Diffuse Cerebral Edema Research Articles

Brain abscess complicating drug abuse

A 29-year-old man was admitted to hospital to undergo a methadone maintenance treatment program as a withdrawal method for illicit drugs. Several hours after the administration of the established dosage of methadone the man showed frequent paroxysmal hypoxia, finally lapsing into a coma. Head computed tomography (CT) scans that were performed shortly before death revealed massive brain swelling with a considerably large ring-enhancing lesion in the right frontal lobe of the brain; the man died shortly thereafter. Police investigation ascertained that the man had been addicted to illegal substances such as a newly synthesized drug named ‘‘krokodil’’ and to heroin. He had no previous medical history. At the medico-legal autopsy, external examination of the body revealed several puncture marks, both old and fresh, on both upper arms, antecubital fossae and forearms. During the internal examination, several firm and obviously swollen lymph nodes were noticed in the neck. The heart was of normal configuration with no evidence of anomaly or endocarditis. Moderate coronary atherosclerosis was observed. The lungs showed massive congestion and edema (weights: left, 1,050 g; right, 1,100 g). Except for the brain, the remaining internal organs showed no pathological changes at gross inspection. The brain weighed 1,530 g and showed diffuse massive cerebral edema and swelling, with uncal and tonsillar herniation. There was no evidence of meningitis. On sequential coronal sectioning of the brain after 3 weeks of formalin fixation, a spherical, well-encapsuled mass with a maximum diameter of 4.2 cm containing a muddy substance was present in the white matter of the right frontal and parietal lobes (Figs. 1, 2). Histopathology revealed a brain abscess characterized by the following: a necrotic center with scattered hemorrhage and gram-positive bacterial colonies surrounded by macrophages; granulation tissue with lymphocytes, plasma cells, fibroblasts and neovascularization surrounded by dense fibrocollagenous tissue and adjacent massive edema of the unaffected brain tissue (Fig. 3). Toxicological analysis of a femoral venous blood sample revealed 0.04 lg/mL of free morphine, 0.1 lg/mL of morphine-3-glucuronide, 0.4 lg/mL of methadone, 0.2 lg/mL of trimipramine and 0.2 lg/mL of N-desmethyltrimipramine. Desomorphine (dihydrodeoxymorphine), a main component of ‘‘krokodil,’’ a newly introduced illegal drug that serves as an inexpensive substitute for heroin, was not detected in the blood or urine. The cause of death was massive brain swelling with uncal and tonsillar herniation due to a cerebral abscess.

Evaluation of acute head injury by computed tomography scan in College of Medical Sciences-Teaching Hospital, Chitwan

This study was conducted to evaluate the computed tomography findings in patient with acute head injury and to emphasize the importance of computed tomography scan in head injury. One hundred consecutive patients presenting to the emergency department with head injury were evaluated by computed tomography scan of the head. Seventy five patients (75%) were male and twenty five (25%) were females. The age of the patients ranged from three to seventy years and the most affected age group was between thirty and forty (40%). The common causes of head injury were motor vehicle accident (70%), fall injury (25% ) and physical assault (5%). The most common computed tomographic findings were: cerebral contusions (52%), skull fractures (41%), intracerebral hematomas (24%), diffuse cerebral edema (23%), midline shift (18%), subdural hematomas (15%), subarachnoid hemorrhage (13%), diffuse axonal injury (8%), intraventricular hemorrhage (6%), extradural hemotomas (4%), pnemocephalus (2%) and normal scans were found in (5%). In conclusion, computed tomography is the mainstay in the imaging of head injury and helps in the patient management. DOI: http://dx.doi.org/10.3126/jcmsn.v7i1.5971 JCMSN 2011; 7(1): 36-39

Risk factors for 1-year mortality in patients with nontraumatic intracranial hemorrhage requiring intensive care

Mortality in patients with intracranial hemorrhage remains high. The aim of this study was to determine the 1-year survival and potential risk factors for 1-year mortality in patients with nontraumatic intracranial hemorrhage requiring intensive care. This was a 3-year (2005-2007) retrospective study in a university-level intensive care unit (ICU). Patient characteristics, level of consciousness, and radiological findings of the primary head computed tomography were recorded on admission. Sequential Organ Failure Assessment scores were recorded during the ICU stay. Patients were divided into two groups: subarachnoid hemorrhage (SAH) group and intracerebral hemorrhage (ICH) group. Kaplan-Meier survival curves were constructed, and independent risk factors were determined using Cox proportional hazards regression analyses. Two hundred twenty-nine patients were analyzed. The 1-year mortality rate was 32% in patients with SAH and 44% in patients with ICH. The risk factors for 1-year mortality in both groups were unconsciousness on admission [SAH: hazard ratio (HR) 6.2, P = 0.017 and ICH: HR 3.0, P = 0.004] and renal failure during the ICU stay (SAH: HR 2.5, P = 0.021 and ICH: HR 3.6, P = 0.021). Risk factors specific to the type of hemorrhage were the presence of ICH (HR 2.0, P = 0.033) and diffuse cerebral edema (HR 2.3, P = 0.017) in the SAH group and a prior use of warfarin (HR 5.1, P = 0.016) in the ICH group. In addition to decreased level of consciousness on admission, renal failure during the ICU stay is an independent risk factor for 1-year mortality in nontraumatic SAH as well as ICH.

Reversible posterior leukoencephalopathy syndrome after blood transfusion in a patient with end-stage renal disease

A 42-year-old female end-stage renal disease (ESRD) patient with reversible posterior leukoencephalopathy syndrome (RPLS) post-transfusion during initiation of hemodialysis is reported. Eleven days after the onset of illness, we diagnosed encephalopathy as a grand mal seizure resulting from diffuse cerebral edema. One reason for the delayed diagnosis was that her symptom, a throbbing headache that occurred during her first dialysis, indicated dialysis disequilibrium syndrome. We must bear in mind that a small amount of transfusion could cause RPLS even during the first dialysis. To our knowledge, this is the first case report on RPLS after blood transfusion in an ESRD patient.

Computed tomography may demonstrate pseudosubarachnoid hemorrhage in diffuse cerebral edema after cardiorespiratory arrest

To report the cases of two children who died from diffuse cerebral edema after cardiorespiratory arrest and who had radiologic findings of subarachnoid hemorrhage on computed tomography, the presence of which was excluded on subsequent postmortem examination. Case notes, clinical records, and postmortem reports of two children who became brain stem dead after cardiorespiratory arrest. Radiologic mimics of subarachnoid hemorrhage have been reported in the adult literature and are termed pseudosubarachnoid hemorrhage. A diagnosis of pseudosubarachnoid hemorrhage, rather than true subarachnoid hemorrhage, should be considered in the context of diffuse cerebral edema after cardiorespiratory arrest. Interpretation of the radiologic finding of subarachnoid hemorrhage in a child after a prolonged cardiac arrest should be cautious to avoid unnecessary and deleterious management and investigation for aneurysms.

Fulminant chemical ventriculomeningitis following intrathecal liposomal cytarabine administration

Intrathecal liposomal cytarabine (ITLC) has shown prolonged time to neurological deterioration in some patients with leptomeningeal spread of breast cancer. We describe a patient with fulminant chemical ventriculomeningitis leading to cerebral edema and death following ITLC administration. A 56-year-old Caucasian female developed progressive headache, depressed level of consciousness and adventitious movements immediately following ITLC. Neurological examination was normal prior to injection. This progressed to loss of all brainstem function and a head CT scan demonstrated diffuse cerebral edema. Due to the absence of neurological function on examination, the family opted to withdraw care. To our knowledge we report the first patient with fulminant chemical ventriculomeningitis leading to cerebral edema and death following ITLC administration. Adjunctive glucocorticoids are recommended. Treatment options are limited and complicated by the liposomal formulation of intrathecal cytarabine.

Cerebral edema and a transtentorial brain herniation syndrome associated with pandemic swine influenza A (H1N1) virus infection

Acute encephalitis, encephalopathy, and seizures are known rare neurologic sequelae of respiratory tract infection with seasonal influenza A and B virus, but the neurological complications of the pandemic 2009 swine influenza A (H1N1) virus, particularly in adults, are ill-defined. We document two young adults suffering from H1N1-associated acute respiratory distress syndrome and renal failure who developed cerebral edema. The patients acutely developed a transtentorial brain herniation syndrome including a unilateral third nerve palsy (dilated and unresponsive pupils), elevated intracranial pressure, coma, and radiological evidence of diffuse cerebral edema. In both patients, neurological deterioration occurred in the context of hyponatremia and a systemic inflammatory state. These patients illustrate that severe neurologic complications, including malignant cerebral edema, can occur in adults infected with H1N1 virus, and illustrate the need for close neurological monitoring of potential neurological morbidities in future pandemics.

Magnetic Resonance Imaging Findings in Reye Syndrome

Magnetic resonance imaging findings in Reye syndrome have been reported only infrequently. A previously well 8-year-old boy presented with repeated episodes of vomiting and abdominal pain followed by altered sensorium and tonic spasms. This occurred 5 days after upper respiratory tract infection. His laboratory data revealed elevated liver enzymes, prolonged prothrombin time, and high blood ammonia levels. Magnetic resonance imaging of the brain done on the day of admission revealed diffuse cerebral edema and signal alterations in brainstem, bilateral thalami, medial temporal lobes, parasagittal cortex, and cerebellar and subcortical white matter. Diffusion restriction was seen in thalami, midbrain, cerebellar white matter, subcortical white matter, and parasaggital cortex in the watershed territory. The patient made a full recovery. Follow-up magnetic resonance imaging after a week revealed complete resolution of all except thalamic lesions. Although diffusion restriction in thalami and midbrain has been reported previously, this is the first report indicating diffusion restriction in subcortical white matter and the parasagittal cortex.

Malignant Course of a Metastatic Melanoma During Pregnancy: A Case Report

Cutaneous melanoma can metastasize to any organ, including brain and spinal cord. A 27-year-old lady, four months after conception presented with generalized seizures and was diagnosed to have subarachnoid hemorrhage. Further investigation did not reveal aneurysm. She underwent right ventriculo-peritoneal shunt for hydrocephalus and MTP for unprotected radiation from CT scan. Six weeks later she came to our institution with symptoms of dorsal compression. Imaging showed multiple intradural extramedullary spinal lesions at D3-D4, D8 and D10-D11. Surgical excision of the lesions was done and histopathology was consistent with metastatic deposits from malignant melanoma which was confirmed by immunohistochemistry studies also. Her conscious level deteriorated on the second postoperative day and CT scan showed multiple small tumor emboli with evidence of right temporal bleed and diffuse cerebral edema. In spite of aggressive treatment she could not be saved. This reported case concludes that pregnancy aggravates the clinical course of metastatic melanoma. doi:10.4021/wjon285w

Correlação entre a escala de coma de Glasgow e os achados de imagem de tomografia computadorizada em pacientes vítimas de traumatismo cranioencefálico

OBJETIVO: Determinar a correlação da escala de coma de Glasgow, fatores causais e de risco, idade, sexo e intubação orotraqueal com os achados tomográficos em pacientes com traumatismo cranioencefálico. MATERIAIS E MÉTODOS: Foi realizado estudo transversal prospectivo de 102 pacientes, atendidos nas primeiras 12 horas, os quais receberam pontuação segundo a escala de coma de Glasgow e foram submetidos a exame tomográfico. RESULTADOS: A idade média dos pacientes foi de 37,77 ± 18,69 anos, com predomínio do sexo masculino (80,4%). As causas foram: acidente automobilístico (52,9%), queda de outro nível (20,6%), atropelamento (10,8%), queda ao solo ou do mesmo nível (7,8%) e agressão (6,9%). No presente estudo, 82,4% dos pacientes apresentaram traumatismo cranioencefálico de classificação leve, 2,0% moderado e 15,6% grave. Foram observadas alterações tomográficas (hematoma subgaleal, fraturas ósseas da calota craniana, hemorragia subaracnoidea, contusão cerebral, coleção sanguínea extra-axial, edema cerebral difuso) em 79,42% dos pacientes. Os achados tomográficos de trauma craniano grave ocorreram em maior número em pacientes acima de 50 anos (93,7%), e neste grupo todos necessitaram de intubação orotraqueal. CONCLUSÃO: Houve significância estatística entre a escala de coma de Glasgow, idade acima de 50 anos (p < 0,0001), necessidade de intubação orotraqueal (p < 0,0001) e os achados tomográficos.

Clinical characteristics and pathophysiological mechanisms of focal and diffuse traumatic brain injury

Traumatic brain injury (TBI) is a frequent and clinically highly heterogeneous neurological disorder with large socioeconomic consequences. TBI severity classification, based on the hospital admission Glasgow Coma Scale (GCS) score, ranges from mild (GCS 13–15) and moderate (GCS 9–12) to severe (GCS ≤ 8). The GCS reflects the risk of dying from TBI, which is low after mild (∼1%), intermediate after moderate (up to 15%) and high (up to 40%) after severe TBI. Intracranial damage can be focal, such as epidural and subdural haematomas and parenchymal contusions, or diffuse, for example traumatic axonal injury and diffuse cerebral oedema, although this distinction is somewhat arbitrary. Study of the cellular and molecular post-traumatic processes is essential for the understanding of TBI pathophysiology but even more to find therapeutic targets for the development of neuroprotective drugs to be eventually used in human beings. To date, studies in vitro and in vivo, mainly in animals but also in human beings, are unravelling the pathological TBI mechanisms at high pace. Nevertheless, TBI pathophysiology is all but completely elucidated. Neuroprotective treatment studies in human beings have been disappointing thus far and have not resulted in commonly accepted drugs. This review presents an overview on the clinical aspects and the pathophysiology of focal and diffuse TBI, and it highlights several acknowledged important events that occur on molecular and cellular level after TBI.

Life-saving decompressive craniectomy for diffuse cerebral edema during an episode of new-onset diabetic ketoacidosis

Diabetic ketoacidosis (DKA), a well-known complication of diabetes mellitus, is associated with severe diffuse cerebral edema leading to brain herniation and death. Survival from an episode of symptomatic cerebral edema has been associated with debilitating neurological sequelae, including motor deficits, visual impairment, memory loss, seizures, and persistent vegetative states. A review of the literature reveals scant information regarding the potential surgical options for these cases. The authors present their case in which they used a craniectomy to treat this life-threatening condition. After reportedly suffering nausea and vomiting, a 12-year-old male presented to the emergency room with lethargy and was diagnosed with acute DKA. After appropriate treatment, the patient became comatose. A CT scan revealed diffuse cerebral edema. To decrease intracranial pressure and prevent further progression of brain herniation, a bifrontal decompressive craniectomy with duraplasty was performed. The patient's neurological function gradually improved, and he returned to school and his regular activities with only minimal cognitive deficits. Given the high mortality and morbidity associated with DKA-related edema, we believe decompressive craniectomy should be considered for malignant cerebral edema and herniation syndrome.

Relative factors for and early treatment of craniocerebral trauma in the elderly

Objective To discuss the relative factors and clinical features of the elderly patients with craniocerebral trauma so as to improve the level of diagnosis and treatment of craniocerebral trauma.Methods A retrospective study was conducted on 139 patients with craniocerebral trauma treated in our department from June 2006 to August 2009. The post-injury pathogenesis, Glasgow Coma Scale (GCS)score, injury type, major complications and treatment method were summarized and analyzed to find the correlation of various factors with prognosis. Results It was revealed that the mortality was closely related with GCS score, injury type and post-tranmatic complications. The lower GCS score induced higher mortality. The high mortality was manifested in patients with craniocerebral trauma who presented diffuse cerebral edema, contusion and laceration combined with multiple hematomas and brain stem injury. The prognosis was impacted by lung infection, failure of respiratory function, hemorrhage in upper digestive tract, or simultaneous 2-3 complications after craniocerebral trauma. Conclusions The prognosis is directly affected by injury severity, injury type and complications of craniocerebral trauma. The elderly patients demonstrate delayed reaction, which deserves active early examinations and treatment to improve the prognosis. Key words: Craniocerebral trauma; Prognosis; Aged

Hipermetioninemia en el recién nacido pretérmino. Estudio de los factores predisponentes

Introduction Excess methionine can cause central nervous system disorders such as diffuse cerebral edema and disorders of myelin. Patients and method A retrospective and prospective (ambispective) observational study in preterm newborns admitted to our hospital over a period of 15 months and who had hypermethioninemia in neonatal screening tests by tandem mass spectrometry. The progress of these infants was monitored during the first year of life, assessing their methionine levels, diet, somatometric parameters and neurodevelopment. Results From a study population of 187 preterm infants, 16 of them showed isolated hypermethioninemia. Weight and feeding the babies with a special formula enriched with methionine is related to an increased number of cases of transient isolated hypermethioninemia (62.6% received a higher contribution of methionine than 97 mg/kg/day). We also found a statistically significant correlation between the days that patients received the formula and the time it takes to normalize the levels of methionine in plasma (R 0.791, p=0.000). There was no correlation between the methionine peak reached in plasma and the score on the Brunet Lézine test, at the corrected age of 6 months. Conclusions This study highlights the importance amino acid supplements, particularly methionine, in premature infants’ formulas due to the impact they may have on neurological development.

Extensive supratentorial hemorrhages following posterior fossa meningioma surgery

Remote supratentorial hematoma soon after posterior fossa surgery for the removal of a space-occupying lesion is a rare but dramatic and dreaded complication, carrying significant morbidity and mortality. A 47-year-old woman presented with headache of 1-year duration that worsened over last 2 months, progressive ataxia of 2 months’ duration, blurring and diminution of vision of 2 months’ duration and forgetfulness of 2 months’ duration. Fundus showed bilateral papille dema, and visual acuity was 6/9 in both eyes. She had left-sided cerebellar signs. There were no focal motor or sensory neurological deficits. MRI brain with contrast showed a large posterior fossa tumor with obstructive hydrocephalus. The patient underwent left paramedian suboccipital craniectomy in prone position with left side up. In the immediate postoperative period, the patient did no recover from anesthesia and was persistently drowsy. Immediate repeat CT scan showed diffuse subarachnoid hemorrhage spread all over the bilateral cerebral hemispheres with diffuse cerebral edema. The patient recovered with conservative management without deficits. This case stresses the importance of early postoperative CT scan and optimal management of the hemorrhage for good outcome.

Underlying prothrombotic states in pregnancy associated cerebral venous thrombosis

The exact pathogenesis of pregnancy associated cerebral venous thrombois is still unsettled. Aims : To identify possible inherited and acquired prothrombotic risk factors and also identify the factors associated with mortality in pregnancy associated CVT. Prospective cohort study to identify prothrombotic risk factors and case control study of influence of local traditional practice of puerperal water restriction on postpartum CVT. Consecutive patients with pregnancy associated CVT seen over a period of three years. Thrombotic workup included genetic markers, protein assays, and other factors. Univariate and chi-square analysis. Of the 41 patients studied during the study period, 71% of patient had a single and 34% had multiple prothrombotic risk factors. Methylene tetrahydro-folate reductase (MTHFR) heterozygosity (19.5%) and factor V Leiden heterozygous (7.3%) were the commonest genetic markers. Hyperhomocysteinemia (34%) and elevated factor VIII levels (14.6%) were the other important risk factors. In this cohort the mortality was 17%. Mortality increased by odds of 1.3 for every additional prothrombotic marker. The factors associated with increased mortality included: status epileptics (P = 0.05, OR 13.2, 95% CI 1.002 - 173), deep venous system involvement (P = 0.016, OR 9.64, 95% CI 1.53 - 60.6), presence of midline shift (P = 0.012, OR 24.7, 95% CI 2.05 - 29.8) and diffuse cerebral edema (P = 0.006, OR 14.5, 95% CI 2.18- 96.4). The traditional practice of decrease intake of water during puerperium was significant in woman with pregnancy associated CVT when compared to control subjects (P < 0.02). In patients with pregnancy associated CVT, prothrombotic markers can be multiple and are associated with increased odds of mortality. Deep venous system involvement, presence of midline shift and diffuse cerebral edema increased mortality. Peuperial water restriction may be a modifiable risk factor.

Hyponatremic Encephalopathy after Excessive Water Ingestion Prior to Pelvic Ultrasound: Neuroimaging Findings

We report two patients with acute hyponatremic encephalopathy which developed after massive water ingestion for pelvic ultrasound and emphasize the findings of magnetic resonance (MR) imaging including diffusion-weighted imaging (DWI). Both subjects had completely recovered within 24 hours following fluid restriction and salt replacement. MR imaging revealed cortical sulcal narrowing, restricted diffusion and sulcal T2 hyperintensity along with diffuse pial enhancement suggesting diffuse cerebral cortical cytotoxic edema and blood-brain barrier breakdown. In addition to the first illustration of multimodality MR imaging features of water-intoxication, these two cases also highlight the need for standardized practice on the quantity of water intake recommended to distend the bladder for pelvic ultrasound, especially in patients at risk for serum inappropriate ADH syndrome-related hyponatremia.

CT Perfusion Evidence of Early Global Cerebral Hypoperfusion After Aneurysmal Subarachnoid Hemorrhage with Cardiac Arrest

Cardiac arrest and aneurysmal subarachnoid hemorrhage both cause sudden, severe cerebral hypoperfusion at ictus. Animal studies indicate that the resultant microvascular dysfunction and cerebral perfusion abnormalities are important determinants of the associated cerebral injury in both conditions. Although this suggests that perfusion imaging might be a useful tool for prognostication in patients with these conditions, this hypothesis has not been thoroughly investigated in humans. Case report. A 49-year-old man developed cardiac arrest upon rupture of an intracranial aneurysm. When he arrived at our institution 10 h later, he was comatose, had neurogenic hyperventilation, absent corneal reflexes, and continuous multifocal myoclonus. Despite normal intracranial pressure, normal cerebral perfusion pressure, normal flow in the proximal cerebral arteries on CT angiography, and a lack of diffuse cerebral edema, CT perfusion imaging performed 12 h after ictus showed severe, diffuse hypoperfusion. After the development of refractory intracranial hypertension, physiologic support was withdrawn and the patient died. Early global cerebral hypoperfusion can be demonstrated by CT perfusion imaging after cardiac arrest associated with high-grade aneurysmal subarachnoid hemorrhage and may be indicative of poor neurologic outcome. CT perfusion should be investigated as a prognostic tool in these conditions.

Intracranial tumor lysis and cerebral edema after administration of intrathecal methotrexate: a case report and discussion

Methotrexate is a common agent used in the management of hematological malignancies, but is often associated with the development of diverse central nervous system adverse events, such as seizures. We present a case of seizures after intrathecal administration of methotrexate, during the management of diffuse large B-cell lymphoma. There was complete resolution of the CNS lesions after chemotherapy along with the interval development of diffuse cerebral edema. We hypothesize that tumor lysis is the underlying mechanism of this untoward event, resulting in the corresponding clinical presentation.

Cerebral angioedema associated with enalapril

Cerebral angioedema associated with enalapril