Geometry.Net - Health_Conditions: Cerebral Edema

JAMA -- Page Not Found
Abstract of a study intended to identify a clinical imaging correlate for HACE and determine whether Category Health Conditions and Diseases Altitude SicknessHighAltitude cerebral edema Evaluated With Magnetic Resonance Imaging Clinical Correlationand Pathophysiology Author Information Peter H. Hackett, MD; Philip
http://jama.ama-assn.org/issues/v280n22/abs/joc61470.html

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Cerebral Edema
Is defined as increased brain water content and can be either intracellular or extracellular.
http://edcenter.med.cornell.edu/CUMC_PathNotes/Neuropathology/Neuropath_I/edema.

Extractions: Intracellular (Cytotoxic) edema Cellular swelling, usually of astrocytes in the grey matter, and classically is seen following cerebral ischema caused by cardiac arrest or minor head injury. The blood brian barrier(BBB) is intact. Intracellular edema is usually not clinically significant, and is reversible in its early phases. Extracellular (vasogenic) edema A consequence of vascular injury with disruption of the BBB. Grossly , the gyri are flattened and the sulci narrowed; the white matter is moist and swollen. Microscopically, there is micro-vacuolization of the white matter, poor staining, and "halo's" around nuclei. Causes include trauma, tumor, and abscess. Ultimately, these changes can lead to herniation. Is a major consequence of cerebral edema. Because of the rigid skull and partitioning of the cranial vault by the falx cerebri and tentorium cerebelli, when the brain swells it is displaced relative to these partitions or is pushed toward the foramen magnum. There are several types of brain herniations - classified by the part that is herniated or the structure under which it has been pushed. Transtentorial herniations are of two main types: Uncal herniation The medial temporal lobe (uncus) herniates through the gap between the cerebral peduncles and the tentorium.
Cerebral Edema
A definition, classifications, pathophysiology and treatment of cerebral edema.
http://brainavm.uhnres.utoronto.ca/staff/Wallace/2000_curriculum/cerebral_edema.

Extractions: The cerebral capillary is the site of the BBB. Interendothelial tight junctions impede the passage of electron-dense markers. Cerebral capillaries lack fenestrations and have tight junctions. They are active in the process of pinocytosis. All these features regulate the passage of highly polar hydrophilic molecules allowing virtually unrestricted passage of lipid-soluble substances. Cerebral capillaries have 2-4X the number of mitochondria as other capillaries. Cerebral capillaries have an array of important enzymes: ATPase, dehydrogenase, monamine oxidase, DOPA decarboxylase, acid and alkaline phosphatase, NAD and others. BBB has both central (cholinergic and aminergic) and peripheral (sympathetic and parasympathetic) innervation.
Krane: DKA And Cerebral Edema
Diabetic Ketoacidosis and cerebral edema Elliot J. Krane, M.D. Departments of Pediatrics and Anesthesiology Stanford University Medical Center In 1922 Banting and Best introduced insulin into clinical practice. A decade later the first reported case of cerebral edema complicating diabetic ketoacidosis (DKA) was reported by Dillon,
http://pedsccm.wustl.edu/FILE-CABINET/Metab/DKA-CEdema.html

Extractions: Stanford University Medical Center In 1922 Banting and Best introduced insulin into clinical practice. A decade later the first reported case of cerebral edema complicating diabetic ketoacidosis (DKA) was reported by Dillon, Riggs and Dyer writing in the pathology literature. While the syndrome of cerebral edema complicating DKA was either not seen, ignored, or was unrecognized by the medical community until 3 decades later when the complication was again reported by Young and Bradley at the Joslin Clinic, there has since been a flurry of case reports in the 1960's and 1970's and basic and clinical research from the 1970's to the 1990's leading to our present day acceptance of this as a known complication of DKA, or of the management of DKA. In fact, we now recognize that the cerebral complications of DKA (including much less frequent cerebral arterial infarctions, venous sinus thrombosis, and central nervous system infections) are the most common cause of diabetic-related death of young diabetic patients (
Acute Illness - Cerebral Edema In DKA
cerebral edema IN DIABETIC KETOACIDOSIS. Fatal cerebral edema has been recognizedwith increasing frequency since the earliest reports in the 1960's.
http://www.mc.vanderbilt.edu/peds/pidl/acute/cerebr.htm

Extractions: PIDL Home/ Contents Development Nutrition Acute Illness ... Psychosocial Acute Illness CEREBRAL EDEMA IN DIABETIC KETOACIDOSIS In spite of advances over the past several decades in the understanding and treatment of diabetes mellitus, the incidence of DKA has not decreased. Ketoacidosis is the leading cause of death in young patients with diabetes. Death is usually due to electrolyte abnormalities, shock, aspiration pneumonitis, or myocardial infarction. Fatal cerebral edema has been recognized with increasing frequency since the earliest reports in the 1960's. The development of cerebral edema in patients with DKA is not heralded by any warning signs, nor are there any predictive indicators. Paradoxically, cerebral edema becomes clinically apparent 6- 10 hours after therapy has begun, at a time when severe acidosis has been partially corrected, the blood glucose level is falling, adequate circulation has been restored, and all indications suggest that the patient is recovering. The occurance of cerebral edema is marked by abrupt changes in mental status, abnormal neurologic signs, and progression to coma. Respiratory arrest may occur. Cerebral edema complicating DKA has a mortality of about 90%.
ClinicalPoints® - Cerebral Edema
Treatments, diagnosis and key points for cerebral edema.
http://mdx.com/products/demos/webready/Professional/ClinicalPoints/data_002.html
Acute Illness - Cerebral Edema In DKA
A good, though brief (less than 1024 chars), description of your site. pneumonitis, or myocardial infarction. Fatal cerebral edema has been recognized with increasing frequency since
http://www.mc.vanderbilt.edu/peds/pidl/acute/cerebr.html

Extractions: PIDL Home/ Contents Development Nutrition Acute Illness ... Psychosocial Acute Illness CEREBRAL EDEMA IN DIABETIC KETOACIDOSIS In spite of advances over the past several decades in the understanding and treatment of diabetes mellitus, the incidence of DKA has not decreased. Ketoacidosis is the leading cause of death in young patients with diabetes. Death is usually due to electrolyte abnormalities, shock, aspiration pneumonitis, or myocardial infarction. Fatal cerebral edema has been recognized with increasing frequency since the earliest reports in the 1960's. The development of cerebral edema in patients with DKA is not heralded by any warning signs, nor are there any predictive indicators. Paradoxically, cerebral edema becomes clinically apparent 6- 10 hours after therapy has begun, at a time when severe acidosis has been partially corrected, the blood glucose level is falling, adequate circulation has been restored, and all indications suggest that the patient is recovering. The occurance of cerebral edema is marked by abrupt changes in mental status, abnormal neurologic signs, and progression to coma. Respiratory arrest may occur. Cerebral edema complicating DKA has a mortality of about 90%.
JAMA -- Page Not Found
281;1794, May 19, 1999, HighAltitude cerebral edema, Buddha Basnyat, MD, MSc MartinI. Surks, MD Ralf W. Baumgartner, MD Peter Hackett, MD; Phil Yarnell, MD.
http://jama.ama-assn.org/issues/v281n19/ffull/jlt0519-3.html

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Cerebral Edema
Slide 38 of 63
http://www.austincc.edu/barnes/head/sld038.htm
Cerebral Edema In DKA References
cerebral edema in DKA References. Mel, JM and Werther, GA Incidence and outcomeof diabetic cerebral oedema in childhood are there predictors?
http://pedsccm.wustl.edu/FILE-CABINET/Metab/DKA_refs.html

Extractions: abstract abstract Rosenbloom, A. L. Intracerebral crises during treatment of diabetic ketoacidosis. Diabetes Care 13: 22-33, 1990. [[ abstract Harris, G. D., Fiordalisi, I., Harris, W. L., Mosovich, L. L. and Finberg, L. Minimizing the risk of brain herniation during treatment of diabetic ketoacidemia: a retrospective and prospective study [published erratum appears in J Pediatr 1991 Jan;118(1):166-7] [see comments]. Journal of Pediatrics 117: 22-31, 1990. [ abstract abstract Duck, S. C. and Wyatt, D. T. Factors associated with brain herniation in the treatment of diabetic ketoacidosis. Journal of Pediatrics 113: 10-14, 1988. [ abstract Hoffman, W. H., Steinhart, C. M., el, G. T., Steele, S., Cuadrado, A. R. and Morse, P. K. Cranial CT in children and adolescents with diabetic ketoacidosis. Ajnr: American Journal of Neuroradiology 9: 733-9, 1988. [ abstract Krane, E. J., Rockoff, M. A., Wallman, J. K. and Wolfsdorf, J. I. Subclinical brain swelling in children during treatment of diabetic ketoacidosis. New England Journal of Medicine 312: 1147-51, 1985. [ abstract Also see:
PedsCCM: EB Journal Club Review
review may have led to an underestimation of the number of cases of cerebral edema because edema can occur subclinically.
http://pedsccm.wustl.edu/EBJ/HARM/Glaser-DKA_CE_risk_factors.html

Extractions: Criteria abstracted from The Users' Guide to Medical Literature , from the Health Information Research Unit and Clinical Epidemiology and Biostatistics, McMaster University Highlighted lines and questions below provide links to the pertinent description of criteria in The EBM User's Guide , now available at the Canadian Centres for Health Evidence Article Reviewed: Risk Factors for Cerebral Edema in Children with Diabetic Ketoacidosis Glaser N, Barnett P, McCaslin I, et al. N Engl J Med 2001;344:264-9. abstract ; full-content for subscribers] Reviewed by Rohit Rao MD and Matthew Scanlon MD, Children's Hospital of Wisconsin Review posted May 4, 2001 The study objective: To identify risk factors for the development of cerebral edema in children with DKA. The study design: Multicenter retrospective case control study. The patients investigated: All children (persons less/than 18 years of age) in whom cerebral edema related to diabetic ketoacidosis developed between 1982 and 1997 at any of 10 pediatric centers.
CNS Pathology
The surface of the brain with cerebral edema demonstrates widened gyri with a flattened surface. The sulci are narrowed.
http://www-medlib.med.utah.edu/WebPath/CNSHTML/CNS056.html
CEREBRAL EDEMA IN HEPATIC FAILURE Slide
Vol. 1, Article 2, Rovira, et al. cerebral edema IN HEPATIC FAILURE Differentcompounds occur in the circulation in increased concentrations
http://foundation.asnr.org/neurographics/Rovira/3.asp

Extractions: Vol. 1, Article 2 Rovira, et al. CEREBRAL EDEMA IN HEPATIC FAILURE Different compounds occur in the circulation in increased concentrations when liver function is impaired and may contribute to hepatic encephalopathy, being ammonia probably the most important. Hyperammonemia induce accumulation of glutamine inside the astrocytes causing its swelling and subsequently an increase in the water content of the whole brain. This cerebral edema is a major cause of intracraneal hypertension and death in patients with fulminant hepatic failure ( Figure 3 ). Brain edema is only rarely a complication of chronic liver failure, although cerebral glutamine increases to a similar extent in both chronic and acute liver failure. The rarity of cerebral edema may be explained by a compensatory decrease of other osmolytes such as myoInositol and taurine ( Figure 4 ). This osmoregulatory mechanism protects the development of massive brain edema and explain the abscence of overt intracranial hypertension in chronic liver failure. It has been suggested that despite the osmoregulatory mechanism a low-grade astrocytic swelling exist in chronic hepatic failure that may be partially responsible to the development of hepatic encephalopathy. The purpose of this scientific exhibit is to show MR data from cirrhotic patients obtained before and after normalization of liver function (liver transplantation) that suppport the presence of a reversible widespread metabolic alteration in the white matter with a slight increase in brain water content. . We obtained MR data, including T1- and T2WI, magnetization transfer imaging and
Radiology In Ped Emerg Med, Vol 5, Case 6
This is the case in generalized cerebral edema, subdural hematoma, epidural hematoma, etc. View compressed ventricles.
http://www2.hawaii.edu/medicine/pediatrics/pemxray/v5c06.html

Extractions: This is a 5-year old female who is brought to the emergency department at 8:00 a.m. because she was poorly responsive when her mother awoke her in the morning. This prompted her mother to drive her to the E.D. There is a history of headache and vomiting during the evening and night. There is no history of trauma. Exam: VS T36.7 (rectal), P92, R32, BP 137/97. She is minimally responsive. Pupils equal and reactive. There are no signs of external trauma. Within minutes of arrival, she exhibits extensor posturing. She is orally intubated using the rapid sequence induction method with atropine, thiopental, and vecuronium. She is hyperventilated. End-tidal CO2 monitoring is used to keep her pCO2 in the 25 mmHg range. A loading dose of phenytoin is administered. An emergency CT scan is ordered. View CT scan. The image on the left is a high CT cut which should show the sulci and gyri well. Due to increased ICP, the cortex is compressed up against the calvarium losing the distinctness of the sulci and gyri. The space between the cortex and the calvarium is obliterated. The sulci/gyri sign cannot be totally relied upon in some instances. In cases of external hydrocephalus or chronic (or subacute) subdural effusions, fluid collects over the cortex. The fluid space between the cortex and the calvarium appears to be increased and the sulci/gyri may appear prominent. View prominent sulci/gyri.
High Altitude Cerebral Edema
High Altitude cerebral edema HACE. Book, Home Page.
http://www.fpnotebook.com/ER16.htm

Extractions: Home About Links Index ... Editor's Choice Paid Advertisement (click above). Please see the privacy statement Emergency Medicine Environmental Injury Traumatic Injury ... Burn Management Assorted Pages High Altitude Sickness Portable Hyperbaric chamber High Altitude Cerebral Edema High Altitude Pulmonary Edema ... Heat Illness Prevention High Altitude Cerebral Edema HACE Book Home Page Cardiovascular Medicine Dental Dermatology Emergency Medicine Endocrinology Gastroenterology General Medicine Geriatric Medicine Gynecology Hematology and Oncology HIV Infectious Disease Jokes Laboratory Neonatology Nephrology Neurology Obstetrics Ophthalmology Orthopedics Otolaryngology Pediatrics Pharmacology Prevention Psychiatry Pulmonology Radiology Rheumatology Sports Medicine Surgery Urology Chapter Emergency Medicine Index Cardiovascular Medicine Dermatology Environmental Injury Examination Fluids, Electrolytes, and Nutrition General Neurology Pharmacology Prevention Procedures Radiology Resources Poisoning and Toxicology Traumatic Injury Page Environmental Injury Index Altitude Altitude Gamow Altitude HACE Altitude HAPE Cold Frostbite Cold Hypothermia Heat Heat Risks Heat Cramps Heat Exhaustion Heat Stroke Trauma Burn Trauma Burn Electrical Trauma Burn Management Symptoms Headache Signs Ataxia Screening: Heal-toe walking in a straight line Focal neurologic deficits Management Gamow Bag Descend Immediately Dexamethasone Initial: 4-8 mg IM/IV/PO Later: 4 mg q6h IM/IV/PO High flow supplemental oxygen Intubation and Hyperventilation if patient comatose Search other websites for this topic
ClinicalPoints® - Cerebral Edema
Treatments, diagnosis and key points for cerebral edema.Category Health Conditions and Diseases cerebral edemaHome Professional ClinicalPoints ® Sample Docs CerebralEdema Select a Sample Document cerebral edema. Treatment.
http://www.micromedex.com/products/demos/webready/Professional/ClinicalPoints/da
DiabetoValens.com - The Diabetes Guide
Risk factors for cerebral edema in children with diabetic ketoacidosis.Introduction. Diabetic Results. Incidence of cerebral edema. Clinically
http://my.diabetovalens.com/complications/cerebral.asp

Extractions: Verify here Diabetic ketoacidosis occurs in 25 to 40 percent of children with newly diagnosed type 1 diabetes mellitus and may later recur in association with illness or noncompliance with treatment. Clinically apparent cerebral edema occurs in approximately 1 percent of episodes of diabetic ketoacidosis in children and is associated with a mortality rate of 40 to 90 percent. Cerebral edema is responsible for 50 to 60 percent of diabetes-related deaths in children. The pathophysiologic mechanism underlying the cerebral edema associated with diabetic ketoacidosis is controversial. In this casecontrol study of children with diabetic ketoacidosis, researchers evaluated the associations between cerebral edema and the following factors: demographic characteristics and initial biochemical characteristics, therapeutic interventions, and changes in biochemical values during treatment. Researchers identified all the children in whom cerebral edema related to diabetic ketoacidosis developed between 1982 and 1997 at any of 10 pediatric centers. To identify these children, the records of all the children who had been admitted because of diabetic ketoacidosis and whose records indicated that they had had cerebral edema, cerebral infarction, coma, seizures, or death, or that they had undergone computed tomographic scanning, magnetic resonance imaging, intubation, or treatment with mannitol were reviewed. The records of all children who died at 10 centers during the study period were also reviewed to ensure that no cases of cerebral edema related to diabetic ketoacidosis had been missed.
HIGH ALTITUDE CEREBRAL EDEMA OR MOUNTAIN SICKNESS - Travel Medicine Program - PP
Population and Public Health Branch. HIGH ALTITUDE cerebral edema ORMOUNTAIN SICKNESS. Travellers to high altitudes, both mountains
http://www.hc-sc.gc.ca/pphb-dgspsp/tmp-pmv/travel/cerebr_e.html

Extractions: HIGH ALTITUDE CEREBRAL EDEMA OR MOUNTAIN SICKNESS Travellers to high altitudes, both mountains climbers and trekkers, should be advised of the potential hazard of acute mountain sickness. Tour companies offer itineraries to Nepal where trekkers climb to over 6,000 metres, to Mount Kilimanjaro in East Africa 6,000 metres, to Andean passes in South Africa 4,000 metres, and to Swiss Alps. These trips are often advertised as being quite easy. However, only those who are healthy and well trained should take part in such expeditions. Anyone in doubt, especially with a history of cardiac or respiratory complaint should undergo medical examination and seek medical advice. Even those who are fit run the risk of acute Mountain sickness during rapid ascent to high altitudes if they spend more than half a day above 2,500 metres. A number of studies have shown a correlation between incidence of that disease and altitude: in the Swiss Alps, high altitude sickness have been observed in 9% of climbers at 2,850 meters, 34% at 3,650 metres, and 53% at 4,559 metres. Having normal heart and lung functions based on examination findings (such as an ECG) does not imply a reduced risk. It is often the young and fit who fall ill.
Cerebral Edema And Brain Swelling
cerebral edema AND BRAIN SWELLING A. Vasogenic cerebral edema (most common form ofedema) 1. Increased permeability of small vessels (breakdown of bloodbrain
http://kobiljak.msu.edu/CAI/Pathology/Intra_F/Intra_2.html
High Altitude Cerebral Edema
HIGH ALTITUDE cerebral edema (HACE). HACE is the result of swellingor brain tissue from fluid leakage. Symptoms can include headache
http://www.triplecitizen.com/Kili/hace.htm

Extractions: HACE is the result of swelling or brain tissue from fluid leakage. Symptoms can include headache, loss of coordination, weakness, decreasing levels of consciousness including disorientation, loss of memory, hallucinations, psychotic behavior, and coma. Severe instances can lead to death if not treated quickly.

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