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Rachel Hudes Benedictine University Dietetic Internship Program CASE STUDY ASSIGNMENT NCP Step 1: Nutrition Assessment Patient Profile Practice Setting in which you are assessing this patient/client Age Gender Race Relevant personal data (e.g. does not speak English, marital status, lives in a nursing home, SES etc.) Symptoms/complaints CURRENT Medical Conditions/Diagnoses Hospital room at Saint Anthony Hospital; general medical floor. 75 y/o Male Caucasian Unable to communicate, resides in a nursing home, single. Dehydration, pressure ulcers, constipation. Multiple contractures of the left extremities, UTI, sepsis, pressure ulcers on left ankle. PAST Medical Conditions/Diagnoses Medical Test(s) conducted or planned Medical procedure(s) conducted or planned Cerebrovascular accident, hypertension, X-Ray Anthropometric Data: Indicator Value for the patient/client Height Weight Weight change UBW IBW % IBW BMI Adjusted Body Weight (if appropriate) Patient Weight Goal 66 inches 167.8 lbs (76.3 kg) None reported n/a 142 lbs 118.2% 27.4 n/a n/a Food/Nutrition Related History Food Allergies None Assessment of patient/client value Overweight Chewing and/or Dental Problems Swallowing Problems Bowel Habits/Problems Recent Changes in Eating Habits Current Appetite Food Preferences Nutrient Malabsorption Problems? N/V/D Past Diet Prescriptions Past Diet Instructions Patient has difficulty chewing. Patient has difficulty swallowing. Currently is constipated. Patient was placed on nutrition support. Pt is on nutrition support. Appetite was not assessed because of this and his inability to communicate. n/a no no NPO, enteral tube feedings. n/a 24 – Hour Recall- N/A (Pt is receiving enteral nutrition support) Meal Type of Food Cooking Method First Meal of Day Snack Second Meal of Day Snack Third Meal of Day Snack Portion Food Recall Assessment- N/A Analyze the recall using MyPyramid Guidelines 1. Analyze the recall using a computer nutrient analysis program of your choice. 2. Attach the computer analysis output to this assignment. 3. Explain the adequacy of the intake below in terms of macro and micro nutrients. Nutrition Focused Physical Assessment Physical Appearance Patient is bedridden and immobile. Lies with his elbows against the bed and head back. Eyes were closed and patient was not in a state to communicate. Appeared to be resting comfortably. Pt was wearing heal protectors. Muscle and fat wasting Swallowing function Appetite Affect (e.g. lethargic, sleeping, coma, energetic, in pain, etc.) He did not show signs of muscle wasting. Poor swallowing function. n/a Sleeping. LABORATORY DATA: Laboratory Test: Diet Order Normal Values: Height Weight Blood Pressure 120/80 Albumin > 3.5 mg/dL I&O Glucose serum 65-110 mg/dL BUN Creatinine BUN/Creatinine ratio CRP ESR GFR Calcium Sodium Potassium Chloride C02 Braden Score 6-20 mg/dL 0.61-1.30 mg/dL 0.60-20.00 mg/dL <1 20 mm/hr >59 8.6-10 mg/dL 136-145 mmol/l 3.5-5.1 mmol/l 98-115 mmol/l 23-29 mmol/l 23/23 Date: 4/6/2011 Values: Date: 4/8/2011 Values: Date: Date: 4/20/2011 Values: Values: Tube feeding: Jevity 1.2 80ml/hr with 300 ml flush q 6hrs Date: Values: Juven BID 66 inches 76.3 kg 105 34 H .71 47.89 H 9.6 H 52 H 115 8.7 140 3.9 98-115 23 6/23 L DISCUSSION of Laboratory Data Instructions: Discuss the relation of laboratory values to disease state and nutritional status. Consider the following: What significance do the abnormal laboratory results have for this patient ( example: type anemia? type hyperlipidemia)? If the case is being completed during a rotation where minimal laboratory data is available (such as WIC), provide a discussion regarding what labs would be helpful in completing a more complete assessment of the patient/client. The patient’s known abnormal labs include blood urea nitrogen (BUN), BUN/Creatinine ratio, C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR). ESR is a marker of inflammation within the body and the high level within this patient may be related to the multiple contractures in his left extremities. The constant tightness and lack of mobility, due to paralysis of this side of his body, resulted in his joints stiffening up and leading to deformities, known as contractures. Joint stiffness and deformity also can occur in people who have severe arthritis, which is what ESR is used to screen for. Because this pt is experiencing similar joint damage as to someone who has severe arthritis, it is likely that this elevated lab is a marker of this pt’s multiple contractures. CRP is elevated in this patient indicating that he is in a state of active inflammation/has infection. This could reflect multiple problems that the patient is experiencing. For example his three pressure ulcers, sepsis, and a urinary tract infection (UTI). BUN is elevated in this patient and not creatinine, which reflects his dehydration status. This also caused his BUN/creatinine ratio to be elevated as well because of his elevated BUN level. In a state of dehydration this happens because the body decreases its urine output, leaving more urea in the body. Kidney function appears to be normal because electrolytes and creatinine are all at normal levels. This patient also has a Braden score of 6 which is very low and indicates that he is at risk for developing pressure ulcers/more pressure ulcers. Other important labs that should have been assessed with this pt are his hemoglobin/hematocrit, albumin, prealbumin, total serum protein, and serum zinc levels. MEDICATIONS: 4/20/2011 Date: Medication &Amount: Desyrel: 150 mg via gastric tube @ HS Purpose or Function: antidepressant Celexa: 40 mg via gastric tube, antidepressant, SSRI daily Heparin: 5000 units via anticoagulant subcutaneous, BID Significant Nutritional Implications: May cause constipation Nausea, increased sweating, diarrhea May cause constipation, subcutaneous and skin necrosis Aspirin: 325 mg via gastric tube, daily Analgesis, antipyretic, antiarthritic, NSAID, to prevent CVA or MI May decrease iron and increase BUN Tylenol: 650 mg via gastric tube, q4-6hrsPRN Omeprazole: 20 mg via gastric tube, daily Analgesic Easy bruising, bleeding, nausea,vomitting Antiulcer, antiGERD May decrease calcium absorption and serum vitamin B 12 Baclofen: 10 mg via gastric tube, TID Skeletal muscle relaxant, antispasmodic Used for brain injury May cause constipation, increase urinary frequency and increase glucose Ensure hydration and vitamin C Albuterol Sulfate: 0.083% via Antiasthma, oral inhalation, q 6hrs pm bronchodilator, Sympathomimetic, beta 2 agonist Diarrhea, indigestion, nausea, upper respiratory infection, urinary tract infection Abilify: 30 mg via gastric tube, Antipsycotic HS Stroke, akathisia (prolonged, abnormal muscle spasms or contractions or a sense of restlessness or need to move), increased blood sugar or diabetes, low blood pressure, low white blood cell count, seizures, nausea, vomiting, constipation Nausea, vomiting, diarrhea, rash, headache, ringing in the ears, decreased hearing Minocycline: 100 mg via gastric tube, q 12hrs X 7 days Used to treat infections of the skin, respiratory tract, and urinary tract Flagyl: 500 mg via gastric Antibiotic: used to treat tube, q 8hrs X 5 days UTIs Clistin: 110 mg via IV, daily X Antihistamine 4 days Vitamin C: 500 mg via gastric Vitamin supplement tube, BID Ipratropium BR: 0.02% Bronchiodilator solution via nasal, q 6hrs pm Naproxen: 375 mg via gastric Antiarthritic, analgesic, tube, BID prn NSAID Apap: 160 mg/5 ml via gastric tube, q 6hrs prn Zosyn: 3.3 gm via IV, q 6hrs X 5 days Zithromax: 500 mg via gastric tube, daily X 5 days Abdominal cramps, constipation, diarrhea, nausea, upset stomach, vomiting Decreased urination, rash Can cause urinary retention, UTI, diarrhea, nosebleeds May cause UTI, increase bun, peripheral edema Pain reliever and fever reducer Antibacterial used t o treat Diarrhea, constipation, nausea, fever, vomiting, infection urinary tract infection, rash Antibacterial used to treat a Diarrhea, nausea, vomiting, upset stomach variety of infections. Infection of the urethra. DISCUSSION of Medications Instructions: Discuss drug-nutrient interactions and side effects the medicines may cause that have nutritional significance. Consider the following: Include whether the patient exhibits any of these side effects. Discuss relevant relations of medications to disease symptom complaints. The drugs that the patient is taking that have the most nutritional significance are aspirin, desyrel, naproxen, flagyl, ipratropium BR, baclofen, and heparin. The medications that may be either contributing to the patients constipation or making it worse include the heparin, baclofen, and desyrel, The medications that may be related to the patient’s increased BUN level and (urinary tract infection) UTI include naproxen and ipratropium BR. The Heparin may also be negativily effecting the patients skin integrity which is also vulnerable and experiencing inflammation from pressure ulcers. In terms of Vitamin C, aspirin may cause a decrease in the absorption of this nutrient but because of this he is receiving additional vitamin C via his gastric tube to compensate for this. This is also important because he may also be losing Vitamin C through wound fluid loss. NCP Step 2: Nutrition Diagnosis PATHOPHYSIOLOGY CURRENT Medical Conditions/Diagnoses List ALL current medical conditions and describe the pathophysiology of each. Add additional rows as needed. Be sure to reference your findings. Diagrams may also be helpful in explaining the pathophysiology of some diseases/conditions. Pressure Ulcers: A variety of factors contribute to putting someone at risk and causing the development of pressure ulcers. Pressure ulcers are areas of damage to the skin and underlying tissue that usually occur over bony protrusions such as over the sacrum, ischial tuberosities, trochanters, malleoli, and heels, primarily due to on-going compression, moisture, friction, and/or shearing forces. The chart above displays these primary/extrinsic factors as well as secondary/intrinsic factors. These situations can lead to reduced blood flow to the skin tissue which can eventually result in erosion, tissue ischemia, and infarction. When blood carrying oxygen and nutrients are not being utilized by skin tissue it can break open. Unrelieved pressure of certain areas of the body due to lack of movement Extrinsic Factors: This image represents a person’s heal resting on a hard surface. The arrow that is labeled with friction is showing how this force is opposite of the direction of the shearing force, taking place between the skin of the heel and the bone. Shearing forces are exerted parallel to the skin and is generated by forces (friction) acting against it and moving in the opposite direction. Moisture also alters the resistance of the epidermis to extend forces by softening the skin’s surface and reducing the tensile strength. Urine, feces, perspiration and/or wound drainage may soften the skin, making it more susceptible to pressure, shear and friction. Friction is resistance to movement between the patient’s skin and the external support surface. This force acts in a direction that is opposite to patient movement. Abrasions of the epidermis and dermis occur as a result of friction between the skin and the bed surface. Tissues, which are attached to the bone, are compressed, obstructed and torn in both shear and friction situations. Shearing and friction occur when the: patient slides in bed/chair patient’s bed-head is elevated beyond 30 degrees (the most common cause of shear injury) patient is pulled across bed/chair as a result of incorrect manual handling, causing friction between the skin and bed/chair’s surface patient is restless or has limb spasms, leading to friction between the skin and the bed surface. This image displays how pressure is transferred from the external surface, through the layers of the skin, toward the underlying bone, as a person sits. Skin, blood vessels, subcutaneous fat and muscle are compressed between the bone (which acts as a counter pressure) and the external surface. This results in a cone, or pyramid shaped, pressure gradient. The apex of the cone equates to the bony surface where tissue interface pressures are highest. This leads to the intensity of pressure being up to five times greater on deep tissues (muscles/bony surfaces) than that on the epidermis. Muscle tissue is more sensitive and less resistant to the pressure then the skin and as a result, deep tissue necrosis often occurs first at the bony interface as a result of this pressure. Pressure exerted at the bony interface then emerges at a point in the surface of the skin. A small, inflamed area, over a bony prominence, may indicate tissue breakdown that is much deeper and wider than indicated at the surface of the skin. Intrinsic Factors: These factors contribute to the risk a person has for developing pressure ulcers because they influence the skin’s supporting structure, and/or lymphatic system. They are individual patient characteristics that affect the ability of skin and soft tissue to withstand unrelieved pressure, friction and shear forces. Therefore, identification of intrinsic risk factors is important when assessing PU risk. They include nutritional status, demographics, pain level, oxygen delivery system, chronic illness, pain levels, and medications. Nutritional status: Poor nutrition has a significant role in PU development. Deficiencies can result from either decreased intake or malabsorption. Research indicates that the following factors increase the risk of developing a PU: malnutrition low levels of protein/albumin recent weight loss or morbid obesity specific deficiencies such as Vitamin C, iron, and zinc. Demographics: Individual characteristics that appear to be associated with increased risk include: > 65 years of age: this automatically puts the pt at risk for depletion of lean body mass since this naturally occurs with age. Older age also results in natural changes to the skin and body. The skin of older adults is generally more fragile, thinner, less elastic, and drier then the skin of young adults. Also new skin cells are usually generated more slowly. All of these conditions make their skin more vulnerable to damage Male Immobility Caucasian Multiple co-morbidities that may result in poor blood flow, immobility, loss of senses. Previous history of PU injury, including reperfusion injury and those extending beyond the level of the dermis. Once injured, the tensile strength of the skin and underlying soft tissues are not restored to their original state and strength. Oxygen delivery system: Decreased supply of oxygen to the area under stress leads to increased risk. Risk conditions include: respiratory disorders cardiovascular impairment smoking autonomic dysfunction (as seen in spinal cord injury) fever or other conditions that lead to increased skin or core body temperature (every degree centigrade rise in temperature leads to a 10% increased demand for oxygen) Pain level: Pain can decrease the amount of physical activity and movement of a person. Chronic Illness: Certain conditions such as diabetes, renal impairment, and metastatic cancer increase risk for developing pressure ulcers. Medications: Drugs that increase the risk of developing pressure ulcers include those that decrease sensation, cause drowsiness which may result in less movement, decrease inflammatory response, and decrease peripheral blood pressure. Dehydration: Can occur when one is not being properly hydrated or is experiencing an increase in fluid loss. When the body is deprived of water, fluid volume decreases and the body works to retain water, which is why a decrease in urination and elevated BUN levels are a marker of dehydration. Urinary Tract Infection: Most are caused my bacterial infections and may occur due to poor hygiene. Normally the bladder is coated with a variety of cationic antimicrobial peptides such as defensins and cathelicidin, which disrupt the integrity of bacterial cell walls. This helps to keep the urinary tract sterile along with mannosylated proteins that interfere with the binding of bacterium to the uroepithelium. When things such as urinary catheter or trauma disturb the protective lining, bacteria can invade the exposed epithelium by binding to it. As bacteria builds up they can form structures that become more difficult for the immune system to battle and antibiotics to treat. Constipation: The patient possesses several factors that may be contributing to his constipation, such as dehydration, lack of mobility and physical activity, and certain medications. During this state there is an increase in colonic luminal pressure. During constipation, stool consistency lacks sufficient water to make it easier to move through the colon. Multiple Contractures of the left extremities: This condition can happen when there is prolonged tightness and immobility of a joint or muscle which leads to the deformity and shortening of it. The joint will lock which is an irreversible situation that only surgery can fix. Sepsis: Inflammatory Cascade: Sepsis can occur from infection at body sites such as the lungs, abdomen, soft tissue, urinary tract or as a result of primary blood stream infection such as meningococcemia. Sepsis can be caused by the signaling of mediators such as the out membrane component of either gram negative or gram positive organisms or fungal, viral, or parasitic components. A family of transmembrane receptors are how these mediators produce their signals. The production of proinflammatory cytokines such as tumor necrosis factor and interkeukin 1 occur due to the activation of nuclear factor-KB in the monocyte. This leads to the production of toxic downstream mediators, including prostaglandins, leukotrienes, platelet-activating factor, and phospholipase A2. Damage to the endothelial lining, leading to increased capillary leakage is caused by these mediators. These cytokines also lead to the production of adhesion molecules on endothelial cells and neutrophils. Neutrophilic endothelial interaction leads to further endothelial injury through the release of the neutrophil components. Activated neutrophils release nitric oxide, a potent vasodilator that then leads to septic shock. Link between inflammation and coagulation: IL-1 and TNF-α also have direct effects on the endothelial surface. As a result of these inflammatory cytokines, tissue factor, the first step in the extrinsic pathway of coagulation, is expressed on the surfaces of the endothelium and of monocytes. Tissue factor leads to the production of thrombin, which is a proinflammatory substance and results in fibrin clots in the microvasculature. Fibrinolysis is also impaired during the septic process due IL-1 and TNF-α causing the production of plasminogen activator inhibitor-1. This is a potent inhibitor of fibrinolysis which therefore reduces the break down of clots. Proinflammatory cytokines, such as antithrombin and activated protein C (ACP), also disrupts the body's naturally occurring modulators of coagulation and inflammation. Protein C circulates as an inactive zymogen but, in the presence of thrombin and the endothelial surfacebound protein thrombomodulin, is converted to the enzyme-activated protein C. Studies have shown that proinflammatory cytokines can shear thrombomodulin from the endothelial surface as well as lead to downregulation of this molecule, thus preventing the activation of protein C. APC and its cofactor protein S turn off thrombin production by cleaving factors Va and VIIIa. APC also restores fibrinolytic potential by inhibiting plasminogen activator inhibitor-1. In vitro studies have revealed that APC has direct anti-inflammatory properties, including inhibiting the production of proinflammatory cytokines by LPS-stimulated monocytes, inhibiting leukocyte adhesion and rolling, and inhibiting neutrophil accumulation. Antithrombin is the second naturally occurring endothelial regulator affected during sepsis. Antithrombin inhibits thrombin production at multiple steps in the coagulation cascade as well as by binding and inhibiting thrombin directly. Antithrombin, when bound to endothelial cell surface glycosaminoglycans (GAGs), leads to the production of the anti-inflammatory molecule prostacyclin (prostaglandin I2 [PGI2]). Evidence exists that neutrophil elastase cleaves GAGs off the surface of the endothelial lining, thus limiting the anti-inflammatory properties of antithrombin Immunoparalysis: CD4 lymphocytes play a key role in the inflammatory response seen in sepsis. Early in the sepsis process, these cells produce large amounts of the proinflammatory mediators, including interferon gamma, TNF-α, and IL-2. CD4 lymphocytes may evolve over time, whereby the CD4 lymphocytes produce anti-inflammatory cytokines, including IL-10, IL4, and IL-13. This is often driven by the release of stress hormones, such as catecholamines and corticosteroids. These cytokines dampen the immune response and can lead to the deactivation of monocytes. Additionally, TNF released early can cause apoptosis of lymphocytes in the gut, leading to further immunosuppression. On-going inflammation and coagulation cardiovascular insufficiency and multiple organ failure can occur and lead to death. PAST Medical Conditions/Diagnoses List ALL past medical conditions and describe the pathophysiology of each. Add additional rows as needed. Be sure to reference your findings. Diagrams may also be helpful in explaining the pathophysiology of some diseases/conditions. Hypertension: Lifestyle factors such as poor diet, limited physical activity, and smoking can lead to this condition and result in disruption of healthy physiological mechanisms that control blood pressure. Inflammation can occur from consuming a diet that is high in sodium, fat, processed foods, and is nutrient poor due to an increase in blood acidity and free radicals. If this is prolonged, endothelial dysfunction can occur and damage to the vascular walls, causing peripheral resistance. The endothelial cells lose their ability to pump blood further and more effectively throughout the vascular system. High blood pressure results from this and in combination with the high levels of sodium and increased water retention due to high sodium content. Normally high blood pressure signals the parasympathetic system to inhibit the systems responsible for increasing blood pressure. The parasympathetic system works to decrease blood pressure, stimulate vasodilation, and excrete sodium. Nitric oxide and natriuretic peptide are involved in doing this. Because endothelial damage results in the decreased production and effect of nitric oxide, vasodilatation of the arteries declines along with sodium excretion, and high blood pressure is prolonged within the body. The continuation of high sodium levels within the body cause high blood pressure because of the signal to continue to reabsorb water in order to dilute the blood, which increases blood volume. Increased blood volume = increased blood pressure. Two of the major systems, when activated, that cause an increase in blood pressure are the rennin-angiotensin-aldosterone system and the sympathetic systems because they work to retain sodium and water. When these systems become hyperactive, hypertension can result. This diagram displays how the rennin-angiotensin-aldosterone system functions. It is normally activated when blood pressure falls. If hyperactive, the kidney will over produce the hormone rennin which will participate in its normal function of converting angiotensinogen to angiotensin 1. Angiotenson-converting enzyme then converts angiotensin 1 to angiotensin 2. Angiotensin 2 is a hormone with powerful effects on blood pressure. It stimulates the adrenal gland to secrete aldosterone, which is another hormone that stimulates the kidneys to reabsorb sodium and water, causing an increase in blood volume. Angiotensin 2 also stimulates vasoconstriction at the same time blood volume is increased, which further increases blood pressure. Normally the kidneys regulate blood pressure by controlling the extracellular fluid (ECF) volume. The major cation in the ECF is sodium. The Kidneys control how much is excreted from the body, which in a healthy individual, is enough to maintain homeostasis and fluid volume. This results in normal blood pressure levels. When a diet high in sodium is consumed, this may disrupt the balance of sodium within the ECF because the level of intake becomes much greater than the output and excretion by the kidneys. When this occurs over a prolonged period of time, vasoconstriction, which decreases the space between the walls of arteries, continue to increase the amount of sodium retained. The systolic pressure will also increase with high sodium intake because the heart is going to pump harder in order to pump the sodium rich blood fast through the body and into the kidneys for excretion. The heart muscle can become over-worked and artery walls can lose elasticity from this process which makes it harder for vasodilatation to occur and increases resistance to blood flow. The lack of accommodation to the high systolic pressure can cause damage arteries Vasoconstriction can also be enhanced by lack of exercise because of the decreased stimulation of vasodilatation. Exercise promotes vasodilatation because the rate that oxygen is transported to tissues is increased because of the need for more oxygen during exercise. In order for blood to deliver oxygen and nutrients to tissue of the body to utilize and produce energy during this active state, the vasoconstriction of arteries is stimulate in order for blood to move through them efficiently. High blood pressure also results from an increase and prolonged sympathetic activity. This system works by secreting norepinephrin which is a vasoconstrictor of arteries, increasing peripheral resistance and high blood pressure. Leukocytosis: White blood cell maturation and release into the circulation are influenced by colony-stimulating factors, interleukins, tumor necrosis factor, and complement components. Within the bone marrow there are white blood cells that are undergoing maturation and those who are mature and in storage. Their release is stimulated by infection or inflammation and the number that circulates can increase by 2-3fold within a couple of hours. This increase is indicative of how the bone marrow responds to infection or inflammation. The white blood cells released called leukocytes are divided into two classes: one pool of cells circulates freely and the second pool is deposited along the margins of blood vessel walls. Cytokines, growth factors, and adhesion molecules control the amount of white blood cells released into the free circulation from the bone marrow, the rate of consumption of cells into the tissues, and the rate of marginating cells out of blood vessels into the tissues. Severe leukocytosis is common in those who have had stroke due to occlusion and ischemia. Cerebral Vascular Accident (CVA): Endothelial cells line the innermost layer of the blood vessel and releases nitric oxide. Nitric oxide is produced by healthy endothelial cells and it works to relax and dilate blood vessels. It also helps to prevent monocytes from sticking under the endothelial wall within the artery. The is important when one has atherosclerosis because diet change that results in lowering blood pressure and stimulating the release of nitric oxide can decrease their build up within the blood vessel walls and therefore, stabilize it. The blood vessel is also made up of the media which is the middle layer, containing smooth muscle cells. It also contains collagen which provides structure to the blood vessel, elastin which provides elasticity, and the smooth muscle which relaxes when nitric oxide is present. A stroke can result from having prolonged hypertension throughout life along with a high fat diet, which can result in blood clot formation that blocks blood flow in an artery that feeds the brain, preventing oxygen and nutrient transportation to the brain. This occurs due to damage of the endothelial cells and artery walls. The damage can lead to atherosclerosis which further causes decrease in elasticity, constriction of blood flow, and thrombus formation. During an ischemic stroke, which happens in about 80% of stroke victims, a thrombus (blood clot) or embolus occludes a cerebral artery, causing hypoxia and neuronal injury. An irreversible neuronal injury occurs when cerebral blood flow (CBF) is very low for longer than 30-60 minutes. Normal CBF is 50-55 ml/100gm/min. If the CBF drops below 18, electrical activity pauses. If the CBF dips below 10, neuronal metabolism stops. The chart above displays the pathway of injury due to lack of fuel to the brain. Due to a lack of fuel and oxygen being transported to the brain cells, excitotoxicity occurs. This results from an over-reaction of the neurotransmitters; primarily glutamate and aspartate. An energy dependant process clears glutamate and aspartate from the synaptic terminals which increases the concentration of both in the extracellular spaces due to membrane pump failure. This occurs in an energy depleted state which causes the receptors, N-methy1-D-asapartate (NMDA) and alpha-amino-3-hydroxy-5-methyl-4-isoxanole propionate to stimulate the opening of calcium channels. This then leads to calcium building up/ influx in the intracellular space. Intracellular calcium is responsible for activating the destructive enzymes (proteases, lipases, and endonucleases) which allow the release of the cytokines and inflammatory mediators. T he most prominent cytokine include interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and IL-6. Shortly after the ischemic attack, leukocytes are recruited to the ischemic areas. The leukocytes end up contributing to the damage as well as aid in improving it. Their beneficial effects include activating vasoactive substances such as nitric acid, oxygen free radicals, and arachidonic acid metabolites (cytokines). These same cellular mediators also cause vasoconstriction, increased permeability, increased platelet aggregation, increased leukocyte adherence to the endothelial wall, and immunoregulation. Endothelial cells react to hypoxia by swelling which causes mechanical plugging by erythrocytes, leukocytes, and platelets in the ischemic area. This interrupts the vasoactive effects of nitric acid and endothelial peptides and leukocyte adherence to the endothelial wall is promoted. The degree and duration of decreased CBF determines the severity of the ischemic injury. Before neuronal death there is a window of opportunity for a reverse in blood flow abnormalities within the brain, called ischemic penumbra. This situation is characterized as having a CBF between 10 and 18. Perfusion/blood flow must be reestablished before 3-6 hours of ischemia or before the CBF drops to 10. After 3-6 hours of ischemia, irreversible damage occurs to the capillary endothelium. The blood-brain barrier becomes dysfunctional and serum proteins and water leak into the interstitial space. This damages the plasma membrane and coagulation necrosis occurs. Hypoxia: Due to an embolism or thrombus, hypoxia can occur. This results from the occlusion of a blood vessel resulting in the blockage of blood flow and oxygen. Hypoxia can from as a result of atherosclerosis. In blood vessels that are experiencing atherosclerosis, blood clots can result in an embolism which is when the blood clot breaks off and travels through the cardiovascular system and ends up blocking a smaller vessel because it is too big to move through it. When there are high levels of LDL present in the circulatory system it can get oxidized which creates injury by burrowing into the artery wall. High blood pressure contributes to this injury because of the damage it can cause to endothelial cells within the vessel wall. In response to the injury, the immune system recruits white blood cells and platelets which turn into marcophages in the artery wall. The macrophages are responsible for getting rid of the LDL-cholesterol but they can build up in the artery. When they become stuffed with LDLcholesterol they form a fatty streak which visibly starts the atherosclerosis process. If this remains ongoing throughout the years, more cholesterol, connective and elastic tissue, calcium, and cell debris accumulate and turn the fatty streak into plaque. As the artery tries to heal itself, smooth muscle cells migrate in to cover the plaque, forming a fibrous cap around it. Macrophages kill the smooth muscle cells within the media, within the blood vessel, and release enzymes that break down the fibrous cap. The cap ruptures which causes more inflammation, causing a blood clot because the body thinks it is an emergency. The blood clot can lead to hypoxia if it occludes an artery. Medical Conditions/Diagnoses INTER-RELATIONSHIPS Describe the inter relationship of the patient/clients disease states. The use of a diagram is encouraged, but the diagram must be accompanied by a narrative explanation. Be sure to reference your findings.. HTN: the pt’s history of HTN may have contributed to his weakened blood vessels. The damage caused by this led to the compromised ability for blood to carry oxygen and nutrients to tissues in his body. Tissues deprived of nutrients and oxygen is a cause of pressure ulcers and also contributed to his past CVA. Hypoxia: when tissue is deprived of oxygen. Direct cause of a pressure ulcer formation because of the occlusion of a blood vessel. This situation is what may have been cause by prolonged hypertension and/or other lifestyle factors. For example, eating a high-fat diet and getting little physical activity throughout life, may have caused constriction of his blood vessels and possible plaque formation, leading to blood clot formation. The chart above is a general representation of what the pt’s past CVA led to. CVA with Hemiplegia: led to paralysis of the left side of the pt’s body because of brain cell necrosis and loss of nerve function. The CVA caused injury to the right side of the brain since he is experiencing paralysis on the left. This caused the patient to be confined to his bed and unable to change positions. Decreased mental awareness also decreased his ability to take care of himself and prevent pressure ulcers. This condition contributed to the development of multiple contractures and inability for anyone to move joints of the lower extremities. A combination of immobility, loss of lean body mass comprising muscle and skin – as well as challenges to the immune system increase the risk of pressure ulcers by 74%. (8) This patient has experienced all of these factors due to being 75 y/o, being immobile, and having inflammation and infection. The UTI may have resulted from the patient being incontinent after his CVA, which caused him to lose all sensation on one side of his body. If the pt is incontinent, it is known that problems with bladder control can greatly increase the risk of pressure sores because the skin may be frequently moist, making it more susceptible to pressure, friction, and break down, especially while the pt is already immobile. Sepsis: Sepsis could have occurred by bacteria entering the blood stream through the broken skin from his pressure ulcers or may have been the result of his urinary tract infection, where the build of bacteria entered his blood stream. Sepsis further increases the pt’s nutritional and energy demands because it is a severe infection, causing inflammation and may interfere with ability for wounds to heal and organs to function normally, if protein stores are depleted due to cytokine release and increased demands. This could lead to the formation of more wounds and complications if aggressive nutritional therapy is not administered, along with other medically appropriate actions. Dehydration: This may be contributing to a disruption in the wound healing process, maintaining healthy skin, and preventing tissue break down, since adequate hydration is needed for this and for bodily reactions to occur. This could also be contributing to the constipation the patient is suffering from. If his wounds have been releasing fluid, this would increase his fluid needs depending on the amount of drainage. In this patient dehydration was possibly caused by his current state of sepsis, not being properly hydrated, or experiencing an increase in fluid loss, possibly from his wound. The patient’s tube feeding alone did not provide him with enough water to meet his needs, so if water flushes were not performed at his nursing home as ordered, this could have resulted in the patient becoming dehydrated. Assessment of Nutrition Needs Calories: 1900-2100 kcals Show your work: (30-35 kcals/kg) 30 X 76.3 = 2290 kcals 35 X 76.3 = 2670 kcals (nutrition care manual) Rationale for calorie level: The patient is not malnourished and has a BMI that classifies him as being overweight. He is also 75 years old and because of this he is experiencing a decline in lean body mass. I would not want restrict or determine his calorie needs based on his BMI because his body is in a state of stress and inflammation due to skin breakdown and pressure ulcers. This would cause an increase in his metabolic rate. I chose 30 because this level will prevent over feeding the patient, will help to maintain his weight, and meet his metabolic needs. Along with other nutrients given to him, the kcals provided should help to provide enough energy to the patient in order for him to utilize additional nutrients given to him for wound healing. It is also important to maintain his weight because the loss of weight in the form of fat and muscle results in less cushioning between bones and a bed. Protein: 115-150 grams Show your work: 1.5-2 grams/kg) 1.5 X 76.3 = 115 grams 2 X 76.3 = 152 grams Rationale for calorie level: He is naturally experiencing a decline in lean body mass due to older age. He also is experiencing skin breakdown from pressure ulcers, causing inflammation and stress. This condition increases his need for protein to promote the fibroblastic response, collagen synthesis, and the wound remodeling processes. I also figured his protein needs based on him having sepsis which would further increase his metabolic needs. Other pertinent macronutrient levels: Show your work: Rationale for calorie level: Other pertinent micronutrient levels: Show your work: Vitamin C: 500-1000 mg/day Arginine: 14 g/day Glutamine: 14 g/day Rationale for calorie level: Preservation of skin tissue, strengthening of tissue resistance, and promoting tissue repair. Research has shown the benefits of maintaining adequate levels of these nutrients in those with pressure ulcers or who are at risk. Arganine: Appears to favorably influence pressure ulcer healing by affecting microvascular and perfusion changes, enhancing collagen production via proline synthesis. (8) One study showed that giving an oral nutrition supplement with this nutrient at 9 g per day and 21 grams of protein total significantly improved the rate of pressure ulcer healing. The 14 grams per day of arginine and the 14 grams of glutamine almost just about equal the 28 grams of total protein given by the oral nutritional supplement in the study. (21 grams pro + 9 grams Arginine = 30 grams total Pro) Glutamine: This amino acid serves as an energy source and for proliferation by inflammatory cells within the wound. It has been shown to maintain mucosal integrity and reduce infection rates. In recent research, it has been included in nutrient mixtures, also containing HMB and arginine. (14 gm glutamine, 14 gm arginine, 2 gm HMB) This mixture showed to be effective in promoting wound healing. Vitamin C: One study showed that giving an oral nutrition supplement made up of a combination of 500 mg Vitamin C, arginine, and zinc, significantly improved the rate of pressure ulcer healing 2.5 fold in PU pts. Because the pt may be experiencing fluid loss from wound drainage, he may also be losing vitamin C since it is water soluble. To be safe I would want to provide 500 -100 mg/day to compensate for any losses. Since the UL is 2g this would be considered safe. Fluid Show your work: 35 mL/kg 35 X 76.3 = 2670.5 mL Rationale for calorie level: The patient does not show any symptoms of kidney problems because electrolytes are all within normal limits, along with creatinine. BUN and BUN/creatinine ratio are likely elevated due to the dehydration the patients is experiencing. Due to the state of stress this patient is experiencing and inflammation due to pressure ulcers I recommend 35 mL/kg of body weight. He may have increased needs because of fluid loss from his wounds, older age, and an increase in protein being given. Which of the following domains is the patient/client presenting with : DOMAIN INTAKE Energy Balance Oral or Nutrition Support Intake Fluid Intake Check () if patient presents with this characteristic Y If checked, explain evidence to support this decision Patient was admitted to the hospital with dehydration and constipation. His BUN and BUN/creatinine ratio also indicate dehydration. Bioactive Substance Intake Nutrient Intake Y Three pressure ulcers on the patient’s body. Lack of nutrients may be contributing to their formation and lack of healing. CLINICAL Functional Y Biochemical Y Paralysis of the left side of the body caused by past CVA, affecting the right side of the brain. Elevated CRP, BUN, BUN/creatinine ratio, and ESR levels. Weight BEHAVIORAL-ENVIRONMENTAL Knowledge and Beliefs Physical Activity & Y Function The patient is immobile and bedridden because of multiple contractures and paralysis of his left side. Food Safety and Access What is the Nutrition Diagnosis for this client/patient? Diagnosis or Etiology Problem Increased Related to Wounds nutrient needs (Protein, Vitamin A, Zinc) Inadequate Related to dehydration fluid intake Related to Related to Signs and/or Symptoms Stage 1, 2, and 4 pressure ulcers. High BUN and BUN/Creatinine ratio and constipation. NCP Step 3: Nutrition Intervention: Nutrition Prescription (Diet Order) Indicate the diet changes and progression since patient’s admission to present Date Diet Prescription/Order 4/09/2011 Enteral Tube Feeding: Jevity 1.2 @ 80ml/hr X 18hrs with 300 ml H20 q 6. 4/13/2011 Enteral Tube Feeding: Jevity 1.2 @ 80ml/hr X 18hrs with 300 ml H20 q 6. 4/20/2011 Juven BID Enteral Tube Feeding: Jevity 1.2 @ 80ml/hr X 18hrs with 300 ml H20 q 6. Juven BID Discussion of Diet Order(s) Consider: Rationale & indications for current diet order Do you agree with the order? Discuss why or why not. Would any other dietary modifications be realistic and appropriate? Discuss why or why not. In the nursing home this patient was receiving enteral nutrition support. Nutrition support in the form of enteral nutrition was chosen as an intervention previously because of lack of neurological and swallowing function, and inability to feed himself, due to his past CVA. He was receiving Jevity 1.2 @ 80mL/hr X 8hrs with 300ml h20 flushes q 6hrs. This tube feeding was providing the patient with a daily intake of 1728 kcals, 80 grams of protein, and 2366 mL of water. Along with his first assessment, the RD recommended that the Dr. order Juven BID for this patient in order to promote wound healing along with keeping his current tube feeding that was provided at his nursing home. I do not agree with his current diet order of Jevity 1.2 @ 80mL/hr X 18 hours because after calculating his calorie and protein needs, this rate does not them. Malnutrition has been found to delay pressure ulcer healing and increase the risk of developing chronic pressure ulcers. Because this patient was not receiving enough enteral formula to meet his needs, this could have contributed to the advancement in the formation of his pressure ulcers. I also calculated how much protein and calories he was getting from the Juven BID which still did not add enough extra calories and protein to meet his daily needs. With the calories from the Juven and the tube feeding (TF), he was receiving 1868 kcals and 95 grams of protein per day. Since he is tolerating the 80mL/hr, I would recommend advancing it to 100mL/hr X 18 hours because this plus the Juven BID would supply him with 2300 kcals and 111 grams of protein, which would be sufficient. At 100mL/hr X 18hrs he would be receiving a total of 1800 mL/day of Jevity 1.2. Because he is dehydrated, fluid losses from his wounds are unkown, and he is getting an increase in protein, I would leave his water flushes at 300 mL q 6 hours which would provide him with a total of 2658 mL/day. His renal function also appears to be good as evidenced by his electrolyte levels which are within normal limits and does not have chronic heart failure which further implies the safety of increasing the fluid given for this specific pt.. I agree with the order of Juven because of the nutrient mixture it provides as well as additional calories for protein which help to meet the energy needs of the patient. The specific nutrients within it have been shown to improve and promote wound healing when given in combination. They include: calcium beta-hydroxy-betamethylbutyrate, arginine, glutamine. (ADA Nutrition Care Manual) Nutrition Intervention Plan Consider the Types of Interventions for this patient/client... Food and/or Nutrient Delivery Nutrition Education Nutrition Counseling Referral to other disciplines will in current setting Referral to other disciplines/services post D/C. Identify each of the short and long term specific nutrition and wellness education needs. Be very specific and very comprehensive. Based on perceived level of current motivation, determine the specific educational goals. Of these goals, which is the most important goal, and why? Also, discuss how you determined the patient’s motivational level, and identify any obstacles which may interfere with diet compliance (i.e. finances, disability, lack of family support, etc.) Nutrition Intervention(s) Intervention #1 1. Provide Juven BID and increase Goal(s) pt’s tube feeding by 10 ml in To see an improvement in and to heal order to meet his needs. the pt’s stage 4, 2, and 1 pressure ulcers. 2. Speaking to the pt’s nursing This is important in order to decrease home about additional nutrition the inflammation cause by these which therapy and educating them on in turn may produce further medical its importance and the goal of and organ problems. promoting pressure ulcer healing and avoiding further skin damage. Problem Intervention #2 Increased nutrient and fluid needs for Goal(s) wound healing. Informing the patient’s nursing home of the patient’s recent order for Juven BID and explaining the importance of this in order to encourage their compliance since the patient is fully dependent on nursing home care. Etiology Related to pressure ulcers. Signs/Symptoms Elevated CRP (9.6), BUN (34) and stage 4, 2, 1 pressure ulcers. Nutrition Prescription Current order: Jevity 1.2 @ 80 ml/hr/18hrs w/ 300mL H20 flushes q 6hrs Your Recommendation: Other wound healing and preventative techniques should also be discussed, such as an individual rotation schedule and change in position of the patient. Intervention #3 Goal(s) Jevity 1.2 @ 100 ml/hr/18hrs w/ 300mL H20 flushes q 6hrs Which goal is the priority at this time? 1. Getting the pt properly hydrated and correcting his dehydration. 2. Maintaining the patient’s weight and nutritional status because he is in a very stressful state and would decline further if his body was not receiving adequate nutrition, energy, and fluid to help with the healing process and his immune system. If instruction was given, who did you instruct? What instructional materials did you use? Where they effective? Why or why not? If patient has been education, what is their motivation/compliance level at this time? Does the patient have any barriers to compliance to the interventions? n n/a n/a n/a – education was inappropriate for this patient. NCP Step 4: Monitoring and Evaluation Health Care Outcomes Based on your Nutrition Intervention indicate below what outcome measurements you will use to monitor progress and success of the interventions. Intervention Juven BID Health & Disease Outcomes Increasing the rate of healing pressure ulcers. Increase to Prevention of Jevity 1.2 @ additional 100mL/hr/18hrs chronic Cost Outcomes Patient Outcomes Less money spent Increased skin on wound and integrity and rate medical care. of wound healing. Prevention of complication associated with non-healing wound. Less hospital Nutritional status trips and medical and weight costs on trying to maintained. illness/meeting nutritional needs and increasing hydration. Monitoring and Evaluation Question to Consider What indices are you using to determine success of your intervention? Did the intervention work? Explain If the intervention is not working, indicate what follow up action you took. What are the causes of initial interventions that did not work? How will you monitor success of your follow up interventions? treat further complications developed from not receiving adequate nutrition. Prevention of quicker decrease of LBM. Adequate hydration to promote wound healing. Answer/Reflection Wound healing status and normalization of his lab values (CRP and BUN especially) The patient was discharged so his dehydration and UTI may have been resolved and/or managed via medications and medical nutrition therapy. N/A – patient was discharged. N/A- there was no proof of recent intervention not working. I would contact the patient’s nursing home to follow up with how he is doing and the status on his pressure ulcers. If they continue to not heal it may indicate the need for the pt to undergo testing for cancer. At this point the patient is not a candidate for surgery because of his current medical state, so managing his wounds and making sure his nursing home is complying with order is crucial in order to promote healing and prevent further complications that may develop as a result of non-healing wounds. DOCUMENTATION Attach all initial and follow up notes for this patient/client to this report. Be sure to delete any data that may identify the patient such as name or room number. References • • • • • • • • • • • • Dorner B, Posthauer ME, Thomas D.(2009)The Role of Nutrition in Pressure Ulcer Prevention and Treatment: National Pressure Ulcer Advisory Panel White Paper. Nutrition White Paper. 1-15. Doley J. (2010) Nutrition Management of Pressure Ulcers. Nutrition in Clinical Practice, (25), 50-60. Desneves KJ, Todorovic BE, Cassar A, Crowe TC. (2005) Treatment with supplementary arginine, vitamin C, and zinc in patients with pressure ulcers: A randomized controlled trial. Clinical Nutrition, (24), 979-987. University of Washington. Taking Care of Pressure Sores. http://www.sci.washington.edu/info/pamphlets/pressure_sores.asp. Mahan KL, Escott-Stump K. (2008) Krause’s Food & Nutrition Therapy: 12th Edition. Saunders Elsevier. St. Louis, MO. 287-295. Victorian Government Health Information. (2008) Pressure Ulcer Basics. http://www.health.vic.gov.au/pressureulcers/pu_basics/module1/topic2/page9.htm American Dietetic Association. ADA Evidence Analysis Library. American Association for Clinical Chemistry. (2001-2011) ESR. Lab Tests Online. http://www.labtestsonline.org Version.pdfhttp://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/infectiousdisease/sepsis/#s0020 American Dietetic Association. Pressure Ulcers. Nutrition Care Manual. Lizaka S, Sanada H, Nakagami G, Sekine R, Koyanagi H, Konya C, Sugama J. (2010) Estimation of protein loss from wound fluid in older patients with severe pressure ulcers. J. Nutrition, (26), 890-895.\ Shah S. Foundation for Education and Research in Neurological Emergencies. http://www.uic.edu/com/ferne/pdf/pathophys0501.pdf.