Combined Intradialytic and Peripheral Parenteral Nutrition: A Case Report

Combined Intradialytic and Peripheral Parenteral Nutrition: A Case Report

Combined Intradialytic and Peripheral Parenteral NutritionA Case Report Scott M. Berry, MD ,* Joseph Lacy, RD, MS,t Marsha Orr, RN, MSN,:f: Robert Bow...

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Combined Intradialytic and Peripheral Parenteral NutritionA Case Report Scott M. Berry, MD ,* Joseph Lacy, RD, MS,t Marsha Orr, RN, MSN,:f: Robert Bower, MD,§ Pamela Schoettker, MS," Kathy Warshawsky, PharmD,1f and Crystal Davis, RN#

Renal failure patients often present with complex metabolic and nutrition management problems. When gastrointestinal dysfunction precludes enteral nutrition, needs must be met with parenteral nutrition (PN) while maintaining volume restrictions. If central access cannot be obtained, intradialytic PN may provide a portion of nutritional needs. However, the amount of time on dialysis limits nutrient provision . Because of volume required to meet nutritional needs, peripheral PN is problematic in the renal failure patient. A renal failure patient with multiple medical problems is described in whom intradialytic and peripheral PN were concurrently employed to approximate nutritional needs (81 % of resting energy expenditure) while minimizing administered fluid volume. © 1994 by the National Kidney Foundation, Inc.

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NTERAL NUTRITION is preferable for patients requiring nutritional intervention . When the gastrointestinal tract is unavailable, parenteral nutrition (PN) is necessary. Central venous administration is preferred for long term, ie, greater than 1 week , PN support ; peripheral PN may be used for short-duration nutrition supplemen*Nutrition Suppor1 Fellow, Depar1ment of Parenteral and Enteral Nutrition, University of Cincinnati Hospital, OH. f e linical Nutritionist, D epartm ent of Parenteral and Enteral Nutrition, University of Cinc innati Hospital, OH. tAssistant Direc tor of the Parenteral and Enteral Nutrition (PEN) Team , Depar1ment of Parenteral and Enteral Nutrition, University of Cinc innati Hospital, OH. §Director of the PEN Team, Depar1ment of Parenteral and Enteral Nutrition, University of Cincinnati Hospital, OH. IIResearc h Assistant, Depar1ment of Parenteral and Enteral Nutrition, University of Cinc innati Hospital, OH. (,IClinical Pharmacist, Department of Parenteral and Enteral Nutrition, University of Cincinnati Hospital, OH. #Nurse Clinician, Depar1ment of Parenteral and Enteral N utrition, University of Cincinnati Hospital, OH. Address reprint requests to Sc ott M Berry, MD, Depar1ment of Parentera l and Enteral Nutrition, SRU G-4 65, University o f Cincinnati Hospital, Cincinnati, OH 45267-0771. © 1994 by the National Kidney Foundation, Inc . 105 1-2276 / 94 / 0401 -0004$03.00 / 0

tation (3 to 5 days). However, because of peripheral venous osmotic limitations , considerable administration volume is required to meet most patient's nutrition needs peripherally , making total nutrient provision by peripheral PN a formidable task in renal failure patients. Intradialytic parenteral nutrition (IDPN) is an option for people who require dialysis and in whom enteral nutrition cannot be fully achieved ; however, the amount of time on dialysis often precludes complete nutrient provision. 1- 3 The following case describes the nontraditional use of traditional feeding modes to meet a malnourished patient 's nutritional requirements parenterally during critical illness while minimizing volume of administration .

CASE REPORT A 57-year-old man with end-stage hypertensive glomerulosclerosis who had undergone renal transplantation 8 years before admission suffered subsequent graft failure 2 years later, which led to uncontrollable hypertension and necessitated graft nephrectomy. One week postnephrectomy he was admitted to the University of Cincinnati Hospital on an emergency basis from an

Journal of Renal Nutrition, Vol 4, No 1 (January) , 1994: pp 15-18

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16 outlying dialysis clinic with dyspnea, hypotension, angina, and a hematocrit level that had decreased from .28 to .07 (28% to 7%). On presentation he was in obvious discomfort. His blood pressure was 152/80 mm Hg , heart rate 95 beats/min, respiratory rate 32 breaths/min , temperature 95.7°F, weight 45 kg, and severe low and sharp, nonradiating, midepigastric back pain without tenderness. He reported having multiple dark, tarry stools over the previous 24 hours. On examination stool was positive for blood both grossly and by guaiac testing . Laboratory tests were significant: hematocrit 0.7 (7%), platelets 297 x 109 /L (297 x 103 /mL) , prothombin time/partial thromboblastin time (PT /PTT) 13.8/27 s , hydrogen 32 nmol/L (pH 7.3) , bicarbonate 9 mmol/L (9 mEq/dL), BUN 5.67 mmol/L (34 mg/dL) , creatinine 720 f.\-mol/L (8 .2 mg/dL), phosphorus 4.5 nmol/L (13.9 mg/ dL) , albumin 42 g i l (4.2 g / dL), total bilirubin 11.9 f.\-mol/L (0.7 mg/dL), and serum glutamic-oxaloacetic transaminase / serum glutamic-pyruvic transaminase (SGOT / SGPT) 280/130 U / L (280/130 U / L) . A 12lead electrocardiogram and chest radiograph showed no acute changes. A computed tomography scan ruled out bleeding from the recent nephrectomy site. During subsequent blood transfusion the patient experienced a cardiopulmonary arrest from which he was successfully revived with 15 to 20 minutes of cardiopulmonary resuscitation. Thereafter, he was taken to the Surgical Intensive Care Unit where he remained intubated and unresponsive . The patient suffered hepatic failure: bilirubin212 f.\-mol/L, SGOT/SGPT8,400/14,100 U/L (8,400/14,100 U/L), lactic acid dehydrogenase 18,300 U/L (18 ,300 U/L), PT/ PTT 39/45 s , ammonia 96 f.\-mol/L (135 f.\-g/dL), and glucose 3.3 mmol/L (60 mg/ dL). In addition, his BUN increased to 9.9 mmol/L (60 mg/dL), his platelets decreased to 65 x 109 /L (65 x 103 / mL) , his fibrinogen was 2 .62 gil (262 mg/dL) , and his fibrin degradation products were 256 mg/L (256 f.\-g/mL). Although hypoactive bowel sounds were present, the patient had multiple grossly bloody bowel movements ,

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which precluded enteral nutrition support. The patient had a hemodialysis arteriovenous fistula in his left upper extremity, which pressurized the central venous system on that side , and he had received multiple temporary dialysis catheters in his right central veins, which had disrupted the normal anatomy on that side. These factors, in addition to low platelets, elevated PT /PTT, and disseminated intravascular coagulopathy, precluded central venous access for PN . The patient underwent daily arteriovenous hemodialysis beginning on hospital day (HD) no. 2. IDPN with hepatic formulation base (high branched-chain amino acids , low-aromatic amino acids) was initiated on HD no. 8, but the length of time on dialysis limited nutrient provision. Peripheral PN was started on HD no . 9 using the maximal allowable volume to more closely approximate the patient's nutritional needs. A metabolic cart on HD no. 9 showed a resting energy expenditure of 2,070 kcal/d, with a respiratory quotient of 0.7. This feeding regimen provided 1,670 total kcal and 72 g amino acids , which met 81 % of the patient's energy need and 83% of his estimated nitrogen need in a total volume of 1,950 mUd (Fig 1) . The patient's overall clinical status slowly began to improve. By HD no. 12, the patient was extubated and had improved liver function tests (decreased ammonia, aminotransferases, bilirubin) and improved mental status . All cultures except sputum were negative . The patient continued on broadspectrum antibiotics (vancomycin, gentamicin, and ceftazidine) . On HD no . 15 a clear liquid diet was started and advanced to a high-calorie, high-protein diet. Hemodialysis was decreased to every other day on HD no. 16, and IDPN and peripheral PN were discontinued. Because of poor oral intake «500 kcal/d), half-strength tube feeding (Magnacal, Sherwood, St Louis, MO) was started on HD no. 22 and advanced to full strength on HD no. 25 . This was continued through HD no. 35 , when the patient was able to meet more than 95% of his daily nutritional needs by mouth .

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Hospital Day FIGURE 1. Percent of resting energy expenditure supplied by various forms of nutritional therapy. IDPN (750 mL/d): amino acids-Hepatamine 4% (McGaw, Irvine, CA); dextrose-25%; vitaminsMVI-12 (Schein, Port Washington, NY); trace elements-MTE (Solopak, Franklin Park, IL); additives-10 U insulin/total volume. Peripheral parenteral nutrition (1,200 mL/ d): Amino acids-Freamine 3.5% (McGaw, Irvine, CA); dextrose-1 0%; Lipid-Intralipid 20% (Kabi Pharmacea, Clayton, NC). Tube feeding: Magnacal (Sherwood, St Louis, MO) 2 kcal/mL. PO: Clear liquid, full liquid, regular, and high-kcal, high-protein diets.

DISCUSSION Many studies have documented the incidence of malnutrition in patients with endstage renal disease (ESRD)4,5 In a patient with underlying renal failure, practical therapeutic nutrition goals are to minimize catabolism, preserve or replete protein and fat stores, reduce uremia, and accelerate recovery of renal function if possible. Metabolic management becomes more difficult in the face of multiorgan impairment. Because of gastrointestinal bleeding, enteral nutrition could not be given to this patient. In addition, the inability to achieve central access in this dialysis-dependent ESRD patient with superimposed acute hepatic insufficiency, coagulopathy and encephalopathy further complicated his nutritional management. Accessing the venous port of

the dialysis machine provides rapid reliable access to the central venous system for PN provision (Tables 1 and 2). Hepatic formulation IDPN was initiated to improve encephalopathy; however, length of dialysis time limited the amount of PN provided to 750 mUd. Peripheral PN was added to more closely approximate the patient's nutritional TABLE 1. IDPN Patient Selection Criteria Malnutrition Unintentional progressive weight loss (loss> 10% normal body weight) Serum albumin ,,;34 giL (34 g/dL) Previous failure with enteral repletion regimens Willingness of patient to participate in this procedure Data from Rothkopf and Harerstick,1 Goldstein and Strom,2 and Feinstein 3

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TABLE 2. IDPN Medicare Coverage Patient has ESRD. Patient cannot eat or has a diagnosis or had a surgical procedure that has caused permanent malabsorption. Patient must receive IDPN for a minimum of 90 days before a claim will be considered. IDPN cannot be considered a supplement to daily nutrition; it must be the only nutrition. Data from Critical Care America North Region Reimbursement Department, Westborough, MA.

requirements; however, volume restrictions limited peripheral PN volume to 1,200 mUd. By providing the maximum achievable volume of IDPN and supplementing peripheral PN as volume status allowed, the authors were able to meet 81 % and 83% of the patient's daily caloric and protein needs, respectively. A branched chain amino acid (BCAA)-enriched IDPN solution was chosen to circumvent exacerbating the patient's encephalopathy.6 A balanced amino acid peripheral PN solution was selected, because it was believed that the peripheral PN's dilute amino acid concentration (3.5%) and low volume infusion (1,200 mUd) ostensibly would not exacerbate the patient's encephalopathy. Moreover, giving BCAAenriched peripheral PN would have resulted in wastage of the expensive amino acid base necessary to achieve proper dilution (3.5%). The patient continued with improved liver function (decreased ammonia, bilirubin, and aminotransferases) and improved mental function on this regimen. Although providing peripheral PN enriched with BCAA may have maximized the intended effect of increasing the BCAA-to-AA ratio, the use of balanced amino acid peripheral formulation did not seem to impede the patient's recovery. It is recommended that patients receive water soluble vitamins to replace losses incurred from hemodialysis. This patient required aggressive nutritional intervention for a defined period of time during acute illness; therefore, he received full multivitamin coverage in each 750 mL of IDPN. When to initiate IDPN requires deft clinical judgment, particularly because nutrition as-

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sessment parameters in dialysis-dependent ESRD patients are unreliable, and clinical markers to predict patient outcome are lacking. IDPN was particularly useful in the previously described patient because of inability to gain enteral or central venous access. Daily dialysis treatment offered convenient access to the venous circulation. Finally, the importance of successfully monitoring transitional feeding was underscored in this case. Nutritional therapy involved "titrating" IDPN, peripheral PN, tube feeding, and modified diet interventions. Care was taken to avoid gross overnutrition or undernutrition and to encourage the patient to take an active role in his nutritional care when he was placed on an oral diet. In summary, this case study employed common nutritional therapies in a novel approach. Both enteral support and central venous PN were precluded early in the patient's clinical course. IDPN and peripheral PN were used in tandem to provide sustenance during the initial management phases of a malnourished critically ill patient until conventional therapy could be instituted. Monitoring transitional feeding modes for adequacy enabled the patient to receive appropriate nutritional prescription until he was able to sustain himself by mouth.

REFERENCES 1. Rothkopf MM, Haverstick L: Metabolic aspects of intradialytic parenteral nutrition (IDPN). Contemp Dial NephroIApril:37-41, 1991 2. Goldstein OJ, Strom JA: Intradialytic parenteral nutrition: Evolution and current concepts. J Renal Nutr 1 :9-22, 1991 3. Feinstein EI: Total parenteral nutritional support of patients with acute renal failure. Nutr Clin Prac 3:9-13,1988 4. Matarese L: Nutrition support in renal failure, in Gottschlich M, Matarese L, Shronts E (eds): Nutrition Support Dietetics Core Curriculum (ed 2). Silver Spring, MD, American SOCiety for Parenteral and Enteral Nutrition Publishers, 1993, pp 327-340 5. Foulks CJ: Nutritional evaluation of patients on maintenance dialysis therapy. Am Nephrol Nurs AssocJ 15:13-16, 1988 6. Hiyama DT, Fischer JE: Nutritional support in hepatic failure: The current role of disease-specific therapy, in Fischer JE (ed): Total Parenteral Nutrition (ed 2). Boston, MA, Little, Brown, 1991, pp 263-298