ich klapper mal die amerikanischen seiten ab.
http://www.braintrauma.org/site/PageServer
ist eine sehr gute seite.
http://www.traumaticbraininjury.com/content/symptoms/severetbisymptoms.html
surgical:
http://www.traumaticbraininjury.com/content/treatmentsfor/surgicaltreatment.html
http://www.cellmedicine.com/braininjury.asp
sehr interresant;
Treatment:
Conventionally, very few treatment options have existed for people with TBI. In the hours and days following trauma to the brain, initial efforts are focused primarily on stabilizing the patient, after which time the therapeutic emphasis is on rehabilitation that may include both physical and occupational therapy, depending on the severity of the TBI. As explained on the website of NINDS,
?Because little can be done to reverse the initial brain damage caused by trauma, medical personnel try to stabilize an individual with TBI and focus on preventing further injury. Primary concerns include insuring proper oxygen supply to the brain and the rest of the body, maintaining adequate blood flow, and controlling blood pressure. Imaging tests help in determining the diagnosis and prognosis of a TBI patient. Patients with mild to moderate injuries may receive skull and neck X-rays to check for bone fractures or spinal instability. For moderate to severe cases, the imaging test is a computed tomography (CT) scan. Moderately to severely injured patients receive rehabilitation that involves individually tailored treatment programs in the areas of physical therapy, occupational therapy, speech/language therapy, physiatry (physical medicine), psychology/psychiatry, and social support.? (From
www.ninds.nih.gov).
Whenever injury is sustained anywhere in the body, swelling is the first response of natural defense mechanisms, and in most parts of the body such defenses expedite the healing process. In the delicate white and gray matter of the central nervous system, however, which includes tissue within the spinal cord as well as the brain, such swelling often causes further, secondary damage. TBI is, in fact, identified most characteristically by the prominent secondary damage that typically results, the precise cellular mechanisms of which are not yet fully understood, but which are believed to be associated with a disruption of calcium regulation in brain cells following an injury. A proper balance of calcium levels is crucial to mitochondrial function and to proper adenosine triphosphate (ATP) synthesis and metabolism, a disruption in which will result in a series of cascading molecular events that end ultimately in necrosis and apoptosis (programmed cell ?suicide?) of neuronal cells. In severe cases of TBI, neuronal shrinkage and gross brain atrophy are visible, precisely for these reasons.
Neurophysiologically, these cellular events are very similar in people who incur moderate to severe TBI and people who suffer from certain other types of neurological maladies. For example, the ?ischemic cascade? which occurs after a stroke, and the inflammatory immunological response following spinal cord injury, are both similar in nature to the swelling that may occur after a TBI, depending upon the severity of the particular TBI. Various cellular and molecular mechanisms that characterize any one of these disorders may therefore be relevant to the others.
The problem of cellular excitotoxicity is one such example, during which an excessive release of excitatory neurotransmitters such as glutamate triggers a series of chemical and cellular processes that cause secondary damage to tissue by overexcitement of the nerve cells. In abnormally high amounts, glutamate disrupts calcium metabolism and related enzymatic activity of the proteases, which in turn disrupts mitochondrial oxidation, thereby damaging glial cells via a number of direct and indirect mechanisms. This phenomenon remains an area of widespread research focus in the treatment of various pathologies involving central nervous system tissue, including not only TBI but also stroke, spinal cord injuries and various neurodegenerative diseases.
In TBI, such cascading cellular events may exacerbate hypoxic and ischemic injury and may require urgent neurosurgical intervention to relieve subdural, extradural or intracerebral hemorrhage. Pathologies of this nature do not always manifest immediately but may develop within days or even weeks following a TBI, and therefore many secondary injuries are not detectable on the same day of injury. Cerebral contusions, for example, are not usually identifiable by CT scan until at least the second or third day following an injury. As already described, continued monitoring of the individual is therefore a crucial aspect of TBI treatment.
Focal injuries in the frontal and temporal lobes are most commonly identifiable, due primarily to the shape of the inner surface of the skull along these regions. While intracranial hematomas may be surgically accessed relatively easily, deep intracerebral hemorrhages, by contrast, which may be caused by arterial damage resulting either from focal or diffuse injury, are virtually inaccessible. In general, diffuse brain injury, known technically as diffuse axonal injury or DAI, is visible on CT scans only in 5 to 10% of the most severe cases, and when it is visible at all it is most commonly recognizable either as intraventricular hemorrhage or as multiple punctate subcortical lesions in and around the corpus callosum and the deep white matter. Symptomatically, DAI manifests as altered states of consciousness, although most DAI patients will not yield any supporting evidence of such damage on CT scans. In the event of coma, the depth and duration of the coma will reflect the extent of the injury, while other clinical markers in the absence of coma may include prolonged retrograde and anterograde amnesia. Certain aspects of an injury increase the risk of DAI, such as a high speed of impact.
Unlike stroke patients, people with DAI that was incurred through TBI seem to maintain more active neural repair mechanisms, and therefore often receive a prognosis that may include some improvement and recovery during the first 5 years following their injury. Such recovery is often the result not merely of natural repair mechanisms but also of various built-in compensatory strategies of neuroplasticity.
Medications that are administered to TBI patients include primarily those that are efficacious in reducing inflammation. To counteract the phenomenon of calcium excitotoxicity described above, calcium channel blockers (CCBs), also known as calcium antagonists, are often employed to help reduce the risk of further injury to damaged nerve cells. CCBs are also routinely prescribed in the treatment of high blood pressure, angina and congestive heart failure and therefore may be contraindicated in certain individuals. Intravenous diuretics are also often prescribed for TBI patients to help reduce brain swelling.
CCBs that have been approved for use in the U.S. include nisoldipine (Sular), nifedipine (Adalat, Procardia), nicardipine (Cardene), bepridil (Vascor), isradipine (Dynacirc), nimodipine (Nimotop), felodipine (Plendil), amlodipine (Norvasc), diltiazem (Cardizem), and verapamil (Calan, Isoptin). Side effects of CCBs most commonly include low blood pressure and other expected consequences of dilated arteries, such as flushing, edema of the lower extremities, increased heart rate and increased palpitations. CCBs are contraindicated in people already diagnosed with heart failure since CCBs reduce the ability of the heart to pump blood. Additional side effects may include flu-like symptoms, fever, nausea, vomiting, headaches, dizziness, nervousness, depression, insomnia, impotence, blurred vision and difficulty breathing. Bepridil in particular slows the ability of cardiac muscle to recover electrically and to prepare for the next contraction, and may therefore cause arrhythmias (abnormal heart rhythm) and should not be taken with other drugs that have similar mechanisms of action, such as quinidine (Quinaglute, Duraquin, Quinidex), procainamide (Procan-SR, Pronestyl), disopyramide (Norpace), flecainide (Tambocor), and tricyclic antidepressants such as amitriptyline (Elavil). Bepridil also increases levels of digoxin (Lanoxin) in the blood and may increase the risk of digoxin toxicity. Bepridil is secreted into breast milk and is also known to cross the placenta and therefore should not be taken by women who are pregnant or nursing. Patients with low serum concentrations of potassium or magnesium, and patients with the electrocardiographic abnormality known as QT prolongation, are at the greatest risk of developing serious arrhythmias from bepridil. Diltiazem has been known to cause elevated liver enzymes.
Recent research has suggested that the drug rivastigmine may improve memory loss in some patients suffering with TBI, according to studies conducted at the New York School of Medicine. Rather than being a calcium channel blocker, rivastigmine falls into the category of medications known as cholinesterase inhibitors, and as such is frequently prescribed for the treatment of Alzheimer?s disease. In clinical trials led by Jonathan Silver, M.D., researchers at the New York School of Medicine have discovered that rivastigmine helps patients who have suffered moderate to severe memory loss from TBI, although the drug does not appear to improve memory in people who have suffered mild TBI. The beneficial effects of this medication are believed to become apparent only when relevant brain regions have incurred a significant depletion of cholinergic activity, which results in the functional impairment of memory and attention that is often seen both in Alzheimer?s disease and in certain types of TBI. Rivastigmine is generally well tolerated with relatively few side effects, as approximately half of all patients who receive the drug complain of nausea, one-third complain of vomiting, and 10% complain of dizziness. Upper respiratory tract infection and headache are also occasionally seen, and approximately 15% of patients choose to discontinue rivastigmine due to such side effects.
It should be noted, however, that anyone who has incurred injury to the brain is unusually vulnerable to adverse effects from medication, as pointed out on the website of the National Institute of Neurological Disorders and Stroke (NINDS), a division of the National Institutes of Health (NIH):
?Great care must be taken in prescribing medications because TBI patients are more susceptible to side effects and may react adversely to some pharmacological agents.? (From
www.ninds.nih.gov).
Whenever brain swelling is too severe to be treated by medication alone, various types of surgery may be warranted. In the absence of hematomas or contusions, a section of the parietal bone on top of the skull may be temporarily removed in order to allow the brain to swell without increasing the risk of further neurological damage from increased intracranial pressure. Neurologists performed this procedure on the ABC News anchor, Bob Woodruff, when he incurred severe TBI from the blast of an IED (improvised explosive device) while reporting from Baghdad in 2006.
National Institute of Neurological Disorders and Strokes
http://www.ninds.nih.gov/
Organizations
Acoustic Neuroma Association
600 Peachtree Parkway
Suite 108
Cumming, GA 30041
info@anausa.org
http://www.anausa.org
Tel: 770-205-8211 877-200-8211
Fax: 770-205-0239/877-202-0239
Brain Injury Association of America, Inc.
8201 Greensboro Drive
Suite 611
McLean, VA 22102
FamilyHelpline@biausa.org
http://www.biausa.org
Tel: 703-761-0750 800-444-6443
Fax: 703-761-0755
Brain Trauma Foundation
523 East 72nd Street
8th Floor
New York, NY 10021
http://www.braintrauma.org
Tel: 212-772-0608
Fax: 212-772-0357
Family Caregiver Alliance/ National Center on Caregiving
180 Montgomery Street
Suite 1100
San Francisco, CA 94104
info@caregiver.org
http://www.caregiver.org
Tel: 415-434-3388 800-445-8106
Fax: 415-434-3508
National Rehabilitation Information Center (NARIC)
4200 Forbes Boulevard
Suite 202
Lanham, MD 20706-4829
naricinfo@heitechservices.com
http://www.naric.com
Tel: 301-459-5900/301-459-5984 (TTY) 800-346-2742
Fax: 301-562-2401
National Stroke Association
9707 East Easter Lane
Suite B
Centennial, CO 80112-3747
info@stroke.org
http://www.stroke.org
Tel: 303-649-9299 800-STROKES (787-6537)
Fax: 303-649-1328
Administering Hypertonic Saline to Patients With Severe Traumatic Brain Injury
Posted 12/06/2006
Diane Schretzman Mortimer; Jon Jancik
Author Information
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Abstract and Introduction
Abstract
Hypertonic saline (HTS) is an osmotic agent that can help patients in the acute phase of severe traumatic brain injury. HTS extracts fluid from swollen cerebral tissue to both control intracranial pressure and diminish the deleterious effects of secondary brain injury. Neuroscience nurses in intensive care and acute care units, who may administer HTS as resuscitation fluid, continuous infusion, or bolus dose, need to be familiar with physiologic actions, potential side effects, and appropriate HTS administration techniques. Neuroscience nurses collaborate with other members of the interdisciplinary team to ensure that HTS is administered safely.
Introduction
Severe traumatic brain injury (TBI) is a major health problem in the United States. There are approximately 50,000 new cases per year, including 17,500 deaths (Narayan et al., 2002). Head injury, which causes significant mortality in all age groups (Bullock et al., 2000), is the leading cause of death in infants and children (Simma, Burger, Falk, Sacher, & Fanconi, 1998). TBI is a contributing factor in more than 60% of all trauma-related deaths (Bullock et al.).
The high mortality rate associated with severe TBI probably is in part due to the deleterious effects of secondary brain injury. The primary injury is often followed by secondary events hours and even days later (Bayir, Clark, & Kochanek, 2003). The occurrence of devastating secondary events accounts for the fact that inpatient mortality rates continue at an alarming 25%?33%, even at the best head injury centers in the country (Narayan et al., 2002). In fact, as many as 90% of patients who die from TBI show some evidence of secondary brain injury (Shackford et al., 1998).
Hypertonic saline (HTS) is an osmotic agent that may diminish the effects of secondary brain injury in patients with TBI. Given during the acute phase of head trauma care, this treatment is inexpensive and has manageable side effects. It has been determined to be safe and effective in multiple human trials. HTS can be given during resuscitation, via continuous infusion, or as a bolus dose (Doyle, Davis, & Hoyt, 2001). Nursing care for patients receiving HTS includes careful administration and close monitoring of laboratory values and patient status (Johnson & Criddle, 2004).
National Institute on Disability and Rehabilitation Research (NIDRR)
U.S. Department of Education Office of Special Education and Rehabilitative Services
400 Maryland Ave., S.W.
Washington, DC 20202-7100
http://www.ed.gov/about/offices/list/osers/nidrr
Tel: 202-245-7460 202-245-7316 (TTY)
http://www.cochrane.org/reviews/en/ab003983.html
Does a procedure that involves removing a section of skull improve the outcome of brain injured patients with raised intracranial pressure (excess pressure within the skull), who have not responded to conventional medical treatments?
An injury to the brain may cause it to swell. In such cases pressure within the skull increases as the brain has no room to expand; this excess pressure (known as intracranial pressure) can cause further injury. High intracranial pressure (ICP) is the most frequent cause of death and disability in brain injured patients. If high ICP cannot be controlled using general maneuvers or first-line therapeutic measures, second-line treatments are initiated. One such second-line measure is a procedure called decompressive craniectomy (DC). DC involves the removal of a section of skull so that the brain has room to expand, and ICP can reduce. There is however clinical uncertainty regarding the use of DC, and a lack of consensus on the optimal management of traumatic brain injury.
This review looked at all high quality trials investigating the effectiveness of DC compared to conventional medical treatments, in terms of the survival and neurological outcome of patients, over the age of 12 months, with raised ICP after traumatic brain injury (TBI).
Only one high quality trial was identified; which involved 27 pediatric patients (less than 18 years old) with TBI, who received either DC or conventional treatment. The results indicate that the risk of death and disability was moderately reduced when DC was used. No trials investigating the effectiveness in adults were found.
The authors of the review conclude that there is no evidence to support the routine use of DC to improve mortality and quality of life in brain injured adults with high ICP. Evidence from one trial indicates that DC may improve survival and neurological outcomes in brain injured pediatric patients with raised ICP, for whom other medical treatments have failed. However, as this one trial involved only a small number of patients, further studies are needed before applying DC as a routine treatment.
Two trials of DC are currently in progress, the results from which may allow further conclusions regarding the effectiveness of the procedure in adults, and will be incorporated into the review on their completion.
search for: severe TBI
Pub MED
http://www.ncbi.nlm.nih.gov/sites/entrez
