INTRODUCTION ------------------------
Woolf (1989) qualitatively divided into two types, namely pain physiological pain and pathological pain. The main difference between the two types of pain is that the pain is physiologically normal sensor that functions as a protective device body, while pain is a sensor of abnormal pathological someone suffer.
Pathological pain is a sensation that arises as a consequence of the existence or tissue damage caused by nerve damage. If the inflammatory process through the normal healing process so that disappeared in accordance with the healing referred to as adaptive pain, commonly known as acute pain. On the other hand, nerve damage in fact develop into intractable pain after healing is completed, referred to as maladaptive pain, and commonly known as neuropathic pain.
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-------------------------- MAIN CONCEPT
Pain can be classified based on patofisiologinya (eg nosiseptif pain and neuropathic pain), etiology (eg, postoperative pain and cancer pain), or influenced areas (eg, headache and low back pain).
Nosiseptif pain caused by the activation or sensitization of peripheral nosiseptor which is a specific receptor that delivers noxious stimuli. Neuropathic pain is the result of an injury or acquired abnormalities in the peripheral or central neural structures.
Acute pain can be defined as pain produced by noxious stimuli because of an injury, disease process or structural abnormality of muscle or viscera. This pain almost always is nosiseptif.
Chronic pain is defined as persistent pain beyond the timeframe of a process of acute or exceed the achievement of a normal period of healing; periods can vary from one to six months. Chronic pain can be nosiseptif, neuropathic, or a combination thereof.
Modulation of peripheral pain occurs on nosiseptor, the spinal cord, or supra-spinal structures. Or the presence of this modulation can be facilitated.
Moderate to severe acute pain, depending on its location, can affect its function in the surrounding organs and has a role in perioperative morbidity or mortality.
Neural blockade with local anesthesia can be used to limit the pain mechanism, but more importantly, this blockade plays an important role in the management of patients with acute or chronic pain.
In general, the main role of antidepressants is to resolve complaints that patients with neuropathic pain such as neuralgia and neuropathy in diabetic postherpetik. This agent showed analgesic effects at lower doses than the doses antidepresannya effects.
Anticonvulsants are usually used in patients with neuropathic pain, particularly trigeminal neuralgia and diabetic neuropathy.
Stimulation of spinal corda most effective for neuropathic pain. The mechanism proposed is the activation and inhibition of descending modulating systems symphatetic outflow. Indications corda spinal stimulation that can be accepted include sympathetically mediated pain, spinal cord lesions with localized segmental pain, Phantom Limb pain, lower limb ischemia due to peripheral vascular penyakt, and adhesive arachnoiditis.
The use of combined local anesthetic and opioids is a very good technique for dealing with postoperative pain after a procedure involving the abdomen, pelvis, thorax and orthopedic.
Serious side effects from the use of epidural or intrathecal opioids is dose-dependent and depressed respiration. Most cases of respiratory depression occurred in patients who received therapy parenteral opioids or sedatives. Old-old patients or those who experience sleep apnea seems to be more susceptible to these side effects, requiring dose reduction.
Physical dependency occurs in all patients using large doses of opioids for long periods. This phenomenon could withdrawl dipresipitasi with opioid antagonist administration.
Multiple triggers can induce the occurrence of sympathetically Maintained pain, which often have overlooked or misdiagnosis. Patients often respond dramatically to the sympathetic block. Cure rate is very high (more than 90%) if therapy is initiated within one month since the discovery of symptoms.
DEFINITION and CLASSIFICATION OF PAIN -------------------
As with many other conscious stimulus, the perception of pain delivered by specialized neurons that act as receptors, detecting the stimulus, reinforcing and penghantar toward the central nervous system. The sensation is often didekripsikan as protopatik (noxious) and epikritik (non-noxious). Epiritik sensation (light touch, pressure, proprioception, and temperature differences) are indicated by a low threshold receptors that are generally delivered by a large nerve fibers bermielin. Conversely, protopatik sensation (pain) receptors characterized by a high threshold is delivered by the nerve fibers of smaller bermielin (A delta) and nerve fibers did not bermielin (C fibers).
According to the IASP (the International Association for the Study of Pain), pain is a "sensory and emotional experience unpleasant associated with tissue damage or potential damage." This definition describes the existence of a combination of an objective component, psychological aspects of pain as well as subjective and emotional factors. Response to pain can vary greatly between one person with another person and the same person at different times.
Terminology of "nosisepsi" taken from the word noci which means "injury", is used to describe the neural response to traumatic or noxious stimuli. All nosisepsi produce pain, but not all pain is the result nosisepsi. Many patients feel pain without a noxious stimulus. Therefore, clinically we divide pain into two categories: (1) acute pain, usually because nosisepsi and (2) chronic pain, perhaps because nosisepsi, but with the psychological and behavioral factors as the main factor.
A. Acute pain
Acute pain can be defined as pain caused by noxious stimuli because of an injury, disease process or abnormal function of muscle and viscera. Nature is almost always nosisepsi. Pain nosiseptif presented to detect, localize and restrict tissue damage. Four physiological processes involved are transduction, transmission, modulation and perception.
-Transduction
Nosiseptor potential changes to the current electro-biochemical / impulses along the axon. Occur due to the release of chemical mediators such as prostaglandins from damaged cells, from plasma bradykinin, histamine from mast cells, Platelet serotonin and substance P from the nerve endings.
-Transmission
Two step process nosiseptor pain impulses from peripheral nerves through the dorsal spinal cord toward Cutaneous cerebral cortex.
-Modulation
Internal control processes by the nervous system, can increase or reduce the pain impulses.
-Perception
SSP reconstruction results of pain impulses received. Reconstruction is the result of sensory nervous system, information on cognitive and emotional experiences.
This type of pain usually associated with a neuro-endocrine stress (sweating, pounding) is proportional to its intensity. This pain may be postoperative pain, obstetric pain, pain in acute medical illness (AMI, pancreatitis, kidney stones), etc.. Most acute pain can heal themselves (self-limited) or cure with medication for several days or weeks. When the pain failed to heal well because of abnormalities in the process of healing and the treatment is not adequate, can develop into chronic pain. Two types of acute pain - pain of somatic and visceral pain - differentiated according to origin of the pain and the clinical picture.
B. Chronic Pain
Chronic pain is defined as pain that settled over the time span of an acute process or a period exceeding the normal achievement of a cure; periods can vary from 1 up to 6 months. Chronic pain can be nosiseptif, neuropathic, or a combination thereof.
ANATOMY and PHYSIOLOGY NOSISEPSI ------------------
Pain pathways
There are three lines of neurons involved in pain
1. First order neurons; deliver the pain from the periphery to the spinal cord
2. Second order neurons; deliver the pain from the medulla to the thalamus spinals
3. Third order neurons; deliver the pain from the thalamus to the cortex,
Physiology Nosisepsi
1. Nosiseptor
- It is free of nerve fibers (free nerve endings / C fibers), the character of afferent (sensory)
- Receptor for temperature stimuli, mechanical and chemical; mainly excitatory on damaged tissue.
- Type:
Mekanonosiseptor; in touch and prick
Silent nosiseptor; on the inflammatory reaction
Polimodal mekano-heat-nosiseptor; the strong pressure, increased temperature (> 42 ° C and 2
Lamotrigine 24 25-400 20-20
Phenytoin 22200-600 10-20
Unknown topiramate 25-200 20-30
Valproic acid 50-100 6-16 750-1250
Corticosteroids
Glucocorticoids are widely used in pain management because of the effects of antiinflammatory and analgesic owned. This agent can be provided by topical, oral, or parenteral (intravenous, subcutaneous, intra-exchange, intraartikular, and epidural). Glucocorticoid excess can cause hypertension, hyperglycemia, increased susceptibility to infections, peptic ulcers, osteoporosis, aseptic necrosis of femoral caput, proximal myopati, cataracts, and (rarely) psychosis.
Route corticosteroid mineralocorticoid activity of glucocorticoid activity equivalent dose (mg) The half-life (hours)
Hydrocortisone O, I, T 1 1 20 8-12
Prednisone O 4 0.8 5 12-36
Prednisolone O, I 4 0.8 5 12-36
Methyl-prednisolone O, I, T 5 0.5 4 12-36
Triamcinolone O, I, T 5 0 4 12-36
Betamethasone O, I, T 25 0 0.75 36-72
Dexamethasone O, I, T 25 0 0.75 36-72
O: oral, I: injectable, T: Topical
Systemic Local Anaesthetics
Local anesthetic can be used systemically with neuropathic pain in patients. These agents produce central effects of sedation and analgesia. Lidocaine, procaine, and klorprokain is most commonly used agent, given the slow bolus and continuous infusion. Lidocaine given intravenously over 50-30 minutes for a total dose of 1-5 mg / kg. procaine 200-400 mg can be given intravenously over 1-2 hours. Klorprokain (i% solution) infused at 1 mg / kg / min for a total dose of 10-20 mg / kg. Monitoring should be done include electrocardiogram (ECG), blood pressure, respiration and mental status. Resuscitation tool should always be available. Signs of toxicity include tinnitus, slurring, and nistagmus esksesif sedation.
