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2.
Arch. argent. pediatr ; 118(5): 332-336, oct 2020. ilus, tab
Article in English, Spanish | LILACS, BINACIS | ID: biblio-1122029

ABSTRACT

Introducción. El edema cerebral (EC) es la complicación más grave de la cetoacidosis diabética (CAD) en niños. La patogénesis del EC no se conoce con exactitud y su aparición ha sido relacionada con la terapia de rehidratación endovenosa en el tratamiento inicial.Objetivos. Estimar la prevalencia de EC en pacientes con CAD tratados en el Hospital General de Niños Pedro de Elizalde mediante rehidratación endovenosa y analizar potenciales factores de riesgo para el desarrollo de EC.Materiales y método. Estudio de diseño transversal para prevalencia y un análisis exploratorio para comparar las características clínicas y de laboratorio entre los pacientes con y sin EC. Se incluyeron pacientes de 1 a 18 años hospitalizados con diagnóstico de CAD desde el 1 de enero de 2005 hasta el 31 de diciembre de 2014.Resultados. Se analizaron 693 episodios de CAD en 561 historias clínicas. En 10 pacientes, se evidenció EC (el 1,44 %; intervalo de confianza del 95 %: 0,8-2,6). Los pacientes con EC presentaron mayor uremia (p < 0,001), menor presión de dióxido de carbono (p < 0,001) y menor natremia (p < 0,001) que aquellos pacientes sin EC.Conclusión. La prevalencia de EC en pacientes con CAD fue del 1,44 %, menor que la reportada en nuestro país (del 1,8 %). Los factores de riesgo al ingresar asociados a su desarrollo fueron la presencia de uremia elevada, hiponatremia e hipocapnia.


Introduction. Cerebral edema (CE) is the most severe complication of diabetic ketoacidosis (DKA) in children. There is no accurate knowledge of CE pathogenesis and its onset has been related to intravenous rehydration therapy during the initial treatment.Objectives. To estimate the prevalence of CE among DKA patients treated at Hospital General de Niños Pedro de Elizalde with intravenous rehydration and analyze potential risk factors for the development of CE.Materials and methods. Cross-sectional prevalence study and exploratory analysis to compare clinical and laboratory characteristics between patients with and without CE. Patients aged 1-18 years hospitalized with the diagnosis of DKA between January 1st, 2005 and December 31st, 2014 were included.Results. A total of 693 DKA events from 561 medical records were analyzed. Ten patients had evidence of CE (1.44 %; 95 % confidence interval: 0.8-2.6). Patients with CE had higher serum urea levels (p < 0.001), lower carbon dioxide pressure (p < 0.001), and lower serum sodium levels (p < 0.001) than those without CE.Conclusion. The prevalence of CE among DKA patients was 1.44 %, smaller than that reported in our country (1.8 %). The risk factors at admission associated with CE development were high serum urea levels, hyponatremia, and hypocapnia.


Subject(s)
Humans , Male , Female , Infant , Child, Preschool , Child , Adolescent , Brain Edema , Diabetic Ketoacidosis/complications , Prevalence , Cross-Sectional Studies , Risk Factors , Diabetic Ketoacidosis/diagnosis , Diabetic Ketoacidosis/therapy
3.
Rev. argent. neurocir ; 34(3): 235-239, sept. 2020. ilus
Article in Spanish | LILACS, BINACIS | ID: biblio-1120967

ABSTRACT

Introducción: Las lesiones durales son complicaciones frecuentes en la cirugía de columna. La fuga de liquidocefalorraquideo (LCR) puede originar hemorragia en todos los compartimientos del cerebro. La mayoría ocurre en venas ubicadas en región cerebelosa.Material y método: Se presenta un caso de hemorragia subaracnoidea posterior a una descompresión lumbar mínimamente invasiva asociada a desgarro dural. Resultados: Evoluciona en el postoperatorio con síntomas neurológicos de cefaleas y trastornos del sensorio por lo que se decide evaluarlo con estudios por imágenes vasculares cerebrales identificándose sangrado subaracnoideo.Discusión: El sitio más frecuente de hemorragia intracraneal posterior a una cirugía de columna es el cerebelo. El mecanismo de acción de este tipo de sangrados es desconocido y controversial, hay algunos reportes que sugieren que se trataría de un sangrado venoso. El síntoma más característico de este síndrome es la cefalea. Aunque se desconoce la etiología exacta, se postula que la pérdida de volumen de LCR causa una caída en la presión intracraneal, lo que lleva a un agrandamiento de los senos venosos durales que predisponen al paciente a un hematoma subdural espontáneoConclusión: La fuga de LCR, las alteraciones asociadas al edema cerebral en la hipotensión cerebral podría ser llave del mecanismo que desencadena una hemorragia subaracnoidea.


compartments of the brain. Most occur in veins located in the cerebellar region.Material and method: A case of subarachnoid hemorrhage after a minimally invasive lumbar decompression associated with dural tear is presented.Results: It evolves in the postoperative period with neurological symptoms of headaches and sensory disorders, so it is decided to evaluate it with studies by cerebral vascular images identifying subarachnoid bleeding.Discussion: The most frequent site of intracranial hemorrhage after spinal surgery is the cerebellum. The mechanism of action of this type of bleeding is unknown and controversial, there are some reports that suggest that it would be a venous bleeding. The most characteristic symptom of this syndrome is headache. Although the exact etiology is unknown, it is postulated that the loss of CSF volume causes a drop in intracranial pressure, which leads to an enlargement of the dural venous sinuses that predispose the patient to a spontaneous subdural hematomaConclusion: CSF leakage, alterations associated with cerebral edema in cerebral hypotension could be key to the mechanism that triggers a subarachnoid hemorrhage.


Subject(s)
Humans , Male , Subarachnoid Hemorrhage , General Surgery , Brain Edema , Intracranial Hemorrhages , Hematoma, Subdural
4.
Article in Chinese | WPRIM | ID: wpr-828505

ABSTRACT

OBJECTIVE@#To investigate the effects of blocking the activation of ERK pathway on the expression of matrix metalloproteinase-9 (MMP-9) and the formation of cerebral edema in SD rats after brain injury.@*METHODS@#Ninety SD rats were randomly divided into 3 equal groups, including a sham-operated group, modified Feeney's traumatic brain injury model group, and ERK inhibition group where the ERK inhibitor SCH772984 (500 μg/kg) was injected via the femoral vein 15 min before brain trauma. At 2 h and 2 days after brain trauma, the permeability of blood-brain barrier was assessed by Evans blue method, the water content of the brain tissue was determined, and the phosphorylation level of ERK and the expression level of MMP-9 mRNA and protein were measured by RT-PCR and Western blotting.@*RESULTS@#Compared with the sham-operated group, the rats with brain trauma exhibited significantly increased level of ERK phosphorylation at 2 h and significantly increased expression of MMP-9 mRNA and protein 2 days after the injury ( < 0.01). Treatment with the ERK inhibitor significantly decreased the phosphorylation level of ERK after the injury ( < 0.01), suppressed over-expression of MMP-9 mRNA and protein 2 days after the injury ( < 0.01). The permeability of blood-brain barrier increased significantly 2 h after brain trauma ( < 0.05) and increased further at 2 days ( < 0.01); the water content of the brain did not change significantly at 2 h ( > 0.05) but increased significantly 2 d after the injury ( < 0.01). Treatment with the ERK inhibitor significantly lowered the permeability of blood-brain barrier and brain water content after brain trauma ( < 0.01).@*CONCLUSIONS@#Blocking the activation of ERK pathway significantly reduced the over-expression of MMP-9 and alleviates the damage of blood-brain barrier and traumatic brain edema, suggesting that ERK signaling pathway plays an important role in traumatic brain edema by regulating the expression of MMP-9.


Subject(s)
Animals , Brain Edema , Drug Therapy , Brain Injuries, Traumatic , Drug Therapy , Gene Expression Regulation, Enzymologic , Indazoles , Pharmacology , Therapeutic Uses , MAP Kinase Signaling System , Matrix Metalloproteinase 9 , Genetics , Piperazines , Pharmacology , Therapeutic Uses , Protein Kinase Inhibitors , Pharmacology , Therapeutic Uses , Random Allocation , Rats , Rats, Sprague-Dawley
5.
Article in Chinese | WPRIM | ID: wpr-828442

ABSTRACT

In this study, Tabu search algorithm was used to analyze the effect of Xingnaojing Injection in the treatment of cerebral hemorrhage in the real world. Through the analysis of the results, the therapies based on the pathogeny of cerebral hemorrhage were screened out: Xingnaojing Injection+hemostatic drugs for promoting blood circulation and removing stasis. Cerebral hemorrhage complicated with brain edema: combined with mannitol or mannitol+aescin. The patients with relevant complications in the acute stage of cerebral hemorrhage could select according to the indications: ①Aminocycline+Oxiracetam+Piperacillin Sodium Sulbactam Sodium+Sodium Lactate Ringer; ②Aminocycline+Oxiracetam+Nifedipine+Captopril+Metoclopramide+Cimetidine; ③Insulin+Pantoprazole+So-dium Nitroprusside. The combined therapies for patients of the stable stage with complicating diseases could select according to the indications: ① Monosialotetrahexosyl Ganglioside Sodium+Deproteinized Calf Blood Serum+Nitroglycerin+Compound Potassium Dihydrogn Phosphate; ② Edaravone+Gangliosides+Captopril+Levofloxacin+Tanreqing Injection+Aminophylline. The analysis of subgroup module of drugs for promoting blood circulation and removing blood stasis suggested that the safety of traditional Chinese medicine should be paid attention to in the treatment of cerebral hemorrhage. This study was based on the data of the real world, but with some problems, such as lack of data and confounding factors. The summarized medication plan is only for the reference of clinicians. The clinical application shall be based on the specific situation of patients and the clinical benefits and risks, and pay attention to the incompatibility.


Subject(s)
Algorithms , Brain Edema , Cerebral Hemorrhage , Drugs, Chinese Herbal , Humans , Medicine, Chinese Traditional
6.
Article in Chinese | WPRIM | ID: wpr-828924

ABSTRACT

OBJECTIVE@#To investigate the effects of blocking the activation of ERK pathway on the expression of matrix metalloproteinase-9 (MMP-9) and the formation of cerebral edema in SD rats after brain injury.@*METHODS@#Ninety SD rats were randomly divided into 3 equal groups, including a sham-operated group, modified Feeney's traumatic brain injury model group, and ERK inhibition group where the ERK inhibitor SCH772984 (500 μg/kg) was injected via the femoral vein 15 min before brain trauma. At 2 h and 2 days after brain trauma, the permeability of blood-brain barrier was assessed by Evans blue method, the water content of the brain tissue was determined, and the phosphorylation level of ERK and the expression level of MMP-9 mRNA and protein were measured by RT-PCR and Western blotting.@*RESULTS@#Compared with the sham-operated group, the rats with brain trauma exhibited significantly increased level of ERK phosphorylation at 2 h and significantly increased expression of MMP-9 mRNA and protein 2 days after the injury ( < 0.01). Treatment with the ERK inhibitor significantly decreased the phosphorylation level of ERK after the injury ( < 0.01), suppressed over-expression of MMP-9 mRNA and protein 2 days after the injury ( < 0.01). The permeability of blood-brain barrier increased significantly 2 h after brain trauma ( < 0.05) and increased further at 2 days ( < 0.01); the water content of the brain did not change significantly at 2 h ( > 0.05) but increased significantly 2 d after the injury ( < 0.01). Treatment with the ERK inhibitor significantly lowered the permeability of blood-brain barrier and brain water content after brain trauma ( < 0.01).@*CONCLUSIONS@#Blocking the activation of ERK pathway significantly reduced the over-expression of MMP-9 and alleviates the damage of blood-brain barrier and traumatic brain edema, suggesting that ERK signaling pathway plays an important role in traumatic brain edema by regulating the expression of MMP-9.


Subject(s)
Animals , Blood-Brain Barrier , Brain Edema , Brain Injuries, Traumatic , MAP Kinase Signaling System , Matrix Metalloproteinase 9 , Rats , Rats, Sprague-Dawley
7.
Acta méd. colomb ; 44(3): 34-38, July-Sept. 2019. tab, graf
Article in English | LILACS, COLNAL | ID: biblio-1098024

ABSTRACT

Abstract Reversible vasoconstriction syndrome is a group of clinical-radiological alterations that are characterized by severe sudden-onset headaches and reversible multifocal narrowing of the cerebral arteries. Most patients do not present with focal neurological deficit, although it can be seen in a small group, associated with cerebral edema, stroke or seizures. It is considered to be a benign process that causes disability and death in a minority of patients. The term 'reversible vasoconstriction syndrome' has been proposed to unify a variety of clinical syndromes which are similar, but have different etiologies, and have originated various eponyms. The apparently low frequency of reversible vasoconstriction syndrome and the way it presents make it a diagnostic challenge in the emergency room, and it may go unnoticed without an adequate medical history. A case probably related to the use of isometeptene is presented. (Acta Med Colomb 2019; 44. DOI: https://doi.org/10.36104/amc.2019.1213)


Resumen El síndrome de vasoconstricción reversible es un grupo de alteraciones clínico-radiológicas que se caracterizan por cefaleas intensas de inicio brusco y estrechamiento multifocal reversible de las arterias cerebrales. La mayoría de los pacientes no presentan déficit neurológico focal, aunque puede verse en un grupo reducido asociándose con edema cerebral, ataque cerebrovascular o convulsiones. Es considerado un proceso benigno, en pocos casos originan discapacidad y muerte en una minoría de pacientes. El término de síndrome de vasoconstricción reversible se ha propuesto para unificar a una variedad de síndromes clínicos similares, pero de etiología diferentes y han originados diversos epónimos. La aparente baja frecuencia del síndrome de vasoconstricción reversible y su forma de presentación hace que se convierta en un reto diagnóstico en los servicios de urgencias y puede pasar desapercibido si no se tiene una historia clínica adecuada. Presentamos un caso probablemente relacionado al uso de isometepteno. (Acta Med Colomb 2019; 44. DOI:https://doi.org/10.36104/amc.2019.1213)


Subject(s)
Humans , Female , Middle Aged , Syndrome , Vasoconstriction , Brain Edema , Cerebral Arteries , Stroke , Headache
8.
Article in Korean | WPRIM | ID: wpr-766747

ABSTRACT

Posterior reversible encephalopathy syndrome (PRES) is characterized by neurotoxic symptoms and neuroimaging finding of reversible cerebral edema in association with various conditions including hypertension, eclampsia, and autoimmune diseases. The author experienced a 47-year-old woman with systemic lupus erythematosus and systemic sclerosis overlap syndrome who developed PRES. The patient presented with alteration of consciousness in association with hypertension and increased autoimmune activity. Magnetic resonance imaging revealed vasogenic edema in the bilateral cerebral cortex, subcortical white matter, basal ganglia, brainstem, and cerebellum.


Subject(s)
Autoimmune Diseases , Basal Ganglia , Brain Edema , Brain Stem , Cerebellum , Cerebral Cortex , Consciousness , Eclampsia , Edema , Female , Humans , Hypertension , Lupus Erythematosus, Systemic , Magnetic Resonance Imaging , Middle Aged , Neuroimaging , Posterior Leukoencephalopathy Syndrome , Pregnancy , Scleroderma, Systemic , White Matter
9.
Article in English | WPRIM | ID: wpr-759975

ABSTRACT

Subarachnoid hemorrhage (SAH) usually occurs due to aneurysmal rupture of intracranial arteries and its typical computed tomography (CT) findings are increased attenuation of cisterns and subarachnoid spaces. However, several CT findings mimicking SAH are feasible in diverse conditions. They are so-called as pseudo-SAH, and this report is a case of pseudo-SAH which is misdiagnosed as aneurysm rupture accompanied by bilateral chronic subdural hematoma (cSDH). A 42-year-old male with severe headache visited our institute. Non-contrast brain CT images showed increased attenuation on basal cistern, and cSDH on both fronto-temporo-parietal convexity with midline shifting. Trans-femoral cerebral angiography was done and we confirmed small aneurysm at right M1 portion of middle cerebral artery. Under diagnosis of SAH, we planned an operation in order to clip aneurysmal neck and remove cSDH. cSDH was removed as planned, however, there was no SAH and we also couldn't find the rupture point of aneurysm. Serial follow-up CT showed mild cumulative cSDH recurrence, but the patient was tolerant and had no neurologic deficit during hospitalization. We have checked the patient via out-patient department for 6 months, there are no significant changes in volume and density of cSDH and the patient also have no neurologic complications.


Subject(s)
Adult , Aneurysm , Arteries , Brain , Brain Edema , Cerebral Angiography , Diagnosis , Follow-Up Studies , Headache , Hematoma, Subdural, Chronic , Hemorrhage , Hospitalization , Humans , Intracranial Hypertension , Male , Middle Cerebral Artery , Neck , Neurologic Manifestations , Outpatients , Recurrence , Rupture , Subarachnoid Hemorrhage , Subarachnoid Space
10.
Laboratory Animal Research ; : 124-131, 2019.
Article in English | WPRIM | ID: wpr-786395

ABSTRACT

Cerebral ischemia is a major cause of neurodegenerative disease. It induces neuronal vulnerability and susceptibility, and leads to neuronal cell death. Resveratrol is a polyphenolic compound that acts as an anti-oxidant. It exerts a neuroprotective effect against focal cerebral ischemic injury. Akt signaling pathway is accepted as a representative cell survival pathway, including proliferation, growth, and glycogen synthesis. This study investigated whether resveratrol regulates Akt/glycogen synthase kinase-3β (GSK-3β) pathway in a middle cerebral artery occlusion (MCAO)-induced ischemic brain injury. Adult male rats were intraperitoneally injected with vehicle or resveratrol (30 mg/kg) and cerebral cortices were isolated 24 h after MCAO. Neurological behavior test, corner test, brain edema measurment, and 2,3,5-triphenyltetrazolium chloride staining were performed to elucidate the neuroprotective effects of resveratrol. Phospho-Akt and phospho-GSK-3β expression levels were measured using Western blot analysis. MCAO injury led to severe neurobehavioral deficit, infraction, and histopathological changes in cerebral cortex. However, resveratrol treatment alleviated these changes caused by MCAO injury. Moreover, MCAO injury induced decreases in phospho-Akt and phospho-GSK-3β protein levels, whereas resveratrol attenuated these decreases. Phosphorylations of Akt and GSK-3β act as a critical role for the suppression of apoptotic cell death. Thus, our finding suggests that resveratrol attenuates neuronal cell death in MCAO-induced cerebral ischemia and Akt/GSK-3β signaling pathway contributes to the neuroprotective effect of resveratrol.


Subject(s)
Adult , Animals , Behavior Rating Scale , Blotting, Western , Brain Edema , Brain Injuries , Brain Ischemia , Cell Death , Cell Survival , Cerebral Cortex , Glycogen , Humans , Infarction, Middle Cerebral Artery , Male , Middle Cerebral Artery , Neurodegenerative Diseases , Neurons , Neuroprotective Agents , Phosphorylation , Rats
11.
Neuroscience Bulletin ; (6): 461-470, 2019.
Article in English | WPRIM | ID: wpr-775428

ABSTRACT

Gastrodin is a phenolic glycoside that has been demonstrated to provide neuroprotection in preclinical models of central nervous system disease, but its effect in subarachnoid hemorrhage (SAH) remains unclear. In this study, we showed that intraperitoneal administration of gastrodin (100 mg/kg per day) significantly attenuated the SAH-induced neurological deficit, brain edema, and increased blood-brain barrier permeability in rats. Meanwhile, gastrodin treatment significantly reduced the SAH-induced elevation of glutamate concentration in the cerebrospinal fluid and the intracellular Ca overload. Moreover, gastrodin suppressed the SAH-induced microglial activation, astrocyte activation, and neuronal apoptosis. Mechanistically, gastrodin significantly reduced the oxidative stress and inflammatory response, up-regulated the expression of nuclear factor erythroid 2-related factor 2, heme oxygenase-1, phospho-Akt and B-cell lymphoma 2, and down-regulated the expression of BCL2-associated X protein and cleaved caspase-3. Our results suggested that the administration of gastrodin provides neuroprotection against early brain injury after experimental SAH.


Subject(s)
Animals , Apoptosis , Astrocytes , Metabolism , Benzyl Alcohols , Blood-Brain Barrier , Metabolism , Brain , Metabolism , Brain Edema , Calcium , Metabolism , Glucosides , Glutamic Acid , Metabolism , Male , Microglia , Metabolism , Neurons , Neuroprotective Agents , Oxidative Stress , Rats, Sprague-Dawley , Subarachnoid Hemorrhage , Metabolism
12.
Article in English | WPRIM | ID: wpr-765922

ABSTRACT

BACKGROUND: Acute ischemic stroke patients with malignant infarct cores were primarily treated with neurocritical care based on reperfusion and hypothermia. We evaluated the predictors for malignant progression and functional outcomes. METHODS: From January 2010 to March 2015 ischemic stroke patients with large vessel occlusion of the anterior circulation with infarct volume >82 mL on baseline diffusion weighted image (DWI) within 6 hours from onset, with National Institutes of Health Stroke Scale ≥15 were included. All patients were managed with intent for reperfusion and neurocritical care. Malignant progression was defined as clinical signs of progressive herniation. Predictive factors for malignant progression and outcomes of decompressive hemicraniectomy (DHC) were evaluated. RESULTS: In total, 49 patients were included in the study. Among them, 33 (67.3%) could be managed with neurocritical care and malignant progression was observed in the remainder. Decompressive surgery was performed in nine patients (18.4%). Factors predictive of malignant progression were initial DWI volumes (odds ratio [OR], 1.01; 95% confidence interval [CI], 1.00 to 1.02; P=0.046) and parenchymal hematoma (OR, 6.77; 95% CI, 1.50 to 30.53; P=0.013) on computed tomography taken at Day 1. Infarct volume of >210 mL predicted malignant progression with 56.3% sensitivity and 90.9% specificity. Among the malignant progressors, 77.7% resulted in grave outcomes even with DHC, while all patients who declined surgery died. CONCLUSION: Acute ischemic stroke patients with malignant cores between 82 to 209 mL can be primarily treated with neurocritical care based on reperfusion and hypothermia with feasible results. In patients undergoing surgical decompression due to malignant progression, the functional outcomes were not satisfactory.


Subject(s)
Brain Edema , Critical Care , Decompression, Surgical , Decompressive Craniectomy , Diffusion , Hematoma , Humans , Hypothermia , Hypothermia, Induced , Infarction, Middle Cerebral Artery , Reperfusion , Sensitivity and Specificity , Stroke , Thrombectomy
13.
Article in English | WPRIM | ID: wpr-761740

ABSTRACT

Primary amebic encephalitis (PAM) is a devastating central nervous system infection caused by Naegleria fowleri, a free-living amoeba, which can survive in soil and warm fresh water. Here, a 43-year-old healthy male was exposed to warm freshwater 5 days before the symptom onset. He rapidly developed severe cerebral edema before the diagnosis of PAM and was treated with intravenous conventional amphotericin B while died of terminal cerebral hernia finally. Comparing the patients with PAM who has similar clinical symptoms to those with other common types of meningoencephalitis, this infection is probably curable if treated early and aggressively. PAM should be considered in the differential diagnosis of purulent meningoencephalitis, especially in patients with recent freshwater-related activities during the hot season.


Subject(s)
Adult , Amoeba , Amphotericin B , Brain Edema , Central Nervous System Infections , Central Nervous System Protozoal Infections , Diagnosis , Diagnosis, Differential , Encephalitis , Encephalocele , Fresh Water , Humans , Male , Meningoencephalitis , Naegleria fowleri , Seasons , Soil
14.
Article in English | WPRIM | ID: wpr-741368

ABSTRACT

Hyperammonemia can be caused by several genetic inborn errors of metabolism including urea cycle defects, organic acidemias, fatty acid oxidation defects, and certain disorders of amino acid metabolism. High levels of ammonia are extremely neurotoxic, leading to astrocyte swelling, brain edema, coma, severe disability, and even death. Thus, emergency treatment for hyperammonemia must be initiated before a precise diagnosis is established. In neonates with hyperammonemia caused by an inborn error of metabolism, a few studies have suggested that peritoneal dialysis, intermittent hemodialysis, and continuous renal replacement therapy (RRT) are effective modalities for decreasing the plasma level of ammonia. In this review, we discuss the current literature related to the use of RRT for treating neonates with hyperammonemia caused by an inborn error of metabolism, including optimal prescriptions, prognosis, and outcomes. We also review the literature on new technologies and instrumentation for RRT in neonates


Subject(s)
Ammonia , Astrocytes , Brain Edema , Coma , Diagnosis , Edema , Emergency Treatment , Humans , Hyperammonemia , Infant, Newborn , Metabolism , Metabolism, Inborn Errors , Peritoneal Dialysis , Plasma , Prescriptions , Prognosis , Renal Dialysis , Renal Replacement Therapy , Urea
15.
Article in English | WPRIM | ID: wpr-739820

ABSTRACT

Decompressive craniectomy (DC) is commonly performed in patients with intracranial hypertension or brain edema due to traumatic brain injury. Infrequently, neurologic deteriorations accompanied by sunken scalp may occur after DC. We report two patients with traumatic subdural hemorrhage who had neurologic deteriorations accompanied by sunken scalp after DC. Neurologic function improved dramatically in both patients after cranioplasty. Monitoring for neurologic deterioration after craniectomy is advised. For patients showing neurologic deficit with a sunken scalp, early cranioplasty should be considered.


Subject(s)
Brain Edema , Brain Injuries , Decompressive Craniectomy , Hematoma, Subdural , Humans , Intracranial Hypertension , Neurologic Manifestations , Scalp , Skin
16.
Geriatr., Gerontol. Aging (Impr.) ; 12(4): 215-218, out.-dez.2018. ilus
Article in English, Portuguese | LILACS | ID: biblio-981852

ABSTRACT

A síndrome da encefalopatia posterior reversível, conhecida como PRES, é rara e pouco descrita em idosos e é caracterizada pelo início subagudo de um conjunto de sinais clínicos e radiológicos e uma variedade de sintomas neurológicos, como cefaleia, crises convulsivas e transtornos da cognição. Na grande maioria dos pacientes, a apresentação clínica inclui pressão arterial elevada e emergência hipertensiva. A ressonância magnética (RM) é o exame padrão-ouro para o diagnóstico imaginológico dessa entidade. O quadro clínico e as alterações de imagens podem se tornar reversíveis caso seja detectada precocemente e tratada a causa base da síndrome. Os autores apresentam o caso clínico de uma idosa de 87 anos, internada para tratamento de pneumonia comunitária retornando ao setor de emergência 24 horas após a alta hospitalar apresentando sintomas neurológicos visuais complexos. Ao exame de RM, observaram-se lesões de hipodensidades occipitais bilaterais, sugestivas de edema vasogênico, compatível com PRES. Após o rigoroso controle da pressão arterial, verificou-se a reversibilidade total dessas lesões cerebrais.


Posterior reversible encephalopathy syndrome (PRES) is a disease rarely described in older adults. It is characterized by subacute onset of a set of clinical and radiological signs and a variety of neurological symptoms, such as headaches, seizures, and cognitive disorders. In the vast majority of patients, clinical presentation includes high blood pressure and hypertensive emergency. Magnetic resonance imaging (MRI) is the gold standard for diagnosing this condition using imaging findings. When the underlying cause is promptly recognized and treated, symptoms and imaging abnormalities may be completely reversible. The authors report the clinical case of an 87-year-old woman first admitted for treatment of community-acquired pneumonia. She returned to the emergency department 24 hours after discharge presenting with complex visual and neurological symptoms. An MRI scan showed lesions of bilateral occipital hypodensities, suggestive of vasogenic edema and compatible with PRES. Complete regression of brain lesions was observed after tight control of hypertension.


Subject(s)
Humans , Female , Aged, 80 and over , Posterior Leukoencephalopathy Syndrome/diagnosis , Posterior Leukoencephalopathy Syndrome/physiopathology , Posterior Leukoencephalopathy Syndrome/therapy , Hypertension/complications , Hypertension/diagnosis , Brain Edema/diagnostic imaging , Magnetic Resonance Imaging/methods , Neurologic Manifestations
18.
Article in English | WPRIM | ID: wpr-765235

ABSTRACT

OBJECTIVE: The beneficial effect of hypothermia after hemicraniectomy in malignant middle cerebral artery (MCA) infarction has been controversial. We aim to investigate the safety and clinical efficacy of hypothermia after hemicraniectomy in malignant MCA infarction. METHODS: From October 2012 to February 2016, 20 patients underwent hypothermia (Blanketrol III, Cincinnati Sub-Zero, Cincinnati, OH, USA) at 34°C after hemicraniectomy in malignant MCA infarction (hypothermia group). The indication of hypothermia included acute cerebral infarction >2/3 of MCA territory and a Glasgow coma scale (GCS) score 10 mm or transtentorial herniation sign (a fixed and dilated pupil). We retrospectively collected 27 patients, as the control group, who had undergone hemicraniectomy alone and simultaneously met the inclusion criteria of hypothermia between January 2010 and September 2012, before hypothermia was implemented as a treatment strategy in Dong-A University Hospital. We compared the mortality rate between the two groups and investigated hypothermia-related complications, such as postoperative bleeding, pneumonia, sepsis and arrhythmia. RESULTS: The age, preoperative infarct volume, GCS score, National institutes of Health Stroke Scale score, and degree of midline shift were not significantly different between the two groups. Of the 20 patients in the hypothermia group, 11 patients were induced with hypothermia immediately after hemicraniectomy and hypothermia was initiated in 9 patients after the decision of hypothermia during postoperative care. The duration of hypothermia was 4±2 days (range, 1 to 7 days). The side effects of hypothermia included two patients with arrhythmia, one with sepsis, one with pneumonia, and one with hypotension. Three cases of hypothermia were discontinued due to these side effects (one sepsis, one hypotension, and one bradycardia). The mortality rate of the hypothermia group was 15.0% and that of the control group was 40.7% (p=0.056). On the basis of the logistic regression analysis, hypothermia was considered to contribute to the decrease in mortality rate (odds ratio, 6.21; 95% confidence interval, 1.04 to 37.05; p=0.045). CONCLUSION: This study suggests that hypothermia after hemicraniectomy is a viable option when the progression of patients with malignant MCA infarction indicate poor prognosis.


Subject(s)
Arrhythmias, Cardiac , Brain Edema , Cerebral Infarction , Glasgow Coma Scale , Hemorrhage , Humans , Hypotension , Hypothermia , Infarction , Infarction, Middle Cerebral Artery , Logistic Models , Middle Cerebral Artery , Mortality , Pneumonia , Postoperative Care , Prognosis , Retrospective Studies , Sepsis , Stroke , Treatment Outcome
19.
Article in English | WPRIM | ID: wpr-788665

ABSTRACT

OBJECTIVE: The beneficial effect of hypothermia after hemicraniectomy in malignant middle cerebral artery (MCA) infarction has been controversial. We aim to investigate the safety and clinical efficacy of hypothermia after hemicraniectomy in malignant MCA infarction.METHODS: From October 2012 to February 2016, 20 patients underwent hypothermia (Blanketrol III, Cincinnati Sub-Zero, Cincinnati, OH, USA) at 34°C after hemicraniectomy in malignant MCA infarction (hypothermia group). The indication of hypothermia included acute cerebral infarction >2/3 of MCA territory and a Glasgow coma scale (GCS) score < 11 with a midline shift >10 mm or transtentorial herniation sign (a fixed and dilated pupil). We retrospectively collected 27 patients, as the control group, who had undergone hemicraniectomy alone and simultaneously met the inclusion criteria of hypothermia between January 2010 and September 2012, before hypothermia was implemented as a treatment strategy in Dong-A University Hospital. We compared the mortality rate between the two groups and investigated hypothermia-related complications, such as postoperative bleeding, pneumonia, sepsis and arrhythmia.RESULTS: The age, preoperative infarct volume, GCS score, National institutes of Health Stroke Scale score, and degree of midline shift were not significantly different between the two groups. Of the 20 patients in the hypothermia group, 11 patients were induced with hypothermia immediately after hemicraniectomy and hypothermia was initiated in 9 patients after the decision of hypothermia during postoperative care. The duration of hypothermia was 4±2 days (range, 1 to 7 days). The side effects of hypothermia included two patients with arrhythmia, one with sepsis, one with pneumonia, and one with hypotension. Three cases of hypothermia were discontinued due to these side effects (one sepsis, one hypotension, and one bradycardia). The mortality rate of the hypothermia group was 15.0% and that of the control group was 40.7% (p=0.056). On the basis of the logistic regression analysis, hypothermia was considered to contribute to the decrease in mortality rate (odds ratio, 6.21; 95% confidence interval, 1.04 to 37.05; p=0.045).CONCLUSION: This study suggests that hypothermia after hemicraniectomy is a viable option when the progression of patients with malignant MCA infarction indicate poor prognosis.


Subject(s)
Arrhythmias, Cardiac , Brain Edema , Cerebral Infarction , Glasgow Coma Scale , Hemorrhage , Humans , Hypotension , Hypothermia , Infarction , Infarction, Middle Cerebral Artery , Logistic Models , Middle Cerebral Artery , Mortality , Pneumonia , Postoperative Care , Prognosis , Retrospective Studies , Sepsis , Stroke , Treatment Outcome
20.
Neuroscience Bulletin ; (6): 951-962, 2018.
Article in English | WPRIM | ID: wpr-777021

ABSTRACT

Fluoxetine, an anti-depressant drug, has recently been shown to provide neuroprotection in central nervous system injury, but its roles in subarachnoid hemorrhage (SAH) remain unclear. In this study, we aimed to evaluate whether fluoxetine attenuates early brain injury (EBI) after SAH. We demonstrated that intraperitoneal injection of fluoxetine (10 mg/kg per day) significantly attenuated brain edema and blood-brain barrier (BBB) disruption, microglial activation, and neuronal apoptosis in EBI after experimental SAH, as evidenced by the reduction of brain water content and Evans blue dye extravasation, prevention of disruption of the tight junction proteins zonula occludens-1, claudin-5, and occludin, a decrease of cells staining positive for Iba-1, ED-1, and TUNEL and a decline in IL-1β, IL-6, TNF-α, MDA, 3-nitrotyrosine, and 8-OHDG levels. Moreover, fluoxetine significantly improved the neurological deficits of EBI and long-term sensorimotor behavioral deficits following SAH in a rat model. These results indicated that fluoxetine has a neuroprotective effect after experimental SAH.


Subject(s)
Animals , Apoptosis , Blood-Brain Barrier , Brain Edema , Drug Therapy , Cytokines , Genetics , Metabolism , Disease Models, Animal , Fluoxetine , Pharmacology , Therapeutic Uses , In Situ Nick-End Labeling , Male , Neuroprotective Agents , Pharmacology , Therapeutic Uses , Pain Measurement , Psychomotor Performance , RNA, Messenger , Metabolism , Rats , Rats, Sprague-Dawley , Subarachnoid Hemorrhage , Drug Therapy , Pathology , Time Factors , Vasospasm, Intracranial , Drug Therapy
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