CHAPTER 42: Postoperative Considerations

Many problems following surgery can be avoided by the preoperative risk assessment and prevention strategies described in Chapter 39. However, despite ideal preparation, complications may still develop, and vigilance for these adverse events can help ensure successful convalescence for most patients.

These written instructions address support of each organ system, while normal function is gradually reestablished. Although orders are customized for each woman, goals are common among all surgical patients—resuscitation, pain control, and resumption of daily activities. Table 42-1 offers a template for both inpatient and outpatient postoperative orders.

Fluid and Electrolytes

Nearly half of the average female body’s weight is water. Two thirds of this water is contained in the intracellular compartment, and the remainder is stored extracellularly. This extracellular compartment is divided into a vascular space filled with plasma and an interstitium, which is the collection of small spaces between cells. Of extracellular fluid volume, 25 percent makes up intravascular plasma, and 75 percent fills the interstitium. This 1 to 3 ratio is relevant during fluid resuscitation. Extracellular compartment osmolarity is controlled primarily by sodium and chloride, whereas potassium, magnesium, and phosphate are the major intracellular electrolytes. Osmotic balance is maintained by the free movement of water between the intra- and extracellular spaces.

To support these fluid volumes, the daily liquid requirement for an average adult approximates 30 mL/kg/day. Urine output and insensible losses offset these requirements (Marino, 2007). Thus, postoperatively, crystalloid fluids are primarily used for maintenance and in some cases for resuscitation. Sodium chloride is the main component of these fluids. Because sodium is most abundant in the extracellular space, the fluid is uniformly distributed between the interstitial areas. With crystalloid resuscitation, the primary effect is interstitial volume expansion rather than plasma volume growth. Two of the most commonly used crystalloid fluids for resuscitation and maintenance requirements are isotonic saline and lactated Ringer solution.

Compared with plasma, isotonic saline, also colloquially called normal saline, has a higher chloride concentration (154 mEq/L versus 103 mEq/L) and lower pH (5.7 versus 7.4). Thus, if isotonic saline is infused at large volumes, it can result in a hyperchloremic metabolic acidosis (Prough, 1999). The saline-induced acidosis usually has no adverse clinical consequences, but differentiating it from lactic acidosis (a marker of tissue necrosis) can be challenging in certain settings. Gastric secretions lost during vomiting or nasogastric tube suctioning are commonly replaced by a 5-percent dextrose in 0.45-percent normal saline solution with 20 mEq/L KCl added.

Also known as Hartmann solution, lactated Ringer solution contains potassium and calcium concentrations similar to plasma, but the sodium concentration (130 mEq) is comparatively reduced to that of isotonic saline to maintain cationic neutrality. The addition of 28 mEq/L of lactate necessitates a reduction in chloride concentrations to a level similar to plasma. In sum, the hyperchloremic metabolic acidosis risk observed with large-volume isotonic saline infusion is avoided. Disadvantageously, lactated Ringer solution leads to increased calcium binding of certain drugs that limits their efficacy (Griffith, 1986). Moreover, calcium can bind the citrated anti­coagulant found in blood products and promote clot formation in donor blood. Advantageously, lactated Ringer solution does not significantly change serum lactate levels because only 25 percent of the infused volume remains intravascular. Therefore lactated Ringer solution is commonly employed in cases of isotonic dehydration, such as bowel sequestration in times of obstruction.

Pain Management

Postoperative pain management remains undervalued, and many patients continue to experience intense pain after surgery. A survey by Apfelbaum and colleagues (2003) revealed that more than 85 percent of respondents following surgery have moderate to severe pain. Poor pain control leads to decreased satisfaction with care, prolonged recovery time, increased use of health care resources, and increased costs (Joshi, 2005; McIntosh, 2009). Options for patient analgesia may be broadly classed as opiate-based or nonopioid.

Nonopioid Treatment Options

The two major classes of nonopioid therapies are acetaminophen and nonsteroidal antiinflammatory drugs (NSAIDs). Multimodal pain control postoperatively using intravenous (IV) NSAIDs and/or acetaminophen can reduce or enhance analgesia, lower narcotic needs, decrease the incidence of postoperative nausea and vomiting by as much as 30 percent, and reduce hospital length of stay (Akarsu, 2004; Chan, 1996; Khalili, 2013; Mixter, 1998; Santoso, 2014). In general, these drugs are well tolerated and carry a low risk of serious side effects. However, acetaminophen can be toxic to the liver in high doses. Thus, patients should avoid total doses exceeding 4000 mg/day and use of alcohol while taking acetaminophen-containing products (Food and Drug Administration, 2011). A list of oral NSAIDs and their dosages are found in Table 10-1.

Opioid Treatment Options

Despite the common side effects that all opiates share—respiratory depression and nausea and vomiting—opiate therapy is the primary choice for managing moderate to severe pain. The three most common opiates prescribed after gynecologic surgeries are morphine, fentanyl, and hydromorphone. Meperidine, although commonly administered in many obstetric units, is avoided in part because of neurologic side effects associated with its active meta­bolite, normeperidine. Normeperidine is a cerebral irritant that can cause effects ranging from irritability and agitation to seizure.

Morphine is prescribed most frequently following gynecologic surgery and is a potent μ-opiate-receptor agonist. Action at this receptor accounts for the analgesia, euphoria, respiratory depression, and decreased gastrointestinal (GI) motility seen with morphine. Onset of action is rapid, and peak effects are seen within 20 minutes of IV administration. Its action typically lasts for 3 to 4 hours. Its active metabolite, morphine-6-glucuronide, is renally excreted and thus is well tolerated in low doses in those with liver disease.

Pruritus is common after administration, although its genesis is poorly understood. Some investigators theorize that central opiate receptors are stimulated, whereas others speculate a histamine release as evidenced by urticaria, wheals, and flushing. In these cases, changing to another pain medication is logical. For pruritus treatment, most evidence-based data derive from studies of regional analgesia. Success has been found with ondansetron, 4 mg IV (George, 2009). Antihistamines, such as diphenhydramine (Benadryl) 25 mg IV, are another option. Naloxone, an opioid antagonist, can be used but may reverse the analgesia provided by morphine.

Fentanyl, a potent synthetic opiate, is more lipophilic than morphine and displays a shorter duration of action and half-life. Peak analgesia is reached within minutes of IV administration and lasts for 30 to 60 minutes. Many conscious sedation protocols used during office gynecologic procedures combine fentanyl with a sedative such as midazolam (Versed).

Hydromorphone (Dilaudid), another semisynthetic analogue of morphine, is less lipophilic than fentanyl. It is available for delivery by multiple routes, including oral, intramuscular (IM), IV, rectal, and subcutaneous (SC). Hydromorphone achieves its peak analgesia 15 minutes after IV administration, and its effects last 3 to 4 hours. Although commonly used during epidural analgesia, hydromorphone is a suitable patient-controlled analgesia (PCA) alternative in patients with a morphine allergy. Table 42-2 provides a summary of various pain medications and dosage equivalents.

Hormone Replacement Therapy

Some women will have significant menopausal symptoms after surgical removal of both ovaries. Symptoms can range from severe hot flashes to headaches or sudden mood swings. In these women, estrogen replacement therapy is considered for those without contraindications (Chap. 22). For women completing surgery for endometriosis, a progestin may be added for those with residual disease, as discussed in Chapter 10.

Broad definitions hinder our ability to accurately assess the incidence of postoperative pulmonary complications, but reported estimates range from 9 to 69 percent (Calligaro, 1993; Hall, 1991). Postoperative pulmonary complications include atelectasis, pulmonary embolism (PE), and less commonly, pneumonia and acute respiratory distress syndrome (ARDS). All can potentially lead to acute respiratory failure.

Acute Respiratory Failure

In the general postsurgical population, acute respiratory failure (ARF) has an incidence ranging from 0.2 to 3.0 percent and an associated mortality rate that can exceed 25 percent (Arozullah, 2000; Johnson, 2007). ARF is classically divided into four subtypes defined by inadequate exchange of oxygen or carbon dioxide or both. Type 1 lesions exchange oxygen poorly, and examples include atelectasis, pneumonia, PE, and ARDS, all discussed subsequently.

Type 2 is typified by hypercapnia. It is seen in anesthesia overdose and muscle fatigue, in which ventilation suffers and carbon dioxide (CO₂) is retained. Also, increased metabolic processes such as fever, severe sepsis, overfeeding, and hyperthyroidism can generate excess CO₂. As a result, ventilatory work increases as the body attempts to maintain appropriate arterial pCO₂ levels. This can ultimately lead to respiratory failure.

Type 3 is similar to type 1 but merits a distinct category because of its common occurrence following anesthesia and surgery. Physiologically, general anesthesia reduces muscle tone to decrease lung volumes and airway diameters. The resulting atelectasis and airway closure can drive abnormal gas exchange and ventilation-perfusion mismatching, which creates a decrease in PaO₂. This hypoxemia is further aggravated by hypoventilation from central decreases in respiratory drive, residual effects of anesthetics, lung edema, or bronchospasm (Canet, 1989). To help circumvent type 3 ARF, important considerations include early treatment of hypoxemia, multimodal approaches to pain management, and chest physiotherapy.

Type 4 stems from shock and its associated cardiopulmonary hypoperfusion. For treatment, circulatory resuscitation, discussed in Chapter 40, accompanies oxygen therapy.

Atelectasis

This reversible closure or collapse of alveoli is seen in 90 percent of surgical patients (Lundquist, 1995). Development is associated with decreased lung compliance, gas exchange abnormalities, and increased pulmonary vascular resistance. Thus, characteristic signs are diminished breath sounds, dullness to percussion over affected lung fields, and decreased oxygenation. Pulse oximetry readings >92 percent represent adequate oxygenation, however, a PaO₂ measurement by arterial blood gas will most accurately assess a patient with hypoxic respiratory failure. In addition to bedside findings, chest radiography typically shows linear densities in the lower lung fields. Classically, atelectasis is associated with low-grade fevers. However, Mavros and colleagues (2011) reviewed eight studies with a total of 998 patients and found no association between atelectasis and postoperative fever.

Prevention using lung expansion therapies is described in Chapter 39, and these can be used for treatment as well. Atelectasis is usually temporary (up to 2 days) and self-limited, and it rarely slows patient recovery or hospital discharge (Platell, 1997). Its importance mainly lies in its clinical similarity to PE and pneumonia. Thus, in women with risks for these more life-threatening complications, atelectasis may ultimately be a diagnosis of exclusion.

Hospital-acquired Pneumonia

This is the second most common nosocomial infection in the United States and carries high associated morbidity and mortality rates (Tablan, 2004). Its incidence in surgical patients varies and ranges from 1 to 19 percent depending on surgical procedure and hospital surveyed (Kozlow, 2003). With these infections, bacterial pathogens most typically include aerobic gram-negative bacilli, such as Pseudomonas aeruginosa, Escherichia coli, Klebsiella pneumoniae, and Acinetobacter species.

Clinically, pneumonia is diagnosed if chest radiography reveals a new or progressive radiographic infiltrate and if two of three clinical features (leukocytosis, fever >38°C, or purulent secretions) are present. Broad-spectrum antibiotic regimens are recommended for hospital-acquired pneumonia treatment (Table 42-3). If aspiration is highly suspected, specific treatment for anaerobes with metronidazole or clindamycin is considered. An algorithm supported by the American Thoracic Society is shown in Figure 42-1. Preventive steps include substituting oral endotracheal and orogastric tubes in place of nasal tubes; elevating the head of the bed 30 to 45 degrees, particularly during feeding; and removing subglottic secretions in those unable to clear these (American Thoracic Society, 2005; Ferrer, 2010).

Pulmonary Embolism

If venous thromboembolism (VTE) is suspected, evaluation begins with clinical examination and risk estimation. Wells and colleagues (1995) described one of the most widely used pretest probability assessments for DVT (Table 42-4). When indicated, duplex sonography is highly sensitive for detecting proximal leg DVTs, with a false-negative rate of 0 to 6 percent (Gottlieb, 1999).

For PE, because symptoms may reflect other cardiopulmonary pathology, clinicians often initially elect chest radiography and electrocardiogram (ECG). The radiograph is typically abnormal but nonspecific, and findings can include atelectasis, elevated hemidiaphragm, cardiomegaly, and small pleural effusions (Worsley, 1993). ECG may display tachycardia or may reflect right heart strain by showing a large S wave in lead I, a Q wave in lead III, and inverted T wave in lead III (Stein, 1991). If suspicion for PE remains, then computed tomographic angiography (CTA) or less frequently, ventilation/perfusion (V/Q) scanning is ordered. These serve as alternatives to the invasive gold standards—pulmonary angiography or contrast venography.

Acute management of VTE involves anticoagulation with intravenous unfractionated heparin or subcutaneous low-molecular-weight heparin (Tables 42-5 and 42-6). After achieving adequate anticoagulation, oral vitamin K antagonists such as warfarin are initiated. To avoid paradoxical hypercoagulability, heparin is continued for at least 5 days after the initiation of warfarin (Houman Fekrazad, 2009). Once the international normalized ratio (INR) reaches a therapeutic range of 2 to 3, then heparin is stopped. Long term, anticoagulation therapy duration is dictated by clinical and patient circumstances. For those with a provoked first DVT or PE, anticoagulants are recommended for 3 months. Provocateurs include surgery, exogenous estrogen, or local trauma. Extended therapy is preferred for both those with unprovoked VTE or with second VTE, unless the risk of bleeding is high, in which case, treatment is halted at 3 months. For those with concurrent cancer, therapy is extended regardless of bleeding risk (Kearon, 2012).

Acute Respiratory Distress Syndrome

Acute lung injury that causes a form of severe permeability pulmonary edema and ARF is termed acute respiratory distress syndrome. This is a pathophysiologic continuum from mild pulmonary insufficiency to dependence on high inspired oxygen concentrations and mechanical ventilation. The theory that multiple insults lead to postoperative ARDS offers insight into modifiable intra- and postoperative alveolar damage prevention (Litell, 2011; Warner, 2000). Intraoperative strategies minimize lung trauma by keeping airway pressure and tidal volumes within set limits and by avoiding repeated alveolar opening and closing (Hemmes, 2013). Other measures strive to prevent infection, limit IV fluid volumes, and avoid blood product transfusion (Güldner, 2013).

Myocardial Infarction

Postoperative myocardial infarction (MI) is rare, and its generally reported incidence ranges from nearly 1 percent to as high as 37 percent among patients with surgery within 3 months following an MI (Mangano, 1990; Tinker, 1978). Declines in oxygen supply and increased demand classically underlie this coronary ischemia. Events that decrease oxygen supply include hypotension, lowered coronary perfusion, or poor carrying capacity caused by anemia. Increased afterload, tachycardia, and increased cardiac contractility can raise myocardial oxygen demands.

Most patients with postoperative MI do not have classic symptoms of chest pain or pressure. These are in part masked by postoperative analgesics (Muir, 1991). Dyspnea is the most common complaint and may be accompanied by acute cardiac failure or hemodynamic instability. ECG changes of postoperative MI tend to be less well defined, and most demonstrate a non-Q wave variant (Badner, 1998). CK isoenzyme (CK-MB) abnormalities are seen within 6 hours, and cardiac troponin I and T are highly specific later for diagnosis of MI (Zimmerman, 1999).

Postoperative MI treatment differs from that of nonsurgical patients, and its main tenets focus on shifting the oxygen delivery and utilization balance. Special attention is given to arrhythmia correction and hemodynamic status improvement. Ideally, these patients are cared for in a unit that provides intense monitoring, cardiopulmonary support, and cardiology consultation.

Hypertension

This is frequently encountered both preoperatively and postoperatively. As standard definitions are lacking, the reported incidence ranges from 3 to 90 percent, depending on the thresholds set and the type of surgery. Patients with poorly controlled hypertension preoperatively tend to have more blood pressure lability compared with normotensive patients or those with well-controlled hypertension. In general, a diastolic blood pressure greater than 110 mm Hg preoperatively best predicts those who will have postoperative hypertension issues.

Several possible triggers may raise blood pressures in the first 24 hours after surgery. First, abrupt withdrawal of β-blocker or of centrally acting sympatholytic agents such as clonidine can cause rebound hypertension. Pain and bladder distention may also contribute. Later in postoperative recovery, sympathetic hyperactivity may stem from inadequate pain management or from alcohol withdrawal. Last, return of excess interstitial fluid back into the vascular space may create fluid overload and hypertension.

Two approaches have been described for blood pressure treatment: fixed thresholds and relative changes from baseline. Charlson and colleagues (1990) demonstrated increased rates of postoperative cardiac and renal complications when the mean blood pressure rose 20 percent or more compared with preoperative levels. Given the paucity of good evidence, it is reasonable to initiate treatment if mean blood pressure readings rise by this percentage. With acute blood pressure management, the mean blood pressure should not be lowered by more than 20 percent or to a level less than 160/100 mm Hg.

Postoperative Nausea and Vomiting

This is one of the most common complaints following surgery, and its incidence ranges from 30 to 70 percent in high-risk patients (Møller, 2002). Those at risk for postoperative nausea and vomiting (PONV) include females, nonsmokers, those with prior motion sickness or prior PONV, and those with extended surgeries (Apfelbaum, 2003).

A multimodal approach to prevention is recommended (Apfel, 2004). Currently, combinations of 4 to 8 mg of dexamethasone prior to anesthesia induction are followed, toward the end of surgery, by less than 1 mg of droperidol (Inapsine) and 4 mg of ondansetron (Zofran). This pretreatment significantly reduces symptoms by 25 percent. However, if symptoms develop within 6 hours of surgery, antiemetics from a different pharmacologic class than previously administered are considered (Habib, 2004). Persistent nausea may benefit from combining agents from different classes (Table 42-7).

Bowel Function and Diet Resumption

Normal GI function requires synchronized motility, mucosal transport of nutrients, and evacuation reflexes (Nunley, 2004). However, following intraabdominal surgery, dysfunction of enteric neural activity typically disrupts normal propulsion. Activity first returns in the stomach and is noted typically within 24 hours. The small intestine also exhibits contractile activity within 24 hours after surgery, but normal function may be delayed for 3 to 4 days (Condon, 1986; Dauchel, 1976). Rhythmic colonic motility resumes last, at approximately 4 days following intraabdominal surgery (Huge, 2000). Passage of flatus characteristically marks this return of function, and stool passage usually follows in 1 to 2 days.

Postoperative feeding is most effective when started early. It improves wound healing, promotes gut motility, decreases intestinal stasis, raises splanchnic blood flow, and stimulates reflexes that elicit GI hormone secretion to shorten postoperative ileus (Anderson, 2003; Braga, 2002; Correia, 2004; Lewis, 2001). The decision to initiate “early feeding” with liquids or with solid food has been studied prospectively (Jeffery, 1996). In patients who were given solid food as the first postoperative meal, the number of calories and amount of protein consumed on the first postoperative day were higher. In addition, the number of patients requiring diet changes to NPO (nil per os) was not statistically different (7.5 percent in regular diet and 8.1 percent in the clear diet groups). The improved tolerance and better palatability of solids makes this a reasonable option.

Ileus

Postoperative ileus (POI) is a transient impairment of GI activity that leads to abdominal distention, hypoactive bowel sounds, nausea and vomiting related to GI gas and fluid accumulation, and delayed passage of flatus or stool (Livingston, 1990).

The genesis of POI is multifactorial. First, bowel manipulation during surgery leads to production of contributory factors. These include: (1) neurogenic factors related to sympathetic overactivity, (2) hormonal factors related to the release of hypothalamic corticotropin-releasing hormone (CRH), which plays a key role in the stress response, and (3) inflammatory factors (Tache, 2001). Second, perioperative opioid use also increases POI rates. Thus, in selecting opiates, clinicians balance the beneficial analgesia produced by central opioid receptor binding against the GI dysfunction that results from peripheral receptor binding effects (Holzer, 2004).

No single treatment defines POI management. Electrolyte repletion and IV fluids to reestablish euvolemia are traditional. In contrast, routine nasogastric tube (NGT) decompression to promote bowel rest has been challenged by multiple prospective randomized trials. A metaanalysis including nearly 5240 patients found routine NGT decompression unsuccessful and inferior to its selective use in symptomatic patients. Specifically, patients without NGTs had significantly earlier return of normal bowel function and decreased risks of wound infection and ventral hernia (Nelson, 2007). Additionally, tube-related discomfort, nausea, and hospital stays were reduced. For these reasons, postoperative NGTs are recommended only for symptomatic relief of abdominal bloating and recurrent vomiting (Nunley, 2004).

Gum chewing after laparotomy as a preventive modality for POI has been the focus of several small but randomized studies. In these, sugarless gum is usually chewed 15 to 30 minutes at least three times daily. In evaluations, this practice is associated with earlier improvement in bowel motility markers (Ertas, 2013; Jernigan, 2014). However, compared with placebo, gum chewing achieves these goals on average only several hours earlier (Li, 2013).

Bowel Obstruction

Obstruction of the small intestines may be partial or complete and can result from adhesions following intraabdominal surgery, infection, or malignancy. Of these, surgical adhesions are the most common cause (Krebs, 1987; Monk, 1994). Small bowel obstruction (SBO) develops following 1 to 2 percent of total abdominal hysterectomies, and nearly 75 percent of obstructions are complete (Al-Sunaidi, 2006). Obstruction may be remote from surgery, and the mean interval between primary intraabdominal procedure and SBO approximates 5 years (Al-Took, 1999).

Initial SBO management is similar to that for POI, but distinguishing between the two is important to prevent serious SBO sequelae. During SBO, the bowel lumen dilates proximal to the obstruction, and decompression may develop distally. Bacterial overgrowth in the proximal small bowel can promote bacterial fermentation and worsening dilation. The bowel wall also becomes edematous and dysfunctional (Wright, 1971). Progressive increases in bowel pressure compromise perfusion to the intestinal segment and can ultimately lead to ischemia or rupture (Megibow, 1991).

Clinical signs that may help distinguish SBO from POI include tachycardia, oliguria, and fever. Physical examination may reveal abdominal distention, high-pitched bowel sounds, and an empty rectal vault during digital examination. Last, leukocytosis with a neutrophil dominance should alert to possible coexistent bowel ischemia.

Computed tomography (CT) scanning is the primary imaging tool to identify SBO. Water-soluble contrast can safely help identify the cause and severity of an obstruction. Gastrografin, the most commonly used water-soluble dye, is a mixture of sodium amidotrizoate and meglumine amidotrizoate and may aid resolution of small bowel edema due to its high osmotic pressure. Gastrografin is also theorized to enhance smooth muscle contractility (Assalia, 1994). Although the use of oral Gastrografin does appear to reduce hospital length of stay, it has no therapeutic benefit in adhesion-related SBO (Abbas, 2007).

Treatment of SBO varies with the degree of obstruction. For partial obstruction, feedings are held, IV fluids and antiemetics are initiated, and an NGT is placed for significant nausea and vomiting. Continued surveillance monitors for signs of bowel ischemia. Symptoms in most cases of partial SBO improve within 48 hours. In contrast, for most of those with complete bowel obstruction, surgery to relieve the obstruction is indicated.

Colonic obstruction is rare following gynecologic surgery but carries a high mortality rate (Krstic, 2014). The colon can be obstructed by intrinsic lesions such as colon cancer or diverticulitis-related strictures or can be compressed by a pelvic mass or foreign body, such as a retained surgical sponge. An enlarged cecum found on an abdominal radiograph requires further evaluation by either a barium enema or colonoscopy. Immediate intervention is necessary when the cecal diameter exceeds 10 to 12 cm to minimize perforation risks.

Diarrhea

Transient episodes of postoperative diarrhea are not uncommon after major gynecologic surgery as the GI tract returns to its baseline motility and function. Protracted episodes and excessive amounts of diarrhea almost always stem from infection and warrant further evaluation. Stool samples are examined for ova and parasites, cultured for bacteria, and assayed for Clostridium difficile toxin. Of potential etiologies, broad-spectrum antibiotics can impair normal GI flora growth and thereby promote C difficile toxin-associated pseudomembranous colitis. If toxin is identified, oral metronidazole or vancomycin is initiated and continued for 10 to 14 days after diarrhea resolution (Cohen, 2010). Regardless of the pathogen, aggressive fluid and electrolyte replacement is critical to prevent further aberrations that can delay recovery.

Nutrition

The primary goals of postoperative nutrition are to improve immune function, promote wound healing, and minimize metabolic disturbances. Despite the additional stress in the immediate postoperative period, underfeeding is accepted for a brief period (Seidner, 2006). Table 42-8 offers a summary of basic immediate postoperative metabolic needs. However, extended protein calorie restriction in a surgical patient can lead to impaired wound healing, diminished cardiac and pulmonary function, bacterial overgrowth within the GI tract, and other complications that increase hospital stays and patient morbidity (Elwyn, 1975; Kinney, 1986; Seidner, 2006). If substantial oral caloric intake is delayed for 7 to 10 days, nutritional support is warranted.

In the absence of contraindications, enteral nutrition is preferred to a parenteral route, especially when infectious complications are compared (Kudsk, 1992; Moore, 1992). Other advantages of enteral nutrition include fewer metabolic disturbances and lower cost (Nehra, 2002).

Oliguria

Prerenal Oliguria

Postoperative oliguria is defined as urine production less than 0.5 mL/kg/hr. Oliguria can be caused by a prerenal, intrarenal, or postrenal insult, and a systematic approach typically allows differentiation among these.

Prerenal oliguria is a physiologic response to hypovolemia, and coexistent tachycardia and orthostatic hypotension usually reflect this volume depletion. Causes of postoperative hypovolemia are varied and include acute hemorrhage, vomiting, severe diarrhea, and inadequate intraoperative volume replacement. In response to hypovolemia, the renin-angiotensin system is activated, and antidiuretic hormone (ADH) is released to prompt reabsorption of sodium and water by the renal tubules. Prerenal oliguria is the result of this sequence.

Treatment focuses on volume replacement. Thus, an accurate assessment of the patient’s fluid deficit is critical. Tallying estimated surgical blood loss and data from the intraoperative fluid logs kept by the anesthesiologist will help begin the calculations. Insensible loss during laparotomy approximates 150 mL/hr.

Intrarenal Oliguria

Ischemic injury can lead to necrosis of the renal tubules and decreased filtration. This damage may be more common in a prerenal setting, in which the renal tubules are more vulnerable to insult from nephrotoxic agents such as NSAIDs, aminoglycosides, and contrast media. In many cases, intrarenal and prerenal oliguria can be differentiated by calculating the fractional excretion of sodium (FENa). Using sodium (Na⁺) and creatinine (Cr) levels from both serum and urine, this is defined as:

A ratio <1 suggests a prerenal source, whereas a ratio >3 indicates an intrarenal insult. Another difference is urine sodium levels. In prerenal oliguria, the level is typically <20 mEq/L, whereas in intrarenal states, it usually is >80 mEq/L.

Postrenal Oliguria

The most common cause of postrenal oliguria is urinary catheter obstruction. In those without a catheter, urinary retention is most likely. More seriously, ligation or laceration to the ureter or bladder may be sources. Importantly, partial or unilateral obstruction may exist despite adequate urine output. With this, associated findings may include hematuria, flank or abdominal pain, or ileus.

For diagnosis, renal sonography is highly sensitive and specific for confirming hydronephrosis. Additional diagnostic tools to identify ureteral obstruction include CT with IV contrast or retrograde pyelography. Importantly, IV contrast can be nephrotoxic, and thus CT with contrast may be a less than ideal choice for those with already elevated creatinine levels. As discussed in Chapter 40, the obstruction may be relieved with ureteral stenting alone or may require surgical repair.

Urinary Retention

Inability to void with a full bladder is common after gynecologic surgery, and incidences range from 7 to 80 percent depending on the definition used and surgical procedure (Stanton, 1979; Tammela, 1986). Overdistention can lead to prolonged difficulty with micturition and even permanent detrusor damage (Mayo, 1973). In addition to patient discomfort, recatheterization to treat retention increases the risk of urinary tract infection and may extend hospitalization.

Keita and colleagues (2005) prospectively evaluated risk factors potentially predictive of early postoperative urinary retention. Three major factors were independently associated with an increased risk—age greater than 50 years, intraoperative IV fluid administration greater than 750 mL, and bladder urine volume greater than 270 mL measured upon entry to the recovery room. Among gynecologic procedures, the risk is higher after laparotomy compared with laparoscopy (Bodker, 2003).

Despite identifiable risks, all women are advised on the need for immediate evaluation of absent or difficult voiding. Clinical markers that include pain, tachycardia, urge to void without success, and bladder enlargement by palpation or percussion are diagnostically equivalent to evaluation using bedside bladder sonography (Bodker, 2003).

Once retention is identified, catheterization and bladder drainage should follow. Lau and Lam (2004) sought to determine the best catheterization strategy for managing postoperative urinary retention. Compared with overnight bladder decompression with an indwelling catheter, episodic in-and-out catheterization is equally effective. Moreover, infectious morbidity rates do not significantly differ between the two.

Voiding Trials

Normal urination requires appropriate bladder contractility in the absence of significant urethral resistance (Abrams, 1999). Objective criteria that define normal function postoperatively vary and may be assessed using either active or passive voiding trials.

With an active voiding trial, the bladder is filled with a set volume, and following patient voiding, residual bladder urine volumes are calculated. To begin, the bladder is completely emptied by catheterization. It may be helpful for a woman to stand upright to clear the most dependent portions of her bladder. Next, sterile water infused under gravity is instilled into the bladder through the same catheter until approximately 300 mL is used or until a subjective maximum capacity is reached. A patient is then given up to 30 minutes to void spontaneously into a urine collection device. The difference between volume infused and volume retrieved is recorded as the postvoid residual.

The only published study evaluating the effectiveness of this strategy was reported by Kleeman and associates (2002). They evaluated women following surgery for incontinence and prolapse. In their study, a postvoid residual of less than 50 percent carried a recatheterization rate of 8 percent. If patients could spontaneously void greater than 70 percent of the instilled volume, there were no failures.

A passive voiding trial serves as an alternative, and residuals may be assessed following passive, physiologic filling of the bladder. To begin, the Foley catheter is removed, and a woman is encouraged to drink increased amounts of liquid. She is encouraged to void spontaneously at her first urge to urinate or after 4 hours, whichever is first. Urine volumes in a collection device are measured. An in-and-out catheterization or bladder sonogram is then performed to measure the postvoid residual (Fig. 23-12).

An easy rule to remember for evaluating either active or passive voiding trials is the “75/75 rule,” which is spontaneously voiding greater than 75 mL and voiding greater than 75 percent of the total volume. This constitutes a successful voiding trial and obviates the need for Foley catheter reinsertion. Alternatively, on the Urogynecology Service at Parkland Memorial Hospital, a postvoid residual of less than 100 mL constitutes a success.

Brief periods of confusion are not uncommon after general anesthesia. Delirium is estimated to complicate approximately 10 to 60 percent of all surgical cases (Ganai, 2007). Elderly patients have an elevated risk, which is associated with longer hospital stays, greater hospital costs, and even risk of death (Bilotta, 2013).

The clinical diagnosis of delirium is based on five criteria as outlined by the Diagnostic and Statistical Manual of Psychiatric Disorders (DSM-5): cognition changes, disturbance in attention and awareness, an acutely fluctuating time course, changes unrelated to a neurocognitive disorder, and a direct physiologic cause that underlies the delirium (American Psychiatric Association, 2013). There is no standard definition of postoperative delirium, but most studies note it between 24 and 72 hours after surgery. The Confusion Assessment Method (CAM) is a simple four-question tool, which has a sensitivity of 94 percent and specificity of 89 percent (Table 42-9) (Inouye, 2014).

Risk factors for postoperative delirium can be categorized as modifiable or nonmodifiable. Risks that can be altered include infection, pain, sodium and potassium electrolyte abnormalities, anemia, hypoxia, polypharmacy, sleep-wake cycle disruption, and certain medication classes (American Geriatric Society, 2015; Sanders, 2011). Notable groups are opiates, antihistamines, anticholinergics, benzodiazepines, and dihydropyridines, which include calcium-channel blocking agents. Nonmodifiable factors are increased age, preexisting cognitive deficits, poor preoperative functional status, and comorbid disease.

Treatment for postoperative delirium engages several strategies. First, oxygenation, electrolyte, and fluid imbalances are corrected. Second, pain and potential infection are carefully assessed. In addition, all nonessential medications are halted to minimize confounding factors. Other strategies incorporate increased activity through physical therapy, establishment of distinct sleep-wake cycles, and even light therapy (de Jonghe, 2011; Ono, 2011).

Hypovolemic Shock

Circulatory dysfunction decreases tissue oxygenation and results in multiorgan failure if not recognized and treated promptly. In gynecology, the most frequent cause of shock is hemorrhage-related hypovolemia, although cardiogenic, septic, and neurogenic shock are considered during patient evaluation. Hypovolemic shock may develop before, after, or during surgery, and a full discussion of the topic is found in Chapter 40.

Hyponatremia

This common imbalance is defined as a serum sodium level <135 mEq/L and may produce symptoms as levels drop below 125 mEq/L. Of causes, hypotonic fluid administration is often implicated. Aggressive IV crystalloid resuscitation with comparatively hypotonic fluids is one example. Another is venous absorption of large volumes of certain distending media during long operative hysteroscopy cases (Chap. 41). Second, pain or drugs can induce water retention through a syndrome of inappropriate ADH (SIADH) (Steele, 1997). Alternatively, excessive renal excretion of sodium is seen with diuretic overuse and adrenal insufficiency. Last, extrarenal sodium losses may follow profuse diarrhea, vomiting, or nasogastric suctioning.

Severe hyponatremia can lead to metabolic encephalopathy with associated cerebral edema, seizures, increased intracranial pressure, and even respiratory arrest. Symptoms are not related to the specific serum sodium level as much as to the rate of change in these levels.

Treatment strategies incorporate the patient’s extracellular volume status and the presence or absence of neurologic symptoms. The speed of correction ideally does not exceed 0.5 mEq/L/hr or a serum sodium goal of 130 mEq/L. Over aggressive correction can result in a specific demyelination disorder known as central pontine myelinolysis. In those without symptoms, careful replacement with isotonic fluids and treatment of underlying conditions will correct most cases. Frequent serum sodium levels are drawn to direct care. With associated hypervolemia, furosemide (Lasix) may be added. In those with acute neurologic symptoms, 3-percent saline can be given in a 100 mL infusion over 30 minutes and repeated an additional two times if needed (Nagler, 2014; Verbalis, 2013).

Hypernatremia

Hypernatremia is defined as a serum sodium concentration exceeding 145 mEq/L. Common causes are loss of hypotonic body fluids such as diarrhea, gastric secretions, and sweat. The resulting plasma hypertonicity draws water out of cells to maintain intravascular fluid compartment volume. Brain cell shrinkage can cause vascular bleeds and permanent neurologic damage. To restore brain cell volume, the brain metabolically generates compensatory compounds, termed idiogenic osmoles, which pull water back into its cells. Therefore, aggressive treatment with hypotonic fluids can overcorrect to create cerebral edema, seizure, coma, and even death (Adrogué, 2000). Volume replacement to correct hemodynamic instability is initiated with isotonic fluids or colloid fluids. Then, hypernatremia is corrected using hypotonic solutions.

Diabetes insipidus is a condition of renal water wasting, and an excessive amount of urine devoid of solutes is produced. Central diabetes insipidus is caused by a failure to release ADH whereas nephrogenic diabetes insipidus is caused by a deficit in the renal responsiveness to ADH. As treatment, the free water deficit is replaced over 2 to 3 days. In cases of central diabetes insipidus, the addition of ADH (vasopressin) prevents ongoing free water loss (Blevins, 1992).

Hypokalemia

This imbalance is defined as serum potassium below 3.5 mEq/L. Hypokalemia is usually caused by diarrhea or by abnormal renal loss secondary to metabolic alkalosis. Mild hypokalemia is often asymptomatic, but nonspecific symptoms seen with progression include generalized weakness and constipation. When the serum levels fall below 2.5 mEq/L, muscle necrosis can begin, and an ascending paralysis can develop with levels below 2.0 mEq/L. Hypokalemia in isolation does not produce cardiac arrhythmia, but it can promote dysfunction in combination with magnesium depletion, myocardial ischemia, and digitalis use (Schaefer, 2005).

The cornerstone of hypokalemia management is potassium replacement. Compared with IV replacement, oral potassium is safer, as it enters the circulation more slowly and reduces the risk of iatrogenic hyperkalemia. The maximum rate of IV potassium replacement is 20 mEq/hr, and the patient’s cardiac rhythm is concurrently monitored (Kruse, 1990). Magnesium depletion can cause hypokalemia refractory to replacement efforts, and magnesium may need to be concomitantly replenished (Whang, 1985).

Hyperkalemia

This imbalance is defined as a serum potassium concentration exceeding 5.0 to 5.5 mEq/L. Pseudohyperkalemia can result from traumatic hemolysis, release from muscles distal to a tourniquet, or cellular release from a clotted specimen tube. Unsuspected findings in an asymptomatic patient should prompt a repeat measurement. Transcellular shifts in potassium are seen with digitalis and β-receptor antagonists. More importantly, medication-induced renal excretion impairment is one of the leading causes of hyperkalemia. The most commonly implicated medication classes are angiotensin-converting enzyme (ACE) inhibitors, potassium-sparing diuretics, and NSAIDs (Palmer, 2004; Perazella, 2000).

Hyperkalemia can slow electrical conduction in the heart. The earliest ECG findings of hypokalemia are narrowing and tenting of the T waves. As hyperkalemia progresses, the PR interval lengthens, P waves disappear, and QRS intervals ultimately widen.

Three principles govern hyperkalemia management: (1) protecting the myocardium, (2) shifting potassium intracellularly, and (3) enhancing potassium excretion. Intravenous calcium gluconate administered as 10 mL of a 10-percent solution over 2 to 3 minutes antagonizes the effect of potassium on myocardial repolarization and the conduction system. If there are no improvements in the ECG, calcium administration can be repeated 5 to 10 minutes later. Also, a combination of IV insulin (10 units) and 50 mL of 50-percent dextrose can temporarily shift potassium to the intracellular compartment. In addition, a β2 agonist, such as inhaled albuterol, can help by activating the Na⁺/K⁺-ATPase channel to also drive a potassium shift. Finally, potassium excretion can be cleared across the GI mucosa using sodium polystyrene sulfonate (Kayexelate), cleared renally using loop diuretics, or cleared with dialysis for those with impaired renal function.

Pathophysiology

Fever is a response to inflammatory mediators, termed pyrogens, which originate either endogenously or exogenously. Circulating pyrogens lead to production of prostaglandins (primarily PGE₂), which elevate the thermoregulatory set point. The inflammatory cascade also produces several cytokines after various events, namely, surgery, cancer, trauma, and infection (Wortel, 1993). Thus, fever is common after surgery and is self-limited in most cases (Garibaldi, 1985). However, for those with persistent symptoms, a systematic approach to patient evaluation helps differentiate inflammatory from infectious etiologies.

Fevers that develop more than 2 days after surgery are more likely to be infectious. More broadly, causes may be categorized by the mnemonic, the “Five Ws,” which represent wind, water, walking, wound, and “wonder” drug. First, pneumonia is considered, and women at greatest risk are those who have been mechanically ventilated for a prolonged period, have an NGT in place, or have preexisting chronic obstructive pulmonary disease (COPD). Second, catheterization places women at risk for urinary tract infection. Logically, catheterization duration correlates positively with this infection risk. Third, VTE may present with low-grade fever and other disease-specific symptoms. For example, women with DVT often complain of unilateral lower-extremity edema and erythema. Those with PE may note dyspnea, cough with blood-tinged sputum, chest pain, tachycardia, and symptoms of hypotension. Fourth, fever related to surgical site infections usually develops 5 to 7 days after surgery. These infections may involve the pelvis or abdominal wall layers. Last, medications commonly used postoperatively—such as heparin, β-lactam antibiotics, and sulfonamide antibiotics—may cause a rash, eosinophilia, or drug fever.

Clinical Evaluation

In multiple studies, fever evaluations that rotely include complete blood count (CBC), urinalysis, blood cultures, and chest radiographs are reported to be ineffective (Badillo, 2002; de la Torre, 2003; Schey, 2005). Thus, initial assessment of a woman with postoperative fever is individualized and begins with a focused history and physical examination. The simple diagnostic algorithm presented in Figure 42-2 can be used as one high-yield, cost-effective strategy. Treatment of wound infections is described in Chapter 3, whereas management of pulmonary complications and VTE were discussed earlier.

Acute Wound Healing

Wound healing has three phases—inflammatory reaction, proliferation, and remodeling (Li, 2007). Hemostasis by coagulation initiates the first step in the inflammatory phase. The infiltration of leukocytes and release of cytokines helps initiate the proliferative phase of wound repair. During this, two activities happen simultaneously–the growth of granulation tissue to fill the wound and the formation of epithelium to cover the wound. The final stage, remodeling, restores the structural integrity and functional aptitude of the new tissue.

Wound Dehiscence

Classification and Incidence

The depth to which a wound may open varies and may involve only the subcutaneous and skin layers. Such superficial separation can result solely from a hematoma or seroma, but more commonly is a consequence of wound infection. The reported incidence of superficial separations ranges from 3 to 15 percent (Owen, 1994; Taylor, 1998).

More seriously, separation can include the abdominal wall fascia. Fascial dehiscence occurs less frequently and is fatal in nearly 25 percent of cases (Carlson, 1997). Infection or sutures held under too much tension are notorious causes and lead to fascial necrosis. Sutures remain poorly anchored in necrotic fascia (Bartlett, 1985). These layers then separate with only minimal increases in intraabdominal pressure.

Prevention

Rates of wound dehiscence are affected by general patient health, surgical technique, and risks associated with wound infections. Of these, patient health factors may or may not be ­modifiable. Characteristics that confer an increased wound disruption risk include age greater than 65 years, pulmonary disease, malnutrition, obesity, malignancy, immunocompromised states, diabetes mellitus, and hypertension (Hodges, 2014; Riou, 1992).

Using proper surgical technique, a surgeon has multiple opportunities to lower wound disruption rates. Described in greater detail in Chapter 40, ideal technique advocates hemostasis, gentle tissue handling, removal of devitalized tissue, closure of dead space, use of monofilament suture in ­tissue at risk for infection, judicious use of closed-suction drains, and sustained normothermia (Mangram, 1999).

Last, infection is a common underlying cause of wound disruption. Risk factors for infection are numerous and are listed in Table 3-18. Of these, many conditions can be improved preoperatively (Table 42-10).

Diagnosis

Superficial wound separations usually present 3 to 5 days after surgery, with wound erythema and new drainage. A delay in evacuating inflammatory exudates from within subcutaneous-layer dead space can lead to fascial weakening and an increased risk of fascial dehiscence.

Fascial dehiscence generally presents within the first 10 days postoperatively. Superficial disruption of the subcutaneous layer and extensive leakage of peritoneal fluid or purulent drainage are indicative. Given the high mortality risk associated with fascial dehiscence and bowel evisceration, examination under anesthesia to estimate the extent of separation is often warranted.

Superficial Wound Dehiscence Treatment

Wet-to-dry Dressing Changes

With initial wound management, all hematomas, seromas, or pus are evacuated, and necrotic tissue is debrided. If needed, underlying infection is treated with antibiotics. As discussed in Chapter 3, most abdominal wound infections that follow clean cases originate from Staphylococcus aureus. In contrast, those after clean-contaminated cases have a greater chance of being polymicrobial. Thus, antibiotic regimens that cover gram-positive and gram-negative organisms are suitable (Table 3-20). In these infections, anaerobes play a lesser role. Importantly, the number of infections caused by methicillin-resistant Staphylococcus aureus (MRSA) has increased dramatically, and coverage for this pathogen is considered.

After evacuation, wounds are typically gently filled with fluffed-out gauze to provide continued wound drainage and access for additional debridement. This dressing is usually removed daily and replaced with new moist gauze. Solutions used in this dressing remove surface bacteria without disrupting normal healing components. Thus, povidone iodine, iodophor gauze, dilute hydrogen peroxide, and Daiken solution, which are cytotoxic to white blood cells, should play a limited role in wound care (Bennett, 2001; O’Toole, 1996). In very necrotic wounds, allowing gauze to dry and pulling tissue adherent to the gauze with each change is acceptable. More frequent dressing changes are avoided as they lead to aggressive debridement of vital tissues and slow wound healing. Table 42-11 lists products used in modern wound care.

Negative-pressure Wound Therapy

This is primarily used for acute wounds to minimize scarring or for chronic wounds that have been resistant to other forms of wound care. The five mechanisms by which this technology aids wound healing are wound retraction, continuous wound cleaning, stimulation of granulation tissue formation, reduction of interstitial edema, and removal of exudates. The external forces create microdefects in individual cells that stimulate the cellular repair process and lead to cell proliferation within the wound. The negative pressure generated by such devices provides three wound care actions: (1) evacuates wound drainage to reduce bacterial colonization, (2) promotes release of cytokines that are helpful in wound healing, and (3) increases blood flow and oxygenation to tissues to uniformly reduce wound size and improve angioneogenesis (Fabian, 2000; Morykwas, 1997; Sullivan, 2009).

The two most commonly used dressings are foam and moistened nonadherent cotton gauze. After the initial application, the dressing is typically changed within 48 hours and then two to three times a week thereafter. After the dressing is covered with an adhesive film dressing, a suction-generating evacuation tube runs through the dressing to help draw excessive exudates away from the wound and into a canister attached at the other end (Fig. 42-3). The vacuum pump offers either continuous or intermittent negative pressure.

Delayed Primary Closure

Approximately 4 days after wound disruption and resolution of subcutaneous infection, a superficial vertical mattress closure with delayed-absorbable suture may be used to reapproximate tissue edges (Wechter, 2005). Depending on wound depth and patient tolerances, this can be completed in the operating room or at the bedside using a local anesthetic complemented by systemic analgesia. Overall, this strategy reduces healing time by 5 to 8 weeks and significantly decreases the number of postoperative visits.

Fascial Dehiscence Treatment

Early recognition of abdominal wall separation is critical in reducing the serious morbidity and mortality rates. Fascial dehiscence is regarded as a surgical emergency, and a gynecologist must first determine if it is associated with evisceration of abdominal content. If abdominal contents are extruded, sterile towels soaked in saline and an outer abdominal binder can be used to cover and gently replace abdominal contents. Broad-spectrum antibiotics are generally recommended to minimize ensuing peritonitis.

The final goal of treatment is fascial closure. For critically ill patients with significant edema, temporarily maintaining anterior abdominal wall integrity with retention sutures until a patient is stable enough to tolerate a definitive operative closure is reasonable. After sufficient debridement of necrotic or infected tissue under general anesthesia, fascial closure may be performed. An interrupted mass closure using a no. 2 permanent suture is typically recommended. However, if primary fascial closure is under significant tension, a synthetic mesh bridge may be required. Typically considered a dirty wound, the subcutaneous layer is often left open. Wet-to-dry dressing changes are performed until the decision is made to proceed with delayed primary closure or allow secondary intention to compete the process (Cliby, 2002).