Which access route is most appropriate for a patient expected to need enteral feeding for many months?
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Clinical Pharmacology · Hepatic and Nutrition Pharmacology
Enteral and Parenteral Nutrition
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Nutrition support feeds patients who cannot eat enough by mouth. The rule is "if the gut works, use it": enteral feeding preserves the gut lining, limits bacteria crossing out of the intestine, and is cheaper and safer than feeding through a vein. Parenteral nutrition, given intravenously, is reserved for when the gut cannot be used at all. Both routes carry real risks, and refeeding a starved patient too fast can trigger refeeding syndrome.
The college version
Enteral Nutrition
Enteral nutrition delivers formula into the stomach or small intestine. Nasogastric or nasojejunal tubes, placed through the nose, suit short-term use; a gastrostomy or jejunostomy tube through the abdominal wall suits feeding expected beyond a few weeks, since it irritates less and tolerates longer use. Formulas are broadly polymeric (intact proteins, fats, carbohydrates, for normal digestion), elemental (predigested nutrients for impaired digestion or absorption), or disease-specific (adjusted for conditions like renal or hepatic disease). Delivery can be bolus (a set volume over minutes), intermittent (given several times daily), or continuous (a slow pump infusion, often for jejunal tubes or critical illness).
Nursing priorities center on safety: verifying placement before feeding and periodically thereafter, since a misplaced tube risks delivering formula into the lungs; keeping the head of the bed elevated during and after feeding to reduce aspiration risk; checking tolerance for distention or excessive residual volume; and flushing the tube before and after each feeding and medication to maintain patency. Extended-release and enteric-coated medications are never crushed, since crushing destroys the timed-release mechanism and can cause a dose dump; an alternate formulation is used instead. Medications are given separately, never mixed into the formula, since mixing can cause clumping or occlusion. Continuous feeding raises two concerns: it can reduce phenytoin absorption, requiring a feeding pause around the dose, and formula's vitamin K can blunt warfarin, requiring closer monitoring. Complications include aspiration, occlusion from poor flushing, dislodgement, and diarrhea, which is often caused by sorbitol-containing liquid medications or antibiotics rather than the formula itself, so reviewing medications often resolves it. Constipation can also occur with low-fiber formulas or reduced mobility.
Parenteral Nutrition
Parenteral nutrition bypasses the gut entirely, for when the tract cannot be used safely, as with bowel obstruction, severe ileus, short bowel syndrome, or inadequate enteral intake. Peripheral parenteral nutrition uses a peripheral vein only briefly, with lower-concentration solutions, because hypertonic mixtures damage smaller veins, causing irritation and thrombophlebitis; higher-osmolarity solutions need central venous access, where a large, high-flow vessel rapidly dilutes the concentrated fluid. The formulation supplies macronutrients (amino acids, dextrose, lipid emulsion) and micronutrients (electrolytes, vitamins, trace elements), tailored to the patient.
Complications reflect composition and access: catheter-related bloodstream infection from the indwelling line; hyperglycemia from the dextrose load, requiring glucose monitoring and sometimes insulin; hypertriglyceridemia from the lipid component; and electrolyte derangements. Long-term use is linked to hepatic steatosis and cholestasis, likely from overfeeding, lipid composition, and reduced enteral stimulation of bile flow. Because the body raises insulin output in response to steady glucose, abruptly stopping the infusion can cause rebound hypoglycemia, so it is tapered off.
Refeeding Syndrome
Refeeding syndrome is the classic hazard of reintroducing nutrition, enteral or parenteral, to a significantly malnourished patient. During prolonged starvation, insulin secretion falls and the body breaks down fat and protein, while intracellular phosphate, potassium, and magnesium become depleted even though blood levels may look normal. When feeding resumes, especially with carbohydrates, insulin surges in response, driving glucose, phosphate, potassium, and magnesium out of the blood and into cells, causing a sudden drop in serum levels. Phosphate depletion is especially dangerous, contributing to cardiac and respiratory muscle dysfunction. Thiamine, needed to metabolize the incoming carbohydrate load, can also become critically depleted, risking neurologic complications. The guiding principle is to start low, go slow, and monitor electrolytes and clinical status closely, replacing thiamine and correcting deficits proactively.
Eli explains
The same idea, in plain words
Explain it like I’m 10
Your stomach and intestines are like a garden hose. If the hose still works, you use it to water the plants, because that is the natural, cheapest, safest way. That is enteral feeding: pouring liquid food through a tube into a working gut. If the hose is broken or blocked, you water the plants a different way, straight from a different pipe. That is parenteral nutrition: feeding straight into a vein because the gut cannot be used. Both ways can go wrong if you are not careful, like feeding too fast or forgetting to flush the tube clean. The scariest problem is refeeding syndrome: if someone has been starving a long time and you suddenly give them a big meal, their body gets so excited it grabs important minerals from the blood and hides them inside cells all at once, which can make the heart and lungs weak. So doctors feed a starved body slowly, like gently turning a squeaky faucet instead of blasting it open.
Check yourself
2 review questions from the chapter. Try each one, then open the answer.
A severely malnourished patient starting nutrition support develops new hypophosphatemia, hypokalemia, and hypomagnesemia within two days. What is happening, and what physiologic trigger explains it?
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Refeeding syndrome, triggered by an insulin surge
Feeding a starved body causes insulin to spike in response to incoming glucose, and that insulin pushes phosphate, potassium, and magnesium out of the blood and into cells at once, dropping their blood levels.
A patient's enteral medication list includes an extended-release tablet. Explain why it cannot simply be crushed and given through the feeding tube, and what should be done instead.
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Crushing destroys the extended-release mechanism, so an alternative form is needed
The coating controls how slowly the drug releases, and crushing breaks that control, dumping the whole dose at once and risking toxicity; the nurse should get an immediate-release or liquid version approved instead.
Quick check
3 questions here. Answers stay hidden until you check.
A patient on continuous enteral feeding starts phenytoin and later has a subtherapeutic level despite no dose change. What is the most likely explanation?
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Why does a hypertonic parenteral nutrition solution require central venous access rather than a peripheral line?
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