NUR 265 ADVANCED MEDICAL-SURGICAL CONCEPTS TEST # 4 CRITICAL CONCEPTS, Exams of Nursing

Download NUR 265 ADVANCED MEDICAL-SURGICAL CONCEPTS TEST # 4 CRITICAL CONCEPTS and more Exams Nursing in PDF only on Docsity! 1 1 NUR 265 ADVANCED MEDICAL-SURGICAL CONCEPTS TEST # 4 CRITICAL CONCEPTS Cancer & Oncological Emergencies (18 Questions) • Cancer Development – Chapter 24 1. Briefly discuss the pathophysiology of cancer. • Cancer cells lack apoptosis (programmed cell death) • Cancer cells are cells that are abnormally, and rapidly multiplying; unlike normal cells. 2. Compare the characteristics of benign and malignant tumor cells. Table 23- 1, pg. 398 • Benign: grow by expansion, specific morphology • Malignant: grow by invasion, and have anaplasia (loss of specific appearance of their parent cell), infinite lifespan, immortal. 3. Discuss the most common routes of cancer cell metastasis. Pg. 399 • 1: Lymphatic System • 2: Blood • 3: Seeding 4. Discuss primary versus secondary prevention of cancer. Table 23-2, pg. 399 • Primary: Avoiding exposure to known causes of cancer (smoking, bad diet, UV exposure) o Tobacco use is a causative or permissive factor in 30% of all cancers • Secondary: Screening of any sort for early detection 5. Identify the most common site(s) of metastasis for the following types of cancer: prostate, breast, lung, colorectal, and melanoma. Table 23-3, pg. 401 2 1 • Prostatebone; especially spine and legs • Breast bone and lung • ColorectalLiver 1 5 • Leukemia is a result of an increased amount of poorly formed, non-functioning WBC’s causing a malfunction with RBC’s (anemia) and platelets (thrombocytopenia) r/t crowding from the WBC’s. • #1 subjective sign is fatigue • #1 objective sign is tachycardia • Observe skin for petichiae, color, or ecchymosis • Ask pt. about fatigue, bruising, bleeding, infections/illnesses, night sweats and unexplained fevers. Bladder • Ask pt. about dysuria, hematuria, cloudy urine, increased frequency or urgency. Lung • Respiratory assessment • Examine mucous membranes for color • How many words can the pt. say between breaths? • Ask pt. about a cough, hoarseness, smoking hx, exposure to inhalation irritants, SOB, activity intolerance, frothy or bloody sputum, pain in the arms or chest, and difficulty swallowing. 12.Briefly discuss racial differences in cancer development, Table 23-11, pg. 406. • Caucasian Lung • African AmericanLung • Asian American Breast • Hispanic AmericanProstate 13.Discuss, in detail, the gene mutations BRCA1 and BRCA2. Pg. 407. • Gene mutations; tests done to determine genetic predisposition • BRCA1: increases the risk for both ovarian and breast cancer • BRCA2: increases the risk for breast cancer Care of Patients with Cancer – Chapter 24 1. Discuss the (4) general disease-related consequences of cancer 1 6 • Reduced Immunity and Blood-Producing FunctionIncreased risks for infection, especially with leukemia and lymphoma; anemia and thrombocytopenia. Pt. feels weak and fatigued and is at risk for bleeding. • Altered GI Structure and Functionmetastasis to livercachexia (malnutrition and extreme body wasting)death. Diet high in proteins and carbohydrates. • Motor and Sensory Deficits Pain, especially chronic pain. • Reduced Oxygenationhypoxia and poor tissue oxygenation. 1. Discuss, in detail, radiation therapy, to include the following concepts: • Gamma rays: high energy photons, used most commonly with radiation because of their ability to deeply penetrate tissue. • Exposure: amount of radiation delivered to the tissue • Radiation dose: amount of radiation absorbed by the tissue. 2. Teletherapy • Radiation delivered from a source outside of the patient. Since the source is external, the pt. is not radioactive and is not hazardous to others. 3. Brachytherapy • With all types of brachytherapy, radiation source is within the pt; therefore, the pt. emits radiation for a period of time and is hazardous to others. • When the isotopes are unsealed, they enter body fluids and eventually are eliminated in waste products, which are radioactive and should not be directly touched by other people. After the isotope is completely eliminated from the body, neither the pt. nor the body wastes are radioactive. • While the solid implants are in place, the pt. emits radiation but excreta are not radioactive and do not pose a hazard to anyone. 4. Care of the Patient with Sealed Implants of Radioactive Sources • TIME, DISTANCE AND SHIELDING !!! THIS DETERMINES EXPOSURE. • Pt. will be on complete bedrest • Pt. must have a private room with a private bath • Place a “Caution: Radioactive Material” sign on the door • If portable lead shields are available, place between the pt. and the door • Keep pts. door closed as much as possible 1 7 • Wear a dosimeter film badge at all times when caring for pt.; badge offers no protection but measure amount of radiation exposure; do not share badge with others. • Wear a lead apron while providing care, do not turn back to pt. to avoid exposure • Pregnant nurses, pregnant women, and children under 16 should not take care of these pts. • Limit each visitor a half-hour each day and advise to stay at least 6 feet away from pt. • Never touch radioactive source with bare hands; if source becomes dislodged, use long-handled lead forceps to grab source and place in lead container in pts. room. • Save all dressing and bed linens in the pts. room until after radioactive source is removed, then dispose of in the usual manner. Other equipment can be removed from the room at any time without special precautions and does not pose a hazard to others. 5. Patient and Family Education: Skin Protection During Radiation Therapy • MAKE SURE PT. HAS ADEQUATE ACTIVITIES TO DO SINCE THEY ARE ISOLATED AND CONFINED. • Wash the irritated are gently each day with water and/or mild soap • Use hand rather than a washcloth to be gentler • Rinse soap thoroughly • If ink or dye markings are present to identify the exactly where the beam of radiation is to be focused, TAKE CARE NOT TO REMOVE THEM • Dry the irritated are by patting rather than rubbing; use a clean, soft cloth • Use only powders, ointments, lotions or creams on your skin at the radiation site that are prescribed by the radiation oncology dept. • Wear soft clothing at the radiation site • Avoid wearing belts, buckles, straps, or any type of clothing that binds or rubs the kin at the radiation site • Avoid sun exposure to radiation site; protect are by wearing clothes over it, go outdoors in the early mornings or evenings to avoid more intense rays; when outdoors, stay under awnings, umbrellas, and other forms of shade during the hours when the sun’s rays are most intense (10am-7pm) • Avoid heat exposure to radiation site. 1 10 mouth sponges, and rinse mouth with ALCOHOL-FREE mouth wash! Use water or saline only !! • Peripheral neuropathy: o loss of sensory or motor function of peripheral nerves associated with exposure to certain anti-cancer drugs. o Protect feet and other areas where sensitivity is reduced, do not wear tight socks, wear shoes, do not wear tight shoes, inspect feet daily, test water with a thermometer before bathing, use pot holders, drink 2-3 liters of fluid daily unless restricted, avoid loose rugs on the floor, use handrails, eat foods high in fiber. Oncologic Emergencies 1. Sepsis 2. DIC 3. SIADH 1 11 • Infec tion of the bloo d; caus es sever e perip heral vaso dilati on (sept ic shoc k) • Blood culture should be obtained if any suspicion is present! • Any increase in temperature should be reported • P t s . w i t h c a n c e r a re at risk for sepsis because of their low WBC count and suppressed immune system. • Disseminated intravascular coagulation • In pts. with cancer, DIC is often caused by gram-negative sepsis, by the release of thrombin or thromboplastin from cancer cells or blood transfusions. • Massive blood clotting that forms micro emboli throughout the body, plugging perfusion to organs; begins during HEMODYNAMIC state of septic shock. • ADMINISTER HEPARIN! • Earliest sign is bleeding from an IV site!! • If not treated, pt. will hemorrhage and die. • Results from a brain tumor • Too much ADH • Fluid volume excess • Dilutional hyponatremia • Fluid restriction of 600ml/day 1 12 • oliguria • Tx: IV hypertonic saline • Prevent fluid overload, monitor for PULMONARY EDEMA (pink, frothy sputum) • Serum sodium 115-120 • Change in LOC 4. Spinal Cord Compression • r/t a tumor or vertebrae metastasis resulting in vertebrae collapsing. • Tx with palliative care and high-dose corticosteroids to reduce swellings and relieve symptoms. 5. Hypercalcemia • Caused by bone metastasisbone begins to crumblereleases calcium into the blood stream • S/S are loss of appetite, N/V, constipation and increased urine output. • Calcium levels greater than 11 6. Superior Vena Cava Syndrome • SVC is compressed or obstructed by tumor or clots in the vessel. • Painful and life-threatening • S/S: venous congestion of head, neck and upper trunk, edema of the face and around the eyes. • Tx is a stent 7. Tumor Lysis Syndrome • Large numbers of tumor cells are destroyed quickly • Complication of successful chemo/radiation • Intracellular contents (potassium and purine (uric acid)) are released into the bloodstream faster than the body can eliminate them • Hyperkalemia occurs causing cardiac dysfunction; tall, peaked t- waves. • Uricemia occurs causing acute kidney failure due to uric crystals. • Tx with allopurinol (tx for gout) and IV insulin for potassium. 8. Diagnostic procedure: frozen section biopsy • Biopsy results are immediate in OR, this can result in tumor removal, partial tumor removal, or a mastectomy if the pt. consented prior too. • If this occurs, pt will be very traumatized when they wake up since they do not know what occurred while they were under. Be supportive. • Can be inconclusive and pt. will only have a biopsy done. 1 15 as soon as possible to lower the chances of the baby contracting the virus. 3. Discuss, in detail, HIV transmission and health care workers. Pg. 363. • Needle stick or “sharps” injuries are the main means of occupation-related HIV infection for heath care workers. • The best prevention for health care providers is the consistent use of Standard Precautions for all patients as recommended by the CDC and required by The Joint Commission. 4. Discuss, in detail, the following laboratory assessment for HIV/AIDS: CD4+ T- cell and CD8+ T-cell counts (normal range for CD4+ T-cells=500-1500); viral load. Pg. 368-369. • CD4+ T-cell counts. Normal range is 500-1500/mm3 . CD4+ t-cell counts will be low when HIV is present. • CD8+ T-cell counts remain normal. 5. Discuss the diagnosis of HIV using the ELISA and Western Blot. Pg. 369 • ELISA is an inexpensive and accurate HIV test. The patient’s serum is mixed with HIV grown in culture. If the patient has antibodies to HIV, they bind to the HIV antigens and can be detected (positive result). However, this test can be negative even when the person has HIV infection if the test is performed before antibodies are made in sufficient amounts. This means that if the patient has an episode of unprotected sex with an HIV positive person one night and comes in for testing a week later, the ELISA will be negative even though the patient may have active HIV. Thus the testing during the window does not provide useful information. • If the ELISA test is POSITIVE then the Western blot is used to confirm the diagnosis 6. Briefly discuss HAART therapy. pg. 370 • goal of HAART therapy is to stop replication of HIV. You can NOT kill HIV. o HAART is termed highly active antiretroviral therapy (combinations of different types of antiretroviral agents, aka “cocktails.”) It is showing 1 16 good results as measured by reduced viral load and improved CD4+ T- cell counts 1 17 o An important issue with HAART is the development of drug-resistant mutations in the HIV organism. When resistance develops, the drugs no longer suppress viral replication. Testing is now possible to determine whether a strain of HIV has developed resistance to specific drugs o DRUG ALERT: ▪ Ensure that HAART drugs are not missed, delayed, or administered in lower-than-prescribed doses in the inpatient setting. Teach patients the importance of taking their drugs exactly as prescribed to maintain the effectiveness of HAART drugs. Even a few missed doses per month can promote drug resistance 7. Discuss specifically the testing for TB with a client with HIV. Pg. 366. See: Nursing Safety Priority:Action Alert. • False negative is possible (even if they are positive) because of Anergy (depressed immune system) • Anergy- inability to have an immune response because CD4 + Tcell count is less than 200mm. • If pt. is experiencing symptoms of TB even with a negative reading and they have HIV, place them on airborne precautions!!! • ANY TEMPERATURE IS A SERIOUS MATTER AND SHOULD BE REPORTED 8. Discuss why the older adult is at risk for HIV/AIDS. o Poor education because hospital staff doesn’t “think” they are having sex. o Inability to get pregnant/ not concerned with getting pregnant therefor they don’t see the need in using protection. Systemic Sclerosis (Scleroderma) – Chapter 20, pg. 347-348 (2 Questions) 1. Briefly discuss the pathophysiology of SSc. Pg. 347 • SSc, also called scleroderma, is an uncommon chronic, inflammatory, autoimmune connective tissue disease. Involving the entire body!!!! 1 20 Care of Patients with Shock – Chapter 39, pg. 808 (8 Questions) 1. Define: shock, pg. 809. • Lack of 02 to the tissues. Oxygen and tissue perfusion needs to maintain cell function are not met. 2. Briefly discuss the common cause of the following types of shock: hypovolemic, cardiogenic, anaphylactic, and septic. Pg. 812. • Hypovolemic – hemorrhage and dehydration • External fluid loss; Internal fluid shifts • Occurs when too little circulating blood volume causes a MAP decrease, resulting in inadequate total body oxygenation • Cardiogenic – direct pump failure • Occurs when the actual heart muscle is unhealthy and pumping is directly impaired. Myocardial infarction is the most common cause of direct pump failure • Distributive – blood distributed to interstitial tissues where it cannot circulate and deliver oxygen (all over body) • e.g. chemical-induced which includes anaphylactic and septic and neural- induced, e.g. spinal cord injury (loss of sympathetic system) • d. Anaphylactic- major VASODILATION. Massive release of histamine causing massive peripheral vasodilation!! (all of the blood runs to the feet) • EX: Allergic reaction to something like bee sting, allergy, latex, severe food allergy, transfusion reaction, penicillin sensitivity. - DOC is Epinpherine • e. Obstructive- Cardiac tampanode (too much fluid in the pericardium. Tx; pericardioscentesis) 3. Discuss the key features of the stages of shock. Pg. 813-814. ****All stages= Metabolic Acidosis from the breakdown of lactic acid*** o Initial Stage (Early Stage): ▪ A heart and respiratory rate increased from the patient’s baseline level or slight increase in diastolic blood pressure may be the only objective manifestation of this early stage of shock! 1 21 o Nonprogressive Stage of Shock (Compensatory-trying to fix itself): 1 22 ▪ Reduction in urine output; tissue hypoxia in nonvital organs; metabolic acidosis with hyperkalemia. o Progressive Stage of Shock (Intermediate Stage): ▪ -HR greater than 150 BPM (tachycardia) ▪ Vital organs develop hypoxia. Life-threatening emergency!!! o Refractory Stage of Shock (Irreversible ): ▪ Therapy is not effective in saving the patient’s life; rapid loss of consciousness, nonpalpable pulse; cold, dusky extremities (mottling), slow, shallow respirations (cheyne stokes), and unmeasurable oxygen saturation. ---these are signs of impending death 4. Briefly discuss multiple organ dysfunction syndrome (MODS). Pg. 814. • EXTREME cell damage caused by the massive release of toxic metabolites and enzymes • Once the damage has started, the sequence becomes a vicious cycle as more dead cells break open and release harmful metabolites. These trigger small clots (microthrombi) to form, which block tissue oxygenation and damage more cells, thus continuing the devastating cycle. • Liver, heart, brain, and kidney functions are lost first. The most profound change is damage to the heart muscle. Once cause of this damage is the release of myocardial depressant factor from the ischemic pancreas. 5. Discuss the outcome of the build-up of lactic acid in shock state. Pg. 813 • -Aerobic= normal metabolism with oxygen • -Anerobic-reduced o2 which then releases lactic acid=METABOLIC ACIDOSIShyperkalemiathis is what occurs in every type of shock 6. Discuss the use of dopamine in the treatment of shock. • **** Therapies for Shock: • OXYGEN THERAPY • IV therapy for fluid resuscitation with NS; RINGERS LACTATE to buffer metabolic acidosis (crystalloids), possibly blood but only with NS!! • DOPAMINEvasopressor Increased HR, BP and UO o Dopamine – see Chart 39-4, pg. 819 – INCREASES RENAL PROFUSION ▪ 5-10 mcg/kg/min IV 1 25 • Microthrombi (blood clots) begin to form in some organsDIC is beginning • DIC (disseminated intravascular coagulation) – microthrombi then uncontrolled bleeding. Monitor IV sites for bleeding. (consequence of septic shock) • Short duration and often missed • Rapid downhill course Example: you would GIVE heparin in the HYPODYNAMINC STATE. ** First sign of DIC is BLEEDING FROM IV SITE (YOU CAN BET THE RANCH ON IT) 8. Discuss DIC as a late complication of septic shock. • By the time DIC occurs in the hyperdynamic state, heparin can no longer be administered due to apparent hemorrhage. Health Promotion and Maintenance – Sepsis/Septic Shock • Older adultsImmunosuppression • Hallmark of sepsis: increasing serum lactate level; normal or low WBC count; decreasing segmented neutrophil level with a rising band neutrophil level (Left Shift) • Infection Precautions: Chart 39-7, pg. 826: Temperature greater than 100 !!! Same precautions as somebody with neutropenia. Concepts of Emergency and Trauma Nursing- Chapter 10 (3 Questions) 1. Discuss, in detail, the components of the Primary survey and resuscitation interventions. Pg. 132-134. o The initial assessment of the trauma patient is called the primary survey, which is an organized system to rapidly identify and effectively manage immediate threats to life. o The primary survey is based on a standard “ABC” mnemonic plus a “D” and “E” for trauma patients: ▪ Airway/cervical spine (A) – PROIORITY PATENT AIRWAY!! ▪ Breathing (B) – this assessment determines whether or not ventilatory efforts are effective by watching BILATERAL CHEST RISE – not only whether or not the patient is breathing. Listen to breath and lung sounds 1 26 and evaluate chest expansion, respiratory effort, and any evidence of chest wall trauma or physical abnormalities. 1 27 ▪ Circulation (C) – the adequacy of heart rate, blood pressure, and overall perfusion becomes the focus on the assessment. ▪ Disability (D) short version of GLASCOWCOME SCALE – Provides a rapid baseline assessment of neurologic status. A simple method to evaluate level of consciousness as a AVPU mnemonic: • A (alert) • V (responsive to voice) • P (responsive to pain) • U (unresponsive). ▪ Exposure (E) – NURSING SAFETY PRIORITY – EVACUATE • Ex: if there is anthrax or fire immediately evacuate. 2. Discuss the client with suicidal potential in ED. • Who should they see – must have a psych consult, psychiatrist, psych nurse practitioner • Ask them if they have a plan. 3. Discuss the presence of family members during resuscitative procedures. • If resuscitation efforts are still underway when the family arrives, one or two family members may be given the opportunity to be present during lifesaving procedures. Family presence during resuscitation is gaining wider acceptance in the health care community. It is actually encouraged. Concept of Emergency and Disaster Preparedness – Chapter 12 (6 Questions) 1. Discuss the concept and purpose of triage. 157. • ***The greatest good for the greatest number. The more resources one may require can take away from others. • A key process in any multi-casualty or mass casualty response is effective triage to rapidly sort ill or injured patients into priority categories based on their acuity and survival potential. 2. Discuss the role of the triage nurse. • The RN is typically the person assigned to perform the triage function in most hospitals. The triage nurse requires appropriate training and experience in both emergency nursing and triage decision-making concepts. 1 30 **Portal HTNpressure transmitted backwards into esophageal veinsesophogeal varicesif varices ruptures, death is imminent. o Hepatic encephalopathy: assess for asterixis -Ascites: Is the collection of free fluid within the peritoneal cavity caused by increased hydrostatic pressure from portal hypertension. o Portal hypertension: a persistent increase in pressure within the portal vein greater than 5 mm Hg is a major complication. (obstruction of the blood flow through the portal vein and its branches, so it seeks other alternative venous channels around the high pressure area) o Esophageal varices: As a result of portal hypertension, the blood backs up from the liver and enters the esophageal and gastric veins. Pressure builds excessively in esophageal veins causing the varices. o Ascites: measure abd girth to assess amt of fluid; daily wts; massive ascites causes pressure on diaphragm making it hard for pt. to breathe, ASSESS lung sounds, and watch for s/s of hypovolemia (increased P, decreased BP) o Diet: modified/decreased protein, fats and carbs o To decrease ammonia levels, administer lactulose (Cephulac) -The liver makes thrombin and fibrinogen (clotting factors); the earliest way to detect if these values are abnormal is to assess the stool for occult blood. 2. Pulmonary Embolism (3) Pathophysiology: o PE is oxygenation failure !!! o Emboli that is either lodged in pulmonary artery or a few small embolis (shower) in bifurcation. o Major risk Factors include: prolonged immobility, surgery, obesity, hx of thromboembolism, central venous catheters, advancing age and conditions that increase blood clotting, DVT!! S/S: o Symptoms SUDDEN ONSET of pleuridic (sharp & stabbing) chest pain and dyspnea, apprehension and restlessness, feeling of impending doom, dyspnea and hemoptysis. o Signs: Low-grade fever, tachypnea and petichiae over axillary and chest. 1 31 o It is important to remember that pts. with PE do not have “the classic” manifestations but instead have vague symptoms resembling the flu, such as N/V, and general malaise. o Assess pts. at risk for PE for the symptom cluster of distended neck veins, syncope, cyanosis, and hypotension; if this cluster is present, notify the rapid response team. Medical and Nursing Interventions: o OXYGEN THERAPY o High-fowlers position o Administer anti-coagulants o The best way to assess efficiency of oxygen therapy is ABG’S o Teach pt: to lose weight if necessary, smoking cessation, and become physically active for prevention of PE. o Pulmonary angiography or CT to diagnose o Heparin: prevent development of existing clots; monitor PTT, monitor for bruising and bleeding, antidote: protamine sulfate o Avoid IM injections, no enemas, apply firm pressure to needle stick site for 10min or longer, avoid straight razors, and hard toothbrushes. 3. ARDS- non cardiogenic pulmonary edemarisk for (1) Pathophysiology: o Acute Respiratory Failure that combines (V/Q) ventilatory and oxygenation failure o ARDS IS NON-CARDIOGENIC PULMONARY EDEMA o Primary Trigger: SYSTEMIC INFLAMMATORY RESPONSE; alveolar-capillary membrane is normally only permeable to small molecules, but when injured, membrane becomes more permeable to large molecules, allowing fluid into the lungs. o 4 Phases: 1 Phase stresses upon early changes of tachypnea and dyspnea; if progressed to 4th stage, pt. mortality is almost 100%, but if survived, pt. will have permanent lung damage and multiple organ dysfunction syndrome which inevitably leads to death. Key Features: o Hypoxemia that persists even with 100% oxygen; Classic sign of ARDS: Also known as Refractory Hypoxemia; FiO2 goes up and Pao2 CONTINUES TO DROP. o Decreased pulmonary compliance o Dyspnea o Noncardiac-associated bilateral pulmonary edema 1 32 o Dense pulmonary infiltrates on x-ray (ground-glass appearance) 1 35 • STEMI: after thrombolytic administration, ST elevation should come down, check troponin levels. o NONSTEMI: check troponin levels and ECG 1 36 o #1 intervention is to decrease pain !!! administer morphine !! o ABC’s are always priority, but pain increases the workload of the heart, obviously something you do NOT want during a heart attack…. o Administer Fibrinloytic (thrombolytic) therapy with reteplase (Retevase), and tenecteplase (TNKase). o Thrombolytic Action: REPERFUSION !!! o Side Effects: once administered, this startles the myocardium, causing ventricular tachycardia, this is normal. o Implication: Most serious outcome is cranial hemorrhage; monitor for signs similar to a stroke (change in LOC, neurological changes) 7. Heart Failure (1) Left Sided (L = Lungs  ) Decreased Cardiac Output: o Angina due to decreased cardiac output causing ischemia o Oliguria during the day, nocturia at night o Confusion and restlessness r/t decreased cardiac output secondary to minimal oxygen and glucose in the brain o Dizziness, fatigue, and weakness o Tachycardia and palpitations o Pallor, weak peripheral pulses, and cool extremities. Pulmonary Congestion: o #1 sign is pink, frothy sputum (pink because blood is bursting through pulmonary capillaries; frothy because of air exchange between capillaries and fluid being there, like blowing bubbles) o Hacking cough, worse at night o Dyspnea/breathlessness o Crackles and/or wheezing o Tachypnea o S3/S4 summation gallop Right Sided Systemic congestion: 1 37 o JVD distension o Enlarged liver and spleen o Anorexia and nausea o Dependent edema in legs and sacrum o Distended abd o Swollen hands and fingers 1 40 • Maintain suction on JP drain or hemovac and compress when empty and measure drainage; notify physician if drainage is more than 30-50ml per shift. • Maintain mechanical ventilation and slight hyperventilation for first 24-48hrs to increase blow off of carbon dioxide and prevent increased ICP • Assess dressing and drainage, notify excess amounts of drainage and monitor for CSF leakage. • Record strict output of I & O. Best way to assess fluid status is daily weights; best way to assess fluid resuscitation is urine output. • Maintain fluid restriction of 1500ml/day, monitor electrolytes (sodium and potassium especially), and monitor for dysrhythmias. • Apply ice packs or cool compresses as prescribed; expect preorbital edema and ecchymosis of one or both eyes, which is not unsual---unlike with basilar skull fx. • Provide ROM to increase circulation and promote mobility • Place antiembolism stockings to prevent DVT • Administer anticonvulsants to prevent seizures, corticosteroids to reduce inflammation, antacids to prevent mucosal irritation from steroids, and ABTs. • Administer only Tylenol or codeine sulfate for pain management; never administer an opiod to a head injury pt so it does not interfere with LOC; Codeine causes constipation, pt. will be on stool softeners; never give aspirin. Basilar skull fracture (unique fracture)* • Fracture at base of skull; causes CSF leakage of the nose (rhinorrhea) and the ears (ottorrhea); CHECK FOR HALO • Risk for INFECTION r/t direct access to subarachnoid spaceMENINGITIS • Potential for hemorrhage: Raccoon eyes (bleeding around orbits of eyes) and Battle Sign (bruising behind ears) 10.Renal Failure (9) **No blood = no urine 1 41 o Prerenal: Any condition that reduces blood flow such as hypovolemia, reduced cardiac output, volume shift, reduced circulation, all reduces blood flow to kidneys. **If dehydration occurs, ADH will kick in; urine specific gravity will be increased. 1 42 o Intrarenal: Caused by nephro-toxic substances: NSAIDS & abtAMINOGLYCOSIDES o Postrenal: Obstruction of urinary tract; nephrolithiasis (kidney stone), BPH, urethral stenosis, etc. **If there is a blockage, urea (uric acid) will build up in the blood stream (uremia); urea is a derivative of ammonia, if this occurs, pt. will have a change in LOC immediately. Urea is the #1 most nitrogenous waste in the body. **S/S or uremia: metallic taste in mouth, muscle cramps, anorexia, N/V, uremic “frost” on skin, itching, fatigue/lethargy, hiccups, edema, dyspnea, and parasthesis. **No contrast dyes **S/S of oliguria and or anuria: Respiratory crackles, SOB, changes in LOC, hypertension, edema, tachycardia, distended neck veins, elevated CVP, wt. gain, anorexia, N/V, and lethargy, o Oliguric phase: Urine output 100-400ml/hr; no response to fluid challenge; Hyperkalemia occurs in this phase, indicator is a peaked narrow t- wave on an EKG, and this means that during ventricular repolarization, the ventricles have less time to fill, resulting in decreased cardiac output. -hyperphophatemia occurs causing inverse hypocalcaemia: s/s are chovstek’s sign (cheek rub twitch) and tress au’s sign (BP twitch), tx w/ calcium gluconate. **never ever push K+ **Best indicator of fluid status is daily wts. **If fluid challenge is performed and is successful, then it is not oliguria, its dehydration. o Diuretic Phase: Often has a sudden onset between 2-6 weeks; urine increases rapidly over a period over several days and can result in up to 10L/24hr period; can cause dehydration due to fluid volume deficit, pt. needs aggressive fluid replacement or else pt. can default back to oliguric phase. o Metabolic acidosis = hyperkalemia; compensation then begins with respiratory system resulting with Kussmal’s respirations 1 45 • Atrial fibrillation: Cardioverted **Before cardioversion, turn oxygen off and away from the pt. Oxygen is combustible, fire will result. Shout “CLEAR” before shock is administered for electrical safety. • Ventricular Tachycardia: Defibrilated • Ventricular fibrillation: Defibrillated **If pt is in VF or pulseless VT, must defibrillate ASAP! After defibrillation, CPR is resumed; CPR must continue at all times except for defibrillation. The terms “push hard-push fast” is used to improve circulation during resuscitation. **Defibrillation must never be delayed for any reason; the earlier the defibrillation, the greater the chance of survival. CARDIOVERSION: • A-fibrilation not responsive to meds • Synchronized countershock (shock must fall on a specific wave) • Amount of joules used is less than 200, always less than amount used for defibrilation DEFRIBRILATION: • V-fibrilation • NOT synchronized (asynchronized) • Higher amount of joules, usually greater than 200 12. Trans-sphenoidal hypophysectomy (1) o Pt at risk for SIADH; follow craniotomy precautions and interventions 13.SIADH and DI (2) ADH is the hormone vasopressin that is released from the posterior pituitary gland; it controls the kidneys by telling them how much water and sodium to reabsorb. DI: this is a deficit in ADH Pathophysiology: o Water metabolism problem caused by an ADH deficiency; results in the excretion of large volumes of dilute urine. Without ADH, distal kidney tubules and collecting ducts do not reabsorb water, leading to polyuria and dehydration. o Primary DI is caused by a defect in the hypothalamus or pituitary gland 1 46 o Secondary DI can result from tumors in or near the hypothalamus/pituitary gland, head trauma, infectious processes, surgical procedures (craniotomy or hypophysectomy) or metastatic tumors. Less often, it is caused by brain hemorrhage, brain disease or cerebral aneurysm. S/S: o The amount of urine excreted in a 24hr. period may vary from 4L to 30L a day. Urine would be diluted with a low specific gravity (less than 1.005) and a low osmolarity (50- 200). Lab Values: o Increased Hemoglobin o Increased Hematocrit o These are increased because the blood volume concentration is increased due to dehydration from polyuria. o Increased BUN Drug Therapy: o Desmopressin (DDAVP): Teach pt. using the inhaled form of the drug to blow the nose prior to taking, sit upight, and hold their breath when spraying or using the rhinal tube. Warn pt. not to drink more than 3L of fluid daily while taking this drug, teach pt. to weigh themselves daily and notify physician if more than 2lbs are gained in a 24hr. period, and let physician know if they experience persistent headaches or acute confusion. o Vasopressin (Pitressin): For hospitalized pt., monitor for water intoxification (listlessness, drowsiness, confusion, weight gain, headache and anuria). Warn pt. not to drink more than 3L of fluid daily while taking this drug, teach pt. to weigh themselves daily and notify physician if more than 2lbs are gained in a 24hr. period, and let physician know if they experience persistent headaches or acute confusion. Management: o Ensure that no pt. suspected of having DI is deprived of fluids for more than 4hrs. They cannot reduce their own urine output; therefore, dehydration will result. o Diabinese and Diamox are sound-alike look-alike drugs. Do not confuse them. Diamox is a type of diuretic, which could increase urine output and the risk for dehydration. 1 47 o The parenteral form of Desmopressin is 10x stronger that the oral form, and the dosage must be reduced. o Tx: medications. SIADH: this is an excess of ADH Pathophysiology: o SIADH is a problem in which ADH is being secreted even when plasma osmolarity is low or normal. A decrease in plasma osmolarity normally inhibits ADH production and secretion. o ADH continues to be released even when plasma is hypo-osmolar; water is retained, which results in dilutional hyponatremia and fluid overload. The increase in plasma volume increases the GFR and inhibits the release of renin and aldosterone. This combined effect leads to an increased sodium loss through urine, resulting in greater hyponatremia. o Caused by certain drugs (SSRI’s) and pathologic conditions (cancer therapy); head trauma, cranial surgeries. o Also known as Schwartz-Bartter Syndrome S/S: o Lethargy, headaches, confusion, hostility, disorientation, and a change in LOC r/t hyponatremia affecting the CNS. o Manifestations can progress from headaches and lethargy to decreased LOC, seizures and coma. o Water retention, NO EDEMA, GI disturbances (loss of appetite, N/V), weight gain, and full bounding pulse from fluid excess. Lab Values: o Serum sodium below 115 o Urine volume decreases, urine osmolarity increases o Plasma volume increases, plasma osmolarity decreases o Elevated specific gravity Drug Therapy: o Tolvaptan (Samsca)or conivaptan (Vaprisol): these drugs are used to treat SIADH when hyponatremia is present. These drugs are vasopressin antagonists that promote water excretion without causing sodium loss. 1 50 o Pt. is at risk for acute adrenal insufficiency r/t surgery o GI bleeding is common with Cushing’s: instruct pt. to not take any NSAIDS, intensifies GI bleeding o Diet: low sodium, high potassium 15.Adrenal Crisis (Addisonian Crisis) (1) Causes: o Usually occurs in response to a stressful event such as surgery, trauma or severe infection, or from sudden withdrawl of medications. Lab Values: o Unless intervention is initiated promptly, sodium levels fall and potassium levels rise rapidly. Severe hypotension results from the blood volume depletion that occurs with the loss of aldosterone. Pharmacological Therapy: o Hormone replacement, hyperkalemia management, hypoglycemia management. o Rapid infusion of NS or dextrose 5% in NShydrocortisone sodium succinate (Solu- Cortef)Insulin with dextrose in NS to shift potassium into cellsKayexalateloop or thiazide diureticsIV glucose (then glucagon as needed)maintain IV access. Medical and Nursing Management: o Monitor I & O, initiate potassium restriction, monitor HR, rhythm and EKG for s/s of hyperkalemia, monitor blood glucose hourly 16.DKA (3) DKA: Caused by lack of insulin and ketosis; usually affects type I DM o Form of metabolic acidosisKussmaul’shyperkalemia o Ketones: acids; derived from improper breakdown of lipids Pathophysiology: 1 51 o Increased glucose  Increased diuresis; Polyuria dehydration and electrolyte imbalance S/S: 1 52 o Earliest sign is dehydration affecting the brain, resulting in LETHARGY o Sudden onset; caused by infection, inadequate insulin dose, or other stressors increasing glucose o Ketosis, Kusmaul’s respirations, “fruity” breath, nausea and abd pain, dehydration and electrolyte imbalance, polyuria and polydipsia, weight loss, dry skin, sunken eyes, soft eyeballs, lethargy, and coma. Lab Values: o Serum glucose greater than 300 o Serum and Urine ketones POSITIVE o Serum Ph less than 7.35 and Serum HCO3 less than 15 Management: o Assess airway, LOC, hydration status, electrolytes and blood glucose o Always ABC’S, hydration status = C ! o Daily weights are the best indicator of fluid status; 1kg of body weights = 1 L of fluid o In the elderly dehydrated patient, skin turgor must be checked on FOREHEAD since rest of body is not reliable due to age- related decreased elasticity. o First outcome of fluid resuscitation is to restore volume and maintain perfusion to the brain, heart and kidneys. o Second outcome of fluid resuscitation is replacing total body fluid loss, this is achieved more slowly. Choice for fluid depends on state of hemodynamics (status of BP), the state of hydration, electrolyte levels, and urine output. In general, hypotonic solution is given, once blood glucose reaches 250, give 5% dextrose in 0.45% NS. This solution prevents cerebral edema hypoglycemia. Drug Therapy: o Tx: Regular insulin IV drip; given concurrently with fluid resuscitation o Assess for signs of hypokalemia including fatigue, malaise, confusion, muscle weakness, shallow respirations, abd distension, paralytic ileus, hypotension and a weak pulse. o Before giving IV potassium, make sure the patient is producing at least 30ml/hr. of urine; if they are not, then pt. is still dehydrated; therefore, they are still hyperkalemic. o Never push potassium. o Sodium Bicarbonate; only systemic antacid; given to treat metabolic acidosis; only given based on ABG’s. Education: