Initials: M.B.P. Occupation: Pastor Admission Date: 02/10/14 Gender: M Socioeconomic Status: Middle Marital Status: Married Age: 56 Residence (Home or LTC): Home Ethnicity: African American
B. Diagnosis: ESRD/Stage 5 CKD (Acute on Chronic Kidney Disease)
C. Medical Problem List: Abdominal pain c ! vomiting 3-4x daily, renal insufficiency
D. Medical/Social Hx: A-fib (pacemaker), HTN, Gout, DM Type 2, CKD
E. Physical/Anthropometric Data (if available):
Date: 02/12/14 Height: 68 UBW: 275# %UBW: 100% Current Wt. 275# IBW: 154 10% %IBW: 179% BMI: 43, Class III Obesity
Note any findings from physical assessment: Pt. appears to have distention of abdomen.
F. Pertinent Laboratory Data: List Normal Values Norm (4.7-6.1) RBC Norm ( 12.1- 15.6 ) ) Hgb Norm (34- 45%) Hct Norm (35-5.0)
Part II: Medical Problems, Laboratory Tests and Medications
Summary of Medical Text Findings Comparison of Patient to Text A. Pertinent Medical Problems: include background of each disease from text and include medical nutrition therapy (MNT) for each; include kcal and protein recommended if noted; highlight information that can relate to this patient. A. Pertinent Medical Problems: include how each disease is affecting patient; what treatments patient is receiving; therapeutic diet PTA and diet order in hospital; how does the kcal/protein recommended for each disease translate for this patient? Do not complete an assessment. A. Renal Failure: Acute on Chronic Kidney Disease
1) Acute Kidney Injury (AKI) Also called Acute Renal Failure (ARF). It is a rapid accumulation of creatinine and urea in blood (azotemia) caused by kidney damage from possible trauma, illness, surgery or intrinsic renal disease (McMillan, 2011, 2436). AKI can occur c! oliguria or normal urine flow. Duration lasts from a few days to several weeks (Wilkens, Juneja & Shanaman, 2012, 808).
Sx of AKI include anorexia, nausea, vomiting c! possibility of seizures and coma if left untreated. Causes of AKI are classified by prerenal, renal or post renal. Prerenal conditions account for 50-80% of AKI cases and they are reversible. Renal causes of AKI involve intrinsic renal disease and attribute to 10-40% of AKI cases and are generally caused by ischemia causing tubule damage. Postrenal instances are caused by obstruction in the
Hx of CKD
Pt. came into ED c! CKD Stage 4. Renal attending believes AKI has further progressed CKD to Stage 5.
urinary system. These cases contribute to a small portion of cases 5-10% (McMillan, 2011, 2436).
AKI is diagnosed by monitoring serum BUN, creatinine, CBC, electrolytes including Ca and phosphate. Serum creatinine can " as much as 2 mg/dL/day. BUN may " by 10-20 mg/dL/day. However, surgery, trauma, corticosteroid usage, burns, transfusion reactions, parenteral nutrition or GI bleeds may affect BUN levels. Urine tests may also be conducted and examined for Na+ and creatinine concentration (McMillan, 2011, 2438).
Prerenal causes of AKI are clinically diagnosed and easily corrected by correcting underlying cause. Postrenal causes are determined by measuring residual urine by use of catheter. If residual urine volume is > 200 mL an obstruction is suspected. Renal ultrasonography sensitivity is only 80-85% of cases. CT can be done to establish obstruction site to help determine treatment. Renal causes are determined by clinical findings. Pts often have edema, proteinuria or signs of arteritis in skin and retina. Often this type of AKI can be diagnosed without a history of intrinsic renal disease (McMillan, 2011, 2439).
MNT for AKI
Energy and macronutrient needs in AKI are determined greatly by the underlying cause of the renal insufficiency (Wilkens et al., 2012, 809).
The amount of protein required can range from 0.5- 0.8 g/kg. Some AKI pts will require hemodialysis (HD) and therefore their protein needs are higher at 1-2 g/kg. If the pt must undergo continuous renal replacement therapy (CRRT), protein needs are even higher due to protein losses during treatment requiring 1.5-2.5 g/kg protein (Wilkens et al., 2012, 809).
Energy needs also take into account any co- morbidity that may be present. If possible, indirect calorimetry can be used to determine needs in an ICU setting. Otherwise, calorie needs can be
BUN " 136, 145, 154 mg/dL on consecutive days
estimated at 30-40 kcal/kg of dry or ideal BW. Be aware of addition of glucose in peritoneal dialysis (PD) and CRRT that can contribute energy. Pts on parenteral nutrition (PN) should receive high amounts of carbohydrate and lipid c! monitored respiratory status (Wilkens et al., 2012, 809).
Fluid and electrolyte intake should balance with output. Fever can account for fluid losses via the skin. When determining fluid needs, IVs, blood and blood products should be taken into consideration. Na+ should be restricted to 20-40 mg/day but difficult to obtain due to antibiotics, blood pressure medication and PN (Wilkens et al., 2012, 809). K+ balance should be monitored and intake should be individualized according to serum K+ levels. HD is used to remove K+ during AKI (Wilkens et al., 2012, 810).
2) Chronic Kidney Disease
Also called Chronic Renal Failure. Chronic Kidney Disease (CKD) is a progressive deterioration of renal function (McMillan, 2011, 2442). CKD causes permanent damage and eventually leads to end-stage renal disease (ESRD) also known as CKD Stage 5. It may result from any cause of renal dysfunction but the most common is diabetic nephropathy followed by hypertensive nephroangiosclerosis (McMillan, 2011, 2442). Diabetic nephropathy is the leading cause of ESRD (Escott-Stump, 2012, 861). Metabolic syndrome is a large and growing cause of renal damage (McMillan, 2011, 2442). About 23 million people have CKD c! moderately or severely reduced glomerular filtration rate (GFR) (Escott-Stump, 2012, 860). Fifty percent of patients with CKD also have DM (Escott-Stump, 2012, 864).
Sx of CKD include: anorexia, nausea, vomiting, stomatitis, dysguesia, nocturia, lasstitude, fatigue, pruritus, decreased mental acuity, muscle twitches, muscle cramps, water retention, undernutrition, GI ulceration, GI bleeds, peripheral neuropathies and seizures (McMillan, 2011, 2442).
Pt. has PMH of DM & HTN
Pts chief complaint was abdominal pain c! nausea & vomiting when admitted.
! renal function interferes c! the kidneys ability to maintain fluid and electrolyte homeostasis. The ability to concentrate urine occurs early on in the disease and is followed by ! in ability to excrete P, acid and K. Soon, the ability to dilute urine is lost and urinary volume does not differ c! " or ! fluid intake (McMillan, 2011, 2443). Na+ and water balance is maintained by " fractional excretion of Na+ and normal fluid intake due to thirst. Therefore, hypervolemia does not occur unless dietary intake of Na+ or water is restrictive or excessive (McMillan, 2011, 2443). K+ levels " when kidney failure becomes more advanced. K- sparing diuretics, ACE inhibitors, beta-blockers, NSAIDs, cyclosporine, tacrolimus or angiotensin II receptor blockers may " K in sooner in the progression of disease (McMillan, 2011, 2443). Ca+, parathyroid hormone, vitamin D metabolism and renal osteodystropy can occur resulting in hypocalcemia, hyperphosphatemia, " or ! bone turnover. Osteopenia or osteomalacia may also occur (McMillan, 2011, 2443).
Moderate acidosis and anemia are often evident. Anemia in CKD is normochromic-normocytic: Hct 20-30% and is caused by ! erythropoietin. CKD pts may also be deficient in Fe, folate, and vitamin B 12 (McMillan, 2011, 2443).
CKD is suspected when creatinine " but initial steps include determining if renal insufficiency is acute, chronic or acute superimposed on chronic. Testing includes urinalysis, electrolytes, BUN, creatinine, phosphate, Ca+ and CBC (McMillan, 2011, 2443).
Staging of CKD: Stage 1: GFR " 90 mL/min/1.73 m 2 (normal) plus albuminuria or known structural or hereditary renal disease Stage 2: GFR 60-89 mL/min/1.73 m 2 Stage 3: GFR 30-59 mL/min/1.73 m 2 Stage 4: GFR 15-29 mL/min/1.73 m 2
Stage 5: GFR < 15 mL/min/1.73 m 2 (McMillan, 2011, 2443).
Pt Rxd Lasix
Hct 28.9%, 27.9%, 27.3%
Folate 12.2 WNL, Vit B12 1174 WNL. Fe 31!
Pts diagnosis by Attending Renal MD.
GFR 14 mL/min/1.73 m 2
GFR indicates pt. is in ESRD; team details he will begin hemodialysis (HD) as an outpatient.
Progression of the disease is determined by degree of proteinuria (McMillan, 2011, 2443). The kidney plays a role in regulation of blood pressure (BP) through the renin-angiotensin system (Escott- Stump, 2012, 860). HTN and other underlying disorders are associated with more rapid progression (McMillan, 2011, 2443). Weight loss and anorexia are associated with mortality (Escott- Stump, 2012, 860).
MNT for CKD
The primary goal in MNT for CKD is to manage sx such as edema, hypoalbuminemia and hyperlipidemia, decrease the risk of progression to renal failure and maintain nutritional stores (Wilkens et al., 2012, 810).
A renal patient needs a detailed nutrition assessment including Subjective Global Assessment (SGA) to monitor physical changes such as weight changes and changes in muscle mass, diet history and gastrointestinal symptoms. Fluid shifts related to edema may cause difficulty in tracking weight losses (Escott-Stump, 2012, 860).
Early nutritional intervention can help to reduce Na+ intake, control BP, manage DM and reduce excessive protein intake that can help slow progression of the disease (Escott-Stump, 2012, 861) and postpone initiation of HD (Escott-Stump, 2012, 869).
Following a HTN diet, such as the DASH diet, low in sodium c! regular exercise can help to reduce BP to goal of <130 mm Hg systolic and <80 mm Hg diastolic. Blood glucose should be under control; aim for HbA1c " 7%. DM pts may have to initiate carbohydrate counting. All pts would benefit from and increase whole grains, fruits and vegetables while limiting processed foods (Escott-Stump, 2012, 869).
It is imperative to maintain or improve nutritional status when possible. Aim to keep serum albumin at 4.0 g/dL. A 10:1 ratio of BUN:creatinine is
CKD may be exacerbated by Type 2 DM, HTN.
Pts alb 3.6, 3.5 g/dL ~27:1 ratio BUN:creat desirable. Urinary creatinine doubles when renal function is <50% (Escott-Stump, 2012, 868). Energy requirements for nondialyzed patients >60 years of age with GFR <25 mL/min need 35 kcal/kg/day. Those <60 years of age need 30-35 kcal/kg/day. Intake from carbohydrates should be 50-60% (Escott-Stump, 2012, 869). If DM or heart disease is present, limit fat to 30% of calories with >10% of total calories from saturated fats (Escott-Stump, 2012, 869).
In CKD stages 1-3, limit protein to 0.8-1.0 g protein/kg IBW. Choose high-quality proteins. In CKD stage 4 reduce protein with GFR <25 mL/min reduce protein to 0.6 g protein/kg IBW/day (Escott-Stump, 2012, 869).
Patients c! DM, HTN or edema should limit their Na+ intake to 2.3 g/day (Escott-Stump, 2012, 869). When monitoring phosphorus and K+, guidelines are based on CKD stage. Phosphorus: Stages 1-2 limit 1.7 g/day. Stages 3-4 limit to 0.8- 1.0 g/day. Phosphate binders are recommended along with limited intake of dairy: 1-2 servings/day (Wilkens et al., 2012, 812). K+: Stages 1-2 keep to >4 g/day. Stages 3-4: 2.4 g/day (Escott-Stump, 2012, 869). Intake and K-depleting medication such as diuretics can affect K+ level (Wilkens et al., 2012, 812). Fluid intake should be restricted to output +500-1000mL (Escott-Stump, 2012, 869).
Patients c! CKD are routinely recommended to take a vitamin to replace water-soluble vitamins lost. There are renal formulations available (Wilkens et al., 2012, 812).
Not everyone requires a strict HD diet and therefore, diet therapy should be personalized to the patient based on his or her needs (Escott-Stump, 2012, 860). In diabetic patients, glycemic control can no longer reverse progression of CKD and instead more importance relies on control of BP and protein restriction when appropriate (Escott-Stump, 2012, 861).
B. Atrial Fibrillation
MNT Goals for Pt based on current status
Not currently on any vitamin/mineral supplements.
Atrial fibrillation (AF or A-fib) is defined as a rapid, irregular artrial rhythm caused by a failure of the atria to contract resulting in inconsistent electrical stimuli. Ventricular rate is also affected but becomes tachycardic. Sx of A-fib are palpitations, weakness, dyspnea and presyncope (Merck, 2011, 2165). AF is often asymptomatic but pts may experience palpitations, chest discomfort or sx of heart failure (Mitchell, 2011, 2166).
AF affects 2.3 million in the US with a higher prevalence in men. Whites are most likely to be affected. Almost 10% of people >80 years old have A-fib (Mitchell, 2011, 2166). It is most often caused by HTN, cardiomyopathy, valvular disorders, hyperthyroidism and binge ETOH drinking. Risk of stroke " in those with rheumatic valvular disorder, hyperthyroidism HTN, DM, left ventricular systolic dysfunction or previous thromboembolic events (Mitchell, 2011, 2166).
AF can cause atrial thrombi, which can lead to embolic stroke. AF is diagnosed by ECG and is treated with anticoagulation medication or other drugs that work to correct sinus rhythm. Sometimes, surgery is required to install a pacemaker that works to correct sinus rhythm (Mitchell, 2011, 2165).
b. MNT for Cardiovascular Disease
Therapeutic Lifestyle Changes (TLC) is helpful for preventing Coronary Heart Disease (CHD) and reducing cardiovascular disease (CVD). These guidelines in conjunction with the Dietary Approaches to Stop Hypertension Diet (DASH), which increases fruits, vegetables, whole grains, lean meats and non-fat dairy products (while decreasing processed foods) are helpful in prevention and treatment (Raymond & Couch, 2012, 753).
Dietary Pattern for TLC: Total fat should be restricted to 25-35% of total calories. Saturated fat should contribute >7% of
calories and trans fatty acids should be kept as close to zero as possible. Therefore, only lean meats, poultry and fish should be included in the diet. Protein in this dietary pattern attributes to 15% of total calories. Polyunsaturated fats (PUFAs) and monounsaturated fats (MUFAs) can help to lower triglycerides and LDL while raising HDL should contribute 10% and 20% of calories respectively. Carbohydrates, mostly fiber rich whole grain, should contribute to 50-60% of the diet. Guidelines recommend 2 g of fiber daily. Cholesterol is restricted to 200 mg/daily. Desirable body weight should be obtained and further weight loss should be prevented. The guidelines also recommend moderate physical activity daily (Raymond & Couch, 2012, 753).
C. HTN
HTN is defined as sustained SBP and DBP greater than 140 and 90 mm Hg (Escott-Stump, 2012, 367). Pre-HTN is defined as SBP between 120-139 mm Hg or DBP b/w 80-89 mm Hg. Stage 1 HTN (140 to 159/90 to 99 mm hg) is the most prevalent level seen in adults this population is most likely to have MI or CVA (Raymond & Couch, 2012, 758). HTN risk increases with age and therefore is prevalent in the elderly. HTN doubles risk for heart attack, stroke, HF (Escott- Stump, 2012, 367). Essential HTN (HTN with unknown cause) is prevalent in 90-95% of pt (Raymond & Couch, 2012, 758).
HTN is asymptomatic until complications develop (Bakris, 2011, 2067). Sx of HTN include frequent headaches, impaired vision, sob, nosebleeds, chest pain, dizziness, failing memory, snoring, sleep apnea and GI distress (Escott-Stump, 2012, 367).
Sleep apnea, drug-related causes, CKD, Cushings syndrome, steroid therapy, pheochromocytoma, reno vascular disease can cause high BP (Escott- Stump, 2012, 368). Lifestyle choices such as poor diet, smoking, physical inactivity, stress, obesity can contribute to HTN. Secondary HTN is a result of another disease, usually endocrine in nature Pts diet PTA " in fat
Pts BP 146/90 mm Hg.
Diet hx reveals diet " in fat, large portion sizes BMI = 43: class III obesity
(Raymond & Couch, 2012, 758).
If left untreated, HTN can lead to stroke, HF, renal failure, MI, accelerated bone loss, increase risk of fracture and LT memory problems (Escott-Stump, 2012, 367).
c. MNT for HTN
For dietary tx of HTN, the DASH diet is recommended. DASH is rich in fiber, includes 5- 10 servings of fruit and vegetables a day and non- fat dairy products. In comparison to BP lowering medication, DASH significantly reduced BP (Escott-Stump, 2012, 368). DASH can reduce SBP 8-44 mg Hg. Sodium should be limited to 2300 mg/day. If target BP is not reached, sodium can be further decreased to 1600 mg/day. Reduction of sodium can reduce SBP 2-8 mm Hg (Raymond & Couch, 2012, 762).
Fish oil rich in omega-3, antioxidants such as vitamin C, folic acid, vitamin K, soy protein and a Mediterranean style diet may also have a positive effect in HTN tx (Escott-Stump, 2012, 368). Including physical activity of 30 min/day on most days can reduce SBP by 4-9 mm Hg Reducing ETOH to 2 drinks/day for men and 1 drink/day for women can reduce SBP 2-4 mm Hg (Raymond & Couch, 2012, 762).
By following DASH and including an exercise regime, weight management can be achieved and possibly reduce SBP by 5-20 mm Hg (Raymond & Couch, 2012, 762).
D. Gout
Gout is a collection of monosodium urate crystals into tissue (McCarty, 2011, 350). The etiology behind gout is unknown (McCarty, 2011, 354), but gout can be induced by diuretics (Bakris, 2011, 2071). Accumulation, called tophi (Winkler & Malone, 2012, 917) usually occurs in and around joints and can cause recurrent acute or chronic arthritis. Diagnosis is determined by clinical criteria and presence of crystals in synovial fluid
Currently consuming " Na+
Pt. is Rxd Lasix.
(McCarty, 2011, 349). Tests performed include synovial fluid analysis, serum urate level and x-rays (McCarty, 2011, 351). Gout occurs more often in men during middle age. If a pt under 30 develops gout, it is often more severe (McCarty, 2011, 350).
Sx of gout include acute pain, tenderness, warmth, redness and swelling in affected areas (McCarty, 2011, 349.) Pain is often nocturnal. The areas most affected is the metatarsophalangeal joint of the great toe but it can occur in the hip, shoulder, sacroiliac, sternoclavicular or cervical spine joints. (McCarty, 2011, 350). Another site for tophi is the helix of the ear (Winkler & Malone, 2012, 917). Tx for gout includes anti-inflammatory drugs, treating co-existing HTN, hyperlipidemia and obesity and prevention of further deposition of crystals by lowering serum urate level (McCarty, 2011, 352).
d. MNT for Gout
Gout has been traditionally treated by a low purine diet, but has since been replaced by drugs, allowing the diet to treat gout to become more liberalized (Gomez & Kaufer-Horwitz, 2012, 917). It is not recommended that pts follow a balanced diet c! limited intake of animal foods, alcohol, avoidance of foods high in purine, fructose and non-complex carbohydrates. Portion control should also be emphasized. Weight loss and glycemic control can help to improve gout. High fluid intake (8- 16 cups daily) should be encouraged to help excrete uric acid and minimize kidney stone formation. Foods high in alkaline such as dairy, eggs, vegetable proteins, cherries and coffee may be protective against uric acid build up since the foods are alkaline in nature (Gomez & Kaufer-Horwitz, 2012, 918).
E. Type 2 Diabetes Mellitus
Total carbohydrate intake eaten regardless of the source is the primary determinant of postprandial Type 2 diabetes mellitus (T2DM) is marked by inadequate insulin secretion. While insulin levels are high in Type 2, peripheral insulin resistance and
Pt. is a middle aged man at age 56.
BMI=43
Indicated for DM as well/in DASH Diet
Not indicated due to CKD.
" in hepatic glucose production make insulin available inadequate to normalize glucose level (Crandall, 2011, 867). T2DM accounts for 90-95% of all DM cases; many undiagnosed (Franz, 2012, 678). Risk factors include genetic and environmental factors, older age, obesity (particularly intraabdominal), physical inactivity, prior hx of gestational DM, race and ethnicity (Franz, 2012, 678).
Blood glucose (BG) levels " after eating, especially after a meal " in carbohydrate. BG levels take longer to return to normal post-prandial (Crandall, 2011, 867). Obesity and weight gain contribute to insulin resistance. Adipose tissue " plasma levels of free fatty acids and adipocytokines impairing glucose transport and muscle glycogen synthase activity (Crandall, 2011, 868).
Symptoms of DM during periods of hyperglycemia include: frequent voiding of urine, polyuria and polydipsia. Dehydration may occur. Weight loss, nausea, vomiting, blurred vision and a predisposition to bacterial or fungal infections may occur (Crandall, 2011, 868).
Complications can result from poorly managed DM, primarily vascular complications, that can result in retinopathy, nephropathy and neuropathy. Microvascular disease also impairs skin healing that can compromise skin integrity. HTN and dyslipidemia are commonly seen in patients with DM (Crandall, 2011, 869). Screening for complications related to DM should become five years after diagnosis including food examinations, funduscopic examinations, urine testing for proteinuria and microalbuminuria and measurement of creatinine and blood lipid profiles (Crandall, 2011, 871).
DM is diagnosed by monitoring fasting plasma glucose levels but sometimes, oral glucose tolerance testing (OGTT) is performed. OGTT is more sensitive but less convenient and therefore often only reserved for diagnosing gestational DM (Crandall, 2011, 871). A random glucose test >
200 mg/dL may be diagnostic but it may also be influenced by a recent meal and must be confirmed by repeat testing if no other symptoms are present. Hemoglobin (Hb) A 1c allows for a retrospective look at glucose levels over the preceding 2-3 months. Urine glucose measurement is no longer used (Crandall, 2011, 871).
Goals for glycemic control: -BG 80-120 mg/dL during the day -BG 100-140 mg/dL at bedtime -HbA 1c levels < 7% (Crandall, 2011, 872).
In the critically ill and hospitalized patients, blood glucose levels should be ~110 mg/dL. Pts in hospital will usually require IV insulin (Escott- Stump, 2012, 548).
e. MNT for Type 2 DM
MNT for T2DM requires an individualized approach. There is no single diabetic diet but a diet prescription based on individual needs and goals (Escott-Stump, 2012, 521). Pts should be educated on self-management via diet and self- monitoring of blood glucose (SMBG) (Franz, 2012, 684). Diet should be reduced in calories and fat, carbohydrate counting or exchange lists with simple meal plans, physical activity and behavioral strategies should be incorporated in treatment (Franz, 2012, 684).
glucose levels (Franz, 2012, 684). Carbohydrate should contribute to 45-65% of total energy intake (Escott-Stump, 2012, 546). Consistency in carbohydrate intake eaten at each mealtime or snack can help to improve glycemic control either solely by diet therapy, or in combination with glucose lowering medications or insulin regimens (Franz, 2012, 684). Carbohydrate counting considers 15 g of carbohydrate to be 1 serving. Exchange lists group foods into list depending on their carbohydrate content. This method utilizes symbols to identify foods high in fiber, fat or sodium (Franz, 2012, 685). Protein should contribute 15-20% of total calories if renal function is normal. If the
No HbA 1c test ordered.
Pts FSBG WNL for hospitalized pt. kidneys are affected, protein restriction to 0.8-1.0 g/kg is recommended (Escott-Stump, 2012, 546). Fat can contribute 25-35% of total calories but saturated fats should be restricted to 7-10%, focusing on a higher intake of PUFAs and MUFAs (Escott-Stump, 2012, 546). The DASH diet principals are useful in planning a DM diet plan, as it will help to manage HTN if present and reduce NA+. Less than 2400 mg Na+ is recommended (Escott-Stump, 2012, 546).
Testing pre-meal and post-meal glucose levels can help pts to make adjustments to their meal planning (Franz, 2012, 685). These diet plans are portion controlled and can lead to weight loss. Moderate weight loss of 5-10% can ! hyperglycemia, dyslipidemia and hypertension (Escott-Stump, 2012, 546).
Part II: continued
Summary of Medical Text Findings Comparison of Patient to Text d. Medications: list medication, indication, effect of food and drug interactions relative to nutrition: factors that can affect nutrition intake/GI/vitamins, minerals and labs. Reference B. Medications: how is medication affecting patient? Is patient experiencing any side effects? 1. Lovenox/heparin Anticoagulant. May cause abdominal pain, GI bleeding, constipation and black tarry stools. Caution c! DM & ESRD. ! Platelets. " AST, " ALT, " PT/INR (Pronsky, 2012, 154).
2. Prinivil Angiotensin Converting Enzyme (ACE) inhibitor, antihypertensive. Used to treat left ventricular dysfunction, CHF post MI, acute MI, diabetic nephropathy. Insure adequate fluid intake, ! Na, ! cal diet may be recommended. Avoid salt substitutes, caution c! K supplements. May cause anorexia. "K, ! Na (Pronsky, 2012, 36).
Heparin is giving prophylactically in hospital. Not likely related to abdominal pain pt was experiencing.
Dx: A-fib, CKD, DM
3. Humalog/insulin lispro Antidiabetic, hypoglycemic. Use c! diabetic meal plan to balance carbohydrate c! doses. " wt. Avoid ETOH. Large wt. gain " insulin needs. ! Glucose, ! HbA1 c, ! K, ! Mg, ! P (Pronsky, 2012, 167).
4. Lopressor/metoprolol Antihypertensive, antiangina, CHF tx (XL), MI tx. Beta-blocker. ! Na, ! Cal diet. Avoid natural licorice. May cause dry mouth, N/V, dyspepsia, diarrhea, constipation. Caution c! DM as it may mask hypoglycemia/may ! insulin release. (Pronsky, 2012, 206).
6. Lasix/furosemide Anti-hypertensive, diuretic (K-depleting). Used for tx of edema associated with CHF, renal or hepatic disease. Take on empty stomach, food ! bioavailability, but may take with food/milk if GI upset occurs. Avoid natural licorice. Limit alcohol. ! BP with possible hypotension. Lab values may indicate ! K, ! Mg, ! Na, ! Cl, ! Ca and " glucose (Pronsky, 2012, 110).
Vomiting likely not caused by medications.
Summary of Medical Text Findings Comparison of Patient to Text C. Laboratory Tests: key tests and their implications relative to patients medical problems; include reasons for increase and decrease for each lab. Reference e. Laboratory Tests: assess patients laboratory values; refer to chart on first page or use values from your facility; note if any medications are affecting lab values. 1. Red Blood Cell Count: Norm (F: 3.9- 5.5, M: 4.7-6.1 million/mm 3 ) " c! polycythemia, dehydration, severe diarrhea. ! c! anemia, hemorrhage, Fe def, systemic disease (Pronsky, 2012, 352).
2. Mean Corpusal Volume: Norm (78-93) " with megaloblastic anemia due to Fol or Vit B12 def, liver disease, reticulocytosis, myelofibrosis Spurious with cold agglutinins. ! with Fe def anemia, hereditary, spherocytosis, thalassemia minor, sideroblastic anemia, Pyr-responsive anemia, lead poisoning (Pronsky, 2012, p. 349).
10. Sodium (Na): Norm (136-144 mEq/L) " (hypernatremia) c ! dehydration & low fluid intake, diabetes insipidus, Cushings syndrome, coma, primary aldosteronism. ! (hyponatremia) c ! edema, severe burns,
Phos WNL
BUN" (136, 145, 154)
Creat " (5.3, 5.6)
Na+ ! (129, 128, 126)
Lasix Rxd severe diarrhea/vomiting, diuretics, SIADH, water intoxication, Addisons disease, severe nephritis, starvation, hyperglycemia, malabsorption, AIDS (Pronsky, 2012, 352).
11. Potassium (K): Norm (3.5-5.0 mEq/L) " (hyperkalemia) c! renal failure, tissue damage, acidosis, Addisons, uncontrolled DM, internal hemorrhage, overuse of K suppl, acute AIDS. ! (hypokalemia) with GI loss, IV fluid with without K suppl, alcohol abuse, malabsorption, malnutrition, diarrhea, vomiting, chronic stress or fever, K depleting diuretic, steroid, estrogen use, hepatic disease with ascites, excessive licorice intake, renal disease (Pronsky, 2012, 351).
GFR 14 " in acromegaly and burns ! in CHF, glomerular disease, eclampsia, gout, multiple myeloma (Pronsky, 2012, 344).
Part III: Nutrition History:
A. Food Intake Pattern/Nutrition History Directions: Record food intake over a 24-hour period including time eaten and portion sizes. Include all food, condiments, alcoholic and carbonated beverages. If eating pattern differs each weekend or due to different work shifts, record on a separate sheet. Food intake can be calculated by hand or computer.
Usual intake at Home or Hospital (circle one)
Meal Intake/Amt Breakfast 2 eggs c! 2 slices cheese, made in bacon fat or salted butter (1 pat) Plus 1 T ketchup 2 slices white toast c! salted butter, 1 T grape jelly 4-5 slices bacon Sometimes: 1 orange or 1 glass ~12 oz. orange juice/apple juice Coffee c! cream and sugar Lunch 2 Egg salad sandwiches c! regular mayonnaise on white bread 1 can Sprite soda 2-3 handfuls potato chips, usually sour cream & onion or plain flavor Snack 2 shortbread cookies & tea made c! whole milk and sugar Dinner 5 Pork roast medallions or 1 large breast of fried chicken Mashed potatoes made c! cream, butter (large portion of late, ~2 cups) Green beans (~15 pcs) Dessert 1 slice apple pie c! vanilla ice cream (1 scoop)
B. Nutritional Analysis
Protein meets recommended quantity, but due to GFR should be restricted from 0.8 to 0.6 g/kg. Na+ is significantly higher than recommended (2.3g/day) (Escott-Stump, 2012, 869). Phosphorus intake is " by 599 mg. K intake is under recommended daily allowance of 2.4 g/day (Escott-Stump, 2012, 869). Pt chooses foods " in fat and does not utilize carbohydrate counting to maintain blood glucose control.
Iron (mg) 8.00 Do not exceed 45 mg * Magnesium (mg) 420.00 Do not exceed 350 mg by supplement * Phosphorus (mg) 700.00 Do not exceed 4000 mg * Potassium (mg) 4,700.00 Sodium (mg) 1,300.00 Less than 2300 mg - lower for some people + Zinc (mg) 11.00 Do not exceed 40 mg * Sources: * Dietary Reference Intakes - For Adult 19-70 years, non-pregnant + 2010 Dietary Guidelines for Americans Bar Graph Report The Bar Graph Report displays graphically the amount of the nutrient consumed and compares that to the dietary intake recommendations. 0 50 100 Percent Nutrient Value 150 DRI Goal Basic Components Calories 3,579.35 110 % 3,249.22 Calories from Fat 1,596.97 176 % 909.78 Calories from SatFat 545.99 187 % 292.43 Protein (g) 110.23 110 % 99.79 Carbohydrates (g) 383.46 86 % 446.77 Sugar (g) 176.93 Dietary Fiber (g) 19.29 42 % 45.49 Soluble Fiber (g) 1.73 InSoluble Fiber (g) 2.57 Fat (g) 177.44 176 % 101.09 Saturated Fat (g) 60.67 187 % 32.49 Trans Fat (g) 1.30 Mono Fat (g) 47.19 131 % 36.10 Poly Fat (g) 15.85 49 % 32.49 Cholesterol (mg) 1,049.98 350 % 300.00 Water (g) 2,145.88 58 % 3,700.00 Vitamins Vitamin A - RAE (mcg) 811.95 90 % 900.00 Vitamin B1 - Thiamin (mg) 1.73 144 % 1.20 Vitamin B2 - Riboflavin (mg) 2.39 184 % 1.30 Vitamin B3 - Niacin (mg) 33.56 210 % 16.00 Vitamin B6 (mg) 2.47 146 % 1.70 Vitamin B12 (mcg) 4.00 167 % 2.40 Vitamin C (mg) 182.30 203 % 90.00 Vitamin D - mcg (mcg) 3.59 24 % 15.00 Vitamin E - Alpha 12.06 80 % 15.00 Folate (mcg) 377.93 94 % 400.00 Minerals Calcium (mg) 915.99 92 % 1,000.00 Iron (mg) 13.74 172 % 8.00 Magnesium (mg) 249.95 60 % 420.00 Phosphorus (mg) 1,599.01 228 % 700.00 Potassium (mg) 3,694.54 79 % 4,700.00 Sodium (mg) 5,499.66 423 % 1,300.00 Zinc (mg) 9.73 88 % 11.00 Other Omega-3 (g) 0.98 Omega-6 (g) 7.02 Alcohol (g) 0.00 Caffeine (mg) 90.72 Spreadsheet Report The Spreadsheet shows all the values for all nutrients. Nutrients are displayed horizontally, with totals at the bottom of the list. Item Day Meal Amount Cals FatCal SatFatCal Prot (g) Fri 01-24- 2014 Breakfast Eggs, whole, lrg, fried (USDA each 2 180.3 126.7 35.5 12.5 Cheese, American, past, proc, each 2 157.5 118.1 74.3 9.3 Butter, salted (USDA SR-21) tbsp 2 203.8 207.3 131.3 0.2 Ketchup (USDA SR-21) tbsp 1 14.6 0.4 0.1 0.3 Bread, white, soft, slice (USDA each 2 133.0 14.8 3.1 3.8 Jelly, concord grape (J.M. tbsp 1 50.0 0.0 0.0 0.0 Bacon, brld/pan fried/rstd, med piece 5 216.4 150.3 49.0 14.8 Juice, orange, 100%, cnd/btl oz 16 206.2 0.0 0.0 0.0 Lunch Sandwich, egg salad, w/white each 2 757.6 430.6 68.5 18.8 Soda, Sprite (Sprite) oz 12 136.1 0.6 0.2 Chips, potato, sour cream & each 2 320.0 180.0 18.0 4.0 Dinner Fried Chicken, breast, each 1 217.6 78.2 21.6 31.2 Mashed Potatoes, prep f/recipe cup 2 474.6 159.1 78.2 7.9 Snap Beans, green, ckd, drained cup 1 43.7 3.1 0.5 2.4 Snack Cookies, shortbread, plain, 1 each 2 80.3 34.6 8.6 1.0 Tea, brewed w/tap water (USDA oz 16 4.5 0.2 0.1 0.0 Sugar, white, granulated (USDA tbsp 1 48.9 0.0 0.0 0.0 Milk, whole, 3.25% (USDA SR-21) tbsp 2 18.3 8.9 5.1 1.0 Apples, pie spiced, w/natural cup 1 140.0 0.0 0.0 0.0 Ice Cream, vanilla (USDA SR-21) oz 3 176.1 84.2 52.0 3.0 Day Total -- 3579.4 1597.0 546.0 110.2 Average Day Total -- 3579.4 1597.0 546.0 110.2 Item Day Meal Carbs (g) Sugar (g) Fiber (g) Fib-S (g) Fib-I (g) Fat (g) Fri 01-24- 2014 Breakfast Eggs, whole, lrg, fried (USDA 0.8 0.8 0.0 0.0 0.0 14.1 Cheese, American, past, proc, 0.7 0.2 0.0 0.0 0.0 13.1 Butter, salted (USDA SR-21) 0.0 0.0 0.0 0.0 0.0 23.0 Ketchup (USDA SR-21) 3.8 3.4 0.0 0.0 0.0 0.0 Bread, white, soft, slice (USDA 25.3 2.1 1.2 1.6 Item Day Meal ExOth ExStar ExVeg ExFat Fri 01-24- 2014 Snack Ice Cream, vanilla (USDA SR-21) 1.3 1.8 Day Total 5.5 12.6 1.7 23.7 Average Day Total 5.5 12.6 1.7 23.7 Calories and Fat The Calories and Fats report is useful for quickly seeing the calorie and fat breakdowns of your intake. The Source of Calories window shows graphically the percentage of calories from protein, carbohydrates, fat, and alcohol. The Source of Fat window shows the breakdown of fat (saturated, monounsaturated, polyunsaturated, and other fats). Source of Calories Calori Gram Percent Protein 12 % Carbohydrates 43 % Fat (Total) 45 % Alcohol 0 % 442 1537 1600 0 Total 3579 110.2 383.5 177.4 0.0 Saturated Fat 546 60.7 15% Mono Fat 425 47.2 12% Poly Fat 143 15.9 4% Trans Fat 12 1.3 0% *The N/A Fat category includes the glycerol portion of the fat molecule (typically 5%), as well as any unavailable values for saturated, mono, poly, and trans fats. Ratios P:S ( Poly Fat / Saturated Fat ) 0.26 : 1 Potassium : Sodium 0.67 : 1 Calcium : Phosphorus 0.57 : 1 CSI ( Cholesterol / Saturated Fat ) 113.77 Source of Fat (approx.) Fat (g) Percent Saturated Fat 34 % Mono Fat 27 % Poly Fat 9 % Trans Fat 1 % 60.7 47.2 15.9 1.3 Total (g) 177.4 *The N/A Fat category includes the glycerol portion of the fat molecule (typically 5%), as well as any unavailable values for saturated, mono, poly, and trans fats. Exchanges Starch 12.60 Other Carbs 5.53 Very Lean Meat Meat Fruit 5.56 Vegetables 1.74 Milk
Part IV: Nutrition Care Process: Assessment, Diagnosis, Intervention, Monitoring and Evaluation (ADIME)
S: Pt. came to the ED c! abdominal pain, nausea and vomiting. Pt. reports that he has a RD that he sees on an outpt basis but admits he has difficulty following his diet at home. Pt. finds it difficult to follow his diet because it is restrictive at times. As a pastor, he attends a lot of events (such as weddings, funerals) that serve catered foods " in carbohydrate and fat. Food being offered to him is hard for him to turn down. He tries to avoid sugar and soda and has attempted to " his vegetable intake. In the hospital, pt has a good appetite and he says he has ate >75% of all meals served. O: 56 y/o #. Dx: acute on chronic kidney disease. PMH: A-fib (pacemaker), HTN, Gout, DM Type 2, CKD Stage 4. Rx: Lovenox, Prinivil, Humalog, Lopressor, Zosyn and Lasix. Ht: 68 Wt: 275# (2/10/14). UBW: 270s. %IBW: 179%. %UBW: 100%. BMI: 43, Class III Obesity. Diet Rx: K2gm, ! Na, ! Chol, 2000 kcal DM providing 1870 kcal, 99 g PRO. Labs: (2/10/14): RBC 4.08 WNL, Hbg 9.9 !, Hct 28.9 !, MCV 70.8 !, Alb 3.6 WNL, Ca++ 9.6 WNL, BUN 136", Creat 5.3", Na+ 129!, K 3.0 !, Glu 214", Cl 85!. (2/11/14) RBC 4.04!, MCV 69.1!, Hgb 9.9!, Hct 27.9!, Alb 3.5 WNL, Phos 3.7 WNL, BUN 145", Creat 5.3", Na+ 128!, Mag 1.8 WNL, Fe 31!, Ferritin 246 WNL, Folate 12.2 WNL, Vit B12 1174 WNL. (2/12/14) RBC 3.86!, MCV 70.1!, Hgb 9.6 !, Hct 27.3!, Ca++ 9.4 WNL, Phos 2.8 WNL, BUN 154", Creat 5.6", Na+ 126!, K+ 3.7 WNL, Glu 56!, Mag 1.8 WNL, Cl 84!. GFR 14. A: PES #1: Not ready for renal/DM diet change related to disinterest in applying knowledge and lack of self-efficacy for making change evidenced by negative body language and defensiveness when discussing renal/DM diet. PES #2: Excessive sodium and phosphorus intake related to lack of application of knowledge of renal diet evidenced by 24-hour diet recall and verbalization of difficulty following renal diet at home. Calorie needs 35 kcal/kg using IBW of 77 kg ~2700 kcal/daily. Current usual intake, evidenced by 24-hour recall provides 3579 kcal/daily: 133% of EEN. Protein needs in CKD Stage 4 are 0.6 g/kg of IBW until initiation of HD. Protein needs are 46 g/day; current diet intake is " in protein providing 240% of protein needs. Protein needs when HD is initiated will " to 77-100 g daily (1.0-1.3 g/kg). Fluid needs are 750-1000 mL. Na+ should be limited to 2.3 g/day and currently Pt is taking in 3.7 g. Phos should be limited to 0.8-1 g, pts diet recall reveals 1.6 g of phos intake. Guidelines for K+ are 2.4 g/daily. K+ intake is within guideline limits; K+ lab values trended up and are now WNL. Pt is at high nutritional complexity due to advancement of CKD to Stage 5 and impending initiation of HD. No edema or s/s of dehydration are noted in this pt, however, his abdomen appears to be distended. Due to ! H&H and ! MCV, Fe deficiency anemia is likely and may be related to CKD or due to blood losses from tests performed while in hospital. BUN/Creat " likely due to renal insufficiency. Gout can also " BUN. ! Na+, ! Cl and ! K+ may be due to Lasix Rx and possibly exacerbated by AKI. Glucose indicates poor glycemic control.
Part IV: Nutrition Care Process continued (Intervention, Monitoring and Evaluation)
Goal 1: Lower serum Na+ and Phos to WNL Plan 1: -Provide reinforcement of nutrition education regarding high/low Na+ and Phos foods -Work c! pt to come up with sample menu including food prefs -Educate for self-monitoring strategies including food diary -Recommend Phoslo phosphate binder -Monitor serum Na+ and Phos on lab reports
Goal 2: " H&H and MCV to WNL Plan 2: -Recommend Epogen & Venofer
Goal 3: Maintain glucose between 80-120 mg/dL
Plan 3: -Provide education reinforcement of carbohydrate counting, incorporating carbohydrates into renal meal plan (mentioned above) -Encourage self-monitoring of blood glucose levels
Long Term (if pt. returns to outpatient clinic):
Goal 4: Encourage 10% wt loss (~30#), 1-2# per week.
Plan 4: -Encourage portion control in combination c! renal & DM diet recommendations -Provide pt c! benefits of wt reduction in Tx of DM, HTN
References
Bakris, G.L. (2011). Arterial hypertension. In R. S. Porter & J. L. Kaplan (Ed.) The Merck Manual. (19 th ed., pp. 2067, 2071). Whitehouse Station, NJ: Merck Sharp & Dohme Corp. Crandall, J.P. (2011). Diabetes mellitus and disorders of carbohydrate metabolism. In R. S. Porter & J. L. Kaplan (Ed.), The Merck Manual. (19 th ed., pp. 867, 868, 869, 871). Whitehouse Station, NJ: Merck Sharp & Dohme Corp. Escott-Stump, S. (2012) Nutrition and diagnosis-related care. (6 th ed., pp. 367, 368, 521, 546, 548, 860, 861, 864, 868, 869). Baltimore: Lippincott Williams & Wilkins. Franz, M. J. (2012). Medical nutrition therapy for diabetes mellitus and hypoglycemia of nondiabetic origin. In Y. Alexopoulous (Ed.), Krauses Food and the Nutrition Care Process (13 ed., pp. 678, 684, 685). St. Louis, MO: Elsevier. Gomez, E.F. & Kaufer-Horwitz, M. (2012). Medical nutrition therapy for rheumatic disease. In Y. Alexopoulous (Ed.), Krauses Food and the Nutrition Care Process (13 ed., pp. 917, 918). St. Louis, MO: Elsevier. McCarty, D.J. (2011). Crystal-induced arthritides. In R. S. Porter & J. L. Kaplan (Ed.), The Merck Manual. (19 th ed., pp. 349, 350, 351, 354). Whitehouse Station, NJ: Merck Sharp & Dohme Corp. McMillan, J. I. (2011). Renal failure. In R. S. Porter & J. L. Kaplan (Ed.), The Merck Manual. (19 th ed., pp. 2436, 2438, 2439, 2442, 2443). Whitehouse Station, NJ: Merck Sharp & Dohme Corp. Mitchell, B. L. (2011). Arrhythmias and conduction disorders. In R. S. Porter & J. L. Kaplan (Ed.), The Merck Manual. (19 th ed., pp. 2166, 2165). Whitehouse Station, NJ: Merck Sharp & Dohme Corp. Pronsky, M. Z. & Crowe, S. J. (2012). Food medication interactions. (16 ed., pp. 36, 110, 154, 167, 206, 340, 342, 343, 344, 345, 346, 348, 349, 350, 351, 352, 354) Birchrunville, PA: Food-Medication Interactions. Raymond, J. L. & Couch, S. C. (2012). Medical nutrition therapy for cardiovascular disease. In Y. Alexopoulous (Ed.), Krauses Food and the Nutrition Care Process (13 ed., p. 753, 758, 762). St. Louis, MO: Elsevier. Wilkens, K.G., Juneja, V. & Shanaman, E. (2012). Medical nutrition therapy for renal disorders. In Y. Alexopoulous (Ed.), Krauses Food and the Nutrition Care Process (13 ed., pp. 808, 809, 810, 812). St. Louis, MO: Elsevier.
Comparison of Cherry Leaves (Mutingia Calabura) As Feed Component Against The Low Density of Lipoprotein Blood, High Blood Lipoprotein Density, Protein and Fat Contents of Mojosari..