|Year : 1960 | Volume
| Issue : 1 | Page : 25-27
Idiopathic recurrent thrombophlebitis with bilateral macular haemorrhage
Y.K.C Pandit, BN Jhaveri
Department of Ophthalmology, Goculdas Tejpal Hospital, Bombay, India
|Date of Web Publication||6-May-2008|
Department of Ophthalmology, Goculdas Tejpal Hospital, Bombay
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Pandit Y, Jhaveri B N. Idiopathic recurrent thrombophlebitis with bilateral macular haemorrhage. Indian J Ophthalmol 1960;8:25-7
|How to cite this URL:|
Pandit Y, Jhaveri B N. Idiopathic recurrent thrombophlebitis with bilateral macular haemorrhage. Indian J Ophthalmol [serial online] 1960 [cited 2020 Aug 15];8:25-7. Available from: http://www.ijo.in/text.asp?1960/8/1/25/40692
The term `Idiopathic Recurrent Thrombophlebitis' was first given by Briggs (1905) to the condition, which from the painful nature of the affliction was commonly called 'Thrombophlebitis Migrans'.. A review of literature shows that jadioux (1845) and Fremy (1864) were the first to report some cases of thrombophiebitis migrans. Paget (1866) described the condition in some detail. Briggs felt that idiopathic recurrent thrombophlebitis was a better term than thrombophlebitis migrans, as it covers phlebitis of tubercular origin as well as phlebitis occurring in thromboangeitis obliternas; whilst migrans is generally associated with syphilis.
Etiology : From the various theories that have been advanced on etiology, it can be seen that it is most obscure. Paget (1866) considered it as a manifestation of gout; Daguillon quoted by Briggs (1905) as a part of arthritic but non-gouty constitution; Briggs (1905) as phlebosclerosis; Herrick (1911) as caused by unknown toxin; Owen (1928) felt it is caused by influenza virus; Ryle (1930) considered it as a bacteracmia; Kletz, Hartfall and Armitage (1932) described mesenteric and pulmonary infarcts with venous lesions of lower extremities; Harkavy (1924) said that there was an allergy of skin to extracts of tobacco; Mc Donnagh (1927) feels it is the 'soil'; the disease depending on obscure alteration in chemico-physiological components of the venous blood.
Age and Sex : 8o per cent of the cases are below the age of 5o and the rest over 5o years. Records of 20 cases collected from the old literature at our disposal suggest the following sex distribution.
The superficial veins of the upper and lower extremity are more commonly affected. In some cases the cerebral vessels are also involved. Barber's case suggested cerebral venous thrombosis as the first sign. Campbell and Morgan (1930) record a case where the first evidence was the thrombosis of the posterior cerebral arteries; Kletz (1932) feels it an uncommon affection with migratory tendency and repeated clottings. No record of ocular complications has been found in the literature at our disposal. Ryle (1930) mentions Campbell and Morgan's case with tubular vision due to complications of the posterior cerebral arteries.
Harkavy (1924) sums up the clinical features as follows :-(a) There is a tendency to involve superficial veins of the upper and lower extremities; (b) there is decidedly a segmental distribution with healthy veins intervening; (c) a progressive spread accompanied by fever and (d) a lesion which gives appearance of a fusiform mass, sensitive to touch, but oedema may or may not occur.
Pathology : Has been studied by necropsy, biopsy, venography, and experimental studies in animals. There is thrombosis and inflammation of all coats of the venous wall. There is a variation in the character of the thrombus. The degree and extent of phlebitis also vary. One of the three types of thrombus may be seen : (i) a red or coagulation thrombus; (ii) a white or agglutination thrombus; and (iii) a mixed thrombus. The red thrombus is homogeneous and resembles a post mortem clot. The thrombocytes and leucocytes are spread in mass of erythrocytes and fibrin. The white thrombus comprises of fibrin and layers of platelets and leucocytes with a few Erythrocytes. We usually come across a mixed thrombus. This develops as follows. There is slowing of blood stream with formation of eddy currents and is accompanied by a change in the plasma platelet stability. The platelets move to the periphery of the blood stream adhere to the endothelium of the blood vessel and disintegrate. Their place is taken by the leucocytes attracted to the place and fibrin precipitates. More fibrin, platelets and leucocytes are deposited. The clot has a red tail towards the heart and a white head distally. The tail may detach and form an embolus. The restoration of the lumen is achieved during involution by partial liquifaction and partial fibrosis. The venous valves are crippled or destroyed. There is destruction of the venous wall but the degree of damage depends upon the cause.
In suppurative thrombophlebitis the bacteria predominate and the leucoytes dominate leading to abscess formation; whilst in spontaneous phlebitis a slow involution occurs. If blood dyscrasia is present there is little reaction in the venous wall. In recurrent idiopathetic thrombophlebitis the lesion involves small and medium sized veins and is segmental. 'I here is a marked periphlebitis and an extensive inflammatory reaction. The lumen of the vessel is completely blocked and healing is slow. The end result is seen as a fibrinous venous cord.
Leriche, Oschner and De Bakey (1946) considered the vasoconstrictor and sympathetic factors in a^dema of periphlebitis and emphasised that a vasoconstrictor impulse is originated by the thrombo;sed segment of the limb which leads to a spasm of both arterioles and venules in the distal part of the limb. Such spasm is observed clinically in a few cases only. There is no doubt a slowing of the venous blood flow and a greater circulation in the collateral but the pressure hardly varies. Vaquez and Laconte (1921) suggest a bacterial cause, blood borne from same cryptic focus. The blood culture in a low grade bacteraemia unless oaken at the onset and from the site of the phlebitis is purely speculative. The leucocyte response is poor.
| Case Record|| |
Hip, a male aged 20, working as an apprentice in industrial trade was admitted to hospital on 5-7-54 with a history of loss of sight and inability to read for the past ii days. He bad a temperature without rigor and felt the loss of vision soon after.
Previous History : There were attacks of pain and swelling in the left thigh with bouts of low ever off and on for the past five years. There was no history of any infectious disease, joint pains, malaria or typhoid. Family history was of no importance to the case.
On examination, the skin along the saphenous vein on the left thigh was pigmented and there was inguinal adenitis. The superficial vein of the left arm was also felt as a cord. Vision in each eye was 6/36. The fundi showed circumscribed haemorrhages at both the macula. The left retina shows some infective haemorrhages with exudates at the periphery probably of infective origin. The right retina showed no peripheral haemorrhages or exudates.
Blood. Total R.B.C.: 4.5 million;
Color Index : o.96.
E.S.R.: 12 mm. at the end of one hour.
Bleeding time : 4 min. 30 sees.
Clotting time : 9 min.
Kahn Test and Menickes Test : Negative.
X-Ray Chest : No active lesion.
E.C.G. No organic lesion-Marked rotation of the heart.
Blood culture - Staphylococcus aureus grown.
Treated with rest and broad spectrum antibiotics the temperature settled down in the course of one week and macular haemorrhages cleared after three weeks. The vision was restored to 6/9 each eye and the patient could read Ji.
A retinal drawing of the left eye is shown in the active stage. The picture of the right eye is after it had cleared.
| Summary|| |
A case of Idiopathic Recurrent Thrombophlebitis with ocular complications is presented. The ocular complications are not found in the records that are available to us. The patient has been observed over a period of 5 years and had some more attacks but no further ocular complications have been observed.
| References|| |
Briggs J. B. (1905) Bull. John Hop kins Hosp. - 16, 228-233.
Campbell and Morgan (1930) Guy's. Hosp. Records, quoted by
Walker. Lancet Lxxx : 3 .
Daguillon. Quoted by Briggs in 1.
Fremy (1861) Quoted by Briggs in I.
Hartfall S. J., Armitage G., (1932),. Guys Hosp. Rep 82, 42.1-36
Harkavy J. (1921) bred. J. and Rec. 120, 64-68.
Herrick W. W. (1911) Amer. J. of fired. Sc. 142, 874-878.
Jadioux : (1845) Quoted by
Briggs. J. B. in 1.
Kletz Norman (1932). Lancet. 2, 938-939.
Leriche Rene (1916) Quoted by Allen Barker Hines Peripheral Vascular Disease- Saunders and Co.
Low G. C. and Cook A.B, (1931). Lancet. 1, 584.
Mc. Donnagh J. E. R.; (1927) Lancet.. 1, 8:15
Owen A. W. (1928) B.M.J.1,690-91.
Oschner., Alton et el (1940) Arch. of Surgery. 40 208-231.
Paget J. (1866) St Barts, Hosp. Rpts. 218 2-92.
Role J. A. (1930). Lancet. 2, 731-33.
Vaquez and Laconte : (1921). Press. Med. 28, 273.
Walker A, B., (1932) Lancet. 2, 938.
[Figure - 1], [Figure - 2]
[Table - 1]