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  1. 1. Disturbances in Inflammatory and Immunologic Process Ma. Tosca Cybil A. Torres, RN
  2. 2. Objectives: At the end of varied teaching and learning activities, the students should be able to: 1. Define related terms: 2. Recall briefly the components and functions of the immune system and the immune response 3. Use assessment parameters appropriate for determining status of clients’ immune system 4. Identify abnormal findings that may indicate impairment in immune function. 5. State the purpose and nature of specific diagnostic procedures Given a situation: 1. Formulate appropriate nursing diagnosis given a set of cues. 2. Use the nursing process as a framework to provide individualized care to clients with altered immune response. Given an actual client in the hospital or community the students should: 1. State the nature, purpose and significance of immunization. 2. Observe the universal precautions when caring for immunocompromised client. 3. Integrate the Dominican teachings on compassion for humanity and demonstrate caring attitude towards the clients.
  3. 3. Definition of terms: • Immune system- group of cells, molecules, and organs that act together to defend the body against foreign invaders that may cause disease such as bacteria, viruses or fungi. • Immunology- the study of our protection from foreign macromolecules or invading microorganisms and our responses to them. • Immunity- ability to resist damage from foreign substances. • Antigen – any molecules that trigger an immune response; a protein that stimulates an immune reaction, causing the production of antibodies. • Antibodies- proteins that fight infections; a globulin produced by B cells as a defense mechanism against foreign materials.
  4. 4. Definition of terms: • Epidemiology – study of how disease is produced, and its distribution in a given population. • Pathogens – microorganisms or proteinaceous substances capable of producing disease. • Virulence – Ability to cause diseases • Nosocomial infections – acquired in a health care setting • Immunocompetent – client whose immune system is able to identify antigens and effectively destroy or remove them. • Immunocompromised - client whose immune system is unable to effectively destroy or remove antigens • Mast cells- tissue cells that resemble a peripheral blood basophil and that contains granules with chemical mediators.
  5. 5. Functions of the immune system: • Defend and protect the body from infection by bacteria, viruses, fungi and parasites. • Removing and destroying damaged or dead cells. • Identifying and destroying malignant cells, thereby preventing their further development into tumors.
  6. 6. Development of cells in the immune system Lymphoblasts Suppressor T- cells
  7. 7. Immune response • Recognition of self and non-self • Antigens • Antibody mediated response (humoral) – produced by B lymphocytes • Cell-mediated response – produced by T lymphocytes. 2 Major Classes of T cells – Effector Cells • Cytotoxic cells (killer T cells) – Regulator Cells • Helper T cells (Majority)- amplify activity of killer T cells • Suppressor T cells
  8. 8. Immune System Components 1. Leukocytes 1. Engulf and destroy pathogens (bacteria) 2. Suppress inflammation 3. Fight parasitic infections 4. Produce antibodies and provide immunity a. Granulocytes- immediate response to cell injury • Neutrophils- phagocytic, first cell to site of cell injury • Eosinophils- hypersensitivity reaction • Basophil-inflammatory response b. Agranulocytes- fight infection • Monocytes – phagocytosis • Lymphocytes- production of immunoglobulins
  9. 9. Immunoglobulin Characteristics And Functions Percentage Class Characteristics and Functions of Total IgG 75% in blood, lymph, and intestines Found Active against bacteria, its toxins and viruses Enhances phagocytosis, crosses placenta and is active in a second response IgA 10-15% Saliva, tears, bronchial, GI, prostatic and vaginal secretions Provides local protection on exposed mucous membrane surfaces and potent antiviral activity Prevents absorption of antigens from food, and protects against respiratory, GI, and GU infections IgM 5-10% decrease during stress Levels Found in blood and lymph First antibody produced with primary immune response High concentrations early in infection, decrease within about a week IgD <1% function, found in blood and lymph Unknown on mast cells and basophils Found IgE <0.1% Involved in immediate hypersensitivity response
  10. 10. Immune System Components 2. The lymphoid system - Lymph nodes - Spleen - Thymus - Bone marrow
  11. 11. Nonspecific inflammatory response - mechanical barriers that cover the body surfaces and to cells and chemicals that act on the initial battlefronts to protect the body from invading pathogens • surface membrane barrier- the first line of defense of the body is an intact skin and mucous membranes • Chemical barriers- acidic gastric juices, enzymes in tears and saliva, sebaceous and sweat secretions • Biologic response modifiers- interferon, a viricidal substance, counters viruses and activates other components of the immune system • Natural killer (NK) cells- lymphocytes responsible for immune surveillance and host resistance to infection • Inflammation – Three stages of inflammatory response: • Vascular response characterized by vasodilation and increased permeability of blood. • Cellular response and phagocytosis • Tissue repair
  12. 12. Three stages of inflammatory response: 1. Vascular response characterized by vasodilation and increased permeability of blood. – Major chemical mediators: 1. Histamine – vasodilation and increased capillary permeability, producing tissue redness, warmth and edema. 2. Kinins 3. Prostaglandins Fluid exudate- fluid that escape from the site of injury  Serous - mild  Sanguineous/serosanguineous- moderate to severe  Fibrinous  Purulent exudate – severe or chronic 2. Cellular response and phagocytosis 3. Tissue repair
  13. 13. Specific Immune Response - A type of immunity effective against specific harmful agents entering the body Types: a. Inborn immunity- inherited immunity of species, races , and individuals to certain diseases b. Acquired immunity- immunity that develops as an individual encounters specific harmful agents. a. Natural- activated by afffected individual a. Active- contact with the disease b. Passive- placenta, breastmilk b. Artificial – activated by vaccine a. active- vaccine: killed, attenuated, toxoid b. passive- immune serum
  14. 14. Assessment of the Immune System • Biographic data • Focused interview - Sensitive in nature – Health Perception-Health management • Perception of general health • Recent illness or changes in health status • Past illness/hospitalizations – BT? Organ transplant? Tissue transplant? – Transfusion reaction? • Allergies • Immunization status • Screening tests. • Occupation • Current medication • Recreational drug use.
  15. 15. Assessment of the Immune System 2 • Focused interview – Nutritional-Metabolic • Usual diet • Recent weight change • Skin lesion, rashes, impaired healing – Activity-exercise • Client’s exercise tolerance and any complaints of excessive unusual fatigue or weakness. • Frequent sore throats or upper respiratory illness • Swollen glands in the neck axilla or groin • Easy bruising or excessive bleeding from injuries or gums
  16. 16. Assessment of the Immune System 3 • Focused interview – Role-Relationship & Sexuality-Reproductive • Living situation including s.o • Sexual relations and practices • Number of sexual partners and their gender. • Specific risk behaviors e.g. anal intercourse • Barrier protection used – Value belief
  17. 17. Physical Assessment • General appearance – Height, weight, ease of movement, evident stiffness, v/s • Skin • Head and neck • Eyes and ears • Respiratory system • CV system • GI System • Urinary system • Nervous system • Musculoskeletal system
  18. 18. Acute Inflammation • Short term reaction • Last <1-2 weeks Chronic Inflammation Slower in onset Occurs over months or years
  19. 19. CAUSES of Inflammation • Mechanical Injuries • Physical damage e.g. burns • Chemical injury from toxins or poisons • Microorganisms • Extremes of heat and cold • Immunologic response e.g. hypersensitivity reaction • Ischemia damage such as stroke or MI
  20. 20. CARDINAL SIGNS OF INFLAMMATION • Erythema • Local heat • Swelling • Pain • Loss of function SYSTEMIC MANIFESTATIONS • T->38C or <36C • P->90/min • R->20/min • WBC- >12,000/mm3 • Enlarged lymph nodes • Loss of Appetite • Fatigue
  21. 21. Factors that may impair healing Factors Effect Malnutrition Protein deficient Prolongs inflammation and impairs healing process Carbohydrates and Impairs metabolic process; proteins are kilocalorie deficient used for energy rather than healing Vitamin deficits Vit. A Limits epithelialization and capillary formation B-complex Inhibits enzymatic reaction that contributes to wound healing Vit. C Impairs collagen synthesis Tissue Hypoxia Associated with an increase risk of infection and impaired healing Impaired blood supply Inadequate delivery of Oxygen and nutrients
  22. 22. Pharmacology • Acetaminophen (Tylenol) – reduces fever and pain – has no anti-inflammatory effect. • Anti-inflammatory Meds 3 GROUPS – Salicylates – NSAID ex. Diclofenac Na (Voltaren), Ibuprofen (Advil), Indomethacin (Indocin), Ketorolac Tromethamine (Toradol) – for pain management only, Naproxen (Naprosyn) – Corticosteroids
  23. 23. Chain of Infection 1 6 Etiologic Susceptible Agent host (microorganism) 5 2 Portal of Entry Reservoir to (Source) susceptible host 4 3 Method of Portal of exit transmission from reservoir
  24. 24. Pathogens • Bacteria – Aerobic – Anaerobic • Viruses - intracellular parasite capable of reproducing outside of a living cell. • Mycoplasma – similar to bacteria and have no cell wall – resistant to antibiotics that inhibit cell wall synthesis • Rickettsiae & Chlamydia- rigid cell wall; with some feature of both bacteria and viruses. – Chlamydia- transmitted by direct contact – Rickettsiae- infect cells of arthropods and are transmitted by these vectors. • Fungi- self-limited, affecting the skin and subcutaneous tissue. • Parasites
  25. 25. Reservoir • -where the pathogen lives and multiplies – Endogenous – Exogenous • Mode of Transmission – Direct contact – Indirect contact • Vector – Droplet or airborne transmission
  26. 26. Host Factors Factors that enable a host to resist infections: • Physical barriers • Hostile environment created by stomach acid secretions, urine & vaginal secretions. • Antimicrobial factors e.g. saliva, tears • Respiratory defenses • Specific and nonspecific immune responses to pathogenic invasion. • Age • Nutrition
  27. 27. Portal of Entry • Respiratory Tract • GI Tract • Genitourinary Tract • Skin and mucous membrane • Bloodstream
  28. 28. Stages of Infectious Process • Incubation period – period begins with active replication but with no symptoms • Prodromal stage – Symptoms first appear • Acute phase – proliferation and dissemination of pathogens • Convalescent stage- containment of infection and pathogens are eliminated • Resolution – total elimination of pathogens without residual manifestation Nosocomial infection – Infection acquired in a health care setting. – Typically manifest after 48 hrs. – UTI most common type
  29. 29. Gerontologic Consideration • Cardiovascular changes • Respiratory system changes • Loss of muscle tone • Gastrointestinal system changes • Skin and subcutaneous changes • Slowed or impaired healing process. FACTORS THAT MAY CONTRIBUTE TO INCREASED RISK FOR INFECTIOUS DISEASE: • Decreased activity level • Poor nutrition • Chronic disease • Hospitalization • Presence of invasive device
  30. 30. Standard precautions • Blood • All body fluids, secretions, excretions, • Non-intact skin • Mucous membranes Essential elements: • Use barrier protection • Prevent inadvertent percutaneous exposure, dispose of needles • Immediate and thorough hand washing
  31. 31. Pharmacology • Check for: – History of hypersensitivity. – Age and childbearing status of the client. – Renal function – Hepatic function – Site of infection • Classification of antimicrobial preparations: – Bacteriostatic – Bactericidal
  32. 32. Five Basic Mechanisms of antimicrobial agents: • Impairing cell wall synthesis, leading to lysis and cell destruction. • Protein synthesis inhibition, impairing microbial function • Altering the permeability of the cell membrane, causing intracellular contents to leak. • Inhibiting the synthesis of nucleic acids • Inhibiting other specific biochemical pathways of the organism.
  33. 33. Classification of Antimicrobials: • Antibiotics – Penicillins • Amoxicillin (Amoxil) Piperacillin (Pipracil) • Ampicillin (Ampicin, Polycillin) Oxacillin (Prostaphlin) • Nafcillin (Unipen) • Amoxicillin and Potassium Clavulanate (Augmentin) – Cephalosporins • Cephalothin (Keflin) Ceftriaxone (Rocephin) • Cefazolin (Ancef) Ceftazidime (Fortaz) • Cefaclor (Ceclor) Cefotaxime (Claforan) – Aminoglycosides • Amikacin (Amikin,Nica) Tobramysin (Nebcin) • Gentamycin (Garamycin) Streptomycin (Stepolin) – Tetracyclines • Doxycycline (Vibramycin) Oxytetracycline (Terramycin) • Minocycline HCl (Minocin) – Erythromycin • Erythromycin (E mycin, Ilosone,Erythrocin)
  34. 34. Antiviral • Amantidine (Symmetrel) – Influenza • Acyclovir (Zovirax) • Ganciclovir (Cytovene) – Herpes virus • Zidovudine (AZT, Retrovir) – HIV • Interferons – Rhinovirus (URI) – HPV Antifungal – Amphotericin B (Fungizone) – Fluoconazole (Diflucan) Antiparasitic – Quinine – Chloroquine (Aralen, Chlorocon) – Metronidazole (Flagyl)
  35. 35. Hypersensitivity Reaction • Altered immune response to an antigen that results in harm to the client CLASSIFICATIONS • Immediate – Type I (anaphylactic )reactions- mediated by IgE antibody, which promotes the release of histamine and other reactive mediators – Type II (cytotoxic) reactions – mediated by IgM and IgG antibodies, which attach to cells and cause cell lysis – Type III (immune complex) reactions- (rheumatoid arthritis) mediated by antigen-antibody complexes that deposit in the lining of blood vessels or on tissue surfaces • Delayed response – Type IV (delayed hypersensitivity) reactions (transplant rejection) are mediated by lymphokines released from sensitized T lymphocytes
  36. 36. Chemical Mediators of Immediate Hypersensitivity reactions • Histamine • Leukotrienes- potent bronchoconstrictor, cause increased venous permeability • Prostaglandins- potent vasodilators and potent bronchoconstrictors • Cytokines- control and/or regulate immunologic functions • Platelet-activating Factor- causes platelet aggregation
  37. 37. Effects of Chemical Mediators 1. Generalized vasodilation, hypotension, flushing. 2. Increased permeability 1. Capillaries of the skin 2. Mucous membrane 3. Smooth muscle contraction 1. Bronchioles 2. Intestines 4. Increased secretions 1. Nasal mucous glands 2. Bronchioles 3. GI 4. Lacrimal 5. Salivary 5. Pruritus 1. Skin 2. Mucous membrane
  38. 38. Asthma • Intermittent and reversible airflow obstruction affecting only the airways, not the alveoli. Occurs in two ways: 1. Inflammation 2. Airway hyperresponsiveness Inflammation Triggered by: Specific allergens Non-allergenic – cold air, dry air, microorganisms Airway hyperresponsiveness may be: Exercise Upper respiratory illness
  39. 39. • Histamine is generated by white blood cells called basophil or mast cells, and is released in allergic reactions. In this false- color electron micrograph of a mast cell, histamine can be seen as red granules on the yellow cell cytoplasm.
  40. 40. Causes of Asthma • The dust mite is a microscopic arthropod that lives in human homes, where it feeds on the dust produced by human and animal skin. • People with pollen allergies may be helped by staying indoors during the midday and afternoon—the times when pollen concentrations are highest. • Pollution • pet hair or cigarette smoke • perfume, hairspray, cosmetics, and household • Intense emotion, such as crying, shouting, or laughing Classic symptoms: • wheezing, coughing, and shortness of breath.
  41. 41. Pathophysiology of Asthma Stimulus Chemical mediator release Bronchospasm Inflammatory cell activation Edema Increased mucus Epithelial damage production Increased airway resistance, obstruction and airflow limitation Acute asthma attack
  42. 42. Diagnostic Test • Skin Testing – Epicutaneous – Intradermal • Radioallergosorbent Test (RAST) TREATMENT MODALITIES: Immunotherapy (desensitization) - indicated for allergic rhinitis and asthma
  43. 43. Anaphylaxis Response that occurs in highly sensitive persons following injection of specific antigen ETIOLOGY:  Immunotherapy  Stinging insects  Skin Testing  Medications  Food  Exercise  Latex
  44. 44. TYPICAL MANIFESTATIONS: Uneasiness Lightheadedness Itching palms and scalp Hives Localized tissue swelling Uvula and larynx swelling Hypotension, tachycardia & syncope
  45. 45. Severe Reaction of Anaphylaxis • Air hunger • Stridor • Wheezing • Barking cough • Anaphylactic shock IMMEDIATE TREATMENT!!:
  46. 46. Assessment • ABC • VS, Degree of respiratory distress • History of onset of symptoms and of exposure to allergen DIAGNOSIS: 1. Impaired breathing pattern 2. Decreased cardiac output 3. Anxiety
  47. 47. Nursing Interventions • Restore effective breathing • Increase cardiac output • Reduce anxiety • Patient education and home maintenance
  48. 48. Allergic rhinitis Manifestations 1. Nasal- mucous membrane congestion, edema, itching, sneezing 2. Eyes- edema, itching, tearing, redness 3. Ears- itching, fullness 4. Others- throat itching, nonproductive cough
  49. 49. Diagnostic Evaluation • Skin testing • Nasal Smear • RAST • Rhinoscopy
  50. 50. Urticaria and angioedema • a skin rash, usually occurring as an allergic reaction, that is marked by itching and small pale or red swellings ETIOLOGY: Ingested substance Infections Insects
  51. 51. SS & DX EVALUATION • Raised red edematous wheals • Intense pruritus • Diffused swelling Dx Evaluation 1. Labs 2. Challenge testing to determine physical cause
  52. 52. FOOD ALLERGIES Common Food Allergens: • Cow’s milk, eggs, shellfish, peanuts, soybeans and wheat. Dx Tests: 1. Skin testing 2. RAST 3. Oral challenge 4. Elimination Diet NSG Diagnosis?
  53. 53. TYPE II CYTOTOXIC HYPERSENSITIVITY • Hemolytic transfusion reaction to blood of an incompatible type. Antigen attached To foreign cell or tissue Plasma cells produce IgG Or IgM antibodies w/c Binds to antigens Binding stimulates Complement activation Cell lysis Phagocytes Killer T cell activation
  54. 54. Serologic testing • BT • Cross matching (compatibility Test) • Direct Coomb’s Test • Indirect Coomb’s Test SCREENING FOR INFECTIOUS DISEASE - Routine lab test - Specific condition screened for: - Hepatitis - HIV (*antibodies not produced at least 6 weeks) - Cytomegalovirus - Syphilis - Bacteria - Malaria
  55. 55. Coombs test The two Coombs tests are: • Direct Coombs test (also known as direct antiglobulin test or DAT). - used to detect if antibodies factors have bound to RBC surface antigens in vivo • Indirect Coombs test (also known as indirect antiglobulin test or IAT). is used to detect in-vitro antibody-antigen reactions
  56. 56. Administration of Whole Blood And Blood Components • Whole Blood – Acute, massive blood loss of greater than 1,000 mL • Packed RBC – Restoration or maintenance of adequate organ oxygenation with minimal expansion of blood volume. – 90-120 min/unit • Platelets concentrates – 5.5 x 1010 platelets and plasma (50-400 mL)
  57. 57. Administration of Whole Blood And Blood Components • Assignment: Other Blood components for administration. – Platelets Concentrates – Plasma (Fresh or Fresh Frozen) – Cryoprecipitate – Fractioned Plasma Products
  58. 58. Blood transfusions can be grouped into two main types depending on their source: • Homologous transfusions, or transfusions using the stored blood of others. • Autologous transfusions, or transfusions using one's own stored blood. • A unit (up to 500 ml) of blood • administered over 4 hours, depending on blood pack. • In patients at risk of congestive heart failure, many doctors administer furosemide to prevent fluid overload. Acetaminophen and/or an antihistamine such as diphenhydramine are sometimes given before the transfusion to prevent a transfusion reaction.
  59. 59. Complications and risks • For the donor – quot;passing outquot; – Bruise at the needle site — 23 percent – Sore arm — 10 percent – Hematoma at needle site — 2 percent – Sensory changes in the arm used for donation (eg, burning pain, numbness, tingling) — 1 percent – Fatigue — 8 percent – Nausea and vomiting — 1 percent
  60. 60. For the recipient • Transfusion reaction • bacterial infection and sepsis • viral infection • volume overload, iron overload (with multiple red blood cell transfusions) • anaphylactic reactions • acute hemolytic reactions (most commonly due to the administration of mismatched blood types).
  61. 61. Objections to blood transfusion • may arise for personal, medical, or religious reasons – Jehovah's Witnesses
  63. 63. ACUTE • May occur the transfusion or within minutes to hours after infusion. • Reactions include allergic, febrile, septic and hemolytic rxns, air embolism and circulatory overload. DELAYED May occur from days to years after the transfusion. Reactions include delayed hemolytic reactions, iron overload (hemosiderosis), infectious diseases.
  64. 64. Immediate Adverse Effects of Transfusion Febrile Reactions Cause: Fever and chills during transfusion are thought to be caused by recipient antibodies reacting with white cell antigens or white cell fragments in the blood product or due to cytokines which accumulate in the blood product during storage. • Fever occurs more commonly with platelet transfusion (10- 30%) than red cell transfusion (1-2%). • Fever may be the initial symptom in a more serious reaction such as bacterial contamination or haemolytic reaction. Management: Symptomatic, paracetamol Investigation: If the fever is accompanied by significant changes in blood pressure or other signs and symptoms, the transfusion should be ceased and investigated
  65. 65. Urticarial (Allergic) Reactions Cause: caused by foreign plasma proteins. On rare occasions they may be associated with laryngeal oedema and bronchospasm. Management: If urticaria occurs in isolation (without fever and other signs), slow the rate or temporarily stop transfusion. If symptoms are bothersome, consider administering an antihistamine before restarting the transfusion. If associated with other symptoms, cease the transfusion and proceed with investigation. Investigation: It is also usually possible to restart the transfusion. Such a decision should be made after assessment by the treating doctor.
  66. 66. Severe Allergic (Anaphylactic) Reactions • Anaphylactic and anaphylactoid reactions have signs of cardiovascular instability including hypotension, tachycardia, loss of consciousness, cardiac arrhythmia, shock and cardiac arrest. Sometimes respiratory involvement with dyspnoea and stridor are prominent. • Cause: In some cases patients with IgA deficiency who have anti-IgA antibodies can have these reactions. • Management: Immediately stop transfusion, supportive care including airway management may be required. Adrenaline may be indicated. Usually given as 1:1000 solution, 0.01mg/kg s.c./i.m. or slow i.v. • Investigation: IgA levels and anti-IgA antibodies. • Prevention: Patients with anti-IgA antibodies require special blood products such as washed red blood cells and plasma products prepared from IgA deficient donors. Manage further transfusion in consultation with the haematologist-on-call.
  67. 67. Acute Haemolytic Reactions • Cause: caused by transfusion of ABO incompatible blood, eg group A, B or AB red cells to a group O patient. • Most haemolytic reactions are the result of human error such as the transfusion of properly labelled blood to the wrong patient, or improper identification of pretransfusion blood samples. • Non-immune haemolysis of RBCs in the blood container or during administration can occur due to physical disruption (temperature changes, non-isotonic fluid) • Symptoms: Chills, fever, pain (along IV line, back, chest), hypotension, dark urine, uncontrolled bleeding due to DIC (Disseminated intravascular coagulation). • Management: Immediately stop transfusion. Notify hospital blood bank urgently (another patient may also have been given the wrong blood!). These patients usually require ICU support and therapy includes vigorous treatment of hypotension and maintenance of renal blood flow. • Prevention: Proper identification of the patient from sample collection through to blood administration, proper labelling of samples and products is essential. Prevention of non-immune haemolysis requires adherence to proper handling, storage and administration of blood products.
  68. 68. Bacterial Contamination • Cause: Bacteria may be introduced into the pack at the time of blood collection from sources such as donor skin, donor bacteraemia or equipment used during blood collection or processing. Bacteria may multiply during storage. • Platelets are more frequently implicated than red cells. • Symptoms: Very high fever, rigors, profound hypotension, nausea and/or diarrhoea. • Management: Immediately stop the transfusion and notify the hospital blood bank. After initial supportive care, blood cultures should be taken and broad-spectrum antimicrobials commenced. Laboratory investigation will include culture of the blood pack. • Prevention: Inspect blood products prior to transfusion. Some but not all bacterially contaminated products can be recognised (clots, clumps, or abnormal colour). Maintaining appropriate cold storage of red cells in a monitored blood bank refrigerator is important. Transfusions should not proceed beyond the recommended infusion time (4 hours).
  69. 69. Transfusion-Related Acute Lung Injury • Transfusion Related acute Lung Injury (TRALI) is a clinical diagnosis of exclusion characterised by acute respiratory distress and bilaterally symmetrical pulmonary edema with hypoxemia developing within 2 to 8 hours after a transfusion. A CXR shows interstitial or alveolar infiltrates when no cardiogenic or other cause of pulmonary oedema exists. • Cause: Pulmonary vascular effects are thought to occur secondary to cytokines in the transfused product or from interaction between patient white cell antigens and donor antibodies (or vice versa). • Management: Symptomatic support for respiratory distress includes oxygen administration and may require intubation and mechanical ventilation. Symptoms generally resolve over 24-48 hours.
  70. 70. Volume Overload • Cause: Patients with cardiopulmonary disease and infants are at risk of volume overload especially during rapid transfusion. • Management: Stop the transfusion, administer oxygen and diuretics as required. • Prevention: Avoid unnecessary fluids and use appropriate infusion rates.
  71. 71. Hypothermia • Cause: Rapid infusion of large volumes of stored blood contributes to hypothermia. Infants are particularly at risk during exchange or massive transfusion. • Prevention and Management: Appropriately maintained blood warmers should be used during massive or exchange transfusion. Additional measures include warming of other intravenous fluids and the use of devices to maintain patient body temperature.
  72. 72. Immediate adverse effects of transfusion and their management Category 1: Mild Reactions Symptom/s Signs Possible Immediate Management Cause Urticaria Pruritus Allergic Assess patient /rash (itching) An antihistamine may be required Transfusion may be restarted if no other signs/symptoms are present If signs/symptoms worsen treat as Category 2.
  73. 73. Category 2: Moderately severe reactions Immediate Signs Symptoms Possible cause Management Allergic moderately- Stop transfusion Flushing Anxiety severe) and maintain Urticaria Pruritus IV line with Febrile non-haemolytic Rigors NSaline transfusion reaction:- Palpitations Fever antibodies to white Contact Medical Mild cells or platelets Officer Restlessness dyspnea antibodies to proteins Patient may require Tachycardia including IgA antihistamine Headache and/or possible contamination paracetamol with pyrogens and /or Further bacteria investigation and management according to clinical features
  74. 74. Category 3: Life threatening reactions Immediate Signs Symptoms Possible cause Management Stop transfusion Anxiety Acute Rigors maintain IV line with intravascular Chest pain Fever NSaline haemolysis Pain at infusion Manage immediate Restlessness (wrong blood) site needs: Bacterial Hypotension fluid for hypotension Respiratory contamination oxygen distress Tachycardia adrenaline for and septic anaphylaxis Loin/back pain shock Dark Urine diuretic for fluid Headache overload Fluid overload Unexplained Dyspnea Anaphylaxis bleeding (DIC) Further management Transfusion according to likely related acute cause lung injury (TRALI)
  75. 75. Delayed and Long Term Averse Effects of Transfusion Delayed Haemolysis • Cause: Patients may develop antibodies to red cell antigens. Antibodies can occur naturally, or may arise as a consequence of previous transfusion or pregnancy. A delayed haemolytic reaction occurs when a patient develops an antibody directed against an antigen on transfused red cells. The antibody may cause shortened red cell survival, with clinical features of fever, jaundice and lower than expected haemoglobin following transfusion. Most delayed haemolytic reactions produce few symptoms and may go unrecognised, however there are reports of serious consequences in critically ill patients. • Prevention: An antibody screen is performed as part of pre- transfusion testing. When an antibody is detected, it is identified and appropriate antigen negative blood is provided. Sometimes antibodies fall below detectable limits and may not be detected by pretransfusion testing.
  76. 76. Drug Category Diuretics -- These agents are used to increase renal blood flow and preserve urinary output in hemolytic transfusion reactions. They also may be used in transfusion-related volume overload • Furosemide (Lasix) Vasopressors -- These agents are used to increase renal blood flow and preserve urinary output in hemolytic transfusion reactions. In severe allergic reactions, epinephrine is used for its inotropic properties and ability to maintain perfusion of vital organs. Dopamine (Intropin) . Lower doses stimulate mainly dopaminergic receptors that produce renal and mesenteric vasodilation. Cardiac stimulation and renal vasodilation produced by higher doses Epinephrine (Adrenalin, Epinal, Epifrin) increased peripheral vascular resistance, hypertension, cardiac activity Antihistamines – Used to treat minor allergic reactions and anaphylaxis. Diphenhydramine (Benadryl, Benylin, Bydramine
  77. 77. • Corticosteroids - These agents have limited benefit in the initial acute treatment of rapidly deteriorating anaphylactic patient. However, they may benefit patients with persistent bronchospasm or hypotension. Onset of action is approximately 4-6 h following its administration. • Methylprednisolone (Solu-Medrol)
  78. 78. IMPAIRED IMMUNE RESPONSE Acquired Immunodeficiency Syndrome (AIDS), “AIDS: Your Problem, Control With Condoms.” • human viral disease that ravages the immune system, undermining the body’s ability to defend itself from infection and disease. • Caused by the human immunodeficiency virus (HIV), AIDS leaves an infected person vulnerable to opportunistic infections.
  79. 79. Human Immunodeficiency Virus • The human immunodeficiency virus (HIV), which causes acquired immunodeficiency syndrome (AIDS), principally attacks CD4 T-cells, a vital part of the human immune system.
  80. 80. • Like all viruses, human immunodeficiency virus (HIV) is comprised of only genetic material, a few proteins, and a protective envelope. • Its genetic material, carried by single-stranded RNA molecules, contains all the information necessary to make more viruses. • HIV can not reproduce itself outside of a cell, but when HIV invades a living cell, it turns the cell into a factory for making more HIV.
  81. 81. Three ways that HIV infections spread: • sexual intercourse with an infected person, • contact with contaminated blood, and • transmission from an infected mother to her child before or during birth or through breastfeeding.
  82. 82. • Left to right, Candy, Robert, Randy, and Richard Ray leave Memorial Elementary School in Arcadia, Florida, on August 24, 1987. It was the boys’ first day at school after having been barred because they were infected with HIV.
  83. 83. Signs and symptoms • Within one to three weeks after infection with HIV, • flu-like symptoms, – such as fever – sore throat, headache, skin rash, tender lymph nodes, and a vague feeling of discomfort. – During this phase, known as acute retroviral syndrome, HIV reproduces rapidly in the blood. – extensive weight loss and fatigue (wasting syndrome), periodic fever, recurring diarrhea, and thrush, a fungal mouth infection. – early symptom of HIV infection in women is a recurring vaginal yeast infection
  84. 84. Diagnostic Evaluation • Enzyme-Linked ImmunoSorbent Assay, or ELISA, is a biochemical technique used to detect the presence of an antibody or an antigen in a sample A 96-well microtiter plate might be used for ELISA
  85. 85. Western Blot test • can detect lower levels of HIV antibodies. In this test a blood sample is applied to a paper strip containing HIV proteins. If HIV antibodies are present in the blood, they bind to the HIV proteins, producing a color change on the paper. • Orasure • Uses saliva rather than blood with result available in about 3 days • Calypte HIV-1 Urine EIA
  86. 86. • Decrease CD4 count • Presence of indicator disease – Pneumocystis carinii pneumonia – Candidiasis of esophagus – Kaposi sarcoma
  87. 87. Specific treatment • Antiretroviral therapy – 3 different classifications of medication to prevent replication – CLASSES – Nucleoside reverse transcriptase inhibitors- zidovudine (AZT), didanosine (ddI),stavudine (d4T) – Non-Nucleoside reverse transcriptase inhibitors- nevirapine (Viramune), efavirenz (Sustiva) – Protease Inhibitors (PI’s) – indinavir (Crixivan), ritonavir (Norvir), saquinavir (Fortovase)
  88. 88. Prevention Therapies • Opportunistic infections • Vaccination – Tuberculosis – yearly screening – Pneumococcal pneumonia- q 5-6 years vax – Influenza- full vaccine
  89. 89. Supportive Care • Treatment of reversible illness • Nutritional support • Palliation of pain • Treatment to relieve symptoms • Antidepressant
  90. 90. STANDARD OF CARE • Universal precautions • Protect confidentiality • Education on prevention of HIV transmission • Develop adherence strategy in taking antiviral drugs • Educate about HIV symptoms and management
  91. 91. Nursing Diagnoses • Fear • Risk for infection • Altered nutrition less than body requirements • Altered oral mucous membrane • Diarrhea • Altered thought process • Hyperthermia Altered breathing pattern
  92. 92. Sjogren's syndrome - an autoimmune disorder in which immune cells attack and destroy the exocrine glands that produce tears and saliva. - defined by its two most common symptoms — dry eyes and a dry mouth.
  93. 93. Causes • heredity • hormones • viral or bacterial infection • white blood cells called lymphocytes target, attack and damage moisture-producing glands • also damage other organs, including lungs, kidneys and liver.
  94. 94. Signs and symptoms • Dry eyes • Dry mouth • Dental cavities • Fatigue • Fatigue • Fever • Enlarged parotid glands • Difficulty swallowing or chewing • Change in sense of taste • Hoarseness • Oral yeast infections, such as candidiasis • Irritation and mild bleeding in your nose • Skin rashes or dry skin • Vaginal dryness • Dry cough that doesn't produce sputum • Joint pain, swelling and stiffness
  95. 95. Complications • Difficulty swallowing. • Dental cavities. • Vision problems. Dry eyes can lead to light sensitivity, blurred vision and corneal ulcers.
  96. 96. Less common complications include: • Inflammation of organs such as your lungs, kidneys or liver. • Heart problems for babies born to mothers with Sjogren's syndrome. • Cancer of the lymph nodes (lymphoma). A small percentage of people with Sjogren's syndrome develop lymphoma. Symptoms include swelling of the salivary glands, fatigue, weight loss and night sweats. • Peripheral nervous system disorders. Peripheral neuropathies are common – legs may be especially affected – may experience symptoms of numbness, tingling and burning. The cranial nerves — such as those relating to the eyes (optic nerve) or face (trigeminal nerve) — can be affected and may cause visual problems or facial pain.
  97. 97. Risk factors • Having a rheumatic disease. • Being female. Women are nine times as likely as men are to have Sjogren's syndrome. • Being a certain age. Sjogren's syndrome is usually diagnosed in people older than 40. • Having a family history of Sjogren's. Sjogren's syndrome sometimes runs in families.
  98. 98. Screening and diagnosis • Blood tests can be done to determine if a patient has high levels of antibodies that are indicative of the condition, such as anti-nuclear antibody (ANA) and rheumatoid factor (because SS frequently occurs secondary to rheumatoid arthritis), which are associated with autoimmune disease • Tear test. measure the dryness of the eyes with a Schirmer tear test, in which a small piece of filter paper is placed under the lower eyelid to measure your tears. In another version of the Schirmer test, a cotton swab is used to stimulate the tear reflex in the nose. A medical eye doctor (ophthalmologist) may also examine the eyes with a slit- lamp after placing a drop of liquid containing a dye in the eye. The dye stains areas of the cornea that have been damaged by the dryness. • Imaging. special X-ray called a sialogram. It detects dye that is injected into the parotid glands. The dye is injected through the opening of a small duct in the mouth. This procedure reveals the flow of saliva into the mouth. • may also perform a parotid gland flow test to determine the amount of saliva that is produce over time. Another imaging test is a salivary scintigraphy, which measures salivary gland function. • Biopsy. lip biopsy to detect the presence of clusters of inflammatory cells. For this test, a small sliver of tissue is removed from salivary glands located in your lip and examined under a microscope. • Slit-lamp exam. use magnifying equipment to determine how dry your eye is and whether the outside of your eye is inflamed.
  99. 99. Medications • Nonsteroidal anti-inflammatory drugs (NSAIDs). This group of medications, which includes aspirin, helps relieve both pain and inflammation. The doctor may recommend these medications if there is painful or swollen joints. Side effects may include indigestion and stomach bleeding. Therefore, always take NSAIDs with food. • Corticosteroids. These medications reduce inflammation and may slow joint damage. In the short term, corticosteroids can make the patient feel dramatically better. But when used for many months or years, they may become less effective and also cause serious side effects. Side effects may include easy bruising, thinning of your bones, cataracts, weight gain, a round face, diabetes and high blood pressure. • Immunosuppressants. These medications, such as cyclophosphamide (Cytoxan), methotrexate (Rheumatrex), mycophenolate (CellCept) and azathioprine (Imuran), suppress the immune system. The doctor may prescribe them for you if problems with the lungs, kidneys, blood vessels or nervous system develops.
  100. 100. Meds continued • Pilocarpine (Salagen). The doctor may prescribe pilocarpine if there is dry- mouth symptoms caused by Sjogren's syndrome. It's not an option if the patient has poorly controlled asthma, inflammation of the iris (acute iritis), glaucoma or significant cardiovascular disease, or if pregnant or breast-feeding. Pilocarpine may cause increased sweating and headaches. • Cevimeline (Evoxac). This prescription medication also is used to relieve symptoms of a dry mouth. The medication works by causing certain mouth glands to produce more saliva. Common side effects may include excessive sweating, nausea, and a runny or stuffy nose. Less common side effects, may include difficulty breathing, fast heartbeat and itching. • Cyclosporine. The ophthalmologist may recommend you use eyedrops containing cyclosporine (Restasis) to treat symptoms of Sjogren's syndrome that affect the eyes.
  101. 101. Surgery Sealing of the tear ducts that drain tears from the eyes (punctal occlusion). Collagen or silicone plugs are inserted into the ducts for a temporary closure. Collagen plugs eventually dissolve, but silicone plugs will keep ducts sealed until they fall out or are removed. Doctor may use a laser to permanently seal your ducts
  102. 102. Systemic Lupus Erythematosus (SLE)
  103. 103. Lupus: Prevalence 1 in 700 (ages 15 -64) women have lupus 1 in 250 are African American Women Asian and Native Americans = ↑ incidence Usually affects women between 15 to 40 In this age group 1:200 will develop lupus Usual onset is during childbearing age Possible hormonal link 8 – 10 times more prevalent in women
  104. 104. Types of Lupus • SLE – Systemic – Chronic, progressive, inflammatory connective tissue disorder that causes organ failure; potentially fatal with a 5-year survival rate of 85% • Drug Induced Lupus – Procainimide – Hydralazine – INH • DLE – Discoid – Affects only the skin
  105. 105. Pathophysiology of Lupus • Autoimmune: Exact Mechanism Unknown – Viruses – Environmental chemicals – Genetic • Antibodies “attack” healthy tissue • Causes inflammation to the organ or to the vessels supplying blood to the organ – Deprives organs of arterial blood supply
  106. 106. Prognosis • Potentially fatal disorder • Increase in survival rate in last 20 years • Now… 85% of clients survive at least 5 years – Leading cause of death are related to infection
  107. 107. Diagnostics • DLE = skin biopsy • Serum ANA, ESR, protein electrophoresis, complement, immunoglobins • Lupus cell prep (LE prep) • CBC • Electrolytes • Liver and cardiac enzymes • Coag studies • Anticardiolipin Antibodies
  108. 108. Diagnostic Criteria • Must have four of the following eleven symptoms or findings: Malar rash Discoid lupus Mouth sores Photosensitivity Arthritis Neurologic disorder +proteinuria Hematologic disorder + ANA Immunologic Disorder Thrombocytopenia, severe anemia, and leukopenia
  109. 109. Signs and Symptoms of Lupus • Skin: – Dry, scaly, raised rash on face – Appears to be in butterfly pattern—the “Bite of the Wolf.” – Individual round lesions • Hair – Hair loss – Change in texture
  110. 110. Signs and Symptoms of Lupus Musculoskeletal  Joints are affected causing painful mobility (Polyarthritis in 90% of SLE patients).  Joint inflammation  Avascular necrosis – after 5 years of diagnosis  Muscle atrophy (results from autoimmune complex invasion—leading to Myositis).  Muscle pain
  111. 111. Sign and Symptoms of Lupus • Renal – Lupus nephritis • Changes in the glomeruli – Decreased urinary output – Proteinuria – Hematuria – Fluid retention – Leading cause of death – 50% of all lupus pts have this
  112. 112. Signs and Symptoms of Lupus • Respiratory – Pleural effusions • Results in restrictive and obstructive changes –Dyspnea –Hypoventilation
  113. 113. Signs and Symptoms of Lupus • Cardiac Pericarditis Raynaud’s Disease • Tachycardia Lack of circulation • Pain to hands and feet • Myocardial ischemia Chest Pain Cardiac Dysrrhythmias
  114. 114. Signs and Symptoms of Lupus • Neurological –Psychoses –Paresis –Seizures –Headaches –Strokes –Peripheral neuropathies
  115. 115. Signs and Symptoms of Lupus • GI Tract • Psychosocial – Abdominal pain – Dealing with illness • Mesenteric arteritis – Fear of death chronic • Pancreatitis – Lack of socialization • Ulcers – Body image changes • Liver enlargement • Rash • Spleenomegaly • Medication related • Sexual Dysfunction • Systemic – Pain – Fever – Fatigue/weakness – Generalized weakness – Self esteem – Fatigue – Decreased desire – Anorexia – Weight loss
  116. 116. Treatment • Medications: • Skin protection – Topical steroids for – Avoid sunlight lesions – Mild soaps – Plaquenil – Cosmetic cover-ups (hydroxychloroquine) - Daily inspection Can damage retina – Steroids • Hair loss – Immunosuppressives – Mild shampoo – Anticoagulants if needed – No chemicals
  117. 117. Nursing management 1. Administer medications which may include NSAIDS and salicylates 2. Maintain skin integrity 3. Perform CV, neurologic and musculoskeletal assessment 4. Provide meticulous mouth care 5. Arrange for dietary consult- soft easily tolerated foods 6. Apply warm packs 7. Collaborate with the PT department 8. Provide client and family teaching • encourage protection from the sun and UV light exposure • avoid people with contagious problems
  118. 118. • end