6.1 Nutrition (01.J)

A neuro ICU patient who cannot eat still has a gut, a liver that must see nutrients, and a brain that pays for both starvation and overfeeding. This section covers enteral nutrition (EN), parenteral nutrition (PN), dysphagia after stroke, post-pyloric versus gastric tubes, conceptual protein goals, refeeding syndrome, stress hyperglycemia including the SHINE trial, and when feeds must stop. Independent OpenExamPrep material here follows topics listed under Nutrition in the ABPN Content Specifications. It is not an ABIM or ABPN product.

Why nutrition items show up on this examination

The trap is rarely "name a brand of formula." It is a middle-aged MCA infarct who is NPO for three days while someone waits for a "real" gastrostomy; a patient on 0.5 mcg/kg/min of norepinephrine whose gastric tube is advanced to goal and who then develops rising lactate and a board-like abdomen; or a chronically starved alcoholic whose phosphate is 1.1 mg/dL twelve hours after a full-calorie start. Those vignettes test timing, route, and when to hold, not calorie arithmetic.

Timing: EN versus PN

If the gastrointestinal tract works and shock is controlled, start EN within 24–48 hours of ICU admission. ASPEN/SCCM adult critical-care nutrition guidance and ESPEN ICU guidance both prefer early EN over waiting a week or starting PN by default. The gut's benefit is not mystical: it preserves mucosal barrier function, avoids central-line infection risk, and supplies the portal circulation. PN is intravenous amino acids, dextrose, and lipid through a central (or, for some short peripheral formulas, a large peripheral) catheter. It is rescue when the gut cannot be used, not a faster way to "catch up" calories on day 1 in a low-risk patient.

Low nutrition risk patients (short expected NPO time, decent prior intake, no severe malnutrition) can wait several days — commonly toward day 7 in ASPEN/SCCM-style algorithms — before supplemental PN if EN is still not feasible. High nutrition risk or frankly malnourished patients (NRS-2002 or NUTRIC in the high range, BMI well below 18.5, weeks of poor intake) should not be left empty if EN is impossible; earlier PN is reasonable while you watch for refeeding. Do not use serum albumin or prealbumin as a nutrition-status stamp. They fall with inflammation and do not tell you whether yesterday's drip met protein needs.

Advance toward goal over 24–48 hours once EN is tolerated. High-risk or malnourished patients are often pushed toward more than 80% of estimated energy and protein within 48–72 hours, with refeeding laboratories in the same window. The first ICU week is also when overfeeding (full predictive-equation calories plus propofol lipid plus dextrose infusions) produces hyperglycemia, lipogenesis, and CO2 load. Indirect calorimetry, when available, beats a chalkboard equation in burns, obesity, and week-long ICU stays. If you lack a cart, many teams use about 25–30 kcal/kg/day as a starting energy frame in non-obese adults and then cut back if the patient is in uncontrolled shock, is refeeding, or is receiving substantial propofol (about 1.1 kcal/mL of 1% emulsion). Those energy figures are planning ranges, not a single official examination constant.

NUTRIREA-2 (Reignier and colleagues, Lancet 2018) randomized ventilated patients on vasopressors to early full EN versus early PN. EN did not improve mortality and produced more vomiting and more bowel ischemia (about 2% versus under 1%). That trial is why "the gut always wins on hour one of septic shock" is a dangerous slogan. Early trophic EN (often 10–20 kcal/h, or up to about 500 kcal/day) in controlled shock on modest, stable vasopressors is a different plan from slamming goal rate in a patient whose norepinephrine is still climbing.

Dysphagia, aspiration, and swallow screens after stroke

Acute ischemic stroke, ICH, and some SAH patients have a high rate of oropharyngeal dysphagia. Silent aspiration is common. A family member saying "he swallowed water in the ambulance" is not a screen.

Nothing by mouth — including oral pills crushed in applesauce — until a swallow screen is passed or a safe alternative route exists. Nursing bedside screens (for example a graded water-swallow protocol such as the Yale Swallow Protocol) are designed to be sensitive, not to replace instrumental testing. Failure sends the patient to a speech-language pathologist. Videofluoroscopic swallow study (VFSS) or fiberoptic endoscopic evaluation of swallowing (FEES) defines the physiology when the bedside examination is unclear, when the stroke is large or brainstem, or when you need to upgrade from NPO to a texture. Until then, give critical medications intravenous or enteric-tube, not "just this one aspirin by mouth."

Aspiration pneumonitis and ventilator-associated or hospital-acquired pneumonia cluster with failed screens, depressed consciousness, vomiting, and supine gastric feeding. Head-of-bed elevation, oral care, and a correct tube position are part of the same problem as formula choice.

Nasogastric tubes first; PEG is not an emergency on day 1

A nasogastric (NG) or orogastric tube is the default early enteric access after stroke. It can be placed at the bedside, checked (radiograph, not auscultation alone), and removed if the swallow returns in days. Percutaneous endoscopic gastrostomy (PEG) creates a durable gastric stoma. It is appropriate when dysphagia is expected to last weeks, when the NG tube keeps coming out and you cannot safely replace it, or when a rehabilitation facility will not accept a nasal tube. It is not an emergency on the afternoon of the infarct.

The FOOD trials (Dennis, Lewis, Warlow, Lancet 2005) tested feeding policy after dysphagic stroke. Early PEG versus nasogastric feeding was associated with an absolute increase of about 7.8% in death or poor outcome at six months. That is the opposite of the reflex "get a PEG tonight so rehab will take them tomorrow." Early tube feeding versus waiting also failed to show a large, clean mortality win for rushing access. In practice, many stroke services keep an NG tube for about 1–2 weeks (sometimes up to about 4 weeks if recovery is clearly underway) and schedule PEG only if a safe oral diet is still unrealistic. Surgical gastrostomy or radiologic gastrostomy is a technical variant of the same delayed decision. Absolute PEG contraindications (uncontrolled coagulopathy, intervening organs, abdominal wall infection) are a gastroenterology problem; the examination point is timing.

Gastric versus post-pyloric EN

Gastric feeding is simpler and uses the stomach as a reservoir. Post-pyloric feeding (nasoduodenal or nasojejunal, or a surgical/endoscopic jejunostomy) delivers formula beyond the pylorus. Choose post-pyloric access when gastric emptying is poor, residual volumes stay high despite prokinetics, the patient must remain flat (unstable spine, some procedures), severe gastroesophageal reflux or documented gastric aspiration keeps recurring, or gastric outlet obstruction leaves the small bowel usable. Severe acute pancreatitis is a classic non-neuro indication for jejunal feeding when EN is used.

Post-pyloric tubes do not abolish aspiration of oropharyngeal secretions. They reduce the chance that a large gastric residual will reflux. Confirm tip position on radiograph before use. Bedside electromagnetic placement systems still need a protocol for confirmation. Do not start a pressor-unstable patient on post-pyloric feeds just because the tube went farther down; ischemia risk follows mesenteric perfusion, not centimeters past the pylorus.

Gastric residual volume (GRV) is a weak isolated stop rule. ASPEN/SCCM-style practice is to avoid holding EN solely for GRV under about 500 mL if the abdomen is soft, there is no vomiting, and the radiograph does not show ileus. Holding for 150 mL residuals is how ICUs starve people. Intolerance looks like vomiting, abdominal distention, rising lactate, diarrhea with a surgical abdomen, or radiographic obstruction — not a single milliliter number.

Protein goals, conceptually

Critically ill adults are catabolic. Published adult ICU ranges commonly put protein at about 1.2–2.0 g/kg actual body weight per day when BMI is under 30, with burns and multitrauma often toward the high end (about 1.5–2.0 g/kg, sometimes higher). Severe TBI is a hypermetabolic state; teams often plan protein in that higher band rather than a ward-diet 0.8 g/kg. In obesity, ASPEN/SCCM-style dosing uses ideal body weight for protein (often ≥2.0 g/kg IBW for BMI 30–40, and up to about 2.5 g/kg IBW for BMI ≥40) while energy is restricted relative to measured or high actual-weight estimates. Continuous renal replacement can remove amino acids; many dietitians push protein toward the top of the range. These are conceptual ranges from nutrition societies, not a single ABPN-published gram number. The examination cares that you do not treat a 100 kg TBI patient as if 40 g of protein a day were enough, and that you do not confuse albumin with a protein prescription.

The EFFORT Protein trial later showed that pushing protein even higher does not automatically improve outcomes and may harm some patients with acute kidney injury. More is not always better. Match the prescription to weight, trauma burden, and dialysis, then reassess.

Refeeding: phosphate and thiamine

Refeeding syndrome is the insulin-driven intracellular shift of phosphate, potassium, and magnesium when carbohydrate returns after starvation. Cardiac arrhythmia, respiratory muscle failure, and delirium follow a phosphate that falls through 1.5 mg/dL toward 1.0. Risk markers include very low BMI, little or no intake for 5–10 or more days, alcoholism, and already-low electrolytes. Thiamine (commonly 100–300 mg IV, then daily) goes in before or with the first dextrose or formula load; Wernicke encephalopathy is the neurologic price of carbohydrate without thiamine. Start calories low (NICE-style teaching often begins near 10 kcal/kg/day in the highest-risk patients) and increase over several days while replacing electrolytes proactively, not after the next morning's panic laboratory. Check phosphate, potassium, and magnesium every 6–12 hours for the first 2–3 days of refeeding. Do not correct hyponatremia with free-water formula boluses while you are also chasing phosphate — those are separate orders.

Stress hyperglycemia and SHINE

Critical illness raises counter-regulatory hormones and insulin resistance. After stroke, hyperglycemia is associated with worse edema, hemorrhagic transformation, and outcome. Association is not a license for tight insulin drips.

NICE-SUGAR (NEJM 2009) compared intensive insulin targeting 81–108 mg/dL with conventional control aiming under 180 mg/dL in ICU patients. Intensive control increased 90-day mortality (27.5% versus 24.9%) and caused more severe hypoglycemia. Adult ICU practice therefore usually targets about 140–180 mg/dL, not a normal fasting glucose.

SHINE (Stroke Hyperglycemia Insulin Network Effort; Johnston and colleagues, JAMA 2019) enrolled 1,151 adults with acute ischemic stroke and hyperglycemia, about 80% with diabetes, within 12 hours of onset. Intensive continuous IV insulin targeting 80–130 mg/dL for up to 72 hours did not improve a favorable 90-day modified Rankin Scale rate versus standard subcutaneous sliding-scale insulin targeting 80–179 mg/dL (20.5% versus 21.6%). Enrollment stopped for futility. Severe hypoglycemia (<40 mg/dL) occurred in 2.6% of the intensive arm and none of the standard arm. Mean on-treatment glucose was about 118 versus 179 mg/dL, so the arms were truly different — the intensive arm just did not help function. AHA/ASA acute ischemic stroke material commonly keeps early glucose in a moderate band near 140–180 mg/dL. Do not order a neuro-ICU insulin drip to 100 mg/dL "because the brain likes euglycemia."

Treat hypoglycemia immediately. A single severe low glucose can erase any theoretical benefit of a pretty glucose chart.

When to hold feeds

Hold or never start EN when the bowel is the ischemic organ or the abdomen is a surgical emergency. Escalating high-dose vasopressors during active, incomplete resuscitation is the other classic hold: the gut is already vasoconstricted. Stable, modest, falling vasopressor doses after source control and volume are not an automatic NPO order; they are a reason to start low and watch the abdomen. Mesenteric ischemia — occlusive or non-occlusive — is a hard stop. Feeding an infarcted bowel is how you get pneumatosis, perforation, and a trip to the operating room that should have happened earlier.

Contraindications to gastric EN

Relative holds that are not automatic PN include isolated GRV under 500 mL, diarrhea without peritonitis, and a single episode of vomiting that stops after a rate reduction and a prokinetic.

Worked bedside scenarios

A 68-year-old with a right MCA occlusion fails a water swallow at 4 hours. The correct nutrition move is NPO, NG tube if they will not eat safely by the next calendar day, and a speech consult — not a same-day PEG "so the floor will take them."

A 55-year-old with septic shock is on rising norepinephrine and a fresh 3 L crystalloid load. Lactate is 6 mmol/L. Do not start goal-rate gastric EN. Finish resuscitation. If the gut is later usable on a stable, modest pressor, begin trophic EN and watch the abdomen.

A 45-year-old with alcoholism, BMI 16, and no food for 10 days has phosphate 2.0 mg/dL. Give thiamine, replace phosphate, potassium, and magnesium, and start a low-calorie EN or dextrose plan — not a 25 kcal/kg jump to "catch up."

Exam traps

Ordering a day-1 PEG after hemispheric stroke. Starting full gastric EN during escalating shock. Treating a GRV of 280 mL as a reason for PN. Using albumin as a nutrition score. Targeting glucose 80–110 mg/dL after SHINE and NICE-SUGAR. Forgetting thiamine in refeeding. Calling post-pyloric feeding a cure for all aspiration.