Briefs: Odontogenic Infections

If you work long enough in the Pediatric Emergency Department – like half a shift – you will see a child with complaints of dental pain. This edition of Briefs focuses on odontogenic infections, including management and complications.

What are some of the odontogenic infections and problems seen in the Pediatric Emergency Department?

Dental caries

Caries are seen at the crown or root of the tooth and develop slowly, not becoming painful until involvement of the pulp. Pain should be managed with Ibuprofen or acetaminophen, oral hygiene and follow up with a dentist. Antibiotics are not needed.


This includes gingivitis. The gums can be swollen, red to purplish. The gums bleed easily after eating and brushing. Patients may also have halitosis. Treatment centers around improved oral hygienic, chlorhexidine mouth rinse and follow up with a dentist.

Pulpitis and periapical abscesses

Early pulpits manifests in toothache exacerbated by temperature changes – like cold drinks. Once the pulp is infected pus can drain through the crown or through the adjacent periodontal tissue (the gums etc,.). Draining pus comes from abscesses. Typically they appear as a pus bubble along the gum line.

From wikimedia commons

Treatment depends on whether or not the abscess is draining. If it is antibiotics are not necessarily warranted. A non-draining abscess should be treated with oral antibiotics and follow up in 1-2 weeks with a dentist. See below for antibiotic recommendations. Resist the temptation to drain the abscess – you can actually do more harm than good. Premature I&D through an area of cellulitis can actually compromise intact barriers to the spread of infection. If you want to drain an abscess through needle aspiration discuss with a pediatric dentist first if possible. They may ask you to wait.


Complications and spread of infection

Abscesses and periodontal disease can extend and cause local and systemic complications. For infections with diffuse spread CT is the imaging test of choice. See the below images for examples;

Patients present with facial swelling pain and redness. Fever is often seen as well. Diagnosis is clinical. Oral antibiotics are appropriate for most patients – see later in this post for admission criteria recommendations. Follow up should be within 72 hours. From

Maxillary sinusitis occurs when the tooth erodes superiorly. These are often associated with significant cellulitis as well.  From wikimedia commons

Ludwig’s Angina – bilateral submandibular cellulitis/abscess that can occlude the airway. it is potentially life threatening and requires a trip to the OR. from Brotherton et al.

Infections can also spread to the brain, the deep spaces of the neck, cause osteomyelitis of the jaw or spread hematogenously. These patients are obviously more ill appearing.

What are the antibiotic recommendations?

  • Amoxicillin is the best first choice – 20-40 mg/kg/day tid
  • Amoxicillin/clavulanate 20 mg/kg bid
  • Clindamycin is preferred in penicillin allergy or infection worsening after 72 hours on amox – 8-20 mg/kg/day tid
  • Azithromycin is an alternative to Clindamycin – 5-12 mg/kg once daily – check local resistance patterns and recommendations as Azithromycin may not adequately cover flora
  • Metronidazole may be used in addition to amoxicillin in a resistant infection – 30 mg/kg/day qid

For admitted patients who need IV antibiotics discuss with the Dentist on call. Common ones used frequently include Ampicillin/Sulbactam and Clindamycin.

Who should be admitted?

Patients with any of the following should be admitted;

  • Toxic appearance
  • Rapid progression
  • Immunocompromised or comorbidities (like diabetes)
  • Difficulty breathing
  • Difficulty swallowing
  • Dehydration
  • Trismus
  • Signs of Ludwig’s Angina or Cavernous Sinus Thrombosis
  • Failed outpatient treatment
  • Cellulitis encroaches upon the orbit, spreads inferior to the body of the mandible, or posterior to the mandibular ramus

Briefs: Serum sickness like reaction (Re-post)

You are seeing a child who is well appearing but has a dramatic rash. The rash appeared this morning and seemed to begin on her torso, later spreading to her limbs. The daycare thought that it was an allergy and was going to give her another child’s EpiPen, despite no respiratory symptoms and no history of previous allergy in the patient. Discretion won out, and the EpiPen was not given and the child was referred to the ED. You learn that she has had a fever to 38.9 C for 2 days, and her feet appear to be slightly swollen. This hasn’t limited her ability to walk, run or jump. Mom denies history of vomiting or diarrhea. there are no respiratory symptoms. She has no involvement of her eyes or mouth. Eight days ago she completed a course of cefdinir for otitis media.Let’s say that the rash in question looks like this:

The rash as it appears on the patient's back. 2014, Brad Sobolewski, MD, MEd

The rash as it appears on the patient’s back. 2014, Brad Sobolewski, MD, MEd

The rash as it appears on the patient's leg. 2014, Brad Sobolewski, MD, MEd

The rash as it appears on the patient’s leg. 2014, Brad Sobolewski, MD, MEd

This rash is characteristic of erythema multiforme in the setting of a serum sickness like reaction. Serum sickness is a heterogeneous clinical entity where you will see variable rash, fever  and polyarthlralgias. It begins 1 to 2 weeks following exposure to an offending agent. The offending agent varies, but the most common identifiable agents are antibiotics, including:

  • Penicillins
  • Trimethoprim-sulfamethoxazole
  • Cephalosporins

Resolution generally occurs within 1-2 weeks after stopping the drug. In other cases it may be viral induced, but good luck discontinuing it. This process is immune complex mediated and results in the development a polymorphous, sometimes pruritic rash that starts in the trunk and spreads peripherally. They appear to be urticarial in some patients and like palpable purpura, maculopapular lesions or erythema multiforme-type exanthema in others. There is no involvement of the mucous membranes or eyes. Most patients develop remittent fever without temporal spikes. Two out of three have arthralgias, most commonly seen in the hands, wrists, feet, ankles and shoulders. The differential diagnosis includes:

  • Viral exanthems (roseola)
  • Hypersensitivity vasculitis
  • Scarlet fever
  • Acute rheumatic fever
  • Meningococcemia
  • Disseminated gonococcemia
  • Reactive arthritis
  • Lyme disease
  • Still’s disease
  • Kawasaki syndrome
  • Stevens-Johnson syndrome

You can generally make the diagnosis clinically in most cases. Treatment consists of stopping the offending agent, NSAIDs for pain, and antihistamines for itching. Glucocorticoids may be useful in patients with severe arthritis/arthralgias or extensive rashes but in general do not have an evidence supported role. If you encounter an ill appearing patient, one with eye/mucous membrane involvement, or those in whom you are not certain about the diagnosis you might want to consider a complete blood count with differential, erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), urinalysis, blood urea nitrogen, creatinine, serum electrolytes, urinalysis and blood culture obtained to exclude other inflammatory or infectious causes. Again, if you are certain about the diagnosis you don’t need to get any labs. You should list the offending agent as an allergy – and if the patient encounters an offending drug again in the future the symptoms may have a more rapid onset. And finally, mucous membrane and eye involvement does not occur in serum-sickness like reactions. These findings should prompt consideration for Stevens-Johnson syndrome, a potentially fatal hypersensitivity reaction and (in my experience) the one reason for a Dermatologist to come in at night.


Fun fact: What was described today is actually serum sickness-like reaction. Classically serum sickness was in response to administration of a non-human species (horse) protein antigen. You may still encounter this today in sheep-derived Fab snake antivenom, heterologous immunomodulators containing murine components (rituximab and infliximab), streptokinase and the human diploid cell rabies vaccine.

Oh No, CO! (Re-post)

Tis the season for flu-like symptoms. Many of you will see multiple members of the same family with the flu. But what if it isn’t the flu? When should one be worried about carbon monoxide poisoning? Let’s take a look at this colorless, odorless, potentially deadly gas.

What exactly is CO poisoning?

CO is a byproduct of the combustion of organic matter – often gasoline powered tools and machinery like older motor vehicles, heaters, generators and cooking equipment and residential fires. CO has a higher diffusion coefficient than oxygen. When it binds to hemoglobin carboxyhemoglobin is formed, thus shifting the oxygen-dissociation curve to the left. Hemoglobin’s affinity for CO is 230 times that of oxygen. The molecular end result is displaced oxygen, and hemoglobin that will not dissociate from CO under atmospheric oxygen partial pressures.

Mild acute poisoning manifests as headache, lightheadedness, confusion and general flu-like symptoms. Greater exposures lead to CNS toxicity, myocardial dysfunction and death. CO readily binds myoglobin which depresses cardiac function and therefore cardiac output. This along with the promotion of free radical formation are responsible for the deleterious CNS effects. Chronic low-level exposure may lead to subacute onset of depressed mood, memory loss and confusion.

When should I obtain co-oximetry? What levels are dangerous?

First of all, a standard pulse oximeter is not an effective diagnostic tool. Carboxyhemoglobin is similar enough to oxyhemoglobin such that a pulse ox can’t tell the difference. Measurement of carboxyhemoglobin levels therefore has utility. Traditionally this is obtained from blood samples, but finger pulse oximeters and breath monitors are available. The breath monitors are not a viable option in obtunded patients, or children, since they require cooperation and deep inhalation with breath holding in order to register. Peripheral pulse-oximeters however are becoming more widespread.

Carboxyhemoglobin levels do not correlate directly with symptoms. However, the higher the level, the worse the symptoms. Headaches can be seen at levels >10%, with 50-75% resulting in seizures, coma and death. It is important to note that some people (smokers) have higher baseline levels of carboxyhemoglobin (two pack/per/day smokers can reach almost 10%).

In the Peds ED it is more difficult to get an arterial sample – especially with the risk of hematoma and other complications increased because of the more compact anatomy. Cannon et al. in the Annals of Emergency Medicine  noted that in general the correlation between venous and arterial samples is excellent. Given that the correlation between level and symptoms is not ironclad I suggest that a venous sample is more than acceptable, especially in kids.

How do I manage patients? What if I don’t have access to hyperbaric therapy?

Start with the ABCs naturally, and consider endotracheal intubation early on. Cardiac monitoring and pulse oximetry are appropriate to start early. Try to get a co-ox as soon as possible. Try to get CO measurements from the local fire or EMS agency if applicable. In general it is a really good idea to continue 100% O2 until patients are asymptomatic. The half life of CO is 30-90 minutes at 100% O2, so one can estimate length of therapy based on initial levels. If you choose to follow serial carboxyhemoglobin levels some authorities recommend discontinuing 100% O2 if the level is <10% in the asymptomatic patient. In patients with cardiopulmonary compromise hedge your bets and treat until the level is <2%.

If you have a local hyperbaric option consider immediate transfer at levels >40%, or if you are seeing cardiac or neurologic dysfunction. Hyperbaric chambers deliver O2 at higher partial pressures than the atmosphere. This further decreases the half life of CO. Admission is warranted for patients with levels >30-40% or >25% if severely symptomatic. However, research has failed to conclusive show that hyperbaric therapy is mandatory – so don’t bend over backwards trying to transport a patient to a chamber out of your facility especially if there is inclement weather.

Even without  the option to dive, management should also include serial neuro exams and CT/MRI in comatose patients to assess for cerebral edema. Do not freak out if your patient is acidotic unless the pH is <7.15. Remember that an acidotic state shifts the oxygen dissociation curve to the right – which we want. Acidosis will get better on its own in most cases with oxygen therapy. In patients exposed to a house fire you may also want to treat with a cyanide kit – which consists of sodium thiosulfate 12.5g IV – which ameliorates a further leftward shift of the dissociation curve.

What about pregnant women? Aren’t they better off? I remember seeing that on an episode of ER.

Mom’s are protected, but at the expense of the fetus. Fetal hemoglobin has an even higher affinity (10-15% greater) for CO than grown up hemoglobin. The fetus cannot efficiently eliminate CO and even in the face of mild maternal symptoms loss of pregnancy may occur. Pregnant patients with levels in excess of 15% are also potential candidates for hyperbaric therapy.

A podcast on kidney stones

It’s an epidemic! OK, so not quite, but we are seeing a rise in the number of kidney stones recently and we’re not quite sure why. This episode of PEMCurrents will focus on diagnosis and treatment of stones and answer such questions as; Which pain medicine should I order first? and which is the better imaging test, ultrasound or CT?

AAP Top 10 2016 #10: RNA biosignatures and SBI

Association of RNA Biosignatures With Bacterial Infections in Febrile Infants Aged 60 Days or Younger

Mahajan P, Kuppermann N, Mejias A, Suarez N, Chaussabel D, Casper TC, Smith B, Alpern ER, Anders J, Atabaki SM, Bennett JE, Blumberg S, Bonsu B, Borgialli D, Brayer A, Browne L, Cohen DM, Crain EF, Cruz AT, Dayan PS, Gattu R, Greenberg R, Hoyle JD Jr, Jaffe DM, Levine DA, Lillis K, Linakis JG, Muenzer J, Nigrovic LE, Powell EC, Rogers AJ, Roosevelt G, Ruddy RM, Saunders M, Tunik MG, Tzimenatos L, Vitale M, Dean JM, Ramilo O; Pediatric Emergency Care Applied Research Network (PECARN)

JAMA, 2016

Links   PubMed   JAMA   pdf

The Bottom Line

RNA biosignatures have the potential to help us distinguish which febrile infants under 60 days have serious bacterial infection

What They Did

  • The authors collected RNA biosignatures from 279 randomly selected infants out of a pool of 1883 total patients
  • They identified 66 genes that helped distinguish SBI vs not – with a sensitivity of 87% (95% CI, 73%-95%) and a specificity of 89% (95% CI, 81%-93%)
  • Ten “classifier” genes distinguished infants with bacteremia from those without bacterial infections 94% (95% CI, 70%-100%) sensitivity and 95% (95% CI, 88%-98%) specificity

What You Can Do

  • Know that this is an emerging area of research – Obviously these arrays are technically complex and not widely available… yet.
  • Cultures are still the gold standard for identifying SBI – and with blood culture false positive rates as high as 10% in some reports new methods that are easier to obtain and are more accurate hold promise