Published on 07/02/2015 by admin
Filed under Anesthesiology
Last modified 22/04/2025
This article have been viewed 1117 times
Robert J. Friedhoff, MD
Pyloric stenosis is one of the most common gastrointestinal abnormalities occurring during the first 6 months of life. The incidence is 1 in 500 live births in whites and 1 in 2000 in blacks, with males having a two to four times increased incidence, compared with females. It is especially common in first-born sons of parents who had pyloric stenosis.
Pyloric stenosis usually presents at 3 to 5 weeks of age in the preterm or term infant. Although the cause is unknown, proposed mechanisms include an imbalance in the autonomic nervous system, humoral imbalances, infection, or edema with muscular hypertrophy. Hirschsprung first described pyloric stenosis in 1888, although he could offer no effective treatment. Ramstedt described the optimal surgical therapy in 1912. Since then, improvements in fluid therapy and anesthetic technique have decreased the mortality rate from 25% to 0.01% to 0.1%.
In pyloric stenosis, a thickening of the circular muscular fibers in the lesser curvature of the stomach and pylorus (from both hypertrophy and an increased number of fibers) causes obstruction of the pyloric lumen. The typical presentation is an infant with persistent bile-free vomiting who is dehydrated and lethargic. The skin is cool to touch, capillary refill is usually greater than 15 sec, and the eyes are sunken. The infant may present at less than its birth weight. Vomiting can be projectile (2 to 3 feet), occurring after every feeding, thus resulting in loss of hydrogen, chloride, sodium, and potassium ions from the stomach.
A metabolic alkalosis develops for several reasons. First and foremost is the loss of hydrogen ions from the stomach. The vomitus does not contain any of the alkaline secretions of the small intestine because the obstruction is proximal (at the gastric outlet). Bicarbonate is one of the ions contained in pancreatic secretions, but because little food reaches the duodenum, pancreatic output is decreased, and bicarbonate remains in plasma (instead of being secreted by the pancreas).
Volume depletion stimulates aldosterone secretion, the distal tubules and collecting ducts retain fluid and sodium and, initially, chloride. As chloride concentration in the plasma and glomerular filtrate decreases, the kidneys begin to retain bicarbonate over chloride, the net result of which is a profound hypokalemic hypochloremic metabolic alkalosis. Eventually, acidic urine is produced because, as the volume and electrolyte concentrations worsen, potassium, rather than hydrogen, is retained preferentially. At this stage, maximal chloride ion conservation in the kidney results in a urinary chloride concentration less than 20 mEq/L.
When examining the infant, the clinician can palpate an olive-sized mass in the midepigastrium. This finding, along with the history, is diagnostic in 99% of cases of pyloric stenosis. Noninvasive diagnostic tests include ultrasound, which can confirm the diagnosis. The “string sign” on barium swallow shows elongation and narrowing of the pyloric canal. Elevated levels of unconjugated bilirubin are seen in 20% of patients with pyloric stenosis.
Pyloric stenosis is a medical emergency, not a surgical emergency. The degree of dehydration may be determined by weighing the infant and measuring bicarbonate and chloride levels. Treatment is instituted with intravenously administered normal saline with 5% dextrose at a rate of 3 L·m−2·day. After urine output is established, 40 mmol of potassium can be added to each liter of fluid. Therapy is aimed at repleting intravascular volume and correcting electrolyte and acid-base abnormalities. A urine chloride concentration greater than 20 mEq/L implies that the volume status has been corrected. The plasma chloride concentration should then be greater than 105 mEq/L.
Anesthetic considerations for pyloric stenosis include the usual neonatal anesthetic concerns; fluid, electrolyte, and glucose balance; anesthesia for a patient with a full stomach who is prone to vomit; and postoperative complications. Patients with pyloric stenosis are at increased risk of vomiting and aspirating gastric contents. After intravenously administering atropine (20 μg/kg) but immediately before inducing anesthesia, the anesthesia provider should empty the patient’s stomach as completely as possible by passing a large-bore (14F multiorifice) orogastric tube two to three times because gastric volume prior to induction averages 96 mL ± 7 mL independent of the fasting interval, prior use of a nasogastric tube, or barium studies. Routine monitors should be applied. The preferred method of induction is either through a rapid sequence or modified rapid sequence intravenous induction using cricoid pressure. Awake oral tracheal intubation, or even intubation after an inhalation induction, has also been described, although these techniques are rarely used.
After general anesthesia is induced, a nasogastric tube should be inserted and left in place during the operation to allow testing of the integrity of the pyloric wall after the surgeon performs the pyloromyotomy. Laparoscopic surgical repair has the advantage of shorter times to full feeding and shorter hospital stays, compared with the traditional open approach. Anesthesia is maintained with inhalation agents without N2O. Skeletal muscle relaxation may not be needed after induction. Additional opioid analgesia may not be necessary in this age group, which has increased respiratory sensitivity. Rectal acetaminophen can be given in the postanesthesia recovery room.
Postoperatively, the infant may be lethargic. Respiratory depression and apnea may occur and are related to cerebrospinal fluid pH and hyperventilation. For these reasons, the infant should be fully awake and able to sustain a regular respiratory pattern before being extubated. Hypoglycemia, which may occur 2 or 3 h after surgical correction of the stenosis, is probably caused by cessation of intravenously administered glucose infusions and the depletion of glycogen stores from the liver. Small frequent feedings are usually begun 4 to 6 h postoperatively. An uneventful recovery should result in discharge from the hospital in 24 to 48 h.
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