الفهرس 
PATHO- PHYSIOLOGY OF BURN
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Abstract
Multiple Oran Failure M.O.F denotes a clinical syndrome that is characterized by a process
of dysfunction and ultimately failure of vital organs (e.g renal, respiratory, haematological and
hepatic).Multiple organ failure (M.O.F) was first diagnosed, as a clinical syndrome in the middle
of the seventies, although its recognition in burned patients was only defined more recently.
Burn injury exerts deleterious effects on all body systems, with the severity and duration of organ
dysfu nction proportionate to the extent of the burn.
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The failure of function m organs hav ing tissues that are
anatomically and functionally different, suggests that a common cellular insult may be the
fundamental pathophysiological event in patients with M.O.F.
Tissue trauma (including burn ) activates non-specific and specific proteolyses in differen t
humoral systems such as the complement, the fibrinol ysis and the coagulati on system, as well as,
the kallikrein cascade. These provoke the release of the mediators responsible for the occurrence
of M.O.F.
The Mediators bf M.O.F. are :
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a - K inins; whicll are polypeptides that increase the capillary permeability, dilate blood vessels
and depress myocardial function.
b - Myocardial depressant factor( M .D.F.); which is a polypeptide released from the pancreas and
leads to a depressant effect on the heart and this exacerbates the shock phase and therefore, is
considered part of the positive feed back deteriorative process that causes progression of the
organ failure .
c - Lysosomes; which are cellular enzymes activated when. the membrane of the cell is disrupted
leading to the reduction in the cellular oxygenation and defect in the sodium pump.
d - Cytoki nes; which are released from different cells , like interleukin IL-1 released from
mononuclear cells which can initiate the coagulation cascade and the inflammatory reaction.
e - Histamine; which is released from mast cells and increases the vascular permeability.
f - Comp lement; which is a group of proteins present in the plasma, activated in a cascade man ner
and has different action in the initi ation of coagul ation , attracting leucocy tes and increasing
capillary permeabi lity.
Intravascular coagulation resu l ts from tissue injury and it is the intermed iary lesion responsi
ble for most of the changes associated with organ fail u re. I t is well kn own
that microaggregates and thrombus formations are important factors in the pathogenesis of M.O.F.
Microaggregates and throm bi may block visceral vasculature and they may release chemical med
iators leading. to increase in the vascular permeability, tissue ischaemia and eventually organ
damage.
The most striking immediate systemic effects following burn injury are related to the haemodynamic
changes that occured. One of these changes is coagulopathy that occured in severe burns with the
presence of thrombocytopenia, increased level of F.D.P and this may lead to the occurence of
D.I.C., respiratory failure, hepatic failure and renal failure.
Fifty male patients. with major burn were included in this study. They were divided into five
groups according to the type of fluid used in the reuscitation and the local management of the bum
wound.
The first group of patients was managed by Brooke’s formula and delayed excision of the burn wound
and skin grafting.
The second group of patients was m anaged by Brooke’s formula and early excision of the burn wound
and skin grafting
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(i.e. 5-7 days).
.The third group of patien ts was man aged by Parkland ’s formula and delayed excision of the bu rn
wou nd and skin grafting.
The fourth group was mana.ged by Parkland’s formula and early excision of the1 bum wound and
skin grafting.
The fifth group was managed by the best combination of fluid resuscitation and the timing of
surgery(least M.O.F. affection)
Each group was further subdivided into three subgrou ps according to the extent of bum :
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Subgroup A : Bums ranged from 30-45% TBSA.
* Subgroup B : Burns ranged from 46-60% TBSA.
* Subgroup C : Burns more than 60% TBSA.
The patients were investigated for respiratory, hepatic, renal and haematological affection and
failure.
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Multiple organ failure was detected , when the following criteria were fulfilled:
PO 2 level less than 75 indicating respiratory Failure. Creatinine more than 2mg indicating renal
Failure.
Double presented level of GOT and GPT indicating Liver Failure.
Criteria for D.I.C indicating haematological Failure.
As regards the timing of surgery, we had two types of interference either early (5-7days post-burn)
or late excision.
Comparison based on the occurence of M.O.F in each group was monitored by the above parameters .
The survival of the patients was also compared between the five groups.
The aim was to select a regimen of both resuscitation and tim ing of surgery which has
the least incidence of M.O.F. occurrence and this regimen was used in group five.
Twenty one patients died in this study, ten of these patients were treated by Brooke’s formula with
a percentage of bu rn ranging from 54-80%. Eight of these patients were treated by Parkland’s
formula wi th a percentage of burn ranging from 60-80%.
The D.I.C was present in 1Oil 0 (100%) in group I and II treated by Brooke’s whereas it was present
in 6/8 (75%) in group III and IV treated by Parkland’s.
Respiratory failure was present in 7/10 (70%) in group Iand II and was noted in 5/8 (62.5%) in
group III and IV.
Renal failure was present in 6/10 (60%) in group I and II and was depicted in 3/8 (37.5%) in group
III and IV.
Liver failure occured in 2/10 (20%) in group I and II where it was found in 1/8 (12.5%) in group
III and IV.
from the results of this study, the haematological failure was present in 88% of the M.O.F.
patients. The respiratory failure was present in 66% of the M.O.F. patients. This was less than
other studies (87,89) because we selected patients having no inhalation injury. Inhalation injury
as a cause of respirator y failure is a problem present in the alveoli and the alveolo-capillary
membrane whereas respiratory failure which occur as a part of M.O.F. is due to microthrombi lodged
in the pulmonary vascular bed. Liver failure occured in 22% of the M.O.F. patients and this was the
least organ to be affected although in the study of Huang in 1992, the occurence of liver failure
was higher when doing pathomorphological studies of liver tissues,than that which abnormal hepatic
function tests could verif y clinicall y. Renal failure occured in 50% of M.O.F. patients and it is
due to tubular necrosis as a part of the M.O.F., and it is not corrected by fluid supplementation.
It is not a pre-renal failure occuring due to inadequate resuscitation.
from the results mentioned, we found that group III and IV had better results than group I and II.
Also, it was concluded from
·this study that the haematological affection had occured from the first day after burn in all the
groups. We used this data in group 5 which is composed of ten patients with major bums. In 6
patients (with burn > 50%) we applied the Parkland’s formula with late excision and grafting . In
the other 4 patients (with burn < 50%) we applied the Parkland’s formula with early excision and
grafting. For all the patients of this group, we used heparin as a prophylactic against the
haematological affection that occured in severe bums. In this group 3 patients died (burn 85% - 78%
- 72%) the first 2 in the seventh day and the third in the tenth day.The D.I.C. was present in
2/10 (20%), respiratory failure was
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present in . 2/10 (20%) and livJi- failure occured in. 1/10 (10%). This group had a better result
in the patient’s survival, as we reduced the haematological affection which trigger M.O.F.
We concluded from this study that M.O.F is a catastrophic outcome of severe burns with a high
incidence of mortality. It’s occurence is related to the percent and depth of the burn.
Parkland’s formula(i.e. formulae using crystalloid) has a better results as regards patients
survival and the occurrence of
M.O.F. as compared to the Brooke’s formula (i.e. formulae using colloid). Early excision is better
than late excision in burns less than 50% as reflected on the patients parameters. This was not the
case in burn > 50% T.B.S.A.
Finally we recommend:
1- The use of heparin in all severly burned patients from the very begining by the dose of 5000 IU
every 8 hours (monitored by P.T, P.T.T.) for 10 days. This will minimize the microthrom bi
formation the main trigger for the occurrence of M.O.F.
2 - The use of crystalloid in the resuscitation .
3 - The early excision for burn < 50%.