Management of lateral sinus thrombosis
Thrombophlebitis can develop in any of the veins adjacent to the middle ear cavity. Of these the lateral sinus, which comprise of the sigmoid and transverse sinuses is the largest and most commonly affected. Initially it is usually preceded by the development of an extradural perisinus abscess. The mural thrombus partly fills the sinus. The clot progressively expands and eventually occlude the lumen.The clot may later become organised, and partly broken down and may even be softened by suppuration. During this stage there is a release of infecting organism and infected material into the circulation causing bacteremia, septicemia and septic embolisation.
Extension / propagation of the thrombus upwards may extend to the confluence of the sinuses, and beyond that to the superior sagittal sinus. Invasion of the superior and inferior petrosal sinuses may cause the infection to spread to the cavernous sinus. This spread of venous thrombophlebitis into the brain substance accounts for the very high association of this complication with brain abscess.Downward progression of thrombus into and through the internal jugular vein can reach the subclavian vein.
The harmful effects are caused by the release of infective emboli into the circulation, and also from the haemodynamic disturbances caused to venous drainage from inside the cranial cavity. The use of antibiotics have greatly reduced the incidence of lateral sinus thrombosis these days.
Formerly it was commonly associated with acute otitis media in childhood; now it is commonly seen in patients with chronic ear disease. In the preantibiotic era the commonest infecting organism was beta hemolytic streptococci. This organism was known to cause extensive destruction of red blood cells causing anaemia. Now a days the infection is by a mixed flora.
Clinical features:
These patients manifest with severe fever, wasting illness in association with middle ear infection. The fever is high and swinging in nature,when charted it gives an appearance of 'Picket fence'. It is always associated with rigors. The temperature rose rapidly from 39 - 40degree Centigrade. Headache is a common phenomenon, associated with neck pain. The patient appear emaciated and anaemic. When the clot extended down the internal jugular vein, it will be accompanied by perivenous inflammation, with tenderness along the course of the vein.This tenderness descended down the neck along with the clot, and would be accompanied by perivenous oedema or even suppuration of the jugular lymph nodes. Perivenous inflammation around jugular foramen can cause paralysis of the lower three cranial nerves. Raised intracranial pressure produce papilloedema and visual loss. Hydrocephalus could bean added complication if the larger or the only lateral sinus is occluded by the thrombus, or if the clot reaches the superior sagittal sinus. Extension to the cavernous sinus can occur via the superior petrosal sinus, and may cause chemosis and proptosis of one eye. If circular sinus is involved it could spread to the other eye. The propagation of the infected emboli may cause infiltrates in the lung fields, and may also spread to joints and other subcutaneous tissues..These distant effects usually developed very late in the disease, these could be the presenting features if the disease is insiduous in onset.Masking by antibiotics could be one of the causes. Patients always feel ill, and persisting fever is usual. The patients may have ear ache, in association with mastoid tenderness, and stiffness along the sternomastoid muscle. The presence of anaemia is rare now a days. Papilloedema is still a common finding. Other coexisting intracranial complications must be expected in more than 50 percent of patients. Extension of infected clot along the internal jugular vein is always accompanied by tenderness and oedema along the course of the vein in the neck, and localised oedema over the thrombosed internal jugular vein may still be seen. One rare finding is the presence of pitting oedema over the occipital region, well behind the mastoid process, caused by clotting within a large mastoid emissary vein, this sign is known as the Griesinger's sign. In fact there is no single pathognomonic sign for lateral sinus thrombosis and a high index of suspicion is a must in diagnosing this condition.
Investigations:
A lumbar puncture must be performed, if papilloedema does not suggest that raised intracranial pressure may precipitate coning. Examination of CSF is the most efficient way of identifying meningitis. In uncomplicated lateral sinus thrombosis the white blood count in the CSF will be low when the cause is chronic middle ear disease, and some what raised in acute otitis media. The CSF pressure is usually normal. The variations in the level of CSF proteins and sugar are not useful.
