Table of Contents

Introduction..1 Objectives..2 Patient`s Profile..3 Health History4 Family Health History4 Past Health History.4 Present Health History5 Health Assessment..6 NAAF (Nurses Admission Assessment Form)...6 Review of Systems11 Laboratory Results13 Patophysiology..15 NCP (Nursing Care Plan) And FDAR (Focus, Data, Action, Response).20 Discharge Plan.. Conclusion..33 References...34

Introduction

Mrs. VA a 66 year old Filipino male. She was the only child. She doesnt know her biological Spanish father. Married and has 2 children. She has a sweet tooth; she likes to eat sweet foods like cakes and other sweetened foods before. She`s fond of baking cakes and pastries Before, Mrs. VA smokes 1-2 packs per year for 30 years and stopped it 18 years ago when she was diagnosed of having Type 2 Diabetes Mellitus. Mrs. VA was diagnosed of Type 2 Diabetes Mellitus for 18 years and Chronic Kidney Disease secondary to Diabetes Nephropathy for 2 years. She has also a controlled secondary hypertension for 2 years. In the developed and industrialized world, diabetes is the leading cause of chronic kidney disease and kidney failure and the numbers of cases are increasing rapidly (Centers for Disease Control [CDC], 2005). Of the new end stage renal disease (ESRD) cases annually in the United States, about 44% are due to diabetes (United States Renal Data System [USRDS], 2007). With type 2 diabetes mellitus prevalence skyrocketing to over 21 million cases in the United States alone (CDC, 2005), catastrophic end organ diseases such as kidney failure will follow. Diabetic nephropathy, or kidney damage due to diabetes, results from changes in blood flow in the small vessels of the glomerular capsule, the functional unit of the kidney (Eknoyan et al., 2003). Each of the approximately 2 million glomerular capsules is composed of thin-walled capillaries that facilitate hydrostatic filtration of toxins and fluid and maintain a delicate balance of vasoconstriction and dilation (Hall, 2006). The pathogenic changes of diabetic nephropathy involve several different complex chains of reactions that culminate in damaging, oxidative remodeling of the vessel walls of the glomerular capsule. The subsequent decreased flow of oxygenated blood, loss of vasodilatory tone, and impairment of vascular wall integrity lead to irreversible damage to glomerular capillaries and, ultimately, to loss of kidney function.

This case study will provide clear understanding of medications, diet, laboratory values, and basic anatomy and physiology that will equip us to deal with the disease effectively. Because kidney failure is quite possibly the most patient-education intensive field for nursing today. With the scope of this disease involving every aspect of the patient's life, constant support and education are essential. Basic education on diabetes should be done for all patients and reinforced at every possible opportunity.

Objectives
For the Nurses: Enhances the assessment skills by practicing head to toe assessment and review of systems. Established knowledge for the nurse regarding Chronic Kidney Disease secondary to DM Nephropathy, the disease process, its management and treatment. Use the nursing process as a framework in utilizing care of the patient with diabetes mellitus and Chronic Kidney Disease. For the Patient: Awareness of the disease and educate them regarding the disease and common management of it. Ensure and provide quality healthcare to them through the knowledge and skills that the healthcare provider possess. Embrace rapport building with the nurse to guarantee harmonious relationship in achieving the desired health goal through the cooperation of the patient in implementing the nursing care plan. For the IANAHP: Evaluate the knowledge and skills of the trainee in assessment and disease process of the case presented (Chronic Kidney Disease Stage V secondary to DM Nephropathy) and how nursing care plan put into action.

Patient`s Profile

Name: Address: Age: Gender: Occupation: Civil Status: Chief Complaint:

Mrs. VA Bugao Bagamnoc Catanduanes 66 years old Female Retired Govt employee Married swelling of left lower leg and infected non-healing wound on 1st and 2nd digit of left foot Chronic Kidney Disease Stage 5 secondary to DM Nephropathy Chronic Kidney Disease Stage 5 secondary to DM Nephropathy March 7, 2011 March 15, 2011 Dr.Santos None

Admitting Diagnosis:

Final Diagnosis:

Date of Admission: Discharged Date: Attending Physician: Referral:

Health History Family History

Grandmother (DM, HPN) Grandfather (HPN) Grandmother? Grandfather?

Mother (DM, HPN)

Father?

Mrs. Verdad

Past Health History

Two years ago Mrs. VA was diagnosed of having CKD stage 5 secondary to DM Nephropathy. Since 2009, she had a maintenance hemodialysis 3 times a week. Mrs. VA was a known case of Type 2 Diabetes Mellitus for 18 years. She takes Metformin and had an insulin injection at home of Novomix, 17 `u` in the morning and 12 `u` in the evening. She had a controlled secondary hypertension for 2 years and had a medication of losartan if her BP is 190/120 mmHg, but her usual BP is 110/60 mmHg. Before Mrs. VA was diagnosed of having Type 2 DM she smokes 1-2 packs per year and stopped it 18 years ago. Mrs. VA underwent Below the Knee Amputation of right foot due to non-healing wound. She was also diagnosed of having Ischemic Heart Disease and Coronary Artery Disease presented by occasional chest pain and dyspnea on exertion. Based also on the result of her 12 Lead ECG there is a diffuse ischemia, non ST segment elevation MI and laboratory test results indicates increased in troponin I. She was treated with MI regimen, Imdur 30 mg tablet and clopidogrel 75 mg tablet. Mrs. VA had also anemia and she had an erethropoitein injection 2 times a week.

Present Health History

Mrs. VA had gangrenous wound on 1st and 2nd digit of left foot with left lower leg swelling. Two weeks prior to admission she noticed that there was blister over her left foot so she consulted her attending physician and aspiration of blister was done. She was given a medication of Augmentin 625mg 2x a day however she noticed that there was progression of blister to gangrenous area over left foot and until 1 week ago there was noted foul smelling discharge on left foot and lower leg swelling. She sought consult and subsequently advised admission for further evaluation and management.

Health Assessment Review of Systems

March 7, 2011

Significant Findings

Analysis
Due to anemia

Eyes

pale palpebral conjunctiva oral thrush/ulcerations

Mouth and oropharynx

Fungal infection due to altered immune system function. (Brunner and Suddarth`s, 2006)

Extremities

>decrease peripheral pulses Symptoms of peripheral of both upper and lower neuropathy or diabetic neuropathy commonly affect extremities

>numbness of left lower foot

>swollen left lower foot

the distal portion of the nerves especially the nerve of lower extremities. Due to elevated blood glucose level over a period of years that may be attributed to either vascular or metabolic mechanism or both, the capillary basement membrane thickens and capillary closure may be present and there may be a demyelinization of the nerve which is thought to be related to hyperglycemia which causes disruption in nerve conduction and this will lead to loss of pain sensation and pressure sensation. ( Brunner and Suddarth`s, 2006)

infected wound and Because of increased blood nd gangrenous 1st and 2 digit glucose level that cause blood to become viscose there is a of left foot

Poor circulation in the lower extremities that contribute to poor wound healing and development of gangrene. (Brunner and Suddarth`s, 2006)

Respiratory

dyspnea on exertion

Caused by stimulation of the sympathetic nervous system and decreased cardiac contractility, compensatory mechanism to meet the increased myocardial oxygen demand in response to physical exertion and emotional stress. (Brunner and Suddarth`s, 2006)

Cardiovascular

Caused by insufficient coronary blood flow which results in decreased oxygen >Coronary Artery Disease supply to meet the increased myocardial demand for oxygen (on Imdur and Clopidogrel) in response to physical exertion Non ST elevation MI or emotional stress.

>occasional chest pain

Hypertension for 2 yrs Secondary hypertension caused (losartan for BP 190/120, by Diabetes Mellitus. usual BP 110/60) Type 2 DM for 18 yrs Abnormally high blood glucose (medication of Metformin level due to DM and Novomix) Usual range of CBG 160 to 180 BUN- 46 mg/dl Creatinine- 4.2 mg/dl
There is an increased amount of metabolic waste due to altered excretory function of the kidney

Endocrine

Renal

Chronic Kidney Disease In hemodialysis a dialyzer stage 5 (on hemodialysis 3x a serves as an artificial kidney replacing the renal glomeruli week)
And tubules as the filter for the impaired kidney which facilitates the excretion of metabolic waste. ( Brunner and Suddarth`s, 2006)

Hematologic

anemia (on epoetien injection 2 times a week)

Kidney is responsible in the regulation of RBC production, it release erythropoietin which

hgb count 11.1 g/dl

stimulates the bone marrow to produce RBC thereby increasing the amount of hemoglobin available to carry oxygen. Anemia is present because of the altered kidney function. (Brunner and Suddarth`s, 2006)

Nutrition/Metabolic

>on full DM and Uremic diet >with 2x a day BGM monitoring every before meals

To determine the amount of insulin to be injected to avoid hypoglycemia/ hyperglycemia.

Musculoskeletal

Surgically amputated right Poor circulation in the lower extremities that contribute to lower leg

poor wound healing and development of gangrene, below the knee amputation was done. (Brunner and Suddarth`s, 2006)

Laboratory Results Complete Blood Count

Date: March 7, 2011 Test Name Result Reference Range

WBC Count Hemoglobin Count Hematocrit PT PTT

10.48 10 3/ul 11.1 g/dl 25.4% 13.6 seconds 37.7 seconds

4.5-11 10 3/ul 13.5- 18 g/dl 40-45% 8.6-12.8 seconds 32.0-36.4 seconds

*Hemoglobin and hematocrit are below normal range: indicates anemia. *PT and PTT are above normal range: indicates that clotting factor and coagulation
are slow, patient are prone to bleeding.

Blood Chemistry
Date: March 8, 2011 Test Name Result Reference Range

BUN Creatinine

46 mg/dl 4.2 mg/dl

6-20 mg/dl 0.5-1.3 mg/dl

*BUN and Creatinine are above normal range: indicates that there is an alteration in
excretion of nitrogenous waste.

References: Patient`s Chart Medical surgical Nursing 10th Edition vol. 1 and 2 by Brunner and Suddarth`s

In this case study, primary disease of Mrs. VA is Type 2 DM. Due to her long term DM she had a complications of CAD, IHD, Diabetic Foot and DM Nephropathy that subsequently progress to Chronic Kidney Disease stage 5. Macro vascular complications result from the changes in the medium to large blood vessel wall. Because of this increase in blood glucose level, this causes blood to become viscose. Diabetes itself is seen as independent risk factor for the development of accelerated atherosclerosis. In Diabetes related atherosclerosis include platelet and clotting factor abnormalities, decreased flexibility of RBC, decreased oxygen release, changes in arterial wall related to hyperglycemia and possibly hyperinsulinemia. Blood vessel wall thicken, scleroses and become occluded by plaque that adheres to vessel wall. Eventually blood flow is blocked. Coronary artery disease, cerebrovascular disease and peripheral vascular disease are the three main types of macrovascular complications that occur more frequently in the diabetic patient. Diabetes has become the primary cause of end-stage renal disease (ESRD).Soon after the onset of diabetes and especially if the blood glucose level is elevated the kidney filtration mechanism is stressed. As a result the pressure in the blood vessel of the kidney increases. Clinically, diabetic nephropathy is characterized by a progressive increase in proteinuria and decline in GFR, hypertension, and a high risk of cardiovascular morbidity and mortality. Initially, due to an impairment of the afferent arteriolar autoregulatory ability, an increase in glomerular filtration pressure develops. This elevated intraglomerular pressure stimulates several responses within the glomerular capillary bed. Endothelial mesangial cells thicken. This, together with the continual deposition of AGEs, eventually leads to thickening of the glomerular basement membrane and loss of selective permeability. Microalbuminuria develops as well as impairment of nitric oxide transport (Eknoyan et al., 2003). The first appearance of microalbuminuria (urine albumin level greater than 50 mg/L) can precede end stage damage by as much as 20 years (Eknoyan et al., 2003). Though micro-vascular damage is irreversible, early intervention in the management of hyperglycemia has been shown to halt the progression of glomerular damage and stabilize kidney function (National Diabetes Information Clearinghouse [NDIC], n.d.). Tight glucose control normalizes the production of AGEs and stabilizes kidney AGE excretion so intimal deposition is prevented (Hall, 2006). Data confirms that for every 1% reduction in glycosylated hemoglobin there is a 37%-40%

reduction in renal failure risk (Hall, 2006). Conversely, at glycosylated hemoglobin level of 8.0% there is a 1.7 /- 2.3 ml/year decline in glomerular filtration rate (United Kingdom Prospective Diabetes Study, [UKPDS], 1998). Severe itching (pruritus) is common. Uremic frost the deposit of urea crystals on the skin is uncommon today because of early and aggressive treatment of dialysis. In the case of Mrs. LA she doesnt experience severe itching and doesnt have uremic frost because of her maintenance Hemodialysis. Thus it should not be assumed that someone with diabetes who has hypertension also has renal disease, other diagnostic criteria must also be presented. In this case of Mrs. Verdad she has hypertension and DM for 18 yrs that lead to Renal Disease from DM Nephropathy to Chronic Kidney Disease. Coronary artery disease is atherosclerosis of the coronary arteries, producing blockages in the vessels which nourish the heart itself. Atherosclerosis occurs when the arteries become clogged and narrowed, restricting blood flow. Without adequate blood flow from the coronary arteries, the heart becomes starved of oxygen and vital nutrients it needs to work properly. Your coronary arteries are blood vessels on the heart. They are smooth and elastic, allowing blood to flow freely. Then, other substances, such as inflammatory cells, proteins, and calcium that travel in your bloodstream start sticking to the inside of the vessel walls. The fat and other substances combine to form a material called plaque, which can narrow the flow of blood in the artery (atherosclerosis). Some plaque deposits are hard on the outside and soft and mushy on the inside. Some plaque is fragile, cracking or tearing, exposing the soft, fatty inside. When this happens, platelets (disc-shaped particles in the blood that aid clotting) come to the area, and blood clots accumulate on the injured vessel wall. This causes the artery to narrow even more. Sometimes, the blood clot breaks apart by itself, and blood supply is restored. Over time, the inside of the arteries develop plaques of different sizes. Eventually, a narrowed coronary artery may develop new blood vessels that go around the blockage to get blood to the heart. However, during times of increased exertion or

stress, the new arteries may not be able to supply enough oxygen-rich blood to the heart muscle. In other cases, the blood clot may totally block the blood supply to the heart muscle, causing what is called an acute coronary syndrome. This is actually a name given to three serious conditions:
y

Unstable angina: chest pain that can often be relieved with oral medications, is unstable, and may progress to a heart attack. Usually more intense medical treatment or a procedure is required to treat this acute coronary syndrome.

Non-ST segment elevation myocardial infarction (NSTEMI) or "non-Q-wave MI": This heart attack, or MI, does not cause typical changes on an electrocardiogram (ECG). However, chemical markers in the blood indicate that damage has occurred to the heart muscle.

ST segment elevation myocardial infarction (STEMI) or "Q-wave MI": This heart attack, or MI, is caused by a prolonged period of blocked blood supply. It affects a large area of the heart muscle, and causes changes on the ECG as well as chemical markers in the blood. Some people have symptoms that tell them that they may soon develop an acute coronary syndrome; others may have no symptoms until something happens, and still others have no symptoms of the acute coronary syndrome at all. When plaque and fatty matter narrow the inside of an artery to a point where it cannot supply enough oxygen-rich blood to meet your organ's needs, cramping of the muscle occurs. This is called ischemia. Ischemia of the heart can be compared to a cramp in the leg. When someone exercises for a very long time, the muscles in the legs cramp up because they're starved for oxygen and nutrients. Your heart, also a muscle, needs oxygen and nutrients to keep working. If its blood supply is inadequate to meet the heart muscle's needs, ischemia occurs, and you may feel chest pain or other symptoms. Ischemia is most likely to occur when the heart demands extra oxygen. This is most common during:

y y

Exertion (activity) Eating

y y

Excitement or stress Exposure to cold Coronary artery disease can progress to a point where ischemia occurs even at rest. When ischemia is relieved in a short period of time (less than 10 minutes) with rest or medications, you may be told you have "stable coronary artery disease" or "stable angina." The most common symptom is of coronary artery disease is angina, called or angina pectoris, or simply chest pain. Angina can be described as a discomfort, heaviness, pressure, aching, burning, numbness, fullness, squeezing or painful feeling. It can be mistaken for indigestion or heartburn. Angina is usually felt in the chest, but may also be felt in the left shoulder, arms, neck, back, or jaw. Other symptoms that can occur with coronary artery disease include:

y y y y y y

Shortness of breath Palpitations (irregular heartbeats, skipped beats, or a "flip-flop" feeling in your chest) A faster heartbeat Weakness or dizziness Nausea Sweating Ischemia, and even a heart attack, can occur without any warning symptoms. This is called silent ischemia. It can occur among all people with heart disease, though it is more common among people with diabetes. Myocardial infarction (MI) is the rapid development of myocardial necrosis caused by a critical imbalance between oxygen supply and demand of the myocardium. This usually results from plaque rupture with thrombus formation in a coronary vessel, resulting in an acute reduction of blood supply to a portion of the myocardium. Although the clinical presentation of a patient is a key component in the overall evaluation of the patient with MI, many events are either "silent" or are clinically unrecognized, evidencing that patients, families, and health care providers often do not recognize symptoms of a MI. The appearance of cardiac markers in the circulation generally indicates myocardial necrosis and is a useful adjunct to diagnosis.

Cardiac markers help to categorize MI, which is considered part of a spectrum referred to as acute coronary syndrome that includes ST-elevation MI (STEMI), nonSTelevation MI (NSTEMI), and unstable angina. This categorization is valuable because patients with ischemic discomfort may or may not have ST-segment elevations on their electrocardiogram. Those without ST elevations may ultimately be diagnosed with NSTEMI or with unstable angina based on the presence or absence of cardiac enzymes. Additionally, therapeutic decisions, such as administering an intravenous thrombolytic or performing percutaneous coronary intervention (PCI), are often made based on this categorization. The most common cause of MI is narrowing of the epicardial blood vessels due to atheromatous plaques. Plaque rupture with subsequent exposure of the basement membrane results in platelet aggregation, thrombus formation, fibrin accumulation, hemorrhage into the plaque, and varying degrees of vasospasm. This can result in partial or complete occlusion of the vessel and subsequent myocardial ischemia. Total occlusion of the vessel for more than 46 hours results in irreversible myocardial necrosis, but reperfusion within this period can salvage the myocardium and reduce morbidity and mortality. Nonatherosclerotic causes of MI include coronary vasospasm as seen in variant (Prinzmetal) angina and in patients using cocaine and amphetamines; coronary emboli from sources such as an infected heart valve; occlusion of the coronaries due to vasculitis; or other causes leading to mismatch of oxygen supply and demand, such as acute anemia from GI bleeding. MI induced by chest trauma has also been reported, usually following severe chest trauma such as motor vehicle accidents and sports injuries. If you have diabetes, your blood sugar levels are too high. Over time, this can damage your nerves or blood vessels. Nerve damage from diabetes can cause you to lose feeling in your feet. You may not feel a cut, a blister or a sore. Foot injuries such as these can cause ulcers and infections. Serious cases may even lead to amputation. Damage to the blood vessels can also mean that your feet do not get enough blood and oxygen. It is harder for your foot to heal, if you do get a sore or infection. Although it can hurt, diabetic nerve damage can also lessen your ability to feel pain, heat, and cold. Loss of feeling often means you may not feel a foot injury. You could have a tack or stone in your shoe and walk on it all day without knowing. You could get a blister and

not feel it. You might not notice a foot injury until the skin breaks down and becomes infected. Nerve damage can also lead to changes in the shape of your feet and toes. Ask your health care provider about special therapeutic shoes, rather than forcing deformed feet and toes into regular shoes. Ulcers occur most often on the ball of the foot or on the bottom of the big toe. Ulcers on the sides of the foot are usually due to poorly fitting shoes. Remember, even though some ulcers do not hurt, every ulcer should be seen by your health care provider right away. Neglecting ulcers can result in infections, which in turn can lead to loss of a limb. If your ulcer is not healing and your circulation is poor, your health care provider may need to refer you to a vascular surgeon. Good diabetes control is important. High blood glucose levels make it hard to fight infection. Poor circulation (blood flow) can make your foot less able to fight infection and to heal. Diabetes causes blood vessels of the foot and leg to narrow and harden. You can control some of the things that cause poor blood flow. Don't smoke; smoking makes arteries harden faster. Also, follow your health care provider's advice for keeping your blood pressure and cholesterol under control. Exercise is good for poor circulation. It stimulates blood flow in the legs and feet. CONCLUSION The single most common cause of ESRD in the United States today is diabetic nephropathy, and the incidence in type 2 DM appears to be increasing. Several factors probably contribute to the renal damage, including hyperglycemia and other metabolic byproducts of elevated glucose, hypertension (both systemic and intrarenal), and a genetic predisposition in some patients. Patients with diabetic nephropathy usually also have diabetic retinopathy and have a much higher mortality from coronary artery disease. Critically important is attention to prevention as preferential to treatment of diabetic nephropathy. Once overt nephropathy is present, progression cannot be avoided, only delayed. The earliest clinical indicator of renal damage is microalbuminuria, which should be screened for at regular intervals with sensitive tests.

Several studies demonstrate the preventive effect of lowered blood glucose on the macrovascular complications of diabetes, including nephropathy, and serve as the rationale for the emphasis on tight rather than casual glycemic control. Before and especially after the onset of early nephropathy, blood pressure control is critical in preventing or slowing the progression of renal damage. First-choice agents for treating microalbuminuria are the ACE inhibitors, but lowered blood pressure by any means is the single most important factor in saving the diabetic kidney from the downward path to ESRD. Access to internet sites and numerous patient education tools put endless resources at the fingertips of all nursing staff and most patients. Basic education on diabetes should be done for all patients and reinforced at every possible opportunity. Because kidney failure is quite possibly the most patient-education intensive field for nursing today. With the scope of this disease involving every aspect of the patient's life, constant support and education are essential. Many people are not diagnosed with chronic kidney disease until they have lost much of their kidney function. There is no cure for chronic kidney disease. Untreated, it usually progresses to endstage renal disease. Lifelong treatment may control the symptoms of chronic kidney disease.

References:
www.emedicine.medscape.com http://care.diabetesjournals.org. Medical surgical Nursing 10th Edition vol. 1 and 2 by Brunner and Suddarth`s Medical surgical Nursing 8th Edition vol. 1 and 2 by Joyce Black Patient`s Chart