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CHAPTER 7
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Self‐Study Answers
1. True: treatment often takes place in multiple
phases which may include infancy, the primary
dentition, transitional dentition, and permanent
dentition
2. False: the timing of bone grafting of the alveolar
cleft is determined primarily by the stage of dental
development
Bibliography andAdditional Reading
American Academy of Pediatric Dentistry. 2018–2019. Policy on the
management of patients with cleft lip/palate and other craniofacial anomalies. In: Clinical Practice Guidelines and Best Practices
(Reference Manual). Pediatr Dent 40:429–30. https://www.
aapd.org/research/oral‐health‐policies‐‐recommendations/
management‐of‐patients‐with‐cleft‐lip‐palate‐and‐other‐
craniofacial‐anomalies
American Cleft Palate–Craniofacial Association. 2018.
Parameters for Evaluation and Treatment of Patients with Cleft
Lip/Palate or Other Craniofacial Differences. Revised edition.
https://acpa‐cpf.org/team‐care/standardscat/parameters‐of‐
care (Accessed 19 June 2019).
3. Autogenous bone grafting from the iliac crest of
the patient’s ilium (hip) is the gold standard for cleft
bone grafting, although bone can also be harvested
from the head, ribs, or leg
4. Orthognathic surgery is typically delayed until
physical maturity is complete in order to minimize
any adverse effects on subsequent growth
Antonarakis GS, Palaska PK, Herzog G. 2013. Caries prevalence
in non‐syndromic patients with cleft lip and/or palate: a
meta‐analysis. Caries Res 47:406–13.
Parker SE, Mai CT, Canfield MA et al.; National Birth Defects
Prevention Network. 2010. Updated National Birth Prevalence
estimates for selected birth defects in the United States, 2004–
2006. Birth Defects Res A Clin Mol Teratol 88(12):1008–16.
Stock NM, Sharratt ND, Heath J etal. 2018. Falling through the
gap: dental treatment experiences of patients affected by
cleft lip and/or palate. Br Dent J 225(3):218–22.
Worth V, Perry R, Ireland T etal. 2017. Are people with an orofa-
cial cleft at a higher risk of dental caries? A systematic
review and meta‐analysis. Br Dent J 223:37–47.
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Medically Compromised Patients
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Paddy Fleming
Kerrod B. Hallett
Richard Balmer
Barbara Sheller
Kerrod B. Hallett
Paddy Fleming
Kirsten FitzGerald
Eleanor McGovern
Paddy Fleming
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
299
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Congenital Heart Disease
• No known food or drug allergies
• Current medications:
Warfarin by mouth (PO) 3 mg daily
Furosemide PO 20 mg daily
• Several past surgeries and hospitalizations
E. Medical Consult
For this patient (see Fundamental Point 1):
• Baseline cardiac function
• Baseline international normalized ratio (INR) range:
2.0–3.0
• Baseline hemoglobin: 11.7 g/dL
• Baseline pulmonary saturations: 97%
• Baseline blood pressure 80/40 mmHg
• Baseline respiratory rate: 20/minute
• Baseline oxygen: 0.5 l/minute
Figure 8.1.1 Facial photograph.
A. Presenting Patient
• Two‐year‐, eight‐month‐old Hispanic female (Figure8.1.1)
• New patient
B. Chief Complaint
• Referred from hospital pediatric cardiac unit for dental
assessment and management of asymptomatic
dental caries
C. Social History
• Single mother is primary caregiver
• Low socioeconomic status
• No siblings
D. Medical History
• Congenital heart defects:
Triscuspid atresia
Hypoplastic right ventricle
Restrictive ventricular septal defect (VSD)
Subpulmonary narrowing
F. Dental History
• No dental home
• Currently bottle feeding with sweetened liquids
• High caloric supplementation to increase weight
• Toothbrushing once a day with fluoridated toothpaste
with little adult supervision
• No systemic fluoride exposure
• No history of dental trauma
G. Extraoral Exam
• No significant findings
H. Intraoral Exam
Soft Tissues
• Generalized erythematous mucosa
• Generalized edematous gingivae
Hard Tissues
• Proximal and smooth surface cavities on maxillary
incisors
• Occlusal cavities on molars
• Smooth surface demineralization on molars
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• Incidence rate of approximately 8–10 cases/1000
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live births
Most lesions occur individually; several form major
•
components of syndromes or chromosomal
disorders such as Down syndrome (trisomy 21),
Turner syndrome (XO chromosome), and 22q11.2
deletion syndrome
•
Known risk factors associated with CHD
include:maternal rubella, diabetes, alcoholism,
irradiation,and drugs such as thalidomide,
phenytoin sodium (Dilantin) and warfarin sodium
(Coumadin)
• Turbulent blood flow is caused by structural
abnormalities of the heart anatomy and presents
clinically as an audible murmur
CHD can be classified into acyanotic (shunt or
•
stenotic) and cyanotic lesions depending on clinical
presentation
•
Acyanotic lesions are characterized by a connection
between the systemic and pulmonary circulations or
stenosis of either circulation (left to right shunts). The
most common anomalies are:
Atrial septal defect (ASD)
Ventricular septal defect (VSD)
Patent ductus arteriosus (PDA) caused by failure
of closure of the ductus connecting the pulmonary artery with the aorta (normally closes soon
after birth)
Coarctation of the aorta
Aortic stenosis
Pulmonary stenosis
•
All cyanotic conditions exhibit right to left shunting
of desaturated blood. Infants with mild cyanosis
may be pink at rest but become very blue during
crying or physical exertion. Children with cyanotic
defects are at significant risk for desaturation
during general anesthesia
• The most common cyanotic lesions are:
Tetralogy of Fallot which includes a VSD, pulmonary stenosis, overriding aorta, and right ventricular hypertrophy
Transposition of great vessels
Tricuspid atresia
• If cardiac failure develops, the infant is digitalized
and prescribed diuretics if necessary.
• Hospitalization, oxygen, nasogastric tube feeding,
and antibiotic therapy for chest infection may also
be required
MEdiCAlly CoMPRoMisEd PATiEnTs
• Current cardiac status:
Blood pressure
Respiratory rate
Oxygen rate
Pulmonary saturations
Blood gases
• Cardiac medications
• Current INR range (normal, without anticoagulant
therapy: –1; target range, with therapy: –2 to 3)
• Previous surgical management
• Future surgical management
Assess risk of cardiac complications under
•
general anesthesia
• Assess risk of infective endocarditis (IE) and
need for antibiotic prophylaxis before invasive
dental procedures
• Assess risk of hemorrhage during dental surgery
• Develop a perioperative anticoagulant manage-
ment plan
Occlusal Evaluation ofPrimary Dentition
• Flush terminal plane
• Anterior open bite
• Generalized severe plaque accumulation
I. Diagnostic Tools
Bacteriology andSaliva Tests
•
Not obtained
Radiographs (Figure 8.1.2)
• Intraoral periapical radiographs (taken at the time of
dental treatment under general anesthesia)
Photographs (Figure 8.1.3)
• Pre‐ and postoperative intraoral photographs (taken at
time of dental surgery)
High Caries Risk perCaries‐Risk Assessment
Tool [CAT] (see Fundamental Point 2):
• Special health needs child
• Visible cavitations
• Enamel demineralizations
• Low socioeconomic status
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BA DC
Figure 8.1.2 (A–G) Preoperative intraoral radiographs.
GFE
Figure 8.1.3
A
D
(A–E) Preoperative intraoral photographs.
B
• Visible plaque score (4/6)
• Dietary chart (more than three sugar exposures/day)
• Medications that impair salivary flow
• Use of fluoridated toothpaste but no fluoridated water
nor fluoride supplements
• Toothbrushing only once a day
C
E
Odontogenic
• Loss of tooth structure due to dental caries
• Dental attrition
• Dental erosion
• Inflammatory
• Pulpal pathology
J. Differential Diagnosis
Developmental
• Enamel hypoplasia/hypomineralization
Infective
• Bacterial and/or fungal
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K. Diagnosis andProblem List
Diagnosis
• Active early childhood caries
• Chronic hyperplastic gingivitis
• Periapical pathology
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MEdiCAlly CoMPRoMisEd PATiEnTs
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• Enamel hypoplasia
• Anterior open bite
Problem List
• Untreated carious lesions with pulp pathology
• Severe plaque accumulation
• Malocclusion
• Poor infant feeding practice
• Parent’s limited understanding of potential medical
complications
• High risk of IE–see Background Information 2
• High risk of increased hemorrhage following dental
extractions–need for local hemostatic measures
following dental extractions
• Behavior assessment: inability of two‐year, eight‐
month‐old child to accept extensive invasive dental
procedures in dental office
• Individuals using this tool should be able to:
Visualize child’s teeth
Access reliable historian for nonclinical elements
Be familiar with footnotes that clarify elements
Understand that each child’s risk classification
is determined by highest risk category where
a risk indicator exists
• Users must understand the following caveats:
Caries risk assessed at one point in time only
Clinical management remains a professional decision
CAT does not render a diagnosis
Advanced technologies (e.g. electronic caries
detection, microbiological tests) are not
essential for using this tool
(American Academy of Pediatric Dentistry [AAPD]
2018–2019a)
Comprehensive Treatment Plan
L.
• Establishment of a dental home and caries
preventionplan:
Cease bottle feeding
Improve and increase frequency of oral hygiene
Limit sugar intake between meals
Brush after oral medicine intake
Commence 1 mg fluoride supplement daily
• Caries control using 0.2% chlorhexidine gel or 0.12%
liquid: apply with cotton tip nightly two weeks prior
toprocedure
Remove any potentially/pulpally involved teeth to
•
reduce future risk of chronic bacteremia
• Comprehensive treatment of carious lesions under
general anesthesia due to the complex medical history,
dental needs, and behavior management issues
• IE Prevention with intravenous antibiotic prophylaxis
• Perioperative anticoagulant plan
Follow‐Up Care
• Postoperative and home care instructions (Figure8.1.4)
Discharge after recommencement of warfarin
Soft cold diet for two days
Recommence tooth brushing after 24 hours
Start prevention plan
• Recall plan
Six weeks postoperative, and three‐ to six‐month
recall thereafter
• Both CHD and rheumatic heart disease can
predispose the scarred internal lining of the
heart to bacterial or fungal infection known as IE
• Bacteremia during or after an invasive dental procedure can lead to the formation of friable vegetations
of blood cells and organisms on the scar tissue
• Streptococcus viridans is most frequently
responsible for chronic IE, while Staphylococcus
aureus is often implicated in the acute fulminating form (Hallett etal. 2013)
• IE may be prevented by antibiotic prophylaxis but
there is little or no evidence to support thispractice
• In 2008, the National Institute for Health and Clinical
Excellence in the UK recommended against IE
prophylaxis for all patients undergoing any type of
dental procedures. Despite a 78.6% reduction in
the number of prescriptions in the two years after
the guideline was introduced, there was no large
increase in the incidence of cases of or deaths from
IE (Douketis et al. 2008; Thornhill et al. 2011)
However, both the American Heart Association
•
and European Society of Cardiology continue to
recommend antibiotic prophylaxis for children at
high risk of IE
• Preoperative antiseptic mouthwash can reduce
oral bacterial load
• Focusing on good oral hygiene practices may be
more important than antibiotic prophylaxis
(Moursi etal. 2018)
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A
D
Figure 8.1.4 (A–E) Postoperative intraoral photographs.
B
M. Prognosis andDiscussion
• Prognosis for limiting caries progression and changing
the diet is guarded in view of limited understanding of
caries risk factors and medical complications by
parent. Prognosis could be improved with additional
home support
N. Common Complications andAlternative
Treatment Plans
• Noncompliance with dietary advice
• Postoperative bleeding or infection
C
E
• Continued caries progression
• Alternative treatment plans may include:
Use of stainless steel crowns in all teeth presenting
with decalfication or white spot lesions
Alternative pulpal management, e.g. extraction vs.
pulp therapy (must consider risks of chronic
bacteremia)
Alternative medications for anticoagulant management (e.g. heparin)
Alternative methods for behavior management
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• Anticoagulants are usually prescribed for children
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with valvular heart disease and prosthetic valves to
reduce the risk of embolization
• If dental extractions are required, it may be necessary to decrease the clotting times to facilitate
adequate coagulation but not to such an extent so
as to cause emboli or clotting around the heart
valves
• Commonly used anticoagulant drugs are oral
warfarin sodium (Coumadin), which is a vitamin K
antagonist depleting factors II, VII, IX, and X, or
heparin sodium (heparin), which inhibits factors IX,
X, and XII
Local hemostatic measures include application of
•
topical thrombin, packing of the socket with
microfibrillar collagen hemostat, oxidized regenerated cellulose, and suturing of attached gingivae.
Splints or stomo‐adhesive bandages may also be of
benefit. There have been recent reports of the
efficacy of a “fibrin sealant” (Tisseel Duo 500) in
the management of coagulopathies, but its use on
moist oral mucosa is limited
• It is recommended to consult with pediatric
cardiologist to discuss if there is a need to modify
anticoagulant therapy before oral surgery. Some
practitioners cease warfarin three to five days prior
to the surgery date, commence enoxaparin sodium
once daily via Insuflon, and admit the patient to the
hospital on the day of the procedure. In this
protocol, recommencement of warfarin and
MEdiCAlly CoMPRoMisEd PATiEnTs
weaning off enoxaparin sodium 24 hours after
surgery is required to re‐establish correct INR,
prothrombin time, and activated partial thromboplastin time
•
However, recent studies on adults who had
multiple dental extractions without modification of
their anticoagulant therapy showed few or no
postoperative complications. American Dental
Association recommendations are that for most
patients there is no need to discontinue warfarin or
antiplatelet therapy prior to dental intervention but
to use local measures to control hemorrhage. A
patient’s coagulation status, based on the INR,
must be evaluated before invasive dental procedures are performed and any changes in their
anticoagulation therapy must be discussed with
the patient’s physician
The American College of Chest Physicians recom-
•
mends that patients who are taking vitamin K
antagonists and are about to undergo minor dental
procedures continue with the therapy because it
does not confer an increase in clinically important
major bleeding. The 2008 College guidelines
further state that it is reasonable to co‐administer
an oral prehemostatic agent at the time of the
procedure until more adequately powered studies
are performed. In patients receiving aspirin, the
College recommends continuing it around the time
of the procedure
• Most guidelines are based on adult studies. More
clinical studies with children are necessary in this area
Self‐Study Questions
Answers are located at the end of the case
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CHAPTER 8
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Self‐Study Answers
portive medications, previous surgical corrections,
future surgical corrections, current cardiac function,
physical activity limitations, risk of IE
usually with a sucrose or sorbitol base
to early childhood caries; high‐caloric diet; use of
sucrose‐rich medications; medications may induce
xerostomia; parental indulgence with sweets, juices,
sodas, etc.
especially those with pulpal involvement, to reduce
the risk of infection and IE
Bibliography andAdditional Reading
American Academy of Pediatric Dentistry. 2018–2019a. Caries‐
risk assessment and management for infants, children, and
adolescents. In: Clinical Practice Guidelines and Best Practices
(Reference Manual). Pediatr Dent 40:205–12. https://www.
aapd.org/research/oral‐health‐policies‐‐recommendations/
caries‐risk‐assessment‐and‐management‐for‐infants‐children‐
and‐adolescents
American Academy of Pediatric Dentistry. 2018–2019b. Antibiotic
prophylaxis for dental patients at risk for infection. In: Clinical
Practice Guidelines and Best Practices (Reference Manual).
Pediatr Dent 40:386–91. https://www.aapd.org/research/oral‐
health‐policies‐‐recommendations/antibiotic‐prophylaxis‐for‐
dental‐patients‐at‐risk‐for‐infection
Brennan MT, Wynn RL, Miller CS. 2007. Aspirin and bleeding in
dentistry: an update and recommendations. Oral Surg Oral
Med Oral Pathol Oral Radiol Endod 104:316–23.
Douketis JD, Berger PB, Dunn AS etal. 2008. The perioperative
management of antithrombotic therapy. American College
of Chest Physicians Evidence‐Based Clinical Practice
Guidelines (8th Edition). Chest 133:299–339S.
Dunn AS, Turpie AGG. 2003. Perioperative management of
patients receiving oral anticoagulants–a systematic review.
Arch Intern Med 163:901–8.
Grines CL, Bonow RO, Casey DE Jr etal. 2007. Prevention of
premature discontinuation of dual antiplatelet therapy in
patients with coronary artery stents. JADA 138(5):652–5.
Hallett KB et al. 2013. Medically compromised children. In:
Handbook of Pediatric Dentistry, 4th Edition. AC Cameron,
RP Widmer (eds). London: Mosby. pp. 329–85.
Jeske AH, Suchko GD. 2003. Lack of a scientific basis for rou-
tine discontinuation of oral anticoagulation therapy before
dental treatment. JADA 134:1492–7.
Lockhart PB, Loven B, Brennan MT, Fox PC. 2007. The evidence
base for the efficacy of antibiotic prophylaxis in dental practice. JADA 138:458–74.
Moursi AM, Truesdale AL, Phoon CK. 2018. Cardiovascular dis-
eases. In: The Handbook of Pediatric Dentistry, 5th Edition.
Nowak AJ, Casamassimo PS (eds). Chicago: American
Academy of Pediatric Dentistry. pp. 371–81.
Napenas JJ, Hong CHL, Brennan MT etal. 2009. The frequency
of bleeding complications after invasive dental treatment in
patients receiving single and dual antiplatelet therapy. JADA
140:690–5.
Perry DJ, Noakes TJC, Helliwell PS. 2007. Guidelines for the
management of patients on oral anticoagulants requiring
dental surgery. Br Dent J 203:389–93.
Thornhill MH, Dayer MJ, Forde JM et al. 2011. Impact of the
NICE guideline recommending cessation of antibiotic prophylaxis for prevention of infective endocarditis: before and
after study. BMJ 342:d2392.
Wahl MJ. 2018. The mythology of anticoagulation therapy inter-
ruption for dental surgery. JADA 149: (1):e1–e10.
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