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RATIONAL: Coronaviruses are RNA viruses that primarily affect the respiratory system. Patients with Coronavirus Disease-19 (COVID-19) pneumonia and respiratory distress often require hospitalization, ICU admission, intubation and/or non-invasive ventilation, and circulatory support. Some experts suggest that the pathophysiology of traditional ARDS and that of the lung disease associated with COVID-19 are different. It is proposed that the severe hypoxemia in COVID-19 patients is the result of hypoxia-induced vasoconstriction and a large burden of microthrombi which result in intrapulmonary shunting. Therefore, COVID-related ARDS-like patterns of disease may not respond to World Health Organization (WHO) recommendations for early intubation and ARDS Network (ARDSNet) recommendations for FiO2-titrated Positive End-Expiratory Pressure (PEEP) administration and ventilator support. Given the distinct pathophysiology of COVID-19-related ARDS, higher PEEP may indicate mechanical over-inflation of the alveoli resulting in volume trauma in addition to compromising preload and decreasing cardiac output, worsening the pulmonary hypoperfusion. The aim of this study was to examine the rate of death associated with initial and subsequent (48-hour) PEEP settings of 10cmH2O and higher in COVID-19 patients. We hypothesized that higher PEEP settings may lead to increased mortality. METHODS: We conducted a retrospective chart review of patients who presented or were transferred to our facility with COVID-19 and were subsequently intubated from March 1st until April 30th, 2020. Charts were reviewed for initial and 48-hour PEEP settings. Mortality, SARS CoV2 results, clinical data and demographics were also recorded. RESULTS: A total of 74 patients were included in the review. Of these, 53 patients had initial PEEP setting of >10cmH2O and 46 patients had PEEP settings >10cmH2O 48 hours after intubation. Thirty-seven patients had PEEP settings >10cmH2O both initially and 48 hours later. Thirty-seven patients who had an initial PEEP setting of >10 cmH220 died, (70%). Forty patients who had PEEP settings >10cmH2O at 48hrs died (87%). Twenty-seven patients who had both a PEEP setting >10 cmH2O initially and at 48 hours died (73%). CONCLUSIONS: There appears to be an association in COVID-19 patients between high mortality rates and high PEEP settings. The marked association is strong enough, in our view, to suggest that conventional ventilator settings recommended by ARDSNet may not apply to patients experiencing COVID-19-associated ARDS and in fact, may be leading to worse patient outcomes.

Background: B-type natriuretic peptide (BNP) is a hormone secreted by cardiomyocytes in response to myocardial ischemia, increased ventricular wall tension, and overload. BNP is utilized as a diagnostic and prognostic marker in congested heart failure (CHF). Its prognostic value in sepsis is unknown. The aim of this study is to determine if BNP correlates with increased in-hospital mortality for septic patients. Methods: This was a retrospective study of 505 patients admitted for sepsis or severe sepsis or septic shock during the period of January 2013 and August 2014. Patients that received > 3 L of intravenous fluids on presentation were included. Intensive care unit length of stay (ICULOS), hospital length of stay (HLOS) and in-hospital mortality were measured. Mean BNP level was calculated and compared to ICULOS and HLOS and in-hospital mortality. Controlled variables included ejection fraction (measured by echocardiogram within 6 months of presentation), glomerular filtration rate (calculated by Cockroft-Gault equation), patient demographics, and lactic acid trends. Exclusion criteria were no echocardiogram within 6 months of admission, no BNP levels on admission, and no repeat lactate or rising lactate levels within 24 h to indicate worsening sepsis. Results: Patients’ mean BNP with in-hospital mortality was 908 pg/mL as compared to mean BNP of 678 pg/mL in survivors. T-test comparisons were statistically significant (P = 0.0375). The Kaplan-Meier curve for BNP as a predictor for in-hospital mortality showed that for the first 25 days, patients with BNP higher than 500 pg/mL had a higher mortality than patients with BNP lower than 500 pg/mL. When comparing HLOS, there is a statistically significant correlation (P = 0.0046). A similar scatter plot was prepared for ICULOS which showed there was a weak positive correlation (r = 0.199). Conclusion: Septic patients with in-hospital mortality had an average BNP of 908 pg/mL and statistically significant higher HLOS. Cardiol Res. 2017;8(6):271-275 doi: https://doi.org/10.14740/cr605w

Duchenne muscular dystrophy (DMD) is characterized by degeneration and atrophy of skeletal, cardiac, and smooth muscles after a latent period of apparently normal development and function. The gastrointestinal manifestations start in the second decade of life and are mainly due to atrophy of smooth muscle layers. Refractory gastroparesis and chronic constipation can lead to severe gastric and small bowel dilatation, which can be life threatening. Here, we present a case of a 21-year-old male with a gigantic stomach secondary to DMD resolved with conservative management and no surgical intervention.

Parkinson’s disease (PD) and dementia with Lewy bodies (DLB) are neurodegenerative disorders of the aging population characterized by the accumulation of α-synuclein (α-syn). The mechanisms triggering α-syn toxicity are not completely understood, however, c-terminus truncation of α-syn by proteases such as calpain may have a role. Therefore, inhibition of calpain may be of value. The main objective of this study was to evaluate the effects of systemically administered novel low molecular weight calpain inhibitors on α-syn pathology in a transgenic mouse model. For this purpose, non-tg and α-syn tg mice received the calpain inhibitors - Gabadur, Neurodur or a vehicle, twice a day for 30 days. Immunocytochemical analysis showed a 60% reduction in α-syn deposition using Gabadur and a 40% reduction using Neurodur with a concomitant reduction in c-terminus α-syn and improvements in neurodegeneration. Western blot analysis showed a 77% decrease in α-spectrin breakdown products (SBDPs) SBDPs with Gabadur and 63% reduction using Neurodur. There was a 65% reduction in the active calpain form with Gabadur and a 45% reduction with Neurodur. Moreover, treatment with calpain inhibitors improved activity performance of the α-syn tg mice. Taken together, this study suggests that calpain inhibition might be considered in the treatment of synucleinopathies.

Synthetic cannabinoids Receptor Agonist (SCRA) intoxication presents with various medical and psychiatric symptoms. The products are sold as K2 or Spice. The symptoms range from agitation, altered mental status (AMS), lethargy, paranoid behavior, psychosis and seizures. In some cases, brief psychiatric or inpatient medicine admission was required for stabilization. Some patients seem to stay longer for observation in the ED. These patients worsen the already problematic ED crowding. To assess K2-related ED presentation, length of stay in the ED and types of disposition over a 5 year period. A retrospective chart review of patients who presented with K2 intoxication. Charts were reviewed from January 1, 2012 until December 31st, 2016 excluding 2016. Demographics, age, gender, past psychiatric illness and other substance abuse history were reviewed. A total of 1405 patients were seen for K2-related ED visits from January 1, 2012 until December 31st, 2016 of which 1279 patients (91%) were male and 126 patients (9%) were female. One hundred thirty nine patients (9.9%) were hospitalized and 1266 patients (90.1%) were either discharged or left from the ED. Twenty-eight (2.0%) stayed more than 16 hours in the ED. Of the 53 patients, whose urine the showed benzodiazepine or opiates 36 patients stayed more than 6 hours in the ED. Most patients with K2 use were male (91%) between the ages of 19 and 50 years (76.4%). There was a surge in K2-related presentation in 2015, particularly in the months of April until November. In addition, K2-related intoxication led to prolonged ED stay, which could affect the ED crowding phenomenon. A concerted effort from public pressure and legislative measures led to a reduction of K2-related visits to the ED.

One aspect of secondary injury in traumatic brain injury is the marked increase in intracellular calcium and resultant over-activation of the calcium-dependent neutral cysteine protease calpain. Gabadur is a novel protease inhibitor with calpain-inhibition properties formulated from the classic protease inhibitor leupeptin linked to a pregabalin carrier. This construction allows the entire compound to cross the blood-brain barrier after peripheral administration to better target the site of injury. In this study, a single intraperitoneal dose of Gabadur was administered immediately following controlled cortical impact injury in rats. Neocortical slices were examined at 48 h post-injury via Fluoro-Jade B staining, revealing an improvement in cortical neurodegeneration in Gabadur treated rats. Levels of detrimental active calpain-2 measured via western blot were also decreased in rats receiving Gabadur. This data supports the benefit of targeted protease inhibition in the treatment of traumatic brain injury.

Background Initial serum potassium (K+) in diabetic ketoacidosis (DKA) often does not reflect the true amount of total body K+ storage, and it is not a good predictor of subsequent hypokalemia. In this study, we tested the hypothesis that a deficiency of the total body K+ storage can be detected initially on surface electrocardiography (ECG). Method Medical records of 350 patients with a diagnosis of DKA were reviewed. Data regarding serial basic metabolic panels, arterial blood gases, serum ketones, and total K+ replacement that patient received during admission were collected. We compared biochemical findings for patients with and without QTU corrected (QTUc) prolongation by using the t test. Patients who were taking medications known to affect QTUc or cause ST-T changes were excluded. Results After exclusion criteria, 61 patients were enrolled in this study. In 38 patients (62.9%), QTUc was more than or equal to 450 milliseconds. Patients with prolonged QTc received statistically more K+ supplementation during admission ( P = .014). They also had lower serum K+ level during their hospital course ( P = .002) compared to patients with normal QTUc intervals. No significant difference was found between initial serum K+, calcium, glucose, anion gap, acidosis, age, or heart rate between these 2 groups. Conclusion The significant relationship between K+ depletion and the ECG changes observed in this study deserves further consideration. Our findings confirm the concept that the ECG is an easy and reliable tool for early diagnosis of hypokalemia in patients with DKA.

Introduction: The burden of stroke is increasing in many low- and middle-income countries. In Ethiopia, stroke has become a major cause of morbidity, long-term disability, and mortality. Time from stroke onset to hospital presentation is a critical factor in acute stroke care. This study aimed to describe risk factors for stroke and clinical presentation of patients presenting to the emergency centre with stroke. Methods: We conducted a cross sectional study conducted from August 2015 to January 2016 in an urban tertiary care centre in Addis Ababa, Ethiopia. Descriptive statistics and multivariable logistic regression models were used to evaluate associations between stroke types and stroke risk factors, and delayed presentation and clinical indicators. P-values less than .05 were considered statistically significant. Results: A total of 104 patients were included. The mean age was 53 years, and 56% were male. Only 30% of patients arrived using an ambulance service. The most common presenting symptoms were altered mental status (48%), hemiparesis (47%), facial palsy (45%), hemiplegia (29%), and aphasia (25%). Hypertension was the most common risk factor (49%), followed by cardiovascular disease (20.2%) and diabetes mellitus (11%). The majority of strokes were haemorrhagic in aetiology (56%). The median arrival time to the emergency centre was 24 h after symptoms onset; only 15% presented within three hours. Patients with hypertension, or presented with loss of consciousness were significantly more likely to have haemorrhagic stroke (p

Although a diagnosis of acute myocardial infarction (AMI) that mandates emergency reperfusion therapy requires ST-segment elevation greater than 1 mm in at least 2 contiguous leads, some of the early electrocardiogram (ECG) changes of AMI can be subtle. Any ST-segment depression or T-wave inversion in lead aVL may be implicated in left anterior descending artery lesion or early reciprocal changes of inferior wall myocardial infarction, particularly when the clinical context suggests ischemia. Early recognition of reciprocal changes and serial ECG help initiate early appropriate intervention. Heightened awareness of ST segment and T-wave changes in lead aVL is of paramount importance to quickly identifying life-threatening condition.

Introduction: Contrast-induced nephropathy (CIN), defined as an increase in serum creatinine (SCr) greater than 25% or ≥0.5 mg/dL within 3 days of intravenous (IV) contrast administration in the absence of an alternative cause, is the third most common cause of new acute renal failure in hospitalized patients. It is known to increase in-hospital mortality up to 27%. The purpose of this study was to investigate the rate of outpatient follow up and the occurrence of CIN in patients who presented to the emergency department (ED) and were discharged home after computed tomography (CT) of the abdomen and pelvis (AP) with IV contrast. Methods: We conducted a single center retrospective review of charts for patients who required CT of AP with IV contrast and who were discharged home. Patients' clinical data included the presence of diabetes mellitus, hypertension, chronic kidney disease (CKD) and congestive heart failure (CHF). Results: Five hundred and thirty six patients underwent CT of AP with IV contrast in 2011 and were discharged home. Diabetes mellitus was documented in 96 patients (18%). Hypertension was present in 141 patients (26.3%), and 82 patients (15.3%) were on angiotensin-converting-enzyme inhibitors (ACEI). Five patients (0.9%) had documented CHF and all of them were taking furosemide. Seventy patients (13%) had a baseline SCr >1.2 mg/dL. One hundred fifty patients (28%) followed up in one of the clinics or the ED within one week after discharge, but only 40 patients (7.5%) had laboratory workup. Out of 40 patients who followed up within 1 week after discharge, 9 patients (22.5%) developed CIN. One hundred ninety patients (35.4%) followed up in one of the clinics or the ED after 7 days and within 1 month after discharge, but only 71 patients (13.2%) had laboratory workup completed. Out of 71 patients who followed up within 1 month, 11 patients (15%) developed CIN. The overall incidence of CIN was 15.3% (17 out of 111 patients). Conclusion: There was a poor outpatient follow up after CT of AP with IV contrast and biochemically CIN appears to be present in some patients. Unlike previous reports that CKD is the major risk factor for CIN, our results demonstrated that risk factors such as advanced age, DM and hypertension seem to predispose patients to CIN rather than abnormal baseline SCr. [West J Emerg Med. 2014;15(3):276–281.]

The electrocardiogram (ECG) is the most important diagnostic tool for acute myocardial infarction (AMI). T wave inversion (TWI) in lead aVL has not been emphasized or well recognized.This study examined the relationship between the presence of TWI before the event and mid-segment left anterior descending (MLAD) artery lesion in patients with AMI.Retrospective charts of patients with acute coronary syndrome between the months of January 2009 and December 2011 were reviewed. All patients with MLAD lesion were identified and their ECG reviewed for TWI in lead aVL.Coronary angiography was done on 431 patients. Of these, 125 (29%) had an MLAD lesion. One hundred and six patients (84.8%) had a lesion50% and 19 patients (15.2%) had a lesion50%. Of the 106 patients who had a MLAD lesion50%, 90 patients (84.9%) had TWI in lead aVL and one additional lead. Of the 19 patients who had an MLAD lesion50%, 8 patients (42.1%) had TWI in lead aVL and one additional lead. Isolated TWI in lead aVL had an overall sensitivity of 76.7% (95% confidence interval [CI] 0.65-0.86), a specificity of 71.4% (95% CI 0.45-0.88), a positive predictive value of 92%, a negative predictive value of 41.7%, a positive likelihood ratio of 2.7 (95% CI 1.16-6.22), and negative likelihood ratio of 0.32 (95% CI 0.19-0.58) for predicting a MLAD lesion of50% (p = 0.0011).TWI in lead aVL might signify a mid-segment LAD lesion. Recognition of this finding and early appropriate referral to a cardiologist might be beneficial. Additional studies are needed to validate this finding.

Background In clinical practice, we progressively rely on biomarkers, without estimating the pretest probability. There is not enough support for the use of cardiac troponin (cTn) I in the management of noncardiac patients. We studied the rate at which this test was ordered, the prevalence of detection of a positive result in noncardiac patients, and the impact of this incidental finding on clinical management. Methodology Patients admitted from December 2011 to 2013 to our community hospital with diagnosis of noncardiac disease who had positive cTn were included. Data collected included final diagnosis, patient disposition, cardiac monitoring, cardiology consult, and cardiac biomarker testing. Results Cardiac troponin I was ordered for 1700 patients in our emergency department. Seven hundred fifty patients had a positive cTn. Of the 750 patients, 412 had a positive cTn without any clinical suspicion of an acute coronary syndrome. An incidental finding of a positive cTn leads to ordering of cTn on average 4 times during admission, cardiac monitoring of 379 (91.99%) patients for at least 1 day, and a cardiac consultation for 268 (63.65%) of these patients. None of these patients was candidates for an invasive cardiac intervention. Seventy-eight (19.17%) patients were admitted to the cardiac care unit and subsequently transferred to the medical intensive care unit. Conclusions A positive cTn in patients diagnosed with a nonacute coronary syndrome was associated with increased cardiac biomarker testing, telemetry monitoring, and cardiology consults. This study supports adherence to national guidelines for the use of cTn, to reduce hospital cost and resource utilization.

Measurement of optic nerve sheath diameter (ONSD) using point of care ultrasound has been used to indirectly assess the intracranial pressure (ICP) particularly in conditions where it is raised. Direct pressure measurements using probes reaching the ventricle system correlated with ONSD using ultrasound. Attempts were made to measure the ONSD pre and post lumbar puncture (LP) after draining cerebrospinal fluid (CSF) as well as post ventricular shunt placement. We report ONSD measurement and demonstrate dynamic changes during LP in a patient with known idiopathic intracranial hypertension (IIH).

Background: The objective of this study was to determine whether a combination of nebulized albuterol and ipratropium with warmed humidified oxygen would be more beneficial when compared to the same combination with humidified oxygen at room temperature. Albuterol alone was tested in the same settings. Methods: All patients between 6 and 17 years of age who presented to a pediatric emergency department in the winter months with acute exacerbation of bronchial asthma were given a combination of nebulized albuterol and ipratropium with warmed or room temperature humidified oxygen. Peak flow was measured before and after the treatment. Results: Sixty patients were enrolled in the study, with 15 subjects in each group. The mean increase in peak flow in the albuterol-ipratropium with warm humidified oxygen group was 52.6, and in the albuterol-ipratropium with humidified oxygen at room temperature group, it was 26.2. The results of the albuterol with warmed humidified oxygen and with humidified oxygen at room temperature groups were 20.6 and 34.3, respectively. The differences between the groups were statistically significant. Conclusion: Our study shows that warmed humidified oxygen given along with the combination of nebulized albuterol and ipratropium is more beneficial for pediatric patients having an acute exacerbation of bronchial asthma in the winter months when compared to nebulized albuterol alone with warmed humidified oxygen, nebulized albuterol alone with room temperature humidified oxygen, or a combination of nebulized albuterol and ipratropium with room temperature humidified oxygen.

Axonal injury is the major correlate of permanent disability in neurodegenerative diseases such as multiple sclerosis (MS), especially in secondary-progressive MS which follows relapsing-remitting disease course. Proteolytic enzyme, calpain, is a potential candidate for causing axonal injury. Most current treatment options only target the inflammatory component of MS. Previous work using calpain inhibitor CYLA in our laboratory showed significant reduction in clinical sign, demyelination and tissue calpain content in acute experimental autoimmune encephalomyelitis (EAE). Here we evaluated markers of axonal injury (amyloid precursor protein, Na(v)1.6 channels), neuronal calpain content and the effect of CYLA on axonal protection using histological methods in chronic EAE [myelin oligodendrocyte glycoprotein (MOG)-induced disease model of MS]. Intraperitoneal application of CYLA (2 mg/mouse/day) significantly reduced the clinical signs, tissue calpain content, demyelination and inflammatory infiltration of EAE. Similarly, markers for axonal injury were barely detectable in the treated mice. Thus, this novel drug, which markedly suppresses the disease course, axonal injury and its progression, is a candidate for the treatment of a neurodegenerative disease such as multiple sclerosis.

We report here 2 cases of methadone induced Torsades de Pointes with a clinical presentation mimicking convulsive seizures in a substance abuser. These cases highlight the importance of being aware of methadone-induced Torsades de Pointes and the occasional atypical clinical presentations of this condition.

Synthetic cannabinoids (SC) have exploded on to the scene. With this rise in SC use, the number of complications and potential adverse effects are also well documented in the literature and is on the rise. The most frequently cited side effects are behavioral in nature and range for severe agitation to psychosis and delirium. We report a case of hyperthermia with severe rhabdomyolysis from SC use. Over the past several years, especially during summer months, synthetic cannabinoids (SC) have exploded onto the scene. Their ease of availability, cloudy legal status, and relatively cheap price make them a popular substance among teens and young adults [1-3]. These SC are often referred to as “K2” or “spice.” With this rise in SC use, the number of complications andpotentialadverse effects are alsowell documented in the literature [3-5]. The most frequently cited side effects are behavioral in nature and range from severe agitation to psychosis and delirium. In popular media, there have been multiple highly publicized cases of deaths directly linked to use of K2 and spice. A 27-year-old African American male with a history of schizophre

Subdural hematoma (SDH) is a rare, but life-threatening complication of spinal anesthesia. Subdural hematoma resulting from this procedure could present with vague symptoms such as chronic headache and could easily be missed. Chronic headache is one of the symptoms of chronic SDH in postpartum women. Diplopia as the presenting complaint in SDH secondary to peripartum spinal anesthesia has not, to our knowledge, been previously reported. Here, we report a case of diplopia secondary to postpartum subacute bilateral SDHs with transtentorial herniation after spinal anesthesia in a healthy primagravid 25-year-old woman. SDH can expand gradually and the initial symptoms might be subtle as in our case, despite critically high intracranial pressure. [West J Emerg Med. 2012;13(1):108–110.]

Background: Wellens’ sign (WS) has been reported as a sign of critical proximal left anterior descending (PLAD) artery lesion with lumen narrowing greater than 90%. Wellens’ ECG signs for critical PLAD lesion are characterized by two different electrocardiogram (ECG) patterns: 1) Deep T wave inversion in leads V2, V3 (approximately 76% of cases); and 2) Biphasic T wave in leads V2, V3 (approximately 24% of cases). The prevalence of the ECG feature of WS ranges from 14-18%. The prognostic significance of WS in detecting significant coronary artery lesion defined as a luminal narrowing of the coronary vessel by more than 70% has not been well studied. Our study’s goal was to evaluate if WS is present in all patients with critical and significant PLAD lesions and is a sensitive or specific sign for critical and significant (>70% stenosis) PLAD lesions. Methods: All patients that underwent percutaneous coronary intervention (PCI) at an urban community hospital between January 2009 and December 2011 were included in the study. Log books from the cardiac catheterization laboratory were reviewed for all lesion types and corresponding demographics. The ECGs of patients with PLAD lesion were reviewed for T wave changes in precordial leads. Additionally, demographics such as age, gender and cardiovascular risk factors were recorded and analyzed. Descriptive statistics were used to analyze the data. Results: A total of 431 patients underwent PCI [emergent PCI 152 (35.3%), elective PCI 279 (64.7%)]. A total of 78 patients (18.1%) from both groups were found to have PLAD lesion. Fifty eight patients were male and 20 patients were female. The average age was 63.7 years. Critical PLAD lesion was present in 26 patients (33.3%) and 52 patients (66.7%) had PLAD lesion less than 90%. Of the 26 patients, 17 (65.4%) had WS. Wellens’ sign for predicting a critical PLAD had a sensitivity of 65.4%, a specificity of 69.2%, a positive predictive value (PPV) of 51.5% and a negative predictive value (NPV) of 80% (p = 0.0069, two-tailed Fisher’s exact test). Of the 42 patients who had PLAD lesion greater than 70%, 21 patients (50%) had WS. Of the 36 patients who had PLAD lesion less than 70%, 11 patients (30.6%) had WS. Wellens’ sign for predicting significant PLAD lesion in this cohort has a sensitivity of 50%, a specificity of 69.4%, a PPV of 65.6% and a NPV of 54.3% ( p = 0.1074). Conclusion: Our results corroborated prior studies showing that WS predicts the presence of critical (90%) PLAD lesion. Unfortunately, the value of WS for detecting/predicting significant CAD in PLAD was weak. Our results indicated that we were not able to predict the presence of significant (70%) PLAD lesion using WS. However, in appropriate clinical settings such as Non-ST elevation MI (NSTEMI) or unstable angina, Wellens’ sign may indicate the need for a more aggressive treatment strategy with patients proceeding to the cardiac catheterization suite sooner than later.

Background Approximately 2% of angioedema (AE) patients have a hereditary or an acquired deficiency of the complement 1 (C1) esterase inhibitor (C1 INH) gene. Some case reports indicate an association between angiotensin-converting enzyme inhibitor (ACEI) use and exacerbation of hereditary AE (HAE). Objective The aim of this retrospective study is to investigate the association between HAE and ACEI use in a larger patient population. Methods A retrospective chart review of patients who presented with AE and patients with diagnostic serum assays for functional C1 INH, C1 INH antigenic protein, C1q, C1q immune complex (C1q IC), and complement 4 (C4) regardless of medical complaint. Descriptive statistics were used to analyze the data. Results A total of 1594 patients had complement levels measured (136 C1 INH, 55 C1q, 10 C1q IC, and 1500 C4), of which 156 (9.7%) patients presented with AE. Angiotensin-converting enzyme inhibitor use was documented in 747 (47%) patients. Low C1 INH was detected in one patient with recurrent AE who was not taking ACEI. Another patient who presented with recurrent AE was found to have systemic lupus erythematosus with abnormal C4, C1q, and C1q IC, but normal C1 INH. A low C4 level was present in 94 patients, 4 of which had AE. Conclusions The risk of exacerbating HAE by ACEI might be present, but we did not find any association in this retrospective study. Further studies are needed to determine the existence of this association.

After an acute ischemia/reperfusion of the rat retina, the activation of cytotoxic proteases, including calpain, results in necrosis and apoptosis of retinal ganglion cells resulting in their degeneration. Using a systemically administered calpain inhibitor that crosses the blood-retinal barrier would provide for novel systemic intervention that protects the retina from acute injury and loss of function. Herein, we study a novel calpain peptide inhibitor, cysteic-leucyl-argininal (CYLA), in an in-vivo rat model of retinal ischemia to determine functional protection using electroretinography. The CYLA prodrug was administered intraperitoneally before and/or after ischemia-reperfusion at concentrations of 20-40 mg/kg. We found that administering 20 mg/kg of CYLA only after ischemia provides significant preservation of retinal function.

Increased anterior chamber pressure also known as intraocular pressure can result from conditions such as glaucoma and trauma. The pressure in the anterior chamber is measured using tonometer. Measurement of the intraocular pressure is essential, as it requires immediate medical attention to alleviate pain and to avoid temporary or permanent damage to intraocular structures. Bedside ocular ultrasound (US) has gained popularity in recent years. It has been used to assess intracranial pressure via optic nerve sheath diameter (ONSD) and evaluate retinal detachment, vitreous hemorrhage, or pupillary reflex in a trauma patient. We report 2 cases of patients with glaucoma and a case of a patient with trauma to the eye with swelling. Anterior chamber depth measurement was conducted and compared with measurements of intraocular pressure (IOP) using a tonometer.

In ischemic preconditioning (IPC), brief sublethal ischemia protects neurons from a subsequent lethal ischemia. In vivo models faithfully display preconditioning, yet, these models are technically challenging, time-consuming and expensive. In vitro models of preconditioning have also been developed that are technically easier and less expensive. A drawback of pre-existing in vitro models is that since susceptibility to ischemic injury is age-dependent; neuroprotection is being studied in neurons that have intrinsic resistance to oxygen-glucose deprivation (OGD). This study introduces a new in vitro model of ischemic preconditioning in hippocampal slice cultures isolated from 20-30-day-old rats. Slice cultures show a high susceptibility and sharp thresholds toward ischemia that is comparable to that found in vivo. A 5-min OGD treatment was not neurotoxic to young adult slice cultures, while a 10-min OGD treatment was neurotoxic. In addition, the sublethal 5-min OGD treatment protected against a 10-min OGD treatment that was delivered 24 h later. Neuroprotection was seen in preconditioned slice cultures stained with propidium iodide (PI) or with antisera against the neuron-specific antigen NeuN. Energy failure is hypothesized to trigger ischemic preconditioning and a 5-min OGD treatment induced transient energy failure in young adult slice cultures. This model may assist in the search for new therapeutics for the prevention and/or treatment of stroke.

During the initial minutes of cerebral ischemia, lactic acid accumulates and acidifies brain pH to 6.0-6.7. Glutamate is also released during ischemia that activates glutamate receptors and induces excitotoxicity. While glutamate excitotoxicity is well established to induce ischemic injury, a role of lactic acidosis in ischemic brain damage is poorly understood. This study analyzes acidosis neurotoxicity in hippocampal slice cultures in the presence or absence of lactate. At pH 6.7, neuronal loss was similar whether or not lactate was present. At pH 6.4, neuronal loss was significantly greater in the presence of lactate suggesting that lactate potentiates the acidosis toxicity. At pH 6.4 in the presence of lactate, NMDA or non-NMDA receptor antagonists reduced neuronal loss, while in the absence of lactate, NMDA or non-NMDA receptor antagonists had little effect. [3H]-Glutamate uptake was inhibited by acidic pH, and the amount of inhibition was significantly greater in the presence of lactate. These findings suggest that lactate plays a role in acidosis neurotoxicity by inducing excitotoxicity. Lactic acidosis and excitotoxicity have been previously thought to be independent events during ischemia. This study suggests that during ischemia, lactic acidosis contributes to excitotoxic neuronal loss.

Background. Angioneurotic edema is a life-threatening medical emergency that requires urgent diagnosis and treatment. Haloperidol is in the butyrophenone class of antipsychotic medications. Acute anaphylaxis to Haloperidol is very rare and no cases have been reported in literature.Objective. To report the association of life-threatening angioneurotic edema with intramuscular Haloperidol.Case Report. We present a case of an adult with no known allergies in whom angioneurotic edema with tongue swelling and protrusion developed after the administration of a single IM dose of Haloperidol.Conclusion. We propose angioneurotic edema in a rare side effect of Haloperidol. The onset of the symptoms is abrupt, but it may take 12–36 hours to resolve completely. Therefore patient should be monitored for 12–36 hrs.

Vogt-Koyanagi-Harada syndrome is an autoimmune disease involving pigmented tissue in the eyes, auditory system, skin, and central nervous system. It often presents as bilateral chronic granulomatous panuveitis. We report the case of a 32-year-old immigrant who presented to the emergency department asking for a second opinion for loss of vision and progressive hearing loss. We also will discuss the issue limited access to health care for a vulnerable population such as undocumented immigrants.

45-year-old man with multiple sclerosis presented with worsening weakness in his right leg and double vision. Neurologic examination revealed horizontal diplopia during lateral gaze in both eyes. The patient had an adduction deficit in the right eye and nystagmus in the left eye on leftward gaze (Panel A). He also had an adduction deficit in the left eye and nystagmus in the right eye on rightward gaze (Panel B). Upward gaze (Panel C), downward gaze (Panel D), and normal primary position (Panel E) were unremarkable (video). Internuclear ophthalmoplegia is characterized by impaired horizontal eye movement that is caused by a lesion in the medial longitudinal fasciculus, a fiber tract that rises from the abducens nucleus in the pons to the contralateral oculomotor nucleus in the midbrain. Lesions in the medial longitudinal fasciculus result in the failure of adduction on attempted lateral gaze. Any brain-stem syndrome can interrupt the medial longitudinal fasciculus and result in impaired horizontal eye movement, but the most frequent underlying cause is multiple sclerosis. This patient had internuclear ophthalmoplegia in both eyes due to demyelinating lesions. Glucocorticoids were administered intravenously, but the deficits did not resolve. On follow-up at 2 months, the patient’s gait had improved, but the internuclear ophthalmoplegia remained.