Chapter 45 Complications of Laparoscopic and Hysteroscopic Surgery

Howard T. Sharp, Tommaso Falcone, William W. Hurd

INTRODUCTION

It has been almost a century since Jacobaeus performed laparoscopy by inserting a Nitze cystoscope (consisting of an incandescent platinum wire loop and a system of lenses) into a patient’s abdomen. Since that time, significant advances in technology have enabled gynecologic surgeons to use laparoscopes to perform procedures that in the past were done exclusively using an abdominal and vaginal approach.

Unfortunately, many laparoscopic advances were developed by trial and error accompanied by significant morbidity and mortality.¹ The application of electrosurgery, automated stapling devices, patient positioning, and trocar use produced unique mechanisms for surgical injury, many of which were not predicted. When can new technologies and procedures be considered safe? How many laparoscopic procedures should be performed before a surgeon is deemed proficient? A recent study of the learning curve associated with laparoscopically assisted vaginal hysterectomies (LAVH) suggests that a gynecologist must perform more than 30 cases before morbidity rates are significantly reduced.¹

This chapter discusses the most common risks associated with laparoscopy and hysteroscopy, including nerve injuries, injuries to structures, including blood vessels, bowel, bladder, and ureters, and electrosurgical injuries related to laparoscopy. The goal is to provide anatomic and technical information that will allow gynecologists to better prevent, recognize, and manage complications associated with laparoscopic and hysteroscopic surgery.

LAPAROSCOPY

Nerve Injury

Mechanisms of Injury

Nerve injuries can occur during laparoscopy by one of three basic mechanisms. The most common mechanism of nerve injury in these patients is related to patient positioning. The dorsal lithotomy position puts many nerves of the lower extremity on stretch or under pressure, resulting in temporary paresthesias on awakening. Unfortunately, prolonged stretch or pressure on nerves during surgery can result in neurologic injury that may take months to resolve or may be permanent. Careful patient positioning, especially during prolonged cases, is important to avoid extreme flexion and abduction, as well as pressure points.

The second mechanism of nerve injury during laparoscopy occurs during port placement through the anterior abdominal wall and the subsequent repair of the incisions. These abdominal wall nerve injuries are uncommon. However, because the nerves involved are not easily identified and their anatomic locations vary greatly, the injuries are difficult to completely prevent. For this reason, diagnosis and treatment become paramount.

The final mechanism of injury is direct trauma to pelvic nerves during retroperitoneal dissections, including resection of severe endometriosis and lymphadenectomy for cancer staging. Surgeons performing these procedures need a thorough understanding of the location of the nerves at risk to minimize injury.

Categories of Nerve Injuries

Nerve injuries are categorized by neurologists according to the degree of injury, which is ultimately reflected in the patient’s subsequent prognosis for recovery. A nerve contusion, referred to as a neurapraxia, is a functional injury in which structural continuity of the nerve is preserved. Diagnostically, it is characterized by a conduction block on electromyelogram. A mild injury results in immediate conduction block at the site of injury with normal conduction distally. A more severe injury results in focal demyelination without disruption of axons, resulting in slowing of conduction velocity across the lesion. Myelin regeneration results in functional recovery within 6 weeks.

The next level of nerve injury is termed axonotmesis and involves separation of axons and myelin sheath of a peripheral nerve with preservation of the nerve’s investing sheaths (i.e., endoneurium, perineurium, and epineurium). This more serious nerve injury results in degeneration of the axon distal to the injury site. Wallerian degeneration occurs, characterized by axonal enlargement and breakdown, as well as schwann cell ingestion of myelin fragments. Spontaneous regeneration of the axon usually results in functional recovery within 6 months to 1 year of injury.

The most serious level of nerve injury is complete division of the nerve, referred to as neurotmesis. After disruption of the axons, myelin sheath, and investing sheaths, wallerian degeneration occurs. Without further treatment there is no recovery. With operative repair of the injured nerve, the prognosis is variable and ranges from complete recovery to permanent disability.

Fortunately, most neurologic injuries associated with patient positioning during laparoscopic surgery do not result in nerve separation and resolve spontaneously with time.² Those associated with radical surgical dissection may be more likely to be serious and permanent.

Specific Nerve Injuries

Femoral Nerve

The femoral nerve is the largest nerve of the lumbosacral plexus and is derived from the posterior divisions of the L2, L3, and L4 nerve roots (Fig. 45-1). It pierces the psoas muscle and runs inferolaterally within the muscle to emerge between the iliacus and psoas muscles. It then courses under the inguinal ligament to enter the femoral sheath lateral to the femoral artery.

Figure 45-1 Schematic representation of nerves that can be injured during laparoscopy.

(Reproduced from Drake R, Vogl W, Mitchell AWM: Gray’s Anatomy for Students. Philadelphia, Elsevier, 2005.)

The femoral nerve contains motor and sensory components. The motor component supplies the iliacus, quadriceps femoris, sartorius, and pectineus muscles, which are hip flexors and leg extensors. Its main sensory branches include the intermediate and medial cutaneous nerves of the thigh and the saphenous nerve, which supplies the medial leg.

Femoral neuropathy during laparoscopy usually results from excessive hip flexion or abduction or from long operating times.² Patients undergoing vaginal or laparoscopic surgery should be placed in a lithotomy position such that the thigh is flexed no greater than 90 degrees and abducted no greater than 45 degrees. If positioning is changed intraoperatively, these relationships should be maintained.

Symptoms of femoral neuralgia include groin pain and weakness of knee extension and thigh flexion. The knee jerk reflex is usually absent. Diagnostic studies such as electromyography and nerve conduction studies can confirm prolonged latencies in the femoral nerve and denervation of the quadriceps muscles.

Obturator Nerve

The obturator nerve arises from the anterior nerve roots of L2, L3, and L4 (see Fig. 45-1). It descends through the psoas muscle, emerging medially at the pelvic brim, and passes through the obturator foramen into the thigh. Its main function is to allow thigh adduction; it supplies motor function to the gracilis, obturator, adductor longus, brevis, and magnus muscles.

The most common cause of obturator neuropathy resulting from gynecologic surgery is direct injury during radical pelvic surgery or lymphadenectomy. The obturator neurovascular bundle is also vulnerable during laparoscopic retropubic dissection, particularly during the paravaginal repair of lateral defects of the anterior vaginal wall. Surgeons who operate in these spaces should be well-versed in the anatomy of the obturator nerve.

Obturator neuropathy can also occur as a result of excessive hip flexion.³ The mechanism whereby excessive hip flexion can cause obturator nerve injury is anatomic. As the obturator nerve leaves the obturator foramen, it lies directly against bone and can become acutely angulated and deformed if the hips are excessively flexed, particularly during prolonged surgery. Injury to the obturator nerve usually manifests as weakness in the hip adductors and sensory loss in the upper medial thigh.

Nerves of the Anterior Abdominal Wall and Inguinal Region: Ilioinguinal, Iliohypogastric, and Genitofemoral

The ilioinguinal, iliohypogastric, and genitofemoral nerves have an overlapping sensory distribution in terms of their cutaneous manifestations, often making it difficult to distinguish between them. The course of these nerves is quite variable. The iliohypogastric and ilioinguinal nerves originate from the T12 and L1 nerve roots of the lumbosacral plexus (see Fig. 45-1). They cross over the quadratus lumborum muscles and pierce the transversus abdominis muscle in parallel at about the level of the anterior superior iliac spine.⁴ The genitofemoral nerve originates from the L1 and L2 nerve roots to pass anterior to the psoas muscles (see Fig. 45-1). The iliohypogastric nerve supplies sensation to the suprapubic region, and the ilioinguinal nerve supplies sensation to the inguinal canal. The genitofemoral nerve provides sensory innervation to the labial skin (genital branch) and the superior thigh (femoral branch).

The most common injury to these nerves is due to abdominal and pelvic incisions with subsequent suture ligature or fibrotic entrapment. With a Pfannenstiel incision, this injury is most likely to occur when the incision extends beyond the fascial aponeurosis to include the medial edge of the internal oblique muscle.⁵ During laparoscopic trocar insertion, the risk of injuring these nerves increases as the trocars are placed inferior to the anterior superior iliac spine.^4,⁶ Palpation of the anterior superior iliac spine before trocar placement is useful for gaining lateral bearings.

Entrapment of these nerves usually manifests as sharp, burning pain and paresthesia. The putative diagnosis is made when local infiltration with a local anesthetic results in pain relief and paresthesia over the sensory distribution of the nerve. Due to the variability of these nerve pathways, entrapment may occur regardless of the precautions taken. For this reason, prompt recognition and treatment are important to avoid prolonged symptoms.

Sciatic Neuropathy

The sciatic nerve, derived from L4 through S3, is the largest peripheral nerve in the body and has tibial and common peroneal divisions. It is located anterior to the piriformis muscle, passing through the greater sciatic foramen to course down the posterior thigh. It supplies motor function to the hamstring muscles, which provide leg flexion and thigh extension. It divides superior to the popliteal fossa. Its tibial branch descends within the posterior leg to supply motor function to the plantar flexors of the foot and intrinsic foot flexors. It supplies sensory innervation to the toes and plantar surface of the foot. The common peroneal nerve continues anteriorly around the fibular head to supply motor function to the dorsiflexor and evertors of the foot. It also provides sensation to the lateral leg and dorsum of the foot.

The most common mechanism of injury to the sciatic nerve during gynecologic surgery is prolonged hip flexion resulting in nerve tension and stretching. Tension is increased with hip flexion when the knee joint becomes straightened or externally rotated. The sciatic nerve can stretch approximately 1.5 inches when the hip is flexed and the leg extended. Therefore, it is important to be cautious not to use excessive hip flexion when placing patients in stirrups, particularly the hanging type. When free-hanging stirrups are used for gynecologic cases, this injury has been reported in procedures lasting as short as 35 minutes.⁷

Patients at greatest risk for sciatic nerve injury are long-legged, obese, or short in stature. In long-legged or obese patients, there is a tendency for the hip to rotate externally; in short patients, there is a tendency to have less knee flexion. Stirrups that support the entire leg are the most appropriate for all but the shortest cases.

Symptoms of sciatic nerve injury depend on the level of injury, as the nerve divides into two separate divisions. Injury to the nerve trunk results in weakness in the hamstrings, presenting as impaired knee flexion. In cases of peroneal nerve injury, dorsiflexion weakness, or footdrop, occurs.

Treatment for Neuropathies

In the case of an apparent neuropathy, the first step is to obtain consultation from a neurologist or physiatrist to assist in both diagnosis and treatment. Treatment typically consists of supportive care with appropriate functional braces and physical rehabilitation.

In patients with pain, oral analgesics, tricyclic antidepressants, and anticonvulsant medications may be helpful. Unfortunately, neuropathic pain is usually refractory to opioids. An effective alternative is tramadol, a synthetic centrally acting analgesic used in doses of 50 to 100 mg every 6 hours. Amitriptyline and desipramine may be useful in doses starting at 25 mg daily, gradually increasing to 150 mg daily in divided doses if needed. Gabapentin, an anticonvulsant drug that causes less somnolence than most tricyclic antidepressants, can be given in a starting dosage of 100 mg three times daily, with a maximum dosage as high as 1200 mg three times daily.

Effect of Carbon Dioxide Insufflation and Venous Gas Embolism

Effect of Carbon Dioxide Absorption

Carbon dioxide (CO₂) gas is the gas of choice for obtaining a pneumoperitoneum for laparoscopy. CO₂ gas is highly soluble in blood and large amounts will dissolve in blood. It is rapidly eliminated from the vascular space. CO₂ gas is readily absorbed through the peritoneum. The partial pressure of arterial CO₂ (PaCO₂) increases during the first 15 to 30 minutes of a laparoscopic procedure with intra-abdominal pressures of less than 15 mm Hg. Typically the anesthesiologist adjusts minute ventilation to compensate for this increase. During laparoscopy in a pregnant patient, this adjustment should take into consideration the lower PaCO₂ typically found (compensated respiratory alkalosis) to avoid fetal acidosis. After the initial rise and plateau of end-tidal CO₂ (ETCO₂), any subsequent rise cannot be attributed solely to the CO₂ insufflation. PaO₂ usually does not change during laparoscopy unless there is a problem.

Capnography (ETCO₂) and pulse oximetry are reliable markers of arterial gases in healthy patients. This may not apply to American Society of Anesthesiologists (ASA) class II and III. Increases in ETCO₂ are usually due to absorption of CO₂ from the peritoneal cavity. However, this may also be due to a variety of clinical circumstances that cause a ventilation/perfusion mismatch (V/Q) that increases the physiologic dead space. A steep Trendelenburg position and increased intra-abdominal pressures can accentuate this mismatch, especially in obese patients. A pneumoperitoneum will decrease pulmonary compliance. Obesity will decrease compliance further ⁸ and increase the airway pressure required to ventilate the patient. Decreased cardiac output will also increase the V/Q mismatch and lead to increase in ETCO_2.

Other clinical events that can increase ETCO₂ are large amounts of CO₂ in the subcutaneous spaces (emphysema), CO₂ pneumothorax, and CO₂ gas embolism. CO₂ pneumothorax is usually the result of CO₂ gas leaking into the pleural space through diaphragmatic defects. Subcutaneous emphysema does not cause desaturation or increases in airway pressure. Swelling and crepitus are usually seen on the abdomen, sometimes tracking down into the labia. A massive CO₂ embolism may initially cause an increase in ETCO_2. However, a drop in ETCO₂ is typically seen in a gas embolism following this initial increase.

Gas Embolism

A gas embolism is a potentially dangerous complication of laparoscopy and hysteroscopy. Direct intravascular injection of CO₂ gas by the pneumoperitoneum needle or trocar can cause a gas embolism. Gas embolization can also occur whenever a significant tear occurs in a large vein during laparoscopy, because the intra-abdominal pressure is higher than the venous pressure. CO₂ gas embolism is occasionally seen during diagnostic hysteroscopy, although the mechanism is unclear. CO₂ should not be used during operative hysteroscopy.

The physical characteristics of CO₂, high solubility and rapid clearance, allow the rapid reversal of clinical symptoms from the embolization. Although there may be an initial increase in ETCO₂, a decrease in ETCO₂ is the most characteristic manifestation of all gas emboli, including CO_2.

Venous air embolism has been reported in many gynecologic procedures, such as hysterectomy, cesarean section, hysteroscopy, and uterine curettage, as well as in normal spontaneous vaginal delivery. The entry of room air into a venous channel usually requires some pressure gradient. As the height above the heart increases at the gas entry point (an open vein), there is a decrease in local pressure. This pressure gradient facilitates gas entry. In theory, air can be introduced into a vein at the hysteroscopic surgical site that is above the level of the heart. It is therefore prudent to not place the patient in Trendelenburg position during an operative hysteroscopy. Insufflation of CO₂ during a hysteroscopy should not commence without purging the tube of room air. Gas should not be used as the cooling system with a laser used for intrauterine surgery.

The basic pathophysiology of a venous gas embolism is V/Q mismatch that results in increase in physiologic dead space and right-to-left shunting. One of the earliest manifestations of a gas embolism is a decrease in ETCO_2. This decrease is thought to be the result of a V/Q mismatch with increases in physiologic dead space. A pneumothorax can also cause a decrease in ETCO_2. Both gas embolism and pneumothorax will cause hypoxemia.

The typical clinical findings of a gas embolism that occurs under anesthesia are abnormal heart murmurs. Typically, it is a systolic murmur and the classic water millwheel murmur only occurs if there is a large amount of air in the right ventricle. Other manifestations include tachycardia, arrhythmias, hypotension, and increases in central venous pressure and pulmonary artery pressure. If the patient is conscious, she may complain of chest pain and breathlessness and may demonstrate altered level of consciousness. Physical examination will show the same classic signs in addition to tachypnea. The anesthesiologist will notice an abrupt fall in ETCO₂. The initial blood gases of a gas embolism are similar to those seen with a venous embolus (a clot) that shows hypoxemia from the V/Q mismatch. A respiratory alkalosis from the tachypnea is also seen if the patient is awake. Treatment consists of the following measures:

• Stop the insufflation.

• Remove the Veress needle.

• Place in steep Trendelenburg position or left lateral decubitus position to reduce right ventricular outflow obstruction.

• Correct hypoxemia with 100% oxygen.

• Remove air from the right atrium using central venous catheter and cardiac massage.

• Carefully search for evidence of venous injury, using laparotomy if necessary.

• If no venous injury is seen, observe the patient overnight.

Successful resuscitations after massive venous CO₂ embolization have been reported.^9,¹⁰

Vascular Injuries during Laparoscopy

The utilization of extremely small abdominal incisions is the primary advantage of laparoscopy. These incisions are also the source of the most serious complications associated with laparoscopy. Techniques used to place primary and secondary laparoscopic ports into the peritoneal cavity are often accompanied by a small but unavoidable risk of injury to blood vessels located in the anterior abdominal wall and the major blood vessels located in the retroperitoneal space. Theses small incisions, which minimize postoperative discomfort, also limit and delay access to treat any vascular injuries. In addition, the use of CO₂ to distend the peritoneal cavity puts patients at the potentially deadly risk of intravascular insufflation. Because of the serious nature of these injuries, every laparoscopic surgeon should develop a plan to deal with these complications before their occurrence. The following is a discussion of methods to avoid injuries and approaches to recognizing and treating injuries should they occur.

The best angle of insertion appears to change according to the patient’s body mass index (BMI=kg/m²) (see Chapter 44). In patients who are either in the ideal weight or overweight groups (corresponding BMI = 25kg/m² and 25 to 30kg/m², respectively), the Veress needle and primary trocar should be inserted through the umbilicus at 45 degrees from horizontal.¹³ A greater angle of insertion in these patients increases the risk of retroperitoneal vessel injury because the bifurcation is beneath the umbilicus in many cases, and the left common iliac vein is beneath the umbilicus in most patients.¹² This is particularly important in the thinnest patients, in whom the distance from the umbilicus to the retroperitoneal vessels may be as little as 2 to 3 cm.¹³

In obese women whose BMI = 30kg/m² (e.g., weight of 200 pounds in a woman who is 67 inches tall), the angle must be increased to as much as 70 to 80 degrees from horizontal to reach the peritoneal cavity, because the thickness of the anterior abdominal wall increases dramatically with weight. Fortunately, the distance between umbilicus and vessels is increased in these patients, and the umbilicus tends to be more caudal in relation to the aortic bifurcation.

When estimating the proper angle of insertion for either the Veress needle or primary trocar, it is important to know the position of the patient in relation to the floor, because it is natural for the gynecologist to use the floor as a point of reference for horizontal. When a patient is placed in the Trendelenburg position with the head lower than the feet, the angle of insertion relative to the floor must be decreased accordingly to avoid the retroperitoneal vessels. Therefore the patient should not be placed in Trendelenburg position before placement of the primary trocar. Open laparoscopy is an alternative method for obtaining peritoneal access that decreases the risk of retroperitoneal vessel injury to almost zero.

Recognition

Immediate recognition of a major vascular injury is necessary to prevent exsanguination. Prompt action must be taken when blood is noted to flow from the open Veress needle or if the patient’s vital signs suggest hemorrhagic shock shortly after the Veress needle or trocar is inserted. In some cases, the first sign of a problem will be a laparoscopic view completely obscured by bright red blood. In other patients, a major vessel injury will manifest as an enlarging retroperitoneal hematoma, which should be approached in an identical manner as a massive intraperitoneal bleeding.

Treatment

Major vessel injuries are a rare but unavoidable laparoscopic complication associated with the closed technique for Veress needle and primary trocar placement. Every laparoscopic surgeon that uses a closed technique should develop a plan of action for major vessel injury. The surgeon should also become familiar with the availability of laparotomy instruments, blood products, vascular clamps, and surgical consultants. This is especially important when these procedures are performed in a freestanding outpatient surgical facility.

When a major vascular injury is suspected, the following steps should be taken without delay:

• Alert nursing personnel to prepare for emergency laparotomy.

• Simultaneously alert anesthesia personnel, who will generally place additional intravenous lines, and call for blood products and additional assistance.

• Immediately perform a laparotomy via a midline incision.

• Control the bleeding using direct pressure over the site of injury.

• Ideally, a trauma surgeon or vascular surgeon can be called in to clearly identify and repair the injury or injuries.

• In the absence of a surgeon experienced in vascular surgery, the laparoscopic surgeon must be prepared to open the retroperitoneal area and stop the bleeding.

• If appropriate personnel and facilities to repair the vascular injury are not available, the patient must be transported to a fully equipped trauma center.

If either the surgeon or facility are not fully prepared to effectively treat a major vascular injury, thought should be given to using only an open laparoscopic technique or performing laparoscopy with a closed technique elsewhere.

Abdominal Wall Vessel Injury

The risk of abdominal wall vessel injury during laparoscopy was extremely uncommon before the widespread use of ports lateral to the midline to perform complex operative procedures. The vessels of the anterior abdominal wall at risk for injury can be divided into two groups: superficial and deep. The superficial vessels consist of the superficial epigastric and circumflex iliac arteries, which are located in the subcutaneous tissue. The deep vessels consist of the inferior epigastric artery and vein, which are located beneath the rectus abdominis muscles immediately above the peritoneum.

Damage to the deep vessels usually leads to immediate and rapid blood loss, whereas damage to the superficial vessels most often results in a persistent external trickle after the port is removed. Postoperatively, a superficial vessel injury (Fig. 45-2) typically presents with pain at the trocar site and a palpable mass. Postoperative deep vessel injury presents with increasing pain and decreasing hematocrit without a palpable mass because the vessels are located behind the rectus abdominis muscle or the bleeding occurs into the peritoneal cavity. A computed tomography scan will demonstrate the correct location of the hematoma.