6.1 Neck Emergencies
6.1.1 Necrotizing Soft Tissue Infections of the Head and Neck
Key Features
Necrotizing fasciitis is a soft tissue infection that causes necrosis of fascia and subcutaneous tissue but initially spares skin and muscle.
It is rare in the head and neck; when it occurs it is usually associated with immunosuppression or odontogenic infection.
Half of patients develop systemic bacteremia.
Necrotizing soft tissue infections require aggressive treatment to combat the associated high morbidity and mortality.
Necrotizing soft tissue infections rarely may involve the face and neck, scalp, and eyelids.
Epidemiology
In the head and neck, dental infections are the most common etiology, followed by trauma, peritonsillar and pharyngeal abscesses, and osteoradionecrosis. Immunocompromised patients are most susceptible. Predisposing conditions include diabetes mellitus, obesity, arteriosclerosis, alcoholism, chronic renal failure, hypothyroidism, malignancy, and poor nutrition. Gas-producing wound infections are usually produced by bacteria of the Clostridia class. Onset of symptoms is usually 2 to 4 days after the insult.
Clinical
Signs
The signs of a necrotizing soft tissue infection include a low-grade fever, and the skin becomes smooth, warm, tense and shiny with no sharp demarcation. The infected skin also develops a dusky discoloration with poorly defined borders. Soft tissue crepitus is common from gas formation (though not necessary for the diagnosis). Later in the disease process, bullae may develop. Systemic symptoms get more severe with typical signs of septicemia. The last stage of the disease is characterized by cyanotic skin discoloration typical of necrosis. Patients may present with a benign clinical picture yet with a leukocytosis not consistent with the clinical picture.
Symptoms
There is sudden severe pain and swelling. There may be anesthesia of the involved skin.
Differential Diagnosis
The differential diagnosis includes other deep neck space infections, pyoderma gangrenosum, radiation necrosis, cellulitis, and erysipelas.
Evaluation
Physical Exam
When clinical hard signs are present (i.e., crepitus, skin necrosis, bullae, hypotension), a physical exam may be helpful. Unfortunately, the signs and symptoms are often very subtle on presentation.
Imaging
Plain soft tissue films of the neck (looking for gas in soft tissue) may be obtained. Computed tomography (CT) is the most useful study to detect gas in areas inaccessible to palpation and to identify areas where the infection has spread. In addition, it can detect vascular thrombosis, erosion of vessels, and mediastinitis. Magnetic resonance imaging (MRI) has also been suggested, as it can demonstrate areas of enhancement or infection that crosses fascial planes.
Labs
Routine blood work is needed to look for metabolic abnormalities such as hyponatremia and hypoproteinemia due to fluid sequestration and hypocalcemia as a result of subcutaneous fat saponification. Additionally, a complete blood count will note a significantly elevated white blood cell count.
Microbiology
Group A hemolytic streptococci and Staphylococcus aureus, alone or in synergism, are frequently the initiating infecting bacteria. However, other aerobic and anaerobic pathogens may be present, including Bacteroides, Clostridium, Peptostreptococcus, Enterobacteriaceae, coliforms, Proteus, Pseudomonas, and Klebsiella species.
Pathology
The pathology shows a localized necrosis of skin that is secondary to thrombosis of nutrient vessels as they pass through involved fascia. Tissue hypoxia resulting from small vessel vasculitis and thrombi and impaired host defenses help facilitate anaerobic bacterial growth.
Treatment Options
Prompt measures offer hope for survival of the patient.
Medical
High-dose intravenous (IV) broad-spectrum antibiotics are recommended. Hyperbaric oxygen therapy is sometimes used in addition to surgical and antimicrobial treatment.
Surgical
Aggressive surgical debridement until there are bleeding viable borders is necessary. This may require multiple trips to the operating room for irrigation and debridement and/or bedside dressing changes and debridement. Initially, it is important not to close the wound with larger defects, due to the progressive nature of the disease process. If the necrotizing process involves the neck, avoid tracheotomy through the infected area.
Outcome and Follow-Up
The overall mortality rate has been reported to be as high as 70%.
6.1.2 Ludwig′s Angina
Key Features
Ludwig′s angina is a rapidly expanding, diffuse inflammation of the submandibular and sublingual spaces.
It is most often caused by dental infections.
The condition is often found in immunocompromised patients, such as those with diabetes or human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS) or drug abusers.
Ludwig′s angina is a rapidly spreading bilateral cellulitis of the sublingual and submaxillary spaces. Before the advent of antibiotics, the mortality associated with Ludwig′s angina approached 50%, but today, mortality rates are in the range of 8 to 10%. The most common cause of death is respiratory compromise.
Epidemiology
Ludwig′s angina represents up to 13% of all deep neck infections. Typically, young adults present with Ludwig′s angina; it is unusual in children. The infection generally spreads from a dental or periodontal infection. Other causes include upper respiratory infections, floor-of-mouth trauma, mandibular fractures, sialadenitis, IV drug abuse, trauma and tonsillitis, and immunocompromised states such as diabetes or HIV/AIDS. Forty percent of Ludwig′s angina cases involve oral anaerobes.
Clinical
Signs
The signs of the infection include an inability to close the mouth, trismus, drooling, sitting upright, inability to swallow and dysphonia, dyspnea, stridor, fever, chills, and tachycardia. Note that stridor, dyspnea, decreased air movement, or cyanosis suggest impending respiratory compromise.
Symptoms
The symptoms of Ludwig′s angina are severe neck pain and tenderness, submandibular and submental swelling, fever, malaise, and dysphagia.
Differential Diagnosis
The differential diagnosis includes other deep neck space infections, an infected cyst, tumor, and cellulitis.
Evaluation
Physical Exam
On physical examination, the patient will often present with carious molar teeth, neck rigidity, and drooling. There is a “woody” or “brawny” induration of involved spaces with little to no fluctuance. The patient′s mouth floor is swollen, and the tongue may be swollen or elevated. The patient may describe difficulty breathing and may have audible breathing.
Imaging
A computed tomography (CT) scan is most useful.
Labs
Blood cultures are usually negative; if the swelling is aspirated or drained, samples should be sent for Gram stain, culture, and sensitivity.
Treatment Options
Airway control is the first priority of treatment, followed by IV antibiotics and timely surgical drainage. Blind oral or nasotracheal intubation or attempts with neuromuscular paralysis are contraindicated in Ludwig′s angina, as they may precipitate an airway crisis.
Medical
Aggressive empiric high-dose, IV antibiotics are recommended—cefuroxime plus metronidazole. If the patient is allergic to penicillin, prescribe clindamycin plus a quinolone. Once culture and sensitivity results have been obtained, antibiotic therapy may be changed accordingly.
Surgical
To establish airway control, a tracheotomy may be indicated. Surgical drainage was once universally required but now may be reserved for cases in which antibiotic treatment fails. On external incision and drainage, often straw-colored material, as opposed to frank purulence, is found. Consider placement of a passive drain to allow continued drainage as the infection resolves.
Complications
A spontaneous rupture may lead to asphyxia, aspiration, or pneumonia. The infection may spread to other deep neck compartments.
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