2 ENT Emergencies Flashcards
What are the ABCDEs of any medical emergency?
A = Airway
B = Breathing
C = Circulation
D = Disability/Drugs (what the patient is taking or what should be given)
E = Exposure/Environmental control
What is acute epiglottitis, pathogens, and why is it an emergency?
Epiglottitis is inflammation of the epiglottis, typically due to an infectious etiology resulting in rapid airway obstruction. Mortality rates can reach 20%, making urgent diagnosis and treatment essential.
The incidence has rapidly declined since the introduction of Haemophilus influenzae type b vaccination. Commonly a childhood disease in the past, it is more common now in adults. The most common bacteria identified include:
- H. influenzae
- beta-hemolytic Streptococcus
- Staphylococcus aureus
- Streptococcus pneumoniae
Current belief is that George Washington died from acute bacterial epiglottitis.
How does the presentation of epiglottitis differ in adults and children?
Children often present with:
- dyspnea
- drooling
- stridor
- fever
Adults often complain of
- severe sore throat
- odynophagia
- hoarseness
Historically, patients presented acutely but now more patients are presenting in a subacute fashion. The “tripod sign” is classically seen on presentation.
How should epiglottitis be diagnosed and treated?
The classic radiographic finding is referred to as the “thumb print sign” described as swelling of the epiglottis on lateral soft tissue neck x-ray.
In children, direct visualization via laryngoscopy in the operating room is recommended. Indirect laryngoscopy (fiber-optic nasopharyngeal laryngoscopy) can be considered in adults if the patient is stable enough to tolerate the procedure.
Once the diagnosis is made, treatment should consist of airway management and prompt antibiotic administration. Patients with respiratory distress should be intubated. Patients who are deemed medically stable from a respiratory standpoint may be observed closely (ICU) with medical management including
- antibiotics with activity against H. influenza (second- or third-generation cephalosporin)
- humidified air
- racemic epinephrine
- intravenous steroids.
It is important to remember that patients who are being observed should always have equipment for intubation and cricothyroidotomy available at the bedside.
Describe angioedema.
Angioedema is the abrupt onset of nonpitting*, *nonpruritic edema involving the reticular dermis, subcutaneous, and sub-mucosal layers of nondependent areas.
This can affect the lips, soft palate, larynx, and pharynx causing airway obstruction.
The duration typically ranges from 24 to 96 hours. Approximately 25% of the U.S. population will have an episode of urticaria and/or angioedema during their lifetime.
Acute angioedema is arbitrarily defined as symptom duration of less than 6 weeks.
What causes angioedema?
The most common causes of acute angioedema include medications, foods, infections, insect venom, contact allergens (latex), and radiology contrast material.
The evaluation of chronic angioedema and/or urticaria can be challenging. In the majority of cases, no etiology is ever found.
What is involved in the workup of angioedema?
In addition to a good history and physical examination, fiber-optic laryngoscopy may be used to determine the degree of laryngeal edema. Patients with angioedema who complain of dyspnea, hoarseness, voice changes, odynophagia, or have stridor on physical exam are likely to have laryngeal involvement. All patients with laryngeal edema require admission to the ICU.
What is the treatment of angioedema?
For patients with both angioedema and urticaria, treatment may consist of:
- Epinephrine
- Antihistamines (2nd Gen H1 + H2)
- Corticosteroids
For the majority of these patients, H1 antihistamines are the cornerstone of therapy. Although effective, they can also cause profound sedation. As a result of this, second-generation H1 antihistamines (loratadine [Claritin], cetirizine [Zyrtec], desloratadine [Clarinex], and fexofenadine [Allegra]) have become the treatment of choice for angioedema. H2 blockers, such as ranitidine [zantac] or famotidine [pepcid], are necessary as well to completely interrupt the histamine cascade.
Corticosteroids are indicated for patients with anaphylaxis, laryngeal edema, and severe symptoms unresponsive to antihistamines.
Isolated angioedema is often caused by medications, most commonly ACE inhibitors.
Patients with recurrent episodes should be evaluated for hereditary angioedema, a deficiency in C1 esterase inhibitor, with laboratory assessment of C1 inhibitor protein and C4 complement factor levels. Danazol has been the mainstay treatment for prophylaxis, although newer drugs with better side effect profiles are in clinical trials. During the acute illness, fresh frozen plasma can be given to replace C1 inhibitor levels.
Describe malignant otitis externa (MOE).
MOE is a potentially life-threatening ENT infection that involves the external auditory canal, temporal bone, and surrounding structures. Typically, MOE has an aggressive course and is associated with a high mortality rate, ranging from 50% to 80%.
MOE typically occurs in immunocompromised elderly patients. The most common comorbid condition associated with MOE is diabetes mellitus (Types 1 and 2).
What are the common bacteria associated with MOE?
Pseudomonas aeruginosa is the causative agent in the majority of cases of MOE. This organism is particularly virulent due to its mucoid coating that deters phagocytosis. In addition, some strains release a neurotoxin that is thought to contribute to a number of intracranial complications.
Patients with malignancy and HIV are at risk for infection with less common organisms, including: [PACKS]
- Proteus mirabilis
- Aspergillus
- Candida species
- Klebsiella oxytoca
- S. aureus
What is the presentation of MOE?
Patients with MOE present with:
- severe, unrelenting ear pain
- temporal headaches
- purulent otorrhea
_The hallmark physical examination finding is the presence of granulation tissue in the inferior portion of the external auditory canal, at the bone-cartilage junction_.
As the infection progresses, patients develop cranial nerve abnormalities, most commonly associated with the seventh cranial nerve. Once cranial nerve abnormalities develop, prognosis is poor. Mortality for patients with MOE and cranial nerve abnormalities approaches 100%.
How is the diagnosis of MOE made?
The diagnosis of MOE is confirmed with imaging studies including computed tomography (CT), magnetic resonance imaging (MRI), technetium bone scanning, and gallium citrate scintigraphy.
CT of the temporal bone is considered by many to be the initial imaging modality of choice to evaluate for bone destruction.
It is important to recognize that anywhere from 30% to 50% of bone must be destroyed before findings are evident on CT. For patients with a normal CT scan and high suspicion for MOE, either a bone scan* or *gallium scintigraphy has a high sensitivity for bone erosion.
Describe the treatment of MOE.
Treatment of MOE centers on antimicrobial therapy. Antipseudomonal antibiotics are the drugs of choice and must be initiated early. Fluoroquinolones [e.g. cipro] and aminoglycosides are considered by many to be the antibiotic of choice with cure rates close to 90%.
In addition to systemic antibiotics, patients should receive good aural toilet with debridement of granulation tissue.
Recent studies have suggested an adjuvant role for hyperbaric oxygen therapy for MOE.
What is acute invasive sinusitis and why is it considered an emergency?
Acute invasive fungal sinusitis (AIFS) is a major cause of morbidity and mortality in the immunocompromised patient population.
It is characterized as an aggressive and often fatal angioinvasive infection of the nose, paranasal sinuses, and neighboring structures. It has been increasingly diagnosed in immunocompromised patients with hematologic malignancies, immunosuppression, and poorly controlled diabetes mellitus.
What are the typical causes of AIFS?
The causative fungal organisms that typically function as saprophytes in the environment can become pathogenic in humans under certain circumstances. The typical species responsible for sinonasal invasive infections are Aspergillus and zygomycetes (Rhizopus, Mucor, Rhizomucor).
What is Ludwig’s angina.
Named after Karl Friedrich Willhelm von Ludwig, it is characterized as a rapidly progressive cellulitis of the soft tissues of the neck and floor of the mouth.
_With progressive swelling of the soft tissues and elevation and posterior displacement of the tongue, airway obstruction is the most emergent concern_. Prior to the development of antibiotics, mortality for Ludwig’s angina exceeded 50%. With antibiotic therapy and improved imaging modalities and surgical techniques, mortality currently averages <10%.
What causes Ludwig’s angina? Pathogens?
The majority of cases of Ludwig’s angina are of odontogenic origin. The submandibular space is the primary site of infection. This space is subdivided by the mylohyoid muscle into the sublingual space superiorly and the submaxillary space inferiorly. Once infection develops, it can spread contiguously to the sublingual space and can also spread to involve the pharyngomaxillary and retropharyngeal spaces, encircling the airway.
Polymicrobial infection occurs in over 50% of cases. The most commonly cultured organisms include:
- Staphylococcus
- Streptococcus
- Bacteroides species
