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426 Roger Saadia
Liver and Biliary Tree
An irreverent classification of hepatic injuries follows:
Grade I: Nothing should be done (treat conservatively)
Grade II: Something should be done (local hemostasis)
Grade III: Too much should not be done (packing only)
Grade IV: Only God can do something (heroic measures)
The following are some practical management principles:
Bleeding from small, superficial capsular tears can be controlled by cautery,
individual vessel ligation, or clipping or by atraumatic suture repair of the fragile
hepatic capsule.
More severe bleeding from a deep or craggy hepatic laceration constitutes a
surgical challenge requiring a stepwise approach. After a quick glance, bimanual
compression of the hepatic parenchyma will control the bleeding temporarily,
allowing the anesthesiologist to catch up with the blood loss. This must be fol-
lowed by rapid mobilization of the liver by division of the falciform and left and
right triangular ligaments—the liver can be literally dislocated into the abdominal incision. Additional exposure via a median sternotomy or right thoracotomy
is rarely indicated. The Pringle maneuver (inflow occlusion of the undissected
triad of portal vein, hepatic artery, and common bile duct) is sometimes useful and safe for up to 60 min. Deep parenchymal bleeding is controlled as well
as possible by clipping visible bleeding vessels and by conservative resectional
debridement. This rarely controls the hemorrhage completely—supplementary
packing is necessary. Packs must be judiciously placed around (not into) the liver.
The aim is to close the laceration by tight packing and thereby tamponade the
bleeding. Excessive packing must be avoided because it can result in inferior vena
cava compression or abdominal compartment syndrome with aggravation of the
hypotension. A return to the operating room (OR) will be necessary in 36–72 hrs
for pack removal. There is always a danger of losing sight of time and the amount
of blood loss that is incurred while trying to achieve an elusive “perfect” result.
More bleeding will require more transfusions and aggravate the coagulopathy in
a well-known vicious cycle. We strongly advise you to look at the clock before
you tackle a nasty liver laceration: you should achieve both vessel control and
packing ideally within 45 min.
Retrohepatic caval injuries are characterized by exsanguinating hemorrhage
despite inflow occlusion. There are probably more techniques described for immediate hemostasis than there are survivors. It is perhaps best to resort to damage
control with packing and come back to fight another day.
Injuries to the porta hepatis require a wide Kocher maneuver for exposure. The
injured portal vein should be repaired, or ligated as a last resort. Hepatic artery ligation
is better tolerated than portal vein ligation. Suture repair or Roux-en-Y biliary enteric
anastomoses are the treatment options for an injured common bile duct; the latter can
39.2 Operative Management of Individual Organ Injuries 427
be performed either at the initial operation or at the reconstruction phase of a damage
control strategy. Unilateral lobar bile duct injuries should be managed by ligation.
An injured gallbladder should be resected.
Spleen
The treatment at laparotomy of an actively bleeding spleen in the adult is
splenectomy. Acrobatic surgical splenic conservation procedures belong to expen-
sive surgical textbooks; they have no place in the OR. The risk of postsplenectomy
sepsis is small and can be further minimized by vaccination, vigilance, and appropriate prophylaxis.
Pancreas
The anterior aspect of the pancreas is exposed through the lesser sac by division
of the gastrocolic omentum; the posterior aspect of the head is exposed by a Kocher
maneuver, while the posterior aspect of the tail is achieved by splenic mobilization.
The state of the pancreatic duct is a crucial determinant of the operative strategy in
the injured pancreas. In some cases, the integrity of the duct may have been assessed
preoperatively in the stable patient by endoscopic (ERCP) or magnetic resonance
cholangiopancreatography (MRCP). If not, intraoperative pancreatography (through
a duodenotomy and cannulation of the ampulla of Vater) is possible, but in practice
it is rarely performed. In superficial pancreatic wounds, the main duct may be presumed to be intact, and drainage alone is sufficient. In deeper parenchymal wounds
of the body or tail, ductal transection is likely, and a distal pancreatectomy (with splenectomy) is warranted. For deeper injuries of the head, wide drainage is indicated; the
management of the inevitable pancreatic fistula in a stable patient is simpler than that
of a leaking enteropancreatic fistula in the aftermath of a fancy, immediate, Rouxen-Y jejunopancreatic reconstruction. The Whipple procedure is reserved for massive injuries of the pancreatic head, with biliary ductal and duodenal disruption. This
procedure is attended by a high mortality; it should be preferably “staged,” with the
definitive reconstruction performed only after the patient has been stabilized.
The following aphorism captures very graphically the management of this
injury:
“For pancreatic trauma, treat the pancreas like a crawfish: suck the head, eat the
tail.” (Timothy Fabian)
Kidney, Ureter, and Bladder (for Much More, see > Chap. 34)
The intraoperative discovery of a perinephric hematoma is usually indicative of renal injury. A large proportion of these are self-limiting. Renal exploration
is indicated in the presence of an expanding or pulsatile hematoma or when a hilar
428 Roger Saadia
injury is suspected. Moderate severity injuries can be controlled usually by cortical
renorrhaphy and drainage; occasionally, a polar nephrectomy may be indicated. A
shattered kidney or a vascular hilar injury is treated by nephrectomy; preliminary
control of the renal artery and vein should not be attempted in the presence of
hemodynamic instability. Attempts at saving a kidney, in these situations, are not
warranted unless the patient has a single kidney.
Lacerations of the renal pelvis are repaired with fine absorbable sutures. An
injured ureter should be carefully exposed, avoiding ischemic damage by overenthusiastic skeletonization. Primary repair with absorbable material over a
stent is the rule. Very proximal or very distal ureteric injuries may require an
expert urologic opinion.
An intraperitoneal bladder injury requires repair with absorbable sutures
and catheter drainage. In an extraperitoneal rupture, catheter drainage alone is
sufficient. A urethral Foley catheter is adequate in most cases. In severe, complex
bladder injuries or significant bleeding, suprapubic drainage may be added to
allow for efficient postoperative bladder irrigation.
Stomach
Most gastric injuries are caused by penetrating trauma and are treated by
simple, one-layer, suture repair. The posterior gastric wall should always be checked
by opening the lesser sac. Blunt injuries are rare, and gastric resection is required
only in exceptional cases.
Duodenum
Intramural duodenal hematomas do not require evacuation; nasogastric decompression, fluid replacement, and adequate nutrition (usually parenteral) need
to be instituted for up to 3–4 weeks.
Small, clean-cut lacerations can be safely repaired primarily. Extensive lacerations, the presence of significant tissue contusion (usually inflicted by blunt
trauma), involvement of the common bile duct, or high-velocity gunshot injuries
should be treated by duodenal repair and pyloric exclusion. This procedure consists of closure of the pylorus (by stapling or suture from inside the stomach) and
re-establishment of gastrointestinal continuity by a gastrojejunostomy; the addition of a truncal vagotomy is not warranted. A feeding jejunostomy is a useful
adjunct for the provision of enteral feeding. There is currently a feeling that this
procedure is overused. In relatively extensive lacerations, we often supplement
primary repair by tube duodenostomy inserted through the corner of the duodenal suture line. [Others insert it away from the suture line; some—us included—
think that this is a gimmick—The Editors].
39.2 Operative Management of Individual Organ Injuries 429
The Whipple operation is reserved for massive combined pancreatoduodenal disruptions. In an unstable patient, you should stage it: resect first and return
another day for reconstruction.
Small Bowel
Most lacerations can be treated with one-layer suture repair. Occasionally, a
segmental resection may be required in injuries involving the mesenteric side of
the intestine or for the treatment of multiple lacerations in close proximity. In the
postresuscitation edematous intestine, hand-sewn anastomoses may be safer than
stapled ones (> Chap. 13). Neglected, long-standing lacerations (more than 24 hrs)
with an established peritonitis may require the fashioning of a temporary stoma
rather than primary repair. Rarely, an extensive mesenteric laceration may endanger a very large segment of bowel, which, if resected, would result in a short-gut
syndrome; it is best then to decide on the extent of resection at a second-look
operation in a well-resuscitated patient.
Colon
Right- or left-sided simple colonic lacerations can be safely treated by suture
repair in most cases. If the severity of the laceration warrants a resection, an ileocolic
anastomosis (after a right hemicolectomy) is usually safe. A colocolic anastomosis
(after a more distal resection) may not be as safe. In any case, a colostomy rather than
repair is recommended in the presence of massive peritoneal contamination, severe
associated injuries, or gross hemodynamic instability. In borderline cases, we advise
you to err on the side of performing a colostomy; the stubborn resort to primary
repair may turn out to be a costly act of surgical bravado: more trauma patients die
from a leaking primary anastomosis than from a subsequent closure of a colostomy
gone wrong. Extensive deserosalization (typical in seat belt injuries of the cecum or
sigmoid colon) should be treated by serosal repair rather than resection.
Rectum (see also Chap. 29)
In the absence of gross fecal contamination, minor lacerations can be treated
by simple suture repair. In all other cases, a proximal diverting colostomy must be
added; a loop sigmoid colostomy is usually adequate. Small lacerations of the intraperitoneal rectal segment do not require extensive mobilization of the rectum
and repair; a diverting colostomy alone is sufficient. Washout of the distal rectal
stump and presacral drainage are unnecessary except in very extensive injuries
with wide dissection and soiling of the perirectal spaces.
430 Roger Saadia
Intra-Abdominal Vascular Injuries
Aorta. A most important step in the management of aortic injuries is expo-
sure to achieve proximal and distal control. Depending on the level, this “medial
visceral rotation” maneuver begins either lateral to the spleen or lower down,
by incising the white line of Toldt lateral to the left colon. The viscera, including spleen, pancreatic tail, left colon, and if necessary left kidney are gradually mobilized medially. The suprarenal aorta can be approached through the
gastrocolic omentum (via the lesser sac) with retraction of the stomach and
esophagus to the left. For injuries of the supraceliac aorta, a left thoracotomy
may be required. Aortic injuries are repaired with 3–0 or 4–0 sutures of polypropylene monofilament.
Infrahepatic vena cava. The exposure is achieved by incision of the white
line of Toldt lateral to the right colon with medial reflection of the right colon,
duodenum, and if necessary right kidney. The bleeding site must be occluded
by direct finger or sponge-stick pressure; vascular clamps may be used, but no
attempt should be made to encircle the vessel. Venorrhaphy can be achieved with
4–0 or 5–0 monofilament vascular suture. Check for the presence of a posterior
laceration: if present, it can be repaired by gentle rotation of the vena cava or from
inside the lumen. In massive disruptions, a synthetic graft may be used, but more
commonly the inferior vena cava is ligated. Ligation above the renal veins is not
well tolerated.
Common or external iliac artery. Suture repair or, if necessary, grafting is
used. A synthetic graft may be used even in the presence of peritoneal soiling.
In this case polytetrafluoroethylene (PTFE) is the preferred material. If gross
contamination is present, consideration should be given to arterial ligation and
restoration of the circulation by means of an extra-anatomical femorofemoral
bypass. The internal iliac artery may be ligated with impunity.
The exposure of the iliac veins is notoriously difficult and may require the
division of the ipsilateral internal iliac artery or even a temporary transection
of the common iliac artery. Iliac veins may be ligated with acceptable morbidity;
compression stockings and limb elevation are indicated postoperatively.
The celiac artery, the retropancreatic portion of the superior mesenteric
artery, and the inferior mesenteric artery may be ligated. The infrapancreatic
portion of the superior mesenteric artery should be repaired. The superior mes-
enteric vein should be repaired if possible since its ligation may cause bowel infarction, severe postoperative intestinal congestion, and intestinal varices. The
inferior mesenteric vein may be ligated without risk.
Heroic attempts at restoring flow by repairing a vessel in a patient in ex-
tremis are to be avoided. At times, ligation with later revascularization may be
possible. A better approach is a temporary shunt across the injury with definitive
grafting over the subsequent 24 hrs.
39.2 Operative Management of Individual Organ Injuries 431
Table 39.2.1. Approach to traumatic retroperitoneal hematoma
Type of hematoma Penetrating injury Blunt injury
Central (Zone I) Explore Explore
Lateral (Zone II) Usually explore Usually do not explore
Pelvic (Zone III) Explore Do not explore
Retroperitoneal Hematomas
The main issue is whether to explore a retroperitoneal hematoma discovered
in the course of a trauma laparotomy.
As a general rule, all retroperitoneal hematomas in penetrating trauma
should be explored, irrespective of size or location. In blunt trauma, a more selective policy can be applied, depending mainly on the location of the hematoma.
A central abdominal location (Zone I), including the main abdominal ves-
sels and the duodenopancreatic complex, always warrants exploration.
Lateral hematomas (Zone II), including kidneys and retroperitoneal
colonic wall, can be left alone unless they are very large, are pulsating, or are
expanding.
Blunt traumatic pelvic hematomas (Zone III) should not be explored.
Breaching the intact retroperitoneum may result in the loss of the tamponade
effect with catastrophic intraperitoneal hemorrhage (see > Table 39.2.1).
Management of Blunt Traumatic Pelvic Hematomas
With the exception of isolated fractures of the iliac crest, fractures involving
the pelvic or obturator rings or sacrum have the potential for significant bleeding
leading to shock and death. The pelvis is always imaged in severe blunt trauma,
either by computed tomographic (CT) scanning (in stable patients) or by a simple
anteroposterior radiograph (in unstable patients). Bleeding from a pelvic fracture
arises from disrupted pelvic veins, from lacerated branches of the internal iliac
arteries, and from cancellous bone, in various combinations.
In an unstable patient with a significant pelvic fracture who does not respond or responds partially to aggressive resuscitation, one must assume that
the source of bleeding is pelvic in origin once an extra-abdominal source of hemorrhage has been ruled out. The first step is then to minimize the pelvic blood
loss by increasing the tamponade effect of the pelvic retroperitoneum; this is best
432 Roger Saadia
achieved by the application of a specially designed pelvic sling (every emergency
department should have one; otherwise, a sheet tightly wrapped around the iliac
crests and tied might do).
This temporary stabilization of the pelvic bony fragments may result in
hemodynamic improvement; if this succeeds, an abdominal CT scan may be
obtained and will enable one to differentiate definitively between abdominal visceral bleeding and pelvic bleeding. The former warrants an emergency laparotomy. If the latter is present alone, a laparotomy should be avoided because it may
increase the bleeding by loss of the tamponade effect. In that scenario, transfer of
the patient to the angiography suite for attempts at angioembolization of pelvic
arterial bleeding is the best strategy; throughout the procedure, maximal resuscitation must be pursued by the trauma team (the radiology staff, while excellent
at what they do, have difficulty spelling the word “resuscitation”). If angiography
facilities are not available, the application of an external pelvic fixator by the
orthopedic team may be beneficial (it works best when the bleeding arises from a
venous or bony source but may fail to make a difference in arterial bleeding).
A grossly unstable patient, unresponsive to resuscitation, is fit only for
transfer to the OR. If pelvic bleeding alone is discovered at operation, the pelvis
should be packed and the patient transferred as a last resort to the angiography
room. The use of either supraumbilical diagnostic peritoneal lavage or abdominal ultrasound has been very disappointing in differentiating between intraperitoneal and pelvic bleeding in the particular setting of profound hemorrhagic
shock. Mortality remains extremely high in that scenario.
The Abbreviated Trauma Laparotomy (Damage Control)
When physiology is severely compromised, attempts at restoring anatomy are
counterproductive.
In a small minority of patients, time-consuming organ repair cannot be undertaken safely when the physiological status is critically impaired. A bailout procedure consisting of essential temporary control of bleeding and contamination is
the only viable option. These cases can be recognized either by a set of physiologi-
cal criteria or by an anatomical pattern of injuries. In the former model, the pres-
ence of coagulopathy, hypothermia, and acidosis is and indication of impending
physiological exhaustion. Each of these amplifies the other two in a vicious cycle
that is aptly referred to as “the triad of death.” In that scenario, a dogged determination to spend the time it takes to achieve definitive organ repair may result in
the patient’s demise. If the latter model is applied, the surgeon makes the decision
for a bailout procedure by a flash assessment of the injury pattern. For example, an
39.2 Operative Management of Individual Organ Injuries 433
injury to a major intra-abdominal vessel associated with a severe duodenopancreatic disruption is recognized immediately as a potential for massive blood loss
should a prolonged, definitive, reconstructive procedure be undertaken. In these
circumstances, there is only a place for a combination of packing, vessel shunting,
tube draining, and the simplest means of preventing peritoneal contamination (by
stapling or tying off with tapes the injured intestine). Abdominal closure consists
of expeditious cutaneous approximation or is avoided altogether—preventing the
commonly associated abdominal compartment syndrome (> Chap. 40). The pa-
tient is then treated in the surgical intensive care unit, where secondary stabilization is conducted over the next 24–48 hrs. Delayed definitive organ repair (or
resection) and abdominal closure are undertaken only in a patient who is hemodynamically more stable, is rewarmed, and has an improved clotting profile.
Summary
Injured organs must be surgically repaired or resected as soon as possible.
This being said, the surgeon should be able to recognize the potential for spontaneous healing of even severe visceral injuries (as in some cases of blunt trauma).
Furthermore, the surgeon should know to temper enthusiasm for immediately
restoring the anatomy in the face of severely impaired physiology.
The Abdominal Compartment
Syndrome
Moshe Schein
In surgery, physiology is the king, anatomy the queen; you can be the prince, but
only provided you have the judgment.
At Thanksgiving, a national holiday here in the United States, many millions of turkeys—also called “Thanksgiving birds”—are tightly stuffed with
various sorts of ingredients (mine would include chickpeas, garlic, wine-soaked
bread, and thyme) and served to the assembled members of American families.
Granted, these large birds are stuffed postmortem, but what would happen if
they were tightly stuffed alive? First, the bird would stop flying, and then gradually it would hypoventilate, collapse, and die. Of course, you could attribute the
death of your stuffed avis to bad lungs, old heart, and toxins produced by the
chickpeas and garlic; as a last resort, you could blame the anesthetist. The reality,
though, proven by a large body of first-grade scientific evidence, is much more
prosaic: intra-abdominal hypertension (IAHT) secondary to increased intra-
abdominal pressure (IAP) caused abdominal compartment syndrome (ACS).
40
Is ACS Real?
Much good evidence now supports the concept that elevated IAP or IAHT
may impair physiology and organ function by producing the ACS. Complex,
adverse physiological consequences of increased IAP develop as the pressure is
transmitted to adjacent spaces and cavities, decreasing cardiac output, restricting
pulmonary ventilation, diminishing renal function and visceral perfusion, and increasing cerebrospinal pressure (> Table 40.1, > Fig. 40.1). If you still doubt the
existence of this condition, ask the anesthetist to monitor the airway pressure the
next time you do a relaparotomy in a ventilated, critically ill patient with abdominal distension. You will note an immediate and dramatic fall as soon as the abdomen is reopened.
Moshe Schein
Marshfield Clinic Ladysmith Center, 906 College Avenue, Ladysmith, WI 54848, USA
M. Schein et al. (eds.), Schein’s Common Sense Emergency Abdominal Surger y,
DOI: 10.1007/978-3-540-74821-2_40, © Springer-Verlag Berlin Heidelberg 2010
435
436 Moshe Schein
Table 40.1. Physiological consequences of intra-abdominal hypertension
Mean blood pressure – – ×
Heart rate × – –
Peak airway pressure × – –
Thoracic/pleural pressure × – –
Central venous pressure × – –
Pulmonary capillary wedge pressure × – –
Inferior vena cava pressure × – –
Renal vein pressure × – –
Systemic vascular resistance × – –
Cardiac output – × –
Venous return – × –
Visceral blood flow – × –
Increased Decreased No change
Gastric mucosal pH ×
Renal blood flow – × –
Glomerular filtration rate – × –
Cerebrospinal fluid pressure ×
Abdominal wall compliance – × –
How Do You Measure IAP?
At the bedside, IAP is best measured through the urinary bladder catheter
connected to a manometer or a pressure transducer. In fact, all you need to measure IAP is a Foley catheter: disconnect it from the urine bag; instill 100 ml saline
into the bladder and elevate the disconnected catheter perpendicular to the supine
patient and the patient’s bed. The height of the water-urine column in the catheter
is the IAP in centimeters of water (1 cm H2O = 0.735 mmHg). The level will fluctuate with the patient’s respiratory cycle—up during inspiration, down during expiration—following the movements of the diaphragm. A neurogenic or small
contracted bladder may render the measurements invalid. Errors can also occur if
the catheter is blocked or if a pelvic hematoma selectively compresses the bladder.
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