Chapter 28: Abdominal Emergencies

The patient is suffering from a gastrointestinal bleed (GIB). Two large-bore intravenous catheters (16 gauge or larger) are necessary to initiate resuscitation with crystalloid and colloid fluids or blood products. When peripheral venous access cannot be obtained, a central venous line such as a Cordis catheter (Cordis Corp, Bridgewater, NJ) should be inserted. An arterial line should be inserted for beat-to-beat monitoring of systemic blood pressure. Four units of packed red blood cells (PRBCs) and 4 units of fresh-frozen plasma should be typed and crossed. Bedside assessment of end-organ perfusion and serial laboratory testing (basic metabolic profile, hemoglobin level, coagulation studies) guide transfusions and prevent delayed resuscitation and hypoperfusion. Vasoactive agents are administered during fluid resuscitation to maintain an adequate perfusion pressure.

This patient has a protected airway, but endotracheal intubation should be considered in patients with massive hemoptysis, shock, or obtundation. A nasogastric tube (NGT) should be placed to assess the site and rate of bleeding. If the abdomen is distended or if the patient complains of abdominal pain, a KUB (kidneys, ureters, and bladder) film should be performed and evaluated.

The differential diagnosis of GI bleeding in critically ill patients is broad (Table 28-1). Observation of bright red blood with coffee grounds appearance on NGT lavage suggests an upper gastrointestinal (UGI) source (originating proximal to the ligament of Treitz). UGI bleeding accounts for approximately 75% of GI bleeds and has a mortality rate of 20% to 30% in hospitalized patients.¹ Intensive care unit (ICU) patients whose lungs are mechanically ventilated for more than 48 hours have coagulopathy, a history of GI ulceration, or bleeding within the last 12 months or two of the following risk factors: sepsis, ICU admission longer than 7 days, occult bleeding of 6 days or longer, or daily use of 250 mg of hydrocortisone or an equivalent are at risk for stress-related mucosal damage.² A history of alcoholism, cirrhosis, or portal hypertension is often elicited in patients with variceal bleeding. Although melena is more common in patients with UGI bleeding, melena is also observed in patients with lower GI bleeding.

Patients whose lungs are mechanically ventilated are at risk for mucosal damage and should be receiving medications to prevent stress gastritis. Prophylactic medications to prevent erosive gastritis include proton pump inhibitors, sucralfate, antacids, and histamine-2 receptor blockers. In patients who suffer from a GIB, a proton pump inhibitor infusion should be initiated. Pepsin is inactivated and cannot effectively lyse clots at pH levels greater than 6. Prescribing proton pump inhibitors with endoscopic hemostasis decreases the risk for rebleeding, the need for surgery, and mortality.^{3, 4} Eighty milligrams of omeprazole or pantoprazole are bolused intravenously to achieve rapid gastric acid suppression. An infusion is started at 8 mg per hour for 72 hours.⁵

Seventy-five to 80% of UGI bleeding ceases with supportive care, but patients who are at high risk for rebleeding or death require endoscopic evaluation and treatment.^{6, 7, 8, 9} The Glasgow Blatchford Scale (GBS) score aids in predicting which patients are high risk. The GBS is an assessment tool developed to predict a patient's need for further medical or endoscopic treatment for UGI bleeding (Table 28-2). The GBS gives scores to multiple clinical and laboratory parameters, and 50% of patients with a score greater than 6 need endoscopic intervention.^{10, 11, 12} Even without a recent BUN (blood urea nitrogen), the patient has a GBS score of 11 and should get an EGD for further evaluation and treatment. EGD identifies the location and type of bleeding in 90% of cases and decreases the mortality from hemorrhage.¹³

EGD also aids in the prognostication of patients with UGI bleeding. Multiple studies have taken into consideration clinical factors and findings on endoscopy to determine the risk of rebleeding and mortality (Table 28-3).^{14, 15, 16} Risk of rebleeding and mortality increases with the number of indicators present.

Experienced endoscopists achieve hemostasis in 90% of patients with UGI bleeding.^{17, 18, 19} In patients who continue to bleed, arterial embolization by interventional radiologists or surgical intervention may be necessary. Surgery for acute GIB carries a mortality rate of 20% to 35%. Therefore, noninvasive intervention is often preferred prior to surgical intervention in unstable patients.^{20, 21}

Interventional radiology should be consulted for an angiogram and possible embolization in this patient. Transcatheter arteriograms are successful in localizing the bleeding vessel in 75% of cases.²² Treatment with hemostatic therapy carries a long-term success rate of up to 65% with a low rate of complications.²³ There are few studies directly comparing efficacy, morbidity, and mortality of transcatheter interventions versus surgery, but transcatheter treatment for UGI bleeding does not increase mortality rate.^{24, 25}

The proton pump inhibitor infusion should be continued for 72 hours to prevent upper GI rebleeding. Hematocrit levels should be evaluated every 4 hours for 24 hours. The patient's coagulation factors should be evaluated. The patient may develop a dilutional coagulopathy secondary to administration of PRBCs without the administration of plasma. A troponin level should be ordered to assess myocardial damage in the setting of his protracted anemia and hemodynamic instability. Urine output and serum creatinine are followed closely. Hypotension places this patient at risk for acute kidney injury (AKI) (Figure 28-1).

A bladder pressure of 15 mm Hg suggests intra-abdominal hypertension (IAH) (Table 28-4). IAH is elevated intra-abdominal pressure (IAP). The normal IAP is 0 to 5 mm Hg, but it varies with body habitus and different disease states (Table 28-5). There are many risk factors for IAH (Table 28-6), and they include sepsis, large-volume resuscitation, abdominal masses, pancreatitis, and abdominal surgery. After aggressive volume resuscitation in patients with a capillary leak syndrome, abdominal and bowel wall edema occurs, increasing abdominal pressure. IAH increases patient morbidity and mortality rates.^{26, 27, 28, 29}

There are several ways to measure IAP. Physical examination alone has not been shown to be sensitive in detecting IAH.^{30, 31} Direct measurement of IAP is possible, but requires placement of either a needle, catheter, or other pressure-monitoring device directly into the abdominal cavity. Direct measurement is complex and invasive. Measuring gastric or rectal pressures can make indirect estimations of IAP, but current standard of care is via bladder pressure measurement. Studies have shown bladder pressure measurements to be a cost-effective, safe, and accurate instrument for identifying IAH and guiding therapy.^{32, 33, 34, 35, 36} Measurements are made by attaching a pressure-monitoring system to the injection port of a Foley catheter (Table 28-7). The Abdominal Compartment Syndrome World Congress currently recommends an intravesicular volume of 25 mL.³⁷ Previous recommendations suggested the use of 50 to 100 mL of normal saline, but studies have shown that larger injection volumes can lead to falsely elevated IAP.^{38, 39, 40} Bladder pressures should be measured regularly in patients with or at risk for IAH to aid in diagnosis and management. The optimal frequency of bladder pressure monitoring has not been determined, but every 4 to 6 hours while critically ill should be sufficient.

The pathophysiology of IAH is complex (Figure 28-2). An increase in IAP limits venous return and decreases left ventricular preload. Abdominal pressure increases systemic vascular resistance, resulting in increased afterload. Decreased preload and increased afterload result in decreased cardiac output. The cardiovascular system initially compensates with an elevation in the heart rate to maintain cardiac output. Abdominal pressure is transmitted to the thoracic cavity, which compresses the lungs and increases airway pressures. These physiologic changes can result in hypotension, which can lead to mesenteric ischemia and AKI and hypoxemia. Unfortunately, aggressive treatment often leads to worsening IAH and continued clinical deterioration (Figure 28-3).

An IAP of 15 mm Hg can affect ICP, CPP, and cerebral blood flow. An increased intrathoracic pressure elevates central venous pressures and decreases venous drainage from cerebral vessels. Cerebral venous congestion leads to elevated ICP, resulting in intracranial hypertension (ICP greater than 20 mm Hg). The pressure inside the cranium is directly proportional to the volume of its contents: blood, cerebrospinal fluid, and brain. Without adequate venous drainage, the volume inside the cranium increases. To compensate, cerebrospinal fluid shifts into the spinal column, but this is only a temporary solution. Eventually, the ICP will rise and stay elevated unless treated. Given her recent craniotomy and tumor removal, this patient needs to be evaluated for elevated ICP.

In nontraumatic brain injury patients, elevated IAP was associated with increased ICP and decreased CPP even at lower abdominal pressures.⁴¹ A study of neurotrauma patients showed that ICP rose by artificially elevating IAP to an average of 15.5 mm Hg.⁴² The concern for intracranial hypertension in this patient population comes from the relationship between ICP and CPP. CPP is the difference between mean arterial pressure (MAP) and ICP (CPP = MAP – ICP). An elevation in ICP without an increase in mean arterial pressure will result in decreased CPP, decreased oxygen delivery to the brain, progressive encephalopathy, and cell injury. Medical management for intracranial hypertension should be initiated in patients with IAH and elevated ICP. Intracranial hypertension secondary to brain injury or IAH may be refractory to medical therapy. Decompressive laparotomy has been shown to be useful in decreasing ICP in traumatic brain injury patients with refractory intracranial hypertension.^{43, 44}

Stratifying IAPs guides management to prevent end-organ damage and clinical deterioration.³⁷ An intra-abdominal pressure of 15 mm Hg is consistent with grade I IAH, and the recommended management is medical therapy (Table 28-8). An increase in IAP to 20 mm Hg indicates clinical deterioration. The patient now has grade II IAH. Suggested treatment is abdominal decompression if end-organ dysfunction is present. Hypotension, elevated airway pressures, and oliguria indicate end-organ dysfunction. The surgical service should be consulted to evaluate this patient.

Until the surgical team is available to evaluate and possibly operate on the patient, medical management of IAH must be initiated (Figure 28-4). Medical management relies on nonoperative interventions to aid in reducing IAP. There are several medical treatment options to improve abdominal wall compliance, beginning with deepening sedation and analgesia. Most heavily sedated patients will relax their abdominal muscles, resulting in less ventilator dyssynchrony. If heavy sedation does not improve peak airway pressures or ventilation, neuromuscular blockade is considered. If abdominal muscle tension complicates IAH, paralysis will reduce the IAP.^{45, 46, 47} The risks of prolonged neuromuscular blockade, namely, myopathy, are weighed against the benefits of IAP reduction. If there are no contraindications, an NGT, suppository, and enema can decompress the GI tract. Diuretics can decrease third spacing and abdominal wall edema but may compromise hemodynamics in a hypotensive patient. If the oliguria persists or anuria develops, initiation of continuous venovenous hemodialysis to aid in fluid removal or correction of acidemia may be necessary. Percutaneous abdominal decompression can decrease IAH or reverse abdominal compartment syndrome (ACS) when the patient has a fluid collection such as ascites, hematoma, or abscess.^{48, 49, 50, 51, 52} Without current abdominal imaging, abdominal drainage carries an unacceptably high risk of accidental visceral perforation or bleeding; therefore, abdominal ultrasound or abdominal CT scanning may be of some benefit. It will help determine if the patient has primary or secondary ACS.

Abdominal perfusion pressure (APP) should be calculated in patients with elevated bladder pressures. APP is calculated from the difference between the MAP and the IAP (APP = MAP − IAP). Hemodynamic therapy targets an APP of 60 mm Hg. In patients with an IAP of 20 mm Hg, a MAP of 80 mm Hg will likely maintain adequate perfusion pressure to the abdominal organs, including the kidneys, liver, and intestines.^{37, 53, 54, 55} Maintaining adequate APP may improve survival, although no prospective randomized controlled trials have been completed. Strategies to maintain APP include fluid administration and vasopressor therapy. Maintaining adequate intravascular volume is an important concept in patients with IAH. Hypovolemia will further aggravate reductions in preload. The use of central venous pressure or pulmonary artery catheter measurements to guide therapy is controversial. The increase in intrathoracic pressure may falsely elevate both central venous and pulmonary pressures, making the use of these indices in fluid administration difficult.

The diagnoses of abdominal abscess, hematoma, perforated viscus, or obstruction of the intestines are unlikely because there is no evidence of a fluid collection, free air, or distention of the small bowel. Based on peripancreatic inflammation and edema, the radiologist confirms the diagnosis of pancreatitis. Several recent studies have suggested that patients with pancreatitis frequently develop IAH with worsening organ dysfunction.^{56, 57} ACS develops when fluid resuscitation for peripancreatic and retroperitoneal inflammation increases visceral edema; pancreatic fluid collections increase abdominal pressure, and paralytic ileus develops.⁵⁸ Patients with pancreatitis undergo surgery for debridement when there is infected necrosis or when an abscess or pseudocyst needs to be drained.

Historically, patients with pancreatitis have been placed on bowel rest, but this is quickly changing. Studies have shown that early enteral feeding may decrease the inflammatory response of pancreatitis.⁵⁹ Enteral feeding may also reduce/prevent the breakdown in gut mucosal defenses, which aid in preventing sepsis in pancreatitis patients.⁶⁰ The data suggest that enteral feeding decreases infection rates, need for surgical intervention, and shortens hospital stay. No effect on mortality has been proved. Pancreatic ileus is common and there are no current recommendations for jejunal versus gastric feedings. There are no specific recommendations to guide enteral feeding for moderate versus severe pancreatitis.⁶¹ This patient has an acute abdominal process that requires the patient to remain supine and may require surgical therapy. Initiating enteral feeding at this time will increase the patient's risk for aspiration.

Head of bed elevation greater than 30 degrees is standard of care for prevention of aspiration pneumonia in intubated and mechanically ventilated patients.^{61, 62} IAP, however, increases with increasing elevation of the head of the bed. Head of bed elevation of 20 degrees caused clinically significant increases in IAP by 2 mm Hg or more.³⁷ Bladder pressure measurements are made in the supine position. If head of the bed is being elevated in between measurements, then the supine measurements of IAP will underestimate the "true" IAP. Prone positioning has also shown to increase IAP, and should not be used in a patient with IAH.^{63, 64, 65} Further research is needed to truly understand the effects of body positioning on IAP. Until then, consider the potential risks of body positioning in patients with mild to moderate IAH.

This patient has ACS. An elevation in lactate suggests abdominal organ hypoperfusion. Acidosis develops from azotemia, hyperlactatemia, and hypercarbia from a decrease in minute ventilation. This patient is developing multisystem organ failure. The patient's AKI has progressed to acute kidney failure. He may require dialysis to manage his fluid balance. Surgical decompression is the gold standard of treatment for ACS. At this point, a delay in surgical decompression increases the patient's mortality.⁵³

After decompressive laparotomy, a temporary abdominal closure device is placed to protect the abdominal viscera and allow for continued expansion. All patients are at risk for recurrent ACS if the device is not large enough to accommodate the expanding viscera. Bladder pressures should continue to be monitored every 4 to 6 hours until the patient is clinically stable. Monitoring renal perfusion pressure and evaluating the patient for acute indications for renal replacement therapy are important.

Increased residual volumes are observed with improper tube placement, feeding tube migration to the proximal stomach or esophagus, gastroparesis, and ileus. Ileus occurs after opioid administration, abdominal infection, and bowel edema. Bilious emesis and abdominal distention should arouse concern for something more serious than feeding tube displacement, ileus, or gastroparesis (Table 28-9). The history of diarrhea followed by absent flatus or bowel movements suggests a bowel obstruction. Intermittent pain and bilious emesis suggest an obstruction of the upper GI system rather than a colonic obstruction, but without imaging it remains unclear. Enteral feeds should be held when residual volumes are greater than 200 mL. Assessment of bowel motility and GI function is performed. Abdominal (upright and supine) films are ordered to evaluate distention of the stomach and intestines. An 18-F nasogastric tube can be inserted to decompress the proximal GI tract via continuous low-wall suction. The patient is assessed for evidence of bowel ischemia.

(Figure 28-5)

The abdominal radiograph shows multiple loops of dilated small bowel, which suggests a small-bowel obstruction. Surgical management considers the clinical picture and classification of the small bowel (Table 28-10). Early treatment (< 36 hours) of a strangulated small-bowel obstruction improves survival.^{66, 67}

The terminology of partial versus complete obstruction is based on abdominal radiographic evidence, and 65% to 80% partial obstructions resolve without surgery.⁶⁸ It can be difficult to determine the degree of obstruction or the etiology from plain films and clinical evaluation (Table 28-11). The clinical feature of continuous abdominal pain is common in patients with strangulated bowel, but its presence is not definitive.

There are a number of radiographic studies and treatments that can aid in evaluating a patient with possible small-bowel obstruction (SBO). A small-bowel enteroclysis, which is a real-time radiographic examination with oral contrast, can be performed at the bedside. This should be performed without barium when there is concern of ischemia or perforation because barium can cause peritonitis if it enters the abdominal cavity.^{69, 70, 71} Contrast-enhanced CT is becoming the study of choice for SBO evaluation. CT scan has a sensitivity and specificity of 82% to 100% for detecting cause of obstruction, location of a transition point, bowel wall edema, signs of ischemia, and extraluminal pathology.^{71, 72, 73}

Postoperative adhesions and hernias cause 70% of SBO, and this patient has had multiple surgeries to repair ventral hernias (Figure 28-6). Postoperative adhesions develop in 95% of adult patients after abdominal surgery.⁷⁴ Common practice for nonstrangulated adhesive SBO involves the administration of Gastrografin. Gastrografin is a water-soluble, radiopaque, hypertonic liquid oral contrast that is used to diagnose and treat adhesive SBOs. It draws fluid into the lumen from the bowel wall, decreasing edema and promoting peristalsis. For patients with possible adhesive SBO, 100 mL of Gastrografin is given via NGT. The NGT is clamped for 2 hours. A repeat abdominal film is taken 4 to 12 hours later. If Gastrografin passed into the colon, then the SBO is partial. If Gastrografin is not in the colon after 6 hours, the obstruction is classified as complete.⁷⁵ Gastrografin passage into the colon is strongly predictive of resolution of SBO. Administration of Gastrografin has been shown to decrease the duration of adhesive SBO and reduce mean hospital length of stay.^{76, 77, 78, 79, 80}

Clinical and laboratory signs of strangulated bowel include increasing intensity and duration of abdominal pain, elevated arterial lactate levels, bloody stool, acidemia, and hemodynamic instability. Concern for strangulated bowel warrants immediate consultation of the surgical service.

Complications such as dehydration, infection, ischemia, and perforation can follow SBO. Increased hydrostatic pressure inside the lumen compresses mucosal lymphatics and causes bowel wall lymphedema. Proteins and electrolytes extravasate across the capillary wall. Decreased venous return from intravascular volume depletion decreases cardiac output. End-organ failure may follow.

Native gut bacteria proliferate proximal to the obstruction. Bacteremia and abscess formation occur from bacterial translocation via the microcirculation to the abdominal cavity and mesenteric lymph nodes. Antibiotic therapy to cover gram-negative and anaerobic organisms is initiated in patients with SBO whose intestine may be compromised and who will be undergoing surgery. There are no data to support antibiotic prophylaxis in patients with an SBO who are managed conservatively.

Radiographic evidence suggests this patient has a partial SBO. This can be treated successfully with conservative management in 73% to 90% of patients (Table 28-12).^{68, 81} Duration of conservative management varies, but may be continued for up to 5 days. If symptoms continue, further diagnostic studies or surgical intervention may be necessary (Figure 28-7).

Leukocytosis, tachycardia, hypotension, and fever are consistent with a systemic inflammatory response. A diagnosis of strangulated small bowel, intestinal perforation, peritonitis, and abscess formation should be considered. Blood cultures should be sent and antibiotic therapy to cover gram-negative rods and anaerobic bacteria should be prescribed. Fluids should be administered to patients who are fluid responsive. Central venous access and direct blood pressure monitoring via an arterial line should be considered. Vasopressors should be titrated to target mean arterial blood pressures greater than 65 mm Hg. A bladder pressure should be measured because the patient is at risk for developing IAH. Further evaluation with a CT scan of the abdomen and pelvis should be performed.

It is more difficult to obtain a history and to perform an abdominal examination in patients whose lungs are mechanically ventilated because they are often sedated and receiving analgesic medications. The patient is at risk for clinical deterioration during manipulation of the bowel during his OR course. The patient should be euvolemic. An arterial line should be placed. Two units of PRBCs should be typed and crossed because dissection of previous adhesions may be associated with intraoperative bleeding.

The patient has an uncomplicated OR course. The appendix was ruptured and the small bowel and proximal colon were distended. A bowel obstruction was not seen.

Perforation of the appendix can cause a paralytic ileus. The ileus appears as a partial SBO with administration of Gastrografin, but does not resolve with conservative therapy. A patient who has a ruptured appendix and peritonitis may have a similar presentation to a patient with strangulated bowel and ischemia. With a complicated abdominal history, partial SBO, and peritonitis, the patient should continue on antibiotics for 3 to 5 days.