\r\n\tThe major pathogenetic mechanisms resulting from RAAS overactivity include activation of the sympathetic nervous system, endothelial dysfunction, proinflammatory, and procoagulant states.
\r\n\tEmerging from basic science evidence, major clinical trials established the beneficial effects of inhibitors of the different components of RAAS such as angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), aldosterone antagonists. These effects range from treatment of hypertension, diabetic nephropathy, CHF, as well as improvement of outcomes after myocardial infarction and improvement in glucose homeostasis and prevention of type 2 diabetes with some agents.
\r\n\tIn this book, written by a world-renowned scholar, we will address the major concepts and topics related to RAAS activation including the pathogenetic mechanisms underlying the deleterious effects of activated RAAS and the role of local tissue RAAS in various organ systems such as the heart and vasculature, the skeletal muscle, adipose tissues, pancreas and the angiotensinergic pathways in the brain. Cutting-edge information is provided that will address the need for a wide range of readers including a medical student, clinical practitioner, and basic science investigators alike. This book will be bridging the gap between basic science and clinical practice regarding the RAAS system, which is imminently critical and highly relevant to the practice of medicine.
\r\n\r\n\tFinally, with data emerging from the COVID-19 pandemic indicating overrepresentation of people with diseases associated with RAAS activation such as hypertension, chronic kidney disease, and diabetes, the role of RAAS activation and RAAS inhibition in the pathogenesis and clinical outcomes in COVID-19 has garnered a great deal of interest. In this book, we will dedicate a chapter addressing this topical and highly critical subject.
\r\n\t
The incidence of Achilles tendon rupture has significantly increased over the last 20 years (Moller, 1996, Young and Maffulli, 2007), achieving, within the tendon diseases, an incidence between 6 and 18% (Rees et al., 2006, Mazzone and McCue, 2002, Shepsis et al., 2002). The risk of the Achilles tendon rupture is greater in the male population with a ratio included between 1.7 : 1 and 30 : 1. This data would be justified by the high prevalence of males subjects in sports considered at risk (Rees et al., 2006, Mazzone and McCue). Despite its high incidence in the context of sports traumatology, the Achilles tendon rupture etiology remains poorly known (Maffulli, 1999; Williams, 1986) and it is essentially based on two main theories: the “degenerative theory” and the “mechanical theory”.
\n\t\t\t\n\t\t\t\t
From a biomechanical point of view, the “degenerative theory” is based on the assumption that a structurally intact tendon, even if subjected to significant tensile forces - however remaining within the physiological request - should not be subject to rupture (Cetti and Christensen, 1983). In fact, since 1959 (Arnero and Lindhom, 1959), we can find in bibliography several studies showing that the majority of patients undergoing Achilles tendon surgical repair, already had rather advanced degenerative processes that were considered responsible for the tendon structural failure (Davidsson and Salo, 1969, Fox et al 1975, Kannus and Jozsa, 1991, Jozsa et al., 1991, Jarvinen, 1997, Jozsa and Kannus, 1997, Waterston, 1997, Waterston and Maffulli, 1997). Although most of these degenerative involutions were not linked to a precise etiologic cause, the majority of the Authors linked these to an alteration in tendon microcirculation subsequent to hypoxia and altered metabolism (Jarvinen, 1997, Jozsa and Kannus, 1997, Waterston, 1997, Waterston and Maffulli, 1997). Others Authors noted that the degenerated tendon tissue showed an increased production of collagen type III and V that disturbs the normal architecture of the tendon tissue making it less resistant against mechanical stress (Waterston, 1997, Waterston et al., 1997).
\n\t\t\t\n\t\t\t\t
Some Authors showed that the Achilles tendon structural failure can occur even if it is subjected to mechanical stress that is within a normal physiological situation but in a situation where the tendon was, or may be, subject to a series of cumulative microtraumatic injuries without having allowed a reasonable time for the biological repair (Knörzer et al., 1986, Selvanetti et al., 1997). Therefore, the complete rupture would be the result of a several number of previous multiple microtraumatic injuries which would lead the tendon just to the point of its structural failure (Knörzer et al., 1986). In such conditions, the situation of greater risk for the tendon integrity would occur when they are present within the same moment three very specific biomechanical factors (Barfred, 1971, Hess et al., 1989).).
\n\t\t\tThe tendon is obliquely loaded in relation to its anatomical axis.
The gastrocnemius-soleus muscle complex is in maximal contraction.
The initial tendon length is reduced.
We can find this combination of factors as a usual situation almost in all sports requiring a "push off” quick action (Selvanetti et al., 1997). The mechanical theory could, at least in part explain the occurrence of the Achilles tendon complete rupture as this event is sometimes observed even in the absence of degenerative processes (Knörzer et al., 1986, Clement et al., 1994). In according with this situation it is interesting to note that some Authors have suggested a relationship between the musculoskeletal disorders and in particular, tendon disorders and subjects’ blood group (Mourant et al., 1978; Lourie, 1983, Joza et al., 1989, Kujala et al., 1992). The scientific rationale for this correlation is based on the fact that subjects belonging to 0 blood groups show an N-acetylgalactosamine transferase activity higher compared to subjects belonging to the A and B group (Kujala et al., 1992). A greater N-acetylgalactosamine transferase activity leads to a collagen type III increased production within the tendon (Waterston and Maffulli, 1997). The type III collagen is less resistant against mechanical stress compared to type I collagen (Waterston and Maffulli, 1997) and would predispose the tendon to spontaneous rupture (Joza et al., 1989; Maffulli, 1999). This may explain the high incidence of Achilles tendon spontaneous ruptures found by some Authors in subjects belonging to the 0 blood group compared to the A and B groups (Joza et al., 1989, Maffulli, 1999).
\n\t\t\tIn addition to these two main theories, the Achilles tendon rupture may result from other different factors that we can assume as follows:
\n\t\t\n\t\t\t\t
The use of corticosteroids are widely used therapeutic practice in a various number of diseases, however their use represents a risk factor for tendon rupture (Fisher, 2004) In literature some Authors report clear associations between rupture of the Achilles tendon and oral assumption and tendinous or peritendinous injections of corticosteroids (Unverferth and Olix, 1973, Newnham et al., 1991). The recommendation to not use corticosteroids in tendinopathy is based over two main points:
\n\t\t\tAn insufficient evidence to justify their use in tendinopathy (Maffulli and Kader, 2002).
\n\t\t\t\n\t\t\t\n\t\t\t\t
The use of some antibiotics such as fluoroquinolone is associated in literature with injury and / or to serious tendon ruptures, especially at Achilles tendon level (Huston, 1994, Royer et al., 1994, Filippucci et al., 2003, Vanek et al., 2003). The first Achilles tendon rupture due to the use of fluoroquinolone was described in 1992 (Ribard et al., 1992). The fluoroquinolone are drugs widely used in clinical practice but their association with corticosteroid drugs, especially in the elderly subjects, is an important risk factor for tendinopathy and/or tendon rupture (Linden Van Der et al., 2003). The most important number of tendon damages caused by fluoroquinolone reported in the literature is caused by the use of ciprofloxacin followed by enoxacin, ofloxacin and enorfloxacin (Huston, 1994; Szarfman et al., 1995; Van der Linden et al., 2002; Filippucci et al., 2003). The fluoroquinolone-induced tendon degeneration would be due to the destruction of the extra cellular matrix, to the inhibition of tenocytes proliferation and to the reduction of collagen synthesis (Szarfman et al., 1995, Corps et al., 2003).
\n\t\tThe intrinsic factors, otherwise defined as endogenous factors, which may give rise to Achilles tendinopathy mainly concern paramorphisms or particular postural aspects that may lead to a functional overload at Achilles tendon level compromising its functionality and structure.
\n\t\t\tAmong these we can mention:
\n\t\t\tThe iper-pronation of the hindfoot associated or not to flat-foot (Ryan et al., 2009, Wyndow et al., 2010).
\n\t\t\tA varus forefoot associated or not to valgus hindfoot (Ajis et al, 2005)
\n\t\t\tA flat-supinated foot (Ryan et al., 2009, Wyndow et al., 2010).
\n\t\t\tA retrocalcaneal spur (Kearney and Costa, 2010)
\n\t\t\tAn Haglund’s deformity (Min et al., 2010)
\n\t\t\tA lower limb asymmetry (Kannus, 1997).
\n\t\t\tA limitation in ankle dorsiflexion (Kaufman et al., 1999).
\n\t\t\tA limitation of the subtalar joint mobility (Kvist, 1991).
\n\t\t\tA poor muscle strength of lower limbs in general and particularly of the calf muscles. In fact, a muscle with a stamina few level cannot effectively protects the tendon structure (Kannus, 1997).
The Dehydration (Hestin et al., 1993, Schwellnus et al., 1997, Gottschalk and Andrish, 2011).The hyperlipidemia (Mathiak et al., 1999, Ozgurtas et al., 2003).
\n\t\t\tThe hyperuricemia (Dodds e Burry, 1984).
\n\t\t\tThe tendon temperature increase resulting from sporting activities (Wilson e Goodship, 1994).
\n\t\t\tChanges in the genes expression regulating the “cell-cell” and the “cell-matrix” interaction, associated to a matrix metal proteinase 3 (MMP-3) down-regulation and to a metal proteinase 2 (MMP-2) and Vascular Endothelian Growth Factor (VEGF). up-regulation (Ajis and Maffulli, 2007).
\n\t\tIn several sports, especially in those where its expected the run and/or the jumps, the injuries and / or the Achilles tendon tears are often associated with errors in the training planning (Hess et al., 1989, Clain and Baxter, 1992, Jozsa and Kannus, 1997, Mahieu et al., 2006). One of the most important causes seems represented by overtraining (Clement e coll, 1984), then follow the changes and / or the increasing in the training program carried out without an appropriate adaptation period (Kvist, 1991, Kwist, 1994, Järvinen et al., 2001) and a lack of specific athletic skill (James e coll., 1978). Others extrinsic factors that may give rise to Achilles tendinopathy that we must remember are: fatigue, poor technique, poor equipment and environment conditions (temperature, humidity, altitude, wind) (Young and Maffulli, 2007).
\n\t\t\tThe aim of this study is to verify, through a retrospective analysis, conducted in an active sports population, the incidence of both Achilles tendons spontaneous ruptures and tendinopathy in relationship to the blood group.
\n\t\tWe considered two different groups composed by 45 caucasian patients belonging to the Northern Italy population whose age, weight and height was respectively 32+7 years, 78+6,7 kg and 178+5,5 cm. In the first group (G1), all subjects attended our medical center complaining of Achilles tendon pain or following a surgery of scarification or open tenorraphy at this level. G1 patients practiced sport activity at professional or amateur level. 24 patients (53,3% of the subjects) followed a conservative program for Achilles tendinopathy, while the two groups of patients surgically treated 15 subjects (equal to 33,3%), with open tenorraphy and 6 subjects, (13,3%) with tendon scarification) were following the specific post-surgery rehabilitation program. In the second group (G2) all subjects. practiced a sport activity at professional or amateur level but none of them had never suffered for tendinopathy during his career. All the subjects were informed of the aim of the study and gave their written consent for the data processing.
\n\t\tAll subjects were required to produce an official document in which their blood group was annotated. The clinical diagnosis of Achilles tendinopathy, formulated for the 20 patients who had not undergone surgical treatment, was confirmed by ultrasonography performed in accordance with the criteria in the following form (Annex A). Both clinical and imaging criteria were adopted in accordance with the protocol already used by the Research Unit for Exercise Science and Sports Medicine, University of Cape Town (Schepsis et al., 2002, Alison et al., 2007, Collins et al., 2010). The clinical criteria allowing us to formulate diagnosis of Achilles tendinopathy were:
\n\t\t\tGradual progressive pain over the Achilles tendon area > 6 weeks
Early morning pain
Early morning stiffness
History of swelling over the Achilles tendon area
Tenderness to palpation over the Achilles tendon
Palpable nodular thickening over the affected Achilles
Positive “shift” test (movement of the nodular area with plantar dorsi-flexion).
For all considered variables the usual statistical indices (average and standard deviation) were calculated. The normality of data distributions was checked with a Kolmorogov-Smirnov test. The difference between the recorded values and the expected values was calculated by a Chi Square Test, the statistic significance was posed to p<0.05.
\n\t\tG1 group
\n\t\t\t30 subjects (66.6%) belonged to group 0. 19 of these 30 subjects (equal to 63.3%) had undergone a chirurgical tenorraphy, 7 subjects (equal to 23.3%) had undergone a chirurgical scarification and the remaining 4 subjects (equal to 13,3%) had undergone a conservative treatment.
\n\t\t\t8 subjects, equal to 17.7%, belonged to group A. 6 of these 8 subject (equal to 75%) had undergone a chirurgical tenorraphy and the remaining 2 subjects (equal to 25%%) had undergone a chirurgical scarification.
\n\t\t\t4 subjects equal to 8.8% belonged to B group. 2 of these 4 subjects (equal to 50%) had undergone a chirurgical tenorraphy while the remaining 2 subjects (equal to the 50%) had undergone a conservative treatment.
\n\t\t\t3 subjects equal to the 6.6% belonged to the group AB. All these subjects had undergone to a chirurgical scarification.
\n\t\t\tAll subjects were male.
\n\t\t\tG2 group
\n\t\t\t18 subjects (equal to 40%) belonged to group 0.
\n\t\t\t20 subjects (equal to 44,4%) belonged to the A group.
\n\t\t\t5 subjects (equal to 11,1%) belonged to the B group.
\n\t\t\t2 subjects (equal to 4.4%) belonged to the AB group
\n\t\t\tAll subjects were male.
\n\t\t\tThe difference between the subjects belonged to group 0 in G1 an G2 group was statistically significant (p<0.005).
\n\t\t\tThe difference between the subjects belonged to group A in G1 an G2 group was statistically significant (p<0.01).
\n\t\t\tThe difference between the subjects belonged to group B in G1 an G2 group was not statistically significant.
\n\t\t\tThe difference between the subjects belonged to group AB in G1 an G2 group was not statistically significant (p<0.01).
\n\t\tAlready in the second half of the last century (Aird et al., 1953) several works showing an association between the blood groups and different types of pathology were published. In this context, we can mention the relationship between blood groups and hip primary osteoarthritis (Lourie, 1983), acute hematogenous osteomyelitis (Eid, 1985), tendon ruptures (Jozsa et al., 1989, Kujala et al., 1992, Mafuli et al., 2000), nail-patella syndrome (Renwich and Lawler, 1955), spondylolisthesis (Wynne-Davies and Scott., 1979), delay in bone healing after fracture (Kujala et al., 1992), just mentioning some studies in a orthopedics context. The hypothesis in patients suffering from generalized tendinopathy (that may include rotator cuff pathology, epicondylopathy, carpal tunnel syndrome, triggering of the long finger flexor tendons and extensor tendon pathology such as de Quervain’s disease) of a “mesenchymal syndrome”, theorizing about a possible genetic component that could cause an abnormal formation of collagen was advanced by Nirshil (Nirshl, 1969). He was comforted in his theory by the fact that in this group, normal routine rheumatologic tests were normal. In general tendinopathy context, Achilles tendon has a particularly important aspect. Achilles tendinopathy and ruptures are increasing among the non-sporting population as well (Young and Maffulli., 2007). In this regard, several etiological hypotheses were formulated (Knörzer et al., 1986, Joza et al., 1989; Selvanetti et al., 1997, Maffulli, 1999, Vanek et al., 2003) but in any case, the etiology remains multifactorial (Bestwick and Maffulli, 2000; Wilson and Goodship, 1994).
\n\t\t\tFrom an anatomical point of view, as in any case, it is important to remember how the Achilles tendon received the blood supply. The tendon vascularity comes from two arteries which run longitudinally to the tendon belly. A part of its blood supply comes from vessels running in the paratenon that are mainly derived from the posterior tibial artery. An additional supply in the proximal part of the tendon is furnished by the muscle bellies that continues into the tendon via the endotenon, (in any case this contribution is not significant). Finally, the distal region receives vessels from an arterial periosteal plexus on the posterior aspect of the calcaneus. The Achilles tendon has, in its downward course, a kind of anatomical twist starting above the point at which is the fusion with the solearis tendon portion. This twist is much more evident as less is important the solearis fusion (Jozsa e Kannus, 1997). This twist causes the emergence of a stress area resulting in a lesser blood flow, displaced about 2-6 centimeters above the tendon heel insertion. For this reason, this area is the site most commonly encountered for pathological risk.
\n\t\t\tFrom a structural point of view, the Achilles tendon shows a tenocytes and tenoblasts percentage equal approximately to 90-95% of its cellular elements. Collagen and elastin are present at levels of about 70 and 2% respectively of the dry weight of the tendon structure and form the most part of the extracellular matrix. The collagen production in the tendon can be affected by many factors, such as the inheritance, the diet, the nerve supply, besides genetic and hormonal factors (Viidik., 1973). Corticosteroids inhibit the new collagen growth while insulin, estrogen and testosterone favor it (O’Brien, 2005). Even the mechanical stimulus related to physical exercise promotes the new collagen synthesis, the increase in the myofibrils number and size and the metabolic enzymes concentration. This will result in increasing the tendon tensile strength (O’Brien, 2005). The Achilles tendon has a high capacity to withstand the tensional forces created by the movements. In vivo peak force of the Achilles tendon has been measured at more than 2.200 Newtons (Fukashiro et al., 1995), namely in the order of 50–100 N/mm (Waggett et al., 1998). However, Achilles tendon transmits forces that are approximately seven times the subject body weight during activity such as running, this represents a huge increase on the forces that normally act during standing which are about half the body weight(Ker et al., 1987). When the Achilles tendon is subjected to tensile stress its wavy configuration disappears and its collagen fibers respond in linear manner to increasing load and a strain level greater than 8% leads to macroscopic rupture due to tensile failure of the tendon collagen fibers (O’Brien, 1992)
\n\t\t\tCollagen type most represented is the type I, with a rate of approximately 95% (Kastelic et al., 1978; Maffulli and Benazzo, 2000). Type I collagen fibrils are grouped into fibers, fiber bundles, and fascicles, so that the Achilles tendon is a very similar to a multistranded cable. However, Achilles tendons which have undergone a complete rupture, show an increase of type III and type V collagen which are known to be less resistant against tensile stress (Coombs et al., 1980, Wren et al., 2000; Koob and Vogel, 1987; Benjamin and Ralphs, 1998). In fact, the type III collagen is mainly present in the tendon during the healing process (Jósza e Kannus, 1997, Myerson and McGarvey, 1999) while type V collagen increases with the tendon aging process and is associated with a decrease in diameter of tendon fibers as well with a decrease in its mechanical properties (Dressler et al., 2002, Goncalves-Neto et al., 2002). In fact, some studies have shown that the tenocytes, following a damaging and / or degenerative event, show an increase in type III and V collagen production that perturb the tendon tissue architecture decreasing its stress resistance (Waterston e coll., 1997). Also other Authors underline that an important proportion of type I collagen increases the strength of the tendon structure (Butler e coll., 1978) and that the minor structural strength of type III and V collagen compared with type I collagen is attributable to the fact that the first two types (III and V) have fewer crosslink than the second one (I) (Józsa e coll., 1990). In addition, some studies indicate an inverse correlation between the type III collagen reactivity and diameter, and thus the structural strength, of tendon fibers (Birk e Maine, 1997). So, a repeated micro-injuries history to the Achilles tendon level may lead to the formation of a hypertrophic tendon tissue which is biologically weaker and which also tends to replace the normal tissue.
\n\t\t\tIn fact, during the normal physiological activity, some microscopic breaks occur in the tendon substance. They are continually remodeled by the formation of new collagen. Obviously, this destruction-remodeling process is particularly emphasized in some sports activities, as for example the run, that strongly stresses the tendon structure (Kirkendall, 1997, Selvanetti et al., 1997). Subjects belonging to blood group 0 shows a N-acetylgalactosamine transferase activity much higher than in subjects in A and B group (Kujala e coll., 1992). This increased N-acetylgalactosamine transferase activity would be result in an increase in type III collagen production within the tendon.
\n\t\t\tSince the type III collagen shows less resistance against mechanical stress compared to type I collagen (Waterston e Maffulli, 1997), its abnormal proliferation may expose to tendinopathy, which could end in tendon spontaneous rupture (Joza et al., 1989, Maffulli, 1999, Maffulli et al., 2000). Is also interesting to note that recently a type III collagen abnormal proliferation and a decreasing in type I collagen are always present in the Achilles tendon calcific insertional tendinopathy (Maffulli et al., 2010). Interesting to note that, since the ABO gene encodes for transferases, some studies have suggested that the different enzymes produced by the ABO gene, could determine not only the glycoprotein antigens structure determination on the red blood cells, but also some types of glycoproteins found within the ground tendons substance (Jozsa et al., 1989). Other studies have proposed that other genes, closely linked to the ABO gene on the tip of the long arm of chromosome 9q32-q34, which encode for components of the extracellular matrix, are more likely associated with Achilles tendon pathology (.Kannus and Natri, 1997, Kujala et al., 1992).
\n\t\t\tTwo of these genes, tenascin-C gene and COL5A1, encode for structural components of tendons (Mokone et al., 2005). The COL5A1 gene encodes for the pro alpha1 (V) collagen chain, found in most of the isoforms of type V collagen (Birk, 2001, Silver et al., 2003).
\n\t\t\tIn literature, we can find other examples concerning other pathologies, such as the nail-patella syndrome, where the LMX1B gene, is closely linked to the ABO gene, encoded for a protein responsible for the pathology (Bongers et al. 2002).
\n\t\t\tHowever, as already suggested by other Authors (Adam and Maffulli, 2007), it is highly unlikely that a single gene, or a group of genes, are exclusively associated with the development of the symptoms of Achilles tendon injury. In fact, it’s more probable that this condition is polygenic, and other genes that encode for important structural components of tendons are also associated with Achilles tendon injury.
\n\t\t\tIn any case, the above could explain the high incidence of the Achilles tendon spontaneous ruptures found by some Authors in individuals belonging to blood group 0 than in A and B group (Joza e al., 1989, Maffulli, 1999). Furthermore, it is interesting to underline that the type III and V collagen high percentage would may explain the occurrence of a spontaneous rupture in tendons that does not show previous degenerative processes.
\n\t\t\tIn our subjects, the group 0 most found frequency (66.6% p<0.005) confirms the hypothesis of an increased susceptibility of individuals belonging to this group in developing tendinopathy at Achilles tendon level and would agree with previous results findings by others Authors (Joza e al., 1989, Maffulli, 1999). Obviously, the limited sample that we considered in our study does not allow us to affirm with certainty this hypothesis which should be confirmed by further studies to be carried out on a larger population. For this reason the results of our study must be interpreted with the greatest attention taking into account this limitation.
\n\t\t\tIn any case, this finding seems particularly interesting in a sporting context, especially concerning its possible use as a preventive measure. In fact, our study may suggest the importance for athletes belonging to 0 group, that practice a sporting activity, such as football, athletics, jogging, running, and/or at least all the other sporting activities which strongly encourage stress to the Achilles tendon, to carry out a regular preventive program based primarily on increasing the Achilles tendon eccentric strength (Allison and Purdam, 2009, Gärdin et al., 2009).
\n\t\t\tIn conclusion, during a sporting activity there is a high incidence of tendon injuries, however, the exact etiology of this condition is not yet fully understood. Some studies, to which our study is a part of, suggest that the genetic component can play an important role; so given the interest and the importance of these problems, we hope that in the future, others studies will further clarify and deepen this exciting topic.
\n\t\tSoft tissue diagnostic ultrasound examination of the Achilles tendon
\n\t\t\t\t\tRight Achilles tendon:
\n\t\t\t\t\tTendon:
\n\t\t\t\t\t•Shape:
\n\t\t\t\t\t•Angular:__
\n\t\t\t\t\t•Fusiform:__
\n\t\t\t\t\t•Margin:
\n\t\t\t\t\t•Sharply defined__
\n\t\t\t\t\t•Poorly defined__
\n\t\t\t\t\t•Contour:
\n\t\t\t\t\t•Smooth__
\n\t\t\t\t\t•Nodular__
\n\t\t\t\t\t•Tapered__
\n\t\t\t\t\t•Max. diameter:
\n\t\t\t\t\t•AP:_____ mm
\n\t\t\t\t\t•TRV:_____ mm
\n\t\t\t\t\t•Internal architecture
\n\t\t\t\t\t•Organised__
\n\t\t\t\t\t•Central hypoechoic foci (med/lat/ant/post)__
\n\t\t\t\t\t•Disrupted fibres (mild/mod/severe)__
\n\t\t\t\t\t•Haematoma__
\n\t\t\t\t\t•Calcification__
\n\t\t\t\t\t•Acoustic shadowing__
\n\t\t\t\t\t•Power Doppler vascularity
\n\t\t\t\t\t•Absent__
\n\t\t\t\t\t•Present__
\n\t\t\t\t\t•Prominent__
\n\t\t\t\t\tParatenon
\n\t\t\t\t\t•Fluid:
\n\t\t\t\t\t•Absent__
\n\t\t\t\t\t•Present
\n\t\t\t\t\t•Site_____
\n\t\t\t\t\t•Amount_____
\n\t\t\t\t\t•Soft tissue swelling
\n\t\t\t\t\t•Absent__
\n\t\t\t\t\t•Present__
\n\t\t\t\t\t•Power Doppler Vascularity
\n\t\t\t\t\t•Absent__
\n\t\t\t\t\t•Present __
\n\t\t\t\t\t•Increased__
\n\t\t\t\t\t•Retrocalcaneal Bursa
\n\t\t\t\t\t•Normal__
\n\t\t\t\t\t•Fluid filled__
\n\t\t\t\t\t•Kager’s fat
\n\t\t\t\t\t•Normal__
\n\t\t\t\t\t•Hyperechogenic__
\n\t\t\t\t\tMyotendinous junction
\n\t\t\t\t\t•Normal__
\n\t\t\t\t\t•Tear__
\n\t\t\t\t\tCalcaneus
\n\t\t\t\t\t•Normal__
\n\t\t\t\t\t•Abnormal__
\n\t\t\t\t\tLeft Achilles tendon:
\n\t\t\t\t\tTendon:
\n\t\t\t\t\t•Shape:
\n\t\t\t\t\t•Angular:__
\n\t\t\t\t\t•Fusiform:__
\n\t\t\t\t\t•Margin:
\n\t\t\t\t\t•Sharply defined__
\n\t\t\t\t\t•Poorly defined__
\n\t\t\t\t\t•Contour:
\n\t\t\t\t\t•Smooth__
\n\t\t\t\t\t•Nodular__
\n\t\t\t\t\t•Tapered__
\n\t\t\t\t\t•Max. diameter:
\n\t\t\t\t\t•AP:_____ mm
\n\t\t\t\t\t•TRV:_____ mm
\n\t\t\t\t\t•Internal architecture
\n\t\t\t\t\t•Organised__
\n\t\t\t\t\t•Central hypoechoic foci (med/lat/ant/post)__
\n\t\t\t\t\t•Disrupted fibres (mild/mod/severe)__
\n\t\t\t\t\t•Haematoma__
\n\t\t\t\t\t•Calcification__
\n\t\t\t\t\t•Acoustic shadowing__
\n\t\t\t\t\t•Power Doppler vascularity
\n\t\t\t\t\t•Absent__
\n\t\t\t\t\t•Present__
\n\t\t\t\t\t•Prominent__
\n\t\t\t\t\tParatenon
\n\t\t\t\t\t•Fluid:
\n\t\t\t\t\t•Absent__
\n\t\t\t\t\t•Present
\n\t\t\t\t\t•Site_____
\n\t\t\t\t\t•Amount_____
\n\t\t\t\t\t•Soft tissue swelling
\n\t\t\t\t\t•Absent__
\n\t\t\t\t\t•Present__
\n\t\t\t\t\t•Power Doppler Vascularity
\n\t\t\t\t\t•Absent__
\n\t\t\t\t\t•Present __
\n\t\t\t\t\t•Increased__
\n\t\t\t\t\t•Retrocalcaneal Bursa
\n\t\t\t\t\t•Normal__
\n\t\t\t\t\t•Fluid filled__
\n\t\t\t\t\t•Kager’s fat
\n\t\t\t\t\t•Normal__
\n\t\t\t\t\t•Hyperechogenic__
Myotendinous junction•Normal__
\n\t\t\t\t\t•Tear__
\n\t\t\t\t\tCalcaneus
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\n\t\t\t\tFour out of every 10 patients are harmed while receiving care; costing payers an average of $8000 per admission [1, 2]. Errors related to diagnosis, medication errors, and unsafe surgical procedures are most frequently reported [1]. Over the past two decades, numerous resources and attention have been devoted to preventing medical errors and adverse events. Yet, in complex, high-risk systems, eliminating errors is unrealistic [3]. Safety practices must incorporate both error prevention and error recovery strategies.
This chapter will focus on error recovery as a critical safety strategy. Topics discussed in this chapter include (1) the error recovery process, (2) the role of health care providers in error recovery, (3) strategies that enhance and prohibit error recovery, and (4) individual and organizational characteristics that influence error recovery.
Health care harm is a top safety concern globally. Medical errors occur when actions (intended or unintended) fail to meet their desired outcome, an action is not completed as intended, or the wrong action is taken to achieve an aim [4, 5]. In other words, errors result from unintended consequences as well as when health care providers make the wrong decision. The Institute of Medicine’s (IOM) seminal report
Research investigating the nature and impact of medical errors within the health care system began in earnest in the 1990s. Initially, human behavior, such as carelessness, poor motivation, and inattention, was blamed as the source of medical errors [6]. However, a shift away from the physiological and psychological limitations of humans and toward system error introduced new safety lessons from areas outside of the traditional health care arena [3, 6, 9]. Strategies adapted from safety-critical industries such as transportation, manufacturing, and aviation brought forward important gains in the fight to improve patient safety.
Aviation safety, for example, depends on managing errors, both through prevention and recovery [9]. In 1995, the US Secretary of Transportation challenged the aviation industry to meet the goal of zero accidents [10]. Interventions such as crew resource management training, checklists, and new technologies were introduced to address attitudes, behavior, and performance with the goal of improving aviation safety. Considerable efforts and resources were invested in the industry to limit opportunities for human error. However, human error is inevitable, particularly in complex, high-hazard organizations, and the goal of zero errors was unrealistic [3]. As a result, the aviation industry recognized the importance of error recovery and began training pilots to identify and remediate errors when they occurred [11].
Still, health care is focused on preventing medical errors, leaving behind important lessons in correcting errors to reduce adverse events. Health care historically equates errors with failure, and failure is unacceptable [12]. Thus, the notion of error management is not easily embraced. Error management involves understanding the nature and extent of errors, changing the conditions that create errors, identifying behaviors and actions that mitigate damage from errors, and training personnel in their use [9]. Error management incorporates two unique aspects [6]. The first aspect is prevention or limiting the incidence of errors. The second aspect is containing the damaging effects of errors, also referred to as error recovery. Error recovery is a highly valued strategy in safety programs outside of health care and is emerging as an important safety strategy in keeping patients safe [13].
Health care systems are highly complex organizations, consisting of numerous interconnected components including the patients and their condition, the procedure, the team’s expertise, the equipment design and use, and the workload [4]. Communication and the urgency in which decisions are made add further complexity to the system. Finally, these complex systems operate in highly variable environments that are impacted by regulatory, fiscal and social considerations.
High-reliability organizations (HROs) are organizations that operate in complex, high-hazard domains for extended periods without serious accidents or catastrophic failures [14]. HROs are not immune to errors and adverse events, instead, they are preoccupied with failure. Defining features of HROs include their heightened sense of vigilance and ability to anticipate and detect problems early in order to prevent adverse events. HROs have learned to make systems as tolerant as possible toward error [6]. Understanding error recovery can support health care organizations on the journey toward high reliability.
In safety-critical systems, error recovery is equally as important as error prevention, as it is often the last barrier of defense before a near miss becomes an adverse event [15]. Error recovery is highly valued in other industries outside of health care, yet it is just beginning to be recognized as an important safety strategy in health care [16]. Both error prevention and error recovery strategies are needed to make greater strides in improving patient safety.
The Eindhoven Model of Near Miss Reporting has been used to explore and define error recovery in safety-critical industries [17]. Errors stem from technical, organizational or human factors that set off a chain reaction that could result in adverse events. When dangerous situations develop, systems are designed with automatic safety mechanisms to prevent negative consequences. In the case of high-risk situations however, automatic safety mechanisms are not always enough to resolve errors. In these instances, human intuition, expertise, and flexibility are needed to intervene and recover the error before harm occurs. If the error is recovered before harm occurs, this is defined as a near miss.
The Eindhoven model offers insight into error recovery processes in health care settings [15]. Henneman and Gawlinski adapted the Eindhoven model to create the Nursing Near-Miss model to better understand the mechanisms nurses use to recover errors at the point of care. In this model, bedside nurses are the final line of defense between a near miss and an adverse event. The researchers pointed out that surveillance is a key strategy nurses use to prevent developing incidents from becoming adverse events. A growing body of literature describes the ingenuity and adaptability of health care providers in recovering errors.
Error recovery is a three-step sequential process incorporating (1) identification, (2) interruption and (3) correction [17, 18, 19]. First, an error must be detected. Error identification or detection is the process of knowing that an error occurred and may be triggered by a mismatch in an expected outcome. This step is aimed at making errors quickly apparent, thereby enabling recovery. Factors such as knowing the patient, players, plan of care, and the environment aid in identifying medical errors [16, 20, 21].
Interrupting an error is the second step in the error recovery process. In this step, participants attempt to understand how the error occurred, the level of importance, and potential countermeasures that may be necessary to return the situation to normal [20, 21, 22, 23]. Health care providers interrupt errors using actions such as offering assistance, clarifying orders, and even verbally interrupting [16].
Perseverance is key to correcting errors, particularly when error identification or interruption was not successful [16]. In this step, the focus is on deploying countermeasures to avert the error and reducing patient harm [20, 21, 22, 23]. Being physically present, reviewing or confirming the plan of care, and involving other experts or leaders are successful strategies in correcting errors [16]. The system returns to its’ safe state and patient harm is averted when errors are successfully recovered [19]. If errors are not successfully recovered, adverse events and potentially catastrophic consequences may occur.
Health care providers rely on flexibility, ingenuity, surveillance, and clinical judgment in recovering errors [16]. Henneman et al. first recognized the importance of surveillance in the error recovery process [15, 20, 21, 24]. Surveillance involves the continuous acquisition, analysis, and synthesis of information from both an individual and organizational perspective. Surveilling the patient and the environment enables providers to recognize developing complications and intervene appropriately. In contrast, when surveillance is lacking dangerous events may develop. Clinical judgment integrates knowledge, skills, expertise, and reasoning to recognize and address potentially dangerous situations [16]. Finally, providers use creativity and flexibility when devising and choosing appropriate strategies to interrupt and correct errors.
Researchers have attempted to quantify the number of errors recovered by health care providers. An integrated review of the literature noted that the magnitude of error recovery among nurses varies from as much as 18 times per 1000 patient days among medical-surgical nurses to as many as two errors per shift among critical care nurses [16]. Perioperative nurses have been known to recover as many as 11 errors per surgical case [22]. Nurses commonly recover errors related to medication errors, mismanagement of aversive systems, mismanagement of coexisting health issues, and improper use of precaution techniques in invasive monitoring [25]. Nurses accept that errors occur and see error recovery as an ongoing part of their job [15]. They regularly identify, interrupt, and correct errors, yet this information is rarely collected and analyzed. Thus, the important role that nurses contribute to patient safety is often invisible [16].
In addition to nurses, others play key roles in error recovery. A growing body of literature has explored strategies pharmacists employ to recover errors [23, 26]. Emergency department pharmacists were found to recover, on average, 7.8 medication errors per 100 patients [26]. A study of error recovery in community pharmacies found that pharmacists recovered numerous e-prescribing errors daily [23]. Most errors were caught at the identification stage of the error recovery process by pharmacists and technicians using strategies such as double checks and highlighting information on the printed e-prescription. Consulting with other pharmacy team members, reviewing the patient’s history, and consulting with patients were strategies used to interrupt medication errors. Finally, pharmacists and technicians contacted prescribers to correct medication errors.
Patients and families also contribute to identifying and interrupting medical errors. A study of families of hospitalized children attempted to quantify the number of errors recovered by families. Benjamin et al. reported that 8% more medical errors were identified and interrupted when families were actively engaged with the health care team during family-centered rounds [27]. Families questioned medication changes, scheduling issues, and adverse drug reactions. The literature supports the notion that patients and families are increasingly involved in early error detection [28]. An analysis of near misses in the National Health Service found many instances of family members reminding staff about lapsed arrangements, pointing out overlooked care plans, and insisting on tests. The literature indicates that patients frequently identify communication and coordination related problems that may lead to adverse events [29]. Key strategies enabling them to prevent adverse events were knowing the patient and plan of care. Patients and families should be encouraged to actively engage in the care process and speak up when concerns arise [28].
While there is no standardized approach to capturing the magnitude of medical errors, front-line providers, as well as patients and families, play critical roles in recovering errors. Patients and families contribute to ongoing surveillance through active engagement in the care process. Effective communication between health care team members, patients and families aids in identifying and interrupting medical errors. Flexibility, creativity, clinical judgment, and surveillance are key strategies enabling health care providers to correct errors.
Health care organizations are striving toward resilience during turbulent times in which they continue to struggle with access, cost and quality issues. Providers are challenged to make intricate decisions in dynamic, fast-paced, complex environments under tight time constraints. Errors are likely to occur under such conditions. Individual characteristics and organizational structures and processes can either help or hinder error recovery.
Individual characteristics that influence error recovery include expertise and workload [16]. Experts, like non-experts, are not immune to errors. However, what is unique about experts, is that they can recover errors more quickly than non-experts [12]. Experts unconsciously organize knowledge into manageable chunks that allow them to access and use critical information when necessary [12, 16, 30, 31, 32]. Experts rely on past experiences to help them identify cues and recognize patterns. They are better able to synthesize explicit and tacit knowledge in meaningful ways as compared to non-experts. Experts separate critical and relevant information from irrelevant information. In the end, experts develop what is known as deep smarts, a special form of wisdom that incorporates social, emotional, formal, and experiential knowledge [32]. As clinicians develop deep smarts, they exhibit greater confidence, perform more efficiently, and achieve higher levels of performance.
In the health care arena, experts use a multi-dimensional approach to integrate clinical judgment with knowledge of the patient, environment, and plan of care that allows them to more readily recover errors [16, 20, 21, 31]. A laboratory study of attending critical care physicians, residents, and medical students exploring the relationship between expertise and error recovery found that experts (physicians) recovered more (75%) errors than residents (61%) [33]. A study exploring the ability of dialysis nurses to recover errors determined that expert nurses detected more errors than non-expert nurses [34]. A study exploring error recovery among medical-surgical nurses found that expert nurses were four times more likely to recover medical errors than non-expert nurses [31].
Another hallmark of expertise is knowing when to deviate from standard protocols and employ shortcuts [35]. The ability to gauge tolerable risk in clinical situations is acquired over time and can only reside within experts. A study of trauma physicians and residents found that expert physicians made fewer errors when deviating from standard protocols than first- and second-year residents [31]. When deviations from standards or countermeasures are required to prevent adverse events the role of expertise should not be underestimated.
Workload is also associated with error recovery. When workload increases, nurses’ ability to recover errors decreases [13, 31]. The notion of workload incorporates the demand placed on one’s cognitive function, physical energy and the work pace itself [36]. Acute care settings are fast-paced, complex environments in which health care providers are constantly combining complex thinking processes with psychomotor and affective skills to deliver appropriate care and interventions [37]. Nurses, in particular, spend a great deal of time providing direct patient care and communicating with patients, families, and team members [38]. Patient care involves nursing process activities such as assessing patients’ clinical conditions, judging the need for nursing care intervention, implementing nursing care measures, and evaluating the effects of therapy. Communication involves consulting with team members, delegating to others, and patient education. Nurses are forced to cognitively shifting between patients based on their condition, medications, therapies, and requests within tight timeframes. As stressors and demands build, the nurse’s thought processes and attention are negatively affected. Error identification and interruption is a complex process that requires significant cognitive resources [39]. Consequently, when nurses are experiencing high cognitive loads, due to heavy patient assignments or workload, their cognitive defenses and capacity to recovery errors are diminished.
In addition to individual characteristics that influence error recovery, there are organizational characteristics as well. These characteristics include a culture of safety and leadership.
A culture of safety is the most important organizational factor contributing to successful error recovery. Organizations with a strong culture of safety recover errors more readily [13, 16]. On average, there are 2.4 recovery opportunities per error [13]. When a recovery opportunity is missed, individuals and organizations have another opportunity to identify, interrupt and correct the error before harm occurs. Organizations that prioritize safety engage in practices and behaviors that enable ongoing surveillance and ultimately error recovery. Practices such as interdisciplinary bedside rounds, effective handoffs, reducing interruptions and facilitating open and ongoing communication enhance early identification and resolution of errors [20, 21, 27, 28, 29].
When organizations do not prioritize safety, errors are more likely to occur, and error recovery opportunities are missed. In this case, important safety checks are skipped, shortcomings in protocols and procedures are noted, and critical knowledge is not transferred between providers making it difficult for errors to be identified [13].
Supportive leadership is also an important organizational characteristic influencing error recovery. Studies noted that when all else fails, involving leadership in the final stage of error recovery is an effective countermeasure to prevent patient harm [20, 21, 31]. But the role of leadership goes well beyond stepping in as the voice of authority to recover errors. Financial constraints, time pressures, and performance constraints put additional strain on organizations and impact error recovery processes [36, 37]. Leadership must develop a portfolio of strategies aimed at managing errors that are coordinated between executives, middle management and frontline staff [40]. Middle managers can act as a buffer for front-line providers and negotiate for solutions to alleviate heavy workloads. Executives can ensure a culture of safety and prioritize safety over other domains when faced with competing pressures. Leadership decisions, at all levels, contribute to creating an environment that either facilitates or hinders error recovery at the point of care.
Organizations striving to consistently provide excellence in quality and safety for every patient, every time must make safety a priority. A key safety strategy in resilient organizations is early error detection and mitigation of medical errors [6]. This strategy must be embraced by the health care industry. Today, health care providers are making critical decisions in complex situations within tight time constraints which contribute to medical errors. When errors occur, expertise and workload are individual characteristics that enhance error recovery. Expertise must be retained and redeployed across the staff. Strategies to facilitate the transfer of expert knowledge or deep smarts to non-experts should be harnessed. Workload and staffing levels must facilitate error recovery. Thus, workload or care models that leverage expertise should be explored. Finally, systems and processes must be adapted to address the strengths and weaknesses of human cognitive functions, particularly as health care becomes more complex.
This chapter described the error recovery process, highlighted the role of health care providers in error recovery, identified strategies that enhance and prohibit error, and explored individual and organizational characteristics that influence error recovery. Health care providers, patients, and families demonstrated ingenuity and adaptability when recovering errors. Flexibility, creativity, surveillance, and clinical judgment of health care providers are key strategies in identifying, interrupting and correcting medical errors. Characteristics that enhance error recovery include individual provider expertise and organizational culture of safety. A burdensome workload is an organizational characteristic that inhibits error recovery.
The value of error recovery in keeping patients safe is clear, although undervalued in health care. Safety-critical industries recognize that errors cannot be fully eliminated and have embraced error recovery as a critical safety strategy. Health care must do the same.
Delivering chemotherapy to cancer patients is a high-risk activity with numerous opportunities for patient harm [41]. Although the incidence of medication errors in chemotherapy is low, the margin of error for administering toxic chemotherapeutic agents to cancer patients is very small. Memorial Sloan Kettering Cancer Center noticed that as the number of chemotherapy orders increased so too did the number of near-miss medication errors. To minimize medication errors, the hospital implemented the new role of a verification nurse (VN) to review all chemotherapy orders. If a discrepancy is noted in the chemotherapy order, VNs investigate the incident by referring to protocols, contacting the health care provider for clarification, referring to the patient’s plan of care for updates or changes and maintaining open and ongoing communication with the team members. Evaluation of the new role noted a direct correlation between an increase in chemotherapy orders and patient volume with error recovery by VNs. While additional complexity added to an increased number of medical errors, the organization embraced the concept of error recovery. This is an example of how one hospital heightened their sense of vigilance and supported strategies to enable health care providers to anticipate and detect problems early to prevent adverse events.
The author has no real or perceived conflicts of interest.
General requirements for Open Access to Horizon 2020 research project outputs are found within Guidelines on Open Access to Scientific Publication and Research Data in Horizon 2020. The guidelines, in their simplest form, state that if you are a Horizon 2020 recipient, you must ensure open access to your scientific publications by enabling them to be downloaded, printed and read online. Additionally, said publications must be peer reviewed.
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