SUBPHARYNGEAL ABSCESS. PHLEGMON OF THE FLOOR OF THE MOUTH, TONGUE AND NECK, SORE THROAT ZHANSUL-LUDWIG. COMPLICATION AND THEIR PREVENTION. TREATMENT PRINCIPLES OF THE MFA INFLAMMATORY PROCESSES.

Retropharyngeal Abscess

Background

Retropharyngeal abscess (RPA) produces the symptoms of sore throat, fever, neck stiffness, and stridor. Retropharyngeal abscess occurs less commonly today than in the past because of the widespread use of antibiotics for suppurative upper respiratory infections. The incidence of RPA in the United States is rising, however. Retropharyngeal abscess, once almost exclusively a disease of children, is observed with increasing frequency in adults. Retropharyngeal abscess poses a diagnostic challenge for the emergency physician because of its infrequent occurrence and variable presentation.

Early recognition and aggressive management of retropharyngeal abscess are essential because it still carries significant morbidity and mortality.

Pathophysiology

The retropharyngeal space is posterior to the pharynx, bound by the buccopharyngeal fascia anteriorly, the prevertebral fascia posteriorly, and the carotid sheaths laterally. It extends superiorly to the base of the skull and inferiorly to the mediastinum.

Abscesses in this space can be caused by the following organisms:

• Aerobic organisms, such as beta-hemolytic streptococci and Staphylococcus aureus

• Anaerobic organisms, such as species of Bacteroides and Veillonella

• Gram-negative organisms, such as Haemophilus parainfluenzae and Bartonella henselae

The high mortality rate of retropharyngeal abscess is owing to its association with airway obstruction, mediastinitis, aspiration pneumonia, epidural abscess, jugular venous thrombosis, necrotizing fasciitis, sepsis, and erosion into the carotid artery.

Epidemiology

Frequency

United States

A review of cases of RPA over an 11-year period at the Children’s Hospital of Michigan revealed a 4.5-times increase in the incidence of RPA when compared with the previous 12 years.^[1] A more recent review at the same hospital reveals that the incidence has increased 2.8-fold over the past 6 years when compared with the previous 11 years.^[2]

In the United States, in 2003, a review of the Kids’ Inpatient Database (KID) revealed 1321 pediatric admissions with retropharyngeal abscess.

An 11-year chart review of 162 pediatric patients with retropharyngeal abscess at St. Louis Children’s Hospital revealed that the number of RPA cases in children increased significantly from 1995 to 2006.

International

A review of deep neck infections (DNI) in children over a 12-year period at a medical center in Taiwan revealed 50 children with DNI. Nine children had DNI in the retropharyngeal space, 17 in the parapharyngeal space, 21 in the peritonsillar region, and 3 were mixed.

A review of RPAs and parapharyngeal abscesses (PPAs) in children presenting to 2 pediatric tertiary care medical centers in Israel over an 11-year period revealed 39 children with RPA or PPA. The incidence increased during the course of the study.^[6]

A retrospective analysis of children diagnosed with RPA and PPA over a 9-year period in a tertiary care medical center in Spain revealed 17 children with RPA, 11 with PPA, and 3 with both.^[7]

Mortality/Morbidity

Once mediastinitis occurs, mortality approaches 50%, even with antibiotic therapy. Retropharyngeal abscess can also cause internal jugular vein thrombosis, carotid artery erosion, pericarditis, and epidural abscess. In addition to invasion of contiguous structures, retropharyngeal abscess can cause sepsis and airway compromise.

Overall mortality rate was 1% in a review of deep cervical space infections in Taiwan.^[8]

In a study of 234 adults with deep space infections of the neck in Germany, the mortality rate was 2.6%. The cause of death was primarily sepsis with multiorgan failure.^[9]

In the United States, in 2003, a review of the Kids’ Inpatient Database (KID) revealed 1321 pediatric admissions with RPA, with no fatalities.^[3]

A case series from Children’s National Medical Center in Washington DC presents 4 children of ages ranging from 8 months to 18 months with RPA who developed mediastinitis. All 4 were treated aggressively with antibiotics and surgical drainage of RPA, and 3 patients required thoracoscopic debridement. All 4 children survived without sequelae.^[10]

Race

• In a 10-year review of retropharyngeal abscess cases treated at Kings County Hospital in Brooklyn, New York, 70% of patients were African American, 25% were white, and 5% were Hispanic.

• A study of pediatric patients with retropharyngeal abscess at Wayne State University in Detroit revealed 43% of cases occurred in blacks, 54% in whites, 1% in Hispanics, and 1% in biracial.^[11]

• In the United States, in 2003, a review of the Kids’ Inpatient Database (KID) revealed 1321 pediatric admissions with retropharyngeal abscess, of which 37.4% were white, 11.7% were African American, 11.1% were Hispanic, 2% were Asian, 3.8% were other races, and the race was not recorded in the rest of the patients.^[3]

Sex

Retropharyngeal abscess is more common in males than in females, with generally reported male preponderance of 53-55%.

• Children’s Hospital of Michigan reports 54% of cases of RPA in males in a 2012 study.^[2]

• A study of children with retropharyngeal abscess in Toronto reported 67% of cases in males.

• A study of retropharyngeal abscess in children in Detroit found 56% of cases in males.^[11]

• A study of adults with deep space infections of the neck in Germany revealed that 56% of patients were male and 44% were female.^[9]

• A study of cases in Nigeria found a male-to-female ratio of 1:1.^[12]

• In the United States, in 2003, a review of the Kids’ Inpatient Database (KID) revealed 1321 pediatric admissions with retropharyngeal abscess, of which 63% were male.^[3]

Age

Initially, retropharyngeal abscess was thought to be a disease limited to children, but now it is being encountered with increasing frequency in adults.

• A review of adults with deep space infections of the neck in Germany revealed a mean age (±standard deviation) of 44.5 (±21.8) years.

• A review of retropharyngeal abscess cases at the Hospital for Sick Children in Toronto revealed that 66% of pediatric cases occurred in children younger than 6 years.

• A review of 30 cases of retropharyngeal abscess over an 11-year period in Nigeria found the median age to be 21 months, and 77% of patients were younger than 5 years. Eighty-three percent of retropharyngeal abscesses occurred in children, and 17% occurred in adults.^[12]

• A 10-year review at Kings County Hospital in Brooklyn, New York, revealed that 30% of the cases were in pediatric patients aged 16 months to 8 years and 70% were in adults aged 21-64 years.

• A 35-year review of cases involving children who were treated for retropharyngeal abscess at the Children’s Hospital of Los Angeles revealed that 50% of patients were younger than 3 years and 71% were younger than 6 years.

• A review or retropharyngeal abscess in children in Detroit found a mean age of 4.1 years, with a range from 2 months to 18 years.

• A review in Sydney, Australia, found that, in 55% of pediatric cases of retropharyngeal abscess, the children were younger than 1 year, with 10% diagnosed in the neonatal period.

• A review of RPA cases in children in Albuquerque revealed a median age of 36 months, with 75% of patients younger than 5 years and 16% of patients younger than 1 year.^[13]

• In the United States, in 2003, a review of the Kids’ Inpatient Database (KID) revealed 1321 pediatric admissions with retropharyngeal abscess, with an average age of 5.1 years (SD, 4.4).^[3]

• An 11-year chart review of 162 pediatric patients with retropharyngeal abscess at St. Louis Children’s Hospital revealed an average age of 4.9 years (range, 6 d to 17 y).^[4]

• A 5-year review of 11 children with parapharyngeal abscess in Portugal revealed an average age of 3.3 years (range, 0-12 y).^[14]

• A 12-year retrospective review of 50 pediatric patients with deep neck infections in Taipei revealed that all of the retropharyngeal abscesses occurred in children younger than 10 years.

Retropharyngeal Abscess Clinical Presentation

History

History is variable, depending on the age group. Symptoms of retropharyngeal abscess are different for adults, children, and infants.

• Symptoms in adults

• Sore throat

• Fever

• Dysphagia

• Odynophagia

• Neck pain

• Dyspnea

• Symptoms in children older than 1 year

• Sore throat (84%)

• Fever (64%)^[14]

• Neck stiffness (64%)^[14]

• Odynophagia (55%)^[14]

• Cough

• Symptoms in infants

• Fever (85%)

• Neck swelling (97%)

• Poor oral intake (55%)

• Rhinorrhea (55%)

• Lethargy (38%)

• Cough (33%)

Physical

Patients with retropharyngeal abscess may present with signs of airway obstruction, but often they do not. Individuals who do not exhibit signs of airway obstruction initially may progress to airway obstruction. The most common presenting signs may be different for adult and pediatric patients.

• Physical signs in adults

• Posterior pharyngeal edema (37%)

• Nuchal rigidity

• Cervical adenopathy

• Fever

• Drooling

• Stridor

• Physical signs in infants and children

• Cervical adenopathy (36%)^[14]

• Retropharyngeal bulge (55%; do not palpate in children)^[14]

• Fever (64%)^[14]

• Stridor (3%)

• Torticollis (18%)

• Neck stiffness (64%)^[14]

• Drooling (22%)

• Agitation (43%)

• Neck mass (55%)^[14]

• Lethargy (42%)

• Respiratory distress (4%)

• Associated signs including tonsillitis, peritonsillitis, pharyngitis, and otitis media

 

Causes

Retropharyngeal abscess develops secondary to lymphatic drainage or contiguous spread of upper respiratory or oral infections. Pharyngeal trauma from endotracheal intubation, nasogastric tube insertion,^[16] endoscopy, foreign body ingestion, and foreign body removal may cause a subsequent retropharyngeal abscess. Patients who are immunocompromised or chronically ill, such as persons with diabetes, cancer, alcoholism, or AIDS, are at increased risk for retropharyngeal abscess.

The most common organisms causing retropharyngeal abscesses include aerobes and anaerobes; gram-negative organisms also may be observed. Often, mixed flora are cultured. The incidence of RPA caused by methicillin-resistant Staphylococcus aureus (MRSA) is increasing.^[2]

• Organisms causing retropharyngeal abscess in adults^[17]

• Beta-hemolytic streptococci

• Streptococcus viridans

• S aureus

• Methicillin-resistant Staphylococcus aureus ( MRSA)^[18]

• Klebsiella pneumoniae

• Bacteroides species

• Staphylococcus epidermidis

• Anaerobic streptococci

• Bartonella henselae

• Eikenella corrodens

• Escherichia coli

• Prevotella species

• Mycobacterium tuberculosis^[19]

• Actinomycetes^[20]

• Cryptococcus neoformans^[21]

• Organisms causing retropharyngeal abscess in children

• S aureus^[11]

• MRSA^{[2, 22, 23, 18]}

• Haemophilus species

• Beta-hemolytic streptococcus (Streptococcus pyogenes)^[11] – The incidence is increasing (54%), according to review of cases at the Children’s Hospital of Michigan.^[1]

• Bacteroides species

• Peptostreptococcus species

• Fusobacterium species

• Prevotella species

• Staphylococcus coagulase negative

• Brucella species

Retropharyngeal Abscess Differential Diagnoses

Differential Diagnoses

• Angioedema

• Dental, Infections

• Epidural and Subdural Infections

• Epiglottitis, Adult

• Esophagitis

• Foreign Bodies, Gastrointestinal

• Foreign Bodies, Trachea

• Kawasaki Disease

• Mediastinitis

• Meningitis

• Mononucleosis

• Otitis Media

• Pediatrics, Croup or Laryngotracheobronchitis

• Pediatrics, Epiglottitis

• Pediatrics, Fever

• Pediatrics, Foreign Body Ingestion

• Pediatrics, Meningitis and Encephalitis

• Pediatrics, Otitis Media

• Pediatrics, Pharyngitis

• Pediatrics, Pneumonia

• Peritonsillar Abscess

• Pharyngitis

• Pneumonia, Bacterial

• Sinusitis

• Torticollis

• Toxicity, Caustic Ingestions

 

Retropharyngeal Abscess Workup

Laboratory Studies

• Complete blood count

• The mean white blood cell (WBC) count in one study was 17,000, with a range of 3100-45,900.

• WBC counts in 18% of the patients were less than 8000; thus, a normal WBC count does not rule out the diagnosis of retropharyngeal abscess.

• In a study in Germany, the mean WBC (±standard deviation was 14,700 [±10,500]), with a range from 200-114,000.

• Blood cultures are indicated before administration of intravenous antibiotics, but culture results may be negative in as many as 82% of retropharyngeal abscess cases.

• A culture of pus, aspirated at the time of surgical drainage of the retropharyngeal abscess, can grow one or more organisms 91% of the time.

• C-reactive protein

• In one study of adults and children with deep cervical space infections, patients with C-reactive protein level greater than 100 had longer hospital stays.

• In a German study, mean (±standard deviation) C-reactive protein level was 15.7 (±12.9), with a range from 0.0-74.

• A study in Taiwan reveals that deep neck infection patients with C-reactive protein values greater than 100 tend to develop complications and have prolonged hospitalizations.

Retropharyngeal Abscess Workup

Imaging Studies

• Lateral neck radiography

• Widening of the retropharyngeal soft tissues was observed in 88% of patients with retropharyngeal abscess in a series that defined soft tissue swelling as more than 7 mm at C2 and more than 14 mm at C6. Most authors define retropharyngeal soft tissue swelling as more than 7 mm at C2 and more than 22 mm at C6; thus, lateral neck radiographs may be considerably less sensitive for detecting retropharyngeal abscess than this study indicates.

• Generally, the anteroposterior diameter of the prevertebral soft tissue space in children should not exceed that of the contiguous vertebral bodies.

• In addition to showing widening of the prevertebral space, the lateral neck radiograph rarely may show a gas-fluid level, gas in the tissues, or a foreign body.

• A hospital in Ireland reports a case series of 3 children with RPA who had negative lateral soft tissue neck x-ray films. Diagnosis was made using CT scan in all 3 cases.

A 5-year-old boy presented to the ED with 2 days of neck pain and fever but with no sore throat. The child had vomited once, and the mother reported that he was irritable. The child’s temperature was 101.7° F, pulse was 118 beats per minute, respirations were 24 per minute, and blood pressure was 122/65 mm Hg. A decreased range of motion of the neck and a right anterior cervical node were observed; the child refused to swallow. Lateral neck radiographic findings show increased retropharyngeal space (white arrow). The CT scan did not demonstrate an abscess. The child was seen by an ear, nose, and throat specialist; he was admitted and started on intravenous clindamycin. He improved for 2-3 days and then worsened. Repeat neck CT scan findings demonstrated a retropharyngeal abscess. Incision and drainage was performed in the operating room. Cultures of the pus grew group A beta-hemolytic streptococci and alpha-streptococci, both sensitive to clindamycin. He improved and was discharged on the tenth hospital day on oral clindamycin.

•   An 8-month-old infant boy presented with fever and a stiff neck. According to the mother, the baby was not moving his neck as much as usual. The mother also reported decreased oral intake. His temperature was 100° F, pulse was 104 beats per minute, respirations were 48 per minute, oxygen saturation was 98% (room air [RA]). The left tympanic membrane (TM) was inflamed and nonmobile. Left submandibular and left postauricular nodes were noted. The lateral neck radiograph shows increased retropharyngeal space. The CT scan demonstrated a small retropharyngeal abscess. The WBC count was 26,000 (24 polymorphonuclear leukocytes [P], 5 bands [B], 63 lymphocytes [L], 8 monocytes [M]). The baby was examined by an ear, nose, and throat specialist; he was admitted and started on intravenous clindamycin. He improved over the next few days and was discharged on the fifth hospital day on oral clindamycin with a plan for repeat CT scans of the neck on an outpatient basis.

  CT scan of the neck

• 
  
  A CT

  scan of the neck with intravenous contrast is very useful in the diagnosis and management of retropharyngeal abscess. Retropharyngeal abscess appears as a hypodense lesion in the retropharyngeal space with peripheral ring enhancement. Other findings on CT scan include soft-tissue swelling, obliterated fat planes, and mass effect.

• Obtain a CT scan of the neck with intravenous contrast when the findings on the lateral neck radiograph are equivocal or if the clinical suspicion for retropharyngeal abscess is high in patients with negative findings on lateral neck radiograph. Lateral neck radiographic findings may be misleading, especially in young children.

• 
  
  A CT

  scan of the neck with intravenous contrast also may be useful if the radiographic findings are positive because the CT scan can differentiate between retropharyngeal abscess and cellulitis. The CT scan also shows the extent of the retropharyngeal abscess and its relation to the great vessels, which is very helpful to the surgeon.

• CT scan of the neck can also differentiate between retropharyngeal abscess and retropharyngeal lymphadenopathy in children, which may help the ear, nose, and throat (ENT) surgeon decide whether to treat with intravenous antibiotics alone or intravenous antibiotics plus surgical drainage.

  A chest radiograph is indicated to look for aspiration pneumonia and mediastinitis.

  An MRI with gadolinium enhancement may demonstrate a retropharyngeal abscess, but this modality has not been used widely.

  Ultrasonography may demonstrate the presence of a retropharyngeal abscess, but its use has not yet been clarified.

 

Procedures

• Nasopharyngolaryngoscopy

• A review of the literature did not reveal a role for nasopharyngolaryngoscopy use in the diagnosis of retropharyngeal abscess.

• Safety of this procedure in the setting of retropharyngeal abscess is unclear.

• Nasopharyngolaryngoscopy has been performed preoperatively in 2 adults; no reports of its use in children exist.

• Endotracheal intubation

• Securing the airway may be required if the patient with retropharyngeal abscess is exhibiting signs of impending upper airway obstruction. Endotracheal intubation may be attempted, but it may be difficult because of distortion of the upper airway.

• Prophylactic intubation for a patient with retropharyngeal abscess but without respiratory distress generally is not indicated unless an interhospital transfer is planned.

• If a patient with signs of upper airway obstruction cannot be intubated, a surgical or needle cricothyrotomy may be required.

• A tracheostomy may be required as definitive airway management in patients with retropharyngeal abscess and respiratory distress.

Retropharyngeal Abscess Treatment & Management

Prehospital Care

• Supplemental oxygen and attention to upper airway patency are the essential components of prehospital care in patients with suspected retropharyngeal abscess.

• If a child exhibits respiratory distress, the sniffing position may be beneficial.

• Occasionally, endotracheal intubation or cricothyrotomy may be required if the patient exhibits signs of upper airway obstruction.

 

Emergency Department Care

ED management of retropharyngeal abscess includes attention to the airway, fluid resuscitation if necessary, antibiotic treatment, and preparation for an emergency operation. Frequent vital sign checks and continuous oxygen saturation monitoring are essential.

• Airway management

• Apply supplemental oxygen. In young children, this can be completed in a nonthreatening way by letting the parent direct blow-by oxygen at the child’s face.

• Endotracheal intubation may be required if the patient has signs of upper airway obstruction. It may be difficult because of upper airway swelling.

• Cricothyrotomy (surgical or needle) may be required in the patient with upper airway obstruction who cannot be intubated. Tracheostomy may be required for definitive airway management.

• Intravenous fluids are required if the patient is dehydrated because of fever and difficulty swallowing.

Consultations

An emergent consultation with an ENT specialist is necessary.

• Consult an ENT specialist as soon as the diagnosis of retropharyngeal abscess is established or as soon as the diagnosis is suspected if the patient is exhibiting signs of upper airway obstruction.

• If an abscess is present, an ENT specialist can drain it in the operating room.

• A prospective study in South Korea compared intravenous antibiotics plus surgical drainage with intravenous antibiotics with or without needle drainage. One case of mediastinitis occurred in the nonsurgical group. The authors concluded that, in conjunction with neck CT scanning, selected cases of parapharyngeal abscesses may be treated conservatively without early open surgical drainage.^[29]

• An 11-year chart review of 162 pediatric patients with retropharyngeal abscess at St. Louis Children’s Hospital revealed that 126 of the patients required surgery initially, and, of the 36 patients treated medically initially, 17 required surgery.^[4]

• Of 24 pediatric RPAs in children treated at Starship Pediatric Hospital in Auckland, Australia, between 1999 and 2005, 10 (41.7%) required surgery, while 14 (58.3%) did not require surgery.^[30]

• An ENT specialist also may perform a tracheostomy.

Retropharyngeal Abscess Medication

Medication Summary

The goals of pharmacotherapy are to eradicate the infection, to reduce morbidity, and to prevent complications. Intravenous broad-spectrum antibiotic coverage is indicated in the treatment of retropharyngeal abscess.

Antibiotics

Class Summary

Gram-positive organisms (including beta-lactamase producing), gram-negative organisms, and anaerobes must be covered. The list of antibiotic regimens in the table below is from The Sanford Guide to Antimicrobial Therapy 2012.^[31]

Some recommend the following regimens, which were not mentioned in The Sanford Guide to Antimicrobial Therapy: penicillin and oxacillin, second- or third-generation cephalosporin and clindamycin, penicillinase-resistant penicillin combined with either clindamycin or metronidazole, or third-generation cephalosporin in combination with clindamycin, nafcillin, or both (triple therapy).

In a review of retropharyngeal infections in children by Wald, the recommendation was to add vancomycin or linezolid to the regimen in patients not responding to clindamycin, and in patients who present with severe disease, in order to cover MRSA.

Clindamycin is a semisynthetic antibiotic produced by 7(S)-chloro-substitution of 7(R)-hydroxyl group of parent compound lincomycin. Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Widely distributes in the body without penetration of CNS. Protein bound and excreted by the liver and kidneys.

Metronidazole is active against various anaerobic bacteria and protozoa. Cells of microorganisms that contain nitroreductase absorb metronidazole. Unstable intermediate compounds are then formed that bind DNA and inhibit synthesis, causing cell death.

Second DOC, penicillin G interferes with the synthesis of cell wall mucopeptide during active multiplication, resulting in bactericidal activity against susceptible microorganisms.

Metronidazole is active against various anaerobic bacteria and protozoa. Cells of microorganisms that contain nitroreductase absorb metronidazole. Unstable intermediate compounds are then formed that bind DNA and inhibit synthesis, causing cell death.

Considered an alternative therapy. A second-generation cephalosporin indicated for the management of infections caused by susceptible gram-positive cocci and gram-negative rods. Many infections caused by gram-negative bacteria resistant to some cephalosporins and penicillins respond to cefoxitin.

Semisynthetic antibiotic produced by 7(S)-chloro-substitution of 7(R)-hydroxyl group of parent compound lincomycin. Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Widely distributes in the body without penetration of CNS. Protein bound and excreted by the liver and kidneys.

Alternative treatment that inhibits biosynthesis of cell wall mucopeptide and is effective during stage of active growth.

Antipseudomonal penicillin plus beta-lactamase inhibitor that provides coverage against most gram-positive organisms, most gram-negative organisms, and most anaerobes.

Antipseudomonal penicillin plus beta-lactamase inhibitor. Inhibits the biosynthesis of cell wall mucopeptide and is effective during the stage of active multiplication.

Retropharyngeal Abscess Follow-up

Further Inpatient Care

• Once the diagnosis of retropharyngeal abscess is established, initiate intravenous antibiotics and admit the patient to the hospital.

• If any signs of respiratory distress are present, admit the patient to the intensive care unit.

• Careful monitoring of airway status is essential and may require intensive care unit admission, even in the absence of respiratory distress in the ED.

• The ENT physician decides whether to incise and drain the abscess in the operating room or whether a trial of medical therapy is indicated first (eg, retropharyngeal cellulitis).

• An 11-year chart review of 162 pediatric patients with retropharyngeal abscess at St. Louis Children’s Hospital revealed that 126 of the patients required surgery initially, and, of the 36 patients treated medically initially, 17 required surgery.^[4]

• Of 24 pediatric RPAs in children treated at Starship Pediatric Hospital in Auckland, Australia, between 1999 and 2005, 10 (41.7%) required surgery, while 14 (58.3%) did not require surgery.^[30]

• Incision and drainage of retropharyngeal abscess in the ED may lead to aspiration and generally is not recommended.

Transfer

• Community hospitals without CT scanning or access to an ENT surgeon may need to transfer patients with suspected or known retropharyngeal abscess.

• Patients with known or suspected retropharyngeal abscess may need to be intubated before transport, depending on their clinical status.

• Intravenous antibiotics may be given prior to transfer but should not delay the transfer.

Deterrence/Prevention

• Good oral hygiene

• Antibiotic therapy of bacterial oral and pharyngeal infections

 

Complications

Complications of retropharyngeal abscess may include the following:

• Airway obstruction

• Mediastinitis

• Pleural involvement

• Atlantooccipital dislocation

• Epidural abscess

• Sepsis

• Acute respiratory distress syndrome (ARDS)

• Erosion of the second and third cervical vertebrae

• Cranial nerve deficits (cranial nerves IX-XII are contained in the cervical fascia)

• Septic thrombosis of jugular vein or hemorrhage secondary to erosion into carotid artery^[33]

• Compression of carotid artery and internal jugular vein^[33]

• Facial nerve palsy

• Esophageal perforation^[34]

• Purulent meningoencephalitis^[35]

 

Prognosis

• Prognosis generally is good if retropharyngeal abscess is identified early, managed aggressively, and complications do not occur.

• The mortality rate may be as high as 40-50% in patients in whom serious complications develop.

 

Patient Education

• Patients should be brought to the ED immediately if they develop the inability to swallow or have difficulty breathing in conjunction with a sore throat.

 

Ludwig’s angina

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Ludwig’s angina is an infection of the floor of the mouth under the tongue. It is due to bacteria.

Causes

Ludwig’s angina is a type of skin infection that occurs on the floor of the mouth, under the tongue. It often develops after an infection of the roots of the teeth (such as tooth abscess) or a mouth injury.

This condition is uncommon in children.

Symptoms

The infected area swells quickly. This may block the airway or prevent you from swallowing saliva.

Symptoms include:

• Breathing difficulty

• Confusion or other mental changes

• Fever

• Neck pain

• Neck swelling

• Redness of the neck

• Weakness, fatigue, excess tiredness

Other symptoms that may occur with this disease:

• Difficulty swallowing

• Drooling

• Earache

• Speech that is unusual and sounds like the person has a “hot potato” in the mouth

Exams and Tests

Your health care provider will do an exam of your neck and head to look for redness and swelling of the upper neck, under the chin.

The swelling may reach to the floor of the mouth. Your tongue may be swollen or out of place.

You may need a CT scan of the neck.  A sample of the fluid from the tissue may be sent to the lab to test for bacteria.

Treatment

If the swelling blocks the airway, you need to get emergency medical help right away. A breathing tube through your mouth or nose and into the lungs to restore breathing. You may need to have surgery called a tracheostomy that creates an opening through the neck into the windpipe.

Antibiotics are given to fight the infection. They are usually given through a vein until symptoms go away. Antibiotics taken by mouth may be continued until tests show that the bacteria have gone away.

Dental treatment may be needed for tooth infections that cause Ludwig’s angina.

Surgery may be needed to drain fluids that are causing the swelling.

Outlook (Prognosis)

Ludwig’s angina can be life threatening. However, it can be cured with getting treatment to keep the airways open and taking antibiotic medicine.

Possible Complications

• Airway blockage

• Generalized infection (sepsis)

• Septic shock

When to Contact a Medical Professional

Breathing difficulty is an emergency situation. Go to the emergency room or call your local emergency number (such as 911) right away.

Call your health care provider if you have symptoms of your condition, or if symptoms do get better after treatment.

Prevention

Visit the dentist for regular checkups.

Treat symptoms of mouth or tooth infection right away.

Alternative Names

Submandibular space infection; Sublingual space infection

What Is Ludwig’s Angina?

Ludwig’s angina is a skin infection that occurs on the floor of the mouth, underneath the tongue. This bacterial infection often follows a tooth abscess (a collection of pus in the center of a tooth) or other mouth infection or injury. This infection is rarely seen in children.

Symptoms include swelling of the tongue, neck pain, and breathing problems. This condition is often cured with antibiotics, but may cause serious complications, such as airway blockage or sepsis (a severe inflammatory response to bacteria).

These complications can be life threatening, but with prompt treatment, most people make a full recovery.

Symptoms of Ludwig’s Angina

Ludwig’s angina often follows a tooth infection or other infection or injury in the mouth. Symptoms include:

• pain or tenderness in the floor of your mouth, underneath your tongue

• difficulty swallowing

• drooling

• problems with speech

• neck pain

• swelling of the neck

• redness on the neck

• weakness, fatigue

• earache

• swollen tongue pushing against your palate

• fever, chills

• confusion

Call your doctor if you have symptoms of Ludwig’s angina. As the infection progresses, you may also experience trouble breathing and chest pain.

If your airway is blocked, you need immediate medical attention. Go to the emergency room or call 911 for help.

Causes of Ludwig’s Angina

Ludwig’s angina is a bacterial infection. It is usually caused by the bacterium Streptococcus or Staphylococcus, and often follows a mouth injury or infection, such as a tooth abscess. Poor dental hygiene, trauma or lacerations in the mouth, or a recent tooth extraction may also contribute to Ludwig’s angina.

Diagnosing Ludwig’s Angina

Your doctor may diagnose this condition with a physical exam, fluid cultures, and imaging tests.

The diagnosis is usually based on clinical observation. The head, neck, and tongue will appear red and swollen. If diagnosis cannot be made with a visual examination, other tests may be used:

• Contrast-enhanced magnetic resonance imaging (MRI) or computed tomography (CT) images can confirm swelling on the floor of the mouth.

• Fluid cultures of tissue from the affected area may also be tested to identify the specific bacterium that is causing the infection.

Treatment for Ludwig’s Angina

If swelling is interfering with breathing, the first goal of treatment will be to clear your airway. Your physician may insert a breathing tube through your nose or mouth and into your lungs. In some cases, an opening can be created through the neck into your windpipe. This procedure is called a tracheotomy, and is performed in emergency situations.

Surgery is sometimes necessary to drain excess fluids that are causing swelling in the oral cavity.

Oral or intravenous antibiotics will be required to fight the infection. Any additional dental infections must also be addressed.

Long-Term Outlook

Your outlook depends on the severity of your infection and how quickly you seek treatment. Delayed treatment increases your risk for potentially life-threatening complications, such as a blocked airway, sepsis (a severe reaction to bacteria or other germs), and septic shock (infection that leads to dangerously low blood pressure).

With proper treatment, most people make a full recovery.

How to Prevent Ludwig’s Angina

You can decrease your risk of developing Ludwig’s angina by:

• practicing good oral hygiene

• having regular dental checkups

• seeking prompt treatment for tooth and mouth infections

 

Named after Karl Friedrich Willhelm von Ludwig, Ludwig’s angina is characterized as a rapidly progressive gangrenous cellulitis of the soft tissues of the neck and floor of the mouth.^[52] With progressive swelling of the soft tissues and elevation and posterior displacement of the tongue, the most life-threatening complication of Ludwig’s angina is airway obstruction. Prior to the development of antibiotics, mortality for Ludwig’s angina exceeded 50%.^[3] As a result of antibiotic therapy, along with improved imaging modalities and surgical techniques, mortality currently averages approximately 8%.^[3,53]

In Ludwig’s angina, the submandibular space is the primary site of infection.^[54] This space is subdivided by the mylohyoid muscle into the sublingual space superiorly and the submaxillary space inferiorly. The majority of cases of Ludwig’s angina are odontogenic in etiology, primarily resulting from infections of the second and third molars. The roots of these teeth penetrate the mylohyoid ridge such that any abscess, or dental infection, has direct access to the submaxillary space. Once infection develops, it spreads contiguously to the sublingual space. Infection can also spread contiguously to involve the pharyngomaxillary and retropharyngeal spaces, thereby encircling the airway.

Odontogenic infections account for over 90% of cases.^[55] Additional etiologies include mandible fracture, neck trauma, tongue piercing, sialdenitis, neoplasm, and other parapharyngeal infections.^[3,52,54] Polymicrobial infection occurs in over 50% of cases.^[54] The most commonly cultured organisms include Staphylococcus, Streptococcus, and Bacteroides species.^[3] Patients with immunocompromising conditions, such as HIV, diabetes, transplant recipients, and alcoholics, are at risk for infection from a variety of atypical organisms. Atypical organisms isolated in these patients include Pseudomonas, Escherichia coli, Klebsiella, Enterococcus faecalis, Candida, and Clostridium.^[54]

The majority of cases of Ludwig’s angina occur in healthy patients with no comorbid diseases.^[3] Nevertheless, there are several conditions that have been shown to predispose patients to Ludwig’s angina. These conditions include diabetes mellitus, alcoholism, acute glomerulonephritis, systemic lupus erythematosus, aplastic anemia, neutropenia, and dermatomyositis.^[3,54]

Ludwig’s angina is a clinical diagnosis. The majority of patients report dental pain, or a history of recent dental procedures, and neck swelling. Less common complaints include neck pain, dysphonia, dysphagia, and dysarthria. Less than one third of adults will present in respiratory distress with dyspnea, tachypnea, or stridor.^[53] On physical examination, over 95% of patients have bilateral submandibular swelling and an elevated or protruding tongue.^[3,53] The submandibular swelling is often characterized as brawny and tense, with overlying erythema.

Airway management is the foundation of treatment for patients with Ludwig’s angina. Unfortunately, the decision to secure the airway continues to rely on clinical judgment and experience. At present, there are no established guidelines for airway control in patients with Ludwig’s angina. Current recommendations are primarily based on individual experience and institution-specific resources.^[56] Clearly, any patient presenting in respiratory distress or impending airway obstruction requires immediate intubation. Recommended techniques include routine orotracheal intubation and fiber-optic nasotracheal intubation. Blind nasotracheal intubation should not be attempted in patients with Ludwig’s angina given the potential for bleeding and abscess rupture.^[54,56,57] Ionintubated patients with Ludwig’s angina, airway equipment, including tracheostomy and cricothyroidotomy instruments, must be at the bedside.

Antibiotics should be initiated as soon as possible. Antibiotics should initially be broad-spectrum and cover gram-positive, gram-negative, and anaerobic organisms. Combinations of penicillin, clindamycin, and metronidazole are typically used.^[3] Recent case reports have advocated the use of intravenous steroids.^[52,54,58] In these reports, corticosteroid administration potentially avoided the need for airway management. To date, there are no randomized controlled trials that demonstrate the efficacy of corticosteroids in patients with Ludwig’s angina.

Up to 65% of patients with Ludwig’s angina develop suppurative complications that require surgical drainage.^[3,53,59] Physical examination alone is insufficient in determining which patients require a surgical procedure. In a recent study of deep neck space infections, the clinical exam underestimated the true extent of infection in 70% of patients.^[60] As a result, imaging is indicated in patients with Ludwig’s angina once antibiotics have been administered and decisions in regard to airway management have been made. Although plain films can demonstrate submandibular soft-tissue swelling, they are inadequate in detecting patients who require surgical drainage. As a result, a CT scan with intravenous contrast is recommended to detect patients who have developed suppurative complications.

Ludwigs angina

Introduction: Ludwigs angina is described as rapidly spreading cellulitis involving the floor of the mouth. It was first described by Wilhelm Friedrich von Ludwig in 1836. This disorder has a potential for airway obstruction.

Synonyms: Cynanche, Carbuculus gangraenosus, Morbus strangulatorius, and Angina maligna.

Anatomy:

This infection involves the submandibular space. The submandibular space can be divided into two spaces: submaxillary and sublingual space. These two spaces are separated from each other by the mylohyoid muscle. These two spaces are connected posteriorly through a cleft known as the mylohoid cleft. The mylohyoid cleft contains the following structures:

1. Tail of submandibular gland

2. wharton’s duct

3. Lingual nerve

4. Hypoglossal nerve

5. Lymphatics

6. Arteries and veins

The floor of the submandibular space is formed by the superficial layer of deep cervical fascia. It is attached from the hyoid bone to the mandible. This space communicates across the midline with that of the space on the opposite side.

Figure showing submaxillary and sublingual spaces

Boundaries of submandibular space:

The submandibular space is bounded by the oral mucosa and tongue superiorly and medially, the mandible superiorly, the superfical layer of deep cervical fascia with its tight attachment to the mandible and hyoid bone laterally, and the hyoid bone inferiorly.

Since the mandible and superficial layer of deep cervical fascia provide unyielding barriers superiorly and laterally, the tongue is forced upward and posteriorly giving rise to airway obstruction. This is the most important danger in Ludwig’s angina.

Figure showing neck spaces

 

Pathophysiology:

Commonest cause of Ludwig’s angina is dental infections. One important factor to be considered is the relationship of mandibular dentition to the attachment of mylohoid muscle (mylohyoid ridge). The anterior teeth and first molars regularly attach superior to this line, and infections arising from these roots commonly result in a limited sublingual abscess. The second and third molar roots are attached routinely below this line. Infections involving these roots cause infections of submaxillary space. One other important relationship is that the roots of the anterior teeth and first molar approximate the lateral mandibular surface, whereas the second and third molar roots approach the lingual surface of the mandible.

Figure showing the relationship of the tooth to the mylohyoid line

 

Criteria for diagnosing Ludwig’s angina:

To diagnose Ludwig’s angina the following features should be present:

1. Rapidly spreading cellulitis with no specific tendency to form abscess.

2. Involvement of both submaxillary and sublingual spaces, usually bilaterally

3. Spread by direct extension along facial planes and not through lymphatics

4. Involvement of muscle and fascia but not submandibular gland or lymph nodes

5. Originates in the submaxillary space with progression to involve the sublingual space and floor of the mouth.

Etiology:

1. Ludwigs angina is commonly caused as a sequlae to dental infections. In fact it is very common in young adults with periodontal disease. Dental causes account for 75% to 80% of these cases.

2. Penetrating injuries involving the floor of the mouth (stab wounds, gun shot wounds etc)

3. Mandibular fractures

CT scan of a patient with ludwigs angina

 

Bacteriology of Ludwig’s angina:

Since a majority of cases of Ludwig’s angina are caused by dental infections, cultures from this infected area show oral cavity flora. The most common aerobes isolated are alpha haemolytic streptococci followed by staphylococci. Anaerobic cultures are difficult to interpret. The anaerobes isolated are peptostreptococcus, peptococcus, fusobacterium nucleatum, and bacteroids. The combination of aerobic and anaerobic organisms has a synergistic effect due to production of endotoxins like collagenase, hyaluranidase, and proteases. These endotoxins contribute to the rapidly spreading cellulitis.

Clinical features:

1. Patient has c/o increasing oral cavity and neck pain.

2. These patients have poor oral hygiene

3. Symptoms are at first unialteral but soon become bilateral

4. The soft tissues of the floor of the mouth swells

5. Tongue gets pushed posteriorly causing air way obstruction

6. These patients are usually febrile

On examination:

These patients have tachycardia, fever, and variable degrees of respiratory obstruction with dysphagia and drooling. The submandibular and submental regions are tense, swollen and tender. The floor of the mouth may become tense swollen and indurated. Fluctuation is not present. The tongue is seen to be pushed backwards.

Diagnosis of Ludwigs angina is based on the clinical features enumerated above. These patients may show leukocytosis. X ray soft tissue neck may show soft tissue oedema. CT scaeck is to be considered in all persistent cases to rule out complications. Xray chest must also be considered to rule out mediastinitis.

 

Management:

Airway management: Since the airway is threatened insertion of oral airway is to be considered. If the patient does not tolerate an oral airway then tracheostomy is to be considered.

Intravenous antibiotics with broad spectrum features (chloramphenicol)may be administered. The drug of choice is amoxycillin with clavulanic acid. Metronidazole must also be administered. Clindamycin can be administered in resistant cases.

Role of surgical drainage: Wide decompression of the supra hyoid region may be considered. The approach is through a median horizontal incision three to four finger breadths below the mandibular margin. The mylohoid muscle is split in the midline, and drainage is established both medially and laterally. Pus is very rarely encountered during this procedure, but starts to drain several days after the procedure.

Complications:

1. Airway compromise

2. Extension to mediastinum causing mediastinitis. This can be suspected if there is persistent swelling in the neck with pain, spiking fever and persistent leukocytosis.

3. Extension into the carotid sheath and retropharyngeal space.

Cellulitis Treatment & Management

Approach Considerations

Antibiotic regimens are effective in more than 90% of patients. However, all but the smallest of abscesses require drainage for resolution, regardless of the microbiology of the infection. In many instances, if the abscess is relatively isolated, with little surrounding tissue involvement, drainage may suffice without the need for antibiotics.

Note that management of cellulitis may be complicated because of the emergence of methicillin-resistant Staphylococcus aureus (MRSA) and macrolide- or erythromycin-resistant Streptococcus pyogenes.^[1] Nonsevere cases of cellulitis may be treated empirically with semisynthetic penicillins, first- or second-generation oral cephalosporins, macrolides, or clindamycin.

Unfortunately, for patients with cellulitis surrounding abscess formation, 50% of MRSA strains also have inducible or constitutive clindamycin resistance.^[1] Of the strains of S pyogenes resistant to macrolides, 99.5% seem to remain susceptible to clindamycin and 100% to penicillin.^[1] Most community-acquired MRSA infections (CA-MRSA) are apparently susceptible to trimethoprim-sulfamethoxazole and tetracycline.

In 2011, the Infectious Diseases Society of American (ISDA) published updated guidelines regarding management of MRSA in adults and children, and in 2012, the updated ISDA guidelines for the Diagnosis and Treatment of Diabetic Foot Infections were published. Readers are encouraged to check the ISDA guidelines Web site for the 2013 updated recommendations for the diagnosis and management of skin and soft-tissue infections, which is expected to be published in the spring of 2013.^{[64, 65]}

Consider consulting an infectious disease specialist if the patient is not improving with standard treatment or if an unusual organism is identified; a critical care specialist for patients who are systemically ill and require admission to a critical care unit; or an ophthalmologist in cases of orbital cellulitis.

Cellulitis without draining or abscess

In cases of cellulitis without draining wounds or abscess, streptococci continue to be the likely etiology,^[1] and beta-lactam antibiotics are appropriate therapy, as noted in the following:

• In mild cases of cellulitis treated on an outpatient basis, dicloxacillin, amoxicillin, and cephalexin are all reasonable choices

• Clindamycin or a macrolide (clarithromycin or azithromycin) are reasonable alternatives in patients who are allergic to penicillin

• Levofloxacin may also represent an alternative, but the prevalence of resistant strains has increased, and fluoroquinolones are best reserved for gram-negative organisms with sensitivity demonstrated by culture^{[5, 1]}

• Some clinicians prefer an initial dose of parenteral antibiotic with a long half-life (eg, ceftriaxone followed by an oral agent)

Recurrent cellulitis

In the occasional patient with recurrent disease usually related to venous or lymphatic obstruction, the cellulitis is most often due to Streptococcus species, and penicillin G or amoxicillin (250 mg bid) or erythromycin (250 mg qd or bid) may be effective.^[66] If tinea pedis is suspected to be the predisposing cause, treat with topical or systemic antifungals.

Severe cellulitis

Patients with severe cellulitis require parenteral therapy, such as the following:

• Usually, cellulitis is presumed to be due to staphylococci or streptococci infection and may be treated with cefazolin, cefuroxime, ceftriaxone, nafcillin, or oxacillin

• Antimicrobial options in patients who are allergic to penicillin include clindamycin or vancomycin^[67]

• Infections associated with diabetic ulcers are often polymicrobial; empiric coverage in this setting should include broad coverage of gram-positive, gram-negative, and anaerobic organisms^[68]

• If the cellulitis appears to be related to a furuncle or an abscess, or if it is a postsurgical situation, including coverage for MRSA is prudent for severe cases until culture and sensitivity information is available

Mammalian bites

CA-MRSA is not commonly associated with bite wounds. Cellulitis associated with mammalian bite wounds is often polymicrobial and should be treated empirically with antimicrobials that target anaerobic bacteria in addition to the common cellulitis pathogens, as described below:

• Mild cases can be treated on an outpatient basis with amoxicillin-clavulanate; in patients with penicillin allergy, combination therapy is usually required; fluoroquinolone plus clindamycin or trimethoprim-sulfamethoxazole (TMP-SMX) plus metronidazole would be reasonable alternatives

• Inpatients can be treated with ampicillin-sulbactam or piperacillin-tazobactam; alternative agents in patients with penicillin allergy would be the same as the above but in parenteral form

Odontogenic cellulitis

Cellulitis of odontogenic origin is typically polymicrobial. Identified organisms include viridans streptococci, Neisseria and Eikenella species, and the anaerobes Prevotella and Peptostreptococcus. Treatment includes the following:

• IV regimens that have demonstrated therapeutic response include clindamycin or ampicillin-sulbactam

• Oral regimens that have demonstrated therapeutic response include clindamycin or amoxicillin-clavulanate

Aquatic lacerations and punctures

Lacerations and puncture wounds sustained in an aquatic environment may be contaminated with bacteria such as Aeromonas hydrophila, Pseudomonas and Plesiomonas species, Vibrio species, Erysipelothrix rhusiopathiae, and others. Treatment in such cases includes the following:

• Antibiotic treatment should address common gram-positive and gram-negative aquatic organisms

• Appropriate antibiotic regimens for saltwater or brackish water include doxycycline and ceftazidime, or a fluoroquinolone

• Appropriate regimens for injuries sustained in freshwater include a third- or fourth-generation cephalosporin (eg, ceftazidime or cefepime) or a fluoroquinolone (eg, ciprofloxacin or levofloxacin)

• Apparent infection that is not responsive to initial courses of antibiotics as above should raise suspicion for Mycobacterium marinum infection; in such situations, wound biopsy for mycobacterial stains and culture should be considered

MRSA

In many communities, CA-MRSA is the most common isolate obtained from abscesses.^[69] Antibiotics used to treat cellulitis associated with abscess or purulent drainage should target CA-MRSA until proven otherwise with culture data. In contrast, for outpatients with nonpurulent cellulitis, the Infectious Diseases Society of America (ISDA) recommends empiric therapy for infection due to beta-hemolytic streptococci, as it is believed that CA-MRSA plays an uncommon role in these scenarios.^[64]

Mild cases that require only outpatient therapy may be treated with TMP-SMX or a tetracycline agent such as doxycycline or minocycline. Available data suggest that doxycycline and TMP-SMX are equivalent for the treatment of mild skin and soft-tissue infections (SSTIs).^[70] It is important to note that TMP-SMX or tetracyclines may not have adequate streptococcal coverage and should not be the first choice unless purulence is present.^[71] Clindamycin may also be a reasonable choice, depending on local sensitivities of CA-MRSA, but the IDSA estimates that up to 50% of MRSA isolates have intrinsic or constitutive resistance to clindamycin in some regions.^[1]

In more severe cases that require parenteral antibiotics to cover MRSA, vancomycin, daptomycin, tigecycline, ceftaroline, and linezolid are appropriate choices. Data are more limited for the newer agents, but they have been shown to have similar efficacy to vancomycin in some clinical trials.^[72] Daptomycin has been associated with more rapid resolution of signs and symptoms of cellulitis in some trials.^{[73, 74]} However, vancomycin continues to be the drug of choice because of its overall excellent tolerability profile, efficacy, and cost.^[72]

If tinea pedis is considered a possible cause of recurrent cellulitis episodes, treatment with a topical antifungal is recommended. Oral antifungals, such as itraconazole or terbinafine, may be considered in cases of refractory chronic changes or if onychomycosis is providing a source for repeated infection

Outpatient Care

Patients with cellulitis who have mild local symptoms and no evidence of systemic disease can be treated on an outpatient basis. Facial cellulitis of odontogenic origin requires extraction or root canal as well as antibiotic therapy. Elevating limbs with cellulitis expedites resolution of the swelling. Cool sterile saline dressings may be used to remove purulent discharge from any open lesion.

Treatment duration for cellulitis is controversial; shorter-duration therapy may be as effective as longer-duration therapy.^[75] In general, consider the following:

• A transient increase in erythema over the first day of treatment is common and represents an inflammatory reaction to cell lysis caused by antibiotics

• The patient should be reassessed with short-interval follow-up—ideally within 48-72 hours—to ensure improvement.

• In patients who respond slowly to therapy, antibiotics may need to be continued until inflammation resolves. If infection does not regress after outpatient treatment, antibiotic resistance or a more serious infection should be ruled out; an alternative diagnosis should also be considered

• Development of systemic symptoms should prompt reevaluation and consideration for admission.

• Concomitant hypotension and tachycardia indicate systemic disease and warrant intensive monitoring

IV Antibiotic Therapy

Severely ill patients and those whose condition is unresponsive to standard oral antibiotic therapy should be treated with inpatient intravenous (IV) antibiotics. The selection of antibiotic therapy should be based on suspicion for likely organisms as well as results of Gram stain, culture, and drug susceptibility analysis, if available.^[1]

In hospitalized patients in which S aureus infection is a concern, it is wise to assume methicillin (oxacillin) resistance because of the high prevalence of community-acquired methicillin-resistant strains (CA-MRSA); administer agents that are usually effective against MRSA, such as vancomycin, linezolid, ceftaroline, or daptomycin.^[1] Step-down treatment for S aureus– related soft-tissue infections may focus upon tetracyclines, trimethoprim-sulfamethoxazole, or other agents, depending on the results of susceptibility tests and following an initial clinical response.

Other individuals who may require inpatient IV antibiotic include the following^[5] :

• Immunosuppressed patients

• Patients with facial cellulitis

• Any patient with a clinically significant concurrent condition, including lymphedema and cardiac, hepatic, or renal failure

• Individuals with newly elevated creatinine, creatine phosphokinase, and/or low serum bicarbonate levels or marked left-shift polymorphonuclear neutrophils

Surgical Examination and Drainage

Urgent consultation with a surgeon should be sought in the setting of crepitus, circumferential cellulitis, necrotic-appearing skin (bronzing), evolving bullae, rapidly evolving cellulitis, pain disproportional to physical examination findings, severe pain on passive movement, or other clinical concern for necrotizing fasciitis. Wong et al have developed a scoring tool to assist in the diagnosis of necrotizing fasciitis.^[76] Cellulitis associated with an abscess requires surgical drainage of the source of infection for adequate treatment.

Serious concern for necrotizing fasciitis and/or the presence of necrotic skin should prompt examination of the fascial planes by immediate computed tomographic imaging or surgical direct observation, which, in most cases, can be performed at the bedside by an experienced surgeon. Circumferential cellulitis may result in compartment syndrome, which may require surgical decompression. Measurement of compartment pressures may be helpful in diagnosis.

Skin and Soft Tissue Infections – Incision, Drainage, and Debridement 

Overview

Background

Skin and soft tissue infections (SSTIs), which include infections of skin, subcutaneous tissue, fascia, and muscle, encompass a wide spectrum of clinical presentations, ranging from simple cellulitis to rapidly progressive necrotizing fasciitis. Diagnosing the exact extent of the disease is critical for successful management of a patient of soft tissue infection.^{[1, 2, 3, 4, 5]}

The various types of SSTIs, listed according to clinical presentation and anatomic location, include the following:

• Impetigo

• Folliculitis

• Furuncles

• Carbuncles

• Erysipelas

• Cellulitis

• Necrotizing fasciitis, also known as hemolytic streptococcal gangrene, Meleney ulcer, synergistic gangrene, and Fournier gangrene (when localized to the scrotum and perineal area)

• Pyomyositis

SSTIs may be caused by any of a formidable number of pathogenic microorganisms, and they may be either monomicrobial or polymicrobial. The following are the most important pathogens:

• Staphylococcus aureus (the most common pathogen)

• Streptococcus pyogenes

• Site-specific infections – Indigenous organisms (eg, gram-negative bacilli in perianal abscesses)

• Immunocompromised hosts and complicated SSTIs – Multiple organisms or uncommon organisms (eg, Pseudomonas aeruginosa, beta-hemolytic streptococci, Enterococcus)

• Polymicrobial necrotizing fasciitis – Mixed infection with both aerobes (eg, streptococci, staphylococci, or aerobic gram-negative bacilli) and anaerobes (eg, Peptostreptococcus, Bacteroides, or Clostridium)

• Monomicrobial necrotizing fasciitis: S pyogenes

Classification of SSTIs

For the purposes of this article, SSTI may be divided into the following categories:

• Uncomplicated SSTI

• Nonnecrotizing complicated SSTI

• Necrotizing fasciitis

Uncomplicated SSTIs include superficial cellulitis, folliculitis, furunculosis, simple abscesses, and minor wound infections. These infections respond well to either source control management (ie, drainage or debridement) or a simple course of antibiotics. These infections pose little risk to life and limb.

Complicated SSTIs involve the invasion of deeper tissues and typically require significant surgical intervention. The response to therapy is often complicated by underlying disease states. Complicated SSTIs include complicated abscesses, infected burn wounds, infected ulcers, infections in diabetics, and deep-space wound infections. They are often limb- or life-threatening.

Necrotizing fasciitis is a progressive, rapidly spreading, inflammatory infection that is located in the deep fascia and is associated with secondary necrosis of the subcutaneous tissues. The inflammation of the deep fascia causes thrombosis of the dermal vessels, and it is this thrombosis that is responsible for the secondary necrosis of the overlying subcutaneous tissue and skin.

It is imperative to distinguish necrotizing infections from nonnecrotizing infections. Early diagnosis and intervention may save a life; delayed diagnosis and treatment may lead to loss of a limb or a life.

Predisposing factors

Factors predisposing to the development of SSTIs include the following:

• Breach in the epidermis

• Dry and irritated skin

• Immunocompromised status – Malnutrition, hypoproteinemia, burns, diabetes mellitus, AIDS

• Chronic venous insufficiency

• Chronic lymphatic insufficiency

• Chronic neuropathy

Indications

Any abscess, however small, must be drained for complete resolution. Any ulcer covered with dead and necrotic tissue must be debrided to promote growth of healthy granulation tissue and healing. Necrotizing fasciitis is a surgical emergency; early surgical treatment optimizes outcomes for these patients.

Contraindications

There are no absolute contraindications for incision, drainage, and debridement of SSTIs. If the patient’s physical condition is compromised, stabilization to render him or her fit for anesthesia should be carried out before these procedures are undertaken.

Technical Considerations

In the drainage of an abscess, the incision should be made at the most prominent part, which has the pus point. If possible, it should be made in a dependent area; however, a dependent incision should not be made if a tubercular etiology is suspected. Ideally, the direction of the incision should be in line with the natural skin crease.

A bold incision must be made that goes all the way into the abscess cavity. However, if there are any major vessels or nerves in the area, additional care should be taken in making the incision, and blunt dissection should be used instead to enter the abscess cavity. Any necrosed or unhealthy skin on the roof of the abscess should be excised completely.

Debridement should be done till healthy dermal bleeding is seen on the edges of the skin. There should be no loose undermined skin edges at the end of surgical debridement. However, overzealous debridement should be avoided in nonnecrotizing SSTIs; a staged debridement should be planned to minimize damage to healthy tissue.

Periprocedural Care

Patient Education and Consent

Consent should be obtained from the patient or family member.^[6] The reason the procedure is being performed (suspected diagnosis); the risks, benefits, and alternatives of the procedure; the risks and benefits of the alternative procedure; and the risks and benefits of not undergoing the procedure. Allow the patient the opportunity to ask any questions and address any concerns they may have. Make sure that they have an understanding about the procedure so they can make an informed decision.

The patient should be counseled about the risks of bleeding (damage to adjacent blood vessels), dissemination of infection (sepsis, endocarditis), and injury of local nerves.

The patient should also be counseled that even if there are no complications, the procedure may not be successful (the abscess may not be completely drained, additional surgery may be necessary).

Discuss how these risks can be avoided or prevented (eg, adequate analgesia, use of ultrasound when possible or indicated, use of antibiotics when indicated).

Preprocedural Planning

Controlling the source of infection is the key to management of SSTIs because it is the fastest way of decreasing the bacterial load. Source control is achieved by means of pus drainage and debridement. The aim of debridement is to create an acute wound milieu so as to trigger the body’s natural wound healing mechanisms and thereby promote healing.

In addition to surgical management of an SSTI, selected investigations, antibiotic therapy, or both may be indicated.

Laboratory tests

Patients with uncomplicated SSTIs usually do not require any investigations and need not be hospitalized. However, patients with symptoms and signs of systemic toxicity, such as tachycardia and hypotension, should undergo the following tests:

• Blood culture and drug susceptibility

• Complete blood count (CBC) with differential

• Creatinine level

• Bicarbonate level

• Creatine phosphokinase level

• C-reactive protein level

Additional investigations may be indicated, depending on the severity of systemic toxicity.

Antimicrobial therapy

Uncomplicated SSTIs with no symptoms or signs of systemic involvement respond well to incision and drainage and appropriate wound care. Patients with such infections usually do not require any antibiotics. However, the extent of abscess must be confirmed and complete drainage ensured at the time of surgical exploration.

A blood sample and a pus sample are sent for culture and antimicrobial sensitivity testing when the patient first presents to the clinician. Oral or intravenous (IV) antimicrobial therapy is then started empirically, depending on the severity of the infection.^[8]

The following are indications for IV antibiotics:

• A severe soft tissue infection is limb- or life-threatening

• The signs and symptoms of systemic illness are present

• The patient is immunosuppressed

• The patient is at the extremes of age

Empirical antimicrobial therapy is administered as follows:

• Semisynthetic penicillins or second-generation cephalosporins are given to cover S aureus

• Site-specific antibiotics are given to cover indigenous organisms

• Appropriate antibiotics are given to cover methicillin-resistant S aureus (MRSA) if suspected

• Broad-spectrum antibiotics are given to patients with complicated SSTIs and immunocompromised status

After identification of the organism or organisms and confirmation of drug sensitivity, appropriate antimicrobials are started.

Equipment

The equipment required for incision, drainage, and debridement is the basic surgical set, which includes the following:

• Sponge-holding forceps

• Surgical blade, Nos. 11 and 15

• Curved artery forceps

• Plane and toothed thumb forceps

• Curette

• Metzenbaum scissors

• Sterile swab stick

• Electrocautery

• Saline

• Hydrogen peroxide

Patient Preparation

Patient preparation includes adequate anesthesia and appropriate positioning.

Anesthesia

Anesthesia for incision and drainage is as follows:

• General anesthesia – This used for large and deep abscesses to facilitate complete and thorough drainage

• Regional anesthesia – This can be used for large and deep abscesses if patient cooperation can be ensured

• Field block – This is used for small abscesses

• Local anesthesia – The overlying skin is anesthetized via a 26-gauge needle, and the anesthetic is infiltrated subcutaneously into the dome of the abscess to achieve anesthesia of the skin to enable painless skin incision; anesthetizing the abscess cavity is not very effective, because the local anesthetic functions poorly in the acidic environment of the abscess

Anesthesia for debridement is as follows:

• General anesthesia – Because debridement is a very painful procedure, and complete analgesia is essential for thorough debridement

• Regional anesthesia – This may be used when general anesthesia is not desirable and patient cooperation can be ensured

Positioning

The patient is positioned in accordance with the location of the lesion. Whichever position is chosen should afford the surgeon easy access to the lesion and should be comfortable for the patient.

Monitoring and Follow-up

Patients with complicated SSTIs or necrotizing fasciitis may have bloodstream infection (BSI) and experience septic shock. Such patients are kept under close monitoring and may require intensive care nursing. Depending on the severity of the BSI and septic shock, the patient may require intensive monitoring, along with supportive measures aimed at maintaining circulation and ventilation.

Technique

Incision and Drainage

After proper positioning and anesthesia (see Periprocedural Care), incision and drainage is carried out in the following manner.

A skin incision is made with a No. 11 or 15 surgical blade in the most prominent and fluctuant part of the abscess. The direction of the incision should parallel the natural skin creases as far as possible so as to prevent unsightly scars. If there is no obvious pus pointing or fluctuant area in the abscess, the incision is made at the dependent portion of the abscess; however, a dependent incision should be avoided if a tubercular pathology is suspected.

In areas where no important neural or vascular structures are expected to be present, a bold incision that cuts through the skin, subcutaneous tissue, and deep fascia may be made to achieve entry into the abscess cavity. However, in areas where important neurovascular structures are present, only skin and subcutaneous tissue are incised. The abscess cavity is entered by insinuating a pair of blunt artery forceps or sinus forceps through a small opening in the deep fascia, then gradually opening the blades.

Once the cavity is entered, pus is seen extruding through the opening. At this point, a pus swab may be sent for microbiologic analysis if indicated. The abscess cavity is explored, and an artery forceps with a gauze piece wrapped around its tip is used to break up all the loculi and drain all the pus pockets. The same result may be achieved with the surgeon’s gloved finger if the presence of a foreign body in the cavity can be ruled out.

The abscess cavity is irrigated with saline solution to flush out all the pus, debris, and blood, then packed with gauze or surgical sponge to achieve hemostasis. After a few minutes, the packing is taken out, and any active bleeding points are cauterized or ligated.

Final dressing is done by loosely packing the cavity with gauze soaked in saline or another commercially available product. This packing acts as a wick to drain any fresh exudate and blood. It is covered with a dry absorbent dressing that soaks up exudate and blood. The dressing is changed after 24 hours and again every 24 hours thereafter until the wound is dry. When healthy granulation tissue is seen in the cavity and no fresh exudate or pus is visible, a simple dressing with gauze is sufficient.

Debridement for Infected Ulcers and Gangrene

Surgery is the most effective method of debridement. Surgical debridement is usually done with the patient under general anesthesia, but local or regional anesthesia may be employed if the lesion is not very extensive. If debridement is being done on a limb, a tourniquet may be used to minimize blood loss.

The lesion is cleaned and draped. The slough over the lesion is then slowly excised off the underlying healthy tissue with a scalpel or scissors (see the images below); smaller areas of dead tissue can be excised using a curette. The slough is excised until the wound starts bleeding, but this must be done without damaging the underlying healthy tissue. The margins of the wound are also freshened. The tourniquet is released, and any active bleeding points are cauterized.

The raw area created by debridement is covered with a nonadherent dressing (eg, tulle gras). The first dressing is changed after 24 hours; regular dressing changes follow at 24-hour intervals. At each dressing, the wound is inspected for any new slough or pus formation. Repeated debridements may be necessary until the wound becomes clean and active infection is controlled by appropriate antibiotics. Once the wound is clean, dressings may be changed at 36-hour intervals.

Other methods of debridement

Debridement methods that may be employed as alternatives to surgical debridement include the following^[9] :

• Mechanical

• Chemical

• Autolytic

• Biological

• Ultrasonic

Mechanical debridement is accomplished by using the wet-to-dry dressing method. The wound is dressed with a wet dressing (usually gauze soaked in saline) covered with a dry dressing. The dressing is then allowed to dry on the wound over the following 24 to 36 hours. When the dry dressing is taken off, it peels the adherent necrotic tissue away from the healthy tissue. This is a very painful method and is not much favored.

Chemical debridement is performed by using certain enzymatic chemicals on the wound which cause lysis of the necrotic tissue in the wound. Commercially available collagenase enzyme granules are sprinkled onto the wound daily until the wound is clear of necrotic tissue. Regular dressings then follow.

Autolytic debridement is a process in which the body sheds the dead necrotic tissue by the use of moisture. This process is helped by the presence of enzymes called matrix metalloproteinases (MMPs), which are produced by damaged tissue and which disrupt the proteins that bind the dead tissue to the body.

This process can be enhanced by applying dressings that encourage a balanced moist environment in the wound. Heavily exuding wounds benefit from the application of alginates, cellulose dressings, and foams; these dressings absorb the excess exudate and prevent maceration of surrounding healthy tissue while still maintaining a moist environment that promotes desloughing. Dry wounds benefit from the application of hydrogels and hydrocolloids, which donate moisture to the dead tissue to facilitate debridement.^[10]

Biological debridement (ie, maggot therapy) involves exposing the wound to the maggots of Lucilia sericata (the greenbottle fly). These organisms digest the necrotic tissue and bacteria in the wound but spare the underlying healthy tissue. This method has not gained much favor among patients.

Ultrasonic debridement involves applying ultrasonic vibrations to the wound bed through a liquid medium. This causes cavitation (ie, the creation and destruction of small bubbles within the fluid surrounding the probe). During cavitation, the bubbles oscillate in size and shape. They expand and rapidly collapse, causing shockwave formation, and this implosion leads to erosion of tissues. Ultrasonic debridement causes necrotic tissue disruption, fragmentation and emulsion.

Debridement for Necrotizing Fasciitis

When a limb is being operated on, a tourniquet is used so as to obtain a bloodless field. The 3 zones of necrotizing fasciitis are delineated (see the images below). A bold incision is made that runs through the entire length of the lesion from normal skin (zone 3) proximally to normal skin distally. The incision should extend to the muscle.

The deep fascia is identified, and a finger is passed along it to probe the extent of its involvement. Healthy deep fascia can be identified by its glistening appearance and its firm attachment to the skin and subcutaneous tissue. Unlike necrosed deep fascia, it does not separate easily from the skin and subcutaneous tissue

At this point, tissue specimens are obtained and sent for aerobic and anaerobic culture and antibiotic sensitivity and for histopathologic examination to establish the diagnosis.

Once the extent of deep fascial involvement has been established, radical excision of the deep fascia is carried out with scissors to expose the underlying healthy muscle. The overlying skin and subcutaneous tissue are then inspected for viability.

Tissues in zone 1 are necrosed and are excised. Tissues in zone 2 are inspected carefully for viability and excised when involved. Viability can be checked by looking for dermal bleeding, calcification and liquefaction of subcutaneous fat, and thrombosed blood vessels.^[11] The involved skin and subcutaneous tissue is excised.

The tourniquet is then deflated, and the tissue is examined for viability. Further debridement is carried out if necessary. Once debridement is complete, hemostasis is achieved by means of electrocauterization, and the wound is washed thoroughly with saline.

The extensive debridement required in cases of necrotizing fasciitis results in a large raw wound. The wound is carefully dressed with a nonadherent dressing and bandaged with absorbent dressing. The dressing is changed after 24 hours.

Complications of Procedures

Bleeding is the most common complication associated with these procedures. Bleeding after debridement (especially debridement for necrotizing fasciitis) may cause rapid deterioration of an already compromised patient. Meticulous hemostasis is hence mandatory. In most cases, pressure dressing is sufficient to control the bleeding; in some cases, the patient may have to be returned to the operating room for control of persistent bleeding.

Drainage of an abscess or debridement of necrotic tissue may result in dissemination of bacteria and bacterial toxins into the bloodstream and thereby cause severe sepsis. Accordingly, it is imperative that these procedures be done under antibiotic coverage.

Injury to underlying nerves and blood vessels is another potential complication. The surgeon must be careful while making the incision and during debridement if the abscess or ulcer is in close proximity to important anatomic structures such as nerves and blood vessels.

Space Infection

 

In order to treat an acute dent alveolar infection as well as a fascial space abscess correctly, the following are considered absolutely necessary:

·         Take a detailed medical history from the patient.

·         Drainage of pus, when its presence in tissues is established.

This is achieved (1) by way of the root canal, (2) with an intraoral incision, (3) with an extraoral incision, and (4) through the alveolus of the extraction. Without evacuation of pus, that is with administration of antibiotics alone, the infection will not resolve.

·      Drilling of the responsible tooth during the initial phase of inflammation, to drain exudate through the root canal, together with heat therapy. In this way, spread of inflammation is avoided and the patient is relieved of the pain. Drainage may also be performed with trephination of the buccal bone, when the root canal is inaccessible.

·         Antisepsis of the area with an antiseptic solution before the incision.

·     Anesthesia of the area where incision and drainage of the abscess are to be performed, with the block technique together with peripheral infiltration anesthesia at some distance from the inflamed area, in order to avoid the risk of existing microbes spreading into deep tissues.

·         Planning of the incision so that:

– Injury of ducts (Wharton, Stensen) and large vessels and nerves is avoided.

– Sufficient drainage is allowed. The incision is performed superficially, at the lowest point of the accumulation, to avoid pain and facilitate evacuation of pus under gravity.

– The incision is not performed in areas that are noticeable, for esthetic reasons; if possible, it is performed intraorally.

·       Incision and drainage of the abscess should be performed at the appropriate time. This is when the pus has accumulated in the soft tissues and fluctuates during palpation, that is when pressed between the thumb and middle finger, there is a wave-like

Incision for drainage of a sublingual abscess. The incision is performed parallel to the submandibular duct and the lingual nerve

Incision for drainage of a palatal abscess, parallel to the greater palatine vessels

Incisions for drainage of a submandibular or parotid (a), and a submasseteric (b) abscess. During cutaneous incisions, the course of the facial artery and vein must be taken into consideration (a), as well as that of the facial nerve (b)

movement of the fluid inside the abscess. If the incision is premature, there is usually a small amountof bleeding, no pain relief for the patient and the edema does not subside.

·       The exact localization of pus in the soft tissues (if there is no fluctuation present) and the incision for drainage must be performed after interpretation of certain data; for example, ascertaining the softest point of swelling during palpation, redness of the skin or mucosa, and the most painful point to pressure. This area indicates where the superficial incision with a scalpel is to be made. If there is no indication of accumulation of pus to begin with, hot intraoral rinses with chamomile are recommended to speed up development of the abscess and toensure that the abscess is mature.

·       Avoid the application of hot compresses extraorally, because this entails an increased risk of evacuation of pus towards the skin (spontaneous drainage)

Superficial incisions on the skin (a) and on the mucosa of the oral cavity (b)

Spontaneous extraoral (undesirable) drainage of an abscess, after the erroneous placement of hot compresses on the skin

·     Drainage of the abscess is initially performed with a hemostat, which, inserted into the cavity of the abscess with closed beaks, is used to gently explore the cavity with open beaks and is withdrawn again with open beaks. At the same time as the blunt dissection is being performed, the soft tissues of the region are gentlymassaged, to facilitate evacuation of pus.

·      Placement of a rubber drain inside the cavity and stabilization with a suture on one lip of the incision, aiming to keep the incision open for continuous drainage of newly accumulated pus.

·        Removal of the responsible tooth as soon as possible, to ensure immediate drainage of the inflammatory material, and elimination of the site of infection. Extraction is avoided if the tooth can be preserved, or if there is an increased risk of serious complications in cases where removal of the tooth is extremely difficult.

·   Administration of antibiotics, when swelling is generally diffuse and spreading, and especially if there is fever present, and infection spreads to the fascial spaces, regardless of whether there is an indication of the presence of pus. Antibiotic therapy is usually empiric, given the fact that it takes time to obtain the results from a culture sample. Because the microorganisms isolatedmost often in odontogenic infections are streptococci (aerobic and anaerobic), penicillin remains the antibiotic of choice for treatment.

Diagrammatic illustrations showing the incision of an intraoral abscess and the placement of a hemostat to facilitate the drainage of pus

Diagrammatic illustrations showing the placement of a rubber drain in the cavity and stabilization with a suture on one lip of the incision.

 

PICTURES OF SUBMANDIBULAR NECK ABSCESS

 

Abscesses of the submandibular neck space are common in children.  The treatment is incision and drainage.  Cultures are obtained and the appropriate antibiotic is administered.

The submandibular abscess was incised and drained.  It contained thick, greenish pus. A drain was left in the wound.

Submandibular abscess in an adult with diabetes mellitus.

Incision and drainage of submental abscess.