Tube feedings in outpatient adult dialysis patients: Two case studies

Tube feedings in outpatient adult dialysis patients: Two case studies

CASE STUDY Tube Feedings in Outpatient Adult Dialysis Patients: Two Case Studies Peggy Harum, RD, CS, LD* Tube feedings are used extensively in hosp...

555KB Sizes 0 Downloads 29 Views

CASE STUDY

Tube Feedings in Outpatient Adult Dialysis Patients: Two Case Studies Peggy Harum, RD, CS, LD*

Tube feedings are used extensively in hospitalized hemodialysis patients with functioning gastrointestinal tracts, but there is little information about outpatients. Two case studies are discussed to show safety and effectiveness of such therapy. The goal was to restore energy and sense of well being and to promote weight gain. Both patients were 60% to 75% of ideal body weight. Enteral trials failed to improve weight loss. Percutaneous endoscopy gastrostomy tubes have been in place 7 to 9 months, respectively. The patients gained 5 to 6 kg with tube feedings containing 2,000 to 2,850 kcal per day. In conclusion, the patients are believed to require a daily calorie-protein intake of more than the recommended 35 kcal and 1.2 g protein/kg to promote weight gain. Tube feedings were effective in maintaining nutritional status and preventing a further decline in the patients’ overall medical condition. o 1997 by the National Kidney Foundation, Inc.

N JANUARY 1996, the Renal Interest Committee of the American Society of Parenteral Nutrition (ASPEN) had its annual meeting in Washington, DC. Presentedat this meeting were the results of a project performed by a group of four physicians and four dietitians. The project involved a literature review that was directed to the identification and treatment of malnutrition in the dialysis patient population.‘-6 A significant amount of data was available on intradialytic parenteral nutrition and intraperitoneal amino acid nutrition, but there wasa void of information regarding the use of enteral tube feedings in the adult hemodialysispatient population. In February 1996, a report was published in Nutrition in Clirzical Practice authored by two of the physicians who participated in the ASPEN project.’ The project and the article, which revealed enteral tube feedings are underutilized, resulted in this present report of two casestudies showing the safety and effectiveness of tube feedings to improve malnutrition in outpatient adult hemodialysis patients with a functioning

I

Journal

ofRerral

Nutrition,

Vol

7, No

1 (January),

1997:

pp 33-38

gastrointestinaltract. The two patients were clearly going to die of malnutrition if something was not done. Thus, the patients were informed that the purpose of this therapy, to which they consented, was to restore energy and a senseof well being, as well asto promote weight gain. Tube feedingsare used extensively in hospitalized hemodialysis patients with a functioning gastrointestinaltract; however, this is not the case in outpatients.7 There are multiple reasonsfor this, including invasiveness of the procedure, presumedpatient discomfort, patient refusal, concern over volume overload, development of mineral and electrolyte imbalances,and the inability to pay for the supplements.7In view of these reasons,it is important that the attitudes of the health professionals,who present the option for therapy to the patient and family, are positive and enthusiastic. According to the Medicare Enteral Policy effective July 1, 1996,8 enteral nutrition is defined as the provision of nutritional requirements through a tube into the stomach or small intestine. The general coverage criteria is asfollows. Enteral nutrition is covered for a patient who has either one of the following conditions that requires a tube feeding to provide sufficient nutrients to maintain weight and strength commensurate with the patient’s overall health status: 33

34

PEGGY

a permanent nonfunction or disease of the structures that normally permit food to reach the small bowel (ie, dysphasia or gastroparesis), or a disease of the small bowel that impairs digestion and absorption of an oral diet (ie, fat malabsorption, gastroparesis, small bowel resection). The patient’s condition could be either anatomic or caused by a motility disorder. Enteral tube nutrition is not covered for patients with a functioning GI tract whose need for enteral nutrition is caused by reasons such as anorexia or nausea associated with a mood disorder or an end stage disease, etc (enteral supplements taken by mouth are not covered by Medicare).

Case Study 1 The patient in case study 1 is a 59-year-old anuric black man who has been on hemodialysis for 4 years. His end-stage renal disease (ESRD) was caused by hypertensive nephrosclerosis. He had a cerebral infarct and has peripheral vascular disease. His ability to communicate is limited. Although he has swallowing dysfunction, there are times when he is able to swallow small amounts of food. Diet history reveals that this patient is able to consume small amounts of food (
Dialysis

Regimen

The patient is on hemodialysis using a Fresenius F8 biocompatible dialyzer (Fresenius USA, Walnut Creek, CA) three times weekly for 3.5 hours, with a blood flow of 350 mL/min and a dialysate flow of 500 mL/min. Bicarbonate dialysis is used with a 2.5 mEq/L calcium, 2.0 mEq/L potassium bath, and 200 mg% dextrose. Each dialyzer had been reused less than 10 times. This is noted because according to Ikizler et al, albumin losses increase significantly after 15 reuses.’

Medications The medications include the following: Liquid Titralac, 1 tablespoon three times daily; Nephrofer, 2 tablespoons at bedtime; Nephrovite, 1 tablespoon daily; Temazepam, 30 mg at bedtime; Cimetidine, 400 mg three times daily; Clonidine 0.2 mg three times daily.

HARUM

Nutrition

Assessment

The following is the physical data for the patient in case study 1: height, 70 inches (178 cm); usual body weight (UBW), 86 kg; ideal body weight (IBW), 76 kg; weight before tube feeding, 59 kg (September 1995) at 68% UBW; current weight, 64.0 kg (May 1996) at 77% IBW. On nutritional physical examinationi the patient had signs of severe malnutrition. He showed a lack of subcutaneous fat under the eyes. There was hollowing at the temples. He lacked fat and muscle tissue on the triceps and biceps. The bones of the clavicle, shoulder, knee, and scapula were prominent. His interosseous muscle was flat. There was no muscle definition on his calf. Before the tube feeding, at 68% of his UBW, he was weak and unable to stand without assistance. He needed a wheelchair after his dialysis treatment. After using the tube feeding for 9 months, he was able to stand alone and did not need assistance. He had no hospitalizations after the tube feeding was initiated. He underwent a series of diagnostic tests including an esophagram, MRI of the brain, and a barium swallow video fluoroscopy in July 1995. These tests concluded that the di5culty in swallowing appeared related to neurological dysfunction with small amounts of aspiration into the larynx with each swallow. With an estimated IBW of 76 kg, his daily calorie and protein needs were estimated as follows: 2,660 cal (35 kcal/kg IBW) and 91 g of protein (1.2 g protein/76 kg IBW).“-‘” Weight loss began in May 1995. By September 1995, he lost 8.5 kg (14% of his weight), despite taking 2 to 3 cans of Nepro (Ross Products Division, Abbott Laboratories, Columbus, OH) a day since May. It is extremely di5cult for patients on long-term hemodialysis to achieve true weight gain.7 It is interesting to note that the level of serum albumin has always remained within normal range. The present investigator is unable to explain this finding. Serum albumin level is only one marker of malnutrition. Weight loss may be a more significant marker of malnutrition. The state of hydration appeared correct because the serum sodium levels remained within the acceptable range, blood pressures were normal, and there were no signs of dehydration, A PEG tube was placed September 28, 1995.

TUBE

FEEDINGS

Six cans of NEPRO were given by bolus to provide 2,850 calories and 105 g of protein. This was 48 kcal/kg body wt at a body weight of 59 kg. There was good family support. Home Health nurses initially instituted the therapy and subsequently trained the wife, who preferred the bolus method to the controlled rate of flow with the pump. Medicare pays for his tube feeding, which has been safely administered. The patient’s dry weight slowly increased 5 kg in 9 months, from 59 kg in September 1995 to 64.0 kg in May 1996. His quality oflife improved; he walks without assistance and is more independent according to his family. He required no more hospitalizations. Blood pressures have remained normal for the past nine months. Clinical parameters are summarized in Table 1.

Case Study 2 The patient in case study 2 is a 68-year-old anuric black man who has been on hemodialysis for 4 years. His ESRD was caused by diabetic glomerulonephrosclerosis and hypertension. Initially his blood sugar was poorly controlled with a glycohemoglobin of 11.6%, indicating an average blood sugar during the past 2 to 3 months of 300 mg% (16.6 mmol/L).‘” Recently, improvement has been noted with a glycohemoglobin of 9.0%, indicating average blood sugars of approximately 210 mg% (11.6 mmol/L).15 He experienced shortterm memory loss, which seems to have influenced his noncompliance with medications and diet. His wife was unsuccessful intervening with his medications or diet because the patient refused her help. Diet history reveals he was only able to ingest small amounts of food < 1000 kcal and 40 g protein/d, which is insufficient to sustain weight or prevent weight loss.

Dialysis Regimen The patient’s hemodialysis prescription is an F8 biocompatible dialyzer three times weekly for 3.5 hours with a blood flow of 450 mL/min and a dialysate flow 500 mL/min (each dialyzer had been reused less than 10 times). Bicarbonate is used with a 2.5 mEq/L calcium, 2.0 mEq/L potassium bath, and 200 mg% dextrose.

IN DIALYSIS

35

PATIENTS

Table 1. Clinical in Case Clinical

Study

Parameters

1995

to 1996

1 September 1995

Parameters

Total protein (g/dL) [g/L] Albumin (g/dL) [g/L] Blood urea nitrogen (mg/dL) [mmol/L] Creatinine (mg/dL) [pmol/L] Bicarbonate (mEq/L) Cholesterol (mg/dL) [mmol/L] KW Urea reduction ratio (%) Sodium (mEq/L) Potassium (mEq/L) Total lymphocyte count

8.2 [82.0] 4.4 [44.0]

50 [17.8]

108 [38.5]

15.4 [1361.3] 25

15.6 [1379.0] 18

207 [5.36] 1.4 68 138 3.3

162 [4.19] 1.7 71 138 3.8 1,714 37.5 13.1 [6.13] 62.5

11 .O [6.82] 59.0

Total protein (g/dL) [g/L] Albumin (g/dL) [g/L] Blood urea nitrogen (mg/dL) [mmolll] Creatinine (mg/dL) [pmol/L] Bicarbonate (mEq/L) Cholesterol (mg/dL) [mmoWL] UW Urea reduction ratio (%) Sodium (mEq/L) Potassium (mEq/L) Total lymphocyte count (mm31 Hematocrit % Hemoglobin (g/dL) [mmol/L] Weight (kg) Note. On January which may explain laboratory results.

6.9 [69.0] 4.1 [41.0]

1,880 33.5

(mm? Hematocrit % Hemoglobin (g/dL) [mmol/L] Weight (kg)

January 1996

March 1996

May 1996

7.6 [76.0] 3.9 [39.0]

8.4 [84.0] 4.2 [42.0]

117 [41.7]

100 [35.7]

19.4 [1714.9] 17

15.8 [1396.7] 25

120 [3.1] 1.5 68 142 4.6

157 [4.0] 1.5 66 136 4.6

1,635 34.6

1,925 33.4

11.4 [7.0] 62.5

1, 1996, a new laboratory some of the variations

11.8 [7.3] 64.0 was used, shown in

Medications The medications include the following: Nephrovite (R&D Laboratories, Marina de1 Roy, CA), 1 tablet daily; NuIron (Mayrand Pharmaceuticals Inc, Greensboro, NC), 150 mg twice daily; Liquid Titralac (3M Personal Healthcare Products, St. Paul, MN), 1 tablespoon with each meal; Catapres (Boehtinger Ingelheim Pharmaceuticals

36

PEGGY

Inc, Ridgefield, CT), .2mg every 8 hours; Norvast (Pfizer Labs Division, Pfizer Inc, New York, NY), 5.0-mg tablet twice daily; Zantac (Glaxo Pharmaceuticals, Research Triangle Park, NC), 150 mg as needed; NPH Insulin (Novo Nordisk Pharmaceuticals Inc, Princeton, NJ), 14 U in morning and 8 U in evening; Epogen (Amgen Inc, Thousand Oaks, CA), 2,000 U each treatment; IV Calcijex Abbot Laboratories, Columbus OH), 1 mcg every treatment (noncompliance with medications is suspected).

Nutrition

Assessment

The following is the data for the patient in case study 2: height, 69 inches (176 cm), UBW, 70 kg, IBW, 75 kg, weight before tube feeding, 45 kg (November 1995) at 64% UBW, and current weight, 51.5 kg (May 1996) at 60% IBW. Nutritional physical examination revealed severe malnutritioni with a lack of fat and muscle tissue on the triceps and biceps. The bones of his clavicle, shoulder, knee, and scapula were protruding. The interosseous muscle was flat. His calfwas without muscle definition. With an estimated IBW of 75 kg, his daily calorie and protein needs were estimated as follows: 2,625 cal (35 kg/75 kg IBW) and 90 g of protein (1.2 g protein/75 kg IBW).“-‘” The patient experienced a weight loss of 10 kg (18%) after August 1995, even though he claimed to consume 8 oz of Sugar Free Re Neph daily (500 kcal/l6 g protein; Nutra Balance Products, Indianapolis, IN). During a hospitalization in November 1995, a PEG tube was placed. His wife was trained on the feeding pump to administer 8 cans (8 oz/can) of Glucerna a day (1,896 kcal and 79.2 g of protein). This was 42 kcal/kg body wt at a body weight of 45 kg. Interdialytic fluid overload was anticipated, but he tolerated the tube feeding well, without fluid overload. In addition to the tube feeding, he consumed small amounts of food, but less than 1,000 kcal and 40 g of protein/d. In 7 months, he gained 6.5 kg with the tube feeding for an estimated total calorie intake of 3,000 kcal/d. Medicare paid for his tube feeding. Immediately before initiation of the tube feeding, he needed assistance to walk after dialysis treatments. After using the tube feeding for 7 months (November 1995 to May 1996), he was able to perform his usual activities of daily living.

HARUM

Table 2. Clinical in Case Clinical

Study

Parameters

1995

to 1996

2

Parameters

Total protein (g/dL) [g/L] Albumin (g/dL) [g/L] Blood urea nitrogen (mg/dL) [mmol/L] Creatinine (mg/dL) [umol/L] Bicarbonate (mEq/L) Cholesterol (mg/dL) [mmol/L] Kt!v Urea reduction ratio (%) Sodium (mEq/L) Potassium (mEq/L) Total lymphocyte count

January 1996

6.8 [68.0] 3.1 [31.0]

7.3 [73.0] 3.1 [31.0]

92 [32.8]

103 136.71

11.5 [1016.6] 29

9.9 [875.1] 18

180 [4.6] 1.2 63 136 5.1

221 [5.7] 1.8 73 132 5.9

2,088 25.9

(mm3) Hematocrit % Hemoglobin (g/dL) [mmol/L] Weight (kg)

8.2 [5.1] 45.0

Total protein (g/dL) [g/L] Albumin (g/dL) [g/L] Blood urea nitrogen (mg/dL) [mmol/L] Creatinine (mg/dL) MW Bicarbonate (mEq/L) Cholesterol (mg/dL) [mmol/L] KtN Urea reduction ratio (%) Sodium (mEq/L) Potassium (mEojL) Total lymphocyte count (mm3) Hematocrit % Hemoglobin (g/dL) [mmol/L] Weight (kg)

November 1995

3,175 35.8 12.3 [7.6] 48.5

March 1996

May 1996

7.6 [76.0] 3.9 [39.0]

7.5 [75.0] 3.3 [33.0]

117 [41.7]

87 [31 .O]

19.4 [1714.9] 28

10.9 [963.5] 20

120 [3.1] 1.5 68 142 4.6

211 [5.4] 1.9 77 139 4.4

1,635 34.6 11.4 [7.1] 49.0

2,930 36.6 12.8 [7.9] 52.5

He had one hospitalization for 2 days in January 1996 for pancreatitis and one more hospitalization in February 1996 for 2 days for a gastrointestinal bleed. Since then, he has required no further hospitalizations. Clinical parameters are summarized in Table 2.

Discussion These two ambulatory anuric hemodialysis patients tolerated enteral feedings well, one via bolus and one with the pump. Both had PEG

TUBE

FEEDINGS

tubes and no discomfort or volume overload was encountered. Common complications have been avoided. No infections, aspirations, or gastrointestinal symptoms occurred. Interdialytic weight gains were <3.5 kg. Both patients were dialyzed using biocompatible noncellulosic dialysis membranes that were used less than 10 times. The patients received more than the recommended calorie protein allowances. Hypercatabolism often characterizes the nutritional state of patients undergoing long-term replacement therapy by dialysis.“~” The process of hemodialysis with exposure of the blood to the extracorporeal hemodialysis circuit enhances the release of monokines, eg, interleukin 1, which can cause anorexia, protein catabolism, negative nitrogen balance, and decreased albumin synthesis. Tumor necrosis factor alfa, otherwise known as cachectin, another monokine activated during hemodialysis, also induces anorexia and weight loss.‘s~‘9 Contact of blood with the dialysis membrane leads to absorption of protein (eg, albumin and fibrinogen) and adhesion of cells (platelets, erythrocytes, and leukocytes) onto its surface.‘” Patients with renal failure associated with metabolic acidosis may have increased protein catabolism,‘8.“” which is associated with muscle wasting. ‘1-23 Recent data show that maintenance hemodialysis patients also have an impaired response to insulin-like growth factor 1 /somatomedin C,“’ which may impair nutrient utilization. The loss of vitamins,a5 amino acids,” and albumin’ into dialysate may also contribute to the development of malnutrition in these patients. The average loss of free amino acids in dialysis fluid has been reported to be 5 to 8 g per dialysis, of which about one third are essential amino acids. Furthermore, 4 to 5 g of peptide-bound amino acids are lost per dialysis. Thus, the total losses of amino acids are about 9 to 13 g per dialysis.“’ There is a relationship between membrane compatibility and protein catabolism. A biocompatible dialysis membrane refers to one that elicits little or no reaction with the biomaterials per se.ls Other membranes such as cuprophan membranes are well-known activators of the complement system.“-as During hemodialysis, especially when using complement-activating membranes, there may be activation of cytokines with an induction of a postdialysis catabolic state. In nonuremic volunteers undergoing sham dialysis with various membranes, use of complement-activating mem-

IN

DIALYSZS

37

PATIENTS

branes caused a net outflow of amino acids from muscle for several hours after completion of dialysis.” Additionally, cuprophan membranes suppress natural killer cell function more than polycarbonate membranes.30 The issue of biocompatibility of the membranes used in the hemodialysis procedure has to be considered in any discussion of protein malnutrition in the hemodialysis patient population.”

Summary The recommended calorie and protein intake of 35 kcal/kg/d and 1.2 g protein/kg/d is for stable hemodialysis patients.“-lq To prevent weight loss and/or to promote weight gain, malnourished hemodialysis patients appear to have calorie and protein needs that exceed this recommendation. The patients received more than the recommended calorie and protein allowances, but failed to achieve desired body weight. This suggests that the catabolic patient undergoing maintenance hemodialysis may require more calories and protein than the stable patient. The tube feedings were effective in maintaining nutritional status and preventing a further decline in the patient’s overall medical condition. Enteral nutrition was safely administered. For these two patients to attain and maintain ideal body weight, it appears they will require longterm tube feeding. Controlled, randomized studies are needed to further define the potential of this therapy as an intervention for the malnutrition in the adult hemodialysis patient population.

References 1. Acchiardo SK, Moore LW. Latour PA: Malnutrition main factor m morbidity and mortalq of hemodialysls Kidney

Int Suppl24:S199-S203,

1983.

(suppl16)

2. Avram MM, Nephrol14:238-244,1994

Mittman

3. Hakim RM. tients. Am J Kidney

Levin N: Malnutrition Dis 21:125-137. 1993

4. Lazarus 21:99-105,1993

JM:

5. Kopple in maintenance 1994

JD:

Nutrition

8. Palmetto

Malnutrition

m hemodialysis.

in uremia.

Semm

m hemodialysis

pa-

Am J &dney

Dis

Effect of nutrition on morbidity and mortality dialysis patient. Am J Kidney Dis 24: 1002-1009,

6. Kaminski MV, Lowrie tion is lethal. diagnosable Transplant Proc 23:1810-1815, 7. Wolfson useful therapy?

N:

as the patxnts.

J, Foulks Nutrition Government

EG. Rosenblatt and trratablr 1991

SG, et al: Malnutnin ESRD patients.

CJ: Intradialyuc parenteral in Clinical Practice 11:s. Benefits

Administration,

nutriuon: 1996 Durable

A

Medical 15, April

Equipment Regional 1996, pp 96-145

9. Ikizler

TA,

Flak011

Carrier PK,

during hemodialysis. Kidney 10. McCann L: Subjective the nutritional

R, Luttgen in maintenance

31:1812-1820.1978 12. Kopple

RA:

Amino

Issue

acid

losses

patvents. FM,

Dial

Cap&mu hemodialysis.

Transplant

to

25:190-

1994 13. Blumenkrantz

MJ:

Handbook

Nutrition,

of Dialysis.

Boston,

in

Daugirdas

MA,

Little,

JT,

Ing

Brown,

TS

1994,

pp374-400 14. Bergstrom patients, in Mitch Boston, 15.

MA, Olson

J: Nutritional WE, Klahr

Little, OC:

Brown, Potpourri,

requirements S (eds): Nutrition

of hemodialysis and the Kidney.

1993, pp 263-289 in: Diagnosis and

17. Wolfson M, Strong CJ, status and lymphocyte function

in hemodialysis 1980

R, Gentile

Appleton&Lange, 19. Lindsay and

nutrition

Dial

Transplant

D (eds): RM,

Clinical

1990, p 69 Bergstrom

in maintenance 9:150-155,

Dialysis. J: Membrane haemodialysis

1994

(suppl2)

lY93(2

Partl)

21. balance

Borah during

of calorie

maintamed

Norwalk,

CT,

patients:

Nephrol

CM,

CRF decreases Am J Physlol

et al: Correc-

protein degrada265:E230-E235,

FA, et al: Nitrogen of uremia. Kidney Int

A, Wahren J, et al: Effect of in and dialysis membranes on protein 1990 of the

interval

suggesting

on

induced 24.

protein

metabolism

catabolism. Fougue D.

AmJ Peng

response

to recombinant

patients.

Kidney

evidence

dialysis-

Kidney Dis SC, Kopple

14:96-100.1989 JD: Impaired

metabolic

insulin-like

growth

in dialysis

Int 47:876-883,

factor-l

1995

Chenoweth

DE,

Cheung

AK,

Henderson

toxin formation during hemodialysis: Effects membranes. Kidney Int 24:764-769, 1983 27. Hakim RM, Fearon DT, Lazarus JM: membranes: Effects of chronic Int 26: 194-2000, 1984

in sham

hemodialysis:

Clin

Nephrol38:20-29, 1992 Lindner A, Farewell B, Sherrard in uremic

ron 27:292-296,

patients 1981

with

Anaphyladialyzer

Biocompatibility

of

activation.

Fehr J. Brihgam KL, et al: Complement pulmonary dysfunction in hemodialysis.

lism

neoplasia

LW: of different

complement

N Engl J Med 296:769-774, 1977 29. Gutierrez A, Bergstrom J, Alvestrand

30.

mterdialytic

Wolfson M: Use ofwater soluble vitamins in patients renal failure. Semin Dialysis 1:28-32, 1988

dialysis Kidney

A,

biocompatibility

SM, Scrimgeour

MF, Schoenfeld PY, Gotch intermittent dialysis therapy

28. Craddock PR, and leukocyte-mediated

in Nlssenson East

D, Channon

catabolism in humans. Kidney Int 38:487-494, 23. Lim VS, Flanigan MJ: The effect

25. chronic

Minturn D, et al: Nutritional in maintenance hemodialysis

patients. Am J Clin Nutr 39:547-555, 1984 18. Cheung AK: Membrane compatibility, Fine

Reaich

of acidosis in humans with and ammo acid oxidation.

26. Management

Diabetes Mellitus. New York, NY, Raven, 1988, p 261 16. Bansal UK, Popli S, Pickering J. et al: Protein malnutrition and cutaneous anergy patients. AmJ Chn Nutr 33:1608-1611,

20. tion tion

14:491-500. I978 22. Gutierrez A, Alvestrand viva contact between blood

T, et al: Protein Am J Clin Nutr

JD: Effect of nutrition on morbidity and mortality dialysis patients. Am J Kidney Dis 24:1002-1009,

in maintenance

(eds):

Parker

Advisory,

Int 46:830-837, 1994 global assessment as it pertains

status of dialysis

225,1996 11. Kluthe requirements

Medicare

The

effect

receiving

A: Protein

of different D: long

High term

catabo-

membranes. incidence dialysis.

of Neph-