f Post graduate mcqs and discussion

Saturday, March 24

Lateral sinus thrombophlebitis

It is an inflammation of inner wall of lateral venous sinus with formation of an intrasinus thrombus.

Fig: lateral sinus thrombophlebitis 

Aetiology :

It occurs as a complication of acute coalescent mastoiditis , masked mastoiditis or chronic suppuration of middle ear and cholesteatoma .


The pathological process can be divided into the following stages :

A. Formation of perisinus abscess :  abscess form in relation to outer dural wall of sinus . It has been destoryed by coalescent bone erosion or cholesteatoma .

B. Endophlebitis and mural thrombosis formation : inflammation spread to inner wall of the venous sinus with deposition of fibrin , platelets and blood cells leading to thrombus formation with in the lumen of sinus. 

C. Obliteration of sinus lumen and intrasinus abscess : mural thrombus enlarges to occlude the sinus lumen completely. Organisms may invade the  thrombus causing intrasinus abscess which may release infected emboli into the blood stream causing septicaemia.

D. Extension of thrombus : though central part of thrombus breaks down due to intrasinus abscess,  thrombotic process continues both proximally and distally . Proximally it may spread to confluence of sinuses and to superior saggital sinus  or cavernous sinus , and distally into mastoid emissary vein , to jugular bulb or jugular vein .

Clinical features :

Hectic picket fence type of fever with rigor : due to septicaemia,  often coinciding with release of septic emboli into blood stream . Usually accompanied by chills and rigor . Clinical pictures resembles malaria but lack of regularity.


Progressive anaemia and emaciation.

Griesingeri' s sign: due to thrombosis of mastoid emissary vein . Oedema appers over the posterior part of mastoid. 

Papilloedema : it's presence depends on the obstructions  of venous return.  It is often seen when right sinus is thrombosed or when clot extend to superior saggital sinus. Fundus may shows blurring of disc margin , retinal haemorrhage or dilated veins .

Tobey - Ayer test:  this is to records CSF pressure by manometer and to see the effect of manual compression of one or both jugular veins .

Compression of veins on the thrombosed side produces no effect while compression of vein on healthy side produces rapid rise in csf pressure which will be equal to bilateral compression of jugular vein.

Crowe-Beck test : pressure on jugular veins on healthy side produces engorgement of retinal vein and supraorbital veins .

Tenderness along the jugular veins : this is seen when thrombophlebitis extends along the jugular veins . There may be associated enlargement and inflammation of jugular chain of lymph nodes and torticollis. 

Investigation :

Blood smear is done to rule out malaria

Blood culture is done to find the causative organisms. Culture should be done at the time of chill when the organism enter into blood circulation.

CSF examination -CSF is normal except for rise in pressure.  It also helps to exclude meningitis. 

X-rays mastoid: May shows clouding of air cells (acute mastoiditis) or destruction of bone ( cholesteatoma)

Imaging studies : shows sinus thrombosis by typical delta sign. It is triangular area with rim enhancement and central low density area is Seen in posterior cranial fossa on axial cuts . MR venography is useful to assess progression or resolution of thrombosis. 

Culture and sensitivity of ear swab.

Complications :

Meningitis and subdural abscess
Cerebellar abscess
Cavernous sinus thrombosis
Ottic hydrocephalus when thrombus extends to saggital sinus via confluens of sinuses.
Septicaemia and pyaemic abscess in the lungs , bone , joints or subcutaneous tissue. 

Treatment :

A. Intravenous antibacterial therapy :

B . Mastoidectomy and exposure of sinus :  A complete cortical or modified radical mastoidectomy is performed,  depending on whether  sinus thrombosis has complicated acute or chronic middle ear disease.  Sinus bony plate is removed to expose the dura and drain the perisinus abscess. 

C. Ligation of internal jugular vein: It is indicated when antibiotics and surgical treatment have failed to control emboli phenomenon and rigors,  or tenderness and swelling along jugular vein is spreading. 

D. Anticoagulant therapy : it is rarely required and used when thrombosis is extending to cavernous sinus .

E. Supportive treatment : repeated blood transfusions may be required to combat anaemia and improve patients resistance.

Friday, March 23

Fat embolism

Most serious complications,  the essential features being occlusion of small vessels by fat globules.

Causes : fat globules may originate from bone marrow or adipose tissue.  Fat embolism is more common following severe injuries with multiple fractures and fracture of major bones . The pathogenesis of the syndrome is not clear but seems likely that two events occur :

(1 ) release of free fatty acids  ( by action of lipases on the neutral fat) , which induces a toxic vasculitis,  followed by platelets -fibrin thrombosis.

(2) actual obstruction of small pulmonary vessels by fat globules.

Consequences : symptoms are evident a day or so after the injury.  Presenting features are in the form of  two or more or less distinct type :

A. Cerebral type : the patients become drowsy,  restless,  and disoriented and gradually goes into state of coma.

B. Pulmonary type: tachypnoea and tachycardia are the most prominent features.

The other common features of fat embolism are petechial rashes, usually on the front of neck , anterior axillary folds , chest and conjuctiva . If untreated and sometimes despite treatment,  the patient develops respiratory failure and dies .

Diagnosis : in a case with multiple fractures,  early diagnosis may be possible by strong suspicion.  In addition to the classic clinical features,  signs of retinal artery emboli ( straited haemorrhages  and exudate ) may be present.  Sputum and urine may reveal the presence of fat globules.  X-rays of chest may show a  patchy pulmonary infiltration
( snow storm appearance ) . Blood po2 of less than 50 mm Hg may indicate impending respiratory failure.

Treatment : this consists of respiratory support,  heparinisation , intravenous low molecular Wight dextran and corticosteroids.  An intravenous 5 percent dextrose solutions with 5 percent alcohol helps in emulsification of fat globules. 

Thursday, March 22

Compartment syndrome

The contain muscles in compartments enclosed by bones , fascia and interosseous membrane. Arise in pressure with in these compartments due to any reason may jeopardize the blood supply to muscles and nerves within the compartment,  resulting in what is known as " the compartment syndrome " .

Fig: osseo-facial compartments 

Causes : the rise in compartment pressure can be due to any of the following reasons :

# any injuries leading to oedema of the muscles
# fracture haematoma within the compartment.
# ischemia to compartment,  leading to muscle oedema.

Consequences : the increased pressure with in the compartment compromises the circulation leading to further muscles ischemia . A viscous cycle is thus initiated and continues until the total vascularity of the muscles and nerves within the compartment is jeopardized.  Results in ischemic muscles necrosis and nerves damage.  The necrotic muscles undergoes healings with fibrosis,  leading to contractures . Nerve damage may result in motor and sensory loss.

In extreme case, gangrene may occur. 

Diagnosis : compartment syndrome can be diagnosed early by high index of suspicion.  Excessive pain not relieve by usual dose of analgesic,  in a patient's with an injury known to cause compartment syndrome must raise an alarm in the mind of treating doctors.  Injuries with high risk of developing compartment syndrome are as follows :

Supracondylar fracture of the humerus
Forearm bone fractures
Closed tibial fracture
Crush injuries to leg and forearms.

Stretch test : this is the earliest sign of impending compartment syndrome.  The ischemic muscles,  when stretched,  give rise to pain . It is possible to stretch the affected muscles by passively moving the joints in a direction opposite to that of the damaged muscles action ( passive extension of fingers produce pain in flexor compartment of forearm. )

Other signs include a tense compartment , hypoanesthesia in the distribution of involved nerves , muscles weakness and etc. It can be conformed by measuring compartments pressure.  A pressure higher than 40 mm of water is indicative of compartment syndrome.  Pulse may remain  palpable till very late in impending compartment syndrome,  and should not provide a false sense of security that all is well.

Treatment : A close watch for an impending compartment syndrome and effective early preventive measures like limb elevation,  active finger movements and etc can prevent this serious complications.  Early surgical decompression is necessary in established cases . This can be performed by the following methods :

Fasciotomy : the deep fascia of compartment is slit longitudinally ( e.g. : forearms )

Fibulectomy : the middle 3rd of fibula is excised in order to decompress all compartment of the legs .
Q. Which of the following does not belongs to axial corneal degeneration.

A. Fatty degeneration
B. Hyaline degeneration
C. Amyloidosis
D. Arcus senilis

Ans : Arcus senilis

List of the axial corneal degeneration are :

 Fatty degeneration
 Hyaline degeneration
 Calcific degeneration ( band keratopathy)
Salzmann's nodular degeneration. 

Tuesday, March 20

Q. Calcific degenerative  ( band shape keratopathy ) changes associated with deposition of calcium salts in which layer of cornea. 

A. Bowmann' s membrane
B. Descemet's membrane
C. Endothelium
D. Stroma

Ans : Bowmann' s membrane


Occular disease complicated by band shape keratopathy includes chronic uveitis in adult,  children with stills disease,  phthisis bulbi, chronic glaucoma,  chronic keratitis and ocular trauma.

Age related band shape keratopathy is common and affects otherwise healthy cornea.

Primary band shape keratopathy is familial.

Metabolic conditions rarely associated with band shaped keratopathy includes hypercalemia, hyperphosphatemia, hyperuricemia, and chronic renal failure .

Clinical features :

It typically presents as band shaped opacity in the interpalpebral zone with a clear interval between the ends of the band and the limbus . The conditions begin at the periphery and gradually progresses towards centre.  The opacity is beneath the epithelium which usually remains intact.  Surface of this opaque band is stippled due to holes in the calcium plaques in the area of nerve canals of Bowmanns membrane.