The Specialist Treatment of Inpatients: Caring for Diabetes in Surgery (STOIC-D Surgery) Trial: A Randomized Controlled Trial of Early Intervention With an Electronic Specialist-Led Model of Diabetes Care.

OBJECTIVE: To investigate the effect of early intervention with an electronic specialist-led "proactive" model of care on glycemic and clinical outcomes. RESEARCH DESIGN AND METHODS: The Specialist Treatment of Inpatients: Caring for Diabetes in Surgery (STOIC-D Surgery) randomized controlled trial was performed at the Royal Melbourne Hospital. Eligible participants were adults admitted to a surgical ward during the study with either known diabetes or newly detected hyperglycemia (at least one random blood glucose result ≥11.1 mmol/L). Participants were randomized 1:1 to standard diabetes care or the intervention consisting of an early consult by a specialist inpatient diabetes team using electronic tools for patient identification, communication of recommendations, and therapy intensification. The primary outcome was median patient-day mean glucose (PDMG). The key secondary outcome was incidence of health care-associated infection (HAI). RESULTS: Between 12 February 2021 and 17 December 2021, 1,371 admissions met inclusion criteria, with 680 assigned to early intervention and 691 to standard diabetes care. Baseline characteristics were similar between groups. The early intervention group achieved a lower median PDMG of 8.2 mmol/L (interquartile range [IQR] 6.9-10.0 mmol/L) compared with 8.6 mmol/L (IQR 7.2-10.3 mmol/L) in the control group for an estimated difference of -0.3 mmol/L (95% CI -0.4 to -0.2 mmol/L, P < 0.0001). The incidence of HAI was lower in the intervention group (77 [11%] vs. 110 [16%]), for an absolute risk difference of -4.6% (95% CI -8.2 to -1.0, P = 0.016). CONCLUSIONS: In surgical inpatients, early diabetes management intervention with an electronic specialist-led diabetes model of care reduces glucose and HAI.

Yield of Investigations in Young Patients Presenting With Transient Monocular Vision Loss: A Prospective Study.

PURPOSE: It is unclear whether transient monocular vision loss (TMVL) warrants the same thorough systemic evaluation for potential embolic sources in young adults as it does in older adults. The objective of the present study was to evaluate the yield of investigations in patients under 45 years of age presenting with TMVL. DESIGN: Prospective cohort study. METHODS: Young adult patients with TMVL presenting to a university-affiliated neuro-ophthalmology clinic were included. All included patients were referred for neuroimaging (computed tomography or magnetic resonance angiography of entire carotid tree and magnetic resonance imaging of the brain) and cardiac investigations (transesophageal echocardiography and 2 weeks of Holter monitoring). RESULTS: A total of 20 participants with TMVL were included in the study. The mean age was 33.1 ± 8.2 years, and 16 of the 20 participants were women. The most common finding on past medical history was migraines, in 5 of 20 cases (25%), and 25% of patients had headaches during their visual loss. Of 17 participants who completed neuroimaging, 1 had fibromuscular dysplasia (this patient also experienced headaches during their symptoms). Two of 13 patients who completed echocardiography had patent foramen ovale. Overall, 3 of 20 participants (15%, 95% CI 3%-38%) had abnormal findings associated with their TMVL. Aspirin treatment was initiated in 2 of 3 patients following investigations. CONCLUSION: In our cohort of young patients presenting with TMVL, 15% of patients had abnormal findings on further investigations. We recommend that young patients presenting with TMVL be referred for neuroimaging and cardiac workup so that appropriate treatments can be initiated to prevent future complications. Headaches during vision loss may not always indicate a benign cause, and retinal migraine should be a diagnosis of exclusion.

Incidence of giant cell arteritis mimicking non-arteritic anterior optic neuropathy.

PURPOSE: Giant cell arteritis (GCA) involving ophthalmic circulation often manifests as anterior ischemic optic neuropathy (AAION), presenting with severe vision loss and pallid optic disc edema. Non-arteritic anterior ischemic optic neuropathy (NAION) classically presents with segmental optic disc edema and corresponding altitudinal visual field defect (VFD) with small cup-to-disc ratio in the fellow eye. Differentiating these two entities is critical as GCA requires immediate treatment to prevent vision loss in the fellow eye. This study investigated how often GCA mimics NAION at presentation. METHODS: Retrospective chart review of patients with temporal artery biopsy (TAB) positive GCA with ocular manifestations seen at a tertiary neuro-ophthalmology practice between 2015 and 2020. Patients presenting with segmental non-pallid optic disc swelling and corresponding altitudinal VFD mimicking NAION were identified. RESULTS: The clinical presentation of 7.1% (3/42) of patients with TAB-positive GCA mimicked NAION. Two of three patients had cup-to-disc ratio of <0.3 in the fellow eye. Two patients were women, mean age was 67.3 ± 6.5 years, and mean presenting visual acuity was 0.45 ± 0.48 LogMAR. Two patients had a normal temporal artery ultrasound. Two of three patients had at least one systemic symptom of GCA at presentation and all had elevation of one or both inflammatory markers. CONCLUSIONS: There should be high index of suspicion for GCA, even in patients highly suspected to have NAION. Inflammatory markers must be checked in every patient with presumed NAION and TAB performed if one or both are elevated to avoid missing GCA.

Visual Recovery in 2 Cases of Central Retinal Artery Occlusion Treated With Prompt Intra-ophthalmic Artery Fibrinolysis.

BACKGROUND: Central retinal artery occlusion (CRAO) rapidly produces inner retinal ischemia and irreversible vision loss. Although many therapeutic interventions have been proposed, no interventions have proven effective in restoring vision in large randomized controlled trials and final visual outcome in most patients is very poor. METHODS: Retrospective case series. RESULTS: We describe 2 cases of CRAO occurring after uncomplicated cataract surgery under topical anesthesia and rapidly diagnosed. Both had very severe vision loss at presentation with dramatic improvement after intra-ophthalmic artery fibrinolysis administered 2.75 and 5.5 hours after symptom onset. CONCLUSIONS: Sudden monocular vision loss is an ophthalmologic emergency as CRAO must be ruled out and if diagnosed, rapid intervention should be performed. Devastating vision loss can be prevented if interventional neuroradiology is trained and available on a 24-hour basis for administration of local intra-arterial thrombolysis.

Low probability of myasthenia Gravis in patients presenting to neuro-ophthalmology clinic for evaluation of isolated ptosis.

BACKGROUND: Concerning causes of ptosis, most notably third nerve palsy and Horner's syndrome, can be ruled out with normal ocular motility and pupillary examination. Myasthenia gravis (MG) however, rarely can present with ptosis as an isolated finding. We reviewed all patients presenting to tertiary neuro-ophthalmology practice with ptosis of unknown etiology to determine the frequency of MG. METHODS: Retrospective chart review of patients referred to a tertiary neuro-ophthalmology practice with undifferentiated ptosis. RESULTS: Sixty patients were included in the study. Twenty eight (47%) patients had ptosis along with various abnormalities of ocular motility and/or alignment and 32 (53%) had isolated unilateral ptosis defined as ptosis with absence of diplopia, or symptoms of generalized MG (GMG). Final diagnosis was aponeurotic ptosis due to levator palpebrae dehiscence in the majority (73%) of patients, while 10 (17%) were diagnosed with MG (6 with OMG, 4 with GMG). Diplopia was present in 9/10 patients with MG and 8/10 had abnormal ocular findings on clinical examination such as orbicularis oculi weakness, Cogan's lid twitch or fatiguability of ptosis on sustained upgaze. Only one patient referred for isolated unilateral ptosis was diagnosed with OMG and this patient had orbicularis oculi weakness. CONCLUSIONS: None of the patients with isolated unilateral ptosis and otherwise normal examination had MG. All patients eventually diagnosed with MG had diplopia or orbicularis weakness on examination. Thus, the yield of investigating patients with isolated ptosis for MG is exceedingly low.

Intracranial rheumatoid nodule causing recurrent transient neurological deficits.

A 67-year-old man with rheumatoid arthritis developed recurrent acute onset of stereotyped focal neurological abnormalities. Cerebral imaging showed a mass lesion in the left parieto-occipital lobe. Imaging did not show the time evolution expected in stroke and so he underwent an extensive workup, which was inconclusive. Brain biopsy identified a rheumatoid nodule causing an extensive inflammatory reaction that mimicked a mass. Following treatment with intravenous corticosteroids and rituximab infusions, his clinical condition improved. While rheumatoid meningitis is well recognised, a rheumatoid nodule in the brain rarely presents as a mass lesion. Nevertheless, it is important to consider rheumatoid nodule in the differential diagnosis of a cerebral mass lesion in patients with rheumatoid arthritis.

Dural Venous Sinus Thrombosis and Papilledema Related to JAK2 Mutation: A Case Series.

BACKGROUND: Dural venous sinus thrombosis (DVST) is an important cause of papilledema. Patients diagnosed with DVST should undergo work-up for underlying hypercoagulable state, including genetic causes. One important prothrombotic mutation is in the JAK2 gene, which is a driver of myeloproliferative neoplasms including polycythemia vera (PV). We aimed to determine the prevalence of JAK2 mutation in patients in presenting to neuro-ophthalmology clinic with DVST and papilledema. METHODS: Retrospective case series of patients seen in a tertiary neuro-ophthalmology practice who presented with papilledema due to DVST and were investigated for presence of JAK2 mutation. RESULTS: Four out of 15 patients with DVST (26%) were found to have JAK2 V617F mutation which led to subsequent diagnosis of PV in 2. One additional patient had a known diagnosis of essential thrombocytosis. We describe the clinical presentation of these four patients with papilledema and JAK2 mutation. CONCLUSIONS: A significant proportion of patients with papilledema secondary to DVST will harbor mutations in the JAK2 gene. Clinicians should be aware of this mutation as early testing will facilitate timely diagnosis and treatment of myeloproliferative disease to improve prognosis and reduce risk of recurrent thrombotic events.

Idiopathic intracranial hypertension in atypical demographics.

BACKGROUND: Idiopathic intracranial hypertension (IIH) is a condition that most often occurs in women of reproductive age with elevated body mass index (BMI) (typical patients). Individuals outside of this demographic group (atypical patients) may have a different pathophysiology underlying raised intracranial pressure (ICP) leading to unique clinical presentations and prognosis. METHODS: Retrospective chart review of patients with IIH in typical and atypical demographic groups: men, those diagnosed at age 40 or older and those with BMI <26.0 kg/m2. RESULTS: 193 typical and 50 atypical patients with IIH were included. Age at diagnosis was higher in men and patients with normal BMI (37.2 ± 11.8 and 32.3 ± 9.8 years versus 27.3 ± 5.6 years). Older patients presented with headache less often than typical patients (42.9% versus 77.2%). Opening pressure on lumbar puncture (LP) and degree of optic disc edema were not significantly different between groups, though men had worse mean deviation (MD) on visual fields (VFs) (10.16 ± 10.40 dB versus 4.52 ± 5.53 dB in typical group). There was no significant difference between the typical and atypical groups in visual outcomes including number of patients requiring surgical treatment, development of optic atrophy and presence of persistent papilledema, though a trend toward worse VF MD was seen in men. In a pooled analysis of all patients, MD on VF at presentation was the only significant predictor of final visual outcome. CONCLUSION: Men and patients with normal BMI are diagnosed with IIH later in life. Clinical presentations of typical and atypical groups are similar, although older patients report headaches less frequently. Final visual outcomes were not significantly different between typical and atypical patients and VF loss at presentation is the most consistent predictor of final visual outcome in all patients.

Horner Syndrome in Giant Cell Arteritis: Case Series and Review of the Literature.

BACKGROUND: Giant cell arteritis (GCA) is a systemic inflammatory vasculitis that affects medium- and large-sized arteries and can result in permanent vision loss. In rare instances, Horner syndrome has been noticed at the time of GCA diagnosis, although the mechanism of both diagnoses occurring at the same time is not entirely understood. We reviewed 53 charts of all patients diagnosed with biopsy-proven GCA in tertiary neuro-ophthalmology practice to find patients who presented with new onset of Horner syndrome at the time of GCA diagnosis. METHODS: Two patients with biopsy-confirmed GCA who presented with concurrent Horner syndrome were found. Data on age, sex, and ophthalmic and neuroradiologic examination findings were collected. RESULTS: Patient 1 was a 67-year-old man who presented with new onset of vertical binocular diplopia and was diagnosed with right fourth cranial nerve palsy. He then developed left ptosis and miosis, and was diagnosed with Horner syndrome by pharmacologic testing. He also had persistently elevated inflammatory markers. Patient 2 was a 71-year-old man who presented with new onset of binocular vertical diplopia, bitemporal headaches, and jaw ache. Both of his inflammatory markers were elevated. On examination, he had left ptosis and myosis, and small comitant left hypertropia. The diagnosis of left Horner syndrome was confirmed on pharmacologic testing and left hypertropia was attributed to skew deviation. Both patients underwent temporal artery biopsy, which confirmed the diagnosis of GCA. Treatment with high dose of oral corticosteroids commenced, and vertical diplopia has completely resolved in both patients. Horner syndrome persisted in Patient 1 and resolved in Patient 2. MRI and MR angiography of the brain and neck were unrevealing in both patients. CONCLUSIONS: This case series describes 2 patients with new diagnosis of GCA and concurrent Horner syndrome, with new diagnosis of likely nuclear/fascicular fourth nerve palsy in one patient and skew deviation in the other. In both patients, vasculitis presumptively affected vertebral arteries and their branches supplying the first-order sympathetic neurons in the brainstem. Considering the severe complication of permanent vision loss in GCA, this diagnosis should be considered in older patients presenting with concurrent new onset of Horner syndrome.

Ischemic ocular manifestations of giant cell arteritis: A Canadian case series.

BACKGROUND: Diagnosing giant cell arteritis (GCA) can be challenging due to the variable clinical presentation and lack of systemic symptoms in approximately 20% of cases, which are termed occult GCA. GCA affects the ocular circulation in more than half of cases and can cause irreversible bilateral blindness if not rapidly recognized and treated. We compared clinical and laboratory findings of patients with occult and systemic temporal artery biopsy (TAB)-positive GCA with ocular manifestations. METHODS: Retrospective chart review of patients with TAB-positive GCA with ocular manifestations seen at a tertiary neuro-ophthalmology practice between 2015 and 2020. RESULTS: GCA was occult in 14.3% (6/42) and systemic in 85.7% (36/42) of patients. Occult GCA affected older patients (average age 84.6 ± 5.3 vs 75.9 ± 8.2). There was no significant difference in ESR or CRP levels between two cohorts. In patients with occult GCA, 83.3% (5/6) presented with AION, and 16.7% (1/6) with isolated cranial nerve six palsy (CN6P). In the systemic GCA cohort, 47.2% (17) presented with AION, 5.6% (2) with CRAO, 2.8% (1) with PION, 2.8% (1) with isolated CWS, 2.8% (1) had both CRAO and AION, 2.8% (1) isolated cranial nerve 4 palsy (CN4P), 2.8% (1) isolated CN6P, 22.2% (8) had history of amaurosis fugax but normal examination, and 11.1% (4) had visual symptoms but a normal exam. Three of the above patients with AION also had CN4P. Of patients diagnosed with AION, presenting visual acuity in the affected eye(s) was significantly worse in patients with occult GCA. Involvement of multiple ocular circulations was seen in six patients in the systemic group but none in the occult group. CONCLUSION: Occult GCA occurs more commonly in older patients who most of the time present with AION. Levels of inflammatory markers were similar in the occult and systemic groups. Though ocular ischemic manifestations were similar in both cohorts, in systemic GCA involvement of multiple ocular circulations is likely more common GCA should always be considered in older patients who present with signs of retinal and/or optic nerve head ischemia (AION and/or CWS) and new onset of CNPs, especially in patients where more than one ocular arterial circulation is involved.

Depression and generalized anxiety symptoms in idiopathic intracranial hypertension: Prevalence, under-reporting and effect on visual outcome.

BACKGROUND: Patients with idiopathic intracranial hypertension (IIH) have been reported to have high prevalence of co-existent mood disorders. We investigated the frequency of symptoms of depression and anxiety in a large cohort of patients with IIH without a known psychiatric diagnosis and compared it with the age- and gender-matched control group. We also studied whether the presence and severity of co-existing mood disorder was related to visual outcome in patients with IIH. METHODS: The Patient Health Questionnaire-8 (PHQ-8) for depression symptoms and the Generalized Anxiety Disorder-7 (GAD-7) questionnaire for symptoms of generalized anxiety were administered via telephone survey to 100 patients with known diagnosis of IIH and 100 control subjects (matched for age and gender) who did not report a history of anxiety or depression during their prior in-person consultations. All participants were also asked whether they had ever been previously diagnosed with a mood disorder during this telephone assessment. Administered questionnaire results were correlated with final visual outcome in IIH cohort. RESULTS: 34 IIH patients and 36 controls self-reported anxiety and/or depression when specifically asked if they had ever been diagnosed with these conditions although this was not reported on clinic intake questionnaires. Mean PHQ-8 depression scale score was 6.5 ± 0.6 in control group and 7.6 ± 0.6 in IIH group (p = 0.18). Mean GAD-7 score was 6.3 ± 0.5 in control group and 7.7 ± 0.6 in the IIH group (p = 0.06). In multivariable regression, scores on both scales were correlated with higher body mass index (BMI), younger age and presence of headache, but not with IIH diagnosis. In the IIH cohort, visual outcomes were not related to GAD-7 or PHQ-8 scores but were predicted by mean deviation on visual fields at presentation. CONCLUSIONS: Pre-existing diagnosis of anxiety and depression are highly under-reported. Symptoms of anxiety and depression are very common in young women with elevated BMI and headache, however, there was no statistical difference in frequency of these symptoms between IIH and control groups. Presence and severity of mood disorder symptoms did not correlate with the final visual outcome in patients with IIH.

Papilledema: A review of etiology, pathophysiology, diagnosis, and management.

Papilledema is optic nerve head edema secondary to raised intracranial pressure (ICP). It is distinct from other causes of optic disk edema in that visual function is usually normal in the acute phase. Papilledema is caused by transmission of elevated ICP to the subarachnoid space surrounding the optic nerve that hinders axoplasmic transport within ganglion cell axons. There is ongoing controversy as to whether axoplasmic flow stasis is produced by physical compression of axons or microvascular ischemia. The most common cause of papilledema, especially in patients under the age of 50, is idiopathic intracranial hypertension (IIH); however, conditions that decrease cerebrospinal fluid (CSF) outflow by either causing CSF derangements or mechanically blocking CSF outflow channels, and rarely conditions that increase CSF production, can be the culprit. When papilledema is suspected clinically, blood pressure should be measured, and pseudopapilledema should be ruled out. Magnetic resonance imaging of the brain and orbits with venography sequences is the preferred neuroimaging modality that should be performed next to look for indirect imaging signs of increased ICP and to rule out nonidiopathic causes. Lumbar puncture with measurement of opening pressure and evaluation of CSF composition should then be performed. In patients not in a typical demographic group for IIH, further investigations should be conducted to assess for underlying causes of increased ICP. Magnetic resonance imaging of the neck and spine, magnetic resonance angiography of the brain, computed tomography of the chest, complete blood count, and creatinine testing should be able to identify most secondary causes of intracranial hypertension. Treatment for patients with papilledema should be targeted toward the underlying etiology. Most patients with IIH respond to weight loss and oral acetazolamide. For patients with decreased central acuity and constricted visual fields at presentation, as well as patients who do not respond to treatment with acetazolamide, surgical treatments should be considered, with ventriculoperitoneal shunting being the typical procedure of choice.

Visual fields and optical coherence tomography (OCT) in neuro-ophthalmology: Structure-function correlation.

Visual field (VF) testing is an essential component of the neurological examination. The differential diagnosis of VF defects depends on relating this measure of afferent visual function to the structure of the visual pathway and optical coherence tomography (OCT) is an invaluable tool for detailed structural evaluation of the optic nerve and retina. This review describes the ways in which interpretation of VF and OCT can be used together to increase the accuracy of the localization of lesions along the visual pathway. Lesions of the anterior visual pathway (originating in ganglion cells or nerve fibre layer of the retina or optic nerve) will typically produce defects that respect the horizontal midline, reflecting the arcuate path of the ganglion cell axons as they travel to the optic nerve. OCT of peripapillary retinal nerve fibre layer and ganglion cell complex (GCC) will typically demonstrate irreversible thinning in compressive and demyelinating lesions affecting anterior visual pathway. Chiasmal lesions produce highly localizable VF defects (junctional scotoma and bitemporal hemianopia) which correspond to the thinning of nasal portion of GCC. Lesions of the optic tract result in incongruous homonymous hemianopia on VF with corresponding hemianopic thinning on GCC developing within months. Lesions affecting optic radiations usually produce more congruous homonymous VF defects and can also produce homonymous thinning on GCC, however, this takes much longer to develop as trans-synaptic degeneration at the lateral geniculate body must occur.