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Damage control surgery is one of the major advances in surgical technique in the past 20 years. The principles of damage control have been slow to be accepted by surgeons around the world, as they contravene most standard surgical teaching practices - that the best operation for a patient is one, definitive procedure.
However it is now well recognized that multiple trauma patients are more likely to die from their intra-operative metabolic failure that from a failure to complete operative repairs. Patients with major exsanguinating injuries will not survive complex procedures such as formal hepatic resection or pancreaticoduodenectomy. The operating team must undergo a shift in their mindset if the patient is to survive such devastating injuries.
Standard surgical teaching
The central tenet of damage control surgery is that patients die from a triad of coagulopathy, hypothermia and metabolic acidosis. Once this metabolic failure has become established it is extremely difficult to control haemorrhage and correct the derangements. If the patient is to survive the operation must be foreshortened so that they can be transferred to a critical care facility where they can be warmed and the hypothermia and acidosis is corrected. Once this is achieved the definitive surgical procedure can be carried out as necessary - the 'staged procedure'.
Damage control approach
The principles of the first 'damage control' procedure then are control of haemorrhage, prevention of contamination and protection from further injury. Damage control surgery is the most technically demanding and challenging surgery a trauma surgeon can perform. There is no margin for error and no place for careless surgery.
Hypothermia. Acidosis. Coagulopathy. These three derangements become established quickly in the exsanguinating trauma patient and, once established, form a vicious circle which may be impossible to overcome.
Hypothermia The majority of major trauma patients are hypothermic on arrival in the emergency department due to environmental conditions at the scene. Inadequate protection, intravenous fluid administration and ongoing blood loss will worsen the hypothermic state. Haemorrhagic shock leads to decreased cellular perfusion and oxygenation and so inadequate heat production. Hypothermia has dramatic systemic effects on the bodies functions but most importantly in this context exacerbates coagulopathy and interferes with blood homeostatic mechanisms.
Acidosis Uncorrected haemorrhagic shock will lead into inadequate cellular perfusion, anaerobic metabolism and the production of lactic acid. This leads to profound metabolic acidosis which also interferes with blood clotting mechanisms and promotes coagulopathy and blood loss.
Coagulopathy Hypothermia, acidosis and the consequences of massive blood transfusion all lead to the development of a coagulopathy. Even if control of mechanical bleeding is achievable, patients may continue to bleed from all cut surfaces. This leads to a worsening of haemorrhagic shock and so a worsening of hypothermia and acidosis, prolonging the vicious cycle.
Some studies have attempted to place threshold levels on these parameters. Some state that conversion to a damage control procedure should take place if the pH is below 7.2, core temperature is below 32C or the patient has received more than one blood volume transfusion. However, once these levels are reached, physiological exhaustion is already established.
The trauma surgeon must make the decision to convert to a limited procedure within 5 minutes of starting the operative procedure. This decision is made on the initial physiological state of the patient and the rapid initial assessment of internal injuries. Do not wait for physiologic exhaustion to set in. This early decision is imperative to the patient's survival.
Damage control surgery
The principles of damage control surgery are abbreviated surgery limited to:
- Control of haemorrhage
- Prevention further contamination
- Avoid further injury
Prehospital and emergency department times should be minimized in these patients. All unnecessary and superfluous investigations that will not immediately affect patient management should be deferred. Cyclic fluid resuscitation prior to surgery is futile and will worsen hypothermia and coagulopathy. Colloid solutions will also interfere with clot quality.
These patients should be transferred rapidly to the operating room without repeated attempts to restore circulating volume. They require operative control of haemorrhage and simultaneous vigorous resuscitation with blood and clotting factors.
Anaesthesia should be induced on the operating table once the patient is prepped and draped and the surgeons ready. The shocked patient usually requires minimal anaesthesia and a careful, haemodynamically-neutral induction method should be used. An arterial line is valuable for patient monitoring peroperatively but small-calibre central venous access is of limited use. Blood, fresh frozen plasma, cryoprecipitate and platelet transfusions should be available but clotting factor therapy should be administered rapidly only once control of major vascular haemorrhage has been achieved. All fluids should be warmed and as much of the patient covered and actively warmed as possible.
Laparotomy: General Conduct and Philosophy
The patient should be rapidly prepped from neck to knees with large abdominal packs soaked in antiseptic skin preparation solution. The incision should be made from the xiphisternum to the pubis. This incision may require extension into the right chest or as a median sternotomy depending on the injury pattern.
Relief of intraperitoneal pressure with muscle paralysis and opening of the abdominal wall may result in dramatic haemorrhage and hypotension. Immediate control is necessary and this is initially achieved with four quadrant packing with multiple large abdominal packs.
If there is continued arterial haemorrhage with packs in place, aortic control may be necessary. This is generally best achieved at the diaphragmatic hiatus with blunt finger dissection and finger pressure by an assistant followed by aortic cross-clamping. The aorta may be difficult to identify in the severely hypovolaemic patient and direct visualization by division of the right crus of the diaphragm may be necessary. Some surgeons prefer to perform a left anterolateral thoracotomy to control the descending thoracic aorta in the chest. However this requires the opening of a second body cavity and further heat loss and is rarely necessary.
The next step is to identify the main source of bleeding. Careful inspection of the four quadrants of the abdomen is necessary. A moment of silence may allow the bleeding to be heard. Immediate control of haemorrhage is with direct, blunt pressure using the surgeons hands, swabs on sticks or abdominal packs. Proximal and distal control techniques are rarely useful in the acute stage. Bleeding from the liver, spleen or kidney can generally be achieved by applying pressure with several large abdominal packs.
Examination of the abdomen must be complete. This includes, where necessary, mobilization and delivery of retroperitoneal structures using several medial visceral rotation manoeuvers. All intraabdominal and most retroperitoneal haematomas require exploration and evacuation. Even a small perienteric or peripancreatic haematoma may mask a serious vascular or enteric injury. Exploration should proceed regardless of whether the haematoma is pulsatile, expanding or stable or due to blunt or penetrating trauma. Nonexpanding perirenal haematomas, retrohepatic haematomas or blunt pelvic haematomas should not be explored and may be treated with abdominal packing. Subsequent angiographic embolization may be required.
Prevention of contamination is achieved by the rapid closure of hollow viscus injury. This may be definitive if there are only a few enterotomies requiring primary suture, but more complex techniques such as resection and primary anastomosis should be avoided and bowel ends stapled, sewn or tied off. Inspection of the ends and reanastomosis is performed at the second procedure.
The basic damage control technique for control of hepatic haemorrhage is peri-hepatic packing. This manoeuver, when performed properly, will arrest most haemorrhage except for major arterial bleeding.
Major hepatic bleeding may be partially controlled with a soft vascular clamp on the portal triad (Pringle's manoeuver). Further vascular isolation (inferior vena cava above and below the liver) may be hazardous and is generally unnecessary in a damage control setting. Full hepatic mobilization and extension into the chest either through a median sternotomy or left thoracotomy may be required to achieve this.
The liver parenchyma can be compressed manually initially, followed by ordered packing. To adequately pack the liver requires compression in the antero-posterior plane. This can only be achieved by mobilization of the right hepatic ligament and systematic placement of packs posterior and anterior to this, as well as one or two in the hepato-renal space. Even retrohepatic venous and inferior vena cava injuries may be controlled in this manner.
Only major arterial bleeds from the liver parenchyma will require further attention. In this case the liver injury can be extended using a finger-fracture technique and the bleeding vessels identified and tied or clipped. In some cases, where the injury is not deep and easily accessible, rapid resectional debridement may be possible by placing large clamps along the wound edges, performing a rapid debridement and the underrunning the clamp with suture to include all the raw surface.
The patient who undergoes hepatic packing should be considered for transfer to the angiography suite immediately after the operation to identify any ongoing arterial haemorrhage which may be controlled with selective angiographic embolization.
Except for minor splenic injuries which may be left alone, splenectomy is the treatment of choice for major spleen injuries. Attempts at splenic conservation are too time-consuming and prone to failure to justify their use in this setting.
A central retroperitoneal haematoma likely represents injury to a major vascular structure. Access to the inferior vena cava or abdominal aorta in this setting is best achieved by complete medial visceral rotation of the right or left side of the abdomen. On the right, the colon is mobilised and an extended Kocher manoeuvre performed to mobilise the duodenum. The root of the small bowel mesentery is mobilised up to the superior mesenteric artery and inferior border of the pancreas.
Right medial visceral rotation (Cattell-Brasch)
The left colon, spleen and kidney are mobilized and the visceral rotated medially to expose the entire length of the abdominal aorta (the Cattell or Mattox manoeuver).
Left medial visceral rotation (Cattell / Mattox)
Occasionally the arteries can be rapidly repaired with direct suture or interposition PTFE graft. However temporary menouevres may be more appropriate in the case of physiologic exhaustion the use of intravascular shunts may be considered. A short of tube thoracostomy tube is used for the abdominal aorta. Iliac injuries are more suitable for shunting and carotid shunts, thoracostomy tubing or large-bore IV tubing may be utilized. These may also be useful for superior mesenteric artery injuries.
Inferior vena cava injuries may be managed by direct suture if amenable, or packing if retrohepatic. Temporary control is best achieved with direct pressure above and below the injury using sponge-sticks. Otherwise venous injuries should be ligated in the damage control setting.
Opening a pelvic retroperitoneal haematoma in the presence of a pelvic fracture is almost universally fatal - even if the internal iliacs are successfully ligated. In this case the retroperitoneum should not be opened but the pelvis packed with large abdominal packs. The pelvis should be stabilized prior to this (a sheet tied tightly around greater trochanters and pubis is adequate) to prevent the packing procedure opening the pelvic fracture and increasing the haemorrhage.
Once control of haemorrhage has been achieved, attention is turned to prevention of further contamination by controlling spillage of gut contents. Small gastrotomies or enterotomies can be rapidly closed primarily with a single layer continuous suture or skin stapler. With extensive damage to the bowel requiring resection, primary anastomosis is required. This may be time consuming and the integrity of the anastomosis is jeopardized in the milieu of generalized hypoperfusion. This may also make decisions about resection margins more difficult to judge.
In this case, especially with colonic injuries, or multiple small bowel lesions, it is wiser to resect non-viable bowel and close the ends, leaving them in the abdomen for anastomosis at the second procedure. The linear stapler is useful to achieve this, but bowel ends may be closed with running suture or even umbilical tapes. Ileostomies or colostomies should preferably not be performed in a damage control setting, especially if the abdomen is to be left open, as control of spillage is almost impossible.
Pancreatic injury rarely requires or allows definitive surgery in the damage control setting. Minor injuries not involving the duct (AAST I,II,IV) require no treatment. If possible a closed suction drain may be placed down to the injury, but this should not be done if the abdomen is packed and left open. If the injury is distal (to the superior mesenteric vein - AAST III) and there is extensive tissue destruction including the pancreatic duct, it may be possible to perform a rapid distal pancreatectomy.
Massive injuries to the pacreaticoduodenal complex (AAST V) are almost always associated with injuries to the surrounding structures. Patients will not survive complex operations such as pancreaticoduodenectomy. The pancreas should be debrided only. Small duodenal injuries can be repaired with a single layer suture, but large duodenal injuries should be debrided and the ends closed temporarily with suture or umbilical tape to be dealt with at the second procedure.
Pulmonary resection may be necessary to control haemorrhage or massive air leaks and to remove devitalised tissue. Formal pulmonary lobar or segmental resection is difficult and unnecessary in the multiply injured patient. The simplest method available should be used. This is usually the linear stapling device which will control most vascular and bronchial injuries. This non-anatomical approach also preserves the maximum amount of functional lung tissue. If necessary the staple line may be overrun with a continuous suture. Take care when controlling superficial injuries with simple suture. Often this controls only superficial haemorrhage and bleeding into deeper tissues continues.
Hilar injuries are best controlled initially with finger pressure. Most patients injuries will then be found to be more distal to the hilum and can be treated accordingly. If hilar control must be achieved this can be done with a vascular clamp (Satinsky) or umbilical tape in the acute setting. Up to 50% of patients will die of acute right heart failure following clamping of hilar structures, so this decision must be based on absolute necessity.
Pulmonary tractotomy may be a useful technique where there is a deep penetrating injury to the lung. Two long clamps are placed through the tract of the injury. The wall of the tract is opened, so exposing the inside of the tract. Any bleeding vessels or bronchi can be tied off. The clamps are then overrun with a suture to control the wound edges.
Abdominal closure is rapid and temporary. Abdominal compartment syndrome is common in these patients and normally the abdomen should be left open as a laparostomy with a silo-bag or vacuum-pack technique.
The priority of the critical care phase of treatment is rapid and complete reversal of metabolic failure. The damage control procedure has controlled life-threatening injury, but the patient requires further surgery to remove packs and/or definitively complete the repairs. The next 24 to 48 hours are crucial if the patient is to be fit for a second procedure. After this time multiple organ dysfunction, especially acute respiratory distress syndrome (ARDS), and cardiovascular failure may render re-operation inadequate.
The intensive care unit must act aggressive to reverse the metabolic failure. The patient must be actively warmed, with blankets, air-warming devices or even continuous arteriovenous warming techniques. This is vital to allow correction of coagulopathy and acidosis.
Acidosis is a reflection of impaired oxygen delivery and utilization. Perfusion must be restored to body tissues by warmed intravenous crystalloid and blood administration as necessary. Massive tissue and bowel oedema may ensue due to the activation and release of inflammatory mediators and large volumes of fluid are required. Right heart catheters should be employed as necessary to monitor cardiac filling pressures and determine oxygen delivery. Vasodilating agents such as dobutamine or the phsophodiesterase inhibitors may be necessary to help open up vascular beds. In the absence of technology that can monitor muscle and gut perfusion, the base deficit or lactate levels should be used to guide resuscitation.
Coagulopathy is treated by the administration of fresh frozen plasma, cryoprecipitate and platelets as necessary, and correcting the hypothermia and acidosis. If correction of metabolic failure is to succeed, all three derangements must be treated simultaneously and aggressively. Take care not to miss the patient who has started to actively bleed again. Large losses from thoracostomy tubes, abdominal distention or loss of control of an open abdomen, or repeated episodes of hypotension all suggest that mechanical bleeding is occurring that will require surgical control.
The principles of reoperation are removal of clots and abdominal packs, complete inspection of the abdomen to detect missed injuries, haemostasis and restoration of intestinal integrity and abdominal wound closure.
Timing of reoperation is critical. There is usually a window of opportunity between correction of metabolic failure and the onset of the systemic inflammatory response syndrome and multiple organ failure. This window usually occurs at 24-48 hours after the first procedure. There is a tradeoff between earlier re-operation, when the patient may be less stable and bowel-well oedema marked, and delaying the procedure to a point where cardiovascular, respiratory and renal failure make the procedure hazardous. Vascular shunts should be removed and grafts inserted at the earliest opportunity as these may dislodge or clot once coagulopathy is corrected. If packs are left in the abdomen it is generally recommended that these are removed at 48-72 hours, although there is little evidence to suggest that leaving them longer is detrimental.
Abdominal packs, especially around the liver or spleen should be removed cautiously as they may be stuck to the parenchyma and removal may lead to further bleeding. Soaking the swabs may aid this process. The bleeding is rarely dramatic however and may be controlled with argon-beam diathermy or fibrin glue. Occasionally repacking will be necessary.
Any intestinal repairs carried out at the first procedure should be inspected to determine their continued integrity. Bowel ends that were stapled or tied off should be inspected, necrotic tissue debrided and primary repair with end-to-end anastomosis undertaken. With a haemodynamically stable, warm patient, colostomy is rarely necessary.
Copious washout should be performed and the abdomen closed with standard mass closure to the sheath and routine skin closure. If the sheath cannot be re-approximated temporary silo closure can be reinstated or an absorbable PDS or vicryl mesh applied which can be skin grafted at a later stage. The resulting incisional hernia can be closed at a later procedure.