CASE STUDY 1 A 72 years old woman with a 15 year history of Type 2 DM, treated
with insulin NPH, 24 units in the morning and 14 units in the evening, presented for the
first time in the Diabetes Clinic for evaluation. She reported that during the last six
months she had been having ‘unexpectedly’ high blood sugar values in her SMBG
measurements. Her weight has been steady (BMI: 29.5 kg/m 2 ). She reported no
symptoms of any disease, neither polyuria nor polydipsia. Her last fundoscopic
examination (two years before) had been normal. She also suffers from mild
hypertension (and is receiving treatment with an ACE inhibitor).
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CASE STUDY 1 A 19 year old man was brought to the Emergency Department in the
early morning hours, in a comatose state. He exhibited tonic-clonic contractions and
was extremely agitated. His family members reported that he was suffering from Type 1
DM and that the previous evening he had attended a party; they did not know what he
had eaten, but reportedly he had drunk quite a lot of alcohol. His mother got worried
when she saw him sleeping very deeply and not responding to her efforts to wake him
up. She tried to feed him because she thought he might be having a hypoglycaemic
episode, but was unsuccessful (he had ‘sealed’ his mouth). The treating physician in the
Emergency Room, after measuring a blood sugar level with a portable meter and
finding it to be 25 mg/ dl (1.4 mmol/L), immediately ordered the intravenous
administration of dextrose infusion. A 10 percent dextrose in water solution was started
and the patient was given an intravenous injection of 5 ampoules 35 percent glucose (10
ml each). What is the diagnosis and cause of this acute situation? How much glucose
must be administered?
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CASE STUDY 1 – DIABETIC KETOACIDOSIS A 25 year old young woman came to
the hospital with fever and mild confusion. During the previous few weeks she had
experienced polydipsia, polyphagia and polyuria, with significant weight loss (12 kg).
She reported pain in her left flank area, with dysuria, for the previous 48 hours. Her
mother reported that her daughter’s breath had a peculiar, uncommon smell, and that
her breaths were more frequent. A physical exam was remarkable for evidence of
dehydration. She had a low supine blood pressure (85/60 mmHg), with increased pulse
rate (120 per min) and respiratory rate (32 breaths per min). Her breath had an acetone
smell. There was mild clouding of sensorium, but without focal neurological signs. She
had fever (37.9 C [100.2 F]) and tenderness on percussion of the left flank area (positive
Giordano sign). A capillary blood glucose measurement showed a very high level: 484
mg/dl (26.9 mmol/L). At the same time, ketone bodies measured in the capillary blood
with a portable meter (Medisense Xtra) were also very high: 4.5 mmol/L (note: these
strips measure only b -hydroxybutyrate [b-HB] and not acetoacetate in the blood; levels
> 3mmol/L are considered a sign of ketosis). Arterial blood gas analysis showed the
following: pH 7.08 (7.35– 7.42); pCO 8 mmHg (35– 45); pO 120 mmHg (80– 100); and
HCO À 2 2 3 6 mmol/L (24– 32). The diagnosis of diabetic ketoacidosis (DKA) was
made. An ECG, a chest X-ray and further laboratory tests were done. The results were:
Blood glucose: Sodium: Potassium: Chloride: 525 mg/dl (29.1 mmol/L) 124 mmol/L 3.8
mmol/L 88 mmol/L (75– 110 mg/dl [4.2– 6.1 mmol/L]) (132– 144) (3.4– 4.8) (93– 108)
Urea: Creatinine: Urinalysis: CBC: 92 mg/dl (15.3 mmol/L) (18 – 36 mg/dl [3.0 – 6.0
mmol/L]) 3.2 mg/dl (282.9 m mol/L) (0.7 – 1.2 mg/dl [61.9 – 106.1 m mol/L]) Urine
cloudy and foul smelling, glucose: þþþþ , ketone: þþþ , many WBCs, abundant
microorganisms, many RBCs. Haematocrit: 44%, WBC: 22,000/ m l
(polymorphonuclear 88%).
What is diabetic ketoacidosis and what is the cause of DKA in this young woman? What
are the therapeutic targets and our immediate priority?
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CASE STUDY 2 – HYPEROSMOLAR NON-KETOTIC HYPERGLYCAEMIC
COMA (HNKHC) A 75 year old woman with a history of residual left hemiparesis due
to a stroke, is transferred to the Emergency Room of the hospital. Recently, the patient
has had intense polyuria and complained of profound thirst, the result of consuming
of large quantities of juices. During the previous week she had experienced a decrease in
her level of consciousness, with gradual clouding of sensorium, slowly deteriorating
until she fell into a coma. Physical examination revealed signs of dehydration, with
blood pressure of 110/80 mmHg and pulse rate of 110 per min. The patient was deeply
comatose, with bilateral positive Babinski sign, unresponsive even to painful stimuli and
with decreased deep tendon re fl exes. Initial impression was that she was suffering
from a very severe stroke, probably in the medulla. A stat-computed tomography of the
brain showed an ischaemic area of the right hemisphere, compatible with the history of
left hemiparesis, but no signs of haemorrhage of recent thromboembolic lesion. The
patient had a temperature of 36 C (96.8 F) (37.2 C [98.9 F] rectally). Laboratory results
were: Na þ 138 mmol/L; K þ 3.6 mmol/L; Cl À 105.0 mmol/L; HCO À 3 30 mmol/L;
urea 92 mg/dl (15.3 mmol/L); creatinine 2.2 mg/dl (194.5 l mol/L). Blood glucose was
1,235 mg/dl (68.5 mmol/L)!! Urinalysis showed 4 þ glucose and 1 þ ketones.
1. What is the diagnosis and where is it based?
What are the circumstances during which HNKHC develops?
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What treatment will you offer to the patient?
1. Fluid administration and restoration of electrolyte disturbances.
2. Correction of hyperglycaemia with insulin administration (lower doses than
needed in DKA
3. Management of underlying diseases
4. Prevention of thromboembolic episodes.
5. Close monitoring in an intensive care unit.
CASE STUDY 3 – LACTIC ACIDOSIS A 74 year old woman presents to the
hospital with complaints of recent high blood glucose levels and a feeling of
progressively deteriorating fatigue. Her family members report episodes of lethargy and
intense sleepiness, as well as confusion during the previous week. The patient suffers
from DM (for 12 years), hypertension, coronary heart disease, dyslipidaemia, heart
failure and atrial fi brillation. An echocardiogram done three months before showed left
ventricular hypertrophy, mitral regurgitation and an ejection fraction of 35 percent.
Her medications include: glimepiride, 6 mg/day; digoxin, 0.125 mg/day; ramipril, 10
mg/day; furosemide, 20 mg twice a day; aspirin, 325 mg/day; and for the last two
months metformin, with a gradual increase of the dose to 1700 mg/day. She does not
smoke or drink alcohol. Physical examination reveals a heart rate of 100/min, blood
pressure of 168/ 72 mmHg, respiratory rate of 18/min and temperature of 36.8 C (98.2
F). An electrocardiogram shows presence of atrial fi brillation with a ventricular rate of
100 beats/min. Laboratory results are as follows: glucose 268 mg/dl (14.9 mmol/L); urea
48 mg/dl (8.0 mmol/L); creatinine 0.9 mg/dl (79.6 l mol/L); HbA 11.5 %; WBC 8600/ l l;
Na þ 138 mEq/L; K þ 4.4 mEq/L; Cl À 1c 95 mEq/L. A chest X-ray is normal, without
signs of cardiac overload or in fl ammatory in filtrates. Blood gas analysis shows pH
7.20 (7.35 – 7.42), pCO 2 28 mmHg (35 – 45), pO 105 mmHg (80 – 100) and HCO À 2 3
15 mmol/L (24 – 32). Anion gap is calculated at 32 mmol/L (increased). Ketone bodies
(measured with the portable meter Medisense Xtra) are 1.6 mmol/L. Given the history
of metformin ingestion and the presence of metabolic acidosis with a high anion gap,
lactate levels are measured in the blood and found to be 6.1 mEq/L (normal values are
0.7 – 2.1 mEq/L). Metformin is discontinued and the patient started on insulin
treatment with a twice a day injection of medium duration insulin. Twenty four hours
later, lactate levels are 1.9 mEq/L. After a few days the patient returns home.
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CASE STUDY 1 A 54 year old man is referred to the urologist by his primary
physician, because of intense dysuric symptoms during the last six months and three
episodes of urinary tract infections. He was examined by the urologist and had an
ultrasound examination of the kidneys, ureter and prostate. A significant hypertrophy
of the prostate gland was found, accompanied by an appreciable amount of residual
urine in the bladder after urination. A transurethral prostatectomy was suggested. The
patient has been suffering from Type 2 DM for the previous six years, treated with
metformin 850 mg tablets, twice a day and nateglinide 120 mg tablets, thrice a day,
before meals. His glycaemic control is satisfactory, as depicted in his SMBG
measurements and his HbA 1c level (6.7 percent). The urologist refers the patient back
to his primary physician, so that pre-operative instructions for optimal control of his
blood glucose before surgery are given. Can the patient be directly operated on, and if
yes, should he be admitted to the hospital before the surgery?
Why should hyperglycaemia be avoided in the surgical diabetic patient?
Metabolic:
Cardiovascular:
CASE STUDY 2 A 42 year old man comes to the hospital because of fever and intense
abdominal pain. He has an increased WBC count of 18,000/ l l and a toxic clinical
picture (he has the face of a sick person, tachycardia, hypotension and high fever).
Hydrops of the gallbladder is detected from radiological examinations. A decision was
made to take the patient immediately to surgery. He is suffering from Type 1 DM, being
treated with an intensive insulin regimen, with 10 – 12 units of rapid-acting insulin
before meals and 36 units of basal insulin (glargine) before bedtime. His blood glucose
level is 283 mg/dl (15.7 mmol/L), and electrolytes, urea, and creatinine concentrations
are within normal limits. How can this patient be managed so that urgent surgery can
be performed?
Were this patient (with Type 1 DM) to undergo a minor surgical procedure, how should
he be managed?
CASE STUDY 1 A 30 year old man with Type 1 DM is under treatment with isophane
insulin (NPH), 10 units in the morning and 14 units in the evening, as well as insulin
Aspart before each meal (at a dose determined based on the carbohydrate content of the
meal and the pre-prandial blood glucose level). The usual daily dose of insulin Aspart is
20– 24 units). His glycaemic control is very good (recent HbA 1c : 6.9 percent). The
patient called his primary physician in the morning because during the previous night
he had four episodes of vomiting, abdominal pains and three episodes of diarrhoea. His
blood glucose level in the morning was 320 mg/dl (17.8 mmol/L). He continued to feel
intense nausea and when attempting to drink water, he vomited again.
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CASE STUDY 2 A 70 year old woman with Type 2 DM for 10 years, smoker, with mild
chronic obstructive pulmonary disease (COPD), is being treated with oral antidiabetic
medicines (glibenclamide 15 mg daily and metformin 850 mg daily). Her glycaemic
control is moderate (last HbA 1c : 7.9 percent). She urgently called her treating
physician because 24 hours ago she developed fever (up to 38.6 C [101.5 F]), cough and
a moderate degree of dyspnoea, which did not improved despite use of inhaled
bronchodilators. Her blood glucose levels were persistently higher than 400 mg/dl (22.2
mmol/L) for the previous 12 hours, despite the fact that she ‘ does not eat nearly
anything ’ and despite the fact that she took the initiative to take one extra pill of
glibenclamide 5 mg and one of metformin 850 mg. She has a dry mouth, intense
polydipsia and polyuria. She is asking for help with management of the high blood
glucose levels.
CASES STUDY 1 A 37 year old man with Type 1 DM since the age of 14, comes to the
diabetes clinic for a routine visit. He is treated with an intensive insulin regimen,
consisting of three injections of rapid-acting insulin analogue before main meals (dose
based on pre-prandial glucose measurements and carbohydrate food counting) and one
injection of long-acting insulin glargine at bedtime. He consumes three main meals and
2– 3 snacks daily. His glycaemic control has generally been quite good for many years
(fasting blood glucose: 80– 110 mg/dl [4.4– 6.1 mmol/L], postprandial < 140 mg/dl [7.8
mmol/L], HbA 1c : 5.7 percent), with relatively few hypoglycaemic episodes, of which he
is always aware. During the last month the patient has started participating in an
exercise programme with some friends, playing tennis three times a week, late in the
afternoon (7– 8 p.m.). He observed that on the days of tennis playing he had severe
hypoglycaemic episodes during the following night. Indicative measurements of the last
five days are shown in Table 9.4 (the units of rapidacting insulin analogue administered
are in parenthesis).
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CASE STUDY 2 A 34 year old man with well controlled diabetes receives six units
rapid-acting (regular) insulin and six units isophane insulin before breakfast (9 a.m.),
four units rapid-acting insulin before lunch (1 p.m.) and four units rapid-acting insulin
with six units isophane insulin before dinner (8 p.m.). He exercises daily (walks around
5 km [3.1 miles] every morning before breakfast). For the previous two days he felt a bit
sick, with mild fever and cough, but decided not to abandon his daily exercise
programme. He woke in the morning (8 a.m.) with blood glucose level 298 mg/dl (16.5
mmol/L) and decided to take his usual walk and administer his morning insulin
afterwards, before breakfast. He noticed he was much more tired today after walking
and was surprised to see his blood glucose level had climbed up to 355 mg/dl (19.7
mmol/L) after walking. Urine ketones were positive.
CASE STUDY 1 A 35 year old healthy woman, with a history of an unexplained
miscarriage six months ago, wishes to become pregnant again. Is there a chance that
this woman will develop gestational diabetes and how will the diagnosis be made?.
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CASE STUDY 3 – MANAGEMENT OF A WOMAN WITH GESTATIONAL
DIABETES A pregnant woman in the 25th week of gestation is subjected to a threehour oral glucose tolerance test with 100 g glucose. The following results are obtained:
fasting plasma glucose: 90 mg/dl (5.0 mmol/L); one hour 198 mg/dl (11.00 mmol/L); two
hours 160 mg/dl (8.9 mmol/L); and three hours 115 mg/dl (6.4 mmol/L). What advice
should she be given and how should she be monitored during pregnancy after these
results?
CASE STUDY 1 A 12 year old boy has lost 6 kg (13.2 lb) over the last six months. At the
same time he exhibited intense polydipsia and polyuria. His paediatrician ordered some
laboratory tests and found that he was suffering from Type 1 DM. Information about
the disease brought up many queries for the child and his parents. The child was not
initially receptive to talking about the problem or getting trained for insulin injections
and self monitoring of blood glucose. Is this anticipated? What is the reaction of a
young person and his or her family to the onset of Type 1 DM?
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CASE STUDY 2 A 15 year old girl is suffering from Type 1 DM. She is treated with
four injections of insulin per day. During the last two days she had vomiting and intense
polyuria and polydipsia. She was admitted to the hospital with diabetic ketoacidosis.
The cause, as the patient herself admitted, was that she had neglected her injections
lately, in an attempt to lose weight. Is this frequent? What are appetite disturbances in
young persons with DM?
CASE STUDY 3 Mrs Anna is 38 years old and is the mother of a 16 year old girl who
suffers from Type 1 DM. During the last two years, the daughter has had very poor
glycaemic control and continues to be extremely disobedient. The mother wants to
discuss the problem with the physician and look for solutions.
CASE STUDY 4 A 7 year old boy is suffering from Type 1 DM. His parents are anxious
and want to ask the physician and the treating health care team what they should know
themselves and what the child should know.
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CASE STUDY 5 A 16 year old boy is suffering from Type 1 DM. His glycaemic control
is poor and his parents are worried because he eats lots of sweets and has started
smoking. Is there reason for worry? Can the problem be dealt with?
CASE STUDY 1 An 85 year old man with Type 2 DM for 20 years, hypertension and
dyslipidaemia, presents with a stroke, that causes left hemiparesis and severe restriction
in his mobility (he can transfer from the bed to the chair only with help, he can dress
with help, he can eat alone but cannot walk alone). His DM is treated with a
combination of oral antidiabetic medicines (metformin at noon) and two doses of a
mixture of insulin (70 percent isophane and 30 percent rapid-acting) in the morning and
night before meals. His glycaemic control prior to the stroke was moderate (HbA 1c 7.5
percent, fasting blood glucose 150– 200 mg/dl [8.3– 11.1 mmol/L], though very rarely
did he measure post-prandial blood glucose levels, usually > 200 mg/dl [11.1 mmol/L]).
Before the stroke he lived alone, but now he lives with his daughter, who works during
the day and has hired a helper to care for her father during her absence. The daughter
reports that her father has become more insular since the stroke and ‘seems to have
declined: he frequently doesn’t eat his food, shows no interest in anything and sleeps all
the time’. She is worried about his glycaemic control, whether it could lead to a second
stroke. She also has difficulties with insulin injections (in the morning she leaves for
work early, before her father eats his breakfast; the helper comes later). She is asking
for the doctor’s advice.
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CASE STUDY 2 A 76 year old woman with Type 2 DM for 15 years comes to the
diabetic clinic for a routine visit. She is treated with maximal doses of sulfonylureas and
metformin. Her blood pressure is 130/80 mmHg and her weight 82 kg (180.8 lb, BMI:
27 kg/m 2 ). She occasionally measures her blood sugar at home (3 – 4 times per week,
usually in the morning or more rarely at noon after lunch – she says that ’ s how her
doctor instructed her). Her measurements are usually high (in the morning 180 – 220
mg/dl [10.0 – 12.2 mmol/L], postprandially at noon always > 200 mg/dl [11.1 mmol/L]).
Her HbA 1c is 8.2 percent. She also receives a statin every night and an ACE inhibitor/
thiazide diuretic combination antihypertensive tablet. She has no complaints except for
nocturia (once or twice a night) and is generally very active. She has mild benign
retinopathy (the ophthalmologist has recommended quarterly follow-ups for the time
being) and no microalbuminuria. What is the proper further management of this
patient?
CASE STUDY 3 A 78 year old man with Type 2 DM for 30 years, and a history of
coronary heart disease (myocardial infarction and coronary artery bypass surgery eight
years ago), hypertension and dyslipidaemia, comes to the diabetic clinic for a routine
follow-up. He uses a mixture of 70/30 insulin, 28 units in the morning and 18 units in the
evening before meals and occasionally rapid-acting insulin before lunch (usually 5 – 6
units before meals) subcutaneously. He says he measures his blood sugar regularly
(always twice and sometimes three times a day) and is unhappy that his glucose control
is not very good (morning blood sugar levels 120 – 220 mg/dl [6.7 – 12.2 mmol/L],
evening 180 – 240 mg/dl [10.0 – 13.3 mmol/L], noon 200 – 340 mg/dl [11.1 – 18.9
mmol/L]). The patient is in very good general health, walks daily for at least 30 – 45
minutes without any problems and is generally very active (he is a retired civil servant
and likes to work in his garden). He reports very frequent hypoglycaemias, usually
around noon. His HbA 1c is 8.4 percent, his weight 92 kg (202.9 lb, BMI: 30.1 kg/m 2 )
and his blood pressure under good control.
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CASE STUDY 1 A 68 year old woman, with poorly controlled DM of 25 years duration,
comes to the diabetes clinic for follow-up. Her fasting blood glucose is around 256 mg/dl
(14.2 mmol/L) and her HbA 1c is 11.2 percent. The patient complains of pricking pains,
burning sensation and numbness in her lower extremities, as well as frequent cramps.
Furthermore, she reports deterioration of her vision lately with decrease in her visual
acuity and blurred vision. She has a history of operated cataract in the left eye. Physical
examination is remarkable only for: BP 170/90 mmHg, a systolic murmur in the apex
and abolition of Achilles tendon re fl exes bilaterally. Her antidiabetic regimen includes:
glibenclamide tablets 5 mg, 1 Â 3, and metformin tablets 850 mg, 1 Â 3 daily.
Fundoscopy reveals diabetic maculopathy bilaterally, without obvious lesions in the rest
of the retina. What would you recommend for this patient?
CASE STUDY 1 A 64 year old woman without previous history of DM presents at the
outpatient clinic with mild xerostomia, polyuria and polydipsia. She reports having
dyslipidaemia and hypertension for a year, treated with cilazapril 5 mg and amlodipine
10 mg daily. She is a smoker, has a moderate alcohol consumption, is obese (weight: 80
kg [176.4 lb], height: 1.62 m [5 ft, 4 in], BMI: 31 kg/m 2 ), and has arterial pressure
170/80 mmHg; otherwise her physical condition is unremarkable. Laboratory fi ndings:
fasting blood glucose 112 mg/ dl (6.2 mmol/L); urinalysis abundant WBCs and urine
protein ( þþþ ). What would you initially recommend for the patient?
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CASE STUDY 1 A 67 year old woman, with a 15 year history of Type 2 DM, comes to
the clinic for a routine visit. She is treated with a mixture of shortand long-acting
insulin in the morning and evening and also rapid-acting insulin before lunch. DM
control is very good (recent HbA 1c : 6.9 percent). The patient reports burning pains in
the soles for the last year, aggravated at night. Sometimes the discomfort is so intense
that she has to get up and walk around or insert her feet in cold water to get some relief.
How are her symptoms explained?