Assessment of Integumentary Function · Review skin alterations such as Jaundice, fissure, ulcers, erosion and how to assess Jaundice>> Yellow color: increased total serum bilirubin level. Hemolysis of RBC, Liver disorders. Fissures>>a crack or tear in the skin extending into the dermis. Ulcers>> open sore caused by poor blood flow, injury, or pressure. Erosion>> eating away of the surface some or all of the epidermis (outer layer). Lesions>>superficial growth or patch of skin that doesn’t resemble the surrounding area. Primary lesions are a direct result of a disease process. Secondary evolve from primary lesion or develop as a consequence from the patient’s activities (ex. Response to topical intervention). Assess lesions or breaks in the skin integrity by color, size, location, shape and presence (or absence ) of odor. · Review overall skin assessment and common abnormalities seen with hypoxia Inspect skin: color, moisture level (presence or absence), edema, lesions (A,B,C,D,E), integrity Asymmetry, Border irregularity, Color variation w/n 1 lesion, Diameter greater than ¼inch or 6mm, Evolving or changing in any feature. Hypoxia causes cyanosis>> increase in deoxygenated blood, bleeding from vessels in tissue, petechiae 1-3mm (localized) thrombocytopenia, ecchymosis >3mm (localized) increased blood vessel fragility. Cyanosis in the nail beds, mucous membranes, or generalized significant in cardiopulmonary disease. Macular= flat Papular= raised Review pressure injury staging, understand common risks for patients and treatments for each stage Stage 1: nonblanchable erythema of intact skin. May be preceded by temp., sensation or firmness changes. Stage 2: Partial-thickness loss with exposed dermis. Wound bed is viable, pink, or red, and moist. May look like intact or ruptured serum-filled blister. Stage 3: Full thickness skin loss with adipose (fat) visible in the ulcer. Tissue and rolled wound edges are often present. Slough and/or eschar may be present. Tunneling may be present. Subq tissues may be damaged or necrotic. Stage 4: full thickness loss of skin and tissue with exposed palpable fascia, muscle, tendon ligament, cartilage, or bone. May have slough or eschar. Unstageable: obscured full-thickness skin and tissue loss. Covered by eschar or slough. Suspected deep tissue injury persistent nonblanchable deep red, maroon, or purple discoloration. Intact or nonintact skin. Mucosal membrane pressure injury: found on mucous membranes where a medical device is in use and these are unstageable ulcers. · Review nutritional requirements for patients with pressure injury Must eat most of every meal; eats a total of four or more servings of meat and dairy products; adequate intake of calories, protein, vitamins, minerals, and water. Citrus fruits, veggies, berries, eggs, beans, green leafy veggies, red meat, dairy, & 6-8 glasses H20 q day to stay hydrated. Management of Patients with Burn Injury · Review top nursing priorities for patients for serious burns Tissue integrity, fluid & electrolyte balance, perfusion, gas exchange, analgesics, emotional support, and maintain body temperature. · Review nursing priorities for smoke inhalation Continuous airway assessment, gas exchange, airway obstruction, edema, maintain patent airway, circulation and perfusion, analgesics. Assess the mouth, throat, and nose for signs of soot. · Review superficial, partial-thickness, full-thickness burns what areas of skin are affected Partial-thickness Burns (1st degree/superficial) erythema [local redness] appears sunburn-like, not included in burn size, and heals by themselves. Partial-thickness Burns (2nd degree) Part of the skin has been damaged or destroyed, blisters w/clear fluid, pink underlying tissue, often heals by themselves. Full thickness Burns (3rd degree) Full skin has been destroyed, deep red tissue underlying blister, presence of bloody blister fluid, muscle, and bone may be destroyed. Requires professional treatment. Full thickness Burns (4th degree) Penetrate deep tissue to fat, muscle, and bone. Requires immediate professional treatment. · Review how to assess and document burns- TBSA and Rule of Nines Rule of Nines to determine TBSA. Factors to also consider in determining burn depth>> how injury occured, causative agent ex. Flame or scalding liquid, duration of contact w/agent & thickness of skin injury. Should be revised w/n first 72 hours b/c demarcation of the wound & depth become more clear. More than 30% is a major burn. 2nd and 3rd degree burns are severe burns. · What are concerning signs and symptoms of patients with serious burns -Fluid & Electrolytes shift -Thermoregulation -Cardiovascular effects (decrease, edema, hypovolemia) -Lungs (edema, vasoconstriction) -airway obstruction or ineffective airway clearance -GI/GU (vasoconstriction kidneys, impaired motility/absorption, increased pH, vasoconstriction) · What electrolyte disturbances do burns cause in emergent and acute phase of injury Emergent phase (resuscitation): begins at the onset of care and continues to 24-48 hours after injury. Acute phase (healing): 36-48 hours after injury when the fluid shifts resolves, and lasts until the wound heals. Emergent Phase Acute Phase -Generalized dehydration interstitial -Fluid reenters vascular space from -Reduced blood vol. & hemoconcentration -Hemodilution -Decreased urine output - Increased urine output -Trauma causes release of K+ into xcell fluid = hyperkalemia -sodium traps in edema shifts into cells hypoK+ -Metabolic acidosis -K+ shifts from xcell fluid into cells: potential as K+ is released= hyponatremia hyponatremia -Sodium loss w/diuresis & dilution = -Systemic response includes release of cytokines and other mediators into systemic circulation · Review nursing interventions for chemical burns First rapid assessment, next remove any particles or debris. Remove clothing but careful manipulating body parts could cause further injury. Fabrics could have been melted into the patient's skin.Then irrigate the burned area and cover with a dry sterile dressing. Help thermoregulate, risk hypothermia once clothing is removed. Provide blankets, heating devices, and infuse warm solutions. Receive emergency care at the nearest ED and then be transferred to a burn center once stable. · Review strategies for a patient with coping issues related to burns -begins early as possible in the emergent phase and extends long after the injury -focus is wound healing, psychosocial support, self-image, lifestyle, and restoring maximal functional abilities. -may need reconstructive surgery to improve function and appearance. -counseling and support groups may help patient · Review how to calculate IVF replacement for burn patients -Calculate fluid needs in the first 24 hours post burn. Starting point is the time of injury and know the time of arrival to the treating facility. -regulated so that one half of the total calculated volume is given in the first 8 hours post burn injury. The second half of the calculated volume is given over the next 16 hours. · Review first aid for burns. Initial emergency treatment & education Nursing Care Acute/Intermediate Phase #1 1 restore fluid balance hypermetabolism 2 prevent infection 4 promote skin integrity 5 relieve pain & discomfort st th 3 modulate nd th rd 6 promote mobility th 7 strengthen coping strategies th Assessment of Neurological Head Trauma · Review age related changes to the nervous system Older adults need more time to retrieve information due to loss of cerebral neurons. Intellect doesn’t decline. Pupil size decreases, sensory perception, and mobility change. Decreased coordination, less sleep during the night. · Review GCS, How to use the tool, what info does it provide the nurse using it The scale informs the nurse of the neurological function/ level of consciousness of the patient · Review epidural, subdural bleeds including S/S and nursing interventions, and education Subdural Hematoma - Venous bleeding into space beneath dura and above arachnoid - Most commonly from tearing of bridging veins w/n cerebral hemispheres or from laceration of brain tissue - Bleeding occurs more slowly, symptoms mirror those of epidural hematoma Treatments: Neuro assessments, reduce ICP, Stop the bleeding, Surgical EVD (external ventricular drain) · Review S/S of increased ICP and intervention to decrease ICP Decrease ICP (Osmotic Diuretics) -Decreasing cellular edema -Caution w/hypovolemic patients · Mannitol · 3% saline · 7% saline · 23% saline Increase ICP (CO2) · · Hypoventilation -Dilation -Increase ICP · Hyperventilation -Constrict decrease flow 35-45 -Maximum perfusion · Review Concussion S/S and nursing interventions, and education Concussions can be caused by a direct blow to the head>> head, faced, neck. Direct impact to the head is NOT REQUIRED. -Less than 10% of concussive injuries result in a loss of consciousness. You do not need to be “knocked –out” to get a concussion. · Review Mannitol, use, side effects, nursing considerations Mannitol is a diuretic/ osmotic agent, reduces swelling and pressure around the brain.High dose 1.2-1.4 g/kg in comatose trauma patients w/ operative acute subdural hematoma or operative intraparenchymal temporal lobe hemorrhage. 0.25-1.0 g/kg to control elevated intracranial pressure in severe head injury patients, bolus rate not to exceed 0.1 g/kg/min Side effects>> dry mouth, excess thirst (polydipsia), headache, N/V, excess urination. Nursing considerations>> closely monitor electrolytes and overall fluid balance, cardiopulmonary complications, and neuro assessments. Before and after administration check fluids, body weight, and I&Os. · Review Kcentra. What it used for, nursing considerations Kcentra is used for adults with acute major bleeding. Reversal of warfarin (anticoagulant). Prothrombin Complex Concentrate, administered by IV infusion @ 0.12 ml/kg/min up to max. 8.4 ml/min. Administered at the same time as vitamin through a separate infusion line Infection, IV management (care) & Sepsis Shock · Review MAP- What it is and its importance in assessment-reasons why its reduced Perfusion is related to mean arterial pressure (MAP). The factors that influence MAP include: • Total blood volume • Cardiac output • Size and integrity of the vascular bed, · especially capillaries Total blood volume and cardiac output are directly related to MAP, so increases in either total blood volume or cardiac output raise MAP. Decreases in either total blood volume or cardiac output lower MAP. The size of the vascular bed is inversely (negatively) related to MAP. This means that increases in the size of the vascular bed lower MAP and decreases raise MAP The Surviving Sepsis Guidelines recommend that a MAP of 65 mmHg should be the initial target The initial stage is present when the patient's baseline MAP is decreased by less than 10 mm Hg.The nonprogressive stage of shock occurs when MAP decreases by 10 to 15 mm Hg from baseline.The progressive stage of shock occurs when there is a sustained decrease in MAP of more than 20 mm Hg from baseline. In septic shock, 5. Administer prescribed vasopressors for hypotension that does not respond to initial fluid resuscitation measures to maintain MAP ≥65 mm Hg Review distributive shock- Signs and Symptoms, Treatments, common medications includes septic shock, neurogenic shock, and anaphylactic shock Distributive shock occurs when blood volume is not lost from the body but is distributed to the interstitial tissues where it cannot perfuse organs. It can be caused by blood vessel dilation, pooling of blood in venous and capillary beds, and increased capillary leak. All these factors decrease MAP and may be started either by nerve changes (neural-induced) or by the presence of some chemicals 1494 (chemical-induced) Neural-induced distributive shock is a loss of MAP that occurs when sympathetic nerve impulses are decreased and blood vessel smooth muscles relax, causing vasodilation and poor PERFUSION. Shock results when vasodilation is widespread. Problems leading to loss of sympathetic tone are listed in Table 37-1. Chemical-induced distributive shock has three common origins: anaphylaxis, sepsis, and capillary leak syndrome. It occurs when certain body chemicals or foreign substances in the blood and vessels start widespread changes in blood vessel walls. The chemicals are usually exogenous (originate outside the body), but this type of shock also can be induced by substances normally found in the body, such as excessive amounts of histamine. Anaphylaxis is an extreme type of allergic reaction. It begins within seconds to minutes after exposure to a specific allergen in a susceptible adult. The result is widespread loss of blood vessel tone, with decreased blood pressure and cardiac output. Chapter 20 describes the pathophysiology, prevention, and care of the patient with anaphylactic shock. Sepsis is a widespread infection that triggers whole-body inflammation. It leads to distributive shock when infectious microorganisms are present in the blood and is most commonly called septic shock. A complete discussion of the pathophysiology, prevention, and care for the patient with sepsis and septic shock begins with the IMMUNITY concept exemplar. Capillary leak syndrome is the response of capillaries to the presence of histamine and other chemicals that enlarge capillary pores and allow fluid to shift from the capillaries into the interstitial tissues. These fluids are stagnant, and no GAS EXCHANGE occurs. Problems causing fluid shifts include severe burns, liver disorders, ascites, peritonitis, large wounds, kidney disease, hypoproteinemia, and trauma. Neurogenic Shock: SNS loses ability to stimulate vessels. Massive vasodilation occurs. Decreased perfusion. Causes: spinal cord injury (cervical or upper thoractic, above T6), spinal anesthesia, or drugs that affect SNS. Decreased cardiac afterload.Decreased preload. Hypotension. Increases DVT risk (blood is just hanging out). Hypothermia due to body losing heat and hypothalamus not working. Cold body but warm extremities (blood hangs out in extremities doesn’t return to body**) Bradycardia due to SNS not · working. LOW filling pressures due to vasodilation (low PAWP). Treatments: keep spine immobilized (cervical collar, logrolling patient, blackboard), Manage airway maybe needs incubation and mechanical ventilation , maintain tissue perfusion so MAP should be 8590, so use fluids with crystalloids (fill dilated vessels, increase venous return to heart, increase preload, and ultimately CO), but use IV fluids with caution since fluid loss isn’t an issue.Signs of fluid overload: crackles, difficulty breathing, edema, high PAWP. If fluids don’t work, use vasoconstors to increase SVR, blood pressure, CO such as DOPAMINE. Use ATROPINE for brachycardia, it blocks PNS-effects on heart, but if brachycardia is SEVERe, patients needs TEMPORARY PACING. For hypothermia, use warming devices. Don’t warm too fast. Use FOLEY PLACEMENT if bladder function is loss, don’t want them to retain urine. And must keep tract of urinary output (at least 30cc/hr). Prevent DVT by using ROM daily, compression stockings, anti-coagulants, avoid leg crossing and avoid pillow under knee Septic Shock: Decrease in perfusion. Cells do not receive enough O2. Hypoxic injury, cell death. Organs die too. Small vessels can’t distribute blood flow due to microorganism invasion. Bacteria most common cause. Hypotension, persistent, systolic less than 90 and won’t go up with fluid. Need vasopressors to (Norepi) keep MAP >65. Serum lactate >2mmol/L. CO is fine but decrease in SVR due to major vasodilation due to exaggerated immune response due to damaging toxins. Causes leaky vessels. Fluid goes to interstitial tissue, leads to relative hypovolemia, limiting blood flow to cells. Inflammation causes clotting, uses up clotting factors, risk for DIC. Clots causes more problems to blood flow. Cytokines increase ejection fraction of heart. Risk factors: SEPSIS → Suppressed immune system, Extreme young (very young or elderly), People who received organ transplant, Surgical procedure, Indwelling devices, Sickness (Chronic conditions) Signs and Symptoms: Early->’warm compensation’ warm flushed skin, low BP, high HR, high RR, fever, anxiety, high or normal CO. Late->cold clammy skin, vasoconstriction (poor perfusion due to failing heart), low CO, severe hypotension, high HR, resp high, low urine output, coma, hypothermia. Treatment: increase perfusion by giving large fluid replacement (crystalloids or colloids, successful if BP goes up CVP goes up to 8-12), then titrate vasopressors like Norepi to constrict vessels to increase MAP over 65, can add Dobutamine to vasopressor to increase perfusion by increasing contractions, make sure oxygenated keep O2Sat >95, mechanical ventilation in respiratory failure risk of ARDs, obtain cultures to fight microorganisms, antibiotic therapy if bacteria, decrease inflammation low-dose corticosteroids if not responding to vasopressors or activated protein C/drotrecogin alfa within 24-48 hrs watch for bleeding (anti inflammatory and antithrombotic), early nutrition (enteral nutrition to preserve GI integrity, nutrition also helps immune health, stress ulcer prevention, Famotidine helps with ulcers), control glucose (insulin drip must be >180). Antibiotics given within 1st hr of shock improves outcome. Cultures are needed FIRST, but don’t delay antibiotic therapy. Anaphylactic Shock: Histamine/inflammatory mediators are released ØCause vasodilation/increased permeability ØFluid shifts from intravascular to interstitial ØDecreases volume within vasculature and increases size. Treatment: Remove causing agent ØO2 ØProtect airway ØInhaled beta-two agonists ØCorticosteroids ØAntihistamines-H2 blockers ØMild (stable BP min. SOB) = IM epi 1:1000 -- 0.2 to 0.5 mg ØSevere= (hypotension, SOB) IV epi 1 mg (1 mL of 1:1000 solution) in 250 mL D5W (4 mcg/mL) and infuse IV at a rate of 1 mcg/min (15 mL/hr) to 10 mcg/min. ØRepeat as needed Review interventions to reduce incidence of septic shock · Prevention is the best management strategy for sepsis and septic shock. Evaluate all patients for their risk for sepsis, especially older adults, because the death rate from sepsis in adults older than 65 years is nearly twice that of younger adults. Table 37-4 lists health problems that increase the risk for septic shock. Use aseptic technique during invasive procedures and when working with nonintact skin and mucous membranes in patients with reduced IMMUNITY. Remove indwelling urinary catheters and IV access lines as soon as they are no longer needed. Ensure that patients receiving mechanical ventilation are weaned from the ventilator as soon as possible Early detection can be made by patients and families, as well as health care personnel. This is especially important for patients discharged to home after invasive procedures or surgery. Teach patients and families the signs and symptoms of local infection (local redness, pain, swelling, purulent drainage, loss of function) and early sepsis (fever, urine output less than intake, lightheadedness). Teach them how to use a thermometer and to take the temperature twice a day and whenever they are not feeling well. Urge those with symptoms of early sepsis to immediately contact their health care provider. Teach them that, if antibiotics are prescribed, to take these drugs as prescribed and to complete the entire course. Review common nursing assessments when infusing vasoactive medication Drug therapy with vasopressors is used when hypotension persists despite fluid resuscitation. Commonly used agents include norepinephrine (Levophed), epinephrine (adrenalin), or dopamine (Intropin). Use of vasopressors should be titrated to keep MAP >65 · Review medication (Norepi)-Levophed-what nursing assessment indicated improvement and medication effectiveness · Assess patient for chest pain because these drugs increase myocardial consumption and can cause angina or ischemia. Monitor urine output hourly because higher doses decrease kidney perfusion and urine output. Assess blood pressure every 15 min because hypertension is a symptom of overdose. Assess patient for headache because headache is an early symptom of drug excess. Assess every 30 min for extravasation; check extremities for color and perfusion because if the drug gets into the tissues, it can cause severe vasoconstriction, tissue ischemia, and tissue necrosis. Assess for chest pain because the drug can cause rapid onset of vasoconstriction in the myocardium and impair cardiac oxygenation. Effective if: Improve mean arterial pressure by increasing peripheral resistance, increasing venous return, and increasing myocardial contractility Review rationales for IV bolus and nursing assessment related to fluid bolus in septic shock · fluid bolus becomes the best means by which cardiac output can be increased, organ blood flow restored and arterial blood pressure improved. It improves BP quickly Check 4 potential fluid overload (ex: if pt develops pulmonary edema à we can intubate them Review stages of shock and signs and symptoms of each Initial Stage • Decrease in mean arterial pressure (MAP) of 5-10 mm Hg from baseline value • Increased sympathetic stimulation • Mild vasoconstriction • Increased heart rate . Compensatory mechanisms are effective at returning systolic pressure to normal at this stage; thus oxygen PERFUSION to vital organs is maintained. Nonprogressive Stage • Decrease in MAP of 10-15 mm Hg from baseline value • Continued sympathetic stimulation • Moderate vasoconstriction • Increased heart rate • Decreased pulse pressure • Chemical compensation • Renin, aldosterone, and antidiuretic hormone secretion • Increased vasoconstriction • Decreased urine output • Stimulation of the thirst reflex • Some anaerobic metabolism in nonvital organs • Mild acidosis • Mild hyperkalemia . Signs and symptoms of this stage include changes resulting from decreased tissue PERFUSION. Subjective changes include thirst and anxiety. Objective changes include restlessness, tachycardia, increased respiratory rate, decreased urine output, falling systolic blood pressure, rising diastolic blood pressure, narrowing pulse pressure, cool extremities, and a 2% to 5% decrease in oxygen saturation. he or she can remain in this stage for hours without having permanent damage. Stopping the conditions that started shock and providing supportive interventions can prevent the shock from progressing. The effects of this stage are reversible when nurses recognize the problem and coordinate the interprofessional health care team to start appropriate interventions. Progressive Stage • Decrease in MAP of >20 mm Hg from baseline value • Anoxia of nonvital organs • Hypoxia of vital organs • Overall metabolism is anaerobic • Moderate acidosis • Moderate hyperkalemia • Tissue ischemia . Objective changes are a rapid, weak pulse; low blood pressure; pallor to cyanosis of oral mucosa and nail beds; cool and moist skin; anuria; and a 5% to 20% decrease in oxygen saturation. Laboratory data may show a low blood pH, along 1497 with rising lactic acid and potassium levels. The progressive stage of shock is a life-threatening emergency. Vital organs tolerate this situation for only a short time before developing multiple organ dysfunction syndrome (MODS) with permanent damage. Immediate interventions are needed to reverse the effects of this stage of shock. The patient's life usually can be saved if the conditions causing shock are corrected within 1 hour or less of the onset of the progressive stage Refractory Stage • Severe tissue hypoxia with ischemia and necrosis • Release of myocardial depressant factor from the pancreas • Buildup of toxic metabolites • Multiple organ dysfunction syndrome (MODS) • Death . The sequence of cell damage caused by the massive release of toxic metabolites and enzymes is termed multiple organ dysfunction syndrome (MODS). Once the damage has started, the sequence becomes a vicious cycle as more dead cells open and release metabolites. These trigger small clots (microthrombi) to form, which block tissue PERFUSION and damage more cells, continuing the devastating cycle. Liver, heart, brain, and kidney functions are lost first. The most profound change is damage to the heart muscle. Signs are a rapid loss of consciousness; nonpalpable pulse; cold, dusky extremities; slow, shallow respirations; and unmeasurable oxygen saturation. Therapy, including fluid replacement, is not ef ective in saving the patient's life, even if the cause of shock is corrected and MAP temporarily returns to normal · Review signs and symptoms of compensated, decompensated and irreversible shock · Review signs and symptoms of inflammation · Inflammation is another important nonspecific defense mechanism for preventing the spread of infection. It occurs when tissue becomes damaged or impaired. Damaged cells release enzymes, and polymorphonuclear (PMN) leukocytes (neutrophils) are attracted to the infected site from the bloodstream. One important substance, histamine, increases the permeability of the capillaries in inflamed tissues, thus allowing fluid, proteins, and white blood cells to enter an inflamed area. Other enzymes activate fibrinogen, which causes leaked fluid to clot and prevents its flow away from the damaged site into unaffected tissue, essentially “walling off” the inflamed tissue. The process of phagocytosis disposes of the invading microorganism and often dead tissue. If inflammation is caused by infection, the end products of inflammation form pus, which is then absorbed or exits the body through a break in the skin Responses at the tissue level cause the five cardinal symptoms of inflammation: warmth, redness, swelling, pain, and decreased function.** Review overall patient education when administering antibiotics Most antibiotics can cause nausea, vomiting, diarrhea, and rashes. Stress the importance 895 of completing the entire course of drug therapy, even if symptoms have improved or disappeared · Review types of isolation and common diseases for each type · For older adults, be sure to teach the need to drink additional fluids if diarrhea occurs as result of antibiotic therapy. Observe older adults in inpatient facilities carefully for signs and symptoms of dehydration as described in Chapter 11. Acute confusion, hypotension, and tachycardia are common indicators of dehydration and require interventions such as IV fluids. Serum electrolyte levels may increase, causing additional risks to the older adult. Airborne Precautions are used for patients known or suspected to have INFECTIONS transmitted by the airborne transmission route. These infections are caused by organisms that can be suspended in air for prolonged periods. Negative-airflow rooms are required to prevent airborne spread of microbes. Enclosed booths with highefficiency particulate air (HEPA) filtration or ultraviolet light may be used for sputum induction procedures. Tuberculosis, measles (rubeola), and chickenpox (varicella) are examples of airborne diseases. 1. Private room required with monitored negative airflow (with appropriate number of air exchanges and air discharge to outside or through HEPA filter); keep door(s) closed 2. Special respiratory protection: • Wear PAPR for known or suspected TB • Susceptible people not to enter room of patient with known or suspected measles or varicella unless immune caregivers are not available • Susceptible people who must enter room must wear PAPR or N95 HEPA filter* 3. Transport: patient to leave room only for essential clinical reasons, wearing surgical mask Droplet Precautions are used for patients known or suspected to have INFECTIONS transmitted by the droplet transmission route. Such infections are caused by organisms in droplets that may travel 3 feet but are not suspended for long periods. Examples of infectious conditions requiring Droplet 885 Precautions include influenza, mumps, pertussis, and meningitis caused by either Neisseria meningitidis or Haemophilus influenzae type B. 1. Private room preferred: if not available, may cohort with patient with same active infection with same microorganisms if no other infection present; maintain distance of at least 3 feet from other patients if private room not available 2. Mask: required when working within 3 feet of patient 3. Transport: as for Airborne Precautions Contact Precautions are used for patients known or suspected to have INFECTIONS transmitted by direct contact or contact with items in the environment. Patients with significant multidrugresistant organism (MDRO) infection or colonization, such as methicillin-resistant Staphylococcus aureus (MRSA) or vancomycin-resistant Enterococcus (VRE), are placed on Contact Precautions. Other infections requiring Contact Precautions include pediculosis (lice), scabies, respiratory syncytial virus (RSV), and C. dif icile. 1. Private room preferred: if not available, may cohort with patient with same active infection with same microorganisms if no other infection present 2. Wear gloves when entering room 3. Wash hands with antimicrobial soap before leaving patient's room 4. Wear gown to prevent contact with patient or contaminated items or if patient has uncontrolled body fluids; remove gown before leaving room 5. Transport: patient to leave room only for essential clinical reasons; during transport, use needed precautions to prevent disease transmission 6. Dedicated equipment for this patient only (or disinfect after use before taking from room) Review the 4 classes of shock hypovolemic, cardiogenic, obstructive, and distributive shock (I went over distributive above) Hypovolemic: Total body fluid decreased (in all fluid compartments). Specific Cause or Risk Factors • Hemorrhage • Trauma • GI ulcer • Surgery • Inadequate CLOTTING • Hemophilia • Liver disease • Cancer therapy • Anticoagulation therapy • Dehydration • Vomiting • Diarrhea • Heavy diaphoresis • Diuretic therapy • Nasogastric suction . Fluid replacement ØCrystalloids –NS & LR •Pass easy across vascular wall •Give at 3:1 replacement ratio •Adult 1-2 liters •Peds 20ml/kg Warm the fluids ØPrevent hypothermia ØPrevent clotting disturbances Safety Practice for Quality and care of Hypovolemic: Ensure a patent airway. • Insert an IV catheter or maintain an established catheter. • Administer oxygen. • Elevate the patient's feet, keeping his or her head flat or elevated to no more than a 30-degree angle. • Examine the patient for overt bleeding. • If overt bleeding is present, apply direct pressure to the site. • Administer drugs as prescribed. • Increase the rate of IV fluid delivery. • Do not leave the patient. Drug Treatment of Hypovolemic: Vasoconstrictors—Improve mean arterial pressure by increasing peripheral resistance, increasing venous return, and increasing myocardial contractility. Dopamine (Intropin, Revimine) Norepinephrine (Levophed) Phenylephrine HCl Assess patient for chest pain because these drugs increase myocardial consumption and can cause angina or ischemia. Monitor urine output hourly because higher doses decrease kidney perfusion and urine output. Assess blood pressure every 15 min because hypertension is a symptom of overdose. Assess patient for headache because headache is an early symptom of drug excess. Assess every 30 min for extravasation; check extremities for color and perfusion because if the drug gets into the tissues, it can cause severe vasoconstriction, tissue ischemia, and tissue necrosis. Assess for chest pain because the drug can cause rapid onset of vasoconstriction in the myocardium and impair cardiac oxygenation. Inotropic Agents—Directly stimulate beta-adrenergic receptors on the heart muscle, improving contractility Dobutamine (Dobutrex) Milrinone (Primacor) Assess for chest pain because these drugs increase myocardial oxygen consumption and can cause angina or infarction. Assess blood pressure every 15 min because hypertension is a symptom of overdose. Agents Enhancing Myocardial Perfusion—Improve myocardial perfusion by dilating coronary arteries rapidly for a short time. Sodium nitroprusside (Nitropress, Nipride) Protect drug container from light because light degrades the drug quickly. Assess blood pressure at least every 15 min because the drug can cause systemic vasodilation and hypotension, especially in older adults Cardiogenic: Overall Cause Direct pump failure (fluid volume not affected). Specific Cause or Risk Factors • Myocardial infarction • Cardiac arrest • Ventricular dysrhythmias • Cardiac amyloidosis • Cardiomyopathies • Myocardial degeneration · Review the stages of shock · Already did - See above Review goal directed therapy for the 4 classes of shock · Signs/Symptoms of Cardiogenic: High PAWP** Treatment for Cardiogenic: Inotropic drugs (dopamine and norepi) ØAntiarrhythmic drugs ØDon’t overload with IVF. May need diuretics to draw some fluid out to decrease workload. Obstructive: Overall Cause Cardiac function decreased by noncardiac factor (indirect pump failure). Total body fluid is not affected, although central volume is decreased. Specific Cause or Risk Factors • Cardiac tamponade • Arterial stenosis • Pulmonary embolus • Pulmonary hypertension • Constrictive pericarditis • Thoracic tumors • Tension pneumothorax Treatment of Obstructive: TX: Relieve obstruction ØTension Pneumothorax = Needle decompression ØCardiac Tamponade = Pericardiocenthesis Once obstruction is relived shock is treated Already did - See above Review IV dressing care assess the skin underneath the dressing especially for signs of medical adhesive– related skin injury (MARSI) (INS, 2016). Lightly palpate the area over the dressing. Assess the integrity of the dressing, making sure that it is clean, dry, and adherent to the skin on all sides. When an implanted port is accessed, the sterile occlusive dressing should cover the entire needle and site. Sterile dressings used over the insertion site protect the skin and puncture site. For a short peripheral catheter, the transparent membrane dressings do not require routine changes. Short peripheral lines do not usually dwell longer than a few days; and, as long as the dressing is dry, clean, and intact, it does not have to be changed. Any VAD dressing should be changed when it is loose or soiled. For central lines and midline catheters, tape and sterile gauze or a transparent membrane dressing may be used. Change tape and gauze dressings every 48 hours; change transparent membrane dressings such as Tegaderm, every 5 to 7 days (INS, 2016). The initial dressing on a midline catheter or PICC is usually tape and gauze, changed within 24 hours after insertion because some bleeding is likely. Transparent membrane dressings can be used for subsequent dressing. For patients who develop erythema (redness) from Tegaderm, the IV3000 dressing from Smith and Nephew may be used. Document when you change the sterile dressing and your IV site assessments in the appropriate electronic health record according to agency policy When changing the dressing, remove it by pulling laterally from side to side. It can also be removed by holding the external catheter and pulling it off toward the insertion site. Never pull it of 519 by pulling away from the insertion site because this could dislodge the catheter! Protect the external catheter, dressing, and all attached tubing from water because it is a source of contamination. Remind unlicensed assistive personnel (UAP) to cover the extremity where the IV line is located when giving the patient a bath. A plastic bag or wrap can be taped over the extremity to keep the dressing and site dry. · Review Central Line Dressing video and care of site · Review PICC line care · Review discontinuing an IV site, Central line, and PICC line · Review MRSA, VRE, and CRE- How they occur, nursing assessments and nursing interventions for each MRSA Staphylococcus aureus (S. aureus) is a common bacterium found on the skin and perineum and in the nose of many people. It is usually not infectious when in these areas because the number of bacteria is controlled by good hygiene measures. However, when skin or mucous membranes are not intact, localized infection such as boils or conjunctivitis may occur. If the organism enters into deep wounds, surgical incisions, the lungs, or bloodstream, more serious or systemic infections occur that 888 require strong antibiotics such as methicillin. Within the past 40 years, more and more S. aureus infections have not responded to methicillin or other penicillin-based drugs. Known as MRSA, these infections are one of the fastest growing and most common in health care today. This type of infection is called health care–associated MRSA, or HAMRSA. Patients who have HA-MRSA have increased hospital stays at a very high cost. To add to this problem, some patients may be colonized with the organism. Health care staff members may also colonize. Patients who develop HA-MRSA pneumonia, abscesses, or bacteremia (bloodstream infection [BSI]) can quickly progress to sepsis and death. MRSA is spread by direct contact and invades hospitalized patients through indwelling urinary catheters, vascular access devices, open wounds, and endotracheal tubes. It is susceptible to only a few antibiotics, such as IV vancomycin (Lyphocin, Vancocin) and oral linezolid (Zyvox). A newer IV antibiotic, ceftaroline fosamil (Teflaro), is the first cephalosporin approved to treat MRSA. Studies show that bathing hospitalized patients with premoistened cloths or warm water containing chlorhexidine gluconate (CHG) solution can significantly reduce MRSA infection by 23% to 32% (Kassakian et al., 2011; Powers et al., 2012). In 2013 the American Association of Critical Care published a recommendation that nurses use CHG to bathe patients in critical care settings as a way to reduce MRSA and other multidrug-resistant organisms. Patients most at risk for HA-MRSA are older adults and those who have suppressed IMMUNITY, have a long history of antibiotic therapy, or have invasive tubes or lines. ICU patients are especially at risk. Check with your agency policy regarding specific MRSA preventive measures. Examples include bathing patients with chlorhexidine wipes and administering nasal mupirocin ointment. Although controversial, some health care facilities have a MRSA-surveillance program in which each patient's nose is swabbed and cultured for MRSA. Staff may also be cultured. All patients with HA-MRSA infection or colonization should be placed on Contact Precautions. Community-associated MRSA, or CA-MRSA, causes infections in healthy, nonhospitalized people, especially those living in college housing and prisons. It is easily transmitted among family members and can cause serious skin and soft-tissue infections, including abscesses, boils, and blisters. The best way to decrease the incidence of this growing problem is health teaching, including: • Performing frequent hand hygiene, including using hand sanitizers • Avoiding close contact with people who have infectious wounds • Avoiding large crowds • Avoiding contaminated surfaces • Using good overall hygiene Minocycline · (Minocin, Apo-Minocycline) and doxycycline (Doryx, Apo-Doxy) are usually effective in treating CA-MRSA. Vancomycin-Resistant Enterococcus (VRE) Enterococci are bacteria that live in the intestinal tract and are important for digestion. When they move to another area of the body, such as during surgery, they can cause an infection, which is usually treatable with vancomycin. However, in recent years many of these infections have become resistant to the drug, and VRE results. Risk factors for this infection include prolonged hospital stays, severe illness, abdominal surgery, enteral nutrition, and immunosuppression. Place patients with VRE infections on Contact Precautions to prevent contamination from body fluids. Unfortunately VRE can live on almost any surface for days or weeks and still be able to cause an infection. Contamination of toilet seats, door handles, and other objects is very likely for a lengthy period. Carbapenem-Resistant Enterobacteriaceae (CRE)Carbapenem antibiotics, most often given for abdominal infections such as peritonitis, have been used extensively for the past 15 years. Examples of this class of antibiotics include imipenem (Cilastin) and meropenem (Merrem IV). Klebsiella and Escherichia coli (E. coli) are types of Enterobacteriaceae that are located within the intestinal tract. Carbapenem-resistant Enterobacteriaceae (CRE) is a family of pathogens that are difficult to treat because they have a high level of resistance to carbapenems caused by enzymes that break down the antibiotics. Klebsiella pneumoniae (KPC) and New Delhi metallo-beta-lactamase are examples of these enzymes. Patients who are high risk for CRE include those in ICUs or nursing homes and patients who are immunosuppressed, including older adults. To prevent the transmission of this infection, place patients who are high risk on Contact Precautions. The CDC (2013) also recommends chlorhexidine (2% dilution) bathing to prevent CRE or decrease colonization and other types of infections from MDROs. Review the sepsis bundle and nursing responsibilities in managing sepsis Within the first 3 hours of suspecting severe sepsis: 1. Measure serum lactate levels. 2. Obtain blood cultures before administering antibiotics. 3. Administer broad-spectrum antibiotics. 4. Administer 30 mL/kg crystalloids intravenously for hypotension or lactate ≥4 mmol/L. Within 6 hours of initial indications of suspected septic shock: 5. Administer prescribed vasopressors for hypotension that does not respond to initial fluid resuscitation measures to maintain MAP ≥65 mm Hg. 6. If arterial hypotension persists despite initial fluid volume resuscitation or lactate remains ≥4 mmol/L (36 mg/dL), reassess volume status and tissue perfusion and document findings (reassessment of volume status and tissue perfusion as outlined below). 7. Remeasure lactate level if initial value was elevated. Document reassessment of volume status and tissue perfusion with EITHER: • Repeat focused examination (after initial fluid resuscitation), including vital signs, cardiopulmonary, capillary refill, pulse, and skin findings OR TWO OF THE THREE FOLLOWING: • Measure of central venous pressure • Measure of central venous oxygen saturation • Bedside cardiovascular ultrasound • Dynamic assessment of fluid responsiveness with passive leg raise or fluid challenge Oxygen therapy is useful whenever poor tissue PERFUSION and poor GAS EXCHANGE are present. The patient with septic shock is more likely to be mechanically · ventilated. Care of the patient being mechanically ventilated is discussed in detail in Chapter 32. Drug therapy to enhance cardiac output and restore vascular volume is essentially the same as that used in hypovolemic shock (see Chart 37-4). In addition, drug therapy is needed to combat sepsis, adrenal insufficiency, hyperglycemia, and clotting problems. Although septic shock can be caused by any organism, the most common agents are gramnegative bacteria. In accordance with the recommendations of The Joint Commission's National Patient Safety Goals (NPSGs), IV antibiotics with known activity against gram-negative bacteria are given before organisms are identified, preferably within 1 hour of a sepsis diagnosis. Multiple antibiotics with broad-spectrum activity are prescribed, based on the site of infection and the most common geographic infections, until the actual causative organism is known (Droege et al., 2016). The stress of severe sepsis can cause adrenal insufficiency. Adrenal support may involve providing the patient with low-dose corticosteroids during the treatment period. Drugs used for this purpose are IV hydrocortisone and oral fludrocortisone (Florinef). Patients with sepsis or septic shock usually have elevated blood glucose levels (>180 mg/dL or >10 mmol/L), which is associated with a poor outcome. Insulin therapy is used to maintain blood glucose levels between 110 mg/dL (6.2 mmol/L) and 150 mg/dL (8.4 mmol/L). Keeping the blood glucose level below 110 mg/dL (6.2 mmol/L) is associated with increased mortality. During severe sepsis, patients have microvascular abnormalities and form many small clots. Heparin therapy with fractionated heparin is used to limit inappropriate CLOTTING and prevent the excessive consumption of clotting factors. Blood replacement therapy is used when poor CLOTTING with hemorrhage occurs and may include clotting factors, platelets, fresh frozen plasma (FFP), or packed red blood cells. Chapter 40 discusses in detail the care of the patient during blood replacement. The use of platelet transfusion is recommended ahead of other blood products for patients with septic shock to improve CLOTTING Review multiple organ dysfunction syndrome (MODS). The effects are temporary and reversible if the cause of shock is corrected within 1 to 2 hours after onset. When shock conditions continue for longer periods without help, the resulting increased metabolites cause so much cell damage in vital organs that they are unable to perform their critical functions. When this problem, known as multiple organ dysfunction syndrome (MODS), occurs to the extent that vital organs die, recovery from shock is no longer possible (see the section on Refractory Stage of Shock. The sequence of cell damage caused by the massive release of toxic metabolites and enzymes is termed multiple organ dysfunction syndrome (MODS). Once the damage has started, the sequence becomes a vicious cycle as more dead cells open and release metabolites. These trigger small clots (microthrombi) to form, which block tissue PERFUSION and damage more cells, continuing the devastating cycle. Liver, heart, brain, and kidney functions are lost first. The most profound change is damage to the heart muscle. Spinal Cord Injury · Review priorities of spinal cord injury · Review the video-These will help you answer the questions 1st Priority: Airway. Assess airway patency. (especially c4 and above, needs respiratory support) Look at RR, depth, pattern. May need ventilation. L3 and above may have weakened respiratory muscles. Neuro Assessment : motor and sensory assessment. Use ROM to help spasticity. Ask for numbness/tingling. And use light touch to see if they can feel it. HR and Blood Pressure: especially for T and above. Usually bradycardic and vasodilation. Give volume and maybe vasopressor to keep MAP >85 Cervical Spine Stabilization: collars , cervical traction Early surgical intervention to decompress and stabilize Temperature Control: C6 and above. Monitor. Will take temperature of environment Mobility: ambulate patients, PT/OT · Review autonomic dysreflexia. What it is, common reasons it occurs, and what nursing can do to fix and educate the patient Autonomic dysreflexia (AD), sometimes referred to as autonomic hyperreflexia, is a potentially lifethreatening condition in which noxious visceral or cutaneous stimuli cause a sudden, massive, uninhibited reflex sympathetic discharge in people with high-level SCI. T6 and above. Hypertensive Crisis due to PAIN. Bladder distention: number 1 reason. Signs: • Sudden, significant rise in systolic and diastolic blood pressure, accompanied by bradycardia • Profuse sweating above the level of lesion—especially in the face, neck, and shoulders; rarely occurs below the level of the lesion because of sympathetic cholinergic activity • Goose bumps above or possibly below the level of the lesion • Flushing of the skin above the level of the lesion—especially in the face, neck, and shoulders • Blurred vision • Spots in the patient's visual field • Nasal congestion • Onset of severe, throbbing headache • Flushing about the level of the lesion with pale skin below the level of the lesion • Feeling of apprehension Causes: The causes of AD are typically GI, gynecologic-urologic (GU), and vascular stimulation. Specific risk factors are bladder distention, urinary tract infection, epididymitis or scrotal compression, bowel distention or impaction from constipation, or irritation of hemorrhoids. Pain; circumferential constriction of the thorax, abdomen, or an extremity (e.g., tight clothing); contact with hard or sharp objects; and temperature fluctuations can also cause AD. Patients with altered SENSORY PERCEPTION are at great risk for this complication. If the patient experiences AD, raise the head of the bed immediately to help reduce the blood pressure. Notify the primary health care provider (PHCP) immediately for drug therapy to quickly reduce blood pressure as indicated. Determine the cause of AD and treat it promptly (Chart 43-3). For example, if the bladder is distended, catheterize the patient to relieve the urinary retention. Check the room temperature and bed coverings and adjust as needed for patient COMFORT. Lack of SENSORY PERCEPTION may prevent the patient from noticing temperature variations Emergency Care of the Patient Experiencing Autonomic Dysreflexia: Immediate Interventions • Place patient in a sitting position (first priority!), or return to a previous safe position. • Notify the primary health care provider or Rapid Response Team. • Assess for and treat the cause: • Check for urinary retention or catheter blockage: • Check the urinary catheter tubing (if present) for kinks or obstruction.If your bladder management program is intermittent catheterization, you may need to drain your bladder by performing a straight cath. This should be done slowly to prevent bladder spasms. ** • If a urinary catheter is not present, check for bladder distention and catheterize immediately if indicated: • Consider using anesthetic ointment on tip of catheter before catheter insertion to reduce urethral irritation. • Determine if a urinary tract infection or bladder calculi (stones) are contributing to genitourinary irritation. • Check the patient for fecal impaction or other colorectal irritation, using anesthetic ointment at rectum. Disimpact if needed. • Examine skin for new or worsening pressure injury symptoms. • Monitor blood pressures every 10 to 15 minutes. • Give nifedipine or nitrate as prescribed to lower blood pressure as needed. • (Patients with recurrent autonomic dysreflexia may receive an alpha blocker prophylactically.) · Review NEXUS Criteria for spinal injury. Mnemonic - NSAID: 1. Neuro deficit. 2. Spinal midline tenderness in C-spine. 3. Alertness. 4. Intoxication. 5. Distracting injury.
