Sensory supply to the ear
II,III=post auricular region
Use 512 Hz against mastoid ask which is louder, it should be air.
Place in middle of forehead
Conductive loss ear will hear better
Opposite of the sensorineural ear will hear better
Acute Otitis Media
Caused by Eustachian tube dysfunction. S. Pneumo, H. flu, m. catarrhalis
Clear wax c 3% Hydrogen Peroxide. In kids diagnose with pneumatic otoscopy
Amoxicillin, Bactrim (kernicterus if <2 mo.) 10 day course
Document no mastoid tenderness
Classic is from an untreated AOM
CT Scan c contrast
Trial of IV ABX and ENT consult for myringotomy
clear or hemorrhagic vesicles on TM
Viral or from mycoplasma
pseudomonas and staph aureus
Presents with itching, pain, fullness in ear, redness and swelling, white cheesy or watery green d/c
Cleanse the ear and fully suction
2% acetic acid (VoSol Otic Solution or VoSol HC) or just have folks mix supermarket white vinegar half and half with warm tap water
If severe give the vinegar and then topical abx (polymyxin B, neomycin, with HC=cortisporin otic solution or suspension.) If TM is perfed, use only the suspension.
A wick may need to be inserted to allow ABX access
Avoid wetting the canal for 2 weeks
If cellulitis is present, give systemic abx as well
Objective 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 213 adults with acute otitis externa.Conclusions 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 2003;327:1201-1205 (22 November), doi:10.1136/bmj.327.7425.1201)
It is actually pseudomonas osteo of the external canal and temporal bone. ENT and IV ABX.
can be seen in diabetics and immuno-compromised folks
pain on the bony/cart border in front of tragus
30% of ct scans can be neg
give iv cipro
infection of auricular cartilage
swollen red pinna
Ciprofloxacin or Augmentin
to cover pseudomonas, proteus, and staph
give abx only if AOM or debris present
follow-up c ENT
Use only suspension
Foreign Bodies or Wax
it is safe to use syringe with canulla to spray eardrums for FB or wax (Emerg Med J 2005; 22:266-268)
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)
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 1ranked 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)
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. The external carotid artery divides into the maxillary and superficial temporal arteries. The maxillary artery has many branches including the sphenopalatine artery. The sphenopalatine artery emerges from the sphenopalatine foramen and further divides into four branches: the posterior septal, inferior turbinate, middle turbinate, and nasopalatine arteries. The inferior and middle turbinate arteries depart from the sphenopalatine artery at right angles. Through its four divisions, the sphenopalatine artery supplies the majority of the blood to the nose (43). The sphenopalatine infuses the posterior aspect of the nose, the septum, and the lateral wall from the middle turbinate caudally. In the anterior region of the septum at about the same level as the middle turbinate is Littles area and within it is Kiesselbachs plexus, a area of vascular anastomosis that is often the site of anterior epistaxis.(Emedhome.com)
Little’s Area=Kiesselbach’s plexus. The anteroinferior portion of the nasal septum. most common ant bleeds.
Posteroinferior turbinate is the most common source of posterior bleeds
Hold for 15 minutes
Silver nitrate if can have 4-5 sec s bleed. Never use for more than 15 sec. Can also try surgicel/gelfoam
Afrin (oxymetazoline) a few squirts up the nose
Soak cotton swabs in lidocaine with epi, put as many as possible into nares (4-5) leave for 10 minutes.
4% Cocaine (still the best, comes in a slurry)
4% Lidocaine mixed 1:1 with 1% phenylephrine
Oxymetazoline 0.05% (Afrin nasal spray) and 4% lidocaine 1:1
A few mils of 1:10,000 epi mixed with some 4% lidocaine
Leave anterior pack for 48 hrs, send home with Keflex
Unless severe hypertension is a problem, first squirt a nasal decongestant
into the affected nares, then have patient hold pressure on anterior nares
for 15 minutes by the clock.
If bleeding persists, using a headlamp, Frasier suction, and speculum put arms in vertical position to avoid compressing the septum)
illuminate the nares and if a bleeding site is apparent, cauterize it with a silver nitrate stick.
If bleeding continues (usually from a site inaccessible for cautery),
pack the anterior and middle nasal passage with an expandable sponge
(Merocel or similar), expanding it with more decongestant or cocaine spray.
May need more than one
If bleeding persists, then usually from a posterior source, remove the
anterior/middle packing, place a small Foley catheter through the nose into
the nasopharynx, blow up the balloon, pull it anteriorly to occlude the
posterior nares and direct all bleeding anteriorly, then repack the entire
nares with petroleum gauze strips using bayonet forceps. Clamp the Foley
where it exits the nose and tape the end of the gauze and Foley to the cheek
in a way that doesn’t pull against the skin of the nares.
Prophylaxis with TMP/SMX or keflex for sinusitis prevention (don’t know
the evidence, but ENT always asks me to), and admit the patient to a
patients may become hypoxic and bradycardiac and can have actual syncope following posterior packing believed to be from a nasopulmonary reflex.
For patients with severe coagulopathies, also consider giving FFP
A loop of BIPP-coated ribbon gauze is inserted into
the nose using Tilley dressing forceps. The forceps
are withdrawn and reinserted below the loop of
BIPP. The dorsal surface of the forceps is then used
to guide the loop into the superior nasal cavity and
to compress it into position. The next loop is
inserted into the nose and likewise compressed,
and this cycle is repeated until the whole nose is
filled by BIPP, extending from the superior limit of
the nose to the floor. This method has two
advantages over the traditional method: the internal
nasal valve does not limit the insertion of BIPP
and with each loop of BIPP inserted the cribriform
plate is further protected from trauma that could
otherwise be inflicted using the forceps.
(Emerg Med J 2009;26:52.)
review article (emerg med australia 2007;18 by lawrence sg)
irritable larynx disease. May have benefit from heliox. May need to be tubed
Paradoxical Vocal Cord Movement
start on PPI
Lidocaine 2% 2 cc in 2 cc NS, nebulize
Cool Mist Nebs
Tell them to sniff, may disappear. May also disappear when reading from a book
Muscle Tension Dysphonia
On scoping, you will see vocal cord adduction
THE DIFFERENTIAL DIAGNOSIS OF PARADOXICAL VOCAL CORD MOVEMENT
Jamie Koufman, MD
This article is reprinted from THE VISIBLE VOICE Vol. 3, No. 3. (July 1994).
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.
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.
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.
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.
TABLE 1: PARADOXICAL VOCAL FOLD MOVEMENT (DIFFERENTIAL DIAGNOSIS)
- Gastroesophageal (laryngopharyngeal) reflux
- Psychogenic stridor (usually in adolescents)
- Respiratory-type laryngeal dystonia
- Drug-induced laryngeal dystonic reactions
- Asthma-associated laryngeal dysfunction
- Abnormalities that affect the brainstem
- Chiari malformation I & II, hydrocephalus, meningomyelocele
- Cerebrovascular accident (stroke)
- Severe closed head injury
Paroxysmal Laryngospasm and PVCM Due to Gastroesophageal Reflux 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
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
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
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.
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
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.
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.
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
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.
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.
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.
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.
Respiratory-Type Adductor Laryngeal Dystonia 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.
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.
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.
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
Drug-Induced Laryngeal Dystonic Reactions
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.)
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
Asthma-Associated Laryngeal Dysfunction
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.
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.
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.
APPROACH TO THE PATIENT WITH PVCM
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.
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.
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.
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.
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.
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.
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.
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.
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.
TABLE 2 SOME DIFFERENTIATING FEATURES OF THE CAUSESOF PARADOXICAL VOCAL CORD MOVEMENT
Airway Support Needed
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.
The work-up of PVCM may require a multidisciplinary approach and a variety of diagnostic methods. Likewise, treatment often must be individualized. Jamie Koufman, M.D.
1. Ward PH, Hanson DG, Berci G: Observations on central neurologic etiology for laryngeal dysfunction. Ann Otol Rhinol Laryngol 90:430-441, 1981
2. Kellman RM, Leopold DA: Paradoxical vocal cord motion: an important cause of stridor. Laryngoscope 92:58-60, 1982
3. Chodosh PL. Gastro-esophageal reflux. Laryngoscope 87:1418-1427, 1977
4. Burton DM, Pransky SM, Kearns DB, et al.: Pediatric airway manifestations of gastroesophageal reflux. Ann Otol Rhinol Laryngol 101:742-749, 1992
5. Koufman JA, Loughlin C: Paroxysmal laryngospasm: an uncommon manifestation of gastroesophageal (laryngopharyngeal) reflux disease (Unpublished data)
6. Bauman NM, Sandler AD, Schmidt C, et al.: Reflex laryngospasm induced by stimulation of distal afferents. Laryngoscope 104: 209-214, 1994
7. Campbell AH, Mestitz H, Pierce R: Brief upper airway (laryngeal) dysfunction. Aust NZ Med 20:663-668, 1990
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)
9. Appleblatt KL, Baker SR: Functional airway obstruction. A new syndrome. Arch Otolaryngol 107:305-307, 1981
10. Snyder HS, Weiss E: Hysterical stridor: a benign cause of upper airway obstruction. Ann Emer Med 18:991-994, 1989
11. George MK, O’Connell JE, Batch AJ: Paradoxical vocal cord motion: an unusual cause of stridor. J Laryngol Otol 105:312-314, 1991
12. Skinner DW, Bradley PJ: Psychogenic stridor. [Review] J Laryngol Otol 103:383-385, 1989
13. Walker FO, Kilgo G, Hunt V, Koufman JA: Induction of psychogenic respiratory distress. (Unpublished data)
14. Blitzer A, Brin MF: Laryngeal dystonia: a series with botulinum toxin therapy. Ann Otol Rhinol Laryngol 100:85-89, 1991
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)
16. Koek RJ, Pi EH: Acute laryngeal dystonic reactions to neuroleptics. Psychosomatics 30:359-364, 1989
17. Stoelting RK: Pharmacology and Physiology in Anesthetic Practice. page 112, Philadelphia, J. B. Lippincott Co., 1987
18. Henderson PS, Cohen JI, Jarnberg P-E, et al.: A canine model for studying laryngospasm and its prevention. Laryngoscope 102:1237-1241, 1992
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
20. Collett PW, Brancatisano T, Konno K: Changes in glottic aperture during bronchial asthma. Am Rev Respir Dis 128:719-723, 1983
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
22. Hesz N, Wolraich M: Vocal-cord paralysis and brainstem dysfunction in children with spina bifida. Dev Med Child Neurol 27:528-531, 1985
23. Charney EB, Rorke LB, Sutton LN, Schut L: Management of Chiari II complications in infants with meningomyelocele. J Pediatrics 111:364-371, 1987
© Copyright, Center For Voice Disorders of Wake Forest University
Must cut both wound edges or will not heal well
Negative rapid strep and worsening pharyngitis raises an interesting differential diagnosis. Remember that the rapid strep test only has a sensitivity of 80-90%. Sometimes we do not get an adequate throat swab. Sometimes we have sampling error. So a negative rapid test does not eliminate group A strep as a possibility.
Next, consider the non-group A strep – groups C and G. In adolescents they cause approximately 1/3 as many sore throats as group A strep (this is not true for pre-adolescents.
Always consider infectious mononucleosis in adolescents with worsening pharyngitis. Also remember that acute HIV infection can present as a sore throat.
Finally, we must consider peritonsillar abscess and Lemierres. We should get clues from a careful physical examination. We should examine the patient for neck swelling or asymmetric tonsillar swelling.
The key point is patient education. We 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.
Can actually involve the supraglottic tissue and spare the epiglottis. Muffled voice and anterior neck tenderness. If there is no respiratory distress, you may perform laryngoscopy. Start 3rd gen. Cephalosporin (or bactrim, zosyn). Consider ICU admit or intubation.
Ducic and colleagues described the vallecula sign, which is easily learned and applied by practitioners at all levels of training [ix]. 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. 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. 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. To do this, first start at the base of the tongue, trace down to the hyoid bone where you should then find the epiglottis. If the air column anterior to this is not deep, sharp, and roughly parallel to the pharyngotracheal air column, then epiglottitis is present. 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. 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). 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). It is noted that the x-ray must be taken with the patients mouth closed, as an open mouth may artificially obliterate the vallecula by epiglottic repositioning.
The Vallecula Sign
Step 1: Ensure that the patients mouth is closed for x-ray. Step 2: Identify the base of the tongue. Step 3: Trace the tongue to the level of the hyoid. Step 4: Locate the epiglottis. Step 5: Locate the air pocket extending nearly to the hyoid. Is the vallecula deep and roughly parallel to the pharyngotracheal air column? YES: No epiglottitis NO: Epiglottitis present
crack or cocaine can cause it in the absence of infection
HIV folks are prone to it
neck masses c sulfa granules.
grey or white pseudomembrane. Can be associated c polyneuritis, tubular necrosis, or myocarditis.
horse anti-toxin, erythromycin
From the Greek for skin or hide
C. diphtheriae (gram +)-humans are the only carriers
Resp tract and skin
Exotoxin induces grayish/brown membrane, which does not effect gingival. Bleeding will occur if removal is attempted.
2-4 day incubation period
can cause cervical nodes extensive enough to give bull neck.
Myocarditis is possible 1-2 weeks after.
Can also give muscle weakness/paralysis 2° to exotoxin which looks like G. Barre
Indigent population can present c cutaneous presentation
Alert lab, b/c special cx is needed.
Give antitoxin (equine) 20000-400000 for pharyngeal disease and 80000-100000 for extensive disease
and 14 days erythromycin or PCN
Can get carrier state.
Booster immunizations every decade.
Pertussis (Whooping Cough)
Means violent cough. Airborne transmission. 7-10 day incubation.
Catarrhal phase-non-specific uri. Most contagious
Paroxysmal-cough, decreased fever. Post-tussive vomiting. Lasts 2-4 weeks
Convalescent-can last months
Complications-aspiration pneumonia, CNS
Presents c very elevated WBC, get nasopharyngeal cx
Erythromycin may help, definitely give to non-immunized exposures
Pertussis component of DPT most likely to cause complications.
cough is usually absent.
Give 60 mg POPrednisone x 1
Oral Dex helps subset of strep + kiddies, but only marginal improvement ((Ann Emerg Med. 2003 May;41(5):601-8))
im or oral dex helps pt >15 y/o (Laryngoscope. 2002 Jan;112(1):87-93)
A randomized clinical trial of oral versus intramuscular delivery of steroids in acute exudative pharyngitis. (Acad Emerg Med. 2002 Jan;9(1):9-14) 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.
only strep worth treating is group A B-hemolytic strep to decrease risk of RF and quinsy. Antibiotics probably do not reduce risk of glomerulonephritis.
Centor criteria (Ann Int Med 2001;134:506)
- Fever (or reliable history thereof): 1 point
- Exudate: 1 point
- Cervical adenitis (tender enlargement of nodes): 1 point
- NO cough: 1 point
4 points: treat with penicillin (Bicillin 1.2 million units)
0,1 or 2 points: do not treat
3 points: flip a coin (trust your instinct, give an antibiotic if the patient
wants one, etc.)
If the Centor score is 4, the percentage of patients who have the disease is
50-70% depending on time of year, current outbreak in the community, etc. Add
a scarletiniform rash (uncommon), and that takes the patient well into the 90’s%.
Sore throat score adds age
One point for age less than 15 years. One point is subtractedif the person is 45 years of age or older
Better than rapid strep (Can J Emerg Med 4 (3):178 2002) Score had sensitivity of 97% and spec. of 78% while rapid strep testing was 75% and 99%. Gold standard was throat cultures
Validated in Kids:
ACP Journal Club. v136(1):p.37, January/February, 2002.
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.
cervical lymphadenopathy, tonsillar swelling (2-category severity scale: absent or mild and moderate or severe), coryza, and scarletiniform rash (present or absent)
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]).
anti-streptolysin-O titers were not done leading to problem of differentiating carrier state
AAP standard evaluated vs. two rapids in a row.
Single Rapid: Sens-88%, Spec 96.2%
Double Rapid: 92% and 95%
Rapid and Cx: 96% and 96%
(Pediatrics 111(6):666, June 2003)
anaerobes, foul breath, pseudomembrane, sub-mandibular nodes. From poor oral hygiene
Rx with Penicillin
gonorrhea and chlamydia
From Epstein Barr Virus (EBV), a herpesvirus
Tender, large anterior or posterior cervical lymph nodes
Get CBC c Diff, Monospot, throat culture and LFTs. Check for hepatosplenomegaly
Give prednisone 40 mg PO for 5 days
If you give ampicillin, they will get rash which is not allergic
Incubation period of 1-2 months, most occur 4-6 weeks after exposure. Can stay contagious for months after the infection. (even years in a small percentage)
Anginose: fever, sore throat, and adenopathy
Typhoidal: prolonged fever, minimal pharyngitis, and delayed lymphadenopathy
Glandular: dramatic LA, with minimal fever and pharyngitis
Splenic Rupture: 1:1000 cases.
Airway Obstruction: from hypertrophied tonsils and lymphoid tissues. Steroid therapy is efficacious.
Occurs only post-tonsillectomy. Pain worsens c tongue movement
R/o epiglotittis, steroids help with quicker recovery
relatively uncommon. etiologies include staph, strep pneumo, and h. flu. Diphtheria, TB, and syphyllis can also be causes.
histoplamsosis, blastomycosis, coccidiomycosis (San Joaquin), and candidiasis
add four tabs (1 gm) of carafate to a bottle of ocean Use QID 3 sprays each time
Most readers know that I have written extensively about pharyngitis. After yesterday’s brief post about a letter I wrote, I received this comment:
so how should a culture be sent, just culture for any species? Our lab does STREP A culture only for throat/tonsil swabs.
Here are the problems for adolescent and adult pharyngitis (caveat pre-adolescents are different in many ways so this rant only focuses on adolescents and adults):
- The Group A strep rapid tests probably only have a sensitivity of around 75% in actual practice this makes reliance on rapid tests less certain than most experts have suggested. Fortunately the specificity is very high, so we can really believe positives but not negatives.
- Group C (and group G) cause approximately 1/3 as many sore throats as group A but I would favor treating those infections. Some labs will culture for these infections, but most only culture for group A.
- Fusobacterium necrophorum probably causes approximately 10% of pharyngitis in this age group. We cannot currently test for this infection.
- All these bacterial infections can cause serious sequelae.
So what is a conscientious clinician to do? I have favored the empiric therapy approach for those patients who look sick. I define looking sick as pharyngitis scores of 3 or 4 (I am still embarrassed to type the eponym).
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.
And that’s my story and I am stickin
Deep Space Infections
Masticator Space Abscess
bounded by masseter and internal pterygoid muscles
from extension of anterior space infection
lateral face swelling and trismus
from the Latin angere: to strangle
Progressive cellulitis of mouth and neck beginning in the submandibular space.
Ludwigs angina is a cellulitis involving the submandibular (sublingual, submaxillary, submental) spaces, rather than simply any perimandibular infection as often erroneously described
Dental disease is the most common cause. Can cause airway obstruction. Neck tenderness, sub-Q emphysema. Cellulitis of connective tissue, not glands. Bilateral.
Microbes associated with Ludwigs angina
Involvement of the sublingual space may result in elevation of the tongue. Clinically, involvement of this space may be excluded by asking the patient to protrude the tongue past the vermillion border of the upper lip. The patients ability to perform this test safely excludes the likelihood of sublingual space compromise (Flynn TR. The Swollen Face: Severe Odontogenic Infections. Emerg Med Clin North Am. August 2000; 18 (3): 481-519)
Neck will have woody edema. If retropharyngeal involvement, can track into mediastinum. Airway compromise is possible. Lateral neck films. Strep or staph.
High dose PCN (4 million units IV q4 hours), add flagyl or clinda for better anaerobic coverage.
Duck quaking voice. Usually seen in 3-6 year olds. Pt supine c neck extended is position of comfort. Lateral neck films, then CT/MRI. Medial or Bilat. Treat as above.
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. Abscesses in the retropharyngeal or prevertebral spaces are collectively known as RPA. 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). 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. Unlike the tripod positioning common in epiglottitis, patients with RPA often lay flat with their neck held in extension. 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
The lateral soft tissue neck x-ray may suggest the diagnosis of RPA. Look for soft-tissue swelling in the retropharyngeal space or retrotracheal space, with the limits described below:
Soft Tissue Measurements
Retropharyngeal space (measured at C2) < 7mm Retrotracheal space (measured at C6)
< 22mm (adults) < 14mm (children < 15 years)
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. 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. 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.
Can cause lemierre
Oropharyngeal infection leading to septic thrombophlebitis of internal jugular vein.
Preceding tonsillar or Peritonsillar infection
Infection usually resolves before presentation, latent period 1-3 weeks
IJV Thrombosis and sepsis develops accompanied by high fever, neck swelling. Pain at angle of mandible and anterior and medial border of sternocleidomastoid muscles. May also have dysphagia and trismus. Infection can met to lung. causing ARDS. Also osteomyelitis, septic arthritis, meningitis, and liver abscess. Most common bacteria is fusobacterium, especially necrophorum
SpRx c Unasyn for 2-6 weeks
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 Patientstypically present with a history of tonsillitis for severaldays, persistent fever, neck pain, and general malaise, followedby signs of sepsissymptoms 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 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 Abnormal radiographswith evidence of infiltrates, pleural effusions, and embolicphenomena are common, but normal findings do not exclude thediagnosis.5,6 Diagnosis is confirmed by demonstrating phlebitisof the internal jugular vein.5 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 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
Championing an orphan disease – Lemierres syndrome
By rcentor on Medical Rants
Despite finishing my residency in 1978 and writing many papers about strep pharyngitis, I first heard of Lemierres syndrome in the late 1990s. During my training, I suspect the incidence of Lemierres syndrome was extremely low. As I slowly became more aware of Lemierres syndrome, I started to put this disease into context.
In 2002, during the early days of this blog, I wrote this rant – Some sore throats are VERY serious.
Very interesting story appears on the BBC site – Warning over killer throat disease. I have done sore throat research early in my career. This article describes a condition so unusual that I know little about it.
It follows a significant rise in the number of cases of Lemierres disease this year.
The disease, which is most common in young adults, can cause serious illness and even death if left untreated.
With this disease patients can go downhill quite quickly
The disease is cause by a bacterium called Fusobacterium necrophorum that normally lives harmlessly in peoples mouths.
However, for reasons unknown to scientists, it can start to attack the body of previously healthy people.
It mostly affects young people between the ages of 16 and 23 and is more common in men.
The disease is rare and affects just a handful of people each year. However, there have been 30 cases so far this year – as much as the total for all of last year.
Most viral sore throats get better of their own accord in a few days but with this disease patients can go downhill quite quickly.
Lemierres disease starts off as a very sore throat and leads to a fever, swollen glands and a general feeling of being unwell.
For the past 30 years, the infectious disease community has worked to decrease the use of unnecessary antibiotics. They have assumed that group A beta hemolytic streptococcal infection is the only pharyngitis cause which needs necessary antibiotics. They have assumed that group C and group G streptococci do not need antibiotics. They have excluded the possibility of unknown bacterial infections. Now it appears that Fusobacterium necrophorum may indeed be an unknown bacterial cause of pharyngitis.
The problem with Lemierres Disease is that it represents a long tail disease. Most sore throats are viral or due to streptococcal disease. At least we thought that until recently. Evidence from 2005 in two articles suggests that the organism thought responsible for most Lemierres Disease – Fusobacterium necrophorum – may cause as much as 10% of pharyngitis.
Hagelskjær Kristensen L, Prag J. Lemierres syndrome and other disseminated Fusobacterium necrophorum infections in Denmark: a prospective epidemiological and clinical survey. European Journal of Clinical Microbiology & Infectious Diseases 2008; 779-789.
Finally we had an epidemiologic study which defined the extent of this disease. I have extrapolated the Danish data to the United States. Assuming the same incidence, I estimate that we have approximately 1000 patients with Lemierres yearly and 100 deaths. I would put the confidence range of these estimates at 50% greater or less than this estimate.
So Lemierres is truly an orphan disease if you just look at the numbers. We have some advantages though in attacking this disease. Routine antibiotics can treat this syndrome very well. We do not need new drugs.
As readers know, I gave my new Grand Rounds presentation on Adult Pharyngitis: Morbidity and Mortality in late July. I am already scheduled to give this talk 4 more times (Oct and Nov.) I hope to find venues to present this talk much more over the next year or two.
My 2007 perspective on adult pharyngitis – Pharyngitis Management: Defining the Controversy – included this paragraph:
Another potential reason for antibiotic therapy for severe pharyngitis is to treat Fusobacterium necrophorum. Recent data suggest that these bacteria may cause endemic acute pharyngitis. F. necrophorum infections can cause Lemierres Disease, peritonsillar abscess and persistent sore throat symptoms. While we do not yet know the probability of progression to these complications, certainly empiric antibiotic treatment would likely decrease their incidence. A recent pediatric paper has documented the increasing incidence of F. necrophorum infections (including Lemierres Syndrome) over a recent 6-year period. The authors speculate that decreased empiric antibiotic use may be contributing to the resurgence of this infection.
1. Lemierre A. On Certain Septicemias due to anaerobic organisms. The Lancet. 1936;1:701-703.2. Eykyn SJ. Necrobacillosis. Scandinavian journal of infectious diseases Supplementum. 1989;62:41-46.3. Golledge CL, Beaman MH, Weeramanthri T, Riley TV. Necrobacillosisprimary anaerobic septicaemia due to Fusobacterium necrophorum. Australian and New Zealand journal of medicine. 1990;20:702-704.4. Harar RP, MacDonald A, Pullen D, Ganesan S, Prior AJ. Lemierres syndrome: are we underdiagnosing this life-threatening infection? ORL J Otorhinolaryngol Relat Spec. 1996;58:178-181. 5. Hagelskjaer LH, Prag J, Malczynski J, Kristensen JH. Incidence and clinical epidemiology of necrobacillosis, including Lemierres syndrome, in Denmark 1990-1995. Eur J Clin Microbiol Infect Dis. 1998;17:561-565.6. Brazier JS, Hall V, Yusuf E, Duerden BI. Fusobacterium necrophorum infections in England and Wales 1990-2000. Journal of Medical Microbiology. 2002;51:269-272.7. Chirinos JA, Lichtstein DM, Garcia J, Tamariz LJ. The evolution of Lemierre syndrome: report of 2 cases and review of the literature. Medicine (Baltimore). 2002;81:458-465.8. Ramirez S, Hild T, Rudolph C et al. Increased Diagnosis of Lemierre Syndrome and Other Fusobacterium necrophorum Infections at a Childrens Hospital. PEDIATRICS. 2003;112:e380-e380.9. Bliss SJ, Flanders SA, Saint S. Clinical problem-solving. A pain in the neck. N Engl J Med. 2004;350:1037-1042.10. Brazier J. Human infections with Fusobacterium necrophorum. Anaerobe. 2006;12:165-172.11. Jensen A, Hagelskjaer Kristensen L, Prag J. Detection of Fusobacterium necrophorum subsp. funduliforme in tonsillitis in young adults by real-time PCR. Clin Microbiol Infect. 2007;13:695-701.12. Riordan T. Human Infection with Fusobacterium necrophorum (Necrobacillosis), with a Focus on Lemierres Syndrome. Clinical Microbiology Reviews. 2007;20:622-659.13. Hagelskjær Kristensen L, Prag J. Localised Fusobacterium necrophorum infections: a prospective laboratory-based Danish study. Eur J Clin Microbiol Infect Dis. 2008;27:733-739.14. Hagelskjær Kristensen L, Prag J. Lemierres syndrome and other disseminated Fusobacterium necrophorum infections in Denmark: a prospective epidemiological and clinical survey. Eur J Clin Microbiol Infect Dis. 2008;27:779-789.15. Lu MD, Vasavada Z, Tanner C. Lemierre syndrome following oropharyngeal infection: a case series. Journal of the American Board of Family Medicine : JABFM. 2009;22:79-83.
named after Andre Lemierre, the first reporter of the disease
high fever, rigors, report on day 5 after sore throat onset,
hallmark is tenderness in the the SCM region of the neck (postgrad med j 2004;80:328)
pulmonary involvement in 80% of the cases
hepatic and splenic abscesses
Can occur even post removal. Drooling, trismus, odynophagia, dysphagia, otalgia, inferior and medial displacement of the tonsil. Usually unilateral. Seen in 20-40 year olds.
CT, MRI, UTS. PCN is drug of choice. Also Unasyn then PO augmentin
Needle aspiration or I/D
feel along teeth and cheeks on both sides
leave 1 cm of needle free of cap
go straight in along the teeth, not from the side.
have assistant hold cheek back
use tape roll as bite block
give steroids and pcn/flagyl
needle apsiration is just as good as scalpel (Otolaryngol Head Neck Surg 2003;128:332)
no published reports of injury to carotid or IJ
Use upside down laryngoscope
cut 1.5 cm off sheath of spinal needle
Master Class on PTA Drainage
Space between c-spine and prevertebral fascia
can lead to cervical osteomyelitis
consider staph or m. tuberculosis
Admit, Abx, Neurosurgical Consult
Frontal, maxillary, ethmoid (can spread to CNS), sphenoid (Can invade sella turcica)
Sphenoid Sinusitis can progress to bacterial meningitis
Mucormycosis-black or grey covering. Invasive to blood vessels.
ACP Guidelines for ABX in Sinusitis
DX: Gold standard for bacterial dx is sinus puncture, but never done
Viral illnesses can last up to 33 days (JAMA 202 1967)
But >7 days of SX c
Purulent nasal discharge; maxillary, dental, or facial pain; unilateral sinus tenderness; or worsening sx after improvement (bacterial superinfection); along with severe SX should be treated with narrow spectrum ABX such as amox, doxy, or bactrim.
Even bacterial sinusitis will self resolve if treated symptomatically so only treat severe sx.
in patients with sx of ~48 hrs with signs of bacterial sinusitis, there was no difference between treatment with augmentin or placebo (Arch Intern Med 2003;163:1793-1798)
5 clinical elements are predictive: maxillary toothache, poor response to decongestants, abnormal transillumination, colored nasal discharge, and purulent nasal mucus. When none are present, 9% had sinusitis, when all are rpesent 92% had sinusitis (Ann Intern Med 117:705, 1992)
Etiology: The microbiology of acute sphenoid sinusitis differs from that of uncomplicated maxillary sinusitis. Whereas maxillary sinusitis is caused predominantly by Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis, sphenoid sinusitis has a different profile. Gram-positive organisms predominate, with Staphylococcus aureus most common, followed by Streptococcus pneumoniae. Chronic sphenoid sinusitis can be caused by both gram-negative and gram-positive organisms, anaerobes, and mixed flora, which are more common. Fungal disease also must be considered, especially in the context of a patient who is immunocompromised. Pathophysiology: The pathophysiology of sphenoid sinusitis involves blockage of sinus ostia and impaired mucociliary clearance leading to stasis and secondary bacterial infection. Several predisposing factors have been implicated. Anatomic differences include variations in the position of the intersinus septum and small or abnormally placed ostia. Blunt, penetrating, or surgical trauma can alter drainage patterns as well as allow entry of pathogenic organisms. Swimming or diving with forceful water entry through the nose also has been implicated in causing disease. Immunosuppression due to long-term steroids, diabetes, or radiotherapy can predispose patients to this disease, as can obstruction of sinus ostia by polyps or tumor. Clinical: Patients with acute sphenoid sinusitis often present with vague nonlocalizing symptoms. Headache is the most common symptom; almost all patients in various studies complain of headache. Although the vertex headache is classic, the pain also can be retroorbital, parietooccipital, or frontal. In general, the headache is described as severe, interfering with sleep, and not relieved by narcotics. Fever and purulent rhinorrhea often are noted, and hypoesthesia of the trigeminal nerve may be present in select cases. Neurologic and ophthalmologic findings suggest impending complications. Decreased mental status, lethargy, and seizures point to intracranial extension or meningitis. Ophthalmologic findings may include abducens nerve palsy or hypoesthesia of V1 and/or V2. Chemosis, proptosis, ptosis, diplopia, or decreased visual acuity and ophthalmoplegia may be noted. Maintain a high index of suspicion for sphenoid sinusitis. A review by Hnatuk et al reported that 78% of cases of sphenoid sinusitis were initially misdiagnosed. Evaluate patients with severe progressive headache, with or without fever, for sphenoid sinusitis. Thoroughly investigate signs of orbital or neurologic complications. Disease in the sphenoid sinus is not always inflammatory in nature. Consider a broad differential diagnosis in a patient with clinical suggestion of sphenoid disease and imaging studies consistent with sphenoid opacification. Isolated sphenoid lesions, for example, merit special consideration. In his review of 132 cases of isolated sphenoid disease, Lawson found that, while inflammatory disease predominates, neoplasms, fibroosseous disease, and other entities were significant. In addition to acute and chronic sinusitis, inflammatory diseases included mucoceles, polyps, retention cysts, and fungal disease. Neoplasms included benign tumors, such as inverting papilloma, myxofibroma, plasmocytoma, and schwannoma. Salivary gland malignancies, such as adenoid cystic carcinoma and epidermoid carcinoma, were present, as well as malignancies including squamous cell, melanoma, and hemangiopericytoma. Extension from adjacent sites, such as the nasopharynx and pituitary, was noted, as was metastatic disease from the prostate, kidney, and tonsil. Several cases of fibrous dysplasia and ossifying fibroma were observed. Miscellaneous entities including foreign bodies, encephaloceles, and even an internal carotid aneurysm were also included. In general, although many clinical cases of sphenoid disease may be inflammatory in nature, consider other entities. INDICATIONS Section 3 of 10 Author Information Introduction Indications Relevant Anatomy And Contraindications Workup Treatment Complications Outcome And Prognosis Future And Controversies Bibliography In general, start medical treatment of acute sphenoid sinusitis once the diagnosis is made. Institute antibiotics and decongestants for 24 hours, and, if the patient does not improve over this time course, schedule surgical therapy. If the patient has evidence of complications, undertake urgent surgical decompression. Some individuals advocate early and aggressive surgical and medical treatment for acute sphenoid sinusitis. Hnatuk comments on the aggressive nature of the disease and concludes that nonoperative medical management is not indicated. These conclusions are based on a small number of patients, all in their teenage years. RELEVANT ANATOMY AND CONTRAINDICATIONS Section 4 of 10 Author Information Introduction Indications Relevant Anatomy And Contraindications Workup Treatment Complications Outcome And Prognosis Future And Controversies Bibliography Relevant Anatomy: The sphenoid sinus is the most posterior of the paranasal sinuses. It is a paired structure, divided asymmetrically by an intersinus septum. Pneumatization begins at age 3 years and progresses rapidly between ages 5 and 7 years. Various degrees of pneumatization exist. While the sphenoid most commonly is fully pneumatized, the structure can be only partially aerated or can be filled completely with bone. Pneumatization also may occur in the bones adjacent to the sinus, such as the greater wing of the sphenoid bone or the vomer or palatine bones. The anterior wall of the sphenoid is adjacent to the sphenoethmoidal recess. The floor of the sinus contributes to the roof of the nasopharynx. Posterior to the sphenoid is the clivus. The inferior aspect where it articulates with the vomer is known as the sphenoid rostrum. The pituitary gland sits superior to the sinus. The sphenoid ostium is membranous but surrounded by bone. It lies approximately 30° from the nasal floor and 7 cm from the nasal vestibule. Lateral to the sphenoid sinus lies the cavernous sinus. The close proximity of the sphenoid to the structures within the cavernous sinus accounts for much of the danger of acute sphenoiditis. Within the cavernous sinus lies the internal carotid artery as well as cranial nerves (CN) II, III, IV, and VI and V3. These structures may lie adjacent to the sphenoid and cause indentations within the wall. The internal carotid artery can be observed indenting the posteroinferior surface of the lateral wall. Cadaver studies have shown that the bony covering is thin in 71% of patients and absent in 4% of patients. The optic nerve also has a significant relationship to the sphenoid sinus. As the optic nerve travels within the optic canal, it passes over the anterolateral region of the sphenoid roof. The bony covering over the nerve has been noted to be absent in 4% of individuals
Phenylephrine drops .5% q 4hours x 3 days
Atrovent Nasal Spray 2 sprays each nostril QID
stimulate the soft palate with tongue blade or cotton tip just short of making patient gag; sugar on base of tongue may do the same
Look in ears, consider chest x-ray. MS can cause intractable hiccups as can hyponatremia
Can try chlorpromazine 25 to 50 po TID or QID (can also be given IM), Haldol 2-5 mg IM then 1-4 mg po TID, Reglan 10 mg IV or IM then 10 to 20 mg PO QID. (Minor Emergencies) My favorite is baclofen.
Dextromethorphan 10-20 mg Q 4-6, at night 30 mg
Demulcents-licorice, glycerin, honey
Expectorants-guaifenesin 100-200 mg TID
guaifenesin was effective in URI subjects and not in healthy subjects (Chest. 2003;124:2178-2181.)
ACCP Guidelines (Chest 2006;129:238)
If cough due to URI or bronchitis, can use ipratropium bromide
Levodropropizine and Moguisteine may be used for short-term relief of bronchitis cough
Cough due to URI does not respond well to cough suppressants or central agents
IN pts with bronchitis, hypertonic saline solution can enhance cough clearance
Arthritis and ankylosis of TMJ joint affects 50-75% and limits the ability to open the mouth. Atlantoaxial cervical spine arthritis, The cricoarytenoid joint can also become arthritic and fix the vocal cords causing upper airway obstruction.
20% have atlantoaxial subluxation making intubation with neck extension risky just like RA patients
Endotracheal Tube Injuries
Most commonly occurs at two levels:
old style cuffs caused circumferential ischemic necrosis resulting in laryngomalacia. This should not be seen with current low pressure cuffs unless over inflated. The other site is at the tip of the tube with mucosal irritation and ulceration leading to subglottic stenosis.
Constant otorrhea, headache, and diplopia, which is attributed to inflammation of the petrous apex, is known as Gradenigo’s syndrome. It is often the result of chronic otitis media with long-standing purulent otorrhea (JEM, In Press, Online 2/27/08).
abnormal bone proliferation in the skull base. causes HA and sinusitis. Nothing to do acutely, most need surgery for debriding.
TXA for Epistaxis
The American Journal of Emergency Medicine Volume 31, Issue 9, September 2013, Pages 1389–1392
and then it was studied and did not work: The Use of Tranexamic Acid to Reduce the Need for Nasal Packing in Epistaxis (NoPAC): Randomized Controlled Trial. Ann Emerg Med. 2021 Jun;77(6):631-640. doi: 10.1016/j.annemergmed.2020.12.