Hemodialysis graft-induced intracranial hypertension

Intracranial hypertension is rarely associated with peripheral hemodialysis shunts, presumably in association with central venous stenosis.1,2 Hemodialysis Reliable Outflow (HeRO) grafts (CryoLife, Inc., Kennesaw, GA) are designed to bypass preexisting central venous stenosis by connecting the brachial artery with the venous circulation through the ipsilateral internal jugular vein (IJV) (figure, C and D).3 We report a case of intracranial hypertension immediately after placement of a HeR

Hypertensive eye disease

Hypertensive eye disease includes a spectrum of pathological changes, the most well known being hypertensive retinopathy. Other commonly involved parts of the eye in hypertension include the choroid and optic nerve, sometimes referred to as hypertensive choroidopathy and hypertensive optic neuropathy. Together, hypertensive eye disease develops in response to acute and/or chronic elevation of blood pressure. Major advances in research over the past three decades have greatly enhanced our understanding of the epidemiology, systemic associations and clinical implications of hypertensive eye disease, particularly hypertensive retinopathy. Traditionally diagnosed via a clinical funduscopic examination, but increasingly documented on digital retinal fundus photographs, hypertensive retinopathy has long been considered a marker of systemic target organ damage (for example, kidney disease) elsewhere in the body. Epidemiological studies indicate that hypertensive retinopathy signs are commonly seen in the general adult population, are associated with subclinical measures of vascular disease and predict risk of incident clinical cardiovascular events. New technologies, including development of non-invasive optical coherence tomography angiography, artificial intelligence and mobile ocular imaging instruments, have allowed further assessment and understanding of the ocular manifestations of hypertension and increase the potential that ocular imaging could be used for hypertension management and cardiovascular risk stratification

Patient Harm Due to Diagnostic Error of Neuro-Ophthalmologic Conditions

PURPOSE: To prospectively examine diagnostic error of neuro-ophthalmic conditions and resultant harm at multiple sites. DESIGN: Prospective, cross-sectional study. PARTICIPANTS: A total of 496 consecutive adult new patients seen at 3 university-based neuro-ophthalmology clinics in the United States in 2019 to 2020. METHODS: Collected data regarding demographics, prior care, referral diagnosis, final diagnosis, diagnostic testing, treatment, patient disposition, and impact of the neuro-ophthalmologic encounter. For misdiagnosed patients, we identified the cause of error using the Diagnosis Error Evaluation and Research (DEER) taxonomy tool and whether the patient experienced harm due to the misdiagnosis. MAIN OUTCOME MEASURES: The primary outcome was whether patients who were misdiagnosed before neuro-ophthalmology referral experienced harm as a result of the misdiagnosis. Secondary outcomes included appropriateness of referrals, misdiagnosis rate, interventions undergone before referral, and the primary type of diagnostic error. RESULTS: Referral diagnosis was incorrect in 49% of cases. A total of 26% of misdiagnosed patients experienced harm, which could have been prevented by earlier referral to neuro-ophthalmology in 97%. Patients experienced inappropriate laboratory testing, diagnostic imaging, or treatment before referral in 23%, with higher rates for patients misdiagnosed before referral (34% of patients vs. 13% with a correct referral diagnosis, P < 0.0001). Seventy-six percent of inappropriate referrals were misdiagnosed, compared with 45% of appropriate referrals (P < 0.0001). The most common reasons for referral were optic neuritis or optic neuropathy (21%), papilledema (18%), diplopia or cranial nerve palsies (16%), and unspecified vision loss (11%). The most common sources of diagnostic error were the physical examination (36%), generation of a complete differential diagnosis (24%), history taking (24%), and use or interpretation of diagnostic testing (13%). In 489 of 496 patients (99%), neuro-ophthalmology consultation (NOC) affected patient care. In 2% of cases, neuro-ophthalmology directly saved the patient's life or vision; in an additional 10%, harmful treatment was avoided or appropriate urgent referral was provided; and in an additional 48%, neuro-ophthalmology provided a diagnosis and direction to the patient's care. CONCLUSIONS: Misdiagnosis of neuro-ophthalmic conditions, mismanagement before referral, and preventable harm are common. Early appropriate referral to neuro-ophthalmology may prevent patient harm

Artificial Intelligence to Detect Papilledema from Ocular Fundus Photographs.

BACKGROUND: Nonophthalmologist physicians do not confidently perform direct ophthalmoscopy. The use of artificial intelligence to detect papilledema and other optic-disk abnormalities from fundus photographs has not been well studied. METHODS: We trained, validated, and externally tested a deep-learning system to classify optic disks as being normal or having papilledema or other abnormalities from 15,846 retrospectively collected ocular fundus photographs that had been obtained with pharmacologic pupillary dilation and various digital cameras in persons from multiple ethnic populations. Of these photographs, 14,341 from 19 sites in 11 countries were used for training and validation, and 1505 photographs from 5 other sites were used for external testing. Performance at classifying the optic-disk appearance was evaluated by calculating the area under the receiver-operating-characteristic curve (AUC), sensitivity, and specificity, as compared with a reference standard of clinical diagnoses by neuro-ophthalmologists. RESULTS: The training and validation data sets from 6779 patients included 14,341 photographs: 9156 of normal disks, 2148 of disks with papilledema, and 3037 of disks with other abnormalities. The percentage classified as being normal ranged across sites from 9.8 to 100%; the percentage classified as having papilledema ranged across sites from zero to 59.5%. In the validation set, the system discriminated disks with papilledema from normal disks and disks with nonpapilledema abnormalities with an AUC of 0.99 (95% confidence interval [CI], 0.98 to 0.99) and normal from abnormal disks with an AUC of 0.99 (95% CI, 0.99 to 0.99). In the external-testing data set of 1505 photographs, the system had an AUC for the detection of papilledema of 0.96 (95% CI, 0.95 to 0.97), a sensitivity of 96.4% (95% CI, 93.9 to 98.3), and a specificity of 84.7% (95% CI, 82.3 to 87.1). CONCLUSIONS: A deep-learning system using fundus photographs with pharmacologically dilated pupils differentiated among optic disks with papilledema, normal disks, and disks with nonpapilledema abnormalities. (Funded by the Singapore National Medical Research Council and the SingHealth Duke-NUS Ophthalmology and Visual Sciences Academic Clinical Program.)

Walsh & Hoyt: Neovascularisation

In eyes with persistent hypoperfusion, further evidence of panocular ischemia becomes evident, including neovascularization of the iris (rubeosis iridis), retina, optic disc, and anterior chamber angle

Walsh & Hoyt: Seizures

Most seizures occur at the onset of intracerebral hemorrhage or within the first 24 hours (819,820). Anticonvulsants can usually be discontinued after the first month in patients who have had no further seizures. Patients who have a seizure more than two weeks after the onset of an intracerebral hemorrhage are at higher risk for further seizures and may require long-term prophylactic treatment with anticonvulsants (820)

Walsh & Hoyt: Pathophysiology

Intracerebral hemorrhages commonly occur in the cerebral lobes, basal ganglia, thalamus, brain stem (predominantly the pons), and cerebellum. Extension into the ventricles occurs in association with deep, large hematomas. Edematous parenchyma, often discolored by degradation products of hemoglobin, is visible adjacent to the clot. Histologic sections are characterized by the presence of edema, neuronal damage, macrophages, and neutrophils in the region surrounding the hematoma. The hemorrhage spreads between planes of white-matter cleavage with minimal destruction, leaving nests of intact neural tissue within and surrounding the hematoma. This pattern of spread accounts for the presence of viable and salvageable neural tissue in the immediate vicinity of the hematoma

Walsh & Hoyt: Pathology

Neurons are more vulnerable to oxygen deprivation than are oligodendroglia and astrocytes, whereas microglia and blood vessels are least vulnerable. After an episode of hypoxia, therefore, structural damage may be limited to neurons (selective neuronal necrosis), or it may include glia and blood vessels. In addition, neurons of the phylogenetically older portions of the CNS are more resistant than neurons of the newer portions (selective vulnerability). The gray matter of the spinal cord and most of the brainstem thus may remainun damaged despite almost total destruction of the cerebral cortex. Infarction