Complications of Pelvic exenteration
Pelvic exenteration (PE) describes a radical surgery involving the en bloc resection of the pelvic organs, including the internal reproductive organs, bladder, and rectosigmoid. Indications include advanced primary or recurrent pelvic malignancies, most commonly centrally recurrent cervical carcinoma, but also other gynecologic tumors and urologic and rectal cancers. Distant metastasis has traditionally been a contraindication to PE with curative intent. As the best chance for disease-free survival is surgical resection of regional disease, this procedure is an opportunity to cure advanced and recurrent cancers conﬁned to the pelvis.
PE has also been used for palliation of symptoms related to radiation necrosis or extensive tumor burden. Both total and partial PE require extensive reconstruction and surgical recovery with signiﬁcant associated morbidity and mortality. Careful patient selection is required to balance the potential goal of cure or symptom palliation with surgical risk.
One of the most common postoperative complications in patients who have undergone pelvic exenteration is fever. Postoperative fever is defined as a temperature above 38°C (100.4°F) on 2 consecutive postoperative days or above 39°C (102.2°F) on any 1 postoperative day. The diﬀerential diagnosis is strongly influenced by the time of onset of the fever. The most common cause of fever within the first 48 hours is a pyretic response to the operation, and this is usually self-limiting.
Studies have shown that the rate of febrile morbidity after pelvic exenteration can be as high as 71%. Among the most common causes of fever are the following:
• Infectious: Surgical site infection, pneumonia, urinary tract infection, and/or intravascular catheter–related infection
• Noninfectious: Hematoma or seroma, deep venous thrombosis (DVT) or pulmonary embolism (PE), inflammatory reaction (pancreatitis), vascular complication (hemorrhage, myocardial infarction, bowel ischemia or infarction), medications.
After pelvic exenteration, sepsis may also be a great cause of morbidity and mortality. To be diagnosed with sepsis, a patient must have two of the following signs plus a confirmed infection: body temperature above 38.3°C (101°F) or below 36°C (96.8°F), heart rate higher than 90 beats per minute, and respiratory rate higher than 20 breaths per minute. Severe sepsis is diagnosed when a patient has one of the following: decreased urine output, abrupt changes in mental status, thrombocytopenia, dyspnea, myocardial dysfunction, or abdominal pain.
Treatment for febrile morbidity should be tailored according to the source of the fever. Patients with persistent postoperative fever should be started on broad-spectrum antibiotics after cultures have been obtained. Coverage should be against aerobic gram-negative enteric bacilli and anaerobic organisms. If a source of fever is not apparent and blood cultures show no growth after 48 hours, then discontinuation of antimicrobials should be considered. If the cultures are positive, then antibiotic coverage should be focused on the known causative organism(s). All unnecessary treatments including medications, nasogastric tubes, and intravascular and urinary catheters should be discontinued, when possible, in the febrile patient.
In the setting of sepsis, all patients should be managed with broad-spectrum antibiotics, hemodynamic support such as crystalloids or albumin, vasopressor therapy, blood product administration, and mechanical ventilation, if needed. Discussion of goals of care and prognosis with the patient or family is paramount. Palliative care principles should be considered when appropriate.
Among women undergoing major gynecologic surgical procedures without thromboprophylaxis, the risk of DVT ranges from 17% to 40%. This risk is even higher among women undergoing operation for gynecologic cancer.
The most common symptoms associated with acute PE include dyspnea, pleuritic chest pain, cough, and hemoptysis. The most common signs are tachypnea, rales, tachycardia, fourth heart sound, accentuated pulmonic component of second heart sound, and circulatory collapse.
The approach to a patient with a thromboembolic event is to ensure that the patient’s condition has been stabilized after assessment of hemodynamic stability. The first steps should be to provide adequate oxygen supplementation (targeting O 2saturation ≥ 90%), obtain peripheral intravenous access, and begin empiric anticoagulation. The ACCP guidelines recommend starting LMWH or subcutaneous heparin. Once-daily treatment is the preferred choice. The length of anticoagulation for DVT is 3 months, and the recommended length of therapy for PE is 6 months.
The ACCP guidelines recommend that thrombolytic therapy should be used in patients with acute PE associated with hypotension (systolic blood pressure BP below 90 mm Hg) who do not have a high risk of bleeding. Embolectomy is recommended in patients with massive PE who have a contraindication to fibrinolysis or who remain unstable after receiving fibrinolysis. It may also be considered in patients with evidence of right ventricular enlargement or dysfunction on transthoracic echocardiogram. Inferior vena cava filters are indicated in the setting of patients with an absolute contraindication to anticoagulant therapy (hemorrhagic stroke or active bleeding). It is also indicated when recurrent embolism is present even after adequate anticoagulant therapy.
Acute Renal Events
Acute kidney injury (AKI) is the abrupt loss of kidney function, resulting in the retention of urea and other nitrogenous waste products and in the dysregulation of extracellular volume and electrolytes. This term has replaced acute renal failure (ARF) after consideration that even small decrements in kidney function are of substantial clinical relevance and are associated with increased morbidity and mortality.
AKI has multiple possible causes, and it is most commonly due to acute tubular necrosis (ATN) from ischemia, nephrotoxin exposure, or sepsis. Other frequent causes include volume depletion, urinary obstruction, rapidly progressive glomerulonephritis, and acute interstitial nephritis. AKI is typically detected by means of an increase in serum creatinine and/or a decrease in urine output. Among hospitalized patients, ATN and pre-renal disease are the most common causes.
Most patients with AKI recover renal function, with recovery manifesting with an increase in urine output and a gradual decrease in the blood urea nitrogen (BUN) and serum creatinine concentration. However, in many patients, including those with previously normal renal function, renal function does not return to baseline levels. In addition, many studies have demonstrated an increase in the risk of chronic kidney disease (CKD) and ESRD in patients who recover from AKI. Even small, acute rises in serum creatinine as low as 0.3 mg/dL (27 μ mol/L) are associated with both short-term and long-term increases in mortality.
Superficial Wound Separation
A frequent complication in patients who undergo pelvic exenteration is wound complication. The rate of such complications has ranged from 5.6% to 29.4% in the largest published series. However, one must consider that these include both abdominal wound complications and perineal wound issues.
Dehiscence and Evisceration
Complete fascial dehiscence is associated with a mortality rate of 10%. Early postoperative fascial dehiscence is a surgi-cal emergency and should be addressed promptly. The risk factors for fascial disruption are advanced age, chronic pulmonary disease, anemia, postoperative coughing, wound infection, and complexity of surgery. Other factors include malignancy, obesity, sepsis, hypoalbuminemia or poor nutrition, and chronic glucocorticoid therapy. Herniation is more common when the incision length exceeds 18 cm.
Dehiscence is most likely due to placement of the suture too close to the edge or under tension. To minimize this complication, elective midline abdominal closure should be performed with continuous absorbable sutures.
Signs and symptoms of complete dehiscence include profuse serosanguineous drainage, fever, and abdominal pain. Most dehiscences occur 4 to 14 days aft er operation. The diagnosis is made primarily based on clinical suspicion. Ultrasonography or CT may be used when the diagnosis is not clear. Once the diagnosis has been confirmed, one should place a moist dressing over the wound at the bedside. When the patient is taken to surgery, the surgeon should perform complete wound opening and subsequent debridement of the fascial edges while ensuring that no bowel injury occurs during the procedure. A mass closure with continuous delayed absorbable sutures should be performed. However, if the fascial defect that remains after proper debridement is too large, use of a wound mesh should be considered.
Necrotizing fasciitis is a rare, life-threatening soft tissue infection primarily involving the fascia and subcutaneous tissue. The reported mortality of necrotizing fasciitis ranges from 20% to 80%. There are three types of necrotizing fasciitis. These are:
• Type I—this is a mixed infection caused by both an-aerobic and aerobic species. Risk factors include diabetes, peripheral vascular disease, immune compromise, or recent operation.
• Type II—this is generally a monomicrobial infection caused by group A streptococci or other β -hemolytic streptococci, either alone or in combination with other species, most commonly Staphylococcus aureus.
• Type III—this is also known as “gas gangrene” and is caused by the organism Clostridium perfringens.
Clinical symptoms include erythema, swelling, changes in skin coloring, intense pain that may be disproportionate to the skin findings, subcutaneous emphysema, fever, nausea, vomiting, and/or malaise. It may oft en be misdiagnosed as cellulitis or abscess.
On physical examination, the patient may appear deceptively well; however, this may significantly delay the diagnosis. Such delay will lead to a rapid deterioration of the patient’s condition, and the patient will suddenly demonstrate a toxic appearance. The redness quickly spreads, with the margins moving rapidly into normal skin near the site of the incision. The skin will then develop a dusky or purplish discoloration, subsequently leading to large areas of gangrenous skin. Ultimately, anesthesia in the involved region may be reflective of the fact that there is thrombosis to the subcutaneous blood vessels that leads to necrosis of the nerve fibers. Local crepitation can occur; however, this is not a common finding.
Postoperative paralytic ileus refers to obstipation and intolerance of oral intake due to nonmechanical factors that disrupt the normal coordinated propulsive motor activity of the gastro-intestinal tract following abdominal or non-abdominal surgical procedures. After abdominal operation, “normal” physiologic postoperative ileus due to postoperative gut dysmotility is widely reported as lasting 0 to 24 hours in the small intestine, 24 to 48 hours in the stomach, and 48 to 72 hours in the colon.
The multiple definitions of “prolonged” postoperative ileus have included:
• No return of bowel function postoperatively (ranging from postoperative days 4 to 6)
• Absence of flatus or stool by postoperative day 6
• Postoperative nausea or vomiting necessitating cessation of oral intake, intravenous support, or nasogastric tube placement by postoperative day 5
• Return of bowel function after postoperative day 5
• Absence of flatus and/or bowel movement prolonging hospitalization beyond discharge goal (ranging from postoperative days 6 to 8)
• Lack of bowel activity more than 5 days after operation
Among the most common nonsurgical risk factors are opioid use, antihypertensive agents, antidiarrheal or antiemetic agents, any drug with an anticholinergic property, muscle relaxants, and atropine products. There are also a number of medical conditions that may predispose the patient to postoperative ileus. These include pancreatitis, gastroenteritis, spinal cord injury, myocardial infarction, stroke, pneumonia, diabetes, diabetic ketoacidosis, botulism, or Parkinson disease.
Small bowel obstruction can be functional or mechanical. The small bowel is involved in about 80% of cases of mechanical bowel obstruction. There are several causes for small bowel obstruction; however, in the postoperative period after pelvic exenteration, the most common cause of small bowel obstruction is adhesion formation. It is imperative to diagnose the bowel obstruction early so that the appropriate management may be initiated.
In simple mechanical obstruction, blockage occurs without vascular compromise. The normal secretory and absorptive functions of the mucosa are depressed, and the bowel wall becomes edematous and congested. There may also be transudative loss of fluid from the intestinal lumen into the peritoneal cavity. Electrolyte loss is common in this setting, leading to metabolic alkalosis, and the fluid loss may result in hypovolemia.
If the bowel obstruction is not recognized and properly addressed, the obstruction will lead to vascular com-promise, and the blood flow to the bowel will diminish. Venous obstruction occurs first, followed by arterial occlusion, resulting in rapid ischemia of the bowel wall. The ischemic bowel becomes edematous and infarcts, leading to gangrene and perforation. Acute mechanical small bowel obstruction is a common surgical emergency.
The overall incidence of anastomotic leaks is approximately 2% to 7%. The lowest leak rates are found with ileocolic anastomosis (1%–3%), and the highest rates are found in coloanal anastomosis (10%–20%). 37 Th e mortality rate for an anastomotic leak in the literature typically is in the 10% to 15% range. In the setting of pelvic exenteration, the anastomotic leak usually occurs as a result of small bowel anastomosis when a segment of ileum is used as the incontinent urostomy. Th e anastomotic leak may also be seen in the setting of ileocolonic anastomosis when a continent conduit is performed aft er the distal ileum and ascending colon have been used for the urinary conduit. Most anastomotic leaks usually become apparent 5 to 7 days postoperatively.