Case Based Pediatrics For Medical Students and Residents
Department of Pediatrics, University of Hawaii John A. Burns School of Medicine
Chapter X.11. Abscesses
Myrna I. Kuo
March 2003

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This is a 4 year old boy who presents to the hospital with a chief complaint of a painful lump in his neck. He has been complaining of progressively worse pain in his ear for the past few days, but now comes to the office because of the development of the neck mass. He has been given acetaminophen for pain relief. He has otherwise been a healthy child and attends pre-school.

Exam: VS T 37.0, P 100, RR 25, BP 100/60, oxygen saturation 99% in room air. He is alert and active, in no distress. He is not toxic and not irritable. Head and eye exam are normal. His right tympanic membrane is bulging and purulent. His left tympanic membrane is normal. His neck exam demonstrates a fluctuant mass on the right side with overlying cellulitis (redness). His mouth exam shows a normal pharynx, mucosa and good dentition. Heart, lung and abdomen exams are normal. He ambulates normally and no neurological deficits are noted. His color and perfusion are good.

A CBC is obtained which shows WBC 12.0, 60% segs, 15% bands. The neck mass is aspirated with an 18 gauge needle for 3 cc's of thick pus. A gram stain of this shows many gram positive cocci. Clindamycin is prescribed and he is seen in follow-up the next day. The culture is positive for Staph aureus. The neck mass continues to enlarge, so he is hospitalized for further management. A surgeon is consulted who performs an incision and drainage. Entry of the abscess cavity reveals thick pus with loculations which does not drain easily so the incision is enlarged and a gauze drain is placed within the cavity. The staph aureus is determined to be methicillin resistant, but sensitive to clindamycin and vancomycin. He is continued on IV clindamycin and he is discharged from the hospital two days later to continue oral clindamycin as an outpatient. The gauze drain is removed three days after the initial incision. The abscess cavity gradually closes and shrinks.

Abscesses are focal collections of purulent material, usually due to bacterial infection, that are contained within a tissue, organ or confined space. Organisms may reach the tissue through various pathways including direct implantation by a foreign object, contiguous spread from an adjacent locus of infection, dissemination via lymphatics or hematogenous routes, and contamination of sterile tissue by normal flora (e.g., perforation of viscera into the abdomen) (1). As an abscess forms, there is an accumulation of necrotic white cells and tissue cells in the center of the abscess surrounded by a layer of preserved neutrophils and a second layer of dilated vessels and fibroblasts. Without spontaneous or surgical drainage, an abscess occasionally resolves slowly after proteolytic digestion of the pus producing a thin, sterile fluid that is resorbed into the bloodstream. Incomplete resorption leaves a cystic loculation within a fibrous wall, where calcium salts sometimes precipitate to form a calcified mass (2). More often, the abscess remains and becomes walled off by a capsule of connective tissue. Risk factors for abscess formation are immunosuppression, the presence of foreign bodies, obstruction to normal drainage of a visceral tract (e.g., respiratory, biliary, or a sweat gland as in acne), areas of low oxygen tension and stasis (e.g., ischemic tissue or hematomas), and trauma (1).

The symptoms associated with abscess formation vary depending on what organ is affected. For superficial or cutaneous and subcutaneous abscesses there is heat, swelling, tenderness, erythema over the affected site, and sometimes fever. Chronic or subacute deep abscesses present more often with local pain, tenderness, and systemic symptoms such as fever, anorexia, weight loss, and fatigue (1). Abscesses can lead to serious complications such as bacteremia, rupture into neighboring tissue, bleeding by erosion into nearby vessels, impaired function of the affected organ or systemic effects. Prompt treatment is generally preferable, but most abscesses are subacute, in that they have often formed over several days or longer. In general, treatment for abscesses is similar regardless of location. For superficial abscesses, incision and drainage with or without antibiotics is indicated. Treatment of a deep-seated abscess consists of drainage and antibiotics active against the responsible bacteria. Without sufficient drainage, antibiotics are ineffective, because the necrotic center of abscesses are not vascularized (i.e., no antibiotic is delivered to organisms within the abscess). Adequate drainage consists of thoroughly removing pus, necrotic tissue, and debris. To prevent reformation of the abscess, loculations (fibrous strands) must be broken and drainage must be permitted to continue. A gauze wick can be used to maintain the patency of the incision site so that fluid within the abscess can continue to drain out of the cavity. Without a wick or drain to keep the cavity open, the incision site will close and fluid will collect within the cavity causing a recurrence of the abscess. Dead space within the cavity can be eliminated by packing with gauze. The leading end of the gauze packing wick is advanced daily to reduce the size of the abscess cavity as it closes. Predisposing conditions, such as obstruction of a duct or the presence of a foreign body, should be corrected or eliminated if possible. Gram stains and cultures followed by susceptibility studies of isolates obtained from the abscess provide a guide to antimicrobial therapy (1).

Each organ is associated with common microbes, with slight differences in pathogenesis and treatment. Some of the more common locations such as brain, lung, liver, neck, pilonidal, and perirectal will be touched upon in this chapter. Additional areas of abscess formation include abdominal, retropharyngeal, peritonsillar, tubo-ovarian, and osteomyelitis Brodie abscesses. These have been covered in other chapters.


Cervical lymphadenopathy, which is defined as enlargement of the cervical lymph nodes due to viral infection or bacterial infections that drain to lymph nodes, is the most common reason for neck masses in children. Up to 90% of children between the ages of 4 and 8 years can have cervical adenopathy without obvious associated infection or systemic illness. Cervical lymphadenopathy should resolve as the primary infection resolves.

Cervical lymphadenitis, on the other hand, occurs when acute infection is present within the lymph node. Acute bilateral cervical lymphadenitis is often due to viral infection, while acute unilateral cervical lymphadenitis is usually due to bacteria. Cervical lymphadenitis and abscess formation commonly occur in children under 5 years old (3). It often follows an upper respiratory illness, pharyngitis, tonsillitis, or otitis media. The bacteria spread from their initial sites of infection to the lymph nodes in the neck. If not contained by the child's immune system, they multiply within the node and evoke an inflammatory response (3). Up to 80% of cervical lymphadenitis is caused by S. aureus and group A streptococci. Less common organisms include anaerobic bacteria (from periodontal disease), H. influenzae, Yersinia pestis, gram-negative bacilli, Francisella tularensis, Actinomyces, and Mycobacterium (3,4). S. aureus is more likely to form an abscess, whereas group A streptococci usually form a general cellulitis or more commonly, a simple reactive lymphadenitis. Bacterial cervical lymphadenitis presents with firm, tender, and warm lymph nodes. Fever may or may not occur. Treatment includes antibiotics and warm soaks. If left untreated, these nodes may become fluctuant with regional cellulitis (3). Needle aspiration should be done on fluctuant masses, and antibiotic treatment should empirically cover Staph aureus, with subsequent therapy based on culture and sensitivity results. If resolution does not occur after needle aspiration and antibiotics, incision and drainage should be done (3). Some would argue that needle aspiration is merely used as a diagnostic test to determine if an abscess is present. Once an abscess is identified by needle aspiration, then incision and drainage should immediately follow.


Cutaneous abscesses primarily form as a result of minor trauma to the skin. The bacterium most frequently involved is S. aureus. Normal skin flora is also commonly involved. The presenting signs are a painful, fluctuant mass that is erythematous and indurated with overlying cellulitis. High fevers may indicate systemic infection and should prompt a more in-depth evaluation. Treatment consists of application of local anesthetic, followed by incision and drainage with probing to remove loculations, irrigating the cavity with saline and sometimes packing with gauze. Because abscess drainage is often very painful and local anesthetics do not penetrate necrotic tissue well, general and regional anesthesia may sometimes be preferable. Elliptical incisions are preferred because they keep the wound from prematurely closing. Applying warm compresses twice a day after drainage is usually recommended. Antibiotic treatment is often used, but it is usually unnecessary (1).

Pyomyositis with subsequent skeletal muscle abscess formation is due to S. aureus in greater than 80% of cases. The accumulation of pus is always intramuscular initially and is not secondary to infection of adjacent skin, soft tissue, or bone. It often occurs after a penetrating wound, prolonged vascular insufficiency in an extremity, or a contiguous infection (5). Often termed tropical myositis due to its geographic distribution, pyomyositis can also be found, though less commonly, in temperate climates. Patients present with fever, chills, malaise, and pain and swelling in the muscle involved (usually large skeletal muscles such as the thigh, psoas and buttocks) (6). The pathogenesis of muscle abscess formation is not clear. One hypothesis is that migrating helminth larvae damage tissue, making it susceptible to bacteria of hematogenous origin or carried by the worm. Treatment of the abscess requires surgical drainage and appropriate antibiotic coverage (usually vancomycin, clindamycin or an anti-staphylococcal penicillin). If group A streptococcus is cultured from a smear of the pus, treatment should be switched to penicillin. Continued fever after drainage and antibiotics may indicate other untreated foci of abscess. A complication of pyomyositis is compartment syndrome (especially when in the anterior tibial compartment), which may require additional treatment including additional surgical drainage, fasciotomy, and debridement (5).


Brain abscesses result from direct extension of cranial infections (e.g., osteomyelitis, sinusitis), from penetrating head wounds, or from hematogenous spread (e.g., bacterial endocarditis, bronchiectasis, congenital heart disease with right-to-left shunt, or IV drug abuse) (7). An abscess in the frontal lobe is often caused by extension from sinusitis or orbital cellulitis, whereas abscesses located in the temporal lobe or cerebellum are frequently associated with chronic otitis media and mastoiditis. Abscesses resulting from penetrating injuries tend to be singular and caused by S. aureus, whereas those resulting from septic emboli, congenital heart disease, or meningitis often have several organisms (8). Bacteria frequently involved include: S. aureus, streptococci (viridans, pneumococci, microaerophilic), anaerobic organisms (gram-positive cocci, Bacteroides, Fusobacterium, Prevotella, Actinomyces, Clostridium) and gram-negative aerobic bacilli (enteric rod, Proteus, Pseudomonas, Citrobacter diversus, and Haemophilus). One organism is cultured from the majority of abscesses (70%), two from 20%, and three or more in 10% of cases. Abscesses due to sinusitis often involve anaerobic bacteria. Once the infection extends into the brain parenchyma, it is encapsulated by glial cells and fibroblasts, forming an abscess (7). The abscess results in increased intracranial pressure, causing symptoms similar to tumors such as headache, vomiting, papilledema, seizures, personality changes, focal neurological deficits, and hemiplegia. Brain abscesses are often fatal unless treated. Treatment consists of prompt administration of appropriate antibiotics: penicillin (for streptococci and anaerobes), metronidazole (for bacteroides), a 3rd generation cephalosporin (for Enterobacteriaceae), vancomycin (for S. aureus infection due to cranial trauma or endocarditis) (7). Clindamycin may also be used for anaerobes and synergistic efficacy with other antibiotics. In many cases, aspiration and drainage of brain abscesses are necessary. Response to antibiotics should be followed by serial CT or MRI scans for a minimum of 4 to 8 weeks. The duration of antibiotic treatment is often about 4 to 6 weeks.


Hepatic abscesses can be divided into two broad categories, pyogenic and amebic. Pyogenic hepatic abscesses are uncommon in immunocompetent individuals, but can occur in immunocompromised persons (9). Biliary tract disease and obstruction, abdominal infections via the portal vein or contiguous spread, and generalized sepsis are usually responsible. However, in up to one half of cases, no definite cause can be found (10). The right lobe is most often infected. Many bacteria are involved in liver abscesses, most commonly S. aureus, E. coli, Salmonella, Klebsiella, Proteus, Pseudomonas, enterococcus and anaerobic organisms (11). Patients may have either an acute or subacute presentation. Acutely, they may experience high fever and chills, RUQ pain, nausea and vomiting (9). Less commonly, once the abscess is encapsulated, the patient may only manifest dull pain over an enlarged liver which is tender to percussion (9). Jaundice is uncommon. Treatment consists of adequate antibiotic coverage and percutaneous drainage. Triple antibiotic coverage with an aminoglycoside or third-generation cephalosporin (gram-negative coverage) plus metronidazole or clindamycin for anaerobes and ampicillin (for streptococcal species) should be used (9).

Amebic abscess occurs by fecal-oral transmission of Entamoeba histolytica, usually involving ingestion of contaminated food or water. Amebae reach the liver after invasion of the intestinal mucosa and enter the liver via the portal vein. The acute presentation is similar to pyogenic hepatic abscess (9). Treatment consists of one week of metronidazole. Most patients will recover with metronidazole alone and percutaneous catheter drainage is only required in complicated cases.


Lung abscesses are usually due to aspiration (e.g., during coma, obtunded from alcohol or other drugs, CNS disease, general anesthesia), bronchial obstruction, periodontal disease, infection secondary to lung infarction or complications of pneumonia. Many different bacteria are responsible for lung abscess. Lung abscess due to aspiration are typically normal flora of the GI tract (anaerobes) (12). Virulent organisms (e.g., S. aureus), cystic fibrosis, or endotracheal intubation may cause failure of microbial clearance mechanisms resulting in bronchial obstruction and abscess formation (13). Lung abscess caused by periodontal disease contain normal anaerobic nasopharyngeal flora. Pneumonia due to Klebsiella, S. aureus, Actinomyces, beta-hemolytic streptococcus, Streptococcus milleri (and other aerobic or microaerophilic streptococci), Legionella, or Haemophilus influenzae can sometimes be complicated by abscess formation. In immunocompromised hosts, Nocardia, Cryptococcus, Aspergillus, phycomycetes, atypical mycobacteria or gram-negative bacilli should also be considered. Blastomycosis, histoplasmosis, and coccidioidomycosis can cause acute or chronic nonputrid lung abscesses in visitors or residents of endemic areas. Finally, pseudomonas should be considered in hospitalized patients and individuals with cystic fibrosis. Cavitary TB is not considered a lung abscess but should be included in the differential diagnosis (12).

Symptoms of a lung abscess may range from minimal fever, anorexia, and weakness, to symptoms of pneumonia, i.e., malaise, sputum-producing cough, sweats, severe prostration and temperatures of 39 to 40 degrees (102 to 104 degrees F) (12). Unless the abscess is completely encapsulated, about 50% of patients will cough up sputum that is purulent and sometimes blood-streaked. In fact, an abscess may not be suspected until it perforates into a bronchus, causing copious purulent sputum to be expectorated over the next few hours or several days. Putrid sputum is indicative of anaerobic bacteria. Chest pain suggests involvement of the pleura. Signs of a subacute or chronic abscess are months of low-grade fever, cough, weight loss and anemia (12,13). Treatment usually consists of 1 to 3 months of the following antibiotic treatments: a) clindamycin, b) penicillin with oral metronidazole, or c) antibiotics determined by sensitivity testing. Vancomycin should be added if S. aureus is suspected. Drainage by aspiration or surgery is usually not required for a lung abscess. Postural drainage may be helpful, but should be done with caution. The risk of perforation and spilling of abscess contents is potentially disastrous and unnecessary, as antibiotic treatment will usually suffice. If, however, the abscess is resistant to drugs, segmental resection or lobectomy is indicated.


Pilonidal abscesses usually occur in hirsute, adolescents. Pilonidal sinuses are common malformations in the sacrococcygeal area that may occur during embryogenesis. They are lined by stratified squamous epithelium and often asymptomatic; however, hair obstructing the sinus can lead to pilonidal cyst formation. Recurrent infection of a cyst, due to foreign body (ingrown hair) granuloma formation, often leads to pilonidal abscess. Due to its location, cultures of pilonidal abscess predominantly contain anaerobic GI flora. Common symptoms include back pain with local tenderness and induration. The abscess, however, may not be superficially obvious. Smaller abscesses only require incision and drainage, which may be done on an outpatient basis under local anesthesia. All hair and pus should be removed, and the lesion should be packed. The area should be repacked every 2 to 4 days and may take weeks to heal. The abscess cavity, however, is often large and recurrence is common. Therefore definitive treatment is removal of the cyst, sinus, and all sinus arborizations once the inflammation has passed. Antibiotics are rarely necessary (14).


There are several common locations for perirectal abscess: >45% perianal, 20% ischiorectal, 12% intersphincteric, and 7% pelvirectal (14). Perianal abscesses occur in healthy infants and adults during the fourth decade of life and more frequently in males (>2:1 ratio). Because they are commonly deep lesions, there is considerable morbidity associated with inadequate treatment of perirectal abscesses. An understanding of anal canal anatomy helps clarify the pathophysiology of perirectal abscesses. The mucosa of the anal canal is loosely attached to the muscle wall. At the dentate line, columnar epithelium transitions into squamous epithelium, and there are vertical folds of tissue called the rectal columns of Morgagni. The columns are connected at their distal end by small semilunar folds (anal valves), and under the valves are invaginations called anal crypts. The crypts contain collections of ducts from anal glands, which are mucus-secreting structures that terminate in the area between the internal and external sphincters. Most perirectal infections begin as a result of blockage and subsequent infection of the anal glands. This causes normal host defense mechanisms to break down resulting in invasion and overgrowth by bowel flora. A mixed infection of GI flora usually occurs, with E. coli, Proteus, streptococci, staphylococci, and bacteroides predominating (14). GI fistulas, inflammatory bowel diseases (Crohn's Disease), episiotomies, or any local trauma that contributes to anal gland infection, predisposes an individual to perirectal abscesses (14). Fistula formation is common in infants, resulting in recurrence of the abscess unless the fistula tract is excised surgically.

Signs and symptoms of superficial perirectal abscesses include: throbbing pain (aggravated by sitting, coughing, sneezing, and straining), swelling, induration, tenderness, and a small area of cellulitis in the perianal region. Deeper abscesses may cause systemic, toxic symptoms, but localized pain may be less severe (14,15). Small, well-defined perianal abscesses are the only perirectal infections that should be treated on an outpatient basis. Incision and drainage result in almost immediate relief of pain and resolution of the infection. However, many perianal abscesses are large and deep resulting in greater morbidity.


Intraabdominal abscesses most frequently occur as a result of GI tract perforation or inflammation (i.e., ruptured appendicitis). Therefore mostly GI flora, a combination of aerobic gram-negative bacilli (E. coli and Klebsiella) and anaerobes (Bacteroides fragilis) are involved. Symptoms of abdominal abscess include fever and minimal to severe discomfort in the area of the abscess. Anorexia, nausea, vomiting, diarrhea, constipation, and paralytic ileus may also occur. Treatment involves: 1) drainage by surgery or percutaneous catheters, and 2) antibiotics which cover all relevant organisms. Treatment regimens include: a) an aminoglycoside (gentamicin) and clindamycin, b) 3rd-generation cephalosporin and metronidazole, or c) single agent cefoxitin or cefotetan. Hospital acquired infections should also cover Pseudomonas (1).


1. True/False: Some abscesses can resolve spontaneously.

2. What is the most common organism involved in abscess formation?

3. True/False: All abscesses are treated by incision and drainage.

4. What is the rationale behind multi-drug antibiotic treatment?

5. Does a person have to be immunocompromised to develop an abscess?

6. What are the complications of untreated abscesses?


1. Chapter 155 Section 3 - Abscesses. In: Beers MH, Berkow R (eds). The Merck Manual of Diagnosis and Therapy, seventeenth edition. 1999, Whitehouse Station, NJ: Merck Research Laboratories, pp. 1135-1136.

2. Chapter 2 - Inflammation. In: MacFarlane PS, Reid R, Callander R (eds). Pathology Illustrated, fifth edition. 2000, Edinburgh: Churchill Livingstone, pp 40-41.

3. McAneney CM, Ruddy RM. Chapter 45 - Neck Mass. In: Fleisher GR, Ludwig S (eds). Textbook of Pediatric Emergency Medicine, fourth edition. 2000, Philadelphia: Lippincott Williams & Wilkins, pp383-390.

4. Peters TR, Edwards KM. Cervical Lymphadenopathy and Adenitis. Pediatrics in Review 2000;21(12):399-405.

5. Swartz M. Chapter 79 - Myositis. In: Mandell G, Bennett J, Dolin R (eds). Mandell: Principles and Practice of Infectious Diseases, fifth edition. 2000, Philadelphia: Churchill Livingstone, Inc, pp. 1058-1060.

6. Jain M. Ch 30 - Common Parasitic Diseases. In: NobleJ (ed). Noble: Textbook of Primary Care Medicine, third edition. 2001, St. Louis: Mosby, Inc, pp. 264.

7. Ch 176 Sec 14 - CNS Infections. In: Beers MH, Berkow R (eds). The Merck Manual of Diagnosis and Therapy, seventeenth edition. 1999, Whitehouse Station, NJ: Merck Research Laboratories, pp. 1440-1441.

8. Haslem R. Chapter 610 - Brain Abscess. In: Behrman R, Kliegman R, Jenson H (eds). Nelson Textbook of Pediatrics, sixteenth edition. 2000, Philadelphia: W. B. Saunders Company, pp. 1857-1858.

9. Guss D. Chapter 85 - Liver and Biliary Tract. In: Marx J, et al (eds). Rosen's Emergency Medicine: Concepts and Clinical Practice, fifth edition. 2002, St. Louis: Mosby Inc, pp. 1262-1264.

10. Maddrey W. Chapter 151 - Parasitic, Bacterial, Fungal, and Granulomatous Liver Diseases. In: Goldman L, Bennett J (eds). Goldman: Cecil Textbook of Medicine, twenty-first edition. 2000, Philadelphia: W. B. Saunders Company, pp. 797.

11. Blistereri W. Chapter 359 - Liver Disease Associated with Systemic Disorders. In: Behrman R, Kliegman R, Jenson H (eds). Nelson Textbook of Pediatrics, sixteenth edition. 2000, Philadelphia: W. B. Saunders Company, pp. 1212.

12. Ch 74 Sec 6 - Lung Abscess. In: Beers MH, Berkow R (eds). The Merck Manual of Diagnosis and Therapy, seventeenth edition. 1999, Whitehouse Station, NJ: Merck Research Laboratories, pp. 616-618.

13. Finegold S. Chapter 83 - Lung Abscess. In: Goldman L, Bennett J (eds). Goldman: Cecil Textbook of Medicine, twenty-first edition. 2000, Philadelphia: W. B. Saunders Company, pp. 439-441.

14. Blumstein H. Chapter 40 - Incision and Drainage. In: Roberts J, Hedges J (eds). Roberts: Clinical Procedures in Emergency Medicine, third edition. 1998, Philadelphia: W. B. Saunders Company, pp. 635-636, 647-651.

15. Ch 35 Sec 3 - Anorectal Disorders. In: Beers MH, Berkow R (eds). The Merck Manual of Diagnosis and Therapy,

16. Malley R. Chapter 44 - Lymphadenopathy. In: Fleisher GR, Ludwig S (eds). Textbook of Pediatric Emergency Medicine, fourth edition. 2000, Philadelphia: Lippincott Williams & Wilkins, pp. 375-382.

17. Ch 112 Sec 10 - Bacterial Infections of the Skin. In: Beers MH, Berkow R (eds). The Merck Manual of Diagnosis and Therapy, seventeenth edition. 1999, Whitehouse Station, NJ: Merck Research Laboratories, pp. 793-795.

18. Pena A. Chapter 344 - Surgical Conditions of the Anus, Rectum and Colon. In: Behrman R, Kliegman R, Jenson H (eds). Nelson Textbook of Pediatrics, sixteenth edition. 2000, Philadelphia: W. B. Saunders Company, pp. 1182.

19. Meislin H, Guisto J. Chapter 131 - Soft Tissue Infections. In: Marx J, et al (eds). Rosen's Emergency Medicine: Concepts and Clinical Practice, fifth edition. 2002, St. Louis: Mosby Inc. pp. 1949-1951.

Answers to questions

1. True

2. Staph aureus

3. False, lung abscesses are not.

4. Abscesses are often mixed infections, therefore antibiotic treatment needs to provide adequate coverage of the common bacteria associated with that type of abscess. Some antibiotics (notably clindamycin) may provide synergistic efficacy as well.

5. No

6. Bacteremia, rupture into neighboring tissue, bleeding by erosion into nearby vessels, impaired function of the affected organ or systemic effects such as cachexia and anorexia.

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