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Ophthalmic Injuries
Published in Ian Greaves, Keith Porter, Jeff Garner, Trauma Care Manual, 2021
Ian Greaves, Keith Porter, Jeff Garner
It is important to note that the eyes may be damaged by remote injury. For example, crush injuries to a limb or the chest can result in retinal damage from emboli or Purtscher’s retinopathy. Episodes of hypo-tension can result in infarction of the occipital cortex or the optic nerves. Optic nerve infarction may occur 24 hours or more after the insult.23
Ophthalmic Issues and the Maternal Eye in Pregnancy
Published in Tony Hollingworth, Differential Diagnosis in Obstetrics and Gynaecology: An A-Z, 2015
This occurs with pre-eclampsia and is rare. It is a risk in a poorly controlled pregnancy-induced hypertension coupled with a hypercoagulability state. In this, the woman presents with acute painless visual loss which is due to micro-vascular problems in the retina and optic nerve. Cortical infarcts may occur as there is occlusion of small arterioles by fibrin clots, platelet and leucocyte aggregation as well as fat or air embolism. Ocular blood flow can be examined with a Doppler examination. Neuroretinitis or malignant hypertension may be considered in the differential diagnosis. There is no known treatment for Purtscher’s retinopathy, although intravenous steroids have been administered in some cases, though without much success in restoring vision. Symptoms disappear at about 6 weeks postpartum but may leave the woman severely visually compromised (Fig. 4).
Trauma from child abuse
Published in David E. Wesson, Bindi Naik-Mathuria, Pediatric Trauma, 2017
Charles S. Cox, Margaret L. Jackson, Benjamin M. Aertker
Fundoscopic examination is critical when assessing for abusive head trauma. Ocular findings must be evaluated and rigorously documented by an ophthalmologist. The validity of clinical information and diagnostic studies in abusive head trauma cases is dependent on the completeness of the retinal examination. A full assessment includes indirect ophthalmoscopy to examine the peripheral retina. One study demonstrated that 29% of patients with retinal hemorrhages were not detected by nonophthalmologists [31]. Complete postmortem ocular evaluation (including the optic nerve) is the gold standard for the diagnosis of retinal hemorrhage [32]. The mechanism that produces retinal hemorrhage is the subject of debate in the literature. One theory postulates that an abrupt increase in intracranial pressure results in venous obstruction and retinal hemorrhage. This may be augmented by abrupt increases in intrathoracic pressure due to thoracic compression. A second theory holds that acceleration/deceleration forces result in traction of the vitreous on the retina with hemorrhagic retinoschisis cavities. Numerous class II and class III studies show that retinal hemorrhages occur only rarely (up to 6%) with severe head trauma and not at all with moderate or mild head trauma [33–35]. In comparison, a retrospective analysis of the National Pediatric Trauma Registry found that retinal hemorrhages were reported in 28% of child abuse cases in children under 5 years of age [36]. Clinically, evidence of retinal hemorrhage is reported to have an approximately 74% sensitivity and 94% specificity for abusive head trauma. This review reports a superior sensitivity for retinal hemorrhage when compared to retinal folds, traumatic retinoschisis, and optic nerve sheath hemorrhage [35]. Other causes of retinal hemorrhage in infants include birth trauma, cardiopulmonary resuscitation (CPR), hematological diseases, and ruptured vascular malformations. With rare exceptions, CPR does not cause retinal hemorrhage [32, 37–39]. Bacon et al. and Kirschner and Stein each reported a case of retinal hemorrhage in an infant after vigorous resuscitation [40, 41]. Purtscher retinopathy, a lesion of diverse pathophysiologic origin, is a rare cause of retinal hemorrhage. However, this is rarely the cause of retinal hemorrhage and should be interpreted in the context of the clinical presentation.
Retinal findings in glomerulonephritis
Published in Clinical and Experimental Optometry, 2022
Heather G Mack, Deborah J Colville, Phillip Harraka, Judith Anne Savige, Alessandro Invernizzi, Samantha Fraser-Bell
Purtscher retinopathy is a constellation of retinal findings including nerve fibre infarcts, retinal haemorrhages, characteristic polygonal areas of retinal whitening (Purtscher flecken) and optic disc oedema. Although first described in trauma, it is now recognised as occurring in many other conditions including acute pancreatitis, systemic autoimmune disease, haemolytic uraemic syndrome and cryoglobulinemia. When seen outside of trauma, it is termed Purtscher-like retinopathy. It has been reported in individuals with atypical haemolytic syndrome93 and lupus nephritis.81 The pathological mechanism of Purtscher and Purtscher-like retinopathy likely involves microembolization of the retinal microvasculature by leucocyte aggregation, platelets, and fibrin. Complement activation may induce the formation of leucocyte aggregates that are large enough to induce precapillary arteriolar occlusion in the retinal vessels.94 Successful treatment of Purtscher-like retinopathy with eculizumab is consistent with the cause being activation of the alternative pathway in atypical haemolytic uraemic syndrome.93 In contrast, no successful treatment of Purtscher-like retinopathy associated with SLE (lectin pathway) has been identified.
Purtscher-like Retinopathy Associated with Crimean-Congo Hemorrhagic Fever: A Case Report
Published in Ocular Immunology and Inflammation, 2022
Duygu Yalinbas, Erman Bozali, Ayse Vural, Husne Kocak, Haydar Erdogan
To our knowledge, Purtscher-like retinopathy in CCHF has not been described before. The probable mechanisms of observing Purtscher-like retinopathy in the course of the CCHF disease are endothelial damage and activation of the coagulation cascade and complement system. It is known that acute lesions resolve spontaneously within 1–3 months in the majority of cases.20 Similarly, we observed resolving of lesions in our case spontaneously at 1 month visit. The cornerstone of Purtscher-like retinopathy treatment is based on the treatment of primary disease and supportive care. Although the use of steroids is controversial, some authors suggested steroid treatment for visual and anatomical improvement. In a systematic review, it was reported that no difference was found in terms of improvement of visual acuity between steroid treatment and observation.7 In a study evaluating the efficacy of Purtscher’s retinopathy treatments, it was indicated that 43% of clinicians advised no treatment and 57% of them administered treatment such as corticosteroids, Traditional Chinese Medicine, or hyperbaric oxygen treatments.21 In our case, we did not recommend any treatment, and we observed approximately two Snellen lines of visual acuity improvement. Although the visual acuity recovery is unpredictable, similar to our case Agrawal et al. reported improvement in at least two Snellen lines in 50% of the cases.6
Dengue Fever Presenting as Purtscher-like Retinopathy
Published in Ocular Immunology and Inflammation, 2018
Luiz H. Lima, Silvana Vianello, Sérgio Pimentel, Gabriel Costa de Andrade, Claudio Zett, Léo Muller, Michel E. Farah, Rubens Belfort
The Purtscher-like lesions are characterized by a constellation of retinal features such as Purtscher flecken, cotton–wool spots, retinal hemorrhages, and optic disc edema.6–8 According to diagnostic criteria, the diagnosis of Purtscher’s retinopathy is conceived in a patient that fits at least three of five criteria (Purtscher flecken, retinal hemorrhages, cotton–wool spots, probable explanatory etiology, and complementary investigation compatible with diagnosis).23 The present clinical cases reported two patients with dengue fever (probable explanatory etiology) diagnosed by specific laboratory exams (complementary investigation compatible with diagnosis) in which retinal manifestations such as cotton–wool and retinal hemorrhages in a Purtscher-like configuration were observed. Therefore, our cases fulfill four out the five diagnostic criteria for Purtscher’s retinopathy. After a follow-up period that varied between 45 days and 4 months, both the cotton–wool spots and retinal hemorrhages totally disappeared and visual acuity improved in all study cases. This outcome corresponds with the natural history of Purtscher’s retinopathy. Typically, a normalization of the retinal appearance on fundoscopic examination is observed in about 40% of Purtscher’s retinopathy patients at 2 months follow-up.23 Although the visual acuity recovery after the onset of disease is unpredictable, spontaneous visual acuity improvement in at least two Snellen lines is identified in approximately 50% of the cases.24