DAMAGE CONTROL

Surgery may need to be limited to the minimum necessary to stop bleeding and
control sepsis. More definitive repairs can be delayed until the patient is
physiologically capable of sustaining the procedure. This concept of tailoring the
operation to match the patient’s physiology and staged procedures to prevent
physiological exhaustion is called ‘damage control surgery’;

Once haemorrhage is controlled, patients should be aggressively resuscitated and

warmed and coagulopathy corrected. Attention should be paid to fluid
responsiveness and the endpoints of resuscitation to ensure that patients are fully
resuscitated and to reduce the incidence and severity of organ failure

Damage control surgery

■ Arrest haemorrhage
■ Control sepsis
■ Protect from further injury
■ Nothing else
Following major injury, protracted surgery in the physiologically unstable patient
with the ‘deadly triad’ – the combination of hypothermia, acidosis and
coagulopathy – carries a very high mortality rate. ‘Damage control’ or ‘damage
limitation surgery’ The application of damage control to the trauma patient has
come from the realisation that minimising surgery until the physiological
derangement can be corrected is the best way of improving outcome. The surgery
is restricted to only two goals:
• stopping any active surgical bleeding;
• controlling any contamination.
The operation is then suspended and the abdomen temporarily closed. The
patient’s resuscitation continues in the intensive care unit. Once the physiology
has been corrected,
the patient warmed and the coagulopathy corrected, the patient is returned to the
operating theatre for any definitive surgery. The key philosophy of damage control
can be summarised as follows:
• to keep the patient alive at any cost, utilising an unconventional approach and
abbreviated surgical technique to limit the depletion of physiological reserve;
• to be part of the resuscitation process, in which there is initial surgical control of
haemorrhage and contamination followed by rapid closure, assisting in the
restoration of normal physiology.
The stages of damage control surgery
Stage
I Patient selection
II Control of haemorrhage and control of contamination
III Resuscitation continued in the intensive care unit
IV Definitive surgery

Damage control resuscitation

This is a new concept that has evolved following recent military experience, in
which the concept of damage control has been broadened to include the
techniques used in resuscitation as well as in surgery. In the group of unstable
trauma patients who are
candidates for damage control surgery the time in the emergency department is
minimised and the resuscitation of the patient is carried out in the operating room
and not in the resuscitation bay. The resuscitation is individualised through
repeated point of care testing in the operating room of haemoglobin level, acidosis
(pH and lactate) and clotting, and is therefore directed towards the early delivery
of biologically active colloids, clotting products, recombinant factor VIIa and whole
blood in order to buy time. The physiological disturbances that are associated with
the downward spiral of acidosis, coagulopathy and hypothermia in these serious
injuries are predicted and attempts are made to avoid them rather than react to
them.
Damage control surgery
The decision that damage control surgery is required should be made at the
earliest opportunity, preferably in the emergency department or at the beginning
of the operation. An early decision improves communication of the strategy with
the whole surgical
and anaesthetic team, expedites time to the operating room, limits time in surgery
and allows earlier admission thereafter to the intensive care unit where the
resuscitation can be best completed. Damage control is a staged process (Table
26.7). Table 26.7
The stages of damage control surgery
Stage
I Patient selection
II Control of haemorrhage and control of contamination
III Resuscitation continued in the intensive care unit
IV Definitive surger
V Abdominal closure

Patient selection is the key to appropriate damage control.This is summarised in

Table 26.8.

Anatomical Inability to achieve haemostasis

Complex abdominal injury, e.g. liver and pancreas
Combined vascular, solid and hollow organ injury, e.g. aortic or caval injury
Inaccessible major venous injury, e.g. retrohepatic vena cava
Demand for non-operative control of other injuries, e.g. fractured pelvis
Anticipated need for a time-consuming procedure

Physiological (decline of Temperature < 34ºC

physiological reserve) pH < 7.2
Serum lactate > 5 mmol l–1 [N (Normal) < 2.5 mmol l–1]
Prothrombin time (PT) > 16 s
 Partial thromboplastin time (PTT) > 60 s
> 10 units blood transfused
Systolic blood pressure < 90 mmHg for > 60 min

Environmental Operating time > 60 min

Inability to approximate the abdominal incision
Desire to reassess the intra-abdominal contents (directed relook)
The initial surgical focus is haemorrhage control, which is followed by control and
limitation of contamination. This is achieved using a range of abbreviated
techniques including
*simple ligation of bleeding vessels, shunting of major arteries and veins,
drainage,
temporary stapling off of bowel, and therapeutic packing.
Following the above the abdomen is closed in a temporary fashion using a sheet
of plastic (e.g. Opsite) over the bowel, an intermediate pack to allow suction, and
a further sheet of adherent plastic drape to the skin to form a watertight and
airtight seal. Suction is applied to the intermediate pack area to collect
abdominal fluid. This technique is known as the ‘Vacpac’ or ‘Opsite sandwich’
(Fig. 26.10).
The closure is not without its own significant morbidity including atmospheric
enteric fistula formation, heat loss and excessive fluid loss and, therefore,
attempts to close the abdomen
should be proactive. Successful closure may require aggressive off-loading of
fluid and even haemofiltration to achieve this if the patient will tolerate it. The
best situation is closure of the abdominal fascia, or, if this cannot be achieved,
then skin closure only. Occasionally, mesh closure can be used, with skin grafting
over the mesh and subsequent abdominal wall reconstruction.
As soon as control has been achieved the patient is transferred from the
operating theatre to the intensive care unit where resuscitation is continued; the
aim of this is the correction of
hypothermia, acidosis and coagulopathy. Following this, further physiological
investigation or radiological intervention can be carried out. The next stage of
damage control is definitive surgery. The team should aim to perform definitive
anastomoses, vascular reconstruction and closure of the body cavity within 24–
72 hours of injury; however, this must be individualised to the patient, the
response to critical care resuscitation and the injury complexes, and must be
judged on its own merits. Undue haste and a premature
return to theatre will convert a definitive second operation into a second damage
control procedure and result in further physiological insult for the patient;
however, undue delay may
increase the risk of intra-abdominal sepsis and the progression of previously
unrecognised injuries.

Damage control
■ Resuscitation is carried out in the operating room using biologically
active fluids
■ Surgery is the minimum needed to stabilise the patient
■ The aim of surgery is control of haemorrhage and limitation of
contamination
■ Secondary surgery is aimed at definitive repair
ABDOMINAL COMPARTMENT SYNDROME AND THE OPEN ABDOMEN
Normal pressures in the abdomen are between 0 and 10mmHg. As the
intraabdominal
pressures rise, dysfunction begins in other organ systems, such as the
pulmonary, renal, and cardiovascular systems , has far-reaching consequences
for the patient; the syndrome that results is known as abdominal compartment
syndrome (ACS
.
Effect of raised intra-abdominal pressure on individual organ function
Organ Effect
Renal Increase in renal vascular resistance leading
to a reduction in glomerular filtration rate
and impaired renal function

Cardiovascular Decrease in venous return resulting in

decreased cardiac output because of both
a reduction in preload and an increase in afterload

Respiratory Increased ventilation pressures because of

splinting of the diaphragm, decreased lung
compliance and increased airway pressures

Visceral perfusion Reduction in visceral perfusion

Intracranial effects Severe rises in intracranial pressures

.
.
Abdominal compartment syndrome results from elevated urinary bladder
pressures. The syndrome occurs most commonly in patients with severe shock
who receive major resuscitation with fluid and blood products. The syndrome
often occurs in patients with massive intra-abdominal or pelvic bleeding.
Intestinal obstruction resulting in distended
bowel, and abdominal distension can cause abdominal compartment syndrome
as well. Untreated cases progress to respiratory failure, renal failure, acidosis,
and shock.
Hallmarks of the syndrome include abdominal distension, oliguria, hypoxia,
hypercarbia, and hypotension.
The diagnosis is made through the demonstration of elevated intra-abdominal
pressures. This is commonly done by taking readings through a Foley catheter.
Clinical signs begin with pressures above 15mmHg. Elevated pressures are
transmitted to the renal parenchyma, negatively impacting venous return and
arterial perfusion. Pulmonary failure results from pressure applied against the
diaphragm, limiting its movement and decreasing ventilation. Airway pressures
become elevated, which prevents adequate ventilation. Decreased venous return
leads to diminished cardiac output and can eventually lead to shock. The need for
surgical intervention is based on the degree of pressure elevation and associated
symptoms

Treatment of abdominal compartment syndrome

involves prompt surgical decompression. During the procedure, the abdominal
wall is opened by creating a new midline incision or by re-entering the original
incision. The abdomen is then closed in a staged fashion, allowing for resolution
of bowel edema and secondary organ dysfunction. Temporary closure can be
achieved with vacuum dressings, mesh placement, or with use of a Bogota bag
(sterilized genitourinary bag). Attempts should be made to have complete fascial
closure within 3 to 4 days.
In all cases of abdominal trauma in which the development of ACS in the
immediate postoperative phase is considered a risk, the abdomen should be left
open and managed as for damage control surgery - abdomen is closed in a
temporary fashion using a sheet of plastic (e.g. Opsite) over the bowel,
anintermediate pack to allow suction, and a further sheet of adherentplastic
drape to the skin to form a watertight and airtight seal. Suction is applied to the
intermediate pack area to collect abdominal fluid. This technique is known as the
‘Vacpac’ or‘Opsite sandwich’ (Fig. 26.10). The closure is not without its own
significant morbidity including atmospheric enteric fistula formation, heat loss
and excessive fluid loss and, therefore, attempts to close the abdomen should be
proactive. Successful closure may require aggressive off-loading of fluid and even
haemofiltration to achieve this if the
patient will tolerate it. The best situation is closure of the abdominal fascia, or, if
this cannot be achieved, then skin closure only. Occasionally, mesh closure can
be used, with skin grafting over the mesh and subsequent abdominal wall
reconstruction

GRADE PRESSURE INTERVENTION

1 10- 14 Intravenous fluid resuscitation

2 15-24 Decompression if pulmonary, renal, or
cardiovascular symptoms occur
3 25-35 Decompression
 4 >35 Surgical exploration

ACS is a major cause of morbidity and mortality in the critically ill patient and its
early recognition is essential

Gas gangrene
It is a rapidly progressive, potentially fatal condition characterised by widespread
necrosis of the muscles and subsequent soft-tissue destruction. The common
causative organism is Clostridium perfringens, a spore-forming, Gram-positive
saprophyte that flourishes in anaerobic conditions.
Other organisms implicated in gas gangrene include
C. bifermentans,
C. septicum and
C. sporogenes.
They are present in the soil and have also been isolated from the human
gastrointestinal tract and female genital tract.
Non-clostridial gas-producing organisms such as coliforms have also been
isolated in 60–85% of cases of gas gangrene.
Risk of gangrene
military woundand traumatic surgery
inadequately treated missile wounds,
crushing injuries and
high-voltage electrical injuries.
colorectal operations.
Patients who are immunocompromised,
diabetic or have malignant disease are at greater risk, particularly if they have
wounds containing necrotic or foreign material, resulting in anaerobic conditions.
Military wounds provide an ideal environment as causes extensive tissue
damage with cavitation. Wounds become contaminated with clostridial spores
and the devitalised tissue, foreign bodies and premature wound closure provide
the anaerobic conditions necessary for spore germination.
The usual incubation period is < 24 hours but it can range from 1 hour to 6
weeks. A vicious cycle of tissue destruction is initiated by rapidly multiplying
bacteria and locally and systemically acting exotoxins., collagenase,
hyaluronidase, other proteases and alpha toxin..
Alpha-toxin, the most important, is a lecithinase, which destroys red and white
blood cells, platelets, fibroblasts and muscle cells.
The phi-toxin produces myocardial suppression whereas the kappa-toxin is
responsible for the destruction of connective tissue and blood vessels.Locally,
this results in spreading necrosis of muscle and thrombosis of blood vessels while
progressive oedema further compromises the blood supply. The typical feature of
this condition is the production of gas (composed of nitrogen, hydrogen sulphide
and carbon dioxide) that spreads along the muscle planes. Systemically, the
exotoxins cause severe haemolysis and, combined with the local effects, this
leads to rapid progression of the disease, hypotension, shock, renal failure and
acute respiratory distress syndrome (ARDS).
The earliest symptom is acute onset of pain that increases in severity as the
myo-necrosis progresses. The limb swells up and the wound exudes a
serosanguinous discharge. The skin is involved secondary to underlying muscle
necrosis, turning brown and progressing to a blue-black colour with the
appearance of haemorrhagic bullae (Fig. 30.17). The characteristic sickly sweet
odour and soft tissue crepitus caused by gas production appear with established
infection but the absence of either does not exclude the diagnosis. These local
signs are accompanied by pyrexia, tachycardia disproportionate to body
temperature, tachypnoea and alteration in mental status.

The diagnosis is made on the basis of history and clinical features:

Gas gangrene wound infections are associated with severe local wound pain and
crepitus (gas in the tissues, which may also be noted onplain radiographs). The
wound produces a thin, brown, sweetsmelling exudate, in which Gram staining
will reveal bacteria without neutrophils.
a peripheral blood smear may suggest haemolysis;
biochemical profile may show metabolic acidosis and renal failure.
Radiography can visualise gas in the soft tissues and computerised tomography
(CT) scans are useful in patients with chest and abdominal involvement

Patients should be admitted to ICU and treated aggressively with careful

monitoring.
High-dose penicillin G and clindamycin, along with third-generation
cephalosporins, should be given intravenously until the patient’s toxicity abates.
The mainstay of management is early surgical excision of the necrotic tissue.
The muscle planes are opened through generous longitudinal incisions and all
devitalised tissue is removed, going beyond the area of induration. Abdominal
involvement may necessitate excision of the wall musculature. Excision should be
continued daily until the process of necrosis has stopped spreading.
In established gas gangrene with systemic toxicity, amputation of the involved
extremity is life saving and should not be delayed. No attempt is made at closure,
amputation stumps are
left open and the wound is lightly packed with saline-soaked gauze and dressed.
The role of HBO is not as clear as in necrotising fasciitis but
it is recommended in severe cases if the facilities are available.

Conclusion
This is a dreaded consequence , if prompt action is not taken systemic
complications with circulatory collapse and MSOF follows. Antibiotic prophylaxis
should always be considered in patients at risk,