Med-Surg Test 2

  1. Perspectives on Care of Children with Special Needs:
    Scope Of Problem
    • can present family with additional tasks, responsibilities, and concerns. Such as child's activity level and developmental opportunities.(days are lost from school, child may be at increased risk for behavior or emotional problems, parents lose days from work, parents may experience financial strain, parents may be challenged emotionally and physically as they cope with care of their sick child, siblings may be affected by feeling guilt, anger, or even jealousy. Secondary losses such as ability to participate in extracurricular activities or social events because of routines imposed by the affected child's chronic condition.

  2. Perspectives on Care of Children with Special Needs:
    Trends in care:
    • – Developmental focus-focus on child's developmental level rather than chornologic age. Normalize experiences, adapt the environment, and promote coping skills.Family development can be affected as well.
    • – Family-centered care- children's physical and emotional health, as well as congnitive and social functioning is strongly influenced by how well their families function. NEED to form a partnership with parents as a nurse. COLLABORATIVE RELATIONSHIPS - communicate, dialogue, active listening, awareness, and acceptance of differences.
    • – “Normalization”- behaviors and intentions of the disabled to integrate into society by living life as persons without a disability would. this would include attending school, pursuing hobbies and recreational interests, and achieving employment and a level of independence. Home care. Mainstreaming- integrating special needs children into regular classrooms. The Education for All HAndicapped Children Act of 1975 and it's amendments which changed the name to Individuals with Disabilities Education Act (IDEA). The Education of the Handicapped Act Amendments of 1986-directs states to develop and implement state wide comprehensive, coordinated, multidisciplinary interagency programs of early intervention services for infants and toddlers with disabilites and support services. Americans with Disabilities Act of 1990.
    • Managed care-major form of health care provision in the US.
  3. Impact of Child’s Chronic Illness or Disability: Parents: anticipated parental stress points
    • Diagnosis of condition-learning about diagnosis along with dealing with emotions.
    • developmental milestones- delayed or impossible for child.
    • start of schooling- stressful because it will not be a regular classroom setting.
    • reaching ultimate attainmentadolescence-accepting that some things just wont happen for the child.
    • future placement-will the child live in a home when they become an adult or when parents are unable to care for them anymore.
    • death of child
  4. Impact of Child’s Chronic Illness or Disability•Parents: adaptive tasks
    • - Accept childs condtion
    • -manage the childs condition on dayto day basis
    • -meet childs norm developmental needs
    • -meet developmental needs of other familt members
    • -cope with ongoing stress and periodic crisis
    • -assist family members to manage feelings
    • -educate others about the childs conditions
    • -establish a support system.
  5. Impact of Child’s Chronic Illness or Disability•Parents
    • Stress of grieving the loss of perfect child.
    • Series of unrewarding experiences can contribute to feelings of inadeuqacy and failure.
    • INTERVENTIONS: Educate parent on what can be expected of child, assist in identifying childs strengths, praise parents for jobs well done, and respite care.
  6. Impact of Child’s Chronic Illness or Disability•Parents: PARENTAL ROLES
    • must perform complex care and symptom management, seek and coordinate health and social services. Then the family must balance their own needs, extended family and friends, personal health and obligations to maintain family function.
    • Often one partner can feel neglected and resentful and incompetent in child's care.
    • Communication and support may be affected.
    • Stressors: burden of care by one parent, finnacial burden, fear od childs death, pressure from relatives, hereditary nature of disease, and fear of pregnancy.
  7. Impact of Child’s Chronic Illness or Disability•Parents: MOTHER-FATHER DIFFERENCES
    mothers are more susceptible to psychologic distress and fatigue, and social isolation. give up job to stay at home with ill child.

    Fathers- role of protector is challenged. may feel depressed weak guilty powerless isolated embarassed and angry may hide emotions and pretend everything is fine.
  8. Impact of Child’s Chronic Illness or Disability•Parents: SINGLE PARENT FAMILIES
    • burden of one person.
    • Find financial and support services to ease burden of care.
  9. Impact of Child’s Chronic Illness or Disability•Siblings
    • negative effect. Report depression and anxiety more often than peers.
    • no more at risk for severe psychiatric problems.
    • Factors that increase negative effects: responsibility for caregiving, diferential treatment by parents, and limitations in family resources and recreational time are often the experience of siblings.
    • IMPORTANT: give child information and knowledge about siblings condition. Promote healthy sibling realtionships, help siblings cope, and involve the siblings.
  10. Coping with Ongoing Stress and Periodic Crises
    • -provide anticipatory guidance
    • -provide emotional support
    • -assist family in assessing and identifying specific stressors
    • -aid family in developing coping mechanisms and problem solving strategies and working collaboratively to help parents become empowered.
  11. Coping with Ongoing Stress and Periodic Crises
    • Concurrent stresses within the family
    • •Coping mechanisms
    • •Parental empowerment
  12. Assisting Family Members in Managing Feelings
    • •Shock and denial- physcian shopping, attributes symptoms of actual illness to a minor condtion, refuses to believe diagnostic test results, delays treatment,acts happy and optimistic, refuses to tell or talk about condition,insists that noone is telling the truth, denying reason for admission, asking no questions.
    • •Adjustment- may experience guilt or self accusation, bitter or angry. May overprotect, reject( detach emotionally from child constantly nag child but provide good physical care), denial, gradual acceptance.
    • •Reintegration and acknowledgment- chronic sorrow(repeated losses as condition worsens)
    • •Establishing a support system
  13. The Child with Special Needs
    • Developmental aspects- impact of illness is influenced by age of onset.
    • Coping mechanisms- develops competence and optimism, feels different and withdraws, is irritable and moody and acts out, complies with tx, seeks support. HOPE- may be life sustaining and satisfying. HEALTH EDU AND SELF CARE. promotes coping.
    • •Responses to parental behavior- one of the greatest predictors of childs pyschologic adjustment.
    • •Type of illness or disability- more severe disorder cope better than those with milder conditions. or more obvious condition are easier to accept becasue limitations are concrete.EX.) blind or physically disabled. as opposed to heart defect.
    • •Americans with Disabilities Act (ADA)
  14. Nursing Care of the Family and Child with Special Needs
    • Assessment knowledge of family's support system. Family's perception of illness. Focus on family members knowledge of condition even before the diagnosis was made, the influence of culture and religion on their thinking, imagined causes of condition, and effects of child's disorder on family.
    • •Nursing diagnoses ineffective coping, compromised family coping, interrupted family processes.
    • •Planningexpected pt. outcomes: child and family will accept support at time of diagnosis, family's emotional reactions will be accepted, child and family will with stresses of the situation, child and family will recieve appropriate info about condition, family will establish an environment of normalization for the child, and family will establish realistic goals.
    • •Implementation Provide support at time of diagnosis, support family's coping methods, parent to parent support, advocate for empowerment, what's the child feel about this, do they understand their illness, provide support when child is ready to accept feelings toward the illness. Same for siblings Educate about disorder, promote normal development, establish future goals, plan palliative care and EOL.
    • •Evaluation the effectiveness of nursing interventions continuously reassses. Assess parents verbalization of feelings and concerns regarding disease or disability. observe parents attitudes, acceptance, and adjustment. determine how family demonstrates understanding of disease and treatment options. Assess family members goals for themselves and child. Observe whether family deomnstrates positive, growth promoting behaviors for the child and other family members.
  15. Identify Family Needs
    • •Provide support at time of diagnosis
    • •Accept family’s emotional reactions:–Denial, guilt, anger
    • •Support family’s coping methods
    • •Advocate for empowerment
    • •Educate about the disorder and general health care
  16. Promotion of Normal Development
    • Early childhood:–Basic trust, separation from parents, beginning independence
    • •School age:–Industry and activity
    • •Adolescence:–Developing independence and autonomy
  17. Developmental tasks and potential effects of chronic illness or disability: Infancy
    • Develop sense of trust multi caregivers and frequent seperations. deprived of consistent nurturing. DO: rooming in, consistent caregivers.
    • Bond delayedb/c of seperation, loss of dream child. DO: emphasize healthy qualities of infant, help parent learn about their child
    • learn through sensorimotor experiences more exposure to pain limited contact with environment. DO: expose infant to pleasurable experiences through all senses. encourage age appropriate developmental skills( hold finger, finger feeding, crawling)
    • begin to develop a sense of seperateness from parent increased dependency on parent, overinvolvment of parent in care DO: encourage all family members to participate i ncare. encourage periodic respite from demands of care.
  18. Developmental tasks and potential effects of chronic illness or disability:toddlerhood
    • -develop autonomy increased dependency on parent DO: encourage independence
    • -master locomotor skills limited opportunity to test own abilities and limits. DO: provide gross motor skill activity and modify toys or equipment.
    • -learn through sensorimotor experience; beginning of preoperational thought increased exposure to painful experiences DO: give choices to allow simple feeling of control. institue age appropriate discipline and limit setting. Recognize that negative and ritualistic behaviors are normal. Provide sensory experiences.(water play, finger paint, sandbox.)
  19. Developmental tasks and potential effects of chronic illness or disability:Preschool
    • Develop intiative and purpose limited opportunites for success in accomplishing simple tasks or masterin self care skills DO: encourage mastery. provide devices to make tasks easier.
    • master self care skills(same as above)
    • begin to develop peer relationships limited opportunites for socialization with peers may appear like a baby to age mates. protection within tolerant and secure family causing child to fear criticism and withdraw.DO: provide age appropriate play, encourage socilalizing,emphasize childs abilities
    • Develop sense of body image and sexual identification- aware of body centering pain, anxiety, and failure. sex-role identification focused primarily on mothering skills DO: encourage relationships with same sex and opposite sex peers and adults
    • Learn through preoperational thought(magical thinking) guilt(thinking he or she casue illness or is being punished for wrongdoing) DO: help child deal with criticisms; realize that too much protection prevents child from realities of world. Clarify child's illness is not their fault!
  20. Developmental tasks and potential effects of chronic illness or disability:School Age
    • develop a sense of accomplishment limited opportunities to achieve and competeDO: encourage school attendecne; schedule medical visits at times other than school; encourage child to make up missed work.
    • form peer relationships limited opportunites for socialization DO: educate teachers classmates about child and needs. encourage sportes and activities.
    • learn through concrete operations incomplete comprehension of imposed physical limits or tx of disorder DO: provide child with info about his or her condition. Encourage creative activities.
  21. Developmental tasks and potential effects of chronic illness or disability:Adolescence
    • Develop personal and sexual identify increase sense of feeling different from peers and reduced ability to compete with peers in appearance, abilities, special skills DO: help child realize that many of the difficulties the teenager is experiecing are part of normal adolescence.
    • Achieve independence from family increased dependency on family; limited job or career opportunities. DO: provide instruction on itnerpersonal and coping skills. Encourage increased responsibility for care and management of disease or condition.Discuss planning for future and how condition can affect choices.
    • Form heterosexual relationships limited opp increased concern with issues such as whydid they get this disorder and can they marry and have a family DO:encourage socialization, activities. Be alert to cues for readiness for info regarding implications of condition on sexuality and reproduction. Emphasize good appearance and wearing stylish clothes use of makeup. understand adolescent has same sexual needs and concerns as any other teenager.
    • Learn through abstract thinking decreased opp DO: provide instruction on decision making, assesrtiveness, and other skills necessary to manage personal plans.
  22. General Concepts of Home Care
    • •Care provided in family’s residence for children with simple to complex health care needs
    • •Purpose: to promote, maintain, or restore health OR to maximize independence and minimize the effects of disability and illness
    • •Different from hospice care (care for the dying patient): Palliative Care active total care of pts whose disease is not responsive to curative treatment. Control of pain and other symptoms and of pyshcological, social, spiritual problems as well.
  23. Home Care Trends
    • •Shift towards home care has many factors:–Parental desire–Advances in medical technology–Desire to improve quality of life–Cost of care
    • •Lack of nurses increases family caregiver role
  24. Discharge Planning and Selection of a Home Care Agency
    • Discharge planning must begin early
    • •Multidisciplinary approach
    • •Identifying appropriate community resources is critical
    • •Involvement of family in discharge plans
    • •Comprehensive written home care instructions
  25. Care Coordination
    • •Cost control
    • •Attainment of desired clinical outcomes
    • •Monitoring and evaluation of care provided
    • •Promote family’s role as primary decision maker
    • •Enhance family’s functioning
  26. Which of the following interventions is most appropriate for encouraging the development of a school-age child with disabilities associated with cerebral palsy?
    Encourage socialization with peers.
  27. Family-Centered Home Care
    • Believing that no one knows the child better than the family is critical to the success of any health care plan
    • •Respect for diversity and family’s values
    • •Parent-professional collaboration
    • •Assessment should address family strengths and resources
  28. Safety Issues in the Home
    • •Priority phone and electrical service provided
    • •Emergency protocols (including CPR)
    • •Care provided by appropriately trained persons
    • •Medications, sharps, hazardous materials
    • •Night safety concerns
    • •Transportation
  29. For case management to be the most effective, who is the most appropriate case manager?
    One nurse
  30. Family-to-Family Support
    • •Evaluate family support systems
    • •Networking with other families of special needs children
    • •Respite care for families
  31. Modifications for Home Care
    The nurse in the home care setting requires expertise to care for a child who is technology dependent.
  32. Establish Realistic Future Goals
    • •Cultivate realistic vocations for the child with chronic illness or disabilities
    • •Prolonged survival leads to new decisions and problems:–Independent living–Marriage, employment, insurance coverage–Reproductive decisions
  33. Perspectives on Care of Children at End of Life
    • •Principles of palliative care:–Focus on symptom control and support.
    • •Decision making at end of life:–Parents,:depend on info given to them by health care pros. they need honest appraisal of childs prognosis to make decisions. Explore their wishes with the physician. Ask "tell me your thoughts on..." Have you considered..."
    • -child: be honest and accurate with info. use clear simple language. Make it a gradual process, increase dialogue between parents, pros and the child. Each child is different must gauge how much info to give and how they should be told. Help parents understand honesty and shared decision making with childs involvement is important to child's and family's emotional health.
    • health care team- made based on progression of disease and amount of truama, availiability of tx options, impact of tx, and overall prognosis.Child's age premorbid go condition, functional status, pain/discomfort, probability of survival, and quality of life.DNR.
    • •Treatment options for the terminally ill child
  34. understanding of and reactions to death :
    infants and toddlers:
    • -Death has least significance to < 6 mo
    • -After parent child attachemnt and trust are established, the loss of significant person is profound.
    • -Cannot comprehend absence of life.
  35. understanding of and reactions to death: preschoolers
    • -Believe their thoughts are sufficient to cause death>they may feel guilt, shame,punishment.
    • -Death is seen as departure;kind of sleep; Seen as temporary and gradual.; No idea of universality and inevitability of death.
    • -
  36. understanding of and reactions to death:School-agers
    • -Still associate misdeeds or bad thoughts with causing death and feel guilt and responsibility.
    • -Respond well to logical explanations.
    • _Understand death in a concrete sense.
    • -Personify death-devil, monster, or bogeyman.
    • -by age 9/10 they have an adult concept of death-inevitable, universal, and irreversible.
  37. understanding of and reactions to death : Adolescents
    • -mature understanding of death.
    • -still influenced by remnants of magical thinking and subject to guilt and shame.
    • -they are likely to see deviations from accepted behavior as reasons for their illness.
  38. Nursing Care of Child and Family at End of Life
    • •Pain and symptom management-
    • -Double Effect: an action that has one good and one bad (unintended) effect that is permissible if following conditions are met: Action must be good in itself, the good effect must not be produced by the bad effect,there must be a compelling reason for permitting the foreseeable bed effect to occur.
    • •Parents’ and siblings’ need for support
  39. Fears at End of Life
    • •Fear of pain
    • •Fear of dying alone or parent’s fear of not being present at time of death
    • •Fear of actual death:–Home vs. hospital.
    • provide info on what the progress of death looks like.
  40. physcial signs of approaching death
    • -loss of sensation or movement in lower extremities, progressing toward upper body.
    • -sensation of heat, although body feels cool.
    • -loss of senses:tactile, sensitivity to light, hearing last sense to fail
    • -confusion, loss of consciousness, slurred speech
    • - muscle weakness
    • - loss of bowel and bladder control
    • - decreased appetite and thirst
    • -difficulty swallowing
    • -change in respiratory pattern- cheyne-stokes(waning of depth of breathing with regular periods of apnea)- Deep Rattle- secretions
    • -Weak, slow pulse; decreased BP
  41. Supporting Child and Family
    For the dying child there is no greater comfort than the security and closeness of a parent.
  42. Organ or Tissue Donation
    • •May be meaningful act to benefit another human being
    • •Common questions asked by families- skin, corneas, bone, kidney, heart, liver, pancreas can be donated.-removal does not mutilate the body or desecrate the body nor does it cause any suffering. Can have open casket does not delay funeral. No cost except their funeral or cremation ceremony responsibilities.
  43. Grief and Mourning
    • •Symptoms of normal grief:–Somatic distress
    • –Preoccupation with image of the deceased
    • –Guilt
    • –Hostility
    • –Loss of usual patterns of conduct
    • •Recognize when grief becomes “complicated” or “abnormal”(more than a year, intense intrusive thoughts, pangs of severe emotion, distressing yearning, feelings of excessive loneliness and emptiness, unusual sleep disturbances, and maladaptive levels of loss of interest in personal activities.)
    • •How long does grief last?- depends on the individual
    • •Nurses’ response to caring for dying children:–Coping strategies
    • –Normal responses
    • –Self-care
  44. Frailty
    •How would you define the term “frail”?“a syndrome of decreased reserve and resistance to stressors, that result in cumulative declines across multiple physiologic systems, causing vulnerability to adverse outcomes.”

    • •What
    • makes a person frail? comorbidities, disability,

    •Are there key components to frailty?


    • •>
    • 10 pounds lost unintentionally in past year

    • –Self-reported
    • exhaustion

    • •Self-report
    • of exhaustion on CES-D questions

    • –Weakness
    • (grip strength)

    • •Grip
    • strength lowest 20% adjusted for gender & BMI

    • –Slow
    • walking speed

    • •Slowest
    • 20% to walk 15 feet

    • –Low
    • physical activity

    • •Lowest
    • quintile of weighted kilocalorie expended per week
  45. Sarcopenia in older adults
    • •Sarcopenia: age-related loss of
    • muscle mass and strength.

    • •Changes in the muscle
    • fiber itself, and an increase in infiltration of fat into the muscle (myosteatosis) also common with
    • aging.

    • •Changes all lead to a
    • decline in muscle function.
  46. Timed Chair Stands(older adults)
    • •Used to evaluate
    • lower body strength and endurance

    • •Instruct to stand
    • from chair without using arms 5 times while being timed.

    • •Normative values
    • available, can identify which older persons may have problems with strength.
  47. Get Up and Go Test( older adults)
    • •The
    • get up and go test asks a person to:

    –stand from a chair without using their arms

    –walk 10 feet

    –turn around and walk back

    –and sit in the chair

    • •Can
    • be timed with a time of ≥ 20 seconds
    • indicating risk for adverse outcomes.

    • Can also observe for
    • unsteady gait
  48. Health literacy in older adults:Contributing Factors in Older Adults
    • •Fewer
    • years of schooling, poorer—fixed incomes

    • •>
    • 50% do not take meds as directed

    • •68%
    • cannot interpret blood sugar value

    • •76%
    • cannot follow Upper GI instructions

    • •100%
    • could not understand Medicaid rights in one study

    • •Non-English
    • speaking

    • •Immigrant
    • status

    • •Ethnic
    • interpretation of illness

    • •Spiritual
    • and religious beliefs

    • •Default
    • answers

    • •Lack
    • of insurance/transportation
  49. What can you do to ensure older adults understand (health literacy).
    • •Always
    • assume and ask in sensitive way

    –”How do you get your information?”

    –“What things do you like to read?”

    –“How satisfied are you with how you read?”

    • •Eyes
    • wandering over page, very slow to finish, sounding out words, look confused

    • •Remember
    • the “pill bottle” prop

    –Ask questions about the dosage and frequency
  50. Changes in Body Composition in older adults
    •There is a net decrease in:

    –Bone mass

    –Lean muscle mass

    –Water content

    •There is a net increase in:

    -Total body fat

    • -Especially intra-abdominal (fat located inside the belly
    • area/abdominal cavity)
  51. Physiological Changes Accounting for Nutrition Risk in
    §Changes in taste, and smell

    §Changes in the gastrointestinal system

    §Impaired thirst sensation

    • §Atrophic gastritis (chronic inflammation of stomach with
    • reduced stomach secretions.
  52. Pathologic Changes Common in Aging
    • •Chronic diseases and
    • restrictive diets
    • •Dental problems
    • •Depression
    • •Alcohol abuse
    • •Medication side
    • effects
  53. Chronic Diseases and Restrictive Diets
    • •Common Restrictive
    • Diets:

    • –Low/no sugar
    • (Diabetes)

    • –Low fat (Elevated
    • cholesterol)

    • –Low sodium
    • (Congestive heart failure)

    • –Combination of above
    • (High blood pressure)

    • •Associated with poor
    • intake

    • •May be seen in
    • specific ethnic groups

    –Decreased meat intake

    • –Other dietary
    • preferences and restrictions
  54. Dental Problems: Tooth Loss
    • •Most
    • common causes of tooth loss:

    • §Inability or unwillingness to access and pay for
    • preventive/restorative treatment

    §Loosening of teeth from periodontal disease

    • §Removal of healthy teeth in preparation for dental
    • prosthesis

    • •Leads
    • to diminished chewing efficiency and reduced range of preferred foods
  55. Dental Problems: Removable Dentures
    • •Can
    • aid in speech

    • •Restores
    • facial contours

    • •Less
    • likely to restore ability to chew (restriction in range of foods)

    • •Requires
    • frequent professional adjustment

    • •Not
    • covered by Medicare
    • -less than 10% of elders have dental coverage!
  56. Screening for Under-nutrition
    or Malnutrition
    • Can use a combination
    • of:

    • §Serial
    • body weight

    • §Weight
    • loss over the past months/yrs

    • §Nutrition
    • history: appetite, # of
    • meals/day, taste & amount of food eaten

    • §Laboratory
    • Values: Low serum cholesterol and/or albumin
  57. Falls Incidence: Community
    •One-third of community-dwelling persons age > 65 years, fall each year

    • •In approximately half of the cases, falls are
    • recurrent

    •Rates increase

    –With age

    –During the month after hospital discharge
  58. Falls Morbidity: Community
    • •10-15% of falls result in injury requiring medical
    • attention

    •Functional deterioration including:

    –Decline in ADLs

    –Fear of falling / loss of confidence

    •40-73% of recent fallers

    •20-46% without recent fall

    –Self-limitation of activities
  59. Falls Mortality: Community
    •Unintentional injury, 5th leading cause of death in those > 65 years

    –Majority due to falls

    –Especially in those > 85 years

    • •Deaths related to consequences after the fall, not the
    • fall itself


    –Decreased activity
  60. Falls Cost: Community
    •Falls account for 6% of ALL medical expenditures

    • •Leading cause of injury-related visits to emergency
    • departments in US

    • •By
    • 2020, annual direct and indirect cost of fall injuries expected to reach $43.8 billion

    •Numbers expected to climb as population ages
  61. Fall Risk Factors : Community
    •Focus of most fall research

    •Falls in community-dwelling older adults tend to be multifactorial in nature

    •As number of risk factors increases, so does risk of falls
  62. Most Common Risk Factors for Falls (AGS Guidelines, 2001)
    Muscle weakness

    History of falls

    Gait deficit

    Balance deficit

    Use asst device

    Visual deficit


    Cognitive impairment
  63. Home environmental risk factors
    • Home
    • •low lighting
    • •poor stairs & rails
    • •unstable furniture
    • •rug/carpet hazards
    • •low beds & toilets
    • •no grab bars
    • •slick floors
    • •obstacles
    • •pets
    • •Medications
  64. Institution risk factors
    • Institution
    • •low lighting
    • •new admission
    • •poor furniture
    • •slick hard floors
    • •low supervision
    • •↓ # of nurses
    • •meal times
    • •no hand rails
  65. outdoors risk factors
    • Outdoors
    • •bad weather
    • •poor sidewalks
    • •traffic activity
    • •street crossings
    • •uneven steps
    • •distractions
    • •obstacles
    • •↑ activity levels
  66. Single-intervention Strategies
    • •Community based balance or strengthening exercise program (Tai chi)
    • •Estimated risk reduction 29-49%

    • •Professionally supervised balance and gait training and muscle strengthening exercise
    • •Estimated risk reduction 14-27%

    • •Gradual discontinuation of psychotropic medications
    • •Estimated risk reduction 39%

    • •Modification of home hazards after hospital discharge
    • •Estimated risk reduction 19%
  67. Multifactorial Risk Assessment
    • •Estimated risk reduction 25-39%
    • •Successful components include:
    • –Review and possible reduction of medications
    • –Balance and gait training, muscle-strengthening exercise
    • –Evaluation of postural blood pressure
    • –Home-hazard modifications
  68. In community-dwelling older persons
    • –Screening for falls should occur yearly
    • –Assessments and Interventions target reversible risk factors
    • •gait and balance deficits
    • •evaluate medication regimen
    • •address postural hypotension
    • •modify environmental hazards
  69. Multifaceted Interventions: Hospitals
    • •A recent meta-analyses showed rate ratio of 0.82 (95% CI 0.68-0.997) for falls
    • •No significant effect on # of fallers or fractures
    • •Multifaceted interventions included:
    • –risk assessment
    • –removal of physical restraints
    • –medical/diagnostic approaches
    • –changes in physical environment
    • –medication review
    • –exercise
    • –care planning
    • –hip protectors
  70. Major Frailty Components
    • •Sarcopenia
    • –Decreased strength
    • –Decreased gait speed
    • –Decreased activity

    • •Undernutrition
    • –Decreased energy expenditure
    • –Aging disease, and medication impact on intake
  71. Nagi’s Disablement Model
    • Active Pathology
    • •Normal cellular processes and homeostatic efforts to return to normal state are interrupted
    • Impairment
    • •Loss or abnormality at the organ or tissue level
    • Functional Limitation
    • •Have physical or mental limitation at the individual level
    • Disability
    • •Have physical or mental limitation in a social context (i.e. socially defined roles or tasks)
  72. lOlder adults will increase from____% to___% of
    the population
    • lOlder adults will increase from 14% to 22% of
    • the population
  73. lOlder adults use roughly____health services
    and this is expected to_____
    • lOlder adults use roughly 1/3 health services
    • and this is expected to increase
  74. lOlder adults are the heaviest consumers of
    ______________ and _____________________.
    • lOlder adults are the heaviest consumers of
    • medication and medical equipment
  75. lOlder adults wish to age in ____________– the
    system often has other ideas
    • lOlder adults wish to age in place – the
    • system often has other ideas
  76. ACUTE Disease
    lRapid onset

    • lAmenable to quick diagnosis and restorative
    • measures

    lCan be completely removed from the body
  77. CHRONIC Disease
    lInsidious onset

    lOften easily diagnosed, can be ameliorated(be made better)but effects cannot necessarily be removed

    lUsually a long term or life long condition
  78. top twelve conditions of the older american
    lAtherosclerosis (Coronary disease and stroke)





    lSensory impairment

    lChronic lung disease

    lKidney failure

    • lDementing
    • illness



  79. medication use in the older population
    • lTake an average of five
    • prescription and four over the counter medications on a daily basis

    • lFill an average of more than
    • twenty different prescriptions in any given year
  80. Adverse drug reactions in the older adult
    • lConsidered a factor in 10-20% of hospital
    • admissions of adults over 65

    • lA more common cause of hospital admission
    • than coronary artery disease

    • lA major contributor to inpatient iatrogenic
    • complications (Up to 35% of older inpatients will have an adverse drug reaction
    • during a hospitalization)
  81. Risk factors for adverse drug reactions
    lChronologic age IS NOT a risk factor

    • lConditions associated with aging can be risk
    • factors

    lChanges in cognition

    lChanges in physical functioning

    Side effect profiles

    lComplexity of medical regimen

    lNumber of prescribing physicians

    lNumber of filling pharmacies

    lChildproof caps

    lCost of medications
  82. Difficulties in understanding adverse drug reactions
    • lSystematic exclusion of elderly from drug
    • studies

    • lDifferences in pharmacokinetics in older
    • patients

    • lLittle controlled research on multiple
    • medications in humans

    lGenetic factors

    • lMinimal research on drugs in the acutely or
    • chronically ill
  83. Basic Pharmacokinetics -
    • lAbsorption
    • across the gut remains normal into tenth decade and beyond

    • lDecrease
    • in gastric acid may lead to decreased breakdown of capsules and coatings

    • lDecreased
    • absorption – Cations,
    • Vitamin B-12
  84. Basic Pharmacokinetics -
    • lLean
    • body mass decreases and fat increases

    lDrugs that are water soluble reach higher unit concentrations

    • lDrugs that are fat soluble have more tissue to spread through
    • and therefore have increased half lives

    lBody protein stores decrease with age

    • lProtein bound medications will
    • have higher free drug levels at standard dosing

    • lMedications that compete for
    • protein binding sites may potentiate each other
  85. Basic Pharmacokinetics -
    • lNormal changes of liver function with age are
    • not well established

    • lThe number of hepatocytes available for metabolism may be
    • reduced

    • lBlood flow through the portal
    • system may be reduced

    • lMultiple medications may compete
    • with each other for limited cellular processes
  86. Basic Pharmacokinetics -
    • lRenal function (GFR and blood flow) are
    • reduced with age

    • lAs lean body mass tends to decline
    • proportionally with GFR, creatinine may remain normal with major impairments

    • lMedications eliminated renally tend
    • to have prolonged half lives
  87. Syndromes of Adverse Drug
    lConfusion and Delirium

    • lDizziness, Vertigo, Orthostasis
    • and Falls

    lAnorexia and Weight Loss


    lUrinary Incontinence

  88. Medications that can cause

    lAlpha Agonists

    • lDopaminergic
    • Drugs


    lH2 Blockers


    lSulfa Drugs

    lBeta Blockers
  89. Medications Linked to










  90. Medications Linked to






    lSSRI antidepressants



  91. Medications Linked to
    lBeta Blockers



    lAlpha agonists
  92. Medications Linked to

    • lAlpha
    • Blockers


    • lAlpha
    • Agonists


    • lMuscle
    • Relaxants

    • lCalcium
    • Channel Blockers

  93. Medications Linked to


    lFiber Supplements


    lH2 Blockers

    lProton Pump Inhibitors
  94. Medication Adherence
    lMore broad based

    • lIncludes factors from providers and the
    • health care system

    lLess paternalistic

    • lViews health care as a partnership between
    • patient and provider
  95. lEstimated____________annual deaths in the US due
    to medication adherence issues
    • lEstimated 125,000 annual deaths in the US due
    • to medication adherence issues
  96. lRoughly _________of nursing facility admissions in
    US based in inability of patients to adhere to medication regimens
    • lRoughly 23% of nursing facility admissions in
    • US based in inability of patients to adhere to medication regimens
  97. lAbout______of acute hospital admission in the
    US due to medication adherence issues
    • lAbout 10% of acute hospital admission in the
    • US due to medication adherence issues
  98. lThe rule of three
    l1/3 of patients take medications correctly

    l1/3 of patients take medications incorrectly

    l1/3 of patients don’t take medications at all
  99. lOf 2 Billion US prescriptions written
    l50% taken incorrectly

    l15-25% never filled at pharmacy
  100. Social and Economic
    Dimensions of medical adherence
    lAvailability of transportation

    lCost of medication

    lCaregiver situation

    • lAvailability and types of prescription
    • insurance
  101. Costs of medication
    Hospital admissions $15.2 billion

    • Nursing home admissions $31.5 billion
    • Lost productivity
    • patients and caregivers $78 billion
  102. Pain in Older Adults
    •25 – 56% community-dwelling elders

    •45 – 85% nursing home residents

    • •30 – 80% cancer
    • patients in treatment

    • •20% of hospitalized patients in their last days of
    • life

    •20% of hospice patients
  103. Nociceptive
    •Sources: organs, bone, joint, muscle, skin, connective tissue

    •Examples: arthritis, tumors, gall stones, muscle strain

    •Character: dull, aching, pressure, tender

    •Responds to traditional pain medicines & therapies
  104. Neuropathic
    • •Source: nerve damage, e.g.,
    • peripheral nerve or CNS pathology

    •Examples: postherpetic neuralgia, diabetic neuropathy, spinal stenosis

    •Character: shooting, burning, electric shock, tingling

    •Requires different types of medications than nociceptive pain
  105. Differences in the Pain Experience of Older Adults with
    • •Tolerance to acute pain possibly
    • increases but pain threshold does not appear to change

    •Dementia may alter response to acute pain

    • •Cognitive impairment may decrease the perceived analgesic
    • effectiveness

    •Pain can negatively affect cognitive function
  106. Behavioral/Observational Cues for pain

    •Grimacing or wincing




    Less Obvious:

    •Changes in activity level

    •Sleeplessness, restlessness

    •Resistance to movement


    •Increased agitation, anger, etc.

    •Decreased appetite

  107. Acetaminophen
    •For mild to moderate pain

    •Best for nociceptive pain

    •First line therapy particularly in the frail elderly

    •Mode of action not well understood

    • Routine dosing up to 2000 – 4000 mg/day in older
    • adults

    • •Scheduled dosing works best for older adults with
    • persistent/ daily pain

    • •Avoid or reduce dose in hepatic compromise or renal
    • disease

    • •Be aware of “hidden” doses of APAP
    • in combination products
  108. NSAIDs
    •Treat Inflammation

    •Effective for mild to moderate pain

    • •Caution in renal, hepatic, gastric, cardiovascular
    • problems

    • •Risk of adverse events( GI bleeding) increases with
    • age
  109. Opioid Side Effects

    •Nausea and vomiting


    •Urinary retention


    •Dysphoria, hallucinations

    •Myoclonus (rare, on low doses)

    •Respiratory depression (rare)
  110. Who 3 step analgesic Ladder
    Image Upload 1
  111. Equianalgesic Dosing
    •Methods for switching from one opioid to another or administration routes

    •Use of equianalgesic tables is necessary but use the data cautiously

    •Keep in mind the issue of “incomplete cross-tolerance”

    •Reduce by 30-50% when changing drugs
  112. Long Acting Medications
    •Sustained release medications

    •Immediate release for breakthrough pain

    •Distinguish types of breakthrough pain
  113. Opioid Rotation
    • •Use when one
    • opioid is ineffective even with adequate titration

    • •Use when adverse
    • effects are unmanageable
  114. Co-analgesics/Adjuvants
    • •Medications developed and marketed for another
    • medical condition (e.g., depression) but found also to be effective for pain

    •Many co-analgesics target neuropathic pain
  115. Adjuvant Analgesics


    • •Local
    • anesthetics

  116. Anticonvulsants
    • Act by reducing conduction of pain signals along
    • damaged nerves

    •Gabapentin (Neurontin®) is commonly used for burning, shooting pains

    •Other anticonvulsants used for neuropathic pain: Levetiracetam (Keppra®), Tiagibine (Gabatril® ), Lamotrigine (Lamictal®), and Pregabalin (Lyrica® )

    • •All these agents can cause unclear thinking, forgetfulness, and other CNS
    • side effects

    • •Slow initiation and taper up is essential – for example, start Neurontin® at 100 mg q hs and
    • move up by 100 mg per day in divided doses once a week
  117. Tricyclic Antidepressants (TCAs)
    •Indicated in neuropathic pain

    • •Believed to work by blocking chemical neurotransmitters for pain in the
    • spinal cord and the brain

    •Significant anticholinergic effects

    •Causes morning grogginess at higher doses

    •Significant postural hypotension in elderly

    •Patient education is important!

    • •Desipramine and nortiptyline are preferred over amitriptyline or doxepin in the
    • older adult because they have less severe anticholinergic effects

    • •TCAs have significant interactions with other drugs that can cause blood
    • levels to be much higher – to check ask the pharmacist to review the resident’s
    • med list
  118. Local Anesthetics
    •Minimal systemic side effects

    • •Indicated for neuropathic pain but can be effective
    • in musculoskeletal pain as well

    •Lidocaine gel, EMLA® & Lidoderm© & Capsaicin
  119. Topical Agents: Lidocaine
    •Lidocaine 5% patch, ointment

    •FDA-approved for post-herpetic neuralgia

    • •Clinical trials show effectiveness in other
    • neuropathic pain syndromes

    •Effective adjuvant for osteoarthritis and back pain

    • •Local side effects: redness, edema, abnormal
    • sensations at site
  120. Topical Agents: Capsaicin
    •Active ingredient of hot chili peppers

    • •Clinical trials show effectiveness for diabetic
    • neuropathy, osteoarthritis, and rheumatoid arthritis

    • •Common adverse effects: burning pain at application
    • site, sneezing and coughing

    • •Dosed q 6h, usually takes 2—4 weeks to achieve
    • therapeutic effect
  121. Cachexia
    • lack of nutrition
    • and wasting
  122. Delirium
    Acute change in cognition/awareness
  123. Agitation -
    accompanies delirium
  124. Confusion
    • disorientation, inappropriate behavior,
    • hallucinations
  125. Epidemiology of Delirium
    •10–40% older adults in medical inpatient units

    •9–44% older adults, post-op

    • •Up to 60% adults ≥ 75 yrs in
    • nursing homes

    • •80–90% imminently dying patients




    •Bladder distention

  126. Neuroleptics( used for delirium)
    Haloperidol (Haldol®)

    •Most commonly recommended drug for managing EOL delirium

    •PO, IV, SQ

    •Short half-life, minimal anticholinergic effects

    •Recommended starting dose for older adults: 0.25–0.5 mg q 4 hours

    •Monitor for extra pyramidal symptoms (EPS)
  127. Benzodiazepines
    •Frequently used, but evidence suggests that they are not effective

    •May worsen delirium

    • •Indicated for agitation with clear anxiety component, delirium due to
    • ETOH or benzodiazepine withdrawal, or for intractable delirium
  128. Complications of Hepatic Failure
    • Liver cell dysfunction
    • Coagulopathy
    • ¡Ascites
    • Hepatic encephalopathy
    • Hepatorenal syndrome
  129. Hepatic failure: NURSING INTERVENTIONS
    • Ascites causes difficulty with breathing
    • Monitor abdominal girth at level of umbilicus
    • Semi-fowler’s position
    • Turn, cough and deep breathing
    • Intubation
    • Bed rest
    • Low-sodium diet
    • Fluid restriction
    • Diuretics
    • Monitor labs – BUN, creatinine, urine output – renal failure
    • Monitor electrolytes
    • Paracentesis –1-2 L of fluid – monitor - too much fluid too quickly
    • can lead to complications – decreased BP, increased HR -Measure abdomen before
    • and after
    • Fluid sent to lab – document color, amount, and
    • characteristics

    • Albumin – increases colloid pressure and decreases loss
    • of fluid into abdomen
    • Peritoneovenous shunting – surgery – shunt fluid from abdomen into superior vena cava
    • Shunt – LeVeen shunt – one end in peritoneum and other end into jugular or superior vena cava – valve opens and closes according to pressure
    • with inspiration
    • Complications:
    • - hemodilution
    • - shunt clotting
    • - wound infection
    • - leakage from incision
    • - bleeding
    • - Increased risk for hepatic encephalopathy
    • Denver shunt has pump to squeeze percutaneously
  130. Hepatic Encephalopathy
    • Four stages :Stage1: tremors, slurred speech, impaired decision making.Stage2:drowsiness, loss of sphincter control, asterixis. Stage 3: Dramatic confusion, somnolence. Stage 4: Profound coma, unresponsiveness to pain, GI alterations
    • ¡Limit protein 20-40 g/day
    • Neomycin or lactulose
    • Restrict meds toxic to liver
    • Sedation
  131. Neomycin
    • antibiotic
    • decreases protein breakdown in bowel by destroying normal bacteria – can be
    • toxic to kidneys
  132. Lactulose
    • makes bowel acidic so ammonia leaves blood and moves to
    • colon where is trapped and eliminated – has laxative effect

    Sedation may be necessary to prevent harm to themselves
  133. Hepatorenal Syndrome
    • Acute renal failure that occurs with hepatic failure –
    • poor prognosis(address end-of-life with family and patient)
    • Nursing interventions should:
    • Improve liver function & support renal function
    • ▪Administer fluids and diuretics
    • ▪Stop meds toxic to kidney
    • ▪Hemodialysis
  134. Hepatic Failure:Prognostic data:
    • Ammonia levels increased
    • Serum bilirubin increased
    • Prothrombin time prolonged levels may be 40-80 seconds above control
    • values
    • Coagulation factors
  135. Hepatic Failure: signs and symptoms
    • Headache
    • Hyperventilation
    • Jaundice
    • Changes in LOC
    • Palmar erythema
    • Spider nevi
    • Bruises
    • Edema
    • Asterixis(a tremor of the wrist when the wrist is extended (dorsiflexion), sometimes said to resemble a bird flapping .)
  136. Hepatic Failure :Medical management
    • Neomycin or lactulose
    • Ulcer prophylaxis
    • Vitamin K, FFP, platelets
    • Antibiotics
    • Treat increased ICP
    • Hemodynamic stability
    • Transplant
    • Decrease ammonia:Limit protein to 20-40 g per day
    • Decrease bacterial breakdown of protein in bowel
    • Neomycin (Antibiotic destroys bacteria) Give PO every 4-6 hours.Toxic to kidneys – daily labs
    • Lactulose Creates acidic environment.Pulls ammonia out of blood into colon .Laxative effect. Give PO or rectal enema.
    • Ulcer prophylaxis – prevent stress ulcer
    • Vitamin K, FFP, platelets – control or prevent bleeding
    • Antibiotics – prophylactic or treatment for infection

    • Treat increased ICP – HOB elevated, mannitol, control BP, correct O2/CO2 balance (intubate),
    • Hemodynamic stability – dialysis (renal failure),
    • fluids, vasoactive meds
  137. Hepatic failure nursing management
    • Protect from injury
    • Comfort measures
    • Monitor for complications
    • Education
    • *Difficult to manage because medications can mask changes
    • in neurological status and increase hepatic encephalopathy. *Can become agitated and combative so may need physical restraint.
    • *Ascites
    • *Monitor abdominal girth at level of umbilicus
    • Semi-fowler’s position
    • Turn, cough and deep breathing
    • Intubation
    • Bed rest
    • Low-sodium diet
    • Fluid restriction
    • Diuretics
    • Monitor labs – BUN, creatinine, urine output – renal failure
    • Monitor electrolytes
    • Paracentesis – 1-2 L of fluid
    • – monitor Albumin
    • Limit needle sticks or invasive procedures – prone to
    • bleeding
    • Peritoneovenous shunting – surgery
    • Monitor : pulse ox, ABGs, neuro assessments at least every hour.
    • Educate causes and treatment, how to prevent recurrence
  138. hepatic failure medical management
    • Liver transplant: Contraindicated if
    • HIV, malignancy, significant heart, lung, or kidney dysfunction
    • Experimental therapies: Extracorporeal liver
    • assist devices to remove toxins
    • To bridge time before transplantation or to allow for time to regenerate
    • Bioartificial liver assist device: Bridge until transplant – removes toxins until transplant or regeneration of tissue
  139. Acute Pancreatitis
    • Assessment: Ascites
    • Vomiting
    • Irritation of pancreas and peritoneum
    • Fat necrosis
    • ▪Grey Turner’s sign or Cullen’s sign( flank bruising and brusing around umbilicus)
    • *Acute inflammatory disease of the pancreas – Most common gallstones, alcohol, meds, idiopathic
    • *Fluid moves into abdomen and is sequestered there – ascites – hypovolemia – can develop shock.
    • *Vomiting due to interruption of blood flow to pancreas – hypovolemia, electrolyte imbalance
    • *Irritation.
    • *Low grade fever – if temp high usually indicates more severe disease – peritonitis, cholecystitis, abcsess
    • *Pain – severe midepigastric pain that is unrelieved by vomiting – generalized or localized in left upper quadrant radiating to back – twisting or knifelike sensation to low back – some comfort when lean forward
    • •Abrupt
    • •After meal or alcohol
    • •Last for several hours
    • •Guarding
    • •Distention
    • *Pseudocysts/Abcess – accumulation of debris from inflammation and pancreatic secretions – can rupture and hemorrhage or become infected – may be able to palpate abdominal mass.
    • *Fat necrosis leads to pancreatic cell necrosis and hemorrhage – increased mortality rate – measure abdominal
    • girth every 4 hours – hypocalcemia, hyperlipidemia
    • *Can have hypoactive bowel sounds and abdominal
    • tenderness and distention.
    • *Hemorrhagic pancreatitis
    • •Grey Turner’s sign – bluish discoloration of flanks
    • •Cullen’s sign – bluish discoloration around umbilicus
    • •Can develop hypovolemic shock due to fluid loss or hemorrhage
    • *May resolve in 5-7 days on its own but may progress and
    • affects every organ
    • *Resp failure and ARDS most common omplications .
    • *Death in first 2 weeks usually due to respiratory or renal
    • complication
  140. Diagnosising Acute Pancreatitis
    • Liver enzymes elevated
    • Elevated WBC
    • Elevated glucose levels
    • Abdominal ultrasound
    • CT scan
    • ERCP (endoscopic retrograde cholangiopancreatography)
    • X-rays
    • *Elevated amylase and lipase •Lipase more specific
    • for pancreas *Best to use urine amylase level - Amylase increased in urine during pancreatitis – urine measurement better than serum because serum levels can be increased in other conditions.
    • – serum levels only elevated for 3-5 days.
    • – organ failure, ARDS, renal failure, septic shock
    • Impaired exocrine and endocrine functions
    • – hyperglycemia or hypoglycemia
    • Abdominal ultrasound
    • Pancreatitis can mimic other diseases
    • CT scan – confirmation of what is suspected by history –
    • complications – perforation, cysts, abcsesses, obstruction

    • ERCP (endoscopic retrograde cholangiopancreatography)
    • x-rays and endoscopy – can cause pancreatitis
    • X-rays – abdomen and chest – r/o other things – ileus,
    • perforation, effusion, lung problems
  141. Severity of Pancreatitis
    Ranson’s Criteria :At admission or on diagnosis: Age >55 yrs(>70), Leukocyte count> 16,000/ microliter (>18,000), Serum glucose level >200 mg/dL (>220), Serum LDH level >350 IU/L (>400), Serum AST level >250 IU/L. During initial 48 hours: decrease in hct> 10%, in crease in blood urea nitrogen level > 5 mg/dL (>2), serum calcium <8 mg/dL, base deficit> 4 MEq/L (>5), Estimated fluid sequestration > 6L (>4), Partial pressure of arterial oxygen < 60 mm Hg.

    • To predict severity & prognosis
    • Criteria on admission
    • 48 hours after diagnosis
    • Mortality increases with number of signs
  142. Nursing interventions for pancreatitis
    • Replacement of fluid and electrolytes
    • Nutritional support
    • Comfort measures
    • Medications
    • Education
    • Treatments for complications of acute pancreatitis: Surgery
    • *Fluids-All patients have some amount of dehydration or
    • shock if severe-Urine output < 30 mL per hour – early sign of hypovolemia
    • -Some patients can hold up to 12 L of fluid in retroperitoneal space.
    • -Priority
    • -Slows progression, prevents renal failure
    • -Colloids, LR, FFP, albumin-May need packed RBCs if
    • hemorrhagic pancreatitis
    • *Maintain SBP > 100 mm Hg-If BP doesn’t respond to fluids may need dopamine or dobutamine
    • *Maintain HR < 100 bpm
    • Electrolytes
    • Hypocalcemia (< 8.5 mg/dl)-Hypocalcemia due to fat necrosis-Calcium needed for nerve and muscle
    • impulses, integrity of cell membranes and vessels, normal clotting, and strong bones and teeth.
    • -Needed for contractility of heart-Low levels - lengthens QT interval
    • -Severe – tetany, seizures, respiratory distress-seizure precautions and respiratory support available.
    • -positive Chvostek’s and -spasm when pressure applied to upper arm (BP cuff)
    • -Trousseau’s signs-– facial muscle spasm when tap on
    • facial nerve
    • -Give replacements
    • -Potassium- Given IV per protocol
    • -Glucose-Elevated due to stress and increased glucagon
    • levels-Transient increase in glucagon-Administer insulin with caution per sliding scale
    • -Monitor for toxicity – lethargy, nausea, shortening of QT interval, decreased excitability of nerves and muscles.
    • -In past rested pancreas- NG tube to suction, NPO until
    • enzymes normal, TPN if would be NPO for > 5 days
    • -Evidence shows – gastric or jejunal feedings if
    • tolerable can prevent septic and metabolic complications, NG tube only if vomiting, distention or obstruction.
    • -Comfort measures - Opiates (morphine) – can cause spasm which increases pain-Demerol used – given routine schedule versus PRN
    • -Medications used in pancreatitis
    • -Prevent stress ulcers - Histamine blockers, antacids
    • -Treatment of inflammation versus prevention of sepsis -
    • Antibiotics
    • -Surgery may be necessary
    • •Pancreatic resection:remove dead or infected tissue (necrosectomy) – may remove entire pancreas
    • •Psuedocysts :
    • •Can become infected(abscess) – may need to be drained
    • •Can resolve themselves
    • •Can rupture leading to peritonitis
    • •Can erode a blood vessel causing hemorrhage
    • •Can cause obstruction– may need to be removed
    • •Cholecystectomy for gallstones
    • Education – prevent recurrence – diet modification and enzyme supplements.
  143. Classification of Acute Renal Failure
    • -Sudden decline in GFR. Categorized by location of insult to kidneys.
    • Prerenal Cause of ARF:Volume of Depletion: Hemorrhage, trauma, surgery, postpartum periof, GI Loss, Diarrhea, NG suction, vomiting, renal loss, diuretics, osmotic diuresis, Diabetes Insipidus, volume shifts, burns, ileus, pancreatitis, peritonitis, hypoalbuminemia.
    • Vasodilation: sepsis, anaphylaxis, meds:antihypertensives , afterload reducing agents, anesthesia.
    • Impaired cardiac performance: heart failure, MI, cardiogenic shock, dysrhythmias, PE, pulmonary HTN, Positive pressure ventilation, pericadial tamponade.
    • Micellaneous:Angiotensisn-converting enzyme inhibitors in renal artery stenosis, inhibition of prostaglandins by non steroidal antiinflammatory drug use during renal hypoperfusion, renal vasoconstriction, norepinephrine, ergotamine, hypercalcemia.
    • Postrenal Causes: Benign prostatic hypertrophy, blood clotsm renal stones or crystals, tumors, postoperative edema, drugs: TCA, ganglionic blocking agents, foley catheter obstruction, ligation of ureter during surgery.
    • Intrarenal/A TN Causes:Glomerular, vascular, or Hematological Problems: Glomerulonephritis(poststreptococcal), vasculitis, malignant htn, systemic lupus erythematosus, hemolytic uremic syndrome, disseminated intravascular, coagulation, scleroderma, bacterial endocarditis, HTN of pregnancy, thrombosis of renal artery or vein.
    • Tubular Problem ( acute Tubular Necrosis or Acute Interstial Nephritis):Ischemia, causues of prerenal azotemia, hypotenision, hypovolemia, obstetric complications( hemmorrhage, abruptio placenta, placenta previa), Meds, radiocontrast dyes( large volume,multiple procedures done), transfusion reaction causing hemoglobinuria, tumor lysis syndrome, rhabdomyolysis, micellaneous: heavy metals(mercury, arsenic) paraquat, snake bites, organic solvents(ethylene glycol, toluene, carbon tetrachloride). pestisides, fungisides, preexisting renal impairment, diabetes mellitus, HHTN, volume depletion, severe heart failure, advanced age.
    • *Azotemia/uremia: retention of nitrogen waste products Elevated BUN – retention of nitrogen waste products normally excreted by kidneys.
    • *Oliguria:< 400 mL in 24 hours Less common
    • *Nonoliguric 2-4 L/day
    • *Anuria: < 100 mL/day
  144. Anuria:
    < 100 mL/day
  145. Nonoliguric
    2-4 L/day
  146. *Oliguria:
    < 400 mL in 24 hours Less common
  147. Azotemia/uremia:
    retention of nitrogen waste products Elevated BUN – retention of nitrogen waste products normally excreted by kidneys.
  148. Prerenal Failure
    • Prerenal-Things that decrease blood flow, blood pressure, or renal perfusion.
    • GFR is decreased leading to decreased urine output.
    • Interruption of renal perfusion.
    • Hypovolemia, Extracellular fluid volume (third spacing), Poor cardiac output, Vasoconstriction of renal blood vessels.
    • Structures of kidneys are intact and are functioning
    • normally they just do not get enough blood. Body tries to correct this by reabsorbing water and sodium. If corrected okay but if prolonged causes kidney
    • damage or necrosis. Need to recognize early.
  149. postrenal failure
    • Obstruction of urine flow.
    • Causes increased tubular pressure.
    • Decreased GRF
    • Abnormal nephron function
    • Sudden onset of anuria
    • Usually resolves once obstruction removed.
    • Only 5=10% of hospital cases of ARF
    • Most common cause benign prostatic hypertrophy
    • Other causes – crystals, bilateral ureteral obstruction,
    • prostate cancer
  150. Intrarenal Failure
    • Direct actions on glomerulus or renal tubules.
    • Acute Tubular Necrosis (ATN) - Most commonly injures
    • proximal tubule and ascending limb of the loop of Henle.
    • Prolonged prerenal ischemia – cell injury – cell death (Can occur after only minutes of hypotension or hypovolemia).
    • Neprotoxins – predisposed if DM, dehydration, elderly
    • – aminoglycosides (mycin antibiotics)
    • - raiological contrasts-When
    • affected by contrast dye see elevated creatinine 24-48 hours after administration. Peak in 7 days and get better within another 3-5 days but may take up to 3 weeks.
    • - Penicillins
    • - Amphotericin B
    • - NSAIDS
    • - blood transfusions
    • - heavy metals(mercury, arsenic)
  151. Phases of Acute Tubular Necrosis
    • Initiation Phase(onset) :
    • Ischemia evolving
    • Decreased GFR
    • Time of injury up to days
    • Urine output begins to decrease
    • Chemical changes
    • Damage not present
    • Can be reversed
    • Maintenance Phase(oliguric/anuric):Lasts 8-14 days
    • Urine output reaches lowest point
    • < 400 mL in 24 hours
    • Can be nonoliguric
    • At risk for hyperkalemia and infection
    • Recovery Phase(diueretic): Increased GFR returns and kidneys can remove volume but not solutes due to scarring and edema.
    • Time it takes for repair – 4-6 months.
    • Urine output gradually increases
    • May have diuretic phase
    • Dialysis may be used
    • Lab values improve
  152. Assessment for Acute Renal Failure
    • 1 History – medical conditions (DM, HTN, Immunological diseases, hereditary disorders) , hypotensive episodes, exposure to nephrotoxins (aminoglycosides, NSIADs) or prolonged use of a drug, infections, volume depletion, increasing age .Symptoms may not occur for 1-2 weeks after exposure.
    • 2 Vital signs:-Changes in blood pressure – hypotension
    • -Tachycardia,arrhythmias (elevated potassium)
    • -Hyperventilation –compensation for metabolic acidosis, Kussmal respirations (DKA)
    • -Altered temp
    • -Decreased – uremic toxins
    • -Increased – infection
    • 3 Physical assessment: (signs of uremia)
    • -Fatigue
    • -Disorientation
    • -Lehtargy
    • -Skin turgor
    • Indicators of fluid balance
    • -Mucous membranes
    • -Edema
    • -Neck vein distension
    • -Weight gain – every 1 lb equals 500 mL extra fluid
    • -Urine output
    • *Systemic manifestations or ARF can occur in any system of the body.
  153. Systemic manisfestations of Acute Renal Failure
    • Cardiovascular:HF- fluid overload and HTN
    • Pulmonary Edema-Increased pulmonary capillary permeability, fluid overload, left ventricular dysfunction.
    • Dysrhythmias-Electrolyte imbalances(hyperkalemia and hypocalcemia).
    • Peripheral edema-Fluid overload.
    • HTN- Fluid overload and increased sodium retention.
    • Hematological:anemia: decreased erythropoietin secretion, loss of RBCs through GI tract, mucous membranes, or dialysis, decrease RBCsurvival time, uremic toxins interfernce with folic acid secretion.
    • Alterations in coagulation:plt dysfunction
    • Increased susceptability to infection: decreased neutrophil phagocytosis
    • Electrolyte imbalances:Metabolic Acidosis: decreased hydrogen ion excretion, decreased bicarb ion reabsorption and generation, decreased excretion of phosphate slats or titratable acids, decreased ammonia synthesis and ammonium excretion.
    • REspiratory: pneumonia: thick tenecious sputum from decreased oral intake, depressed cough reflex, decreased pulmonary macrophage activity.
    • Pulmonary edema:Increased pulmonary capillary permeability, fluid overload, left ventricular dysfunction.
    • GI:Anoriexia, nausea, vomiting,Stomatitis and uremic halitosis and Gastritis and Bleeding: uremic toxins, decompesition of urea releasing ammonia that irritates mucosa
    • Neuromuscular:Drowsiness, confusion, irritability, and coma: uremic toxins produce encephalopathy, metabolic acidosis, and electrolyte imbalances.
    • Tremors, twitching, and convulsions: uremic toxins produce encephalopathy, decreased nerve conduction from uremic toxins.
    • Psychosocial:decreased mentation, decreased concentration , and altered perceptions(psychosis):uremic toxins produce encephalopathy, electrolyte imbalances, metabolic acidosis, tendency to develop cerebral edema.
    • Integumentary:Pallor: anemia. Yellowness:retained urochrome pigment. Dryness: decreased secretions from oil and sweat glands.Pruritius:dry skin, calcium and/or phosphate deposits in skin, uremic toxins effect on nerve endings. Purpura: increased capillary fragility, plt dysfunction. Uremic Frost: Urea or urate crystal excretion.
    • Endocrine:Glucose intolerance: peripheral insensitivity to insulin, prolonged insulin halflie from decreased renal metabolism.
    • Skeletal:Hypocalcemia:Hyperphosphatemia from decreased excretion of phosphates, decreased GI absorption of vitamin D, depostion of calcium phosphate crystals in soft tissues.
  154. Nursing Assessment of ARF
    • Daily labs: BUN – norm 5-21 mg/dl (reflects protein
    • metabolism – least reflective measurement of renal function because is not a constant. Can be affected by dehydration, high-protein diet, starvation, GI bleeding, steroids,fever)
    • Creatinine – norm 0.5-1.5 mg/dl(reflects
    • GFR – (95%) by-product of muscle metabolism Increased levels indicate decrease in GFR – usually a constant level)
    • Ratio – norm 10:1 to 20:1( indicates more than
    • just renal failure.found in prerenal ARF. Increased absorption of urea but creatinine not reabsorbed due
    • to decreased GFR.Normal ratio in ATN (intrarenal).
    • Ratio not elevated because urea and creatinine levels rise proportionally. Increased reabsorption and decreased clearance.)
    • Creatinine clearance: norm 84-138 mL/min(creatinine levels reflect changes in renal function, estimate of GFR. Most accurate measurement of renal function. Normal 84-138 mL per minute. GFR decreases 10% every 10 years of age after 40. 1.Empty bladder –record time – discard.2.Collect all urine for next 24 hours - refrigerate. 3.At exactly 24 hours –voids and save. 4.Serum creatinine level drawn.Saved urine sent to lab.)
    • *Urine : Prerenal: specific gravity: >1.020
    • Urine osmality: >500 mOsm/L
    • Urine sodium: <10 mEq/L
    • Few hyaline casts possible
    • BUN/CR Ratio: elevated
    • FENa: <1%
    • Intrarenal: specific gravity: 1.010
    • Urine osmality: <350 mOsm/L
    • Urine sodium: >20 mEq/L
    • Epithelial cast RBC casts, pigmented granular casts
    • BUN/CR Ratio: normal
    • FENa: >1%:
    • Postrenal: specific gravity: normal to 1.010
    • Urine osmality: variable
    • Urine sodium: normal to 40 mEq/L
    • may have stones, crystals, sediment, clots or bacteria
    • BUN/CR Ratio: normal
    • FENa: >1%
  155. Diagnostic tests for ARF
    • Non-invasive: X-ray of kidneys, ureters,
    • and bladder (KUB):Size, shape and position of kidneys
    • Stones, cysts, or tumors

    • Renal ultrasound:Obstruction. Kidney size differentiates between acute and chronic RF. Also used for biopsy and placement of nephrostomy tubes
    • Invasive:Intrvenous pyleography: to visualize the renal parenchyma, calyces, renal pelvis, ureters, and bladder to botain info regarding size, shape, position, and function of the kidneys. *Can result in hypersensitivity reaction to contrast medium, or acute renal failure.
    • Computed tomography:to visualize the renal parenchyma to obtain data regarding size, shape, and presence of lesions, cysts, masses, calculi, obstructions, congenital anomalies, and abnormal accumulations of fluid. *Can result in hypersensitivity reaction to contrast medium.
    • Renal angiography:to visualize the arterial tree, capillaries, and venous drainage of the kidneys to obtain data regarding the presence of tumors, cysts, stenosis infarction, aneurysms, hematoma, lacerations, and abcesses. *Can result in hypersensitivity reaction to contrast medium, hemorrhage or hematoma at the catheter insertion site, or ARF.
    • Renal scanning:to determine renal function by visualizing the appearance and disappearance of the radioisotopes within the kidney; also provides some anatomical info. *Can result in hypersensitivity reaction to contrast medium.
    • Renal Biospy:To obtain data for making a histological diagnosis to determine the extent of the pathology, the appropriate therapy, and the possible prognosis. * Can result in Hemorrhage or Post-biopsy hematoma.
  156. Invasive diagnostic procedures for assessing renal system Nurses responsibilities:
    • Explain procedure (reinforce info from MD) – explain pt
    • responsibilities
    • •Notify MD of allergies especially IVP dye
    • •Prep pt for procedure – bowel prep, Ivs, pre-op meds or fluids, labs, consent forms
    • •Provide emotional support
    • •Assist with procedure
    • •Monitor for complications
    • •Document
  157. Nursing interventions for ARF
    • -Normal UO – 0.5-1 mL per kg per hour
    • -Hydrate prior to
    • surgery or invasive procedures
    • -Fluids restricted to UO/24 hrs + insensible loss = 600-1000mL/dy
    • -Allow for insensible loss
    • -non ventilated patient needs 500-700 mL/dy more than input to be equal
    • -Ventilated I & O should be equal
    • -Weight – same scale, time, clothing
    • •Want wgt. within 2 lbs of dry wgt.
    • •1kg = 2.2 lbs = 1000 mL fluid gain
    • -Infection
    • •Strict aseptic techniques
    • •No catheters – oliguric for 8-14 days
    • Monitor peak & trough levels to prevent nephrotoxic effects
    • -Peak – 1-2 hours after drug given.
    • -Trough – just before next dose is given
  158. Management of ARF
    • Prerenal - key goals to prevent ATN – irreversible RF – maintain cardiac function and intravascular volume.
    • Hypovolemia – replace fluids
    • Hydrate before surgery, invasive procedures and contrast dye procedures.
    • Cardiac – IABP, positive inotropes, antidysrhythmics, preload or afterload reducers
    • Intrarenal: Diet:•Adequate calories – 25-35 cal/kg/day
    • •Adequate protein – 1.5-2 g/kg/day - catabolism
    • •Sodium, potassium, calcium
    • •Fluid – UO + 600-1000 mL/day
    • •Dialysis pt – needs vitamins, amino acids, possibly
    • feedings with enteral or TPN
    • Medications:•Diuretics can lead to electrolyte imbalances – mannitol most used if brain injury or increased ICP or renal failure due to rhabdomyolysis.
    • *Controversial – 1) increases mortality and delays
    • recovery, 2) increases UO but no improvement in survival or recovery, 3) may cause excess diruesis and renal hypoperfusion leading
    • *Should correct hypovolemia before using diuretics
    • •Inotropes – dobutamine, dopamine – maintain
    • renal blood flow – controversial because decreases T cell count making susceptible to infection.
    • •Mucomyst (acetylcysteine) – used for pts with
    • elevated serum creatinine levels before
    • radiologic procedure using contrast – also hydration
    • 600 mg orally bid day before procedure & day of procedure
    • •Fenoldopam, theophylline – also used to
    • prevent contrast induced renal failure
    • Postrenal:Catheter
    • Ureteral stent
    • Surgery
  159. Medical Management ARF:Hyperkalemia
    • Hyperkalemia – decreased GFR < 6.5, no symptoms
    • Decrease intake
    • Increase urine loss – diuretics
    • >6.5, not taking digitalis
    • IV Calcium over 2-5 minutes – short lived 30-60 minutes
    • §Decrease body content
    • §Kayexalate
    • §Lasix
    • §Dialysis
    • §Shift intracellulary
    • §Insulin/Dextrose
    • §Sodium bicarbonate
    • §Antagonize membrane effect
    • §Albuterol
  160. Medications to treat hyperkalemia: Kayexalate(sodium polystyrene sulfonate)
    • Mechanism of Action:Increased fecal excretion of potassium by exchanging sodium ions for potassium ions.
    • Dosage: Oral: 15 g 1-4 times daily by mouth. Rectal: 30-50 g via enema every 6 hours
    • Side Effects: Constipation, hypkalemia, hypernatremia, nausea and vomiting, fecal impaction in the elderly
    • Nursing Implications:Available as a powder or suspension. Mix powder with full glass of liquid and chill to increase palatabilty. Do not mix oral powder with OJ. May be mixed with sorbitol to facilitate movement thgouh the intestinal tract.
  161. Medications to Treat Hyperkalemia: Sorbitol
    • Mechanism of Action:Hyperosmotic laxative
    • Dosage: 20-100mL rectally via enema every 6 hr
    • Side Effects: Hpergylcemia, diarrhea, edema, abdominal discomfort, hypokalemia
    • Nursing Implications:Administer as retntion enema in combo with Kayexelate.
  162. Medications to Treat Hyperkalemia: Furosemide(Lasix)
    • Mechanism of Action:Increases Renal excretion of potassium
    • Dosage:Oral: 20-80mg daily twice /day
    • IV: 20-40 mg/dose every 6-12 hours
    • Continuous Infusion: 10-40 mg/hr
    • Side Effects: Orthostatic hypotension, hypokalemia, urinary, dizziness, ototoxicity
    • Nursing Implications: Administer IV dose over several minutes; ototoxicity is associated with rapid administration. Assess for allergy to sulfonylurea before giving. Monitor for dehydration, hypokalemia, hypotension. Diuretics only work if the patient is nonoliguric.
  163. Medications to Treat Hyperkalemia: Insulin/dextrose
    • Mechanism of Action:Shifts potassium temporarily from extracellular fluid(blood) into the intracellular fluid; the dextrose helps prevent hypoglycemia
    • Dosage: 10 units regular insulin and 50 mL of 50% dextrose as a bolus IV
    • Side Effects:Hyperglycemia, Hypoglycemia, hypokalemia
    • Nursing Implications: if the serum glucose is >300 mg/ dL, the physician may order only insulin.
  164. Medications to Treat Hyperkalemia: Sodium Bicarbonate
    • Mechanism of Action:Shifts potassium temporarliy from extracellular fluid (bllod) to the intracellular fluid
    • Dosage: 50-100mEq/L IV push
    • Side Effects:hypernatremia, hypokalemia, pulmonay edema
    • Nursing Implications:Do not mix with any other meds to avoid precipitation. helpful if patient has a sever metabolic acidosis.
  165. Medications to Treat Hyperkalemia: Albuterol
    • Mechanism of Action: Adrenergic agonist increases plasma insulin concentration; shifts potassium to intracellular space
    • Dosage:Inhalation:10-20mg over 10 minutes
    • IV:0.5 mg over 15min
    • Side Effects: Tachycardia, angina, palpiatations, hypertension, nervousness, irritability.
    • Nursing Implications: note that the dose used is much higher than that used in treating pulmonary conditions. Use concentrated form(5mg/mL) so the volume to be inhaled is minimized.
  166. Medications to Treat Hyperkalemia: Calcium gluconate
    • Mechanism of Action: Electrolyte replacement
    • Dosage: 10 mL IV over 5 min
    • Side Effects: Bradycarida, hypotension, syncope, necrosis if infiltrated
    • Nursing Implications: has no effect on actually lowering serum potassium. Will see almost immediate effect on ECG. Be sure IV is patent; Avoid extravasation( leakage)
  167. Medical Management of ARF: Hyponatremia
    • Be careful – sodium can be lost with diuretic use.
    • Fluid restriction – loss of free water.
    • Nurse should check output and electrolytes hourly.
    • Hyponatremia_Due to water overload
    • Inability to conserve sodium – due to tubular damage
    • Restrict fluids – free water < 1000 mL/24 hr
    • Diuretics with saline infusion (3 or 5%)
    • Monitor I & Os and electrolytes hourly
    • Can lead to osmotic demyelination syndrome
    • Dialysis – change sodium in dialysate
    • Osmotic demyelination syndrome
    • Hypocalcemia – hyperphosphatemia – inverse
    • relationship – abnormal excreteion, absorption, and
    • metabolism
    • Hypermagnesemia – decreased excretion
  168. Osmotic demyelination syndrome:
    • Osmotic demyelination syndrome (previouslycalled central pontine myelinolysis) may followtoo-rapid correction of hyponatremia.
    • Demyelination may affect the pons and other areas ofthe brain. Lesions are more common in patients with alcoholism, malnutrition,or other chronic debilitating illness. Flaccid paralysis, dysarthria, and dysphagia can evolve over afew days or weeks. The lesion may extend dorsally to involve sensory tracts andleave the patient with a locked-in
    • syndrome (an awake and sentient state inwhich the patient, because of generalized motor paralysis, cannot communicate, exceptpossibly by coded
    • eye movements). Damage often is permanent. If Na isreplaced too rapidly (eg, > 14 mEq/L/8 h) and neurologic symptoms start to develop, it is critical to prevent further plasma Na increases bystopping hypertonic fluids.In such cases, inducing hyponatremia with hypotonic fluidmay
    • mitigate the development of permanent neurologic damage.
  169. Medical management of ARF:Management of Acid-Base Balance
    • Metabolic acidosis in ARF : Etiology: Inability of kidney to excrete hydrogen ions; decreased production of ammonia by the kidney( normally assists with hydrogen ion excretion). Retention of acid end-products of metabolism which use available buffers in the body; inability of kidney to synthesize bicarbonate.
    • Signs and Symptoms: Low pH of arterial blood( pH<7.35)
    • Low serum bicarbonate
    • Increased rate and depth of respirations to excrete carbon dioxide from the lungs( compensatory mechanism) KUSSMAUL's Respirations.
    • Low PaCO2
    • Lethargy and coma if severe.
    • ▪ Kussmaul’s respirations
    • ▪ Serum bicarbonate level
    • ▪ < 15 mEq/L & pH < 7.2
    • ▪Dialysis
  170. Normal Bicarb level
    24-28 mEq/L
  171. Chronic Kidney Disease (CKD)
    • Irreversible damage to nephrons of both kidneys
    • Defined – damage to kidney or GFR < 60 ml/min
    • Systemic disease –affects every body organ
    • Staged according to level of kidney function –
    • Stage 5 – end-stage kidney disease (ESKD)
    • ▪Needs dialysis or transplant
    • Numerous causes – 2 main causes hypertension and
    • diabetes
    • End-stage-kidney disease (ESKD) - kidney function unable to sustain life.
    • By stage 4 (severe CKD) getting ready for dialysis
    • In stage 5 GFR < 15 ml/min measured by creatinine clearance (normal 85-135 ml/min) and require dialysis or renal replacement – may need transplant
    • Normally our body can compensate until about 90% of nephrons are lost (born with 2 million)
    • *1972 Social Security Act made CKD a disability to allow
    • for access to health care through Medicare and Medicaid
    • -All patients must be offered dialysis unless medically
    • contraindicated or refuses treatment.
  172. Normal GFR
    > 90 ml/min
  173. CKD: Systemic manifestations: Electrolyte imbalances and hematological
    • Electrolyte and acid-base imbalances
    • Urea –elevated BUN (by-product of protein metab in diet
    • – kidney unable to excrete), creatinine protein
    • breakdown from muscle – kidneys unable to excrete
    • Hyperkalemia – fatal if 7 to 8 mEq/L
    • Potassium can come from:
    • •Decreased excretion, Breakdown of protein, Bleeding, Metabolic acidosis, Food, drugs, IV infusions
    • Treatment:•Restrict diet
    • •IV glucose and insulin or calcium gluconate
    • •Kayexalate (sodium polystyrene) – mixed in sorbitol – laxative – diarrhea – avoid if hypoactive bowel sounds
    • •Dialysis –arrhythmias
    • Hyponatremia – water retention, dilutes sodium-not
    • due to not enough sodium but too much water, or decreased reabsorbtion - Edema, HTN, CHF - Restricted to 2 g per day
    • Metabolic acidosis – unable to excrete acids (ammonia) and reabsorb or regenerate bicarb - Kussmaul respirations
    • Hyperphosphatemia/Hypocalcemia – inverse relationship – renal osteodystrophy – bones demineralize in an
    • attempt to increase calcium levels.
    • Treatment for Hyperphosphatemia
    • •Calcium-based phosphate binders – bind to phosphate for excretion in stool – give with each meal
    • Tums – calcium carbonate, PhosLo – calcium acetate, Renagel (sevelamer hcl) or Fosrenol(lanthanum carbonate) – does not contain calcium
    • *DO NOT USE ALUMINUM HYDROXIDE GELS OR ANTACIDS – associated with dementia and osteomalacia
    • *DO NOT GIVE MAGNIESIUM-CONTAINING ANTACIDS – need kidneys to excrete
    • •Limit phosphorus in diet
    • •Provide Vitamin D supplements – need to make sure phosphate level is down first to prevent soft tissue calcification if Calcium and phosphorus both elevated – monitor for hypercalcemia
    • Hematological: Anemia – decreased kidney production of erythropoietin – decreased erythropoiesis
  174. CKD systemic manifestations: Cardiovascular, GI, and respiratory.
    • Cardiovascular system:
    • Hypertension:aggravated
    • by sodium and water retention – leads to vascular changes,
    • Accelerates atherosclerosis, left ventricular hypertrophy, CHF, pulmonary edema, MI, stroke. Increased risk if diabetic.Retinopathy,encephalopathy, nephropathy. Diuretics & ß-adrenergic blockers – initially.ACE inhibitors – decrease proteinuria & RF progression.
    • -Hyperlipidemia
    • -Heart failure
    • -Pericarditis
    • GI system
    • Inflammation due to excessive urea.
    • Ulcers, stomatitis, uremic fetor (breath smells of
    • urine), GI bleeding.
    • Anorexia, N & V -weight loss, malnutrition.
    • Diarrhea from hyperkalemia &change in calcium metabolism or constipation from fluid restrictions ormedications (iron or calcium-containing-phosphate binders)
    • Respiratory: Uremic lung – uremic
    • pneumonitis – interstitial edema on CXR – treat with dialysis
    • Kussmaul resp,dyspnea, pulmonary edema, pleurisy, pleural effusion, infections

  175. CKD: Systemic manifesations: Integumentary andNeurologic
    • Neurologic system
    • Increased BUN, electrolyte imbalances, metabolic
    • acidosis
    • CNS depression –lethargy, apathy, decreased concentration, fatigue, irritability, AMS(altered mental status)
    • Seizures and coma –elevated BUN and hypertensive encephalopathy
    • Peripheral neuropathy– restless leg syndrome, burning sensation, foot drop, muscle atrophy, muscle twitching, jerking, asterixis(Hand-flapping tremor), nocturnal leg cramps
    • *Treatment – dialysis or transplant

    • Integumentary:
    • §Yellow-gray discoloration
    • §Pruritis, itching
    • §Uremic frost – urea crystallizes on skin
    • §Dry, brittle hair
    • §Thin, brittle, ridged nails
    • §Petechiae and ecchymoses -platelets
  176. CKD medication considerations
    • *Drugs – some must be avoided or dosages reduced
    • Digitalis:loading dose okay
    • maintenance dose: 0.125 mg every other day
    • not affected by dialysis – can decrease potassium levels – potentiates digitalis
    • Antibiotics: Aminoglycosides, PCN, tetracycline – nephrotoxic
    • Vancomycin, gentamicin –excreted by kidneys
    • Pain medication:NEVER give Demerol (meperidine)
    • accumulation of normeperidine – seizures - Liver
    • metabolizes Demerol into normeperidine to be
    • excreted by kidneys
    • Others may just need smaller doses and less frequent – effects last longer
    • Avoid NSAID – worsen renal hypoperfusion -NSAIDs –
    • block synthesis of renal prostaglandins that promote vasodilation
    • Antacids– avoid if contain magnesium – cannot excrete
    • Insulin –not metabolized or excreted well – reduce dosages – monitor BS qid
  177. Dietary Restrictions for CKD
    • Protein:0.55 to 0.60 g/kg/day Hemodialysis:1-1.5 g/kg/day Peritoneal Dialysis:1.2-1.5 g/kg/day
    • Calories: To prevent negative nitrogen balance. Hemodialysis:To prevent muscle loss &
    • malnutrition .Peritoneal:High calorie supplements
    • Sodium:1-3 g/day. Hemodialysis:2-4 g/day.Peritoneal:No table salt.
    • Potassium: Avoid salt substitutes Hemodialysis:60-70 mEq/day.Peritoneal: No restriction
    • Phosphate:Restrict dietary phosphorus – protein.Phosphate
    • binders.
    • Water:Equal to urine output
    • Hemodialysis:500-700 mL + urine output
    • Peritoneal: I & O, symptoms

    • *When not on dialysis Protein is increased in diet if
    • lost in urine – measured on actual body weight not ideal body weight
    • On dialysis “dry” weight is used.
    • Suggested protein sources – milk, eggs, meat.Decreased albumin levels indicate poor protein intake
    • Restricting phosphorus also restricts calcium – may need calcium and vitamin D supplements
    • Fluid – daily weight – 1 kg = 1 l fluid = 2.2 lbs.
  178. Hemodialysis:Before procedure nurse assess?
    • – weight, baseline
    • vital signs, edema, lung and heart sounds, vascular access site, condition of skin
    • End weight at last treatment and this weight determines
    • weight to be removed. Ideally no more than 1 to 1.5 kg should be gained between treatments to avoid large quantities to be removed – can cause hypotension
    • *Elderly pt with ESRD most commonly die from MI or
    • stroke, followed by withdrawal
    • *Dialysis should not be withheld can enhance quality of
    • life and has been shown to have good success rates
    • *During procedure VS are taken every 30-60 min – lasts 3-5 hours
    • CAn be done at Hospital, clinic or at home
  179. Hemodialysis: Procedure
    2 needles placed in fistula or graft, or two blood lines.Needle closest to fistula (red) pulls blood with help ofpump at 200 to 500 ml/min to dialyzer (primed with 1000 ml saline) Heparin is added to blood as it goes through dialyzer –prevents clotsDialysate(body temperature) flows from bottom at 300-900 ml/minBlood returns to patient through second needle (blue)Alarms on dialysatedelivery system Blood leaking into dialysateAir leaking into bloodAltered temp of dialysateExtreme changes in BPAt end of procedure dialyze is flushed with saline toreturn all bloodNeedles removed and pressure applied until bleedingstops – not too hard can cause thrombosis If has lines they are clamped and removed
  180. Vascular access for hemodialysis
    • AVF – usually radial or ulnar artery and cephalic vein are used – can’t use for 4 to
    • 6 weeks – prefer to wait 3 months if possible

    • Arterial blood flow is established through vein –
    • increased pressure dilates vein and becomes tough – is able to withstand numerous punctures

    • Best patency rates and least number of complications –
    • need healthy vessels – not placed very often because harder to place, lack of expertise, time consuming

    AVG – usually brachial artery and antecubital vein – can use in 2 to 4 weeks – self-healing (seal over punctures) – infection and thrombosis complications

    Cannulated with 14-16 gauge needles

    Thrill felt

    Bruit auscultated

    NO BP, IV, venipunctures

    • Steal syndrome – distal ischemia because too much
    • arterial blood shunted from extremity

    Anuerysms – increased pressure

    • Nursing care
    • •Palpate thrill, auscultate bruit every 8 hours
    • – assess distal pulses
    • •Never draw blood, take BPs, IM injections or start IVs in arm with graft/fistula
    • •Strict aseptic
    • technique
    • •Inspect for infection
    • •Inject with heparin
    • •Clamp when not in use
  181. Temporary Access for Hemodialysis
    • -internal jugular of femoral vein
    • -subclavian used as last resort
    • -Jugular or subclavian catheters can stay in for 1-3 weeks
    • -Femoral catheters can stay in for up to 1 week

    • Complications
    • •Jugular –uncomfortable, less risk of thrombosis
    • Subclavian – pneumothorax, neuropathies, hemothorax, central stenosis
    • Femoral – more at risk for kinking, not clean area, only stay short time, thrombosis, pulmonary emboli, immobility, hematoma
  182. Hemodialysis: Complications:
    • Hypotension – rapid removal of fluid
    • -Decrease rate and give 100 to 300 ml 0.9% saline
    • -Hold BP meds before dialysis
    • -Reassess dry weight

    • Muscle cramps – rapid removal of sodium and water
    • -Decrease rate of filtration
    • -Give saline bolus

    Loss of blood –

    Dialyzer not completely rinsed

    Accidental separation of tubing

    Membrane rupture

    Bleeding after needles removed – heparinized

    • Hepatitis
    • – B and C
    • – blood transfusion or exposure (IV drug abuse, unprotected sex)
    • -Isolation if infected with B
    • -Disposable equipment
    • -Hepatitis B vaccine
    • -Infection control
    • Sepsis–vascular access site or poor technique
    • Aseptic technique

    • Disequilibriumsyndrome – rapid changes in composition of extracellular fluid from blood but not as fast from brain – fluid moves into brain causing edema
    • -Stop or slow dialysis
    • -Give hypertonic saline, albumin or mannitol to shift fluid from brain to systemic circulation
  183. Continuous Renal Replacement Therapies
    • -24 hours per day
    • -Gradually removes solute
    • -Decreased risk of complications
    • -Bed bound
    • -One-to-one nursing care
    • Four types of CRRT – (continuous ultrafiltration & clearance of waste products )
    • -Slow Continuous Ultrafiltration (SCU)
    • -Continuous Venovenous Hemofiltration (CVVH)
    • -Continuous Venovenous Hemodialysis (CVVHD)
    • -Continuous Venovenous Hemodiafiltration (CVVHDF)
    • Complications: Same as for hemodilaysis – more vulnerable to filter clotting, air embolism, and
    • hypothermia.
  184. Nursing care for CRRT
    • VS every hour¡
    • Monitor I & O – replace if needed
    • Assess filter for clots
    • Monitor lytes, PTT, Hgb, Hct, ABGs
    • Assess system –kinks, warm tubing
    • Monitor for blood in filtrate
    • Maintain sterile technique – samples, changes, dressing changes
    • Continuous heparin infusion
    • Collaboration with physician
  185. CRRT Complications
    • Imbalances of fluid, electrolytes, acidbase
    • Hemorrhage
    • Infection
    • Hypothermia
    • Clotting of filter
    • Air embolism
    • Failure of vascular access
  186. Nephrotic Syndrome
    • *Glomerulus more permeable to plasma protein Multisystem diseases, infections, neoplasms, allergens, drugs 1/3 of patients have another condition – diabetes, lupusOthers – idiopathic
    • Characteristics:Peripheral edema – decreased serum protein – severe ascites and anasarca Massive proteinuria – hypercoagulable state – renal or pulmonary emboli – 40% of cases HypertensionHyperlipidemia Hypoalbuminemia
    • Labs:Decreased serum albumin Decreased total serum proteinElevated cholesterol
    • Treat symptoms
    • §Relieve edema
    • §Control or cure disease
    • §ACE inhibitors
    • §NSAIDS
    • §Low sodium (2-3 g/day), low protein diet (0.5-0.6 g/kg/day)
    • §Lipid-lowering agents
    • §Corticosteroids
  187. Neurogenic Bladder
    • *Abnormal or absent innervation to the bladder Hyperreflexic, spastic – corticospinal lesion – SCI, brain tumor or trauma, CVA, MS – no inhibition, empties in response to stretching of wall Areflexic, flaccid – Lower motor lesion – trauma S2-S4, pelvic nervies, cauda equina – acts as paralysis of all motor funcion, fills without emptying Dyssynergia - damage to sensory spinal reflex arc, MS, DM – Lack of sensation to void Common problems:Urgency, frequency, incontinence, inability to void, high bladder pressure – reflux into kidneys
    • Classifications: ¡Reflexic – spastic, uninhibited, upper motor neuron¡Arereflexic – autonomous, flaccid, lower motor neuron¡Sensory

    Symptoms : ¡Incontinence, frequency, urgency, unpredictable ¡No control – overdistension, overflow incontinence¡Poor sensation, infrequent voiding
  188. Neurogenic Bladder Treatment
    • ¡Treatment determined by:§Upper extremity function§Caregiver strain§Lifestyle choices
    • *Intermittent catheterization
    • External catheter
    • Indwelling catheter
    • Antiucholinergic
    • Intravesical capsaicin
    • Botulinum A toxin
    • *Usually intermittent catheter or indwelling catheter Risk for UTI
    • Fistula formation
    • Diverticula
    • Need adequate hydration
    • Nurses must teach – select intervals – usually q 4 hours Assess bladder before cath - < 200 mL may extend time - > 500 mL time interval shortened
    • Usually 5 or 6 times a day
    • May need urinary diversion surgery if repeated UTIs
  189. Abdominal injuries
    • Usually due to blunt trauma or penetration injuries.
    • Blunt – MVA, falls
    • Compression – direct blow
    • Sheering – rapid deceleration
    • Penetrating gunshot or stabbing – open
    • Solid organ – profuse bleeding
    • Hollow organs – causes peritonitis
  190. Abdominal injuries Manifestations
    • Guarding or splinting – peritonitis
    • §Hard & distended – bleeding
    • §Decreased or absent bowel sounds – peritonitis §Contusions, abrasions, bruising
    • ▪Grey Turner’s sign▪ Cullen’s sign §Pain▪Abdominal▪Scapula – phrenic nerve
    • §Hematemesis or hematuria
    • §Shock

    • *Retroperitioneal hemorrhage:
    • Grey Turner’s – bruising of flanks
    • Cullen’s sign – bruising around umbilicus Pain over scapula caused by irritation of the phrenic nerve by free blood in abdomen
  191. abdominal injuries: diagnostic
    • ¡Diagnostic:
    • §CBC, ABGs, PT, lytes, BUN, creatinine, T & C §Urinalysis
    • § Abdominal ultrasound
    • §Abdominal CT scan
    • §Peritoneal lavage
    • *Lavage – most sensitive for detecting injury to hollow organs. Local anesthetic – large catheter – aspirate – < 10 mL give 1 L of slaine into abdomen and drained
  192. abdominal injuries: what to do
    • ¡Ensure airway¡
    • Fluid replacement ¡
    • Prevent shock ¡
    • NG tube ¡
    • Close monitoring ¡
    • Never remove impaled object
  193. Immunosuppressive therapy
    • Commonly used immunosuppressive drugs include corticosteroids, cyclosporine, tacrolimus (Prograf), and mycophenolate mofetil (CellCept).
    • §Calcineurin inhibitors
    • §Sirolimus
    • §Mycophenolate mofetil
    • §Polyclonal antibodies (antithymocyte globulin and antilymphocyte globulin)
    • §Monoclonal antibodies
  194. Organ Transplantation
    • ¡Tissue Typing§HLA typing
    • §Panel of reactive antibodies
    • §Crossmatch
    • ¡Transplant Rejection§Hyperacute rejection
    • §Acute rejection
    • §Chronic rejection
    • *The human leukocyte antigen (HLA) system is responsible for rejection of genetically unlike tissues. It consists of a series of linked genes that occur together on the sixth chromosome in humans. Because of its importance in the study of tissue matching, the chromosomal region incorporating the HLA genes is termed the major histocompatibility complex.
  195. Graft vs. host disease
    In graft-versus-host disease (GVHD), the immunocompetent cells in a transplant graft attack or destroy vulnerable host or recipient tissue. Once the reaction is started, little can be done to modify its course. The target organs for the GVHD phenomenon are the skin, liver, and gastrointestinal tract; the biggest issue is infection.
  196. Congenital HYPOthyroidism: Manifestations:
    Permanent – can be hereditary (15%) or non-heredity Most common thyroid dysgenesis of unknown cause World-wide due to iodine deficiency Transient – assoc with maternal Grave’s Disease treated with antithyroid meds or hypothalamic and pituitary immaturity.

    • Manifestations :
    • BIRTH :Poor feeding, lethargy, jaundice, resp difficulties, cyanosis, constipation, bradycardia, hoarse cry, large fontanels, postterm, birth weight > 8.8 lbs
    • 6-9 WEEKS: Depressed nasal bridge, short forehead, puffy eyelids, large tongue, thick, dry skin, coarse hair, abdominal distention, umbilical hernia, hyporeflexia, bradycardia, hypothermia, hypotension, anemia, widely patent cranial sutures.
    • OLDER:Short stature, obesity, intellectual deficits, abnormal tendon reflexes, slow, awkward movements.
  197. Congenital Hypothyroidism:
    • —Early identification and treatment needed to prevent mental retardation (before 6 months)—
    • Neonatal screening – mandatory in US.
    • —Filter paper blood spot thyroxine (T4)—TSH if low T4– heel stick between 2-6 days of age, usually between 24-48 hours before discharge (can result in false positive)Decreased T4 and high TSH indicate CH – need further testing for cause
  198. Congenital Hypothyroidism: Treatment, signs of overdose and inadequate treatment
    • —Treatment —:Lifelong thyroid hormone replacement —Synthroid, Levothroid —Regular measurement of thyroxine levels—,Bone-age surveys —
    • Signs of overdose:—Tachycardia, dyspnea, irritability, insomnia, fever, sweating, weight loss —
    • Signs of inadequate treatment —Fatigue, sleepiness, decreased appetite, constipation

    *Can have normal physical and intellectual growth if treatment started early. MUST stress importance of compliance. Crushed in put in formula or food – if missed dose, twice dose should be given next day. If diagnosed late – mental retardation is inevitable – treatment may prevent further damage. Genetic counseling may be needed.
  199. Endocrine Emergencies
    • —Hyperglycemia
    • —Hypoglycemia—
    • Diabetic Ketoacidosis (DKA)—
    • Hyperosmolar
    • Hyperglycemic State (HHS)—
    • Diabetes Insipidus —
    • Adrenal crisis

    *Stress during critical illness changes the excretion of endocrine glands. Hyperglycemia normal finding – research shows aggressive treatment of BS lessens infection, renal failure, transfusion needs, stroke, MI in the critically ill. Control for BS 110-180 Hypoglycemia – results from abrupt d/c of nutrition, too much insulin, sepsis, drugs
  200. Adrenal Crisis
    • —Insufficient aldosterone & cortisol
    • —Long-term use of steroids – abrupt withdrawal—
    • Acute stress – trauma, infection, surgery
    • —Occult – sepsis, septic shock, or severe trauma—
    • Life-threatening—
    • Symptoms vary

    • Primary hypoadrenalsim – intrinsic failure to produce glucocorticosteroid
    • Secondary hypoadrenalism – administration of steroids stops prodction of instrinic glucocorticosteroids. Cortisol – helps with defense mechanisms and response to stress – inhibits the immune and inflammatory responses
    • Deficiency:•Decreased glucose production•Decreased protein and fat metabolism•Decreased appetite•Decreased intestinal motility and digestion•Decreased vascular tone•Diminished effects of catecholamines
    • Aldosterone helps to regulate fluid and electrolyte balance – increases sodium and water reabsorption and potassium and hydrogen excretion.
    • Deficiency:•Decreased retention of sodium and water•Decreased circulating volume•Increased reabsorption of potassium and hydrogen ionsBecause symptoms vary should be considered in any patient with shock, fever, vomiting, low sodium, high potassium, hypoglycemia, hypotension
  201. Adrenal Crisis Manifestations:
    • Cardiovascular—Hypovolemia
    • —Decreased vascular tone—
    • Hyperkalemia .•Decreased vascular tone – decreased effectiveness of catecholamines •Hypotension is not responsive to fluids and requires vasopressors.•EKG changes with hyperkalemia •Can lead to hemodynamic collapse and shock.
    • žNeurological—Decreased: glucose, protein, volume, perfusion, sodiumž.•Headache•Fatigue – worse at end of day•Severe weakness•Confusion, listlessness, lethargy, apathy, psychotic, emotional roller coaster
    • Gastrointestinal—Decreased intestinal enzymes—Decreased motility and digestionž•Vague symptoms – loss of appetite, nausea, vomiting, diarrhea
    • Genitourinary—Decreased renal perfusion—Decreased GFR. Decreased urine output.
  202. Adrenal Crisis: Diagnosis and interventions
    • —Diagnosis—Diagnosis made by cortisol level—Adrenal failure - < 15 mcg/dl—Suspected – 15-34 mg/dl—Normal in stressed patient—
    • .*Adrenal crisis should be suspected in anyone acutely ill w/ fever, vomiting, hyptension, shock, decreased sodium, increased potassium, or hypoglycemia. •Decreased or normal cortisol levels indicates adrenal insufficiency - should be increased during stress Cosyntropin test – synthetic ACTH – to check for adrenal insufficiency – check cortisol level, give cosyntropin 250 mcg IV, recheck level in 30 and 60 minutes. Looking for ability to raise coritsol levels. If rise < 7 mcg/dl adrenal gland not able to respond to stress (nonresponder) – increased risk of mortality.If rise > 9 or total > 20 mcg/dl normal function (responder) Nursing Interventions—Fluids•Use NS snd 5% dextrose – need sugar – until s/s improve•Potassium usually corrects itself with glucose and volume – may actually decrease levels – hypokalemia •Metabolic acidosis usually corrects itself also
    • Hormones-Give cortisol to nonresponders – 50 mg hydrocortisone q 6 hrs with 50 mg fludrocortisone (optional) NG tube daily – do not withdraw abruptly. •May give Decadron (dexamethasone phosphate) while waiting on cosyntropin testing – doesn’t interfere with testing.
    • Education•About meds – take daily, don’t stop without guidance – life-long•Call MD for stress – may need double dose – define stress•Small frequent meals•Restrict activity – frequent periods of rest
  203. Thyroid crisis
    • —Hyperthyroidism - Suspect if unexplained rapid heart rate—
    • Thyroid Storm—-following illness, general anesthesia, surgery, or infection.
    • Due to untreated or undertreated hyperthyroidism. Hyperdynamic, hypermetabolic state
    • Produces excessive thermal energy and fever
    • Severe fever (up to 106), marked tachycardia, heart failure, tremors, delirium, stupor, and coma.
    • Death can occur in 48 hours if not treated – from fever and cardiovascular collapse
    • Precipitated by stress—
    • Systemic effects
    • —Labs —
    • Hypothyroidism—:Myxedema Coma:hypometabolic state – gradual – suspected if known hypothyroidism, scar on neck, sensitive to medications.
    • Usually crisis does not occur in properly treated diagnosed thyroid disease.
    • Can be precipitated by stress or if undiagnosed.
    • Life-threatening.
    • Goiters most common cause.
  204. Thyroid Storm Nursing Management
    • -—Safe environment
    • —-Monitor cardiac status—
    • -Support breathing—
    • -Monitor and treat fever—
    • *Administer medications:Antagonize Peripheral Effects of Thyroid Hormone: Propanol(Inderal)
    • Inhibit Hormone Biosynthesis: Propylthiouracil and Methimazole.
    • Block Thyroid Release: Saturated solution of potassium iodie and Lugol' solution
    • Secondary Options:Laponic acid, Ipodate(oragrafin), and Lithium carbonate.
    • Supportive Therapy: Hydrocortisone or dexamethasone.
    • (Medications •Antagonize peripheral effects of thyroid hormone – work within 1 hour•Inhibit hormone biosynthesis – may take weeks to months to lower thyroid hormone•Block thyroid hormone release – given 1-2 hours after antithyroid meds – effects stabilize in 3-6 days)
    • -Manage fluid and electrolyte imbalances—
    • -Nutrition—Education
  205. Treatment of Myedema Coma
    • —-Treat cause—
    • -Thyroid replacement—: levothyroxine sodium(200-500 mcg IV loading dose,) then 50 mcg/ day IV; or liothyronine sodium(25mcg IV every 8 hrs)
    • -Restore fluid & electrolytes: Hyponatremia: <115 mEq/L, hypertonic saline; <120 mEq/L, fliud restriction.
    • Hypoglycemia: IV glucose
    • —-Supportive care—
    • -Blankets: passive warming
    • —-Respiratory assistance
    • -Avoid sedation—( narcotics)
    • -Adrenal hormone replacement: hydrocortisone(100 mg IV bolus, then 50- 100 mg every 6-8 hr for 7-10 days)
    • -CXR, echo—
    • -Family & patient education

    • *Levothyroxine is drug of choice
    • Hyponatremia – responds to thyroid replacement and fluid restriction, may need hypertonic saline w/ or w/o lasix
    • Glucose in IV fluids
    • Hydrocortisone – adrenal hormone replacement
  206. Diabetes Insipidus
    • —Neurogenic – inadequate ADH – rare —*Central (neurogenic) – congenital or idiopathic – more common in critical care from head injury, tumors or neurosurgery, IICP, brain death, infections, encephalitis, and meningitis.
    • Nephrogenic – insensitive to ADH – most common*Nephrogenic - Adequate levels of ADH are made and released but kidneys are not able to conserve water – usually due to long-term use of lithium carbonate
    • —Primary – water intoxication—.*compulsive drinking > 5 L/day causes polyuria or excessive IV fluids or drug induced
    • Causes (Lewis Box 50-3 page 1261): —Head injury or surgery—
    • Genetic—
    • Chronic renal disease—
    • Drugs

    *No matter what the cause the patient has impaired renal conservation of water resulting in polyuria.Severe dehydration occurs if unable to respond to thirst or if thirst is not present.
  207. Diabetes Insipidus: Diagnosis
    • —Sudden abrupt onset of polyuria —
    • Polydipsia if conscious—
    • Signs of hypovolemia
    • —Laboratory findings:—Low urine osmolality – high serum osmolality —Hypercalcemia or hypokalemia —Elevated BUN & creatinine
    • *Dilute urine without diuretics, fluid challenge or hyperglycemia
    • Labs:Serum sodium > 145 mEq/L
    • Serum osmolarity > 295 mOsm/L
    • Urine osmolarity < 300 mOsm/L
    • Determine if neurogenic or nephrogenic
    • Give demopressin 1 mcg SubQ
    • Collect urine at 30 minute intervals
    • Neurogenic DI – urine output decreased
    • Nephrogenic DI – urine unchanged
    • Be careful that patient does not become dehydrated or hypotensive In neurogenic DI the pt does not secrete enough ADH or vasopressin which causes them to secrete diluted urine. When you give vasopressin this decreases the flow of urine and increases the osmolality. Nephrogenic DI does not respond to vasopressin
  208. Diabetes Insipidus Treatment
    • Discover and treat cause
    • Replace fluids PO or IV
    • Hourly VS & UO
    • Accurate I & O, daily weight
    • Monitor Neuro status
    • Medications - Hormones can be given IV, IM, intranasally, or SubQ. More potent when injected, more reliable if IV.Neurogenic Desmopressin (DDAVP) 1-2 mcg IV or SC q 12 hrs– synthetic vasopression - DDAVP most commonly used – SE: Headache, nausea, mild abdominal cramps. – stronger antidiuretic than pitressin. Vasopressin (Pitressin) 5-10 U IM q 3-4 hrs – SE: hypertension, vasospasm of cardiac, cerebral or mesenteric arteries. Nephrogenic – hyrochlorothiazide 12.5 to 25 mg 1-2 times per day - decrease sodium diet – decreases sodium and GFR so fluid is reabsorbed and urine is less diluted.
    • Education – patho of DI, medications, daily weights, Medic-Alert bracelet, drinking according to thirst not over drinking.
  209. Syndrome of Inappropriate Antidiuretic Hormone (SIADH): What is it, causes, S/S
    • —*SIADH – TOO much ADH so unable to dilute urine, retain fluid, hyponatremia due to increased fluids.
    • Excessive ADH secreted
    • —Excess water resorbed —
    • Water intoxication—
    • Causes :•Malignant cells make, store and release ADH
    • •Head trauma, infections – meningitis, encephalitis, lupus, Guillain-Barre
    • •Drugs – amiodarone, morphine, fentanyl, acetaminophen
    • •PEEP – stimulates barroreceptors to release ADH
    • S/S
    • CNS – weakness, lethargy, restlessness, headaches, seizures, coma, cerebral edema – increased ICP
    • GI – decreased motility from hyponatremia – N & V , anorexia, muscle cramps, decreased BS
    • CV – JVD, HTN, increased wedge press.
    • Pulmonary – fluid overload – SOB, pink, frothy sputum, increased resp.
  210. Syndrome of Inappropriate Antidiuretic Hormone (SIADH): Lab findings
    • —Lab findings—:
    • Hyponatremia
    • —Serum hypo-osmolality
    • —Elevated sodium in urine—
    • Decreased BUN, creatinine, albumin—
    • *Hallmark findings – hyponatremia and hypo-osmolality in presence of inappropriately concentrated urine. Osmotic gradient causes shift of water into brain cells causing cerebral edema and IICP - Neurologic symptoms not seen until serum sodium < 120 mEq/L in 48 hours or less. Urine sodium is elevated because kidneys functioning appropriately so sodium is not conserved. BUN, creat, and albumin low because of hemodilution
    • Water load test—:
    • Not done in critical care— and Only if stable.*Need to correct sodium level to at least 125 mEq.L before water load test.
  211. Syndrome of Inappropriate Antidiuretic Hormone (SIADH): Treatment
    • Prevention: monitor those at risk
    • Treat cause
    • Fluid balance:800-1000 mL/day w/ liberal salt intake. Hypertonic saline 3% used if Na < 120 – can be dangerous if given too rapidly - diuretics may be given with this solution to prevent overload. End infusion when-Symptoms gone-Safe serum Na level reached > 120-Total correction of 20 mEq/L achieved. Risk of osmotic demyelination – severe neurologic damage and possibly death. Check Na levels q 4 hrsNeuro checks q 1 hr – seizure precautions
    • Medications:Demeclocycline – 600-1200 mg/day for several days - derivative of tetracycline - decreases renal tubule response to ADH – rarely used because is nephrotoxic and risk of infection. Tolvaptan – new drug Mouth care, I & O, Weigh daily
  212. Diabetic Ketoacidosis (DKA):CAuses and insulin deficiency
    • —Insulin deficiency:
    • —Type I DM—
    • Medications—
    • Failure to give themselves enough insulin or increase their insulin requirements—
    • Insulin pump malfunction—:Malfunctioning pump can cause symptoms within 12 hours.
    • Lack of knowledge
    • —Noncompliance
    • Causes :Most common stress or infection
    • Medications – steroids, thiazide diuretics, beta-blockers, calcium channel blockers, etc
    • Develops over short period
    • Greater incidence in females and adolescents Precipitated by:Change in type of insulin,Change in dosage of insulin,Something triggers response,May be first indication of Type I – undiagnosed,Drugs trigger insulin deficiency,Known DM fail to give themselves enough insulin or increase their insulin requirements,If using a pump can malfunction
  213. DKA:Osmotic Diuresis, Protein breakdown, lipolysis, Kussmal respiration
    • —Osmotic diuresisHyperglycemia—-Pancreas cannot keep up with insulin demand and glucose cannot be used so body breakdown protein for energy•Elevated extracellular glucose levels cause fluid to move out of cells through osmosis
    • Glycosuria -•Elevated levels of glucose in the serum causes glycosuria – loss of glucose in urine
    • —Polyuria-•kidneys excrete water, sodium, potassium, magnesium, calcium, and phosphorus. •Total water loss 6 L•Dehydration
    • —Dehydration
    • —Protein breakdown—Hyperglycemia—
    • Elevated BUN—
    • Hyper/Hypokalemia
    • *•amino acids, glucose and nitrogen•Unable to use without insulin – hyperglycemia and elevated BUN•Potassium moves from inside cell to plasma – hyperkalemia •Potassium may be lost during diuresis – hypokalemia
    • —Lipolysis: —Ketones
    • —Metabolic acidosis
    • *•Breakdown of fats – free fatty acids •Increased production of ketones – hydrogen ions dissociate from ketones - metabolic acidosis
    • —Kussmal respiration—:Fruity breath*•compensation – to blow off CO2 •Acetone is formed and produces fruity breath
  214. Hyperosmolar Hyperglycemic Syndrome (HHS):
    —*Able to produce enough insulin to prevent DKA (breakdown of proteins) but not enough to prevent severe hyperglycemia, osmotic diuresis, and extracellular fluid depletion. Produces fewer symptoms so can go undetected and BS can rise higher

    • Inadequate insulin secretion or action —
    • Newly diagnosed Type II DM
    • Major illness-Infection> Stress >Overproduction of glucose
    • High-calorie feedings -Unable to metabolize
    • Decreased fluid intake-Decreased thirst – impaired sensation>Decreased access – functional ability
    • Medications – corticosteroids, phenytoin, thiazide diuretics, beta blockers, dobutamine, antipsychotics
  215. DKA Versus HHSManifestations
    • —DKA—:Blood sugar > 250 mg/dl—
    • Metabolic acidosis
    • —Ketones in urine and blood
    • —Kussmaul’s respirations
    • —Fluid loss 6 L
    • —
    • HHS—:Blood sugar > 600 mg/dl—
    • More “normal” ABGs—
    • Minimal or no ketonemia and ketonuria —
    • Higher serum osmolarity than DKA—
    • Fluid loss > 9 L
  216. DKA Versus HHS: Manifestations:Explainations
    • Manifestations are due to dehydration, acidosis and electrolyte abnormalities.
    • Hyperglycemia and ketosis contribute to delayed gastric emptying causing nausea and vomiting.
    • Abdominal pain common in DKA – disappears with reversal of dehydration. May be underlying disease process also.
    • Altered LOC ranges from restlessness, confusion, agitation, somnolence to coma – worse in HHS Seizures in HHSCells without glucose starve and move to proteins and fat to get sugar.
    • Metabolic acidosis caused by ketones and impaired bicarbonate buffering
    • Ketones caused by breakdown of fatty acids
    • Kussmaul’s resp due to increase in carboinc acid and compensatory mechanism to blow off CO2 as acid CNS affected by dehydration and acidosis HHS – less fatty acids so no ketones but higher BS, osmolarity and dehydration than DKA HHNC – pH > 7.3 and bicarb > 15 mEq/L
  217. DKA & HHS Nursing Interventions
    • —Respiratory support:Assess ABCs,Oral airways, Oxygen, Intubation, Prevent aspiration - Elevate HOB, Nasogastric suction
    • —Fluid replacement—
    • Insulin administration
    • —Electrolyte replacement—
    • Correction of acidosis—
    • Prevent complications—
    • Teaching and support
  218. DKA & HHS: What to do specifically and watch for!
    • Assess ABCs
    • Oral airways, Oxygen, Intubation
    • Prevent aspiration - Elevate HOB, Nasogastric suction
    • IV access - Normal saline 0.9% Bolus 1 L/hr – 10-20 mL/kg 1st hr then0.45% (if hypernatremic) or 0.9% per sodium/osmolarity levels
    • When BS reaches 250 change to D5 0.45% NaCl at 150-200 ml/hr
    • Can develop shock – altered mental status may be indication – monitor VS q 15 minutes, RA pressure or PAP
    • Measure I & O – daily wgt - Should replace volume deficit within 24 hours
    • Assess for overload – breath sounds - Crackles cardiovasccular symptoms – Tachypnea, JVD, tachycardia, elevated PAOP, decreased LOC
    • Monitor BS q 1-2 hrs – insulin bolus then infusion - should lower BS by not more than 75-100 per hour – too rapid can result in cerebral edema.Once stable change to subQ w/ BS q 6-8 hrs.Potassium usually added to each liter of IV fluid
    • Phosphate- Acidosis usually corrected after fluids replaced
  219. Educations for HHS and DKA
    • —Medication—
    • Monitoring hemoglobin A1C levels 2-3 times per year—(Glycosated or glycated hemoglobin – reflects long-term control of blood sugars)
    • Eating—
    • Exercise—
    • Rest and sleep—
    • Relaxation
  220. HYPOglycemia
    • —*Insulin shock, insulin reaction
    • * —Glucose < 70 mg/dl
    • *Glucose not made as fast as being used
    • *Increased counterregulatory hormones to increase glucose levels
    • Diabetics at risk-children
    • -elderly – unable to recognize signs and symptoms dementia Thirst
    • -other illness
    • -beta blockers decrease awareness
    • Causes: Too much insulin, Tumors, Liver or renal disease, Autoimmune phenomenon, Medications, Hormones, Alcohol, Dietary deficiency, Surgery, Exercise
    • S & S: Alteration in LOC – glucose preferred energy source for brain, Headache,Impaired mental status, inability to concentrate, Irritability, Dizziness, Unconsciousness, Seizures, If prolonged – brain damage and coma
    • Systemic signs:Pale, Cool, clammy skin, Tremors, Palpitations, Tachycardia
  221. Hypoglycemia: interventions:
    • —Stop insulin—
    • Give carbohydrates (Lewis Table 49-20 page 1246):Route you give carbohydrates depends on LOC.Carbs are given in 15 g increments—
    • Reassess in 15-20 minutes :Neurological status is best indication that treatment is working.
    • —If BS < 70 mg/dl repeat
    • —Seizure precautions—
    • Educate patient and family
  222. —Insulin therapy is a critical intervention in the treatment of DKA. What crucial parameters must be monitored to ensure optimal patient outcomes?
    Ongoing assessment of ABCs and oxygenation is a priority. ABGs are needed to assess the degree of acidosis. Hourly blood sugar assessment during insulin infusion is essential in titrating therapy. Fluid administration and assessment of patient response is required. When the blood sugar reached 300 mg/dl, it is important to change to an IV solution that contains dextrose to prevent hypoglycemia.
  223. —What is the critical assessment parameter to differentiate DKA from HHS?
    ABGs will show metabolic acidosis (often severe) in DKA. Patients in HHNC usually are not acidotic. Ketonuria will be present in DKA and absent in HHNC. Kussmaul’s respirations may be seen in DKA secondary to the metabolic acidosis.
  224. —Which organ system is most affected by a slower, more prolonged fall in serum glucose, and what nursing interventions are most critical to prevent harm to this patient?
    The central nervous system is most affected by decreases in serum glucose. A progressive decrease in glucose activates the sympathetic nervous system to release epinephrine. Epinephrine is an insulin-antagonistic hormone that results in a higher glucose level. Epinephrine release causes cool, clammy skin; pallor; tremors; and tachycardia. The nurse should be alert to these critical signs of hypoglycemia and provide prompt intervention. Inadequate glucose to the brain will result in brain cell damage, coma, and even death.
  225. Thyroid Storm: Alterations in level of conciousness
    • Symptoms can be confused with other disorders.
    • Provide a safe environment.
    • Assess for orientation, agitation, inattention.
    • Control environmental influences
    • Implement seizure precautions.
  226. Thyroid Storm: Increased Cardiac workload due to hypermetabolic state; decreased cardiac output
    Can lead to heart failure and collapse

    • Assess for chest pain, palpitations
    • monitor for cardiac dysrhythmias and tachycardia
    • monitor blood pressure for widening pulse pressure
    • auscultate for development of S 3
    • monitor hemodynamic status: CI, SVR. PAOP.
    • Assess urine output
    • Evaluate response to therapy
  227. Thyroid storm: increased o2 demand due to hypermetabolic state; ineffective breathing pattern
    • Increased RR and drive can lead to fatigue and hypoventilation
    • provide supplemental o2 or mechanical ventilation as needed.
    • Monitor RR and effort
    • Monitor O2 sat via pulse oximeter
    • minimize activity
  228. Thyroid storm: Loss of ability to regulate with temperature
    • inability to respond to fever exacerbates hypermetabolic demands
    • monitor temp and treat with acetaminophen and/or a cooling blanket as needed
  229. Myxedema coma: Decreased cardiac function
    • Hypotension and potential to develop pericadial effusion.
    • perfusion cradiac monitoring( look for decreased voltage, indicating effusion.
    • auscultate for diminshed heart sounds
    • monitor BPfor sigs of hypotension
  230. myxedma Coma: Muscle weakness, hypoventilation, pleural effusion; ineffective breathing
    • potential for respiratory acidosis and hypoxemia
    • Auscultate the lungs frequently. monitor respiratory effort (rate and depth) and pattern
    • Maintain I and O
    • monitor ABGs/ pulse oximtery and CBC for anemia
    • position for optimum respiratory effort
  231. Myxedema Coma :Alterationd in LOC
    • Ranges from difficulty concentrating to coma Seizures can occur
    • Assess and maintain patient safety
  232. Myxedema Coma: Loss of ability to regulate temperature
    • Inability to respond to cold
    • monitor temp
    • control room temp and provide rewarming measures
  233. Thyroid Storm: Lab Tests
    T3, Free (triiodothyronine): >0.52 ng/dL(HYPERTHYROIDISM)

    T3, resin uptake : > 35% of total

    T4(thyroxine): >12 mcg/dL

    TSH: <0.01 mU/L

    • Glucose: >200mg/dL ( 2 hr postprandial or random) > 140 mg/dL( fasting)

    • Sodium: >150mEq/L
    • BUN: 20 mg/dL

    • CBC :Decreased RBCs and Increased WBCs
    • Calcium: >10.2 mg/dL
Card Set
Med-Surg Test 2
Peds considerations,Chronicity issues, Alt in nutrition, metabolic and elimination,and Alt in endocrine function