What are the key aspects of localized abscesses. How are abscesses diagnosed and treated. What are the indications and contraindications for abscess incision and drainage. How is the abscess incision and drainage procedure performed. What materials are needed for abscess drainage. What are the important considerations for aftercare and patient education following abscess treatment.

Understanding Localized Abscesses: Causes and Formation

A localized abscess is a collection of pus that forms beneath the skin’s surface. But how does this condition develop? Typically, an abscess begins as a localized superficial cellulitis after a breach in the skin’s protective barrier. As the infection progresses, cellular debris accumulates, leading to necrosis and liquefaction. This process results in a walled-off collection of pus beneath the epidermis.

What are the primary causes of abscesses? The most common culprit in Emergency Department (ED) cases is Staphylococcus aureus, particularly community-acquired methicillin-resistant S. aureus (MRSA). Patients often mistakenly identify these infections as “boils” or “spider bites.” Other causative organisms can include:

• Group A β-hemolytic streptococci (more commonly associated with cellulitis without abscess formation)
• Eikenella or Pasteurella (following animal bites)
• Vibrio (after saltwater exposure)
• Pseudomonas (following whirlpool exposure)
• Anaerobic bacteria (in perineal or oral regions)
• Various bacteria in IV drug users (including strep, staph, anaerobic, and gram-negative bacteria)

Diagnosis of Localized Abscesses: Clinical and Imaging Techniques

How can healthcare providers accurately diagnose a localized abscess? The diagnosis often relies on careful physical examination and, when necessary, imaging techniques. Let’s explore the key diagnostic approaches:

Physical Examination

What are the characteristic signs of an abscess on physical examination? Typically, an abscess presents as:

• A tender, erythematous (red), and warm mass
• Fluctuance: a tense area of skin with a wave-like or boggy feeling upon palpation

It’s important to note that surrounding cellulitis can sometimes mask the presence of an abscess, making diagnosis more challenging.

Bedside Ultrasound

When physical examination findings are unclear, how can bedside ultrasound assist in diagnosis? Ultrasound imaging can effectively differentiate between simple cellulitis and an abscess requiring drainage. What are the key ultrasound findings?

• Cellulitis: Hyperechoic appearance with thickened lobules of subcutaneous fat interwoven with hypoechoic strands of fluid (often described as “cobblestoning”)
• Abscess: Well-defined collection of anechoic fluid, sometimes containing loculations and whirling debris

Indications and Contraindications for Abscess Incision and Drainage

When is incision and drainage (I&D) of an abscess indicated? The primary indication for I&D is the presence of a confirmed abscess. Without adequate evacuation of the accumulated pus, the infection can continue to worsen and potentially lead to disseminated or systemic infection.

Are there any contraindications to abscess I&D? While there are few absolute contraindications, certain situations warrant careful consideration and potential consultation with surgical specialists:

• Large or complex abscesses
• Abscesses in sensitive areas (face, hand, breast, genitalia)
• Abscesses in close proximity to vital structures such as blood vessels

When should healthcare providers consider alternative approaches or specialist consultation? In cases where abscesses do not resolve despite repeated adequate drainage, providers should consider:

• Possibility of a retained foreign body
• Underlying osteomyelitis or septic arthritis
• Presence of unusual organisms (e.g., fungi or mycobacteria)
• Patient immunodeficiency (e.g., uncontrolled or undiagnosed diabetes)

Abscess Incision and Drainage Procedure: Step-by-Step Guide

How is the abscess incision and drainage procedure performed? Let’s break down the process into key steps:

Preparation

1. Gather necessary materials and equipment
2. Ensure proper personal protective equipment (PPE) is worn
3. Prepare the skin by cleaning with alcohol swabs, betadine, or chlorhexidine

Anesthesia

What are the options for anesthesia during abscess I&D? Local anesthesia is typically sufficient for most abscesses. This can be achieved using:

• Injectable anesthetic (e.g., lidocaine with or without epinephrine, bupivacaine)
• Field block or ring block technique for larger abscesses

Incision and Drainage

1. Make an incision using a #11 blade scalpel
2. Express pus using gentle pressure
3. Explore the cavity using a curved hemostat to break up loculations
4. Irrigate the cavity with sterile saline

Packing and Dressing

1. Pack the cavity loosely with thin packing gauze (e.g., iodoform)
2. Apply a sterile dressing over the wound

Essential Materials and Equipment for Abscess I&D

What materials are needed to perform an abscess incision and drainage procedure? Here’s a comprehensive list of essential items:

• Personal protective equipment (eye shield, mask, gloves)
• Injectable anesthetic (lidocaine +/- epinephrine, bupivacaine)
• 10cc syringe, 18g & 25g needles
• #11 blade scalpel
• Curved hemostat
• 4×4 gauze pads
• Saline and syringe with 18-gauge angiocatheter or splash shield
• Thin packing gauze (e.g., iodoform)
• Scissors
• Forceps
• Tape

Aftercare and Patient Education: Ensuring Proper Healing

What are the crucial aspects of aftercare following abscess I&D? Proper aftercare is essential for promoting healing and preventing complications. Key components include:

Wound Care

• Instructions for daily dressing changes
• Guidance on packing removal and replacement (if applicable)
• Signs of proper healing to monitor

Pain Management

How can patients manage pain following abscess drainage? Recommendations may include:

• Over-the-counter pain relievers (e.g., acetaminophen, ibuprofen)
• Application of warm compresses to the area
• Elevation of the affected area (if appropriate)

Follow-up Care

What follow-up care is necessary after abscess I&D? Patients should be advised to:

• Schedule a follow-up appointment for wound check and possible packing removal
• Return to the ED if signs of worsening infection or complications develop

Prevention of Recurrence

How can patients reduce the risk of future abscesses? Education should include:

• Proper hygiene practices
• Avoidance of sharing personal items
• Prompt treatment of minor skin injuries

Complications and Special Considerations in Abscess Management

What potential complications can arise from abscess I&D, and how can they be managed? While incision and drainage is generally a safe procedure, healthcare providers should be aware of possible complications:

Bleeding

How can excessive bleeding be managed during or after the procedure?

• Apply direct pressure to the site
• Consider the use of hemostatic agents or sutures if bleeding persists
• Be cautious when draining abscesses near major blood vessels

Incomplete Drainage

What steps can be taken if an abscess doesn’t fully resolve after initial I&D?

• Reassess the wound for proper packing and drainage
• Consider repeat I&D if necessary
• Evaluate for underlying causes of persistent infection

Spread of Infection

How can healthcare providers prevent and manage the spread of infection during abscess drainage?

• Use proper sterile technique during the procedure
• Consider antibiotic therapy for high-risk patients or extensive infections
• Monitor patients closely for signs of systemic infection

Special Populations

What unique considerations apply to abscess management in special populations?

Diabetic Patients

• Higher risk of complications and delayed healing
• May require more aggressive treatment and closer follow-up
• Importance of glycemic control in wound healing

Immunocompromised Patients

• Increased susceptibility to unusual pathogens
• May require broader spectrum antibiotic coverage
• Closer monitoring for systemic infection

Pediatric Patients

• Consideration of sedation for procedure
• Tailored approach to wound care and follow-up
• Age-appropriate pain management strategies

Emerging Trends and Future Directions in Abscess Management

What new developments are shaping the future of abscess treatment and management? The field of abscess care continues to evolve, with several emerging trends and areas of research:

Antibiotic Stewardship

How is the approach to antibiotic use in abscess management changing?

• Increasing focus on judicious use of antibiotics to prevent resistance
• Development of guidelines for when antibiotics are truly necessary
• Research into targeted antibiotic therapies based on local resistance patterns

Advanced Imaging Techniques

What role will advanced imaging play in future abscess management?

• Exploration of high-resolution ultrasound for more precise diagnosis
• Potential use of AI-assisted imaging interpretation
• Investigation of novel imaging modalities for deep tissue abscesses

Minimally Invasive Techniques

How might minimally invasive approaches change abscess treatment?

• Development of advanced needle aspiration techniques
• Exploration of catheter-based drainage systems for complex abscesses
• Research into novel drainage devices and materials

Wound Healing Technologies

What new technologies are being developed to promote wound healing after abscess drainage?

• Investigation of advanced wound dressings and packing materials
• Exploration of growth factors and other biological agents to enhance healing
• Research into negative pressure wound therapy for complex abscess cavities

As research in these areas continues, healthcare providers can expect to see ongoing improvements in abscess diagnosis, treatment, and management. Staying informed about these developments will be crucial for providing the most effective and up-to-date care for patients with localized abscesses.

Abscess incision and drainage

Author: Heidi Ludtke, MD, Medical College of Wisconsin

Editor: Rahul Patwari, MD, Rush University Medical Center

Objectives

1. To understand the indications and contraindications for incision and drainage (I&D) of abscesses in the ED
2. To describe the procedure of abscess I&D, including appropriate anesthesia.
3. To recognize the importance of after care and patient education about abscess I&D.

 Introduction

What may begin as a localized superficial cellulitis after a compromise of the epithelium can result in an abscess.  Necrosis and liquefaction occur as cellular debris accumulates, becomes loculated and walled off as a collection of pus beneath the epidermis. Staphylococcus aurues, especially community-acquired methicillin resistant S. aureus (MRSA), is the most common cause of abscesses in the Emergency Department (ED) population. Patients may present to the ED complaining of a “boil” or “spider bite”, but it’s frequently a MRSA abscess. Group A b-hemolytic streptococci most often cause cellulitis without abscess.  Abscesses associated with specific environmental exposures may be caused by organisms such asEikenella or Pasteurella after an animal bite, Vibrio after saltwater exposure and Pseudomonas after whirlpool exposure.  Anaerobic bacteria can contribute to abscesses in perineal or oral regions.  Abscesses in IV drug users most frequently form abscesses containing strep and staph but may also form abscess that contain anaerobic and gram negative bacteria.

Indications

Diagnosis of abscess is often made by observation of a tender, erythematous, warm, fluctuant mass on physical examination such as that noted in Figure 1.  Fluctuance can be described as a tense area of skin with a wave-like or boggy feeling upon palpation; this is the pus which has accumulated beneath the epidermis.   Without adequate evacuation of this pus, the infection will continue to to accumulate and can lead to disseminated or systemic infection.

Figure 1: Abscess in an African American patient

Because there may be surrounding cellulitis, induration can make an abscess less apparent on physical exam.  In these cases, bedside ultrasound can be helpful in differentiating a simple cellulitis from an abscess which requires drainage.  When reviewing ultrasound, areas of cellulitis are hyperechoic with thickened lobules of subcutaneous fat interwoven with hypoechoic strands of fluid; this is referred to as “cobblestoning.” (Figure 2)  In contrast, abscesses have a more well defined collection of anechoic fluid sometimes containing loculations and whirling debris. (Figure 3) There may be overlying findings of cellulitis or a hyperechoic rim.

Figure 2: Ultrasound image demonstrating cobblestoning often seen in cellulitis

Figure 3: Ultrasound image demonstrating fluid collection consistent with abscess

If there is a localized area of induration but no fluctuance on exam or fluid collection on ultrasound, home care with application of heat via warm compresses or soaks along with antibiotics may be attempted.   However, it may be the very early development of an abscess which will be ready to drain within 24-36 hours, so these patients should be well educated on the signs of abscesses and reasons to return to the ER for re-evaluation.

There are few contraindications to this procedure, however, certain situations should prompt consideration of consultation of general or specialty surgical services: large or complex abscesses, those in sensitive areas (face, hand, breast, genitalia) or in regions in close proximity to structures such as blood vessels.  Abscesses that do not resolve despite repeated adequate drainage should prompt consideration of a retained foreign body, underlying osteomyelitis or septic arthritis, unusual organisms such as fungi or mycobacteria, or immunodeficiency of the patient (i.e.: uncontrolled or undiagnosed diabetic).

Occasionally, needle aspiration may be attempted by the Emergency Physician or subspecialist with a smaller abscess in these situations.  However, the success rate of needle aspiration is lower for multiple reasons: the inability to aspirate pus does not necessarily mean there is no purulence to be drained and some will later require repeat drainage (either again by needle or later by I&D. )

Materials/supplies

• Personal protective equipment (eye shield, mask, gloves)
• Injectable anesthetic such as lidocaine +/- epi, bupivacaine
• 10cc syringe, 18g & 25g needles
• #11 blade scalpel
• Curved hemostat
• 4×4 gauze pads
• Saline and syringe with 18-gauge angiocatheter or splash shield
• Thin packing gauze such as iodoform
• Scissors
• Forceps
• Tape

Technique

Preparation

Prepare the skin by cleaning with either alcohol swabs, betadine or chloraprep.  Clean gloves and sterile equipment should be used, though this is a procedure that is impossible for sterility to be maintained (given the draining of infected contents.)

Prophylactic antibiotics are recommended in patients at high risk for infective endocarditis (prosthetic valves, previous endocarditis and certain cases of congenital heart disease or cardiac transplantation. )

Anesthesia & analgesia

Local anesthetic such as lidocaine or bupivacaine should be injected within the roof of the abscess where the incision will be made.  Care should be taken to avoid injecting anesthetic into the abscess cavity, as this will increase pressure (and thus pain for the patient) and is unlikely to successfully anesthetize.  Many emergency physicians also inject a ring of anesthetic into the subcutaneous tissue approximately 1cm around the circumference of the abscess.  However, the maximum safe dose of anesthetic should not be exceeded.

Achieving adequate anesthesia of abscesses can be challenging, as even the best technique will prevent the sensation of sharp but not the tension and pressure of breaking up adhesions.  Parenteral or oral analgesics should be given in the ED.  Depending on the abscess size and location, as well as the patient’s individual characteristics and preferences, procedural sedation may be necessary.

Incision and Drainage

Make a linear incision across the diameter of the fluctuant area, ensuring appropriate depth to have reached the cavity of purulence as in Figure 4 and 5.   It’s also important to ensure the length of the incision will allow adequate drainage and room to use hemostats; this is typically between 2/3rd to the full length of the diameter of the fluctuant area.  After initial drainage of purulence, probe the incision with hemostats, opening them up at varying angles in multiple different directions within the cavity to break up all loculations.

Figure 4 and 5: Incision, drainage and use of hemostats to break up loculations

Normal saline is often used via a syringe (which may have an attached angiocatheter or splash-shield) to irrigate the cavity, though current evidence makes this is of questionable benefit.

It is also optional to pack the wound, as this can be a source of increased discomfort for the patient and appears to be of limited utility in the current literature.  However, some emergency physicians still opt to pack larger abscess cavities with the intent of allowing adequate drainage by preventing premature closure in the days following I&D.   Thin, continuous, plain or iodoform gauze should be placed gently into the cavity with 2 cm extruding and taped to the skin.  It should not be packed tightly as this increases pain for the patient and is not necessary.  The wound can then be covered with a dressing.

Post-procedure care

For many abscesses, the initial I&D is curative.

However, antibiotics are recommended for cutaneous abscesses (in addition to I&D) by the Infectious Disease Society of America in the following instances:

• Severe or extensive disease (i.e.: abscesses in multiple sites, recurrences)
• Rapid disease progression with cellulitis
• Associated systemic illness (i.e.: fever)
• Immunosuppression or complicating co-existing conditions
• Extremes of age
• Abscess in area that is difficult to drain (i.e.: genitalia, face)
• Septic phlebitis
• Lack of response to I&D alone

In those cases in which antibiotic therapy is initiated, coverage should be directed at MRSA with antibiotics such as oral trimethroprim-sulfamethoxazole, doxycycline or clindamycin.   It’s important to be aware of local resistance patterns as community-acquired MRSA resistance to commonly used antibiotics, such as clindamycin, has increased in some regions.

At home, patients may change their dressing as needed.  They should soak the area in warm water or with warm compresses to encourage evacuation of all purulence.  Pain should be treated at home with analgesics such as acetaminophen and ibuprofen.  Patients who had packing placed may be taught how to replace the packing as indicated.  Occasionally, there may be residual purulence requiring further drainage and/or packing replacement.  For this reason, a follow-up recheck visit in 1-3 days is recommended.  The patient should be instructed to return to the ER sooner for worsening pain, swelling, erythema or for signs of systemic illness such as a fever, vomiting and myalgias.

Summary

Abscess I&D is a relatively simple procedure commonly performed in the ED.  It is often curative and antibiotics are rarely indicated.   Patients should be instructed on home care and the importance of a recheck in approximately 2 days.

References

1. Holtzman LC, Hitti E, Harrow J.  Roberts and Hedges’ Clinical Procedures in Emergency Medicine.  Chapter 37 Incision and Drainage. 719-757.  E3
2. O’Malley GF, Dominici P, Giraldo P, Aguilera E, Verma M, Lares C, Burger P, Williams E.  Routine Packing of Simple Cutaneous Abscesses is Painful and Probably Unnecessary.  Academic Emergency Medicine 2009; 16:470-473.
3. Reichman.  Emergency Medicine Procedures.  Chapter 106 Subcutaneous Abscess Incision and Drainage.
4. Singer AJ, Talan DA.  Management of Skin Abscesses in the Era of Methicillin-Resistant Staphylococcus aureus.  New England Journal of Medicine. 370;11: 1039-1047.

Abdominal Abscess – StatPearls – NCBI Bookshelf

Continuing Education Activity

Abdominal abscesses contain cellular debris, enzymes, and liquid and can be from an infectious or non-infectious source. They are a common and serious condition and can develop almost anywhere in the abdomen. However, most are confined to some part of the peritoneal cavity. To avoid the high morbidity and mortality associated with this condition, it must be promptly diagnosed and treated. This activity reviews the evaluation and treatment of abdominal abscesses and the importance of the interprofessional team in recognizing and treating this condition.

Objectives:

• Identifywhen an abdominal abscess should be suspected and what evaluation should be done.

• Review the most definitive imaging test for an abdominal abscess and describe what this imaging might show in a patient with an abdominal abscess.

• Describe the treatment strategy for an abdominal abscess.

• Explain how careful patient monitoring and strong communication amongst the interprofessional team will improve patient outcomes in those with an abdominal abscesses.

Access free multiple choice questions on this topic.

Introduction

An abdominal abscess is a collection of cellular debris, enzymes, and liquefied remains which can be from an infection or non-infectious source. An intra-abdominal abscess usually signals that something serious is happening to the patient. An abscess can develop almost anywhere in the abdomen but are usually confined to some part of the peritoneal cavity. In many cases, the omentum, viscera, or mesentery may wall off an intraabdominal abscess. An abdominal abscess is quite common and is a serious condition. To avoid the high morbidity and mortality, the condition must be promptly diagnosed and treated. In general, sepsis that occurs after perforation in the upper gastrointestinal (GI) tract or leak is often associated with less morbidity and mortality compared to leaks that result from a colonic perforation or injury.[1][2][3]

Etiology

The most common organisms involved in an abdominal abscess include a mixture of aerobic and anaerobic bacteria that originate from the gastrointestinal tract. Causes of an intraabdominal abscess include perforation of a gastric ulcer, perforated appendicitis, diverticulitis, ischemic bowel disease, pancreatic necrosis, or gangrenous cholecystitis. Other common causes include penetrating abdominal trauma, surgical trauma, anastomotic leaks, volvulus, intussusception, or a missed gallstone during a cholecystectomy. Less frequently sterile abscess can result from the injection of a drug.[4]

Organisms involved in an abdominal abscess include the following:

• Escherichia coli

• Bacteroides

• Neisseria

• Chlamydia

• Candida

Epidemiology

In most cases, intra-abdominal abscesses derive from an intra-abdominal organ and often develop after operative procedures. It is estimated that about 70% are postsurgical and that 6% of patients undergoing colorectal surgery may develop a postoperative abscess. Hepatic abscesses account for 13% of all intra-abdominal abscesses. Most hepatic abscesses involve the right lobe, probably due to the larger size and greater blood supply.

Pathophysiology

An intra-abdominal abscess may be confined or generalized within the peritoneal cavity. Localized collections of pus may have a barrier that may include adhesions, omentum or other adjacent viscera. In almost all cases, abdominal abscesses contain a polymicrobial collection of both aerobic and anaerobic organisms from the GI tract. The bacteria usually incite an inflammatory reaction that often results in a hypertonic environment that continues to expand as an abscess cavity. If left untreated, an abdominal abscess can lead to septic shock.[5][6]

History and Physical

Patients with an intra-abdominal abscess may present with abdominal pain, fever anorexia, tachycardia, or prolonged ileus. The presence of a palpable mass may or may not be present. If the presentation is delayed, some individuals may appear in septic shock.

If the abscess is retroperitoneal or located deep in the pelvis, there may be no clinical signs. In such cases, the only suspicion may be a fever, mild liver dysfunction, or prolonged ileus.

In post-surgery patients, the diagnosis of an abdominal abscess is difficult because of analgesia and antibiotics which often mask the signs of an infection.

A subphrenic abscess may present with shoulder tip pain, hiccups, or atelectasis.

Most patients with an abdominal abscess will show signs of dehydration, oliguria, tachycardia, tachypnea, and respiratory alkalosis.

Evaluation

Blood work is not specific for an intra-abdominal abscess but may reveal leukocytosis, abnormal liver function, anemia or thrombocytopenia. These are features that signal an infection. Blood cultures are often negative but when positive may reveal predominantly anaerobic organisms, the most common being Bacteroides fragilis.

Plain abdominal x-rays are not sensitive for identifying an intraabdominal abscess and hence a CT scan is required and is considered to be the most definitive test to rule out an intra-abdominal abscess. A CT scan can reveal the location, size, and presence of bowel thickening, thumbprinting, and ileus. Intra-abdominal abscess almost always requires intravenous (IV) antibiotics. If the abscess is localized, CT-guided aspiration can be performed to drain the abscess. CT scan has the advantage that it avoids general anesthesia and wound complications. It also prevents contamination of other parts of the abdominal cavity.[7][8][9]

In some patients, ultrasound may help identify abdominal abscess.

Nuclear scans are rarely used today to detect abscesses because the technique is time-consuming and has a high rate of false positives.

Treatment / Management

Broad-spectrum antibiotics and hydration are essential. Once cultures become, available one can use specific antibiotics as noted by their sensitivity. Intravenous hydration is required. A nasogastric tube may help decompress bowel and lower the emesis.[10][11][12]

Percutaneous CT guided drainage is widely used to drain abdominal abscesses. The procedure can be done under local anesthesia and decreases the duration of hospitalization. In most patients, improve occurs within 48 hours after drainage. In localized abscesses, CT-guided drainage has a success rate of over 90%.

If the patients fail to improve within 24 to 48 hours, surgical consultation is required. Both laparoscopic, interventional radiology and open procedures can be used to evacuate the abdominal abscess. However, if surgery is required, the necrotic tissue will be removed, and all adhesions can be lysed. Most of these patients require monitoring in the intensive care unit (ICU) and need aggressive resuscitation with fluids. If the abscess is localized and promptly treated, the prognosis is good.

Abscesses located in the pelvis may be drained transrectally or transvaginally, and the results are excellent.

Open surgery for an abdominal abscess is a difficult undertaking and can be difficult because of adhesions and lack of proper anatomical pathways to separate bowel.

Differential Diagnosis

• Prolonged ileus

• Fever of unknown origin

• Crohn disease

• Ulcerative colitis

Prognosis

The prognosis of patients with an abdominal abscess prior to the era of the CT scan was very high. Today, with the availability of CT scans the diagnosis is made much earlier, and in fact in many cases, CT guided drainage has helped lower the morbidity. However, if an abdominal abscess is misdiagnosed and not treated, the mortality is very high. Risk factors that increase mortality and morbidity include the following:

Complications

An abdominal abscess can lead to the following complications:

Postoperative and Rehabilitation Care

Patients with an abdominal abscess usually require a stay in the hospital. Repeat imaging is often done to ensure that there is no more residual abscess after treatment.

Depending on the complexity of the abscess, some patients may require total parenteral nutrition.

Because the patients are often frail, physical therapy is recommended to help recover muscle strength and flexibility.

Consultations

Once a diagnosis of an abdominal abscess is done, a general surgeon and a radiologist should be consulted.

Pearls and Other Issues

Those with gross contamination of the abdominal cavity can develop multiorgan failure and consequently have a high mortality rate.

Today with the availability of CT scan, both diagnosis and drainage can be accomplished with very low morbidity.

A complex abscess may require a laparoscopic or an open approach.

Enhancing Healthcare Team Outcomes

An abdominal abscess is not an uncommon presentation on the general surgery ward or to the emergency department. Because of its vague clinical presentation, the disorder is best managed by an interprofessional group of health professional that includes a surgeon, dietitian, pharmacist, radiologist, gastroenterologist, and a wound care nurse. An abdominal abscess has significant morbidity and can rapidly become fatal if left untreated. To improve outcomes, communication between the interprofessional team is highly recommended.

While initial antibiotics are broad-spectrum, the pharmacist and clinicians need to watch the blood cultures to determine the type of organisms growing and their sensitivity. In many cases, patients with an abdominal abscess may not be able to eat and may require peripheral or central parenteral nutrition and hence, a dietary consult should be involved. While there are no universal guidelines on the management of an abdominal abscess, the current consensus indicates that percutaneous drainage by a radiologist has low morbidity compared to an open procedure.

All patients with an abdominal abscess need close monitoring as they can quickly become septic. The nursing responsibility lies with measuring vital signs, urine output, pressure sore prevention, DVT prophylaxis, ambulation, and timely antibiotics. Any change in the patient’s clinical status should be immediately communicated to the clinician.

There should not be any delay in consulting with the surgeon, as delay can lead to adverse outcomes and significant healthcare costs. Many of these patients also develop wound infections that do not heal. Hence a consult with a wound care nurse for daily dressings is necessary.

The progress and monitoring of patients with an abdominal abscess are made by regular physical exams, vital signs, and imaging tests. Often these patients have drainage devices that also need to be monitored for the type and amount of fluid discharge. Only through a systematic clinical interprofessional team approach can the morbidity and mortality of an abdominal abscess be lowered. [13][14](Level III)

Outcomes

The outcomes after an abdominal abscess depend on patient morbidity, the cause, extent of contamination and age. When multiple organs are involved and the patient is septic, the outcomes are poor. However, for localized abscesses from a rupture of an appendix or sigmoid diverticulitis, the outcomes are good. Many of these patients have significant comorbidity which affects their long-term survival. The key to improving mortality is an interprofessional approach with prompt diagnosis, close monitoring, and early treatment. [Level 5}  [15][4] (Level V)

References

1.

Sarychev LP, Sarychev YV, Pustovoyt HL, Sukhomlin SA, Suprunenko SM. Management of the patients with blunt renal trauma: 20 years of clinical experience. Wiad Lek. 2018;71(3 pt 2):719-722. [PubMed: 29783255]

2.

Son DJ, Hong JY, Kim KH, Jeong YH, Myung DS, Cho SB, Lee WS, Kang YJ, Kim JW, Joo YE. Liver abscess caused by Clostridium haemolyticum infection after transarterial chemoembolization for hepatocellular carcinoma: A case report. Medicine (Baltimore). 2018 May;97(19):e0688. [PMC free article: PMC5959397] [PubMed: 29742715]

3.

Serraino C, Elia C, Bracco C, Rinaldi G, Pomero F, Silvestri A, Melchio R, Fenoglio LM. Characteristics and management of pyogenic liver abscess: A European experience. Medicine (Baltimore). 2018 May;97(19):e0628. [PMC free article: PMC5959441] [PubMed: 29742700]

4.

Cirocchi R, Afshar S, Shaban F, Nascimbeni R, Vettoretto N, Di Saverio S, Randolph J, Zago M, Chiarugi M, Binda GA. Perforated sigmoid diverticulitis: Hartmann’s procedure or resection with primary anastomosis-a systematic review and meta-analysis of randomised control trials. Tech Coloproctol. 2018 Oct;22(10):743-753. [PubMed: 29995173]

5.

Göbel T, Rauen-Vossloh J, Hotz HG, Boldt A, Erhardt A. [Conservative treatment of an aseptic abscess syndrome with splenic abscesses in Crohn’s disease]. Z Gastroenterol. 2017 Dec;55(12):1313-1317. [PubMed: 29212102]

6.

Lentz J, Tobar MA, Canders CP. Perihepatic, Pulmonary, and Renal Abscesses Due to Spilled Gallstones. J Emerg Med. 2017 May;52(5):e183-e185. [PubMed: 28174034]

7.

Li PH, Tee YS, Fu CY, Liao CH, Wang SY, Hsu YP, Yeh CN, Wu EH. The Role of Noncontrast CT in the Evaluation of Surgical Abdomen Patients. Am Surg. 2018 Jun 01;84(6):1015-1021. [PubMed: 29981641]

8.

Zens TJ, Rogers AP, Riedesel EL, Leys CM, Ostlie DJ, Woods MA, Gill KG. The cost effectiveness and utility of a “quick MRI” for the evaluation of intra-abdominal abscess after acute appendicitis in the pediatric patient population. J Pediatr Surg. 2018 Jun;53(6):1168-1174. [PubMed: 29673611]

9.

Guizzetti L, Zou G, Khanna R, Dulai PS, Sandborn WJ, Jairath V, Feagan BG. Development of Clinical Prediction Models for Surgery and Complications in Crohn’s Disease. J Crohns Colitis. 2018 Jan 24;12(2):167-177. [PMC free article: PMC5881746] [PubMed: 29028958]

10.

Chen CY, Lin MJ, Yang WC, Chang YJ, Gao FX, Wu HP. Clinical spectrum of intra-abdominal abscesses in children admitted to the pediatric emergency department. J Microbiol Immunol Infect. 2020 Apr;53(2):283-291. [PubMed: 30150137]

11.

Bakopoulos A, Tsilimigras DI, Syriga M, Koliakos N, Ntomi V, Moris D, Bistarakis D, Schizas D. Diverticulitis of the transverse colon manifesting as colocutaneous fistula. Ann R Coll Surg Engl. 2018 Aug 16;:e1-e3. [PMC free article: PMC6204519] [PubMed: 30112933]

12.

Yoshioka T, Kondo Y, Fujiwara T. Successful wound treatment using negative pressure wound therapy without primary closure in a patient undergoing highly contaminated abdominal surgery. Surg Case Rep. 2018 Aug 01;4(1):85. [PMC free article: PMC6070448] [PubMed: 30069647]

13.

Holubar SD, Hedrick T, Gupta R, Kellum J, Hamilton M, Gan TJ, Mythen MG, Shaw AD, Miller TE., Perioperative Quality Initiative (POQI) I Workgroup. American Society for Enhanced Recovery (ASER) and Perioperative Quality Initiative (POQI) joint consensus statement on prevention of postoperative infection within an enhanced recovery pathway for elective colorectal surgery. Perioper Med (Lond). 2017;6:4. [PMC free article: PMC5335800] [PubMed: 28270910]

14.

Seifarth C, Kreis ME, Gröne J. Indications and Specific Surgical Techniques in Crohn’s Disease. Viszeralmedizin. 2015 Aug;31(4):273-9. [PMC free article: PMC4608647] [PubMed: 26557836]

15.

Zani A, Hall NJ, Rahman A, Morini F, Pini Prato A, Friedmacher F, Koivusalo A, van Heurn E, Pierro A. European Paediatric Surgeons’ Association Survey on the Management of Pediatric Appendicitis. Eur J Pediatr Surg. 2019 Feb;29(1):53-61. [PubMed: 30112745]

Dental abscess: A microbiological review

Dent Res J (Isfahan). 2013 Sep-Oct; 10(5): 585–591.

Shweta

¹Department of Microbiology, Maulana Azad Medical College, New Delhi, India

S Krishna Prakash

¹Department of Microbiology, Maulana Azad Medical College, New Delhi, India

¹Department of Microbiology, Maulana Azad Medical College, New Delhi, India

Address for correspondence: Dr. Shweta, Department of Microbiology, Maulana Azad Medical College, New Delhi – 110 002, India. E-mail: moc.liamg@201atewhs

Received 2012 Jun; Accepted 2013 Mar.

This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

This article has been cited by other articles in PMC.

Abstract

Dental abscess is a frequently occurring infectious process known to the health practice. The fate of the infection depends on the virulence of the bacteria, host resistance factors, and regional anatomy. Serious consequences arising from the spread of a dental abscess lead to significant morbidity and mortality. Acute dental abscess is polymicrobial, comprising of strict anaerobes, such as anaerobic cocci, Prevotella, Fusobacterium species, and facultative anaerobes, such as viridans group streptococci and the Streptococcus anginosus group. Numerous novel, uncultivable and fastidious organisms have been identified as potential pathogens with the use of non-culture techniques. The majority of localized dental abscesses respond to surgical treatment while the use of antimicrobials is limited to severe spreading infections. There is a need for good-quality clinical trials of sufficient size to identify the ideal treatment. The microbiology of the acute dentoalveolar abscess and its treatment in the light of improved culture and diagnostic methods are reviewed.

Keywords: Antibiotic sensitivity, dental abscess, diagnosis, microbiology, therapy

INTRODUCTION

Dental abscess was a poorly discussed topic of medical science until the late 1900s. This clinical entity was frequently underestimated in terms of its morbidity and mortality. Dental or dentoalveolar abscess is a denomination used to describe localized collection of pus in the alveolar bone at the root apex of the tooth. It usually occurs secondary to dental caries, trauma, deep fillings or failed root canal treatment. Once the intact pulp chamber is breached, colonization of the root canals occurs with a diverse mix of bacteriological agents. These microorganisms are capable of forming biofilms in root canals, hence making application of the “biofilm concept” plausible in such infections.[1] After entering the periapical tissues via the apical foramen, these bacteriae are capable of inducing acute inflammation leading to pus formation. The pathogenesis of dentoalveolar abscess is polymicrobial in nature, comprising of various facultative anaerobes, such as the viridans group streptococci and the Streptococcus anginosus group, and strict anaerobes, especially anaerobic cocci, Prevotella and Fusobacterium species.[2] If not treated at an early stage it may rapidly evolve and spread to adjacent anatomic structures, leading to serious complications such as septicemia, cavernous sinus thrombosis, brain abscess, shock, and occasionally to death. Possibility of development of complications and the associated morbidity and mortality makes it an important public health problem. In this paper, current knowledge of the pathogenesis, diagnosis, and management of dental abscess is reviewed.

EPIDEMIOLOGY AND RISK FACTORS

In the early 1600s, the London Bills of Mortality began listing the causes of death with teeth being continually listed as the fifth or sixth leading cause of death.[3] By 20^th century, the potential of dental abscesses to spread and cause severe sepsis leading to death was recognized. An audit carried out at the Hull Royal Infirmary between 1999 and 2004 showed an increase in the number of patients presenting to oral and maxillofacial surgery services with dental sepsis.[4] In the United States, a large prospective study reported that 13% of adult patients sought treatment for dental pain and infection over a 24 month follow-up.[5] The incidence of dentoalveolar abscess was 6.4% among children attending an outpatient dental clinic in Nigeria.[6] In India, dental caries affect 60-65% of the general population.[7] In addition, periodontal disease is estimated to occur in 50-90% of the population in India, depending on age.[8] Improved methods of diagnosis and reporting of this common problem are required to allow exhaustive epidemiological analysis and its implications on health-care system. Nevertheless, oral diseases have been identified as one of the priority health conditions because, in late stages, they cause severe pain and are expensive to treat. This translates into a loss of man-hours, which has a significant negative impact on economic productivity.[9]

The various host factors play a significant role in pathogenesis of dental infections and their complications. It has been observed that there are specific “at-risk” population groups. In a retrospective series of 185 cases, Huang et al. found a statistically significant correlation of acute dental infections, complications and death with medically compromising diseases, such as diabetes, renal insufficiency, hepatic cirrhosis, myeloproliferative disorders, and chemotherapy.[10] Most studies report a male preponderance of the severe odontogenic infections in both adult[11] and pediatric[6] populations.

CAUSATIVE AGENTS

Bacteriological agents implicated in causation of dental abscesses comprise of the complex mix of strict anaerobes and facultative anaerobes. Datasets from culture and molecular studies show that over 460 unique bacterial taxa belonging to 100 genera and 9 phyla have been identified in different types of endodontic infections.[12] Depending upon the recovery and cultural conditions, strict anaerobes outnumber facultative by a ratio which varies between 1.5 and 3:1 in mixed infections.[13,14] The mean number of species recovered by culture from dentoalveolar aspirates is four with a range of between 1 and 7.5.[13,15,16] Dental abscesses caused solely by strict anaerobes occur in approximately 20% of cases. Although there is a wide range depending upon recovery conditions (6-63%) it has been observed that pure cultures from an acute dental abscess are unusual[15,16,17,18,19] and mixed aerobic infections are also uncommon, accounting for 6% of abscesses.[19] Polymicrobial nature of such infections and presence of cultivable and uncultivable microbes may pose a challenge toward diagnostic analysis in routine microbiological laboratories.

STRICT ANAEROBES

The most commonly isolated genera include anaerobic streptococci, Fusobacterium species and the black-pigmented anaerobes such as Prevotella and Porphyromonas species.[20]Prevotella species have been reported as the most frequent isolates in numerous studies, found in 10-87% of dentoalveolar abscesses.[12,14,15,21]Prevotella intermedia, Prevotella nigrescens and Prevotella pallens, Porphyromonas endodontalis, and Porphyromonas gingivalis are the commonly detected pathogens.[22]

Bacteroides fragilis, a more common isolate from intra-abdominal infections, has only infrequently been reported from acute dentoalveolar infections and is not regarded as an oral commensal. The member of the Bacteroides genus most likely to be recovered from an acute dental abscess is Bacteroides forsythus (now transferred to a new genus as Tannerella forsythia). [23]

Fusobacterium periodonticum and Fusobacterium nucleatum (which includes subsp. nucleatum, subsp. polymorphum, subsp. animalis, subsp. vincentii, and subsp. fusiforme) are frequently detected with F. nucleatum recovered most frequently from the acute dental abscess.[24,25] Baumgartner et al. performed polymerase chain reaction for F. nucleatum on samples from endodontic origin and found prevalence of 73%.[26]

Studies have shown the presence of Clostridium species causing dentoalveolar abscess in a range varying from 2% to 20%. Important species isolated include Clostridium hastiforme, Clostridium histolyticum, Clostridium perfringens, Clostridium subterminale, and Clostridium clostridioforme.[13,27] Some infrequent pathogens in the oral cavity belonging to Clostridium genus are Clostridium sporogenes, Clostridium bifermentans, Clostridium botulinum, “Clostridium oedematiens,” and “Clostridium welchii. ”[28]

With the help of Polymerase Chain Reaction, high prevalence of Treponema species has been reported within the acute dental abscess. It was found that Treponema denticola was present in up to 79% of dental abscesses.[29] Other Treponema species were found in lower numbers, including Treponema socranskii, Treponema pectinovorum, Treponema amylovorum, and Treponema medium.

Certain unusual or new bacteria isolated from cases of dental abscess include members of the genus Atopobium (Gram-positive strictly anaerobic coccobacilli), for example, Atopobium parvulum and Atopobium rimae. Other anaerobic Gram-positive rods include Bulleidia extructa, Cryptobacterium curtum, Eubacterium sulci, Mogibacterium timidum and Mogibacterium vescum,[30] Pseudoramibacter alactolyticus, and Slakia exigua.[31] While unfamiliar anaerobic Gram-negative rods include Filifactor alocis, Dialister pneumosintes,[23,32,33] Centipeda periodontii and Selenomonas sputigena. [34] Catonella morbi, a Gram-negative anaerobe formerly known as Bacteroides D42, was found in 16% of 19 aspirates, and Granulicatella adiacens, a facultative anaerobic Gram-positive coccus formerly known as nutritionally variant streptococci, was present in 11% of 19 aspirates.[35,36] The detection of these unfamiliar species has expanded our insight into the potential of virulence and pathogenicity of these organisms in acute dental abscess and interactions with more commonly isolated and better understood pathogens.

FACULTATIVE ANAEROBES

Facultative anaerobes belong to the viridans group streptococci and the anginosus group streptococci are commonly implicated in dental abscess. The viridans group streptococci includes mitis group, oralis group, salivarius group, sanguinis group, and the mutans group.[37] The anginosus group (formerly referred to as “Streptococcus milleri” or S. anginosus) has also been reported with varying degrees of accuracy.

Staphylococcus aureus has been frequently reported from acute dental abscess, ranging from 0.7% to 15%.[17,19,27,38] Recovery rates of coagulase-negative strains of staphylococci (usually reported as Staphylococcus epidermidis) are generally higher with figures ranging from 4% to 65%.[14,17,19,30,38,39]

CLINICAL FEATURES

The signs and symptoms of the acute dental abscess are pain, swelling, and erythema usually localized to the affected tooth, although the suppuration can frequently spread to the nearby tissues causing fatal complications. Fever, extraoral and intraoral swelling, erythema, tenderness to palpation are notable. Trismus in addition to any changes in the voice such as hoarseness and drooling should prompt the dentist to an emergency situation. The clinical examination should focus on the general status of the patient such as lethargy or extreme sickness. Deep neck and descending necrotizing mediastinal abscesses are a rare complication of the dental abscess and spread of odontogenic infections accounts for a large number of deep neck abscesses. [40] Delay of diagnosis owing to vagueness of early symptoms is one of the primary reasons for the high mortality. The literature describes mortality rate of mediastinitis up to 40% despite aggressive use of antibiotics and advances in intensive care facilities.[41] Death usually occurs due to sepsis and multiorgan failure although airway occlusion is also a significant complication and requires early management by tracheostomy.

MICROBIOLOGICAL ANALYSIS

Sample collection

In the past, inappropriate methods of sampling hampered correct identification of the causative pathogens involved in the development of the dental abscess. The studies using swabs of purulent material have demonstrated poor recovery of strict anaerobes and low mean numbers of isolates per sample (range 1.0-1.6)[42] choice of sample type and method of sampling are crucial to optimal diagnostic efficacy. Ideally, an aspirate through intact mucosa after disinfection by an appropriate antiseptic mouthwash, e. g., chlorhexidine should be collected. This will reduce contamination from the normal oral flora. Some researchers have also sampled purulent exudates from within infected canals.[24,42]

Cultural and non-cultural techniques

Significant improvement in the routine diagnostic yield from acute dental abscesses has occurred with employment of meticulous specimen collection and processing on selective and nonselective agars under appropriate atmospheric conditions. However, despite the close attention to detail, it is apparent that many genera of bacteria have yet to be cultured. A major limitation of past cultural studies is that a large percentage of the oral microflora does not grow on conventional artificial culture media in the laboratory.[43]

Introduction of molecular techniques has helped us to understand the microbial bionomics of dental abscesses. Use of PCR or deoxyribonucleic acid (DNA) – DNA hybridization chequerboard techniques and more recently 16S rRNA gene sequencing and species-specific primers have helped in searching for the presence of specific microbes. [30,32,35,44,45] The use of 16S rRNA gene sequence analysis for the identification of isolates and clones has greater precision to discriminate between taxa and recognize novel taxa than conventional identification methods.[30] Genetic methods of identification have also helped in detection and speciation of fastidious organisms like Treponemes in samples from dental abscesses.[29] Culture-independent, molecular analysis has revealed a more diverse microflora associated with endodontic infections than that revealed by cultural methods alone.

ANTIBIOTIC RESISTANCE

Antimicrobials must never be used as a replacement for appropriate surgical drainage and/or debridement. The maintenance of an airway and abscess drainage is a condition sine qua non. However, antimicrobial therapy initiated soon after diagnosis and before surgery can shorten the period of infection and minimize associated risks like bacteremia.

Penicillins and cephalosporins

Historically, the penicillins have been used as first-line agents in the treatment of odontogenic infections. Increasing rates of penicillin resistance and treatment failures have been reported. The highest rates of penicillin resistance have been observed with the members of the genus Bacteroides and Prevotella.[46,47,48]

Penicillin resistance in these pathogens has been correlated with β-lactamase production. Heimdahl et al. reported on a series of patients with orofacial infections who failed to respond to penicillin therapy due to β-lactamase producing Bacteroides.[49] Using an animal model, β-lactamase production by strains of Prevotella. melaninogenicus in a mixed infection has been shown to protect both Prevotella. melaninogenicus and other bacteria from penicillin.[50]

Reduced susceptibility to penicillin is more prevalent in the mitis group streptococci than in the anginosus group. In susceptibility test to antibiotics, imipenem was the most active molecule tested, confirming its general good activity against oral streptococci. Also, third generation cephalosporins such as ceftriaxone and fourth generation cephalosporins like cefepime, showed good activity. Chinolones, glycopeptides, and rifampicin confirmed a good activity against oral streptococci.[51]

Macrolides

Macrolide resistance is most commonly due to acquisition of one of a number of erm genes (erythromycin methylases resulting in reduced binding of macrolides to the 50S ribosomal subunit). Resistance to macrolides appears to have a higher prevalence in the “viridans group streptococci,” anaerobic streptococci, and Prevotella species. The newer macrolides, clarithromycin and azithromycin, offer improved pharmacokinetics compared to erythromycin.[38,52,53] Erythromycin has adequate activity against the majority of odontogenic pathogens, but up to 50% of Fusobacterium are resistant to erythromycin.[54,55] The macrolides should not be considered as first-line therapy in treating odontogenic infections and should be reserved for patients with penicillin allergy.

Metronidazole

Metronidazole is a bactericidal agent that is highly active against most anaerobes, but it lacks activity against aerobic bacteria. Similarly, although it retains activity against penicillin-resistant anaerobic Gram-negative bacilli, it only has moderate activity against microaerophilic Gram-positive cocci. In serious infections, metronidazole is best used in conjunction with penicillin to ensure coverage against aerobic Gram-positive bacteria. However, a combination of two drugs with different dosing schedules may lower patient compliance. The development of resistance to this agent by common odontogenic pathogens is rare.

Clindamycin

Clindamycin has excellent activity against Gram-positive organisms, including anaerobes and β-lactamase producing strains. Low concentrations of the drug are bacteriostatic, but bactericidal activity is achieved clinically with the usual recommended doses. A number of clinical trials have demonstrated clindamycin’s efficacy in treating odontogenic infections. Gilmore et al. demonstrated comparable activity between clindamycin and penicillin V in the treatment of moderate to severe odontogenic infections.[56] von Konow et al. reported similar findings, but the clindamycin group had a shorter duration of fever, pain, and swelling.[57] In one study, moxifloxacin was significantly more effective in reducing pain at days 2-3 of therapy than clindamycin.[58] Clindamycin has recently been considered for the management of odontogenic infections because of the bacterial susceptibility to this drug, great oral absorption, low emergence of bacterial resistance and good antibiotic levels in bone.

NEED OF GOOD QUALITY CLINICAL TRIALS

There is a lack of sufficient evidence to support the use of one antibiotic regimen over another or to indicate one treatment modality over another. Clinical trials in the treatment of the dental abscess are often flawed in design, limiting validity and applicability of results. Many studies are inadequately blinded and do not have appropriate inclusion criteria. Measurement of the primary outcome is also faulty due to lack of standardization. Some studies rely on clinical assessment of relatively crude parameters that is failure, slight improvement, cure[56,59,60] while others a combination of both patient responses and clinical examination with well-defined but subjective criteria.[15,57,61,62] This has resulted in patients receiving multiple surgical and medical interventions making it impossible to analyze the relative contributions of each intervention to the success of treatment.

Nonetheless, there are a number of recommendations which can be suggested based on the current evidence. If empirical antibiotics are required, the following may be considered. Amoxicillin remains the antimicrobial of first choice. If local patterns of antimicrobial resistance indicate a high prevalence of resistance to amoxicillin then the use of either metronidazole[27] or amoxicillin in combination with clavulanic acid[63] should be considered as alternatives. Clindamycin remains an alternative in individuals who are allergic to the penicillin group of antibiotics.[56,64]

CONCLUSION

Dental abscess and its complications position a substantial burden on individuals, communities, and the health-care system; hence, early diagnosis and appropriate intervention are extremely important. Determination of various host and environmental factors that put an individual at risk for development of dental abscess, influence the spread of infection from a localized collection at the apex of a tooth to a cellulitis and further life-threatening sepsis would aid treatment decisions. Increased reliance on novel molecular techniques has enriched our knowledge of the diverse polymicrobial collection that constitutes a dental abscess. At present, there is no consensus over the gold standard treatment as evidenced by the wide variety of surgical protocols and prescription of antibiotic. Nevertheless, available data suggest that at present most isolates are still susceptible to first-line β-lactam agents. Antimicrobials should be reserved for patients with evidence of cellulitis and signs of sepsis. Most of the evidence pointing toward a key role for prompts surgical intervention and timely review.

Footnotes

Source of Support: Nil.

Conflict of Interest: None declared.

REFERENCES

1. Shu M, Wong L, Miller JH, Sissons CH. Development of multi-species consortia biofilms of oral bacteria as an enamel and root caries model system. Arch Oral Biol. 2000;45:27–40. [PubMed] [Google Scholar]2. Nair PN. Pathogenesis of apical periodontitis and the causes of endodontic failures. Crit Rev Oral Biol Med. 2004;15:348–81. [PubMed] [Google Scholar]4. Carter L, Starr D. Alarming increase in dental sepsis. Br Dent J. 2006;200:243. [PubMed] [Google Scholar]5. Boykin MJ, Gilbert GH, Tilashalski KR, Shelton BJ. Incidence of endodontic treatment: A 48-month prospective study. J Endod. 2003;29:806–9. [PubMed] [Google Scholar]6. Azodo CC, Chukwumah NM, Ezeja EB. Dentoalveolar abscess among children attending a dental clinic in Nigeria. Odontostomatol Trop. 2012;35:41–6. [PubMed] [Google Scholar]7. Kaur J. Dental education and oral health problems in India. Indian J Dent Educ. 2009;2:167–71. [Google Scholar]8. Agarwal V, Khatri M, Singh G, Gupta G, Marya C, Kumar V. Prevalence of periodontal diseases in India. J Oral Health Community Dent. 2010;4:7–16. [Google Scholar]10. Huang TT, Liu TC, Chen PR, Tseng FY, Yeh TH, Chen YS. Deep neck infection: Analysis of 185 cases. Head Neck. 2004;26:854–60. [PubMed] [Google Scholar]11. Flynn TR, Shanti RM, Hayes C. Severe odontogenic infections, part 2: Prospective outcomes study. J Oral Maxillofac Surg. 2006;64:1104–13. [PubMed] [Google Scholar]12. Siqueira JF, Jr, Rôças IN. Diversity of endodontic microbiota revisited. J Dent Res. 2009;88:969–81. [PubMed] [Google Scholar]13. Khemaleelakul S, Baumgartner JC, Pruksakorn S. Identification of bacteria in acute endodontic infections and their antimicrobial susceptibility. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2002;94:746–55. [PubMed] [Google Scholar]14. Külekçi G, Inanç D, Koçak H, Kasapoglu C, Gümrü OZ. Bacteriology of dentoalveolar abscesses in patients who have received empirical antibiotic therapy. Clin Infect Dis. 1996;23:S51–3. [PubMed] [Google Scholar]15. Fazakerley MW, McGowan P, Hardy P, Martin MV. A comparative study of cephradine, amoxycillin and phenoxymethylpenicillin in the treatment of acute dentoalveolar infection. Br Dent J. 1993;174:359–63. [PubMed] [Google Scholar]16. Reader CM, Boniface M, Bujanda-Wagner S. Refractory endodontic lesion associated with Staphylococci aureus. J Endod. 1994;20:607–9. [PubMed] [Google Scholar]17. Brook I, Frazier EH, Gher ME. Aerobic and anaerobic microbiology of periapical abscess. Oral Microbiol Immunol. 1991;6:123–5. [PubMed] [Google Scholar]18. Spijkervet FK, Vissink A, Raghoebar GM. The odontogenic abscess. Aetiology, treatment and involvement in the orofacial region. Ned Tijdschr Tandheelkd. 2004;111:120–7. [PubMed] [Google Scholar]19. Goumas PD, Naxakis SS, Papavasiliou DA, Moschovakis ED, Tsintsos SJ, Skoutelis A. Periapical abscesses: Causal bacteria and antibiotic sensitivity. J Chemother. 1997;9:415–9. [PubMed] [Google Scholar]20. Jacinto RC, Gomes BP, Shah HN, Ferraz CC, Zaia AA, Souza-Filho FJ. Incidence and antimicrobial susceptibility of Porphyromonas gingivalis isolated from mixed endodontic infections. Int Endod J. 2006;39:62–70. [PubMed] [Google Scholar]21. Kuriyama T, Absi EG, Williams DW, Lewis MA. An outcome audit of the treatment of acute dentoalveolar infection: Impact of penicillin resistance. Br Dent J. 2005;198:759–63. [PubMed] [Google Scholar]22. Tomazinho LF, Avila-Campos MJ. Detection of Porphyromonas gingivalis, Porphyromonas endodontalis, Prevotella intermedia, and Prevotella nigrescens in chronic endodontic infection. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2007;103:285–8. [PubMed] [Google Scholar]23. Gomes BP, Jacinto RC, Pinheiro ET, Sousa EL, Zaia AA, Ferraz CC, et al. Molecular analysis of Filifactor alocis, Tannerella forsythia, and Treponema denticola associated with primary endodontic infections and failed endodontic treatment. J Endod. 2006;32:937–40. [PubMed] [Google Scholar]24. Gomes BP, Pinheiro ET, Gadê-Neto CR, Sousa EL, Ferraz CC, Zaia AA, et al. Microbiological examination of infected dental root canals. Oral Microbiol Immunol. 2004;19:71–6. [PubMed] [Google Scholar]25. Sassone LM, Fidel RA, Faveri M, Guerra R, Figueiredo L, Fidel SR, et al. A microbiological profile of symptomatic teeth with primary endodontic infections. J Endod. 2008;34:541–5. [PubMed] [Google Scholar]26. Baumgartner JC, Siqueira JF, Jr, Xia T, Róças IN. Geographical differences in bacteria detected in endodontic infections using polymerase chain reaction. J Endod. 2004;30:141–4. [PubMed] [Google Scholar]27. Roche Y, Yoshimori RN. In-vitro activity of spiramycin and metronidazole alone or in combination against clinical isolates from odontogenic abscesses. J Antimicrob Chemother. 1997;40:353–7. [PubMed] [Google Scholar]28. Ledezma-Rasillo G, Flores-Reyes H, Gonzalez-Amaro AM, Garrocho-Rangel A, Ruiz-Rodriguez Mdel S, Pozos-Guillen AJ. Identification of cultivable microorganisms from primary teeth with necrotic pulps. J Clin Pediatr Dent. 2010;34:329–33. [PubMed] [Google Scholar]29. Siqueira JF, Jr, Rôças IN. Treponema species associated with abscesses of endodontic origin. Oral Microbiol Immunol. 2004;19:336–9. [PubMed] [Google Scholar]30. Sakamoto M, Rôças IN, Siqueira JF, Jr, Benno Y. Molecular analysis of bacteria in asymptomatic and symptomatic endodontic infections. Oral Microbiol Immunol. 2006;21:112–22. [PubMed] [Google Scholar]31. Siqueira JF, Jr, Rôças IN. Pseudoramibacter alactolyticus in primary endodontic infections. J Endod. 2003;29:735–8. [PubMed] [Google Scholar]32. Siqueira JF, Jr, Rôças IN. Detection of Filifactor alocis in endodontic infections associated with different forms of periradicular diseases. Oral Microbiol Immunol. 2003;18:263–5. [PubMed] [Google Scholar]33. Siqueira JF, Jr, Rôças IN. Simultaneous detection of Dialister pneumosintes and Filifactor alocis in endodontic infections by 16S rDNA-directed multiplex PCR. J Endod. 2004;30:851–4. [PubMed] [Google Scholar]34. Siqueira JF, Jr, Rôças IN. Nested PCR detection of Centipeda periodontii in primary endodontic infections. J Endod. 2004;30:135–7. [PubMed] [Google Scholar]35. Rôças IN, Siqueira JF., Jr Detection of novel oral species and phylotypes in symptomatic endodontic infections including abscesses. FEMS Microbiol Lett. 2005;250:279–85. [PubMed] [Google Scholar]36. Siqueira JF, Jr, Rôças IN. Catonella morbi and Granulicatella adiacens: New species in endodontic infections. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2006;102:259–64. [PubMed] [Google Scholar]37. Fowell C, Igbokwe B, MacBean A. The clinical relevance of microbiology specimens in orofacial abscesses of dental origin. Ann R Coll Surg Engl. 2012;94:490–2. [PMC free article] [PubMed] [Google Scholar]38. Kuriyama T, Nakagawa K, Karasawa T, Saiki Y, Yamamoto E, Nakamura S. Past administration of beta-lactam antibiotics and increase in the emergence of beta-lactamase-producing bacteria in patients with orofacial odontogenic infections. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2000;89:186–92. [PubMed] [Google Scholar]39. Niazi SA, Clarke D, Do T, Gilbert SC, Mannocci F, Beighton D. Propionibacterium acnes and Staphylococcus epidermidis isolated from refractory endodontic lesions are opportunistic pathogens. J Clin Microbiol. 2010;48:3859–69. [PMC free article] [PubMed] [Google Scholar]40. González-García R, Risco-Rojas R, Román-Romero L, Moreno-García C, López García C. Descending necrotizing mediastinitis following dental extraction. Radiological features and surgical treatment considerations. J Craniomaxillofac Surg. 2011;39:335–9. [PubMed] [Google Scholar]41. Jarboui S, Jerraya H, Moussi A, Ben Moussa M, Marrakchi M, Kaffel N, et al. Descending necrotizing mediastinitis of odontogenic origin. Tunis Med. 2009;87:770–5. [PubMed] [Google Scholar]42. Lewis MA, MacFarlane TW, McGowan DA. A microbiological and clinical review of the acute dentoalveolar abscess. Br J Oral Maxillofac Surg. 1990;28:359–66. [PubMed] [Google Scholar]43. Blome B, Braun A, Sobarzo V, Jepsen S. Molecular identification and quantification of bacteria from endodontic infections using real-time polymerase chain reaction. Oral Microbiol Immunol. 2008;23:384–90. [PubMed] [Google Scholar]44. Riggio MP, Lennon A. Development of a novel PCR assay for detection of Prevotella oris in clinical specimens. FEMS Microbiol Lett. 2007;276:123–8. [PubMed] [Google Scholar]45. Siqueira JF, Jr, Rôças IN, Souto R, de Uzeda M, Colombo AP. Actinomyces species, streptococci, and Enterococcus faecalis in primary root canal infections. J Endod. 2002;28:168–72. [PubMed] [Google Scholar]46. Snydman DR, Jacobus NV, McDermott LA, Golan Y, Goldstein EJ, Harrell L, et al. Update on resistance of Bacteroides fragilis group and related species with special attention to carbapenems 2006-2009. Anaerobe. 2011;17:147–51. [PubMed] [Google Scholar]47. Snydman DR, Jacobus NV, McDermott LA, Ruthazer R, Golan Y, Goldstein EJ, et al. National survey on the susceptibility of Bacteroides fragilis group: Report and analysis of trends in the United States from 1997 to 2004. Antimicrob Agents Chemother. 2007;51:1649–55. [PMC free article] [PubMed] [Google Scholar]48. Boyanova L, Kolarov R, Gergova G, Dimitrova L, Mitov I. Trends in antibiotic resistance in Prevotella species from patients of the University Hospital of Maxillofacial Surgery, Sofia, Bulgaria, in 2003-2009. Anaerobe. 2010;16:489–92. [PubMed] [Google Scholar]49. Heimdahl A, von Konow L, Nord CE. Isolation of beta-lactamase-producing Bacteroides strains associated with clinical failures with penicillin treatment of human orofacial infections. Arch Oral Biol. 1980;25:689–92. [PubMed] [Google Scholar]50. Hackman AS, Wilkins TD. Influence of pencillinase production by strains of Bacteroides melaninogenicus and Bacteriodes oralis on pencillin therapy of an experimental mixed anaerobic infection in mice. Arch Oral Biol. 1976;21:385–9. [PubMed] [Google Scholar]51. Pasquantonio G, Condò S, Cerroni L, Bikiqu L, Nicoletti M, Prenna M, et al. Antibacterial activity of various antibiotics against oral streptococci isolated in the oral cavity. Int J Immunopathol Pharmacol. 2012;25:805–9. [PubMed] [Google Scholar]52. Kuriyama T, Karasawa T, Nakagawa K, Saiki Y, Yamamoto E, Nakamura S. Bacteriologic features and antimicrobial susceptibility in isolates from orofacial odontogenic infections. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2000;90:600–8. [PubMed] [Google Scholar]53. Soares GM, Figueiredo LC, Faveri M, Cortelli SC, Duarte PM, Feres M. Mechanisms of action of systemic antibiotics used in periodontal treatment and mechanisms of bacterial resistance to these drugs. J Appl Oral Sci. 2012;20:295–309. [PMC free article] [PubMed] [Google Scholar]54. Karlowsky J, Ferguson J, Zhanel G. A review of commonly prescribed oral antibiotics in general dentistry. J Can Dent Assoc. 1993;59:292. [PubMed] [Google Scholar]55. Senhorinho GN, Nakano V, Liu C, Song Y, Finegold SM, Avila-Campos MJ. Occurrence and antimicrobial susceptibility of Porphyromonas spp. and Fusobacterium spp. in dogs with and without periodontitis. Anaerobe. 2012;18:381–5. [PubMed] [Google Scholar]56. Gilmore WC, Jacobus NV, Gorbach SL, Doku HC, Tally FP. A prospective double-blind evaluation of penicillin versus clindamycin in the treatment of odontogenic infections. J Oral Maxillofac Surg. 1988;46:1065–70. [PubMed] [Google Scholar]57. von Konow L, Köndell PA, Nord CE, Heimdahl A. Clindamycin versus phenoxymethylpenicillin in the treatment of acute orofacial infections. Eur J Clin Microbiol Infect Dis. 1992;11:1129–35. [PubMed] [Google Scholar]58. Cachovan G, Böger RH, Giersdorf I, Hallier O, Streichert T, Haddad M, et al. Comparative efficacy and safety of moxifloxacin and clindamycin in the treatment of odontogenic abscesses and inflammatory infiltrates: A phase II, double-blind, randomized trial. Antimicrob Agents Chemother. 2011;55:1142–7. [PMC free article] [PubMed] [Google Scholar]59. Adriaenssen CF. Comparison of the efficacy, safety and tolerability of azithromycin and co-amoxiclav in the treatment of acute periapical abscesses. J Int Med Res. 1998;26:257–65. [PubMed] [Google Scholar]60. Hanna CB., Jr Cefadroxil in the management of facial cellulitis of odontogenic origin. Oral Surg Oral Med Oral Pathol. 1991;71:496–8. [PubMed] [Google Scholar]61. Fouad AF, Rivera EM, Walton RE. Penicillin as a supplement in resolving the localized acute apical abscess. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1996;81:590–5. [PubMed] [Google Scholar]62. Paterson SA, Curzon ME. The effect of amoxycillin versus penicillin V in the treatment of acutely abscessed primary teeth. Br Dent J. 1993;174:443–9. [PubMed] [Google Scholar]63. Lewis MA, Carmichael F, MacFarlane TW, Milligan SG. A randomised trial of co-amoxiclav (Augmentin) versus penicillin V in the treatment of acute dentoalveolar abscess. Br Dent J. 1993;175:169–74. [PubMed] [Google Scholar]64. Mangundjaja S, Hardjawinata K. Clindamycin versus ampicillin in the treatment of odontogenic infections. Clin Ther. 1990;12:242–9. [PubMed] [Google Scholar]

Common Dental Emergencies – American Family Physician

ALAN B. DOUGLASS, M.D., Middlesex Hospital, Middletown, Connecticut

JOANNA M. DOUGLASS, B.D.S., D.D.S., University of Connecticut School of Dental Medicine, Farmington, Connecticut

Am Fam Physician. 2003 Feb 1;67(3):511-517.

Dental caries, a bacterial disease of teeth characterized by destruction of enamel and dentine, is often the underlying cause of dental pain. When a carious lesion impinges on the dental pulp, pulpitis follows and, ultimately, necrosis of the pulp occurs. Untreated necrosis may lead to a localized abscess or a spreading infection into the surrounding soft tissue that results in cellulitis. Immediate treatment involves antibiotic therapy for cellulitis, perhaps with drainage of abscesses, while definitive treatment requires root canal therapy or extraction of the involved tooth. Pericoronitis is an inflammation of the soft tissue overlying a partially erupted tooth. Localized cases respond to irrigation. Secondary cellulitis can develop. Definitive treatment may require surgical extraction of the underlying tooth or excision of the gum flap. Avulsion of a permanent tooth secondary to trauma is a true dental emergency. The tooth should be reimplanted on the spot, and the patient should be seen immediately by a dentist for splinting and antibiotic prophylaxis. Most dental problems can be prevented with regular dental care and steps to minimize risks of oral trauma.

Dental emergencies (Table 1) are extremely common in America. In one recent survey,1 22 percent of the general population had experienced orofacial pain in the preceding six months, and 12 percent experienced toothache. In 1996, American students missed 1,611,000 school days because of acute dental problems.2

View/Print Table

TABLE 1

Common Dental Emergencies

TABLE 1

Common Dental Emergencies

Dental Anatomy

All human teeth are composed of three structural layers3 (Figure 1). The outer layer of enamel is an extremely hard, highly mineralized, crystalline structure that covers and protects the crown of the tooth. The core structure of the tooth is composed of dentine. At the center of the tooth is the pulp chamber, which contains blood vessels and nerves that connect to the jaw’s vascular and nervous supply through the tooth apices. The tooth roots are attached to the surrounding alveolar bone of the tooth socket via the periodontal ligament.

FIGURE 1.

Normal tooth anatomy.

Dental Pain

The first step in the evaluation of oral pain should be to determine its etiology. Dental sources are most common. However, pain arising from nondental sources such as myofascial inflammation, migraine headache, maxillary sinusitis, nasal tissues, ears, temporomandibular joints, and neuralgias always must be considered and excluded.4

CARIOUS ORIGIN

Dental caries is a bacterial disease of teeth characterized by demineralization of tooth enamel and dentine by acid produced during the fermentation of dietary carbohydrates by oral bacteria, predominately Streptococcus mutans.5,6 Dental decay presents visually as opaque white areas of enamel with grey undertones (Figure 2) or, in more advanced cases, as brownish, discolored cavitations (Figure 3). Caries is initially asymptomatic. Pain does not occur until the decay impinges on the pulp, and an inflammatory process develops.

View/Print Figure

FIGURE 2.

Caries presenting as opaque white areas with central cavitations.

FIGURE 2.

Caries presenting as opaque white areas with central cavitations.

FIGURE 3.

Caries in the primary dentition.

Reversible pulpitis is mild inflammation of the tooth pulp caused by caries encroaching on the pulp. Pain is triggered by hot, cold, and sweet stimuli, lasts for a few seconds, and resolves spontaneously.7 Treatment involves removal of the carious tissue and placement of a dental restoration, or filling.

If a carious lesion causing reversible pulpitis is not treated, the condition will progress to irreversible pulpitis, a severe inflammation of the pulp (Figure 4). Pain becomes severe, spontaneous, and persistent, and is often poorly localized.7 The only way to definitively treat the discomfort is root canal treatment (removal of the pulp and filling of the empty pulp chamber and canal) or extraction of the tooth. The urgency of referral to a dentist should be determined by the patient’s level of discomfort, but examination should not be delayed for more than a few days. The pain should be managed with appropriate analgesia such as a nonsteroidal anti-inflammatory drug (NSAID) or a weak opioid combined with an NSAID or acetaminophen in an appropriate quantity to last until the dental appointment. Patients should be warned of the risks of further complications if they do not have prompt definitive treatment and advised to return to their physician if symptoms change or worsen before they see the dentist.

FIGURE 4.

Irreversible pulpitis.

A severely inflamed pulp will eventually necrose, causing apical periodontitis, which is inflammation around the apex of the tooth (Figure 5). Pain is severe, spontaneous, and persistent, but unlike that of irreversible pulpitis, localizes to the affected tooth. The tooth is sensitive to percussion with a metal object.7 Regional lymphadenopathy can be present. Management is root canal treatment or extraction. Referral to a dentist should occur as soon as possible, with provision of appropriate pain medication. Antibiotics are not necessary, but patients should be warned to return to the physician immediately if swelling or other evidence of spreading infection occurs.

FIGURE 5.

Apical periodontitis, periapical abscess, and cellulitis.

Apical abscess is a localized, purulent form of apical periodontitis (Figures 5 and 6). It may present clinically as a fluctuant buccal or palatal swelling, with or without a draining fistula. Regional adenopathy is usually present. If pus is draining, pain usually is not severe. Antibiotics are not necessary unless concurrent cellulitis is present. Acute incision and drainage of a fluctuant area by an appropriately trained physician would be reasonable. Definitive therapy is root canal treatment or extraction. Patients should be seen by a dentist within one to two days and provided with appropriate pain medication in the meantime.

FIGURE 6.

Abscess adjacent to primary tooth.

Cellulitis may follow apical periodontitis if the infection spreads into the surrounding tissues (Figure 5). Diffuse, tense, painful swelling of the affected tissues occurs. Regional lymphadenopathy is common, and fever may be present. The infection can spread into the major fascial spaces of the head and neck,8 with the attendant risk of airway compromise. Maxillary infection also may spread to the periorbital area, increasing the risk of serious complications that include loss of vision, cavernous sinus thrombosis, and central nervous system involvement.8

The examination should focus on determining if the cellulitis remains localized or has spread regionally. Patients with localized cellulitis that is deemed appropriate for outpatient therapy should be treated by the physician with antistreptococcal oral antibiotics, such as oral penicillin in a dosage of 500 mg three times daily in adults or 50 mg per kg per day divided into three doses in children.

In the event of true penicillin allergy, erythromycin or clindamycin (Cleocin) may be substituted. Appropriate pain medication should be provided. Definitive therapy is root canal treatment or extraction, which in selected cases may be delayed until swelling has subsided. Patients should be evaluated by a dentist within one to two days but warned to return earlier if swelling or pain worsens.

If infection extends regionally into the deep spaces of the head and neck as evidenced by severe swelling, the risk of life-threatening complications such as airway compromise is substantial. Generally, these patients should be hospitalized and provided with surgical and infectious disease consultation. Imaging, usually with computed tomographic scanning, is mandatory, as is surgical drainage if abscess formation is detected. Intravenous broad-spectrum antibiotic treatment should be started immediately and should include coverage for anaerobes.8

In general, the same principles of initial evaluation and management apply to the primary and permanent dentition. However, carious lesions of the primary teeth less frequently cause pain and abscesses and more frequently drain cutaneously than lesions of the permanent dentition. The systemic effects of infection are more pronounced in children, with rapid temperature elevations, greater risk of dehydration, and more rapid spread of infection.8

PERIODONTAL ORIGIN

Periodontal disease is an inflammatory destruction of the periodontal ligament and supporting alveolar bone. The main etiologic agent is bacterial plaque. Multiple bacteria are implicated, but as the disease progresses, gram-negative anaerobes predominate.5 Patients with chronic periodontal disease or patients who have a foreign object lodged in the gingiva may present with an acute periodontal abscess. Symptoms include throbbing pain with erythema and swelling over the affected tissue. The tooth is normally tender to percussion and shows increased mobility.

If left untreated, the abscess may rupture or, less commonly, progress to cellulitis. Patients require referral to a dentist within 24 hours for drainage and debridement of the infected periodontal area. Antibiotics are not normally indicated if debridement is successful, but their use remains controversial.9

WISDOM TOOTH ORIGIN

Pericoronitis is inflammation of the soft tissues surrounding the crown of a partially erupted tooth, most commonly a wisdom tooth (Figure 7). It occurs when bacterial plaque and food debris accumulate beneath the flap of gum covering the partially erupted tooth. Inflammatory edema, often complicated by trauma from the opposing tooth, leads to swelling of the flap, pain, tenderness, and a bad taste caused by pus oozing from beneath the flap.7 Regional lymphadenopathy is common, and cellulitis and trismus (inability to open the mouth fully) can occur. In severe cases, the oral airway can be compromised.

FIGURE 7.

Pericoronitis.

If pericoronitis is well localized, hot salty mouthwashes and irrigation under the flap can resolve symptoms in the majority of cases.10 Localized cases that do not respond to mechanical therapy and more severe disseminated cases with spreading cellulitis should be treated with penicillin and appropriate pain medication as described in the section on carious origin of pain. Referral to a dentist should occur as quickly as possible so the patient can be evaluated to see if symptomatic treatment can suffice until eruption is complete or if surgical therapy to remove the gum flap or underlying tooth is necessary.

Dental Trauma

Dental trauma is extremely common. Children are particularly affected, with one third of five year olds having suffered injury to their primary teeth, and one fourth of 12 year olds having suffered injury to their permanent teeth.11 Injuries to teeth and their supporting structures can be classified as fractures, lateral or extrusive luxation (loosening and displacement of the tooth), intrusion (displacement of the tooth vertically into the alveolar bone), and avulsion (complete displacement of the tooth out of its socket).12

The mechanism of injury and timeline are particularly important aspects of the history because they define the risk of associated injuries and available treatment options. Examination should focus on related soft tissue injuries and the need for suturing, signs of tooth loosening, displacement or fracture, and disturbance in the bite or other signs of alveolar fracture. Complete diagnosis requires at least one dental radiograph in all cases.

All patients with traumatized teeth ultimately need follow-up with a dentist for complete diagnosis and long-term care. Long-term sequelae can include pulp death, root resorption, and displacement or developmental defects of permanent tooth successors.

Tooth fractures may involve the crown, the root, or both, with or without exposure of the pulp. Fractures limited to the enamel and small amounts of dentine that are not sensitive may not require immediate treatment but should be checked by a dentist. Fractures exposing the pulp are often painful, and patients with this condition require timely referral to a dentist. Tooth fragments should be kept hydrated as they could possibly be reattached. Definitive treatment may involve root canal therapy or extraction.

Fractures of the root usually require a radiograph for detection (Figure 8) unless the tooth is particularly loose and the fracture occurred close to the gingival margin. Treatment may involve root canal therapy, splinting, or extraction, depending on the exact nature of the root fracture.

FIGURE 8.

Fractured root shown on radiograph.

Teeth subject to lateral or extrusive luxation have been displaced and are loose. In the primary dentition, if the traumatized teeth are so loose that they are in danger of being aspirated or if they interfere with normal occlusion, immediate referral to a dentist for extraction is required.12 Luxated permanent teeth require dental referral for repositioning, splinting, or root canal therapy, along with long-term follow-up.13 Any luxated tooth that interferes with normal occlusion requires immediate dental evaluation and treatment to avoid pain and further complications.

Teeth subject to intrusive luxation have been intruded into the alveolar bone, which may occur to the point that the teeth are not visible. With regard to injuries to the primary dentition, dental referral is required for monitoring to determine if the teeth will re-erupt. For injuries to the permanent teeth, dental referral is required for monitoring or treatment to promote re-eruption (surgical or orthodontic), often coupled with root canal therapy.13

Avulsed teeth are a true dental emergency. Primary teeth are never reimplanted.12 In the case of permanent teeth, time is of the essence. Immediate on-scene reimplantation is the preferred method of treatment. If the tooth is visibly contaminated, it should be gently rinsed in cold running tap water and then reimplanted. Care should be taken not to touch, rub, or clean the root, which could remove periodontal ligament fibers and reduce the chance of successful reimplantation. The patient should then see a dentist immediately for splinting and antibiotic prophylaxis.

If immediate on-scene reimplantation is not possible, the tooth should be transported in the patient’s buccal sulcus, milk, or a specialized tooth transport container to the physician’s or dentist’s office. The tooth should then be immediately reimplanted. If rinsing is required, normal saline should be used, and any clot present in the socket should be flushed out before reimplantation.

Antibiotic prophylaxis with penicillin should be prescribed, tetanus vaccine should be administered if the patient has not received it in the past five years,14 and the patient should be immediately referred to a dentist for splinting and further therapy. Avulsed teeth that have not been managed in an appropriate and timely fashion should not be discarded. Alternative, but less optimal, treatments are available.13

Prevention

Dental caries and periodontal disease can be prevented by decreasing ingestion of sugar-containing food items and employing regular tooth brushing and appropriate fluoride use. Regular dental examinations with early treatment of carious lesions can substantially reduce the risk of serious complications.

Most dental trauma occurs in children, and its occurrence can be reduced substantially. Family physicians should advocate the use of appropriate mouthguards and face shields in organized sports.15

Dental Referral

Family physicians often ask the question, “What sort of dentist should I refer this patient to?” In most cases, a general dentist can meet the needs of patients with the problems described in this article. Children younger than three years and children who may present a behavior problem in the dental chair should be referred to a dentist with significant experience in managing children. Adults who do not wish to attempt to keep their teeth or who have significant facial swelling should be referred to an oral surgeon.

Dental abscess – Symptoms, diagnosis and treatment

Dental abscess covers a clinical spectrum from minor well-localized infection to severe life-threatening complications involving multiple fascial spaces.

The vast majority of otherwise healthy patients presenting with a dental infection can be managed on an outpatient basis.

Common presenting symptoms include dental pain/toothache; intraoral and/or extraoral edema, erythema, or discharge; and thermal hypersensitivity.

A major consideration is the potential for airway obstruction as a consequence of extension of the infection into fascial spaces surrounding the oropharynx.

Panoramic dental x-ray reveals the source of infection in most cases; however, a periapical x-ray may also be helpful. A computed tomography scan is recommended if there is suspicion of a fascial space infection or if panoramic or periapical x-rays are not available.

Prompt operative intervention to identify and eliminate the source of infection and provide a path for drainage, along with antibiotic therapy and supportive care, is required. Operative treatment is considered the cornerstone of successful management.

Immunocompromised patients must be treated in a timely fashion as tooth-related infections may spread rapidly.

A dental abscess is the final product of an inflammatory process, a suppurative collection associated with the structures surrounding the teeth. It is a type of odontogenic infection (i.e., an infection that originates within a tooth).

An abscess may remain localized (damaging only the adjacent tissues) or it may develop into a diffuse cellulitis, which can lead to the development of potentially life-threatening systemic complications.

The vast majority of otherwise healthy patients have localized infections which can be managed on an outpatient basis.

The most common types of dental abscess are periapical, periodontal, and pericoronal. Other less common types include gingival or combined periodontal-endodontic. This topic primarily deals with the most common types of dental abscess.

5 Stages, Symptoms, Pictures & Treatment

What is a Dental Abscess?

A dental abscess can also be called an oral abscess or tooth abscess. It is a localized infection that results in a collection of pus.

The long-term build-up of pus inside the gums or teeth triggers an abscess, which forms due to a bacterial infection. The infection affects the surrounding structures of teeth and can cause persistent toothaches and other symptoms.

There are three main types of oral abscesses that can form in different regions around a tooth, including:

Gingival Abscess (Gum Abscess)

A Gingival abscess can also be called a gum abscess. It is a painful and rapidly expanding lesion that forms between the gums and teeth. It is the result of a bacterial infection.

The most common cause of a gingival abscess is the impact of a foreign object. This could be popcorn, a toothpick splinter, or something else.

In the beginning stages, a gum abscess appears as a red swelling with a shiny, smooth surface. After about 48 hours, the abscess becomes pointed and has a higher risk of erupting as it progresses.

Periodontal Abscess

A periodontal abscess is a pocket of pus that forms in the gum tissue. This abscess appears as a shiny, smooth swelling that protrudes out of the gums and is sensitive to the touch. The tooth or teeth around the abscess may also become sensitive or loosen.

A periodontal abscess typically develops in patients who have periodontal disease. This is the advanced stage of gum disease that results in permanent bone loss.

The long-term build-up of dental plaque and hardened tartar (calculus) initiates periodontitis. The calculus is located beneath the gums (subgingival), between the gums, and along the gum line. The calculus can only be removed with scaling and root planing treatment.

Periapical Abscess

A periapical abscess forms at the root of a tooth. It consists of a pocket of pus that develops due to a bacterial infection. Bacteria first enters the innermost part of the tooth (dental pulp) through a cavity, crack, or chip.

The dental pulp contains the nerve, blood vessels, and connective tissues. It provides sensory innervation (stimulation) through a tooth’s nerve. Once the bacteria pass through the pulp, it can spread all the way down to the root, creating an abscess.

Inflammation, swelling, and pain typically occur at the tip of a tooth’s root where the abscess forms.

Summary

A tooth abscess is a painful pocket of pus that develops from a bacterial infection in the mouth. There are three types: gingival, periodontal, and periapical abscesses.

Pictures of Dental Abscesses (Warning: Medical Images)

5 Dental Abscess Stages

A tooth abscess is one of the later stages of tooth decay. Tooth abscess stages include:

1. Enamel Decay

The first stage is damage to the first layer of your teeth (enamel). Enamel decay is often caused by plaque build-up on your teeth. Some people may not experience any symptoms. Others may experience tooth sensitivity or develop spots on their teeth.

2. Dentin Decay

If you don’t treat your enamel decay, it will progress to the next layer of your tooth. Dentin is the yellowish second layer. Many people will experience increased tooth sensitivity in this stage. In others, a small hole in your tooth may develop.

3. Pulp Decay

The soft inner pulp is the deepest layer of your tooth structure. If bacteria reach this layer, they can attack the nerve of the tooth. This often causes severe tooth pain. Eventually, the tooth’s nerve dies, which is when the abscess begins to form.

4. Abscess Formation

Once the bacteria makes its way to your pulp, it can start to spread deeper into your gums or jaw bone. Your gums may begin to swell and you may see a small bump on your gums. This may feel like throbbing pain in your teeth, gums, and surrounding tissue.

5. Serious Complications

If you do not treat your tooth abscess, it could lead to serious symptoms. The most common are:

• Tooth loss — severe tooth decay can cause your tooth to break or fall out
• Sepsis — bacteria can spread to your bloodstream and cause sepsis, which is a life-threatening infection

Summary

The six stages of a dental abscess include enamel decay, dentin decay, pulp decay, abscess formation, and complications. Serious complications like sepsis (a deadly blood infection) and/or tooth loss can occur if left untreated.

What Causes Dental Abscesses?

The primary cause of dental abscesses is from plaque build-up due to neglected oral care. This includes not brushing, flossing, or using fluoride regularly. Other risk factors associated with tooth abscesses include:

Injuries & Damage

Injuries, dental damage, or deep tooth cracks allow bacteria to spread to deeper parts of the teeth or gums. This can cause an abscess.

Underlying Medical Conditions & Medications

People with weaker immune systems or those taking medications for serious health conditions are at a higher risk of developing abscesses. This includes chemotherapy patients, steroids, and people with diabetes.

Poor Diets High in Sugar

Eating sugary and processed foods results in the build-up of dental plaque and calculus. Without proper brushing, cleaning, and flossing, tooth decay may develop. Untreated decay can result in a dental abscess later on.

Summary

Dental abscesses are caused by poor oral hygiene/untreated dental infections. Risk factors include mouth trauma, weakened immune systems, poor diets, and tooth cracks, among others.

Symptoms of a Dental Abscess

Depending on the type of dental abscess and how long it has been progressing, common symptoms may include:

• Severe toothache and throbbing near the affected tooth. This can include the gums, tooth root, or the tooth directly. The pain typically comes and goes suddenly
• Painful, swollen lymph nodes in the neck and/or jaw
• Redness, swelling, and inflammation near the abscess
• Swollen, inflamed, and shiny gums
• Pain that worsens when lying down and interrupts sleep
• Tooth sensitivity to cold, sweet, or hot substances
• Consistent bad breath, even after brushing or rinsing the mouth
• A loose tooth or multiple loose teeth near the infection site
• Severe ear, neck, and/or jaw pain
• Pain when biting down or chewing
• Difficulties swallowing and breathing
• Face swelling
• Fever

If the abscess ruptures, you may notice a foul taste (salty fluid) and smell in your mouth. You will also feel pain relief in the infected tooth. If this occurs, call your general dentist immediately.

If you experience severe pain and difficulty breathing, call your local emergency department or 9-1-1.

Summary

The primary symptom of a dental abscess is severe pain near the infection site. Swelling, redness, and inflammation around the abscess are also common.

Dental Abscess Treatment

Depending on the type and severity of the infection, there are three treatment options available. They include:

Abscess Draining

If the abscess is treated early and hasn’t progressed, abscess draining is typically recommended. During the procedure, a dentist will make a small incision into the abscess to drain the pus. A dentist cleans the infected area and prescribes antibiotics post-op.

Root Canal Treatment

Root canal treatment is necessary when the bacteria spreads to the dental pulp and tooth roots. Or if there is an abscess at the root of a tooth (periapical abscess).

During the procedure, a dentist removes the infected dental pulp in the patient’s tooth and also drains the abscess. Then the root canal is cleaned, shaped, sealed, and restored with a dental crown.

The root canal procedure itself is typically performed in one to two appointments. If you add the crown on top of that, it can be three to four appointments. However, if you’re seeing an endodontist, it’s usually just one visit for the root canal treatment. Then two visits with a general dentist for the crown.

Tooth Extractions

Tooth extractions might be necessary after teeth are damaged from an injury, disease, or tooth decay. If an abscessed tooth cannot be saved, extraction is necessary. During the procedure, local anesthesia is administered and the tooth is removed using small instruments.

After extraction, the tooth socket is covered with sterile gauze, and pressure should be applied for about 20 minutes. Stitches may also be necessary. A dental implant can be placed after the extraction site heals.

Summary

Tooth abscesses must be treated quickly to prevent spreading. Your dentist must drain the infection (never try to do this at home). Root canal treatment and tooth extraction may also be necessary (depending on the severity).

Best Antibiotics For Dental Abscesses

Commonly prescribed antibiotics for dental abscesses include amoxicillin and penicillin. These antibiotics also treat many other types of general infections and tooth infections.

Your dentist may prescribe you metronidazole and penicillin to treat bacterial infections.

Antibiotics alone do not cure dental abscesses. Instead, they are taken after the root canal or extraction procedure to help clear up the infection.

Tips for Managing Pain

Ibuprofen and similar painkillers can help control dental abscess pain before you see your dentist for treatment.

Many of these medications can be purchased over-the-counter and do not require a prescription. You can also take them in combination with the antibiotics your dentist prescribes after treatment.

Summary

Amoxicillin and penicillin can be used to treat the underlying bacterial infection. However, antibiotics will not cure an abscess. Professional drainage is still necessary. Over-the-counter medications can be used to manage pain before/after your appointment.

Risk Factors of an Untreated Dental Abscess

Dental abscesses should be treated promptly or there is a risk for serious complications. If you ignore your tooth infection or wait too long to get treatment, you may experience:

• Tooth loss — if the abscessed tooth becomes severely infected or weak, a root canal will not be able to save it. If this is the case, you must get the tooth removed and replaced with a dental implant and dental crown (artificial tooth).
• Bone infection — leaving the tooth untreated can result in an infection that affects the surrounding facial bones.
• Sinus infections — frequent and painful sinus infections and/or oral soft tissue infections can develop as well.
• Septicemia — this is a life-threatening condition that occurs when your entire bloodstream becomes infected. A dental abscess can trigger septicemia if left untreated long-term.
• Brain abscess — a dental abscess infection can travel to the brain, resulting in another abscess. This is relatively rare but can occur if the infection becomes severe enough. A brain abscess is dangerous and requires a visit to the emergency room or hospital for treatment.

Summary

A tooth abscess is serious and can be life-threatening (if left untreated). It can lead to tooth loss, bone/sinus infections, septicemia (a deadly blood infection), or a brain abscess (rare).

Prevention Tips

Practicing good oral hygiene is the best way to prevent the development of any oral condition and disease. Dental abscess prevention tips include:

• Brush your teeth twice a day with fluoride toothpaste. You can either use a regular or electric toothbrush
• Replace your toothbrush or toothbrush head every 3 to 4 months
• Floss between your teeth daily with dental floss, floss sticks, or a water flosser
• Use a fluoride or antiseptic mouth rinse daily to help prevent plaque buildup and tooth decay
• Keep up with professional dental care. This includes visiting your dentist for routine teeth cleanings, x-rays, and dental exams every six months
• Drink fluoridated water often
• Eat a balanced, healthy diet and reduce sugar intake

Summary

Optimal oral hygiene is essential for abscess prevention. Also, make sure you keep up with professional teeth cleanings and dental exams every six months.

Dental Abscess FAQs

Can a tooth abscess go away on its own?

A tooth abscess will not go away on its own. If the abscess is not drained by a dentist, it can spread to other areas of your body, including the jaw, head, or neck.

Can I pop an abscess on my gum?

You should never try to pop or squeeze a dental or gum abscess. Doing so can push the infection into deeper tissues in your mouth.

How can I treat a gum abscess at home?

You cannot drain a gum abscess at home. However, you can minimize the pain by applying a warm compress to the area 4 times a day for 30 minutes at a time.

How do I know if my tooth abscess is spreading?

Symptoms that a tooth abscess has spread to other parts of your body include fever, swelling, dehydration, increased heart rate, increased breathing rate, and stomach pain.

Is a gum abscess an emergency?

It is difficult to predict how a dental infection will spread, so it is best to assume that a tooth abscess is an emergency. Any visible swelling in the gums, whether it causes pain or not, could be dangerous, and you should seek urgent dental care. 

What does a tooth abscess look and feel like?

Most abscesses are warm and soft to the touch. In some cases, they can be firm to the touch.

Will a tooth abscess go away with antibiotics?

Antibiotics alone cannot treat a tooth abscess. An abscess has to be professionally drained by a dentist. Antibiotics may be prescribed if the infection has spread or is very severe.

Abdominal Abscess: Background, Anatomy, Pathophysiology

Author

Alan A Saber, MD, MS, FACS, FASMBS Director of Bariatric and Metabolic Surgery, University Hospitals Case Medical Center; Surgical Director, Bariatric Surgery, Metabolic and Nutrition Center, University Hospitals Digestive Health Institute; Associate Professor of Surgery, Case Western Reserve University School of Medicine

Alan A Saber, MD, MS, FACS, FASMBS is a member of the following medical societies: American College of Surgeons, American Society for Gastrointestinal Endoscopy, American Society for Metabolic and Bariatric Surgery

Disclosure: Nothing to disclose.

Coauthor(s)

Raymond D LaRaja, MD, FACS Clinical Professor of Surgery, Icahn School of Medicine at Mount Sinai; Director, Department of Surgery, Cabrini Medical Center

Raymond D LaRaja, MD, FACS is a member of the following medical societies: American College of Surgeons, American Medical Association, New York Academy of Medicine, New York County Medical Society

Disclosure: Nothing to disclose.

Chief Editor

John Geibel, MD, MSc, DSc, AGAF Vice Chair and Professor, Department of Surgery, Section of Gastrointestinal Medicine, Professor, Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director of Surgical Research, Department of Surgery, Yale-New Haven Hospital; American Gastroenterological Association Fellow; Fellow of the Royal Society of Medicine

John Geibel, MD, MSc, DSc, AGAF is a member of the following medical societies: American Gastroenterological Association, American Physiological Society, American Society of Nephrology, Association for Academic Surgery, International Society of Nephrology, New York Academy of Sciences, Society for Surgery of the Alimentary Tract

Disclosure: Nothing to disclose.

Acknowledgements

H Scott Bjerke, MD, FACS Clinical Associate Professor, Department of Surgery, University of Missouri-Kansas City School of Medicine; Medical Director of Trauma Services, Research Medical Center; Clinical Professor, Department of Surgery, Kansas City University of Medicine and Biosciences

H Scott Bjerke, MD, FACS is a member of these medical societies: American Association for the History of Medicine, American Association for the Surgery of Trauma, American College of Surgeons, Association for Academic Surgery, Eastern Association for the Surgery of Trauma, Midwest Surgical Association, National Association of EMS Physicians, Pan-Pacific Surgical Association, Royal Society of Medicine, Southwestern Surgical Congress, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Michael A Grosso, MD Consulting Staff, Department of Cardiothoracic Surgery, St Francis Hospital

Michael A Grosso, MD is a member of the following medical societies: American College of Surgeons, Society of Thoracic Surgeons, and Society of University Surgeons

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Reference Salary Employment

Qualified treatment of abdominal abscess in NEARMEDIC

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Causes of occurrence

Any abscess is a localized inflammatory process limited by the capsule. In this case, the capsule may consist of an omentum, inflammatory adhesions and adjacent tissues. The abscess cavity most often contains aerobic and anaerobic bacteria that migrated to this area from the gastrointestinal tract.

The direct sources of abscess formation are infectious agents and inflammatory factors that affect the state of tissues.Bacteria can penetrate into the structures of the abdominal organs from the external environment during surgery, the gastrointestinal tract and other areas. Often we are talking about secondary peritonitis against the background of rupture of the walls of the intestine or pancreas.

Main reasons:

1. Inflammation of the appendix of the cecum (appendicitis). In this case, a purulent exudate is formed in the closed intestinal cavity. If treatment is not carried out in a timely manner, perforation of the intestinal wall with the penetration of pus is possible.
2. Inflammation of the tissues of the pancreas with subsequent necrosis. Exudate can also enter the free abdominal cavity and form an abscess.
3. Rupture of the duodenal wall in case of organ peptic ulcer.
4. Inflammation of the gallbladder and its complications such as gangrenous cholecystitis.
5. Mesenteric ischemia and development of tissue necrosis.
6. Purulent inflammation of the female genital organs.
7. Complication of surgical intervention in the gastrointestinal tract, severe trauma.
8. Other sources of exudate include ruptured diverticulum, leaky intestinal anastomosis, and ruptured hematoma.

The composition of the pathogenic microflora of the abscess depends on the source of inflammation. Most often, Escherichia coli is found in the pus. In patients who have taken antibiotics for a long time, inflammation can be caused by pathogenic and opportunistic fungal microorganisms.

Classification

Doctors describe different forms of the disease based on the source of the inflammatory process.It is very important to establish the localization of the abscess at the early stages of diagnosis for effective surgical treatment.

Basic Shapes:

• Metastatic abscess – the formation of a secondary pyogenic capsule containing pus as a result of the spread of infection from distant sites. Bacteria and fungal microorganisms can spread through the blood and lymph flow.
• Postoperative abscesses are pathological areas that form as a result of surgical treatment of diseases.In this case, the pathology may be due to an incompetent interintestinal anastomosis, infection, or a mistake during the removal of the appendix.
• Perforated abscess. An inflammatory focus is formed as a result of rupture of the walls of the inflamed anatomical structure. This can be a rupture of the walls of the appendix, pancreas with pancreatic necrosis, or another organ.
• Post-traumatic abscess resulting from trauma to the abdominal organs.

Imaging and diagnostic operations can identify the source of the inflammation.

Symptoms

In the early stages, this inflammatory disease can be detected by symptoms. This may be an exacerbation of the symptoms of a previously diagnosed pathology or the spontaneous appearance of unpleasant sensations in the abdominal region.

Possible attributes:

• Severe abdominal pain;
• tension of the abdominal muscles;
• nausea and vomiting;
• lack of appetite;
• dizziness and weakness.
• increase in body temperature;
• heart palpitations;
• chills;
• intestinal obstruction.

The nature of the symptoms depends on the location of the abscess. When a subphrenic abscess forms, the patient may complain of cough, fever, and pain that occurs during inhalation.

Diagnostics

If purulent inflammation is suspected, the patient will need the help of a surgeon. The doctor will ask the patient about the complaints in detail and study the anamnestic data. A physical examination, including palpation of the abdomen, can help localize the inflammation. The required method of treatment is selected after receiving the results of instrumental and laboratory diagnostics.

Possible survey methods

1. Blood test. An increase in the number of leukocytes testifies to the inflammatory process.
2. Visualization of organs with contrast radiography or computed tomography. The resulting image gives the specialist the opportunity to see the location of the purulent capsule.
3. Ultrasound imaging.
4. Examination with minimally invasive intervention (diagnostic laparoscopy).

The data obtained through visual and laboratory examinations are used for the operation and the prescription of medications.

Treatment

The patient requires hospitalization in the clinic for timely treatment and close medical supervision. The abscess can only be removed with the help of an operation, however, in addition to surgical treatment, patients are prescribed medications.

Treatment methods

1. Opening and draining the abscess. The type of surgical access depends on the location of the abscess. If multiple foci of inflammation are found, a wide dissection may be required.
2. Intravenous administration of broad-spectrum antimicrobial drugs to suppress the infectious process.
3. Percutaneous drainage of small abscesses.

Antimicrobial therapy must be continued after surgery. If, as a result of inflammation and subsequent treatment, the functions of one or another organ have been impaired, the patient will need additional rehabilitation. With timely surgical intervention, the prognosis is positive.

Tooth abscess treatment in Moscow

Tooth abscess is a disease of an infectious nature, localized in the area of ​​the roots of the teeth and proceeding quite hard.

If measures to stop the process are not taken in a timely manner, the infection often spreads to the tissues responsible for keeping the tooth in the alveolus. Often, the jaw bone is also affected, the consequences of this can be very serious – for example, the patient can get phlegmon of the oral cavity.

Causes of tooth abscess

• Not completely cured dental diseases – gingivitis, pulpitis, highly developed caries, granuloma, etc.
• May develop after influenza, sore throat, other infectious diseases as a result of transmission of infection by the bloodstream.
• In case of mechanical injury, the resulting chips, fractures can cause an abscess.
• Damage to the mucous membrane in the mouth.
• Development of boils in the jaw region.
• As a result of an infection resulting from injections into the gums, which are not uncommon in dental treatment.

The above factors can provoke a violation of the integrity of the enamel of the teeth. This facilitates the penetration of pathogens into the dental pulp by pathogens and promotes the development of inflammation.

Signs of dental abscess

• Frequent bitter taste in the mouth;
• pain when chewing or touching a tooth;
• tooth becomes sensitive to temperature changes;
• there is often acute pain in the tooth – aching or throbbing;
• the patient feels discomfort, frequent ailments;
• there are appetite disorders, sleep disorders, body temperature rises;
• from the mouth smells rotten, unpleasant;
• gums redden and swell;
• cervical lymph nodes are enlarged;
• open ulcers appear on the surface of the gums, from which pus is released;
• in the jaw area, edema appears, the soft tissues of the face swell.

If you start the course of the disease, the abscess can break out on its own or into the oral cavity. After that, an improvement in the patient’s well-being is noted, pain decreases, the severity of manifestations is smoothed out, the face takes a natural shape. But improvement should not be the reason for discontinuation of treatment. A breakthrough of an abscess means the transition of an acute form of the disease to a chronic one. In the future, an exacerbation may begin anew, often with the formation of a fistulous tract.

Treatment of dental abscess

Already at the initial examination, it is possible to establish a tooth abscess by external manifestations, such as pain when tapping, swelling and redness of the gums, ulcers on them, suppuration.

If necessary, the dentist will ask the patient to take an X-ray. This study will help to find out if the patient really has an abscess, or to determine another disease with similar symptoms.

All measures taken to treat an abscess are aimed at eliminating the focus of infection. This helps to preserve the tooth and prevents the complications of the disease.

Often the abscess needs to be drained, for this purpose the doctor works on the root canal. During the procedure, dying root tissue is removed.Then the tooth is filled, sometimes crowns are installed.

With a serious and prolonged development of the infection, there is a high risk of complications. In many cases, it is not possible to save a tooth; more often, a decision is made to remove it, since it is a source of infection. When removed, drainage is carried out through the alveolus of the extracted tooth.

Another method used to treat an abscess can be described. An incision is made on the gum near the site of infection, through which drainage is carried out.

Now a laser with a low intensity of radiation is also used in treatment – its use helps to influence the problem area and perform procedures with greater comfort than with conventional methods.

During the treatment of abscesses, patients are prescribed antibiotic drugs in order to suppress the infection.

Prevention measures for dental abscess

Preventive measures for dental diseases overlap in many ways. Any diseases must be treated in a timely manner – this approach will help prevent their complications.Oral hygiene must be observed.

In case of injury to the jaw apparatus, as a result of which tooth enamel is chipped off or loosening of one or more units occurs, you should contact your dentist as soon as possible. Getting advice on time and the help provided by doctors will certainly prevent the development of infection.

Timely contact to the clinic “Center for Family Dentistry” for the treatment of tooth abscess will provide professional dental care without pain.And may your teeth be healthy!

90,000 Publications in the media

Amoebic liver abscess – abscess of the liver parenchyma caused by hematogenous dissemination Entamoeba histolytica through the portal vein in acute or recurrent intestinal amebiasis. The predominant localization is the right lobe of the liver (90% of cases).

Etiology • Causative agent – Entamoeba histolytica • 50% of patients have a history of intestinal amebiasis • The disease is endemic in tropical and subtropical regions (Africa, Southeast Asia, Mexico). Risk group – homosexuals.

Pathogenesis • Complication of acute or recurrent intestinal amebiasis • Entamoeba histolytica enters the intestine through the mouth and then through the portal vein to the liver. Pathomorphology • A single large abscess • The contents of the abscess are liquid, red-brown in color (fragments of liver tissue and products formed as a result of liver necrosis).

Clinical picture • Pain in the right hypochondrium • Hepatomegaly • Increased body temperature, but to a lesser extent than with bacterial abscesses • Pleural pain • Chills • Night sweats • Nausea, vomiting • Unproductive cough.

Laboratory data • In 75% – leukocytosis at the onset of the disease • The level of transaminases in serum is increased at the beginning of the disease, the activity of serum alkaline phosphatase (ALP) is increased in chronic course • Serological tests. The method of choice is the detection of class G immunoglobulins to Entamoeba histolytica in an enzyme-linked immunosorbent assay (ELISA; sensitivity 99%, specificity over 90%).

Special studies • Ultrasound reveals hypoechoic masses in the liver (sensitivity 75–80%) • CT is more sensitive (88–95%), but less specific than ultrasound.CT is informative for detecting small abscesses and extrahepatic lesions • Radioisotope scanning of the liver using ^99m Tc allows differentiating between bacterial (hot focus) and amoebic (cold focus) liver abscesses • The contents of the abscess are usually sterile, pathogens can be found in scrapings from the abscess wall (method not very informative)

Diagnostic tactics • Enlarged painful liver in a young man against the background of fever staying in an endemic area, detection of class G immunoglobulins to Entamoeba histolytica in the ELISA reaction, corresponding changes in ultrasound, CT and radioisotope scanning make it possible to diagnose • ELISA in case a negative result must be repeated after 1 week.

Differential diagnosis • Bacterial liver abscess • Liver cyst • Hemangioma • Tumors.

Treatment • Restriction of physical activity in the first days of the illness • General table • The drug of choice – metronidazole 750 mg 3 r / day for 10 days • In case of metronidazole intolerance or ineffectiveness for 5 days – chloroquine 500 mg / day in for 2 days, then 250 mg / day for 3 weeks • If conservative therapy is ineffective for 3-5 days, puncture of the abscess cavity under the control of ultrasound or CT with aspiration of the contents is shown share.

Complications • Breakthrough of an abscess into the pleural cavity and lung leads to the development of empyema, hepatobronchial fistula, lung abscess • Breakthrough of an abscess into the peritoneal cavity leads to the development of peritonitis • An abscess of the left lobe can break into the pericardial cavity, which, as a rule, leads to death …

Prevention • Monitoring the condition of water and food.

Course and prognosis – mortality up to 5%, due to the development of complications.

MKB-10 • A06.4 Amoebic liver abscess.

90,000 symptoms and removal at the Star clinic

An abscess on the gums is a swelling caused by purulent inflammation. There can be two reasons for the development of such a state:

1. Infectious process localized at the apex of the tooth root;
2. Inflammation of the gums with periodontitis or traumatic injury.

Clinical signs

The main symptoms of gum abscess are swelling and soreness.Depending on the severity of the condition and the cause of the development of the abscess, the clinical symptoms are somewhat different. Additional signs may be swelling of the cheeks and lips, the presence of a fistula with purulent or cloudy discharge. An increase in body temperature is often noted.

Inflammation caused by a complication of caries or poor-quality root canal treatment develops gradually, may be asymptomatic for a certain time or be characterized by slight pain when biting.Aggravation of the process is manifested by constant pain and swelling of the gums.

If the cause of the gum abscess was an inflammatory process caused by periodontitis, then the symptoms are usually less pronounced. There is a swollen gum that bleeds easily when brushing teeth. Pus may be discharged from the gingival groove.

Treatment methods

Therapeutic tactics depends on the cause that caused the development of the abscess, and consists in ensuring the outflow of purulent contents, as well as eliminating the source of infection.Removal of an abscess on the gum after opening it can include both conservative treatment methods and surgical intervention. Complex impact is often used, which consists of

• carrying out anti-inflammatory measures;
• antibiotic therapy;
• Root canal filling or re-filling;
• resection of the apex of the tooth root.

In case of periodontitis, the treatment tactics for removing an abscess on the gums consists in removing dental plaque, anti-inflammatory therapy, and performing surgical curettage.

Any purulent focus localized in the oral cavity is dangerous by further spread and involvement of nearby tissues in the process, the development of osteomyelitis, phlegmon, damage to the sinuses and meninges. When the first signs of the disease appear, it is necessary to seek qualified help from a dentist, who will clarify the pathology and conduct appropriate treatment.

In Zelenograd, any type of dental care can be obtained at the Star clinic, which is the Innovation Center of the Russian Dental Association.Thanks to the high professionalism of specialists, excellent material and technical base, the impeccable quality of all types of services is guaranteed here.

You can make an appointment by phone. +7 (495) 023-17-71

Treatment of Periodontal Abscesses – STOMWEB.RU

Author: Philip R. Melnick and Henry H. Takei

ABSCESS CLASSIFICATION

Periodontal abscess is a localized purulent inflammation of the periodontal tissues.It was divided into three diagnostic groups: gingival abscess, periodontal abscess, and pericoronal abscess. Gingival abscess includes marginal gingival and interdental tissues. Periodontal abscess is an infection that comes into contact with a periodontal pocket and can lead to destruction of the periodontal ligament and alveolar bone. Pericoronal abscess associated with the crown of a partially erupted tooth.

Periodontal Abscess

Periodontal abscess usually occurs in patients with untreated periodontitis and in association with periodontal pockets of moderate depth.Periodontal abscesses often occur as exacerbations of an existing pocket (Fig. 42-1).

Figure 42-1 A. Deep furcation defects are a common site of a periodontal abscess. B. The anatomy of furcations often interferes with complete removal of calculus and microbial plaque.

First of all, associated with incomplete removal of calculus, periodontal abscesses have been associated with a number of clinical situations. They have been identified in patients after periodontal surgery, after supportive prophylaxis (Figure 42-2), after systemic antibiotic therapy, and as a result of recurrent disease.

Figure 42-2. Periodontal abscess after preventive measures, caused by partial healing of the periodontal pocket over the remaining calculus.

Conditions in which a periodontal abscess is not associated with inflammatory periodontal disease include perforations or fractures of the teeth (Figure 42-3) and foreign body retention.

Figure 42-3 A, Found a fistulous tract in the attached gingiva in the region of the right maxillary canine.B, A detached flap shows the cause – a root fracture.

Poorly controlled diabetes mellitus is considered a predisposing factor for the formation of a periodontal abscess (Fig. 42-4).

Figure 42-4 Localized periodontal abscess in the right canine of the lower jaw of an adult male with poorly controlled type 2 diabetes. Some patients have pho

A chronic abscess is … What is a chronic abscess?

Chronic abscess

Abscess, proceeding slowly, with little expressed general and local symptoms of purulent inflammation; occurs with some infectious diseases (tuberculosis, actinomycosis, etc.) or with the penetration of low-virulent pathogens of purulent infection.

1. Small Medical Encyclopedia. – M .: Medical encyclopedia. 1991-96 2. First aid. – M .: Great Russian Encyclopedia. 1994 3. Encyclopedic Dictionary of Medical Terms. – M .: Soviet encyclopedia. – 1982-1984

• Cold abscess
• Abscess Chitelli

See what “Chronic abscess” is in other dictionaries:

• chronic abscess – (a.chronicus) A., proceeding slowly, with little expressed general and local symptoms of purulent inflammation; occurs with some infectious diseases (tuberculosis, actinomycosis, etc.) or with the penetration of low-virulent pathogens purulent … … Big Medical Dictionary

• Chronic lung abscess – long-term suppurative process, which is the outcome of an acute abscess. Symptoms and course. Chronic lung abscess proceeds with exacerbations and improvements.During remission, complaints of cough with a small amount of sputum, sometimes … Disease Handbook

• Lung abscess – Lung abscess … Wikipedia

• LUNG ABSCESS – honey. Lung abscess An abscess localized within the pulmonary parenchyma. Divided into acute and chronic (duration more than 2 months). Localization: more often the posterior segment of the upper lobe (S2), the upper segment of the lower lobe (S6). Etiology • Contact … … Disease Handbook

• Abscess of the brain – Abscess of the brain … Wikipedia

• Chronic pancreatitis – ICD 10 K86.086.0 K86.186.1 ICD 9 577.1 … Wikipedia

• Lung abscess – Lung abscess Picture of lung abscess on computed tomography. A cavity is visible in the lung tissue. ICD 10 J … Wikipedia

• Lung abscess – Lung abscess Picture of lung abscess on computed tomography. A cavity is visible in the lung tissue. ICD 10 J … Wikipedia

• Lung abscess – Lung abscess Picture of lung abscess on computed tomography.A cavity is visible in the lung tissue. ICD 10 J … Wikipedia

• BRAIN ABSCESS – honey. Brain abscess is a delimited accumulation of pus in the brain that occurs secondarily in the presence of a focal infection outside the central nervous system; the simultaneous existence of several abscesses is possible. May occur as a complication of injuries … Disease Handbook

• SOFT TISSUE ABSCESS – honey. A soft tissue abscess is a cavity filled with pus and delimited from the surrounding tissues by a pyogenic membrane, localized in the subcutaneous tissue, muscles.