The abdomen is both a primary source of disease conditions that require care in the intensive care unit (ICU) and, frequently, a secondary source of additional pathophysiology for children in the ICU being treated for other conditions.
In either case, early recognition of these conditions and the judicious use of medical and surgical intervention can be key to a successful outcome in critically ill children with abdominal disease or injury.
Anatomic and physiologic considerations
The peritoneum provides a protective environment for the intraabdominal organs and, because of its marked sensitivity, a valuable window for the examining healthcare provider. It is composed of a single layer of mesothelial cells lining the abdominal cavity along the abdominal wall (the parietal peritoneum) and the intraabdominal 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. The peritoneum’s sensitivity to inflammation, ischemia, and necrosis is mediated by the fluid in the peritoneum that contains macrophages and other leukocytes. Thus, with a focus of inflammation anywhere in the peritoneal cavity, these leukocytes release inflammatory mediators, 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 (GI) 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. However, disease states that result in full-thickness inflammation of the bowel wall can stimulate the visceral peritoneum, inciting the release of leukocytic and tissue macrophage–derived inflammatory mediators, resulting in pain. Patients who are receiving immunosuppressive drugs or are in an immunocompromised state have reduced production of these peritoneal inflammatory mediators. Consequently, they can have deceptively little pain despite a significant intraabdominal disease. 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. 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 associated reflexes, on GI hormones, and on GI vasoactive mediators, such as adenosine, endothelin-1, and nitric oxide. In pathologic states such as sepsis alone or shock—whether from sepsis, hemorrhage, or cardiac failure—visceral blood flow is reduced. This can lead to ischemia of the intestinal mucosa and submucosa. Even with restoration of blood pressure and cardiac output following 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, 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 (see also Chapter 111 ). Whether the translocation of bacteria or endotoxin from gut lumen to splanchnic drainage is the chicken or the egg can be debated. Regardless, this perturbation of intestinal blood flow contributes to the pathophysiology of shock and sepsis.
Other conditions in the intensive care unit (ICU) can affect splanchnic blood flow, especially mechanical ventilation with high inspiratory pressures, high positive end-expiratory pressure (PEEP), or high tidal volumes. ,
Physical examination of the abdomen
One should always start the examination of the child by assessing vital signs. Fever is common in patients presenting with significant abdominal disease, but it may not always present early in the disease process. Tachycardia is seen with fever, pain, or anxiety but is also a sensitive indicator of serious underlying illness, often seen in patients with early compensated shock. Hypotension may indicate a decompensated patient who needs immediate attention and intervention for likely sepsis.
The examination of a child’s abdomen should begin with keen observation, patience, and sensitivity to the patient’s fears and the parents’ anxiety. One should first notice the child’s position and demeanor. Children with peritonitis do not move or writhe about the bed, as this only worsens their pain. They will remain quite still and avoid movement or any rapid changes in position. A child with visceral ischemia that has not progressed to peritonitis may be actively seeking a more comfortable position with multiple positional adjustments.
The abdomen should initially be evaluated for any skin changes that can give clues to the underlying process. Bruises or patterned abrasions and petechiae can indicate trauma with significant underlying organ lacerations or blood loss. Seat belt restraints can often leave a significant lesion on a child’s chest and abdomen after a motor vehicle accident and should prompt further evaluation for intraabdominal injury. In the absence of reported trauma, the provider must consider nonaccidental trauma in the differential diagnosis, particularly in very young, nonverbal children. Grey Turner sign is significant bruising in the flanks, which indicates significant retroperitoneal bruising and is often associated with severe pancreatitis or pancreatic necrosis. Bruising around the umbilicus, Cullen sign, is also an indicator of significant intraabdominal bleeding and pancreatic disease. Neonates with necrotizing enterocolitis often have skin changes of the abdominal wall ranging from localized or diffuse erythema to a dusky blue or purple discoloration.
Observation of the patient’s facial expressions is important throughout the physical examination, as young children may not be able to express what they are feeling or simply are too anxious to give clear responses. Once the manual examination is to begin, the examiners should make certain that their hands and stethoscope are warm. For the verbal child who has localized the pain to a specific portion of the abdomen, the examiners should start the palpation in the opposite quadrant. If palpation in one area causes referred pain in a different location (Rovsing sign), this is suggestive of localized peritonitis in the area of pain, classically seen in appendicitis but also seen in other localized abdominal conditions.
In generalized peritonitis, spasm of the rectus abdominis can be detected regardless of where the source of the inflammation is located. When rectus spasm is detected on one side of the abdomen, a comparison to the rectus on the other side is helpful. When both are in spasm, it could be a manifestation of guarding by an anxious child; therefore, distraction should be employed. Distraction can often be created by engaging in conversation with the verbal child or by using the warmed stethoscope to listen with light pressure over the area of the abdomen in question, followed by gradually increasing the pressure to elicit a response. Asking the child to take a deep breath and blow it all the way out while feeling the rectus can overcome the spasm if it is due to voluntary guarding, while a child with peritonitis will fail to relax the rectus spasm.
Testing for rebound tenderness is valuable only in older children. It should be avoided in children younger than adolescence, as it is too startling and thus has a high false-positive rate. Gently shaking the bed, asking the child to cough, or moving the child’s hips from side to side will cause a painful response in conditions with peritonitis and is much less threatening to younger children. As mentioned earlier, pain out of proportion to the findings on physical examination in an ICU patient suggests ischemia independent of the location in the body. Bowel sounds are highly variable; thus, their assessment is not usually useful in the ICU patient.
Significant abdominal distention may also indicate considerable underlying illness and can make the physical examination more challenging. Differentiation between apparent tenderness from distention and peritonitis requires patience and gentle palpation. Assessing the rectus muscles for spasm may facilitate the diagnosis of peritonitis. Distention from hepatomegaly or splenomegaly can be due to end-stage liver disease, malignancy, or masses. Fluid in the abdomen could indicate significant blood loss requiring immediate attention and resuscitation. Ascites with abdominal pain may be an indicator of spontaneous bacterial peritonitis, particularly in patients with end-stage renal or liver disease.
Medications can interfere with the reliability of the physical examination of the abdomen. As mentioned, steroids can blunt an inflammatory response in the peritoneum and lead to decreased pain sensation despite a significant intraabdominal disease process. Patients receiving opiates may have a diminished response to painful stimuli; however, significant intraperitoneal pathology can still be ascertained by careful observation and examination. Patients who are receiving paralytic drugs are particularly challenging because the rectus abdominis spasm associated with peritonitis may be substantially decreased. Observation of the face, heart rate, or blood pressure can still be valuable, especially by comparing these findings during examination to other areas of the body. Just as in the nonsedated, non-ICU patient, beginning the examination on another portion of the body gives the examiner a baseline for comparison.
Assessment of possible intraabdominal conditions should include blood and serum tests that measure inflammation, acid-base abnormalities, possible coagulopathy, and those focused on suspected involved organs. The leukocyte count and differential, hematocrit, and platelet counts should always be checked for patients with suspected abdominal disease. Leukocytosis, especially with an increased percentage of neutrophils or immature forms (bandemia, left shift), should raise concern about an infectious process. Neutropenia suggests a more severe infection or a suppression of the patient’s bone marrow from medications or from the infection; such a situation might make clearance of a bacterial infection more difficult. Similarly, both an increased and decreased platelet count can indicate an intraabdominal infection. Serial declines in the platelet count are particularly suggestive of a continuing inflammatory consumption seen in conditions such necrotizing enterocolitis. Hematocrits must be followed in any child in the ICU because they can demonstrate intraabdominal bleeding or hemolysis related to disseminated intravascular coagulopathy (DIC). Other coagulation tests should be considered, especially in children with severe infections or those with liver dysfunction. In such situations, the prothrombin time (PT), partial thromboplastin time (PTT), D-dimers, and fibrin split products are helpful to characterize and monitor the coagulopathy. C-reactive protein (CRP) is elevated in states of inflammation and/or infection and may be useful for trending the body’s response to therapy.
Abnormalities of acid-base balance should be monitored regularly in a child hospitalized in the ICU with an abdominal disease process. The source of increased acid can either be an overproduction, such as ongoing lactate generation by ischemic bowel, or decreased acid clearance by the liver or kidneys in conditions associated with shock and decreased visceral blood flow. Lactate is a sensitive measure of intestinal ischemia, especially when monitored serially for trends. Arterial blood samples are more reliable than venous samples in that measurement. Hyperlactemia is not specific to intestinal ischemia and can be associated with any tissue necrosis or underperfusion of organs. Elevated serum lactate is also associated with a worse prognosis in patients with sepsis, and the normalization of lactate levels after resuscitation is associated with improved prognosis in patients with sepsis.
Liver function tests, more accurately termed liver injury tests , include transaminases (alanine transaminase [ALT] and aspartate transaminase [AST]), bilirubin, and γ-glutamyltransferase (GGT). These can be elevated with trauma to the liver, active hepatic inflammation, hepatic ischemia, or obstruction of the hepatic venous outflow, known as Budd-Chiari syndrome. The latter can result in extremely elevated transaminase levels. Elevation of the GGT without a significant rise in transaminase suggests a biliary condition such as common bile duct obstruction or cholecystitis.
Amylase is a valuable diagnostic test for children with abdominal pain or unexplained intraabdominal sepsis, as hyperamylasemia can indicate pancreatitis. Elevated amylase is not specific to pancreatic insults—it can be elevated with head trauma, decreased renal clearance, and intestinal obstruction. Serum lipase can be an additive test to the assessment of the pancreas. It is more specific to the pancreas but can be mildly elevated in intestinal obstruction as well. When both amylase and lipase are markedly elevated, pancreatitis is most likely. Children with a past history of severe or chronic pancreatitis might not have marked elevations; thus, the level of the enzyme does not always correlate with the severity of the disease.
The reliability of abdominal examination is subjective, highly variable, and may depend on the experience of the observer, the fluctuating status of the patient, the patient’s medications, the patient’s level of anxiety, and many other factors. Consequently, most ICU providers use imaging studies to ascertain whether intraabdominal pathology warrants intervention. For reasons of resource efficiency as well as considerations about the potential risks of ionizing radiation and patient comfort/safety, prudence needs to be exercised before ordering expensive and potentially obfuscating imaging studies. The following factors should always be evaluated before performing each study:
Specifically, what is one looking for—that is, what is the differential diagnosis?
How reliably will this study rule in or rule out those diagnoses—that is, what is the specificity and sensitivity of the study?
Will the results of this study change the management—that is, will a negative result prompt the termination of a drug regimen or life-supporting technology, and will a positive study necessitate surgical intervention or initiation of a new therapy?
Are the risks—such as ionizing radiation, transportation of a heavily medicated or unstable patient from the ICU to the radiology suite, the administration of intravenous (IV) contrast, and so on—offset by the value of the study?
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 the assessment of visceral blood flow to kidneys, pelvic organs, and GI 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. The presence of a whirlpool sign can be diagnostic of malrotation with midgut volvulus. However, neither finding is sensitive enough to exclude the diagnosis of malrotation, necessitating an upper GI contrast study to clearly determine the position of the duodenal-jejunal junction. Assessments of gallbladder wall thickening suggestive of acalculous cholecystitis or biliary tree dilation are particularly accurate. Intraabdominal and pelvic fluid collections can be identified, making ultrasound useful in the setting of traumatic injury or suspected intraabdominal abscess. It can be used as an adjunct to guide fluid drainage either surgically or percutaneously. Recently, ultrasonography has gained popularity for its usefulness in assessing for pneumatosis intestinalis, portal venous gas, and bowel wall perfusion, specifically in infants suspected to have necrotizing enterocolitis. In experienced hands, studies have shown that ultrasonography is more sensitive than plain films in this regard. This can be particularly useful in patients who are critically ill with an unknown but suspected abdominal source of sepsis who are too unstable to transport for computed tomography (CT) imaging (see also Chapter 15 ).
The use of ultrasound is limited in patients with bowel obstruction or severe paralytic ileus, as intestinal distention creates ultrasonic distortion, minimizing the value of this imaging modality. Accuracy of images is also highly dependent on having a skilled and experienced technician.
Abdominal plain radiographs
Plain radiographs of the abdomen can be revealing and 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 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 and instead a consequence of air dissecting through mediastinal and diaphragmatic tissue planes. Other plain radiograph findings suggestive of intestinal disease include thumbprinting, pneumatosis intestinalis, and portal venous gas.
Abdominal CT scans are accurate, fairly rapid, and can be used to guide interventional procedures such as percutaneous biopsies or drainage of intraabdominal 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 children who receive serial radiographs. 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 IV 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. That risk can be minimized as well by using nonionic contrast materials or with the administration of sodium bicarbonate and N -acetylcysteine prior to the administration of the IV 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 effective at identifying the condition of all the intraabdominal organs and 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 IV 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 as 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 earlier for CT scans. The added challenges posed by MRI include the slower speed of the image capture, which 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 these issues, MRI enterography and cholangiography are now capable of generating revealing images of the GI and hepatobiliary tracts. Thus, if the value of the images can offset the risks of transporting a sick child to the MRI suite, it should be considered.
Abdominal conditions requiring treatment in the intensive care unit
Children with perforation of the GI 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, it is unusual for it to result in serious intraabdominal 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 GI tract include gastric or proximal intestinal perforation from severe gastritis, peptic ulcer disease, gastric ischemia, or following 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 intraabdominal 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. Interestingly, some gastric formulas now contain probiotics that, if leaked into the peritoneum, can elicit a septic response.
Ingested foreign bodies can lead to perforation anywhere in the GI tract, with common items being sharp materials such as pins or nails, fish bones, disc batteries, and magnets. Magnet ingestion incidents, in particular, have dramatically risen since the early 2000s and have led to serious injury and death. If more than one magnet is ingested, the magnets can pinch loops of bowel and lead to ischemia, necrosis, perforation, and death.
Trauma can also result in perforation. The lap portion of a seat belt can cause an abrupt and significant increase in intraabdominal pressures during motor vehicle accidents. Patients may sustain intestinal perforation, organ lacerations, or significant intraabdominal hematomas requiring ICU care. Abdominal injury is the second most common cause of death in abused children after head injury. A punch or kick can compress the small bowel against the vertebral column, causing a jejunal perforation. So characteristic is this mechanism 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. Sports injuries, from skateboarding to all-terrain vehicle use, can all lead to significant injury requiring resuscitation.
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. With venous congestion as an early component of these obstructive volvulus conditions, there may be less release of lactate into systemic circulation, potentially leading to a falsely reassuring normal lactate level despite significant intestinal 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 difficult to diagnose, as neither contrast enema radiographs nor antegrade upper GI contrast studies are likely to reach the involved area of volvulus. In addition, these children will often not have impressive physical examination 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 the pediatric ICU (PICU), 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 following cardiac surgery, manifested as pneumatosis intestinalis on radiographs or ultrasonography, 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 (NEC), which 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, as 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 following 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 NEC 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.
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 it is labeled neutropenic enterocolitis , as it can affect other portions of the intestinal tract as well. It may be preceded by mucositis and enteropathy 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. Treatment includes early initiation of broad-spectrum antibiotics, bowel rest/decompression with a nasogastric tube, fluid resuscitation, hemodynamic support if needed, serial abdominal and radiographic examinations, and a cessation of chemotherapy. Surgical treatment is reserved for patients with clinical instability or deterioration after appropriate resuscitation and those with free air on CT or plain film. Neutropenic enterocolitis is becoming more common with the expanding use of bone marrow transplantation as an adjunct to the treatment of many childhood diseases, including cancer. Additionally, the use of new, targeted immunotherapy for the treatment of childhood cancers has increased, and it is yet unclear what risk these drugs pose in the development of neutropenic enterocolitis.
Severe pancreatitis can require intensive care in children. Etiologies for 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, though rare in children, can require repeated surgical debridement to eradicate the ongoing source of sepsis.
Intraabdominal hemorrhage can result from trauma or following 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 PICU 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 following 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 Haemophilus influenza , Streptococcus pneumoniae , and meningococcus.
The liver is also a commonly injured organ in blunt abdominal trauma; it, too, can usually be managed nonoperatively. The development of hemobilia several weeks after nonoperative management of a hepatic laceration is uncommon. However, when it occurs, it can result in significant GI bleeding. This can usually be managed with arteriographic embolization or endoscopic biliary stent placement, but it sometimes requires resection of the involved hepatic segment or lobe.
Other specific conditions
Gallstones are increasingly common in children, perhaps because of the increased use of parenteral nutrition with its associated risk of cholestasis or the increasing prevalence of childhood obesity. Gallstones 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 doses of opiates that lead 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 gallbladder with a thickened gallbladder wall and pericholecystic fluid are diagnostic. However, a radionuclide study, such as a hepatobiliary iminodiacetic acid scan, is the most accurate functional imaging study.
Empiric antibiotic coverage for common biliary pathogens—including Gram-negative organisms such as Klebsiella , Pseudomonas , or E. 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 gallbladder, performed with ultrasound guidance in the ICU, can be an effective temporizing procedure.
Spontaneous bacterial peritonitis
Spontaneous bacterial peritonitis (SBP) is an acute bacterial infection of ascitic abdominal fluid that may present with fever, abdominal pain, altered mental status, or persistent vomiting. Enteric organisms have traditionally been isolated from more than 90% of infected ascites fluid in SBP, suggesting that the GI tract is the source of bacterial contamination. This is thought to be due to direct transmural migration of bacteria from an intestinal or hollow organ lumen. An alternative proposed mechanism for bacterial inoculation of ascites is via hematogenous transmission in conjunction with an impaired immune system. The debate continues, and the exact mechanism of bacterial displacement from the GI tract into ascites fluid remains controversial. If suspected, broad-spectrum antibiotics should be initiated to cover GI flora until culture results can guide therapy further. Interventional radiology–guided paracentesis can be both diagnostic and therapeutic.
Abdominal compartment syndrome
Intraabdominal hypertension (IAH) is defined as intraabdominal pressure (IAP) greater than 12 mm Hg. Although this is relatively uncommon in PICU patients, it can be associated with a high morbidity and mortality. If the IAP reaches a point where perfusion to intraabdominal organs is compromised, a constellation of organ dysfunctions may occur, including renal insufficiency, intestinal ischemia, hepatic dysfunction, elevated diaphragms, and respiratory insufficiency. This constellation is termed abdominal compartment syndrome (ACS). Risk factors for ACS include massive fluid resuscitation for any illness, IAH, intraabdominal inflammation or infection from any cause, obesity, and tight abdominal wall closures following laparotomy. Like compartment syndrome in extremities, there is no absolute pressure to define the presence of ACS; 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 IAP. An abdominal perfusion pressure (APP) can be calculated as mean arterial pressure minus IAP. If the APP is greater than 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 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 practical measurement can be obtained using a closed system composed of a Foley bladder catheter connected to a fluid column and a pressure measuring device, such as a tube manometer or pressure transducer. Ultrasound evaluation—including Doppler imaging of renal, portal, and mesenteric blood flow—can be helpful in assessing end-organ perfusion as well as estimating intraabdominal venous pressure by assessing the caliber of the inferior vena cava (IVC). CT scans can also reveal poor perfusion of these organs and a flattened IVC 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. Practitioners should avoid the reverse Trendelenburg or prone positions, as these can increase IAP. Effective decompression of the GI tract is important—it can be optimized by effective nasogastric tube drainage, administration of prokinetic medications, and colonic decompression by either enemas, rectal irrigation, or rectal tube. Supporting renal function is also important, which includes liberal use of diuretics along with volume resuscitation. If these maneuvers have not improved 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, and mortality rates higher than 50% have been reported, especially if treatment is delayed until multisystem organ failure develops. After decompression, and once 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 that serve as a protein matrix for tissue ingrowth.
Intraabdominal abscesses are highly variable in presentation. Patients may present with significant abdominal pain, spiking fevers, prolonged ileus after a surgical procedure, or leukocytosis. Classic physical findings may be absent in a deep abscess, where the only clues may be persistent fevers, tachycardia, and mild persistent GI dysfunction. Postoperative analgesics and incisional pain frequently mask abdominal findings. In addition, antibiotic administration may mask abdominal tenderness, fever, and leukocytosis.
In patients with subphrenic abscesses, irritation of the diaphragm may lead to shoulder pain, persistent episodes of hiccups, or unexplained pleural effusions, atelectasis, or pneumonia. With pelvic abscesses, frequent urination, diarrhea, or tenesmus may occur. If these abscesses go unrecognized, patients may develop a significant septic response that can lead to multiple-organ failure and death.
Intestine as a source of sepsis
The intestine is an organ endowed with large quantities of both lymphatic tissue and bacteria. Consequently, it can be a central organ in the systemic inflammatory response in children hospitalized in the ICU. The role of the gut’s immune system is not fully understood but may play a key role in some intestinal inflammatory diseases such as Crohn disease. In addition, the interplay between the gut-associated lymphoid tissue and bacteria present in the bowel lumen is important in critical illness. The sick child with decreased visceral blood flow and under severe stress likely has alterations in the mucosal integrity of the intestine. That loss of integrity can lead to bacterial invasion of the bowel wall with subsequent entry of the bacteria/toxins into the lymphatic or portal venous circulation. Once in the circulation, these bacteria/toxins can trigger a severe systemic inflammatory response, even if the bacteria are not detectable as a bloodstream infection. Use of enteral antibiotics to decrease potentially pathologic gut bacteria has proved effective in reducing intestinal sources of sepsis in some settings, whereas replacement of gut flora using probiotics or synbiotics has been used with some success in others.
The decision to perform a laparotomy or laparoscopy in a pediatric ICU patient can be challenging. There are indeed times when a patient can be too sick to go to the operating room and other times when the patient is so sick that only an immediate operation will provide a chance for successful treatment.
With the possible exception of patients with continued IAH or ACS, delaying operative treatment with time spent on preoperative resuscitation is often valuable. Induction of general anesthesia in a hypovolemic or acidotic patient with cardiogenic or septic shock can be dangerous. An understanding of the differential diagnosis can be most helpful in planning the appropriate antibiotic coverage and timing of the surgical treatment. Most of the conditions that require laparotomy in ICU patients have an infectious component; thus, empiric broad-spectrum antibiotics should be administered early in the resuscitation. Depending on the disease, resuscitation and antibiotics alone may obviate the need for emergent laparotomy. Therefore, effective communication between the surgical and ICU teams is essential. To optimize the timing of the operation, the surgical team should be ready to go immediately once the preoperative resuscitation is sufficient. In situations in which physical examination or radiographs do not provide localization, bedside imaging can help localize the disease. Image-guided drainage of localized infection may be a successful strategy in lieu of a full laparotomy with its incumbent risks , or may help to improve the physiology so that a definitive operation can be more safely performed after the condition has stabilized.