Despite the increased focus on improving patient safety and minimizing medical errors, it is impossible to eliminate human error entirely. Individual errors can cause minor or major complications during or after a surgical procedure. Although these types of errors may not be publicized as much as wrong-site surgery or a retained surgical item, they can still lead to surgical complications that prolong the course of illness, lengthen hospital stay, and increase morbidity and mortality rates.
Complications in Minor Procedures
Central Venous Access Catheters
Complications of central venous access catheters are common. Improvements in ultrasound technology and mass education surrounding the use and techniques in ultrasonography have led to increased employment and enthusiasm for its use in central venous catheter placement. Numerous institutions have recently begun to mandate use of ultrasound for placement of all central venous lines. Anecdotally, many subclavian catheters have been alternatively placed at the internal jugular position due to a perceived benefit of decreasing complications. Literature exists that there is some merit to this; however, one should proceed with caution as the decrease in pneumothoraces may not be balanced by the increase in line infections as the neck is difficult to keep the site clean and the dressing intact. Steps to decrease complications include the following:
Ensure that central venous access is indicated.
Experienced personnel should insert the catheter or should supervise the insertion.
Use proper positioning and sterile technique.
Ultrasound is recommended for internal jugular vein insertion.
All central venous catheters should be assessed on a daily basis and should be exchanged only for specific indications (not as a matter of routine).
All central catheters should be removed as soon as possible.
Common complications of central venous access include the following.
Occurrence rates from both subclavian and internal jugular vein approaches are 1% to 6%. Prevention requires proper positioning of the patient and correct insertion technique. A postprocedure chest x-ray is mandatory to confirm the presence or absence of a pneumothorax, regardless of whether a pneumothorax is suspected. Pneumothorax rates are higher among the inexperienced but occur with experienced operators as well. If the patient is stable, and the pneumothorax is small (<15%), close expectant observation may be adequate. If the patient is symptomatic, a thoracostomy tube should be placed. Occasionally, pneumothorax will occur as late as 48 to 72 hours after central venous access attempts. This usually creates sufficient compromise that a tube thoracostomy is required.
Arrhythmias result from myocardial irritability secondary to guidewire placement and usually resolve when the catheter or guidewire is withdrawn from the right heart. Prevention requires electrocardiogram (ECG) monitoring whenever possible during catheter insertion and rapid recognition when a new arrhythmia begins.
Inadvertent puncture or laceration of an adjacent artery with bleeding can occur, but the majority will resolve with direct pressure on or near the arterial injury site. Rarely will angiography, stent placement, or surgery be required to repair the puncture site, but close observation and a chest x-ray are indicated. Ultrasound guided insertion has not mitigated this complication, but may decrease the incidence of arterial puncture. Ultrasound has also been shown to decrease the number of attempts and the time it takes to complete insertion.
A guidewire or catheter that inadvertently migrates further into the vascular space away from the insertion site can be readily retrieved with interventional angiography techniques. A prompt chest x-ray and close monitoring of the patient until retrieval are indicated.
Although estimated to occur in only 0.2% to 1% of patients, an air embolism can be dramatic and fatal. If an embolus is suspected, the patient should immediately be placed into a left lateral decubitus Trendelenburg position, so the entrapped air can be stabilized within the right ventricle. Auscultation over the precordium may reveal a “crunching” noise, but a portable chest x-ray will help confirm the diagnosis. Aspiration via a central venous line accessing the heart may decrease the volume of gas in the right side of the heart and minimize the amount traversing into the pulmonary circulation. Subsequent recovery of intracardiac and intrapulmonary air may require open surgical or angiographic techniques. Treatment may prove futile if the air bolus is larger than 50 mL, however.
Flow-directed, pulmonary artery (“Swan-Ganz”) catheters can cause pulmonary artery rupture due to excessive advancement of the catheter into the pulmonary circulation. There usually is a sentinel bleed with coughing noted when a pulmonary artery catheter balloon is inflated, followed by uncontrolled hemoptysis. Reinflation of the catheter balloon is the initial step in management, followed by immediate airway intubation with mechanical ventilation, an urgent portable chest x-ray, and notification of the OR that an emergent thoracotomy may be required. If there is no further bleeding after the balloon is reinflated, the x-ray shows no significant consolidation of lung fields from ongoing bleeding, and the patient is easily ventilated, then a conservative nonoperative approach may be considered. However, more typically a pulmonary angiogram with angioembolization or vascular stenting is required. Hemodynamically unstable patients rarely survive because of the time needed to initiate and perform interventional procedures or a thoracotomy and to identify the ruptured branch of the pulmonary artery.
Central Venous Line Infection
The CDC reports mortality rates of 12% to 25% when a central venous line infection becomes systemic, with a cost of approximately $25,000 per episode.52,53,54 The CDC does not recommend routine central line changes, but when the clinical suspicion is high, the site of venous access must be changed. Nearly 15% of hospitalized patients will acquire central venous line sepsis. In many instances, once an infection is recognized as central line sepsis, removing the line is adequate. Staphylococcus aureus infections, however, present a unique problem because of the potential for metastatic seeding of bacterial emboli. The required treatment is 4 to 6 weeks of tailored antibiotic therapy. Using a checklist when inserting central venous catheters has been shown to significantly decrease rates of line infections.55 Following a checklist strategy and close monitoring of catheters has resulted in significant reductions in infection rates for numerous institutions and many are now reporting zero annual infection rates.
Arterial lines are placed to facilitate arterial blood gas sampling and hemodynamic monitoring. The use of ultrasound to assist in placement of these catheters has become commonplace and markedly reduces the number of attempts and time for insertion completion.
Arterial access requires a sterile Seldinger technique, and a variety of arteries are used, including the radial, femoral, brachial, axillary, dorsalis pedis, or superficial temporal arteries. Although complications occur less than 1% of the time, they can be catastrophic. Complications include thrombosis, bleeding, hematoma, arterial spasm (nonthrombotic pulselessness), and infection. Thrombosis or embolization of an extremity arterial catheter can result in the loss of a digit, hand, or foot, and the risk is nearly the same for both femoral and radial cannulation. Thrombosis with distal tissue ischemia is treated with anticoagulation, but occasionally surgical intervention is required. Pseudoaneurysms and arteriovenous fistulae can also occur.
Endoscopy and Bronchoscopy
The principal risk of gastrointestinal (GI) endoscopy is perforation. Perforations occur in 1:10,000 patients with endoscopy alone, but have a higher incidence rate when biopsies are performed (up to 10%). This increased risk is due to complications of intubating a GI diverticulum (either esophageal or colonic), or from the presence of weakened or inflamed tissue in the intestinal wall (e.g., diverticulitis, glucocorticoid use, or inflammatory bowel disease).
Patients will usually complain of diffuse abdominal pain shortly after the procedure, and then progress with worsening abdominal discomfort and peritonitis on examination. In obtunded or elderly patients, a change in clinical status may take 24 to 48 hours. Radiologic studies to look for free intraperitoneal air, retroperitoneal air, or a pneumothorax are diagnostic. Open or laparoscopic exploration locates the perforation and allows repair and local decontamination of the surrounding tissues.
The occasional patient who may be a candidate for nonoperative management is one in whom perforation arises during an elective, bowel-prepped endoscopy and who does not have significant pain or clinical signs of infection. These patients must be closely observed in a monitored setting, on strict dietary restriction and broad-spectrum antibiotics.
Complications of bronchoscopy include bronchial plugging, hypoxemia, pneumothorax, lobar collapse, and bleeding. When diagnosed in a timely fashion, they are rarely life threatening. Bleeding usually resolves spontaneously and rarely requires surgery, but may require repeat endoscopy for thermocoagulation or fibrin glue application. The presence of a pneumothorax necessitates placement of a thoracostomy tube when significant deoxygenation occurs or the pulmonary mechanics are compromised. Lobar collapse or mucous plugging usually responds to aggressive pulmonary toilet, but occasionally requires repeat bronchoscopy. If biopsies have been performed, the risk for these complications increases.
Tracheostomy facilitates weaning from a ventilator, may decrease length of ICU or hospital stay, and improves pulmonary toilet. Tracheostomies are performed open, percutaneously, with or without bronchoscopy, and with or without Doppler guidance. Arguments for percutaneous tracheostomy largely side with efficiency and cost containment over open tracheostomy. A recent literature review examining early (<3–7 days) vs. late (>14 days) tracheostomy demonstrates little difference in outcomes but does demonstrate greater patient comfort in those patients with tracheostomy than those with an endotracheal tube. Complications and outcomes between the two different methods remain largely equivalent.
Recent studies do not support obtaining a routine chest x-ray after percutaneous or open tracheostomy.56,57 However, significant lobar collapse can occur from copious tracheal secretions or mechanical obstruction. The most dramatic complication of tracheostomy is tracheoinnominate artery fistula (TIAF) (Fig. 12-7).58,59 This occurs rarely (~0.3%) but carries a 50% to 80% mortality rate. TIAFs can occur as early as 2 days or as late as 2 months after tracheostomy. A sentinel bleed occurs in 50% of TIAF cases, followed by a large-volume bleed. Should a TIAF be suspected, the patient should be transported immediately to the OR for fiberoptic evaluation. If needed, remove the tracheostomy and place a finger through the tracheostomy site to apply direct pressure anteriorly for compression of the innominate artery while preparation for a more definitive approach is organized.
This illustration depicts improper positioning of the percutaneous needle. It is possible to access the innominate artery via the trachea, thus placing the patient at risk for early tracheoinnominate artery fistula.
A misplaced percutaneous endogastrostomy (PEG) tube may lead to intra-abdominal sepsis with peritonitis and/or an abdominal wall abscess with necrotizing fasciitis. As in other minor procedures, the initial placement technique must be fastidious to avoid complications. Transillumination of the abdomen may decrease the risk for error, but this is unsubstantiated in the literature. Inadvertent colotomies, intraperitoneal placement of the tube and subsequent leakage of tube feeds with peritonitis, and abdominal wall abscesses require surgery to correct the complications and to replace the PEG with an alternate feeding tube, usually a jejunostomy.
A dislodged or prematurely removed PEG tube should be replaced as early as possible after dislodgment because the gastrostomy site closes rapidly. A contrast x-ray (sinogram) should be performed to confirm the tube’s intragastric position before feeding. If there is uncertainty of the tube location, conversion to an open tube placement procedure is required.
Chest tube insertion is performed for pneumothorax, hemothorax, pleural effusions, or empyema. In most patients, a chest tube can be easily placed with a combination of local analgesia and light conscious sedation. Common complications include inadequate analgesia or sedation, incomplete penetration of the pleura with formation of a subcutaneous track for the tube, lacerations to the lung or diaphragm, intraperitoneal placement of the tube through the diaphragm, and bleeding related to these various lacerations or injury to pleural adhesions. Additional problems include slippage of the tube out of position or mechanical problems related to the drainage system. In patients with bullous disease, there can be significant intrapleural scarring and it can be easy to mistakenly place the chest tube into a bullae. All of these complications can be avoided with proper initial insertion techniques, plus a daily review of the drainage system and follow-up radiographs. Tube removal can create a residual pneumothorax if the patient does not maintain positive intrapleural pressure by Valsalva’s maneuver during tube removal and dressing application.
Complications of Angiography
Intramural dissection of a cannulated artery can lead to complications such as ischemic stroke from a carotid artery dissection or occlusion, mesenteric ischemia from dissection of the superior mesenteric artery, or a more innocuous finding of “blue toe syndrome” from a dissected artery in a peripheral limb. Invasive or noninvasive imaging studies confirm the suspected problem. The severity of ischemia and extent of dissection determine if anticoagulation therapy or urgent surgical exploration is indicated.
Bleeding from a vascular access site usually is obvious, but may not be visible when the blood loss is tracking into the retroperitoneal tissue planes after femoral artery cannulation. These patients can present with hemorrhagic shock; an abdominopelvic CT scan delineates the extent of bleeding along the retroperitoneum. Initial management is direct compression at the access site and resuscitation as indicated. Urgent surgical exploration may be required to control the bleeding site and evacuate larger hematomas.
Renal complications of angiography occur in 1% to 2% of patients. Contrast nephropathy is a temporary and preventable complication of radiologic studies such as CT, angiography, and/or venography. Intravenous (IV) hydration before and after the procedure is the most efficient method for preventing contrast nephropathy. Nonionic contrast also may be of benefit in higher-risk patients. Close communication between providers is often required to resolve the priorities in care as well as to balance the risks versus benefits of renal protection when managing patients in need of angiographic procedures.
Complications of Biopsies
Lymph node biopsies have direct and indirect complications that include bleeding, infection, lymph leakage, and seromas. Measures to prevent direct complications include proper surgical hemostasis, proper skin preparation, and a single preoperative dose of antibiotic to cover skin flora 30 to 60 minutes before incision. Bleeding at a biopsy site usually can be controlled with direct pressure. Infection at a biopsy site will appear 5 to 10 days postoperatively and may require opening of the wound to drain the infection. Seromas or lymphatic leaks resolve with aspiration of seromas and the application of pressure dressings, but may require repeated treatments or even placement of a vacuum drain.
Organ System Complications
Neurologic complications that occur after surgery include motor or sensory deficits and mental status changes. Peripheral motor and sensory deficits are often due to neurapraxia secondary to improper positioning and/or padding during operations. Treatment is largely clinical observation, and the majority of deficits resolve spontaneously within 1 to 3 months.
Direct injury to nerves during a surgical intervention is a well-known complication of several specific operations, including superficial parotidectomy (facial nerve), carotid endarterectomy (hypoglossal nerve), thyroidectomy (recurrent laryngeal nerve), prostatectomy (nervi erigentes), inguinal herniorrhaphy (ilioinguinal nerve), and mastectomy (long thoracic and thoracodorsal nerves). The nerve injury may be a stretch injury or an unintentionally severed nerve. In addition to loss of function, severed nerves can result in a painful neuroma that may require subsequent surgery.
Mental status changes in the postoperative patient can have numerous causes (Table 12-12). Mental status changes must be continually assessed. A noncontrast CT scan should be used early to detect new or evolving intracranial causes.
Table 12-12Common causes of mental status changes ||Download (.pdf) Table 12-12 Common causes of mental status changes
Closed head injury
Venoms and poisons
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Poor glycemic control
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Corticosteroids, anabolic steroids
Atherosclerotic disease increases the risk for intraoperative and postoperative stroke (cerebrovascular accident). Postoperatively, hypotension and hypoxemia are the most likely causes of a cerebrovascular accident. Neurologic consultation should be obtained immediately to confirm the diagnosis. Management is largely supportive and includes adequate intravascular volume replacement plus optimal oxygen delivery. Advents in interventional radiology by radiologists and vascular and neurologic surgeons have proven successful alternatives in patients requiring diagnostic and therapeutic care in the immediate and acute postoperative period. Catheter-directed therapy with anticoagulants such as the kinases and tissue plasminogen activator (tPA) has potential benefit in postoperative thrombosis where reoperation carries significant risk. In addition, endoluminal stents with drug-eluting stents (DESs) or non-DESs have been used with some degree of success. DESs do require systemic antiplatelet therapy due to the alternative coagulation pathway. Duration of antiplatelet therapy of 1 year is routine.
Corneal abrasions are unusual, but are due to inadequate protection of the eyes during anesthesia. Overlooked contact lenses in patients occasionally may cause conjunctivitis.
Persistent epistaxis can occur after nasogastric tube placement or removal, and nasal packing is the best treatment option if prolonged persistent direct pressure on the external nares fails. Anterior and posterior nasal gauze packing with balloon tamponade, angioembolization, and fibrin glue placement may be required in refractory cases. The use of antibiotics for posterior packing is controversial.
External otitis and otitis media occasionally occur postoperatively. Patients complain of ear pain or decreased hearing, and treatment includes topical antibiotics and nasal decongestion for symptomatic improvement.
Ototoxicity due to aminoglycoside administration occurs in up to 10% of patients, and is often irreversible. Vancomycin-related ototoxicity occurs about 3% of the time when used alone, and as often as 6% when used with other ototoxic agents.60,61
Vascular Problems of the Neck
Complications of carotid endarterectomy include central or regional neurologic deficits or bleeding with an expanding neck hematoma. An acute change in mental status or the presence of localized neurologic deficit requires an immediate return to the OR. An expanding hematoma may warrant emergent airway intubation and subsequent transfer to the OR for control of hemorrhage. Intraoperative anticoagulation with heparin during carotid surgery makes bleeding a postoperative risk. Other complications include arteriovenous fistulae, pseudoaneurysms, and infection, all of which are treated surgically.
Intraoperative hypotension during manipulation of the carotid bifurcation can occur and is related to increased tone from baroreceptors that reflexly cause bradycardia. Should hypotension occur when manipulating the carotid bifurcation, an injection of 1% lidocaine solution around this structure should attenuate this reflexive response.
The most common delayed complication following carotid endarterectomy remains myocardial infarction. The possibility of a postoperative myocardial infarction should be considered as a cause of labile blood pressure and arrhythmias in high-risk patients.
Thyroid and Parathyroid Glands
Surgery of the thyroid and parathyroid glands can result in hypocalcemia in the immediate postoperative period. Manifestations include ECG changes (shortened P-R interval), muscle spasm (tetany, Chvostek’s sign, and Trousseau’s sign), paresthesias, and laryngospasm. Treatment includes calcium gluconate infusion and, if tetany ensues, chemical paralysis with intubation. Maintenance treatment is thyroid hormone replacement (after thyroidectomy) in addition to calcium carbonate and vitamin D.
Recurrent laryngeal nerve (RLN) injury occurs in less than 5% of patients. Of those with injury, approximately 10% are permanent. Dissection near the inferior thyroid artery is a common area for RLN injury. At the conclusion of the operation, if there is suspicion of an RLN injury, direct laryngoscopy is diagnostic. The cord on the affected side will be in the paramedian position. With bilateral RLN injury, the chance of a successful extubation is poor. If paralysis of the cords is not permanent, function may return 1 to 2 months after injury. Permanent RLN injury can be treated by various techniques to stent the cords in a position of function.
Superior laryngeal nerve injury is less debilitating, as the common symptom is loss of projection of the voice. The glottic aperture is asymmetrical on direct laryngoscopy, and management is limited to clinical observation.
Surgical complications that put the respiratory system in jeopardy are not confined to technical errors. Malnutrition, inadequate pain control, inadequate mechanical ventilation, inadequate pulmonary toilet, and aspiration can cause serious pulmonary problems.
Pneumothorax can occur from central line insertion during anesthesia or from a diaphragmatic injury during an abdominal procedure. Hypotension, hypoxemia, and tracheal deviation away from the affected side may be present. A tension pneumothorax can cause complete cardiovascular collapse. Treatment is by needle thoracostomy, followed by tube thoracostomy. The chest tube is inserted at the fifth intercostal space in the anterior axillary line. The anterior chest wall is up to 1 cm thicker than the lateral chest wall, so needle decompression is more effective in the lateral position. Attempted prehospital needle decompression in the traditional anterior position results in only 50% needle entry into the thoracic cavity.
Hemothoraces should be evacuated completely. Delay in evacuation of a hemothorax leaves the patient at risk for empyema and entrapped lung. If evacuation is incomplete with tube thoracostomy, video-assisted thoracoscopy or open evacuation and pleurodesis may be required.
Pulmonary atelectasis results in a loss of functional residual capacity (FRC) of the lung and can predispose to pneumonia. Poor pain control in the postoperative period contributes to poor inspiratory effort and collapse of the lower lobes in particular. The prevention of atelectasis is facilitated by sitting the patient up as much as possible, early ambulation, and adequate pain control. An increase in FRC by 700 mL or more can be accomplished by sitting patients up to greater than 45°. For mechanically ventilated patients, simply placing the head of the bed at30 to 45° elevation and delivering adequate tidal volumes (8–10 mL/kg) improves pulmonary outcomes.
Patients with inadequate pulmonary toilet are at increased risk for bronchial plugging and lobar collapse. Patients with copious and tenacious secretions develop these plugs most often, but foreign bodies in the bronchus can be the cause of lobar collapse as well. The diagnosis of bronchial plugging is based on chest x-ray and clinical suspicion with acute pulmonary decompensation with increased work of breathing and hypoxemia. Fiberoptic bronchoscopy can be useful to clear mucous plugs and secretions.
Aspiration complications include pneumonitis and pneumonia. The treatment of pneumonitis is similar to that for acute respiratory distress syndrome (see later in this section) and includes oxygenation with general supportive care. Antibiotics are not indicated. Hospitalized patients who develop aspiration pneumonitis have a mortality rate as high as 70% to 80%. Early, aggressive, and repeated bronchoscopy for suctioning of aspirated material from the tracheobronchial tree will help minimize the inflammatory reaction of pneumonitis and facilitate improved pulmonary toilet. Forced diuresis to overcome anasarca and over-resuscitation remains controversial and unsubstantiated. Complications of forced diuresis include electrolyte disturbances, replacement of those electrolytes, metabolic alkalosis, hypotension, and acute kidney injury.
Pneumonia is the second most common nosocomial infection and is the most common infection in ventilated patients. Ventilator-associated pneumonia (VAP) occurs in 15% to 40% of ventilated ICU patients, with a probability rate of 5% per day, up to 70% at 30 days. The 30-day mortality rate of nosocomial pneumonia can be as high as 40% and depends on the microorganisms involved and the timeliness of initiating appropriate antimicrobials Protocol-driven approaches for prevention and treatment of VAP are recognized as beneficial in managing these difficult infectious complications.
Once the diagnosis of pneumonia is suspected (an abnormal chest x-ray, fever, productive cough with purulent sputum, and no other obvious fever sources), it is invariably necessary to initially begin treatment with broad-spectrum antibiotics until proper identification, colony count (≥100,000 colony-forming units [CFU]), and sensitivity of the microorganisms are determined.62 The spectrum of antibiotic coverage should be narrowed as soon as the culture sensitivities are determined. Double-coverage antibiotic strategy for the two pathogens, Pseudomonas and Acinetobacter spp., may be appropriate if the local prevalence of these particularly virulent organisms is high. One of the most helpful tools in treating pneumonia and other infections is the tracking of a medical center’s antibiogram every 6 to 12 months.63
Epidural analgesia decreases the risk of perioperative pneumonia. This method of pain control improves pulmonary toilet and the early return of bowel function; both have a significant impact on the potential for aspiration and for acquiring pneumonia. The routine use of epidural analgesia results in a lower incidence of pneumonia than patient-controlled analgesia.64
Acute lung injury (ALI) was a diagnosis applied to patients with similar findings to those with acute respiratory distress syndrome (ARDS). The Berlin definition of ARDS developed by the American-European Consensus Conference of 2012 effectively not only simplifies the definition of ARDS, but eliminates the term ALI from critical care vernacular. ARDS is now classified by partial pressure of oxygen in arterial blood (Pao2)/fraction of inspired oxygen (Fio2) ratios as mild (300–201 mmHg), moderate (200–101 mmHg), and severe (<100 mmHg). Elements of modification of the definition include the following: less than 7 days of onset; removal of pulmonary artery occlusion pressure; and clinical judgment for characterizing hydrostatic pulmonary edema is acceptable, unless risk factors for ARDS have been eliminated, in which case objective analysis is necessary.65,66,67,68
The definition of ARDS traditionally included five criteria (Table 12-13). The multicenter ARDS Research Network (ARDSnet) research trial demonstrated improved clinical outcomes for ARDS patients ventilated at tidal volumes of only 5 to 7 mL/kg.69 This strategy is no longer prescribed solely for patients with ARDS, but is also recommended for patients with normal pulmonary physiology as well who are intubated for reasons other than acute respiratory failure. The beneficial effects of positive end-expiratory pressure (PEEP) for ARDS were confirmed in this study as well. The maintenance of PEEP during ventilatory support is determined based on blood gas analysis, pulmonary mechanics, and requirements for supplemental oxygen. As gas exchange improves with resolving ARDS, the initial step in decreasing ventilatory support should be to decrease the levels of supplemental oxygen first, and then to slowly bring the PEEP levels back down to minimal levels.70 This is done to minimize the potential for recurrent alveolar collapse and a worsening gas exchange.
Table 12-13Inclusion criteria for the acute respiratory distress syndrome ||Download (.pdf) Table 12-13 Inclusion criteria for the acute respiratory distress syndrome
Pao2:Fio2 <200 (regardless of positive end-expiratory pressure)
Pulmonary artery occlusion pressure <18 mmHg
No clinical evidence of right heart failure
Not all patients can be weaned easily from mechanical ventilation. When the respiratory muscle energy demands are not balanced or there is an ongoing active disease state external to the lungs, patients may require prolonged ventilatory support. Protocol-driven ventilator weaning strategies are successful and have become part of the standard of care. The use of a weaning protocol for patients on mechanical ventilation greater than 48 hours reduces the incidence of VAP and the overall length of time on mechanical ventilation. Unfortunately, there is still no reliable way of predicting which patient will be successfully extubated after a weaning program, and the decision for extubation is based on a combination of clinical parameters and measured pulmonary mechanics.71 The Tobin Index (frequency [breaths per minute]/tidal volume [L]), also known as the rapid shallow breathing index, is perhaps the best negative predictive instrument.72 If the result equals less than 105, then there is nearly a 70% chance the patient will pass extubation. If the score is greater than 105, the patient has an approximately 80% chance of failing extubation. Other parameters such as the negative inspiratory force, minute ventilation, and respiratory rate are used, but individually have no better predictive value than the rapid shallow breathing index.73
Malnutrition and poor nutritional support may adversely affect the respiratory system. The respiratory quotient (RQ), or respiratory exchange ratio, is the ratio of the rate of carbon dioxide (CO2) produced to the rate of oxygen uptake (RQ = Vco2/V.o2). Lipids, carbohydrates, and protein have differing effects on CO2 production. Patients consuming a diet of mostly carbohydrates have an RQ of 1 or greater. The RQ for a diet of mostly lipids is closer to 0.7, and that for a diet of mostly protein is closer to 0.8. Ideally, an RQ of 0.75 to 0.85 suggests adequate balance and composition of nutrient intake. An excess of carbohydrate may negatively affect ventilator weaning because of the abnormal RQ due to higher CO2 production and altered pulmonary gas exchange.
Although not without risk, tracheostomy decreases the pulmonary dead space and provides for improved pulmonary toilet. When performed before the tenth day of ventilatory support, tracheostomy may decrease the incidence of VAP, the overall length of ventilator time, and the number of ICU patient days.
The occurrence of PE is probably underdiagnosed. Its etiology is thought to stem from DVT. This concept, however, has recently been questioned from Spaniolas et al.74 The diagnosis of PE is made when a high degree of clinical suspicion for PE leads to imaging techniques such as ventilation:perfusion nuclear scans or CT pulmonary angiogram. Clinical findings include elevated central venous pressure, hypoxemia, shortness of breath, hypocarbia secondary to tachypnea, and right heart strain on ECG. Ventilation:perfusion nuclear scans are often indeterminate in patients who have an abnormal chest x-ray and are less sensitive than a CT angiogram or pulmonary angiogram for diagnosing PE. The pulmonary angiogram remains the gold standard for diagnosing PE, but spiral CT angiogram has become an alternative method because of its relative ease of use and reasonable rates of diagnostic accuracy. For cases without clinical contraindications to therapeutic anticoagulation, patients should be empirically started on heparin infusion until the imaging studies are completed if the suspicion of a PE is high.
Sequential compression devices on the lower extremities and low-dose subcutaneous heparin or low molecular weight heparinoid administration are routinely used to prevent DVT and, by inference, the risk of PE. Neurosurgical and orthopedic patients have higher rates of PE, as do obese patients and those at prolonged bed rest.
When anticoagulation is contraindicated, or when a known clot exists in the inferior vena cava (IVC), decreasing risk for PE includes insertion of an IVC filter. The Greenfield filter has been most widely studied, and it has a failure rate of less than 4%. Newer devices include those with nitinol wire that expands with body temperature and retrievable filters. Retrievable filters, however, must be considered as permanent. In most studies, the actual retrievable rate only reached about 20%. Some studies recognize the benefit of automated reminders and diligence of outlying patient follow-up, where higher retrieval rates have been achieved.75 Patients with spinal cord injury and multiple long-bone or pelvic fractures frequently receive IVC filters, and there appears to be a low, but not insignificant, long-term complication rate with their use. However, IVC filters do not prevent PEs that originate from DVTs of the upper extremities.
Arrhythmias are often seen preoperatively in elderly patients but may occur postoperatively in any age group. Atrial fibrillation is the most common arrhythmia76 and occurs between postoperative days 3 to 5 in high-risk patients. This is typically when patients begin to mobilize their interstitial fluid into the vascular fluid space. Contemporary evidence suggests that rate control is more important than rhythm control for atrial fibrillation.77,78 The first-line treatment includes β-blockade and/or calcium channel blockade. β-Blockade must be used judiciously, because hypotension, as well as withdrawal from β-blockade with rebound hypertension, is possible. Calcium channel blockers are an option if β-blockers are not tolerated by the patient, but caution must be exercised in those with a history of congestive heart failure. Although digoxin is still a standby medication, it has limitations due to the need for optimal dosing levels. Cardioversion may be required if patients become hemodynamically unstable and the rhythm cannot be controlled.
Ventricular arrhythmias and other tachyarrhythmias may occur in surgical patients as well. Similar to atrial rhythm problems, these are best controlled with β-blockade, but the use of other antiarrhythmics or cardioversion may be required if patients become hemodynamically unstable.
Cardiac ischemia is a cause of postoperative mortality. Acute myocardial infarction (AMI) can present insidiously, or it can be more dramatic with the classic presentation of shortness of breath, severe angina, and sudden cardiogenic shock. The workup to rule out an AMI includes an ECG and cardiac enzyme measurements. The patient should be transferred to a monitored (telemetry) floor. Morphine, supplemental oxygen, nitroglycerine, and aspirin (MONA) are the initial therapeutic maneuvers for those being investigated for AMI.
Surgery of the esophagus is potentially complicated because of its anatomic location and blood supply. Nutritional support strategies should be considered for esophageal resection patients to maximize the potential for survival. The two primary types of esophageal resection performed are the transhiatal resection and the transthoracic (Ivor-Lewis) resection.79 The transhiatal resection has the advantage that a formal thoracotomy incision is avoided. However, dissection of the esophagus is blind, and anastomotic leaks occur more than with other resections. However, when a leak does occur, simple opening of the cervical incision and draining the leak is all that is usually required.
The transthoracic Ivor-Lewis resection includes an esophageal anastomosis performed in the chest near the level of the azygos vein. These have lower leak rates, but leaks result in mediastinitis and can be difficult to control. The reported mortality is about 50% with an anastomotic leak, and the overall mortality is about 5%, which is similar to transhiatal resection.
Postoperative ileus is related to dysfunction of the neural reflex axis of the intestine. Excessive narcotic use may delay return of bowel function. Epidural anesthesia results in better pain control, and there is an earlier return of bowel function and a shorter length of hospital stay. The limited use of nasogastric tubes and the initiation of early postoperative feeding are associated with an earlier return of bowel function.80 The use of chewing gum and other oral stimulants to minimize ileus remains controversial.
Pharmacologic agents commonly used to stimulate bowel function include metoclopramide and erythromycin. Metoclopramide’s action is limited to the stomach and duodenum, and it may help primarily with gastroparesis. Erythromycin is a motilin agonist that works throughout the stomach and bowel. Several studies demonstrate significant benefit from the administration of erythromycin in those suffering from an ileus.81 Alvimopan, a newer agent and a mu-opioid receptor antagonist, has shown some promise in many studies for earlier return of gut function and subsequent reduction in length of stay.82,83 Neostigmine has been used in refractory pan-ileus patients (Ogilvie’s syndrome) with some degree of success. It is recommended for patients receiving this type of therapy to be in a monitored unit.84 0
Small bowel obstruction occurs in less than 1% of early postoperative patients. When it does occur, adhesions are usually the cause. Internal and external hernias, technical errors, and infections or abscesses are also causative. Hyaluronidase is a mucolytic enzyme that degrades connective tissue, and the use of a methylcellulose form of hyaluronidase, Seprafilm, has been shown to result in a 50% decrease in adhesion formation in some patients.85,86 This should translate into a lower occurrence of postoperative bowel obstruction, but this has yet to be proven.
Fistulae are the abnormal communication of one structure to an adjacent structure or compartment and are associated with extensive morbidity and mortality. Common causes for fistula formation are summarized in the mnemonic FRIENDS (Foreign body, Radiation, Ischemia/Inflammation/Infection, Epithelialization of a tract, Neoplasia, Distal obstruction, and Steroid use). Postoperatively, they are most often caused by infection or obstruction leading to an anastomotic leak. The cause of the fistula must be recognized early, and treatment may include nonoperative management with observation and nutritional support, or a delayed operative management strategy that also includes nutritional support and wound care.
GI bleeding can occur perioperatively (Table 12-14). Technical errors such as a poorly tied suture, a nonhemostatic staple line, or a missed injury can all lead to postoperative intestinal bleeding.87,88 The source of bleeding is in the upper GI tract about 85% of the time and is usually detected and treated endoscopically. Surgical control of intestinal bleeding is required in up to 40% of patients.89
Table 12-14Common causes of upper and lower gastrointestinal (GI) hemorrhage ||Download (.pdf) Table 12-14 Common causes of upper and lower gastrointestinal (GI) hemorrhage
UPPER GI BLEED
LOWER GI BLEED
Peptic ulcer disease
Inflammatory bowel disease
When patients in the ICU have a major bleed from stress gastritis, the mortality risk is as high as 50%. It is important to keep the gastric pH greater than 4 to decrease the overall risk for stress gastritis in patients mechanically ventilated for 48 hours or greater and patients who are coagulopathic.90 Proton pump inhibitors, H2-receptor antagonists, and intragastric antacid installation are all effective measures. However, patients who are not mechanically ventilated or who do not have a history of gastritis or peptic ulcer disease should not be placed on gastritis prophylaxis postoperatively because it carries a higher risk of causing pneumonia.
Complications involving the hepatobiliary system are usually due to technical errors. Laparoscopic cholecystectomy has become the standard of care for cholecystectomy, but common bile duct injury remains a nemesis of this approach. Intraoperative cholangiography has not been shown to decrease the incidence of common bile duct injuries because the injury to the bile duct usually occurs before the cholangiogram.91,92 Early recognition and immediate repair of an injury are important, because delayed bile duct leaks often require a more complex repair.
Ischemic injury due to devascularization of the common bile duct has a delayed presentation days to weeks after an operation. Endoscopic retrograde cholangiopancreatography (ERCP) demonstrates a stenotic, smooth common bile duct, and liver function studies are elevated. The recommended treatment is a Roux-en-Y hepaticojejunostomy.
A bile leak due to an unrecognized injury to the ducts may present after cholecystectomy as a biloma. These patients may present with abdominal pain and hyperbilirubinemia. The diagnosis of a biliary leak can be confirmed by CT scan, ERCP, or radionuclide scan. Once a leak is confirmed, a retrograde biliary stent and external drainage are the treatment of choice.
Hyperbilirubinemia in the surgical patient can be a complex problem. Cholestasis makes up the majority of causes for hyperbilirubinemia, but other mechanisms of hyperbilirubinemia include reabsorption of blood (e.g., hematoma from trauma), decreased bile excretion (e.g., sepsis), increased unconjugated bilirubin due to hemolysis, hyperthyroidism, and impaired excretion due to congenital abnormalities or acquired disease. Errors in surgery that cause hyperbilirubinemia largely involve missed or iatrogenic injuries.
The presence of cirrhosis predisposes to postoperative complications. Abdominal or hepatobiliary surgery is problematic in the cirrhotic patient. Ascites leak in the postoperative period can be an issue when any abdominal operation has been performed. Maintaining proper intravascular oncotic pressure in the immediate postoperative period can be difficult, and resuscitation should be maintained with crystalloid solutions. Prevention of renal failure and the management of the hepatorenal syndrome can be difficult, as the demands of fluid resuscitation and altered glomerular filtration become competitive. Spironolactone with other diuretic agents may be helpful in the postoperative care. These patients often have a labile course, and bleeding complications due to coagulopathy are common. The operative mortality in cirrhotic patients is 10% for Child class A, 30% for Child class B, and 82% for Child class C patients.93
Pyogenic liver abscess occurs in less than 0.5% of adult admissions, due to retained necrotic liver tissue, occult intestinal perforations, benign or malignant hepatobiliary obstruction, sepsis, and hepatic arterial occlusion. The treatment is long-term antibiotics with percutaneous drainage of large abscesses.
Pancreatitis can occur following injection of contrast during cholangiography and ERCP. These episodes range from a mild elevation in amylase and lipase with abdominal pain, to a fulminant course of pancreatitis with necrosis requiring surgical débridement. Traumatic injuries to the pancreas can occur during surgical procedures on the kidneys, GI tract, and spleen most commonly. Treatment involves serial CT scans and percutaneous drainage to manage infected fluid and abscess collections; sterile collections should not be drained because drain placement can introduce infection. A pancreatic fistula may respond to antisecretory therapy with a somatostatin analogue. Management of these fistulae initially includes ERCP with or without pancreatic stenting, percutaneous drainage of any fistula fluid collections, total parenteral nutrition (TPN) with bowel rest, and repeated CT scans. The majority of pancreatic fistulae will eventually heal spontaneously.
Renal failure can be classified as prerenal failure, intrinsic renal failure, and postrenal failure. Postrenal failure, or obstructive renal failure, should always be considered when low urine output (oliguria) or anuria occurs. The most common cause is a misplaced or clogged urinary catheter. Other, less common causes to consider are unintentional ligation or transection of ureters during a difficult surgical dissection (e.g., colon resection for diverticular disease) or a large retroperitoneal hematoma (e.g., ruptured aortic aneurysm).
Oliguria is initially evaluated by flushing the urinary catheter using sterile technique. Urine electrolytes should also be measured (Table 12-15). A hemoglobin and hematocrit level should be checked immediately. Patients in compensated shock from acute blood loss may manifest anemia and end-organ malperfusion as oliguria.
Table 12-15Urinary electrolytes associated with acute renal failure and their possible etiologies ||Download (.pdf) Table 12-15 Urinary electrolytes associated with acute renal failure and their possible etiologies
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Acute tubular necrosis (ATN) carries a mortality risk of 25% to 50% due to the many complications that can cause, or result from, this insult. When ATN is due to poor inflow (prerenal failure), the remedy begins with IV administration of crystalloid or colloid fluids as needed. If cardiac insufficiency is the problem, the optimization of vascular volume is achieved first, followed by inotropic agents, as needed. Intrinsic renal failure and subsequent ATN are often the result of direct renal toxins. Aminoglycosides, vancomycin, and furosemide, among other commonly used agents, contribute directly to nephrotoxicity. Contrast-induced nephropathy usually leads to a subtle or transient rise in creatinine. In patients who are volume depleted or have poor cardiac function, contrast nephropathy may permanently impair renal function.94,95,96,97
The treatment of renal failure due to myoglobinuria has shifted away from the use of sodium bicarbonate for alkalinizing the urine, to merely maintaining brisk urine output of 100 mL/h with crystalloid fluid infusion. Mannitol and furosemide are not recommended. Patients who do not respond to resuscitation are at risk for needing renal replacement therapy. Fortunately, most of these patients eventually recover from their renal dysfunction.
A compartment syndrome can develop in any compartment of the body. Compartment syndrome of the extremities generally occurs after a closed fracture. The injury alone may predispose the patient to compartment syndrome, but aggressive fluid resuscitation can exacerbate the problem. Pain with passive motion is the hallmark of compartment syndrome, and the anterior compartment of the leg is usually the first compartment to be involved. Confirmation of the diagnosis is obtained by direct pressure measurement of the individual compartments. If the pressures are greater than 20 to 25 mmHg in any of the compartments, then a four-compartment fasciotomy is considered. Compartment syndrome can be due to ischemia-reperfusion injury, after an ischemic time of 4 to 6 hours. Renal failure (due to myoglobinuria), tissue loss, and a permanent loss of function are possible results of untreated compartment syndrome.
Decubitus ulcers are preventable complications of prolonged bed rest due to traumatic paralysis, dementia, chemical paralysis, or coma. Unfortunately, they are still occurring despite extensive research and clinical initiatives that demonstrate successful prevention strategies. Ischemic changes in the microcirculation of the skin can be significant after 2 hours of sustained pressure. Routine skin care and turning of the patient help ensure a reduction in skin ulceration. This can be labor intensive, and special mattresses and beds are available to help. The treatment of a decubitus ulcer in the noncoagulopathic patient is surgical débridement. Once the wound bed has a viable granulation base without an excess of fibrinous debris, a vacuum-assisted closure dressing can be applied. Wet to moist dressings with frequent dressing changes is the alternative and is labor intensive. Expensive topical enzyme preparations are also available. If the wounds fail to respond to these measures, soft tissue coverage by flap is considered.
Contractures are the result of muscle disuse. Whether from trauma, amputation, or vascular insufficiency, contractures can be prevented by physical therapy and splinting. If not attended to early, contractures will prolong rehabilitation and may lead to further wounds and wound healing issues. Depending on the functional status of the patient, contracture releases may be required for long-term care.
The transfusion guideline of maintaining the hematocrit level in all patients at greater than 30% is no longer valid. Only patients with symptomatic anemia, who have significant cardiac disease, or who are critically ill and require increased oxygen-carrying capacity to adequately perfuse end organs require higher levels of hemoglobin. Other than these select patients, the decision to transfuse should generally not occur until the hemoglobin level reaches 7 mg/dL or the hematocrit reaches 21%.
Transfusion reactions are common complications of blood transfusion. These can be attenuated with a leukocyte filter, but not completely prevented. The manifestations of a transfusion reaction include simple fever, pruritus, chills, muscle rigidity, and renal failure due to myoglobinuria secondary to hemolysis. Discontinuing the transfusion and returning the blood products to the blood bank is an important first step, but administration of antihistamine and possibly steroids may be required to control the reaction symptoms. Severe transfusion reactions are rare but can be fatal.
Infectious complications in blood transfusion range from cytomegalovirus transmission, which is benign in the nontransplant patient, to human immunodeficiency virus (HIV) infection, to passage of the hepatitis viruses (Table 12-16).
Table 12-16Rate of viral transmission in blood product transfusionsa ||Download (.pdf) Table 12-16 Rate of viral transmission in blood product transfusionsa
Patients on warfarin (Coumadin) who require surgery can have anticoagulation reversal by administration of fresh-frozen plasma. Each unit of fresh frozen plasma contains 200 to 250 mL of plasma and includes one unit of coagulation factor per milliliter of plasma.
Thrombocytopenia may require platelet transfusion for a platelet count less than 20,000/mL when invasive procedures are performed, or when platelet counts are low and ongoing bleeding from raw surface areas persists. One unit of platelets will increase the platelet count by 5000 to 7500 per mL in adults. It is important to delineate the cause of the low platelet count. Usually there is a self-limiting or reversible condition such as sepsis. Rarely, it is due to heparin-induced thrombocytopenia I and II. Complications of heparin-induced thrombocytopenia II can be serious because of the diffuse thrombogenic nature of the disorder. Simple precautions to limit this hypercoagulable state include saline solution flushes instead of heparin solutions and limiting the use of heparin-coated catheters. The treatment is anticoagulation with synthetic agents such as argatroban.
For patients with uncontrollable bleeding due to disseminated intravascular coagulopathy (DIC), a potentially useful drug is factor VIIa, but its use should be judicious.98,99,100 Originally used in hepatic trauma and obstetric emergencies, this agent was lifesaving in some circumstances. The CONTROL Trial,101 however, has largely decreased overuse of this agent because investigators demonstrated no benefit over simple factor replacement in severely coagulopathic patients. Factor VIIa use may also be limited due to its potential thrombotic complications. For some situations, the combination of ongoing, nonsurgical bleeding and renal failure can occasionally be successfully treated with desmopressin.
In addition to classic hemophilia, other inherited coagulation factor deficiencies can be difficult to manage in surgery. When required, transfusion of appropriate replacement products is coordinated with the regional blood bank center before surgery. Other blood dyscrasias seen by surgeons include hypercoagulopathic patients. Those who carry congenital anomalies such as the most common factor V Leiden deficiency, as well as protein C and S deficiencies, are likely to form thromboses if inadequately anticoagulated, and these patients should be managed in conjunction with a hematologist.
Abdominal Compartment Syndrome
Multisystem trauma, thermal burns, retroperitoneal injuries, and surgery related to the retroperitoneum are the major initial causative factors that may lead to abdominal compartment syndrome (ACS). Ruptured AAA, major pancreatic injury and resection, or multiple intestinal injuries are also examples of clinical situations in which a large volume of IV fluid resuscitation puts these patients at risk for intra-abdominal hypertension. Manifestations of ACS typically include progressive abdominal distention followed by increased peak airway ventilator pressures, oliguria followed by anuria, and an insidious development of intracranial hypertension.102 These findings are related to elevation of the diaphragm and inadequate venous return from the vena cava or renal veins secondary to the transmitted pressure on the venous system.
Measurement of abdominal pressures is easily accomplished by transducing bladder pressures from the urinary catheter after instilling 100 mL of sterile saline into the urinary bladder.103 A pressure greater than 20 mmHg constitutes intra-abdominal hypertension, but the diagnosis of ACS requires intra-abdominal pressure greater than 25 to 30 mmHg, with at least one of the following: compromised respiratory mechanics and ventilation, oliguria or anuria, or increasing intracranial pressures.104,105,106
The treatment of ACS is to open any recent abdominal incision to release the abdominal fascia or to open the fascia directly if no abdominal incision is present. Immediate improvement in mechanical ventilation pressures, intracranial pressures, and urine output is usually noted. When expectant management for ACS is considered in the OR, the abdominal fascia should be left open and covered under sterile conditions (e.g., a vacuum-assisted open abdominal wound closure system) with plans made for a second-look operation and delayed fascial closure. Patients with intra-abdominal hypertension should be monitored closely with repeated examinations and measurements of bladder pressure, so that any further deterioration is detected and operative management can be initiated. Left untreated, ACS may lead to multiple system end-organ dysfunction or failure and has a high mortality.
Abdominal wall closure should be attempted every 48 to 72 hours until the fascia can be reapproximated. If the abdomen cannot be closed within 5 to 7 days following release of the abdominal fascia, a large incisional hernia is the net result. A variety of surgical options have evolved for prevention and closure of the resultant hernias, but no standard approach has yet evolved.
Wounds, Drains, and Infection
Wound (Surgical Site) Infection
No prospective, randomized, double-blind, controlled studies exist that demonstrate antibiotics used beyond 24 hours in the perioperative period prevent infections. Prophylactic use of antibiotics should simply not be continued beyond this time. Irrigation of the operative field and the surgical wound with saline solution has shown benefit in controlling wound inoculum.107 Irrigation with an antibiotic-based solution has not demonstrated significant benefit in controlling postoperative infection.
Antibacterial-impregnated polyvinyl placed over the operative wound area for the duration of the surgical procedure has not been shown to decrease the rate of wound infection.108,109,110,111,112 Although skin preparation with 70% isopropyl alcohol has the best bactericidal effect, it is flammable and could be hazardous when electrocautery is used. The contemporary formulas of chlorhexidine gluconate with isopropyl alcohol remain more advantageous.113,114,115
There is a difference between wound colonization and infection. Overtreating colonization is just as injurious as undertreating infection. The strict definition of wound (soft tissue) infection is more than 105 CFU per gram of tissue. This warrants expeditious and proper antibiotic/antifungal treatment.63,116 Often, however, clinical signs raise enough suspicion that the patient is treated before a confirmatory culture is undertaken. The clinical signs of wound infection include rubor, tumor, calor, and dolor (redness, swelling, heat, and pain). Once the diagnosis of wound infection has been established, the most definitive treatment remains open drainage of the wound. The use of antibiotics for wound infection treatment should be limited.117,118,119,120
One type of wound dressing/drainage system that is gaining popularity is the vacuum-assisted closure dressing. The principle of the system is to decrease local wound edema and to promote healing through the application of a sterile dressing that is then covered and placed under controlled suction for a period of 2 to 4 days at a time. Although costly, the benefits are frequently dramatic and may offset the costs of nursing care, frequent dressing changes, and operative wound débridement.
The four indications for applying a surgical drain are:
To collapse surgical dead space in areas of redundant tissue (e.g., neck and axilla)
To provide focused drainage of an abscess or grossly infected surgical site
To provide early warning notice of a surgical leak (either bowel contents, secretions, urine, air, or blood)—the so-called sentinel drain
To control an established fistula leak
Open drains are often used for large contaminated wounds such as perirectal or perianal fistulas and subcutaneous abscess cavities. They prevent premature closure of an abscess cavity in a contaminated wound. More commonly, surgical sites are drained by closed suction drainage systems, but data do not support closed suction drainage to “protect an anastomosis” or to “control a leak” when placed at the time of surgery. Closed suction devices can exert a negative pressure of 70 to 170 mmHg at the level of the drain; therefore, the presence of this excess suction may call into question whether an anastomosis breaks down on its own or whether the drain creates a suction injury that promotes leakage (Fig. 12-8).121
This illustration demonstrates typical intraoperative placement of closed suction devices in pancreatic or small bowel surgery, where there may be an anastomosis. At negative pressures of 70 to 170 mmHg, these devices may actually encourage anastomotic leaks and not prevent them or become clogged by them.
On the other hand, CT- or ultrasound-guided placement of percutaneous drains is now the standard of care for abscesses, loculated infections, and other isolated fluid collections such as pancreatic leaks. The risk of surgery is far greater than the placement of an image-guided drain.
The use of antibiotics when drains are in place is often unnecessary as the drain provides direct source control. Twenty-four to 48 hours of antibiotic use after drain placement is prophylactic, and after this period, only specific treatment of positive cultures should be performed, to avoid increased drug resistance and superinfection.
Several complications of urinary catheters can occur that lead to an increased length of hospital stay and morbidity. In general, use of urinary catheters should be minimized and every opportunity to expeditiously remove them should be encouraged. If needed, it is recommended that the catheter be inserted its full length up to the hub and that urine flow is established before the balloon is inflated, because misplacement of the catheter in the urethra with premature inflation of the balloon can lead to tears and disruption of the urethra.
Enlarged prostatic tissue can make catheter insertion difficult, and a catheter coudé may be required. If this attempt is also unsuccessful, then a urologic consultation for endoscopic placement of the catheter may be required to prevent harm to the urethra. For patients with urethral strictures, filiform-tipped catheters and followers may be used, but these can potentially cause bladder injury. If endoscopic attempts fail, the patient may require a percutaneously placed suprapubic catheter to obtain decompression of the bladder. Follow-up investigations of these patients are recommended so definitive care of the urethral abnormalities can be pursued.
The most frequent nosocomial infection is urinary tract infection (UTI). These infections are classified into complicated and uncomplicated forms. The uncomplicated type is a UTI that can be treated with outpatient antibiotic therapy. The complicated UTI usually involves a hospitalized patient with an indwelling catheter whose UTI is diagnosed as part of a fever workup. The interpretation of urine culture results of less than 100,000 CFU/mL is controversial. Before treating such a patient, one should change the catheter and then repeat the culture to see if the catheter was simply colonized with organisms. Cultures with more than 100,000 CFU/mL should be treated with the appropriate antibiotics and the catheter changed or removed as soon as possible. Undertreatment or misdiagnosis of a UTI can lead to urosepsis and septic shock.
Recommendations are mixed on the proper way to treat Candida albicans fungal bladder infections. Continuous bladder washings with fungicidal solution for 72 hours have been recommended, but this is not always effective. Replacement of the urinary catheter and a course of fluconazole are appropriate treatments, but some infectious disease specialists claim that C. albicans in the urine may serve as an indication of fungal infection elsewhere in the body. If this is the case, then screening cultures for other sources of fungal infection should be performed whenever a fungal UTI is found.
One of the most debilitating infections is an empyema, or infection of the pleural space. Frequently, an overwhelming pneumonia is the source of an empyema, but a retained hemothorax, systemic sepsis, esophageal perforation from any cause, and infections with a predilection for the lung (e.g., tuberculosis) are potential etiologies as well. The diagnosis is confirmed by chest x-ray or CT scan, followed by aspiration of pleural fluid for bacteriologic analysis. Gram’s stain, lactate dehydrogenase, protein, pH, and cell count are obtained, and broad-spectrum antibiotics are initiated while the laboratory studies are performed. Once the specific organisms are confirmed, anti-infective agents are tailored appropriately. Placement of a thoracostomy tube is needed to evacuate and drain the infected pleural fluid, but depending on the specific nidus of infection, video-assisted thoracoscopy may also be helpful for irrigation and drainage of the infection. Refractory empyemas require specialized surgical approaches.
Postsurgical intra-abdominal abscesses can present with vague complaints of intermittent abdominal pain, fever, leukocytosis, and a change in bowel habits. Depending on the type and timing of the original procedure, the clinical assessment of these complaints is sometimes difficult, and a CT scan is usually required. When a fluid collection within the peritoneal cavity is found on CT scan, antibiotics and percutaneous drainage of the collection is the treatment of choice. Initial antibiotic treatment is usually with broad-spectrum antibiotics such as piperacillin-tazobactam or imipenem. Should the patient exhibit signs of peritonitis and/or have free air on x-ray or CT scan, then re-exploration should be considered.
For patients who present primarily (i.e., not postoperatively) with the clinical and radiologic findings of an abscess but are clinically stable, the etiology of the abscess must be determined. A plan for drainage of the abscess and decisions about further diagnostic studies with consideration of the timing of any definitive surgery all need to be balanced. This can be a complex set of decisions, depending on the etiology (e.g., appendicitis or diverticulitis), but if the patient exhibits signs of peritonitis, urgent surgical exploration should be performed.
Postoperative infections that progress to the fulminant soft tissue infection known as necrotizing fasciitis are uncommon. Group A streptococcal (M types 1, 3, 12, and 28) soft tissue infections, as well as infections with Clostridium perfringens and C. septicum, carry a mortality of 30% to 70%. Septic shock can be present, and patients can become hypotensive less than 6 hours following inoculation. Manifestations of a group A Streptococcus pyogenes infection in its most severe form include hypotension, renal insufficiency, coagulopathy, hepatic insufficiency, ARDS, tissue necrosis, and erythematous rash.
These findings constitute a surgical emergency, and the mainstay of treatment remains wide débridement of the necrotic tissue to the level of bleeding, viable tissue. A gray serous fluid at the level of the necrotic tissue is usually noted, and as the infection spreads, thrombosed blood vessels are noted along the tissue planes involved with the infection. Typically, the patient requires serial trips to the OR for wide débridement until the infection is under control. Antibiotics are an important adjunct to surgical débridement, and broad-spectrum coverage should be used because these infections may be polymicrobial (i.e., so-called mixed-synergistic infections). S. pyogenes is eradicated with penicillin, and it should still be used as the initial drug of choice.
Systemic Inflammatory Response Syndrome, Sepsis, and Multiple-Organ Dysfunction Syndrome
The systemic inflammatory response syndrome (SIRS) and the multiple-organ dysfunction syndrome (MODS) carry significant mortality risks (Table 12-17). Specific criteria have been established for the diagnosis of SIRS (Table 12-18), but two criteria are not required for the diagnosis of SIRS: lowered blood pressure and blood cultures positive for infection. SIRS is the result of proinflammatory cytokines related to tissue malperfusion or injury. The dominant cytokines implicated in this process include interleukin (IL)-1, IL-6, and tissue necrosis factor (TNF). Other mediators include nitric oxide, inducible macrophage-type nitric oxide synthase, and prostaglandin I2.
Table 12-17Mortality associated with patients exhibiting two or more criteria for systemic inflammatory response syndrome (SIRS) ||Download (.pdf) Table 12-17 Mortality associated with patients exhibiting two or more criteria for systemic inflammatory response syndrome (SIRS)
2 SIRS criteria
3 SIRS criteria
4 SIRS criteria
Table 12-18Inclusion criteria for the systemic inflammatory response syndrome ||Download (.pdf) Table 12-18 Inclusion criteria for the systemic inflammatory response syndrome
Temperature >38°C or <36°C (>100.4°F or <96.8°F)
Heart rate >90 beats/min
Respiratory rate >20 breaths/min or Paco2 <32 mmHg
White blood cell count <4000 or >12,000 cells/mm3 or >10% immature forms
Sepsis is categorized as sepsis, severe sepsis, and septic shock. Sepsis is SIRS plus infection. Severe sepsis is sepsis plus signs of cellular hypoperfusion or end-organ dysfunction. Septic shock is sepsis plus hypotension after adequate fluid resuscitation.
MODS is the culmination of septic shock and multiple end-organ failure.122 Usually there is an inciting event (e.g., perforated sigmoid diverticulitis), and as the patient undergoes resuscitation, he or she develops cardiac hypokinesis and oliguric or anuric renal failure, followed by the development of ARDS and eventually septic shock with death.
The international Surviving Sepsis Campaign (http://www.sccm.org/Documents/SSC-Guidelines.pdf) continues to demonstrate the importance of early recognition and initiation of specific treatment guidelines for optimal management of sepsis. Management of SIRS/MODS includes aggressive global resuscitation and support of end-organ perfusion, correction of the inciting etiology, control of infectious complications, and management of iatrogenic complications.123,124,125 Drotrecogin-α, or recombinant activated protein C, appears to specifically counteract the cytokine cascade of SIRS/MODS, but its use is still limited.126,127 Other adjuncts for supportive therapy include tight glucose control, low tidal volumes in ARDS, vasopressin in septic shock, and steroid replacement therapy.
Nutritional and Metabolic Support Complications
A basic principle is to use enteral feeding whenever possible, but complications can intervene such as aspiration, ileus, and to a lesser extent, sinusitis. There is no difference in aspiration rates when a small-caliber feeding tube is placed post-pyloric or if it remains in the stomach. Patients who are fed via nasogastric tubes are at risk for aspiration pneumonia, because these relatively large-bore tubes stent open the gastroesophageal junction, creating the possibility of gastric reflux. The use of enteric and gastric feeding tubes obviates complications of TPN, such as pneumothorax, line sepsis, upper extremity DVT, and the related expense. There is growing evidence to support the initiation of enteral feeding in the early postoperative period, before the return of bowel function, where it is usually well tolerated.
In patients who have had any type of nasal intubation who are having high, unexplained fevers, sinusitis must be entertained as a diagnosis. CT scan of the sinuses is warranted, followed by aspiration of sinus contents so the organism(s) are appropriately treated.
Patients who have not been enterally fed for prolonged periods secondary to multiple operations, those who have had enteral feeds interrupted for any other reason, or those with poor enteral access are at risk for the refeeding syndrome, which is characterized by severe hypophosphatemia and respiratory failure. Slow progression of the enteral feeding administration rate can avoid this complication.
Common TPN problems are mostly related to electrolyte abnormalities that may develop. These electrolyte errors include deficits or excesses in sodium, potassium, calcium, magnesium, and phosphate. Acid-base abnormalities can also occur with the improper administration of acetate or bicarbonate solutions.
The most common cause for hypernatremia in hospitalized patients is underresuscitation, and conversely, hyponatremia is most often caused by fluid overload. Treatment for hyponatremia is fluid restriction in mild or moderate cases and the administration of hypertonic saline for severe cases. An overly rapid correction of the sodium abnormality may result in central pontine myelinolysis, which results in a severe neurologic deficit. Treatment for hyponatremic patients includes fluid restriction to correct the free water deficit by 50% in the first 24 hours. An overcorrection of hyponatremia can result in severe cerebral edema, a neurologic deficit, or seizures.
In 2001, Van den Berghe and colleagues demonstrated that tight glycemic control by insulin infusion is associated with a 50% reduction in mortality in the critical care setting.128 This prospective, randomized, controlled trial of 1500 patients had two study arms: the intensive-control arm, where the serum glucose was maintained between 80 and 110 mg/dL with insulin infusion; and the control arm, where patients received an insulin infusion only if blood glucose was greater than 215 mg/dL, but serum glucose was then maintained at 180 to 200 mg/dL.
The tight glycemic control group had an average serum glucose level of 103 mg/dL, and the average glucose level in the control group was 153 mg/dL. Hypoglycemic episodes (glucose <40 mg/dL) occurred in 39 patients in the tightly controlled group, while the control group had episodes in six patients. The overall mortality was reduced from 8% to 4.6%, but the mortality of those patients whose ICU stay lasted longer than 5 days was reduced from 20% to 10%. Secondary findings included an improvement in overall morbidity, a decreased percentage of ventilator days, less renal impairment, and a lower incidence of bloodstream infections. These finding have been corroborated by subsequent similar studies, and the principal benefit appears to be a greatly reduced incidence of nosocomial infections and sepsis. It is not known whether the benefits are due to strict euglycemia, to the anabolic properties of insulin, or both, but the maintenance of strict euglycemia between 140 and 180 mg/dL appears to be a powerful therapeutic strategy.128,129,130 A number of studies followed this sentinel publication of tight glycemic control. NICE-SUGAR131 and COIITSS132 revisited the Van den Berghe study and found that the glycemic goals found initially to improve outcomes in critically ill patients were now found to be associated with a higher mortality when glucose was kept below 180 mg/dL, due to an increase in incidents of hypoglycemia. When targeted goals of 180 mg/dL are achieved, less occurrences of hypoglycemia have been documented and improved survivorship has been achieved. In addition, some studies find no relationship between glycemic control and improved outcomes. Thus, glycemic control in the critically ill still remains unclear and elusive at best.133,134 Part of the difficulty in achieving “tight glycemic control” is the necessity for frequent (every 1–2 hours) blood glucose determinations. When this is performed, glycemic control is enhanced and hypoglycemia is avoided.
“Stress dose steroids” have been advocated for the perioperative treatment of patients on corticosteroid therapy, but recent studies strongly discourage the use of supraphysiologic doses of steroids when patients are on low or maintenance doses (e.g., 5–15 mg) of prednisone daily. Parenteral glucocorticoid treatment need only replicate physiologic replacement steroids in the perioperative period. When patients are on steroid replacement doses equal to or greater than 20 mg per day of prednisone, it may be appropriate to administer additional glucocorticoid doses for no more than 2 perioperative days.135,136,137
Adrenal insufficiency may be present in patients with a baseline serum cortisol less than 20 μg/dL. A rapid provocative test with synthetic adrenocorticotropic hormone may confirm the diagnosis. After a baseline serum cortisol level is drawn, 250 μg of cosyntropin is administered. At exactly 30 and 60 minutes following the dose of cosyntropin, serum cortisol levels are obtained. There should be an incremental increase in the cortisol level of between 7 and 10 μg/dL for each half hour. If the patient is below these levels, a diagnosis of adrenal insufficiency is made, and glucocorticoid and mineralocorticoid administration is then warranted. Mixed results are common, but the complication of performing major surgery on an adrenally insufficient patient is sudden or profound hypotension that is not responsive to fluid resuscitation.123
Thyroid hormone abnormalities usually consist of previously undiagnosed thyroid abnormalities. Hypothyroidism and the so-called sick-euthyroid syndrome are more commonly recognized in the critical care setting. When surgical patients are not progressing satisfactorily in the perioperative period, screening for thyroid abnormalities should be performed. If the results show mild to moderate hypothyroidism, then thyroid replacement should begin immediately and thyroid function studies should be monitored closely. All patients should be reassessed after the acute illness has subsided regarding the need for chronic thyroid replacement therapy.
Problems with Thermoregulation
Hypothermia is defined as a core temperature less than 35°C (95°F) and is divided into subsets of mild (35–32°C [95–89.6°F]), moderate (32–28°C [89.6–82.4°F]), and severe (<28°C [<82.4°F]) hypothermia. Shivering, the body’s attempt to reverse the effects of hypothermia, occurs between 37 and 31°C (98.6 and 87.8°F), but ceases at temperatures below 31°C (87.8°F). Patients who are moderately hypothermic are at higher risk for complications than are those who are more profoundly hypothermic.
Hypothermia creates a coagulopathy that is related to platelet and clotting cascade enzyme dysfunction. This triad of metabolic acidosis, coagulopathy, and hypothermia is commonly found in long operative cases and in patients with blood dyscrasias. The enzymes that contribute to the clotting cascade and platelet activity are most efficient at normal body temperatures; therefore all measures must be used to reduce heat loss intraoperatively.138
The most common cardiac abnormality is the development of arrhythmias when body temperature drops below 35°C (95°F). Bradycardia occurs with temperatures below 30°C (86°F). It is well known that hypothermia may induce CO2 retention, resulting in respiratory acidosis. Renal dysfunction of hypothermia manifests itself as a paradoxic polyuria and is related to an increased glomerular filtration rate, as peripheral vascular constriction creates central shunting of blood. This is potentially perplexing in patients who are undergoing resuscitation for hemodynamic instability, because the brisk urine output provides a false sense of an adequate intravascular fluid volume.
Induced peripheral hypothermia for hyperpyrexia due to infection (not to include neurologic or cardiac disease) is likely deleterious and does not appear to be beneficial. Placing cooling blankets on or under the patient or ice packs in the axillae or groin may be effective in cooling the skin, and when this occurs, a subsequent feedback loop triggers the hypothalamus to raise the internally regulated set point, thus raising core temperature even higher. This paradoxical reaction may be why outcomes for those who feel the need to treat a fever in the ICU by cooling the skin and arguably the core have worse outcomes. Cooling core temperatures can be achieved reliably with catheter-directed therapy with commercially available devices. Whether this is a worthwhile practice or not may be controversial. Poor data exist in support of treating fevers lower than 42°C in any fashion.133,134,139,140,141,142
Adult trauma patients who underwent induced hypothermia had poor outcomes in a recent investigation, and thus, this remains a procedure to be avoided. In a similar vein, pediatric patients who were induced did not show any improvement, and therefore, induced hypothermia is not recommended. Complications with induced hypothermia include, but are not limited to, hypokalemia, diuresis, DVT (due to catheter-related vein injury), arrhythmias, shivering, undiagnosed catheter-related bloodstream infection, and bacteremia.143,144,145,146
Neurologic dysfunction is inconsistent in hypothermia, but a deterioration in reasoning and decision-making skills progresses as body temperature falls, and profound coma (and a flat electroencephalogram) occurs as the temperature drops below 30°C (86°F). The diagnosis of hypothermia is important, so accurate measurement techniques are required to get a true core temperature.
Methods used to warm patients include warm air circulation over the patient and heated IV fluids, and more aggressive measures such as bilateral chest tubes with warm solution lavage, intraperitoneal rewarming lavage, and extracorporeal membrane oxygenation. A rate of temperature rise of 2 to 4°C/h (3.6–7.2°F/h) is considered adequate, but the most common complication for nonbypass rewarming is arrhythmia with ventricular arrest.
Hyperthermia is a core temperature greater than 38.6°C (101.5°F) and has a host of etiologies (Table 12-19).147 Hyperthermia can be environmentally induced (e.g., summer heat with inability to dissipate heat or control exposure), iatrogenically induced (e.g., heat lamps and medications), endocrine in origin (e.g., thyrotoxicosis), or neurologically induced (i.e., hypothalamic).
Table 12-19Common causes of elevated temperature in surgical patients ||Download (.pdf) Table 12-19 Common causes of elevated temperature in surgical patients
Neuroleptic malignant syndrome
Malignant hyperthermia occurs after exposure to agents such as succinylcholine and some halothane-based inhalational anesthetics. The presentation is dramatic, with rapid onset of increased temperature, rigors, and myoglobinuria related to myonecrosis. Medications must be discontinued immediately and dantrolene administered (2.5 mg/kg every 5 minutes) until symptoms subside. Aggressive cooling methods are also implemented, such as an alcohol bath, or packing in ice. In cases of severe malignant hyperthermia, the mortality rate is nearly 30%.
Thyrotoxicosis can occur after surgery due to undiagnosed Graves’ disease. Hyperthermia (>40°C [104°F]), anxiety, copious diaphoresis, congestive heart failure (present in about one fourth of episodes), tachycardia (most commonly atrial fibrillation), and hypokalemia (up to 50% of patients) are hallmarks of the disease. The treatment of thyrotoxicosis includes glucocorticoids, propylthiouracil, β-blockade, and iodide (Lugol’s solution) delivered in an emergent fashion. As the name suggests, these patients are usually toxic and require supportive measures as well. Acetaminophen, the cooling modalities noted in the previous paragraph, and vasoactive agents often are indicated.