Diabetes Final
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Good practices for treating Diabetes Mellitus in a developing country Based on a thesis submitted in partial fulfillment of the University’s requirements for the Master of “International Medicine – Health Crisis Management” by GEORGIOS PAPADAKIS, MD, MSc Authors THEOFILOS ROSENBERG, MD, PhD, Associate Professor of Surgery ELENI KAKALOU, MD, MSc Internal Medicine specialist GEORGIOS PAPADAKIS, MD, MSc, resident in Endocrinology AUGUST 2010 The University of Athens in Collaboration with the NGO “Médecins du Monde” – Greece
Transcript of Diabetes Final
Good practices for treating Diabetes Mellitus
in a developing country
Based on a thesis submitted in partial fulfillment
of the University’s requirements for the Master of
“International Medicine – Health Crisis Management”
by GEORGIOS PAPADAKIS, MD, MSc
Authors
THEOFILOS ROSENBERG, MD, PhD, Associate Professor of Surgery
ELENI KAKALOU, MD, MSc Internal Medicine specialist
GEORGIOS PAPADAKIS, MD, MSc, resident in Endocrinology
AUGUST 2010
The University of Athens in Collaboration with
the NGO “Médecins du Monde” – Greece
© 2010 – Athens, Medical School, University of Athens, Greece
PAGE EDITING: ∂vangelia Stamatellou
Abstract .............................................................................................................................. 5
Intoduction ...................................................................................................................... 7
1. Objectives .................................................................................................................... 9
Monitoring and Evaluation .............................................................................................. 11
2. Methods of therapeutic approach .......................................................... 15
2.1 The profile of the Therapist ...................................................................................... 15
2.2 Barriers to the process of therapeutic work .............................................................. 16
2.3 Approaches and Methods for patient empowerment and improved adherence .... 17
3. Features of the disease .................................................................................. 19
3.1. Pathophysiology of diabetes mellitus ...................................................................... 19
3.2. Types of diabetes ...................................................................................................... 21
3.3. Chronic complications of Diabetes Mellitus ............................................................ 25
Diabetic neuropathy ................................................................................................ 26
Diabetic nephropathy .............................................................................................. 27
Diabetic retinopathy ................................................................................................ 27
Gastrointestinal /genitourinary dysfunction ............................................................ 28
Infections .................................................................................................................. 28
3.4. Diagnosis of Diabetes Mellitus ................................................................................ 29
4. Treatment of diabetes .................................................................................... 35
4.1. The role of the patient .............................................................................................. 35
4.2. DM and Travel .......................................................................................................... 36
4.3. Diabetic Ketoacidosis, Hyperosmolar Coma ............................................................ 36
4.4. Hypoclycemia ............................................................................................................ 40
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Contents
4.5. Antihypertensive Therapy ........................................................................................ 44
4.6. Antidiabetic agents .................................................................................................. 47
4.7. Insulin Therapy .......................................................................................................... 52
General information about insulin .......................................................................... 52
Insulin pens ................................................................................................................ 54
Needles-Syringes ...................................................................................................... 55
Choosing the right insulin ........................................................................................ 56
Insulin dosage ............................................................................................................ 57
Blood Glucose Meters .............................................................................................. 58
4.8. Common practices in the treatment with insulin .................................................... 59
4.9. Lipohypertrophy ........................................................................................................ 60
4.10. Storage of insulin .................................................................................................... 60
4.11. Diabetic Foot .......................................................................................................... 61
4.12. Diabetes and physical activity ................................................................................ 62
4.13. Dietary intervention ................................................................................................ 63
4.14. Diabetes and Obesity .............................................................................................. 66
4.15. Fasting and Diabetes .............................................................................................. 67
4.16. Diabetes and lack of food ...................................................................................... 68
5. Diabetes in patients of special categories ...................................... 71
5.1. Diabetes in children and adolescents ...................................................................... 71
5.2. Diabetes in pregnancy and gestational diabetes .................................................... 73
5.3. Diabetes and surgical procedures ............................................................................ 76
5.4. Diabetes and the elderly patients ............................................................................ 77
Discussion and conslusions ................................................................................ 79
Literature ........................................................................................................................ 81
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DIABETES MELLITUS (D.M.) is a chronic disease with a worldwide impact in both the
developed as well as the developing world. In poor countries where hygiene problems
overwhelm populations and guide the priorities of local Health systems, diabetes mellitus may
not be well treated and this can result in worsening the patient’s condition. A good number
of factors may contribute to it since the patients themselves are quite unaware of their health
condition. The Health System on the other hand might prove unable to cope due to lack of
health professionals as well as lack of medicines, health materials and supplies.
This text attempts to provide basic and concise knowledge on the disease taking into
account the realities of everyday life in resource poor settings. It aims also at describing a
proposed care delivery model designed for a rural area of a developing country. The model is
based on a concept of an outpatient clinic established at district hospital level .Cultural
differences, specific problems related to people’s daily lives, their socioeconomical status and
educational background must be taken into account in order to set up an effective care delivery
model. Methods of attracting patients and raising awareness in the community, have to be
developed as integral parts of care for DM. Moreover, a treatment algorithm based on simple
steps is presented in order to be used by local health workers such as Clinical Officers and nurses.
Special references to needed interventions such as nutrition and physical activity of
patients are presented. Specific issues concerning groups such as children, the elderly and
pregnancy are also included. Although, the golden standard of care as practiced in resource
abundant environments is presented, adapted clinical care pathways more appropriate for
resource poor settings are emphasised.
By no means does this text aims at substituting neither National guidelines nor more
detailed Medical textbooks. For anyone wishing to get more in depth and accurate information
on any subject, Medical textbooks on Internal Medicine or DM are recommended. This text aims
at concentrating basic background clinical knowledge and perspectives on clinical care of DM
in a resource poor setting in a short, easy to use introductory reference for starting to address
DM care. Any feedback remarks from readers will be much appreciated by the authors.
Corresponding address for comments:
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Abstract
THE RAPIDLY INCREASING incidence of D.M. poses a threat to health systems so much in
developed as in a developing countries being faced with a new challenge (2009a).
Incidenence of D.M. is increasing at a higher rate in developing countries in recent years (Gersh
et al., 2010). At the beginning of the 20th century diabetes was quite rare in Africa but
urbanisation and change of lifestyle brought about a rise in the disease and its complications.
More than 70% of diabetic sufferers live in countries of average to low income. It is
estimated that in 15 years, from 1995 to 2010, the number of people suffering from diabetes
in Africa has almost doubled. In 2025 there will be approximately 18,4 million diabetics in
Africa with the potential to reach 3,5% of the population. An even higher increase will be
noted in developing countries up to 2030 (69% rise in adult with D.M.) (Shaw et al., 2010).
It is estimated that 285 million of people suffer from D.M. or 6.4% of adult population
worldwide. According to WHO, 76% of the diabetics will be found in developing countries by
2030. The life expectancy of a person diagnosed with D.M. (diabetes type 1) may be 1 year
in some African countries where the disease remains uncontrolled (WDF, 2010).
Treatment of D.M. varies from country to country in Africa but Health Systems in overall
are focused on more serious problems resulting in undertreatment. Chronic diseases tend to
be neglected in the developing world where illnesses such as hypertension or diabetes are not
a priority (Unwin et al., 1999). Health-care systems in Africa are traditionally geared to the
management of acute illnesses and infectious diseases, such as tuberculosis, malaria and
gastroenteritis. The HIV-AIDS epidemic has further strained the available but inadequate
resources. Even though the HIV-AIDS epidemic is unfolding in sub-Saharan Africa, it is clear
that the relative importance of non-communicable diseases will rise, driven by an ageing
population, increasing urbanisation and other risk factors, such as tobacco smoking, obesity
and physical inactivity.
At the same time, successes at treating HIV/AIDS in resource poor settings in recent years
brought about by a combination of reduced prices through competition by generic drugs,
mobilisation of local communities, international support and funding as well as novel
approaches to chronic disease management, have opened a way for other chronic diseases to
appear manageable in even the most deprived of communities. Piloting efforts in this area,
emerges as a top priority ethical obligation of medical, academic and corporate world.7
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Introduction
Our initial goal is to establish quality and comprehensive care for D.M. in rural Tanzania
(Ifakara St Francis Hospital). DM care will first be integrated in the services of St Francis
Hospital. At a later stage it will be decentralized to at least four points of care in the District,
along with development of a referral system. Involvement of patients, their families and the
community will be crucial at all stages of design, implementation and scaling up care for
DM. Support groups, trained peer educators and expert patients will play a pivotal role in the
effort to introduce quality care of DM in Ifakara District.
A secondary goal is to record and analyze epidemiological data on prevelance, incidence,
immunological-genetic background, complications, morbidity, mortality and all other relevant
indexes for DM in a rural African setting. These data will allow the project to set and evaluate
impact indicators. Such estimations are impossible for the beginning of the project as very
little is yet known for DM in that setting and the country in general. The information that will
be produced will permit us to properly evaluate our intervention as the project evolves and
scales-up DM care within Ifakara District.
Research projects to be developed should be able to directly produce positive impact for
patients’ lifes, answering to the needs of poor rural communities. Research should never be
prioritised over patient’s care. This kind of information is also relevant to any other effort
aiming at introducing DM care within the health system in Tanzania. Cost-effectiveness of9
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A proposed model of comprehensive DMcare in a rural resource poor setting
chapter 1
various interventions has to be estimated, in order to develop a model of care relevant to the
needs of the target population.
Our ultimate ambition however is for DM to join the agenda of priorities of the Ministry
of Health. Contributing to this, by sharing lessons learnt and possible successes of the model
established in Ifakara for DM care, is of major importance for multiplying synergies and impact
of our limited in time and space intervention. The result of this work may in future be used
to strengthen the discussion on the treatment of diabetes.
Sharing successes, failures and capacity built at Ifakara Health Structures and local
community with other actors at National and International level1 could be a very positive
contribution of the project. Certain actors such as IDF (International Diabetes Federation) or
even associations such as the TDA (Tanzanian Diabetes Association) are of paramount
importance and much has to be gained by seeking both to learn from them but also to share
any experience on possible successes and failures.
General Objective
Reducing the morbidity and mortality of D.M. in a rural community (Ifakara, Tanzania).
Specific objectives
1. Design, implementation and evaluation of a comprehensive prevention and holisticcare package for DM
➠ Introducing availablility of basic diagnostic, treatment and follow-up means for
offering free access to clinical care for DM patients (oral antidiabetics, insulin,
glucometres and other diagnostics and consumables)
➠ Ensuring availability of staff for DM care on a daily basis at outpatient level
➠ Linking of hospital services to DM clinic
➠ Decentralization of services to at least four points of care within the district and
establishment of a rigorous referral system
➠ Ensuring uninterrupted logistic supply lines (medicines, diagnostics, consumables etc)
2. Record the epidemiological profile of DM in the rural setting of Ifakara, Tanzania andassess cost effectiveness of various interventions
➠ Assessment surveys of prevalence, incidence, mortality and morbidity rates
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1. Beran et al., 2005.
➠ Clinical cohort data analysis (complication rates, deaths)
➠ Cost-effectiveness analysis of interventions introduced by the project
3. Ensure quality care within a model, appropriate for piloting approaches for introducingDM care in resource poor settings
➠ Development and evaluation of a simplified medical algorithm for managing DM,
relevant to the needs and particularities of a rural community in Sub-Saharan Africa
➠ Staff training
➠ Education of patients and families
➠ Raising awareness and involvement of community in the care of DM
4. Raising awareness, interest and commitment of the health system at local, Nationaland International level
Financial restrictions
Access to adequate and quality health services affordable and accessible to patients must
be established. Quality treatment has to be offered and applied in a way that it becomes
effective at the lowest possible cost (Abbas and Archibald, 2007).
Monitoring and Evaluation
We aim to assess prevalence and incidence of D.M. along with the complications in Ifakara
region and compare the rates with those of previous studies (McLarty et al., 1989) (Ahren and
Corrigan, 1984).
Measuring quality of care and coverage is extremely important for assessing the project’s
success and for respecting patient and community rights. A rigorous follow up of implementation,
program outputs, transparency and good management practices is essential for both ethical
as well as accountability reasons.
Thus, the following sets of indicators are proposed for monitoring and evaluation of the
project:
A. Process indicators:
➠ Number of new patients enrolled at the program on monthly basis
➠ % of patients under follow up at 3, 6, 12, 18 and 24 months after initial diagnosis and
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➠ % of patients missing >1 appointment per year2
➠ % of patients on treatment with insulin
➠ % of patients receiving treatment for hypertention
➠ % of patients receiving treatment for hyperlipidemia
➠ % of patients following introductory training in disease management and lifestyle
modifications (offered at a weekly basis, initially in the hospital and later at community level)
➠ Number of patients recruited in the program
➠ Number of patients on insulin treatment
➠ Number of staff trained
➠ Number of peer educators and expert patients trained
➠ % of trained peer educators and expert patients still active in the program one year
after their initial training and involvement in the program
➠ Number of patients diagnosed following referral from general uptake of health structure
➠ Number of meetings with health actors at National level (on a six month basis)
B. Output indicators
➠ % of patients achieving Gluc<110-130 mg/dl or HbA1C < 7-8%3
➠ % of patients with BP values < 140/80
➠ % of patients with BMIs <25 kg/m2
➠ % of patients with values:
➠ LDL <130 mg / dl,
➠ HDL> 40 mg / dl for men and> 50 mg / dl for women
➠ Triglycerides <150 mg/dl.
➠ % of lost to follow up patients at 1 year
➠ % of limp amputations for patients under treatment and follow up
➠ % of deaths due to DM emergency or treatment complications (diabetic ketoacidosis
or hyperosmolar non ketosis coma or hypoglycaemia)
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2. Kalyango et al., 2008 and Kengne et al., 2009.
3. Specific values for Gluc, HbA1C, BP, BMI, Lipids to be decided based on recording such values for
first 1-3 months of program rolling out. Based on the fact that we are operating in a resource poor
setting, less rigorous targets of such values could be set for measuring program outputs. This is a point
necessitating further debate.
C. Means of collection
➤ Specifically designed patient data base
RISK STRATIFICATION OF COMPLICATIONS IN RELATION TO DIFFERENT VALUES OF GLUCOSE,
BP AND LIPIDS
In more detail, the targets for glucose and lipids regulation are shown below
Tables A and B:
∞. Goals of blood glucose levels to reduce the risk of DM complications:
B. Lipids goals for reducing the risk of complications:
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Low risk High risk Low risk for macrovascular for microvascular
complications complications
HbA1C (%∏b) <6 >6 >7
(normal = 4-6%)
Fasting plasma glucose <110 >110 >125
before meal (mg/dl)
Glucose of self-control
postprandial (mg/dl) <135 >135 >160
Risk LDL-Chol. (mg/dl) HDL-Chol. (mg/dl) Triglycerides (mg/dl)
High >130 <35 (men) >200
<45 (women)
Middle 100 -129 35-45 (men) 150 -200
45-55 (women)
Low <100 >45 (men) <150
>55 (women)
2.1. The profile of the Therapist
The clinical therapist in charge plays the most important role in the D.M. treatment team.
He/she will have to instruct the patients on how to regulate their D.M. and guide them with
their choices in order to enable them to adjust with the disease in their daily lives. The
therapist may be a health worker but not necessarily a medical doctor. He/she could be a
health carer with the basic knowledge of D.M. and should be able to properly guide the
patients (Gill et al., 2008). Preferably the therapist has to be close to the local community
(Culica et al., 2008). Finally, control of DM can be guided by experienced patients themselves
(trained expert patients) who can provide important advice and guidance to other patients
who will get for the very first time an organized medical treatment. (Seung et al., 2008).
The therapist must assist patients in making the necessary adjustments concerning diet,
physical activity, adherence to treatment and other behavioural issues so as to be able to
master themselves control of this chronic disease. Other members of staff, fellow patients
(expert patients and peer educators) and the entire community should play an integral part
in assisting the clinical care team to support patients.
Skills necessary for clinical therapists:
➠ He/she must have basic knowledge of epidemiology, pathophysiology, diagnosis,
complications, treatment and prevention of D.M.
➠ He/she must be skilled in techniques such as giving injections, checking sugar levels
and providing foot care.
➠ He/she should demonstrate good communication skills 15
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Methods oftherapeutic approach
chapter 2
➠ He/she should be surrounded by a team of people who could undertake a part of
treatment. But in poor resources countries the options and possibilities of ensuring
availability of a multidisciplinary team (nutritionist, psychologist, paediatrician,
surgeon, eye expert, nephrologist, health promotion expert ) could be limited .For
this the therapist should be prepared to undertake multiple roles within the
program.
2.2. Barriers to the process of therapeutic work
During clinical care the therapist may be met with limitations in his attempt to introduce
his patients to an ideal behaviour concerning D.M. The obstacles may be physical disabilities
which hinder communication or even psychological problems since it is extremely difficult for
some patients to accept confinements entailed by the disease (Neuhann et al., 2002). It is not
uncommon for patients to undergo through several stages until they finally accept their
condition, therefore the therapist will be asked to cope with the patient’s denial, anger and
depression, before acceptance which usually finally occurs.
People with diabetes are very likely to develop depression which is associated with a
higher mortality rate. Depression affects negatively a person’s ability to manage his/her
diabetes and follow the appropriate diabetes care. Moreover, diabetes-related stress is
common, particularly the fear of hypoglycaemia and long-term complications
Many patients fear the financial side of their disease (Khuwaja et al., 2010). Not everybody
can buy medication and insulin nor can they adopt a special diet. Also D.M. as a disease
requires frequent visits to the doctor and transfers to the hospitals (Mbanya and Mbanya,
2003). In some countries as in Tanzania for instance, there is legislation for free medication
but that has never been put to practice (Shiraishi et al., 2006). In the private sector the prices
of the medicines remain very high while in public hospitals serious shortages often exist
(Justin-Temu et al., 2009), (Beran, June 2004). Finally there is always the concern whether a
patient would be able to continue with his work or his normal life.
Additionally, lack of family and social support along with the social stigma can act as
obstacles in the therapist’s efforts. And yet there are always different cultures and attidutes
among people suffering from the disease (Belue et al., 2009).
Illiteracy proves to be an additional obstacle in the teaching process. Each educational
approach must aim at the individual profile of the patient so as to meet needs and particular
circumstances of individual patients (Smide et al., 1999).
The therapist might also encounter distorted views, prejudice and misconceptions. He/she
should thus obtain a good understanding of what is considered true or appropriate by the
community. In some communities in Africa for instance, obesity is regarded as a sign of health
and prosperity. That might negatively affect the dietary interventions of the therapist. In other16
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places there are myths and beliefs concerning the disease and there are populations who
regard it as a result of magic.
In many cases herbs and magic are preferred to medicines. Misunderstandings still occur
as far as the pathogenesis of the disease is concerned. Some believe that it is a result of
poisoning or of excessive sugar consumption. Thus, honey they believe, should be consumed
rather than sugar. In other traditions the consumption of bitter tree leaves is believed to help
lower blood glucose. Traditional healers are the ones to bring upon cure by use of alternative
therapies which are more preferable to conventional medicine for most people (2004)
(Famuyiwa, 1993). It is also a common belief that the disease is contagious, confined to white
populations, the elderly and the rich. Some practices again could be dangerous such as, for
instance, to walk barefoot inorder to ‘’reduce the temperature’’ of ‘’burning’’ foot. Some
beliefs are also quite harmful such as the one arguing that diabetics cannot be operated
on since the wounds are expected never to heal. In some populations those myths and beliefs
are solid into the conscious mind of people and very hard to overcome (Rai and Kishore,
2009).
To sum up, the therapist will be faced with the ethical, social and financial aspects of the
disease (Bal, 2000).
2.3. Approaches and Methods for patientempowerment and improved adherence
Teaching approaches can apply in groups or individually.
When in groups, various methods can be used
There can be lectures on D.M. where many people can participate. The disadvantage
though is the passive participation and low turn-out. Another approach might be through
group discussions where participants and therapists can openly exchange ideas and
experiences. Although this approach can prove quite flexible, it might not be well focused and
become influenced by the interpersonal relations of the participants. Teaching should also
include demonstration of some techniques such as giving insulin injections, measuring glucose
or foot care. Finally activities, role play and discussions should be included in teamwork
(International Diabetes Federation (IDF), 2008). Instructing in groups can be applied to a wider
number of people not only to patients but to relatives as well. The teaching project can be
realised with the collaboration and liaison of local organisations or institutions if these exist
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insulin storage and changes in lifestyle. It will all be within the frame of the basic health
care package offered (Beaglehole et al., 2008).
Apart from team work, the therapist will have to meet his patientsin private.
This will allow to individualise the programme and allow the patient to learn in his own
pace. Restrictions occur when the therapist has a little time in his hands and a large number
of patients to deal with. For this reason, nurses must be gradually trained so as to implement
routine clinical care and follow up tasks and only the more complicated cases will be reported
to doctors. Various approaches to task-shifting have to be developed, so as to better use scare
resources (eg. MDs)
“Peer to peer education” is of utmost importance.
The term refers to the mutual knowledge shared among the diabetics. Usually the patient
chosen is a “gifted” member of the community with good communication skills and it is his
responsibility to lead the other patients to the clinic to seek help. Experience exchange among
patients is vital. Problems concerning their health in their daily routine are discussed. This
encourages passing on knowledge and experience among the patients which is sometimes
more effective that the theoretical lectures of the health professionals to whom the illness
is not a personal experience (2007) (Wientjens, 2008).
Brochures, posters and fliers in local language can be used to enhance learning. Different
leaflets giving information about diet, ways of insulin administration or foot care must be
distributed so that the patient can refer to them easily. Finally information technology and
interactive boards can also be used as efficient ways of teaching. However, something like
that in a resource poor environment with high illiteracy rates might sound irrelevant.
However, theatre, dance and role playing exercises can be easily introduced in many
cultures in the developing world with the active participation and involvement of local
communities.
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3.1. Pathophysiology of diabetes mellitus
Diabetes is a chronic disease characterized by hyperglycaemia due to lack of insulin, resistance
to insulin action or combination of both. Diabetes mellitus comprises a group of common
metabolic disorders that share the phenotype of hyperglycemia. The knowledge on the effect
of beta-cells in the pancreas, the relationship between glucose, insulin and contra-reacting
hormones in glucose homeostasis is important so as to understand the pathophysiology of
the disease.
Chronic hyperglycemia leads to many complications affecting the whole body. The body
receives energy from food. Carbohydrates, proteins and fats are the main nutrients. As food
gets chemically degraded by enzymes, glucose molecules, amino acids, fatty acids and glycerol
are being produced. These are absorbed by the walls of the intestine organ and transported
into the bloodstream. The elevated glucose levels stimulate the pancreas to secrete insulin
which enables body cells to absorb glucose and turn it into energy.
Insulin acts on the liver so that glucose is stored as glycogen which remains as an inactive
form of glucose. It also inhibits gluconeogenesis, which is the conversion of non-carbohydrates
into glucose. It facilitates the transport of glucose through cell membranes with insulin
receptors, such as skeletal cells or heart cells and adipose tissue. Insulin also acts on the
metabolism of proteins supporting the transport of amino acids into the cells, thereby
enhancing protein synthesis particularly in muscle tissue. In relation to the metabolism of fats,
insulin stimulates adipose cells to synthesize and store fat while reducing release of fatty acids
from the adipose tissue. By all these ways, insulin reduces the concentration of glucose in
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Features of the disease
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A number of hormones are secreted responding to low plasma glucose. Glycogen is converted
into glucose (glycogenolysis) and fats and amino acids are converted into glucose
(gluconeogenesis), thus increasing blood glucose. The hormone that mainly compensates the
action of insulin is glucagon which is produced by the alpha cells of the pancreas. Glucagon
converts glycogen into glucose, and non-carbohydrates such as amino acids into glucose
(gluconeogenesis). It also stimulates the degradation of fats into fatty acids and glycerol
(lipolysis). As insulin levels decrease between meals or during the night, the secretion of
glucagon is activated. When the levels of glucose are rising glycogen is not produced.
Growth hormone, cortisone and adrenaline can increase the levels of blood glucose
through alternative biochemical pathways. When insulin is absent glucose levels increase and
so glucose is not stored in the form of glycogen. The use of glucose by muscle and adipose
tissue is reduced and the lack of glucose in the cells results in the production of energy from
the degradation of fats and proteins. This leads to the production of ketoacids which result
in ketoacidosis a condition which can be life threatening.
The secretion of insulin from beta cells of the pancreas is biphasic. The first rapid phase
lasts 5-10 minutes and then a prolonged second stage lasts as long as the duration of the
stimulus. The half-life of circulating insulin is 4-5 minutes and when insulin is bound to
receptors it is longer. The ‚-cells respond to hyperglycaemia in glucose concentration from
5 mmol/lt to about 9 mmol/lt. Above these prices hyperglycemia has negative effects on beta
cells.
Type 1 diabetes mellitus (T1DM) is characterised by loss of insulin producing beta cells of
the Langerhans islets in the pancreas leading to insulin deficiency. This type of diabetes can
be further classified as immune-mediated or idiopathic. Viruses and other environmental
factors may lead to the production of autoantibodies (GAD, IA-2, ICA antibodies). Patients
with permanent insulin deficiency tend to develop ketoacidosis. Idiopathic type by which there
is no obvious mechanism of autoimmune reaction is frequent in Africa and Asia. Another type
of diabetes can also occur in Africa where patients may periodically develop ketoacidosis.
T1DM is less common among black Africans in Sub-Saharan Africa compared to people
from other tribes in this region. The average age of the Africans is 23 years, which is a much
older age compared to whites. This fact is related to prolonged breastfeeding which is more
common in Africa. Moreover, the frequency of GAD antibodies and IA-2 antibodies were found
to be significantly rarer in black adults, something that shows that non-autoimmune T1DM is
the most common type (Lutale et al., 2007).
Type 2 diabetes mellitus (T2DM) is characterised by insulin resistance which may be
combined with relatively reduced insulin secretion. The defective responsiveness of body
tissues to insulin is believed to involve the insulin receptor. Genetic background,
environmental factors, rich in fats diet and reduced physical activity are also related to the
development of the disease. There is also strong correlation with obesity of central type and
with resistance to insulin. T2DM is caused due to delayed and eventually reduced production20
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of insulin by beta cells of the pancreas and increased insulin resistance of cells with insulin
receptors (Osei et al., 2003).
The failure of beta cells may be due to a defect in insulin secretion which leads to high
postprandial plasma glucose levels. Other abnormalities may be associated with high levels of
inactive forms of insulin release and gradual but steady damage of beta cells.
Insulin resistance is associated with dysfunction of insulin receptors. This leads to reduced
sensitivity of cells to insulin action and as a result reduced absorption of glucose into cells,
while glucose levels in blood stream remain high. As a consequence of elevated glucose, beta
cells are stimulated to secrete more insulin. Eventually, the beta cells lose gradually their ability
to secrete more insulin to overcome the resistance of peripheral targets and thus
hyperglycemia and clinical symptoms worsen.
3.2. Types of diabetes
A most recent classification of diabetes divided the two types of D.M. into insulin and non
insulin dependent according to the pathogenesis of the disease. The term “type 1 diabetes”
has replaced several former terms, including childhood-onset diabetes, juvenile diabetes,
and insulin-dependent diabetes mellitus (IDDM). Similarly, the term “type 2 diabetes” is
used instead of several former terms, including adult-onset diabetes, obesity-related
diabetes, and non-insulin-dependent diabetes mellitus (NIDDM).Another type is the
gestational diabetes.
The main characteristic of T1DM is its early development due to destruction of beta cells
of the pancreas. Most of the patients are diagnosed before the age of 35 years and the onset
of the disease may be acute or less acute, depending on the reduction rate of beta-cells of the
pancreas. The majority of T1DM is of immune-mediated nature, with beta cell loss being a
T-cell mediated autoimmune process. There is also a category of autoimmune destruction of
cells in adults at a slower pace (LADA-latent autoimmune diabetes in adults). Usually people
with T1DM are of normal or reduced body weight. No preventive measure is known against
T1DM, which causes approximately 10% of diabetes mellitus cases. At the beginning of the
disease people affected are mostly healthy and of normal weight, while sensitivity and
responsiveness to insulin are usually normal. T1DM was traditionally found under the term
“juvenile diabetes” because it represents a majority of diabetes cases in children but it can
affect both children and adults. In children and young people the first sign of T1DM may be
the diabetic ketoacidosis or a coma. People with T1DM depend on insulin for survival in order
to prevent dehydration, ketoacidosis and generalized catabolism.
The classic symptoms of hyperglycaemia may roughly translate to polyuria (frequent
urination), nocturnal enuresis, polydipsia (increased thirst) and polyphagia (increased hunger),
weight loss, headaches, fatigue, and blurry vision disorders (Roche et al., 2005). There may21
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also be numbness at hands, legs and feet and recurring infections. Symptoms may develop
rapidly (weeks or months) in T1DM while in T2DM they usually develop much more slowly and
may be subtle or absent. The production of ketoacids is associated with symptoms such as
abdominal pain, nausea and vomiting. Under conditions of intense stress and infection the
body tends to develop more severe hyperglycemia. Usually, in the diagnosis of T1DM no
chronic complications are present. In many countries the mortality can be high and patients
may die undiagnosed.
Many patients may develop the disease at the beginning of puberty. However in a 10%
DM occurs after the age of 65. There are variations depending on origin. Worldwide it is
estimated that 5% of the population has T1DM with increasing trends for the future. In Africa
the rate is about 2.5% of the total population, estimated by 2025 to raise up to 2.8%. DM
is less common in indigenous Africans living in sub-Saharan region. Men seem to have a
greater prevalence of the disease compared with women (IDF, 2005).
Regarding T2DM, it develops mostly in people older than 40 years, but it can also be found
in younger patients. T2DM is the most common type. There is no absolute dependence on
insulin for survival. Usually, T2DM is treated with diet, exercise and antidiabetic tablets. After
a few years T2DM, may not be controlled by oral drugs and consequently insulin has to be
used to achieve good metabolic control. We can categorize patients with T2DM, depending
on whether they are obese or not. In Western societies the obese amounted to 80% of the
population. In Southern Africa the rate of obesity in T2DM patients is between 20-30%.
Nevertheless, there is a genetic component to the expression of disease (Mengesha and
Abdulkadir, 1997). T2DM often remains undiagnosed for many years because hyperglycaemia
develops gradually.
Although T2DM can be considered characteristic of Western lifestyle, it appears to be
emerging as an epidemic over the developing world. Only half of the patients may experience
the classic symptoms of the disease. The disease can be diagnosed accidentally during a
routine check in only a third of cases. Repeated infections may herald the onset of the disease.
Finally, it can be diagnosed late, when long-term complications of the disease such as sores
on the foot, gangrene, myocardial infarction, peripheral vascular disease and renal disease
have already developed. The likelihood of ketoacidosis is not high and certainly much lower
compared to T1DM. Diabetic nephropathy in Africa entails a poor prognosis because of lack
of treatment means and lack of dialysis units (Rolfe, 1988). The same applies for retinopathy
or myocardial ischaemic disease.
Average age of onset for T2DM is around 55-60 years. The ratio of men/women is 3/2. The
percentage of diabetics is larger in urban areas than in rural areas (Alemu et al., 2009). Diets
rich in fats and low in carbohydrates and fibres, high stress levels and the limitation of physical
activity are all related to T2DM development. There is also a genetic background. T2DM was
not common in younger age groups, but lately it affects younger people too. Childhood
obesity is also related to DM, later in life. T2DM is often combined with hypercholesterolemia
and hypertriglyceridemia (Mengesha, 2006). 22
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Besides, the metabolic syndrome or syndrome X is quite common in Africa (Longo-Mbenza
et al., 2010) (Makuyana et al., 2004). For the diagnosis the following must be present:
➠ central type obesity waist circumference> 102 cm for men and> 88 cm for women or
BMI> 30 kg/m2
plus two of the following criteria:
➠ triglycerides> 150 mg / dl, HDL cholesterol <40 mg / dl for men and <50 mg / dl for
women
➠ blood pressure values BP> 130/85 mmHg
➠ fasting plasma glucose> 100mg/dl
These criteria have not been adjusted for indigenous Africans (Gaillard et al., 2009).
The table below highlights the main differences between T1DM and T2DM:
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Features T1DM T2DM
Onset Acute Slow, it develops gradually.
Patients may remain
undiagnosed for too long
Age Usually <30-35 years old >40-45 years old
Symptoms Yes, severe or less severe Patient might be asymptomatic
for too long
Weight Thin person, usually big loss Normal or overweight
of weight before diagnosis
Insulin secretion Lack of insulin which is Reduction of ‚-cells, low secretion
necessary for survival and/or abnormality of insulin
receptors in the peripheral
tissue, insulin resistance
Complications at the time Rare Common, because of late
of diagnosis diagnosis
Insulin resistance No Yes
Ketoacidosis Yes, usually sets the diagnosis More rare than T1DM
Autoantibodies anti-GAD, ICA, 1A-2 No
Genetic background-susceptibility May be present Stronger correlation
Syndrome X No Yes
Therapeutic choices Insulin Lifestyle, antidiabetics, insulin
Complications Mostly microvascular Mostly macrovascular and later
in course of disease
microvascular as well
Finally, there is also another category, gestational diabetes (GDM) which first appears
during pregnancy. Gestational diabetes can occur at any stage during pregnancy. It usually
occurs during the second or third trimester of pregnancy. Typically the rate is estimated
between 1-3% in expectant mothers.
Women entering pregnancy with pre-existing diabetes are also included in this group.
Gestational diabetes is associated with increased rate of perinatal complications. Risks to
the baby include macrosomia (high birth weigh), increasing the risk for children of diabetic
mothers to become themselves diabetic in later life. Early diagnosis is essential to avoid
complications (Iqbal et al., 2009). Age (over 35 years) and obesity are factors to be taken
into account for higher risk of gestational diabetes (Hossein-Nezhad et al., 2007).
Finally, diabetes may be the result of pancreatic disease in any case where there may be
inflammation (pancreatitis), trauma, infection, cancer and post-pancreatectomy. Furthermore,
chronic pancreatitis, cystic fibrosis and hemochromatosis destroy beta cells of the pancreas,
leading to decreased insulin secretion. Additionally, diabetes may occur as a result of
endocrine disorders involving other hormones or as a result of drugs, chemicals and toxins.
Congenital diabetes, which is due to genetic defects of insulin secretion, cystic fibrosis-related
diabetes, steroid diabetes induced by high doses of glucocorticoids, and several forms of
monogenic diabetes are other forms included in D.M disorders.
The table below shows etiological classification of D.M.
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T1DM (‚-cell destruction, usually leading to absolute insulin deficiency)
(a. Immune mediated, b. Idiopathic)
T2DM (may range from predominantly insulin resistance with relative insulin deficiency to a predo-
minantly insulin secretory defect with insulin resistance)
Other specific types of diabetes mellitus:
➣ Genetic defects of ‚-cell function
➣ Genetic defects in insulin action
➣ Diseases of the exocrine pancreas-pancreatitis, pancreatectomy, neoplasia, cystic fibrosis,
hemochromatosis, fibrocalculous pancreatopathy
➣ Endocrinopathies – acromegaly, Cushing’s syndrome, glucagonoma, pheochromocytoma,
hyperthyroidism, somatostatinoma, aldosteronoma
➣ Drug- or chemical-induced – Vacor, pentamidine, nicotinic acid, glucocorticoids, thyroid
hormone, diazoxide, ‚-adrenergic agonists, thiazides, phenytoin, ·-interferon, protease
inhibitors, clozapine, beta blockers
➣ Infections- congenital rubella, cytomegalovirus, coxsackie
➣ Uncommon forms of immune-mediated diabetes
➣ Other genetic syndromes sometimes associated with diabetes – Down’s syndrome, Klinefelter’s
syndrome, Turner’s syndrome, Wolfram’s syndrome, Friedreich’s ataxia, Huntington’s chorea,
Laurence-Moon-Biedl syndrome, myotonic dystrophy, porphyria, Prader-Willi syndrome
Gestational diabetes mellitus (GDM)
3.3. Chronic complications of Diabetes Mellitus
Diabetes mellitus indicates a condition where various organs fail over the years. People with
diabetes should be regularly checked for signs of complications. These chronic complications
include damage caused to various organs and systems:
➠ Eyes (eg diabetic retinopathy)
➠ Nervous system (eg diabetic neuropathy)
➠ Heart and blood vessels (eg diabetic microangiopathy)
➠ Kidneys (eg, diabetic nephropathy).
If complications are not diagnosed early and treated properly, they can lead to vision loss,
amputations, kidney failure or premature heart disease. The risk of chronic complications
increases by the duration of hyperglycemia and they usually become apparent in the second
decade of disease. Diabetes can also cause complications during pregnancy. Complications
occur in both types of diabetes, irrespectively whether the patient receives insulin or
antidiabetic drugs.
There are two main categories of complications:
➠ Diabetic microvascular disease:
It affects capillary blood vessels and damage presents as diabetic eye disease (retinopathy,
nonproliferative/proliferative, macular edema), neuropathy (sensory, motor mono/polyneuro-
pathy and autonomic neuropathy) and nephropathy.
DIABETIC MACROVASCULAR DISEASE:
It is characterized by early appearance of severe atherosclerosis and it is associated with
increased incidence of coronary heart disease (acute myocardial infarction, stroke, cere-
brovascular disease and peripheral arterial disease).
Other complications include:
➠ Gastrointestinal (diarrhea, gastroparesis due to autonomic neuropathy)
➠ Genitourinary (uropathy / sexual dysfunction)
➠ Infectious
➠ Dermatologic (skin ulceration, protracted wound healing)
➠ Glaucoma
➠ Cataract
MANAGEMENT OF COMPLICATIONS:
Basic diabetes management skills are necessary. These may include good blood glucose
control, treatment of hypertension, control of increased cholesterol levels and generally good
medical care in order to prevent or delay complications. Good adjustment and long-term
regulation of glucose should slow down the process of the disease. As a precaution, people25
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with diabetes should undergo periodic special examinations regularly to detect early damage
caused by diabetes in order to prevent the worst (eg regular eye examination for diabetic
retinopathy, etc.). In a resource poor setting environment, periodic screening for possible
complications could be performed avoiding use of sophisticated means that are not available
Diabetic neuropathy
Approximately 50% of patients with long-standing T1 and T2DM may suffer from diabetic
neuropathy. Diabetic microvascular injuries involving small blood vessels that supply nerves
(vasa nervorum) in addition to macrovascular conditions can accumulate contributing to
development of diabetic neuropathy. Common conditions related to and/or associated with
diabetic neuropathy include 3rd nerve palsy, mononeuropathy, mononeuropathy multiplex,
diabetic amyotrophy, (a painful polyneuropathy), autonomic neuropathy and thoraco-
abdominal neuropathy.
All peripheral nerves can be affected by diabetic neuropathy. In autonomic nerves, pain
fibers and motor neurons can be damaged. Since all organs and systems are innervated they
can be seriously affected by diabetic neuropathy. Several distinct syndromes -based on organ
systems- can appear in the form of autonomic and/or sensorimotor neuropathy. Symptoms
usually unfold gradually and they vary depending on the nerve(s) affected including symptoms
other than those listed.
Symptoms may include:
➠ Numbness and tingling of extremities
➠ Fasciculation (muscle contractions)
➠ Diarrhea
➠ Dysesthesia (decrease or loss of sensation to a body part)
➠ Impotence
➠ Difficulty swallowing
➠ Erectile dysfunction
➠ Urinary incontinence (loss of bladder control)
➠ Dizziness
➠ Muscle weakness
➠ Facial, mouth and eyelid drooping
➠ Vision changes
➠ Anorgasmia
➠ Speech impairment
➠ Burning or electric pain
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Diabetic nephropathy
Angiopathy of capillaries in the kidney glomeruli causes Diabetic Nephropathy Chara-
cterised by nephrotic syndrome and diffuse glomerulosclerosis.
Kidney failure may be caused by glomerulosclerosis and it results in fluid filtration deficits
and other various disorders of kidney function. Edema can be caused by hypertension and
fluid retention in the body with a reduced plasma oncotic pressure, along with other
complications such as proteinuria, and arteriosclerosis of the renal artery.
At its onset, diabetic nephropathy shows little symptoms, since they develop gradually
in late stages. They may be due to renal failure or a result of excretion of high amounts of
protein in the urine. Symptoms may include:
➠ edema: swelling, usually around the eyes in the morning; later, general body edema
may result, such as in the legs
➠ foamy appearance or excessive frothing of the urine (caused by the proteinuria)
➠ unintentional weight gain (from fluid accumulation)
➠ nausea and vomiting
➠ anorexia (poor appetite)
➠ malaise (general ill feeling)
➠ fatigue
➠ headache
➠ frequent hiccups
➠ generalized itching
The first abnormality that can be detected by a special lab test is microalbuminuria. Mostly
the diagnosis is suspected when proteinuria occurs in a routine urinalysis of a person with
diabetes. As kidney damage progresses and blood glucose is poorly controlled there are signs
of glucose in the urine, plus increase in serum creatinine and blood urea levels.
Diabetic nephropathy continues its destructive course, especially when complications of
chronic kidney failure occur earlier and progress more rapidly. Even transplantation or dialysis
do not seem to work so effectively in diabetes patients.
Diabetic retinopathy
Diabetic retinopathy is ocular manifestation of systematic disease. It is caused by
complications of diabetes mellitus and it can lead to blindness. Diabetic retinopathy can affect
the 80% of all patients with diabetes for 10 years or more.
No early warning signs may herald diabetic retinopathy. However, a person with macular
edema, who is likely to have blurred vision, does not have any warning signs even though
macular edema causes vision loss quite rapidly.27
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In part proliferate diabetic retinopathy consists of new blood vessels which form in the
eye and they can bleed and blur vision. This may not be too severe the first time it happens.
Just a few specks of blood or spots are left in a person’s visual field and most probably they
will clear away a few hours later.
Gastrointestinal/ genitourinary dysfunction
Motility and function of gastrointestinal and genitourinary systems may be affected by T1
and T2DM. Gastroparesis (delayed gastric empting) and either constipation or diarrhea (altered
small and large bowel motility) are the most prominent gastrointestinal symptoms. Symptoms
of vomiting, early satiety, anorexia, nausea and abdominal bloating may be present with
gastroparesis. Genitourinary dysfunction including erectile dysfunction, female sexual
dysfunction and cystopathy can be caused by autonomic neuropathy.
Infections
Frequent and severe infections are a common phenomenon within the diabetic population.
Incompletely defined abnormalities in cell-mediated immunity and phagocyte function
associated with hyperglycemia as well as diminished vascularization are some of the reasons.
Colonization and growth of various organisms (Candida and other fungal species) are
favored by hyperglycemia. While many common infections are more frequent and severe in
diabetic patients, there are also several rare infections detected almost exclusively in the
diabetic population.
Some examples of this latter category may be emphysimatous infections of the gall
bladder and urinary tract, rhinocerebral mucormycosis, and “malignant” or invasive otitis
externa. Invasive otitis externa –usually secondary to P. aeruginosa infection of the soft tissue
surrounding the external auditory canal- may first begin with pain and discharge before it
rapidly leads to osteomyelitis and meningitis. Other more common infections within the
diabetic population are pneumonia, urinary tract infections, and skin and soft tissue infections.
It is a fact though that the organisms which cause pulmponary infections are very alike those
found in the nondiabetic populations.
Pathogens considered more frequent among diabetic patients are:
Gram (-) negative organisms
Staphylococcus aureus
Mycobacterium tuberculosis
Several commonly observed yeast species such as Candida parapsilosis, glabrata
Bacterial agents like Escerichia coli, resulting from urinary tract infections (either lower
or pyelonephritis). 28
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Emphysematous pyelonephritis and emphysematous cystitis are also complications of
urinary tract infections. Patients with diabetic cystopathy are often faced with bacteriuria,
superficial candidal infections and vulvovaginitis. These patients also appear to have an
increased rate of colonisation by S. aureus at skin folds. A common denominator among these
patients is poor glycemic control.
3.4. Diagnosis of Diabetes Mellitus
Diagnosis of diabetes is usually based on clinical suspicion when certain symptoms are present.
Along with late diagnosis, long-term health problems have already been established and
this is the main reason why early diagnosis is important (Ambady and Chamukuttan, 2008).
All risk factors related to the disease should be taken into consideration by the therapist
and the health professionals working in the local clinic. Thus diagnosis of new diabetic
patients –even of those unaware of their disease-can be reached.
Risk factors for DM are:
➠ Family history of diabetes (i.e., parent or sibling with type 2 diabetes)
➠ Previously identified impaired fasting glyceamia or impaired glucose tolerance
➠ History of gestational DM or delivery of baby >4 kg (>9 lb)
➠ Habitual physical inactivity
➠ Obesity (Body Mass Index > 25 kg/m2)
➠ Hypertension (blood pressure >140/90 mmHg)
➠ HDL cholesterol level < 35 mg/dL (0.90 mmol/L) and/or a triglyceride level >250 mg/dL
(2.82 mmol/L)
➠ Polycystic ovary syndrome or acanthosis nigracans
➠ Race/ethnicity
➠ History of vascular disease
Laboratory tests of blood glucose or/and the glucose tolerance test confirm the diagnosis.
Usually a fasting blood glucose level >126 mg / dl is diagnostic, unless an infection or any
other health problem co-exist which cause temporal rise in blood sugar. Random plasma
glucose measurement level should be >200mg/dl (Krein et al., 2009). A single measurement
is not sufficient to rely on therefore it must be repeated. The second test can be done after
consultation on an empty stomach. An additional glucose tolerance test can be made for
further confirmation. If the results are inconclusive then further periodical tests are suggested
till a certain diagnosis is reached.
Glycated haemoglobin (glycosylated hemoglobin, hemoglobin A1c, HbA1c, A1C, or Hb1c,
sometimes also HbA1c) is a form of haemoglobin used primarily to identify the average plasma
glucose concentration over prolonged periods of time. It is formed in a non-enzymatic29
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pathway by haemoglobin’s normal exposure to high plasma levels of glucose. High levels of
HbA1c have been associated with cardiovascular disease, nephropathy, and retinopathy.
Monitoring the HbA1c in type-1 diabetic patients may improve treatment. Glycosylated
haemoglobin test (HbA1c), which represents the average blood glucose for a period of weeks
(8-12 weeks) can be used but it is not always available as a method, it is expensive and the
biochemical instruments require special storage conditions (Wikblad et al., 1998). A kit to
measure HbA1c is also available (Rector et al., 2001). In an environment of limited resources
such kits could be donated by sponsors so that glycosylated haemoglobin test can be
integrated in diabetes diagnosis and care. Approximate correlation between HbA1c
values and
eAG (estimated Average Glucose) measurements is given below:
The glucose tolerance test is a more complicated test especially for a poor resources
environment, but it can assist to ascertain diagnosis. The patient doesn’t eat anything for 8-
14 hours. After the first blood sample the person receives per os glucose (75 gr for adults and
1.75 g / kg for children). Two hours later the plasma glucose is rechecked. Glu >126 mg/dl
before glucose intake and 200mg/dl after glucose intake sets the diagnosis. Fasting
glucose=110-126mg/dl and glucose level after 2h=140-199mg/dl represent a state of poor
glucose tolerance. These glucose levels indicate that there is a high chance of development of
diabetes in the future.
Glucosuria testing with a urine stick might also be helpful to set the diagnosis. However,
it is not the main test because of its low sensitivity and specificity. It can be preferred,
however, if no alternative tests can be conducted (van der Sande et al., 1999).
A combination of screening method that uses multiple tests would certainly reach higher
sensitivity and specificity for the diagnosis of diabetes (WHO, 2003), but in an environment
of limited resources this case stands little chance.
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HbA11cc eAG (estimated Average Glucose)
(%) (mmol/L) (mg/dL)
5 5.4 (4.2–6.7) 97 (76–120)
6 7.0 (5.5–8.5) 126 (100–152)
7 8.6 (6.8–10.3) 154 (123–185)
8 10.2 (8.1–12.1) 183 (147–217)
9 11.8 (9.4–13.9) 212 (170–249)
10 13.4 (10.7–15.7) 240 (193–282)
11 14.9 (12.0–17.5) 269 (217–314)
12 16.5 (13.3–19.3) 298 (240–347)
TO SUM UP, THE CRITERIA FOR THE DIAGNOSIS OF DIABETES ARE:
● Symptoms of diabetes with random plasma glucose level> 200 mg / dl. The random test
means that the sample of blood is taken at any time of the day, regardless of the time
of the latest meal.
● Fasting plasma glucose >126 mg / dl. That means that there is no caloric intake for at least
eight hours.
● 2-hour plasma glucose after receiving 75 gr glucose >200 mg / dl.
CRITERIA FOR DIAGNOSING DISORDERS OF GLUCOSE HOMEOSTASIS ARE:
● Impaired fasting glyceamia (IFG): fasting plasma glucose from venous blood sample =
110-125 mg / dl.
● Impaired glucose tolerance (IGT): 2-hour plasma glucose from venous blood sample =
140-199 mg / dl.
If at a random monitoring test glucose> 100 mg / dl, we check fasting plasma glucose (FPG).
● If FPG > 125 mg / dl in two different measurements _ T2DM
● If FPG > 110 mg / dl _ Glucose tolerance test (OGTT-75gr)
● If FPG > 90 mg / dl _ Annual testing, take into account other cardiovascular risk factors
Conducting OGTT 75gr and measuring plasma glucose after 2 hours
● If Glucose after 2 hour > 200 mg /dl in two different measurements _ T2DM
● If Glucose after 2 hour 140-199 mg / dl _ Impaired glucose tolerance
● If Glucose after 2 hour <140 mg / dl and FPG> 110 mg / dl _ Impaired fasting glycaemia
The following algorithm (page 36) shows how we can figure out whether the patient is
diabetic or if he has IFG or IGT as early stages of diabetes:
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Random plasma glucose > 100 mg/dl person with risk factors (hypertension,
hypercholesterolemia, obesity, a first grade relative with DM, history gestational diabetes
or birth of a child weighting over 4 kg, age over 45 years) or presence of classic symptoms
Glu 2 h < 140 mg/dl
and FPG > 100 mg/dl?
IFG (Impaired Fasting
Glycaemia)
Glu 2 h = 140-199 mg/dl
& FPG = 100 mg/dl-125
mg/dl IGT (Impaired
Gluocose Tolerance)
Annual fasting plasma
glucoseAnnual OGGT 75 gr
Glu 2 h > 200 mg/dl
and FPG > 125 ?
DM
Check fasting plasma glucose (FPG) twice
110-125 mg/dl. Perform OGGT 75 gr
Initial fasting plasma glucose. Give 75g of anhydrous glucose. Repeat plasma glucose
in 2 hours. If FPG < 100 mg/dl and Glu after 2h < 140 mg/dl it is normal. Otherwise:
< 100 mg/dl? No DM >125 mg/dl? DM
If the number of diabetic patients grows rapidly there will not be any chance for multiple
diagnostic testing and so we will use the following simplified algorithm:
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Person with risk factors (hypertension, hypercholesterolemia, obesity, family history of
diabetes, history of gestational diabetes and born of overweight child, age over 45 years)
or presence of classic symptoms
Determine plasma glucose. Is it over 126 mg / dl?
Yes: Determine in two other
measurements. Is it still above
126 mg/dl?
No: Is it above 110 mg/dl
or are there any other risk factors
present?
Possible diagnosis of DMYes: Check regularly,
give lifestyle advices
4.1. The role of the patient
The patient develops a personal attitude towards his illness determined by social, psycho-
logical and financial factors (Hurwitz, 2006). The disease can cause problems both in the
patient’s life and his family’s since there are hindrances often related to lack of family and peer
support, prejudice, impoverishment, depression, ageing, impaired vision and last but not least
lack of motive and distortion of the right information.
Diabetes is a chronic disease which demands constant patient adherence to treatment,
vital for the patient’s understanding and motivation. The patient must be taught in a simple
language adapted to meet his needs. He/she must also learn how to change his eating habits,
include physical activity in his daily routine, examine his feet and receive medication following
instructions.
It is important that patient records be kept. The patient must check his blood sugar or
his urine on indicated times of a day before meals or 2 hours later. In cases of irregulation
or high levels of hyperglycemia during pregnancy, stressful periods, or other illness, a multiple
administration of injections is recommended. Glucometers and sugar tapes must be
recommended according to availability.
It can also be possible to check ketones in the urine when glucose is inadequate to cover
body energy needs. Thus, alternative sources are recruited from lipids and proteins. Ketones
check is essential in cases where blood sugar cannot be regulated, insulin injections have been
neglected or when the patient is under stress.
Clinical and lab examination is also highly recommended where possible. Eye and35
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Treatment ofdiabetes
chapter 4
neurological examination, cardio screening, urea and creatinine must be checked annually, so
as to diagnose levels of kidney failure and/or harm on feet.
The patient must understand that he must reach set targets such as BMI <25 kg/m2,
plasma glucose (Glu) <110 mg / dl, HbA1C <7%, blood pressure (BP) <130-140/80 mmHg, and
normal cholesterol levels (LDL <100-130 mg / dl, HDL> 40 mg / dl for men and> 50 mg / dl
for women and total cholesterol <230 mg / dl) and triglycerides (<150 mg / dl). Lipid
examination is desirable but not affordable in a poor resource setting environment in most
cases. It is important to understand that the patient should visit a doctor at scheduled
meetings and is not to neglect the state of his health.
At each visit, the doctor will check the weight, the blood pressure, the glucose level, the
veins of the feet and their pulse, as well as urine for ketones.
4.2. DM and Travel
People with diabetes need special preparation and planning when travelling. In Africa, many
factors such as the transportation means or the infrastructure make journeys quite difficult
for the diabetic traveller especially when long distances have to be covered so as to meet with
his therapist or family and for business related reasons . Travelling patients must follow
specific instructions for additional food, water, sweets, while sugar must be available
especially for the ones who are under insulin treatment and they have to carry their
medication. It is recommended that they be accompanied by a person with basic knowledge
of the disease. Proper foot wear -customised if possible- must be worn to prevent the walking
traveller from injuries. The sedentary traveller must move periodically. In the Western world
distinctive bracelets stating the disease are worn to indicate the condition to responding
health workers in case of coma.
During the journey insulin must be kept in cool temperatures away from direct sunlight.
If ice is used, it must be well wrapped in cloth and plastic bags so that insulin is not in direct
contact with it. It is also wise to keep insulin wrapped in plastic bags. When the patient
reaches his destination he must either keep his insulin in a refrigerator or in the coolest part
of the room.
4.3. Diabetic Ketoacidosis, Hyperosmolar Coma
Diabetic ketoacidosis (DKA) and non-ketonic hyperglycemic hyperosmolar coma are the most
serious acute metabolic complications of diabetes mellitus. Diabetic ketoacidosis occurs more
frequently in patients with T1DM, but it can also occur in patients with T2DM. Hyperglycemic36
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hyperosmolar coma occurs mainly in patients with T2DM aged over 50 years. In both
complications frequent trigger factors can be illness (eg, infections, cardiovascular disease,
etc.), omission of insulin injection, new-onset diabetes etc.
DKA most frequently occurs in those who have already had diabetes but also in those
diagnosed for the first time. A particular underlying problem usually leads to the DKA
episode. Concurrent conditions such as inadequate insulin administration, myocardial
infarction, stroke, pregnancy or the use of drugs may be some of the underlying problems.
Recurrent episodes of DKA in young patients may be due to eating disorders or insufficient
use of insulin. Young patients are particularly concerned about weight gain, thus prone
to reduce insulin dosing.
The presence of large amounts of ketones in blood and urine as well as marked metabolic
acidosis distinguish diabetic ketoacidosis from other diabetic emergencies. A more common
state in T2DM is the Hyperosmolar Hyperglycemic State (HHS or HONK) which features
increased plasma osmolarity (above 320 mOsm/kg) due to profound dehydration and
concentration of the blood. The phenomenon of mild acidosis and ketonemia which can also
occur in this state is not so extensive as in DKA. In spite of the fact that osmolarity may also
be increased in DKA there is a degree of overlap between DKA and HHS which makes it
possible for the case to be classified into either DKA or HHS.
Ketoacidosis does not always result from diabetes since alcohol excess and starvation- in
which case glucose level is normal or low- can also lead to the condition. In diabetic patients,
other reasons such as poisoning with ethylene glycol or paraldehyde can lead to metabolic
acidosis. A rare side affect of lactic acidosis must be mentioned for T2 diabetics who take
metformin.
The annual incidence of diabetic ketoacidosis is 4.6 to 8 cases per 1000 diabetic patients,
while the annual incidence of hyperglycemic hyperosmolar non-ketonic coma is less than 1
case per 1000 diabetic patients. The mortality of patients with diabetic ketoacidosis is less
than 5%, while the mortality of patients with hyperglycemia hyperosmolar non-ketonic coma
remains high (15%) (Sotiropoulos, 2008). The main disorders in both metabolic complications
are lack of insulin and increased levels of contra-acting hormones (glucagon, catecholamines,
cortisol, growth hormone).
Diabetic ketoacidosis is characterized by hyperglycemia (> 300 mg / dL), reduced levels
of bicarbonates (<15 mEq / L) and acidosis (pH <7,30) as well as ketonaimia and ketonouria.
The non-ketonic hyperglycemic hyperosmolar coma is characterized by significant
hyperglycemia (>600 mg / dL), high plasma osmolarity >320 mOsm/kgH2O, severe
dehydration (9L) as a result of osmotic diuresis, bicarbonate >15 mEq / L, absence or middle
ketonaimia and disorders of consciousness.
The treatment of both disorders is based on fluid replacement, insulin restorage, the
correction of metabolic acidosis (in diabetic ketoacidosis) and electrolyte disturbances. It is
based also on the treatment of trigerring factors and the related complications such as
hypoglycemia, low potassium restorage, cerebral edema, acute pulmonary edema, adult37
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respiratory distress syndrome or vascular thrombosis. Through proper education of the
patient, and effective communication with the therapist - especially during the acute phase
of the disease- many cases of diabetic ketoacidosis and hyperglycemic hyperosmolar non-
ketonic coma can be prevented.
The aim is, however, that all patients learn how to prevent diabetic ketoacidosis. An
infection may disturb glucose metabolism and result in a hyperglycemic crisis. Bad psycho-
logical disposition or even an injury can have the same outcome. Other hormones such as
glucagon, growth hormone, epinephrine and cortisone are released. All these hormones
acting in combination result to insulin tolerance leading to hepatic glucose production
and reduced use of circulating blood glucose (Fasanmade et al., 2008). Under these
circumstances ketonaimia and ketonouria are likely to occur. Gradually diabetic ketoacidosis,
related to significant mortality without appropriate treatment (Mbugua et al., 2005) may
appear.
Attacks of DKA can be prevented in known diabetics to an extent by adherence to “sick
day rules”. These are clear-cut instructions to patients how to treat themselves when unwell.
The patient must never firstly omit insulin doses and secondly be dehydrated. Also, any
possible disease should be treated promptly and more intensive laboratory testing should
be performed Availability of such testing or the need for patients to bear the related costs
could have a negative impact on mortality in poor resources settings. If lab support is limited
or even inexistent, the use of validated clinical algorithms based on research data, could raise
the effectiveness of treatment. Additional insulin may be given and, if necessary, admission
to hospital is required before the diabetic coma takes place (Otieno et al., 2005). Long
distances and associated travel costs could present a major obstacle in poor communities.
Innovative approaches have to be developed (eg funds for bearing travel costs for patients or
community involvement along with project funding for referral system costs).
The hydration is important and fluids should be given that contain sodium and potassium
to replace electrolytes. Fluids can also contain sugar to ensure the intake of carbohydrates.
Losing weight can be a warning sign of dehydration for someone who is going to develop
diabetic ketoacidosis. In such case, the control should be regular and glucose must be checked
every four hours as well as ketones in the urine. The patient must rest and supplementary
insulin should be provided. Furthermore, a 10-20% of normal dose can be given so that the
level of glucose remains below 240 mg / dl as shown in the following table (page 43).
Signs which are alarming and raise the suspicion for admission to hospital may be signs of
dehydration such as dry mouth and dry lips, sunken eyes and weight loss, multiple episodes
of vomiting, abdominal pain, hyperventilation, nausea and drowsiness. Deep breathing
(emitting acetone smell) known as Kussmaul breathing and altered states of consciousness
make good signs for hospital admission. Also reason for admission may be a blood glucose
value> 240 mg / dl and ketonouria for over 12 hours.
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Therapeutic algorithms in the hospital now for any kind of coma as follows:
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Level of glucose Ketones detectable Quantity of supplementary insulinin mg/dl in urine, not just a trace
Below 80 mg/dl Yes or No skip the usual insulin and reduce insulin
analogues by 20%. Check after 3-4 hours
80-240 mg/dl Yes or No No supplementary insulin. Check after 3-4 hours
240-400 mg/dl No 10% of addition supplementary dose of insulin,
check after 3-4 hours, repeat dose if no
improvement
240-400 mg/dl Yes 20% of addition supplementary dose of insulin,
check after 3-4 hours, repeat dose if no
improvement
>400 mg/dl Yes or No 20% of addition supplementary dose of insulin, check
after 3-4 hours, repeat dose if no improvement
Treatment algorithm for hyperosmolar coma (Stoner, 2005)
4.4 Hypoclycemia
Hypoglycemia is the lack of glucose in the blood occurring when insulin levels are high
therefore allowing glucose to rapidly enter the blood cells. Respectively, when glucose levels
fall to extremely low levels, loss of consciousness or even permanent brain damage may be
established leading to hypoglycaemic coma. Hypoglycemia may also occur as a complication
of treatment with either insulin or oral medication of diabetes mellitus. Although
hypoglycemia is not common in non-diabetic persons it can occur at any age and be related
to many causes. Common causes are excessive insulin produced in the body, inborn errors,
medications and poisons, alcohol, hormone deficiencies, prolonged starvation, alterations
of metabolism associated with infection, and organ failure. Children may also experience it
since they are engaged in more physical activity and they tend to neglect the dietary
requirements of their disease. 40
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Treatment algorithm of diabetic ketoacidosis (Kitabchi and Wall, 1999)
Throughout a 24 hour period blood plasma glucose levels are generally maintained
between 4-8 mmol/L (72 and 144 mg/dL). Although 3.3 or 3.9 mmol/L (60 or 70 mg/dL) is
commonly cited as the lower limit of normal glucose, symptoms of hypoglycemia usually do
not occur until 2.8 to 3.0 mmol/L.
Hypoglycemic coma can be installed quickly and is characterized by normal or rapid
breathing, pale and sticky skin, profuse sweating, dizziness and headache, rapid pulse,
impaired level of consciousness that can take any form of aggression, lethargy, changed
behaviour and hunger. In more severe cases there are seizures, fainting, coma, or weakness in
one side of the body.
The manifestations of hypoglycaemia are listed below:
ADRENERGIC MANIFESTATIONS
➠ Palpitations, tachycardia
➠ Shakiness, anxiety, nervousness,
➠ Sweating, feeling of warmth (although sweat glands have muscarinic receptors, thus
“adrenergic manifestations” is not entirely accurate)
➠ Dilated pupils (mydriasis)
➠ Pallor, coldness, clamminess
➠ Feeling of numbness “pins and needles” (parasthaesia)
GLUCAGON MANIFESTATIONS
➠ Headache
➠ Hunger, borborygmus
➠ Nausea, vomiting, abdominal discomfort
NEUROGLYCOPENIC MANIFESTATIONS
➠ Abnormal mental status, impaired judgment
➠ Personality change, emotional change
➠ Paresthesias, headache
➠ Irritability, belligerence, combativeness, rage
➠ Nonspecific dysphoric feeling, anxiety, moodiness, depression, crying
➠ Ataxia, incoordination, sometimes mistaken for “drunkenness”
➠ Fatigue, weakness, apathy, lethargy, daydreaming, sleep
➠ Amnesia, confusion, delirium, dizziness
➠ Staring, “glassy” look, blurred vision, double vision
➠ Difficulty speaking, slurred speech
➠ Automatic behavior, also known as automatism
➠ Stupor, coma, abnormal breathing
➠ Focal or general motor deficit, paralysis, hemiparesis
➠ Generalized or focal seizures41
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Newborns can experience hypoglycemia demonstrating several symptoms such as:
irritability, jitters, myoclonic jerks, cyanosis, respiratory distress, apneic episodes, sweating,
hypothermia, somnolence, hypotonia, refusal to feed, and seizures or “spells”. Hypoglycemia
can resemble asphyxia, hypocalcemia, sepsis, or heart failure.
In spite of neuroglycopenic impairment there is reduction of noticeable symptoms in
both young and old patients when the brain habituates to low glucose levels. This
phenomenon is termed hypoglycemia unawareness and it proves to be a significant clinical
problem when improved glycemic control is attempted especially in insulin-dependent
diabetic patients.
In each case where the patient does not feel well and enters a hypoglycemic coma, he
should be given sugar by mouth, or a sugary juice. Alternatively the patient can take honey.
Overtreatment should very carefully be avoided as far as this is possible because the blood
glucose can usually be raised to normal within minutes with 15-20 grams of carbohydrate.
This can be taken as food or drink and it is contained in approximately 100-120 ml of
orange, grape or apple juice, or in one slice of bread and in about one serving of most
starchy foods.
If hypoglycemic coma is established and the patient is unconscious with impaired ability
to swallow, he should be given intravenous dextrose serum (in particular, a serum 50%
dextrose 50 ml intravenously). (Infants are given 2cc/kg Dextrose 10%, Children Dextrose
25%, and Adults Dextrose 50%). If no response there must be given a second dose. If the
patient feels better and becomes conscious and the glucose is above 70 mg/dl, he should
be rechecked regularly. We continue to provide dextrose serum 10% with a rate of one litre
at 6 hours.
If a vein route for intravenous serum proves difficult to find or no skilled personnel is
available then a glucagon injection in the form of prepared syringe can be used. Glucagon is
a hormone that rapidly counters the metabolic effects of insulin in the liver, causing release
of glucose and glycogenolysis into the blood. It can raise the glucose by 30-100 mg/dl within
minutes in any form of hypoglycemia caused by insulin excess (including all types of diabetic
hypoglycemia). It requires no fridge storing and is readily available in the event of
hypoglycemia (Vermeulen et al., 2003). 1gr is given intramuscularly which takes 10-15
minutes to reach maximum levels in blood. Common side-effects include headache and
nausea. It is recommended that patients with a recent hypoglycaemia episode or patients
with previous admission in hospital -for the same reasons- are provided with a prefilled
syringe of glucagon. Both patients and relatives must be trained how to use the kit for
preventive reasons.
If the patient shows no signs of improvement after 30 minutes when all the steps have
been made then we should search for other potential causes of coma.
Typically, the treatment algorithm of hypoglycemia is as follows:
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Assess if MILD/MODERATE (Blood Glucose 41-70 mg/dl) or SEVERE HYPOGLYCEMIA
(Blood Glucose 41-70mg/dl with mental status changes, OR, Blood Glucose ≤ 40mg)
Recognize HYPOGLYCEMIA SYMPTOMS
(Adrenergic = Shakiness, anxiety, nervousness, tremor, palpitations, tachycardia, sweating,
feeling of warmth, pallor, coldness, clamminess, dilated pupils, Hunger, Neuroglycopenic
= abnormal mentation, impaired judgment, moodiness, depression, irritability, personality
change, labile emotions, fatigue, weakness, lethargy, slurred speech, confusion, staring,
blurred or double vision.)
Treat for hypoglycemia
Moderate Hypoglycemia:
Give a fruit juice or honey
or gel/tab of glucose per os
Repeat after 45 minutes. If still Glu
<70 mg/dl extra medical attention
is necessary. Otherwise be sure that
the patient will receive a satisfying
quantity of regular meals for the
rest of the day.
Redefine the blood glucose after
15-20 min. If Glu<70 mg/dl give extra
juice or honey until Glu> 70 mg/dl.
Severe Hypoglycemia: If the patient
can swallow, we can provide treat-
ment per os, as in the treatment of
moderate hypoglycaemia.
Is it possible for intravenous fluids
(Is the patient inside hospital)?
NO: Give glucagon injection 1gr.
intramuscularly. Check Glu level in
15-20 minutes. If the patient remains
unconscious attempt to secure
intravenous route and contact a
health professional.
YES: Give a single serum 50%
dextrose 50 ml. Check in 15-20
minutes and if the Glu level has not
risen give a second dose of serum
dextrose 10% at a rate of one liter
at 6 hours.
4.5. Antihypertensive Therapy
High blood pressure or hypertension may develop in patients suffering from D.M. for
several years and so hypertension may coexist with D.M. (Mugusi et al., 1995). The
combination of D.M. treatment and that of hypertension can prove quite effective.
The objectives of therapeutical levels of BP in people with diabetes are:
➠ Adults: <130 / 80 mmHg
➠ Adolescents: <90th percentile for age
➠ Systolic blood pressure<160 mmHg. If the objective is achieved, and BP is well re-
gulated then a further reduction in the levels of 140 mmHg should be pursued.
Typically, the effectiveness of antihypertensive drugs used in a diabetic patient is as follows
(Konzem et al., 2002):
Angiotensin converting enzyme A inhibitors (ACE inhibitors): Beneficial effects have
been displayed in patients diagnosed with either myocardial ischemia, congestive heart failure
or diabetic nephropathy. These drugs have been proven first line therapy for patients with
hypertension and diabetes (Gandhi and Isley, 2007). Deterioration of renal function is slowed
down (Papadakis, 2001). Patients with D.M. and hypertension tend to increase insulin
sensitivity while reducing cardiovascular events as well as the risk of stroke and coronary heart
disease.
Diuretics: The thiazide diuretics have been shown to benefit patients with diabetes and
high blood pressure. They reduce cerebrovascular and cardiovascular events in non-insulin-
dependent diabetic patients who also have high blood pressure. They can be used in
combination with ACE inhibitors. Preferably hydrochlorothiazide is used at a dose of 12,5 mg
daily to 25 mg daily. Thiazide diuretics are not very effective in patients with renal
insufficiency. In these patients loop diuretics are preferred.
Calcium channel blockers (CCBS): They represent alternative options in the treatment
of hypertension in patients with diabetes, especially the dihydropyridines (eg amlodipine,
nifedipine). The calcium channel blockers alone or in combination with another
antihypertensive agent were associated with reduced cardiovascular risk mainly due to
reduction of high blood pressure. In many patients it is required to add one ACE inhibitor or
another antihypertensive agent so as to achieve the desired levels of blood pressure. The
combination of an ACE inhibitor and one dihydropyridines calcium channel blocker has shown
to reduce proteinuria.
Angiotensin II receptors blockers: They are highly recommended especially after side
effects are present of the ACE inhibitors. Treatment with losartan has positive effects not only44
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on the kidneys but also on reducing blood pressure in diabetic patients with nephropathy.
Similarly irbesartan reduces microalbuminuria levels even more than amlodipine.
Beta-adrenergic blockers: Traditionally, the use of beta blockers in patients with diabetes
has been constrained due to adverse metabolic effects and the masking of the hypoglycaemic
symptoms. Atenolol is correlated with greater weight gain compared with captopril but when
compared in relation to hypoglycemic episodes, there is no difference. Yet, there is no
corresponding reduction in risk of cardiovascular complications. Alternatively, Carvedilol (b-
blocker and peripheral a-blocking activity) causes fewer changes in lipid and glucose levels
compared to traditional beta-blocked but can cause dizziness and hypotension (due to it’s
a-blocking action). Thus, dosage increases should be achieved at a slower rate.. Beta-blockers
seem to have a positive effect on atherosclerosis (heart disease).
Alpha-adrenergic blockers: They are not considered first line drugs for the treatment of
hypertension in patients with diabetes. These drugs can be combined with other antihyperten-
sives for the treatment of poorly controlled hypertension but special should be given to avoid
hypotension.
Combination therapy: Most patients with coexisting hypertension and diabetes require
more than one antihypertensive tablets to achieve adequate control of blood pressure. The
combination of ACE inhibitors and CCBs is associated with reduction of cardiovascular events
and reduction of proteinuria. Extra caution should be given when CCBs which do not belong
to the dihydropyridines are combined with ß-adrenergic blockers, due to possible negative
inotropic action on myocardium. The combination of beta-blocker and ACE has also been
associated with additional effects on blood pressure when administered to patients with heart
rate below 83 beats per minute. The combination therapy may have proved more effective
but there is a risk of mistakes involved on behalf of the patient who might fail to maintain
the appropriate combined treatment (Etuk et al., 2008).
Treatment algorithm of hypertension in diabetic patients:
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Many times the cost of drugs will determine our final choice (Salako, 1993). Generally,
in the private sector the value of drugs is higher. Hydrochlorothiazide is relatively
inexpensive and can be used more often (Twagirumukiza et al., 2010). Apart from the
widespread use of diuretics ACE-inhibitors are also of wide use (Olanrewaju et al., 2010). In
any case it should be recommended to the patients to avoid consumption of salt and salty
foods in general.
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BP still not at goal levels (130/80 mmHg): Add long acting CCB, titrate or moderate
dosage, if BP goal is achieved, convert to fixed dose combination using an ACE inhibitor
and a CCB or an ACE inhibitor and a diuretic
BP still not at goal levels (130/80 mmHg)
BP still not at goal levels (130/80 mmHg)
Add night long acting alpha- adrenergic blocking agent, titrate dosages to moderate
dosages, or refer patient to a hypertension experienced specialist
ACE inhibitor /thiazide diuretic. If serum creatinine level is >1,8 mg per dL
(159 Ìmol per L), use long acting loop diuretic
Baseline pulse rate >84 beats per
minute. Add beta- adrenergic
blocking agents or alpha- and beta-
adrenergic blocking agents
Baseline pulse rate <84 beats per
minute. Add another subgroup
of CCB (i.e. amplodipine-like agent
if verapamil or diltiazem is already
being used, or the converse)
4.6 Antidiabetic agents
In T2DM there are several alternatives in relation to the release and efficacy of insulin in the
tissue region. Treatment with antidiabetic tablets along with exercise and nutrition is likely to
achieve a good control of glucose metabolism and of complications of the disease. Medication
can rely on a single drug or on a combination of several drugs. When monotherapy does not
achieve therapeutic goal a second drug must be used, that belongs to another category. The
choice must be made according to some characteristics, such as lifestyle of the patient, the
level of glycemic control, access to medicines, and financial costs.
Monotherapy is usually the first choice, but as the disease develops we may add sup-
plementary medications. Sulphonylureas and metformin are used more.
If the person is overweight (BMI> 25 kg/m2) metformin from the category of biguanides
is the first choice. Alternatively we can use theiazolidinediones.
Specifically, sulphonylureas are drugs that stimulate insulin secretion through the
stimulation of beta cells in the pancreas. If the number of beta cells is significantly reduced
then the action of insulin is also reduced respectively. Sulphonylureas are chosen for T2DM
when diet alone is not enough. As for side effects, sulphonylureas can lead to low blood sugar
and hypoglycemia in cases of insufficient food intake. There are also signs of increased
appetite and weight gain. Long-acting sulphonylureas should be avoided in elderly patients
because of the risk of hypoglycemia. Short-acting sulphonylureas, or glitazones may be used
instead. They must be avoided in T1DM, cases during pregnancy and in liver or kidney
disorders.
Metformin is preferred in overweight people and it can be combined with a sulphonylurea.
It should be prescribed with caution in the elderly people over 75 years of age. It is also
contraindicated in patients with impaired renal function and high levels of plasma creatinine.
It is also contraindicated in the case of liver and severe heart or lung diseases as well as in
pregnancy. Metformin is considered as the only widely used oral drug that does not cause
weight gain amongst the commonly used oral diabetic drugs.
Theiazolidinediones (pioglikazone, rosiglitazone) are a new class of drugs that act similarly
by reducing insulin resistance and increasing insulin action on glucose and lipid metabolism.
They also reduce the hepatic glycogenesis and they increase glycogen synthesis in muscle
tissue as well as lipogenesis. However, they are associated with weight gain and have are
contraindicated in pregnancy, and hepatic or cardiac dysfunction.
Meglitinides are related to insulin secretion (repaglinide and nateglinide). These are called
“short-acting secretagogues” and their major role is to help the pancreas to produce insulin.
These drugs should only be taken before a meal and they help to control postprandial
hyperglycemia. Repaglinide is preferred in cases of renal failure, but it can cause hypoglycemia.
The increased cost versus metformin and sulphonylurea is prohibitive for use in communities
or health systems where financial resources are limited.
Finally, inhibitors of alpha-glucosidase are another category of drugs that inhibit the47
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absorption of glucose. Alpha-glucosidase inhibitors are “diabetes pills” which are not
technically hypoglycemic agents since they lack in a direct effect on insulin secretion or
sensitivity. These agents act by slowing down the digestion of starch in the small intestine
in a way that glucose from the starch enters the bloodstream more slowly so a much more
effective result is achieved even though impaired insulin response or sensitivity is present.
Acarbose which belongs to this class, inhibits the breakdown of polysaccharides to
oligosaccharides and thus reduces the postprandial increase of blood sugar.
Alternatively, the newer drugs used to treat T2DM is the GLP-1 analogue (Glucagon-like
peptide-1) or “similar to the glucagon peptide-1” (liragloutide). GLP-1 analogues are admi-
nistered with a daily injection and reduce the weight of patients. They can slow down the pace
of disease progression and they can be combined with antidiabetic tablets and insulin, while
they do not cause hypoglycaemia. Increased cost makes them unavailable in most settings.
The following table shows the characteristics of some antidiabetic agents with their brand
names in Tanzania, as determined by Tanzania Food and Drug Authority (TFDA):
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Name of drug Starting Max. Major side effects Contraindicationsdose dose
SULPHONYLUREAS
Glibenclamide 2,5 mg 20 mg Hypoglycemia, weight Pregnancy, use with
(Glibenclamide- gain, skin rashes caution in liver and
Novartis) renal disease
Gliclazide 40 mg 320 mg » »
(Diabetron – Glaxo-
SmithKline Egypt)
Glipizide (Glynase 5 mg 40 mg » »
–USV Limited –Korea)
Glimepiride 1 mg 8 mg » »
(Amaryl- Aventis)
Chlorpropamide 100 mg 500mg » »
(Diabinese – Pfizer
NV Belgium)
Tolazomide (not 500 mg 2500 mg » »
available in Tanzania)
Acetoexamide (not
available in Tanzania) 250 mg 1500 mg » »
Tolbutamide 500 mg 2500 mg » »
➜
Out of all those drugs, metformin and sulphonylureas are appropriate for use in poor
resource settings due to cost issues. Generally, the algorithm for treatment of diabetes has to
be based on the availability of drugs, their cost and cost-benefit criteria. Metformin and
sulfonylurea are relatively cheap drugs and can be integrated into the treatment algorithm of
a DM clinic in rural African communities.
Attention has to be paid to avoid any drug which is substandard or counterfeit (Chauve,
2008).
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Name of drug Starting Max. Major side effects Contraindicationsdose dose
BIGUANIDES
Metformin 500 mg 2250 mg Abdominal pain, Renal, heart and
(Rolab Metformin- nausea, loose bowel liver failure
Novartis), (Metformin motions, lactic acidosis pregnancy
–Alpharma Limited UK)
THIAZOLIDINE DIONES
Rosiglitazone (not 4 mg 8 mg Liver impairment, Renal, heart and
available in Tanzania) fluid retention, liver failure,
weight gain, pregnancy
dilutional anaemia
Pioglitazone 15 mg 45 mg » »
(Diavista- Dr. Reddy’s
Laboratories Limited,
India)
MEGLITINIDES
Nateglinide (not 180 mg 360 mg Hypoglycaemia, weight Heart and liver
available in Tanzania) gain, dyspepsia failure, pregnancy
Repaglinide 0,5 mg 16 mg » »
(Novonorm-Novo
Nordisk, Denmark)
ALPHA-GLUCOSIDASE INHIBITORS
Acarbose (Glucobay- 25 mg 300 mg Dyspepsia, loose None
Bayer, Germany) bowel motions
Meglitole (not 25 mg 300 mg » »
available in Tanzania
Patients will receive treatment in relation to some constraints such as:
1. Initially and based on glucose levels, patients will be advised to make lifestyle changes,
start exercising, and avoid smoking and alcohol consumption. Although alcohol use is
widely popular in most poverty hit communities, obedity, lack of exercise and smoking are
less common in such communities. However, urbanization is rapidly changing daily habits
at a fast rate among many deprived communities.
2. If after this period euglucemia levels are not achieved, regular check-ups to ensure that
the patient has succeeded in maintaining good glucose metabolism are needed. If glycemic
goal is not achieved, sulphonylureas treatment has to start for patients with normal
weight and metformin is given for obese patients, as monotherapy. We start with a low
dose and we can increase dosages after the first month of treatment.
Metformin is given as tablets of 500 mg every day and we can double the dose. If
necessary, it can be given at a dose of 850 mg twice daily or even three times daily.
Sulphonylureas are adequate for non-obese patients and chlopropramide and
tolbutamide are the most common ones which are given per os once daily with
breakfast. If it is necessary we can increase the dosing to two tablets daily. The above
mentioned sulphonylureas are more easily to be found in Tanzania (Justin-Temu et al.,
2009).
3. If after three months we achieve metabolic goal we check the patient regularly to make
sure that he maintains this. Otherwise we add another hypoglycaemic agent, first at a low
dose and we can increase it after 3 months (combined oral therapy).
4. If after three months we haven’t reached euglycemia levels, we add intermediate-acting
insulin. ( Liraglutide could be used istead but cost is prohibitive).
5. If after three months euglycemia is not achieved, we choose a combination of multiple
insulin injections.
In general, treatment phases of diabetes are as follows (International Diabetes
Federation (IDF):
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MEDICATION NONADHERENCE:
Medication nonadherence highly prevails among patients with chronic conditions. Diabetic
patients, for instance, have to face at least two comorbidities and they often require multiple
medications. Therefore, one of the reasons for nonadherence is the cost of medication.
Medication nonadherence is associated with public health issues and higher health care costs.
This makes it important for health care professionals to detect cost related nonadherence since
it can lead to strategies to assist patients especially in poor resource environments.. Strategies
to reduce non adherence are pill-splitting, and the use of generic drugs. Free access to
treatment is the strategy to achieve the greatest impact on the health of the population51
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Therefore reductions in diabetes morbidity and mortality along with significant cost savings
to the health care system, can be reached through appropriate and relevant interventions
so that nonadherence can improve.
4.7. Insulin Therapy
Insulin is the main treatment for patients with T1DM and for many patients with T2DM. In
T1DM there is a lack of beta cells of the pancreas which produce insulin for survival.
About Insulin:
A healthy normal weight person produces between 18-40 units of insulin every day. Half
of it is produced between meals or at night (basal insulin) and the other half is excreted during
meals (bolus insulin). This occurs in two phases:
a. During the first phase the secretion of insulin is rapid and it lasts 15-20 minutes. In ∆2DM
this phase is absent or incomplete.
b. During the second phase, insulin secretion lasts longer while glucose is released into the
bloodstream, for instance during a meal. In T2DM this phase is delayed or incomplete,
leading to hyperglycemia.
General information about insulin
Insulin is mostly available in injectable form. This makes it one of the few medicines that
cannot be taken in the form of a pill at the present time. Insulin, like many other proteins
introduced into the gastrointestinal tract, is reduced to fragments (even single amino acid
components) whereupon all “insulin activity” is lost. Although there has been some research
into ways to protect insulin from the digestive tract (so that it can be administered in a pill)
this remains entirely at an experimental stage so far.
Insulin is either of animal origin or biosynthetic insulin by genetic engineering. The most
recently introduced forms of insulin are insulin analogues. Usual forms available are of 40 IU
/ ml and 100 IU / ml vials. There are three types of insulin:
Regular fast acting insulin
Insulin isophane (medium acting)
Premixed insulin (30% regular /70% isophane) Abnsulin analogues: insulin molecules are
attracted to each other and exist as bilateral or six-parts in the solution. For insulin to be
absorbed, six parts must break down to monomers. This process can take up to 30 minutes.
Insulin analogues are not present in the body, but are produced by a molecular change in52
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an amino acid. This change makes them act differently according to the initiation and duration
of action of insulin.
Insulin analogues help overcome the obstacles of soluble (regular) insulin. Soluble insulin
slows the degradation of six parts to two and one part delays the onset of action when
injected subcutaneously. Thus, soluble insulin must be injected up to about 30 minutes
before lunch, allowing the monomers of insulin to rise in the circulation before glucose
levels rise. This time limitation makes it sometimes difficult for the patients to keep the
30 minutes time gap between injection and lunch. They cannot eat before 30 minutes pass.
As a result, maximum postprandial insulin level is delayed, as insulin concentrations have
risen slowly after subcutaneous injection. This may also introduce higher risk of
hypoglycemia, as long as insulin levels may increase before the rise of glucose, or remain at
high levels after the postprandial hyperglycemia has passed. In this way there is no
simulation of the endogenous insulin secretion. On the other hand, insulin analogues act
quickly and do not require this time gap of 30 minutes between time of injection and lunch.
They mimic endogenous insulin secretion, allowing a better control of postprandial and 24-
hour glucose levels. They also increase the risk for hypoglycemia. For all these reasons they
allow more flexibility in patient’s lifestyle but their cost is a lot higher. Analogues are mostly
used as: Short acting (bolus), Long-acting (basal 17-24 hrs of action) The premixed analogue.
Insulin analogues are more expensive and rather difficult to use in a poor resource settings
environment.
Regular short acting is human soluble insulin. When it enters the body, it works in the
same way as natural insulin and increases overall ability for the body to uptake glucose.
Soluble insulin is fast-acting (usually between 30 minutes and an hour) and lasts for
approximately eight hours depending on dose. Soluble insulin is usually used before a meal,
and controls postprandial blood glucose levels. Regular insulin can sometimes be combined
with other types of insulin (longer-lasting) to provide overall control through the day. With all
insulin types it is worth bearing in mind that the stricter control exercised over diabetes, the
less likely it is to develop into serious complications.
Intermediate-acting insulin helps to control blood glucose throughout the day.
Premixed Insulin in mixtures of 10/90, 20/80, 30/70, 40/60 and 50/50 mixtures of short
acting regular and intermediate acting preloaded pens and also in penfill cartridges and vials.
All of these medicines are based around human biphasic isophane insulin. Mixtard is based
around soluble insulin and isophane insulin. Pre-mixed insulin such as this acts both rapidly
(soluble) and at an intermediate level.
The following table shows the main characteristics of the most commonly used
insulins:
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Insulin pens
An insulin pen is used to inject insulin for the treatment of diabetes. It is composed of
an insulin cartridge (integrated or bought separately) and a dial to measure the dose, and is
used with disposable Pen needles to deliver the dose.
Insulin pens are currently available on the market as insulin delivery system apart from
conventional syringes. When the patient learns how to handle the pens properly there is no
other financial cost compared with that of vials and syringes (Baser et al., 2010). They can
be particularly useful to patients with blurred vision. 54
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The fact that pens can be used by the trained patient in an easy way and the fact that
they can be kept out of the refrigerator (even after opening) are among the main
advantages.
The use of insulin pens can increase the cost of treatment for many patients in an
environment of limited resources and it is difficult to implement it in a diabetes clinic of a
developing country. The vial-syringe system is cheaper and can have wider application in such
a program.
Needles-Syringes
The needles used with pens are described by two numbers. The first referred in mm refers
to the length of the needle. The second expressed in G refers to the thickness of the needle
(the higher the number, the thinner the needle). Eg. 6mm (31G) and 80mm (30G).
These needles are used with pens. When the patient uses vials and syringes instead of pens
and needles he/she can reuse syringes in order to reduce costs and avoid buying large supplies
of syringes. This is very important in a poor resource settings environment. Some useful tips
we the therapist should give to the patients when reusing syringes are:
➠ Keep the needle clean by keeping it capped when you are not using it.
➠ Never let the needle touch anything but clean skin and the top of the insulin bottle.
➠ Never let anyone use a syringe you have already used, and do not use anyone else’s
syringe.
➠ Cleaning it with alcohol removes the coating that helps the needle slide into the skin
easily.
An important part of good injection technique is to inject at the proper depth. Insulin
should be injected in the subcutaneous fat –the layer of fat just below the skin- is highly
recommended by most professionals. If the injection goes too deep, the insulin could go
into muscle, where it is absorbed faster but it might not last long enough and it is much more
painful. The onset and duration of action of insulin is also affected when the injection is not
deep enough and the insulin goes into the skin.
Most people pinch up a fold of skin and insert the needle at a 90Æ angle to the skin fold.
To pinch the skin properly, the patient should follow the steps below:
➠ Squeeze a couple of inches of skin between the thumb and two fingers, pulling the
skin and fat away from the underlying muscle. (If a 5 millimeter mini-pen needle is used
to inject, the patient doesn’t have to pinch up the skin when injecting at a 90Æ angle,
with this shorter needle, there is no to fear of injecting into muscle.)
➠ Insert the needle.
➠ Hold the pinch so the needle does not go into the muscle.
➠ Push the plunger (or button if a pen is used instead) to inject the insulin. 55
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➠ Release the grip on the skin fold.
➠ Remove the needle from the skin.
Note that not everyone injects at a 90Æ angle. If the body has less fat, it might be necessary
to inject at less than a 45Æ angle, to avoid injecting into a muscle.
Choosing the right insulin
There are several problems with insulin as a clinical treatment for diabetes:
➠ Selecting the right dose and timing.
➠ Mode of administration.
➠ Selecting an appropriate insulin preparation (typically on “speed of onset and duration
of action” grounds).
➠ Adjusting dosage and timing to fit exercise undertaken.
➠ Adjusting dosage and timing to fit food intake timing, amounts, and types.
➠ Adjusting dosage, type, and timing to fit other conditions, for instance the increased
stress of illness.
➠ Variability in absorption into the bloodstream via subcutaneous delivery
➠ It is dangerous in case of mistake (most especially “too much” insulin).
➠ It is not highly recommended that patients inject whenever they eat carbohydrate or
show a high blood reading.
The choice of the appropriate type of insulin depends on the patient’s lifestyle. If the person
requires maximum flexibility in his daily activity, it is recommended that he inject insulin four
times daily (basal and bolus). This allows the patient to match the insulin injections to his
lifestyle. Alternatively, he can apply a figure of two insulin injections daily from premixed insulin.
Some features that should be taken into account before choosing the appropriate types
of insulin administration have to do with the patient’s eating habits. The quantity and quality
of the meals as well as the dietary preferences of the patient must also be considered. Other
important factors are the level of physical activity, age, or certain disabilities. Patients unwilling
to undergo multiple injections or reluctant to cooperate should also attract our attention. The
level of perception and adaptability as well as the level of health support in the region should
also be considered before we start someone on insulin injections.
The proper insulin regimen should imitate as much as possible the endogenous insulin
secretion characterized by a basal secretion which suppresses the hepatic glucose production,
and an increased secretion in response to meals. The most rapidly absorbed and fast acting
analogues of insulin reduce the risk of postprandial hypoglycemia. The basic levels of insulin
can be achieved with intermediate-acting insulin injection at bedtime with or without reduced
morning doses. Long-acting insulin given once a day can produce the same result. A number
of dosing regimens can be applied for each patient.56
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Insulin dosage
A. In the multiple injection regimen we combine bolus and basal insulin. The starting dose
for T1DM is 0,6 IU / kg of total body weight per day and for T2DM 0.2 IU / kg of total body
weight per day. 60% of the total daily dose should be administered as a short dose insulin
(bolus) (ins. Actrapid) before meals for example, 20% before breakfast, 20% before lunch and
20% before dinner. The remaining 40% should be used as an intermediate-acting insulin
(basal) before bedtime (eg at 22:00 hours).
B. The double regimen is simpler and it uses premixed insulin (eg 30/70). The initial dose
is for T1DM is 0,6 IU / kg of body weight per day, and for T2DM 0.2 IU / kg of body weight
per day. The two thirds of the total dose should be given before breakfast and the remaining
one third before the evening (Ministry of Health, 2009).
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C. For people with T2DM bolus insulin can be administered in combination with anti-
diabetic tablets. In cases of shortage of glycemic control, exclusive insulin analogues can be
used instead.
a. Additional treatment: Basal insulin in combination with antidiabetic tablets. The dose of
antidiabetic drugs is increased gradually and basal insulin is added (long acting) at 10:00
a.m. at a dose equivalent to 0,2 IU / kg of body weight.
b. Replacement therapy: If no glycemic control is successfully reached with antidiabetic
tablets, a double insulin regimen is introduced . The total daily dose is 0.2 IU / kg of body
weight and it is used 2/3 in the morning and the rest 1/3 in the evening. It consists of
premixed insulin analogues.
Attention must be paid when we increase or decrease the dose of insulin. We should not
exceed more than 2-4 IU above or below the previous total dose. Moreover, we should do not
change insulin regiments more than once per week. Only if there are ketones present, can we
adjust doses more rapidly.
There are also several factors that influence insulin absorption, as shown in the table
below. Variability of insulin absorption is perhaps the greatest obstacle to replicating
physiologic insulin secretion.
In developed countries pumps for insulin secretion can be used. Their implementation
requires good health system support which is unlikely to find in a poor settings environment.
Blood Glucose Meters
A glucose meter (or glucometer) is a medical device for determining the approximate
concentration of glucose in the blood. It is a key element of home blood glucose monitoring58
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Factor Effects
Site of injection Abdominal injection (particularly if above the umbilicus) results in the
quickest absorption, arm injection results in quicker absorption than thigh or
hip injection
Depth of injection Intramuscular injections are absorbed more rapidly than subcutaneous
injections
Exercise Exercising a muscle group before injecting insulin into that area increases the
rate of insulin absorption.
Heat application Local application of heat or massage after an insulin injection increases the
or massage rate of insulin absorption
by people with diabetes mellitus or hypoglycemia. A small drop of blood, obtained by pricking
the skin with a lancet, is placed on a disposable test strip that the meter reads and uses to
calculate the blood glucose level. The meter then displays the level in mg/dl or mmol/l.
It would be desirable for patients injecting insulin to have a device for measuring blood
sugar at home. Unfortunately, many of them cannot afford to buy one together with the
strips. When resources are limited projects should prioritize patients more prone to benefit
from a more tight control and able to do this as well as to families with diabetic children. (Cho
et al., 2006). Patients or relatives to be given such a device should be taught how to use it
properly.
4.8. Common practices in the treatment with insulin
Rebound hyperglycemia: A state of hypoglycemia, symptomatic or asymptomatic, which stimulates the secretion of
insulin antagonistic hormones. In a normal person increased pancreatic insulin secretion will
neutralize the action of these hormones. In a person with insulin deficiency these hormones
can cause hyperglycemia, which is a phenomenon known as Somogyi. As a result elevated
blood glucose levels can be observed during the morning wake-up.
The Dawn phenomenon:Dawn effect is defined as an increase in the blood sugar in the morning and is typically
invoked in the context of diabetes. It is different from chronic Somogyi rebound in that Dawn
effect is not associated with nocturnal hypoglycemia. In a person without diabetes during
sleep insulin levels are low, especially at 3 am. Insulin levels gradually increase by dawn in
order to counteract the rising levels of cortisone and growth hormone. For insulin-dependent
diabetic patients the insulin pattern should preferably be similar, ie low insulin dose at 3 am
and high at 6am. The increase in insulin requirements is called “the Dawn phenomenon”, and
thus we try to provide the evening dose of basal insulin as late as possible in the evening,
for example at 22:00. The later the insulin injection is given, the later is the peaking time of
insulin.
As a result for a person who wakes up with morning hyperglycemia his levels of blood
glucose should be checked during the night around 02.00-03.00 hrs in the morning. If glucose
is low, the person experiences hypoglycemia followed by rebound hyperglycemic reaction.
In this case, we need to reduce the evening dose of insulin and to add a snack at 22:00. If
glucose is normal or high, the person may develop the Dawn phenomenon and in this case
we must add insulin at 22:00 or choose a basal insulin with a more delayed peak.
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4.9. Lipohypertrophy
The injection sites which are mostly used are the abdomen, the thigh, and the buttock. The
arm can also be used, although it is difficult to access. The rate of absorption is fastest on the
abdomen and slowest on the unexercised thigh. The thigh should be avoided when exercise
follows, as this will increase the rate of absorption of the insulin. One area should be used for
an injection at a particular time of day, e.g. the abdomen is the site for the morning injection,
and the thigh is the site for the evening injection.
Lipohypertrophy is a medical term that refers to a lump under the skin caused by
accumulation of extra fat at the site of many subcutaneous injections of insulin. It may be
unsightly, mildly painful, and may change the timing or completeness of insulin action. It is
a common, minor, chronic complication of diabetes mellitus.
In the site of injection hypertrophy of adipose tissue can be observed. It is characterized
by appearance of large, elevated, spongy masses of fatty fibrous tissue (lumps) at the injection
site. Easily accessible sites, such as the thighs, are most commonly affected. The injection in
these areas is relatively painless, so the patient usually continues to inject insulin at the same
site. The absorption of insulin is also reduced in these areas. The necrosis of the skin can occur
if injections are done into the skin rather than subcutaneously. In any such a case we should
advise the patient to change the site of injection.
4.10. Storage of insulin
Insulin should be stored in a refrigerator at 4-8 Æ C. Human insulin is stable for 30 months from
the date of manufacture in these temperatures and the insulin analogues for 24 months.
Insulin should be stored in a separate section at the bottom of the refrigerator, away from the
ice and not at the door where the temperatures are not stable. Insulin should never be
freezed. On rare occasions which this happens and insulin has to be defrosted, the crystal
structures will most probably be destroyed, so it is best to be discarded. We should always
check the expiring date and examine the bottle closely to make sure the insulin looks normal
before we draw the insulin into the syringe.
Shortly used insulin does not need to be stored in the refrigerator. If there is no refrigerator
or no electricity available, insulin may be stored in a cool place or in special containers, away
from sunlight (Allen, 1982) (Gill et al., 2002). A cold injection would also hurt more. At 25 Æ
C insulin is stable for 6 weeks and at 37 Æ C for 4 weeks. It should however be kept away from
the sun. Analogues remain stable for four weeks at temperatures of 30 Æ C and lower. We
should shake the vial gentle before use and avoid the intense shaking that can damage the
molecular structures. 60
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Insulin pens should be stored in the refrigerator before opening and after opening they
can be left outside the refrigerator, but in temperatures below 30 Æ C.
4.11. Diabetic Foot
Diabetic foot is an umbrella term for foot problems in patients with diabetes mellitus. Due to
arterial abnormalities and diabetic neuropathy, as well as a tendency to delayed wound
healing, infection or gangrene of the foot is relatively common. Ten to fifteen percent of
diabetic patients develop foot ulcers at some point in their lives and foot related problems are
responsible for up to 50% of diabetes related hospital admissions.
Micro and macro ischemia as well as diabetic neuropathy are the two main risk factors that
cause diabetic foot ulcer. Due to several metabolic and neurovascular factors, diabetic patients
often suffer from diabetic neuropathy. Peripheral neuropathy –a type of neuropathy- causes
loss of pain or feeling in the toes, feet, legs and arms due to distal nerve damage and low
blood flow. On numb areas of the feet and legs (such as metatarso-phalangeal joints and
the heel region) pressure or injuries may go unnoticed, that may also happen with blisters and
sores which eventually become portal of entry for bacteria and infection. Diabetes can reduce
both the movement and the sensation in the foot. This can cause loss of sensitivity, touch and
temperature. The diabetic foot in conditions of reduced care may have high mortality (Gulam-
Abbas et al., 2002). The patient’s foot should be examined for any sores, redness, blisters,
cellulite, injuries, necrotic tissue, discoloration, reduced peripheral pulse at the legs. The
injuries to the foot of patients in developing countries need preventive treatment, otherwise
it is difficult to deal with them (Unwin, 2008). We also need to protect feet from rodent
bites and stings which can deteriorate the state of the foot (Abbas et al., 2005).
Early detection of foot at risk and appropriate treatment reduced the risk of amputations
in a program in Tanzania from 9% to 6,5% (WDF, 2008). The costs for the treatment of
diabetic foot is proportionately high compared to the total cost of treating diabetes. (Karel
Bakker, 2009)
Patients are recommended not to walk barefoot (Jayasinghe et al., 2007). They should also
wear socks that are not too tight and avoid contact with cold or hot objects. They must
examine their toes regularly and they must dry the feet after washing them. Moreover, they
must cut nails straight and pay attention to the skin, and if there are wounds they should
be covered with gauze and elastic bandage.
Multidisciplinary assessment by diabetes specialists and surgeon is requires for foot ulcers
in diabetes. Foot ulcers are usually treated with appropriate bandages, antibiotics (against
staphylococcus, streptococcus and anaerobe strains), debridement and arterial revascula-
risation. Flucloxacillin from 500 mg to 1000 mg, amoxicillin of 1g and metronidazole to tackle
the putrid smelling bacteria are also used in treatments.61
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Projects should aim to increase the level of knowledge about the risks of damage on the
foot. Patients and health professionals should be taught all the good practices to reduce the
risk of diabetic foot (Matwa et al., 2003). It should also provide appropriate care for patients
who have already undergone amputation, as the reinfection rate is often high in patients from
Africa (Viswanathan et al., 2010).
Finally, in many populations of tropical regions there are observed hands injuries similar
to those of the diabetic foot, due to microangiopathy. This complication is considerably rarer
than the well-known diabetic foot, but may be more likely to meet in Africa (TDHS, 2002).
4.12. Diabetes and physical activity
Physical activity is an important factor in the treatment of diabetes type 1 and 2. The aim
is that all patients learn the benefits of physical activity, and potential risks of intense
physical exercise. We must also take into consideration all the physical problems that make
it difficult for some patients to exercise, and in each case we must give special recommend-
ations. It seems that the urban population exercises less than the rural population (Kuga
et al., 2002).
Exercise increases insulin sensitivity and peripheral glucose utilization and improves blood
glucose control. In addition, it improves cardiovascular function, it reduces high blood pressure
and lipids level that frequently coexist with diabetes, while reducing hepatic glucose release.
Exercise also helps the patient to control body weight and gain a feeling of well being.
Improvement of muscle strength, increase of bone density and energy level, release of tension
and anxiety, while enhancing work capacity are only some of the benefits the patient enjoys
after exercising.
The risk of intense physical activity on the other hand, is that patients may develop
hypoglycemia, mainly the patients on insulin. Also, strenuous physical exercise should be
avoided because it can have a bad influence on cardiovascular system, particularly in elderly
diabetics. The exercise which is usually recommended is aerobics, a relaxed pace, especially
walking or light running, with adequate protection of the feet in order not to be injured. So
as to control blood sugar, the patient should try to exercise at the same time for the same
duration at least 3 times a week for approximately 30-45 minutes. As far as insulin injection
is concerned, insulin must be reduced or avoided if the patient has an intense physical
activity.
An obstacle for people with diabetes can be the presence of another illness, physical
disability, eg polio, blindness, also problems related to the legs such as neuropathy or joints
problems. Other possible barriers may be lack of space, time, safety or motivation. Exercise
is not recommended when blood sugar level is over 300 mg/dl and if the patient feels sick,
short of breath, is experiencing any tingling, pain or numbness in the legs. Diabetics should62
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also refrain from exercising when ketones appear in their urine and when the medication
is peaking.
The concept of physical activity may also vary from region to region. Sure there are
populations in the developing country that have adopted a more urbanized way of life which
is characterized by obesity and reduced physical activity. But when a person suffering from
diabetes is involved in a job which requires strenuous physical activity, many hours of work,
or a long way commuting on foot, then the dose of insulin must be adjusted accordingly in
order to avoid possible hypoglycemia episodes. In such cases it is essential that special
footwear for protection (eg custom made shoes that follow the shape of the feet ) and some
food rich in carbohydrates are available.
If the patient intends to exercise after he has eaten, a snack high in carbohydrates is much
more preferable than a proper meal. Of course, if the patient does heavy aerobic exercise or
strenuous work, it is wise to eat a bit more. If the patient hasn’t eaten for over an hour or
if blood sugar is less than 100 to 120 mg/dl, he should have an apple or glass of milk before
working out. In all cases the patient should have a snack with him. Insulin dependent patients
should work out after eating and not before. Testing blood sugar before, during and after
exercising could be ideal but unfortunately this is not always possible especially in poor
resource settings environment.
4.13. Dietary intervention
A change in dietary habits of the patient is an important factor of the treatment of diabetes.
The diet should be tailored according to age, needs, religion, cultural characteristics and
lifestyle of the patient.
The objective of dietary changes is that the patient receives all the necessary calories and
nutrient elements which ensure growth and health. The patient should also maintain or
achieve the appropriate weight with proper nutrition. In addition euglycemia levels should be
reached according to their metabolic needs, physical activity and medication of the patient.
In any case, the patient should learn the importance of nutrition in regulating the disease,
although health professionals sometimes lack in this knowledge (Abioye-Kuteyi et al., 2005).
It is essential that clinical nutritionists are involved in DM care.
The diet for diabetes should be applied according to concept of a healthy diet. The diabetic
patient can eat a variety of dishes. As a general rule fatty food and sugar should be reduced.
Moreover the patient should eat 2-4 fruits daily and avoid sugary juices. Sugar could be
replaced by sweeteners. Proposed diets should be tailored to the particular eating habits
and food availability at local level.
The patient’s eating habits, time and frequency of main and smaller meals should also
be taken into account. Possible allergies must also be considered. The patient must be checked63
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for signs of malnutrition, excessive food surplus and alcohol. Each case requires specific diet
arrangements according to age, gender, socioeconomic status, ethnicity and occupation. The
patient’s level of perception as well as his willingness to change his dietary habits play an
important role. The recommended diet must also depend on the type of diabetes, the
prescribed treatment, the level of physical activity, the body mass index, waist circumference
and blood pressure. If biochemical control is possible, the lipid profile, liver enzymes, urea and
electrolytes must also be checked.
After considering all these aspects the therapist can discuss the appropriate changes to
be made with the patient. The therapist must keep a follow-up even after his first session with
the patient so as to ensure that the patient follows the recommendations. Sometimes further
diet changes and adjustments are also required. Specific groups such as pregnant women and
patients with renal problems must be checked more regularly. It is common practice within
the African culture for the family to gather and eat together from the same dish. The therapist
here must emphasize the need for the diabetic member of the family to follow his own
specific diet. The understanding of the family can help especially if they all decide to adopt
the same healthy eating habits as the patient. This can provide a way out when there is no
possibility of cooking separate dishes for the diabetic member of the family.
The basic elements of nutrition are discussed below:
Carbohydrates are essential for all people with diabetes. In Africa, many diets are rich
in carbohydrates and they contribute best for glycemic control. Foods consumed in large
quantities are hard porridge, bread, rice, beef, milk, oranges and sunflower oil. The main
beverage is water, tea and milk (Hoffmeister et al., 2005). It is recommended that
approximately 60% of all calories come from carbohydrates. They are found mainly in cereals,
grains, dairy, fruits and vegetables. Fresh fruits are preferred to juice as they contain fibres.
Sugar increases blood glucose levels faster compared to starch, and therefore it is suggested
that sugar be replaced by other sources of carbohydrates. Sugar is preferred during exercising
or when the patient enters a phase of hypoglycemia. The quantity of insulin dosage should
also be regulated depending on the level of carbohydrates on the diet. Furthermore, fibres
intake is crucial.
The glycemic index (GI) is a measure of the effects of carbohydrates on blood sugar
levels. Carbohydrates that break down quickly during digestion and release glucose rapidly
into the bloodstream have a high GI, carbohydrates that break down more slowly,
releasing glucose more gradually into the bloodstream, have a low GI. GI values can be
interpreted intuitively as percentages on an absolute scale and are commonly interpreted
as follows:
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A lower glycemic index suggests slower rates of digestion and absorption of the foods
carbohydrates and may also indicate greater extraction from the liver and periphery of the
products of carbohydrate digestion. A lower glycemic response usually corresponds to a lower
insulin demand but not always, and may improve long-term blood glucose control and blood
lipids. A low-GI food will release glucose more slowly and steadily. A high-GI food causes a
more rapid rise in blood glucose levels and is suitable for energy recovery after endurance
exercise or for a person experiencing hypoglycemia.
Proteins are found mainly in foods of animal origin. The influence of proteins in blood
sugar depends on the availability of insulin. In well-regulated diabetes proteins do not increase
blood sugar levels, but in T2DM proteins are likely to stimulate the secretion of insulin.
Proteins require insulin for metabolism. Approximately 15-20% of calories should come from
protein (about 0,8 gr / kg body weight). However, a diet high in protein and low in
carbohydrates is not recommended because it is usually accompanied by large quantities of
saturated fats.
The fats are found mainly in foods of animal origin and cooking oils. They should not
exceed 30% of total calories. Fat provides more calories per gram (total 9 kcal / gr). They
are distinguished to “good” and “bad” fats depending on their effect on cholesterol meta-
bolism.
Saturated fats, the bad ones, raise cholesterol levels in blood. They are found mainly in red
meat. The fats from coconuts and palms fruits which are often found in Africa belong to
this category. They are in solid form at room temperature with the exception of coconut and
palm fats.
Unsaturated or “good” fats are divided into monounsaturated and polyunsaturated. If
saturated fats are replaced in the diet of the patient that will help to lower cholesterol. It is
in liquid phase at room temperature. Source of polyunsaturated fats are sunflower, corn,
soybeans and fish fats. Monounsaturated fat source are olive oil, nuts (peanuts and nuts) and
avocados. A diet high in monounsaturated consumption reduces the risk of cardiovascular
disease, whereas polyunsaturated and omega-6 fats reduce triglyceride levels. Finally, trans65
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Classification Examples
Low GI most fruits and vegetables (except potatoes and watermelon), whole-grain
breads, pasta, legumes/pulses, milk, yogurt, products extremely low in
carbohydrates (some cheeses, nuts), fructose
Medium GI whole wheat products, sweet potato, table sugar
High GI corn flakes, baked potatoes, watermelon, white bread, extruded breakfast
cereals, most white rices, straight glucose
fats, found mainly on butter products and fried foods, increase LDL cholesterol and should be
avoided. Imported foods rich in conservatives and trans fats are found in Africa, especially
in urban settings and their use should be highly discouraged.
Preferring dairy products low in fats and removing the visible fat from meat and the skin
from chicken make the basic rules for reducing fats in food. Baking food should be preferred
instead of frying. Also vegetable oils rich in polyunsaturated and monounsaturated should be
consumed, as well as fish. Vegetables should preferably be cooked without butter.
To simplify the type and quantity of food recommended for DM we could use the food
pyramid. The body needs more cereals, rice, bread and other carbohydrates which are on
the basis of the pyramid and less sweets and fats which are on the top of the pyramid.
So every day the body needs 6 to 11 parts of starchy foods or bread. This is about a
slice of bread, half cup of cooked rice or grains. The body also needs 3-5 parts of
vegetables (each part is a cup of raw vegetables), 2-4 parts of fruit (each part is a cup of
fruit or half cup of fresh juice without sugar), 2-3 parts of milk products (each part
corresponds to a cup of milk or cup of yogurt), also 2-3 parts of meat (a part corresponding
to 57-85gr meat, two eggs and two pieces of cheese) and the total fat should be limited
to a spoon of margarine.
Important is the willingness of the patient to choose the right foods for him and avoid
foods of low nutritional value (Macmullan, December 2009).
Moderation is advised with regards to consuming alcohol and the use of some drugs.
Alcohol inhibits the glycogenesis in the liver and some drugs inhibit hunger symptoms. This,
together with impaired judgment, memory and concentration caused by some drugs can lead
to hypoglycemia.
4.14. Diabetes and Obesity
A large number of people with T2DM living in the developing countries are obese (Delpeuch
and Maire, 1997), particularly in urban areas (Aspray et al., 2000). Obesity is also no longer
a condition that just affects older people, although the likelihood does increase with age,
and increasing numbers of young people have been diagnosed with obesity. Obesity is
associated with poor prognosis of the disease and its complications. The reduction in body
weight has a positive effect on the disease. Obesity is a major factor of the metabolic
syndrome. The waist circumference is also a sign of obesity, which we should take into
account.
We should set realistic targets for reducing weight in an overweight patient, and in order
to achieve this we should change the diet and increase the physical activity level. Generally,66
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it is difficult for patients to lose weight and maintain the ideal body mass index. Also, in many
cases obesity is accepted by a large proportion of the population as it is considered a sign
of prosperity or beauty. In such cases it is not easy to convince them to reduce their body
weight.
4.15. Fasting and Diabetes
Many people fast for religious or cultural reasons. According to estimates coming from
religious leaders and sociologists the Christian and Muslim communities in Tanzania are
approximately equal in size, each accounting for 30 to 40 percent of the population, with
the remainder consisting of practitioners of other faiths, indigenous religions, and
atheists.
The culture of each nation carries the values, beliefs about what is good and bad, and
suggests ways of behavior. It is important to take into account these cultural characteristics
to understand better the daily lives of these people. According to this many diabetics follow
their religious beliefs and fast in contrast to the advice and knowledge of the therapist.
Therefore we should be careful to adjust treatment to a man who fasts.
In such cases the general principle is to recommend to the patients to avoid fasting if it
is not absolutely necessary. If they want to follow “hard” diets, they should not exclude water
in any case. There are certain groups of people and circumstances where you may be exempt
from fasting. For example:
➠ children (under the age of puberty)
➠ the elderly
➠ the sick
➠ those with learning difficulties
➠ those who are travelling
➠ pregnant, breastfeeding and menstruating women
➠ anyone who would be putting their health at serious risk by fasting, eg people who
treat their diabetes with insulin or have diabetic complications (damage to eyes, kidney
or the nerves in your hand and feet).
Religion leaders should allow patients to be exempted from fasting. If the person takes
insulin or hypoglycaemic drugs, special administration is required to match the reduced calorie
intake and to avoid episodes of hypoglycemia. In these patients we should check more
regularly blood glucose levels. The complete exclusion of food is not recommended for anyone
with diabetes. The necessary hydration of the patient is necessary even during the fasting
period. Strenuous physical activity during the period of fasting should be avoided. In cases67
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of hypoglycemia or persisting infections the patient should be advised to stop fasting. The
same thing is also necessary for patients with renal or heart problems.
Muslims fast for one month during Ramadan. From sunrise until sunset they do not eat
any kind of food or even water, nor do they smoke or drink. They only eat between sunset
and sunrise.
Patients who are treated with antidiabetic tablets and diet may fast. The usual dietary
advice should also be followed during this period. Patients who take metformin, and alpha-
glucocidase can continue taking their usual doses, the usual hours. Patients prescribed with
chlopropramide (of the sylphonylureas family) should replace it with a shorter acting
antidiabetic agent. If they take a second or third generation sulphonylureas (glibenclamide,
gliklazide, glipidine) they should take them before the fast ending and not before dawn. If
the patient is receiving tolbutamide, he may take both the morning and the afternoon dose,
but the lower dose should be taken before dawn.
Patients with T2DM who receive insulin injections once daily at bedtime hour they may
continue as before. If they take two doses daily, a short and an intermediate acting insulin,
the hours should be changed and the patient should receive the usual evening dose of short
acting insulin before meals by dawn. Also before dinner the patient should receive the usual
dose of the intermediate acting insulin that he used to take before fasting in the morning.
It is also useful to measure blood glucose regularly to adjust insulin dosages. Patients with
T1DM can receive a long acting insulin by 70% and the rest 30% of short acting. The total
dose of insulin before fasting can be reduced up to 85%. The double dose before and after
sunset is another alternative (Kassem et al., 2005)
Fasting in many religions, especially Christianity can have various forms. Thus, the
absolute fasting requires complete abstention from food and water, as during Easter, for
instance. It is recommended that this does not last more than three days and it is absolutely
not recommended to patients receiving insulin. In some forms of fasting the person abstains
from meat, but he can drink water and follow a vegetarian diet. In these forms of diet the
patient should receive all the calories and nutrients. If this happens there is no special
treatment adjustments needed. The patients can continue to take metformin tablets with
meals as well as sulphonylureas and insulin before meals.
4.16. Diabetes and lack of food
Often the therapist will encounter people with low body mass index. This may be due either
to malnutrition or it may be the result of T1DM (Lester, 1993). Malnutrition is not related to
future development of D.M. in an undernourished person (Swai et al., 1992).
In many developing countries due to poverty, wars, or poor crops, patients with diabetes
may not have access to food. The body then tries to save energy. The fat stores are consumed68
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first and then the proteins and the muscle tissues follow. Primarily the body places an
emphasis on providing the brain and the heart with the appropriate energy. The risk of
ketoacidosis is high, and this occurs especially to patients with T1DM.
In such cases, the therapist has a limited potential to act. The doses of insulin to patients
who are malnourished are reduced drastically. Dietary restrictions are not valid anymore and
the person is recommended to eat all kinds of food that he finds available. When some meals
are found only small doses of short-acting insulin may be given. Hydration of the patient is
also essential.
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5.1. Diabetes in children and adolescents
Throughout the world, incidences of diabetes are on the rise, and consequently so is diabetes
amongst children. Most children are affected by T1DM in childhood. However, the number of
children and young adults affected by T2DM is also beginning to rise. Life expectancy for a
child with T1DM in Africa may be just one year. This is due to incapability of the health system
to detect and treat the disease, the limited resources available and the heavy cost of
treatment of a child with diabetes for a poor family (Elrayah et al., 2005). In addition, for
children already diagnosed the glycemic control reached by the applied treatment is not
always satisfactory (Majaliwa et al., 2007).
Children and adolescents require special treatment specifically during the periods of their
growth and development. The program aims to help children and their families to regulate
diabetes and achieve a normal development and maturity. Also while emergency
complications such as ketoacidosis and hypoglycemia need to be avoided, the knowledge
of the community in relation to the risk of diabetes in children should be increased (Bassili
et al., 2001).
To meet all these needs we should check the environment of the child or adolescent, his
stage of development, the family and social support received. The program followed at school
and the level of physical activity should be taken into account as well. Sometimes the family
regards the child with diabetes as cursed or bewitched. Therefore the child faces the family
rejection as well (Bucci, 2008).
There is often a family history of children with diabetes and the autoimmune nature of71
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Diabetes in patients of special categories
chapter 5
diabetes is confirmed, often with the presence of specific autoantibodies (Fakhfakh et al.,
2008).
The typical appearance of diabetes in children may include polydipsia, polyuria (often with
a recurrence of nocturnal enuresis), tachypnea (typical deep breathing Kussmaul), fatigue and
weight loss. Amongst children, specific symptoms may include stomach aches, headaches and
behavioral problems. Recurrent tummy pains and an unexplainable history of illness should
be treated as possible heralds of diabetes. The delay in diagnosis leads to vomiting, abdominal
pain, dehydration, ketoacidosis, drowsiness and coma. Diabetic ketoacidosis has a mortality
rate of 10%. The patient emits sweet breathing smell typical of “ketones emittance” which
makes a clinical sign for the diagnosis of ketoacidosis.
In addition, fever occurrence suggests coexisting infections and abdominal tenderness can
mimic surgical abdomen problems. You should check for the presence of glucose in urine in
all children with polydipsia or urinary symptoms. The glucose tolerance test has little value
in diabetic children who suffer mostly from T1DM and so it is important to measure blood
sugar.
The admission to hospital is required in case of diabetic ketoacidosis or dehydration. Insulin
is administered subcutaneously or intravenous if there is an intravenous route. When
ketonouria is treated, insulin is administered subcutaneously once again. The method of
insulin injection should be completely understood by the child’s environment. Children who
are diagnosed for the first time with diabetes require insulin dose 0.5 to 1 IU / Kg / day. Usually
after a few weeks or days the insulin requirements are reduced and sometimes stopped. This
period is called “honeymoon period”. The therapist should be very observant to adjust the
dose and avoid possible hypoglycemia episodes.
Because type 1 typically means that the vast majority of islet cells have been destroyed
and insufficient or zero insulin can be produced, the only certain method of treating diabetes
in children is insulin treatment. As a general rule the pre-adolescent dosage is 0,5-0,8 IU /
kg / day, adolescent dose 0.8 IU / kg / day and the dose for adults 0.6 IU / kg / day. Insulin
can be administered twice daily in a typical treatment regimen, or three times daily in an
intensive regimen that offers flexibility on meals and physical activity. The triple regimen may
be better applied to older children, with special care to avoid hypoglycemia. Insulin should
always be adjusted according to measured blood glucose levels and in relation to physical
activities especially when children are concerned.
At the same time, we must teach the child’s environment to recognize signs of
hypoglycemia and ketoacidosis. Such warning signs may be irritability, abnormal behavior
or constant complaints of hunger. Children themselves should be trained to avoid
hypoglycemia and if possible they should carry a snack rich in glucose, in case they need it.
The children also can make more frequent laboratory testing. For example, we can check
their urines for ketones with a urine stick, and we need more frequent tests of blood glucose.
Ideal levels of fasting glucose are <110 mg / dl, postprandial <150 mg/dl and glycated
hemoglobin (HbA1c) 7-9% in children under 5 years, while for older children 7 to 8%.72
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We should also check the development of the child and if there are any abnormalities
we should proceed to intervention as soon as possible. Exercise is also important for a child
with diabetes. Nevertheless, children need to understand the impact that the exercise may
have on their blood glucose. So, if they undergo a strenuous physical activity they should
consume food rich in carbohydrates before exercising. The diet they follow needs to cover
all the essential nutrients so as to achieve a healthy development. We nevertheless follow the
general instructions concerning dietary interventions and we suggest 4-6 meals every day
to avoid hypoglycemia.
The family is also an important factor when we treat a child with diabetes. Sometimes
parents may be absent or unable to care for their child. These children are in need of special
care. Parents or other members of the family must be aware that children with diabetes have
diet restrictions and that their activity levels need to be closely monitored. Initially, and
throughout the lifetime of the disease, diabetes can be a serious strain. We always try to find
someone from the child’s environment to work closely with the therapist. Finally, therapists
must be prepared in cases that children change their behavioral or sleep pattern, react
unpredictably, mainly where their diet is concerned and suffer from infections or viral diseases
more frequently. Children are also a more vulnerable group with a smaller body site available
for insulin injections.
5.2. Diabetes in pregnancy and gestational diabetes
Gestational diabetes mellitus (GDM) bears resemblance to T2DM in several respects, involving
a combination of relatively inadequate insulin secretion and responsiveness. It occurs in about
2%–5% of all pregnancies and may improve or disappear after delivery. Gestational diabetes
is fully treatable but requires careful medical supervision throughout pregnancy. About
20%–50% of affected women develop T2DM later in life.
During the perinatal period, women with pre-existing diabetes and women with
gestational diabetes have special needs. The overall medical checkup that should be done in
these women includes medical and gynecological history, especially the history of a large sized
baby. Blood pressure should be below 130/80 mmHg. This can be regulated medically. Also,
women with diabetes may suffer from complications in the eyes, which can be verified by
ophthalmologic examination. In such cases a caesarean section is recommended in order to
avoid bleeding of the vessels in the retina. Additionally, women who have T2DM and treated
with anti-diabetic tablets may not be regulated only by them and must take additional insulin.
If they are already treated with insulin, hypoglycemic episodes are more likely to occur during
the first trimester of pregnancy, whereas during the second and third trimester, the dose of73
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insulin will increase due to the contra-acting hormones of pregnancy that resist to the action
of insulin.
The test for gestational diabetes should be performed on women who have a greater
chance to develop it. Women over 35 are at increased risk, as well as those with a history of
delivering an overweight baby over 4 kgr, women with a family history of diabetes revealing
a first degree relative with T2DM, those who had a history of pregnancies that had many
complications. Classical risk factors are a previous diagnosis of gestational diabetes or
prediabetes, impaired glucose tolerance, or impaired fasting glycaemia. The ethnic background
is quite important since those with higher risk factors are found amongst African-Americans,
Afro-Caribbeans, Native Americans, Hispanics, Pacific Islanders, and people originating from
South Asia. Additionally, being overweight, obese or severely obese increases the risk by a
factor 2.1, 3.6 and 8.6, respectively and finally another risk factor is the previous poor obstetric
history.
Smokers run a double risk of GDM according to statistics. Although relevant evidence
remains controversial, the polycystic ovarian syndrome is considered as a risk factor. More
controversial potential risk factors are also studied. There is a wide advocation of all women
being screened because the 40-60% of women with GDM have no demonstrable risk factor.
Typically women with gestational diabetes exhibit no symptoms (another reason for universal
screening), but some women may demonstrate increased thirst, increased urination, fatigue,
nausea and vomiting, bladder infection, yeast infections and blurred vision.
The medical examination includes oral glucose test and the measurement of blood glucose.
A general monitoring of pregnant women by measuring blood glucose may cost less than
having to deal with the complications of gestational diabetes in a whole community (Larijani
et al., 2003).
If blood glucose is not regulated during pregnancy there is an increased risk of early birth,
polyhydramnion, hypertension, fetal death or still-born, rapid development renal failure,
damage to the cornea of the eye, vaginal and urinary infections.
All children born by diabetic mothers are more likely to be large sized and they can easily
develop hypoglycemia in the first 72 hours of life, hyperbilirubinemia, polycythemia,
hypokalemia, hypomagnesemia and respiratory distress syndrome. There are also related risks
of trauma at birth, delayed growth and prematurity along with birth defects and fetal death
in case of diabetic ketoacidosis of mother (Coetzee, 2009).
In normal circumstances the fetus is dependent on its mother for glucose which passes
through the placenta. Glucose and ketones are passed with filtration through the placenta
from the mother to the fetus. Insulin is not permeable through the placenta. In a normal
pregnancy there is an increase of basic and postprandial insulin secretion. The need for insulin
is lower in the first three months, but as the pregnancy progresses and the hormones of
pregnancy cause significant insulin resistance, the demand for insulin increases accordingly.
In women with diabetes the embryo receives excessive amounts of glucose, less amino
acids and more fatty acids due to hyperglycemia. Under these metabolic changes it is likely74
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that abnormality may develop. Especially during the third trimester the fetus is at increased
risk of developing disorders of the central nervous system and behavioral disorders later as
a child.
Maternal hyperglycemia may also result in large sized babies. Through the mother’s
placenta glucose can pass while insulin cannot. From the tenth week of pregnancy the fetal
pancreas starts working and producing insulin when it detects high levels of glucose. If the
mother is hyperglycemic, glucose also is given to the fetus as well as an additional stimulus
to the pancreas receptors and so fat tissue is developed additionally to the muscle tissue.
Problems can be caused during delivery and if the baby is too large it is recommended to
proceed to a caesarean section.
Hypoglycemia also after birth is the result of the interrupted supply of glucose from the
umbilical cord. The enhanced beta-cells of fetal pancreas still produce extra insulin, thus
decreasing immediately after birth the levels of glucose. That is why it is recommended that
the baby be fed soon after birth.
The respiratory distress syndrome also develops when the surfactant agent is produced
at a reduced quantity while there is excess insulin in the circulation of the fetus. To avoid this,
blood glucose levels should be at normal level before birth.
The desired blood glucose level is 60-90 mg/dl for fasting glucose, 60-104 mg/dl before
meals, 101-140 mg/dl one hour after meals, 90-121 mg/dl, two hours after meals and during
sleep, and between 2:00 to 6:00 a.m. desired blood glucose is 60-121 mg/dl. If the price of
sugar is above 140 mg/dl there is an increased risk for problems in the fetus or the mother.
A morning urine test for ketones is also necessary since insufficient calorie intake or poor
meals can result in the catabolism of fat. In such a case a meal before bedtime must be added
and the patient should not be left hungry for more than 10 hours.
Women with T2DM who fail to achieve regulation of blood sugar should take insulin.
For a woman who takes for the very first time insulin, the dose should be calculated at 0.5
IU/kg/24h. Preferably mixed insulin may be used. Moreover, 30% of the dose should be short-
acting and 70% long-acting insulin. The best site for injection is around the belly because the
absorption is faster there. As the pregnancy progresses the injections should not be done in
the thighs since the vascular circulation is affected over there because of pressure from the
uterus. The dose of insulin is 0,5 IU/kg/24h the fifth month, 0,6 IU/kg/24h the sixth month,
0,7 IU/kg/24h the seventh month, 0,8 IU/kg/24h the 8th and 0,9 IU/kg/24h the ninth month.
If a woman with T1DM was used to injecting insulin before her pregnancy, doses should
be adjusted upwards accordingly. It is desirable that the expectant mother has the appropriate
supplies and learns to control her own blood glucose levels. The best time to check the
patients glucose is by testing both fasting and one hour postprandial glucose.
At birth, the level of blood glucose can be reduced. That is why we should check blood
glucose every hour and give dextrose intravenous fluids if hypoglycemia occurs. The chance
of developing T2DM is two times higher. After birth tight control is necessary. In women with
T1DM the dose of insulin is gradually reduced so as to reach the same levels as before75
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pregnancy. Gestational diabetes generally resolves after delivery. A high rate of recurrence
is involved in a second pregnancy within one year of the previous one.
During lactation, glucose is reduced at the mothers. The woman should stop taking any
anti-diabetic tablets as their substances are absorbed by milk and can cause hypoglycemia
to the baby.
5.3. Diabetes and surgical procedures
Operational patients often suffer from diabetes. A surgery may affect the normal blood
glucose levels and so we should rearrange meals and treatment. Surgical stress stimulates the
secretion of various hormones and inhibits the secretion of insulin. These changes enhance
the catabolism and can quickly cause hyperglycemia and ketosis.
Hypoglycemia can occur especially in patients who fast before surgery. There is an
increased risk for hypoglycemia in patients under anaesthesia.
Additionally, patients with diabetes have more postoperative complications such as
myocardial injuries and contaminated sections infarcts. Often deterioration of renal function
takes place, particularly if diabetic nephropathy existed before the surgery. Diabetics are
also characterized by poor and/or slow wound healing, weak skin and tissue at site of surgery.
The approach of D.M. treatment at home differs greatly to that in hospital. One good
example is the use of regular insulin given intravenously, rather than other types available.
Most professionals would avoid administering oral medication or long acting types of insulin.
Regular insulin works within a short time allowing the surgeons and staff to have a much
better idea of the glucose level. This allows them to treat elevated levels, or low levels
immediately. In some cases, blood glucose testing will be done as frequently as every two
hours, with medication coverage provided as needed.
After surgery, the need for high quality nutrition and tight glycemic control is still present.
Nutrition will provide the building blocks for healing and a normal glucose level will promote
a faster recovery. Tight control of glucose levels could potentially save days or even weeks
of the recovery period when compared to recovery times with elevated blood glucose.
Once the surgery is over and the patient is into the recovery phase, it is necessary to
aggressively check for signs of infection in the healing wound, in addition to the normal
checks (such as checking the feet for problems).
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5.4. Diabetes and the elderly patients
As people get older ability to confront and deal with everyday problems is reduced. Life
expectancy in the developing world might be lower compared to the developed countries but
gradually African countries seem to have an increased number of elderly (Nordberg, 1997).
Treating and diagnosing diabetes amongst the elderly requires a flexible and unique approach.
Older people may have other coexisting problems that must be taken into account before
trying to treat DM (Kesavadev et al., 2003).
Elderly people are often more frail and susceptible to illness. Some of the most common
problems are hearing problems, poor vision, physical disabilities, impaired memory, coexisting
medical diseases, especially hypertension, reduction of cardiac and renal function, extensive
use of multiple medications, lack of social and family support, depression, dental problems
and malnutrition. Many elderly diabetic patients are pre-disposed to hypoglycemia
A good number of physiological changes take place as our bodies grow and adapt to new
conditions. The expected classic symptoms may not be exhibited in elderly people at risk of
developing the disease or with already developed D.M. Age-related changes can mean that
some symptoms will be masked, or harder to spot.
In any case we have tailor-made program for every elderly patient in order to treat D.M.
properly.
77
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WE WILL REGULARLY TRY TO ASSESS and evaluate whether the objectives of the clinic
are reached. So, our first objective is to increase the number of patients visiting the
diabetes clinic. It is also very important to detect new diagnosed patients with D.M. who were
unaware about their medical condition. Moreover, it is important to determine how
widespread the disease is in the region, as well as how to achieve better clinical results with
the least possible means and with limited personnel and laboratory tests. Finally, taking into
account all the cultural characteristics of the population our ultimate goal to raise “health
seeking behavior” among the community will be assessed.
The personal data of each patient will remain anonymous and confidential in any case. The
patients will not be obliged to come to the clinic and they will not be given any motives rather
than that of the therapeutical benefit of their medical condition. Medical treatment is the
primary goal over any other objectives such as possible research conclusions or even financial
efficacy of the clinic. We will act respectfully towards the cultural and religious features of the
patients in their background. According to this, the therapist will adapt to the particular
profile of patients rather than patients to the cultural characteristics of the therapist. We will
also be discreet when dealing with the patients and we have to make sure that treatment
in the diabetes clinic is not associated with any kind of stigma and discrimination between
community members. In addition, there will be no discrimination in choosing the patients, but
there will be an increased awareness about vulnerable groups such as pregnant women and
children.
Our objectives will be evaluated on a monthly basis so that amendments can be made.
In any case we will try to come up with innovative proposals, suggestions, and ideas for
further investigation or action.
The effectiveness of our intervention in quality terms is a priority. We will examine if it
introduces the correct behaviours to local health institutions and organizations of diabetics
(Beran et al., 2006).
The ultimate aim of this project is to contribute to the effort for a new global strategy for
diabetes appropriate for the developing world. New strategies should place diabetes on the
agenda of global health systems. Global donors must be convinced that millions of people
around the world are in immediate need of education and access to D.M. treatment. Above
all, it is vital to understand that poverty and underdevelopment are the main obstacles to79
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Discussion and conclusions
proceed to the establishment of good care practices, reducing morbidity and mortality due to
chronic diseases on top of the battle against infectious diseases and public health inter-
ventions.
Therefore the main aim of the project is to establish a DM care clinic aiming at an
innovative program that apart from a valuable service to the local community, will also
contribute to better understanding the problem of DM in poor rural communities. Medicine
is the art of assisting people to survive with dignity in good health. Every effort has to be
made to offer good quality and accessible health services to poor people by strengthening
health systems all over the world.
80
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