Lessons in timely recognition of laparoscopy-related bowel injury
Be diligent about inspecting the bowel in the area of surgical intervention and quick to suspect intestinal injury when the patient doesn’t improve postop
IN THIS ARTICLE
The author reports no financial relationships relevant to this article.
In Part 1 of this article, I outlined circumstances in which abdominal adhesions should be anticipated and described strategies to prevent intestinal injury during operative procedures. Here, I describe ways to identify intestinal injury as soon as possible after it occurs, which is vital to prevent serious sequelae such as sepsis and even death.
During operative laparoscopy, a quick search for injury through the laparoscope cannot assure any surgeon that the intestinal wall has not been seriously denuded. A damaged muscularis—even if it is not recognized as transmural injury—may subsequently rupture if it is not appropriately repaired intraoperatively.
Following dissection of adhesions, irrigate the neighboring intestine with sterile saline, and perform a detailed inspection of the intestine to ascertain integrity of the bowel wall. The color of the intestine is important, as it can indicate whether the abundant vascular supply has been compromised. Include a detailed description of the intestines in the operative note.
Avoid stapling or vascular clips when repairing any wound; careful suturing is preferred.
Why early diagnosis is critical
The most favorable time to diagnose an iatrogenic intestinal perforation is within the intraoperative period. Prompt recognition and repair of bowel perforation offers several advantages:
- A second or third operation is less likely (<50% probability)
- The risk of abdominal sepsis is decreased.
- The volume of peripheral injury to the intestine is reduced.
- The patient can be followed for subsequent complications more precisely, permitting earlier diagnosis, more timely and effective treatment, and lower morbidity.
If the diagnosis is missed intraoperatively, then early postoperative diagnosis—less than 48 hours after the termination of surgery—is infinitely more beneficial for the patient than late diagnosis. Clearly, the longer diagnosis is delayed into the postoperative period, the greater the risk of serious morbidity and associated mortality.
The 130 intestinal injuries reported by Baggish reflect the clinical significance of timely diagnosis.1 Seventy percent of small bowel and 51% of large bowel perforations were correctly diagnosed more than 48 hours postoperatively. Sepsis was present in a majority of these cases at the time of diagnosis.
Effects of intestinal perforation?
Infection, fluid-electrolyte imbalance, sepsis syndrome
The principal derangements that arise as a result of bowel perforation are 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:
- Contamination of the abdominal cavity leads to inflammation of the peritoneum
- In turn, subperitoneal blood vessels become porous, causing interstitial fluid to leak into the third space
- 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
- Fluid of inflammatory origin may accumulate in the chest as 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 injuries are:
- peritonitis (98% of cases)
- ileus (92%)
- pleural effusion (84%)
- colostomy (80%)
- intra-abdominal abscess (78%).
The most common sequelae after small-bowel perforation are:
- peritonitis (100% of cases)
- ileus (89%)
- intra-abdominal abscess (63%)
- pleural effusion (59%).1
Reasons for diagnostic delay
- The gynecologic surgeon fails to place intestinal injury at the top of the differential diagnosis.
- A surgical consultant is delayed in making a correct diagnosis. Surgeons have less experience with perforation than do gynecologists, and invariably consider the postoperative abdominal problem to be ileus or intestinal obstruction. The presence of postoperative pneumoperitoneum is incorrectly thought to be lingering CO2 gas from the initial laparoscopy rather than air from a perforated viscus.
- Ancillary diagnosis confuses the primary physician. Pleural effusion, chest pain, and tachypnea are usually thought to indicate pulmonary embolism; as a result, the gynecologist and consulting pulmonologist focus on pulmonary embolus and deep-vein thrombosis. Only a spiral computed tomography (CT) scan, a ventilation perfusion (VQ) scan, or arteriogram quickly rules pulmonary embolus in or out. Peritonitis associated with ileus or third-space fluid leakage resulting in diaphragmatic elevation also creates pleural effusion, tachypnea, and dyspnea.
Presumptive diagnosis is critical
Definitive diagnosis of intestinal perforation happens at the operating table under direct vision and is corroborated by the pathology laboratory if bowel resection is performed. However, presumptive diagnosis helps overcome inertia and gets the patient to the operating room sooner.
The process by which the presumptive diagnosis is made is the most important issue in this article. The shorter the process, the lower the patient’s morbidity, and vice versa.
Look for steady improvement. Worry when it is absent
After any laparoscopic operation, the postoperative course should be one of steady clinical improvement. When a patient deviates from this model, the foremost presumptive diagnosis should be laparoscopy-associated injury, and the intestine should top the list of organs that may be injured. Other diagnoses should be subordinate to the principal presumptive diagnosis; these include ileus, bowel obstruction, pulmonary embolus, gastroenteritis, and hematoma, to name a few.
I do not mean to imply that a potentially life-threatening complication such as pulmonary embolus should not be ruled in or out, but that the necessary imaging should be performed in a timely fashion. The abdominal-pelvic CT scan will offer clues to the presence of free air, free fluid, air-fluid levels, and foreign bodies. It also is useful in detecting intra-abdominal—specifically, subphrenic—abscess. If necessary, a VQ scan or spiral CT scan can then be performed without delaying the diagnosis of the primary intra-abdominal catastrophe responsible for the pulmonary symptoms.
In the opening case, before making an improbable presumptive diagnosis, the surgeon should have questioned why an otherwise healthy woman would coincidentally develop gastroenteritis after laparoscopic surgery. The same can be said for diagnoses of intestinal obstruction or vascular thrombosis involving the intestinal blood supply.
Typical presentation of the injured patient
An injured patient does not experience daily improvement and a return to normal activity. Instead, the postoperative period is marked by persistent and worsening pain, often compounded by nausea or vomiting, or both. The patient may complain of fever, chills, weakness, or simply not feeling normal. Breathing may be labored. As time elapses, the symptoms become worse.
Reports of more than one visit to an emergency care facility are not uncommon. When examined, the patient exhibits direct or rebound tenderness, or both. The abdomen may or may not be distended, but usually is increased in girth. Bowel sounds are diminished or absent.
Vital signs initially reveal normal, low-grade, or subnormal temperature, and tachycardia, tachypnea, and normal blood pressure are typical. As time and sepsis progress, however, fever and hypotension develop. Most other symptoms and signs become progressively more abnormal in direct proportion to the length of time the diagnosis is delayed.
Seminal laboratory values for sepsis include a lower than normal white blood cell (WBC) count, elevated immature white-cell elements (e.g., “bandemia”), elevated liver chemistries, and an elevated serum creatinine level.
Mortality is most often the result of overwhelming and prolonged sepsis, leading to multiorgan failure, bleeding diathesis, and adult respiratory distress syndrome.
Among 130 laparoscopic surgical cases complicated by bowel injury and reported by Baggish, sepsis was diagnosed in 100% of colonic perforations and 50% of small-bowel perforations when the diagnosis was delayed more than 48 hours after surgery.1
TABLE 1 lists the signs and frequency of sepsis in these 100 cases, and TABLE 2 collates the signs and symptoms that were observed. Peritoneal cultures obtained at the time of exploratory laparotomy revealed multiple organisms (polymicrobial) in 60% of cases.
Frequency of signs of sepsis among 130 patients with colon or small-bowel injury
Colon (49 patients)
Small bowel (81 patients)
Normal or subnormal temperature
Depressed WBC count
Elevated WBC count
Elevated creatinine and blood urea nitrogen levels
*Number of patients.
Watch for signs and symptoms of intestinal injury
Direct or rebound tenderness
Diminished bowel sounds
Elevated or subnormal temperature
Pallor, hypotension, diminished consciousness
Concurrent injuries to neighboring structures
A number of collateral injuries may occur in conjunction with intestinal perforation, depending on the location of the trauma. The most dangerous combination includes indirect laceration of one of the major retroperitoneal vessels. A through-and-through perforation of the cecum can also involve one or more of the right iliac vessels. A trocar perforation of the ileum may continue directly into the presacral space or pass above it and penetrate the left common iliac vein or aorta. Similarly, perforation of the sigmoid colon may penetrate the left iliac vessels.
Careful inspection of the posterior peritoneum for tears and evidence of retroperitoneal hematoma is required to avoid missing a serious collateral injury. More likely, however, is a penetrating injury to the small bowel presenting with collateral mesenteric damage and compromise of the blood supply of an entire segment of bowel. The ureter and bladder may also be injured when dissection along the pelvic sidewall, or a trocar thrust, deviates to the right or left of midline. In thin patients, the stomach may be perforated as well as the small intestine or transverse colon.
In one memorable case, a primary trocar penetrated the omentum, injuring several underlying structures. In its transit, the trocar passed through both the anterior and posterior walls of the duodenum and finally entered the superior mesenteric artery. The gynecologic surgeon performing the laparoscopic tubal ligation failed to recognize any of these injuries. The patient went into shock in the recovery room and was returned to the operating room. Fortunately, a transplant surgeon from a neighboring theater was immediately available to consult and repair the damage.
Another danger: intestinal ischemic necrosis
Abnormalities in splanchnic blood flow are sometimes caused by elevations in intra-abdominal pressure. Caldwell and Ricotta inflated the abdomens of nine dogs and reported a significant reduction of blood flow to omentum, stomach, duodenum, jejunum, ileum, colon, pancreas, liver, and spleen, but not to the adrenal glands.2 The splanchnic flow reductions essentially shunted blood away from abdominal viscera with auto-transfusion to the heart, lungs, and systemic circulation.
Eleftheriadis and colleagues studied 16 women randomized to laparoscopic versus open cholecystectomy.3 Significant depression of the hepatic microcirculation during the period of CO2 gas insufflation was noted in the laparoscopy cohort but not in the control group. Gastric mucosal ischemia also was observed in the laparoscopy group.
Recently, however, Hasson and colleagues reported a case of possible ischemic necrosis of the small intestine following laparoscopic adhesiolysis and bipolar myolysis.8 The authors emphasized that CO2 pneumoperitoneum reduces splanchnic blood flow, predisposing the patient to ischemia, but that ischemia with infarction requires an underlying vasculopathy or inciting factors such as traction on a short mesentery, atherosclerosis, or thrombosis.
A high index of suspicion for bowel ischemia following laparoscopic surgery should occur when, postoperatively, a patient experiences inordinately severe abdominal pain associated with tachypnea, tachycardia, and alterations in the WBC count. A paucity of physical abdominal signs in the early phases of this disorder should alert the clinician to the possibility of bowel ischemia.
A CT scan with contrast can suggest ischemia, but angiography is usually required for definitive diagnosis.
Treatment begins with infusion of papaverine into the intestinal vasculature via angiography cannula. In some cases, anticoagulation may be indicated. Surgery by laparotomy is clearly indicated for patients who fail to respond to vasodilatation measures.