The Peritoneum

The peritoneum provides a protective environment for the intra-abdominal organs, and, because of its marked sensitivity, a valuable “window” for the examining health care provider. It is composed of a single layer of mesothelial cells lining the abdominal cavity along the abdominal wall (the parietal peritoneum) and the intra-abdominal viscera (the visceral peritoneum). The space between these is the peritoneal cavity. Beneath the mesothelium is a submesothelial layer of extracellular matrix, capillaries, and lymphatics.¹ The peritoneum’s sensitivity to inflammation, ischemia, and necrosis is mediated by the fluid in the peritoneum that contains macrophages and other leukocytes.² Thus, with a focus of inflammation anywhere in the peritoneal cavity, inflammatory mediators are released by these leukocytes, often resulting initially in poorly localized, generalized pain. With irritation of the peritoneum associated with early appendicitis, for example, the patient interprets the inflammation as periumbilical pain. This is related to the embryologic development along dermatomes. As more inflammatory cytokines are secreted throughout the peritoneal cavity, the pain becomes more generalized and will eventually result in spasm of the overlying muscles of the abdominal wall, interpreted by the examiner as guarding.

Pain in the gastrointestinal tract is mainly limited to conditions that result in distention of the organ. Inflammation or irritation of the mucosa is generally not the cause of pain, except in the stomach. Disease states that result in full-thickness inflammation of the bowel wall, however, can stimulate the visceral peritoneum, inciting the release of leukocytic and tissue macrophage derived inflammatory mediators that results in pain. Patients who are receiving drugs such as steroids, which blunt the immune response, have reduced production of these peritoneal inflammatory mediators, and consequently can have deceptively little pain despite a significant intra-abdominal disease. Just as in other parts of the body, ischemia associated with any abdominal condition results in severe pain, often out of proportion to what is detected on physical examination.

Visceral Blood Flow

The regulation of visceral blood flow is a tightly controlled balance of neural, humoral, paracrine, and metabolic factors.³ In the gut, enteral feeding increases the blood flow and the metabolic demands on the intestinal mucosa. Some of these effects are directly related to the nutrients in the intestinal lumen, whereas others are dependent on the enteric nervous system and the associated refexes, on gastrointestinal hormones, and on gastrointestinal vasoactive mediators such as adenosine, endothelin-1, and nitric oxide.⁴ In pathologic states such as sepsis alone or shock, whether from sepsis, hemorrhage, or cardiac failure, visceral blood flow is reduced, which can lead to ischemia of the intestinal mucosa and submuscosa. Even with restoration of blood pressure and cardiac output after treatment of shock, microvascular perfusion of the intestine may remain impaired resulting in mucosal ischemia and persistent lactate production.

Such ischemia can lead to altered integrity of the mucosal barriers to bacteria and other pathogens, thus increasing the entry of endotoxins into the splanchnic venous and lymphatic systems. These pathogens can fuel the inflammatory response. This finding has fostered the theory of “the gut as a central organ of sepsis or multisystem organ failure.”⁵ Whether the translocation of bacteria or endotoxin from gut lumen to splanchnic drainage is the chicken or egg can be debated; regardless, this perturbation of intestinal blood flow contributes to the pathophysiology of shock and sepsis.

Other conditions in the ICU can affect splanchnic blood flow, especially mechanical ventilation with high inspiratory pressures, high positive end-expiratory pressure, or high tidal volumes.^6,7

Ultrasonography

Ultrasonography has several advantages over other imaging studies, most notably its portability, which obviates the need for moving the patient and its lack of ionizing radiation exposure. In addition, the use of Doppler modality permits assessment of visceral blood flow to kidneys, pelvic organs, and the gastrointestinal tract. When the relative positions of the mesenteric vein and artery can be accurately determined, an abnormal orientation suggests an increased risk of malrotation, even without midgut volvulus.⁹ The presence of a “whirlpool sign” can be diagnostic of malrotation with midgut volvulus.¹⁰ Neither finding is sensitive enough to exclude the diagnosis of malrotation. Thus, if suspected, malrotation requires an upper gastrointestinal contrast study to assess the position of the duodenal-jejunal junction.¹¹ Assessment of gall bladder wall thickening suggestive of acalculous cholecystitis or biliary tree dilation are particularly accurate. Intra-abdominal and pelvic fluid collections can be identified and characterized well with ultrasonography, suggesting collections that would be suitable for drainage, either surgical or percutaneous, via ultrasound guidance. In the patient with bowel obstruction or severe paralytic ileus, the resultant intestinal distention creates ultrasonic distortion, minimizing the value of this imaging modality.

Abdominal Plain Radiographs

Plain radiographs of the abdomen can be revealing and also are portable, relatively inexpensive, involve small amounts of radiation, and require minimal patient movement. To be of greatest value, however, the abdominal radiograph should be done with the patient in at least two different positions, such as supine and upright, and ideally as lateral decubitus as well. Cross-table laterals can also add value. These different views facilitate the identification of air-fluid levels suggestive of small bowel obstruction, and the presence of pneumoperitoneum indicating likely visceral perforation. Pneumoperitoneum in a patient with high inspiratory pressures on a mechanical ventilator can sometimes be unrelated to abdominal pathology, but rather a consequence of air dissecting through mediastinal and diaphragmatic tissue planes. Other plain radiograph findings suggestive of intestinal disease include “thumb printing,” pneumatosis intestinalis, and portal venous gas.

Computed Tomography

Abdominal computed tomography (CT) scans are accurate, fairly rapid, and can be used to guide interventional procedures such as percutaneous biopsies or drainage of intra-abdominal fluid collections. Except in institutions where CT scans are located in the ICU or those that have mobile CT units, patients must be transported to access imaging with this modality. That requirement can be a significant challenge with children who are ventilated or hemodynamically unstable. In addition to the transport challenges, the radiation exposure of a CT scan may pose a risk for developing malignancies later in life, especially for those children who receive serial radiographs.¹² That risk can be reduced by using directed scans (i.e., limiting the scan to the portion of the abdomen in question). Other risks include the administration of intravenous contrast material that can cause anaphylaxis in those who are allergic, or renal injury, especially in those who might already be hypovolemic or receiving nephrotoxic drugs.¹³ That risk can be minimized as well, by using nonionic contrast materials, or with the administration of sodium bicarbonate and N-acetylcysteine before the administration of the intravenous contrast. Administration of enteral contrast can result in aspiration if there is intestinal obstruction or delayed gastric emptying with vomiting or gastroesophageal reflux.

The abdominal CT scan can be very effective at identifying the condition of all the intra-abdominal organs, and the retroperitoneal spaces. It is being used with increasing success to assess for bowel obstruction. Identification of fluid collections and their characteristics can help ascertain whether blood, bile, or pus is present and whether it can be drained percutaneously. To make certain that nonopacification of fluid-filled loops of bowel is not misconstrued for pathologic collections of fluid, enteral contrast should be given as long as no contraindications exist. With intravenous contrast and carefully timed image capture, conclusions about organ perfusion can be assessed as well. Colonic and intestinal ischemia, necrotizing pancreatitis, and decreased renal perfusion can all be seen reliably.

Magnetic Resonance Imaging

Magnetic resonance imaging (MRI) of the abdomen can be valuable, especially because the risks of radiation can be obviated, but the logistical challenges of moving an ICU patient to the MRI suite are similar to those mentioned previously for CT scans. The added challenges posed by MRI include the slower speed of the image capture that interferes with accessing the unstable patient for interventions, as well as the restrictions for certain MRI-incompatible ICU equipment to be in the MRI scanning room. Despite this, MRI enterography and cholangiography are now capable of generating very revealing images of the gastrointestinal and hepatobiliary tracts.¹⁴ Thus, if the value of the images can offset the risks of transporting a sick child to the MRI suite, it should be considered.

Perforated Viscera

Children with perforation of the gastrointestinal tract will frequently require either preoperative resuscitation or postoperative stabilization in the ICU. The most common condition resulting in perforation is appendicitis. Although perforated appendicitis is common, occurring in 30% to 50% of children who present to children’s hospitals with appendicitis,¹⁵ it is unusual for it to result in serious intra-abdominal sepsis. Nevertheless, deaths do still occur in such children, related most often to septic shock with cardiovascular collapse or severe acute respiratory distress syndrome.

Other sites of perforation in the gastrointestinal tract include gastric perforation from either severe gastritis, gastric ischemia, or after manipulations such as insertion of gastric tubes or transpyloric feeding tubes. In children with chronic gastrostomies, accidental dislodgements or manipulations of the gastrostomy site can result in separation of the stomach from the abdominal wall, leading to spillage of gastric contents into the peritoneal cavity. Because the acidic gastric pH results in lower bacterial counts, such perforations do not usually result in serious intra-abdominal sepsis. However, chronically hospitalized children, or children with gastroesophageal reflux on chronic acid suppression therapies may be colonized with resistant bacterial or fungal organisms such as Candida species that can lead to serious septic consequences.

Ingested foreign bodies can lead to perforation anywhere in the gastrointestinal tract, with common items being sharp materials such as pins or nails, fish bones, disc batteries, and magnets.¹⁶ Trauma can also result in perforation, notably in lap seat belt injuries from motor vehicle accidents, or in cases of nonaccidental trauma where a punch or kick can compress the small bowel against the vertebral column causing a jejunal perforation. Therefore, characteristic in this mechanism is that the intraoperative finding of a jejunal perforation in the absence of a known trauma history should prompt an evaluation by the hospital’s child abuse team.¹⁷

Ischemia

Volvulus of a loop of small intestine can occur when a segment of bowel, typically distal ileum, becomes entrapped beneath an omphalomesenteric remnant. This particular lesion can be very difficult to diagnose as neither contrast enema radiographs nor antegrade upper gastrointestinal contrast studies are likely to reach the involved area of volvulus. In addition, such children will often not have impressive physical exam findings until the bowel has become ischemic. At that point, systemic sepsis can occur rapidly. Similar pathophysiology can develop from a twist of bowel within an internal hernia.

In children with intestinal malrotation, the entire intestine supplied by the superior mesenteric artery (i.e., from jejunum to right transverse colon) can twist, resulting in midgut volvulus. In a somewhat similar manner, the colon alone can twist when there is sufficient redundancy in the mesocolon, typically in the cecum or the sigmoid colon. In any of these situations with intestinal and mesenteric twisting, the resultant venous congestion can compromise the capillary inflow to the bowel wall, ultimately leading to irreversible ischemia if the bowel is not untwisted promptly.

In the pediatric ICU, another cause of intestinal ischemia is low cardiac output or hypoxemia. Children with congenital heart disease, particularly those with single ventricle physiology or severe cyanotic heart disease, can develop mucosal ischemia after cardiac surgery, manifested as pneumatosis intestinalis on radiographs, bloody stool, metabolic acidosis with elevated serum lactate, and sepsis. Children on potent vasoactive pressors such as epinephrine or norepinephrine, and those receiving extracorporeal support, can develop ischemia as well. This is a variant of necrotizing enterocolitis and can involve the entire small intestine, and less commonly the colon. If the diminished cardiac output or hypoxemia is corrected and the ischemia is limited to the mucosa, surgical treatment may be avoided. Resection is necessary if the acidosis or systemic perturbations are refractory or if perforation results. Unfortunately, because this disease can involve the entire gut, the utility of resection may be limited.

Other causes of intestinal ischemia include small bowel obstruction, usually from adhesions after previous laparotomies, or, less commonly, related to incarcerated inguinal hernias. If the bowel becomes sufficiently distended, the intraluminal pressure can exceed the intramural perfusion pressure of the microcirculation, resulting in ischemia. Other, less common causes of intestinal ischemia include conditions that alter the microcirculation of the bowel wall such as vasculitis or hemolytic uremic syndrome.

The systemic physiologic insult of intestinal ischemia is usually proportional to the degree of ischemic tissue. Thus, midgut volvulus or total intestinal involvement with necrotizing enterocolitis can be the most catastrophic of these disease states acutely, and can have the most devastating long-term consequences, with short bowel syndrome and intestinal failure a common consequence if the ischemia is irreversible.

Neutropenic Enterocolitis

Children who have significant neutropenia, whether drug-induced from chemotherapy for malignant diseases or as a primary disease, may develop inflammation of the intestinal tract. The most common location is the right colon. Historically, this has been termed typhlitis, but more accurately is labeled neutropenic enterocolitis, because it can affect other portions of the intestinal tract as well. It may be preceded by mucositis that permits the intestinal bacteria to invade the bowel wall. Affected children exhibit fever, abdominal pain and tenderness, abdominal distention, ileus or diarrhea, radiographic signs of inflammation, and sometimes hemodynamic instability. The diagnosis is made best by CT scan or ultrasound.¹⁸ Surgical treatment is reserved for those patients with peritonitis or hemodynamic instability after appropriate resuscitation.

Pancreatitis

Severe pancreatitis can require intensive care in children. Etiologies for the pancreatitis are most often idiopathic in children, but anatomic causes such as gallstones, pancreatic trauma, or pancreas divisum can also be responsible. Drugs and hemolytic uremic syndrome can be unusual causes of severe pancreatitis. In severe cases, pancreatitis can lead to significant third-space fluid losses, pleural effusions, retroperitoneal hemorrhage, abscess formation, and hypocalcemia. Necrotizing pancreatitis, although rare in children, can require repeated surgical debridement to eradicate the ongoing source of sepsis.

Hemorrhage

Intra-abdominal hemorrhage can result from trauma or surgical procedures or manipulations. In blunt trauma, the spleen is the most commonly injured abdominal organ. To avoid the risk of overwhelming postsplenectomy infection, nonoperative management is attempted as long as hemodynamic stability can be maintained. Hospitalization in the pediatric ICU with strict bed rest is indicated when the splenic injury is Grade IV or V, or if there are other significant injuries. The risk of delayed splenic rupture after nonoperative management is extremely low. If surgery is necessary, attempts to salvage the spleen with splenorrhaphy are important. Before surgery, if time permits, the child should be immunized for encapsulated bacterial organisms including Hemophalus influenza, Streptococcus pneumoniae, and meningococcus.

The liver is also a commonly injured organ in blunt abdominal trauma, and it too can usually be managed nonoperatively. The development of hemobilia several weeks after nonoperative management of hepatic laceration is uncommon, but when it occurs it can result in significant gastrointestinal bleeding. This can usually be managed with arteriographic embolization or endoscopic biliary stent placement,¹⁹ but sometimes requires resection of the involved hepatic segment or lobe.

Cholecystitis

Gall stones are increasingly common in children, perhaps because of the increased use of parenteral nutrition with its associated risk of cholestasis. Gall stones can result in cholecystitis, biliary obstruction, or pancreatitis that can complicate an ICU course for a child. Acalculous cholecystitis can be seen in children who are hospitalized in the ICU, particularly those who are receiving large does of opiates that leads to biliary dyskinesia, or those who have decreased perfusion of the abdominal organs because of hypotension. Acalculous cholecystitis can be associated with a significant systemic inflammatory response, and should be considered as a source of unexplained sepsis in a child. Ultrasonographic and CT scan findings of a dilated gall bladder with a thickened gall bladder wall and pericholecystic fluid are diagnostic, although a radionuclide study such as a hepatobiliary iminodiacetic acid scan is the most accurate functional imaging study.

Empiric antibiotic coverage for common biliary pathogens such as Gram negative organisms like klebsiella, pseudomonas, or Escherichia coli should be started immediately. Cholecystectomy would be definitive therapy. In critically ill children who might not tolerate a trip to the operating room, percutaneous drainage of the gall bladder done by ultrasound guidance in the ICU can be an effective temporizing procedure.

Abdominal Compartment Syndrome

Intra-abdominal hypertension (IAH) is defined as intra-abdominal pressure (IAP) that is >12 mm Hg. Although this is relatively uncommon in pediatric ICU patients, it can be associated with a high morbidity and mortality. If the IAP reaches a point where perfusion to intra-abdominal organs is compromised, a constellation of organ dysfunctions may occur including renal insufficiency, intestinal ischemia, hepatic dysfunction, elevated diaphragms, and respiratory insufficiency.^20–22 This constellation is termed abdominal compartment syndrome (ACS). Risk factors for ACS include massive fluid resuscitation for any illness, intra-abdominal hemorrhage, intra-abdominal inflammation or infection from any cause, obesity, and tight abdominal wall closures following laparotomy. As with compartment syndrome in extremities, there is no absolute pressure to define the presence of ACS; the intravascular volume status, blood pressure, and systemic vascular resistance are all factors that can impact the perfusion pressure of the abdominal organs and minimize the effect of the IAP. An abdominal perfusion pressure can be calculated as the mean arterial pressure minus the IAP. If abdominal perfusion pressure is > 60 mm Hg, a higher survival rate has been reported. The diagnosis of ACS is made when there is a sustained increased IAP in combination with signs of organ dysfunction such as decreased cardiac output, oliguria, and respiratory insufficiency. Other organ systems that can be affected by IAH include the reduction of portal and mesenteric venous flow, potentially leading to hepatic dysfunction and intestinal edema and ischemia. In addition, the increased intrathoracic pressure that can result from the elevated diaphragms can raise intracranial pressure.

When signs of IAH are evident in the setting of abdominal distention, pressure measurements can be made using nasogastric tubes, rectal catheters, bladder catheters, and peritoneal drainage tubes such as peritoneal dialysis catheters. The most reliable and easily practical measurement can be obtained using a closed system of a Foley bladder catheter connected to a fluid column and a pressure measuring device such as a tube manometer or a pressure transducer. Ultrasound evaluation, including Doppler imaging of renal, portal, and mesenteric blood flow can be helpful in the assessment of end-organ perfusion, as well as estimating the intra-abdominal venous pressure by assessing the caliber of the inferior vena cava. CT scan can also reveal poor perfusion of these organs and a flattened inferior vena cava, as well as increased abdominal girth, especially in the anterior to posterior dimension.

If the diagnosis of ACS is suspected, efforts to augment perfusion must be initiated. Avoid the reverse Trendelenburg or prone positions because these can increase IAP. Effective decompression of the gastrointestinal tract is important and can be optimized by effective nasogastric tube drainage, administration of prokinetic medications, and colonic decompression by either enemas or colonoscopy. Supporting renal function is also important and includes liberal use of diuretics along with volume resuscitation. If these maneuvers have not improved the organ function, temporary decompression by insertion of an abdominal drain to decrease the amount of fluid in the abdomen may be necessary. If this does not adequately decompress the IAH, laparotomy is necessary with placement of a sterile patch or silo that may provide sufficient compliance to reverse the ACS.

The morbidity of ACS is significant, with mortality rates of >50% reported, especially if treatment is delayed until multisystem organ failure develops. After decompression, and after resolution of any end-organ dysfunction occurs, and after the underlying causes of the IAH have abated, delayed closure of the abdomen can be considered. Sometimes that closure will require abdominal wall reconstruction techniques such as skin flap closure without fascial repair or skin grafts. Primary or delayed primary fascial repair may be feasible, sometimes requiring separation and release of the muscle groups, or insertion of prosthetic patches such as synthetic mesh, Gore-tex, or biologic sheet materials made from human dermal grafts or porcine intestinal submucosa.