Stress ulceration has been a well-recognized complication of surgery and trauma since 1932, when Cushing reported gastric bleeding accompanying head injury. With later research in gastric physiology and shock, it has been recognized that the appearance of gastric erosion results from failure of the protective function of gastric mucosa and back diffusion of hydrogen ion, enabling gastric acid to injure the mucosa. Once the mucosa is injured, the defenses are further weakened, leading to further injury in a vicious cycle. The protective functions of the mucosa rely on the stomach's rich blood flow to maintain high oxygen saturation. The most critical factor in the development of erosive ulceration now appears to be mucosal ischemia. Once the rich blood supply of the mucosa is compromised, the protective mechanisms are impaired, and gastric acid causes erosion, bleeding, and perforation.
In the late 1970s, the incidence of gastric bleeding in critically ill patients was 15%. Recognition of the importance of organ perfusion has resulted in decreased rates of erosive stress gastritis. Factors often cited for this observation are: improvement in resuscitation and monitoring technology, nutritional support, and effective agents for medical prophylaxis. The prophylactic medicines are targeted to reduce gastric acidity. Antacids have been shown to provide effective protection against erosive ulceration; however, there is some risk of aspiration pneumonia. Antagonists of the histamine-2 (H2) receptors of the parietal cells impair gastric acid secretion and also are effective prophylaxis for erosive ulceration. Due to ease of use, H2-blockers have become the mainstay of stress ulcer prophylaxis in abdominal surgery.83
In the setting of elective operations when the patients are not critically ill, the incidence of stress ulceration is now very low and routine use of ulcer prophylaxis medication has been questioned. In addition, the routine use of H2-antagonists in this setting may lead to increased risk of pneumonia because of failure of the gastric juices to kill bacteria.
Ileus is a condition of generalized bowel dysmotility that frequently impairs feeding in the postoperative setting. Ileus typically occurs after abdominal surgery, even if the bowel itself is not altered. It has been shown that laparotomy alone, without intestinal manipulation, leads to impaired gastrointestinal motility. The small bowel is typically affected the least, and can maintain organized peristaltic contractions throughout the perioperative period. The stomach usually regains a normal pattern of emptying in 24 hours, and the colon is last to regain motility, usually in 48–72 hours.
The exact mechanism that causes postoperative ileus is not known; however, physiologic studies have demonstrated the significant contribution of both inhibitory neural reflexes and local mediators within the intestinal wall. Inhibitory neural reflexes have been shown to be present within the neural plexuses of the intestinal wall itself, and in the reflex arcs traveling back and forth from the intestine to the spinal cord. These neural pathways may account for the development of ileus during laparotomy without bowel manipulation. In addition, inflammatory mediators such as nitric oxide are present in manipulated bowel and in peritonitis and may play a role in the development of ileus.
Ileus can be recognized from clinical signs, such as abdominal distension, nausea, and the absence of bowel sounds and flatus, which should prompt the diagnosis. Abdominal x-ray imaging typically shows dilated loops of small bowel and colon. Bowel obstruction must also be considered with these clinical findings, however, and CT or other contrast imaging may be required to rule out obstruction.
Ileus can also appear following nonabdominal surgery, and can result from the effects of medications (most often narcotics), electrolyte abnormalities (especially hypokalemia), and a wide variety of other factors.
Occasionally, the patient sustains a prolonged period of postoperative ileus. This can be due to a large number of contributing factors, such as intra-abdominal infection, hematoma, effects of narcotics and other medications, electrolyte abnormalities, and pain. In addition, there can be prolonged dysmotility from certain bowel operations, such as intestinal bypass.
The role of laparoscopic surgery in prevention of ileus is controversial. In theory, with less handling of the bowel laparoscopically and with smaller incisions, there should be less stimulation of the local mediators and neural reflexes. Animal studies comparing open and laparoscopic colon surgery indicate earlier resumption of normal motility studies and bowel movements with the laparoscopic approach. Human trials have not been conclusive. Several series demonstrate earlier tolerance of postoperative feeding with the laparoscopic approach to colon resection; however, these have been criticized for selection bias, and such studies are impossible to conduct in a blind fashion.
Early mobilization has long been held to be useful in prevention of postoperative ileus. While standing and walking in the early postoperative period have been proven to have major benefits in pulmonary function and prevention of pneumonia, mobilization has no demonstrable effect on postoperative ileus.
In the expected course of uncomplicated abdominal surgery, the stomach is frequently drained by a nasogastric tube for the first 24 hours after surgery, and the patient is not allowed oral intake until there is evidence that colonic motility has returned, usually best evidenced by the passage of flatus. Earlier feeding and no gastric drainage after bowel surgery can be attempted for healthy patients undergoing elective abdominal surgery, and has a high rate of success provided clinical symptoms of ileus are not present. In such patients, the use of effective preventive strategies is highly effective. These include maintenance of normal serum electrolytes, use of epidural analgesia, and avoidance of complications such as infection and bleeding. The routine use of nasogastric tubes for drainage in the postoperative period after abdominal surgery has come into question since the mid-1990s.
The most effective strategy for management of postoperative ileus following abdominal surgery has been the development of epidural analgesia. Randomized trials have shown that the use of nonnarcotic (local anesthetic–based) epidural analgesia at the thoracic level in the postoperative period results in a decreased period of postoperative ileus in elective abdominal surgery. Ileus reduction is not seen in lumbar level epidural analgesia, suggesting that inhibitory reflex arcs involving the thoracic spinal cord may play a major role in postoperative ileus.
Narcotic analgesia, while effective for postoperative pain, has been shown to lengthen the duration of postoperative ileus, especially when used as a continuous infusion or as PCA. Patients report better control of postoperative pain with continuous infusion or PCA as compared to intermittent parenteral dosing. Many studies have been done comparing various types of opioid analgesics, in attempts to find a type that does not prolong ileus. There has been no clearly superior drug identified; all currently available opioids cause ileus. Opioid antagonists such as naloxone have been used in trials to decrease ileus in chronic narcotic use, and there is evidence that antagonists are effective in that setting; however, in postoperative ileus, the antagonists have not been shown to be clinically useful, again suggesting that other mechanisms are contributing to postoperative ileus.
Early Postoperative Bowel Obstruction
Early postoperative bowel obstruction refers to mechanical bowel obstruction, primarily involving the small bowel, which occurs in the first 30 days following abdominal surgery. The clinical picture may frequently be mistaken for ileus, and these conditions can overlap. The clinical presentation of early postoperative bowel obstruction is similar to that of bowel obstruction arising de novo: crampy abdominal pain, vomiting, abdominal distention, and obstipation. The incidence of early postoperative bowel obstruction has been variable in published series, due to difficulty in differentiating ileus from early postoperative bowel obstruction, but the reported range is from 0.7% to 9.5% of abdominal operations.
Retrospective large series show that about 90% of early postoperative bowel obstruction is caused by inflammatory adhesions. These occur as a result of injury to the surfaces of the bowel and peritoneum during surgical manipulation. The injury prompts the release of inflammatory mediators that lead to formation of fibrinous adhesions between the serosal and peritoneal surfaces. As the inflammatory mediators are cleared and the injury subsides, these adhesions eventually mature into fibrous, firm, and bandlike structures. In the early postoperative period, the adhesions are in their inflammatory, fibrinous form, and as such do not usually cause complete mechanical obstruction.
Internal hernia is the next most common cause of early postoperative bowel obstruction, and can be difficult to diagnose short of repeat laparotomy. Internal hernia occurs when gaps or defects are left in the mesentery or omentum, or blind gutters or sacs are left in place during abdominal surgery. The typical scenario is colon resection involving extensive resection of the mesentery for lymph node clearance. If the resulting gap in the mesentery is not securely closed, small bowel loops may go through the opening and not be able to slide back out. A blind gutter may be constructed inadvertently during the creation of a colostomy. When the colostomy is brought up to the anterior abdominal wall, there is a space between the colon and the lateral abdominal wall, which may also trap the mobile loops of small bowel. Defects in the closure of the fascia during open or laparoscopic surgery can cause obstruction from incarcerated early postoperative abdominal wall hernia. Fortunately, internal hernia is a rare occurrence in the early postoperative period; however, it must be suspected in cases where bowel anastomoses or colostomies have been constructed. Unlike adhesive obstruction, internal hernia requires operative intervention due to the high potential for complete obstruction and strangulation of the bowel.
Intussusception is a rare cause of early postoperative bowel obstruction in adults, but occurs more frequently in children. Intussusception occurs when peristalsis carries a segment of the bowel (called the lead point) up inside the distal bowel like a rolled up stocking. The lead point is usually abnormal in some way, and typically has some intraluminal mass, such as a tumor or the stump of an appendix after appendectomy. Other rare causes for early postoperative bowel obstruction include missed causes of primary obstruction at the index laparotomy, peritoneal carcinomatosis, obstructing hematoma, and ischemic stricture.
Management of early postoperative bowel obstruction depends on differentiation of adhesive bowel obstruction (the majority) from internal hernia and the other causes, and from ileus. Clinicians generally rely on radiographic imaging to discern ileus from obstruction. For many years, plain x-ray of the abdomen was used: if the abdominal plain film showed air-distended loops of bowel and air-fluid levels on upright views, the diagnosis of obstruction was favored. However, plain radiographs can be misleading in the postoperative setting, and the overlap of ileus and obstruction can be confusing. Upper GI contrast studies using a water-soluble agent has better accuracy, and abdominal CT using oral contrast has been shown to have 100% sensitivity and specificity in differentiating early postoperative bowel obstruction from postoperative ileus.
Once the diagnosis is made, management is tailored to the specific needs of the patient. Decompression via nasogastric tube is usually indicated, and ileus can be treated as discussed. Adhesive bowel obstruction warrants a period of expectant management and supportive care, as the majority of these problems will resolve spontaneously. Most surgical texts recommend that the waiting period can be extended to 14 days. If the early bowel obstruction lasts longer than 14 days, less than 10% resolve spontaneously, and exploratory laparotomy is indicated. The uncommon causes of early postoperative bowel obstruction, such as internal hernia, require more early surgical correction, and should be suspected in the setting of complete obstipation, or when abdominal CT suggests internal hernia or complete bowel obstruction.
Patients without a clinical history suggesting renal disease have a low incidence of significant electrolyte disturbances on routine preoperative screening.84 However, those patients with renal or cardiac disease who are taking digitalis or diuretics, or those with ongoing fluid losses (ie, diarrhea, vomiting, fistula, and bleeding) do have an increased risk of significant abnormalities and should have electrolytes measured and replaced preoperatively.
Preoperative urinalysis can be a useful screen for renal disease. Proteinuria marks intrinsic renal disease or congestive heart failure. Urinary glucose and ketones are suggestive of diabetes and starvation in the ketotic state, respectively. In the absence of recent genitourinary instrumentation, microscopic hematuria suggests calculi, vascular disease, or infection. A few leukocytes may be normal in female patients, but an increased number signifies infection. Epithelial cells are present in poorly collected specimens.
Patients with renal insufficiency or end-stage renal disease often have comorbidities that increase their overall risk in the perioperative period. Hypertension and diabetes correlate with increased risk of coronary artery disease and postoperative MI, impaired wound healing, wound infection, platelet dysfunction, and bleeding. Preoperative history should note the etiology of renal impairment, preoperative weight as a marker of volume status, and timing of last dialysis and the amount of fluid removed routinely. Evaluation should include a cardiac risk assessment. Physical examination should focus on signs of volume overload such as jugular venous distention and pulmonary crackles. In patients with clinically evident renal insufficiency, a full electrolyte panel (calcium, phosphorus, magnesium, sodium, and potassium) should be checked preoperatively, along with blood urea nitrogen and creatinine levels. Progressive renal failure is associated with catabolism and anorexia. Such patients need aggressive nutritional support during the perioperative periods to minimize the risk of infection and poor healing.
Dialysis-dependent patients should have dialysis within 24 hours before surgery, and may benefit from monitoring of intravascular volume status during surgery. Blood samples obtained immediately after dialysis, before equilibration occurs, should only be used in comparison to predialysis values to determine the efficacy of dialysis.85
Postoperatively, patients with chronic renal insufficiency or end-stage renal disease will need to have surgical volume losses replaced, but care should be taken to avoid excess. Replacement fluids should not contain potassium, and early dialysis should be employed to address volume overload and electrolyte derangements. Patients with impaired creatinine clearance should have their medications adjusted accordingly. For example, meperidine should be avoided because its metabolites accumulate in renal impairment and can lead to seizures.
The choice of postoperative fluid therapy depends on the patient's comorbidities, the type of surgery, and conditions that affect the patient's fluid balance. There is no evidence that colloid is better than crystalloid in the postoperative period, and it is considerably more expensive.86 Sepsis and bowel obstruction will require ongoing volume replacement rather than maintenance. Ringer's solution provides six times the intravascular volume as an equivalent amount of hypotonic solution. In patients with normal renal function, clinical signs such as urine output, heart rate, and blood pressure should guide fluid management. Once the stress response subsides, fluid retention subsides and fluid is mobilized from the periphery, and fluid supplementation is unnecessary. This fluid mobilization is evident by decreased peripheral edema and increased urine output. Diuretics given in the period of fluid sequestration may cause intravascular volume depletion and symptomatic hypovolemia.
Postoperative management includes close monitoring of urine output and electrolytes, daily weight, elimination of nephrotoxic medications, and adjustment of all medications that are cleared by the kidney. Hyperkalemia, hyperphosphatemia, and metabolic acidosis may be seen and should be addressed accordingly. Indications for renal replacement therapy include severe intravascular overload, symptomatic hyperkalemia, metabolic acidosis, and complicated uremia (pericarditis and encephalopathy) (Table 2-5).
Table 2-5: Guidelines for Perioperative Management of Antithrombotic Medications ||Download (.pdf)
Table 2-5: Guidelines for Perioperative Management of Antithrombotic Medications
|Standard Anticoagulation||Antiplatelet Therapy||Should Warfarin or Antiplatelet Be Stopped Pre-operatively?||Is Bridging Anticoagulation Indicated?||When Should Anticoagulant or Antithrombotic Be Restarted Postoperatively?|
|Low-risk atrial fibrillation||Warfarin goal INR 2.0||None||Yes, 5 days||No||When taking orals|
|Moderate/High-risk atrial fibrillation||Warfarin goal INR 2.0||None||Yes, 5 days||No||When taking orals|
|Mechanical mitral valve||Warfarin goal INR 2.5–3.0||None||Yes, 5 days||Yes||Low bleeding risk: 24 hours High bleeding risk: 48–72 hours|
|Mechanical aortic valve||Warfarin goal INR 2.0||None||Yes, 5 days||Yes||Low bleeding risk: 24 hours High bleeding risk: 48–72 hours|
|Coronary stent||None||Clopidogrel Aspirin||Yes, 5–10 daysNo||No||Low bleeding risk: 24 hours High bleeding risk: 48–72 hours|
|Bare metal coronary stent within 6 weeks||None||Aspirin and Clopidogrel||No||No||Low bleeding risk: 24 hours High bleeding risk: 48–72 hours|
|Drug-eluting stent within 12 months||None||Aspirin and Clopidogrel||No||No||Low bleeding risk: 24 hours High bleeding risk: 48–72 hours|
|History of VTE||Warfarin goal INR 2.0 for at least 3 months||No||Yes, 5–7 days||Low risk: No Moderate/high risk: yes|
Postoperative renal failure increases perioperative mortality. Risk factors for postoperative renal failure include intraoperative hypotension, advanced age, congestive heart failure, aortic cross-clamping, administration of nephrotoxic drugs or radiocontrast, and preoperative elevation in renal insufficiency. Up to 10% of patients may experience acute renal failure after aortic cross-clamping. Postoperative renal failure rates are higher in hypovolemic patients, so preoperative dehydration should be avoided. Contrast nephropathy is a common cause of hospital-acquired renal failure, and manifests as a 25% increase in serum creatinine within 48 hours of contrast administration.
Nephropathy is caused by ischemia and direct toxicity to the renal tubules. Diabetes and chronic renal insufficiency are the greatest risk factors for dye nephropathy. Recent trials87 have shown that patients receiving contrast have a lower incidence of contrast-induced nephropathy when treated with a sodium bicarbonate infusion. N-acetylcysteine given orally on the day prior to contrast exposure also decreases the incidence of radiocontrast nephropathy.88
Rising blood urea nitrogen and creatinine and postoperative oliguria (<500 mL/d) herald the onset of postoperative renal failure. Management is determined by the cause of renal insufficiency. Acute renal failure is classified into three categories: prerenal, intrarenal, and postrenal. Prerenal azotemia is common in the postoperative period. It is caused by decreased renal perfusion seen with hypotension and intravascular volume contraction. Intrarenal causes of oliguric renal failure include acute tubular necrosis (from aortic cross-clamping, shock, or renal ischemia), and less commonly, acute interstitial nephritis from nephrotoxic medication. Postrenal causes include obstruction in the collecting system (from bilateral ureteral injury, Foley catheter occlusion, or urethral obstruction). Workup should include urinalysis, serum chemistries, and measurement of the fractional excretion of sodium. Invasive monitoring and cardiac echocardiogram may be employed to evaluate volume status. Ultrasound is indicated if obstruction is suspected.
Initial management of oliguria in adults includes placement of a bladder catheter, and a challenge with isotonic fluids (500 mL of normal saline or Ringer's lactate). If a bladder catheter is already present, it should be checked to ensure that it is draining properly. A urinalysis should be obtained with special attention to specific gravity, casts, and evidence of infection. Hematocrit should be evaluated to exclude bleeding and blood pressure measured to rule out hypotension as causes. The fractional excretion of sodium can help determine the etiology of the renal failure (Table 2-6). Serum creatinine is used to follow the course of acute renal failure. Patients who have been adequately resuscitated or who are in CHF require evaluation to rule out cardiogenic shock. Urinary retention can be treated with a Foley catheter, and ureteral obstruction can be addressed with percutaneous nephrostomy.
Table 2-6: Oliguria in the Perioperative Patient ||Download (.pdf)
Table 2-6: Oliguria in the Perioperative Patient
|UOsm||>500 mOsm/L||Equal to plasma||Variable|
|UNa||<20 mOsm/L||>50 mOsm/L||>50 mOsm/L|
Intravascular volume depletion adversely affects cardiac output, tissue perfusion, and oxygen delivery. Monitoring includes total body weight, urine output, vital signs, and mental status. However, body weight should not be used alone because total volume overload can be seen in the setting of intravascular volume depletion. Most cases of postoperative renal failure are associated with an episode of hemodynamic instability,47 and perioperative hemodynamic optimization has been shown to decrease acute kidney injury and mortality.89 Invasive monitoring to measure cardiac filling pressures may be utilized when clinical assessment is unreliable.
Fluid overload may be seen in patients with renal, hepatic, and cardiac disease, and is associated with increased morbidity.90 Critically ill patients may develop anasarca. It is difficult to determine volume status by observation alone, and invasive monitoring may be required.
Electrolyte abnormalities are common in the perioperative period. Serum sodium reflects intravascular volume status. Hyponatremia signifies excess free water in the intravascular space, and is caused by excess antidiuretic hormone in the postoperative period. It occurs in the setting of normo-, hypo-, or hypervolemia. It may be avoided by judicious use of isotonic fluids. Conversely, hypernatremia suggests a relative deficit of intravascular free water. Patients who are unable to drink, or those with large insensible losses, are most at risk. Treatment includes free water replacement.
Diuretics, malnutrition, and gastrointestinal losses may cause postoperative hypokalemia. Metabolic alkalosis shifts potassium into the intracellular compartment. Serum potassium levels less than 3 mEq/L warrant ECG monitoring and replacement in patients who are not anuric. Replacement in patients with renal insufficiency may be complex. Hyperkalemia is more commonly seen in renal patients. It may also be seen in myonecrosis, hemolysis, and acidosis. Cardiac arrhythmias are seen at levels above 6.5 mEq/L and death is associated with levels greater than 8 mEq/L. These patients should have cardiac monitoring until their levels normalize. ECG will show widened QRS interval, peaked T waves, and absent P waves. Hyperkalemia should be treated with sodium bicarbonate to stimulate acidosis, as well as intravenous calcium and insulin with glucose to drive potassium into the intracellular compartment. Cation exchange resins can be administered orally or per rectum to bind ions in the gastrointestinal tract, but care should be taken for the patient who is post–GI surgery or has underlying gastrointestinal problems. Dialysis can by employed if other measures fail.