trigem=ant canal<\/p>\n
VII=post canal<\/p>\n
IX=lower canal<\/p>\n
X=TM<\/p>\n
II,III=post auricular region<\/p>\n
Hearing Testing<\/p>\n
Rinne<\/p>\n
Use 512 Hz against mastoid ask which is louder, it should be air.<\/p>\n
Weber<\/p>\n
Place in middle of forehead<\/p>\n
Conductive loss ear will hear better<\/p>\n
Opposite of the sensorineural ear will hear better<\/p>\n
<\/span>Acute Otitis Media<\/span><\/h2>\nCaused by Eustachian tube dysfunction.\u00a0 S. Pneumo, H. flu, m. catarrhalis<\/p>\n
Clear wax c 3% Hydrogen Peroxide.\u00a0 In kids diagnose with pneumatic otoscopy<\/p>\n
Amoxicillin, Bactrim (kernicterus if <2 mo.)\u00a0 10 day course<\/p>\n
Document no mastoid tenderness<\/p>\n
Mastoiditis<\/h4>\n
Classic is from an untreated AOM<\/p>\n
CT Scan c contrast<\/p>\n
Trial of IV ABX and ENT consult for myringotomy<\/p>\n
Bullous Myringitis<\/p>\n
clear or hemorrhagic vesicles on TM<\/p>\n
Viral or from mycoplasma<\/p>\n
Sx treatment<\/p>\n
<\/span>Otitis Externa<\/span><\/h2>\npseudomonas and staph aureus<\/p>\n
Presents with itching, pain, fullness in ear, redness and swelling, white cheesy or watery green d\/c<\/p>\n
Cleanse the ear and fully suction<\/p>\n
2% acetic acid (VoSol Otic Solution or VoSol HC) or just have folks mix supermarket white vinegar half and half with warm tap water<\/strong><\/p>\nIf severe give the vinegar and then topical abx (polymyxin B, neomycin, with HC=cortisporin otic solution or suspension.)\u00a0\u00a0 If TM is perfed, use only the suspension.<\/strong><\/p>\nA wick may need to be inserted to allow ABX access<\/p>\n
Avoid wetting the canal for 2 weeks<\/p>\n
If cellulitis is present, give systemic abx as well<\/p>\n
Objective<\/strong> To compare the clinical efficacy of ear drops containingacetic acid, corticosteroid and acetic acid, and steroid and antibiotic in acute otitis externa in primary care.Participants<\/strong> 213 adults with acute otitis externa.Conclusions<\/strong> Ear drops containing corticosteroids are more effectivethan acetic acid ear drops in the treatment of acute otitisexterna in primary care. Steroid and acetic acid or steroidand antibiotic ear drops are equally effective.(BMJ\u00a0\u00a02003;327:1201-1205\u00a0(22\u00a0November), doi:10.1136\/bmj.327.7425.1201)<\/p>\n <\/p>\n
<\/p>\n
Malignant Externa<\/h4>\n
It is actually pseudomonas osteo of the external canal and temporal bone.<\/strong>\u00a0 ENT and IV ABX.<\/p>\ncan be seen in diabetics and immuno-compromised folks<\/p>\n
pain on the bony\/cart border in front of tragus<\/p>\n
30% of ct scans can be neg<\/p>\n
give iv cipro<\/p>\n
<\/span>Perichondritis<\/span><\/h3>\ninfection of auricular cartilage<\/p>\n
swollen red pinna<\/p>\n
Ciprofloxacin or Augmentin<\/p>\n
to cover pseudomonas, proteus, and staph<\/p>\n
<\/span>TM Perforation<\/span><\/h3>\ngive abx only if AOM or debris present<\/p>\n
follow-up c ENT<\/p>\n
![\"\"](\"\/wp-content\/images\/part1\/perfed%20tm_small.jpg\")
<\/a><\/p>\nUse only suspension<\/p>\n
<\/p>\n
<\/span>Foreign Bodies or Wax<\/span><\/h3>\nit is safe to use syringe with canulla to spray eardrums for FB or wax (Emerg Med J<\/em> 2005; 22<\/em>:266-268)<\/p>\nInsects: Kill the insect before attempting to remove it Mineral oil or lidocaine (2%), or isopropyl alcohol (Suggest baby oil, isopropyl alcohol, or cooking oil if patient is frantically calling the ED)<\/p>\n
Insecticidal activity of common reagents for insect foreign bodies of the ear Antonelli PJ, Ahmadi A, Prevatt A, Laryngoscope. 2001;111:15-20 Conclusion: Many agents commonly available in the EMS may be used to kill insect foreign bodies in the ear canal. Antiseptic agents and microscope oil were the most effective against the most common insect foreign body, the cockroach. Ticks were the most resistant to all agents tested. Comment: What is the best agent to grab when you have a distraught patient severely agitated by the presence of a live insect in the ear? Mineral oil has been commonly recommended, but it tends to create a gooey mess, making foreign body removal more difficult. Isopropyl alcohol would be my drug of choice. Although it is only number 2 on the quick-kill list, it is probably more readily available than the number 1\u0096ranked ethyl alcohol. Liquid anesthetics are a nice thought, but take at least 3 or 4 times longer to achieve the desired lethal effect on the bug. (From ACEP)<\/p>\n
<\/p>\n
<\/p>\n
<\/span>Epistaxis<\/span><\/h2>\nGreater understanding and visualization of nasal anatomy revealed that the nose receives blood from many different sources and a large amount of vascular redundancy exists.\u00a0 The external carotid artery divides into the maxillary and superficial temporal arteries.\u00a0 The maxillary artery has many branches including the sphenopalatine artery.\u00a0 The sphenopalatine artery emerges from the sphenopalatine foramen and further divides into four branches: the posterior septal, inferior turbinate, middle turbinate, and nasopalatine arteries.\u00a0 The inferior and middle turbinate arteries depart from the sphenopalatine artery at right angles.\u00a0 Through its four divisions, the sphenopalatine artery supplies the majority of the blood to the nose (43).\u00a0 The sphenopalatine infuses the posterior aspect of the nose, the septum, and the lateral wall from the middle turbinate caudally.\u00a0 In the anterior region of the septum at about the same level as the middle turbinate is Little\u0092s area and within it is Kiesselbach\u0092s plexus, a area of vascular anastomosis that is often the site of anterior epistaxis.(Emedhome.com)<\/p>\n
<\/p>\n
![\"\"](\"\/wp-content\/images\/part1\/epistaxis_small.JPG\")
<\/a>![\"\"](\"\/wp-content\/images\/part1\/epistaxis2_small.JPG\")
<\/a>![\"\"](\"\/wp-content\/images\/part1\/epistax_small.jpg\")
<\/a><\/p>\n <\/p>\n
Little’s Area=Kiesselbach’s plexus.\u00a0 The anteroinferior portion of the nasal septum.\u00a0 most common ant bleeds.<\/p>\n
Posteroinferior turbinate is the most common source of posterior bleeds<\/p>\n
<\/p>\n
Hold for 15 minutes<\/p>\n
Silver nitrate if can have 4-5 sec s bleed.\u00a0 Never use for more than 15 sec.\u00a0 Can also try surgicel\/gelfoam<\/p>\n
<\/p>\n
Afrin (oxymetazoline) a few squirts up the nose<\/p>\n
<\/p>\n
Soak cotton swabs in lidocaine with epi, put as many as possible into nares (4-5) leave for 10 minutes.<\/p>\n
4% Cocaine (still the best, comes in a slurry)<\/p>\n
4% Lidocaine mixed 1:1 with 1% phenylephrine<\/p>\n
<\/p>\n
Oxymetazoline 0.05% (Afrin \u0096 nasal spray) and 4% lidocaine 1:1<\/p>\n
<\/p>\n
A few mils of 1:10,000 epi mixed with some 4% lidocaine<\/p>\n
<\/p>\n
Leave anterior pack for 48 hrs, send home with Keflex<\/p>\n
Unless severe hypertension is a problem, first squirt a nasal decongestant<\/p>\n
into the affected nares, then have patient hold pressure on anterior nares<\/p>\n
for 15 minutes by the clock.<\/p>\n
<\/p>\n
If bleeding persists, using a headlamp, Frasier suction, and speculum put arms in vertical position to avoid compressing the septum)<\/p>\n
illuminate the nares and if a bleeding site is apparent, cauterize it with a silver nitrate stick.<\/p>\n
<\/p>\n
If bleeding continues (usually from a site inaccessible for cautery),<\/p>\n
pack the anterior and middle nasal passage with an expandable sponge<\/p>\n
(Merocel or similar), expanding it with more decongestant or cocaine spray.<\/p>\n
May need more than one<\/p>\n
<\/p>\n
If bleeding persists, then usually from a posterior source, remove the<\/p>\n
anterior\/middle packing, place a small Foley catheter through the nose into<\/p>\n
the nasopharynx, blow up the balloon, pull it anteriorly to occlude the<\/p>\n
posterior nares and direct all bleeding anteriorly, then repack the entire<\/p>\n
nares with petroleum gauze strips using bayonet forceps. Clamp the Foley<\/p>\n
where it exits the nose and tape the end of the gauze and Foley to the cheek<\/p>\n
in a way that doesn’t pull against the skin of the nares.<\/p>\n
<\/p>\n
Prophylaxis with TMP\/SMX or keflex for sinusitis prevention (don’t know<\/p>\n
the evidence, but ENT always asks me to), and admit the patient to a<\/p>\n
monitored bed.<\/p>\n
patients may become hypoxic and bradycardiac and can have actual syncope following posterior packing believed to be from a nasopulmonary reflex.<\/p>\n
<\/p>\n
For patients with severe coagulopathies, also consider giving FFP<\/p>\n
<\/p>\n
TECHNIQUE<\/p>\n
A loop of BIPP-coated ribbon gauze is inserted into<\/p>\n
the nose using Tilley dressing forceps. The forceps<\/p>\n
are withdrawn and reinserted below the loop of<\/p>\n
BIPP. The dorsal surface of the forceps is then used<\/p>\n
to guide the loop into the superior nasal cavity and<\/p>\n
to compress it into position. The next loop is<\/p>\n
inserted into the nose and likewise compressed,<\/p>\n
and this cycle is repeated until the whole nose is<\/p>\n
filled by BIPP, extending from the superior limit of<\/p>\n
the nose to the floor. This method has two<\/p>\n
advantages over the traditional method: the internal<\/p>\n
nasal valve does not limit the insertion of BIPP<\/p>\n
and with each loop of BIPP inserted the cribriform<\/p>\n
plate is further protected from trauma that could<\/p>\n
otherwise be inflicted using the forceps.<\/p>\n
(Emerg Med J 2009;26:52.)<\/p>\n
![\"\"](\"\/wp-content\/images\/part2\/img5_small.jpg\")
<\/a><\/p>\n <\/p>\n
<\/span>Laryngeal Dyskinesia<\/span><\/h2>\nreview article (emerg med australia 2007;18 by lawrence sg)<\/p>\n
<\/span>Spasmdomic Dysphonia<\/span><\/h3>\nirritable larynx disease.\u00a0 May have benefit from heliox.\u00a0 May need to be tubed<\/p>\n
<\/p>\n
<\/span>Paradoxical Vocal Cord Movement<\/span><\/h3>\nyoung women<\/p>\n
start on PPI<\/p>\n
benzos<\/p>\n
Lidocaine 2% 2 cc in 2 cc NS, nebulize<\/p>\n
Cool Mist Nebs<\/p>\n
Tell them to sniff, may disappear. May also disappear when reading from a book<\/p>\n
<\/p>\n
Muscle Tension Dysphonia<\/p>\n
<\/p>\n
On scoping, you will see vocal cord adduction<\/p>\n
<\/p>\n
<\/p>\n
THE DIFFERENTIAL DIAGNOSIS OF PARADOXICAL VOCAL CORD MOVEMENT<\/strong><\/p>\nJamie Koufman, MD<\/p>\n
This article is reprinted from THE VISIBLE VOICE Vol. 3, No. 3. (July 1994).<\/p>\n
\n ABSTRACT<\/strong><\/p>\nParadoxical vocal cord movement (PVCM) producing airway obstruction is a relatively uncommon, and sometimes confusing, condition that affects the larynx. PVCM occurs when there is inappropriate closure of the vocal cords during inhalation, and the resultant respiratory obstruction may be intermittent or continuous, mild or severe, depending on the cause. The differential diagnosis of PVCM also includes congenital, inflammatory, traumatic, neoplastic, and neurological causes. Contrary to popular belief, relatively few cases are “functional,” i.e., psychogenic. This article presents the clinician with a differential diagnosis for PVCM and the clinical features that differentiate its various causes.<\/p>\n
INTRODUCTION<\/strong><\/p>\nDuring the respiratory cycle of most higher animals and of human beings, the vocal cords partially abduct (open) with inhalation and partially adduct (close) with exhalation. This phasic vocal cord movement is physiologic, and it allows the unimpeded movement of air into the lungs during inspiration while helping to maintain the alveolar patency (of the lungs) by providing positive airway pressure during expiration. Thus, the larynx serves as an upper airway valve to help keep the lungs expanded.<\/p>\n
Some patients who present with stridor (noisy breathing), dyspnea (difficulty breathing), and upper airway obstruction have paradoxical vocal cord movement (PVCM), characterized by inappropriate adduction (closure) of the vocal cords during inhalation. The persistence and the degree of inappropriate glottic closure determines the degree of the airway obstruction, and hence the severity of respiratory symptoms experienced by the patient. In some patients, the problem is constant and severe, requiring prompt remedial treatment, and in other patients, the problem is intermittent and relatively mild. Few articles1,2 address the differential diagnosis of this condition or provide an approach to the management of these challenging patients.<\/p>\n
DIFFERENTIAL DIAGNOSIS<\/strong><\/p>\nThe differential diagnosis of PVCM is shown in Table 1. Three key elements of the history quickly limit the possibilities in each case: (1) Is the stridor constant or intermittent? (2) Is there any history of head trauma, stroke, or other brainstem problem? (3) Are there any other associated symptoms, such as hoarseness, dysphagia, globus pharyngeus, or cough? In addition, as discussed below, the findings on fiberoptic laryngeal examination are crucial in making the diagnosis.<\/p>\n
<\/p>\n
TABLE 1: PARADOXICAL VOCAL FOLD MOVEMENT (DIFFERENTIAL DIAGNOSIS)<\/strong><\/p>\n\n- Gastroesophageal (laryngopharyngeal) reflux<\/li>\n
- Psychogenic stridor (usually in adolescents)<\/li>\n
- Respiratory-type laryngeal dystonia<\/li>\n
- Drug-induced laryngeal dystonic reactions<\/li>\n
- Asthma-associated laryngeal dysfunction<\/li>\n
- Abnormalities that affect the brainstem\n
\n- Chiari malformation I & II, hydrocephalus, meningomyelocele<\/li>\n
- Cerebrovascular accident (stroke)<\/li>\n
- Severe closed head injury<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n
Paroxysmal Laryngospasm and PVCM Due to Gastroesophageal Reflux<\/strong> Gastroesophageal reflux can cause a true intermittent type of PVCM, laryngospasm, or both, in which adduction predominates and abduction is temporarily lost during “attacks.”3-5 Thus, laryngospasm may be considered a specific variation of PVCM. Using this definition, reflux appears to be the most common cause of PVCM.5 In either case, the attacks of respiratory obstruction are paroxysmal and the result of direct contact of gastric fluids with laryngopharyngeal structures.5 It is postulated that some additional form of vagal dysfunction may prolong the episodes for minutes, hours, or sometimes days.6,7<\/p>\nPatients with this frightening condition describe intermittent, sudden-onset, noisy, obstructed breathing, which some describe as “choking episodes.” Attacks of stridor may follow a pattern, e.g., occurring after a meal, after the start of exercise, or after bending over. Sometimes, the attacks may awake the patient from sound sleep. Often, the attacks are truly paroxysmal, occurring without any pattern or identifiable precipitating events. Some patients have one or more attacks per day, and others have their attacks as infrequently as a few each year. The duration of attacks is variable, but “a few minutes” is typical.5<\/p>\n
Two-thirds of the patients deny ever having heartburn; however, all complain of some other symptom(s) of laryngopharyngeal reflux, such as chronic or intermittent hoarseness, difficulty swallowing, a sensation of a lump in the throat, chronic throat clearing and cough, or simply too much throat mucus and\/or “post-nasal drip.”5<\/p>\n
Within the past two years, the author has diagnosed this condition in 15 adult patients.5 Of these, 12 underwent pH monitoring, which yielded abnormal findings in 11 (92%), five of whom had laryngopharyngeal reflux demonstrated by a pH probe in the hypopharynx behind the laryngeal inlet.5 All fifteen patients were treated with dietary and life-style modification as well as omeprazole 20 mg b.i.d., and, within four weeks, all attacks of laryngospasm had ceased in all patients.<\/p>\n
H2-blockers appear to be inadequate treatment for reflux in this group of patients.5,8 For some patients under age 40 years, fundoplication should be considered as an alternative long-term treatment after the symptoms of laryngospasm have been initially corrected by omeprazole therapy; that is, antireflux surgery should be considered in patients who subsequently fail maintenance on H2 blocker therapy.5,8<\/p>\n
Patients with the respiratory type of adductor laryngeal dystonia (discussed below), may also have reflux disease. When these two conditions occur together, the attacks of PVCM tend to be prolonged and severe, and the patient may require airway intervention, e.g. intubation or tracheotomy. Such a patient usually requires treatment with both botulinum toxin and omeprazole.<\/p>\n
The clinician caring for patients with PVCM due to causes other that reflux should realize that reflux may be a secondary initiating or complicating factor. When laryngopharyngeal reflux is suspected, by the history or by the laryngeal findings, ambulatory 24-hour double-probe pH monitoring is indicated. Long-term medical treatment or surgical fundoplication is usually necessary in such patients.<\/p>\n
Psychogenic Stridor<\/strong><\/p>\nAfter reflux, psychogenic stridor appears to be the second most common cause of PVCM. (The author sees approximately 2 to 3 such cases each year.) Usually, this group of patients is easily diagnosed. First, almost all are teenagers. Second, PVCM occurs with a sudden onset and offset. Third, such patients are usually unconcerned (blase) about their noisy breathing and airway obstruction. Fourth, it is usual for the clinician to be able to “fool” the patient during fiberoptic examination, thus making the PVCM go away. (In most cases, when the patient is asked to read a long passage loudly, the stridor may disappear and phasic respiratory activity of the vocal cords may become normal.) Fifth, the PVCM attacks often can be precipitated and ameliorated by injections of placebo.9-13<\/p>\n
The history of each patient will often suggest an underlying psychologic or psychiatric problem, manipulative behavior, and family problems, alone or in various combinations, and the stridor usually occurs at “times of significance” for the patient. In one patient, for example, the stridor only occurred when she was sent to the school principal’s office for misbehaving. Characteristically, her stridor was so loud and disturbing that it demanded medical attention.<\/p>\n
A word of caution about this diagnosis. Even though the criteria for psychogenic stridor are fairly well-established — (1) periods of normal phasic vocal cord movement during the fiberoptic examination, (2) induction of stridor and response to placebo, and (3) a psychological or psychiatric disorder — still, this is almost a diagnosis of exclusion. A review of the literature makes clear that many cases of “psychogenic stridor” probably actually had an organic basis, e.g., reflux or dystonia.<\/p>\n
Patients with presumed psychogenic PVCM should be approached by the otolaryngologist and the psychologist and\/or psychiatrist as a team, and should be completely evaluated before the team reaches a final diagnosis.<\/p>\n
In the author’s experience, none of the patients diagnosed as having psychogenic stridor have subsequently developed one of the other conditions associated with PVCM. On the other hand, patients with another presumed cause of PVCM, such as respiratory-type laryngeal dystonia, are sometimes eventually diagnosed as having psychogenic stridor. In other words, the differentiation between dystonia-related and psychogenic PVCM sometimes may be difficult.<\/p>\n
Respiratory-Type Adductor Laryngeal Dystonia<\/strong> The most common type of focal laryngeal dystonia causes a voice disorder known as spasmodic dysphonia (SD). SD occurs in women five times more frequently than in men, is rarely seen in people under age 20 years, and usually affects the voice very severely, but does not affect respiration. The most common pattern is the adductor type, in which glottal overclosures create a “strain-strangled” sounding voice. Patients with this type of SD do not usually experience difficulty breathing, although some patients with severe non-focal dystonia involving the larynx and pharynx (Meige’s syndrome) do have severe, inappropriate laryngeal hyperadduction, which causes airway obstruction. There also is a small group of patients with a respiratory type of adductor laryngeal dystonia in whom the vocal cords inappropriately hyperadduct during inspiration but the voice is normal. Stridor in these patients is present throughout the day, but disappears during sleep, a characteristic of most dystonias.<\/p>\nBlitzer and Brin 14 reported a large series of patients with laryngeal dystonia, most of whom had the well-recognized adductor-type SD. However, they did report that approximately 1% had a respiratory type of adductor laryngeal dystonia, as described above.<\/p>\n
Within the past five years, the author has seen five patients with this type of laryngeal dystonia; these patients represent 2% of the author’s laryngeal dystonia patient population.15 None of the five have significant abnormality of voice, but two actually presented with tracheotomy tubes in place.15 On fiberoptic examination, the vocal cords characteristically close during inspiration, and when the patient is asked “take a deep breath,” the degree of overclosure worsens, increasing the respiratory obstruction.<\/p>\n
Of the five patients in the author’s series, all have responded well to treatment with botulinum toxin, although this group of patients appears to need larger doses of botulinum toxin than those required by typical SD patients.15<\/p>\n
Drug-Induced Laryngeal Dystonic Reactions<\/strong><\/p>\nTemporary drug-induced PVCM has been reported after administration of neuroleptic drugs, including chlorpromazine and haloperidol.16 (Obviously, this cause of PVCM needs to be considered only in patients receiving such medications.) The stridor is usually associated with extrapyramidal symptoms, muscle stiffness, and dystonias of the head and neck, e.g., torticollis. The airway obstruction (PVCM) and the other dystonias are relatively short-lived (hours), and are reversible with intravenous administration of an anticholinergic drug.16 (The author’s experience is in agreement with this report.)<\/p>\n
Thiopental, an anesthetic, also may have some such effects at certain doses.17 This may explain the relatively high incidence of “laryngospasm” observed during the induction of anesthesia. It has been shown experimentally that such laryngospasm can be prevented by the administration of topical lidocaine.18<\/p>\n
Asthma-Associated Laryngeal Dysfunction<\/strong><\/p>\nPatients who present with PVCM are frequently misdiagnosed as having asthma as the cause of the airway obstruction, even though anti-asthma medications are ineffective. Nevertheless, there appears to be a subset of patients with asthma who also have PVCM.19 Although the mechanism of PVCM in these patients is unknown, glottal aperture changes have been observed in asthma patients20; and vagal reflex dysfunction may be the cause.20 In any asthma patient, when inspiratory stridor is present, the diagnosis of PVCM should be considered. The finding of PVCM on transnasal fiberoptic laryngoscopy is diagnostic.<\/p>\n
Brainstem Abnormalities<\/strong><\/p>\nMany central neurological (usually brainstem) abnormalities can cause PVCM, in addition to or complicated by bilateral abductor paralysis, apneic episodes, and central sleep apnea syndrome.21 23 Severe closed head injury, Chiari malformations I and II, meningomyelocele, and cerebrovascular accidents (strokes of the posterior circulation) may all produce PVCM. In these cases, the obstruction and inappropriate vocal cord movement may be inconsistent and variable, and may appear to change with multiple fiberoptic examinations; what is important, however, is that the stridor does not disappear during sleep. This point is critical, since with all the other causes of PVCM, the stridor is paroxysmal or improves during sleep. Early (days or weeks) after closed head injury, extubation may fail and the patient may require multiple intubations, and then, later on, a tracheotomy. With time, as the cerebral and brainstem edema subsides, the vocal cord movement may return to normal and the stridor will disappear. Similarly, some patients with congenital lesions of the brainstem may experience a normalization of vocal cord function after surgical treatment of the lesion.<\/p>\n
In the evaluation of patients with PVCM due to brainstem abnormalities, computerized tomographic scanning, magnetic resonance imaging (or both), as well as neurologic consultation is recommended. The prognosis should be guarded. For instance, patients with Chiari malformations who undergo surgical treatment of the malformation may have improvement of their PVCM postoperatively, while others may require a permanent tracheotomy.<\/p>\n
APPROACH TO THE PATIENT WITH PVCM<\/strong><\/p>\nAfter a thorough history is obtained, the first examination of the stridulous patient should include transnasal fiberoptic laryngoscopy (TFL). During this examination, the patient should be asked to: (1) alternatively phonate the vowel \/i\/ and sniff, in rapid alternating succession; (2) take deep breaths; (3) cough, throat clear, and chuckle; (4) count to fifty, rapidly and loudly; (5) read a written passage in a loud voice; and (6) sing.<\/p>\n
These maneuvers may reveal a pattern of adduction and abduction consistent with PVCM and a specific diagnosis. Patients with an organic cause of the PVCM, that is, a non-psychogenic cause, usually demonstrates consistent fiberoptic findings, whereas patients with psychogenic PVCM do not. Patients with psychogenic stridor, for example, will often revert to normal phasic vocal cord movement when asked to count or read out loud.<\/p>\n
PVCM is therefore usually diagnosed by TFL, and the diagnosis should be considered when there are findings of: (1) inappropriate vocal fold adduction during inspiration; (2) paroxysmal inability to abduct the vocal cords (“transient abductor paralysis”); or (3) a combination of these findings. There is, however, one group of patients that comprises a notable exception: patients with reflux-induced paroxysmal laryngospasm may have normal phasic vocal fold movement on TFL. In these patients, other findings characteristic of laryngopharyngeal reflux (edema, erythema, posterior commissure hypertrophy, and granulation) are almost always observed.<\/p>\n
A firm diagnosis of reflux-induced PVCM can be made when the history (pattern and associated symptoms), the laryngeal findings, and the pH monitoring data all support the diagnosis. In addition, complete resolution of the laryngospastic episodes during a therapeutic trial of omeprazole (20 mg b.i.d.) confirms of the diagnosis.<\/p>\n
Unlike patients in the other PVCM groups, patients with respiratory-type laryngeal dystonia describe a progressive onset of the PVCM over a period of days, weeks, or months. In addition, such patients usually deny having hoarseness or other reflux symptoms. On TFL, their PVCM is consistent and worsens when the patient is asked to take a deep breath, although the PVCM may improve when the patient reads a written passage or sings. However, improvement is only partial and transient.<\/p>\n
On occasion, differentiating dystonic from psychogenic PVCM can be a difficult task. When the clinician is faced with this diagnostic dilemma, neuropsychological testing, psychiatric consultation, and trial injections of botulinum toxin may all be indicated. In some cases, it may take months for the clinical team to reach a diagnosis.<\/p>\n
Except for patients in the brainstem abnormality group (who often require tracheotomy), patients with PVCM usually do not have respiratory obstruction severe enough to warrant emergency airway intervention. Of the other groups of patients with PVCM, dystonia patients appear next in terms of the frequency of need for airway support, followed in decreasing order by the psychogenic group, the asthma group, and the reflux group. Table 2 summarizes some of the differentiating features of PVCM.<\/p>\n
The diagnostic work-up for each patient with PVCM should be individualized and may include some or all of the following: serial fiberoptic examinations, pH monitoring, neuropsychiatric evaluation, placebo injections, audio-recordings of the patient’s breathing during sleep, and radiographic examinations. In selected cases, therapeutic trials of omeprazole and\/or laryngeal injections of botulinum toxin also may be used.<\/p>\n
Finally, PVCM can be confused with other causes of laryngeal obstruction, at least on the initial clinical examination. Inspiratory stridor, for example, may be seen in patients with bilateral vocal cord paralysis, and in patients with laryngeal stenosis or fixation. These conditions may be differentiated from PVCM because, in the former group of conditions, examination shows that vocal cord abduction does not occur. Although abduction may be inconsistent, inappropriate, or incomplete, it must occur some of the time in order for the diagnosis of PVCM to be made.<\/p>\n
\n TABLE 2<\/strong> SOME DIFFERENTIATING FEATURES OF THE CAUSESOF PARADOXICAL VOCAL CORD MOVEMENT<\/p>\n \u00a0<\/strong><\/p>\n Pattern<\/strong><\/p>\n Duration<\/strong><\/p>\n Hoarseness<\/strong><\/p>\n Airway Support Needed<\/strong><\/p>\n Reflux <\/strong><\/p>\nparoxysmal<\/p>\n
minutes<\/p>\n
usually<\/p>\n
almost never<\/p>\n
Dystonia <\/strong><\/p>\ndaytime<\/p>\n
hours<\/p>\n
rarely<\/p>\n
sometimes<\/p>\n
Psychogenic <\/strong><\/p>\nparoxysmal<\/p>\n
variable<\/p>\n
never<\/p>\n
sometimes<\/p>\n
Brainstem <\/strong><\/p>\ncontinual<\/p>\n
continual<\/p>\n
sometimes<\/p>\n
usually<\/p>\n
\n SUMMARY<\/strong><\/p>\nPVCM presents the clinician with an interesting and challenging differential diagnosis. Only abnormalities of the brainstem produce a constant (day and night) stridor and respiratory obstruction, whereas all of the other causes are intermittent or occur only during the daytime. The causes of PVCM, in the author’s experience, in order of frequency of occurrence are: gastroesophageal reflux, followed by psychogenic stridor, respiratory-type laryngeal dystonia, and abnormalities of the brainstem. In the last group, closed head injuries are most common.<\/p>\n
The work-up of PVCM may require a multidisciplinary approach and a variety of diagnostic methods. Likewise, treatment often must be individualized. \u0080 Jamie Koufman, M.D.<\/p>\n
REFERENCES<\/strong><\/p>\n1. Ward PH, Hanson DG, Berci G: Observations on central neurologic etiology for laryngeal dysfunction. Ann Otol Rhinol Laryngol 90:430-441, 1981<\/p>\n
2. Kellman RM, Leopold DA: Paradoxical vocal cord motion: an important cause of stridor. Laryngoscope 92:58-60, 1982<\/p>\n
3. Chodosh PL. Gastro-esophageal reflux. Laryngoscope 87:1418-1427, 1977<\/p>\n
4. Burton DM, Pransky SM, Kearns DB, et al.: Pediatric airway manifestations of gastroesophageal reflux. Ann Otol Rhinol Laryngol 101:742-749, 1992<\/p>\n
5. Koufman JA, Loughlin C: Paroxysmal laryngospasm: an uncommon manifestation of gastroesophageal (laryngopharyngeal) reflux disease (Unpublished data)<\/p>\n
6. Bauman NM, Sandler AD, Schmidt C, et al.: Reflex laryngospasm induced by stimulation of distal afferents. Laryngoscope 104: 209-214, 1994<\/p>\n
7. Campbell AH, Mestitz H, Pierce R: Brief upper airway (laryngeal) dysfunction. Aust NZ Med 20:663-668, 1990<\/p>\n
8. Koufman JA: Gastroesophageal reflux and voice disorders. In Diagnosis and Treatment of Voice Disorders Editors: Gould WJ, Rubin JS, Korovin G, Sataloff R. Igaku-Shoin Publishers, New York (In press)<\/p>\n
9. Appleblatt KL, Baker SR: Functional airway obstruction. A new syndrome. Arch Otolaryngol 107:305-307, 1981<\/p>\n
10. Snyder HS, Weiss E: Hysterical stridor: a benign cause of upper airway obstruction. Ann Emer Med 18:991-994, 1989<\/p>\n
11. George MK, O’Connell JE, Batch AJ: Paradoxical vocal cord motion: an unusual cause of stridor. J Laryngol Otol 105:312-314, 1991<\/p>\n
12. Skinner DW, Bradley PJ: Psychogenic stridor. [Review] J Laryngol Otol 103:383-385, 1989<\/p>\n
13. Walker FO, Kilgo G, Hunt V, Koufman JA: Induction of psychogenic respiratory distress. (Unpublished data)<\/p>\n
14. Blitzer A, Brin MF: Laryngeal dystonia: a series with botulinum toxin therapy. Ann Otol Rhinol Laryngol 100:85-89, 1991<\/p>\n
15. Koufman JA, Blalock PD: Diagnosis and subclassification of spasmodic dysphonia: the value of “unloading” and of spectral analysis. Presented at the American Laryngological Association annual meeting, Los Angeles, California, April 18, 1993. (Submitted for publication)<\/p>\n
16. Koek RJ, Pi EH: Acute laryngeal dystonic reactions to neuroleptics. Psychosomatics 30:359-364, 1989<\/p>\n
17. Stoelting RK: Pharmacology and Physiology in Anesthetic Practice. page 112, Philadelphia, J. B. Lippincott Co., 1987<\/p>\n
18. Henderson PS, Cohen JI, Jarnberg P-E, et al.: A canine model for studying laryngospasm and its prevention. Laryngoscope 102:1237-1241, 1992<\/p>\n
19. Hayes JP, Nolan MT, Brennan N, FitzGerald MX: Three cases of paradoxical vocal cord adduction followed up over a 10-year period. Chest 104:678-680, 1993<\/p>\n
20. Collett PW, Brancatisano T, Konno K: Changes in glottic aperture during bronchial asthma. Am Rev Respir Dis 128:719-723, 1983<\/p>\n
21. Holinger PC, Holinger LD, Reichert TJ, Holinger PH: Respiratory obstruction and apnea in infants with bilateral abductor vocal cord paralysis, meningomyelocele, hydrocephalus, and Arnold-Chiari malformation. J Pediatrics 92:368-373, 1978<\/p>\n
22. Hesz N, Wolraich M: Vocal-cord paralysis and brainstem dysfunction in children with spina bifida. Dev Med Child Neurol 27:528-531, 1985<\/p>\n
23. Charney EB, Rorke LB, Sutton LN, Schut L: Management of Chiari II complications in infants with meningomyelocele. J Pediatrics 111:364-371, 1987<\/p>\n
\n \u00a9 Copyright, Center For Voice Disorders of Wake Forest University<\/strong><\/p>\n <\/p>\n
<\/span>Earlobe Lacs<\/span><\/h2>\nMust cut both wound edges or will not heal well<\/p>\n
<\/p>\n
<\/span>Sore Throat<\/span><\/h2>\n ![\"\"](\"\/wp-content\/images\/part1\/pharyngitistail_small.jpg\")
<\/a><\/h3>\nNegative rapid strep and worsening pharyngitis raises an interesting differential diagnosis. \u00a0Remember that the rapid strep test only has a sensitivity of 80-90%. \u00a0Sometimes we do not get an adequate throat swab. \u00a0Sometimes we have sampling error. \u00a0So a negative rapid test does not eliminate group A strep as a possibility.<\/p>\n
Next, consider the non-group A strep – groups C and G. \u00a0In adolescents they cause approximately 1\/3 as many sore throats as group A strep (this is not true for pre-adolescents.<\/p>\n
Always consider infectious mononucleosis in adolescents with worsening pharyngitis. \u00a0Also remember that acute HIV infection can present as a sore throat.<\/p>\n
Finally, we must consider peritonsillar abscess and Lemierre\u0092s. \u00a0We should get clues from a careful physical examination. \u00a0We should examine the patient for neck swelling or asymmetric tonsillar swelling.<\/p>\n
The key point is patient education. \u00a0We should tell patients that if they are worsening in 3-5 days that we should re-examine them, perhaps do further testing and generally view the patient as having a potentially serious infection.<\/p>\n
<\/span>Adult Epiglottitis<\/span><\/h3>\nCan actually involve the supraglottic tissue and spare the epiglottis.\u00a0 Muffled voice and anterior neck tenderness.\u00a0 If there is no respiratory distress, you may perform laryngoscopy.\u00a0 Start 3rd gen. Cephalosporin (or bactrim, zosyn).\u00a0 Consider ICU admit or intubation.<\/p>\n
<\/p>\n
![\"\"](\"\/wp-content\/images\/part1\/news120103b_small.JPG\")
<\/a><\/p>\nDucic and colleagues described the vallecula sign, which is easily learned and applied by practitioners at all levels of training [ix]<\/a>.\u00a0 In this prospective, blinded study involving 26 laryngoscopically-proven cases of epiglottitis and 26 controls, staff emergency physicians, radiology and otolaryngology residents, and senior medical students were asked to evaluate randomly mixed radiographs for epiglottitis, both before and after a 5-minute tutorial on the vallecula sign.\u00a0 The sign increased sensitivity and specificity from 78.5% and 82.8% to 98.2% and 99.5% respectively, with no difference between evaluator groups.\u00a0 This sign is based on evaluating the vallecula, which appears as an air pocket at the level of the hyoid that should be roughly parallel to the pharyngotracheal air column.\u00a0 To do this, first start at the base of the tongue, trace down to the hyoid bone where you should then find the epiglottis.\u00a0 If the air column anterior to this is not deep, sharp, and roughly parallel to the pharyngotracheal air column, then epiglottitis is present.\u00a0 In this study, the vallecula was deemed abnormal in all cases of epiglottitis, including those patients with minor symptoms, as well as those that needed urgent airway intervention.\u00a0 Furthermore, the vallecula was deemed abnormal in cases where the epiglottis itself was difficult to evaluate (and hence signs like the thumb sign could not be applied).\u00a0 A normal appearing vallecula accurately predicted a normal epiglottis (see Figure 4 below of a normal vallecula and an abnormal vallecula found with epiglottitis, both outlined in red<\/em>). It is noted that the x-ray must be taken with the patient\u0092s mouth closed, as an open mouth may artificially obliterate the vallecula by epiglottic repositioning.<\/p>\nThe Vallecula Sign<\/p>\n
Step 1:\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Ensure that the patient\u0092s mouth is closed for x-ray. Step 2:\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Identify the base of the tongue. Step 3:\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Trace the tongue to the level of the hyoid. Step 4:\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Locate the epiglottis. Step 5:\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Locate the air pocket extending nearly to the hyoid. \u00a0 Is the vallecula deep and roughly parallel to the pharyngotracheal air column? \u00a0\u00a0\u00a0\u00a0 YES: No epiglottitis \u00a0\u00a0\u00a0\u00a0\u00a0 NO: Epiglottitis present<\/p>\n
crack or cocaine can cause it in the absence of infection<\/p>\n
HIV folks are prone to it<\/p>\n
<\/p>\n
<\/p>\n
<\/span>Actinomyces<\/span><\/h3>\nneck masses c sulfa granules.<\/p>\n
<\/span>Diphtheria<\/span><\/h3>\ngrey or white pseudomembrane.\u00a0 Can be associated c polyneuritis, tubular necrosis, or myocarditis.<\/p>\n
horse anti-toxin, erythromycin<\/p>\n
From the Greek for skin or hide<\/p>\n
C. diphtheriae (gram +)-humans are the only carriers<\/p>\n
Resp tract and skin<\/p>\n
Exotoxin induces grayish\/brown membrane, which does not effect gingival.\u00a0 Bleeding will occur if removal is attempted.<\/p>\n
2-4 day incubation period<\/p>\n
can cause cervical nodes extensive enough to give bull neck.<\/p>\n
Myocarditis is possible 1-2 weeks after.<\/p>\n
Can also give muscle weakness\/paralysis 2\u00b0 to exotoxin which looks like G. Barre<\/p>\n
Indigent population can present c cutaneous presentation<\/p>\n
Alert lab, b\/c special cx is needed.<\/p>\n
Give antitoxin (equine) 20000-400000 for pharyngeal disease and 80000-100000 for extensive disease<\/p>\n
and 14 days erythromycin or PCN<\/p>\n
Can get carrier state.<\/p>\n
Booster immunizations every decade.<\/p>\n
<\/span>Pertussis (Whooping Cough)<\/span><\/h3>\nMeans violent cough.\u00a0 Airborne transmission.\u00a0 7-10 day incubation.<\/p>\n
Bortedella pertussis<\/p>\n
Catarrhal phase-non-specific uri. Most contagious<\/p>\n
Paroxysmal-cough, decreased fever.\u00a0 Post-tussive vomiting.\u00a0 Lasts 2-4 weeks<\/p>\n
Convalescent-can last months<\/p>\n
Complications-aspiration pneumonia, CNS<\/p>\n
Presents c very elevated WBC, get nasopharyngeal cx<\/p>\n
Erythromycin may help, definitely give to non-immunized exposures<\/p>\n
Pertussis component of DPT most likely to cause complications.<\/p>\n
<\/span>Strep Pharyngitis<\/span><\/h3>\ncough is usually absent.<\/p>\n
Give 60 mg <\/strong>PO<\/strong>Prednisone x 1<\/strong><\/p>\n(or Decadron)<\/p>\n
Oral Dex helps subset of strep + kiddies, but only marginal improvement ((Ann Emerg Med. 2003 May;41(5):601-8))<\/strong><\/p>\n <\/p>\n
im or oral dex helps pt >15 y\/o (Laryngoscope. 2002 Jan;112(1):87-93)<\/strong><\/p>\n <\/p>\n
A randomized clinical trial of oral versus intramuscular delivery of steroids in acute exudative pharyngitis. (Acad Emerg Med. 2002 Jan;9(1):9-14)\u00a0 They are the same and help im dex. (Ann Emerg Med. 1993 Feb;22(2):212-5) Dexamethasone as adjuvant therapy for severe acute pharyngitis. \u00a0<\/strong><\/p>\n <\/p>\n
only strep worth treating is group A B-hemolytic strep to decrease risk of RF and quinsy.\u00a0 Antibiotics probably do not reduce risk of glomerulonephritis.<\/p>\n
Centor criteria (<\/strong>Ann Int Med 2001;134:506)<\/h4>\n\n- Fever (or reliable history thereof): 1 point<\/li>\n
- Exudate: 1 point<\/li>\n
- Cervical adenitis (tender enlargement of nodes): 1 point<\/li>\n
- NO cough: 1 point<\/li>\n<\/ul>\n
<\/p>\n
4 points: treat with penicillin (Bicillin 1.2 million units)<\/p>\n
0,1 or 2 points: do not treat<\/p>\n
3 points: flip a coin (trust your instinct, give an antibiotic if the patient<\/p>\n
wants one, etc.)<\/p>\n
<\/p>\n
If the Centor score is 4, the percentage of patients who have the disease is<\/p>\n
50-70% depending on time of year, current outbreak in the community, etc.\u00a0 Add<\/p>\n
a scarletiniform rash (uncommon), and that takes the patient well into the 90’s%.<\/p>\n
<\/p>\n
<\/p>\n
Sore throat score adds age<\/h4>\n
One point for age less than 15 years. One point is subtractedif the person is 45 years of age or older<\/p>\n
Better than rapid strep (Can J Emerg Med 4 (3):178 2002)\u00a0 Score had sensitivity of 97% and spec. of 78% while rapid strep testing was 75% and 99%.\u00a0 Gold standard was throat cultures<\/p>\n
<\/p>\n
<\/p>\n
Validated in Kids:<\/p>\n
ACP Journal Club. v136(1):p.37, January\/February, 2002.<\/p>\n
<\/p>\n
Culture after Negative Rapid Strep is not necessary or cost effective (Preventative Medicine 35 25-257, 2002) Reviewed Source Attia MW, Zaoutis T, Klein JD, Meier FA. Performance of a predictive model for streptococcal pharyngitis in children. Arch Pediatr Adolesc Med. 2001 Jun;155:687-91.<\/p>\n
<\/p>\n
cervical lymphadenopathy, tonsillar swelling (2-category severity scale: absent or mild and moderate or severe), coryza, and scarletiniform rash (present or absent)<\/p>\n
<\/p>\n
218 children (37%) had positive culture results for GABHS. The prediction model did better than the physicians’ probability estimates and was comparable to the rapid antigen detection test . The model did not differ in performance according to setting (emergency department vs outpatient clinic) or study period (in season [January to March] vs off season [April to December]).<\/p>\n
<\/p>\n
anti-streptolysin-O titers were not done leading to problem of differentiating carrier state<\/p>\n
<\/p>\n
AAP standard evaluated vs. two rapids in a row.\u00a0 <\/strong><\/p>\nSingle Rapid: Sens-88%, Spec 96.2%<\/p>\n
Double Rapid:\u00a0 92% and 95%<\/p>\n
Rapid and Cx:\u00a0 96% and 96%<\/p>\n
(Pediatrics 111(6):666, June 2003)<\/p>\n
<\/p>\n
<\/span>Vincent\u0092s angina<\/span><\/h3>\nanaerobes, foul breath, pseudomembrane, sub-mandibular nodes.\u00a0 From poor oral hygiene<\/p>\n
Rx with Penicillin<\/p>\n
<\/span>STDs<\/span><\/h3>\ngonorrhea and chlamydia<\/p>\n
<\/span>Mononucleosis<\/span><\/h3>\nFrom Epstein Barr Virus (EBV), a herpesvirus<\/p>\n
Tender, large anterior or posterior cervical lymph nodes<\/p>\n
Get CBC c Diff, Monospot, throat culture and LFTs. Check for hepatosplenomegaly<\/p>\n
Give prednisone 40 mg PO for 5 days<\/p>\n
If you give ampicillin, they will get rash which is not allergic<\/p>\n
Incubation period of 1-2 months, most occur 4-6 weeks after exposure. Can stay contagious for months after the infection.\u00a0 (even years in a small percentage)<\/p>\n
Three forms:<\/p>\n
Anginose:\u00a0 fever, sore throat, and adenopathy<\/p>\n
Typhoidal:\u00a0 prolonged fever, minimal pharyngitis, and delayed lymphadenopathy<\/p>\n
Glandular:\u00a0 dramatic LA, with minimal fever and pharyngitis<\/p>\n
Complications:<\/p>\n
Splenic Rupture:\u00a0 1:1000 cases.<\/p>\n
Airway Obstruction:\u00a0 from hypertrophied tonsils and lymphoid tissues.\u00a0 Steroid therapy is efficacious.<\/p>\n
<\/span>Lingual Tonsillitis<\/span><\/h3>\nOccurs only post-tonsillectomy.\u00a0 Pain worsens c tongue movement<\/p>\n
<\/span>Laryngitis<\/span><\/h3>\nR\/o epiglotittis, steroids help with quicker recovery<\/p>\n
<\/span>Laryngotracheitis<\/span><\/h3>\nViral<\/h4>\nBacterial<\/h4>\n
relatively\u00a0 uncommon.\u00a0 etiologies include staph, strep pneumo, and h. flu.\u00a0 Diphtheria, TB, and syphyllis can also be causes.<\/p>\n
Fungal<\/h4>\n
histoplamsosis, blastomycosis, coccidiomycosis (San Joaquin), and candidiasis<\/p>\n
<\/p>\n
<\/p>\n
add four tabs (1 gm) of carafate to a bottle of ocean Use QID 3 sprays each time<\/p>\n
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<\/span>From Centor<\/span><\/h3>\nMost readers know that I have written extensively about pharyngitis.\u00a0 After yesterday’s brief post about a letter I wrote, I received this comment:<\/p>\n
so how should a culture be sent, just culture for any species? Our lab does STREP A culture only for throat\/tonsil swabs.<\/p><\/blockquote>\n
Here are the problems for adolescent and adult pharyngitis (caveat \u0096 pre-adolescents are different in many ways so this rant only focuses on adolescents and adults):<\/p>\n
\n- The Group A strep rapid tests probably only have a sensitivity of around 75% in actual practice \u0096 this makes reliance on rapid tests less certain than most experts have suggested.\u00a0 Fortunately the specificity is very high, so we can really believe positives but not negatives.<\/li>\n
- Group C (and group G) cause approximately 1\/3 as many sore throats as group A \u0096 but I would favor treating those infections.\u00a0 Some labs will culture for these infections, but most only culture for group A.<\/li>\n
- Fusobacterium necrophorum<\/em>\u00a0probably causes approximately 10% of pharyngitis in this age group.\u00a0 We cannot currently test for this infection.<\/li>\n
- All these bacterial infections can cause serious sequelae.<\/li>\n<\/ol>\n
So what is a conscientious clinician to do?\u00a0 I have favored the empiric therapy approach for those patients who look sick.\u00a0 I define looking sick as pharyngitis scores of 3 or 4 (I am still embarrassed to type the eponym).<\/p>\n
I tell all patients that they should be improved in 3-5 days. If their symptoms worsen or if they develop neck swelling they should return for further evaluation.<\/p>\n
And that’s my story \u0096 and I am stickin<\/p>\n
<\/p>\n
<\/span>Angioedema<\/a><\/span><\/h2>\n <\/p>\n
<\/span>Deep Space Infections<\/span><\/h2>\n<\/span>Masticator Space Abscess<\/span><\/h3>\nbounded by masseter and internal pterygoid muscles<\/p>\n
from extension of anterior space infection<\/p>\n
lateral face swelling and trismus<\/p>\n
<\/span>Ludwig\u0092s Angina<\/span><\/h3>\nfrom the Latin angere: to strangle<\/p>\n
odontogenic infections<\/p>\n
Progressive cellulitis of mouth and neck beginning in the submandibular space.<\/p>\n
Ludwig\u0092s angina is a cellulitis involving the submandibular (sublingual, submaxillary, submental) spaces, rather than simply any perimandibular infection as often erroneously described<\/p>\n
Dental disease is the most common cause.\u00a0 Can cause airway obstruction.\u00a0 Neck tenderness, sub-Q emphysema.\u00a0 Cellulitis of connective tissue, not glands.\u00a0 Bilateral.<\/p>\n
<\/p>\n
![\"\"](\"\/wp-content\/images\/part1\/ludwigs_small.jpg\")
<\/a>![\"\"](\"\/wp-content\/images\/part1\/ludwigs2_small.jpg\")
<\/a><\/p>\n <\/p>\n
Microbes associated with Ludwig\u0092s angina<\/p>\n
Viridans streptococci<\/p>\n
<\/p>\n
Streptococci <\/em> species<\/p>\n <\/p>\n
Bacillus fragilis<\/em><\/p>\n\u00a0<\/em><\/p>\nAnearobic species<\/p>\n
\u00a0<\/em><\/p>\n Staphylococcus aureus<\/em><\/p>\n 35%<\/strong><\/p>\n\u00a0<\/strong><\/p>\n 25%<\/strong><\/p>\n\u00a0<\/strong><\/p>\n 13%<\/strong><\/p>\n\u00a0<\/strong><\/p>\n 13%<\/strong><\/p>\n\u00a0<\/strong><\/p>\n8%<\/strong><\/p>\n(Emedhome.com)<\/p>\n
<\/p>\n
Involvement of the sublingual space may result in elevation of the tongue.\u00a0 Clinically, involvement of this space may be excluded by asking the patient to protrude the tongue past the vermillion border of the upper lip.\u00a0 The patient\u0092s ability to perform this test safely excludes the likelihood of sublingual space compromise (Flynn TR. \u0093The Swollen Face: Severe Odontogenic Infections.\u0094 Emerg Med Clin North Am. August 2000; 18 (3): 481-519)<\/p>\n
<\/p>\n
Neck will have \u0093woody\u0094 edema.\u00a0 If retropharyngeal involvement, can track into mediastinum.\u00a0 Airway compromise is possible.\u00a0 Lateral neck films.\u00a0 Strep or staph.<\/p>\n
High dose PCN (4 million units IV q4 hours), add flagyl or clinda for better anaerobic coverage.<\/p>\n
<\/span>Retropharyngeal Abscess<\/span><\/h3>\nDuck quaking voice.\u00a0 Usually seen in 3-6 year olds.\u00a0 Pt supine c neck extended is position of comfort.\u00a0 Lateral neck films, then CT\/MRI.\u00a0 Medial or Bilat.\u00a0 Treat as above.<\/p>\n
Local extension of oropharyngeal infections such as tonsillitis, pharyngitis, or adenitis in children can lead to retropharyngeal lymph node infection. These infections may progress from cellulitis to phlegmon and finally to retropharyngeal abscess (RPA), which requires drainage.\u00a0 Abscesses in the retropharyngeal or prevertebral spaces are collectively known as RPA.\u00a0 As the retropharyngeal lymph nodes typically regress by age 4 to 6, the main cause of RPA in older children and adults is either extension of odontogenic infection or local trauma (as with a fish bone or holding an object in the mouth).\u00a0 Patients with an RPA may present with symptoms and signs similar to that of acute epiglottitis, including dysphagia, odynophagia, hoarse voice, fever, and neck extension or unusual positioning.\u00a0 Unlike the tripod positioning common in epiglottitis, patients with RPA often lay flat with their neck held in extension.\u00a0 When severe, there may be enough local swelling and pharyngeal pain to cause reluctance in swallowing solids, liquids or secretions, which therefore leads to drooling<\/p>\n
<\/p>\n
The lateral soft tissue neck x-ray may suggest the diagnosis of RPA.\u00a0 Look for soft-tissue swelling in the retropharyngeal space or retrotracheal space, with the limits described below:<\/p>\n
Soft Tissue Measurements<\/strong><\/p>\nRetropharyngeal space (measured at C2) < 7mm Retrotracheal space (measured at C6)<\/p>\n
< 22mm (adults) < 14mm (children < 15 years)<\/p>\n
The retropharyngeal space is measured from the anteroinferior aspect of C2 to the posterior pharyngeal wall, and should not exceed 7mm in children or adults.\u00a0 The retrotracheal space, measured from the anteroinferior aspect of C6 to the posterior pharyngeal wall, should not exceed 22mm in adults or 14mm in children.\u00a0 The most reliable x-rays are taken during deep inspiration with the neck extended. Films taken during expiration (particularly in children less than 24 months) or that are rotated can increase the apparent width of neck soft tissues.<\/p>\n
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<\/span>Parapharyngeal Abscess<\/span><\/h3>\nCan cause lemierre<\/p>\n
<\/span>Lemierre Syndrome<\/span><\/h3>\nOropharyngeal infection leading to septic thrombophlebitis of internal jugular vein.<\/p>\n
Preceding tonsillar or Peritonsillar infection<\/p>\n
Infection usually resolves before presentation, latent period 1-3 weeks<\/p>\n
IJV Thrombosis and sepsis develops accompanied by high fever, neck swelling.\u00a0 Pain at angle of mandible and anterior and medial border of sternocleidomastoid muscles.\u00a0 May also have dysphagia and trismus.\u00a0 Infection can met to lung. causing ARDS.\u00a0 Also osteomyelitis, septic arthritis, meningitis, and liver abscess.\u00a0 Most common bacteria is fusobacterium, especially necrophorum<\/p>\n
<\/p>\n
SpRx c Unasyn for 2-6 weeks<\/p>\n
<\/p>\n
The classic Lemierre’s syndrome has been characterizedby four findings: a primary infection of the oropharynx, septicemiadocumented by at least one positive blood culture, clinicalor radiographic evidence of thrombosis of the internal jugularvein, and at least one metastatic focus of infection.3<\/a> Patientstypically present with a history of tonsillitis for severaldays, persistent fever, neck pain, and general malaise, followedby signs of sepsis\u0097symptoms that are all present in thiscase. Delays in diagnosis are common because of a low indexof suspicion probably due to its rarity or to atypical prodromes.4<\/a> The key to diagnosis is to have a high level of suspicion in older children and adolescents who have fever and neck painor swelling after pharyngitis or tonsillitis.5<\/a> Abnormal radiographswith evidence of infiltrates, pleural effusions, and embolicphenomena are common, but normal findings do not exclude thediagnosis.5<\/a>,6<\/a> Diagnosis is confirmed by demonstrating phlebitisof the internal jugular vein.5<\/a> The proposed pathogenesis inthis case is as follows: disruption of the mucosal barrier of the oropharynx leads to hypoxia and tissue destruction, whichcreates the oxygen-free environment necessary to maintain thelow oxidation-reduction potential necessary for bacterial proliferation.5<\/a> The anatomy of the lateral pharyngeal space (an inverted cone extending from the base of the skull to the hyoid bone bounded medially by the superior pharyngeal constrictor and laterallyby the medial pterygoid) allows invasion of the internal jugularvein either by direct extension or by lymphatic or hematogenousspread from the peritonsillar vessels.7<\/a><\/p>\n <\/p>\n
<\/span> Championing an orphan disease – Lemierre\u0092s syndrome<\/a><\/span><\/h3>\nBy rcentor on Medical Rants<\/p>\n
<\/p>\n
Despite finishing my residency in 1978 and writing many papers about strep pharyngitis, I first heard of Lemierre\u0092s syndrome in the late 1990s.\u00a0 During my training, I suspect the incidence of Lemierre\u0092s syndrome was extremely low.\u00a0 As I slowly became more aware of Lemierre\u0092s syndrome, I started to put this disease into context.<\/p>\n
In 2002, during the early days of this blog, I wrote this rant – Some sore throats are VERY serious<\/a>.<\/p>\n
pseudomonas and staph aureus<\/p>\n
Presents with itching, pain, fullness in ear, redness and swelling, white cheesy or watery green d\/c<\/p>\n
Cleanse the ear and fully suction<\/p>\n
2% acetic acid (VoSol Otic Solution or VoSol HC) or just have folks mix supermarket white vinegar half and half with warm tap water<\/strong><\/p>\n If severe give the vinegar and then topical abx (polymyxin B, neomycin, with HC=cortisporin otic solution or suspension.)\u00a0\u00a0 If TM is perfed, use only the suspension.<\/strong><\/p>\n A wick may need to be inserted to allow ABX access<\/p>\n Avoid wetting the canal for 2 weeks<\/p>\n If cellulitis is present, give systemic abx as well<\/p>\n Objective<\/strong> To compare the clinical efficacy of ear drops containingacetic acid, corticosteroid and acetic acid, and steroid and antibiotic in acute otitis externa in primary care.Participants<\/strong> 213 adults with acute otitis externa.Conclusions<\/strong> Ear drops containing corticosteroids are more effectivethan acetic acid ear drops in the treatment of acute otitisexterna in primary care. Steroid and acetic acid or steroidand antibiotic ear drops are equally effective.(BMJ\u00a0\u00a02003;327:1201-1205\u00a0(22\u00a0November), doi:10.1136\/bmj.327.7425.1201)<\/p>\n <\/p>\n <\/p>\n It is actually pseudomonas osteo of the external canal and temporal bone.<\/strong>\u00a0 ENT and IV ABX.<\/p>\n can be seen in diabetics and immuno-compromised folks<\/p>\n pain on the bony\/cart border in front of tragus<\/p>\n 30% of ct scans can be neg<\/p>\n give iv cipro<\/p>\n infection of auricular cartilage<\/p>\n swollen red pinna<\/p>\n Ciprofloxacin or Augmentin<\/p>\n to cover pseudomonas, proteus, and staph<\/p>\n give abx only if AOM or debris present<\/p>\n follow-up c ENT<\/p>\n Use only suspension<\/p>\n <\/p>\n it is safe to use syringe with canulla to spray eardrums for FB or wax (Emerg Med J<\/em> 2005; 22<\/em>:266-268)<\/p>\n Insects: Kill the insect before attempting to remove it Mineral oil or lidocaine (2%), or isopropyl alcohol (Suggest baby oil, isopropyl alcohol, or cooking oil if patient is frantically calling the ED)<\/p>\n Insecticidal activity of common reagents for insect foreign bodies of the ear Antonelli PJ, Ahmadi A, Prevatt A, Laryngoscope. 2001;111:15-20 Conclusion: Many agents commonly available in the EMS may be used to kill insect foreign bodies in the ear canal. Antiseptic agents and microscope oil were the most effective against the most common insect foreign body, the cockroach. Ticks were the most resistant to all agents tested. Comment: What is the best agent to grab when you have a distraught patient severely agitated by the presence of a live insect in the ear? Mineral oil has been commonly recommended, but it tends to create a gooey mess, making foreign body removal more difficult. Isopropyl alcohol would be my drug of choice. Although it is only number 2 on the quick-kill list, it is probably more readily available than the number 1\u0096ranked ethyl alcohol. Liquid anesthetics are a nice thought, but take at least 3 or 4 times longer to achieve the desired lethal effect on the bug. (From ACEP)<\/p>\n <\/p>\n <\/p>\n Greater understanding and visualization of nasal anatomy revealed that the nose receives blood from many different sources and a large amount of vascular redundancy exists.\u00a0 The external carotid artery divides into the maxillary and superficial temporal arteries.\u00a0 The maxillary artery has many branches including the sphenopalatine artery.\u00a0 The sphenopalatine artery emerges from the sphenopalatine foramen and further divides into four branches: the posterior septal, inferior turbinate, middle turbinate, and nasopalatine arteries.\u00a0 The inferior and middle turbinate arteries depart from the sphenopalatine artery at right angles.\u00a0 Through its four divisions, the sphenopalatine artery supplies the majority of the blood to the nose (43).\u00a0 The sphenopalatine infuses the posterior aspect of the nose, the septum, and the lateral wall from the middle turbinate caudally.\u00a0 In the anterior region of the septum at about the same level as the middle turbinate is Little\u0092s area and within it is Kiesselbach\u0092s plexus, a area of vascular anastomosis that is often the site of anterior epistaxis.(Emedhome.com)<\/p>\n <\/p>\n <\/p>\n Little’s Area=Kiesselbach’s plexus.\u00a0 The anteroinferior portion of the nasal septum.\u00a0 most common ant bleeds.<\/p>\n Posteroinferior turbinate is the most common source of posterior bleeds<\/p>\n <\/p>\n Hold for 15 minutes<\/p>\n Silver nitrate if can have 4-5 sec s bleed.\u00a0 Never use for more than 15 sec.\u00a0 Can also try surgicel\/gelfoam<\/p>\n <\/p>\n Afrin (oxymetazoline) a few squirts up the nose<\/p>\n <\/p>\n Soak cotton swabs in lidocaine with epi, put as many as possible into nares (4-5) leave for 10 minutes.<\/p>\n 4% Cocaine (still the best, comes in a slurry)<\/p>\n 4% Lidocaine mixed 1:1 with 1% phenylephrine<\/p>\n <\/p>\n Oxymetazoline 0.05% (Afrin \u0096 nasal spray) and 4% lidocaine 1:1<\/p>\n <\/p>\n A few mils of 1:10,000 epi mixed with some 4% lidocaine<\/p>\n <\/p>\n Leave anterior pack for 48 hrs, send home with Keflex<\/p>\n Unless severe hypertension is a problem, first squirt a nasal decongestant<\/p>\n into the affected nares, then have patient hold pressure on anterior nares<\/p>\n for 15 minutes by the clock.<\/p>\n <\/p>\n If bleeding persists, using a headlamp, Frasier suction, and speculum put arms in vertical position to avoid compressing the septum)<\/p>\n illuminate the nares and if a bleeding site is apparent, cauterize it with a silver nitrate stick.<\/p>\n <\/p>\n If bleeding continues (usually from a site inaccessible for cautery),<\/p>\n pack the anterior and middle nasal passage with an expandable sponge<\/p>\n (Merocel or similar), expanding it with more decongestant or cocaine spray.<\/p>\n May need more than one<\/p>\n <\/p>\n If bleeding persists, then usually from a posterior source, remove the<\/p>\n anterior\/middle packing, place a small Foley catheter through the nose into<\/p>\n the nasopharynx, blow up the balloon, pull it anteriorly to occlude the<\/p>\n posterior nares and direct all bleeding anteriorly, then repack the entire<\/p>\n nares with petroleum gauze strips using bayonet forceps. Clamp the Foley<\/p>\n where it exits the nose and tape the end of the gauze and Foley to the cheek<\/p>\n in a way that doesn’t pull against the skin of the nares.<\/p>\n <\/p>\n Prophylaxis with TMP\/SMX or keflex for sinusitis prevention (don’t know<\/p>\n the evidence, but ENT always asks me to), and admit the patient to a<\/p>\n monitored bed.<\/p>\n patients may become hypoxic and bradycardiac and can have actual syncope following posterior packing believed to be from a nasopulmonary reflex.<\/p>\n <\/p>\n For patients with severe coagulopathies, also consider giving FFP<\/p>\n <\/p>\n TECHNIQUE<\/p>\n A loop of BIPP-coated ribbon gauze is inserted into<\/p>\n the nose using Tilley dressing forceps. The forceps<\/p>\n are withdrawn and reinserted below the loop of<\/p>\n BIPP. The dorsal surface of the forceps is then used<\/p>\n to guide the loop into the superior nasal cavity and<\/p>\n to compress it into position. The next loop is<\/p>\n inserted into the nose and likewise compressed,<\/p>\n and this cycle is repeated until the whole nose is<\/p>\n filled by BIPP, extending from the superior limit of<\/p>\n the nose to the floor. This method has two<\/p>\n advantages over the traditional method: the internal<\/p>\n nasal valve does not limit the insertion of BIPP<\/p>\n and with each loop of BIPP inserted the cribriform<\/p>\n plate is further protected from trauma that could<\/p>\n otherwise be inflicted using the forceps.<\/p>\n (Emerg Med J 2009;26:52.)<\/p>\n <\/p>\n review article (emerg med australia 2007;18 by lawrence sg)<\/p>\n irritable larynx disease.\u00a0 May have benefit from heliox.\u00a0 May need to be tubed<\/p>\n <\/p>\n young women<\/p>\n start on PPI<\/p>\n benzos<\/p>\n Lidocaine 2% 2 cc in 2 cc NS, nebulize<\/p>\n Cool Mist Nebs<\/p>\n Tell them to sniff, may disappear. May also disappear when reading from a book<\/p>\n <\/p>\n Muscle Tension Dysphonia<\/p>\n <\/p>\n On scoping, you will see vocal cord adduction<\/p>\n <\/p>\n <\/p>\n THE DIFFERENTIAL DIAGNOSIS OF PARADOXICAL VOCAL CORD MOVEMENT<\/strong><\/p>\n Jamie Koufman, MD<\/p>\n This article is reprinted from THE VISIBLE VOICE Vol. 3, No. 3. (July 1994).<\/p>\n ABSTRACT<\/strong><\/p>\n Paradoxical vocal cord movement (PVCM) producing airway obstruction is a relatively uncommon, and sometimes confusing, condition that affects the larynx. PVCM occurs when there is inappropriate closure of the vocal cords during inhalation, and the resultant respiratory obstruction may be intermittent or continuous, mild or severe, depending on the cause. The differential diagnosis of PVCM also includes congenital, inflammatory, traumatic, neoplastic, and neurological causes. Contrary to popular belief, relatively few cases are “functional,” i.e., psychogenic. This article presents the clinician with a differential diagnosis for PVCM and the clinical features that differentiate its various causes.<\/p>\n INTRODUCTION<\/strong><\/p>\n During the respiratory cycle of most higher animals and of human beings, the vocal cords partially abduct (open) with inhalation and partially adduct (close) with exhalation. This phasic vocal cord movement is physiologic, and it allows the unimpeded movement of air into the lungs during inspiration while helping to maintain the alveolar patency (of the lungs) by providing positive airway pressure during expiration. Thus, the larynx serves as an upper airway valve to help keep the lungs expanded.<\/p>\n Some patients who present with stridor (noisy breathing), dyspnea (difficulty breathing), and upper airway obstruction have paradoxical vocal cord movement (PVCM), characterized by inappropriate adduction (closure) of the vocal cords during inhalation. The persistence and the degree of inappropriate glottic closure determines the degree of the airway obstruction, and hence the severity of respiratory symptoms experienced by the patient. In some patients, the problem is constant and severe, requiring prompt remedial treatment, and in other patients, the problem is intermittent and relatively mild. Few articles1,2 address the differential diagnosis of this condition or provide an approach to the management of these challenging patients.<\/p>\n DIFFERENTIAL DIAGNOSIS<\/strong><\/p>\n The differential diagnosis of PVCM is shown in Table 1. Three key elements of the history quickly limit the possibilities in each case: (1) Is the stridor constant or intermittent? (2) Is there any history of head trauma, stroke, or other brainstem problem? (3) Are there any other associated symptoms, such as hoarseness, dysphagia, globus pharyngeus, or cough? In addition, as discussed below, the findings on fiberoptic laryngeal examination are crucial in making the diagnosis.<\/p>\n <\/p>\n TABLE 1: PARADOXICAL VOCAL FOLD MOVEMENT (DIFFERENTIAL DIAGNOSIS)<\/strong><\/p>\n Paroxysmal Laryngospasm and PVCM Due to Gastroesophageal Reflux<\/strong> Gastroesophageal reflux can cause a true intermittent type of PVCM, laryngospasm, or both, in which adduction predominates and abduction is temporarily lost during “attacks.”3-5 Thus, laryngospasm may be considered a specific variation of PVCM. Using this definition, reflux appears to be the most common cause of PVCM.5 In either case, the attacks of respiratory obstruction are paroxysmal and the result of direct contact of gastric fluids with laryngopharyngeal structures.5 It is postulated that some additional form of vagal dysfunction may prolong the episodes for minutes, hours, or sometimes days.6,7<\/p>\n Patients with this frightening condition describe intermittent, sudden-onset, noisy, obstructed breathing, which some describe as “choking episodes.” Attacks of stridor may follow a pattern, e.g., occurring after a meal, after the start of exercise, or after bending over. Sometimes, the attacks may awake the patient from sound sleep. Often, the attacks are truly paroxysmal, occurring without any pattern or identifiable precipitating events. Some patients have one or more attacks per day, and others have their attacks as infrequently as a few each year. The duration of attacks is variable, but “a few minutes” is typical.5<\/p>\n Two-thirds of the patients deny ever having heartburn; however, all complain of some other symptom(s) of laryngopharyngeal reflux, such as chronic or intermittent hoarseness, difficulty swallowing, a sensation of a lump in the throat, chronic throat clearing and cough, or simply too much throat mucus and\/or “post-nasal drip.”5<\/p>\n Within the past two years, the author has diagnosed this condition in 15 adult patients.5 Of these, 12 underwent pH monitoring, which yielded abnormal findings in 11 (92%), five of whom had laryngopharyngeal reflux demonstrated by a pH probe in the hypopharynx behind the laryngeal inlet.5 All fifteen patients were treated with dietary and life-style modification as well as omeprazole 20 mg b.i.d., and, within four weeks, all attacks of laryngospasm had ceased in all patients.<\/p>\n H2-blockers appear to be inadequate treatment for reflux in this group of patients.5,8 For some patients under age 40 years, fundoplication should be considered as an alternative long-term treatment after the symptoms of laryngospasm have been initially corrected by omeprazole therapy; that is, antireflux surgery should be considered in patients who subsequently fail maintenance on H2 blocker therapy.5,8<\/p>\n Patients with the respiratory type of adductor laryngeal dystonia (discussed below), may also have reflux disease. When these two conditions occur together, the attacks of PVCM tend to be prolonged and severe, and the patient may require airway intervention, e.g. intubation or tracheotomy. Such a patient usually requires treatment with both botulinum toxin and omeprazole.<\/p>\n The clinician caring for patients with PVCM due to causes other that reflux should realize that reflux may be a secondary initiating or complicating factor. When laryngopharyngeal reflux is suspected, by the history or by the laryngeal findings, ambulatory 24-hour double-probe pH monitoring is indicated. Long-term medical treatment or surgical fundoplication is usually necessary in such patients.<\/p>\n Psychogenic Stridor<\/strong><\/p>\n After reflux, psychogenic stridor appears to be the second most common cause of PVCM. (The author sees approximately 2 to 3 such cases each year.) Usually, this group of patients is easily diagnosed. First, almost all are teenagers. Second, PVCM occurs with a sudden onset and offset. Third, such patients are usually unconcerned (blase) about their noisy breathing and airway obstruction. Fourth, it is usual for the clinician to be able to “fool” the patient during fiberoptic examination, thus making the PVCM go away. (In most cases, when the patient is asked to read a long passage loudly, the stridor may disappear and phasic respiratory activity of the vocal cords may become normal.) Fifth, the PVCM attacks often can be precipitated and ameliorated by injections of placebo.9-13<\/p>\n The history of each patient will often suggest an underlying psychologic or psychiatric problem, manipulative behavior, and family problems, alone or in various combinations, and the stridor usually occurs at “times of significance” for the patient. In one patient, for example, the stridor only occurred when she was sent to the school principal’s office for misbehaving. Characteristically, her stridor was so loud and disturbing that it demanded medical attention.<\/p>\n A word of caution about this diagnosis. Even though the criteria for psychogenic stridor are fairly well-established — (1) periods of normal phasic vocal cord movement during the fiberoptic examination, (2) induction of stridor and response to placebo, and (3) a psychological or psychiatric disorder — still, this is almost a diagnosis of exclusion. A review of the literature makes clear that many cases of “psychogenic stridor” probably actually had an organic basis, e.g., reflux or dystonia.<\/p>\n Patients with presumed psychogenic PVCM should be approached by the otolaryngologist and the psychologist and\/or psychiatrist as a team, and should be completely evaluated before the team reaches a final diagnosis.<\/p>\n In the author’s experience, none of the patients diagnosed as having psychogenic stridor have subsequently developed one of the other conditions associated with PVCM. On the other hand, patients with another presumed cause of PVCM, such as respiratory-type laryngeal dystonia, are sometimes eventually diagnosed as having psychogenic stridor. In other words, the differentiation between dystonia-related and psychogenic PVCM sometimes may be difficult.<\/p>\n Respiratory-Type Adductor Laryngeal Dystonia<\/strong> The most common type of focal laryngeal dystonia causes a voice disorder known as spasmodic dysphonia (SD). SD occurs in women five times more frequently than in men, is rarely seen in people under age 20 years, and usually affects the voice very severely, but does not affect respiration. The most common pattern is the adductor type, in which glottal overclosures create a “strain-strangled” sounding voice. Patients with this type of SD do not usually experience difficulty breathing, although some patients with severe non-focal dystonia involving the larynx and pharynx (Meige’s syndrome) do have severe, inappropriate laryngeal hyperadduction, which causes airway obstruction. There also is a small group of patients with a respiratory type of adductor laryngeal dystonia in whom the vocal cords inappropriately hyperadduct during inspiration but the voice is normal. Stridor in these patients is present throughout the day, but disappears during sleep, a characteristic of most dystonias.<\/p>\n Blitzer and Brin 14 reported a large series of patients with laryngeal dystonia, most of whom had the well-recognized adductor-type SD. However, they did report that approximately 1% had a respiratory type of adductor laryngeal dystonia, as described above.<\/p>\n Within the past five years, the author has seen five patients with this type of laryngeal dystonia; these patients represent 2% of the author’s laryngeal dystonia patient population.15 None of the five have significant abnormality of voice, but two actually presented with tracheotomy tubes in place.15 On fiberoptic examination, the vocal cords characteristically close during inspiration, and when the patient is asked “take a deep breath,” the degree of overclosure worsens, increasing the respiratory obstruction.<\/p>\n Of the five patients in the author’s series, all have responded well to treatment with botulinum toxin, although this group of patients appears to need larger doses of botulinum toxin than those required by typical SD patients.15<\/p>\n Drug-Induced Laryngeal Dystonic Reactions<\/strong><\/p>\n Temporary drug-induced PVCM has been reported after administration of neuroleptic drugs, including chlorpromazine and haloperidol.16 (Obviously, this cause of PVCM needs to be considered only in patients receiving such medications.) The stridor is usually associated with extrapyramidal symptoms, muscle stiffness, and dystonias of the head and neck, e.g., torticollis. The airway obstruction (PVCM) and the other dystonias are relatively short-lived (hours), and are reversible with intravenous administration of an anticholinergic drug.16 (The author’s experience is in agreement with this report.)<\/p>\n Thiopental, an anesthetic, also may have some such effects at certain doses.17 This may explain the relatively high incidence of “laryngospasm” observed during the induction of anesthesia. It has been shown experimentally that such laryngospasm can be prevented by the administration of topical lidocaine.18<\/p>\n Asthma-Associated Laryngeal Dysfunction<\/strong><\/p>\n Patients who present with PVCM are frequently misdiagnosed as having asthma as the cause of the airway obstruction, even though anti-asthma medications are ineffective. Nevertheless, there appears to be a subset of patients with asthma who also have PVCM.19 Although the mechanism of PVCM in these patients is unknown, glottal aperture changes have been observed in asthma patients20; and vagal reflex dysfunction may be the cause.20 In any asthma patient, when inspiratory stridor is present, the diagnosis of PVCM should be considered. The finding of PVCM on transnasal fiberoptic laryngoscopy is diagnostic.<\/p>\n Brainstem Abnormalities<\/strong><\/p>\n Many central neurological (usually brainstem) abnormalities can cause PVCM, in addition to or complicated by bilateral abductor paralysis, apneic episodes, and central sleep apnea syndrome.21 23 Severe closed head injury, Chiari malformations I and II, meningomyelocele, and cerebrovascular accidents (strokes of the posterior circulation) may all produce PVCM. In these cases, the obstruction and inappropriate vocal cord movement may be inconsistent and variable, and may appear to change with multiple fiberoptic examinations; what is important, however, is that the stridor does not disappear during sleep. This point is critical, since with all the other causes of PVCM, the stridor is paroxysmal or improves during sleep. Early (days or weeks) after closed head injury, extubation may fail and the patient may require multiple intubations, and then, later on, a tracheotomy. With time, as the cerebral and brainstem edema subsides, the vocal cord movement may return to normal and the stridor will disappear. Similarly, some patients with congenital lesions of the brainstem may experience a normalization of vocal cord function after surgical treatment of the lesion.<\/p>\n In the evaluation of patients with PVCM due to brainstem abnormalities, computerized tomographic scanning, magnetic resonance imaging (or both), as well as neurologic consultation is recommended. The prognosis should be guarded. For instance, patients with Chiari malformations who undergo surgical treatment of the malformation may have improvement of their PVCM postoperatively, while others may require a permanent tracheotomy.<\/p>\n APPROACH TO THE PATIENT WITH PVCM<\/strong><\/p>\n After a thorough history is obtained, the first examination of the stridulous patient should include transnasal fiberoptic laryngoscopy (TFL). During this examination, the patient should be asked to: (1) alternatively phonate the vowel \/i\/ and sniff, in rapid alternating succession; (2) take deep breaths; (3) cough, throat clear, and chuckle; (4) count to fifty, rapidly and loudly; (5) read a written passage in a loud voice; and (6) sing.<\/p>\n These maneuvers may reveal a pattern of adduction and abduction consistent with PVCM and a specific diagnosis. Patients with an organic cause of the PVCM, that is, a non-psychogenic cause, usually demonstrates consistent fiberoptic findings, whereas patients with psychogenic PVCM do not. Patients with psychogenic stridor, for example, will often revert to normal phasic vocal cord movement when asked to count or read out loud.<\/p>\n PVCM is therefore usually diagnosed by TFL, and the diagnosis should be considered when there are findings of: (1) inappropriate vocal fold adduction during inspiration; (2) paroxysmal inability to abduct the vocal cords (“transient abductor paralysis”); or (3) a combination of these findings. There is, however, one group of patients that comprises a notable exception: patients with reflux-induced paroxysmal laryngospasm may have normal phasic vocal fold movement on TFL. In these patients, other findings characteristic of laryngopharyngeal reflux (edema, erythema, posterior commissure hypertrophy, and granulation) are almost always observed.<\/p>\n A firm diagnosis of reflux-induced PVCM can be made when the history (pattern and associated symptoms), the laryngeal findings, and the pH monitoring data all support the diagnosis. In addition, complete resolution of the laryngospastic episodes during a therapeutic trial of omeprazole (20 mg b.i.d.) confirms of the diagnosis.<\/p>\n Unlike patients in the other PVCM groups, patients with respiratory-type laryngeal dystonia describe a progressive onset of the PVCM over a period of days, weeks, or months. In addition, such patients usually deny having hoarseness or other reflux symptoms. On TFL, their PVCM is consistent and worsens when the patient is asked to take a deep breath, although the PVCM may improve when the patient reads a written passage or sings. However, improvement is only partial and transient.<\/p>\n On occasion, differentiating dystonic from psychogenic PVCM can be a difficult task. When the clinician is faced with this diagnostic dilemma, neuropsychological testing, psychiatric consultation, and trial injections of botulinum toxin may all be indicated. In some cases, it may take months for the clinical team to reach a diagnosis.<\/p>\n Except for patients in the brainstem abnormality group (who often require tracheotomy), patients with PVCM usually do not have respiratory obstruction severe enough to warrant emergency airway intervention. Of the other groups of patients with PVCM, dystonia patients appear next in terms of the frequency of need for airway support, followed in decreasing order by the psychogenic group, the asthma group, and the reflux group. Table 2 summarizes some of the differentiating features of PVCM.<\/p>\n The diagnostic work-up for each patient with PVCM should be individualized and may include some or all of the following: serial fiberoptic examinations, pH monitoring, neuropsychiatric evaluation, placebo injections, audio-recordings of the patient’s breathing during sleep, and radiographic examinations. In selected cases, therapeutic trials of omeprazole and\/or laryngeal injections of botulinum toxin also may be used.<\/p>\n Finally, PVCM can be confused with other causes of laryngeal obstruction, at least on the initial clinical examination. Inspiratory stridor, for example, may be seen in patients with bilateral vocal cord paralysis, and in patients with laryngeal stenosis or fixation. These conditions may be differentiated from PVCM because, in the former group of conditions, examination shows that vocal cord abduction does not occur. Although abduction may be inconsistent, inappropriate, or incomplete, it must occur some of the time in order for the diagnosis of PVCM to be made.<\/p>\n TABLE 2<\/strong> SOME DIFFERENTIATING FEATURES OF THE CAUSESOF PARADOXICAL VOCAL CORD MOVEMENT<\/p>\n \u00a0<\/strong><\/p>\n Pattern<\/strong><\/p>\n Duration<\/strong><\/p>\n Hoarseness<\/strong><\/p>\n Airway Support Needed<\/strong><\/p>\n Reflux <\/strong><\/p>\n paroxysmal<\/p>\n minutes<\/p>\n usually<\/p>\n almost never<\/p>\n Dystonia <\/strong><\/p>\n daytime<\/p>\n hours<\/p>\n rarely<\/p>\n sometimes<\/p>\n Psychogenic <\/strong><\/p>\n paroxysmal<\/p>\n variable<\/p>\n never<\/p>\n sometimes<\/p>\n Brainstem <\/strong><\/p>\n continual<\/p>\n continual<\/p>\n sometimes<\/p>\n usually<\/p>\n SUMMARY<\/strong><\/p>\n PVCM presents the clinician with an interesting and challenging differential diagnosis. Only abnormalities of the brainstem produce a constant (day and night) stridor and respiratory obstruction, whereas all of the other causes are intermittent or occur only during the daytime. The causes of PVCM, in the author’s experience, in order of frequency of occurrence are: gastroesophageal reflux, followed by psychogenic stridor, respiratory-type laryngeal dystonia, and abnormalities of the brainstem. In the last group, closed head injuries are most common.<\/p>\n The work-up of PVCM may require a multidisciplinary approach and a variety of diagnostic methods. Likewise, treatment often must be individualized. \u0080 Jamie Koufman, M.D.<\/p>\n REFERENCES<\/strong><\/p>\n 1. Ward PH, Hanson DG, Berci G: Observations on central neurologic etiology for laryngeal dysfunction. Ann Otol Rhinol Laryngol 90:430-441, 1981<\/p>\n 2. Kellman RM, Leopold DA: Paradoxical vocal cord motion: an important cause of stridor. Laryngoscope 92:58-60, 1982<\/p>\n 3. Chodosh PL. Gastro-esophageal reflux. Laryngoscope 87:1418-1427, 1977<\/p>\n 4. Burton DM, Pransky SM, Kearns DB, et al.: Pediatric airway manifestations of gastroesophageal reflux. Ann Otol Rhinol Laryngol 101:742-749, 1992<\/p>\n 5. Koufman JA, Loughlin C: Paroxysmal laryngospasm: an uncommon manifestation of gastroesophageal (laryngopharyngeal) reflux disease (Unpublished data)<\/p>\n 6. Bauman NM, Sandler AD, Schmidt C, et al.: Reflex laryngospasm induced by stimulation of distal afferents. Laryngoscope 104: 209-214, 1994<\/p>\n 7. Campbell AH, Mestitz H, Pierce R: Brief upper airway (laryngeal) dysfunction. Aust NZ Med 20:663-668, 1990<\/p>\n 8. Koufman JA: Gastroesophageal reflux and voice disorders. In Diagnosis and Treatment of Voice Disorders Editors: Gould WJ, Rubin JS, Korovin G, Sataloff R. Igaku-Shoin Publishers, New York (In press)<\/p>\n 9. Appleblatt KL, Baker SR: Functional airway obstruction. A new syndrome. Arch Otolaryngol 107:305-307, 1981<\/p>\n 10. Snyder HS, Weiss E: Hysterical stridor: a benign cause of upper airway obstruction. Ann Emer Med 18:991-994, 1989<\/p>\n 11. George MK, O’Connell JE, Batch AJ: Paradoxical vocal cord motion: an unusual cause of stridor. J Laryngol Otol 105:312-314, 1991<\/p>\n 12. Skinner DW, Bradley PJ: Psychogenic stridor. [Review] J Laryngol Otol 103:383-385, 1989<\/p>\n 13. Walker FO, Kilgo G, Hunt V, Koufman JA: Induction of psychogenic respiratory distress. (Unpublished data)<\/p>\n 14. Blitzer A, Brin MF: Laryngeal dystonia: a series with botulinum toxin therapy. Ann Otol Rhinol Laryngol 100:85-89, 1991<\/p>\n 15. Koufman JA, Blalock PD: Diagnosis and subclassification of spasmodic dysphonia: the value of “unloading” and of spectral analysis. Presented at the American Laryngological Association annual meeting, Los Angeles, California, April 18, 1993. (Submitted for publication)<\/p>\n 16. Koek RJ, Pi EH: Acute laryngeal dystonic reactions to neuroleptics. Psychosomatics 30:359-364, 1989<\/p>\n 17. Stoelting RK: Pharmacology and Physiology in Anesthetic Practice. page 112, Philadelphia, J. B. Lippincott Co., 1987<\/p>\n 18. Henderson PS, Cohen JI, Jarnberg P-E, et al.: A canine model for studying laryngospasm and its prevention. Laryngoscope 102:1237-1241, 1992<\/p>\n 19. Hayes JP, Nolan MT, Brennan N, FitzGerald MX: Three cases of paradoxical vocal cord adduction followed up over a 10-year period. Chest 104:678-680, 1993<\/p>\n 20. Collett PW, Brancatisano T, Konno K: Changes in glottic aperture during bronchial asthma. Am Rev Respir Dis 128:719-723, 1983<\/p>\n 21. Holinger PC, Holinger LD, Reichert TJ, Holinger PH: Respiratory obstruction and apnea in infants with bilateral abductor vocal cord paralysis, meningomyelocele, hydrocephalus, and Arnold-Chiari malformation. J Pediatrics 92:368-373, 1978<\/p>\n 22. Hesz N, Wolraich M: Vocal-cord paralysis and brainstem dysfunction in children with spina bifida. Dev Med Child Neurol 27:528-531, 1985<\/p>\n 23. Charney EB, Rorke LB, Sutton LN, Schut L: Management of Chiari II complications in infants with meningomyelocele. J Pediatrics 111:364-371, 1987<\/p>\n \u00a9 Copyright, Center For Voice Disorders of Wake Forest University<\/strong><\/p>\n <\/p>\n Must cut both wound edges or will not heal well<\/p>\n <\/p>\n Negative rapid strep and worsening pharyngitis raises an interesting differential diagnosis. \u00a0Remember that the rapid strep test only has a sensitivity of 80-90%. \u00a0Sometimes we do not get an adequate throat swab. \u00a0Sometimes we have sampling error. \u00a0So a negative rapid test does not eliminate group A strep as a possibility.<\/p>\n Next, consider the non-group A strep – groups C and G. \u00a0In adolescents they cause approximately 1\/3 as many sore throats as group A strep (this is not true for pre-adolescents.<\/p>\n Always consider infectious mononucleosis in adolescents with worsening pharyngitis. \u00a0Also remember that acute HIV infection can present as a sore throat.<\/p>\n Finally, we must consider peritonsillar abscess and Lemierre\u0092s. \u00a0We should get clues from a careful physical examination. \u00a0We should examine the patient for neck swelling or asymmetric tonsillar swelling.<\/p>\n The key point is patient education. \u00a0We should tell patients that if they are worsening in 3-5 days that we should re-examine them, perhaps do further testing and generally view the patient as having a potentially serious infection.<\/p>\n Can actually involve the supraglottic tissue and spare the epiglottis.\u00a0 Muffled voice and anterior neck tenderness.\u00a0 If there is no respiratory distress, you may perform laryngoscopy.\u00a0 Start 3rd gen. Cephalosporin (or bactrim, zosyn).\u00a0 Consider ICU admit or intubation.<\/p>\n <\/p>\n Ducic and colleagues described the vallecula sign, which is easily learned and applied by practitioners at all levels of training [ix]<\/a>.\u00a0 In this prospective, blinded study involving 26 laryngoscopically-proven cases of epiglottitis and 26 controls, staff emergency physicians, radiology and otolaryngology residents, and senior medical students were asked to evaluate randomly mixed radiographs for epiglottitis, both before and after a 5-minute tutorial on the vallecula sign.\u00a0 The sign increased sensitivity and specificity from 78.5% and 82.8% to 98.2% and 99.5% respectively, with no difference between evaluator groups.\u00a0 This sign is based on evaluating the vallecula, which appears as an air pocket at the level of the hyoid that should be roughly parallel to the pharyngotracheal air column.\u00a0 To do this, first start at the base of the tongue, trace down to the hyoid bone where you should then find the epiglottis.\u00a0 If the air column anterior to this is not deep, sharp, and roughly parallel to the pharyngotracheal air column, then epiglottitis is present.\u00a0 In this study, the vallecula was deemed abnormal in all cases of epiglottitis, including those patients with minor symptoms, as well as those that needed urgent airway intervention.\u00a0 Furthermore, the vallecula was deemed abnormal in cases where the epiglottis itself was difficult to evaluate (and hence signs like the thumb sign could not be applied).\u00a0 A normal appearing vallecula accurately predicted a normal epiglottis (see Figure 4 below of a normal vallecula and an abnormal vallecula found with epiglottitis, both outlined in red<\/em>). It is noted that the x-ray must be taken with the patient\u0092s mouth closed, as an open mouth may artificially obliterate the vallecula by epiglottic repositioning.<\/p>\n The Vallecula Sign<\/p>\n Step 1:\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Ensure that the patient\u0092s mouth is closed for x-ray. Step 2:\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Identify the base of the tongue. Step 3:\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Trace the tongue to the level of the hyoid. Step 4:\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Locate the epiglottis. Step 5:\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Locate the air pocket extending nearly to the hyoid. \u00a0 Is the vallecula deep and roughly parallel to the pharyngotracheal air column? \u00a0\u00a0\u00a0\u00a0 YES: No epiglottitis \u00a0\u00a0\u00a0\u00a0\u00a0 NO: Epiglottitis present<\/p>\n crack or cocaine can cause it in the absence of infection<\/p>\n HIV folks are prone to it<\/p>\n <\/p>\n <\/p>\n neck masses c sulfa granules.<\/p>\n grey or white pseudomembrane.\u00a0 Can be associated c polyneuritis, tubular necrosis, or myocarditis.<\/p>\n horse anti-toxin, erythromycin<\/p>\n From the Greek for skin or hide<\/p>\n C. diphtheriae (gram +)-humans are the only carriers<\/p>\n Resp tract and skin<\/p>\n Exotoxin induces grayish\/brown membrane, which does not effect gingival.\u00a0 Bleeding will occur if removal is attempted.<\/p>\n 2-4 day incubation period<\/p>\n can cause cervical nodes extensive enough to give bull neck.<\/p>\n Myocarditis is possible 1-2 weeks after.<\/p>\n Can also give muscle weakness\/paralysis 2\u00b0 to exotoxin which looks like G. Barre<\/p>\n Indigent population can present c cutaneous presentation<\/p>\n Alert lab, b\/c special cx is needed.<\/p>\n Give antitoxin (equine) 20000-400000 for pharyngeal disease and 80000-100000 for extensive disease<\/p>\n and 14 days erythromycin or PCN<\/p>\n Can get carrier state.<\/p>\n Booster immunizations every decade.<\/p>\n Means violent cough.\u00a0 Airborne transmission.\u00a0 7-10 day incubation.<\/p>\n Bortedella pertussis<\/p>\n Catarrhal phase-non-specific uri. Most contagious<\/p>\n Paroxysmal-cough, decreased fever.\u00a0 Post-tussive vomiting.\u00a0 Lasts 2-4 weeks<\/p>\n Convalescent-can last months<\/p>\n Complications-aspiration pneumonia, CNS<\/p>\n Presents c very elevated WBC, get nasopharyngeal cx<\/p>\n Erythromycin may help, definitely give to non-immunized exposures<\/p>\n Pertussis component of DPT most likely to cause complications.<\/p>\n cough is usually absent.<\/p>\n Give 60 mg <\/strong>PO<\/strong>Prednisone x 1<\/strong><\/p>\n (or Decadron)<\/p>\n Oral Dex helps subset of strep + kiddies, but only marginal improvement ((Ann Emerg Med. 2003 May;41(5):601-8))<\/strong><\/p>\n <\/p>\n im or oral dex helps pt >15 y\/o (Laryngoscope. 2002 Jan;112(1):87-93)<\/strong><\/p>\n <\/p>\n A randomized clinical trial of oral versus intramuscular delivery of steroids in acute exudative pharyngitis. (Acad Emerg Med. 2002 Jan;9(1):9-14)\u00a0 They are the same and help im dex. (Ann Emerg Med. 1993 Feb;22(2):212-5) Dexamethasone as adjuvant therapy for severe acute pharyngitis. \u00a0<\/strong><\/p>\n <\/p>\n only strep worth treating is group A B-hemolytic strep to decrease risk of RF and quinsy.\u00a0 Antibiotics probably do not reduce risk of glomerulonephritis.<\/p>\n <\/p>\n 4 points: treat with penicillin (Bicillin 1.2 million units)<\/p>\n 0,1 or 2 points: do not treat<\/p>\n 3 points: flip a coin (trust your instinct, give an antibiotic if the patient<\/p>\n wants one, etc.)<\/p>\n <\/p>\n If the Centor score is 4, the percentage of patients who have the disease is<\/p>\n 50-70% depending on time of year, current outbreak in the community, etc.\u00a0 Add<\/p>\n a scarletiniform rash (uncommon), and that takes the patient well into the 90’s%.<\/p>\n <\/p>\n <\/p>\n One point for age less than 15 years. One point is subtractedif the person is 45 years of age or older<\/p>\n Better than rapid strep (Can J Emerg Med 4 (3):178 2002)\u00a0 Score had sensitivity of 97% and spec. of 78% while rapid strep testing was 75% and 99%.\u00a0 Gold standard was throat cultures<\/p>\n <\/p>\n <\/p>\n Validated in Kids:<\/p>\n ACP Journal Club. v136(1):p.37, January\/February, 2002.<\/p>\n <\/p>\n Culture after Negative Rapid Strep is not necessary or cost effective (Preventative Medicine 35 25-257, 2002) Reviewed Source Attia MW, Zaoutis T, Klein JD, Meier FA. Performance of a predictive model for streptococcal pharyngitis in children. Arch Pediatr Adolesc Med. 2001 Jun;155:687-91.<\/p>\n <\/p>\n cervical lymphadenopathy, tonsillar swelling (2-category severity scale: absent or mild and moderate or severe), coryza, and scarletiniform rash (present or absent)<\/p>\n <\/p>\n 218 children (37%) had positive culture results for GABHS. The prediction model did better than the physicians’ probability estimates and was comparable to the rapid antigen detection test . The model did not differ in performance according to setting (emergency department vs outpatient clinic) or study period (in season [January to March] vs off season [April to December]).<\/p>\n <\/p>\n anti-streptolysin-O titers were not done leading to problem of differentiating carrier state<\/p>\n <\/p>\n AAP standard evaluated vs. two rapids in a row.\u00a0 <\/strong><\/p>\n Single Rapid: Sens-88%, Spec 96.2%<\/p>\n Double Rapid:\u00a0 92% and 95%<\/p>\n Rapid and Cx:\u00a0 96% and 96%<\/p>\n (Pediatrics 111(6):666, June 2003)<\/p>\n <\/p>\n anaerobes, foul breath, pseudomembrane, sub-mandibular nodes.\u00a0 From poor oral hygiene<\/p>\n Rx with Penicillin<\/p>\n gonorrhea and chlamydia<\/p>\n From Epstein Barr Virus (EBV), a herpesvirus<\/p>\n Tender, large anterior or posterior cervical lymph nodes<\/p>\n Get CBC c Diff, Monospot, throat culture and LFTs. Check for hepatosplenomegaly<\/p>\n Give prednisone 40 mg PO for 5 days<\/p>\n If you give ampicillin, they will get rash which is not allergic<\/p>\n Incubation period of 1-2 months, most occur 4-6 weeks after exposure. Can stay contagious for months after the infection.\u00a0 (even years in a small percentage)<\/p>\n Three forms:<\/p>\n Anginose:\u00a0 fever, sore throat, and adenopathy<\/p>\n Typhoidal:\u00a0 prolonged fever, minimal pharyngitis, and delayed lymphadenopathy<\/p>\n Glandular:\u00a0 dramatic LA, with minimal fever and pharyngitis<\/p>\n Complications:<\/p>\n Splenic Rupture:\u00a0 1:1000 cases.<\/p>\n Airway Obstruction:\u00a0 from hypertrophied tonsils and lymphoid tissues.\u00a0 Steroid therapy is efficacious.<\/p>\n Occurs only post-tonsillectomy.\u00a0 Pain worsens c tongue movement<\/p>\n R\/o epiglotittis, steroids help with quicker recovery<\/p>\n relatively\u00a0 uncommon.\u00a0 etiologies include staph, strep pneumo, and h. flu.\u00a0 Diphtheria, TB, and syphyllis can also be causes.<\/p>\n histoplamsosis, blastomycosis, coccidiomycosis (San Joaquin), and candidiasis<\/p>\n <\/p>\n <\/p>\n add four tabs (1 gm) of carafate to a bottle of ocean Use QID 3 sprays each time<\/p>\n <\/p>\n <\/p>\n Most readers know that I have written extensively about pharyngitis.\u00a0 After yesterday’s brief post about a letter I wrote, I received this comment:<\/p>\n so how should a culture be sent, just culture for any species? Our lab does STREP A culture only for throat\/tonsil swabs.<\/p><\/blockquote>\n Here are the problems for adolescent and adult pharyngitis (caveat \u0096 pre-adolescents are different in many ways so this rant only focuses on adolescents and adults):<\/p>\n So what is a conscientious clinician to do?\u00a0 I have favored the empiric therapy approach for those patients who look sick.\u00a0 I define looking sick as pharyngitis scores of 3 or 4 (I am still embarrassed to type the eponym).<\/p>\n I tell all patients that they should be improved in 3-5 days. If their symptoms worsen or if they develop neck swelling they should return for further evaluation.<\/p>\n And that’s my story \u0096 and I am stickin<\/p>\n <\/p>\n <\/p>\n bounded by masseter and internal pterygoid muscles<\/p>\n from extension of anterior space infection<\/p>\n lateral face swelling and trismus<\/p>\n from the Latin angere: to strangle<\/p>\n odontogenic infections<\/p>\n Progressive cellulitis of mouth and neck beginning in the submandibular space.<\/p>\n Ludwig\u0092s angina is a cellulitis involving the submandibular (sublingual, submaxillary, submental) spaces, rather than simply any perimandibular infection as often erroneously described<\/p>\n Dental disease is the most common cause.\u00a0 Can cause airway obstruction.\u00a0 Neck tenderness, sub-Q emphysema.\u00a0 Cellulitis of connective tissue, not glands.\u00a0 Bilateral.<\/p>\n <\/p>\n <\/p>\n Microbes associated with Ludwig\u0092s angina<\/p>\n Viridans streptococci<\/p>\n <\/p>\n Streptococci <\/em> species<\/p>\n <\/p>\n Bacillus fragilis<\/em><\/p>\n \u00a0<\/em><\/p>\n Anearobic species<\/p>\n \u00a0<\/em><\/p>\n Staphylococcus aureus<\/em><\/p>\n 35%<\/strong><\/p>\n \u00a0<\/strong><\/p>\n 25%<\/strong><\/p>\n \u00a0<\/strong><\/p>\n 13%<\/strong><\/p>\n \u00a0<\/strong><\/p>\n 13%<\/strong><\/p>\n \u00a0<\/strong><\/p>\n 8%<\/strong><\/p>\n (Emedhome.com)<\/p>\n <\/p>\n Involvement of the sublingual space may result in elevation of the tongue.\u00a0 Clinically, involvement of this space may be excluded by asking the patient to protrude the tongue past the vermillion border of the upper lip.\u00a0 The patient\u0092s ability to perform this test safely excludes the likelihood of sublingual space compromise (Flynn TR. \u0093The Swollen Face: Severe Odontogenic Infections.\u0094 Emerg Med Clin North Am. August 2000; 18 (3): 481-519)<\/p>\n <\/p>\n Neck will have \u0093woody\u0094 edema.\u00a0 If retropharyngeal involvement, can track into mediastinum.\u00a0 Airway compromise is possible.\u00a0 Lateral neck films.\u00a0 Strep or staph.<\/p>\n High dose PCN (4 million units IV q4 hours), add flagyl or clinda for better anaerobic coverage.<\/p>\n Duck quaking voice.\u00a0 Usually seen in 3-6 year olds.\u00a0 Pt supine c neck extended is position of comfort.\u00a0 Lateral neck films, then CT\/MRI.\u00a0 Medial or Bilat.\u00a0 Treat as above.<\/p>\n Local extension of oropharyngeal infections such as tonsillitis, pharyngitis, or adenitis in children can lead to retropharyngeal lymph node infection. These infections may progress from cellulitis to phlegmon and finally to retropharyngeal abscess (RPA), which requires drainage.\u00a0 Abscesses in the retropharyngeal or prevertebral spaces are collectively known as RPA.\u00a0 As the retropharyngeal lymph nodes typically regress by age 4 to 6, the main cause of RPA in older children and adults is either extension of odontogenic infection or local trauma (as with a fish bone or holding an object in the mouth).\u00a0 Patients with an RPA may present with symptoms and signs similar to that of acute epiglottitis, including dysphagia, odynophagia, hoarse voice, fever, and neck extension or unusual positioning.\u00a0 Unlike the tripod positioning common in epiglottitis, patients with RPA often lay flat with their neck held in extension.\u00a0 When severe, there may be enough local swelling and pharyngeal pain to cause reluctance in swallowing solids, liquids or secretions, which therefore leads to drooling<\/p>\n <\/p>\n The lateral soft tissue neck x-ray may suggest the diagnosis of RPA.\u00a0 Look for soft-tissue swelling in the retropharyngeal space or retrotracheal space, with the limits described below:<\/p>\n Soft Tissue Measurements<\/strong><\/p>\n Retropharyngeal space (measured at C2) < 7mm Retrotracheal space (measured at C6)<\/p>\n < 22mm (adults) < 14mm (children < 15 years)<\/p>\n The retropharyngeal space is measured from the anteroinferior aspect of C2 to the posterior pharyngeal wall, and should not exceed 7mm in children or adults.\u00a0 The retrotracheal space, measured from the anteroinferior aspect of C6 to the posterior pharyngeal wall, should not exceed 22mm in adults or 14mm in children.\u00a0 The most reliable x-rays are taken during deep inspiration with the neck extended. Films taken during expiration (particularly in children less than 24 months) or that are rotated can increase the apparent width of neck soft tissues.<\/p>\n <\/p>\n Can cause lemierre<\/p>\n Oropharyngeal infection leading to septic thrombophlebitis of internal jugular vein.<\/p>\n Preceding tonsillar or Peritonsillar infection<\/p>\n Infection usually resolves before presentation, latent period 1-3 weeks<\/p>\n IJV Thrombosis and sepsis develops accompanied by high fever, neck swelling.\u00a0 Pain at angle of mandible and anterior and medial border of sternocleidomastoid muscles.\u00a0 May also have dysphagia and trismus.\u00a0 Infection can met to lung. causing ARDS.\u00a0 Also osteomyelitis, septic arthritis, meningitis, and liver abscess.\u00a0 Most common bacteria is fusobacterium, especially necrophorum<\/p>\n <\/p>\n SpRx c Unasyn for 2-6 weeks<\/p>\n <\/p>\n The classic Lemierre’s syndrome has been characterizedby four findings: a primary infection of the oropharynx, septicemiadocumented by at least one positive blood culture, clinicalor radiographic evidence of thrombosis of the internal jugularvein, and at least one metastatic focus of infection.3<\/a> Patientstypically present with a history of tonsillitis for severaldays, persistent fever, neck pain, and general malaise, followedby signs of sepsis\u0097symptoms that are all present in thiscase. Delays in diagnosis are common because of a low indexof suspicion probably due to its rarity or to atypical prodromes.4<\/a> The key to diagnosis is to have a high level of suspicion in older children and adolescents who have fever and neck painor swelling after pharyngitis or tonsillitis.5<\/a> Abnormal radiographswith evidence of infiltrates, pleural effusions, and embolicphenomena are common, but normal findings do not exclude thediagnosis.5<\/a>,6<\/a> Diagnosis is confirmed by demonstrating phlebitisof the internal jugular vein.5<\/a> The proposed pathogenesis inthis case is as follows: disruption of the mucosal barrier of the oropharynx leads to hypoxia and tissue destruction, whichcreates the oxygen-free environment necessary to maintain thelow oxidation-reduction potential necessary for bacterial proliferation.5<\/a> The anatomy of the lateral pharyngeal space (an inverted cone extending from the base of the skull to the hyoid bone bounded medially by the superior pharyngeal constrictor and laterallyby the medial pterygoid) allows invasion of the internal jugularvein either by direct extension or by lymphatic or hematogenousspread from the peritonsillar vessels.7<\/a><\/p>\n <\/p>\n By rcentor on Medical Rants<\/p>\n <\/p>\n Despite finishing my residency in 1978 and writing many papers about strep pharyngitis, I first heard of Lemierre\u0092s syndrome in the late 1990s.\u00a0 During my training, I suspect the incidence of Lemierre\u0092s syndrome was extremely low.\u00a0 As I slowly became more aware of Lemierre\u0092s syndrome, I started to put this disease into context.<\/p>\n In 2002, during the early days of this blog, I wrote this rant – Some sore throats are VERY serious<\/a>.<\/p>\nMalignant Externa<\/h4>\n
<\/span>Perichondritis<\/span><\/h3>\n
<\/span>TM Perforation<\/span><\/h3>\n
![\"\"](\"\/wp-content\/images\/part1\/perfed%20tm.jpg\")
<\/a><\/p>\n<\/span>Foreign Bodies or Wax<\/span><\/h3>\n
<\/span>Epistaxis<\/span><\/h2>\n
<\/a><\/a><\/a><\/p>\n<\/a><\/p>\n<\/span>Laryngeal Dyskinesia<\/span><\/h2>\n
<\/span>Spasmdomic Dysphonia<\/span><\/h3>\n
<\/span>Paradoxical Vocal Cord Movement<\/span><\/h3>\n
\n\n
\n
\n
\n
\n<\/span>Earlobe Lacs<\/span><\/h2>\n
<\/span>Sore Throat<\/span><\/h2>\n
<\/a><\/h3>\n<\/span>Adult Epiglottitis<\/span><\/h3>\n
<\/a><\/p>\n<\/span>Actinomyces<\/span><\/h3>\n
<\/span>Diphtheria<\/span><\/h3>\n
<\/span>Pertussis (Whooping Cough)<\/span><\/h3>\n
<\/span>Strep Pharyngitis<\/span><\/h3>\n
Centor criteria (<\/strong>Ann Int Med 2001;134:506)<\/h4>\n
\n
Sore throat score adds age<\/h4>\n
<\/span>Vincent\u0092s angina<\/span><\/h3>\n
<\/span>STDs<\/span><\/h3>\n
<\/span>Mononucleosis<\/span><\/h3>\n
<\/span>Lingual Tonsillitis<\/span><\/h3>\n
<\/span>Laryngitis<\/span><\/h3>\n
<\/span>Laryngotracheitis<\/span><\/h3>\n
Viral<\/h4>\n
Bacterial<\/h4>\n
Fungal<\/h4>\n
<\/span>From Centor<\/span><\/h3>\n
\n
<\/span>Angioedema<\/a><\/span><\/h2>\n
<\/span>Deep Space Infections<\/span><\/h2>\n
<\/span>Masticator Space Abscess<\/span><\/h3>\n
<\/span>Ludwig\u0092s Angina<\/span><\/h3>\n
<\/a><\/a><\/p>\n<\/span>Retropharyngeal Abscess<\/span><\/h3>\n
<\/span>Parapharyngeal Abscess<\/span><\/h3>\n
<\/span>Lemierre Syndrome<\/span><\/h3>\n
<\/span> Championing an orphan disease – Lemierre\u0092s syndrome<\/a><\/span><\/h3>\n