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Acute traumatic myofascitis is a very painful condition that can affect any area
of the body. The most prevalent area affected is the area over the shoulder bla
de (scapula). This muscle pain syndrome will affect almost everyone at one time
or another. Very often this condition will be misdiagnosed as being related to a
rthritis. Acute traumatic myofascitis is not due to arthritis and is a myalgia,
meaning muscle pain.
Very often the trauma causing a myofascitis can be of such a minimal degree that
it can be unrecognized at the time of occurrence. At other times the individual
will be quite aware of it happening due to the severity of the trauma. The occu
rring pain can be on a scale of 1 to 10, from slight to severe, again depending
on the trauma sustained.
The pain can start on the low number of the scale and if left unattended, it can
become more painful as time goes on. The longer the pain exits, inflammation an
d possible swelling and redness of the tissues will become a serious factor in t
he condition. Inflammation is the body’s response to tissue damage. There is als
o a very good chance that at this stage the condition can become chronic. As thi
s develops into the chronic stage, treating the condition becomes more difficult
and can take longer to resolve.
Several areas of the body can be affected at the same time. Should this occur, t
he condition might be diagnosed as polymyositis, an inflammation of many muscles
? In the older patient it is often called polymyalgia rheumatica. Muscles are co
vered by sheets of tissue, and is called fascia, a fibrous tissue. The fascia fa
cilitates the movement of the muscles between other structures. When the inflamm
ation occurs in the fascia it is called fibrositis. An injury can occur affectin
g only the fascia and not the muscle itself. An injury or damage to the fascia w
ill impact the movement of the underlying muscle. There are many types of injuri
es that can cause an acute traumatic myofascitis. There are several ways these i
njuries can occur. An example would be pushing an object, pulling an object, rea
ching above your head for something, lifting a package (no matter how light), or
even a whiplash injury. Household chores, gardening, etc. can also be a source
of getting injured. Occupations where repetitive actions are necessary are ferti
le ground for injuries to muscles.
When an injury occurs, a “knot” forms in the muscle itself. This knot is called
a “trigger point”. A trigger point can cause pain, not only at the injured site,
but can also send a radiating pain to points emanating far from the site that w
as injured. A pain caused by a trigger point in the area of the shoulder blade (
scapula), top of the shoulder or upper arm, can cause pains radiating into the c
hest. Very often these pains have been mistaken for heart problems and even a po
ssible heart attack. Trigger points can also be caused by poor posture, lack of
exercise, repetitive motion injuries and even poor nutrition.
As previously mentioned, inflammation is natures first step to the healing proce
ss. When this occurs, there is a proliferation of certain cells called “fibrobla
sts” that act as patches to the injured muscle fibers, much like a patch on a le
aking tire tube. These patches result in the formation of scar tissue and adhesi
ons, causing the loss of flexibility of normal muscle tissue. As the healing pro
cess progresses, the muscle will lose its full range of motion because of the sc
ar tissue formation and adhesions.
Treatment at the earliest stages of an injury is extremely important so that pre
vention of the scar tissues and adhesions will be lessened or completely prevent
ed. It is therefore advisable to see your healthcare provider as soon as possibl
e. The longer the condition is left unattended, the greater the possibility of e
xtensive scar tissue and adhesions forming, and a greater loss of normal range o
f motion. At this stage, more extensive treatment will become necessary to resto
re normalcy. Treatments by the healthcare provider, may consist of several types
of treatment such as, electric muscle stimulation (EMS), ultrasound (US), and m
assage therapy. If the injury occurred within a 48-hour period, cold packs or ic
e massage may also be used. If, after the 48-hour period, heat packs (preferably
moist) can be used. The healthcare provider will also instruct the patient on s
tretching exercises to help prevent loss of range of motion and restore normal r
ange of motion.
The individual must also take an active role immediately after an injury and at
the onset of pain. Here too, they should use ice packs, or they can even apply i
ce massage to the injured area. This should be applied for 15 to 20 minutes on a
nd an hour off, several times daily. After the 48-hour period they should use he
at, preferably moist heat, applied 20 to 30 minutes, several times daily. From t
he onset of injury the patient should also use a good analgesic gel applied 3 to
4 times daily. This will prove very soothing and help relieve pain. It also inc
reases circulation to the injured area, helping the healing process to begin.
As the pain lessens, stretching exercises can be started, slowly at first and gr
adually increased as pain tolerance permits. The bottom line is that when an inj
ury occurs, it should not be ignored. First see your healthcare provider to have
it examined and evaluated. If they do not feel they have to take an active role
in treating the injury, then the patient should definitely follow through by tr
eating the condition as mentioned above. Many individuals will just take an atti
tude that in time it will just go away. True, the pain may lessen as time goes o
n, but there will definitely be remaining scar tissue and adhesions left to some
degree. Most of this is preventable by devoting a little time to your own care.
Necrosis (from the Greek νεκρός, "d ad") is th p matu d ath of c lls ad liv
ig tissu . N c osis is caus d by xt al facto s, such as if ctio, toxis o
t auma. This is i cot ast to apoptosis, which is a atu ally occu ig caus
of c llula d ath. Whil apoptosis oft p ovid s b ficial ff cts to th o ga
ism, c osis is almost always d t im tal, ad ca b fatal.
C lls which di du to c osis do ot usually s d th sam ch mical sigals to
th immu syst m that c lls ud goig apoptosis do. This p v ts a by phag
ocyt s f om locatig ad gulfig th d ad c lls, l adig to a build up of d ad
tissu ad c ll d b is at o a th sit of th c ll d ath. Fo this aso, i
t is oft c ssa y to mov c otic tissu su gically.
Caus s
C llula c osis ca b iduc d by a umb of xt al sou c s, icludig iju
y, if ctio,cac , ifa ctio, poisos, ad iflammatio. Fo xampl , a i
fa ctio (bloc ag of blood flow to muscula tissu ) caus s c osis of muscl t
issu du to lac of oxyg to th aff ct d c ll, such as occu s i amyoca dial
ifa ctio -- a h a t attac . C tai spid (b ow clus ) ad sa ( attl s
a , Both ops) v oms ca caus c osis of th tissu a th bit woud, as
ca a G oup A st ptococcus if ctio (o of th "fl sh- atig" bact ia).
N c otic tissu do s ot ud go th sam ch mical actios that "o mally" dyi
g apoptotic tissu do s. Th sudd failu of o pa t of th c ll t igg s a
cascad of v ts. I additio to th lac of ch mical sigals to th immu sys
t m, c lls u d goi g c osis ca l as ha mful ch micals ito th su oudi
g tissu . I pa ticula , c lls cotai small o ga ll s call d lysosom s, which
a capabl of dig stig c llula mat ial. Damag to th lysosom m mb a ca
t igg l as of th cotai d zym s, d st oyig oth pa ts of th c ll. Wo
s , wh th s zym s a l as d f om th o-d ad c ll, th y ca t igg a
chai actio of fu th c ll d ath. If a suffici t amout of cotiguous tissu
c otiz s, it is t m d gag . P op ca ad t atm t of wouds o aim
al bit s plays a y ol i p v tig this typ of wid sp ad c osis. Du ig
a su gical biopsy, this c osis chai- actio is halt d by fixatio o f zi
g.
N c osis typically b gis with c ll sw llig, ch omati dig stio, dis uptio of
th plasma m mb a ad o ga ll m mb a s. Lat c osis is cha act iz d by
xt DNA hyd olysis, vacuolatio of th doplasmic ticulum, o ga ll b
siv
a dow , a d c ll lysis. Th l as of it ac llula cot t aft plasma m mb
a uptu is th caus of iflammatio i c osis.
Mo phologic patt s
Th a s v distictiv mo phologic patt s of c osis:
Coagulativ c osis is typically s i hypoxic (low oxyg ) vi om
ts, such as a ifa ctio. C ll outli s mai aft c ll d ath ad ca b obs
v d by lightmic oscopy.
Liqu factiv c osis (o colliquativ c osis) is usually associat d w
ith c llula d st uctio ad pus fo matio ( .g. p umoia). This is typical of
bact ial o , som tim s, fugal if ctios b caus of th i ability to stimulat
a iflammato y actio. Cu iously, isch mia ( st ictio of blood supply) i
th b ai p oduc s liqu factiv , ath tha coagulativ , c osis, du to th l
ac of ay substatial suppo tiv st oma.
Gummatous c osis is st ict d to c osis ivolvig spi ocha tal if
ctio s ( .g.syphilis).
Ha mo hagic c osis is du to bloc ag of th v ous d aiag of a o
ga o tissu ( .g. i t sticula to sio ).
Cas ous c osis is a sp cific fo m of coagulatio c osis typically ca
us d bymycobact ia ( .g. tub culosis), fugi, ad som fo ig substac s. It
ca b cosid d a combiatio of coagulativ ad liqu factiv c osis.
Fatty c osis sults f om th actio of lipas s o fatty tissu s ( .g.
acut pac atitis, b ast tissu c osis).
Fib ioid c osis is caus
d by immu
-m diat d vascula damag . It is m
a d by d positio of fib i -li p ot i ac ous mat ial i a t ialwalls, whic
h app a s smudgy ad osiophilic o light mic oscopy.
A achog ic c osis
Spid bit s a cit d as causig c osis i som a as, but such claims a wi
d ly disput d. I th US, oly b ow clus spid s (g usLoxosc l s) hav b
p ov to cosist tly caus c osis.[1] Oth spid s of th sam g us, such
as th Chil a clus i South Am ica, hav simila ly b show to caus c
osis i oth cout i s.[2][3]
Claims of c osis caus d by oth spid s' bit s a commo, but suppo tig vi
d c is lac ig. Coclusiv vid c is difficult to obtai, pa tly b caus ma
y spid bit s a iitially pail ss ad thus th sp ci s go s uid tifi d, a
d pa tly b caus may docto s will p mptiv ly mov v possibly c otic fl
sh
ath tha is fu th tissu damag . A f w spid s commoly susp ct d (but o
t coclusiv ly p ov ) of havig c otic v om iclud :
Hobo spid i o thw st USA[4]
Sac spid i Uit d Stat s ad Aust alia[5]
Whit -tail d spid s i Aust alia ad N w Z alad[6]
R clus spid
How v , a study of 130 cofi m d whit -tail d spid bit s foud that th ff c
ts w lativ ly mild, ad coclud d that th i bit is v y uli ly to caus
c osis.[6]
T atm t
T atm t of c osis typically ivolv s two distict p oc ss s. Usually, th u
d lyig caus of th c osis must b t at d b fo th d ad tissu itslf ca
b d alt with. Fo xampl , a s a o spid bit victim will c iv a ti-v
om to halt th sp ad of th toxis, whil a if ct d pati t will c iv ati
biotics.
Ev aft th iitial caus of th c osis has b halt d, th c otic tissu
will mai i th body. Th body's immu spos to apoptosis, th automati
c b a ig dow ad cyclig of th c ll mat ial, is ot t igg d by c otic
c ll d ath.
Th stada d th apy of c osis (wouds, b dso s, bu s tc.) is su gical mo
val of c otic tissu . D p dig oth s v ity of th c osis, this may ag
f om moval of small patch s of s i, to compl t amputatio of aff ct d limb
s o o gas. Ch mical moval, via a zymatic d b idig ag t, is aoth optio
. I s l ct d cas s, sp cial maggot th apy has b utiliz d with good sults
.
Fascia
Fascia (făsh'ē-ə), pl. fas•ci•a (făsh'ē-ē), adj. fascial (făsh'ē-əl) (f om lati
: a bad) is th soft tissu compo t of th co ctiv tissu syst m that p
m at s th huma body. It it p t at s ad su ouds muscl s, bo s, o gas,
v s, blood v ss ls ad oth st uctu s. Fascia is a uit upt d, th -di
m sioal w b of tissu that xt ds f om h ad to to , f om f ot to bac , f om
it io to xt io . It is sposibl fo maitaiig st uctu al it g ity; fo
p ovidig suppo t ad p ot ctio; ad acts as a shoc abso b . Fascia has a
ss tial ol ih modyamic ad bioch mical p oc ss s, ad p ovid s th m dium
that allows fo it c llula commuicatio. Fascia fuctios as th body's s co
d li of d f s agaist pathog ic ag ts ad if ctios aft th si[citat
io d d]. Aft iju y, it is th fascia that c at s a vi om t fo tiss
u pai .
Lay s of th fascia
NA 1983 TA 1997 D sc iptio Exampl
Sup ficial fascia
This is foud i th subcutis i most gios of th body, bl dig with
th ticula lay of th d mis. [3]
Fascia of Sca pa
D p fascia
Fascia of muscl s
This is th d s fib ous co ctiv tissu that it p t at s ad su ouds t
h muscl s, bo s, v s ad blood v ss ls of th body. T asv salis fa
scia
isc al fascia
isc al fascia,pa i tal fascia
This susp ds th o gas withi th i caviti s ad w aps th m i lay s of co
ctiv tissu m mb a s.
P ica dium
Th a may ci cumstac s i which sutu s a us d to pai tissu ad fac
ilitat h alig. Th t chiqu s that you us , th sutu mat ial you us , ad t
h sp cific typ of dl you us will va y d p dig o wh th you a closi
g a simpl lac atio o th foot, a compl x lac atio o th fac , a gast oit
stial aastomosis, a vascula aastomosis, o closig a m dia st otomy.
Tissu R spos to Iju y:
Th Phas s of H alig
• h mostasis ad iflammatio
• fib oplasia
• woud matu atio
Th is cosid abl ov lap amog th s phas s.
Phas I – H mostasis adIflammatio
With vascula dis uptio th is t asi t vasocost ictio, follow d by vasodi
latatio ad ic as d capilla y p m ability. Cotact of plat l ts with collag
ad g oud substac caus s activatio ad agg gatio of plat l ts. Th it i
sic ad xt isic coagulatio cascad s a t igg d, ad ch motaxis att acts i
flammato y c lls.
N ut ophils, which a th fi st ucl at d c lls to com ito play, iitiat pha
gocytosis ad atimic obial d f s , but by th 3 d o 4th day mac ophag s hav
plac d th ut ophils as th domiat c ll typ .
• Mac ophag s play a c t al ol i woud h alig. Th y mov mic ob s
a d c llula d b is th ough phagocytosis ad zymatic b a dow of th xt ac l
lula co ctiv tissu mat ix, ad th y labo at cyto i s which stimulat ag
iog sis ad fib oplasia.
Phas II – Fib oplasia
Th iflammato y spos abat s as th iflammato y stimuli a mov d, ad th
fib oplastic phas is usually w ll stablish d by th 5th day. Th is fib ob
last mig atio ad p olif atio that is m diat d by a va i ty of ch motactic fa
cto s ad g owth facto s ( .g., fib o cti, C5A, PDGF, ad FGF). As fib oblasts
populat th woud, th y b gi to syth siz ad s c t p ot oglycas, collag
, ad lasti.
In contrast, the tip of cutting needlesis triangular in shape, and the apex form
s a cutting surface, which facilitates penetration of tough tissue, such as skin
. Cutting needles make it much easier to penetrate tough tissue. Penetrating ski
n with a taper needle is very difficult and causes excess trauma to the skin bec
ause of difficulty in penetration and the need to grasp the skin edge very tight
ly with forceps. Consequently, you should never use taper needles to suture skin
.
The tip of the needle holder should grasp the needle about 2/3 of the way back f
rom the point. The needle holder and needle should be roughly perpendicular.
The far skin edge is elevated with the forceps in the left hand, while the rig
ht hand is pronated to “cock” the needle in preparation for taking the first “bi
te”. The tip of the needle should penetrate the skin perpendicularly about 5-10
mm from the wound edge, and the needle should be rotated all the way through the
epidermis and dermis by supinating the right hand to rotate the needle through
its arc.
A Key Maneuver:
The tip of the needle should now be seen protruding into the wound fro
m the subcutaneous tissue. At this point, it is important to maintain the positi
on of the skin edge using the forceps. A common error here is to release the for
ceps from the skin edge, but this allows the skin to retract, and the needle may
move and retract beneath the skin edge.
The key is to maintain the position of the skin edge while releasing the needle
from the needle holder. This will maintain the position of the needle tip. After
the needle is released from the needle holder, the right hand should be fully p
ronated before regrasping the needle. The “bite” can then be completed by supina
ting the right hand in order to complete the rotation of the needle through the
skin.
If it is necessary to reposition the needle in the needle holder before taking
the second “bite,” the needle should be grasped with the forceps, not with your
fingers.
The forceps then elevate the near skin edge in preparation for the second “bite.
” Once again, the right hand is cocked by pronating it, and the needle is passed
upward through the near skin edge by supinating the right wrist in order to kee
p the body of the needle perpendicular to the tissue it is passing through at al
l times. The needle should emerge about 4-5 mm from the wound edge (equidistant
on both sides of the wound).
Scissors:
Scissors are generally held with the thumb slightly in one ring and the ring fin
ger in the other. The index finger stabilizes the instrument by resting on the s
haft.
When cutting sutures, some recommend sliding the tips of the scissors down the s
trands to the point where they will be cut, but it probably makes more sense to
simply move the tips of the scissors directed to the point where the cut will be
made. For external non-absorbable sutures it is important to leave 4-5 mm “ears
” to facilitate suture removal.
Suture Removal:
When?
Face: 3-4 days
Scalp: 5 days
Trunk: 7 days
Arm or leg: 7-10 days
Foot 10-14 days
How?
Many patients are very apprehensive about suture removal, so the first
step is to reassure the patient that the procedure is not painful. The skin sho
uld be cleansed. Hydrogen peroxide is a good choice for gently removing dried bl
ood and exudate.
Then grasp one of the “ears” of the suture with a forceps to elevate the suture
just enough to slip the tip of a small scissor under the suture in order to cut
it. This should be done close to the skin edge in order to minimize the amount o
f contaminated suture that will be dragged through the stitch path. The suture i
s then gently removed by pulling with the forceps. It is frequently a good idea
to reinforce the wound with Proxi-Strips. These are narrow adhesive strips that
are placed perpendicularly across the wound at intervals.