Diabetic Emergencies – paramedics regularly attend a variety of diabetic emergencies. Many diabetic emergencies can be avoided through good diabetic education. This is why it is so important for paramedics to have a thorough understanding of the disease process of diabetes, so that you can provide good basic diabetic advice.
What organs are involved in diabetes?
Pancreas – Is both an exocrine and endocrine gland. The exocrine portion functions in digestion. Its endocrine functions are relevant to the pathophysiology of diabetes.
It is a flattened organ of 12.5-15cm length, consisting of a head, body and tail. It is located posteriorly to the stomach and is attached to the small intestine and the spleen.
The majority of the pancreas (99%), is made up of clusters called acini which are the exocrine portion. It has 700 000 – 1000 000 small endocrine glands, the pancreatic islets (islets of Langerhans) which are scattered throughout the organ and consist of:
Alpha cells (20%) that secrete glucagon
Beta cells (70%) that secrete insulin
Delta cells (5%) that secrete somatostatin
F cells that secrete pancreatic polypeptide
In the average adult the liver weighs between 1200-1600gms.
It is located in the right upper quadrant below the diaphragm and consists of two lobes.
It has numerous functions. The functions related to diabetic crises are described below.
The liver stores excess glucose in the form of the polymer glycogen. When stimulated by certain hormones the liver performs glycogenesis and gluconeogenesis.
Some terms about diabetes
Glycogenolysis– the breakdown of glycogen into glucose.
Gluconeogenesis – the creation of glucose from lactate, amino acids (not including leucine and lysine) and glycerol.
Diabetes – “comes from the Greek word meaning to siphon”
Mellitus – “comes from a the Latin word that means sweet like honey” (Lundstrom & Rossini, 1998)
It was first described by Ebers Papyrus in 1500 BC.
In 10 AD Celsus developed a clinical description and in 20 AD Aretaeus gave it the name diabetes.
In 1869 Langerhans describes the clusters of cells in the pancreas.
In 1921 Banting and Best discovered that insulin injections lowers blood sugar levels in animals.
There are two types of diabetes mellitus.
Type 1 Diabetes Mellitus (DM1) is one of the most common childhood diseases and accounts for 10% of DM.
Other names include, insulin dependent diabetes mellitus (IDDM), juvenile onset diabetes, brittle diabetes and ketosis-prone diabetes.
Its peak onset is between ages 11 and 13, with onset usually earlier for girls than boys. It rarely occurs before the age of 1yr or after 30yrs.
The person is usually of normal weight or underweight.
DM1 results from the complete lack of insulin due to a loss of Beta Cells.
Though it is both alpha and beta cells that are abnormal. Hyperglycaemia is not caused simply by insulin, rather and imbalance between insulin and glucose in the portal vein.
The destructions of the islets of Langerhans is related to:
Chemicals eg the drug streptozocin, an antibiotic and antineoplastic.
Illness eg mumps and rubella.
DM1 is controlled by regular daily insulin injections and regular self monitoring of BSL.
Types of insulin used in diabetes mellitus type 1
Insulin for treating diabetes with exogenous forms of insulin began in the 1920’s. The majority of these were made from either pork or beef pancreas.
As technology has progressed, genetic engineering has allowed for the manufacture of insulin closer to that of human insulin.
Both animal insulin and “human” insulin are classified by their onset of action.
Rapid-acting – have a fast onset and short duration.
Short acting – have a longer onset time but about the same duration as rapid-acting.
Intermediate-acting – have a longer onset time, but a much longer duration.
Long-acting – Again have a longer onset time, and an even longer duration
Premixed insulins – have a moderately rapid onset time and a long intermediate time of duration.
Type two diabetes DM2, results due to a relative lack of insulin. 90% of people with diabetes have this type.
Other names include, non-insulin dependant diabetes mellitus (NIDDM), maturity-onset diabetes, adult-onset diabetes, ketosis-resistant diabetes, stable diabetes.
It usually has an onset in people over the age of 40 and who are over weight, but this trend appears to be changing to affect younger people also in their early twenties, as diet and seddentary lifestyles are changing.
It is more prevalent in some racial groups including, Pacific Islanders, Japanese, Puerto Ricans, Hispanics, and African Americans all have a higher likelihood of developing Diabetes Mellitus Type 2
DM2 results from a genetic predisposition and environmental and other risk factors, such as long term obesity.
DM2 is controlled by diet and sometimes oral medication is also needed. These medications fall under five categories.
Sulfonylureas – stimulate the secretion of insulin from the pancreas.
Meglitinides – act like sulfonylureas only they are faster acting.
Biguanide – reduces hepatic glucose production.
Alpha-glucosidase inhibitors – delay carbohydrate absorption from the small intestine.
Thiazolidinediones – increase insulin receptor sensitivity to insulin.
Differentiating Type DM type 1 and type 2
Onset is acute with symptoms of:
Polyuria, polydipsia (excessive thirst), and polyphagia,
There may be a sweet odour in the breath,
Occasionally diabetic coma is the initial symptom.
Onset is insidious with nondescript symptoms including:
Some of the classic symptoms of DM1 may be present.
Gestational diabetes arises when there is glucose intolerance that occurs during pregnancy.
Risk factors include:
Familial history of diabetes
Increased age of mother
Mother who has had five or more children
Previous complicated pregnancy.
Once the baby is born, the abnormal blood glucose levels usually return to normal.
Although it is not related to the emergencies that will be discussed, it is another form of diabetes worth mentioning.
Diabetes insipidus differs from DM as it does not involve insulin and glucose. Instead there is either unresponsiveness of the kidneys to ADH or a lack of ADH secretions from the pituitary.
It is typified by copious urination and excessive polydipsia.
Its cause can be:
Idiopathic (basically means we have no idea why this happens)
Blood glucose level, or blood sugar level (BSL) reflects the balance of glucose absorbed by the intestines, the amount released by the liver into the bloodstream and the amount going from the blood- stream into the tissues.
When blood glucose becomes to high, the kidneys try to correct the hyperosmolarity by excreting the excess. However water will follow by way of osmosis, hence the polyuria. Polyuria causes the brain to send a thirst message, hence the polydipsia. This continued will lead to dehydration and hence dry skin, pruritus and blurred vision.
What drugs are involved?
Is a catabolic water soluble hormone.
Insulin is the only hormone which directly promotes cell uptake of glucose.
All cells need glucose for energy provision, however, glucose does not easily enter the cell. Insulin links with the plasma membrane receptor tyrosine kinase instigating autophosphorylation of tyrosine kinase which activates glucose transporters.
Insulin also promotes the synthesis of proteins, carbohydrates, lipids and nucleic acids.
The extracellular transport of ions such as K+, PO4 and Mg+ is also promoted by insulin.
When there is no insulin to assist glucose movement into the cells they starve, hence the symptom of polyphagia.
Glucagon is an anabolic hormone, produced by the alpha cells of the pancreas and in the cells that line the GIT. It stimulates both glycogenolysis and gluconeogenesis and raises blood sugar levels within a few minutes. Its release is stimulated by high glucose levels and sympathetic stimulation.
Adrenaline (ADR) has fast acting effects promoting glycogenolysis and gluconeogenesis. It also has more delayed effects of suppressing insulin release and decreasing cell reception of insulin.
Is secreted by the adrenal glands.
Acts more slowly and stimulates gluconeogenesis and decreases cell response to insulin.
Growth Hormone (Somatotropin)
Is secreted from the pituitary gland and acts in the same way as cortisol.
Glucagon, Adrenaline, Cortisol and Growth Hormone are all Counterregulatory Hormones
Inhibits the secretion of insulin and glucagon.
Slows absorption of nutrients from the GIT.
Inhibits somatostatin secretion, gallbladder contraction and secretion of pancreatic digestive enzymes.
If a person with diabetes takes to much insulin, exercises or drinks alcohol without taking precautions, there can be a decrease in blood glucose levels.
It is believed that the hypothalamus is responsible for detecting a critical decrease in systemic glucose levels (about 70mg/dL). The counterregulatory hormones are released.
Adrenaline then causes the classic symptoms of hypoglycaemia, ie. nervousness, tachycardia, shakes etc.
As the brain requires a high amount of glucose, if the levels are not increased to a sufficient level, then more severe symptoms such as seizure and coma can occur.
Signs and symptoms of hypoglycaemia
Increases heart rate
Mostly attributed to the release of adrenaline.
The Central Nervous System (CNS)
These symptoms are directly related to the brain being starved of glucose.
Hypoglycaemic unawareness is when a person with diabetes does not get obvious warning signs when they have a low blood glucose level.
Some people with diabetes develop hypoglycaemic unawareness because they have repeated episodes of hypoglycaemia and their body becomes accustomed to the decreasing levels of glucose. The level of glucose has to become severely low for the release of adrenaline to occur, hence, a lack of symptoms. At the same time however, the brain still suffers at the same decrease in glucose level. So the decrease in glucose level to cause symptoms is lower than that which will cause a decrease in level of consciousness.
Some more terms to know
Hyperglycaemia – “a greater than normal amount of glucose in the blood” (Anderson 2002, p 844)
Ketoacidosis – “acidosis accompanied by an increase of ketones in the body, resulting from extensive breakdown of fats because of faulty carbohydrate metabolism” (Anderson 2002, p 8954)
Pathophysiology of hyperglycaemia and keto-accidosis
As insulin promotes glucose uptake from the blood stream into the tissues, a lack of insulin or its inability to perform its function, will cause a hyperosmolarity of glucose in the blood. As the cells are being starved of glucose there is an increase in consuming of food and therefore the entry of more sugars, causing a vicious cycle.
Due to the lack of intracellular glucose the cells use fats and proteins for energy. Fats undergoing this process create ketones which the body tries to excrete via urination and in the breath (hence Kussmauls respirations); proteins create ammonia and shows as an increase in ammonia in the urine.
Hypoglycaemia versus Hyperglycaemia
Cool, moist skin
Full bounding pulse
May appear intoxicated, irrational.
Dry, warm skin
Rapid and weak pulse
Normal to low BP
Kussmauls respirations, sweet odour to breath.
Appear very sick.
Hyperosmolar Hyperglycaemic Nonketotic Coma (HHNC)
HHNC can occur in individuals when hyperglycaemia occurs with the presence of some residual insulin.
The insulin is in sufficient concentrations to prevent ketogenesis but in insufficient concentrations to enable glucose use in the peripheral tissues, or decrease gluconeogenesis.
Underlying cardiac or renal disease.
Decrease in either insulin secretion or action.
Increase insulin requirement eg physical or mental stress.
Use of medications such as diuretics, beta blockers, dilantin and sympathomimetics.
Supplemental nutrition, either parenteral or enteral.
Signs and Symptoms
Flushed dry skin
Dry mucous membranes
Loss of consciousness
HHNC presentation differs from hyperglycaemia/ketoacidosis as:
There is intense thirst due to the bodies attempt to dilute the hyperosmolarity of blood glucose.
Vomiting is uncommon
Breathing is shallow and tachypnoeic. Not deep and tachyopnoeic.
There is no sweet odour of the breath.
Seizures and coma can occur, which is rare in hyperglycaemia/ketoacidosis
Diabetic emergencies present with a myriad of signs and symptoms which mimic other common problems. The Ambulance Officer needs to be weary of this.
Diabetic ketoacidosis rarely causes coma, keep in mind other possible causes.
Hypoglycaemia can happen rapidly whatever the person is doing, even driving cars. As a result accidents can happen.
Look for med alerts, but don’t discard the possibility someone has diabetes just
because they do not have a med alert.
Take a thorough history and assessment.
Compliance to medication, use of other drugs, illness eg. infection, last meal and events leading up to onset eg. exercise/stressful situation are all specifically important questions when attending a patient with diabetes.
It is essential to take a blood glucose level test.
BEWARE of the silent infarct. Diabetes has effects on the nervous system and cardiovascular system resulting in neuropathies and an increased risk of cardiac complications. These two factors combined can lead to a silent infarct ie, an asymptomatic AMI.
Summary of Diabetic Emergencies
There are a few different types of diabetes.
DM2 is the more common of the two, mostly effects the older population and can be controlled by diet, exercise and oral medications.
DM1 is less common and usually has an onset in childhood or adolescence. Management requires regular insulin injections.
Gestational diabetes occurs during pregnancy, but usually dissipates after parturition.
Diabetes insipidus differs from the others as it is related to the bodies response to ADH
The liver and the pancreas are the two main organs involved.
The major clinical factor of diabetes mellitus is the difficulty in maintaining glucose level homeostasis.
The hormones insulin, glucagon, ADR, cortisol, somatotropin, somatostatin and pancreatic polypeptide are all involved either directly or indirectly.
Insulin non-existence or insufficiency being causes, Glucagon, ADR, Cortisol and Somatotropin being the counterregulatory hormones which, act when glucose levels drop, causing the early symptoms.
Hypoglycaemia occurs with low blood glucose levels. After many episodes a person with diabetes may develop hypoglycaemic unawareness.
Hyperglycaemia occurs with high blood glucose levels. It can occur with or without ketoacidosis.
The treatment of hypoglycaemia and hyperglycaemia is outlined in protocol 40.
Hypoglycaemia treatment depends on the Patient’s LOC. If they are conscious they should be given food or drink with sugar in it followed by a carbohydrate. If they have a decreased LOC then either glucacon or dextrose should be administered.
Hyperglycaemia administer Hartmanns if the BSL is 17mmol or more. Be wary of other associated conditions.
Most importantly, take a thorough history and assessment at all times to make sure you identify the presenting problem correctly.
Diabetic emergencies can appear like other common problems.
Patients with diabetes can have neuropathies and other underlying problems that can complicate the presenting problem.
Alcoholic diabetic patients may have a Vitamin B1 deficiency that will need supplementation when given dextrose.
The management of diabetes is personalised and can be effected by subtle changes in health diet and activity, therefore can be common pre-hospital patients. Knowing adequate information on the complexities of diabetes will assist in better pre-hospital care and patient outcomes.