Case study 1: Tracy Shield, is a 19 year old with type 1 diabetes diagnosed age 9 years. She has no other medical conditions. She smokes a packet of cigarettes a day and drinks “occasionally”. Since leaving school she has worked in retail and hospitality, two months previously she moved from her parent’s home to shared rental accommodation. Over the last year she has had two hospital admissions with diabetic ketoacidosis. Her current medications are: insulin glargine 22 units daily and insulin aspart with meals (variable dose).
Tracy’s last HbA1C was 13. 2% and she monitors her capillary blood glucose infrequently. Pharmacological rationale for using long acting and rapid acting insulin for treatment of type 1diabetes and the principles of glucose monitoring Type 1 diabetes is also known as insulin dependent diabetes or juvenile diabetes. It occurs at any age but is commonly found among adolescents, children and young adults. In type 1 diabetes, insulin, the hormone necessary for moving blood sugar into cells is produced in very little amounts or is absent.
In the absence of insulin, there is build up of glucose in the bloodstream in place of the glucose going in to the cells (Hannas and Hithchock, 2005, p10). The body is thus unable to utilize glucose in the production of energy. The exact cause of type 1 diabetes remains unknown but it is believed that there could be an environmental or viral trigger in people who are genetically predisposed. This trigger is responsible for an immune reaction that causes the white blood cells in the body to attack the beta cells that produce insulin in the pancreas.
Diabetes is usually diagnosed using fasting blood glucose levels (FBS), random blood glucose levels (RBS), the oral glucose tolerance test (OGTT) and ketone testing which is done especially for type 1 diabetes. Diabetes is diagnosed when the glucose levels for FBS, RBS and OGTT are higher than 126 mg/dl, 200mg/dl and 200mgdl respectively (Hannas and Hithchock, 2005, p10). Ketones are substances produced when muscle and fat are broken down. When they increase to high levels they become toxic.
Insulin is a hormone produced by the pancreas which lowers the levels of sugar in circulation by allowing the blood to leave the bloodstream and get into cells. In type 1 diabetes, insulin is unavailable for use due to autoimmune destruction of the beta cells. Patients with type 1 diabetes have a high incidence of acidosis and ketosis. Thus the person with type 1 diabetes has to take insulin daily. The insulin is taken in various ways, it can be injected under the skin or it can be delivered as a continuous infusion via a pump. Preparations of insulin are different in their speed of action and how long their effect lasts.
The type of insulin to be used is determined by the glucose levels of the patient. Insulin of various types can be mixed together to achieve optimum control of glucose. Blood glucose serves as the most effective stimulus for the secretion of insulin (Polonsky et al, 1988, pp 443). When there is an increase in the level of blood sugar, the secretion of insulin is increased. Insulin production usually returns to baseline in normal individuals. Analysis of twenty four hour insulin levels in normal individuals shows the secretion pattern of insulin to be pulsatile (Polonsky et al, 1988, pp 444).
According to the study the most prevalent distribution of pulses was three pulses after dinner and lunch and two pulses after breakfast (Polonsky et al, 1988, pp444-445). Studies have shown that both subcutaneous and intravenous injections of insulin are equally effective in the management of sugar levels within normal or near normal levels (Drop et al, 1977, pp738). Insulin levels are also known to peak at night which creates a potential for developing hypoglycemia. Various factors influence glycemia with the administration of insulin.
These include length of time between insulin administration and meal consumption. When regular insulin is used, it needs to be given within 20 or 30 minutes of consumption of food. The lag time is usually increased when lispro insulin is used as it is quicker acting (Hirsch, 1999, p2; Skyler, 1998, p191). Short acting insulin (regular insulin), it has a peak effect of about two to four hours following injection. The duration of action ranges from six to eight hours and its activity still continues after food has been absorbed. Rapid acting insulin (insulin lispro) self aggregates in subcutaneous tissue.
Lente insulin has an onset of action of one to three hours. It peaks in four to eight hours and has a duration of action of twenty two hours. Other forms of insulin include utralente insulin and NPH insulin. NPH insulin peaks in one to three hours and ultralente insulin peaks in two to four hours. The duration of action for NPH insulin is thirteen to eighteen hours while that of ultralente insulin is twenty to twenty four hours (Hirsch, 1999, p2). For a flexible diabetes therapy to be effective, the mealtime and basal components should be identified.
The basal component is useful in restraining production of hepatic glucose. This allows for the glucose to be kept in equilibrium with tissues like the brain tissue which are obligate glucose consumers. Mealtime insulin offers stimulation for uptake of glucose while it inhibits the output of hepatic glucose. The basal insulin may be provided as intermediate acting insulin during bedtime or morning intermediate acting insulin (Hirsch, 1999, p2). It can also be provided as ultralente insulin which is administered two times in a day or it can be administered as an insulin pump (Hirsch, 1999, p2).
Dosing is determined by assessing the levels of blood glucose after insulin has been administered at meal time and it has dissipated when the food is digested. To provide insulin that is sufficient throughout the 24hours various regimens are used. Some of the regimens include two daily injections where intermediate acting insulin and short acting insulin are mixed, three daily injections where a mixture of intermediate acting and short acting insulin given before breakfast, an afternoon snack or before the main evening meal (Hirsch, 1999, p2).
The basal bolus regimen gives short acting insulin of about twenty to thirty minutes before the main meal and long acting or intermediate insulin at bedtime. Another possible regimen for the basal-bolus regimen is an analog of rapid acting insulin before the main meal and long acting or intermediate insulin at bed time, occasionally at lunch time and before breakfast. Insulin pump regimens are used to give bolus doses with meals or variable doses. For optimum use of the regimens mentioned it is necessary to conduct thorough blood gas monitoring.
The dose of insulin to be given varies depending on certain factors such as weight, age, the condition of injection sites, exercise patterns, daily routine, intercurrent illnesses, and results of blood glucose monitoring (including glycated hemoglobin). High levels of glycated haemoglobin indicate poor control of blood glucose. The recommended range for good diabetes control is glycated haemoglobin values below 6. 5% (Sperling, 2003, p210). Insulin can be administered by syringe injections which are given deep into the subcutaneous tissue.
The skin is usually pinched to avoid administering the insulin intramuscularly. The pen injector technique is also used to administer insulin subcutaneously. The patient should ensure that there is no blockage in the form of airblock or otherwise in the needle. The pen injector eliminates the need for drawing insulin from a vial; it makes use of a digital scale on which the dose is dialled up and the diabetic person can then self administer. The pump delivers insulin over twenty four hours. It usually delivers short acting insulin. The pump is changed after two or three days.
The pump has a cannula which is placed subcutaneously on the abdomen through which insulin is delivered. It is important to consider previous insulin treatments and past adherence before deciding to use the pump as it is hazardous due to the use of a smaller depot of subcutaneous insulin which increases the risk for ketoacidosis. Case Study 2: You are called to a cafe because a customer has had a seizure. On arrival you find Tracy lying on the floor and unresponsive. Her airway is intact, she is breathing and she has a palpable radial pulse. Her GCS is 7(E=1:V=2:M=4).
An OPA is inserted and 100% O2 via BVM is administered by your partner. Your note she is wearing a medic alert bracelet “type 1 diabetes, on insulin” with no mention of epilepsy. You check her capillary blood glucose, it is “low” on your meter. You administer glucagon 1mg IM, establish IV access and administer 50% glucose, 50ml IV. Observations include a blood pressure of 175/100 mm Hg, heart rate 115 beats/min, and respiratory rate 8 to 10 breaths/min. Tracy rapidly recovers consciousness (GCS 15) and is able to drink the lemonade provided by cafe staff.
There is an empty drink glass on the table and a plate of untouched food. The waiter tells you he had just delivered her food, he saw her take a cell phone call shortly afterwards, then five minutes later she had a seizure. In her purse she has an insulin pen injector containing insulin aspart and a capillary glucose meter, the most recent reading on the meter is 22. 3 mmol/L 25 minutes previously. She reports that because of her high capillary glucose she’d taken 12 units of insulin aspart rather than her usual 6 units with her evening meal.
She had had two glasses of vodka and orange over the preceding hour. You observe her eat some food. She declines transport to hospital, her housemate arrives and offers to drive her home. Reasons for occurrence of seizures Hypoglycaemia results from a mismatch between food, exercise and insulin. Some of the factors that could lead to the development of hypoglycaemia include, low HbA1c, defective counter-regulation of catecholamine and glucagons, alcohol ingestion, altered routines such as missing meals, changes in physical activity and alterations in insulin doses.
Tracy has had a seizure because she was hypoglycaemic. Hypoglycaemia presents with signs and symptoms of anxiety, pallor, sweating, palpitations, convulsions, confusion and coma (Sperling, 2003 p325). As the concentration of blood glucose falls, symptoms referred to as autonomic symptoms. These symptoms include palpitations, sweating, pallor, anxiety which serve as a warning sign for the hypoglycaemic episode. When glucose concentrations continue to fall, the patient starts to develop neutroglycopenic symptoms. The blood glucose threshold for neuroglycopenia is a blood glucose between 2. and 3. 5mmol per litre.
Sometimes neuroglycopenia occurs before autonomic activation which may cause hypoglycaemic unawareness. Tracy’s symptoms were mainly those for neuroglycopenia which indicates that she may also have had hypoglycaemic unawareness. Tracy has developed hypoglycaemia as a result of insulin overdose. In most young adults, the most common cause of severe hypoglycaemia is insulin injection (Sperling,2003, p325). Tracy used more insulin than she usually does; she used 12IU in place of the usual 6IU.
The intake of two glasses of vodka could have contributed to Tracy’s development of hypoglycaemia. There are differences in the capillary glucose readings on Tracy’s meter and on the paramedics reading. This means that there must have been an error in the reading which led to the development of hypoglycaemia following the injection of insulin. When insulin administration does not mimic the normal secretion pattern of insulin, a person is predisposed to hypoglycaemia. Effect of alcohol on glucose levels Alcohol has a varied effect on the levels of hypoglycaemia in different individuals.
Oxidation of ethanol leads to increased levels of the ratio of NADH: NAD. This impairs the level of gluconeogenesis. In the early stages, glucose concentrations are maintained by the breakdown of glycogen in the liver. Individuals who have type 1 diabetes are predisposed to developing hypoglycaemia in the period following twelve hours of ingestion of alcohol (Sperling,2003, p327). Additionally, alcohol intake causes deficits in cognition which can lead to errors in food consumption, insulin administration and a reduced awareness of hypoglycaemia. Reasons for administering glucagon
To manage hypoglycaemia it is necessary to immediately raise the blood sugar levels, to identify the cause of hypoglycaemia and to take measures that will prevent future occurrence of hypoglycaemia. Hypoglycaemia can be managed using glucagon and administering intravenous glucose. The blood glucose is raised quickly using 50% dextrose. 50% dextrose was used in Tracy’s case because she was unconscious and thus could not feed orally. Glucagon works to restore the concentrations of glucose in blood by increasing the processes of gluconeogenesis and glycogenolysis (Sperling,2003, p323).
How to administer glucose 50% glucose is a monosaccharide which increases the serum blood glucose levels. It should be given intravenously through a large vein. The use of small veins can cause local irritation to occur. The intravenous line should be patent to prevent the occurrence of infiltration which is likely to cause necrosis (Sperling,2003, p328). The fluid should be run wide open when dextrose 50% is administered and the venous patency should be checked frequently. Risk of hypoglycaemia Tracy is at higher risk of getting another episode of hypoglycaemia.
This is because neuroglycopenia usually causes cognitive impairment such that the affected individual becomes incapable of reacting correctly to an impending episode of hypoglycaemia. Conditions of hypoglycemia unawareness like the one experienced by Tracy have the effect of blunting the ability to detect decreasing levels of glucose concentrations (Sperling,2003, p328). In experimental settings patients who have a history of recurrent hypoglycaemia, show defective counterregulation when they are challenged with infusions of intravenous insulin. Thus Tracy is at high risk of having another episode of hypoglycaemia.
University/College: University of Chicago
Type of paper: Thesis/Dissertation Chapter
Date: 24 September 2016
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