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NSAIDs and Musculoskeletal Treatment: What is the Clinical Evidence?



Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly prescribed for musculoskeletal injuries because the conditions are believed to be inflammatory in nature. However, because inflammation is a necessary component in the healing process, decreasing inflammation may prove counterproductive. Also, many tendon injuries called 'tendinitis' are, in fact, degenerative and not inflammatory conditions. An analysis of the pathophysiology and healing of musculoskeletal injuries questions the use of NSAIDs in many treatment protocols. Because NSAIDs have profound side effects, they should not automatically be the first choice for treating musculoskeletal injuries.
NSAIDs and Musculoskeletal Treatment
What Is the Clinical Evidence?
Steven D. Stovitz, MD
Robert J. Johnson, MD
In Brief: Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly prescribed for musculoskeletal injuries
because the conditions are believed to be inflammatory in nature. However, because inflammation is a necessary
component in the healing process, decreasing inflammation may prove counterproductive. Also, many tendon
injuries called 'tendinitis' are, in fact, degenerative and not inflammatory conditions. An analysis of the
pathophysiology and healing of musculoskeletal injuries questions the use of NSAIDs in many treatment
protocols. Because NSAIDs have profound side effects, they should not automatically be the first choice for
treating musculoskeletal injuries.
Musculoskeletal concerns rank with upper respiratory illness as the most common reason patients seek medical
attention in family practice. [1] Treatment algorithms for musculoskeletal injuries tend to reflexively include the
use of nonaspirin, nonsteroidal anti-inflammatory drugs (NSAIDs). Currently, NSAIDs are among the most
widely prescribed drugs in this country . [2]
Despite the widespread use of NSAIDs, we question their role in many treatment protocols for musculoskeletal
complaints--in particular, the clinical value of their anti-inflammatory properties. Although originally marketed as
the "safe" alternative to aspirin, NSAIDs are known to have serious gastrointestinal toxicity and other side
effects. We review the pathophysiology and healing of musculoskeletal injuries and the clinical evidence regarding
the efficacy of NSAIDs in treating a variety of nonrheumatic musculoskeletal injuries.
Mechanism of Action
NSAIDs are used for their analgesic, anti-inflammatory, and antipyretic properties. Their therapeutic actions are
thought to stem primarily from their ability to block the formation of certain prostaglandins through inhibition of
the cyclooxygenase (COX) enzymes (Figure 1 ). In general, COX-1 catalyzes the production of several
cytoprotective prostaglandins that coat the stomach lining with mucus and aid platelet aggregation, among other
functions. COX-2 catalyzes the conversion of arachidonic acid into the inflammatory prostaglandins that are
involved in three key biological functions: sensitizing skin pain receptors, elevating body temperature through the
hypothalamus, and recruiting inflammatory cells toward injured body parts. (The delineation between COX-1 and
COX-2 enzymes may be more complex, as described in the section on COX-2 inhibitors below.)
In addition to their effects on prostaglandins, NSAIDs exhibit other properties that have uncertain clinical
relevance (eg, inhibition of neutrophil migration, oxidative phosphorylation, and lysosomal enzyme release). [3]
Inflammation and Healing
A major rationale for using NSAIDs in the treatment of musculoskeletal injuries has been their anti-inflammatory
quality. The prev ailing argument is that healthy tissue is not inflamed; therefore, if we stop the inflammation in
an injured tissue, the tissue will be healthy. The problem with this v iewpoint is that, in addition to being a sign of
injury, inflammation is a necessary component of the healing process. As noted by Leadbetter, [4] "inflammation
can occur without healing, but healing cannot occur without inflammation."
Whether the injured tissue is a ligament, tendon, or muscle, the body responds to injury with a sequence of events
that begins with an influx of inflammatory cells and blood. The inflammatory cells remove debris and recruit
cytokines and other growth factors toward the injury site. This inflammatory phase is partly mediated by the
same prostaglandins that are blocked by NSAIDs. In a healthy healing process, a proliferative phase consisting of
a mixture of inflammatory cells and fibroblasts naturally follows the inflammatory phase. The fibroblasts build a
new extracellular matrix and persist into the final phase of repair, the maturation phase, where, if all goes well,
functional tissue is laid down. The key point is that each phase of repair is necessary for the subsequent phase. By
blocking the inflammatory phase, NSAIDs can, at least theoretically, delay the healing of musculoskeletal injuries.
NSAIDs and Musculoskeletal Injuries
NSAIDs are commonly prescribed for the treatment of musculoskeletal complaints such as muscle injuries,
ligament sprains, tendon injuries, low-back pain, and osteoarthritis. However, an examination of the
pathophysiology and healing of such injuries, as well as a remarkable dearth of clinical trials supporting the
efficacy of NSAIDs, raises questions about their use in many treatment protocols.
Muscle injuries. Whether caused by direct trauma or excessive strain, muscle injury is the
most common sports injury. [5] Although NSAIDs are commonly recommended in treatment
protocols, clinical studies documenting their efficacy are notably lacking. We searched MEDLINE
(1966 to 2002) using keywords "anti-inflammatories, nonsteroidal," "NSAIDs," "skeletal muscle," or
(1966 to 2002) using keywords "anti-inflammatories, nonsteroidal," "NSAIDs," "skeletal muscle," or
"athletic injuries" and "randomized controlled trials" and found none involving oral NSAIDs. A recent
review of studies on strains, contusions, and delayed-onset muscle soreness revealed minimal benefit
at best when NSAIDs are compared with placebo. [5]
While some literature [6,7] suggests that NSAIDs may delay the rate of muscle fiber regeneration, the
clinical ramifications of this remain unclear. Clinical outcome studies of muscle injuries are difficult to
conduct because the injuries tend to heal within days without intervention. Many clinicians in our
sports medicine community are turning to short (24- to 48-hour) courses of NSAIDs, hoping to
combine the benefits of pain relief and decreased swelling without affecting the regenerative phases of
healing. Furthermore, several physicians in our community are now advocating the newer COX-2
inhibitors (discussed below) for muscle injuries with the idea that the drugs' lack of platelet inhibition
might further diminish bleeding and swelling in the injured tissue. We are unaware of any studies to
substantiate these claims.
Interestingly, users of anabolic steroids anecdotally report that these drugs--which actually increase
inflammation--hasten the healing of muscle injuries. A recent animal study [8] supports these claims.
If anabolic steroids prove helpful for tissue healing in humans, the medical profession may be faced
with some interesting ethical decisions.
Ligament injuries. Data on the efficacy of NSAIDs in the treatment of ligament sprains is
extremely limited. In 1990, a review by Almekinders [9] found only 15 studies that he felt were
"carried out in a scientifically appropriate manner," and 8 of those focused on a single joint. NSAIDs
were beneficial in half of these single-joint studies (2 of the 6 that examined ankle ligament sprains
and the 2 that focused on knee ligament injuries). In 1995, a clinical review [10] on treatment
modalities for soft-tissue injuries of the ankle stated that "NSAIDs tended to offer significant
improvement in recovery time and sy mptomatic relief over placebo." However, the authors do not
state how the papers were selected for review or assessed for validity. Our own search of MEDLINE
(1966 to 2002) using keywords "anti-inflammatories, nonsteroidal" or "NSAIDs," "ligaments," and
"clinical trials" revealed no studies using oral NSAIDs in the outpatient setting. A 1997 study [11] of
364 Australian army recruits who had ankle sprains showed that the group given NSAIDs returned to
activity sooner, but had increased instability and decreased range of motion, compared with those
given placebo.
The study of ligament sprains is limited, because sprains tend to heal with time and because the
outcomes are subjective and favor NSAIDs, which are excellent analgesics. Controlled mobilization of
injured ligaments assists healing, [1 2] and, in this context, if NSAIDs decrease pain and thus
encourage activity, they may provide some therapeutic benefit. It is unknown whether a similar effect
could be obtained with other analgesics, including simply ice.
Tendon injuries. When it comes to tendinitis, the use of NSAIDs as anti-inflammatory agents
becomes especially controversial. Contrary to what their name implies (the suffix "itis" denotes an
inflammatory process), these injuries may not be inflammatory in nature. Indeed, several experts in
this area have pointed out this misnomer and emphasized its unfortunate effect of furthering a false
perception that an anti-inflammatory medicine should be used in treatment. [13-1 5]
Several large studies [14,16,17] have looked at tissue biopsies from chronic injuries of the extensor
carpi radialis brevis ("tennis elbow"), Achilles, patellar, and rotator cuff tendons. Results show the
tendons to be degenerative and lacking in inflammatory cells. Thus, a more proper term would be
either "tendinosis," meaning tendon degeneration, or "tendinopathy," signifying nonspecific tendon
pathology. Some have argued that a poor inflammatory process is the precipitant that causes tendon
degeneration. [13,16]
Controlled trials of NSAID use have not resolved this issue. A review [1 5] of MEDLINE from 1 966 to
1996 found only 9 prospective studies comparing NSAIDs with placebo. The review noted that
NSAIDs provided better pain relief in 5 of the 9 studies. This result is hardly unexpected, given the
potent analgesic effect of NSAIDs. The maximum study follow-up was only 1 to 4 weeks; therefore,
the long-term effect of NSAIDs on these tendons is unknown.
Low-Back Pain and Osteoarthritis
NSAIDs are frequently used to treat common musculoskeletal conditions, such as low-back pain and
osteoarthritis, though they are not classically sports-related injuries.
Low-back pain. The study of treatments for low-back pain is limited by its multiple and poorly
understood causes. Two large meta-analyses [18,19] were recently conducted, including a Cochrane
review in 2000. Both searched MEDLINE for literature from the 1960s to the 1990s; the Cochrane
study [19] also included Embase studies from 1988 to 1998. Both found very few well-designed trials,
and those that were found had small numbers of patients. T here were some subtle differences in the
reviews, but overall their methods and conclusions were similar.
Koes et al [18] found 1 0 acceptable trials comparing NSAIDs with placebo and concluded that NSAIDs
"might be effective for short-term sy mptomatic relief in patients with uncomplicated low-back pain."
The Cochrane review [19] identified 11 controlled studies of adequate design and concluded that there
is "conflicting evidence that NSAIDs provide better pain relief than placebo for acute low-back pain."
The Cochrane review found 5 "acceptable" studies comparing NSAID efficacy to that of
acetaminophen and only 1 that was considered "high quality." This high-quality study included only
30 patients. It concluded that there is, at best, level 3 (ie, conflicting or limited) ev idence that NSAIDs
are more effective than acetaminophen for acute or chronic low-back pain.
Osteoarthritis. Eighty percent of individuals older than 65 have radiographic signs of
osteoarthritis (OA), and a large percentage have sy mptoms. [20] Given the chronic nature of the
disease and the high incidence of medication side effects in the elderly, an understanding of the risks
and benefits of NSAIDs in treating OA is crucial. T he two main issues are pain relief and disease
In reviews of clinical trials on OA of the hip and knee, NSAIDs perform significantly better as
analgesics compared with placebo. [21,22] Most studies comparing different NSAIDs have found no
significant difference in their analgesic effects and provide no strong basis for recommending one
NSAID over another. A recent randomized controlled trial [23] comparing NSAIDs with
acetaminophen found a significant benefit in using NSAIDs for moderate-to-sev ere OA. Previously,
only two studies on OA had compared an NSAID with acetaminophen; neither supported a benefit for
either medication. Given that the adverse effects of NSAIDs (see below) tend to disproportionately
strike the elderly (hence, sufferers of OA), numerous guidelines, including those put forth by the
American College of Rheumatology, recommend trying acetaminophen before an NSAID. [24-26] An
increasing number of small trials are being conducted that compare glucosamine and chondroitin
sulfate with NSAIDs. The emerging evidence suggests a trend whereby pain relief during the first 4
weeks is superior with an NSAID, but then plateaus after 1 month. [27,28]
Whether NSAIDs hasten, attenuate, or have no effect on the progression of OA is unknown. In vitro
studies are beginning to show evidence that certain NSAIDs stimulate the synthesis of
glycosaminoglycan, whereas others either have no effect or degrade it. [29,30] Given this variation in
response among NSAIDs, their effects on articular cartilage are likely mediated by a mechanism other
than prostaglandin inhibition. If certain NSAIDs prove beneficial to articular cartilage while others
prove harmful, future treatment recommendations could change dramatically.
Weighing Side Effects
Although strong and consistent evidence is lacking that NSAIDs clinically benefit the healing of musculoskeletal
injuries, they remain potent pain relievers. Their use in this capacity, however, is limited by notable side effects;
gastrointestinal (GI) effects are the most common and serious.
GI bleeding secondary to NSAID use is the 15th leading cause of death in the United States. [31] Unfortunately,
dyspepsia cannot be used as a screening criterion, because only 40% of those who have NSAID-induced GI
bleeding report abdominal symptoms before the bleed. [32] T his might be due to their analgesic effects. Perhaps
as a result of their inhibition of platelet aggregation, individuals who have GI bleeding while taking NSAIDs have a
as a result of their inhibition of platelet aggregation, individuals who have GI bleeding while taking NSAIDs have a
significantly higher mortality than those with GI bleeds who are not taking NSAIDs. [32]
The renal and cardiovascular systems are also affected, because prostaglandins are necessary for renal blood flow
and the secretion of sodium and chloride. Prostaglandin inhibition has been shown to raise mean arterial blood
pressure by an av erage of 3 to 5 mm Hg, a small but potentially harmful amount. [33] Endurance athletes are
often hypohydrated as a consequence of prolonged training. NSAIDs can superimpose further decreases in renal
blood flow through prostaglandin inhibition. T his combination has been implicated in case reports of acute renal
failure in marathoners. [34,35] NSAIDs have historically been perceived to be either neutral or beneficial
regarding cardiovascular occlusive events. However, a recent study [36] suggests that the drugs' temporary
platelet inhibition may limit the cardioprotective effects of aspirin by antagonizing aspirin's irreversible platelet
Another potential complication for athletes involves the respiratory system. Blocking cyclooxygenase can shunt
arachidonic acid toward the formation of the bronchoconstricting leukotrienes (see figure 1 ). It is estimated that
10% of patients who have asthma experience a decline in their respiratory function as a result of NSAID inhibition
of cyclooxygenase. [37]
COX-2 Inhibitors
The new COX-2 inhibitors are being marketed as the safe alternative to other NSAIDs. Given the recent entry of
COX-2 inhibitors into the market, little is known about their in vivo effects (either intended or adverse). Data
from clinical trials suggest that their analgesic effects are similar to traditional NSAIDs. [38]
As their name implies, the COX-2 inhibitors preferentially block the COX-2 enzyme while allowing the pathways
catalyzed by COX-1 to proceed. Theoretically, this inhibits the formation of the inflammatory prostaglandins
while allowing the production of the homeostatic prostaglandins. Unfortunately, as Oscar Wilde said, "the pure
and simple truth is rarely pure and never simple." [39] In fact, increasing evidence indicates that the COX-2
enzyme also has some homeostatic functions.
Breyer and Harris [40] suggest that the COX-2 enzyme plays an integral role in kidney function and will likely
affect blood pressure to an ex tent similar to traditional NSAIDs. COX-2 inhibitors seem to cause fewer new GI
ulcers, although this has not been definitively shown to decrease the number of complications from GI bleeds.
[41] Interestingly, this might be because the inflammatory pathway is necessary for healing preexisting ulcers.
A concern is that selective inhibition of antithrombotic prostaglandins might increase cardiovascular ev ents.
Patients receiving rofecoxib during the VIGOR study [42] suffered cardiovascular events at a higher rate than
those in the naproxy n group. This prompted a meta-analysis of trials with COX-2 inhibitors [43] to state that
"the available data raise a cautionary flag about the risk of cardiovascular events with COX-2 inhibitors." A more
recent analysis [44] suggests that the increased rate of cardiovascular ev ents noted above was actually due to a
cardioprotective effect of naproxen and not to increased events in the rofecoxib group.
The expense of COX-2 inhibitors is another major concern; treatment can cost as much as $70 or more than
generic NSAIDs per month. [45] Certainly, if this decreases other medical costs, this might prove beneficial.
Finally, given their inhibition of the inflammatory pathway, all of the concerns regarding delayed healing of
injured tissues remain the same when using COX-2 inhibitors.
Clarifying the Role of NSAIDs
Reviewing the most current updates on the use of NSAIDs in the treatment of musculoskeletal injuries is
challenging. Although we mention randomized controlled trials, or lack thereof, this review is not intended to be a
meta-analysis. Any attempt at a meta-analysis on this topic would be fraught with either a tremendous lack of
data (if stringent criteria were used) or controversy (if criteria were loosened).
Given the paucity of data, we are unable to draw any definitive conclusion in support of or against the use of
NSAIDs. We realize that many clinicians use anti-inflammatories for musculoskeletal conditions so routinely that
NSAIDs. We realize that many clinicians use anti-inflammatories for musculoskeletal conditions so routinely that
any suggestion that little evidence supports their use is interpreted as a condemnation. This discussion is meant
to clarify, not simply diminish, the role of NSAIDs. To effectively treat musculoskeletal injuries, the clinician must
have realistic expectations about the capabilities of NSAIDs and convey them to the patient. NSAIDs are rarely a
substitute for rehabilitation and activity modification.
When used properly, NSAIDs can be a useful, but limited, adjunct. T hey certainly play a key therapeutic role in
the treatment of the crystalline and rheumatoid arthritides and may be beneficial in treating pathologic edema of
bursa and synovial tissue (eg, tenosynovitis). For most common sprains, strains, and overuse injuries, however,
their therapeutic properties are unproven. It is crucial to keep a proper perspective regarding the role of NSAIDs,
especially given their risk of side effects and their potential to blunt the normal healing response. Too many
physicians and patients view NSAIDs as critical to recovery. Additional research is needed to define more
explicitly the role of NSAIDs in interfering with or delaying healing and the role of other, potentially safer, means
to control the pain of musculoskeletal injuries.
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The authors thank Anne Marie Weber-Main, PhD, for her editorial assistance with this manuscript.
Dr Stovitz is an assistant professor and coordinator of sports medicine education in the department of family
practice and community health at the University of Minnesota in Minneapolis. Dr Johnson is the director of
primary care sports medicine in the department of family practice at Hennepin County Medical Center in
Minneapolis and is president of the American Medical Society for Sports Medicine. Address correspondence
to Steven D. Stovitz, MD, Smiley's Clinic, 2615 E Franklin Ave, Minneapolis, MN 55406; e-mail to
Disclosure information: Drs Stovitz and Johnson disclose no significant relationship with any manufacturer of
any commercial product mentioned in this article. No drug is mentioned in this article for an unlabeled use.
... Common brand names of NSAIDs include Ibuprofen, Motrin, Aleve, or Advil. However, it is important to note that the use of NSAIDs will not accelerate, and may actually delay, the recovery process (44). NSAIDs inhibit the synthesis of prostaglandins, which initiate inflammation (44). ...
... However, it is important to note that the use of NSAIDs will not accelerate, and may actually delay, the recovery process (44). NSAIDs inhibit the synthesis of prostaglandins, which initiate inflammation (44). Campbell (6) suggests Tylenol as an alternative, as it is not an NSAID and will not disrupt the inflammatory process. ...
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... Similar findings have been demonstrated when NSAIDs were compared to opioids for management of post-fracture pain in children. 23 A 2016 review demonstrated that the analgesic effects of NSAIDs were equivalently efficacious as opioids when treating musculoskeletal pain. 24 In addition, studies have demonstrated that ...
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... The use of NSAIDs in acute musculoskeletal injuries has become more controversial as it can hinder the natural process of healing [61,71,72]. In ankle sprain, the clinician must weight on the benefits and risks of using NSAIDs and consider if the goal can be obtained with other type of medicine or modality [72]. ...
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Purpose of the Review Ankle sprains are one of the most common sports injuries, resulting in sequelae that can ultimately affect function, return to play, and increase the risk of re-injury. This narrative review analyzes the scientific literature regarding acute ankle sprains in the athletic population and provides an overview of the clinical management as well as secondary prevention of this injury. Recent Findings A detailed clinical assessment is necessary to confirm diagnosis, establish the severity of the sprain, and document associated injuries. The rehabilitation program can include functional and early mobilization, manual therapy, and cryotherapy followed by a progression of strengthening, sports-specific exercises, and plyometrics. Topical and oral NSAIDs can be helpful in pain control. Return to sports should be a shared decision, encompassing both subjective and objective measures. Secondary preventive strategies should be incorporated in the treatment protocol as recurrence of this injury is common. Summary Ankle sprains are frequently seen by clinicians who care for athletes with sports injuries, particularly in the sideline and training room settings. These clinicians should be acquainted with the treatment and prevention of this condition.
... 8,9 NSAIDs are commonly prescribed for the treatment of musculoskeletal complaints such as muscle injuries, ligament sprains, tendon injuries, low-back pain. 10 additionally, "prophylactic use" of analgesics by the athletes is also prevalent. 11 Among Italian professional soccer players, the prevalence of using NSAIDs in a year was as high as 92.6%, 12 while more than half of the players used ...
Background: Although the high prevalence of analgesic use in various sports disciplines is well-known, it has not been reported among Olympic-style weightlifters yet. We aimed to determine; (1) the frequency of the nonsteroidal anti-inflammatory drugs (NSAIDs) and paracetamol use in elite-level Olympic-style weightlifters, (2) weightlifters' attitudes towards NSAIDs and paracetamol use, and (3) the total daily, weekly and monthly doses of NSAIDs and paracetamol. Methods: A total of 166 (46 female, 120 male) Olympic-style weightlifters enrolled for this study. Data was collected through an interviewer-administered questionnaire distributed during national championships. The Assessment of Spondyloarthritis International Society-NSAID equivalent score, total doses of acetylsalicylic acid and paracetamol were calculated daily, weekly, and monthly. Results: The mean age of participants was 18.9 ± 4.7 years. Only 11.4% of athletes stated that they used the drug only when the physician prescribed it. More than half of the athletes (57.2%) stated that they used at least one of the analgesics the day before the competition day. The most common form reported by the athletes was the concomitant use of medications (31.3%). The mean total acetylsalicylic acid, NSAID and paracetamol doses of 95 athletes using analgesics were daily: 500.0 ± 95.0 mg / 105.0 ± 71.4 mg / 555.6±160.1 mg, weekly: 1166.0 ± 899.4 mg / 145.2 ± 176.6 mg / 1166.7 ± 892.8 mg, and monthly: 3461.1 ± 4940.7 mg / 201.5 ± 274.0 mg / 2750.0 ± 3841.9 mg, respectively. Conclusions: The frequency of analgesic and anti-inflammatory medication use among the elite-level Olympic-style weightlifters is very high.
Background: The early identification of factors that increase risk of poor recovery from acute low back pain (LBP) is critical to prevent the transition to chronicity. Although most studies of risk factors for poor outcome in LBP tend to investigate the condition once it is already persistent, there is evidence to suggest that this differs from risk factors measured during the early-acute stage. This study aimed to identify early risk factors for poor outcome in the short- and long-term in individuals with acute LBP, and to compare this with factors identified at 3 months in the same cohort. Methods: One hundred and thirty-three individuals were recruited within 2 weeks of an acute LBP episode and completed questionnaires related to their sociodemographic, psychological, clinical and history/treatment status at baseline and 3 months later, and their pain-level fortnightly for 12 months. Results: Of the 133 participants recruited, follow-up data was provided by 120 at 3 months, 97 at 6 months, 85 at 9 months and 94 at 12 months. Linear regression identified various factors at baseline (acute phase) and 3 months later that predicted short- and long-term outcome (pain level, change in pain). Key findings were that: (1) depressive symptoms at baseline most consistently predicted worse outcome; (2) psychological factors in general at 3 months were more predictive of outcome than when measured at baseline; (3) early health care utilisation predicted better outcome, whereas use of pain medication later (3 months) predicted worse outcome; and (4) sex and BMI predicted outcome inconsistently over 12-months. Conclusions: The results highlight the multidimensional nature of risk factors for poor outcome in LBP and the need to consider time variation in these factors.
Ankle sprains are among the most frequent injuries related to sports participation. The practice of sports has been rising in both genders and all ages, at any level of competition. As awareness of patient-related and non patient-related risk factors is essential in defining the best approach regarding diagnostics, treatment, and the risk of potential concomitant injury, this chapter outlines the current concepts for ankle sprains.
Acute ankle sprain is the most common lower limb injury in athletes and accounts for 16%-40% of all sports-related injuries. It is especially common in basketball, American football, and soccer. The majority of sprains affect the lateral ligaments, particularly the anterior talofibular ligament. Despite its high prevalence, a high proportion of patients experience persistent residual symptoms and injury recurrence. A detailed history and proper physical examination are diagnostic cornerstones. Imaging is not indicated for the majority of ankle sprain cases and should be requested according to the Ottawa ankle rules. Several interventions have been recommended in the management of acute ankle sprains including rest, ice, compression, and elevation, analgesic and anti-inflammatory medications, bracing and immobilization, early weight-bearing and walking aids, foot orthoses, manual therapy, exercise therapy, electrophysical modalities and surgery (only in selected refractory cases). Among these interventions, exercise and bracing have been recommended with a higher level of evidence and should be incorporated in the rehabilitation process. An exercise program should be comprehensive and progressive including the range of motion, stretching, strengthening, neuromuscular, proprioceptive, and sport-specific exercises. Decision-making regarding return to the sport in athletes may be challenging and a sports physician should determine this based on the self-reported variables, manual tests for stability, and functional performance testing. There are some common myths and mistakes in the management of ankle sprains, which all clinicians should be aware of and avoid. These include excessive imaging, unwarranted non-weight-bearing, unjustified immobilization, delay in functional movements, and inadequate rehabilitation. The application of an evidence-based algorithmic approach considering the individual characteristics is helpful and should be recommended.
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A Abstract clinical study was carried out to scientifically validate the analgesic effect and safety of Unani pharmacopoeial formulations Ùabb-i-Süranjän and Rawghan-i-Süranjän in the patients of Waja' al-Mafäñil (Joint Pain) at Regional Research Institute of Unani Medicine (RRIUM), Bhadrak (Odisha) during 2013-2014. All the cases (49) registered for the study completed the trial. After 14 days of treatment, the symptoms of the disease, like joint pain, tenderness, swelling and restriction of movements were found decreased by 64.70%, 47.83%, 50% and 50% respectively as compared to the baseline. The variations in the values of liver function tests and kidney function tests before and after the treatment were found within normal limits. The study drugs were found well-tolerated and no adverse reaction was observed during the study. The study findings confirm the safety and efficacy of Unani pharmacopoeial formulations in the treatment of Waja' al-Mafäñil (Joint Pain).
Conference Paper
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HASTANE ÖNCESİ ALANDA RESÜSİTASYON UYGULAMALARI Giriş Kazalar ve acil durumlar ani gelişen olaylar olup can ve mal kayıplarına yol açabilirler. Acil durumlarda olayın en az zararla atlatılması büyük önem arz etmektedir. Bu noktadan hareketle hastane öncesi alanda olayları yönetebilmenin oldukça zor olduğu düşünülmektedir. Özellikle kardiyak arrest olguları sistematik yaklaşımı beraberinde gerektiren durumlardır. Arrest olgularının başarılı bir şekilde yönetilebilmesi için acil olgu yönetim basamaklarının uygulayıcılar tarafından iyi bilinmesi ve uygulanması gerekmektedir. Acil olgu yönetimi; acil sağlık hizmeti gereksinimine ihtiyaç duyan hastaların yaşamsal fonksiyonlarının devam ettirilmesi, durumun daha kötüye gitmesinin önlenmesi, acil girişim uygulamalarının başlatılması ve hastaların ilgili sağlık kuruluşuna transportunu içeren amaçlar doğrultusunda, ekip liderinin koordinasyonunda, acil sağlık hizmeti sunan ekiplerce, ekip bazlı yürütülen çalışmalar bütünüdür. Acil olgu yönetimi ön hazırlık gerektiren ve süreklilik arz eden bir süreçtir. Acil olgu yönetiminin basamakları aşağıda verilmiştir:  Olay yeri güvenliği,  İletişim ve onam alma,  Ekip ve malzeme yerleşimi,  Birincil değerlendirme,  İkincil değerlendirme (tam muayene, vital parametre izlenimi, tıbbi öykü),  Tanılama,  Tedavi,  Yeniden değerlendirme,  Nakil ve teslimdir. Olay yeri güvenliği; olay yerine ulaşıldığında öncelikli olarak olay yeri güvenliği sağlanmalıdır. Olay yeri hızlı bir şekilde değerlendirilmeli ve tehlikeler belirlenmelidir. Olay yerinin güvenliği sağlandıktan sonra yaralıla¬rın/ kazazedelerin sayısı belirlenmeli, hastalar öncelik sırasına göre kategorize edilmeli ve uy¬gulanacak girişimler bir plan dahilinde gerçek¬leştirilmelidir. İletişim ve onam alma; olay yerine ulaşıldığında ekip lideri kendisini ve ekibini hızlı şekilde tanıtır. Fakat arrest olgularında tanıtım işlemi hasta yakınlarını gerginliğe sürükleyebileceği için öncelikli olarak vakaya müdahale edilmelidir. Bu davranış doğrudan iletişim kanallarının açılmasına yol açabileceği için olayın yönetilmesi daha da kolaylaşabilir. Olay yerinde hastayı veya hasta yakınlarını suçlayıcı davranışlardan kaçınılmalıdır. Ekip ve malzeme yerleşimi; olgunun niteliğine göre ekip yerleşiminde minimal düzeyde modifikasyonlar yapılabilmektedir. Hastanın bilinci açık ve olay yeri uygunsa ekip lideri, hastanın sağ yanından yaklaşarak birincil ve ikinci değerlendirmeyi gerçekleştirir. Ekibin diğer üyeleri ise vital parametreleri alabilecek ve tedavi protokolünü rahat gerçekleştirebilecekleri şekilde yerleşirler. Hastanın bilincinin kapalı veya hastayla iletişimin sağlanamadığı durumlarda ekip lideri hastanın baş tarafında yer alabilir. Fakat ekip lideri gerekli durumlarda yer değişikliğine gidebilir. Medikal vakalarda ekip malzeme yerleşimi ile arrest vakalarında ekip malzeme yerleşimi Şekil 1.’de ve Şekil 2.’de verilmiştir. Şekil 1. Medikal Vakalarda Ekip Üyeleri ve Malzeme Yerleşimi (20) Şekil 2. Arrest Vakalarında Ekip Üyeleri ve Malzeme Yerleşimi (20) Ekip çalışmasının önemi Ekip oluşumu, örgütsel stratejiyi geliştirmek için çok iyi bir yoldur. Bireyler başarı için genellikle ekip bazlı yapıları benimsemektedir. Ancak bireylerin örgütsel karar vermeyi yavaşlatan fazla hiyerarşili yapıları ise tercih etmedikleri görül¬mektedir. Ekip çalışmasının avantajlarına ilişkin görüşlerden bazıları aşağıda sunulmuştur:  Görev dağılımının net şekilde yapılmış olması ve ekip liderinin kardiyopulmoner resüsitasyon uygulamasını (KPR) etkili yönetmesi başarıyı artırır.  Ekip liderinin yönlendirmesi ile birlikte KPR uygulamalarındaki standart görevler daha kısa sürede ve doğru zamanda gerçekleştirilir (örneğin, entübasyon uygulama süresi daha kısadır).  Ekibin deneyimli olması zamanın etkili kullanılmasını sağlar.  Esnek, uyarlanabilir, koordine edilmiş dinamik ekiplerin, resüsitasyon uygulamasındaki standart görevlerini doğru zamanda, daha az hatayla ve daha hızlı gerçekleştirdiği bilinmektedir. Birincil değerlendirme; birincil değerlendirme; her hasta/yaralı için hızlı ve tekrarlanabilir bir fiziki muayene yaparak, ya¬şamı tehdit eden durumları teşhis ve tedavi etmek için tasarlanmıştır. Birincil değerlendirmede ABCDE yaklaşımı uygulanır. Uygulama basamaklarına ilişkin veriler aşağıdaki şekildedir: Airway (A) : Havayolu açıklığının değerlendirilmesi ve sağlan¬ması, Breathing (B) : Solunumun değerlendirilmesi ve sağlanması, Circulation (C) : Dolaşımın değerlendirilmesi ve sağlanması, Disability (D) : Nörolojik durumun değerlendirilmesi, Exposure (E) : Hastanın tamamen soyul¬masıdır. İkincil değerlendirme; birincil değerlendirmeden sonra hasta/ yaralının baştan aşağıya detaylı şekilde değerlendirilmesi esasına dayanır. İkincil değerlendirmenin amacı, yaralanmaları tam olarak belirlemek ve gizil problemleri ortaya çıkarmaktır. İkincil değerlendirmenin aşamaları “Hasta/ yaralının öyküsünü alma, vital bulguları alma ve baş¬tan aşağı muayene” basamaklarını içerir. Tanılama; yapılan değerlendirmeler sonucunda (birincil ve ikincil değerlendirme) elde edilen verilere göre ön tanı veya ta¬nılama işlemi gerçekleştirilir. Ekibin lideri hekim ise tanılamaya gidilir. Ekip içinde hekim yok ise danışman hekim yönlendirmesiyle ön tanı-lamaya ve tanı önerisine gidilebilir. Yapılan de¬ğerlendirmeler ve planlamalar sonucunda uygun tedavi akış şeması uygulanabilir. Tedavi; yapılan değerlendirmelere ve belirlenen tanıya göre Sağlık Bakanlığı’nın belirlemiş olduğu tedavi akış şemalarına göre uygun tedavi protokolü uygulanabilir. Ancak çocuk hastalarda dikkat edilmesi gereken önemli noktalar; çocuğun yaş grubuna, özelliklerine ve klinik tablosuna göre ilaç dozlarının uygun şekilde hesaplanması ve uygulanmasıdır. Yeniden değerlendirme; bu basamakta tedavinin sonuçları değerlendirilir. İlk aşamada ertelenen işlemlerinin tamamlanması ve uygulanan müdahalelerin stabilizasyonu sağlanır. Nakil ve teslim; gerekli uygulamalar yapıldıktan sonra Komuta Kontrol Merkezi (KKM) ile iletişime geçilerek uy¬gun hastaneye nakil sağlanır. Olay yerinde, ambulansta yapılan uygulamalar ve girişimler sözel ve yazılı olarak teslim alan sağlık ekibine aktarılır. Yapılan her işlem yazınsal olarak kayıt altına alınmalıdır. Arrest Ritimlerini Tanıma ve Yönetim Hastane öncesi alanda hasta/ yaralıların ri¬timlerinin doğru ve hızlı tanınması ile uygun tedavi algoritmalarının uygulanması mortalite açısından oldukça önemlidir. Alanda karşılaşılabilecek ölümcül ritimler 4 adet olup bunlar “şoklanabilir ve şoklanamaz” ritimler olarak iki grupta toplanır. Şoklanamaz ritimler “asistoli ve nabızsız elekt¬riksel aktivite (NEA)” olarak ikiye ayrılır. Şoklanabilir ritimler “ventriküler fibrilasyon (VF) ve nabızsız ventriküler taşikardi (nVT)” olarak ikiye ayrılır. Kardiyak arrestten sonra sağ kalımı iyileştirmeye katkıda bulunan tartışma götürmeyen uygulamalar olayı görenlerin uyguladığı hızlı ve etkili temel yaşam desteği, kesintisiz yüksek kaliteli göğüs basıları ve VF/nVT için erken defibrilasyondur. Yapılan çalışmalar Adrenalin kullanımının ROSC’u artırdığını göstermiştir. Ayrıca uzun dönem nörolojik sağ kalımı kötüleştirebileceğine dair bir olasılığın olduğu da bilinmektedir. Benzer şekilde ileri yaşam desteği (İYD) uygulaması sırasında ileri havayolu uygulamalarının kullanımını destekleyen kanıtlar halen kısıtlıdır. Bu nedenle her ne kadar ilaçlar ve ileri havayolu uygulamaları İYD uygulamalarının içine dahil edilseler de, erken defibrilasyon ve yüksek kaliteli göğüs basıları karşısında önemlilikleri ikinci sıradadır. Yetişkin ileri yaşam desteği algoritması Şekil 3.’de verilmiştir. Şekil 3. Yetişkin İleri Yaşam Desteği Algoritması (3, 21) Adrenalin Uygulaması Adrenalin uygulaması günümüz koşullarında İYD algoritmalarının temel ilaçları arasında yerini korumaktadır. Adrenalin uygulamasına ilişkin bazı bilgiler aşağıda verilmiştir:  Herhangi bir nedenle kardiyak arrestte ilk tercih edilen ilaçtır: İYD algoritmasında her 3- 5 dakikada bir kullanılır.  Anafilaksi tedavisinde tercih edilir.  Kardiyojenik şokta ikinci basamak tedavidir.  KPR sırasında doz: Kardiyak arrest sırasında adrenalinin başlangıç intravenöz (IV)/ intraosseoz (IO) dozu 1 mg’dir.  Dirençli kardiyak arrestlerde yüksek doz adrenalin ile sağkalımda veya nörolojik seyirde iyileşme olduğunu gösteren herhangi bir çalışma yoktur.  ROSC’u takiben adrenalinin düşük dozları bile (50- 100 μgr) taşikardi, miyokard iskemisi, VT ve VF’yi tetikleyebilir.  Perfüzyon ritmi sağlandıktan sonra eğer daha fazla adrenalin gerekli görülüyorsa uygun kan basıncını sağlayabilmek için doz dikkatlice titre edilir.  Çoğu hipotansif hasta için genellikle 50μgr IV doz yeterlidir. Antiaritmik Uygulaması Vazopressörlerde olduğu gibi antiaritmik ilaçların kardiyak arrestlerde yararı sınırlıdır. İnsanlarda uzun dönem seyir verilerinin yokluğuna rağmen kanıtlardaki denge kardiyak arrestte aritmi yönetiminde antiaritmik ilaçların kullanımı yönündedir. Amiodaron; Amiodaron, atriyal ve ventriküler miyokardda aksiyon potansiyeli ve refrakter periyodun süresini artıran membran stabilize edici bir antiaritmik ilaçtır. Amiodaronun orta derecede negatif inotrop etkisi vardır. Yarışmasız alfa bloker etkisi ile periferal vazodilatasyona neden olur. İntravenöz amiodaron ile oluşan hipotansiyon uygulama hızına ve daha çok da ilacın kendisinden çok histamin salınımına neden olan çözücüye bağlıdır (polisorbat 80 ve benzil alkol). Şoklanabilir ritimlerde 3. şoktan sonra 300 mg Amiodaron 300 mg (20ml %5 Dekstroz ile sulandırılarak) bolus şeklinde verilir. 5. şok¬tan sonra ise 150 mg olacak şekilde uygulanır. Çocuklarda Uygulama; şoklanabilir ritim algoritmasına göre 3. ve 5. şoklardan sonra uygulanır. Doz: 5 mg/kg’dir. Tekrar edilmesi gerekiyorsa 5. Şoktan sonra 5 mg/kg’dir. Max. Doz 15 mg/kg’dir. En yüksek tek doz 300 mg’dır. En yüksek toplam doz 15mg/kg olacak şekilde gerektiğinde 5mg/kg doz, iki kere tekrarlanabilir. Lidokain Uygulaması; İYD sırasında amiodaronun olmadığı durumlarda kullanımı önerilir. Lidokain miyozit refrakter periyodunu artırarak etki gösteren bir membran stabilize edici antiaritmiktir. Ventriküler otomatisiteyi azaltır ve lokal anestezik etkisi ventriküler ektopik aktiviteyi baskılar. Lidokain normal dokuların elektriksel aktivitelerini minimal etkilerken depolarize, aritmojenik dokuların aktivitesini baskılar. Bu nedenle lidokain depolarizasyonla ilişkili aritmileri (ör, iskemi, dijital toksisitesi) baskılamada etkilidir, ama normal polarize hücrelerde oluşan aritmilerde (ör, atriyal fibrilasyon/ flutter) nispeten etkisizdir. Endikasyonları: Lidokain dirençli VF/ nVT’de endikedir (amiodaronun mevcut olmadığı durumlarda). Dozu: Amiodaronun olmadığı durumlarda üç şoka dirençli VF/ nVT’de başlangıçta 100mg (1- 1.5mg/kg) lidokain düşünülür. Eğer gerekliyse ek olarak 50mg bolus daha verilir. Toplam doz ilk 1 saat içinde 3mg’yi geçmemelidir. Çocuklarda İleri Yaşam Desteği Çocuklarda acil olgu yönetim ba¬samakları standart planını korumuş olsa da uygulamada bir takım farklılıkların olduğu gö¬rülmektedir. Çocuk ve bebeklerin anatomik/ fizyolojik durumu, yapılan uygulamaların mo¬difiye edilmesine yol açmaktadır. Çocuklarda “Şoklanamaz ve Şoklanabilir” ritimlerin tedavi algoritması Şekil 4’de ve Şekil 5.’de verilmiştir. Şekil 4. Şoklanamaz Ritimlerin Yönetimi (3) Şekil 5. Şoklanabilir Ritimlerin Yönetimi (3) KPR Sırasında Mekanik Kompresyon Cihazlarının Kullanımı Temel ve İleri Kardiyak Yaşam Desteğine ilişkin yapılan çalışmaların ana hedefi, kaliteli Kardi¬yopulmoner Resüsitasyon (KPR) işlemininin gerçekleştirilmesi ve sağlıklı sağ kalım oranı¬nın artırılmasıdır. Fakat bazı durumlarda temel ve ileri yaşam desteği uygulamalarında göğüs kompresyon uygulamasının etkin şekilde gerçekleştirilemeyeceği öngörülmektedir. Bu durumlarda mekanik kompresyon cihaz kullanımının faydalı olacağı düşünülmektedir. Yapılan çalışmalar mekanik kompresyon cihazlarının rutin olarak manuel göğüs kompresyonlarının yerini almaması gerektiğini önermektedir. Fakat zorunlu hallerde kullanımın faydalı olabileceğini önermektedirler. Uzun süreli KPR uygulaması, personel yetersizliği, yorgunluk ve hareketli ambulans ortamı göz önüne alındığında me¬kanik kompresyon cihazlarının hastane öncesi alanda da kullanılmasının mantıklı olacağı dü-şünülmektedir (zorunlu hallerde). Hipotermi Durumlarında Kardiyak Arrest Oluşan hipotermik durumda düşük vücut sıcaklığı beyinde 10 kata kadar daha uzun süre koruyucu etki gösterdiği için uzamış KPR’ye yanıt ihtimali çok daha yüksektir. Bu nedenle resüsitasyona, vücut sıcaklığı normal seviyeye gelene kadar devam edilmelidir. KPR esnasında ısıtma uygulamaları devam etmelidir. Uygulama esnasında tüm sıvılar ve O2 ısıtılarak kullanılmalıdır. Nabız kontrolü için ana arterler kullanılmalı ve mümkünse atım olmadığına karar verilmeden önce, 1 dakika süreyle EKG ve yaşam belirtileri değerlendirilmelidir. Nabız yokluğunda, hemen göğüs kompresyonlarına başlanılmalıdır. İlaçlar, mümkünse santral veya geniş proksimal venlerden verilmelidir. Vücut ısısının 30 derecenin altında olduğu durumlarda ilaç uygulaması yapılmamalıdır. Vücut ısısı 30-35 derece arasında ilaçlar ya düşük dozlarda uygulanmalı, ya da uygulamalar arasındaki süre (2 kat) daha uzun tutulmalıdır. 35 derecenin üstündeki vücut sıcaklıklarında standart İYD yaklaşımı uygulanmalıdır. Vücut sıcaklığı ölçümünde rektal, tympanic ya da oral yol tercih edilmelidir ve sürekli aynı metotla ölçülmelidir. Gebelik Durumlarında Resüsitasyon Sağlık personelleri gebelik ile ilişkili resüsitasyon çalışmalarında iki potansiyel hasta grubu ile karşı karşıya kalmaktadır. Yapılacak uygulamalar gebelik haftasına göre, sadece anneye, anne ve fetüse veya sadece fetüse yö¬nelik yapılabilmektedir. Bu durumlar göz önüne alındığında bakım standartlarını ilgilendiren bazı durumlar aşağıda verilmiştir: Kritik olarak gebe hastalarda bakım standartları;  İnferior vena cava’nın basısını engellemek için gebe, tam sol yana yatırılır veya elle uterus sola kaydırılır.  %100 oksijen verilir; pulse oksimetre ile takip sağlanır.  IV yol diyafragmanın yukarısından açılmaya çalışılır.  Hasta hipotansiyon açısından değerlendirilir; tedavi gerektiren maternal hipotansiyon sistolik kan basıncı 100mmHg’ya da bazal değerin %80’i olarak tanımlanır.  Erken dönemde uzman yardımı istenir (Kadın doğum, yenidoğan uzmanı)  Altta yatan nedenler tespit edilir ve tedavi planlaması yapılır. Gebelikte Kardiyak Arrest Gebe travma hastalarında uterus elle yer değiştirilir ya da hastayı sol yana yatırmak gerekir (vena kava inferiora basıncı azaltarak venöz dönüşüm sağlanır). Sol yana yatırmalarda spinal kord güvenliğine dikkat edilmelidir. Gebelerde kardiyak arrest yönetimine ilişkin dipnotlar aşağıda verilmiştir:  Göğüs basısı, diyafragmanın yükselmesi ve gebe uterusun neden olduğu abdominal içeriğe göre ayarlanması açısından sternum üzerinde normalde önerilenden hafifçe yukarı uygulanmalıdır.  Gebelerde OED kullanımı çalışılmamıştır, fakat kullanımı mantıklıdır.  Şoklanabilir ritimlerde (VF/ nVT) mümkün olan en kısa sürede defibrilasyon uygulanır.  Gebelikte kardiyak arrestin müdahelesi sırasında ilaçlar ve dozlarının değiştirilmesine dair kanıtlar yoktur.  Kardiyak arrestin geri döndürülebilir nedenleri ve gebelikte gelişebilecek nedenler belirlenip tedavi edilmelidir.  Mide regürjitasyonu ve aspirasyon riski oluşabileceğinden gebe hastalarda erken entübasyon düşünülür.  Tedavide öncelik annededir (24 hafta öncesi).  Genel prensipler diğer hastalar ile aynıdır.  PAŞG sadece bacak kısımları şişirilerek kullanılabilir.  Perimortem Sezeryan (PS) akılda tutulmalıdır (24-26 hafta). Geriatrik Hastalarda Resüsitasyon KPR uygulamasında herhangi bir modifikasyon olmamakla birlikte bazı durumların sık görüldüğü veya anatomik/ fizyolojik durumların resüsitasyon çalışmasını etkilediği bildirilmiştir. Örneğin; dişler olmadığı için ağızdan ağıza suni solunum oldukça güçtür. Boyun eklemlerindeki dejenerasyon sebebiyle endotrekeal entübasyon uygulaması zorlaşmaktadır. Bu nedenle yaşlılarda non invaziv havayolu yöntemleri öncelikle tercih edilmelidir. İleri kardiyak yaşam desteği uygulamaları standart erişkin uygulamaları ile aynıdır. Ancak yaşlılar akciğer ödemine kolay girebileceklerinden, gerektiğinde sıvı resüsitasyonu kontrollü bir şekilde yapılmalıdır. Karotis arterde aterom plakları oluşma ihtimali yüksek olduğu için nabız kontrolü femoral arterden yapılmalıdır. Obez Hastalarda Resüsitasyon Standart yaklaşım önerilmektedir. Fakat etkili KPR uygulanmasının zor olabileceği vurgulanmaktadır. Hastanın fiziki özelliklerine bağlı olarak IV erişimin zorluğu, havayolu yönetimi sorunları, nakil esnasındaki sorunlar vb. durumlar KPR etkinliğini olumsuz yönde etkilemektedir. Özellikle hastane öncesi alanda obez hastalar için tasarlanmış özel araçlara ihtiyaç duyulmaktadır. Diş Cerrahisi Sırasında Kardiyak Arrest Diş cerrahisi sırasında kardiyak arrest olan kişilerde KPR’ye başlamak için hastayı diş hekimliği koltuğundan hareket ettirmemek gerekir. Koltuk hızla horizontal pozisyona getirilir ve baş bölgesinin altına KPR uygulaması esnasında stabiliteyi sağlamak için arkalıksız bir sandalye yerleştirilir. Suda Boğulmalar ve Resüsitasyon Alkol alımı sonrası suya girenler ile çocukların daha fazla boğulma tablosuyla karşı karşıya kaldıkları bildirilmiştir. Boğulma vakalarının görülme sıklık¬ları bölgeden bölgeye değişmektedir. Boğulma va¬kalarında kararlı ve agresif tedavilerin kullanımı sağ kalım oranını arttırmaktadır. Suda boğulmalarda klinik seyrin ana belirleyicisi suyun altında kalma süresidir. 10 dakikadan daha uzun süre suyun altında kalma, zayıf klinik seyir ile ilişkilidir. Olayı görenler erken kurtarma ve resüsitasyonda kritik rol oynamaktadır. Solunumsal veya kardiyak arrest olgularının resüsitasyon stratejilerinde halen oksijenizasyon ve ventilasyon önceliğini korumaya devam etmektedir. Sonuç Klinik veya hastane öncesi alanda kardiyak arrest yönetiminin genel standartları aynı olmakla birlikte mekânsal koşulların ve imkanların olgu yönetimini etkilediği düşünülmektedir. Özellikle hastane öncesi dönemde olgu yönetiminin daha zor olduğu kanısına varılmıştır. Bu durumun temel nedenleri arasında; olay yerinin kaotik yapıda olması, mekânsal sorunların varlığı, çevresel baskının oluşumu, personel durumu vb. durumların yer aldığı düşünülmektedir. Kaynakça 1. Adams, K.F., Schatzkin, A., Harris T.B., et al. 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Çuvalcı, B , Hintistan, S . (2017). DNR Order and El¬derly. Middle Black Sea Journal of Health Science, 3 (3), 32-40. DOI: 10.19127/mbsjohs.338904. 8. Ersoy, G. (2019). Geriatrik Hastalara Hastane Öncesi Yaklaşım. Cander Başar (Ed.), Hastane Öncesi Acil Tıp ve Paramedik içinde (s.807-823). İstanbul. İstanbul Tıp Kitabevleri. 9. Fraga, G. P., Bansal, V., & Coimbra, R. (2010). Transfusion of blood products in trauma: an update. The Journal of Emergency Medicine, 39(2), 253-260. 10. Gruber E, Beikircher W, Pizzinini R, et al. Non- extracorporeal rewarming at a rate of 8oC per hour in a deeply hypothermic arrested patient. Resuscitation 2014;85:e119–20. 11. Hans, F. P., Hoeren, C. J., Kellmeyer, al. (2016) Pos¬sibly preventable cardiac arrest in a morbidly obese patient a comment on the 2015 ERC guidelines. Scand J Trauma Resusc Emerg Med. Oct 4;24(1):116. DOI: 10.1186/s13049-016-0306-4 12. Korkmaz İ, (2019). Çevresel Aciller, Editörler: Yavuz S, Yavuz G. Paramedikler İçin Hastane Öncesi Acil Tıp. 2.Baskı. Ankara: Ankara Nobel Tıp Kitapevleri. Bölüm 28, s523-524. 13. Kruska, P., Kappus, S., Kerner, T. (2012) Obesity in prehospital emergency care. Anasthesiol Intensivmed Notfallmed Schmerzther 47:556–62. DOI: 10.1055/s- 0032-1325286. 14. Kundra, P., Khanna, S., Habeebullah, S., & Ravishan¬kar, M. (2007). Manual displacement of the uterus du¬ring caesarean section. Anaesthesia, 62(5), 460-465. 15. Nanson, J., Elcock, D., Williams, M., & Deakin, C. D. (2001). Do physiological changes in pregnancy change defibrillation energy requirements?. British Journal of Anaesthesia, 87(2), 237-239. 16. Osborne Christina (2008). Understanding Leadership, Essential Managers New York: DK Publishing, p[6]. 17. Quan L, Mack CD, Schiff MA. Association of water temperature and submersion duration and drowning outcome. Resuscitation 2014; 85:790. 18. S. Cooper. Developing leaders for advanced life sup¬port: evaluation of a training programme Resuscitati¬on, 49 (2001), pp. 33-38 19. Safar P. Resuscitation from clinical death: Pathophysiologic limits and therapeutic potentials. Crit Care Med. 1988;16:923-941 20. Sağlık Bakanlığı, Acil Sağlık Hizmetleri Genel Müdür¬lüğü, Erişkin İleri Yaşam Desteği Eğitimi Ders Notları. Ankara. 2017 21. Tek, E. (2016). ERC 2015 Yetişkin ve Pediatrik İleri Yaşam Desteği Algoritmaları, Erişim Linki: Erişim Tarihi: 07.10.2019 22. Tobin JM, Ramos WD, Pu Y, et al. Bystander CPR is associated with improved neurologically favourable survival in cardiac arrest following drowning. Resus-citation 2017; 115:39. 23. Venema AM, Groothoff JW, Bierens JJ. The role of bys¬tanders during rescue and resuscitation of drowning victims. Resuscitation 2010; 81:434. 24. Wang HE, Szydlo D, Stouffer JA ve ark. ROC Investigators. (2012), Endotracheal intubation versus supraglottic airway insertion in out-of hospital cardiac arrest, Resuscitation 83(9):1061-6 25. Yücel, N. Ve Pepele, M.S. (2019). Pediatrik İleri Kardiyak Yaşam Desteği. Cander Başar (Ed.), Hastane Öncesi Acil Tıp ve Paramedik içinde (s.313-326). İstanbul. İstanbul Tıp Kitabevleri.
Ankle sprains affect athletic populations at high rates. Athletes who suffer an ankle sprain frequently go on to develop persistent symptoms, resulting in significant resources spent toward treatment, rehabilitation, and prevention. A thorough clinical evaluation is necessary to ensure an accurate diagnosis and appropriate treatment prescription. This narrative review aims to present an approach to evaluation of high and low ankle sprains for athletes of all levels. The authors review the current evidence for ankle sprain treatment and rehabilitation. Strategies for prevention of recurrent sprains and return to play considerations also are discussed.
In some patients with asthma, aspirin (ASA) and all nonsteroidal anti-inflammatory drugs that inhibit cyclooxygenase enzymes (cyclooxygenase-1 and -2) precipitate asthmatic attacks and naso-ocular reactions. This distinct clinical syndrome, called aspirin-induced asthma (AIA), is characterized by a typical sequence of symptoms, intense eosinophilic inflammation of nasal and bronchial tissues, combined with overproduction of cysteinyl-leukotrienes (Cys-LTs). At baseline, cys-LT urinary excretion is augmented, and ASA administration leads to its further temporary increase. After ASA challenge, cys-LTs are released into nasal and bronchial secretions and can be collected in the urine. LTC4 synthase, the terminal enzyme for cys-LT production, is markedly overexpressed in eosinophils and mast cells from bronchial biopsy specimens of most patients with AIA. An allelic variant of LTC4 synthase that enhances enzyme transcription is associated with AIA. Avoiding ASA and nonsteroidal anti-inflammatory drugs does not prevent progression of the inflammatory disease. Corticosteroids continue to be the mainstay of therapy, and anti-LT drugs are also indicated for treatment of the underlying disease. After ASA desensitization, daily ingestion of high doses of ASA reduces inflammatory mucosal disease symptoms, particularly in the nasal passages, in most patients with AIA.
Tendon disorders are a major problem for participants in competitive and recreational sports. To try to determine whether the histopathology underlying these conditions explains why they often prove recalcitrant to treatment, we reviewed studies of the histopathology of sports-related, symptomatic Achilles, patellar, extensor carpi radialis brevis and rotator cuff tendons. The literature indicates that healthy tendons appear glistening white to the naked eye and microscopy reveals a hierarchical arrangement of tightly packed, parallel bundles of collagen fibres that have a characteristic reflectivity under polarised light. Stainable ground substance (extracellular matrix) is absent and vasculature is inconspicuous. Tenocytes are generally inconspicuous and fibroblasts and myofibroblasts absent. In stark contrast, symptomatic tendons in athletes appear grey and amorphous to the naked eye and microscopy reveals discontinuous and disorganised collagen fibres that lack reflectivity under polarised light. This is associated with an increase in the amount of mucoid ground substance,which is confirmedwithAlcian blue stain. At sites of maximal mucoid change, tenocytes, when present, are plump and chondroid in appearance (exaggerated fibrocartilaginous metaplasia). These changes are accompanied by the increasingly conspicuous presence of cells within the tendon tissue, most of which have a fibroblastic or myofibroblastic appearance (smooth muscle actin is demonstrated using an avidin biotin technique). Maximal cellular proliferation is accompanied by prominent capillary proliferation and a tendency for discontinuity of collagen fibres in this area.Often, there is an abrupt discontinuity of both vascular and myofibroblastic proliferation immediately adjacent to the area of greatest abnormality. The most significant feature is the absence of inflammatory cells. These observations confirmthat the histopathological findings in athletes with overuse tendinopathies are consistent with those in tendinosis — a degenerative condition of unknown aetiology. This may have implications for the prognosis and timing of a return to sport after experiencing tendon symptoms. As the common overuse tendon conditions are rarely, if ever, caused by ‘tendinitis’, we suggest the term ‘tendinopathy’ be used to describe the common overuse tendon conditions.We conclude that effective treatment of athletes with tendinopathiesmust target the most common underlying histopathology, tendinosis, a noninflammatory condition.
Atherosclerosis is a process with inflammatory features and selective cyclooxygenase 2 (COX-2) inhibitors may potentially have antiatherogenic effects by virtue of inhibiting inflammation. However, by decreasing vasodilatory and antiaggregatory prostacyclin production, COX-2 antagonists may lead to increased prothrombotic activity. To define the cardiovascular effects of COX-2 inhibitors when used for arthritis and musculoskeletal pain in patients without coronary artery disease, we performed a MEDLINE search to identify all English-language articles on use of COX-2 inhibitors published between 1998 and February 2001. We also reviewed relevant submissions to the US Food and Drug Administration by pharmaceutical companies.Our search yielded 2 major randomized trials, the Vioxx Gastrointestinal Outcomes Research Study (VIGOR; 8076 patients) and the Celecoxib Long-term Arthritis Safety Study (CLASS; 8059 patients), as well as 2 smaller trials with approximately 1000 patients each. The results from VIGOR showed that the relative risk of developing a confirmed adjudicated thrombotic cardiovascular event (myocardial infarction, unstable angina, cardiac thrombus, resuscitated cardiac arrest, sudden or unexplained death, ischemic stroke, and transient ischemic attacks) with rofecoxib treatment compared with naproxen was 2.38 (95% confidence interval, 1.39-4.00; P = .002). There was no significant difference in cardiovascular event (myocardial infarction, stroke, and death) rates between celecoxib and nonsteroidal anti-inflammatory agents in CLASS. The annualized myocardial infarction rates for COX-2 inhibitors in both VIGOR and CLASS were significantly higher than that in the placebo group of a recent meta-analysis of 23 407 patients in primary prevention trials (0.52%): 0.74% with rofecoxib (P = .04 compared with the placebo group of the meta-analysis) and 0.80% with celecoxib (P = .02 compared with the placebo group of the meta-analysis).The available data raise a cautionary flag about the risk of cardiovascular events with COX-2 inhibitors. Further prospective trial evaluation may characterize and determine the magnitude of the risk.
Gastrointestinal (GI) toxicity induced by nonsteroidal anti-inflammatory drugs (NSAIDs) is among the most common serious adverse drug events in the industrialized world. Gastroduodenal ulcers can be demonstrated by endoscopy in 10% to 20% of patients who take NSAIDs on a regular basis, and the annual incidence of clinically important GI complications approaches 2%.1 The impact of NSAIDs on public health is significant and has provided the impetus to search for safer but equally effective anti-inflammatory agents.
Muscle injury presents a challenging problem in traumatology and is frequently encountered in sports medicine. The injury can occur via a variety of mechanisms, ranging from direct mechanical deformation (as in contusions, lacerations, and strain) to indirect causes (such as ischemia and neurological damage). Injured muscle usually undergoes a process of degeneration and regeneration. The injured muscle fibers first undergo necrosis, during which the damaged myofibers are removed by macrophages. New muscle fibers regenerate within the connective tissue framework of the damaged muscle. Even though muscles retain their ability to regenerate after injury, the healing process is very slow and often leads to incomplete functional recovery. We, along with others, have observed that injured muscle promptly initiates the process of healing; however, it is often inefficient and hindered by fibrosis (ie, scar tissue formation). This review is intended to increase the reader's understanding of the muscle healing process and will cover the events that occur after muscle injury including: (1) the pathological processes of degeneration and inflammation, (2) the biological repair process of muscle regeneration, and (3) the development of muscle fibrosis during the repair process. We will also discuss potential biological approaches to enhance muscle regeneration and prevent muscle fibrosis, which can eventually be used to improve muscle healing after injuries. This chapter should further our understanding of the muscle healing process and may help to develop novel and innovative therapies to promote efficient muscle healing for complete functional recovery after injuries.
Overuse tendinopathies are common in primary care. Numerous investigators worldwide have shown that the pathology underlying these conditions is tendinosis or collagen degeneration. This applies equally in the Achilles, patellar, medial and lateral elbow, and rotator cuff tendons. If physicians acknowledge that overuse tendinopathies are due to tendinosis, as distinct from tendinitis, they must modify patient management in at least eight areas. These include adaptation of advice given when counseling, interaction with the physical therapist and athletic trainer, interpretation of imaging, choice of conservative management, and consideration of whether surgery is an option.
There is no doubt that nonsteroidal anti-inflammatory drugs (NSAIDs) cause gastrointestinal injury. The most serious consequences are gastric and duodenal ulcers which can cause bleeding and perforation, and which may lead to the premature death of 3000 to 4000 patients in the UK annually. The immediate actions of NSAIDs operate at a subcellular level; in particular altering of mitochondrial function which causes depletion of ATP and renders the cell vulnerable to oxidant stress. Secondary consequences follow, such as the inhibition of prostaglandin synthesis which delays cellular repair. While adaptation can be shown in volunteers despite continued NSAID ingestion, studies in patients suggest mucosal damage develops continuously and cumulatively even with low doses of aspirin. Histamine H2-receptor antagonists and proton pump inhibitors heal NSAID-related ulcers, though healing rates with H2-antagonists are slower in patients who continue NSAID treatment. They have little role in preventing damage. In addition to acid suppression, prostaglandin analogues cause bicarbonate secretion and enhance mucosal blood flow. They have a specific role in both prevention and treatment of NSAID-related damage. The use of misoprostol offers a rational approach to reduce the high prevalence of unwanted gastroduodenal damage from NSAIDs. On a purely financial basis more information is needed before routine coprescribing can be recommended. However, for any patient on NSAIDs with a previous ulcer or for patients aged over 60 years (where the risks and seriousness of complications are markedly increased), the use of misoprostol should be considered. Further developments in prostaglandin analogues may reduce their adverse effects and perhaps thereby improve their efficacy at symptom control.
This article provides a background for the use of nonsteroidal anti-inflammatory drugs (NSAIDs) in sports medicine, including the nature of the drugs, the settings and rationale for their use, and concerns about their general safety. The criteria for the ideal study to examine the efficacy and safety of NSAIDs after acute injury is then enumerated, including a review of how many of the published studies have met each of the major criteria. Selected studies are described to demonstrate those that have or have not provided the basis for a rational decision on the use of NSAIDs in sports medicine and in the treatment of tendinitis. Finally, this article draws conclusions based on these published studies.