Enteral feed obstructing its own way Case

Esophageal obstruction due to solidi ﬁ ed enteral feeds is a rare but distressful complication in intensive care unit (ICU) patients. It has been suggested that gastroesophageal re ﬂ ux, very low gastric pH, decreased pepsin and pancreatic enzyme secretions may be responsible for the solidi ﬁ cation of casein containing enteral formulas. Recognition and avoidance of these factors will prevent such complication.


Introduction
Early enteral feeding in critically ill patients in intensive care unit (ICU) is a fairly well-established approach. Amongst various complications associated with naso-gastric (NG) feeding, "diarrhea" and "tracheal aspiration" are the most common. [1,2] Esophageal obstruction due to the feed solidifi cation is infrequent and has seldom been reported.
A patient in our ICU developed esophageal obstruction due to solidifi cation of enteral feed, which led us to review our experience in the light of published literature. This case report and overview of pertinent literature intends to facilitate physicians to re-evaluate their approach to enterally fed patients, aiming to identify factors responsible for feed solidifi cation.

Case Report
A 71-year-old Caucasian man was admitted to our ICU with type 2 respiratory failure and severe hyponatremia. His past medical history included hypertension, gout, unilateral nephrectomy for renal tuberculosis and carotid endarterectomy.
The patient was intubated on the day of ICU admission for worsening respiratory failure and altered sensorium. A 14-French salem sump NG feeding tube was placed and NG tube tip position was confi rmed on low chest radiograph to be in the stomach. Continuous infusion of polymeric, isotonic, fi ber-mixed suspension (1 kcal/ml, Jevity ® , Abbott Nutrition) was commenced and target feeding rate of 2000 kcal/day was achieved in 12 hours. The NG tube was fl ushed every 4-hourly with 30 ml of water. Medications administered through the NG tube during his ICU stay were metoprolol, lercanidipine, amlodepine, omeprazole, amiodarone, temazepam, folic Acid, coloxyl with senna and lactulose.
The patient underwent tracheostomy on the 18 th ICU day after a failed extubation trial. Simultaneously, the NG tube was changed to 12-French polyurethane fi ne-bore tube. On the 47 th ICU day, a computerized tomography (CT) scan was done to delineate lung opacities seen on chest X-ray, and coincidentally, an intra-luminal space-occupying lesion in the esophagus was observed [ Figure 1].
Concurrently, blockage of the NG tube necessitated its removal and a new NG tube could not be inserted beyond the hypopharynx. Fiber-optic esophagoscopy showed a white caseous substance with fi rm cheesy consistency completely obstructing the lumen of the distal esophagus [ Figure 2]. This material could not be removed with the fi ber-optic instrumentation, although at one time the esophagoscope went beyond the obstruction into the stomach with no evidence of any obstruction distally.
It took considerable time and three sittings over the next 3 days to scrap out the concretions from the lower 2/3 rd of esophagus with biopsy forceps, suction and repeated washouts performed through a rigid esophagoscope. The obstructing material was not adherent to the esophageal mucosa [ Figure 3]. The naked eye appearance of the removed material was the same as the solidifi ed enteric feed.
Subsequently, a new NG tube was inserted and enteral feed recommenced. Over the next 2 weeks, the patient could be weaned from ventilator, was decannulated and discharged to the ward.
We could conclude that the esophageal obstruction had been caused by solidifi ed enteric feed, as no other reason could account for such a clinical picture.

Discussion
We searched Medline, Embase and Cumulative Index to Nursing and Allied Health Literature (CINAHL) from January 1980 to February 2009, using the following search terms: "nasogastric feed", "enteral feed", "oesophageal obstruction" and "oesophageal bezoar". The literature appeared to be scattered and pointing toward various hypotheses postulated for the esophageal obstruction due to enteral feeding:

Altered esophageal tone and motility coupled with gastroesophageal refl ux
In mechanically ventilated patients, some degree of gastroesophageal refl ux is unavoidable. Nasogastric tube can lead to loss of sphincter action of gastroesophageal junction with subsequent refl ux of gastric acid and food contents from stomach. [3] Likewise, altered esophageal tone and motility will cause enteral feed stasis and precipitation. [4] By performing in vitro tests, Irgau et al. [5] demonstrated that stasis of the enteral feed formula and its fi ber contents is not responsible for solidifi cation by itself but is due to gastroesophageal acid refl ux.  The factors that led to the formation of esophageal bezoar in our patient were casein-rich tube feeding, gastric stasis and acid refl ux.
We recommend the following strategies to prevent esophageal obstruction caused by solidifi cation of enteric feed: 1. The proximal side-port and the distal tip of the NG tube should be visualized on a radiograph to be within the stomach before commencing and continuing enteral feeds. 2. Simple measures such as 30° head-up position will help prevent gastroesophageal refl ux and gastric pooling. 3. Periodic fl ushing of the feeding tube will reduce the incidence of food stasis. 4. Avoid combining enteral formula and sucralfate. 5. In patients with peptic ulcer disease, signifi cant gastroesophageal refl ux and diseases with abnormal pepsin or pancreatic secretion; avoid caseincontaining feeds and use adequate doses of acid lowering medications.