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Necrotizing fasciitis
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Necrotizing fasciitis
Synonyms
Flesh-eating bacteria, flesh-eating bacteria syndrome,[1] necrotizing soft tissue infection (NSTI),[2] fasciitis necroticans
Person with necrotizing fasciitis. The left leg shows extensive redness and tissue death.
Pronunciation
/ˈnɛkrəˌtaɪzɪŋ ˌfæʃiˈaɪtɪs/ or /ˌfæs-/
Specialty
Infectious disease
Symptoms
Severe pain, fever, purple colored skin in the affected area[3]
Usual onset
Sudden, spreads rapidly[3]
Causes
Multiple types of bacteria[4]
Risk factors
Poor immune function such as from diabetes or cancer, obesity, alcoholism, intravenous drug use, peripheral vascular disease[2][3]
Diagnostic method
Based on symptoms, medical imaging[4]
Prevention
Wound care, handwashing[3]
Treatment
Surgery to remove the infected tissue, intravenous antibiotics[2][3]
Prognosis
~30% mortality[2]
Frequency
0.7 per 100,000 per year[4]
Necrotizing fasciitis (NF), commonly known as flesh-eating disease, is an infection that results in the death of the body's soft tissue.[3] It is a severe disease of sudden onset that spreads rapidly.[3] Symptoms include red or purple skin in the affected area, severe pain, fever, and vomiting.[3] The most commonly affected areas are the limbs and perineum.[2]
Typically the infection enters the body through a break in the skin such as a cut or burn.[3] Risk factors include poor immune function such as from diabetes or cancer, obesity, alcoholism, intravenous drug use, and peripheral vascular disease.[2][3] It is not typically spread between people.[3] The disease is classified into four types, depending on the infecting organism.[4] Between 55% and 80% of cases involve more than one type of bacteria.[4] Methicillin-resistant Staphylococcus aureus (MRSA) is involved in up to a third of cases.[4] Medical imaging is helpful to confirm the diagnosis.[4]
Necrotizing fasciitis may be prevented with proper wound care and hand washing.[3] It is usually treated with surgery to remove the infected tissue and intravenous antibiotics.[2][3] Often a combination of antibiotics are used such as penicillin G, clindamycin, vancomycin, and gentamicin.[2] Delays in surgery are associated with a higher risk of death.[4] Despite high quality treatment, the risk of death is between 25% and 35%.[2]
Necrotizing fasciitis affects 0.4 to 1 person per 100,000 per year.[4] Both sexes are affected equally.[2] It becomes more common among older people and is very rare in children.[4] Necrotizing fasciitis has been described at least since the time of Hippocrates.[2] The term "necrotising fasciitis" first came into use in 1952.[4][5]
Contents
[hide]
1 Signs and symptoms
2 Cause
2.1 Risk factors
2.2 Bacteria
3 Diagnosis
3.1 Medical imaging
3.2 Scoring system
4 Prevention
5 Treatment
5.1 Surgery
5.2 Antibiotics
5.3 Others
5.4 Definitive management
6 Epidemiology
7 History
7.1 Notable cases
8 See also
9 References
10 External links
Signs and symptoms[edit]
The start of necrotizing fasciitis.
Symptoms may include fever, swelling, and complaint of excessive pain when compared to a small, benign swelling on the skin. The initial skin changes are similar to cellulitis and abscess, thus making the diagnosis of necrotising fasciitis at early stages difficult. Induration (hardening of the skin and soft tissue) and swelling beyond the area of skin changes are commonly present in those with early necrotizing changes.[2] The redness and swelling usually blends into surrounding normal tissues. The overlying skin may appear shiny and tense.[6] Other signs which are more suggestive of necrotising changes (but present in later stages in 7% to 44% of the cases) are: formation of bullae, skin ecchymosis which is present before skin necrosis[2] (skin turning from red to purple and black due to thrombosis of blood vessels),[6] presence of gas in tissues and reduced or absent sensation over the skin[2] (due to the necrosis of the underlying nerves).[6] Rapid progression to shock despite antibiotic therapy is another indication of necrotizing fasciiitis. When necrotising changes affects the groin it is known as Fournier gangrene.[2]
However, those who are immunocompromised (malignancy, corticosteroid usage, radiotherapy, chemotherapy, HIV/AIDS, prior organ or bone marrow transplantation) may not show normal signs and symptoms. Immunocompromised persons also have two fold higher risk of death from necrotising infections. Therefore, higher suspicion should be maintained in this group.[2]
Cause[edit]
Risk factors[edit]
More than 70% of cases are recorded in people with at least one of the following clinical situations: immunosuppression, diabetes, alcoholism/drug abuse/smoking, malignancies, and chronic systemic diseases. For reasons that are unclear, it occasionally occurs in people with an apparently normal general condition.[7]
Necrotising fasciitis can occur at any part of the body but it is more commonly seen at the extremities, perineum, genitals. Only few of such cases arises from chest and abdomen. Trauma is the usual cause of the infection such as intravenous drug injection, insulin injection, animals and insect bites, catheter insertion over the skin, or a fistula connecting skin to the internal body organs. Skin infections such as abscess, ulcers can also complicates into necrotising fasciitis. Spreading of infection through blood has been suggested for those with Streptococcal pharyngitis. For infection of the perineum and genitals (Fournier gangrene), trauma, surgery, urinary tract infection, stones, and Bartholin gland abscess are the usual causes.[2]
Bacteria[edit]
Types of soft tissue necrotising infection can be divided into four classes according to the types of bacteria infecting the soft tissue. This classification system was first described by Giuliano and his colleagues in 1977.[4][2]
Type I infection - This is the most common type of infection which accounts for 70 to 80% of the cases. It is caused by a mixture of bacterial types, usually in abdominal or groin areas.[4] This type of infection is usually inhabited by various species of gram positive cocci,(Staphylococcus aureus, Streptococcus pyogenes and enterococci) gram negative rods, (Escherichia coli, Pseudomonas aeruginosa) and anaerobes, (Bacteroides and Clostridial species).[4] Population of those affected are typically older with medical co-morbidities such as diabetes mellitus, obesity, and immunodeficiency.[4] Usually, trauma is not the cause of such infections. Previous history of abscess infection, gut perforation with bacterial translocation may be elicited. Clostridial infection accounts for 10% of Type I infection. Types of Clostrdium species involved are: Clostridium perfringens (typically causes gas gangrene), Clostridium septicum, and Clostridium sordellii. Clostrodium species produces two types of deadly toxins: alpha-toxin and theta-toxin. Alpha toxins causes excessive platelet aggregation which blocks blood vessels and deprive the vital organs of oxygen supply. This creates an acidic, oxygen deficient environment for the proliferation of bacteria. When alpha-toxin is absorbed by soft tissues, it can inhibits the migration of white blood cells from the blood vessels into the soft tissue, thus impairing phagocyte function. These two toxins together can cause destruction of red blood cells in blood vessels, damages the integrity of the blood vessels and suppress heart function. These species are usually found in the heroin injection users. Those with Clostridial infection typically have severe pain at the wound site; where the wound typically drains foul smelling blood mixing with serum (serosanguinous discharge). Shock can progress rapidly after initial hours injury or infection, and once the state of shock is established, the chance of dying exceeds 50%. Another bacteria with similar rapid progression is Group A streptococcal infection (mostly Streptococcus pyogenes). Meanwhile, other bacterial infections requires two or more days to become symptomatic.[2]
Type II infection - This infection accounts for 20 to 30% of the cases, mainly involving the extremities.[4][8]This infection mainly involves the Streptococcus pyogenes bacteria or in combination with Staphylococcal infections. Both types of bacteria can progress rapidly and manifests as toxic shock syndrome. Streptococcus has M protein which acts as superantigen, thus stimulating a massive systemic immune response which is not effective against the bacteria antigen, precipitating shock. Type II infection more commonly infects young, healthy adults with history of injury.[2]
Type III infection - Vibrio vulnificus, a bacterium found in saltwater, is a rare cause of this infection. Infection occurs through a break in the skin. Disease progression can be as rapid as Type II infection without any visible skin changes.[2]
Type IV infection - Some authors have described the Type IV infection as fungal infection.[4]
Diagnosis[edit]
Necrotising fasciitis producing gas in the soft tissues as seen on CT scan
Play media
Necrotizing fasciitis as seen on ultrasound[9]
Micrograph of necrotizing fasciitis, showing necrosis (center of image) of the dense connective tissue, i.e. fascia, interposed between fat lobules (top-right and bottom-left of image). H&E stain
Early diagnosis is difficult as the disease often looks early on like a simple superficial skin infection.[4] While a number of laboratory and imaging modalities can raise the suspicion for necrotizing fasciitis, the gold standard for diagnosis is a surgical exploration in the setting of high suspicion. When in doubt, a small incision can be made into the affected tissue, and if a finger easily separates the tissue along the fascial plane, the diagnosis is confirmed and an extensive debridement should be performed.[2]
Medical imaging[edit]
Imaging has a limited role in the diagnosis of necrotizing fasciitis. The time delay in performing imaging is a concern. Plain radiography may show subcutaneous emphysema (gas in the subcutaneous tissue) which is strongly suggestive of necrotising changes, but it is not sensitive enough to detect all the cases. This is because necrotising skin infections caused by the bacteria other than clostridial infections usually do not show subcutaneous emphysema. If the diagnosis is still in doubt, computed tomography (CT scan) and magnetic resonance imaging (MRI) are more sensitive modalities than plain radiography. However, both the CT scan and MRI are not sensitive enough rule out necrotizing changes completely.[2] CT scan may show fascial thickening, edema, subcutaneous gas, and abscess formation.[2] In MRI,when there is fluid collection with deep fascia involvement, thickening or enhancement with contrast injection, necrotising fasciitis should be strongly suspected. Meanwhile, ultrasonography can show superficial abscess formation but is not sensitive enough to diagnose necrotizing fasciitis.[2] CT scan is able to detect approximately 80% of cases while MRI may pick up slightly more.[10]
Scoring system[edit]
A white blood cell count less than 15,000 cells/mm3 and serum sodium level greater than 135 mmol/L has a sensitivity of 90% in detecting the necrotising soft tissue infection. It also has 99% chance of ruling out necrotising changes if the values has shown otherwise. There are various scoring system being developed to determine the likelihood of getting necrotising fasciitis but a scoring system developed by Wong and colleagues in 2004 is the most commonly used. It is the Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC) score which can be utilized to risk stratify people having signs of severe cellulitis or abscess to determine the likelihood of necrotizing fasciitis being present. It uses six labolatory values: C-reactive protein, total white blood cell count, hemoglobin, sodium, creatinine and glucose.[2] A score greater than or equal to 6 indicates that necrotizing fasciitis should be seriously considered.[11] The scoring criteria are as follows:
CRP (mg/L) ≥150: 4 points
WBC count (×103/mm3)
<15: 0 points
15–25: 1 point
>25: 2 points
Hemoglobin (g/dL)
>13.5: 0 points
11–13.5: 1 point
<11: 2 points
Sodium (mmol/L) <135: 2 points
Creatinine (umol/L) >141: 2 points
Glucose (mmol/L) >10: 1 point[11][12]
However, the scoring system has not been validated. The values would be falsely positive if there is any other inflammatory conditions present. Therefore, the values derived from this scoring system should be interpreted with caution.[2] 10% of patients with necrotizing fasciitis in the original study still had a LRINEC score <6.[11] A validation study done in 2008 showed that patients with a LRINEC score ≥6 have a higher rate of both death and amputation.[13]
Prevention[edit]
Prevention is by good wound care and handwashing.[3]
Treatment[edit]
Surgical debridement (cutting away affected tissue) is the mainstay of treatment for necrotizing fasciitis. Early medical treatment is often presumptive; thus, antibiotics should be started as soon as this condition is suspected. Given the dangerous nature of the disease, a high index of suspicion is needed. Cultures are taken to determine appropriate antibiotic coverage, and antibiotics may be changed when culture results are obtained. Besides, blood pressure and hydration support should be initiated for those with unstable vital signs with low urine output.[2]
Treatment for necrotizing fasciitis may involve an interdisciplinary care team. For example, in the case of a necrotizing fasciitis involving the head and neck, the team could include otolaryngologists, speech pathologists, intensivists, infectious disease specialists, and plastic surgeons or oral and maxillofacial surgeons.[14] Maintaining strict asepsis during any surgical procedure and regional anaesthesia techniques is vital in preventing the occurrence of the disease.[15]
Surgery[edit]
In necrotizing fasciitis, aggressive wound debridement (removal of unhealthy tissues) is always necessary to keep it from spreading and is the only treatment available. Surgical incisions should extend beyond the area of induration because dermal lymphatic blockage and thrombosis of small veins are the causes of such induration. However, cellulitic soft tissue can be spared from debridement for later skin coverage of the wound. The subcutaneous tissue should be debrided until the healthy, bleeding tissue is seen. A second look operation maybe planned within 24 hours to remove additional necrotic tissue and an average of 3 to 4 operations is required for one person. Sometimes, amputation of the affected limb or the debridement of internal organs may be necessary. After the wound debridement, adequate dressings should be applied to prevent exposure of bones, tendons, and cartilages so that such structures would not dry out and to promote wound healing.[2]
For necrotising infection of the perineal area (Fournier gangrene), wound debridement and wound care in this area can be difficult because of the excretory products that often renders this area dirty and affect the wound healing process. Therefore, regular dressing changes with a faecal management system can help to keep the wound at the perineal area clean. Sometimes, colostomy maybe necessary to divert the excretory products to keep the wound at the perineal area clean.[2]
Necrotic tissue from the left leg surgically removed
Post surgical debridement and skin grafting
Post knee disarticulation amputation
Antibiotics[edit]
Broad spectrum antibiotics that covers the gram positive, gram negative and anaerobes should be used with the consideration of Methicillin-resistant Staphylococcus aureus (MRSA) coverage. Examples of antibiotics used are: penicillin G, clindamycin, vancomycin, and gentamicin. Penicillin G is effective against the Streptococcal and Clostridial infections. Clindamycin is effective in reducing the alpha toxins produced by Clostridial species, reducing the production of M protein by Streptococcal species, and reducing the production of tumor necrosis factor alpha production by monocytes. Vancomycin is the treatment of choice for MRSA. Meanwhile, gentamicin is useful against many gram negative rods and anaerobic bacteria. Fluoroquinolone may be used instead of gentamicin for those with acute kidney injury for kidney protection. Antibiotics are typically continued until the cultures come back for appropriate narrowing of antibiotic spectrum or until the completion of wound debridement and the person's vital signs are stable with normal white blood cell count.[2]
Others[edit]
Hyperbaric oxygen treatment is sometimes used to treat necrotizing soft tissue infection in combination with antibiotics and debridement. A person is placed inside a high pressure chamber where oxygen is delivered a t 2 to 3 times the atmosphereic pressure. This resulted with arterial oxygen tension of 2000 mmHg and tissue oxygen tension of 300 mmHg as compared with 300 mmHg arterial oxygen tension and 75 mmHg tissue oxygen tension when breathing 100% oxygen. Humana and animal studies has shown that high oxygen tension in tissues help to reduces oedema, stimulate fibroblast growth, increasing the killing ability of white blood cells, toxic effects on anoerobes, inhibit bacterial toxin release and increase antibiotics efficacy.[2] However, there is a lack of compelling evidence regarding its efficacy for this purpose.[16][17] Therefore, hyperbaric oxygen therapy is only limited for those with stable vital signs in conditions where surgical debridement will not be delayed.[2]
Intravenous immunoglobulin is considered for the treatment of necrotising soft tissue infection. This is because the immunglobulins can bind to the exotoxins produced by Streptococcal and Staphylococcal infections, which subsequently limits immune response of the human body. However, there is limited data on the efficacy of this therapy. Therefore, such therapy is limited only for those who are critically ill.[2]
Definitive management[edit]
Wound dressings applied on the should allow for ambulation in order to prevent hospital acquired pneumonia, urinary tract infection, and deep vein thrombosis. The use of Mafenide (2.5 or 5% dilution) or Dakin solution, pulse lavage (wound irrigation using pressurised jets of normal saline to remove fibrinous material and bacteria), and negative-pressure wound therapy (vacuum dressing; promotes vascularisation of wound bed). Wound closure should be delayed if there is hypoperfusion of the tissues due to hypotension. Wound closure can be started once the wound bed is clean with good tissue perfusion.[2]
Pain control is another important modality in wound management as pain can affect wound healing. The severity of pain can be assessed by Wong-Baker Faces Pain Rating Scale and Numeric Rating Scale according to the age and cultural background of the those in pain. Pain can be divided into three types: background pain, breakthrough pain, and procedural pain. Background pain is relatively constant and may be started before the onset of necrotising fasciitis which can range from mild to moderate pain. Such pain can be treated by methadone. Breakthough pain is the sudden worsening of pain in addition to background pain which is precipitated by movements or emotions. This type of pain can be treated by morphine, or oxycodone with combination of nonsteroidal anti-inflammatory drug (NSAID). Procedural pain the intense burning or stinging pain when procedures are performed such as wound debridement, changing of dressings, or physiotherapy. Morphine or oxycodone, in combination with short acting anxiolytic drugs such as midazolam and lorazepam. Gabapentin, an anticonvulsant, can be used to control neuropathic pain in surgical debridements and ampuatations. Skin graft and tissue rearrangement can be used to achieve wound closure.[2]
Epidemiology[edit]
Necrotizing fasciitis affects about 0.4 in every 100,000 people per year in the United States.[4] There were about 1,000 cases of necrotising fasciitis cases per year in the United States, however, the rates have been increasing. This could be due to increasing awareness of this condition, leading to increased reporting, or there could be increasing bacterial virulence, or increasing bacterial resistance against antibiotics.[2] In some areas of the world it is as common as 1 in every 100,000 people.[4]
Higher rates of necrotising fasciities are seen in those with obesity, diabetes, immunocompromised, alcholic, or with peripheral vascular disease. However, such disease may also occurs in young healthy adults with no underlying illnesses. Non-steroidal anti-inflammatory drug (NSAIDs) may have increase the rates of necrotising infections due to the modification of immune response in the body. This is because NSAIDs inbihits the cycloxygenase -1 and cycloxygenase-2 enzymes which are important in producing thromboxane and prostaglandin E2. Prostaglandin has been responsible for fever, inflammation, and pain. The inhibition of prostangladin E2 production reduces inflammatory response and leukocyte adhesion, thus reduces immune response against bacterial invasion, giving rise to soft tissue infection.[2]
History[edit]
In the 5th century BC, Hippocrates described necrotising soft tissue infection as a disease which was the complication of Streptococcal infection where those affected would have "erysipelas all over the body while the cause was only a trivial accident. Bones, flesh, and sinew (cord, tendon, or nerve) would fall off from the body and there were many deaths". The first English description for necrotising soft tissue infection was by British surgeon Leonard Gillespie and British physicians Gilbert Blaine and Thomas Trotter in the 18th century. At that time, necrotising soft tissue infection was known as phagedaenic (gnaw - biting or chewing which gradually make a hole or destroying it) ulcer, phagedena gangrenous, gangrenous ulcer, malignant ulcer, putrid ulcer, or hospital gangrene. Later the word "hospital gangrene" become more commonly used. In 1871, Confederate States Army surgeon Joseph Jones reported 2,642 cases of hospital gangrene with mortality rate of 46%. In 1883, Dr Jean-Alfred Fournier described the necrotising infection of the perineum and scrotum which termed as Fournier gangrene today. The term "Necrotising fasciitis" was first coined by Wilson in 1952. The definition of necrotising fasciitis has become broader, to include not only infection of fascia, but also other soft tissue infection.[2]
Notable cases[edit]
1994 Lucien Bouchard, former premier of Québec, Canada, who became infected while leader of the federal official opposition Bloc Québécois party, lost a leg to the illness.[18]
1994 A cluster of cases occurred in Gloucestershire, in the west of England. Of five confirmed and one probable infection, two died. The cases were believed to be connected. The first two had acquired the Streptococcus pyogenes bacteria during surgery, the remaining four were community-acquired.[19] The cases generated much newspaper coverage, with lurid headlines such as "Flesh Eating Bug Ate My Face".[20]
1997 Ken Kendrick, former agent and partial owner of the San Diego Padres and Arizona Diamondbacks, contracted the disease. He had seven surgeries in a little more than a week and later fully recovered.[21]
2004 Eric Allin Cornell, winner of the 2001 Nobel Prize in Physics, lost his left arm and shoulder to the disease.[22]
2005 Alexandru Marin, an experimental particle physicist, professor at MIT, Boston University and Harvard University, and researcher at CERN and JINR, died from the disease.[23]
2006 Alan Coren, British writer and satirist, announced in his Christmas column for The Times that his long absence as a columnist had been caused by his contracting the disease while on holiday in France.[24]
2009 R. W. Johnson, British journalist and historian, contracted the disease in March after injuring his foot while swimming. His leg was amputated above the knee.[25]
2011 Jeff Hanneman, guitarist for the thrash metal band Slayer, contracted the disease. He died of liver failure two years later, on May 2, 2013, and it was speculated his infection might be the cause of death. However, on May 9, 2013, the official cause of death was announced as alcohol-related cirrhosis. Hanneman and his family had apparently been unaware of the extent of the condition until shortly before his death.[26]
2011 Peter Watts, Canadian science fiction author, contracted the disease. On his blog, Watts reported, "I’m told I was a few hours away from being dead...If there was ever a disease fit for a science fiction writer, flesh-eating disease has got to be it. This...spread across my leg as fast as a Star Trek space disease in time-lapse."[27]
2014 Daniel Gildenlöw, Swedish singer and songwriter for the band Pain of Salvation spent several months in hospital after being diagnosed with necrotizing fasciitis on his back in early 2014. After recovering he went to write the album 'In the Passing Light of Day',[28] a concept album about his experience during the hospitalization.[29]
2015 Edgar Savisaar, Estonian politician. His right leg was amputated. He got the disease during a trip to Thailand.[30]
See also[edit]
Mucormycosis, a rare fungal infection that can resemble necrotizing fasciitis.
Toxic shock syndrome
Gangrene
Noma (disease)
Fournier gangrene, another name for necrotizing fasciitis of the groin region
References[edit]
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External links[edit]
Classification
V · T · D
ICD-10: M72.6
ICD-9-CM: 728.86
MeSH: D019115
DiseasesDB: 31119
External resources
MedlinePlus: 001443
eMedicine: emerg/332 derm/743

Wikimedia Commons has media related to Necrotizing fasciitis.
Necrotizing fasciitis at Curlie (based on DMOZ)
LRINEC Score Online
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Soft tissue disorders / Rheumatism / Connective tissue arthropathy (M65–M79, 725–728)
Capsular joint
Synoviopathy
Synovitis/Tenosynovitis
Calcific tendinitis
Stenosing tenosynovitis
Trigger finger
De Quervain's syndrome
Transient synovitis
Ganglion cyst
osteochondromatosis
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NFL Scouting Combine
From Wikipedia, the free encyclopedia
Jump to: navigation, search
The NFL Scouting Combine is a week-long showcase occurring every February at Lucas Oil Stadium (and formerly at the RCA Dome until 2008) in Indianapolis, where college football players perform physical and mental tests in front of National Football League coaches, general managers, and scouts. With increasing interest in the NFL Draft, the scouting combine has grown in scope and significance, allowing personnel directors to evaluate upcoming prospects in a standardized setting. Its origins have evolved from the National, BLESTO,[1] and Quadra Scouting organizations in 1977 to the media event it has become today.
Athletes attend by invitation only. Implications of an athlete's performance during the combine can affect their draft status and salary, and ultimately their career. The draft has popularized the term "workout warrior", whereby an athlete's "draft stock" is increased based on superior measurable qualities such as size, speed, and strength, despite having an average or sub-par college career.[2][3][4] The 2018 NFL scouting combine is scheduled for February 27 to March 5.[5]
Contents
[hide]
1 History
2 Tests and evaluations
3 Bench press records
4 Scouting organizations
5 Combine invitations
6 Criticism
7 Television
8 Regional combines
9 Veteran combine
10 References
11 External links
History[edit]
Tex Schramm, the president and general manager of the Dallas Cowboys from 1960 to 1989, proposed to the NFL competition committee a centralization of the evaluation process for NFL teams. Prior to 1982, teams had to schedule individual visits with players to run them through drills and tests.[6] The national invitational camp (NIC) was first held in Tampa, Florida, in 1982.[7] It was originated by National Football Scouting, Inc. as a means for member organizations to look at NFL draft prospects. For non-member teams, two other camps were created and used 1982–1984. The NIC was renamed the NFL scouting combine following the merger of the three camps in 1985 to cut the cost of running the extra camps. The NIC was held in New Orleans, Louisiana, in 1984 before the merger. It was held in Arizona in 1985 and once again in New Orleans in 1986 before permanently moving to Indianapolis in 1987.
Tests and evaluations[edit]
Tests/evaluations include:
40-yard dash[8]
Bench press (225 lb repetitions)[8]
Vertical jump[8]
Broad jump[8]
20-yard shuttle[8]
3 cone drill[8]
60-yard shuttle[8]
Position-specific drills[8]
Interviews – each team is allowed 60 interviews in 15-minute intervals[9]
Physical measurements[9]
Injury evaluation[9]
Drug screen[9]
The Cybex test[9]
The Wonderlic test[10]
Sports writers question whether these tests have any relationship with future NFL performance.[11] Empirical research conducted by Brian D. Lyons, Brian J. Hoffman, John W. Michel, and Kevin J. Williams (2011) found that the 40-yard dash, vertical jump, 20-yard shuttle, and 3 cone drill tests have limited validity in predicting future NFL performance.[12] In fact, the Lyons et al. (2011) study suggests that a prospect's past performance in college is a better indicator of future NFL performance than the aforementioned physical ability tests.
Bench press records[edit]
At the NFL combine, bench press is used as a test of strength and stamina, in which athletes lift 225 pounds (102 kg) as many times as possible.[13] Since 1998, only eighteen men at the combine have managed to achieve more than 40 "reps" (repetitions).
51 reps: Justin Ernest (1999)[14]
49 reps: Stephen Paea (2011)[15]
45 reps: Mike Kudla (2006), and Mitch Petrus (2010) Leif Larsen (2000)[16]
44 reps: Brodrick Bunkley (2006), Jeff Owens (2010), and Dontari Poe (2012)
43 reps: Scott Young (2005) and Kyle Harrington (2010)
42 reps: Isaac Sopoaga (2004), Tank Tyler (2007), Russell Bodine (2014), Harrison Phillips (2018)
41 reps: Igor Olshansky (2004), Terna Nande (2006), David Molk (2012), and Vita Vea (2018).
Scouting organizations[edit]
The NFL's first scouting organization, LESTO (Lions, Eagles and Steelers Talent Organization), was started in 1963 by the teams mentioned in its name with headquarters in Pittsburgh, Pennsylvania.[17] It became BLESTO when the Bears joined the following year and BLESTO-V when the Vikings came on board later in the decade; by 1971 the Bills, Colts and Dolphins had joined and the group was known as BLESTO-VIII.[18] It is now known simply as BLESTO despite the fact that the Bears and Eagles are no longer members.[19] The group's offices stayed in Pittsburgh until 2007 when the headquarters moved to Jacksonville, Florida, with support offices remaining in Pittsburgh.[17]
CEPO (Central Eastern Personnel Organization), formed in 1964, was a joint venture of the Colts, Browns, Packers and Cardinals. Its name was changed to United Scouting after the Falcons, Giants and Redskins joined, then to National Football Scouting in 1983 to avoid confusion with the United States Football League, which began operations that year. National Football Scouting is now known simply as The National.[19]
Another scouting organization formed in 1964 was Troika, launched by the Cowboys, Rams and 49ers. It was renamed Quadra when the Saints joined in 1967.[19] Quadra no longer exists; its former members now all belong to The National.
As of the 2015 season, eighteen franchises participate in The National (Arizona Cardinals, Atlanta Falcons, Carolina Panthers, Cincinnati Bengals, Dallas Cowboys, Denver Broncos, Green Bay Packers, Houston Texans, Kansas City Chiefs, New Orleans Saints, New York Jets, Philadelphia Eagles, Los Angeles Rams, Los Angeles Chargers, San Francisco 49ers, Seattle Seahawks, Tampa Bay Buccaneers, and Tennessee Titans), with eight served by BLESTO (Buffalo Bills, Detroit Lions, Jacksonville Jaguars, Miami Dolphins, Minnesota Vikings, New York Giants, Pittsburgh Steelers, and Washington Redskins). Each of the six non-affiliated teams (Baltimore Ravens, Chicago Bears, Cleveland Browns, Indianapolis Colts, New England Patriots, and Oakland Raiders) relies on its in-house scouting staffs.[19][20]
Combine invitations[edit]
In a typical year, there are about 330 invited players. About 250 invitations are sent before bowl games are completed to those who have completed their seasons. However, underclassmen have until mid-January to confirm their draft status. Invitations are made to those receiving supermajority support from the selection committee.[21]
Criticism[edit]
The combine however is not without its critics. Sports writer Steve Silverman explains, in an article he wrote, what happened to Terrell Suggs in 2003. Suggs was a star player for Arizona State but when Suggs ran a slow 4.83 40 he was downgraded. Later, he became a star player for the Ravens.[22] Doug Tatum of Times-Picayune argues that it is unlikely players will be asked to run a 40-yard dash again during their career.[23] Silverman says that the best way to scout is to simply watch them play.[22] Others think the value in the 40 depends on the position; Daniel Jeremiah, a former scout and an analyst on the NFL Network says "The position where the 40 holds the most weight is cornerback. If you're a receiver who runs a 4.6 like (Anquan) Boldin, but you have short-area quickness and strong hands, the 40 isn't a big deal. But if you're a cornerback who runs a 4.6 and you're facing a receiver who runs a 4.4, it doesn't matter how good your ball skills are."[24]
Television[edit]
The NFL scouting combine was first shown on television in 2004. Media and cameras were historically prohibited, but with the launch of NFL Network on November 4, 2003, six installments of one-hour shows to recap the day's events aired in February 2004.[25] NFL Network has exclusive access to the Scouting Combine, whereas ESPN, a competitor network, does not.[26] NFL Network aired two hours of combine workouts for each workout day in 2005,[27] 26 total hours of coverage in 2006,[28] 27 hours in 2007,[6] and 25 hours in 2009.[29] It began airing over 30 hours of Combine coverage starting in 2010,[30] which received 5.24 million viewers.[31]
Regional combines[edit]
Beginning in 2011, a series of eleven regional combines for players not invited to the main scouting combine, as well as other free agents, were held in eight cities (Los Angeles, Houston, Baltimore, Tampa, East Rutherford, Chicago, Atlanta, and Cleveland) from January to March. The best players from these regional combines were invited to the NFL super regional combine at Ford Field in Detroit in late March.[32] In 2016, the NFL went away from this format only holding five Combines in Houston, Arizona, Baltimore, Minnesota and New Orleans.[33]
Veteran combine[edit]
The first NFL Veteran Combine was scheduled on March 22, 2015 at the Arizona Cardinals's team facility. The combine corresponded with the NFL owners' meetings also being held in Phoenix from March 22–24, 2015. The combine featured veteran free agents, and all 32 clubs in attendance. There were over 2,000 applications from players to participate, although only a select few were chosen. Some of the notable players included Adam Carriker, Felix Jones, Michael Sam, and Brady Quinn.[34] However, only two players participating in the combine (linebacker Brandon Copeland and tight end Ifeanyi Momah) were still on NFL rosters by Week 1 of the 2015 regular season.[35]
The NFL cancelled the planned 2016 Veteran Combine, citing a lack of player interest.[36]
On December 16, 2016, the NFL announced it would bring back the veteran combine renaming it the Pro Player Combine and focus its attention on younger players instead of veterans trying to get another chance in the NFL.[37]
References[edit]
Jump up ^ "Beaver County Times – Google News Archive Search". google.com.
Jump up ^ Schoenfield, Dave (April 27, 2006). "The 100 worst draft picks ever". ESPN.com. Retrieved February 25, 2012.
Jump up ^ Cheifetz, Isaac (2007). Hiring Secrets of the NFL: How Your Company Can Select Talent Like a Champion. p. 68.
Jump up ^ Eisen, Rich (2007). Total Access: A Journey to the Center of the NFL Universe. p. 128.
Jump up ^ "Schedule". nflcombine.net. Retrieved January 12, 2018.
^ Jump up to: a b Crouse, Karen (February 23, 2007). "Players Are Seen and Unseen At N.F.L. Scouting Combine". New York Times. Retrieved February 26, 2012.
Jump up ^ Mitchell, Fred (February 5, 1991). "Where millionaires are separated from the boys". Chicago Tribune. Retrieved February 25, 2012.
^ Jump up to: a b c d e f g h "Workout & Drills". NFL.com. Retrieved February 25, 2012.
^ Jump up to: a b c d e "The NFL Scouting Combine". theredzone.org. Retrieved February 25, 2012.
Jump up ^ Casserly, Charley (February 24, 2012). "Wonderlic Test is helpful, but certainly not a foolproof tool". NFL.com. Retrieved February 25, 2012.
Jump up ^ Ledbetter, D. Orlando (February 25, 2011). "NFL's physical testing methods scrutinized". Atlanta Journal-Constitution. Retrieved February 25, 2012.
Jump up ^ Lyons, B. D.; Hoffman, B. J.; Michel, J. W.; Williams, K. J. (2011). "On the Predictive Efficiency of Past Performance and Physical Ability: The Case of the National Football League". Human Performance. 24 (2): 158. doi:10.1080/08959285.2011.555218.
Jump up ^ "Combine events: Bench press". NFL.com. Archived from the original on April 18, 2012.
Jump up ^ https://sports.yahoo.com/nfl/news?slug=ycn-7663872
Jump up ^ "bench press – NFL Combine Results". nflcombineresults.com.
Jump up ^ "McClain: 40 times fuel combine conversation". Houston Chronicle.
^ Jump up to: a b "Butler's retirement marks the end of a BLEST career – Pittsburgh Post-Gazette". Pittsburgh Post-Gazette. June 10, 2007.
Jump up ^ "Computer Makes NFL Draft Selections" (PDF). The Daily Gazette. 1971.
^ Jump up to: a b c d "Who Are BLESTO & The National?". DraftDaddy.com. Retrieved February 25, 2012.
Jump up ^ Marino, Tom (December 10, 2008). "The Scouting Combine's Role in Pro Scouting". Scout.com. Retrieved February 25, 2012.
Jump up ^ Gabriel, Greg (December 30, 2011). "Q A on NFL Scouting Combine invites". National Football Post. Archived from the original on January 8, 2012. Retrieved January 19, 2012.
^ Jump up to: a b Silverman, Steve (February 21, 2012). "Silverman: NFL Combine Is Overrated". CBS Chicago. Retrieved February 3, 2014.
Jump up ^ Tatum, Doug (March 15, 2009). "40-yard dash is just a waste of time for NFL prospects". The Times-Picayune. Retrieved February 3, 2014.
Jump up ^ "NFL draft: Is the 40-yard dash really that important?". mercurynews.com.
Jump up ^ Wood, Skip (February 18, 2004). "NFL opens combine to curious cameras". USA Today. Retrieved February 26, 2012.
Jump up ^ Sandomir, Richard (February 3, 2005). "The NFL Network Wants You to Want It". New York Times. Retrieved February 26, 2012.
Jump up ^ Clayton, John (February 25, 2005). "Combine should be one of the busiest ever". ESPN.com. Retrieved February 26, 2012.
Jump up ^ "NFL Combine accompanied by hazy labor outlook". USA Today. February 23, 2006. Retrieved February 26, 2012.
Jump up ^ "Exclusive coverage of NFL Combine on NFL Network, NFL.com". NFL.com. 2009. Retrieved February 26, 2012.
Jump up ^ "NFL Network, NFL.com to provide exclusive combine coverage". NFL.com. 2010. Retrieved February 26, 2012.
Jump up ^ Hiestand, Michael (February 25, 2011). "Combine: NFL niche that runs way over". USA Today. Retrieved February 26, 2012.
Jump up ^ Vensel, Matt (February 11, 2012). "Regional combine provides another road to the NFL". Baltimore Sun. Retrieved February 25, 2012.
Jump up ^ https://nflcommunications.com/Pages/2016-NFL-Regional-Combines-Schedule-Announced.aspx
Jump up ^ Breech, John (January 15, 2015). "NFL adds event: Veteran combine for free agents to be held in March". cbssports.com. Archived from the original on January 16, 2015. Retrieved January 16, 2015.
Jump up ^ Alex Putterman. "NFL cancels veteran combine due to lack of interest". Yardbarker. Retrieved April 8, 2016.
Jump up ^ Michael David Smith. "NFL shelves the veteran combine". Pro Football Talk. Retrieved April 8, 2016.
Jump up ^ "NFL reboots veteran's combine as Pro Player Combine". NFL.com.
External links[edit]
Official website
Combine on NFL.com
NFL Regional Combines website
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