Chapter 199 Medical Complications
Thromboembolic Disease
Incidence
Thromboembolic disease is one of the most significant potential complications after spine surgery, with rates of acute deep venous thrombosis (DVT) ranging from 0.3% to 31%, with an overall DVT incidence of 2.2%.1 These rates vary substantially depending on a number of factors. Overall, as expected, the lowest rates occur in younger patients undergoing simple elective procedures, whereas the highest reported rates are those in patients with preexisting risk factors that predispose them to DVT.
Risk Factors
Virchow’s triad of venous stasis, endothelial injury, and hypercoagulability is the classic description of the combination of factors that may predispose a person to DVT. In addition, general clinical risk factors include advanced age, trauma, previous DVT, stroke, malignancy, smoking, and exogenous estrogen replacement. While numerous systems have been developed to attempt stratification of DVT risk in surgical patients, many are cumbersome and therefore not of practical utility for most surgeons. However, one of the simpler systems involves assignment of a patient into one of four categories on the basis of complexity of procedure (major vs. minor), age, and additional risk factors such as prior DVT, hypercoagulability, and malignancy.2 In general, spine surgery patients are at a higher risk than general surgery patients secondary to the postoperative immobility that may occur due to pain or neurologic deficits.3,4 Conversely, the risk is significantly lower than that for patients undergoing lower-extremity surgery such as total hip or knee replacement, which can be associated with DVT rates as high as 50%.2 While the overall risk of DVT in spine surgery patients can be described as moderate, the degree of immobility, and thus the risk of DVT, can be directly correlated with the type of spine procedure being performed. For example, patients undergoing a single-level anterior cervical discectomy and fusion are often treated in outpatient surgical centers and discharged home the same day, thereby minimizing the amount of postoperative bedrest and risk of DVT. Patients undergoing more extensive and complex surgery, particularly those with traumatic spinal cord injury (SCI), are at the highest risk. With regard to acute SCI, the incidence of DVT has been reported as ranging from 10% to 100% without prophylaxis and from 0% to 7% with prophylaxis. Interestingly, no correlation has been observed between level of injury, American Spinal Injury Association (ASIA) grade, or spasticity and the incidence of DVT.1
Unfortunately, there is a limited amount of evidence regarding the specific risks of DVT in spine surgery patients. One study that used routine venography in patients undergoing spine surgery who did not receive any prophylaxis reported an incidence of 15.5%.4 It is important to note that none of these patients had any clinical evidence of DVT, underscoring the low sensitivity of physical signs in the diagnosis of DVT. Furthermore, the same authors found that lumbar surgery carries a much higher risk of DVT (21%) as compared to cervical surgery (6%).4 As was previously noted, the risk of DVT may also increase with the complexity of the procedure because more complex operations have longer operative times and often increased postoperative immobility. The use of ventral and lateral approaches further elevates the risk by requiring manipulation of vessels, particularly major veins, and thus increasing the chance for endothelial disruption. Dearborn et al. reported an incidence of 6% in patients undergoing combined ventral/dorsal approaches compared to 0.5% in patients in whom only a dorsal approach was employed.5
Prevention
Recommendations for DVT prophylaxis for patients undergoing spine procedures are varied and inconsistent. This inconsistency stems largely from the lack of rigorous supporting evidence for many of the prophylactic measures that are employed. Available prophylactic modalities include the use of gradient compression stockings (GCSs) or intermittent pneumatic compression devices (ICDs), administration of low-dose unfractionated heparin (LDUH) or low-molecular-weight heparin (LMWH), and the placement of a caval filter. The first step in determining appropriate DVT prophylaxis for an individual patient is assessing the risk of DVT using the criteria described previously. This risk depends heavily on the procedure being performed and the patient’s age and comorbid conditions. In 2004, the American College of Chest Physicians published guidelines for prevention of venous thromboembolism.2 These recommendations are summarized in Box 199-1.
BOX 199-1 Recommendations for Deep Venous Thrombosis Prophylaxis in Patients Undergoing Spine Surgery
• For spine surgery patients with no additional risk factors, the routine use of any thromboprophylaxis modality, apart from early and persistent mobilization, is not recommended.
• Some form of prophylaxis may be used in patients undergoing spinal surgery who exhibit additional risk factors, such as advanced age, known malignancy, presence of a neurologic deficit, previous venous thromboembolism (VTE), or a ventral surgical approach.
• For patients with additional risk factors, any of the following prophylaxis options is recommended: postoperative low-dose unfractionated heparin (LDUH) alone, postoperative low-molecular-weight heparin (LMWH) alone, or perioperative intermittent pneumatic compression devices (ICDs) alone.
• In patients with multiple risk factors for VTE, combining LDUH or LMWH with gradient compression stockings (GCSs) and/or ICDs is recommended.
• Thromboprophylaxis should be provided for all patients with acute spinal cord injury (SCI).
• The use of LDUH, GCSs, or ICDs as single prophylaxis modalities in patients with acute SCI is not recommended.
• In patients with acute SCI, we recommend prophylaxis with LMWH, to be commenced once primary hemostasis is evident. The combined use of ICDs and either LDUH or LWMH as alternatives to LMWH is recommended.
• The use of ICDs and/or GCSs when anticoagulant prophylaxis is contraindicated early after injury is recommended.
• The use of an inferior vena cava filter as primary prophylaxis against pulmonary embolism is not recommended.
• During the rehabilitation phase following acute SCI, the continuation of LMWH prophylaxis or conversion to an oral anticoagulant agent (international normalized ratio [INR] target, 2.5; INR range, 2–3) is recommended.
Based on 2004 American College of Chest Physicians Guidelines.
While the risk of DVT may be further decreased with the use of pharmacologic anticoagulation, the controversy surrounding its use is significant. Several small studies have demonstrated the effectiveness of LDUH and LMWH in spine surgery patients. In a double-blind randomized controlled trial, Agnelli and Becattini demonstrated a reduction in DVT incidence from 30% in patients treated with ICD alone to 17% in patients treated with ICD plus LMWH.6 The paucity of sufficient evidence to definitively support the use of medical anticoagulation combined with concerns for increased intraoperative blood loss and postoperative epidural hematoma formation has led to a lack of standardized guidelines for DVT prophylaxis in spine surgery patients.1
Screening and Diagnosis
Clinical diagnosis of DVT remains a concern as less than 50% of patients will exhibit clinical signs.1,7 This raises the question of whether routine screening should be employed as a method of early detection. While there are some authors who advocate routine screening, there does seem to be at least a majority consensus that routine screening for DVT with ultrasound or venography is not clinically indicated after spine surgery. Similarly, a comprehensive review by Furlan and Fehlings concluded that there is insufficient evidence to support routine screening for DVT in patients with acute SCI.7
If routine screening is not indicated, the question arises as to the most sensitive and cost-effective method for diagnosis of DVT in patients in whom DVT is suspected. Lower-extremity pain and tenderness, leg edema, and low-grade fevers can be nonspecific indicators of DVT. While DVT is confirmed in only 10% to 25% of patients in whom it is suspected clinically, clinical suspicion remains an important first step in the initiation of more accurate diagnostic testing.8
Beyond clinical suspicion, objective confirmatory tests remain mandatory for accurate diagnosis of DVT. Contrast venography continues to be the gold standard for diagnosis of DVT against which other tests are measured. No other modality is as sensitive and specific for both proximal and distal DVT. However, high cost, limited availability, patient discomfort, and contrast reactions have led to the increased use of less invasive diagnostic modalities. By using a pressurized cuff, impedance plethysmography measures the change in electrical impedance of the lower extremity in response to occlusion of the deep venous system. The sensitivity and specificity are high for proximal DVT and lower for distal DVT on single examinations. The accuracy can therefore be increased with serial examinations. By comparison, B-mode ultrasonography is as sensitive as plethysmography for proximal DVT and more sensitive for distal DVT. The addition of Doppler flow analysis in conjunction with ultrasonography has demonstrated sensitivity and specificity of 95% to 100% and has therefore become the diagnostic modality of choice in most clinical settings.9–11
Treatment
Management of acute DVT is directed toward reducing both the short-term (pulmonary embolism [PE], clot propagation) and long-term (postphlebitic syndrome) complications. General management includes bedrest, elevation of edematous extremities, and administration of appropriate analgesics (non–platelet-active agents). Definitive management of acute proximal DVT requires a decision regarding risk of anticoagulation to the patient. If the risk for systemic anticoagulation is acceptable, treatment of established DVT may be initiated in several ways. Because the risks of using oral anticoagulation agents alone have been well documented, a safe and effective treatment strategy must include an initial course of continuous intravenous unfractionated heparin (IVUH), subcutaneous LMWH, or subcutaneous fondaparinux. The need for an initial course of heparin has been demonstrated in a double-blind, randomized trial with a threefold reduction in recurrent venous thromboembolic events compared with oral anticoagulants alone.12 This is thought to be the result of the long half-life of factor II (compared to proteins C and S), which results in an initial hypercoagulable state at the onset of oral anticoagulant therapy. Recommendations for treatment of acute DVT, summarized in Box 199-2, are based on the ACCP guidelines for patients with DVT.13
BOX 199-2 Recommendations for Treatment of Deep Venous Thrombosis
Anticoagulation
• Treatment should begin simultaneously (day 1) with both oral anticoagulants and intravenous unfractionated heparin (IVUH), low-molecular-weight heparin (LMWH), or fondaparinux.
• IVUH, LMWH, or fondaparinux should continue until the international normalized ratio (INR) is ≥2 for 24 hours.
• IVUH, LMWH, or fondaparinux should continue for a minimum of 5 days.
• For both inpatients and outpatients, LMWH is preferred over IVUH.
• For patients treated with LMWH, routine monitoring of antifactor Xa levels is not recommended.
• Target INR of 2–3 should be maintained throughout the duration of treatment.
Inferior Vena Cava Filter
• The routine use of an inferior vena cava filter (IVCF) in addition to anticoagulation is not recommended.
• If anticoagulation is contraindicated due to risk of bleeding, an IVCF should be placed for the prevention of pulmonary embolism. In these patients, anticoagulation therapy should be initiated once the risk of bleeding resolves.
Duration of Treatment
• For patients with first-time deep venous thrombosis (DVT) and known transient risk factors, anticoagulation should be continued for 3 months.
• For recurrent DVT or in patients for whom risk factors cannot be identified or have not resolved, long-term anticoagulation is recommended, with reassessment at periodic intervals.
• Graduated compression stocking should be initiated as soon as possible after initiation of anticoagulation and should be continued for at least 2 years.
Based on 2004 American College of Chest Physicians Guidelines.
The aforementioned regimen remains our preferred means of managing thromboembolism. It does, however, carry risks of morbidity. The medical and surgical literature contains numerous reports of complications related to heparin therapy. These complications include thrombocytopenia and thrombotic disorders, skin necrosis, priapism, spontaneous hemorrhage, gastrointestinal bleeding, and epidural hematoma formation.14,15 Decortication of portions of the vertebral column and the creation of large potential dead space during exposure predisposes the spine surgery patient to an even higher risk of hemorrhagic complications and hematoma formation.16 Furthermore, following decompressive surgery, hematomas are often in direct continuity with the thecal sac, placing neural structures at risk of injury, thus necessitating further surgical intervention and its additional risks.
Pulmonary Embolism
The diagnosis and treatment of DVT and PE are often discussed separately, but there is increasing evidence that these two entities should be considered the same disease process. The incidence of PE in spine surgery has been reported as ranging from 0% to 13%, with a mean incidence of 2.5%.17 As with DVT, the risk of development of PE is lowest in patients undergoing simple elective surgery (i.e., microdiscectomy) and highest with ventral or combined thoracolumbar/lumbar procedures.17
Initial Evaluation
Common clinical manifestations of PE include tachypnea, dyspnea, and pleuritic chest pain. The initial evaluation for clinical suspicion of PE includes chest radiograph, arterial blood gas measurements, and electrocardiogram. The arterial blood gas measurement is useful to demonstrate alterations of oxygen transfer that accompany the ventilation of lungs that have a reduction of pulmonary vascular inflow (ventilation/perfusion mismatch). Arterial blood gases typically reveal respiratory alkalosis, variable reduction in partial arterial oxygen pressure, and widening of the alveolar-arterial oxygen pressure gradient. Chest radiographs and electrocardiograms are more important and are used to rule out other diagnoses, such as pneumonia, pneumothorax, myocardial infarction, or pulmonary edema. Occasionally, the electrocardiogram may reveal right axis deviation or a right bundle branch block that may aid in the diagnosis of PE. Most commonly, chest radiographs reveal nonspecific findings such as pleural effusion, infiltrate, atelectasis, or elevation of the hemidiaphragm or are negative. Measurement of brain natriuretic peptide (BNP) is sensitive but not specific for diagnosis of PE.18 Similarly, measurements of serum d-dimer (by enzyme-linked immunosorbent assay) have a high sensitivity but low specificity, particularly in postoperative patients, as the d-dimer may be elevated from the procedure.19 However, the utility of d-dimer assays remain in that the negative predictive value of levels below threshold (<500 ng/mL) are sufficient to exclude PE in patients with low or moderate pretest probability.
Diagnostic Modalities
If suspicion remains high for PE after initial evaluation, further diagnostic workup is recommended. The choice of diagnostic tests depends on multiple factors, including clinical probability of PE, availability of modality, patient condition, and cost. While pulmonary angiography remains the gold standard for diagnosis of PE, its invasive nature and the development of modern imaging techniques have dramatically decreased its utility. The widespread availability of spiral CT scanners has allowed for the increasing use of a CT pulmonary angiogram in the diagnosis of PE. The diagnostic sensitivity and specificity of a CT pulmonary angiogram are 83% and 96%, respectively.20 In patients who are intolerant to IV contrast or those with prohibitively poor renal function, a ventilation/perfusion scan remains an option for the diagnosis of PE. The diagnostic accuracy of the ventilation/perfusion scan appears to be similar to that of the CT pulmonary angiogram both in overall sensitivity and in the observation that results must be correlated with clinical suspicion. Specifically, a negative scan in a patient with low pretest probability virtually excludes the diagnosis of PE.
Treatment
The treatment of patients with “nonmassive” PE is exactly the same as that previously described for DVT. However, IVUH is recommended over LMWH for the treatment of massive PE and in patients with significant renal impairment.21 Massive PE with significant hemodynamic compromise requires urgent intervention with acute thrombolysis, surgical embolectomy, or, more recently, percutaneous transvenous fragmentation or removal of emboli.
Disseminated Intravascular Coagulation
Spine surgery and, in particular, deformity surgery have been associated with an increased incidence of disseminated intravascular coagulation. Several mechanisms may contribute to this, including injury to soft tissue, muscle, and bone, which releases tissue thromboplastin and may lead to disseminated intravascular coagulation.22 Disseminated intravascular coagulation is a consumptive coagulopathy in which microvascular thrombosis results in end-organ damage and depletion of clotting factors and platelets. The result is a mixed picture of organ ischemia and hemorrhage. Laboratory findings included depletion of platelets, prolongations in both prothrombin time and partial thromboplastin time, and increased d-dimer. However, many of these may be nonspecific, as they can arise from surgical blood loss with inadequate repletion. Treatment involves replacement of platelets and clotting factors with both fresh-frozen plasma and cryoprecipitate. Transfusion of platelets should be based on bleeding or a high risk of bleeding. Included in this group are postoperative patients with a platelet count of less than 50,000 µL. In patients with a predominantly thrombotic picture, anticoagulation with IVUH should be considered. As with DVT and PE, the benefits of anticoagulation must be carefully weighed against the risks of significant bleeding.23
Other Pulmonary Complications
Pneumonias, respiratory failure, and prolonged intubation are all common in patients undergoing major spine procedures, especially those with SCI. Immobility, particularly when combined with neurologic injury, can lead to atelectasis, stasis of respiratory secretions, and pneumonia. Bacterial pneumonia may be either an early-onset (within 4 days) or a late-onset complication. Organisms associated with early-onset pneumonia are similar to those found in community-acquired pneumonia, mainly Streptococcus pneumoniae, Haemophilus influenzae, and methicillin-sensitive Staphylococcus aureus. Late-onset pneumonia is often more severe and associated with more virulent and resistant organisms, including Pseudomonas and Acinetobacter.24
Severe and diffuse lung injury has also been documented following spine surgery, including acute respiratory distress syndrome (ARDS) and transfusion-related acute lung injury. Risk factors for ARDS in patients undergoing spine surgery include aspiration, pulmonary contusion, hypotension, multiple transfusions, infection, and sepsis.25 Clinically, ARDS presents with hypoxemia that is resistant to increasing oxygen therapy. The diagnosis of ARDS is established by the following criteria: chest radiograph demonstrating multiple diffuse infiltrates, pulmonary capillary wedge pressure greater than 18 mmHg, and Pao2 to Fio2 ratio of 200 or less. ARDS is treated with mechanical ventilation that trades increased positive end expiratory pressure to decrease Fio2 requirements and uses low tidal volumes and plateau pressures of 30 mm H2O or less. Additional measures include frequent changes in body/bed position, bronchodilators, and sufficient sedation to prevent asynchronous ventilation.26 Even with aggressive treatment, the mortality associated with ARDS is greater than 30%.27
In patients with a complete SCI above C4, phrenic nerve function is lost; therefore, diaphragmatic function is typically absent. These patients require mechanical ventilation. With injury at C4 and C5, the patient has compromise of diaphragm function and may require short-term ventilatory support (long-term support if there is preexisting pulmonary disease). At lower cervical and thoracic levels, the loss of innervation to the accessory muscles of respiration and to the intercostal muscles can impair respiratory function. Because of the recumbent position in postoperative patients and patients with unstable spines, the respiratory capacity is decreased.
Cardiac and Vascular Complications
Cardiac complications, including myocardial infarction, are the most common cause of perioperative death in spine surgery patients. The overall incidence of myocardial infarction in patients without known coronary artery disease who are undergoing lumbar fusion procedures is 0.8%.28 It is important to consider that these complications can occur in patients with no history of coronary artery disease and that the incidence of silent myocardial ischemia is estimated to be as high as 15%. The specific risks for development of perioperative myocardial infarction include age over 60 years, male gender, abdominal obesity, smoking, hypertension, diabetes mellitus, reduced high-density lipoprotein, and calcified atherosclerosis in the aorta or common iliac vessels. Asymptomatic myocardial ischemia can be identified with dobutamine echocardiography, thallium perfusion scintigraphy, or continuous 24-hour electrocardiographic monitoring.29 In patients with multiple risk factors, we recommend preoperative screening with one of these modalities. Interestingly, one study of lumbar fusions found no correlation between cardiac complications and factors related to surgery, including approach, type of surgery, operating time, and blood loss.30
Gastrointestinal Complications
Stress Ulcerations
The stress resulting from a complicated surgery, traumatic injury, and mechanical ventilation as well as preoperative use of steroidal and nonsteroidal anti-inflammatory drugs can predispose a patient to ulcer formation. Stress ulcerations appear to be related to ischemia of gastric capillary beds, resulting in diminished resistance of the gastric lining to the digestive secretions of the stomach. The incidences of gastritis and ulcer formation in spine surgery patients are 0.33% and 0.08%, respectively.31 There has been a gradual reduction in the incidence of severe bleeding from stress ulcerations. This is thought to result from a combination of routine prophylaxis (antacids, H2 blockers, proton pump inhibitors, or sucralfate) and improved attention to tissue oxygenation.32 We advocate standard administration of either an H2 blocker or a proton pump inhibitor for all patients undergoing spine surgery.
Adynamic Ileus
Adynamic ileus is a well-known complication of spine surgery, with an incidence of 5% to 12%.33 Ileus is characterized by abdominal distention and absent bowel sounds. Nausea and vomiting, respiratory distress, a feeling of constipation, or abdominal tenderness may be present. Copious gas is diffusely distributed through the intestine and colon, often with fluid levels. The diaphragm may be elevated and have diminished motion. If the clinical picture and plain radiography provide an inconclusive diagnosis, contrast medium can be given orally. In adynamic ileus, some contrast medium should reach the cecum in 4 hours; a stationary column for 3 to 4 hours indicates complete obstruction. Ileus usually persists for 36 to 48 hours, and treatment includes restriction of oral intake and administration of bowel stimulants, enemas, or laxatives. In some cases, nasogastric suction and replacement of electrolytes may be required.
Ogilvie Syndrome
Ogilvie syndrome, or pseudo-obstruction of the colon, is characterized by massive abdominal distention with a cecal diameter greater than 9 cm. Nausea and vomiting, constipation, diarrhea, and pain are all more common in Ogilvie syndrome than in adynamic ileus. The diagnosis is made by the clinical findings, including high-pitched bowel sounds, and radiographic findings of marked distention of the proximal colon with distal cutoff of colonic gas. The radiographic findings may be difficult to distinguish from those of cecal volvulus.
Colonic pseudo-obstruction is a major contributor to morbidity and lengthened hospital stays, occurring in as many as 12% of all spine surgery patients.34 Delayed diagnosis can result in serious complications, including spontaneous perforation in up to 3%, with an attendant mortality rate of 50%.35 Patients at increased risk are those who have had previous abdominal surgeries, more extensive dissections, retroperitoneal hematomas, major intraoperative fluid shifts, and excessive narcotic use.33 Initial treatment for Ogilvie syndrome includes nasogastric suction, insertion of rectal tubes, cessation of oral intake, and cessation of narcotics. Patients who fail to respond to these measures may undergo pharmacologic interventions, if they are not contraindicated, before the clinician considers colonoscopic decompression. Numerous studies have reported the use of the acetylcholinesterase inhibitor neostigmine for treatment of refractory postoperative spine surgery ileus.36,37 The obstruction is thought to result from an imbalance in the autonomic motor system via excess parasympathetic suppression. Thus, neostigmine acts to increase parasympathetic stimulation, thereby normalizing autonomic stability. Cure rates have been reported to range from 86% to 94% following a single 2-mg IV bolus infusion in appropriately selected patients.37–40 Side effects following infusion have been reported to occur in fewer than 5% of patients; however, it is essential to note the contraindications to using parasympathetic agents, which includes patients with bradyarrhythmias and bronchospasm. Patients must be monitored by experienced personnel and with telemetry during neostigmine infusion, and atropine must be readily available at the bedside. At our institution, patients are transferred to the intensive-care unit for monitoring if neostigmine is administered.
If pharmacologic means fail or are contraindicated, endoscopic decompression may be performed, though undoubtedly under suboptimal conditions in an unprepared and distended colon, further complicating and increasing the morbidity and mortality of the procedure.41 Endoscopic decompression is reported to be successful in approximately 70% of cases, although approximately one third of patients require multiple endoscopic procedures for complete resolution.42 Failure of colonoscopic decompression requires surgical laparotomy and tube cecostomy with a concomitant mortality rate reported as high as 26%.43
Superior Mesenteric Artery Syndrome
Superior mesenteric artery syndrome has been described in patients undergoing correction of kyphotic deformity, with an incidence of 0.5% to 1%.44,45 While more common in adolescents, superior mesenteric artery syndrome has also been described in adults.46 Crowther et al. proposed two possible mechanisms: disruption of autonomic supply to the bowel from retroperitoneal dissection and compression of the duodenum between the aorta and the superior mesenteric artery after gain of height (resulting in reduction of the angle between the aorta and the superior mesenteric artery).47 The onset of superior mesenteric artery syndrome is usually more than 1 week after surgery, and it presents with epigastric distention and tenderness accompanied by present bowel sounds and tympanic percussion. The administration of oral contrast will demonstrate a blockage at the level of the third part of the duodenum. Conservative management is similar to that for ileus, including restriction of oral intact, nasogastric suction, and intravenous alimentation. Failure of these measures warrants a general surgery consultation and may require surgical mobilization or division of the ligament of Treitz.
Pancreatitis
Acute pancreatitis has been reported in patients who have undergone spine surgery. Leichtner et al. reported elevated pancreatic enzymes in 14% of adolescents who had undergone surgery for correction of scoliosis.48 Up to 70% of these may have associated signs or symptoms. Risk factors include both significant blood loss and intraoperative hypotension. Clinical presentation includes abdominal and back pain, nausea, vomiting and fever, accompanied by tachycardia and leukocytosis. Because these symptoms are relatively nonspecific, a high index of suspicion is necessary for diagnosis. Specific laboratory abnormalities include elevation of amylase and lipase. As isolated elevation of amylase is somewhat common, a diagnosis of clinical pancreatitis requires that the signs and symptoms should be present as well as elevations in both amylase and lipase. While the mechanism of pancreatitis associated with spine surgery remains unknown, treatment is mostly conservative. If pancreatitis is suspected, a consultation from general surgery is recommended along with observation in the intensive care unit.22 Initial management includes nothing by mouth (NPO) status, aggressive IV fluid resuscitation, and, if necessary, total or partial parenteral nutrition. It is important to differentiate patients with pancreatitis from the more common postoperative ileus; in general, the diagnosis of pancreatitis should be considered in patients with prolonged or severe abdominal pain. If pancreatitis is undiagnosed, the resulting morbidity can be significant. Bragg et al. reported a 50% incidence of subsequent complications, including pancreatic pseudocyst, abscess, or fistula. Furthermore, the same authors reported mortality from pancreatitis in 2 of 15 patients.49
Genitourinary Complications
Urinary complications related to retention, infections, and acute renal failure continue to be significant sources of morbidity after spine surgery. The most common genitourinary complication in spine surgery patients is postoperative urinary retention, with an incidence of 38%.50 Risk factors include advanced age and preoperative use of beta-blockers, while preoperative administration of NSAIDs and narcotic analgesics may reduce the risk. SCI patients are at a particularly high risk, as SCI usually results in a period of spinal shock resulting in the absence of detrusor motor function and bladder sensation, as well as compromise of sphincteric activity. Incomplete emptying of the bladder is common, and elevated bladder pressures may result. This can lead to renal damage from hydroureteronephrosis or vesicoureteral reflux if an appropriate bladder routine is not followed. Initially, placement of a Foley catheter is recommended. If voluntary control of urination is not established at the time the Foley catheter is removed, intermittent clean catheterization is instituted every 4 hours, with the goal of keeping the bladder volume to less than 500 mL.
The overall incidence of urinary tract infection (UTI) in spine surgery patients is 9%.51 In addition to their importance in increasing cost and length of hospital stay, UTIs are the most common source of sepsis in the postoperative patient. The majority of these UTIs are due to Escherichia coli and other gram-negative rods such as Proteus, Enterobacter, and Klebsiella. Fungal UTIs with Candida species are also common. Although routine surveillance cultures are not recommended, fever or other signs, including dysuria and urgency, should prompt a diagnostic workup.52 Urine must be sampled by using aseptic technique and should be sent for laboratory analysis. According to the Centers for Disease Control and Prevention, diagnostic criteria include positive nitrites, positive leukocyte esterase, pyuria, or positive Gram stain.53 Upon diagnosis, the Foley catheter should be removed or exchanged, and antibiotic therapy should be initiated. Initial therapy should provide broad-spectrum coverage with an antibiotic such as a fluoroquinolone or third-generation cephalosporin. Antibiotic coverage may be narrowed according to culture and sensitivity results. Prevention of UTIs is extremely important, including hand washing prior to insertion and early removal of Foley catheters.
Acute renal failure (ARF) has been reported in up to 1.2% of spine surgery patients and usually results from either prerenal failure or acute tubular necrosis (ATN).54 Hypotension and hypovolemia that result from long operative times and significant blood loss can often lead to prerenal ARF following spine surgery. Risk factors for prerenal ARF include age, diabetes mellitus, and preexisting chronic renal failure. ARF is defined by an increase in creatinine to 1.65 mg/dL in previously normal patients or a doubling of creatinine in patients with a baseline of more than 2 mg/dL. Adequate volume resuscitation and maintenance of normotension can significantly decrease the risks even in predisposed patients. Similarly, prerenal ARF is readily treated with volume resuscitation and restoration of renal perfusion. Delay in treatment can result in acute tubular necrosis.55 Additional causes of acute tubular necrosis in spine surgery patients include exposure to nephrotoxins, rhabdomyolysis, and intravenous contrast administration. The treatment of ARF involves reversal or removal of inciting causes, including restoration of normovolemia and discontinuation of nephrotoxic agents. In severe cases, hemodialysis may be required.
Sexual dysfunction is well recognized as a complication following complex spine surgery, particularly with ventral approaches. The reported incidence varies by author but has been found to account for as many as 20% of spine surgery–related complications.33,56 Retrograde ejaculation in particular has been reported by numerous studies, with an incidence ranging from 9% to 24% following anterior lumbar interbody fusion procedures.33 This is conceivably the result of injury to the superior hypogastric plexus of the sympathetic chain located ventral to the L5-S1 vertebrae.56 The incidence appears to be higher following transperitoneal and laparoscopic as opposed to retroperitoneal approaches.57 With regard to complications related to great vessel manipulation and DVT formation secondary to retraction injuries, periodic release of pressure cannot be overemphasized to help minimize the incidence of neural injury. Interestingly, Hagg et al. reported an increase in sexual performance and pleasure in both men and women who had undergone dorsal spine surgery.57
Miscellaneous Complications
Delirium
Alterations in mental status are known to occur following spine surgery, particularly in older patients undergoing larger procedures. This is compounded by administration of narcotics and muscle relaxants. One study reported an incidence of delirium of 12.5% in spine surgery patients over 70 years old.58 Risk factors associated with postoperative delirium include anemia, hypercarbia, hypoxemia, hypoglycemia, UTI, and sepsis.59 Accordingly, prevention includes maintenance of hematocrit greater than 30%, avoidance of benzodiazepines and anticholinergics, administration of supplemental oxygen, and normalization of glucose and electrolyte balance.60
Perioperative Blindness
Acute visual loss is a rare but significant complication following spine surgery. Proposed mechanisms include central retinal artery occlusion, ischemic optic neuropathy, and occipital stroke. Being in a prone position for a long time may result in central retinal artery occlusion by direct compression.22,61 Risk factors for ischemic optic neuropathy include anemia, dehydration, and hypotension. Prevention is essential; this is achieved by avoiding pressure on the eyes while in the prone position (proper padding around the orbits and placing the table in some reverse Trendelenburg position), maintenance of euvolemia and normotension by anesthetists, and mindfulness concerning the length of the operative procedure.61 Should visual loss occur, an urgent neuro-ophthalmology consultation is indicated.
Decubitus Ulceration
Sacral and other pressure ulcerations may occur with increased frequency in spine surgery patients. These ulcerations result from prolonged immobility, especially in patients with SCI. Avoidance requires constant vigilance, frequent changes in position, early stabilization and mobilization, and specialized mattresses or air beds that decrease pressure on vulnerable sites. Consultation from a wound care specialist may aid in treatment, including cleansing, prevention of infection, maintenance of adequate nutrition, and protection of adjacent skin.62
Conclusions
Medical complications following spine surgery are common and span the entire spectrum of organ systems. More lengthy and complicated procedures place patients at higher risk of suffering these complications and threaten patients’ well-being. High clinical suspicion and knowledge of the literature are the keys to early recognition and treatment. Through increased awareness of the possible range of complications, we must work toward minimizing these problems to effect better outcomes for our patients and to control the increasing medical expenditures associated with spine procedures.
Baron E.M., Albert T.J. Medical complications of surgical treatment of adult spinal deformity and how to avoid them. Spine (Phila Pa 1976). 2006;31:S106-S118.
Harmanci A., Harmanci O., Akova M. Hospital-acquired pneumonia: challenges and options for diagnosis and treatment. J Hosp Infect. 2002;51:160-167.
Lee D.Y., Lee S.H., Jang J.S. Risk factors for perioperative cardiac complications after lumbar fusion surgery. Neurol Med Chir (Tokyo). 2007;47:495-500.
O’Grady N.P., Barie P.S., Bartlett J., et al. Practice parameters for evaluating new fever in critically ill adult patients: Task Force of the American College of Critical Care Medicine of the Society of Critical Care Medicine in Collaboration with the Infectious Disease Society of America. Crit Care Med. 1998;26:392-408.
Stein P.D., Woodard P.K., Weg J.G., et al. Diagnostic pathways in acute pulmonary embolism: recommendations of the PIOPED II investigators. Radiology. 2007;242:15-21.
1. Glotzbecker M.P., Bono C.M., Wood K.B., Harris M.B. Thromboembolic disease in spinal surgery: a systematic review. Spine (Phila Pa 1976). 2009;34:291-303.
2. Geerts W.H., Pineo G.F., Heit J.A., et al. Prevention of venous thromboembolism: the seventh ACCP conference on antithrombotic and thrombolytic therapy. Chest. 2004;126:338S-400S.
3. Ferree B.A., Wright A.M. Deep venous thrombosis following posterior lumbar spinal surgery. Spine (Phila Pa 1976). 1993;18:1079-1082.
4. Oda T., Fuji T., Kato Y., et al. Deep venous thrombosis after posterior spinal surgery. Spine (Phila Pa 1976). 2000;25:2962-2967.
5. Dearborn J.T., Hu S.S., Tribus C.B., Bradford D.S. Thromboembolic complications after major thoracolumbar spine surgery. Spine (Phila Pa 1976). 1999;24:1471-1476.
6. Agnelli G., Becattini C. Treatment of DVT: how long is enough and how do you predict recurrence? J Thromb Thrombolysis. 2008;25:37-44.
7. Furlan J.C., Fehlings M.G. Role of screening tests for deep venous thrombosis in asymptomatic adults with acute spinal cord injury: an evidence-based analysis. Spine (Phila Pa 1976). 2007;32:1908-1916.
8. Cogo A., Lensing A.W., Koopman M.M., et al. Compression ultrasonography for diagnostic management of patients with clinically suspected deep vein thrombosis: prospective cohort study. BMJ. 1998;316:17-20.
9. Goodacre S., Sampson F., Thomas S., et al. Systematic review and meta-analysis of the diagnostic accuracy of ultrasonography for deep vein thrombosis. BMC Med Imaging. 2005;5:6.
10. Tan M., van Rooden C.J., Westerbeek R.E., Huisman M.V. Diagnostic management of clinically suspected acute deep vein thrombosis. Br J Haematol. 2009;146:347-360.
11. Grady-Benson J.C., Oishi C.S., Hanson P.B., et al. Routine postoperative duplex ultrasonography screening and monitoring for the detection of deep vein thrombosis: a survey of 110 total hip arthroplasties. Clin Orthop Relat Res. 1994;307:130-141.
12. Brandjes D.P., Heijboer H., Buller H.R., et al. Acenocoumarol and heparin compared with acenocoumarol alone in the initial treatment of proximal-vein thrombosis. N Engl J Med. 1992;327:1485-1489.
13. Houman Fekrazad M., Lopes R.D., Stashenko G.J., et al. Treatment of venous thromboembolism: guidelines translated for the clinician. J Thromb Thrombolysis. 2009;28:270-275.
14. Clark S.K., Tremann J.A., Sennewald F.R., Donaldson J.A. Priapism: an unusual complication of heparin therapy for sudden deafness. Am J Otolaryngol. 1981;2:69-72.
15. Demasi R., Bode A.P., Knupp C., et al. Heparin-induced thrombocytopenia. Am Surg. 1994;60:26-29.
16. Cain J.E.Jr., Major M.R., Lauerman W.C., et al. The morbidity of heparin therapy after development of pulmonary embolus in patients undergoing thoracolumbar or lumbar spinal fusion. Spine (Phila Pa 1976). 1995;20:1600-1603.
17. Schizas C., Neumayer F., Kosmopoulos V. Incidence and management of pulmonary embolism following spinal surgery occurring while under chemical thromboprophylaxis. Eur Spine J. 2008;17:970-974.
18. Sohne M., Ten Wolde M., Boomsma F., et al. Brain natriuretic peptide in hemodynamically stable acute pulmonary embolism. J Thromb Haemost. 2006;4:552-556.
19. Crowther M.A., Cook D.J., Griffith L.E., et al. Neither baseline tests of molecular hypercoagulability nor D-dimer levels predict deep venous thrombosis in critically ill medical-surgical patients. Intensive Care Med. 2005;31:48-55.
20. Stein P.D., Woodard P.K., Weg J.G., et al. Diagnostic pathways in acute pulmonary embolism: recommendations of the PIOPED II investigators. Radiology. 2007;242:15-21.
21. Kearon C., Kahn S.R., Agnelli G., et al. Antithrombotic therapy for venous thromboembolic disease: American College of Chest Physicians evidence-based clinical practice guidelines (8th edition). Chest. 2008;133:454S-545S.
22. Baron E.M., Albert T.J. Medical complications of surgical treatment of adult spinal deformity and how to avoid them. Spine (Phila Pa 1976). 2006;31:S106-S118.
23. Levi M., Toh C.H., Thachil J., Watson H.G. Guidelines for the diagnosis and management of disseminated intravascular coagulation: British Committee for Standards in Haematology. Br J Haematol. 2009;145:24-33.
24. Harmanci A., Harmanci O., Akova M. Hospital-acquired pneumonia: challenges and options for diagnosis and treatment. J Hosp Infect. 2002;51:160-167.
25. Kane C., Galanes S. Adult respiratory distress syndrome. Crit Care Nurs Q. 2004;27:325-335.
26. Bernard G.R., Artigas A., Brigham K.L., et al. Report of the American-European Consensus Conference on Acute Respiratory Distress Syndrome: definitions, mechanisms, relevant outcomes, and clinical trial coordination consensus committee. J Crit Care. 1994;9:72-81.
27. Santacruz J.F., Diaz Guzman Zavala E., Arroliga A.C. Update in ARDS management: recent randomized controlled trials that changed our practice. Cleve Clin J Med. 2006;73:217-219. 223–225, 229 passim
28. Faciszewski T., Jensen R., Rokey R., Berg R. Cardiac risk stratification of patients with symptomatic spinal stenosis. Clin Orthop Relat Res. 2001;384:110-115.
29. Katzel L.I., Sorkin K.D., Colman E., et al. Risk factors for exercise-induced silent myocardial ischemia in healthy volunteers. Am J Cardiol. 1994;74:869-874.
30. Lee D.Y., Lee S.H., Jang J.S. Risk factors for perioperative cardiac complications after lumbar fusion surgery. Neurol Med Chir (Tokyo). 2007;47:495-500.
31. Faciszewski T., Winter R.B., Lonstein J.E., et al. The surgical and medical perioperative complications of anterior spinal fusion surgery in the thoracic and lumbar spine in adults: a review of 1223 procedures. Spine (Phila Pa 1976). 1995;20:1592-1599.
32. Reusser P., Gyr K., Scheidegger D., et al. Prospective endoscopic study of stress erosions and ulcers in critically ill neurosurgical patients: current incidence and effect of acid-reducing prophylaxis. Crit Care Med. 1990;18:270-274.
33. Rajaraman V., Vingan R., Roth P., et al. Visceral and vascular complications resulting from anterior lumbar interbody fusion. J Neurosurg. 1999;91:60-64.
34. Caner H., Bavbek M., Albayrak A., Altinors T.C. Ogilvie’s syndrome as a rare complication of lumbar disc surgery. Can J Neurol Sci. 2000;27:77-78.
35. Rex D.K. Acute colonic pseudo-obstruction (Ogilvie’s syndrome). Gastroenterologist. 1994;2:233-238.
36. Althausen P.L., Gupta M.C., Benson D.R., Jones D.A. The use of neostigmine to treat postoperative ileus in orthopedic spinal patients. J Spinal Disord. 2001;14:541-545.
37. Amaro R., Rogers A.I. Neostigmine infusion: new standard of care for acute colonic pseudo-obstruction? Am J Gastroenterol. 2000;95:304-305.
38. Althausen P.L., Gupta M.C., Benson D.R., Jones D.A. The use of neostigmine to treat postoperative ileus in orthopedic spinal patients. J Spinal Disord. 2001;14:541-545.
39. Paran H., Silverberg D., Mayo A., et al. Treatment of acute colonic pseudo-obstruction with neostigmine. J Am Coll Surg. 2000;190:315-318.
40. Ponec R.J., Saunders M.D., Kimmey M.B. Neostigmine for the treatment of acute colonic pseudo-obstruction. N Engl J Med. 1999;341:137-141.
41. Vantrappen G. Acute colonic pseudo-obstruction. Lancet. 1993;341:152-153.
42. Rex D.K. Colonoscopy and acute colonic pseudo-obstruction. Gastrointest Endosc Clin N Am. 1997;7:499-508.
43. Vanek V.W., Al-Salti M. Acute pseudo-obstruction of the colon (Ogilvie’s syndrome): an analysis of 400 cases. Dis Colon Rectum. 1986;29:203-210.
44. Altiok H., Lubicky J.P., DeWald C.J., Herman J.E. The superior mesenteric artery syndrome in patients with spinal deformity. Spine (Phila Pa 1976). 2005;30:2164-2170.
45. Zhu Z.Z., Qiu Y. Superior mesenteric artery syndrome following scoliosis surgery: its risk indicators and treatment strategy. World J Gastroenterol. 2005;11:3307-3310.
46. Derincek A., Wood K.B., Muench C.A. Superior mesenteric artery syndrome following correction of kyphosis in an adult. J Spinal Disord Tech. 2004;17:549-553.
47. Crowther M.A., Webb P.J., Eyre-Brook I.A. Superior mesenteric artery syndrome following surgery for scoliosis. Spine (Phila Pa 1976). 2002;27:E528-E533.
48. Leichtner A.M., Banta J.V., Etienne N., et al. Pancreatitis following scoliosis surgery in children and young adults. J Pediatr Orthop. 1991;11:594-598.
49. Bragg L.E., Thompson J.S., Burnett D.A., et al. Increased incidence of pancreas-related complications in patients with postoperative pancreatitis. Am J Surg. 1985;150:694-697.
50. Boulis N.M., Mian F.S., Rodriguez D., et al. Urinary retention following routine neurosurgical spine procedures. Surg Neurol. 2001;55:23-27. discussion 27–28
51. van Dam B.E., Bradford D.S., Lonstein J.E., et al. Adult idiopathic scoliosis treated by posterior spinal fusion and Harrington instrumentation. Spine (Phila Pa 1976). 1987;12:32-36.
52. O’Grady N.P., Barie P.S., Bartlett J., et al. Practice parameters for evaluating new fever in critically ill adult patients: Task Force of the American College of Critical Care Medicine of the Society of Critical Care Medicine in Collaboration with the Infectious Disease Society of America. Crit Care Med. 1998;26:392-408.
53. Garner J.S., Jarvis W.R., Emori T.G., et al. CDC definitions for nosocomial infections, 1988. Am J Infect Control. 1988;16:128-140.
54. Carmichael P., Carmichael A.R. Acute renal failure in the surgical setting. ANZ J Surg. 2003;73:144-153.
55. Jarnberg P.O. Renal protection strategies in the perioperative period. Best Pract Res Clin Anaesthesiol. 2004;18:645-660.
56. Tiusanen H., Seitsalo S., Osterman K., Soini J. Retrograde ejaculation after anterior interbody lumbar fusion. Eur Spine J. 1995;4:339-342.
57. Hagg O., Fritzell P., Nordwall A., et al. Sexual function in men and women after anterior surgery for chronic low back pain. Eur Spine J. 2006;15:677-682.
58. Kawaguchi Y., Kanamori M., Ishihara H., et al. Postoperative delirium in spine surgery. Spine J. 2006;6:164-169.
59. Marcantonio E.R., Goldman L., Orav E.J., et al. The association of intraoperative factors with the development of postoperative delirium. Am J Med. 1998;105:380-384.
60. Palmer R.M. Perioperative care of the elderly patient. Cleve Clin J Med. 2006;73(Suppl 1):S106-S110.
61. Wolfe S.W., Lospinuso M.F., Burke S.W. Unilateral blindness as a complication of patient positioning for spinal surgery: a case report. Spine (Phila Pa 1976). 1992;17:600-605.
62. Bansal C., Scott R., Stewart D., Cockerell C.J. Decubitus ulcers: a review of the literature. Int J Dermatol. 2005;44:805-810.