|Posted on May 17, 2015 at 4:20 PM||comments (6387)|
Narcotics refer to a class of prescription pain killers derived from opiates. Narcotics blocks pain signal from the brain to reduce pain. Narcotics reduce the feeling of pain by blocking pain signal from the brain and the central nervous system. Opioids are a type of narcotic pain medication when you have a mild headache or muscles ache. An over- the-counter pain reliever is usually enough to make you feel better-but if your pain is more severe you doctor might recommend something stronger which is opioid-varieties of narcotic include codeine, morphine, hydromorpone, oxycodone and hydrocodone, which is commonly know by it brand name of vicodin.
Narcotics work by binding to receptor in the brain, which blocks the feeling of pain. When use carefully and under doctors direct care, they can be effective at reducing pain. These drugs can be abused and addictive and have been associated with accidental overdose death. Your doctors may suggest that you take your medicine only when you feel pain, so always take narcotics as prescribed.
Narcotics attach to receptors on nerves in the brain that increase the threshold to pain and reduce the perception of pain. Some adult have chronic pain which require proper pain management since long term use can lead to drug addiction and tolerance. Most men and women take narcotic analgesic for short period until pain lessen or goes away.
Side effect of narcotic and pain medication
The following are the side effect of narcotics and pain medication
1. Weak or shallow breathing, weak pulse, slow heartbeat
2. A lightheaded feeling like you might pass out
3. Signs of too much serotonin in the body-agitation, hallucination, fever, fast heart rate, over active, reflexes, nausea, vomiting, diarrhea, loss of coordination and fainting
4. Constipation, mild nausea, stomach pain
5. Severe drowsiness or dizziness, confusion, problem with speech
6. Headache, tired feeling, mild drowsiness or dizziness: drowsiness is most common just after you begin to take the drugs or increase the dose. Like 20% to 60% of pain patient will experience a small increase in sleepiness when taking opioid medicine. Any drowsiness will usually fade away as you become used to the medication.
7. Sedation, dry mouth, chest pain and abnormal heart beats
8. Sexual side effect: living with chronic pain often takes a toll on your sex life. Opioids- and not the pain itself- may be at least partly to blame. The drug appears to lower testosterone level, and cause erectile dysfunction in men and difficulty with orgasm for both sexes.
9. Common side effect of pain medication and narcotic include, drowsiness, leading to an inability to-safely-operate machinery or drive. Other less common but more side effect include sweating, shortness of breath, nausea, decreased hunger and vomiting.
10. Itching is also a side effect of narcotic and constipation. Between 10% of opioid user may find themselves itching all over. The side effect is most common when morphine is-administered via an injection into the spine. The itching might seem like an allergic reaction, but allergies to opioids are rare.
|Posted on September 1, 2014 at 5:25 PM||comments (3306)|
Wound can be defined as a disturbance or commotion of normal anatomical structure of a tissue and its specific function affiliated with loss of body fluid leading to infection. Healing can be defined as the restoration of anatomical continuity and function through a very well- orchestrated dynamic process regulated by certain biological molecules such as cytokines, and growth factors . Systematic progression of cells through four known phases of healing namely haemostasis, inflammation, proliferation and remodelling or maturation are thus becoming very essential for the successful acute healing process.
These chronic wounds results in both noteworthy patient morbidity and high cost to both affected individuals and the health care system. In the United States alone there were about 5 million patients suffering from chronic non-healing wounds, costing the health system $20 billion annually; this is projected to grow a further 10% each year . Some of the cost coverage is for diagnostic and surgical procedures of wounds, pharmaceuticals, wound closure devices and hospital and physician charges.
The wounds can be caused by trauma, disease, and environmental stresses or insults. The ability of the body to heal these wounds is one of the most essential defense mechanisms of the human body. However there are situations where this defense mechanism is impaired and the wounds either heal very slowly or not at all. The chronicity of the wounds is characterized by tissue destruction and impaired blood circulation that deprives the wound site of cells vital for wound healing. Such cells include macrophages, endothelial cells and fibroblasts. Examples of chronic wound include pressure ulcers, ischemic ulcers and venous ulcers .
CURRENT STANDARD TREATMENTS:
For several years there had been numerous treatments formulated to combat chronic wounds. Usually, debridement and moist wound healing are still commonly practiced treatments today. The importance of appropriate management of the wound bed is recognized as an essential part of the treatment approach to chronic wounds . Several novel approaches to managing and treating chronic wounds are continually being proposed, encompassing chemical, biological or physical treatments or even combinations of these different methodologies .
COLD LASER THERAPY:
A promising novel approach to acute and chronic wound management is through high powered laser therapy. For over 35 years, in the EU, Australia, Asia and Russia low level laser therapy (LLLT) had been an established treatment for pain and tissue repair. Regulatory approval for LLLT in the United States was given in 2002.
EFFECT OF LASER ON CELLS:
This relatively new technology has been utilized to enhance acute and chronic wound healing .The Laser and light is absorbed at the cellular level and converted into biochemical energy, thereby enhancing normal cell function and tissue repair .
MECHANISM OF ACTION:
The following sequenced events occur to bring about normal or cellular haemostasis. There is reduction of inflammation and increase collagen fibre synthesis, endothelial cell migration, proliferation and NO excretion [9, 10]. Laser light also increases the vascularity of the regenerating tissues that in turn results in more blood flow to the injury site and an increase rate of healing and tissue regeneration. As a result there is reduced scarring and control of suppurative diseases of skin or other opportunistic infections.
TREATMENT OF WOUND AREA WITH LASER:
The cold Laser therapy is accomplished using our standard wound therapy laser treatment protocols. The laser source is capable of delivering uniform power and our standard wavelength distribution covering the entire wound area under treatment. The treatment sessions are done with illumination with single exposure of pre-assigned parameters that is monitored before and after exposure to ensure proper energy delivery to the wounded site. Before each session it was confirmed that the laser beam was spread out uniformly over the entire wound including the wound boundaries. Histological samples are taken where necessary such as from chronic pressure ulcers, diabetic foot ulcers etc. etc. to monitor the healing process. Additionally the wounds are measure before and after a certain number of therapy sessions to evaluate the progress of wound healing.
All the previously mentioned sequence of event in wound healing is accomplished through optimal and effective settings of the cold laser through extensive research and patient feedback .It is very essential to utilize the combination of optimal laser treatment parameters for the most effective collagen remodelling that is a major protein responsible for normal skin tensile strength, integrity and structure. Tensile strength regeneration is one of the vital elements for successful wound healing and due to its direct role; periodic and accurate monitoring of collagen in this regard may be of direct relevance
1. J.L. Monaco and W.T. Lawrence. (2003).Clin.Plast.Surg.30, 1-12.
2. A.C.Gloria, F.D.Robert and S. S.Gregory. Wound Healing (Taylor and Francis, Florida, 2005), p.3.
3. Ablaza V & Fisher J. (1998).Telemedicine and wound care management. Home care Provid. 3(4):206-11; quiz.12-3.
4. Vodovnik I. & Karba R.(1992).Treatment of chronic wounds by means of electric and electromagnetic fields. Part 1:Literature review .Med Biol Eng Comput;30(3);257-66.
5. Schultz GS, Sibbald RG, Falanga V et al (2003). Wound bed preparation: a systematic approach to wound management. Wound Repair Regen; 11 Suppl 1:S1-28.
6. Poole-Warren I A &LyM. Wound healing. In: Akay M(Ed). Encyclopedia of BME. Hoboken. N.J: John Wiley& Sons Inc., 2006, p.3862-70.
7. Tuner J, Hode L. The Laser Therapy Handbook, Prima Books; Grandsberg, Sweden, 2002.
8. Tuner J, Hode L. The Laser Therapy Handbook, Prima Books; Grandsberg, Sweden, 2002.
9. Yasukawa A, Hrui H, Koyama Y, Nagai M & Takakuda K. The effects of low reactive-level laser therapy (LLLT) with helium-neon laser on operative wound healing in a rat model.J Vet Med Sci 20 SH07; 69(8); 799-806.
10. Chen CH, Hung HS & Hsu SH. Low-energy laser irradiation increases endothelial cell proliferation, migration and eNOS gene expression possibly via PI3K signal pathway. Lasers Surg Med 2008; 40(1):46-54.
METHICILLIN-RESISTANT S. AUREUS (MRSA) SKIN ABSCESS AND VARIOUS OTHER SKIN CONDITIONS TREATED WITH NON-INVASIVE COLD LASER THERAPY.
|Posted on September 1, 2014 at 5:05 PM||comments (27205)|
The extensive and inappropriate use of antibiotics in the early 1980s gradually led to the buildup of universal antimicrobial resistance. Penicillin was first widely used in the early 1940s and by 1944 half of all clinical Staphylococci spp isolates were resistant to this proclaimed “miracle drug . In recent times infectious disease has become the second most important killer in the world, number three in developed nations and fourth in the USA . Additionally it is one of the leading cause of death in Europe, mostly in elderly and debilitated populations, and despite existing antibiotic therapies and vaccines, infectious diseases remain the leading cause of mortality and morbidity . Worldwide, 17 million people die each year from bacterial infections .In addition to that, five classes of antibiotic-resistant pathogens are emerging as major threats to public health: methicillin-resistant Staphylococcus aureus (MRSA), vancomycin-resistant Enterococcus faecalis (VRE), multidrug-resistant mycobacteria, Gram-negative pathogens and fungi .
As the efficacy of antibiotics reduces and the end of the “antibiotic era” gets closer, major international research efforts to discover new ways to eradicate bacteria are evolving. Antibiotic therapy failure can result in variants of Staphylococcus aureus that are more resistant to antibiotics and can lead to persistent infections, necessitating the development of more effective antimicrobial strategies to combat small colony variant infections.
CAUSES AND RISK FACTORS FOR MRSA:
S. aureus small colony variants (SCVs) are clinically important owing to their reduced susceptibility to antibiotics. SCVs are commonly auxotroph’s for hemin, menadione or thymidine, resulting in electron transport chain defects and consequently reduced membrane potential and reduced uptake of cationic antibiotics . Resistance to cell wall–active antibiotics such as β-lactams occurs due to the slow growth rate and reduced cell wall metabolism of SCVs . Given their persistent nature and their selection by and resistance to conventional antibiotics, there is a need to identify effective therapies for SCV infections. One relatively new potential novel strategy is high powered non-invasive laser therapy.
STANDARD TREATMENT METHODS FOR MRSA RELATED SKIN CONDITIONS:
Primary topical anti-microbial and antiseptic agents are indicated in both prophylaxis and treatment of superficial skin infections. One advantage of topical application of anti-microbial agents is their low systemic absorption, consequently the reduced exposure of the commensal gastrointestinal flora to these antibiotics and low systemic toxicity . The principles of anti-microbial treatment of infected skin wounds are discussed extensively by Filius et al. . Today topical therapy with antibiotics has become unpopular because of the development of resistance .
Colsky and colleagues made a comparison of antibiotic resistance profiles using data collected from 1992 to 1996 from patients with skin wounds and revealed a marked increase in oxacillin and ciprofloxacin resistance in S. aureus and P. aeruginosa. In leg ulcers, an increase from 24% to 50% oxacillin resistance in S. aureus and from 9% to 24% ciprofloxacin resistance in P. aeruginosa. In superficial wounds, an increase from 24% to 36% ciprofloxacin resistance in P. aeruginosa [11, 12]. This study demonstrated the rapid increase of antibiotic resistant bacterial pathogens due to the systemic use of antibiotics in dermatology and highlights the importance of searching for alternatives.
USE OF NON-INVASIVE COLD LASER THERAPY:
In a first report, Hamblin et al. showed the use of a photochemical approach to destroy bacteria infecting a wound in an animal model without damaging the surrounding host tissue . After topical application of achlorin (e6) photosensitizer conjugated with poly-Lysine, E. coli was rapidly killed upon exposure to selected visible light wavelengths.
MECHANISM OF ACTION OF LASER INACTIVATION OF MICROORGANISMS:
Upon irradiation with light from a high powered non-invasive laser using parameters of 1275 nm or 1064 nm wavelength and within the 750 mW to 2.8 watts per cm2range , the photosensitizer (PS) or chromosphere undergoes a transition from a low energy ground state to a higher energy triplet state. This triplet state photosensitizer can react directly with biomolecules to produce free radicals and/or radical ions (type I reaction), or with molecular oxygen to produce highly reactive singlet oxygen (type II reaction) as shown is figure. Various studies showed that there is a difference in susceptibility to anti-bacterial PDT between gram-positive and gram-negative bacteria [14, 15, 16]. Anionic and neutral photosensitizers were found to bind efficiently to gram-positive bacteria to induce growth inhibition or killing by visible light, whereas gram-negative bacteria were not killed. Growth inhibition of E. coli by porphyrin photosensitization was possible only in the presence of membrane disorganizing substances, e.g. the nona-peptide polymyxin or Tris–EDTA . However, direct photo killing of gram-negative bacteria is also possible. In recent years, different chemical classes of positively charged PS, including phthalocyanines and porphyrins, were successfully tested as photo inactivating agents against gram-positive and gram-negative bacteria so far [17, 18, 19, 15, 20]. In general, photosensitizers with an overall cationic charge and meso-substituted cationic porphyrins and water-soluble cationic zinc phthalocyanines can efficiently kill gram negative bacteria by photosensitization even in the absence of additives. This resistance of gram-negative bacteria against efficient killing by anti-bacterial photodynamic therapy is due to the different outer membrane structures of gram-positive and gram-negative bacteria, which is discussed in detail elsewhere . Inactivation of S. aureus, E. coli and P. aeruginosa is accompanied by alterations of the ultra-structure of the cells, e.g. disordered cell wall structure; elongated cells connected together without separation of the daughter cells and different low density areas in the cytoplasm [16, 22].
The current research work provides sufficient evidence that cold laser therapy can be an effective tool in the management of non-healing MRSA abscess or related skin conditions. Such results prove that there is still hope for the cure and even prevention of MRSA infection complications. The research to develop a standard guideline for the use of such laser therapy should be continued and promoted so that a larger number of patients can benefit from laser therapy.
1. Livermore DM. Antibiotic resistance in staphylococci. Int J Antimicrob Agents 2000; 16:3-10; PMID:11137402; http://dx.doi.org/10.1016/S0924- 8579(00)00299-5.
2. Kraus CN. Low hanging fruit in infectious disease drug development. Curr Opin Microbiol 2008; 11:434-8; PMID:18822387;http://dx.doi.org/10.1016/j.mib.2008.09.009.
3. Vicente M, Hodgson J, Massidda O, Tonjum T,Henriques-Normark B, Ron EZ. The fallacies of hope: will we discover new antibiotics to combat pathogenic bacteria in time? FEMS Microbiol Rev 2006; 30:841-52; PMID:17064283; http://dx.doi. org/10.1111/j.1574-6976.2006.00038.x.
4. Butler MS, Buss AD. Natural products—the future scaffolds for novel antibiotics? Biochem Pharmacol 2006; 71:919-29; PMID:16289393; http://dx.doi. org/10.1016/j.bcp.2005.10.012.
5. Nicolau DP. Current challenges in the management of the infected patient. Curr Opin Infect Dis 2011; 24:1-10; PMID:21200179; http://dx.doi.org/10.1097/01. qco.0000393483.10270.ff.
6. Proctor RA, von Eiff C, Kahl BC, Becker K, McNamara P, Herrmann M, et al:Small colony variants: a pathogenic form of bacteria that facilitates persistent and recurrent infections. Nat Rev Microbiol 2006, 4:295–305.
7. Proctor RA, Kahl B, von Eiff C, Vaudaux PE, Lew DP, Peters G:Staphylococcal small colony variants have novel mechanisms for antibiotic resistance. Clin Infect Dis 1998, 27(suppl 1):S68–S74.
8. Kaye ET (2000) Topical antibacterial agents: role in prophylaxis and treatment of bacterial infections. Curr Clin Top Infect Dis 20:43–62.
9. Filius PM, Gyssens IC (2002) Impact of increasing antimicrobial resistance on wound management. Am J Clin Dermatol 3:1–7.
10. Wyatt TD, Ferguson WP, Wilson TS, McCormick E (1977) Gentamicin resistant Staphylococcus aureus associated with the use of topical gentamicin. J Antimicrob Chemother 3:213–217.
11. Colsky AS, Kirsner RS, Kerdel FA (1998) Analysis of antibiotic susceptibilities of skin wound flora in hospitalized dermatology patients. The crisis of antibiotic resistance has come to the surface. Arch Dermatol 134:1006–1009.
12. Colsky AS, Kirsner RS, Kerdel FA (1998) Microbiologic evaluation of cutaneous wounds in hospitalized dermatology patients. Ostomy Wound Manage 44:40–42, 44, 46.
13. Hamblin MR, O’Donnell DA, Murthy N, Contag CH, Hasan T(2002) Rapid control of wound infections by targeted photodynamic therapy monitored by in vivo bioluminescence imaging. Photochem Photobiol 75:51–57.
14. Merchat M, Bertolini G, Giacomini P, Villanueva A, Jori G(1996) Meso-substituted cationic porphyrins as efficient photosensitizers of gram-positive and gram-negative bacteria.J Photochem Photobiol B 32:153–157.
15. Minnock A, Vernon DI, Schofield J, Griffiths J, Parish JH,Brown ST (1996) Photoinactivation of bacteria. Use of a cationic water-soluble zinc phthalocyanine to photoinactivate both gram-negative and gram-positive bacteria. J PhotochemPhotobiol B 32:159–164.
16. Nitzan Y, Gutterman M, Malik Z, Ehrenberg B (1992) Inactivation of gram-negative bacteria by photosensitized porphyrins. Photochem Photobiol 55:89–96.
17. Maisch T, Bosl C, Szeimies RM, Lehn N, Abels C (2005).Photodynamic effects of novel XF porphyrin derivatives on prokaryotic and eukaryotic cells. Antimicrob Agents Chemother 49:1542–1552.
18. Merchat M, Spikes JD, Bertoloni G, Jori G (1996) Studies on the mechanism of bacteria photosensitization by meso-substitutedcationic porphyrins. J Photochem Photobiol B 35:149–157.
19. Minnock A, Vernon DI, Schofield J, Griffiths J, Parish JH,Brown SB (2000) Mechanism of uptake of a cationic watersoluble pyridinium zinc phthalocyanine across the outer membrane of Escherichia coli. Antimicrob Agents Chemother44:522–527.
20. Segalla A, Borsarelli CD, Braslavsky SE, Spikes JD, Roncucci G, Dei D, Chiti G, Jori G, Reddi E (2002) Photophysical,photochemical and antibacterial photosensitizing properties of a novel octacationic Zn(II)-phthalocyanine. Photochem Photobiol Sci 1:641–648.
21. Maisch T, Szeimies RM, Jori G, Abels C (2004) Antibacterial photodynamic therapy in dermatology. Photochem PhotobiolSci 3:907–917.
22. Malik Z, Faraggi A, Savion N (1992).Ultrastructural damage in photosensitized endothelial cells: dependence on hematoporphyrin delivery pathways. J Photochem Photobiol B 14:359–368.
|Posted on August 31, 2014 at 8:55 PM||comments (4426)|
Laser therapy is usually the last resort for people suffering from back pain. At this present time of writing, many people reach for laser therapy as one of the latest technology revelations that can ease back pain and discomfort with minimal to no side effects. Various researches have proven laser therapy to be both effective and worthy investment. However, when considering laser therapy, always look for a licensed and skilled doctor or therapist. Nonetheless, it is safe to say that low level laser therapy can be used for both a quick fix and a long term solution for chronic back pain.
Back pain:An unrelenting health problem
•Many people from the outside think that people suffering from back pain sometimes exaggerate. The truth is, the pain is very much real and severe, and more often than not, it is chronic, lasting for more than 3 months.
•Living with chronic back pain can be a real challenge, since even the simplest everyday routines seem hard to do and taxing. When faced with patient with chronic back pain, doctors focus on treating the cause of the pain (which can be either an injury or a disease).
•The thinking behind it is that, once the cause is healed, the pain diminishes. What is even more challenging for dealing with chronic back pain is the fact that there are no measures for the level of pain.
•Many times, there is no clear cause of back pain, and patients go from one doctor to another, struggling to identify the culprit of the physical suffering.
Cold laser in action
Benefits of cold laser therapy in treating back pain
Low laser therapy treats back pain in three ways:
(1) it eases pain,
(2) it reduces inflammation, and
(3) it enhances tissue healing.
Light emitted from low laser therapy influences muscles, ligaments and even, bones. In its essence, laser therapy enhances microcirculation; therefore, stimulating red blood cells flowing to the designated area, and there is increase inthe blood flow in that area. Low level laser therapy also stimulates oxygenation in the tissue, and finally, stimulates cytochrome oxidase enzyme, which targets injured cells providing them extra energy for recovery and rejuvenation.
Studies that prove the efficiency of cold laser therapy:
Different studies have shown different results of the effectiveness of laser therapy. The upshot has always been and always, will be pain relief. This has been substantiated by numerous studies including a research conducted by John Zhang and Eric Malisali from Logan University, published in the Journal of Chiropractic Education (vol 23, 2009). The study revealed that laser stimulation on acupuncture points is effective and safe treatment for low back pain. Thirty two people were part of the study, who have reported satisfying results.
Another study that supports laser therapy is the one done by the Department of Animal Clinical Sciences, in cooperation with the College of Veterinary Medicine, and the University of Florida. Their study proved that low level laser therapy encourages ambulation faster than surgery alone. Their study was conducted on dogs. Results showed that the time to achieve a modified Frankel score of 4 was significantly lower in the laser therapy (3-5 days) than in the surgery alone group (14 days).
Moreover, a group of scientists, Felix Adah, Hamed Benghuzzi, Michelle Tucci, Ashraf Ragab, and Neva Greenwald from the University of Mississippi Medical Center conducted a study in 2008. Their subjects were rats, and the intention of the study was to prove the effect of low power laser treatment on a traumatized disc in a rat model. It was disclosed that the group that underwent a laser treatment showed healing and cellular re-organization.
Kennedy-Spaien E.K.S, (2013). The challenge of chronic low back pain. 1st ed. USA: OTR/L.
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Chen Y-J, Wang Y-H, Wang C-Z, Ho M-L, Kuo P-L, et al. (2014) Effect of Low Level Laser Therapy on Chronic Compression of the Dorsal Root Ganglion. PLoS ONE 9(3): e89894. doi:10.1371/journal.pone.0089894
Gina Shaw, (2012). Let There Be Light. 1st ed. USA: American Chiropractic Association.
Felix Adah, Hamed Benghuzzi, Michelle Tucci, Ashraf Ragab, and Neva Greenwald., (2008). EFFECT OF LOW POWER LASER TREATMENT ON A TRAUMATIZED DISC IN A RAT MODEL. University of Mississippi Medical Center. 1 (1), pp.1-10
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Saime Ay & Şebnem Koldaş Doğan & Deniz Evcik, (2010). Is low-level laser therapy effective in acute or chronic low back pain?. Clin Rheumatol. 29 (29), pp.905-910
W. E. Draper, T. A. Schubert, R. M. Clemmons and S. A. Miles, (2012). Low-level laser therapy reduces time to ambulation in dogs after hemilaminectomy: a preliminary study. Journal of Small Animal Practice. 1 (53), pp.465-469
Marienke van Middelkoop • Sidney M. Rubinstein • Ton Kuijpers • Arianne P. Verhagen • Raymond Ostelo • Bart W. Koes • MauritsW. van Tulder, (2010). A systematic review on the effectiveness of physical and rehabilitation interventions for chronic non-specific low back pain. Eur Spine J. 1 (20), pp.19-39
Júlia S. Diniz & Renata Amadei Nicolau & Natália de Melo Ocarino & Fernanda do Carmo Magalhães & Renato Dornas de Oliveira Pereira & Rogéria Serakides, (2009). Effect of low-power gallium-aluminum-arsenium laser therapy