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University of Mississippi Medical Center School of Nursing

Monica Nichols White

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acute kidney injury kidney failure renal function medical education

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This document discusses acute kidney injury, including causes, diagnostic studies, and risk factors. It also describes the differences between acute and chronic kidney injury and the effects of aging on the urinary system. Different types of kidney injury like prerenal, intrarenal, and postrenal and how to treat them are presented.

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Acute Kidney Monica Nichols White, MSN, RN Injury / Assistant Professor University of MS Medical Acute Renal Center School of Nursing N460 Adult Health II Failure Kidney and Urinary Systems Regulates fluid and...

Acute Kidney Monica Nichols White, MSN, RN Injury / Assistant Professor University of MS Medical Acute Renal Center School of Nursing N460 Adult Health II Failure Kidney and Urinary Systems Regulates fluid and Structures electrolytes Kidneys Removes wastes Ureters Bladder Provides hormones Urethra involved in: red blood cell production (dysfunction can cause anemia – erythropoietin) bone metabolism Control of blood pressure Kidneys, Ureters, and Bladder Diagnostic Studies Urinalysis and urine culture Biopsies: used to help diagnose and evaluate the Urinalysis: provide import clinical info about kidney extent of kidney disease. function & helps diagnose other diseases Indications include unexplained acute kidney injury, Urine culture determines whether bacteria are present persistent proteinuria or hematuria, transplant in urine rejection, and glomerulopathies. Renal function tests IV urography: may be used as the initial (refer to Table 47-5) assessment of many suspected urologic conditions, Ultrasonography: noninvasive method of especially lesions in the kidneys and ureters. measuring urine volume in the bladder. Retrograde pyelography: catheters are May be indicated for urinary frequency, inability to advanced through the ureters into the renal pelvis void after removal of an indwelling urinary catheter, measurement of postvoiding residual urine volume, by means of cystoscopy. A contrast agent is then inability to void postoperatively, or assessment of the injected. need for catheterization during the initial stages of an Cystography (see back flow of urine up to intermittent catheterization training program. ureters): aids in evaluating vesicoureteral reflux CT and MRI: used to evaluate genitourinary (backflow of urine from the bladder into one or masses, nephrolithiasis, chronic renal infections, both ureters) and in assessing for bladder injury. renal or urinary tract trauma, metastatic disease, A catheter is inserted into the bladder, and a contrast and soft tissue abnormalities. agent is instilled to outline the bladder wall. Nuclear scans (radiocontrast inserted to patient IV Renal angiography (imagining of renal arteries): – helps visualize renal structures) used to evaluate renal blood flow in suspected Endoscopic procedures: can be performed in one renal trauma, to differentiate renal cysts from of two ways: using a cystoscope inserted into the tumors, and to evaluate hypertension. urethra, or percutaneously, through a small incision. It is used preoperatively for renal transplantation. Acute Kidney Injury AKI / ARF page: 1564-1570 CHARACTERIZED ALMOST A ACUTE RENAL BY A SUDDEN COMPLETE LOSS FAILURE CAN ONSET AND OF FUNCTION IN HAVE MANY RAPID DECLINE A PERIOD OF ETIOLOGIES OF RENAL HOURS TO DAYS FUNCTION ARF / AKI Kidneys unable Cannot to remove perform Substances metabolic regulatory accumulate wastes functions Fluid, Disruptions in electrolyte and both endocrine acid-base and metabolic problems functions develop Acute vs Chronic Acute – lethargic, ill, dry skin & mucous membranes, central nervous symptom s/s, decreased GFR of sudden onset (GFR- 125mL/min/1.73m2) Chronic – progressive, irreversible loss of function, eventually affects other organ systems leading to end- stage renal disease (ESRD) AKI Characterized by a rapid loss of kidney function. Rise in serum creatinine level and/or a reduction in urine output. Serum creatinine: 0.6-1.2 mg/dL (male) 0.4-1.0 mg/dL (female) (table 47-5) Can develop over hours or days Wide range of possibly Risk Factors life threatening metabolic Hx of HTN, DM issues Recent use/exposure to Metabolic acidosis nephrotoxic agents, heavy Fluid / electrolyte Acute metals or organic solvents imbalances Recent severe hypotensive Renal episode Failure Presence of tumor or obstruction Recent infections Idiopathic / unknown Effects of Aging on Urinary System/Gerontologic Considerations Physiologic changes The etiology of AKI in older adults Loss of elasticity and muscle includes prerenal causes such as support dehydration, intrarenal causes Decreased renal blood flow such as nephrotoxic agents, and Results in decreased GFR Altered hormonal levels result complications of major surgery in Between ages 30 and 90 Decreased ability to Size and weight of kidneys concentrate urine Altered excretion of water, decrease 20% to 30% sodium, potassium, and acid By seventh decade Prostate enlargement (cause Loss of 30% to 50% of post renal damage) glomerular function Atherosclerosis accelerates decrease of renal size with age Gerontologic Considerations More susceptible to AKI Dehydration due to polypharmacy- diuretics & laxatives Illness and immobility Hypotension (can cause decreased perfusion to kidneys) Aminoglycoside therapy Obstructive disorders Surgery Infection Under normal conditions, the aging kidney is able to maintain homeostasis. However, after abrupt changes in blood volume, acid load, or other insults, the kidney may not be able to function effectively because much of its reserve has been lost. High doses of aspirin can cause injury to kidney Suppression of thirst, enforced bed rest, lack of access to drinking water, and confusion all contribute to the older patient’s failure to consume adequate fluids and may lead to dehydration, further compromising already decreased renal function. Categories of ARF/Chart 54-4 Intrarenal Prerenal failure (a.k.a. Postrenal failure intrinsic failure failure) Damage to Damage results Damage to the kidneys results from tissue of from a problem something glomeruli or ABOVE the BELOW tubules kidneys kidneys Causes: Prerenal, Intrarenal, Postrenal Prerenal Causes o Is the result of impaired blood flow that leads to hypoperfusion of the kidney commonly caused by volume depletion (burns, hemorrhage, GI losses), hypotension (sepsis, shock), and obstruction of renal vessels, ultimately leading to a decrease in the GFR o Volume depletion o Hemorrhage, overuse of diuretics, excessive GI losses (vomiting, diarrhea), severe dehydration (common reason for older adults to have AKI) o Impaired cardiac function o Heart failure, MI, cardiogenic shock, valve disease, damage to renal artery o Vasodilation o Medications (antihypertensives), anaphylaxis, sepsis o Prerenal azotemia is treated by optimizing renal perfusion, whereas postrenal failure is treated by relieving the obstruction. Intrarenal Causes o Is the result of actual parenchymal damage to the glomeruli or kidney tubules. o Prolonged renal ischemia o Myoglobinuria (burns, massive trauma, injuries involving a large amount of muscle damage); hemoglobinuria o Nephrotoxic agents o Aminoglycosides antibiotics , NSAIDS, radiopaque contrast agents o Infection o Pyelonephritis, glomerulonephritis, etc. (e. coli, various bacteria, fungi, protozoan or viral causes) Intrarenal or intrinsic azotemia is treated with supportive therapy, with removal of causative agents, aggressive management of pre- and postrenal failure, and avoidance of associated risk factors. Intrarenal Failure o Acute tubular necrosis (ATN) (damage to the kidney tubules) is the most common intrinsic renal disorder o 30% of incidences are r/t to aminoglycosides / radiocontrast agents / chemotherapy drugs o 50% are related to ischemia from decreased perfusion o Potentially reversible o Characteristics of ATN are intratubular obstruction, tubular back leak (abnormal reabsorption of filtrate and decreased urine flow through the tubule), vasoconstriction, and changes in glomerular permeability. o Result in a decrease of GFR, progressive azotemia, and fluid and electrolyte imbalances. o CKD, diabetes, heart failure, hypertension, and cirrhosis can contribute to ATN. o Know renal function of patient before giving radiocontrast agents (if not good – should not have procedure) Postrenal Causes Usually results from obstruction distal to the kidney by conditions such as renal calculi, strictures, blood clots, benign prostatic hyperplasia, malignancies, and pregnancy. Pressure rises in the kidney tubules, and eventually the GFR decreases. Obstruction in flow of urine from ureters to external urethral opening Urolithiasis (stones), blood clots or stricture Tumors (prostate, ovarian or cervical or colon cancer) Bladder dysfunction Obstruction (benign prostatic hyperplasia, obstructed indwelling urinary catheter, ureteral obstructions) Trauma to bladder Obstructio ns to urine outflow Obstruction Pressures Increased pressure interfere with in kidney function structures Can’t filter or regulate wastes / fluids Tissue injury Hydronephrosis occurs Kidney Failure GFR decreases AKI may progress RIFLE classification Acute through phases: Risk (R) Kidney oliguric, diuretic, and recovery. Injury (I) Failure (F) Injury When a patient does not recover from Loss of function AKI, then CKD may (L) develop. End-stage renal The RIFLE classification disease (E) is used to describe the stages of AKI (Table 54- 2). Definitions to KNOW Oliguria: UOP < 400 mL/day Minimum amount of urine required to rid the body of waste products is 400 mL/day Anuria: UOP < 50 mL/day Uremia: excess of urea and other nitrogenous wastes in blood Azotemia – abnormal concentration of nitrogenous wastes in blood Diagnostics Requires a thorough history for risk factors UOP, specific gravity, osmolality Renal US/Scan, CT, MRI, biopsy Labs BUN (normal 8 – 20) CR (normal.7 – 1.4) CBC, electrolytes Calcium (normal 8.8-10.5) Metabolic ABG’s for acidosis __________________ Urinalysis First morning void Examine urine within 1 hour Urine Creatinine clearance Collect 24-hour urine specimen Studies (throw out 1st void) Creatinine clearance closely approximates GFR Urodynamics Study of storage and flow of urine thru urinary tract Radio-contrast induced nephropathy Hospital acquired Contrast-induced nephropathy Some contrast agents can result in nephrotoxic injury Major cause of hospital acquired ARF Identify patients at risk before procedures Baseline Cr > 2.0 mg/Dl = high risk Recommendations pre-procedure hydration may Radio- be considered Use of other diagnostic contrast procedures - ultrasound Client receiving metformin induced Should be held 48 hours prior and post procedure to nephropat decrease risk of lactic acidosis* hy Follow your institution’s policy. Guidelines and opinions vary Initiation Period Phase Initial insult Oliguric Phase s of Goal: support renal function, keep client stable until injury AKI / heals / resolves Diuretic Phase (2-3 L/day) Goals: maintain hydration, ARF prevention electrolyte imbalances, support renal function Recovery Oliguric Phase Injury or damage to kidneys is manifested in labs & patient presentation Most common initial manifestation is oliguria Occurs within 1-7 days after injury & last 10-14 days Urinalysis may show casts, RBCs, WBCs This period is accompanied by an increase in the serum concentration substances usually excreted by the kidneys Urea, creatinine, uric acid, organic acids, phosphorus, potassium, and magnesium The minimum amount of urine needed to rid the body of normal metabolic waste products is approximately 400 mL in 24 hours or 0.5 mL/kg/h over 6 hours In this phase, uremic symptoms first appear & life-threatening conditions such as hyperK develops Oliguric Phase: Clinical Manifestations Fluid overload Elevated BUN, Neuro Contributes to heart failure, pulmonary edema, CR symptoms Fatigue, difficulty concentrating, seizures, pericardial or pleural stupor, coma effusions Oliguric Phase: Clinical Manifestations Hypermagnesemia Kidneys cannot excrete magnesium Hypocalcemia: kidneys cannot produce the active component of vit D in order to absorb calcium through GI tract Hyperphosphatemia Low calcium = high phosphorus Oliguric Phase: Clinical Manifestations Progressive metabolic acidosis occurs in kidney disease because patients cannot eliminate the daily metabolic load of acid-type substances produced by the normal metabolic processes. In addition, normal renal buffering mechanisms fail. This is reflected by decreased serum carbon dioxide (CO2) and pH levels. Metabolic acidosis Impaired kidney cannot excrete hydrogen ions Serum bicarbonate decreases Existing levels depleted attempting to buffer acids Also production is affected Severe acidosis develops Kussmaul respirations Diuretic Phase: Clinical Manifestations The diuresis period is marked by a gradual increase in urine output, which signals that glomerular filtration has started to recover. Begin to see increases in UOP 1 to 3 L (can get up to 5 L / a day!) Glomerular filtration is recovering Improvement in ability to excrete wastes BUT – can’t concentrate urine Lab values begin to normalize Uremic symptoms may still be present The patient must be observed closely for dehydration during this phase; if dehydration occurs, the uremic symptoms are likely to increase, and an elevated serum BUN and creatinine will be noted. Diuretic Phase: Clinical Manifestations Volume may reach normal or elevated levels At risk for excess fluid loss WHY? Hyponatremia Monitor for: Hypokalemia Dehydration Recovery Phase The recovery period signals the improvement of renal function and may take 3 to 12 months. Laboratory values return to the patient’s normal level. However, in those patients with preexisting CKD, an episode of AKI may necessitate beginning CRRT. Lab values return to patient’s normal levels May have some reduction in GFR – usually not significant. Although a permanent 1% to 3% reduction in the GFR may occur, it is not clinically significant. Recovery can take several months (up to a year in some cases) Goals: patient education, follow up, preventive measures If don’t make it to recovery phase will go into chronic kidney disease Complications Metabolic acidosis Kidneys’ inability to excrete hydrogen ions Loss of renal bicarbonate buffering capabilities Electrolyte imbalances CHF, pulmonary edema, hypertension Due to: Retention of sodium and water; activation of the renin- angiotensin system, fluid therapy Prevention of AKI/ARF Treat Adequate Prevent / treat hypotension hydration shock promptly promptly Meticulous Monitor use of Prevent / treat urine catheter toxic infections care! medications / promptly Remove as soon dosages as possible! Medical Management Objectives of treatment for AKI: restore normal chemical balance and prevent complications until repair of renal tissue and restoration of renal function can occur. Correcting precipitating events Management includes eliminating the underlying cause; maintaining fluid balance; avoiding fluid excesses; and, when indicated, providing RRT. Support Body systems Because pulmonary edema may be caused by excessive administration of parenteral fluids, extreme caution must be used to prevent fluid overload. Fluid excesses can be detected by the clinical findings of dyspnea, tachycardia, and distended neck veins, moist crackles. Prevention or treatment of complications Restoring blood flow to kidneys (fluids, transfusions, albumin infusions) Maintenance of fluid balance is based on daily body weight, serial measurements of central venous pressure, serum and urine concentrations, fluid intake and output, blood pressure, and the clinical status of the patient. Adequate renal blood flow in patients with prerenal causes of AKI may be restored by IV fluids or transfusions of blood products. If AKI is caused by hypovolemia secondary to hypoproteinemia, an infusion of albumin may be prescribed. Dialysis may be initiated to prevent complications of AKI, such as hyperkalemia, metabolic acidosis, pericarditis, and pulmonary edema. Dosages of medications eliminated through kidneys must be adjusted Nutritional Therapy Maintain adequate caloric intake Primarily carbohydrates and fat Caloric requirements are met with high-carbohydrate meals because carbohydrates have a protein-sparing effect (so in a high carb diet, protein is not used for meeting energy requirements but is spared for growth and tissue healing Limited protein Restrict sodium Foods and fluids containing sodium, potassium, or phosphorus (e.g., bananas, citrus fruits and juices, dairy foods) are restricted. Increase dietary fat Enteral nutrition Nursing Management Physical (cardiopulmonary, renal and overall hemodynamic status) Focused Previous renal problem history Recent use of nephrotoxic substances Renal Recent exposure to heavy metals or organic solvents Assessme Hypotensive episode of > 25 minutes nt Tumors or clots in renal area Presence of infection Mental status/level of consciousness Oral mucosa (dryness, inflammation) Nursing Lung sounds Assessme Heart rhythm (ECG, nt dysrhythmias) Laboratory values Diagnostic test results Pulmonary Cardiac Nursing Patient should be Assess for signs of Assessme assisted to turn, cough, and take deep breaths decreased cardiac frequently to prevent output nt atelectasis & respiratory tract infections Auscultate heart Assess for signs of sounds for presence of third heart sound circulatory overload. (could indicate heart Decreased urine output, JVD, restlessness, failure) shortness of breath Nursing Diagnoses and Collaborative Problem Activity Intolerance Excess fluid Risk for High risk for infection volume infection Asepsis is essential with invasive lines and catheters to minimize the risk of infection and increased metabolism. High Risk for Injury Fatigue Anxiety High Risk for Altered Mucous Membranes High Risk for Altered Skin Integrity Potential Pain Ineffective complicatio tissue n: Anxiety perfusion dysrhythmi Knowledge Deficit a Nursing Interventions Monitor fluid / electrolytes Monitor heart rhythms, serum I’s and O’s (include all emesis, electrolytes – ECG changes (tall, drainage, stools) tented, or peaked T waves) Lab values S/sx of hyperkalemia (cardiac* and Monitor s/sx metabolic acidosis musculoskeletal systems) (confused, restless, fatigue, heart (potassium value greater than 5.0 mEq/L [5 racing) mmol/L]) Sx of hyperkalemia: irritability, abdominal If peripheral edema is present, cramping, diarrhea, paresthesia, and generalized muscle weakness. move the patient gently and Muscle weakness may present as slurred reposition often. speech, difficulty breathing, paresthesia, and paralysis. As the potassium level increases, both cardiac and other muscular function declines, making this a medical emergency. Weigh daily Fluid excess findings: dyspnea, tachycardia, distended neck veins, lung crackles, generalized edema Nursing Interventions Give oral and IV fluids as Client may require renal prescribed BUT administer IV replacement therapy if medications in least amount of fluid possible. indicated. Administer medications (e.g., Therapy clears the body of diuretics) as prescribed. excess fluid and waste Diuretic therapy requires products. close supervision because Renal replacement therapy reduced blood volume can may be needed to clear result in inadequate renal perfusion. solutes, and dehydration should be treated. Nursing Interventions: Hyperkalemia If the patient is experiencing ECG changes, IV dextrose 50%, insulin, and calcium replacement may be given to shift potassium back into the cells. Glucose and/or insulin drip Insulin shifts potassium back into the cells Glucose given to prevent hypoglycemia Sodium bicarbonate Treat acidosis & hyperkalemia Promotes a shift of potassium INTO cells and out of vascular Eventually the potassium will move out of cell again – The shift of potassium into the intracellular space is temporary, so arrangements for dialysis need to be made on an emergent basis. Nursing Interventions: Hyperkalemia Calcium carbonate Increases the threshold at which lethal rhythms occur Temporarily stabilizes myocardium Sodium polystyrene sulfonate (Kayexalate) Binds to potassium and is excreted through feces Given via retention enema Place rectal tube after (inflate balloon – 30 cc) Cleansing enema after rectal tube removed to help decrease impaction risk Don’t give if patient has no active bowel sounds Treatment Options for Renal Failure Hemodialysis – a procedure that circulates the patient’s blood through an artificial kidney [dialyzer] to remove waste products and excess fluid Peritoneal dialysis – a procedure that uses the patient’s peritoneal membrane (the lining of the peritoneal cavity) as the semipermeable membrane to exchange fluid and solutes Continuous renal replacement therapies (CRRT) – methods used to replace normal kidney function by circulating the patient’s blood through a hemofilter Renal Replacement Therapy (RRT) Alternative or adjunctive method for treating ARF Means by which uremic toxins & fluids are removed Acis-base status/electrolytes adjusted slowly & continuously Indications Volume overload Elevated serum potassium level Metabolic acidosis BUN level > 120 mg/dL (43 mmol/L) Significant change in mental status Pericarditis, pericardial effusion, or cardiac tamponade Evaluation The expected outcomes are that the patient with AKI will Regain and maintain normal fluid and electrolyte balance Adhere to the treatment regimen Experience no complications Have complete recovery Health Promotion Identify & monitor populations at high risk Control exposure to nephrotoxic drugs & industrial chemicals Prevent prolonged episodes of hypotension & hypovolemia Measure daily weight Monitor intake and output Monitor electrolyte balance Replace significant fluid losses Provide aggressive diuretic therapy for fluid overload Use nephrotoxic drugs sparingly Chapter 49 Urolithiasis and Nephrolithiasis Urolithiasis and Nephrolithiasis Refers to calculi (stones) in the urinary tract or kidney Pathophysiology: Stones are formed in the urinary tract when urinary concentrations of substances such as calcium oxalate, calcium phosphate, and uric acid increase. Stones may be found anywhere from the kidney to the bladder and may vary in size from minute granular deposits, called sand or gravel, to bladder stones as large as an orange. Causes: may be unknown Depends on location and presence of obstruction or infection Pain and hematuria Diagnosis non-contrast CT scan Blood chemistries and a 24-hour urine test for measurement of calcium, uric acid, creatinine, sodium, pH, and total volume Stone analysis – when stones are recovered, chemical analysis is carried out to determine their composition. (can provide a clear indication of the underlying disorder) Will strain all urine and save stones Potential Sites of Urinary Calculi Medical management Urolithiasis and Nephrolith Goals: eradicate the stone, determine the stone type, prevent nephron destruction, control infection, and relieve any obstruction that may be present. The immediate objective of treatment of renal or ureteral colic is to relieve the pain until its cause can be eliminated. Unless the patient is vomiting or has heart failure or any other condition requiring fluid restriction, fluids are encouraged. Increases the hydrostatic pressure behind the stone, assisting it in its downward passage. A high, around-the-clock fluid intake reduces the concentration of urinary crystalloids, dilutes the urine, and ensures a high urine output. Nutritional therapy Calcium stones – Liberal fluid intake is encouraged. Medications such as ammonium chloride may be used, therapy with thiazide diuretics may be beneficial in reducing the calcium loss in the urine and lowering the elevated parathormone levels. Uric acid stones – patient is placed on a low-purine diet to reduce the excretion of uric acid in the urine. Foods high in purine (shellfish, anchovies, asparagus, mushrooms, and organ meats) are avoided, and other proteins may be limited. Allopurinol may be prescribed to reduce serum uric acid levels and urinary uric acid excretion, and to dissolve or reduce the size of existing stones Cystine stones (decrease protein, want value less than 6/7)- Low-protein diet may be prescribed Oxalate stones (increase fluid intake, decrease foods high in oxalate) – dilute urine is maintained through increasing fluid intake, and the intake of oxalate is limited. Many foods contain oxalate including spinach, Swiss chard, chocolate, peanuts, and pecans Urolithiasis and Nephrolithiasis Interventional Procedures Ureteroscopy Extracorporeal shock wave lithotripsy Percutaneous stone removal (considered surgical) Surgical Management: may be indicated if the stone does not respond to other forms of treatment. It may also be performed to correct anatomic abnormalities within the kidney to improve urinary drainage. Nephrolithotomy: performed if stones are within the kidney (incision into the kidney with removal of the stone) Urterolithotomy: removes stones in the ureter Cystotomy: removes stones in bladder are Pyelolithotomy: removes stones in the kidney pelvis Nephrectomy: performed if the kidney is nonfunctional secondary to infection or hydronephrosis. Ureteroscopy Involves first visualizing the stone and then destroying it. Access to the stone is accomplished by inserting a ureteroscope into the urethra up to ureter and then inserting a laser, electrohydraulic lithotripter, or ultrasound device through the ureteroscope to fragment and remove the stones. A stent may be inserted and left in place for 48 hours or more after the procedure to keep the ureter patent Can expect hematuria (pink tinged urine) due to broken up stones – patient will pass stone causing Extracorporeal Shock Water Lithotripsy o Noninvasive procedure used to break up stones in the calyx of the kidney. o Use shock waves to break up stone, after stones broken up patient must pass stone – will see hematuria – watch out for infection – may have bruising in area o When the shock wave encounters a substance of different intensity (a renal calculus), a compression wave causes the surface of the stone to fragment. o Repeated shock waves focused on the stone eventually reduce it to many small pieces that are excreted in the urine. o The patient is observed for obstruction and infection resulting from blockage of the urinary tract by stone fragments. o All urine is strained after the procedure; voided gravel or sand is sent to the laboratory for chemical analysis. o Discomfort from the multiple shocks may occur, although the shock waves usually do not cause damage to other tissue. o May need multiple treatments to ensure disintegration of stones. Percutaneous Nephrolithotomy oNephroscope is introduced through a percutaneous route into the renal parenchyma. oDepending on its size, the stone may be extracted with forceps or by a stone retrieval basket. oIf the stone is too large to initially be removed, an ultrasound probe inserted through a nephrostomy tube is used to pulverize the stone. oSmall stone fragments and stone dust are then removed. oPuncture skin near stone area, place probe with Patient Education for Renal Calculi Signs and symptoms to report: fever, chills, flank pain, hematuria, decreased urine volume, bloody or cloudy urine, and pain Follow-up care Urine pH monitoring Measures to prevent recurrent stones Importance of fluid intake: The patient is encouraged to follow a regimen to avoid further stone formation, including maintaining a high fluid intake because stones form more readily in concentrated urine. A patient who has shown a tendency to form stones should drink enough fluid to excrete greater than 2000 mL (preferably 3000 to 4000 mL) of urine every 24 hours Dietary education Medication education as needed (opioids in hospital, NSAIDs for home) Opioid analgesic agents may be prescribed and given to provide rapid relief along with an IV NSAID. Preventing renal calculi – Chart 49-11 Nursing Interventions Assess Increase fluid intake encouraged to prevent dehydration and increase Pain hydrostatic pressure within the urinary tract to promote passage of the stone. n/v/d If the patient cannot take adequate fluids Abd Distention orally, IV fluids are prescribed. The total urine output and patterns of UTI – urgency, chills, fever voiding are monitored. Monitor vital signs (temperature) Ambulation is encouraged as a means of moving the stone through the urinary tract. Obstruction Monitor I/O Renal calculi increase the risk of Monitor for infection infection, sepsis, & obstruction Strain urine to determine the Sudden increase in pain type of calculi the patient has VS formed Patient education Objectives 1. Discuss the etiology of common burn injuries. 2. Describe prehospital care for the client with burn injuries. 3. Describe factors that affect the severity of a burn and the potential for recovery. 4. Discuss the classification system related to the depth of burn injury for the client with burn injuries. 5. Demonstrate how to calculate: a. The extent of total body surface area (TBSA) involved b. Fluid replacement requirements during the emergent/resuscitative phase (Parkland Formula) 6. Describe gerontological considerations in the care of the older adult with burn injuries. 7. Describe emergent / resuscitative care for adult client with burn injuries. 8. Describe the potential complications for the emergent / resuscitative phase of burn recovery. 9. Describe the acute / rehabilitative care for adult clients with burn injuries. Care of the Adult Client with a Burn Injury N460 Adult Health II Chapter 57: Management of patients with burn injuries Lisa Hosey MSN RN What is a burn? Why is knowing about burns important? Type​​ Cause​​ Special Considerations​​ Thermal​​ Superficial heat , hot liquid splashes Severity (depends on temp of burning agent that you encountered) Chemical​​ Toxic substances, bleach, gas, paint Direct contact with the skin with the thinner causative agent Flush exposed area with clean tepid water Radiation​​ Chemotherapy patients, fluoroscopy, Damage to epidermal cell and DNA sunburn Inhalation​​ Inhaling smoke Damage to respiratory system, carbon monoxide poisoning – travels faster than oxygen (binds to RBCs cause carbon hypoxemia) Cold​​ Frost bite Monitor temp for hypothermia, temp less than 95 F causes vasoconstriction, which increases tissue ischemia & necrosis Electrical​​ Direct contact with voltage – current Severity may not be indicated by outer passes through body causing internal appearance, causes release of Burn Classifications / Burn Depth Burns are classified according to depth of tissue destruction Superficial – 1st degree Partial thickness – 2nd degree Full thickness – 3rd degree Full thickness that includes fat, fascia, muscle, and / or bone – 4th degree *** Graphic Images Ahead *** First-degree burns are superficial injuries that involve only the outermost layer of skin. These burns are painful and erythematous, but the epidermis is intact If rubbed, the burned tissue does not separate from the underlying dermis. (known as a negative Nikolsky’s sign.) A typical first-degree burn is a sunburn or superficial scald burn. Superficial 1st Degree Burns Partial Thickness 2nd Degree Burns Second-degree (partial-thickness) burns involve the entire epidermis and varying portions of the dermis. They are painful and typically associated with blister formation. Healing time depends on the depth of dermal injury, typically ranging from 2 to 3 weeks. Hair follicles and skin appendages remain intact. The wound bed is moist due to serous leakage from the peripheral microcirculation. Full Thickness 3rd Third-degree Degree Burns burns involve total destruction (full-thickness) of the epidermis, dermis, and, in some cases, damage of underlying tissue. Wound color ranges widely from pale white to red, brown, or charred. The deeply burned area lacks sensation because the nerve fibers are damaged. The wound appears leathery and dry due to the destruction of the microcirculation. Skin organelles such as hair follicles and sweat glands may be affected. The severity of this burn is often deceiving to patients because they have no pain in the injury area 4th Fourth-degree burns (deep burn necrosis) Degree are those injuries that extend into deep tissue, muscle, or bone Burns Includes fat, fascia, muscle, and / or bone Practice Time! The nurse is caring for a client with a large burned area on the right arm. The area appears pink, has blisters, and is very painful. How will the nurse categorize this injury? A. Full thickness B. Superficial C. Partial thickness D. Full thickness deep Practice Time! The nurse is caring for a client that experienced an electrical burn of both lower extremities. What is the priority assessment? A. ROM of lower extremities B. Heart rate & rhythm C. Respiratory rate & 02 saturation D. Orientation & LOC Rule of Nines Rule of nines – most common method, based on dividing anatomic regions, each representing approximately 9% of the TBSA – Total Body Surface Area TBSA Practice Anterior chest / abdomen 18% Left arm 9% Left leg 18% TBSA 45% TBSA Practice Anterior & posterior chest/abdomen 36% Anterior Left Arm 4.5% Anterior Left leg 9% TBSA = 49.5% Fluid Resuscitation To facilitate fluid administration, peripheral IV access may be obtained initially In larger burns, central venous access is recommended due to the large volumes required. Large amounts of fluid replacement may be required in short period of time Replacement volume is calculated based on affected TBSA and patient's body weight Most commonly used fluid replacement: Lactated ringers (crystalloid solution) – is the crystalloid of choice because its pH and osmolality most closely resemble human plasma. Urine output Thermal & Chemical injuries: urine output of 0.5 to 1 mL/kg/h in adults indicates appropriate resuscitation Electrical injuries: urine output of 75 to 100 mL/h is desired Daily weights and trends in laboratory test results require close monitoring in the immediate postburn (resuscitation) period to monitor This Photo by Unknown author is licensed under CC BY-SA. fluid status. The Parkland Formula Used to calculate total volume of fluid replacement in 1st 24 hours after 2nd & 3rd degree burns 2 ml to 4 ml weight in kilograms TBSA burned = TOTAL amount of fluid needed in 1st 24 hours after burn How do you administer? – IV Parkland Formula Practice #1 Burn injury occurred at 8:00 a.m. Patient admitted to hospital at 10:00 a.m. When would the first 8-hour period end? 4:00pm #2 TBSA involved 40% Weight 60 kg Calculate 2 ml and 4 ml rates Parkland Formula Practice #3 At 2 ml, how much fluids would be administered in the first 8 hours? ________ Remember, the burn occurred at 8:00 a.m. and patient was admitted at 10:00 a.m. How many hours are left to infuse fluids? ____________ How many ml / hr would you set the IV pump? __________ How would you calculate the remaining fluids over the next 16 hours? ______________ Facial Edema Before & After Fluid Resuscitatio n Fluid Resuscitation Care / Interventions What type of IV is needed? 15% - Large bore (maybe 2) – greater than 30% TBSA need a central line What type of fluids? Based on size & depth of wound , lactated ringer Strict monitoring of urine output – what is best method? Foley An indwelling catheter is inserted to allow accurate monitoring of urine output & fluid needs while also providing a measure of kidney function for patients with moderate to severe burns What are frequent nursing assessments? Cardiac, respiratory, I/Os, temperature, electrolytes, BUN, Creatinine, total protein, albumin Monitor for symptoms of fluid overload – Edema in places with no burns , daily weights, SOB, crackles, dyspnea, tachycardia, third spacing – fluid moving to abnormal levels Are diuretics beneficial for fluid volume overload? Why or why not? No If burn exceeds 20-25% TBSA, a NG tube is inserted & connected to low/intermittent suction All patients who are intubated should have a NG tube in place to decompress the stomach & prevent vomiting & aspiration The patients' temp is monitored because hypothermia may develop rapidly A temp superficial thickness The burn injury itself produces systemic release of cytokines and other substances that cause leukocyte and endothelial cell dysfunction. Skin disruptions/ impaired skin integrity – skin is the largest barrier to infection Integumentary losses cause inabilities to regulate body temperature leading to hypothermia Patients with burns often experience low body temps in the early hours after injury from the amount of TBSA involved, the IV resuscitation fluids administered, and exposure resulting in increased evaporative heat loss Increases risk for infection Practice Time A client asks the nurse why they are experiencing so much edema after sustaining a burn. How should the nurse respond? A. "Fluid shifts occur from an increased amount of circulating whole blood." B. "Fluid shifts occur from an increase in intravascular plasma amounts." C. "Fluid shifts occur from an increase in permeability of capillary walls." D. "Fluid shifts occur from an increase in permeability of kidney tubules." Acute & Rehabilitative Phases of Burn Care Phases of burn management Acute / Intermediate (wound healing) Beginning of diuresis to near completion of wound closure Rehabilitative (restorative) Major wound closure to return to individual’s optimal level Acute Phase Begins 48 – 72 hours after injury Priorities Prevention or treatment of complications Pain management Early positioning / mobility Nutritional support Wound care & closure Potential Complications Pulmonary: pneumonia, respiratory failure, airway obstruction caused by upper airway edema Late pulmonary complications secondary to inhalation injuries include mucosal sloughing of the airway and cast formation from cellular debris, which can lead to obstruction, increased secretions, inflammation, atelectasis, airway ulceration, pulmonary edema, and tissue hypoxia. Ventilator-associated pneumonia (VAP) is a common complication of any patient who is hospitalized and mechanically ventilated and is particularly exacerbated in the patient with an inhalation injury. Cardiovascular, Renal & Fluid Imbalances: overload, HF Gastrointestinal: diarrhea, ileus, constipation (opioids) Neurologic system: stress, hyponatremia, sleep disturbances, confusion/delirium Musculoskeletal system: decreased ROM, contractures, muscle loss Potential Complications: Endocrine Increased blood glucose levels Due to stress-mediated cortisol and catecholamine release Hyperglycemia may also be caused by the increased caloric intake necessary to meet metabolic requirements Treat with IV or subcutaneous insulin, do not decrease feeding Check blood glucose levels frequently What is an acceptable blood glucose level? < 180 Potential Complications: Infection Leading cause of death Partial-thickness burns can change to full-thickness wounds in the presence of infection Watch for signs and symptoms: systemic & local How do you know?? Infected wound with colony count of 105 (life threatening even with ABX therapy – may need surgical excision) If sepsis suspected: cultures are obtained from where? Broad spectrum antibiotics & Tetanus Aminoglycosides Cephalosporins Pain Control Pharmacologic treatment for the management of burn pain includes the use of opioids, nonsteroidal anti-inflammatory drugs, anxiolytics, and anesthetic agents Frequent assessment of pain is required, and analgesic and anxiolytic medications are administered as prescribed. To increase its effectiveness, analgesic medication is provided before the pain becomes severe. Continuous background pain IV infusion of an opioid Or slow release, twice a day oral opioid Treatment induced wound care/dressing changes Analgesics (prior to treatment) Anxiolytics Nonpharmacologic therapies include relaxation techniques, distraction, guided imagery, hypnosis, therapeutic touch, humor, music therapy, and virtual reality techniques. Nutrition o Daily weights o Alert to trends, especially losses of 10% or more o Evaluate & modify diet plan o Enteral feedings o When are enteral feedings started? Within 4 hours of given fluid resuscitation o What are the benefits of enteral feedings? Increase gut motility o When is TPN used? Present GI motility issue o When client begins oral nutrition o Assess preferences o Feed at client’s schedule o May continue with frequent high calorie/ high protein supplemental feedings o If caloric goals cannot be met by oral feeding, a feeding tube is inserted and used for continuous or bolus feedings of specific formulas. o The volume of residual gastric secretions should be checked periodically to ensure absorption. o The patient should be weighed each day and the results tracked to properly assess appropriate weight parameters and to attenuate catabolism of lean muscle mass. Positioning Flexibility Deep breathing, turning, and proper positioning are essential Both passive and active range-of-motion nursing practices that prevent atelectasis and pneumonia, control edema, and prevent pressure injuries and exercises are initiated from the day of contractures. admission and are continued after grafting Specialty beds may be useful, and early mobility is strongly within prescribed limitations. encouraged Splints or functional devices applied to the If the lower extremities are burned, elastic pressure extremities may lessen contractures through bandages should be applied before the patient is placed in an upright position to promote venous return and minimize compression and stretch. edema formation. The nurse monitors the splinted areas Head / neck: position of hyperextension for signs of vascular insufficiency, nerve No pillow; use towel roll under neck or shoulder compression, and skin breakdown. Elbow: position of extension & supination Active ROM Keep joint in extended position at least 3 times a day Ankle: position of dorsiflexion Padded footboard; heels free of pressure Assist with Passive ROM where needed Legs: position of abduction (15-20) Hands: Small pillow between legs Perform exercises for hand, thumb and fingers every hour while awake Gloves during any & all contact with open wounds Cross-contamination Change gloves when handling wounds on different areas Change gloves between old and new dressings Wound Care Topical Medications Silver sulfadiazine (Silvadene, Flamazine) Mafenide acetate (Sulfamylon) Silver Nitrate Do not apply to freshly grafted area Inhibits cell growth Wound Care: Goal of care is to remove non-viable Cleaning ofwound tissue and woundsexudate, – mild soaps agents and previously applied topical Ranges from gentle cleaning with mild soap and water to use of shower carts / tubs Hydrotherapy (1 to 2 times daily) Cleanses wounds, allows visualization of burns and tissue Immersion in tub or showering on a specially designed shower table Washing small areas at bedside During treatment Assess for signs of additional StudyPK (2021) skin breakdown, infection, hypothermia Wait 24 hours before Dressings Standard Biologic Multiple layers of gauze Human tissue applied over topical agents on wound Promotes healing; helps # layers – r/t depth, amount of prepare for a permanent drainage expected, area, client’s skin graft mobility, frequency of dressing Homograft (human skin – fresh changes or frozen from cadaver) Held in place with roll-type Heterograft (another species; gauze bandages (Kerlix) pig skin most common / Distal to proximal direction compatible with human skin) Elastic wraps cover arms / legs Debridement Mechanical Surgical tools used to separate and remove eschar Done with daily dressing changes Wet to dry dressings are not advised because they can remove viable epithelial cells along with necrotic tissue. Wet to wet or wet to moist dressings may be used instead Natural (autolysis) Devitalized tissue separates from underlying viable tissue spontaneously Bacteria present at the interface of the burned tissue & healthy viable tissue gradually liquefy the collagen that holds eschar in place May take weeks to months Surgical Occurs before the natural separation of eschar transpires from bacterial lysis of collagen fibers at the dermal–eschar junction. This may be performed as soon as possible after the burn, once the patient is hemodynamically stable and edema has decreased Remove devitalized tissue & early burn wound closure (increases survival rates) Covered with skin graft if necessary and dressing The use of surgical excision carries with it risks and complications, especially with large burns. The procedure creates a high risk of extensive blood loss with lengthy operating and anesthesia times. Wound Graftin Placed on clean granulated bed that has been surgically excised to promote healthy growth Autografts – use patient's own skin & are not rejected by immune system They can be split-thickness, full-thickness, or epithelial grafts. Because the donor site (the area from which skin is taken to provide the autograft) for a full-thickness graft includes both the epidermis and dermis, its use must be cautiously considered because the donor site cannot heal spontaneously. Sheet grafts or mesh grafts Split-thickness autografts are most used and can be applied in sheets or they can be expanded by meshing so that they cover more than a given donor site area. Skin meshers enable the surgeon to cut tiny slits into a sheet of donor skin, help to expand, covering larger areas with smaller amounts of donor skin. Any kind of graft other than a sheet graft contributes to scar formation as it heals. The use of widely meshed (largely expanded) grafts may be necessary in large wounds but should be viewed as a compromise in terms of cosmesis. Homograft (allograft) - recently deceased or living human other than patient – intended as temporary wound coverage Xenograft (heterograft) - animal skin – temporary wound coverage – immune response will eventually reject ^< Graft site – 1st change done 3-5 days after surgery – look for signs of bleeding and infection Occlusive dressings in bulky gauze wraps to support humid environment Splints may be used Elevate site to reduce edema Donor site hemostatic agent such as thrombin or epinephrine may be applied directly to the donor site to promote hemostasis. Typically a Partial thickness wound so usually painful Heals spontaneously in 7 – 14 days normally with proper care MedScape (2021) Practice Time! The nurse has an order to administer Morphine Sulfate to a client experiencing pain that was admitted for extensive burns. What route would the nurse administer the medication? A. Oral B. Intravascular C. Intramuscular D. NG tube Practice Time! What are appropriate nursing interventions when providing burn wound care & dressing changes? Select all that apply. A. Change gloves between old & new dressings B. Apply silver nitrate to graft site C. Wrap roll-type dressings distal to proximal D. Wear 1 pair of sterile gloves for all burn wounds E. Medicate patient after wound care for pain control Rehabilitation Phase: Rehabilitation begins immediately after the burn has occurred and often extends for years after the initial injury. Goals for client: Work toward resuming a functional role in society Rehabilitation for any functional and cosmetic post burn reconstructive surgery that might be necessary. The ultimate goal is to return patients to the highest level of function possible within the context of their injuries. Newly healed areas can be hypersensitive or hyposensitive to cold, heat and touch Skin may never completely regain its original color due to destruction of melanocytes Scar contour elevates and enlarges; What's flaking occurs as old epithelium is replaced Happening Client experiences discomfort due to itching Discoloration of scar fades with time Contractures may occur Post-traumatic stress disorder Severe depression Psychosocia Dealing with reaction of others to sight of l healing wounds & scars Adjustment Visits from friends; short public appearances / before discharge can help to begin adjusting Community programs Teaching Proper use of prosthetic / positioning devices / splints Correct application and care of pressure garments Comfort measures to reduce pruritus Follow-up appointments

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