Red lips Pale Face… and the story behind

img_2345There was a point in my life where exam stress could have killed me. But it didn’t and I survived the battle. Reminiscing the moment I stood outside the viva-voce room on the last day of my Masters final exam, I was reminded of how terrified I felt inside. I pulled an outer strong face because I knew I just had to pass. But I guess it still showed, because one of the coordinators said “The examiners better call this candidate now, her face already turned pale and vanishing and only her red lips are seen”. Did I really turn cyanosis?? I managed to put on my red lipstick that morning because someone told me that will increase your confidence level. *lies* *cries* Well, it didn’t and I still felt like crap. (I still love my red lipstick though)

So to cut the story short, immediately after it was announced that I passed my Master final exam with flying colours, I went completely blacked out. People were congratulating me and I stood there feeling numb and blanked for no reason. Actually, there was a plenty of reason and I’m sure it could possibly be because I had fragmented sleep for nearly 2 weeks and I dosed up on caffeine like every 2-3 hours.

Like every other people who experience PTSD (that’s Post Traumatic Stress Disorder I’M TELLING YOU), the aftermath is no joke. But with every hardship there comes ease, like there is a silver lining in every cloud… And suddenly here comes the better days where I don’t have to swallow books and sleep on my notes anymore. I still have to update my knowledge once a while (learning process is a never ending process my teachers already warned me… pftGgr#%!!) but at least I can do it at my own timing and with a lot less pressure.

So what’s next?

Here’s my plan:

  1. Start a family
  2. Travel
  3. Write a blog about fashion, travel, style, beauty, food and everything that is NOT medical and NON academics.

May the odds be in my favour… Ameen. Xoxo.


ENT Conjoint Final Exam 2005 – Short Notes


Image result for lingual thyroid


Lingual thyroid is caused by a rare developmental disorder due to aberrant embryogenesis during the descent of thyroid gland to the neck.

It is the most frequent ectopic location of thyroid gland.

The incidence of LT is reported as 1:100,000.

It is 7 times higher in females.

Hickmann recorded the first case of lingual thyroid in 1869. Montgomery stressed that for a condition to be branded as lingual thyroid, thyroid follicles should be demonstrated histopathologically in tissues sampled from the lesion



Early in embryogenesis, thyroid gland appears as proliferation of endodermal tissue in the floor of the pharynx between tuberculum impar and hypobranchial eminence (this area is the later foramen caecum).Normally thyroid gland descends along a path from foramen cecum in the tongue, passes the hyoid bone, to the final position in front and lateral to the second, third, and fourth tracheal rings by 7 weeks gestation. During this descent thyroid tissue retains its communication with foramen cecum. This communication is known as thyroglossal duct. Once the thyroid reaches its final destination, the thyroglossal duct degenerates.

Persistence of thyroglossal duct even after birth leads to the formation of thyroglossal cyst. These cysts usually arise from the remnants of thyroglossal duct and can be found anywhere along the migration site of thyroid gland. This descent may arrest anywhere along this path and this condition may remain unnoticed until puberty. Any functioning thyroid tissue found outside of the normal thyroid location is termed ectopic thyroid tissue. Although it is usually found along the normal path of development, ectopic tissue has also been noted in the mediastinum, heart, esophagus, and diaphragm. Lingual thyroid is the result of failure of descent of the thyroid anlage from the foramen cecum of the tongue. The reasons for the failure of descent are unknown.


Clinical presentations:

Majority of these patients are asymptomatic.

oropharyngeal obstruction may include dysphagia (mild or severe), dyspnea and dysphonia, fullness in the throat, sleep apnoea.

Stridor is most common in neonates.

About 33% of the patients show hypothyroidism findings.

Bleeding is rarely described.


The clinical presentation of LT could be classified into two groups according to the appearance of the symptoms: infants and young children whose lingual thyroid is detected via routine screening may suffer from failure to thrive and mental retardation, or even severe respiratory distress, resulting in a medical emergency. Other cases may present with onset of slowly progressing dysphagia and symptoms of oropharyngeal obstruction before or during puberty. This occurs as a response to the increased demand for thyroid hormone in these hypermetabolic states. Similar response is also encountered during other metabolic stress conditions like pregnancy, infections, trauma, menopause, etc.


head and neck examination :

midline, nodular pinkish mass in the base of the tongue. On palpation this mass could be felt as solid firm and fixed mass. It would be seen attached to the tongue at the junction of anterior 2/3 and posterior 1/3. approximately foramen cecum is supposed to be present. palpate the neck in the region of thyroid to ascertain whether normal thyroid tissue is present in the neck.




  1. thyroid function tests (often demonstrate normal gland functions).
  2. USG neck no thyroid in neck, Xray neck (globular mass at tongue base hyoid region), CT scan neck
  3. Technetium scanning confirms the presence of ectopic thyroid tissue at the base of tongue.
  4. FNAC, LT resembles normal thyroid tissue.



1.Suppressive therapy with exogenous thyroid hormone should be tried first in order to decrease the size of the gland.

  1. surgical removal if emergency. levothyroxine therapy should be initiated after as the lingual thyroid is the only functioning thyroid tissue found in 70% of these patients.



Short Note 2005

-A fistula is an abnormal communication between two epithelialized surfaces.

-Pharyngocutaneous fistula is the most common non-fatal complication following total laryngectomy.

– It creates a communication between the pharynx and cervical skin around the surgical incision or, less frequently, the stoma of the tracheostomy.

– Billroth was also the first person to report PCF as one of the complications of total laryngectomy (he performed first total laryngectomy)

– INCIDENCE reported extremely variable ranging from 3.6% to 65%


-Total laryngectomy w or w/o pharyngectomy
-Partial laryngectomy
-Commando procedure



-a complication that appears in the early post-operative period after total laryngectomy.

-Usually around 3th to 8th post operative day.

-Pharyngeal contents, usually saliva, flow through the fistula emerging from the cutaneous orifice

– Mean hospitalization time is usually 13 – 15 days in comparison to 3 – 5 days for other patients.

-increased morbidity, delay in adjuvant treatment, prolonged hospitalization, and high treatment costs

-More common in males than females



  1. Time of oral feeding Initiating oral feeding within 48 hours of total laryngectomy without partial pharyngectomy; who have not had a previous surgical resection of the upper aerodigestive tract; and who have either not received previous therapeutic irradiation to the head and neck region; does not increase the frequency of PCF. Oral feeding especially with solid food encourages granulation tissue formation along the fistula tract and eventually results in more spontaneous closure of the fistula tract.
  2. Age – > 60 yrs more predisposed.
  3. Gastroesophageal reflux disease(GORD) Prophylactic use of ranitidine (H2 receptor blocker) and metoclopramide (prokinetic) has decreased the incidence of pharyngo-cutaneous fistula
  4. Preoperative tracheostomy contributes to post total laryngectomy PCF fistula formation
  5. Tumor stage and laryngeal site Glottis Ca > Supraglottis > Pyriform sinus > Subglottis
  6. Preoperative Hb:  Low preoperative Hb increases the incidence of PCF nine-fold
  7.  Preoperative radiation: Related to increase of the radiation field size, dose increment and a change from continuous to fractionated radiation therapy 8. Malnutrition
  8. Suture material: There is a statistically significant difference in the formation of PCF between vicryl and catgut groups in favor of vicryl which has greater tensile strength, less inflammatory reaction and has a longer half- life Staples have shown a much lesser incidence of PCF
  9. Positive surgical margins: Presence of infiltrated margins may explain the higher frequency of fistula formation as a result of deficient healing process occurring at the surgical wound, where the presence of the tumor cells may negatively influence the healing process and wound closure. 11. Vascular diseases related to smoking and alcohol drinking


Early diagnosis is important:
Less risky for sepsis and major vessel rupture
More conservative and easy management
Early sign of impending Pharyngocutaneous fistula:
Persistent low-grade fever: 38.5C
wound erythema and edema
localized tenderness in central neck near the wound
wound infection unresponding to conservative treatment
saliva seen at wound or in the drain tube
esophagogram: sinus tract> 2 cm
barium methyl blue swallowing test (+)
definitive fistula formation
Conservative management:
Residual tumor should be excluded firstly
Surgical intervention is reserved when failed by Conservative management
Saliva accumulation ->abscess formation ->flap necrosis and sepsis
Goal: infection control and prevention of large fistula
If suction drain tube (+), delay removal or shift to penrose for drainage
If no drain tube:
Small: Repeated aspiration
Large with abscess formation: open drain:
Away from the stoma: prevention of aspiration
Temporal pharyngostoma-> secondary reconstruction
Silicone septal button with stoma bag (khan 1993)
Removal and curettage of necrotic tissue
Pressure dressing for flap down
Tube feeding with adequate nutrition
Infection control: systemic antibiotics: aerobic and anaerobic.
Time: small fistula without infection< 2-3 weeks
Most: less than 40 days
Surgical management:

PCF have been classified according to source of tissue used in reconstruction to three types:
Type I: two layers are repaired locally
Type II: one locally, one distantly
Type III: both layers repaired distantly
Surgical options:
Direct primary closure: 2 layer: inner mucosa and outer skin
Reconstruction methods with local flap and free flap
Local adjacent flap:
Myocutaneous flaps

The pectoralis major flap offers the benefit of an excellent vascular pedicle.

The latissimus dorsi and the trapezius flaps much less advantageous than the versatile, durable pectoralis major.

Muscle flaps Sternocleidomastoid muscle flap is also used for fistula closure which has advantages of workable mass, good coverage and single stage reconstruction.
Free flap:
Forearm flap
Jejunal free graft


Short Note 2003



Procedure whereby  fistula of the lacrimal sac into the nasal cavity is created.

The operative approach to the sac may be external or endoscopic. The latter approach may use rigid telescopes or the microscope.



Endonasal approach to correct nasolacrimal obstruction was described way back in 1800 by Caldwell, West and later during the begining of 1900 by Mosher.

McDonogh was the first to perform endoscopic dacryocystorhinostomy in 1989.



  • Socially unacceptable epiphora caused by anatomic or functional lacrimal sac or nasolacrimal duct obstruction
  • Chronic dacryocystitis with purulent drainage from the canaliculi
  • Inflammation of the skin overlying the lacrimal sac in the region of the medial canthus
  • Dacryolith formation
  • Benign lacrimal sac mass


Advantages of endoscopic DCR:

  • better aesthetic result , no external scar.
  • any concomittant intranasal pathology causing epiphora can be addressed
  • avoids injury to the medial canthus and/or pathologic scar formation.
  • preserves the pumping mechanism of the orbicularis oculi muscle.
  • active infection of the lacrimal system is not a contraindication to surgery.
  • It is especially superior to the external approach in revision surgery.
  • less bloody than the external approach.
  • the perioperative time is shorter.
  • success rate is comparable to the external approach.


Disadvantages of endoscopic DCR:

  • It requires specialized training in nasal endoscopic surgery.
  • The endoscopic equipment is an expense.


Contraindications of endoscopic DCR:
–  Presence of a firm indurated mass above the level

of medial canthus.
–  Bloody epiphora
–  Presence of bony destruction as seen in

radiological films
–  Pseudoepiphora: is essentially reflux tearing: the

main gland over compensates secretion because

of lack of secretion from minor glands of along the

lid margin.


Surgery technique:

– Patient under GA

– Nasal packing with decongestants

– Localisation of lacrimal sac:  the anterior portion of middle turbinate, the sac lies just lateral to it.  The lacrimal fossa is bounded by the anterior lacrimal crest, which consists of the frontal process of the maxillary bone. The posterior lacrimal crest is made up of the lacrimal bone itself.

– Mucosal incision:  lateral wall mucosa is incised with a sickle knife and is elevated using a Freer elevator.  The incision is made vertically from inferior to superior.  After elevation the mucosa is removed using a Blakesley forceps.

– Bone removal:  To expose the lacrimal sac, the bony lacrimal fossa must be uncovered first.  Bone removal can be performed using a Kerrison’s punch forceps or by using a burr.

– Opening of lacrimal sac:  After overlying bone removal the lacrimal sac can be incised using a sickle knife.  An assistant could tent out the medial wall of the sac with lacrimal probes introduced through the canaliculi.  The whole of the medial wall of the sac is removed.

– Topical mitomycin can be applied to the site of surgery to prevent restenosis of the sac.




  • Instil one drop of fluorescein into the conjunctival sac
  • Put a cotton bud soaked in anaesthetic in the inferior meatus.
  • If fluorescein is detected after five minutes, the system is patent (positive Primary Jones Test)
  • If no fluorescein is discovered, this is a negative Primary Jones Test and the functional obstruction could be anywhere from the punctum to the Valve of Hasner.
  • Next, wash the excess fluorescein from the conjunctival sac and syringe. If fluorescein is detected, then this shows it had entered the sac and constitutes a positive Secondary Jones Test and suggests a functional obstruction of the nasolacrimal duct.
  • If no dye is found on the cotton bud after syringing, this is termed a negative Secondary Jones Test, because fluorescein had not entered the sac and, thus, there is stenosis of the puncta or canalicular system.
  • If no saline appears in the nose, there is a complete obstruction somewhere in the lacrimal drainage system.


Hard stop

If the cannula touches the medial wall of the lacrimal sac and lacrimal bone, a definite end point is reached. It indicates that there is no complete obstruction in the canalicular system


Soft stop

If a spongy end point is felt, this indicates that the cannula has been prevented from entering the lacrimal sac. Therefore, there is a blockage in the canalicular system and there will be no distension of the lacrimal sac when the plunger is pressed.



A.K.A: Adamantinoma of the jaw  ( Short Note 2003 )


Benign, locally aggressive tumours that arise from the mandible, or less commonly from the maxilla.



Ameloblastomas are the second most common odontogenic tumour (odontoma is the most common)

3rd to 5th decades of life

No gender predilection


Clinical presentation:

Hard painless slow growing mass near the angle of the mandible in the in the region of the 3rd molar tooth (48 and 38)

Can occur anywhere along the alveolus of the mandible (80%) and maxilla (20%).

When the maxilla is involved, the tumour is located in the premolar region, and can extend up in the maxillary sinus.

Although benign, it is a locally aggressive neoplasm with a high rate of recurrence. Approximately 20% of cases are associated with dentigerous cysts and unerupted teeth.



Arise from  ameloblasts, which are part of the odontogenic epithelium, responsible for enamel production and eventual crown formation.


Three variants are described:

simple (no nodule): best prognosis

luminal: single nodule projecting into the cyst

mural: multiple nodules (often only microscopic) in the wall of the cyst


Radiographic features

Plain film and CT

It is classically seen as a multiloculated (80%), expansile “soap-bubble” lesion, with well demarcated borders and no matrix calcification.


In general ameloblastomas demonstrate a mixed solid and cystic pattern, with a thick irregular wall, often with papillary solid structures projecting into the lesion.


Treatment and prognosis

surgical en-bloc resection.

Local curettage is associated with a high rate of local recurrence (45-90%).

Simple unicystic lesions are less common but have a better prognosis. Simple (no nodule) variant will not be diagnosable on radiography, as it will be indistinguishable form other more common cysts. Luminal variant, has a single nodule projecting into the cyst.

Mural variant has multiple nodules (often only microscopic) in the wall of the cyst. has an elevated risk of recurrence.



Malignant behaviour is seen in two forms :

  1. ameloblastic carcinoma
  • frankly malignant histology
  1. malignant ameloblastoma
  • metastases despite well differentiated ‘benign’ histology


Differential diagnosis

  1. dentigerous cyst: the relationship between ameloblastomas and dentigerous cysts is a controversial one, 20% of ameloblastomas thought to arise from pre-existing dentigerous cysts
  2. odontogenic keratocyst (OKC): usually unilocular with thin poorly enhancing walls
  3. odontogenic myxoma: can be almost indistiguishable
  4. aneurysmal bone cyst (ABC)
  5. fibrous dysplasia


Short Note 2003



  • Formation of a blood clot within the cavernous sinus, a cavity at the base of the brain which drains deoxygenated blood from the brain back to the heart.



Usually from a spreading infection in the nose, sinuses, ears, or teeth.

Nasal furuncle (50%), sphenoidal or ethmoidal sinuses (30%) and dental infections (10%).

Less common primary sites of infection include tonsils, soft palate, middle ear, or orbit (orbital cellulitis).

The highly anastomotic venous system of the paranasal sinuses allows retrograde spread of infection to the cavernous sinus via the superior and inferior ophthalmic veins (valveless veins).

Causative organism: Staphylococcus infectious 70% of the cases. Streptococcus is the second leading cause. Gram-negative rods and anaerobes, rarely Aspergillus fumigatus and mucormycosis.







-abrupt onset of unilateral periorbital edema, headache,

photophobia and proptosis

– Ptosis, chemosis, cranial nerve palsies (III, IV, V,VI).

Sixth nerve palsy is the most common. ( it is the content of cavernous sinus while others are located at lateral wall)

– Sensory deficits of the ophthalmic and maxillary branch of the fifth nerve are common.

– Periorbital sensory loss and impaired corneal reflex

– Papilledema, retinal hemorrhages, and decreased visual acuity and blindness may occur from venous – congestion within the retina.

– Fever, tachycardia and sepsis may be present.

– Headache with nuchal rigidity may occur.

– Pupil may be dilated and sluggishly reactive.

– Infection can spread to contralateral cavernous sinus within 24–48 hours of initial presentation.



FBC, ESR, blood cultures, and sinus cultures

Lumbar puncture TRO meningitis.

CT BRAIN/ PNS: Opacification, sclerosis, and air-fluid levels, thickening of the superior ophthalmic vein, and irregular filling defects within the cavernous sinus.

MRI,  MR venogram : more sensitive than a CT scan & imaging studies of choice. Findings may include deformity of the internal carotid artery within the cavernous sinus, and an obvious signal hyperintensity within thrombosed vascular sinuses on all pulse sequences.





  • IV Antibiotics: IV Rocephine 2g OD

+/-  IV Metronidazole 500mg TDS

  • Anticoagulation with heparin is controversial.
  • Steroid therapy is also controversial.


Surgical drainage with sphenoidotomy is indicated if the primary site of infection is thought to be the sphenoidal sinuses.


All patients with CST are usually treated with prolonged courses (3–4 weeks) of IV antibiotics. If there is evidence of complications such as intracranial suppuration, 6–8 weeks of total therapy may be warranted.





A.k.a: Malignant Otitis Externa



Rare complication of Otitis Externa

Severe infection of temporal and adjacent bone

May lead to osteomyelitis of temporal bone and skull base

Commonly caused by Pseudomonas aeruginosa

Typically seen in immunocompromised and DM patients








A-    MicroAbscess A – Age (elderly)
B-   Bone scan positive B – Bacterial culture (pseudomonas – 98%)
C-   Cruciating pain C – Cranial nerve palsy
D-   Discharge D – DM/ debilitating illness
E-   Edema E – ESR raised
G-  Granulation tissue  
F-   Failed medical therapy  




Lab: ESR, swab c&s, HPE of granulation tissue, TWC, Glucose, Creatinine level


CT scan – to exclude temporal bone SCC. Findings: soft tissue enhancement in EAC +/- abscess

Technetium 99 – for diagnosis (absorbed by osteoclast and osteoblast)

Galium 67 – for prognosis (absorbed by macrophages)



Medical – IV abx (anti-pseudomonal): Ciprofloxacin 1/12, sugar control, pain control, ear toileting

Surgical – mastoidectomy + debridement of granulation tissue

Neck mass – long case / short case


  1. Site
  2. Duration
  3. Onset
  4. Progress
  5. Pain
  6. Secondary changes – ulceration/ discharge
  7. Aggravating factor
  8. Relieving factor
  9. Assoc symtoms: Dyspnea/ Dysphagia/ Trismus / Change of voice
  10. Fever
  11. URTI hx
  12. LOA / LOW
  13. H/o Trauma
  14. Any other swelling elsewhere
  15. Similar hx in the past



  1. Number
  2. Site
  3. Size
  4. Shape
  5. Surface
  6. Edge
  7. Skin changes – colour / ulcer / punctum/ discharge/ necrotic patch
  8. Scar – transcervical / schobinger/ modified blair
  9. Trachea deviation
  10. Pulsatile
  11. Movement on deglutition
  12. Movement on protrusion of tongue


  1. Local rise of temperature
  2. Tenderness
  3. Confirm inspector findings – number / site/ size/ shape/ surface
  4. Consistency
  5. Mobility
  6. Fixity to overlying skin
  7. Pulsation – expansile/ transmitted
Special tests on swelling:
– Transillumination test
– Retrosternal extension
– Bruit: vascular
Examination of regional lymph nodes

Relative Prevalence of Neck Mass Etiologies

Type Common Uncommon Rare

Cytomegalovirus infection

Epstein-Barr virus infection

Staphylococcal or streptococcal infection


Viral upper respiratory infection

Acute sialadenitis

Arteriovenous fistula

Bartonella henselae infection


Human immunodeficiency virus infection

Mycobacterium tuberculosis infection

Parotid lymphadenopathy



Squamous cell carcinoma of the upper aerodigestive tract



Metastatic cancer

Parotid tumor


Sjögren syndrome

Castleman disease

Kikuchi disease

Kimura disease

Rosai-Dorfman disease


Thyroid pathology

Branchial cleft cyst

Carotid body tumor

Glomus jugulare tumor

Glomus vagale tumor



Thyroglossal duct cyst


Parathyroid carcinoma


1. Soo-Geun Wang. Differential Diagnosis and Treatment of Neck Masses. J Korean .Med Assoc. 2007 Jul;50(7):613-625.

Sudden Sensorineural Hearing Loss

– hearing loss more 30 db
– 3 consecutive frequencies
– within 3 days
1- Vascular : Inner ear stroke- cochlear artery branch (thrombosis) of labyrinthine artery branch of AICA)
2- Inflammation,infection :
  • labyrinthitis
  • autoimmune disease (eg: Cogan’s syndrome)
3- Neoplasia: CP angle tumour – usually progressive. sudden onset may be due to bleeding tumour).
  • Acoustic neuroma grows 1mm/year grow ,unilateral (bilateral in Type 2 Neurofibromatosis)
  • Meningioma
4- Ototoxic drug: bilateral ear affected
  • Vestibulotoxic: gentamicin(aminoglycoside), dietatic, aspirin, quinolone(antimalaria)
  • Cochleotoxic: streptomycin, kanamycin,neomycin
5- Trauma
  • FBC – anemia, polycythemia, high twc
  • ESR
  • RP
  • Fasting serum lipid
  • FBS, HbA1c
  • Autoimmune screening c3/4
  • TFT -hypothyroid
  • VDRL -syphilis
  • PTA
  • MRI- do later
Clinical presentation
Elderly f>m
99% unilateral, 1- 2% bilateral
Inpatient vs outpatient
  • DM patient – monitor sugar as steroid started, vertigo, logistic —> treat in patient
  • Others treat as outpatient
1) Start steroid-tab prednisolone( to start within 7 days of onset–>1mg/kg/day) and taper down in 2 weeks
2) LMW (heparin) dextran- reduce viscosity of blood – 2 pints a day for 3 days
3) methylcobalamine
4) acyclovir if hx suggestive of viral infection ( eg URTI)
5) carbogen ( 5% co2- vasodilator effect,95% o2) 30mins for 5days
6) hyperbaric o2 (100% o2)
SHOTGUN regime
Latest management:
Intratympanic dexamethasone
  • inject dexamethasone through TM under LA  (use EMLA) n lie down for 30 minutes- every week once for 3 weeks
  • dose: 4 mg ( 1ml) each injection
– higher succession  rate
– less systemic steroid effect
  • Age: Young <10 years old and >60 years old: bad
  • Esr > 25: bad
  • Vertigo: bad
  • Comorbid: bad
  • Severity: Severe to profound HL: bad, mild / moderate: good
  • Bilateral: bad
  • Tinnitus: good (protective)
Unilateral —> do nothing/ CROS/ BAHA/ CI
Bilateral—> HA/ CI