Hypertensive Encephalopathy Research Articles

Hypertensive encephalopathy in a patient with unconsciousness

Hypertensive encephalopathy in a patient with unconsciousness

Status Epilepticus as a Presenting Feature in Posterior Reversible Encephalopathy Syndrome: Tertiary Care Center Experience.

Though epileptic seizures are common in posterior reversible encephalopathy syndrome (PRES), status epilepticus (SE) as the presenting feature is rare. To study the clinical spectrum and outcome of patients with SE as presenting feature of PRES. This is a retrospective study. PRES was diagnosed based on the clinical features and imaging findings on brain MRI (n = 40) which became normal after 6 months follow-up imaging. Patients with SE as the initial manifestation of PRES were identified. Baseline information regarding the clinical presentation, etiology, past history of illness, treatment history, imaging findings, EEG and long-term clinical outcome. Seizure was the most common presentation seen in 31 patients (77.5%). The etiologies in PRES were preeclampsia, or eclampsia [n = 33 (82.5%)], hypertensive encephalopathy [n = 3 (7.5%)], systemic lupus erythematosus (SLE), AIP, and chronic renal failure (CRF) in one patient each [n = 01 (2.5%)]. Brain MRI showed the involvement of parieto-occipital lobes (n = 33 [82.5%]) mostly. Status epilepticus (generalized convulsive) was the presenting feature in eight cases (20%). Among them, five cases (0.5%) had a history of chronic epilepsy. In the remaining three patients, SLE and acute intermittent porphyria, CRF precipitated the SE. The study highlights the clinico-etiological spectrum of PRES and the identification of SE within its context leading to the early diagnosis and management if treated early. The role of antenatal care is important for the identification and treatment of etiologies, blood pressure, proper antiepileptic drug compliance and appropriate counseling. Prasad P. Status Epilepticus as a Presenting Feature in Posterior Reversible Encephalopathy Syndrome: Tertiary Care Center Experience. Indian J Crit Care Med 2023;27(7):488-492.

Epidemiological Profile and Complications of Patients on the Waiting List for Liver Transplantation

Objective: To identify the epidemiological profile of candidates for liver transplantation and the complications that occurred up to the sixth month of admission to the waiting list. Method: Descriptive-exploratory study conducted in a liver transplant program located in a city in the interior of the state of São Paulo. Candidates aged ≥ 18 of both genders who entered the waiting list between January 1, 2018, and February 28, 2019, made up the study sample, totaling 51 patients. Data analysis was performed using descriptive statistics. Results: The average age of the participants was 52.7 years, most male (60.8%) with incomplete primary education (58.8%). Arterial hypertension was the most frequent comorbidity (51.4%). Most participants had blood type O (58.8%). The average Body Mass Index was 28.8 Kg/m²(overweight). Alcoholic cirrhosis was the most frequent indication for transplantation (31.4%). The average MELD score when joining the waiting list and six months later was 17.9 points. Class B of the Child-Pugh score had the highest frequency at the patient’s admission and the first follow-up. Ascites were the most frequent complication (56.9%), followed by portal hypertension (52.9%) and hepatic encephalopathy (33.3%). At the end of the study, 29 patients remained on the waiting list (56.9%), ten patients were transplanted (19.6%), and 12 died (23.5%).Conclusion: As for the epidemiological profile, the study’s results were in line with other studies, that is, participants with a predominance of male biological sex, most frequent age group of 50 to 59 years and low level of education. Concerning the identified complications, ascites were the most frequent. Among participants who did not remain on the waiting list, the number of deaths was more significant than the number of transplants performed, evidence that differs from other studies.

Characteristics and Prognosis of Patients With Hypertensive Encephalopathy: A French Nationwide Cohort Study.

Hypertensive encephalopathy (HE) constitutes a serious condition, usually observed in patients with long-lasting hypertension. Hypertension-associated HE is sometimes differentiated from the stroke-associated hypertensive emergency. Whether prognosis of hypertension-associated and stroke-associated HE is different is unclear. Characteristics and prognosis of HE were assessed in this nationwide retrospective cohort study in all patients with an administrative code of HE compared with age-, sex- and year of inclusion-matched controls admitted to French hospitals during the 2014 to 2022 period. HE was identified in 7769 patients. Chronic kidney disease (19.3%), coronary artery disease (13.8%), diabetes (22.1%), and ischemic stroke (5.2%) were frequent but thrombotic microangiopathy, hemolytic-uremic syndrome, systemic sclerosis or renal infarction were <1%. HE prognosis was poor (death: 10.4%/y, heart failure: 8.6%/y, end-stage kidney disease: 9.0%/y, ischemic stroke: 3.6%/y, hemorrhagic stroke: 1.6%/y, dementia: 4.1%/y). The risk of death was increased to a similar extent in patients with HE, regardless of the presence of known hypertension or concomitant stroke (versus patients without HE). Among patients with HE, known hypertension was significantly associated with increased risks of ischemic stroke, hemorrhagic stroke, heart failure, vascular dementia, and all-cause dementia and to a lesser extent with chronic dialysis in multivariable analyses including adjustment on concomitant stroke. HE remains a considerable health burden and is associated with a poor prognosis. The distinction between hypertension- versus stroke-associated HE is relevant as these 2 situations convey different risks of stroke, heart failure, vascular dementia, and end-stage kidney disease.

V-034 SPONTANEOUS EVISCERATION THROUGH AN UMBILICAL HERNIA

Abstract Aim Umbilical hernia in the cirrhotic patient is frequently seen in the setting of refractory ascites. Nevertheless, spontaneous evisceration is an unusual and potentially life-threating event. This hernia rupture has a high mortality and morbidity and presents many challenges in medical and surgical management. Material &amp; Methods We present a case of a 58 years-old man with personal history of alcoholic cirrhosis with multiple ascites drainages, portal hypertension and hepatic encephalopathy. The patient went to the emergency department suffering from an umbilical hernia with spontaneous rupture and evisceration. Results An urgent umbilical hernioplasty was conducted. We performed a hernia sac and suprafascial dissection. We verified that the vascularization of the hernia content was correct. We close peritoneum with double suture (transfixion ligature and continuous suture techniques) and fascia defect. We finally placed an onlay mesh. In the postoperative period, the patient had no complications related to dehiscence of suture or peritoneal fluid leakage, but stayed hospitalized for 25 days due to the decompensation of the cirrhosis. After six months of follow-up, there are no signs of recurrence. Conclusions Cirrhotic patients undergoing abdominal surgery are prone to complications, especially in hernias with spontaneous evisceration. One of de most frightening surgical complications in cirrhotic patients is the leakage of peritoneal fluid. In our case, this leakage could not have been produced because we used double suture and transfixion ligation to close peritoneum.

An Unusual Case of Posterior Fossa Predominant Posterior Reversible Encephalopathy Syndrome (PRES) Leading to Acute Hydrocephalus (P10-7.002)

<h3>Objective:</h3> To discuss acute hydrocephalus as an unusual complication of Posterior Reversible Encephalopathy Syndrome. <h3>Background:</h3> Posterior Reversible Encephalopathy Syndrome (PRES) is a well-recognized clinical and radiologic syndrome typically characterized by parieto-occipital vasogenic edema along with neurological symptoms, that improves after management or withdrawal of offending factor, in most cases being acute uncontrolled hypertension. However, clinical presentation and radiological findings are variable and may encompass different cerebral structures. Although pathophysiology is not well established, failure of sympathetic autoregulation in the vertebrobasilar system is thought to be related. This failure leads to breakdown of the blood-brain barrier, hence the vasogenic-type edema appreciated on imaging. Acute obstructive hydrocephalus is a rare and potentially fatal complication of PRES. <h3>Design/Methods:</h3> A 56-year-old Caucasian female who presented due to encephalopathy, headache and falls in the setting of hypertensive emergency. CT (Computed Tomography) head showed hypodense pons, midbrain, cerebellum, and bilateral thalami with effacement of the fourth ventricle, ventriculomegaly in the lateral and 3rd ventricles with associated trans-ependymal edema. Due to initial concern of posterior fossa mass leading to acute hydrocephalus, neurosurgery was consulted, and extra ventricular drain (EVD) was placed for emergent CSF diversion. <h3>Results:</h3> MRI Brain with and without contrast showed no evidence of acute ischemia or enhancing lesions. Severe edema was redemonstrated within the pons, midbrain, bilateral thalami, and cerebellum. Susceptibility weighted imaging showed microhemorrhages confined to the brainstem. The patient’s clinical exam improved after blood pressure management and EVD placement. Repeat head CT showed decreased cerebral edema and improvement of fourth ventricle obstruction. Based on presentation of hypertensive encephalopathy with posterior circulation vasogenic edema that improved with blood pressure management, PRES diagnosis was made. <h3>Conclusions:</h3> Posterior fossa predominant PRES is an uncommon presentation that if overlooked may lead to life threatening complications. Early recognition of clinical manifestations and radiological findings may lead to favorable outcomes. <b>Disclosure:</b> Dr. Morales-Nunez has nothing to disclose. Dr. Baez-Lugo has nothing to disclose. Dr. Yalcin has nothing to disclose. Dr. Shah has nothing to disclose. Dr. Garcia has nothing to disclose. Dr. Nichols has nothing to disclose.

Concomitant Occurrence of Non cirrhotic Portal Hypertension Multiple Acute Cerebral Infarcts, and Lupus Nephritis in a Patient with Systemic Lupus Erythematosus

Systemic lupus erythematosus (SLE) is an autoimmune disease that is characterized by multiple organ involvement with extremely variable and heterogeneous clinical presentations. Patients with SLE do not often experience multiple acute ischemic strokes, and liver involvement caused by SLE itself, such as cirrhosis, portal hypertension, or hepatic encephalopathy, is even rarer. In this paper, we report on a 35-year-old woman with SLE simultaneously presenting with multiple acute ischemic strokes, portal hypertension, nodular regenerative hyperplasia and lupus nephritis. To our knowledge, such a concomitant occurrence has rarely been reported in SLE patients before.

The impact of uncontrolled hypertension on the CNS.

The brain is a target of organ damage due to hypertension. In addition to acute damage in the form of hypertensive encephalopathy, ischaemic stroke, and intracerebral haemorrhage, hypertension causes chronic changes in the brain tissue that, over the course of years, will be manifested by impaired brain functions including cognitive deficit. Hypertension is also a risk factor for progression of cognitive disorder to overt dementia. It is commonly accepted that the earlier in life hypertension occurs, the greater the risk of developing dementia in old age. The pathophysiological mechanism underlying this effect of hypertension is microvascular damage which causes changes in the brain tissue and brain atrophy. A favourable fact is that the treatment with antihypertensive drugs demonstrably reduces the risk of developing dementia in individuals with hypertension. A more profound preventive effect was found in intensive blood pressure control and in RAAS system inhibitors. Therefore, hypertension has to be controlled since its onset, even in younger patients.

Managing severe hypertension in children.

Severe childhood hypertension is uncommon and frequently not recognised and is best defined as a systolic blood pressure (SBP) above the stage 2 threshold of the 95th centile + 12mmHg. If no signs of end-organ damage are present, this is urgent hypertension which can be managed by the slow introduction of oral or sublingual medication, but if signs are present, the child has emergency hypertension (or hypertensive encephalopathy if they include irritability, visual impairment, fits, coma, or facial palsy), and treatment must be started promptly to prevent progression to permanent neurological damage or death. However, detailed evidence from case series shows that the SBP must be lowered in a controlled manner over about 2days by infusing short-acting intravenous hypotensive agents, with saline boluses ready in case of overshoot, unless the child had documented normotension within the last day. This is because sustained hypertension may increase pressure thresholds of cerebrovascular autoregulation which take time to reverse. A recent PICU study that suggested otherwise was significantly flawed. The target is to reduce the admission SBP by its excess, to just above the 95th centile, in three equal steps lasting about ≥ 6h, 12h, and finally ≥ 24h, before introducing oral therapy. Few of the current clinical guidelines are comprehensive, and some advise reducing the SBP by a fixed percentage, which may be dangerous and has no evidence base. This review suggests criteria for future guidelines and argues that these should be evaluated by establishing prospective national or international databases.

Manifestations of hypertensive encephalopathy in cats.

Hypertensive encephalopathy in cats is an important entity but is underestimated in clinical practice. This could be explained, in part, by non-specific clinical signs. The objective of this study was to characterise the clinical manifestations of hypertensive encephalopathy in cats. Cats with systemic hypertension (SHT) recognised by routine screening, associated with underlying predisposing disease or a clinical presentation suggestive of SHT (neurological or non-neurological), were prospectively enrolled over a 2-year period. Confirmation of SHT was based on at least two sets of measurements of systolic blood pressure >160 mmHg by Doppler sphygmomanometry. Fifty-six hypertensive cats with a median age of 16.5 years were identified; 31 had neurological signs. In 16/31 cats, neurological abnormalities were the primary complaint. The other 15 cats were first presented to the medicine or ophthalmology service, and neurological disease was recognised based on the cat's history. The most common neurological signs were ataxia, various manifestations of seizures and altered behaviour. Individual cats also showed paresis, pleurothotonus, cervical ventroflexion, stupor and facial nerve paralysis. In 28/30 cats, retinal lesions were detected. Of these 28 cats, six presented with a primary complaint of visual deficits, and neurological signs were not the primary complaint; nine presented with non-specific medical issues, without suspicion of SHT-induced organ damage; in 13 cats, neurological issues were the primary complaint and fundic abnormalities were detected subsequently. SHT is common in older cats and the brain is an important target organ; however, neurological deficits are commonly ignored in cats with SHT. Gait abnormalities, (partial) seizures and even mild behavioural changes should prompt clinicians to consider the presence of SHT. A fundic examination in cats with suspected hypertensive encephalopathy is a sensitive test to support the diagnosis.

Natural history and prognosis of pediatric PSC with updates on management.

Natural history and prognosis of pediatric PSC with updates on management.

Feohromocitom kao potencijalni uzrok napada epilepsije

Epileptic seizures are defined as the transient appearance of signs or symptoms due to excessive or synchronous neuronal activity in the cerebral cortex. Pheochromocytomas and paragangliomas (PPGL) are tumors of chromaffin cells that arise from the medulla of the adrenal gland in 80-85% of patients and from the extra-adrenal sympathetic tissue of the abdomen, pelvis and chest in 10-20% of patients. The clinical picture of PPGL is variable and ranges from the absence of symptoms to severe clinical picture, depending on the biochemical profile. They are most often manifested by paroxysmal hypertension, followed by episodes of severe headache or diaphoresis, while epileptic attacks are rare. Neurological symptoms are present in many patients with PPGL. Also, paroxysmal neurological conditions such as vasodilating headache, intracranial tumors, diencephalic-autonomic epilepsy, hypertensive encephalopathy, focal arterial disease of the brain and anxiety state have been described, which may have similar clinical manifestations with pheochromocytomas. We present a 44-year-old woman, who has been diagnosed with pheochromocytoma as possible etiological basis of epileptic seizures. Pheochromocytoma, with its low incidence and "chameleon" clinical spectrum, should be considered as a potential etiological factor of convulsions.

Beneficial effects of the phytoestrogen genistein on hippocampal impairments of spontaneously hypertensive rats (SHR).

Hippocampal neuropathology is a recognized feature of the spontaneously hypertensive rat (SHR). The hippocampal alterations associate with cognitive impairment. We have shown that hippocampal abnormalities are reversed by 17β-estradiol, a steroid binding to intracellular receptors (estrogen receptor α and β subtypes) or the membrane-located G-protein coupled estradiol receptor. Genistein (GEN) is a neuroprotective phytoestrogen which binds to estrogen receptor β and G-protein coupled estradiol receptor. Here, we investigated whether GEN neuroprotection extends to SHR. For this purpose, we treated 5-month-old SHR for 2 weeks with 10mg kg-1 daily s.c injections of GEN. We analyzed the expression of doublecortin+ neuronal progenitors, glial fibrillary acidic protein+ astrocytes and ionized calcium-binding adapter molecule 1+ microglia in the CA1 region and dentate gyrus of the hippocampus using immunocytochemistry, whereas a quantitative real-time polymerase chain reaction was used to measure the expression of pro- and anti-inflammatory factors tumor necrosis factor α, cyclooxygenase-2 and transforming growth factor β. We also evaluated hippocampal dependent memory using the novel object recognition test. The results showed a decreased number of doublecortin+ neural progenitors in the dentate gyrus of SHR that was reversed with GEN. The number of glial fibrillary acidic protein+ astrocytes in the dentate gyrus and CA1 was increased in SHR but significantly decreased by GEN treatment. Additionally, GEN shifted microglial morphology from the predominantly activated phenotype present in SHR, to the more surveillance phenotype found in normotensive rats. Furthermore, treatment with GEN decreased the mRNA of the pro-inflammatory factors tumor necrosis factor α and cyclooxygenase-2 and increased the mRNA of the anti-inflammatory factor transforming growth factor β. Discrimination index in the novel object recognition test was decreased in SHR and treatment with GEN increased this parameter. Our results indicate important neuroprotective effects of GEN at the neurochemical and behavioral level in SHR. Our data open an interesting possibility for proposing this phytoestrogen as an alternative therapy in hypertensive encephalopathy.

HYPERTENSIVE ENCEPHALOPATHY: TO BE DIAGNOSED AND TREATED IMMEDIATELY

It is important to have a good understanding of the pat­hogenetic diagnosis and treatment features of the severe complication with high mortality – hypertensive encepha­lopathy (HE) because of the amount of people suffering from chronic arterial hypertension is constantly increa­sing. Thus, this article briefly reviews the mechanism of cerebral blood flow autoregulation, HE pathophysiology, and the main aspects of diagnosis and treatment. An HE episode is caused by a sudden and significant increase in arterial blood pressure, when the autoregulatory mecha­nism of cerebral blood flow becomes ineffective. Along with increased blood pressure, the patient gradually deve­lops neurological symptoms ranging from intense heada­che to vision loss, loss of consciousness, and convulsions. The diagnosis of HE is based on the clinical signs – acute arterial hypertension and the subsequent neurological symptoms. Also, the diagnosis of HE can be determined retrospectively when the neurological symptoms rapi­dly disappear with effective antihypertensive treatment. Computed tomography is important in differentiating HE from intracerebral hemorrhage and ischemic stroke. In management of HE it is recommended to return to the limits of cerebral blood flow autoregulation by immedi­ately reducing mean arterial blood pressure by 20-25%. In order to achieve the maximum rapid antihyperten­sive effect, it is suggested to administer the medication only intravenously. Labetalol and sodium nitroprusside are currently recommended first-line drugs for the treat­ment of HE. Patients with HE should be hospitalized in the intensive care unit for continuous control of decre­asement of arterial blood pressure while observing the cautious dynamics of the neurological condition. The outcome of patients depends on the urgency and effici­ency of treatment in returning arterial blood pressure to the limits of cerebral blood flow autoregulation, as well as on comorbidities, the severity of the condition and possible complications.

STATE OF COCHLEOVESTIBULAR DISORDERS IN PATIENTS WITH ARTERIAL HYPERTENSION

The article presents the otoneurological characteristics of pre-stroke cerebrovascular disorders in patients with essential hypertension. Among the problems of modern otorhinolaryngology, one of the leading places belongs to cochleovestibular disorders in some cardiovascular diseases, in particular, hypertension. The state of vestibular function in arterial hypertension was studied by many authors who noted a decrease in resistance in such patients. It has been established that one of the reasons for the formation of secondary cochleovestibular disorders is chronic hypertensive encephalopathy, which develops in patients with arterial hypertension, often already in the early stages of the disease. In the study of the peculiarities of the pathogenesis of cochleovestibular disorders, certain results have made it possible to study the nature of the vestibulo-vascular interaction. It is shown, in particular, the difference in vestibulo-vascular reactions in the case of central and peripheral lesions of the vestibular analyzer, which is important for the differential diagnosis of these pathological conditions.

Эпигеномные изменения в лейкоцитах периферической крови у пациентов с гипертонической болезнью и дисциркуляторной энцефалопатией

В настоящее время эпигеномный ландшафт, лежащий в основе гипертонической болезни и дисциркуляторной энцефалопатии, мало изучен. Идентификация эпигенетического паттерна в комплексе с генетическим паспортом индивида может предоставить дополнительную информацию об этиологии заболеваний и риске развития осложнений, а также о выборе стратегии и тактики лечения. В представленной работе проведена количественная оценка уровня полногеномного метилирования ДНК и степени компактизации хроматина в лейкоцитах периферической крови у пациентов с гипертонической болезнью и дисциркуляторной энцефалопатией и здоровых добровольцев из Санкт-Петербурга. У пациентов с гипертонической болезнью выявлены гендерные различия в риске развития дисциркуляторной энцефалопатии. По сравнению с контролем при гипертонической болезни повышены уровень метилирования ДНК и степень компактизации хроматина. В исследованных группах у мужчин и женщин обнаружена различная эпигеномная реакция лейкоцитов на лекарственную терапию при данных заболеваниях. Currently, the epigenomic landscape underlying hypertension and dyscirculatory encephalopathy is poorly understood. Identification of the epigenetic pattern in combination with genetic passport can provide additional information about the etiology of diseases and the risk of complications, as well as the choice of strategy and tactics of treatment. We carried out a quantitative assessment of the level of genome-wide DNA methylation and the degree of chromatin compaction in peripheral blood leukocytes in patients with hypertension and dyscirculatory encephalopathy, and also in healthy volunteers from St. Petersburg. Gender differences in the risk of developing dyscirculatory encephalopathy were revealed in patients with hypertension. It was found that the level of DNA methylation and the degree of chromatin compaction are increased in hypertension (compared to control). In the studied groups, men and women showed different epigenomic reactions of leukocytes to drug therapy in these pathologies.

PSAT051 Posterior Reversible Leukoencephalopathy Syndrome Associated With Cushing's Syndrome

Abstract Background Corticosteroids can induce hypertension through a variety of mechanisms such as vasoconstriction, increased hepatic production of angiotensinogen, sympathetic activity, and possible direct cardiotoxic effect. Posterior reversible leukoencephalopathy syndrome (PRES), a syndrome with unclear pathogenesis, can be the consequence of blood pressure elevation in these patients, which can present with headaches, altered consciousness, visual disturbances, or seizures. CASE REPORTA 57-year-old African American woman with a history of hypertension on Lisinopril 40mg as an outpatient, who was brought to the emergency department (ED) by family members due to altered mental status (AMS). Daughter reports that a day prior to the admission the patient has complained of feeling unwell, with mild shortness of breath and anxiety. On admission, she was found to be on sinus tachycardia with heart rate between 100-140bpm and severely hypertensive at 203/107mmHg. Toxicology screen was positive for cannabinoids, which the patient admitted to vapping the night prior. At the ED, Stroke alert was called due to altered mentation and weakness, however CT brain showed no large infarct or hemorrhage. MRI was obtained and showed patchy t2/flair hyperintense signal abnormality predominantly of the subcortical white matter in the bilateral frontoparietal lobes, most conspicuous at the vertex. Findings could reflect acute hypertensive encephalopathy (PRES). The patient had a Cushingoid appearance, with truncal obesity, moon face and reported easy bruising. Given the clinical findings and severe hypertension, serum cortisol was obtained at night and was found to be elevated at 34. 08UG/DL (3.44 - 16.76 ug/dl). ACTH was mildly low at 5 pg/mL (6-50pg/mL). 24-hour urine cortisol was then ordered and also found to be elevated at 818mcg/24h (4-50mcg/24h). Blood pressure was controlled with antihypertensive medications (nifedipine 60mg and carvedilol 12.5mg), AMS resolved and patient was discharged home with follow up with endocrinology for further Cushing's workup. Conclusion Cushing Syndrome is a known cause of secondary hypertension that should not be neglected. Patients that present with severe or resistant hypertension regardless of age should be worked up for possible secondary cases. Patients with Cushing syndrome are at elevated cardiovascular risk and the sooner the diagnosis is made, the better, so they can receive appropriate treatment. Hypertensive crisis can present as PRES syndrome and patients with clinical suspicion for Cushing should be worked up for the condition. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.

Features of the bioelectrical activity of the brain and cerebral hemodynamics in patients with hypertensive dyscirculatory encephalopathy and hypothyroidism

Encephalopathy is common in people of working age. In the last decade there was an important question the relationship of thyroid and cerebrovascular disease. The aim of the study was to investigate the characteristics of the brain’s elektorogenezis and cerebral hemodynamics in patients with hypertensive encephalopathy and related dyscirculatory hypothyroidism.&#x0D; We examined 97 patients, including 60 people with the HDE and the associated hypothyroidism and 37 - with the HDE without hypothyroidism.&#x0D; The fact, that bioelectrical activity of the brain in patients with hypothyroidism and related HDE was mostly characterized by desynchronization and disorganization of the cortical rhythm, was revealed during the study. Changes revealed by the EEG reflected the presence of metabolic and hemodynamic disturbances of the brain. Also, in patients with GDE and accompanying hypothyroidism, according to the duplex scanning of cerebral vessels, there is a significant decrease in cerebral blood supply and structural changes in vessels with a decrease in the elasticity of the common carotid artery and vertebral arteries and a decrease in cerebral reactivity accordingly. Thus, the comorbidity of HDE and hypothyroidism appears credible changes in the functional activity of the brain and decrease in cerebral reactivity.

40 30-day Outcomes of Hypertensive Emergency Department Patients Discharged With Antihypertensive Therapy

Hypertension (HTN) is extremely common among emergency department patients (ED) and carries an elevated risk of stroke, myocardial infarction, aortic dissection, hypertensive encephalopathy, and death. Additionally, discharged ED patients with HTN have a high short-term revisit rate to the ED. It is currently unclear if prescribing antihypertensive therapy to discharged ED patients affects their short-term revisit rate or their short-term risk of severe adverse outcomes. We aimed to assess whether ED prescription of oral anti- hypertensive therapy on discharge for hypertensive patients decreases their 30-day risk of the severe adverse outcomes of aortic dissection, hypertensive encephalopathy, heart failure, myocardial infarction, stroke, and death as well as the 30-day risk of ED revisit.

Clinical and metabolic features of diabetic encephalopathy

BACKGROUND: Actual mindset, concerning the pathogenesis of type 2 diabetes mellitus and its complications, is described in the glucocentric, lipocentric and lipokine theories. At the same time, it is known, that acute cerebrovascular disorder in type 2 diabetes mellitus can also develop with normoglycemia. The mechanism of association between obesity and type 2 diabetes mellitus in metabolic syndrome has not yet been studied, and 40% of diabetic patients are not obese. In the physiological state hyperglycemia is prevented by pancreatic regulatory oligopeptides rather than insulin, and protein glycation occurs before the development of diabetes symptoms. That facts indicate the need to continue investigation of the pathogenesis in general and diabetic encephalopathy in particular from the standpoint of metabology in order to substantiate the peptidergic theory of the diabetes mellitus and dyscirculatory encephalopathy pathogenesis.&#x0D; AIM: To consider little-known clinical, morphological and metabolic manifestations of diabetic encephalopathy from the standpoint of improving the disease diagnosis.&#x0D; MATHERIALS AND METHODS: Among 162 elderly and senile patients in the pre-stroke and stroke stages of diabetic encephalopathy, modern methods of radiological, laboratory, histological, psychometric and clinical analysis have been used: the relationship between low total cholesterol and disease progression has been determined according to Schulte and MMSE psychometric tests with the same hyperglycemia in different age groups sick; cases of amyloid angioencephalopathy on magnetic resonance imaging in the ultrasensitive weighted imaging mode and amyloidosis have been identified.&#x0D; Staining post-mortem ultrathin tissue biopsy sections with Congo red allowed to find amyloid deposition in 12% of autopsy cases in the absence of diagnosing amyloidosis during life; preparations, in which Congo red staining was positive for the presence of amyloid, were taken for inspection in polarizing light and typing of amyloid. Staining of histological preparations with hematoxylin-eosin and Van Gieson revealed a morphological characteristic of diabetic encephalopathy different from that of atherogenic and hypertensive dyscirculatory encephalopathy; using immunological studies, a statistically significant increased content of induced interleukin-1 production, a trigger for the serum amyloid analogue in the liver synthesis, was determined, and an experimental method for beta-amyloid peptide adhesion by monocytes and the density of amyloid expression on the surface of monocytes in patients with diabetic encephalopathy at senile age at 23 times higher than the density of the peptide in the elderly and in the patients with dyscirculatory encephalopathy of the same old age.&#x0D; RESULTS: It has been established that a fairly frequent and early manifestation of metabolic disorders in diabetic encephalopathy is a violation of protein metabolism with its final conformation into toxic amyloid tissue components. These observations indicate the multifactorial nature of diabetic encephalopathy. Literature data on the parametabolism of the serotonin mediator and tryptophan in the pathogenesis of diabetic encephalopathy are presented.&#x0D; CONCLUSIONS: Modern immunological, morphological, and histochemical capabilities make it possible to diagnose the conformation of the protein matrix and develop a protein-centric hypothesis of diabetic encephalopathy.