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The Crush Syndrome in Ophthalmology*
660
PAUL WEINSTEIN
20. Bannon, R. E., Cooley, F. H., Fisher, H. M., and Textor, R. T.: The stigmatoscopy method of determining the binocular refractive status. Am. J. Optometry, 27 :371-384 (Aug.) 1950. 21. Fincham, E. F.: The accommodation reflex and its stimulus. Brit. J. Ophth., 35 :381-393 (July) 1951. 22. Ogle, K. N., Imus, H. A., Madigan, L. F., Bannon, R. E., and Wilson, E. C.: Repeatability of ophthalmoeikonometer measurements. Arch. Ophth., 24:1179-1189 (Dec.) 1940.
THE CRUSH SYNDROME IN OPHTHALMOLOGY* PAUL WEINSTEIN,
M.D.
Budapest, Hungary
During the Second World War, British authors (Bywaters and Beall1) described a strange complication which occurred in per sons who had been covered by debris from ruined buildings during air raids and who, although at the time seemingly free from injury, had later developed renal troubles which have come to be known as the "crush" syndrome. Trueta and his co-authors2 explained the origin of this syndrome. They compressed the lateral extremities of experimental ani mals by applying elastic tourniquets and observed that, several hours after the tourni quet had been removed, the distal part of the femoral artery remained contracted, that the renal arteries were also spastically con tracted, and that the renal cortex appeared to be ischemic. Trueta described similar alterations as a sequence of toxicity from staphylococcus. They also followed irritation of the central stump of the ischiatic nerve or the distal stump of the splanchnic nerve, after irrita tion of the renal hilus and following injection of adrenalin and pituitrin. Farkas 3 reports similar effects following the use of histamine. Alterations of the retina may also be found as a belated sequela of injury. Trau matic edema of the retina and traumatic angiopathy of the retina are examples. Trau matic edema may follow contusions of the globe and is associated with a distinct, al though transitory, opacity of the retina. * From the Department of Ophthalmology of the Jewish Hospital.
Traumatic retinal angiopathy usually follows injury of the skull and chest. Cases of retinitis stellata occurring in the same eye after lesions of the cornea should also be included in this group. The origin of these eyeground alterations is rather obscure. However, considering the findings of Trueta, 2 and his explanation that crushing injuries may be followed by distant neurovascular effects, the etiology of the fundus changes becomes more apparent. The subjects of my study were persons with apoplexy who showed hemorrhages of the eyegrounds. Within 24 hours after death, autopsies were performed. I regard the cerebral hemorrhages as resulting from a crushing injury to the brain and the retinal hemorrhages as the distant neurovascular effect. CASE REPORTS
In all, 12 cases were studied, four in detail with Trueta's theory in mind. Reports of these four cases follow: CASE 1
A man, aged 60 years, had blood pressure of 120/75 mm. Hg. He showed retinal edema and retinal hemorrhage in both eyes. Autopsy findings. Ischemic dura. Coagulated blood covered large parts of the left hemisphere and laterally at the occipital area, partly extending toward the base. The circle of Willis and extensive areas in the occipital and temporal lobes showed an emolliated and brittle substance. The intact parts of the brain were extremely ischemic CASE 2
A woman, aged 58 years, had blood pressure of 180/100 mm. Hg. Examination of the eyegrounds showed retinal edema and hemorrhages.
CRUSH SYNDROME IN OPHTHALMOLOGY Autopsy findings. The dura and substance of the brain were ischemic. At the base, around the chiasm, there was a small quantity of coagulated blood. The vessels at the base were rigid and wide open, with numerous yellow plaques. The floor of the third chamber was distended and liquefied. The distended fourth cerebral chamber contained a clot of blood the size of a walnut which pressed the cerebral hemispheres aside. CASE 3
A man, aged 50 years, had blood pressure of 290/120 mm. Hg. Eyeground examination revealed a hypertonic fundus and retinal hemorrhages. Autopsy findings. The dura was ischemic. The vessels of the outer layer of the soft brain were hyperemic. The right hemisphere was swollen, soft, and decidedly larger than the left. Coagulated blood, which filled the chamber of the right hemi sphere, had entirely destroyed and emolliated the substance of the brain. The chambers were filled with bloody liquid, and there was a plastic coagu late in the fourth chamber. CASE 4
A woman, aged 60 years, had blood pressure of 140/85 mm. Hg. Fundus examination showed wide, meandering veins and numerous hemorrhages. Autopsy findings. The pia was extraordinarily hyperemic. The substance of the brain was also hyperemic with pointlike, open vessels at the cut surface. Histologically, the brain substance ap peared to be distended with edema. There were small thrombotic vessels and small amounts of extravasated blood. COMMENT
The findings in these four cases would seem to show that anemic cerebral mem branes follow cerebral hemorrhage. Various areas of the brain are also anemic, with ex tensive hemorrhages in the depth of the brain. The cerebral membranes may be ex tremely hyperemic and the substance of the brain may be swollen with edema even though the hemorrhages are microscopic in size. It would seem that, as a sequela of the tissue shock, angiospasm develops within the precapillaris of the brain, the membranes, and the retina. If this angiospasm persists for a considerable time, it causes dilatation within the capillaries and veins, followed by local edema. This, by the way, is generally known (Elwyn 4 ). Trueta describes a case of ischemia of the renal cortex in which the blood of the
661
arterial lobes was directed into the so-called vasa recta spuria through the juxtamedullary glomeruli. This juxtaconduction brings to mind the arteriovenous anastomoses of Clara and Spanners. The anatomy of the retinal circulation has been considerably advanced by Michaelson and Campbell,5 Ballantyne and Loewenstein,8 Evans, 7 and Friedenwald.8 The essential re sult of these investigations is that two capil lary networks surround the papilla; the one at the level of the fibrils of the optic nerve shows a more or less rectangular pattern, with the long axis parallel to the fiber bundles of the nerve. A deeper, more irregular net work mainly appears at the level of the inner nuclear layer (Friedenwald). Usually retinal hemorrhages and retinal edema originate within the superficial capil lary network because the superficial plexus is "higher up" in the vascular circuit and is more continuous with the arterial capil laries than is the deep plexus. Vessels carrying the blood from the super ficial to the deep plexus are of definite length and, in many places, pass nearly vertically through the inner molecular layers. The consequence of these anatomic relationships is that the impact of an increased pressure within the arterial system is felt more quickly and more strongly in the superficial plexus than in the deep one (Michaelson and Camp bell). Evans noted, in retina and choroid, a pe culiar narrowing of certain capillaries where they joined the next larger vessel. If such capillary sphincters really exist, their con traction would conspicuously influence circu lation in the capillary plexus. When a capil lary sphincter that was connected to the arterioles contracted, it should reduce the flow of blood in the capillary network; con traction of a capillary sphincter connected to the venuoles should cause stasis and distention of the plexus. The same line of reasoning would lead one to assume that, in cases of injury, the neurovascular reflex mechanism affected by
662
PAUL WEINSTEIN
trauma in a distant part of the body might produce arterial spasm in certain layers of the retina, followed by dilatation, hemor rhage, and edema in other layers. (Feigenbaum.) The development of a one-sided retinitis stellata following localized ischemia might be explained as the result of the corneal in jury producing a neurovascular reflex which increased the retinal arterial pressure. Tran sient amblyopias which sometimes follow local use of novocaine-adrenalin in the ton sils or nasal septum could have a similar explanation.
should be regarded as the result of vascular spasm and subsequent retinal edema (Vanysek,9 Magitot,10 Samoiloff11). If recognized early, this progressive loss of vision may be reversed; later, it is irreversible. Sudden increase in ocular tension is a shock to the retinal vessels and it is within reason to assume that the changes credited to the crush syndrome take place within them. This deduction is especially reasonable in the light of Evans's finding that, because the sphincter of the retinal capillaries in glaucomatous eyes is constricted, a marked stasis is visible within the capillaries.
GLAUCOMA AND THE CRUSH SYNDROME
SUMMARY
It is known that a late complication of general injury is the development of trau matic glaucoma, always congestive in type, which is characterized by an increased intra ocular pressure and vascular alterations in the optic nerve and retina. A relationship between the crush syn drome and the development of traumatic glaucoma may be postulated when one con siders the following facts: the intraocular volume of blood is regulated by the blood supply of the choroid; the circulation of the optic nerve depends on the central retinal artery. It is conceivable that, following injury in another part of the body and at a later time, the sudden overfilling of the choroidal vessels might precipitate an acute glaucomatous at tack. A progressive decrease of vision in a glaucomatous eye (sometimes occurring in the presence of normal ocular tension)
A new explanation for spastic atonic alterations in ocular circulation is offered. An attempt has been made to explain such angiospastic-atonic conditions as Berlin's retinal edema, Purtscher's retinal lesions, traumatic glaucoma, and so forth, by apply ing to the ocular lesions the deductions made by Trueta in his report of the crush syn drome. He described renal cortical ischemia as a distant effect of trauma. The analogy between Trueta's renal and my ocular findings was verified by autopsy study of cerebral areas in four cases of apo plexy and by correlation of the postmortem findings with eyeground findings before death. Anatomic studies of the retinal circulation lend weight to the point-of-view herein re ported. V., Szemelynok-u.
9-ll.%-3.
REFERENCES
1. Bywaters, E. G., and Beall, D.: Brit. M. J., 2 ATI, 1941. 2. Trueta, J., Barclay, A. E., Daniel, K. J., Franklin, M. S., and Pritchard, T.: Studies of Renal Circulation. London, Oxford, 1947. 3. Farkas, K , and Szasz, G.: Orv. Het., 1948, p. 1501. 4. Elwyn, H.: Diseases of the Retina. Philadelphia, Blakiston, 1946, p. 128. 5. Michaelson, I. C, and Campbell, C. P.: Tr. Ophth. Soc. U. Kingdom, 60:71, 1940. 6. Ballantyne, A. J., and Loewenstein, A: Tr. Ophth. Soc. U. Kingdom, 63 :9S, 1944. 7. Evans, J. N.: Arch. Ophth., 37 :182, 1947. 8. Friedenwald, J. S.: Tr. Am. Acad. Ophth., 1948, p. 73. 9. Vanysek, J.: Brit. J. Ophth., 30:742,1946. 10. Magitot, A.: Ann. d'ocul., 180:321,1947. 11. Samoiloff, A. J. S.: In: Modern Trends in Ophthalmology. London, Hoeber, 1948, p. 331.
PAUL WEINSTEIN
20. Bannon, R. E., Cooley, F. H., Fisher, H. M., and Textor, R. T.: The stigmatoscopy method of determining the binocular refractive status. Am. J. Optometry, 27 :371-384 (Aug.) 1950. 21. Fincham, E. F.: The accommodation reflex and its stimulus. Brit. J. Ophth., 35 :381-393 (July) 1951. 22. Ogle, K. N., Imus, H. A., Madigan, L. F., Bannon, R. E., and Wilson, E. C.: Repeatability of ophthalmoeikonometer measurements. Arch. Ophth., 24:1179-1189 (Dec.) 1940.
THE CRUSH SYNDROME IN OPHTHALMOLOGY* PAUL WEINSTEIN,
M.D.
Budapest, Hungary
During the Second World War, British authors (Bywaters and Beall1) described a strange complication which occurred in per sons who had been covered by debris from ruined buildings during air raids and who, although at the time seemingly free from injury, had later developed renal troubles which have come to be known as the "crush" syndrome. Trueta and his co-authors2 explained the origin of this syndrome. They compressed the lateral extremities of experimental ani mals by applying elastic tourniquets and observed that, several hours after the tourni quet had been removed, the distal part of the femoral artery remained contracted, that the renal arteries were also spastically con tracted, and that the renal cortex appeared to be ischemic. Trueta described similar alterations as a sequence of toxicity from staphylococcus. They also followed irritation of the central stump of the ischiatic nerve or the distal stump of the splanchnic nerve, after irrita tion of the renal hilus and following injection of adrenalin and pituitrin. Farkas 3 reports similar effects following the use of histamine. Alterations of the retina may also be found as a belated sequela of injury. Trau matic edema of the retina and traumatic angiopathy of the retina are examples. Trau matic edema may follow contusions of the globe and is associated with a distinct, al though transitory, opacity of the retina. * From the Department of Ophthalmology of the Jewish Hospital.
Traumatic retinal angiopathy usually follows injury of the skull and chest. Cases of retinitis stellata occurring in the same eye after lesions of the cornea should also be included in this group. The origin of these eyeground alterations is rather obscure. However, considering the findings of Trueta, 2 and his explanation that crushing injuries may be followed by distant neurovascular effects, the etiology of the fundus changes becomes more apparent. The subjects of my study were persons with apoplexy who showed hemorrhages of the eyegrounds. Within 24 hours after death, autopsies were performed. I regard the cerebral hemorrhages as resulting from a crushing injury to the brain and the retinal hemorrhages as the distant neurovascular effect. CASE REPORTS
In all, 12 cases were studied, four in detail with Trueta's theory in mind. Reports of these four cases follow: CASE 1
A man, aged 60 years, had blood pressure of 120/75 mm. Hg. He showed retinal edema and retinal hemorrhage in both eyes. Autopsy findings. Ischemic dura. Coagulated blood covered large parts of the left hemisphere and laterally at the occipital area, partly extending toward the base. The circle of Willis and extensive areas in the occipital and temporal lobes showed an emolliated and brittle substance. The intact parts of the brain were extremely ischemic CASE 2
A woman, aged 58 years, had blood pressure of 180/100 mm. Hg. Examination of the eyegrounds showed retinal edema and hemorrhages.
CRUSH SYNDROME IN OPHTHALMOLOGY Autopsy findings. The dura and substance of the brain were ischemic. At the base, around the chiasm, there was a small quantity of coagulated blood. The vessels at the base were rigid and wide open, with numerous yellow plaques. The floor of the third chamber was distended and liquefied. The distended fourth cerebral chamber contained a clot of blood the size of a walnut which pressed the cerebral hemispheres aside. CASE 3
A man, aged 50 years, had blood pressure of 290/120 mm. Hg. Eyeground examination revealed a hypertonic fundus and retinal hemorrhages. Autopsy findings. The dura was ischemic. The vessels of the outer layer of the soft brain were hyperemic. The right hemisphere was swollen, soft, and decidedly larger than the left. Coagulated blood, which filled the chamber of the right hemi sphere, had entirely destroyed and emolliated the substance of the brain. The chambers were filled with bloody liquid, and there was a plastic coagu late in the fourth chamber. CASE 4
A woman, aged 60 years, had blood pressure of 140/85 mm. Hg. Fundus examination showed wide, meandering veins and numerous hemorrhages. Autopsy findings. The pia was extraordinarily hyperemic. The substance of the brain was also hyperemic with pointlike, open vessels at the cut surface. Histologically, the brain substance ap peared to be distended with edema. There were small thrombotic vessels and small amounts of extravasated blood. COMMENT
The findings in these four cases would seem to show that anemic cerebral mem branes follow cerebral hemorrhage. Various areas of the brain are also anemic, with ex tensive hemorrhages in the depth of the brain. The cerebral membranes may be ex tremely hyperemic and the substance of the brain may be swollen with edema even though the hemorrhages are microscopic in size. It would seem that, as a sequela of the tissue shock, angiospasm develops within the precapillaris of the brain, the membranes, and the retina. If this angiospasm persists for a considerable time, it causes dilatation within the capillaries and veins, followed by local edema. This, by the way, is generally known (Elwyn 4 ). Trueta describes a case of ischemia of the renal cortex in which the blood of the
661
arterial lobes was directed into the so-called vasa recta spuria through the juxtamedullary glomeruli. This juxtaconduction brings to mind the arteriovenous anastomoses of Clara and Spanners. The anatomy of the retinal circulation has been considerably advanced by Michaelson and Campbell,5 Ballantyne and Loewenstein,8 Evans, 7 and Friedenwald.8 The essential re sult of these investigations is that two capil lary networks surround the papilla; the one at the level of the fibrils of the optic nerve shows a more or less rectangular pattern, with the long axis parallel to the fiber bundles of the nerve. A deeper, more irregular net work mainly appears at the level of the inner nuclear layer (Friedenwald). Usually retinal hemorrhages and retinal edema originate within the superficial capil lary network because the superficial plexus is "higher up" in the vascular circuit and is more continuous with the arterial capil laries than is the deep plexus. Vessels carrying the blood from the super ficial to the deep plexus are of definite length and, in many places, pass nearly vertically through the inner molecular layers. The consequence of these anatomic relationships is that the impact of an increased pressure within the arterial system is felt more quickly and more strongly in the superficial plexus than in the deep one (Michaelson and Camp bell). Evans noted, in retina and choroid, a pe culiar narrowing of certain capillaries where they joined the next larger vessel. If such capillary sphincters really exist, their con traction would conspicuously influence circu lation in the capillary plexus. When a capil lary sphincter that was connected to the arterioles contracted, it should reduce the flow of blood in the capillary network; con traction of a capillary sphincter connected to the venuoles should cause stasis and distention of the plexus. The same line of reasoning would lead one to assume that, in cases of injury, the neurovascular reflex mechanism affected by
662
PAUL WEINSTEIN
trauma in a distant part of the body might produce arterial spasm in certain layers of the retina, followed by dilatation, hemor rhage, and edema in other layers. (Feigenbaum.) The development of a one-sided retinitis stellata following localized ischemia might be explained as the result of the corneal in jury producing a neurovascular reflex which increased the retinal arterial pressure. Tran sient amblyopias which sometimes follow local use of novocaine-adrenalin in the ton sils or nasal septum could have a similar explanation.
should be regarded as the result of vascular spasm and subsequent retinal edema (Vanysek,9 Magitot,10 Samoiloff11). If recognized early, this progressive loss of vision may be reversed; later, it is irreversible. Sudden increase in ocular tension is a shock to the retinal vessels and it is within reason to assume that the changes credited to the crush syndrome take place within them. This deduction is especially reasonable in the light of Evans's finding that, because the sphincter of the retinal capillaries in glaucomatous eyes is constricted, a marked stasis is visible within the capillaries.
GLAUCOMA AND THE CRUSH SYNDROME
SUMMARY
It is known that a late complication of general injury is the development of trau matic glaucoma, always congestive in type, which is characterized by an increased intra ocular pressure and vascular alterations in the optic nerve and retina. A relationship between the crush syn drome and the development of traumatic glaucoma may be postulated when one con siders the following facts: the intraocular volume of blood is regulated by the blood supply of the choroid; the circulation of the optic nerve depends on the central retinal artery. It is conceivable that, following injury in another part of the body and at a later time, the sudden overfilling of the choroidal vessels might precipitate an acute glaucomatous at tack. A progressive decrease of vision in a glaucomatous eye (sometimes occurring in the presence of normal ocular tension)
A new explanation for spastic atonic alterations in ocular circulation is offered. An attempt has been made to explain such angiospastic-atonic conditions as Berlin's retinal edema, Purtscher's retinal lesions, traumatic glaucoma, and so forth, by apply ing to the ocular lesions the deductions made by Trueta in his report of the crush syn drome. He described renal cortical ischemia as a distant effect of trauma. The analogy between Trueta's renal and my ocular findings was verified by autopsy study of cerebral areas in four cases of apo plexy and by correlation of the postmortem findings with eyeground findings before death. Anatomic studies of the retinal circulation lend weight to the point-of-view herein re ported. V., Szemelynok-u.
9-ll.%-3.
REFERENCES
1. Bywaters, E. G., and Beall, D.: Brit. M. J., 2 ATI, 1941. 2. Trueta, J., Barclay, A. E., Daniel, K. J., Franklin, M. S., and Pritchard, T.: Studies of Renal Circulation. London, Oxford, 1947. 3. Farkas, K , and Szasz, G.: Orv. Het., 1948, p. 1501. 4. Elwyn, H.: Diseases of the Retina. Philadelphia, Blakiston, 1946, p. 128. 5. Michaelson, I. C, and Campbell, C. P.: Tr. Ophth. Soc. U. Kingdom, 60:71, 1940. 6. Ballantyne, A. J., and Loewenstein, A: Tr. Ophth. Soc. U. Kingdom, 63 :9S, 1944. 7. Evans, J. N.: Arch. Ophth., 37 :182, 1947. 8. Friedenwald, J. S.: Tr. Am. Acad. Ophth., 1948, p. 73. 9. Vanysek, J.: Brit. J. Ophth., 30:742,1946. 10. Magitot, A.: Ann. d'ocul., 180:321,1947. 11. Samoiloff, A. J. S.: In: Modern Trends in Ophthalmology. London, Hoeber, 1948, p. 331.