How Are Dental Abscesses Treated?

Patient Presentation
A 15-year-old male came to clinic because of right ear pain. Initially he said it was only for a couple of days but when asked again he said that he had been having oral pain that now seems to have moved to his ear. He denied fever or chills. The ear did not hurt when he pressed on the tragus and he denied discharge. He recently had moved to the area and had not established health or dental care.

The pertinent physical exam showed he had normal vital signs and his weight was at the 10%. HEENT showed potentially slight swelling near the lower jaw on the right side. He had normal tympanic membranes but he complained when the otoscope speculum was inserted. Oral examination was difficult because the patient would not open the mouth widely due to pain. It showed an extensive dental caries of the last right-sided mandibular molar with just a rim of tooth remaining that looked like a crater. No specific suppuration was seen. The adjacent gingiva looked reddened. The next to last right molar also had two separate brown lesions with one on the lingual surface and the other on the articular surface. There were several other teeth with similar small brown caries throughout the mouth. There was significant tarter and overall poor hygiene but no other area had redness or swelling. The two molars were painful with tapping of the teeth. Palpation of the jaw itself did not elicit pain. There were two submandibular and anterior cervical lymph nodes on the right side that were ~1 cm in size. Movement of the neck did not exacerbate the symptoms. The rest of his examination was normal.

The diagnosis of poor oral hygiene, significant dental caries and possible dental abscess was made. The patient’s clinical course revealed that the father stated that he had been trying to get his son dental treatment before and since moving but it had been challenging because of few providers accepting his insurance. The pediatrician consulted the on call dentist who recommended starting Augmentin® for possible abscess and he would arrange to see the patient the following day. The pediatrician also arranged to provide care to the boy and other children in the family. The sister was seen 6 weeks later for routine care and the boy had had to have the last molar extracted but the second molar was being treated.

Discussion
Dental caries are one of the most common infections. It is usually caused by Streptococcus viridans. Dental caries are also quite preventable with brushing the teeth at least twice a day with a fluoridated dentifrice, use of dental floss, and preventative dental appointments with application of fluoride varnish and sealants as appropriate. Additionally, fluoridation of the community water supply has significantly decreased dental caries and is a very effective public health measure. Fluoride binds within the dental matrix to strength it.

Dental abscesses are usually caused by poor oral hygiene but others are at risk because of malformations and deformation of the dental structure or underlying medical conditions (a review can be found here). Dental abscess often contain poly-organisms with combinations of anaerobic and fastidious organisms. Other odontogenic infections include gingivitis, periodontitis, pulpitis and various periodontal abscesses. They can also lead to regional and systemic infections such as osteomyelitis, deep fascial infections of the head and neck, and hematogeneous spread including bacteremia and sepsis.

Diagnosis is by history, clinical examination and may be aided by panoramic imaging and/or computed tomographic evaluation of osseous structures. Magnetic resonance imaging may be needed if deep tissue infections are suspected. General pain, pain with pressure, eating, temperature changes, and trismus are indications for possible dental disease. Careful inspection of the area may help in diagnosis including for foreign bodies such as popcorn or corn husks or other foreign bodies (e.g. trapped dental floss, plastic piece) Tapping of teeth to try to localize the dental disease can be helpful but isn’t always specific especially in children.

Healthcare providers should also consider if the dental disease is part of a larger health or socio-economic problem. As parents are responsible for children’s dental care for many years and also oversee it when they are older, significant dental disease could be a sign of child neglect and should be evaluated if suspected. Families with lack of resources or knowledge may need social service interventions to be able to locate and receive needed overall health and welfare services and specifically dental services.

Learning Point
Treatment for dental caries depends on the extent of the disease. Usually antibiotics are not necessary for dental caries but more extensive disease may need oral antibiotics or even intravenous antibiotics especially for suspected abscess. Initial outpatient oral antibiotics used for children is amoxicillin but if more expensive disease or abscess is suspected then amoxicillin-clavulanic acid or clindamycin are used to cover the common organisms. Mechanical debridement of the area such as scaling of the teeth, or foreign body removal, or appropriate filling of caries can fix many caries. Abscess however can need surgical debridement of the affected area, and even more extensive care (e.g. root-canal). Patient education and institution of meticulous oral care at home may save the teeth. However, periodontic abscesses are well known as “hopeless” teeth and still with extensive treatment, may need to be extracted.

Questions for Further Discussion
1. What is included in the differential diagnosis of different colored teeth? A review can be found here
2. What are indications for referral to a dentist?
3. What is the difference between a dentist, oral surgeon, and orthodontist?

Related Cases

To Learn More
To view pediatric review articles on this topic from the past year check PubMed.

Evidence-based medicine information on this topic can be found at SearchingPediatrics.com and the Cochrane Database of Systematic Reviews.

Information prescriptions for patients can be found at MedlinePlus for these topics: Tooth Decay and Child Dental Health.

To view current news articles on this topic check Google News.

To view images related to this topic check Google Images.

To view videos related to this topic check YouTube Videos.

Herrera D, Roldan S, Sanz M. The periodontal abscess: a review. J Clin Periodontol. 2000;27(6):377-386. doi:10.1034/j.1600-051x.2000.027006377.


Seow WK. Diagnosis and management of unusual dental abscesses in children. Aust Dent J. 2003;48(3):156-168. doi:10.1111/j.1834-7819.2003.tb00026.


Jenkins GW, Bresnen D, Jenkins E, Mullen N. Dental Abscess in Pediatric Patients: A Marker of Neglect. Pediatr Emerg Care. 2018;34(11):774-777. doi:10.1097/PEC.0000000000001611

Author
Donna M. D’Alessandro, MD
Professor of Pediatrics, University of Iowa

What Are the Main Acyanotic Congenital Heart Diseases?

Patient Presentation
An 8-year-old male was referred to the nephrology clinic of a regional children’s hospital for hypertension. The patient had been seen at a mobile free medical clinic and was noted to have an elevated blood pressure when taken several times with measurements in the 140s-150s systolic and 100-110s diastolic. The past medical history showed he had little medical care previously because he was relatively well per his parents, and he was partially vaccinated. The family history was negative for cardiac or renal disease. There was diabetes and possibly a stroke in two paternal family members. The social history revealed a pleasant immigrant family with limited educational and economic resources. The review of systems found no frequent infections, dyspnea, fatigue, lethargy, facial or extremity swelling, cyanosis, or failure to thrive (although the physicians suspected food insecurity). The patient did complain of intermittent headache but the family could not provide additional details.

The pertinent physical exam showed a thin male with height and weight in the 10%. Parents were also small individuals. Blood pressure was 158/112 in right upper extremity, 134/98 in left upper extremity, 138/104 in right lower extremity, and 128/96 in left lower extremity. HEENT was normal but it was difficult to see the optic discs. His cardiac examination had no murmurs, bruits or jugulovenous distension. His abdominal examination had no masses or hepatosplenomegaly. There was no peripheral edema.

The diagnosis of hypertension with abnormal four-point blood pressures made the diagnosis of coarctation of the aorta a strong possibility. The laboratory evaluation with normal urinalysis, electrolytes and full chemistry panel and thyroid studies was eventually normal. The nephrologist consulted the cardiologists who saw him that afternoon. Echocardiogram confirmed coarctation of the aorta. The patient was started on antihypertensive medication and was taken to the interventional cardiology suite 3 days later for angiography and balloon dilatation. He was followed for the next three months and was weaning down on the hypertensive medication. He missed his next appointment and the clinic social worker was told by his school that the family had moved out of the area.

Discussion
Congenital heart diseases (CHD) are malformations of the heart and great vessels. It occurs in about 5-8/1000 live births. Cyanotic congenital heart disease is often noted perinatally because of cyanosis, respiratory distress and/or poor feeding or other distress type problems. A review can be found here.

Acyanotic congenital heart disease (ACHD) can present at birth but often is seen in older children or adults unless the lesions are severe, especially obstructive lesions. Severe lesions may also cause cyanosis and distress type problems in patients also.

  • Shunting lesions cause problems by diverting blood flow into an abnormal location with frequent overflow of blood in that area.
    • Atrial septal defects (ASD)
      • Defect in the atrial septum. Occurs in 8-12% of CHD.
      • There are 4 types: ostium primum, ostium secundum, sinus venosus and coronary sinus.
      • Blood is shunted from left to right with right sided volume overload which causes dilatation of right sided structures.
      • Clinical
        • Patients are often asymptomatic with incidental murmur.
        • Murmur – Normal S1, fixed split S2, systolic ejection murmur in pulmonic area.
      • Evaluation
        • Electrocardiogram can show right bundle branch block with right atrial enlargement.
        • Chest radiograph shows cardiomegaly with pulmonary artery dilatation and increased pulmonary vascular markings.
      • Treatment – They can spontaneous close but this is not common after age 2 or if defect is > 8 mm. Small ones can be closed with devices. Larger ones may need percutaneous or cardiac surgery.
    • Ventricular septal defects (VSD)
      • Defect in the ventricular septum. Occurs in 8-12% of CHD.
      • Types are perimembraneous, muscular, inlet or outlet. Perimembraneous and muscular may spontaneous close.
      • Blood is shunted from left to right with right sided volume overload which causes dilatation of right sided structures.
      • Clinical
        • Patients are often asymptomatic with incidental murmur, but can have failure to thrive, congestive heart failure, recurrent pulmonary infections, or Eisenmenger syndrome.
        • Murmur – Normal S1, normal S2, harsh pansystolic murmur at lower left sternal border. Mid-diastolic murmur may also be heard.
        • Evaluation
          • Electrocardiogram can be normal or show left ventricular hypertrophy.
          • Chest radiograph shows cardiomegaly with pulmonary artery dilatation and increased pulmonary vascular markings.
        • Treatment – Perimembraneous and muscular may spontaneous close. Small ones can be closed with devices. Larger ones may need percutaneous or cardiac surgery.
    • Patent ductus arteriosis (PDA)
      • The ductus arteriosus (DA) connects the aorta to pulmonary artery during fetal life effectively shunt fetal circulation away from the lungs. It usually closes after birth by 24 hours of life and becomes a fibrous remnant.
      • If closure fails then a PDA is the result. The DA is purposely kept open in some cases of CHD to maintain circulation. Examples would be pulmonary stenosis, tetrology of fallot, tricuspid atresia or transposition of the great veins.
      • It is a left to right sided shunt
      • Clinical
        • Patients may be asymptomatic or have recurrent respiratory infections, congestive heart failure or failure to thrive.
        • Murmur – Normal S1, normal S2, with a continuous murmur in left upper sternal border. A loud P2 may be also heard.
        • Evaluation
          • Electrocardiogram is normal or has left ventricular hypertrophy.
          • Chest radiograph shows cardiomegaly with pulmonary artery dilatation, aorta that is prominent and increased pulmonary vascularity.
        • Treatment – device closure or surgical treatment.
  • Obstructive lesions impair the blood flow through the heart and great vessels. Hypertrophy is seen proximal to the lesion and dilatation is seen distal to it.
    • Right ventricular outflow tract obstruction (RVOT)
      • Occurs in pulmonary arteries and its branches. Occurs at the valvular, or sub- or supra-valvular areas.
      • Valvular pulmonic stenosis is the most common type of RVOT (7-9% of all CHD).
      • Clinical
        • Mild to moderate obstruction often is asymptomatic with an incidentally noted murmur. Severe probably will be cyanotic.
        • Right heart failure may be seen such as hepatomegaly or pedal edema.
        • Murmur – Normal S1, S2 may be wide split with decreased P2 intensity. Systolic ejection murmur present at left upper sternal border with radiation to the back.
        • Longer duration or increased intensity murmurs may indicate more severe stenosis.
        • Evaluation
          • Electrocardiogram shows right ventricular hypertrophy with monophasic R waves in precordial leads.
          • Chest radiograph shows normal cardiac silhouette but with dilated pulmonic artery.
        • Treatment – balloon dilatation with surgery.
    • Left ventricular outflow tract obstruction (LVOT)
      • Occurs in aorta and its branches. Occurs at the valvular, or sub- or supra-valvular areas. Ventricular septal defect is a common accompanying lesion.
      • Valvular aortic stenosis is the most common type of LVOT (5-6% of all CHD). Valvular aortic stenosis most commonly occurs in bicuspid aortic stenosis.
      • Clinical
        • Mild to moderate obstruction often is asymptomatic. Severe stenosis may have cyanosis and/or heart failure in neonates. Older children and adults may have dyspnea, chest pain and/or presyncope or syncope.
        • Murmur – Normal S1, Normal S2 may have paradoxically split S2 when severe. Systolic ejection murmur and click present at the right upper sternal border with radiation to the back.
        • Longer duration or increased intensity murmurs may indicate more severe stenosis.
        • Evaluation
          • Electrocardiogram shows left ventricular hypertrophy with T wave inversion in lateral leads.
        • Treatment – percutaneous valvuloplasty or surgical valvuloplasty.

    Learning Point
    Coarctation of the aorta(CoA) is a congenital (present at birth) condition where there is narrowing of the aorta (the main blood vessel that carries oxygen-rich blood from the heart to the body). The narrowed segment (coarctation) is typically short, with the aorta opening up to normal size past the coarctation. However, the coarctation can cause problems with increased work of the heart and high blood pressure.

    • Coarctation of the aorta
      • Narrowing of the descending thoracic aorta distal to the left subclavian origin near the ductus arteriosus.
      • Occurs in 5-8% of all CHD but is likely underdiagnosed.
      • Clinical
        • Patient’s are often asymptomatic. Palpitation of the femoral artery and right upper brachial artery may show differences in delay of the beat and pressure indicating potential CoA. Hypertension on routine blood pressure check or for headache evaluation may indicate presence.
        • Neonates may have congestive heart failure and/or shock when the ductus arteriosus closes.
        • Murmur – May be normal or have continuous murmur in interscapular area which reveals significant collateral blood flow.
        • Evaluation
          • Electrocardiogram may be normal or have left ventricular hypertrophy.
          • Chest radiograph may show rib notching in older children and adults.
        • Treatment – balloon angioplasty, stenting in older children and adults, potentially surgery. The earlier patients receive treatment the more likely that patients become normotensive.

    CoA is not the same as an interrupted aortic arch (IAA) which is caused by a discontinuous aorta obstructing blood flow to the descending aorta. Blood flow is dependent on a PDA. There are 3 different types of IAA and it is commonly associated with LVOT and VSDs. Because of the severe obstruction and other accompanying CHD, patients usually present early and with more severe problems.

    Questions for Further Discussion
    1. What are indications for interventional versus open-heart cardiac procedures for CHD?
    2. What are the causes of hypertension? A review can be found here
    3. What are complications of hypertension?

    Related Cases

    To Learn More
    To view pediatric review articles on this topic from the past year check PubMed.

    Evidence-based medicine information on this topic can be found at SearchingPediatrics.com and the Cochrane Database of Systematic Reviews.

    To view current news articles on this topic check Google News.

    To view images related to this topic check Google Images.

    To view videos related to this topic check YouTube Videos.

    Sarrechia I, Miatton M, Francois K, et al. Neurodevelopmental outcome after surgery for acyanotic congenital heart disease. Res Dev Disabil. 2015;45-46:58-68. doi:10.1016/j.ridd.2015.07.004

    Rohit M, Shrivastava S. Acyanotic and Cyanotic Congenital Heart Diseases. Indian J Pediatr. 2018;85(6):454-460. doi:10.1007/s12098-017-2454-6

    Riggs KW, Tweddell JS. How Small Is Too Small? Decision-Making and Management of the Small Aortic Root in the Setting of Interrupted Aortic Arch. Semin Thorac Cardiovasc Surg Pediatr Card Surg Annu. 2019;22:21-26. doi:10.1053/j.pcsu.2019.02.004

    Author
    Donna M. D’Alessandro, MD
    Professor of Pediatrics, University of Iowa

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    What Are Common Fatty Acid Oxidation Metabolic Disorders?

    Patient Presentation
    A 4-week-old male came to clinic for his well child visit. He had been a full-term infant with no known problems, but his parents had been called on day 3 of life for a possible fatty acid oxidation defect on his neonatal screening test. The genetic team evaluated him and additional testing had been sent and eventually was negative. He had always been a vigorous feeder and occasionally would have an effortless emesis after feeding. He did have mild jaundice in the first few days of life that resolved. The family history was negative for any neonatal or infant deaths. There was a paternal second cousin who died in a car accident but no unexplained sudden deaths. The mother had 1 previous first trimester spontaneous abortion. The review of systems was negative.

    The pertinent physical exam showed a healthy appearing male with growth parameters in the 10-50%. Weight was 25-50%. He had no obvious abnormal stigmata on his face, head or extremities. Cardiac examination had normal S1, S2 without murmurs. Abdominal examination had no masses or hepatosplenomegaly. Tone and strength were normal.

    The diagnosis of a healthy male was made. The parents related their story to the pediatrician and noted there had “been a lot of crying” about the possible diagnosis. “I’m still pretty vigilant watching him. I know that he doesn’t have it, but I worry about any little spit up or funny movement. I guess most parents do, and I know I’ll probably stop doing that as he gets bigger,” the mother stated. The pediatrician offered that these reactions were totally normal for a healthy baby, but with any child who has or could have a health problem, it usually makes the parents more concerned.

    Discussion
    All cells and particularly their mitochondria need an energy source. Glucose is one of the most common ones, but also fatty acids, lactate, pyruvate, ketones, and amino acids. Fatty acids are formed with a carboxylic acid with a long aliphatic carbon chain usually with even numbers of carbon atoms (usually 4-28 most commonly). Most are unbranched and in foods are usually found in the form of esters.

    Fatty acids are important energy sources for the heart (50-70%) but also skeletal muscle where resting muscle uses both glucose and fatty acids. During fasting or increased stress fatty acids become a major source of energy in skeletal muscle. Regulation is by several factors including physiological state, organ system, substrate and co-substrate availability (such as oxygen or carnitine), blood supply, hormones, etc. Long-chain fatty acids need the carnitine transfer system to transport the substance across the outer mitochondrial membrane. Medium and short-chain fatty acids enter the mitochondria directly. Therefore carnitine availability and metabolism is vital for long-chain fatty acids metabolism but not for shorter ones.

    Health problems occur when there is insufficient energy production and also build up of precursor metabolites.

    With the increase and expansion of neonatal screening programs, especially the use of tandem mass spectrometry, in the US, most infants are screened at birth for fatty acid metabolism problems and therefore can be treated very early in life. However patients can present with arrhythmias, Reye’s syndrome like illnesses and/or even sudden death. Other people may not present until later with more exercise fatigue. Symptoms are generally worsened by stress including fasting, exercise, and illness.

    Learning Point
    Common fatty acid inborn errors of metabolism include:

    • Very-long chain acyl-CoA dehydrogenase deficiency (VLDCASD)
      • Initial step of β-oxidation of long-chain fatty acids for carbon lengths of 14-20
      • ADVL genes (autosomal recessive) with elevated metabolites with carbon chain lengths of 12, 14, and 16
      • Presents in first months of life usually if severe but can present later
        • Heart – cardiomyopathy and arrhythmias
        • Skeletal – hypotonia, later disease often with muscle fatigue and/or rhabdomyolysis
        • Liver – hypoglycemia, hepatomegaly, hyperammonemia, lactic acidosis, elevated transaminases
      • Treatment
        • Frequent feeding, glucose infusion, low fat formulas and increased medium-chain triglycerides
    • Medium-chain acyl-CoA dehydrogenase deficiency (MCAD)
      • **Most commonly diagnosed fatty acid oxidation disorder on neonatal screening
      • Initial step in dehydrogenation of fatty acids for carbon lengths of 4-12
      • ACADM with elevated metabolites with carbon chain lengths of 8 and 10
      • Presents in 3-24 months with “Reye-like” presentation
        • Liver – hypoketotic hypoglycemia, hepatomegaly, elevated transaminase
        • Neurological – lethargy, seizures
        • Sudden death
      • Treatment
          Avoid fasting, frequent feeding, glucose infusion, uncooked starch
    • Short chain acyl-CoA dehydrogenase deficiency (SCAD)
      • ACADS with elevated metabolites with carbon chain lengths of 4
    • Carnitine palmitoyltransferase I
      • CPT1A with elevated carnitine and decreased carbon chain lengths of 16 and 18
      • Presents < 24 months
        • Heart – cardiomyopathy and arrhythmias
        • Liver – hypoketotic hypoglycemia, hepatomegaly, elevated transaminase, hyperammonemia
        • Neurological – lethargy, seizures
        • Sudden death
      • Treatment
        • Carnitine supplementation, avoid fasting, frequent feeding, glucose infusion
    • Carnitine palmitoyltransferase II
      • CPT2 with decreased carnitine and decreased carbon chain lengths of 16 and 18
      • Presents neonatal to first year usually
        • Heart – cardiomyopathy and arrhythmias
        • Liver – hypoketotic hypoglycemia, hepatomegaly
        • Skeletal – hypotonia, later disease often with muscle fatigue and/or rhabdomyolysis
        • Neurological – lethargy, seizures
        • Sudden death
        • Cystic kidneys
      • Treatment
        • Avoid fasting, frequent feeding, glucose infusion, increased medium-chain triglycerides
    • Systematic primary carnitine deficiency
      • SLC22A5 with decreased total carnitine

    Questions for Further Discussion
    1. What are common presentations for inborn errors of metabolism? A review can be found here
    2. What causes hyperammonemia? A review can be found here
    3. What are emergency treatment plan elements that needed to be listed for a patient with a suspected or known inborn error of metabolism?

    Related Cases

    To Learn More
    To view pediatric review articles on this topic from the past year check PubMed.

    Evidence-based medicine information on this topic can be found at SearchingPediatrics.com and the Cochrane Database of Systematic Reviews.

    Information prescriptions for patients can be found at MedlinePlus for this topic: Lipid Metabolism Disorders

    To view current news articles on this topic check Google News.

    To view images related to this topic check Google Images.

    To view videos related to this topic check YouTube Videos.

    El-Hattab AW. Inborn errors of metabolism. Clin Perinatol. 2015;42(2):413-439, x. doi:10.1016/j.clp.2015.02.010

    Longo N, Frigeni M, Pasquali M. Carnitine Transport and Fatty Acid Oxidation. Biochim Biophys Acta. 2016;1863(10):2422-2435. doi:10.1016/j.bbamcr.2016.01.023

    El-Gharbawy A, Vockley J. Defects of Fatty Acid Oxidation and the Carnitine Shuttle System. Pediatr Clin North Am. 2018;65(2):317-335. doi:10.1016/j.pcl.2017.11.006

    Fatty acid. In: Wikipedia. ; 2020. https://en.wikipedia.org/w/index.php?title=Fatty_acid&oldid=947595395.

    Author
    Donna M. D’Alessandro, MD
    Professor of Pediatrics, University of Iowa