MNT Case Study: 63-year-old Woman with Sepsis and Decreased Renal Fxn

Introduction to the Problem:

Renal failure is a consequence of kidney malfunction and their inability to excrete all

nitrogenous wastes from ones body. (1) A change in terminology now describes what was

previously known as an acute renal failure to acute kidney injury or AKI. As the name

describes, an AKI is caused by an incident that inhibits the kidneys capability to function at

100%, or by a decrease in the glomerular filtration rate. (2) Better defined as, a rapid

decrease of the glomerular filtration rate, with concurrent losses of the homeostatic

functions of the kidney, including the purification of blood, maintenance of acid-base

equilibrium and of water and electrolyte balance by the renin-angiotensin aldosterone

system, synthesis of erythropoietin, and neoglucogenesis. (7) Chronic kidney disease is

seen among those who have long-term diseases that will directly hinder proper kidney

function whereas an acute injury likely occurs to a kidney that had been healthy

beforehand. (6)

There are several causes of Acute Kidney Injuries, as classified in Krauses Food and

Nutrition Therapy text, into three categories, inadequate renal perfusion, diseases within

the renal parenchyma, and obstruction.(4) The etiology ranges from toxic drug exposure, a

drug allergen, progressive glomerulonephritis, and ischemic acute tubular necrosis and

tissue destruction, acidosis, uremia, and hyperkalemia making up the pathophysiology of

an acute kidney injury. Medical and nutritional interventions must not be taken likely in

either mild or severe cases. Treatment options include but are not limited to drug

withdraw, dialysis, TPN, and electrolyte replacement (4).

 Although, defined as acute, this should not be taken lightly, as one study

discovered nearly 18,870, 662 admissions from 2001-2011 were those suffering from an

Acute Kidney Injury (2) and another study stating a 50-60% mortality rate (1). Treatment

should also not be taken lightly. There are several different types of dialysis, for this

particular diagnosis a continuous method is often initiated. Continuous Renal Replacement

Therapy, also known as, CRRT has been around since 1980s. (1) This form of dialysis is

commonly seen in an intensive care unit; acting as ones external 24-hour kidney, removing

unwanted toxins and excess fluid without ever taking a break or slowing down. CVVH, a

type of CRRT is defined as a method of acute renal failure management in which an

ultrafiltration membrane, powered by the patients own blood pressure or a pump,

produces an ultra filtrate that can then be removed and replaced by parenteral nutrition

fluids. (6) The VV in CVVH stands for vein to vein, CVVH removing bad fluid and

replacing with good, filtered fluid vein to vein. While this seems like the perfect solution to

an otherwise failed or injured kidney it often causes many different nutritional

ramifications for the already critically ill patient.

As we know, most critically ill and physiologically stressed patients are at increased

needs, however, not all of patients can get adequate intake considering their current state

and need nutritional intervention such as TPN or EN. For a patient population such as

those with AKI, nutritional intervention can become somewhat complicated when taking

into consideration the presence of uremia, metabolic acidosis, and fluid and electrolyte

imbalance. (6) AKI can alter metabolism of macro/micronutrients, increase loss of water

soluble vitamins, electrolytes, and trace elements, reduce clearance of potassium,

magnesium, and phosphorous, causes hyperglycemia, increase triglycerides, protein

catabolism, and cause on to become deficient in selenium, zinc, vitamin C and vitamin E. (7)

With treatment/CVVH, comes many potential nutritional ramifications.

According to Schneeweiss et al (1990), patients are at increased nutritional needs

with an infection such as sepsis and renal failure. (6) The problems here are, while these

patients are at increased needs, they may also be facing nausea, vomiting, and diarrhea.

Hyperglycemia is often seen in patients with such critical illness, as Weisen et al (2011)

states,(these patients) are more prone to exacerbated insulin resistance because of the

losses of renal gluconeogenesis and hormonal clearance (pp218). Blood glucose is

affected depending on the dialysate composition.

The presence of an AKI causes an increase in protein breakdown because of

compromised transportation of amino acids across the cell membrane. (7) According to the

A.S.P.E.N. Clinical Guidelines on Nutrition Support in Adult Acute and Chronic Renal Failure,

up to 2.5 g/kg/day of protein may be the key to achieving positive nitrogen balance in a

patient on a continuous therapy. Protein goals of 1.5g/kg bw/day would be appropriate

with non-protein intake of 25kcal/kg bw/day (3). While for every 1 g increase in nitrogen

balance, patient survival increased by 21%(1, pp 374). Proteins needs vary depending on

the etiology of the AKI, use of dialysis, and other conditions present and CVVH can actually

increase protein catabolism (7). As stated by Cano et al (pp 300), There is a loss of about

0.2g amino acids/l filtrate, giving a total daily loss of 10-15g amino acids, to which

(depending on the type of therapy and the membrane material used) a protein loss of 5g

and 10g/day has to be added. (3) Most generally, ICU patients with kidney injuries are also

on strict input/output observation. Potassium, magnesium, and phosphorous can become

excessive in the body of an AKI patient because of the kidneys incapability to excrete the
excess. (7)

One must agree that medical nutrition therapy for such patients can become quite

complicated and must be completely tailored to them based on their treatment in which

they are receiving.

Introduction of the Subject:

The patient being examined, PD, is a 63-year-old white female. With a history

significant for Congestive Heart Failure, Myocardial Infraction, Coronary Artery Disease,

COPD, Diverticulitis, and Type 2 Diabetes Mellitus. The patients daughter was present

among admission and stated that the patients bother has cancer but much of the family

history is otherwise unknown. After speaking with the patient once able, I learned that the

patient lives alone in a trailer.

Patient History:
In October 2016, PD was admitted to DuPont Hospital with a perforated

diverticulum when a segmental colectomy when a colostomy was preformed. In March

2017, the patient arrived for an elective reversal of the colostomy, where she had an

elongated stay due to elevated troponin, hypoxemia, and COPD exacerbation. Not long

after discharge, the patient was then readmitted on April 3rd, with an anastomosis leak,

pelvic perianastamotic abscess along with nausea, abdominal bloating, orange stools and

inability to urinate. To correct this, an exploratory laparotomy and drain was completed,

inevitability leading to septic shock, causing the patient to ultimately transfer into

Lutherans Intensive Care Unit for further observation and use of CVVH, of which was not

available at DuPont Hospital.

 Upon arrival on April 11th, to Lutheran Hospital, PD was vented due to respiratory

failure, sedated, with septic shock, multiple system organ failure, fever, anemia, oliguria

AKI, and lastly peritonitis. A preliminary round of CVVH started on April 12th, of which

clotted off, was restarted, and lasting until the 14th, followed by chest tube placement on

April 13th to help resolve the peritonitis, Total Parental Nutrition. TPN, was started by

pharmacy, with the help of our recommendations, on April 14th providing 1900 calories, 90

grams of protein, with added magnesium and potassium phosphate. Besides potassium

and phosphorous, PDs electrolytes where reasonably normal, for which she received

supplementation for. By April 15th, PD was finally without sepsis and by the 16th was

extubated and was likely to advance to a liquid diet, still diuresing due to fluid overload,

and third spacing, however her AKI was getting worse. For PD, it is more or less one step

forward and two steps back; by Monday, April 17th she was reintubated and sedated with

Versed. On April 19th PD was transitioning from receiving full nutrition from TPN to trickle

feeds of EN in which she met her goal rate of 65ml/hr on the 21st. Her chest tube has been

removed and she was extubated as of the 22nd. PD had advanced to a Renal Diet order on

April 24th,eating more than 50% of her meals with plans for physical therapy/occupational

therapy and to transfer out of the ICU.

Surgical History:
Cholecystectomy
Bilateral arm surgeries
Spleenectomy
Right Heart Cath
Left wrist surgeries
OR for anast leak and L&D abscess 4/2017
Colostomy s/p reversal 3/15/2017
Right leg surgery
Right lymph nodes X2 removed
Social History:
 Smoker for most of her life-quit 20 years ago.
Allergies: Naproxen and Zoloft
Initial Diagnosis:
Septic Shock:
o Severe Sepsis syndrome
Abdominal abscess w/drain
AKI causing Metabolic acidosis
o Oliguric Acute Kidney Injury-less than 400-500ml/24 hrs.
ARF
o Ischemic acute tubular overload.
Pleural effusions (right chest tube to suction)

Anthropometric Measurements:
Upon admission, PD was 62 inches tall and weighed approximately 182 pounds

making her Body Mass Index 33.3, of which falls under the Obesity Grade 2 category. With a

history of Congestive Heart Failure and now Acute Kidney Injury this admission weight

could be skewed due to fluid retention. PDs ideal body weight is 110 pounds, 72 pounds

less than her initial weight, placing her around 165% her ideal body weight. Due to the

patients level of sedation since admit and lack of history, it was uncertain if this weight is

what she, herself, would consider her usual body weight but after getting to speak with

her I found 147 pounds is what she would consider normal. Since her admission on April

11th, PDs weight has fluctuated quite a bit.

Weight History:

Date Weight (lbs) Edema

Prior to admit: 147
4/12/2017 182 No edema noted
4/14/2017 177 Generalized 3+
pitting
4/18/2017 195 Generalized 3+
pitting, BUE, BLE
3+4+ pitting.
4/21/2017 169 Generalized 2+
pitting, BUE 3+4+
 pitting, bilat ankle
and feet 1+ pitting.
4/24/2017 147 Generalized
1+2+,BLE 1+2+
pitting.

Laboratory Values:
Lab 4/12 4/14 4/18 4/19 4/21 4/24

Glucose 89-121 198 121-155 130 (H) 119 (H) 95-142

Albumin 1.3 (L) 1.1 (L) 1.2(L) 1.8(L) 1.8 (H) 2.1 (L)
BNP 566.7(H) - 553.9 (H) 553.9 (H) - -
BUN 25 (H) - 52(H) 65(H) 90(H) 109 (H)
Creatinine 2.2 (H) - 2.3 (H) 2.4 (H) 2.6 (H) 2.1 (H)
GFR 21 (L) 25 (L) 23 (L) 20 (L) 19 (L) 24
Sodium 147 (H) 140 139 137 139 136
Chloride 118 (H) 111 (H) 100 99 95 (H) 93
Phosphorus 1.4 (L) 1.5 (L) 3 2.8 4.0 5.8 (H)
Magnesium - - 2.1 1.8 1.8 2.2
Potassium - 3.2 (L) 3.4 (L) 4.0 4.1 5.4 (H)
Hemoglobin 9.1 (L) 10.0 (L) 10.5 (L) 8.4 (L) 8.6 (L) 7.8 (L)
Hematocrit 27.5 (L) 28.6 (L) 31.4 (L) 23.8 (L) 25 (L) 22.6 (L)
AST 51 (H) - - - - -
ALT 8 (L) - - - - -
NRBC - 7.4 (H) 0.8 (H) 0.6 (H) 0.0 -
HgbA1c N/A - - - - -
WBC - 17.6 (H) 19.3 (H) 18.5 (H) 10.9 -

Medical Tests and Procedures:

CT Abdomen/ Pelvic @ DuPont
o Decreased size of pelvic abscess-fluid accumulation in right upper abdomen
o Collapsed bladder
o 5-6cm renal cyst
Chest tube placement 4/11/2017 @ DuPont
o Chest x-ray: after placement
CV Cath placement 4/11/2017
CVVH with 35ml/kg replacement 4/12/2017-4/14/2017
Oral endotracheal reintubation: 4/17/2017
o Chest x-ray: postop
Medications:
Medication Purpose
Antibiotics Treat infection/sepsis
 Humulin R Patient history significant for Type 2 DM
Protonix Decreases stomach acid
Precedex Sedative
Fentanyl Pain Management
Kphos rider For renal function
Propofol (140kcal Sedative
4/17-4/19)
Proventil Bronchodilator
Lasix Drip (IVF) Diuretic
Norepinephrine Blood pressure support
infusion (IVF)
Diprivan (IVF) Anesthetic

TPN
o 4/14: TPN @ 43.4 (46)ml/hr w/ CA, Mg, KPh, Adult trace minerals, thiamin,
1900kcal, 90grams Pro
o 4/21: TPN @ 46ml/hr being weaned,
TPN decreased to 20g Pro, 730kcal
Vital AF 1.2 @40ml/hr providing 1152kcal, 75grams protein, and 779
ml free water
o 4/21-22 (early morning/after TPN bag was finished): EN NG tube @ 65ml/hr
continuous Vital AF 1.2 with 5ml residuals.

Diet Assessment:
Due to PD, lengthy sedation, I was unable to obtain a diet history until April 24th.

For the first half of PDs stay, starting on April 14th, she was on TPN at 46ml/hour with

added calcium, magnesium, potassium phosphate, adult trace mineral, and thiamin,

providing 1900 calories and 90 grams of protein. During this time PD was also receiving

propofol, a sedative that provided 1.1kcal/ml, adding another 140kcals overall. By April

21st the decision was made to begin weaning the TPN and start the initiation of enteral

nutrition; TPN was then decreased to 730 calories and 20 grams of protein. At this point

the Registered Dietitian was consulted for an enteral nutrition tube feeding

recommendation of which provided PD with 1152 calories, 75 grams of protein, and 779
milliliters of free water. After the last bag of TPN on April 21st was finished, Vital AF 1.2 via

NG tube was increased to full strength of 65ml/hour providing 1872 calories, 117 grams of

protein and 1265mlilliliters of free water was started. At one point during PDs stay, she

had been extubated with thoughts of starting a liquid diet but less than 24 hours later, she

was reintubated. I will continue to monitor PDs tolerance of the enteral nutrition,

residuals, and labs and make changes as needed with the assistance of the Registered

Dietitian. After PD was extubated and passed her swallow study, she was able to advance

her diet order to a Renal Diet. After observing her intake over roughly 24hours, I saw that

she was eating able half of her order. I met with PD and we discussed Nepro and Glucera, in

which she decided she would like to try Glucera with her meals.

Nutrition Diagnosis and PES Statement:

Increased nutrient needs related to physiological problems impairing nutrient

utilization as evidenced by NPO diet, TPN orders, and use of CVVH.

Inadequate oral intake related to decreased appetite as evidenced by estimated

energy intakes from diet are currently less than recommended levels indicating

need for supplementation with meals.

Interventions:
Upon admission to Lutheran, PD was already intubated and sedated from her stay at

DuPont Hospital. After a few days it had been decided that TPN would be the best

option for this patient given the medical interventions taken place.

o 4/14: TPN @ 43.4 (46)ml/hr w/ CA, Mg, KPh, Adult trace minerals, thiamin,

1900kcal, 90grams Pro

o This decision was made from pharmacy with the help of the RD and I.
 As I followed that patient throughout I noticed that her weight had been fluctuating

as well as the presence of edema. With the help of the Dietitian we decided it would

be best to calculate her needs with her admit weight, which was with the littlest

presence of edema, close to a dry weight. Using the ASPEN Critical Care Guidelines,

we calculated PDs nutritional needs at 25kcal/kg, and 2.5 grams protein per

kilogram bodyweight (50kg). Making her overall nutritional needs 1895kcal/day

and 125g protein/day.

o 4/21:Vital AF 1.2 EN was started @ 65ml/hour providing 1872 calories, 117

grams of protein and 1265mlilliliters of free water was started.

o Although this was coming up a little short on the calories and protein, the RD

and I found it most suitable for this patient.

After being extubated and passing her swallow study over the weekend by Monday,

PD had a Renal Diet order in place from the doctor. I completed her follow-up on

Monday afternoon and observed her oral intake. By April 25th, I met with the patient

to discuss her diet history, social history, usual weight, and if she felt she was

meeting her needs currently. After some discussion PD and I decided to add

Glucerna to her meal trays.

o 4/25: Glucera TID with meals.

Proposed Outcomes to Monitor and Evaluate:

As my MNT experience is coming to an end, I will remain following this patient until

she is discharged. During this time I will continue to complete her reassessments every

three days while paying close attention to her tolerance of her tube feeds, if she is meeting

the goal rate, diet advancement, percent oral intake, lab values, input/output, medication
changes, and lastly I will monitor her weight changes and presence of edema. Specific labs

that I will continue to monitor include but are no limited to GFR, blood glucose, BUN,

creatinine, albumin, potassium, magnesium, sodium, calcium, and phosphorous. Most of

these labs directly related to kidney function or her past medical history and should be

monitored until she is medically stable. As long as PD remains getting her nutrition from

tube feeding, residuals produced, tolerance, and meeting the goal rate/receiving adequate

nutrition must be monitored as well. Along with intake must come output and in this case

monitoring the patients output after such problems are incredibly important. Monitoring

the patients diet and the advancement therefore of will be something that we will continue

to monitor until discharge while also providing nutrition education/educational handouts

for the patient to go home with.

Conclusion:

This patient has had a very interesting past eight months. After getting a colostomy,

followed by a reversal, pelvic abscess, nausea, abdominal bloating, orange stools and an

exploratory laparotomy inevitability leading to septic shock PD found herself in the Medical

Surgical Intensive Care Unit at Lutheran Hospital. Her initial diagnoses included septic

shock, severe sepsis syndrome, peritonitis, multiple system organ failure, abdominal

abscess w/drain, AKI causing metabolic acidosis, anemia, respiratory failure, oliguric Acute

Kidney Injury-less than 400-500ml output/24 hrs, ARF/Ischemic acute tubular overload

and pleural effusions with a right chest tube to suction. Medical/nutrition intervention

included CVVH 24-hour dialysis, TPN, electrolyte replacement, and intubation/sedation.

After nearly 10 days, PD was making advancements, she was extubated and advanced from

enteral nutrition via NG tube and now on a Renal diet order.

To conclude, renal failure and the associated nutrition intervention must be closely

monitored throughout. It is crucial that we remain current in our research on best

practice/nutritional needs and interventions for patients on CRRT/CVVH. Although each

patient is different, we should always determine if our provided plan was effective in its

goal for this patient and establish future implementations for later cases.
 Citation:

1. Brown R, Compher C, American Society for Parenteral and Enteral Nutrition Board of
Dierectors. A.S.P.E.N. Clinical Guidelines: Nutrition Support in Adult Acute and
Chronic Renal Failure. Journal of Parenteral and Enteral Nutrition. 2010;34(4):36-
377. doi:10.1177/0148607110374577.

2. Brown JR, Rezaee ME, Marshall EJ, Matheny ME. Hospital Mortality in the United States
following Acute Kidney Injury. BioMed Research International. 2016;2016:1-6.
doi:10.1155/2016/4278579.

3. Cano N, Fiaccadori E, Tesinsky P, et al. ESPEN Guidelines on Enteral Nutrition: Adult

Renal Failure. Clinical Nutrition. 2006;25(2):295-310.
doi:10.1016/j.clnu.2006.01.023.

4.- Mahan LK, Escott-Stump S. Krause's Food and Nutrition Therapy. 12th ed. Philadelphia,
PA: Saunders Elsevier ; 2008.

5. McClave S, Taylor B, Martindale R, et al. Guidelines for the Provision and Assessment of
Nutrition Support Therapy in the Adult Critically Ill Patient (A.S.P.E.N). Journal of
Parenteral and Enteral Nutrition. 2016;40(2):159-211.
http://pen.sagepub.com/content/40/2/159.full. Accessed April 20, 2017.

6. Schneeweiss, B., Graninger, W., Ferenci, P., Eichinger, S., Grimm, G., Schneider, B., ... &
Kleinberger, G. (1990). Energy metabolism in patients with acute and chronic liver
disease. Hepatology, 11(3), 387-393.

7. Wiesen P, Overmeire LV, Delanaye P, Dubois B, Preiser J-C. Nutrition Disorders During
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Enteral Nutrition. 2011;35(2):217-222. doi:10.1177/0148607110377205.