Things aren't always what they seem at first

Now that 4D IMRT is all the buzz, we are seeing more and more studies on the volume changes of tumors througout the course of chemoradiation. This is imaging science at its best, monitoring progress and titrating treatment according to burden of disease. Perhaps we can learn something in managing other pathologies; like infection for example.

Weekly volume and dosimetric changes during chemoradiotherapy with intensity-modulated radiation therapy for head and neck cancer: a prospective observational study. (http://www.ncbi.nlm.nih.gov/pubmed/20338474)
Bhide SA, Davies M, Burke K, McNair HA, Hansen V, Barbachano Y, El-Hariry IA, Newbold K, Harrington KJ, Nutting CM.
Int J Radiat Oncol Biol Phys. 2010 Apr;76(5):1360-8.

The Master speaks

When it comes to surgical management of NPC, William Wei always has the last word.

So, it's good that he issues refreshers like this one to keep our management strategies abreast with latest developments.

This appears as the article 'Current management strategy of nasopharyngeal carcinoma' in Clin Exp Otorhinolaryngol. 2010 Mar;3(1):1-12
(http://www.ncbi.nlm.nih.gov/pubmed/20379395)

Other review articles of relevance are linked as well.
(http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=link&linkname=pubmed_pubmed&uid=20379395)

New in OSA

This is music to my ears.

Authors Xu H, Huang W, Yu L, and Chen L. published in Acta Otolaryngolica this week an article entitled 'Sound spectral analysis of snoring sound and site of obstruction in obstructive sleep apnea syndrome.'
(http://www.ncbi.nlm.nih.gov/pubmed/20377505)

They showed objectively what we have known intuitively, that the higher the obstruction the lower the pitch of noise generated. In fact they found that lower obstructions had a greater proportion of >800Hz and >2000Hz first-snore sounds than higher obstructions.

This confirms the way we clinically differentiate stertor and stridor, and might even spawn a new wave of polysomnogram parameters.

Post exposure prophylaxis for Varicella?

The author of this blog is currently in day 7 of illness, suffering from a moderate form of varicella. In spite of starting acyclovir (thanks to vigilant and quick-acting wife) on the day of eruptions, the disease process was not halted and vesicles are florid. While we are taking precautions against pneumonia, encephalitis, and other adult-onset associated complications, it is my 2yr old that I agonise about.

He is an 'exposed' individual. Varicella infections in children are mild and rarely complicated. Being an otolaryngologist, however, we know that Ramsay-Hunt (herpes zoster oticus; i.e. reactivation of virus in facial nerve) syndrome causes debilitating facial palsy - sometimes irreversible. Shingles is painful, too. My question is, should I bother vaccinating him now? He was planned for his jab next week, but now that he is exposed, shouldn't I just wait and see if he develops the infection which would obviate vaccination altogether?

Well, this is where the evidence is really useful:

According to the Cochrane review of randomized trials evaluating varicella vaccine in children and adults; from 3 trials with 110 healthy siblings of household contacts where they received post-exposure prophylaxis (PEP) within 3 days of exposure or not at all:
- varicella developed in 18% (PEP) vs. 78% (no PEP) (p < 0.05)
- moderate to severe varicella developed in 2% (PEP) vs. 76% (no PEP) (p < 0.05)
- PEP group who developed varicella had mild disease (< 50 skin lesions)
- no trials reported on adverse events following immunization

Also, for all my healthcare worker friends out there, don't be a hero (or a chicken, depending why you're delaying.) Get yourself jabbed now! Varicella vaccine is recommended for those who have never had chickenpox and are seronegative for varicella antibodies. The caveat (or bonus) is 1-5% adult develop varicella-like rashes that shed the virus and should be removed from patient contact (perfect excuse for holiday, no?) [Am Fam Physician 1997 Dec;56(9):2291]

Unilateral hearing loss: To MR or not to MR?

The occasional case of unilateral hearing loss sometimes poses a dilemma. Should we order MRIs to rule out acoustic neuroma for every case of unexplained unilateral SNHL when the incidence is only 1 in 100,000?

Perhaps our suspicion index can be guided by the symptom profile of acoustic neuroma where there is:
93.4% hearing impairment
75.5% tinnitus
40.6% vertigo
38.8% unsteadiness

Hearing loss can be sudden (12-47%) or insidious

Ho & Kveton, 2002, recommended a protocol for investigation:
- for patients with limited symptoms (isolated vertigo, historically explained unilateral hearing loss or tinnitus, or symmetrical hearing loss; estimated risk of acoustic neuroma < 5%): ABR as initial test and MRI if abnormal ABR
- for patients with intermediate symptoms (sudden sensorineural hearing loss or unexplained persistent unilateral tinnitus; estimated risk of acoustic neuroma 5-30%): MRI as initial test
- for high-risk patients with combination of unilateral asymmetric sensorineural hearing loss, tinnitus and decreased speech discrimination (estimated risk of acoustic neuroma > 30%): MRI with gadolinium initially and periodic ABR testing if negative MRI


On the other hand, it is worth remembering that tumor growth is on average 1-2.3 mm/year and less than 30% grow > 2 mm/year so that serial MRIs are hardly helpful and may not require any intervention in the elderly.

References
Arch Otolaryngol Head Neck Surg 2004 Feb;130(2):216
Neurosurgery 2006 Jul;59(1):67
J Laryngol Otol 1994 Feb;108(2):116
Am J Otolaryngol 1999 May-Jun;20(3):157
Neurosurgery 1997 Jan;40(1):1
Otolaryngol Clin North Am. 2002 Apr;35(2):393-404, viii

Risk of CA in MNG

I was asked this by a friend who has a progressively enlarging non-toxic goitre and a CT scan that showed a huge multinodular goitre with tracheal compression: do I need surgery and why? Should the whole thyroid be removed or can some be spared?

My quick answer was YES you need surgery, and a total thyroidectomy, both because of the risk of occult carcinoma. An FNAC can easily miss malignant foci, MNGs have a risk of malignant change, imaging has no reliable sign of malignancy, and compression heralds worse complications (with or without op).

But what's the risk exactly, and what does evidence say about how much of thyroid to remove? This is what the evidence says:

1)In a review of 317 patients operated for multinodular goiter, the incidence of occult micro-carcinoma was 3.3% (Wahl RA, Goretzki P, Meybier H, Nitschke J, Linder M, Roher HD. Coexistence of hyperthyroidism and thyroid cancer. World J Surg 1982; 6: 385-390)
2) Another review of 98 total thyroidectomies done for MNGs revealed an incidence of 10 cases (10.2 percent) occult carcinomas - seven patients were diagnosed with papillary carcinoma, two with the follicular variant of papillary and one with follicular carcinoma.
http://www.ispub.com/ostia/index.php?xmlFilePath=journals/ijs/vol17n1/goiter.xml
2) Total thryoidectomy may avoid need for reoperation in case of incidental thyroid
cancer; a study of 218 patients with euthyroid multinodular goiter and no suspicion for malignancy were randomized to total or near-total thyroidectomy (remnant tissue < 1 g) vs. bilateral subtotal thyroidectomy (remnant tissue> 5g); no significant differences in rates of temporary unilateral vocal cord dysfunction (0.9% vs. 0.9%), hypoparathyroidism (1.8% vs.0.9%) or finding of papillary cancer (9.2% vs. 7.3%) (Arch Surg 2004 Feb;139(2):179 in JAMA 2004 May 5;291(17):2058)

So, with a risk of somewhere between 3-10% occult carcinoma (papillary still being the commonest) and near-total also mean could-miss; I think it's still right to say MNGs should be treated with total thyroidectomies unless surgically difficult; upon which post-operative suppressive thyroxine may be an option.

Combined Approach to Paranasal Sinuses

Summary of article: Combined anterior-to-posterior and posterior-to-anterior approach to paranasal sinus surgery: an update. Schaefer SD, Li JC, Chan EK, Wu ZB, Branovan DI.Laryngoscope. 2006 Apr;116(4):509-13

This article first reviews the historical development of FESS, from Wigand's postero-anterior approach (expose posterior ethmoids, open face of spehnoid, and retrograde ethmoidectomy) to the antero-posterior approach of Messerklinger & Stammberger (anterior ethmoidectomy followed by antegrade dissection posteriorly, extent determined by disease.) Kennedy's FESS is built on these antecedent techniques with the aim of 'reestablishing sinus drainage & mucosal recovery through restoration of obstructing sinus ostium and removal of devitalised mucous membrane or bone.'

The obvious advantage and disadvantage of the P-A approach is that
1. it avoids the skull base
2. surgery is excessive in cases of limited disease

As for the A-P approach:
1. surgery is selective and limited to pathologic sinus
2. there is potential for penetrating the posterio-inferiorly sloping skull base

The author's (Schaeffer) CAPS (combined approach to paranasal sinuses) is introduced and discussed. It is claimed that CAPS aims to 'bring together the salient features of the AP and PA approaches while observing the concept of functional endoscopic sinus surgery' and is therefore a 'minimally invasive surgery.. seeking the least disruption of form and function of the paranasal sinuses'

Key tenets of the combined approach are :
1. It is a 'disease-and-anatomy-oriented surgical approach'
2. It's goal is to 'conserve sinus anatomy'
3. Surgical principles utilizes 'anatomic relationships'

(It is disease-oriented in that surgery is targeted to 'relieve medically irreversibly obstruction of sinus outflow tracts' and it is anatomy-oriented in that anterior and posterior ethmoid sinuses are approached separately, in view that they are 'embryologically distinct structures... separated by the basal lamella of the middle turbinate.')

The key surgical principles include:
1. Complete uncinectomy necessary for anterior ethmoidectomy and prevent recurrence
2. Identification of MSO necessary to find plane of lamina papyracea
3. Anterograde (AP) dissection of anterior ethmoid cells up to basal lamella, retrograde (PA) dissection of posterior ethmoid cells

The authors' experience indicates that CAPS can be performed under local or general anesthesia, as permitted or tolerated. In this review of 2,344 patients, 'the overall complication rate was 3.4%. The minor complication rate was 2.6% (6 of 2,344 patients), and the major complication rate was 0.8% (2 of 2,344 patients).' Evidence that underscores how this 'hybrid technique' succesfully combines 'the conservation goals of the AP approach and anatomic virtues of the PA approach to ethmoidectomy.'

PubMed link

Blame it all on GERD!

'Heavner et al., in two animal studies, have demonstrated that exposure of the eustachean tube to simulated gastric content in rodents creates eustachean tube dysfunction. Velepic et al., in two separate studies, have demonstrated a strong correlation of otitis media and GERD. Using a 24-h double pH probe, they found that approximately 60% of the patients had pathologic GERD. In a 2002 study, Tasker et al. demonstrated that middle-ear effusions taken from 54 children contained pepsin/pepsinogen at concentrations up to 1000-fold greater than those in serum 83% of the time. These data suggest that the reflux of gastric juices could be a major cause for otitis media with effusion in children. The link between otitis media with effusion and pharyngeal reflux was further strengthened in a 2004 study by Keles et al. This dual-probe pH study demonstrated that 48% of the children with chronic otitis media effusion had GERD and 64% of the children had pharyngeal reflux. This study suggests that pharyngeal reflux may play an important role in the causes of chronic otitis media with effusion and also that standard single-channel pH probes evaluating for gastroesphageal reflux frequently will miss pharyngeal reflux.'

Should we blame everything on GERD? The above discussion, excerpted from 'SPECIAL COMMENTARY: Should otolaryngologists perform pH probe studies?' by Craig W. Senders in Current Opinion in Otolaryngology & Head and Neck Surgery 2006, 14:38–40 seems to say so.

In the past decade or so, more and more 'mysterious' diseases of ENT are finding its origin in acid. From globus pharyngicus, recurrent tonsillitis, chronic pharyngitis to sinusitis. Now, good old 'glue ear' has a new culprit to blame. And which otolaryngologist hasn't been wondering along those lines? It seems in the fragmented world of subspecialised medicine, diseases are pulling us back together!

Heavner SB, Hardy SM, White DR, et al. Function of the eustachian tube
after weekly exposure to pepsin/hydrochloric acid. Otolaryngol Head Neck
Surg 2001; 125:123–129.
Velepic M, Rozmanic V, Velepic M, Bonifacic M. Gastroesophageal reflux, allergy
and chronic tubotympanal disorders in children. Int J Pediatr Otorhinolaryngol
2000 Oct 16; 55 (3):187–190
Velepic MM, Velepic MS, Starcevic R, et al. Gastroesophageal reflux and sequelae
of chronic tubotympanal disorders in children. Acta Otolaryngol 2004
Oct; 124 (8):914–917
Tasker A, Dettmar PW, Panetti M, et al. Is gastric reflux a cause of otitis
media with effusion in children? Laryngoscope 2002 Nov; 112 (11):1930–
1934
Keles B, Ozturk K, Gunel E, et al. Pharyngeal reflux in children with chronic
otitis media with effusion. Acta Otolaryngol 2004 Dec; 124 (10):1178–
1181

HIgh frequency hearing loss from low frequency noise

It has long been believed that the spectrum of hearing loss closely matches that of the presenting noise. An antiquated study by Mill et al showed that this is not always true.

Human subjects were exposed to an octave-band noise for 24 hours. Temporary threshold shifts increased for the first eight hours of exposure and then were asymptotic. While threshold shifts were largest at about one-half octave above the center frequency of the noise, a second maximum was observed at higher test frequencies. The exact frequency of this second maximum decreased from 7.0 kHz, for a noise centered at 2.0 kHz, to 5.5 kHz for a noise centered at 0.5 kHz. This result could be caused by the travelling wave pattern along the cochlear partition or to the production of distortion products.

PubMed

Effects of gastroesophageal reflux disease in laryngeal carcinoma

GERD as a contributory factor to laryngeal carcinoma is much appreciated in the ORL community, but just how strong is it as a risk? Should it be aggresively investigated and treated if the risk is high?

An Italian retrospective investigates the association with 36 consecutive non-smoking and non-drinking patients with histologically confirmed SCC of the larynx vs a control, a group of 125 lifetime non-smoking and non-drinking cancer-free subjects. Patients with laryngeal cancer had a higher prevalence of gastroesophageal reflux disease than the control subjects (P < 0.0001).

PubMed

Medical management of middle ear disease in children less than 2 years of age with sensorineural hearing loss

'Pneumatic otoscopy should be used to diagnose middle ear effusion. Clearance of OME may be prolonged in children with craniofacial abnormalities. Antibiotics provide a small short-term increase in the resolution of OME and may be warranted in children with coexisting SNHL and OME for 4 to 6 weeks. If OME persists for 8 to 12 weeks, bilateral myringotomy and tube placement (BM&T) with short-term tubes will improve hearing and help resolve OME. AOM in children less than 2 years of age should be treated with a 10-day course of antibiotics. Prophylactic antibiotics may be useful in avoiding tube placement in children less than 2 years of age with recurrent AOM. BM&T with short-term tubes are recommended if recurrent AOM persists. Pneumococcal vaccination can decrease episodes of AOM by 6 to 7%.'

Above are the recommendations based on a meta-analytic study by Westerberg BD, et al. in J Otolaryngol. 2005 Aug;34 Suppl 2:S64-9.

Laryngopharyngeal reflux reviewed

'Over the last 3 decades, many reports have implicated refluxed gastric acid as a cause of, or as a contributory factor in, development of chronic laryngeal and pharyngeal disorders. Although this putative cause-effect relationship has been strengthened by more recent evidence, the body of evidence on causation, diagnosis, and treatment of these increasingly diagnosed disorders is still evolving. A variety of symptoms, functional and structural abnormalities involving the larynx, and other contiguous structures positioned proximal to the esophagus constitute the spectrum of these disorders (see the list below). Various terms such as supraesophageal gastroesophageal reflux disease (GERD), atypical GERD, laryngopharyngeal reflux (LPR), and extraesophageal complications of GERD have been used to describe this group of symptoms and signs.'
- Jeegar Jailwala and Reza Shaker reviews the theory and literature regarding laryngopharyngeal reflux at emedicine.com.

Rhinosinusitis - Review of January 2005

by Y.Y.Yap, MD

Our understanding of rhinosinusitis and how we can best treat this ambiguous condition is in rapid evolution.

Fungal etiology for RSS
First off we have Gosepath J and Mann WJ. take a closer look at the role of fungi role in initiating and maintaining CRSS. While fungi are ubiquitously present in ALL, an immunologic sensitization in RSS patients is evidenced by specific cytokine production in blood-derived lymphocytes not found in controls. Sasama J, et.al also supports this theory showing from literature that eosinophilic inflammation in the nasal mucosa seems to be a specific reaction to certain molds in the nasal and paranasal cavities. Hence the shift from a bacteria-driven etiology to a fungal based one for RSS. It's implications for research and treatment is pressing and is reviewed in these articles. As though to dispel all doubt, Ponikau JU, et.al boldy instituted a clinical trial and showed that intranasal amphotericin B reduces inflammatory mucosal thickening on both CT scan and nasal endoscopy and decreases the levels of intranasal markers for eosinophilic inflammation in patients with CRS.

Recurrent Rhinosinusitis - something different?
Bhattacharyya N, Lee KH. try to distinguish Chronic Recurrent (CRRSS) from Chronic Persistent Rhinosinusitis (CPRSS) by looking at a distinct group of patients who have symptom free periods between at least 4 episodes of RSS symptoms a year. Interestingly the chronic recurrents (CRRSS) seem to suffer more, require more antibiotics and miss work more than the chronic persistents.

FESS for children?
Lieser JD, Derkay CS review the role of FESS in children. Present consensus for FESS in children are 'when maximal medical therapy, adenoidectomy, and culture-directed systemic antibiotics have all failed with persistence of sinonasal disease, when anatomic abnormalities predispose to chronic rhinosinusitis by obstructing normal sinonasal drainage pathways, in sinonasal polyposis to facilitate application of topical steroids', among others. The debate for the best timing for surgery and the fine balance between interfering with facial growth vs. quality of life continues.

No limits!
The greats have spoken! Cohen NA and Kennedy DW. have come forward to defend a larger role for the endoscopic surgeon, stating: 'Endoscopic sinus surgery is no longer exclusively for the management of chronic rhinosinusitis and nasal polyposis. Sinonasal malignancies, as well as anterior skull base lesions have become part of the rhinologist's responsibility. Furthermore, selective lesions managed through traditional craniotomies may now be accessed via trans-sinonasal transcranial endoscopic routes.' They attribute this increased scope, safety and efficacy to advancements in imaging technology including image acquisition, three-dimensional reconstruction, stereotactic navigation, and CT-MRI fusion.

Rapid steps forward are being made on the basic science, pharmacotherapeutics and surgical fronts in rhinology. The future is bright!