Editor:I read with interest the Editorial by Forbes1discussing the article by Sturm,2 which states that the optical coherence tomography (OCT) findings in cases of presumed Shaken Baby syndrome (SBS) “provide further support for the substantial role that shearing forces at the vitreoretinal interface play in the generation of the retinal hemorrhages seen in SBS.” However, as Sturm and associates correctly pointed out, “Preretinal blood applies pressure on the vitreous body leading to an indentation and localized vitreous detachment with consecutive vitreoretinal traction in the surrounding area.” Thus, it is the hemorrhage, not vitreous traction, that creates the schisis cavity and retinal folds seen on OCT. These schisis cavities are clearly shown by OCT to be bubbles. Traction does not produce bubbles. Traction at a point produces a tent; traction along a line, a ridge (as seen at the edge of these cavities). For vitreous traction to cause the smooth, dome-shaped elevation of the internal limiting membrane (ILM) seen on OCT, the vitreous would need to contract maximally at the apex of the dome and then gradually less so as the edge was approached. This is unlikely if not impossible. Even Forbes, in a previous article,3 noted the folds to be the edge of a schisis cavity. The retinoschisis cavities seen in presumed SBS are similar to premacular hemorrhages seen in adults in conditions such as valsalva retinopathy and Terson syndrome, conditions with altered intravascular pressure. A brief literature search revealed no premacular hemorrhages attributed to acceleration-deceleration forces. Indeed, vitreous traction for the production of retinal hemorrhage seems unlikely since the vitreous can only act on and through the ILM. The ultimate in ILM traction, the surgical peeling of the ILM, causes little to no hemorrhage. Numerous retinal hemorrhages are usually seen with changes in intravascular pressure such as retinal vein occlusions and Terson syndrome.Noting “it is the shaking itself, with resultant repetitive acceleration and deceleration that induces shearing forces at the vitreoretinal interface, that is the primary factor in the generation of retinal hemorrhages seen in SBS,” Forbes incorrectly states, “Such schisis lesions are not observed in single-impact accidental trauma,” ignoring the cases of Lantz and associates,45 and Watts and Obi,6 where such lesions were noted with single or no impact. In the Lantz and Watts cases, gravitational acceleration of the child’s head, perhaps augmented by the TV set in Lantz’s case and the mother’s body in the Watts case, gives a single acceleration. When the head collided with the floor, a much more sudden deceleration occurred. In either case, there was no repetitive acceleration/deceleration. In the Lueder case, the child was already on the floor and this appears to be almost all head crush with little or no acceleration/deceleration of the head. Thus, “repetitive” vitreoretinal traction forces do not resuscitate the shaking theory. Lueder and associates,
Optical coherence tomography has not brought us closer to determining the cause of the vascular disruption in these cases.References1. 1Forbes BJ. Clues as to the pathophysiology of retinal hemorrhages in Shaken Baby syndrome determined with optical coherence tomography. Am J Ophthalmol. 2008;146:344–345. Full Text Full-Text PDF (48 KB) | CrossRef |2. 2Sturm V, Landau K, Menke MN. Optical coherence tomography findings in Shaken Baby syndrome. Am J Ophthalmol. 2008;146:363–368. Abstract | Full Text | Full-Text PDF (2229 KB) CrossRef |3. 3Forbes BJ, Christian CW, Judkins AR, Kryston K. Inflicted childhood neurotrauma (Shaken Baby syndrome): ophthalmic findings. J Pediatr Ophthalmol Strabismus. 2004;41:80–88. MEDLINE4. 4Lantz PE, Sinal SH, Stanton CA, Weaver RG. Evidence-based case report (Perimacular retinal folds from childhood head trauma). BMJ. 2004;328:754–756.5. 5Lueder GT, Turner JW, Paschall R. Perimacular retinal folds simulating nonaccidental injury in a infant. Arch Ophthalmol. 2006;124:1782–1783. MEDLINE | CrossRef6. 6Watts P, Obi E. Retinal folds and retinoschisis in accidental and non-accidental head injury. Eye. 2008;22:1514–1516. CrossRefSource:
American Journal Of Ophthalmology
Further response by Dr. Horace B Gardner
I read with interest the article by Sturm and associates,1 which notes one “theory of vitreoretinal traction from repeated acceleration-deceleration postulates a direct mechanical effect of the shaking or impact itself” and indicates the optical coherence tomography (OCT) findings in cases of presumed Shaken Baby syndrome (SBS) lend support for this. However, as they correctly pointed out, “Preretinal blood applies pressure on the vitreous body leading to an indentation and localized vitreous detachment with consecutive vitreoretinal traction in the surrounding area.” Thus, it is the hemorrhage, not the proposed vitreous traction caused by shaking, that causes the configuration of the schisis cavity and retinal folds seen on OCT. This was assumed by Madarov and associates2 and again postulated by Emerson and associates.3 These OCT findings have been previously published in adults with premacular hemorrhages.4, 5 These hemorrhages can occur either between the vitreous and the internal limiting membrane (ILM) (true “preretinal” or subhyaloid hemorrhages) or between the ILM and the nerve fiber layer (NFL) (sub-ILM) or both.6 If the blood is between the vitreous and the ILM, the vitreous elevates the ILM. If the blood is between the ILM and the NFL, the ILM elevates the NFL. The blood obscures the visible retinal vessels, proving it is superficial to the NFL, but clinically it is difficult, if not impossible, to tell which layer it is in. Emerson and associates3 noted all their cases to be sub-ILM. Sturm’s cases appear to also be sub-ILM, the structure identified as epiretinal membrane (ERM) most likely being the ILM. (ERMs are indeed “epi,” ie, on top of, the retina and take some time to form.)
Just as flame-shaped hemorrhages only tell us the location (in the NFL) of the blood, not the mechanism causing the vascular disruption leading to the hemorrhage, these schisis cavities and their associated elevated edges (folds) only tell us where the hemorrhage lies (either just in front of or just under the ILM), not what caused the hemorrhage. The premacular hemorrhages cited above were from Valsalva retinopathy and Terson cases, supporting the retinal venous pressure theory mentioned by Sturm.
Sturm’s labeling of the small retinal hemorrhages seen on OCT as “schises” is apt to lead to confusion. Madjarov and associates2 used 2.0 mm as the lower end of size for a schisis cavity and Yanoff (Yanoff M, Fine BS. Ocular Pathology. Hagerstown: Harper and Row, 1975:416) used 1.5 mm (a common number in ophthalmology, since it is one disc diameter). Even a single red blood cell outside a blood vessel must interpose itself between existing structures, thus separating, splitting, or “schising” them. These are perhaps better labeled as dot and blot hemorrhages and are indeed beautifully depicted by OCT.
Optical coherence tomography appears to offer much in the clinical diagnosis of eye conditions. Unfortunately, it doesn’t tell us the cause of retinal hemorrhages, only their location and configuration.
References1. 1Sturm V, Landau K, Menke MN. Optical coherence tomography findings in Shaken Baby syndrome. Am J Ophthalmol. 2008;146:363–368. Abstract | Full Text | Full-Text PDF (2229 KB) |CrossRef
2. 2Madjarov B, Hilton GF, Brinton DA, Lee SS. A new classification of the retinoschises. Retina. 1995;15:282–285. CrossRef
3. 3Emerson MV, Jakobs E, Green WR. Ocular autopsy and histopathologic features of child abuse. Ophthalmology. 2007;114:1384–1394. Abstract | Full Text | Full-Text PDF (3010 KB) | CrossRef
4. 4Shukla D, Naresh KB, Kim R. Optical coherence tomography in Valsalva retinopathy. Am J Ophthalmol. 2005;140:134–136. Abstract | Full Text | Full-Text PDF (202 KB) | CrossRef
5. 5Meyer CH, Mennel S, Rodrigues EB, Schmidt JC. Persistent premacular cavity after membranectomy in Valsalva retinopathy evident by optical coherence tomography. Retina. 2006;26:116–118. CrossRef
6. 6Srinivasan S, Kyle G. Subinternal limiting membrane and subhyaloid haemorrhage in Terson syndrome: the macular ‘double ring’ sign. Eye. 2006;20:1099–1101. CrossRef