Updated: Apr 2, 2008
Mediastinitis is an infection involving the mediastinum. It is a surgical emergency with a high mortality rate. Mediastinitis may begin primarily from structures in the mediastinum, or it may be the result of an infection extending downward from the oropharynx, in which case it is called descending necrotizing mediastinitis.
The criteria for the diagnosis of descending necrotizing mediastinitis include the following:
Infection of the mediastinum is typically polymicrobial in nature resulting from a disruption of normal mucosal and tissue barriers. Infection may result from a rupture of the esophagus or trachea or from surgical intervention. When infection extends from the head and neck downward into the mediastinum, the condition is described as descending necrotizing mediastinitis because the infection uses the fascial planes in the neck to gain access to the mediastinum. It is necrotizing, as the infection is often polymicrobial in etiology with gas-producing organisms. The potential spaces that can allow infections from the head or neck to enter the mediastinum include the following:
Carotid space
The carotid sheath is a thick, matted, fibrous investment over the main longitudinal vessels of the neck. Lymph nodes are contained within the sheath, and infection in these nodes potentially could spread downward into the mediastinum. The carotid sheath extends from the arch of the aorta to the base of the skull.
Prevertebral space
This space is bounded anteriorly by the prevertebral fascia, which overlies the prevertebral muscles in the neck. The prevertebral fascia extends from the base of the skull to the lower limit of the longus colli muscle, which is approximately at the level of T3 vertebra.
Danger space
This potential space lies between the alar and prevertebral fasciae. It is patent from the skull base to the diaphragm. Its upper part is the retropharyngeal space, which lies between the prevertebral fascia and the buccopharyngeal fascia on the outer surface of the pharynx. Lymph nodes are present in this space.
Pathological walling-off of infection usually occurs in the retropharyngeal space, but no anatomical barrier exists to the spread of infection downward into the mediastinum. The lower part of this potential space extends behind the esophagus, through the superior mediastinum, and into the posterior mediastinum.
More than 90% of cases of acute mediastinitis are caused by esophageal rupture. This may be due to trauma (eg, MVA, chicken bone), neoplasm, surgery, or endoscopy. See Esophageal Perforation, Rupture and Tears for more detail on this subject.
Comorbid conditions (eg, diabetes) may make certain patients highly susceptible to spreading cellulitis. Mediastinitis may also result from direct extension from an adjacent source of infection including osteomyelitis of the sternoclavicular junction. Pulmonary infections may also extend into the mediastinal space. Mediastinitis may also result from extension of granulomatous disease from mediastinal lymph nodes.
Pathogens
This is often a mixed infection, with facultative and strict aerobes acting together. Obligate anaerobes usually outnumber facultative organisms by 10:1. Streptococcus species are the most common facultative organisms, while Bacteroides species are the most common strict aerobes. Other organisms implicated include Pseudomonas aeruginosa and species of Fusobacterium, Peptostreptococcus, and Staphylococcus. Case reports have identified Eikenella corrodens and species of Prevotella, Haemophilus, and Salmonella as responsible pathogens. Histoplasmosis and tuberculosis have also been implicated in mediastinitis. As the incidence of iatrogenic mediastinitis rises compared with infections acquired outside the hospital, methicillin-resistant Staphylococcus aureus infections become a cause for great concern.
Candidal species and even aspergillus have been implicated in cases of meningitis.
Esophageal rupture is the most common cause of mediastinitis currently. Descending necrotizing infection is relatively rare in the era of antibiotic use.
In developing countries, mediastinitis still is a common devastating potential complication of head and neck infections.
Prevalence is higher among males than females, with a male-to-female ratio of 6:1.
Patients usually have experienced symptoms for a few days before presentation to the ED. Occasionally, patients present with a fulminant course and symptoms that have lasted only a few hours.
A complete examination of the head and neck, including the oral cavity, is essential. Such an examination may yield findings such as the following:
| CBRNE - Anthrax Infection | Pharyngitis |
| Cellulitis | Pneumonia, Empyema and Abscess |
| Esophageal Perforation, Rupture and
Tears | Shock, Septic |
| Necrotizing Fasciitis | Superior Vena Cava Syndrome |
Ludwig angina
Mediastinitis may result in airway compromise. Protection of the airway is vital. Since patients may present in septic shock, adequate volume resuscitation is essential.
Because mediastinitis usually is a mixed growth infection, wide antimicrobial coverage is required. The cause of infection should be determined. Extension of a Staphylococcus aureus osteomyelitis should be managed differently from an esophageal rupture; however, in the absence of a source and definitive microbiological data, broad-spectrum therapy is indicated. Combinations such as piperacillin-tazobactam with vancomycin or ceftazidime with vancomycin or vancomycin with a fluoroquinolone and clindamycin should be used. An aminoglycoside may be added to broaden gram-negative coverage.
Therapy must cover all likely pathogens in the context of the clinical setting.
Third-generation cephalosporin that has broad-spectrum gram-negative activity, lower efficacy against gram-positive organisms, and higher efficacy against resistant organisms. By binding to one or more of the penicillin-binding proteins, it arrests bacterial cell wall synthesis and inhibits bacterial growth.
1-2 g IV qd; not to exceed 4 g/d
50-75 mg/kg/d IV divided bid
Probenecid may increase levels; coadministration with ethacrynic acid, furosemide, and aminoglycosides may increase nephrotoxicity
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in renal impairment; caution in breastfeeding women and allergy to penicillin
Lincosamide that is useful treatment of serious skin and soft tissue infections caused by most staphylococcal strains. Effective against aerobic and anaerobic streptococci, except enterococci. Inhibits bacterial protein synthesis by inhibiting peptide chain initiation at the bacterial ribosome where it preferentially binds to the 50S ribosomal subunit, causing bacterial growth inhibition.
600-1200 mg/d IV divided bid/tid/qid
For very severe infections, dose range may be 1200-2700 mg/d IV
Doses as high as 4800 mg/d have been given in exceptional circumstances
<1 month: 15-20 mg/kg/d IV divided tid/qid
1 month to 16 years: 20-40 mg/kg/d IV divided tid/qid
Increases duration of neuromuscular blockade, induced by tubocurarine and pancuronium; erythromycin may antagonize effects; antidiarrheals may delay absorption
Documented hypersensitivity; regional enteritis: ulcerative colitis; hepatic impairment; antibiotic-associated colitis
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in severe hepatic dysfunction; no adjustment necessary in renal insufficiency; associated with severe and possibly fatal colitis by allowing overgrowth of Clostridium difficile
Used for treatment of multiple organism infections in which other agents do not have wide spectrum coverage or are contraindicated because of their potential for toxicity.
500-1000 mg IV q6h
Patients with impaired renal function need lower doses
50 mg/kg/d IV divided tid/qid
Coadministration with cyclosporine may increase CNS adverse effects of both agents; coadministration with ganciclovir may result in generalized seizures
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Adjust dose in renal insufficiency; avoid use in children <12 years because they may be prone to neurotoxicity of drug
Active against various anaerobic bacteria and protozoa. Appears to be absorbed into the cells and the intermediate metabolized compounds that bind DNA are then formed and inhibit synthesis, causing cell death.
15 mg/kg IV over 1 h initially, followed by 7.5 mg/kg q6h IV infusion; not to exceed 4 g/d
15-30 mg/kg/d IV divided bid/tid for 7 d, or 40 mg/kg PO once; not to exceed 2 g/d
May increase toxicity of anticoagulants, lithium, and phenytoin; cimetidine may increase toxicity; disulfiram reaction may occur with orally ingested ethanol
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in hepatic disease; monitor for seizures and development of peripheral neuropathy
An aminoglycoside antibiotic effective against Pseudomonas aeruginosa, Escherichia coli, Proteus, Klebsiella, and Staphylococcus species.
Numerous dosing regimens are available, and they are adjusted based on creatinine clearance and changes in the volume of distribution. The dose of gentamicin may be given IV or IM.
3 mg/kg/d IV divided tid
>1 week: 6-7.5 mg/kg/d IV divided tid
Coadministration with other aminoglycosides, cephalosporins, penicillins, and amphotericin B may increase nephrotoxicity; aminoglycosides enhance effects of neuromuscular blocking agents, thus prolonged respiratory depression may occur
Coadministration with loop diuretics may increase auditory toxicity of aminoglycosides; possible irreversible hearing loss of varying degrees may occur (monitor regularly)
Documented hypersensitivity; non–dialysis-dependent renal insufficiency
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Narrow therapeutic index (not intended for long-term therapy); caution in renal failure (not on dialysis), myasthenia gravis, hypocalcemia, and conditions that depress neuromuscular transmission; adjust dose in renal impairment
Antipseudomonal penicillin plus beta-lactamase inhibitor. Inhibits the biosynthesis of cell wall mucopeptide and is effective during the stage of active multiplication. This medication has a broad antimicrobial spectrum that is effective again most oral, respiratory, and GI bacterial pathogens. Used in concert with gentamicin, strong anti-gram-negative activity occurs.
3.375 g IV q6h; adjust to 2.25 g IV q6h for creatinine clearance <20
<6 months: Not established
>6 months: 240-400 mg/kg/d IV divided q6h
Tetracyclines may decrease effects of piperacillin; high concentrations of piperacillin may physically inactivate aminoglycosides if administered in same IV line; effects when administered concurrently with aminoglycosides are synergistic; probenecid may increase penicillin levels; high-dose parenteral penicillins may result in increased risk of bleeding
Documented hypersensitivity; severe pneumonia, bacteremia, pericarditis, emphysema, meningitis, and purulent or septic arthritis should not be treated with an oral penicillin during the acute stage
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Perform CBCs prior to initiation of therapy and at least weekly during therapy; monitor for liver function abnormalities by measuring AST and ALT levels during therapy; exercise caution in patients with hepatic insufficiencies; perform urinalysis, and BUN and creatinine determinations during therapy and adjust dose if values become elevated; monitor blood levels to avoid possible neurotoxic reactions; caution when administering medication to patients on heparin or warfarin
Drug combination of beta-lactamase inhibitor with ampicillin. Interferes with bacterial cell wall synthesis during active replication, causing bactericidal activity against susceptible organisms.
1.5 (1 g ampicillin + 0.5 g sulbactam) to 3 g (2 g ampicillin + 1 g sulbactam) IV/IM q6-8h; not to exceed 4 g/d sulbactam or 8 g/d ampicillin
<3 months: Not established
3 months to 12 years: 100-200 mg ampicillin/kg/d (150-300 mg Unasyn) IV divided q6h
>12 years: Administer as in adults; not to exceed 4 g/d sulbactam or 8 g/d ampicillin
Probenecid and disulfiram elevate ampicillin levels; allopurinol decreases ampicillin effects and has additive effects on ampicillin rash; may decrease effects of oral contraceptives
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in renal failure; evaluate rash and differentiate from hypersensitivity reaction
Inhibits cell wall synthesis. Accomplished by binding to carboxyl units on peptide subunits containing free D-alanyl-D-alanine.
Effective against methicillin-resistant S aureus.
500 mg to 1 g (ie, 10 mg/kg DBW) IV q8-24h (based on CrCl)
40 mg/kg/d IV divided q6h
Erythema, histaminelike flushing, and anaphylactic reactions may occur when administered with anesthetic agents; taken concurrently with aminoglycosides, risk of nephrotoxicity may increase above that with aminoglycoside monotherapy; effects in neuromuscular blockade may be enhanced when coadministered with nondepolarizing muscle relaxants
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in renal failure, neutropenia; red man syndrome is caused by too rapid IV infusion (dose given over a few min) but rarely happens when dose given IV over 2 h administration or as PO or IP administration; red man syndrome is not an allergic reaction
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descending necrotizing mediastinitis, oropharynx, oropharyngeal infection, mediastinum, mediastinitis, infection of the mediastinum, head and neck infection, head infection, neck infection
Ethan S Brandler, MD, MPH, Clinical Assistant Instructor, Staff Physician, Departments of Emergency Medicine and Internal Medicine, University Hospital of Brooklyn, Kings County Hospital
Disclosure: Nothing to disclose.
Richard Sinert, DO, Associate Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center
Richard Sinert, DO is a member of the following medical societies: American College of Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Eric Kardon, MD, FACEP, Associate Staff, Division of Emergency Medicine, Athens Regional Medical Center
Eric Kardon, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians
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Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
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Jeter (Jay) Pritchard Taylor III, MD, Compliance Officer, Attending Physician Emergency Medicine Residency, Department of Emergency Medicine, Palmetto Richland Memorial Hospital, University of South Carolina
Jeter (Jay) Pritchard Taylor III, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, and Society for Academic Emergency Medicine
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John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
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Jonathan Adler, MD, Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital; Division of Emergency Medicine, Harvard Medical School
Jonathan Adler, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
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