(Papilledema) articles in PubMed
- Predictors of admission and shunt revision during emergency department visits for shunt-treated adult patients with idiopathic intracranial hypertension. [Journal Article]
- J Neurosurg 2016 Sep 23; :1-7JN
- OBJECTIVE Factors associated with emergency department admission and/or shunt revision for idiopathic intracranial hypertension (IIH) are unclear. In this study, the associations of several factors w...
OBJECTIVE Factors associated with emergency department admission and/or shunt revision for idiopathic intracranial hypertension (IIH) are unclear. In this study, the associations of several factors with emergency department admission and shunt revision for IIH were explored. METHODS The authors performed a retrospective review of 31 patients (169 total emergency department visits) who presented to the emergency department for IIH-related symptoms between 2003 and 2015. Demographics, comorbidities, symptoms, IIH diagnosis and treatment history, ophthalmological examination, diagnostic lumbar puncture (LP), imaging findings, and data regarding admission and management decisions were collected. Multivariable general linear models regression analysis was performed to assess the predictive factors associated with admission and shunt revision. RESULTS Thirty-one adult patients with a history of shunt placement for IIH visited the emergency department a total of 169 times for IIH-related symptoms, with a median of 3 visits (interquartile range 2-7 visits) per patient. Five patients had more than 10 emergency department visits. Baseline factors associated with admission included male sex (OR 10.47, 95% CI 2.13-51.56; p = 0.004) and performance of an LP (OR 3.10, 95% CI 1.31-7.31; p = 0.01). Contrastingly, older age at presentation (OR 0.94, 95% CI 0.90-0.99; p = 0.01), and a greater number of prior emergency department visits (OR 0.94, 95% CI 0.89-0.99; p = 0.02) were slightly protective against admission. The presence of papilledema (OR 11.62, 95% CI 3.20-42.16; p < 0.001), Caucasian race (OR 40.53, 95% CI 2.49-660.09 p = 0.009), and systemic hypertension (OR 7.73, 95% CI 1.11-53.62; p = 0.03) were independent risk factors for shunt revision. In addition, a greater number of prior emergency department visits (OR 0.86, 95% CI 0.77-0.96; p = 0.009) and older age at presentation (OR 0.93, 95% CI 0.87-0.99; p = 0.02) were slightly protective against shunt revision, while there was suggestive evidence that presence of a programmable shunt (OR 0.23, 95% CI 0.05-1.14; p = 0.07) was a protective factor against shunt revision. Of note, location of the proximal catheter in the ventricle or lumbar subarachnoid space was not significantly associated with admission or shunt revision in the multivariable analyses. CONCLUSIONS The decision to admit a shunt-treated patient from the emergency department for symptoms related to IIH is challenging. Knowledge of factors associated with the need for admission and/or shunt revision is required. In this study, factors such as male sex, younger age at presentation, lower number of prior emergency department visits, and performance of a diagnostic LP were independent predictors of admission. In addition, papilledema was strongly predictive of the need for shunt revision, highlighting the importance of an ophthalmological examination for shunt-treated adults with IIH who present to the emergency department.
- Gaze Evoked Deformations of the Peripapillary Retina in Papilledema and Ischemic Optic Neuropathy. [Journal Article]
- Invest Ophthalmol Vis Sci 2016 Sep 1; 57(11):4979-4987IO
- CONCLUSIONS: Horizontal eye movements affect the shape of the ppBM layer. The deformation in normals and AION, in adduction, causes posterior displacement temporal to the BMO. In contrast, the deformations in papilledema are larger, involving temporal and nasal sides, presumably because of shifts in cerebrospinal fluid pressure against the scleral flange and hydraulic stiffening of the optic nerve sheath. The clinical importance of gaze-induced deformations is unknown but repetitive motion may be a factor in the genesis or progression of a variety of optic neuropathies.
- Chronic Headaches After a Concussion in an Obese 16-Year-Old Girl. [Journal Article]
- J Dev Behav Pediatr 2016 Sep 20JD
- Jennifer is a 16-year-old Latina girl who is new to your practice. During her first well visit, she mentions that she has had daily headaches for 2 years. They began after sustaining a concussion in ...
Jennifer is a 16-year-old Latina girl who is new to your practice. During her first well visit, she mentions that she has had daily headaches for 2 years. They began after sustaining a concussion in a car accident. Typically, her headaches are bilateral and "squeezing"; they occur in the afternoons and last for a few hours. Her concussion also resulted in depressed mood, which has improved over time.When you ask if her headaches have changed recently, she says that they have been worse for the last few days. The quality and severity are unchanged; however, they now occur first thing in the morning, are worse when supine, and no longer remit. In the last 2 days, she has developed new-onset blurry vision, nausea, dizziness, photophobia, and sonophobia. Although she previously experienced sadness with her concussion, she now feels irritable. She has never used tobacco, alcohol, or drugs, and she takes no medications.On examination, her body mass index is above the 99th percentile. You note mild papilledema bilaterally. She has no focal neurological deficits. The remainder of her examination is normal.You send her to an emergency department. Her head computed tomography is normal. A lumbar puncture demonstrates an opening pressure of 32 cm H2O; she feels relief after the procedure. She is admitted with a diagnosis of benign intracranial hypertension and is started on acetazolamide. What is the differential diagnosis of chronic headaches in an obese adolescent? How should a busy community pediatrician manage Jennifer acutely? What follow-up care should Jennifer receive?
- Wernicke's encephalopathy due to hyperemesis gravidarum: Clinical and magnetic resonance imaging characteristics. [Case Reports]
- J Postgrad Med 2016 Sep 21JP
- Hyperemesis gravidarum-induced Wernicke's encephalopathy (WE) is an underestimated condition. The purpose of this study is to improve its awareness and early diagnosis. We report five cases of WE sec...
Hyperemesis gravidarum-induced Wernicke's encephalopathy (WE) is an underestimated condition. The purpose of this study is to improve its awareness and early diagnosis. We report five cases of WE secondary to hyperemesis gravidarum. Classic triad of encephalopathy, ataxia, and ocular signs was seen in four out of five patients. Two unusual features noted in this series were papilledema in one patient and severe sensory-motor peripheral neuropathy in one patient. Magnetic resonance imaging (MRI) was abnormal in all the five patients, and high signal in medial thalamus and surrounding the aqueduct was the most common abnormality (5/5). Involvement of caudate nucleus was seen in two patients with severe psychosis, and two patients had bilateral cerebellar peduncle involvement. Median time delay between onset of neurological symptoms and diagnosis was 7 days. All patients improved with thiamine, but minor sequelae were seen in four patients at 12 months follow-up. One patient had a fetal demise. Hyperemesis gravidarum-induced WE is a common cause of maternal morbidity. Typical MRI findings of symmetric medial thalamic and periaqueductal signal changes may permit a specific diagnosis. A delay in diagnosis, therefore treatment, leads to worse prognosis.
- ED 08-4 DIAGNOSIS AND TREATMENT OF HYPERTENSIVE EMERGENCY IN CHILDREN. [Journal Article]
- J Hypertens 2016; 34 Suppl 1:e373-4JH
- According to the seventh report of Joint National Committee (JNC 7), hypertensive emergency (HE), a kind of hypertensive crisis, is defined as a sudden and abrupt elevation in blood pressure so as to...
According to the seventh report of Joint National Committee (JNC 7), hypertensive emergency (HE), a kind of hypertensive crisis, is defined as a sudden and abrupt elevation in blood pressure so as to cause acute target organ dysfunctions, including central nervous system, cardiovascular system or kidneys. Patients with HE require immediate reduction in markedly elevated blood pressure. Currently, there are no international guidelines for children HE, so the JNC definition is commonly used. Hypertensive emergency in children is rare but a life-threatening emergency. Generally, secondary hypertension is the most common reason of hypertensive emergency. We analyzed clinical features of 16 patients with HE who were diagnosed as HE from Jan 2007 to Dec 2015 in our hospital. Results showed that all patients were diagnosed as secondary hypertension, including 10 cases associated with renal diseases, 3 cases with Takayasu arteritis,1case with hypercortisolism, 1 case with migraine, and 1 case with unknown reason. The pathophysiologic mechanisms of HE involve sympathetic hyperactivity and increasing of vasoconstricting substances, activation of renin-angiotensin system (RAS), decreasing in auto-regulation of target organs, and chronic endothelial damage and remodeling. There is strong evidence that the renin-angiotensin system plays an important role in the genesis of hypertensive crisis. Target organ dysfunctions may be manifested as hypertensive encephalopathy, acute left ventricular failure, acute renal failure and papilledema, etc. Hypertensive encephalopathy is the most common one with the symptoms of persistent headache, nausea, vomiting, altered mental status, convulsion and coma. Some patients may be revealed as reversible posterior leukoencephalopathy. Among 16 patients involved in our study, 13 patients had encephalopathy with 4 cases of reversible posterior leukoencephalopathy, 4 patients had acute heart failure with 1 case of fundus exudation, and 2 case of acute renal failure. 2 patients died with 3 target organ dysfunctions, including encephalopathy, acute heart failure, and acute renal failure, which showed that multiple organ dysfunction may increase the mortality of HE, so earlier identification of target organ dysfunction to take steps is important. As to the key points of diagnosis of HE, one is the level of blood pressure and its elevation speed, the other is to identify target organ dysfunction earlier. Detailed medical history and complete physical examination are important. Additionally, serum electrolytes, complete blood counts, blood urea nitrogen, creatine, urinalysis, chest radiography, electrocardiogram, enchocardiography, brain MRI and fundoscopy may be needed in some situation. It is worth mentioning that 8 patients had hypokalemia, and hypokalemia is associated with the activation of RAS. It indicates the possibility that hypokalemia may be a predictive factor of HE. The treatment of HE is based on the differentiation of acute, chronic or acute attack on chronic hypertension. Once HE is confirmed, intravenous drugs should be emergently applied. It is suggested that the targeted drop of mean arterial pressure in the first 6∼8 hours should reach 25% of the difference between the original value and the target value, and should be followed by a gradual reduction to the target value within 24∼48 hours. Safe and efficacious drugs with rapid onset of action are favorable. According to our experience, sodium nitroprusside and phentolamine are the most useful and effective in our hospital. It's notable that lowering intracranial pressure is more important than decreasing blood pressure for those patients with a high intracranial pressure who are diagnosed as encephalopathy. However, rapidly decreasing blood pressure levels may result in decreasing blood flow of brain, causing ischemia and infarction. To patients with acute left heart failure, management including sedation, oxygen supplement, cardiotonics, diuresis, and vascular dilation should be necessary. Long-acting oral anti-hypertensive medications should be introduced in conscious child after the blood pressure has been reasonably controlled within 24-48 hours. According to our experience, these patients with HE should need more than 2 kinds of anti-hypertensive drugs. In summary, the key points of diagnosis and treatment of HE are earlier identification and effective therapy to control the development of acute target organ dysfunctions.
- Idiopathic intracranial hypertension following surgical treatment of Cushing disease: case report and review of management strategies. [Journal Article]
- World Neurosurg 2016 Sep 12WN
- CONCLUSIONS: Symptomatic IIH is very rare in adult patients, but can be severe and result in permanent vision loss. A high index of suspicion should be maintained and a fundus exam is necessary to exclude papilledema, whenever there are suggestive symptoms that initially may overlap with AI. It is possible that some cases of mild IIH are misdiagnosed as GC withdrawal and/or AI, however further studies are needed. Treatment consists of re-initiation of higher steroid doses together with acetazolamide with or without cerebrospinal fluid diversion and the priority is to preserve vision and reverse any visual loss.
- [Optic disc swelling : A compilation of relevant differential diagnoses]. [Journal Article]
- Ophthalmologe 2016 Sep 13O
- Optic disc oedema describes blurred optic disc margins. It describes an unspecific clinical sign with various possible underlying causal mechanisms. The correct diagnosis and the detection of the und...
Optic disc oedema describes blurred optic disc margins. It describes an unspecific clinical sign with various possible underlying causal mechanisms. The correct diagnosis and the detection of the underlying disease is however of special clinical importance. This article summarizes the most important differential diagnoses and gives advice to find the correct diagnosis.
- Pseudo-Foster Kennedy Syndrome as a Rare Presentation of Vitamin B12 Deficiency. [Journal Article]
- Iran Red Crescent Med J 2016; 18(6):e24610IR
- CONCLUSIONS: Demyelinating disease, anterior ischemic optic neuropathy, non-arteritic anterior ischemic optic neuropathy, autoimmune disease, and hereditary optic neuropathy could cause optic neuropathy. Normal CBC parameters and the absence of clinical manifestations of vitamin B12 deficiency could not rule out its diagnosis. Careful physical examinations and history-taking with a classical approach led us to the diagnosis of vitamin B12 deficiency and its treatment.
- Analysis of Potential Ischemic Effect of Intravitreal Bevacizumab on Unaffected Retina in Treatment-Naïve Macular Edema Due to Branch Retinal Vein Occlusion: A Prospective, Interventional Case-Series. [Journal Article]
- PLoS One 2016; 11(9):e0162533Plos
- CONCLUSIONS: This study analysed the effects with a single injection of bevacizumab. However, whether ischemic adverse effects will emerge with repeated IVB injections as a consequence of cumulative dosing needs further investigation. The setting of our study being a tertiary care centre, the numbers of fresh BRVO cases without prior intervention were limited. Thus, the limitations of our study include a small sample size with a small follow-up period. No major ocular/systemic adverse event was observed in the study period.No evidence of progressive ischaemia attributable to single bevacizumab treatment was observed in this study. However, a larger prospective study involving subjects with cumulative dosing of bevacizumab and a longer follow-up could provide a better understanding of the potential ischaemic effects of bevacizumab or other anti-VEGF agents.
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- Starling resistors, autoregulation of cerebral perfusion and the pathogenesis of Idiopathic Intracranial Hypertension. [Journal Article]
- Panminerva Med 2016 Sep 6PM
- Two critical functions for the control of intracranial fluids dynamics are carried on the venous side of the perfusion circuit: the first is the avoidance of cortical veins collapse during the physio...
Two critical functions for the control of intracranial fluids dynamics are carried on the venous side of the perfusion circuit: the first is the avoidance of cortical veins collapse during the physiological increases of cerebrospinal fluid (CSF) pressure in which they are immersed. The second, is the generation of an abrupt venous pressure drop at the confluence of the cortical veins with the dural sinuses that is required to allow a CSF outflow rate balanced with its production. There is evidence that both of these effects are ensured by a Starling resistor mechanism (a fluid dynamic construct that governs the flow in collapsible tubes exposed to variable external pressure) acting at the confluence of cortical veins in the dural sinus. This implies that, in normal circumstances of perfusion balance, a certain degree of venous collapse physiologically occurs at the distal end of the cortical vein. This is passively modulated by the transmural pressure of the venous wall (i.e. the difference between internal blood pressure and external CSF pressure). The mechanism provides that the blood pressure of the cortical vein upstream the collapsed segment is dynamically maintained a few mmHg higher than the CSF pressure, so as to prevent their collapse during the large physiological fluctuations of the intracranial pressure. Moreover, the partial collapse of the vein confluence also generates a sharp pressure drop of the blood entering into the sinus. The CSF is drained in dural sinus through arachnoid villi proportionally to its pressure gradient with the sinus blood. The venous pressure drop between cortical veins and dural sinus is therefore needed to ensure that the CSF can leave the cranio-spinal space with the same speed with which it is produced, without having to reach a too high pressure, which would compress the cortical veins. Notably, the mechanism requires that the walls of the dural sinuses are rigid enough to avoid the collapse under the external cerebrospinal fluid pressure, and predicts that in the presence of excessively flexible dural sinuses, the system admits a second point of balance between cerebral fluid pressure and dural sinus pressure, at higher values. The second balance state is due to the triggering of a self-limiting venous collapse feedback loop between the CSF pressure, that compresses the sinus, and the subsequent increase of the dural sinus pressure, that further raises the intracranial pressure. The loop may stabilize only when the maximum stretching allowed by the venous wall is reached. Then, a new relatively stable and self-sustaining balance state is achieved, at the price of a higher CSF and dural sinus pressure values. We propose that this model is crucially involved in Idiopatic Intracranial Hypertension pathogenesis with and without papilledema, a condition that could be described as a pathological new balance state, relatively stable, between intracranial and dural venous pressure, at higher absolute values.