MEDSURG NOTES
Lecture 1 - January 9th
A: Introduction to Medical Surgical Nursing Practice
Introduction
- The Canadian Health Act was established to promote, restore and maintain the physical and
mental health of all Canadians
Healthcare Initiatives
- Health Canada (2019) has prioritized the following initiatives
- Expand resources to cope with national opioid crisis and create harm reduction strategies
- Promote smoking cessation (including vaping)
- Improve access to affordability of and the appropriate use of prescription medications
- Increased access to home, community and mental health services
- Implement a multi year Healthy Eating Strategy
- Support implementation of Indigenous Service Canada programs
Challenges in Healthcare
- Rapidly changing technology
- Significant increases in knowledge of disease, disorders, medication, treatments
- Human genome project
- Diverse populations
- Canadians are living longer: aging population
- Increase in the number of patients with chronic disease
- Strain on resources/healthcare system
- More culturally and ethnically diverse populations
Medical Surgical Nursing
- Interprofessional teams
- Nurses are critical for coordinating care among team members to facilitate optimal
patient outcomes
- Communication among healthcare team members
- SBAR: situation, background, assessment, and recommendations
- Delegation and Assignment: formal process guided by CNO standards
- Delegation
- Right task
- Right circumstances
- Right person
- Right direction and communication
- Right supervision and evaluation
- Assignment: allocation of nursing care providers in order to meet patient needs
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Informatics and Technology
- Integration of nursing science, computer science and information technology
- Use of relevant information and knowledge to support delivery of evidence based
practice
- In accordance with professional and regulatory standards
- Use of ICT (informatics computer technology) in the delivery of patient care
- Electronic health record
- Use of computerized record of patient health information
The Nursing Process
- An assertive, problem solving approach to the identification and treatment of patient health
problems
- Provides an organizing framework for the knowledge,
judgements, and actions that nurse bring to patient care
- Phases of the nursing process
- Assessment (subjective and objective, focused then
general)
- Foundation for appropriate diagnosis, planning,
and intervention
- Database must be accurate and complete
- Diagnosis
- The process of identifying actual and potential
health issues
- Planning
- Priority setting (ABCs: Airway, Breathing,
Circulation)
- Identifying outcomes
- Determining interventions
- Implementation
- Carrying out the specific, individualized plan
- Nurse may designate activities to and supervise qualified others
- Evaluations
- Determine if patient outcomes have been met
- Determine whether plan should be maintained, modified, revised, or discontinued
Evidence Based Practice
- Evidence-based nursing (EBN) is an approach to
making quality decisions and providing nursing
care based upon personal clinical expertise in
combination with most current, relevant research
available on the topic
- Four primary elements of evidence based
practice
- Clinical state, setting, and circumstances
- Patient preferences and actions
- Best research evidence
- Healthcare resources
- Goal: to produce better outcomes in the most
effective and efficient way
- Use of EBI to guide clinical practice in
healthcare
B: Chronic Illness
Chronic Illness
- Chronic illness refers to health conditions that persist over extended period of time
- Often associated with
- Activity limitations (disability)
- Tobacco use
- Unhealthy diet
- Harmful use of alcohol
- WHO considers non communicable diseases such as cardiac disease (top cause of death),
respiratory disorders, stroke, cancer and diabetes, to be responsible for 70% of deaths world
wide
- Canadian healthcare is still largely built around an acute, episodic model of care, which does not
meet the needs of patients with chronic health conditions
Epidemiology of Chronic Diseases
- Almost ¾ of all non communicable disease occur in low and middle-income countries
- Canada is part of G7 so high-income country
- In 2018, globally, cardiovascular disease was responsible for the highest proportion of all deaths
- About ⅔ of deaths in Canada each year result from chronic diseases
- Cardiovascular: 1.6 million Canadians are living with heart disease, 70,000 die yearly
- Cancer: 2 in 5 Canadians will develop cancer in their lifetime; 78,000 die yearly
- Diabetes: 1 in 16 Canadians (6.2%) have diabetes and 0.9% of the population is
undiagnosed
- Respiratory: over 3 million live with chronic respiratory disease
Epidemiology of Chronic Disease Indigenous Peoples
- Indigenous people in Canada have higher risk factors and number of chronic diseases when
compared to the national average
- Diabetes: 19.2% of Indigenous population vs 5.2% national average
- Kidney failure: 2-4 items higher than national average
- Three (3) times higher rates of Hepatitis C and HIV
Chronic Illness
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Health Canada tracks chronic disease prevalence and incidence rates using Canadian Chronic
Disease Surveillance System (CCDSS)
Epidemiology Terminology
- Morbidity: rates of disease in a population
- 2 in 5 Canadians will develop cancer during their lifetime
- Mortality: rates of death
- 1 in 4 Canadains diagnosed with cancer will die from the disease
- Most common cancers in Canada are
- Lung (causes more deaths than the next three combined)
- Breast
- Colorectal
- Prostate
Health-Wellness Continuum
- Health: a state of complete physical, mental, and social well-being and not merely the absence of
disease or infirmity
- Disease: a disorder of structure or function in a human, especially one that has a known cause and
a distinctive group symptoms, signs, or anatomical changes
- Illness is the human experience or the reaction of the body to the disease
- Refers to how the disease is perceived, lived with, and responded to by individuals and
their families
- Signs: objective manifestations of a condition
- Symptoms: subjective reports of the patient
Acute vs Chronic
- Acute
- Is typically characterized by a sudden onset with signs and symptoms relative to the
disease process
- Usually self-limiting
- Responds well to treatment
- Complications are infrequent
- Patient returns to previous level of functioning
- Chronic
- Disease that is prolonged, does not resolve spontaneously and is rarely cured completed
- Permanent impairments or deviations from normal
- Irreversible pathological changes
- Residual disability
- Need for long term medical or nursing care
Chronic Diseases
- Comorbidity: presence of two or more disorders that are not directly related to each other in a
person at the same time
- Multimorbidity: simultaneous occurrence of several chronic medical conditions in the same
person, may or may not be related to each other
Chronic Disease: Risk Factors
- Lifestyle choices can be harmful to an individual’s health
- Individual factors
- Background: sex, age, level of education and genetic factors (nonmodifiable)
- Behavioural: smoking, diet, physical activity (modifiable)
- Community factors: social and economic conditions
- Poverty, employment
- Climate and air pollution
- Access to products and services (rural)
Health and Illness
Disability in Chronic Illness
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Chronic illness is often associated with disability
- However, many people are not disabled by their chronic illness
Disability
- Disability is a phenomenon where there is a complex interaction between the individual
with physical or developmental issues and the physical environment that surrounds them
- Cannot complete ADLs
- Supreme Court of Canada definition is “includes a wide and evolving range of
permanent, temporary or intermittent impairments, both physical and mental,
which can result in functional limitations as the person interacts with others and
potentially with socially constructed barrier”
- Medical model of view is disability as directly caused by disease, trauma, or another
health condition to be medically corrected
- Social model of disability sees it as a socially created problem and not an inherent
attribute of individuals
International Classification of Functioning
Concepts Critical to Chronic Illness
- Self-efficacy: it is the optimistic self-belief in our competence or changes of successfully
accomplishing a task and producing a favourable outcome
- Self-efficacy management in healthcare is an approach in which the individual works in
partnership with the healthcare team to find solutions to issue with the patient’s chronic
condition (it has shown to be highly effective in reducing symptoms and facilitating
behaviour change)
- Mastery: ability to master needed skills to care for their condition, i.e., calculate
heart rate
- Vicarious experience: learn through modeling, learn to walk with a walker
- Verbal persuasion and other social influences: verbal support systems, i.e.,
encouragement
- Physiological and affective states (stress): examine and find resources to cope
with alternative states to improve outcomes
- How to manage stress and or anxiety
- Health related hardiness: personality resource that helps to buffer stress and allow people to
manage high degrees of stress without fallin gill
- Control: belief that people can influence the events of their experience
- Choose to look at their experience in a positive way
- Commitment: ability to feel committed to their activities of life
- To remain committed to doing their ADLs as possible
- Challenge: is the anticipation of change
- Attitude to move forward regardless “I can do this”
Chronic Illness Associated Challenges
- Mood disorders
- Illness related anxiety and stress can trigger depression
- Estimated that ⅓ of all individuals with chronic illness experience depression
- Research has indicated that inflammation is an important etiological factor in mood
disorders
- Patients with rheumatoid arthritis, COPD and multiple sclerosis higher rates of
depression
- Nurses need to be aware and assess for signs of depression in this patient population
- Fatigue: commonly associated with chronic illness
- Symptom of the disease process and or an outcome of the condition
- Pain, mood disorders, sleep issues, deconditioning and metabolic abnormalities can
contribute to fatigue
- Nurses need to assess their patients ability to do ADLs and implement measures to reduce
fatigue
- Space ADLs out and allow time between to rest and regain energy
- Stigmatization: how they are regarded by other as having less worth and or value
- Older patients and chronically ill patients are often viewed negatively in the healthcare
setting, impact the healthcare they receive
- Example: patients with obesity, viewed negatively
- Need to be aware of this bias and treat patient with dignity and respect
- Quality of life: is the perceived quality of an individual’s daily life, that s, an assessment of their
well-being or lack thereof
- This includes all emotional, social and physical aspects of the individual’s life
- Health-related quality of life is an assessment of how the individual’s well-being may be
affected over time by a disease, disability or disorder
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Nurses need to monitor patient responses and questions about quality of life to ensure
patient needs and requests are being met
- Chronic illness impacts both the patient and their immediate social circle can lead to caregiver
stress
- Informal caregiver: anyone who provides care without pay
- Many patients with chronic illness are community based
- Caregiver stress can impact finances, physical and emotional health
- Increase in physical care required oer time
- Lack of time to provide self-care
- Fatigue, anxiety, and depression
- Nurses have role in assessing caregiver abilities and news, coordinating supportive care
Chronic Disease Self Management
- Four tasks must be mastered in order to achieve successful self-management
- Processing emotions
- Adjusting to changes to self and life
- Integrating illness into daily life
- Determining the meaning of illness
- Self-management comprises the daily activities that individuals undertake to
- Keep the illness under control
- Minimize its impact on physical health status and functioning
- Cope with the psychosocial sequelae of the illness
- Self-management involves for nurses includes
- Empowering the patient: teaching and follow up
- Ensuring some autonomy with respect to adjusting the treatment regimen as necessary
- Encouraging adherence and self-care
Summary
- Our health care system
- Organized around an acute, episodic model of care
- Fails to meet the needs of many patients, including those with chronic illnesses
- A new model of care must enacted that better addresses the needs of person with chronic illness
- Nurses play a vital role in helping to im[rove the care of persons living with chronic illness
Lecture 2 - January 16th
A: Integumentary System
Introduction
- The integumentary system is the largest organ of the body
- It is comprised of the skin, hair, nails and glands
- VIDEO
- Your skin gives insight on what’s happening inside the body
Integumentary Structures
- Skin: comprised of three (3) layers
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Epidermis (outer layer)
- Relatively skin
- No vascular or lymphatic structures
- Contain keratinocytes which form the basal layer: undifferentiated cells when
they mature (keratinize) as they move to the body’s surface and the cells flatten
and form the outermost layer of skin
- Takes 14 days for the cells to move from the basal layer to the outermost layer
and the cells will remain there for approximately 14 days
- Outer layer is replaced every 28 days
- If not intact then it could be entry course for an infection
- Wants to close the top and could leave hole that could tunnel
- Epidermis also contains melanocytes deep in the basal layer
- Melanocytes contain melanin, a pigment that gives colour to the skin and hair
- Melanin also protects the body from ultraviolet (UV) sunlight
- People with darker skin tones have increased numbers of melanocytes which
produce more melanin = increased protection from harmful UV rays
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Dermis
- Connective tissue below the epidermis
- Is highly vascular
- Contains nerves, lymphatic vessels, hair follicles, sebaceous glands
- Nerves have a hard time regenerating
- Contains specialized cells, i.e., mast cells (initiate inflammatory response)
- Contains collagen, gives skin toughness and strength, critical in wound healing
- Subcutaneous tissues
- Attaches the skin to underlying tissues such as muscle and bone
- Contain loose connective tissue and fat cells
- Deeper wound = increased risk for infection
- High probably muscle is injured or skin detaches from muscle
- Healing needs to go from bottom to top
- Skin appendages include hair, nails and glands (sebaceous, apocrine and eccrine)
- All of these have roots in the dermis layer and receive nutrients (fluid, electrolytes) from the
dermis
- Hair and nails form from specialized keratin
- Sebaceous glands (secrete sebum) which waterproofs and lubricates the skin
- Thinning skin from age decreased sebum and dry out, more prone to injury
- Eccrine sweat glands (function to cool the body by evaporation)
- Can also excrete waste products and moisturize surface cells
- Adults get brain injury with temperature over 102℉
- Need to kept body temp down → needs fluid to lose heat → ice behind knees and
in armpits → antipyretics, acetaminophen, ibuprofen
- Nursing
- Why have stuff slowed
- Losing hair = cell division slowing down
- Chemo effects hair, nails, guts
Functions of the Integumentary System
- Primary roles include:
- Protect underlying tissues from the external environment
- Insulate the body and provide a cushion from trauma
- Melanin screens and absorbs ultraviolet rays
- Nerve endings provide sensory information about the environment
- Help to regulate body temperature
Assessment: Subjective
- Health history questions
- Past medical history
- Medications: prescription and OTC
- Immunosuppressant
- Family history (skin cancer,
- Nutritional history
- Social, environment, and occupational health history (exposure)
- Cognitive: perceptual (sense changes in temperature and tactical function
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Coping abilities
- Burns
- Body image (blank poker face when opening bandages)
Assessment: Objective
- Normal physical assessment of the integumentary system includes
- Skin: evenly pigmented, no petechiae, purpura, lesions, or excoriations, warm, good
turgor
- Capillary refill: body pulls/shunts blood to core and lets the extremity “go”
- Nails: pink, oval, adhere to nail base with 160 degree angle
- Hair: shiny and full, amount and distribution appropriate for age and gender, no flaking
scalp, forehead or pinna
- Physical examination
- Inspection
- General colour and pigmentation
- Pallor, poor perfusion (BP, heart rate), cyanosis (hypoxia, pulse oxygen)
- Vascularity (capillary refill, less than 3 seconds)
- Bruising (ask where they got it to help patient)
- May photograph injuries, wounds, surgical sites, burns, etc. if patient
gives consent
- Lesions or discolourations (rashes, scarlet fever)
- Purpura (purple colours spots/patches), petechiae (tiny, flat pinpoint),
need good assessment
- Changes in skin colour and temperature, problem with perfusion
- Palpation
- Temperature: warm
- Turgor and mobility: elasticity of the skin
- Clavicle, sternum, back of hands
- Slow = dehydrated (rehydrate normal saline or lactated ringers)
- Moisture: dry
- Texture: skin is fine or coarse
- Thickness = callous
- Concerned when on feet because could impair immobility and
cause falls
Assessment of Patient with Dark Skin Tones
- Patient with darker skin tones have increased levels of melanin pigment that are produced by the
melanocytes in the epidermis
- Assessment of skin colour is easier for injury or perfusion in areas where the epidermis is thin and
pigmentation is lighter
- For example mucous membranes, nail beds, palmar surface
- Patient with vitiligo: total loss of pigment in an affected area
Different Skin Conditions on Lighter and Darker Skin Tones
Cyanosis
Lighter Skin Tones
Darker Skin Tones
Greyish-blue tone mucous
Ashen or greyish colour mucous
membranes, lips, earlobes
membrane, nail beds
Ecchymosis
Dark red, purple yellow, green
depending on age of bruise
Purple to brownish-black,
difficult to visualize
Erythema
Reddish tone, increase in skin
temperature
Deeper brown or purple tone,
increase in skin temperature
Pallor
Pale skin colour, white, ashen
May be yellow, ashen or grey
Petechiae
Small reddish pinpoints
Difficult to see, palpate skin
Scar
Usually white or pink, narrow
Higher increase of keloids,
thickened raised scar
Genetic component?
B: Inflammation and Wound Healing
Introduction
- Cells are the smallest unit in the body
- Cells form tissues → organs → body systems → individual
Cell Adaptation to injury
- Sublethal Injury: alters function without causing cell destruction
- Hypertrophy: expansion in size of cells, increased tissue mass without cell division
- Hyperplasia: multiplication of cells as a result of increased cellular division
- Atrophy: decrease in size of tissue or organ as result of reduction in the number or size of
individual cells
- Dysplasia: abnormal differentiation of dividing cells that results in changes in their size,
shape, and appearance
- Anaplasia: cell differentiation to a more immature or embryonic form
- Lethal injury: irreversible process that causes cell death
- Apoptosis/Programmed cell death: normal anticipated event that occurs in some
regenerating tissues to create homeostasis
- Necrosis: tissue death that occurs as a result of a traumatic injury, infection, ischemia or
exposure to toxic chemical
Inflammation
- Inflammation: a biological response to cell injury and/or stress which can be caused by
pathogens, irritants or chronic health condition (i.e., arthritis)
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The intensity of the response depends on the extent and severity of the injury
Two mechanisms that respond to cell injury are:
- Vascular response
- After cell injury, the sympathetic nervous system (SNS) causes a brief
vasoconstriction of blood vessels
- Platelets then begin to adhere to the vessels, initiates clot formation
- Blood staring to be lost
- During this process, inflammatory mediators (histamines) will be released =
vasodilation
- With vasodilation the capillaries become permeable = plasma fluid (serous)
moves into cellular space = warmth and redness
- Swelling and edema
- Albumin (plasma protein) also enters into the injured area, this then attracts more
plasma fluid = edematous tissue = fluid exudate
- Cellular response
- Mast cells release mediators which stimulates vasodilation and also signals for
white blood cells to enter the injured area
- With the vasodilation in the blood vessels, chemotaxis begins (pathological term
for)
- This is the process of moving specific cells to the site of injury begins
- Each type of cell has mediator that attracts it to the area of injury
- Example neutrophil chemotactic factors attract neutrophils
- Increased produced because the move fast
Inflammation
- Chemotaxis: the process of moving specific cells to the site of injury
- Each type of cell has a mediator that attracts to the area of injury
- Cellular adherence: is the binding of needed cells to the endothelial wall of the blood vessel
- Receptors located onto each cell, helps to lock the needed cells into place
- Cellular migration: the process of cells migrating or moving across the endothelial cells into the
injured area
- Due to chemotaxis the following cells arrive at the site of injury (arrival order)
- Neutrophils: first leukocyte to arrive (first responder)
- CBC will show increase of WBC
- Neutrophils increased in CBC if acute infection
- Macrophages increased in CBC if chronic infection
- Monocytes: larger WBC, arrive later, become macrophages
- Both perform phagocytosis, engulfs and breaks down foreign substances, cellular
exudate
- Lymphocytes arrive later to the site of injury and stimulates humoral and cell mediated
immunity processes
- Reads code for pathogen such as COVID
- Signs of Inflammation
- Local signs
- Redness and edema
- Warmth and pain
- decrease/loss of function (varies)
- Systemic signs
- Leukocytosis (rising WBC count)
- Malaise
- Nausea and/or anorexia
- Increased heart rate and respiratory rate
- Fever
- Eventually becomes sepsis, loss of control
Inflammation Treatment Minor Injuries
- Management of inflammation (RICE)
- Rest: injured area
- Ice: cool and cold therapies
- Compression: wrap injuries to limit swelling and drainage
- Elevation: reduce blood flow, elevated the injured area
- Management of pain
- Antipyretic medications
- Aspirin, acetaminophen
- NSAIDs: ibuprofen (not with blood thinners)
- Anti-inflammatory medications
- Aspirin
- NSAIDs: ibuprofen (not with blood thinners)
- Corticosteroids
- Antihistamines
- Vitamins A, B complex, C, D
Inflammation Acute vs Chronic
- Acute
- Healing occurs in 2-3 weeks
- No residual damage
- Neutrophils dominate cellular response
- Chronic
- Lasts for weeks to months
- Repeated tissue injuries
- Lymphocytes and macrophages dominate cellular response
Healing Process
Two types of wound healing
- Regeneration: is the replacement of lost cells and tissues
- Is impacted by the type of cell injured
- Cells that regenerate rapidly lymphoid organs, bone marrow and mucous
membranes of GI, urinary and reproductive tracts
- Labile cells (skin, lymphoid organs, bone marrow and mucous membranes)
divide constantly so injury to these organs is followed by rapid regeneration
- Stable cells (liver, pancreas, kidney and bone cells) only regenerate if they organ
is injured
- Permanent cells (neurons of CNS and cardiac muscles) do not regenerate so
permanent loss is sustained and healing is through repair
- Repair: is healing as the result of lost cells being replaced by connective tissue
- More common
- Can result in scar tissue
Wound Healing
- Repair: comprised of three phases
- Inflammatory phase (initial)
- Acute inflammatory response (vascular and
cellular)
- 3-5 days after injury
- Granulation (proliferative/reconstructive) phase
- Takes from 5 days to 3 (4) weeks
- Fibroblasts migrate to the area and secrete
collagen
- Young capillaries begin to develop (tissue in pink)
- Surface epithelial cell regenerate
- May have scarring or differing pigmentation
- Epithelium thickens begins to mature
- Maturation phase
- Overlaps with granulation phase
- Beings about 7 days post injury (some overlapping)
- Collagen fiber become more organized (remodeling)
- Myofibroblasts cause contraction within the wound, closing the edges
- Scar tissue is maturing, pale, less vascular
Healing by Intention
- Primary: healing where the margins are neatly
approximated
- Surgical incision, usually sutured or stapled in
place
- Secondary: wounds with wide irregular margins
- Healing must take place from the bottom of
the wound to the top (too deep)
- Pack a dressing into the wound (pressure
ulcer) to allow it to heal
- Chronic wounds such as venous leg ulcers,
trauma or pressure
- Debrided common
- Tertiary: wound is left open
- Allows for drainage of fluid, pus and cellular debris
- Closed later (surgically)
Wound Assessment
- Location
- Size: length, depth and width
- Appearance
- Drainage: amount, colour, consistency and odour
- REEDDA
- Pain (describe it and rate it)
- Functionality
- Vital signs: fever
- Comorbidities: age, weight, diabetes mellitus
Wound Treatment
- Wound healing: is dependent on the adequate blood supply to bring oxygen and nutrients to cells
for regeneration and repair
- Prevention of infection: frequent assessment and monitor lab (neutrophils)
- Minimize inflammation: treat with rest (some exercise to prevent DVTs), warmth and
cool therapies, address increases in temperature and pain (pain management control)
- Adequate nutrition: proteins (the need for cellular respiration, fuel) at every stage of
healing, vitamin A (carrots, leafy greens, fish, dairy, eggs) &C (orange, tomato) (shown
to support re-epithelization and collagen synthesis), glucose is important for healing,
nutrition is a concern for very young and old
- Dressing: per physician orders (packing, irrigation, when to change)
Complications of Wound Healing
- Infection
- Excessive redness, edema and warmth in wound
- Presence of pus
- Culture to determine cause
- Treated with medications, antibiotics
- Hemorrhage
- Occurs at initial injury
- Treated with compression, dressings
- Monitor Hgb and Hct
- Fluid as needed
- *patients on blood thinners are at risk
- Adhesions
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Bands of scar tissue that form around organs
Reduce organ functionality
High risk
- Lungs
- Trauma, rib fracture, pleural space sticks
- Tx: incentive spirometry, ambulate, sit up, cough and deep breathing
- GI tract
- Peristalsis is impaired
- Listen to bowel sounds, last BM, I/Os
- Surgical repair
- Contractures
- Shortening of muscle or skin due to scar tissue (rheumatoid arthritis)
- Frequently occurs in burn victims
- Loss of mobility, impacts ADLs
- Nursing: ensure range of motion, monitor wound
- Dehiscence
- Separation of previously joined wound edges
- Nursing: clean and cover the wound then notify the HCP
- Evisceration
- When the wound edges separate and intestine protrude through the wound
- Nursing: apply sterile moist dressing
- Do not manipulate organs
- Notify HCP
- Surgical repair
- Keloids
- Protrusion of scar tissue beyond the wound edges
- Occurs more commonly in patient with darker skin tones
- Feel tenderness, pain in scar area
- Aware of body image
- Can try to prevent it by compression dressing to prevent overgrowth
- Hypertrophic scars
- Large, red, raised and hard scar within wound edges
- May regress in time
- Fistula formation: abnormal passage that forms between organs or a hollow organ and the skin
- Excess Granulation tissue: hypergranulation that protrudes above the surface of the healing
wound, may be cauterized or cut off to promote normal healing
- Delay of healing: some factors may delay healing (nutrition deficiencies [vitamin C, protein,
zinc], smoking, inadequate blood supply, corticosteroid medications, infection, anemia, advanced
age, obesity, diabetes mellitus, poor general health, mechanical friction on wound, cold
temperature, excessive moisture)
Pressure Injuries
- Localized injury to skin/or underlying soft tissue as a result of excessive or prolonged pressure,
shear and tissue deformation
- 2.4% of cases in long term care home in Ontario
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Causes
- Pressure (intensity and duration)
- Shearing force
- Friction
- Excessive moisture
Risk factors
- Advanced age, anemia, contractures (short or weird position), diabetes mellitus,
immobility, impaired circulation (vascular disease), neurological disorders, nutritional
deficiencies, prolonged use of steroids (immunocompromised)
Prevention
- Perform a risk assessment for pressure injuries
- Braden Scale (Table 14.14 p. 236)
- Routine skin assessment while in care
- Repositioned frequently every 2 hours
- Monitor ensure hydration and nutrition
- Dehydration = dry skin = risk for breakdown
- Encourage mobility
- Uses devices to reduce pressure and shearing
- Therapeutic mattresses
- Lift sheets, wheelchair cushions
- Heel boots
Clinical manifestations
- Depend on extent of the tissue involved
- Staged according to deepest level of tissue damage
- EPUAP/NPIAP/PPPIA (2019) pressure injury staging
guidelines
- If a stage 3 ulcer is now a stage 2 it is called
“healing stage 3 ulcer”
Nurses are responsible for assessing and managing pressure injuries
Deep tissue injuries
- Intact or non-intact skin with localized area of persistent
non-blanchable deep red, maroon, or purple discolouration
due to pressure
- Commonly from traumatic injuries (ex. fall)
- Time, rest and RICE will resolve
- Pain and temperature change often precede skin colour changes.
Staging
- Stage 1
- Early stages, presence of blanchable erythema with changes in sensation and
temperature or firmness
- Intact skin with localized area of non-blanchable erythema
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Stage 2
- Partial thickness skin loss with exposed dermis
- Wound bed is pink or red and moist
- May appear as intact or ruptured serum filled blister
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Stage 3
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Full thickness loss of skin in which adipose tissue is visible in the ulcer
Granulation tissue and epibole (rolled edges) are often present
Slough or eschar (black) may be visible
Depth of injury varies depending on location
- Skin not perfused
Stage 4
- Full thickness skin and tissue loss with exposed or directly palpable fascia,
muscle, tendon, ligament, cartilage or bone in the ulcer
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Slough undermining and tunneling or combination of these are often present
Depth varies by location
Unstageable
- If eschar obscures the extent of tissue loss
Assessment
- Review health information
- Health history: surgery, prolonged bed rest, diabetes
- Medication use: corticosteroids, nicotine
- Symptoms
- pain/discomfort
- Presence of sensation
- Physical assessment
- Location, staging
- Wound measurement: depth and max length
- Photograph and document
Treatment
- Dressing changes as ordered by the physician
- Wound care cleaning and debriding as appropriate
- If irrigation ordered, non-toxic solution, normal saline (NS)
- Debridement
- Surgical: surgery to clean and debride the wound
- Mechanical: wet to dry dressing, lift away debris
- Autolytic: moist dressing to soften eschar for removal (hydrogel dressing)
- Enzymatic: medication contain proteolytic enzymes to breakdown necrotic tissue
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Bio surgical: medical grade maggots in a controlled environment to breakdown
necrotic tissue
Negative Pressure Wound Therapy
- Application of negative pressure (suction) to wound bed
- Will remove exudate, fluids and infectious material
- Promotes blood flow
- Wound is packed with foam or gauze dressing and then semi-occlusive is applied
and connected to suction
Hyperbaric treatment
- Patient is placed in an enclosed chamber and 100% oxygen is administered at 2-3
times atmospheric pressure
- Accelerates healing
- Electrical stimulation
- Electrodes are attached to wounds and electrical current is used to stimulate
healing
- Limited in patient with cancer, implantable devices (pacemaker) and
osteomyelitis)
- Psychological Implications
- Patients may have fears or distress about the wound and/or possibility of scarring
- Patient teaching must focus on the healing process and the changes that will occur as the
wound heals
- Nursing must be careful not to react to the wound, adding to the patient’s fears or anxiety
- Use therapeutic communication
- Provide emotional support
- Provide care for the whole patient, not just the wound itself
Ambulatory and Home Care
- More and more patients are being treated in the outpatient setting
- Patients and families need to be taught how to care for wounds and pressure injuries
- Promote adequate rest and good nutrition
- Educate patient what to monitor for in term of complications i.e., infection
- Redness, edema, warmth, change in drainage
- Signs of abnormal healing
- Teaching about how to take medications, orally and with dressings
- Assess cultural implications
- Connect patient without patient resources, home health
Lecture 3 - January 23rd
Fluid and Electrolytes
Body fluids
- Water is the most important nutrient for life
- Water is the primary body fluid
- Adult weight is 55-60% water
- Loss of 10% body fluid = 8% weight loss is SERIOUS
- Loss of 20% body fluid = 15% weight loss is FATAL
- Fluid gained each day should equal (=) fluid lost each day (2-3L/day average)
- Loss fluid via: sweating, vomiting, blood loss, diarrhea
- Water imbalance symptoms may show faster in patients with a lower tolerance levels
(pediatrics, older adults) than patients with a higher tolerance level
Special Populations
- The pediatric client
- Newborn: 77% weight is
water
- In children less than 2, they
lose more water through the
skin than through the kidneys
- can desaturate quickly if
dehydrated
- less than 2 month olds with
lethargy are an emergency
- Need to measure diapers
- The older adult population
- Normal physiological aging results in
- Decrease thirst mechanism
- Decreased number of sweat glands
- Decreased renal function
- There als be o may be decreased mobility and/or cognitive function which
impacts their ability to get adequate fluid intake
Fluid Compartments
- Intracellular fluid (ICF): located inside cells
- 42% of body weight
- Extracellular fluid (ECF): found outside cells
- 30% of body weight
- Intravascular (plasma)
- Interstitial
- Lymph
- Transcellular
Fluid Spacing
- First spacing
- Normal distribution of fluid in ICF and ECF
- Second spacing
- Abnormal accumulation of interstitial fluid (edema)
- Third spacing
- Fluid accumulation in part of the body where it is not easily exchanged with ECF; fluid
trapped and unavailable for functional use (ascites)
- Ascites: fluid in abdomen space (liver failure patients)
- Hard to reabsorb so they have to drain third spacing fluid medically/surgically
- Scrotal swelling, pitting edema, periorbital edema
Fluid Movement
- Diffusion
- Movement of particles from high to low concentration
- the movement of individual molecules of a substance through a semipermeable barrier
from an area of higher concentration to an area of lower concentration
- Path of least resistance
- Osmosis
- The tendency of a fluid, usually water to pass through a semipermeable membrane into a
solution where the solvent is lower and the solute concentration is higher
- Facilitated Diffusion
- the passive movement of molecules along the concentration gradient using a protein
carrier
- Active Transport
- the movement of molecules across a cell membrane from a region of lower concentration
to a region of higher concentration—against the concentration gradient and requires
cellular energy
- Filtration
- the removal or filtering of the toxins and waste products from a liquid (blood, water, etc.)
Capillary Hemodynamics
-
Hydrostatic pressure correlates with blood pressure so if BP is increased hydrostatic pressure will
increase
- Hydrostatic pressure is the force within a fluid compartment
- Oncotic pressure (colloidal osmotic pressure) is osmotic pressure exerted by colloids in
solution
- If pushing pressure is more than pulling then you will have edema
- Edema is correlated to high blood pressure
- Ideally you want equal pushing and pulling pressure
- Reabsorption pressure is oncotic pressure
- Proteins and sodium will pull water towards the venous end
- Arterial = pushing, Venous = pulling
- Shifts of Plasma to Interstitial Fluid
- Elevation of venous hydrostatic
pressure
- Decrease in plasma oncotic pressure
- Elevation of oncotic pressure
- Capillary fluid movement is determined by
- Capillary hydrostatic pressure
- Plasma oncotic pressure
- Interstitial hydrostatic pressure
- Interstitial oncotic pressure
Regulation of Fluid Balance
- Baroreceptors
- Pressure receptor
- Decreased pressure tells brain to release aldosterone
- Aldosterone holds on to water
- Osmoreceptors
- Osmoreceptors regulate sodium and water balance in a manner that maintains the osmotic
pressure of the extracellular fluid (ECF)
- Osmolarity receptor
-
Found in the hypothalamus, when
osmolarity/Na+ concentrations rise
Stimulates thirst
Stimulates release of ADH
Stimulates kidneys to reabsorb water
blood flows through so it tells your
body to hold to pee (too high
osmolarity, aka too many solvents so
you do not want to remove the water)
or pee (to low, too little solvents so you
want to bring the concentration up so
pee and get rid of some water)
Osmolarity
- Concentration of particles
- Plays a huge role of concentration in blood
- SERUM OSMOLARITY: 285-295 mmol/Kg
- 10 on either side is still normal
- 150 mmol/Kg: low concentration, oncotic pressure too low, very diluted, edema, need to
get rid of fluid
- 500 mmol/Kg: very concentrated, need to give fluids, dehydration
- Osmolality: a measurement of the osmotic force of solute per unit of weight of solvent (mOsm/kg
or mmol/kg)
- Osmolarity: a measurement of the total milliosmoles of solute per unit total of volume solution
(mOsm/L)
Renal Regulation
- Primary organs for regulating fluid and electrolyte balance
- Adjusting urine volume
- Selective reabsorption of water and electrolytes
- Renal tubules are sites of action of ADH and aldosterone
Renin-Angiotensin Cycle
Extracellular Fluid Volume Imbalances
- ECF volume deficit (hypovolemia)
- Abnormal loss of normal body fluids (diarrhea, fistula drainage, hemorrhage, polyuria),
inadequate intake, or plasma-to-interstitial fluid shift
- Treatment: replace water and electrolytes with balanced IV solutions
- Straight water will cause dilution
- Fluid volume excess (hypervolemia)
- Excessive intake of fluids, abnormal retention of fluids (CHF), or interstitial-to-plasma
fluid shift
- Treatment: remove fluid without changing electrolyte composition or osmolality of ECF
- Diuretics, keep on electrolytes
- Pay attention to I/Os (looking at imbalance)
- Nursing Management
- Nursing implementation
- I/O
- Intake: fluids, food, oxidation = about 2500mL
- Output: skin and lungs (insensible loss) -900mL, feces -100mL, urine
-1500L = 2500mL
- Excess fluid likes to shift in lungs, skin between alveoli and
membrane is very thin for diffusion but will also cause fluid into
lungs
- Urine gravity should be measured 1.005-1.030 is normal
- Monitor cardiovascular changes (increased heart rate, edema, cold hands, BP,
pulse force, jugular venous visibility, orthostatic hypertension)
- Assess respiratory changes (hear crackles aka excess fluid, especially at base,
SOB)
- Neuro assessment (LOC, cerebral edema, pupil reaction, voluntary movements)
- Daily weights (same time of day, 1 Kg = 1 L of fluid)
- Skin assessment (turgor/mobility, tenting = dehydration, leaky fluid, edema
assessment, mild: dry and wrinkled, severe: cold and moist)
Gerontologic Considerations
-
Structural changes in kidneys decrease ability to conserve water (put out a lot more fluid, leads to
dehydration)
- Hormonal changes lead to decrease in ADH
- Loss of subcutaneous tissue leads to increased loss of moisture
- Reduced thirst mechanism results in decreased fluid intake
Diuretics
- Need to give fluids or get rid of fluid
- Need to keep close eye on electrolytes
- K+ sparing diuretics are used if loop diuretics are causing a loss of K+
Osmotic Movement of Fluids
- Cells are affected by osmolality of the fluid
that surrounds them
- Isotonic
- Fluid with same osmolality as cell
interior
- Sae as intravascular fluid
- Very little fluid movement
- Hypotonic (hypoosmolar)
- Solutes are less concentrated than
cells
- Has lower osmolality
- More diluted, less solubles than our
intravascular fluid
- Hypertonic
- More concentrated, more solutes
- Solutes more concentrated than in cells
- Has higher osmolarity
Types of IV Solution
- Isotonic solution
- An isotonic solution has an osmolarity about equal to that of serum
- Because it stays in the intravascular space, it expands the intravascular compartment
- + or - 20 mmol/L from normal range (285-295)
- Hypotonic
- A hypotonic solution has an osmolarity lower than that of serum
- It shifts fluid out of the intravascular compartment, hydrating the cells and the interstitial
compartments
- Hypertonic solution
- A hypertonic solution has an osmolarity higher than that of serum
- It draws fluid into the intravascular compartment from the cells and the interstitial
compartments
IV Solution Examples
- Isotonic
- Lactated ringer’s (275 mmol/L)
- Ringers (275 mmol/L)
- Normal saline (308 mmol/L)
- Dextrose 5% in water D5W (260 mmol/L)
- 5% Albumin (308 mmol/L)
- Hetastarch (310 mmol/L)
- Normosol (295 mmol/L)
- Hypotonic
- Half-normal saline (154 mmol/L)
- 0.33% sodium chloride (103 mmol/L)
- Dextrose 2.5% in water (126 mmol/L)
- Hypertonic
- Dextrose 5% in half-normal (406 mmol/L)
- Dextrose 5% in normal saline
(560 mmol/L)
- 3% sodium chloride (1025
mmol/L)
- 25% albumin (1500 mmol/L)
- 7.5% sodium chloride (2400
mmol/L)
Plasma Expanders
- Stay in vascular space and increase
osmotic pressure (pull more fluid in)
- Colloids (protein solution)
- Packed RBCs
- Albumin
- Plasma
Electrolytes
Electrolytes
- Solutes
- Are substances dissolved in a solution
- Classified as electrolytes (have a charge) or nonelectrolytes (proteins, no charge)
Extracellular vs Intracellular
- Extracellular (blood sample taken from here)
- +
- Na+, K+, Ca++, Mg++
- - Cl-, HCO3-, HPO4- Intracellular
- +
- K+, Mg++, Na+, Ca++
- - HPO4-, HCO3-, ClElectrolytes
-
Regulation of electrolytes (most)
- Distal nephron
- Regulation of
electrolyte balance
- Different areas
are sensitive to
different
electrolytes
- Nonelectrolytes
- Solutes without an electrical
charge
- Nonelectrolytes found in body
fluids include
- Glucose
- Proteins
Sodium (Na+)
- NORMAL RANGES: 136-145
- Major Role in the Body
- Maintain concentration and volume ECF (where sodium goes water follows)
- Nerve impulse generation (Na+/K+ pump)
- Muscle concentration
- Acid-base balance
- Hypernatremia (>145)
- Na+ Increases or Water Decreases
- Because Na+ is the major determinant of ECF osmolality, hypernatremia causes
hyperosmolarity which then causes a shift of fluid out of the cells and causes
cellular dehydration
- Common in people who aren’t able to react to their thirst center, people with
decreased level of consciousness or inability to obtain fluids for reasons such as
cognitive impairment
- Causes:
- Increase water loss (heat)
- Diabetes insipidus (deficiency in the synthesis of ADH or its release or decrease
in kidney responsiveness to ADH)
- Na IV (hypertonic saline, sodium bicarbonate, sodium containing drugs,
- Excessive oral intake
- Primary aldosteronism (hypersecretion of aldosterone)
- Administration of concentrated hyperosmolar tube feedings, and osmotic
diuretics (mannitol), hyperglycemia from uncontrolled DM can cause
hyperosmolarity
- S&S
- Thirsty
- Excessive sweat
- Lethargy, weakness
-
- Seizures
- Tremors, twitching
- Hypertension
- Nausea
- Weight gain
- Agitation, restlessness
- Coma
- Neurons become more easily excitable
- Edema (peripheral, pulmonary)
- Flushed skin
- NSG Interventions
- Reduce sodium gradually (slowly, too quick could result in cerebral edema)
- Treat underlying causes (replace fluid orally or by IV, D5W)
- Sodium restriction
- Strict intake and output
- Daily weights
- BP management
Hyponatremia (<136)
- Na+ decreases or water increases
- Usually associated with hypoosmolality
- Causes:
- Sodium loss (GI, diarrhea, NG)
- Diuretics
- Wound drainage
- Water gain: heart failure, excessive hypotonic IV
- S&S
- Dizziness, irritability, confusion
- Headache, hypotension
- Muscle cramps
- Nausea
- Vomiting
- Seizure
- Rapid pulse (tachycardia)
- NSG Interventions
- Monitor IV fluids
- Fluid restriction
- Hypertonic IV solution (if severe ex. seizures, 3% NaCl)
- Avoid rapid overcorrection
- Accurate intake/output
- Gatorade (at home)
-
Food sources
- Cheese, salt, seafood, processed meats, canned vegetables, canned soups, ketchup, snack
foods, noodles
Potassium (K+)
- NORMAL RANGES: 3.5-5.1
- Role
- Promotes membrane potential
- Nerve impulse generation
- Muscle contraction
- Normal heart conduction/contraction
- Acid-base balance
- Inverse relationship with sodium reabsorption in kidneys (more sodium less potassium or
less sodium more potassium)
- Hyperkalemia (>5.1)
- K+ increases or water decreases
- Causes:
- Excessive intake
- Excessive IV administration
- Increased intake
- K+ meds
- Shift out of cells
- Massive cell destruction (traumatic injury)
- Metabolic acidosis
- Failure to excrete
- Renal failure (most common cause)
- Potassium sparing meds
- S&S
- Irregular heart rate
- Cardiac failure
- Muscle weakness
-
- Leg cramping (1st sign)
- Tall “T” waves (most significant clinical issue)
- Abdominal cramping
- Diarrhea
- NSG Interventions
- Eliminate oral or parenteral K+ intake
- Increase K+ elimination
- Diuretics
- Dialysis
- Kayexalate (med exchanges electrolytes
but is slow)
- It is easy to give potassium but
hard to get it out of the cell
- Increase fluid
- Force K+ to ICF
- IV Insulin
- Given with glucose to not cause hypoglycemia
- Carriers K+ into the cell, could use IV drip but as soon as it stops
K+ will come back out of the cell
- Reverse membrane effects
- Calcium gluconate IV
- Minimize bad levels
- Monitor with ECG for severe cases
Hypokalemia (<3.5)
- K+ decrease or water increases
- Causes
- Potassium loss
- Kidneys are the primary source of potassium loss (90%)
- Inversely related to sodium, if the kidneys are reabsorbing
sodium then they are excreting potassium
- Diuretics
- Shift of Potassium into cells
- Insulin
- Alkalosis (exchanges for hydrogen)
- B-Adrenergic meds
- Rapid cell building
- Lack of potassium intake
- Lack in diet
- Insulin
- B-Adrenergic
- S&S
- Muscle cramps
- Arrhythmias
- Weak, irregular pulse
- Loss of appetite
- Decreased reflexes
- Hyperglycemia
- NSG Interventions
- Administration of KCl (oral/IV)
- Check urine output
- Should be red on the IV bag, it is also hard on the veins and sometimes
patients will have a cardiac monitor on during administration
- Monitor closely
- Food Sources
- Bananas
- Spinach
- Acorn squash
- Yogurt
- Fish
- Backed potato
- White bans
- Dried apricots
- Oranges
- Tomatoes
- Avocados
- Mushrooms
Calcium
- NORMAL RANGES: 2.10-2.50
- Role
- Part of bone and teeth, muscle contraction, nerve impulse transmission and regulates
enzyme activity, blood clotting (is pulled out of bones and teeth when needed)
- Calcium is obtained from ingested foods
- Only 30% is absorbed in the GI tract
- More than 99% of the body’s calcium is combined with phosphorus in the skeletal system
- Inverse relationship, when one increases the other decreases
- Hypercalcemia (>2.50)
- Causes:
- Prolonged immobilization (demineralization, increases risk for osteoporosis and
fractures)
- hyperparathyroidism** (90% of cases are hyperparathyroidism and malignancy)
- Calcium is controlled by parathyroid hormone (PTH), its production and
release are stimulated when serum calcium is low to increase calcium
levels so hyperparathyroidism would increase calcium levels
- Milk-alkali syndrome (too many medications with calcium in them, ex. TUMS,
rarely happens)
- Vitamin D overdose
- S&S
- Lethargy
-
- Weakness
- Confusion
- Anorexia
- Nausea/vomiting
- Fractures
- Polyuria
- Dysrhythmias
- Impaired memory, disorientation, fatigue, constipation, renal calculi
- NSG Interventions
- Promotion of excretion of calcium in urine
- Diuretic (loop diuretics)
- IV NS (fluid overload if patient has impaired renal function and cannot
excrete excess sodium)
- Calcitonin (synthetic)
- Mobilization (weight-bearing)
- Low calcium diet
- If associated with malignancy, bisphosates are used to inhibit the activity of
osteoclasts (zoledronic acid)
Hypocalcemia (<2.10)
- Causes:
- Decrease production of PTH (parathyroid or thyroid surgery)
- Acute pancreatitis (lipolysis, produces fatty acids that combine with calcium ions
- Low calcium diet
- Multiple blood transfusions because the citrate used to anticoagulant the blood
binds with calcium
- S&S
- Nerve irritability
- Tetany
- Decreased cardiac
contractility
- ECG changes
- Depression
- Seizures
- Laryngeal spasm
- NSG Interventions
- Check for tetany
- Trousseau’s sign
(BP inflation for
1-4 minutes,
claw spasm is +)
- Chvostek’s sign (tap below and in front of ear, grimace is +)
- If multiple blood transfusions
- Check calcium levels
- Calcium rich diet
-
Vitamin D supplement
Oral supplement
- Calcium carbonate
IV calcium gluconate for severe symptoms
- Food sources
- Soy milk
- Bok choy
- Fortified orange juice
- Kale
- Collard
- Tofu
- Edamame
- Sesame seeds
- Almond
- Fortified breakfast cereal
- Rice
- Broccoli
Magnesium (Mg++)
- NORMAL RANGES: 0.65-1.05
- Role
- Promotes protein synthesis, role in energy generation, role in sodium-potassium pump
(decrease = delay in nerve impulse)
- 60% of magnesium is contained in bone
- Must be assessed with calcium and potassium, cannot be looked at on its own
- Hypermagnesemia (>1.05)
- Causes:
- Renal failure
- Increased ingestion (Maalox, milk of magnesia)
- Pregnant women who are taking magnesium sulphate for eclampsia
- S&S
- Impaired muscle contraction
- Paralysis
- Hypotension
- Facial flushing
- Lethargy, urinary retention, deep tendon reflexes are lost, coma
- NSG Interventions
- Avoid magnesium medications
- Limit diet intake
- Increase fluids and diuretics
- Dialysis
- Calcium gluconate (symptomatic, IV)
- Hypomagnesemia (<0.65)
- Resembles hypocalcemia
- Causes
-
S&S
-
Limited magnesium ingestion
Increased gastrointestinal or renal loss, IBD, proton pump inhibitors
Prolonged TPN w/o magnesium supplementation
Diuretic medications
Uncontrolled diabetes
Chronic alcoholism
Resembles hypocalcemia (can contribute to hypocalcemia as a result of the
decreased action of PTH)
- Muscle tetany
- Muscle cramps, tremors, hyperactive deep tendon reflexes, Chvostek’s
sign and Trousseau’s sign
- Confusion
- Vertigo
- Seizures
- Dysrhythmias (V-Fib)
- NSG Interventions
- Oral supplements
- Magnesium rich diet
- Monitor vital signs with magnesium supplements
- Must use infusion pump
- Severe cases: parenteral IV or intramuscular magnesium should be administered
- Food Sources
- Yogurt
- Pumpkin seeds
- Lentils
- Bananas
- Whole grains
- Dark chocolate
- Spinach
- Figs
- Almonds
- Black beans
- Avocados
- Fish
Phosphate (PO4 3-)
- NORMAL RANGES: 1.00-1.50
- Role
- Promotes bone formation, muscle contraction, is part of ATP, DNA, RNA, and cell
membranes
- Important for the function of RBCs
- the acid–base buffering system, in the mitochon-drial energy production of ATP,
in cellular uptake and use of glucose, and as an intermediary in the metabolism of
carbohydrates, proteins, and fats.
-
-
-
Hyperphosphatemia (>1.50)
- Causes:
- Renal failure
- Certain enemas (fleet)
- Excessive milk intake
- Large vitamin D intake
- Chemotherapeutic agents
- Hypothyroidism
- S&S
- Hypocalcemia
- Tetany
- Calcium-phosphate precipitates on skin
- NSG Interventions
- Identify and treat the underlying cause
- Restrict dairy products
- Adequate hydration
- Correction of hypocalcemic conditions (enhances renal excretion of phosphate)
- Patients with renal failure: calcium supplements, phosphate binding agents or
gels, dietary phosphate restrictions
Hypophosphatemia (<1.00)
- Causes;
- Malabsorption
- Glucose administration
- TPN
- Phosphate-binding antacids
- Nutritional recovery syndrome
- Alcohol withdrawal
- Recovery from diabetic ketoacidosis
- Respiratory alkalosis
- S&S
- Confusion
- Rhabdomyolysis
- Muscle weakness
- Cardiac dysrhythmias
- Coma
- Renal tubular wasting Mg2+, Ca2+, HCO3- Decreased stroke volume
- Osteomalacia
- NSG Interventions
- Oral supplements
- High phosphorus diet (dairy)
- IV administration of IV phosphate (not common, sodium phosphate or potassium
phosphate)
Food sources
-
Yogurt
Seeds
Cheese
Pork
Poultry
Beans
Nuts
Tofu
Shellfish
Beef
Fish
Proteins
- Composed of combinations of
- Amino acids, nitrogen, hydrogen, oxygen
- Proteins have complex functions
- Cell membranes (so important because if it breaks electrolytes will come out)
- Formation and maintenance of cells, tissues and organs
- Considered “building blocks” as they contribute to structure of
- Enzymes, hormones, antibodies, hemoglobin of RBC
- Maintenance of osmotic pressure
- Source of energy
- Protein synthesis and degradation is an ongoing process
- Under stress, protein catabolism increased
- Can lead to malnutrition, diminished resistance to infection and fluid imbalances
- Hypoproteinemia can over time
- Causes:
- anorexia, malnutrition, starvation, fad dieting and imbalance diets
- Poor absorption
- GI malabsorptive diseases (pancreatic insufficiency and inflammatory
bowel disease)
- S&S
- Edema, slow healing, anorexia, fatigue, anemia and muscle loss
- Vascular oncotic pressure decrease as it won’t pull water in
- Management
- High-carb, high protein diet
- Dietary protein supplements
- Enteral nutrition or total parenteral nutrition
- Hyperprotetinemia is rare but can occur with dehydration-induced hemoconcentration
Blood Disorders
Anemia
-
Definition
-
A deficiency in the number of erythrocytes (Red Blood Cells [RBC]), the quantity or
quality of hemoglobin, and the volume of packed RBCs (hematocrit, how tightly packed),
or a combination of these
- Identified by a thorough history and physical examination, and then classified on the
basis of laboratory review of the complete blood count
- 3 main “types” of anemia
- Caused by decreased erythrocyte production
- Caused by blood loss
- Caused by erythrocyte destruction
Anemia Symptoms
- Anemia symptoms are related to tissue hypoxia because anemia affects RBCs transport of oxygen
throughout the body
- Hb is used to determine the severity of Anemia
- S&S
- Mild (100-120 g/L Hb): Palpitations,
asymptomatic most of the time (usually
compensation for heavy exercise, other
underlying disease)
- Moderate (Hb 60-100 g/L Hb): cardio
symptoms are increased and are present at
resting, palpitations (bounding pulse),
dyspnea, fatigue
- Severe (Hb <60 g/L):
- Skin: pallor, jaundice, pruritus,
night sweats
- Eyes: icteric conjunctiva and sclera, retinal hemorrhage, blurred vision
- Mouth: glossitis, smooth tongue
- Cardio: tachycardia, increased pulse pressure, systolic murmurs, intermittent
claudication, angina, heart failure, myocardial infarction
- Pulmonary: tachypnea, orthopnea, dyspnea at rest, SOB
- Neurological: headache, vertigo, irritability, depression, impaired thought
processes
- GI: anorexia, hepatomegaly, splenomegaly, difficulty swallowing, sore mouth,
nausea and vomiting, decreased urine output, diarrhea, constipation
- Musculoskeletal: bone pain
- General: sensitivity to cold, weight loss, lethargy
- Nursing Goals
- Assume normal activities of daily living
- Maintain adequate nutrition
- Develop no complications related to anemia
Age-Related Considerations: Anemia
- Signs and symptoms of anemia in older adults may include pallor, confusion, ataxia, fatigue,
worsening cardiovascular and respiratory problems
-
Anemia may go unrecognized in the older adult because manifestations may be mistaken
as normal aging changes or overlooked because of another health problem
Anemia Caused by Decreased
Erythrocyte Production
Iron-Deficient Anemia
- Most common nutritional disorder
in the world
- Populations at risk: very young,
nutritionally inadequate diets and
women in reproductive years
- Decrease in RBC production
- Iron is needed to form RBC
and carry oxygen
- Blood loss is the major cause of iron deficiency
- Dietary
- Malabsorption
- Blood loss (GI/GU bleed, peptic ulcer, gastritis,
esophagitis, diverticular, hemorrhoids and
neoplasia, menstrual bleeding)
- Hemolysis
- Common S&S: pallor, glossitis (inflammation of the
tongue), headache, paresthesia, burning sensation of the
tongue
- NSG Interventions: identify and treat underlying disease,
dietary changes, oral (ferrous sulphate or gluconate) or
parenteral iron supplements (iron dextran, iron sucrose,
sodium ferric gluconate), transfusion if acute blood loss,
education to people at risk,
Thalassemia
- A GROUP of disease involving inadequate production of
normal hemoglobin - RBCs
- Reduced globulin protein
- Not common in Canada
- Mostly mediterranean/Asia/Africa
- Hereditary
- S&S: frequently asymptomatic, mild to moderate anemia symptoms
- Microcytosis (small RBCs), hypochromia (pale cells), mild splenomegaly,
bronze-coloured skin and bone marrow hyperplasia
- Symptoms develop by age 2
- NSG Interventions
- Minor requires no treatment because the body adapts
-
Major: blood transfusions, chelating agents that bind to iron (deferasirox oral,
deferiprone, subcutaneous/IV deferoxamine), ascorbic acid supplement, zinc
supplementations, folic acid
- Iron supplements should not be given
- Hematopoietic stem cell transplantation (HSCT), only cure but not a good option for all
patients
Megaloblastic Anemia
- Group of disorders caused by impaired DNA synthesis
- Large RBCs (macrocytic)
- Destroyed easily
- Results in cobalamin (vitamin B12) and folic acid deficiencies
- Cobalamin Deficiency
- Pernicious anemia: absence of intrinsic factor (IF) and is the most common cause of
cobalamin deficiency, middle age or later
- IF is required for cobalamin absorption
- S&S
- GI: Sore, red, shiny tongue, anorexia, nausea, vomiting, abdominal pain
- Neuro: symptoms are due to progressive demyelination of nerve fibers,
weakness, paresthesias of feet and hands, reduced vibratory and position senses,
ataxia, muscle weakness, and impaired thought processes ranging from confusion
to dementia
- Takes several months for manifestations to develop
- NSG Interventions
- Parenteral or intranasal administration of cobalamin
- Consistently starting with IM for 2 weeks then weekly until HB is
normal then every month for life
- Patient will die within 1-3 years without ^^
- High- dose oral cobalamin and sublingual cobalamin are also available for those
whose GI absorption is intact. As long as supplemental cobalamin is used, the
anemia can be reversed.
- Neurological complications may not be reversible
- Folic Acid Deficiency
- S&S are similar to cobalamin deficiency
- Expect for the neurological findings, Folic Acid Deficiency does not get these
symptoms so it is a way to differentiate the two
- NSG Interventions
- Replacement therapy, 1mg/day by mouth, malabsorption or chronic alcoholism
may need up to 5mg/day by mouth
Anemia of Chronic Disease
- Aka anemia of inflammation, can be caused by cancer, autoimmune and infectious disorders, HF
or chronic inflammation, bleeding episodes can also contribute
- Usually develops 1-2 months after the disease activity has an immune basis
- Cytokines released with inflammatory, autoimmune, infectious, or malignant disease cause an
increased uptake and retention of iron within macrophages. This leads to a diversion of iron from
the circulation into storage sites and subsequent limitation of the availability of iron for
erythropoiesis.
- High serum ferritin and increased iron stores distinguish it from iron-deficiency anemia. Normal
folate and cobalamin blood levels distinguish it from megaloblastic anemias secondary to folate
and cobalamin deficiencies.
- Correct underlying disease
Aplastic Anemia (Page 709)
- Peripheral blood pancytopenia (decrease of all blood cell types - RBCs, WBCs, platelets), usually
acquired from bone marrow damage (hypocellular bone marrow)
- Low incidence
- Etiology
- Prone to infection
- 70% due to autoimmune activity by autoreactive T lymphocytes
- Other may be acquired from toxic injury to bone marrow stem cells or result
from congenital stem cell defect
- Clinical Manifestations
- General manifestations: fatigue, dyspnea, cardiovascular and cerebral responses
- Patients with neutropenia (low neutrophil counts) are susceptible to infection and at risk
for septic shock, a low-grade fever is a medical emergency
- Diagnostic Studies
- Laboratory studies: Hb, WBC, platelet values, RBC is generally normal
- Bone marrow biopsy, aspiration, and pathological examination
- The serum iron and total iron-binding capacity (TIBC) may be elevated as indicating
signs of erythropoiesis suppression
- Management
- Identify and remove causative agent and providing supportive care until the pancytopenia
- Prognosis is poor
- HSCT and immunosuppressive therapy with antithymocyte globulin, steroids,
cyclosporine, cyclophosphamide
- ATG can cause anaphylaxis, but with premedications and careful infusion
Anemia caused by Blood Loss
-
RBCs are being produced not
destroyed and are functional but we
are losing them
Acute Blood Loss
- Acute blood loss and chronic blood
loss
- Causes a decrease in RBCs
- Acute could be caused by
traumatic injury, surgical
complications and
conditions/diseases that
disrupt vascular integrity
-
Pulse SPO2 could be 100% because the RBCs that are left are at 100% oxygen levels
around 1000mL we would begin blood transfusions to replace loss
Diagnostic studies: RBC count may seem normal or fight for 2-3 days
Management
- Replacing blood volume to prevent shock (IV Fluids [minor loss] or blood
transfusion [major loss])
- Blood transfusions usually packed RBCS, but may also include platelets,
plasma and cryoprecipitate
- Identifying the source of the hemorrhage and stopping the blood loss
Chronic Blood Loss
- Sources of chronic blood loss are similar to those of iron-deficiency anemia (e.g., bleeding ulcer,
hemorrhoids, menstrual and postmenopausal blood loss)
- Effects of chronic blood loss are usually related to the depletion of iron stores and are usually
considered as iron-deficiency anemia
- Management
- Identifying the source and stopping the bleed
- Supplemental iron
Anemia of Chronic Disease
- Associated with an underproduction of RBCs and mild shortening of RBC survival
- Chronic inflammation, autoimmune, infectious, or malignant disease can lead to anemia of
chronic disease
Anemia caused by Erythrocyte Destruction
- Also known as hemolytic anemia
Sickle Cell Disease (SCD)
-
Inherited, autosomal recessive disorders characterized by the presence of an abnormal form of Hb
in the RBC
Abnormal hemoglobin S (HbS) cause erythrocyte to stiffen and elongate and take on a “sickle”
shape in response to low levels of O2 in the blood
Usually discovered in infancy or early childhood
Causes irreversible damage to the lungs, kidneys, brain, retina or bones that significantly reduce
the patient’s quality of life
-
-
-
-
Common in African-descended population
Etiology and Pathophysiology
- Types: sickle cell anemia (most common and severe,
two sickle cell genes), sickle cell-thalassemia and sickle
cell-HbC is when you have one sickle cell gene and the
other is abnormal (thalassemia or HbC), sickle cell trait
is when you have a sickle cell gene and a normal gene
Sickling episodes
- Sickling episodes are most commonly triggered by low
O2 tension in blood
- Other causes are hypoxia or deoxygenation from viral or bacterial infection, high altitude,
emotional or physical stress, surgery or blood loss
- Sickled RBCs become rigid and take on elongated, crescent shape, they cannot easily
pass through capillaries or other small vessels and cause vascular occlusion, leading to
acute or chronic tissue injury
- The resulting hemostasis promotes a self-perpetuating cycle of local hypoxia
deoxygenation of more erythrocytes, and more sickling
- Initially it is reversible but eventually becomes irreversible
Sickle Cell Crisis
- Severe, painful, acute exacerbation of RBC sickling causing a vaso-occlusive crisis
- Blood flow is impaired vasospasm occurs further restricting blood flow
- Severe capillary hypoxia causes changes in membrane permeability, leading to plasma
loss, hemoconcentration, the development of thrombi, further circulatory stagnation
- Tissue ischemia, infraction and necrosis eventually occur from lack of O2
- Shock is a life threatening consequence
- Can begin suddenly and persist for days to weeks
Clinical manifestations
- You have to look at trends for patients with sickle cell anemia
-
-
Hypovolemic, hypoxia and decreased
in BP
- Need to compare vital signs you have
taken with past vitals
- Heart rate increased signals increase in
pain
- Patients could have chronic health
conditions and pain because of organ
tissue hypoxia and damage (e.g.,
involving the kidneys or liver)
- Typical patient is anemic but
asymptomatic until sickling episodes
- Pallor is examined in mucus
membranes
- Jaundice is common (because of
hemolysis) and patients are at risk for
gallstones
- Primary symptom with sickling is pain
- Could be accompanied by fever, swelling, tenderness, tachypnea, hypertension,
nausea, vomiting
Complications
- Gradual involvement of all body systems throughout repeated sickling episodes
(especially spleen, lungs, kidneys, brain)
- Infection is a major cause of morbidity and mortality in patients with SCD
- the failure of the spleen to phagocytize foreign substances as it becomes infarcted and
dysfunctional (usually by 2 to 4 years of age) from the sickled RBCs.
- Becomes small because of repeated scarring, autosplenectomy
- Pneumonia is most common infection can cause aplastic and hemolytic crisis and
gallstones
- An aplastic crisis can be so severe to cause a temporary shutdown of RBC
production in bone marrow
- Acute chest syndrome: acute pulmonary complications (pneumonia, tissue infarction, fat
embolism)
- characterized by fever, chest pain, cough, pulmonary infiltrates, and dyspnea, and
may be life-threatening
- Pulmonary infarction may cause pulmonary hypertension, MI, and cor pulmonale
- Heart may become ischemic and enlarged leading to HF
- Retinal vessel obstruction may result in hemorrhage, scarring, retinal detachment, and
blindness.
- The kidneys may be injured from the increased blood viscosity and the lack of O2, which
can lead to renal failure
- Chronic leg ulcers can result from hypoxia and are especially prevalent around the
ankles.
- Priapism (persistent penile erection) may occur if penile veins become occluded.
-
Pulmonary embolism or stroke can result from thrombosis and infarction of blood
vessels.
- Bone changes may include osteoporosis and osteosclerosis after infarction
- Diagnostic Studies
- Peripheral blood smear
- Hb electrophoresis
- Increased bilirubin levels
- Other abnormal laboratory test results
- Skeletal x-rays show bone and joint deformities and flattening
- MRI can identify stroke caused by blocked cerebral vessels
- Doppler studies can assess for DVT
- Chest x-ray diagnose infection or organ malfunction
- NSG Management
- Goals
- Preventing sequelae from the disease
- Alleviating manifestations from the complications
- Minimize end-target organ damage
- Promptly treating serious sequelae
- Education
- Minimize trigger
- Ongoing screening (retinopathy at 10 years, brain scans)
- Immunizations
- Avoid dehydration
- Prophylaxis antibiotics potentially
- Assessment
- Respiratory status as respiratory failure is most common cause of death for these
patients
- Encourage rest, DVT prophylaxis
- Fluids and electrolytes administration to reduce blood viscosity and maintain renal
function
- Pain management
- Transfusion of packed RBC if aplastic crisis occurs
- those with thalassemia major, may require chelation therapy to reduce
transfusion-produced iron overload
- Hydroxyurea is the ONLY medication that has been shown clinically beneficial in
anti-sickling and increased production of fetal hemoglobin (HbF) which alters adhesion
of sickle erythrocytes to the endothelium
- Haematopoietic stem cell transplantation (HSCT) is not common but is possible
Hemolytic anemia
- A condition caused by the destruction or hemolysis of RBCs at a rate that exceeds production
- Could be physical destruction, immune reactions (isoimmune or autoimmune) or
infectious agents and toxins
- General supportive care until causative agent is eliminated or at least rendered less
injurious to RBCs
-
Corticosteroids, blood products, removing the spleen
Chronic: folate replacement and immunosuppressive medications such as
rituximab
- A hemolytic crisis is a potential consequence
- Aggressive hydration and electrolyte replacement to reduce risk for kidney injury
caused by Hb clogging the kidney tubules and subsequently shock
Hemochromatosis: iron overload disorder, genetic defect or secondary to diseases such as sideroblastic
anemia, liver disease, or multiple blood transfusions
Polycythemia: abnormal condition characterized by increased RBCs this can increase RBCs to be so great
that blood circulation is impaired as a result of increased blood viscosity (hyperviscosity) and volume
(hypervolemia)
Leukemia
-
-
-
-
A group of malignant disorders affecting the blood and blood-forming tissues of
- Bone marrow
- Lymph system
- Spleen
Accumulation of dysfunctional cells due to loss of regulation in cell division
Fatal if untreated
Often thought of as a childhood disease but it affects all age groups
- Quite prevalent in older adults
ETIOLOGY AND PATHOPHYSIOLOGY
- No single causative agent
- Combination of genetic and environmental influences (research recently)
- Associated with development
- Chemicals agents
- Chemotherapeutic agents
- Viruses
- Radiation
- Immunological deficiencies
CLASSIFICATION
- Acute versus chronic
- Cell maturity and nature of disease onset
- Acute: clonal proliferation of immature hematopoietic cells, quick
symptoms
- Chronic: mature forms of WBC, and onset is more gradual, virus
symptoms then weaker
- Identifying type of leukocyte involved, whether it is of myelogeous origin or of
lymphocytic origin
TYPES
- Acute lymphocytic leukemia (ALL)
- 25% of all leukemias
- 80% of the acute leukemias in adults
- Abrupt, dramatic onset
-
-
-
Serious infection or abnormal bleeding
- Can be any area
- Uncontrolled proliferation of myeloblasters, the precursors of granulocytes
- Clinical Manifestations
- Fatigue, weakness, headache, mouth sores, anemia, bleeding, fever,
infection, sternal tenderness, gingival hyperplasia, mild
hepatosplenomegaly
- Diagnostic Findings: Low RBC count, Hb, Hct; low platelet count; low to high
WBC count with myeloblasts; high LDH; greatly hypercellular bone marrow
with myeloblasts
Acute myelogenous leukemia (AML)
- Most common in children, 20% of adults
- Immature, small lymphocytes proliferate in the bone marrow; most are of B-cell
origin
- Signs and symptoms may appear abruptly
- Fever
- Bleeding (nose possibly)
- Pallor, anorexia, generalized lymphadenopathy, infections, weight loss,
hepatosplenomegaly (liver and spleen enlargement), headache, mouth
sores
- Insidious with progressive weakness, fatigue, pain (bone, joint, abdo), bleeding
tendencies
- CNS manifestations
- Especially common in ALL
- Serious problem
- Breathing issues??
- Increased intracranial pressure secondary to meningeal infiltration
(leukemic meningitis caused by arachnoid infiltration)
- Diagnostic findings: low RBC count, Hb, Hct, and platelet count,
low/normal/high WBCs, high LDH, hypercellular bone marrow with
lymphoblasts and could be in cerebrospinal fluid, presence of Philadelphia
chromosome
Chronic myelogenous leukemia (CML)
- Excessive development of mature neoplastic granulocytes by the bone marrow
that then move into peripheral blood in massive numbers and infiltrate the liver
and spleen
- Clinical Manifestations
- No symptoms early in disease; then fatigue and weakness, fever, sternal
tenderness, weight loss, joint pain, bone pain, massive splenomegaly,
increase in sweating
- Diagnostic Findings: Low RBC count, Hb, Hct; high platelet count early, lower
count later; increase in polymorphonuclear neutrophils, normal number of
lymphocytes, and normal or low number of monocytes in WBC differential; low
-
-
leukocyte alkaline phosphatase; presence of Philadelphia chromosome (90% of
patients)
- Course: chronic stable phase followed by the development of a more acute,
aggressive phase referred to as the blastic phase
- Chronic lymphocytic leukemia (CLL)
- Most common in adults in western countries
- Production and accumulation of functionally inactive but long-lived,
mature-appearing lymphocytes usually b-cell that then infiltrate bone marrow
spleen and liver
- Infection common because of T-cell deficiencies or hypogammaglobulinemia
- Lymphadenopathy is common and can cause complications such as pain and
paralysis
CLINICAL MANIFESTATIONS
- Manifestations relate to problems caused by bone marrow failure and formation of
leukemic infiltrates due to bone marrow overcrowding by abnormal cells and inadequate
production of normal marrow elements
- Inadequate marrow elements cause
- Anemia
- Thrombo-cytopenia
- Decreased number and
function of WBCs
- Cannot fight
infection
- Older adults die
from infection
- Leukemic cells cause
- Splenomegaly
- Hepatomegaly
- Lymphadenopathy
- Bone pain
- Meningeal irritation
- Oral lesions
- Solid masses (chloromas)
DIAGNOSTIC STUDIES
- To diagnose and classify
- Peripheral blood evaluation
- Bone marrow elevation
- Morphological,
histochemical,
immunological, and
cytogenetic methods are
all used to identify cell
subtypes, stage of
development, and
-
-
significant genetic mutations
- That’s how you know for sure
- Bone marrow transplant
- CT and Lumbar Punctures are used to determine presence of leukemia cells
outside of the blood and the bone marrow
Collaborative care
- Goal is to attain remission
- Prognosis is directly related to ability to maintain a remission
- Complete remission: no evidence of overt disease on physical exams, bone
marrow/peripheral blood smear are normal
- Partial remission: lack of symptoms + normal blood smear but bone marrow has
disease
- Minimal residual disease: tumours cells that cannot be detected by morphological
examination but can be detected during molecular testing
- Molecular remission: all molecular studies are negative for residual leukemia
- Different types of chemotherapy alongside multiple medications are usually used
- Induction therapy: aggressive chemo to destroy leukemic cells everywhere
- Intensification therapy: high dose therapy immediately after induction for several
months
- Consolidation therapy: after remission is achieved, one or two additional courses
- Maintenance therapy: lowe doses every 3-4 weeks for prolonged period of time
- Corticosteroids and radiation can be used, HSCT
- Emotional support for family and patient
- Education
- Important nursing interventions
- Maximizing the patient’s physical function
- Teaching patients that acute adverse effects of treatment are usually temp.
- Encouraging patients to discuss their quality-of-life issues
- Advocate and educate
Hematopoietic Stem Cell Transplant
- Goal
- Totally eliminate leukemic cells using combinations of chemotherapy
with/without total body irradiation
- Eradicates client’s hematopoietic stem cells
Blood Transfusions
Blood Transfusions
- The transfusion of blood and blood components restores and maintains quality of life for patients
with hematological disorders, cancer, injury or surgical intervention
- Increases oxygen carrying capacity
- Must know the complexities of the ABO and Rh system
- Very important to get the right type of blood
- (+, -) antigen, negative cannot get positive
-
Most know numerous components of blood that can be transfused and the serious negative
outcomes that can occur
Principles for Practices
- Intravenous (IV) administration
- Whole blood (traditionally what blood transfusion referred to)
- Blood components
- Plasma-derived product
- Allogeneic transfusion or autotransfusion
- Sometimes patients will give blood leading up to surgery and then are able to just have their own
blood if needed
Blood Values
- Hemoglobin
- Protein in red blood cells
- Normal: Male: 140-180 b/L
- Female: 120-160 g/L
- Hematocrit
- Percentage of red blood cells
in your body
- Normal 37-54%
ABO System
- Uses the presence or absence of
specific antigens on the surface
of red blood cells
- A antigen = type A
- B antigen = type B
- A and B antigen = type
AB
- No antigen = type O
Person-Centered Care
- Consider a patient’s values and
cultural beliefs about blood
therapy
- Allay patient anxieties when
possible
- Some religions do not allow
blood transfusions
- Parents have primary obligation to make decisions for minor children
- Prevent transfusion-related complications
-
Type and screen before
Have to stay for the first 15 minutes to ensure there are no severe reactions
Start slow then speed up
Only primary can be normal saline
18 or 20G needle to ensure you do not break the blood cells
SAFETY ALERT
- Dextrose solutions or lactate ringer’s solution must not be used for administering blood
because the will cause RBC hemolysis
- Additives (including medications) must not be given via the same tubing as the blood
unless the tubing is first cleared with saline solution
Acute Transfusion Reactions
- Range from mild to severe (most minor)
- Usually develop in the initial 15 minutes of the transfusion (or 50mL)
- Take vitals before and at 15 minutes (or 50mL)
- Every 30 minutes and then an hour after transfusion is done
- Includes
- Acute hemolytic reaction
- ABO-incompatible blood
- Antibodies in the recipient’s plasma attach to antigens on transfused
RBCs, causing RBC destruction
- Leads to AKI, DIC and death
- Usually develop within 15 minutes
- Mild or severe
- Improper product-to-patient identification causes 90% of hemolytic
transfusion reactions
- Clinical Manifestations
- Fever (w or w/o chills), low back/abdo/chest/flank pain, flushing,
tachycardia, dyspnea, tachypnea, hypotension, vascular collapse,
hemoglobinuria, acute jaundice, dark urine, bleeding
-
-
-
-
-
-
-
Management
- Treat shock and DIC
- Draw blood samples + urine
- Maintain BP with IV colloid solutions and give diuretics to monitor
hourly output
- Dialysis may be required if renal failure
- Do not transfuse until blood bank has provided newly cross-matched
units
Febrile nonhemolytic reaction (most common)
- Can be delayed
- Sensitization to donor WBCs, platelets, or plasma proteins
- Clinical Manifestations
- Sudden chills and fever (rise in temperature of >1℃), headache,
flushing, anxiety, vomiting
- Treatment: give antipyretics and do not transfuse unless doctor orders
Mild allergic reaction
- Sensitivity to foreign plasma proteins (common in people with allergies)
- Flushing, itching, pruritus, urticaria (hives)
- Treatment: antihistamines, corticosteroid, epinephrine, transfusion may be
continued, observe for fever or pulmonary symptoms
severe allergic reaction
- Sensitivity to plasma proteins or IgA proteins in blood product and recipient has
IgA antibodies
- Clinical manifestations
- Anxiety, urticaria, dyspnea, wheezing, progressing to cyanosis,
bronchospasm, hypotension, shock, and possible cardiac arrest
- Treatment: CPR if cardiac arrest, administer O2, epinephrine injection,
antihistamines, corticosteroids, B2-agonists, DO NOT RESTART
TRANSFUSION
Circulatory overload reaction
- Fluid administered faster than the circulation can accommodate
- Risk factor is people with cardiac or renal disease
- Clinical manifestations: cough, dyspnea, pulmonary congestion, adventitious
breath sounds, headache, hypertension, tachycardia, distended neck veins
- Treatment: upright position with feet in dependent position, chest x-ray stat,
administer prescribed diuretics, O2 and/or morphine
Sepsis reaction
- Transfusion of bacterially infected blood components
- Clinical manifestations: rapid onset of chills, high fever, vomiting, diarrhea,
marked hypotension or shock
- Management: cultures from patient blood and bag then send bag back to bank,
treat septicemia as directed (IV fluid, antibiotics, vasopressors)
TRALI (transfusion reaction of acute lung injury)
-
-
Reaction between transfused anti leukocyte antibodies and recipient’s leukocytes,
causing pulmonary inflammation and capillary leak
- Clinical manifestations: fever, chills, hypotension, tachypnea, frothy sputum,
dyspnea, hypoxemia, respiratory failure, noncardiogenic pulmonary edema,
leading cause of transfusion related deaths
- 1-6 hours of transfusion
- Management: draw blood, chest x-ray stat, O2, corticosteroids, CPR and
ventilation as needed
- Massive Blood Transfusion Reaction
- Replacement of 10 units or more within 24 hours that do not contain clotting
factors, albumin, and platelets
- Clinical manifestations: hypothermia, cardiac dysrhythmias, citrate toxicity,
hypocalcemia, hyperkalemia
- Management: monitor clotting and electrolyte levels
- ABO compatibility is not a prereq for platelet transfusion however after multiple platelet
transfusions a patient may develop anti-HLA antibodies to transfused platelets so the use
of lymphocyte typing to match HLA types of the donor and recipient are required for
multiple transfusion patients and patients with hx of platelet transfusions may be
premedicated with an antihistamine and hydrocortisone to decrease the possibility of
reaction
What to do if reaction occurs:
- Stop transfusion → maintain a patient IV line with saline → notif blood bank and HCP
→ recheck identifying tags/numbers → monitor vital signs and urine output → treat
symptoms per HCP order → save and return blood bag and tubing to the blood bank for
examination → collect blood and urine samples at intervals as per policy → document
Evidence-Informed Practice
- Acute hemolytic transfusion reaction is the leading cause of transfusion-related death
(TRALI in the new textbook apparently has surpassed and is now the leading cause of
transfusion-related death pg. 744); 80% are related to error with ABO incompatibility
- Advances in technology help to decrease errors
-
Bar-code technology
International standard for labeling of blood components
Radiofrequency transponder microchips
Advanced laboratory screening procedures
Blood alternatives
Lecture 4 - January 30th
Chronic Neurological Conditions
Chronic Neurological Conditions
- Neurological disorders involve the central and/or peripheral nervous system
- This can include the brain, spinal cord, cranial nerves, peripheral nerves, nerve roots, autonomic
nervous system, neuromuscular junctions, and muscles
- Chronic diseases, also known as noncommunicable diseases (NCDs), are diseases that are often
persistent, are generally slow in progression, and can be treated but not cured (Public Health
Agency of Canada), we need to find ways to help patients manage
- Multiple sclerosis
- Parkinson disease
- Seizures
- Gullian-barré syndrome
- Bell’s Palsy
- Trigeminal neuralgia
Multiple Sclerosis
-
Chronic, progressive, degenerative autoimmune disorder of the central nervous system (CNS)
Characterized by disseminated demyelination of nerve fibers of the brain (axon sheath becomes
damaged), spinal cord, and the optic nerves
Autoimmune process driven by activation of T cells
The disease usually affects those between 20 and 50 years of age
Average onset is 30-35 years of age
Women are affected more than men
MS has relatively high prevalence rates in regions with temperate climates, this includes large
parts of Europe, Canada and the northern United States
Canada has one of the highest prevalence rates of MS in the world
- 77,000 Canadians are diagnosed with MS and 75% are women (2019)
- May have genetic component but unsure
- Screen ahead of time treat early and early identification
Cause
- The cause of MS is unknown
- Theory is that MS develops in a genetically susceptible person following an environmental
exposure
- Gene + exposure = MS
- Precipitating factors include
- Infection (COVID, RSV)
- Smoking
- Physical injury
- Emotional stress
- Excessive fatigue
- Pregnancy
3 Phases
1. Chronic inflammation
- An unknown trigger activates T cells to attack the
neurons, often in the brain barrier
- The body attacking itself (autoimmune)
- Immune system goes on overdrive, sees
sheath as foreign
- CNS activates an inflammatory responses
2. Demyelination
- Neurons in the brain and spinal cord are
attacked by the immune system
- Myelin sheath is damaged, exposing the nerve
axon, which then becomes disrupted
- Impulses are disrupted, going in or out
- MS likes to attack the optic nerves
3. Gliosis in CNS
- The damaged myelin is replaced by a glial scar
tissue which then forms into hard plaques
- This disrupts nerve conduction; occurs in
multiple parts of the brain
- As more and more nerves become damaged
- As it grew it cannot differentiate or
specialized so it becomes lesions
Clinical Manifestations
- The onset is slow and progressive
- Many patients experience periods of
remission and exacerbation
- The overall trend is progression
- After exacerbations patient cannot
go back to baseline, residual
symptoms
- Common signs
- Motor: weakness, fatigue
- Sensory: blurred vision, numbness,
tingling, patchy blindness, vertigo,
tinnitus, decreased hearing, neuropathic pain
-
-
Cerebellar: nystagmus (involuntary eye movement), dysarthria (slurred speech, scanning
speech), spastic (uninhibited) bladder or faccid (hypotonic) bladder,
Emotional: liability (euphoria or depression)
- Mood swings, not as acute as a person with bipolar
Lose proprioception: Cannot sense or calculate next step
Loss of ADL independence over time
Ataxia movement, trouble walking
Lhermitte sign: transient sensory symptom described as an electric shock radiating down
the spine or into the limbs with flexion of the neck
Assessment
- Patient’s history and presenting symptoms
- There is remission and exacerbation
- Weight loss, dysphagia (difficulty swallowing)
- Muscle weakness or fatigue, tingling or numbness
- Comes and stays for long periods, gets worse progressively
- Blurred or lost vision, diplopia (double vision)
- Vertigo, tinnitus
- Changes in libido, sexual functioning
- Emotional changes: mood swings
- Physical assessment
- Scanning speech and/or dysarthria (slurred speech)
- Looking for word but cannot find it
- Tremors and/or hyperactive reflexes
- Nystagmus (involuntary eye movement)
- Decreased hearing
- Paresis (muscular weakness) and/or paralysis
- Ataxia (impaired coordination), foot dragging
Diagnostic Testing
- Based primarily on history (how long, how often), clinical manifestations, and presence of
multiple lesions over time measured by MRI
- 1) Need to have two (2) demyelinating lesions in two different locations in the brain
- 2) Damage or attacks at different times
- 35-40 years of age
- Susceptible people will see it easier
- Need to rule out other diseases
- 3) all other possible diagnoses ruled out
- Laboratory tests can be used as an adjunct to a clinical
examination
- Lumbar puncture
- Increased in oligoclonal immunoglobulin G (IgG)
- Presence of oligoclonal banding = inflammation in SC
Treatment
- No cure currently exists
- Medication therapy
- Corticosteroids: reduce inflammation (high doses, decreased immune system, susceptible
to infection and hyperglycemia)
- Immunomodulators: modifies your immune systems response to disease
- Tries to tell immune system that we like the myelin sheaths
- Used to reduce exacerbations and slow progression of the disease
- Interferon 1b (betaseron), Interferon 1a (Avonex), Glatiramaer acetate
(Copaxone)
- Anticholinergics: act on the neurotransmitter acetylcholine, prevent impulses from
reaching smooth muscle, reduce cramps/spasms (antispasmodic properties)
- Helps with mobility of smooth muscles
- Muscle relaxants (Baclofen?)
- Help skeletal muscles
- Side effects: sedation
- Other medication to treat symptoms - meds for vertigo, depression, pain …
- Cholinergics
- Acetylcholinesterase inhibitor
- Sphing-1-Phosphate Receptor Modulator
- Therapies to target/manage symptoms
- Physical therapy
- To help prolong ADL independence
- Exercises to maintain mobility, balance and strengthen (mobility and grip)
- Use of adaptive devices: cane, walker
- remission/exacerbations and progression
-
Stem cell therapy
- Research is examining the cells ability to reduces brain inflammation
- Can we get them into the brain and will that help stop the T-cells to prevent/stop
attacking myelin sheaths
- Nutrition
- Well balanced diet
- Reduce sodium
- Risk of tinnitus
- Will help hearing, sense of proprioception, reduce risk factors of muscles due to
increase/decrease potassium = irritability of muscle contraction, it is the same
with sodium and neurons, reduced firing a capacity of neurons (sodium) which is
what we want
- Causes you to hold onto more fluid
Patient Teaching
- No cure, focus is on symptom management
- Take medications as prescribed
- Teach the importance of building general resistance to illness
- Avoiding fatigue, extremes of hot and cold, exposure to infection
- Good balance of exercise and rest
- Don’t overdue to exhaustion
- Minimize caffeine intake and nutritious well-balanced meals
- Abdominal problems increased overtime and during exacerbations
- Teach adequate intake of fiber to aid in regular bowel habits
- Paralytic ileus is what MS causes
- Foods: greens veggies, whole grains, oats
- Teach self-catheterization if necessary
- Late stages
- Encourage and provide referrals for counseling as needed
- Connect to support groups
- Home safety: handrails, no loose rugs, reduce stairs
Parkinson’s Disease
-
-
Parkinson’s disease is a slow progressive degenerative disorder of the central nervous system
(CNS)
- Dopamine is not being produced and levels drop
- The start and stop mechanism or impulses
- “Shaking palsy”
Characterized by delayed initiation and execution of movement (bradykinesia), muscle rigidity,
tremors at rest and impaired gait
Others signs include pill rolling of fingers, mask like facies (no facial expressions due to lack of
ability to move facial muscles), muscle rigidity, tremors at rest and impaired gait
No known cause and no cure currently
We have significant rates in Canada but not as much as MS
2013-2014 data per Public Health Agency of Canada
-
-
Approximately 84,000 Canadians aged 40 years and older were living with diagnosed
parkinsonism (prevalence 0.4%)
10,000 Candians were newly diagnosed with this condition (incidence: 55.1 per 100,000
population)
Pathological process of PD involves degeneration of dopamine
(DA)-producing neurons in the substantia nigra of the midbrain
- PD is cognitive deterioration characterized by Lewy bodies in the
substantia nigra
- DA is a neurotransmitter essential for the motor system, including
control of posture, support, and voluntary motion and contributes to
feelings of motivation and reward (leads to depression)
- Disrupts dopamine-acetylcholine balance in basal ganglia
- PD patient’s often have a decrease in dopamine that allows acetylcholine to take over
(acetylcholine starts, dopamine stops, without dopamine acetylcholine has no stopper)
- When this occurs, muscles become too “excited,” which leads to symptoms such as jerking
movements and tremors
- Symptoms of PD do not occur until 80% of neurons in the
substantia nigra are lost
- Very difficult to treat because isn’t noticed early
- The onset of PD is gradual, with ongoing progression
Four Cardinal Signs of PD
1. Tremor
- Often the first sign
- Beginning stages may involve only a mild tremor,
slight limp, or decreased arm swing (hard to
notice)
- Becomes more prominent at rest and is aggravated
by emotional stress or increased concentration
-
Described as “pill rolling” because the thumb and forefinger appear to move in rotary
fashion
- Later stages may have shuffling, propulsive gait with arms flexed and loss of postural
reflexes
- Lean forward and shuffle, jerky movements
2. Rigidity
- Increased resistance to passive motion when limbs are moved through range of motion
(ROM, poor ROM)
- Rigidity is typified by a jerky quality (cogwheel rigidity) when the joint is moved
- Caused by sustained muscle contraction and results in the following
- Muscle soreness
- Feeling tired and achy
- Pain in the upper body, spine, or legs
3. Bradykinesia
- Evident in slowing of autonomic movements
- Slowing down of blinking (eyes dry), swinging of arms while walking
- Difficulty swallowing of saliva = drooling (aspiration risk)
- Decreased self-expression with facial movement (impaired communication)
- Minor movements of postural adjustment lessened
- Can advance to AKINESIA: absence or loss of control of voluntary muscle movements
4. Postural instability
- Propulsion or retropulsion with gait
- Mobility issues
Assessment
- There is no definitive test for Parkinson’s
- Health history
- CNS trauma (concussion,
- Cerebrovascular disorders (
- Exposure to metals and carbon monoxide (
- Encephalitis (infection, West Nile Virus)
- Medications (is it a drug [EPS] or is it parkinsons)
- Tranquilizers (haloperidol [Haldol] and phenothiazines)
- Methyldopa
- Amphetamines
- Physical Assessment
- Examine ability to smile, make facial
expressions (blank faces, infrequent
blinking)
- Examine range of motion: tremors, poor
coordination, impaired gait
- Assess vital signs: looking for postural
hypotension (orthostatic hypotension
assessment)
- Difficulty with chewing, swallowing and/or drooling
- Look for “Pill rolling” behaviours (rolling thumb and finger movements)
- Subtle signs of dementia as disease worsens
- Diagnostic Tests
- No specific tests
- Diagnosis is based solely on history and clinical features, and if the patient responds to
antiparkinsonian medications (levodopa or dopamine agonist)
- Clinical diagnosis requires presence of TRAP
- Tremor
- Rigidity
- Akinesia (bradykinesia)
- Postural instability
Treatment
- Medications therapy
- Dopaminergics:
- Levodopa with carbidopa (Sinemet) is often the first medication used
- Precursor of DA and crosses blood-brain barrier
- Converted to DA in the basal ganglia
- Carbidopa inhibits an enzyme that breaks down levodopa before it
reaches the brain
- Medication alert: monitor for signs of dyskinesia, short-term adverse
effects of nausea, vomiting and light-headness, stress that effects may be
delayed for weeks to months, educate about the importance of reporting
any uncontrolled movement of face, eyelids, mouth, tongue, arms, hands,
or legs, mental changes, palpitations and difficulty urinating, DO NOT
GIVE WITH FOOD as protein reduces absorption
- For bradykinesia, tremor, rigidity
- Antiviral agent (amantadine): exact mechanism is unknown (but we know it works)
- Reduces tremors, bradykinesia, rigidity
- Anticholinergics are also used in management (Benztropine)
- Decreases activity of acetylcholine
- For tremors
- Antihistamines with anticholinergic or B-adrenergic blockers are used to manage tremors
(Diphenhydramine - Benadryl) and rigidity
- Monoamine Oxidase Inhibitor
- Bradykinesia, rigidity, tremor
- Catechol-O-Methyltransferase (COMT) inhibitor (slows breakdown of levodopa thus
prolonging the action of levodopa)
- Surgical therapy
- Comorbidities are taken into account
- Ablation surgery
- Stereotactic thalamotomy works by destroying part of the thalamus (relay system
to the brain) to block the abnormal brain activity from reaching the muscles and
causing tremors
-
-
- Brain surgeon consciously sedated the patient and
- Goal: bring the tremoring down
- Deep brain stimulation (DBS)
- Involves placing an electrode in the thalamus, globus pallidus, or subthalamic
nucleus
- Connected to a generator placed in the upper chest (like pacemaker)
- The device is programed to delivery specific current to a targeted brain location
which can then block impulses that lead to tremors
- If there is a part of the brain that is over firing it sends shock to that part
- Transplantation of fetal neural tissue into the basal ganglia provides dopamine-producing
cells in the brains of patients
- Fetal neural tissue is by donation
- Earlier research was largely abandoned after mixed results but the recent
improvements in transplant techniques have renewed interest in this as a potential
option
- Try to grow tissue to increase dopamine tissue
- Nursing will be responsible for post operative care with a focus on neurological
assessment and functioning
- Pupil, cranial nerves, sensory and motor function, LOC (GCS)
Nutritional therapy
- Aspiration precautions
- Food should be cut into bite-sized pieces
- Place patient in high fowler’s positions
- Evaluate the use of straws (thickened liquids)
- Keep upright for 30-45 minutes post meal
- Several small meals should be taken to prevent fatigue
- Patients can burn a lot of calories while eating
- Provide ample time to avoid frustration
- Suction equipment present (safety)
- In case of aspiration or choking
Physical therapy
- Goal: maintain mobility
Occupational therapy
- Goal: ability to complete ADLs
Speech therapy (keep muscles strong)
- Dysphagia (difficulty with swallowing) is common with PD as it progresses
Monitor for signs of depression
Connect to support groups
Safety in the home environment: reduce fall risk
- Get out of a chair by using arms and placing the back legs on small blocks
- Remove rugs and excess furniture
- Simplify clothing by wearing clothing without buttons and hooks
- Use elevated toilet seats and handrails in shower
- Push up with hands
Complications
- As disease progresses, complications can increased
- Neurological conditions
- Urinary retention: assess for bladder function (may need catheter)
- Constipation: diet high in fruits and fibers
- Neuropsychiatric conditions: memory changes, depression, dementia
- Encourage cognitive exercises to maintain brain activity as possible
- If caught early you want to keep brain active, learning and use
Seizure Disorders
-
Seizures disorders are a group of neurological diseases marked by recurring seizures
Seizure: a hyperexcitation of neurons in the brain leading to abnormal electrical activity that
causes sudden violent involuntary series of contraction of muscle groups
- Epilepsy: is a type of seizure disorder in which at least 2 spontaneous seizures occur more than 24
hours apart (unrelated to trauma or other conditions/complications)
- Affects approximately 0.06% of Canadians
Etiology
- Seizures are often symptoms of an underlying condition
- In adults the most common reason are structural lesions (growth; malignant or benign) and/or
injury (car accidents)
- Trauma, brain tumors or vascular disease (stroke)
- Metabolic disturbances can also cause seizures to occur
- Acidosis and electrolyte disturbances (sodium)
- hypOglycemia
- Hypoxia
- Alcohol and/or barbiturate withdrawal
- Heart disease, liver or kidney failure and lupus can also result in seizures
Pathophysiology
- A seizure disorder is characterized by abnormal neurons that undergoing spontaneous firing
- Multiple stimuli can trigger the firing sequence which then can spread along neural pathways
within the brain
- If activity involves the whole brain, generalized seizure occurs
- If the firing remains in a limited or focal area = localized seizure
- Astrocytes are now believed to play a key role in recurring seizures (send nutrients and remove
waste from neurons, connect blood vessels to neurons)
- Astrocytes release glutamate (need for impulse) which triggers synchronous firing of
neurons
- Possible that over stimulation or lower threshold triggering in occuring
- Research: indicating the presence of abnormal receptor antibodies in cerebrospinal fluid
- Emerging concept of autoimmune disorder
Diagnostic Studies
- Review the patient’s health history
- CNS trauma, tumors, metabolic disorders
- Alcoholism, exposure to metals or carbon monoxide
- Hepatic or renal failure (imbalance of electrolytes)
- An electroencephalogram (EEG) is a test that measures electrical activity in the brain using small,
metal discs (electrodes) attached to the scalp
- Difficult to catch the abnormal activity in progress
- Would need seizure to happen during testing
- Computerized tomography (CT) scan
- Magnetic resonance imaging (MRI)
- Any physical/structural features
Types of Seizures (we need to know for the exam)
- General onset
- Tonic-clonic seizures
- Focal onset
- Focal aware seizures
- Focal impaired awareness seizures
Focal Onset Seizures
- Focal Aware
- Simple motor or sensory phenomena with elementary symptoms with NO loss of
consciousness
- Often last less than 1 minute
- Weakness, numbness, tingling sensations (afterwards)
- Only a small area of the brain is over-firing
- Can still see HCP (you) and can turn toward person talking, they have awareness of
environment and can react to stimuli
- Focal Impaired Seizures
- Patients have a loss of consciousness or are in a dream-like state (cannot interact)
- LOC is effected
- Eyes are open but cannot follow commands or interact with others
- Can last 1-2 minutes, patients are left confused and tired
- May experience muscle stiffening or jerking motion the extremities, lip smacking
(repetitive behaviours)
- May or may not have an emotional component (fear, strange feelings) when seizure is
finished
Generalized Onset Seizures
- Whole brain is involved/affected, may or may not be a warning
- Characterized by bilateral synchronous epileptic discharges in the brain
- In most cases the patient will lose consciousness somewhere between a few seconds to several
minutes
- Most common generalized seizure is Tonic-Clonic (used to be grand mal)
Clinical Manifestations
- The process of a seizure can go through several phases
- Most common with generalized seizures
1. Prodrome: signs or activities that provoke a seizure (i.e., flashing lights)
2. Aural phase: sensory warning about an impending seizure (headache, visual - light)
3. Ictal phase: seizure activity
4. Postictal phase: period of recovery following the seizure (drowsiness to decreased LOC)
Tonic Clonic Seizures
- Are characterized by the body stiffening (tonic) for 10-20 seconds and then the extremities for
30-40 seconds, the process then repeats
- Can also see poor respiratory effort (cyanosis, become hypoxic, using a lot of O2), excessive
salivation (aspiration) or cheek biting (injury) and incontinence (over-firing causes smooth
muscle to release)
- Patient cannot breathe well
-
In the postictal phase (recovery)
- Patient will have muscle soreness
- Fatigue and may sleep for several hours
- May not feel well for several hours to several days
- Patient may have no memory of the event
-
Acute interventions: observation and treatment of seizure
- Maintain patient airway, support head, turn the patient to their side (prevents aspiration),
loosen constrictive clothing, ease to floor
-
Don’t retrain the patient (fight or flight will be activated making patient worse)
Don’t put anything in patient’s mouth (even to support airway)
Stay with patient at all times (cannot leave or delegate)
Establish an IV access (if possible, hopefully already have IV)
Anticipate administration of benzodiazepine or phenytoin to control/stop seizure (must
be IV)
- Apply oxygen as needed
- Have suction equipment present (you can suction without going into mouth)
- Put patient in side-lying position to avoid possible aspiration if the patient vomits
- Protect the patient’s head
- Care immediately following the seizure
- Assess heart rate/rhythm and depth of respirations (1st priority)
- SPO2 saturation
- Assess neurological status: cognition, ability to follow commands
- Do not assess pupils because the light could trigger more seizures
- Ask things like “can you hear me” “squeeze my hand”
- Glasgow coma scale
- Assess skin for signs of injury
- Look in mouth for signs of cheek to tongue biting
- Close observation (patient will need rest) in a quiet environment
- May need to draw lab (blood work) to evaluate medication levels (ex. Phenytoin levels),
electrolytes
- Documentation: the nurse should carefully observe and record details of the event
because the diagnosis and subsequent treatment often rest solely on the seizure
description
- Time, physical movement, triggers, postictal responses
- The patient cannot tell you what happened
- Ongoing monitoring
- Vital signs (stability)
- Level of consciousness (LOC, GCS)
- Oxygen saturations
- IV fluid (dextrose if hypoglycemic)
- Reassure and orient patient as needed
- LAMP (look at me please)
Treatment
- Medical therapy
- Aimed at prevention
- Stabilize nerve cell membranes and prevent spread of epileptic discharge
- 70% of patients are controlled with medication
- Monitor medication serum levels
- Caution patients that they should not take alcohol or any other CNS depressants
- Phenytoin (Dilantin)
- Limits seizures by altering ion transport, decrease synaptic transmission
- Monitor for development of rash, occurs within the first two weeks
-
- May tolerate at first
- Monitor for behavioural changes, worsening or development of suicidal thoughts
- Monitor mental status: sedation
- Medications
- Carbamazepine (Tegretol): decreases synaptic nerve transmission, affecting
sodium channels
- Monitor for behavioural changes: worsening of suicidal thoughts
- Monitor CBC: overtime increased risk of bone marrow depression
- Increased risk for infection
- Monitor ionized calcium levels and thyroid function
- Phenobarbital: anticonvulsant, causes CNS depression and inhibits neural
transmission
- More complications with sedation
- Monitor respiratory status, pulse and BP
- Monitor for sedation
Surgical Options
- Patients whose epilepsy cannot be managed by medications, who meet stringent
requirements may be offered a surgical option
- Focal impaired awareness seizures: reaction of epileptogenic tissue (take a section of
tissue out)
- Generalized seizures: sectioning of the corpus
callosum (CC function is to allow R to L
communication)
- Bundle of nerve fibers in the longitudinal
fissure of the brain that enables
corresponding regions of the left and right
cerebral hemispheres to communicate
- Limits firing to one side
- Vagal nerve stimulation: an electrode is placed in the vagal
nerve and when the patient's sense that a seizure is imminent,
they activate the device
- The device delivers electrical stimuli to the vagal nerve,
increasing blood flow and neurotransmitters to the
hyperresponsive area, decreasing the patterns and
reducing seizure activity
- Responsive neurostimulation (RNS): similar to cardiac pacemaker and continually
monitors the EEG to detect abnormalities and responds to seizure activity by delivering
electrical stimulation to a precise stimulation, placed under skin outside skull with
electrodes over the area of seizure focus
- Alternative Treatments
- Ketogenic diet: special high fat, low carbohydrate diet help control seizures in some
patients
- Uses ketones as an energy source (as carbs could potentially trigger seizures)
- Long term effects not clear
-
Biofeedback: involves attaching sensors to the patient’s skin to monitor for signs of a
seizure
- To help the patient to learn what their triggers are and to maintain a brain wave
pattern that is refractory to seizure activity
Complications
- Status epilepticus: a state of continuous seizure activity, neurological emergency
- Causes the brain to use more energy than is supplied
- Then they stop working
- 5 minutes MAX
- Neurons become exhausted and cease to function
- Permanent brain damage can result, then death
- Emergency care
- Maintain patent airway, support head, turn patient to their side
- Loosen constrictive clothing
- Ease to floor and/or remove side rails if not padded
- Don’t restrain the patient
- Don’t put anything into the patient’s mouth
- Apply oxygen (mask, all the way up)
- Ensure suction present
- Establish IV access and prepare to administer benzodiazepines or phenytoin IVP
- Notify healthcare provider
Patient Teaching
- Home care
- Instruct patient on importance of adherence to medication, not to adjust dose without
consulting healthcare provider
- Need to take meds as prescribed
- Keep regular appointments
- Teach family members emergency management
- Emotional support and identification of coping mechanisms
- Medical alert bracelets/necklaces and ID card
- Referrals to agencies and organizations
- Health promotion
- Wear helmet if risk for head injury
- Promote good general health habits (diet, exercise)
- Assist patient in identifying events or situations precipitating seizures and to avoid them
if possible
- Instruct patient to avoid alcohol intake and minimize fatigue
- Promote a sleep-activity balance
Cranial and Peripheral Nerve Conditions
Cranial Nerves
- 12 pairs of nerves that emerge through the various opening in the skull
- Originate in the base of the brain
-
-
Carry impulses for smell, vision, ocular
movement, pupil contraction, muscular sensibility,
mastication, facial expression, hearing
Causes of cranial nerve problems include:
- Tumors, inflammatory processes, trauma,
infection, idiopathic conditions
Trigeminal Neuralgia
-
Neurological condition of the trigeminal facial
nerve (V) caused by degeneration or pressure on
the nerve (inflammation, infection and trauma)
- Characterized by stabbing like pain along the
nerve branches which recurs in clusters (2hr
window, then stops and starts again) lasting from
several seconds to several minutes
- Around the eyes and over the forehead
- Upper lip, nose, cheek
- Side of tongue, lower lip and jaw
- Triggers for nerve stimuli can include: chewing, teeth
purple, cold air, face washing and yawning
- Diagnosis: bilateral face pain, MRI, neurological
assessment, electromyography (EMG)
Treatment
- Medication therapy
- 1st line: carbamazepine (Tegretol): is an
anticonvulsant medication used primarily in the treatment of epilepsy and neuropathic
pain
- Can cause bone marrow suppression so CBC need to be routine
- 2nd line: baclofen (Lioresal): muscle relaxant
- 3rd line: gabapentin (Neurontin) and pregabalin (Lyrica): is used to treat neuropathic
pain (nerve pain) by blocking pain messages from reaching the brain
- Conservative Therapy
- Local anesthetics
- Biofeedback
- Surgery
- Percutaneous radiofrequency rhizotomy: ablate the nerve
- Minimal motor and sensory deficit
- Nursing post-op care
- Routine post op care (PACU)
- Ice pack to operative site for 3-5 hours (inflammatory
response will trigger pain)
- Do not chew on operative side until sensation has
returned (side of face would be numbed)
-
Keep environmental stimuli to minimum for a few weeks (same NSG Tx as
below)
Nursing Care
- Pain relief: drug therapy
- Non pharmacological pain management: biofeedback
- Ways to manage nutrition: high protein, soft foods
- Ways to manage hygiene: lukewarm water, warm mouth rinse (to prevent triggers)
- Ways to manage oral care: soft toothbrush, warm mouth rinse
- Alternate communication during acute episodes (talking
will use muscles thus cause pain, so iPad, texting/typing
and whiteboard can be used)
- Apply artificial tears to eyes (blinking sensation will be
decreased)
Bell’s Palsy
-
Is unilateral paralysis of the facial nerve (VII)
Possible causes include trauma, compression or infection (herpes
simplex virus) of the nerve
- Any or all the branches may be impacted
- Usually resolves over weeks although some can leave permanent
damage
- Cause unknown but may be linked to immune, infective, and ischemic
mechanisms, reactivation of herpes simplex virus
Clinical Manifestations
- Onset is often acute, affecting the muscles of the upper and lower face
- Facial drooping, inability to close eyelid, inability to frown or smile,
loss or excessive tearing
- Diagnosis is based on clinical manifestations, CT/MRI used to rule out
other diseases
Treatment and NSG Care
- Corticosteroids (prednisone) given for 2-3 weeks
- Analgesic for pain management (mild)
- If herpes simplex virus, antivirals, acyclovir for 5-10 days
- Hot wet packs (opposite of trigeminal neuralgia)
- Chew on unaffected side
- Artificial tears and sunglasses (protect dropping eyes, cannot close so cannot protect from sun)
- Therapeutic communication for change in appearance
- Oral care, straw for drinking, mastication techniques
Guillain Barre Syndrome (GBS)
-
Acute rapidly progressing and potentially fatal form of polyneuritis
This syndrome impacts the peripheral nervous system
The etiology is unknown but research supports an autoimmune response following an infection
-
Potential pathogens include
- Campylobacter jejuni: common cause of intestinal infection i.e., food poisoning
- Cytomegalovirus: related to herpes virus, mild fever, swollen glands, muscle aches
- Epstein Barr virus: infectious mononucleosis
- Varicella zoster virus: herpes virus family, chicken pox or in adults reactivation =
shingles
Pathophysiology
- Acute inflammatory demyelinating
polyneuropathy is the most common
type
- Phase 1: due to a trigger or exposure
the immune system goes into
overdrive and T lymphocytes, which targeted the original infection, begin to attack the myelin
sheath surrounding peripheral nerves
- Results in demyelination, edema and inflammation of the nerves themselves
- Manifests as symmetrical ascending paralysis (ground to brain)
- Phase 2: as the demyelination occurs neural impulses are slowed down and/or stopped
- Muscles that are innervated by the PNS will atrophy and are unable to function properly
- Phase 3: in the recovery phase, the nerves will remyelinate slowly, which will allow a very slow
return to function
- Functionality returns in a proximal to distal pattern (from brain to ground)
Clinical Manifestations
-
GBS symptoms can range from mild to severe
Characterized by
- Symmetrical muscle weakness, feet to legs to abdomen to
chest
- Mild distal sensory paresthesia
- Loss of deep tendon reflexes
- Pain: neurologic, paresthesia (prickling) burning, stabbing
- Worse at night
-
Weakness can progress to complete paralysis in the worst cases
As the nerves become demyelinated both the sympathetic and parasympathetic systems are
impacted
- Severe dysfunction can include fluctuating blood pressure, cardiac arrhythmias, gastrointestinal
stasis (incontinence), urinary retention and pupillary changes (won’t respond to light, cannot
contract
- Can also progress to the lower brainstem, impacting cranial nerves
- Signs: facial weakness, difficulty with eye movements, dysphagia (cannot swallow) and
paresthesia (pin and needle sensations) of the face
Diagnostic Studies
- Diagnosis based on patient’s history and clinical signs
- Lumbar puncture: assess protein levels, 7-10 days will be elevated
- EMG and nerve conduction studies: to assess the health of muscles and the nerve cells that
control them (motor neurons)
Assessment
- Acute phase
- Assessing for muscle weakness and ability to sense
- Respiratory function
- (decreased) ability to speak and swallow
- Vital signs (unstable)
- Corneal reflexes
- Pain
- Frequent assessment at the demyelination process moves up the body
- A: airway, B: breathing, C: circulation
- As it moves up we worry about respiratory function (respiratory failure)
Treatment
- Is primarily supportive
- Oxygen: intubation and mechanical ventilator as needed
- Prevention of DVTs: low molecular weight heparin, stocking, repositioning
- IV fluid: keep the patient hydrated
- Nutritional
- Aspiration precautions in patients with mild dysphagia
- Feeding tubes and/or TPN infusion: patient with facial paralysis or who are intubated
- Pain management: medications that address neuropathic pain
- Bowel and bladder management: catheterization
- Physiotherapy: range of motion, attention to body position
- If facial paralysis: artificial tears
- Skin care: hygiene, prevent pressure injuries
- Monitor for secondary infection: respiratory (nosocomial)
- Occupational and speech therapies
- Alternative form of communication: speech boards
- Clinical guidelines support
1. Use of IV immunoglobulins (IVIG): within 2 weeks diagnosis
- Used to treat antibody deficiencies due to inflammatory responses
-
The IVIG infusions are derived from thousands of healthy blood plasma
donations
2. Plasmapheresis a method of removing blood plasma from the body by withdrawing
blood, separating it into plasma and cells, and transfusing the cell back into the
bloodstream
- Dialysis procedure to remove antibodies in treating autoimmune conditions
- Special dialysis that pulse out the bad antibodies
- Used within 3 weeks of onset
-
-
Psychosocial needs: patient and families often experience fear and anxiety
- Provide clear communication with the patient and family
- Clarify misconceptions
- Address communication needs
- Connect with support services
Recovery can take months: many patients can experience residual pain
Lecture 5 - February 6th
Pre/Intra/Post Op Care
Pre-op
Surgery
- Performed for (could be emergency or planned)
- Diagnosis (biopsy, endometriosis)
- Cure or repair (appendectomy, orthopedic, trauma)
- Palliation (not treating, mass that causes pain)
- Prevention (vasectomy, mastectomy/hysterectomy for BRCA)
- Exploration (internal bleeding, laparoscopic vs actual surgery)
- Diagnosis and exploration are like a venn diagram)
- Cosmetic improvement (nose jobs, lasik)
Surgical Settings
- Emergency (unexpected)
- Elective (planned)
- Inpatient (ICU or surgery unit)
- Usually same-day admission
- Ambulatory (same-day surgery) - discharged same day
- Procedures usually take less than 2 hours
- Usually less than 3-4 hours in post-anesthesia care unit (PACU) or
post-anesthesia recovery room (PARR)
Patient Interview
- Pre-operative appointment
-
Check documented information prior to interview to avoid repetition
Occurs in advance or day of surgery
Purposes
- Obtain health information (medical conditions, allergies, family history)
- Determine patient expectations (goals,
- Provide and clarify information on procedure (consent signed by patient and doctor)
- Assess emotional state and readiness (TLC)
- Begin discharge planning and post-operative teaching (starts as soon as they come into
the hospital)
NSG Assessment of the Patient Before Surgery
- Risk factors
- pre-existing conditions
- fasting (NPO 8 hrs is regular)
- aspiration (causes pneumonia)
- medications (blood thinners, vitamins ex. St John’s Wort)
- Patient safety
- Confirm patient
- Blood type and Rh factor
- Type and screen (mix patient’s and donor’s blood together and check for reactions)
- Allergies (especially latex, make sure patient has bracelet with the allergy and reaction
type, the protein in latex that is the allergen is a lot like banana and kiwis)
- LATEX ALLERGY: Persons allergic to foods like bananas, avocados, passion
fruit, kiwi, tomatoes, melons, celery and chestnuts which resemble a protein
element in latex
- Crossmatch blood (donor and patient blood mixed together)
- Malignant hypothermia reaction
- Psychological status
- Reinforce coping strategies
- Common Patient Fears
- Stress and anxiety
- Death or disability
- Pain and discomfort
- mutilation/alteration in body image
- Anesthesia
- Disruption of life functioning/patterns
- Cultural and ethnic
- Receipt of adequate information from surgeon
- Psychosocial needs of the patient (stairs, travel type, etc.)
- Influencing factors
- Age (as they get older the more medications [blood thinners])
- Past experience
- Current health
- Socioeconomic status
- Past health history
-
Diagnosed medical conditions (sleep apnea, snoring, loose teeth [aspiration risk], diabetes
[insulin - NPO], malignant hypothermia)
- Previous surgeries and problems
- menstrual/obstetric history (last period, pregnancy)
- Reactions/problems to anaesthesia (patient or family)
- Current medications
- Prescription and
OTC
- Herbal products
- Vitamins
- Recreational
- Drugs
- Alcohol
- Tobacco
- Each System
- Nervous system
(LOC, GCS,
cognition function,
follow commands,
heading and vision, concentration, delirium risk, history)
- Cardiovascular system (radial pulse, regularity, EKG, pre-existing conditions, pacemaker
or implanted devices, lab tests, anticoagulants, edema, blood pressure)
- Respiratory system (listen to lungs, recent/chronic respiratory infections, asthma,
smoking, RR, SPO2)
- Urinary system (output, pregnancy test, renal function tests, enlarged prostate, catheter)
- Hepatic system (liver enzymes, if the liver can metabolize anesthetics, substance misuse)
- Integumentary system (pre-existing wounds/cuts, colour, ulcers, rashes, hx of pressure
injuries, mucous membranes, temperature, moisture, turgor)
- Musculoskeletal system (ROM, mobility, gait, balance, pain)
- Endocrine system (diabetes, insulin, blood glucose check, thyroid dysfunction)
- Immune system (WBC,
- Any lab testing
- Fluid and electrolyte status
- Nutritional status
- Gastrointestinal System (weight, dentures, recent weight loss/gain
Laboratory and Diagnostic Testing
- Nurses document relevant findings and report to perioperative team
- Nurses obtain and evaluate results of laboratory tests
- Nurses monitor blood glucose for diabetics
- ABGs, oximetry, Blood urea nitrogen, creatinine, CBCs, ECG, Electrolytes, hCG, PT, PTT, INR,
Platelet count, Pulmonary function studies, serum albumin, type and cross math, urinalysis
Preoperative Teaching
- Patient has right to know what to expect and how to participate
- Increases patient satisfaction
-
Reduces fear, anxiety, stress, pain
and vomiting
- Limited time available
- Address needs to highest priority
- Include information focused on
safety
- Provide written material
Legal Preparation for Surgery
- All required forms are signed and in chart
- Informed consent (dr. is responsible
for signing, the nurse is just ensuring
it is correct, informed = voluntary,
capacity and information)
- Blood transfusions (different and
separate than consent form)
- Advance directives and power of
attorney
- Surgeon is responsible for obtaining consent
- Nurse may witness signature
- Verify patient has understanding
- Nurse must inform surgeon if patient
has questions or did not understand
- Patient’s permission may be
withdrawn at any time
Day of Surgery Preparation
- Final preoperative teaching
- Assessment and report of pertinent findings
- Verify signed consent
- Labs
- Type and screen (valid for 96 hours)
- History and physical examination
- Baseline vitals
- Consultation records
- Nurse’s notes
- NSG role
- Patient should not wear any cosmetics
- valuables returned to family member or locked up
- Dentures, contacts, prostheses are removed
- Identification and allergy bands on wrist
- Void before surgery
Preoperative medications
- Provide analgesia
- Prevent nausea and vomiting
- Promote sedation and amnesia
-
1000mL of clear fluids 2-3 hours before
decreases rates of nausea/vomiting,
decrease risk of paralytic ileus, tolerate the
anesthetics
- Fasting Recommendations:
- 2hr: clear liquid
- 4hr: breast milk
- 6hr: light meal, formula or
nonhuman milk
- 8hr: meal including meat, fried or
fatty food
- Decrease anesthetic requirements
- Facilitate induction of anesthesia
- relieve apprehension and anxiety
- Other medications may be administered
preoperatively
- Antibiotics
- Eye drops
- Routine prescription drugs
- Benzodiazepines, anticholinergics,
opioids, antibiotics, antacids
- Oral meds should be given 60-90 minutes
before surgery
Age-Related Considerations
- Nurse must be particularly alert in assessing and
caring for older adult surgical patients
- Consider patient’s physiological condition, not just
his or her chronological age
- Consider sensory deficits
Intraoperative Care
Intraoperative care
- Nursing care requires understanding of
- Anesthesia
- Pharmacology
- Surgery
- Surgical interventions
- Allows you to monitor patient’s response
- Historically took place in OR
- Current trend to decreased in-hospital surgery and increased ambulatory procedures
- Healthier patients
- Shorter procedures
Surgical Team
- Perioperative nurse (umbrella term)
- Prepares room with team
- Patient advocate throughout surgical experience
- Circulating nurse
- Not scrubbed, gowned, or gloved
- Remains in unsterile field
- Documents
- Scrub nurse (sterile entire procedure)
- Follows designated scrub procedure
- Gowned and gloved in sterile attire
- Remains in sterile field
- RPN or surgical technician (not licensed)
- Performs scrubbed or circulating function
- Passes instruments and implements other technical functions during procedure
- Supervised by RN
- Surgeon (may have residents, also 1st assist nurse, PA)
- Physician who performs the procedure
- Responsible for
- Preoperative medical history
- Physical assessment
- Patient safety
- Post Op management
- Anaesthesiologist
- Administered anesthesia
- Maintenance of physiological homeostasis throughout intraoperative period
- Prescribes preoperative and adjunctive medicines
- Monitors cardiac and respiratory status and vital signs throughout procedures
Nursing Management
- Before surgery
- Chart review
- History and physical examination
- urinalysis
- CBC
- Serum electrolytes
- Chest x-ray
- ECG
- Admitting patient
- Reassessment
- Last-minute questions
- Review of chart
- Final questioning about valuables, prostheses, contacts, last intake of food/fluid (mark the
correct limb for amputations)
- Room preparation
- Surgical attire worn by all persons entering OR suite
- Electrical and mechanical equipment checked for proper function (overheat, bulbs falls)
-
-
Scrubbing, gowning and gloving (sterile)
- Mask (AGMP: aerosol generating medical procedures, wear N95 especially if intubate,
shoe covers)
- Cleanse hands and arms by scrubbing with detergent and brush
- Eliminates dirt and oil
- Decreases microbes
- Inhibit rapid regrowth of microorganisms
- Standard procedure for personnel
- Waterless products are sometimes used
- Sterile gown and gloves are put on after scrub
Basic aseptic technique
- Centre of sterile field is site of surgical incision
- Only sterilized items in sterile field
- Protective equipment
- Face shields, caps, gloves, aprons and eyewear
Postoperative Care
Post-op care in the PACU
- While in the PACU, priority care includes monitoring and management of
- Respiratory and circulatory function
- Pain
- Temperature
- Surgical site
- Patient’s response to anesthetic reversal
Initial Assessment
- AIRWAY, BREATHING, CIRCULATION
(ABC)
- A: airway patency (tongue, can the
patient protect their airway on their
own, muscle spasms if taken out too
fast, decreased O2 states, increased
HR to compensate, choking, gasp,
chin up (open) chin down (closed),
cyanosis, muscle spasm if taken out
too fast)
- B: rate and quality of respirations
(opiates can cause respiratory distress (OD risk, antidote = narcan), cyanotic, decreased
LOC, decreased RR)
- Auscultate breath sounds in all fields
- O2 saturation (pulse oximetry)
- Supplemental oxygen (nasal prongs most common, flow/rate, consistent O2 sats)
- C: ECG monitoring (throughout procedure, rate and rhythm [of pulse slights decreases do
to opiates, should be regularity])
- Measure BP and compare to baseline
-
-
-
- Temperature and colour of skin (cool, pulses)
- Peripheral pulses (especially if surgery was on a limb)
Conduct initial neurological assessment (PACU assessment q15m x4, q2hx2, full vitals,
supplements oxygen, should be A+Ox3, should not still be sleepy or in and out of sleep)
Assess intakes and outputs
Assess surgical site and condition of dressing (do not touch bandage until ordered to prevent
infection, mark pen around any discharge to track,
- bleeding is #1 post op complication
- 1st signs: visual and vasoconstriction (cold, fast HR, thready pulse, irregular
pulse, increased RR)
- 2nd: compensation fails and hypovolemic shock
Assess pain (might not be in pain at first, OPQRSTUV [O is onset, V is values])
- ** EXAM QUESTION: A nurse is assessing a patient’s pain, she asks “how would you
rate your pain from 1-10” what is wrong with this? ANSWER: 1-10, to assess severity
0-10, must have 0
Assess for emergency delirium
Explain all activities from admission as hearing is first sense to return (decreased LOC)
PACU Report
(also estimated blood loss)
Initial Post-op Assessment
- After verbal report and patient transferred into bed…
- Check patient ID/record time of return
- Should always begin with A, B, Cs
- Airway
- A of ABC
- Patency
- Spinal patient should not have their chin have their chin up for
airway patency
- Most will have a cervical collar preventing this movement
anyways so for those patients you would use the
tongue/nasal airway that would be in the emergency
resuscitation kit
- Complication: obstruction
- Breathing
- B of ABC
- Respiratory rate and quality
- Auscultation
- Oxygen saturation
- Any supplement oxygen?
- First hours post-op
- Obstruction
- Positioning
- Laryngospasm
- Retained secretions
-
-
Hypoxemia: a below-normal level of oxygen in your blood, specifically in the
arteries
- PaO2 <60 mm Hg
- O2 sat <90-92% (this is the normal range for post op patients)
- Hypoventilation: breathing that is too shallow or too slow to meet the needs of
the body
- Atelectasis: a complete or partial collapse of the entire lung or area (lobe) of the
lung
- Bronchial secretions
- High risk of pneumonia
- Atelectasis and pneumonia commonly occur after abdominal and
thoracic surgery
- Related to mucous plugs and decreased surfactant,
hypoventilation, recumbent position, ineffective coughing, and
smoking
- Bronchospasm
- Most at risk?
- NSG Management: Respiratory Complications
- Nursing assessment
- Assessment of temperature, oximetry, respiratory rate, patterns, and
breath sounds is essential (crackles, or wheezes)
- Evaluate airway patency: chest symmetry, and depth, rate, and character
of respirations
- Breath sounds auscultated anteriorly, laterally, and posteriorly
- Notify anesthesiologist of crackles or wheezes
- Nursing implementation
- Proper positioning to facilitate respirations and protect airway
- Lateral position unless contraindicated
- Client allowed in supine with head of bed elevated once
conscious
- Deep breathing and coughing techniques
- Help prevent alveolar collapse
- Help move respiratory secretions to larger airway passages for
expectation
- Three to four deep breaths every 5-10 minutes
- Incentive spirometer is helpful in providing visual feedback of
respiratory effort
- Splinting abdominal incision provides support to the incision and
aids in coughing
- Condition: respiratory insufficiency (hypoxemia, hypercarbia [too much CO2 in
bloodstream])
C: Circulation
- Heart rate (quality, rate, regular?)
- BP (compare to pre-op/PACU)
-
- Capillary refill
- Temperature
- Skin colour
- Peripheral pulses
Potential Alterations in Cardiovascular Function
- Most common complications initially
- Hypotension (bleed [not epidural or spinal] treat with blood, only epidurals or
spinals = spinal shock [accidentally hit those nerves parasympathetic system
causes hypotension and bradycardia] treat with IV fluids)
- Most common cause is unreplaced fluid (spinal shock) and blood loss
- Other causes include dysrhythmias, decreased low systemic vascular
resistance, and incorrect cuff
- Hypertension
- Results from sympathetic stimulation from
- Pain, anxiety, bladder distension, respiratory compromise
- Dysrhythmias (ECGs)
- Often result from identifiable cause (as opposed to myocardial injury)
- Leading cause include
- Hypokalemia (potassium)
- Hypoxemia
- Hypercarbia
- Alterations in acid-base status
- Circulatory instability
- Pre-existing heart disease
- Other post op complications
- Postoperative fluid and electrolyte imbalances
- Contribute to alterations in cardiovascular function
- May result from combination of the body’s normal response to the stress
of surgery, excessive fluid losses, and improper IV fluid replacement
- Stress response can cause fluid retention during the first 2-5 days after
surgery
- Fluid loss resulting from surgery decreased kidney perfusion,
stimulating the renin-angiotensin-aldosterone system and causing
release of aldosterone
- Fluid overload is possible when
- IV fluids are administered too rapidly
- Chronic (e.g., cardiac or renal) disease exist
- Client is an older adult
- Fluid deficit may result from inadequate fluid replacement
- Decreased cardiac output and tissue perfusion
- Stress response contributes to increased clotting factors
- Can take a couple days to work
-
-
Deep vein thrombosis (hip surgery increased vs appendectomy
decreased) and pulmonary embolism (can be fatal, DVT moves to heart,
brain or lungs)
- Ambulation decreases risk of DVT
- If you do have a DVT ambulation is important
- Signs and Symptoms: swelling, warmth
- Syncope may indicate decreased cardiac output, fluid deficits, or deficits in
cerebral perfusion
- Frequently occurs from postural hypotension on ambulation
Those at greatest risk
- Altered respiratory function
- Cardiac history
- Older adults
- Debilitated or critically ill
- Nursing Assessment
- Frequently monitor vital signs
- Compare to baseline
- Assess apical, radial pulse carefully and report irregularities
- Assess skin colour, temperature, and moisture
- Notify anesthesiologist if:
- Systolic <90 mm Hg or >160 mm Hg
- Pulse pressure difference between systolic and diastolic
- Pulse <60 or >120 beats per minute
- Pulse pressure narrows
- BP gradually decreases
- Irregular cardiac rhythm develops
- Significant variation from preoperative readings
- Nursing Implementation
- Treatment begins with administration of oxygen therapy (loss blood lose
hemoglobin, you might actually have 100% oxygen but you have less
blood)
- Volume status assessed
- IV fluid boluses to normalize BP
- Spinal shock: have all the blood they need the veins are
just so dilated that they need fluid to move blood around
- Drug intervention
- Hypertension: address and eliminate cause of sympathetic nervous
system stimulation (NOT TESTING)
- Analgesics, voiding, correction of respiratory problems
- Rewarming corrects hypothermia-induced hypertension
- Accurate intake and output
- Part of q15m assessment in PACU, wound loss would be
included in output
- Monitor laboratory findings
-
-
-
Assessment of infusion rate of fluid replacement and infusion
site
- Adequate mouth care
- Leg exercises (compressive socks)
- Unfractionated or low-molecular-weight heparin
Clinical Unit
- Ambulation
- Slowly progress, monitor pulse, assess for feelings of
faintness (supervise, orthostatic hypertension)
- With spinal you need to check the dermatomes, need
movement and sensation not just movement
Neurological
- Level of consciousness
- Orientation
- Sensory and motor status
- Especially if epidural/spinal anesthesia
- Delayed awakening
- Commonly caused by prolonged drug action
- POTENTIAL ALTERATIONS
- Emergency delirium (or violent emergence)
- Can induce restlessness, agitation, disorientation, thrashing, and shouting
- Caused by anesthetic agent, hypoxia, bladder distension, pain, electrolyte
abnormalities, or anxiety, sensory and cognitive impairments
- Nursing Assessment
- Level of consciousness
- Orientation
- Ability to follow commands
- Size, reactivity, and equality of pupils
- Sensory and motor status
- Nursing Implementation: PACU
- Attention on evaluation of respiratory function
- Hypoxemia causes postoperative agitation
- Sedation may be beneficial for controlling agitation and providing safety
- Nursing Implementation
- Side rails up
- Secure IV lines artificial airways
- Verify presence of ID and allergy bands
- Monitor physiological status
- Some alterations in neurological function may be related to pain medication sleep
deprivation or sensory overload
- Complete a CNS assessment
- Ensure clients receiving pain medication are responsive and oriented to
person, place, and time
-
-
Assess sensation and motor function on any client who has received a
spinal or epidural anaesthetic
Potential Alterations in Temperature
- Hypothermia
- Core temperature less than 36℃
- Occurs when heat loss exceeded production
- Loss of heat to cold or the use of cold irrigation fluids
- Rewarm slowly to not cause a seizure
- Increased risk associated with
- Age (elderly; less than two years; neonates)
- Long surgical procedures (>12 hours)
- Prolonged anesthetic administration
- If using an external warming device take temperature q15m
- Hyperthermia:
- Temperature elevation provides information about client’s status
- Mild elevation (up to 38℃ in first 48 hours) may result from stress
response
- Moderate elevation (>38℃) usually caused by respiratory congestion or
atelectasis, and rarely by dehydration
- After 48 hours, a moderate to marked elevation (higher than 37.7℃)
usually indicates infection
- Ex.
- Wound, respiratory tract, urinary tract (secondary to
catheterization), hospital-associated diarrhea caused by
Clostridium difficile, septicemia
- Nursing Assessment
- Vital signs (oral, tympanic or axillary temperature)
- Assess colour and temperature of skin
- Frequent temperature assessment
- Observe for early signs
- Nursing Implementation
- Passive rewarming raises basal metabolism
- Active rewarming requires application of warming devices
- Blankets, radiant warmers, heated water mattresses
- Monitor body temperature at 15-minute intervals when using an external
warming device
- Closely monitor client with increased in temperature for symptoms of malignant
hyperthermia: severe reaction to certain drugs used for anesthesia, typically
includes dangerously high body temperature, rigid muscles or spasms, a rapid
heart rate (blood family history risk, increased trend in temperature is fatal)
- Symptoms may not be evidence until the postoperative phase
- Dantrolene antidote?
- Measure temperature a4h for first 48 hours postoperatively
- Encourage airway clearance
-
-
Chest x-rays and cultures if infection suspected
Antipyretics and body cooling for fever over 39.4℃
Potential Gastrointestinal Problems
- Nausea and vomiting are significant problems in postoperative period
- Responsible for unanticipated admission, increased discomfort, delays in
discharge, and dissatisfaction with surgical experience
- Nausea and vomiting are most pronounced after abdominal surrey
- Treatment: ondansetron (Zofran), transcutaneous electrical nerve stimulation,
acupuncture, acupressure, acupoint stimulation, and aromatherapy
- The following clients are predisposed to PostOperative Nausea and Vomiting
(PONV)
- Age <50 years
- Female clients
- Clients with motion sickness
- Non-smokers
- Nausea and vomiting caused by:
- Volatile anesthetic agents
- Nitrous oxide
- Opioids
- Duration of surgery < 1 hour
- Type of surgery, e.g., laparoscopy (ports to inflate the abdomen so lots of gas
pain)
- Abdominal distension from deceased peristalsis is caused by handling of bowel
during surgery
- Swallowed air and gastrointestinal secretions may accumulate in colon,
producing distension and gas pains
- PostOperative Ileus (PO) is a transient cessation of bowel motility that prevents effective
passage of intestinal contents and may affect the client’s tolerance of oral intake
(peristalsis)
- Stomach motility returns 1-2 days, and bowel motility in 3-5 days
- Bowel sounds need to be present in all quadrants before eating, usually
come back 2-4 hours post op clear fluid 1st
-
-
Paralytic ileus
- Impairment of intestinal motility (small or large intestine), not mechanical
obstruction
- Postoperative ileus last >3 days
- Small bowel obstruction results when peristalsis stops
- Bowel lumen remains patent, but contents of intestine are not propelled forward,
producing severe nausea and vomiting
- Usually seen on the clinical unit postoperatively
- Nurses assess for abdominal distension and a reduction or absence of bowel
sounds
- Abdominal distension may require NG tube for symptomatic relief
(decompression NG connected to suction)
- S&S: absent BS, abdominal distension, abdominal pain, nausea, vomiting, poor
appetite
- Nursing Assessment (paralytic ileus/abdominal distension)
- Auscultate abdomen in all four quadrants to determine the presence, frequent,
and characteristics of the bowel sounds (if you are passing gas you do not need to
listen to the bowel sounds)
- Can be absent or diminished in immediate postoperative period
- Return of the bowel motility accompanied by flatus
- Nursing Implementation
- Antiemetic drugs
- Oral fluids as tolerated
- Suction at bedside
- Turn client’s head to side to protect from aspiration
- Upright position
- Slow, deep breathing
- May resume intake upon return of gag reflex (aspiration risk)
- NPO until return of bowel sounds for client with abdominal surgery (IV, NG for
decompression)
- Clear liquids (advance as tolerated)
- Regular mouth care when NPO
- Antiemetics administered for nausea
- Ambulation
Potential Alterations in Urinary Function
- Low urinary output may be expected in the first 24 hours, regardless of intake
- Urinary output of about 30mL/hour is expected in the first few hours
- Increased aldosterone and ADH from stress of surgery, fluid restriction, fluid
losses during surgery, drainage, or diaphoresis
- Anticholinergic, antispasmodic, and opioid drugs may also interfere with ability to
initiate voiding or fully empty bladder
- Retention more likely with lower abdominal or pelvic surgery
- Pain may alter perception so filling bladder (may not feel the need to pee)
- Nursing Assessment
-
Urine examined for quantity and quality
- Note colour, amount, consistency, and odour
- Assess in-dwelling catheters for patency
- Urine output should be at least 30mL/hour
- If no catheter, client should be able to void 200mL within 6-8 hours after surgery
- If no voiding, abdominal contour inspected and bladder palpated and
percussed/scanned for distension
- Nursing Implications
- Position client for normal voiding
- Reassure client of ability to void
- Use techniques such as running water, drinking water, pouring water over
perineum, ambulation, or use of bedside commode
- Potential Alterations in the Integument
- Incision disrupts skin barrier and healing is a major concern during postoperative period
- SSIs (surgical site infection) occur within 30 days after surgery or within 1 year of
implant surgery
- Characterized by
- A combination of purulent discharge
- The isolation of organisms, most commonly Staphylococcus aureus (skin
flora)
- Physician or radiological diagnosis
- Nursing Assessment for Surgical Wounds
- Appearance (REEDDA): periwound: area around wound
- Size
- Exudate
- Edema (some is normal at first)
- Pain
- Drains (active use gravity/suction ex. JPs, passive = Penrrose, Hemovac drains in
thoracics)
- Dressing (change only if you do need to or it is ordered, keep dressing on as
much as possible to decrease risk of infection)
- Wound dehiscence: separation and disruption of previously joined wound edges
- May be preceded by a sudden discharge of brown, pink, or clear drainage
- Wound evisceration: protrusion of the visceral organs through a wound opening)
- This is an EMERGENCY and will be surgery
- apply sterile moist dressing, moist soaked gauze in sterile water or saline
- Nursing Implementation
- Note type, amount, colour, consistency, and odour of drainage
- Notify surgeon of excessive or abnormal drainage and significant
changes in vitals
- Note number and type of drains when changing dressing
- Examine incision site
- Clean gloves and sterile technique
Postoperative Complications
-
Urinary retention: common for epidural or spinal
Emergence delirium
Antibiotics and gravol are good for nausea and vomiting
Hemorrhage: blood loss
Pain
What is pain?
- Pain is a complex constellation of
unpleasant sensory, emotional,
psychological and certain autonomic
(involuntary) responses and
behavioural reactions provoked by
tissue damage
Pain Management
- Remember: effective pain
management
- Promotes optimal healing
- Prevents complications
- Allows clients to participate
in necessary activities
- Should be timed to
ensure it is in effect
-
during painful activities (e.g., ambulating)
Without effective pain management body focuses on stress not healing
Nociceptive Pain
- Mediators of nociceptive pain
- Nociceptors are specifically designed receptors to detect stimuli that may cause harm to
the body, which may be mechanical, chemical or thermal in nature
- Most common type of pain
- Physiologic response when nociceptors respond to noxious or potentially harmful stimuli
- Protective role
- Transient duration
- May be acute or chronic
- May vary in intensity, quality and may be referred
- Somatic: originates from musculoskeletal, joint or cutaneous and often localized
- Visceral: originates from hollow organs and smooth muscles, often referred
- Heart attack: arm pain
- Ectopic pregnancy and uterine bleeding: shoulder pain
- Assessments
- Visual analogue
- Numerical rating scale
- Verbal rating scale
- Wong-baker FACES Pain Rating Scale (useful in children <7 years)
Neuropathic Pain
- Pathological nerve pain resulting from impaired processing of pain due to nerve damage
- Chronic pain disorders caused by a lesions in peripheral or central somatosensory system
- Occurrence in 35% of chronic pain patients
- 5% of population suffer from neuropathic pain
- Varied presentation: can be intermittent, constant, spontaneous or provoked
- Nerve damage
- Central: associated with stroke or spinal cord injury/ischaemia
- Peripheral: diabetic peripheral neuropathy and postherpetic neuralgia
Referred pain
-
-
Associated comorbidities with neuropathic pain
- disability/changes in activity patterns or routines
- Increased confusion
- Changes in sleep periods
- Irritability
- Appetite changes
- Increased wandering
- Mental status changes/crying
Mixed pain
- Cases with both nociceptive and neuropathic type of pain
- Herniated lumbar disc patient with radiculopathy
- Malignant tumour pain
- Diabetic foot syndrome
Characteristics
Nociceptive Pain
Neuropathic Pain
Mechanism
Physiologic activation of
peripheral nociceptors
Lesions in somato-sensory
system
Localization
local and referred pain
Confined to innervations
territory of the nerves
Quality of symptoms
Ordinary painful sensation
New strange sensations
Description of pain
Varied (throbbing, aching,
pressure-like pain)
Burning, lancinating, tingling,
associated with numbness
Difference
- Pain threshold: the lowest intensity of a painful stimulus that is perceived by a person as pain
- Similar for everyone
- Pain tolerance: the amount of pain a person is willing ito endure
- Different for everyone
Pain Treatment: Principles
1) Client must always be believed: subjective experience
2) Every client has a right to the best possible pain management
3) Treatment must be based on client’s goals
4) Treatment plans should use a combination of drug and non-drug therapies
5) A multidisciplinary approach is necessary to address all dimensions of pain
6) All therapies must be evaluated to ensure that they are meeting the client’s goals
7) Drug side effects must be prevented and/or managed
8) Client and family teaching should be a cornerstone to the treatment plan
Pain
- Nociceptive pain management
- The first line management NSAIDs like paracetamol, ibuprofen and aspirin
- For more severe pain: opioids as tramadol, fentanyl may be required
- Neuropathic pain management
- Combination of opioid analgesics, antidepressants and anticonvulsants
- Non-pharmacological methods like TENS, acupuncture
- Invasive methods like sympathetic blocks
- Treatment is different for both
Pain: Take home message
- Chronic pain can turn into neuropathic pain if inadequately treated
- Differentiation of chronic nociceptive pain from neuropathic pain is essential to guide proper
therapy
- A multimodal approach (including non-pharmacological) targeting the various elements of pain
should be tried in all patients
- Choice of drugs for various types of neuropathic pain may varies according to different guidelines
and underlying condition of the patient
WHO Principles of Pain Management
- Use WHO Analgesia ladder
- PO route preferred
- By the clock and PRN
- Adjuvant therapies as needed
- Anticipate and prevent side effects
- STEP ONE: mild pain (1-3/10)
- Non-opioid and adjuvant
- Acetaminophen, NSAIDs
- STEP TWO: moderate pain (4-6/10)
- Weak opioid and adjuvant
- Codeine, tramadol
- STEP THREE: severe pain (7-10/10)
- Strong opioids and adjuvant
- First line: morphine,
hydromorphone, oxycodone
- Second line: fentanyl
- Third line: methadone
- Terms
- Tolerance: larger doses needed for adequate pain control over time (NOT addiction)
- Dependence: withdrawal symptoms if a chronically used opioid is suddenly discontinued
or reduced
- Addiction: psychological dependence, used for a “high”
Patient-Controlled Analgesia
- “Demand” analgesia
- Allows patient to self-administer a dose of opioid through a pump, when needed
- Patient teaching extremely important
- Asses: pain, vitals, use, meds used, IV site
- Lockout: even with 17 pushes you do not get to have 17 doses
Epidural Analgesia
- Infusion of pain-relieving medication through a catheter placed into the epidural space
surrounding the spinal cord (not spinal)
- Provides excellent pain reduction and/or relief of long duration (8-24 hours) without causing
sympathetic motor nerve blockade
- Sometimes can only impact sensory nerves, walking epidural
- Local anesthetics can be combined with opioids
- Continuous or intermittent administration
- About 10x stronger than IV medication (therefore smaller doses)
- Very closely monitored
Intrathecal Pump
- Administration in the spinal area, into the CSF
- “Nerve” block
- Prevents pain signals from traveling down the spinal cord
- For severe chronic pain that does not respond to traditional analgesia
- Can also be used to delivered muscle relaxants (i.e., Baclofen) to reduce spasticity
Nonpharmacetual/natural interventions
- Massage therapy
- Non-opioid medications: like acetaminophen, ibuprofen and NSAIDs
- Physical therapy and exercise
- Yoga
- Interventional treatments: like nerve blocks, epidurals and joint injections
- Cognitive behavioural therapy (CBT): a form of talk therapy designed to change negative
thoughts and behaviours
Pain in the PACU
- Analgesic medications and pain-relieving techniques
- IV opioids are used for rapid relief
- Medications are administered slowly and titrated to allow for optimal pain management with
minimal to no adverse side effects
- Around-the-clock (ALC) use of NSAIDs, Cox-2 inhibitors or acetaminophen can be used to
decreased opioid requirements
- Sustained relief options: epidural catheters, PCA or regional anesthetic blockade
- Non-pharmacological pain management strategies include touch, application of heat or cold,
massage, imagery, music and biofeedback
Lecture 6 - GI Disorders
Lecture 7 - Diabetes Mellitus
Diabetes
- Diabetes mellitus (DM): is a complex disorder of carbohydrate, fat and protein metabolism that is
primary the result of a deficiency or complete lack of insulin secretion by beta cells of the
pancreas or a resistance to insulin
- Type 1: occurs due to progressive destruction of beta cells in the pancreas due to an
autoimmune process and results in little to no insulin production
- More common in people younger than 30 years of age
- Type 2: the pancreas does not produce enough insulin and therefore fewer glucose
molecules enter the cells. In addition, some body cells respond poorly to insulin and
therefore less glucose is absorbed (insulin resistance)
- More common in adults
- Gestational diabetes: is a type of diabetes that develops during pregnancy
- Often between the 24th and 28th week of pregnancy
- Can resolve but increases risk of developing type 2
- Diabetes: 1 in 16 Canadians (6.2%) have diabetes and 0.9% of the population is undiagnosed
Health Screening
- Type 1 DM: no screening is recommended for healthy individuals
-
- Monitor patients who have a first generation relative with diabetes mellitus
Type 2 DM
- Screening every 3 years in patients > 40 years of age or those at high risk
- Lab: fasting blood glucose levels of Glycated hemoglobin A1C >6.5% (shows three
month average)
- Oral glucose tolerance test (OGTT) > 7.8 mmol/L (usually used for T1)
Risk Factors
- Type 1: first generation relative
- Type 2
- High risk populations: latin americans, indigenous, asian or african descent
- Overweight: abdominal obesity (glucose not going in cell so glucose is stored in adipose
tissue)
- History of gestational diabetes
- Impaired fasting glucose or glucose intolerance
- Delivered a macrosomic infant (> 8 lbs. 13 oz)
- Have hypertension, vascular disease or dyslipidemia (fat stays in blood causing
atherosclerosis, burn fats for fuel rather than glucose)
- Have polycystic ovary disease or schizophrenia (check these patients regularly)
Pancreas and Insulin
- Pancreas is both an exocrine and endocrine gland
- Produces trypsin, amylase and lipase (needed to breakdown fuels, fats, carbs, etc.), which
are secreted into the duodenum and are necessary for digestion and absorption of
nutrients
- Within the pancreas, the the isles of Langerhans contain beta cells that are responsible for the
production of insulin
-
Insulin facilitates the transport of glucose from the bloodstream across cell membranes
into the cells, lock and key mechanism
Glucagon (hormone) triggers the liver to convert stored glucose (glycogen) into a usable
form and then release it into your bloodstream, glycogenolysis
- Occurs when the blood glucose is low or failing
- When blood glucose decreases storage needs to be used
Insulin
- If it cannot get in then your body thinks that is starving
Diabetes Mellitus
- Glucose homeostasis
- Diabetes and the body
Onset of Diabetes
- Up to 6 million Canadians have prediabetes
- Prediabetes, impaired glucose tolerance
- Diagnostic studies
- Fasting (4-6 mmol/L) > 6.1 mmol/L (12 hours fasting)
-
-
2 hour plasma glucose level > 7.8 mmol/L (they have glucose but it cannot get into the
cells)
Elevated glucose levels can damage blood vessels, increasing the risk for:
- Heart disease and stroke (glucose is so large it hurts the vascular system, plaque
formation)
- Kidney injury, leads to renal insufficiency and failure (molecules are large and damage
nephrons, kidneys will diaphoresis glucose to get it out, urine should never have glucose)
- Eye injuries, impaired vision to blindness (very fine vessels to retina, glucose damages
these, cause retinopathy, leading cause of blindness)
Type 1 Diabetes
-
occurs due to the destruction of beta cells within the pancreas often due to an autoimmune
condition
Research support a genetic predisposition (first generation relative [siblings and parents])
Occurs more commonly in people < 30 years of age
Peak onset is 11-13 years of age
Signs and symptoms are often abrupt but the disease process may be present for several years
before diagnosis
Pathophysiology
- Absence of or low levels of insulin
- Glucose builds up in the blood (cannot enter the cells) - hyperglycemia
- Glucose (fasting) 4-6 mmol/L (normal range)
- Leads to fluid and electrolyte imbalances
- Kidney: excrete excess glucose = loss of large volumes of fluid, litres (polyuria)
- Result is dehydration - triggers thirst mechanism (polydipsia)
- Cells are not receiving glucose - trigger need for “food” (polyphagia)
- Patients experience weight loss - burning fats and proteins for fuel
- No glucose entering the cells, body begins to breakdown fats, into fatty acids for energy
- Conversion produces ketones (small acids), as they build up in the blood, metabolic
acidosis (serum pH <7.35, metabolic alkalosis is >7.45 pH)
- The increased acidity in the blood, trigger respiratory center to increase the respiratory
rate to blow off more CO2 (waste product) attempt to keep pH WNL (7.35-7.45)
- Kussmaul respirations = increase in depth and rate (get rid of extra CO2)
- Acetone is exhaled = fruity odor
- Polyuria (fluid loss): potassium being excreted in the urine, hypokalemia
- Due to the low levels in the serum, potassium moves out of the cells to compensate
- Due to the continued polyuria to remove excess glucose, more and more potassium is lost
- Leads to skeletal muscles weakness and can progress to intercostal muscles causing
respiratory arrest
- Also at increased risk for cardiac dysrhythmia (heart rhythm abnormalities)
Type 2 Diabetes
-
Occurs most commonly in people over 35 years of age and 80-90% of those patients are
overweight
Risk factors
- Indigenous, South Asian, Latin American Ethnicity
- Risk increases with age
- Obesity
-
The pancreas is able to produce some insulin, however it is insufficient, poorly utilized by the
tissues or both
1. Insulin resistance (the body tissues do not respond to insulin)
- Majority of insulin receptors are located in skeletal muscle, fat and liver cells
- When glucose cannot enter the cells = hyperglycemia and hyperinsulinemia (rises)
2. Over time the pancreas becomes fatigued and insulin production falls
a. Cannot keep it up, gets overwhelmed, gives up
3. Liver: which contains a large number of insulin receptors, fails to properly respond to serum
glucose levels, elevated glucagon levels = increase in blood glucose
- Onset is gradual, usually has for years and you have no idea
- The patient may go for years with undetected hyperglycemia
- These patients are often diagnosed due to routine lab testing
- Clinical signs
- Nutritional status, overweight (got glucose but cannot get in cells)
- Fatigue, recurring infections (bacteria likes sugar, uses glucose as fuel to replicate)
- Prolong wound healing
- Visual acuity changes
- Peripheral neuropathy (neurons are damaged by glucose
- Please review table 52.1 Characteristics of Type 1 and 2 Diabetes, p. 1271
Diagnostic Testing
- Glycated hemoglobin A1C >6.5% (12 weeks average or 3 months)
- Glucose attaches to hemoglobin, reflection of glycemic control over time
- Fasting blood glucose > 7/0 mmol/L (NPO for 8 or 12 hrs
prior to testing)
- Random plasma glucose > 11.1 mmol/L
- 2 hours plasma glucose > 11.1 mmol/L
- Tests need to be repeated for confirmation
-
If the patient is acutely ill the glucose gets released to help fight whatever is causing the
illness, hyperglycemia
Assessment
-
Subjective
- Frequent urination
- Increased thirst and appetite
- Muscle weakness, fatigue
- Poor wound healing
- Changes in vision
- Weight loss (type 1), gain (type 2)
- Objective
- Cardiovascular: hypotension, diminished peripheral pulses, increased pulse, fee cool to
the touch
- Respiratory: increased respiratory rate (deep and rapid), fruity breath, kussmauls
- Muscle weakness and fatigue
- Vision changes
- Warm, dry skin, loss of hair in extremities
- Assess for weight loss or gain
Treatment
- Medication therapy
- Insulins
- Oral antihyperglycemic agents
- Nutritional therapy
- Exercise
- Monitoring blood glucose
Insulin
- Patient who have little to no insulin production to meet metabolic needs will require exogenous
(injected insulin)
- In Canada biosynthetic insulin is the most widely used type
- Several different types of insulin
- Rapid acting
- Short acting
- Intermediate acting
- Extending or long acting
Insulin
Onset
Peak
Duration
Rapid acting:
Lispro (Humalog)
Aspart (Novo
rapid)
10-15
minutes
60-90
minutes
3-5 hours Given 10 minutes before meals
Will need long acting with it to manage
basal background insulin
Decreased pos meal hyperglycemia
Increased flexibility
Multiple injections for patients
Short acting:
Regular (Novolin)
½-1
hour
2-4 hours
5-8 hours Given 30 minutes before meals
May need a longer acting insulin needs
Multiple injections daily
Intermediate
Acting: NPH,
cloudy Humulin
or Novolin
1-3
hours
6-8 hours
12-16
hours
Has a peak 4-10 hours, monitor for
hypoglycemia
Can be mixed with rapid and short acting
insulins
No
pronounced
peak
24+
hours
May be given to patients who require basal
insulin for control of hyperglycemia
Clear insulin, careful not to confuse with
short/rapid acting insulins
Many cannot be mixed with other insulins
Extended or long
1-2
acting: glargine
hours
(Lantus), Determir
(Levemir),
Degludec
(Tresibal)
-
-
-
Insulin is inactivated by gastric juices, cannot be taken orally
Must be taken by subcutaneous injection:
- Syringe
- Pen
- Infusion pump (device)
Insulin vials, pens are stored in fridge until open, then they can remain at room temperature for 28
days
- Never above 30℃
Insulin Administration: Patient Teaching
- Wash hands thoroughly
- Check insulin type and expiration date
- Wipe off top with alcohol sponge or remove cap
- Pull plunger on syringe down to the number of units required
- With the vital upside down, inject the air from the syringe and then pull the plunger down
to achieve the required number of units (check to ensure no bubbles are present)
- Clean and the inject into the proper site at a 90° angle and leaving the needle in place for
5 seconds
- Dispose of the syringe properly
cloudy then clear air, then clear to cloudy draw
rotate sites
- Alternative forms of delivery: insulin pump
- Directly affixed to the body
- The pump is connected to a catheter within the subcutaneous tissue
- Every 2-3 days the insertion site is changed and the pump is refilled
- Program to delivery a basal rate of rapid acting insulin or regular
- Use can activate the pump to deliver a bolus amount prior to meals
- Good for patients who inject multiple times a day
Insulin Complications
- Allergic reactions (rare)
- Local inflammation at injection site, redness, edema, warmth
- Promote site rotation
- Lipodystrophy
-
- Hypertrophy (thickening) of subcutaneous tissue
- Atrophy (loss) of subcutaneous tissues
- Impairs absorption (not getting insulin they need), rotate and avoid injured sites
Somogyi effect: associated with the decline of blood glucose in response to too much insulin
- Patient experienced hyperglycemia in the morning = increase in insulin does
- However, patient experiences hypoglycemia at night due to the increased dose
- Growth hormone and cortisol are contributing factors
Medications
-
-
Oral antihyperglycemic medication work to improve the mechanism by which insulin and glucose
are produced and used by the body
Primarily work on
- Insulin resistance
- Decreased insulin production
- Increased hepatic glucose production
Primarily used to treat Type 2 diabetes
When a patient is NPO you hold these meds
1st Line Therapy
- Biguanides: reduced glucose production by the liver and enhances the insulin sensitivity
at the tissue level which improves glucose transport into the cells
- Metformin (Glucophage)
- Does not promote weight gain
- Can be used to treat pre-diabetes and patients’ with obesity who have impaired
fasting glucose
-
Must be discontinued for patient undergoing surgery or radiological procedure involving
contrast mediums
- Must be held for several hours post procedure or until serum creatinine levels are normal
- 2nd Line Therapies
- Insulin secretagogues/Sulfonylureas: stimulate increased beta cell production of insulin
from the pancreas
- Glimepiride (Amaryl), Glyburide (Diabeta)
- Used cautiously in older patients and those with renal impairment due to
increased risk of hypoglycemia
- Meglitinides: increase insulin production from the pancreas
- Repaglinide (Gluconorm)
- Rapidly absorbed and eliminated = increased risk of hypoglycemia
- Taken 30 minutes before a meal
- Thiazolidinediones: improve insulin sensitivity and uptake in muscle and fats cells and
inhibit hepatic glucose production
- Insulin sensitizers
- Secondary benefit: it lowers triglyceride level and improved high density lipid
levels (HDDLs)
- Side effects: weight gain, edema (not recommended for patients with heart
failure)
Nutritional Therapy
- Based on a plan of health eating (review table 52.8 page 1284)
- Canadian Diabetes Association Recommendations
- Eat three meals a day at regular intervals
- Limit sugars and sweets
- Limit high-fat foods (fried)
- Eat more high fiber foods (whole grains…)
- Drink water, not sweet fluids
- Add physical activity to the lifestyle
Diabetes: Exercise
- Regular and consistent exercise is an essential part of the DM management
- Exercise increases insulin sensitivity and can have a direct effect on lowering blood glucose
(could cause hypoglycemia)
- Regular exercise also lowers triglyceride and low density lipids, reduces blood pressure and
improves circulation = heart benefits
- Type 1 diabetes: should slowly start an exercise program once medical clearance has been
attained
- Type 2 diabetes: 150 minutes of moderate exercise/week
- Type 1 diabetes and those that take Sulphonylureas or meglitinides are at an increased risk of
hypoglycemia when they experience an increase in their physical activity
- If a patient exercises at a peak time of a medication or food id not sufficient to maintain
adequate glucose levels = hypoglycemia
- Patient are encouraged to take a 10-15g carbohydrate snack before exercising
- Small apple, orange, pear; ½ banana, 1 cup of a sports drink, 15 grapes
-
For those at risk need to carry or have access to juice, glucose tablets or candy in the event they
experience hypoglycemia
- Monitoring glucose levels before and after exercise is key (especially type 1)
Monitoring Blood Glucose Levels
- Self-monitoring is critical to DM management
- Allows patient to make self-management decisions about diet, exercise and medications
- Used to determine hyper and hypoglycemia states
- Supplies immediate information about serum glucose levels
- Types
- Portable glucose monitors
- Continuous glucose monitors
- Portable glucose monitors
- Require the patients to use a disposable lancet to obtain a drop of capillary blood which is
then placed on a glucose strip and inserted into a machine for analysis
- See table 52.10, page 1287
- Nurse’s provide teaching to new diabetes about how to correctly the machine
- Patient will also need to taught how to use control solution to ensure the machine is
calibrated
- Patients’ are encourage to carry their machine with them at all time sot evaluate change
sin the blood glucose levels
- Continuous glucose monitoring (CGM) systems are becoming more widely used
- Uses a sensor placed under the skin and it sends values to a receiver every 5 minutes
- Can be integrated into cell phone
- Alerts the patient to episodes of hypo and hyperglycemia
- Sensor is inserted by the patient at regular intervals
- Provides trending data
- Site rotation is still important
Hypoglycemia
- Occurs when there is too much insulin in proportion to available glucose in serum
- Serum glucose levels < 4 mmol/L
- Hypoglycemia stimulates the autonomic nervous system to suppress insulin production and
initiate glucagon, stimulates the liver to release glucose
- In addition, epinephrine (fight or flight hormone lost fuel need to fix) is released = diaphoreses,
hunger, tremors, nervousness, anxiety, pallor, palpitations
- Often related to mismatch timing of food intake and the peak action of insulin or other
medications
- Alcohol intake with food and too much exercise without a snack → lethargy, stuporous,
comatose
- Signs and Symptoms
- Changes in vision
- Cool-cold clammy skin
- Faintness, dizziness
- Headache
- Hunger
- Tremors, unsteady gait
- Slurred speech
- Interventions
- Ingestion of 15-20g of simple carbohydrates
- Focused assessment, respiratory rate, heart rate, LOC (can be comatose)
- Ensure safety, lie down or sit down
- Reassess blood glucose, 15 minutes
- Repeat ingestion of 15-20g of simple carbohydrates if serum glucose not improving
- Fruit juice, hard candies, sport drink
Hyperglycemia
- An excess of glucose in the bloodstream
- If there is not enough insulin, glucose can not enter the cells = cells do not have fuel to work
properly
- Body begins to break down fats for fuel = ketones
- This alters the pH levels in the bloodstream, becoming acidic (pH < 7.35)
- Kidneys try to compensate by increasing diuresis to remove the ketones and excess glucose
molecules = polyuria
- Also experience a loss of potassium
- Body is also breaking down protein for fuel, production of amino acids into fuel (glucose)
increased hyperglycemia, glucose still cannot enter the cells
- Causes
- Corticosteroids
- Emotional or physical stress
- Illness, infection (immune system
needs a lot of food)
- Inactivity
- Poor absorption or lack of insulin
- Too much food
- Signs and Symptoms
- Polyuria
- Polyphagia
- Nausea, vomiting
- Acetone (fruity) breath
- Blurred vision
- Abdominal cramps
- Weakness, fatigue
- Interventions
- Assess serum glucose level
frequency
- Get medical care (depend on the elevated level)
- Increased fluid intake, water
- Assess urine for ketones
- Administer medications as prescribed
- Sliding scale insulin (short or regular acting)
- Treat the cause, infection, stress
Diabetic Ketoacidosis (DKA)
- Acute metabolic complication of DM that
occurs when fats are metabolized for fuel in the
absence of insulin
- Life threatening complication
- More common in Type 1 diabetes but can occur
due to severe illness or stress in type 2 DM
patients
- Characterized by
- Hyperglycemia
- Ketosis
- Metabolic acidosis (pH < 7.35)
- Dehydration (due to polyuria)
- Signs and Symptoms
- Polyuria (volume depleted, losing
litres)
- Polydipsia
- Decreased skin turgor, dry mucous
membranes
- Tachycardia
- Orthostatic hypotension → severe
hypotension (less than 100 systolic)
- Kussmaul’s respirations 30+ RPM
- Fruity breath (acetones)
- Diagnostics
- Serum glucose > 14 mmol/L
- Serum pH < 7.35
- Serum sodium bicarbonate < 15 mmol/L
(base, have used stores to balance
ketones)
- Anion gap > 12 mmol/L
- The difference between the
positively and negatively
charged electrolytes in your
blood
- Treatment
1. Fluid balance
2. Hyperglycemia
- Administer IV fluids (isotonic), large bore IVs or a central line (18 gauge)
- Administer short acting insulin (regular) IV initially (gets glucose into cells)
- 1:1 ratio, 100mL IV fluid (NS):100 units of insulin
- Frequent assessment of serum glucose (1 hr)
- Frequent assessment of blood and urine for ketones
-
Frequent assessment of cardiovascular and respiratory status
Frequent assessment of LOC and neurological function (confusion, disoriented,
irritability)
- Heart (ECG) monitor
- Electrolyte replacements - potassium (IV, hard on veins, 10 mEq/hr IV, 20 mEq/hr central
line)
- Strict intake and output monitoring
- Urinary catheterization (for balance)
- Initially NPO, clear liquids (probably have nausea, food increases blood sugar)
- If pH is really low they may get a little sodium bicarb but once fluid comes back adult
body will correct itself
- Ongoing assessment
- Monitoring for fluid volume overload (crackles, edema, hypertensive)
- Monitor serum glucose, pH and serum potassium
- Monitor vital signs and LOC
- Strict intake and output monitoring
- Heart monitor, rate and rhythm
- Once glucose level is decreasing, monitor for hypoglycemia, may need to change IV
fluids to D5 ½ NS
- Because they have been getting IV insulin
Hyperosmolar Hyperglycemic State (rare)
- Occurs in patients who are able to produce enough insulin to prevent DKA but not enough to
prevent severe hyperglycemia, osmotic diuresis and extracellular fluid depletion
- Older type 2 DM patients with sensory or cognitive impairment, high risk
- Elevated serum glucose levels, 34 mmol/L, but ketones are absent or minimal in urine and blood
samples
- Signs and Symptoms
- are often seen late (cannot tell us)
- Lethargy → Somnolence → stuporous → coma
- Seizures
- Hemiparesis, weakness on one side of the body
- Aphasia, impaired expression and understanding of language
- Treatment (a lot like DKA but no ketones)
- IV, isotonic
- Regular insulin, IV initially
- Electrolyte monitoring and replacement (K+)
- Frequent vital signs
- Heart monitor
- Strict intake and output, monitor for fluid volume overload
- Frequent serum glucose levels
Complications
- Chronic complications of DM are commonly the result of damage to marco (large) and micro
(small) blood vessels that occur due to chronic hyperglycemia
- Possible causes
- By products of glucose metabolism (i.e., sorbitol) are associate with nerve damage
- Formation of abnormal glucose molecules in small blood vessels
- Oxidative stress in RBCs results in damage to tissue
- Microvascular complications results from thickening of the vessel (lining) membranes (becomes
hypoxia tissue) in the capillaries and arterioles in response to chronic hyperglycemia
- Types
- Retinopathy (eyes)
- Nephropathy (kidneys)
- Neuropathy (nerves)
- Clinical manifestations of these conditions may not appear until 10-20 years after the
onset of DM
- Control of serum glucose levels is key to reducing the impact of these
pathophysiology processes
- Macro
- Cardiovascular disease
- Cerebrovascular disease
- Peripheral vascular disease
Diabetic Retinopathy
- Diabetic Retinopathy: is the process of microvascular damage to blood vessels in the retina due to
chronic hyperglycemia, nephropathy and hypertension in patients with DM
- After 15 years with DM, nearly all patients with Type 1 and 80% with Type 2 will have
some form this disease
- Diabetic retinopathy is estimated to be the most common cause of new cases of blindness
in working adults
-
-
Non-proliferative retinopathy: partial occlusion of small blood vessels in the
retina causing microaneurysms in capillary walls = results in capillary leaking =
retinal edema = loss of vision due to hemorrhage (once damage is there there is
nothing we can do)
Proliferative retinopathy: retinal capillaries become occluded, new vessels are
formed but they are extremely fragile = hemorrhage easily = retinal tear or
complete retinal detachment = vision loss
-
Health promotion
- Type 1: annual eye exam, especially starting 5 years post onset
- Type 2: eye exam every 1-2 years, if normal
- Screening for glaucoma and cataracts
- Treatment
- Maintain good glucose control
- Maintain good blood pressure control
- Treatment: laser photocoagulation, destroy ischemic tissue, preventing growth of
new capillaries
- Treatment: intraocular injection of medications
Diabetic Nephropathy
- Damage to the small blood vessels that
supply the nephrons within the kidney which
impact filtration = renal insufficiency = renal
failure
- Risk factors
- Hypertension
- Genetic predisposition
- Smoking
- Chronic hyperglycemia
- Kidneys will compensate for a long time but
then they will just give up one day
- Health promotion and treatment
- Serum glucose control
- Aggressive blood pressure control
- ACE inhibitors: prevent the conversion of angiotensin I to angiotensin II =
arteries remain open, lisinopril, ramipril
- Does not vasodilate arteries prevent vasoconstriction
- Angiotensin receptor blockers - prevent angiotensin II from connecting with
blood vessels = arteries remain open, losartan, valsartan
- Yearly screening for microalbuminuria (urine)
-
- Protein is not filtered
24hr urine collection: assess creatinine clearance (better than BUN)
Lab, serum glomerular filtration rate (GFR)
- Takes into account age + ethnicity
Neuropathy
- Diabetic neuropathy: is nerve damage that occurs due to metabolic derangements associated with
DM
- 40-50% of patients with diabetes will have some degree of neuropathy
- Most common is peripheral neuropathy, leads to a loss of sensation in the lower extremities,
increases the risk of injury and amputation
- Signs and symptoms include
- Paresthesia, difficulty walking
- Abnormal sensations, tingling, burning and itching
- Pain, neuropathic, burning, cramping
- Loss of sensation
- Due to the breakdown of different fats and proteins, different waste products are circulating
which cause ______________
- Health Promotion and Treatment
- Maintaining control of serum glucose
- Medication of pain management
- Gabapentin, pregabalin (anticonvulsants)
- Topical creams (capsaicin) must be applied with gloves
- Tricyclic antidepressants
- Assess extremities for injuries
- Proper footwear, reduce the risk of falls and injuries
- Educate on importance to check feet everyday and importance of proper footwear
Foot Care
- Complications of the foot and lower extremities for diabetes is complicated by both micro and
macro vascular diseases which increase risk of injury, infection and amputation
- Sensory neuropathy adds to the complexity as patients cannot sense when an injury occurs
- Poor perfusion (ischemia) and chronic hyperglycemia impair the healing process
-
Patient teaching
- Wash feet daily with mild soap and warm water
- Pat dry gently, especially between the toes
- Examine the feet daily for injuries
- Use lanolin to prevent dryness and cracking
- Cut toes nails evenly with a rounded contour
- Clean injuries with soap and water, avoid iodine, rubbing alcohol and strong adhesives
- Wear clean cotton soaks
- Avoid open toe shoes and heels
- Do not use hot water bottles or heating pads
- Exercise daily, walking with supportive footwear
Infection
- A patient with diabetes is more susceptible to infection
- Staphii most common
- Contributing factors
- Body response to infection by mobilizing glucose
stores to increase fuel supply which allows the body to
fight the infection = increased hyperglycemia
- Decreased circulation, slower immune response
- Pathogens can thrive in a glucose rich environment
- Loss of sensation in extremities will delay the detection
Sick days
- Patient teaching
- Check your glucose levels every 3-4 hours
- Increase your fluid intake (water)
- If you cannot eat, ensure adequate fluid intake with fluids high in carbohydrates
- Get plenty of rest and have someone checking in on you (decreased LOC)
- Do not omit or skip insulin or oral medications
- Immune needs glucose so body can increase blood glucose
- Call your physician if:
- Have vomiting or diarrhea for > 6 hours
- Urine self, test show positive for ketones (early detection of DKA)
-
Glucose level significantly elevated or you are unable
to resolve an episode of hypoglycemia
Signs of severe hyperglycemia
Significant chest or abdominal pain
Ill for several days not improving
Macro Complications
- Marco complications with diabetes are complications in the larger
blood vessels
- Occur with greater frequency and the onset is much earlier
- Atherosclerosis: a condition where the arteries become narrowed and
hardened due to buildup of plaque (fats) in the artery wall
- Research supports a genetic predisposition with DM the altered lipid
metabolism (using fats for fuel) contributes to increase plaguing in
arteries
- Risk of MI and stroke
Cardiovascular Disease
- Insulin resistance is implicated in the development of hypertension of
hypertension and dyslipidemia
- Not well understood
- All patients with DM should be screened for dyslipidemia routinely
and considered high risk for vascular events
- Atherosclerosis, coronary artery disease (CAD)
Myocardial infarction
- Cerebrovascular disease (stroke)
- Peripheral vascular disease, poor
perfusion, gangrene and amputation
- Patient teaching (like a heart disease
patient)
- Heart healthy diet, decreased
sodium and fats
- Weight modification as necessary
- Smoking cessation
- Increased physical activity
- ACE inhibitory (lisinopril)
- Antiplatelet therapy (81 mg ASA)
- Fluids, water
Lecture 8 - Endocrine Disorders
Lecture 9 - Hypertension and Stroke
Hypertension
-
Hypertension: characterized by elevated blood pressure (BP) over normal values
Hypertension is most significant modifiable risk factor for cardiovascular disease and mortality in
Canada
- As BP increased, so does the risk for:
- Myocardial infarction (MI)
- Heart failure
- Stroke
- Renal disease
- Plays a role in a number of diseases (strokes, cardio, renal)
- Muscle (if thickens it cannot pump as well unlike skeletal, muscle that works all the time and has
to work hard against the pressure)
- About 25% of all Canadians are affected by hypertension
- Normal BP: SBP < 120 mm Hg and DBP < 80 mm Hg (perfect numbers)
- Persistent (doesn’t rise and fall) elevation of
- Systolic blood pressure (SBP) > 140 mm Hg or
- Diastolic blood pressure (DBP) > 90 mm Hg or
- Current use of antihypertensive medication(s)
- Prevalence increases with age (comorbidities)
- Hypertension is more prevalent in older women than older man
Anatomy and Physiology
- Blood Pressure (BP) is the tension or pressure of the blood within the systemic arteries
- BP is needed to continuously perfused organs and tissues and is measured in mm Hg
- Systolic BP: the amount of pressure exerted during contraction of the left ventricle and results in
the ejection of blood into the aorta
- Activities that can increase SBP include exercise, smoking, cardiovascular disease
(atherosclerosis) and stress (sympathetic response, fight or flight)
- Exercise is okay because it brings it back down too
- Diastolic BP: is the amount of blood that remains in the aorta during the resting phase of the
cardiac cycle
- Allowing the ventricles of the heart to fill
- Elevations in DBP indicate that the heart is not relaxing during the resting phase = underlying
pathophysiological process i.e., heart disease, stress
- Needs to call physician especially at rest 90+ is a red flag
- Pulse pressure: is the difference between the SBP and DBP
- Narrowing of pulse pressure indicates the heart is having a harder time overcoming
pressure in systemic system and resting (refilling) about 40 mm Hg
- Tends to narrow high SBP increase, DBP extremely increased,
- Decreases volume in vascular system and beats capillaries down
- The autonomic nervous system (ANS) impacts regulation and control of BP
-
-
-
-
The autonomic nervous system is a network of nerves that regulates unconscious body processes
- Such as apical pulse, blood flow, respiration, digestion
Autonomic nervous system is made up of
- Sympathetic nervous system (SNS), fight or flight (stimulates as increase in HR and BP)
- Parasympathetic nervous system (PNS), rest and relax (decreases HR and BP, rest and
digest)
Baroreceptors are located in the aortic arch and carotid arteries, if they sense pressure changes,
send messages to the medulla oblongata (cardiac center in the brainstem) which trigger
compensatory mechanisms
- If they sense a decrease in pressure, stimulate the sympathetic nervous system (SNS)
- Stimulate Beta 1 receptors (increase heart rate)
- Stimulates Beta 1 receptors (increased cardiac output)
- Alpha 1 receptors, causes vasoconstriction of arteries
- **when optimal pressure is resumed
(baroreceptors sense the BP-WNL) =
SNS stimulation is turned off
Renin-Angiotensin-Aldosterone System (RAAS)
and Kidneys
- The RAAS is a hormone system within
the body that is essential for the
regulation of blood pressure and fluid
balance
- The system is mainly comprised of the
three hormones: renin, angiotensin and
aldosterone
- Primarily it is regulated by the rate of renal artery blood flow (25% of blood from heart)
If the kidneys sense a decrease in blood flow through the renal arteries
- Kidney’s will produce the hormone renin which is secreted into the vascular system
- Renin, converts the plasma protein angiotensinogen from the liver to angiotensin 1
- Angiotensin 1 is converted to angiotensin 2 by an enzyme within the lungs
- Angiotensin 2 stimulates the adrenal glands to produce aldosterone
- Aldosterone stimulates the kidneys to reabsorb water and sodium = increasing volume
and therefore pressure in the vascular system
- Also stimulates vasoconstriction of blood vessels, increasing blood pressure
- Fluid spills and goes into third space if not needed
-
-
-
Kidneys, osmoreceptors and the hypothalamus
If osmoreceptors in the hypothalamus sense a decrease in arterial
pressure or volume
- Signals the thirst center to trigger the thirst response
- Hypothalamus also signals the posterior pituitary to release
antidiuretic hormone (ADH)
- ADH: triggers the kidney to reabsorb water in the
collecting ducts of the nephrons
- Result an increase in fluid volume in the vascular system =
more pressure
- Decrease in urine production
- Potassium and toxins are not being excreted
- Attempts to fill vascular system to increased
pressure
If the mechanisms that control BP are impaired = increased
pressure
- SNS: overstimulation = chronic vasoconstriction
- RAAS: increased fluid retention = increased blood volume = increased pressure
- High sodium level: kidney retain more water to dilute the salt and prevent hypernatremia
- Decreased urine output may happen over time so it may be overlooked
This chronic high pressure can lead to injuries in the lining of arteries
Compensatory mechanisms
-
Chronic hypertension can lead to injuries in the intima (inner lining) of blood vessels, which
results in an inflammatory response
Inflammatory response, vasodilation and capillary permeability further injury’s the lining of the
blood vessels
Result of the injury is hypertrophy and hyperplasia of the blood vessels, narrowing and increased
pressure
-
Hypertrophy and hyperplasia
Injury that may not reversible
Primary Hypertension
-
-
-
Primary (essential) is the most common
Contributing factors include
- Over-production of sodium intake and/or elevate serum lipids
- Greater than ideal body weight, obesity
- Diabetes mellitus
- Excessive alcohol intake
- Smoking
- Sedentary lifestyle
- Family history, ethnicity (black especially, needs early screening to prevent nephrotic
damage)
Clinical Manifestations
- Hypertension is a silent killer, signs appear very late
- At this point significant injury has occured
- Secondary signs are due to tissue and organ damage that have occurred over time
- Fatigue
- Reduced activity tolerance
- dizziness/palpitations (heart cannot manage it)
- Angina (chest pain)
- Dyspnea (shortness of breath)
Diagnostic studies
- Diagnosis is not based on a single elevated reading (white coat syndrome), but requires
multiple readings over several weeks
- Lab
-
-
-
Blood chemistry: potassium, sodium, BUN, creatinine , nitrogen levels (how well
kidneys are working)
- Lipid panel
- Fasting glucose (common in diabetes)
- Urinalysis
- ECG - assess heart rate and rhythm
Treatment
- Home BP monitoring (electronic BP machine at home)
- Especially if on medication because do not want hypotension and over correct
- Nutritional therapy
- Low sodium, low cholesterol and fat diet
- Adequate intake of potassium, magnesium and calcium
- Weight management
- Regular moderate activity - 30 minutes/daily
- Stop smoking
- Moderate alcohol consumption, 2 glass/week
- Stress management
Medications
- Diuretics: thiazides (category, ex. hydrochlorothiazide)
- Work by inhibiting the absorption of sodium (Na+) in the distal convoluted tubule in the
nephrons
- More sodium is secreted = more water is secreted
- Lowers fluid volume in vascular system = lower pressure
- Nursing considerations
- Monitor for orthostatic hypotension
- Monitor for hypokalemia (potassium loss with urination)
- Impacts digoxin = toxic
levels and hypokalemia
- Need to monitor,
can cause cardiac
arrest
- Loop diuretics: furosemide (lasix)
- Inhibits sodium reabsorption in the
loop of Henle = less water is
reabsorbed = increase urine output
- Nursing considerations
- Orthostatic hypotension
- Hypokalemia (monitor
electrolytes especially
potassium)
- Dehydration
- Potassium: sparing diuretics ex.
Spironolactone
-
-
-
-
Inhibits the effects of sodium and potassium excreting effects of aldosterone in
the distal tubule and collecting ducts
- Nursing considerations
- Orthostatic hypotension
- Hyperkalemia
- Not for renal failure patients
- Not appropriate as it will cause hyperkalemia
- Need to do pt. Teaching because diuretics usually recommend
increase in K+ in diet BUT not with this drug
Angiotensin converting enzyme (ACE) inhibitors:
captopril, lisinopril
- Prevents vasoconstriction but does NOT cause
vasodilation
- 5% of population gets chronic cough on this
medication
- Inhibit the conversion of angiotensin 1 to
angiotensin 2
- Prevents vasoconstriction in blood
vessels (keeping blood vessels open)
- No stimulation of aldosterone, some
fluid loss (water and sodium)
- Side effects: hypotension, frequent
cough, hyperkalemia
- Nursing considerations
- Monitor blood pressure
- Monitor potassium levels
- Monitor kidney function
Angiotensin 2 Receptor Blockers (Losartan,
Valsartan)
- Prevents angiotensin 2 from connecting
with blood vessels
- Prevents vasoconstriction = less
pressure
- Nursing considerations
- Monitor blood pressure
- Monitor for hyperkalemia
- Monitor kidney function
Beta Adrenergic Blockers (Carvedilol,
metoprolol)
- When hypertension the SNS may be overstimulated = chronic vasoconstriction
and increased heart rate
- Will block beta 1 receptors = decrease heart rate and reduce sympathetic
vasoconstrictive tone = decrease in pressure
- Nursing considerations
-
- Monitor heart rate and BP
- Risk for bronchospasm
- May exacerbate heart failure
- There are beta receptors in lungs, risk for
patients with asthma or COPD
Calcium channel blockers: amlodipine, felodipine
- Also diltiazem and verapamil
- Block the movement of calcium into the cells =
causing vasodilation and decreased systemic
vascular resistance (SVR)
- Nursing considerations
- Use with caution in patient with
HF
- Monitor for bradycardia (60 bpm)
- Abdominal discomfort (calcium
effects muscles)
- Peripheral edema, headache
(neurons are impacted)
Complications
- Hypertension is a major risk factor for coronary artery disease
- HTN contributes to atherosclerosis development which decreases blood flow to the myocardium
= angina
- Increases the risk for myocardial infarction (MI)
- Heart cells cannot regrow
- HTM also speeds up the process of atherosclerosis in the peripheral arteries, contributing to poor
perfusion
-
-
Increased risk of
- Aortic aneurysms (low chance of survival, needs to monitor and
intervene early)
- Peripheral artery disease
- Intermittent claudication, ischemic muscle pain precipitated by
activity and relieved with rest
- Not enough oxygen and glucose to muscles
Heart Failure
- The left ventricle of the heart has to
pump against the resistance in the
systemic arteries
- Elevated SBP require the ventricles to
work harder and harder and as results
the myocardium layer will
hypertrophy
- This weakens the heart’s ability to
pump and narrows the chamber of the
left ventricle = heart failure
- Chest pain and shortness of breath
- Failure leads to arrest
- Significant changes in ventricle cells, unlike skeletal
muscle the heart doesn’t get stronger with additional
weight and time so it must stay lean
- Nephrosclerosis
- HTN is one of the leading causes of end stage renal
disease (ESRD)
- The elevated pressure and atherosclerosis of renal
arteries damage the nephrons within the kidney, unable
to filter = more toxins in the bloodstream
- Earliest signs, microalbuminuria, presence of protein in
the urine
- Later signs, elevated BUN (fluctuates a little), serum creatinine (kidneys will
compensate) and microscopic hematuria (blood in urine that you cannot see)
- Stage 4 = dialysis, kidneys are great at compensating but then they just give up
- Retinal damage
- Elevated pressure and development of
atherosclerosis damage the blood vessels of the
retina and plaque formation
- Blurred vision, retinal hemorrhage
(increased pressure, significantly impacts
vision)
Patient Teaching
- Teach the patient what hypertension is
-
Although it can be asymptomatic there are long term consequences for poor management
Teach specific about medications (action, dosage, adverse reactions), critical importance of taking
medications as prescribed, no skipping dose (gentleman, erectile dysfunction due to less pressure)
Caution about the use of OTC medications, can increase BP (epinephrine, cough med, stimulants)
Teach nutritional therapy, low sodium, low fat diet
Taking high potassium foods if taking thiazide or loop diuretics (bananas, leafy greens spinach,
lentils, avocados, potatoes)
Monitor blood pressures at home (randomly throughout the day)
Stop smoking
Moderate exercise, 30 minutes/day
Stroke
Stroke
- Stroke or cerebrovascular accident (CVA) occurs due to
ischemia in parts of the brain or hemorrhage into the brain
- The brain cannot store oxygen and if blood flow is disrupted
then the cells of the brain become hypoxic and can die, as a
result brain function is impaired
- The severity of loss of function varies according to the
location and extent of the injury to the brain
Public Health
- An estimated 62,000 persons in Canada will suffer a stroke annually
- Over 13,000 deaths occur annually from stroke
- Third most common cause of death, behind heart disease and cancer
- The direct and indirect costs of strokes are estimated to be greater than $3.6 billion per year in
Canada
- More than 400,000 people are currently living with the effects of a stroke, leading cause of
disability in adults
Health Promotion
- Teach patients the importance of hypertension control and management
- Uncontrolled hypertension is the primary cause of stroke
- Diabetic patients develop atherosclerosis more quickly than general
population
- Control of glucose levels and activities to reduce the
development of cardiovascular complications is critical
- Teach everyone the signs of stroke
- Promote healthy active lifestyle (heart health)
Types of Strokes
- Ischemic: inadequate blood flow (blockage) to the brain
from partial or complete occlusion of an artery
- The majority of all strokes are ischemic stroke
- No perfusion to that part of brain past blockage
-
Hemorrhagic: result from bleeding into the brain tissue itself or into the subarachnoid space or
ventricles
- Increased intracranial pressure
- Vasoconstriction cause global issues throughout the brain
Risk Factors
- Modifiable factors
- Hypertension
- Diabetes mellitus
- Heart disease
- Increased serum cholesterol
- Heavy alcohol consumption
- Oral contraceptive use (DVT, clots, estrogen imbalance)
- Physical activity
- Smoking
- Substance abuse
- Obesity
- Non-modifiable factors
- Stroke risk increases with age, doubling each decade after 55 years of age
- ⅔ of all strokes occur in individuals >65 years of age
- Sex: men at high risk but as women age risk level increases
- Ethnicity and race
- heredity/family history (black due to hypertension)
- Personal circumstances (genetics)
- Arteriovenous malformation (circle of wilms)
Transient Ischemic Attack (TIA)
-
Temporary neurologic dysfunction from a brief interruption in cerebral blood flow
Can be caused by micro emboli or plaque that temporarily blocks an artery (partial occlusion)
Easy to ignore as symptoms are mild or resolve with 30-60 minutes
Symptoms include
- Visual deficits: blurred or double vision, tunnel vision or blindness in one eye (depends
on part of your brain affected)
- Motor deficits: weakness in arms, legs and hands, facial droop, ataxia
- Sensory perception: numbness (hands, face, arms, legs), vertigo
- Speech deficits: aphasia, dysarthria (slurred speech)
Assessment
- Initially assessment
- Vital signs, ABCs, focused neurological assessment
- Complete neurological workup along with an ECG and CT scan (embolism will
eventually end up in the left ventricle thus the ECG)
- TIA:
- Patients not at a higher risk for stroke requiring additional assessments
- MRI to assess carotid and cerebral arteries and brain tissues (more fine tuned tissues)
Treatment
- Reducing blood pressure (as appropriate)
- Aspirin or antiplatelet medication (as appropriate, risk for bleeding, age, if clots, need to stop or
slow down)
- Assessment of serum cholesterol and medications (as appropriate)
- Controlling diabetes and/or chronic illnesses
- Promoting healthy lifestyles:
- Smoking cessation
- Heart healthy diet
- Active lifestyle
- TIAs are a warning sign that a stroke could happen so we need to make changes
Ischemic Stroke
Pathophysiology
- Ischemic stroke results from inadequate blood flow to the brain from a partial or complete
occlusion of an artery
- Thrombotic stroke
- Occurs when a blood clot (thrombus) forms in a diseased or narrowed blood vessels in
the brain or brain stem
- If atherosclerosis is present in a blood vessel then the plaque narrows the vessel and is
often rough
- Platelets stick to the plaque and a clot can form rapidly = occludes the blood vessel
- As a result the cells do not receive oxygen and nutrients = hypoxia which can then
become anoxic = tissue death (necrosis)
- Two-thirds of thrombotic strokes are associated with hypertension or diabetes mellitus,
both of which accelerate atherosclerosis
- In 30-50% of individuals, thrombotic strokes have been preceded by a TIA
- Most patients with ischemic stroke do not have a decreased level of consciousness in the
first 24 hours, unless it is due to a brainstem stroke or other conditions such as seizures,
increased intracranial pressure (ICP), or hemorrhage
- Embolic stroke
- Occurs when an embolus lodges in and occludes a cerebral artery, resulting infarction and
edema in the area supplied by the artery
- Second most common cause of stroke
-
Majority of emboli originate in the heart and travel through the carotid arteries to the
brain
Valvular disease (blood moves back and forth) and irregular (heart shakes) heart rhythms
are primary causes of emboli (platelets stick)
Onset of embolic stroke is usually sudden and is characterized by severe neurological
deficits
Hemorrhagic Stroke
-
-
-
Hemorrhagic strokes account for 15% of all strokes
Results from bleeding into the brain tissue itself, the
subarachnoid space or the ventricles
Risk factors
- Hypertension
- Vascular malformations
- Coagulation disorders
- Trauma
- Tumors
- Aneurysms
Intracerebral Hemorrhage: bleeding into the brain
- Severe headache with nausea and vomiting
- Hemiparesis (weakness on one side of the body)
- Slurred speech
- Deviation of the eyes
- Abnormal body posturing
Subarachnoid hemorrhage: bleeding between the
arachnoid and pia mater membranes of the brain
- Commonly caused by rupture of cerebral
aneurysm
- LOC ranges from alert to comatose
(dependent on the size of vessel and where)
- Focal neurological deficits
- Nausea, vomiting, seizures
- Stiff neck (pressure)
Left vs Right Strokes
- Right brain affects L body and L brain affects R body
Clinical Manifestations
-
-
Clinical manifestations are related to
where in the brain the injury is occuring
- Motor function
- Communication
- Affect
- Intellectual function
- Spatial: perceptual alterations
- Elimination
Motor function
- Mobility impairment: weakness or
paralysis
- Hemiparesis: muscular weakness or partial paralysis restricted to one side of the
body
- Hemiplegia: total or partial paralysis of one side of the body that results from
disease or injury to the motor centers of the brain
- Impaired respiratory function (risk for bacterial/viral illness)
- Difficulty with speech and swallowing (aspiration)
- Impaired gag reflex
- Impaired self care abilities due to muscular weakness or hemiplegia (ADLs)
-
Communication
- Aphasia refers to the difficulty related to the comprehension or use of language
- Four categories
- Expressive: difficulty expressing thoughts through speech
- Receptive: difficulty understanding the spoken word
- Anomic/amnesic: difficulty finding the correct names or words
- Global: loss of all expressive and receptive abilities
- Many patients experience dysarthria: disturbance in the muscular control of speech
- Impairments may involve
- Pronunciation
- Articulation
- Phonation
- Affect
- Patients who suffer a stroke may have difficulty controlling their emotions
- Emotional responses may be exaggerated or unpredictable
- Depression and feelings associated with changes in body image and loss of function can
make this worse
- Intellectual function
- Both memory and judgement may be impaired as a result of stroke
- A left-brain stroke is more likely to result in memory problems related to language
- Tend to be more cautious in making judgements
- A right-brain stroke patient tends to be impulsive and to move quickly
- Both left and right side injuries can impact the patients’ ability to learn
- Break activities into steps
- Patients cannot comprehend stuff at a normal speed, may have to go slower
- Spatial: Perceptual Alterations
- Stroke on the right side of the brain is more likely to cause problems in spatial-perceptual
orientation
- Spatial-perceptual problems may be divided into four categories
- Deny illness or own body parts (anosognosia)
- Erroneous perception of self in space
- Inability to recognize an object by sight, touch or hearing (agnosia)
- Inability to carry out learned sequential movements on command (apraxia)
- GI/GU
- Most conditions with urinary and bowel elimination occur initially and are temporary
- When a stroke affects one hemisphere of the brain, the prognosis to regain normal
bladder function is excellent
- Although motor control of the bowel is usually not a problem, patients are frequently
constipated
- Constipation is associated with immobility, weak abdominal muscles, dehydration, and
diminished response to the defecation reflex
Diagnostics
- When symptoms of a stroke occur, diagnostic studies are done to
- Confirm that it is a stroke
- Identify the likely cause of the stroke
- Computed tomography (CT), non-contrast (because when you inject IV contrast it will increased
ICP)
- Magnetic resonance imaging (MRI)
- Other diagnostic tools
- Computed tomography angiography (CTA): blood flow through the brain
- Magnetic resonance angiography (MRA): blood flow through carotid and/or cerebral
arteries
- Transcranial doppler ultrasonography: noninvasive study that measures the velocity of
blood flow in the major cerebral arteries
- Lumbar puncture: blood in cerebrospinal fluid (CSF)
Assessment
- Airway, Breathing, Circulation
- Vital signs (_____ need to relisten)
- Conduct an initial neurological assessment
- Level of consciousness
- Complete GCS (under 8 you intubate the patient)
- Ability to move and follow commands
- Speech: facial drooping
- Pupils: visual assessment
- Obtain health history from patient or family
- Perform a full head to toe assessment
- Priority is to do a head CT
- Motor
- Compare one side of the body to the other
- Assess strength and the patients’ ability to follow commands
- Hands, arms, legs, feet
- Pronator drift, ability to stand and gait (if possible)
- Sensory
- Evaluates the patient’s response to touch, painful stimuli
- Assess for pain perception with a dull (cotton tip applicator) and sharp (needle,
blunt tip)
- Patient closes their eyes ask if the sensation is sharp or dull
- Gently tap on extremities asking about touch
- WHERE not do you feel this
- Visual
- Damages to the carotid artery can cause pupillary constriction or dilation
- Check pupils (PERRLA): pupil equal in size, round and regular in shape and
react to light and have accommodation
- Examine face for symmetry
- Ptosis (eyelid drooping)
- Hemianopsia, blindness in ½ the visual field, from injury to the optic nerve
- Pressure on nerve
- Need to know baseline for this
Treatment
Acute Treatment
- Frequent assessment of vital signs including pulse oximetry
- Place on heart monitor (rate and rhythm)
- Contact facility stroke team
- Establish IV access and infuse isotonic fluids (for medication)
- Obtain CT scan immediately
- Baseline lab, chemistry, CBC, random glucose, coagulation studies (PT, PTT, INR - bleed vs
thrombus, ischemic vs hemorrhage)
- Position the head midline and elevated the head of bed 30° (unless a spinal cord injury with
trauma, gravity will drain blood, herniation of brain stem especially)
- Keep the patient NPO
- Initiate seizure precautions (suction, O2, bed rails up, dentures out, gown)
- Remove dentures, clothing
Ischemic Stroke: Acute Care
- Must know the time the signs and symptoms of the stroke started
- Patients with ischemic stroke can receive thrombolytic therapy if they are within 4.5 hours of the
start of symptoms
- Recombinant tissue plasminogen activator (tPA), clot buster, used to re-establish perfusion in the
brain MUST meet specific criteria to be eligible
- Nothing can turn it off once it is administered (no antidote)
- Cannot be given if
- Post-op
- Blood disorders
- Ulcers
- Patient is already on blood thinner
- During infusion
- Frequent vital signs
- Hemorrhage from auto BP cuff, must do manually to have more control
- No anticoagulation or antiplatelet meds for 24 post treatment
- Close observation for any type of bleeding
- Number one area is the nose (epistaxis)
- Fresh frozen plasma
- Endovascular surgical intervention
- Vascular surgeon will thread a specialized
catheter into the artery, which hooks and
removes the blood clot, often a balloon at
the end of the catheter to prevent any clot
fragments from traveling through the
vasculature
- Main therapy is hypertensive management
- Oral and IV agents keep BP < 160 mmHg (anything above causes injury)
- BP is allowed to run a bit high to ensure brain perfusion initially
- Surgical therapy
-
Immediate evacuation of an aneurysm, induced
hematoma or cerebellar hematomas > 3 cm
- Craniotomy, the cranium is opened and hematoma is
removed
Hemorrhagic Stroke: Surgical Therapy
- Aneurysm treatment includes clipping or coiling
- Coiling is an endovascular procedure when a metal
coil is inserted into the lumen of vessel providing
protection against hemorrhage, eventually thrombus
forms and aneurysm is sealed off from the parent
vessel
- Aneurysm clipping the surgeon
- Opens a window of bone in the skull
- Isolates the blood vessel and aneurysm from the
surrounding brain tissue
- Places a metal clip across the aneurysm’s neck
- Replaces the bone and closes the incision
- The clip effectively cuts off blood flow from the artery to the
aneurysms
Post-Operative Care
- Patients who have had any surgical treatment for a stroke will require
extensive post-op care
- Frequent vital signs
- Frequent neurological assessment (q1h)
- Close monitoring for signs of infection (brain)
- Monitor and treat any fluid or electrolyte imbalances
- Prevent complications, postoperative pneumonia, DVT, pressure injuries
- When stable, initiate rehabilitative therapies
- Regain ADLs, learn to use assistive devices
Acute Care
- Hypertension is common immediately after stroke
- Medications to lower BP are used only if BP is markedly increased
- The fluid and electrolyte balance must be controlled carefully
- Adequate hydration promotes perfusion and decreases further brain injury
- Interventions: Ongoing
- Monitor vital signs and neurological status
- Level of consciousness
- Motor and sensory function
- Pupil size and reactivity
- O2 saturation (supplemental oxygen, need to get oxygenated blood to brain)
- Cardiac rhythm
Complications
ICP
-
Monitoring for increased intracranial pressure (ICP) which can result from edema in the brain,
especially the first 72 hours post CVA
- More ICP the more cell damage
- Reassess these patients q1-4 h depending on the severity of the stroke
- Signs and symptoms
- First sign is a decreased in LOC
- Headache, nausea, vomiting
- Changes in speech
- Changes in sensorimotor status (pupillary constriction, cranial nerve dysfunction,
ataxia)
- Seizures
Ongoing Assessments and Interventions
- Respiratory (autonomic nervous system is in the brainstem)
- Frequent respiratory assessment
- Encourage deep breathing and coughing
- Incentive spirometry (as appropriate)
- Increased risk of aspiration due to impaired LOC or dysphagia
- Aspiration precautions
- Cardiovascular
- Frequent vital signs, close BP monitoring (keep pressure reasonable)
- Medications to reduce hypertension
- Monitor fluid status
- Assess extremities for edema (do not overhydrate)
- I&O, daily weight
- Monitor perfusion in extremities
- Capillary refill, skin colour and temperature
- Risk
- Nervous system
- Frequent neurological assessment
- LOC (mental status)
- Pupillary responses
- Extremity movement and strength
- Glasgow coma scale (neuro status)
- Canadian neurological scale
- Designed to evaluate stroke patients
- Monitor for increased intracranial pressure (ICP)
- Decreased LOC = increased ICP, raised head of bed 30°
- Musculoskeletal
- Assess the patient’s muscle tone for strength, compare right vs left
- Interventions
- Range of motion exercises, proper body alignment in bed and with activity
- Splints to maintain alignment, physical therapy and occupational therapy consults
- Promote independence as possible
- Sensory: evaluates the patient’s response to touch, painful stimuli
-
-
-
-
-
-
Assess for pain perception with a dull (cotton tip applicator) and sharp (needle,
blunt)
Interventions: provide a safe environment, monitor external temperature
Integumentary
- Skin assessment daily and PRN
- Interventions:
- Position changes q2h and PRN
- Proper use of pressure relieving devices
- Provide good skin hygiene
- Promote early mobility
- Monitor for pressure injury development
Gastrointestinal
- Perform abdominal assessment
- Common complication constipation
- Assess fluid balance (in vs out)
- Increase fiber intake
- Ambulation promotes regularity
- Stool softeners or laxatives as appropriate
Urinary
- Acute: indwelling urinary catheter (increases risk of infection)
- Promote normal bladder function
- Intermittent catheterization
- Bladder retraining program
- Toileting q2h
- Monitor intake and output
- Monitor daily weight
Nutrition
- Acute care: may receive IV fluids and electrolytes until stable
- Impaired swallow and/or gag reflex, enteral or parenteral nutrition
- Bedside study by nurse, assess ability to sip 3 tbsp of water
- Speech therapist to conduct swallow study
- Diet based on patient’s ability to swallow
- If impaired, pureed food and/or thickened liquids
- Aspiration precautions
- Do not rush patients, PSW may feed some patients
Communication
- Assessment of patient’s ability to understand and speak
- Nurse to speak slowly and calmly, normal tone of voice
- Use simple words or sentences
- Use yes or no questions
- Can mimic or use gestures as appropriate
- Allow time for the patient to process information and give a response
- Use touch as a way to express feelings
- Follow a routine as possible
- Aphasia worsens with fatigue, have patient, allow rest
- Sensory Perceptual Alterations
- Visual disturbances
- Arrange environment, placing objects within visual field (biggest issue is falls)
- Create a self environment
- Close observation of patient (line of sight)
- Use of sitter or family member
- Bed alarms and bed rails x 3
- Teach to rise slowly
- Implement safety measure, call don’t fall
- Coping
- Stroke can impact the whole family, emotionally, socially, and financially
- Can result in changing roles and responsibilities
- Teach the patient and family, use therapeutic communication techniques
- What has happened, diagnosis
- Therapeutic procedures
- Prognosis
- Arrange for community and healthcare supports
- Medications for depression as necessary
Community Based Care
- Skilled nursing unit: assist with ADLs and supervision to prevent injury or accidents
- Rehabilitation facility: receive additional nursing care plus OT and PT
- Teach the use of adaptive equipment, cane, walker, larger utensils
- Home: topics related to patient safety
- Free from scattered rugs and obstacles in pathways
- Grab bars in bathroom, non skid surfaces in shower and bath
- Training and use of assistive devices as needed
- Modification of the home (ramp or larger doors)
- Medications, following prescriptions
Lecture 10 - Respiratory Disorders
Respiratory System Physiology
- Respiratory system functions primarily to maintain the exchange of oxygen and carbon dioxide in
the lungs and tissues
- Ventilation and Perfusion (V/Q ratio)
- Ventilation (V) is the movement of air into and out of the lungs
- Air must reach the alveoli to be available for gas exchange
- Perfusion (Q) is the filling of the pulmonary capillaries with blood
- Adequate gas exchange depends on an adequate V/Q ratio, a match of ventilation
and perfusion
- Nose → larynx → epiglottis → trachea → bronchi (2) → bronchioles → alveoli (exchange gas)
Respiratory Assessment
- Subjective
-
History
- Current health status and respiratory risk factors
- Smoking (tobacco/cannabis): mucus, carbon, can damage alveoli
- Occupations (construction, dust + debris, asbestos, mine, firefighters, nail
salons, clowns, drag)
- Auscultation (clothing, breast/fatty tissue, bone)
- Use of accessory muscles and/or signs of respiratory distress
- Higher up retractions are more concerning
- Tracheal tug, xiphoid process, nasal flaring, tripod position
- Vital signs
- SPO2
- Respiration rate
- Objective
- Normal breath sounds
- Vesicular (peripherally)
- Bronchial (centrally)
- Abnormal (adventitious)breath/sounds
- Wheezing (inflammation, narrowing, obstruction partial, mucus, ventilation
issue)
- Stridor/rub (turbulence in airway or friction within pleural space there is
lubricant, stridor is not enough)
- Crackles (fluid in lungs, COPD, pneumonia)
- Absent (full obstruction, collapsed lung)
- Physical assessment
- Auscultation
- Breathing patterns
- Symmetry
- Vital signs
- skin/nail beds (appropriate for ethnicity, hair on peripheries, not clubbing,
pink/moist mucous membranes, no cyanosis, peripheral less concerning than
central)
Diagnostic Tests
- Pulmonary function tests (especially COPD)
- Arterial blood gases (oxygen in arteries, SPO2 is oxygen in capillaries)
- Sputum tests (infection, antibiotic resistance decreased, especially TB)
- Chest x-ray (pneumothorax, fibrosis [TB, COVID], fluid accumulation, rib fractures, heart bigger
for compensation)
- Computer tomography (CT)
- Magnetic resonance imaging (MRI)
- Fluoroscopic studies and angiography
- Radioisotope procedures (lung scans - cancer)
- Bronchoscopy and Thoracoscopy (camera)
- Thoracentesis (fluid in lungs or extra air)
- Biopsies
Pulse Oximetry
- A noninvasive method to monitor the oxygen saturation of the blood
- Normal level is 95-100%
- Hypoxia (not enough oxygen in the tissues)
- Hypoxemia (not enough O2 in blood)
- Heart and brain need blood
Nursing Care of Patients with Upper Airway Disorders
- Upper airway disorders may be minor and treated outside of the health care setting, or they may
be severe and life-threatening
- Require good assessment skills, an understanding of the variety of disorders that affect the upper
airway, and the impact that those disorders may have on the patient
- Patient teaching is an important aspect of care
Tuberculosis (TB)
History of TB
- TB has affected humans for millennia
- Historically known by
- Consumption, wasting disease, white plague
- TB was a death scene for many
- Until mid-1800s, many believed that TB was hereditary (intergenerational housing, physically
small spaces)
- 1865 Jean Antonie-Villemin showed TB was contagious (airborne)
- 1882 Robert Koch discovered M. tuberculosis
- Sanatoriums
- Before TB antibiotics, many patients were sent to sanatoriums (if they could afford it so
only the rich)
- Patients followed a regimen of bed rest, open air, sunshine
- TB patients who could not afford sanatoriums often died at home
- Drugs that could kill TB bacteria were discovered in 1940s and 1950s
- Streptomycin (SM) discovered in 1943 (antibiotic of choice, TB rates decreased
significantly)
- Isoniazid (INH) and p-aminosalicylic acid (PAS) discovered between 1943 and 1952
- TB death rates in US/Canada began to drop dramatically
- Each year, fewer people died from TB
- Most TB sanatoriums in US/Canada had closed by mid 1970s
- Increased in TB in mid 1980s
- Contributing factors
- Inadequate funding for TB control programs
- HIV epidemic (immunocompromised)
- Increased immigration from countries where TB is common
- Spread of TB in homeless shelters and correctional facilities
- Increase and spread of multidrug-resistant TB
Transmission
-
-
TB is spread person to person through the air via droplet nuclei
M. tuberculosis may be expelled when an infectious person
- Cough, speaks, signs
Transmission occurs when another person inhales droplet nuclei
Probability that TB will be transmitted depends on
- Infectiousness of the TB patient (active can spread, latent no probs)
- Environment in which the exposure occurred
- Frequency and duration of the exposure
- Susceptibility (immune status) of the exposed individual
- The best way to stop transmission
- Isolate infectious persons
- Provide treatment to infectious persons as soon as possible
Latent TB Infection (LTBI)
- Goal of TB management is to get it to latent
- LTBI occurs when tubercle bacilli are in the body, but the immune system is keeping them under
control
- LTBI is detected by the Mantoux tuberculin skin test (TST, intradermal injection looking
induration, >10mm = +ve then chest x-ray then culture) or by an interferon-gamma release assay
(IGRA), such as:
- QuantiFERON-TB Gold In-Tube (QFT-GIT)
- T-Spot.TB test (T-SPOT)
- To prove latency: +ve mantoux, scarring of the lungs, -ve sputum culture
- People with LTBI are not infectious
TB Disease
- TB disease develops when the immune system cannot keep tubercle bacilli under control
- May develop very soon after infection or many years after infection
- About 10% of all people with normal immune systems who have LTBI will develop TB disease at
some point in their lives
- People with TB disease are often infectious
People at High Risk for Exposure to or Infection with M. tuberculosis
- People who have come to Canada within the last 5 years from areas of the world where TB is
common
- People who visit areas with a high prevalence of TB disease
-
People who live or work in high-risk congregate settings
- Correctional facilities
- Homeless shelters
- Nursing homes
- Healthcare facilities
- Healthcare workers who serve patients at increased risk (especially northern communities)
High-Risk Groups for TB Infection
- Populations defined locally
- Low-income is linked to higher risk of TB exposure
- Possible reasons include factors associated with low income
- Inadequate living conditions
- Crowding
- TB rates are 10 times higher for people experiencing homelessness
Infectiousness
- Infectiousness is directly related to number of tubercle bacilli TB patients expel into air
- TB patients generally expel more tubercle bacilli if their cough produces a lot of sputum
- Only people with TB of the lungs, airways, or larynx are infectious
- Factors generally associated with infectiousness
- Presence of cough
- Cavity in the lung (fibrosis)
- Acid-fast bacilli on sputum smear
- TB of lungs, airway or larynx
- Not covering mouth when coughing
- Not receiving adequate treatment or prolonged illness
- Undergoing cough inducing procedures
- Infectiousness appears to rapidly decline after adequate treatment is started however
- How quickly infectiousness declines varies from patient to patient (weeks to months)
- Patients with drug-resistant TB may not respond to initial drug regimen
- Meaning they may remain infectious for longer
- Drugs are also hard on the liver so you may not be able to drink
- Patients can be considered non-infectious when they meet all of the following criteria:
- Received adequate treatment for 2 weeks or longer
- Symptoms have improved
- Three consecutive negative sputum smears from sputum collected in 8-24 hour intervals
(at least one early morning specimen)
TB Infection Control Program
- Main goals of a TB infection-control program are to ensure early and prompt (has to be reported
to public health)
- Detection of TB disease
- Airborne precautions (e.g., isolation of people who have or are suspected of having TB
disease)
- Treatment of people who have or are suspected of having TB disease
- Detection of TB Disease
- HCWs should suspect TB disease in anyone with any of these symptoms
- Persistent cough
- Chest pain
- Bloody sputum (never normal, could be related to cancer)
- Weight loss or loss of appetite
- Fever
- Chills
- Night sweats
- When a healthcare worker suspects that a patient has TB disease, the patient should be
- Placed in an area away from other patients and evaluated
- Given a surgical mask to wear
- Given tissues and asked to cover nose and mouth when coughing or sneezing
- Airborne Precautions
- Airborne precautions should be taken for any person who has signs or symptoms of TB
disease
- If facility has a ventilation room, TB suspects and TB patients should be placed there
- Healthcare settings, such as TB clinics, should implement a respiratory-protection
program
Management
- Most patients can be treated on outpatient basis (direct observational therapy ensures compliance
with meds)
- Hospitalization maybe needed for the severely ill patients
- Mainstay (basis) is drug therapy
- Monitoring for complications is a key for successful treatment
- Difficulty breathing, low O2 saturation, bloody sputum
- Avoid hepatic meds, alcohol, tylenol
Medical management
- Treated primarily with chemotherapeutic agents (antituberculosis agents) for 6-12 months
- A prolonged treatment duration is necessary to ensure eradication of the organisms and to prevent
relapse
- A worldwide concern and challenge in TB therapy is the continuing (since the 1950s) and
increasing resistance of M. tuberculosis to TB management
Chronic Obstructive Pulmonary Disease (COPD)
- Incurable, need to quit smoking
- You cannot reverse damage from smoking
Cardinal Symptoms
- Dyspnea
- Shortness of breath (SOB)
- Limitations in activity
- All of their energy goes to breathing
- Cannot complete ADLs
- Insidious in onset and progressive
Advanced Symptoms
-
Initially confined to lungs
Skeletal muscle dysfunction
Right-sided heart failure
- Cannot keep up with hypoxia
- Secondary polycythemia
- Increased RBCs causing thickened blood and microclots
- Depression
- Altered nutrition
- All energy goes to O2
- Lose weight rapidly because it goes to lungs
Other Causes
- Occupational chemicals and dusts (ie: mining and asbestos, tobacco, dust)
- Recurrent infections make bronchioles/alveoli more susceptible to injury (HIV, TB)
- Maybe genetic factors
AI- Antitrypsin Deficiency
- Genetic abnormality that leads to COPD
- Condition in which the body does not make enough of AAT, a protein that protects the lungs and
liver from damage
Aging (relisten to this slide*******)
- Changes in lung structure and respiratory muscles cause gradual loss of elastic recoil
- Lungs become smaller and stiffer
- Loss of alveolar structure/functional alveoli
- osteoporosis/calcification
- Increase work of breathing
Pathophysiology
- Chronic inflammation airways, lung parenchyma, lung blood vessels
- Airflow limitations during forced exhalation caused by loss of elastic recoil
- Airway obstruction caused by mucus hypersecretion, mucosal edema and bronchospasm
- Not only hyperinflammation but also hypersecretion
- Ventilation issue but can also be perfusion
Pulmonary Vascular Changes
- Pulmonary hypertension
- Compensates causing weakened arteries
-
Body puts more pressure in the pulmonary artery so it can get more blood to lungs to get
oxygenated
- Pulmonary arteries undergo vasoconstriction and thickening of walls in response to hypoxemia
- We do
- Hypertrophy right ventricle
- We don’t have oxygen supply
- Cor pulmonale (right sided heart failure)
Emphysema vs Chronic Bronchitis
- COPD was previously classified as one or other, now COPD had elements of both
- Emphysema (perfusion)
- Destruction of alveoli
- Warm undertone, secondary polycythemia common to see here, increased hematocrit
- “Pink puffers”
- Alveoli are effected and destroyed
- No mucus production
- Right ventricle gets bigger
- Chronic bronchitis (ventilation)
- Presence chronic productive cough x 3 months in 2 years
- “Blue bloaters”
- Right sided heart failure
- A lot of work due to mucus
- Bloated = peripheral edema
- Daily weights are important
- A lot of mucus
Clinical Manifestations
- Asthma and COPD (age) cause diagnostic confusion
- Patient may have both
- See table 31-12 for comparison of clinical features
COPD Symptoms: Early
- Cough, sputum production or dyspnea
- History of smoking or risk exposure
- Intermittent cough in morning with small amount
- Productive “winter cough” x three months (especially in morning)
- Dyspnea on exertion
COPD Symptoms Progressive
- Dyspnea more severe, at rest
- Anxiety
- As more alveoli become distended, trapping air, hyperinflation, diaphragm flattens and AP
diameter of chest increases, “barrel shape,” AP ratio 1:1, ratio normal 5:7
- Weight loss despite adequate caloric intake
- Fatigue that affects ADLs
- Getting ready in the morning
Physical Examination
- Prolonged expiratory phase
- Wheezes (bronchitis) and decreased BS (emphysema) or combination of both
- Tripod position
- Pursed-lip breathing (helps expel extra CO2, may be autonomic or taught by therapist)
- Accessory muscle use neck to aid with inspiration (very common)
- Ankle edema (right sided heart failure)
- Bluish-red colour (cyanosis/polycythemia)
Normal ABG Values
pH 7.35-7.45
PaO2 80-100 mmHg
O2 Saturation > or = 95%
PaCO2 35-45 mmHg
Bicarbonate HCO3 21028 mmol/L