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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_20_библиотеки_им_акад_М_И_Перельмана
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Crohn’s Disease
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A
B
MEdiCAlly CoMPRoMisEd PATiEnTs
Middle class family
•
• Maternal aunt has Crohn’s disease (CD)
D.
Medical History
• Hospitalized because of weight loss, abdominal
cramps, and diarrhea. Gastroenterologists undertaking investigations to determine if child has CD
• Three‐month history of abdominal cramps, diarrhea,
anorexia, and weight loss
• No medications present during medical work‐up
• No known allergies to foods or medications
• Vaccinations are up to date
Figure 8.8.1 (A, B) Facial photographs at six‐month follow‐up visit.
A. Presenting Patient
Seven‐year‐, four‐month‐old Caucasian female
•
(Figure8.8.1)
B. Chief Complaint andHistory
• New patient referred from pediatric gastroenterology
for assessment of swollen lower lip and angular
cheilitis as part of a diagnostic work‐up of inflammatory bowel disease
• Mother noted progressive swelling of lower lip for the
past three to four months concurrently with abdominal cramps and diarrhea
C. Social History
• Lives at home with both parents
• Sister (five years old) and brother (two years old)
Specific Exams
• Weight: 21.5 kg (below the 25th percentile)
• Hemoglobin: 9.7 g/dl (normal range: 11–14)
9
• Platelets: 507 × 10
/l (normal range: 140–400)
• C-reactive protein: 13 mg/l (normal range: <10)
• Albumin: 26 g/l (normal range: 35–50)
• Barium meal and follow‐through showed irregular
stricture involving the distal portion of the terminal ileum
• Upper endoscopy and colonoscopy reveal multiple
regions with inflammation but mainly involvement of
terminal ileum with large ulcers
Histopathology
Biopsies from stomach, terminal ileum, and colon
•
show focal areas of acute and chronic inflammation
• Gingival biopsy (mandibular incisor labial gingiva)
shows marked chronic inflammation and non‐
necrotizing granulomas, which, in combination with
acute and chronic inflammation in the other biopsies,
supports the clinical diagnosis of CD with involvement
of multiple regions of the gastrointestinal tract
(seeBackground Information 1 and 2)
E. Medical Consult
• Pediatric gastroenterologist
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• Inammatory bowel disease (IBD) can be subclassied as ulcerative colitis (UC) or CD. Indeterminate
colitis is the term used when unable to clearly
discriminate between UC and CD
• Incidence of pediatric onset IBD is increasing
worldwide
• Chronic granulomatous inammatory disorder of
unknown etiology, likely the result of an inappropriate
inammatory response in a genetically susceptible
individual to an environmental stimulus
• May affect any part of the gastrointestinal tract
from the mouth to the anus
Typically involves the terminal segment of the
•
small intestine (ileum) and first segment of the
large intestine (colon)
• Peak incidence is in the second and third decades
of life with up to one‐third of cases occurring
before 20 years of age
• There is familial clustering with a history of IBD in
approximately 15% of cases of CD
•
There are probably several genes involved in
conferring susceptibility to IBD and there may be
genetic heterogeneity, with different genes having
similar phenotypic expressions
• NOD2 is the best characterized susceptibility
gene, mutations of which confer increased risk
for CD. The gene encodes for a protein that is
involved in recognizing pathogens and intracellular signaling of the innate immune response
Treatment ofCrohn’s Disease
• Medical induction and maintenance of remission of
intestinal inflammation
Nutritional support may require nasogastric infu-
•
sion of formulated food in severe cases with
malnourishment and growth retardation, to
increase caloric intake
• Medical treatment of relapses and acute exacerbations
• Surgical intervention if there are intractable symptoms despite medical therapy or if there are
intestinal complications such as obstruction,
infection, fistula, perforation, or hemorrhage
• Abdominal pain
• Diarrhea ± blood in stools
• Poor appetite
• Weight loss
• Impaired growth and pubertal delay
Anemia due to malabsorption and blood loss
•
• Elevated erythrocyte sedimentation rate (ESR)
or C‐reactive protein (CRP) and high platelet
count are indicative of an inflammatory process
• Low albumin due to protein losing enteropathy
• Elevated fecal calprotectin
• Oral soft tissue manifestations
F. Dental History
• One previous dental visit at six years of age and
dentist noted caries‐free primary dentition
• Poor oral hygiene during last two weeks due to illness;
difficult to brush teeth because of swollen lower lip
• Reduced appetite during last three months but good
diet prior
348 Clinical Cases inPediatric Dentistry
Figure 8.8.2 Swelling and angular cheilitis of lower lip.
• Uses toothpaste containing fluoride, supervised by
parents
• Lives in optimally fluoridated area
• No history of dental trauma
G. Extraoral Exam
• Bilateral angular cheilitis (Figure8.8.2)
• Gross swelling of lower lip with vertical fissures
• Dry lips
H. Intraoral Exam
• Soft tissues: swelling of lower labial mucosa, soft
tissue tags, and ulcers in lower labial sulcus, and
swelling of marginal and attached gingiva around
mandibular incisors (see Fundamental Point 1)
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• Early mixed dentition with class I relationship of
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permanent first molars
• Mandibular permanent lateral incisors erupting
lingual to permanent central incisors with retention
of both mandibular primary lateral incisors and the
mobile mandibular left primary central incisor
(Figure8.8.3)
• Generalized plaque accumulation, particularly on labial
aspect of incisors
• Caries‐free dentition
I. Diagnostic Tools
• Gingival biopsy when under general anesthesia for
endoscopy and colonoscopy (see Fundamental
Point2)
MEdiCAlly CoMPRoMisEd PATiEnTs
Figure 8.8.4 Histological image of gingival granuloma,
formed by an aggregate of epithelioid macrophages. To the
right of the center of the image is a multinucleated giant cell.
Figure 8.8.3 Intraoral soft tissue inflammation and ulcerations,
and retained mandibular primary incisors.
• Up to 40% of children may have one or more of
the following oral manifestations of CD at initial
presentation:
Lip and/or cheek swelling
Angular cheilitis
Mucogingivitis (inflammation of marginal and
attached gingiva), most commonly in the
anterior region
Irregular nodular swelling or “cobblestoning”
of buccal mucosa
Long, deep ulcers in mandibular buccal sulcus
Mucosal tags
Multiple aphthous ulcers
• A non‐necrotizing granuloma is a key histopathological nding in CD. It consists of an aggregate
of epithelioid macrophages (“epithelioid”: lots of
pink cytoplasm similar to squamous epithelial
cells) and multinucleate giant cells (Figure8.8.4)
• Serial sections of a specimen must be examined by
a pathologist to nd loosely formed non‐necrotizing
granulomas that are scattered in affected tissue
• Biopsy of a gingival or mucosal tag lesion, if
present, is recommended because non‐necrotizing granulomas should be found in a biopsy from
these sites
Biopsy of the lower lip is not recommended
•
because there is a risk of damage to the labial
branches of the mental nerve. Furthermore,
granulomas in an extensively edematous lip will
be sparse and scattered and may not be captured in a biopsy specimen
J. Differential Diagnosis
• Orofacial granulomatosis (OFG) that may be associated with hypersensitivity to foods or additives (see
Background Information 3)
• UC: inflammatory bowel disease affecting the colon in
which there may be associated oral aphthous ulceration. Pyostomatitis vegetans with tiny yellow pustules
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Anti‐inflammatory Glucocorticoids
Prednisolone
Budesonide
Enteral nutrition
Aminosalicylates (ASA)
Sulfasalazine
Mesalamine
Antibiotic Metronidazole
Ciprofloxacin
Immunomodulator 6‐Mercaptopurine
Azathioprine
Biologic Infliximab
Adalimumab
in the oral mucosa has been reported in individuals
with UC and CD
• Hereditary angioedema
• Allergic angioedema
K. Diagnosis
• CD with oral lesions
• Retained primary incisors
L. Comprehensive Treatment Plan
Initial Medical Treatment Following Diagnosis
ofCD (see Table 8.8.1)
• 6‐Mercaptopurine 25 mg daily
• Prednisolone 25 mg daily for four weeks. Then reduce
dosage by 5 mg each week until tapered course is
completed
• Iron supplements for treatment of anemia: 6 mg/kg
daily of elemental iron
Dental Treatment
• Gingival biopsy to obtain histological confirmation of
granulomatous inflammation and diagnosis of CD
• Delay treatment in the dental office until medical
improvement in CD
• Extraction of retained mandibular primary incisors
• Oral hygiene instruction
• Monitor developing occlusion
• Frequent preventive dental visits to encourage improved
oral hygiene and application of fluoride varnish
• Fissure sealant application to permanent first
molars when erupted sufficiently to isolate for
moisture control
Conventional corticosteroid, initial high dose to control
disease
Typically exclusive use of elemental or semi‐elemental diet
for six to eight weeks
Active component, 5‐ASA, acts locally in intestinal mucosa
to inhibit inflammation
Antibacterial effect on intestinal flora
Immunosuppressant
Steroid‐sparing
Monoclonal antibodies that neutralize bioactivity of the key
inflammatory cytokine, tumor necrosis factor‐alpha
(TNF‐α)
• OFG is a condition characterized by orofacial
swelling with biopsy‐positive non‐necrotizing
granulomas in a patient without CD or other
systemic disease
• May be associated with a hypersensitivity to
certain food and drink additives such as benzoates, cinnamon, and tartrazine
• OFG that is associated with hypersensitivity to
food additives may improve or resolve with an
exclusion diet; however, compliance with such a
diet may be very difficult
• Intralesional steroids may be required to treat lip
swelling in OFG
A child with OFG may not have overt symptoms
•
or signs of CD but may subsequently develop
intestinal CD
• A child with OFG should be referred to a specialist in oral medicine. Review by a pediatric
gastroenterologist may also be required because
OFG may precede the development of CD
M. Prognosis andDiscussion
• Regression of oral lesions anticipated with treatment
of CD
• Oral lesions may reappear if there is relapse of
systemic CD
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MEdiCAlly CoMPRoMisEd PATiEnTs
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If general anesthesia is planned, prednisolone therapy
•
may result in suppression of the normal adrenocortical response, with a risk of developing hypotension.
Hydrocortisone should therefore be administered IV
at induction of anesthesia by an anesthesiologist if
Self‐Study Questions
general anesthesia is administered within three to six
months of glucocorticoid therapy. There is no need for
IV hydrocortisone or glucocorticoid medication prior to
providing dental treatment under local anesthetic in a
dental office
Answers are located at the end of the case
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Self‐Study Answers
tis, mucogingivitis, cobblestoning of buccal mucosa,
mucosal tags, aphthous ulceration, and long, deep
ulcers in the mandibular buccal sulcus are some of
the possible orofacial manifestations of CD
nutrition, aminosalicylates), immunomodulators, biologics, and antibiotics may be used in the
management of CD in children
ates, cinnamon, and tartrazine
Additional Reading andResources
Challacombe SJ. 1997. Oro‐facial granulomatosis and oral
Crohn’s disease: are they specific diseases and do they predict systemic Crohn’s Disease? Oral Dis 3:127–9.
Harty S, Fleming P, Rowland M etal. 2005. A prospective study
of the oral manifestations of Crohn’s disease. Clin Gastroenter
Hepatol 3:886–91.
Hussey S, Fleming P, Rowland M etal. 2011. Disease outcome
for children who present with oral manifestations of Crohn’s
disease. Eur Arch Paediatr Dent 12:167–9.
Kammermeier J, Morris M‐A, Garrick V etal. 2016. Management
of Crohn’s disease. Arch Dis Child 101: 475–80.
Leao JC, Hodgson T, Scully C etal. 2004. Review article: orofacial
granulomatosis. Aliment Pharmacol Ther 20:1019–27.
Levine A, Koletzko S Turner D etal. 2014. ESPGHAN revised
Porto criteria for the diagnosis of inflammatory bowel disease in children and adolescents. J Pediatr Gastroenterol
Nutr 58:795–806.
Scully C. 2014. Scully’s Medical Problems in Dentistry,
7thEdition. Edinburgh: Elsevier.
White A, Nunes C, Escudier M et al. 2006. Improvement in
orofacial granulomatosis on a cinnamon‐ and benzoate‐free
diet. Inflamm Bowel Dis 12:508–14.
352 Clinical Cases inPediatric Dentistry
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9
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Patients withDisabilities
Nancy Dougherty
Case 1: Down Syndrome (Trisomy 21) ................................................................................................................354
Nancy Dougherty, Farah Alam, and Sheena Nandi
Case 2: Cerebral Palsy, Bronchopulmonary Dysplasia ........................................................................................359
Nancy Dougherty and Farah Alam
Case 3: Attention Deficit Hyperactivity Disorder ................................................................................................365
Nancy Dougherty
Case 4: Seizure Disorder, Intellectual Disability ..................................................................................................371
Nancy Dougherty and Farah Alam
Case 5: Autism Spectrum Disorder ....................................................................................................................377
Nancy Dougherty
Case 6: Sickle Cell Anemia, Intellectual Disability ...............................................................................................383
Nancy Dougherty and Sheena Nandi
Clinical Cases in Pediatric Dentistry, Second Edition. Edited by Amr M. Moursi.
© 2020 John Wiley & Sons, Inc. Published 2020 by John Wiley & Sons, Inc.
Companion website: www.wiley.com/go/moursi/pediatrics
353
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Case 1
Down Syndrome (Trisomy 21)
BA
Patient was hospitalized at age three for
•
myringotomy and placement of tympanostomy
tubes. Due to postoperative complications, patient
was required to stay in the hospital for three days
postoperatively
BACKGROUND INFORMATION 1
Figure 9.1.1 (A, B) Facial photographs.
A. Presenting Patient
• Six‐year‐, six‐month‐old, African‐American male
(Figure9.1.1)
• Diagnosed with Down syndrome (trisomy 21)
(seeBackground Information 1)
• New patient visit
B. Chief Complaint
• Mother states, “My son has been to other dentists,
but they were not able to take care of him”
Social History
C.
• Patient attends school; in class for children with
special educational needs
• Mother is primary caregiver
• Lower mid‐level socioeconomic status
• Patient has two sisters, ages eight and 11
D. Medical History
• Cardiac: Ebstein’s anomaly (congenital defect of tricuspid
valve). Patient’s defect is mild and has not required surgical
repair. He is not currently on any medications and is
followed by pediatric cardiology on an outpatient basis (see
Fundamental Point 1)
• History of frequent otitis media and upper respiratory
infections
Down Syndrome (Trisomy 21)
• Down syndrome consists of a characteristic
group of cognitive and physical ndings that result
from having an extra copy of chromosome 21
• Most individuals with Down syndrome function in
the range of mild to moderate intellectual disability
• Craniofacial characteristics include:
Hypoplastic midface and maxilla
Mild microcephaly
Upslanting palpebral fissures
Short neck
• Health conditions frequently seen in individuals
with trisomy 21 include:
Congenital heart disease
Hypotonia
Compromised immune function
Hearing problems
Thyroid dysfunction
Skeletal abnormalities
Eye problems, especially cataracts
Increased risk for development of leukemia
Early development of senile dementia
(American Academy of Pediatrics 2011; Jones
etal. 2013)
E.
Medical Consult
• Cardiology consult requested. Patient cleared for routine
dental treatment. Antibiotic prophylaxis not required
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PATiEnTs wiTHDisAbiliTiEs
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FUNDAMENTAL POINT 1
Medical History forDown Syndrome
• It has been estimated that the frequency of
congenital cardiac defects in individuals with
trisomy 21 is 40–50%
• A medical history should include questions on:
History of cardiac problems
Symptoms of cardiac problems
Any surgeries for cardiac problems
Medications for cardiac problems
Restrictions on activities
• Due to anatomic variations and compromised
immune systems, individuals with trisomy 21
are at increased risk for upper airway infections.
(Freeman et al. 1998; Mitchell et al. 2003)
F. Dental History
• Mother has taken patient to three other dentists, but
she was dissatisfied with care provided
• Patient’s behavior was uncooperative for previous
dental examinations
• Optimal water fluoridation levels
• Patient is not a frequent snack eater, but does drink
large amounts of sugary beverages
• Patient does not brush teeth himself. Allows mother
to brush his teeth under duress
G. Extraoral Exam (Figure9.1.1)
• Patient has characteristic facies of trisomy 21, as
discussed in the Background Information
• No other significant findings
H. Intraoral Exam (Figure9.1.2
andFundamentalPoint 2)
• Early mixed dentition
• Erupting mandibular central incisors
• Poor oral hygiene
• Generalized marginal gingival inflammation
• Caries‐free dentition
• Class III skeletal relationship, mesial step primary molars
I. Diagnostic Tools
• Radiographs were not obtained for the following reasons:
Patient was unable to cooperate for radiographic exam
No carious lesions were noted during clinical exam
It was determined that the patient would require
sedation for radiographic exam; due to absence of
caries and the patient’s past history of
A
C
Figure 9.1.2 (A–C) Intraoral photographs showing generalized
marginal gingival inflammation.
B
postanesthesia complications, the practitioner did
not feel sedation presented an appropriate risk/
benefit balance for this patient at this time
(seeFundamental Point 3)
FUNDAMENTAL POINT 2
Oral–Facial Presentation ofTrisomy 21
• Individuals with trisomy 21 may present with a
number of oral–facial abnormalities and dental
anomalies. These include:
Class III malocclusion (due to maxillary
hypoplasia)
Relative macroglossia due to the small size of
the oral cavity
Delayed dental eruption
Hypodontia
Microdontia, taurodontism, and other
anatomic anomalies of teeth
Ectopic eruption and impaction of teeth
Increased risk for periodontal disease (due to
compromised immune response)
(Pilcher 1998)
J. Differential Diagnosis
• Not applicable
K. Diagnosis andProblem List
Diagnosis
• Trisomy 21
• Congenital heart defect (triscuspid valve prolapse)
• Frequent otitis media
• Gingivitis
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