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ARTICLE
Year : 1960  |  Volume : 8  |  Issue : 1  |  Page : 25-27

Idiopathic recurrent thrombophlebitis with bilateral macular haemorrhage


Department of Ophthalmology, Goculdas Tejpal Hospital, Bombay, India

Date of Web Publication6-May-2008

Correspondence Address:
Y.K.C Pandit
Department of Ophthalmology, Goculdas Tejpal Hospital, Bombay
India
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Source of Support: None, Conflict of Interest: None


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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 May 30];8:25-7. Available from: http://www.ijo.in/text.asp?1960/8/1/25/40692

Table 1

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Table 1

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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 Top


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.

Investigations

Urine; normal.

Blood. Total R.B.C.: 4.5 million;

Hb.: 82%;

Color Index : o.96.

W.B.C.: 6,800;

Neutrophils 70%.

Eos.: 5%;

Lympho.: 23%;

Mono.: 2%;

E.S.R.: 12 mm. at the end of one hour.

Bleeding time : 4 min. 30 sees.

Clotting time : 9 min.

Platelets 240,000.

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.[18]


  Summary Top


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 Top

1.
Briggs J. B. (1905) Bull. John Hop kins Hosp. - 16, 228-233.  Back to cited text no. 1
    
2.
Campbell and Morgan (1930) Guy's. Hosp. Records, quoted by Walker. Lancet Lxxx : 3 . 1.  Back to cited text no. 2
    
3.
Daguillon. Quoted by Briggs in 1.  Back to cited text no. 3
    
4.
Fremy (1861) Quoted by Briggs in I.  Back to cited text no. 4
    
5.
Hartfall S. J., Armitage G., (1932),. Guys Hosp. Rep 82, 42.1-36  Back to cited text no. 5
    
6.
Harkavy J. (1921) bred. J. and Rec. 120, 64-68.  Back to cited text no. 6
    
7.
Herrick W. W. (1911) Amer. J. of fired. Sc. 142, 874-878.  Back to cited text no. 7
    
8.
Jadioux : (1845) Quoted by Briggs. J. B. in 1.  Back to cited text no. 8
    
9.
Kletz Norman (1932). Lancet. 2, 938-939.  Back to cited text no. 9
    
10.
Leriche Rene (1916) Quoted by Allen Barker Hines Peripheral Vascular Disease­- Saunders and Co.  Back to cited text no. 10
    
11.
Low G. C. and Cook A.B, (1931). Lancet. 1, 584.  Back to cited text no. 11
    
12.
Mc. Donnagh J. E. R.; (1927) Lancet.. 1, 8:15  Back to cited text no. 12
    
13.
Owen A. W. (1928) B.M.J.1,690-91.  Back to cited text no. 13
    
14.
Oschner., Alton et el (1940) Arch. of Surgery. 40 208-231.  Back to cited text no. 14
    
15.
Paget J. (1866) St Barts, Hosp. Rpts. 218 2-92.  Back to cited text no. 15
    
16.
Role J. A. (1930). Lancet. 2, 731-33.  Back to cited text no. 16
    
17.
Vaquez and Laconte : (1921). Press. Med. 28, 273.  Back to cited text no. 17
    
18.
Walker A, B., (1932) Lancet. 2, 938.  Back to cited text no. 18
    


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