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A 71-year-old obese female with no previous esophageal or gastric dysfunction was admitted for elective coronary artery bypass grafting. Postoperatively an 18-Fr. Argyle(r) Salem Sump(r) (Sherwood Medical, St. Louis, MO) orogastric tube was placed. Full strength Nutren-2.0 feed (Nestle Clinical Nutrition Company, Mississauga, Ont.) was initiated on the third postoperative day at 25 ml/hr, and increased to a final rate of 45 ml/hr. The patient remained intubated, ventilator dependent and was subsequently transferred from the cardiac surgery unit to the ICU on the fifth postoperative day. Neither H2 receptor blockers nor omeprazole was administered. Several times during day 6 and 7 the patient vomited small amounts of formula-like material after oral suctioning. Tube tip position was repeatedly checked by air injection and auscultation, by the ability to obtain gastric returns and by review of the chest radiographs. Blue food coloring was added to the formula and enteral nutrition continued. During days 8 and 9, two further episodes of emesis containing yellow/green formula-like fluid occurred with oral suctioning. However, visualization of the side port was hampered by the presence of midline surgical staples. This, together with poor film quality due to motion artifact and underexposure, resulted in misdiagnosis of the true tube tip position. Attempts at tube advancement and removal were met with resistance. A more forceful attempt at removal dislodged the tube, the esophageal portion of which was completely encrusted by a mass of inspissated formula-like material (Figures 1).
An additional large solid mass of this material was suctioned from the oral cavity. A new 14-Fr. Salem Sump(r) tube was inserted nasally without resistance and the position confirmed radiologically. Enteral nutrition was resumed, and continued uneventfully over the next 17 days until the patient died following a cardiac arrest.
A 66-year-old male with 35 % burns and no known history of esophageal or gastric dysfunction was admitted to the ICU, from the burn unit, following 3 days of enteral feeding with Osmolite HN(r) (Ross Products Division, Columbus OH) via an 18-Fr. Argyle(r) Salem Sump(r) nasogastric tube. On admission to the ICU, a chest radiograph revealed the proximal side port of the tube to be situated at the level of the gastroesophageal junction. Several attempts were made to either reposition or remove the tube, but each attempt was met with resistance. The tube was finally removed with the application of gentle force. Numerous attempts were made to insert a new tube but each insertion met with resistance. Endoscopy revealed a creamy white semi-solid concretion extending throughout the length of the esophagus. Using the endoscope, the mass was pushed through the esophagus into the stomach. An 18 Fr. Salem Sump(r) nasogastric tube and a 12 Fr. Entriflex(r) (Sherwood Medical, St. Louis, MO) nasoduodenal feeding tube were subsequently inserted and feeding resumed. No further problems arose with enteral feeding over the remainder of the ICU stay. On day 10, the severity of the burn injury and multiple organ failure resulted in withdrawal of active treatment.
A 52-year-old female was admitted to the ICU following a high-speed motor vehicle accident. Injuries included transection of the thoracic aorta, multiple rib fractures, pulmonary contusions, a left subdural hematoma and several small liver lacerations. After urgent surgery to repair the aorta and pericardium, the clinical course was complicated by pneumonia and progressive multiple organ failure including acute respiratory distress syndrome. Although initially tolerant of gastric feeding via a Salem Sump(r) orogastric tube, gastric stasis impeded enteral feeding on the ninth postoperative day. On day 10 an attempt was made to manually position a 12 Fr. Entriflex(r) nasoenteric feeding tube into the duodenum. The initial attempt met with resistance in the nasopharynx. During a second attempt by another operator the tube was passed with minimal resistance. Straw colored fluid with some blood streaking was aspirated. Injected air was auscultated in the midepigastrium. A low chest radiograph (Figure 2) showed that the nasoenteral tube followed the same course as the original nasogastric tube but the distal tip of the new feeding tube was not visualized.
Osmolite HN(r) was administered through the new tube and the infusion titrated up towards the goal rate. Over the next 24 hours the patient continued to deteriorate, with increased inotropic requirements and progression to anuric renal failure. The abdomen became more distended but because of sedation and neuromuscular blocking agents clinical assessment was difficult. An abdominal ultrasound on day 12 revealed free peritoneal fluid. Peritoneocentesis yielded thick cream-colored fluid, which looked like formula and was negative for pus or organisms on Gram stain. Tube feedings were immediately discontinued and the patient was taken for urgent exploratory laparotomy.
A diffuse chemical peritonitis was present and 1.5 liters of thick cream-colored fluid with fibrin deposits were removed from the abdominal cavity. The Entriflex(r) feeding tube was seen emerging from the mid-anterior stomach and an intramuscular tract could be traced to the level of the gastroesophageal junction. Intraoperative endoscopy demonstrated that air, which was insufflated into the oropharynx, passed into the peritoneal cavity via the tract formed by the Entriflex(r) tube. On day 13, progressive severe acidosis, refractory shock and multiple organ failure resulted in the withdrawal of active treatment. At postmortem examination, chemical peritonitis was present along with the expected evidence of injury and multiple organ failure. A Zenker’s diverticulum was discovered but the feeding tube had actually perforated the piriform sinus creating a subserosal tract along the esophagus with an exit site in the mid-anterior stomach.
In the first two case reports, the tube was retrospectively determined to be in poor position with the proximal side port at the level of the gastroesophageal junction despite repeated clinical and radiological “confirmation” of proper tube placement. In the first case report, the true position of the tube was ascertained from radiographs and measurement of tube discoloration (indicating contact with body tissues). The position of the tube was further confirmed by the location of the concretion around the tube.
For enterally fed patients who are not receiving medications known to be associated with concretion formation it is believed that tube feeding formula remaining in contact with gastric acid can result in the precipitation of casein and the subsequent formation of a solid mass. It is also believed that a large-bore tube passing through the gastroesophageal junction enhances gastric reflux thus allowing gastric acid to reach the lower esophagus. We were able to rule out a break in the integrity of the tube. This further supported the fact that formula extravasation occurred at the gastroesophageal junction. This was the position of the proximal port of the nasogastric tube. Therefore the primary factor in esophageal concretion formation in the first two patients was the malpositioned tube, which allowed esophageal extravasation of formula, and its subsequent contact with refluxed gastric acid.
The second tube complication has not been previously described. Sedation and neuromuscular blockade may have masked early warning signs of feeding tube malposition in this patient. Tube placement was assessed by aspiration of gastric-type contents and by auscultation in the epigastrium of insufflated air. As well, the chest radiograph showed the new tube traveling beside the previously placed nasogastric tube and passing below the level of the diaphragm. This was felt to be adequate information to confirm tube placement and tube feedings were started. However, the distal metallic tip was not included on the radiograph. The use of sedatives and neuromuscular blockade led to a delay in the correct diagnosis of nasoenteral tube malposition with chemical peritonitis resulting from the presence of formula in the peritoneal cavity.
Another unusual feature of this case is the path that the Entriflex(r) tube had taken. The most common site of perforation by small-bore tubes is into the thoracic cavity (12-14) after endobronchial misplacement. This problem is readily identified by radiography. The one case of submucosal dissection reported in the literature is that of a patient undergoing elective cholecystectomy where placement of the gastric tube met resistance after 10 centimeters. Direct visualization showed the tube to be passing submucosally and it was withdrawn without complication (22). There seemed to be no predisposing factors in that case. It is unclear as to why the nasoenteral tube dissected submucosally in our patient.
Feeding tube malposition may be associated with serious complications in the critically ill patient. Clinical signs of feeding tube malposition may be absent in the critically ill and so radiologic visualization remains the gold standard in the placement of both large bore and flexible small diameter feeding tubes. The correct radiographic technique and careful inspection of the radiograph for the proximal side port and distal tip is mandatory.