Major Complications Associated With Laparoscopic Surgery

A number of complications may be associated with laparoscopic surgery. Several of these iatrogenic injuries are unique and peculiar to the laparoscopic procedure itself (i.e., separate from the major surgical objective). For example, total abdominal hysterectomy is associated with the risk of a number of complications inherent to the surgical procedure, whereas laparoscopic hysterectomy has risks associated with the laparoscopic approach plus the hysterectomy portion of the operation.

Vascular and Intestinal Injury

The two most serious laparoscopic complications are major vascular injury and intestinal damage. The former results in massive intra-abdominal hemorrhage and hypovolemic shock. This catastrophe must be managed in a timely, appropriate manner; otherwise, the patient will die as exemplified in case one autopsy photographs ( Fig. 119.1A to C ). A second case showing autopsy photographs illustrates the cataclysmic outcome of retroperitoneal great vessel injury. In this case delayed surgical intervention led to this young woman’s demise ( Fig. 119.1D to H ). Small or large intestinal injury inevitably leads to immediate or delayed perforation ( Fig. 119.2A and B ). Fig. 119.2C details a compound injury created by injudicious supraumbilical trocar placement. In the case illustrated the trocar creates a through-and-through perforation of the transverse colon, which is coupled with even worse collateral damage inflicted to the superior mesenteric artery. The failure to promptly identify and treat the laceration of a great retroperitoneal vessel injury led to the patient’s death by exsanguination. In some instances, significant damage to the bowel mesentery or directly to the blood vascular supply will result in ischemia followed by intestinal necrosis ( Fig. 119.3A to D ). As bowel contents spill into the abdominal cavity and then into the bloodstream, infection and sepsis follow. Sepsis syndrome is manifested by systemic inflammatory response syndrome (SIRS) ( Tables 119.1 and 119.2 ). A cascade of events triggered by bacteremia and bacterial endotoxins and exotoxins eventuates in multiple organ failure. Necrotizing fasciitis may further complicate the picture in these cases. The condition progresses rapidly and is hallmarked by inordinate wound pain with cellulitis-like signs. Radiologic studies may show air within the abdominal wall ( Fig. 119.3E and F ). The bottom run of the downward spiral of events is septic shock (hypotension) and death. It is most convenient to subdivide these complications into those associated with the laparoscopic approach and those associated with the operative procedure ( Table 119.3 ). Electrosurgical technology has become the principal methodology for hemostasis during laparoscopic operations. These techniques use either monopolar or bipolar circuits. The latter clearly offer greater safety compared with the former (see Chapter 6 ’s discussion of energy devices). Both types of circuitry, however, can create damage to surrounding intra-abdominal structures by thermal conduction through tissues beyond the target point of electrode contact. Fig. 119.4A to E illustrates the progression of an intestinal burn from initial impact to full perforation. Figs. 119.5A and B and 119.6A and B illustrate a thermal injury to the colon, which subsequently results in a colonic-vaginal fistula.

FIG. 119.1, A. Autopsy of a young woman who sustained a through-and-through trocar injury of the left common iliac artery and vein and died of massive blood loss. The area below the forceps shows the laceration on the posterior wall of the artery. B. The probe passed by the coroner enters the posterior wall of the artery and exits through the anterior wall. Vascular clips can be seen on the left common iliac vein. C. The probe points to a laceration in the left common iliac vein. This was the fatal wound. D. Autopsy showing massive injury to left common iliac artery with Gore-Tex graft. E. Magnified view of D. F. Removed aorta and trunks of common iliac arteries; note graft interposed between aortic bifurcation and left iliac artery. G. Magnified view of aorta and iliacs. A segment of the vena cava is opened and contained two puncture wounds and sutures. H. The aorta has been opened; the doublet holes on the posterior wall are perforating vessel openings.

FIG. 119.2, A. The forceps has been placed in a trocar wound of the omentum. B. The transverse colon has been elevated, permitting the scissors to trace the trajectory into a trocar-induced perforation of the duodenum. C. In preparation for a robotic procedure the initial entry incision was made 4 to 5 cm above the umbilicus. The trocar was directed at an angle close to 90°. The razor-sharp trocar created a through-and-through perforation of the transverse colon and continued a deep trajectory into the superior mesenteric artery. The patient died of massive hemorrhage as a result of failure to find the injured artery and lack of measures to repair the laceration.

FIG. 119.3, A. This 28-year-old para 3-0-0-3 underwent a postlaparoscopy emergency laparotomy. At the time of the laparotomy, the patient had extensive peritonitis and multiple small-bowel interloop abscess formations. Note the swollen, edematous small intestine. The patient also exhibited clinical signs of septic shock. B. The mesentery of the small intestine had been coagulated by plasma kinetic forceps and torn away from the intestine by blunt dissection during attempted adhesiolysis. Note the extensive ischemic and necrotic small bowel. C. Close-up at the necrotic segment of the small intestine shown in Fig. 119.3B . D. The small bowel is covered with fibrin secondary to extensive peritonitis. E. Necrotizing fasciitis is a by-product of intestinal perforation and sepsis, particularly in obese patients. Group “A” streptococci or methicillin-resistant staphylococci rapidly spread along tissue planes while their toxins digest fat and fascia. This is clearly shown in this photo. The fat becomes grayish as the tissue undergoes cell death. F. Treatment consists of radical debridement of all dead or dying tissue. Frequent returns to the operating room are the rule before the infection is terminated. In this photo, most of the fat of the anterior abdominal wall is gone, including the rectus sheath.

TABLE 119.1

Definitions of Sepsis

From Goldman L, Ausiello D: Cecil Textbook of Medicine, 22nd ed. Philadelphia, Saunders, 2004. With permission.

Infection: Phenomenon characterized by an inflammatory response to the presence of microorganisms or the invasion of normally sterile host tissue by those organisms.
Bacteremia: Presence of viable bacteria in the blood.
Systemic inflammatory response syndrome: Systemic inflammatory response to a variety of severe clinical insults. The response is manifested by ≥2 of the following conditions:
- Temperature: >38°C or <36°C
- Heart rate: >90 beats/min
- Respiratory rate: >20 breaths/min or PaCO ₂ <32 mm Hg @ 4.3 kPa
- White blood cell count: >12,000 cells/mm ³ , <4000 cells/mm ³ , or >10% immature (band) forms
Sepsis: Systemic response to infection. This systemic response is manifested by ≥2 of the following conditions as a result of infection:
- Temperature: >38°C or <36°C
- Heart rate: >90 beats/min
- Respiratory rate: >20 breaths/min or PaCO ₂ <32 mm Hg @ 4.3 kPa
- White blood cell count: >12,000 cells/mm ³ , <4000 cells/mm ³ , or >10% immature (band) forms
Severe Sepsis: Sepsis associated with organ dysfunction, hypoperfusion, or hypotension. Hypotension and perfusion abnormalities may include, but are not limited to, lactic acidosis, oliguria, or an acute alteration in mental status. Patients who are on inotropic or vasopressor agents may not be hypotensive at the time that perfusion abnormalities are measured.
Hypotension: Systolic blood pressure <90 mm Hg or reduction >40 mm Hg from baseline in the absence of other causes for hypotension.
Multiple organ system failure: Presence of altered organ function in an acutely ill patient such that homeostasis cannot be maintained without intervention.

TABLE 119.2

Effects of Intestinal Perforation: Infection, Fluid-Electrolyte Imbalance, Sepsis Syndrome

From Baggish MS: Ob-Gyn Management 20:47-60, 2008. With permission.

The principal derangements that arise as a result of bowel perforation include infection and fluid-electrolyte imbalance and their sequelae. Intestinal fluid and feces contain a variety of bacteria, such as Escherichia coli, Enterococcus, Klebsiella, Proteus, Pseudomonas, and Clostridium, to name a few. These bacteria produce toxins that facilitate entry of bacteria into the circulation and contribute to a downward spiral of events, referred to as sepsis syndrome, as well as intra-abdominal abscess:

1.
Contamination of the abdominal cavity leads to inflammation of the peritoneum.
2.
In turn, subperitoneal blood vessels become porous, causing interstitial fluid to leak into the third space.
3.
Paralytic ileus and an accumulation of intra-abdominal fluid push the diaphragm upward, lowering the capacity for lung expansion within the thorax and contributing to partial lung collapse.
4.
Fluid of inflammatory origin may accumulate in the chest as a pleural cavity effusion.

A number of progressive complications are predictable but may occur at variable intervals after the initial perforation. The most frequent complications associated with colonic injury include the following:

Peritonitis (98% of cases)
Ileus (92%)
Pleural effusion (84%)
Colostomy (80%)
Intra-abdominal abscess (78%)

The most common sequelae after small-bowel perforation are as follows:

Peritonitis (100% of cases)
Intra-abdominal abscess (63%)
Ileus (89%)
Pleural effusion (59%)

TABLE 119.3

One-Hundred Thirty Cases of Intestinal Injury Associated With Laparoscopic Surgery

Baggish MS: J Gynecol Surg 23:83-95, 2007. With permission.

Approach	Percentage	Small Intestine	Percentage	Colon
Entry related	77%	62	41%	20
Primary trocar		(57)		(18)
Secondary trocar		(3)		(1)
Other		(2)		(1)
Operative related	23%	19	59%	29
With energy		(10)		(11)
Without energy		(9)		(18)
Total	100%	81	100%	49