|Year : 1954 | Volume
| Issue : 1 | Page : 19-26
A case of bilateral papilloedema after fat embolism
Y.K.C Pandit1, RD Munshi2
1 Department of Ophthalmology, G.T. Hospital, Bombay, India
2 Dept of Pathology and Bacteriology, Sasson Medical College, Poona, India
Department of Ophthalmology, G.T. Hospital, Bombay
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Pandit Y, Munshi R D. A case of bilateral papilloedema after fat embolism. Indian J Ophthalmol 1954;2:19-26
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Pandit Y, Munshi R D. A case of bilateral papilloedema after fat embolism. Indian J Ophthalmol [serial online] 1954 [cited 2021 Feb 25];2:19-26. Available from: https://www.ijo.in/text.asp?1954/2/1/19/33590
We have not been able to trace any case in the literature at our disposal of papilloedema following fat embolism. In recording such a case it would not be out of place to review the literature on the subject.
The literature is found mostly in the form of case records and has been reviewed by Grosskloss (1935).
Wilson and Salisbury (1944) define fat embolism as "a state in which lobules of fat are present in circulation, of sufficient size to produce blockage of the intimate vascularities of the various organs. The local action of the fat particle on the capillary wall may be a feature of the pathology of the condition."
Most of the cases of fat embolism are due to fractures particularly of long bones, the death rate being very high when fat embolism has occurred-75% Wilson and Salisbury (1944). The death is due to pulmonary or cerebral embolism.
| Age Incidence|| |
Warren S. (1946) gives the age groups as follows :
18 - 25 ... ... 59%
26 - 35 ... ... 25%
36 and over......6%
This indicates a considerably higher frequency in lower age groups.
| Ocular Fat Embolism|| |
Cases of fat embolism have been studied and described by Meyer A. (1941), Rob Smith (1941-42), and Dorothy Russel (1941), but there is no indication that eye-grounds were observed ophthalmoscopically. Only J. Evans (1940) records ocular findings in fat embolism as consisting of a diffuse oedema of the retina more marked on the macular side by a crescentic pallor and sub-hyaloid hemorrhages along with segmentation of blood columns.
Devoe (1949) mentions that ocular fat embolism can occur in a (a) gross trauma-most frequent cause, (b) burns, (c) surgical manipulation of joints, (d) therapeutic injections of oily substances, (e) injection of paraffin in orbital operations and (f) as complication following poisoning with ammonia and alkalis. He attributes the rarity of the ocular disease in the first place, to the cerebral form of the disease in which widespread dissemination of globules is uncommon.
Secondly, generally speaking an ophthalmoscopic examination is not likely to be requested unless cerebral changes are obvious. Thirdly, it is possible to have fat in the retinal vessels without fundal changes being detectable.
| Pathogenesis|| |
Sources of Fat : According to Robb-Smith ( 1941-42) there is considerable disagreement as regards the course of the fatty material and its mode of entry through the circulation. He observes that (1) it is rare to find a rupture of a large vein with considerable amount of fat going into the circulation; (2) as most of the cases occur in patients who have sustained a fracture of bones specially the long ones it is suggested that (a) fat from the marrow is forced into the veins of the medullary cavity at the time of impact, (b) extracellular fat around the fracture seeps through the lymphatics and veins and (c) certain substances are liberated at the site of the fracture which enter circulation and cause a change in the physical state of the plasma lipids or lipoproteins.
The essentials for entry of embolic fat into circulation are: mobilised fat, a vein which is disrupted and patent and local pressure. All these three are operative in cases with bone injury. If fat is derived from the blood, no portal of entry is necessary: if from the site of injury, a local pressure drives it into the veins, capillaries or lymphatics. Some suggest that it is sucked due to negative pressure. In the opinion of Warren ( 1946 ), however, the total amount of body fat has little relation to fat embolism and blood pressure plays no role in producing fat embolism. According to Nightingale (1941) fat globules going from the lung into the heart receive a churning action.
Fat circulates in blood in the form of globules of a size sufficient to obstruct capillaries. This block leads to anoxaemia. Effects of breakdown products resulting from this and their toxic action on the tissues become evident.
According to Macfarlane, Oakley and Anderson (1941), claustridium Welchii produces a lipoproteolytic agent which splits the lipoprotein content of blood. A similar agent is released by traumatised tissue and may be responsible for fat embolism to occur. Wakeley (1941) found fat embolism in 40% of fatal burn cases.
One can thus understand that fat embolism may take place either (1) by mobilization of fat from the traumatised region or (2) by the liberation of a lipoproteolytic agent.
| Pathology|| |
Robb-Smith (1941-42) has made a careful study of pulmonary fat embolism. The right heart is dilated and contains a considerable amount of fat. The lungs are heavy and firm and have similar consistency all over. Visceral pleural surface has a marbled appearance with alternate zones of haemorrhages and emphysema. Emphysema, oedema, haemorrhage, froth and globules of fat are seen on the cut surfaces. There is no infarction.
Dorothy Russel (1941 ) describes macroscopic changes in the brain. There are diffuse pinkish areas of hyperaemia all over the cortex, the subcortical white matter and basal ganglia. The surface of the cortex is covered with petechial haemorrhages. Meyer (1941) records selective softening of the globus pallidus in the brain of a child. There is no mention of the optic nerve in the literature at our disposal. The frequency of fat embolism in the central nervous system is 31% of all the cases of fat embolism, but there is no correlation between cerebral and pulmonary embolism.
Histopathology : The precapillary arterioles are occluded with fat, the capillaries are blocked with thrombus or leucocytes and are found damaged in section. This damage may be due to the fatty acids leading to the necrosis of the tissue. A non-specific irritative reaction is set up attracting the histiocytes, monocytes, fibroblasts and epithelioid cells. Microscopically fat droplets are seen in small vessels. These fat droplets predominate in lungs and glomeruli of the kidney-Warren (1946). Fat staining should be carried out on frozen sections of fresh autopsy material. In paraffin sections we find a number of vacuoles within the tuft of capillaries or alveolar vessels. [Figure - 1].
| Clinical Picture|| |
Bdurger as quoted by Warren (1946) distinguishes three forms of fat embolism. (1) the peracute form where death occurs in a few seconds, (2) acute form in which symptoms appear immediately after the injury and death occurs in hours to days, (3) subacute form where a free period intervenes between trauma and the onset of symptoms. In the last type the lucid interval is followed by a train of symptoms-dyspnoea, pallor, sweating, cyanosis. The pulse rate, temperature and respiration rate are raised. This may be followed by cough with sputum which may be blood-stained. Cerebral symptoms may supervene with stupor and irritability, the condition may be mistaken for surgical shock or internal haemorrhage. The cerebral symptoms may be confused with or simulate contusion. Death in fat embolism may be caused by (a) general anoxaemia due to interference with respiratory function, (b) local anaemia of vital centres due to fat emboli, (c) cardiac failure from physical obstruction. Sputum and urine examination can give some valuable information but this is generally after one week. The specimen should be collected without an oily lubricant. Lipuria, however, rarely develops before the fourth day. Scriba as quoted by Warren (1946) found fat in urine in 80% of his cases, 2 to 6 days after injury to the bones.
| Experimental Work|| |
Zeker (1862) was the first to recognize the condition in man. Lower (1664) and Majendie (1821) tried to produce fat embolism experimentally. Harris, Parret and Maclachlin ( 1939) showed that the minimum lethal dose of human fat for rabbits was 0.9 c.c. per Kg. In their opinion hydrolysed human fat is more toxic. A tissue lipase splits the fatty acids and irritates the tissues. Von Czerny (1875) injected fatty material in the jugular veins of dogs and found congestion of the retinal veins and oedema of the retina the next day. Preretinal haemorrhages occurred after 1-7 days. Lehman and Moore quoted by Wilson and Salisbury (1943) expe-imented with cotton seed oil on dogs and suggest that even if the whole fat of the femur is injected it will not lead to fat embolism.
| Case Record|| |
Patient's name: Corporal W. Nationality: British. Occupation: heavy motor truck driver. Aged 22. Employed at a British Ordnance Unit in Andemishk in South Persia in the year 1944 during World War II.
Notes : Patient was involved in a motor accident and a 3-ton motor vehicle which he was driving overturned in a field and he was thrown out. He sustained a simple fracture of the left femur and was admitted to the C.G.H. at Andemishk. He showed no signs of shock or serious internal injuries except a fracture of the left femur at the middle of the shaft. He was transferred to Ahwaz for a radiological examination of his fracture. A distance of over 100 miles was covered in an ambulance.
The patient arrived in Ahwaz in an unconscious state. There was no paralysis, no fever. The fundi were examined and showed haziness of the inner margins of the discs with engorged veins, the pupils were reacting to light. Reexamination of the optic discs after 4 hours showed that the oedema of the discs had generalised, and the margins were indistinct. Surrounding retina was oedematous. The disc surface was raised by about 1.5 D. In the evening there was a joint consultation with surgeons from the American Army Hospital and papilloedema had increased to 3.0 D. It was decided to perform an exploratory craniotomy to exclude subdural or extradural haematoma. At the operation the cerebro-spinal fluid was not found under increased tension and petechial haemorrhages were found on the brain surface. The same night the patient expired.
Post mortem report : The patient was found to be a very well built young man. No external injuries of importance could be found. Post mortem examination revealed nothing of importance except the brain which showed profuse pin point haemorrhages all over the subcortical region, and the dura was intensely congested. The white matter was free from haemorrhages.
Heart showed a large antemortern clot.
Histopathological examinations of sections of the brain as well as the liver, lungs, heart and adrenals showed extensive fat embolism.
A small portion of the brain is presented herewith though with the passage of time the effects of the preservative fluid has obliterated most of the pin point haemorrhages. Unfortunately the whole brain could not be acquired as orders were received to send all the organs to the Royal College of Surgeons, England.
The optic nerve was removed for sections. As frozen sections were not possible in the field, paraffin sections were prepared. The section of the optic nerve shows[Figure - 2],[Figure - 3] that the optic nerve fibres are separated due to oedema. At a few places a few dilated spaces can be seen, some of which show partial endothelial lining. The vessel supplying the nerve show a change of mild sclerosis. There is increased round cell infiltration.
| Discussion|| |
(1) The case is of a subacute type of fat embolism with a latent period. It is likely that movement during transfer from one hospital to another might have been a contributory factor.
(2) Bilateral papilloedema is difficult to explain. It can be hypothetically considered to be clue to several factors, such as: (a) a rapidly developing increased intracranial tension due to several fat emboli in the cerebral vessels, (b) increased tension may be the result of increased production of C.S.F. caused by innumerable emboli studding the brain tissue, (c) it may be the result of concomitant injury to the brain tissue, (d) emboli may produce a partial venous blockage, impeding the return of venous blood from the eyes, leading to the development of papilloedema on both sides.
The special features we would like to emphasise in this case are: (1) the rapid development and increase of papilloedema, (2) the cerebro-spinal fluid was not found to be under tension, (3) extensive pin point haemorrhages and the intensely congested dura, (4) the optic nerve under the microscope.
Taking each probable cause of papilloedema separately, for papilloedema to occur the embolic process should be so heavy as to cause an increase in the bulk of the brain. In our case, widespread dissemination of the globules seems to have occurred and that was perhaps the reason why ocular manifestations were found in this case as remarked by Devoe. Can fat emboli, however numerous, lodging in the huge vascular cerebral bed displacing the blood within it cause an increase in cerebral bulk? It seems a little unlikely. In our case the cerebrospinal fluid was not under tension. It is already commented upon that it is possible to get fat embolism in the retinal vessels without getting ophthalmoscopic changes, and as the retinal and cerebral vessels are similar it is unlikely that the embolic process itself will cause an increase in the size of the brain, though it can cause death. If ophthalmoscopic findings should be in proportion to the cerebral changes seen at post mortem, then papilloedema should be a more frequent ophthalmoscopic finding, since the post-mortem findings were extremely typical of cerebral fat embolism, but as can be ascertained from the literature, papilloedema is an unrecorded finding. It appears possible that ophthalmoscopic examination may not have been called for and the ocular condition may have remained unrecorded. Looking to all the facts it seems unlikely that the cause of papilloedema was due to increase in brain-bulk from the intrusion of fat emboli.
Increased production of the cerebro-spinal fluid by the choroid plexus again appears a remote possibility, since the cerebro-spinal fluid was not found under increased pressure both at operation and at post-mortem.
The probability of a concomitant cerebral injury also appears to be ruled out from the post-mortem findings which do not show an\ primary cerebral damage.
The possibility of a venous blockage especially in the presence of numerous petechial haemorrhages and a congested dura has to be specially considered and seems to be the most likely cause especially because the onset and progress of papilloedema seemed rather rapid.
There is yet one more probability and that is the cerebral hemorrhages and papilloedema-like condition may be due to the toxic effect of secondary changes resulting from the setting up of a lipoproteolytic process discussed in the paper. One would expect some fever in such a condition. but it was not present in our case.
Speculating on the cause of death would be even more difficult since the patient was subjected to a major cerebral operation and surgical shock was added to whatever lethal process may be working. It seems however that the mere embolism of fat particles themselves cannot cause death unless it occurs in one of the vital centres of the brain or a vital organ. The comatose condition of the patient on reaching Ahwaz suggests a toxic condition resulting from lysis of lipoproteins as mentioned under papilloedema.
| Summary|| |
A rare case of bilateral papilloedema in fat embolism following a fracture of a long bone is presented.
Literature on fat embolism as at our disposal is briefly reviewed.
The possible causes of papilloedema and death are commented upon.
| References|| |
von Czernv: Berl Klin Wchnscher (1875 ) 12:
593-605 as quoted by Devoe in 2.
Devoe A. G.: ( 1949) Trans. of Am. Ophth. Soc. ( 1949) 254-262.
Evans J. J.: ( 1940) Brit. Jour. of Ophth. 24:
Grosskloss H. H.: (1935) Jour. of Biol. Med. Yale 59: 175-197.
Harris R. I.. Perret T. S., and Maclachlin A.: ( 1939) Annals of Surg. 110:
Lehman and Moore: as quoted in 19 below.
Lower R. R.: ( 1664) Tractus de Corde Amsterdam as quoted by Robb-Smith in 12.
Magendie F.: (1821) Jour, of Exp. Physiol. 1 : 37 as quoted by Robb-Smith in 11,
Macfarlane, Oakley and Anderson: (1941) as quoted by Robb-Smith in 12.
Meye A.: (1941) Proceedings of the Royal Society of Medicine 34: 639-656.
Robb-Smith A. H. J., Hunt A. H.. Russel D., and Grenfield G. J., ( 1941 ). Proceedings of the Roy. Soc. Med. 34:
Robb-Smith A. H. J.: ( 1941) Lancet 1 : 135-141.
Russel D.: ( 1941) Proc. Roy. Soc. Med. Sect. of Neur. 34: 639-656.
Scriba J.: as quoted by Warren S. in 17.
Vance B. M.: (1931) Arch. of Surg. 23: 426-465.
Meyer A.: (1941) Proceedings of the Royal Society of Medicine 34:
Warren S.: ( 1946) Am. Jour. of Path. 22: 69-87.
Wilson J. V., and Salisbury C. V.: ( 1943) Br. Jour. Surg. 31:
Zeker F. A.: as quoted by Robb-Smith in 12.
[Figure - 1], [Figure - 2], [Figure - 3]