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BACKGROUND AND PURPOSE: Aneurysmal subarachnoid hemorrhage occurs in approximately 30,000 patients annually in the United States. Uncontrolled blood pressure is a major risk factor for aneurysmal subarachnoid hemorrhage. Clinical guidelines recommend maintaining blood pressure control until definitive aneurysm securement occurs. It is unknown whether racial differences exist regarding blood pressure control and outcomes (HLOS, discharge disposition) in aneurysmal subarachnoid hemorrhage. Here, we aim to assess whether racial differences exist in 1) presentation, 2) clinical course, and 3) outcomes, including time to blood pressure stabilization, for aSAH patients at a large tertiary care medical center. METHODS: We conducted a retrospective review of adult aneurysmal subarachnoid hemorrhage cases from 2013 to 2019 at a single large tertiary medical center. Data extracted from the medical record included sex, age, race, insurance status, aneurysm location, aneurysm treatment, initial systolic and diastolic blood pressure, Hunt Hess grade, modified Fisher score, time to blood pressure control (defined as time in minutes from first blood pressure measurement to the first of three consecutive systolic blood pressure measurements under 140mmHg), hospital length of stay, and final discharge disposition. RESULTS: 194 patients met inclusion criteria; 140 (72%) White and 54 (28%) Black. While White patients were more likely than Black patients to be privately insured (62.1% versus 33.3%, p < 0.001), Black patients were more likely than White patients to have Medicaid (55.6% versus 15.0%, p < 0.001). Compared to White patients, Black patients presented with a higher median systolic (165 mmHg versus 148 mmHg, p = 0.004) and diastolic (93 mmHg versus 84 mmHg, p = 0.02) blood pressure. Black patients had a longer median time to blood pressure control than White patients (200 minutes versus 90 minutes, p = 0.001). Black patients had a shorter median hospital length of stay than White patients (15 days versus 18 days, p < 0.031). There was a small but statistically significant difference in modified Fisher score between black and white patients (3.48 versus 3.17, p = 0.04).There were no significant racial differences present in sex, Hunt Hess grade, discharge disposition, complications, or need for further interventions. CONCLUSION: Black race was associated with higher blood pressure at presentation, longer time to blood pressure control, but shorter hospital length of stay. No racial differences were present in aneurysmal subarachnoid hemorrhage associated complications or interventions.
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Hipertensión , Hemorragia Subaracnoidea , Adulto , Humanos , Presión Sanguínea , Estudios Retrospectivos , Factores de Riesgo , Hipertensión/complicacionesRESUMEN
Subperiosteal orbital hemorrhage usually occurs in the setting of facial or orbital trauma. Non-traumatic subperiosteal orbital hemorrhage (NTSOH) has rarely been reported in literature. The proposed mechanism of NTSOH is the transmission of sudden increase in cranial venous pressure to the orbital veins, which are valveless. We present a case of a 37 year old right-handed woman with a past medical history significant for type 1 diabetes, end-stage renal disease, peripheral artery disease and hypertension who developed NTSOH following an elective revision of a clotted right upper extremity arteriovenous fistula. During this procedure, she had acute eye pain, bilateral complete vision loss and emesis. CT of the orbits revealed large heterogeneously hyperdense lesions in the bilateral orbital apex extending anteriorly along the roof of the orbit, concerning for hemorrhage. Cultures obtained through nasal endoscopy were negative for a bacterial or fungal infection involving the sinuses. Ophthalmology was consulted and she underwent bilateral canthotomy and lateral cantholysis. Postoperatively, she was started on systemic and topical ocular antihypertensives, as well as prophylactic antibiotics. Visual acuity remained poor with finger counting on the right eye and lack of consistent response to light on the left eye. This case highlights periprocedural increase in systemic venous pressure secondary to a fistula repair procedure as a potential cause of NTSOH.
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Altered mental status in immunosuppressed patients has a wide differential diagnosis. In this case, a 27-year-old man presented with encephalopathy, nausea, vomiting, and fevers. His medical history was significant for acute myeloid leukemia in remission after allogenic hematopoietic stem cell transplantation 17 months prior complicated by graft vs host disease affecting his skin treated with sirolimus. A lumbar puncture was performed with a lymphocytic pleocytosis, mildly elevated protein, and negative Gram-stain and bacterial and fungal cultures. His examination deteriorated, and he became comatose with loss of pupillary and corneal reflexes. An MRI of his brain demonstrated T2/fluid-attenuated inversion recovery signal abnormality involving the bilateral basal ganglia, mesial temporal lobes, and entire brainstem along with bilateral temporal parenchymal and leptomeningeal enhancement. Ultimately, diagnosis was made through metagenomic PCR sequencing from his CSF. This case highlights diagnostic challenges in immunosuppressed patients because antibodies against the causative antigen were negative (potentially related to decreased antibody production in the setting of immunosuppression).
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Encefalomielitis Equina Oriental , Masculino , Humanos , Huésped Inmunocomprometido , Encéfalo , Imagen por Resonancia Magnética , Trasplante de Células Madre/efectos adversosRESUMEN
INTRODUCTION: Patient-centered care, particularly shared medical decision making, is difficult to measure in critically ill patients where decisions are often made by a designated surrogate, often receiving information from multiple providers with varying degrees of training. The purpose of this study was to compare short-term satisfaction with care and decision making in patients or surrogates between two neurocritical care units [one staffed by a neurocritical care attending and advanced practice providers (APPs) and one staffed by a neurocritical care attending and resident/fellow trainees] using the Family Satisfaction in the ICU (FS-ICU) survey. METHODS: Over a 6-month period, the FS-ICU was administered on a tablet device to patients or surrogates at least 24 h after admission and stored on REDCap database. RESULTS: One hundred and thirty-four patients or surrogates completed the FS-ICU. The response rates were 59.97% and 46.58% in the APP and trainee units, respectively. There were no differences in patient age, sex, ventilator days or ICU length of stay. Overall, there were no differences in satisfaction with care or perceived shared medical making between the units. Respondents who identified their relationship with the patient as "other" (not a spouse, parent, nor a sibling) were less satisfied with care. Additionally, surrogates who identified as parents of the patient were more satisfied with degree of shared medical decision making. CONCLUSION: This study showed that: (1) collecting FS-ICU in a neurocritical care unit is feasible, (2) overall there is no difference in short-term satisfaction with care or shared decision making between a NICU staffed with trainees compared to one staffed with APPs, and (3) parents of patients have a higher short-term satisfaction with degree of shared medical decision making.
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Toma de Decisiones , Satisfacción Personal , Enfermedad Crítica , Humanos , Unidades de Cuidados Intensivos , Recursos HumanosRESUMEN
INTRODUCTION: Carbon dioxide (CO2) as a contrast agent has been in use as early as the 1920s for visualization of retroperitoneal structures. Digital subtraction angiography (DSA) using CO2 as a contrast agent for vascular imaging was developed in the 1980s. Currently, CO2 angiography is an alternative agent in patients with chronic kidney disease (CKD) and those who are at risk of developing contrast-induced nephropathy. However, CO2 causes neurotoxicity if the gas inadvertently enters the cerebrovascular circulation leading to fatal brain injury. CASE PRESENTATION: A 71-year-old female with h/o sickle cell trait, hypertension, obesity, metastatic renal cell cancer status post nephrectomy, bone metastasis, chronic kidney disease was admitted for elective embolization of the humerus bone metastasis. Given the high probability of contrast-induced nephropathy, CO2 angiography was chosen for embolization of the metastasis. During the procedure, the patient became unresponsive. Emergent medical management with hyperventilation, 100% fraction oxygen inhalation was performed. Her neuroimaging showed global cerebral edema. An intracranial pressure monitor was placed which confirmed intracranial hypertension. Hyperosmolar therapy was administered with no improvement in clinical examination. She progressed to brain stem herniation. Given poor prognosis, the family opted for comfort measures and the patient expired. DISCUSSION AND CONCLUSIONS: Inadvertent carbon dioxide entry into cerebrovascular circulation during angiography can cause fatal brain injury. Caution must be exercised while performing CO2 angiography in blood vessels above the diaphragm.
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Angiografía/efectos adversos , Neoplasias Óseas/diagnóstico por imagen , Edema Encefálico/inducido químicamente , Dióxido de Carbono/efectos adversos , Medios de Contraste/efectos adversos , Embolia Aérea/inducido químicamente , Húmero/diagnóstico por imagen , Neoplasias Renales/patología , Anciano , Neoplasias Óseas/secundario , Neoplasias Óseas/terapia , Edema Encefálico/diagnóstico por imagen , Edema Encefálico/terapia , Dióxido de Carbono/administración & dosificación , Medios de Contraste/administración & dosificación , Embolia Aérea/diagnóstico por imagen , Embolia Aérea/terapia , Embolización Terapéutica , Resultado Fatal , Femenino , Humanos , Húmero/patologíaRESUMEN
Cerebral hyperperfusion and reperfusion injuries are not infrequently encountered following in reperfusion of ischemic or hypoperfused brain. Mechanism of injury could be related to tissue plasminogen activator toxicity, oxidative stress, and hyperperfusion due to impaired cerebral autoregulation in already maximally dilated cerebral vasculature and compromised cerebral hemodynamic reserve. Reperfusion injury can present as headaches and seizures in mild forms and as subarachnoid hemorrhage, intracranial hemorrhage, cerebral edema, and encephalopathy in its most severe manifestation. Prevention and identifying those at risk of hyperperfusion syndromes are the best strategy. Active treatment includes basic neurocritical care with reduction of blood pressure to a reperfused brain and timely neuroprotection and cerebral edema control measures are the mainstay of its management approach.
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Isquemia Encefálica/patología , Isquemia Encefálica/fisiopatología , Circulación Cerebrovascular/fisiología , Daño por Reperfusión/patología , Presión Sanguínea/fisiología , Isquemia Encefálica/terapia , Trastornos Cerebrovasculares/terapia , Endarterectomía Carotidea/efectos adversos , Humanos , Hemorragias Intracraneales/etiología , Factores de Riesgo , Stents , Terapia Trombolítica/efectos adversosRESUMEN
We examined the role of heme oxygenase (HO)-1 in morphine-induced decrease in macrophage migration. Morphine promoted expression of HO-1 in murine macrophages. Morphine-receiving mice (MRCs) showed decreased (P<.001) macrophage migration and increased (P<.001) occurrence of macrophage apoptosis. In in vitro studies, peritoneal macrophages harvested from MRCs also showed decreased (P<.001) migration, compared with those from control mice. Bone marrow cells isolated from MRCs showed not only decreased (P<.001) migration but also increased apoptosis. Pretreatment of MRCs with hemin not only decreased migration of macrophages further but also enhanced the apoptosis of peritoneal macrophages. On the other hand, pretreatment of MRCs with zinc protoporphyrin attenuated the effect of morphine on both macrophage migration and the occurrence of apoptosis. In in vitro studies, pretreatment of macrophages with hemin exacerbated morphine-induced apoptosis, whereas pretreatment with zinc protoporphyrin attenuated morphine-induced macrophage apoptosis.
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Apoptosis/efectos de los fármacos , Hemo Oxigenasa (Desciclizante)/fisiología , Macrófagos/efectos de los fármacos , Morfina/farmacología , Animales , Movimiento Celular/efectos de los fármacos , Quimiocina CCL2/biosíntesis , Relación Dosis-Respuesta a Droga , Hemo-Oxigenasa 1 , Hemina/farmacología , Macrófagos/fisiología , Masculino , Proteínas de la Membrana , RatonesRESUMEN
BACKGROUND: Angiotensin II (ANG II) has been shown to play a role in the induction of glomerular injury. In the present study, we evaluated the effects of ANG II on mesangial cell apoptosis and the involved molecular mechanism. MATERIALS AND METHODS: The effect of ANG II on apoptosis of mouse mesangial cells (MC) was evaluated by morphologic, DNA fragmentation and TUNEL assays. To evaluate the role of oxidative stress and involved mechanisms, we studied the effect of antioxidants, anti-TGF-beta antibody, inhibitors of nitric oxide synthase and modulators of cytosolic calcium/heme oxygenase (HO) activity. In addition, we studied the effect of ANG II on the generation of reactive oxygen species (ROS) by MCs. RESULTS: ANG II promoted apoptosis of MCs in a dose dependent manner. This effect of ANG II was not only associated with ROS production, but also inhibited by antioxidants. Both Anti-TGF-beta antibody and propranolol inhibited ANG II-induced ROS generation and apoptosis. BAPTA inhibited both ANG II- and TGF-beta-induced apoptosis. On the other hand, thapsigargin stimulated MC apoptosis under basal as well as ANG II/TGF-beta stimulated states. ANG II receptor types 1 and 2 antagonists attenuated the proapoptotic effect of ANG II. Hemin inhibited but zinc protoporphyrin enhanced the proapoptotic effect of ANG II. Propranolol increased HO activity; whereas pre-treatment with propranolol prevented ANG II-induced apoptosis. CONCLUSIONS: ANG II promotes MC apoptosis. This effect of ANG II is mediated through downstream signaling involving TGF-beta, phospholipase D, and Ca(2+), contributing to the activation of NADPH oxidase and generation of ROS. HO activity plays a modulatory role in ANG II- induced MC apoptosis.