CLINICAL CASE REPORT: NUTRITIONAL

MANAGEMENT OF END STAGE RENAL

DISEASE ON HEMODIALYSIS
AMAL EL-ROWMEIM

QUEENS COLLEGE DIETETIC INTERN

10/27/17
TYPE 1 DIABETES

• 5 – 10% of diabetics; can occur at any age, mainly under 30 yrs

• Risk factors: genetic predisposition, autoimmune, environmental
• Caused by autoimmune destruction of pancreatic beta cells which causes decreases
insulin production, resulting in hyperglycemia.
• Hyperglycemia present only after 90% of beta cells destroyed.
• Asymptomatic for many years.
• 5 – 10 years after onset total loss of beta cells. Completely dependent on exogenous insulin for
survival.
TYPE 2 DIABETES

• Disease that is characterized by elevated glucose due to insulin resistance, decreased

insulin secretion, and or increased glucagon secretion.
• Initially, before the diagnosis of diabetes, the body produces more insulin to overcome insulin
resistance and maintain normal or prediabetic levels of glucose, but pancreas can’t keep this
up and hyperglycemia ensues.
DIABETES

• Diagnosis: • Symptoms:
• A1C of >6.5% • Excessive hunger/thirst
• FPG > 126 mg/dl • Fatigue
• 2 hr > 200 mg/dl • Increase urination
• Casual glucose > 200 mg/dl + symptoms • Slow healing sores/cuts
• Testing for autoantibodies distinguishes • Pain/numbness in feet
between type 1 and 2 • Blurry vision
DIABETES

• Complications:
• DKA (diabetic ketoacidosis)
• Glu >300
• Ketones and acidosis present à not enough insulin, fat breaks down
• Kussmaul breathing; heavy breathing to expel CO2, fruity scent (ketones)
• Causes: not enough insulin; more common with type 1
• Tx: rehydration, insulin, electrolyte replacement
DIABETES

• Complications:
• HHS (hyperosmolar hyperglycemic state)
• Glu >600 -> high osmolarity, dehydration
• Altered mental state --> confusion; coma, seizure possible
• No/few ketonesà just enough insulin present to suppress ketogensis
• Tx: rehydration, insulin, electrolyte replacement
• Causes: infection/illness/dehydration/uncontrolled diabetes/imparied kidney function/heart
attack/stroke/drugs that impair glu tolerance (steroids) or increase fluid loss (diuretics)
DIABETES

• Complications:
• Hypoglycemia
• Excess glucose damages blood vessels and can cause
• Nephropathy -> reduced kidney function
• Retinopathy -> leading cause of blindness
• CHD
• Peripheral vascular disease
• Neuropathy -> if damage to nerves in GI -> esophagitis, gastropareis. Damage in peripheral
nerves -> numbess/pain
HTN

• Blood pressure: measure of cardiac output x peripheral vascular resistance

• Systolic BP: measures pressure on arterial walls as heart contracts and forces blood out
• Diastolic BP: measures pressure on arterial walls as heart relaxes and refills with blood
• Regulated by kidneys, SNS, adrenal medulla, parasympathetic NS
HTN
HTN

• Types:
• Essential/primary HTN ~90% of cases
• Unknown cause; risk factors: smoking, DM, dyslipidemia, age, diet, obesity, stress
• Secondary HTN~10% cases
• Caused by another disease, cured by treating primary disease

• Complications:
• Renal disease; decrease in blood flow activates RAAS which will further increase BP and exacerbate
problem
• Retinopathy
• Can lead to heart disease, CVA
CHRONIC KIDNEY DISEASE

• Characterized by a decline in renal function,

minimum 3 mo.
• Stages 1-3 are usually asymptomatic.
• Clinical manifestations typically don’t appear
until stages 4-5.
CHRONIC KIDNEY DISEASE
CKD

• Potential Complications:
• ESRD
• Renal osteodystrophy
• Hyperkalemia
• Uremia
• Hyperphosphatemia
• Proteinuria
• Anemia
 ESRD

• Hemodialysis:
• Dialysate used is similar to fluid and
electrolyte content to normal plasma.
• Permanent catheter
• Waste products and excess fluid removed
by diffusion
• 3-5 hours 3x week
CASE PRESENTATION

• African American male

• Brought in by EMS, following a seizure episode.
• Admitted for management of:
• Acute respiratory failure 2/2 aspiration pneumonia
• HHS -> arrived to ED with Glu >700 mg/dl
• Hypertensive emergency
• Seizure 2/2 HHS
• ESRD
CLIENT HISTORY

• PMH: DM Type 1, HTN, ESRD on dialysis

• Social hx: denies toxic habit. Independent; able to care for self.
• Family hx: Mother with HTN and osteoporosis. Father with high cholesterol and HTN.
• Diet hx: unrestricted
• Food allergies: strawberries
• Home medications: Bumetanide and Lasix, both diuretics; Humalog, a rapid acting insulin
and Toejeo, a long acting insulin
NUTRITION AND DIET HISTORY

• Based on 24 hr recall, pt does not follow any kind of diet and eats out a few times a
week.
• Pt takes vitamin D supplements.
• Pt gives himself insulin injections before meals. Does not have a strong grasp of
carbohydrate counting.
• Physical activity: is not physically active.
CLIENT - ANTHROPOMETRICS

• Nutrition focused physical exam:

• Pt appears WNL, good muscle definition.

• Admit ht/wt: indicative of normal wt status.

• IBW 94.5 kg, IBW%: 83%
• Wt history: unknown
BIOCHEMICAL DATA

• Removed to ensure anonymity of patient.

• Labs indicated HHS (elevated glucose, electrolytes, few ketones).
• Also elevated A1C.
NUTRIENT NEEDS:

• Estimated using admit wt with considerations for pt intubated, critical care setting,
comorbidities:
• Kcals: 1975 – 2370 kcals/day via 25 - 30 kcals/kg
• Protein: 95 – 119 gm/day via 1.2 – 1.5 gm/kg
• Fluids: 1000 ml + urine output

• Nepro @ goal rate of 55 ml/hr x 24 hrs to provide: 2376 kcals, 106 gm protein, 959 ml of
free water.
NUTRITION DIAGNOSES

• Predicted suboptimal energy intake (NI-1.4) related to planned medical

therapy/intubation as evidenced by pt currently NPO, to receive EN to meet estimated
needs, currently receiving 0% calorie/protein needs. (resolved)
• Altered nutrient related labs (NC-2.2) related to endocrine/kidney dysfunction as
evidenced by elevated glucose, A1C, fingersticks x 24 hrs, BUN, and Cr.
• Food and nutrition related knowledge deficit (NB-1.1) related to lack of prior nutrition
related knowledge as evidenced by pt appears resistant to change.
MEDICAL INTERVENTIONS:

• Pt intubated, given IV fluids and insulin

• NGT placed
• Vancomycin 2/2 aspiration pneumonia
• Nifedipine and metopropol for HTN
• Hemodialysis – remove excess fluid/waste
NUTRITION INTERVENTION:

• Nepro @ goal rate of 55 ml/hr x 24 hrs to provide: 2376 kcals, 106 gm protein, 962 ml free
water.
• After extubation energy needs re-estimated:
• Kcals: 2370 – 2765 kcals/day via 30-35 kcals/kg
• Protein: 95 – 119 gm/day via 1.2 – 1.5 gm/kg
• Fluids: 1000 ml + urine output
• Diet change to Renal (80 gm protein, 2gm Na, 2 gm K, 1g P) + High CCD + Nepro daily (425 kcals,
19 g protein)
• Educate pt on diabetic/renal diet and it’s importance
• Refer patient to outpatient dietitian
MONITORING

• Monitor:
• Rate of EN feeds and subsequent PO intake after extubation to assess for adequacy
• Nutrition related labs including glu, electrolytes, BUN, Cr
• Weight and I/O charts to assess fluid retention
EVALUATION

• Short term goals:

• Pt will identify 3 high potassium and 3 high phosphorous foods in current diet and swap out for appropriate
alternatives.
• Pt will identify 5 high sodium foods in current diet and eliminate in a month’s time.
• Pt will try Mrs. Dash salt substitute and other means of flavoring food in one wk

• Long term goals:

• Pt will strictly follow Renal/diabetic diet.
• A1C levels <7%
• Blood pressure goals <140/90
• Pt will regularly visit outpt dietitian for counseling.
• Prevent complications: renal osteodystrophy, uremic sarcopenia etc.
DISCHARGE:

• Patient was discharged against medical advice.

• Patient had not finished antibiotic course. Glucose levels were also spiking to dangerous
levels on day of discharge.
• Limited education was achieved. The patient seemed reluctant to change current eating
habits.
 REFERENCES

• Statistics About Diabetes. (n.d.). Retrieved November 06, 2017, from http://www.diabetes.org/diabetes
basics/statistics/?referrer=https%3A%2F%2Fwww.google.com%2F
• Mahan, L. K., Raymond, J. L., & Escott-Stump, S. (2011). Medical Nutrition Therapy for Diabetes Mellitus and
Hypoglycemia of Nondiabetic Origin. In Krause's Food & the Nutrition Care Process (13th ed., pp. 676-706).
Elsevier.
• Kitabchi, A. E., & Fisher, J. N. (2008). Hyperglycemic Crises: Diabetic Ketoacidosis (DKA) and Hyperglycemic
Hyperosmolar State (HHS). Acute Endocrinology,119-147. doi:10.1007/978-1-60327-177-6_6
• Division for Heart Disease and Stroke Prevention. (2016, June 16). Retrieved November 06, 2017, from
https://www.cdc.gov/dhdsp/data_statistics/fact_sheets/fs_bloodpressure.htm
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In Krause's Food & the Nutrition Care Process (13th ed., pp. 758-767). Elsevier.
 REFERENCES

• Kidney Disease Statistics for the United States. (2016, December 01). Retrieved November 06, 2017, from
https://www.niddk.nih.gov/health-information/health-statistics/kidney-disease
• Mahan, L. K., Raymond, J. L., & Escott-Stump, S. (2011). Medical Nutrition Therapy for Renal Disorders. In Krause's Food & the
Nutrition Care Process (13th ed., pp. 799-813). Elsevier.
• Batuman, V. (2017, October 23). Diabetic Nephropathy. Retrieved November 01, 2017, from
https://emedicine.medscape.com/article/238946-
overview?pa=uNKy%2FL5pyZZsBJWzilH0NTezfS42GOKFYK9ey250K5qfnoDfcUkMig4p4alB%2BVbevZSDM%2FR183mDl7Oyf
kcBR6VWPnT09k%2B5rrSiOMPj9A0%3D#a3
• Hemodialysis. (2017, February 14). Retrieved November 06, 2017, from https://www.kidney.org/atoz/content/hemodialysis
• Stoner, G. D. (2005). Hyperosmolar Hyperglycemic State. Am Fam Physician. Retrieved from
http://www.aafp.org/afp/2005/0501/p1723.html
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