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Holzheimer RG, Mannick JA, editors. Surgical Treatment: Evidence-Based and Problem-Oriented. Munich: Zuckschwerdt; 2001.

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Surgical Treatment: Evidence-Based and Problem-Oriented.

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Damage control

, M.D. and , M.D.

Department of Surgery Denver Health Medical Center Denver, CO, U.S.A.

The most common causes of death for trauma patients are head injury, massive blood loss, and multiple organ failure. Since the late 1970's surgeons have been able to operate upon the most severely injured patients until a constellation of metabolic derangements developed. This is characterized by the triad of coagulopathy, hypothermia, and acidosis (1). Hypothermia is caused by evaporative and conductive heat loss and diminished heat production. The metabolic acidosis of shock is aggravated by aortic clamping, vasopressors, massive transfusion, and impaired myocardial performance. Coagulopathy is caused by consumption dilution, hypothermia and acidosis. Each of these factors reinforces the others resulting in a critically ill patient who is at high risk for cardiac failure or a fatal arrhymia. This downward spiral has been referred to as the bloody vicious cycle (1). Stone was the first to address this issue clinically and emphasized the treatment of coagulopathy as the pivotal issue (2). Rapidly closing the abdomen, he believed, would aid in the tamponade of bleeding since abdominal pressure would increase. While this is probably correct, increased intraabdominal pressure can be associated with serious or even lethal consequences. It is now recognized that heat loss is the central event since neither of the other components can be corrected until core temperature returns toward normal. Laboratory and mathematical heat exchange models have demonstrated that evaporative heat loss from an open abdomen is by far the greatest source of hypothermia (3). A concomitant open thoracic cavity greatly accelerates the rate of the patient's deterioration and can cause the syndrome by itself Immediate abdominal closure halts additional heat loss, interrupts the vicious cycle, and is the cornerstone of damage control surgery.

The term “damage control” was coined by the United States Navy during World War II (4). It was defined as those procedures and skills employed to maintain or restore the watertight integrity, stability or offensive power in a warship (5). It is remarkable how appropriate this military term is when used to describe the management of the surgical equivalent of a sinking ship. Other terms which have been used synonymously include staged laparotomy and abbreviated laparotomy (68). Damage control operations should be considered when a coagulopathy develops and core temperature drops below 34 °C. The goal is to complete the procedure as soon as possible or the patient will certainly die. Several methods can be used to expedite wound closure. Bleeding raw surfaces, often of the liver, are packed with laparotomy pads. Small enteric injuries are closed with staples, and large ones are stapled on both sides with the GIA stapling device and the damaged segment removed. Clamps may be left on unrepaired vascular injuries, or the vessels are ligated. Vessels which cannot be ligated without loss of life or limb can be treated with temporary indwelling shunts. Injuries of the pancreas and kidneys are not treated if they are not bleeding. No drains are placed, and the abdomen is closed with sharp towel clips placed two centimeters apart which include only the skin. Towel clips are used because they do not cause bleeding as needles do and they can be applied very rapidly, usually in 60–90 seconds. The closure of just the skin allows for the abdominal or thoracic cavities to accommodate a greater volume without increased pressure. The clips are covered with a towel, and a plastic adhesive sheet is placed over the towel to prevent excessive fluid from draining onto the patient's bedding. Cold wet drapes are removed, and the patient is covered from head to toe with layers of warm blankets. It should be noted that many of these unorthodox treatments, including the creation of closed loop bowel obstructions and unrepaired injuries are not compatible with survival. However, reoperation is planned within 24 hours, and the treatments are tolerated well within that time frame. The time between initial abdominal closure and reoperation may be as short as 30 minutes to distinguish between residual mechanical bleeding versus a diffuse capillary bleeding from a coagulopathy. If the surgeon believes that the patient's metabolic problems can be corrected in a short time (2 hours or less), the patient may remain in the operating room while additional blood products are administered and rewarming measures are instituted. Patients who are in very poor condition and will require several hours for metabolic corrections should be transferred to the SICU. If the patient's condition improves as evidenced by normalization of coagulation studies, the correction of acid/base balance, and a core temperature of at least 36 °C, he should be returned to the operating room for removal of packs and definitive treatment of his injuries. There are several complications associated with damage control procedures. Failure to identify noncoagulopathic hemorrhage can lead to exsanguination. Most patients with coagulopathic hemorrhage will have a gradual decrease in the need for blood components and an improvement in coagulation studies as temperature rises. Patients with vascular hemorrhage will require continuous or increasing transfusions and must be returned to the operating room for reexploration.

A second complication is referred to as the abdominal or thoracic compartment syndrome (9). These entities are caused by an acute increase in intracavitary pressure. In the abdomen the compliance of the abdominal wall and the diaphragm permit the accumulation of several liters of fluid before intraabdominal pressure (IAP) increases. There are primarily two sources for this fluid, blood and edema. Blood accumulates due to the coagulopathy or missed vascular injury described above. The cause of edema is multifactorial. Ischemia and reperfusion cause capillary leakage; loss of oncotic pressure occurs; and in the case of the small bowel which is often eviscerated, prolongation and narrowing of veins and lymphatics caused by traction impairs venous and lymphatic drainage. The resulting edema may be dramatic. Similar phenomena occur in the chest. As fluid continues to accumulate, the compliance limit of the abdominal cavity is eventually exceeded; and IAP increases. When IAP exceeds 15 mmHg, serious physiologic changes begin to occur. The lungs are compressed by the upward displacement of the diaphragm. This causes a decrease in functional residual capacity, increased airway pressure and ultimately, hypoxia. Cardiac output decreases due to diminished venous return to the heart and increased afterload. Blood flow to every intraabdominal organ is reduced due to increased venous resistance. As IAP exceeds 25 mmHg, life threatening hypoxia and anuric renal failure occur. Cardiac output can be returned toward normal with volume expansion and inotropic support. However, the only method for treating hypoxia and renal failure is to decompress the abdominal cavity by opening the incision. This results in an immediate diuresis and a resolution of hypoxia. Failure to decompress the abdominal cavity will eventually cause lethal hypoxia or progressive organ failure. There have been a few reports of sudden hypotension when a hypertensive abdomen is opened. However, volume loading to enhance cardiac output has largely eliminated this problem. IAP is measured using the Foley catheter. Since the bladder is a passive reservoir at low volumes (50–100 ml), it imparts no intrinsic pressure but can transmit IAP. 50 ml of saline are injected into the aspiration port of the urinary drainage tube with an occlusive clamp placed across the tube just distal port. The saline is used to create a standing column of fluid between the bladder and port which can transmit IAP to a recording device. The needle in the port is connected to a CVP manometer using a three way stopcock. The manometer is filled with saline and opened to the drainage tube. IAP is read at the meniscus with a manometer zeroed at the pubic symphysis. Bladder pressures measured in this fashion are both reliable and consistent.

In the chest similar phenomena occur. Edema of the heart and lungs develops and the heart may also dilate. Blood accumulation is rarely a problem because of the use of chest tubes. However, the diagnosis is usually apparent in the OR since the heart tolerates compression poorly. Attempts to close the chest in this setting are associated with profound hypotension, and it becomes obvious that an alternative method of closure is necessary.

At present the most popular material used to accommodate the addition of volume in the chest or abdomen is a three liter plastic urologic irrigation bag which has been cut open and sterilized. The bag is sewn to the skin or fascia using heavy nylon suture with a simple running technique. As many as four bags may need to be sewn together to cover a large defect. Closed suction drains are placed beneath the plastic to remove blood and serous fluid which inevitably accumulate. The entire closure is covered with a iodinated plastic adhesive sheet to simplify nursing care. Definitive wound closure can usually be performed in 48 to 72 hours.

Patients who develop early multiple organ failure (MOF) may be problematic because they do not resolve their edema until the hyperinflammation resolves. This may require several weeks. The bags have been left in place up to three weeks with the patient surviving. However, the authors make every effort to at least close the skin over the viscera to decrease protein and heat loss and to inhibit infection. If these attempts are unsuccessful and the abdomen remains open with granulating tissue exposed, lateral tractive forces of the abdominal wall will eventually cause an enteric fistula. The risk of developing a fistula increases rapidly after two weeks with an open abdomen. These problems are extremely difficult to treat. Several approaches have been used to avoid this catastrophic complication including silastic, latex, PTFE, polyglycolic acid or polypropylene mesh sewn to the fascia, split thickness skin grafts placed directly on the bowel, musculocutaneous flaps and traction devices. Of these options skin grafts appear to have the greatest success although the abdominal wall hernia will eventually require reconstruction.

Results

Results of recent damage control series are shown in table I. Mortality rates are usually around 60% in larger series. Complications are frequent in survivors and include ARDS, multiple organ failure, sepsis, pneumonia, intraabdominal abscess and abdominal compartment syndrome. Unfortunately, all data available regarding the efficacy of damage control techniques is retrospective in nature. Further more, randomized, prospective studies are unlikely to be performed since most trauma surgeons believe in the effectiveness of damage control and would consider such studies unethical.

Table I. Results of damage control series.

Table I

Results of damage control series.

References

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Kashuk J L, Moore E E, Millikan S. et al. Major abdominal vascular trauma-A unified approach. J Trauma. (1982);22:672–678. [PubMed: 6980992]
2.
Stone H H, Strom P R, Mullins R J. Management of the major coagulopathy with onset during laparotomy. Ann Surg. (1983);195:532–535. [PMC free article: PMC1353025] [PubMed: 6847272]
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Griffin A (1943) A ship to remember. Howell Soskin Publishers .
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Gaynor F (1951) The new military and naval dictionary. Philosophical Library Publishers, NY .
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Rotondo M F, Schwab C W, McGonigal M D. et al. ‘Damage control’: An approach for improved survival in exsanguinating penetrating abdominal injury. J Trauma. (1993);35:375–383. [PubMed: 8371295]
9.
Burch J M, Moore E E, Moore F A. et al. The abdominal compartment syndrome. Surg Clin North Am. (1996);76:833–842. [PubMed: 8782476]
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Carrillo C, Fogler R, Shaftan G. Delayed gastrointestinal reconstruction following massive abdominal trauma. J Trauma. (1993);34:233. [PubMed: 8459461]
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Garrison J, Richardson D, Hilakos A. et al. Predicting the need to pack early for severe intraabdominal hemorrhage. J Trauma. (1996);40:923. [PubMed: 8656478]
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Cosgriff N, Moore E E, Sauaia A. et al. Predicting life-threatening coagulopathy in the massively transfused trauma patient: Hypothermia and acidoses. J Trauma. (1997);42:857. [PubMed: 9191667]
Copyright © 2001, W. Zuckschwerdt Verlag GmbH.
Bookshelf ID: NBK6905
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