AKI POST cardiac cath with blurred vision and skin lesions

General

Heent

Neck

Cardiovascular

Lungs

Abdomen

Extremities

Skin

Neurological Exam

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Discussion

Cholesterol crystal embolism (CCE) is a severe disorder that usually affects several organs. It results from a massive release of cholesterol crystals from widespread ulcerative atherosclerotic disease of the aorta and/or its first branches [11, 12]. The main difference with atherosclerosis is the severity and the quantity of the embolic events that occur during the course. It mostly affects white Caucasians, more frequently men in their sixth decade, with cardiovascular risk factors and multiple manifestations of atherosclerosis [12, 13]. Embolization can occur spontaneously but an iatrogenic triggering event is noticed in up to 79% of cases (e.g., transluminal angioplasty, angiography, vascular surgery, and anticoagulant or fibrinolytic treatment) [12].

From a pathogenic point of view, CCE behaves like small vessels vasculitis. Crystals are too small to obstruct the artery in which they are located and induce an endothelial inflammatory reaction which leads to a complete obstruction within weeks or months [8, 12, 13]. The vasculitis may be associated with biologic features of inflammation and eosinophilia. Locations of emboli are multiple and thus cause proteiform clinical manifestations. The diagnosis is classically suspected in case of an acute renal failure associated with livedo reticularis and blue toe with preserved distal pulses, following any type of endovascular procedure [11]. Beside these typical settings, chronic forms of the disease may occur, with multiple embolizations, delayed from the triggering event. Masquerading presentations with essentially symptoms of vasculitides have been reported [8]. These multiple patterns make CEE a diagnostic challenge, and the diagnosis is often made only with autopsy [8, 9, 12]. The prognosis is poor, with death in up to 73% of the cases, secondary to multisystemic ischaemic complications, renal failure, sepsis, and cardiac arrest [7].

Ophthalmologic findings are the consequences of retinal emboli (monocular transient or definitive vision loss and visual field defects) or may be related to secondary vasculitis (diplopia caused by neurologic or muscular lesions and central neuro-ophthalmologic symptoms caused by visual paths lesions) [8, 9]. The ocular complications of CEE have seldom been described in the ophthalmologic literature, despite the putative role of fundus examination to confirm the diagnosis. Prevalence of retinal emboli varied from 10% to 25% [10]. Emboli can be multiple and disseminated or unilateral [8–10]. This heterogeneity can be explained by the locations of the plaques (retinal emboli occurs only if the plaques are located either on the carotid arteries or on the aorta), but also by the mobile nature of these emboli. Fundus examination has a double interest in suspected cases of CEE. In a patient with visceral failure, it confirms the hypothesis and makes useless invasive biopsies, as it was the case in our patient and in those reported by Gittinger and Kershaw [10]. Systematic fundus examination also enables exploring the CEE hypothesis in case of vasculitis or unexplained neuro-ophthalmologic signs, which could be initially misdiagnosed as giant cell arteritis, for example, as reported by Jacobson [8].

Since retinal emboli of CEE appear as usual cholesterol emboli detached from carotid atheromatous plaques, it is of crucial importance to ask the patient for a previous history of vascular procedure. The main differences lie both in the short-term prognosis and the management: CEE can quickly lead to multivisceral failure, whereas usual retinal emboli are only associated with a higher risk of stroke and delayed mortality [1, 2, 14]. Once the diagnosis of CEE is established, any form of anticoagulation or endovascular procedure should be banned. Some authors have used steroids and/or statins [13, 15]. Although a particular dialysis option is not contraindicated, some investigators suggest that peritoneal dialysis, which avoids anticoagulation, could be the preferred treatment modality [12]. Prospective studies reported an improvement of the survival rate with supportive and adapted treatments [15].

Fundoscopic examination may be the key test to diagnose cholesterol crystal embolism. When typical emboli are seen in the retina, it obviates the need for invasive investigations, thus saving precious time to manage this potentially lethal disease.