Gastroesophageal Reflux
Gastroesophageal reflux (GER) is a term used to describe a leaky lower esophageal sphincter that causes a child to regurgitate recently ingested meals. It is common in the first year of life, especially in children born premature, and usually resolves during early childhood. Children with GER related to neuromuscular disorders, such as cerebral palsy, will continue to reflux throughout childhood. Because of weakened airway protective mechanisms, these children often demonstrate chronic pulmonary aspiration that results in repeated episodes of pneumonitis and hypoxemia. Some children require a Nissen fundoplication, a surgical “tightening” of the lower esophageal sphincter, to prevent GER.
Many anesthesiologists assume that children with GER are at risk for pulmonary aspiration on induction of anesthesia and will opt for a rapid sequence induction. But to do so, an IV catheter must be placed preoperatively, which is not a routine procedure in many pediatric centers. This practice also obligates the placement of an endotracheal tube instead of a face mask or a supraglottic airway (SGA). No data exist to justify this practice. Studies that assessed residual gastric volumes after a normal preanesthetic fast have demonstrated no differences between children with GER and normal controls. The authors’ opinion is that GER occurs only when there is food in the stomach of susceptible children. When these children are fasted normally, gastric volumes at induction of anesthesia are low and do not pose an increased risk for pulmonary aspiration.
There are additional valid reasons for not performing a rapid sequence induction in children with GER. First, the performance of cricoid pressure reflexively decreases lower esophageal pressure, thus promoting passive regurgitation of gastric contents. Second, paralysis or relaxation of the cricopharyngeus muscle (a striated skeletal muscle) that forms the upper esophageal sphincter may allow passively regurgitated gastric contents to reach the larynx. Lastly, acid reflux into the lower third of the esophagus reflexively causes an increase in upper esophageal sphincter tone, which would not occur in the presence of neuromuscular blockade.
Inflammatory Bowel Disease
Inflammatory bowel disease (IBD) primarily consists of Crohn disease and ulcerative colitis (UC). Crohn disease is a chronic inflammatory bowel disease that is seen in children and young adults, but it is also increasingly seen in very young children. (This “very early onset” IBD is seen primarily in children with IBD associated with genetic syndromes.) Clinical manifestations, among others, include diarrhea, abdominal pain, rectal bleeding, anal fistulas, anemia, and weight loss. Extraintestinal manifestations include joint pain and swelling, growth failure, and delayed puberty. Therapy includes administration of 5-aminosalicylic acid (5-ASA) preparations, nutritional therapy, corticosteroids, immunosuppressants like methotrexate and 6-mercaptopurine, and biologic medications (i.e., monoclonal antibodies such as infliximab, vedolizumab, and ustekinumab).
Ulcerative colitis is characterized by inflammation of the large intestine that manifests clinically as abdominal cramping, diarrhea, and bloody stools. Associated systemic findings include anorexia, weight loss, low-grade fever, and anemia. Severe cases of colitis can result in severe anemia requiring blood transfusion, hypoalbuminemia, and toxic megacolon. Approximately 20% of cases of UC occur during childhood. As with Crohn disease, the primary therapeutic options are antiinflammatory therapy with 5-ASA preparations, corticosteroids, and biologic therapy, depending on disease severity.
Children with IBD require repeated esophagogastroduodenoscopies and colonoscopies during the course of their disease, for which general anesthesia is usually required. In Crohn disease surgery is indicated in select cases when medical therapy has failed. For example, when microperforations have resulted in a phlegmon, in cases of intestinal strictures which result in obstruction, or with perforation. Intestinal or colonic resections are palliative but not curative. Surgery is indicated for intractable colitis and toxic megacolon with peritonitis. Because UC is confined to the large intestine, colectomy is considered curative.
There are no unique anesthetic considerations for children with IBD. Anecdotal data indicate that these children require higher than usual amounts of opioids. This may be related to tolerance from intermittent or chronic opioid use.
Neonatal Hyperbilirubinemia
Some neonates manifest jaundice in the first week of life. Unconjugated (indirect) hyperbilirubinemia occurs because of the breakdown of fetal erythrocytes in combination with low activity of glucuronyl transferase, the enzyme responsible for conjugation of bilirubin to glucuronic acid. It manifests clinically as jaundice of the skin and sclera and is most prominent after the third day of life, especially in prematurely born infants and in term breast-fed infants. Concomitant medical disorders that cause hemolysis and contribute to hyperbilirubinemia in an additive fashion include hemolytic disease of the newborn, spherocytosis, G-6-PD deficiency, and presence of a cephalohematoma.
Treatment is indicated when serum bilirubin levels are excessively high. The potential for neurotoxicity of the developing brain (kernicterus) is historically associated with bilirubin levels greater than 20 mg/dL in full-term infants. Prematurity, hypoxemia, acidosis, and hypothermia increase the likelihood of kernicterus in the presence of hyperbilirubinemia. Phototherapy is the initial treatment; exchange transfusions are required in accelerated cases. Bilirubin values that trigger phototherapy or exchange transfusion vary between institutions.
Chronic Liver Disease
Chronic liver disease is associated with congenital biliary atresia for which a Kasai procedure or liver transplant is required. Other possible causes include α 1 -antitrypsin deficiency, cystic fibrosis, tyrosinemia, and Wilson disease, among others. Clinical manifestations will depend on the remaining degree of liver function and will include ascites, portal hypertension (with esophageal varices), and coagulopathy. Respiratory insufficiency in children with advanced liver disease is caused by loss of functional residual capacity from the mass effect of ascites or hepatomegaly, and creation of intrapulmonary shunts (hepatopulmonary syndrome). Fulminant hepatic failure is associated with encephalopathy and increased intracranial pressure.
Principles of anesthetic management for children with liver disease include avoidance of medications that are metabolized in the liver (e.g., steroidal neuromuscular blockers) that will have an increased duration of action. All inhaled agents have minimal liver metabolism and reduce hepatic blood flow to a similar extent.
Achalasia
Achalasia is a rare esophageal motor disorder characterized by loss of organized peristalsis in the body of the esophagus, along with elevated lower esophageal sphincter (LES) tone, both of which lead to esophageal stasis. The annual incidence is estimated at 1.6 in 100,000 individuals, with less than 5% of those occurring in children. It is caused by a loss of inhibitory ganglion cells in the myenteric plexus in the esophageal wall. Symptoms include dysphagia for both solids and liquids, chest pain, regurgitation, poor weight gain, and respiratory symptoms such as cough and breathing difficulties, especially when supine. Diagnosis is confirmed by esophagram, which shows a dilated esophagus that tapers at the LES, and by esophageal manometry.
The initial management of achalasia in children includes endoscopy with pneumatic dilation of the LES and is repeated if symptoms recur. Advanced surgical management, after one or more dilations, consists of peroral endoscopic myotomy, or Heller myotomy via laparoscopy.
Induction of anesthesia in these children carries a significant risk of pulmonary aspiration as a result of esophageal stasis and requires strategies to mitigate this risk. Prolonged fasting times may decrease the food burden in the esophagus but do not guarantee an empty esophagus. Awake (or sedated) nasogastric tube placement with esophageal evacuation before induction can further decrease esophageal content. Nebulized lidocaine beforehand can help facilitate this process. Rapid sequence induction should be performed by an experienced laryngoscopist with the head of the bed elevated.
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