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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 23-year-old woman presented with disturbance of consciousness and seizure. Her blood pressure was remarkably high, and brain magnetic resonance imaging (MRI) showed high-intensity T2 signals in the bilateral basal ganglia, corpus callosum, cerebral white matter, and cortex. With the administration of angiotensin II receptor blocker, the symptoms and MRI findings improved, along with normalization of blood pressure, and a diagnosis of posterior reversible leukoencephalopathy syndrome (PRES) was made. Plasma renin activity was high, and the right kidney was severely atrophic. Results from renal and adrenal vein sampling revealed renal vascular hypertension derived from the right renal artery stenosis. The right kidney was then removed by laparoscopic nephrectomy. Pathological examination of the kidney confirmed the diagnosis of fibromuscular dysplasia (FMD). In juvenile-onset encephalitis/encephalopathy, PRES due to FMD should be included in the differential diagnosis.
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PMID:A case of posterior reversible leukoencephalopathy syndrome caused by fibromuscular dysplasia. 2758 Jul 65

A 70-year-old African American man suffered anoxic encephalopathy following a choking episode. He had a history of hypertension, which was being treated with lisinopril, an angiotensin-converting enzyme inhibitor (ACEI). Soon after the patient's admission to an intensive care unit, his tongue began to swell until it reached more than twice its normal size and extended almost 2 inches outside his mouth. When the swelling did not diminish after 2 weeks, a diagnosis of ACEI-induced angioedema was determined. ACEIs have the potential to cause angioedema through an uncommon effect on the angiotensin-renin vascular control system. Lingual angioedema can be life-threatening due to the possibility of severe compromise of the airway and thus may require immediate intubation. After the ACEI is discontinued, swelling may remain if there is continued pressure from the maxillary and mandibular incisors on the dorsal and lingual surfaces of the tongue. In this case, the patient was comatose and unable to voluntarily move the tongue; therefore, relief from pressure was easily accomplished, and the edema was eventually diminished through a team effort in which a dentist instructed the nursing personnel on proper placement of Molt mouth props.
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PMID:Management of persistent lingual angioedema: a team approach. 2868 84

When aortic dissections extend to the renal arteries, reductions in renal blood flow can cause marked increases in renin production. The resultant rise in angiotensin II can lead to difficult-to-control blood pressure, despite normal postdissection antihypertensive agents. We highlight a case of a postdissection patient with malignant hypertension refractory to eight different enteral antihypertensives. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers had been held due to postoperative acute kidney injury. A single dose of valsartan, administered on day 12, produced a marked drop in blood pressure, alleviation of encephalopathy, and allowed for cancellation of a planned tracheostomy. A serum renin level was found to be 50 times the normal upper limit. In patients with aortic dissection and renal artery involvement, angiotensin-modifying agents may warrant earlier administration to combat this unique cause of hypertension.
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PMID:Valsartan Effective for Malignant Hypertension after Aortic Dissection with Renal Artery Involvement. 2948 21

We present a case of a 39-year-old G8P6 Pacific Islander woman who at 15+5 weeks' gestation had an out-of-hospital cardiac arrest secondary to profound hypokalaemia which was associated with severe hyperemesis gravidarum (HG). Her clinical course after arrest was complicated by a second 5-minute cardiac arrest in the Intensive Care Unit (ICU) (pre-arrest potassium 1.8), anuric renal failure requiring dialysis, ischaemic hepatitis, and encephalopathy and unfortunately fetal demise and a spontaneous miscarriage on day 2 of admission. Despite these complications, she was discharged home 4 weeks later with a full recovery. Following a plethora of inpatient and outpatient investigations, the cause of her cardiac arrest was determined to be profound hypokalaemia. The hypokalaemia was presumed second to a perfect storm of HG with subsequent nutritional deficiencies causing electrolyte wasting, extracellular fluid (ECF) volume reduction, and activation of the renin-angiotensin-aldosterone axis (RAAS). This combined with the physiological changes that promote potassium wasting in pregnancy including volume expansion, increased renal blood flow, increased glomerular filtration rate, and increase in cortisol contributed to the patient having a profoundly low total body potassium level. This diagnosis is further strengthened by the fact that her pre- and post-pregnancy potassium levels were within normal limits in the absence of supplementary potassium. This case highlights the potentially life-threatening electrolyte imbalances that can occur with HG and the importance of recognising the disease, comprehensive electrolyte monitoring, and aggressive management in pregnancy.
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PMID:Profound Hypokalaemia Resulting in Maternal Cardiac Arrest: A Catastrophic Complication of Hyperemesis Gravidarum? 3015 Dec 87

Coronavirus disease 2019 (COVID-19) is a highly infectious pandemic caused by a novel coronavirus called severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). It frequently presents with unremitting fever, hypoxemic respiratory failure, and systemic complications (e.g., gastrointestinal, renal, cardiac, and hepatic involvement), encephalopathy, and thrombotic events. The respiratory symptoms are similar to those accompanying other genetically related beta-coronaviruses (CoVs) such as severe acute respiratory syndrome CoV (SARS-CoV) and Middle East Respiratory Syndrome CoV (MERS-CoV). Hypoxemic respiratory symptoms can rapidly progress to Acute Respiratory Distress Syndrome (ARDS) and secondary hemophagocytic lymphohistiocytosis, leading to multi-organ system dysfunction syndrome. Severe cases are typically associated with aberrant and excessive inflammatory responses. These include significant systemic upregulation of cytokines, chemokines, and pro-inflammatory mediators, associated with increased acute-phase proteins (APPs) production such as hyperferritinemia and elevated C-reactive protein (CRP), as well as lymphocytopenia. The neurological complications of SARS-CoV-2 infection are high among those with severe and critical illnesses. This review highlights the central nervous system (CNS) complications associated with COVID-19 attributed to primary CNS involvement due to rare direct neuroinvasion and more commonly secondary CNS sequelae due to exuberant systemic innate-mediated hyper-inflammation. It also provides a theoretical integration of clinical and experimental data to elucidate the pathogenesis of these disorders. Specifically, how systemic hyper-inflammation provoked by maladaptive innate immunity may impair neurovascular endothelial function, disrupt BBB, activate CNS innate immune signaling pathways, and induce para-infectious autoimmunity, potentially contributing to the CNS complications associated with SARS-CoV-2 infection. Direct viral infection of the brain parenchyma causing encephalitis, possibly with concurrent neurovascular endotheliitis and CNS renin angiotensin system (RAS) dysregulation, is also reviewed.
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PMID:Central nervous system complications associated with SARS-CoV-2 infection: integrative concepts of pathophysiology and case reports. 3275 57

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) uses Angiotensin- converting enzyme 2 (ACE2) receptors to infect host cells which may lead to coronavirus disease (COVID-19). Given the presence of ACE2 receptors in the brain and the critical role of the renin-angiotensin system (RAS) in brain functions, special attention to brain microcirculation and neuronal inflammation is warranted during COVID-19 treatment. Neurological complications reported among COVID-19 patients range from mild dizziness, headache, hypogeusia, hyposmia to severe like encephalopathy, stroke, Guillain-Barre Syndrome (GBS), CNS demyelination, infarcts, microhemorrhages and nerve root enhancement. The pathophysiology of these complications is likely via direct viral infection of the CNS and PNS tissue or through indirect effects including post- viral autoimmune response, neurological consequences of sepsis, hyperpyrexia, hypoxia and hypercoagulability among critically ill COVID-19 patients. Further, decreased deformability of red blood cells (RBC) may be contributing to inflammatory conditions and hypoxia in COVID-19 patients. Haptoglobin, hemopexin, heme oxygenase-1 and acetaminophen may be used to maintain the integrity of the RBC membrane.
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PMID:Impact of COVID-19 on the cerebrovascular system and the prevention of RBC lysis. 3309 Apr 38


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