Foundation Degree in Paramedic Science

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Your Name: Daniel Dodd

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Module Code and level: Level 5 FP2011X
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Module Title: Gastro-Urinary Endocrine
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handbook)
Start Date of Module: 31st January 2011
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handbook)
Assignment Type: Case study Assignment
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Word Count: 1974
Due Date: 18th March 2011

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Signature: D.J.Dodd Date: 17/03/2011

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 Table of Contents

1.0 The Case study 3

2.0 Reasons for choosing the case study 3
3.0 Diabetes Pathophysiology 3
3.1 The Pancreas 4
3.2 Genetic Link 4
4.0 Clinical Presentation 5
5.0 Psychosocial 5
6.0 Out Of Hospital Management 6
6.1 Complications – Diabetic Ketoacidosis 6
6.2 Clinical Presentation 7
7.0 Discussion 7
7.1 Cardiovascular Effect 7
7.2 Fluid Management 8
7.3 Oxygen Therapy 9
8.0 Future Treatment 9
9.0 Conclusion 10
10.0 Reference List 11

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 1.0 The Case study

This assignment is based on a case study of 31 year old James Longley, a design

engineer who lives with his girlfriend. Over the last few weeks James has been feeling

very tired and thirsty and also got up four times per night to urinate. He has had some

recent weight loss and also complains of a number of boils under his right axilla. Last week

he spent time on the sofa feeling exhausted. He visited his GP and was diagnosed with

Type 1 Diabetes.

2.0 Reasons for choosing the case study

I have chosen this case study as I have a specific interest in diabetes, and the out of

hospital management of diabetes. I also feel that as practitioners it is important to

understand the initial symptoms associated with the disease. It has been recognised since

the 1950's that early diagnosis of the symptoms of diabetes is vital. (Fajans, 1959) Studies

show that type 1 diabetes is most common cause of diabetes worldwide; however some

data from certain countries was unreliable. At puberty the incidence peaks, however still

remains high in adult males up to the age of 29 to 35. (Soltesz et al, 2007) This has an

impact on clinical practice as it is important to understand the age that people are at risk of

developing diabetes and understand the “red flags” that associate with the progression of

the disease.

3.0 Diabetes Pathophysiology

Diabetes occurs due to either a lack of production of insulin or because of the presence of

factors that oppose the action of insulin. This results in an increase of blood glucose level,

known as hyperglycaemia. (Watkins, 2003) Glucose provides the body with a source of

fuel for cellular function. Insulin acts as a transport hormone to transport glucose from the

circulating blood volume into the cells for oxidation and energy production. (British

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Paramedic Association, 2008)

3.1 The Pancreas

The pancreas is both an endocrine and exocrine gland. The endocrine function is vital in

the regulation of blood glucose. The pancreas is a flattened organ that measures about

12.5cm – 15cm. It is located in the curve of the duodenum. 99% of the pancreas is

arranged in clusters called acini, responsible for production of digestive enzymes. Within

the acini there are clusters of islets of Langerhans. The Beta Cells of the islets of

Langerhans are responsible to the secretion of insulin. (Tortora, 2008)

It is not fully clear on what causes type 1 diabetes. There has been evidence to suggest

that the islet Beta cells are susceptible to damage by the Coxsackie B virus, causing either

direct damage to the islet cells or autoimmune cytotoxic damage. (Fairweather, D 2002)

3.2 Genetic Link

Many chromosomal loci associated with type 1 diabetes have been located; however few

true genes have been identified. (Atkinson, D 2001) The most important genes are located

within the major histocompatibility complex (MHC) HLA class II region on chromosome

6p21, formally termed IDDM1. This accounts for about 45% of genetic susceptibility for the

disease. (Bruzetti, 1998)

A study by O'Connor et al (2006) concluded that in almost one third of patients, (32.2%)

had symptoms of hyperglycaemia upon diagnosis. This can be analysed that two thirds of

patients were symptom free of hyperglycaemia. This poses the question that is it difficult to

diagnose type 1 diabetes as there are not often the associated symptoms.

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 4.0 Clinical Presentation

As practitioners it is important to recognise the symptoms that are associated with type 1

diabetes as they may not present in such an acute manner compared to a hypoglycaemic

coma. I will review and evaluate the sensitivity and specificity to the disease where

possible. A study of 283 paediatric patients concluded that polyuria and polydipsia was

present in 97% of patients. Weight loss was present in 46% of patients. Polyuria is the

excessive production of urine; Polydipsia describes excessive thirst. (Roche, E 2005)

Gastric emptying has been shown to be reduced in patients with hyperglycaemia, a

protective effort from the body to slow absorption of sugar. (Worle et al, 2008) Adults,

compared to children tend to have a longer duration of symptoms and higher C-Peptide

concentration and are less likely to to exhibit ketonuria and ketoacidosis. Symptom

duration in children was 3-4 weeks where as in adults it was 7-8 weeks. (Vandewalle, C et

al 1997)

5.0 Psychosocial Aspect

Psychological treatments, for example counselling, cognitive behaviour therapy, family

system therapy and psycho-dynamic therapy, can slightly improve glycemic control in

paediatrics but not in adults. (Winkley, et al 2006) A meta-analysis of 25 controlled studies

concluded that psychological studies improved glycemic control but had no effect on

weight loss or blood glucose concentration. This was for type 2 diabetes where the stress

of self medicated insulin is not a factor. (Ismail et al 2004)

Penckofer, et al (2007) researched into the psychological impact of living with diabetes.

They concluded that women with type two diabetes experience feelings of depression,

anxiety and anger having a negative effect on their health and overall quality of life.

Evaluation from the study can be drawn that it is also important to view the psychological

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impact of the disease, taking into account the patients age, gender and social situation.

This can be incorporated into the out of hospital element of treatment, where a holistic

approach is not as common. Ranebennur (2004) concluded that training for medical

doctors and paramedic staff is an effective way of dealing with the more simple health

issues. This may have an important impact on the psychosocial impact of diabetes.

Studies have concluded that cohabitants of patients with type 1 diabetes recall significantly

more episode of hypoglycaemia than the patients. It concludes that severe hypoglycaemic

episodes have a negative psychological effect on a spouse. (Jorgensen, H et al 2003)

6.0 Out of Hospital Management

The management of hyperglycaemia depends on the severity and any complications that

the patient is encountering. It is important as a practitioner to ensure you are aware of the

complication and immediate emergencies that can occur from a high blood glucose level.

The JRCALC sets out UK ambulance practice guidelines. There is an emphasis on the

initial assessment to focus on the history. It is important to gain a good history, including

family history and medication history. As with all patients it is important to ensure that the

airway, breathing and circulation is assessed, and importantly in the case of this patient,

blood glucose is assessed. (JRCALC, 2006)

6.1 Complications – Diabetic Ketoacidosis (DKA)

Diabetic Ketoacidosis (DKA) is a life threatening condition where there is a reduction in

effective glucose circulating in the blood stream and increased counter-regulatory

hormones. Glucose is unable to be synthesized for cellular metabolism. The insulin

deficiency causes a release in catecholamine’s, lipdolysis and the metabolism of free fatty

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acids and subsequently ketone body release and metabolic acidosis. (Dunning 2007)

Karges et al, 2011 concluded that DKA prevalence at diabetes onset was constantly about

21% during the last 15 years. This study is on children and adolescents but not adults.

However the study is strong and reliable, and used a large sample source of 16562

patients and was a meta-analysis.

6.2 Clinical Presentation

DKA can be recognised in the early signs by polydipsia, polyuria, fatigue, weight loss,

nausea and vomiting, abdominal pain, myalgia, tachycardia and Kassumaul's respiration.

There can be factors that precipitate DKA including eating disorders, severe emotional

distress and acute illness, for example myocardial infarction or trauma. (Dunning, 2007)

Tokuda, et al (2010) researched into a triage screening tool for DKA. Within their research

of 1070 patients across two hospitals there were various symptoms that as paramedics

can be easily obtained. Systolic blood pressure had a mean difference of 22mmHg with a

P value of 0.003. This showing that marked hypotension can be a good predictor of DKA.

An increased mean of 27bpm in pulse rate is also in a good indicator, and increase is

respiratory rate of 5 respirations per minute. Again with a P value of 0.001. Temperature

had a no strong indication of DKA, and had a poor P value of 0.95. This tool would be

useful in the out of hospital environment in recognising DKA as recognition is a priority in

treatment.

7.0 Discussion

7.1 Cardiovascular effect

Roberts and Levin (2009) report that some patients can present with respiratory distress,

myocardial dysfunction, elevated troponin levels, ECG changes and pulmonary oedema.

They go onto to stress the importance of closely monitoring a patients cardiac function

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when DKA is present or suspected.

7.2 Fluid Management

The Joint British Societies guideline for the management of DKA suggests that the most

important initial therapeutic intervention is fluid replacement. The initial doses of fluids are

to correct hypotension by restoring the circulatory volume; clear ketones and to correct

electrolyte imbalances. It recommends that in patients with a systolic blood pressure under

90mmHg that 500ml of normal saline 0.9% over 10 – 15 minutes. Patients with a blood

pressure of above 90mmHg should be given 1000ml over 60 minutes.

There are studies to suggest that rapid fluid administration in DKA can lead to cerebral

oedema in adolescents. Hom, J (2008) found that there is a lack of strong evidence to

suggest that volume or rate is a preceptor for cerebral oedema in the case of DKA. This

research is limited as there is a low incidence of this, and it is also observational research.

The American Diabetes Association released a consensus on the management of

hyperglycaemic crisis. They state that fluid therapy is directed towards expansion of the

intra-vascular and extra vascular volume and restoration of renal perfusion. It recommends

that isotonic saline 0.9% should be infused at a rate of 15-20ml/kg or 1 – 1.5L per hour.

(Kitabachi A et al 2006)

There is still some debate over what fluid is best for the management of Diabetic

Ketoacidosis, which is reported in journals. JRCALC rules against the use of Hartmanns

for DKA. Dhatariya (2007) explains that the use of hartmanns can lead to an increase in

lactate and exacerbate this and lead to adverse outcomes. It causes a raise in serum

lactate and generates more glucose from this. Hyperkalemia may be present with DKA,

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and administering Hartmanns may lead to fatal cardiac This is clear evidence that sodium

chloride 0.9% is a suitable choice in the out of hospital environment. (Dhatariya, K 2007)

7.3 Oxygen Therapy

JRCALC advocates the use of oxygen in the use of a medical emergencies, especially in

patients with oxygen saturations below 95%. Blood chemistry affects the affinity of oxygen

to haemoglobin. Acidosis shifts the dissociation curve to the right. The loose bonds means

that haemoglobin has more difficulty in binding with oxygen in pulmonary alveoli, but it is

easier for the oxygen to dissociates from haemoglobin for tissue cells to use.(Xiong, L

2010) From the literature search I was unable to find any evidence that supplementary

oxygen in acidosis is beneficial to a patients outcome. I would draw a personal conclusion

that if there is more oxygen available for external respiration then there is more chance of

gas exchange, however this is not evidence based. In accordance with the British Thoracic

Society, oxygen saturations should be maintained between 94-98% in acute illness or 88-

92% with patients at risk of hypercapnic respiratory failure.(Driscoll, B et al, 2008)

8.0 Future Treatment

In my view it is important to always look for future developments, delivering the best and

most immediate care to a patient safely. As there is insufficient insulin circulating in the

patient’s blood stream, resulting in the increasing state of metabolic acidosis. The Joint

British Societies guideline for the management of DKA states that insulin should be given

on a weight basis until the ketoacidosis is resolved. Upon review if this can be started in

the out of hospital environment I found that serum potassium level should be investigated

before insulin started as hypokalemia can occur upon insulin administration and can cause

fatal cardiac arrhythmia. (Arora et al, 2011)

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 9.0 Conclusion

Upon conclusion it is important to ensure a good history is a vital part of the treatment,

measure blood glucose levels and vital signs. Give IV fluids dependent on cardiovascular

state, ensure a 12 lead ECG is completed and monitor the patient en route. A pre-alert to

the hospital is important to ensure that the patient blood chemistry is restored to normal as

soon as possible. The adoption of a screening school for the pre-hospital setting would

improve diagnosis and speed up treatment. Education of possible side effects and other

associated problems that can occur with hyperglycaemia is important to delivering high

levels of care and immediate treatment to diabetic patients.

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10.0 Reference List

Atkinson, D. (2001). Type 1 diabetes: new perspectives on disease pathogenesis and

treatmen. The Lancet. 358 (9277), 221 - 229.

British Paramedic Association. (2008). Endocrine Emergencies. In: Wieting, M Nancy

Caroline's Emergency Care in the Streets. 6th ed. Sudbury: Jones and Bartlett Publishers.
29.2.

Bruzetti, C. (1998). Dissecting the genetics of type 1 diabetes: relevance for familial
clustering and differences in incidence. Diabetes & Metabolism. 14 (1), 111 - 128

Dhatariya, K. (2007). Diabetic ketoacidosis. BMJ . 334 (1), 1284.

Driscoll, B et al. (2010). Guideline for emergency oxygen use in adult patients. Thorax. 63
(vi), 1-81.

Dunning, T (2009). Care of People with Diabetes: A Manual of Nursing Practice. 3rd ed.
Oxford: Wiley-Blackwell. 188 - 193.

Fairweather, S; Rose N. (2002). Type 1 diabetes: virus infection or autoimmune disease.

Nature Immunology. 3 (1), 338 - 340.

Fajans, S. (1959). The early recognition of diabetes melitus. Annals of the New York
Academy of Sciences. 82 (1), 208-218.

Hom, K. (2008). Is Fluid Therapy Associated With Cerebral Edema in Children With
Diabetic Ketoacidosis?. Annals of Emergency Medicine. 52 (1), 69 - 75.

Ismail et al. (2004). Systematic review and meta-analysis of randomised controlled trials of
psychological interventions to improve glycaemic control in patients with type 2 diabetes .
The Lancet. 363 (9621), 1589 – 1597

Jørgensen, H et al. (2003). The Impact of Severe Hypoglycemia and Impaired Awareness
of Hypoglycemia on Relatives of Patients With Type 1 Diabetes . Diabetes Care . 26 (4),
1106 - 1109.

Kitabachi, A et al. (2006). Hyperglycemic Crises in Adult Patients With Diabetes A

consensus statement from the American Diabetes Association . Diabetes Care. 29 (12),
2739 - 2748.

O'Connor et al. (2006). Diabetes: How Are We Diagnosing and Initially Managing It? .
Annals of Family Medicine. 4 (1), 15-22.

Ranebennur, V. (2004). Role of Medical Doctors and Paramedics in Counselling Services.

Jounral of Family Welfare. 50 (1), 38 - 41

Roberts, K; Levin D. (2009). Diabetic ketoacidosis, respiratory distress and myocardial

dysfunction. BMJ Case Reports. 10 (1), 1530.

Roche, E et al. (2005). Clinical presentation of type 1 diabetes. Peadiatric Diabetes. 6 (1),
75 - 78.
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Sotelsz et al. (2007). Worldwide Childhood Type 1 Diabetes, What can we learn from
epidemiology?. Peadiatric Diabetes. 8 (6), 6-14.
Tokuda, Y et al. (2010). Vital sign triage to rule out diabetic ketoacidosis and non-ketotic
hyperosmolar syndrome in hyperglycemic patients . Diabetic Research and Clinical
Practice. 87 (3), 366 - 371.

Vandewalle, C et al. (1997). Epidemiology, clinical aspect and biology of IDDM pateints
under the age of 40. Diabetes Care. 20 (1), 1556 - 1561.

Watkins, P (2003). ABC of Diabetes. 5th ed. London: BMJ Publications.

Winkley, K et al. (2006). Psychological interventions to improve glycaemic control in

patients with type 1 diabetes: systematic review and meta-analysis of randomised
controlled trials . BMJ. 333 (7558),

Woerle et al. (2008). Impaired Hyperglycemia-Induced Delay in Gastric Emptying in

Patients With Type 1 Diabetes Deficient for Islet Amyloid Polypeptide . Diabetic Care. 31
(12), 2325 - 2331.

Xiong, L. (2010). Interpreting and using the arterial blood gas analysis. Nursing Critical
Care. 5 (3), 26 - 36.

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