Understanding Pulmonary Embolism: Causes, Symptoms, and
School
Grambling State University**We aren't endorsed by this school
Course
NUR 219
Subject
Nursing
Date
Dec 10, 2024
Pages
51
Uploaded by Lateria1
MED SURG 2 EXAM 2ππ’Sad Adventures of the Lung, Liver and Pancreasπ’πβAre you ok? Youβre breathing WEIRDβTHIS IS THE BEST TITLE YET!Pulmonary embolism - PathophysiologyβBlockage in one of the pulmonary arteries in the lungsβCaused by blood clots that travel to the lungs from deep veins in the legs or (rarely) other parts of the body. = DEEP VEIN THROMBOSISβWhen thrombus completely or partially obstructs a pulmonary artery or branches the alveolar dead space is increasedβGas exchange is impaired or then absent in the areaβMassive PE is best defined by the degree of hemodynamic instability βOcclusion of outflow tract of the main pulmonary arteryβBlood clot that forms in a blood vessel in one area of the body, breaks off, and travels to another area of the body called an EMBOLUS.βEmbolus can lodge itself in the blood vessel and block blood supply to organsβThe blockage of a blood vessel by an embolus is called an EMBOLISM.βSlower blood flow leads to clot formationβVTE- Venous thromboembolism = blood clots - umbrella term that includes DVT and PE (1)βRISK FACTORS-βSurgery - LEADING CAUSEβIntervention- medication to prevent blood clots may be given before and after major surgeryβImmobility or reduced mobility, Oral contraceptive/hormone replacement therapy, prolonged air travel, pregnancyβKidney disease can also increase risk for blood clotsβHeart disease, Cancer (malignancy), clotting disorders, obesity, Hx of DVT, cigarette smoking, HFPulmonary embolism- Clinical Manifestations SATA(2)βHypoxemia- low O2 in the bloodβA clot in the lung somewhere is blocking the blood and canβt pass O2 = low O2 in bloodβDyspnea- shortness of breathβBlood carries O2 which need to breathe (gasping for air)1
βMost frequent sign and appears suddenly, worse with exertion**βTachycardia- Fast heart rate - 140βThe heart kicks in to compensate by pumping faster to move blood faster through the body to increase O2.βTachypnea- Fast breathing - 32?it fastβNot enough O2, breathing gets fasterβMost frequent sign**- very rapid respiratory rateβCough-βBloody or blood streaked sputum, pink tinged (Hemoptysis)βChest Pain-βInflammation from the clotβSudden and pleuritic**βAnxiety-βRacing heart, gasping for air, chest pain, canβt breathe.βOTHER S/S: HYPOXIAβIrregular heartbeatβSyncopeβLightheadedness or dizzinessβExcessive sweatingβFeverβLeg pain or swellingβClammy or discolored skinβDiagnostic Tests-βV./Q. - ***MOST IMPORTANT TEST**βAlso called a Ventilation (V) Perfusion (Q) scanβMade up of two scans that examine air flow and blood flow to lungsβUses a small amount of radioactive substance called a tracer that helps look for diseases in the bodyβCompares the amount of perfusion in a lung segment with the degree of ventilation in that segmentβWhat do you hear from patients when they breathe out? βPulmonary Angiogram- GOLD STANDARD for diagnosis**βChest X-Ray- atelectasisβECHO- Enlarged right-sided heart chambers, tricuspid regurgitationβECG- rule out MIβPulse ox- hypoxic?βABG Analysis- hypoxemia and hypocapnia2
βD-Dimer- fibrin (a small protein fragment present in the blood after a blood clot is degraded by fibrinolysis)Pulmonary embolism- TreatmentsβMassive PE is a LIFE-THREATENING EMERGENCYβImmediate action is to stabilize the cardiopulmonary systemβOxygen is given IMMEDIATELY to relieve hypoxemia(3)βIV infusion linesβPrompt vasopressor therapyβPulse ox, ABGs are preformedβECG, Lab draw, Indwelling catheter is placedβIV morphine or sedatives are givenβ**Patient c/o chest pain and trouble breathing = 1st action is to elevate HOB!!βThe treatment goal is to dissolve (lyse) the existing emboli and prevent new ones fromforming**βLong term anticoagulation is also indicated from 10 days - 3 months following the PE and is critical in the prevention of recurrence of VTE.βHeparin-βAnticoagulation prevent clots from formingβAfter thrombosis has developed, it can inhibit additional coagulation by inactivating thrombinβPREVENTS FURTHER THROMIβaPPT should be maintained at therapeutic level of 45-70 seconds (normal-25-35 seconds)βThrombolytics-βUsed in patients with an acute PE who have hypotension and do not havea contraindication for potential bleeding risk.βRecombinant tissue plasminogen activator (activase)- tPAβKabikinase (Streptase)βDissolve clotsβNot to be used with stroke patientsβEmbolectomy-βArtery in neck or groin to retrieve the clotβIVC filters-βPlaced to prevent further emboli in patients who remain at high risk and for patients who have a contraindication to anticoagulationβLooks like a head scratching/massage device from walmart3
Pulmonary embolism- PreventionNursing Care-βPrevent Venous StasisβEncourage ambulation and active and passive left exercises to prevent venous stasis.βAvoid sitting still for too longβEncourage leg pumps in bed(4)βDO NOT dangle legsβCompression stockings and/or compression devices while in bedβManage oxygen therapyβAssess for S/S of hypoxemiaβMonitor the pulse ox valueβBed rest in a semi-fowlerβs position to facilitate breathingβIncentive spirometerβMaintain IV line for meds and fluid therapy, monitor VS, cardiac dysrhythmias (tele)βMonitor thrombolytic therapyβINR or PTT- performed every 3-4 hours after infusion has startedβTherapy causes lysis of deep vein thrombi and PE which helps dissolve clotsβTeaching about long-term anticoagulant therapyβReinforce the need for follow-up exams and lab drawsβManage painβTurn patients frequently and reposition to improve ventilation-perfusion ratio.βSemi-fowlers position to help breathing βPreventing Thrombus FormationβMajor nursing responsibility- we encourage ambulation and active/passage leg exercisesARDS (Acute Respiratory Distress Syndrome)- DiagnosticsβPhysical ExamβHealth HxβBNP levels - rule out pulmonary edemaβEcho or TEEβEKG - assess for any arrhythmias or ischemiaβPulmonary artery catheterizationβChest xray - rule out edema, effusion, and pneumonia4
βBronchoscopy - help ID causeβUrine- rule out infection or kidney issuesβSputum culture - look for bacteria or infectionβABG - hypoxemiaARDS- Clinical manifestationsβInitially it closely resembles severe pulmonary edemaβAcute phase- marked by rapid onset of severe dyspnea βThen progresses to fibrosing alveolitis with persistent, severe hypoxemiaβPt has increased alveolar dead space (ventilation to alveoli but poor perfusion)βPt has decreased pulmonary compliance (Stiff lungs- difficult to ventilate) βIntercostal retractions and crackles may be present as the fluid begins to leak into the alveolar interstitial spaceβ***Severe ARDS does NOT respond to supplemental O2***(5)βSOBβFast breathing, or taking lots of rapid, shallow breathsβFast heart rateβCoughing that produces phlegmβBlue fingernails or blue tone to the skin or lipsβExtreme tirednessβFeverβCrackling sound in the lungsβChest pain, especially when trying to breathe deeplyβLow blood pressureβConfusionARDS - TreatmentβSupplemental Oxygen - intubation or ventilationβProviding ventilatory PEEP (prevents alveoli collapse)(6) - Respiratory therapistβGoal is PaO2 greater than 60mm Hh or an oxygen saturation level of greater that 90% at the lowest possible FiO2βInotropic or vasopressor agentsβProne positionβSedationβParalysisβDiuretics - prevent fluid overload5
βNutritional supportβRequire 35-45kcal/kg/day to meet caloric requirementsβEnteral feeding is the first considerationβParenteral nutritionβHigh fat, low carbARDS- Mechanical VentilationβPEEP π£π£π£ - positive pressure maintained by the ventilator at the end of exhalationβPEEP causes increased end-expiratory pressure- unnatural pattern of breathing and feels strange to the ptβPt may become anxious and try to fight the ventilatorβUsed for pts with ARDS to help maintain airway/respiratory functionβHigh amounts of PEEP needed bc of collapsed sacs, stiffening of the lung and pulmonary edemaβThis high amount of pressure will open the sacs, improve gas exchange and help keep them clear of fluidβHigh amounts can cause issues with intrathoracic pressure and decrease cardiac output βTo increase functional residual capacityβImproves oxygenation with a lower fraction of inspired oxygenβFraction of inspired oxygen (FiO2): concentration of oxygen delivered (1.0=100% oxygen)βA mechanical ventilator - positive or negative pressure breathing device - maintains ventilation and oxygen delivery for a prolonged period***βICU - critically illβGeneral medical-surgical unitsβExtended care facilitiesβAt homeARDS- Nursing Care of Patients on VentilatorsβICU unitβOxygen administrationβNebulizer therapyβChest physiotherapyβEndotracheal intubation or tracheostomyβMechanical ventilation, suctioning6
βBronchoscopyβFrequent turning- Prone positioning may be necessaryβReduce anxietyβPromote restβVAP- Ventilator-Associated PneumoniaβKeep HOB elevated (30-45 degrees)βDaily sedation vacations and readiness to extubateβPeptic ulcer disease prophylaxis- ProtonixβDeep venous thrombosis (DVT) prophylaxis- Heparin, Warfarin, LovenoxβDaily oral care with chlorhexidineβWeaningβPhysiologically and hemodynamically stable**βDemonstrates spontaneous breathing capability**βRecovering from the acute stage of medical and surgical problemsβCause of respiratory failure is sufficiently reversed βPatients may be anxious and βfight ventilatorβ**βAssess for unnatural breathing pattern - vents feel strange to the patientβAssess for tube blockage by kinking or retained secretions**βAssess for other acute respiratory problems (pneumothorax and pain)βObserve for a sudden decrease in oxygen level (dyspnea)**βObserve for ventilator malfunctionMechanical Ventilators- Medicationsβ***ASSESS AIRWAY*** βSedationβThe need for sedative therapy in critical care adults receiving mechanical ventilation is established to be 85% of ICU patientsβThey are given IV sedatives to help alleviate anxiety, pain and agitationβSedativesβLorazepam (Ativan)βMidazolam (Versed)βDexmedetomidine (Precedex)βPropofol (Diprivan)βShort-acting barbituratesβRegionalβPeripheral nerve blocks, spinal anesthetics, epidural anesthetics, general anesthesia7
βBenzodiazepines produce amnesia, anxiolysis, sedation, and have anticonvulsant properties βNot paralyzed* they can still hear youβNeuromuscular Blocking Agents (muscle relaxants)- paralyze ptβVecuronium (Norcuron)***Know this medication!!***βMaximum neuromuscular blockade occurs within 3-5 minutesβDuration of action is 25-40 minutesβDose-dependent βPancuronium ( Pavulon)βAtracurium (Tracrium)βRocuronium (Zemuron)βπ£ Train-of-four test may be used to measure the level of neuromuscular blockadeβRed electrode is closest to the heartβFind out what level the patient responds to using Train of 4.βNeuromuscular stimulator level = sedation levelβWatch so patient does not become disconnected from the ventilator, because respiratory muscles are paralyzed and the patient will be apneic***βAct by temporarily suspendingnerve impulses at the neuromuscular junction do the nerve test thing(7) βCan be titrated to produce weakness through complete paralysisβHelps to facilitate easy tracheal intubation and mechanical ventilation byrelaxingthe vocal cords, jaw, and associated respiratory muscles effects of Vecuronium(8)β***Assessing patients airway and respiratory function following the administration is the most important nursing implication***βThe anesthetists ensures respiratory function during the period of anesthesiaMechanical Ventilators- Nursing Considerationsβ***Talk to your patient -> let them know whatβs going on. Patient is still be able to hear and it is scary for them to be in situation and not know whats going on***βNurse should say to bratty colleague : Patient is critically ill on a vent, there is plenty to assess and to reposition frequently(9)βUnconscious - loses motor functionβCannot breathe, talk or blink independently βRetains sensation and is awake and able to hearβMake sure they do not become disconnected from the ventilator8
βAlarms must be on at all timesβEyecare - may not be able to blink independentlyβVTEβSkin breakdown - reposition frequently (Does not have to be major changes)Acute Respiratory FailureβIn acute respiratory failure, the ventilation or perfusion mechanisms in the lung are impaired.***βFluid builds up in the air sacs in your lungsβLungs can't release oxygen into your bloodβThus, organs cannot get enough oxygen-rich blood to function (HYPOXEMIA)βCan also develop acute respiratory failure if your lungs cant remove CO2 from your blood (HYPERCARBIA)βCapillaries or tiny blood vessels, surrounding your air sacs can't properly exchange carbon dioxide for oxygenβCondition can be either acute or chronicβAcute- you experience immediate symptoms from not having enough oxygen in your bodyβChronic- In most cases, this failure may lead to death if its not treated quicklyβCentral nervous systemβDrug overdose, head trauma, infection, hemorrhage, sleep apneaβNeuromuscular dysfunctionβMyasthenia gravis, guillain-barre syndrome, amyotrophic lateral sclerosis, spinal cord traumaβMusculoskeletal dysfunctionβChest trauma, kyphoscoliosis, malnutritionβPulmonary dysfunctionβCOPD, asthma, cystic fibrosisβOxygenation failure mechanismsβPneumonia, ARDS, heart failure, COPD, PEβRestrictive lung diseasesβdiseases that cause a decrease in lung volumeβPost-op medicationsβRespiratory depressionβCan be too much or high of a doseβPainβMay interfere with deep breathing and coughingβPatient cannot remove crap from lungs9
βPain may not be managed enoughβDrug or alcohol abuseβStroke Acute Respiratory Failure - SymptomsβEarly SymptomsβRestlessnessβFatigueβHeadacheβDyspneaβAir hungerβTachycardiaβIncreased BPβAs hypoxemia progressesβConfusionβLethargyβTachypneaβCentral cyanosisβDiaphoresisβRespiratory arrestβInability to complete full sentencesβAccessory muscle use- strainingβAltered mental status Acute Respiratory Failure - TreatmentβVentilationβIntubation Acute Respiratory Failure - Nursing ConsiderationsβRespiratory statusβABGβsβVitalsβTurning scheduleβMouth careβSkin careβRange of motion extremities10
Acute Respiratory Failure - PharmacologyβFurosemide or other loop diuretic - whichever question has the word furosemide in it, pick that lol we think its a pulmonary edema one(10)βIV push orf as a continuous infusionβRapid therapeutic effectβBlood pressure is monitored closely - be alert for hypotensiveβI&OβsβDaily weightsβMonitor serum electrolytes and creatinineβVasodilatorsβIV nitroglycerin or nitroprussideβSymptom relief in pulmonary edema βBUFFER SYSTEMAcid-base BalanceβBody's balance between acidity and alkalinity is referred to as acid-base balanceβBloods acid-base balance is precisely controlled because even a minor deviation from the normal range can severely affect many organsβBody uses different mechanism to control the bloods acid-base balanceManagement of Acid-base balance- CompensationsβThe pulmonary and renal systems compensate for each other to return pH to normalβBlood gas analysis - specific acid-base problemβ1st line of defense - BuffersβSoaks up hydrogen ions when too many are present or squeezing out hydrogen ions when too few are presentβ2nd line of defense- respiratory system 6 to 12 hoursβHyperventilation and hypoventilation will change amounts of arterial CO2β3rd line of defense - renal system MOST POWERFULβTakes days to work completelyβKidney movement of bicarbonate, formation of acids, formation of ammonium compensate depending on direction of pH changesMetabolic Acidosis11
βThe buildup of acid in the body due to kidney disease or kidney failureβWhen your body fluids contain too much acid meansβyour body is either not getting rid of enough acidβMaking too much acidβCannot balance the acid in your bloodβKidneys are unable to remove enough acid from your bloodβLow calcium levelsβManifestationsβHeadacheβConfusionβDrowsinessβIncreases respiratory rate and depthβNausea and vomitingβDecreased blood pressureβCold and clammy skinβDysrhythmiasβShockβDiagnosticsβEKGβABGβhyperkalemia/hypokalemia (monitor closely)βMedical ManagementβCorrect imbalanceβGive bicarbβIn chronic metabolic acidosis, treat calcium levels first(11)βAvoid tetanyβAnion GapβNormal anion gap: DIRECT LOSSβDiarrheaβFistulasβRenal insufficiencyβParenteral nutrition w/o bicarbβLactateβHigh anion gap acidosis: excessive accumulation of fixed acidβMetabolic acidosisβKetoacidosis and lactic acidosis βLate phase of salicylate poisoningβUremia12
βMethanol or ethylene glycol toxicityβKetoacidosis with starvationβPharmacologyβGiving bicarb - what to watch for? βWatch for hypernatremia, hyperkalemia,( its one of these 2) (12) hypocalcemiaMetabolic AlkalosisβHigh pH (decreases H+ concentration)βHigh plasma bicarbonate concentrationβProduced by a gain of bicarbonate or a loss of H+βCausesβGastric suctioningβVomiting (13)βPyloric stenosisβPotassium loss- diuretic useβCushing's syndromeβLong term antacid useβManifestationsβHypercalcemiaβTingling of the fingers and toes (tetany)βDizzinessβHypertonic musclesβRespirations are depressedβAtrial tachycardiaβHypokalemia developsβVentricular disturbancesβDecreased motility and paralytic ileusβChronic metabolic alkalosis symptomβLong term diuretic use(14)βPotassium decreases - PVCβs or U waves are seen on ECGβDiagnosticsβABG - pH greater than 7.45 and a serum bicarbonate concentration greater than 26mEq/LβMedical ManagementβCorrect underlying problemsβI&Oβs - GI lossβRestore fluid volume13
βGive electrolytes as neededβGive tagametβHypoventilationβThe PaCO2 increases as the lungs attempt to compensate for the excess bicarbonate by retaining CO2βHypokalemiaβUrine chloride - ID the cause βPharmacologyβSodium chlorideβPotassium chlorideβTagamet Respiratory AcidosisβpH is less than 7.35 and the PaCO2 is greater than 42 mm Hg and a compensatory increase in HC03βCausesβHypoventilation - inadequate excretion of CO2βAcute pulmonary distressβAspiration of a foreign objectβAtelectasisβPneumothoraxβOverdose of sedativesβSleep apneaβChronic hypercapnia (Excessive CO2 in blood)βSevere pneumonia and acute respiratory distress syndromeβMuscular dystrophyβMultiple sclerosisβMyasthenia gravisβGuillain-barre syndromeβAcuteβSudden spike in CO2 levelsβMedical emergencyβWithout treatment, symptoms will get progressively worse and become life threateningβManifestationsβBreathlessnessβHeadingβWheezing14
βAnxietyβBlurred visionβRestlessnessβCyanosis in the hands and feetβWithout treatment or severeβSleepiness or fatigueβLethargyβDelirium or confusionβInvoluntary muscle movements and twitchingβPossible seizureβPersonality changesβComaβTreatmentsβLook for underlying causeβBronchodilatorsβVentilation - BiPAPβChronicβMay not have symptomsβLong time to developβChemoreceptors in your brain alerted to elevated CO2 ventilationβReceptors- less sensitive - miss the elevationβManifestationsβMemory lossβCoordination problemsβPolycythemiaβPulmonary hypertensionβHeart failureβSleepiness and headaches (obstructive sleep apnea)βEmphysema (15)βTreatmentβLook for underlying causeβAntibioticsβDiureticsβBronchodilatorsβCorticosteroidsβMechanical ventilationβDiagnosticsβABGβs15
βUrinalysisβCBC- electrolytesβDrug screen - ODβChest xrayβECGβLung function tests - ISβPharmacologyβSodium bicarbβBronchodilatorsβAlbuterolβSalmeterolβlevalbuterolβVentilationβAntibioticsβThrombolyticsβanticoagsRespiratory AlkalosisβpH is greater than 7.45 and the PaCO2 is less than 38mm HgβOccurs when you breathe too fast or too deep and carbon dioxide levels drop too lowβCausesβHyperventilation- panic attack or anxiety (16)βHeart attackβPainβDrug useβAsthmaβFeverβCOPDβInfectionβPulmonary embolismβPregnancyβManifestationsβDizzinessβBloatingβLightheadednessβNumbness or muscle spasms (hands/feet)βDiscomfort in chest area16
βConfusionβDry mouthβTingling in armsβHeart palpitations/tachycardiaβSOBβDiagnosticsβABGβsβElectrolytesβToxicology screenβTreatmentβBreathe into bag - raise CO2βReassure patientβPursed lip breathingβPharmacologyβPaper bag - rebreathe CO2βAnxiety meds - valium or benzos Management of Acid-base balance - Nursing ConsiderationsβNursing ConsiderationsβAssess patient and labsβAssess what patient vital signs are telling youβCount patient's respirations for a full minuteβWhat are the rate and depth?βAre they clues to impending or underlying respiratory or metabolic problems?βWhat is the patient's LOC?βConfusion can be early sign of an acid-base disturbanceβCorrelate your patients fluid balance and creatinine levels with kidney functionβCorrelate assessment findings with patients dxβDo they match?βIs some clue pointing you in a different direction?βDouble check implications and adverse effects of all drugs you administer Management of Acid-base balance- ABG interpretation17
Management of Acid-base balance- Electrolyte imbalances with ABG imbalancesPulmonary edema/failure - PathophysiologyβAbnormal accumulation of fluid in the interstitial spaces and alveoli of the lungsβAn acute event that results from left ventricular failureβIt can occur following acute MI or as an exacerbation of chronic HFβWhen the left ventricle begins to fail, blood backs up into the pulmonary circulation, causing pulmonary interstitial edemaPulmonary edema/failure - SymptomsβDifficulty breathing (dyspnea) or extreme SOB that worsens with activity or lying down**βFeeling of suffocating/drowning that worsens lying down**βCough - frothysputum tinged with blood (pink)** - Sit up and dangle feet (17)βWheezing or gasping for breathβCold, clammy skinβAnxietyβRestlessness or sense or apprehensionβBluish lipsβTachycardia18
βIrregular heartbeat (palpitations)βJVDβConfusion/stuporPulmonary edema/failure - DiagnosticsβMake sure to differentiate if this is pneumonia or pulmonary edemaβABGβElectrolytesβBUN, creatinineβBNPβChest x-rayβCTβEKG, ECHOβUSPulmonary edema/failure - PreventionβDiureticsβGet rid of fluid accumulation in bodyβMorphineβManage painβUpright positionβManage weightβLosing weightβLimit salt intakeβWhere salt goes, water goesβBP medicationsPulmonary edema/failure- Nursing interventionsβDangle feet**βPosition uprightβI&OβDaily weightsβTelemetryPulmonary edema/failure- Complications19
Pulmonary edema/failure- TreatmentsβO2βDiureticsβvasodilatorsHepatitis (A,B,C,D,E)- Modes of transmissionβProdromal-βGradual onset of anorexia, malaise, and fatigueβConvalescent-βViral hepatitis begins with the disappearance of jaundice and major symptoms.βMalaise and susceptibility to fatigue may persist for weeks and even months following viral hepatitis.βIcteric-βMay note dark urine, followed by pale-colored stools with GI symptoms- malaise,and develop right upper quadrant pain with hepatomegaly.βViral- MOST COMMON TYPEβHep A, B, C, D, EβAlcoholic- βCaused by heavy alcohol useβToxic-βCaused by poisons, chemicals, medicines, or supplements. βAutoimmune-βChronic type in which your body's immune system attacks your liver. βThe cause is not known, but genetics and environment may play a role.Hepatitis (A,B,C,D,E)- PreventionβHepatitis A20
βFecal Oral routeβIngestion of food or liquids infected with the virusβMore prevalent in countries with overcrowding and poor sanitationβVirus has been found in stool of infected patients before the onset of symptoms and during the first few days of illness.βIncubation period is estimated between 2-6 weeks.βHepatitis A Symptoms-βResemble those of a mild, flu like upper respiratory tract infection with low grade fever.βAnorexia (early sign), jaundice, dark urine, vague epigastric distress, nausea, heartburn, flatulence.βStrong aversion to taste of cigarettes or smoke/strong odorsβFatigue, sudden nausea/vomiting, abdominal pain/discomfort, clay colored BM, low-grade fever, joint pain.βThe liver and spleen are often moderately enlarged for a few days after onset.βThe antigen may be found in the stool 7-10 days before illness and for 2-3 weeks after symptoms appear. βHepatitis A Prevention-βVaccinations - 2 doses (6-12 months apart)βTRaveling, high risk groups, IV drug users, daycare workers(18), healthcare workers, hand hygiene, safe water supplies, proper control of sewage disposal. βHepatitis A Interventions-βBedrestβDiet- small feedings are given frequentlyβIV fluids with glucoseβPhysical activity restrictionsβBut ambulation is still encouragedβHepatitis BβBlood and Body FluidsβMost people who contract HBV develop antibodies and recover spontaneously in6 months.βFor some people Hep B infection can become chronicβIncreases risk for developing liver failure, liver cancer, and cirrhosis.βInfants and children are more likely to develop a chronic Hep B infectionβA VACCINE CAN PREVENT HEP B, but THERE IS NO CURE IF YOU HAVE THE CONDITION21
βHepatitis B Symptoms-βFever, fatigueβJaundice (skin/eyes), dark urine, N/VβClay-colored BM, joint pain, loss of appetiteβHepatitis B Nursing Care-βCoping skills for patient and family diet-βantacids or antiemeticsβNeed protein in the diet to repair the tissuesβBed rest, follow up appointments, blood work,βNo ALCOHOLβGood hygiene (hands/body)βEntecavir, tenofovir, alpha-interferon, pegylated interferonβHepatitis B Prevention- SATA - tattoos, sex, needles - i selected all five(19)βVaccinations β3 doses (over 6 months)βTravelingβHigh risk groupsβIV drug usersβDaycare workers, Healthcare workersβEnd stage renal diseaseβChronic liver disease patients βDISPOSE SYRINGES, NEEDLES, LANCETS. USE GLOVESβHepatitis B Intervention-βKnow the HBV status of any sexual partnersβUse a new latex condom every time you have sexβDonβt use illegal drugsβUse sterile needle each time you inject illicit drugsβNever share needlesβBe cautious about body piercings and tattoosβAsk about Hep B vaccine before you travelβGiven in series of 3 injections over 6 months22
βHepatitis B Medical Intervention-βInjection- immunoglobulin (antibody) within 12 hours of exposureβRest/fluidsβChronic - antiviral medicationsβEntecavir, (baraclude), tenofovir (viread), lamivudine (epivir), adefovir (Hepsera), and telbivudine (Tyzeka), InterferonβLiver transplantβCan form scars and scabs on liver - canβt filter things - liver transplantβHepatitis C-βMost COMMON CHRONIC BLOOD-BORNE INFECTION***βA combination of 2 antiviral agents (peginterferon and ribavirin) effect in producing improvement in patients with Hep C and in treating relapses.βHepatitis D-βInterferon alpha is the only licensed drug available in the treatment of HDV infectionβHigh dose, long duration therapy for at least a year is recommended.βWater soluble Vitamins - A, D, E, KβYou can't have Hep D without having Hep B.βHepatitis E-βFecal- Oral routeβSimilar to Hep BβAbrupt onsetβJaundiceβCanβt have Hep E without having Hep AβHepatitis E Prevention-βImmunoglobulins βHand hygieneHepatitis (A,B,C,D,E)- Risk Factors βHepatitis A-βFood contaminated with fecal matter, consuming water or shellfish from sewage-contaminated waters, poor hygiene, sexual activity.βHepatitis B-23
βHaving sex with an infected personβSharing dirty needles βBeing in direct contact with infected blood, saliva, semenβGetting needle stick injuries βBeing transferred from mother to unborn child (birth)βAll pregnant women should be tested for hepatitis BβWithin 24 hours of birth, infants born to mothers with Hep B need to receive treatment with Hep B antibody and Hep B vaccine.βHepatitis C-βSharing needlesβBeing in direct contact with infected bloodβGetting needle stick injuries or mucosal exposure to bloodβHaving sex with an infected person is LESS COMMONβLONG TERM DRUG USAGE***βNO BENEFIT FROM REST, DIET, VITAMIN SUPPLEMENTS***βChildren born to women infected with Hep C virusβMultpile sex partners, history of sexually transmitted infections, unprotected sexβPast/current illicit IV/injection drug useβHepatitis D-βIV or injection drugsβPatients undergoing hemodialysisβRecipients of multiple blood transfusionsβSexual contact with those who ahve Hep B.βHepatitis E-βEating, drinking food, or water contaminated with the virus undercooked foodsβPork, venison, shellfishβUncommon in the Us but can occur after travel to a country where this infection is commonβDangerous or fatal in pregnant womenHepatitis- NutritionβBed rest during acute stage and nutritious diet are important aspects of treatmentβSmall frequent feedings, supplemented by IV fluids with glucose if necessary 24
Dietary Management of HepatitisβAdvise patient to avoid substances (medications, herbs, illicit drugs, and toxins) that may affect liver function, such as St. John wort in patients taking hepatitis C virus protease inhibitors.βBe aware that that enteral feedings may be necessary if anorexia, nausea, and vomiting persist.βCarefully monitor fluid balance.βInstruct patient to abstain from alcohol during acute illness and for at least 6 months after recovery.βProvide intake of 25β30 kcal/day.βProvide protein intake of 1.2β1.5 g/kg/day.βRecommend small, frequent meals; minimize periods without food intake.Hepatitis Medications-********βNucleoside Analogs -Hep BβPegylated interferon and antiviral agentsβLamivudine-βPatients who have evidence of Hep B viral replication and active inflammation of the liverβPost exposureβRibavirin-βOral antiviral drug administered in combination with peginterferon alpha-2a or peginterferon alpha-2bβAcute HCV Therapy-βPegylated interferonβSupportive therapy-βAntiemeticsβDo not use phenothiazines βSedative/HypnoticsβChronic HCV-βPegylated a-interferon given with ribavirinβDirect acting antivirals (DAA)βChronic HBV)-25
βFocus on decreasedβPegylated interferonβEntecavirβTenofovirHepatitis- Medication InducedβToxic-βExposure to hepatotoxic chemicals, medications, botanical agents, or other toxic agents in the early treatments and removal of the causative agentβSigns and Symptoms-βAnorexia, N/V - usual symptomsβJaundice and hepatomegaly βClotting issuesβDelirium, coma, seizureβSymptoms are more intense for these patientsβDrug Induced - Can Be Severe-SATA(20)βChills, fever, rash, pruritus, arthralgia, anorexia, headache, nausea ***βLater- jaundice, dark urine, enlarged/tender liverβAfter offending medication is withdrawn, symptoms may gradually disappearβAnesthetic agentsβMedications used to treat rheumatic.musculoskeletal diseaseβAntidepressants (WE ARE SCREWED) βPsychotropic medicationsβAnticonvulsant, antituberculosis agents βCORTICOSTEROIDSβOVERALL PREVENTIONβGet the vaccines for HEP A AND HEP B**βUse a condomβDonβt share needlesβPRACTICE GOOD HAND HYGIENE (SOAP AND WATER) **βDon't use infected persons itemsβTake precautions when getting any tattoos or body piercings26
βTake precautions when traveling to areas of the work with poor sanitation (makesure you get vaccines before you go)βDrink BOTTLED WATER while traveling (or you will be in the shitter)Pancreatitis- PathophysiologyβPancreas is a long, skinny gland located in the upper abdomen (epigastric region) behindthe stomachβCan be mild or severe (necrotizing) another name for pancreatitis.(21)βCan be acute or chronicβThe most common cause of pancreatitis is stones in the gallbladder.βStones pass through the common bile duct to enter small intestines, stones get stuck and cause obstruction of normal flow of pancreatic fluid leading to pancreatic injuryβPlays a role in endocrine - insulin/glucagon that are secreted into the bloodstreamβPlays a role in exocrine - digestive enzymes secreted into duodenum to digest food.βEnzymes break down macromoleculesβCarbohydrates, lipids, proteinsβIf cause is not found, IDIOPATHIC. ** NO IDEA WHAT IS GOING ONPancreatitis- Clinical manifestationsβAlcoholism- most common cause in men(22)βGallbladder disease- biliary stones - most common in womenβASK ABOUT HISTORY OF ETOH βAbdominal pain - midepigastric βRigid, indicates peritonitis (very painful) - Most cause for concern in acute(23)βProgressive abdominal distentionβDecreased bowel activityβN/V, low grade fever, leukocytosis, hypotension, tachycardia, βJaundice (possibly)βLUQ OR MID EPIGASTRIUM COMMONLY RADIATES TO THE SHOULDER OR BACKβOFTEN OCCURING 24-48 HOURS AFTER FATTY MEAL OR HEAVY ALCOHOL INTAKEβCAN HAVE ABDOMINAL TENDERNESS WITH GUARDING AND RIGIDITY27
βCAN BE DEEP, SEVERE, PIERCING, CONTINUOUS PAIN, FREQUENT ONSET WHENPATIENT IS LYING DOWNβCullen Sign-βCircle pattern βAround umbilicusβGrey-Turner Sign-βNo pattern/shape βIn the flank area.βDiagnostic Tests-βSerum amylase and lipase- PRIMARY TESTS***βSerum glucoseβSerum calcium - will be decreasedβLiver functions testsβMRI, CT, X-RAY - show enlargementPancreatitis- TreatmentβNPO to reduce pancreatic secretions - initiallyβNO ALCOHOLβSmall frequent feeding - once they can eatβHigh carbohydratesβBland diet with no stimulants - NO CAFFEINEβSupplemental fat-soluble vitamins (A, D, E, K)βTPN in severe malnutritionβREMEMBER PATIENTS CANNOT DIGEST PROTEIN AND FATSβBland dietβRest pancreas to digestβRELIEF OF PAIN - non stop pain meds - Give IV morphine (24)βPrevention/control of shockβReduction of pancreatic secretionsβControl of fluid and electrolyte imbalances28
Pancreatitis- Nursing Management-β#1 priority - relieve pain and decrease secretion of pancreatic enzymesβParenteral opioids- morphine, hydromorphone, fentanylβPCA pump or bolusβPain assessmentsβComfort care and effectiveness of medicationsβOral feeding is withheldβFluids are givenβGastric enzymesβNG tube insertion and maintenance, oral hygieneβBedrest- Semi Fowlers- most comfortableβMonitor ABGs, pulse Ox, daily weights, I&OβMonitor/measure abdominal girth for distention **βMonitor labs- low calcium and magnesium**Pancreatitis Medications-βCimetidine (Tagamet)/Ranitidine (Zantac)βDecrease pancreatic activity by inhibiting the secretion of gastric acidβPantoprazole (Protonix) Proton Pump Inhibitors-βMay be used for patients who do not tolerate H2 antagonists or for whom this therapy is ineffectiveβMorphine, Fetanyl, Dilaudid-βIV for severe painβZofran-βNauseaβAntibiotics-βInfectionβGlucose Levels-βPancreas is affected/not eatingPancreatitis- ComplicationsβRespond quickly to changes in patient status - think SHOCK!βHypovolemicβHemorrhageβSepticβMultiple Organ Dysfunction Syndrome (MODS)βIncreasing pain needs to be reported to MD immediately.29
Chronic Pancreatitis- CausesβThe most common cause is long-term alcohol abuseβMenβ70% are linked to alcohol consumptionβMalnutritionβDiabetesβObstructionβMetabolic disturbancesβTrauma, pseudocysts, Systemic diseases (Lupus/CF)Chronic Pancreatitis- Clinical manifestationsβPain in upper abdomen - recurring and severeβDiarrhea/Fatty stools-βSmelly, loose, pale, doesnβt flush away easily (malabsorption)(25)βNausea/vomitingβSOB, fatigue, excessive thirst, unexplained weight loss (fear of eating)βProgressive to more severe symptoms-βPain - more severe, more frequent, longer duration, constant pancreatic fluids in your abdomenβJaundice, internal bleeding, intestinal blockageβDiagnostic tests-βSerum amylase and lipaseβSerum bilirubinβAlkaline phosphatase, mild leukocytosis, increased sed rate, secretin stimulation test, blood glucose levels, ERCP, X-rays, ultrasounds, CT, US.βSurgical-βThe goal is to restore drainage reduce, pain, and attacks.(26)βPancreaticojejunostomyβEndoscopic or laparoscopic interventionβStentsChronic Pancreatitis- TreatmentβEffective pain management 30
βIV morphine, fentanyl, hydromorphoneβLow-fat, bland dietβSupplemental pancreatic enzymesβELIMINATE ALCOHOLβBile salts to facilitate absorption of fat-soluble vitamins (ADEK)βControl diabetes and teach to monitor blood glucoseβAntacids and anticholinergics to decrease gastric acidsβSmall frequent meals, patients do not tolerate fatty, rich, and stimulation foods.Enteral NutritionβRefer to any method of feeding that uses the GI tract to deliver part or all of a person caloric requirementsβIt can include-βNormal oral dietβUse of liquid supplementsβDelivery of part or all the daily requirements by use of a tubeβNG tube (tube feeding)Parenteral Nutrition-βIV administration (blood stream) of nutrition for patients that cannot eat or absorb enough food through tube feeding formula or by mouth to maintain good nutrition statusβProteinβCarbohydratesβFatsβMinerals/VitaminsβElectrolytesβDelivers concentrated nutrients/solutions IV to maintain or supplement nutritional balance when oral or enteral nutrition is inadequate or not possible.Components of TPN-βCarbohydratesβFat emulsion (lipids) VERY STICKYβProtein (amino acids)βWater31
βElectrolytesβVitamins and trace mineralsAspiration Prevention-βCheck residual every 4-6 hours and before feeding to see if tolerating the feeding.βWill hold feeding if residual is too highβThese patients need to be at 30 angle or higher when receiving tube feedingβMinimizes aspirationβDo not lay patients flat while tube feeding is infusing and before a procedureβTurn off tube feeding when going to CT, MRI about 30 minutes before goingTypes of Tubes-βNG Tube-βStarts in the nose and ends in the stomachβOrogastric Tube (OGT)-βStarts in the mouth and ends in the stomachβGastroenteric Tube-βStarts in the nose and ends in the intestinesβSubtypes are: nasojejunal and nasoduodenal tubesβOroenteric Tube-βStarts in the mouth and ends in the intestinesβGastrostomy Tube (G- Tube)-βPlaced through the skin of the abdomen straight into the stomachβSubtypes are: PEG, PRG, button tubeβJejunostomy Tube (J-Tube)-βPlaced through the skin of the abdomen straight through into the intestinesβSubtypes are: PEJ, PRJ tubesThings to Know About Feedings-βBag should only hang for 24 hours βMade in pharmacy using aseptic technique and sent up/placed in the refrigerator.βTubing gets changed every 24 hours for lipids β72 hours for regular without lipidsβIf TPN sits out beyond the time it should, fat emulsion portion at room temp becomes a medium for microorganism growth32
βPatients can become extremely ill with fevers and vomitingβIf TPN is completed before new bag arrives, hang 5% dextrose solution βD5W, 5%, 10%, 20% dextroseβWatch for hypoglycemia!!Cirrhosis- PathophysiologyβLate stage liver disease where healthy liver tissue is replaced with scar tissue and the liver is permanently damaged. βScar tissue keeps your liver from working properly.βScar tissue blocks the flow of blood through the liver and slows the liver's ability to process nutrients, hormones, drugs, and natural toxins (poisons)βMany types of liver diseases and conditions can injure healthy liver cells, causing cell death and inflammation, followed by cell repair and finally tissue scarring as a result from the repair process.βReduces the production of proteins and other substances made by the liverβCirrhosis eventually keeps the liver from working properlyβLate stage cirrhosis is life-threateningTypes of Cirrhosis-βAlcoholic cirrhosis-βScar tissue characteristically surrounds the portal areas.βMost frequently caused by alcoholism and is the MOST COMMON TYPE OF CIRRHOSIS.βPostnecrotic cirrhosis-βBroad bands or scar tissue is a late result of a previous bout of acute viral hepatitis.(27)βBiliary cirrhosis- (less common)βScarring occurs in the liver around the bile ducts.βResults from chronic biliary obstruction and infection (cholangitis)Cirrhosis- Treatments βTreatment is usually symptomaticβIncluding antacids or H2 antagonists to decrease gastric distress and minimize the possibility of GI bleedingβVitaminsβOrganic compounds that help to release energy from carbohydrates, fats and proteins33
βUsed to improve health and prevent or treat illnessβEarly recognition and treatment with vitamins can prevent mild deficiency βMineralsβThese maintain acid-base balance and osmotic pressureβOccur in the body and foods mainly in ionic formβNutritional productsβEnteral nutritionβParenteral nutritionβ Hopefully used for short term (3-5 days) the goal is to provide adequate amounts of fluids and electrolytes β For long term use the goal is to provide nutrients required for normal body functioning (including tissue repair)βPotassium-sparing DiureticsβSpironolactone (Aldactone):reduces retention of sodium and waterβ Adverse effects: dizzy, headache, abdominal cramping, diarrheaβAmiloride (Midamor) and TTriamterene (Dyrenium)β These drugs decrease the exchange of sodium for potassium and have similar diuretic activityβThiazolidinediones βRosiglitazone maleate (Avandia)β Stimulates receptors on muscle, fat and liver cellsβIncreasing or restoring the effectiveness of circulating insulinβ Adverse effects include liver injury and diarrheaCirrhosis- Clinical manifestationsβFever- MildβEpistaxis - NosebleedβHypotensionβJaundiceβWeight lossβBruisingβWeaknessβLate stage symptoms- (28 Sata quizlet)βEasy bruising and bleedingβJaundiceβItchy skin34
βEdemaβAscites - abdominal girth measurementsβSpider-like blood vessels surround small, red spots on skin (telangiectasia) βIN MEN:βLoss of sex drive, enlarged breasts (gynecomastia), shrunken testiclesβIN WOMEN:βPremature menopause (no longer having your period)βBrownish or orange color urineβLight colors stoolβConfusion- difficulty thinking, memory loss, personality changesβBlood in stoolβRedness - palms of the handsCirrhosis- Complications-βEdema and ascitesβInfectionsβMalnutritionβBuildup of toxins in the brainβHepatic encephalopathyβJaundiceβBone Disease- calcium - fracturesβIncreased risk of liver cancerβMultiorgan failureCirrhosis- Nursing Care-βRestβI&OsβDaily weightsβFluid volume excess βSalt and fluid restrictionsβAbdominal girthβAssess for edemaβFluid volume excessβProtection of the side railsβSeizuresβBleeding precautions-βClotting factorsβAssess mental status35
βAssess for oliguriaβOnce eating and stronger-βActivity followed by rest periods.Cirrhosis- TreatmentβMedications to alleviate symptoms- NO CURE (awww booo)(29)βSpironolactone (Aldactone)βReduces retention of salt and waterβGive with foodβMax effect takes 6 weeks βSame time every morningβRosiglitazone maleate (Avandia)βRestoring effectivement of circulating insulinβMonitor liver enzymes q2mo for 1 yearβTake with mealsβGlucose checksβAssess cardiac and lung soundsβHistamine 2 Receptor Antagonists (Cimetidine, famotidine, nizatidine, ranitidine)βInhibits secretion of gastric acid, decreasing the acidity of gastric juicesβPrevent and treat heartburn PUD, GERD, esophagitis, GI bleeding due to stress ulcers.βProton Pump Inhibitors (Omeprazole, esomeprazole, lansoprazole, pantoprazole,rabeprazole)-βBinds irreversibility to the gastric proton pump to prevent the release of gastric acid.βProtonix- Decrease gastric acidβHerbals-βMilk Thistle just document in patient chart(30)36
βTreats jaundice and other symptomsβMay be okay to takeCirrhosis- Patient EducationβProvide dietary instruction, including exclusion of alcoholβRefer to alcoholics anonymous (AA), psychiatric care counseling, spiritual advisor if indicated βContinue sodium restrictionβStress avoidance of raw shellfishβEducate patient and family using written instructions, reinforcement, supportβEncourage rest and probably change in lifestyle βAdequate dietary intake and elimination of alcoholβInstruct family about symptoms of impending encephalopathy and possible bleeding tendencies and susceptibility to infectionβOffer support and encouragement to the patient and provide positive feedback when the patient experiences success.βRefer patients to home care nurses, and assist in transition from hospital to home.Acute renal failure- ClassificationβAlso called Acute Kidney InjuryβSudden episode of kidney failure or kidney damage that happens within a few hours or daysβRapid loss of renal funcion due to damaged kidneysβAKI causes a buildup of waste products in your blood and makes it hard for your kidneys to keep the right balance of fluid in your bodyβInjury (structural damage)βImpairment (loss of function)βA syndrome that rarely has a sole and distinct pathophysiology βUnderlying causes need to be addressed promptly before kidney injury developsβConditions that reduce blood flow to the kidney and impair kidney functionβHypovolemiaβHypotensionβReduced cardiac output and heart failure βObstruction of kidney or lower urinary tract by tumor, blood clot or kidney stoneβBilateral obstruction of the renal arteries or veins37
βGOAL: treat and correct before the kidneys are permanently damaged, the increased BUN and creatinine levels, oliguria and other signs may be reversedClassifications of Acute Kidney Injury (RIFLE) (31)βR: riskβI: injuryβF: failureβL: lossβESKD: end stage kidney diseaseβ1) risk, injury, and failure are considered grades of AKI severityβ2) loss and ESKD are considered outcomes of loss that require some form of renal replacement therapyAcute renal failure- Pre/Intra/Post renalβPrerenal - sudden and severe drop in blood pressure (shock) or interruption of blood flow to the kidneys from severe injury or illness (hypoperfusion of kidneys)(32)βIntrarenal- direct damage to the kidneys by inflammation, toxins, drugs, infection, or reduced blood supply (acute damage)βPostrenal- sudden obstruction of urine flow due to enlarged prostate, kidney stones, bladder tumor, or injury4 Phases of AKI1)Theinitiation period begins with the initial insult and ends when oliguria develops2)The oliguriaperiod is accompanied by an increase in urea, creatinine, uric acid, organic acids, as well as potassium and magnesiuma)Minimum amount of urine needed to rid the body of normal metabolic waste products is 400mL in 24 hours or 0.5mL/kg/hrb)In this phase, uremic symptoms first appear and life threatening conditions such as hyperkalemia developβ Oliguria - <400mL/day - occurs w/n 1-7 days of kidney injuryβ Urinalysis - casts, RBC, WBC, sp gr fixated at 1.010β Metabolic Acidosisβ Hyperkalemia and Hyponatremiaβ Elevated BUN and Creatinineβ Fatigue and Malaise3)The diuresis period - a gradual increase in urine output, which signals that glomerular filtration has started to recover. Laboratory values stabilize and eventually decreaseβ Gradual increase in urine output - 1-3 L/day, may reach 3-5 L/day38
β Hypovolemia, Dehydrationβ Hypotensionβ BUN and Creatinine levels begin to normalize4)The recovery period signals the improvement of renal functions and may take 3 to 12 months. Laboratory values return to normal β Begins when GFR increasesβ BUN and Creatinine levels plateau, then decreaseAcute Renal Failure Symptomsβ**You might not notice any symptoms of AKI at first**βNot enough urine (oliguric)βSwelling in legs, ankesl, feet - retentionβFeeling tired or drowsyβTrouble catching breathβFeeling confusedβNauseaβPain or pressure in chestβDry mucous membranesβTwitchingβLethargicβJVDβSEVERE AKI- seizures or fall into comaβRadiocontrast-induced nephropathy (CIN)βMajor cause of hospital acquired AKIβPreventableβ1% require dialysis or hospitalizationβAssessβbaseline levels of creatinine greater than 2 mg/dl (high-risk patient)βPreventionβLimit exposureβMonitor medications - nephrotoxicβPrehydrate before procedure with NS - creatinine level 4 so give IV(33)βAdminister bicarb before the procedure GRF decrease = creatinine increase(34)Acute renal failure diagnostics/labs39
βDiagnosticsβUS, CT, MRIβUrinalysisβRenal scan - how kidney is working - IRβBiopsy βEarly detection (3 Rβs)βRecognition βResponseβReferral βLabsβLow specific gravityβHematuriaβPrerenal azotemia - decreased sodiumβIntrarenal azotemia - increased sodiumβBUN level - increases steadilyβSerum creatinine levelsβDecreased GFR, oliguria, anuria, - high risk for hyperkalemiaβPhosphates increased - calcium decreasedβLow hemoglobinAcute renal failure- PrecautionsβRestore balanceβEliminate the underlying causeβMaintain fluid balanceβAvoid fluid excessβRehydrateβStop post op hemorrhageβGI losses (V/D) - give medicationsβRelieve obstructionβBlood transfusionβDialysisβMedication βshould be monitored closely - canβt filter them outβAminoglycosidesβGentamicinβTobramycinβColistimethate40
βCyclosporineβNSAIDSβmay cause interstitial nephritisβContrast dyeβLimit exposureβN-acetylcysteine and sodium bicarbonate before and during procedures reduce riskβPrehydration with salineβDehydrationβMake fluids available to elderly patientsβBowel PrepsβWatch for dehydrationChronic Renal Failure Nursing CareβDaily weightsβI&OβHigh calorie, low protein, low potassium, low sodium dietβAvoid high potassium foods and sports drinks - high sodiumβAvoid potassium or phosphorus (bananas, citrus fruits and juices, coffee)βAfter diuretic phase βhigh protein, high calorie dietβEncourage to resume activities graduallyβMonitor fluid and electrolytes - hyperkalemiaβReduce metabolic rate- bed rest may be neededβAlterations in heart sounds and breath soundsβEdema- can lead to skin breakdownβJVDβIncreased difficulty in breathingβCough and IS useβMaintain bedrestβFoley care - *prevent infections* - avoid catheter if possible Chronic renal failure- Clinical manifestationsβBegins with a slow decline in renal function and is irreversibleβWhen damaged kidneys have been unable to process waste efficiently for longer than 3 months, as indicated by abnormal creatinine levels41
βUnless preceded by AKI initially, there may not be any signs or symptoms of kidney disease and substantial damage can occur before the disease is detected in the early stakes of CKDβSerum creatinine levels may even be normal, but the kidneys begin leaking protein or red blood cells into the urineβBy the time the disease is detected, the GFR can be substantially reducedβPsychologicalβWithdrawnβBehavior changesβDepressionβNeurologicalβWeakness/fatigueβConfusion βHematologicalβAnemiaβBleeding tendenciesβIncreased serum KβCardiovascularβIncreased BPβIncreased CVPβPitting edemaβPeriorbital edemaβPericarditisβSkinβDry flakyβPruritusβEcchymosisβPurpuraβYellow-gray skin colorβPulmonaryβSOBβDepressed coughβThick sputumβGIβAmmonia odor to breathβMetallic tasteβMouth/gum ulcerationsβAnorexia42
βNausea/vomiting βMusculoskeletalβCrampsβRenal osteodystrophyβBone painβHemodialysisβEvaluate access site for patency and signs of infectionβDO NOTtake blood pressure or obtain blood samples from extremity that has access siteESRD - End Stage Renal DiseaseβMost severe stage of chronic kidney diseaseβYour kidneys are no longer working well enough for you to live without dialysis or kidneytransplant - need one or the otherβBest way to prevent ESRD (kidney failure) is to prevent CKDβPreventable factors βDiabetesβHTNβHeart diseaseβNon Preventable factorsβFamily hxβAfrican American, Hispanic, Native American, AsianChronic renal failure- DiagnosticsβGFR - decreases (due to non functioning glomeruli)βCreatinine clearance - decreasesβSerum creatinine and BUN levels increaseβUrine tests - check the level of protein albumin in your urineβImaging tests:βUltrasoundβMRIβCT scanβKidney tissue biopsyChronic renal failure - Clinical Manifestationsβ*d/t accumulation of uremic waste products*βNausea/ vomiting43
βLoss of appetiteβFatigue and weaknessβChanges in how much you urinateβChest pain - if fluid builds up around the lining of heartβSOB - if fluid builds up in the lungsβSwelling of feet and anklesβHigh blood pressure (hypertension) - difficult to controlβHeadacheβDifficult sleepingβDecreased mental sharpnessβMuscle twitches and crampsβPersistent itchingβMetallic tasteβAsterixis - (35)βperson loses motor control of some parts of bodyβCommonly called flapping hand tremor βLoss of muscle control and irregular jerking movement in hands 5 Stages of Kidney DiseaseβStage 1βGFR >90βNormal or high functionβStage 2β89>GFR>60βMildly decreased functionβStage 3Aβ59>GFR>40βMild to moderately decreased functionβStage 3Bβ44>GFR>30βMild to moderately decreased functionβStage 4β29>GFR>15βSeverely decreased functionβStage 5βGFR<15βKidney failure44
Chronic renal failure- NutritionβDietβRegulation of protein intakeβFluid intake to balance fluid lossesβSodium intake to balance sodium lossesβRestriction of potassiumβAvoid alcohol βSATA: dont pick calories and calcium - pick the other three(36)Chronic renal failure- TreatmentsβMedicationsβCalcium phosphorus bindersβAntihypertensivesβAnticonvulsants βErythropoietinβDialysisChronic Renal failure - Nursing educationβWorsening signs and symptoms of kidney diseaseβNauseaβVomitingβChange in usual urine outputβAmmonia odor on breathβSigns and symptoms of hyperkalemiaβMuscle weaknessβDiarrheaβAbdominal crampsβSigns and symptoms of access problemsβClotted fistula or graftβInfectionβFollow up examsβDiet and restrictions The Kidney Bean - Some considerations45
βThe aging kidney is less able to compensate for changes in fluid volume, solute load, cardiac outputβMore susceptible to AKIβDehydration is associated with:βPolypharmacyβDiuretics, laxatives, drugs that suppress appetite or consciousnessβAcute febrile illnessβBeing bedriddenβCardiovascular disease or diabetes mellitus can increase the risk of developing AKIβAminoglycosides, gentamicin can be nephrotoxicβMonitor kidney function with creatinine labs Dialysis- IndicationsβGOALSβRemove excess fluid and toxinsβBalance electrolytes(37)βManage and correct acidosis Dialysis- HemodialysisβHemodialysisβAcutely ill and require short term dialysis for days to weeks until kidney function resumes βLong-term or permanent renal replacement therapy βPrevents death but does not cure kidney disease and does not compensate for the loss of endocrine or metabolic activities of the kidneysβ3 times a weekβ3 to 5 hours in an outpatient settingβHome - time & frequency can be different per patientβRequires a vascular access siteβArteriovenous shuntβPortβFistulaβAdvantagesβHome and/or at a dialysis centerβRemoves fluid rapidlyβExcellent for potassium removal46
βLess protein lossβLowers serum triglycerides quickly βQuickly removes urea and creatinineβTemporary access may be obtained quicklyβDisadvantagesβProblems obtaining vascular accessβVery strict diet and fluid limitsβHeparin may be required to keep access openβBlood loss, which contributes to anemiaβTrained personnel requiredβPermanent access requires a surgical procedureβSeveral hours to recover from treatmentβStrict diet maintaining low phosphorus and potassium intakeβ AV FistulaβMust have good veinsβFistula is a connection of the vein to the artery directlyβAfter the operation the vein needs to mature and get bigger and thicker in size before it can be successfully used for dialysisβMost durable option because if it matures successfully, it lasts much longer than an AV graftsβAV fistulas are much less likely to clot than graftsβMake sure you are checking a patient's fistula βListen for bruit βPalpate for thrillβPresence of a thrill and bruit indicate adequate blood flow through fistula β AV GraftβIf veins are not good qualityβThere is a synthetic Teflon graft connecting the artery to the vein βAdvantageβcan be used as early as 2 weeksβDisadvantageβGraft does not last as long as a fistula 47
βHalf of these grafts will clot off in the first yearβ***If a patient β pain and coldness on the arm of the graft, make sure you report the patients symptoms to the doctor***βCan be an indication of distal ischemia that may require revisionββ Hemodialysis Nursing CareβAssess for toxic levels of medicationsβWater solubleβFat solubleβPromote good nutrition and fluid intake βPrevent uremiaβProtein restriction β1.2 to 1.3 g/kg dailyβFluid restrictions βDaily urine output plus 500 mL/dayβSodium restrictions β2 to 3 g/dayβPotassium restrictionβPhosphorus restrictionβMonitor vitalsβPsychological needs βPatient βFamily Dialysis Types - PeritonealβPeritonealβRequires access via an implanted port with a catheter placed in the anterior wall of the abdomenβAutomated peritoneal dialysis (APD)βAccomplish dialysis while they sleepβMachine cycles four or more exchanges per night β1 to 2 hours per exchange βContinuous ambulatory peritoneal dialysis (CAPD)βManuallyβ1.5 to 3 L of peritoneal dialysate48
βAt least four times daily - dwell times averaging 4 hoursβEx: one schedule exchanges at 7:00am, 12:00pm, 5:00pm, 10:00pmβAdvantagesβNo need for vascular accessβLess dietary and fluid restrictionsβBetter BP controlβNot as complicated as hemodialysisβCan be done at homeβCauses fewer cardiovascular problemsβIncreased mobilityβEasier to manage for patients with diabetes βDisadvantagesβInfections risk (peritonitis) βChronic back pain or herniaβRisk of hyperglycemiaβSurgery needed for catheter placementβCatheter may migrateβContraindicated for patients with abdominal surgeriesβTransporting solutions and pump needed for travelβIncreased risk of hyperlipidemiaβMust be done dailyβNutritional complicationsβPatients tend to gain weight overtime d/t calories from dextrose in the dialysateβ***if a patient is struggling to drain dialysate from the abdomen, gentle massagecan help***β***warm the dialysate to prevent cramps*** β Peritoneal Nursing Care βPsychological needsβPatientβFamilyβWatch electrolytesβPruritus and pain secondary to neuropathyβVitalsβPrevent infectionβDaily or 3-4 times weekly routine catheter site care is typically performed during showering or bathing49
βWarm dialysate to body temperature with a heating pad to prevent discomfort(38) βDiet restrictions - Limit SATA(39)βProteinβSodiumβPotassiumβPhosphorusβFluidsDialysis- ProcessβDialyserβHollow-fiber device containing thousands of tiny capillary tubes that carry the blood through the artificial kidneyβSemipermeable membrane allows toxins, fluids, and electrolytes to pass across the membraneβBlood crosses the membrane into the dialysate solution where wastes are removed and discarded Dialysis- Safety Pharmacological treatment- ComplicationsβHyperkalemiaβKayexalate(40)βBicarbβCalcium gluconateβGlucose50
βInsulinβConstipationβSorbitol βRenal impairmentβCalciumβPulmonary edemaβLasixβEdema - renal, hepaticβLasixβBumexβHydrochlorothiazideβSpironolactone - this might be on there for cirrhosis βFluid volume excessβMannitolβAnemiaβEpogenβProcrit 41: question 150mL/hr IV fluids for kidney pt in hospital with infection42: offer palliative care to old conservative ladyTwo - abg Two or 3 - med math 51