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Swine flu


Swine influenza, also called pig influenza, swine flu, hog flu and pig flu, is an infection caused by any one of several types of swine influenza viruses.


Virus- Cause- Influenza A known as H1N1, H1N2, H2N1, H3N1, H3N2, and H2N3.

Mode of Infection

Entry-Enters through mouth or nose
Spread- Through coughing or sneezing
Transmission- Through humans,Pigs(swine) or Birds (Avians).


Most people have production of antibodies, while some may develop zoonotic infection.

The symptoms are similar to Influenza-like illness:

1.Nausea- Feeling of vomiting
4.Sudden fever
5.Body ache
7.Sore throat

Cause of death

Most common- Respiratory failure


  • Pneumonia(leading to sepsis)
  • High fever (leading to neurological problems)
  • Dehydration (from excessive vomiting and diarrhea)
  • Electrolyte imbalance and kidney failure


Best methods include having lots of water throughout day and avoiding contact to virus as:-

1.Avoid touching nose or mouth
2.Wash hands everytime before meal or touching nose/mouth
3.Do jal neti kriya or try cleaning your nose with salt water and cotton. This flushes out colonies of virus.
4.Try handwash instead of soap.
5.Avoid crowded areas
6.Wear masks if you are low on immunity
7.Have lots of vitamin C(Amla)


The vaccines will be available in Delhi and NCR by next month,i.e,by march.

Though injectable vaccines (Influvac, Agrippal, Vaxigrip, Vaxiflu-S and Fluarix) against swine flu are available, the Government has ruled out universal vaccination for now and has recommended that it be used only for people who are actively treating the swine flu patients (doctors and other medical practitioners).


If you have sudden fever for more than two days and breathlessness,contact your doctor.

Swine flu can only be diagnosed for sure in labs. It is diagnosed by identifying the particular antigens associated with the virus type. In general, this test is done in a specialized laboratory and is not done by many doctors’ offices or hospital laboratories. However, doctors’ offices are able to send specimens to specialized laboratories if necessary.


  • Drink alot of water(prevent dehydration) and stay warm(prevent chills) since this is one of the best options.
  • Paracetamol for fever and ibuprofen for pain(Combiflam for both) and other symptomatic treatment can be done.
  • There are certain antiviral drugs which help treat swine flu – Zanamivir (Relenza) and Oseltamivir (Tamiflu).One should take these only with a doctor’s prescription since indiscriminate use could lead to resistance to the virus.
  • The patient will need to be hospitalized, isolated and put on a ventilator in severe cases.



Dengue is derived from African word “Denga” which means fever with haemorrhage. And what are those 9 things about dengue disease everyone should know?


Dengue is spread by Female mosquito AEDES AEGYPTI which sucks blood from infected body and during sucking her meal, she sucks DENGUE VIRUS. The disease is considered mostly in monsoon or rainy season when mosquito have easy supply of stagnant water to reproduce.

Mosquito- Aedes Aegypti, Virus- DENV (Dengue virus)

Aedes Egypti

Dengue virus or DENV is an RNA virus of five serotypes- DENV-1,DENV-2,DENV-3,DENV-4 and DENV-5 (DENV-5 announced in 2013).

Sign and Symptoms

Most dengue affected people are without any symptoms or mild fever. Children are most susceptible to dengue and develop life-threatening conditions. This is the most important part. The early you suspect you have dengue, better the result from treatment.

Dengue fever triad = Fever + Rash + Headache

Dengue should be immediately suspected if you have:-

Fever (40°C/104F) 

with any 2 of following:

  • Severe headache
  • Pain behind eyes
  • Muscle and joint pain
  • Vomiting
  • Tiredness
  • Black stool
  • Nose or gum bleeding 

These symptoms will start within few hours of mosquito bite and last for upto 14 days.

What not to do?

Dengue reduces your platelet count and causes dehydration. Following things should be AVOIDED in all cases:-

  • Taking Aspirin or Disprin
  • Taking any antibiotic
  • Taking any NSAID for pain and fever

(These are contraindicated as these cause further platelet damage and worsen dengue.)

  • Getting dehydrated- As dengue fever warms up body and causes blood loss from body, there are chances of several dehydration. One should always try to keep him hydrated with drinks.
  • Ignoring symptoms and avoiding visit to physician- The earlier you know,the better you survive.

Clinical diagnosis

Once you reach the physician, he will immediately order the following tests:-

  • Complete blood test (CBC)
  • X-ray Chest (CXR)
  • Plasma thromboplastin time and prothrombin time

Why all these test? These tests reveal following to physician:-

>Complete blood test- Reveal marked reduction in platelet count (<100,00/cubic mm) called Thrombocytopenia. Also reveal Haemoconcentration.

>X-ray chest- This reveals pleural effusion in lung,mostly on right side. Bilateral (both sided) pleural effusion occurs in very severe cases of Dengue Shock Syndrome.

>Plasma thromboplastin time and prothrombin time- These are prolonged and thus mean prolonged bleeding time.

The lab diagnosis of dengue,though, differs from the clinical diagnosis.The approach is highly specific.

Lab diagnosis

The most specific tests for Dengue fever include:-

  • ELISA- MAC-ELISA is done
  • IgM/IgG ratio- It is increased
  • Haemagglutination inhibition test- it reveals 4 fold rise in antibody response
  • Other tests- Include Neutralization tests like serum dilution,virus constant,plaque-reduction test, Dot-blot immunoassay and Complement fixation test (CFT).


Dengue is caused by a virus, hence, no specific management of dengue is available till now (not even anti-viral drugs). However, only symptomatic treatment is done.

The symptomatic treatment of dengue involves:-

Management of pain and fever

Paracetamol is the only drug of choice in dengue. However, doses guidelines as per WHO are as follows:-

1 year 60 mg/dose
1–3 years 60–120 mg/dose
3–6 years 120 mg/dose
6–12 years 240 mg/dose

A dose should be administered when body temperature is greater than 39°C, but no more than 6 doses should be administered in a 24-hour period.

Maintaining Fluid levels

This is done by I.V fluids to prevent patient from going into shock stage.

A dose should be administered when body temperature is greater than 39°C, but no more than 6 doses should be administered in a 24-hour period.

Administration of I.V (intravenous fluid) is necessary as the patient has a >20% increase in haematocrit and early signs of circulatory disturbance (i.e. rapid pulse and worsening condition).


It becomes only solution when-

  • Cool, mottled or pale skin
  • Reduced peripheral pulses
  • Changes in mental status
  • Increased heart beat (Tachycardia)
  • Increased capillary refill time (.2s)
  • Oliguria
  • Sudden rise in haematocrit or continuously elevated haematocrit despite administration of fluids
  • Narrowing of pulse pressure (<20 mmHg (2.7 kPa) )
  • Hypotension (a late finding representing uncorrected shock)


Dengue presents in three stages from the time of biting by mosquito,.i.e., entry of dengue virus into human body. These stages are:-

Symptomatic stage (Febrile stage)

This is where the fever and other symptoms start. It peaks and remains for 2-7 days.

Dengue hemorrhagic fever (Critical stage)

Fever comes down to normal body temperature. The plasma from blood capillaries starts leaking. This results in fluid accumulation in chest (pleural effusion) and abdominal cavity (ascites) while decreased blood supply to vitals. Cutaneous and intestinal hemorrhages are features of DHF.

Dengue shock syndrome (DSS)

This is the most serious manifestation of dengue and results in untreated patients or vulnerable children. This is the cause of death.

Noting point is, in most people,dengue is less serious as :-

  • Stage A can occur without symptoms (asymptomatic).
  • Stage B can occur as Dengue Fever (DF) Syndrome which is self-limiting febrile illness affecting muscles and joints with severe back pain due to myalgia (and hence the name ‘break-bone’ fever).


The cause of death is the end stage, Dengue Shock Syndrome (DSS) which is characterised by:

  • Bluish coloration of skin
  • Cold, clammy skin and restlessness
  • Rapid and weak pulse
  • Narrow pulse pressure
  • Hypotension

The patient starts feeling lethargy, which follows by shock and coma and finally, death in untreated patients.


The last and tricky question that comes is- CAN I HAVE DENGUE AGAIN?

The answer to question is YES. Since Dengue has 5 seroptypes, any other can affect you even if you have been affected. Moreover, the condition is more serious if this happens. This is called Secondary infection.

Dengue is always a hot topic during monsoon season, and you don’t want to miss out such an important endemic around you.  Hope we helped you. Feel free to share the page. Any doubts or suggestions or feedback is always welcome.




In this blog thread, we will be discussing first about normal physiology and anatomy of eye to make understanding clear as quick as we can, which includes anterior chamber angles and trabecular meshwork, normal aqueous humour flow, and flow of aqueous humour by schlemn’s canal. Later, we will discuss deeply about the GLAUCOMA, which includes Congenital Glaucoma, Primary Glaucoma and Secondary Glaucoma. Surgeries will be discussed as closing ceremony of this blog.


Glaucoma is a group of disorders characterized by optic neuropathy associated with visual field defects and elevated intraocular pressure.

So, here is the look of what we should know about Glaucoma:-

In this article, we will be establishing a base before we proceed to Glaucoma and its types. This will just take few minutes to understand the concept.

Anatomy of eye

The most significant structure of eye when dealing with glaucoma is the Anterior chamber angle followed by trabecular meshwork.

Angle of anterior chamber

The mechanism of various types of glaucoma including open angle and angle closure glaucoma depends on width of this angle.

Trabecular meshwork (Trabeculum)

It is sieve like structure through which aqueous humour passes into schlemn’s canal.

These can be well-observed in the following images :-

anterior chamber angles
Note Anterior chamber angle and Trabeculum
Note Anterior chamber angle and Trabeculum
The Shaffer’s system grades the angle width for glaucoma as follows:-
SL, Schwalbe’s line; TM, trabecular meshwork; SS, scleral spur; CBB, ciliary body band; ROI, root of iris
Some of the configurations can be noted in eye as:-
Very narrow-angle of the anterior chambern (Grade I)
Open-angle of the anterior chamber (Grade III)
Wide open angle of the anterior chamber  (Grade IV) a- Iris root, b- Ciliary body, c- Scleral spur, d- Trabecular meshwork

Aqueous Humour Flow

Intraocular pressure(IOP) is determined by three factors:
1. The rate of aqueous humor production
2. Resistance to aqueous outflow across the trabeculum, especially in the juxtacanalicular meshwork, and
3. The level of episcleral venous pressure.
The Aqueous humour outflow before glaucoma is easy to understand:-
Aqueous humour, derived from plasma, is produced from ciliary process. From there, it passes to posterior chamber and then around iris to anterior chamber. From here (anterior chamber), it either drains into schlemn’s canal via trabecular meshwork [Trabecular outflow] or goes back into ciliary process towards venous circulation [Uveoscleral outflow]. Trabecular outflow is conventional outflow (90%).
uveoscleral outflow aqueous humor pathway
The initial steps are always the flow of aqueous humour from ciliary process to anterior chamber as:-

Aqueous humour in Schlemn’s canal

It is a part of trabecular outflow and is best explained by vacuolation theory. The below diagram will quickly explain the steps of vacuolation theory in schlemn’s canal:-
1. Non-vacuolated stage; 2. Stage of early infolding of basal surface of the endothelial cell; 3. Stage of macrovacuolar structure formation; 4. Stage of vacuolar transcellular channel formation;5.Stage of occlusion of the basal infolding
This was all about understanding the anatomy and physiology of eye. We have indeed used more images than text, to establish a strong base before we proceed to the original topic, Glaucoma.

Otosclerosis: Causes, Types, Pathology, Symptoms, Diagnosis, Treatment


Otosclerosis or Otospongiosis is primary disease of bony labyrinth or the inner ear. The irregularly laid spongy bone replace the normal enchondral layer of bony otic capsule. Otosclerosis can cause Conductive deafness mostly, or sensorineural deafness or none depending on the region of disease.

  • Oto – Ear
  • Sclerosis- Hardening of tissue

Therefore, literally meaning hardening of ear tissue.


Otosclerosis can be attributed to various facts:

  1. Anatomical basis- Bony labyrinth is indeed hard, made of enchondral bone, which changes rarely. But sometimes, some cartilaginous areas in this bony labyrinth can form new spongy bone, hence hardening the normal structural composition of inner ear.
  2. Hereditary- Otosclerosis has autosomal dominant trait and 50% cases have positive family history.
  3. Race- White races are more prone to otosclerosis and it is common in india but rarely found in chinese and japanese.
  4. Sex- Female:Male is 2:1 but reverse in india.
  5. Age of onset- As disease progresses, hearing loss generally occurs at 2nd-3rd decade of life.
  6. Viral infection- Presence of otosclerotic foci has relation with measles virus just like Paget’s disease.


Otosclerosis can be classically categorised into 3 types as follows:

1. Stapedial Otosclerosis

Hardening at stapes causes stapedial otosclerosis. Fixation of stapes result in Conductive deafness. The hardening occurs most commonly at “Fistula ante fenestram” which is present just in front of oval window and can occur at other foci too. The different sites of stapedial otosclerosis can be better understood by the following image:

stapedial otosclerosis types
Types of Otosclerosis: (A) Anterior focus (B) Posterior focus (C) Circumferential (D) Biscuit type (E) Obliterative

2. Cochlear Otosclerosis

Hardening occurs around round window. Liberation of toxic materials into inner ear fluid causes Sensorineural hearing loss.

3. Histologic Otosclerosis

Asymptomatic, there is neither conductive nor sensorineural hearing loss.


Grossly- Chalky white, greyish or yellow when inactive but red (due to increased vascularity) when active.

Microscopically- In immature active lesion, there are plenty osteoblasts and osteoclasts with cement substance, while mature lesion has more layered bone and fibrilllar substance than cementum.


  1. Hearing loss- The patient presents with bilateral (both sides) conductive hearing loss without any pain.
  2. Paracusis Willsii- The patient hears better in noisy surrounding as compared to quiet surrounding. This can be attributed to hardened ear ossicles which respond well to stronger vibrations than normal optimal vibrations.
  3. Tinnitus- Ringing sound in ear appears commonly in cochlear otosclerosis active lesion.
  4. Vertigo- Uncommon though
  5. Speech- Patient has monotonous, well-modulated and soft speech.


  1. Otoscopy- Tympanic membrane is normal; Schwartze sign can be demonstrated, i.e, reddish hue on promontory through tympanic membrane.
  2. Tuning fork tests- Negative rinne test (i.e, Bone conduction > Air conduction) for 256,512 and 1026 Hz when stapes fixation is complete.
  3. Weber test- Lateralized to ear with greater conductive loss.
  4. ABC (Absolute Bone Conduction)- Normal, decreased in cochlear otosclerosis.
  5. Pure tone audiometry shows loss of air conduction for lower frequencies. Carhart’s notch appears best at 2000hz when there is highest hearing loss. Carhart’s sign disappears after stapedectomy.

    Carhart's notch
    Carhart’s notch: Notice sharp notch at 2000Hz
  6. Speech audiometry- Normal
  7. Tympanometry- In later stages, curve of ossicular stiffness is seen.

Treatment of Otosclerosis

1. Medical

There is no medical treatment that cures otosclerosis. Bisphosphonate and sodium flouride have been tried but proved ineffective.

2. Hearing aids

Less risky and efficient, BIHA (Bone Implanted Hearing Aids) are most convenient.

3. Surgical

TOR (Total Ossicular Replacement) is performed which involves removal of otosclerotic stapes called Stapedectomy (removal of stapes) /Stapedotomy creation of hole in stapes) followed by placement of a prosthesis between incus and oval window.

Total ossicular replacement
(A) Pre-stapedectomy (B) Post-stapedectomy

The Prosthesis so inserted can be either Teflon piston, Stainless steel piston, Platinum-teflon or Titanium teflon piston. The improvement is noteworthy, but may fail for reasons like erosion of incus, displacement of prosthesis or reclosure of window.

Types of prosthesis
Types of prosthesis: (A) Teflon piston (B) Platinum-teflon piston (C) Titanium-teflon piston

Selection of Patient for Stapedectomy

Conductive hearing loss should be around 25-30dB with average air-borne gap of atleast 15dB with Rinne test negative for 256 and 512Hz. The patient should be hearing better with hearing aids and speech discrimination should be more than 60% to exclude any substantial sensory component.

Contraindications of Stapedectomy

  1. Only hearing ear
  2. Associated with Menieres disease- Sensorineural hearing loss can occur
  3. Young children- Repeated eustachian tube dysfunction can displace prosthesis.
  4. Profession of athletes, frequent air travelers, divers and construction workers- Post-operative vertigo can cause hindrance in their jobs.
  5. Noisy surrounding occupation- Can cause snsorineural hearing loss due to trauma.
  6. Pregnancy
  7. Otitis externa, TM perforation and exostosis(syn. osteoma, benign overgrowth of per-existing bone)

Steps of Stapedectomy

  1. Incision- A Rosen’s incision (most common type of meatal incision for stapedectomy) is made.

    Rosen's incision
    Rosen’s incision
  2. Typmpanomeatal flap is elevated

    Tympanomeatal flap elevation
    Tympanomeatal flap elevated, notice dotted lines represent posterosuperior bony hang
  3. Removal of posterosuperior bony overhang of canal

    Overhang removal
    Removal of Posterosuperior bony overhang
  4. Removal of Superstructure of stapes

    Superstructure removal
    Removal of superstructure
  5. Stapedotomy (creation of fenestra or hole in stapes footplate) or Stapedectomy (removal of part of stapes footplate)
  6. Prosthesis placement

    Stapedotomy and prosthesis placement
    Stapedotomy/Stapedectomy with prosthesis placement
  7. Tympanomeatal flap repositioning

Complications of Stapedectomy

  1. Post-operative complications of stapedectomy are:-
  2. Tympanomeatal flap tea and TM perforation
  3. Taste disturbance due to chorda tympani injury
  4. Facial nerve injury
  5. Incus bone dislocation
  6. Vertigo
  7. Perilymph granuloma/fistula
  8. Conductive loss becauseof prosthesis damage
  9. Sensorineural hearing loss- rare
  10. Dead ear- rare

Atticoantral Chronic Suppurative Otitis Media


So far, we have discussed Chronic Suppurative Otitis Media in general and its one type- Tubotympanic CSOM. In this section, we will be dealing with its second type, i.e, Atticoantral CSOM. Atticoantral is unsafe type of CSOM with several complications. Lets head to it and explain it.


The causes of of Atticoantral CSOM are quite indifferent than Cholesteatoma which has following theories:

  • Congenital- Presence of congenital cell rests
  • Primary acquuired cholesteatoma- Invagination of tympanic membrane from attic or posterosuperior part of pars tensa in for Retraaction Pockets.
  • Theroy of Basal Cell hyperplasia
  • Epithelial invasion
  • Metaplasia of middle ear mucosa

Some points can be understood by the following images:

Congenital CSOM

Congenital csom
Congenital CSOM
Congenital CSOM
Note the white pearly mass behind intact tympanic membrane

Retraction pockets/Primary acquired

Retraction pockets in CSOM
Invagination Tympanic membrane


  • Cholesteatoma

    Cholesteatoma in Atticoantral CSOM
  • Osteitis and granulation tissue
  • Ossicular necrosis- causes conductive deafness

    Ossicular necrosis in CSOM
    Ossicular necrosis in CSOM
  • Cholesterol granuloma-It is a mass of granulation tissue with foreign body giant cells surrounding cholesterol  crystals.


Same as tubotympanic type

  1. Aerobic- Pseudomonas aeruginosa, proteus, E.coli, Staph aureus
  2. Anaerobic- Bacteriodes fragilis and anaerobic streptococci


  • Ear discharge- Scanty but always foul smelling due to bone destruction
  • Hearing loss- Ossicular destruction causes Conductive deafness,sometime sensorineural, but hearing is normal when ossicular chain is intact or when cholesteatoma bridges gap between ossicular chain.

    Bridging of gap CSOM
    Hearing loss in Atticoantral CSOM
  • Bleeding- It may occur from granulation or the polyp when cleaning ear.


  • Perforation- Either attic or Posterosuperior perforation.
    Perforation in atticoantral csom
    Perforation in Atticoantral CSOM
    Postero-superior perforation in atticoantral csom
    Postero-superior perforation in atticoantral csom

    Posterosuperior perforation in atticoantral csom 2
    Posterosuperior perforation in atticoantral csom
  • Retraction pockets- An invagination of tympanic membrane is seen in attic or posterosuperior area of pars tensa.
  • Cholesteatoma- Pearly white flakes of cholesteatoma can be sucked from retraction pockets.
    Attic perforation Cholesteatoma in CSOM
    Attic Cholesteatoma in CSOM

    Congenital CSOM
    Pearly white cholesteatoma in Atticoantral CSOM


  • Examination under microscope- may reveal cholesteatoma, evidence of bone destruction, granuloma, condition of ossicles and pockets of discharge.
  • Tuning fork tests and Audiogram- Essential for pre-operative assessment and to confirm degree and type of hearing loss.
  • X-ray mastoid or CT scan temporal bone- indicate extent of bone destruction and degree of mastoid pneumatisation.
  • Culture and sensitivity of ear discharge- for proper selection of antibiotic.

Features indicating complications

  1. Pain- Indicates extradural, perisinus or brain abscess or otitis media externa with discharging ear.
  2. Vertigo- Indicates erosion of lateral semicircular canal which may progress to labyrinthitis or meningitidis.
  3. Persistent headache- Intracranial complication
  4. Facial weakness- erosion of facial canal
  5. A listless child refusing to take feeds- extradural abscess
  6. Fever, nausea and vomitting (F+N+V)- intracranial infections
  7. Irritability and neck rigidity- Meningitidis
  8. Diplopia- Gradenigo syndrome,i.e, petrositis
  9. Ataxia- Labyrinthitis or cerebellar abscess
  10. Abscess around ear- Mastoiditis


This part is confusing to many about where and what is the exact difference between canal up and canal down procedures. We will explain that as we proceed:-


Primary aim is to remove disease and render ear safe while second aim is to preserve or reconstruct hearing but never at cost of primary aim.

There are two types of procedures which are followed in atticoantral csom surgeries:-

Canal wall down procedure

It leaves mastoid cavity open into external auditory canal so that  diseased area is fully exteriorized.

It is named as canal wall down because posterior wall of external auditory canal is  removed during the surgery. This removal of posterior wall makes ear canal and mastoid a single cavity called mastoid bowl. From this cavity, the cholesteatoma is allowed easy passage out of the ear.

Examples include Atticotomy, modified radical mastoidectomy and radical mastoidectomy.

Canal wall down procedure
Radical mastoidectomy- Note open mastoid cavity is formed

Canal wall up procedure

Posterior bony meatal wall is kept intact while disease is removed through meatus and/or mastoid, thus, an open mastoid cavity is avoided. Reconstruction of hearing is easy but risk of leaving behind some cholesteatoma is high and hence, 6 months re-exploration is necessary.

Intact canal wall mastoidectomy > Cortical mastoidectomy + Posterior tympanoplasty

Let’s explain this abit deeper. First of all, the canal wall up procedure is to done such that posterior wall is intact, hence, we approach to FACIAL RECESS for this. This can be better explained by following images and do read the captions written just below each image:

Canal wall up mastoidectomy
External ear canal reached through facial nerve and hence leaving posterior wall intact
Mastoidectomy posterior tympanotomy
Cortical mastoidectomy followed by posterior tympanotomy

Difference between canal wall up and canal wall down procedures

The simplest difference is that in canal wall down, the posterior wall is damaged and hence more invasive type whereas in canal wall up, there is minimal invasion. This, in turn, is complicated as in canal wall down, with more invasion, the cholesteatoma is generally removed to full with better prognosis whereas in canal wall up, with less invasion, the cholesteatoma can be left behind, hence a need for 6-month re-exploration is usually required to check cholesteatoma again.

Reconstructive Surgery

Myringoplasty (closure of the perforation of pars tensa of the tympanic membrane) pr tympanoplasty (myringoplasty with ossicular reconstruction) is done.

Conservative treatment

Repeated suction clearance, aural toilet and other measures for mild cholesteatoma cases or in elderly or in a patient refusing for surgery can be tried.

Tubotympanic Chronic Suppurative Otitis Media


We discussed about CSOM or Chronic Suppurative Otitis Media in general in our previous section. Let’s take a deeper look into its first type, i.e, Tubotympanic CSOM, also called safe CSOM or benign CSOM. Click to jump to Atticoantral CSOM.


The Etiology of Tubotympanic CSOM is as follows:

  1. Sequela of Acute Otits Media following exanthematous (eruptive) fever and leaving behind a large central perforation which becomes permanent and permits repeated infections from external ear.
  2. Ascending infections via Eustachian tube like from tonsils, adenoids and infected sinuses.
  3. Persistent mucoid otorrhoea is sometimes result of allergy to ingestants such as milk,eggs,fish etc.


Pathology of CSOM Chronic Suppurative Otits Media
Pathology of CSOM Chronic Suppurative Otits Media

It remains localized to mucosa and mostly to anteroinferior part of middle ear. Pathological changes seen in Tubotympanic CSOM is as follows:are:

  1. Perforation of pars tensa- Central perforation
  2. Middle ear mucosa- Normal when disease is inactive but oedematous and velvety when active
  3. Polyp- Pale
  4. Ossicular chain- usually intact and mobile but may show some degree of necrosis, especially of long process of incus.
  5. Tympanosclerosis- It is hyalinisation and subsequent calcification of subepithelial connective tissue. It is seen as white chalky deposits on promontory, ossicles, joints, tendons, oval and round windows. It interferes with mobility of these structures, hence, causing conductive deafness.
  6. Fibrosis and adhesion- They are result of healing process and may further impair mobility of ossicular chain or block eustachian tube.


The bacteriology of Tubotympanic CSOM is as follows:

  1. Aerobic
  2. Pseudomonas aeruginosa, proteus, E.coli, Staph aureus
  3. Anaerobic
  4. Bacteriodes fragilis and anaerobic streptococci

Clinical features

The Clinical Features of Tubotympanic CSOM are as follows:

  1. Ear discharge- Non-offensive, mucoid or mucopurulent, constant or intermittent. Discharge appears mostly at time of upper respiratory tract infection or accidental entry of water into ear.
  2. Hearing loss- Conductive type and rarely exceeds 50dB. Sometimes, patient reports of paradoxical effect, i.e, hears better in presence of discharge than when ear is dry. This is due to ’round window shielding effect’ produced by discharge which helps to maintain phase differential. In dry ear with perforation, sound waves strike both oval and round windows simultaneously, thus, cancelling each others effect.

    Shielding effect in CSOM Chronic Suppurative Otitis Media
    Shielding effect in CSOM Chronic Suppurative Otitis Media
  3. Perforation- Always central which is anterior,posterior or inferior to handle of malleus or subtotal/extending upto annulus.

    Perforation in Tubotympanic CSOM Chronic Suppurative Otitis Media
    Perforation in Tubotympanic CSOM Chronic Suppurative Otitis Media
  4. Middle ear mucosa- Pale pink and moist on normal but when inflamed, it looks red, oedematous and swollen and occasionally with polyps.


Investigations done in Tubotympanic CSOM are as follows:

  1. Examination under microscope- can reveal granulation, ingrowth of squamous epithelium, status of ossicular chain, tympanosclerosis and adhesion.
  2. Audiogram- Conductive deafness but sensorineural deafness element may be present.
  3. Culture and sensitivity of ear discharges- may help to select proper antibiotic ear drugs.
  4. Mastoid Xrays/CT scan temporal bone- Mastoid is usually sclerotic but may be pneumatized with clouding of air cells. There’s no evidence of bone destruction (which is a feature of atticoantral csom)


The aim of treatment is to control the infection and eliminate ear discharge and at a later stage, surgery may be done to assist hearing loss. Following are treatment regimes for Tubotympanic CSOM:

  1. Aural toilet- All discharge and debris from is ear is removed to enhance effect of topical antibiotics.
  2. Ear drops- Neomycin, Polymysin and gentamycin are used.
  3. Systemic antibiotics- Only in acute cases.
  4. Precautions- Avoiding hair washing, water in ears or blowing nose hard can be helpful.
  5. Surgical treatment- Polyps in ear or granulation is removed to facilitate ear toilet though avulsion is strictly avoided.
  6. Treatment of contributory causes- Corrects of infection of adenoids, maxillary antra and nasal allergy.
  7. Reconstructive surgery- Once ear is dry, myringoplasty with/without ossicular reconstruction and closure of perforation can stop recurrent infections.

Chronic Suppurative Otitis Media | CSOM


Chronic Suppurative Otitis Media or CSOM is a long standing infection of a part or whole of the middle ear cleft characterized by Ear discharge and a permanent Perforation. A perforation becomes permanent when it’s edges are covered by squamous epithelium and it does not heal spontaneously. A permanent perforation can be likened to an epithelium-lined fistulous track.

Word wise Meaning of CSOM:

  • Chronic- Long standing
  • Suppurative- Related with pus (containing or discharging pus)
  • Otitis- Inflammation of ear
  • Media- Middle ear

Types of CSOM

Clinically, it can be divided into two types:-


  • Also called the safe or benign type.
  • It involves anteroinferior part of middle ear cleft ,i.e, eustachian tube and mesotympanum.
  • It is associated with central perforation.
  • There is no risk of serious complication.


  • Also called unsafe or dangerous type.
  • It involves posterosuperior part of middle ear cleft, i.e, attic, antrum and mastoid.
  • It is associated with an attic or marginal perforation.
  • This disease is often associated with a bone-eroding process such as cholesteatoma, granulation or osteitis and risk of complication is very high.

Difference between Atticoantral and Tubotympanic CSOM

tubotympanic vs atticoantral csom
Difference between Tubotympanic and Atticoantral CSOM
Features Tubotympanic Atticoantral
Discharge Profuse Mucoid




Foul Smelling

Perforation Central Attic/Marginal
Granulation Uncommon Common
Polyp Pale Red and fleshy
Cholesteatoma Absent Present
Complications Rare Common
Audiogram Mild to moderate conductive deafness Conductive deafness or mixed deafness
polyp in ear canal csom
Polyp in Ear Canal in CSOM

This was general about Chronic Suppurative Otitis Media. There are its two types- Tubotympanic and Atticoantral CSOM.

Basics of Reading Chest X ray


Xray is a type of radiography and most widely used investigation. It first appears too complicated to read the chest xrays because we barely know what lies where and what to make out of it. But the basics of Chest Xray here will guide you through various aspects, including Counting ribs, PA vs AP view, Inspiratory vs Expiratory Xray, Erect vs Supine, Lucency and Opacity and some common terms like Consolidation and Pleural Effusion.

Part 1: Basics First

Best Chest Xray

PA vs AP view

AP vs PA view of Chest Xray

  • AP or Anteroposterior view- The view is from front to back.
  • PA or Posteroanterior view- The view is from back to front

Difference between PA vs AP view Chest Xray

PA vs AP view Chest Xray

Features PA view AP view
Position of clavicle Oblique Horizontal
Scapula Away from lung field Over the lung field
Spirolamina angle Inverted ‘V’ Not significant

PA is most common X-Ray done where AP is usually done when patient cannot stand and XRay machine is brought to him on bed and view taken from anterior to posterior.

The point to add is that there is apparent Cardiomegaly in AP view as compared to PA view because there is slight magnification of heart since heart is away from view capturing film.

This can be well understood by the following:-

The approach to cardiomegaly on Chest Xray is as follows:

Chest xray cardiomegaly

  • A/B x 100 = cardio ratio
  • In PA view, Cardiomegaly when ratio is more than 50%
  • In AP view, Cardiomegaly when ratio is more than 60%

Erect vs Supine position

erect vs supine cxrThere is fundal view in erect position because all the air in stomach comes in fundus when the patient is standing.

Inspiratory vs Expiratory

inspiratory vs expiratory chest xrayinspiratory vs expiratory chest xray 2If anterior end of 6th or 7th rib reaches mid-clavicular line of diaphragm, it is Inspiratory Xray.

Counting Ribs in Chest Xray

Counting ribs CXRTwo points can just help you quickly count ribs from top to bottom:

  • The front opaque appearing side of ribs is actually it’s posterior side.
  • Ribs are counted from anterior sides.

Counting ribs chest xrayBefore we proceed, let us see what structures lie in a normal Chest Xray:

Best Chest XrayThe Chest Xray is usually divided into three zones as:

Zones in Chest xray

  • Upto 2nd rib- First zone
  • 2nd to 4th rib- Second zone
  • 4th to 6th rib- Third zone

Now let’s proceed to start studying the Xray.

Lucency and Opacity in Chest Xray


Anything that appears dark or black on chest xray is said to be lucent.

  • This is because of less density.
  • Black color appears because of AIR.


Anything that appears light or white on chest xray is said to be Opaque.

  • This is because of high density.
  • White color appears because of Bones and soft tissues.

Therefore, we can conclude the following easily:-

Increase in lucency:

  • Increase in air
  • Decrease in soft tissues or absence of bone

Increase in Opacity:

  • Increase in soft tissue or abnormal bone
  • Decrease in air

The basic approach when seeing a chest xray always sequentially as:-

  1. Define whether xray is normal or abnormal
  2. If xray is abnormal, where is this abnormality
  3. Extent of abnormality
  4. What is the final diagnosis

Before we proceed to pathological approaches to Chest X-Rays, let’s see what layers the xrays hit when they enter the body. Note this strengthens further basics:-

Muscle> Ribs> Pleura> Lung

Talking about when Hyperlucency (increase in blackness) or Hyperopacity (increase in whiteness) occurs:-

Unilateral Lung Hyperopacity

Hyperopaque lung

  1. Consolidation- Replacement of air by something abnormal
  2. Atelectasis- Collapse of lung resulting in loss of air

Also seen in Plethora, i.e, increase i vascularity.

The differential diagnosis of three important causes if unilateral (one side) opaque thorax are:-

1. Atelectasis- collapse of lung

  • Displacement of interlobar fissure: because the lobes of lung collapse, the fissures in between the lobes move up or down because of hyperinflation of normal lobe against collapsed lobe. This is the most reliable direct sign of Collapse.
  • Mediastinal shift: The structures on mediastinum shift to side of collapsed lung
  • Crowding of ribs
  • Elevation of hemidiaphragm
  • Sharp defined margins of opacity

2. Consolidation- replacement of air


  • No mediastinal shift
  • Ill defined margins of opacity
  • Airbronchogram sign: visualization of air in bronchus sorrunded by alveolar opacity

Positive Airbronchogram sign is seen in:

  • All except interstitial (viral) pneumonia
  • Pulmonary oedema (water replace air)
  • ARDS (Acute respiratory distress syndrome)
  • Goodpasture syndrome (blood)
  • HMD (Hyaline membrane disease)
  • Pulmonary alveolar proteinosis (macrophages congested in alveoli making crazy paving pattern)

Airbronchogram sign is NOT seen in:

  • Lung abscess
  • All except bronchoalveolar carcinoma

3. Pleural effusion-accumulation of fluid

Normally, there is no air in pleura. But effusion in pleura can occur.

  • Mediastinal shift: which is on opposite side, i.e, structures shift to opposite side of pleural effusion.

Note: Pleural effusion and Haemothorax cannot be differentiated because soft tissue cannot be differentiated on Chest Xray.

Unilateral Lung Hyperlucency

hyperlucent lung

  • Rotation: apparent increase in air gap
  • Scoliosis
  • Masectomy
  • Poland syndrome (absent pectoralis major muscle)
  • Airway obstruction
  • Large pulmonary embolus
  • Pneumothorax

A small mnemonic to quickly grab the names:


  • P- Poland syndrome/Pneumothorax
  • O- Oligemia/Obstruction (like Pulmonary embolism)
  • E- Emphysema
  • M- Mastectomy/Mucous plug
  • S- Swyer’s james syndrome

Enjoyed reading? In our upcoming blog of Chest xray, we will be explaining Silhoutte sign (where exactly the abnormality is in the lung relating with intervening border of an organ or its part) and some pathological diseases observed on chest xrays like pulmonary embolism, left ventricular failure, bronchogenic carcinoma, bronchiectasis, and lots more. Stay tuned.

Part 2: ABCDEF Approach to Reading Chest X-Ray

Before Analyzing

Before Analyzing Chest Xray, ABCDEF approach for preliminary check can be used as:

A: AP or PA view

B: Body Position

C: Confirm Name of patient on film

D: Date of Xray

E: Exposure adequate?

F: Films for comparison

Analysis of Chest XRay

Again, an ABCDEFGHI approach can be used to recall the steps of Analysis of Chest Xray. It can be related as:

A: Airways- Initially check tracheal deviation, and then check for hilar adenopathy or enlargement

B: Bones / Breast Shadows- Check for fracture of ribs, scapula or clavicle)

C: Cardiac Silhouette- Cardiac Enlargement/ Costophrenic Angles- Check for sharp angles, if blunt could be pleural effusion

D: Diaphragm- Check for free air, could mean perforation peritonitis/ Digestive tract

E: Extra-thoracic tissues / Edges- Apices for fibrosis, pneumothorax, pleural thickening or plaques)

F: Fields- Check for alveolar filling in lung fields / Failure- Alveolar air space disease with prominent vascularity with or without pleural effusions

G: Gastric Bubble- Visible at left upper abdomen

H: Hilum- Check for lymph node enlargement

I: Insertion / Artefacts: Check for any external object appearing in xray film

Types of Headache


Headache is indeed the most common symptom everyone suffers in his day to day life. But rather than going all type approaches for headache, we will be explaining today what are the types of headaches and what possible information a medico should have about headache.

Headache is a symptom which appears as pain occurring anywhere in the region of head and neck. Cutting off the causes of headache, we will just discuss types of headaches as shall be learn by a medical officer.

Types of Headache

There are basically 5 types of headaches that we will be dealing about in this blog. These are:

  1. Migraine
  2. Tension headache
  3. Cluster headache
  4. Hypnic headache
  5. Pseudotumour cerebri

Let’s have a closer look on all the types we just pin pointed:-


Migraine is basically a female predominant type of headache. Most common age in which females face migraine has been found to be 10-25 years of age.


  1. It is commonly unilateral (meaning one sided)
  2. Throbbing pain in nature
  3. Severe in intensity
  4. Starts and peaks at 3-4 hours
  5. Associated with photophobia and phonophobia (fear of light and sound)
  6. Associated with nausea and vomiting
  7. Associated with aura

Just to explain, Aura is feeling before migraine actually starts. Visual disturbances are more common in the contralateral eye.

Migraine, again can be of two types, depending whether the aura was present or not.

  • Headache with Aura- 25% – also known as classical migraine.
  • Headache without aura- 75% – common migraine



Clinical/ diagnosis of exclusion is done to find out migraine following the symptoms. Other features of migraine include:

  • Xray PNS (paranasal sinus) – normal
  • MRI Brain – normal
  • Fundus examination – normal



Depends whether the migraine is acute migraine or chronic migraine:

1. Acute migraine

  • First drug- NSAID (Non steroidal anti inflammatory drug)
  • Best drug- sumatriptan ( sumatriptan,though, has 10-13% chances of sudden cardiac death)
  • Other drug- ergotamine

2. Chronic migraine

  • Propanolol
  • Valproate
  • Flunarizine
  • Caramazepine
  • Topirimate
  • TCA (Tricyclic antidepressants)
  • cGRP antagonist which is calcitonin related peptide, eg. OLCAGEPENT
  • PIEZOTIFEN which causes vasoconstriciton and is 5HT2 antagonist


Tension headache

There is constant gripping sensation on forehead. Moreover, there is no anxiety and stress. This headache is less severe in intensity and thus mild headache. Therefore, it usually doesn’t interfere with normal life.

The tension headache is further divided into two types as acute and chronic.

  • Acute Tension Headache- less than 15 episodes per month
  • Chronic Tesnion Headache- more than 15 episodes per month



  • Acute Tension Headache- Nsaids
  • Chronic Tesnion Headache- TCA like amitryptiline


Cluster headache

It is a male predominant type of headache and commonly occurs at age of 30-40 years.
Features of cluster headache include:

  1. Rhinnorrhoea- unilateral
  2. Lacrimation- unilateral
  3. Intake of alcohol- on/off effect which is pathognomic of cluster (patient complains of increased intensify and frequency of headache with 3 episodes per day for 1-2 months and then a gap of 1 year)
  4. Tearing type of headache which hampers normal life
  5. Unilateral type
  6. Very severe in intensity
  7. Chemosis which is unilateral
  8. Nasal congestion which is unilateral
  9. Peaks in 10-15 minutes and remains for 45-60 minutes



The diagnosis is again made on clinical basis.


1. For acute cluster headache:

  • O2 inhalation
  • Application of lignocaine to base of inferior nasal turbinate which blocks pterygopalatine ganglion

2. For chronic cluster headache:

  • DOC,namely verapamil
  • lithium
  • steroids
  • ergotamine


Hypnic headache

It is more prominent in elderly females where the mean age is 60 years. The headache occurs within 1-2 hours of sleep and remains for more than 15 minutes. Pathophysiology of  hypnic headache is yet unknown but hypertension may be related since hypothalamic nucleus may have a role.


  1. Occurs 1-2 hrs after sleep
  2. Very severe- patient awakes of headache
  3. Lasts more than or equal to 15 minutes (upto 1 hour)
  4. Frequency should be more episodes per month
  5. Associated with hypertension
  6. Associated with hypothalamic inflammation which gives circadian rhythmic type of headache
  7. MRI of brain is normal
  8. EEG explains REM sleep onset



  • For acute attacks- NSAID like indomethacin
  • For chronic attacks- Lithium is used


PseudoTumour cerebri

It is also known as benign intracranial hemorrhage. It is more predominant in females than males. Common age is 35-50 years of age. The pseudo tumour cerebri is more common in obese patients.

Risk factors of pseudotumour cerebri

  • Addison’s disease
  • Hypoparathyroidism
  • Oral contraceptive pills
  • Hypervitaminosis A



  1. Incidentally mild headache which doesn’t hamper daily activity
  2. Maybe unilateral or bilateral
  3. No focal neurological deficit (FND)
  4. Fundus- pappiloedema
  5. MRI brain is normal
  6. CSF examination reveals pressure increased and cells,protein and sugar are normal



  • For chronic pseudotumour, the approach is either medical or surgical.
  • Medically, we give acetazolamide or sterouds like prednisolone.
  • Surgically, in order to reduce CSF pressure, we perform either optic nerve fenestration or Ventriculo peritoneal shunt is performed.

So that was all about the five types of headache from the medical point of view.

Medical Trade Fair Pragati Maidan 2015


Medical Fair-India led many visitors to enjoy the exquisite opportunities of learning about the new medical technology around the globe.

Though the statement about the visits to medical fair was like:

Only for business visitors

This statement was indeed, upsetting for medical students and other aspirants who had wish to visit the medical fair without actually buying or dealing with the exhibitionist.

But later on, it was observed that the students and other visitors are allowed to visit. All that was required was an identification proof. And the entry was ABSOLUTELY FREE!

Featured Exhibitions

After visits to Hall 11,12 & 12A of pragati maidan fair, some of the wonderful and eye-catching exhibition were:



This is one technology that helps in transferring medical equipment,cash and other important things from one place to another with secured and wonderful speed. It can be used in hospitals to deliver medical equipment and others to patients and doctors.

Student-friendly Surgical models

Surgical Models

These models actually help students aspiring for surgery or orthopedics.

Wound Hub

Wound Hub
Wound Hub

This technology helps heal the wounds by spraying medic over the burns or wounds. Since you are not touching the wound, pain and chances of infection are very less.

Sliding Stair Chair

Sliding Stair Chair
Sliding Stair Chair

This can be set up at home for people who cannot walk the stairs or those are unable to walk to top floors with no access to lift or any other reason.

Wrist bands

Wrist bands

These wrist band can be used in hospitals on patients. This will easily identify the patient important details like blood group, sensitivity to penicillin, etc. without need of carrying files of individual patients.

Medical fair 2015 Pragati maidan was indeed fun, let’s see what they have planned for 2016 Mumbai!

And like the theme said:
Hope to see you soon in Medical Fair,Mumbai,2016.

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