Otolaryngology (ENT)

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).

ABSTRACT

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.

INTRODUCTION

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.

DIFFERENTIAL DIAGNOSIS

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.

Psychogenic Stridor

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.

Brainstem Abnormalities

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

SUMMARY

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.

REFERENCES

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

Earlobe Lacs

Must cut both wound edges or will not heal well

Sore Throat

Adult Epiglottitis

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 patient’s mouth closed, as an open mouth may artificially obliterate the vallecula by epiglottic repositioning.
 

crack or cocaine can cause it in the absence of infection

HIV folks are prone to it

Actinomyces

neck masses c sulfa granules.

Diphtheria

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.

Bortedella pertussis

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.

Strep Pharyngitis

cough is usually absent. 

Give 60 mg PO Prednisone x 1 (or Decadron)

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 subtracted if 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)

Vincent’s angina

anaerobes, foul breath, pseudomembrane, sub-mandibular nodes.  From poor oral hygiene

Rx with Penicillin

STDs

gonorrhea and chlamydia

Mononucleosis

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)

Three forms:

Anginose:  fever, sore throat, and adenopathy

Typhoidal:  prolonged fever, minimal pharyngitis, and delayed lymphadenopathy

Glandular:  dramatic LA, with minimal fever and pharyngitis

Complications:

Splenic Rupture:  1:1000 cases. 

Airway Obstruction:  from hypertrophied tonsils and lymphoid tissues.  Steroid therapy is efficacious. 

Lingual Tonsillitis

Occurs only post-tonsillectomy.  Pain worsens c tongue movement

Laryngitis

R/o epiglotittis, steroids help with quicker recovery

Laryngotracheitis

Viral

Bacterial

relatively  uncommon.  etiologies include staph, strep pneumo, and h. flu.  Diphtheria, TB, and syphyllis can also be causes. 

Fungal

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

Angioedema

Deep Space Infections

Masticator Space Abscess

bounded by masseter and internal pterygoid muscles

from extension of anterior space infection

lateral face swelling and trismus

Ludwig’s Angina

from the Latin angere: to strangle

odontogenic infections

Progressive cellulitis of mouth and neck beginning in the submandibular space. 

Ludwig’s 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.

(Emedhome.com)

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 patient’s 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. 

Retropharyngeal Abscess

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:
 

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.
 

Parapharyngeal Abscess

Can cause lemierre

Lemierre Syndrome

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 characterized by four findings: a primary infection of the oropharynx, septicemia documented by at least one positive blood culture, clinical or radiographic evidence of thrombosis of the internal jugular vein, and at least one metastatic focus of infection.³ Patients typically present with a history of tonsillitis for several days, persistent fever, neck pain, and general malaise, followed by signs of sepsis—symptoms that are all present in this case. Delays in diagnosis are common because of a low index of 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 pain or swelling after pharyngitis or tonsillitis.⁵ Abnormal radiographs with evidence of infiltrates, pleural effusions, and embolic phenomena are common, but normal findings do not exclude the diagnosis.^5,6 Diagnosis is confirmed by demonstrating phlebitis of the internal jugular vein.⁵ The proposed pathogenesis in this case is as follows: disruption of the mucosal barrier of the oropharynx leads to hypoxia and tissue destruction, which creates the oxygen-free environment necessary to maintain the low 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 laterally by the medial pterygoid) allows invasion of the internal jugular vein either by direct extension or by lymphatic or hematogenous spread from the peritonsillar vessels.⁷

Championing an orphan disease - Lemierre’s syndrome

By rcentor on Medical Rants

Peritonsillar Abscess

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

Prevertebral Infection

Space between c-spine and prevertebral fascia

can lead to cervical osteomyelitis

consider staph or m. tuberculosis

Admit, Abx, Neurosurgical Consult

Sinusitis

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)

Sphenoid Sinusitis

from emedicine

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

Common Cold

Motrin

Phenylephrine drops .5% q 4hours x 3 days

Or

Atrovent Nasal Spray 2 sprays each nostril QID

H1 Blocker

Hiccups (Singultus)

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.

Cough

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

Rheumatoid Arthritis

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.  

Trisomy 21

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. 

Gradenigo's Syndrome

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).