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This list is not a guarantee of final exam content. It is meant to help the student focus study time on important content, but may not include all elements of final exam questions. The final exam is cumulative and the student is responsible for all material covered in the course. Remember the emphasis is on assessment and nursing interventions. 50-60 Questions 2 hours The following are the topics to be covered on the final and general areas of concentration: Med-Math calculations dosage calculations drip factor flow rates intake and output Give amikacin 800 mg IVPB, now Available: Amikacin 500 mg/2 ml Set and solution: D W 150 ml minibag and a drop factor of 15 gtt/ml set Instructions: Infuse over 60 min 5 a. Drug dose? b. Flow rate? I and O’s: 1 ounces = 30 ml Any items that is liquid form at room temperature: ex. pudding, jello, ice cream, ice Intravenous Infusions and Blood Transfusions care and assessment of IV sites and tubing Complication Finding Treatment Prevention Infiltration pallor, local swelling at the site, decreased skin temperature around the site, damp dressing, slowed infusion • stop the infusion and remove the catheter. • elevate the extremity. • encourage active range of motion. • apply warm compresses three to four times/day. • restart the infusion proximal to the site or in anoth • Carefully select site and catheter. • secure the catheter. phlebitis/ thrombophlebitis edema; throbbing, burning, or pain at the site; increased skin temperature; erythema; a red line up the arm with a palpable band at the vein site; slowed infusion • promptly d/c the infusion and remove the catheter. • elevate the extremity. • apply warm compresses three to four times/day. • restart the infusion proximal to the site or in another extremity. • Culture the site and catheter if drainage is present. • rotate sites at least every 72 hr. • avoid the lower extremities. • use hand hygiene. • use surgical aseptic technique. hematoma ecchymosis at site • do not apply alcohol. • apply pressure after iv catheter removal. • use warm compress and elevation after bleeding stops. • minimize tourniquet time. • remove the tourniquet before starting iv infusion. • maintain pressure after iv catheter removal. Cellulitis pain; warmth; edema; induration; red streaking; fever, chills, and malaise • promptly d/c the infusion and remove catheter. • elevate the extremity. • apply warm compresses three to four times/day. • Culture the site and cannula if drainage is present. • administer: - antibiotics - analgesics - antipyretics • rotate sites at least every 72 hr. • avoid the lower extremities. • use hand hygiene. • use surgical aseptic technique. fluid overload distended neck veins, increased BP, tachycardia, SOB, crackles in the lungs, edema • stop infusion. • raise the HOB • assess vital signs. • adjust rate as prescribed. • administer diuretics if prescribed. • use an infusion pump. • monitor i&o. Catheter embolus missing catheter tip when discontinued; severe pain at the site with migration, or no symptoms if no migration • place the tourniquet high on the extremity to limit venous flow. • prepare for removal under x-ray or via surgery. • save the catheter after removal to determine the cause • do not reinsert the stylet into the catheter. steps in transfusion of blood and blood products BEFORE DIFFUSION During Infusion Post infusion 1) The nurse will assess laboratory values. Many institutions have specific guidelines for blood product transfusions (e.g platelet count <20,000 or hemoglobin <6g/dL). Hematocrit – 7) The nurse will administer the blood product using the appropriate filtered tubing. The filters remove aggregates and possible contaminants. • Obtain the pt's VS upon completion of the transfusion • Dispose of the blood- Females: 37%-47% Increased: Fluid shift, dehydration Decreased: Hemorrhage Hemoglobin Females: 12-16 g/dL Increased: Fluid shift, dehydration Decreased: Hemorrhage Potassium Females: 3.5-5.0 m/Eq/L or mmol/L Increased: dehydration, acidosis 8) If dilution is necessary, dilute with normal saline only. Other IV solution will destroy the blood product. Infuse blood product at the prescribed rate. Begin the infusion slowly 2) The nurse will verify the medical prescription. Legally, a blood transfusion requires physician’s prescription. The prescription will have the type of product, dose and transfusion time. 3) The nurse will explain the procedure to the patient. The nurse will assess the patient’s vital signs before beginning the transfusion and then assess urine output, skin color, and history of transfusion reactions. Assess whether or not the patient is able to handle the infusion. Gather prior data about previous infusion allows a nurse to be aware of signs of transfusion reaction. 4) The nurse will obtain venous access. Ideally, the nurse will use a central catheter or at least a 20-gauge needle. This prevents the cells from getting stuck. 5) The nurse will obtain blood products from a blood bank. Then transfuse immediately. Transfusion must occur ASAP once the blood product leave the blood bank. 6) Two nurses must verify the patient by name and number, check blood compatibility, and note expiration time. The nurse explains the procedures to the patient. This decreases the chance of ABO incompatibility reactions. Remain w/pt for the first 15-30 min & monitor: - VS (then q1hr afterward). For older adult pts, assess VS more frequently b/c changes in pulse, B/P, & RR may indicate fluid overload or may be the sole indicators of a transfusion rxn. Older adult pts w/cardiac or renal dysfunction are at an increased risk for heart failure & fluid-volume excess when receiving a blood transfusion. - rate of infusion - respiratory status - sudden increase in anxiety - breath sounds - neck-vein distention administration set appropriately (biohazard bags) • Monitor blood values as prescribed (CBC, H+H; Hgb levels should rise by ~1 g/dL w/each unit transfused) • Complete paperwork & file in the appropriate places Document the pt's response Ask pt to report unusual sensations (like chills, SOB, hives, or itching) Notify the primary health care provider immediately if any signs of a rxn occur If there are no signs of a rxn, increase transfusion rate to 1 unit in about 2 hrs depending on pt's cardiac status Complete the transfusion w/in a 2-4 hr time frame to avoid bacterial growth. know reactions and interventions for blood transfusions When Given How Supplied How Given Nursing Considerations Whole Blood To restore blood volume (to maintain b/p). Excessive blood loss caused by injury or surgery. Hgb 6-10 g/dL, depending on symptoms 450-500 mL usually from blood donors of the same blood type Transfusions take 1 to 4 hours, depending on how much blood and what type is given, and no special recovery time is needed. Most of the time whole blood is not used because the patient's medical condition can be treated with a blood component and too much whole blood can raise a recipient's blood pressure. High blood pressure can have medical side effects Packed RBCs Most common blood component given. Given to replace cells lost due to trauma, surgery or conditions that destroy RBCs or impair RBC maturation. Anemia (Hgb 6-10 g/dL, depending on symptoms) Chronic renal failure Supplied in 250ml bags. Infuse with special tubing. Given to patients with HGB < 8g/dL or who are hypoxemic. Actually a transplant of tissue. Platelets Given to pts with: PLT counts < 10,000 mm3 or who have thrombocytopenia or platelet dysfunction (platelets < 20,000 or < 80,000) and have active bleeding. or are scheduled for an invasive Packed in bags of 300ml from pooled donors or 200ml from a single donor. Requires ABO compatibility. Infused over 15-30minute period. Infuse with special tubing. Include on the labels: • either: platelets, pooled, buffy coat derived, leukocyte-depleted or: platelets, apheresis, leucocyte-depleted; • volume; • blood component producer’s name; • either: a unique pool or batch number procedure. Granulocytes or: the donation number of all contributing units or: the donation number and, if subdivided, the sub batch number; • the ABO group; • the RhD group stated as positive or negative; • the expiry date; • the blood pack lot number. • store at 22˚C ± 2˚C with continuous gentle agitation; • always check the patient ⁄ component compatibility ⁄ identity; • inspect pack for signs of deterioration or damage; • risk of adverse reaction ⁄ infection. For clients with infections. Suspended in 400ml plasma. Infuse in 45-60 minutes. Take VS q15min throughout the transfusion. Transfusion Reactions and Complications: Febrile 30 min – 6 hr after transfusion Cause Manifestations Occur most often in pts w/antiWBC antibodies, which can develop after multiple transfusions Chills, tachycardia, fever, hypotension, & tachypnea Priority Nursing Action 1. D/C the transfusion immediately. 2. Give antipyretics as ordered. 3. Notify the physician. 4. KVO w/a NS infusion. Hemolytic Onset may be immediate (acute- ) or after subsequent units have been transfused Blood type or Rh incompatibility. When blood containing antigens different from the pt's own antigens is infused, antigen-antibody complexes are formed in his/her blood. These complexes destroy the transfused cells & start inflammatory responses in the blood vessel walls & organs. Mild: fever & chills Life-threatening: disseminated intravascular coagulation (DIC: a pathological activation of coagulation mechanisms → formation of small blood clots inside the blood vessels throughout the body. Small clots consume coagulation proteins and platelets, normal coagulation is disrupted and abnormal bleeding occurs from the skin (e.g. from sites where blood samples were taken), the GI tract, resp tract, and surgical wounds. The small clots also disrupt normal blood flow to organs (such as the kidneys), which may malfunction as a result. Occurs acutely but also on a slower, chronic basis. Common in the critically ill, and may participate in the development of multiple organ failure which may lead to death) & circulatory collapse Other manifestations: – apprehension – headache – chest pain 1. D/C the transfusion immediately. When the transfusion is d/c, the blood tubing must be removed as well. Use new tubing for the NS infusion. Treatment Giving leukocytereduced blood or singledonor HLA-matched platelets reduces the risk for this type of rxn WBC filters may be used to trap WBCs & prevent their infusion into the pt 2. KVO w/NS, or according to agency protocol. Replace donor blood w/ NS Furosemide may be administered to increase renal blood flow. Low-dose dopamine may be considered to improve renal blood flow. Maintain urine output at 30-100 mL/hr 3. Send the remaining blood, a sample of the client’s blood, and a urine sample to the laboratory. To prevent a hemolytic rxn, check the blood type or Rh compatibility with another RN before transfusion. 4. Notify the physician immediately. 5. Monitor VS. 6. Monitor fluid I&O. – low back pain – tachycardia – tachypnea – hypotension – hemoglobinuria – a sense of impending doom Allergic Mild: during or up to 24 hr after transfusion Mild: sensitivity to infused plasma proteins. ------------------------------Severe: antibody-antigen reaction Mild: Flushing, itching, urticaria, bronchial wheezing --------------------------------Severe: Dyspnea, chest pain, circulatory collapse, cardiac arrest Mild: 1. Stop/slow the transfusion, depending on agency protocol. 2. Notify the physician. 3. Administer medication (antihistamines) as ordered. ------------------------Severe: 1. Stop the transfusion 2. KVO w/NS 3. Notify the physician immediately. Mild: Administer antihistamines. Although the necessity of stopping the transfusion is unclear, in more severe cases and in uncertain cases, the transfusion should be stopped. Pts w/a hx of allergy can be given leukocytereduced or washed RBCs in which the WBCs & plasma have been removed. This procedure reduces the possiblity of an allergic rxn. 4. Monitor VS Administer CPR if needed. 5. Administer medications and/or oxygen as ordered. Anaphylaxis or -phylactic Immediate onset Type I hypersensitivity reaction (in this case, to whole blood, cryoprecipitate, immune serum globulin—all of which is probably a result of direct mast cell degranulation rather than an IgE-mediated hypersensitivity event) Occurs systematically (affects many organs) w/in secondsminutes of exposure to allergen o Wheezing, dyspnea, chest tightness, cyanosis, & hypotension. Stop the transfusion immediately. Maintain airway; give O2 & IV fluids Administer epinephrine, antihistamines (diphenhydramine), corticosteroids, & vasopressors. Maintain intravascular volume. Administer epinephrine, antihistamines (diphenhydramine), corticosteroids, & vasopressors. Chart 22-2 Emergency Care of the Pt w/ Anaphylaxis Immediately assess the respiratory status, airway, and oxygen saturation of pts who show any symptom of an allergic reaction Call Rapid Response Team Ensure that intubation and tracheotomy equipment is ready Apply oxygen using a high-flow, non-rebreather mask at 40% to 60% Immediately discontinue the IV drug of a pt having an anaphylactic reaction to that drug. Do not discontinue the IV, but change the IV tubing and hang normal saline. If the pt does not have an IV, start one immediately and run normal saline Be prepared to administer diphenhydramine (Benadryl) and epinephrine IV Diphenhydramine 25 mg to 50 mg IV push Epinephrine 1:1000 concentration, 0.3 to 0.5 mL IV push Repeat as needed every 10 to 15 min until the pt responds Keep the head of the bed elevated about 10 degrees of hypotension is present; if BP is normal, elevate the HOB to 45 degrees or higher to improve ventilation Raise the feet and legs Stay w/ the pt Reassure the pt that the appropriate interventions are being instituted steps in transfusion of blood and blood products know reactions and interventions for blood transfusions ~ focus on BLOOD. Packed RBCS, whole blood, ~ not cryoprecipitate, fresh frozen plasma Clients Having Surgery pre-op assessment of high risk for intraoperative complication o ~ what would keep pt from going to surgery post-op complications o ~ pt gets out of surgery, o “RESTLESS” THINK ABOUT HYPOXIA. Don’t assume… look for hypoxia. If not there, don’t put it there. pre- and post-op pt teaching o ~ know before surgery o ~ during d/c Clients with Pain assessment of pain influences on pt perception of pain o ~ culture o ~ age old people have potential to not feel pain (neuropathy) o ~ liver, kidney o ~ old people refuse pain meds – not wanting to admit – seem frail; want independence. o ~ psychosocial - culture pharmacological and non-pharmacological interventions o ~ not pharm class. Don’t memorize but be familiar w/ opiates – assessment, giving meds. Older Adult Pain PREVALENCE OF PAIN • Recognize that older adults are at great risk for undertreated pain. • Consider the older adult at risk for the undertreatment of cancer pain because of inappropriate beliefs about pain sensitivity, tolerance, and ability to take opioids. Beliefs about pain: • In addition to receiving less analgesia, older adults tend to report pain less often than do younger adults. These findings may be related to beliefs and concerns about pain and the reporting of pain. Many older people hold these beliefs and concerns about pain: • Pain is something that must be lived with. • Expressing pain is unacceptable or is a sign of weakness. • Reporting pain will result in being labeled as a "bad" patient. • Nurses are too busy to listen to reports of pain. • Pain signifies a serious illness or impending death. • Nurses should be aware of the beliefs of older patients regarding pain management. Nurses and other caregivers often under-medicate these patients and are sometimes reluctant to administer the prescribed analgesics. ASSESSMENT • Ask about present pain only. • Use a standard scale, such as the numerical FACES rating scales. • Explain the scale each time it is used. • Use verbal descriptions such as "ache," "sore," and "hurt," rather than the word "pain." -Use visual representations of pain measures rather than mental images of pain rating scales. Be sure that the patient is wearing glasses and hearing aids if needed and available. - Alter a written pain scale to include large lettering, adequate space between lines, nonglossy paper, and color for increased visualization. -Provide adequate lighting and privacy to avoid distracting background noise. CONSIDERATIONS FOR COGNITIVELY IMPAIRED PATIENTS -Assess for nonverbal indicators of pain (facial expressions, grimacing, vocalizations, body movement, behavioral changes). - Remember to "assume pain is present" (APP) in cognitively impaired patients with diseases and condition commonly associated with pain. MANAGEMENT OF PAIN -Use around-the-clock dosing of analgesics. .-Consider an analgesic trial in a cognitively impaired patient - Beware of adverse effects of acetaminophen (hepatotoxity, nephrotoxicity) and NSAIDs (Gl bleeding, nephrotoxicity). - Start low and go slow with opioid dosing. -Avoid the use of meperidine (Demorol), codeine, and propoxyphene (available in combination with acetaminophen, as Darvocet) -Use methadone and tramadol with caution. -Older adults and those with renal disease should not take meperidine because of the prolonged half-life of its drug metabolite, normeperidine. -Use nondrug pain relief measures. pharmacological and non-pharmacological interventions Non-pharmacological interventions: Cutaneous stimulation: Pain relief is generally sustained only as long as the stimulation continues. Stimulation itself may aggravate preexisting pain or may produce new pain. - heat/cold/pressure -therapeutic touch, massage, vibration -Transcutaneous electrical nerve stimulation (TENS) also known as percutaneous electrical nerve stimulation (PENS). *Not widely use but older adults can benefit from this. It's safer and just as effective as medications. Cognitive-behavior measures: Distraction, imagery, hypnosis. Other: Acupuncture Glucosamine for arthritis. Nursing Interventions to Prevent Side Effects Opioids Constipation Nausea/vomiting Sedation/confusion Respiratory distress . Assess previous bowel habits. . Use measures to prevent this problem because constipation is the most common side effect (push fluids, encourage activity, give foods high in bulk and roughage). . Keep a record of bowel movements. . Administer stool softeners and stimulant laxatives. . if ineffective, try suppository or Fleet's enema. Assess actual cause of nausea. Recognize that N/V may be only an initial, temporary side effect for the first 24 to 48 hours because tolerance seems to develop quickly to this side effect. . Try an antiemetic prophylactically before administration, as prescribed. . Treat with prochlorperazine (Compazine) 5 mg orally every 4 hours, as prescribed. • Give metoclopramide (Reglan) 10 mg before meals and at bedtime, or ondansetron (Zofran) 4 mg IV. • Assess actual cause of sedation because the patient may also be on hypnotics and antianxiety agents; eliminate unnecessary sedating medications of Opioids • Recall that tolerance to this side effect generally occurs after 2 to 3 days. • Be aware that stimulants such as caffeine may counteract opioid-induced sedation. • Consider opioid rotation using an equianalgesic chart. • Be aware that clinically significant respiratory depression is rarely seen in patients with severe pain caused by cancer, even when large doses of opioids are given. • Recognize that pain and stress seem to counteract the respiratory depression effects of opioids. • Recall that respiratory depression is usually preceded by sedation. • Monitor sedation level and respiratory status frequently for the first 24 to 48 hours, especially in opioid-naive patients. • If increased sedation occurs, decrease opioid dose and attempt to stimulate patient. • Be aware that respiratory rate alone is not indicative of respiratory status. • If absolutely necessary in an unresponsive patient, administer naloxone (Narcan) 0.4 mg diluted in 10 mL of normal saline; push 0.5 mL IV slowly for 2 minutes and observe the patient. Management of Clients with Fluid & Electrolyte Imbalances risk for (causes of) and assessment for fluid volume overload, deficiency o ~ dehydration o o o o o o Extracellular Fluid Volume Deficit: Dehydration Average daily fluid intake 1500 to 2500 ml Etiology Lack of fluid intake Excess fluid loss Alteration in the fluid balance regulators o Thirst o Hormones o Lymphatic system o Kidneys Excess Fluid Losses Potential causes of excess fluid loss Unmonitored use of diuretics Severe vomiting and persistent diarrhea Fever and diaphoresis Gastrointestinal suction and fistula drainage Blood loss and burns Third spacing of fluids Compensation for excess fluid loss Interstitial fluid moves to restore volume ADH & aldosterone increase, causing reabsorption of sodium, water Baroreceptors are stimulated -> vasoconstriction & increased HR Osmoreceptors signal thirst mechanism When compensation fails, the individual experiences a fluid deficit Types of Extracellular Fluid Volume Deficits Hypertonic deficit Water loss is greater than electrolyte loss Increases the osmolarity of the remaining plasma, making it hypertonic or hyperosmolar increased osmotic pressure that causes water to move from the ICF into the plasma and interstitial fluid spaces leads to cellular dehydration and shrinkage also causes the plasma volume to increase to normal or greater than normal levels Iso-osmolar or isotonic deficit Water and electrolyte losses are equal ECF osmolarity remains normal while volume is reduced does not cause a shift of fluids between spaces, so intracellular fluid (ICF) volume remains normal. Hypotonic deficit Electrolyte loss is greater than fluid loss The remaining fluid is dilute, with hyponatremia and hypokalemia causing skeletal muscle weakness. Clinical Manifestations of a Fluid Deficit Loss of body weight Changes in intake and output Changes in vital signs Decrease in blood pressure (particularly orthostatic hypotension), central venous pressure (CVP), etc. Increased heart rate and temperature Other: dry mucous membranes, decreased skin turgor, etc. Diagnostic Findings During a Fluid Deficit Indicators of hemoconcentration Osmolality above 295 mOsm/kg Plasma sodium above 145mEq/L Blood urea nitrogen above 25 mg/dl Plasma glucose above 120 mg/dl Hematocrit above 55% Urine specific gravity above 1.030 Outcome Management of a Fluid Deficit Fluid restoration Oral or IV rehydration Monitor for complications Decreased cardiac output o o o Dysrhythmias Electrolyte imbalances Impaired mucous membranes Correct the underlying problem Nursing management Assessments o Vital signs o Peripheral vein filling o Intake, output, and daily weights o Lab values o Oral cavity o Skin turgor Restore fluids Control underlying problem Interventions for Fluid Deficits Teach Appropriate fluid replacement Exercise with adequate fluid replacement o Cool water before exercise o 150 to 200 ml every 15 minutes during exercise Do not decrease fluid intake for incontinence Drink fluids even in the absence of thirst Extracellular Fluid Volume Excess: Fluid Overload Fluid overload or overhydration Hypervolemia o Excess fluids in the vascular system Third-spacing o Excess fluids in the interstitial spaces Etiology Simple overloading of fluids Failure to excrete fluids o Renal failure o Edema Types of Extracellular Fluid Volume Overload Isotonic overhydration AKA hypervolemia: caused by problems that arise from excessive fluid in ECF isotonic fluids are ingested or retained, so that osmolarity remains normal only the ECF compartment expands and fluid does not shift between the spaces Hypotonic overhydration AKA water intoxication excess fluid is hypotonic to normal body fluids the osmolarity of the ECF decreases and hydrostatic pressure increases fluid moves into the intracellular space because of the decreased plasma osmotic pressure all fluid spaces expand. Hypertonic overhydration rare, caused by an excessive sodium intake hyperosmolarity of the plasma and interstitial compartments draws fluid from the intracellular fluid (ICF) compartment the ECF volume expands and the ICF volume contracts. o o o o Clinical Manifestations of Fluid Excess Respiratory and cardiovascular Cough, dyspnea, crackles, pallor, etc. Bounding pulse, elevated blood pressure (BP), CVP Other Peripheral edema Weight gain Confusion, seizure, coma Diagnostic Findings During a Fluid Excess Indicators of hemodilution Osmolality less than 275 mOsm/kg Sodium less than 135 mEq/L Hematocrit less than 45% Specific gravity less than 1.010 Blood urea nitrogen less than 8 mg/dl Outcome Management of Fluid Excess Restrict sodium Restrict fluids Promote urine output Diuretics and digitalis Improve myocardial function Angiotensin-converting enzyme (ACE) inhibitors and beta-blockers Nursing management Assessments o Vitals, lung sounds o Edema o Intake and output o Lab values Reduce sodium and fluid Intake Mobilize fluids Control underlying problem patient teaching and nursing interventions for patients with fluid imbalances o ~ if pt dehydrated, want to know if they have heart problems ~ CHF, renal failure… ~ assess electrolytes o ~ Blood pressure – what fluid? o ~ Pt teaching – weight gain/loss.. Teach o o Appropriate fluid replacement Exercise with adequate fluid replacement Cool water before exercise 150-200 ml every 15 minutes during exercise o Do not decrease fluid intake for incontinence o Drink fluids even in the absence of thirst A. fluid volume excess (overhydration) –pg. 182 Monitor for indicators of increased fluid overload (bounding pulse, increasing neck vein distention, presence of crackles in lungs, increasing peripheral edema, reduced urine output) o Pulmonary edema can occur very quickly and lead to death Assess for skin breakdown esp. coccyx, elbows, hips, heels, nares, and ears (oxygen cannula) & turn patient every 2 hours Diuretics and digitalis to increase water and sodium excretion Restrict sodium intake in nutritional therapy Monitor I&O Take weight daily o Fluid retention may not be visible but rapid weight gain is BEST indicator of fluid retention/overload Improve myocardial function (PPT) o Angiotensin-converting enzyme (ACE) inhibitors and beta-blockers Na+ B. fluid volume deficit (dehydration) –pg. 180 Administer IV therapy, as prescribed Give fluids, as appropriate Promote oral intake (e.g. providing a drinking straw, offer fluids between meals, change ice water routinely), as appropriate Distribute the fluid intake over 25 hours, as appropriate Encourage significant other to assist patient with feedings, as appropriate Offer snacks (e.g. frequent drink and fresh fruits/fruit juice), as appropriate Signs of decreased level (hypo) • Sodium less than 135 mEq/L – Neurologic: headache, confusion, etc. Treatment of decrease Signs of increased level (hyper) Treatment of increase • Medical and nursing management – Restore sodium levels: replacement • Early symptoms –Polyuria, anorexia, weakness, restlessness • Late symptoms Medical/nursing outcome mgmt -replace fluid loss -sodium restriction K- – Cardiovascular: decreased BP, tachycardia, thready pulse, etc. – Pulmonary: crackles, dyspnea, etc. – Gastrointestinal: nausea, vomiting, etc. – Other: dry skin and mucous membranes – Reduce sodium loss: prevent vomiting and diarrhea – Restore sodium balance • Outcomes – The nurse will monitor sodium and chloride levels and for clinical manifestations of hyponatremia – Confusion, seizures, coma, tremors, muscle twitching, rigid paralysis • Cardiovascular – Electrocardiogram (ECG) changes, dysrhythmias, arrest, etc. • Gastrointestinal – Anorexia, abdominal distention, etc. • Musculoskeletal – Weakness, flabbiness, leg cramps, etc. • Neurologic – Confusion, convulsions, coma, etc. Restore potassium levels • Potassium is given intravenously for severe hypokalemia. • Maximum recommended infusion rate is 5 to 10 mEq/hr. • This rate is never to exceed 20 mEq/hr under any circumstances. • Potassium is a severe tissue irritant and is never given by intramuscular injection or subcutaneous injection. Ongoing assessments • Cardiopulmonary –Hypotension, cardiac and respiratory arrest due to muscle paralysis • Gastrointestinal – Intestinal colic, diarrhea • Musculoskeletal – Paresthesias, muscle irritability Mg++ Myocardial irritability, Replacement convulsions, etc. Ca++ • Neuromuscular • Medical/nursing – Numbness and management tingling of hands, toes, – Restore calcium and lips balance – Facial twitching, • Replacement tetany, seizures (test – Educate regarding for Trousseau’s and calcium-rich foods Chvosteck’s signs) – Move client with • Cardiovascular caution – Hypotension, – Careful assessments dysrhythmias, weak pulse • Skeletal – Spontaneous fractures ClPhos Cardiovascular Musculoskeletal (acute muscle breakdown, or rhabdomyolysis) CNS Restore phosphate balance Muscle weakness, areflexia, respiratory paralysis, sedation • Urinary – Polyuria related to an osmotic diuresis • Gastrointestinal – Anorexia, constipation, nausea, abdominal distention • Neuromuscular – Fatigue, depression, muscle weakness Outcomes -the nurse will monitor plasma sodium and chloride levels and for clinical manifestations of hypernatremia • Medical/nursing management – Restore potassium balance • Administer fluids and encourage diuresis • Utilize cation exchange resin (Kayexelate) • Outcome – The nurse will monitor potassium levels and report abnormal findings and symptoms of hyperkalemia IV hydration and diuretics • Medical/nursing management – Restore calcium balance • IV hydration and diuretics • Avoid calciumcontaining products – Safety precautions – Educate to avoid calcium intake Problems caused by The management of hyperphosphatemia center on hyperphosphatemia entails the hypocalcemia that results the management of when serum phosphate levels hypocalcemia increase Eliminate excess phosphate Early: tachycardia, palpitations Late: tetany, hyperreflexia Direction of fluid Isotonic fluid Isotonic fluids in the vasculature will stay there and will NOT move Hypotonic fluid Water moves from the IVS to ISC dilutes interstitial fluid osmolarity decreases water drawn into cells Hypertonic fluid ~They draw water into the vasculature Uses (to treat what problems) • Fluids remain IVS & expand volume. – Hypotensive – Hypovolemic • Cellular dehydration – Dialysis – Diuretics – DKA (high serum glucose causes fluid to move out of the cells into the vascular and interstitial compartments). • Stabilizing blood pressure • Increasing urine output • Correcting hypotonic hyponatremia and decreasing edema • ~For patients who have vascular dehydration Potential complications • • Risk of fluid overloading exists. – Left ventricular dysfunction, history of CHF or hypertension. Avoid volume hyper-expansion in patients with intracranial pathology or space occupying lesions. • Caution Sudden fluid shifts from IVS to cells • Cardiovascular collapse • Increased ICP in certain patients. These can be dangerous in the setting of cell dehydration Management of Clients with Acquired Immunodeficiency Syndrome spread of HIV o ~who’s at risk? When? How? Transmission o Sexual: genital, anal, or oral sexual contact with exposure of mucous membranes to infected semen or vaginal secretions o Parenteral: sharing of needles or equipment contaminated with infected blood or receiving contaminated blood products o Perinatal: from the placenta, from contact with maternal blood and body fluids during birth, or from breast milk from an infected mother to child o Teach everyone about the transmission routes and ways to reduce their exposure (discussed next). Also stress that HIV is not transmitted by casual contact in the home, school, or workplace. Sharing household utensils, towels and linens, and toilet facilities does not transmit HIV. In addition, HIV is not spread by mosquitoes or other insects. o Anal intercourse in which the semen depositor (inserting or active partner) is infected is a very risky sexual practice regardless of whether the semen receiver (receiving partner) is male or female. o Although there is less virus in seminal or vaginal fluids of people receiving HAART, the risk for transmission still exists o o ~ Need to have pt’s blood in contact w/ your blood system ~ Hollow bore needles. Inside the bore is where the blood can stay. ~ can get anti-retroviral drugs right away so it doesn’t have opportunity to replicate. ~ standard precautions – everyone assumed to have something that can cause harm to health care worker Diagnostic testing o Chart 21-6 Key Features AIDS Immunologic Manifestations • Low white blood cell counts: o CD4+/CD8+ ratio < 2 o CD4+ count < 200/mm3 • Hypergammaglobulinemia • Opportunistic infections • Lymphadenopathy • Fatigue Integumentary Manifestations • Dry skin • Poor wound healing • Skin lesions • Night sweats Respiratory Manifestations • Cough • Shortness of breath Gastrointestinal Manifestations • Diarrhea • Weight loss • Nausea and vomiting Central Nervous System Manifestations • Confusion • Dementia • Headache • Fever • Visual changes • Memory loss • Personality changes • Pain • Seizures Test for HIV antibodies ~ may not be positive right after exposure b/c body hasn’t developed enough antibodies to get detected. Get tested q6months Home testing Salivary and urine testing Interpreting test results Positive, negative, or indeterminate ~ positive – have enough antibodies for HIV ~ negative test doesn’t guarantee that they don’t have the virus ~ repeat testing important HIV viral load testing ~ more direct but more expensive ~ detect how much virus is in blood ~ used for treatment, not diagnostic. We know pt is (+). Want to know how disease is progressing. If treatments are working. “Lower Limit” – want viral load to be undetectable. Not that there isn’t any virus in their body but we want very small amount. Laboratory Assessment Lymphocyte counts ~ best indicator for viral infection AIDS: < 3500 WBCs/mm3 (leukopenic); <1500 lymphocytes/mm3 (lymphopenic) CD4/CD8 counts ~ CD4+ and viral count = inverse Normal ratio of CD4+ to CD8+ is 2:1. In HIV and AIDS, b/c of low number of CD4+ T-cells, the ratio is low. Antibody tests Enzyme-linked immunosorbent assay (ELISA) Western blot, viral culture, viral load ELISA and Western blot tests antibodies to HIV Quantitative RNA assays p24 antigen assay ways to see extent of the virus and extent of the effect on the immune system Everyone who has AIDS has HIV infection; however, not everyone who has HIV infection has AIDS. A diagnosis of AIDS requires that the person be HIV positive and have either a CD4+ T-cell count of less than 200 cells/mm3 or an opportunistic infection. o o o o o o o o testing/diagnosis for HIV/AIDS o ~ some tests for presence – HIV+ ELISA, western blotter CD4+ o ~ how well treatment is working [viral load testing] nursing interventions/patient teaching for clients with HIV/AIDS o ~ not too much detail Management of clients with Gastrointestinal Disorders gastritis/reflux care & pt teaching o ~ heartburn o ~ not hiatal hernias clinical manifestations and nursing care of peptic/duodenal ulcer disease o ~ how to diagnose, sx, tx o ~ gastric – lose weight Mucosal barrier o ~ duodenal – o *** difference b/t tx for two is so minor that don’t get caught up into details. GERD Assessment Physical o o Diagnostic tests Occurs as a result of the backward flow (reflux) of GI contents into the esophagus Reflux produces sx by exposing the esophageal mucosa to the irritating effects of gastric or duodenal contents, resulting in inflammation A person w/ acute sx of inflammation is often described as having reflux esophagitis, which may be mild or severe. The degree of inflammation is r/t the acid concentration of the refluxed material, the # of reflux episodes, and the length of time that the esophagus is exposed to the irritant Reflux esophagitis (excessive relaxation of LES) –avoid fatty foods, caffeine, chocolate, citrus, peppermint, etc. Key features: o Dyspepsia (heartburn)** main symptom substernal or retrosternal burning sensation that tends to move up and down the chest in a wavelike fashion; severe heartburn may radiate to the neck or jaw or may be felt in the back. It can resemble angina… o Regurgitation (may lead to aspiration or bronchitis) o Coughing, hoarseness, or wheezing at night o Water brash (hypersalivation) o Dysphagia o Odynophagia (painful swallowing) o Epigastric pain o Belching and flatulence o Nausea o Pyrosis (retrosternal burning) o Globus (feeling of something in back of throat) o Pharyngitis o Dental caries (severe cases) Most accurate method: 24-hour ambulatory esophageal pH monitoring EGD evaluating reflux esophagitis (biopsy may be performed) GASTRIC ULCER Occurs when there is a break in the mucosal barrier and HCl injures the epithelium. Gastric emptying is delayed, causing regurgitation of duodenal contents. Gastric ulcers are deep and penetrating, and they usually occur on the lesser curvature of the stomach near the pylorus DUODENAL ULCER Chronic break in the duodenal mucosa that extends through the muscularis mucosa and leaves a scar after healing. Characterized by high gastric acid secretion and is the most common type of peptic ulcer PUD is associated primarily w/ NSAIDs use and H. pylori o o o o o o o o Epigastric tenderness (midline between umbilicus and xyphoid process) If perforation, rigid, board-like abdomen with rebound tenderness ~peritonitis Dyspepsia (indigestion) –discomfort in upper abdomen (sharp, burning, gnawing) Assess for fluid volume deficit (orthostatic hypotension, dizziness) H&H low due to bleeding Stool specimen positive for occult Testing methods for H. pylori If perforation suspected, chest and abdominal x-ray Esophageal manometry: motility testing (not as common) Treatment Meds Drug therapy: take before meals! o Antacids: increase pH of gastric content by deactivating pepsin o Histamine receptors: decrease gastric acid production (shortacting) o Prokinetic drugs: increase gastric emptying o Proton pump inhibitors: decreases gastric acid production (long-acting) Other Nonsurgical management o Most important role of nurse it pt and family education and ongoing mgmt. o Nutritional therapy: eliminate foods to decrease LES pressure: chocolate, alcohol, fatty foods (esp fried), caffeine, and carbonated beverages, orange juice, tomatoes –spicy or acidic foods also, small portions, and no bed time snacks (avoid eating for 3 hrs (or more) before bedtime) o Right side lying position to decrease effects of nighttime episodes of reflux, sleep with 612 inch pillow o Manage obesity, avoid heavy lifting, straining, and working over in bent-over position Surgical management o Laparoscopic Nissen Fundoplication (LNF) o Very small percentage require anti-reflux surgery; manage lifestyle to prevent GERD* Complications Increase risk for cancer with prolonged GERD Serious complications are hemorrhage and aspiration pneumonia Dental decay Associated w/ cardiac disease o Most accurate test is EGD** –direct visualization of ulcer crater and allows H. testing biopsy Acute pain; chronic pain o Drug therapy triple therapy including PPI, Prevacid, plus 2 antibiotics (PPI’s are drug of choice for pts with acid-related disorders) H2-receptor antagonists inhibit gastric acid secretion Prostaglandin analogues are effective in treating duodenal ulcers Antacids buffer gastric acid and prevent formation of pepsin (1 hr before, and 2-3 hrs after) Sucralfate is mucosal barrier fortifier (protector) ~ don’t give levothyroxine Acute pain; chronic pain o Nutrition therapy Management of nutrition is controversial Eat bland diet with no caffeine o CAM Hypnosis and imagery, yoga (reduce stress and anxiety) Herbs and vitamins (slippery elm and marshmallow root, quercetin, and licorice, vitamin A, B, C, chamomile, ginger, dandelion, cranberry) –heal inflamed tissues Potential for GI bleeding o Nonsurgical management Emergency: upper GI bleeding (prevent hypovolemic shock –ABC’s) NG tube placement and lavage –lavage is withdrawn until clear or light pink and without clots (place client on left side) Endoscopic therapy –for clients with active bleeding, signed consent, NPO 6 hrs, do not resume preprocedure diet until gag reflex intact Acid suppression –used to prevent rebleeding Surgical management o Not indicated unless medical therapy not working or they develop PUD complication o MIS via laparoscopy Subtotal gastrectomy (partial stomach removal) Pyloroplasty (open pylorus) Vagotomy (vagus nerve cutting) Hemorrhage – most serious o Hematemesis (vomits bright red or coffee-ground blood) o Melena (occult blood in tarry stool) Perforation, w/ the gastroduodenal contents emptying through the anterior wall of the stomach or duodenum into the peritoneal cavity o Tender, rigid, and board-like (peritonitis) o Surgical emergency and life threatening! Pyloric obstruction – abd bloating, N/V Intractable disease, which is characterized by lack of response to conservative management and w/ symptoms that interfere w/ ADLs priority assessment of inflammatory and non-inflammatory GI problems Pancreatitis* ACUTE PANCREATITIS Serious and, at times, life-threatening inflammatory process of the pancreas caused by premature activation of pancreatic enzymes and resulting in autodigestion and fibrosis of the pancreas The extent of the inflammation and tissue destruction ranges from mild involvement, characterized by edema and inflammation, to severe, necrotizing hemorrhagic damage leading to diffusely bleeding pancreatic tissue w/ fibrosis and tissue death Many factors can cause injury to the pancreas: o Biliary tract disease w/ gallstones o Excessive alcohol ingestion [most frequent cause] o Postop trauma from surgical manipulation after biliary tract, pancreatic, gastric, and duodenal procedures o External blunt trauma o Metabolic disturbances o Kidney failure or kidney transplant o Drug toxicities, including opiates, sulfonamides, thiazides, steroids, and oral contraceptives o Other medical diseases In acute pancreatitis, four major pathophysiologic processes occur: lipolysis, proteolysis, necrosis of blood vessels, and inflammation Assessment Physical Abdominal pain (most frequent symptom), including sudden-onset pain in a midepigastric or LUQ location w/ radiation to the back, aggravated by a fatty meal, ingestion of a large amount of alcohol, or lying in the CHRONIC PANCREATITIS Progressive, destructive disease o the pancreas w/ remissions and exacerbations Inflammation and fibrosis of the tissue contribute to pancreatic insufficiency and diminished exocrine and endocrine function Characterized by the loss of exocrine function, which causes a decreased output of enzymes and bicarbonate; loss of endocrine unction results in diabetes mellitus Chart 62-3 Key Features Chronic Pancreatitis Intense abd pain (major clinical manifestation) that is continuous and burning or gnawing Diagnostic tests Treatment Meds recumbent position; intense, boring, and continuous and is worsened by lying in supine position. E: Pain that worsens when lying supine and the presence of jaundice are the only assessment findings indicative of acute pancreatitis. E: Pain associated with pancreatitis is usually located in the mid-epigastric or upper left quadrant, and jaundice is present. E: Pain associated with acute pancreatitis usually has an abrupt onset E: Pain associated with pancreatitis usually lessens with sitting up. Weight loss, w/ N and V Jaundice Gray-blue discoloration of the abd and periumbilical area (Cullen’s sign) Gray-blue discoloration of the flanks (Turner’s sign) Absent or decreased bowel sounds Abd tenderness, rigidity, and guarding Dull sound on abd percussion, indicating ascites Elevated temp w/ tachycardia and decreased BP Adventitious breath sounds, dyspnea, or orthopnea Elevated serum amylase and lipase levels Significant changes in VS may indicate shock. Hypotension and tachycardia may result from pancreatic hemorrhage, excessive fluid volume shifting, or the toxic effects of abd sepsis from enzyme damage. Observe LOC that may be r/t alcohol withdrawal, hypoxia, or impending sepsis w/ shock. Serum lipase , amylase , alkaline phosphatase , alanine aminotransferase (ALT) , bilirubin , WBC , HGB, HCT, coagulation factors, Na+, Ca2+, Mg2+, triglycerides, and albumin ~ Ca2+ and Mg2+ low Imaging of the pancreas and gallbladder w/ ultrasound or CT scan Opioids such as morphine or hydromorphone, often w/ PCA device Proton pump inhibitors or H2-histamine receptor blockers to decrease gastric hydrochloric acid production during fasting Antibiotics for pts w/ acute necrotizing pancreatitis Other Relief of pain by assuming the fetal position or by sitting upright and bending forward. Diet therapy: o Withhold foods and fluids in the acute period; maintain hydration w/ IV fluids o NG intubation to decrease gastric distention and suppress pancreatic secretion o Initiating nasojejunal enteral nutrition o Assess frequently for presence of bowel sounds Comfort measures include: o Side-lying position to decrease abd pain o Avoiding oral stimulation while providing measures to keep mucous membranes from drying ~ NPO Abd tenderness Ascites Possible LUQ mass (if pseudocyst or abscess is present Resp compromise manifested by adventitious or diminished breath sounds, dyspnea, or orthopnea Steatorrhea; clay-colored stools Weight loss Jaundice Dark urine Polyuria, polydipsia, polyphagia (diabetes mellitus) ~ Fatigue and muscle wasting Elevated serum amylase, bilirubin, and alkaline phosphatase Identification of calcification of pancreatic tissue in biopsy specimen Opioid analgesia Non-opioid analgesics Pancreatic-enzyme replacement therapy (PERT) is the standard of care to prevent malnutrition, malabsorption, and excessive weight loss Insulin or oral hypoglycemic agents to control diabetes H2-histamine receptor antagonist or proton pump inhibitor to decrease gastric aclid Diet therapy includes: fasting to avoid recurrent pain exacerbated by eating and providing jejunal or TPN Surgical management – not the primary intervention o Indicated for intractable pain, incapacitating pain relapses, or complications such as pseudocyst and abscess o I&D for abscesses or pseudocysts o Laparoscopic cholecystectomy or cholechotomy for underlying biliary tract disease o Sphincterotomy (incision of the sphincter) for ibrosis o Pancreatojejunostomy (pancreatic Complications E: Enzyme preparations should not be mixed with foods containing protein because the enzymes will dissolve the food into a watery substance. duct is opened and anastomosed to the jejunum, relieving obstruction) to relieve pain and preserve pancreatic tissue and fxn) o Partial pancreatectomy, which may be performed for advanced pancreatitis or disabling pain o Vagotomy w/ gastric antrectomy to alter nerve stimulation and decrease pancreatic secretion Chart 62-5 Prevention of Exacerbations of Chronic Pancreatitis Avoid things that make your sx worse, such as drinking caffeinated beverages Avoid alcohol ingestion Avoid nicotine Eat bland, low-FAT, high-PRO, moderate-CHO meals; avoid gastric stimulants, such as spices Eat small meals and snacks high in calories Take pancreatic enzymes that have be prescribed for you w/ meals Rest frequently; restrict your activity to one floor until you regain your strength E: Pancrelipase (Cotazym) is a pancreatic enzyme used for enzyme replacement for clients with chronic pancreatitis. To avoid skin irritation and breakdown from residual enzymes, the lips should be wiped. Pseudocyst Abscess Table 62-3 Potential Complications of Acute Pancreatitis Pancreatic infection (most common cause of death) Hypovolemia Hemorrhage Acute renal failure Paralytic ileus – peritoneal irritation and seepage of pancreatic enzymes into the abd cavity Hypovolemic or septic shock – shock results from peripheral vasodilation form the released vasoactive substances and the retroperitoneal loss of protein-rich fluid form proteolytic digestion. Hypovolemia results from decreased renal perfusion and acute renal failure. Pleural effusion Acute resp distress syndrome (ARDS) – disruption of the aveolar capillary membrane Atelectasis Pneumonia Multi-organ system failure – caused by necrotizing hemorrhagic pancreatitis Disseminated intravascular coagulation (DIC) – involves hypercoagulation of the blood, w/ consumption of clotting factors and development of microthrombi Diabetes mellitus Appendicitis* APPENDICITIS Acute inflammation of the vermiform appendix, the small finger-like pouch attached to the cecum of the colon Inflammation of the appendix can occur when the lumen of the appendix is obstructive Inflammation leads to infection as bacteria invade the wall of the appendix Most common cause of acute inflammation of RLQ of abd Peak incidence is b/t 20 and 30 yrs; may occur at any age Not common for older adults Assessment Physical Abd pain originating in the epigastric or periumbilical area and shifting to the RLQ (McBurney’s point); pain may Diagnostic tests Treatment Meds Other Complications not be localized N/V Anorexia after the initial diagnosis of pain Urge to defecate or pass flatus Muscle rigidity and rebound tenderness Normal or slightly elevated temp Abd pain that increase w/ cough or movement and is relieved by flexion of the right hip or knees suggests a perforated appendix w/ peritonitis ~ pain before N/V Increased WBC w/ possible increased segmented neutrophils – 10,000 to 18,000/mm3 w/ a “shift to the left” (increased # of immature WBCs) WBC elevation > 20,000/mm3 may indicate peritonitis Ultrasound study may show presence of enlarged appendix If sx are recurrent or prolonged, a CT scan can be used for diagnosis and may reveal the presence of a fecalith Keep pt w/ suspected or known appendicitis on NPO to prepare for the possibility of emergency surgery and to avoid making the inflammation worse The pt w/ suspected appendicitis should NOT receive laxatives or enemas, which can cause perforation of the appendix. Heat should NEVER be applied to the abd b/c this may increase circulation to the appendix and result in increased inflammation and perforation Keep pt in semi-Fowler’s position so that abd drainage, if any, can be contained in the lower abd Appendectomy may be performed as a traditional procedure through a small incision or, if not ruptured, by means of laparoscopy If the process occurs slowly, an abscess may develop Rapid process may result in peritonitis Perforated appendix w/ peritonitis All complications of peritonitis are serious. Gangrene can occur w/in 24 to 36 hrs, is life threatening, and is one of the most common indications for emergency surgery. Perforation may develop w/in 24 hrs, but the risk rapidly rises after 48 hrs Perforation is more common in older people, causing a higher mortality rate. The diagnosis of appendicitis is difficult to establish in older adults b/c sx of pain and tenderness may not be as pronounced in this age-group, resulting in tx delay and an increased risk for perforation, peritonitis, and death Peritonitis* PERITONITIS Life-threatening, acute inflammation of the visceral/parietal peritoneum and endothelial lining of the abd cavity Primary – acute bacterial infection that develops as a result of contamination of the peritoneum through the vascular system; rare Secondary – bacterial invasion as a result of perforation or a penetrating wound, such as appendicitis, diverticulitis, peptic ulcer, ascending genital infection, or a gunshot injury to the abd. Chemical peritonitis is the result of leakage of bile, pancreatic enzymes, and gastric acid Most often caused by contamination of the peritoneal cavity by bacteria or chemicals (secondary) Assessment Physical Chart 60-1 Key Features Peritonitis Rigid, boardlike abd (classic) Abd pain (localized, poorly localized, or referred to the shoulder or chest) Distended abd N, anorexia, V Diminishing BS Inability to pass flatus or feces Rebound tenderness in the abd High fever Tachycardia Dehydration from high fever (poor skin turgor) Decreased urine output Hiccups Possible compromise in resp status Diagnostic CBC: WBC elevated to 20,000/mm3 w/ high neutrophil count tests Blood culture – determine whether septicemia has occurred and to ID the causative organism Serum electrolytes, BUN, creat Abd x-rays or CT to determine presence of dilation, edema, and inflammation of the intestines Treatment Meds Other Complications IV fluids and antibiotics Pain management w/ IV analgesics, anticipate use of PCA pump Keep pt NPO Administer O2 as prescribed according to pt’s resp status Surgical Management: may be necessary to ID and repair underlying cause of the peritonitis o Focused on controlling the contamination, removing foreign material from the peritoneal cavity, and draining fluids collections o During surgery, the peritoneum is irrigated w/ antibiotic solution, and drainage catheters are inserted o Exploratory laparotomy – usual approach to remove or repair inflamed or perforated organs o Maintain the pt in semi-Fowler’s position to promote drainage of peritoneal contents into the lower region of the abd cavity o Monitor LOC, VS, resp status (RR and breath sounds), and I&O at least hourly immediately after surgery Shock Resp problems Paralytic ileus ~ kidney failure ~ bacteremia, septicemia Crohn’s vs. ulcerative colitis* CROHN’S Regional enteritis, idiopathic inflammatory disease that occurs anywhere in the GI tract but most often affect the terminal ileum w/ patchy lesions that extend through all bowel layers Chronic nonspecific inflammation of the entire intestinal tract occurs, and eventually deep fissure and ulcerations develop and often extend through all bowel layers, predisposing the pt to development of bowel fistulas Chronic pathologic changes include thickening of the bowel wall, resulting in narrowing of the bowel lumen and strictures Assessment Physical Fever, abd pain (RLQ), loose stools ULCERATIVE COLITIS Creates widespread inflammation of mainly the rectum and rectosigmoid colon but can extend to the entire colon Characterized by hyperemic intestinal mucosa (increased blood flow) w/ resultant edema. In more severe inflammation, the lining can bleed and small erosions, or ulcers, occur. Abscesses can form in these ulcerative areas and result in tissue necrosis. Continued edema and mucosa thickening can lead to a narrowed colon and possibly a partial bowel obstruction Stool typically contains blood and mucus Diagnostic tests Treatment Meds Blood in stool Periumbilical pain before and after BM Weight loss (indicates serious nutritional deficiencies) Distention, masses, or visible peristalsis Ulcerations or fissures of the perianal area Bowel sounds diminished or absent in the presence of severe inflammation High-pitched or rushing sounds over the areas of narrowed bowel loops Diarrhea w/ steatorrhea (stool does not usually contain blood but is fatty, frothy, foul-smelling) Anemia – slow bleeding and poor nutrition Low folic acid and cobalamin (vit B12 group) serum levels b/c of malabsorption, further contributing to anemia Decreased albumin – amino acid malabsorption and protein-losing enteropathy C-reactive protein and ESR elevated – indicate inflammation WBCs in urine – infection (pyuria), caused by uretal obstruction or an enterovesical (bowel to bladder) fistula Electrolyte losses, K+ and Mg2+ - if severe diarrhea present X-rays – show narrowing, ulcerations, strictures, and fistulas Abd ultrasound, CT scan Biopsies obtained via colonoscopy may verify the diagnosis Aminosalicylates – anti-inflammation Glucocorticoids – during exacerbation Immunomodulatory therapy, used for pts w/ refractory disease Metronidazole (Flagyl, Novonidazol) – fistulas * bowel rest, TPN, Other Malnutrition: high-calorie, high-PRO, high-vitamin, low-fiber meals; oral supplements such as Ensure and Vivonex Electrolyte therapy: F&E replacement by oral liquids, nutrients, IV fluids Impaired skin integrity results from fistula formation: apply pouch, cover area w/ skin barrier, clean and keep dry Surgical Management: bowel rsn and anastomosis w/ or w/o colon rsn Stricturoplasy – for bowel strictures Abd cramping, pain, and distention Bloody diarrhea, tenesmus (unpleasant and urgent sensation to defecate) Lower abd colicky pain relieved w/ defecation Low-grade fever, tachycardia Malaise, anorexia, weight loss are common Anemia occurs less often Extraintestinal manifestations such as: migratory polyarthritis, ankylosing spondylitis, and erythema nodosum Gallstones Abnormal lab values: HCT, HGB, WBC, ESR, Creactive protein, and electrolytes Results from most recent colonoscopy Aminosalicylates – reduce inflammation Glucocorticoids – during exacerbation Anti-diarrheal drugs – symptomatic management of diarrhea; given cautiously, b/c they can precipitate colonic dilation and toxic megacolon Immunomodulators – alter immune response and are commonly given w/ glucocorticoids. Inliximab (Remicade) or adalimumab (Humira) may be given for refractory disease or for severe complications such as toxic megacolon. E: adalimumab (Humira) - The client should avoid being around large crowds to avoid developing an infection; The client should not take the medication if he or she is allergic to certain proteins. Sulfasalazine (Azulfidine) is one of the primary treatments for UC. It is thought to inhibit prostaglandin synthesis and thereby to reduce inflammation. E: Lactose-containing foods are often poorly tolerated and should be reduced or eliminated from the diet of clients with UC. E: Raw vegetables and high-fiber foods can cause GI symptoms in clients with UC. Diet therapy may include: o NPO status for pt w/ severe sx o TPN while NPO o Elemental formulas, which are absorbed in the upper bowel thereby minimizing bowel sitmulation o Avoiding high-fiber foods such a nuts and fresh fruits or vegetables Avoiding carbonated beverages, pepper, nuts and corn, dried fruits, and smoking, b/c these are common GI stimulants that could cause discomfort Complementary and alternative therapies used as a supplement to traditional therapies may include herbs such as flaxseed, selenium, vit C, biofeedback, yoga, acupuncture, and Ayurveda (combination of diet, herbs, and breathing exercises) Surgical procedures: total proctocolectomy w/ permanent ileostomy, total colectomy w/ a continent ileostomy (Kock’s ileostomy) or ileal reservoir, creation of ileoanal reservoir (aka Resorative Proctocolectomy w/ Ileal Pouch Anal Anastomosis (RPC-IPAA) Intestinal perforation w/ peritonitis and fistula formation Toxic megacolon Toxic megacolon is characterized by an enlarged colon with fever, leukocytosis, and tachycardia. Hemorrhage Increased risk for colon cancer Malabsorption Extraintestinal clinical manifestations o Complications Malabsorption Fistulas Hemorrhage Abscess formation Bowel obstruction Increased risk for cancer Severe malnutrition Diverticulitis vs diverticulosis* DIVERTICULITIS Inflammation of one or more diverticula, results when the diverticulum retains undigested food, which compromises the blood supply to that area and facilitates bacterial invasion of the diverticular sac, which may then perforate A perforated diverticulum can progress to intraabd perforation w/ generalized peritonitis DIVERTICULOSIS Pouchlike herniations of the mucosa through the muscular wall of any portion of the gut, but it most commonly refers to diverticula of the colon Can occur in any part of the intestine but most common in sigmoid colon High intraluminal pressure forces the formation of a pouch in the weakened area of the mucosa, commonly near blood vessels Assessment Physical Diagnostic tests Treatment Meds Other Abd pain that may begin as intermittent and may progress to continuous o pain may be localized to the LLQ and increased w/ coughing, straining, or lifting o generalized abd pain is a sign of perforation and peritonitis Fever N/V Abd distention Palpable, tender abd or rectal mass Hypotension and dehydration occur if massive bleeding occurs Signs of septic shock occur if peritonitis has occurred Blood in stool (microscopic to larger amounts) Elevated WBC, reduced HCT and HGB if bleeding occurs Flat plate x-ray to evaluate for free air and fluid outside the GI tract CT scan to diagnose abscess or thickening of lumen caused by repeated inflammation and injury Serum electrolytes I, O, and pt fluid status If a NGT is used for gastric decompression or to manage vomiting, check output for amount and quality or color broad-spectrum antibiotics such as metronidazole (Flagyl) plus trimethoprim/sulfamethoxazole (Bactrim, Septra), or ciprofloxacin (Cipro) implement management for mild or moderate pain; if pain is severe, use opioids laxatives and enemas are not given, b/c they increase intestinal motility NGT inserted if N, V, or abd distention is severe Recommend rest Diet AVOID FIBER Surgical management: colon rsn w/ end-to-end anastomosis or temporary or permanent colostomy Chart 60-6 Nursing Focus On The Older Adult Diverticulitis • Provide antibiotics, analgesics, and anticholinergics as prescribed. Observe older patients carefully for side effects of these drugs, especially confusion (or increased confusion), urinary retention or failure, and orthostatic hypotension. • Do not give laxatives or enemas. Teach the patient and the family about the importance of avoiding these measures. • Encourage the patient to rest and to avoid activities that may increase intra-abdominal pressure, such as straining and bending. • While diverticulitis is active, provide a low-fiber diet. When the inflammation resolves, provide a high-fiber diet. Teach the patient and family about these diets and when they are appropriate. • Because older patients do not always experience the w/o inflammation, diverticula are asymptomatic unless pain or bleeding develops, the condition may go undiagnosed intermittent pain in LLQ history of constipation Lab studies are not indicated colonoscopy barium enema (rectal) upper GI tract series (small intestine) Use a bulk-forming laxative such as psyllium (Metamucil) to increase fecal size and consistency if the recommended fiber requirements cannot be tolerated Eat diet high in cellulose and hemicellulose, which are found in wheat bran, whole-grain breads, and cereals. HIGH FIBER! Foods containing seeds or indigestible material that may block a diverticulum, such as nuts, corn, popcorn, cucumbers, tomatoes, figs, and strawberries, may be eliminated Complications typical pain or fever expected, observe carefully for other signs of active disease, such as a sudden change in mental status. • Perform frequent abdominal assessments to determine distention and tenderness on palpation. • Check stools for occult or frank bleeding. Require emergent surgery: o Rupture of the diverticulum w/ subsequent peritonitis o Pelvic abscess o Bowel obstruction o Fistula o Persistent fever or pain after 4 days of medical tx o Uncontrolled bleeding colon cancer o ~ who’s at risk? Older adults, ulcerative colitis, high fat, red meat o ~ what do you do for colon cancer? Colectomy (take out portion of colon), may have colostomy [know concept, not specific] o ~ s/p colon cancer: complications/problems? Recurrence, imbalanced nutrition ~ think about time – 3 hrs? 1 days? 3 days? ~ what happens in colon? Water absorption. Be worried about F&E imbalance. ~ another complication ADHESIONS risk for obstruction ~ psychosocial – colostomy COLON CANCER Most CRCs are adenocarcinomas arising from the glandular epithelial tissue of the colon an develop as a multistep process, resulting in loss of key tumor suppressor genes and activation of certain oncogenes that alter colonic mucosa cell division Increased proliferation of the colonic mucosa first forms polyps that can transform into malignant tumors Tumors occur in all areas of the colon and can spread by direct invasion and through the lymphatic and circulatory systems Most common sites of metastasis: liver, lungs, brain, bones, and adrenal glands E: Genetic testing is the only definitive way to determine whether the client has a predisposition to develop CRC. A higher incidence of the disease has been noted in families who have a history; however, it is not the responsibility of the nurse to engage in genetic counseling, and this client might not be predisposed to developing CRC. Assessment Physical Rectal bleeding (most common manifestation) Change in stool pattern or appearance Cachexia (late sign) – (weight loss, muscle atrophy) Guarding or abd distention (late sign) Abd mass (late sign) Diagnostic Anemia (low HGB and HCT; stool positive for occult blood) tests Fecal occult blood test (FOBT) ~ avoid aspirin, vit C, and red meat 48hrs before stools specimen is collected to avoid false positive Carcinoembryonic antigen (CEA) blood test ~ elevated, but not specific to CRC Colonoscopy ~ definitive test for diagnosis of colorectal cancer CT or MRI of chest, abd, pelvis, lungs, or liver E: Carcinoembryonic antigen may be elevated in many clients diagnosed with CRC. Treatment Meds E: 5-FU cannot discriminate between cancer and healthy cells; therefore the side effects are diarrhea, mucositis, leukopenia, mouth ulcers, and skin ulcers. E: Cetuximab (Erbitux), a monoclonal antibody, may be given for advanced disease. This drug works by binding to a protein (epidermal growth factor receptor) to slow cell growth. E: Clients with advanced colorectal cancer and metastasis also receive drugs such as analgesics and antiemetics for relief of symptoms, specifically pain and nausea. Other Non-surgical Management o Radiation therapy: local or regional control of the disease; used postoperatively as a palliative measure to reduce pain, hemorrhage, bowel obstruction, or metastasis o Chemotherapy o Targeted biotherapy – Bevacizumab (Avastin), Cetuximab (Erbitux) Surgical Management Colon rsn – bowel segment containing tumor is removed along w/ several inches of bowel beyond tumor margin and regional lymph nodes, and an end-to-end anastomosis – open method or MIS o Colectomy (colon removal) w/ temporary or permanent colostomy o Abd peritoneal (A-P) rsn – sigmoid colon and rectum are removed, anus is closed, and a permanent colostomy is formed ~ asc = liquid, transverse = pasty, desc = solid Bowel perforation w/ peritonitis Abscess Fistula formation – to vagina or bladder Frank hemorrhage – tumor may invade neighboring blood vessels and cause frank bleeding Complete intestinal obstruction – tumors growing into bowel lumen can gradually obstruct and eventually block intestine o Complications GI obstruction o ~ risk: previous GI surgery BOWEL OBSTRUCTION Can be partial or complete; intestinal contents accumulate at or above the obstruction Mechanical obstruction bowel is physically obstruction by disorders outside the intestine (adhesions or hernias) or blockages in the lumen of the intestine (tumors, fecal impactions, and stricture) Non-mechanical obstruction (paralytic or adynamic ileus) peristalsis is decreased or absent, resulting in a slowing of the movement or a backup of intestinal content caused by physiologic, neurogenic, or chemical imbalances: paralytic ileus is associated w/ trauma, abd surgery, hypokalemia, MI, or vascular insufficiency Strangulated obstruction obstruction w/ compromised blood flow. SURGICAL EMERGENCY! Assessment Physical E: A small bowel obstruction is characterized by upper or epigastric abdominal distention, metabolic alkalosis, and a great amount of vomiting. Chart 59-5 Key Features Small-Bowel and Large-Bowel Obstructions o Small-Bowel Obstructions Abd discomfort or pain possibly accompanied by visible peristaltic waves in upper and middle abd Upper or epigastric abd distention N and early, profuse V (may contain fecal material) Obstipation (no passage of stool) Severe F&E imbalances Metabolic alkalosis o Large-Bowel Obstructions Intermittent lower abd cramping Lower abd distention Minimal or no vomiting Obstipation or ribbon-like stools No major F&E imbalances Metabolic acidosis (not always present) Early cramping - borborygmi (high-pitched BS) – intestine tries to push the mechanical obstruction forward Later BS absent, esp distal to the obstruction Nonmechanical obstruction: pain described as constant, diffuse discomfort. Abd distention. Decreased BS in early obstruction and absent BS in later stages. V of gastric contents and bile is frequent, but vomitus rarely has a foul odor and is rarely profuse. Diagnostic Laboratory Assessment tests o WBC normal unless there is a strangulated obstruction in which case there may be leukocytosis (increased WBCs) o HGB, HCT, creat, and BUN often elevated, indicating dehydration o Na+, Cl-, K+ reduced b/c of loss of F&E o Elevation in serum amylase levels may be found w/ strangulating obstructions, which can damage the pancreas o High obstruction in small intestine have ABG values indicative of metabolic alkalosis o Obstruction in large intestine may show values suggestive of metabolic acidosis Imaging Assessment o Flat-plate and upright abd x-rays and CT scan o Distention w/ fluid and gas in small intestine w/ absence of gas in colon = obstruction in small intestine o X-ray findings often normal when a strangulated obstruction exists in small intestine Other o Abd ultrasound to evaluate potential cause of obstruction o Endoscopy (sigmoidoscopy or colonoscopy) to determine cause of obstruction, except when perforation or complete obstruction is suspected Treatment Meds Other Complications Pain management – opioid analgesics withheld in diagnostic workup period so that clinical manifestations of perforation or peritonitis are not masked Broad-spectrum antibiotics if strangulation is suspected Non-surgical Management o NPO o Semi-Fowler’s position helps alleviate pressure of abd distention on the chest o Decompress GI tract by inserting or maintaining a gastric or intestinal tube, which can be inserted nasally or orally o Obstruction caused by fecal impaction resolves after disimpaction and enema o Intussusception (telescoping of bowel) may result w/ hydrostatic pressure changes during a barium enema or w/ manipulation under fluoroscopy o Administer F&E replacement o * changes from a colicky, intermittent pain to a constant discomfort can indicate perforation of the intestine or peritonitis ~ administer fluids… Surgical Management o Required for complete obstruction and for many cases of incomplete mechanical obstruction o Exploratory laparotomy to locate obstruction and determine nature of the problem o Examples of procedures: lysis of adhesions colon rsn w/ anastomosis for obstruction resulting from tumor or diverticulitis embolectomy or thrombectomy for intestinal infarction colon rsn and colostomy Prevention of fecal impaction o High fiber diet – raw vegetables, fruits, whole grain o Drink adequate fluids esp water o Do not routinely use laxatives –b/c it decreases abd muscle tone and contributes to atonic colon o Exercise regularly o Use natural foods to promote peristalsis like warm beverages and prune juice o Take bulk forming products such as Metamucil to provide fiber o Sit on toilet or bedtime commode o Check stool for oozing, meaning obstruction Absorption of F&E into the vascular space is compromised and can lead to reduced circulatory blood volume and electrolyte imbalances Hypovolemia Perforation of intestine Peritonitis Sepsis, shock Management of Clients with Musculoskeletal Disorders, Trauma or Overuse osteomyelitis causes and care o ~ who’s at risk? What you do for it. Risk factors and treatment. RA/OA OSTEOARTHRITIS Most common type of arthritis Joint pain and loss of function characterized by progressive deterioration and loss of cartilage in the joints Osteophytes Synovitis Subluxation Assessment Physical Diagnostic tests Treatment Meds Other Joint involvement Heberden's nodes – DIP joints – painful and red Bouchard’s nodes – PIP joints – “ Joint effusions – excess joint fluid Atrophy of skeletal muscle – pain discourages movement of painful joints Spine, esp L3-4 or C4-6 – radiating pain, stiffness, and muscle spasms in one or both extremities Middle-aged or older women Chronic joint pain and stiffness Early: pain diminishes after rest and worsens after activity Later: pain occurs w/ slight motion or even when at rest Crepitus w/ ROM Joint stiffness lasts <30 min after period of inactivity ESR and high-sensitivity C-reactive protein (hsCRP) slightly elevated when secondary synovitis (synovial inflammation) occurs ESR tends to rise w/ age and infection Analgesics Glucosamine = decrease inflammation; careful w/ HTN, diabetics, anticoagulants Chondroitin = increase/strengthen cartilage Acetaminophen (Tylenol, Atasol) as the primary drug of choice because OA is not a primary anti-inflammatory disorder. NSAIDS Opioids Cortisone injection Non-Surgical Management Analgesics Rest – local (immobilize unstable joint), systemic (nap), psychological Positioning – position joints in their functional position Thermal modalities – heat (decrease muscle tension), cold (numbing nerve endings and decreasing secondary joint inflammation) Weight control – less stress on weight-bearing joints, decrease pain, slow joint degeneration Integrative therapies Surgical Management Total joint arthroplasty (TJA) Total joint replacement (TJR) Arthroscopy Osteotomy PP: Sequestrectomy - Because bone cannot heal in the presence of necrotic tissue, a sequestrectomy may be performed to débride the necrotic bone and allow revascularization of tissue. The excision of dead and infected bone often results in a sizable cavity, or bone defect. Bone grafts - The excision of dead and infected bone often results in a sizable cavity, or bone defect. The use of bone grafts to repair bone defects is also widely used. Bone segment transfers - When infected bone is extensively resected, reconstruction with microvascular bone transfers may be done. Reserved for larger skeletal defects. Most common donor sites are the patient's fibula and iliac crest. Muscle flaps - The bone graft may have an attached muscle or skin flap, if necessary. Amputation Neurovascular (NV) assessments must be done frequently because the patient experiences increased swelling after the surgical procedure. Elevate the affected extremity to increase venous return and thus control swelling. ~ fractures ~ DVT, VTE, PE Complications RHEUMATOID ARTHRITIS One of the most common connective tissue diseases and the most destructive to the joints Chronic, progressive, systemic inflammatory autoimmune disease affecting primarily the synovial joints Autoantibodies (rheumatoid factors) formed that attack healthy tissue, especially synovium, causing inflammation Affects synovial tissue of any organ or body system Assessment Physical Early disease manifestations—joint stiffness, swelling, pain, fatigue, and generalized weakness and morning stiffness Late disease manifestations—as the disease worsens, the joints become progressively inflamed and quite painful Frequent morning stiffness (gel phenomenon) which lasts for 45 min to several hours after awakening PIP and MCP – slightly reddened, warm, stiff, swollen, tender or painful Bilateral and symmetric Migratory arthritis: migrating symptoms Chart 20-7 Key Features The Patient with Rheumatoid Arthritis Early Manifestations Joint • Inflammation Systemic • Low-grade fever • Fatigue • Weakness • Anorexia • Paresthesias Late Manifestations Joint • Deformities (e.g., swan neck or ulnar deviation) • Moderate to severe pain and morning stiffness Systemic Diagnostic tests Treatment Meds Other Complications • Osteoporosis • Severe fatigue • Anemia • Weight loss • Subcutaneous nodules • Peripheral neuropathy • Vasculitis • Pericarditis • Fibrotic lung disease • Sjögren's syndrome (dry eyes/mouth/vagina) • Renal disease • Felty's syndrome (RA, hepatosplenomegaly, leukopenia) rheumatoid factor (+) = rheumatoid disease antinuclear antibody titer (+) = autoimmune disease erythrocyte sedimentation rate = inflammatory disease serum complement serum protein electrophoresis serum immunoglobulins Other diagnostic assessments— x-ray – visualize joint changes an deformities CT – may help determine presence and degree of cervical spine involvement Arthrocentesis – monitor site for bleeding or leakage of synovial fluid. Notify physician. bone scan – asses extent of joint involvement NO GLUCOSAMINE OR CHONDROITIN (1) Disease-modifying antirheumatic drugs – inflammation (2) NSAIDs - inflammation Biologic response modifiers Other drugs: Glucocorticoids (3) Immunosuppressive agents Gold therapy – don’t worry about this Analgesic drugs Non-pharmacologic Interventions Adequate rest Proper positioning Ice and heat applications Plasmapheresis Gene therapy Complementary and alternative therapies Promotion of self-care Carpal tunnel syndrome Systemic Complications Moderate to severe weight loss, fever, and extreme fatigue in late disease exacerbations Subcutaneous nodules – ulnar surface of the arm, fingers, Achilles tendon Vasculitis; periungal lesions – don’t worry about brown spots Paresthesias – peripheral neuropathy associated w/ decreased circulation can cause foot drop and paresthesias Respiratory complications: pleurisy, pneumonitis, diffuse interstitial fibrosis, and pulm HTN Cardiac complications: pericarditis, myocarditis Eye involvement: iritis, scleritis Associated sydromes: o Sjogren’s syndrome (dry eyes/mouth/vagina), o Felty’s syndrome (RA, hepatosplenomegaly, leukopenia), o Caplan’s syndrome (rheumatoid nodules in lungs and pneumoconiosis) nursing management for patients with skin and skeletal traction o ~ skin – boot, Velcro strap o ~ skeletal – bone, infection issue o o o o o o Traction Application of a pulling force to the body to provide reduction, alignment, and rest at that site Types of traction: skin, skeletal Table 54-2 Types of Traction Traction care: Maintain correct balance between traction pull and countertraction force Care of weights Skin inspection Pin care Assessment of neurovascular status Traction is the application of a pulling force to a part of the body to provide reduction, alignment, and rest. It is also used as a last resort to decrease muscle spasm (thus relieving pain) and prevent or correct deformity and tissue damage. A patient in traction is often hospitalized, but in some cases, home care is possible even for skeletal traction. Skin traction involves the use of a Velcro boot (Buck's traction) (Fig. 54-5), belt, or halter, which is usually secured around the affected leg. The primary purpose: decrease painful muscle spasms that accompany hip fractures. The weight is used as a pulling force and is limited to 5 to 10 pounds (2.3 to 4.5 kg) to prevent injury to the skin. In skeletal traction, pins, wires, tongs (e.g., Crutchfield), or screws are surgically inserted directly into bone. These allow the use of longer traction time and heavier weights—usually 15 to 30 pounds (6.8 to 13.6 kg). Skeletal traction aids in bone realignment. Pin site care is an important part of nursing management to prevent infection. The nurse may set up or assist in the setup of traction if specially educated. In larger or specialty hospitals or units, orthopedic technicians or physician assistants often set up traction. Once traction is applied, maintain the correct balance between traction pull and countertraction force. Nursing Safety Priority Action Alert When patients are in traction, weights usually are not removed without a prescription. They should not be lifted manually or allowed to rest on the floor. Weights should be freely hanging at all times. o o Teach this important point to UAP on the unit, to other personnel such as those in the radiology department, and to visitors. Inspect the skin at least every 8 hours for signs of irritation or inflammation. When possible, remove the belt or boot that is used for skin traction every 8 hours to inspect under the device. Check traction equipment frequently to ensure its proper functioning. Inspect all ropes, knots, and pulleys at least every 8 to 12 hours for loosening, fraying, and positioning. Check the weight for consistency with the health care provider's prescription. Sometimes one of the weights is accidentally removed by a staff member or visitor who bumps into it. Replace the weights if they are not correct, and notify the health care provider or orthopedic technician. If the patient reports severe pain from muscle spasm, the weights may be too heavy or the patient may need realignment. Report the pain to the health care provider if body realignment fails to reduce the discomfort. Assess neurovascular status of the affected body part to detect circulatory compromise and tissue damage. The circulation is usually monitored every hour for the first 24 hours after traction is applied and every 4 hours thereafter. Interventions include: Emergency care: assess for respiratory distress, bleeding and head injury Nonsurgical management: closed reduction and immobilization with a bandage, splint, cast, or traction post op care and assessment after musculoskeletal surgery (hips, knees, fracture) Management of Clients with Peripheral & Central Nervous System Disorders assessment & care of pts with spinal cord injury o ~ complications? Incontinence, paralysis (skin, move regularly, CONTRACTURES, ROM), ***Alignment*** respiratory – what kind of movement do you expect pt to have bowel care b/c they can’t go on their own. Need muscles of peristalsis to move bowel out of colon. Incontinence… Psychosocial – depression, ROLE conflict KNOW DIFF B/T AUTONOMIC DYSREFLEXIA AND SPINAL SHOCK Spinal shock – right after surgery. SWELLING 48-72 hrs?? Nutrition – physically not putting food in mouth, depression, metabolic needs MS/ALS/ MG/Guillain-Barré – priority care, meds, interventions o ~ which one does this pt have? (assessment) o ~ safety issues r/t diseases? o ~ how to prevent complications that will kill pt o ~ distinguish o ~ psychosocial issues First priority: ABC After the airway is established, assess the patient’s breathing pattern. Spinal nerve (C3-5) innervate the phrenic nerve, which controls the diaphragm. A significant head injury, pneumothorax, hemothorax, and fracture may also cause respiratory distress. C2 injury are common in older who fell from a low height. Assessing motor function in Spinal cord injury: -To assess C4-5, apply downward pressure while the patient shrugs his or her shoulders upward. -To assess C5-6, apply resistance while the patient pulls up his or her arms. -To assess C7, apply resistance while the patient straightens his or her flexed arms. -To assess C8, make sure the patient is able to grasp an object and form a fist. -To assess L2-4, apply resistance while the patient lifts his or her legs from the bed. -To assess L5, apply resistance while the patient dorsiflexes his or her feet. -To assess SI, apply resistance while the patient plantar flexes his or her feet. The Patient with a Spinal Cord Injury intervention Airway Management: Facilitation of patency of air passages. Positioning: Neurologic: Achievement of optimal, appropriate body alignment for the patient experiencing or at risk for spinal cord injury or vertebral irritability. • Position patient to maximize ventilation potential. • Identify patient requiring actual/potential airway insertion. • Insert oral or nasopharyngeal airway, as appropriate. • Perform chest physical therapy, as appropriate. • Remove secretions by encouraging coughing or by suctioning. • Encourage slow, deep breathing; turning; and coughing. • Instruct how to cough effectively. • Assist with incentive spirometer, as appropriate. • Auscultate breath sounds, noting areas of decreased or absent ventilation and presence of adventitious sounds. • Perform endotracheal or nasotracheal suctioning, as appropriate. • Administer humidified air or oxygen, as appropriate. • Regulate fluid intake to optimize fluid balance. • Position to alleviate dyspnea. • Monitor respiratory and oxygenation status, as appropriate. • Immobilize or support the affected body part, as appropriate. • Place in the designated therapeutic position. • Maintain proper body alignment. • Position with head and neck in alignment. . Turn using the log roll technique. • Apply an orthosis collar. • Instruct on orthosis collar care, as needed. • Apply and maintain a splinting or bracing device. . Monitor skin integrity under bracing device/orthosis collar. • Instruct on pin site care, as needed. • Monitor traction pin insertion site. • Perform traction/orthosis device pin insertion site care. • Monitor traction device setup. Spinal shock, also called spinal shock syndrome, occurs immediately as a concussion response to the injury. The patient has flaccid paralysis and loss of reflex activity below the level of the lesion. It often lasts less than 48 hours but may continue for several weeks. Muscle spasticity begins in patients with cervical or high thoracic injuries when spinal shock is resolved. Spinal shock, also called spinal shock syndrome, occurs immediately as the cord’s response to the injury. The patient has complete but temporary loss of motor, sensory, reflex, and autonomic function Often lasts less than 48 hours but may continue for several weeks. Several manifestations include: absence of tactile sensation absence of reflexes* flaccid paralysis (inability to move) of all voluntary muscles* hypoesthesia (decreased sensation) hyperesthesia (increased sensation) bladder incontinence parasthesia or dull pain. Autonomic dysreflexia Symptoms Emergency intervention • Sudden onset of severe, throbbing headache • Severe, rapidly occurring hypertension • Bradycardia • Flushing above level of lesion (face and chest) • Pale extremities below level of lesion • Nasal stuffiness • Sweating • Nausea • Blurred vision • Piloerection (goosebumps) • Feeling of apprehension -Place patient in sitting position (first priority!). -Page/notify health care provider. - Loosen tight clothing on the patient. -Assess for and treat the cause. -Check the urinary catheter tubing (if present) for kinks or obstruction. -If a urinary catheter is not present, check for bladder distention and catheterize immediately if indicated. -Place anesthetic ointment on tip of catheter before insertion -Check the patient for fecal impaction; if present, disimpact immediately using anesthetic ointment. -Check the room temperature to ensure that it is not too cool or drafty. -Monitor blood pressures every 10 to 15 minutes. -Give nitrates or hydralazine (Apresoline, Novo-Hylazin*) as prescribed. Disease Brief pathophysiology/etiology Manifestations GuillainBarre Syndrome is an acute inflammatory Motor Manifestations: demyelinating • Ascending symmetric muscle polyneuropathy (AIDP) weakness → flaccid paralysis that affects the peripheral without muscle atrophy nervous system, causing • Decreased or absent deep motor weakness and sensory tendon reflexes (DTRs) abnormalities. It is an • Respiratory compromise uncommon disorder, (dyspnea, diminished breath affecting both genders sounds, decreased tidal volume equally and peaking after age and vital capacity) and 55 years. As a result of respiratory failure demyelination (destruction of • Loss of bowel and bladder the myelin sheath) of the control (less common) peripheral nerves, • Ataxia progressive motor weakness and sensory abnormalities Sensory Manifestations occur. Symptoms typically •Paresthesias begin in the legs and spread • Pain (cramping) to the arms and upper body. This is referred to as an Progression Nursing interventions Progression of GBS changes depending on the variant of the disease. The three different types of GBS are: (1) ascending, (2) pure motor (3) descending. - Managing the airway and respiratory status. - Monitor the ABG values - keep emergency airway equipment supplies at easy access. - managing cardiac function - pain management. - improving mobility and preventing effects of immobility. - Tx – plasmapheresis The ascending affects the nervous system functionality (paresthesias) from the feet rising up to the head. The pure motor presents itself and follows the same path PP: Ineffective breathing pattern interventions: - chest physiotherapy - IS - O2 - monitor ABG and vital capacity - keep equipment for endotracheal intubation at the bedside ascending paralysis. Cranial Nerve Manifestations Paralysis can increase in • Facial weakness intensity until the muscles •Dysphagia cannot be used at all and the • Diplopia patient is almost totally • Difficulty speaking immobile. As a result, some patients require mechanical Autonomic Manifestations ventilation because of weak • Labile (~easily altered) blood or paralyzed respiratory pressure muscles. Healing occurs in • Cardiac dysrhythmias reverse; the neurons affected •Tachycardia last are the first to recover. GBS is the result of a variety PP: of related immune-mediated * muscle weakness and P have pathologic processes. The abrupt onset; cause remains immune system starts to obscure destroy the myelin sheath * cerebral function or pupillary that surrounds the axons of signs are NOT affected the peripheral nerves or * the most common clinical attacks the axons themselves. pattern is that the immune Segmental demyelination system starts to destroy the (the destruction of myelin myelin sheath surrounding the between the nodes of axons. Ranvier) is the major * weakness and paresthesia pathologic finding in GBS. begin in LE and progress upward This destruction affects the toward trunk, arms, and cranial transmission of impulses nerves in ascending GBS from node to node by slowing it down. Also, the ***COGNITIVE STATUS brain receives fewer sensory NOT AFFECTED. signals, affecting the patient's ability to feel textures, heat, ***REVERSIBLE and pain. On the other hand, the brain may receive altered ~ weakness. Takes naps a lot. signals that cause the tingling or “crawling-skin” sensation many patients report. * as the ascending GBS however this version is absent of sensory manifestations. Descending GBS starts in the face of the patient usually affecting the jaw muscles making its way downward. This type can be more life threatening due to the fact that it affects respiratory function soon in the disease process. Interventions for cardiac dysfunction: - can affect both the sympathetic and parasympathetic systems - client placed on cardiac monitor b/c of risk for arrhythmias - HTN treated w/ beta blocker or nitroprusside - IV fluids for hypotension; client placed in supine position - atropine may be used for bradycardia Drug Therapy - plasmapheresis (remove immune complexes and then give blood back) or IV immunoglobulin - plasma exchange - IV immunoglobulin - NO corticosteroids EVOLVE * has three acute stages * demyelination of peripheral neurons * affect resp status and muscle function Myasthenia Gravis (MG) “gravity” is an acquired autoimmune disease characterized by fatigue and weakness primarily in muscles innervated by the cranial nerves, as well as in skeletal and respiratory muscles. This autoimmune disease of the neuromuscular junction may take many forms—from mild Motor Manifestations • Progressive muscle weakness (proximal) that usually improves with rest • Poor posture • Ocular palsies • Ptosis • Weak or incomplete eye closure • Diplopia The onset of MG is usually insidious. This starts with a rapid onset of fatigue. In more severe cases all muscle groups are affected, in most all cases some facial component is always affected. - Provide respiratory support - promote mobility with pt doing as much as possible. - Rx therapy: anticholinesterases and immunosuppressants - Teach the patient and family to monitor for these two types of crises: - Myasthenic crisis—an exacerbation (flare-up or worsening) disturbances of the ocular muscles to a rapidly developing, generalized weakness that may lead to death from respiratory failure. It has remissions and exacerbations (worsening or “flare-ups”). Although MG can present at any age, it is less commonly seen in the United States than GuillainBarré syndrome. The incidence is equal between men and women. MG is caused by an autoantibody attack on the acetylcholine receptors (AChRs) in the muscle end plate membranes. As a result, nerve impulses are not transmitted to the skeletal muscle at the neuromuscular junction and the muscles cannot contract. EVOLVE * autoimmune disease w/ ocular symptoms * characterized by exacerbations and remissions * affect resp status and muscle function * should not take OTC drugs w/o checking w/ health care provider Amyotrophic Lateral Sclerosis (ALS) Lou Gehrig’s disease Patho: -adult onset upper and lower motor neuron disease. -characterized by progressive weakness, muscle wasting and spasticity eventually leading to paralysis PP: There is loss of anterior horn cells, so that patients present with progressive weakness that proceeds to paralysis from neurogenic muscular atrophy. Because of the loss • Respiratory compromise Sensory Manifestations • Muscle achiness • Paresthesias • Decreased sense of smell and taste *** assess muscle strength in FACE & NECK! *** biggest concern is AIRWAY b/c problem swallowing (dysphagia) *** diplopia, trouble focusing b/c decrease control of muscles that move eyes. *** associated w/ thymus. Thymectomy. *** like MS, worse w/ exertion and exercise. Schedule rest periods. ***Eye muscles, speech ability and patterns. * AChR – Tensilon Testing. Diagnostic Test ~ Tensilon Test vagus nervous system decreases HR (vagal response, then you are positively diagnosed w/ MG. Tensilon test we administer cholinergic agent to see if you have positive response to cholinergic agent. If you have positive test, you are positive for MG. of the myasthenic symptoms caused by not enough anticholinesterase drug - Tx- maintaining adequate respiratory function. *** give the meds Characteristics: Increase P and resp Rise in BP Anoxia Cyanosis Bowel and bladder incontinence Decreased urine output Absence of cough and swallow reflex - Cholinergic crisis—an acute exacerbation of muscle weakness caused by too many anticholinesterase drugs - Tx- immunosuppression with corticosteroids. ***Hold the meds Characteristics: N/V Diarrhea Abd cramps Blurred vision Pallor Facial muscle twitching Pupillary miosis hypotension PP: - cholinesterase-inhibitor drugs - immunosuppressants - corticosteroids for immunosuppression - plasmapheresis PP: Early symptoms: -fatigue while talking, -tongue atrophy -dysphagia -weakness of the hands and arms -fasciculations -nasal quality of speech Dysarthria Drooling PP: - no known cure, no treatment, no preventive measures - Riluzole, only drug approved by FDA to extend survival time (monitor kidney) - exercise and mobility program - management of swallowing difficulties - respiratory support PNS - SKIN - feeding tube - DVT Pt cannot move! ****DOESN’T AFFECT MENTAL STATUS DIFFERENTIATES ALS AND of anterior horn cells, the anterior (ventral) spinal motor nerve roots demonstrate atrophy M.S. no cognitive involvement. You know everything going on but you can’t speak… Motor neurons are SCARRED Later, muscles of respirations. Riluzole – 50 mg bid on an empty stomach. Monitor for liver toxicity. Inability to walk. All b/c of weakness. Hyporeflexivity – twitching. Fasciculations. Speech b/c inability to use muscles necessary. Senses and cognition will remain. No specific test. Usually follow a viral infection and onset of GBS but we don’t really know. Acts much like MS in which in demyelinates the sheaths. Multiple Sclerosis (MS) “myelin sheaths” Patho: autoimmune disease. characterized by an inflammatory response that results in diffuse random or patchy areas of plaque in the white matter (axons). In Particularly it affects optic nerves, pyramidal tracts, posterior columns, brainstem nuclei, and periventricular region of brain. Myelin sheath damaged and its thickness reduced (demyelinated). Slows down electrochemical transmission of impulses between the brain and spinal cord. Can lead to complete blockage over time. Etiology: cause unknown. thought to be d/t viral, immunologic, and genetic (first-degree) and environmental etiologic factors. Pre disposition determined by antigens (HLA DR2 and DQ6). tends to affect family members, especially siblings. Things that exacerbate Ability to move increased fatigue and stiffness of the extremities particularly in the legs, continuous sensitivity to temperature, flexor spasm at night, increased or hyperactive deep tendon reflexes , clonus, positive Babinski’s reflex, absent abdominal reflexes, gait unsteady because of weakness Cerebellar: intention tremor (tremor when performing an activity), dysmetria (inability to direct or limit movement), dysdiadochokinesia (inability to stop one motor impulse and use another, clumsy motor movements, loss of balance, poor coordination Cranial nerves and brainstem tinnitus (ringing in both ears), vertigo (dizziness), hearing loss, facial weakness and dysphagia, dysarthria ( slurred speech) Vision: blurred vision, diplopia (double vision), decreased visual acuity, scotomas (changes in peripheral vison, scotomas (changes in Chronic and progressive disease with no cure. Symptoms progress in severity over time. Initial symptoms so vague that most of the time goes unnoticed for years. disease does not affect life expectancy. monitor effects on immune system, prevent exacerbations, manage symptoms, improve function. requires collaborative care. The onset is usually between 20-40 years of age, and occurs twice as often in women. -immunosupressive agents to reduce the frequency of relapses -antispasmodics to treat muscle spasticity -immunodulators to prevent relaspse -anticonvulsants for paresthesia -stool softeners for constipation -anticholinergics for bladder dysfunction -beta-blockers for tremors 4 types: relapsing-remitting MS (RRMS) -most common -mild to moderate, depends on the degree of disability -symptoms develop and resolve in a few weeks to months -patient returns to baseline primary progressive Drug therapy: one or more of: -interferon beta -natalizumab -glatirame Promoting mobility and managing symptoms -team with PT -include ROM, stretching, and strengthening Health teaching -promote community resources and respite services for patient and family relapse: -viruses and infectious agents -living in a cold climate -physical injury -emotional stress -pregnancy -fatigue -overexertion -temperature extremes -hot shower/bath peripheral vision), nystagmus (involuntary, rapid eye movement) Sensory: hypalgesia (diminished sensitivity to pain), paresthesia, facial pain, decreased temperature perception, numbness tingling, burning, crawling sensations If demyelination has occurred: -bowel and bladder dysfunctions -alterations in sexuality -flexic bladder -frequency -urgency -nocturia PP: Common physical assessment - key feature is muscle weakness and spasticity Findings include: - flexor spasms at night - intention tremor - dysmetria - blurred vision, diplopia, decreased visual acuity - tinnitus, vertigo - hypalgesia, numbness, tingling or burning - bowel and bladder dysfunction - Cognitive changes come later in the disease *** assess mental status MS (PPMS) -steady and gradual neurological deterioration without remission of symptoms -progressive disability with no acute attacks -usually 40-60 yrs old during onset secondary progressive MS (SPMS) -begins with relapsing-remitting course -later becomes rapidly progressive -functioning continues to decline with no clear times of remission progressiverelapsing (PRMS) -frequent relapses with some partial recovery, but never back to baseling -progressive and cumulative symptoms and deterioration occur over several years -avoid overexertion , stress, extremes in temperature, humidity, people with upper respiratory tract infections -explain all medications upon discharge -how to differentiate side effects from adverse or allergic reactions -devices to promote ADL’s -include information about bowl and bladder management, skin care, nutrition, and positioning techniques -importance of adequate rst -engage in regular social activities -coping strategies **** quality of life. ADLs. #1 goal. Longer, better functioning life. Helping support immune system. Management of clients with Functional and Structural Cardiac Disorders clinical manifestations associated with selected structural abnormalities of the heart (valves and cardiomegaly) VALVULAR DISORDERS (General) includes mitral stenosis (valve thickening by fibrosis and calcification), mitral regurgitation (prevents valve from closing Mitral stenosis- fatigue, dyspnea on exertion, orthopnea, neck vein distention, pitting edema, afib, paroxysmal nocturnal Nonsurgical management focus on drug therapy & rest (~don’t wanna overwork heart to reduce risk of HF) -monitor ECG for development of irregular ENDOCARDITIS completely during systole which allows for backflow of blood), mitral prolapse ( valvular leaflets enlarge and prolapse into left atrium), aortic stenosis (orifice narrows and obstructs left ventricular outflow and the resistance leads to ventricular hypertrophy, and aortic regurgitation ( valve leaflets don’t close properly during diastole which allows backflow from aorta back into L ventricle.. dyspnea, hemoptysis, hepatomegaly, apical diastolic murmur Mitral regurg.- fatigue, dyspnea on exertion, orthopnea, neck vein distention, pitting edema, afib, palpitations, high-pitched holosystolic murmur Mitral Prolapse- atypical chest pain, dizziness, syncope, palpitations, atrial tachycardia, ventricular tach., systolic click Aortic stenosis- dyspnea on exertion, angina, syncope on exertion, orthopnea, paroxysmal nocturnal dyspnea, harsh systolic crescendo decrescendo murmur Aortic regurg.- fatigue, dyspnea, orthopnea, paroxysmal nocturnal dyspnea, angina, sinus tach, blowing decrescendo diastolic murmur heart rhythm and notify doctor if one develops. -a balance of rest and exercise is needed to prevent skeletal muscle atrophy and fatigue. -Surgery such as valvuloplasty (opens stenosis valve) may be needed and it is the nurses priority afterwards to observe for bleeding from the catheter insertion site and institute post-angiogram precautions. -assess for signs of regurgitant valve by monitoring heart sounds, CO, and heart rhythm. -observe for signs of systemic emboli (~**thromboemboli: give anticoagulants) ~prophylactic antibiotics (prevent infection) ~cardiac diet (low salt diet to decrease volume and decrease pressure) ~diuretics to decrease fluid volume (monitor F&E for imbalance) refers to a microbial infection involving the endocardium. Occurs primarily in patients who abuse IV drugs, have had valve replacements, have experienced systemic infection or have natural cardiac defects. With Cardiac defect, blood may flow rapidly from a high pressure area to a low pressure zonem eroding section of the endocardium. Platelets and fibrin adhere to the denuded endocardium, forming a vegetative lesion. For bacteremia, bacteria becomes trapped in the low pressure sinkhole and are deposited in the vegetation. Additional platelets and fibrin are deposited, which causes the vegetative lesions to grow. The endocardium and valve are destroyed. Valvular insufficiency may result when the lesions interfere with normal alignment of the valve. if vegetations become so large that blood flow through the valve is obstructed the valve appears stenotic and then likely to embolize. almost all endocarditis develop heart mumurs. heart failure is the most common cause of ineffective endocarditis. Assess for right sided HF (as evidenced by peripheral edema weight gain and anorexia) and left sided as evidenced by fatigue shortness of breath, and crackles on auscultation of breath sounds). -fever associated with chills night sweats, malaise, and fatigue -anorexia and weight loss -cardiac murmur -development of heart failure -evidence of systemic embolization -petechiae -splinter hemorrhages -oslers nodes ( on palms and soles of feet) -janesways lesions (flate reddened macules on hands and feet) care of the patients with endocarditis usually includes antimicrobials, rest balanced with activity, and supportive therapy for HF. if not successful then surgery is required. antimicrobials are the main treatment with the choice of drug depending on the specific organism involved. because vegetative surround and protect the offending microorganisms an appropriate drug must be given in a sufficiently high dose to ensure its destruction. Most are given 4-6 weeks. balance the patients activities with adequate rest. consistently use appropriate aseptic technique to protect the patient from contact with potential infective organisms. Group Study o mitral stenosis – under 45, rheumatic fever physical manifestations of and assessment of pts with CHF o Left ventricular failure is associated with decreased cardiac output and elevated pulmonary venous pressure. It may appear clinically as: • Weakness • Fatigue • Dizziness • Acute confusion • Pulmonary congestion • Breathlessness • Oliguria (scant urine output) o The pulse may be tachycardic, or it may alternate in strength (pulsus alternans). Take the apical pulse for a full minute, noting any irregularity in heart rhythm. An irregular heart rhythm resulting from premature atrial contractions (PACs), premature ventricular contractions (PVCs), or atrial fibrillation (AF) is common in HF o Chart 37-1 Key Features Left-Sided Heart Failure • DECREASED CARDIAC OUTPUT Fatigue Weakness Oliguria during the day (nocturia at night) Angina Confusion, restlessness Dizziness Tachycardia, palpitations Pallor Weak peripheral pulses Cool extremities • PULMONARY CONGESTION Hacking cough, worse at night Dyspnea/breathlessness Crackles or wheezes in lungs Frothy, pink-tinged sputum Tachypnea - respiratory rate typically exceeds 20 breaths/min. S3/S4 summation gallop - often the first sign of HF o Laboratory Assessment • Electrolyte imbalance may occur from complications of HF or as side effects of drug therapy, especially diuretic therapy. Regular evaluations of a patient's serum electrolytes, including sodium, potassium, magnesium, calcium, and chloride, are essential. • Any impairment of renal function resulting from inadequate perfusion causes elevated blood urea nitrogen and serum creatinine and decreased creatinine clearance levels. • Hemoglobin and hematocrit tests should be performed to identify HF resulting from anemia. • If the patient has fluid volume excess, the hematocrit levels may be low as a result of hemodilution. • B-type natriuretic peptide (BNP) is used for diagnosing HF (in particular, diastolic HF) in patients with acute dyspnea. As discussed earlier, it is part of the body's response to decreased cardiac output from either left or right ventricular dysfunction. An increase in BNP, in conjunction with history and physical, best differentiates between the dyspnea of HF and that associated with lung dysfunction (Wexler et al., 2009). However, patients with renal disease may also have elevated BNP levels (Chen et al., 2010). • Urinalysis may reveal proteinuria and high specific gravity. • Microalbuminuria is an early indicator of decreased compliance of the heart and occurs before the BNP rises. It serves as an “early warning detector” that lets the health care provider know that the heart is experiencing early signs of decreased compliance, long before symptoms occur. • Arterial blood gas (ABG) values often reveal hypoxemia (low blood oxygen level) because oxygen does not diffuse easily through fluid-filled alveoli. Respiratory alkalosis may occur because of hyperventilation; respiratory acidosis may occur because of carbon dioxide retention. Metabolic acidosis may indicate an accumulation of lactic acid. • CXR heart enlarged (cardiomegaly), representing hypertrophy or dilation • Echocardiography is considered the best tool in diagnosing heart failure. Cardiac valvular changes, pericardial effusion, chamber enlargement, and ventricular hypertrophy can be diagnosed using this noninvasive technique. The test can also be used to determine ejection fraction. o ~ Interventions: • Vavluloplasty - Open stenosis valve o Chart 37-2 Key Features Right-Sided Heart Failure • Systemic Congestion Jugular (neck vein) distention Enlarged liver and spleen Anorexia and nausea Dependent edema (legs and sacrum) Distended abdomen Swollen hands and fingers Polyuria at night Weight gain Increased blood pressure (from excess volume) or decreased blood pressure (from failure) o TABLE 37-1 COMMON CAUSES AND RISK FACTORS FOR HEART FAILURE • Hypertension • Coronary artery disease • Cardiomyopathy • Substance abuse (alcohol and illicit/prescribed drugs) • Valvular disease • Congenital defects • Cardiac infections and inflammations • Dysrhythmias • Diabetes mellitus • Smoking/tobacco use • Family history • Obesity • Severe lung disease • Sleep apnea • Hyperkinetic conditions (e.g., hyperthyroidism) nursing interventions and patient teaching for patients with CHF o Chart 37-4 Home Care Assessment The Patient with Heart Failure • Assess for signs of heart failure, including: Changes in vital signs (heart rate >100 beats/min at rest, new atrial fibrillation, blood pressure <90 or >150 systolic) o o o Indications of poor tissue perfusion: o Fatigue o Angina o Activity intolerance o Changes in mental status o Pallor or cyanosis o Cool extremities Indications of congestion: o Presence of cough or dyspnea o Weight gain o Jugular venous distention and peripheral edema • Assess functional ability, including: Performance of ADLs Mobility and ambulation (review frequency and duration of walking, development of symptoms, and pulse rate) Cognitive ability Assess nutritional status, including: Food and fluid intake Intake of sodium-rich foods Alcohol consumption Skin turgor Assess home environment, including: Safety hazards, especially related to oxygen therapy Structural barriers affecting functional ability Social support (family, home health services) Assess the patient's adherence and understanding of illness and its treatment, including: Signs and symptoms to report to health care provider Dosages, effects, and side or toxic effects of medications When to report for laboratory and health care provider visits Ability to accurately weigh self on scale Presence of advance directive Use of home oxygen, if appropriate • Assess patient and caregiver coping skills TABLE 37-4 HEART FAILURE SELF-MANAGEMENT HEALTH TEACHING (MAWDS) • Medications: •Take medications as prescribed, and do not run out. •Know the purpose and side effects of each drug. •Avoid NSAIDs to prevent sodium and fluid retention. • Activity: •Stay as active as possible, but don't overdo it. - When exercise is indicated, teach the patient to begin walking 200 to 400 feet per day. At home the patient should try to walk at least three times a week and should slowly increase the amount of time walked over several months. •Know your limits. •Be able to carry on a conversation while exercising. • Weight: •Weigh each day at the same time on the same scale to monitor for fluid retention. • Diet: •Limit daily sodium intake to 2 to 3 grams as prescribed. •Limit daily fluid intake to 2 liters. • Symptoms: •Note any new or worsening symptoms, and notify the health care provider immediately. Nursing Safety Priority Action Alert • Per the HF Core Measure for discharge instructions, teach the patient and caregiver to immediately report to the health care provider the occurrence of any of these symptoms, which could indicate worsening or recurrent heart failure: • •Rapid weight gain (3 lb in a week or 1 to 2 lb overnight) • •Decrease in exercise tolerance lasting 2 to 3 days • •Cold symptoms (cough) lasting more than 3 to 5 days • •Excessive awakening at night to urinate - nocturia • •Development of dyspnea or angina at rest or worsening angina • •Increased swelling in the feet, ankles, or hands Chart 37-5 Patient and Family Education: Preparing for Self-Management Beta Blocker/Digoxin Therapy • • Establish same time of day to take this medication every day. • • Continue taking this medication unless your health care provider tells you to stop. • • Do not take digoxin at the same time as antacids or cathartics (laxatives). • • • • o o • Take your pulse rate before taking each dose of digoxin. Notify your health care provider of a change in pulse rate (60 to 100 beats/min is normal) or rhythm, as well as increasing fatigue, muscle weakness, confusion, or loss of appetite (signs of digoxin toxicity). • If you forget to take a dose, it may be delayed a few hours. However, if you do not remember it until the next day, you should take only your usual daily dose. • Report for scheduled laboratory tests (e.g., potassium and digoxin levels). • If potassium supplements are prescribed, continue the dose until told to stop by your health care provider. The priority problems for patients with heart failure (HF) include: • 1. Impaired Gas Exchange related to ventilation/perfusion imbalance • 2. Decreased Cardiac Output related to altered contractility, preload, and afterload • 3. Fatigue and weakness related to hypoxemia • 4. Potential for pulmonary edema related to left-sided HF diagnostic studies used to assess clients with cardiac disorders o valves o Cardiomyopathy - subacute or chronic disease of cardiac muscle, and the cause may be unknown Etiologies: ETOH Hypertension CAD idiopathic Heart enlarged, muscle thickens and stiffens Weaken the ability to pump blood TYPES: Dilated - DCM involves extensive damage to the myofibrils and interference with myocardial metabolism. Ventricular wall thickness is normal, but both ventricles are dilated (left ventricle is usually worse) and systolic function is impaired. Causes may include alcohol abuse, chemotherapy, infection, inflammation, and poor nutrition. Decreased CO from inadequate pumping of the heart causes the patient to experience dyspnea on exertion (DOE), decreased exercise capacity, fatigue, and palpitations. o Most common o Stasis in the ventricles o Treat like CHF o Inotropics o Diuretics o Antidysrhythmics o Rest o Signs and symptoms Fatigue and weakness HF (left side) Dysarhythmias or heart block Systemic or pulmonary emboli S3 and S4 gallops Moderate to severe cardiomegaly o Treatment Symptomatic treatment of HF Vasodilators Control of dysrhythmias Surgery: heart transplant o Hypertropic - asymmetric ventricular hypertrophy and disarray of the myocardial fibers. Left ventricular hypertrophy leads to a stiff left ventricle, which results in diastolic filling abnormalities. Obstruction in the left ventricular outflow tract is seen in most patients with HCM. In about half of patients, HCM is transmitted as a single-gene autosomal dominant trait o Usually under age 30 o Sudden death in professional athletes o Hank Gathers o Reggie Lewis Restrictive - characterized by stiff ventricles that restrict filling during diastole. Symptoms are similar to left or right heart failure (HF) or both. The disease can be primary or caused by endocardial or myocardial disease such as sarcoidosis or amyloidosis. The prognosis for this type of cardiomyopathy is poor. o Infiltrative process o Fibrosis & thickening o Inpaired diastolic stretch o Ventricular stretch cardiac infections infective endocarditis o Assess the patient's cardiovascular status. Almost all patients with infective endocarditis develop murmurs. Carefully auscultate the precordium, noting and documenting any new murmurs (usually regurgitant in nature) or any changes in the intensity or quality of an old murmur. An S3 or S4 heart sound also may be heard. o Heart failure (HF) is the most common complication of infective endocarditis. Assess for rightsided HF (as evidenced by peripheral edema, weight gain, and anorexia) and left-sided HF (as evidenced by fatigue, shortness of breath, and crackles on auscultation of breath sounds). See discussion of HF earlier in this chapter. o Arterial embolization is a major complication in up to half of patients with infective endocarditis. Fragments of vegetation break loose and travel randomly through the circulation. When the left side of the heart is involved, vegetation fragments are carried to the spleen, kidneys, GI tract, brain, and extremities. When the right side of the heart is involved, emboli enter the pulmonary circulation. o Splenic infarction with sudden abdominal pain and radiation to the left shoulder can also occur. When performing an abdominal assessment, note rebound tenderness on palpation. The classic pain described with renal infarction is flank pain that radiates to the groin and is accompanied by hematuria (red blood cells in the urine) or pyuria (white blood cells in the urine). Mesenteric emboli cause diffuse abdominal pain, often after eating, and abdominal distention. o The most reliable criteria for diagnosing endocarditis include positive blood cultures, a new regurgitant murmur, and evidence of endocardial involvement by echocardiography. o A positive blood culture is a prime diagnostic test. Both aerobic and anaerobic specimens are obtained for culture. Some slow-growing organisms may take 3 weeks and require a specialized medium to isolate. Low hemoglobin and hematocrit levels may also be present. Chart 37-8 Key Features Infective Endocarditis • Fever associated with chills, night sweats, malaise, and fatigue • Anorexia and weight loss • Cardiac murmur (newly developed or change in existing) • Development of heart failure • Evidence of systemic embolization • Petechiae • Splinter hemorrhages • Osler's nodes (on palms of hands and soles of feet) • Janeway's lesions (flat, reddened maculae on hands and feet) • Positive blood cultures Interventions: o Antimicrobials – main treatment; 4-6 weeks; STREP. o Rest, balanced with activity o Supportive therapy for heart failure o Anticoagulants o Surgical management •Removing the infected valve (either biologic or prosthetic) •Repairing or removing congenital shunts •Repairing injured valves and chordae tendineae •Draining abscesses in the heart Rheumatic Carditis (AKA Rheumatic heart disease Rheumatic carditis, also called rheumatic endocarditis, is a sensitivity response that develops after an upper respiratory tract infection with group A beta-hemolytic streptococci ~ mitral valve stenosis Rheumatic carditis is one of the major indicators of rheumatic fever. The common manifestations are: o •Tachycardia o •Cardiomegaly (enlarged heart) o •Development of a new murmur or a change in an existing murmur o • Pericardial friction rub o • Precordial pain o • Electrocardiogram (ECG) changes (prolonged PR interval) o • Indications of heart failure (HF) o • Evidence of an existing streptococcal infection Primary prevention is extremely important. Teach all patients to remind their health care providers to provide appropriate antibiotic therapy if they develop the indications of streptococcal pharyngitis: o •Moderate to high fever o •Abrupt onset of a sore throat o •Reddened throat with exudate o •Enlarged and tender lymph nodes Penicillin is the antibiotic of choice for treatment. Erythromycin (Eryc, Erythromid ) is the alternative for penicillin-sensitive patients. Pericarditis Chart 37-9 Best Practice for Patient Safety & Quality Care - Care of the Patient with Pericarditis o •Assess the nature of the patient's chest discomfort. (Pericardial pain is typically substernal. It is worse on inspiration and decreases when the patient leans forward.) o •Auscultate for a pericardial friction rub. o •Assist the patient to a position of comfort. o •Provide anti-inflammatory agents as prescribed. o •Explain that anti-inflammatory agents usually decrease the pain within 48 hours. o •Avoid the administration of aspirin and anticoagulants because these may increase the possibility of tamponade. o •Auscultate the blood pressure carefully to detect paradoxical blood pressure (pulsus paradoxus), a sign of tamponade: o •Palpate the blood pressure, and inflate the cuff above the systolic pressure. o •Deflate the cuff gradually, and note when sounds are first audible on expiration. o •Identify when sounds are also audible on inspiration. o •Subtract the inspiratory pressure from the expiratory pressure to determine the amount of pulsus paradoxus (>10 mm Hg is an indication of tamponade). o •Inspect for other indications of tamponade, including jugular venous distention with clear lungs, muffled heart sounds, and decreased cardiac output. o •Notify the physician if tamponade is suspected. Acute pericarditis is most commonly associated with: o •Infective organisms (bacteria, viruses, or fungi) (usually respiratory) o •Post–myocardial infarction (MI) syndrome (Dressler's syndrome) o •Post-pericardiotomy syndrome o •Acute exacerbations of systemic connective tissue disease Chronic constrictive pericarditis occurs when chronic pericardial inflammation causes a fibrous thickening of the pericardium. It is caused by tuberculosis, radiation therapy, trauma, renal failure, or metastatic cancer. In chronic constrictive pericarditis, the pericardium becomes rigid, preventing adequate filling of the ventricles and eventually resulting in cardiac failure. Assessment o Assessment findings for patients with acute pericarditis include substernal precordial pain that radiates to the left side of the neck, the shoulder, or the back. Pain is classically grating and oppressive and is aggravated by breathing (mainly on inspiration), coughing, and swallowing. The pain is worse when the patient is in the supine position and may be relieved by sitting up and leaning forward. Ask specific questions to evaluate chest discomfort to differentiate it from the pain associated with an acute MI (see Chapter 40). o A pericardial friction rub may be heard with the diaphragm of the stethoscope positioned at the left lower sternal border. This scratchy, high-pitched sound is produced when the inflamed, roughened pericardial layers create friction as their surfaces rub together. o Patients with acute pericarditis may have an elevated white blood cell count and usually have a fever. Therefore blood culture and sensitivity may be analyzed in the laboratory. The ECG usually shows ST-T spiking with the onset of inflammation, which returns to baseline with treatment. Atrial fibrillation is also common. Echocardiograms may be used to determine a pericardial effusion. o Patients with chronic constrictive pericarditis have signs of right-sided HF, elevated systemic venous pressure with jugular distention, hepatic engorgement, and dependent edema. Exertional fatigue and dyspnea are common complications. Thickening of the pericardium is seen on echocardiography or a computed tomography (CT) scan. Interventions o The focus of collaborative management is to relieve pain and treat the cause of pericarditis before severe complications occur. o NSAIDS for pain CAD - broad term that includes chronic stable angina and acute coronary syndromes. It affects the arteries that provide blood, oxygen, and nutrients to the myocardium. When blood flow through the coronary arteries is partially or completely blocked, ischemia and infarction of the myocardium may result. Ischemia occurs when insufficient oxygen is supplied to meet the requirements of the myocardium. Infarction (necrosis, or cell death) occurs when severe ischemia is prolonged and decreased perfusion causes irreversible damage to tissue. Cardiovascular Disease Leading single cause of death Risk Factors o Nonmodifiable Age, gender, family history, ethnic background, Age is the most important risk factor for developing CAD in women. - When they are older than 40 years, women are more likely than men to die within 1 year after their MI o Modifiable - diet, exercise, smoking •Elevated serum lipid levels •Tobacco use •Limited physical activity •Hypertension •Diabetes mellitus •Obesity •Excessive alcohol •Stress o Chart 40-1 Patient and Family Education: Preparing for Self-Management o Prevention of Coronary Artery Disease o Smoking • If you smoke, quit. • If you don't smoke, don't start. o Diet • Consume sufficient calories for your body to include: •Less than 7% from saturated fats •Avoiding trans fatty acids • Limit your cholesterol intake to less than 200 mg/day. • Limit your sodium intake as specified by your health care provider. o o Cholesterol • Have your lipid levels checked regularly. • If your cholesterol and LDL levels are elevated, follow your health care provider's advice. o Physical Activity • If you are middle-aged or older or have a history of medical problems, check with your health care provider before starting an exercise program. • Appropriate exercise should be enjoyable, burn 400 calories per session, and sustain a heart rate of 120 to 150 beats/min, depending on your age. • Exercise periods should be at least 20 to 30 minutes long with 10-minute warm-up and 5-minute cool-down periods. • If you cannot exercise moderately three to five times each week, walk daily for 30 minutes at a comfortable pace. • If you cannot walk 30 minutes daily, walk any distance you can (e.g., park farther away from a site than necessary; use the stairs, not the elevator, to go one floor up or two floors down). Diabetes • Manage your diabetes with your health care provider. o Blood Pressure • Have your blood pressure checked regularly. • If your blood pressure is elevated, follow your health care provider's advice. • Continue to monitor your blood pressure at regular intervals. o Obesity • Avoid severely restrictive or fad diets. • Restrict intake of saturated fats, simple sugars, and cholesterol-rich foods. • Increase your physical activity. o Reducing Elevated Serum Lipid Levels • 130-159 mg/dL—borderline high • 160-189 mg/dL—high • ≥190 mg/dL—very high The desired LDL level in patients who are at high risk or have existing CAD is less than 70 mg/dL. For patients at low or moderate risk, LDL should also be substantially less than 100 mg/dL (AHA, 2010). HDL cholesterol levels should be above 40 mg/dL, although this recommendation may soon be changed to a higher level. The recommended triglyceride level is less than 135 mg/dL in women 150 mg/dL in men (Pagana & Pagana, 2010). Approaches to decrease lipids are focused on diet, exercise, and drug therapy that lowers cholesterol and triglyceride levels. Teach patients with elevated lipid levels to: •Reduce intake of saturated fats to less than 7% of total calories •Avoid trans fatty acids •Consume less than 200 mg per day of cholesterol •Participate in daily physical activity •Manage weight Contributing Risk Factors Stable Angina Pectoris - chest discomfort that occurs with moderate to prolonged exertion in a pattern that is familiar to the patient. The frequency, duration, and intensity of symptoms remain the same over several months. CSA results in only slight limitation of activity and is usually associated with a fixed atherosclerotic plaque. It is usually relieved by nitroglycerin or rest and often is managed with drug therapy. Rarely does CSA require aggressive treatment. ~ exertion, exercise Relieved by rest Nitroglycerin sublingual Stable – fine Unstable – relieved by rest Unrelieved by rest or nitroglycerin for 15, go to ER Acute Coronary Syndromes - unstable angina or an acute myocardial infarction atherosclerotic plaque in the coronary artery ruptures, resulting in platelet aggregation (“clumping”), thrombus (clot) formation, and vasoconstriction (Fig. 40-1). The amount of disruption of the atherosclerotic plaque determines the degree of coronary artery obstruction (blockage) and the specific disease process. The artery has to have at least 40% plaque accumulation before it starts to block blood flow. Unstable angina (the most commonly used term) is chest pain or discomfort that occurs at rest or with exertion and causes severe activity limitation. An increase in the number of attacks and in the intensity of the pressure indicates unstable angina. The pressure may last longer than 15 minutes or may be poorly relieved by rest or nitroglycerin. Unstable angina describes a variety of disorders, including new-onset angina, variant (Prinzmetal's) angina, and pre-infarction angina. Patients with unstable angina will present with ST changes on a 12-lead ECG but will not have changes in troponin or creatine kinase (CK) levels. Ischemia Infarction – troponin (up to 21 days?, if there is damage), CKMB (first 24 hrs, last 3 days, how much damage), myoglobin Acute MI: Sudden loss of blood supply to an area of the heart causing permanent heart damage or death Most serious acute coronary syndrome Occurs when myocardial tissue is abruptly and severely deprived of oxygen Dynamic process that does not occur instantly but evolves over several hours ***EKG changes associated w/ MI – T wave inversion, ST elevation, abnormal Q wave are all EKG results that you will see w/ pt w/ MI!!! o o Outcome Management: Interventional Therapy o Reduce risk factors o Antiplatelet aggregation therapies o Restore blood supply – PTCA o Coronary atherectomy o Stent placement o Cardiac surgery o Laser revascularization ~ break up plaque heart failure ^ PVD - arterial, venous Peripheral Vascular Disease Disorders that alter the natural flow of blood through the arteries and veins of the peripheral circulation Manifestation of systemic atherosclerosis: a chronic condition in which partial or total arterial occlusion deprives the lower extremities of oxygen and nutrients Arterial Physical Assessment (Arterial) o Intermittent claudication o Pain that occurs even while at rest; numbness and burning o Hair loss and dry, scaly, mottled skin and thickened toenails o Arterial ulcers Management o Nonsurgical Exercise Positioning Promoting vasodilation Drug therapy Angioplasty o Surgical Arterial bypass Amputation Venous Insufficiency o Result of prolonged venous hypertension, stretching veins and damaging valves o Stasis dermatitis, stasis ulcers o Management of edema o Management of venous stasis ulcers o Drug therapy o Surgical management Varicose Veins o Distended, protruding veins that appear darkened and tortuous o Collaborative management includes: Elastic stockings Elevation of extremities Sclerotherapy Surgical removal of veins Radio frequency energy to heat the veins Chart 38-5 Home Care Assessment The Patient with Peripheral Vascular Disease Assess tissue perfusion to affected extremity(ies), including: •Distal circulation, sensation, and motion •Presence of pain, pallor, paresthesias, pulselessness, paralysis, poikilothermy (coolness) •Ankle-brachial index Assess adherence to therapeutic regimen, including: •Following foot care instructions •Quitting smoking •Maintaining dietary restrictions •Participating in exercise regimen •Avoiding exposure to cold and constrictive clothing Assess ability to manage wound care and prevent further injury, including: •Use of compression stockings or compression pumps as directed •Use of various dressing materials •Signs and symptoms to report to nurse Assess coping ability of patient and family members. Assess home environment, including: •Safety hazards, especially related to falls Chart 38-6 Patient and Family Education: Preparing for Self-Management Foot Care for the Patient with Peripheral Vascular Disease • Keep your feet clean by washing them with a mild soap in room-temperature water. • Keep your feet dry, especially the ankles and between the toes. • Avoid injury to your feet and ankles. Wear comfortable, well-fitting shoes. Never go without shoes. • Keep your toenails clean and filed. Have someone cut them if you cannot see them clearly. Cut your toenails straight across. • To prevent dry, cracked skin, apply a lubricating lotion to your feet. • Prevent exposure to extreme heat or cold. Never use a heating pad on your feet. • Avoid constricting garments. • If a problem develops, see a podiatrist or physician. • Avoid extended pressure on your feet or ankles, such as occurs when you lean against something. o o 5 Million Lives – Seven Key Interventions 1. Left ventricular systolic (LVS) heart function assessment (CMS,JCAHO,ACC,AHA) 2. ACE inhibitor or ARB at discharge for CHF patients with systolic dysfunction (LVEF<40) (CMS,JCAHO,ACC,AHA) 3. Anticoagulant at discharge for CHF patients with chronic/recurrent atrial fibrillation (ACC,AHA) o o 4. Influenza immunization (ACIP) 5. Pneumococcal immunization (ACIP) 6. Smoking cessation counseling (CMS,JCAHO,ACC,AHA) 7. Discharge instructions that address all of the following: activity level, diet, discharge medications, follow-up appointments, weight monitoring, and what to do if symptoms worsen (CMS,JCAHO,ACC,AHA) Tips for Transition Planning o Focus on discharge at admission o Use a discharge checklist with nurse-patient/family/caregiver face time Assure health literacy; use teach back to insure understanding; test using “Ask-Me-3” Reconcile medications; use teach back to ensure understanding of purpose, regimen, and side effects Provide real-time information transfer to next provider(s) Speak with emergency contact for high risk patients Schedule follow-up phone calls to patient/family to occur within 48 hours and physician visit within one week for average risk patients Schedule, before patient leaves, follow-up visit (home or office) for high risk patients to occur within 48 hours after discharge The Six Interventions AMI Interventions in the ACC clinical guidelines & measured by JCAHO and CMS 1. Early administration of aspirin 2. Aspirin at discharge 3. Beta-blocker at discharge 4. ACE-inhibitor or angiotensin receptor blockers (ARB) at discharge for patients with systolic dysfunction 5. Timely initiation of reperfusion (thrombolysis or percutaneous intervention) 6. Smoking cessation counseling Heart attack 6 steps: The 100,000 Lives Campaign asked hospitals to implement the following six interventions: 1) Deploy Rapid Response Teams at the first sign of patient decline. 2) Deliver reliable, evidence-based care for acute myocardial infarction to prevent deaths from heart attack. 3) Prevent adverse drug events by implementing medication reconciliation. 4) Prevent central line infections by implementing a series of scientifically grounded steps. 5) Prevent surgical site infections by reliably delivering the correct preoperative antibiotics at the proper time. 6) Prevent ventilator-associated pneumonia by implementing a series of interdependent, scientifically grounded steps. Management of Clients with Cancer characteristics of normal cells and cancer cells. o ~ 2 slide chart… don’t just memorize; what does this contribute to? Normal adhere; cancer don’t adhere. r/t to metastasis – can break off. Normal apoptosis; cancer don’t have time clock. Contributes to tumor growth. Normal Have limited cell division Undergo apoptosis (programmed cell death) Show specific morphology Have a small nuclear-cytoplasmic ratio Perform specific differentiated functions Adhere tightly together Non-migratory Grow in an orderly and well-regulated manner Contact inhibited Euploid w/ 23 pairs of chromosomes Cancer Have rapid or continuous cell division Do not respond to signals for apoptosis Show anaplastic morphology Have a large nuclear-cytoplasmic ratio Lose some or all differentiated functions Adhere loosely together Able to migrate through embryonic cells Grow by invasion Are aneuploidy (> or < 23 chromosomes) Side effects of cancer treatment – radiation vs. chemotherapy o ~ radiation – o ~ brachytherapy… o ~ who gets it, side effects, nursing care o ~ no surgery! radiation therapy as a treatment for neoplastic disorders, its potential side effects, and nursing care. chemotherapy as a treatment modality for neoplastic disorders, its side effects, and nursing care. o Radiation – types, pt care, side effects Types External beam – beam comes from outside and targets particular tissue Brachytherapy – “short” or “close” therapy - radiation source comes into direct, continuous contact w/ the tumor tissues for a specific period of time o Ex) Radioactive iodine Side Effects site dependent – in head and neck can cause permanent facial hair; destroy salivary glands Long-term sequelae Patient Consider time, distance and shielding (little time, far away, use shield like iron Care vest) Teach accurate objective facts to help client cope. (be realistic) Do not remove markings. (allows radiation in right place each time) Administer skin care. (protect, cover, moisturize) no lotion before RT Do not use lotions or ointments. o Brachytherapy: With all types of brachytherapy, the radiation source is within the patient. Therefore the patient emits radiation for a period of time and is a hazard to others Side Vary according to treatment site and is dependent on the total absorbed dose Effects o Local skin changes and hair loss o Altered taste sensations (head and neck) o Fatigue related to increased energy demands o Inflammatory responses that cause tissue fibrosis and scarring o Avoid direct exposure of the skin to the sun. o Care for xerostomia (dry mouth). o Bone exposed to radiation is more vulnerable to fracture. Chemotherapy – types, pt care, side effects Types Antimetabolites Antitumor antibodies Alkylating agents Antimitotic agents Topoisomerase inhibitors Miscellaneous chemotherapeutic agents Combination chemotherapy [check Table 24-2 categories] Patient Care Side Effects Administration Verification of agent, dose, schedule Safe preparation, handling, and disposal Routes of administration Intravenous, regional, oral, etc. Adverse reactions Hypersensitivity reaction and extravasation Safe preparation, handling, and disposal Myelosuppression (Neutropenia, Thrombocytopenia, Anemia) -- leading to infection, anemia, bleeding ~ decreasing immune system. Monitor CBC. Nausea and vomiting ~ irritation of meds to GI tissues Mucositis in the entire gastrointestinal tract Diarrhea/ Constipation Fatigue Alopecia or hair loss Fertility problems ~ extravasation, PPE, fluids b/c vomiting and bleeding, peripheral neuropathy, memory… (?) Management of Clients with Respiratory Disorders hypoxemia and hypoxia symptoms and treatment tracheostomy care o ~ not types o ~ assessing for: cuff pressure, WEANING off a trach. The steps. o Care o Weaning Chart 30-3 Best Practice for Patient Safety & Quality Care Tracheostomy Care 1 Assemble the necessary equipment. 2 Wash hands. Maintain Standard Precautions. 3 Suction the tracheostomy tube if necessary. 4 Remove old dressings and excess secretions. 5 Set up a sterile field. 6 Remove and clean the inner cannula. Use half-strength hydrogen peroxide to clean the cannula and sterile saline to rinse it. If the inner cannula is disposable, remove the cannula and replace it with a new one. 7 Clean the stoma site and then the tracheostomy plate with half-strength hydrogen peroxide followed by sterile saline. Ensure that none of the solutions enters the tracheostomy. 8 Change tracheostomy ties if they are soiled. Secure new ties in place before removing soiled ones to prevent accidental decannulation. If a knot is needed, tie a square knot that is visible on the side of the neck. One or two fingers should be able to be placed between the tie tape and the neck. 9 Wash hands. 10 Document the type and amount of secretions and the general condition of the stoma and surrounding skin. Document the patient's response to the procedure and any teaching or learning that occurred. Chart 30-4 Focused Assessment The Patient with a Tracheostomy • Note the quality, pattern, and rate of breathing: •Within patient's baseline? Tachypnea can indicate hypoxia. Dyspnea can indicate secretions in the airway. • Assess for any cyanosis, especially around the lips, which could indicate hypoxia. • Check the patient's pulse oximetry reading. • If oxygen is prescribed, is the patient receiving the correct amount, with the correct equipment and humidification? • Assess the tracheostomy site: •Note the color, consistency, and amount of secretions in the tube or externally. •If the tracheostomy is sutured in place, is there any redness, swelling, or drainage from suture sites? •If the tracheostomy is secured with ties, what is the condition of the ties? Are they moist with secretions or perspiration? Are the secretions dried on the ties? Is the tie secure? •Assess the condition of the skin around the tracheostomy and neck. Be sure to check underneath the neck for secretions that may have drained to the back. Check for any skin breakdown related to pressure from the ties or related to excess secretions. •Assess behind the faceplate for the size of the space between the outer cannula and the patient's tissue. Are any secretions collected in this area? • If the tube is cuffed, check cuff pressure. • Auscultate the lungs. • Are a second (emergency) tracheostomy tube and obturator available? Weaning is a gradual decrease in the tube size and ultimate removal of the tube. Cuff is deflated as soon as the patient can manage secretions and does not need assisted ventilation. Change from a cuffed to an uncuffed tube. Size of tube is decreased by capping; use a smaller fenestrated tube. Tracheostomy button has a potential danger of getting dislodged. Button maintains stoma patency and assists spontaneous breathing. types of tracheostomies System FiO2 Delivered When Used Nasal Cannula 24%-40% at 1-6 L/min Chronic lung disease and for any pt needing long-term O2 therapy Simple Facemask 40%-60% at 5-8 L/min; flow rate must be sat at least at 5 L/min to flush mask of CO2 Nursing Responsibilities - ensure that prongs are in the nares properly - provide water-soluble jelly to nares PRN - assess the patency of the nostrils - assess the pt for changes in resp rate and depth - be sure mask fits securely over nose and mouth - assess skin and provide skin care to the area covered by the mask - monitor the pt closely for risk of aspiration Partial Rebreather Mask - provide emotional support to the pt who feels claustrophobic - make sure that the reservoir does not twist or kink, which results in a deflated bag - adjust the flow rate to keep the reservoir bag inflated 60%-75% at 6-11 L/min, a liter flow rate high enough to maintain reservoir bag two-thirds full during inspiration and expiration 80%-95% at liter flow to maintain reservoir bag two-thirds full NonRebreather Mask Venturi mask (venti mask) 45%-50% w/ flow rates as recommended by the manufacturer, usually 4-10 L/min; provides high humidity Pt w/ chronic lung disease b/c it delivers a more precise O2 concentration Aerosol mask, face tent, tracheostomy collar 24%-100% w/ flow rates of at least 10 L/min; provides high humidity Face tent: facial trauma or burns Aerosol mask: high humidity needed after extubation or upper airway surgery or for thick secretions Tracheostomy collar: high humidity and the desired O2 to the pt w/ tracheostomy T-piece 24%-100% w/ flow rates of at least 10 L/min; provides high humidity Noninvasive Positive Pressure Ventilation CPAP Can deliver O2 or may just use room air Transtracheal Oxygen Delivery Long-term method of delivering O2 directly into the lungs Home Oxygen Therapy Concentrated from room air and is delivered at more than 90% - interventions as for partial rebreather mask; this pt requires close monitoring - make sure that valves and rubber flaps are patent, functional, and not stuck. Remove mucus or saliva - closely assess the pt on increased FiO2 via non-rebreather mask. Intubation is the only way to provide more precise FiO2 - provide constant surveillance to ensure an accurate flow rate for the specific FiO2 - keep the orifice for the Venturi adaptor open and uncovered - provide a mask that fits snugly and tubing that is free of kinks - assess the pt for dry mucous membranes - change to a nasal cannula during mealtime - assess that aerosol mist escapes from the vents of the delivery system during inspiration and expiration - empty condensation from the tubing - empty condensation from the tubing - keep the exhalation port open and uncovered - position the T-piece so that it does not pull on the tracheostomy or endotracheal tube - make sure the humidifier creates enough mist. A mist should be seen during inspiration and expiration Those w/ atelectasis after surgery or cardiac-induced pulm edema; sleep apnea More cosmetically acceptable Least expensive, does not need to be filled. Nurse or RT teaches the pt about the equipment needed for home O2 therapy, including the O2 source, delivery devices, humidity sources, and safety aspects of using and maintaining the equipment No smoking. Candles, gas burners, and fireplaces (or other open flames) are not to be used in the same room that O2 is being used. suctioning techniques and complications o Suctioning Chart 30-2 Suctioning the Artificial Airway 1 Assess the need for suctioning (routine unnecessary suctioning causes mucosal damage, bleeding, and bronchospasm). 2 Wash hands. Don protective eyewear. Maintain Standard Precautions. 3 Explain to the patient that sensations such as shortness of breath and coughing are to be expected but that any discomfort will be very brief. o Complications Complication and description Tracheomalacia: constant pressure exerted by the cuff causes tracheal dilation and erosion of cartilage Tracheal stenosis: narrowed tracheal lumen is due to scar formation from irritation of tracheal mucosa by the cuff Tracheoesophageal fistula (TEF): excessive cuff pressure causes erosion of the posterior wall of the trachea. A hole is created b/t the trachea and the anterior esophagus. the pt at highest risk also has a NG tube present 4 Check the suction source. Occlude the suction source, and adjust the pressure dial to between 80 and 120 mm Hg to prevent hypoxemia and trauma to the mucosa. 5 Set up a sterile field. 6 Preoxygenate the patient with 100% oxygen for 30 seconds to 3 minutes (at least three hyperinflations) to prevent hypoxemia. Keep hyperinflations synchronized with inhalation. 7 Quickly insert the suction catheter until resistance is met. Do not apply suction during insertion. 8 Withdraw the catheter 0.4 to 0.8 inch (1 to 2 cm), and begin to apply suction. Use a twirling motion of the catheter during withdrawal. Never suction longer than 10 to 15 seconds. 9 Hyperoxygenate for 1 to 5 minutes or until the patient's baseline heart rate and oxygen saturation are within normal limits. 10 Repeat as needed for up to three total suction passes. 11 Suction mouth as needed, and provide mouth care. 12 Wash hands. 13 Describe secretions, and document patient's responses. Manifestations Management Prevention - an increased amount of air is required in the cuff to maintain the seal - a larger tracheostomy tube is required to prevent an air leak at the stoma - food particles are seen in tracheal secretions - pt does not receive the set tidal volume on the ventilator - stenosis is usually seen after the cuff is deflated or the tracheostomy tube is removed - pt has increased coughing, inability to expectorate secretions, or difficulty in breathing or talking No special management is needed unless bleeding occurs - use an uncuffed tube ASAP - monitor cuff pressure and air volumes closely, and detect changes Similar to tracheomalacia: - food particles are seen in tracheal secretions - an increased amount of air is required in the cuff to maintain the seal - increased coughing and choking while eating - does not receive the set tidal volume on the ventilator - manually administer O2 by mask to prevent hypoxemia - use small, soft feeding tube instead of NG tube for tube feedings. A gastrostomy or jejunostomy may be performed by the physician - monitor the pt w/ a NG closely; assess for TEF and aspiration - remove trach tube immediately - apply direct pressure to the innominate artery at the stoma site - prepare the pt for immediate repair surgery Keep cuff pressure 14-20 mmHg Tracheal dilation or surgical intervention is used - prevent pulling of and traction on the tracheostomy tube - properly secure the tube in the midline position - maintain proper cuff pressure - minimize oronasal intubation time - maintain cuff pressure - intor the amount of air needed for inflation, and detect changes. Progress to a deflated cuff or cuffless tube ASAP Trachea-innominate artery - trach tube pulsates in - correct the tube size, length, fistula: a malpositioned synchrony w/ heartbeat and midline position tube causes its distal tip to - heavy bleeding from stoma - prevent pulling or tugging push against the lateral - life-threatening complication on trach tube wall of the tracheostomy. - immediately notify Continued pressure causes physician of the pulsating necrosis and erosion of the tube innominate artery. This is a medical emergency. Possible complications assessment: o Tube obstruction Difficulty breathing; noisy respirations; difficulty inserting a suction catheter; thick, dry secretions; and unexplained peak pressures (if a mechanical ventilator is in use). Assess the patient at least hourly for tube patency. o o o o o Prevent obstruction by helping the patient cough and deep breathe, providing inner cannula care, humidifying the oxygen source, and suctioning. If tube obstruction occurs as a result of cuff prolapse over the end of the tracheostomy tube, the physician or advanced practice nurse repositions or replaces the tube. Tube dislodgment—accidental decannulation This problem can be prevented by securing the tube in place. This action reduces movement and traction on the tube from oxygen or ventilator tubing or accidental pulling by the patient. Tube dislodgment in the first 72 hours after surgery is an emergency because the tracheostomy tract has not matured and replacement is difficult. The tube may end up in the subcutaneous tissue instead of in the trachea. If the tube is dislodged on an immature tracheostomy, ventilate the patient using a manual resuscitation bag and facemask while another nurse calls the Rapid Response Team. Pneumothorax (air in the chest cavity) can develop during the tracheotomy procedure if the chest cavity is entered. When pneumothorax occurs during tracheotomy, it usually does so at the apex of the lung. Chest x-rays after placement are used to assess for pneumothorax. Subcutaneous emphysema occurs when there is an opening or tear in the trachea and air escapes into fresh tissue planes of the neck. Air can also progress throughout the chest and other tissues into the face. Inspect and palpate for air under the skin around the new tracheostomy. * crepitus Bleeding constant oozing is abnormal. Wrap gauze around the tube and pack gauze gently into the wound to apply pressure to the bleeding sites. Sterile technique Infection In the hospital, use sterile technique to prevent infection during suctioning and tracheostomy care. Assess the stoma site at least once per shift for purulent drainage, redness, pain, or swelling. Tracheostomy dressings may be used to keep the stoma clean and dry. These dressings resemble a 4 × 4 gauze pad with an area removed to fit around the tube. If tracheostomy dressings are not available, fold standard sterile 4 × 4s to fit around the tube. Do not cut the dressing because small bits of gauze could then be aspirated through the tube. Change these dressings often because moist dressings provide a medium for bacterial growth. Careful wound care prevents most local infections. Management of Clients with Endocrine Disorders hypo/hyper thyroid o ~ diagnosis o ~ lab values [increased/decreased] beyond TSH, T3, T4 antibodies!!! o ~ interventions o ~ s/sx HYPOTHYROID • Myxedema ~ mucous and fluid • Causes • Primary • Pituitary gland • Hypothalamus • Older • Females – 30-60 yrs Assessment Physical Chart 66-6 Key Features Hypothyroidism Skin Manifestations o • Cool, pale or yellowish, dry, coarse, scaly skin o • Thick, brittle nails o • Dry, coarse, brittle hair o • Decreased hair growth, with loss of eyebrow hair o • Poor wound healing Pulmonary Manifestations o Hypoventilation o Pleural effusion o Dyspnea Cardiovascular Manifestations [DECREASED] o • Bradycardia o • Dysrhythmias o • Enlarged heart o • Decreased activity tolerance o • Hypotension Metabolic Manifestations o • Decreased basal metabolic rate o • Decreased body temperature o • Cold intolerance Musculoskeletal Manifestations o • Muscle aches and pains o • Delayed contraction and relaxation of muscles Neurologic Manifestations o • Slowing of intellectual functions: •Slowness or slurring of speech •Impaired memory •Inattentiveness o • Lethargy or somnolence o • Confusion o • Hearing loss o • Paresthesia (numbness and tingling) of the extremities o • Decreased tendon reflexes Psychological/Emotional Manifestations o • Apathy o • Depression – most common reason for seeking medical attention o • Paranoia o • Withdrawal Gastrointestinal Manifestations o • Anorexia o • Weight gain o • Constipation o • Abdominal distention Reproductive Manifestations o Women • Changes in menses (amenorrhea or prolonged menstrual periods) o • Anovulation • Decreased libido Men • Decreased libido • Impotence Other Manifestations o • Periorbital edema o • Facial puffiness o • Nonpitting edema of the hands and feet o • Hoarseness o • Goiter (enlarged thyroid gland) o • Thick tongue o • Increased sensitivity to opioids and tranquilizers o • Weakness, fatigue o • Decreased urine output o • Anemia o • Easy bruising o • Iron deficiency o • Folate deficiency o • Vitamin B12 deficiency Diagnostic tests Treatment Meds Other T3/T4 - DECREASED TSH - INCREASED Lifelong thyroid hormone replacement: levothyroxine sodium (Synthroid, T4) – start at lowest dose o Weight loss indicates a need for a decreased dose o If the client is gaining weight and continues to feel tired, that is an indication that the dose may need to be increased. Chart 66-7 Best Practice For Patient Safety & Quality Care - Emergency Care of the Patient During Myxedema Coma • Maintain a patent airway. • Replace fluids with IV normal or hypertonic saline, as prescribed. • Give levothyroxine sodium IV as prescribed. Complications • Give glucose IV as prescribed. • Give corticosteroids as prescribed. • Check the patient's temperature hourly. • Monitor blood pressure hourly. • Cover the patient with warm blankets. – b/c cold intolerance • Monitor for changes in mental status. • Turn every 2 hours. • Institute Aspiration Precautions. Myxedema coma = overall metabolism slows to the point that cardiac and resp arrest can occur o Coma o Respiratory failure o Hypotension o Hyponatremia o Hypothermia o Hypoglycemia Myxedema coma can lead to shock, organ damage, and death. Assess the patient with hypothyroidism at least every 8 hours for changes that indicate increasing severity, especially changes in mental status, and report these promptly to the health care provider ~ hyperthyroidism (with hormone replacement therapy) HYPERTHYROID – THYROTOXICOSIS • Etiology • Graves Disease (autoimmune) • Excess TSH from pituitary • Neoplasms • Thyroiditis • Excessive thyroid replacement Assessment Physical Chart 66-1 Key Features Hyperthyroidism Skin Manifestations o • Diaphoresis (excessive sweating) o • Fine, soft, silky body hair o • Smooth, warm, moist skin o • Thinning of scalp hair o ~ pretibial myxedema – dry waxy swelling in front of tibia Neurologic Manifestations o • Blurred or double vision o • Eye fatigue o • Corneal ulcers or infections o • Increased tears o • Injected (red) conjunctiva o • Photophobia o • Eyelid retraction, eyelid lag* [Graves’ disease only] o • Globe lag* [Graves’ disease only] o • Hyperactive deep tendon reflexes o • Tremors o • Insomnia Metabolic Manifestations o • Increased basal metabolic rate o • Heat intolerance o • Low-grade fever o • Fatigue Psychological/Emotional Manifestations o • Decreased attention span o • Restlessness o • Irritability o • Emotional lability o • Manic behavior Reproductive Manifestations o • Amenorrhea o • Decreased menstrual flow o • Increased libido Other Manifestations o • Goiter o • Wide-eyed or startled appearance (exophthalmos)* [Graves’ disease only] o • Decreased total white blood cell count o • Enlarged spleen Pulmonary Manifestations o • Shortness of breath with or without exertion o • Rapid, shallow respirations o • Decreased vital capacity Cardiovascular Manifestations o • Shortness of breath with or without exertion o • Rapid, shallow respirations o • Decreased vital capacity GI Manifestations o • Weight loss o • Increased appetite o • Increased stools o • Hypoproteinemia Musculoskeletal Manifestations o • Muscle weakness o • Muscle wasting Serum antibodies – positive = Graves TSH ~ used to guide treatment, not T3/T4 - DECREASED T3 & T4 INCREASED Uptake tests Suppression tests Thyroid scan evaluates the position, size, and functioning of the thyroid gland. • Anti-Thyroid meds • Tapazole • PTU Beta adrenergic blockers Radioactive iodine Thyroidectomy • Preoperative Meds • PTU (propylthiouracil) or Tapazole - Block T3 & T4 production by inhibiting thyroid binding of iodide and by preventing the conversion of T4 to T3 • Assess for liver problems for PTU • Dark urine may indicate liver toxicity or failure. The client must notify the provider immediately. • Methimazole needs to be taken every 8 hours for an extended period of time. Levels of T3 and T4 will be followed and dosages adjusted as levels fall. • Methimazole is an iodine preparation that decreases blood flow through the thyroid gland. This action reduces the production and release of thyroid hormone. The client should see some effects within 2 weeks; however, it may take several more weeks before metabolism • The client should avoid large crowds and people who are ill. Propylthiouracil reduces blood cell counts and the immune response, which increases the risk for infection. The client does not, however, need to remain completely at home. • The client must notify the provider of weight gain because this may indicate hypothyroidism. A lower drug dose may be required. • SSKI or Lugol’s Solution - Decrease vascularity of the thyroid gland • Iodine preparations – short term therapy before surgery • Decrease blood flow through the thyroid gland, reducing the production and release of thyroid hormone • Lopressor - Block adrenergic effects of hyperthyroidism • relieve diaphoresis, anxiety, tachycardia, and palpitations but do not inhibit thyroid hormone production Thyroidectomy o Post-Operative Respiratory Distress Mucous, laryngeal edema Vocal cord paralysis Diagnostic tests Treatment Meds Other • • • Complications Humidify air Trach tray, suction available Hemorrhage Check behind neck Expect ~50 ml drainage in first 24 hours Verify proper functioning of drain ~ check H&H; lethargy, pale, pulse ox go down, make sure dressing not too tight Hypocalcemia Tetany + Chvostek’s sign + Trousseau’s sign Calcium Gluconate at the bedside ~ early: tingling around fingers and mouth, small muscle twitching, numbness Thyroid Storm Tachycardia, HTN, Hyperthermia Reduce fever Anticipate a beta blocker PTU ~ temperature change (early), increase HR (early), sweating, HTN, hyperactive BS, diarrhea ~ late: seizures, coma Chart 66-5 Best Practice For Patient Safety & Quality Care Emergency Care of the Patient During Thyroid Storm o Maintain a patent airway and adequate ventilation. o Give antithyroid drugs as prescribed: methimazole (Tapazole), up to 60 mg daily; propylthiouracil (PTU, Propyl-Thyracil ), 300 to 900 mg daily. o Administer sodium iodide solution, 2 g IV daily as prescribed. o Give propranolol (Inderal, Detensol ), 1 to 3 mg IV as prescribed. Give slowly over 3 minutes. The patient should be connected to a cardiac monitor, and a central venous pressure catheter should be in place. o Give glucocorticoids as prescribed: hydrocortisone, 100 to 500 mg IV daily; prednisone, 4 to 60 mg IV daily; or dexamethasone, 2 mg IM every 6 hours. o Monitor continually for cardiac dysrhythmias. o Monitor vital signs every 30 minutes. o Provide comfort measures, including a cooling blanket. o Give non-salicylate antipyretics as prescribed. o Correct dehydration with normal saline infusions. o Apply cooling blanket or ice packs to reduce fever. Nonsurgical Management o Monitor apical pulse, BP, temp q4h Increase in temp may indicate thyroid storm Immediately report temp increase of even one degree Fahrenheit o Reduce stimulation o Promote comfort Cushing’s/ Addison’s o ~ adrenal gland o ~ meds – esp cortisol, glucocorticoids, steroids (steroids most pharm info you’ll need) ADDISON’S DISEASE (Adrenal Insufficiency) Highest levels of ACTH is after sleep b/c of regeneration Assessment Physical Adrenal Crisis: Clinical Signs o Thorough history essential to look for cause o Symptoms of hypovolemia o Fluid and electrolyte imbalances o Postural hypotension o Change level of consciousness o Hyperkalemia o Fatigue, weakness o Gastrointestinal complaints o Decreased renal perfusion and decreased urine output o Skin changes (hyperpigmentation) o Decreased libido o Hyperkalemia, hyponatremia, hypotension, hypoglycemia, shock o Sex, salt, sugar, skin Sex – decreased libido Salt – hyponatremia; decreased volume Sugar – decreased glucose – decreased ability to respond to stress Skin – hyperpigmentation Diagnostic tests Chart 65-8 Key Features Adrenal Insufficiency Neuromuscular Manifestations • Muscle weakness • Fatigue • Joint/muscle pain Gastrointestinal Manifestations • Anorexia • Nausea, vomiting • Abdominal pain • Bowel changes (constipation/diarrhea) • Weight loss • Salt craving Skin Manifestations • Vitiligo • Hyperpigmentation Cardiovascular Manifestations • Anemia • Hypotension • Hyponatremia • Hyperkalemia • Hypercalcemia • Laboratory values • Hyponatremia • Hyperkalemia • Azotemia (elevated BUN) • Hypoglycemia • Low plasma cortisol levels and urinary metabolites • ACTH (cosyntropin) stimulation test • Give ACTH, doesn’t respond – adrenal gland! • If cortisol levels don’t go up very much, we know problem is w/ adrenal gland. • Give ACTH, cortisol levels rise, then problem is hypothalamus or pituitary. Treatment Meds • • • • Cortisol and aldosterone deficiencies are corrected by replacement therapy. Hydrocortisone corrects glucocorticoid deficiency (Chart 65-10). Oral cortisol replacement regimens vary. The most common drug used for this purpose is prednisone. o Generally, divided doses are given, with two-thirds given in the morning and one-third in the late afternoon to mimic the normal release of this hormone. Other • • • • Nursing interventions focus on promoting fluid balance, monitoring for fluid deficit, and preventing hypoglycemia. Weigh the patient daily, and record intake and output. Assess vital signs every 1 to 4 hours, depending on the patient's condition and the presence of dysrhythmias or postural hypotension. Monitor laboratory values to identify hemoconcentration (e.g., increased hematocrit or BUN). Chart 65-7 Best Practice For Patient Safety & Quality Care Emergency Care of the Patient with Acute Adrenal Insufficiency Hormone Replacement • Start rapid infusion of normal saline or dextrose 5% in normal saline. • Initial dose of hydrocortisone sodium succinate (Solu-Cortef) is 100 to 300 mg or dexamethasone 4 to 12 mg as an IV bolus. • Infuse additional 100 mg of hydrocortisone sodium succinate by continuous IV drip over the next 8 hours. • Give hydrocortisone 50 mg IM concomitantly every 12 hours. • Initiate an H2 histamine blocker (e.g., ranitidine) IV for ulcer prevention. Hyperkalemia Management • Administer insulin (20 to 50 units) with dextrose (20 to 50 mg) in normal saline to shift potassium into cells. • Administer potassium binding and excreting resin (e.g., Kayexalate). • Give loop or thiazide diuretics. • Avoid potassium-sparing diuretics, as prescribed. • Initiate potassium restriction. • Monitor intake and output. • Monitor heart rate, rhythm, and ECG for manifestations of hyperkalemia (slow heart rate; heart block; tall, peaked T waves; fibrillation; asystole). Hypoglycemia Management • Administer IV glucose, as prescribed. • Administer glucagon, as needed and prescribed. • Maintain IV access. • Monitor blood glucose level hourly. Complications CUSHING’S DISEASE (HYPERCORTISOLISM) • Excessive secretion of cortisol from the adrenal cortex – problem in adrenal cortex, anterior pituitary gland, or hypothalamus • Cushing’s disease is a condition in which the anterior pituitary gland releases too much adrenocorticotropic hormone (ACTH). Oversecretion of ACTH can result from a pituitary adenoma, an adrenal adenoma, or drug therapy with corticosteroids (aka glucocorticoids) for another health problem) • Adrenal Cortex Disorder • Hyperaldosteronism • Primary hyperaldosteronism (rare) • Secondary hyperaldosteronism • Cushing’s Syndrome • Pheochromocytoma – tumor on adrenal medulla Assessment Physical Key Features • Elevated plasma cortisol levels • Weight gain • Truncal obesity • “Moon face” • Extremity muscle wasting • Loss of bone density • Hypertension • Hyperglycemia • Purple striae • Acne • Thin, easily damaged skin • Hyperpigmentation • PP – Hyperaldosteronism: Clinical Signs • Thorough history essential to look for cause • Hypertension • Hypokalemia • Weight gain and fatty deposits • Slow wound healing • Glucose intolerance that may lead to diabetes Fatigue and muscle weakness Depression, anxiety and irritability; loss of emotional control For Women: • Hirsutism (increased hair growth) • Irregular or absent menstrual periods • For Men: • Decreased libido, • Decreased fertility • Erectile dysfunction • Other signs and symptoms include: • Striae on the abdomen, thighs, breasts and arms • Thinning, fragile skin that bruises easily • Acne • Headache • Bone loss, leading to fractures over time Chart 65-11 Key Features Hypercortisolism (Cushing’s Disease/Syndrome) • General Appearance • • Fat redistribution: • Moon face • Buffalo hump • Truncal obesity • • Weight gain • Skin Manifestations • • Thinning skin (“paper-like” appearance, especially on the back of the hands) • • Striae • • Increased pigmentation (with ectopic or pituitary production of ACTH) • Cardiovascular Manifestations • • Hypertension • • Increased risk for thromboembolic events • • Frequent dependent edema • • Capillary fragility: • Bruising • Petechiae • Immune System Manifestations (b/c high levels of corticosteroids kill lymphocytes and shrink organs containing lymphocytes, such as liver, spleen, and lymph nodes) • • Increased risk for infection • • Decreased immune function: • •Decreased circulating lymphocytes • •Decreased production of immunoglobulins (antibodies) • • Decreased inflammatory responses: • Decreased eosinophil count • Slight increase in neutrophil count but activity is reduced • • Decreased production of proinflammatory cytokines, histamine, and prostaglandins • • Manifestations of infection/inflammation may be masked • Musculoskeletal Manifestations • • Muscle atrophy (most apparent in extremities) • • Osteoporosis (bone density loss) • Pathologic fractures • Decreased height with vertebral collapse • Aseptic necrosis of the femur head • Slow or poor healing of bone fractures ACTH o Pituitary Cushing’s disease: ACTH elevated o Adrenal Cushing’s disease or when Cushing’s syndrome results from chronic steroid use: ACTH low Increased blood glucose! Decreased lymphocyte Increased sodium Decreased serum calcium level Decreased potassium level • • • • Diagnostic tests • • • • • • Treatment Meds • • Fluid overload o Administer drugs to interfere w/ ACTH production or adrenal hormone synthesis: aminoglutethimide (Elipten, Cytadren), Metyrapone (Metopirone), Cyproheptadine (Periactin), Mitotane (Lysodren) Risk for injury Other • • • Complications • Risk for infection • ~ restrict fluid, glucocorticoid inhibitors Fluid overload o Pt safety includes preventing fluid overload becoming worse pulmonary edema and heart failure o Watch for signs of overload: increased pulse quality, increase neck vein distention, presence of crackles in lungs, increase peripheral edema, reduce UO) –checked every 2 hours o Pulmonary edema can occur quickly and can lead to DEATH o Assess skin pressure areas and changed position every 2 hrs o Drug therapy that interferes with ACTH production or adrenal hormone synthesis for temporary relief o Nutrition may involve both fluid and sodium restriction o Monitor I&O and daily weight o Check urine specific gravity (<1.005 may indicate fluid overload) o Radiation therapy for pituitary adenomas o Surgery for removal of pituitary gland or partial or complete removal of adrenal gland Risk for injury – risk for skin breakdown, bone fractures, and GI bleeding -Use soft toothbrush and an electric shaver -Caution using adhesive tape -Exert pressure over site of venipuntures to prevent bleeding and bruising -Use drawsheets -Milk, cheese, yogurt, and green leafy and root vegetables add calcium and promote bone density -Monitor for GI bleeding -Antacids to protect GI mucosa -H2 receptor to prevent formation of hydrochloric acid Risk for infection -Thorough handwashing* -Hypercortisolism may not show manifestations of infection -Monitor CBC with differential WBC and absolute neutrophil count (ANC) -Assess for temperature elevation of even 0.5 F (or 0.5 C) above baseline –significant! • -Pulmonary hygiene every 2-4 hrs Potential for acute adrenal insufficiency Cortisol replacement therapy o Chart 65-12 Patient And Family Education: Preparing For Self-Management Cortisol Replacement Therapy o • Take your medication in divided doses—the first dose in the morning and the second dose between 4 and 6 pm. o • Take your medication with meals or snacks. o • Weigh yourself daily. o • Increase your dosage as directed for increased physical stress or severe emotional stress, including surgery, dental work, influenza, fever, pregnancy, and family problems. o • Never skip a dose of medication. If you have persistent vomiting or severe diarrhea and cannot take your medication by mouth for 24 to 36 hours, call your physician. If you cannot reach your physician, go to the nearest emergency department. You may need an injection to take the place of your usual oral medication. o • Always wear your medical alert bracelet or necklace. o • Make regular visits for health care follow-up. o • Learn how to give yourself an intramuscular injection of hydrocortisone. Be aware of lab values Management of Clients with Renal/Urinary Disorders Polycystic kidney disease POLYCYSTIC KIDNEY DISEASE Inherited disorder Fluid-filled cysts develop in nephrons - develop anywhere in the nephron as a result of abnormal kidney cell division. Assessment Physical Diagnostic tests Treatment Meds Chart 70-1 Key features Polycystic Kidney Disease o Abdominal or flank pain – pain often first manifestations Dull, aching increased kidney size w/ distention or by infection w/in cyst Sharp, intermittent cyst ruptures or stone is present When a cyst ruptures, the patient may have bright red or cola-colored urine. o Hypertension – r/t kidney ischemia from the enlarging cysts. As the vessels are compressed and blood flow to the kidneys decreases, the renin-angiotensin system is activated, raising blood pressure. o Increased abdominal girth – distended abd o Constipation o Bloody or cloudy urine o Kidney stones Infection is suspected if the urine is cloudy or foul smelling or if there is dysuria (pain on urination). Nocturia (the need to urinate excessively at night) is an early manifestation and occurs because of decreased urine concentrating ability. As kidney function further declines, the patient has increasing hypertension, edema, and uremic manifestations such as anorexia, nausea, vomiting, pruritus, and fatigue Because berry aneurysms often occur in patients with PKD, a severe headache with or without neurologic or vision changes requires attention. Psychosocial: While obtaining the family history, listen carefully for spoken and unspoken feelings of anger, resentment, futility, sadness, or anxiety. Urinalysis shows proteinuria (protein in the urine) once the glomeruli are involved. Hematuria (blood in the urine) may be gross or microscopic. Bacteria in the urine indicate infection, usually in the cysts. Obtain a urine sample for culture and sensitivity testing when there is evidence of infection. As kidney function declines, serum creatinine and blood urea nitrogen (BUN) levels rise. With decreasing kidney function, creatinine clearance decreases. Changes in kidney handling of sodium may cause either sodium losses or sodium retention. Diagnostic studies include: o Renal sonography, computed tomography (CT), and magnetic resonance imaging (MRI). o Small cysts are detected by sonography, CT, or MRI. o Renal sonography shows evidence of PKD, with minimal risk. Managing Pain o NSAIDs are used cautiously because of their tendency to reduce kidney blood flow. Aspirin-containing compounds are avoided to reduce the risk for bleeding. o If cyst infection causes discomfort, antibiotics such as trimethoprim/sulfamethoxazole (Bactrim, Septra, Trimpex) or ciprofloxacin (Cipro) are prescribed. Monitor the serum creatinine levels because antibiotic therapy can be nephrotoxic. Preventing Constipation o Advise him or her about the use of stool softeners and bulk agents, including the careful use of laxatives, to prevent chronic constipation. Controlling Hypertension and Preventing End-Stage Kidney Disease o Antihypertensive agents: Angiotensin-converting enzyme (ACE) inhibitors - may help control the cell growth aspects of PKD and reduce microalbuminuria Calcium channel blockers Beta blockers Vasodilators (see Chapter 38) o Diuretics Other Assessment Physical Control of hypertension is a top priority because proper treatment can disrupt the process that leads to further kidney damage Managing Pain o Apply dry heat to the abdomen or flank to promote comfort when kidney cysts are infected. o When pain is severe, cysts can be reduced by needle aspiration and drainage; however, they usually refill. Preventing Constipation o Teach the patient who has adequate urine output how to prevent constipation by maintaining adequate fluid intake, increasing dietary fiber when fluid intake is more than 2500 mL/24 hr, and exercising regularly. Controlling Hypertension and Preventing End-Stage Kidney Disease o When kidney impairment results in decreased urine concentration with nocturia and low urine specific gravity, urge the patient to drink at least 2 L of fluid per day to prevent dehydration, which can further reduce kidney function. o Restricting sodium intake may help control blood pressure. Chart 70-2 Patient And Family Education: Preparing for Self-Management Polycystic Kidney Disease o Measure and record your blood pressure daily, and notify your health care provider for consistent changes in blood pressure. o Take your temperature if you suspect you have a fever. o Weigh yourself every day at the same time of day and with the same amount of clothing; notify your physician or nurse if you have a sudden weight gain. o Limit your intake of salt to help control your blood pressure. o Notify your physician or nurse if your urine smells foul or has blood in it. o Notify your physician or nurse if you have a headache that does not go away or if you have visual disturbances. o Monitor bowel movements to prevent constipation. Complications HTN cerebral aneurysms (outpouching and thinning of an artery wall) is higher in patients with PKD Heart valve problems (e.g., mitral valve prolapse), left ventricular hypertrophy, and colonic diverticula also are common in patients with PKD. Hydronephrosis, hydroureter HYDRONEPHROSIS, HYDROURETER Hydronephrosis the kidney enlarges as urine collects in the renal pelvis and kidney tissue. Obstruction w/in the pelvis or ureteropelvic junction results in renal pelvic distention, and extensive damage to the vasculature and renal tubules can result. Hydroureter (enlargement of the ureter) the obstruction of the ureter at the point of the iliac vessel crossing or the ureterovesical entry. Dilation of the ureter occurs at the point proximal to the obstruction as urine accumulates. Urethral stricture the obstruction is very low in the urinary tract, causing bladder distention before hydroureter and hydronephrosis Causes of hydronephrosis or hydroureter include tumors, stones, trauma, structural defects, and fibrosis. Urethral stricture occurs from chronic inflammation Obtain a history from the patient, focusing on known kidney or urologic disorders. A history of childhood urinary tract problems may indicate previously undiagnosed structural defects. Ask about his or her usual pattern of urination, especially amount, frequency, color, clarity, and odor. Ask about recent flank or abdominal pain. Diagnostic tests Treatment Meds Other Chills, fever, and malaise may be present with a urinary tract infection (UTI). Inspect each flank to identify asymmetry, which may occur with a kidney mass Gently palpate the abdomen to locate areas of tenderness. o Palpate and percuss the bladder to detect distention, or use a bedside bladder scanner. Gentle pressure on the abdomen may cause urine leakage, which reflects a full bladder and possible obstruction. Urinalysis may show bacteria or white blood cells if infection is present. When urinary tract obstruction is prolonged, microscopic examination may show tubular epithelial cells. Blood chemistries are normal unless glomerular filtration decreases. Blood creatinine and blood urea nitrogen (BUN) levels increase with a reduced glomerular filtration rate (GFR). Serum electrolyte levels may be altered with elevated blood levels of potassium, phosphorus, and calcium along with a metabolic acidosis (bicarbonate deficit). IV urography shows ureteral or renal pelvis dilation. Urinary outflow obstruction can be seen with sonography (renal echography) or computed tomography (CT). Urinary retention and potential for infection are the primary problems. Failure to treat the cause of obstruction leads to infection and end-stage kidney disease. Radiologic Interventions o When a stricture is causing hydronephrosis and cannot be corrected with urologic procedures, a nephrostomy is performed. This procedure diverts urine externally and prevents further damage to the kidney. o After nephrostomy, notify the physician immediately when the drainage decreases or stops, drainage becomes cloudy or foul-smelling, the nephrostomy site leaks blood or urine, or the patient has back pain. Complications Pyelonephritis PYELONEPHRITIS Bacterial infection in the kidney and renal pelvis (upper urinary tract) Acute pyelonephritis is the active bacterial infection Chronic pyelonephritis results from repeated or continued upper urinary tract infections or the effects of such infections. Often occurs with a urinary tract defect, obstruction, or, most commonly, when urine refluxes from the bladder back into the ureters. Assessment Physical Increased risk: pregnancy, DM, and chronic renal calculi Key features include: ◦ Fever, chills, tachycardia, and tachypnea ◦ Flank, back, or loin pain ◦ Abdominal discomfort ◦ Turning, nausea and vomiting, urgency, frequency, nocturia ◦ General malaise or fatigue Chart 70-3 Key Features Acute Pyelonephritis • Fever • Chills • Tachycardia and tachypnea • Flank, back, or loin pain Diagnostic tests Treatment Meds Other • Tender costovertebral angle (CVA) • Abdominal, often colicky, discomfort • Nausea and vomiting • General malaise or fatigue • Burning, urgency, or frequency of urination • Nocturia • Recent cystitis or treatment for urinary tract infection (UTI) Chart 70-4 Key Features Chronic Pyelonephritis • Hypertension • Inability to conserve sodium • Decreased urine concentrating ability, resulting in nocturia • Tendency to develop hyperkalemia and acidosis Urinalysis shows a positive leukocyte esterase and nitrite dipstick test and the presence of white blood cells and bacteria. Blood cultures are obtained for specific organisms. Other blood tests include the C-reactive protein and erythrocyte sedimentation rate to determine the presence of inflammation. An x-ray of the kidneys, ureters, and bladder (KUB) and IV urography are performed to diagnose stones or obstructions. A cystourethrogram is indicated for some patients. Broad spectrum antibiotics Nutrition therapy involves ensuring that the patient's nutritional intake has adequate calories from all food groups for healing to occur. Fluid intake is recommended at 2 L/day unless another health problem requires fluid restriction. Surgical Procedures: o Pyelolithotomy (removal of a stone from the renal pelvis) o Nephrectomy (removal of a kidney) o Ureteral diversion or reimplantation of the ureter to restore the bladder drainage mechanism) Maintain sufficient perfusion to the kidneys to prevent acute (hypotensive) or chronic (hypertensive) kidney injury Maintain sufficient fluid intake to promote urine output greater than 1 mL/kg/hr Assess for signs of acute kidney injury such as increasing BUN or CREAT level or decreased urinary output Complications Abscess formation Septicemia Glomerulonephritis/nephrotic syndrome GLOMERULONEPHRITIS/NEPHRITIC SYNDROME (ACUTE) GLOMERULONEPHRITIS/NEPHRITIC SYNDROME (CHRONIC) Glomerulonephritis may be caused by problems with the body's immune system. Damage to the glomeruli causes blood and protein to Develops over 20 to 30 years or even longer be lost in the urine. Changes in the kidney tissue result from hypertension, infections and inflammation, or The condition may develop quickly, and kidney function is lost within weeks or months poor blood flow to the kidneys. Onset of symptoms is about 10 days from the time of infection. Chronic glomerulonephritis always leads to end-stage kidney disease Assessment Physical Common symptoms Mild proteinuria and hematuria, hypertension, o Blood in the urine (dark, rust-colored, or fatigue, and occasional edema are often the brown urine) only manifestations. o Foamy urine (due to excess protein in the Ask about other health problems, including urine) systemic diseases, kidney or urologic disorders, o Swelling (edema) of the face, eyes, ankles, infectious diseases (e.g., streptococcal feet, legs, or abdomen infections), and recent exposures to infections. Fluid overload and circulatory congestion (which Ask about changes in urine color, odor, or may accompany the sodium and fluid retention clarity and whether dysuria or incontinence occurring with acute GN) has occurred. Ask about any difficulty in breathing or shortness Nocturia also is a common symptom. of breath. Assess for systemic circulatory overload. Assess for crackles in the lung fields, an S3 heart Auscultate lung fields for crackles, observe the sound (gallop rhythm), and neck vein distention. respiratory rate and depth, and measure blood Dysuria, Oliguria pressure and weight. Fluid retention – check weight Auscultate the heart for rate, rhythm, and the presence of an S3 heart sound. Mild to moderate HTN as a result of Na+ and fluid retention Inspect the neck veins for venous engorgement, and check for edema of the foot and ankle, on Fatigue, a lack of energy, anorexia, nausea, and/or vomiting if uremia from severe kidney impairment The less common manifestations of acute GN are more likely to occur in older adults. Circulatory congestion often is present, causing acute GN to be easily confused with congestive heart failure. Nausea, vomiting, or anorexia indicates that uremia is present. TABLE 70-1 PRIMARY GLOMERULAR DISEASES AND SYNDROMES o Acute glomerulonephritis o Rapidly progressive glomerulonephritis (RPGN) o Chronic glomerulonephritis o Nephrotic syndrome o Persistent, vague urinary abnormalities with few or no symptoms TABLE 70-2 SECONDARY GLOMERULAR DISEASES AND SYNDROMES o Systemic lupus erythematosus (SLE) o Schönlein-Henoch purpura o Goodpasture's syndrome o Systemic necrotizing vasculitis o Wegener's granulomatosis o Periarteritis nodosa (also called polyarteritis nodosa) o Amyloidosis o Diabetic glomerulopathy o HIV-associated nephropathy o Alport's syndrome o Multiple myeloma o Viral hepatitis B o Viral hepatitis C o Cirrhosis o Sickle-cell disease o Nonstreptococcal postinfectious acute glomerulonephritis o Infective endocarditis o Hemolytic-uremic syndrome o Thrombotic thrombocytopenic purpura TABLE 70-3 INFECTIOUS CAUSES OF ACUTE GLOMERULONEPHRITIS o Group A beta-hemolytic Streptococcus o Staphylococcal or gram-negative bacteremia or sepsis o Pneumococcal, Mycoplasma, or Klebsiella pneumonia o Syphilis o Visceral abscesses o Infective endocarditis o Hepatitis B o Infectious mononucleosis o Measles o Mumps o Rocky Mountain spotted fever o Cytomegalovirus infection o Histoplasmosis o Toxoplasmosis o Varicella o Chlamydia psittaci infection o Coxsackievirus infection o Any bacterial, parasitic, fungal, or viral infection (potentially) Most causes of acute GN are infectious (Table 70-3) or are related to other systemic diseases the shin, and over the sacrum. Assess for uremic symptoms, such as slurred speech, ataxia, tremors, or asterixis (flapping tremor of the fingers or the inability to maintain a fixed posture with the arms extended and wrists hyperextended). Inspect skin for a yellowish color, texture, bruises, rashes, or eruptions. Ask about itching, and document areas of dryness or any excoriation from scratching. Diagnostic tests Treatment Meds Other Urinalysis shows red blood cells (hematuria) and protein (proteinuria). The glomerular filtration rate (GFR) decreased to 50 mL/min. BUN are usually increased. The older patient may have a greater decline in GFR. The protein excretion rate for patients with acute GN may be increased from 500 mg to 3 g/24 hr in most patients. Serum albumin levels are decreased because of the protein lost in the urine and because of fluid retention causing dilution. Specimens from the blood, skin, or throat are obtained for culture, if indicated. Other serologic tests include antistreptolysin-O titers, C3 complement levels, cryoglobulins (immunoglobulin G [IgG]), antinuclear antibodies (ANAs), and circulating immune complexes. A kidney biopsy provides a precise diagnosis of the condition, assists in determining the prognosis, and helps outline treatment Penicillin, erythromycin, or azithromycin is prescribed for GN caused by streptococcal infection. For patients with fluid overload, hypertension, and edema, diuretics and a sodium and water restriction are prescribed. Antihypertensive drugs may be needed to control hypertension (see Chapter 38). The usual fluid allowance is equal to the 24-hour urine output plus 500 to 600 mL. Patients with oliguria usually have increased serum levels of potassium and blood urea nitrogen (BUN). Potassium and protein intake may be restricted to prevent hyperkalemia and uremia as a result of the elevated BUN. Drug therapy to control the problems from uremia. Diet changes, fluid intake sufficient to prevent reduced blood flow volume to the kidneys, and Eventually, the patient requires dialysis or transplantation to prevent death from uremia. Sodium restriction Water restriction Diuretics Protein restriction – til they’re not losing protein in urine Urine output decreases, but the urine appears normal unless a urinary tract infection (UTI) also is present. Urinalysis shows protein, usually less than 2 g in a 24-hour collection. The specific gravity is fixed at a constant level of dilution (around 1.010). Red blood cells and casts may be in the urine. GFR low. The serum creatinine level is elevated, usually greater than 6 mg/dL but may be as high as 30 mg/dL or more. The BUN is increased, often as high as 100 to 200 mg/dL. Sodium retention is common, but dilution of the plasma from excess fluid can result in a falsely normal serum sodium level (135 to 145 mEq/L) or a low sodium level (less than 135 mEq/L). When oliguria develops, potassium is not excreted and hyperkalemia occurs when levels exceed 5.4 mEq/L. Hyperphosphatemia, hypocalcemia Acidosis The kidneys are abnormally small on x-ray and on IV urography and when measured by sonography or computed tomography (CT). Complications Nephrotic Syndrome NEPHROTIC SYNDROME Condition of increased glomerular permeability that allows larger molecules to pass through the membrane into the urine and then be excreted. Severe loss of protein into the urine, edema formation, and decreased plasma albumin levels. Most common cause of glomerular membrane changes an immune or inflammatory process. Defects in glomerular filtration can also occur as a result of genetic defects of the glomerular filtering system, such as Fabry disease. Altered liver activity may occur with nephrotic syndrome, resulting in increased lipid production and hyperlipidemia. Assessment Physical Chart 70-5 Key Features Nephrotic Syndrome Sudden onset of these manifestations: o •Massive proteinuria (> 3.5 g protein in 24 hrs) o •Hypoalbuminemia (< 3 g/dL) o •Edema (especially facial and periorbital) o •Lipiduria o •Hyperlipidemia o •Increased coagulation o Diagnostic tests Treatment Meds Other ◦ ◦ ◦ ◦ ◦ •Reduced kidney function Immunosuppressive agents (corticosteroids) ~ b/c immune related disorder Angiotensin-converting enzyme inhibitors (to keep BP down and decrease protein lost in the urine) Heparin (may reduce urine protein loss and improve kidney function) Diet changes (low salt ) Mild diuretics (control edema and hypertension) ONLY RENAL DISORDER IN WHICH YOU INCREASE PROTEIN IN PT! [PROTEIN REPLACEMENT] If the glomerular filtration rate (GFR) is normal, dietary intake of complete proteins is needed. If the GFR is decreased, dietary protein intake must be decreased. Complications risks for renal failure o Causes of Renal Failure Unrecognized acute renal failure Diabetes Trauma Chronic Med Use Anomalies ~ structural problems Genetics ~ polycystic disease, genetic disorders DISEASE Assessment Physical ACUTE ◦ Sudden onset ◦ Reversible ◦ AKI (formerly known as acute renal failure), is a rapid decrease in kidney fxn leading to the accumulation of metabolic wastes in the body ◦ Can result from: ◦ conditions that reduce blood flow or O2 to the kidneys (prerenal failure); ◦ damage to the glomeruli, interstitial tissue, or tubules (intrarenal or intrinsic renal failure); ◦ obstruction of urine flow (postrenal failure). CHRONIC - also known as End Stage Renal Disease (ESRD) ◦ End Stage Kidney Disease (ESKD) ◦ Insidious, chronic ◦ Irreversible ◦ Requires dialysis for survival Chart 71-1 Key Features Acute Kidney Injury Chart 71-6 Key Features Severe Chronic Kidney Disease Prerenal Azotemia • Hypotension • Tachycardia • Decreased cardiac output • Decreased central venous pressure • Decreased urine output • Lethargy Intrarenal (Intrinsic) AKI and Postrenal Azotemia • Renal manifestations: •Oliguria or anuria •Increased urine specific gravity Cardiac manifestations: •Hypertension •Tachycardia •Jugular venous distention •Increased central venous pressure •ECG changes: tall T waves Respiratory manifestations: •Shortness of breath •Orthopnea •Crackles •Pulmonary edema •Friction rub Gastrointestinal manifestations: •Anorexia •Nausea •Vomiting •Flank pain Neurologic manifestations: •Lethargy •Headache •Tremors •Confusion General manifestations: •Generalized edema •Weight gain Neurologic Manifestations • Lethargy and daytime drowsiness • Inability to concentrate or decreased attention span • Seizures • Coma • Slurred speech • Asterixis (jerky movements or “flapping” of the hands) • Tremors, twitching, or jerky movements • Myoclonus • Ataxia (alteration in gait) • Paresthesias Cardiovascular Manifestations • Cardiomyopathy • Hypertension • Peripheral edema • Heart failure • Uremic pericarditis • Pericardial effusion • Pericardial friction rub • Cardiac tamponade Respiratory Manifestations • Uremic halitosis • Tachypnea • Deep sighing, yawning • Kussmaul respirations • Uremic pneumonitis • Shortness of breath • Pulmonary edema • Pleural effusion • Depressed cough reflex • Crackles Hematologic Manifestations • Anemia (fatigue, pallor, lethargy, weakness, SOB, dizziness) • Abnormal bleeding and bruising (brusing, petechiae, purpura, MM bleeding in nose or gums, intestinal [melena]) Gastrointestinal Manifestations • Anorexia • Nausea • Vomiting • Metallic taste in the mouth • Changes in taste acuity and sensation • Uremic colitis (diarrhea) • Constipation • Uremic gastritis (possible GI bleeding) • Uremic fetor (breath odor) • Stomatitis Urinary Manifestations • Polyuria, nocturia (early) • Oliguria, anuria (later) • Proteinuria • Hematuria • Diluted, straw-colored appearance (early) • Concentrated and cloudy appearance (later) Integumentary Manifestations - UREMIA • Decreased skin turgor • Yellow-gray pallor • Dry skin • Pruritus • Ecchymosis • Purpura • Soft-tissue calcifications • Uremic frost (late, premorbid) Musculoskeletal Manifestations Diagnostic tests Similar to those occurring in chronic kidney disease (CKD) (Chart 71-2) Rising BUN and serum creatinine levels and abnormal blood electrolyte values. Patients with AKI, however, usually do not have the anemia associated with CKD unless there is hemorrhagic blood loss or unless blood urea levels are high enough to break (lyse) red blood cells. X-rays help determine the cause of AKI. An abdominal x-ray is used to check the size of the kidneys. Enlarged kidneys, possibly due to obstruction, may result from hydronephrosis. Xrays may show stones obstructing the renal pelvis, ureters, or bladder. Renal ultrasonography useful in the diagnosis of urinary tract obstruction. Dilation of the renal calyces and collecting ducts, as well as stones, can be detected. CT scans without contrast dye can identify obstruction or tumors. • Muscle weakness and cramping • Bone pain • Pathologic fractures • Renal osteodystrophy Reproductive Manifestations • Decreased fertility • Infrequent or absent menses • Decreased libido • Impotence How is CKD Diagnosed? Astute clinician Sees the big picture Knows who is at risk Advocates for the patient Collaborates with the team Treatment Meds Other In the early stages of CKD, urinalysis may show excessive protein, glucose, red blood cells (RBCs), white blood cells (WBCs), and decreased or fixed specific gravity. Urine osmolarity is usually decreased. GFR 24 creatinine clearance As CKD progresses, the urine output decreases dramatically. In severe CKD, measurements of the serum creatinine and BUN levels may be used to determine the presence and degree of uremia. Serum creatinine levels may increase gradually over a period of years, reaching levels of 15 to 30 mg/dL or more, depending on the patient's muscle mass. BUN levels are directly related to dietary protein intake. Prerenal azotemia fluid challenges and diuretics are often used to promote kidney blood flow. Diuretics such as furosemide (Lasix) also may be prescribed along with a fluid bolus. If oliguric kidney injury is diagnosed, the fluid challenges and diuretics are d/c. Patients often require central venous pressure (CVP) monitoring or measurement of pulmonary arterial pressure by means of a pulmonary artery catheter for accurate evaluation of their hemodynamic status. They also require constant nursing supervision for assessment of the response to fluid and drug therapy. Carefully monitor for signs of possible fluid overload. Calcium channel blockers may be used to treat AKI resulting from nephrotoxic acute tubular necrosis (ATN) prevent the movement of calcium into the kidney cells, maintain kidney cell integrity, and improve the glomerular filtration rate (GFR) by improving kidney blood flow. Chart 71-7 Best Practice for Patient Safety & Quality Care - Managing Fluid Volume •Weigh the patient daily at the same time each day, using the same scale, with the patient wearing the same amount and type of clothing, and graph the results. •Observe the weight graph for trends (1 liter of water weighs 1 kilogram). •Accurately measure all fluid intake and output. •Teach the patient and family about the need to keep fluid intake within prescribed restricted amounts and to ensure that the prescribed daily amount is evenly distributed throughout the 24 hours. •Monitor for these manifestations of fluid overload at least every 4 hours: •Decreased urine output •Rapid, bounding pulse •Rapid, shallow respirations •Presence of dependent edema •Auscultation of crackles or wheezes •Presence of distended neck veins in a sitting position •Decreased oxygen saturation •Elevated blood pressure •Narrowed pulse pressure •Assess level of consciousness and degree of cognition. •Ask about the presence of headache or blurred vision. Nursing Considerations Infection Monitor drug levels Alterations in nutrition ◦ Limit protein, sodium, and potassium Potential injury (mentation changes from uremia, electrolyte changes, acidosis) Monitor electrolytes Fatigue and weakness Monitor ECG changes Neurological assessment Preparation for dialysis Monitor hematocrit and hemoglobin Assist with ADL’s Administration of epogen Impaired skin integrity ~ Prioritize: Meds diet EKG HCT/HGB Treatment of Hyperkalemia Dialysis Cation Exchange Resin ◦ Kayexalate ~ rid of excess K+ Shift intracellularly ◦ Glucose and insulin ◦ Alkali (sodium bicarbonate) ◦ Antagonize cellular membrane effect ◦ Calcium gluconate for membrane stabilizing effect Complications Systemic Manifestations – End Stage Renal Disease o Neurological confusion, lethargy, decreased level of consciousness, stupor Gastrointestinal nausea, vomiting, anorexia, distention, constipation, or diarrhea Respiratory crackles, pulmonary edema, pleural effusion, risk for infection Cardiovascular tachycardia, dysrhythmias, rub, pericarditis, increased blood pressure Integumentary dry skin, pruritus, edema, bruising, pallor, uremic frost Fluid/Electrolyte Imbalances Hyperkalemia: low excretion Hyponatremia: fluid retention Hypocalcemia: low excretion of phosphorus Hyperphosphatemia o Hematological??? Patient teaching for renal failure pts – including diet and meds o Chart 71-5 Patient and Family Education: Preparing for Self-Management Prevention of Kidney and Urinary Problems Be alert to the general appearance of your urine. Note any changes in its color, clarity, or odor. Changes in the frequency or volume of urine passage occur with changes in fluid intake. More frequent or infrequent voiding not associated with changes in fluid intake may signal potential problems. Any discomfort or distress with the passage of urine is not normal. Pain, burning, urgency, aching, or difficulty with initiating urine flow or complete bladder emptying is of some concern. The kidneys need 1 to 2 quarts of fluid a day to flush out your body wastes. Water is the ideal flushing agent. Reduce your intake of carbonated soft drinks. Changes in kidney function are often silent for many years. Periodically ask your health care provider to measure your kidney function with a blood test (serum creatinine) and a urinalysis. If you have a history of kidney disease, diabetes mellitus, hypertension (high blood pressure), or a family history of kidney disease, you should know your serum creatinine level and your 24-hour creatinine clearance. At least one checkup per year that includes laboratory blood and urine testing of kidney function is recommended. If you are identified as having decreased kidney function, ask about whether any prescribed drug, diet, diagnostic test, or therapeutic procedure will present a risk to your current kidney function. Check out all nonprescription drugs with your physician or pharmacist before using them. o Health Promotion and Maintenance The health-promotion activities to prevent or delay the onset of CKD focus on controlling the diseases that lead to its development, such as diabetes and hypertension. Identifying patients who have these disorders at an early stage is critical to CKD prevention. Teach patients to adhere to drug and diet regimens and engage in regular physical activity to prevent the blood vessel changes that lead to kidney damage. Instruct patients with diabetes to keep their blood glucose levels within the prescribed range. Teach patients with hypertension that drug therapy is not a cure and must be continued along with lifestyle changes. Urge patients with diabetes or hypertension to have yearly testing for microalbuminuria. Teach everyone treated for an infection anywhere in the kidney/urinary system to take all antibiotics as prescribed. Urge everyone to drink at least 3 L of water daily unless a health problem requires fluid restriction. Caution people who use over-the-counter NSAIDs to avoid abusing these drugs because they reduce blood flow to the kidney and their long-term use reduces kidney function Hemodialysis o what should you do as nurse about medications Hemodialysis Nursing Care Many drugs, such as antibiotics, are dialyzable (i.e., can be partially removed from the blood during dialysis) and should not be administered just before or during dialysis. Vasoactive drugs can cause hypotension during HD and may also be held until after treatment. Coordinate with the physician to assess the patient's drug regimen and determine which drugs should be held until after HD treatment. Table 71-12 lists common dialyzable and vasoactive drugs that should be given after rather than before HD. o *Post hemodialysis symptoms Post-Dialysis Care Closely monitor the patient immediately and for several hours after dialysis for any side effects from the treatment. Common problems include hypotension, headache, nausea, malaise, vomiting, dizziness, and muscle cramps. Obtain vital signs and weight for comparison with pre-dialysis measurements. Blood pressure and weight are expected to be reduced as a result of fluid removal. Hypotension may require rehydration with IV fluids, such as normal saline. The patient's temperature may also be elevated because the dialysis machine warms the blood slightly. If he or she has a fever, sepsis may be present and a blood sample is needed for culture and sensitivity. The heparin required during HD increases the clotting time, which increases the risk for excessive bleeding. All invasive procedures must be avoided for 4 to 6 hours after dialysis. Continually monitor the patient for hemorrhage during and for 1 hour after dialysis o *Dialysis disequlibrium syndrome Complications of Hemodialysis – disequilibrium syndrome and viral infections o o o o o Dialysis disequilibrium syndrome may develop during HD or after HD has been completed. The cause appears to be the rapid decrease in fluid volume and blood urea nitrogen (BUN) levels during HD. The change in urea levels can cause cerebral edema and increased intracranial pressure. Neurologic symptoms can result (e.g., headache, nausea, vomiting, restlessness, decreased level of consciousness, seizures, coma, or death). The problem may be PREVENTED by starting HD for short periods with low blood flows so that rapid changes in plasma composition are avoided. ***Assess for and document symptoms of disequilibrium syndrome (headache, nausea, vomiting, restlessness, decreased level of consciousness, seizures, coma) during and after HD, because early recognition and treatment with anticonvulsants and barbiturates may prevent a life-threatening situation. o Chart 71-9 Best Practice for Patient Safety & Quality Care Caring for the Patient Undergoing Hemodialysis Weigh the patient before and after dialysis. Know the patient's dry weight. Discuss with the health care provider whether any of the patient's drugs should be withheld until after dialysis. Be aware of events that occurred during previous dialysis treatments. Measure blood pressure, pulse, respirations, and temperature. Assess for symptoms of orthostatic hypotension. Assess the vascular access site. Observe for bleeding. Assess the patient's level of consciousness. Assess for headache, nausea, and vomiting. o Hemodialysis Nursing Care (PP) Drugs Post-dialysis assess for hypotension, headache, nausea, malaise, vomiting, dizziness, and muscle cramps or bleeding Dialysis disequilibrium syndrome Complications: o Thrombosis or stenosis o Infection – most serious are hepatitis and HIV o Aneurysm formation o Ischemia o Heart failure o Chart 71-8 Best Practice for Patient Safety & Quality Care Caring for the Patient with an Arteriovenous Fistula or Arteriovenous Graft • Do not take blood pressure readings using the extremity in which the vascular access is placed. • Do not perform venipunctures or start an IV line in the extremity in which the vascular access is placed. • Palpate for thrills and auscultate for bruits every 4 hours while the patient is awake. • Assess the patient's distal pulses and circulation in the arm with the access. • Elevate the affected extremity postoperatively. • Encourage routine range-of-motion exercises. • Check for bleeding at needle insertion sites. • Assess for manifestations of infection at needle sites. • Instruct the patient not to carry heavy objects or anything that compresses the extremity in which the vascular access is placed. • Instruct the patient not to sleep with his or her body weight on top of the extremity in which the vascular access is placed. Nursing Considerations (PP) o Planning for dialysis o o o Medications Meals Activities Procedures Dialysis nurse relies on accurate nursing data Determines “dry weight” Blood pressure baseline Lab values Other considerations Patient requires close surveillance post-dialysis Procedure is exhausting Peritoneal dialysis How it’s done Procedure • Each PD exchange process consists of three phases: fill, dwell, and drain. • A siliconized rubber (Silastic) catheter is surgically placed into the abdominal cavity for infusion of dialysate (Fig. 71-10). • Usually 1 to 2 L of dialysate is infused by gravity (fill) into the peritoneal space over a 10- to 20minute period, according to the patient's tolerance. • The fluid stays (dwells) in the cavity for a specified time prescribed by the physician. • The fluid then flows out of the body (drains) by gravity into a drainage bag. • The peritoneal outflow contains the dialysate and the excess water, electrolytes, and nitrogen-based waste products. • The dialyzing fluid is called peritoneal effluent on outflow. • The three phases of the process (infusion, or “fill”; dwell; and outflow, or drain) make up one PD exchange. • The number and frequency of PD exchanges are prescribed by the physician, depending on manifestations and laboratory data. • The more hypertonic the solution, the greater the osmotic pressure (pulling pressure) for water filtration and fluid removal from the patient during an exchange. Dialysate Additives • Heparin may be added to the dialysate to prevent clotting of the catheter or tubing. Usually intraperitoneal (IP) heparin is needed only after new catheter placement or if peritonitis occurs. IP heparin is not absorbed systemically and does not affect blood clotting. • Other agents that may be given in the dialysate include potassium and antibiotics. Commercially prepared dialysate does not contain potassium. Some patients need potassium added to the dialysate to prevent hypokalemia. Antibiotics may be given by the IP route when peritonitis is present or suspected. Potassium and antibiotics are not mixed in the same dialysate bag because interactions may reduce the antibiotic effect. Nursing care before, during, after Potential complications o Peritoneal Dialysis (PP) Uses the peritoneal membrane as filter Less efficient High risk of peritonitis Procedure involves siliconized rubber catheter placed into the abdominal cavity for infusion of dialysate. Types of peritoneal dialysis: Continuous ambulatory peritoneal dialysis (CAPD) Performed by the patient with the infusion of four 2-L exchanges of dialysate into the peritoneal cavity. Each time, the dialysate remains for 4 to 8 hours, and these exchanges occur 7 days a week (Fig. 71-11 through 7113). Automated peritoneal dialysis Intermittent peritoneal dialysis Continuous-cycle peritoneal dialysis May be used in the acute care setting, the outpatient dialysis center, or the patient's home. APD uses a cycling machine for dialysate inflow, dwell, and outflow according to preset times and volumes. A warming chamber for dialysate is part of the machine (Fig. 71-14). The functions are programmed for the patient's specific needs. A typical prescription calls for 30-minute exchanges (10/10/10 for inflow, dwell, and outflow) for a period of 8 to 10 hours. The machines have many safety monitors and alarms and are relatively simple to learn to use (Fig. 71-15). Combines osmotic pressure gradients with true dialysis. Form of automated dialysis that uses an automated cycling machine. The patient usually requires exchanges of 2 L of dialysate at 30- to 60-minute intervals, allowing 15 to 20 minutes of drain time. For most patients, 30 Exchanges occur at night while the patient sleeps. The final exchange of the night is left to dwell through the day and is drained the next During the dwell period, the patient can use a continuous connect system or a disconnect system. Advantages Permits in-home dialysis while the patient sleeps, allowing him or her to be dialysis-free during waking hours. The incidence of peritonitis is reduced with APD because fewer connections and disconnections are needed. Also, APD can be used to deliver larger volumes of dialysis solution for patients who need higher clearances. to 40 exchanges of 2 L three times weekly are needed. IPD treatments can be automated or manual. evening as the process is repeated. Advantages Permits 24-hour dialysis, as in CAPD, but the sterile catheter system is opened less often. Complications of Peritoneal Dialysis (PP) Peritonitis – most common cause is connection site contamination; use meticulous sterile technique when caring for PD catheter and when hooking up or clamping off dialysate bags • Manifestations: cloudy dialysate outflow (effluent), fever, abdominal tenderness, abdominal pain, general malaise, nausea, and vomiting. • Cloudy or opaque effluent is the earliest sign of peritonitis. Examine all effluent for color and clarity to detect peritonitis early. When peritonitis is suspected, send a specimen of the dialysate outflow for culture and sensitivity study, Gram stain, and cell count to identify the infecting organism. Pain - during the inflow of dialysate is common when patients are first started on PD therapy. • Usually this pain no longer occurs after a week or two of PD. • Cold dialysate increases discomfort. Warm the dialysate bags before instillation by using a heating pad to wrap the bag or by using the warming chamber of the automated cycling machine. [Microwave ovens are not recommended for the warming of dialysate.] Exit site and tunnel infections - should be clean, dry, and without pain or inflammation. • can lead to peritonitis, catheter failure, and hospitalization. • Dialysate leakage and pulling or twisting of the catheter increase the risk for ESIs. Poor dialysate flow - usually related to constipation. • To prevent constipation, a bowel preparation is prescribed before placement of the PD. • An enema before starting PD may also prevent flow problems. • Teach patients to eat a high-fiber diet and use stool softeners to prevent constipation. • Other causes of flow difficulty include kinked or clamped connection tubing, the patient's position, fibrin clot formation, and catheter displacement. • Ensure that the drainage bag is lower than the patient's abdomen to enhance gravity drainage. • Turning the patient to the other side or ensuring that he or she is in good body alignment may help. • Having the patient in a supine low-Fowler's position reduces abdominal pressure. • Increased abdominal pressure from sitting or standing or from coughing contributes to leakage at the PD catheter site. • Fibrin clot formation may occur after PD catheter placement or with peritonitis. • Milking the tubing may dislodge the fibrin clot and improve flow. • An x-ray is needed to identify PD catheter placement. If displacement has occurred, the physician repositions the PD catheter. Dialysate leakage - seen as clear fluid coming from the catheter exit site • Leakage occurs more often in obese patients, those with diabetes, older adults, and those on longterm steroid therapy. • During periods of catheter leak, patients may require hemodialysis (HD) support. Other complications - include bleeding, which is expected when the catheter is first placed, and bowel perforation, which is serious. • When PD is first started, the outflow may be bloody or blood tinged. This condition normally clears within a week or two. • After PD is well-established, the effluent should be clear and light yellow. • Observe for and document any change in the color of the outflow. Brown-colored effluent occurs with a bowel perforation. If the outflow is the same color as urine and has the same glucose level, a bladder perforation is probable. Cloudy or opaque effluent indicates infection. Nursing Care During Peritoneal Dialysis (PP) Before treating, evaluate baseline vital signs, weight, and laboratory tests. Continually monitor the patient for respiratory distress, pain, and discomfort. - Check the dressing around the catheter exit site every 30 minutes for wetness during the procedure. Monitor prescribed dwell time, and initiate outflow. Observe the outflow amount and pattern of fluid. Chart 71-10 Best Practice for Patient Safety & Quality Care Caring for the Patient with a Peritoneal Dialysis Catheter Mask yourself and your patient. Wash your hands. Put on sterile gloves. Remove the old dressing. Remove the contaminated gloves. Assess the area for signs of infection, such as swelling, redness, or discharge around the catheter site. Use aseptic technique: o Open the sterile field on a flat surface, and place two precut 4 × 4–inch gauze pads on the field. o Place three cotton swabs soaked in povidone-iodine on the field. Put on sterile gloves. Use cotton swabs to clean around the catheter site. Use a circular motion starting from the insertion site and moving away toward the abdomen. Repeat with all three swabs. Apply precut gauze pads over the catheter site. Tape only the edges of the gauze pads. TABLE 71-9 A COMPARISON OF HEMODIALYSIS AND PERITONEAL DIALYSIS AS RENAL REPLACEMENT THERAPY OPTIONS Hemodialysis Peritoneal Dialysis Advantages More efficient clearance Easy access Short tie needed for tx Few hemodynamic complications Complications Disequilibrium syndrome Protein loss Muscle cramps Peritonitis ~ HIGH RISK Hemorrhage Hyperglycemia Air embolus Respiratory distress Hemodynamic changes (hypotension, anemia) Bowel perforation Cardiac dysrhythmias Infection Infection Contraindications Hemodynamic instability Extensive peritoneal adhesions Peritoneal fibrosis Recent abdominal surgery Access Vascular access route Intra-abdominal catheter Procedure Complex Simple Specially trained RN required Training less complex than for hemodialysis Nursing Implications Vascular access care Abdominal catheter care Restrict Diet More flexible diet LAB TESTS GFR o o The glomerular filtration rate (GFR) is used as an indicator of kidney function and as a guide to safe levels of protein intake. A patient with a severely reduced GFR who is not undergoing dialysis is usually permitted 0.55 to 0.60 g of protein per kilogram of body weight (e.g., 40 g of protein daily for a 150-pound [about 70-kg] adult). If protein is lost in the urine, protein is added to the diet in amounts equal to that lost in the urine. Protein requirements are calculated based on actual body weight (corrected for edema), not ideal body weight. o Best measure of CKD Creatinine o Adult o Female: 0.5-1.1 mg/dL or 44-97 μmol/L (SI units) o Male: 0.6-1.2 mg/dL or 53-106 μmol/L (SI units) o Elderly: decrease in muscle mass may cause decreased values o This test measures the amount of creatinine in the blood. o Creatinine is a catabolic product of creatine phosphate, which is used in skeletal muscle contraction. The daily production of creatine, and subsequently creatinine, depends on muscle mass, which fluctuates very little. Creatinine, as with blood urea nitrogen (BUN, see p. 993), is excreted entirely by the kidneys and therefore is directly proportional to renal excretory function. Thus, with normal renal excretory function, the serum creatinine level should remain constant and normal. o Besides dehydration, only such renal disorders as glomerulonephritis, pyelonephritis, acute tubular necrosis, and urinary obstruction will cause abnormal elevations in creatinine. There are slight increases in creatinine levels after meals, especially after ingestion of large quantities of meat. Furthermore, there may be some diurnal variation in creatinine—nadir at 7 AM and peak at 7 PM. o The serum creatinine test, as with BUN, is used to diagnose impaired renal function. Unlike BUN, however, the creatinine level is affected very little by hepatic function. The creatinine test is used as an approximation of glomerular filtration rate (GFR). The serum creatinine level has much the same significance as the BUN level but tends to rise later. Therefore, elevations in creatinine suggest chronicity of the disease process. In general, a doubling of creatinine suggests a 50% reduction in GFR. The creatinine level is interpreted in conjunction with the BUN test. These tests are referred to as renal function studies. The BUN/creatinine ratio is a good measurement of kidney and liver function. The normal adult range is 6-25, with 15.5 being the optimal adult value for this ratio. BUN o Adult: 10-20 mg/dL or 3.6-7.1 mmol/L (SI units) o Elderly: may be slightly higher than those of adult o The BUN measures the amount of urea nitrogen in the blood. o Urea is formed in the liver as the end product of protein metabolism. During ingestion, protein is broken down into amino acids. In the liver these amino acids are catabolized, and free ammonia is formed. The ammonia is combined to form urea, which is then deposited into the blood and transported to the kidneys for excretion. Therefore, BUN is directly related to the metabolic function of the liver and the excretory function of the kidney. It serves as an index of the function of these organs. Patients who have elevated BUN levels are said to have azotemia. o Nearly all renal diseases cause inadequate excretion of urea, which causes the blood concentration to rise above normal. If the disease is unilateral, however, the unaffected kidney can compensate for the diseased kidney, and BUN may not become elevated. o BUN also increases in conditions other than primary renal disease. For example, when excess amounts of protein are available for hepatic catabolism (from a high-protein diet or gastrointestinal [GI] bleeding), large quantities of urea are made. o BUN levels also may vary according to the state of hydration, with increased levels seen in dehydration and decreased levels seen in overhydration. o Finally, one must be aware that the synthesis of urea depends on the liver. Patients with severe primary liver disease will have a decreased BUN. With combined liver and renal disease (as in hepatorenal syndrome), BUN can be normal not because renal excretory function is good but because poor hepatic functioning has resulted in decreased formation of urea. DISEASE Assessment Physical Diagnostic tests Treatment Meds Other Complications