Critical Pathway: Case Study of Chronic Renal Failure

Advanced Pathophysiology
NURS 5104

October 4, 2013

Critical Pathway: Case Study of Chronic Renal Failure
I. Introduction Mr. P. J., a 38-year-old African American male, presented to the Emergency Department by the rescue squad team, with a six day old complaint of increased swelling of the bilateral lower extremities, unusual weight gain, and a feeling of ‘I can not breathe’ per patient. Patient was sent as a direct admit to the Intensive Care Unit (ICU) and placed on 2 liters NC with hydration and adult special care monitoring. Vital signs were taken by the paramedic enroute revealing the following: Ambulance Vitals: * BP 202/112 * Pulse 101 * Respirations 20 * O2 86% before O2 * Temp. 98.4 * Height 5’10 Patient stating * Weight 222 lbs. Patient stating (weighed the day before)
The paramedic started a 20 gauge IV into Mr. J’s right antecubital and started him on 2 liters nasal cannula; due to the “presence of crackles no Procardia was administered” (J. Madden, personal communication, August 14, 2013). The paramedic monitored the vitals and reported to medical control the situation and estimated time of their arrival in five minutes. Mr. P. J. has been married to K for twenty years and they have one child, a twelve-year-old daughter. Mr. P. J. has worked in construction for twenty years; Mr. J stated working on his feet all day he noticed the swelling six days ago, but had assumed it would go away like before. Mr. P stated that with a weekend of rest and relaxation the swelling had diminished in time for work. This past Monday morning the swelling was worse and his shoes were beginning to get tight P stated. By Wednesday he was no longer able to wear his work boots and took a weight of himself noting that 222 lbs. was 18 lbs. heavier than his normal weight. P then stated that when he awoke this morning there was a severe shortness of breath, as if he was smothering, and when he attempted to get out of bed he found he was unable to ambulate due to the heaviness felt in his legs. Mr. P. J.’s wife, K, stated she called 911 for she feared she would not be able to assist him to the car from a second level bedroom. They both agreed that the emergency services arrived 4 minutes later to transport. Upon admission into the ICU, a complete assessment was performed and notations were made in regards to the following findings:
Assessment
Vital Signs * BP 208/99 * Pulse 122 auscultated hearing S3 and S4 gallop * Respirations 20 Bibasilar crackles are present * O2 Sats 98% on 2 liters Nasal Cannula * Temp. 98.4 oral
General. Mr. J, a 38-year-old African American male, showed himself alert, cooperative, and well groomed. Mr. J communicates well, answering appropriately to all questions asked. Eye contact made during assessment and Mr. J expressed appropriate concern through out history.
Mental Status. Mr. J is oriented to time, place and person; his reasoning and arithmetic calculations intact evidenced by answering his personal thoughts on what may be going on within his body, multiplication, and division problems. Memory intact, Mini-mental score = 30; Mr. J’s speech is clear, smooth and enunciates each word. When asked to point to his wife he completed without error showing comprehension of directions.
Skin, hair, and nails. Mr. J is African American with skin deviations apparent by sight. Skin is light brown and when asked Mr. J placed his palm supination to reveal skin to palm is callused and dry. Upon pinching the forearm the turgor had instant recoil. Mr. J’s forearm was nontender with slight non-pitting edema; nail beds pale without clubbing, pigmented bands visible, uniform thickness. Proudly P had showed his nails, smiling he stated that K takes very good care of his nails. The nails are smooth, firmly adhered to nail bed, with a brisk capillary refill. K had stated she prefers bald men when RN made note regarding early stage baldness. P’s skin to lower extremities taught and shiny, no weeping edema, 3+ pitting edema present.
Head. P’s head was easily examined revealing an erect and midline structure, scalp light brown, freely movable without lesions or tenderness. Mr. J squeezed K’s hand while allowing an overview of facial features that revealed to be well spaced and symmetric. Mr.J’s temporal arteries assessed as soft and non-tender to touch.
Eyes. P’s brows, lids, and lashes even another perfection he gave K praise for. P’s eyes were without tearing; sliding the lower lid down to allow view of conjunctiva, P’s appeared pink without discharge. Mr. J asked not to leave the light in his eye long because of sudden onset headaches bright light caused. Briskly running the light over the pupils there was an equal reaction/accommodation bilaterally to light. Extraoccular movements intact, no lid lag, nor nystagmus, P’s visual field equals examiner’s; corneal light reflex equal bilaterally, red reflex present, discs brownish in color with well-defined border bilaterally; arterial-venous ratio 2:5, no crossing changes noted; cornea, lens, and vitreous clear; retina brownish, no hemorrhages noted or exudates; macula yellow.
Ears. Mr. J’s auricles in proper alignment, without lesions, masses, or tenderness; canals with small amount dry cerumen; tympanic membrane gray, translucent, light reflex and bony landmarks present; no perforations, and P easily repeats whispered words at 2 feet bilaterally.
Nose and sinuses. P is a mouth breather, therefore no flaring of nares, and his septum slightly to the left of midline, patent bilaterally, mucosa pink and moist, no polyps or discharge. Upon palpitation P stated that no frontal or maxillary sinus tenderness present. O2 saturations fell to 87% without the use of nasal cannula for testing. Replaced and spoke with wife regarding P’s normal diet. K stated P eats meat and potatoes each day with no green vegetables. P loves to eat pasta with cheese and has soup beans with fried cornbread once a month. Noted the O2 saturation back up to 98%, explained to P when mask comes off to open mouth wide and continue breathing. P performed task without incident.
Throat and mouth. P’s buccal mucosa appeared pale/pink and slightly moist, no lesions, salivary glands nontender; 28 teeth in good repair, no movement; teeth 1, 16, 17 and 32 missing; gingivae slightly erythematous and spongy; tongue in midline without fibrillation, no lesions; uvula midline with elevation of soft palate; gag reflex intact; slight ammonia smell noted, pharynx without erythema; no hoarseness; excluded the taste test for management of his normal mouth breathing pattern.
Neck. P’s trachea is midline, with no tracheal tug, thyroid and cartilages move with swallowing, hyoid noted in tact, thyroid lateral borders palpable, no enlargement or nodules noted, lymph nodes, lymph nodes nonpalpable, full range of motion and appropriate strength. Jugular vein distention not found; “A mean jugular venous pressure greater than 10 cm H2O usually indicates volume overload” (Applefeld, 1990, para. 13) and issues with the right ventricle.
Chest and lungs. P could not stand on his own so with assistance from the nurse’s aide and K, back of the bed had been lowered and gown removed to reveal upper portion of body. AP diameter less than lateral with 1:2 ratio; muscle and respiratory effort symmetric bilateral revealing use of accessory muscles; inspiration-to-expiration is 1:2. Breath sounds with bibasilar crackles present, do not clear with coughing. Left ventricular heave noted at the Apex.
Breast. P’s chest appeared as symmetric with no retraction, discharge, or lesions. P had no masses or tenderness, no lymphadenopathy.
Heart. P’s apical rate was122 an irregular rate and rhythm with S2 & S3 gallop present. RN had noted apical pulse timed with radial pulse for accuracy.
Abdomen. P had been assisted into a supine position when he stated to quickly do this because lying down completely caused ‘an uncomfortable feeling with breathing’ at home he uses three pillows for elevation to ‘comfortably breathe and rest’ he had revealed. Abdomen was distended, hard, and P had winced with the deep palpation. P’s abdominal skin with no lesions, scars, or striae and bowel sounds present in all four quadrants. K had notified the RN that the last bowel movement had been this morning. Organomegaly noted to bilateral kidneys.
Extremities. Skin color is light brown, no redness, cyanosis, or lesions. P was unable to ambulate due to 3+ pitting edema to bilateral lower extremities, edema noted in upper extremities with no pitting. P was not showing signs of anxiety but tachypnea present. O2 Sats at 98% on non-rebreather however, peripheral pulses bounding bilaterally.
Musculoskeletal. P showed no issues with the temporomandibular joint no slipping or crepitation, neck full ROM and the vertebral column no tenderness, no deformity or curvature. P was unable to stand therefore omitted the bending head to toe test. Arms symmetric with a 1 rating for edema, full ROM, muscle strength 3+ bilaterally when asked to squeeze hands. Legs symmetrical with 3+ pitting edema. P unable to lift legs from bed, wiggle toe, and stated tender with palpation.
Neurologic. P was not able to neither stand safely nor ambulate at this time. This RN was unable to evaluate gait, balance, or deep tendon reflexes of lower extremities. P showed upper extremity, hand to eye coordination as unremarkable.
CBC, BMP, urinalysis, and CMP were ordered. The doctor also requested an electrocardiogram to be completed STAT, IV Lasix 20 mg now, non-rebreather mask and a Foley catheter to be placed. With the insertion of a 14 French Foley Catheter 30 cc brownish colored, strong smelling urine was released and sent for urinalysis.
II. Precipitating Factors
Lab results CMP: * Glucose 60-110 108 * Bun 8-24 mg/dL 41 mg/dL * Creatinine 0.9-1.6 mg/dL 23.2 mg/dL * Calcium 8.4-10.7 mg/dL 7.8 mg/dL * Sodium 132-142 mmol/L 127 mmol/L * Potassium 3.6-5.0 mmol/L 6.1 mmol/L * Chloride 101-111 mmol/L 89 mmol/L * Carbon Dioxide 21-31 mmol/L 9.9 mmol/L * Anion Gap 6-16 26 * Magnesium 1.8-2.5 mg/dL 2.7 mg/dL * Phosphorus 49-142 IU/L 640 IU/L * Albumin 3.2-5.5 g/dL 2.9 IU/L * AST 7-21 U/L 21 * ALT 0-30 U/L 15 * GFR 125-150 mL/min 3 mL/min
CBC:
* WBC 3.8-11.0 THO/MM3 19 THO/ THO/MM3 * RBC 4.2-5.6 M/L 4.0 M/L * Platelets 140-400 Thousand 142,000 * MCV 80-99 FI 81 FI * MCH 27-34 uug 27 uug * MPV 7.3-10.1 7.4 * Amylase 25-125 U/L 78 U/L * Lipase 25-51 U/L 38 U/L
ABG’s:
* pH 7.38-7.42 7.0 * PaO2 75-100 mm/Hg 40 mm/Hg * PaCO2 38-42 mm/Hg 22.9 mm/Hg * HCO3 22-28 mEq/L 12 mEq/L * Base Excess 0- -4 mmol/L -10 mmol/L
Random:
* Uric Acid 3.8-8.9 mg/dL 18 mg/dL
Coagulation:
* Hemoglobin 13.0-17.0 g/dL 11.4 g/dL * Hematocrit 38-50% 25% * PT 10.5-13.8 sec 10.8 sec * PTT 22.0-37.0 sec 23.4 sec * INR 2-3 2.2
Urinalysis
* 4+ protein * 2+ hematuria
Electrocardiogram
* Revealed left ventricular hypertrophy and ST- T waves consistent with a strain pattern. Patient and family history is obtained from Mr. J and his wife K. Mr. J’s history is significant for hyperlipidemia diagnosed in 2000, diagnosed with hypertension in 2010, in 2011 Mr. J was diagnosed with Restless Leg Syndrome and placed on Melatonin 3 mg before bed to assist in his altered sleep patterns due to the issue. Mr. J is current on immunizations and tetanus in 2010. No history of surgeries, allergies or severe illness. Patient smokes 1 pack of cigarettes a day and drinks a six-pack on the weekends. K stated she has not noticed any neurological changes in her husband; but his sudden weight gain, chronic headaches and complaint of not being able to breathe did disturb her. Family History reveals a history of hyperlipidemia and hypertension in his mother and his father had been diagnosed with hypertension, gout, and kidney disease. His father passed away from a heart attack three years ago. Mr. J has one sister recently diagnosed with glomerulonephritis. There is no other family history identified.
Current Medications * Melatonin 3 mg PO before bed * Simvastatin 20 mg PO before bed * Amlodipine 5 mg PO daily * Clonidine 0.01 mg PO q 6 hours as needed for systolic BP > 160
The attending doctor, after a review of labs and diagnostic, immediately consulted for a Nephrologist to join the care team. Knowing that time was of the greatest importance the doctor had the nurse to gather educational material regarding kidney failure, symptoms, and treatment options available.
Three hours after Mr. J’s completed admission and lab work the vitals revealed to be correcting and the labs were returned and reviewed by the attending doctor.
Vitals
* BP 168/84 * Pulse 90 * Respirations 18 * O2 98% 2 liters nasal cannula * Temp 98.6 oral * Pain 5/10 to bilateral lower extremities * Foley output 0 (the 30 cc previously out used for lab)
III. Symptoms Upon physical assessment, review of labs and diagnostics, and adding the relevant symptoms of the diagnosis not present; the following list represents the physiological effects and abnormal lab representations of Chronic Renal Failure: * Hypertension * Headaches and jugular vein distention * Arteriovenous nicking and hemorrhage * Edema * Jugular vein distention (JVD) (not diagnosed/relevant sign of disease) * Dyspnea * Metabolic Acidosis * Oliguria * Pain * Restless Leg Syndrome * Dysrhythmia * Crackles bilaterally * Dry skin (not diagnosed/relevant symptom/sign of disease) * Anemia * Weight gain * Hyperkalemia * Hypocalcaemia * Proteinuria * Uremia (not diagnosed/relevant symptom of disease) * GFR < 15 mL/min Mr. J’s GFR = 3 mL/min * Hyponatremia * Anemia * Decreased RBC * Decreased hemoglobin * Decreased hematocrit * Hypochloremia * Anion Gap * Hypermagnesium * Hyperhosphatemia * Hypoalbuminemia * Decreased WBC * Decreased RBC * Hyperuricemia * Smoker * ETOH use
IV. Cellular Analysis The most definitive laboratory indicator for kidney function is the estimated GFR. Chronic kidney failure is defined by the National Kidney Foundation (NKF) as, “Kidney damage of GFR <60 mL/min/1.73m2 for 3 months” (National Kidney Foundation website, 2002, table 11). The kidneys are the regulators of many body functions and control complex processes that keep homeostasis throughout the body’s system. In the kidneys, blood is filtered through the functioning units, nephrons. When 90% of the functioning units are lost the functioning ability of the kidneys is severely impaired. The following are results of this malfunction.
Hypertension. “Hypertensive nephrosclerosis is a vaguely defined clinical entity, most commonly applied to African Americans with hypertension and advanced chronic kidney disease (CKD) in the absence of other causes for renal failure” (Freedman & Sedor, 2008, p. 2048). Hypertension is the product of NaCl retention, dangerously high renin levels for expended extracellular fluid volume (ECFV), stimulation of the sympathetic system through the afferent renal reflexes, and damaged renal endothelial function with less than needed nitric oxide and increased endothelin production (Med education: Chronic Renal Failure website, 2010). Renin is released from the juxtaglomerular cells, acts on Angiotensinogen and converts it to Angiotensin I. In the lungs angiotensin-converting enzyme (ACE) converts Angiotensin I to Angiotensin II. The production of Angiotensin II causes vasoconstriction briefly, followed by an increase in blood pressure due to the stimulation of the adrenal cortex. Upon stimulation the adrenal cortex releases aldosterone, which causes sodium and water reabsorption by the kidneys. The end result is the inability of tissue perfusion due to the lack of the peripheral vascular bed to meet the demands of resistance (McCance et. al., 2010). Left ventricular hypertrophy was noted on the electrocardiogram, this is an important sign of hypertension (Frohlich, 2009, para. 4). Mr. J stated symptoms of sudden onset headaches; this would be justified by the hypertensive state. “Physical damage from high pressures may act directly, and may also induce arteriolitis in systemic hypertension, creating twofold abnormality” (Schneiderman, 1990, para. 8), of arteriovenous nicking and hemorrhages. Although these were not observed during the fundoscopy, this manifestation is a significant indicator of hypertension and will be monitored for. “Elevated blood pressure also increases proteinuria due to transmission of the elevated pressure to the glomeruli” (Porth, 2009, p. 867).
Edema. “Sodium retention contributes to hypertension, edema, and heart failure” (McCance et al., 2010, p. 1394). The alteration of fluid volume occurs when the kidney loses the function to excrete water due to damaged nephrons and with damaged nephrons the decreased GFR. “One of the most important clinical causes of edema is the so-called nephrotic syndrome” (Hall, 2011, p. 377). In nephrotic syndrome, the loss of protein into the filtrate and the urine due to increased glomerular capillary permeability decreases the plasma protein. Once the plasma protein level <1/3 the normal and the oncotic pressure falls the process of fluid shifting from the intravascular space to the interstitial space occurs throughout the body resulting in edema and a decreased plasma volume (Hall, 2011, p. 377).
Jugular vein distention (JVD). JVD is a clear indicator of fluid volume overload and hypertension. Although Mr. J did not have this sign monitoring of the jugulars and maintaining the head of bed elevation to 45-65 degrees will be a priority for the nurse.
Dyspnea. ‘The uncomfortable sensation of breathing” where the etiology is so complex and not tied to any one issue makes this manifestation a remarkable hallmark of complications to this writer. A mechanism of the body to assist in an abnormal decrease in pCO2 is the breathing rate. The central and peripheral chemoreceptors along with the carotid and aortic bodies respond to the pO2, pCO2 and pH of the blood creating dyspnea. The pH, pCO2, and HCO3 are monitored by the respiratory and urinary systems to maintain a balance. “ J-receptors also trigger dyspnea in individuals with pulmonary edema and pulmonary microemboli” (McCance et al., 2010, p. 1267).
Metabolic Acidosis. When kidneys fail to get rid of metabolic acids formed in the body normally or an excess production of metabolic acids throughout the body (Hall, 2011). Renal tubular acidosis, “This type of acidosis results from a defect in renal secretion of H+ or in reabsorption of HCO3 or both” ((Hall, 2011, p. 392). Mr. J’s metabolic acidosis was diagnosed by a pH=7.0, PaO2=40 mm/Hg, PaCO2= 22.9 mm/Hg, and HCO3=12 mEq/L. The base excess was = -10 mmol/L. Metabolic acidosis is a result of increased noncarbonic acids or with a loss of bicarbonate from the extracellular fluid (McCance et al., 2010). The domino effect begins with a decreased pH related to a decreased bicarbonate that is related to decreased renal regeneration of the bicarbonate, metabolic processes, bodily losses (i.e. diarrhea, emesis), or the ingestion of acids (Hall, 2011). The built in mechanism of the body to compensate is hyperventilation.
Oliguria. Defined as urine excretion of less than 400ml/day or 30ml/hr., which represents a decrease from the normal. As GFR decreases the urine output will decrease as well. The 30cc of brownish urine that appeared upon insertion of the foley was all that came out during his hospital stay.
Pain. Manifested pain from bright lights can be associated with headaches, fluid volume overload leading to the edema of bilateral lower legs which gives the heavy feeling P stated he had. Uremic toxins leading to pain and burning in the lower extremities can cause gouty arthritis.
Dysrhythmia. P’s electrocardiogram showed left ventricular hypertrophy and ST- T waves consistent with a strain pattern. P’s potassium level was elevated at 6.1 mmol/L. The high potassium level increased the risk for fatal dysrhythmias.
Left ventricular hypertrophy. “Anemia, in particular, has been correlated with the presence of left ventricular hypertrophy” (Porth, 2009, p. 865). Augmented pulse pressure is a loss of elasticity of the vessels and to vascular calcifications; “anemia and the retention of sodium and water secondary to decreased renal function are responsible for volume overload, determining a hyperdynamic state” (Taddei et al., 2011, p. 615). Using erythropoietin to correct anemia a patient has a better chance of reducing LVH (Taddei et al., 2011).
Crackles bilaterally. The sound of pulmonary edema with etiology of heart disease, in Mr. J’s case the Left ventricular hypertrophy found with the electrocardiogram. With the failure of the left ventricle, pressure will increase on the left side causing a movement of vascular volume into lung space that leads to an increase of hydrostatic pressure into the pulmonary capillaries (McCance et al., 2010).
Dry Skin. Pruritus often occurs in chronic kidney failure due to waste and phosphate products using the skin to get out due to decreased GFR (McCance et al., 2010). The sweat and oil glands have less activity and skin color may change due to anemia or urinary pigment (McCance et al., 2010). Any of these changes can lead to itching and led to impaired skin integrity.
Restless leg syndrome (RLS). In Mr. J’s case this was diagnosed previously yet no other labs or checks were completed to verify etiology. An etiology of (RLS) is from the demyelination of the nerves from uremic toxins and electrolyte imbalances caused in renal failure. “RLS is also related to environmental factors and genes; the single largest known environmental factor is low iron levels” (John Hopkins Center website, n.d., para. 8). The low labs of RBC’s, hemoglobin and hematocrit represented low iron levels.
Weight gain. Mr. J stated to the paramedic he had noted an 18lb weight gain from when he weighed the day before. Mr. J normally weighed once a month therefore his statement is used subjectively. The 3+ pitting edema and crackles audible in lung sounds verified additional fluid retention due to the decreased GFR.
Hyperkalemia. Increased serum potassium is the effect of damage to the renal function causing oliguria, excess potassium intake, or a potassium shift from cells to the ECF (McCance et al., 2010). Due to the presence of acidosis, H+ shift into the cells and intracellular potassium and sodium move into the extracellular fluid (McCance et al., 2010). Hypoxia can result in hyperkalemia due to insufficient cell membrane active transport leading to the leakage of potassium into the ECF (McCance et al., 2010).
Hypocalcaemia. Due to the decrease in GFR the levels of calcium and phosphorus are related. When levels of phosphorus are high it is relevant that calcium will be decreased. Calcium is found in three forms in the blood, free or ionized, attached to proteins (therefore, when albumin is decreased so is calcium and P’s albumin was 2.9 IU/L), or attached to other complexes. Due to the renal insufficiency vitamin D can not be converted to active form 1.25 dihydroxycholecalciferol, hence the absorption of calcium in the GI tract can not occur (McCance et al., 2010). Low serum hypocalcaemia, and hyperphosphatemia can start PTH synthesis and secretion. In Chronic kidney failure, PTH secretion becomes nonproductive and the parathyroid glands, that first hypertrophy, become hyperplastic and the continued elevation of PTH levels exacerbate hyperphosphatemia from bone resorption of phosphate (National Kidney Foundation website, 2002).
Proteinuria. “Proteinuria is consequence of two mechanisms: the abnormal transglomerular passage of protein due to increased permeability of glomerular capillary wall and their subsequent impaired reabsorption by the epithelial cells of the proximal tubuli” (Sato et al., 2011, p. 326).
Uremia. Uremia is a state where there is urine in the blood. This will occur after 2/3 of the nephrons are destroyed. P is close to this stage yet he has not began to exhibit the severe signs of altered mental status through uremic encephalopathy, extreme weakness, loss of needed hydration through vomiting and lethargy (Porth, 2009). If treatment is not received soon when this begins P faces coma and death (Porth, 2009). High levels of uremic toxins are also a cause of sexual dysfunction in men and women.
Sexual dysfunction. High levels of uremic toxins, luteinizing and prolactin hormone levels with a decrease in testosterone levels will decrease the sperm count and can cause erectile dysfunction in men (Porth, 2009). Though P and K stated there was any issue in this area questions pertaining to this issue are to be monitored for as a red flag of an issue.
GFR. Normal GFR in men is 125 to 150 ml/min per 1.73 m2 and is defined by the KDOQI as having” kidney damage lasting for 3 months or more or having a GFR less than 60 mL/min per 1.73 m2 for 3 months or more with or without kidney damage” (National Kidney Foundation website, 2002, table 139). Mr. J’s GFR was calculated to be 3mL/min. The calculator used for the actual calculation is located at the National Kidney Disease Education Program website: http://www.nkdep.nih.gov. Damage to the glomeruli causes proteinuria and increased renin. Mr. J has a family history of kidney disease, he has hypertension, also he is ethnic American and according to the National Kidney Foundation GFR education should be given to him or other individuals who fall into that category (2002).
Hyponatremia. Mr. J’s sodium level was 127 mmol/L. In this case Mr. P had dilutional hyponatremia. Advanced chronic kidney disease defined as a glomerular filtration rate GFR<15ml/min is one reason of hyponatremia. Low intra-arterial filling caused by low cardiac output due to hypoalbuminemia in nephrotic syndrome (JAPI, n.d.). “Activation of the neurohormonal compensatory mechanisms (renin-angiotensin-aldosterone, ADH and norepinephrine) causes water and salt retention leading to hyponatremia and hypervolemia. (JAPI, n.d., para. 12). A response from the decreased GFR causes the adrenal cortex to release aldosterone, which then causes the kidneys to reabsorb sodium and water. All the fluid that is retained causes edema and trouble with the cardiovascular system and the respiratory system. These were evidenced by S3 and S4 heart sounds found in examination, the hypertension, sinus tachycardia, the crackles in the lungs and the decreased sodium level. A decreased sodium level leads to a decrease in chloride proven by Mr. J’s chloride level. Impairment of the renal water excretion path and ADH are critical factors of hyponatremia.
Hypochloremia. Hypochloremia is a direct result from Hyponatremia. The job Mr. J has is a continuous moving, hard labor work that has him sweating profusely from morning until night. Loosing large amounts of sweat can be an issue for Mr. J as well. Chloride is needed in the body for metabolism. Mr. J’s level was 89.
Anion gap. The calculation for the Anion gap = Na+ - (Cl− + HCO3-)=26 mEq/L the normal range is 8-16 mEq/L (Anion Gap Calculator website, 2013, table 1). Mr. J’s is showing a widening in the Anion gap therefore this lab supports the metabolic acidosis to kidney failure. When the glomeruli are damage sulfuric acid and phosphoric acids are retained causing the widening of the anion gap.
Anemia. “Anemia of CKD is due to several factors, including chronic blood loss, hemolysis, bone marrow suppression due to retained uremic factors, and decreased red cell production due to impaired production of erythropoietin and iron deficiency” (Porth, 2009, p. 864). Normochromic normocytic anemia principally develops from decreased renal synthesis of erythropoietin (National Kidney Foundation website, 2002). Red blood cells are created in the kidneys by a hormone called erythropoietin (EPO) that stimulates the bone marrow to produce more red blood cells (UNC Kidney Center, n.d.). “When kidney function is reduced, not enough EPO is produced, thus causing anemia. Symptoms of anemia include fatigue, tiredness, shortness of breath, headache and inability to concentrate” (UNC Kidney Center, n.d., p. 4). Uremia will stop erythropoietin production and also causes a shorter life span for RBC’s. “Anemia, in particular, has been correlated with the presence of left ventricular hypertrophy” (Porth, 2009, p.865) and also contributes to the further damage of the nephrons that are left in the kidneys by “increased hypoxic and oxidative stress” (Porth, 2009, p.865).
Hypermagnesium. Mr. J’s level of magnesium had risen to 2.7 mg/dL. Magnesium is excreted through the renals. The kidneys have the ability to regulate reabsorption of magnesium similar to that of the intestinal uptake of magnesium by way of passive paracellular fashion (De Francisco & Rodriguez, 2013). The distal convoluted tube is where magnesium-specific transporters reabsorb magnesium in a specified range with excretion amounts varying and in CKD stages 1-3 renal loss can be compensated with a small increase of magnesium however in advanced CKD this mechanism fails and hypermagnesium occurs (De Francisco & Rodriguez, 2013).
Hypoalbuminemia. Mr. J has proteinuria this loss of albumin has contributed to the decreased level of calcium. Albumin is more than 80% of the excreted protein in proteinuria and according to the lab work it is evident Mr. J has proteinuria. A small amount of albumin is catabolized in the “proximal tubule of the kidney after reabsorption of filtered albumin” (Brenner & Rector, 2011, para. 3). Hypoalbuminemia occurs from the large urinary loss, decreased hepatic synthesis and the large amounts of albumin catabolism (Brenner & Rector, 2011).
Increased WBC. The lab results show WBC at 19. The increase is due to cell-mediated immunity. The glomeruli have damage and the lymphocytes have arrived on the scene to correct what they can.
Decreased RBC. Decreased lab values of hemoglobin, hematocrit and GFR are indicators of low RBC. The kidney produces erythropoietin that produces RBC’s. When function is hindered there cannot be any erythropoietin released for production.
Glycemic control. Patient is not a diabetic but with renal failure the Hemoglobin A1C needs to be monitored. After dialysis a patient can bottom out with a low blood sugar due to the ‘cleansing’ of the blood; alternately, a patient may become hyperglycemic due to the solute of the dialysate.
Bone phosphate and Calcium abnormalities. Patient did not show any signs of bone disorders, however this is a common occurrence in Chronic Renal Failure patients due to hypocalcaemia and Hyperhosphatemia. Symptoms should be monitored for and test completed to monitor for breakdown. One type of bone abnormality is osteodystrophy. This is seen by a low number of osteoblasts and the osteoclast average being just below range to normal range (Porth, 2009). “Adynamic osteodystrophy bone disease is characterized by reduced bone volume and mineralization that may result, in part, from excessive suppression of PTH production with calcitriol hyperuricemia” (Porth, 2009, p. 864).
Hyperuricemia. The end result of purine metabolism from filtration in the glomeruli, which is secreted into the distal tubule, is uric acid. When function of the glomeruli is damaged high levels of uric acid build up and can lead to gouty arthritis. P’s level was elevated so the monitoring for gout is a necessity.
Smoking. P smokes daily and this is a habit that can lead to serious effects with the lungs, kidneys by “increasing intraglomerular pressure and urinary albumin excretion” (Porth, 2009), heart and will enhance the chance for hypertension.
ETOH use. P has admitted to the use of alcohol each weekend. Drinking can cause a depletion of the much-needed electrolytes in the body and “chronic drinking has further detrimental effects on the kidneys, including impaired sodium and fluid handling and even acute kidney failure” (Epstein, 1997, p. 84).

V. Nursing & Medical Management
Non-pharmacological Measures * Nephrology Consult * Vein Mapping for access site * Immediate insertion of temporary and permanent dialysis access/ once Hypertension is corrected. Temporary access, a trialysis, to be placed in the right internal jugular vein allowing access of the left arm for the arterial-venous fistula. Temporary access can be used for three months allowing the permanent access time to mature and be accessed once for verification of usage then pull the temporary access. * Echocardiogram * Stat EKG * Continuous Adult Special Care Monitoring in ICU * Basic Metabolic Panel every A.M. * Monitoring potassium levels for dialysis treatment is essential in mixing of the dialysate * Complete Blood Count every A.M * Monitoring the Hemoglobin and Hematocrit levels is essential before any type of surgery. If the level drops below 7 for Hemoglobin, according to the Johnson City Medical Center Hospital Nephrologist, two units of PRBC are to be administered. * Strict Input and Output daily * The patient may have reached the stage of anuria due to the stage of CKF * Daily weight * Doctor to determine the necessity of glycemic monitoring if patient is not a diabetic * Strict Renal diet of 60 g of protein, 2 g sodium & 1000cc Fluid restriction * NPO 12 hours prior to placement of temporary and permanent access * Dietary Consult * Education on need for monitoring new diet restrictions (potassium rich foods) * Each shift to complete Neurological checks * Non-Rebreather to be titrated as patient tolerates to 2 liters on a nasal cannula while maintain O2 saturations >96% * Stat ABG and if breathing gets distressed * Foley catheter to be placed and if no output within 24 hours remove to avoid infection
Pharmacological Methods * Captopril (Capoten) 25mg PO to start may repeat every 30 minutes to reduce Hypertensive emergency then stop (Skidmore-Roth, 2009). * This ACE inhibitor is used for hypertension and CHF (Left Ventricular dysfunction). * Nifedipine (Procardia) 40 mg PO once daily * This Calcium Channel Blocker is used to reduce blood pressure by relaxing “the coronary vascular smooth muscle, dilates coronary arteries, increases myocardial oxygen delivery and dilates the peripheral arteries” (Skidmore-Roth, 2009, p. 752). Another use of this drug is the “inhibition of calcium ion influx across cell membrane during cardiac depolarization” (Skidmore-Roth, 2009, p. 752). * Multivitamin one pill once daily * This vitamin will help replace a multitude of diminished vitamins. The use of Sesame Street vitamins is acceptable for treatment. * Ferrous Sulfate 0.25 grams tid * This hematinic drug “replaces iron stores needed for red blood cell development” (Skidmore-Roth, 2009, p. 472). * Aranesp 60 mcg/ml SQ given once a week in the lower abdominal area * Hematopoietic agent that “stimulates erythropoiesis by the same mechanism as endogenous erythropoietin” (Skidmore-Roth, 2009, p. 337). Used to treat anemia associated with chronic renal failure for patients on and not taking dialysis (Skidmore-Roth, 2009). * Sevelamer 800 mg- 1600 mg PO with each meal according to doctor order. * Polymeric phosphate binders that help reduce serum phosphate in adults to be monitored and readjusted according to phosphate level (Skidmore-Roth, 2009). * Sensipar 30mg PO once daily * This calcium receptor agonist is used to treat secondary hyperparathyroidism in chronic kidney disease on dialysis (Skidmore-Roth, 2009). * Calcitrol 0.25 mcg PO once pre dialysis on dialysis days * This parathyroid agent is used in renal dysfunction to treat hypocalcaemia to assist with “intestinal absorption of calcium provides calcium for bones” (Skidmore-Roth, 2009, p. 216). * Calcium Chloride 30 ml IV as indicated by calcium levels * This electrolyte replacement, a calcium product, is used in prevention and treatment of hypermagnesium, Hyperhosphatemia, vitamin D deficiency, and cardiac toxicity caused by hyperkalemia (Skidmore-Roth, 2009). * Calcium Carbonate (Phos-Lo) 1 gm PO once daily * An antacid to assist with calcium supplement, treat Hyperhosphatemia Treatment: Secondary hyperparathyroidism and osteitis fibrosa are prevented by reducing serum phosphate levels by restricting diet with phosphates, and by giving phosphate binding agents like calcium carbonate, and calcium acetate, some times short course of aluminum hydroxide with calcium carbonate are used. Give after dialysis on dialysis days (Skidmore-Roth, 2009). * Vitamin E 60 units PO once daily * “Supplement for malabsorption syndrome” (Skidmore-Roth, 2009, p. 1098). * Lisinopril PO 10 mg daily * ACE Inhibitors are very effective in treating kidney disease, especially if there is an increase in the amount of protein in the urine. ACE inhibitors help the muscles around the blood vessels relax and enlarges the blood vessels, which reduces blood pressure. The National Institute of Diabetes and Digestive and Kidney Diseases sponsored the African American Study of Kidney Disease and Hypertension (AASK) in 2003 and found that ACE Inhibitors were better than other drugs at slowing kidney disease in African Americans (Davita website, 2013, para. 15). Given in low doses this medication can assist with systolic CHF. * Lasix 40 mg IV once stat then 40 mg PO as needed for fluid volume overload * A diuretic that will help alleviate edema and potassium overload by inhibiting “reabsorption of sodium and chloride at the proximal and distal tubule and in the loop of Henle” (Skidmore-Roth, 2009, p. 509). Mr. J was having hypertensive crisis due to the severe fluid volume overload and visual signs of 3+ pitting edema bilaterally to the lower extremities. * Metoprolol Succinate XL 50 mg PO BID daily * A Beta-blocker will reduce the heart rate and the heart’s output of blood, reduces elevated renin plasma levels, “blocks B2-adrenergic receptors in bronchial, vascular smooth muscle only at high doses” (Skidmore-Roth, 2009, p. 693). Metoprolol will also benefit Mr. J by preventing migraines. * Simvastatin 20 mg PO before bed * This medication will be continued for antilipidemic treatment of hyperlipidemia. * Melatonin 3 mg PO before bed * Herbal supplement to assist in sleeping and aide with hypertension * Sarna Lotion with 45% menthol ointment * Given for pruritus and itching due to kidney failure/dialysis treatment * Insulin if doctor requires patient to begin monitoring and assisting body to adjustment of dialysis treatment * Medications to inquire about before taking if not ordered by doctor * Ibuprofein * Stop taking: * Amlodipine 5 mg PO daily * Clonidine 0.01 mg PO q 6 hours as needed for systolic BP > 160 * Will re-evaluate upon discharge for home usage
Nursing Diagnosis * Excess fluid volume overload related to compromised regulatory mechanisms secondary to renal failure. * Monitor daily weight * Strict input and output monitoring * Monitor breath sounds each shift * Monitor for electrolyte imbalances * Monitor for bone breakdown (i.e., osteodystrophy) * Monitor vital signs for: * Increased respirations * Increased heart rate * Increased blood pressure * Decreased O2 saturations * Ineffective breathing patterns related to edema secondary to renal failure as evidenced by dyspnea and patient stating, “I can not breathe”. * ABG Stat * O2 with hydration maintain O2 saturation >96% * Reposition patient with elevation 45 to 60 degrees for effective breathing with education on maintaining elevation at home with the use of pillows * Monitor with oxygen oximetry * Encourage deep breathing with focus on breathing in the nose and long deep breaths out the mouth * Monitor for signs and symptoms of metabolic acidosis * Headaches, nausea and vomiting, rapid and shallow respirations * Re-check ABG’s every other day or as symptoms arise * Monitor for signs of confusion * Ineffective ventricular perfusion related to interruption of the ventricular blood flow secondary to ventricular failure * Monitor cardiac rate and rhythm * Monitor for abnormal heart sounds * Monitor vital signs continuously on ASC * Assess peripheral pulses every four hours * Knowledge deficit related to new diagnosis as evidenced by patient not understanding the significance of symptoms occurring * Education regarding: * Vision/visual deficit * Monitoring BP as directed by doctor * Monitoring for mental status changes * Monitoring for bone breakdown (ie, osteo * Monitoring for ammonia breath * Monitoring for weight gain * Impaired skin integrity of upper extremities related to dry skin and itching * Space fluids, allowing for 300 cc from 0600 to 1200, 300 cc from 1200 to 1800, 200 cc from 1800 to 2300, and 200 from 2300 to 0600. This allows for 1000 cc a day according to doctor order. * Strict input and output each shift * Daily morning weight * Sarna lotion for itching to be applied at least bid patient can have as needed * Provide mouth care every 4 hours and after every meal * Provide daily antiemetic one hour prior to meals * Assist with promoting daily hygiene care * Risk for infection related to compromised immune response secondary to renal failure * Monitor CBC, BMP daily * Monitor temperature every four hours * Monitor for signs and symptoms of chills, tremors, fatigue * Risk for infection related to new trialysis access as evidenced by patient asking, “Do I need to keep this bandaged”? * Educate on the necessity to keep dry, sterile bandage in place * Educate on proper dressing change procedure if dressing becomes wet or begins to peel off * Send supplies home with patient for dressing changes (at least three) until patient can obtain correct supplies * Educate patient on signs and symptoms of infection to monitor for * Set up home health for assistance in dressing changes the first few times * Educate on the necessity of checking for a +bruit and thrill and how to properly check for these * Risk for ineffective therapeutic regimen management related to change in life status and dependency on dialysis * Determine factors that may interfere with patient’s ability to adhere to treatment plan * Education for both patient and spouse regarding: * New diet * Smoking cessation * Alcohol use * Possible change in current occupation * Arrange for mental status evaluation regarding unexpected changes in mid-life * Prepare patient and family for disruption, expenses, and considerable alterations in family routines * Refer to a community outpatient dialysis center close to home * Have case management work with patient and family regarding expenses, transportation, and any equipment/ medications that may be needed at home * Refer family to a support group
VI. Outcomes The Nephrologist determined the patient was last stage chronic renal failure. Immediate access would need to be placed to alleviate body breakdown. A trialysis was place in the right internal jugular for immediate temporary use and plans discussed with family regarding a permanent access in the left arm. The doctor, patient and spouse agreed upon the insertion of an Arterial Venous fistula (AVF) to his non-major arm, the left. Patient underwent the first procedure and had his first dialysis treatment immediately following. 4.3 kilos of fluid removed and patient’s edema began to diminish. Pulse came down to 91, BP 167/78, respirations 18, temperature 98.0 orally, and O2 saturation maintained at 96% on 2 liters nasal cannula. Two days later the AVF was placed without incident to his left arm. The AVF had a +bruit and thrill palpitated and no excessive bleeding incurred. The KDOQI guidelines base the focus of treatment in CKF specifically with dialysis for Mr. J’s situation (National Kidney Foundation website, 2002). Outcomes will include adequate hemodialysis based on before and after treatment evaluations. The correction of electrolytes, fluid volume overload and acid-base imbalances will correct with accurate treatment and compliance by the patient. “Dialysis disequilibrium can occur in first few weeks of dialysis due to the reduction of urea leading to cerebral edema and increased intracranial pressure due to rapid shift of osmolality and pH” (C. Crissostimo, personal communication, September 20, 2013). Mr. J received dialysis daily for three days having a total of 12.1 kilos of fluid removed bringing his dry weight back to normal of 195.3 lbs. This correction of fluid imbalance will correct Mr. J’s impaired gas exchange, assist in maintaining a proper blood pressure along with proper diet and exercise. Mr. J has had his medications altered to assist in his new lifestyle. The benefit of iron supplements, multivitamins and the aranesp injections will assist in maintaining proper hemoglobin and hematocrit levels. The addition of phosphate binders taken with each meal will help decrease the phosphorus levels and increase the calcium levels. The addition of antihypertensive medications after dialysis will prevent hypotension due to the loss of fluid the body has been compensating for (C. Crissostimo, personal communication, September 20, 2013). Education Mr. J and K receive from the dietician will be a benefit in maintaining an adequate protein supply which in turn results in fluid balance, healing of skin integrity, and immune function.
Dialysis has been set up for the patient on Tuesday, Thursday and Saturday. K has spoken with their church group and has arranged for transportation to and from the center for her husband. The trialysis will be removed in two months after an initial use of the AVF. Mr. J and his family have several changes to cope with, through counseling and support groups these changes can be managed and over time grasped as a part of natural life they will be leading.

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