Diagnosis is based on symptoms and physical examination findings and confirmed by serial neuroimaging (computed tomography scans and magnetic resonance imaging). The treatment of cerebral edema depends on the cause and includes monitoring of the person's airway and intracranial pressure, proper positioning, controlled hyperventilation, medications, fluid management, steroids. Extensive cerebral edema can also be treated surgically with a decompressive craniectomy. Cerebral edema is a major cause of brain damage and contributes significantly to the mortality of ischemic strokes and traumatic brain injuries. As cerebral edema is present with many common cerebral pathologies, the epidemiology of the disease is not easily defined.
Introduction
Cerebral edema
Cerebral edema | Introduction
Brain injuries from ischemic stroke, subarachnoid hemorrhage, traumatic brain injury etc Acute brain injuries from a variety of origins It is frequently encountered in acute brain injuries from a variety of origins. Cerebral edema is frequently encountered in acute brain injuries from a variety of origins
who is elwyn roy king?
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A fighter ace in the Australian Flying Corps (AFC) during World War I
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has he been a part of any other war?
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Yes - World War II
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how did he die?
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cerebral oedema
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did he get a military funeral service?
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Yes - his funeral service was attended by hundreds of mourners from the military and civil aviation world
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did an air staff chief attend it?
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Yes - Sir Charles Burnett
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the flying corps that king served, when was it formed?
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1912
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do they provide trainings?
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Yes - they conduct both pilot and mechanic training
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what are the causes of the disease king had?
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Cerebral edema is excess accumulation of fluid (edema) in the intracellular or extracellular spaces of the brain. This typically causes impaired nerve function, increased pressure within the skull, and can eventually lead to direct compression of brain tissue and blood vessels. Symptoms vary based on the location and extent of edema and generally include headaches, nausea, vomiting, seizures, drowsiness, visual disturbances, dizziness, and in severe cases, coma and death. Cerebral edema is commonly seen in a variety of brain injuries including ischemic stroke, subarachnoid hemorrhage, traumatic brain injury, subdural, epidural, or intracerebral hematoma, hydrocephalus, brain cancer, brain infections, low blood sodium levels, high altitude, and acute liver failure.
Cerebral edema | Introduction
The incidence of this disorder should be considered in terms of its potential causes and is present in most cases of traumatic brain injury, central nervous system tumors, brain ischemia, and intracerebral hemorrhage. For example, malignant brain edema was present in roughly 31% of people with ischemic strokes within 30 days after onset.
Cerebral edema | Introduction
His career was curtailed by ankylosing spondylitis.
Michael King (golfer) | Introduction
Diagnosis is based on symptoms and physical examination findings and confirmed by serial neuroimaging (computed tomography scans and magnetic resonance imaging). The treatment of cerebral edema depends on the cause and includes monitoring of the person's airway and intracranial pressure, proper positioning, controlled hyperventilation, medications, fluid management, steroids. Extensive cerebral edema can also be treated surgically with a decompressive craniectomy. Cerebral edema is a major cause of brain damage and contributes significantly to the mortality of ischemic strokes and traumatic brain injuries. As cerebral edema is present with many common cerebral pathologies, the epidemiology of the disease is not easily defined.
Cerebral edema | Introduction
Cerebral edema is frequently encountered in acute brain injuries from a variety of origins, including but not limited to:
Cerebral edema | Causes
Cerebral edema is a severe complication of acute brain injuries, most notably ischemic stroke and traumatic brain injuries, and a significant cause of morbidity and mortality.
Cerebral edema | Outcomes
As cerebral edema is present with many common cerebral pathologies, the epidemiology of the disease is not easily defined. The incidence of this disorder should be considered in terms of its potential causes and is present in most cases of traumatic brain injury, central nervous system tumors, brain ischemia, and intracerebral hemorrhage.
Cerebral edema | Epidemiology
A 1998 MRI study of nine climbers with HACE clearly demonstrated vasogenic edema. Data about HACE are lacking because it generally occurs in remote areas, far from hospitals and is generally rare. It is uncommon for doctors to be able to study victims within six days of the condition's development. Animal models of HACE have not been developed. Several genes are being examined for the role they may play in the development of the condition. Increased education and helicopter capabilities have combined to cut the number of deaths from the condition. Symptoms of HACE have been reported in many cases of deaths while descending Mount Everest, although HACE may not be the only problem they suffered.
High-altitude cerebral edema | History
Hydrostatic extracellular brain edema is typically caused by severe arterial hypertension. A difference in the hydrostatic pressure within the arterial system relative to the endothelial cells allows ultrafiltration of water, ions, and low molecular weight substances (such as glucose, small amino acids) into the brain parenchyma. The blood-brain barrier is intact usually and the extent of the edema depends on the arterial pressure. The regulatory processes of the brain circulation can function up to systolic arterial pressures of 150 mm Hg and will have impaired function at higher blood pressures.
Cerebral edema | Hydrostatic
Then intracellular sodium and osmolarity increase, and there is an influx of water that causes cellular swelling. After the failure of the ATPase pumps, free radicals form and cause damage that complicates the edema. Evidence against cytotoxic edema includes the high levels of hypoxemia (low bloodstream oxygen) needed to cause it.
High-altitude cerebral edema | Cause and mechanism
Diagnosis of cerebral edema relies on the following:
Cerebral edema | Diagnosis
MRI scans of patients with HACE showed increased T2 in the corpus callosum, although grey matter was unchanged. This demonstrated that the blood-brain barrier was broken by cerebral blood vessels, thus interfering with white matter metabolism. Another study looked at the brains of HACE sufferers several months after their recovery; it showed hemosiderin deposits in the corpus callosum, evidence of vascular permeability. While there is strong evidence that vasogenic edema plays a major role in HACE, cytotoxic edema, cellular retention of fluids, may contribute as well. Cytotoxic edema may be caused by the failure of cellular ion pumps, which results from hypoxia.
High-altitude cerebral edema | Cause and mechanism
Posterior reversible encephalopathy syndrome (PRES) is a rare clinical disease characterized by cerebral edema. The exact pathophysiology, or cause, of the syndrome is still debated but is hypothesized to be related to the disruption of the blood-brain barrier. The syndrome features acute neurological symptoms and reversible subcortical vasogenic edema predominantly involving the parieto-occipital areas on MR imaging. PRES in general has a benign course, but PRES-related intracranial hemorrhage has been associated with a poor prognosis.
Cerebral edema | Posterior Reversible Encephalopathy Syndrome
Patients are usually given supplemental oxygen and dexamethasone as well. HACE can be prevented by ascending to heights slowly to allow the body more time to acclimatize. Acetazolamide also helps prevent the condition. Untreated patients usually die within 48 hours. Those who receive treatment may take weeks to fully recover. It is a rare condition, occurring in less than one percent of people who ascend to . First described in 1913, little was known about the cause of the condition until MRI studies were performed in the 1990s.
High-altitude cerebral edema | Introduction
The use of specific MRI techniques has allowed for some differentiation between the mechanisms.
Cerebral edema | Combined types of cerebral edema
Edgar Samuel John King CMG DSc FRACP FRACS MCPA FAA, (10 June 1900, Mosgiel, Otago, New Zealand – 31 January 1966, East Melbourne, Victoria, Australia), was an Australian surgeon and pathologist.
Edgar King | Introduction
HACE also posed a threat to workers on the Qinghai–Tibet Railway.
High-altitude cerebral edema | History
He was transported to Northern Cumberland Hospital in Bridgton and then flown by air ambulance to Central Maine Medical Center (CMMC) in Lewiston. His injuries—a collapsed right lung, multiple fractures of his right leg, scalp laceration and a broken hip—kept him at CMMC until July 9. His leg bones were so shattered that doctors initially considered amputating his leg, but stabilized the bones in the leg with an external fixator. After five operations in 10 days and physical therapy, King resumed work on "On Writing" in July, though his hip was still shattered and he could sit for only about 40 minutes before the pain became unbearable.
Stephen King | Car accident and aftermath
The blood–brain barrier becomes more permeable, leading to "vasogenic" cerebral edema (swelling of the brain due to fluid leakage from blood vessels). Large numbers of white blood cells enter the CSF, causing inflammation of the meninges and leading to "interstitial" edema (swelling due to fluid between the cells). In addition, the walls of the blood vessels themselves become inflamed (cerebral vasculitis), which leads to decreased blood flow and a third type of edema, "cytotoxic" edema. The three forms of cerebral edema all lead to increased intracranial pressure; together with the lowered blood pressure often encountered in acute infection, this means that it is harder for blood to enter the brain, consequently brain cells are deprived of oxygen and undergo apoptosis (programmed cell death).
Meningitis | Mechanism
King died in a midair collision on 24 January 1919 over Sedgeford, Norfolk, while serving as a combat instructor with 33 Squadron. His death notice stated his parents lived at Springfield Dukes, Chelmsford. He is buried at the churchyard of St Mary the Virgin at Docking, Norfolk.
Cecil Frederick King | Death
Doctors at University of California at Davis, where the necropsy also was performed, originally thought that tumor to be about one foot long. 'It went all the way from his pelvis to invade and erode his diaphragm and chest cavity', said Dr. David Wilson, director of UCD's large-animal clinic, who was part of a team of veterinarians and specialists who worked with the horse. 'It also involved his arteries, kidneys and intestinal organs. It actually invaded one kidney and compressed both. It came right up against his aorta', Wilson added. "He had experienced swelling in his hind legs and that was no doubt caused by the tumors pressing on blood vessels'.
Lost in the Fog | Death
King died unexpectedly of cerebral oedema on 28 November 1941, aged 47. Survived by his wife and children, he was cremated at Fawkner Crematorium, Melbourne. His funeral service at South Yarra was attended by hundreds of mourners from the military and civil aviation world, including the Chief of the Air Staff, Air Chief Marshal Sir Charles Burnett, and a representative of the Minister for Air; the pallbearers included Air Vice Marshal Henry Wrigley, Air Commodore Raymond Brownell, Group Captain Allan Walters, and Wing Commander Henry Winneke. Elwyn Roy King's name appears on panel 97 in the Commemorative Area of the Australian War Memorial, Canberra.
Elwyn Roy King | Death and legacy
Cytotoxic, osmotic, and vasogenic edema exist on a continuum. The mechanism of the cause of cerebral edema can often overlap between these types. In most instances, cytotoxic and vasogenic edema occur together. When the two edema types evolve simultaneously, the damage of one type reaches a limit and will bring about the other type of injury. For example, when cytotoxic edema occurs in the endothelial cells of the blood-brain barrier, oncotic cell death contributes to loss of integrity of the blood-brain barrier and promotes the progression to vasogenic edema. When brain edema types are combined, there is typically a primary form and the edema type and context of the cause must be determined in order to start appropriate medical or surgical therapy.
Cerebral edema | Combined types of cerebral edema
Finding the optimal head position in persons with cerebral edema is necessary to avoid compression of the jugular vein and obstruction of venous outflow from the skull, and for decreasing cerebrospinal fluid hydrostatic pressure. The current recommendation is to elevate the head of the bed to 30 degrees to optimize cerebral perfusion pressure and control the increase in intracranial pressure. It is also worth noting that measures should taken to reduce restrictive neck dressings or garments as these may lead to compression of the internal jugular veins and reduce venous outflow.
Cerebral edema | Positioning
"I couldn't walk without stumbling, and completely lost the ability to think or speak. It was a really strange feeling. I'd have some word in my mind, but I couldn't figure out how to bring it to my lips. So Scott and Neal had to get me dressed and make sure my harness was on correctly, then Scott lowered me down the fixed ropes." By the time Kruse arrived in Base Camp, he says, "it was still another three or four days before I could walk from my tent to the mess tent without stumbling all over the place."’ Patients with HACE have an elevated white blood cell count, but otherwise their blood count and biochemistry are normal.
High-altitude cerebral edema | Signs and symptoms
In the paper which was to give Kellie lasting eponymous fame he describes the post mortem appearances in the bodies of two individuals found dead after lying outside after a storm. He was asked by local magistrates to try to establish the cause of death. Kellie noted that the veins in the meninges and surface of the brain were congested and the associated arteries were relatively bloodless while the brain was otherwise normal. In concluding that the individuals died from exposure he quotes a similar case described by Samuel Quelmalz (1696–1758) where exposure results in a progression through weariness, lassitude, drowsiness, coma and death which he ascribes to disordered cerebral circulation.
George Kellie | Paper on intracranial circulation
Interstitial edema can be best characterized by in noncomunnicating hydrocephalus where there is an obstruction to the outflow of cerebrospinal fluid within the ventricular system. The obstruction creates a rise in the intraventricular pressure and causes CSF to flow through the wall of the ventricles into the extracellular fluid within brain. The fluid has roughly the same composition of CSF. Other causes of interstitial edema include but are not limited to communicating hydrocephalus, and normal pressure hydrocephalus.
Cerebral edema | Interstitial (Hydrocephalic)
HACE was first described by a medical officer stationed in Chile in 1913, but few took note of it. Later, access to air travel made the condition more common because it allowed more people access to high mountains, such as those in the Himalayas. One early description of HACE may have been published in 1969 after a group of Indian soldiers made a rapid ascent to almost . It is not definitely established whether they had HACE or acute decompression sickness. MRI has been used to study the effects of high altitude on the brain, providing the best evidence about the condition.
High-altitude cerebral edema | History
As reported by Alan Michie in "God Save The Queen," published in 1952 (see pages 194 and following), King George VI was diagnosed with the disease on 12 November 1948. Both legs were affected, the right more seriously than the left. The king's doctors prescribed complete rest and electric treatment to stimulate circulation, but as they were either unaware of the connection between the disease and smoking (the king was a heavy smoker) or unable to persuade the king to stop smoking, the disease failed to respond to their treatment. On 12 March 1949, the king underwent a lumbar sympathectomy, performed at Buckingham Palace by James R.
Thromboangiitis obliterans | Notable sufferers
Cerebral edema is a present with many common cerebral pathologies and risk factors for development of cerebral edema will depend on the cause. The following were reliable predictors for development of early cerebral edema in ischemic strokes.
Cerebral edema | Risk Factors
King died in Opelousas in his early 60s.
George Rogers King | Introduction
This proved fortunate when an error by launch pad technicians caused one of the CM's Teflon fuel tank bladders to rupture, and the entire space vehicle had to be returned to the Vehicle Assembly Building. Slayton noted that "there wasn't even any discussion of replacing him; that was one of the lessons we'd learned on 13."
Charles Duke | Training
There are several clinical conditions in which vasogenic edema is present:
Cerebral edema | Vasogenic
Cerebral edema is mainly classified into cytotoxic edema, vasogenic edema and interstitial edema. Cytotoxic edema affects both the white and gray matter and results from the swelling of cellular elements such as neurons, glia and endothelial cells. Vasogenic edema affects white matter and results from blood brain barrier (BBB) breakdown. Interstitial edema results from lack of proper cerebrospinal fluid (CSF) absorption.
Osmotherapy | Cerebral edema
Cerebral edema, or unusual swelling of the brain, is commonly caused by anoxic episodes. If it is severe enough, it is known to cause preferential damage to cerebral white matter due to excessive swelling of glial cells while leaving many other tissues unharmed. This theory suggests that hypoxia and carbon monoxide induce a form of edema resulting in white matter necrosis. Evidence for this theory comes from the observation of pathological lesions mimicking those of carbon monoxide poisoning where hypoxia and dehydration along with too-rapid rehydration have taken place without carbon monoxide present.
Grinker myelinopathy | Cerebral edema
Building work began in 1913 with the foundation stone being laid by the Duchess of Norfolk. W.A. Kenyon was the architect and despite delays caused by the First World War the hospital opened early in 1916 and had around 120 beds along with the associated treatment rooms and operating theatre. The hospital was known as the King Edward VII Hospital for Crippled Children until 1948 and it treated patients with tuberculosis, rickets, congenital deformities and poliomyelitis. The hospital pioneered Ultraviolet ray and vitamin treatment under the orthopaedic surgeon Dr. Creswell Lee Pattison. In 1944 some of the children were moved out of the hospital to allow treatment of wounded soldiers; in the same year the hospital was recognised as a nurse training hospital.
King Edward VII Orthopaedic Hospital, Sheffield | History
Extracellular brain edema, or vasogenic edema, is caused by an increase in the permeability of the blood-brain barrier. The blood-brain barrier consists of astrocytes and pericytes joined together with adhesion proteins producing tight junctions. Return of blood flow to theses cells after an ischemic stroke can cause excitotoxicity and oxidative stress leading to dysfunction of the endothelial cells and disruption of the blood-brain barrier. The breakdown of the tight endothelial junctions that make up the blood–brain barrier causes extravasation of fluid, ions, and plasma proteins, such as albumin, into the brain parenchyma. Accumulation of extracellular fluid increases brain volume and then intracranial pressure causing the symptoms of cerebral edema.
Cerebral edema | Vasogenic
At the same time, improvement of radiographic markers, biomarkers, and analysis of clinical monitoring data is essential in treating cerebral edema. Many studies of the mechanical properties of brain edema were conducted in the 2010s, most of them based on finite element analysis (FEA), a widely used numerical method in solid mechanics. For example, Gao and Ang used the finite element method to study changes in intracranial pressure during craniotomy operations. A second line of research on the condition looks at thermal conductivity, which is related to tissue water content.
Cerebral edema | Research
The operating table is on display at Westminster Hospital, while Dr Cyril F. Scurr donated the ECG machine to the British Oxygen Company Museum at the Association of Anaesthetists of Great Britain.
Clement Price Thomas | Memorabilia of the king's surgery
The King Edward VII Orthopaedic Hospital owed its existence to the fondness that the people of Sheffield had for King Edward VII who died in 1910. On his death a fund was set up and the population of the City raised £18,000 in his memory with the organisers expressing a desire that the money should be used to build a hospital school for crippled children. Sheffield City Council provided extra funds when it was found that £18,000 was not sufficient to build the hospital and the Duke of Norfolk presented the land in the Rivelin Valley on which it was to be built free of charge.
King Edward VII Orthopaedic Hospital, Sheffield | History
Price Thomas led the team that removed a cancerous left lung from King George VI. His Times obituary noted that despite his huge fame and international reputation "the more honours that befell him, the more did his innate modesty came to the fore". The king had been unwell in 1951, and was advised by his physicians Sir Daniel Davies, Sir Horace Evans, Geoffrey Marshall and Sir John Weir, to return to London from Balmoral and confine himself to his room. He was described as having 'catarrhal inflammation', and rest may improve it. However, he did not improve and was considerably weak, thin and pale with little exercise tolerance due to intermittent claudication.
Clement Price Thomas | King George VI lung operation
He contributed the neurological section to "Practice of Medicine" (12th edn, 1922 ed. Sir Frederick Taylor). In Boston, he described subarachnoid haemorrhage in 1924, in which year he was elected a Fellow of the Royal College of Physicians (FRCP). He returned to the National Hospital in London in 1926, and was also appointed consultant in neurology to the Royal National Throat, Nose and Ear Hospital. From his observations of patients in these hospitals he published his description of what he named "otitic hydrocephalus" in 1931. The condition is now known as idiopathic intracranial hypertension.
Charles Symonds | Inter-war years
A study of samples of the King's hair published in 2005 revealed high levels of arsenic, a possible trigger for the disease. The source of the arsenic is not known, but it could have been a component of medicines or cosmetics. The King may have had a brief episode of disease in 1765, but a longer episode began in the summer of 1788. At the end of the parliamentary session, he went to Cheltenham Spa to recuperate. It was the furthest he had ever been from London—just short of 100 miles (150 km)—but his condition worsened. In November he became seriously deranged, sometimes speaking for many hours without pause, causing him to foam at the mouth and making his voice hoarse.
George III | William Pitt
In 2014 King suffered an intracranial aneurysm from which he recovered after hospital treatment. In September 2017, along with his 'Hairy Bikers' partner Dave Myers he was initiated into the showbusiness charity the Grand Order of Water Rats. King is a supporter of Premier League football team Newcastle United F.C.
Si King | Personal life
Shortly after receiving an M.D. and PhD in physiology from the University of Minnesota medical school under the mentorship of Professor Maurice B. Visscher, MD, Wood became a key member of a team, working in a, what was then top secret, laboratory at the Mayo Clinic, tasked with helping military pilots and flight crew survive and function in high G-force environments. Based upon extensive physiologic testing via use of the human centrifuge installed at the Mayo Clinic, it was determined that blackout and then unconsciousness was caused by reduction of blood flow to the eyes first and then the brain.
Earl Wood | <a href="G-Suit">G-Suit</a>
Bones" on the ends. He died in New York City from cerebral edema in 1868.
George Christy | Introduction
King was diabetic and in 1986 one of her toes was amputated as a result of the disease. In 1990, King suffered a stroke and entered the Motion Picture & Television Country House and Hospital in Woodland Hills, California. In 1991, King's diabetes resulted in the amputation of her left leg. In 1994, her right leg was also amputated. King would also lose one of her arms to diabetes. Her son, Larry, died in 1996. King died on November 9, 1999 at age 66.
Mabel King | Later years and death
He was diagnosed with "cavernous hemangioma" and "venous angioma" (blood vessel tumours) in the brain.
Frederick Ma | Government years
High-altitude cerebral edema (HACE) is a medical condition in which the brain swells with fluid because of the physiological effects of traveling to a high altitude. It generally appears in patients who have acute mountain sickness and involves disorientation, lethargy, and nausea among other symptoms. It occurs when the body fails to acclimatize while ascending to a high altitude. It appears to be a vasogenic edema (fluid penetration of the blood–brain barrier), although cytotoxic edema (cellular retention of fluids) may play a role as well. Individuals with the condition must immediately descend to a lower altitude or coma and death can occur.
High-altitude cerebral edema | Introduction
King was born on May 11, 1925 in Chelsea, Massachusetts. During his teens, King worked as a pinsetter in a Revere Beach bowling alley to help pay for his schooling. Toward the end of World War II he served in the United States Navy. He was given a medical discharge due to a broken ankle.
Edward J. King | Early life
Royal developed Alzheimer's disease in his later years. He died from a myocardial infarction on February 3, 2002, at the age of 66.
Nelson Royal | Death
An increase in cerebral water content is called cerebral edema and it usually results from traumatic brain injury (TBI), subarachnoid hemorrhage (SAH), intracerebral hemorrhage (ICH), subdural hematoma, ischemic stroke, brain tumors, infectious disorders and intracranial surgery. Cerebral edema may result in compromised regional cerebral blood flow (CBF) and intracranial pressure (ICP) gradients which could lead to death of the affected. Increased ICP leads to increased intracranial volume. Unmonitored ICP leads to brain damage by global hypoxic ischemic injury due to reduction in cerebral perfusion pressure (CPP) which is found by subtracting the ICP from mean arterial pressure(MAP), cerebral blood flow, and mechanical compression of brain tissue due to compartmentalized ICP gradients.
Osmotherapy | Cerebral edema
His diagnosis was that the King had suffered as a young man from "social and sexual inadequacy". He ended "The stage was set for disaster".
Bernard Armitage | Career
In connection with this, the young Kenessey was expected to request an audition with the King in order to thank for the ring, a request that was usually granted, but in this case, possibly due to the tense political situation and/or the advanced age of the monarch, the occasion did not materialize, to Kenessey's later regret. Kenessey had decided to become a surgeon and he started working as assistant-in-training at the surgical clinic of Budapest. When in 1914 the First World War broke out he had to go to the front. He soon earned the Signum Laudis award for bravery but in 1915 he contracted typhoid fever.
Albert Kenessey | Early life and education
The cause of the prince's death is unknown: at the time, it was believed to be "brain fever" or meningitis. Later speculation has included appendicitis.
Kamehameha IV | Reign
Nutritional support is necessary in all patients with acute brain injury. Enteral feeding, or through mouth via tube, is the preferred method, unless contraindicated. Additional attention must be placed on the solute concentration of the formulations to avoid free water intake, decreased serum osmolality, and worsening of the cerebral edema. Elevated blood glucose, or hyperglycemia, is associated with increased edema in patients with cerebral ischemia and increases the risk of a hemorrhagic transformation of ischemic stroke. Maintaining a normal blood glucose level of less than 180 mg/dL is suggested. However, tight glycemic control of blood glucose under 126 mg/dL is associated with worsening of stroke size.
Cerebral edema | Nutrition
Numerous students and trainees have trained under Edwards. Dwight Harken from the USA, took up a visiting fellows post with Tudor Edwards in 1942 later, ironically competing with another trainee, Sir Russell Brock. Edwards was the inspiration for Clement Price Thomas, the surgeon who performed the thoracotomy on King George VI in 1951. He was known as the "operator of supreme skill and beautiful technique". In 1948, his colleagues organised a memorial fund to endow a lecture in his memory. Administered by both the Royal College of physicians and Royal College of Surgeons, the lecture is an honour to give.
Tudor Edwards | Legacy
Her attending physician was Norton Folsom, who indicated the "form of her disease was mania, which was manifested by excitement, irascibility, incoherence of speech and violent conduct", and that her condition was "caused by some disease peculiar to females". He indicated that by 10 May 1867, she appeared better. She was discharged on 10 September 1867. From then until 1873, she worked as a milliner and teacher in New York City, Philadelphia, and Hartford, not returning to her hometown during this period.
Lizzie Lloyd King | Early life
According to the "autoregulation breakthrough" conception, cerebral arterioles are forced to dilate, leading to vasogenic edema. Cerebral edema can be generalized or focal. Brain ventricles are compressed, cortical gyri flattened.
Hypertensive encephalopathy | Pathogenesis
Sir Maurice Alan Cassidy GCVO CB (29 February 1880 – 22 October 1949) was a British doctor, physician to the King from 1937 until his own death. Maurice was born the eldest son of David McKay Cassidy, a doctor at the Lancaster Mental Hospital in Lancashire and was educated at Lancaster Grammar School and Clare College, Cambridge. He then entered St Thomas' Hospital in London as a medical student, qualifying M.B. in 1906 and M.D. in 1909. After working there for several years, including two as Resident Assistant Registrar, he was elected in 1913 a Fellow of the Royal College of Surgeons and joined the honorary staff of St Thomas'.
Maurice Cassidy | Introduction
Despite injury to the left recurrent laryngeal nerve and an effect on the king's voice, the cancerous lung was successfully removed. Price Thomas declined the fee for the surgery, considering it an honour to have been of service to his king. The king honoured him with the KCVO, in December 1951, barely two months before he died from the effects of arterial disease.
Clement Price Thomas | King George VI lung operation
King died on March 24, 1958 of heart failure. King was inducted into the AQHA Hall of Fame in 1989.
King (horse) | Death and honors
Before long, however, he decided he wanted to return to the theatre and learned how to walk well with a prosthetic leg in order to do so. While he was recovering at St. Thomas' in London, King George V visited the hospital. When asked to pick which of the actor's legs he thought was artificial, the king chose the wrong one. Throughout his career, Marshall largely managed to hide the fact that he had a prosthetic limb, although it was occasionally reported in the press. Marshall suffered from his war injury for the rest of his life, both from phantom pain common to amputees and from the prosthesis.
Herbert Marshall | War injury
If a lumbar puncture is performed, it will show normal cerebral spinal fluid and cell counts but an increase in pressure. In one study, CT scans of patients with HACE exhibited ventricle compression and low density in the cerebellum. Only a few autopsies have been performed on fatal cases of HACE; they showed swollen gyri, spongiosis of white matter, and compressed sulci. There was some variation between individuals, and the results may not be typical of HACE deaths.
High-altitude cerebral edema | Signs and symptoms
Homer Duncan King, who was born in 1897, began his journalism career as a young man, first on the "Hemet News," then the "Redlands Daily Facts" and the "San Bernardino Sun-Telegram" before becoming managing editor of the "Nevada State Journal" and finally of the "Hollywood Citizen-News." He held all those positions before he was age 30. Homer King and his sister, Helen, a schoolteacher, were both afflicted with multiple sclerosis. While King was working at the "Citizen-News" "a creeping paralysis first manifested itself," according to King's obituary in the "Long Beach Independent." "A physician prescribed that he should be placed in a cast for two years." Instead, in 1926, he returned to Hemet and took over operation of the family's newspaper.
John E. King and Homer D. King | Homer D. King
Neurosurgery Department pioneers spinal cord stimulation in Pakistan. Pakistan's first Spinal Cord Stimulation surgery was done by Neurosurgery Department of King Edward Medical University / Mayo Hospital Lahore in August 2018. Medtronic Spinal Cord Stimulation (SCS) system was purchased via tender. The team included Professor Shahzad Shams (Chairman Neurosurgery King Edward Medical University / Mayo Hospital Lahore), Dr Muhammad Tariq (Asst Prof Neurosurgery King Edward Medical University, Lahore), Dr Ammar Anwer (Research Fellow ANFN-DBS Pakistan) and Dr Rupesh Jung Raut (R 3, Neurosurgery Department King Edward Medical University / Mayo Hospital Lahore). The patient was suffering from phantom limb syndrome and Medtronic Prime Advance™ SCS system was implanted bilaterally in cervical spine.
King Edward Medical University | Surgery and allied departments
On the following day at noon, a telegram marked "OFFICIAL" was dispatched around the Empire, with the news that the coronation was postponed and that the King was undergoing an operation. Shortly afterwards, a bulletin was released from Edward's medical team, stating that "The King is suffering from . The condition on Saturday was so satisfactory that it was hoped that with care His Majesty would be able to go through the Coronation ceremonies. On Monday evening a recrudescence became manifest, rendering a surgical operation necessary today". It was undersigned by, among others, Lord Lister and Sir Frederick Treves, who actually carried out the operation on a table in the Music Room at Buckingham Palace, to drain his abdominal cyst.
Coronation of Edward VII and Alexandra | Illness and postponement
This case also demonstrates Hill's understanding of the clinical features of cerebral compression: ‘The smallest compression brought on a stupor, a low intermittent pulse, nausea, vomiting and sometimes convulsive twitches.’ From case 3 onwards he avoided dressings which compressed the trepanned area. In case 3 he again relieved the features of cerebral compression by a trepan with drainage of an EDH. In case 5 drainage of a large EDH resulted in restoration of consciousness and resolution of a right sided weakness. His account of this case also shows that he appreciated the concept that paralysis on one side of the body indicated compression on the opposite side of the brain.
James Hill (surgeon) | Head injuries
He had been excused from military service during World War II due to a duodenal ulcer. He and his family—first wife Victoria Florence (née Harris) and daughter Margaret—and Taunton's school were evacuated to Bournemouth from Southampton in 1940. Among the many pupils was 15-year-old Benny Hill. King was always a keen musician, playing the piano, piano-accordion and organ. During the Second World War he formed various concert parties—"The V Concert Party" was one—which toured the smaller outlying military bases and entertained troops not often reached by ENSA. He also raised funds by organising concerts to "buy" Spitfires and send aid to Russia.
Horace King, Baron Maybray-King | Early life
In general, cytotoxic edema is linked to cell death in the brain through excessive cellular swelling. During cerebral ischemia for example, the blood–brain barrier remains intact but decreased blood flow and glucose supply leads to a disruption in cellular metabolism and creation of energy sources, such as adenosine triphosphate (ATP). Exhaustion of energy sources impairs functioning of the sodium and potassium pump in the cell membrane, leading to cellular retention of sodium ions. Accumulation of sodium in the cell causes a rapid uptake of water through osmosis, with subsequent swelling of the cells. The ultimate consequence of cytotoxic edema is the oncotic death of neurons.
Cerebral edema | Cytotoxic
On the morning of July 26, 1981, Turner was driving on Indiana State Road 46 near Columbus, Indiana, when his car lost control on a curve and flipped. He was driving to the Kings Island amusement park in Ohio with three friends, who were all also injured in the crash. Turner had not been wearing a seat belt when he crashed. Turner was taken to Bartholomew County Hospital in Columbus before he was transferred to Indiana University Health Methodist Hospital later that same day. Knight, who was on a summer fishing vacation in Idaho, flew back to Indiana to be with Turner and his family.
Landon Turner (basketball) | Paralysis
Cerebral edema is commonly present in a variety of neurological injuries. Thus, determining a definitive contribution of cerebral edema to the neurological status of an affected person can be challenging. Close bedside monitoring of a person's level of consciousness and awareness of any new or worsening focal neurological deficits is imperative but demanding, frequently requiring admission into the intensive care unit (ICU). Cerebral edema with sustained increased intracranial hypertension and brain herniation can signify impending catastrophic neurological events which require immediate recognition and treatment to prevent injury and even death. Therefore, diagnosis of cerebral edema earlier with rapid intervention can improve clinical outcomes and can mortality, or risk of death.
Cerebral edema | Diagnosis
Keplinger was 13 when the filmmakers met him as part of their federally funded documentary projects on mainstreaming children with disabilities. The cerebral palsy means Keplinger has little control over the muscles of his arms, legs or mouth. He uses a paintbrush attached to his head to paint. He could neither speak nor dress himself when the filmmakers met him. "They recorded Keplinger's move from a state school for disabled children into Parkville High School. They filmed him moving from his mother's home into his first apartment. His first art show, his friendship with a young woman hired to help him with homework, his senior prom and his tears at his college graduation -- all were captured on film," according to "The Baltimore Sun".
King Gimp | The journey begins
Kingwell later suffered from arthritis, requiring one stick, then two, then crutches, and ultimately confined to a bath-chair. He died on 10 November 1949 at The Nursing Home, Beech Hill, Hadley Wood. He left an estate of £22,611. Kingwell Road in Hadley Wood is named after him. Eva died on 16 January 1950 at 1 Crescent West, Hadley Wood. The house was demolished in the 1960s and replaced by other buildings.
Albert Kingwell | Health and death
Autoregulation of cerebral blood flow is impaired, and is associated with anaerobic glycolysis and oxidative stress. Neuronal cell astrocytes are susceptible to these changes, and they swell up, resulting in increased intracranial pressure. Inflammatory mediators also play important role. Unfortunately, signs of elevated intracranial pressure, such as papilledema and loss of pupillary reflexes, are not reliable, and occur late in the disease process. CT imaging of the brain is also unhelpful in detecting early cerebral oedema, but is often performed to rule out intra-cerebral bleeding. Invasive intracranial pressure monitoring via subdural route is often recommended; however, the risk of complications must be weighed against the possible benefit (1% fatal haemorrhage).
Acute liver failure | Encephalopathy and cerebral edema
If the swelling is untreated, it causes death by brain herniation. The brain swelling is likely a result of vasogenic edema, the penetration of the blood–brain barrier by fluids. This process has been observed in MRI studies. Hypoxia increases extracellular fluid, which passes through the vasogenic endothelium in the brain. The leaking may be caused by increased pressure, or it may be caused by inflammation that makes the endothelium vulnerable to leaking. An MRI study found microhemorrhages in the corpus callosum of HACE patients, and hypoxia may also cause microvascular permeability. It has been hypothesized that vascular endothelial growth factor may cause the vascular permeability at the root of HACE.
High-altitude cerebral edema | Cause and mechanism
The extent and severity of the symptoms of cerebral edema depend on the exact etiology but are generally related to an acute increase of the pressure within the skull. As the skull is a fixed and inelastic space, the accumulation of cerebral edema can displace and compress vital brain tissue, cerebral spinal fluid, and blood vessels, according to the Monro-Kellie doctrine. Increased intracranial pressure (ICP) is a life-threatening surgical emergency marked by symptoms of headache, nausea, vomiting, decreased consciousness. Symptoms are frequently accompanied by visual disturbances such as gaze paresis, reduced vision, and dizziness. Increased pressures within the skull can cause a compensatory elevation of blood pressure to maintain cerebral blood flow, which, when associated with irregular breathing and a decreased heart rate, is called the Cushing reflex.
Cerebral edema | Signs and symptoms
King was one of the original Fellows of the Royal College of Surgeons of England upon its establishment in December 1843. At that time, he was living and practising at 36 Bedford Square in London. He died of tuberculosis in 1847.
Thomas Wilkinson King | Later life and death
He was chairman of the Test and County Cricket Board's Finance and General Purposes Sub-committee from 1968 until 1980.
Edmund King (cricketer, born 1906) | Introduction
King Gimp is a 1999 documentary that was awarded the 2000 Oscar for Best Short Subject Documentary and 2000 Peabody Award. "King Gimp" follows the life of artist Dan Keplinger of Towson, Maryland, who has cerebral palsy. Filmmakers Susan Hannah Hadary and William A. Whiteford, of the University of Maryland Video Press and Tapestry International Productions produced the film. Geof Bartz, A.C.E. edited the final version.
King Gimp | Introduction
Together with Gordon Butler Iles he made major advances on flight simulators for the RAF and did major studies on the effects of fatigue on pilots. He died at the age of 31 following an accident, where a car struck his bicycle on the Kings Parade in Cambridge on the 7 May 1945. He died in hospital on the following day: VE Day. He is buried in the northern section of Dean Cemetery. His parents Marie Sylvia Craik and James Craik were later buried with him.
Kenneth Craik | Life
By Lord Peterborough's advice he paid a second visit to the bedchamber, and at the moment that he entered Charles fell down in a fit. King bled him immediately, and Charles gradually regained consciousness. The other physicians who arrived approved the bleeding, and the privy council advised that King should receive a reward of £1,000; but King received no fee.
Edmund King (physician) | Life
King died, aged 81, in Toronto, reportedly from complications of emphysema.
Charmion King | Death
He also scored three more times in March.
Cecil Frederick King | Aerial service
The Cushing reflex often indicates compression of the brain on brain tissue and blood vessels, leading to decreased blood flow to the brain and eventually death.
Cerebral edema | Signs and symptoms
Sir Edmund King (c.1630–1709), also Edmund Freeman, Edmond King, was an English surgeon and physician. He is known as an experimentalist, and also for his attendance on Charles II of England.
Edmund King (physician) | Introduction
CTE is caused by repeated concussions and subconcussive head injuries. Martin's body was cremated and his remains were flown to his family in his hometown of Whitby, Ontario.
Test (wrestler) | Death
Under their management, the treatment of patients with spinal injuries was revolutionised.
Harold Henry Blake | Introduction
In October 1981, Cochrane was involved in a single-vehicle accident on his way home from his job at a manufacturing plant when the motorcycle he was riding veered off of an exit ramp. He suffered a traumatic brain injury. Upon arrival at a hospital, Cochrane was experiencing clonic epileptic seizures and was unconscious. Surgery to remove a left-side subdural hematoma was successful. After a few days in the hospital, Cochrane was able to respond to simple commands. After one week he was able to recognize his mother. A follow up CT scan revealed a chronic bilateral frontal subdural hematoma, enlarged ventricles and sulci, and left occipital lobe infarction.
Kent Cochrane | Accident and neurological damage
Although cerebral edema is closely related to increased intracranial pressure (ICP) and cerebral herniation and the general treatment strategies above are useful, the treatment should ultimately be tailored to the primary cause of the symptoms. The management of individual diseases are discussed separately. The following interventions are more specific treatments for managing cerebral edema and increased ICP:
Cerebral edema | Specific Measures
Prince Leopold had haemophilia diagnosed in childhood, and in early years had various physicians in permanent attendance, including Arnold Royle and John Wickham Legg. In February 1884, Leopold went to Cannes on doctor's orders: joint pain is a common symptom of haemophilia and the winter climate in the United Kingdom was always difficult for him. His wife, pregnant at the time, stayed at home but urged him to go. On 27 March, at his Cannes residence, the 'Villa Nevada', he slipped and fell, injuring his knee and hitting his head. He died in the early hours of the next morning, apparently from a cerebral haemorrhage.
Prince Leopold, Duke of Albany | Illness and death
King has received annual chest X-rays to monitor his heart condition. During his 2017 examination, doctors discovered a cancerous tumor in his lung. It was successfully removed with surgery.
Larry King | Heart disease
Sepulchre. Also in 1666 he was elected a Fellow of the Royal Society. Gilbert Sheldon, the archbishop of Canterbury, created him M.D., a Lambeth degree; he was incorporated at Cambridge in 1671, and in 1677, on bringing a commendatory letter from the king, was admitted an honorary fellow of the College of Physicians of London. He was admitted a regular fellow 12 April 1687, one of the nominees of James II's charter. He was knighted and sworn physician to the king in 1676. On the morning of 2 February 1685 King was sent for by Charles II. Charles talked incoherently, but King did not discover the morbid change at work.
Edmund King (physician) | Life
Coroner Gary Evans released a report into the deaths of the children in July 2012. He found that the twins had suffered the brain injuries which led to their deaths during the afternoon or early evening of 12 June 2006, at a time "whilst they were in the sole custody, care and control of their father", Kahui. He said there was no evidence or fact to support that injuries being caused by King. Kahui, who gave evidence to the coroner's inquest, attempted to prevent the publication of the report.
Cris and Cru Kahui homicides | Coroner's report
King joined the Royal Flying Corps in February, 1917. In the fall of 1917, he was assigned to No. 43 Squadron RFC to fly Sopwith Camels. In conjunction with fellow ace Lieutenant William MacLanachan, he drove down an Albatros D.III out of control on 12 November 1917. King did not score again until February 1918; in the latter half of the month, he ran off a string of three more enemy craft driven down out of control, then became an ace by destroying an Albatros D.V on the 26th. By March 1918, he had advanced to B Flight Commander. On 22 March 1918, he was awarded the Military Cross.
Cecil Frederick King | Aerial service
The condition is commonly associated with vascular and cardiac changes associated with aging but can be caused by many other conditions, including congestive heart failure, kidney failure, liver cirrhosis, portal hypertension, trauma, alcoholism, altitude sickness, pregnancy, hypertension, sickle cell anemia, a compromised lymphatic system or merely long periods of time sitting or standing without moving. Some medicines (e.g. amlodipine, pregabalin) may also cause or worsen the condition.
Peripheral edema | Cause
King was born in 1809 and was educated in London and Paris. He became a doctor like his father, who practised in Dover, and began training at Guy's Hospital as a teenager in 1824. He was appointed curator of the Guy's Hospital museum, a position previously held by Thomas Hodgkin, in 1837, and three years later became a lecturer in comparative anatomy and comparative physiology. He also lectured in anatomical pathology and wrote prolifically in the "Guy's Hospital Reports", particularly about cancer.
Thomas Wilkinson King | Early life and education
Cerebral edema has been traditional classified into two major sub-types: cytotoxic and vasogenic cerebral edema. This simple classification helps guide medical decision making and treatment of patients affected with cerebral edema. There are, however, several more differentiated types including but not limited to interstitial, osmotic, hydrostatic, and high altitude associated edema. Within one affected person, many individual sub-types can be present simultaneously. The following individual sub-types have been identified:
Cerebral edema | Classification
Most people who travel to high altitudes acclimatize. Acclimatization precludes the development of HACE by maintaining adequate levels of cerebral oxygen. The primary cause of HACE is hypoxia (oxygen deprivation). This occurs after the body is exposed to a low-oxygen environment and before it acclimatizes. The rate of change from a normal oxygen environment and how little oxygen is in the new environment can be used to predict the chance of developing HACE. Prolonged exertion in low oxygen also causes serious hypocapnia, lower carbon dioxide in the bloodstream, which may play a role in HACE. These factors cause the brain to swell with fluid, resulting in severe impairment.
High-altitude cerebral edema | Cause and mechanism
Deep brain stimulation (DBS) is effective treatment for several neurological and psychiatric disorders, most notably Parkinson's disease. DBS is not without risks and although rare, idiopathic delayed-onset edema (IDE) surrounding the DBS leads have been reported. Symptoms can be mild and nonspecific, including reduction of the stimulation effect, and can be confused for other causes of edema. Thus, imaging is recommended to rule out other causes. The condition is generally self-limiting and the exact mechanism of the cause is unexplained. Early identification can help persons affected avoid unnecessary surgical procedures or antibiotic treatments.
Cerebral edema | Idiopathic delayed-onset edema