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| ARTICLE |
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| Year : 1967 | Volume
: 15
| Issue : 5 | Page : 189-192 |
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Cavernous sinus thrombophlebitis due to a boil on ALA NASI
ML Agarwal
M.G.M. Medical College, Indore, India
| Date of Web Publication | 21-Jan-2008 |
Correspondence Address:
M L Agarwal
M.G.M. Medical College, Indore
India
 Source of Support: None, Conflict of Interest: None  | Check |
How to cite this article:
Agarwal M L. Cavernous sinus thrombophlebitis due to a boil on ALA NASI. Indian J Ophthalmol 1967;15:189-92 |
Cavernous sinus thrombophlebitis results as a complication of a prior orbital cellulitis or may be a starting point of such an infection. In either event, the inflammation originates in the neighbourhood. The known avidity for the orbit to share the troubles of the neighour is due to free venous communication, anteriorly with the facial vein through angular vein and posteriorly with the cavernous sinus through the Ophthalmic veins. Thus any suppuration in the vast area drained by these veins should be eyed suspiciously and dealt with caution, as the prognosis is mostly fatal, because of the involvement of the cavernous sinus in the absence of proper therapy. With modern chemo-therapy the cases are seen rarely and only as a result of inadequate attention and care of a seemingly harmless inflammation and or a resistant strain of organism.
The case presented below of cavernous sinus thrombosis developed from inadequate treatment of a boil on the left ala nasi. Though he recovered fully, he got the complication of blindness in one eye, a very rare complication in those cases that do recover.
| Case Report | |  |
Mr. M. Hanif, 55 yrs. had a small boil on the left ala nasi 12 to 15 days ago. It became very painful, swollen and tender in 4 days. A day or two later, he felt pain and heaviness in the left eye. In the next three days, the left eye was proptosed with marked swelling of the lids and surrounding area. A day later, he felt similar pain and heaviness in the right eye and similar swelling appeared within the next two days. He had temperature and was getting drowsy with complete loss of vision in the left eye, for which he was admitted to the hospital on 26-11-64.
Examination
The patient was well built. The face was swollen with a discharging boil on left alanasi. He was having a temperature of 102° F was drowsy but could answer questions. The skin was hot and tender.
Right Eye
The lids were swollen, with oedema on forehead and side of nose. The eye was proptosed with conjunctival chemosis and had restriction of all the ocular movements. The cornea was clear with a normal anterior chamber. The pupil reaction to direct light was brisk. The consensual light reflex was absent. Visual acuity was finger counting 15-20 feet. Fundus copy showed a hyperaemic disc with full veins.
Left Eye:-
The oedema was marked involving almost the whole of the left side of the face. The skin was hot, shiny and tender. The chemosed conjunctiva was protruding outside the lids. The eye was proptosed with complete immobility. The cornea was a little hazy. The anterior chamber was normal. The pupil was moderately dilated with no reaction to light. The consensual light reflex was present. Funduscopy showed swollen hyperaemic disc, dilated veins and arteries and retinal edema. He had lost perception of light for the last 3 days.
Investigations-
...The total R.B.C. count was 12,250 with polymorphs 78 per cent and lymphocytes 18 per cent. The urine was free of sugar and albumin. Kahn's test was negative.
Treatment-
Intravenous injections of Reverine (rolitetracyclin) was given daily for 5 days, followed by Subamycin (tetracyclin hydrochlor) capsules 250 mgm. 4 hourly for 3 days, 6 hourly for 4 days and then 8 hourly for six days.
B Vitamin Complex tablets and vitamin C 300 mgm daily, were given throughout his stay. Achromycin oil suspension was instilled in the eyes 4 hourly.
The patient's temperature and his drowsy state improved on the second day. He showed clinical improvement on the fourth day and then a gradual improvement was noticed.
14-12-1964- The right eye was perfectly normal with 6/6 vision and free ocular movements. In the left eye, there was ptosis with restriction of ocular movements, (edema was much less. Fundoscopy showed a pale-white optic disc with thin sheathed vessels.
31-12-1964-The right eye was normal. The left eye had ptosis and some restriction of ocular movement and showed a post neuritic optic atrophy on fundus examination.
He was discharged with advice to continue achromycin oil-suspension, 3 times a day, injection, B1 100 mg, B 12 , 500 mic. g once a week for 8 weeks, tablets of vitamin B Complex and vitamin C 200 mg daily and to report every week.
In another fortnight the ptosis in the left eye had disappeared and all the movements had returned.
| Discussion and Comments | | |
Infection:
The free venous communication, involving a vast drainage area, the peculiar anatomic structure of the cavernous sinus, lethargic flow of blood and an absence of valves in the veins, which allows the deflection of the blood current in the opposite direction with a change in the pressure relations (Mac NEAL et al, 1943), all contribute to spreading of a facial infection.
As a source, nasal infections top the list because of profuse and intimate venous connections between plexuses of turbinates and sinuses with the cavernous sinus. In 98 cases collected by TAYLOR (1957) 25 had furuncle of nose and 14 cases had sinusitis. DHIR AND RATHORE (1964) reported a case due to a boil on nose.
Cavernous sinus thrombophlebitis of septic origin, has been described to develop in two ways (TAYLOR 1957). (1) The thrombus is infected from the start or arises from a septic embolus or (2) The thrombus is initially free and gets secondarily infected. MAC NEAL et al say that thrombus is sometimes propagated along the lumen of a tributary, to reach the cavernous sinus by continuous extension and may be infected, or if free of infection, is liable to get infected if the patient survives long enough. A second and more malignant type of thrombosis is, a discontinuous form in which the blood carries a toxic substance which induces swelling of the endothelial lining of the tortuous venous channels and the bacteria are caught by the swollen cells, initiating a thrombus which is infected from its beginning. In such a thrombus, infection tends to spread through the walls of vessels and sets up purulent inflammation of the surrounding structures. Such cases where the thrombus is infected from the start, proved invariably fatal in pre-sulfonamide days. Even in this era of modern anti-biotics, the danger arises when there is a resistant strain of organism.
This case had a boil on the left ala nasi. It was an acute infection thus producing a generalised toxemia and bacteremia. The full clinical picture was evident 7 days after the acute stage of the boil, which suggests an extension to the sinus by local spread.
Ophthalmoplegia-
Ophthalmoplegia with proptosis and chemosis at the peak of cavernous sinus thrombophlebitis, constitute the diagnostic trio. At the subsidence of acute symptoms, ophthalmoplegia disappears but the resolution takes a few days to weeks.
The case presented showed a complete resolution in the right eye within a period of 3 weeks while the left eye took nearly 7 weeks for complete resolution. TAYLOR'S (1957) case showed ocular movements in 7 weeks, and took a further 3 months for full recovery.
SMITH (1918) considered that the cause was involvement of the nerves within the cavernous sinus. In more acute cases, the rising intra-orbital pressure might cause displacement and fixation of the globe and its muscle, before any distinct nerve palsies could be recognised.
The ophthalmoplegia which recovers fully at the subsidence of symptoms can be attributed to the reactive oedema and raised intra-orbital pressure, which on relief, leaves the eyeball free to move. An additional nerve paresis can be the cause in ophthalmoplegia with partial resolution which recovers with the passage of time.
Blindness due to optic atrophy-
WALSH (1957) states that septic thrombosis of cavernous sinus is regularly associated with papilloedema which characteristically appears late. DUKE ELDER (1952), has mentioned that some times papillcedema and visual failure are early signs and at other times the fundus remains normal. He further states that involvement of optic nerve in orbital cellulitis may be in the form of papilloedema or neuritis with rapidly progressing atrophy.
In a series of 98 cases (TAYLOR 1957), out of 60 cases which recovered, only one had blindness of both eyes and three had blindness of one eye. How is it that only few cases develop affection of the optic nerve? Cases that become blind due to affection of the optic nerve, are those where the nerve and the vision are affected early, where the infection is acute, and the thrombus is infected from the beginning.
NICHOLSON AND ANDERSON (1944), while reporting a case of blindness in cavernous sinus thrombosis described the fundus condition as one of secondary optic atrophy, with engorged veins and sheathing with narrowing of retinal arteries. They comment that the inflammatory reaction may be due to a direct extension of the inflammation along the wall of the internal carotid to that of the ophthalmic artery, since the internal carotid comes in very close contact with infection, lying within the infected cavernous sinus, or the same fundus appearance may be due to a reflex constriction in the proximal portion of the arterial tree from irritation of the sympathetic in the carotid sheath of the sinus.
TAYLOR (1957) suggested two possible causes, a toxic neuritis of the optic nerve due to adjacent purulent inflammation or an inflammatory arteritis. One of his cases showed optic atrophy on the 25th day with marked haziness of the ocular media.
Our case already had a fixed and dilated left pupil with no perception of light on the day of admission and ophthalmoscopy showed a hyperemic swollen disc with dilated veins and arteries and retinal edema. The postneuritic type of optic atrophy with thinned sheathed vessels was clearly visible a month after admission which closely resembles the case described by NICHOLSON and ANDERSON above and may be attributed to the causes suggested by them.
The history and acuteness of symptoms suggest an early involvement of the left nerve. Cases in which the thrombus is infected from the beginning tend to spread, the infection to the surrounding structures, through the walls of the vessels. A possible explanation for the toxic or inflammatory neuritis of the papilla, can be based on simultaneous occurrence of orbital cellulitis, an additional factor being the mechanical pressure due to raised intra-orbital pressure.
| Conclusion | | |
1. The generalised toxaemia and bacteraemia associated with acute infection with the peculiar anatomic structure and slow blood stream helps in establishing an infected thrombus.
2. A complete resolution of an ophthalmoplegia, occurs in cases with reactive oedema. An added nerve paresis is responsible for partial and late resolution.
3. Blindness had been attributed to the affection of optic nerve (toxic or inflammatory) at the papilla, the orbital cellulitis and increased orbital pressure being contributory factors.
4. The case reported developed the complication of blindness in one eye which is very rare in cases that recover.
| Summary | | |
A case of cavernous sinus thrombophlebitis due to boil on ala nasi has been reported. It resulted in blindness in one eye from secondary optic atrophy.
The mechanism of infection, ophthalmoplegia and blindness due to optic atrophy, has been discussed.[7]
| References | | |
| 1. | DUKE ELDER S. W. (1952) Text book of Ophthalmology-ocular adnexa Vol. V. Henry Kimpton, London, pp. 5429, 5444.  |
| 2. | DHIR, B. K. and RATHORE U. G. (1964) J. of the Indian Med. Ass. 43: 393. |
| 3. | Mac NEAL W. J., FRISBEE F. C. and BLEVINS Anne. (1943) A.M.A. Arch. of Ophthalmology (Chicago), 29, 231. |
| 4. | NICHOLSON, W. M. and ANDERSON, W. B. (1944), J. Amer. Med. Assn., 126, 12. |
| 5. | SMITH D. (1918), Arch. of Ophthal. (Chicago), 47, 482. |
| 6. | TAYLOR, P. J. (1957), Brit. J. Ophthal.. 41, 22. |
| 7. | WALSH, F. B. (1957), Clinical Neuro-Ophthalmology, II Ed. The Williams and Wilkins Co., Baltimore, p. 292. |
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