Case Study Of A Complicated UTI

PBL Scenario: A young woman with a complicated urinary tract infection

Miss KP was a 24-year-old hospital cleaner with Type 1 diabetes which she had developed at the age of 18. Her usual treatment was Actrapid insulin, 8 units 3 times daily 30 minutes before meals and Actraphane insulin, 16 units at bedtime. On the day of admission to hospital she had presented to the A&E department with a three day history of dysuria, loin pain and feeling feverish. She felt unwell, had lost her appetite and because she was not eating she had not taken any insulin for 24 hours.

In A&E the casualty officer noted that she was disorientated in time and space, she had Kussmaul’s respiration and he could smell ketones on her breath, He diagnosed a urinary tract infection and arranged some blood tests and a dipstix urine test which showed:

Plasma

Glucose – 28mmol/L (normal fasting, 3.9-6.1)

Na+ – 145mmol/L (normal range, 136-146)

K+ – 3.7mmol/L (normal range, 3.5-5.1)

Arterial blood

pH – 7.1 (normal range, 7.38-7.44)

HCO3- – 8.0 (normal range, 22-29)

PO2 – 13kPa (normal range, 10-13.4)

PCO2 – 3.6kPa (normal range, 5-5.5)

Urine

Ketones – ++++

Blood – ++

Protein – ++

She remained in hospital for 5 days receiving treatment. Although she usually attended the Diabetic Clinic regularly, prior to discharge from hospital she had a further education session with the diabetes specialist nurses.

Group agreed learning objectives.

Discuss the mechanisms of action of insulin in normal health and in diabetes.

Discuss different regimes of treatment for people with diabetes.

Outline how patients can be educated in the management of their diabetes.

Describe the effects of diabetes on the immune system and whether patients are more susceptible to opportunistic infections.

Describe DKA in the context of the investigations and results presented in this case.

Relate the signs and symptoms to the test results.

Discuss the management of DKA in hospital.

For the purposes of improving the flow of the write up I have combined objectives 5 and 6 in order to avoid repetition.

Introduction

Learning objectives.

Discuss the mechanisms of action of insulin in normal health and in diabetes.

Insulin is a 51 amino acid protein formed of 2 chains linked by disulphide bonds, created following the cleavage of proinsulin to functional insulin. Insulin synthesis and secretion occurs in the endocrine pancreas, specifically in the Beta cells. The cleavage of proinsulin to form the functional molecule occurs within the secretory vesicles just prior to release from the beta cell. Insulin may be considered as a hypoglycaemic hormone.

In normal health, insulin has actions on blood glucose levels, protein and fat metabolism. Insulin acts to lower blood glucose in three ways:

Acts to enhance cellular uptake of glucose by increasing release of GLUT4 transporters from cytosolic vesicles to the plasma membrane. This particularly occurs in fat and muscle cells.

Acts to inhibit the breakdown of glycogen to glucose to prevent an increase in blood glucose supplied by stored glycogen.

Inhibits conversion of amino acids/fats to glucose.

These actions occur through the initiation of a signalling cascade activated by insulin acting on its receptor, which is a tyrosine kinase. Generally, cell energy needs are supplied and excess glucose is converted to glycogen. If further glucose is available it is converted to fat. Insulin acts muscle cells to increase the uptake of amino acids, thereby stimulating protein synthesis.

The release of insulin can be stimulated by many factors but the most common, is the elevated blood glucose which occurs following a meal. Other release stimulators are rising plasma amino acids or fatty acids levels. Insulin release can be stimulated through parasympathetic mechanisms. Insulin is also stimulated when hyperglycaemic hormones such as glucagon promote increases in blood glucose.

In type 1 diabetes, there is a pancreatic insufficiency, meaning that little or no insulin is produced. Such insufficiency occurs as a result of autoimmune destruction of pancreatic beta cells by T cells but the causes of this appear to be polygenic with additional environmental determinants.

In type 2 diabetes, the pancreas may be able to produce insulin in response to blood glucose but this is resisted and the 1st phase of this response is impaired. This condition is not relevant to the subject of this PBL and it thus not discussed further.

Discuss different regimes of treatment for people with diabetes.

Conventional insulin therapy: Patients will inject premixed insulins 2-3 times/day. The mixtures contain short acting and intermediate acting insulin. Lifestyle is rigidly controlled as mealtimes are scheduled to coincide with the anticipated peaks of insulin following injection. It is more difficult to acheive fine control thus blood glucose targets are higher. This regimen is more suited to people with a very regular lifestyle who do not want to test and inject regularly.

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Basal bolus insulin therapy: Patients use a combination of long and short acting insulin. The long acting insulin forms the basal component, typically given once per day. This works over 24 hours, mirroring the way that background levels of insulin would control blood glucose in the fasting state. When patients eat a meal, they inject a bolus of fast acting insulin to respond to the anticipated rise in glucose. One benefit to this regimen, is that patients are not restricted to eating at set times; insulin can be taken at any time in response to a meal. The patients can also vary daily activities and therefore insulin as necessary The DCCT and UKPDS trials demonstrated that patients using this therapy regimen were able to achieve levels of glucose control closer to that of a healthy person and better than patients using conventional insulin therapy. In addition, retinopathy and nephropathy occurred with less frequency and severity. However, patients require more education and the cost of medication is higher.

Continuous subcutaneous insulin infusion (CSII) is a type of basal bolus therapy. A small cannula is inserted into the subcutaneous tissue and infuses small amounts of insulin continuously (basal), mimicking the normal action of the human pancreas. When the patient eats a meal, a bolus dose can be infused, in the same way that the pancreas releases a large amount of insulin following a meal. For some patients, the pump improves glycaemic control and minimises the frequency of hypos that a person will experience. It is therefore useful in patients who are prone to hypos and whose blood glucose is particularly variable. However, blood glucose has to be measured regularly to tightly control insulin dose requiring high patient adherence. In addition some people don’t like the idea of being hooked up to the pump continuously. Currently, NICE reccomends the use of the pump, where multiple daily injections have failed to maintain HbA1c at an appropriate level or where hypoglycaemia is disabling.

Outline how patients can be educated in the management of their diabetes.

Current NHS reccomendations suggest that all patients with diabetes, or either type 1 or 2, are offered specialist education to promote good self-management. These are known as Structured Education sessions. This is in addition to regular contact with the multidisciplinary team which patients may access in either primary or secondary care.

There are several important points of education for people with diabetes.

Learning to test their blood glucose, understanding the result and making appropriate dietary modifications.

Learning to inject insulin and vary their dose according to carbs (carb counting).

Learning the risks of poor management and the benefits of tight glucose control.

Learning the benefits of regular health contact review and of self checks (e.g. feet).

Sick day rules – as the body upregulates glucose production as part of the normal response to infection, it is particularly important to maintain insulin dosing during illness, even when the patient isn’t eating. Advice is – to stick to normal diet and insulin regime where possible but to maintain insulin dosing even in the absence of food. Drink lots of fluids, test blood glucose regularly and test urine for presence of ketones. Seek help if glucose levels remain high even with extra insulin, ketones present in urine consistently, unable to eat or drink, recurrent vomiting/diarrhoea leading to fluid loss, confusion or drowsiness.

Describe the effects of diabetes on the immune system and whether patients are more susceptible to opportunistic infections.

At present, patients with good glycaemic control are not thought to be at increased risk of infections. Patients with poor control are at risk of infections in:

Skin – staphylococcal infections such as boils and abscesses. Mucocutaneous candidiasis.

GI tract – chronic peridontitis, rectal and ischiorectal abcess formation.

Urinary tract – urinary tract infections in women, pyelonephritis, perinephric abscess.

Lungs – staphylococcal and pneumococcal pneumonia, gram negative bacterial pneumonia and TB.

This is thought to be because high glucose concentrations impair the actions of some leucocytes. Infections can precipitate DKA as patients need to increase insulin dosing during infection. This is due to increased glycogenolysis and gluconeogenesis which occurs during a period of infection.

Describe DKA in the context of the investigations and results presented in this case and relate the signs and symptoms to the test results.

Normal range

Miss KP’s results

Result

Interpretation

Plasma

Glucose

3.9-6.1mmol/L

28mmol/L

High

DKA

Na+

136-146mmol/L

145mmol/L

Normal

N/A

K+

3.5-5.1mmol/L

3.7mmol/L

Normal

N/A

Arterial blood

pH

7.38-7.44

7.1

Low

Acidotic

HCO3-

22-29mmol/L

8.0mmol/L

Low

Compensation

PO2

10-13.4kPa

13.0kPa

Normal

PCO2

5-5.5kPa

3.6kPa

Low

Compensation

Urine

Ketones

–

++++

Present

DKA

Blood

–

++

Present

UTI

Proteins

–

++

Present

UTI

On presentation, Miss KP described dysuria and loin pain. She had also been feeling feverish. These symptoms were present 3 days prior to her seeking medical advice and are likely to result from her urinary tract infection.

Discuss the management of DKA in hospital.

Following a diagnosis of DKA, through tests to confirm hyperglycaemia, ketonaemia and acidosis as described in objective 5, hospital management moves through a three stage process with additional measures if necessary. The table below, shows in detail the measures necessary at each stage. As the DKA has been precipitated by the urinary tract infection in this case, it will be important to treat Miss KP with antibiotics. A good choice would be the antimicrobial agent, Trimethoprim which interferes with folate acid synthesis in bacteria and is particularly effective in UTI.

Initially, diagnosis is confirmed with simple tests of blood glucose to confirm hyperglycaemia, blood ketones to confirm ketonaemia and arterial blood gases to measure pH and show acidosis.

Phase

Investigations

Other considerations

Phase 1

Blood glucose

Blood pressure

Blood [K+]

Arterial pH

Phase 2

Blood glucose

Phase 3

Blood glucose

4x daily insulin, given subcutaneously. Dose according to previous 24 hour requirements and anticipated consumption of food.

Conclusion