Saturday, July 15, 2006

Damage Control Surgery

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 paradigm shift in their 'mindset' if the patient is to survive such devastating injuries.
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'.
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.
Metabolic Failure
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.
HypothermiaThe 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.
AcidosisUncorrected 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.
CoagulopathyHypothermia, 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, it is already too late.
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 metabolic failure to set in. This early decision is imperative to the patients survival.
Damage Control Laparotomy
The principles of damage control surgery are:
1. Control haemorrhage
2. Prevention contamination
3. Avoid further injury
PreparationPrehospital 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.
General Conduct and PhilosophyThe 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.
Aortic control may be necessary at this stage. 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.
Abdominal closureAbdominal closure is rapid and temporary. If possible, the skin only is closed with a rapid continuous suture or even multiple towel clips. Abdominal compartment syndrome is common in these patients and if there is any doubt the abdomen should be left open as a laparostomy with a silo-bag or vacuum-pack technique.
LiverThe 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 transferred to the angiography suite immediately after the operation to identify any ongoing arterial haemorrhage which may be controlled with selective angiographic embolization.
Critical Care
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.
Abdominal Compartment Syndrome
Massive intestinal oedema often follows laparotomy for major tra uma where there has been prolonged shock. Crystalloid resuscitation, capillary leakage due to activated inflammatory mediators and reperfusion injury all contribute to this tissue swelling. Combined with intra-abdominal packing or retroperitoneal haematomas this may render the abdomen difficult or impossible to close. If the abdomen is closed, intra-abdominal pressure may rise to a level (>25 cmH2O) where it leads to significant cardiovascular, respiratory, renal and cerebral dysfunction.
CardiovascularA rise in the intra-abdominal pressure leads to a fall in cardiac output, due mainly to compression of the inferior vena cava and reduction in venous return to the heart. Cardiac output is reduced despite apparent rises in central venous pressure, pulmonary artery occlusion pressure and systemic vascular resistance. This distortion of standard monitoring modalities makes adequate and appropriate resuscitation difficult.
RespiratoryRaised intra-abdominal pressure will effectively splint the diaphragm and lead to a rise in peak airway pressure and intra-thoracic pressure and subsequently a reduced venous return to the heart. The increase in airway pressures may also exacerbate barotrauma and contribute to the development of acute respiratory distress syndrome.
RenalAn acute increase in intra-abdominal pressure leads to oliguria and anuria probably due to compression of the renal vein and renal parenchyma. Renal blood flow, glomerular filtration are decreased with a corresponding increase in renal vascular resistance.
CerebralThe rise in intra-abdominal pressure, intrathoracic pressure leads to a rise in central venous pressure which prevents adequate venous drainage from the brain, leading to a rise in intracranial pressure and worsening of intracerebral oedema.
Diagnosis of Abdominal Compartment SyndromeThe abdominal compartment should be suspected and sought for in any multiple trauma patient who has undergone a period of profound shock. Clinically it is characterized by a fall in urine output associated with an elevated central venous pressure. The diagnosis can be confirmed by the measurement of intra-abdominal pressure. This may be done either through a foley catheter in the bladder or a nasogastric tube in the stomach. Simple water-column manometry is used at 2 to 4 hourly intervals, although it is possible to connect a pressure transducer to a foley catheter.
Normal intra-abdominal pressure is zero or subatmospheric. A pressure of over 25cmH2O is suggestive, and over 30cmH2O diagnostic, of the abdominal compartment syndrome.
ManagementIt is better to anticipate the development of abdominal compartment syndrome and use an alternate wound closure technique to prevent its occurrence. If the abdomen is at all difficult to close, this procedure should be abandoned at alternative techniques applied. A good rule of thumb is that if, when looking at the abdomen horizontally, the guts can be seen above the level of the wound, the abdomen should be left open and temporary closure utilized.
The easiest method to control the open abdomen is to use a silo-bag closure. A 3 litre plastic irrigation bag is emptied and cut open so it lies flat. The edges are trimmed and sutured to the skin, away from the skin edges, using a continuous 1 silk suture. It is useful to place a sterile absorbent drape inside the abdomen to soak up some of the fluid and ease control of the laparostomy.
An alternative technique is the 'vacuum-pack' technique. Here the 3 litre bag is opened and placed into the abdomen to protect the gut contents, under the sheath. Two large calibre suction drains are placed over this, and a large adherent steridrape placed over the whole abdomen. The suction catheters are connected to high-displacement suction to provide control of fluid losses and create the 'vacuum-pack' effect.
Do not suture material to the sheath. Repeated suturing of the sheath damages it and makes definitive closure impossible. If the sheath cannot be closed at a subsequent operation, the defect may be closed with an absorbable mesh system.
Sudden release of the abdominal compartment syndrome may lead to an ischaemia-reperfusion injury causing acidosis, vasodilatation, cardiac dysfunction and arrest. Prior to release the patient should be pre-loaded with crystalloid solution. Mannitol and vasodilators such as dobutamine or the phosphodiesterase inhibitors may have a place here.
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.


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