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Abdominal Compartment Syndrome

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OsamuYoshino, NicholasLee, andZsoltJ.Balogh

The application of damage control surgery (DCS) principles and aggressive uid resuscitation made it possible to save critically injured penetrating trauma patients by the early 2000s. These survivors suffer whole-body ischemia/reperfusion injury (hemorrhagic shock followed by resuscitation), which is associated with bowel edema, abdominal wall swelling, retroperitoneal swelling, and ascites formation. The abdominal packing and the formal closure of the abdomen together with the increased volume of the abdominal content can cause signicantly increased abdominal pressure, which compromises the function of vital organs (kidneys, liver, lung, heart, and intestines). Abdominal compartment syndrome (ACS, increased intra-abdominal pressure with organ dysfunction/failure) has emerged as a life-threatening complication among survivors of DCS. Prevention of ACS is a solution, but when it is attempted, the abdominal decompression and use of temporary abdominal closure is required. The liberal use of open abdomen strategy has decreased the incidence of ACS and mortality from ACS but created a new challenge: the management of the open abdomen, which is a condition with signicant morbidity and potential mortality. More recently the renement of hemostatic resuscitation has further improved to outcomes and minimized the need for prolonged open abdomen. Nowadays, severe traumatic shock patients are less likely to have systemic edema, and even when open abdomen strategy is utilized, the fascial closure is typically achieved within 48–72h.

60.1 Denitions

Abdominal compartment syndrome (ACS) is dened as sustained increased intra-abdominal pressure (IAP>20mmHg), also known as intra-abdominal hypertension (IAH), and is

O. Yoshino · N. Lee · Z. J. Balogh (*) Department of Traumatology, John Hunter Hospital and University of Newcastle, Newcastle, NSW, Australia e-mail: zsolt.balogh@health.nsw.gov.au

Table 60.1 Causes of abdominal compartment syndrome in penetrating trauma

Primary abdominal compartment syndrome

Severe penetrating abdominal trauma+shock

Aortic, mesenteric, portal cross-clamping

Abdominal sepsis as late complication

associated with newly developed organ dysfunctions. While IAH is graded [from grade I (12–15 mmHg) to grade IV (over 25mmHg)], ACS is considered as an “all or nothing” phenomenon. ACS can be classied based on the etiology (e.g., postinjury, postburn, after abdominal aortic surgery, pancreatitis, septic patients) and the acuity of the syndrome (acute, subacute, and chronic). This chapter focuses on acute postinjury abdominal compartment syndrome, which can be further classied as primary (injury to the abdomen) or secondary (extra-abdominal trauma only) ACS (Table60.1).

Secondary abdominal compartment syndrome

Severe extra-abdominal bleeding requiring massive resuscitation

Extra-abdominal sepsis requiring massive resuscitation

60.2 When toExpect ACS inPenetrating Trauma?

ACS, a potentially lethal complication of penetrating injuries, can develop in both abdominal and extra-abdominal penetrating trauma. ACS typically develops in patients who present with severe shock and require urgent hemostasis and uid resuscitation.

Typical presentations of ACS after penetrating trauma are

listed in Table60.1 and described below:

1. Penetrating abdominal trauma with shock (Figs.60.1 and

60.2): This is the classic pattern; patients with major

abdominal injuries, especially with abdominal vascular trauma or major solid organ injury such as AAST grade V liver injury, are at high risk of developing primary ACS. Hemorrhagic shock and subsequent resuscitation

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Fig. 60.1 Multiple stab wounds requiring damage control surgery, high risk for abdominal compartment syndrome. (Courtesy of Michael Sugrue)

Fig. 60.2 Isolated stab wound without hemodynamic compromise, suitable for denitive surgery, low risk for abdominal compartment syndrome. (Courtesy of Michael Sugrue)

are whole-body ischemia-reperfusion injury, which is associated with generalized and localized (intestinal) edema. The venous return from abdominal organs is further compromised by the space-occupying nature of the packs used for hemorrhage control. Open abdomen strategy is a proven approach to prevent ACS, in most of the cases. Fascial closure of the abdomen after damage control surgery (DCS) is not feasible because it can cause ACS, and in any case, a second look is necessary to remove the packs and any potential necrotic tissue and to restore the continuity of the intestinal tract. Urgent need to go to the operating room and the presence of damage control physiology (acidosis, coagulopathy, and hypothermia) are independent predictors of the primary ACS.

O. Yoshino et al.

2. Penetrating chest or extremity trauma with shock: This is

the classic example of secondary ACS, as there is no abdominal injury or pathology, but the whole-body ischemia- reperfusion injury is present and driving the pathophysiology. The intestinal tract has a signicantly lower anti-edema capacity than other vital organs like the brain, lung, or heart. Secondary ACS has the same symptoms (increased airway pressures, decreased urine, and cardiac output) like primary ACS, but secondary ACS is much more elusive since there is no obvious abdominal cause. Massive resuscitation is always present as a major independent predictor. Secondary ACS can be present as early as at the time of the initial surgery on extraabdominal bleeding sources. Reassessment on the operating table for potential ACS is important, and while a distending non-injured abdomen with high airway pressures could be a clue, measuring the intra-abdominal pressure is always helpful in the differential diagnosis.

3. In examples 1 and 2, the common confounder is delay to

denitive hemorrhage control and uncontrolled resuscitation, more than optimal volumes of crystalloids and low ratios of clotting factors administered with blood transfusion.

4. After closure of the open abdomen: Premature closure of

the open abdomen at the time of the second look laparotomy can result in recurrent ACS.Intraoperative measurement of the IAP during closure and reassessment on the operating table are advisable when the desired level of closure is achieved. It is important to remember that the IAP is most likely to be at its lowest while the patient is on the operating table (anesthetized, paralyzed, at, and supine), and it will be higher in the intensive care unit (elevation of the head of bed, avoidance of neuromuscular paralysis, nursing). It is hard to measure the IAP at the end of surgery unless there is a femoral line reaching into the inferior vena cava or a urinary catheter is in situ and connected to the OR monitor via a pressure transducer. If there is no IAP measurement available when you close the abdomen, airway pressures as a guide should be discussed with the anesthesiologist.

5. Late presentation compounded with sepsis: ACS can

present in penetrating trauma patients later as a complication of uncontrolled abdominal (primary ACS) or extraabdominal (secondary ACS) sepsis. Remember that treating the sepsis will also treat the ACS.

60.3 Diagnosis

The presentation of ACS after penetrating trauma with shock is very rapid; most of the cases develop within 12h of hospital admission representing a second life-threatening insult

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Table 60.2 The common scenarios and avoidable scenarios, which could lead to abdominal compartment syndrome in penetrating trauma patients

Prehospital Delay to denitive care

Poor control of external hemorrhage Uncontrolled crystalloid resuscitation

Emergency department

Operating room Aortic, mesenteric, portal cross-clamping

Intensive care unit

Delay to hemorrhage control Uncontrolled large volume crystalloid

resuscitation Extensive imaging with uncontrolled

resuscitation Underestimation of non-cavity bleeders Poor control of the environment (hypothermia)

Delay to hemorrhage control Uncontrolled resuscitation Inability to improve hypothermia, acidosis, and

coagulopathy Tight packing with fascial closure Inadequate temporary abdominal closure Poor control of abdominal bleeding Prolonged surgery Chasing supranormal resuscitation endpoints Crystalloid boluses to maintain lling pressures

or for Starling curve assessment Not measuring IAP Inability to recognize rebleeding

after the potential exsanguination. In some extreme cases, ACS can develop on the operating table while thoracic or skeletal life-/limb-saving operation is performed. For the prevention of the syndrome, it is essential to be aware of the common scenarios and avoidable situations when ACS could develop (Table60.2).

The diagnosis of ACS involves the measurement of the IAP. Clinical examination is unreliable in estimating the IAP.The most feasible method is the intravesical route, originally described by Kron and modied by many. The measurement can be done with improvised devices, but today there are several reliable proprietary devices available. Most of these techniques require saline instillation into the bladder before measurement. Historically, the recommended instilled volume was 50mL and above. However, recent research has shown that there is no need for more than 25mL of saline through a safe closed system. The limitation of the technique is the intermittent nature and the 5–8min required to perform each measurement. The IAP can be monitored continuously via a three-way urinary catheter in the most critical patients, where the timely recognition of increased IAP is crucial.

The other component of the diagnosis is the organ dysfunction, which is related to the increased IAP.The differentiation of the IAP-related organ dysfunctions can be difcult from the ongoing circulatory, respiratory, and renal dysfunction of an acute penetrating trauma patient. Acute penetrat-

ing trauma patients are not necessarily anuric or oliguric when they develop ACS.The urine output has to be judged in the context of the magnitude of the uid resuscitation (100mL/h in a patient who is in 10L positive balance does not necessarily indicate adequate urine output). Young healthy trauma patients are expected to have a hyperdynamic response after major trauma and resuscitation. Close to normal cardiac output in these scenarios can mean compromised circulation. The lling pressures (central venous pressure and pulmonary capillary wedge pressure) can be falsely normal or elevated in patients with increased IAP.Many factors can directly and/or indirectly affect ventilation during the initial phase of shock resuscitation. If no signicant lung or intrapleural injury/pathology exists, high airway pressures and low compliance associated with increased IAP can be diagnostic as well.

60.4 Treatment

Recent reports suggest that postinjury ACS, especially in blunt trauma cohorts, is largely preventable with judicious hemostatic resuscitation. The treatment of a compartment syndrome is decompression; in postinjury ACS, this involves a full midline laparotomy. The nonoperative measures, which are more frequently described in acute general surgical and medical literature, are unlikely to be helpful in critically ill penetrating trauma patients, where the syndrome is evident within a few hours of ICU admission. In this scenario, there is no time for you to wait and see the potential modest decreases of IAP due to nonoperative measures (positioning, neuromuscular paralysis, evacuation of gastric and intestinal intraluminal contents). These patients are dying. Your immediate, efcient action is required. In obvious secondary ACS cases (no intra-abdominal injury), bedside ultrasound-guided drainage of the acutely developed ascites might be a solution, but, in most cases, not only the peritoneal uid but rather the intestinal edema which is the main component of the increased IAP.If intra-abdominal injury is excluded, you can even perform decompression in the ICU by using sterile technique (ICU procedure team). In primary ACS cases, usually rebleeding is present, which requires you to perform further formal exploration of the abdomen and control of the hemorrhage preferably after transfer of the patient to the operating room.

After decompression or reexploration, you need to apply a temporary abdominal closure to prevent evisceration and contamination but allow space for potential progressive swelling. Historically, this was done with skin-only closure with running stitch, towel clips, or with the “Bogota bag.” The latter is a large sterile infusion bag (arthroscopic or cystoscopic 3L normal saline bag) fashioned and stitched into the fascia or to the skin of the abdominal wound edges. The

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skin-only closures do not provide enough room for swelling during the acute resuscitation. These measures can be utilized in the operating room after quick packing to gain hemostasis and prevent further heat loss while allowing time to the anesthesiologist to “catch up” with the blood loss and coagulation factors. The patient abdomen should be reassessed (repacked as required) and temporary abdominal closure applied. The Bogota bag allows room for swelling, but its control of the peritoneal uids is poor and potentially ruins the skin/fascia, which could prevent future fascial closure. Most of the centers prefer to use some elastic self-adhesive coverage with abundant drainage. This can be performed with commercial vacuum-assisted devices or with a homemade (hand towel, adhesive foil, and suction drains) vacuum pack method. For rst dressing after DCS, probably, a homemade technique is ne (cheaper and readily available) and less likely to cause ongoing blood loss due to low suction. Commercial devices are denitively benecial from the rst relook laparotomy and dressing change, but many institutions use them successfully from day one. Please note that “ongoing bleeding” is usually listed as contraindication in the proprietary devices’ user manuals. If stomas are indicated at the time of the relook laparotomy, you should place them as lateral (further away from the midline) as possible, to prevent potential interference with fascial closure.

60.5 Open Abdomen

The open abdomen is the recognized preventive and therapeutic measure of postinjury ACS.The liberal application of the open abdomen strategy has led to a decrease in the incidence of lethal ACS but has created signicant morbidity and resource utilization. Temporary abdominal closure is efcient in preventing ACS, but in low-risk patients, it leads to unnecessary morbidity and cost. From the rst relook laparotomy, the goal should be to achieve fascial closure or at least minimize the size of the hernia. Most preventive open abdomens can be closed with one or two extra trips to the operating room. Vacuum-assisted techniques are very effective in controlling the local edema, evacuating ascites rich with inammatory mediators, improving nursing care, preventing contamination, and preventing the retraction of the abdominal wall. Fascial closure should occur within less than 10days. Dynamic closure systems may help with this. The earlier that closure or cover is achieved, the less the risk of stula formation. Since the areas above the costal margin and below the iliac crests are difcult to cover with component separation, extra attention must be given to close the fascia as soon as it is safe. If the fascial edges are retracted, the options for short term are insertion of a mesh or skin

grafting over the granulating bowel or skin-only closure. The closure over the intestines is important to prevent further protein loss, stula formation, peritonitis, or anastomosis breakdown. The quality of life with open abdomen patients is generally poor, and the continued restoration of the abdominal wall signicantly improves it. Late reconstruction is usually not considered before 6months, and component separation, non-resorbable mesh, or pedicled muscle aps are the main options.

60.6 Outcomes

Early recognition and preventative strategy are essential to optimize outcomes in severely shocked penetrating patients at the highest risk of developing ACS.Clinicians must be vigilant when monitoring the clinical course of patients and laboratory studies to anticipate the possibility of ACS in penetrating trauma and avoid its sequelae with appropriate patient management. Liberal application of hemostatic resuscitation, permissive hypotension to minimize uid volume before denitive surgery if possible, and open abdomen management and monitoring IAP from the early phase are imperative.

Once ACS is developed, outcomes depend on the amount of time elapsed prior to performing decompression. With timely surgical decompression, organ dysfunction could improve rapidly, improving diaphragmatic excursion, improving ventilation-perfusion mismatch, and reducing peak airway pressures. Additionally, compression of the IVC is relieved, leading to improved cardiac output and ability to wean patients off vasopressor support, and compression of the renal vessels is relieved, leading to resolution of acute kidney injury.

Developing ACS within 48h of admission is associated with an increased 30-day mortality rate, increased length of stay in the ICU under ventilation, increased overall hospital length of stay, and increased risk to discharge to a long-term support facility for care instead of home. Not only does ACS lead to poorer patient outcomes and delayed recovery, but it is also associated with increased resource utilization.

Important Points

• Abdominal compartment syndrome only develops in live

patients, so at rst, you need to save them from imminent

exsanguination.

• It is imperative to think about it even before the patients

come to the ER—never mind the OR!

• Abdominal compartment syndrome is dened by elevated

intra-abdominal pressure and organ dysfunction/failure

associated with it.

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• Abdominal compartment syndrome can develop in penetrating trauma without penetration to the abdomen (secondary abdominal compartment syndrome).

• Abdominal compartment syndrome after major penetrating trauma usually develops within a few hours after ICU admission, if not earlier.

• Do not be fooled and try to overcome the abdominal compartment syndrome-related organ dysfunctions/failures with uid resuscitation and with the ventilator. Preloaddriven resuscitation in impending abdominal compartment syndrome is the recipe for making the situation worse. As a surgeon, use a scalpel rather than salty water.

• The damage control physiology (hypothermia, acidosis, coagulopathy): The urgent need for operative hemorrhage control and the amount of crystalloids used (>3L until the operating room and more than 7L until ICU admission) are independent predictors of postinjury abdominal compartment syndrome. Remember to watch out for polycompartment syndrome.

• The open abdomen is one efcient method for prevention of abdominal compartment syndrome. It is most important to control the hemorrhage and avoid excessive resuscitation.

• After damage control laparotomy, fancy temporary abdominal closures are not necessary. The main principles to follow are ensuring plenty of room for swelling, good seal, control of the peritoneal uids, and abdominal wall friendliness.

• Abdominal compartment syndrome can develop in patients with open abdomen.

• Saving a patient with abdominal decompression is a satisfying experience, but managing the subsequent open abdomen can be challenging and less rewarding.

• While the decompression of the abdominal compartment syndrome is an urgent life-saving intervention, the management of the open abdomen is a quality-of-life- restoring activity, where consultation with experts should occur in a timely fashion.

• A strategy which ensures the timely and safe (stula, abscess, peritonitis, and hernia-free) management of the open abdomen at your institution with the aim of fascial closure within 7–10days should be developed.

• Early treatment or preferably the prevention of ACS leads to better patient outcomes, faster recovery, and less resource utilization.

Acknowledgment The authors are grateful to Michael Sugrue for his contribution to the previous versions of this chapter and providing opportunities in this version for younger generation of trauma surgeons to contribute.

The current chapter is a revision of the original chapter written by

Zsolt J.Balogh, Osamu Yoshino, and Michael Sugrue in the previous edition of the book (all this meets the requirement of TPR team).

Suggested Reading

ABRA® Literature Compendium. Use of ABRA abdominal, ABRA sur-

gical, and ABRA adhesive in clinical practice. ACell. 2019.

Ball CG, Dente CJ, Shaz B, Wyrzykowski AD, Nicholas JM,

Kirkpatrick AW, etal. The impact of a massive transfusion protocol (1:1:1) on major hepatic injuries: does it increase abdominal wall closure rates? Can J Surg. 2013;56(5):E128–34.

Balogh Z, McKinley BA, Cocanour CS, etal. Secondary abdominal

compartment syndrome is an elusive early complication of traumatic shock resuscitation. Am J Surg. 2002;184:538–43.

Balogh Z, McKinley BA, Cocanour CS, Kozar RA, Cox CS, Moore

FA.Patients with impending abdominal compartment syndrome do not respond to early volume loading. Am J Surg. 2003;186:602–7.

Balogh Z, McKinley BA, Cox CS Jr, et al. Abdominal compartment

syndrome: the cause or effect of postinjury multiple organ failure. Shock. 2003;20:483–92.

Balogh Z, McKinley BA, Holcomb JB, etal. Both primary and second-

ary abdominal compartment syndrome can be predicted early and are harbingers of multiple organ failure. J Trauma. 2003;54:848–59.

Balogh Z, Jones F, D’Amours S, Parr M, Sugrue M. Continuous

intra-abdominal pressure measurement technique. Am J Surg. 2004;188:679–84.

Balogh Z, Moore FA, Moore EE, Bif WL. Secondary abdominal

compartment syndrome: a potential threat for all trauma clinicians. Injury. 2007;38:272–9.

Balogh ZJ, van Wessem K, Yoshino O, Moore FA.Postinjury abdom-

inal compartment syndrome: are we winning the battle? World J Surg. 2009;33:1134–41.

Balogh ZJ, Martin A, van Wessem KP, King KL, Mackay P, Havill

K. Mission to eliminate postinjury abdominal compartment syndrome. Arch Surg. 2011;146:938–43.

Balogh ZJ, Lumsdaine W, Moore EE, Moore FA.Postinjury abdominal

compartment syndrome: from recognition to prevention. Lancet. 2014;384(9952):1466–75.

Cheatham ML, Safcsak K, Llerena LE, Morrow CE Jr, Block EF.Long-

term physical, mental, and functional consequences of abdominal decompression. J Trauma. 2004;56:237–41; discussion 41–2.

Cheatham ML, Malbrain ML, Kirkpatrick A, etal. Results from the

international conference of experts on intra-abdominal hypertension and abdominal compartment syndrome. II.Recommendations. Intensive Care Med. 2007;33:951–62.

Diaz JJ Jr, Mejia V, Subhawong AP, et al. Protocol for bedside lapa-

rotomy in trauma and emergency general surgery: a low return to the operating room. Am Surg. 2005;71:986–91.

Hirshberg A, Wall MJ Jr, Mattox KL.Planned reoperation for trauma:

a two year experience with 124 consecutive patients. J Trauma. 1994;37:365–9.

Ivatury RR.Update on open abdomen management: achievements and

challenges. World J Surg. 2009;33:1150–3.

Kirkpatrick AW, Roberts DJ, De Waele J, etal. Intra-abdominal hyper-

tension and the abdominal compartment syndrome: updated consensus denitions and clinical practice guidelines from the World Society of the Abdominal Compartment Syndrome. Intensive Care Med. 2013;39:1190–206.

Kron IL, Harman PK, Nolan SP.The measurement of intra-abdominal

pressure as a criterion for abdominal re-exploration. Ann Surg. 1984;199:28–30.

Mayberry JC, Mullins RJ, Crass RA, Trunkey DD. Prevention of

abdominal compartment syndrome by absorbable mesh prosthesis closure. Arch Surg. 1997;132:957–61; discussion 61–2.

Miller PR, Meredith JW, Johnson JC, Chang MC. Prospective evalu-

ation of vacuum-assisted fascial closure after open abdomen: planned ventral hernia rate is substantially reduced. Ann Surg. 2004;239:608–14; discussion 14–6.

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Moore EE.Thomas G. Orr Memorial Lecture. Staged laparotomy for

the hypothermia, acidosis, and coagulopathy syndrome. Am J Surg. 1996;172:405–10.

Offner PJ, de Souza AL, Moore EE, et al. Avoidance of abdominal

compartment syndrome in damage-control laparotomy after trauma. Arch Surg. 2001;136:676–81.

Raeburn CD, Moore EE, Bif WL, etal. The abdominal compartment

syndrome is a morbid complication of postinjury damage control surgery. Am J Surg. 2001;182:542–6.

Rodas EB, Malhotra AK, Chhitwal R, Aboutanos MB, Duane TM,

Ivatury RR. Hyperacute abdominal compartment syndrome: an

unrecognized complication of massive intraoperative resuscitation for extra-abdominal injuries. Am Surg. 2005;71:977–81.

Subramonia S, Pankhurst S, Rowlands BJ, Lobo DN.Vacuum-assisted

closure of postoperative abdominal wounds: a prospective study. World J Surg. 2009;33:931–7.

Sugrue M. Intra-abdominal pressure and intensive care: current con-

cepts and future implications. Intensivmed. 2000;37:529–35.

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SNOM: Conservative Management

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ofSolid Viscera

PradeepH.Navsaria

The selective nonoperative management (SNOM) of hemodynamically stable, clinically evaluable patients with abdominal stab and low-velocity gunshot wounds without an intra-abdominal injury is safe. The high success rates of the nonoperative management of patients with blunt solid organ injuries have been extended to select patients with documented penetrating liver, kidney, and spleen injuries. While this is not a universally accepted mode of treatment, there is a small, but growing body of evidence to support the SNOM of penetrating solid organs.

The concept of the SNOM of penetrating solid organs is

one that deals with patients who have sustained a penetrating abdominal injury, who do not have an emergent indication for laparotomy (hemodynamic instability or peritonitis), who are neurologically (centrally and peripherally) intact, who have undergone computerized tomography (CT) documenting a solid organ injury, and who are then managed non- operatively, without a laparotomy.

61.1 SNOM: Liver

Patients with penetrating injury to the right thoracoabdomen and right upper quadrant with injury to the right lung, right diaphragm, and liver may be safely observed in the presence of stable vital signs, minimal or no abdominal tenderness, and reliable clinical examination.

61.1.1 The Patient

• Right thoracoabdominal/right upper quadrant penetrating injury.

61.1.2 Clinical Findings

• Stable vital signs.

• No central or spinal cord neurological decit.

• Minimal or no abdominal tenderness.

61.1.3 Plain Chest Radiograph

• Normal.

• Right pneumothorax.

• Right hemothorax.

• Right hemo-/pneumothorax.

• Right-sided pulmonary opacity signifying lung contusion and/or intrapulmonary hematoma.

61.1.4 Special Investigation

Contrasted computerized axial tomography essential (lower chest and upper abdomen).

• CT scan conrms lung and liver injury (diaphragm injury by inference).

• Grades liver injury.

• Determines the amount of pleural uid and degree of lung contusion.

• Any contrast “blush” on CT scan is considered a nding of bleeding or false aneurysm and must be followed up immediately by angiography and angioembolization, provided the patient remains hemodynamically stable.

• Free air, free uid with no solid organ involvement, localized bowel wall thickening, mesentery stranding, and hematoma/free air surrounding hollow viscus suggest hollow viscus injury—proceed to laparotomy.

P. H. Navsaria (*) Department of Surgery, Trauma Centre, Groote Schuur Hospital, Observatory, Cape Town, South Africa e-mail: pradeep.navsaria@uct.ac.za

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61.1.5 Management

• Admit to high observation unit for at least 48–72h.

• Two-hourly blood pressure and hemoglobin estimation for 24h, then four-hourly.

• Four-hourly serial abdominal examination.

• Nil per mouth for 24h, then feed; if tolerated, hollow visceral injury unlikely.

• Transfer to general surgical ward.

61.1.6 Complications

Failed abdominal observation: Development of peritonitis and hypotension warrants immediate surgery. Pyrexia and raised leukocyte count must be taken in context of clinical abdominal ndings and not necessarily imply failure of nonoperative management.

Infected uid (bile and/or blood) collections: Infected

subphrenic, subhepatic, and intrahepatic collections usually manifest 3–5days post-injury. Patients are usually generally well, but have a swinging pyrexia, elevated leukocyte count, and maybe some increase inlocalized tenderness to the right upper quadrant. Repeat CT scan is essential for diagnosis, and treatment consists of percutaneous drainage and broadspectrum antibiotic cover (antistaphylococcal agent and anaerobic cover is essential). Patients without drainable collections should be empirically commenced on broadspectrum antibiotics for suspected infected liver “tract hematoma.”

61.2 Thoracobiliary Fistulae

All patients with a liver gunshot traversing the diaphragm treated nonoperatively are at risk of thoracobiliary (pleurobiliary and bronchobiliary) stulae. Diagnosis is usually suspected with bilious drainage from tube thoracostomy or reaccumulation of pleural uid collections that are bilestained and bile-stained sputum. Management consists of adequate pleural drainage, percutaneous drainage of any peri-/intrahepatic collections, endoscopic retrograde cholangiography with sphincterotomy, and placement of a biliary stent.

61.3 The Evidence

ries who were successfully managed nonsurgically without any liver-related complications. In the following year, Chmielewski etal. described successful NOM in 12 patients with RUQ gunshot wound, of which eight sustained grade II–III liver injuries. Demetriades etal. reported lower success rate (69%) for selective NOM in GLI.They managed to treat 11 of 16 patients nonsurgically successfully and concluded that particular patients with simple (grade I/II) liver injuries can be managed nonoperatively. Later in 2005, in a relatively larger series of patients by Omoshoro-Jones etal. described 97% success rate of NOM for GLI.In their series of 33 patients, 8, 14 and 11 patients had grade I/II, grade III and grade IV/V liver injuries, respectively. Only two patients failed conservative management and required delayed laparotomy unrelated to liver trauma. More recently, in 2009, Navsaria etal. described 92% success of NOM for both simple and complex GLI.They treated 58 of 63 patients nonoperatively with overall liver-related complications seen in only 9.5% (three liver abscesses and three biliary stulas) of patients. The overall success rate of NOM for GLI 93%. This is similar to the most recent prospective series by Navsaria etal. (94.4%). In this study of 195 liver gunshot injuries, 81/195 (41.5%) liver injuries required no treatment at laparotomy, and 63/195 (32.3%) patients were considered for nonoperative management without laparotomy. Hence, a total of 144/195 (73.8%) of all liver gunshot injuries in their series were managed conservatively. The constant high success rate could be ascribed to the fact that most isolated GLI requires no treatment. The surgeon, however, must recognize the risks of SNOM of penetrating liver injuries and have the resources (angiography with angioembolization, percutaneous interventional techniques and endoscopic interventional cholangiography) available to address potential complications. Arterial phase contrast extravasation may predict failure of SNOM and adjunctive angioembolization should be considered for this group. SNOM of penetrating abdominal wounds, with or without liver injury, with or without advanced CT technology, is still based largely on the ndings from serial clinical examinations.

61.4 SNOM: Kidney

The mandatory exploration of all patients with penetrating renal trauma is not necessary.

The reports of NOM related to GLI appeared more frequently since the 1990s. Renz etal. are attributed to reporting rst successful NOM of GLI.In their small series of 13 patients with a RTA gunshot, 7 had CT conrmed liver inju-

61.4.1 The Patient

• Penetrating abdominal trauma, particularly to the ank and posterior abdomen.

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61.4.2 Clinical Findings

• Stable vital signs.

• No central or spinal cord neurological decit.

• Minimal or no abdominal tenderness.

• Hematuria (microscopic/macroscopic).

61.4.3 Special Investigation

Contrasted computerized axial tomography is essential.

• CT scan conrms renal injury.

• CT grades renal injury.

• Ureteric injuries require surgical intervention.

• Nonperfusing kidneys require nephrectomy. Note that parenchymal contrast extravasation is not an absolute contraindication to nonoperative treatment.

• Any contrast “blush” on CT scan is considered a nding of bleeding or false aneurysm and must be followed up immediately by angiography and angioembolization, if the patient remains hemodynamically stable.

Free air, free uid with no solid organ involvement, local-

ized bowel wall thickening, mesentery stranding, and hematoma/free air surrounding hollow viscus suggest hollow viscus injury—proceed to laparotomy.

61.4.4 Management

• Admit to high observation unit for at least 48–72h.

• Two-hourly blood pressure and hemoglobin estimation for 24h, then four-hourly.

• Four-hourly serial abdominal examination and daily urine dipstick.

• Nil per mouth for 24h, then feed; if tolerated, hollow visceral injury unlikely.

• Transfer to general surgical ward.

61.4.5 Complications

1. Failed abdominal observation: Development of peritoni-

tis and hypotension warrants immediate surgery.

2. Pyrexia and raised leukocyte count must be taken in con-

text of clinical abdominal ndings and not necessarily implies failure of nonoperative management.

3. Perinephric infected hematoma/urinoma: Infected peri-

nephric collections usually manifest 3–5days post-injury. Patients are usually generally well, but have a swinging pyrexia, elevated leukocyte count, and some ank and/or renal angle tenderness. Repeat CT scan is essential for

diagnosis, and treatment consists of percutaneous drainage and broad-spectrum antibiotic cover. Persistent urinary leaks can be managed by retrograde ureterogram and endoscopic stent placement.

4. Persistent hematuria/recurrent macroscopic hematuria: Persistent macroscopic hematuria (>72h) and those who present with delayed-onset macroscopic hematuria (usually 10–14days post-injury) are an indication for renal angiography and embolization of intrarenal arteriovenous stulae or false aneurysms.

5. Blocked urinary catheters: Usually occurs in the presence of macroscopic hematuria and blood clots in the bladder. An ultrasound of the bladder will conrm blood clots in the bladder and bladder irrigation should be commenced using a three-way hematuria catheter.

61.4.6 The Evidence

The only absolute criterion for emergency surgery in kidney trauma is hemodynamic instability. Patients with vascular pedicle and renal pelvis and ureter injuries require immediate exploration. The percentage of kidney stab wounds amenable to nonoperative management ranges between 51 and 77% with success rates of greater than 95%. It has been reported though that gunshot wounds are signicantly more likely to result in severe kidney injuries than stab wounds and thence the reluctance maybe to manage gunshot wounds to the kidney nonoperatively. Penetrating trauma is associated with a high nephrectomy rate (24%); however, a high nonoperative success rate approaching 100% is achievable with minimal morbidity. It has also been suggested that the threshold for exploring urinary extravasation for gunshot wounds should be lower than that for stab wounds because of the increased risk of delayed complications because of extensive tissue damage from the projectile’s blast effect. Most studies on conservatively managed gunshot wounds have been retrospective in nature. While there is some evidence to support that with accurate preoperative imaging and grading of the kidney injury, grades I–III need not be explored at the time of laparotomy for other injuries. The evidence to support the nonoperative management of isolated kidney gunshot injuries is few. Overall, nonoperatively managed kidney gunshot injuries have a success rate of almost 95%. McAninch and colleagues reported a series of 87 gunshot kidney units, of which ten were not explored at laparotomy for associated injuries and eight (9.2%) patients were managed with a 100% success rate without a laparotomy. Similarly, Velmahos etal. managed four patients in a series of 52 consecutive kidney gunshot injuries successfully nonoperatively without laparotomy. Complications that may occur with expectant management are ongoing bleeding or rebleeding (increase in perinephric hematoma or appearance

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P. H. Navsaria

of macroscopic hematuria or persistent microscopic hematuria), infected perinephric uid collections, and persistent urinary leaks. Therefore, the surgeon must recognize the risks of SNOM of penetrating kidney injuries and have the resources (angiography with angioembolization and percutaneous radiological interventional techniques) available to address potential complications. However, SNOM of penetrating abdominal wounds, with or without kidney injury, with or without advanced CT technology, is still based largely on the ndings from serial clinical examinations.

61.5 SNOM: Spleen

The vast majority of penetrating splenic trauma requires urgent operative management. In a recent study from LACUSC trauma center, a group of 38 patients without hemodynamic instability, peritonitis, or radiologic evidence of hollow viscus injury (free air, free uid and bowel wall edema) was managed conservatively. Hollow viscus injury was responsible for SNOM failure in up to a fth of these cases and typically presented within 24h of injury. Delayed laparotomy, within this limited time period, did not appear to increase mortality nor preclude successful splenic salvage. The authors further emphasize the role of diagnostic laparoscopy to evaluate and repair occult diaphragm injury in patients with penetrating left thoracoabdominal trauma. They conclude that as SNOM for penetrating abdominal trauma becomes more common, multicenter data is needed to dene the principles of patient selection and the limitations and consequences of SNOM more accurately of penetrating splenic injury. Presently, there is very little evidence to support the nonoperative management of splenic injuries.

Important Points

• SNOM is for hemodynamically stable, clinically evaluable patients without an intra-abdominal injury.

• SNOM is still based largely on the ndings from serial

clinical examinations.

• With or without advanced CT technology, you need to see your patient regularly.

• It takes time to see your patient regularly.

• Clinical serial examination is best done by the same person.