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Case Study:Medical Nutrition Therapy for Paralytic Ileus 914400265430Lara SneadSodexo Mid-Atlantic Dietetic InternFebruary 1, 2013Abstract The following case study report provides detailed information on the complex gastrointestinal (GI) complications of GG, a patient at Washington Adventist Hospital. GG was initially admitted to the Intensive Care Unit (ICU) for respiratory distress, and while there was diagnosed with a small bowel obstruction (SBO) that was later identified as an ileus (a non-mechanical obstruction of the GI tract.1 Throughout GG’s hospital course of over two months, GI complications occurred related to the ileus/SBO. Nutrition support in the form of total parenteral nutrition (TPN) and enteral nutrition (EN) via a nasogastric tube (NGT) were provided during the earlier parts of the hospital stay, and a PO diet was eventually cleared by the Speech Language Pathologist (SLP). In collaboration with the medical care team, nutrition interventions were implemented by the Registered Dietitians (RD) and dietetic intern. The following report will go into further detail of GG’s hospital course.IntroductionGG is a 64 year old male initially admitted to Washington Adventist Hospital (WAH) on November 12, 2012 with possible COPD exacerbation, generalized weakness, and shortness of breath. GG subsequently was transferred to the Intensive Care Unit (ICU) and intubated because of dropping pressure and respiratory distress. There in the ICU, the he was initially seen by Meagan McClure RD, LDN, CNSC on November 13th as a nursing screen referral. Since admission, GG has been seen by a Registered Dietitian ten times and nine times by the dietetic intern accompanied with an RD. At present time, GG remains an inpatient at WAH. Past Medical History & Social HistoryGG’s past medical history is significant for COPD, HTN, anemia, PVD, cellulitis of the lower extremities, and rashes. A brief social history comprises of living with his elderly parents, smoking about one pack of cigarettes per day, and drinking alcohol almost every day.Anthropometric DataHeightAdmit WeightIBW%IBWBMI5’7” (67”)139# (63 kg)148# (67 kg)94%21.8 kg/m2**BMI within normal weight categoryHospital CourseOn the day GG was admitted to WAH, he developed an acute arterial occlusion of the right lower extremity and an emergency right femoral enarterectomy and embolectomy were performed, as well as fasciotomies of the lower part of the right leg. The following day when the RD saw the patient, he was intubated, sedated, on two pressors (Levophed and Vasopressin), and was nonresponsive to voice or questions. His abdomen appeared distended, he was NPO, and it was recommended to initiate enteral nutrition once he became more hemodynamically stable. Upon the next visit by the RD, GG had become more hemodynamically stable despite developing acute renal insufficiency; nevertheless enteral nutrition had been initiated via a nasogastric tube (NGT). In the follow-up visit on Nov. 15th, GG remained intubated and was receiving and tolerating Nepro @ 20 mL/hr. Abdominal distention was noted, though not significant enough to hold or discontinue the feeds, and blood glucose levels were slightly elevated so it was recommended to change the tube feeding (TF) to Glucerna 1.2 @ 45 mL/hr.The next visit on Nov. 19th, GG had been extubated, was alert and responsive, though delirious. He had been tolerating the feeds running with Glucerna 1.2 @ 35 mL/hr, so it was recommended to advance the rate to 60 mL/hr to better meet his needs. Unfortunately, when visited again eight days later on Nov. 27th, GG was NPO, had been reintubated and was on full vent support with an oral gastric tube (OGT) on low continuous suction (LCS). According to an abdominal CT performed three days prior, it showed free air consistent with a perforated viscus. Per discussion with the ICU team, there was no plan for surgery at that time. A portable x-ray (KUB) also showed a small bowel obstruction (SBO), thus indicating the need for total parenteral nutrition (TPN)2 and discontinuing any enteral nutrition. Fortunately, three days later, GG had another KUB which showed additional loops of small bowel with gaseous distention more consistent with an ileus versus a SBO. The abdominal x-ray showed contrast able to exit the small bowel; therefore the ICU team believed GG had a localized ileus. GG had gone into cardiac arrest two days prior and general surgery suspected a small rupture of the stomach secondary to vigorous bagging. The plan was to do gastrografin via the NGT and if there was no extravasation, or leaking of stomach, GG could restart enteral nutrition at a slow, trophic rate, and then advance as tolerated to the new goal of Osmolite 1.5 @ 35 mL/hr with one ProStat (providing a total of 1332 kcal, 68 gm protein). In the interim time, GG was to continue receiving TPN and monitored for restarting tube feeding and possible TPN weaning.Literature ReviewAccording to an article in a 2009 issue of the Cleveland Clinic Journal of Medicine, an ileus is the “absence of intestinal peristalsis without mechanical obstruction.”3 Among surgeons, it is believed that despite having an abdominal or non-abdominal surgery, the GI tract’s motility is disrupted due to the body’s normal physiological response to surgery. Normal times for the small bowel to resume activity are 0-24 hours, 24-48 hours for the stomach, and 48-72 hours for the colon.1 When the postoperative ileus continues longer, it is called a paralytic ileus. Though not usually life-threatening, an ileus can still be painful and uncomfortable for the patient, and is costly as it delays hospital discharge. Postoperative ileuses have been associated with many clinical conditions, but all are connected with GI dysmotility through four possible factors: a sympathetic-parasympathetic imbalance, chemical mediators of bowel activity, inflammation, and narcotic analgesics. 3 The sympathetic nervous system acts by inhibiting the small bowel, whereas the parasympathetic nervous system stimulates it. Since the parasympathetic nervous system has little impact of small bowel activity, and the sympathetic activity is increased, thus the inhibition response is more dominant. Nitric oxide, vasoactive intestinal polypeptide, and possible substance P are chemical mediators that are thought to inhibit neurotransmitters in the gut which slow bowel motility. 1 A postoperative ileus also results from the inflammatory response following surgery, intestinal manipulation, or trauma. One of the most common causes and modifiable risk factor for an ileus is the use of narcotic analgesics, or opiates, to treat postoperative pain. A major disadvantage to using opiates is the effect they have on the GI tract – opiates delay motility, emptying, and colonic movements. Fortunately the effect can be reversed with the use of narcotic antagonists, such as naloxone (Narcan).Signs and symptoms of an ileus include abdominal distention, persistent abdominal pain, nausea and/or vomiting, and inability to tolerate food. Image studies are imperative to exclude an obstruction; however, abdominal radiographs often show multiple dilated loops of small bowel, air-fluid levels, and colonic gas that can indicate both an ileus and SBO. A CT with oral contrast is 90-100% more effective in differentiating an ileus from a complete SBO, although less reliable in differentiating an ileus from a partial SBO.1 Many strategies are used for treating a postoperative ileus. The most common methods include a nasograstric tube for decompression, early postoperative enteral feeding, gum-chewing, and medications such as erythromycin and metoclopramide (Reglan).3 Nasogastric tube placement for decompression has been shown to provide a faster return in bowel function, manage intractable vomiting and prevent aspiration of gastric contents, and improves patient comfort.1 Early enteral nutrition (EN) has been shown to be beneficial as it promotes gut motility, and according to the Journal of Parenteral and Enteral Nutrition (JPEN), it is safe to feed a patient through a mild to moderate ileus.4 Even simply chewing gum can help with an ileus as it stimulates the parasympathetic nervous system without any oral intake. Erythromycin is an antibiotic that is a motilin receptor agonist and Reglan works as an antiemetic and prokinetic that stimulates gastric emptying. It has actually been shown through multiple trials that there is no benefit of these medications in accelerating postoperative GI recovery.1 Hospital Course, ContinuedAt GG’s last follow-up by an RD, it was recommended to continue TPN and initiate tube feedings at a trophic rate and advance as tolerated to new goal. Unfortunately, when GG was seen again four days later on December 4th, the tube feedings had been stopped three days before as he had residuals of 1200 mL. The day of the follow-up, he had vomited, had 300 mL NGT output, had a distended, firm abdomen, and had started Reglan. The RD noted his albumin level to be low at 0.9 g/dL (normal range: 3.4-5.0 g/dL) possibly indicating protein malnutrition despite receiving what was thought adequate support via TPN. Therefore, it was recommended to check his prealbumin and determine if he was meeting his needs with the current nutrition support by conducting a 24 hour metabolic cart as he remained on full vent support and was planning on receiving a tracheostomy on Dec. 6th.Indirect Calorimetry Known as the “gold standard,” indirect calorimetry (IC) is the most accurate method for determining energy needs for critically ill patients in the ICU. IC determines both resting energy expenditure (REE), and respiratory quotient (RQ) by measuring respiratory gas exchange between oxygen (VO2) and carbon dioxide (VCO2).5 It has been long believed that critically ill patients are in hypermetabolism, thus requiring more calories; however, further studies with IC have provided adequate data concerning negative pulmonary consequences associated with increased carbon dioxide production from overfeeding. Patients who were receiving 300-500 less calories a day did not display negative effects during an ICU stay of 7 to 10 days; on the other hand, extended hospital stay of weeks or months and inadequate nutrition support may negatively affect the patient’s clinical course.6 In GG’s case, he had been hospitalized for almost one month, and had failed previous weaning from mechanical ventilation, indicating the appropriate use of IC in the form of WAH’s metabolic cart.Interpreting the RQ better determines the utilization of substrate. An RQ <0.82 suggests underfeeding or predominant lipid catabolism, indicating the need for increased calories. An RQ > 1 with excessive CO2 production suggests overfeeding, lipogenesis, and increased respiratory demand.5 Reviewing the respiratory charting, GG’s RQ was consistently <0.8, indicating the current TPN (1434 kcal, 84 gm protein) was not meeting his needs. The average recorded REE was 2200 calories. Based on that amount, GG was receiving about 65% of his needs. The TPN order was changed to 2L Non-Standard: 19% Dextrose, 4.5% AA, 275 mL Lipids, providing 2206 kcal and 90 gm protein, thus adequate meeting his needs.Along with the new TNP order, it was recommended to trial TF with Jevity 1.2 @ 10 mL/hr if NGT output remained <400 mL over the next 24 hours. Three days later, the RD was asked by the ICU team to reassess GG’s TPN formula because his labs were showing high sodium (Na+) and high chloride (Cl-) levels likely due to the increased calories in the same amount of volume of TPN. The TPN was adjusted accordingly to a greater volume: 2.5L Non-Standard: 15% Dextrose, 3.6% AA, 275 mL Lipids, providing 2185 kcal and 90 gm protein.GG was seen by the same RD the next day for a follow-up visit. He had not tolerated the trial of TF previously recommended as he had 800 mL of NGT output overnight (though NGT was clamped during visit), increased stool output likely increasing his Na+, Cl-, and BUN lab values, and his abdomen remained distended though less than before. An abdominal x-ray on Dec. 10th determined he did not have a SBO that a previous abdominal CT on Dec. 5th had shown, instead the x-ray showed normal transit time and dilated small and large bowel consistent with an ileus. It was recommended to continue with the current TPN order, add ? NS (Normal Saline) IV fluids until stooling improves and labs return to normal, trial Reglan, and if the NGT output was <500 mL in the next 24 hours, trial TF with Jevity @ 10 mL/hr.Follow-Up: December 14, 2012 Since the last visit, GG had been transferred to the IMCU (Intermediate Medical Care Unit) where the dietetic intern started to follow him. Upon GG visit, he continued to receive TPN with the larger volume previously prescribed, and was receiving TF with Jevity @ 20 mL/hr per the RD’s recommendation. During the visit and physical assessment, GG was alert, nonverbal but was responding to questions with nods, and remained on full vent support with the tracheostomy. His abdomen was distended though he denied any pain when palpated and his bowel sounds (BS) were hyperactive. His Flexiseal contained 500 mL of brown liquid stool that had come out in just 3? hours. According to his Registered Nurse (RN), he did not have any residuals. It was also noted that his right toes were necrotic and his inner and outer right calf had staples from the procedure on the day of admission.Medications:Medications were reviewed (see Appendix 1 for an entire list of medications with classification/pharmacological action). The pertinent medications he was receiving on the day of the follow-up were Pepcid and Reglan.Labs:In respect to simplicity and space, only abnormal and symptom-specific lab values are listed and explained below (see Appendix 3 for additional lab values). Prealbumin21-43 mg/dLZn60-130 mcg/dLHgb13.5-18 g/dLHct39-52%WBC4.5-11.0 K/uL8.0 L47 L6.4 L19.6 L20.1 HSerum prealbumin levels have commonly been used to assess protein levels and adequacy of nutrition support. Low prealbumin could indicate protein-energy malnutrition, but according to the Journal of Parenteral and Enteral Nutrition (JPEN), prealbumin is not an appropriate marker for evaluating the adequacy of nutrition support in critically ill patients with inflammation.7 Seeing how GG’s white blood cells (WBC) are high, possibly indicating an infection or inflammation, his prealbumin was likely low due to inflammation. Checking the C-reactive protein (CRP) that is synthesized by the liver during times of inflammation can better explain a low prealbumin. Another lab value that could have possibly been affected by inflammation was zinc (Zn). Zinc is transported bound to albumin, and levels are depressed during inflammation, thus measured zinc levels may be reduced in patients with hypoalbuminemia. Another possible reason for low zinc levels is the amount of diarrhea GG was having. Subclinical zinc deficiency may increase the incidence of diarrhea. Zinc is actively absorbed throughout the small intestines and zinc deficiency has been described in malabsorption syndromes. Also, patients receiving chronic TPN with solutions lacking adequate zinc supplementation or with underlying conditions such as diarrhea, have been shown to have zinc deficiency.8 Both low hemoglobin (Hgb) and low hematocrit (Hct) (referred to as H&H) indicate anemia; there was a pending order for a blood transfusion that day to stabilize his H&H levels. The nutrition problem at the time of the follow-up was questionable malabsorption versus the hypermotility side effect of Reglan as evidenced by 500 mL/stool out over 3? hours. The plan was to continue the TPN, change TF to the elemental formula Vivonex @ 20 mL/hr, recommend discontinuing Reglan, check the CRP, and add 25 mg of Zn to the TPN for 10 days.Elemental FormulasElemental formulas are specially designed enteral nutrition formulas comprised of individual amino acids, glucose polymers, and medium-chain triglycerides (MCT) that require minimal digestive function.9 Vivonex?RTF is an elemental formula that provides 1.0 kcal/mL. It is indicated for transitional feeding, bowel resection, malabsorption, select trauma/surgery, early post-op, and Crohn’s disease.Follow-Up: December 18, 2012Upon the follow-up visit, GG continued receiving the same TPN solution, although his TF with Vivonex @ 20 mL/hr had been on hold due to vomiting and an abdominal x-ray on Dec. 17th was consistent with an ileus. During the dietetic intern’s visit and physical assessment, GG remained on full vent support, was nonverbal, kept his eyes closed, and appeared slightly agitated. His NGT was clamped with no output that day per discussion with the RN; however, he did have a total of 1300 mL out the previous day. The Flexiseal contained 500 mL of liquid brown stool out over eight hours. The physical assessment showed a less distended abdomen compared to previous visit, it was soft and he denied abdominal pain, and there were hyperactive BS in the left lower quadrant. It was also noted that his right toes remained necrotic and skin was peeling off the heel of his right foot.Medications:Medications were reviewed. Reglan had been discontinued as recommended in the previous note. GG remained on Pepcid; Ativan had been added due increased agitation, and potassium chloride (KCl) was added for replete low levels as seen below.Labs:K+3.5-5.1 mEq/LCl-98-107 mmol/LCO221-32 mmol/LHgb13.5-18 g/dLHct39-51%WBC4.5-11 K/uL3.1 L115 H18 L6.7 L ↑20.5 L ↑14.0 H ↓Potassium (K+) levels are likely low due to NGT output and diarrhea. Often times, hypokalemia causes muscle weakness and dysfunction of gastrointestinal muscles, resulting in an ileus as evidenced by distention, anorexia, nausea, and vomiting. Like GG, hypokalemia in patients with ileuses is caused by concomitant diarrhea.10 High chloride (Cl-) and low carbon dioxide (CO2) indicate acidosis likely related to vomiting the previous day. GG’s WBC remained high but was lower than the value at the previous assessment, and his H&H remained low despite a blood transfusion several days before; there was a pending order for another blood transfusion that day to stabilize his H&H levels. The nutrition problem remained the same, malabsorption as evidenced by 500 mL of liquid stool in eight hours. The plan was to continue with the current TPN, recommend restarting Reglan due to vomiting and large amounts of NGT output the previous day, recommend starting Imodium as it is an antidiarrheal medication, and lastly recommend a GI consult to evaluate the patient.Follow-Up: December 21, 2012Three days later, the dietetic intern visited GG for another nutrition follow-up. He continued to receive TPN with the same solution and had an order to resume TF 48 hours prior but due to issues with the feeding pump and opening the bottle, the feedings had not restarted. During the physical assessment, GG remained on full vent support with the tracheostomy, had his eyes open, and was able to respond to questions with nods, though remained nonverbal. The NGT was clamped and no output had been recorded. His abdomen was soft, non-distended/non-tender (ND/NT), and he had active BS. The Flexiseal contained 200 mL of liquid brown stool when had come out in about one hour before the dietetic intern’s visit as the RN stated it had just been changed. Per discussion with GG’s RN and Acute Care Nurse Practitioner (ACNP), he had about 800 mL of stool output over the past 24 hours. Due to the amount of diarrhea GG was having, his stool had been tested for Clostridium difficile on Dec. 19th which results came out negative. It was discussed with the ACNP that GG was not started on Imodium as previously recommended because they were waiting for GI input. GG had been seen by a gastroenterologist but there were no plans to do anything because Reglan had been resumed, even though it has been noted that output was not different when on or off Reglan. Also during the physical assessment, it was noted GG’s bilateral upper extremities were anasarcic and he had a rash all over his body with the majority on this trunk. His weight had not been recorded since he had been admitted; when weighed during the visit, it was 184 pounds which was a 45 pound weight gain likely related to the upper extremity edema.Medications:Medications were reviewed. GG remained on Pepcid; Reglan at 10 mg BID (twice a day) had been restarted per recommendation; Benadryl and fluconazole were added for the rash on his body; and magnesium sulfate (MgSO4) was given the previous day due to low magnesium (Mg) levels.Labs:Na+135-145 mEq/LK+3.5-5.1 mEq/LCO221-32 mmol/LcCa8.2-10.6 mg/dLMg1.8-2.4 mg/dL145 ←149* H↓3.6 ↑28 ↑11.58 H1.7 LIt was noted the previous day that GG’s Na+ level was high, so an RD was asked to adjust his daily TPN order. Looking at GG’s additional IV fluids, it was noted he was receiving D5/NS + NaHCO3 for previously low CO2 levels related to metabolic acidosis secondary to diarrhea. HCO3- is lost through the GI tract with severe diarrhea, and treatment in the form of sodium bicarbonate (NaHCO3) is used to correct the ongoing GI losses.11 GG’s calcium was corrected as calcium is bound to albumin and his albumin was severely low (see below for further details). With the correction, his calcium was actually high indicating hypercalcemia as the total serum value was > 11 mg/dL. Clinical signs of hypercalcemia include nausea, vomiting, ileus, polyuria, confusion, etc. 11 The planned treatment for the high level of calcium was to simply eliminate it from the TPN. The other electrolyte noted at an abnormal level was magnesium (Mg). One predisposing factor for low magnesium levels related to GG’s case includes malabsorption. Recommendation for repletion depends on the severity of the depletion and may take up to 1 or 2 days to replete. 11 In GG’s case, he had been given MgSO4 via IV supplementation the previous day. Looking back, it would have been beneficial to recommend additional Mg supplementation during the follow-up visit as the serum Mg level remained low.It was discussed with the ACNP to check the prealbumin and CRP levels as they had not been checked as previously recommended. Below are the lab results and discussion:CRP<0.9 mg/LPrealbumin21-43 mg/dLAlbumin3.4-5.0 g/dLWBC4.5-11.0 K/uL12.6 H2.1 L↓0.9 L12.1 H ↓As discussed previously, prealbumin is often used to assess adequate nutrition support in acute care settings as it is preferred over albumin which has a shorter half-life. Prealbumin is a negative acute-phase protein that decreased in response to inflammation, and CRP is a marker for inflammation that changes rapidly as the half-life is about 19 hours.7 Changes in prealbumin do not reflect changes in percent calories or percent protein delivered; instead the changes reflect the presence of an inflammatory condition. In GG’s case, his CRP is high and prealbumin remained low despite receiving adequate calories determined by indirect calorimetry; and his WBCs remain high, further indicating the presence of inflammation. Seeing how GG was continuing to have large amounts of diarrhea, and his zinc levels were not rechecked as recommended, the nutrition problem continued to be altered GI function related to possible zinc deficiency versus an unknown etiology as evidenced by 800 mL of liquids stool in 24 hours. The plan was to recommend the medications Cholestyramine and Octreotide. Cholestyramine is often used to treat osmotic diarrhea because it works by binding to bile acids, that if in large amounts, when entered into the colon can cause an increased osmotic load with subsequent diarrhea. Octerotide is also used to treat diarrhea, but mainly in the secretory form. 12 It was later noted that GG had osmotic diarrhea, not secretory, so Octreotide was not added. Another recommendation was to add Lactinex, the probiotic lactobacillus, as there is strong evidence for the use of probiotics in the management of diarrheal diseases and in reducing the duration of diarrhea. 13 Additional plans of care were discussed with the ACNP included adding 25 mg Zn to TPN for 10 days, removing the calcium from the TPN, decreasing the dose of Reglan to 5 mg BID in hopes of reducing amount of diarrhea, another GI consult was recommended, trial trophic feeds of Vivonex @ 20 mL/hr with no advancement, and monitor strict I’ & O’s (input & output).Follow-Up: December 24-26, 2012During the holiday break, GG was followed by one of WAH’s RDs. The RD was asked to reassess him on Dec. 24th due to a probable central line infection to his right subclavian vein. The plan was to remove the right sublavian line and place a new line in the left subclavian vein. GI had been previously consulted and recommended discontinuing Reglan. Per RD note, GG had 1200 mL of stool output on Dec. 23rd and 770 mL output on 12/22 (none documented on the 24th) and no significant residuals with Vivonex running at 20 mL/hr. The RD recommended continuing TPN with the added Zn, a trial increase of Vivonex @ 40 mL/hour if stool decreases, and again recommend Imodium and Cholestyramine.Two days later on Dec. 26th, GG was seen again by the same RD. Due to the central line infection, no new line was placed so he was no longer receiving TPN, and fortunately he was tolerating the Vivonex @ 40 mL without significant residuals. Lactinex had been added as previously recommended several days prior, and Imodium and Cholestyramine were started on Dec. 24th and he only had 550 mL of stool output on Dec. 25th (again his stool was tested for Clostridium difficile and results remained negative). The plan was to increase the rate of Vivonex to 60 mL/hour and if there were no significant changes in stooling over the next 14-48 hours, change the TF to the semi-elemental formula Impact 1.5 @ 60 mL/hr. It was also recommended to check the zinc level again as TPN had been stopped, and if still low add zinc sulfate (ZnSO4) for 10 days to replenish zinc stores. Semi-Elemental FormulasSemi-elemental formulas are another type of specially designed enteral nutrition formula comprised of hydrolyzed proteins (as opposed to free amino acids in elemental formulas) that are absorbed more efficiently. Semi-elemental formulas contain peptides of varying chain lengths, simple sugars, glucose polymers or starch, and fat in the form of medium-chain triglycerides (MCT). 9 Impact? Peptide 1.5 is a type of semi-elemental formula that contains 1.5 kcal/mL. It has been indicated for mechanically ventilated, chronically ill patients, trauma patients, burn injuries, wounds, and stage 3 and 4 pressure ulcers.Follow-Up: January 2, 2013Upon GG’s follow-up by the dietetic intern, his TF had been changed to Impact 1.5 @ 60 mL/hr and had been tolerated with no residuals per discussion with his RN. He was also receiving autoflushes with his feeds, providing an additional 600 mL of water a day. During GG’s visit, he was more alert, though continued to respond to questions with nods, and was being weaned off the vent support as he was breathing with a trach collar and using the vent at night as tolerated. He had a SLP swallow evaluation that day and it was recommended to remain NPO except ice chips. His physical assessment showed a soft, ND/NT abdomen with positive bowel sounds, and the staples on his right shin had been removed and the skin was healing (proving adequate calories and protein had been provided despite low prealbumin levels as previously noted). The Flexiseal contained 400 mL of liquid brown stool out during that shift, and his RN stated he had an additional 300 mL out overnight. Medications:Medications were reviewed. GG remained on Pepcid, Benadryl, Imodium, Cholestyramine, and Lactinex; ZnSO4 had previously been added due to the discontinuation of TPN and likelihood of low zinc level, and Methylprednisolone was added for his rash.Labs:Na+135-145 mEq/LCl-98-107 mmol/LCO221-32 mmol/LBUN7-20 mg/dLWBC4.5-11 K/uLZn60-130 mcg/dL146 H ↑116 H ↑20 L36 H ↑15.4 H ↑58 L ↑The high sodium (Na+), chloride (Cl-), and BUN levels are likely related to the ongoing significant GI losses GG was having in the form of diarrhea; thus indicating the need for increased water intake.14 The lower carbon dioxide (CO2) level was also likely related to the diarrhea. GG had been receiving ZnSO4 for several days when his zinc level was rechecked; it level remained low, though had increased since the last time it was measured.The problem at this follow-up was inadequate fluid intake related to diarrhea as evidenced by his lab values mentioned above. The plan was to continue with the current TF and autoflushes and to add additional water flushes of 210 mL every six hours to provide a total of 2549 mL of free water.Follow-Up: January 8, 2013Upon the next follow-up by the dietetic intern, on Jan. 4th, GG was taken off vent support as apparently he “coughed” out the vent. The same day his NGT was removed and he had a modified barium swallow study (MBSS) by the SPL. The results of the MBSS showed mild to moderate pharyngeal dysphagia with delayed swallow and silent aspiration. A mechanical soft, nectar thick liquid diet was subsequently recommended. During the visit, GG was alert and able to converse. He reported being hungry, by when discussed with his RD and SLP, he was not eating a lot of solid foods and instead drinking all the liquids on the tray. He was however willing to try a supplement. GG denied any nausea, vomiting, or abdominal pain. The physical examination showed his abdomen was soft, ND/NT, had positive bowel sounds. The Flexiseal had 350 mL of liquids green stool out during the entire shift. It was noted his upper extremities were less anasarcic and he had a bandage over his throat stoma. He was reweighed at 138 pounds, a 19 pound weight loss since Jan. 2nd (157 pounds) likely related to less edema.Medications:Medications were reviewed; GG remained on Benadryl, Haldol for agitation, and Cholestyramine, which was later discontinued that day.Labs:GG’s Basic Metabolic Panel (BMP) was within normal range except for high Cl- at 110 mmol/L; his WBC also remained high at 12.2 K/uL.Eosinophils0-6%13.6 HIt was discussed with the Acute Care Physician Assistant (ACPA) the discontinuing of Cholestyramine due to high eosinophils. Eosinophils are a form of leukocytes, or white blood cell, that become active and accumulate during allergic or inflammatory disorders. Eosinophils normally stay in tissues including the respiratory, gastrointestinal, and lower genitourinary tracts and their lifespan can last for weeks.15 Looking back at GG’s medications, Cholestyramine was added around the same time his eosinophils were noted to be high, thus questioning whether or not he was having an allergic reaction to the medication. The other possible explanation for the high levels was his ongoing rash all over his body.The nutrition problem at the time was inadequate intake as he was only meeting about 30% of his estimated need when choosing to drink only liquids and not eating solid foods. The plan was to continue with the ordered diet per SLP’s recommendation, add Resource Shake Thickened three times a day (TID) as the supplement was at nectar consistency, and to add an appetite stimulant.Follow-Up: January 10, 2013The last follow-up visit to be discussed in detail was two days later on Jan. 10th. GG remained on the same diet (mechanical soft and nectar thick liquids) and he was receiving the Resource Shake Thickened TID. During the visit, GG reported having a good appetite, stating he ate about 50% of his lunch and had been drinking all the supplements. He denied any abdominal pain; his abdomen was soft, ND/NT, had positive bowel sounds; he stated no nausea, vomiting, constipation, and his Flexiseal contained 550 mL of light brown stool out over the entire shift, 500 mL of which was in the bag at the start of the shift. However, it was noted he did have 840 mL of stool output the previous day and it was discussed with the ACPA to restart Imodium. Another weight was taken and remained stable at 137 pounds.Medications:Medications were reviewed; GG remained on Benadryl and Haldol, and had been receiving the appetite stimulant Marinol for about two days as previously recommended.Labs:CO221-32 mmol/LWBC4.5-11.0 K/uLEosins0-6%17 L ↓15.2 H ↑21.0 H ↑The low CO2 was likely related to the large amount of stool GG had the previous day. The WBC remained high and despite discontinuing Cholestyramine, the eosinophil count increased, likely indicating he was not having a reaction to the medication and in fact the stool output had increased.There was no acute nutrition problem at the time of the follow-up as GG was meeting his needs with his current intake of meals and supplements, and he remained on an appetite stimulant. The goal was for him to consume ≥75% of his current diet and supplements ordered.Patient UpdateGG remains an inpatient at WAH. His hospital course took a turn when he had significant vomiting and NGT output, likely related to an ileus or SBO. An abdominal CT on Jan. 14th showed a high-grade SBO and an additional CT two days later showed persistent dilated SB loops. He had been made NPO, had large amounts of NGT output, Flexiseal contained 450 mL of dark green stool (again, negative for Clostridium difficile), and had restarted Reglan. If his SBO did not resolve in the next 24-48 hours, TPN was recommended with a different solution that did not include lipids due to a lipid shortage at WAH’s pharmacy. When he was followed-up five days later, his PO diet had been restarted and was well tolerated. Several days prior, another abdominal CT on Dec. 19th was suspicious for SBO or high-grade SBO, but his NGT was removed the next day, and the diet was resumed. When seen, GG reported having a good appetite and was drinking the supplements.Nine days later, GG was followed up by the dietetic intern on Jan. 31st, and unfortunately was NPO as he continued to have a SBO though the abdominal CT on Jan. 30th showed resolving SBO and no free air. It was discussed with the ACNP that General Surgery is following GG as he will possibly need surgery to remove the section of SB if symptoms persist; and looking back at his hospital course, there is a good chance they will persist. GG’s case, to be continued…ReferencesLitkouhi B, Soybel DI, Collins KA. Postoperative Ileus. Nov. 2012. Available from: UpToDate. Accessed on January 9, 2013.Madsen H, Frankel E. The Hitchhicker’s Guide to Parenteral Nutrition Management for Adult Patients. Practical Gastroenterology. July 2006: 47.Johnson MD, Wash RM. Current therapies to shorten postoperative ileus. Cleveland Clinic Journal of Medicine. November 2009:76(11):641-647. McClave SA, et al. Guidelines for the Provision and Assessment of Nutrition Support Therapy in the Adult Critically Ill Patient. JPEN. 2009;33(3):292-296.Indirect Calorimetry. The A.S.P.E.N. Nutrition Support Core Curriculum. 2007:22-24Krenisky J, Willcutts K. Indirect Calorimetry: Clinical Applications in Critically Ill Patients. Support Line. October 2006:28(5)13,16-18.Davis CJ,?Sowa D,?Keim KS,?Kinnare K,?Peterson S. The use of prealbumin and C-reactive protein for monitoring nutrition support in adult patients receiving enteral nutrition in an urban medical center. JPEN. March 2012;36(2):197-204.Pazirandeh S, Burns DL, Griffin IJ, Lipman TO, Hoppin AG. Overview of dietary trace minerals. October 2012. Available from: UpToDate. Accessed on January 9, 2013.Makola D. Elemental and Semi-Elemental Formulas: Are They Superior to Polymeric Formulas? Practical Gastroenterology. December 2005:60,62.Mount DB, Sterns RH, Emmet M, Forman JP. Clinical manifestations and treatment of hypokalemia. June 2011. Available from: UpToDate. Accessed on January 10, 2013.Kingley, J. Fluid and Electrolyte Management in Parenteral Nutrition. Support Line. December 2005;27(6):13,16-22.Smith MH. Descriptive Clinical Evaluation of Stool Output. Support Line. October 2009: 20-26.Boyle?RJ, Robins-Browne RM, Tang MLK. Probiotic use in clinical practice: what are the risks? Am J Clin Nutr. 2006; 83(6):1256-1264. Available at: 1256.full. Accessed January 8, 2012.Sterns R, Emmet M, Forman JP. Maintenance and replacement fluid therapy in adults. September 2012. Available from: UpToDate. Accessed on January 14, 2013.Kliegman RM, Stanton BF, St. Geme JW, Schor NF, Behrman RE. Eosinophils. Nelson Textbook of Pediatrics. 19th ed. Saunders; 2011:739-741. Available from: Clinical Key. Accessed on: January 16, 2013.Pronsky ZM, Crowe SRJ. Food-Medication Interactions. 17th ed. Birchrunvill, PA; 2012.AppendixesAppendix 1MedicationsClassification, Pharmacologic ActionAtivan (lorazepam)AntianxietyBenadrylAntihistamineCholestryramineAntidiarrheal, bile acid sequestrantDiflucan (fluconazole)Antifungal, anticandidiasisHaldolAntipsychoticImodiumAntidiarrheal, antiperistaltic agentPotassium Chloride (KCl)Electrolyte, potassium supplementLactinex (lactobacillus)Biotherapeutic agent, antidiarrheal, live microbial supplementMarinolAppetite stimulant, antiemeticMethylprednisoloneCorticosteroid, anti-inflammatoryMagnesium Sulfate (MgSO4)Mineral supplement, antacid, laxativePepcidAntacid, histamine H2 receptor antagonistReglan (metoclopramide)Prokinetic agent, dopamine antagonistZinc Sulfate (ZnSO4)Mineral supplementPronsky ZM, Crowe SRJ. Food-Medication Interactions. 17th ed. Birchrunvill, PA; 2012.16Appendix 2Appendix 3LabReference RangeDateDec. 14th Dec. 18th Dec. 21st Dec. 26th Jan. 2nd Jan. 8th Jan. 10th Na+135-145 mEq/L140144145139146 H143137K3.5-5.1 mEq/L4.23.1 L3.64.04.23.74.0Cl-98-107 mmol/L110 H115 H111 H110 H116 H110 H107CO221-32 mmol/L2118 L2820 L20 L2317 LBUN7-20 mg/dL23 H30 H1324 H36 H1932 HCr0.6-1.3 mg/dL1.11.30.91.21.21.21.9 HGluc74-105 mg/dL82108 H8375156 H9178Ca8.2-10.6 mg/dL7.8 L9.1 (cCa=11.6 H)8.0 L8.58.78.6Alb3.4-5.0 g/dL1.0 L0.9 L1.0 LPrealbumin21-43 mg/dL8.02.1 LWBC4.5-11 K/uL20.1 H14.0 H12.1 H9.615.4 H12.2 H15.2 HHgb13.5-18 g/dL6.4 L6.7 LHct39-52%19.6 L20.5 LMg1.8-2.4 mg/dL2.01.7 L1.5 L2.42.4Zn60-130 mcg/dL47 L58 LCRP<0.9 mg/L12.6 HEosin0-6%13.6 H21.0 HHighLowAppendix 4: Nutrition Care PlansDecember 14, 2012Dx: Altered GI function R/T ?malabsorption vs. hypermotility side effect of Reglan AEB 500 mL liquid stool out over 3.5 hours.Goal: Stool output <400 mL/dayPlan:Cont. TPN Δ TF to Vivonex @ 20 mL/hr (480 kcal, 24 g prot)Rec. d/c Reglan Check CRPAdd 25 mg Zn to TPN x 10 daysRec. SLP consult for swallow eval Monitor: TF tolerance, stool output, labs December 18, 2012Dx: Altered GI function R/T ?malabsorption AEB >500 mL stool output/8 hours.Goal: Stool output <400 mL/dayPlan:Cont. TPN Rec. restarting Reglan Rec. ImodiumRec. GI consultMonitor: Stool output, labs, ileus status December 21, 2012Dx: Altered GI function R/T ?zinc deficiency vs. unknown etiology AEB stool output of 800 mL/24 hrs.Goal: Decrease stool output to <600 mL/24 hrsPlan:Rec. Octreotide & Cholestyramine Rec. Lactinex Add 25 mg Zn to TPN x 10 daysRemove Ca from TPNDecrease Reglan to 5 mg BIDRec. GI consultTrial trophic feeds of Vivonex @ 20 mL/hr – do not advanceStrict I/O’sMonitor: Stool output, labs, wt, GI input, TF tolerance, I/O’s January 2, 2013Dx: Inadequate fluid intake R/T diarrhea AEB Na+-146 H, Cl--116 H, BUN-36 H.Goal: Normal lab valuesPlan:Cont. Impact @ 60 mL/hr + autoflushes Add 210 mL H2O flushes q6hrs (total 2549 mL free H20)Monitor: Stool output, TF tolerance, labs, hydration January 8, 2013Dx: Inadequate protein-energy intake R/T pt choosing to drink liquids and not eat solid foods AEB meeting ~30% of est. needs.Goal: ≥50% PO intakePlan: Cont. current dietAdd Resource Shake Thickened TIDAdd appetite stimulantMonitor: PO intake, stooling January 10, 2013Dx: No acute nutrition problems @ this time.Goal: ≥75% PO intake Plan:Cont. current diet & supplementsAdd Imodium – d/w ACPAMonitor: PO intake, stooling ReferencesLitkouhi B, Soybel DI, Collins KA. Postoperative Ileus. Nov. 2012. Available from: UpToDate. Accessed on January 9, 2013.Madsen H, Frankel E. The Hitchhicker’s Guide to Parenteral Nutrition Management for Adult Patients. Practical Gastroenterology. July 2006: 47.Johnson MD, Wash RM. Current therapies to shorten postoperative ileus. Cleveland Clinic Journal of Medicine. November 2009:76(11):641-647. McClave SA, et al. Guidelines for the Provision and Assessment of Nutrition Support Therapy in the Adult Critically Ill Patient. JPEN. 2009;33(3):292-296.Indirect Calorimetry. The A.S.P.E.N. Nutrition Support Core Curriculum. 2007:22-24Krenisky J, Willcutts K. Indirect Calorimetry: Clinical Applications in Critically Ill Patients. Support Line. October 2006:28(5)13,16-18.Davis CJ,?Sowa D,?Keim KS,?Kinnare K,?Peterson S. The use of prealbumin and C-reactive protein for monitoring nutrition support in adult patients receiving enteral nutrition in an urban medical center. JPEN. March 2012;36(2):197-204.Pazirandeh S, Burns DL, Griffin IJ, Lipman TO, Hoppin AG. Overview of dietary trace minerals. October 2012. Available from: UpToDate. Accessed on January 9, 2013.Makola D. Elemental and Semi-Elemental Formulas: Are They Superior to Polymeric Formulas? Practical Gastroenterology. December 2005:60,62.Mount DB, Sterns RH, Emmet M, Forman JP. Clinical manifestations and treatment of hypokalemia. June 2011. Available from: UpToDate. Accessed on January 10, 2013.Kingley, J. Fluid and Electrolyte Management in Parenteral Nutrition. Support Line. December 2005;27(6):13,16-22.Smith MH. Descriptive Clinical Evaluation of Stool Output. Support Line. October 2009: 20-26.Boyle?RJ, Robins-Browne RM, Tang MLK. Probiotic use in clinical practice: what are the risks? Am J Clin Nutr. 2006; 83(6):1256-1264. Available at: 1256.full. Accessed January 8, 2012.Sterns R, Emmet M, Forman JP. Maintenance and replacement fluid therapy in adults. September 2012. Available from: UpToDate. Accessed on January 14, 2013.Kliegman RM, Stanton BF, St. Geme JW, Schor NF, Behrman RE. Eosinophils. Nelson Textbook of Pediatrics. 19th ed. Saunders; 2011:739-741. Available from: Clinical Key. Accessed on: January 16, 2013.Pronsky ZM, Crowe SRJ. Food-Medication Interactions. 17th ed. Birchrunvill, PA; 2012. ................
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