Research Topics: Pain Examples

Describe the pathways responsible for modulation of painful stimuli in the central nervous system

Describe the pathways responsible for modulation of painful stimuli in the central nervous system Introduction             Pain is caused by threatened or actual tissue damage that stimulates nociceptive (pain sensitive) neural receptors. Pain may also be caused by damage to the transmission system itself. However, thee stark statements do not actually help us understand and actual person’s pain experience. It is like describing a sunset in terms of the physical stimulation of the retina! We do need to know about the pain receptors and their pathways to the brain. Pain Receptors             The train of events that leads to pain begins when pain receptors are stimulated by mechanical, chemical or thermal sources. Nerve receptors for pain (nociceptors) differ from the complex receptors for vision and other senses. Nociceptors are simply free nerve endings occurring in almost all type of tissue. Nociceptors react only to changes very close to them and they require a relatively high level of stimulation to be activated. However, once their threshold is exceeded they continue to actively communicate the presence of the painful stimulus (slow adaptation). Nociceptors can also become sensitized so that continues to discharge long after the stimulus is removed. Most is known about pain coming from receptors in the skin. It is assumed that pain receptors in deeper tissue are similar, but they may operate differently. Pain Experience             Once nociceptors are stimulated, the impulse they discharge travels as electrical activity to the spinal cord and on to the brain. This electrical activity becomes the experience of pain when it reaches the brain. There are no “pain impulses” as such. However, if the neural pathway for these impulses is blocked, pain is also blocked since the impulses do not reach the brain. Pain pathways can be blocked by (a) surgically cutting the, (b) drugs that inhibit the activity of the pathway’s fibers, and (c) natural (endogenous) methods of blocking portions of the pain pathway. Nerve Pathways             Nerve Fibers that carry somatosensory information from the body periphery to the spinal cord include A-beta, A-delta, and C fibers. A-type fibers have a myelin sheath that speeds up information transmission. A-delta fibers transmit pain. A-beta fibers are larger and carry other sensory information. C fibers transmit pain more slowly because they have no myelin sheath.             Pain sensation following stimulation of A-delta fibers differs from that following C-fiber stimulation. A-delta activity is experienced as sharp, easily localized pain. C-fiber activity is felt more slowly after painful stimulation. It is persistent, dull, and aching and is difficult to localize. Recall when you received an injection or stubbed your toe. A sharp, well-localizes sensation occurred first (a-delta activation) followed by a persistent, dull, aching sensation (C-fiber activation).     Spinal Cord Pathways             Different transmissions pathways in the spinal cord contribute to the experience of various qualities of pain. The major spinal tract carrying painful information to the brain is the spinothalamic tract. Some fibers of this tract go directly to the thalamus. From there they pass to the somasensory cortex, which involved in discriminating the quality and localization of pain. Other fibers branch diffusely out to the many areas of the brain associated with emotion and motivation. The direct path of pain from spinal cord thalamus to somasensory cortex is sometimes called the neospinothalamic tract (neo means new). This appears to be of more recent evolutionary development. The diffuse path of pain goes to more diverse brain centers. It is called the paleosinothalamic tract, since it seems to be an earlier evolutionary development. The receptors for pain and various areas of the brain activated by pain dictate a complex response to painful stimuli. Painful stimulation provides (A) information (about the character, intensity, and location of the insult, (B) motivation to behave. Gate-Control Model of Pain             The physiology of pain transmissions and perception is less well understood than the underlying physical structure (anatomy). There are various theoretical models attempting to explain how neural units interact during the experience of pain.             In 1965,  and  presented the first version of the gate control theory. They suggested the existence of a “gate” that could either facilitate or inhibit the transmissions of pain signals. The gate is controlled by the dynamic function of certain cells in the spinal cord’s dorsal horn. The fibers bringing information about pain from tissue synapse for the first time in laminae of the dorsal horn. Laminae II is known as the substantia gelatinosa. The SG is visually distinct from other laminae when the spinal cord is inspected in cross section.  and  proposed that the SG is the anatomic location of the gate. Both small fibers and large fibers converge in SG. The theory suggests that the excitatory and inhibitory links from the SG to the transmission cells as well as descending inhibitory control from brain-stems. The action may be presynaptic, postsynaptic, or both. All connections are excitatory, except the inhibitory link from SG to T cell. Pain Therapy – Non-analgesic Medication             Much pain therapy is conducted by administering medications that act specifically on the particular end organ that is the source of pain. Such medications act directly on the pain-producing organ itself. Rather than on the higher centers responsible for pain perception. For example, medications such as nitroglycerin relieve the pain of angina pectoris by affecting the heart – the painful end organ; atropine may relieve pain caused by smooth muscle spasm by relieving the muscle spasm; ergotamine constricts overdistended arteries in the brain, thereby relieving the pain of some migrane headaches. Such medications are not analgesics, analgesics act peripherally or centrally to modify pain perception or reaction. Placebos             Placebos, or pharmacologically inactive substances, e.g. sodium bicarbonate, vitamins and lactose. Currently they are used extensively as a control in experiments examining the effects of medication.   Recorded history allows us to see that pain has been an integral component of the human experience. When a person is in pain, the person will try to find every measure that can lessen that pain and give him or herself comfort. What could be considered as comfort could not be considered comfort to another person. This mirrors that both pain and comfort are subjective. Traditionally, pain has been viewed simply as a symptom of an illness or condition. However, at present, pain itself is considered to be a separate disease and merits special consideration. Knowing that pain affects every aspect of a client’s life, pain management and the provision of comfort from that pain is one of the most researched concepts in nursing ( & , 2004).   Reference:       Credit:ivythesis.typepad.com

Describe the pathways responsible for modulation of painful stimuli in the central nervous system

Describe the pathways responsible for modulation of painful stimuli in the central nervous system Introduction Pain is cause...

DISCUSSION ON THE DIAGNOSIS OF STABLE ANGINA PECTORIS

DISCUSSION ON THE DIAGNOSIS OF STABLE ANGINA PECTORIS   Chest discomfort or pain, which is often perceived as originating from the heart, may be due to many conditions. Angina pectoris, a type of chest pain, signals that the heart muscle is not getting sufficient blood flow and, specifically, sufficient oxygen. The muscles of the heart, like all muscles, depend upon the constant flow of oxygen-rich blood into the tissues in order to perform their required work and sustain their health (2000). The blood vessels which supply the heart with blood are the coronary vessels. Any change in the caliber of these significant vessels, such as sudden narrowing or blockage, will seriously obstruct the flow of oxygen and nourishment to the cardiac muscle.             When the heart beats at a very rapid rate, the myocardium may receive an inadequate blood supply because the relaxation periods (when the blood is able to flow to the heart tissue) are shortened (2004). Ordinarily, a person cannot “feel” his or her heart, but when the cardiac muscle undergoes ischemia (inadequate supply of blood to a part of the body, caused by partial or total blockage of an artery), pain sensations are often exhibited. Situations in which the myocardium is deprived of oxygen often result in crushing chest pain called angina pectoris (an-ji’nah pek’tor-is). Angina pectoris classically refers to chest pain or pressure produced by myocardial ischemia (2003). Angina pectoris is the clinical term used to describe chest pain resulting from a relative oxygen deficiency in heart muscle. It occurs when cardiac work and myocardial oxygen demand exceed the ability of the coronary arterial system to supply oxygen. The heart muscle does not receive enough blood (nutrients and oxygen) resulting in chest pain. This lack of blood supply to the heart muscle to sustain various levels of work required of the heart is called myocardial ischemia. This pain is a warning that should never be ignored because, if angina is prolonged, the ischemic heart cells may die, forming an infarct. The resulting myocardial infarction is commonly called a “heart attack” or “coronary” (2004). The coronary heart disease syndromes are stable angina pectoris, unstable angina pectoris, variant angina (Prinzmetal’s angina), acute myocardial infarction, non-Qwave infarction (usually nontransmural), and Q-wave infarction (usually transmural) (2002). It is common for the severity of the symptoms of angina to vary with time, or even from day to day. At the same time, underlyingcoronary plaque accumulations in the artery may progress, either by an increase in the severityof pre-existing lesions or by the formation of new stenoses.Under certain circumstances coronary plaque accumulations can be induced to regress. “Stable” angina is a relative term used in contrast to”unstable” angina where symptoms are progressively increasingin severity over a short time period, and there is an increasedrisk of complications such as death or myocardial infarction. Most individuals with angina have underlying atherosclerotic coronary artery disease (CAD). Atherosclerosis in human beings is a process in which the intimal layer of the large muscular and elastic arteries is thickened as a result of intra- and extracellular accumulation of plasma lipids, cellular proliferation, and macrophage migration ( 2000). The resulting lesions generally progress through several stages of severity from fatty streaks to complicated, fibrous plaques. The presence of severe lesions in the coronary arteries often culminates in a disease spectrum that includes angina pectoris, myocardial infarction, and disturbances of performance, rhythm, and electrical activity of the heart ( 1994). Arteriosclerotic disease of the coronary arteries may present in three ways, depending on the rate of narrowing of the lumina of the arteries: (a) as a general degeneration and fibrosis of the myocardium, which occurs over many years and is caused by a gradual narrowing of the coronary arteries; (b) as angina pectoris, cardiac pain that occurs on exertion and is relieved by rest; in this condition, the coronary arteries are so narrowed that myocardial ischemia occurs on exertion but not at rest; and (c) as myocardial infarction, in which coronary flow is suddenly reduced or stopped and the cardiac muscle undergoes necrosis (2000). However, angina may also develop in some patients with ventricular hypertrophy, left ventricular (LV) outflow obstruction, severe aortic valvular regurgitation or stenosis, cardiomyopathy, or a dilated ventricle or ventricles in whom coronary artery stenosis is not present. This angina occurs because even normal coronary arteries may not adequately supply oxygen to hypertrophied, dilated, or failing heart muscle ( 2002). On occasion, a limited coronary vasodilator reserve may explain angina, especially in some patients with ventricular hypertrophy associated with LV outflow obstruction, including valvular aortic stenosis and hypertrophic obstructive cardiomyopathy, and in patients with poorly controlled systemic arterial hypertension (2002). Angina occurs when the blood flow to the heart is enough for normal needs but not enough for increased needs such as occurs in physical exercise, strong emotions or extreme temperatures. For example running to catch a bus could trigger an attack of angina where walking to the bus stop might not. Angina pectoris typically occurs in the setting of exertion resulting in increased demand that cannot be met adequately by diseased coronary arteries, thus leading to ischemia. In most persons, exertion or emotion precipitates the attack. Under these circumstances, the heart muscle beats more rapidly and needs a faster, richer supply of oxygen and blood. If the coronary vessels are partially blocked by fatty deposits, as in arteriosclerosis, the circulation is not able to cope with the increased demands by the heart and angina results. The diagnosis of angina is usually made on the basis of the clinical history, including a clinical assessment of risk factors forcoronary plaque leading to blockage of blood flow to and from the heart. An assessment of risk factors should include a recording of a family history of angina pectoris, hypertension or diabetes; recordingof body mass index; measurement of blood pressure; urine testingfor glucose; and measurement of plasma lipids, preferably includinghigh density lipoprotein (HDL) cholesterol and triglycerides. The 12 lead Electrocardiogram is also useful in determining presence of angina pectoris. One useful index of myocardial ischemia is a demonstration of myocardial lactate production by sampling the coronary sinus during angina or stress. As the myocardium becomes ischemic, coronary sinus blood pH falls, there is cellular potassium loss, lactate production replaces utilization, ECG abnormalities appear, and ventricular performance deteriorates. Angina pectoris results in chest pain that is aching, sharp, tingling, or burning, or that feels like pressure ( 2004). Its severity could be mild to moderate, sometimes perceived as discomfort rather than pain ( 2003).             The discomfort of angina pectoris is highly variable. It may be a vague, barely troublesome ache, or it may rapidly become a severe, intense precordial crushing sensation. The patient usually describes stable angina pectoris symptoms in one or several of the following terms: heaviness, pressure, squeezing, and sensation of strangling or constriction in the chest. It may also be described as aching or indigestion. Angina pain typically leads to a pressure-like sensation in the chest, but the pain may radiate to the left arm, jaw, teeth, or throat. Some patients describe a burning sensation (2001). A clenched fist over the sternum suggests angina pectoris ( 2003). This pain is usually felt beneath the upper sternum and in addition is often referred to distant surface areas of the body, most commonly to the left arm and left shoulder but also frequently to the neck and even to the side of the face or to the opposite arm and shoulder (2000). Retrosternal chest pain is the most characteristic clinical feature of angina pectoris. The reason for this distribution of pain is that the heart originated during embryonic life in the neck, as do the arms. Therefore, both of these structures receive pain nerve fibers from the same spinal cord segments (2000).  The more severe the attack is, the greater the radiation of the pain. In some clients anginal pain may not radiate ( 2004). Associated symptoms can be dyspnea and nausea (2003). Accompanying symptoms also often include tachycardia (rapid heart rate), and diaphoresis (sweating) (2001). The pain is typically caused by relative ischemia of the heart. No pain usually is felt as long as the person is quiet, but as soon as he or she overworks the heart, the pain appears (2000). The pain usually is of short duration. The symptoms usually begin at a low intensity, increase over 2 to 3 minutes and last less than 15 minutes. Angina can also occur at rest, or it can be due to vasospasm of the coronary arteries ( 2001). The pain can last from 1 to 15 minutes. The pain of angina pectoris is typically brief, lasting seldom more than three or four minutes. When longer, the cause may be something else. In most people who develop progressive constriction of their coronary arteries, cardiac pain or angina pectoris, begins to appear whenever the load on the heart becomes too great in relation to the coronary blood flow. Factors that aggravate the pain are exertion, especially in the cold; meals; and emotional stress ( 2004). Angina frequently occurs after a heavy meal, because of the increased work load digestion places on the heart. A man who may be able to walk rapidly without distress at a time when he has no food in his stomach may be unable to walk even a hundred feet after he has had a heavy meal. The attack of angina pectoris is likely to occur following a meal which is eaten too hastily, in which case considerable air is taken in with the food. It may also follow a meal which is indigestible or eaten when one is too tired. Patients with stable angina have symptoms usually after physical activity or during periods of emotional stress. Any strong emotion may precipitate an attack of angina, especially grief, anger, or worry. Coronary artery vasoconstriction occurring with exercise or stress may also be a contributing factor. Most humans without coronary heart disease or ventricular hypertrophy do not develop angina, probably because the heart is protected from an important imbalance between oxygen supply and demand by other factors that limit physical activity, such as dyspnea and fatigue (2002). The condition of angina pectoris may also occur at rest. Clients report that pain is often precipitated by activities that increase myocardial oxygen demand (e.g., exercise, anxiety, or stress). The pain is usually relieved with rest and coronary vasodilators, the most common being a nitroglycerin preparation ( 2004). It may also occur in any occupation, though less commonly to laborers because of their better muscular development. Angina pectoris is more prevalent in cities, probably because of the faster paced life associated with cities.             Any increase in heart rate, blood pressure, contractile state, or ventricular wall tension can raise myocardial oxygen demand. When supply lags behind demand, angina results. When stable angina is diagnosed, pharmacologic therapy can be prescribed to reduce myocardial oxygen demand and to increase blood flow to ischemic areas of the myocardium. However, a patient’s risk factors and the extent of underlying disease must be determined before a specific treatment decision is made (2002). The standard Electrocardiogram (ECG) is a critical tool in the diagnosis of angina pectoris. In fact a 12-lead ECG recorded at rest in the absence of pain is normal in about half of the patients with typical angina. However, an ECG taken in the presence of pain may yield a great deal more information because it may document the presence of transient ST segments depression, a characteristic sign of subendocardial ischemia. In an ECG recording, a current of injury sometime occurs during an attack of severe angina pectoris because the coronary insufficiency then becomes great enough to prevent adequate repolarization of the membranes in some areas of the heart during diastole (2000). The acute pain experienced in angina pectoris may be related to decreased myocardial blood flow, increased cardiac workload/oxygen consumption, possibly evidenced by verbal reports, narrowed focus, distraction behaviors (restlessness, moaning), and autonomic responses like diaphoresis and changes in vital signs (2004).             The decreased cardiac output may be related to inotropic changes (transient/prolonged myocardial ischemia, effects of medication), alterations in rate/rhythm and electrical conduction, possibly evidenced by changes in hemodynamic readings, dyspnea, restlessness, decreased tolerance for activity, fatigue, diminished peripheral pulses, cool/pale skin, changes in mental status, and continued chest pain (2004). Women report higher prevalence of angina than men, despite the lower prevalence of ischemic electrocardiograms (ECGs) ( 1996). High-strung, active people are most commonly subject to it, and in 90 percent of cases, arteriosclerosis, or hardening of the arteries, is noted. Persons with diabetes, high blood pressure, rheumatic heart disease, and anemia are more susceptible than others to angina pectoris. The excess of abnormal ECGs in men is greater for probable ischemia, Q waves, than it is for possible ischemia, S-T- and T-wave changes (1996). Although angina is more common in women than in men, it is also more commonly associated with normal coronary arteries,microvascular angina, and other noncoronary causes of chest pain, such as mitral valve prolapse.This is in contradistinction to angina in men, which more commonly is associated with coronary artery disease. In addition, chest pain syndromes in women are more likely to be attributed to noncardiac (and possibly psychogenic) etiologies by physicians, as related diagnoses (e.g., depression and panic attacks) are more common in women. These circumstances in turn may lead physicians to less aggressively pursue the evaluation of complaints of chest pain by women (2000). The pathophysiology of the pain is uncertain, because studies that have used Holter monitors to examine ischemia during activities of daily living demonstrate that the majority of ischemic episodes are clinically silent ( 2001). Exactly what causes the pain is not known, but it is believed that ischemia causes the muscle to release acidic substances, such as lactic acid, or other pain-promoting products, such as histamine, kinins, or cellular proteolytic enzymes, that are not removed rapidly enough by the slowly moving coronary blood. The high concentrations of these abnormal products then stimulate the pain endings in the cardiac muscle, and pain impulses are conducted through the sympathetic sensory afferent nerve fibers into the central nervous system (2000). Presumably the accumulation of active substances during ischemia stimulates the sensory nerves encircling the heart, producing the deep visceral sensation of angina. Moderation is of the greatest importance in controlling angina pectoris. At the first sign of chest pain, the person should immediately cease what he is doing and sit down and rest. Relief of pain will often come in a few minutes. To persist in exertion after the onset of pain is extremely hazardous, and in this respect the pain is a significant symptom which informs the patient that he is overexerting himself and needs rest. Most people who have chronic angina pectoris feel pain when they exercise and when they experience emotions that increase metabolism of the heart or temporarily constrict the coronary vessels because of sympathetic vasoconstrictor nerve signals. The pain usually lasts for only a few minutes. However, some patients have such severe and lasting ischemia that the pain is present all the time. The pain is frequently described as hot, pressing, and constricting; it is of such quality that it usually makes the patient stop all activity and come to a complete state of rest (2000). Many conditions cause pain in the chest and must be considered in the differential diagnosis (e.g. abnormalities of the cervicodorsal spine, costochondral separation, and non-specific chest wall pain). However, few truly mimic angina, and the syndrome of angina is so characteristic in most individuals that errors in diagnosis are usually the result of careless history taking. Fortunately many drugs are available which give immediate relief to those with angina pectoris or a tendency to narrowing of the coronary vessels for whatever reason. The improvements in the treatment of coronary heart disease have mainly occurred in relation to the management of angina (1991). Medical therapy for angina is directed at decreasing myocardial oxygen demand, increasing myocardial blood flow, or both (2001). Diagnosis of angina and decisions about the most appropriate form of treatment have been assisted by the development of a range of investigative techniques such as exercise testing and invasive investigations such as coronary angiography. One common method of treating angina is through drug therapy where the aim is to increase the blood flow to the heart or to decrease the work of the heart (1991). A large number of drugs are used to treat angina. Patients with stable angina can benefit from treatment with nitrates, beta blockers, calcium antagonists, antiplatelet agents (aspirin either alone or in combination with clopidogrel), and, possibly, ACE inhibitors ( 2002). These groups of drugs are currently used alone and sometimes in combination for treatment of angina. The beta blockers, calcium channel blockers, and vasodilators are also used to treat hypertension and some cardiac arrhythmias. Several vasodilator drugs, when administered during an acute anginal attack, usually give immediate relief from the pain. Commonly used vasodilators are nitroglycerin and other nitrate drugs (2000). Nitroglycerine causes dilation or widening of the coronary vessels during an attack and thus permits more blood to flow through. Nitroglycerine, taken as a small tablet slipped under the tongue during an attack, brings relief almost immediately, and seldom later than two or three minutes. Although they improve symptoms, nitrates have not been shown to reduce mortality or the future development of myocardial infarction (MI) in patients with coronary artery disease (2002). A second class of drugs that are used for prolonged treatment of angina pectoris is the beta blockers, such as propranolol. They block the sympathetic beta receptors, which prevents sympathetic enhancement of heart rate and cardiac metabolism during exercise or emotional episodes. Therefore, therapy with a beta blocker decreases the need of the heart for extra metabolic oxygen during stressful conditions ( 2000). Because of their positive effects on morbidity and mortality, beta blockers should be strongly considered as initial therapy for chronic stable angina (2002).             There is growing evidence that angiotensin-converting enzyme (ACE) inhibitors may also be beneficial, especially in reducing future risks of coronary events. Immediate-release or short-acting dihydropyridine calcium antagonists have been reported to increase the risk of adverse cardiac events, although these reports remain controversial. Long-acting or slow-release dihydropyridines, or nondihydropyridines, have the potential to relieve symptoms without increasing the risk of adverse events (2002). Amylnitrate, a medicine which is inhaled during an attack, can also be taken. Other drugs of a similar nature may be regularly prescribed for two or three times a day to prevent attacks. No drugs should be taken without consulting a doctor, as they may have unpleasant or serious side-effects. Surgery is the alternative method of treating angina. Surgical and interventional cardiology procedures to treat CAD include angioplasty, arthrectomy, and coronary artery by pass graft surgery. Promising techniques currently under evaluation for treatment of angina and CAD include angiogenesis (induction of the growth of new blood vessels) and laser therapy to increase collateral blood flow ( 2001). The form of treatment which has been the recent focus of a lot of interest and debate is coronary artery bypass grafting (CABG). CABG is a technique in which a blocked or narrowed section of a coronary artery is bypassed using part of a vein or artery from elsewhere in the patient’s body. The objective of the treatment in addition to the relief of angina is the prolongation of life. The development of coronary angiography (X-ray examination of blood vessels) which allowed the precise identification of the size and extent of the disease paved the way for CABG (1991). Heart attack resulting from cardiovascular disease is the leading cause of death in the industrialized world and one of the most common causes of disabilities. Angina pectoris is one of its three clinical manifestations, myocardial infarction (heart attack or death of heart muscle because of a lack of oxygen), and sudden cardiac death the other two. These outcomes now seem almost inevitable accompaniments of modern lifestyles (2001). The person who suffers from angina pectoris should not despair of his or her situation. It is not a disease, but a warning of danger from the heart. Relief of the acute attack, though momentarily significant, is not the entire solution to angina pectoris. The person’s daily life must be regulated so as to avoid situations liable to affect adversely the circulation of the heart. It is quite possible to live a fairly normal existence if the person takes proper care of himself and always heeds the warning signal of pain. Credit:ivythesis.typepad.com

DISCUSSION ON THE DIAGNOSIS OF STABLE ANGINA PECTORIS

DISCUSSION ON THE DIAGNOSIS OF STABLE ANGINA PECTORIS Chest discomfort or pain, which is often perceived as originating from the hear...

Literature Review on Reflective Practice with Pain Control after Surgery

PAIN CONTROL AFTER SURGICAL OPERATION         There are many reasons why people must need to undergo surgical operation and whatever the case maybe the doctors who advice their patients about surgery understand that this is the only way or probably the last procedure they need to be cured. Surgical operation cause a lot of depression on the part of the patient even in their family considering the financial aspect, time they are going to spend and most of all the risk of going through any surgical operation.       Patients who undergone surgical may feel a slight physical and emotional changes during the operation but unfortunately the consequence they are going to suffer from surgical operation extend even more after the surgical proceedings. That is why doctors will need to advice the patients and their family about medicines and other procedures to lessen the pain after the operation. The person who suffer from operation may require utmost important in care and medication and doctors need to specify and  inform their patient about their condition and how they are going to deal with the pain for the next few days to safely minimize the pain of their patients.       This information about pain management after the surgical operation must be strictly followed or the patient may suffer even more consequence due to negligence or improper medication. Doctors also advice their family to give them enough attention to care especially for the elderly patients who are experiencing the pain, it is also important to inspect all the medicine and their tools such so as not to create complication on the part of the patient. The nurse or the care taker must inform their doctor immediately if the patient is suffering any abnormal behavior such as allergy or infection.       The patient will be the one to acknowledge his movement or behavior if he feels comfortable about the pain and the medicine. There are surgical procedures that require minimal movement of the patient to best prevent complication after the operation. Walking and proper breathing is also somehow a doctor’s discretion but basically patients should be the one to control this activity according to their condition, in case of children who always have a varying tendency to excessive movement must absolutely need assistant to lookup all the time.       Depending on surgical procedure and disease of the patients, they may feel various pains such as; Muscle pain, movement pain and conditional pain from various body parts. Pain can also be measure according to severity, patients may say it hurts a bit, it hurts bit more or it hurts much. Doctors from acute pain management will review you surgical history to give you a corresponding cure about your situation. Usually they may give you to report for a specified period of time.       Depending on your disease, doctors may give you various pain management treatments. 1. Intravenous pain controlled Analgesia – this is a computerized pump method that when pushed will give you a small intravenous medicine and this will control your pain. 2. Patient Control Epidural Analgesia – A thin plastic tube that puts on your back, this is often used for maternal care or patients suffering from heart or lung disease. This will give you a more comfortable position though his may require a certain procedure to be used and medical personnel will be the one to put it on to the patients back. They may also give you a 3. Nerve block – to keep you sleepy and relax for a moment, this control can be used before and after surgical operation to reduce the pain that causes nausea and drowsiness. There are also 4. Oral pain medication or medicine – that can control you from pain suffering, usually this medicine is to be taken every 3 to four hours or depending on the severity and prescription of your physician. This is the less stressful type of pain management because if doesn’t require any cooperation or push on the part of the patient and they can take it without much conditioning unlike any other types of pain management.       Home pain management medication can also be given by your physician, by this time the patient is in a more stable condition and can be cured at home. Generally doctors would give you advice for the proper diet about your eating habit, enough rest, use clean bed and pillows, prevent excessive movement, listen to soft music and relax your mind. Be sure to take note of the medication and additional prescription that is given by your doctor so that the cure of the patient is easily regulated and basically immediate healing will take place sooner in less time. Most importantly don’t self medicate, if you are not sure what to do on a given situation always consult a medical advice from an authorized medical professionals.         Credit:ivythesis.typepad.com

Literature Review on Reflective Practice with Pain Control after Surgery

PAIN CONTROL AFTER SURGICAL OPERATION There are many reasons why people must need to undergo surgical operation and whatever the...

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