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AACN PCCN Webinar

Session 7

Endocrine & Multisystem

Presenter: Carol A. Rauen, RN, MS, CCNS, CCRN, PCCN, CEN

Independent Clinical Nurse Specialist & Education Consultant [email protected]

mailto:[email protected]

Session 7: Endocrine & Multisystem

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Table of Contents Endocrine ........................................................................................................................................ 2

Multisystem .................................................................................................................................... 6


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Endocrine

I. INTRODUCTION Disorders of the Endocrine System are Related to Either an Excess or a Deficiency of a Specific Hormone or Defect at its Receptor Site.

PCCN Test Plan

Endocrine, GI, Heme & Renal: 18% a. Diabetes Mellitus b. Diabetic Ketoacidosis c. Hyperglycemic Hyperosmolar Syndrome (HHS) d. Hypoglycemia e. Metabolic Syndrome Every Cell in the Body is Under Endocrine Influence

II. DIABETES MELLITUS

Type I vs Type II Diabetes Mellitus

Characteristic Type I Type II Etiology Destruction of beta cells Insulin resistance Prevalence 10-15% 80-90% Insulin No insulin production Insulin deficiency and/or resistance Age Before age 35 After age 35 Onset Rapid Gradual Ketosis Common Uncommon Glucose Goal Fasting 100-125mg/dl

Pre-prandial 70-130 Post-prandial <180 Hgb A1C < 6%

Same

Signs &Symptoms Polyuria Polydipsia polyphagia

Polyuria Polydipsia Polyphagia Blurred vision Fatigue

Treatment Diet & weight management Exercise Glucose control Insulin

Diet & weight management Exercise Glucose control Oral medications GLP-1 agonist injectables (exenatide,

liraglutide) Insulin


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Severe

Hyperglycemia Diabetic Ketoacidosis Hyperglycemic Hyperosmolar Non

Ketotic Syndrome

Complications of Diabetes Mellitus (increased risk of) a. Stroke b. Retinopathy, cataracts, blindness c. Heart Disease d. Vascular Disease (arterial and venous) e. Hypertension f. Renal Insufficiency/Failure/Disease g. Peripheral neuropathy h. Immunosupression (increase risk of infection)

Treatment a. Nutrition: balance diet – primarily low carb and calorie b. Exercise: improves insulin utilization and increases metabolism c. Insulin:

Insulins

Type Brand Onset Peak Duration Pearls Very Rapid Novolog (Aspart)

Humalog (Lispro)

< 15 min 30min – 2 hr 3-5 hr “Seefood” MUST take w food.

Used to Correct

Rapid Humulin R (regular)

Novolin R (regular)

30-60 min 2-4hr 4-8hr Can be used for IV infusion

Meal time dosing Intermediate NPH

Humulin N

Novolin N Lente

Lumulin L Novolin L

2-4hr 1-4hr

4-12hr 4-14hr

12-16hr 15-25hr

Basal dosing

Long Lantus (glargine)

Levemir (detemir)

1-2hr No real Peak 24hr Basal dosing

Acute Hypoglycemia Serum Glucose < 50mg/dL

Causes a. Too Much Insulin b. Not Enough Calories


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Signs & Symptoms a. Tachycardia b. LOC: Irritable, Confused, Unconscious c. Skin: Pale, Cool, Clammy d. Seizures e. Blurred Vision

Treatment a. Give Glucose b. Enteral c. Parental (if BG < 20mg/dL) d. Determine Cause

Diabetic Ketoacidosis (DKA)

Diagnosis a. Metabolic derangement resulting from absolute or relative insulin deficiency b. Blood Glucose > 500mg/dl c. pH < 7.32 d. HCO3 < 15mEq/L e. Increase Anion Gap f. + Ketones in Urine g. Azotemia

Signs & Symptoms a. Hypotension b. Tachycardia c. Tachypnea d. Kussmaul’s Respirations e. Decreased Skin Turgor f. Dry Mucous Membranes g. Abdominal Pain, Nausea & Vomiting

Fluid Therapy a. Restore Circulating Volume b. 1-2 L of Isotonic Saline in 2 hr c. D5 .45%NS after BS down to 250mg/dl d. May get 8-10L in 1st 24 hr

Drug Therapy a. Continuous IV or Bolus Regular Insulin b. Lower 100mg/dl/hr c. Monitor K+ levels Carefully d. Bicarbonate for Severe Acidosis


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Hyperglycemic Hyperosmolar Syndrome (HHS) A hyperosmolar state from severe hyperglycemia without ketosis. Predominantly older adults and type II DM.

Diagnosis a. Glucose > 800mg/dL b. Osmolality > 350mlOsm c. Ketones neg d. pH > 7.3 e. Severe Dehydration

Fluid Therapy a. 2 L of Normal Saline in 1 hr b. Followed by Fluid Replacement

Drug Therapy a. Continuous IV Regular Insulin (10U/hr) b. Monitor K+ Closely

III. METABOLIC SYNDROME A term used for a collection of physical assessment findings that carry with them an increased risk of developing DM and cardiovascular disease. A dx is confirmed when a person has three or more of the following conditions. a. Fasting Blood Glucose > 100mg/dL b. HDL < 40mg/dL in Men, < 50 mg/dL in Women c. Triglycerides > 150mg/dL d. Waist Circumference > 102cm (41in) in Men, > 88cm (35in) in Women e. SBP > 130mmHg or DBP > 85mmHg, or on medication for HTN


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Multisystem

I. INTRODUCTION

PCCN Test Plan

Neurological, Multisystem & Behavioral: 15% a. Complex Wounds and Pressure Ulcers b. Healthcare-Acquired Infections

Catheter-Associated Urinary Tract Infections (CAUTI)

Central-Line-Associated Blood Steam Infections (CLABSI) c. End of Life (e.g., comfort care measures, hospice) d. Infectious Diseases

Influenza

Multi-Drug Resistant Organisms (e.g., MRSA, VRE) e. Pain f. Palliative Care g. Sepsis Continuum

Systemic Inflammatory Response Syndrome (SIRS)

Sepsis

Severe Sepsis

Septic Shock h. Shock States (hypovolemic and anaphylactic)

II. HOLISTIC CARE

Pain

Definitions “A personal, private sensation of hurt. A harmful stimulus which signals current or impending tissue damage. A pattern of responses to protect the organism from harm.” -- Sternback (1979) “Pain is whatever the experiencing person says it is and exists whenever he/she says it does.” -- McCaffery (1979)

Physiologic Bases for Pain a. Somatic Pain

Cutaneous or deep skin, bone or muscles b. Visceral Pain

Organs (poorly localized)


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c. Referred Pain

Left arm pain perceived for chest pain, right shoulder pain perceived for gall bladder pain

d. Neuropathic Pain

Injury or damage to nerves (phantom limb pain) e. Neurotransmitters

Acetylcholine

Norephinephrine

Epinephrine

Dopamine

Types of Pain a. Acute b. Chronic Malignant c. Chronic Non-Malignant

Pain Assessment Subjective a. Precipitation Factors b. Aggravating Factors c. Localization of Pain d. Character and Quality of Pain e. Duration of Pain Physiological Acute Pain - Sympathetic Response Measurement Tools a. Visual Analog Scales VAS b. Verbal Descriptors c. Facial Expressions d. Oucher Scale

Principles of Pain Management ABC Principle of Assessment and Planning a. Ask about pain regularly, Assess pain systematically b. Believe the patient and family in their reports of pain and what relieves it. c. Choose pain control options appropriate for the patient, family, and setting d. Deliver interventions in a timely, logical and coordinated fashion. e. Empower patients and their families. Enable them to control their course to the greatest

extent possible.


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Pharmacology a. Narcotic b. Anti-inflammatory c. Non-Narcotic d. Adjuvant Physical Treatments a. Massage b. Heat or Cold c. BioFeedback d. TENS e. Elevation Alternative/Complimentary Therapies a. Acupuncture b. Aroma Therapy c. Therapeutic Touch d. Prayer e. Mental Imaging

Palliative Care A significant and legitimate part of acute care. This is more than just ‘comfort care.’ There are standards and guidelines. We, as the direct care provides are an important member of this team. Our patients and their loved ones depend on us.

End of Life Care

III. WOUNDS AND INFECTIONS

Major Functions of the Skin a. Barrier From Environment b. Absorption of Vitamins (Vit D) c. Temperature Regulation d. Sensory Perception e. Shock Absorber f. Appearance and Identity g. Assists with Blood Pressure Regulation


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Pressure Ulcers a. Stage I: Skin intact with nonblanchable erythema b. Stage II: Partial thickness epidermis open, superficial –not depth c. Stage III: Full thickness through dermis d. Stage IV: Full thickness through dermis with exposure of underlying structures (muscle,

bone) e. Unstageable: Unable to assess thickness (eschar or covered) f. Prevention, Assessment and Appropriate Tx are KEY!

Infections a. Bacterial b. Viral: Warts, Herpes Zoster c. Parasite: ex Scabies d. Fungal: Candidiasis e. Dermatitis: Contact

Wound Healing

Types a. Primary Intention: surgical incisions b. Secondary Intention: heal from inside out by granulation tissue c. Tertiary Intention: heal from inside out by granulation tissue, typically delayed because of

infection, inflammation and/or large open wound. May require skin grafting

Contributing Factors a. General Health b. DM c. Infection d. Nutrition e. Activity f. Age g. Obesity

Drains a. Hemovac b. Jackson-Pratt - JP c. Penrose d. Vacuum Assisted Closure - VAC


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Dressings a. Dry b. Wet-to-Dry c. Moisture Retentive – hydrogel d. Debrideing Agents: Granulex, Zymase, AccuZyme

Hospital-Acquired Infections a. Catheter-Associated Urinary Tract Infections (CAUTI) b. Central-Line-Associated Blood Steam Infections (CLABSI)

IV. SHOCK

Definition The inability of the circulatory system to supply oxygen and nutrients to the cells of the body. The oxygen demands are greater than the supply.

Sepsis Continuum

1992 ACCP/SCCM Definitions (Bone, R. et al (1992) Chest, 101, pg 1644-1655)

Sepsis The systemic response to infection, manifested by two or more of the following conditions as a result of infection: a. Temperature > 38o C or < 36oC b. Heart Rate > 90 beats per minute c. Respiratory Rate > 20 bpm or PaC02 < 32mmHg d. WBC > 12,000 or < 4,000, or > 10% immature (bands) forms Systemic Inflammatory Response Syndrome (SIRS) The systemic inflammatory response to a variety of severe clinical insults. The response is manifested by two or more of the following conditions: a. Temperature > 38o C or < 36oC b. Heart Rate > 90 beats per minute c. Respiratory Rate > 20 bpm or PaC02 < 32mmHg d. WBC > 12,000 or < 4,000, or > 10% immature (bands) forms Severe Sepsis Sepsis associated with organ dysfunction, hypoperfusion, or hypotension. Hypoperfusion and perfusion abnormalities may include, but are not limited to a. Lactic acidosis b. Oliguria c. Acute alteration in mental status


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Septic Shock Sepsis-induced with hypotension despite adequate fluid resuscitation along with the presence of perfusion abnormalities that may include, but are not limited to: a. Lactic Acidosis b. Oliguria c. Acute alteration in mental status Pt who is receiving inotropic or vasopressor agents may not be hypotensive at the time that perfusion abnormalities are measured.

2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference Levy, M., et al. (2003). 2001 SCCM/ESICM/ATS/SIS International sepsis definitions conference. CCM 31(4), 1250-1256.

Approved and supported 1992 definitions. Offered S&S for sepsis and staging system (lacks evidence at this time). General Variables a. Fever (core >38.3C) b. Hypothermia (core < 36C) c. Heart Rate > 90min or > 2 SD above the normal value for age d. Tachypnea e. Altered mental status f. Significant edema or positive fluid balance (20ml/kg over 24 hr) g. Hyperglycemia (plasma glucose >120) in absence of DM Inflammatory Variables a. Leukocytosis (WBC > 12,000) b. Leukopenia (WBC < 4,000) c. Normal WBC with >10% immature forms (bands) d. Plasma C-Reactive Protein > 2 SD above normal value e. Plasma Procalcitonin > 2 SD above normal value (IL-6) Hemodynamic Variable a. Arterial Hypotension (SBP < 90mmHg, MAP < 70, or SBP decreased >40mmHg in adults

or < 2SD below normal for age) b. Sv02 > 70% c. CI > 3.5L/min Organ Dysfunction Variables a. Arterial Hypoxemia (Pa02/Fi02 <300) b. Acute Oliguria (UO < 0.5mL/kg/hr) c. Creatinine Increase > 0.5mg/dL


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d. Coagulation Abnormalities (INR > 1.5 or APT > 60sec) e. Ileus (absent bowel sounds) f. Thrombocytopenia (platelet count < 100,000) g. Hyperbilirubinemia (plasma total bilirubin > 4mg/dL) Tissue Perfusion Variables a. Hyperlactatemia (>1mmol/L) b. Decreased capillary refill or mottling

Causes Infection is the cause of sepsis. The infective agent can be a bacteria (gram positive or negative), virus or fungi. Once the infection moves from a local to a systemic problem, sepsis and septic shock can result.

Clinical Presentation Although initiated by a localized infection, once the patient is septic they present with a systemic inflammatory response. This response is a systemic reaction to the release of endotoxin and biochemical mediators stimulated by inflammation and inadequate oxygen delivery. The patient will present with a relative hypovolemia secondary to massive vasodilation. a. Relative Hypovolemia and Hypoperfusion b. Increased Capillary Permeability and Edema c. Myocardial Depression d. Lactic Acidosis e. Pulmonary Capillary Leak Leading to ARDS f. Activation of Complement System Leading to Microthrombi g. Platelet Abnormalities h. Gluconeogenesis and Insulin Resistance

Therapeutic Goal Identify and stop the causative agent. Block the effects of the inflammatory mediators. Treatment options typically include: a. Antibiotics b. Fluid Resuscitation c. Vasopressors d. Ventilation and Oxygenation e. Restore Hemopoietic Balance Dellinger, P. et al (2013). Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock: 2012. Critical Care Medicine, 41(2), 296-327.

Hypovolemia Shock Hypovolemic Shock is the most common type of shock. It also is the easiest to treat if identified early. Shock develops when blood volume is insufficient to fill the intravascular space causing a preload deficit and ultimately a decreased cardiac output.


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Cause a. Absolute/Direct or Relative/Indirect Loss of Volume b. Relative/Indirect Losses

Clinical Presentation Patient presentation will depend a. Percent Volume Loss b. Duration of Hypovolemia c. Activation and Response of Compensatory Mechanisms

Therapeutic Goal Restore adequate intravascular volume as quickly as possible and stop losses. The fluid options and crystalloid vs colloid controversy will be addressed in the management section of this seminar.

Anaphylactic Shock

Definition Massive vasodilation occurs because of an antigen-antibody reaction which activates mast cells and basophils triggering the release of vasoactive mediators (histamine, serotonin, bradykinin, eosinophil chemotactic factor, prostaglandlins, heparin, leukotrinenes, platelet-activating factors, adenosine and various proteolytic enzymes) which stimulates a systemic response. This results in tremendous vasodilation and increased capillary permeability, with loss of fluid into the interstitial space and resultant hypotension from the relative hypovolemia.

Cause The initial activating response can be immunoglobulin E (IgE) or non-IgE mediated. Anaphylaxis is IgE mediated and is typically the result of a specific antigen exposure. An anaphylatoid response is mediated by a non-IgE reaction. There is direct activation of the mediators listed above (not antigen-antibody) from a source. A wide range of agents can cause this response: anti-inflammatory drugs, contrast media, opiates, polysaccharide volume expanders and anesthetics.

Clinical Presentation The release of the vasoactive mediators cause an array of systemic effects which lead to decreased oxygen delivery and shock. a. Hypotension b. Generalized Edema (increased capillary permeability) c. Laryngeal Edema d. Severe Bronchoconstriction e. Difficulty Breathing f. Coronary Vasoconstriction


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g. Urticaria h. Angioedema i. Itching j. Fever k. Flushed or Warm Skin l. Anxiety

Therapeutic Goal: Identify and stop the exposure to the causative agent. Block the effects of the vasoactive mediators. Treatment options are typically anti-histamines, vasoconstrictors, bronchodilators, and fluid resuscitation.

Stages of Shock All of the shock states cause hypoperfusion. There is inadequate oxygen supply to the tissue resulting from hypoperfusion, decreased blood pressure, and inadequate cardiac output. A supply/demand imbalance develops and the patient moves into anaerobic metabolism and lactic acidosis. Many physiologic mechanisms in the body delay this occurrence by compensating for the perfusion deficit. -- Rauen & Munro, 1998

Aerobic vs Anaerobic Metabolism

Aerobic Metabolism: a. C02 b. H20 c. 38 ATP

Anaerobic Metabolism: a. 2 ATP

b. Lactate

Cytoplasm

Glycogen Glucose Pyruvic Acid

2 ATP

Lactate

Anaerobic Glycolysis

Mitochondria

Citric

Acid

Cycle

02

C02

H20

36

ATP

Aerobic

Glycolysis


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Stage 1 – Compensatory Stage As inadequate perfusion persists and significant numbers of cells are affected, an imbalance of oxygen supply and demand occurs. Hypoxemia, hypotension, and acidosis activate the body’s compensatory mechanisms. The physiological goal of compensation is to supply or improve oxygenation and perfusion to the cells. a. Neural Response b. Hormonal Response c. Chemical Response Goal Improve Cardiac Output and Oxygen Delivery Mechanisms a. Activated Sympathetic Nervous System b. Renin/Angiotensin/Aldosterone System

Stage 2 – Decompensatory Stage As shock progresses, the compensatory mechanisms begin to fail. The progression of shock is evident at the cellular, organ, and system levels; and extensive physiological dysfunctions occur. The arteriolar and precapillary sphincters require sufficient energy in the form of adenosine triphosphate (ATP) to maintain a vasoconstrictive state. As energy dissipates with the progression of shock, the sphincters relax, allowing blood to flow into organs and sequester. Sludging of the blood in these capillary beds occurs, and the microcirculation becomes blocked. Metabolic waste products, microaggregates of platelets, white blood cells, and clots accumulate, further enhancing sludging and contributing to the development of metabolic acidosis. In response to these events chemical mediators are released that are harmful to the microciruculation and general system function. This will be reviewed in more detail in the cellular response to shock section.

Stage 3 – Irreversible Stage This is the final stage of shock. It is also referred to as the refractory phase because the body systems are no longer responsive to treatment. As each organ system decompensates and requires more and more support, they reach a point where therapeutic measures are no longer effective in maintaining function. The term irreversible is appropriate because it is at this point when several, if not all, of the systems cross the line from organ dysfunction to organ failure.

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