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Non-arteritic anterior ischemic optic neuropathy as the only manifestation of a malignant hypertensive crisis: Report of a case
Neuropatía óptica isquémica anterior no arterítica como única manifestación de una crisis hipertensiva maligna: presentación de un caso
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Miralles Pechuan, J. González-Martín-Moro, M. Castro Rebollo, R. Cobo Soriano" "autores" => array:4 [ 0 => array:4 [ "nombre" => "V." "apellidos" => "Miralles Pechuan" "email" => array:2 [ 0 => "vicentemirallesp@hotmail.com" 1 => "vicentemipe@gmail.com" ] "referencia" => array:2 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] 1 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">*</span>" "identificador" => "cor0005" ] ] ] 1 => array:3 [ "nombre" => "J." "apellidos" => "González-Martín-Moro" "referencia" => array:2 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] 1 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "aff0010" ] ] ] 2 => array:3 [ "nombre" => "M." "apellidos" => "Castro Rebollo" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] ] ] 3 => array:3 [ "nombre" => "R." "apellidos" => "Cobo Soriano" "referencia" => array:2 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] 1 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "aff0010" ] ] ] ] "afiliaciones" => array:2 [ 0 => array:3 [ "entidad" => "Departamento de Oftalmología, Hospital Universitario del Henares, Coslada, Madrid, Spain" "etiqueta" => "a" "identificador" => "aff0005" ] 1 => array:3 [ "entidad" => "Facultad de Ciencias de la Salud, Universidad Francisco de Vitoria, Madrid, Spain" "etiqueta" => "b" "identificador" => "aff0010" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "<span class="elsevierStyleItalic">Corresponding author</span>." ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Neuropatía óptica isquémica anterior no arterítica como única manifestación de una crisis hipertensiva maligna: presentación de un caso" ] ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:8 [ "identificador" => "fig0005" "etiqueta" => "Fig. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 1165 "Ancho" => 1333 "Tamanyo" => 152830 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0005" "detalle" => "Fig. " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Ultra-widefield photograph showing thinning of the retinal arteries and optic disc edema.</p>" ] ] ] "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Introduction</span><p id="par0005" class="elsevierStylePara elsevierViewall">Nonarteritic anterior ischemic optic neuropathy (NAION) is the most frequent optic neuropathy above the age of 50 years, after glaucoma.<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> The pathogenesis of this entity is not well understood, but it is believed that hypoperfusion of the optic nerve head sets in motion a compartment syndrome that eventually leads to infarction of a good portion of the optic nerve axons, thus producing a very significant impairment of the patient's visual function.<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> Before reaching a diagnosis of NAION, a differential diagnosis must be made with other potential causes of visual loss in this context: ischemic stroke (associated cardiovascular risk factors and usually binocular visual loss), systemic vasculitis (elevated erythrocyte sedimentation rate [ESR] and probably a positive autoimmune study) and accelerated-malignant hypertension (associated with other retinal lesions such as exudates and hemorrhages and symptoms of acute renal failure).<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">NAION is an atypical infarction, and still poorly understood, in which the classic cardiovascular risk factors have less weight than in cerebrovascular pathology. Predisposing factors for the development of this neuropathy are known to be diabetes mellitus, hyperlipidemia, antiphospholipid antibody syndrome and arterial hypertension (AHT) maintained for years.<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">Likewise, it has been postulated that nocturnal systemic arterial hypotension could be an important trigger. This theory is justified because patients subjected to excessive antihypertensive treatment are at greater risk and because patients with NAION have lower systolic blood pressure than healthy subjects throughout the day, with the most notable difference occurring in the early morning, before awakening.</p><p id="par0020" class="elsevierStylePara elsevierViewall">However, the most important risk factor is anatomical. Patients with small and “<span class="elsevierStyleItalic">crowded</span>” optic <span class="elsevierStyleItalic">discs</span> (<span class="elsevierStyleItalic">crowed optic disc</span> or <span class="elsevierStyleItalic">disc at risk</span>) have a much higher risk of developing this neuropathy. Even so, there continues to be debate about what exactly is a disc at risk. Some recent studies suggest that the papillary area of patients with this neuropathy and controls is the same, defining the at-risk disc as one that has a smaller volume because it has a more anteriorized lamina cribrosa.<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">Papillary edema is a known manifestation of hypertensive retinopathy and chronic arterial hypertension is a proven risk factor for the development of NAION.<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> However, we believe that this is one of the few published cases of anterior ischemic optic neuropathy in the setting of a hypertensive crisis in a young patient with no other risk factors.</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Presentation of the case</span><p id="par0030" class="elsevierStylePara elsevierViewall">A 32-year-old male patient admitted to the intensive care unit for a hypertensive emergency with blood pressure of 227/168 mmHg reported acute loss of vision in the left eye. He had no ophthalmologic history of interest. Regarding systemic history, he was only on treatment with low molecular weight heparin since the onset of the hypertensive emergency. He did not have diabetes, nor had he been diagnosed with systemic arterial hypertension or dyslipidemia previously. He was not a smoker and did not consume toxic substances.</p><p id="par0035" class="elsevierStylePara elsevierViewall">Basal computed tomography (CT) and angioCT of the supra-aortic trunks and the polygon of Willis were performed, with no space-occupying lesions. The CT angiography showed a correct repletion of contrast material without images of stenosis or dissections. CT only showed a dubious left occipital hypodensity and CT angiography showed no evidence of carotid dissection or findings suggestive of aneurysmal subarachnoid hemorrhage. An MRI was also performed, which showed no evidence of demyelinating lesions in the brain or optic nerve.</p><p id="par0040" class="elsevierStylePara elsevierViewall">Ophthalmologic examination produced a best uncorrected visual acuity (BCVA) of 0.65, improving with pinhole to 1 in the right eye and 0.5 improving with pinhole to 0.65 in the left eye. Anterior segment examination was normal. She had a severe relative afferent pupillary defect in the LE. Fundus examination revealed some arteriolar thinning (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>), a papilla at risk (small and unexcavated) in the RE, while the LE showed an elevated, moderately blurred papilla with a splinter hemorrhage on the temporal side (<a class="elsevierStyleCrossRef" href="#fig0010">Fig. 2</a>.1). The autorefractometer showed mild ametropia in both eyes (RE (–0.25D, –0.75D at 102°); LE (–0.75D, –1D at 77°).</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0045" class="elsevierStylePara elsevierViewall">Optical coherence tomography (OCT) was performed, which showed the presence of a very significant thickening of the peripapillary nerve fiber layer of the RO (<a class="elsevierStyleCrossRef" href="#fig0010">Fig. 2</a>.2). The visual field revealed the presence of a very severe peripheral defect in the RO with preservation of the islet of central vision (<a class="elsevierStyleCrossRef" href="#fig0015">Fig. 3</a>). At the end of 3 months the visual field had not changed but the papillary edema had subsided.</p><elsevierMultimedia ident="fig0015"></elsevierMultimedia><p id="par0050" class="elsevierStylePara elsevierViewall">Fundus examination revealed the presence of a pale, excavated papilla, and OCT revealed the presence of severe atrophy. The stability of the visual field and the substitution of papilla edema for atrophy suggested that the patient had suffered a NAION in his LE.</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Discussion</span><p id="par0055" class="elsevierStylePara elsevierViewall">Although the pathophysiology of NAION is not yet known exactly, the most accepted theory at present suggests that it is caused by hypoperfusion of the short posterior ciliary arteries supplying the optic nerve, leading to ischemia. This ischemia induces edema in the axons of the optic nerve head, which is tightly packed by the surrounding meninx.<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a> It is believed that the edema thus sets in motion a compartment syndrome that leads to apoptosis and death of the ganglion cells whose axons compose the optic nerve.<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a></p><p id="par0060" class="elsevierStylePara elsevierViewall">Therefore, the presence of a “disc at risk” is nowadays considered the most important risk factor for developing NAION. However, there are also other intraocular and systemic factors that may favor this pathology. A recent meta-analysis that included 48 studies and integrated the clinical characteristics of 10 million patients found that the following risk factors were associated with an increased risk of causing NAION: hyperlipidemia, arterial hypertension, diabetes mellitus, coronary artery disease, sleep apnea, Leiden factor V, and surgical procedures with significant blood loss.<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a> However, malignant arterial hypertension is not considered a risk factor.<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a></p><p id="par0065" class="elsevierStylePara elsevierViewall">The case presented is interesting because NAION has not been considered to be part of the spectrum of manifestations of malignant hypertension. Anterior ischemic optic neuropathy is not uncommon in the context of acute arterial hypotension, but is infrequent in hypertensive crises. In previous literature we have found only four cases of ischemic optic neuropathy secondary to hypertensive crisis.<a class="elsevierStyleCrossRefs" href="#bib0020"><span class="elsevierStyleSup">4,5</span></a> One was a posterior optic neuropathy.<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a> The remaining cases were earlier forms, and the visual loss occurred in the context of hyperaldosteronism, and the cause of the hypertension was not clear. Although we do not have a clear explanation of the associated pathophysiology, it is likely to be related to autoregulation of blood flow in the optic nerve. It is possible that the rise in blood pressure may induce vasospasm of the short posterior ciliary arteries leading to hypoperfusion of the optic nerve head. In an at-risk disc this edema may lead to the onset of this compartment syndrome.</p><p id="par0070" class="elsevierStylePara elsevierViewall">The case we report presents some limitations. It is not possible to completely exclude other neuropathies as a cause of the visual loss, but the evolution towards papillary atrophy is more typical of NAION than of an inflammatory neuropathy, and the temporal coincidence with the hypertensive crisis leads us to suspect a vascular rather than an inflammatory origin.</p><p id="par0075" class="elsevierStylePara elsevierViewall">In summary, we present an association infrequently described in the biomedical literature. It is difficult to understand why papillary edema with an ischemic mechanism that frequently accompanies hypertensive crises does not evolve more frequently in at-risk discs toward the development of NAION. The cases we have found have been published mostly in non-ophthalmologic journals and have not been as well documented from an ophthalmological point of view as the one we present. A better understanding of this fact could help in the future in the development of new therapies that could prevent or improve the prognosis of this neuropathy.</p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Funding</span><p id="par0080" class="elsevierStylePara elsevierViewall">This research has not received specific support from public sector agencies, commercial sector or non-profit entities.</p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Conflict of interest</span><p id="par0085" class="elsevierStylePara elsevierViewall">No conflicts of interest were declared by the authors.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:10 [ 0 => array:3 [ "identificador" => "xres2254509" "titulo" => "Abstract" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0005" ] ] ] 1 => array:2 [ "identificador" => "xpalclavsec1885535" "titulo" => "Keywords" ] 2 => array:3 [ "identificador" => "xres2254508" "titulo" => "Resumen" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0010" ] ] ] 3 => array:2 [ "identificador" => "xpalclavsec1885536" "titulo" => "Palabras clave" ] 4 => array:2 [ "identificador" => "sec0005" "titulo" => "Introduction" ] 5 => array:2 [ "identificador" => "sec0010" "titulo" => "Presentation of the case" ] 6 => array:2 [ "identificador" => "sec0015" "titulo" => "Discussion" ] 7 => array:2 [ "identificador" => "sec0020" "titulo" => "Funding" ] 8 => array:2 [ "identificador" => "sec0025" "titulo" => "Conflict of interest" ] 9 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "fechaRecibido" => "2023-05-02" "fechaAceptado" => "2024-04-23" "PalabrasClave" => array:2 [ "en" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec1885535" "palabras" => array:5 [ 0 => "Malignant hypertension" 1 => "NAION" 2 => "Optic disc edema" 3 => "Hypertensive neuropathy" 4 => "Hypertensive retinopathy" ] ] ] "es" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec1885536" "palabras" => array:5 [ 0 => "Hipertensión maligna" 1 => "NOIANA" 2 => "Edema depapila" 3 => "Neuropatía hipertensiva" 4 => "Retinopatía hipertensiva" ] ] ] ] "tieneResumen" => true "resumen" => array:2 [ "en" => array:2 [ "titulo" => "Abstract" "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">Non-arteritic anterior ischemic optic neuropathy (NAION) is after glaucoma the most common optic neuropathy in patients over 50 years. It is known that high blood pressure (HBP) is an important risk factor for the development of NAION. It is also known that malignant arterial hypertension (MAH) could be accompanied by optic disc edema. However, MAH has not classically been considered a cause of NAION. We report the case of a 32-year-old patient who presented irreversible visual loss with a pattern compatible with NAION as the only manifestation of a hypertensive crisis.</p></span>" ] "es" => array:2 [ "titulo" => "Resumen" "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">La neuropatía óptica isquémica anterior no arterítica (NOIANA) es, después del glaucoma, la neuropatía óptica más frecuente por encima de los 50 años. Se sabe que la hipertensión arterial (HTA) es un factor de riesgo importante para el desarrollo de NOIANA y que la HTA maligna se acompaña de edema de papila. Sin embargo la HTA maligna no se ha considerado clásicamente una causa de NOIANA. Presentamos el caso de un paciente de 32 años de edad que sufrió una pérdida visual irreversible compatible con NOIANA como única manifestación de daño orgánico en el contexto de una crisis hipertensiva.</p></span>" ] ] "multimedia" => array:3 [ 0 => array:8 [ "identificador" => "fig0005" "etiqueta" => "Fig. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 1165 "Ancho" => 1333 "Tamanyo" => 152830 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0005" "detalle" => "Fig. " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Ultra-widefield photograph showing thinning of the retinal arteries and optic disc edema.</p>" ] ] 1 => array:8 [ "identificador" => "fig0010" "etiqueta" => "Fig. 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr2.jpeg" "Alto" => 4153 "Ancho" => 2895 "Tamanyo" => 631602 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0010" "detalle" => "Fig. " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">1) Retinograms showing the evolutionary sequence of the optic disc of the LE (from initial papilla edema to pallor). 2) Optical coherence tomography report showing the evolution of the peripapillary nerve fiber layer of the LE.</p>" ] ] 2 => array:8 [ "identificador" => "fig0015" "etiqueta" => "Fig. 3" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr3.jpeg" "Alto" => 2356 "Ancho" => 2716 "Tamanyo" => 310499 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0015" "detalle" => "Fig. " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Image of the visual field showing a peripheral defect with respect to the central area.</p>" ] ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:9 [ 0 => array:3 [ "identificador" => "bib0005" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Non-arteritic anterior ischaemic optic neuropathy: a review and update" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:3 [ 0 => "N.M. 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