Archive for March, 2007

Intranasal Fentanyl Comparable to IV Morphine for Acute Pain in Children

Posted by Jeff Hugus, MD — published on March 26th, 2007

NEW YORK (Reuters Health) Mar 23 - Intranasal fentanyl achieves pain relief comparable to intravenous (IV) morphine for emergency department management of acute pain in children who have sustained long bone fractures, Australian researchers report in the March issue of Annals of Emergency Medicine. Intranasal fentanyl can also be administered more easily and rapidly, and has potential use in general practice and other out-of-hospital settings.

“The introduction of intranasal fentanyl has revolutionized the provision of analgesia to children in the initial presentation of any acutely painful conditions, not just in the trauma setting,” lead investigator Dr. Meredith Borland told Reuters Health.

In the pediatric emergency department, rapid, effective, and painless delivery of analgesia is desirable. It is routine in many facilities to give IV morphine to children in pain.

However, Dr. Borland of the Princess Margaret Hospital for Children, Subicao, and colleagues note that insertion of an IV cannula requires special skills, is time and staff dependent, and can cause pain and anxiety in some children.

To evaluate an alternative approach, the team conducted a prospective, double-blind, placebo-controlled, trial with 67 children between 7 and 15 years old. The subjects, who had “clinically deformed closed long-bone fractures,” were randomized to intravenous morphine (10 mg/mL) and intranasal placebo or intranasal concentrated fentanyl (150 mcg/mL) and intravenous placebo.

There were no significant differences in analogue pain scores before treatment or from 5 to 30 minutes after receiving analgesia. The mean total fentanyl dose was 1.7 mcg/kg and the mean total morphine dose was 0.11 mg/kg.

Having adopted the method, continued Dr. Borland, “we can now give effective analgesia within minutes of arrival without the distress of needles. In our department,” she concluded, “we now insert fewer IV cannulas and do not hold back on giving opiate analgesia for fear of causing distress.”

Ann Emerg Med 2007;49:335-340.

Reuters Health Information 2007. © 2007 Reuters Ltd.

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categories: Emergency Medicine

Aspirin Plus Clopidogrel Debated for ACS Patients in ED

Posted by Jeff Hugus, MD — published on March 26th, 2007

“There is a great deal of controversy regarding the combination therapy of aspirin (ASA) plus clopidogrel” for patients with acute coronary syndromes, according to Amal Mattu, MD, FAAEM, associate professor of the department of emergency medicine at the University of Maryland School of Medicine in Baltimore. While there is “no doubt” that aspirin should be given to everyone except those with true allergies, he said, “the debate is whether to give [patients presenting with non-ST segment elevation] aspirin plus clopidogrel.”

Dr Mattu and others at the 13th annual meeting of the American Academy of Emergency Medicine (AAEM) discussed the latest recommendations regarding combination antiplatelet treatment by emergency physicians of patients with acute non–ST segment elevation ACS (NSTE-ACS).

The benefit of ASA in patients with what was then referred to as unstable angina was proven 20 years ago, with studies showing a reduction in early and late myocardial infarction and death rates of between 50% and 70%. With benefits of aspirin this profound, there have been many advocating desensitization of allergic patients, according to Dr. Mattu.

“Aspirin should be in the water,” David DuBois, MD, a session attendee and emergency medicine specialist in Pinehurst, North Carolina, told Medscape.

When it comes to treating patients with clopidogrel in addition to ASA in the emergency department (ED) before knowing with certainty whether or not they will require coronary artery bypass graft (CABG) surgery, the current recommendations vary. “There are certain benefits to giving clopidogrel, and it should be given to patients that have a true, severe allergy to aspirin, instead of aspirin,” Dr. Mattu said.

Benefits of early administration (within 24 hours) followed by subsequent use is associated with a 1% absolute decrease in the risk of death, stroke or myocardial infarction by 9 months, and carries a 1% absolute increase in the risk of major bleeding, according to the findings a study by Fitchett and colleagues in the June 2006 issue of the Canadian Journal of Cardiology.

Patients who end up requiring CABG surgery within 5 days of presenting in the ED and placed on clopidogrel plus aspirin combination therapy have an increased risk of perioperative bleeding.

“There have been no good criteria that have been proven to predict that NSTE-ACS patients will not need a CABG,” said Dr. Mattu, highlighting the current dilemma for the ED physician in knowing which patient might be a risk for bleeding complications with clopidogrel on board.

Clopidogrel tends to work best in ACS patients who are truly high risk (eg, positive troponins, ST-segment depression), but those are also the patients who are most likely to need CABG, explained Dr. Mattu.

To date, there is insufficient evidence to make definite recommendations about whether these medications should be initiated in the ED or wait for the interventional cardiologist start the medications in the cath lab.

“We don’t give clopidogrel before it is discussed with the cardiologist,” Mary Burns, MD, an emergency medicine specialist at Northshore Medical Center affiliated with Harvard University in Boston, told Medscape.

At Lenox Hill Hospital in New York City, “the cardiologists prefer us to give [clopidogrel] right away,” Robert Glatter, MD, attending emergency physician at the hospital, told Medscape. “We’ve not seen higher bleeding rates in our patients here,” he said.

None of the quoted physicians report any relevant financial disclosures.

Medscape Medical News

Karen Dente, MD
AAEM 13th Annual Scientific Assembly: Plenary Session Lecture. Presented March 12, 2007.

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categories: Emergency Medicine

ENT Emergencies Review

Posted by Paul Rega, MD — published on March 8th, 2007

Evidence-Based Diagnosis and Management of ENT Emergencies

by

Michael Winters, MD

Medscape Emergency Medicine.  2007; ©2007 Medscape

Posted 02/15/2007

  

Introduction

Emergency physicians (EPs) diagnose and treat a variety of ear, nose, and throat (ENT) disorders on a daily basis. Although the majority of these conditions are benign, there are several critical ENT disorders that must be immediately recognized and treated. The following article discusses these potentially life-threatening ENT conditions, namely, acute epiglottitis, angioedema, malignant (necrotizing) otitis externa (MOE), Ludwig’s angina, and tracheoinnominate (TI) fistula. In recent years, numerous reviews, trials, and recommendations have been published that have advanced the understanding of the pathophysiology and clarified the appropriate diagnostic work-up and management of these conditions. With this information, the EP can more effectively recognize these disorders and provide current, evidence-based treatment.

Epiglottitis in Adults

Although still debated by some historians, it is believed that George Washington died from a case of acute bacterial epiglottitis.[1] In fact, his is probably the first recorded death from this disorder.[2] Epiglottitis is defined as inflammation of the epiglottis, most often due to an infectious etiology. Rapid airway obstruction can result from progressive inflammation and edema of the epiglottis. Mortality rates for epiglottitis range from 7% to 20% in adults and are directly related to the development of airway obstruction.[2,3] Thus, urgent diagnosis and treatment are essential. Unfortunately, delays in diagnosis are common. It is estimated that epiglottitis is missed by primary care physicians in all but 35% of cases.[2,4]

Early descriptions of epiglottitis consisted primarily of case reports in the adult population.[2] Since the 1960s, however, epiglottitis has been described as largely a childhood disease. Then, with the widespread application of the Haemophilus influenzae type b vaccination, the incidence of the disease in the pediatric population markedly declined.[2,5,6] As a result of this decline, acute epiglottitis is now more common in adults, and not only is it more common in adults; recent reports indicate that the incidence is rising.[7,8] The current annual incidence of epiglottitis in adults ranges from 1.0 to 3.1 per 100,000 persons per year.[7,8] The average age at presentation ranges from 42 to 50 years, with the peak incidence occurring from ages 35 to 39.[3,9] Depending on the study, there is a slight male predominance that ranges from 2:1 to 4:1.[2,10,11]

The most common cause of acute epiglottitis is infection. A variety of bacteria have been implicated in the disease. The most common bacteria identified include H influenzae, beta-hemolytic Streptococcus, Staphylococcus aureus, and Streptococcus pneumoniae.[3] Although viruses are considered by many to be a common cause, only herpes simplex has been positively identified on histologic specimens.[2,12] Patients with immunosuppressive conditions, such as those with HIV, are at risk for infection from atypical organisms. Atypical organisms linked to epiglottitis in the immunocompromised population include Aspergillus, Candida, and Klebsiella.[2,13] In many cases, a causative organism is not isolated.

In addition to infection, there are a number of noninfectious etiologies of epiglottitis. Perhaps most important is the development of epiglottitis from thermal inhalation injury. Recent reports have illustrated the inhalation of crack cocaine as an etiology of noninfectious epiglottitis.[14,15] Additional noninfectious etiologies include neck trauma and caustic ingestions.[3,16]

The clinical presentation of epiglottitis in adults is different from that in children. In contrast to children, adults are less likely to present with dyspnea, drooling, stridor, or fever. Adults are more likely to report severe sore throat, odynophagia, and hoarseness. In fact, the combination of severe sore throat and odynophagia is present in over 90% of adults with epiglottitis.[3] Delays in presentation are common. Typically, adults present an average of 2 days after the onset of symptoms.[3] Carefully exam the neck in adults with severe sore throat. Up to 80% of adults with epiglottitis have marked anterior neck tenderness on physical examination.[8,17,18] Suspect epiglottitis in any adult with severe sore throat, odynophagia, and tenderness of the larynx.

The gold standard for diagnosis is direct visualization of the epiglottis and surrounding structures. Direct visualization is accomplished through laryngoscopy. In contrast to children, indirect laryngoscopy is considered a safe procedure in adults with suspected epiglottitis.[2] Fiber-optic nasopharyngeal laryngoscopy (NPL) can also be used to visualize the posterior elements of the hypopharynx, including the epiglottis. It is important to recognize that radiographs are of limited value. Depending on the study, the overall sensitivity of plain films for epiglottitis can be as low as 75%.[3] The classic radiographic finding is swelling of the epiglottis on lateral soft-tissue neck x-ray, commonly referred to as the “thumb sign”. This sign is absent in 14% to 27% of cases.[3] In a recent study, Ducic and colleagues[19] described the “vallecula sign”. The vallecula sign is characterized by a decrease in the vallecular air space as the epiglottis swells.[9] With appropriate training, the investigators were able to diagnose epiglottitis with plain films with 98.8% accuracy.[19] Although promising, the initial study involved only a small number of positive plain films, and further study is needed before widespread clinical application. Arterial blood gas analysis and the white blood cell count are nonspecific and of no diagnostic or prognostic value in epiglottitis.

Once the diagnosis is confirmed, treatment centers on airway management and prompt antibiotic administration. Up to one third of patients with epiglottitis eventually require endotracheal intubation.[9] Any patient with respiratory distress should be immediately intubated. Recognize that intubation is often difficult due to significant swelling of the epiglottis and surrounding structures, and any attempts at blind intubation must be avoided. Up to 15% of patients in whom blind intubation is attempted require emergent tracheotomy.[9,17] For patients without respiratory distress, the literature is less clear. A number of retrospective reviews have attempted to identify clinical features that predict airway deterioration. Unfortunately, there is no particular sign or combination of signs that has been shown to consistently identify patients who will require airway support.[3] For patients who are being observed, always have equipment for intubation and cricothyroidotomy available at the bedside.

The majority of adults with epiglottitis will respond to medical management with antibiotics and close observation. Current recommendations are that patients receive a second- or third-generation cephalosporin with activity against H influenzae.[2,3] At present, there are no controlled trials that demonstrate the benefit of aerosolized racemic epinephrine, corticosteroids, or humidified air. Given the potential for airway compromise, all patients with epiglottitis require admission to an intensive care unit (ICU).

Angioedema

Angioedema is characterized by the abrupt onset of nonpitting, nonpruritic edema involving the reticular dermis, subcutaneous, and submucosal layers.[20-22] Lesions are well defined, asymmetric, and located in nondependent areas. Common locations include the lips, periorbital area, extremities, abdominal viscera, and genitalia. The duration of individual lesions typically ranges from 24 to 96 hours. Most patients present with the combination of urticaria and angioedema. In fact, up to 25% of the US population will have an episode of urticaria and/or angioedema during their lifetime.[23,24] Of these patients, up to 10% will have isolated angioedema.

Angioedema is caused by either mast cell-mediated or nonmast cell-mediated mechanisms. Mast cell-mediated mechanisms typically present with the combination of urticaria and angioedema. Regardless of the exact mechanism, there is degranulation of mast cells and the release of vasoactive substances. Patients with isolated angioedema usually have symptoms as a result of a nonmast cell-mediated mechanism. The two most common nonmast cell-mediated mechanisms include alterations in the bradykinin pathway, ie, angiotensin-converting enzyme (ACE) inhibitor-induced angioedema and abnormalities in the complement system — hereditary angioedema.

The evaluation of patients with angioedema centers on the history, and one of the most important aspects of the history is to determine symptom duration. Acute angioedema is arbitrarily defined as symptom duration of less than 6 weeks. The most common causes of acute angioedema include medications, foods, infections, insect venom, contact allergens (latex), and radiocontrast material.[22,24,25] Of these, medications, foods, and viral infections account for the majority of cases. Patients with angioedema must be questioned about medications, new foods, and infectious symptoms. Less common etiologies of acute angioedema include physical stimuli, environmental triggers, and endocrine disorders. Patients with symptoms longer than 6 weeks are classified as having chronic angioedema. The evaluation of chronic angioedema and/or urticaria can be challenging. In the majority of cases, no etiology is ever found.

Unless suggested by findings from the history and/or physical examination, there is no role for “routine” labs (complete blood count, basic metabolic panel, liver function tests, erythrocyte sedimentation rate, and urinalysis) in the evaluation of acute angioedema. Laboratory testing, in an attempt to detect occult disease, is typically deferred until at least 6 weeks of persistent symptoms. Even in patients with protracted symptoms, laboratory testing yields little additional information. In a recent study of over 6400 patients with angioedema and/or urticaria with at least 6 weeks of symptoms, laboratory testing detected occult disease in just 1.6% of patients.[26]

In addition to a good history and physical examination, fiber-optic NPL is often used. It is well known that angioedema of the larynx is a marker of severe disease and can result in rapid airway obstruction. Fiber-optic NPL provides the physician the ability to determine the presence of laryngeal edema. On the basis of recent studies, patients with angioedema who complain of dyspnea, hoarseness, voice changes, odynophagia, or have stridor on physical exam are likely to have laryngeal involvement.[27,28] Patients with angioedema and these symptoms should undergo fiber-optic NPL. All patients with laryngeal edema require admission to the ICU.

For patients with the combination of angioedema and urticaria, treatment may consist of epinephrine, antihistamines, and corticosteroids. Patients presenting in severe respiratory distress or with marked laryngeal edema on NPL should be given epinephrine subcutaneously at a dose of 0.3 mg (0.3 mL of 1:1000 solution). For the majority of these patients, H1-antihistamines are the cornerstone of therapy. In addition to relieving pruritus, these medications reduce the number, size, and duration of lesions.[29] Although effective, the first-generation H1-antihistamines (diphenhydramine, hydroxyzine) are limited by the side effect of profound sedation. As a result, second-generation H1-antihistamines (loratadine, cetirizine, desloratadine, and fexofenadine) have become the agents of choice.[30] These medications have less central nervous system penetration, thereby producing less sedation. There are currently no controlled trials that demonstrate the superiority of any second-generation H1-antihistamine.[31] For patients whose symptoms are not controlled with an H1-antagonist, an H2-antagonist may be added to the medical regimen. Up to 15% of histamine receptors in the skin are of the H2 subtype. The combination of an H1- and H2-antagonist has been shown to be beneficial in some patients.[24] Corticosteroids are indicated for patients with anaphylaxis, laryngeal edema, and severe symptoms unresponsive to antihistamines.[32] Recommended corticosteroid doses for patients with severe angioedema and urticaria range from 0.5 to 1.0 mg/kg/day.[32]

Management of the patient with isolated angioedema is controversial. As discussed, these patients typically have nonmast cell-mediated mechanisms of angioedema. The majority of patients have isolated angioedema secondary to an ACE inhibitor. In fact, up to 68% of cases of isolated angioedema are due to an ACE inhibitor.[33-36] Treatment of ACE inhibitor angioedema focuses on discontinuation of the drug, airway management, and supportive care. In addition to severe laryngeal edema on NPL, indications for intubation of the patient with ACE inhibitor angioedema include tongue edema and edema of the floor of the mouth.[33,34,37] Although epinephrine, antihistamines, and corticosteroids can be given to these patients, there are no controlled trials that demonstrate their efficacy in ACE inhibitor angioedema.[22,38,39] All intubated patients, patients with laryngeal edema, and those with severe symptoms require admission to the ICU.

Finally, it is important to recognize and avoid medications that can exacerbate angioedema and/or urticaria. Medications that have been shown to exacerbate symptoms are aspirin, nonsteroidal anti-inflammatory drugs, opiates, and estrogen-containing compounds in any patient with angioedema..[22,25] In addition, any patient with ACE inhibitor angioedema should not be switched to an angiotensin receptor blocker (ARB). Although the incidence is less than that with ACE inhibitors, ARBs have been shown to also cause angioedema. A recent study illustrated that 32% of patients with angioedema due to an ARB had a prior episode of ACE inhibitor angioedema.[40] ARBs should not be considered a safe alternative in patients with ACE inhibitor angioedema.

MOE

MOE is a potentially life-threatening ENT infection that involves the external auditory canal, temporal bone, and surrounding structures. Although case reports can be traced to the early 1800s, it was not until the late 1960s that MOE was defined as a clinical disease. Typically, MOE has an aggressive course and is associated with a high mortality rate. Depending on the complications, mortality rates for MOE range from 50% to 80%.[41,42]

MOE almost always occurs in immunocompromised patients. The most common comorbid condition associated with MOE is diabetes mellitus. In one study, up to 90% of patients with MOE were diabetic.[43] There is no difference in predisposition between type 1 and type 2 diabetes mellitus. Recent reports have highlighted the rising incidence of MOE in patients with HIV.[44-46] It is important to recognize that HIV patients with MOE tend to be younger than diabetic patients with the disorder. In addition to HIV, lymphoproliferative disorders and medication-induced immunosuppression have been identified as risk factors for MOE.[42]

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 from less common organisms. These include Aspergillus, S aureus, Proteus mirabilis, Klebsiella oxytoca, and Candida species.

Patients with MOE present with severe, unrelenting ear pain. The pain is usually worse at night and aggravated with chewing. It is often associated with temporal headaches and 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. The presence of cranial nerve abnormalities other than with cranial nerve 7 should raise suspicion for intracranial complications, namely, abscess and cerebral sinus thromboses. Unfortunately, once cranial nerve abnormalities develop, prognosis is poor. Mortality for patients with MOE and cranial nerve abnormalities approaches 100%.[42]

The diagnosis of MOE is confirmed with imaging studies. Laboratory studies, such as white blood cell counts, are nonspecific and can be normal even in patients with extensive disease. Imaging studies used in the evaluation of MOE include 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. It is important to recognize that anywhere from 30% to 50% of bone must be destroyed before findings are evident on CT. As such, CT can be normal early in the disease process. For patients with a normal CT scan and high suspicion for MOE, obtain either a bone scan or gallium scintigraphy. Although not specific, these studies have high sensitivity for bone erosion. MRI and CT demonstrate equivalent sensitivity and specificity for soft-tissue complications.

Treatment of MOE centers on antimicrobial therapy. Antipseudomonal antibiotics are the drugs of choice and must be initiated early. Fluoroquinolones, primarily ciprofloxacin, are considered by many to be the antibiotic of choice. Cure rates of 90% have been achieved through the use of fluoroquinolones.[47] There are recent reports of MOE from ciprofloxacin-resistant Pseudomonas; however, as of yet, no increase in mortality has been seen in these patients.[48] Initial doses should be given intravenously. There is no role for topical antibiotics in the treatment of MOE. In addition to systemic antibiotics, patients should receive good aural toilet with debridement of granulation tissue. Biopsy of granulation tissue is indicated in most cases to rule out squamous cell malignancy. Recent studies have suggested an adjuvant role for hyperbaric oxygen therapy for MOE.[49,50] To date, there are no randomized controlled trials that demonstrate a benefit to adjunctive hyperbaric oxygen therapy in patients with MOE.[51]

Ludwig’s Angina

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] In nonintubated 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.[60]

TI Fistula

TI fistula is a rare but life-threatening complication of tracheostomy, long-term mechanical ventilation, neck tumors, and tracheal surgery. In patients with a tracheostomy, the incidence of TI fistula ranges from 0.6% to 0.7%.[61] Even with aggressive treatment, mortality approaches 80%.[62]

Patients with a TI fistula secondary to tracheostomy typically present between the first and second week following the procedure.[61,63] Risk factors for TI fistula include tracheal infection, steroid use, and an anomalous innominate artery.[61] The most common site for fistula formation is at the level of the endotracheal cuff. Fifty percent of patients present with massive hemorrhage. The remainder will report a brief episode of bright red blood from the tracheostomy site, referred to as a “sentinel bleed”. A sentinel bleed can occur anywhere from hours to days before the onset of catastrophic bleeding. It is imperative that clinicians recognize a sentinel bleed because this may be the only opportunity to intervene while the patient remains hemodynamically stable.

Definitive treatment of a TI fistula requires median sternotomy and ligation of the innominate artery. For patients with massive hemorrhage, a variety of temporizing measures can be performed at the bedside in an attempt to get the patient to the operating room. Because the most common site for hemorrhage is at the level of the endotracheal cuff, the first maneuver is to overinflate the tracheostomy. This technique is reportedly successful in almost 85% of cases.[61,64] In patients in whom overinflation is unsuccessful, replace the tracheostomy with a cuffed endotracheal tube. Ensure that the cuff is placed distal to the site of bleeding to protect the airway. If the endotracheal balloon does not tamponade bleeding, a final maneuver is simply to place a finger in the airway and compress the innominate artery against the posterior sternum.

Maintain a high index of suspicion for a sentinel bleed in tracheostomy patients presenting with hemoptysis or peritracheal bleeding. Patients with a sentinel bleed require urgent thoracic surgery consultation for bronchoscopy. Rigid bronchoscopy is recommended over flexible bronchoscopy for its superior visualization and ability to apply direct pressure. Rigid bronchoscopy should always be performed in the operating room.[61]

Summary

Epiglottitis, angioedema, malignant otitis externa, Ludwig’s angina, and tracheoinnominate fistula are potentially life-threatening ENT disorders that must be recognized and treated promptly. On the basis of the information provided, the EP can more effectively diagnose and deliver current, evidence-based therapies.

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  26. Kozel MM, Bossuyt PM, Mekkes JR, Bos JD. Laboratory tests and identified diagnoses in patients with physical and chronic urticaria and angioedema: a systematic review. J Am Acad Dermatol. 2003;48:409-416. Abstract
  27. Ishoo E, Shah UK, Grillone GA, Stram JR, Fuleihan NS. Predicting airway risk in angioedema: staging system based on presentation. Otolaryngol Head Neck Surg. 1999;121:263-268. Abstract
  28. Bentsianov BL, Parhiscar A, Azer M, Har-El G. The role of fiberoptic nasopharyngoscopy in the management of the acute airway in angioneurotic edema. Laryngoscope. 2000;110:2016-2019. Abstract
  29. Simons FE. Advances in H1-antihistamines. N Engl J Med. 2004;351:2203-2217. Abstract
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  31. Lee EE, Maibach HI. Treatment of urticaria. An evidence-based evaluation of antihistamines. Am J Clin Dermatol. 2001;2:27-32. Abstract
  32. Dibbern DA Jr. Urticaria: selected highlights and recent advances. Med Clin North Am. 2006;90:187-209. Abstract
  33. Agah R, Bandi V, Guntupalli KK. Angioedema: the role of ACE inhibitors and factors associated with poor clinical outcome. Intensive Care Med. 1997;23:793-796. Abstract
  34. Chiu AG, Newkirk KA, Davidson BJ, Burningham AR, Krowiak EJ, Deeb ZE. Angiotensin-converting enzyme inhibitor-induced angioedema: a multicenter review and an algorithm for airway management. Ann Otol Rhinol Laryngol. 2001;110:834-840. Abstract
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  36. Megerian CA, Arnold JE, Berger M. Angioedema: 5 years’ experience, with a review of the disorder’s presentation and treatment. Laryngoscope. 1992;102:256-260. Abstract
  37. Sondhi D, Lippmann M, Murali G. Airway compromise due to angiotensin-converting enzyme inhibitor-induced angioedema: clinical experience at a large community teaching hospital. Chest. 2004;126:400-404. Abstract
  38. Agostoni A, Cicardi M. Drug-induced angioedema without urticaria. Drug Saf. 2001;24:599-606. Abstract
  39. Vleeming W, van Amsterdam JG, Stricker BH, de Wildt DJ. ACE inhibitor-induced angioedema. Incidence, prevention and management. Drug Saf. 1998;18:171-188. Abstract
  40. Warner KK, Visconti JA, Tschampel MM. Angiotensin II receptor blockers in patients with ACE inhibitor-induced angioedema. Ann Pharmacother. 2000;34:526-528. Abstract
  41. Amorosa L, Modugno GC, Pirodda A. Malignant external otitis: review and personal experience. Acta Otolaryngol Suppl. 1996;521:3-16. Abstract
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  48. Berenholz L, Katzenell U, Harell M. Evolving resistant pseudomonas to ciprofloxacin in malignant otitis externa. Laryngoscope. 2002;112:1619-1622. Abstract
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  50. Mader JT, Love JT. Malignant external otitis. Cure with adjunctive hyperbaric oxygen therapy. Arch Otolaryngol. 1982;108:38-40. Abstract
  51. Phillips JS, Jones SE. Hyperbaric oxygen as an adjuvant treatment for malignant otitis externa. Cochrane Database Syst Rev. 2005;(2):CD004617.
  52. Saifeldeen K, Evans R. Ludwig’s angina. Emerg Med J. 2004;21:242-243. Abstract
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  58. Freund B, Timon C. Ludwig’s angina: a place for steroid therapy in its management? Oral Health. 1992;82:23-25.
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Michael Winters, MD, Assistant Professor of Emergency Medicine and Medicine; Program Director, Combined Emergency Medicine/Internal Medicine Residency Training Program, University of Maryland School of Medicine, Baltimore, Maryland

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categories: Emergency Medicine

Some Medical Devices Might Flummox with DST Change

Posted by Paul Rega, MD — published on March 8th, 2007

The upcoming change in the beginning and end of daylight saving time (DST) may adversely affect medical equipment that uses date and time information for diagnosis or treatment, according to the US Food and Drug Administration (FDA). The new DST will begin 3 weeks earlier and end one week later this year.

Medical equipment that uses, creates, or records time or date information about a patient’s diagnosis or treatment may register the wrong dates for the start and end of DST when the changes are implemented, according to an alert sent Friday from MedWatch, the FDA’s safety information and adverse event reporting program.

The FDA notes that most devices currently in use are likely to be affected, unless they were manufactured after the DST change was approved (Energy Policy Act of 2005) or have been updated by the manufacturer.

Adverse effects associated with their use might include incorrect dose prescribing, dose administration at the wrong time, missed doses, extra doses, unintended increased/decreased duration of therapy, and incorrectly recorded treatment/diagnostic results.

Healthcare professionals are advised to check with manufacturers for available patches/fixes for medical devices, hospital networks, and associated information technology systems; the time on these products should be verified on each of the critical DST dates: March 11 (new start date), April 1 (old start date), October 28 (old end date), and November 4 (new end date). Vigilance should be exercised when making clinical decisions or using medical devices on these days.

Unpredictable medical device events or medical device–related problems related to DST should be reported to the manufacturer and to the FDA’s MedWatch reporting program by phone at 1-800-FDA-1088, by fax at 1-800-FDA-0178, online at http://www.fda.gov/medwatch, or by mail to 5600 Fishers Lane, Rockville, MD 20852-9787. 

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categories: Emergency Medicine

Death in Severe Trauma May Be Result of Exhausted Cytokine Response

Posted by Jeff Hugus, MD — published on March 7th, 2007

February 22, 2007 (Orlando) — Danish researchers say there is an almost immediate release of the cytokines interleukin-6 (IL-6) and interleukin-10 (IL-10) in trauma patients. Cytokine levels reflect severity of injury and open the door to better treatment of severely injured patients and prevention of the complications that stem from the body’s response to trauma, they say.

Results of a study indicating that cytokine release occurs within minutes of trauma were reported here at the 36th Critical Care Congress of the Society of Critical Care Medicine, being held this week.

Jakob Stensballe, MD, PhD, of the Department of Anesthesia at Copenhagen University Hospital in Denmark, presented results from a study of 265 consecutive adult trauma patients admitted to his institution directly from the trauma scene. Patients were admitted between 2003 and 2004. Length of the observation period was 18 months.

Dr. Stensballe’s team serially measured levels of IL-6, a pro-inflammatory cytokine, and IL-10, an anti-inflammatory cytokine. The first sample was taken within 40 minutes of the accident. Subsequent samples were taken at 6, 12, and 24 hours after the trauma.

“Cytokine levels have not been [previously] evaluated in the very early phase of trauma,” Dr. Stensballe explained in an interview with Medscape.

At 30 days after the trauma, the mortality rate was 10.9%. The injury severity score was significantly correlated with IL-6 and IL-10 levels at all time points and levels had increased at all time points, Dr. Stensballe reported.

“Nonsurvivors had the highest scores,” he added. “IL-6 scores were 4 times higher than baseline and IL-10 levels were 10 times higher than baseline” at the time of death.

“Death could be the result of an exhausted IL-10 response,” Dr. Stensballe speculated. “The body doesn’t have the ability to prioritize its response” to inflammation after a certain point. “This is a part of a cytokine storm that happens in trauma.”

“I can’t say if [IL-6 and IL-10 secretion] is a good response or a bad one. All I can say is that it happens in trauma,” Dr. Stensballe said in response to questions raised by several meeting attendees.

“A clinical implication might be to stimulate the IL-10 response by giving corticosteroids” to improve survival, he offered.

Jonathon Dean Truwit, MD, chief of the Pulmonary and Critical Care Division at the University of Virginia in Charlottesville, Virginia, told Medscape that cytokine response in early trauma, before the development of acute respiratory distress syndrome (ARDS), is an area that hasn’t been adequately investigated.

He believes Dr. Stensballe’s idea of starting drug therapy before lung damage occurs “makes sense…. Most drug trials in ARDS have failed.”

In the setting of acute trauma, “an approach might be an anti-inflammatory drug,” Dr. Truwit said. “But there are all kinds of inflammatory mediators and all kinds of anti-inflammatory drugs…and treatment with anti-inflammatory drugs may increase the risk of infection.”

Dr. Stensballe said a randomized trial of corticosteroids and IL-10 response might offer insight into the treatment of acute trauma patients.

“There has been some talk of a clinical study of [ibuprofen in this setting],” Dr. Truwit said. “Just like treatment of a heart attack with a baby aspirin to stop the inflammatory process, that [approach] might make sense here, too.”

Drs. Stensballe and Truwit report no relevant financial relationships.

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categories: Emergency Medicine