlier age and at a lower body mass index level, so requires particular attention to prevent type II diabetes.
In the critical/emergency situation, type I and type II diabetes are associated with diabetic ketoacidosis (DKA) and hyperglycaemic, hyperosmolar syndrome (HHS), respectively. In order to treat either of these two medical emergencies, an understanding of the pathophysiology of diabetes is necessary.
Physiology of blood glucose control
Glucose (a carbohydrate) is one of the body's principal fuel sources, with the majority coming from ingested food. Foods particularly high in glucose include starch-rich foods such as potatoes, rice, bread, and pasta (Kamel et al, 2016).
In the small intestine, glucose is absorbed into the blood and travels to the liver via the hepatic portal vein. The hepatocytes (liver cells) absorb much of the glucose and convert it into glycogen, an insoluble polymer of glucose. This glycogen is stored in the liver and can be reconverted into glucose when blood glucose levels fall (Kitabchi, 2009).
The control and maintenance of blood glucose levels are regulated by the pancreas. The pancreas itself is a heterocrine gland as it has both endocrine and exocrine characteristics. Exocrine refers to the secretion of substances by way of a duct to an epithelial surface, while endocrine refers to the secretion of hormones into the circulatory system to target a distant organ. While the exocrine function plays a role in digestive glucose production, mentioned earlier, the endocrine function is of primary concern in glucose homeostasis. The endocrine tissue within the pancreas responsible for blood sugar maintenance is the Islets of Langerhans, which are divided into five subsets:
While all five subsets of cells within the Islets of Langerhans secrete hormones that play important roles in metabolism and growth, alpha and Beta cells play the primary roles in glucose maintenance and homeostasis (Mitchell and Medzon, 2005).
After glucose is ingested and subsequently absorbed, there is an increase in blood glucose levels. This increase is detected by the beta cells of the pancreatic islets, causing them to increase the release of insulin. Insulin stimulates cells, especially adipose and muscle cells, to take up glucose from the bloodstream.
Conversely, several hours after the absorption of glucose, in what is termed a post-absorptive state, blood glucose levels fall, along with those of insulin. This state results in the hormone glucagon being released by the alpha cells of the pancreas. Glucagon has the opposite effect to insulin in that it increases blood glucose levels.
It is therefore the case that beta and alpha cells, together with their respective hormones (insulin and glucagon) regulate blood glucose levels (Gosmanov et al, 2018).
Diabetes is a complex metabolic disorder of glucose metabolism regulation and is associated with an increased risk of microvascular and macrovascular disease (Robert et al, 2015). The two main types of diabetes, along with their associated acute clinical complications, are discussed in the next section but what is important to acknowledge here is that the main clinical characteristic of diabetes is hyperglycaemia; the fundamental ‘problem’ in diabetes is an inadequate control of blood glucose levels (Handelsman et al, 2016).
Pathophysiology of diabetes
Until recently, and since 1979, the two types of diabetes have been classified as ‘type I’ and ‘type II’. These replaced the former ‘insulin-dependent’ (type I) and ‘non-insulin-dependent’ (type II) terms previously used.
Type I diabetes is an autoimmune disease that causes the insulin-producing beta cells in the pancreas to be destroyed, preventing the body from being able to produce insulin, thus preventing adequate blood glucose control (Robert et al, 2015). In the more common type II diabetes, the pathophysiological mechanism is either that the pancreas produces some (but not enough) insulin or that cells become resistant to the action of insulin, or both (Rosenstock and Ferrannini, 2015). The causes of type II diabetes are not fully understood but are thought to involve genetics, environmental factors, age, diet and obesity (Dalfrà et al, 2016).
It is worth noting that Zaccardi et al (2016) maintain that in the last 10 years, the limitation of a simple distinction between ‘type I’ and ‘type II’ diabetes has been increasingly recognised, with many patients now showing the coexistence of insulin resistance and immune activation against b-cells. However, a full exploration of this ‘coexistence of type I and type II diabetes’ is outside the scope of this paper.
Pathophysiology of diabetic emergencies
Evidence shows that DKA HHS are associated with ‘type I’ and ‘type II’ respectively (Gosmanov et al, 2014). Both are classified as ‘hyperglycaemic emergencies’ that derive from either an absolute or relative insulin deficiency (Eledrisi et al, 2006; Dalfrà et al, 2016). Thus, the basic cause of DKA and HHS is insufficient insulin effect.
DKA is mainly a complication of type I diabetes (Rosenstock and Ferrannini, 2015). DKA is characterised by hyperglycaemia, hyperosmolality, ketoacidosis and volume depletion, and has mortality of between 2–5% (Al-Jaghbeer and Kellum, 2015). According to Gosmanov et al (2014) and Dalfrà et al (2016), along with insulin deficiency, increased insulin counter-regulatory hormones (cortisol, glucagon, growth hormone, and catecholamines) and peripheral insulin resistance also contribute to the development of severe hyperglycaemia, severe intracellular dehydration, ketosis, and electrolyte imbalance—all of which should be considered in the pathophysiology of DKA.
The specific acidosis mechanism seen in DKA is caused by free fatty acids. Because there is increased lipolysis and decreased lipogenesis, this results in the production of free fatty acids, which are then converted to acidic ketone bodies: b-hydroxybutyrate (b-OHB) and acetoacetate, with these then causing acidosis (Basnet et al, 2014).
Hyperglycaemia results in a rise in the blood's osmotic pressure, leading to glycosuria and osmotic diuresis; that is—increased urination due to the presence of glucose in the fluid filtered by the kidneys. The hyperosmolar state seen in DKA also causes intracellular dehydration and a global fluid deficit (Gosmanov et al, 2018). The resultant hypovolaemia is of particular concern for paramedics and emergency department staff (Cardoso et al, 2017; Fadini et al, 2017).
A diagnosis of DKA can be made using the following diagnostic criteria: presence of blood hyperglycaemia of >8 mmol/litre, acidosis with an arterial pH of ≤7.30, a bicarbonate level of ≤18 mEq/litre, and adjusted for albumin anion gap of >10–12 (Benoit et al, 2018). Although paramedics do not currently undertake blood gas analysis, the patient history, clinical presentation and blood glucose measurement should be enough to diagnose a hyperglycaemic emergency and DKA.
HHS, characterised by marked hyerglycaemia, hyperosmolality and severe dehydration, is usually associated with type II diabetes, and presents with minimal lipolysis and ketoacidosis (Al-Jaghbeer and Kellum, 2015; Kamel et al, 2016; Cardoso et al, 2017). It has a slower onset than DKA and mortality rate ranges from 10–35%. The reason why hyperosmolar, non-ketotic syndrome (HONK) was renamed hyperglycaemic, hyperosmolar syndrome (HHS) is because a small sub-set of patients with type II diabetes, and who develop HHS, do experience some form of (mild) ketoacidosis (Gosmanov et al, 2018; Lindner et al, 2018). Thus, hyperglycaemic hyperosmolar syndrome better reflects the condition's pathophysiology. Because acidosis is not usually present in HHS, the main pathophysiological mechanism leading to patient collapse is osmotic diuresis-induced intravascular and intracellular fluid depletion (Kamel et al, 2016; Benoit et al, 2018). As mentioned, hyperglycaemia-induced hypovolaemia is of particular concern for paramedics and staff in the emergency department (Cardoso et al, 2017; Fadini et al, 2017).
Paramedic management of DKA/HHS
The goals for treating hyperglycaemic emergencies such as DKA and HHS include:
Currently all paramedics in the UK do not routinely administer insulin, but fluid replacement can mitigate against the hyperglycaemic environment. Indeed, one of the most important initial interventions made by the paramedic, in hyperglycaemic emergencies, is appropriate fluid replacement. This can then be followed by insulin administration in the emergency department. In terms of paramedic interventions(s) for hyperglycaemic emergencies, the following is recommended (NICE, 2015):
The aim of fluid replacement is re-establishment of circulatory volume, ketone clearance and electrolyte imbalance correction. The fluid of choice is a crystalloid, generally 0.9% Sodium Chloride with the aim to correct any hypotension, replenish the deficit in intravascular volume, and correct the electrolyte disturbance as a result of the osmotic diuresis. Sodium Chloride 0.9% with pre-mixed potassium chloride can also be used dependent on plasma concentrations (NICE, 2015).
Conclusion
According to Gosmanov et al (2018), the underlying defects in DKA and HHS are:
As paramedics do not routinely administer insulin, prehospital DKA/HHS management is focused on fluid replacement and mitigating against the effects of dehydration (NICE, 2015). The paramedic has a vital role in fluid replacement therapy, which is based upon a thorough ABCD survey and swift admission to hospital.