1. RSD / CRPS & The 4 Stages of Hell ( this is a long read but something we all need to be aware of , I think it is very important ! )
REFLEX SYMPATHETIC DYSTROPHY (RSD)
To define Reflex Sympathetic Dystrophy (RSD) one should understand the terminology of sympathetic and parasympathetic nervous systems. There are two different types of nervous systems controlling the body. One is the so-called "somatic" nervous system which has clear-cut anatomical structures and is controlled by the cerebral cortex (cerebral hemispheres) in a relatively volitional manner. We see, hear, touch, taste or smell something, and volitionally and knowingly respond positively or negatively towards the stimulus. We can influence our response through the judgment of higher centers of the brain (cerebral hemispheres). This is the "somatic" system which is strongly influenced and controlled by our conscious mind.
The other system is the so-called autonomic system. The name implies that it is autonomous (kind of having a mind of its own). It is almost autonomous but it can be influenced to a certain extent by conscious brain as well. This system is quite primitive and old (from evolutional standpoint). Even a worm has an autonomous nervous system. If one does an experiment by warming up one end of a fish tank water and cooling the other end of the; the worm will go from one extreme to the other and eventually will reside halfway between the two extremes of temperature in the mid portion of the fish tank. The worm does not need a brain to decide where to retire. The autonomic system does the job for it.
The autonomic nervous system concerns itself with preservation and protection of the "Internal Environment". For example, in warm blooded animals the autonomic nervous system keeps the temperature inside the body around 99º Fahrenheit (37 ºC).
To protect the internal environment, the autonomic nervous system has two main components.
1.The sympathetic system.
The sympathetic system is a fight component of the "Fight and Flight" reflexes of the autonomic nervous system. On the fight end part of it the sympathetic system increases the internal temperature, raises the blood pressure, strengthens the protective function of the skin, makes the skin cold so that there would be no waste of temperature, makes the skin sweat excessively (so that there would be no extreme increase of the internal temperature); and increases muscle metabolism, bone circulation, circulation of the brain and guts. The end result is the animal is ready to fight. On the other hand, the parasympathetic system that is the balancer of the other end of the autonomic system (the flight system), drops the blood pressure, slows down the pulse, relaxes the muscles, and preserves energy by cutting down the calories burned in the body. As such, the parasympathetic system works the opposite of the sympathetic system. The two systems are totally independent and one cannot give a patient parasympathetic enhancing medications in the hope of cooling the sympathetic and vice-versa.
THEN WHAT IS RSD?
RSD is one form of disturbance of the function of the autonomic nervous system. Simply having a hyperactive sympathetic nervous system does not make RSD. The disturbance of the autonomic system comprises several diseases, some acquired, some genetic, some metabolic, some traumatic, etc.
Some examples of dysautonomias "disturbances of the autonomic nervous system" are attacks of hypotension (low blood pressure), congenital absence of sweating, and neuropathic pain syndrome.
The latter category of chronic neuropathic pain syndrome refers to the conditions that are not exactly necessarily reflex sympathetic dystrophy, but have an abnormal sympathetic component to them. They share sympathetically maintained pain (SMP) with RSD but they are not RSD.
Examples of such chronic neuropathic pain are post-hepatic neuralgia (pain accompanying and following shingles), neuropathic diabetic neuropathy, acute neuropathic pain accompanying bee stings, snake bites or spider venom stings as well as involvement of the sympathetic nerves due to the systemic AIDS infection.
The neuropathic pains are not at all synonymous with RSD. They do not even in any way resemble RSD. In some cases, however, they can end up with RSD.
The chronic neuropathic pain syndrome is far more common than the true clinical picture of RSD.
CAN RSD BE MORE CLEARLY DEFINED?
RSD is a definitive chronic pain syndrome called by several different names such as reflex sympathetic dysfunction, (stage I), reflex sympathetic dystrophy (stage II), reflex sympathetic atrophy (stage III), late stage RSD complicated by disturbance of immune system, suicidal and fetal tendency, cancer, heart attack or stroke (stage IV), complex regional pain syndrome (CRPS) which encompasses all different forms of RSD as well as the causalgic RSD, causalgia (burning, stabbing, constant pain, acting more like an epileptic seizure), shoulder-hand syndrome, sudeck's atrophy (circa 1900), traumatic vasospasm of Lehman (1934), mimocausalgia (1973), minor causalgia (1940), and half a dozen other names.
In medicine there is a trend. When a disease becomes confusing, the physicians become desperate and give it new names. Each of the above almost dozen names reflect some features of RSD.
Merskey and Bogduk in January of 1994 defined the syndrome as follows (IASP Press, Seattle classification of chronic pain 2nd edition): CRPS TYPE I is a syndrome that usually develops after an initiating noxious event, is not limited to the distribution of a single peripheral nerve, and is apparently disproportionate to the inciting event. It is associated at some point with evidence of edema, changes in skin blood-flow, abnormal sudomotor activity (sweating) in the region of the pain, or allodynia or hyperalgesia. They also clarify in the main features of CRPS (RSD). "The symptoms and signs may spread proximally or involve other extremities. Impairment of motor function is frequently seen". They clarify associated symptoms and signs and specify "atrophy of the skin, nails, and other tissues, alterations in hair growth, and loss of joint mobility may develop. Impairment of motor function can include weakness, tremor, and in rare instances, dystonia. Symptoms and signs fluctuate at times. Sympathetically maintained pain may be present and may be demonstrated with pharmacological blocking or provocation techniques. Affective symptoms of disorders occur secondary to the pain and disability. Guarding of the affected part is usually observed".
This is a long but relatively comprehensive definition of RSD. Building on the basis of this comprehensive definition of RSD, one can come to the conclusion that RSD is a syndrome with multiple manifestations which require the following minimal symptoms and signs for the condition to be called RSD (CRPS).
1. Pain: constant, burning pain, and in some forms at times during the course of the disease, stabbing type of pain (causalgic). The pain is relentless and is invariably accompanied by allodynia (even simple touch or breeze aggravating the pain) and hyperpathia (marked painful response to even a simple stimulation).
2. Spasms in the blood vessels of the skin and muscles of the extremities. The spasms in the blood vessels result in a cold extremity. The muscle spasms result in tremor, movement disorders such as dystonia, flexion spasm, weakness and clumsiness of the extremities, and tendency to fall.
3.RSD is accompanied by a certain degree of inflammation in practically all cases. This inflammation may be in the form of swelling (edema), skin rash (neurodermatitis), inflammatory changes of the skin color (mottled or purplish, bluish or reddish or pale discolorations), tendency for bleeding in the skin, skin becoming easily bruised, inflammation and swelling around the joints as well as in the joints (such as wrists, shoulders, knee, etc.) which can be identified on MRI in later stages, and secondary freezing of the joints.
4.The fourth component and pre-requisite of diagnosis of RSD is insomnia and emotional disturbance. The fact that the sympathetic sensory nerve fibers carrying the sympathetic pain and impulse up to the brain terminate in the part of the brain called "limbic system". This limbic (marginal) system which is positioned between the old brain (brainstem) and the new brain (cerebral hemispheres) is mainly located over the temporal and frontal lobes of the brain. The disturbance of function of these parts of the brain results in insomnia, agitation, depression, irritability, and disturbance of judgment. Insomnia is an integral part of an untreated RSD. So are problems of depression, irritability and agitation.
So the clinical diagnosis of RSD is based on the above four principles rather than simply excluding RSD and finding some other cause for the patient's pain.
Other laboratory and ancillary tests are helpful in confirming the diagnosis but if the results are negative they don't rule out RSD. For example, bone scan has 55 to 65% sensitivity of positive results in RSD so the other 35% of the patients still have RSD in the face of negative bone scan.
The thermography may be positive and helpful in confirming the diagnosis of RSD but at least 10% of RSD patients do not have the positive thermographic test. This is because of symmetrical involvement of RSD in both extremities. Thermography also has the handicap of tests such as MRI in that it can show false-positive results showing temperature changes in the absence of the symptoms and signs of RSD.
Phentolamine IV nerve block test is probably the most sensitive test to confirm RSD in the earlier stages (stages I and II within the first two to three years of the disease). However, as the disease becomes chronic, the longstanding constriction of the blood vessels causes disturbance of the circulation in the peripheral somatic nerves with resultant involvement of the somatic sensory nerves as well. As a result, the patient does not show a pure sympathetically mediated pain (SMP) but can show sympathetically independent pain (SIP) with no relief from Phentolamine in late stages of RSD.
In conclusion, RSD is a clinical bedside diagnosis. Not every hyperpathic pain is RSD. Not every SMP is RSD. SMP can be due to a simple post-herpetic neuralgia or diabetic neuropathy but that does not make RSD.
"Now that RSD has been diagnosed by the above criteria, what is the nature of the illness, manifestations, and treatment of RSD?"
RSD, as defined above, usually develops after a minor trauma. There are precipitating factors that enhance the development of RSD. These consist of immobilization of the extremity with cast or brace, application of ice, and inactivity due to strong addictive narcotics and tranquilizers.
The application of ice plays a major role. In experiments regarding the conductibility of the nerve impulse to the nerves, cold has shown to play a major role. If the temperature of the extremity drops from 37ºcentigrade to 10º centigrade, then the larger somatic sensory nerves stop conducting electricity through the nerve fibers. It takes the temperature to drop to 0º centigrade (freezing temperature) for the sympathetic nerves which are small thin fibers to stop conducting. The reason is the smaller the nerve fiber the less fatty sheath of myelin (insulator) surrounds the nerve. The fat in the myelin freezes more readily with the drop of temperature and stops the conduction of the nerve impulse.
What the above implies is the fact that once the extremity is cooled down with ice to 10º temperature or lower, the normal conduction of the somatic nerves (touch, vibration, and position sense) is blocked off and the extremities left with purely the sympathetic nerve fibers function (constant burning pain).
The above clearly indicates that cooling of the extremity that had minor injury will tilt the scale towards the hyperactive sympathetic burning pain function at the expense of excluding the
normal good senses of touch, vibration and position senses.
The somatic and sympathetic sense counteract each other. The somatic sensory system inhibits and stops the provocation of the exaggerated burning pain at the spinal cord level. Cooling of the extremity selectively knocks out the inhibition of the good sensory input (somatic) and causes sympathetically mediated pain (SMP) to be the sole modulation of the sensation in the RSD extremity.
It becomes obvious that not only application of ice aggravates RSD but plays a major role in the development of RSD as well.
The application of brace type cast, wheelchair and crutches also reduces the proper sensory input and results in immobilization of the extremity. The extremity that has become immobile loses its surface temperature. The body considers that extremity inactive and not needing blood on the surface so the body constricts the surface blood vessels to preserve heat and not to waste it on an immobile extremity. This second factor of immobilization aggravates the first factor of burning pain by increasing the degree of constriction of blood vessels to the skin of the extremity.
The use of addicting narcotics and benzodiazepines (tranquilizers), results in withdrawal pain every 4 to 5 hours. The use of such addicting medications puts an end to the brain manufacturing its own narcotics and BZs. As a result, 4 to 5 hours after the administration of such medications, even though the patient does not have a new injury affecting his body, feels withdrawal pain because of the lack of endorphines and endoBZs.
The combination of the above three factors, use of ice, immobilization and addicting drugs, exaggerates the SMP (sympathetically maintained pain) due to the original minor trauma.
As the condition becomes chronic, the other aspects of this syndrome complete the clinical picture. Inflammation develops, insomnia, agitation and depression affect the patient's diurnal cycle, deprive the patient of resting well and sleeping normally at night and the end result is the full-blown picture of RSD.
The original injury may involve any part of the body, but the most common areas affected by this type of sympathetic pain (i.e. constant burning pain, accompanied by severe anxiety, depression and muscle spasm) are the hand, elbow, knee, and foot.
In the United States, over five million patient suffer from this extremely painful and disabling illness called by many names, including reflex sympathetic dystrophy (RSD), sympathetic dysfunction syndrome (SDS), and causalgia, to name a few. This unusual, but severe painful condition is caused by disturbance of the function of the sympathetic nervous system (SNS).
Normally, the sense of pain is perceived through two separate channels in the body. The most common type of pain is transmitted through the nerves that end up in the cortex of the brain, over the vertex of the head (parietal lobe). This somatic pain is temporary, clear-cut and focalized. As the area of nerve damage is healed, the pain disappears.
In contrast to the somatic pain, the sympathetic pain terminates in a more primitive part of the brain, called the limbic system .This is the area of the brain at the margin of brain stem and neocortex (frontal and temporal lobes). It controls emotion, memory, and judgment. The end result is insomnia, agitation, irritability, poor judgment and depression
As the condition becomes more persistent and chronic, the physician unknowingly perpetuates and aggravates the condition by the good intention of trying surgical procedures in the area affected by RSD.
The disease was first recognized by the Civil War surgeon from Atlanta (Dr. S.W. Mitchell); however, even a century later, this condition remains enigmatic, and is often diagnosed too late for successful treatment; not infrequently, it is complicated by unnecessary surgical operations, along with addicting narcotic and tranquilizer treatment. Any operation in the injured area can result in new scar formation and therefore a new source of pain. The treatment with narcotics and tranquilizers deprives the brain of it's own endogenous hormones (endorphines); this causes a new source of pain due to drug dependence. The scar of surgical procedure, added to drug dependency causes rapid deterioration; at this point, the treatment becomes the source of the disease.
Eventually, the four major manifestations of RSD evolve (see RSD Components, Table 2).The combination of a constant burning pain, which is instigated by even a simple touch (allodynia, muscle spasm and tremor, anxiety, depression and agitation, may result in a confusing, confounding and frustrating clinical picture, making the diagnosis and proper treatment quite difficult.
As a result, the source of this condition is mistaken for "psychological causes; e.g., malingering, hysteria and hypochondriasis.
In 1992, Doctor Mary E. Lynch had found no significant pre-existing psychopathology in RSD patients.
As the disease becomes chronic, it goes through four stages; these stages are not distinctive or clear-cut, but develop in an overlapping fashion. Stages I and II are the earliest and easiest to treat. If the disease is diagnosed and properly treated in the first six months, then stages III and IV shall be aborted. Any attempt at proper treatment, in the form of physical therapy or sympathetic block, will prevent serious complications seen in stage III and IV. (Table 3) As a result, because the classical advanced complications are not seen in partially treated patients, the clinician does not arrive at the proper diagnosis of RSD.
The staging of RSD is not as critically done on the basis of dysfunction (stage I) meaning abnormal function of the sympathetic system in the extremity, dystrophy (stage II , meaning trophic and inflammatory changes, skin changes and other signs of inflammation), atrophy (stage III, meaning usually minimal degree of atrophy in the involved muscles), or stage IV (meaning disturbance of the immune system, suicidal attempts, stroke, heart attacks, intractable hypertension and chest pain, and in some cases development of cancer). The prognosis is more related to the temporal development of the above four stages.
Stages of RSD
Stage I: A sympathetic dysfunction with thermatomal distribution of the pain. The pain may spread in a mirror fashion to contralateral extremity or to adjacent regions on the same side of the body. In stage one, the pain is usually SMP in nature.
Stage II: The dysfunction changes to dystrophy manifested by edema, hyperhidrosis, neurovascular instability with fluctuation of livedo reticularis and cyanosis causing change of temperature and color of the skin in matter of minutes. The dystrophic changes also include bouts of hair loss, ridging, dystrophic, brittle and discolored nails, skin rash, subcutaneous bleeding, neurodermatitis, and ulcerative lesions (Fig. 5). Due to the confusing clinical manifestations, the patient may be accused of self-mutilation and even "Münchausen syndrome." All these dystrophic changes may not be present at the same time nor in the same patient. Careful history taken is important in this regard.
Stage III: Inflammation becomes more problematic and release of neuropeptides from c-fiber terminals results in multiple inflammatory and immune dysfunctions. The secondary release of substance P may damage mast cells and destroy muscle cells and fibroblasts.
Stage IV: Identifies the final stage of RSD / CRPS manifested by:
1. Failure of the immune system, reduction of helper T-cell lymphocytes and elevation of killer T-cell lymphocytes. This is in contrast to the opposite, up-regulated function of immune system in early stages.
2. The hypertension in early stages due to alpha-1 up-regulation reverses to eventual exhaustion and to the common occurrence of orthostatic hypotension in this late stage. Blood pressure changes in this stage are due to autonomic failure. The failure of the sympathetic system exaggerates the response to drugs that lower or raise the blood pressure.
3. Intractable generalized extremity and visceral edema involving the abdomen, pelvis, lungs, and extremities due to long-standing disturbance of sodium-potassium and calcium magnesium pumps usually left untreated for several years. The same organs may eventually be subject to multiple abscesses due to failure of immune function.
4. Ulcerative skin lesions.
5. High risks of cancer and suicide.
6. Multiple surgical procedures seem to be precipitating factors for development of stage IV.
This late stage is almost the flip side of earlier stages, and points to exhaustion of sympathetic and immune systems. Ganglion blocks in this stage are useless and treatment should be aimed at improving the edema and the failing immune system.
The use of addicting narcotics and benzodiazepines (tranquilizers), results in withdrawal pain every 4 to 5 hours. The use of such addicting medications puts an end to the brain manufacturing its own narcotics and BZs.
As a result, 4 to 5 hours after the administration of such medications, even though the patient does not have a new injury affecting his body, feels withdrawal pain because of the lack of endorphines and endoBZs.
The combination of the above three factors, use of ice, immobilization and addicting drugs, exaggerates the SMP (sympathetically maintained pain) due to the original minor trauma.
As the condition becomes chronic, the other aspects of this syndrome complete the clinical picture. Inflammation develops, insomnia, agitation and depression affect the patient's diurnal cycle, deprive the patient of resting well and sleeping normally at night and the end result is the full-blown picture of RSD.
The one extreme in the case of major causalgia with significant damage to the sympathetic nerve, the status 1 through 3 can develop in a matter of weeks or a few months.
On the other extreme, for example in the case of heart attack or stroke causing RSD, the stages evolve in a very slow fashion and it may take a few years before stages III and IV are seen.
The faster the stages develop, the more severe the RSD and the treatment should be applied in a more aggressive fashion.
On the other hand, even a partial or minimal treatment of chronic stages of RSD can change the clinical picture of stage III (atrophy) back to stage II or stage I. That is a good sign, but that does not mean that the patient's condition is mild just because the patient is in stage I. The more chronic the disease the more likely the persistence of the symptoms and complications even though the bed side examination shows reversal to stages I and II from stages III and IV.
If properly treated with extensive physical therapy, heat, mobilization, exercise and sympathetic nerve blocks, the success rate for full recovery in the first six months (stages I and II) is better than 80% .
SPREAD OF THE DISEASE
Even in the early stages, laboratory tests such as triphasic bone scanning or thermography show a spread of the disease from one side to the other. The headache and facial pain becomes bilateral, the facial pain is complicated by dizziness, tinnitus (buzzing in the ear). In the later stages of the disease, the spread is both horizontal and vertical (e.g., from right arm to left, down the legs). The reason for this spread is the anatomical structure of the sympathetic nervous system. The majority of the Sympathetic nerve fibers do not allow the standard somatic nerve fibers, but follow the wall of the blood vessels and end up in the chain of clumps of the nerve cells, called sympathetic ganglia", which are present on each side of the spine. Input of pain into any part of these chains of nerves causes the impulse to spread both vertically and horizontally. This is the main reason sympathectomy or removal of the ganglia is fraught with an extremely high percentage of failure.
This complex clinical picture of the spread of this disease has played a major role in confusing and delaying the proper diagnosis and treatment of RSD. to begin with, the injury causes such a small scar that may be barely visible. This is followed by a constant burning pain, severe neck pain and headache, spread of pain to the opposite side, followed by dizziness, fatigue, insomnia, agitation and irritability.
On this background, the patient may develop pain in the arm, tremor of the hand, may have trouble walking, spasms in the legs, and may end up in a wheelchair. It is obvious that such a patient may be viewed as a neurotic, depressed, and a hypochondriac.
The condition is further compounded by the fact that the patient has normal MRI, CAT scans, and x-rays. The pain is a physiological phenomenon, due to the disturbance of small sympathetic nerve fibers; CAT scan and MRI will not show such an abnormality. An individual who suffers a heart attack and goes to the emergency room, has a normal CAT scan and MRI in the face of a potentially fatal disease. By the time MRI is abnormal, showing fluid in the involved joints or damage to the bone due to increased circulation in the deep structures, the disease is quite advanced and easy to diagnose.
Eventually, the spasm may spread to the truncal muscles; as a result, an accordion-like jamming effect of the vertebrae evolves, with resultant bulging of the lower lumbar discs noted on MRI. This may result in unnecessary surgical operation. The RSD causes constriction of blood vessels to the hands; in this clinical picture, the patient is often mis-diagnosed as carpal tunnel syndrome, tardy ulnar nerve palsy, or thoracic outlet syndrome.
Not infrequently, such patients undergo multiple operations over the arms and cervical and lumbar spine regions, with rapid acceleration and deterioration of the RSD.
The worst risk factor, and the cardinal sin, is amputation of a limb. If the patient has any sympathetic mediated pain, amputation is going to multiply the disease by several times, due to the fact that the stump of the Amputation causes scar formation at the cut ending of the nerves with marked exacerbation of RSD in the most severe form, called "Causalgia".
Even without application, surgical procedure over the inflamed area of involvement of the RSD (such as ankle, knee or wrist), is a major aggravator of RSD which overnight changes as stage I RSD to stage III or later.
The Three areas that are most commonly and unfortunately operated on are:
1.Wrist according to the diagnosis of carpal tunnel syndrome. This has already discussed in the RSD quiz related to carpal tunnel syndrome. Simply put, carpal tunnel syndrome rarely causes RSD but in rare cases of RSD the inflammation of the soft tissue at the wrist results in a clinical picture identical to carpal tunnel syndrome (CTS). This form of carpal tunnel syndrome is the effect not the cause. It is the result of RSD rather than being the cause of RSD. In this type of CTS, the entire hand, wrist and forearm are quite hypopathic, allodynic and sensitive to touch in contrast to the true somatic carpal syndrome. In this form of RSD, treatment with nerve blocks and anti-inflammatory medications Baclofen, moist heat and Epsom salt clears up the symptoms and signs of CTS. On the other hand, surgery ends up with disastrous results.
2.The same is true in the case of so-called tarsal tunnel syndrome which is over-diagnosed and over-treated universally by the podiatrists and surgery over the tarsal tunnel on the ankle rapidly deteriorates the already existing RSD.
3.The same is true with a lot of minor injuries to the knee with full-blown clinical picture of cold extremity, flexion, weakness and atrophy of the muscles around the knee, difficulty with weight bearing, severe constant burning pain, all of which prompt the surgeon to explore the knee with obvious disastrous results.
Opposite to the prevalent notion of "treat the source" the proper principle should be treat the RSD and then see what happens to the so-called source.
Even nerve blocks should not be done in the area of inflammation of RSD (over the wrist, ankle, dorsum of the foot, dorsum of the hand or the knee). Instead the nerve blocks which are very effective in treatment of RSD, should be done in axial area (over the spine) where the nerves enter and exit from the spinal cord to the involved part of the extremity.
Simply said, do not needle, amputate, or operate the area of inflammation of the RSD.
The diagnosis is achieved by the physician's familiarity with the triad of RSD, as mentioned above. Confirmatory tests, such as beneficial effect from sympathetic nerve block, as well as the use of bone scan or thermography are quite helpful. None of the above tests yield 100% positive diagnostic proof. Even sympathetic nerve block is positive and relieves the pain in early stages of the disease. In the later stages, there has been enough damage - due to vasoconstriction - in the involved area, that non-sympathetic pain contaminates the clinical picture and the patient does not receive 100% relief from the nerve block.
Early diagnosis in the first six months to maximal two years is the key to successful treatment . Surgical procedures have no place in treatment of RSD. Sympathectomy or removal of a part of the chain of sympathetic ganglia on the side of the spine) has an extremely high rate of failure. It has been reported to help the war type of RSD, which is quite different from civil type. In the war type, the soldier is a young teenager who responds favorably to treatment, regardless of the mode of treatment. The war time RSD is due to high velocity damage to the nerves in the proximal parts of the extremities and sympathectomy, even in these cases, has a high rate of failure in the long run. The civil type of RSD is due to a small damage of the sympathetic nerves in the central or peripheral nervous system.
If the patient lives longer than five years, the rate of failure from sympathectomy is over 80%. The scar of the surgical procedure becomes a new source of RSD. Removal of a part of sympathetic ganglia does not prevent spread of the disease in the areas of the body where the sympathetic nerves have been removed. This is due to the fact that the adjacent sympathetic nerves eventually compensate for the lack of sympathetic function due to surgery.
Insertion of epidural spinal stimulators has been quite vogues. In our comparison of 41 RSD patients treated with spinal stimulators vs. 40 non-RSD chronic pain patients who received the same treatment, the RSD group of patients had only maximum three and one half to four months relief of pain. Afterwards, the stimulator acted as a foreign body and became a new source of RSD. The reason may be due to the fact that the stimulators are digital in nature with predicted rhythmic stimulation, whereas the pain of RSD is practically constant and analog (variable) in nature.
No single physician is smart and potent enough to treat RSD. Successful treatment requires a teamwork of physical medicine, anesthesiology, and neuropharmacology physicians. The keys to successful treatment are early diagnosis, early mobilization and extensive physical therapy, and early detoxification of the patient from addicting narcotics, alcohol and addicting tranquilizers.
The anesthesiologist should interrupt the sympathetic hyperactivity by doing repetitive, successive (six) nerve blocks, combined in the same day with physical therapy and exercise. Discontinuation of ice and all other assistive devices, such as wheelchair, brace, cast, walker, etc., is essential.
The addicting drugs should be replaced with the treatment of choice for chronic pain in the form of newer-generation antidepressants, Paxil, Zoloft, and Trazodone, which are not trycyclic antidepressants. Trazodone is the treatment of choice to replace the tranquilizers and sleeping pills. It provides normal sleep, as well as prevention of chronic pain. The patient can be detoxified quickly and easily by discontinuation of the narcotics and replacement with nonaddicting ones, such as Stadol. The use of muscle relaxant, Baclofen, which selectively works on the spinal cord, counteracts the spasm, clumsiness and tremor.
In severe brain or spinal cord injuries that result in severe crippling spasticity, the infusion pump can be very effective in the treatment of spasticity. Unfortunately, not enough infusion pumps are being used for treatment of severe head and spinal cord injuries. With the use of Baclofen in the pump, such victims of severe crippling spasticity can become mobilized and can be spared from life-threatening inactivity and bed sores.
The infusion pump has been used for treatment of severe pain. In our studies of over 400 cases of advanced RSD, over three dozen patients have been treated with infusion pump, with close to 90% success rate. Through the pump, a drip irrigation form of pain medication is introduced to the spinal fluid. The pain medication given in one month is equivalent to the amount of medication given in two to three days by mouth or by IM injection.
Infusion pump should not be mistaken with other forms of narcotic administration. The infusion pump is totally different and practically opposite to administration of narcotics in the muscle (IM), IV, by skin patch, or simply in the epidural space.
The intrathecal infusion pump (administration of the medication directly to the spinal fluid that surrounds the brain and spinal cord), provides direct access to the brain and spinal cord bypassing liver, kidney and other organs. As a result, the patient requires only 1/20 monthly dose of the narcotic to provide complete relief of pain. In addition, when the pain is optimally achieved by use of as little as 1 to 7 mg a day (usually 3mg a day) of Morphine sulfate, if the patient for other reasons has pain (such as drinking alcohol or simultaneously taking other addicting narcotics by mouth), increasing the dosage of Morphine in the spinal fluid over and above 9mg per day, causes recurrence of severe pain. This is because the system is so flooded by such a strong dose of narcotics that the brain does not form its own endorphines, and the large doses of Morphine in the pump only causes drowsiness, causes the patient respiratory trouble, but does not completely control the pain.
The above phenomenon emphasizes the importance of optimal small dose of narcotic infusion in the spinal fluid which is obviously non-addicting. When distress is violated by increasing the dosage of medicine in the pump, then it becomes like any other form of addicting narcotic administration. The patient develops severe pain due to the fact that the brain cannot form its own endorphines. If the brain manufactures its own endorphine in the face of large doses of narcotic applied in the spinal fluid, then the patient faces the risk of dying from arrest of respiration. So it becomes obvious that the infusion pump is not just another form of giving addicting medications. It works because a very small amount (usually 1/20 to 1/30 dose) of pain medication is given in the form of drip irrigation directly in the spinal fluid with complete control of pain and complete relief of symptoms and signs of RSD.
The use of proper diet, with avoidance of chocolate (phenyletholamine), hot dog, liver and sausage, and alcohol is essential in management of RSD.
1. Merskey H, Bogduk N.: Classification of Chronic Pain: Descriptions of Chronic Pain Syndromes and Definitions of Pain Terms. Second Edition. Task Force on Taxonomy of the International Association for the Study of Pain. Merskey H, Bogduk N, Editors. IASP Press. Seattle, WA 1994.
2.Benarroch EE: The central autonomic network: functional organization, dysfunction, and perspective. Mayo Clin Proc 68:988-1001 1993.
3. Schwartzman RJ, Kerrigan J: The movement disorder of reflex sympathetic dystrophy. Neurology 40:57-61 1990.
4. Yokota T, Furukawa T, Tsukagoshi H: Motor paresis improved by sympathetic block a motor form of reflex sympathetic dystrophy? Arch Neurol 46: 683-687 1989.
5.Lynch ME: Psychological aspects of reflex sympathetic dystrophy : a review of the adult and pediatric literature. Pain 49:337-47 1992.
6. Poplawski ZJ, Wiley AM, Murray JF: Post traumatic dystrophy of the extremities. J Bone Joint Surg [Am] 65:642-655, 1983.
7. Appenzeller O: The Autonomic Nervous System: An introduction to basic and clinical concepts, 4th rev, Elsevier 1990.
H. Hooshmand, M.D.
where i found this info. http://www.rsdrx.com/rsdpuz4.0/puz_1.htm
T cells belong to a group of white blood cells known as lymphocytes, and play a central role in cell-mediated immunity. They can be distinguished from other lymphocyte types, such as B cells and natural killer cells by the presence of a special receptor on their cell surface called T cell receptors (TCR). The abbreviation T, in T cell, stands for thymus, since this is the principal organ responsible for the T cell's maturation. Several different subsets of T cells have been discovered, each with a distinct function.
Abdominal Compartment Syndrome
ACS is a condition that elevates intra-abdominal pressure (IAP), adversely affects end-organ physiology, and disrupts patient homeostasis. ACS was described as early as the 1800s; however, only in the last 10-15 years has ACS been consistently recognized in the surgical and medical patient population. The reported incidence of ACS is 10-15%, and, if left untreated, it is uniformly fatal. With diagnosis and treatment, the mortality rate is 46-66%.
ACS is most often encountered during the early postoperative course and commonly discovered in patients who have undergone damage-control celiotomy with primary fascial closure and intra-abdominal packing for coagulopathy.
ACS may be found in people with the following conditions:
Massive ascites/massive intraperitoneal hemorrhage
Ruptured abdominal aortic aneurysm
The aforementioned conditions may lead to decreased blood flow to the abdominal wall and organs. This derangement of cellular perfusion initiates cytokine release, destabilizing cell membranes and ultimately leading to cellular edema and cell death if not reversed. This process is clinically manifested by organ swelling, leading to secondary pressure effects on the respiratory, cardiovascular, and central nervous system when the IAP rises above a critical level.
Additional causes of IAP include the following:
Free intraperitoneal blood
Capillary leak syndrome
Mesenteric venous ligation/thrombosis
Positive pressure ventilation/positive end expiratory pressure
Application of military antishock garment trousers
The aforementioned conditions either directly or indirectly increase IAP in patients who are critically ill with ACS.
Elevated IAP results in elevated intrathoracic pressure, leading to elevated central venous pressure and causing an increase in intracerebral pressure. The Monroe-Kellie doctrine states that this increase in intracranial blood volume results in elevation of intracranial pressure. During resuscitation and vascular volume expansion, intracerebral pressure and cerebral perfusion pressure may increase transiently; however, these pressures will ultimately fall if abdominal pressure continues to increase. Due to a concomitant decrease in caval venous return, this will ultimately cause a fall in cardiac output that will negatively impact intracerebral perfusion pressure.
This fall in ICP may be transient as well if intrathoracic pressure increases due to increased IAP. This can cause increased intracerebral pressure due to increased internal jugular/superior caval venous pressure.
In a porcine model, Bloomfield et al have demonstrated significant effects of elevated IAP upon the central nervous system (CNS); elevated IAP resulted in increased intracranial pressure (ICP) and decreased cerebral perfusion pressure (CPP).1 The mechanism is a functional obstruction of jugular venous drainage due to the elevated pleural pressures and CVP. As previously mentioned, the increase in intracranial blood volume results in elevation of the ICP (the Monroe-Kellie doctrine). Abdominal decompression has resulted in a return toward baseline for ICP and an improvement in the CPP. Head injury and concomitant abdominal injury is a frequently encountered clinical scenario. This observation (confirmed clinically) is important. Decompressive celiotomy in patients such as these has resulted in a dramatic reduction in ICP. Abdominal decompression in these patients has resulted in a return toward baseline for ICP and an improvement in CPP.
Increased IAP can cause the rupture of retinal capillaries, resulting in the sudden onset of decreased central vision (Valsalva retinopathy). Valsalva retinopathy has been described in a number of settings in which a sudden increase in IAP or intrathoracic pressure has occurred. The retinal hemorrhage usually resolves within days to months, and no specific treatment is necessary. If a patient with ACS develops visual changes, Valsalva retinopathy should be considered and an appropriate ophthalmic examination should be performed.
Increased IAP may cause the following problems:
Compression of splanchnic capacitance vessels (When IAP is at least or between 10-15 mm Hg, compression of splanchnic capacitance vessels may occur, causing temporary auto transfusion [approximately 250-500 mL].)
Decreased cardiac output
Increased heart rate
Unchanged mean arterial pressure
Artificial elevation of capillary wedge pressures and central venous pressure
An increase of IAP to greater than 15 mm Hg results in the following:
Increased systemic vascular resistance
Decreased venous return
Decreased stroke volume
Decreased cardiac output
ACS may lead to pulmonary complications.
Diaphragm is forced cephalad.
Chest wall expansion is restricted.
Dynamic and static compliance decrease.
Peak and plateau pressures increase.
Physiologic dead space and intrapulmonary shunting increase.
Combined respiratory/metabolic acidosis is a common finding.
ACS can lead to acute renal failure.
Oliguria occurs when IAP is greater than 20 mm Hg.
Anuria occurs when IAP is greater than 30 mm Hg.
Increased IAP causes the following:
Increased renal parenchymal pressure
Direct pressure on renal veins
Shunting of blood from renal cortex to the medulla
Decreased renal blood flow/glomerular filtration rate
Ureteral obstruction does not occur with increased IAP.
Increased IAP up-regulates the juxtaglomerular apparatus, causing the following:
Rennin, angiotensin (I and II)
Abdominal Wall/Viscera Changes
Increased IAP results in the following:
Markedly reduced blood flow to the abdominal wall (IAP >40 mm Hg = blood flow 20% of normal. IAP of 30-40 mm Hg causes blood flow in celiac, hepatic, and mesenteric arteries and in portal and mesenteric veins.)
Decreased perfusion of every intra-abdominal organ, except the adrenal gland
Severely decreased splanchnic flow with concomitant decreased cardiac output
Ischemia in the gastric, duodenal, and intestinal mucosa
Monitoring and Measuring IAP
The most direct and accurate measurements of IAP are via a cannula placed percutaneously into the peritoneum.
Indirect IAP is monitored through transfemoraly placed inferior-caval venous lines, nasogastric tubes, rectal tubes, and, most commonly, Foley catheters. The most accurate and simple way to determine the IAP is indirectly by measurement of the bladder pressure using a Foley catheter. The bladder pressure is essentially equivalent to the IAP.
To measure the bladder pressure, the following steps must be completed:
Inject 50-100 mL of sterile saline into the Foley catheter via the aspiration port.
Cross-clamp the sterile tubing of the urinary drainage bag just distal to the culture aspiration port.
Connect the end of the drainage bag tubing to the indwelling Foley catheter.
Release the clamp just enough to allow the tubing proximal to the clamp to fill with fluid from the bladder.
Reapply the clamp.
Y-connect a pressure transducer to the drainage bag via the culture aspiration port of the tubing using a 16-gauge needle.
Determine the IAP from the transducer using the top of the symphysis pubis bone as the zero point with the patient in the supine position. (A handheld manometer connected to the Foley catheter via the column of fluid in the tubing may be used instead of a transducer.)
Release of ACS
Morris et al and other investigators have noted that the sudden release of ACS may lead to an ischemia-reperfusion injury, causing acidosis, vasodilatation, cardiac dysfunction, and cardiac arrest. Morris et al have also recommended that, prior to the release of the abdominal cavity, the patient should be preloaded with 2 L of 0.45% normal saline, 50 g/L of mannitol, and 100 mEq of sodium bicarbonate crystalloid solution.2 Vasodilators, such as dobutamine or phosphodiesterase inhibitors, may also be beneficial.
Prevention and Treatment of ACS
Leaving the abdominal incision open during surgery prevents ACS. ACS more commonly presents in the early postoperative period (24-72 h); however, it can present later than this time frame.
Temporary Abdominal Closure
The techniques of temporary abdominal closure (TAC) are varied, each with its own advantages and disadvantages. All techniques face a similar challenge: the management of the open abdomen. No prospective randomized studies are available to compare the effectiveness of these various techniques or to validate the concept of the open abdomen protocol. However, retrospective data in the form of case and cohort studies do exist. These data consistently show that maintaining the open abdomen protocol in high-risk groups has been effective in reducing mortality in a clinical setting.
The benefits of TAC include the following:
Allows viscera to expand and prevent abdominal hypertension
Allows the patient to return to the critical care setting for further resuscitation and restoration of physiologic reserve, tissue perfusion, normothermia, correction of acid base balance, and normalization of coagulation
Allows the trauma team to further assess the patient and to define other potential life- or limb-threatening injuries
Damage-control celiotomy: The trauma surgeon must decide to convert to a limited procedure within 5 minutes of starting the operative procedure. This decision is based on the initial physiological state of the patient and a rapid initial assessment of the internal injuries. The surgeon must not wait for evidence of metabolic failure to manifest. This decision is imperative to the patient's survival. The intent of damage-control surgery is to accomplish the following:
Avoid further injury
TAC: The trauma surgeon should be familiar with different TAC techniques, including their indications, their advantages, and their disadvantages.
Reevaluate in 24-36 hours: The trauma surgeon must maintain a low index of suspicion for delayed or occult injuries, particularly in patients with blunt polytrauma.
Spare the fascia: Repeated attempts at TAC that use the aponeurotic fascia cause recurrent direct and indirect (ischemic) tissue damage. This damage degrades the native tissue, decreasing its tensile and elastic capacity, and increases the potential for delayed incisional hernia.
Attempt definitive closure within 7-10 days: Loss of abdominal domain and lateral retraction of the recti and aponeurotic edges tend to be maximal after this time frame.
Types of Temporary Abdominal Closures
Towel Clipping the Skin Edges
One of the simplest and fastest forms of temporary closure of the abdomen is towel clipping the skin edges. Towel clips are placed 1 cm apart and 1 cm away from each side of the skin edge. Up to 30 standard perforating towel clips may be required to close an incision. The incision may then be covered with an adherent plastic drape (eg, Vi-Drape, Steri-Drape). Covering the incision decreases manipulation of the towel clips while transferring the patient. This technique may be used in the rapid temporary closure of thoracic or groin incisions in patients with trauma injuries who are in unstable condition and in patients undergoing general surgery.
Open Packing of the Abdomen
Open packing of the abdomen, a form of TAC, has been used for more than 2 decades at the Detroit Receiving Hospital. The abdominal wall defect and the exposed viscera are covered with rayon cloth. This rayon cloth is then covered with gauze dressing. Widely spaced, retention-type sutures are placed, encompassing all layers of the abdominal wall, and tied above the gauze packing. As bowel edema diminishes, the gauze dressing is removed and the retention sutures are gradually tightened until the incision can be closed. Bender et al reported successful fascial closure in 15 of 17 patients who survived beyond the initial 24 hours.
First described by Leguit in 1982, zipper closures were popularized by Stone et al in their open abdomen approach for pancreatic abscess.
The approach using the Wittmann Patch (STARSURGICAL, Inc, Burlington, Wis) was first reported by Teichman et al, Wittmann et al, and Aprahamian et al.As bowel edema resolves, the excess Velcro-biocompatible patch material is removed and the fascial edges are approximated. Tension closure is accomplished by the adherence of the overlapping Velcro-like sheets.
The major advantage of this approach is the ease of access for repeated surgical interventions and the capacity to apply tension to the midline fascia, which helps prevent lateral retraction of the aponeurotic edges, allowing for definitive delayed primary closure in most cases .
Synthetic Mesh Closure
The polytetrafluoroethylene (PTFE) 2-mm biocompatible prosthetic abdominal wall graft is strong and watertight and creates a bed for granulation tissue, which may be covered with a split-thickness skin graft when the prosthesis is removed. PTFE is expensive, and similar outcomes may be achieved with less costly absorbable mesh or silastic (silo) dressing changes.
Marlex Mesh (Polypropylene)
Several authors have reported the use of marlex mesh in the setting of a contaminated wound (eg, fasciitis, intra-abdominal sepsis). Healing has been reported, even in wounds where frank purulent discharge is present. Although short-term successes have occurred, numerous long-term complications have been reported with marlex mesh. These complications include increased incidence of postoperative wound sepsis, increased incidence of enteric fistulas, and significant decreased survivability of split-thickness skin grafts. The experience recorded by Voyles et al, Stone et al, and Jones et al strongly suggests that permanent rigid-type prosthetic mesh should not be inserted in the setting of abdominal wall defects with associated contamination from the gastrointestinal tract secondary to trauma, intra-abdominal sepsis, or necrotizing infections involving the abdominal wall.
Synthetic absorbable mesh has been used extensively in TACs. Polyglactin (Vicryl) and polyglycolic acid (Dexon) have been in the surgical armamentarium for approximately 25 years. This type of prosthetic mesh implant has been used in the repair of traumatic liver, splenic, and renal injuries and in pelvic floor repair in the setting of abdominal peroneal resection of the rectum. Although early burst strength (at 8 wk) is comparable to that of permanent mesh, as the mesh is absorbed (at 10-12 wk), hernias inevitably develop in most patients.
As described by Bender et al, the mesh is applied loosely over the abdominal contents and then covered with fine mesh gauze packing, maintaining the bowel below the absorbable mesh and within the abdominal contents. This may decrease bowel wall distention, thinning, and subsequent desiccation, which may decrease the incidence of enterocutaneous fistula.
The choice between the use of either Vicryl mesh or Dexon mesh is primarily determined by the surgeon's preference. However, Brasel et al have reported some advantage in the use of Dexon mesh. This mesh has wider interstices that Brasel et al believe may allow for more efficient drainage of intra-abdominal fluid and, thus, may decrease potential delayed complications (eg, abdominal distention, ileus, abscess).
Silastic (Plastic) Closures
A presterilized (gas), soft 3-L plastic cystoscopy fluid irrigation bag is cut and shaped to cover the abdominal incision and extruded viscera. This bag is either stapled or sutured to the skin edges of the wound with a standard (wide) skin stapling device or monofilament, nonabsorbable suture, thus preserving the fascia. Sterile, antibiotic-soaked towels (using Kantrex) may be applied over the silo, which is then covered with an iodine-impregnated adhesive plastic drape.
An alternative is to apply sterile towels over the silo and to secure them with a Montgomery abdominal wound binder, being careful not to create increased abdominal pressure while securing the dressing. The wound is inspected and the dressing is changed every 24 hours (or as needed). Intravenous (IV)/cystoscopy bag silos may be replaced in the ICU setting using standard sterile surgical technique and equipment. This technique is a variation of the silon (silo) closure used for the repair of gastroschisis and omphalocele. In hospitals in Colombia, South America, IV bag closure (also known as the Bogotá Bag) has been used extensively and successfully.
Silastic closures are fast and effective temporary closure modes and have some significant cost benefits, as reported by Fernandez, Norwood, and Roettger .
Methods of Definitive Abdominal Wall Reconstruction
Primary Delayed Fascial Closure
Primary delayed facial closure (between 5-10 d) may be attempted if the abdominal cavity can be closed without significant elevation of IAP. A high index of suspicion for recurrent ACS must be maintained. Elevated peak airway pressure or plateau pressures (>30 mm Hg), increased urinary catheter bladder pressures (>25 mm Hg), and accompanying deteriorating clinical parameters (eg, abdominal distension, decreased urine output) should prompt a careful reevaluation of the patient and consideration for decompressive celiotomy.
Fabian et al have published their experience with their eponymous protocol.13 The patients are subsequently brought back for definitive reconstruction, usually within 6-12 months.
Stage I - Prosthesis placement (polyglactin 910 [Vicryl] or polyglycolic acid [Dexon])
Stage II - Mesh removal or allowance of granulation tissue to cover the mesh
Stage III - Split-thickness skin graft applied when granulation tissue is adequate
Stage IV - Definitive abdominal wall reconstruction (6 mo to 1 y)
Closure of Abdominal Wall (Creation of Ventral Hernia)
The Sure-Closure Skin Stretching System is a patented, disposable, molded device made of stainless steel and plastic parts and used to provide sufficient skin in advance of closures for fasciotomies and trauma repairs of various types, including closure of the open abdomen. Use of the Sure-Closure Skin Stretching System can minimize the need for more extensive secondary wound closure techniques. The device is attached intraoperatively by first inserting needles parallel to the wound edges. These needles serve to distribute tension forces over the length of the incision. Gauges on the device monitor the applied forces, ensuring a safe and permanent skin stretching. The device allows the surgeon to take advantage of the inherent viscoelastic properties of the skin by mechanically stretching the skin and allowing it to relax under tension; the surgeon then has sufficient skin to affect a suitable closure.
The device comes in sizes of 50 mm and 75 mm. The 50-mm device is designed for smaller skin defects with uneven surfaces, while the 75-mm device is designed for larger skin defects with relatively flat, even surfaces.
The Sure-Closure Skin Stretching System was first described by Hirshowitz et al and has been used extensively in the plastic, orthopedic, cancer, general surgical, and trauma patient population.
In a comparative clinical study of the Sure-Closure Skin Stretching System with more conventional wound closure techniques, Narayanan et al found that, in their study cohort, they were able to demonstrate a cost reduction trend . In their cost analysis, they included the costs of the following: operating room time, operating room supplies, anesthesia, monitoring, recovery room time, wound care supplies, pharmacy charges, and hospital room and board. They also noted above average healing of the wounds at 1 month and 3 months, with better cosmesis than comparable conventionally closed wounds. This experience has been confirmed by other reported clinical studies.
Using the Sure-Closure device potentially offers the following:
Relatively fast closure, usually in 30-60 minutes, with healthy skin and subcutaneous tissue
Cosmetically superior appearance when compared with that of split-thickness skin grafts
Decreased need for future scar reduction
Shorter hospital stay
Reduced overall cost
By using the Sure-Closure Skin Stretching System, the surgeon is able to close most cases of skin defects that would more commonly require secondary wound closure techniques, such as myocutaneous flaps or skin grafts.
Sure-Closure System Application
The Sure-Closure device accomplishes skin stretching by using 2 intradermal needles in conjunction with a tension rod that connects 2 self-aligning U-arms. The device contains a graduated tension indicator that registers after 1 kg of force is applied. The Sure-Closure system has a built-in safety clutch mechanism that prevents excessive tension by limiting the total force to 3 kg. The device is used in the setting of the following:
Skin cancer resections
Closure of traumatic wounds (including open abdomen)
Delayed primary closures
Vacuum Assisted Closure®
Fascial Vacuum Assisted Closure® (V.A.C.®) therapy (Kinetic Concepts, Inc, San Antonio, Tex) is a relatively new concept in the management of the open abdomen that allows for fascial closure as long as 1 month after the initial laparotomy. This avoids the need and attendant operative risks incurred with abdominal wall reconstruction in the future.
The main functional component of V.A.C.® is the use of a nonadherent, polyethylene sheet to cover the exposed viscera and the placement of a polyurethane sponge under controlled negative pressure. The polyethylene sheet helps prevent visceral-abdominal wall adhesions that inhibit movement of the abdominal wall. The polyurethane sponge, when placed under negative pressure (suction), provides the countertraction required to inhibit abdominal wall retraction and creates an environment where approximation of the abdominal wall may occur.
Miller et al reported excellent results in the use of this system. They reviewed 646 patients with trauma injuries who underwent laparotomies, of which 148 patients required management of an open abdomen over a 5-year period (1996-2001). Of these 148 patients, 85 survived to closure. Patients treated with the open abdomen technique who were unable to undergo fascial closure by early postoperative period (POD 9) were treated with a fascial V.A.C.® technique. Patients treated with planned hernia (HERNIA group, Fabian protocol) were compared with those undergoing fascial closure 9 or more days after the initial laparotomy (LATE group). All of the patients in the LATE group underwent fascial V.A.C.® therapy.
Fifty-nine patients underwent fascial closure, 37 patients before postoperative day 9 and 22 patients on or after postoperative day 9. Mean time to fascial closure in the LATE group was 21 days (range, 9-49 d). Injury severity scores, admissions base deficit, number of fistulas, number of operations, and mortality were similar between the HERNIA group and the LATE group. The incidence of abscess, wound dehiscence, and fistula in the LATE group and the HERNIA group were nearly identical. In both groups, the differences were not significant with respect to time in the intensive care unit, total hospital stay, incidence of acute respiratory distress syndrome, multiple organ failure, and death. The fascial closure rate (71.08%) reported compares favorably with the results previously published by Barker et al in their large review of fascial closure rates using the standard vacuum pack technique; the fascial closure rate in the previous study was 70%.Case Study
In the following case study, Dennis E. Weiland, MD, and John M. Stein, MD (Scottsdale Health Care-Osborn, Scottsdale, Arizona), illustrate the abdominal V.A.C.® capabilities.
A 25-year-old man was admitted with 2 gunshot wounds to the abdomen. Repair of liver laceration with abdominal washout was accomplished . Postoperatively, the patient developed severe abdominal distention and respiratory distress. He required a decompression laparotomy for ACS. He was placed on suction drainage for 2 days. V.A.C.® therapy was initiated on day 3. The wound was closed by delayed primary closure 12 days after the initial decompression laparotomy.
The diagnosis was ACS secondary to a gunshot wound to the abdomen.
The prognosis was excellent once the skin was closed over the fascia.
V.A.C.® therapy was as follows:
8/25/01 - Laparotomy, cholecystectomy, and repair of liver laceration with drainage
8/28/01 - Laparotomy, abdominal decompression with drainage tubes and plastic abdominal dressings, and release of abdominal adhesions
8/30/01 - Removal of decompressive dressings and application of V.A.C.® therapy
9/05/01 - Removal of V.A.C.® system, partial closure of the wound, and reapplication of V.A.C.® therapy
9/09/01 - Removal of V.A.C.® system and delayed primary closure of the abdominal wound
After discharge, the patient continued to have follow-up visits in the wound clinic.
The open skin over the fascia will be closed either by contraction or by secondary closure. The original wound measured 30 cm X 15 cm at the time of the decompression laparotomy. The wound now measures 20 cm X 3-4 cm.
ACS and Abdominal Hypertension Not Present, Patient Requires Reoperation
Among the trauma patient population, the more common indications for reoperations include bleeding, infection, presence of ACS, and reassessment of the abdomen for bowel viability or possible missed or delayed injury. The management of the severely contaminated abdomen, severe peritonitis, and intra-abdominal sepsis by an open approach has been discussed in the literature. First proposed by Steinberg, the intraperitoneal silo approach has been applied in several settings and surgical patient groups.
Fernandez et al described a technique that evolved from their experience with the use of the silastic silo closure for patients with ACS.They used the extraperitoneal silo in the intraperitoneal (IP) position in selected patients who did not have ACS and whose injuries would benefit from a second look procedure. Their patient population was summarized The approximate total hospital cost of the silo was $15.94 with an approximate patient cost of $57 Fernandez et al reported one death in the group (patient 3). They also reported one IP silo failure (patient 1) that developed a small bowel dehiscence. This patient underwent IP silo replacement in the ICU.Placement of IP Silo
The technique of IP silo placement is simple and straightforward.
A presterilized (gas), soft, 3-L, plastic, cystoscopy fluid irrigation bag is commonly used.
A small epigastric slit incision is made at the cephalad portion of the silo. This incision allows placement of the IP silo around the falciform ligament and round ligament of the liver (if still present after initial damage-control celiotomy) without causing injury.
The inferior corners and lateral edges of the silo are gently tucked into the right and left lower abdominal quadrants and the lateral pericolic gutters, respectively.
Finally, the skin is approximated with skin clips, and a sterile dressing is applied.
Several techniques in the surgical armamentarium are available to affect temporary closure of the open abdomen. One of the least expensive and rapid is the gas sterilized, 3-L, plastic, cystoscopy irrigation bag. This bag is commonly available, and its application is straightforward. In the author's opinion, it is the preferred initial method of temporary closure, particularly in patients who may require multiple reoperative interventions.
Of the techniques described within this article, the Sure-Closure Skin Stretching System has the potential to obviate split-thickness skin grafting in the setting of the open abdomen, particularly if approximation of the skin can be achieved within the first 7-10 days. This Sure-Closure device facilitates the creation of a ventral hernia that may be repaired at a later date in an elective fashion.
The Wittmann Patch and the abdominal V.A.C.® are inherently designed to affect not only a temporary closure but also a permanent fascial closure in most patients. The relative cost of these devices is small in comparison to the potentially decreased associated cost and morbidity of a second, planned abdominal wall reconstructive procedure commonly required in this patient population. The Wittmann Patch and the abdominal V.A.C.® system represent major advancements in surgical theory and are a welcome addition to the extant surgical doctrine.
temporary abdominal closure, TAC, trauma damage-control celiotomy, damage control, damage-control celiotomy, damage-control surgery, damage control celiotomy, trauma damage control celiotomy, damage control surgery, abdominal compartment syndrome, ACS, intra-abdominal pressure, IAP, positive pressure ventilation, positive end expiratory pressure, intrathoracic pressure, central venous pressure, intracerebral pressure, intracranial pressure, abdominal wall, viscera, fascia, zipper closure, Wittmann Patch, synthetic mesh closure, polytetrafluoroethylene closure, marlex mesh, absorbable mesh, silastic closure, primary delayed fascial closure, Fabian protocol, Sure-Closure system, Sure-Closure Skin Stretching System, vacuum-assisted closure, VAC, vacuum-assisted fascial closure, VAFC, intraperitoneal silo, IP silo
Acidosis is an increased acidity(i.e. an increased hydrogen ion concentration). If not further qualified, it usually refers to acidity of the blood plasma.
Acidosis is said to occur when arterialpH falls below 7.35, while its counterpart (alkalosis) occurs at a pH over 7.45. Arterial blood gas analysis and other tests are required to separate the main causes.
The term acidemia describes the state of low blood pH, while acidosis is used to describe the processes leading to these states. Nevertheless, physicians sometimes use the terms interchangeably. The distinction may be relevant where a patient has factors causing both acidosis and alkalosis, where the relative severity of both determines whether the result is a high or a low pH.
The rate of cellular metabolic activity effects and, at the same time, is affected by the pH of the body fluids. In mammals, the normal pH of arterial blood lies between 7.35 and 7.50 depending on the species (e.g. healthy human-arterial blood pH varies between 7.35 and 7.45). Blood pH values compatible with life in mammals are limited to a pH range between 6.8 and 7.8. Changes in the pH of arterial blood (and therefore the extracellular fluid) outside this range result in irreversible cell damage.
where i found this info... http://en.wikipedia.org/wiki/Acidosis
Diet, Exercise, Stress and the Immune System
The immune system and its role in chronic fatigue syndrome (CFS)
The immune system is our body's protective network designed to fend off invasion by harmful substances, including bacteria, viruses, and harmful chemicals, and to act as a surveillance system against the development of cancer.
Under normal circumstances, the immune system is highly efficient, providing multiple defenses against the onslaught of outside invaders. These defenses include physical barriers (such as skin); the non-specific inflammatory response, which is brought about by changes in blood flow that bring chemical substances to the injured area; and specific immune responses, in which the body learns to recognize specific invaders and destroy them after subsequent exposures.
In many diseases, ranging from autoimmune diseases to AIDS and CFS, there is evidence of mild to severe dysfunction of the immune system. An impaired immune system weakens the body's ability to fend off infection and malignancy, but the immune system can also produce symptoms such as fever, weight loss, musculoskeletal pain and fatigue. In fact, many of the symptoms of the flu (such as achy muscles and joints, fever, and headache) are caused by the immune system's response to the infection.
Functions of the immune system suspected to be impaired in CFS include those of the B-lymphocytes (B cells) and T-lymphocytes (T cells), as well as those of the phagocytic and complement systems. B cells and T cells carry out specific immune responses. B cells, a type of white blood cell, can recognize foreign proteins (antigens) and make specific proteins (antibodies) to destroy the antigens (humoral immunity). T cells, other types of white blood cells, do not produce antibodies, but can perform a number of functions, including recognizing foreign antigens, attaching to them and destroying the invader cells (cell-mediated immunity).
The phagocytic and complement systems bring about non-specific inflammatory responses. In the phagocytic system, numerous types of white blood cells (phagocytes) engulf and digest foreign particles. The complement system is a group of proteins that become activated when they come into contact with antigen/antibody complexes, the combination of the antibody attached to the antigen. Once activated, these proteins attach to the invader and destroy it. The complement system can bring about a host of non-specific inflammatory responses.
How can I strengthen my immune system?
While it is difficult to enhance a normal functioning immune system, there are things that you can do to protect and strengthen your immune system during periods of illness or in the face of chronic disease. The three areas that are most important in protecting and bolstering the immune system are diet and nutrition, exercise, and stress reduction. Diet, nutrition, and immunity
There have been many excellent books written about the relationship between diet, nutrition, and immunity. (Please refer to the reading list below.) There are two major changes you can make in your diet to help your immune system. First, you can enrich your diet with antioxidants and, second, you can make sure you are getting enough nutrients and micronutrients. Antioxidants
Antioxidants are vitamins and minerals, found in foods and available as supplements, that remove harmful oxidants from the bloodstream. Oxidants, also known as free radicals, are the toxic byproducts our bodies make when we turn food into energy. They are also byproducts of cigarette smoke, pollution, sunlight exposure, and other environmental factors. Free radicals are capable of damaging DNA and suppressing the body's immune system.
Free radicals also play an important role in the development of many human diseases. In fact, there are several journals now dedicated to their study and investigation. Nearly all types of cancers have been related to diets that are poor in antioxidants. Data from some research also suggest that a diet high in antioxidants might also protect against cancer.
Heart disease and atherosclerosis (hardening of the arteries) are also brought about, in part, by free radicals. Certain diseases of the central nervous system — such as dementia and some forms of kidney, gastrointestinal, and skin disease — also involve free radicals. You cannot prevent these diseases simply by taking antioxidants. You can, however, ensure that you are doing everything possible to lessen their effects. Most importantly, you should eliminate environmental factors that promote the production of free radicals. Nutrients and micronutrients
Marginal nutrient deficiencies in the diet can also weaken the immune system. Marginal deficiency is a state of gradual vitamin loss that can lead to a general lack of well being and impairment of certain biochemical reactions. Marginal deficiencies of micronutrients (nutrients required only in a small amount) do not cause obvious symptoms of disease, but they can affect your mental abilities, your coping abilities, and your body's ability to resist disease and infection. They might also slow your recovery from surgery.
Marginal nutrient deficiencies are very common in both younger and older individuals. The typical American diet is often deficient in a variety of nutrients including calcium, iron, vitamin A, and vitamin C. Furthermore, the recommended daily allowance (RDA) for many nutrients might be well below what is needed to optimally protect the immune system. For this reason, vitamin and mineral supplements are used to protect us against micronutrient deficiencies. Foods
You can further modify your diet by eating less saturated fat and animal protein (particularly red meat), by limiting dairy products (particularly those with fat), by modifying your use of oils and fats, and by eating more fresh fruits, vegetables, and whole grains.
Take a minute to examine your diet. How many times a week do you eat fried foods or red meat? What types of oils do you use in your cooking? Do these oils include cooking oil as well as butter and margarine? What types of garnishes and sauces do you use? Do they contain egg yokes or oils? What types of dairy are you consuming? If you drink milk, which is good for you, is it anything less than skim or 1%? Do the yogurts and cheeses you eat contain a lot of fat?
Try eliminating red meat from your diet or, if necessary, eat it no more than once every 10 days. Also eliminate or reduce your intake of fried meats. Try to replace the meats in your diet with servings of fish, particularly oily fish such as salmon. Salmon contains a rich form of an oil known as omega-3 fatty acids, which has natural anti-inflammatory properties.
Use only olive oil in your cooking. Olive oil is rich in mono-saturated fats. All other oils, with the possible exception of canola oil, have unfavorable types of fats for the immune system. Avoid excessive use of margarine. Though most margarines are unsaturated in their fat content they are artificially prepared and the long-term effects of their use are not known. Try to minimize the use of all fats, but wherever possible use olive oil in cooking and for dressing salads.
Eat more fruits and vegetables. Green leafy vegetables such as broccoli are very rich in antioxidants. Add several servings a week to your diet. Do not overcook them and think of creative ways to prepare them. Add more servings of other fruits and vegetables to your diet, as they are rich sources of antioxidants as well.
Add fiber to your diet. Fiber can be found in many types of whole grains. If you are going to add rice, which is healthy, try to add brown rice. Brans and cereals are also helpful, but avoid those with any form of artificial sugar.
Drink plenty of water.
If you follow these guidelines, you will move your diet in the proper direction toward protecting your immune system. As an added benefit, you will be following a diet that is also good for your cardiovascular system. (These recommendations are similar those of the STEP II diet promoted by the American Heart Association.)
Ideally, fat should account for less than 30 percent of your total calories. Less than 7 percent of your total calories should come from saturated fats. In addition, you should try to eat less than 200 milligrams (mg) of cholesterol per day.
Much has been said about nutritional supplements and their ability to enhance or protect health. While there is a lot of debate in the medical literature, and many doctors do not discuss their use with their patients, some CFS specialists believe that nutrients can provide a measure of protection for the immune system. No matter how well you design your diet for nutrition, you can still augment it with supplemental antioxidants. Some of the best studied and most readily available as supplements are beta carotene, selenium, vitamin C, vitamin E, and vitamin A.
Supplementing your diet with a balanced multivitamin is essential. To do this, you should add beta carotene in a dose of 25,000 international units (IU) twice per day. In addition, vitamin C in doses of at least 500 to 1000 mg a day is recommended. Why these vitamins? Beta carotene is one of the most potent nutrients and can protect the body from oxidative stress. Populations that have diets high in beta carotene have a lower incidence of certain forms of cancer.
Several studies have shown that beta carotene supplements can do little to reduce cancers in people who smoke cigarettes. This fact should not be surprising. Dietary modifications are made to bring back a failing immune system or to protect a healthy immune system, not to overcome overwhelming toxic effects of activities such as smoking.
Vitamin C is also an extraordinarily important antioxidant. While many studies have shown that daily ingestion of vitamin C does little to protect you from the common cold, it can reduce the severity of colds. Furthermore, there are several controlled studies performed in populations of people working under heavy stress that have shown a profound protective effect of vitamin C in terms of common colds and pneumonia.
Other nutrients that might be helpful include selenium in doses of 200 micrograms (mcg) per day and vitamin E in doses of 400 IU per day. Many over-the-counter vitamins with similar doses are available. There is no difference between natural vitamins and synthetic vitamins.
Exercise and immunity
Even more so than nutrition, exercise has the capacity to protect and even enhance the immune response. Experimental studies have shown that a regular exercise program of brisk walking can bolster many defenses of the immune system, including the antibody response and the natural killer (T cell) response.
Fortunately, the intensity and duration of exercise needed to support the immune system is less than that needed to provide the best cardiovascular training. Thus, even relatively low levels of aerobic exercise can protect your immune system. Twenty to 30 minutes of brisk walking five days per week is an ideal training program for maintaining a healthy immune response.
Exercise can also improve your mental wellness. Regular aerobic exercise can help relieve mild to moderate degrees of depression and anxiety. People who exercise also have less loneliness and anger, and are better able to control their own destiny. It is not clear whether exercise boosts the immune system directly or works through a link with the brain and nervous system.
Stress and immunity
The final component for fine-tuning your immune system is reducing the stress in your life by achieving a higher level of spiritual harmony. Altered mood states such as depression, anxiety, and panic are harmful to the body in many ways. Secondary symptoms such as fatigue, difficulties with memory and concentration, aches and pains, and problems with sleep are common in people with mood disorders. Mood disorders also harm the immune system.
There are many techniques you can use to reduce stress and anxiety in your life. Guided imagery involves focusing on mental images, such as a serene setting. You can also try yoga or tai chi, which combine both mental and physical exercise, and can help heal the mind and the body. You might consider using biofeedback, a process in which you monitor certain functions of the body, such as blood pressure, and learn to alter these functions through relaxation. Other simple techniques include breathing exercises or taking a walk and appreciating the beauty in the world around you.
For people who have severe mood disorders, antidepressants and other psychotropic medicines, as well as counseling, are essential.
Putting it all together
Diseases such as chronic fatigue syndrome, fibromyalgia, and many other poorly understood illnesses should no longer be viewed as disorders of either the mind or the body. The mind and body act as one unit and thus we must approach them together.
To maintain the strongest immune system possible, you must have a nutritious diet, get regular exercise, and reduce stress in your life. You must attend to all three of these areas to achieve your optimum health.
Some people eat a nutritious diet and exercise regularly, but are so keyed up in their lives that their stress levels overcome all of the success they achieve in the first two areas. Other people might have successfully modified their mental and spiritual state but are eating unhealthy diets or are sedentary. Others might make significant advances in all three areas, but are doing foolish and harmful things to their bodies, such as smoking or using excessive alcohol, which take away from their achievements.
Dr. Andrew Weil, noted author and director of the program in integrative medicine at the University of Arizona, has written extensively about the body's ability to heal itself. Many health care providers have witnessed people overcome complex medical illnesses without the assistance of medicine. Though medicines are vital for overcoming many acute illnesses, they might be less important in overcoming chronic diseases.
You can take advantage of the body's inner ability to heal by eating well, exercising regularly, and striving for spiritual well-being. Eliminate other negative factors such as drugs, alcohol, tobacco, and other insults to the your body. Only you can put it all together and it cannot be achieved overnight. There is no better time to start than now.where i found this info... http://my.clevelandclinic.org/disorders/chronic_fatigue_syndrome/hic_Diet_Exercise_Stress_and_the_Immune_System.aspx
The third diagnostic principle is neuropathic pain, including CRPS I, is complicated by inflammation in varying degrees. This inflammation was first reported by Mitchell (1864)as "shiny skin" and, later on, by Sudeck (1942). The neurogenic inflammation results in bullbous lesions, sterile abscess, edema and impingement of the nerves at the wrist, elbow, thoracic outlet and ankle areas - resulting in the disease being mistaken for conditions such as carpal tunnel, thoracic outlet (TOS), tarsal tunnel syndromes, and myofascial syndrome. The well-intended surgical procedure to relieve such entrapment neuropathies may in turn aggravate the inflammation by virtue of surgical trauma becoming a new source of neuropathic pain.
The inflammation is another manifestation of dysfunctional sympathetic system. The sympathetic system is responsible for immune system regulation (Arnason, 1993). As a result, the patient may develop bouts of unexplained fever, edema, attacks of subcutaneous bleeding, neurodermatitis, bulbous lesions , pelvic inflammatory disease (PID), or interstitial cystitis. Inflammation may cause development of subcutaneous skin nodules, pulmonary nodules, laryngitis, difficulty with phonation, attacks of hacking cough and hematemesis. In late stages it can cause elephantiasis, subcutaneous bleeding, bullous deep ulcerative lesions involving the skin as a manifestation of disturbance of the immune system. It can be mistaken for infection, osteomyelitis, dermatitis, and cystitis. Treatment with antibiotics provides no relief.
The inflammation is usually intermittent, and is not consistently present. Only a careful history taking can document previous attacks of inflammation.
where i found this info... http://rsdrx.com/CRPSABSTRACT.htm
Hematemesis or haematemesis (see American and British spelling differences) is the vomiting of blood. The source is generally the upper gastrointestinal tract. Patients can easily confuse it with hemoptysis (coughing up blood), although the former is more common.
Signs of the onset of hematemesis may include:
Any esophago-gastric symptoms, such as nausea or vomiting
Brown or black vomit
Vomit that looks like coffee grounds
Dark colored, tar like stools (a condition known as melena)
Causes can be:
Ingested blood (for example, swallowed after a nosebleed)
Vascular malfunctions of the gastrointestinal tract
History of Smoking
Minimal blood loss
If this is not the case, the patient is generally administered a proton pump inhibitor (e.g. omeprazole), given blood transfusions (if the level of hemoglobin is extremely low, that is less than 8.0 g/dL or 4.5-5.0 mmol/L), and kept nil per os(nil by mouth) until endoscopy can be arranged. Adequate venous access (large-bore cannulas or a central venous catheter) is generally obtained in case the patient suffers a further bleed and becomes unstable.
Significant blood loss
In a "hemodynamically significant" case of hematemesis, that is hypovolemic shock, resuscitation is an immediate priority to prevent cardiac arrest. Fluids and/or blood is administered, preferably by central venous catheter, and the patient is prepared for emergency endoscopy, which is typically done in theatres. Surgical opinion is usually sought in case the source of bleeding cannot be identified endoscopically, and laparotomy is necessary. ( more can be read at this web site )This page was last modified on 23 March 2009where i found this info... http://en.wikipedia.org/wiki/Hematemesis
Causes and symptomsMany different agents cause abscesses. The most common are the pus-forming (pyogenic) bacteria like Staphylococcus aureus, which is nearly always the cause of abscesses under the skin. Abscesses near the large bowel, particularly around the anus, may be caused by any of the numerous bacteria found within the large bowel. Brain abscesses and liver abscesses can be caused by any organism that can travel there through the circulation. Bacteria, amoeba, and certain fungi can travel in this fashion. Abscesses in other parts of the body are caused by organisms that normally inhabit nearby structures or that infect them. Some common causes of specific abscesses are:
skin abscesses by normal skin flora
dental and throat abscesses by mouth flora
lung abscesses by normal airway flora, pneumonia germs, or tuberculosis
abdominal and anal abscesses by normal bowel flora
Retropharyngeal, parapharyngeal, peritonsillar abscess. As a result of throat infections like strep throat and tonsillitis, bacteria can invade the deeper tissues of the throat and cause an abscess. These abscesses can compromise swallowing and even breathingDiagnosis
The common findings of inflammation--heat, redness, swelling, and pain--easily identify superficial abscesses. Abscesses in other places may produce only generalized symptoms such as fever and discomfort. If the patient's symptoms and physical examination do not help, a physician may have to resort to a battery of tests to locate the site of an abscess, but usually something in the initial evaluation directs the search. Recent or chronic disease in an organ suggests it may be the site of an abscess. Dysfunction of an organ or system--for instance, seizures or altered bowel function--may provide the clue. Pain and tenderness on physical examination are common findings. Sometimes a deep abscess will eat a small channel (sinus) to the surface and begin leaking pus. A sterile abscess may cause only a painful lump deep in the buttock where a shot was given.Prognosis
Once the abscess is properly drained, the prognosis is excellent for the condition itself. The reason for the abscess (other diseases the patient has) will determine the overall outcome. If, on the other hand, the abscess ruptures into neighboring areas or permits the infectious agent to spill into the bloodstream, serious or fatal consequences are likely. Abscesses in and around the nasal sinuses, face, ears, and scalp may work their way into the brain. Abscesses within an abdominal organ such as the liver may rupture into the abdominal cavity. In either case, the result is life threatening. Blood poisoning is a term commonly used to describe an infection that has spilled into the blood stream and spread throughout the body from a localized origin. Blood poisoning, known to physicians as septicemia, is also life threatening.
Of special note, abscesses in the hand are more serious than they might appear. Due to the intricate structure and the overriding importance of the hand, any hand infection must be treated promptly and competently
The phonatory process, or voicing, occurs when air is expelled from the lungs through the glottis, creating a pressure drop across the larynx. When this drop becomes sufficiently large, the vocal folds start to oscillate. The minimum pressure drop required to achieve phonation is called the phonation threshold pressure, and for humans with normal vocal folds, it is approximately 2–3 cm H2O. The motion of the vocal folds during oscillation is mostly in the lateral direction, though there is also some superior component as well. However, there is almost no motion along the length of the vocal folds. The oscillation of the vocal folds serves to modulate the pressure and flow of the air through the larynx, and this modulated airflow is the main component of the sound of most voiced phones.
The sound that the larynx produces is a harmonic series. In other words, it consists of a fundamental tone (called the fundamental frequency, the main acoustic cue for the percept pitch) accompanied by harmonic overtones which are multiples of the fundamental frequency. According to the Source-Filter Theory, the resulting sound excites the resonance chamber that is the vocal tract to produce the individual speech sounds.
The vocal folds will not oscillate if they are not sufficiently close to one another, are not under sufficient tension or under too much tension, or if the pressure drop across the larynx is not sufficiently large. In linguistics, a phone is called voiceless if there is no phonation during its occurrence. In speech, voiceless phones are associated with vocal folds that are elongated, highly tensed, and placed laterally (abducted) when compared to vocal folds during phonation.
Fundamental frequency, the main acoustic cue for the percept pitch, can be varied through a variety of means. Large scale changes are accomplished by increasing the tension in the vocal folds through contraction of the cricothyroid muscle. Smaller changes in tension can be effected by contraction of the thyroarytenoid muscle or changes in the relative position of the thyroid and cricoid cartilages, as may occur when the larynx is lowered or raised, either volitionally or through movement of the tongue to which the larynx is attached via the hyoid bone. In addition to tension changes, fundamental frequency is also affected by the pressure drop across the larynx, which is mostly affected by the pressure in the lungs, and will also vary with the distance between the vocal folds. Variation in fundamental frequency is used linguistically to produce intonation and tone.
There are currently two main theories as to how vibration of the vocal folds is initiated: the myoelastic theory and the aerodynamic theory. These two theories are not in contention with one another and it is quite possible that both theories are true and operating simultaneously to initiate and maintain vibration. A third theory, the neurochronaxic theory, was in considerable vogue in the 1950s, but has since been largely discredited. ( This page was last modified on 21 February 2009 )
where i found this info ... http://en.wikipedia.org/wiki/Phonation
The traditional approach to the study of acid-base physiology has been the empiric approach. The main variants are the base excess approach and the bicarbonate approach. The modern quantitative approach introduced by Peter A Stewart in 1978 is now emerging as the most correct approach
The reason is that acids become negatively electric charged in basic fluids, since they donate a proton. On the other hand, bases become positively electric charged in acid fluids, since they receive a proton.
Since electric charge decrease the membrane permeability of substances, once an acid enters a basic fluid and becomes electrically charged, then it cannot escape that compartment with ease and therefore accumulates, and vice versa with bases.
where i found this info... http://en.wikipedia.org/wiki/Acid-base_physiology
When blood volume is low, the kidneys secrete renin. Renin stimulates the production of angiotensin. Angiotensin causes blood vessels to constrict resulting in increased blood pressure. Angiotensin also stimulates the secretion of the hormone aldosterone from the adrenal cortex. Aldosterone causes the tubules of the kidneys to retain sodium and water. This increases the volume of fluid in the body, which also increases blood pressure.
If the renin-angiotensin-aldosterone system is too active, blood pressure will be too high. There are many drugs which interrupt different steps in this system to lower blood pressure. These drugs are one of the main ways to control high blood pressure (hypertension), heart failure, kidney failure, and harmful effects of diabetes
Patil Jaspal et al. have shown local synthesis of Angiotensin II in neurons of sympathetic ganglia.
It is believed that Angiotensin I may have some minor activity, but angiotensin II is the major bio-active product. Angiotensin II has a variety of effects on the body:
In the kidneys, it constricts glomerular arterioles, having a greater effect on efferent arterioles than afferent. As with most other capillary beds in the body, the constriction of afferent arterioles increases the arteriolar resistance, raising systemic arterial blood pressure and decreasing the blood flow. However, the kidneys must continue to filter enough blood despite this drop in blood flow, necessitating mechanisms to keep glomerular blood pressure up. To do this, Angiotensin II constricts efferent arterioles, which forces blood to build up in the glomerulus, increasing glomerular pressure. The glomerular filtration rate (GFR) is thus maintained, and blood filtration can continue despite lowered overall kidney blood flow.
In the adrenal cortex, it acts to cause the release of aldosterone. Aldosterone acts on the tubules (e.g the distal convoluted tubules and the cortical collecting ducts) in the kidneys, causing them to reabsorb more sodium and water from the urine. Potassium is secreted into the tubules in exchange for the sodium, which is excreted. Aldosterone also acts on the central nervous system to increase an individual's appetite for salt, and to stimulate the sensation of thirst.
Release of Anti-Diuretic Hormone (ADH), also called vasopressin -- ADH is made in the hypothalamus and released from the posterior pituitary gland. As its name suggests, it also exhibits vaso-constrictive properties, but its main course of action is to stimulate reabsorption of water in the kidneys.
These effects directly act in concert to increase blood pressure.
The renin-angiotensin system is often manipulated clinically to treat high blood pressure.
Other uses of ACE
Interestingly, ACE cleaves a number of other peptides, and in this capacity is an important regulator of the kinin-kallikrein system.
Fetal renin-angiotensin system
In the fetus, the renin-angiotensin system is predominantly a sodium-losing system, as angiotensin II has little or no effect on aldosterone levels. Renin levels are high in the fetus, while angiotensin II levels are significantly lower — this is due to the limited pulmonary blood flow, preventing ACE (found predominantly in the pulmonary circulation) from having its maximum effect.
where i found this info... http://en.wikipedia.org/wiki/Renin-angiotensin_system
Please feel free to email us if you have any questions or comments at