NCM 118 Finals Lecture on Acute Renal Failure PDF

NCM 118 FINALS LECTURE CLINICAL MANIFESTATIONS ACUTE RENAL FAILURE  A syndrome of varying causation that results in a 1. PRERENAL sudden decline in renal function... It is frequently...

NCM 118 FINALS LECTURE CLINICAL MANIFESTATIONS ACUTE RENAL FAILURE  A syndrome of varying causation that results in a 1. PRERENAL sudden decline in renal function... It is frequently  Decreased tissue turgor associated with an increase in BUN and creatinine,  Dryness of mucous membranes oliguria (less than 500 mL urine/24 hours),  Weight loss hyperkalemia, and sodium retention.  Hypotension  Results in retention of toxins, fluids, and end products  Oliguria or anuria of metabolism  Flat neck veins  Usually reversible with medical treatment.  Tachycardia  Also called ACUTE KIDNEY INJURY. 2. INTRARENAL ETIOLOGY Edema usually present PRERENAL 3. POSTRENAL -result from conditions that decrease renal blood flow such  Obstruction to urine flow as:Hypovolemia, shock, blood loss, embolism, burns,  Obstructive symptoms of BPH (Benign Prostatic cardiovascular disorders, sepsis Hyperplasia or Hypertrophy)  Possible nephrolithiasis INTRARENAL - result from injury to renal tissue and are usually 4. CHANGES IN URINE VOLUME AND SERUM associated with: Nephrotoxic agents, infections, ischemia CONCENTRATIONS OF BUN, CREATININE, and blockages,polycystic kidney disease POTASSIUM POSTRENAL SUBJECTIVE SYMPTOMS - arise from obstruction or disruption to urine flow  Nausea anywhere along the urinary tract.  Loss of appetite Stones, blood clots, BPH, urethral edema from invasive  Headache procedures.  Lethargy  Tingling in extremities OTHER MAJOR CAUSES  Vascular Disease OBJECTIVE SYMPTOMS  Glomerular Disease  Diuretic phase  Interstitial/Tubular Disease  Increased UOP  Obstructive Uropathy  Gradual decline in BUN and creatinine  Hypokalemia CLINICAL COURSE  Hyponaturmia  Tachycardia ONSET: begins when the kidney is injured and lasts from  Improved LOC hours to days. DIAGNOSTIC EVALUATION OLIGURIC-ANURIC PHASE:  Urinalysis- reveals proteinuria, hematuria, casts (urine volume less than 400 to 500 mL /24 hours).  Rising serum creatinine and BUN levels a) Accompanied by rise in serum concentration of  Urine chemistry examinations to distinguish various elements usually excreted by kidney (urea, creatinine, forms of acute renal failure; decreased sodium organic acids, and intracellular cations- potassium  Renal Ultrasonography- for estimate of renal and magnesium). size and to exclude a treatable obstructive uropathy b) There can be a decrease in renal function with increasing nitrogen retention even when the patient is excreting more than 2-3 L of urine daily- called non- PATHOPHYSIOLOGY oliguric or high-output renal failure. Prerenal, Intrarenal, Post renal causes ↓ DIURETIC PHASE: Hypoperfusion of the kidneys begins when the 24-hour urine volume exceeds 500 mL ↓ and ends when the BUN and serum creatinine levels stop Alteration in kidney function rising. ↓ Decreased glomerular filtration rate ↓ RECOVERY PHASE: Retention of fluids and urinary sediments a. Usually lasts several months to 1 year. ↓ b. Probably some scar tissue remains, but the functional Increase in serum concentration of renal substances loss is not always clinically significant. ↓ Kidney damage Transcribed by: Taño, Sirilan & Yu BSN 4-J 1 TREATED 8. Pay special attention to draining wounds, burns,  Restricted diet and fluid intake which can lead to dehydration and sepsis and  Medications and careful monitoring progressive renal damage. ↓ 9. Avoid infection; give meticulous care to patients with Recovery of kidney and return of normal filtering Function indwelling catheter or I.V.lines. ↓ Wellness CORRECTIVE AND SUPPORTIVE MEASURES 1. Corrective reversible cause of acute renal failure (e.g, UNTREATED improve renal perfusion, maximize cardiac output, surgical relief of obstruction). - Progressive renal failure 2. Be alert for and correct underlying fluid excesses or - Coma deficits - Death 3. Correct and control biochemical imbalances- treatment of hyperkalemia. NURSING ASSESSMENT 4. Restore and maintain blood pressure. 1. Determine if there is a history of cardiac disease, 5. Maintain nutrition. malignancy, sepsis, or intercurrent illness. 2. Determine if patient has been exposed to potentially COMPLICATIONS nephrotoxic drugs (antibiotic, NSAIDs, contrast  Infection agents, solvents).  Arrhythmias due to hyperkalemia 3. Conduct ongoing physical examination for tissue  Electrolyte (sodium, potassium, calcium, phosphorus) turgor, pallor, alteration in mucous membranes, blood  abnormalities pressure, heart rate changes, pulmonary edema, and  Gl Bleeding due to stress ulcers peripheral edema.  Multiple organ systems failure 4. Monitor intake and output. NURSING INTERVENTIONS NURSING DIAGNOSIS  Excessive Fluid Volume related to decreased glomerular filtration rate and sodium retention ACHIEVING FLUID AND ELECTROLYTE  Risk for infection related to alterations in immune BALANCE system and host defenses  Monitor for signs and symptoms of hypovolemia or  Imbalanced Nutrition: Less Than Body hypervolemia  Requirements related to catabolic state, anorexia,  Monitor urinary output and urine specific gravity; and malnutrition associated with acute renal failure. measure and record intake and output including urine,  Risk for Injury related to Gl Bleeding gastric suction, stools, wound drainage, perspiration.  Disturbed Thought Processes related to the effects of  Monitor serum and urine specific concentrations. uremic toxins on the central nervous system (CNS).  Weigh patient daily to provide an index of fluid balance; expected weight loss is ½ to 1 lb (0.25 - 0.5 MEDICAL MANAGEMENT kg) daily.  Fluid and dietary restrictions  Adjust fluid intake to avoid volume overload and  Maintain Electrolytes dehydration.  May need dialysis to jump start renal function  Evaluate for signs and symptoms of hyperkalemia  May need to stimulate production of urine with IV and monitor serum potassium levels. (Notify health fluids, Dopamine, diuretics, etc. care provider of value above 5.5mg/L)  Watch for cardiac arrhythmia and heart failure from hyperkalemia, electrolyte imbalance, or fluid overload. MANAGEMENT Have resuscitation equipment on hand in case of cardiac arrest. PREVENTIVE MEASURES  Instruct patient about the importance of following 1. Identify patients with preexisting renal disease.Initiate prescribed diet, avoiding foods high in potassium. adequate hydration before, during, and after any  Administer blood transfusions during dialysis to procedure requiring NPO status. prevent hyperkalemia from stored blood. 2. Avoid exposure to nephrotoxins. Be aware that the majority of drugs or their metabolites are excreted by PREVENTING INFECTION the kidneys.  Monitor for all signs of infection. Be aware that renal *DRUG ALERT: Nonsteroidal anti-inflammatory failure patients do not always demonstrate fever and drugs(NSAID's) including COX-2 inhibitors, may reduce leukocytosis. glomerular filtration rate in people at risk for renal  Remove bladder catheter as soon as possible; insufficiency, causing renal failure. monitor for UTI. 3. Monitor chronic analgesic use-some drugs may  If antibiotics are administered, care must be taken to cause interstitial nephritis and papillary necrosis. adjust the dosage for renal impairment. 4. Prevent and treat shock with blood and fluid replacement. PREVENTING GI BLEEDING 5. Prevent long periods of hypotension.  Examine all stools and emesis for gross and occult 6. Monitor urinary output and CVP hourly in critically ill blood. patients to detect onset of renal failure at the earliest  Administer H2-receptor antagonist, such as moment. cemetidine (Tegamet) or ranitidine (Zantac), or 7. Schedule diagnostic studies requiring dehydration so nonaluminum or magnesium antacids as prophylaxis there are "rest days", especially in aged who may not for gastric stress ulcers. have adequate renal reserve.  Prepare for endoscopy when Gl bleeding occurs. Transcribed by: Taño, Sirilan & Yu BSN 4-J 2 MAINTAINING ADEQUATE NUTRITION PERITONEAL DIALYSIS HEMODIALYSIS No vascular access & heparin Requires vascular access and  Work collaboratively with dietitian to regulate protein (except placement heparin intake according to impaired renal function. peritoneal catheter)  Offer high carbohydrate feedings because No rapid fluctuation of in Rapid fluid/electrolyte shift; done carbohydrates have a greater protein-sparing power extracellular fluid; continuous only 3-4 times a week; 3-5 hours and provide additional calories. process  Weigh daily Diet liberalized; more protein, Diet more restrictive; only means  Be aware that food and fluids containing large personal adjustment of fluid intake to control fluids is by by increasing amount of dextrose in dialysis 3-4 times week and amounts of potassium, sodium, and phosphorus may dialysate personal regulation fluid need to be restricted. (osmosis to cause loss of fluid) *still intake should control Na,Mg, Phosphorous PRESERVING NEUROLOGIC FUNCTION intake & fluid May require less insulin; add insulin Onset of dialysis may allow control  Speak to the Patient in simple orienting statements, to dialysate of diabetes to using repitition when necessary. improve  Maintain predictable routine, and keep change to a Potential increased risk for infection Still at risk for infection; blood minimum. (peritonitis) borne due to dialysis and vascular  Watch for and report mental status changes- access (Hepatitis, HIV) Slower process; less effective in Rapid improvement in fluid and somnolence, lassitude, lethargy, and fatigue waste elimination electrolyte status progressing to irritability, disorientation, twitching, Increased serum triglycerides Improved control of serum seizures. triglycerides  Correct cognitive distortions.  Use seizure precautions-padded side rails, airway Altered body image; weight gain Minimal body image change and suction equipment at bedside. (increased glucose  Encourage and assist patient to turn and move (dextrose intake because drowsiness and lethargy may prevent activity. STAGES OF CKD  Use music tapes to promote relaxation. STAGES STAGE 1 STAGE 2 STAGE 3 STAGE 4 STAGE 5 AMOUNT OF More than 60%- 30%- 15%- Less CHRONIC KIDNEY KIDNEY FUNCTION 90% 89% 59% 29% than 15% REMAINING DISEASE DESCRIPTI ON Early kidney Worse kidney Even worse Severe kidney Severely impaired  Chronic kidney disease (CKD) is defined by the damage damage kidney damage kidney. presence of kidney damage for three or more months with normal with damage with poor The and thelevel of kidney function or even reduced with less functions kidneys increased function function that the not  End stage renal disease (ESRD) represents a clinical kidney kidneys working state in which there has been an irreversible loss of function are well renal function. barely enough  #CKD often will lead to ESRD. able to to keep keep the the person person DEFINITIONS alive alive Symptom Uremia: The presence of excessive amounts of urea may in the blood, which may be a sign of kidney disease or include failure. poor SYMPTOMS No No Early Tirednes sleeping Azotemia: An elevation of blood urea nitrogen (BUN) symptom symptom symptom s, poop at night, and serum creatinine levels. The reference range for BUN observed. observed occur appetite difficulty is 8-20 mg/dL, and the normal range for serum creatinine Urea and Urea and and may and breathing creatinine creatinin include itching ,itchiness is 0.7-1.4 mg/dL. levels are e levels tiredness may get and Glomerular filtration rate (GFR) is the volume of normal are itching worse frequent plasma filtered in the glomeruli per unit time, usually normal, and poor vomiting. or mildly appetite. High reported in mL/min. elevated Creatinin levels of -e level creatinin- rises, e and excess urea are ureaand present anemia begin to occur eGFR 90 ml/min 60-89 30-59 15-29 15 (Estimated or more ml/min ml/min ml/min ml/min or Glomerular less Filtrate Rate) TREATMEN- Identify Monitor Continue Plan and Start T OPTIONS cause and creatinin to stop or create replacem try to e level, slow the access ent renal reverse it blood worsenin site for therapy; pressure, g kidney dialysis. dialysis general function. Receive or health Patient assessm transplan and well learns ent for tation being. more possible Try to about the transplan stop or disease t slow the and the worsenin treatment g kidney options Transcribed by: Taño, Sirilan & Yu BSN 4-J function 3  CAUSES AND CONTRIBUTING CLINICAL MANIFESTATIONS FACTORS OF CKD EARLY STAGE Weakness UNCONTROLLED DIABETES Decreased appetite Nausea Glomerular hyperfiltration-increase in GFR and Renal Loin pain blood flow. Elevated BP Chronic hyperglycemia lead to diabetic Change in urination (nocturia, polyuria,frequency) nephropathy. LATE STAGE SYSTEMIC HYPERTENSION Elevated BP cause vascular and glomerular  General - Lassitude, fatigue, high BP, decreased damage- lead to tubular atrophy and chronic mental acuity interstitial nephritis → tubular and glomerular  Skin - Pale due to anemia, dry, scaly, bruises easily loss and in the end nephron loss. due to platelet abnormalities, uremic frost.  Pulmonary - Dyspnea, pleural effusion, pulmonary NEPHROTOXINS edema, uremic lung. Toxic agent or substance (NSAIDs) that inhibits,  Cardiovascular - Pericardial friction rub, damages or destroys the cells or tissues of the pericarditis. congestive heart failure. kidneys.  Gastrointestinal - Anorexia, nausea, vomiting, weight loss, stomatitis, unpleasant taste in the mouth DECREASED PERFUSION (BLOOD FLOW) (first symptom for ESRD patient), GI bleeding due to From severe dehydration or episodes of shock. GI irritation.  Neuromuscular - Muscle cramps, restless legs, sleep disorders, seizures, coma. PROTEINURIA  Central, peripheral and autonomic Presence of abnormal quantities of protein in the urine, which may indicate damage to the neuropathy. kidneys.  Endocrine - Elevated uric acid level(gout), menstrual irregularities, hypothyroidism HYPERLIPIDEMIA  Hematologic - Anemia, bleeding diathesis, iron High lipid levels can cause blockage in arteries deficient. HYPERPHOSPHATEMIA WITH CALCIUM DIAGNOSTIC TESTS PHOSPHATE DEPOSITION 1. Urinalysis: fixed specific gravity 1.010 (low); Electrolyte disturbance, meaning abnormally excess protein, blood cells, cellular casts elevated level of phosphate in blood. 2. Urine culture; identify infection 3. BUN and serum creatinine; evaluate kidney ETIOLOGY function Diseases and conditions that often lead to CKD include: Mild azotemia: BUN 20-50 mg/dl  Type 1 or type 2 diabetes Severe renal impairment: BUN > 100 mg/dl  High blood pressure Uremic symptoms: > BUN 200 mg/dl  Glomerulonephritis, an inflammation of the kidney's *Creatinine levels >4 mg/dl = serious renal filtering units (glomeruli). impairment (**better indicator than BUN  Interstitial nephritis, an inflammation of the kidney's of renal function); elevated BUN -responsible for tubules and surrounding structures. neurological symptoms  Polycystic kidney disease. 4. Creatinine clearance: reflects GFR and renal  Prolonged obstruction of the urinary tract, function (most accurate; need 24 hour urine collection) fromconditions such as enlarged prostate, calculi 5. Serum electrolytes: monitored throughout course  and some cancers. of CKD  Vesicoureteral reflux, a condition that causes urine to back up into your kidneys. 6. CBC: moderately severe anemia with hematocrit20-  Recurrent kidney infection, also called 30%; low hemoglobin, reduced RBC's and platelets pyelonephritis. 7. Renal ultrasonography: CKD; decreased renal size RISK FACTORS 8. Kidney biopsy: diagnose underlying disease Factors that may increase the risk of chronic kidney process; differentiate acute from chronic. disease:  Diabetes MANAGEMENT (attempt to delay onset  High blood pressure of ESRD)  Heart disease  Smoking 1. MEDICATIONS  Obesity General effects of CKD on medication effects  High cholesterol Increased half-life and inc. plasma levels of meds  Family history of kidney disease excreted by kidneys; monitor carefully  Age 65 or older Dosage may change when in renal failure; do not give demerol to patients on dialysis (toxic); digitalis excreted largely by kidney* Dec. drug absorption if phosphate-binding agents administered concurrently Transcribed by: Taño, Sirilan & Yu BSN 4-J 4  "Low plasma protein levels > lead to toxicity when RENAL REPLACEMENT THERAPIES protein-bound drugs are given Used when medications and diet are no longer effective Avoid nephrotoxic drugs (Aminoglycosides, penicillin in high doses, carefully monitor vancomycin due to toxic HAEMODIALYSIS (AV FISTULA OR GRAFT) accumulation); Amphotericin B very nephrotoxic also  the most common type of dialysis. contrast-media induced nephrotoxicity  During the procedure, a tube is attached to a needle If on dialysis; many drugs removed by dialysis; varies in your arm. Blood passes along the tube and into an with hemodialysis and peritoneal dialysis: CHECK before external machine that filters it,before it's passed back serving. into the arm along another tube. Typically do not serve antihypertensive drugs before  usually carried out three days a week, with each hemodialysis (BP may drop); give after dialysis. session lasting around four hours. PERITONEAL DIALYSIS MEDICATIONS uses the inside lining of abdomen (the peritoneum) as the filter, rather than a machine.Like the kidneys, the 1.) DIURETICS peritoneum containsthousands of tiny blood vessels, eg. furosemide 20-80mg PO OD/20-40mg IV/IM once making it auseful filtering device. To reduce extracellular fluid volume and edema 1. Warmed sterile dialysate instilled into peritoneal cavity via catheter inserted into peritoneal cavity 2.)ANTIHYPERTENSIVE AGENTS (ACE 2. Metabolic waste products and excessive electrolytes diffuse into dialysate while it remains in abdomen INHIBITORS 3. Water diffusion controlled by glucose (dextrose) PREFERRED) concentration in the dialysate which acts as an eg. perindopril 4-8mg PO QID "osmotic" agent To lower blood pressure 4. Amount of solution removed determined by glucose concentration of the dialysate! Excess fluid/solutes 3.) ANTACIDS removed more gradually; less risk for unstable client To treat gastric irritation 5. Fluid drained by gravity into sterile bag at set interval- No magnesium based, can cause magnesium removing waste products/ excess fluid toxicity 1. "Clear" solution 'fills" abdomen 2. "Yellow" urine appearing fluid drains out (looks like urine, should be clear) 4.) ALKALINIZING AGENTS eg. sodium bicarbonate 325 to 2000 mg PO OD to QID to correct serum pH in metabolic acidosis TYPES OF PERITONEAL DIALYSIS A.CAPD: 5.) ORAL PHOSPHORUS BINDING AGENTS  most common eg. calcium carbonate 1-1.2 g PO QID  continuous ambulatory peritoneal dialysis Act as binding agent to lower phosphate level  exchanges 4-5 times a day As calcium supplement  treatments-ongoing 24 hours a day; 7 days a week  2 liters solution in peritoneal cavity except during 7.)SUPPLEMENTS AND HORMONE drain time; independent treatment REPLACEMENT B. CCPD: ✓ Vitamin D ✓ Folic acid and iron tablets  continuous cycler peritoneal dialysis; ✓ EPO inj.  uses delivery devise (cycler) during nighttime hours Improve calcium absorption and continuous dwell during day To combat anemia KIDNEY TRANSPLANT MANAGEMENT  involves surgically placing a healthy kidney from a donor into body.  can come from deceased or living donors DIETARY RESTRICTIONS  need to take medications for the rest of life to keep *Early in CRF: diet modification-slow kidney failure body from rejecting the new organ. avoid uremic symptoms Restrict proteins (40gm/day) of high biologic NURSING CARE PLAN: NURSING value. Increase carbohydrate intake (35kcal/kg/day) INTERVENTIONS & RATIONALE: Limit fluid to 1-2 L per day; limit sodium to 2 NURSING DIAGNOSIS: RISK FOR INEFFECTIVE g/day (usual guideline is 500-600 ml more than RENAL PERFUSION previous' day's 24 urine output) 1. Monitor intake and output, vital signs including Restrict potassium to (60-70 mEg/day; no salt orthostatic blood pressures and weight. substitutes); avoid bananas, prunes, raisins, To identify changes in fluid volume orange juice, tomatoes, deep green and yellow 2. Restrict fluids as ordered. vegetables To promote elimination of excess fluid. Restrict phosphorus food (especially milk, ice 3. Report manifestations of electrolyte imbalances cream, cheese; also meat, eggs, dairy products) To determine further action. to 1000 mg/day. 4. Time activities and procedures to allow rest periods. To prevent patient from having others complication such as fatigue. 5. Administer medications as prescribed by doctor. To treat electrolyte imbalances. Transcribed by: Taño, Sirilan & Yu BSN 4-J 5  NURSING DIAGNOSIS: IMBALANCED 3. CARDIOVASCULAR RISK  Hypertension is the most common complication of NUTRITION RELATED TO DISEASE CKD and ESRD. PROCESS.  It may develop early during the course of 1. Monitor food and nutrient intake. hypertension in uremia. To determine the adequacy of intake.  Volume overload is the major cause of hypertension 2. Assist with mouth care prior to meals and at bedtime. in uremia. To improve taste and stimulate appetite.  Rarely, patient may develop malignant hypertension. 3. Serve small meals and provide between-meal snacks. To prompt nausea and help improve food 4.GASTROINTESTINAL AND NUTRITIONAL intake. ABNORMALITIES 4. Encourage family members to bring food as dietary restrictions allow.  Gastrointestinal symptoms (abdominal pain,nausea, To provide preferred foods within restrictions vomiting) usually may the first symptomfor ESRD promotes intake. patients. 5. Administer antiemetic agents as ordered by doctor 30  Uremic toxins is associated with an unpleasant to 60 minutes before eating. metallic taste ESRD patient. To prevent nausea and vomiting wit food intake.  Gastritis, peptic disease are common in ESRD patient. NURSING DIAGNOSIS: RISK FOR INFECTION RELATED TO DISEASE 5. DYSLIPIDEMIA PROCESS  A major risk factor for cardiovascular morbidity and mortality, and is very common in CKD. 1. Monitor temperature and vital signs at least every 4  Lipid profiles in CKD patients reflect the level of hours. kidney function and the degree of proteinuria. To detect low-graded fever and prevent itfrom  Prevalence of hyperlipidemia ↑, as renal function ⇓ getting worse.  The degree of hypertriglyceridemia and elevation of 2. Use standard precautions and good hand hygiene LDL cholesterol is proportional to severity of renal technique all times. impairment. To prevent the transfer of organisms. 3. Culture urine, peritoneal dialysis fluid and other drainage as indicated To verify the presence of pathogens. SIRS AND MODS 4. Teach patient coughing and deep breathing exercise. To improve clearance of respiratory secretions. SIRS 5. Teach the patient and family members about therisk ♥ Systemic inflammatory response syndrome (SIRS) is for infection a systemic inflammatory response to a variety of To reduce the spread of infection. insults. ♥ Generalized inflammation in organs remote from the COMPLICATIONS initial insult 1. ANEMIA  Anemia is a reduction in one or more of themajor red TRIGGERS blood cell measurements: hemoglobin concentration,  Microbial invasion: bacteria, viruses, fungi hematocrit, or red blood cell count.  Endotoxin release: gram-negative bacteria  A hemoglobin level less than 13 g/dL in men and  Global perfusion deficits: post-cardiac resuscitation, post-menopausal women, and less than 12 g/dL in shock states pre-menopausal women. (World Health Organization)  Regional perfusion deficits: distal perfusion deficits  The significant mechanism of anemia in CKD: - Insufficient production of EPO by the diseased kidneys. ODS - In CKD, tubular atrophy generates tubulointerstitial ♥ Multiple organ dysfunction syndrome (MODS) is the fibrosis, whichcompromises renal erythropoietin synthetic failure of two or more organ systems. capacity and results in anemia*  Homeostasis cannot be maintained without intervention. 2. CKD-ASSOCIATED MINERAL AND BONE  Results from SIRS DISORDERS.  Mortality rates are linearly related to the number of failed organ systems  "CKD-associated mineral and bone disorders" comprises abnormalities in bone and mineral metabolism and/or extra-skeletal calcification STAGE 1 secondary to CKD pathophysiology  Increased volume requirements  Four types of bone phenotypes (renal osteodystrophy)  Mild respiratory alkalosis which is accompanied by can be diagnosed in CKD patients: oliguria, hyperglycemia and ↑ insulin requirements. ➔ OSTEITIS FIBROSA CYSTICA (high bone turnover with secondary hyperparathyroidism), STAGE 2 ➔ OSTEOMALACIA (low bone turnover and inadequate  Tachypneic, hypocapnio and hypoxemio. mineralization, primarily related to diminished vitamin D  Moderate liver dysfunction synthesis)  Possible hematologic abnormalities ➔ ADYNAMIC BONE DISORDER (low bone turnover from excessive suppression of the parathyroid glands) STAGE 3 ➔ MIXED OSTEODYSTROPHY (with elements of both  Shock with ↑ BUN/creatine, acid-base disturbances. high and low bone turnover).  Significant coagulation abnormalities.  Cause bony pain, proximal muscle weakness, and spontaneous bone fracture. Transcribed by: Taño, Sirilan & Yu BSN 4-J 6 STAGE 4 CARDIOVASCULAR SYSTEM  Vasopressor dependent and ↓ UO.  Myocardial depression and massive vasodilation  Ischemic colitis and lactic acidosis follow. NEUROLOGIC SYSTEM  Mental status changes due to hypoxemia, inflammatory mediators, or impaired perfusion  Often early sign of MODS RENAL SYSTEM  Acute renal failure  Hypo-perfusion  Release of mediators  Activation of renin-angiotensin- aldosterone systen  Nephrotoxic drugs, especially antibiotics GI SYSTEM  Motility decreased: abdominal distention and paralytic ileus  Decreased perfusion: risk for ulceration and GI bleeding  Potential for bacterial translocation HYPERMETABOLIC STATE  Hyperglycemia-hypoglycemia  Insulin resistance  Catabolic state  Liver dysfunction  Lactic acidosis HEMATOLOGIC SYSTEM -DIC ELECTROLYTE IMBALANCES METABOLIC ACIDOSIS COLLBORATIVE CARE  Prognosis for MODS is poor.  Goal: prevent the progression of SIRS to MODS  Vigilant assessment and ongoing monitoring to detect early signs of deterioration or organ dysfunction are critical. PREVENTION AND TREATMENT OF INFECTION  Aggressive infection control strategies to decrease SIRS AND MODS risk for nosocomial infection PATHOPHYSIOLOGY  Once an infection is suspected, institute interventions to control the source. CONSEQUENCES OF INFLAMMATORY MAINTENANCE OF TISSUE OXYGENATION RESPONSE  Decreased 02 demand  Release of mediators  Sedation  Direct damage to the endothelium  Mechanical ventilation  Hypermetabolism  Paralysis  Vasodilation leading to decreased SVR  Analgesia  Increase in vascular permeability  Activation of coagulation cascade NUTRITIONAL AND METABOLIC NEEDS ORGAN AND METABOLIC DYSFUNCTION  Goal of nutritional support: preserve organ function  Total energy expenditure is often increased  Hypotension  1.5 to 2.0 times.  Decreased perfusion  Use of the enteral route is preferred to parenteral  Formation of microemboli nutrition.  Redistribution or shunting of blood  Monitor plasma transferrin and prealbumin levels to assess hepatic protein synthesis. RESPIRATORY SYSTEM SUPPORT OF FAILING ORGANS  Alveolar edema  ARDS: aggressive 02 therapy and mechanical  Decrease in surfactant ventilation  Increase in shunt  DIC: appropriate blood products  V/Q mismatch  Renal failure: continuous renal replacement therapy  End result: ARDS or dialysis Transcribed by: Taño, Sirilan & Yu BSN 4-J 7  NURSING MANAGEMENT SUBTYPES: ♥ Reduce chance of infection ♥ Dressing changes on all invasive line sites and A. THROMBOTIC STROKE surgical wounds according to protocol  occurs when an artery becomes blocked by the ♥ Maintain aseptic technique with all dressing changes formation of a blood clot (thrombus) within it. and manipulation of intravenous lines.  Atherosclerosis is the primary cause wherein ♥ Institute the measures that are necessary to prevent fatty material deposit and form plaques on vessel aspiration when patients are placed on enteral walls. feedings.  Total blockage may subsequently occur due to ♥ Keep the head of the bed elevated, and check for clumping together of blood cells (platelets) or other residual volume and tube placement every 4 hours substances normally found in the blood. ♥ Oral care if on ventilator ♥ Provide frequent rest periods ♥ Create a quiet environment whenever possible. B. EMBOLIC STROKE ♥ Schedule procedures and nursing care interventions  It is the occlusion of a cerebral artery by an embolus so that the patient has periods of uninterrupted rest that is formed outside the brain, detaches and travels ♥ Manage situations of increased metabolic demand- through the cerebral circulation until if lodges in and such as fever, agitation, alcohol withdrawal, and pain- occludes a cerebral artery. promptly so that the patient conserves energy and  These materials could be blood clots (e.g. from the limits oxygen consumption. heart) or fatty materials (e.g. from another artery ♥ Monitor bony prominences and areas of high risk for in the neck- carotid artery disease). skin breakdown.  Causes: Chronic atrial fibrillation, mechanical prosthetic heart valves, bacterial and non bacterial endocarditis, tumor, fat, bacteria and air. CEREBROVASCULAR 2. HEMORRHAGIC STROKE ACCIDENT/STROKE - caused by the rupture of arteriosclerotic and hypertensive vessels which cause bleeding into brain tissue. EPIDEMIOLOGY SUBTYPES: STROKE MORTALITY In 2021, there were 68,180 deaths from stroke in the A. INTRACEREBRAL HEMORRHAGE (ICH) Philippines despite of Covid-19. The average number of  Is most often due to high blood pressure. deaths from stroke over the previous 10 years was 63,804  The sudden increase in pressure within the brain due per year. (DOH) to the bleeding can cause damage to the brain cells surrounding the blood. STROKE INCIDENCE AND PREVALENCE B. SUBARACHNOID HEMORRHAGE (SAH)  The national stroke incidence rate in the Philippines ranges from 3.95% to 5.61%, while the prevalence  Occurs when a blood vessel lying just rate ranges from 0.486% to 6.0%. (DOH)  Outside the brain ruptures. The fluid-filled space  Cerebrovascular disorders are the third leading cause surrounding the brain (the subarachnoid space) of death in the United States (Saunders, 2017) rapidly fills with blood.  It is most often caused by abnormalities of the arteries called aneurysms. PREVALENCE: Ischemic Stroke - 83% ISCHEMIC STROKE Hemorrhagic Stroke - 17%  Also known as cerebral infarction due to blockage of an artery DEFINITION  Accounts for about 80% of cases  A stroke, also called a "brain attack", occurs when a  May either be : Thrombotic or Embolic portion of the brain is damaged due to a lack of blood  Transient ischemic attack (TIA) are very similar to supply to that part of the brain. ischemic stroke but all signs and symptoms usually  It is caused by either a blockage (ischemic) or rupture disappear within 1 hour of the blood vessel (hemorrhagic) in the brain.  Due to the lack of oxygen and nutrients carried by the HEMORRHAGIC STROKE blood, brain cells (called "neurons") die and the Are due to rupture of an artery connections between neurons (called "synapses" or Accounts for about 20% of cases junctions) are lost. May either be: Intracerebral or Subarachnoid TYPES TRANSIENT ISCHEMIC ATTACK (TIA)  Aka "mini stroke" are episodes in which a person has 1. ISCHEMIC STROKE signs or symptoms of a stroke (e.g, numbness; inability to speak) that last for a short time, but - Occur as a result of an obstruction within a blood vessel without any sign of stroke on brain scans such as supplying blood to the brain. MRI or CT.  Symptoms of a TIA usually last between a few minutes and a few hours. A person may have one or many TIAs. People recover completely from the symptoms of a TIA. Transcribed by: Taño, Sirilan & Yu BSN 4-J 8  ATA is a waning sign that a person is at high risk for  Sudden trouble seeing in one or both eyes a stroke; immediate treatment can decrease or  Sudden trouble walking, dizziness, loss of balance or eliminate this risk. coordination  Sudden severe headache with no known cause PATHOPHYSIOLOGY STROKE ASSESSMENT SCALE NATIONAL INSTITUTES OF HEALTH STROKE SÇALE, OR NIH STROKE SCALE (NIHSS)  Is a tool Used by healthcare providers to objectively quantify the impairment caused by a stroke.  Is Composed of 11 items, each of which scores a specific ability between a 0 and 4.  For each item, a score of 0 typically indicates normal function in that specific ability, while a higher score is ETIOLOGY: indicative of some level of impairment.  The maximum possible score is 42, with the minimum MODIFIABLE score being a 0.  Blood pressure  Heart disease NIHSS  Blood cholesterol  Diabetes SCORE STROKE SEVERITY  Clotting problem 0 -No stroke symptoms  Cigarette smoking 1-4 -Minor stroke  Heavy alcohol intake 5-15 - Moderate stroke  Obesity 16-20 -Moderate to severe stroke  Sedentary lifestyle 21-42 -Severe stroke NON-MODIFIABLE STROKE ASSESSMENT SCALE  Age (> 40 years old)  Gender (Female > Male) CINCINNATI PREHOSPITAL STROKE SCALE  Race (African American) (CPSS)  Genetics  Is a system used to diagnose a potential stroke in a  Previous stroke prehospital setting.  It tests three signs for abnormal findings which may indicate that the patient is having a stroke. SYMPTOMS  If any one of the three tests shows abnormal findings. the patient may be having a stroke and should be transported to a hospital as soon as possible.  The CPSS was derived from the National Institutes of Health Stroke  Scale developed in 1997 at the University of Cincinnati Medical Center for prehospital use. THE GLASGOW COMA SCALE (GCS)  Is a neurological scale which aims to give a reliable and objective way of recording the conscious state of a person for initial as well as subsequent assessment.  A patient is assessed against the criteria of the scale, and the resulting points give a patient score between 3 (indicating deep unconsciousness) and either or 15 (normal level of consciousness). ♥ Face Drooping Does one side of the face droop or is it numb? Ask the person to smile. ♥ Arm Weakness Is one arm weak or numb Ask the person to raise bothmarms. Does one arm drift downward? ♥ Speech Difficulty Is speech slurred, are they unable to speak, or are they hard to understand? Ask the person tO repeat a simple sentence, like "the sky is blue." Is the sentence repeated correctly ♥ Time to call 911 If the person shows any of these symptoms, even if the symptoms go away, call 9-1-1 and get them to the hospital immediately. OTHER CLINICAL MANIFESTATIONS:  Sudden confusion or trouble understanding Transcribed by: Taño, Sirilan & Yu BSN 4-J 9  LABORATORY AND DIAGNOSTIC  Intra-arterial thrombolysis - Doctors may insert a long, thin tube (catheter) through an artery in your PROCEDURES groin and thread it to your brain to deliver tPA directly into the area where the stroke is occurring CRANIAL CT SCAN:  Removing the clot with a stent retriever -  CT scanning combines special x-ray equipment with beneficial for people with large clots that can't be sophisticated computers to produce multiple images completely dissolved with PA or pictures of the inside of the body. Physicians use CT of the head to detect a stroke from a blood clot or bleeding within the brain.  MRI uses a powerful magnetic field, radio frequency MEDICAL MANAGEMENT pulses and a computer to produce detailed pictures of (HEMORRHAGIC STROKE) organs and virtually all other internal body structures.  MRI is also used to image the cerebral vessels and Focus: Control bleeding and reducing pressure in the cerebral blood flow. Physicians use MRI of the head to assess brain damage from a stroke. brain. BLOOD TESTS SURGICAL BLOOD VESSEL REPAIR. a. CBC  Surgery may be used to repair blood vessel b. Anticoagulation studies- PT, APTT abnormalities associated with hemorrhagic strokes. c. Blood lipid tests: Cholesterol, total lipids, HDL, and LDL  Surgical clipping. A surgeon places a tiny clamp d. Blood Chemistry- Glucose, Na, K, BUN, Creatinine at the base of the aneurysm, to stop blood flow to it. e. Homocysteine level tests This clamp can keep the aneurysm from bursting, f. C- Reactive Protein level tests or it can prevent re-bleeding of an aneurysm that has recently hemorrhaged.  Coiling (endovascular embolization). A ECHOCARDIOGRAM (ECG) surgeon inserts a catheter into an artery in your groin  An echocardiogram Uses sound waves to create and guides it to your brain using X-ray imaging. Tiny detailed images of your heart. An echocardiogram detachable coils are guided into the aneurysm can find a source of clots in your heart that mnay (aneurysm coiling). The coils fill the aneurysm, which have traveled from your heart to your brain and blocks blood flow into the aneurysm and Causes caused your stroke. the blood to clot.  Surgical AVM removal. Surgeons may remove a smaller AVM if it's located a in an accessible area of MEDICAL MANAGEMENT your brain, to eliminate the risk of rupture and lower the risk of hemorrhagic stroke. However, it's not PILLARS OF STROKE THERAPY always possible to remove an AVM if its removal 1. IV/IA Thrombolysis would cause too large a reduction in brain function, or 2. Thrombectomy if it's large or located deep within your brain. 3. Stroke Unit  Stereotactic radiosurgery. Using multiple 4. Antiplatelets and anticoagulants beams of highly focusedradiation, stereotactic 5. Antihyperlipidemic radiosurgery is an advanced minimally 6. Antihypertensives invasivetreatment used to repair vascular 7. Decompressive Hemicraniectomy malformations. 8. Neurorestoration and neuroprotectants NURSING MANAGEMENT (PREVENTIVE) MEDICAL MANAGEMENT HEALTH EDUCATION a. DIET - Low-fat, high-fiber, low salt diet (ISCHEMIC STROKE) b. EXERCISE - at least 150 minutes (2 hours and 30 minutes) of moderate-intensity aerobic activity every Focus: Restore blood flow to the brain week (e.g. cycling or fast walking) A. Emergency treatment with medications. Therapy with c. STOP SMOKING clot-busting drugs must start within 4.5 hours if they d. CUT DOWN ON ALCOHOL are given into the vein - and the sooner, the befter. INTRAVENOUS INJECTION OF TISSUE NURSING MANAGEMENT (CURATIVE) PLASMINOGEN ACTIVATOR (IPA) 1. Use assistive ambulatory devices  This injection of recombinant tissue plasminogen  Facilitates ambulation/transfers safely activator (IPA), also called alteplase, is considered 2. Frequent neurological assessments (per orders) the gold standard treatment for ischemic stroke.  Alerts nurse to neurological changes as early as  An injection of tPA is usually given through a vein in possible, enables them to notify MD and the arm. intervene when needed  This potent clot-busting drug ideally is given within 3 - 3. HOB at 30 degrees unless otherwise indicated 4.5 hours  Increases venous return, decreases ICP  This drug restores blood flow by dissolving the 4. Initiate DVT prophylaxis (mechanical and/or blood clot causing your stroke. chemical)  Decreases risk for subsequent stroke, as patient B. Emergency endovascular procedures. Doctors most likely will not be as mobile as they are at sometimes treat ischemic strokes with procedures baseline performed directly inside the blocked blood vessel. Transcribed by: Taño, Sirilan & Yu BSN 4-J 10  18. Facilitate communication; promote family coping 5. Ensure PT/OT/ST is ordered and communication  Rehab is essential in stroke recovery; all must  Having a stroke is a major life event. Roles within complete a baseline assessment and provide families and support systems may change, recommendations especially if the patient played a caregiving role 6. Fall prevention measures (non-skid socks, bed in within their family structure lowest locked position, call bell within reach, and so forth) NURSING MANAGEMENT  Injury prevention; patient will most likely not be able to ambulate as they could prior to stroke (REHABILITATIVE) and will require assistance 7. Prevent contractions PHYSICAL ACTIVITIES  Extremities that are now paralyzed are at risk for  Motor-skill exercises. These exercises can help becoming contracted; ensure pillow supports are improve your muscle strength and coordination. in place as well as rolled towels and adaptive You might have therapy to strengthen your devices swallowing. 8. Prevent aspiration: follow ST (Speech Therapy) recommendations, keep HOB at 45 degrees  Mobility training. You might learn to use mobility during oral intake and keep patient upright after a aids, such as a walker, canes, wheelchair or ankle meal, have suction available, assess lung sounds brace. The ankle brace can stabilize and strengthen and body temp your ankle to help support your body's weight while  Stroke patients frequently have impaired you relearn to walk. swallowing, and are at high risk for aspiration  Constraint-induced therapy. An unaffected from their own oral secretions and oral intake. limb is restrained while you practice moving the 9. Cluster care; promote rest affected limb to help improve its function. This  Maximizes time with the patient so they can rest therapy is sometimes called forced-use therapy. when care is not being provided  Range-of-motion therapy. Certain exercises and 10. Monitor vital signs appropriately: know BP limits treatments can ease muscle tension (spasticity)  Closely monitoring BP is essential in managing and help you regain range of motion. ICP 11. Prevent edema: elevate limbs, utilize COGNITIVE AND EMOTIONAL ACTIVITIES compression stockings, promote ambulation,  Therapy for cognitive disorders. Occupational promote complete bladder emptying  Patients who are in bed more will have a harder therapy and speech therapy can help you with lost fime clearing fluid out, especially if they have any cognitive abilities, such as memory, processing, underlying heart condition causing a decreased problem-solving, social skills, judgment and safety cardiac output (like atrial fibrillation) awareness. 12. Promote self-care  Therapy for communication disorders.  Patients will have a decreased ability to care for Speech therapy can help you regain lost abilities in self due to new deficits; promote confidence and speaking, listening, writing and comprehension. participation in caring for themselves as much as  Psychological evaluation and treatment. possible Your emotional adjustment might be tested. You 13. Promote cerebral tissue perfusion (interventions might also have counseling or participate in a support per orders, as this can differ depending on kind group. of stroke, location, and other factors)  Medication. Your doctor might recommend an  This prevents additional neurological damage antidepressant or a medication that affects alertness, 14. Facilitate safe swallowing: ensure bedside agitation or movement. swallow screening completed and/or speech therapy assessment prior to oral intake PALLIATIVE CARE  Frequently, brain injury results in an impaired  Pain management ability to swallow safely. This is not always  Emotional turmoil and grief apparent as patients don't always cough when aspirating and have silent aspiration.  Physical limitations such as loss of strength or 15. Promote adequate nutrition balance  Nutrition and nutrition disorders caused by stroke  Once a patient is cleared to eat, do what you can to encourage appropriate intake... as patient cannot heal if they don't eat 16. Initiate discharge planning  Stroke patients typically require multiple needs at discharge (follow up appts, rehab/therapy, and may need to go to long-term care or inpatient rehab, depending on the situation) begin getting your mind around their discharge needs at the beginning even if it's not clear yet what their needs will be 17. Prevent skin breakdown: turn q2hrs, ensure adequate protein intake, off-loading, pillow support, keep linen clean and dry  There are many reasons why a stroke patient will be at risk for skin breakdown... from an inability to feel or move extremities, incontinence, inability to communicate needs/pain/discomfort, decreased nutritional status. Transcribed by: Taño, Sirilan & Yu BSN 4-J 11