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10.3 · Diabetic Syndromes
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10
Wolfram Syndrome (DIDMOAD)
Wolfram syndrome (WS) is a rare disease characterized by
d iabetes i nsipidus, d iabetes m ellitus, o ptic a trophy, and sen-
sorineural d eafness, making the acronym DIDMOAD.
WS has an autosomal recessive mode of inheritance, and
it is caused by mutation in chromosome 4. Incidence of WS
is estimated to be 1in 100,000 live births.
Diagnostic and key features of DIDMOAD include:
Ophthalmologic Clinical Findings
Bilateral progressive optic atrophy (98 % of cases) ( diagnostic
criterion )
Auditory Clinical Findings
Bilateral sensorineural hearing loss is found in up to 12 % of
cases ( diagnostic criterion ).
Metabolic and General Clinical Findings
5 Diabetes insipidus (35 % of cases) ( diagnostic criterion )
5 DM (99 % of cases) ( diagnostic criterion )
5 Hypogonadism (occasionally)
Renal Clinical Findings
5 Dilatation of the urinary tract with unknown cause
( diagnostic criterion )
5 Testicular atrophy (occasionally)
Neurological Clinical Findings
5 Ataxia due to cerebellar atrophy.
5 Short-term memory loss and dementia.
5 e mean age at death is 30 years, most commonly due
to brain stem atrophy and central respiratory failure.
5 Dysmorphic facial features, with large ears ( diagnostic
criterion )
5 Generalized hypertrichosis, with coarse head hair
5 Genital (phallic) enlargement ( diagnostic criterion )
5 Premature dentition
Renal Clinical Findings
5 Bilateral renal enlargement with medullary sponge
kidney may be found. Medullary sponge kidney is a
congenital disease characterized by dilatation of the
collecting tubules in one or more renal papillae, a ecting
one or both kidneys. ere is a high incidence of renal
calculi formation in medullary sponge kidney, with
hypercalciuria found in up to 50 % of patients. Gross
hematuria can be found in 10–20 % of patients.
5 Nephrocalcinosis.
Dermatological Clinical Findings
Typically, there are areas of hyperpigmentation and papillary
hypertrophy on the neck and exor creases (acanthosis
nigricans).
Signs on IVU
Sponge kidney is diagnosed by the presence of typical
cystic collection of contrast material in the collecting
ducts in a form of “bouquet of fl owers or paintbrush
appearance” (
. Fig. 10.3.3 ).
Signs on Brain MRI
5 Generalized brain atrophy, especially in the
cerebellum, medulla, and pons.
5 Loss of the posterior pituitary signal.
5 Atrophy of the optic nerves, tracts, and radiations.
5 Patchy areas of white matter demyelination may
be seen occasionally.
Rabson–Mendenhall Syndrome
Rabson–Mendenhall syndrome (RMS) is a rare genetic disease with various somatic abnormalities, characterized by
noninsulin-dependent DM due to severe insulin resistance,
caused by insulin receptors mutation. e disease has an
autosomal recessive mode of inheritance.
Diagnostic and key features of RMS include:
Metabolic and General Clinical Findings
5 Noninsulin-dependent DM, postprandial hypoglycemia,
and hyperinsulinemia ( diagnostic criterion )
. Fig. 10.3.3 Intravenous urography radiograph of a patient
with sponge kidney shows the classical collecting duct
paintbrush appearance ( arrowheads )
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Chapter 10 · Diabetology
10
Further Reading
Barrett TG.Mitochondrial diabetes, DIDMOAD and other
inherited diabetes syndromes. Best Prac Res Clin
Endocrinol Metab. 2001;15(3):325–43.
Benso C, etal. ree new cases of Alström syndrome. Graefe’s
Arch Clin Exp Opthalmol. 2002;240:622–7.
Bin-Abbas B, et al. Wolcott-Rallison syndrome: clinical,
radiological, and histological ndings in a Saudi child.
Ann Saudi Med. 2001;21(1–2):73–4.
Cohen Jr MM.Syndromology: an updated conceptual over-
view. V.Aspects of aneuploidy. Int J Oral Maxillofac Surg.
1998;18:333–8.
Dippell J, etal. Early sonographic aspects of kidney morphol-
ogy in Bardet-Biedl syndrome. Pediatr Nephrol.
1998;12:559–63.
Donohue WL, etal. Leprechaunism. A Euphuism for a rare
familial disorder. J Pediatr. 1954;45(5):505–18.
Fralick RA, etal. Early diagnosis of Bardet-Biedl syndrome.
Pediatr Nephrol. 1990;4:264–5.
Galluzzi P, etal. MRI of Wolfram syndrome (DIDMOAD).
Neuroradiology. 1999;41:729–31.
Genis D, et al. Wolfram syndrome: a neuropathological
study. Acta Neuropathol. 1997;93:426–9.
Gupta S, etal. Medullary sponge kidney. Indian J Pediatr.
2002;69(12):1091–2.
Harris AM, etal. Rabson-Mendenhall syndrome: medullary
sponge kidney, a new component. Pediatr Nephrol.
2007;22:2141–4.
Hatori M, etal. Multiple epiphyseal dysplasia– report of two
families. Arch Orthop Trauma Surg. 2000;120:372–5.
Makaryus AN, etal. A rare case of Alström syndrome pre-
senting with rapidly progressing severe dilated cardiomyopathy diagnosed by echocardiography. J Am Soc
Echocardiogr. 2003;16:194–6.
Miller J, etal. Neurocognitive ndings in Prader-Willi syn-
drome and early-onset morbid obesity. J Pediatr.
2006;149:192–8.
Morgan J, etal. US, CT, and MRI imaging of hepatic masses
in Alström syndrome: a case report. Clin Imaging.
2008;32:393–5.
Papavramidis ST, et al. Prader-Willi syndrome-associated
obesity treated by biliopancreatic diversion with duodenal
switch. Case report and literature review. J Pediatr Surg.
2006;41:1153–8.
Parveen BA, et al. Rabson-Mendenhall syndrome. Int J
Dermatol. 2008;47:839–41.
Rubin EL, etal. Cystic disease of the renal pyramids (‘sponge
kidney’). J Fac Radiol. 1959;10(3):134–7.
Sebik A, etal. e orthopaedic aspects of multiple epiphyseal
dysplasia. Int Orthopaed (SICOT). 1998;22:417–21.
Shannon P, etal. Evidence of widespread axonal pathology in
Wolfram syndrome. Acta Neuropathol. 1999;98:304–8.
Stöß H, etal. Wolcott-Rallison syndrome: diabetes mellitus
and spondyloepiphyseal dysplasia. Eur J Pediatr.
1982;138:120–9.
Summitt RL, etal. Leprechaunism (Donohue’s syndrome): a
case report. J Pediatr. 1969;74(4):601–10.
Tekgül S, etal. Urological manifestations of the observation
in 14 patients. J Urol. 1999;161:616–7.
Tobin JL, etal. Bardet-Biedl syndrome: beyond the cilum.
Pediatr Radiol. 2007;22:926–36.
Urben SL, etal. Otolaryngologic features of Laurence-Moon-
Bardet-Biedl syndrome. Otolaryngol Head Neck Surg.
1999;120:571–4.
Verri A, etal. A case of Wolfram syndrome: neurological fea-
tures. Ital J Neurol Sci. 1982;4:351–3.
10.4 Diabetes Insipidus
Diabetes insipidus (DI) is a disease characterized by increased
frequency of urination (polyuria), with increased uid intake
(polydipsia) secondary to inappropriate secretion of the
antidiuretic hormone (ADH) vasopressin from the posterior
pituitary gland.
ADH is secreted by the supraoptic and paraventricular
hypothalamic nuclei and stored in the terminals within the
posterior pituitary. Neurohypophysis is a term used to describe
the posterior pituitary, the infundibular stalk, and the
supraoptic and paraventricular hypothalamic nuclei. ADH
regulates uid and electrolytes balance within the body by
promoting water reabsorption in the distal tubules in the
kidneys.
According to its origin, DI is classi ed into three types:
5 Neurogenic DI can be idiopathic (50 %), genetic (5 %),
secondary to tumor (e.g., craniopharyngioma), or
secondary to in ammatory reactions (e.g., Langerhans
cell histiocytosis).
5 Nephrogenic DI can be due to primary renal disease or
secondary to chronic renal failure or hypercalcemia.
5 Dipsogenic DI arises due to compulsive polydipsia or due
to hypothalamic disorders a ecting the thirst center.
DI has a prevalence of 1:25,000 of the population. Patients
typically present with polyuria and polydipsia. e polyuria
is not reduced by cessation of uid intake. Signs of
dehydration, such as dry skin, hypotension, and tachycardia,
are o en found. Serum electrolyte investigations show high
plasma osmolarity, hypernatremia, hypokalemia,
hyperglycemia, and hypercalcemia.
e most common hypothalamic tumors associated with
DI are metastases, germinoma, and craniopharyngioma.
Craniopharyngioma is a benign, slow-growing tumor that
arises from the remnant of Rathke ’ s pouch (craniopharyngeal
duct). It can occur in children between 6 and 15 years of age
and adults between 50 and 60 years of age. Up to 50 % of
suprasellar lesions in children are craniopharyngiomas.
Patients usually present with visual disturbance (bitemporal
quadrantanopia), headache, and hypothalamic dysfunction.
As previously mentioned, the neurohypophysis is composed of the posterior pituitary lobe, the infundibular
stalk, and the median eminence of the hypothalamus. e
normal posterior pituitary shows high signal intensity on
native T1W images (
. Fig. 10.4.1 ). It is thought that this
10.4 · Diabetes Insipidus
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. Fig. 10.4.1 Sagittal nonenhanced T1W MRI of the sella shows the
physiological bright signal of the posterior hypophysis ( arrowhead )
413
5 Craniopharyngioma : on CT, the main bulk of the
lesion is located in the suprasellar region and has
cystic (90 %) and solid components with rim-like or
nodular calcifi cations in up to 80 % of cases
(
. Fig. 10.4.3 ). The solid component enhances after
contrast administration. On MRI, the lesion has high
T1 signal and high/low T2 signal according to the fat
and thick protinaceous (motor oil) consistency
within the lesion. The solid component enhances
after contrast administration.
5 Langerhans cell histiocytosis : there is typical
enlargement of the central part of the
infundibulum (>2.5 mm) when Langerhans cell
histiocytosis is the main cause of DI (
5 Bilateral, symmetrical brain calcifications within
the basal ganglia and the subcortical area have
been reported as unusual manifestations of
DI. These findings are best evaluated on CT.
5 Ectopic posterior pituitary is seen as a bright spot,
typically located in the hypothalamic eminence
(
. Fig. 10.4.5 ) .
. Fig. 10.4.4 ).
10
bright spot is due to the macrogranules composed of the
ADH neurophysin complex. Ectopic posterior pituitary is a
condition where the posterior pituitary bright signal spot
on MR imaging is not located in the posterior pituitary
lobe but is typically seen in the median hypothalamic eminence.
e anterior pituitary gland ( adenohypophysis ) normally
shows the same signal characteristic as the rest of the brain
on T1W images. However, the adenohypophysis can show a
bright signal on native T1W images during the rst 2 years of
life, due to secretory activity, or in preterm babies during the
rst 2 months of life. e bright signal of the adenohypophysis is best demonstrated with the magnetization transfer MR
sequence.
Signs on Brain MRI (Done in Patients with Suspected
Neurogenic DI)
5 Genetic cause : there is loss of the typical posterior
pituitary hyperintensity signal on T1W
contrast-enhanced images (
However, the neurohypophysis bright spot can be
absent in 10–20 % of normal individuals.
. Fig. 10.4.2 ).
. Fig. 10.4.2 Sagittal nonenhanced T1W MR illustration of
the sella shows loss of the physiological posterior pituitary
bright spot, which is a characteristic fi nding in idiopathic or
genetic diabetes insipidus
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Chapter 10 · Diabetology
a
. Fig. 10.4.4 Sagittal nonenhanced T1W MR illustration of
the sella shows thickened infundibulum due to Langerhans cell
histiocytosis ( arrowhead )
10
b
. Fig. 10.4.3 Axial nonenhanced brain CT ( a ) and sagittal
contrast-enhanced T1W MRI of the sella show
craniopharyngioma in a 40-year-old patient. In ( b ), the main
bulk of the lesion is located in the suprasellar area, with
infi ltration of the sella turcica and the sphenoid sinus. The lesion
is mostly solid, with anterior cystic component located in the
inferior frontal region ( arrowhead ). In ( a ), a calcifi ed rim that
surrounds the lesion is nicely illustrated
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a
415
Mavrakis AN, etal. Diabetes insipidus with de cient thirst:
report of a patient and review of the literature. Am J
Kidney Dis. 2008;51(5):851–9.
Mitchell LA, etal. Ectopic posterior pituitary lobe and peri-
ventricular heterotopia: cerebral malformation with the
same underlying mechanism. AJNR Am J Neuroradiol.
2002;23:1475–81.
Saeki N, etal. MRI of ectopic posterior pituitary bright spot
with large adenomas : appearances and relationship to
transient postoperative diabetes insipidus. Neuroradiology.
2003;45:713–6.
Schmitt S, etal. Pituitary stalk thickening with diabetes insip-
idus preceding typical manifestations of Langerhans cell
histiocytosis in children. Eur J Pediatr. 1993;152:399–401.
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b
. Fig. 10.4.5 Sagittal ( a ) and axial ( b ) T1W MRI shows an
ectopic high signal intensity spot located at the proximal part of
the infundibulum (ectopic posterior pituitary)
Obesity is a disease characterized by an increase in the size
and number of fat cells. Fat cell size di ers from region to
region within the body, and the number of fat cells may
increase three- to vefold during adolescence. Overweight
is de ned as a body weight of 101–120 % of the ideal, while
obesity is de ned as fat accumulation >120 % of the ideal.
Obesity is de ned by the World Health Organization
(WHO) as the ratio of body mass to body height (kg/m 2 ), the
so-called body mass index (BMI). A BMI of 25–30kg/m 2 is
considered “overweight,” >30 kg/m 2 is de ned as “obesity,”
and >40kg/m 2 is de ned as “morbid obesity.” BMI is used as
a marker for estimating the risks for diseases such as diabetes
mellitus and cardiovascular diseases. Women usually have
gynecoid fat distribution around the hips, while men have
android fat distribution where adiposity is predominantly
central.
Patients with obesity su er from many systemic diseases
such as diabetes mellitus and insulin insensitivity, cardiovascular diseases, obstructive sleep apnea, osteoarthritis, venous
stasis and varicosities, and gout.
ere are di erent causes of obesity. Apart from a sedentary lifestyle and high-carbohydrate food intake, hormonal,
syndromic/pathologic, and drug-induced lipomatoses are
other common causes of obesity. Each cause induces obesity
by a di erent mechanism.
Further Reading
Al-Kandari SR, etal. Intracranial calci cation in central dia-
betes insipidus. Pediatr Radiol. 2008;38:101–3.
Hadjizacharia P, etal. Acute diabetes insipidus in severe head
injury: a prospective study. J Am Coll Surg. 2008;207:477–84.
Jane Jr JA, etal. Neurogenic diabetes insipidus. Pituitary.
2006;9:327–9.
Kassebaum N, etal. Diabetes insipidus associated with pro-
pofol anesthesia. J Clin Anesth. 2008;20:466–8.
Maghnie M, etal. Central diabetes insipidus in children and
young adults. N Eng J Med. 2000;343:998–1007.
Maria IA.MRI of the hypothalamic-pituitary axis in chil-
dren. Pediatr Radiol. 2005;35:1045–55.
Hormonal Obesity
5 Hypothalamic obesity : obesity that arises a er
paraventricular ventromedial hypothalamic injury,
causing hyperphagia due to loss of the serum leptin level
sensitization.
5 Cushing ’ s syndrome : obesity is a cardinal sign of
Cushing’s syndrome. Patients classically present with
truncal (android) obesity.
5 Hypothyroidism : obesity in hypothyroidism is mainly due
to a slow metabolic rate. e weight gain is o en modest,
without marked obesity.
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5 Polycystic ovary disease : up to 50 % of patients with
polycystic ovary disease are overweight with insulin
resistance.
5 Growth hormone de ciency : growth hormone de ciency
causes a reduction in lean body mass and an increase in
fat body mass.
Syndromic/Pathologic Obesity
5 Lipoma is de ned as the localized, encapsulated
accumulation of fat. It can be single or multiple and can
be seen in any part of the body (. Fig. 10.5.1 ). Multiple
lipomas can be seen in Ma ucci syndrome and
neuro bromatosis type 1 ( von Recklinghausen disease ).
5 Lipomatosis is a condition characterized by proliferation
of nonencapsulated fat cells (. Fig. 10.5.2 ).
5 Liposarcoma is a rare malignant tumor characterized by
neoplastic proliferation of fat cells (. Fig. 10.5.3 ).
5 Lipodystrophy is a condition characterized by loss of body
fat in one or more areas. It can be genetic or acquired
(e.g., HIV drug-induced lipodystrophy).
5 Binge - eating disorder is a psychiatric disorder,
characterized by uncontrolled episodes of eating, usually
in the evening.
5 Night - eating syndrome is a psychiatric disorder,
characterized by consumption of at least 25 % of daily
energy between the evening meal and the next morning.
Patients o en awake at night to eat, three or more times
per week.
5 Dercum ’ s disease ( lipomatosis dolorosa ) is a rare disease,
characterized by painful subcutaneous fatty tissue with
in ammatory characteristics. Patients are typically young
obese women 25–40 years of age, presenting with vague
pain that can be focal or generalized. Many patients live
with this disease while being unaware of it, either
because the disease sometimes shows mild symptoms or
because patients receive a wrong diagnosis.
Lipomatosis dolorosa can be mistaken for bromyalgia
rheumatica. Unlike bromyalgia rheumatica, the pain in lipomatosis dolorosa increases with body weight gain. e pain
o en has insidious onset and progresses with time. e pain in
lipomatosis dolorosa is chronic (>3months duration), aching,
stabbing, or burning and usually symmetrical (. Fig. 10.5.4 ).
However, localized pain may be seen in the upper limbs or
around the knee. e face and hands are typically not involved.
e pain characteristically arises from the subcutaneous
fat. e pain may worsen on any light touch or pressure (allodynia), wearing tight clothes, or taking a shower. Also, the pain
is temperature and humidity dependent and usually reduces
when the weather is hot and dry. Hot baths may reduce the
pain but only temporarily. e pain is thought to be caused by
. Fig. 10.5.2 Axial abdominal postcontrast CT shows retroperitoneal
lipomatosis, with increased fat content of the retroperitoneum
pushing the kidneys anteriorly in a bilateral fashion ( arrowheads )
. Fig. 10.5.1 Axial nonenhanced chest CT shows left chest wall
lipoma, seen as a typically well-circumscribed mass with fat
attenuation ( arrowhead )
. Fig. 10.5.3 Axial abdominal postcontrast CT shows severe
abdominal fatty proliferation that pushes the left kidney and the
intestines to the left abdominal cavity region ( arrowhead ) due to
proliferating retroperitoneal liposarcoma
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fat masses pressing upon the nerve root endings or by releasing
cytokines that induce pain (e.g., tumor necrosis factor-α).
ree types of lipomatosis dolorosa are described: type 1
( juxta - articular ), with painful subcutaneous folds around the
knees or the hips; type 2 ( di use ), which a ects the whole
body symmetrically; and type 3 ( nodular ), characterized by
intense pain around lipomas.
5 We b er – Christian disease ( WCS ) is a disease characterized
by painful subcutaneous nodules found mainly on the
trunk and the extremities, with constitutional symptoms
like fever, fatigue, polymyalgia, and arthralgia. e
subcutaneous nodules are composed of lobular
panniculitis (subcutaneous tissue in ammation). When
the panniculitis is systemic, WCS can be fatal in up to 10 %
of patients. Patients commonly show elevated erythrocyte
sedimentation rate and C-reactive protein levels.
5 Madelung ’ s disease ( benign symmetric
lipomatosis / Launois – Bensaude syndrome ) is a rare
condition, characterized by massive symmetric deposits
of nonencapsulated adipose tissue in the head, the neck,
and the upper trunk.
Madelung’s disease (MD) is typically seen in middle-aged
males of Mediterranean origin with a history of excessive
alcohol consumption (90 % of cases). Patients with MD typically consume more than 80g of alcohol per day for more
than 10 years. MD is considered a “sight diagnosis” because
of the typical patterns of fat distribution in the head and neck
region. Lipomatosis is typically seen accumulating in both
parotid regions (hamster cheek appearance), cervical region
(horse collar appearance), and the posterior neck region
(bu alo hump appearance) (. Fig. 10.5.5 ). e disease is
divided into two types: type 1 MD is characterized by sym-
metric body lipomatosis that gives the patient a “pseudoathletic” appearance (. Fig. 10.5.5 ). Type 2 MD is
characterized by di use lipomatosis that gives the patient a
generalized obese appearance.
Sensory, motor, or autonomic polyneuropathy is seen in
up to 85 % of patients with MD.Rarely, the tongue or the
mediastinum is involved in lipomatosis, resulting in dysphagia and dyspnea.
5 Metabolic syndrome ( syndrome X ) is de ned by the WHO
as the presence of impaired glucose regulation or
. Fig. 10.5.4 An illustration
demonstrates the typical pain
distribution in dercum dolorosa
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diabetes, with two of the following risk factors:
hypertension, dyslipidemia, central obesity, and
microalbuminuria. ere is a strong association between
the development of metabolic syndrome and increase in
visceral adipose tissue (VAT).
5 Fröhlich syndrome is a rare hypothalamic disorder,
characterized by obesity, stunned growth, and genital
hypoplasia.
5 Obesity hypoventilation ( Pickwickian ) syndrome is a
disease characterized by the triad of morbid obesity,
a
hypoventilation, and irresistible hypersomnolence
(drowsiness). Hypoventilation in Pickwickian syndrome
is de ned clinically by an arterial blood gas as a
PaCO 2 > 45 and/or a PO 2 < 55in the presence of morbid
obesity. is hypoventilation is attributed to obstructive
sleep apnea in these patients and by the ventilation/
perfusion mismatch that results from the irregular
shallow breathing with or without compression by a thick
chest wall.
b
c
. Fig. 10.5.5 An illustration demonstrates the typical clinical signs of Madelung’s disease: ( a ) hamster cheeks appearance, ( b ) horse collar
appearance, ( c ) buff alo hump appearance, and ( d ) pseudo-athletic appearance
d
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Drug-Induced Obesity
5 Glucocorticoids use : glucocorticoids cause fat
accumulation in the body in a similar fashion to people
with Cushing’s syndrome. Glucocorticoid obesity is seen
in patients with chronic prednisolone intake >10mg/day
or its equivalent.
5 Cessation of smoking : patients who quit smoking can gain
up to 4–5kg on average, and it is partly mediated by
nicotine withdrawal.
Evaluation of Fat Within the Body
ere are several techniques used to estimate body fat.
Anthropometry is a technique used to estimate BMI by measuring waist circumference and skinfold thickness. BMI is a
good indicator of obesity, but it provides indirect measurement of body fat and is unable to di erentiate lean body mass
from body fat. e inability of BMI to discriminate lean body
mass from fat body mass leads to de ning lean, muscular
individuals as obese.
The metabolism of adipocytes varies with fat sites. Fat
deposits in the abdomen and flank are more metabolically
active than fat deposits in the buttocks or thighs. Upperbody obesity is more associated with hypertension, glucose intolerance, and serum cholesterol levels than is
lower-body obesity. Recent research emphasizes the high
risks of cardiovascular diseases and metabolic abnormalities associated with increased intra-abdominal VAT.VAT
is defined as the fatty tissue that accumulates beneath the
abdominal muscle wall and surrounding the abdominal
viscera. VAT mass is pathologically more important than
subcutaneous fat thickness over the trunk. Also, visceral
fat is a major determinant of whole body insulin resistance.
Adipose tissue is a specialized loose connective tissue that
is laden with adipocytes. It works as a source of energy, thermal insulation (e.g., brown fat), and as a mechanical cushion
in mammals. A 70-kg man normally has 15kg of adipose
tissue, representing 21 % of body mass. In contrast, fat is a
term used to describe the chemical lipid component in the
form of triglycerides. It can be found within adipocytes or in
pathological conditions like fatty liver. Modern methods use
ultrasound, CT, and MRI as useful and accurate tools for
VAT quanti cation.
Quantitative Assessment of Visceral Fat by US
Ultrasound can be used as a fast and easy method to quantify
visceral and subcutaneous fat. Although it is not as standard
as CT quanti cation, it is reported by many investigators to
be an accurate method to quantify the abdominal wall fat
thickness and preperitoneal fat thickness.
Quantitative Assessment of Visceral Fat by CT
and MRI
An axial body section is taken at the level of the navel or (L4/
L5), and assessment is done via a computer so ware program
to calculate the percentage of visceral fat distribution
. Fig. 10.5.6 An axial CT section obtained at the level of L4/L5
vertebra
(. Figs. 10.5.6 and 10.5.7 ). Excess visceral fat typically sepa-
rates the intra-abdominal structures. e drawbacks of the
CT method are the use of radiation and the limited gantry
diameter to patients less than 70cm wide (the standard CT
gantry diameter). MRI, on the other hand, is radiation-free
but more expensive in its use as a regular monitoring method.
e MRI method uses the same procedures as the CT method
of quanti cation.
Gastric Banding
Gastric banding is a widely performed surgical procedure as
a surgical therapy for morbid obesity. e procedure consists
of placing a silicon band around the upper part of the stomach to create a small gastric pouch that works as a stomach
(neostomach). e pouch is connected to the rest of the
stomach via a narrow stoma. e silicon band contains an
adjustable inner balloon that can be in ated with air or uid
up to 5cm 3 , and it is connected to a reservoir that is typically
sutured to the anterior rectus sheath. e stoma width normally should be within 3–4mm.
e gastric banding procedure controls obesity by
restricting food administration to the stomach into a small
gastric pouch and narrow stoma, which creates early satiety
when the pouch is full. Although gastric banding is a
relatively safe procedure, several complications may arise
later in up to 35 % of cases. Additional surgery may be
required in up to 11 % of cases.
Early complications of gastric banding include esophageal
perforation (0.5 % of cases), dysphagia (14 % of cases),
gastroesophageal re ux disease, and early slippage of the
band (1 % of cases). Late complications include eccentric
pouch dilatation (25 %), slippage of the band (24 %),
intragastric band migration, and gastric necrosis (<0.3 %).
Patients with diabetes show early gastric dilatation due to
diabetic gastroparesis.
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b
10
c
. Fig. 10.5.7 Computer-generated histogram segmentation of the same CT section as (. Fig. 10.5.6 ) done by using image analysis software
(Image J). The image in ( a ) refl ects fat density (represented in white ), and the other nonfatty tissues are removed (represented in black ). Image
( b ) represents total body volume, image ( c ) represents subcutaneous tissue volume (in back after inversion of the original white color ), and
image ( d ) represents VAT volume (in black ). The volume of VAT or subcutaneous tissue in this image is gained in cm 2 . The volume must be
multiplied by the slice thickness of the original image to get the fat volume in cm
Fluoroscopic barium meal examination is performed to
detect abnormalities and complications of gastric banding.
Initially, a scout supine abdominal image is taken to identify
the place of the band and the reservoir. Water-soluble contrast media is initially administered in the early stages to
d
3
con rm the absence of leakage. e normal images should
reveal a small upper gastric pouch, a narrow stoma extending through the gastric band, and opaci cation of the rest of
the stomach (. Fig. 10.5.8 ). CT can be performed a er the
uoroscopic examination to detect other abnormalities.
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