Dr. IA. Ratih Wulansari M,SpPD-KR,M.

Kes,FINASIM

Lahir : Surabaya, 21 April 1970

Pendidikan:
S1 Fak. Kedokteran UNUD(1995)
SP1 Spesialis Penyakit Dalam
FKU UNUD (2003)
S2 Magister Manajemen Rumah
Sakit, FK UGM (2006)
SP2 Konsultan Rheumatologi,
FK UI (2009)
FINASIM Kolegium PAPDI (2016)

Kegiatan :
Praktek : RS Manuaba, RS Prima Medika, RS Puri Raharja
Dosen: S1 Kep Stikes Bali, S2 MM Undiknas, S1 Fisioterapi IIK Medika Persada
 Inflammation & Healing
DR.IA.RATIH WULANSARI MANUABA,SPPD-KR,M.KES,FINASIM
Inflammation

 complex protective reaction

 caused by various endo- and exogenous stimuli
 injurious agents are destroyed, diluted or walled-off
 without inflammation and mechanism of healing could
organism not survive
 can be potentially harmfull
Mechanisms

 local - in cases of mild injury

 systemic
 3 major:
 1. alteration
 2. exsudation - inflammatory exsudate
 liquid (exsudate)
 cellular (infiltrate)
 3. proliferation (formation of granulation and fibrous tissue)
usualy - all 3 components - not the same intensity
 Classification

several points of view

 length:
 acute × chronic (+ subacute, hyperacute)
 according to predominant component
 1. alterative (predominance of necrosis - diphtheria)
 2. exsudative (pleuritis)
 3. proliferative (cholecystitis - thickening of
the wall by fibrous tissue)
 Classification

 according to histological features

 nonspecific (not possible to trace the etiology) - vast majority
 specific (e.g. TB)

 according to causative agent

 aseptic (sterile) - chemical substances, congelation, radiation - inflammation has a
reparative character
 septic (caused by living organisms) - inflammation has a protective character
Acute inflammation

 important role in inflammation has microcirculation!

 supply of white blood cells, interleukins, fibrin, etc.
 Local symptomatology

 classical 5 symptoms
 calor - heat
 rubor - redness
 tumor – swelling
 dolor – pain
 functio laesa - loss (or impairment) of
function
 Systemic symptomatology

 fever (irritation of centre of thermoregulation)

 TNF, IL-1, IL-6, high erythrocyte sedimentation rate
 leucocytosis - increased number of WBC
 bacteria – neutrophils
 parasites – eosinophils
 viruses - lymphocytosis
 leucopenia - decreased " "
 viral infections, salmonella infections, rickettsiosis
 immunologic reactions - increased level of some substances (C-reactive protein)
Vascular changes

 vasodilation
 increased permeability of vessels due to widened intercell.
junctions and contraction of endothelial cells (histamin, VEGF,
bradykinin)
 protein poor transudate (edema)
 protein rich exsudate
 leukocyte-dependent endothelial injury
 proteolysis – protein leakage
 platelet adhesion  thrombosis
 Cellular events

 leukocytes margination  rolling  adhesion  transmigration

 emigration of:
 neutrophils(1-2 days)
 monocytes (2-3 days)

 chemotaxis
 endogenous signaling molecules - lymphokines
 exogenous - toxins

 phagocytosis - lysosomal enzymes, free radicals, oxidative burst

 passive emigration of RBC - no active role in inflamm. - hemorrhagic
inflammation
Phagocytosis

 adhesion and invagination into cytoplasm

 engulfment
 lysosomes - destruction
 in highly virulent microorganisms can die leucocyte and not the
microbe
 in highly resistant microorganisms - persistence within macrophage
- activation after many years
 Outcomes of acute inflammation

 1. resolution - restoration to normal, limited injury

 chemical substances neutralization
 normalization of vasc. permeability
 apoptosis of inflammatory cells
 lymphatic drainage
 2. healing by scar
 tissue destruction
 fibrinous inflammtion
 purulent inflamation  abscess formation (pus, pyogenic membrane, resorption - pseudoxanthoma
cells - weeks to months)
 3. progression into chronic inflammation
 Chronic inflammation

 chronic inflammatory cells ("round cell" infiltrate)

 Lymphocytes : plasma cells, cytotoxic (NK) cells, coordination with
other parts of immune system
 plasma cells : production of Immunoglobulin
 monocytes/macrophages activation of macrophages by various
mediators - fight against invaders - specialized cells (siderophages,
gitter cells, mucophages)
Morphologic patterns of inflammation

 1. alterative
 2. exsudative
serous
fibrinous
suppurative
pseudomembranous
necrotizing, gangrenous
 3. proliferative
primary (rare) x secondary (cholecystitis)
Morphologic patterns of inflammation

 serous - excessive accumulation of fluid, few proteins -

skin blister, serous membranes - initial phases of
inflamm.
 modification - catarrhal - accumulation of mucus
 fibrinous- higher vascular permeability - exsudation of
fibrinogen -> fibrin - e.g. pericarditis (cor villosum, cor
hirsutum - "hairy" heart
 fibrinolysis  resolution; organization  fibrosis 
scar
 suppurative (purulent) - accumulation of neutrophillic leucocytes -
formation of pus (pyogenic bacteria)
 interstitial
 phlegmone – diffuse soft tissue
 abscess - localized collection
 acute – border – surrounding tissue
 chronic – border - pyogenic membrane
 Pseudoabscess – pus in lumen of hollow organ
 formationof suppurative fistule
 accumulation of pus in preformed cavities - empyema (gallbladder, thoracic)
 complications of suppurative inflamm.:
 bacteremia (no clinical symptoms!; danger of formation of secondary
foci of inflamm. (endocarditis, meningitis)
 sepsis (= massive bacteremia) - septic fever, activation of spleen,
septic shock
 thrombophlebitis - secondary inflammation of wall of the vein with
subsequent thrombosis - embolization - pyemia - hematogenous
abscesses (infected infarctions)
 lymphangiitis, lymphadenitis
 pseudomembranous - fibrinous pseudomembrane (diphtheria -
Corynebacterium, dysentery - Shigella) - fibrin, necrotic mucosa, etiologic
agens, leucocytes
 necrotizing - inflammatory necrosis of the surface - ulcer (skin, gastric)
 gangrenous - secondary modification by bacteria - wet gangrene -
apendicitis, cholecystitis - risk of perforation - peritonitis
SUMMARY
The Basics of Healing -
Understanding the Inflammation
Process
The Healing Process

 It is practical to have a sense of the healing process - this will give you insight
into why some injuries take longer than others to recover

 In an ideal world, we would let the process take over and allow the athlete to
heal properly

 In athletics, we do not have the luxury in many cases to allow this to happen
The Healing Process

 Consists of 3 phases:

1) Inflammatory response phase

2) Fibroblastic repair phase
3) Maturation - remodeling phase

• Anything done when treating an athlete that interferes with this

process will likely slow the return to full activity
The Healing Process

 There is little that can be done to speed up physiology

 But we can provide the optimal environment for healing or do the
opposite and impair the process
 Understand these phases, although discussed separately, do overlap
and sometimes are tough to distinguish
The Healing Process

 Inflammatory Response Phase

 The initial inflammatory response is critical to the
entire healing process. If this response does not
accomplish what it is supposed to do, normal healing
cannot take place
 The body often overreacts in this phase
 This is an individual process - each of us are different
 The Healing Process

 The inflammatory response phase

 Signs we are in this phase:
5 signs of inflammation:
Redness
Swelling
Tenderness
Increased temperature
Loss of function
 How long does this phase last?
Typically 72 hrs if treated correctly
 The Healing Process

 Inflammatory Response Phase

 How do we treat this correctly and allow it to do its thing?
 R.I.C.E.
 Rest = Do not use the part (crutches, slings, splints, etc)
 Ice = Used for pain and vasoconstriction (slow down the body’s overreaction)
 20 min on and 1 hr off
 Hunting response - a slight temperature increase during cooling
 A reaction against tissue damage from too cold exposure. This is important to educate athletes on how long they
should leave ice on
 Compression = elastic wrap will help control edema and reduce space for fluids to develop
 Elevation = help the lymphatic system by using gravity to return the damaged cells to the core for removal
The Healing Process

 Fibroblastic Repair Phase

 How do I know?
Generally, signs and symptoms of inflammatory period
subside
Tenderness and pain with function remain
 How long does it last?
Starts few hours after injury and can last as long as four to
six weeks depending on tissue and trauma done
The Healing Process

 Maturation - Remodeling Phase

 Tensile strength begins to increase
 Wolff’s Law states that bone and soft tissue will
respond to the physical demands placed on them to
remodel or realign along the lines of the tensile force
 This is why most patients are now treated with
controlled mobilization rather than complete
immobilization
 The Healing Process

 How do I know?

 Clinical signs and symptoms will now begin to disappear

 As healing progresses to remodeling, controlled activity is warranted with a

gradual return to normal flexibility and strength

 Usually, this is the time to tape, wrap and brace to allow activity while supporting
the structure
 The Healing Process

 Factors that impede healing:

1. Extent of injury or separation of tissue
2. Amount of edema - increased pressure impedes healing process
3. Hemorrhage
4. Poor blood supply
5. Muscle spasm
6. Infection
7. Health, age and nutrition
Allowing activity too early may allow these things to happen!
 The Healing Process

 Methods used to modify healing:

 Drugs: Non-steroidal anti-inflammatory drugs (NSAIDs): ibuprofen, advil,
motrin, etc.- combat out of control inflammation
 Thermal agents - cold first 72 hrs, usually a combo thereafter
 Modalities - Electrical Stimulation = helps with pain and inflammation,
Ultrasound = aids in blood flow and healing in later stages
 Exercise - trend now is early range of motion (ROM) to aid in maturation-
remodeling and avoid adverse biochemical changes
 The Healing Process “Apply our Knowledge”

In general:
 Sprains and Strains:
 RICE for first 72 hrs
 “R” may include brief period of immobilization
 After 72 hrs, introduce heat (hot packs, ultrasound, whirlpool) and range of motion (ROM)
exercises
 When symptoms begin to subside and ROM returns - begin strengthening and return to functional
 If we handle properly, expected length of recovery:
 1st degree = 3-6 wks
 2nd degree = months
 3rd degree = months to years
 The Healing Process
 In general:
 Fractures
 Immobilize 6-8 wks depending on severity
 Then we begin the process
 Expected length of recovery:
 2-4 months
 “itis” -
 Begin healing modalities, stretching and massage right away in combo with ice and electrical
stimulation
 Stimulate blood flow
 Monitor stages and modify as needed
 Generally, we are not going to heal this, we want to keep athlete in functional stages
SUMMARY
SUMMARY