[libribook.com] Traumatic Scar Tissue Management 1st Edition
Prolonged InflammationInflammation will persist as long as debris is present at the wound site.Ineffective ‘clean-up’ during the inflammatory stage may prolong healing. Bothbacteria and endotoxins can lead to the prolonged elevation of pro-inflammatorycytokines (e.g. interleukin-1 (IL-1)) extending this stage beyond its normallength of time. Consequently this can result in the wound transitioning intochronic state with failure to heal. In vitro evidence suggests that the presence ofmacrophages delays wound contraction, therefore the withdrawal ofmacrophages from the wound site may be essential for subsequent stages tooccur in normal sequence and timing. Prolonged inflammation can lead to anincreased level of matrix proteases (e.g. collagenase) that are known to degradethe ECM or conversely the excessive/prolonged presence of cytokines thatstimulate excessive collagen production – resulting in pathophysiological scars(Edwards & Harding 2004, Menke et al. 2007).
Clinical ConsiderationDrainage of excess fluid from interstitial spaces reduces the concentrationof pro-inflammatory cytokines (Fryer & Fossum 2009).
- Page 412 and 413: Wound HealingThe NS plays an import
- Page 414 and 415: Clinical ConsiderationNeural and ci
- Page 416 and 417: Compression SyndromesAlthough perip
- Page 418 and 419: Pathophysiological ConsiderationIf
- Page 420 and 421: Pathophysiological ConsiderationUni
- Page 422 and 423: Clinical ConsiderationAs is the cas
- Page 424 and 425: Pathophysiological ConsiderationFas
- Page 426 and 427: Damasio AR, Grabowski TJ, Bechara A
- Page 428 and 429: Magee DJ (2008) Orthopedic physical
- Page 430 and 431: Stecco C, Porzionato A, Macchi V et
- Page 432 and 433: CHAPTER 5Wound healing and scarsNev
- Page 434 and 435: Wound HealingWound healing, a compl
- Page 436 and 437: Table 5.1Stages of wound healing
- Page 438: Clinical ConsiderationBecause thera
- Page 441 and 442: fibroblast growth factor (FGF), epi
- Page 443 and 444: Clinical ConsiderationDuring wound
- Page 445 and 446: Clinical ConsiderationAlthough the
- Page 447 and 448: Pathophysiological ScarsPathophysio
- Page 450 and 451: Figure 5.3Adapted from Huang et al.
- Page 452 and 453: Pathophysiological considerationFib
- Page 454 and 455: Table 5.2Important pathophysiologic
- Page 456 and 457: According to Klingler (2012):… pa
- Page 458 and 459: Table 5.3Scar types and related ter
- Page 460 and 461: unyielding or pliable and mobile. R
- Page 464 and 465: ImmobilizationThe impact of immobil
- Page 467 and 468: Figure 5.4The fall-out associated w
- Page 469 and 470: Clinical ConsiderationHere we see t
- Page 471 and 472: Pathophysiological ConsiderationAcc
- Page 473 and 474: Pathophysiological ConsiderationNeu
- Page 475 and 476: The diverse biological effects of N
- Page 477 and 478: Clinical ConsiderationCareful appli
- Page 479 and 480: Clinical ConsiderationSome patholog
- Page 481 and 482: Pathophysiological ConsiderationSom
- Page 483 and 484: compressive effect in the keloidal
- Page 485 and 486: alterations in the mechanical envir
- Page 487 and 488: Clinical ConsiderationMechanical fo
- Page 489 and 490: Table 5.4Role of neuropeptides (NP)
- Page 491 and 492: Fitch P (2005) Scars of life. Journ
- Page 493 and 494: Langevin HM (2006) Connective tissu
- Page 495 and 496: active scars. Journal of Bodywork a
- Page 497 and 498: trauma.
- Page 499 and 500: Clinical ConsiderationPostsurgical
- Page 501 and 502: following burn injury,bacterial col
- Page 503 and 504: Table 6.1Comparison of scars (Ogawa
- Page 505 and 506: Pathophysiological ConsiderationAcc
- Page 507 and 508: BurnsA burn injury to the skin or o
- Page 510 and 511: Figure 6.1Depth of burn trauma and
Prolonged Inflammation
Inflammation will persist as long as debris is present at the wound site.
Ineffective ‘clean-up’ during the inflammatory stage may prolong healing. Both
bacteria and endotoxins can lead to the prolonged elevation of pro-inflammatory
cytokines (e.g. interleukin-1 (IL-1)) extending this stage beyond its normal
length of time. Consequently this can result in the wound transitioning into
chronic state with failure to heal. In vitro evidence suggests that the presence of
macrophages delays wound contraction, therefore the withdrawal of
macrophages from the wound site may be essential for subsequent stages to
occur in normal sequence and timing. Prolonged inflammation can lead to an
increased level of matrix proteases (e.g. collagenase) that are known to degrade
the ECM or conversely the excessive/prolonged presence of cytokines that
stimulate excessive collagen production – resulting in pathophysiological scars
(Edwards & Harding 2004, Menke et al. 2007).