Oxygenation and perfusion Diagnoses and interventions

Lung cancer

-Diagnosis Diagnosis is made through several methods: • Chest x-ray • Computed tomography (CT) scan of the chest • Sputum for cytology • Bronchoscopy • Positron emission tomography (PET) scans • Bone scans and abdominal scans • Mediastinoscopy A chest x-ray or a CT scan of the chest may identify a pulmonary lesion. A cytology test on sputum may identify specific tumor cells. Bronchoscopy or mediastinoscopy allows direct visualization of the tissues to aid in the diagnosis of lung cancer. Bronchoscopy is the assessment of the larger airways, the trachea and bronchi, through a scope inserted through the mouth or nose. Mediastinoscopy is a surgical procedure that allows for direct visualization of the mediastinum. A scope is inserted through an incision in the chest that allows direct examination and collection of samples for biopsy. Bone scans and abdominal scans are performed to look for metastatic lesions. The PET scan is used to identify changes in the body's metabolism and function rather than structure. A PET scan can detect areas of increased metabolic activity as occurs with rapidly dividing cancer cells. • Oxygen saturation Decreased SpO2 is due to poor gas exchange. An SpO2 of less than 90% indicates significant oxygenation problems. • Temperature Increased temperature is a sign of infection. • Breath sounds The presence of wheezes may indicate airway obstruction. Rhonchi indicate increased secretions in the upper airways. • Cough Cough indicates an irritation of the tracheobronchial tree. The presence of hemoptysis indicates the rupture of small blood vessels. • Pain Pain increases respiratory rate; anxiety decreases quality of life. • Appetite/weight Appetite may be decreased because of the side effects of chemotherapy or loss of energy due to increased work of breathing. Monitoring the weight helps to identify nutritional deficiencies. • Focused postoperative assessment: • Vital signs Hypotension and/or tachycardia may indicate excessive blood or fluid loss. • Breath sounds Diminished or absent breath sounds may indicate postoperative atelectasis. • Suture line A suture line that is reddened, warm to touch, and/or draining thick, yellow drainage indicates infection. • Chest tube • Monitor amount and color of chest tube drainage. Excessive bloody drainage may indicate a bleed within the chest. Cloudy drainage may indicate infection. • Monitor water-seal chamber. Persistent bubbling in the water-seal chamber indicates an air leak in the chest tube system. -Treatment The treatment for lung cancer is interprofessional and is dependent on the type, size, location, and stage of the tumor. The components of nonsurgical treatment typically consist of a combination of radiation and chemotherapy. Pain management is also an important focus in treatment. The chemotherapeutic agent used to treat lung cancer is dependent on the type and/or size of the tumor. It may be used in conjunction with surgery (discussed in the following section), or it may be the primary treatment option for more advanced cancers or if the patient is too ill for surgery. Radiation therapy used in lung cancer treatment has great versatility. In situations where surgery is not an option, radiation can be used. Radiation can also be used palliatively to relieve symptoms or for pain control. Pain control is a major component in lung cancer management. A pain relief ladder developed by the World Health Organization is helpful as a guideline for pain control (see Chapter 11, Fig. 11.7). Step 1 involves the use of nonopioid analgesics (acetaminophen or NSAIDs) for mild to moderate pain. Step 2 consists of a moderately potent opioid (codeine, hydrocodone, and oxycodone) plus a nonopioid for persistent pain or pain not controlled by Step 1. Step 3 includes the use of stronger opioids (morphine, fentanyl) plus a nonopioid for uncontrolled or severe pain. The use of adjuvant or additional medications is important to consider at all levels of treatment to relieve patient anxiety. Pain medication needs to be administered around the clock rather than on demand to avoid peaks of pain. Palliative care services are appropriate to consider with the diagnosis of a life-threatening illness like lung cancer. Palliative care improves the quality of life of patients and their families. In addition to providing pain relief, palliative care can also help in the management of other distressing and debilitating symptoms, such as shortness of breath, nausea, and vomiting. Surgery is the preferred treatment if there is no metastasis. Surgery is primarily used for non-small-cell tumors. There are several types of pulmonary surgery depending on the tumor site and size (Fig. 26.6): • Lobectomy is the removal of an entire lobe of the lung. • Pneumonectomy is the removal of the entire lung. • Wedge resection is the removal of a small section of a lobe of the lung. Chemotherapy may be administered prior to surgery to reduce the size of the tumor to aid in resection. The administration of a chemotherapeutic agent in an effort to shrink the tumor prior to surgery is a type of neoadjuvant therapy. Additionally, chemotherapy can be used as adjuvant therapy after surgery to kill any remaining cancer cells. Similar to chemotherapy, radiation is also used to shrink the tumor prior to surgery or after surgery to kill any remaining cancer cells. • Provide oxygen. Increase the SpO2 to 90%. • Administer medications as ordered. • Pain medications/Anti-anxiety medications Pain and anti-anxiety medications provide relief from both pain and anxiety, allowing better relaxation, increased expansion of the lungs to improve oxygenation, and improved quality of life. • Bronchodilators Bronchodilators, bronchial smooth muscle relaxants, open the airway and decrease the work of breathing. • Provide small, frequent meals with dietary supplements. Small, frequent meals avoid excessive pressure on the diaphragm associated with a large meal. Dietary supplements increase nutritional caloric intake, providing energy for the work of breathing. • Position—semi-Fowler's The semi-Fowler's position increases oxygenation by allowing full lung expansion. • Focused postoperative actions • Maintain a closed chest tube system. A closed system prevents any inadvertent air leaks. • Never clamp the chest tube. Clamping the chest tube may result in increased air or fluid in the pleural space, worsening the pneumothorax, and may lead to a tension pneumothorax.

Guillain-Barré syndrome (GBS)

-Diagnosis The patient with GBS is admitted to the inpatient setting for a thorough evaluation. Established diagnostic criteria for GBS include progressive weakness of two or more limbs caused by neuropathy, areflexia, and history of recent viral or bacterial infection. Additionally, a lumbar puncture is performed to obtain cerebrospinal fluid (CSF). Cerebrospinal fluid findings include elevated protein and normal cell count. Electromyography results reveal slowed nerve conduction velocity soon after the patient develops paralysis. • Perform respiratory assessment with vital capacity measurement. Respiratory assessment is a priority because respiratory compromise secondary to weakness of the diaphragm and intercostal muscles may require intubation. Vital capacity measurement is an important function to monitor. The provider should be notified of a value below 1 L. Diaphragmatic weakness results in hypoxemia. • Cranial nerves VII, IX, X, XI, and XII Cranial nerve assessment should be performed to identify deficits. Focus on facial expression, speech, gag, and swallow. • Motor and sensory assessment Motor and sensory impairment may develop related to slowing of impulses or a conduction block secondary to demyelination of peripheral nerves. • Pain assessment Patients often complain of pain. This may be due to sensory nerve fiber involvement. -Treatment Management of GBS focuses on supportive care and reducing the severity, potential complications, suffering, and recovery time. Although GBS is an autoimmune disorder, steroids have not been found to help speed recovery. The use of steroids is debatable, and current research is leaning toward patients with GBS not receiving corticosteroid therapy. There are two main approaches used for treatment. These modalities are IVIG and plasmapheresis. Intravenous immunoglobulin therapy can shorten the length of the recovery phase by 50%, and this therapy is recommended for patients who need help to walk within 2 to 4 weeks of clinical presentation of GBS. This treatment may work by several mechanisms, which include blocking of macrophage receptors, the inhibition of antibody production, the inhibition of complement binding, and the neutralization of pathological antibodies. The dosing is 2 g/kg intravenously over 5 days. Typical adverse effects of this medication include flu-like symptoms. Rare adverse reactions are aseptic meningitis and acute renal failure. Fluid overload may occur in patients with heart failure or renal insufficiency. The American Academy of Neurology recommends plasmapheresis for nonambulatory adult patients with GBS who start treatment within 4 weeks of onset of neuropathic symptoms. Plasmapheresis is also recommended for ambulatory patients who start treatment within 2 weeks of the onset of neuropathic clinical manifestations. This therapy can reduce recovery time, yet requires the insertion of a plasmapheresis catheter, skilled nursing staff, and specialized equipment that may not be available at all healthcare facilities. Plasmapheresis diminishes the length of hospitalization and the need for mechanical ventilation if initiated within the first week of clinical manifestations. There is an increased risk of infection and hemorrhage as a result of the removal of immunoglobulins and clotting factors. Adverse reactions the patient may experience include hypotension, bradycardia, fever, chills, and rash. Additional complications from this treatment include septicemia, pneumonia, cardiac arrhythmias, malaise, bleeding/clotting abnormalities, and hypocalcemia. • Turn frequently and perform range of motion every shift to maintain joint and muscle integrity. Immobility places the patient at risk for contractures, skin breakdown, and VTE. • Consult with the provider on the need for VTE prevention (subcutaneous heparin, antiembolism hose, sequential compression devices). Prolonged immobility leads to venous stasis and the development of VTE. • Reposition patient frequently. Measures are implemented to promote comfort and prevent complications of immobility, including thromboembolism and impaired skin integrity. • Consult with provider regarding use of analgesics or nonopioids. Carbamazepine or gabapentin may be used to relieve neuropathic pain. • Offer diversions such as music or other relaxation techniques. Pain management is addressed with pharmacological as well as nonpharmacological methods. • Establish a method of communication, and provide a method to call the nurse (e.g., soft call bell). Because of limb weakness, the patient may not have the strength to locate and use the call light. A soft squeeze call bell allows the patient to call the nurse with only a gentle squeeze.

Idiopathic (immune) thrombocytopenia purpura

-Diagnosis The treatment of ITP depends on the level of thrombocytopenia present. If platelet counts remain above 100,000/mm3, an observational strategy is usually employed through routine CBC analyses. A CBC with a manual differential can confirm the diagnosis of thrombocytopenia, which is defined as platelets less than 150,000/mm3. In addition to the CBC, a bone marrow biopsy confirms the diagnosis of ITP. Prolonged prothrombin time, partial prothrombin time, and thrombin time are helpful in diagnosing DIC, as well as a reduced fibrinogen level, elevated fibrin split products, and elevated dimers (cross-linked fibrin fragments). Clotting factors (e.g., factors VIII, IX) may aid in the diagnosis of both hemophilia and DIC. A blood smear is helpful in determining the morphology of the platelets. An additional test, in addition to a CBC to diagnose HIT, is the enzyme-linked immunosorbent assay (ELISA), which is an immunoassay test to determine the presence of the antibodies. • Platelet count A decreased platelet count is seen on the CBC. Further testing indicates whether it is due to increased platelet destruction or decreased platelet production. In pregnant patients, monitor liver function tests and platelet count during the pregnancy. Monitor for easy bruising, and report any clinical manifestations of bleeding to the healthcare provider. Watch for excessive postpartum hemorrhage or clots. Place patient on bleeding precautions if the platelet count is below normal, hematocrit is low, or liver function tests are elevated. • Ecchymosis Ease of bruising increases as the number of platelets decreases and tissue injury increases with contact. • Petechiae/purpura Intradermal bleeding occurs as a result of platelet reduction. • Frank bleeding (nosebleeds; bleeding gums; black, tarry stools; or hematuria) Parts of the body where mucous membranes are thin or cells rapidly divide are more prone to bleeding when platelet counts are decreased. -Treatment If the thrombocytopenia becomes more profound, treatment with glucocorticoids has proven to be beneficial. Glucocorticoids increase platelet counts by decreasing the antiplatelet antibody production, improving production of platelets by the bone marrow, and decreasing the phagocytosis that is consuming the platelets. In extreme cases, performing a splenectomy has improved platelet counts because the spleen is the primary site of platelet destruction. In hemophilia cases, depending on the type of hemophilia, replacement of the missing clotting factors is indicated. Replacement of factor VIII resolves bleeding in hemophilia A, whereas factor IX is used in hemophilia B. These clotting factors are delivered intravenously from recombinant DNA products, which do not contain human blood components. For minor injuries, treatment should be obtained as soon as possible with as many as three treatments (one treatment daily). Major traumas need replacement of clotting factors for 7 to 10 days or until healing is assured. Prophylactic treatment with clotting factors may be indicated for some surgeries with factor replacement for up to 7 to 10 days postoperatively. Prompt treatment with clotting factors minimizes complications caused by bleeding, such as joint deformities, which were prevalent prior to factor replacement. Resolution of the underlying condition that initiates the clotting cascade is imperative in treating DIC, for example, immediate antibiotic therapy to treat the sepsis. Providing supportive care in the form of administering blood, platelets, fresh frozen plasma, and cryoprecipitate (plasma product rich in factor VIII) may be employed to maintain hemostasis. These patients are managed in an intensive care setting where they can be closely observed with hemodynamic monitoring equipment. Mortality rates are high in patients who develop DIC, although exact numbers are not known because the cause of death is usually attributed to the underlying disorder. Stopping the heparin administration is the first step in treating HIT. However, because the formation of additional thrombi occurs frequently in these patients, an anticoagulant is required to prevent further thrombus formation and the production of the antibodies, allowing the platelet count to recover. Warfarin should not be used because it can cause skin gangrene in this population. Three anticoagulants have been approved for use in patients diagnosed with HIT: danaparoid (not available in the United States), lepirudin, and argatroban. Platelet transfusions are discouraged because they may increase thrombus formation. • Implement bleeding precautions (see Box 34.1). Due to decreased platelet count, the patient is at increased risk of bleeding from minor injuries, venepuncture, and so forth. • Minimize blood loss from lacerations or venipuncture. If bleeding occurs, apply direct pressure and/or application of ice to cause vasoconstriction to stop bleeding. This includes direct pressure on sites after blood draws and venipuncture. • Avoid intramuscular injections. Intramuscular injections can cause bleeding into the muscle, and the bleeding can be difficult to manage. • Avoid rectal temperatures, enemas, suppositories, and douches. These procedures can tear the thin mucosa of the rectum, anus, and vagina, leading to bleeding. • Provide a safe environment. Keep the patient's room clutter-free to minimize patient injury that leads to bruising. • Use minimal inflation when assessing blood pressure. Overinflation of the blood pressure cuff can cause bruising. Inflate the cuff only until the pulse is obliterated. Avoid automatic blood pressure cuffs. • Minimize blood draws. Blood draws should be kept to a minimum. The use of venous access devices should be considered if frequent blood draws are necessary to prevent the need for multiple venipuncture. Report low platelet counts to the healthcare provider.

Peripheral arterial disease

-Diagnosis The vascular assessment for PAD includes pulse palpation, auscultation for femoral bruits, and inspection of the legs and feet. To confirm the diagnosis of PAD, abnormal physical examinations findings must be confirmed with diagnostic testing. Specifically, other comorbid causes of atypical leg pain should be ruled out before diagnosing PAD. Noninvasive testing for arterial disease has become a common method of diagnosis. This includes the ankle-brachial index (ABI), plethysmography, and graded-exercise treadmill test. These tests provide information about the arterial system with minimal risk. Anatomical imaging studies, including duplex ultrasound, computed tomography angiography, magnetic resonance angiography, and invasive angiography, are other diagnostic tools but are sometimes reserved for highly symptomatic patients who are being considered for revascularization. • Bilateral blood pressures Patients with diagnosed PAD have an increased risk of subclavian artery stenosis. Upper arm blood pressure difference of greater than 15 to 20 mm Hg is abnormal and suggestive of subclavian stenosis. Use the higher blood pressure measurement when calculating ABI and titrating blood pressure medications. • Palpate all pulses in both legs Weak or absent pulses indicate poor blood flow through the extremity. The most sensitive indicator of arterial function is the quality of the posterior tibial pulse. • Visual assessment of feet and limbs Signs of ulcer formation: sluggish capillary refill; dry, scaly, dusky, pale, or mottled skin; thickened toenails. Loss of hair on the lower calf, ankle, and foot indicate poor peripheral blood flow. • Temperature Cool or cold temperature in the extremities indicates poor flow. • Assess bilateral muscle tone Muscle atrophy can accompany prolonged chronic arterial disease. • Assess pain Pain in the affected extremity with activity that is relieved with rest is indicative of PAD. -Treatment The primary goals of medical treatment and nursing care for patients with PAD are to provide relief of symptoms, prevent the progression of arterial disease and cardiovascular complications, improve quality of life, and provide education about the disease. Medications and nonsurgical and surgical interventions are options for treatment. The majority of patients with PAD are elderly with a significantly increased risk of myocardial infarction, stroke, and cardiovascular death. Nonpharmacological interventions such as weight reduction, smoking cessation, exercise, and adherence to a low-fat diet are first-line actions. Medication therapies target the risk factors driving the progression of atherosclerosis in PAD. They include antihypertensive, antiplatelet, and statin agents. All of these medications have been associated with significant reductions in mortality in patients with PAD. Beta blockers can be used for BP control. They were previously thought to exacerbate intermittent claudication but are now currently recommended to achieve BP goals in PAD. Antiplatelet agents such as acetylsalicylic acid (aspirin) and clopidogrel (Plavix) are commonly prescribed in patients with chronic PAD. Another antiplatelet agent, cilostazol, is an effective medical therapy for treatment of leg symptoms and walking impairment due to claudication. In addition to antiplatelet aggregation properties, it is also a vasodilator which can help improve blood flow through affected extremities. Unfortunately, significant side effects of headache, diarrhea, dizziness, and palpitations cause some patients to discontinue their treatment with that medication. Statin therapy is also recommended for all patients with PAD. The goal is to achieve a target LDL-C level less than 100 mg/dL. A more stringent LDL-C target is recommended (less than 70 mg/dL) in patients with PAD with multiple risk factors, especially diabetes, or severe and poorly controlled risk factors such as smoking, high triglycerides, or acute coronary syndrome. • Administer medications as ordered • Antihypertensives Controlling hypertension is necessary to help manage comorbidities, and it can improve tissue perfusion by maintaining pressures that are adequate to perfuse the periphery but not constrict the blood vessels. • Antiplatelet agents Patients with PAD and no contraindications to antiplatelet therapy should receive either aspirin or clopidogrel to inhibit clot formation. • Cilostazol Cilostazol has antiplatelet and vasodilation properties that can improve PAD symptoms. • Proper positioning Keep the affected extremity dependent to facilitate blood flow.

Folic acid deficiency anemia

-Diagnosis A CBC confirms the diagnosis of anemia with decreased hemoglobin levels; however, the specific etiology of the anemia must be identified. Serum folate levels may or may not be decreased. Because folate is absorbed in the proximal segment of the small intestine and is quickly available for cell metabolism, serum folate levels should be a fasting blood test; otherwise, the level may be falsely elevated. A more reliable indicator is the RBC folate level. Folate that enters the RBC remains there for the life span of that cell. Thus, an RBC folate level reflects the serum folate level over the past 3 months. However, because 50% of patients with a vitamin B12 deficiency also have low RBC folate levels, this is not a definitive test. Serum MMA and homocysteine levels are the best laboratory tests used to differentiate between anemia caused by a folic acid deficiency and those secondary to a vitamin B12 deficiency. Vitamin B12 and folate are cofactors in the methylation cycle converting methylmalonyl coenzyme A to homocysteine to methionine as part of the Krebs cycle. In a vitamin B12 deficiency, the serum MMA level is more sensitive and is elevated, whereas the homocysteine level remains normal. A folic acid deficiency causes the reverse: The homocysteine level is elevated, whereas serum MMA levels remain normal. Some conditions, such as renal insufficiency, may affect these results, so it is always important to consider the complete clinical presentation and not rely on one test to make a differential diagnosis. • Vital signs Tachycardia and tachypnea are secondary to the heart and lungs compensating for decreased oxygenation of body tissues caused by the reduced production of heme and RBC maturation demonstrated by decreased hemoglobin levels. • Fatigue, pallor, and shortness of breath Fatigue, pallor, and shortness of breath worsen with increasingly decreased levels of hemoglobin causing inadequate tissue perfusion. • Confusion, disorientation Neurological clinical manifestations are caused by decreased oxygenation to the central nervous system. • Hemoglobin levels, serum folate levels, RBC folate levels, and increased serum homocysteine levels Folic acid deficiency causes incomplete DNA synthesis that is necessary for the formation of heme, RBC maturation, and folate levels in the serum and RBCs and influences the metabolic pathway, which results in increased homocysteine levels. -Treatment Fortification of cereals and grains with folic acid helps to reduce the incidence of this specific deficiency. In certain patient populations, however, oral supplementation is recommended. Folic acid supplementation is recommended in pregnant women, children in the first year of life, patients with a history of gastrointestinal resections, and individuals with a history of chronic alcohol use. It is recommended that pregnant women consume at least 400 mcg (normal recommendation for adult women) of folic acid daily in order to reduce the occurrence and severity of neural tube defects and some orofacial abnormalities in infants. For patients on certain medications that can interfere with folate absorption, such as oral contraceptives, metformin, and certain chemotherapeutic agents, oral or parental supplementation may be recommended. Short- or long-term supplementation depends on the length of treatment with the medication. • Ensure adequate folate/folic acid intake. Ensuring adequate intake of dietary sources of folate and folic acid through food fortification prevents anemia and neural tube defects (see Table 34.2). • Administer folic acid supplements. Folic acid is the synthetic form for supplementation. Supplementation is needed when the body has increased folate demands, such as in pregnancy, early childhood, or alcoholism. It is also needed when malabsorption of folate occurs because of disorders such as Crohn's disease, gastrointestinal resections, and the use of medications that interfere with folate absorption. • Differentiate anemia caused by folic acid deficiency versus vitamin B12 deficiency. Supplementation of folic acid may reverse the anemia caused by vitamin B12 but will not stop the neurological degenerations that occur with vitamin B12 deficits. These neurological changes may become irreversible if misdiagnosed.

Malignant lymphoma k. Multiple myeloma

-Diagnosis A detailed history and physical examination are the first steps to diagnosing a malignant lymphoma, usually followed by radiological testing that may include a routine chest x-ray, computed tomography (CT) scan, positron emission tomography (PET) scan, or magnetic resonance imaging (MRI). A lymph node biopsy usually provides a definitive diagnosis. Examination of the tissue and determining the presence of the RS-H cells determine whether the patient has HD or NHL. A CBC may show evidence of bone marrow involvement with possible anemia and abnormal WBC count. If bone marrow involvement is suspected, a bone marrow biopsy may be indicated. A lumbar puncture is performed if central nervous system involvement is suspected. • Vital signs Low-grade fever, drenching night sweats, weight loss, and fatigue are a result of B-cell involvement, which causes systemic clinical manifestations. • Pain, breathing pattern, face/neck Shortness of breath, chest pain, dysphagia, and edema of the face and/or arms may indicate SVC syndrome with resulting venous congestion. • Neurological status The expanding lymphoma may cause spinal cord or nerve root compression. • Cervical, axillary, and inguinal lymph nodes Enlarged lymph nodes are a result of the expanded lymphoma, and the swelling may be painless. • Skin Generalized pruritus/itching can increase the risk of bleeding. • CBC results A CBC may show bone marrow involvement with impaired blood cell production, resulting in decreased RBCs, WBCs, and platelets. • Lower extremities Pain or swelling may occur secondary to thrombus formation if lymphoma compresses veins, slowing blood flow and increasing venous stasis. • Serum calcium levels If metastasis of the lymphoma involves the bones, the resulting bone breakdown releases calcium, causing hypercalcemia. • Activity tolerance Fatigue may develop as a result of the anemia caused by myelosuppression. -Treatment Treatment of malignant lymphomas usually involves the use of chemotherapeutic agents and/or radiation therapy to destroy the tumor cells. Surgical intervention to remove the tumor may also be indicated. If the individual has been diagnosed with an indolent NHL, a wait-and-see approach may be used initially because of the slow growth of the tumor. Stem cell transplantation may be indicated in some patients, but this depends on the type and stage of the disease. The rationale for transplantation is to destroy the mutant lymphoid stem cells with chemotherapy/radiation and then replace them with healthy donor cells. The success of stem cell transplantation in the lymphoma population varies and may depend on the aggressiveness of the underlying disease. If a splenectomy is required to treat lymphomas, respiratory problems may occur because of the spleen's proximity to the diaphragm and the need for a high abdominal incision. Pneumonia and atelectasis are possible complications due to postoperative pain and the patient's reluctance to cough and deep breathe. Development of pancreatitis may occur because the tail of the pancreas is near the spleen and may be damaged during surgery. Because of the spleen's role in the immune system, infection is a serious postoperative complication. Overwhelming post-splenectomy infection is a serious complication that has a high mortality rate because sepsis can quickly occur and is usually a result of streptococci, Neisseria spp., or influenza. Patients should maintain lifetime vaccinations against these organisms if a splenectomy is performed. • Administer blood products as ordered. Transfusions may be required as blood counts drop because of the myelosuppression that occurs as a result of the treatment regimens. • Administer chemotherapeutic agents. Patients will be started on chemotherapy as a primary treatment of lymphoma. • Administer IV fluids as prescribed. Increased insensitive fluid loss may develop secondary to fevers and drenching sweats. Additionally, in patients with hypercalcemia secondary to bone breakdown, increased fluids decrease the calcium concentration in the kidneys and decrease the risk of calcium-containing renal calculi. • Symptom management Symptom management of the disorder itself, as well as symptoms that may occur as a result of the chemotherapy and radiation, is the focus of nursing care. Easing the discomfort of itching and the drenching night sweats is important to the comfort of the patient with Hodgkin's disease, as is managing any clinical manifestations of therapy such as nausea and vomiting. • Obtain routine CBCs. Myelosuppression may be a result of chemotherapy or radiation therapy. Hemoglobin and WBC counts need to be monitored closely, as does the platelet count. • Provide emotional support. Emotional support is essential to patients with a cancer diagnosis. Helping them to deal with fears of death and dying and referring them to needed resources are essential to helping them manage the course of the disease.

Aortic artery disease (aneurysms)

-Diagnosis A number of imaging modalities can be used to detect and diagnose aortic dilation. Computed tomography scanning with IV contrast is considered the gold standard for assessing the size and location of an abdominal or thoracic aneurysm. Abdominal ultrasound or transthoracic echocardiography (TTE) have also been preferred screening modalities because they can be done quickly and efficiently at the bedside and because of their noninvasive nature and lack of radiation. Cardiac MRI is an imaging modality that has shown improved sensitivity and specificity versus TTE in detecting aortic dilation. The lack of radiation exposure with MRI compared with CT may make it the imaging modality of choice for aortic dilation. An ECG is also routinely done to rule out an MI because complications of aneurysm usually involve chest pain. • Vital signs Hypotension and tachycardia may indicate hypovolemia secondary to a loss of circulating volume. Blood pressure may vary between extremities if dissection is occurring because of the lessening of blood flow distal to the dissection. Hypertension, elevated diastolic pressure, and tachycardia can further weaken the vessel wall, increasing the risk that the aneurysm will enlarge, dissect, or rupture. • Neurological assessment An aneurysm of the aortic arch can cause neurological symptoms similar to those of a TIA or stroke. The bulging aorta exerts pressure on the subclavian artery, decreasing blood flow through the common carotid arteries to the brain, causing neurological effects. • Pain Persistent abdominal, chest, or back pain indicates that the aneurysm is pushing on adjacent organs and structures and may help pinpoint the location. Pain is also an indicator of a change such as dissection or rupture. • Peripheral pulses, skin color, and temperature Weak peripheral pulses, poor color, and cool extremities indicate lack of arterial flow, potentially because of dissection or thrombus formation in the aneurysm. • Peripheral sensation and motor response Paresthesias or paralysis may indicate pressure against the arteries supplying the spinal cord. • Gentle abdominal auscultation and palpation Pulsatile abdominal masses may indicate an AAA. A bruit is caused by turbulent flow through the aneurysm. -Treatment Treatment is focused on reducing the growth rate and preventing the complications of aneurysms. Hypertension is an important risk factor for rupture, so BP is aggressively managed with antihypertensive medications such as angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers (ARBs), and/or beta blockers. In addition to antihypertensive medications, macrolides and tetracyclines, antibiotics that may inhibit secondary infections implicated in aneurysm development, have been proposed as a treatment for AAA with varying rationales and degrees of success. There is also evidence from a number of studies suggesting that statins may influence aneurysm growth rate by reducing the progression of atherosclerosis The size and location of the aneurysm along with the presence of symptoms are the determining factors for patient management (Table 31.12). Currently, surgical intervention is shown to be the only treatment effective in preventing AAA rupture and aneurysm-related death. The most common surgical procedure for AAA has traditionally been a resection and repair (aneurysmectomy). In this procedure, the aneurysm is excised, and a graft is applied. Surgical repair is associated with risks that include bleeding, infection, MI, renal failure, and graft occlusion. Benefits versus risks should be weighed when considering an elective surgical repair of the aneurysm. More recently, endovascular aneurysm repair (EVAR) has gained acceptance as an alternative to open surgical repair with reduced periprocedural risks. The endovascular alternative is an endothelial stent graft or EVAR, which involves the transluminal placement and attachment of a sutureless aortic graft prosthesis across an aneurysm. The aneurysm eventually shrinks down onto the stent graft Most people with an aneurysm less than 5 cm in diameter are advised not to have immediate surgery. The goal for patients who do not require immediate surgical intervention is to monitor the growth of the aneurysm over time and to maintain the BP at a normal level to decrease the risk of rupture. For those with small or asymptomatic aneurysms, regular ultrasounds or CT scans are necessary to monitor the growth of the aneurysm. Patients with TAAs measuring 2.8 in. (7 cm) in diameter or with AAAs measuring 2 in. (5 cm) in diameter or those with smaller aneurysms that are producing symptoms are advised to have elective surgery (see Geriatric/Gerontological Considerations). A small aneurysm that expands more than 0.5 cm over a 6-month period of time should also be repaired surgically. • Administer antihypertensives as ordered Antihypertensives control high BP, which is a major risk factor for aneurysm rupture. • Administer statins as ordered Statins lower cholesterol and therefore reduce the risk of atherosclerosis, which may reduce the aneurysm growth rate. • Administer tetracyclines and macrolides as ordered These types of antibiotics may inhibit AAA progression by reducing secondary infections within the aortic wall. • Administer stool softeners as ordered Prevent strain on the aneurysm during defecation • Create calm environment to reduce stress Reduction in stress has been shown to reduce BP and therefore lessen stress on the aneurysm.

Coronary artery disease

-Diagnosis As stated previously, the formation of plaque within the blood vessels is a silent process. Often CAD is suspected only when the individual presents with clinical symptoms. The diagnosis is made on the basis of clinical presentation and diagnostic findings. Timely recognition of ischemia related to CAD is essential for prompt treatment and improved patient outcomes, particularly in cases where CAD has progressed to acute coronary syndrome or myocardial infarction. Delays in diagnosis can result in more myocardial damage from ischemia. When time is muscle, every minute counts. Many of the blood tests performed assess for the presence of risk factors for CAD development, such as lipid profiles, inflammation, and coagulation studies. Lipid profiles evaluate total cholesterol and triglyceride levels as well as LDL and high-density lipoprotein (HDL). Specific cardiac biomarkers are used to rule out MI. Creatine kinase (CK) or creatine kinase-muscle/brain (CK-MB) and troponin (I or T) levels rise when myocardial injury occurs and are used to identify when ischemia has led to tissue damage. Because these biomarkers do not immediately rise with chest pain, they are measured every 6 hours after admission to the hospital to evaluate chest pain. This is known as serial cardiac enzyme or biomarker testing. Although most acute care facilities use both biomarkers, hospitals are increasingly using troponin alone as recommended in national guidelines. Recent evidence suggests that women may have a lower troponin threshold, which may be contributing to underdiagnosis of MI and worse outcomes. Laboratory tests diagnostic for CAD are summarized in Table 28.3 in Chapter 28. An electrocardiogram (ECG) is often the initial test when CAD is suspected. During anginal episodes or symptoms of ACS, the ECG may show ST segment depression of greater than 0.5 mm or flat or inverted T waves that are indicative of ischemia. These changes return to normal when chest pain is relieved. It is important to note that ischemia in some patients may be electrically silent, with an ECG that appears normal. Serial ECGs may be done with cardiac biomarkers to rule out an infarction. If cardiac biomarkers and ECGs are normal, a patient may then undergo an exercise stress test. This is done to assess the function of the heart during exercise. Alternatively, for those who are unable to use a treadmill or stationary bicycle, pharmacological agents such as dobutamine can be used to increase heart rate, mimicking the effects of exercise on the heart. Stress echocardiograms are another option. Stress testing can be combined with nuclear imaging, such as thallium or technetium studies, to further evaluate perfusion to the heart. The goals of the stress test are (a) to determine whether there is reduced oxygen-rich blood flow to the heart tissue during physical activity and (b) to determine what parts of the heart are affected by the decreased blood flow. Descriptions of these tests can be found in Chapter 28. The gold standard for diagnosing CAD is coronary angiography, a left-sided cardiac catheterization with the purpose of evaluating the coronary arteries for blockage. This is performed to determine the location of the plaque within the coronary circulation, the degree of occlusion, and whether the area can be treated with percutaneous transluminal coronary angioplasty. The lack of major plaque limits the diagnostic value of this test in patients with nonobstructive CAD. Coronary computed tomography (CT) angiography, magnetic resonance angiography, and stress imaging techniques can be useful instead. • Vital signs Tachycardia and tachypnea can be manifestations of cardiac ischemia. Hypertension is a CAD risk factor. Nitroglycerin and morphine administration can result in hypotension. • Pain assessment utilizing provoking factors, quality, region/radiation, severity, time (PQRST) Angina can be nonspecific in some patients; establishing location and quality can aid in the diagnosis of cardiac chest pain and disease progression. Headache can result from nitroglycerin administration. • Electrocardiogram and continuous cardiac monitoring Depressed ST segment or flat or inverted T waves are indicative of ischemia; ST elevations are indicative of acute injury. Cardiac dysrhythmias may result from ischemia or infarction. • Physical assessment Pallor, clamminess, nausea, vomiting, shortness of breath, and diaphoresis may indicate cardiac ischemia. Xanthomas are associated with hypercholesterolemia. • Patient history Evaluate CAD risk factors and anginal patterns. Fatigue and weakness may be indicative of CAD. Identify potential noncardiac causes of chest pain, such as gastroesophageal reflux or respiratory disorders. • Recreational drug use Illicit drug use (i.e., cocaine) can cause vasospasm, obstructing blood flow and causing symptoms that resemble CAD. • Depression screening Depression may increase morbidity and mortality. • Laboratory values • Cardiac biomarkers: troponin, CK/CK-MB Cardiac enzymes and troponin levels rise when the heart sustains an acute injury—can help differentiate between angina and MI pain. • Creatinine, blood urea nitrogen Assess renal function. The contrast dye used during heart catheterization is nephrotoxic. • Glycosylated hemoglobin (HgbA1c) Hyperglycemia occurs with diabetes and is a risk factor for CAD. • Lipid profiles: cholesterol, triglycerides, LDL, HDL Assess for hyperlipidemia, a risk factor for CAD development. -Treatment Medications for patients with CAD are often prescribed with the goals of (a) stopping the aggregation of blood components to the injured endothelium, (b) controlling factors that led to damage of the endothelium, and (c) relieving symptoms (Table 30.2). Patients with stable angina at low risk for ACS are often prescribed aspirin and nitroglycerin along with medications to reduce risk factors, such as antihypertensives, antidiabetic agents, and cholesterol-lowering medications. Aspirin prevents thrombus formation in the coronary artery. Nitroglycerin, a vasodilator, is used to manage anginal episodes, both at home and in the hospital. Nitroglycerin can be administered as sublingual tabs, as a spray or powder, intravenously, through transdermal patches, as an ointment, and by mouth with extended-release capsules. During anginal episodes, the sublingual and IV routes are preferred to restore blood flow promptly. Blood pressure should be monitored carefully due to the adverse effect of hypotension. Headaches can also occur and are best treated with nonopioid analgesics such as acetaminophen. Treatment of ACS in the acute care setting includes aspirin, supplemental oxygen, nitroglycerin, and morphine and can be referred to by the acronym MONA. Morphine can be given for angina pain in patients not responsive to nitroglycerin, but its use can be associated with hypotension, nausea, and vomiting. Beta blockers, additional anticoagulants, and possibly calcium channel blockers are also prescribed in ACS management. Treatment for nonobstructive CAD is being studied. Statins, angiotensin-converting enzyme (ACE) inhibitors, and beta blockers may be beneficial. Percutaneous transluminal coronary angioplasty (PTCA) is the procedure most commonly performed to relieve symptoms caused by atherosclerotic changes in the coronary vessels. During this procedure, after the patient receives monitored anesthesia care (MAC), a catheter with a small balloon on its tip is advanced under fluoroscopy through a suitable artery, commonly the femoral or radial, to the area with atherosclerotic plaque. The balloon is inflated and deflated to open the lumen of the artery. During this time, patients may experience chest pain due to vessel occlusion. Once the lumen is open, a stent may be advanced to the location to hold the artery open and maintain adequate blood flow. Stent options include bare metal stents (BMS), drug-eluting stents (DES) to prevent clots, or the newer bioabsorbable stents. Patients frequently return from the procedure with a vascular closure device, such as an angioseal, applied to the access site to maintain hemostasis. This allows early ambulation. If no closure device is applied, strict bedrest for 6 to 8 hours is required until hemostasis is achieved. Figure 30.3 illustrates stent placement within the artery. Bleeding at the insertion site, abrupt vessel closure, dysrhythmias, and ruptured arteries are uncommon but potential complications from PTCA (see Genetic Connections: Pharmacogenetics and Anticoagulants). Care of the patient receiving a PTCA is outlined in Chapter 28. A more invasive surgical treatment is coronary artery bypass grafting (CABG). With CABG, blockages in coronary arteries are bypassed using other arteries from the chest or arm or veins from the legs. In the traditional CABG, patients undergo general anesthesia. A large incision through the sternum is made, and a cardiopulmonary bypass (CPB) is begun through large catheters in the vena cava or right atrium and aorta. A CPB provides continuous gas exchange and perfusion while the heart is stopped to provide a still, bloodless field for surgery. Then arteries or veins being used as bypasses are surgically attached to the diseased coronary artery, creating an alternate path for blood to flow around the blockage. Common vessels used are the internal thoracic (mammary) and saphenous vein. Bypasses made from arteries have greater longevity, but more bypasses can be made with saphenous veins, which require an additional incision in the leg. Multiple blockages may be bypassed in the same surgery. For example, a patient with four large coronary artery blockages would undergo a quadruple bypass. inimally invasive coronary surgery (MICS CABG) may be an alternative to CABG. MICS CABG involves a left chest incision and multiple smaller incisions that act as ports for instruments. A CBP is used, and multiple vessels can be bypassed. Minimally invasive direct coronary artery bypass (MIDCAB) is an option for some patients, in which incisions similar to those in MICS CABG are made. A pressor device placed through the chest incision immobilizes a part of the heart while the internal thoracic artery is used to bypass a single blockage. A similar procedure through a sternotomy incision allows for additional vessels to be bypassed. Because both procedures do not require a CPB, they are called off-pump or "beating heart surgery." Potential advantages of all these procedures include faster recovery times and fewer complications. Patients who undergo CABG are sent to a critical care unit for intensive monitoring and care. Multiple hemodynamic monitoring catheters, chest tubes, an endotracheal tube, mechanical ventilation, a nasogastric tube, an indwelling bladder catheter, and a temporary pacemaker wire may all be needed postoperatively. Nursing care of the patient undergoing CABG is described in Chapter 32. The decision between PTCA and CABG is made by the healthcare team and patient based on degree of disease, surgical risk, hemodynamic stability, and symptom severity. Other, less common invasive treatment strategies, such as atherectomy and transmyocardial laser revascularization (TMLR), may be performed in patients meeting limited criteria. During an atherectomy, plaque within the coronary artery is shaved and removed through a specialized catheter during cardiac catheterization. In TMLR, a patient's heart is surgically exposed, and a laser is used to create 20 to 40 tiny channels from the outside of the left ventricle to the chamber within. The outside openings are closed by clots, but the channels stay open on the inside. The procedure is also thought to stimulate angiogenesis; the formation of new blood vessels from pre-existing vessels. • Administer oxygen to keep oxygen saturation greater than 93%. Supplemental oxygen optimizes oxygen delivery to the myocardium. Cardiac dysrhythmias, especially tachycardia, and anxiety increase myocardial oxygen consumption. • Obtain ECG with the occurrence of chest pain. Evaluates new anginal episode for evidence of ischemia or injury. In cases of acute chest pain, an ECG within 10 minutes is recommended. • Administer nitroglycerin as ordered. Dilates the coronary arteries to improve flow to the heart and relieve pain • Administer aspirin as ordered. Prevents platelet aggregation • Administer morphine as ordered if nitroglycerin does not relieve pain. Minimizes pain and decreases the workload on the heart. Monitor for adverse effects of hypotension, nausea, vomiting, and respiratory depression. • Administer beta blockers/calcium channel blockers as ordered. Inhibit cardiac response to physical activity, decrease oxygen consumption; may consider holding prior to exercise test • Administer statin medications as ordered. Reduce cholesterol level and decrease the risk of increased plaque formation

Vitamin B12 and pernicious anemia

-Diagnosis Because of the slow progression of a vitamin B12 deficiency and delayed clinical manifestations, the results of a CBC may be the first indication that a problem exists, and further investigation is needed to determine the cause. The diagnosis of vitamin B12 deficiency is made based on a history and physical examination and a vitamin B12 serum assay blood test. Serum vitamin B12 is not low in all individuals with a deficiency because there are inborn errors of vitamin B12 metabolism that may cause serum levels to be normal, but low cellular levels may have already resulted in damage. Therefore, the vitamin B12 serum assay test has its limitations and has a wide normal range (200 to 1,000 pg/mL). Patients with liver disease, lymphoma, and myeloproliferative disorders may have false-negative results. A more sensitive test for vitamin B12 deficiency is to measure the level of methylmalonic acid (MMA), part of the methionine conversion, in the patient's urine or blood. An excess of MMA indicates a lack of vitamin B12 in the tissues. Because patients with renal failure, dehydration, or hypovolemia can have falsely elevated serum MMA levels, a urinary MMA test is needed for accurate diagnosis in individuals with these disorders. Other relevant blood tests that may assist in determining vitamin B12 deficiency include gastrin levels, intrinsic factor levels, and in rare instances, the Schilling's test, a radionuclide 24-hour urine test that indirectly measures intrinsic factor. • Vital signs Vitamin B12 deficiency impairs RBC production, with a resulting decrease in tissue perfusion. Tachycardia and tachypnea occur as the heart attempts to compensate for the decrease in tissue perfusion. • Fatigue, pallor, and shortness of breath Fatigue, pallor, and shortness of breath worsen with increasingly decreased levels of RBCs, causing inadequate tissue perfusion. • Numbness, tingling, or burning of the hands or feet; confusion; mood swings Neurological clinical manifestations occur because of the impairment of DNA synthesis of myelin sheath and neurotransmitters. • Decreased hemoglobin/hematocrit levels, decreased vitamin B12 levels, elevated serum and urine MMA levels A CBC shows decreased hemoglobin and hematocrit levels. The serum vitamin B12 assay is decreased due to the lack of vitamin B12 needed for synthesis. • Fall risk (safety) Confusion, dementia, coordination and balance impairment, and visual disturbances make these patients at risk for falls. Paresthesia and tingling (peripheral neuropathy) can affect ambulation, gait, and stability. Severe neuropathy may take time to recover. • Intake and output Constipation, diarrhea, and/or anorexia affect the absorption of vitamin B12 and may worsen the problem. -Treatment Prevention of vitamin B12 deficiency is important, and animal proteins provide the only source of vitamin B12 in the world. Vitamin B12 has not been discovered in any plants. Dietary sources of vitamin B12 include meat, seafood, eggs, and dairy products. Long-term vegans/vegetarians or those of low socioeconomic status are at increased risk of deficiency and may need to take a daily supplement of vitamin B12. Oral supplementation of vitamin B12 may not be sufficient once the deficiency is profound and the patient has developed clinical manifestations such as fatigue, weakness, and paresthesias. Once severe deficiency is determined, weekly vitamin B12 injections are required. • Ensure adequate vitamin B12 intake. Ensuring that the patient has an adequate intake of vitamin B12 prevents clinical manifestations of anemia and degenerative neurological changes (see Table 34.3). • Administer vitamin B12 therapy. Oral supplementation in mild cases of vitamin B12 deficiency may be helpful. In more severe cases, supplementation with parenteral therapy is required. Parenteral supplementation may be necessary for patients who lack intrinsic factor and cannot absorb oral supplementation. Vegetarians can prevent or treat this deficiency with oral supplements, vitamins, or fortified soy milk. When the deficiency is due to pernicious anemia or the absence of intrinsic factor, the replacement of vitamin B12 involves I-mg IM injections of cyanocobalamin vitamin B12. • Monitor use of folic acid. Before starting a patient on folic acid, confirm that the patient does not have a vitamin B12 deficiency. Folic acid resolves the anemia by escaping the methylfolate trap, but neurological degeneration due to vitamin B12 deficiency continues. • Monitor use of nitrous oxide. Nitrous oxide inactivates vitamin B12 in the body. Prior to using for anesthesia, confirm that the patient is not vitamin B12 deficient. • Assess pain and activity levels due to peripheral neuropathy. Peripheral neuropathy may develop because of vitamin B12 deficiency. Increasing pain may interfere with functional abilities. Because position sense, coordination, and balance are affected, physical therapy and occupational therapy should be considered along with the use of assistive devices.

Polycythemia vera

-Diagnosis Because the onset of PV is insidious, the disorder is often discovered during routine blood tests. Complete blood count results include an increased RBC count of greater than 6 million/mm3, and the hematocrit can exceed 60%. Because splenomegaly is often seen in about 75% of patients, the bone marrow becomes fibrotic and is unable to produce sufficient cells. To make the diagnosis, the World Health Organization (WHO) recommends hemoglobin levels of greater than 16.5g/dL in men and greater than 16.0g/dL in women. In PV, elevated WBC and platelet counts may also be present as a result of the gene mutation's effect on the bone marrow production of blood cells. In secondary polycythemia, the WBCs and platelets remain in the normal range. Other laboratory tests that may aid in diagnosis are an erythropoietin level, blood smear, bone marrow biopsy, and genetic testing. A complete history and physical examination are often keys to diagnosing the cause of the polycythemia. • Shortness of breath/dyspnea, especially when supine Because of decreased oxygen delivery to the tissues, respiratory effort increases in an attempt to improve oxygen delivery. • Headache Headache is a result of the increased blood volume and hyperviscosity in PV. A sudden, severe headache may be a clinical manifestation of a CVA as the result of clot formation. • Dizziness Dizziness in PV occurs because of impaired tissue perfusion as the blood flow slows secondary to blood hyperviscosity. • Generalized pruritus, especially after a warm bath The itchiness in PV is most likely due to the vascular dilation and capillary engorgement as a result of the increased blood cell production with resulting increased blood volume. This can be painful due to swelling from the histamine release and increased number of basophils and may be triggered by the exposure to water (aquagenic pruritus). • Flushing of the face Flushing in PV occurs secondary to capillary engorgement caused by the increased blood volume. This plethora causes a ruddy complexion. • Feeling of fullness in the left upper abdomen The abdominal fullness (which may become painful) is due to the organ congestion secondary to the hyperviscosity and increased blood volume. • Fatigue Fatigue occurs because of the increased workload of the heart and poor tissue perfusion secondary to the hyperviscosity. Angina and intermittent claudication can occur. • Vision problems Blurred vision or blind spots occur from poor tissue perfusion or vascular damage to small vessels in the eye secondary to hyperviscosity. • Weight loss The feeling of fullness in the abdomen in the left upper quadrant is caused by organ congestion that leads to abdominal pain, early satiety, and/or anorexia. Patients with elevated hemoglobin and hematocrit should be checked for an enlarged spleen on physical exam by the healthcare provider. • RBCs, hemoglobin, and hematocrit Overproduction of RBCs is a result of stimulation of the bone marrow secondary to either a gene mutation or the body's hypoxic state. This may lead to angina, hypertension, and thrombophlebitis, especially if the patient has cardiac disease. • Bone marrow biopsy results Examination of the bone marrow shows the panmyelosis (overproduction of RBCs, WBCs, and platelets) in PV. • Erythropoietin level In secondary polycythemia, the hypoxic state stimulates the release of erythropoietin by the kidneys. • Vital signs during therapeutic phlebotomy If blood loss is not too fast, the patient may develop signs of hypovolemia, including hypotension and tachycardia. • Uric acid level The rapid turnover of red blood cells associated with PV may result in an elevated uric acid level. This increase in uric acid can cause gout and kidney stone formation. -Treatment Treatment of PV is aimed at reducing the hyperviscosity and preventing hemorrhage. Therapeutic phlebotomy involves removing blood to decrease blood volume and viscosity. A unit of blood (350 to 500 mL) is removed weekly until the hematocrit is less than 45%, then only as needed. The patient usually feels more comfortable immediately because this reduces congestion of organs such as the spleen and liver. Repeated phlebotomies may cause iron-deficiency anemia, so serum ferritin levels are monitored as well as CBCs. Phlebotomy, however, does not decrease WBC or platelet levels if elevated in PV, and chemotherapeutic agents such as hydroxyurea or interferon may be given to suppress bone marrow production. Radiation may also be employed to suppress the bone marrow. These treatments may have the undesirable side effect of causing leukemia. Antiplatelet medications, such as anagrelide or low-dose aspirin, may be prescribed to reduce the risk of thrombosis. When secondary polycythemia is appropriate, treatment of the underlying condition usually resolves the polycythemia. Prevention of secondary polycythemia includes the cessation of activities such as smoking or mountain climbing, which deprive the body of oxygen. Maintaining a healthy lifestyle contributes to preventing conditions that cause polycythemia. Symptom management in patients with PV is important to maintain quality of life. Regular moderate exercise to improve circulation and decrease thrombosis is emphasized. Medications to minimize itching may be prescribed, as well as interventions focused on avoiding extreme temperatures, taking extra care of the hands and feet, guarding against injury, drinking at least 3 L of fluid daily, avoiding tight clothing, elevating the feet while at rest, and reporting any chest pain or dyspnea. • Obtain routine CBCs. If the patient is undergoing therapeutic phlebotomy, blood count checks are done to maintain a hematocrit below 45% in men and below 42% in women. If the patient is on chemotherapeutic agents, CBCs are indicated to monitor the degree of myelosuppression. • Increase fluid intake. Increased fluid intake may reduce the hyperviscosity of the blood. • Ensure adequate rest. Frequent rest periods may be needed to help the patient deal with the increased workload on the heart due to the hyperviscosity and the patient's subsequent shortness of breath. • Elevate lower extremities when sitting. Elevation of the lower extremities aids the circulation in returning to the heart and minimizes the risk of thrombus formation secondary to venous stasis. • Modify cardiovascular risk factors. Obesity, hypertension, diabetes, and smoking can increase the risk of thrombosis, CVA, MI, or deep vein thrombosis (DVT). Avoid restrictive clothing and crossing legs. Encourage smoking cessation. Implement DVT prophylaxis.

Laryngeal trauma

-Diagnosis Diagnosis is completed by conducting a physical inspection of the neck for signs of swelling, discoloration, subcutaneous emphysema, tracheal deviation, and open wounds. Diagnostic studies include cervical CT, fiberoptic laryngoscopy, or flexible bronchoscopy. During a laryngoscopy or flexible bronchoscopy, the provider uses a flexible tube with a fiberoptic system to view structures in the upper and lower airways • Vital signs Increases in respiratory and heart rates, decreased oxygen saturation, and tachypnea indicate respiratory distress. • Physical assessment of the neck and upper airway Identify risk for laryngeal trauma if discoloration, change in voice, stridor, use of accessory muscles for breathing, or restlessness indicating hypoxia are present. -Treatment The priority of care in patients with laryngeal trauma is to ensure and maintain a patent airway. Maintenance of the airway may include endotracheal intubation or tracheostomy. Because of the potential of cervical spine injury in addition to laryngeal trauma, stabilization of the cervical spine is vital. Diagnostics wait until the airway is protected and the cervical spine is stabilized. Surgical interventions, if necessary, include evacuation of hematoma, repair of lacerations, and stabilization/repair of fractures. • Have tracheostomy insertion tray and emergency equipment at the bedside. The patient may have a sudden loss of the airway requiring emergency tracheostomy. • Provide humidified air via a face mask or face tent. Cool humidified air will help decrease airway edema. • Keep the head of the bed elevated at 45 degrees or greater. Elevation of the head of the bed will assist in decreasing edema and maintaining a patent airway. • Aspiration precautions Maintain nothing-per-os (NPO) status to protect the airway in the presence of edema and/or bleeding. Also, maintain NPO status until the need for surgery has been evaluated.

Rhinosinusitis

-Diagnosis Diagnosis is primarily based on a physical examination and starts with the completion of a history and physical examination focusing on the ears, nose, throat, teeth, sinuses, and chest. During the physical examination, the provider is looking for signs of inflammation, tenderness, firmness, or redness. Light palpation or percussion of the sinuses using the index finger is done to evaluate the presence of pain. A vital sign assessment also needs to be completed to identify temperature elevation. Diagnostic testing may include radiographical imaging of the sinuses, computed tomography (CT), and magnetic resonance imaging (MRI) if patients do not meet clinical diagnosis criteria. On radiographical studies, fluid; thickening of the mucous lining of the sinuses; and the presence of polyps, opacities, or foreign objects may be found, indicating rhinosinusitis. • Vital signs Temperature elevation may indicate the presence of infection. Increased blood pressure may be a side effect of the decongestants. • Physical examination of the mouth, nose, and face Facial pressure, a sense of fullness or pain or nasal obstruction, and the presence of purulent (yellow-green) nasal discharge indicate impaired nasal drainage. Swelling, redness, and pain around the eyes may indicate an abscess or cellulitis. • Percussion of sinuses Identifies presence of fluid within the sinus cavity, which results in pain -Treatment The focus of treatment in acute rhinosinusitis is based on the etiology. Treatment goals include pain relief, reduction of nasal mucosal inflammation, and treating infection if present. Normal saline irrigation has local effects that reduce symptoms in acute rhinosinusitis. In this procedure, the patient pours or sprays normal saline into one nostril; it flows through the nasal cavity and pours out the other nostril. Irrigation is beneficial in the removal of infectious debris, bacteria, allergens, and inflammatory mediators. It also decreases edema of the nasal mucosa and the viscosity of nasal secretions. Caution must be taken to prevent antibiotic use in nonbacterial illnesses such as viral rhinosinusitis to prevent the development of antibiotic resistance, but in bacterial infections, antibiotic therapy is required. A delay in initiating antibiotic therapy may be indicated if the patient presents with symptoms of nonsevere illness (temperature less than 101°F [38.3°C] or with mild pain). If after 7 days the patient fails to improve or worsens at any time, antibiotics are prescribed. Amoxicillin or amoxicillin-clavulanate is the first-line therapy for most patients with ABRS because of its efficacy, safety, narrow microbiological spectrum, and low cost. In patients with penicillin allergies, doxycycline or a respiratory fluoroquinolone such as moxifloxacin or Levofloxacin is used. In patients who fail to respond within 48 to 72 hours of treatment or who have persistent symptoms, second-line antibiotics may be required. Second-line antibiotics most commonly used include second- or third-generation cephalosporins (cefuroxime [Ceftin], cefpodoxime [Vantin]), macrolides (clarithromycin [Biaxin]), fluoroquinolones (ciprofloxacin [Cipro], levofloxacin [Levaquin], moxifloxacin [Avelox]), and clindamycin (Cleocin). Antipyretics and analgesics are used as needed to control temperature elevation and pain. The use of intranasal corticosteroids is recommended in patients with a history of allergic rhinitis. The use of decongestants can be helpful in reducing obstruction of the osteomeatal complex (the bony structures around the drainage openings of the sinuses), facilitating drainage of the sinuses. Patients with hypertension should use caution when taking oral decongestants due to their action of vasoconstriction to reduce stuffiness, which can increase blood pressure. Medications typically used for symptomatic relief that should be used with caution include antihistamines that may cause drying of secretions, thus impairing mucus drainage, and topical decongestant sprays that, if used for more than 3 days, may result in rebound nasal congestion when discontinued. This is also referred to as rhinitis medicamentosa. Rhinitis medicamentosa results in nasal congestion without rhinorrhea or sneezing and is known as rebound rhinitis or chemical rhinitis. Treatment of rhinitis medicamentosa is the cessation of topical nasal decongestants.

Carpal tunnel syndrome

-Diagnosis Diagnosis starts with a detailed patient history. The history includes the patient's occupation, factors responsible for generating the wrist pain, and medical history. The Phalen's test aids in diagnosis of CTS and is performed by having the patient relax his or her hand in the flexed position for 60 seconds or by placing the back of the hands together while flexing both wrists. This compresses the median nerve. Patients with CTS experience numbness and tingling during the Phalen's test. Tinel's sign, tapping the median nerve over the carpal tunnel at the wrist, will also elicit paresthesia over the median nerve region of the wrist. Nerve conduction studies and electromyographies are frequently ordered to determine the severity of CTS and rule out any potential spinal cord lesions or tumors. Cervical spine radiography eliminates any possible cervical disorders that could cause radiating pain in the hands. Occasionally, MRI and ultrasound may be used to isolate the cause of CTS. • Patient work or activity history A work or activity history of repetitive movements such as computer or assembly-line work puts patients at risk for CTS. • Physical assessment of injured extremity via inspection and palpation Numbness and tingling during the Phalen's test or paresthesias with a Tinel's test may indicate CTS caused by compression of the median nerve. • Pain, paresthesia Pain is caused by inflammation and edema, resulting in compression of the median nerve. -Treatment Treatment of CTS can be done with conventional nonoperative measures such as modifying the work environment to eliminate repetitive motion and promote ergonomics. Ultrasound therapy, NSAIDs, steroid injections, night splinting, and acetaminophen are other treatment options. • Splinting at night or with symptoms Immobilizes the joint, decreasing irritation and inflammation on the median nerve • Exercise/ROM therapy as tolerated Prevents atrophy, strengthens muscles, and promotes mobility • Administer anti-inflammatory medications as ordered Inhibits prostaglandin (mediators of pain and inflammation) formation reducing pain and inflammation • Collaborate with occupational therapist An occupational therapist can evaluate the work area and make recommendations for modifications to eliminate causative factors.

Laryngeal cancer

-Diagnosis Diagnosis starts with the completion of a thorough health history, including general health information, other medical conditions, onset of symptoms, risk factors, and family history. Physical assessment of the neck, thyroid, lymph nodes, and muscle movement of the neck can indicate if tumor growth has invaded these structures. If these initial findings are suspicious for laryngeal cancer, a referral to an otolaryngologist (ear, nose, and throat specialist) or a head and neck surgeon is made. Further diagnostic procedures include endoscopy and imaging. Visualization and examination of the pharynx and larynx are performed by an otolaryngologist with the use of a direct laryngoscopy with a flexible endoscope. Laryngoscopy allows for assessment of the vocal folds and glottis for the presence of ulcerations, nodules, polyps, strictures, bleeding, or tumors. Laryngoscopy may also be performed under general anesthesia, at which time samples or biopsies of suspicious tissue are obtained for evaluation (Fig. 25.8). Diagnostic imaging includes a barium swallow, chest x-ray, CT, MRI, and positron emission tomography (PET). A barium swallow evaluates the throat and the ability to swallow. Chest x-rays are obtained to evaluate the lungs for the presence of lung cancer. The CT, MRI, and PET scans are completed to determine the presence of metastasis into the surrounding and distant soft tissues and for regional adenopathy, or lymph node involvement. The information obtained through biopsy and diagnostic imaging is used to determine the stage of the tumor and disease progression. Stages of laryngeal cancer are based on the size of the tumor, the involvement of the lymph nodes, and whether the cancer has spread to other sites within the body. Diagnostic laboratory testing is also done to provide information about the overall health status of the patient. A complete blood count, blood chemistry profile, coagulation studies, and urinalysis provide vital information about the potential spread of laryngeal cancer, nutritional status, and organ function, such as the kidneys and liver. At present, there is no specific blood test or marker to assist in diagnosing laryngeal cancer. • Complete a review of risk factors Focus on risk factors for laryngeal cancer, such as smoking, alcohol use, and occupational exposure to chemicals. • Review of symptoms/complaints Hoarseness, earache, and sore throat lasting several weeks need further evaluation. • Skin/vocal/swallowing assessment Red, tender, peeling skin may result from radiation therapy. Radiation therapy may also cause worsening hoarseness and difficulty swallowing. • Laboratory assessments: electrolytes, white blood cell (WBC) and platelet count Patients on chemotherapy may have alterations in their electrolyte balance. Also, they can become immunosuppressed, resulting in neutropenia, making them more susceptible to infection. Platelet counts may decrease, resulting in bleeding risk. • Vital signs Decreased blood pressure may occur with blood loss; increased heart rate may be due to hypovolemia or pain. • Oxygenation status Edema and increased secretions postoperatively may cause shortness of breath and decreased oxygenation. • Patency of tracheostomy Bleeding or edema may occur postoperatively, impairing the patency of the tracheostomy. • Weight, nutritional intake, calorie count Swallowing impairments postoperatively may impact adequate nutritional intake. -Treatment Treatment of laryngeal cancer is based on factors such as the stage of the disease, the location and size of the tumor, and whether the current tumor is a reoccurrence. Treatment includes radiation therapy, surgery, and chemotherapy. Radiation therapy is used to eliminate cancer cells and maintain the structure and function of the larynx. It is used to treat small tumors, to reduce tumor size prior to surgery, or in patients who are unable to undergo surgery. Radiation therapy is usually given 5 days a week for 6 to 8 weeks. Side effects of radiation include increased hoarseness; prolonged tissue healing; sore throat; difficulty swallowing; and if the salivary glands are involved, dry mouth (xerostomia). Chemotherapy can be used in several different ways. It can be given at the same time as radiation therapy (chemoradiation) to improve the effectiveness of the radiation therapy. It can be given before radiation therapy to shrink larger tumors and make radiation therapy more effective. It can also be given prior to surgery to shrink larger tumors that are not easily excised. Finally, it can be used palliatively to help to control the cancer and relieve symptoms (palliative chemotherapy). Surgical procedures used to treat laryngeal cancer include laser surgery, cordectomy, partial laryngectomy, and total laryngectomy. The goal of surgical treatment is to remove the tumor and maintain the function of the larynx, speech, swallowing ability, and breathing. Laser microsurgery is used to treat early forms of glottic cancers and is now considered the standard approach at many institutions. It utilizes a beam of light to remove the tumor. A cost-effective alternative to an open surgical procedure, laser microsurgery results in good functional outcomes and causes minimal morbidity. Cordectomy is the removal of part or all of a vocal cord through the use of a transoral laser. If laryngeal cancer is present unilaterally on the vocal cords and is in the early stages, this option may be considered. Partial laryngectomy is performed to remove part of the larynx in the early stages of laryngeal cancer. This includes removal of part of the larynx, only one vocal cord, and the tumor. Preservation of the voice, which may be slightly altered or hoarse, is achieved because of the presence of the remaining structures. Patients will retain normal breathing and swallowing ability. A temporary tracheostomy may be required after partial laryngectomy to protect the airway. Total laryngectomy is the complete removal of the larynx. In advanced stages of laryngeal cancer where the cancer has spread beyond the vocal cords, a total laryngectomy is a curative procedure. In this procedure, the larynx and several rings of the trachea are removed. Swallowing ability will remain normal after total laryngectomy, but the surgery results in the inability to speak. The creation of a tracheostomy is required for breathing and because of the risk of aspiration of fluids and food after the removal of the epiglottis • Administer chemotherapy as ordered. Chemotherapy is used in combination with radiation and/or surgery in an effort to destroy cancer cells and reduce tumor size. • Institute bleeding precautions as necessary. Chemotherapy may increase bleeding risk due to decreased platelet count. • Tracheostomy care: use of humidified oxygen via a trach collar; pulmonary hygiene such as turning, coughing, deep breathing, and mobility; suctioning equipment, replacement tracheostomy tube (same size and one smaller), and obturator at bedside; tracheostomy care twice daily and as needed; management of oral secretions with a Yankauer suction tip (Fig. 25.10) Post-laryngectomy patients will have a permanent tracheostomy tube placed (Figs. 25.11 and 25.12). Good care is essential to maintain patency and decrease infection. Humidity, which will assist in moistening respiratory secretions, and pulmonary hygiene will facilitate secretion removal. Replacement equipment is necessary in case of unintended dislodgement of the tracheostomy. See Chapter 7 for more detailed information on tracheostomies. • Institute aspiration precautions. Postoperatively, the patient is at risk for aspiration because of the removal of upper airway structures/epiglottis. • Provide means for communication. Post-laryngectomy, the patient will not be able to speak due to the removal of the larynx. Provide pen and paper and a picture board. • Nutritional consultation Swallowing impairments may result in inadequate nutritional intake. Placement of a gastric or percutaneous esophageal gastrostomy tube may be required if the patient cannot maintain adequate nutritional intake.

Obstructive sleep apnea

-Diagnosis Diagnostic testing begins with a sleep history, which includes gathering information on sleep patterns, a history of snoring, and daytime sleepiness. Polysomnography (a sleep study) is performed to diagnose OSA and can be conducted in an overnight sleep laboratory or using home portable monitoring. Numerous biophysiological measurements are obtained during sleep, including an electrocardiogram, pulse oximetry, respiratory airflow, eye and skeletal muscle movement, and an electroencephalogram. A key value obtained during the sleep study is the apnea-hypopnea index value, the number of apneic events each hour. It can be used to characterize the severity of OSA. • Vital signs Hypertension and dysrhythmias are common findings in OSA due to the hypoxia and release of inflammatory mediators as a result of the apneic episodes. • Height and weight Obesity is a risk factor for OSA. • Sleep, rest, and activity history Disruptive sleep patterns, daytime fatigue, increased sleepiness, and the presence of snoring indicate OSA. • Assess for edema, bleeding, and respiratory distress postoperatively if a surgical option is pursued. Surgical procedures put the patient at risk for bleeding. Additionally, procedures in that area may cause respiratory distress if swelling occurs. • Diagnostic testing Patient may undergo a sleep study, electrocardiogram, and echocardiogram. -Treatment Treatment of OSA requires multiple interventions and the active participation of the patient. The use of continuous positive airway pressure (CPAP) is the treatment of choice (Fig. 25.5). Continuous positive airway pressure prevents collapse of the upper airway through the use of pressure delivered through the use of a nasal, oral, or oronasal mask during sleep (Fig. 25.6). A CPAP machine delivers a continuous stream of positive pressure, keeping the airway open and providing an unobstructed airway. Patients are taught about the operation, care, and maintenance of the CPAP machine. Follow-up care is conducted for problem solving and to evaluate the effectiveness of therapy. Weight management and loss are encouraged as a first-line intervention in conjunction with the use of CPAP. Positioning during sleep in a nonsupine position by using pillows is an effective secondary intervention. The avoidance of alcohol and sedatives before bedtime is an additional intervention. Oral appliances that are custom-made for the patient may be used to maintain airway patency. Oral appliances assist with mandibular repositioning to hold the mandible in a forward position to keep the airway open. Forward positioning of the tongue is accomplished with tongue-retaining devices.

Glucose-6-phosphate dehydrogenase (G6PD) deficiency

-Diagnosis Diagnostic testing for G6PD deficiency includes CBC, reticulocyte count, and blood smear analysis for Heinz bodies (accumulation of degraded Hbg in RBCs). The CBC in patients with this disorder reveals a mild to severe anemia. In patients with G6PD deficiency, the increased reticulocyte count reflects the production of new red blood cells secondary to hemolysis. The blood smear analysis may reveal RBC abnormalities, including the presence of Heinz bodies. Liver enzymes may be elevated in G6PD deficiency due to RBC destruction. Direct DNA testing and sequencing of the G6PD gene are also important to the diagnosis of this disorder. • Vital signs The G6PD enzyme is required for RBC development, and in its absence, anemia may develop. With the decreased oxygen-carrying capacity of the Hgb, tachycardia and tachypnea may develop as a compensatory mechanism. • Shortness of breath, pallor, and fatigue These clinical manifestations are exacerbated by the decreased oxygen-carrying capacity of the lysed RBCs. • CBC and reticulocyte count Decreased RBCs, hematocrit, and hemoglobin result due to hemolysis. The reticulocyte count may be increased in an attempt to replace the lysed cells. • Oxygenation saturation With severe anemia leading to insufficient hemoglobin to carry oxygen, oxygen saturation levels may decrease. • Blood smear analysis The G6PD deficiency results in RBC abnormalities and the accumulation of degraded Hgb (Heinz bodies). When a Heinz body is identified by macrophages in the spleen, the macrophage engulfs the Heinz body and a small piece of the RBC membrane, resulting in misshapen RBCs, called bite cells, in the RBC analysis. • Liver enzymes and bilirubin levels The excessive amounts of heme released from RBC destruction are catabolized to bilirubin concentrations that exceed the liver's ability to conjugate. This also results in the accumulation of indirect bilirubin. • Skin color and urine color The bilirubin accumulation in the circulation leads to jaundice and dark urine color. -Treatment Once definitively diagnosed, prevention is the key to the management and treatment of G6PD deficiency. Avoiding foods and medications that cause hemolysis is indicated. In the case of severe hemolysis, blood transfusions may be necessary because these transfused RBCs are not G6PD deficient and have a normal life span. Folic acid may also be prescribed to support RBC synthesis. Splenectomy may be indicated in patients with an enlarged spleen due to frequent episodes of hemolysis. • Provide supplemental oxygen. Supplemental oxygen is needed to treat decreased oxygenation and perfusion secondary to decreased Hgb. • Implement bleeding precautions. Decreased platelets increase the risk of bleeding, and bleeding precautions include the use of soft toothbrushes and direct pressure to venipuncture and injection sites until bleeding stops, among others. • Administer folic acid. Folic acid facilitates RBC production; G6PD places the patient in a state of high RBC synthesis.

Aplastic anemia

-Diagnosis Diagnostic testing for aplastic anemia includes a CBC, coagulation tests, iron levels, hemoglobin electrophoresis, and a bone marrow biopsy. The CBC results reveal pancytopenia, including decreased reticulocyte, WBC, and platelet counts. Due to the potential for thrombocytopenia, coagulation testing is important to evaluate the risk for bleeding. Patients with aplastic anemia are typically treated with blood transfusions, and repeated transfusions may lead to increased iron levels. Hemoglobin electrophoresis is often used in the evaluation of anemias because it is used to identify different forms of hemoglobin (Hgb). In aplastic anemia, there may be an increase in Hgb F, which is normally found in small amounts in adults. Bone marrow results typically demonstrate a lack of hematopoietic cells with a predominance of fat cells. • Vital signs Tachycardia and tachypnea are secondary to heart and lung compensation for the decreased oxygen-carrying capacity of RBCs. Temperature may be elevated due to inflammatory or infectious processes. • CBC results Bone marrow suppression caused by aplastic anemia results in pancytopenia, leading to decreased RBCs, WBCs, and platelets • Bone marrow results Aplastic anemia leads to a lack of hematopoietic cells, with a predominance of fat cells. • Oxygen saturation Severe anemia leads to insufficient hemoglobin to carry oxygen; oxygen saturation levels may decrease. • Signs of bleeding Due to decreased platelets, the patient is susceptible to bleeding gums, nosebleeds, and increased time to stop bleeding from trauma, venipuncture, injections, and other causes. • Fatigue and pallor Decreased oxygen to tissues secondary to decreased RBCs leads to fatigue, particularly on exertion, and pallor due to decreased perfusion. • Dizziness and headache Decreased oxygen may lead to dizziness and headache. -Treatment During the diagnostic evaluation phase of aplastic anemia, blood transfusions are a primary treatment. However, the goal of treatment is to minimize transfusions to decrease the sensitization that ultimately increases the risk for bone marrow transplantation rejection. The preferred treatment for aplastic anemia is bone marrow transplantation from an HLA-matched sibling donor. Other treatments focus on stimulating bone marrow with medications such as filgrastim (Neupogen®) and epoetin-alfa (Epogen®), which stimulate the bone marrow production of cells and relieve symptoms. In patients over the age of 60, immunosuppressive therapy is preferred. This therapy is also used in patients with no HLA-matched sibling donor. In patients who develop aplastic anemia secondary to chemotherapy or radiation treatments, Epogen or Neupogen may be used to stimulate bone marrow activity; however, the bone marrow usually recovers once these treatments are completed. • Provide supplemental oxygen. Supplemental oxygen is needed to treat decreased oxygenation and perfusion secondary to decreased Hgb. • Administer blood products. Blood components, including packed red blood cells and platelets, may be required for the treatment of symptomatic pancytopenia. • Implement bleeding precautions. Decreased platelets increase the risk of bleeding, and bleeding precautions include the use of soft toothbrushes and direct pressure to venipuncture and injection sites until bleeding stops, among others. • Protect from injury. Due to pancytopenia, the patient is at risk for decreased tissue perfusion that can result in dizziness and falls. The patient is also at risk for bleeding and infections.

Carotid artery disease

-Diagnosis Diagnostic testing involves physical assessment and noninvasive and/or invasive procedures. Physical assessment of carotid artery disease includes auscultation over the blood vessels in the neck. When the bell of the stethoscope is placed over the side of the neck anterior to the sternocleidomastoid muscle, a carotid bruit may be heard. This sound occurs when blood flow becomes turbulent while it hits an obstruction at the carotid bifurcation. Noninvasive tests include carotid duplex scanning, computed tomography angiography (CTA), and magnetic resonance angiography (MRA). Duplex ultrasound is the most commonly used screening tool to evaluate for atherosclerotic plaque and stenosis of the external carotid artery (Fig. 31.7). An invasive test, conventional carotid angiography, is the gold standard for diagnosis of the severity of carotid artery disease. This test involves inserting a catheter into an artery, typically the femoral artery, and guiding it up to the carotids. Contrast dye is injected through the catheter that allows visualization of the carotid arteries via radiographical imaging. Because of the invasive nature of the test and the risks associated with it, noninvasive tests are more commonly used for diagnosis. See Table 31.9 for information on noninvasive diagnostic tests. • Vital signs Hypertension is a risk factor for carotid artery disease. Fluctuations in blood pressure and bradycardia may be complications of treatment. • Neurological assessment Difficulty speaking, weakness, facial droop, acute vision problems, and acute headache may be signs of stroke. • Auscultation of the carotid arteries Asymptomatic carotid artery stenosis may be identified by the presence of carotid bruits, sounds created by blood flow through a stenosed vessel, on auscultation. • Stroke history/signs of stroke Determines if patient is symptomatic or asymptomatic which impacts treatment Postprocedure CEA/CAS • Respiratory rate, SpO2, stridor, tracheal deviation In CEA—Hematoma formation at the incision site can cause tracheal pressure resulting in respiratory distress, which can escalate rapidly as the hematoma enlarges. • Vital signs: HR, BP In CEA—Prior to treatment, the carotid baroreceptor sensed a low pressure in the stenotic carotid artery. Following CEA, a new "normal" pressure may be sensed as a high pressure signalling the vagus nerve to respond, resulting in vasodilation, bradycardia, and hypotension. Prolonged hypertension may result in damage to the arterial graft, causing hemorrhage as well as placing the patient at risk of intracerebral haemorrhage. In CAS—Bradycardia, related to manipulation of the carotid sinus baroreceptors located in the carotid bulb, may occur during the procedure just after the stent implantation; Persistent hypotension can be caused by the effect of the stent on the carotid sinus baroreceptors. • Post-CEA—Cranial nerves, specifically VII, X, XI, and XII (see Table 31.10) Retraction on the lower cranial nerves during surgery can result in temporary or permanent nerve damage due to trauma or edema. • Post-CAS - Renal function Angiogram dye is nephrotoxic, especially in those patients who already have kidney disease. -Treatment Treatment for patients with carotid artery stenosis depends on the severity of the occlusion and whether the individual is symptomatic or asymptomatic. An asymptomatic patient is without a prior history of stroke or TIA. A symptomatic patient is one who presents with TIA, stroke in evolution, or completed stroke. The management of asymptomatic patients starts with optimal medical therapy (OMT) which includes a combination of healthy lifestyle changes such as weight management, smoking cessation, limited alcohol consumption, and control of comorbidities such as diabetes and hypertension, and use of medications to manage the cause of atherosclerotic vascular disease. Medication management includes antiplatelet therapy with aspirin. Clopidogrel is an option if aspirin in contraindicated. Antihypertensive therapy for blood pressure control is essential. The AHA recommends maintaining blood pressure below 140/90 mm Hg. Many classes of medications, such as calcium channel blockers, angiotensin-converting enzyme inhibiters, and angiotensin receptor blockers, are effective in blood pressure control. Lipid-lowering therapy with statins is also recommended. Without stating an LDL-C target level as evidence, current guidelines suggest that the use of high-intensity statins shows a 50% reduction in LDL-C levels. Somewhat controversial is the use of invasive procedures to treat the obstruction itself. Patients would benefit from either surgical or endovascular revascularization but are at risk for the complications of the procedures, which include stroke. Current guidelines suggest revascularization in medically stable patients with carotid endarterectomy (CEA) or carotid artery stenting (CAS). Both procedures will be discussed below in detail. The management of symptomatic patients includes OMT but requires revascularization with CEA or CAS due to the presence of stroke or stroke symptoms unless excessive comorbidities put the patient at unreasonable risk of death. • Administer antihypertensive medication as ordered to maintain BP below 140/90 mm Hg Prolonged increases in BP may cause vessel rupture, which leads to hemorrhage and stroke. • Administer lipid-lowering medication as ordered Reducing LDL-C helps reduce plaque formation in the carotid vessels. • Administer antiplatelet aggregates as ordered Antiplatelet therapy helps reduce platelet aggregation, resulting in decreased risk of obstruction in the vessel. • Manage diabetes mellitus/maintain blood glucose within normal levels Poorly controlled diabetes mellitus results in increased plaque formation in the vessels due to the breakdown of fats for energy, increasing the risk for ischemic stroke.

Valvular disease

-Diagnosis Diagnostic tests used to diagnose valvular disease include: • Echocardiogram to identify valve abnormalities and ejection fraction • Chest x-ray to identify left or right heart hypertrophy and pulmonary edema • Stress testing to identify functional capacity • Heart catheterization as a definitive test for stenosis done prior to corrective surgery • CT or MRI • Vital signs Hypertension, tachycardia, and tachypnea are indicative of HF due to increased resistance to flow and backflow of blood to the pulmonary system. Tachycardia occurs as a compensatory mechanism to increase cardiac output and oxygenation. Fever is indicative of infection and increases metabolic demands. Decreased SpO2 occurs with pulmonary congestion. • Pain assessment Chest pain and palpitations may occur with some murmurs. • Monitoring for irregular heart rhythm Dysrhythmias, specifically atrial fibrillation, are common in valve disease. • Peripheral vascular assessment Poor color, cool extremities, weak peripheral pulses, delayed capillary refill, and edema can indicate inadequate cardiac output. • Breath sounds Crackles and orthopnea indicate pulmonary congestion. • Activity tolerance Dyspnea on exertion, weakness, and fatigue indicate worsening HF. • Auscultate heart sounds. Murmurs are typically the initial manifestation of valvular disease. • Daily weights, intake and output Weight increases and intake greater than output can be indicative of HF. • Monitor international normalized ratio (INR). Patients with valve replacements on warfarin need to maintain an INR that is two to three times normal. -Treatment Medication management for valvular disease is dependent on the etiology and degree of the disease. Valvular diseases with infectious etiology require antimicrobial therapy, whereas advanced valvular diseases require general HF management. That includes: • Angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARBs), or angiotensin receptor-neprilysin inhibitors (ARNIs) with beta blockers to reduce heart rate and blood pressure • Diuretics to decrease preload and pulmonary congestion (see Safety Alert) Medication management is also determined by the type of valve utilized in valve replacement, if necessary. Replacement valves are generally categorized as mechanical or tissue/bioprosthetic. Patients who undergo valve replacement with a mechanical prosthetic valve will need to be anticoagulated for life to prevent thrombotic events such as strokes. Tissue valves have recommended anticoagulation for only 6 months after placement but have less longevity. They are typically considered in patients who are older or cannot be anticoagulated. • Provide supplemental oxygen and elevate the head of the bed. Oxygen and positioning increase oxygenation and ventilation. • Administer medications as ordered: diuretics, ACE inhibitors, ARBs, ARNIs, beta blockers, antibiotics, anticoagulants. Medications are indicated for the relief of symptoms, not as a curative measure. Diuretics help decrease fluid overload; ACE inhibitors, ARBs, ARNIs, and beta blockers decrease heart rate and blood pressure, thus decreasing myocardial workload. Antibiotics are indicated if the valvular disease is caused by an infection such as IE. Anticoagulation decreases the risk of thrombus formation in patients with a prosthetic valve or patients in atrial fibrillation. • Restrict sodium and fluids. To decrease fluid overload and reduce HF symptoms

Deep vein thrombosis

-Diagnosis Diagnostics include a combination of pre-test probability (PTP) testing, D-dimer testing, and compression ultrasonography (CUS). These have proven to be the most accurate, safe, and effective diagnostic tools for DVT. The evaluation of a patient with a suspected DVT begins with an assessment of a set of clinical prediction rules, pre-risk probability, for DVT. The Wells score is a PTP scoring system that categorizes patients as high, moderate, or low probability. This is based on the presence of clinical features commonly associated with DVT and identification of an alternative diagnosis. Box 31.3 outlines both the PTP and DVT risk classification. In patients with a low or moderate probability the next step is D-dimer testing. The D-dimer test is a global marker of coagulation activation by measuring fibrin degradation products produced from fibrinolysis (clot breakdown). A negative D-dimer test can exclude DVT without an ultrasound. Conversely, an elevated D-dimer suggests DVT but requires further testing to confirm the diagnosis because of the low specificity of the test. This low specificity is caused by the increase of the D-dimer level in other conditions, including infection, inflammation, cancer, surgery and trauma, extensive burns or bruises, ischemic heart disease, stroke, PAD, ruptured aneurysm or aortic dissection, or pregnancy. In the presence of a positive D-dimer or high probability PTP the next step is compression ultrasonography (CUS). It allows rapid and clear visualization of thrombi, including identification of unstable or floating thrombi, which may cause emboli. Contrast venography, CT venography and MRI venography are other diagnostic tools but are rarely needed or utilized. These alternatives to ultrasound may be beneficial in selective cases, such as in the morbidly obese or when pelvic or abdominal thrombosis is suspected. • Vital signs with oxygen saturation Hypotension, tachycardia, and decreased oxygen saturation could indicate the presence of a PE or bleeding, especially if the patient is anticoagulated. • Assess extremity for pain, tenderness, warmth, redness, or swelling Common symptoms of DVT that occur because of obstruction of blood flow and may indicate location of the clot • Compare right and left calf, thigh, or arm circumferences Localized edema due to obstruction to blood flow in one extremity may suggest a DVT. • Gentle palpation to inspect for induration Induration (hardening) helps to locate the placement of the clot in the blood vessel. • D-dimer test Measures fibrin degradation products produced from clot breakdown. A positive result stratifies the patient into a high-risk category for DVT. • Laboratory values: INR, PT/aPTT, hemoglobin, and hematocrit • The INR and PT/aPTT should be prolonged. • The hemoglobin and hematocrit should be within normal limits. The PT/INR evaluates the extrinsic coagulation cascade and is used to evaluate the effectiveness of warfarin. The aPTT evaluates the intrinsic coagulation cascade and is used to evaluate the effectiveness of heparin. • Assess for signs of bleeding such as bruising, petechiae, hematuria, bloody stools Signs of bleeding may indicate a need to modify or decrease anticoagulation therapy. -Treatment The first step in treatment is prevention. In low risk patients, early ambulation may be all that is necessary. Venous thromboembolism (VTE) prophylaxis is indicated in at-risk hospitalized populations. In patients with a low bleeding risk pharmacological prevention is recommended. Preferred medications include low molecular weight heparin (LMWH), unfractionated heparin, or, in patients with heparin-induced thrombocytopenia (HIT), fondaparinux can be used. In patients with a higher risk of bleeding mechanical VTE prophylaxis is indicated. This includes the use of graduated compression stockings, venous foot pumps, and active external intermittent compression devices. The benefits of these methods include their effectiveness, ease of application, and safety especially in respect to bleeding. Intermittent compression devices apply external pressure to the limb which promotes blood flow velocity, reduces venous stasis, and increases levels of systemic fibrinolysis. Despite widespread use, there is limited evidence regarding the use of graduated compression stockings, venous foot pumps, or combined medical and mechanical prophylaxis. • Early ambulation Bedrest has been recommended in the past, but recent studies show early ambulation does not result in more complications (see Evidence-Based Practice) and is key to prevention. • Leg elevation When at rest, the affected extremity should be elevated at least 10 to 20 degrees above heart level to enhance venous return and reduce swelling. • Compression stockings Should be worn at all times. Compression promotes venous return and decreases leg swelling. • Avoid use of sequential compression devices (SCDs) in affected extremity An SCD may cause the thrombus to break away, resulting in an embolus. • Encourage adequate fluid intake Prevents dehydration and sluggish blood flow, which exacerbates DVT growth • Administer anticoagulation medications as ordered Anticoagulation with unfractionated heparin followed by long-term oral anticoagulation prevents the formation of new thrombi and inhibits the growth of the existing thrombi. • Administer thrombolytic agent as ordered Thrombolytic agents dissolve existing thrombi and decrease the instance of vascular damage.

COPD

-Diagnosis Inspection is the first step in the assessment of the respiratory system. Abnormalities in the patient's level of consciousness and orientation status may indicate hypoxia. During inspection, the nurse should also assess the patient's speech. Patients should be able to speak freely and in full and complete sentences. Patients in respiratory distress may have difficulty speaking because of shortness of breath. The characteristics of the patient's fingernails may also indicate chronic respiratory dysfunction. Clubbing of the fingernails (Fig. 23.11) is a sign of chronic hypoxia and is a common assessment finding in patients with COPD. The diagnosis of COPD is based on patient history, physical assessment, and spirometry. Generally, a chest x-ray is obtained to rule out other causes of respiratory distress. A computed tomography (CT) scan may be considered when the lungs need to be viewed in more detail. Pulmonary function tests also aid in diagnosis. The most commonly performed pulmonary function test (PFT) is spirometry. Spirometry is the measurement of lung volumes and airflow. The two tests done by spirometry are forced vital capacity (FVC) and forced expiratory volume in 1 second (FEV1). Forced vital capacity is the maximum volume of air exhaled during a forced expiration; FEV1 is the volume of air expired in the first second of maximal expiration after a maximal inspiration. It is a measurement of the lung's ability to empty quickly. Diagnosis is based on both the value of FEV1 and FEV1/FVC. Using normal values for the sex, age, and height of the patient, the FEV1 is measured, then calculated as a percentage of a normal value. The FEV1/FVC is computed as a percentage of normal. Patients with COPD show a decrease in both the FEV1 and the FEV1/FVC. Chronic obstructive pulmonary disease is a progressive disease. As the disease progresses, FEV1 and FEV1/FVC deteriorate, and exacerbations become more frequent and life threatening. The severity and progression of the disease correlate to the degree of abnormality of the tests. The Global Initiative for Obstructive Lung Disease has identified stages or grades of the disease: Grade I, mild; Grade II, moderate; Grade III, severe; and Grade IV, very severe. • Oxygen saturation An SpO2 of less than 90% indicates a significant oxygenation problem. The goal is to maintain the SpO2 at 90% or above. • Respiratory rate Monitor respiratory rate to avoid hypoventilation—the respiratory drive in COPD is hypoxemia, not hypercapnia. See Safety Alert. • Breath sounds The presence of crackles and wheezes may indicate airway obstruction. Crackles indicate the premature closing of the airways. • Pursed-lip breathing Patients with COPD display pursed-lip breathing to keep the airways open longer and prolong exhalation, allowing for increased time for oxygen and carbon dioxide exchange. • Cough Cough is a cardinal sign of pulmonary disease. It is a protective mechanism for the tracheobronchial tree. • Temperature Increased temperature is a sign of an infectious trigger. • Dyspnea Use of the visual analog dyspnea scale allows the patient to identify his or her own level of dyspnea because dyspnea is a subjective experience. • Weight Monitoring weight identifies nutritional deficiencies—with prolonged increased work of breathing and decreased energy, the ability to eat decreases. -Treatment The management plan for COPD has four goals: assess and monitor the disease, reduce modifiable risk factors, manage stable COPD, and manage exacerbations. Assessment includes regular pulmonary function tests and chest x-rays with an exacerbation to identify other thoracic abnormalities or progressive changes within the structure of the lungs. Additional important biological measurements in the COPD management plan include pulse oximetry (SpO2) to determine the severity of hypoxemia during an exacerbation and ABGs to measure the lungs' ability to clear carbon dioxide, as evidenced by PaCO2 and acid-base balance. The ABGs also evaluate oxygenation through PaO2 values and help identify the patient's response to oxygen therapy and medications. Finally, sputum cultures are assessed to identify organisms causing an infectious trigger to an exacerbation. Reducing modifiable risk factors includes, if possible, decreasing or eliminating exposure to chemicals, dust, and air pollutants, especially smoke. The single most important modifiable risk factor is smoking cessation. Managing stable COPD includes health education regarding the risks and the warning signs of an exacerbation, oxygen therapy, moderate exercise as tolerated, and the mainstay of medical management: medications. The cornerstone of pharmacological management is bronchodilators: beta2-adrenergic agonists and anticholinergics used individually or in combination on an as-needed or regular basis to control symptoms. A way to evaluate the effectiveness of treatment and determine a course of therapy is to administer a bronchodilator treatment after the initial spirometry and then repeat the test. This approach helps determine how the lungs respond to the bronchodilator or how the pulmonary obstruction is reversed with the medication. Medication management progresses as the disease progresses and begins with inhaled bronchodilators on an as-needed basis. As the disease worsens, long-term bronchodilators are added. Inhaled glucocorticoids are added when and if the patient experiences frequent exacerbations. Identifying and quickly managing exacerbations is essential because they can dramatically impair pulmonary function and accelerate disease progression. Inhaled bronchodilators and oral glucocorticoids are used, as well as antibiotics if the cause of the exacerbation is infection. Noninvasive positive-pressure ventilation can be used to improve oxygenation and ventilation as well as reduce the need for endotracheal intubation and ventilation. • Administer bronchodilators as ordered. Bronchodilators are bronchial smooth muscle relaxants that help open the airway. Beta2-agonists (short-acting beta-agonists [SABAs] and long-acting beta-agonists [LABAs]) relax the smooth muscles of the airway by stimulating beta-adrenergic receptors, resulting in antagonism to bronchoconstriction. Anticholinergics relax and enlarge the airways in the lungs, making breathing easier. Anticholinergics can also protect the airways from bronchospasm and may reduce the amount of mucus produced by the airways. • Provide oxygen. Increase the SpO2 to 90%. Patients may be placed on continuous oxygen therapy if the SpO2 is less than or equal to 88% or the PaO2 is less than or equal to 60 mm Hg. • Position—semi-Fowler's The semi-Fowler's position increases oxygenation by allowing adequate lung expansion. • Provide small, frequent meals with dietary supplements. Small, frequent meals take less energy to consume and avoid excessive pressure on the diaphragm that may be associated with a large meal.

Leukemia

-Diagnosis Often a patient presents to the healthcare provider with complaints of flu-like symptoms such as fatigue, low-grade fever, and pallor, although many times a patient is asymptomatic, and a routine CBC reveals the leukemia. A CBC not only reveals the leukocytosis, or increased WBC count, but also demonstrates anemia and thrombocytopenia that occurs as a result of the congested bone marrow. A history and physical examination are performed. Confirmation of the diagnosis of leukemia usually follows a bone marrow biopsy that shows the type of leukemia and extent of the malignancy. Genetic testing can be performed on these cells to determine any chromosomal abnormalities. • Vital signs Low-grade fevers in response to minor infections by cuts, abrasions, sores, and so forth occur because of the decrease in mature neutrophils needed to produce a more pronounced temperature elevation. • Fatigue, pallor, dizziness, shortness of breath These clinical manifestations of anemia occur as a result of decreased erythrocytosis because the bone marrow is congested with WBCs. • Excessive bruising, petechiae (different from a rash—when you push, petechiae do not blanch) These clinical manifestations of thrombocytopenia occur as a result of decreased production of platelets because the bone marrow is congested with WBCs, and there may be spontaneous bleeding into the subcutaneous tissues. • CBC values Leukocytosis of leukemic WBCs occurs from a single mutation. The excessive WBCs clog the bone marrow, resulting in decreased production of RBCs and platelets. -Treatment Systemic chemotherapy is initiated to destroy the leukemic cells and induce a remission that indicates that the bone marrow is free of leukemic cells and is able to produce healthy blood cells. Remission does not indicate a cure. Radiation therapy is sometimes used as part of this treatment. There are many different chemotherapeutic agents employed today in the treatment of leukemia, and they may be administered solely or in combination regimens. Numerous clinical trials are ongoing, all with the goal of inducing remission. Treatment strategies consist of two main phases: remission induction and post-remission maintenance. Remission induction includes the initial administration of chemotherapeutic agents. High doses of chemotherapy are given and may be accompanied by radiation therapy. This usually causes the patient to become acutely ill. This is very difficult on the patient, especially if asymptomatic at the time of diagnosis, because the patient may feel the treatment is worse than the disease. Education regarding the progression of the disease and the need for chemotherapy, as well as helping the patient to establish a good support system, is crucial in the early stages of treatment. Routine CBCs to monitor the progression of myelosuppression caused by chemotherapy is indicated to prevent complications. Transfusions of RBCs and/or platelets are usually an aspect of the supportive care for these patients. In the past, chemotherapy almost always led to infection as a result of the neutropenic state that these medications produce. The advent of granulocyte colony-stimulating factors (GCSFs) has changed this because they are frequently given post-chemotherapy to stimulate the bone marrow to produce neutrophils. Filgrastim (short-acting) and pegfilgrastim (long-acting) are given as subcutaneous injections. In many cases, these medications prevent some patients from developing post-chemotherapeutic infections. After the induction phase, which may lead to a state of remission or partial remission, the patient usually enters a post-remission maintenance phase of care. Chemotherapy may continue at lower doses and/or less frequently in order to suppress the formation of leukemic cells. This may continue for months or years. Transplantation is currently the only possibility for a cure from leukemia. Previously, bone marrow transplantation (BMT) was the only type of transplantation, but peripheral stem cell transplantation (PSCT) or hematopoietic stem cell transplantation (HSCT) are now more often used. With both procedures, donor cells are needed to transplant into the bloodstream of the patient, either the patient's own (autologous) or from a donor (allogeneic). The advantage of PSCT over BMT is primarily one of comfort for the donor. In a BMT, bone marrow is harvested via a large needle inserted into the iliac bone. (The bone marrow biopsy procedure is described in Chapter 33). The stem cells in a PSCT are gathered in a manner similar to donating blood from a peripheral vein. The stem cells are then separated in an apheresis machine (a machine that separates the stem cells from the rest of the blood components), and the blood is returned to the donor minus the stem cells. The success rate of transplantation is approximately the same for both procedures. A transplantation is not without its potential complications in the form of graft-versus-host disease (GVHD) when donor bone marrow or stem cells attack the recipient. Managing GVHD is complicated and requires maintaining a balance between allowing the body some degree of immune response and suppressing this response to the extent that it can be fatal if the body's immune system successfully destroys the new stem cells. Despite enduring a transplantation, there is also the possibility that the leukemia can return, causing a relapse. • Administer chemotherapy as prescribed. The patient is started on chemotherapy to destroy the leukemic cells. • Institute neutropenic precautions. The patient needs to take extra precautions to prevent infection due to low neutrophil counts. • Prophylactic use of antibiotics, antivirals, and antifungals as ordered A prophylactic regimen of antibiotics, antivirals, and antifungals is often initiated to provide added protection against infection when the neutrophil count is low. • Administer IV antibiotics. When the ANC is less than 1,000, it is imperative to start IV antibiotics immediately in order to prevent sepsis and possible death. • Symptom management (nausea/vomiting/diarrhea, ulcerations of the mouth) Post-chemotherapy/post-radiation symptom management is continuously assessed to maintain the patient's quality of life. Antiemetics or antidiarrheal medication are indicated to minimize discomfort as well as to decrease fluid loss. • Administer ordered blood products. The patient may require blood products as cell counts (RBCs and platelets) drop because of the myelosuppression caused by chemotherapy.

Myocarditis

-Diagnosis Patient history, C-reactive protein, troponin, brain natriuretic peptide (BNP), ECG, echocardiography, and magnetic resonance imaging (MRI) are used in the diagnostic process. Myocardial biopsy, also called endomyocardial biopsy, is the definitive test but is reserved for more acute cases. • Vital signs Hypotension, hypertension, tachycardia, tachypnea, and hypoxia are signs of heart failure. Fever is indicative of infection. • Cardiac rhythm Dysrhythmias are a common and dangerous clinical manifestation and must be identified and treated promptly. • Assess for crackles, edema, jugular vein distention (JVD), weight gain, and decreased urine output. These are evidence of the weakened heart muscle seen with heart failure. -Treatment Some cases of myocarditis resolve within days, whereas others progress to heart failure and acute dilated cardiomyopathy that require significant intervention, which may include heart transplantation, implanted cardiac defibrillators, or mechanical circulatory support (see Chapter 32). Medical treatment focuses on the management of heart failure, dysrhythmias, and dilated cardiomyopathy. Antiviral immunosuppressants (prednisone and azathioprine) and immunotherapies such as immunoglobulin IgG may be used but have limited evidence of effectiveness. • Administer antivirals, antimicrobials, immunosuppressives, and immunoglobulins as ordered. Medications are administered depending on the cause of myocarditis. • Administer heart failure medications as needed. Heart failure is a common manifestation and must be treated to optimize cardiac output and tissue perfusion. • Provide emotional support. The diagnosis of myocarditis can cause fear and anxiety.

Infectious endocarditis

-Diagnosis Tests used to confirm the diagnosis of IE are blood cultures, two sets from different sites, and transthoracic echocardiogram (TTE) or transesophageal echocardiogram (TEE). Echocardiography can identify valve dysfunction, vegetative growth, abscesses, and changes in heart size and pumping ability that can occur with IE. Echocardiography is described in more detail in Chapter 28. An elevated white blood cell count may also be indicative of infection. • Vital signs Fever is indicative of ongoing acute infection. Hypotension, tachycardia, tachypnea, and low SpO2 can be signs of sepsis or heart failure. • Auscultate breath sounds. Crackles may be a sign of heart failure related to valve dysfunction. • Auscultate heart sounds. A new or worsening murmur may occur due to valve damage. • Assess neurological function. Neurological changes or deficits in pupils, grips, foot pushes, facial droop, and speech may be signs of CNS embolization. • Assess extremities. Cyanosis or pallor, delayed capillary refill, and decreased peripheral pulses may indicate peripheral embolization. Edema could be a sign of heart failure related to valve dysfunction. • Skin assessment Osler's nodes, Janeway lesions, and splinter hemorrhages are indicative of IE. • Monitor diagnostic test results. Repeated culture reports are used to evaluate the effective treatment of IE. White blood cell (WBC) counts can indicate responsiveness to infection. Echocardiograms can evaluate the size of vegetation and valve function and can be used to predict the risk of complications. • History of drug use, invasive procedures, implanted vascular or cardiac devices, or valve replacement surgery Common risk factors for IE -Treatment Medication management consists primarily of IV antibiotic therapy. The increasing trend of microbial resistance has led to the use of combination therapy. The standard duration of treatment is 4 to 6 weeks but may be longer for prosthetic valves. Patients are often discharged to home on IV antimicrobial therapy. Shorter duration is recommended for some combination therapies. Oral antimicrobial agents are rarely used as initial treatment. Repeated blood cultures may be obtained until results are negative, indicative of adequate bactericidal effects. Prophylactic use of oral antibiotics is not routinely recommended but is used for patients at high risk (see Safety Alert). The choice of antimicrobial agents is complex and based on the organism cultured and the sensitivity report, right-sided versus left-sided IE, native versus prosthetic valve involvement, patient comorbidity, and other factors. Infectious disease specialists are often consulted. Penicillin G, ceftriaxone, vancomycin, nafcillin, and gentamicin may be considered in various combinations for the treatment of IE. Supportive treatment for the common complications of IE, especially HF, is also indicated to optimize cardiac output and tissue perfusion. • Administer antibiotics as prescribed. Treatment for IE is long-term IV antibiotic treatment. • Maintain IV access for antibiotic administrations. Intravenous access is essential for antibiotic administration. Long-term venous access, such as a peripherally inserted central catheter (PICC), may be considered. • Administer heart failure medications as needed. Heart failure treatment optimizes cardiac output and tissue perfusion. • Provide social support during prolonged hospitalization. Social isolation due to hospitalization may contribute to depression, anxiety, and anger. • Refer patient to addiction counseling services if drug use has caused the disease. Stopping recreational IV drug use may help limit the reoccurrence of IE and lead to a better quality of life.

Pericarditis

-Diagnosis Tests used to diagnose pericarditis include ECG, chest x-ray, echocardiogram (transthoracic or transesophageal), cardiac CT scan, and MRI. The hallmark ECG changes include widespread ST-segment elevation or PR-segment depression (Fig. 30.6). The finding of cardiomegaly and clear lung fields on chest x-ray may indicate a pericardial effusion (fluid buildup in the pericardial sac) and might be supportive of the pericarditis diagnosis. Pericardial effusion might also be evident on an echocardiogram, CT scan, or MRI. Laboratory tests include serial cardiac biomarkers to rule out MI. Positive blood cultures, a complete blood count with a high WBC count, and positive inflammatory markers such as C-reactive protein or sedimentation rates may indicate the presence of infection or inflammation, leading to the diagnosis of pericarditis when combined with the associated clinical manifestations. • Vital signs Hypotension, tachycardia, tachypnea, and pulsus paradoxus are indicative of cardiac tamponade, which is due to an excessive or sudden buildup of pericardial effusion. Fever is indicative of an ongoing infection. • Pain Chest pain that is relieved by sitting up and leaning forward distinguishes pericarditis pain from the pain associated with MI. • Auscultate heart sounds. A friction rub is a common finding in pericarditis. Muffled heart tones may indicate pericardial effusion or cardiac tamponade. • ECG ST elevation or PR depression in all or most leads can be associated with pericarditis. -Treatment Medication management goals are to alleviate pain and stop the inflammatory process. Aspirin and other NSAIDs are indicated. Colchicine may be used as an additional anti-inflammatory medication with acetylsalicylic acid (ASA) or NSAIDS. If pain or inflammation is not relieved by ASA or NSAIDs, corticosteroids may be used. Additional treatment may be warranted depending on the etiology of the disease. For example, in addition to the use of anti-inflammatory agents, antimicrobial therapy may be instituted for bacterial pericarditis. • Keep the head of the bed elevated. Pericardial effusion exerts pressure on surrounding organs, resulting in orthopnea (shortness of breath when lying down) and dyspnea. Raising the head of the bed relieves shortness of breath. Pain is also relieved by sitting in the upright position. • Administer NSAIDs or ASA and colchicine medications as prescribed. Pain relating to pericarditis is associated with inflammation, so control is largely managed with anti-inflammatories. Steroids are added if necessary. • Provide emotional support. Anxiety can occur because of the fear that the pain is from a heart attack.

Asthma

-Diagnosis The diagnosis and assessment of asthma include a detailed patient history, pulmonary function tests, chest x-ray, and pulse oximetry and possibly arterial blood gases (ABGs). The detailed patient history should include childhood illnesses, family history of allergies or asthma, eczema, smoking history, occupational history, and exposure to environmental triggers. Additionally, the patient history should include the frequency of symptoms, whether they are triggered by any specific activity or time (day, evening, spring, or fall), how long the symptoms last, and mechanisms the patient uses to relieve the symptoms. The chest x-ray is needed to rule out any other respiratory conditions and to monitor progressive changes in the chest. Pulmonary function tests (PFTs) are a predominant feature in evaluating asthma. PFTs are a group of tests used to evaluate the functioning of the respiratory system. Some of the more commonly used PFTs are spirometry, peak expiratory volume, and pulse oximetry. There are other PFTs available for use in confirming a diagnosis of asthma when routinely used tests or exams do not provide a clear diagnosis of asthma. Spirometry is a test that measures airflow and lung volumes, such as the forced expiratory volume (FEV). One of the major tests of pulmonary function is the forced expiratory volume in 1 second (FEV1). The FEV1 measures the amount of air forced out of the lungs after a full inspiration. The volume is measured at 1 second. The measurement is compared to a normal person's predicted volume based on age and gender. A decrease in this test of 15% to 20% below the predicted value for age and gender is diagnostic of asthma. An increase of 12% after administration of a bronchodilator is also diagnostic of asthma. Peak expiratory flow readings measure the maximum airflow expired during a forced expiration. The patient's peak flow readings are compared to the personal best reading with a reading obtained during an exacerbation or "asthma attack." Patients are encouraged to monitor their peak flow values. The reading done during an exacerbation as compared to a personal best allows the patient to recognize the severity of the respiratory distress. The patient's asthma action plan (discussed later) is based on the peak flow readings (Box 26.1). Both noninvasive and invasive methods can be used to obtain oxygen saturation levels in the blood. Pulse oximetry is a noninvasive method of measuring oxygen saturation (SpO2). It can be used to help determine the severity of the respiratory distress. The normal pulse oximetry value is 95% to 100%. Pulse oximetry monitoring detects desaturation of the hemoglobin before the patient exhibits symptoms. Arterial blood gas monitoring is an invasive sampling of arterial blood to measure the oxygenation of the blood (PaO2), acid-base balance, and the partial pressure of carbon dioxide (PaCO2). PaO2 is an important term and component of ABGs. PaO2 is the partial pressure of oxygen in arterial blood. PaO2 reflects a more accurate measure of oxygen in the arterial blood than SpO2. Once the PaO2 in arterial blood falls below the threshold of 60 mm Hg, there is a steep reduction in SpO2. Although a PaO2 of 60 mm Hg is considered acceptable, a more acceptable range for PaO2 is 80 to 95 mm Hg. Arterial blood gases provide the best information with regard to identifying the patient's response to oxygen and ventilation therapy and medications. Once asthma is diagnosed, the disease is classified based on the frequency and severity of the symptoms. One approach through the Global Initiative for Asthma guidelines identifies the level of control and the treatment recommended for asthma. Asthma is classified as "mild asthma," "moderate asthma," "severe asthma," and "uncontrolled asthma." Asthma severity may be assessed retrospectively through close evaluation of the treatment required to manage symptoms. • Vital signs—pulse rate, temperature, respiratory rate, peak flow measurement Increased pulse rate may be a sign of poor oxygenation or anxiety or a side effect of treatment with bronchodilators; increased temperature is a sign of infection; a respiratory rate greater than 30 breaths per minute is due to increased anxiety and increased work of breathing due to bronchial constriction; peak flow values indicate the severity of the asthma attack and help monitor recovery. • Oxygen saturation Oxygen saturation of less than 90% indicates significant oxygenation problems. The goal is to maintain the SpO2 at 90% or above. Hypoxemia causes restlessness, anxiety, and increased blood pressure and pulse rate. • Arterial blood gas The patient initially exhibits respiratory alkalosis caused by hyperventilation (decreased PaCO2). As respiratory difficulty increases, respiratory acidosis develops (increased PaCO2). • Breath sounds The presence of wheezing indicates narrowing of the airway—expiratory first, then inspiratory. Absent or diminished breath sounds signify a decrease in the movement of air due to increased obstruction or respiratory exhaustion. • Level of consciousness Changes in level of consciousness are indicators of hypoxemia. • Ability to speak in full sentences This demonstrates the ability to move air throughout the tracheobronchial tree; inability to speak in full sentences is an indicator of respiratory distress. • Cough Irritation causes stimulation of the cough receptors. • Use of accessory muscles Use of accessory muscles demonstrates respiratory fatigue. • Position—tripod position (sitting upright with arms propped on a table) or semi-Fowler's position The patient may assume the tripod position in an attempt to decrease the work of breathing. • Monitor dyspnea Use of the visual analog dyspnea scale allows the patient to identify his or her own level of dyspnea because dyspnea is a subjective experience (Fig. 26.2). • Previous intubation The need for intubation in past asthma attacks is an indicator of severity. -Treatment The patient and healthcare provider develop an asthma action plan, which assists with decision making. The plan provides information and instructions on how the patient can manage his or her asthma based on peak expiratory flow readings, medications, an awareness or recognition of worsening symptoms and when to seek emergency care. The treatment of asthma includes assessment, monitoring, control of environmental factors, pharmacological treatment, and education. The patient's frequency of symptoms and triggers should be noted. Pulmonary function tests should be conducted regularly to track the patient's response to therapy. During an acute exacerbation, peak flow readings, pulse oximetry, and ABGs (in a very severe attack) are used to determine the severity of the attack. Control of environmental factors is a necessary part of the education program for the patient with asthma. Irritant exposure should be reduced once the irritant has been identified. Patient history or sensitivity testing will often reveal the likely irritant. Environmental smoke is associated with increased symptoms and decreased lung function. Patients should be advised not to smoke and to avoid "second-hand" smoke exposure. The patient should be counseled on the importance of being aware of the levels of air pollution and to avoid outside activities if the level is high. There are many air-monitoring apps available to assist patients in becoming more informed about the air quality in their area. Patients should avoid fumes from wood-burning stoves, fireplaces, aerosol sprays, and strong perfumes. They should also remove animals and/or birds from their home if they are sensitive to the dander. Stress and depression may also be factors that can precipitate an asthma attack. • Provide oxygen. Increase SpO2 to 90% or greater. • Administer bronchodilators as ordered. Bronchial smooth muscle relaxants help open the airway. • Administer anti-inflammatory medication/steroids as ordered. Anti-inflammatory medication decreases the inflammation causing the airway obstruction. • Administer anticholinergics as ordered. Anticholinergics relax the muscles around the larger airways or bronchi. • Pursed-lip breathing Pursed-lip breathing keeps the airways open longer and prolongs exhalation, allowing increased time for oxygen and carbon dioxide exchange. -Medications Pharmacological treatment of the patient with asthma is based on the patient's response to previous treatment(s) and the level of engagement in the self-management plan. Patients are seen frequently when they begin a new medication (1-3 months) and when they experience an acute exacerbation (within a week). There are several classifications of medications that are used to treat asthma: anti-inflammatories, bronchodilators, anticholinergics, and leukotriene modifiers. Anti-inflammatories, typically inhaled corticosteroids, reduce mucus production and swelling, making the airways less sensitive and less likely to react to asthma triggers that cause asthma symptoms. Bronchodilators such as beta2-adrenergic agonists relax the bronchial smooth muscle, helping to open the airway and decreasing obstruction. Anticholinergics are another group of bronchodilators. Different from beta2-adrenergic agonists, which relax the bronchioles or small airways, anticholinergics relax the muscles around the larger airways or bronchi. Leukotriene receptor antagonists are another class of medications that may be used to enhance asthma control if the usual medications are not effective. They are not steroids; they inhibit the leukotriene-mediated inflammatory process. Medications also fall into two categories: long-term control medications and "rescue" medications. Long-term control medications are used daily regardless of the symptoms a patient is experiencing to achieve and maintain control of the asthma. The most effective long-term control medications for asthma are inhaled anti-inflammatories. Another long term control medication option for poorly controlled asthma or when inhaled gluccocorticoids are difficult to manage, such as in young children, is oral theophylline, a bronchodilator with anti-inflammatory effects. "Rescue" medications are those medications used once an asthma attack has started; these are usually short-acting bronchodilators. Short-acting beta2-adrenergic agonists are the gold standard because they are most effective. Short-acting beta2-adrenergic agonists should be used for acute exacerbations of asthma only. Studies have shown that regular use of short-acting beta2-adrenergic agonists results in more frequent and earlier exacerbations, tolerance, decreased baseline pulmonary function, and increased hyperresponsiveness. Oral anti-inflammatories such as prednisone may also be used in an acute exacerbation. As the attack subsides, oral anti-inflammatory medications are not abruptly stopped but decreased in dosage until they are discontinued. New medications for poorly controlled asthma include anti-interleukin 5 (anti-IL5) and anti-immunoglobulin-E (anti-IgE) therapy. Anti-IL5 medications reduce the production and survival of eosinophils involved in the asthma attack. Anti-IgE medications help prevent the inflammatory response in allergic asthma. Figure 26.1 illustrates a stepwise approach to the treatment of asthma.

Heart failure

-Diagnosis The diagnosis of HF is heavily dependent on history and physical assessment. The symptoms are fairly nonspecific, so diagnostic tests are done to rule out other disorders and determine the underlying cause. Diagnostic tools include chest x-ray, echocardiogram, and ECG to assess the presence of structural disease, ejection fraction, heart size, pulmonary congestion, or dysrhythmias. Multigated acquisition (MUGA) scans can also determine EF. Nuclear imaging studies, stress testing, and coronary angiography to evaluate blood flow to the heart are performed when coronary artery disease is suspected. In severe acute heart failure, hemodynamic monitoring with a pulmonary artery catheter can be useful. Laboratory testing includes cardiac biomarkers, serum electrolytes, a complete blood count, urinalysis, glucose level, fasting lipid profile, liver function testing, and renal function tests. Electrolytes can be outside the normal range as a result of decreased kidney perfusion or medication. For example, potassium might be low because of diuretic therapy. Also, inadequate flow to the kidneys may impair renal function, resulting in elevated creatinine and blood urea nitrogen (BUN) levels. Decreased hemoglobin and hematocrit levels may indicate anemia, which may be a result of decreased blood flow to the kidneys that reduces the production and function of erythropoietin in the kidneys. Cardiac biomarkers such as troponin I or T are used to rule out an acute ischemic event. Other biomarkers, BNP and N-terminal pro-B-type natriuretic peptide (NT-proBNP), are increased because of the overstretching of the ventricles. Increased values in these tests can be used to diagnose HF; BNP and NT-proBNP can also guide clinical decision making and track a patient's response to therapy as well as indicate disease progression. • Vital signs Hypertension is present because of the increased afterload. Hypotension may be caused by acute heart failure or be an adverse effect of medications. Tachycardia can be present as the heart attempts to compensate for decreased cardiac output. Tachypnea and decreased oxygen saturation may be present when fluid accumulates in the lungs because of left-sided HF. • Breath sounds Crackles indicate pulmonary congestion. • Monitoring for irregular heart rhythm or dysrhythmias Dysrhythmias are a common adverse effect of HF and medications used to treat HF. • Skin color, temperature, peripheral pulses, and capillary refill time Pale or cyanotic color, cool extremities, weak peripheral pulses, and sluggish refill time result from inadequate cardiac output. • Dry, persistent cough Common complication of ACE inhibitors • Activity tolerance Dyspnea on exertion, weakness, and fatigue indicate decreased cardiac output and worsening heart failure. • Urine output Output may be reduced with decreased renal perfusion. It can also be used to assess the effectiveness of diuretic therapy. Less than 30 mL/hr should be reported to the provider. • Daily weight To evaluate fluid retention and effectiveness of diuresis • Laboratory data Elevated BNP and NT-proBNP indicate overstretching of heart tissue. Elevated creatinine and BUN may be indicative of prerenal failure due to decreased cardiac output or overdiuresis. Elevated hepatic enzymes can be indicative of hepatomegaly; hypokalemia is a common complication of diuretic administration. Anemia can be caused by reduced kidney perfusion resulting in decreased erythropoietin production and function • Depression screening High rates of depression and anxiety are noted in the HF population. These can impact self-management. • Social support Social isolation has been shown to be an independent predictor of mortality among HF patients. -Treatment The medical management described here is predominantly for patients with HFrEF. These strategies have not been efficacious for patients with HFpEF. Management of patients with HFpEF focuses on the treatment of the underlying cause, blood pressure control, diuretics for fluid volume overload, and symptom management. The goals of HFrEF management are the reduction of risk factors, manipulation of the critical components of cardiac output (preload, afterload, and contractility), and control of the compensatory mechanisms. Successful management slows disease progression, prevents complications, reduces morbidity and mortality, and improves quality of life. Risk-factor management may include blood pressure and glucose control, weight loss, optimizing serum lipids, and smoking cessation. Beta blockers are used to control the sympathetic nervous system compensatory response in HF, such as tachycardia, in order to decrease cardiac workload. Ivabradine, a new medication that slows sinus-node firing, can be added for greater control of heart rate in patients taking maximal doses of beta blockers or who do not tolerate beta blockers. Preload is the amount of stretch in the heart at the end of diastole and is affected by the amount and pressure of blood returning to the heart. Aldosterone antagonist diuretics such as spironolactone (Aldactone) as well as loop diuretics such as furosemide (Lasix) are essential medications to decrease preload in patients with fluid retention. The use of spironolactone should be cautioned in patients with renal insufficiency because of the potential complication of hyperkalemia. In contrast, furosemide can cause hypokalemia and is often paired with a potassium replacement medication. Afterload refers to the resistance within the vasculature. Increased afterload intensifies the workload on the heart, further impairing cardiac output. Afterload reduction is a main goal of medical management. Angiotensin-converting enzyme (ACE) inhibitors are usually the first line of medications used to control the RAAS compensatory response and reduce afterload. Angiotensin receptor blockers (ARBs) have a similar effect and can be used in patients who are intolerant of ACE inhibitors. Angiotensin receptor-neprilysin inhibitors (ARNIs) are a new class of medications that combine an ARB with a neprilysin inhibitor (valsartan with sacubitril) and can be used in place of an ACE inhibitor or ARB. Neprilysin is an enzyme that breaks down natriuretic peptides (BNP), which produces natural diuresis and vasodilation. By blocking neprilysin, natriuretic peptides remain active in increasing urine output and dilating blood vessels. Other medications that may be prescribed to reduce afterload include vasodilators such as hydralazine and isosorbide dinitrate. Calcium channel blockers, with the exception of amlodipine, should be avoided in HF due to their myocardial depressant effect and lack of demonstrated efficacy. Contractility is the force of the myocardial muscle contraction. A past mainstay of HF management has been digoxin (Lanoxin), an oral positive inotropic medication used to increase cardiac contractility and reduce heart rate. Its use is being questioned. Although patients realize a reduction in symptoms, overall mortality is not decreased. Patients on digoxin (Lanoxin) are prone to toxicities, with symptoms such as nausea and vomiting and visual disturbances (e.g., yellow halos around lights). Care must be taken to monitor patients closely to avoid the later signs of toxicity, such as bradycardia and dysrhythmias. See Table 30.7 for a summary of medications used in the treatment of HF. Medical management of heart failure often requires multiple medications from different classes to achieve optimal results. For instance, patients can be prescribed spironolactone, furosemide, and carvedilol to manage their HF along with their other routine medications. In combination, these medications have been shown to improve survival in patients with HF by slowing or stopping the progression of ventricular remodeling and dysfunction. An acute exacerbation of HF is typically treated with IV medications that can more quickly and effectively decrease preload and afterload and increase contractility. Nitroglycerin and nitroprusside (Nitropress), potent vasodilators, are commonly used. Intravenous inotropic agents (e.g., dopamine) can be used to increase contractility, whereas inodilators, agents with both positive inotropic and vasodilator effects (e.g., dobutamine and milrinone), provide positive inotropic effects and reduce afterload. All these medications require careful monitoring of blood pressure, heart rate, and cardiac rhythm and frequent assessments to guide therapy and avoid adverse effects. • Oxygen therapy To maintain adequate oxygenation • Elevate the head of the bed and provide a fan for dyspnea. Maximize oxygenation and promote comfort • Medication administration as ordered: • Administer diuretics. Diuretics decrease volume, thus preload. • Administer ACE inhibitors, ARBs, ARNIs, and vasodilators. Angiotensin-converting enzyme inhibitors, ARBs, ARNIs, and vasodilators decrease afterload, which helps to decrease the workload on the heart and decrease myocardial oxygen consumption. • Administer beta blockers. Beta blockers decrease the sympathetic response (heart rate), thus reducing myocardial oxygen consumption. • Administer inotropic agents. Enhance contractility • Fluid and sodium restriction To prevent fluid overload

Iron-deficiency anemia

-Diagnosis The diagnosis of IDA is confirmed by specific blood tests. A complete blood count (CBC) demonstrates decreased hemoglobin and hematocrit levels. Low serum ferritin levels, which reflect the body's iron stores, are a confirmation of IDA. Serum ferritin levels less than or equal to 100 ug/L indicate IDA 100% of the time. Additional diagnostic studies to confirm IDA include serum iron, total iron-binding capacity (TIBC), serum transferrin receptors, and mean corpuscular volume (MCV). • Vital signs Tachycardia and tachypnea are secondary to the heart and lungs compensating for decreased oxygenation of body tissues caused by decreased iron levels, which leads to decreased hemoglobin levels. • Serum hemoglobin and ferritin levels With an iron deficiency, reflected by low ferritin levels, there is insufficient hemoglobin to deliver oxygen to the body tissues. Decreased hemoglobin and serum ferritin levels indicate IDA. • Fatigue, pallor, and shortness of breath Fatigue, pallor, and shortness of breath worsen with increasingly decreased levels of iron, resulting in inadequate oxygen-carrying capacity. • Level of consciousness Alterations in level of consciousness occur as a result of decreased iron levels that cause decreased oxygenation to the brain. If prolonged IDA is present in a child's developing brain, cognitive impairment could be permanent. • Blood loss, if present The greater the blood loss, the worse the clinical manifestations are as a result of decreasing iron stores and decreased hemoglobin levels leading to inadequate tissue perfusion. -Treatment Adjusting the diet to increase iron intake is the easiest and best way to prevent IDA, especially long term. Good dietary sources of iron include meat (especially red meat), dark green leafy vegetables (spinach, broccoli, peas), beets, dried beans, iron-fortified breakfast cereals and breads, and Cream of Wheat (Table 34.2). Ingesting citrus fruits such as oranges or grapefruits increases the vitamin C intake and may improve iron absorption. If diet alone cannot restore iron levels, then iron supplementation is needed, and this can be done through iron preparations administered orally, intramuscularly, or intravenously. Oral supplementation is the first line of therapy. During iron therapy, patients must be monitored for nausea, abdominal discomfort, constipation, and/or diarrhea. Iron supplementation by parenteral means is indicated only in cases of severe gastrointestinal distress secondary to oral administration, malabsorption disorders, or in acute cases of IDA in which levels need to be increased more rapidly. Parenteral supplementation may be given by intramuscular (IM) or IV routes. In the past, iron dextran was the only IV supplement; however, because it often causes cardiotoxic side effects, and patients need to be closely monitored while infusing, newer formulations of IV iron supplements are now available. These newer solutions do not have major cardiac risks, and although they are much safer to administer to the patient, vital signs still need to be monitored while the iron preparation is being infused. • Increase dietary iron. Increasing iron intake through dietary sources increases the body's iron stores and results in increased hemoglobin levels, thus increasing tissue perfusion. • Increase intake of vitamin C. Increasing vitamin C intake may increase iron absorption. • Administer iron-supplement therapy. Iron-supplement therapy is necessary if iron stores need to be increased quickly or if malabsorption disorders are present, which interfere with the body's ability to incorporate iron from dietary sources. • Minimize blood loss. Any obvious hemorrhaging needs to be controlled immediately to minimize blood loss. Excessive bleeding with menstruation may be controlled by various hormonal medications.

Myasthenia gravis (MG)

-Diagnosis The diagnosis of MG is based on clinical assessment as well as analysis of diagnostic tests. Serological tests, electromyography, and the edrophonium (Tensilon) test all aid in establishing a diagnosis of MG. An assay for AChR antibodies is essential for making a diagnosis of MG. The AChR-binding antibodies are found in roughly 80% of patients with generalized MG but only 55% of patients with ocular MG. The AChR-binding antibody assay is very specific, and positive antibody studies verify MG in the presence of a clinical picture that is consistent with MG. The AChR antibodies compete for the neurotransmitter's ACh binding sites. Additionally, antibodies to MuSK are found in about one-third of patients with generalized MG. Patients with MuSK are generally females with prominent bulbar clinical manifestations, shoulder girdle weakness, and respiratory weakness. • Assess breath sounds and observe the patient's respiratory effort. Obtain vital capacity per provider's order. This is usually obtained immediately prior to a dose of pyridostigmine to obtain a trough value and then 1 hour post-dose to evaluate peak effect. If the value is below 1 L, the patient is at risk for respiratory compromise. Notify the provider. Respiratory deterioration may lead to respiratory arrest. Patients often require intubation and mechanical ventilation in an intensive care setting. • Vital capacity measurement Vital capacity is an important respiratory function to monitor. If the value is below 1 L, notify the provider. In MG, the patient develops weakness of the diaphragm and intercostal muscles. Weakness of the respiratory muscles results in diminished forced vital capacity. • Cranial nerves IX, X, XI, and XII Bulbar symptoms are the first to appear in about 16% of MG patients and place the patient at risk for aspiration due to difficulty swallowing. • Dysphagia Weakness of the oropharyngeal muscles places the patient at risk for dysarthria and dysphagia. • Nutritional intake, intake and output, and daily weight Cranial nerve weakness can make it difficult for the patient to chew and swallow. The patient may become fatigued during the meal. • Dysarthria Patients may have a nasal quality to the speech and be at risk for aspiration because of weakness of these muscles. This is related to impairment of CNs V, VII, IX, X, XI, and XII. -Treatment The treatment of MG is individualized to meet the needs of each patient (Table 38.2). The healthcare provider considers the severity of the patient's illness, age, and lifestyle, as well as the financial demands of long-term therapy. Treatments are aimed at (1) symptomatic treatment to increase the availability of ACh, (2) immunosuppression, (3) approaches to alter the immunopathogenic mechanism underlying MG, and (4) immunomodulatory effect with thymectomy. • Administer medications at prescribed times and prior to activities requiring swallowing. Pyridostigmine must be administered exactly at the prescribed hour to maintain optimal muscle strength. Patients often take pyridostigmine 30 to 60 minutes before meals to minimize difficulty with chewing and swallowing. • Elevate the head of the patient's bed with eating or drinking. Weakness of the oropharyngeal muscles increases the risk of aspiration, and elevating the head of the bed may decrease aspiration. • Establish effective communication method with the patient. Consult with speech language pathology to obtain a picture communication board because verbal communication is impaired by dysarthria. • Plan meals when medications are at peak levels. Timing the meals with peak medication levels decreases the risk of aspiration. Small, frequent meals will help maintain calorie intake. Weight loss may result from poor nutritional intake. • Offer soft foods and thickened liquids as recommended by the speech language pathologist. A temporary feeding tube may be necessary if swallowing is impaired or if the patient deteriorates and requires intubation and mechanical ventilation. • Plan for rest periods between activities of daily living. Use energy conservation techniques, such as sitting while activities of daily living are completed, to minimize fatigue and muscle weakness.

TB

-Diagnosis The diagnosis of TB infection is made by laboratory testing, a skin test, and chest x-ray. Laboratory testing consists of a sputum test for culture and acid-fast staining. Suspicious cavitating lesions (resulting from pathologic processes leading to necrosis and formation of a "gas-filled" space within the lung tissue) are seen on chest x-rays. The skin test is a positive purified protein derivative (PPD) screen skin test, also called a Mantoux test. The Mantoux tuberculin skin test is the standard method for determining if an individual is infected with the TB-causing organism. The test is administered by injecting 0.1 mL of PPD intradermally into the tissue of the forearm. Within 48 to 72 hours after injection, the administration site should be observed for any reaction (Table 24.7). Individuals who have received a bacille Calmette-Guérin (BCG) immunization may show a false-positive PPD when not infected with the TB bacteria. Further testing in these individuals is required, such as a chest x-ray and/or blood testing using an interferon gamma release assay (IGRA). There are currently two IRGAs approved for use by the U.S. Food and Drug Administration (FDA): QuantiFERON®-TB Gold In-Tube (QTF-GIT) and T-SPOT® TB test (T-SPOT). These blood tests can determine if an individual has been infected with TB bacteria. A negative result indicates unlikely TB infection. A positive test confirms TB infection, and further work-up is necessary to establish whether the infection is latent TB or TB disease. • Oxygen saturation Decreased oxygen saturation occurs with the destruction of lung tissue, lessening the available surface area for air exchange. • Temperature Fever is a result of the inflammatory process. • Sputum Blood-tinged or rusty-colored sputum is present as a result of the destruction of lung parenchyma tissue. • Breath sounds Wheezing from irritated airways; rales and rhonchi from fluid/exudates -Treatment According to the American Thoracic Society, the CDC, and the Infectious Diseases Society of America, the goals of treatment for TB infection are (1) to cure the patient and (2) to minimize the transmission of M. tuberculosis to other persons. A basic four-drug combination is recommended for the treatment of TB and should continue for 9 to 12 months (Table 24.8). The basic recommended treatment for TB is broadly applicable, but modifications may be necessary in special circumstances, such as HIV+, pregnancy, drug resistance, and children. Immediate isolation of the patient with suspected or confirmed TB infection in a private room with negative airflow capabilities is a priority. Negative airflow occurs when air moves into the contaminated area or into the patient's room from bordering areas. The institution of airborne precautions, the use of an N95 mask respirator for healthcare personnel entering the patient's room (requires fit-testing), and a snug-fitting surgical mask for visitors are essential interventions. The patient's movement and transportation to other departments should be limited to essential needs only. Patients who must leave the negative-pressure room should also wear a surgical mask. • Humidified oxygen Humidified oxygen helps ensure adequate oxygen delivery to the tissues and maintains the integrity of the mucous membranes. • Institute airborne isolation (see Table 24.4). Tuberculosis is an extremely contagious disease. Care must be taken to avoid transmission to other individuals, especially other hospitalized individuals with an increased risk for infection. • Administer antibiotics as ordered. Antibiotics are the definitive treatment for TB and are essential in controlling the spread of the disease. • Ensure adequate nutrition. Adequate caloric intake to maintain optimum body weight is necessary for recovery. Often, patients report substantial weight loss during the time prior to diagnosis.

Fractures

-Diagnosis The diagnosis of fractures is based on a thorough history of how the injury occurred, a physical assessment, and is confirmed by radiography or computed tomography (CT). When the patient's history is obtained, it is important to note the specific mechanism of force that caused the injury. Other imperative information includes the patient's medical history and any chronic illnesses, medications, and potential substance abuse. Medications and substance abuse can impair mental judgment and function and contribute to motor vehicle accidents and falls, thus producing bone fractures and other traumatic injuries. If a chronic illness is suspected as having a major role in the injury, a bone scan and MRI may be needed to confirm the diagnosis. • Vital signs Excessive bleeding leads to symptoms of hemorrhagic shock: low blood pressure, tachycardia, and tachypnea. Tachycardia, tachypnea, and decreased pulse oximetry with chest pain may indicate pulmonary embolus. An elevated temperature may indicate infection. • Physical assessment of the site of injury via inspection and palpation. Palpate the injured extremity noting the six Ps: pain, pressure, paralysis, pallor, paresthesia, and pulselessness. Complete the neurovascular assessment by checking movement and sensation. The presence of one or several of the six Ps may indicate neurovascular compromise that can lead to hemorrhage, compartment syndrome, infection, or permanent loss of function. The absence of the six Ps indicates that proper treatment is being provided and that there is no neurovascular compromise. • Verify proper positioning, application, and stability of traction/splinting/immobilization devices Immobilization, traction, casts, and splints secure the fractured bone segments to promote healing. Occasionally, immobilization devices become loose, compromise circulation, or move out of position. Frequent assessment is needed to ensure that the devices are secure and are not hindering the healing process. • Laboratory tests • Myoglobin Myoglobin is released from damaged muscle and may indicate the presence of rhabdomyolysis, which may lead to renal compromise or failure. • Creatine phosphokinase (CPK) CPK is released with any muscle breakdown, increased levels are seen with rhabdomyolysis • Complete blood count (CBC), metabolic profile, and renal studies Rhabdomyolysis is frequently complicated by multiple electrolyte disorders including hyperkalemia, hypophosphatemia, and hypo/hypercalcemia as well as renal failure. Blood loss and infection are potential complications of fractures. A complete blood count (CBC), metabolic profile, and renal studies are used to detect signs of infection (increased white blood cell count), blood loss (decreased hemoglobin and hematocrit), electrolyte disturbances (metabolic profile) and indications of renal failure (increased blood urea nitrogen [BUN] and creatinine). • Urine appearance Urine may be tea colored in rhabdomyolysis because of ruptured blood cells that clog the nephrons. Acute kidney injury is the most serious and even life-threatening complication of rhabdomyolysis. • Intake and output All fractures result in blood loss. Adequate volume replacement is necessary to prevent hypovolemic shock. Blood loss from drains, incisions, and wounds should be monitored closely. Also, hypovolemia and rhabdomyolysis may result in decreased urine output. -Treatment Definitive treatment of fractures is highly dependent on their type and location and may require either surgical or nonsurgical intervention. Table 54.1 describes various fractures and their treatment. In the case of open fractures with contaminated wounds, antibiotics are implemented to prevent osteomyelitis and other wound infections. Effective pain management is an important aspect in treating fractures. Narcotics and anti-inflammatory medications are effective in controlling pain and inflammation. These medications allow the patient to gradually regain movement and function of the injured area. After definitive treatment, movement and function are key in preventing muscle atrophy and contractures. • Maintain pulmonary hygiene Incentive spirometry exercises and coughing and deep breathing expands alveoli, helping maintain adequate alveolar gas exchange • Administer analgesia as ordered Administration of scheduled narcotic and anti-inflammatory medications inhibits prostaglandin formation, thus reducing pain and allowing the patient to reestablish function and mobility. • Administer antibiotics as ordered Reduce the risk of infection, especially in patients with open fractures • Administer anticoagulants as ordered Patients with fractures are highly susceptible to VTE and pulmonary emboli. Anticoagulants help prevent blood clots and emboli. • Wound/Pin care Providing daily pin site and wound care using strict aseptic technique reduces the risk of infection and promotes healing. • Elevation Elevating the affected extremity above the level of the heart minimizes pain and edema. *If a crushing injury is suspected, do not elevate the limb because elevation reduces arterial pressure. • Apply ice Promotes therapeutic vasoconstriction and decreases edema and pain • Range-of-motion exercises and ambulation using available assistive devices Ambulation and movement as soon as ordered prevent muscle atrophy and contractures, promote function and mobility, and promote healing and strength. Early ambulation as possible helps prevent VTE through the action of muscle contraction, which discourages blood from pooling. Assistive devices are very helpful in allowing the patient to perform self-care. (Box 54.2) • Repositioning Patients in traction, casts, and other immobilization devices have an increased risk of skin breakdown and decubitus ulcers. Provide the patient with a trapeze that is set up to encourage mobility while in bed. • Provide hydration and nutrition Metabolic demands increase during bone and wound healing. Extra protein, calcium, and vitamins A/D/C are needed for adequate bone repair. Adequate fluid intake is essential to ensure adequate "flushing" of the kidneys to prevent the complications of rhabdomyolysis. Iron supplements may be required for the treatment of anemia after surgery. • Positive feedback and encouragement Empower the patient to continue with treatment/rehabilitation and boost self-confidence

Hypertension

-Diagnosis The diagnosis of hypertension is made on the basis of the average of two or more properly measured BP readings on two or more office visits. Treatment is indicated at that time but may begin immediately if two consecutive readings during a single visit indicate an extreme elevation. New (2017) ACC and AHA guidelines for the detection, prevention, management and treatment of high blood pressure lower the definition of high blood pressure to account for complications that can occur at lower numbers and to allow for earlier intervention. See Table 31.2 for the classifications of hypertension for adults aged 18 and older. Once the diagnosis of hypertension has been made, providers attempt to identify the underlying cause on the basis of risk factors and other symptoms. Laboratory tests are performed to identify possible causes of secondary hypertension. Additional tests for diabetes and high cholesterol levels are performed because they are risk factors for the development of heart disease that require treatment. Tests typically performed in a hypertension work-up are classified in Table 31.3. A thorough history and physical examination are done to detect TOD. The search for the presence of subclinical target organ damage (TOD) is strongly recommended because it allows a better stratification of cardiovascular risk, encourages the achievement of a lower BP target than usual, and helps with the selection of the most appropriate medication regimen. To that end, testing is done to determine if hypertension has caused damage to the heart, eyes, or kidneys. • Neurological assessment It is important to assess signs and symptoms that could indicate TOD and cerebrovascular disease leading to possible complications such as stroke and aneurysm. • Blood pressure Early detection and treatment of hypertension can prevent or minimize TOD. Measurements determine the treatment regimen prescribed. • Heart rate Increased PVR can lead to increased HR or increased SV to compensate for the increased PVR. • Examination of the optic fundi Hypertension may lead to retinal damage and eventually retinal hemorrhage because of the vascular changes caused by hypertension. • Auscultation for carotid, abdominal, and femoral bruits Bruits are sounds created by blood flow through a stenosed or narrow vessel. • Palpation of the lower extremities for edema and pulses Weak pulses and peripheral edema can indicate kidney disease and/or HF. • Serum creatinine, blood urea nitrogen (BUN), estimated glomerular filtration rate, and 24-hour urine collection for creatinine clearance Abnormal levels indicate renal disease, which may develop in patients with hypertension. • Albumin excretion rate Microalbuminuria is a significant marker of early cardiac, renal, and retinal structural and functional changes in essential hypertension. • Calculation of BMI and waist circumference Obesity and diet are major risk factors in hypertension. -Treatment An increase in recent years of illness and death due to hypertension has prompted experts to urge more effective BP control. To bring high blood pressure down to a healthy level, treatment guidelines recommend healthy lifestyle changes, medication, or both. Lifestyle changes alone may be the first step in patients with mildly elevated (systolic between 120-129 and diastolic < 80) blood pressure readings. The new guidelines recommend only prescribing medication beginning at Stage I hypertension if a patient has already had a cardiovascular event such as a heart attack or stroke or is at high risk of heart attack or stroke based on age, the presence of diabetes mellitus, chronic kidney disease or calculation of atherosclerotic risk. If medications are necessary, there are a variety of medications used to treat high BP. Which medications are initially prescribed to a patient depends on numerous factors including ease of use, side effects, and coexisting medical conditions that may necessitate use of one agent versus another. Diuretics are commonly included in the treatment plan. Clinical trials have shown they enhance the antihypertensive efficacy of multiple medication regimens, are useful in achieving BP control, and are more affordable than other antihypertensive medications. Combination therapy regimens can facilitate achievement of BP goals. Table 31.4 gives an overview of the antihypertensive medications that may be used individually or in combination with one another. When a treatment plan is considered for the patient, socioeconomic status and psychosocial stress as risk factors for high blood pressure should be considered in a patient's plan of care. • Administer antihypertensive medications as ordered Clinical outcome trial data prove that lowering BP with a combination of one or several classes of medications reduces the complications of hypertension. • Provide patient with DASH diet for meals A 1,600-mg sodium DASH eating plan has effects similar to those of antihypertensive single-medication therapy.

Laryngitis

-Diagnosis The diagnosis of laryngitis is based on patient complaint of hoarseness related to a current or recent upper respiratory infection. In patients with risk factors for developing cancers of the throat and lungs, further diagnostic evaluation may be warranted. Patients may require visual examination of the larynx by an ear, nose, and throat specialist through the use of a laryngeal mirror or fiberoptic laryngoscopy. A flexible fiberoptic laryngoscopy involves inserting a thin, flexible scope into the mouth or nose to the larynx to allow direct visualization. If polyps, inflammation, or tumors are present, x-rays or CT may be required. • Vital signs Temperature elevation may indicate an infection. • Assessment of throat structures Increased edema of the throat structures could compromise the patency of the airway. • Assess for the presence of stridor after extubation. Stridor indicates acute obstruction of the airway and is a medical emergency that may require reintubation. -Treatment Treatment consists of voice rest, adding moisture to the air in the home with a humidifier or vaporizer, and drinking plenty of fluids. Avoidance of smoking and exposure to second-hand smoke is also important. The use of antibiotics is indicated in the setting of bacterial infection. If laryngitis lasts greater than 5 days after appropriate treatment and voice rest, evaluation for the presence of malignancy should be considered. • Administer humidification as prescribed. Humidification may be ordered to reduce inflammation. • Administer antibiotics as ordered. Antibiotics may be ordered to treat infection if present. • Have emergency airway equipment readily available, especially if laryngitis occurs after extubation. Hoarseness and stridor after extubation indicate acute obstruction of the airway and are a medical emergency. • Provide alternatives for communication (pen and paper or a communication board with pictures). Patients should be encouraged to rest the voice to prevent further trauma.

Meniscus injuries

-Diagnosis The diagnosis of meniscus injuries is based on physical examination using either the McMurray's test, in which the knee is supported and flexed while the lower leg is rotated internally and externally (Fig. 54.11), or Steinman's test, in which the knee is flexed and extended. A positive result is indicated when either test reveals an audible/palpable "click," an inability to extend the knee, or the presence of pain. Radiography may be needed to rule out degenerative joint diseases. An MRI can further help isolate and characterize the extent of the tear. • Physical assessment of injured extremity via inspection and palpation An assessment revealing adequate pulses, color, and temperature ensures that there is no emergent or permanent damage to circulation, movement, and sensation. • Vital signs Tachycardia and hypotension may result because of hypovolemia due to hemorrhage. Increased temperature is an indicator of infection. Tachycardia and hypertension may indicate increased pain. • Neurovascular check Poor pulses, pallor, and cool extremities indicate problems with increased swelling, which can compress the nerves, blood vessels, and muscle. • Wound site/dressing Blood on the dressing indicates bleeding. Purulent drainage and/or a red, warm incision indicate postoperative infection. • Pain Increased pain may indicate further injury or edema. Well-controlled pain indicates effectiveness of pain interventions. -Treatment Treatment of meniscus tears is dependent on the size and severity of the tear. Smaller tears often heal within a few months and are treated with limited rest, ice, and administration of NSAIDs. Total immobility and resting of the affected joint is not recommended because it may cause muscle atrophy, stiffness, and further movement problems. Patients are encouraged to continue daily activities as tolerated. • Apply ice or cold compress to wound Cryotherapy causes vasoconstriction, which decreases further bleeding and inflammation and helps manage pain. • Elevation Elevation decreases edema, which eases pain and promotes mobility of the injured area. • Exercise/ROM therapy as tolerated Prevents atrophy, strengthens muscles, and promotes mobility • Administer anti-inflammatory and analgesia medications as ordered Inhibits prostaglandin (mediators of pain and inflammation) formation reducing pain and inflammation

Strains and sprains

-Diagnosis The diagnosis of sprains and strains is based on a thorough history and physical examination of the affected area and is often confirmed by radiography, ultrasound, or magnetic resonance imaging (MRI). Ultrasounds are low cost and highly effective in identifying strains and sprains, but an MRI may be more definitive in the final diagnosis. • Physical assessment of injured extremity via inspection and palpation: palpate the injured extremity noting the six Ps to include pain, pressure, paralysis, pallor, paresthesia, and pulselessness. Complete the neurovascular assessment by checking movement and sensation. Inspection and palpation are done to assess circulation, movement, and sensation in the injured area. The presence of the six Ps may indicate neurovascular compromise of the injured area and may necessitate immediate medical intervention to prevent permanent damage. Extreme pain may indicate the presence of a fracture. • Patient history of injury Appropriate medical management is dependent on an accurate patient history to include determination of a chronic versus acute injury. -Treatment Treatment of first- and second-degree strains and sprains involves RICE, a common acronym referring to the treatment plan for strains and sprains: • Rest the injured extremity for as long as 72 hours to allow the ligaments or tendon time to heal. • Ice applied for no longer than 30 minutes three to five times per day for 24 to 72 hours after injury. This promotes vasoconstriction and decreases bleeding and fluid collection in the injured area. • Compression by means of an Ace wrap or similar compression dressing to minimize further swelling, which can delay healing. The dressing should be wrapped tightly but not enough to alter neurovascular function. Ensure that circulation, movement, and sensation remain intact. • Elevate the affected area to minimize dependent swelling. Functional supports in the form of braces may be used for 4 to 6 weeks and are preferred versus immobilization. Exercise therapy programs may be prescribed and consist of neuromuscular and proprioceptive exercises. In addition to the therapies mentioned previously, NSAIDs are usually prescribed to minimize pain and inflammation. Third-degree strains may require surgical repair of the torn tendon or muscle. Surgical repair typically involves an open incision and the use of thick suture material to reattach the torn muscle and tendons. Occasionally, either a graft from the patient's healthy tendon or a donor graft can also be used for surgical repair. Third-degree sprains may necessitate the need for arthroscopic surgical repair. Arthroscopic surgery uses small scopes to visualize and repair the injured area. Musculoskeletal allografts are gaining popularity for ligamentous reconstruction by orthopaedic surgeons while their safety and efficacy continue to improve. Postoperative treatment for strains and sprains involves immobilization of the affected extremity for 4 to 6 weeks and physical therapy. • Rest the injured extremity Minimizing activity promotes healing. • Ice applied to the injury Cryotherapy causes vasoconstriction, which decreases further bleeding and inflammation. • Compression via ace wrap Compression reduces the inflammation that causes pain and delays healing. • Elevation Elevation decreases edema, which eases pain and promotes mobility of the injured area. • Administer anti-inflammatory and analgesia medications as ordered Inhibit prostaglandin (mediators of pain and inflammation) formation, which can reduce pain and inflammation

Trigeminal neuralgia

-Diagnosis The diagnosis of trigeminal neuralgia is primarily based on the clinical presentation and ruling out other pathophysiological processes, such as direct injury to CN V or tumors. In addition to a comprehensive neurological assessment, including trigeminal reflex testing, a magnetic resonance imaging (MRI) scan of the head is also performed. Blood work may include a sedimentation rate (ESR), antinuclear antibody titer (ANA), or complete blood cell (CBC) count to look for hematological abnormalities. • Pain, including onset, character, and exacerbating factors It is important to identify the pain rating as well as aggravating factors. The pain is believed to be related to irritation of the nerve fibers in CN V. • Oral intake Pain may impair oral intake, so it is important to assess oral intake and fluid-volume status. • Weight If pain significantly interferes with nutritional intake, the patient may have weight loss. • History of exacerbations and remissions Because the time between attacks appears to shorten as the patient ages, it is important to establish any pattern of attacks. -Treatment Medications are used in the treatment of trigeminal neuralgia, including the use of antiepileptic drugs (AEDs) such as carbamazepine, oxcarbazepine, or gabapentin. Carbamazepine is the first line of medication therapy used in the treatment of trigeminal neuralgia, and it works by reducing the excitability of neurons by inhibiting neuronal sodium channels. Additionally, baclofen may also be prescribed, particularly in patients with MS, because it works as a muscle relaxant. Although medications can be helpful in abating the pain, some patients do not receive optimal relief and seek surgery. Table 38.4 presents a summary of the surgical approaches for the management of trigeminal neuralgia. Microvascular decompression is the most effective surgical treatment for this disorder; facial pain is usually relieved within 24 to 48 hours, and the patient does not have residual facial numbness. • Administer medications as ordered. Medication is taken at prescribed intervals to assist with pain relief. Antiepileptic medications have been found to have an analgesic effect on neuropathic pain. • Nonpharmacological strategies including meditation, diversional activities, support groups, and acupuncture. Suggest meditation or diversional activities. Seek a support group so that members may share their experiences. Acupuncture has been found to have efficacy similar to that of carbamazepine. These interventions are implemented to address pain management through alternative measures. Acupuncture has been found to have efficacy similar to that of carbamazepine in some patients.

Amputations

-Diagnosis Traumatic Amputations Due to the life-threatening nature of traumatic amputations, it is imperative to immediately control the bleeding and replace the blood lost from the injury. A tourniquet should be applied to the remaining portion of the limb to stop both arterial and venous bleeding. The tourniquet can remain in place for as long as 6 hours before the tissue becomes necrotic. Typically, patients with traumatic amputations also demonstrate polytrauma based on the same mechanism of injury. As a result, a rapid but thorough injury assessment should be conducted on the patient's arrival to the hospital. A coagulation panel and CBC can establish the need for immediate blood transfusion. A serum lactate level, an indicator of anaerobic metabolism, helps determine the level of hypoxemia and gauge the success of resuscitative efforts. To preserve life and maintain limb function in traumatic amputations, salvage surgery may be required to control hemorrhage, reattach limbs (Box 54.5), or remove/reconstruct the damaged tissue. Elective Amputations All possible medical interventions to reestablish perfusion are used before performing elective amputations. Radiography is used to determine the extent of bone damage or infection, whereas venograms and arteriograms are done to assess the level of peripheral circulation. Cultures and sensitivities isolate infective organisms in the wound and allow for accurate implementation of antibiotics. Medical interventions include hyperbaric therapy (100% oxygen administered under pressure in a hyperbaric chamber), percutaneous transluminal angioplasty (insertion of a balloon-tipped catheter into the affected artery that can be expanded to open the artery and restore blood flow), and anticoagulant therapy. In the case of neoplasms of the bone, resection of the tumor and bone grafting can often eliminate the need for surgical amputation. Once all other efforts have been exhausted, elective amputations are performed to salvage the remaining function of viable tissue. • Vital signs Hypotension and tachycardia may occur secondary to hemorrhage and sepsis. Increased temperature is an indication of infection. Decreased SpO2 indicates problems with oxygenation. • CBC Hemorrhage in traumatic amputation causes loss of red blood cells (RBCs), and low hemoglobin and hematocrit. • Pulses, temperature, color, movement, and sensation of affected extremity Weak pulses, pale color, a cool temperature, and limited movement or sensation indicate inadequate blood flow and tissue perfusion in the affected limb that may indicate the potential need for elective amputation. • Pain Phantom limb pain is a common side effect due to remapping of impulses from the amputated extremity to the spinal cord, causing continued pain sensations. • Wound/incision site Warm, red tissue with purulent drainage is a sign of wound infection. -Treatment • Insert large bore IV The massive blood loss associated with traumatic amputation necessitates IV blood and fluid resuscitation. • Transfusion of IV fluids and blood products as ordered Replace fluid and blood lost in traumatic amputation • Administer analgesia as ordered Improved pain control promotes movement, function, increasing the ability to participate in rehabilitation. • Alternative pain management techniques Alternative pain management modalities such as TENS unit or CAM therapies are synergistic in conjunction with analgesic medications. • Refrain from using a pillow under the remaining portion of the lower extremity Prevents the development of flexion contractures that can occur if a pillow is left under the extremity • Application of ice for no longer than 15 to 20 minutes Promotes vasoconstriction and decreases painful edema • Nutrition: maintain adequate intake and output The increased metabolic demands of healing require additional protein and carbohydrates. • Range of motion Strengthens muscles and prevents contractures in the residual limb fostering improved self-care • Application of rigid splint Minimizes edema by compressing residual limb for a better fit into the prosthesis

Pneumonia

-Diagnosis • Elevated WBC count (leukocytosis) with elevated bands (immature neutrophils) on differential indicating acute inflammation • Elevated C-reactive protein level, an accurate, sensitive, and historically used test to detect the presence of inflammation and infection. Values can range from 30 to 300 mg/dL in cases of bacterial and viral pneumonia. • Arterial blood gases may initially reflect a primary respiratory alkalosis (decreased CO2, increased pH) due to tachypnea. As the condition progresses, a primary respiratory acidosis with hypoxemia (elevated CO2, decreased PaO2, and decreased pH) will occur. • Sputum cultures will reveal a preliminary category of the offending organism by Gram stain and confirm the specific organism after 24 to 48 hours of incubation in the laboratory. Expectorated sputum specimens yield little information because of contamination with normal oral bacteria. Specimens obtained by deep tracheal suctioning or bronchoscopy offer the best yield for confirming a diagnosis and directing the choice of antimicrobial management. Imaging studies reveal: • Chest x-rays may or may not show infiltrates and can be up to 72 hours behind in their ability to reveal an infectious process. • Computed tomography scans of the chest may better demonstrate consolidation (solidification of lung tissue) and the presence of pleural effusions. As noted previously with clinical manifestations, prompt diagnosis is essential in providing timely and effective treatment. • Vital signs Tachypnea: The body's first compensatory mechanism to a decreased oxygen delivery is increased respiratory rate and depth. Tachycardia: The body's second compensatory mechanism for a continued impairment of oxygen delivery is to raise the heart rate. Decreased oxygen saturation: Impaired gas exchange at the alveolar level results in hypoxia. Tachypnea and tachycardia decrease cardiac output, reducing perfusion and peripheral oxygen saturation. Fever occurs as a part of the inflammatory response. • Neurological function Agitation, restlessness, anxiety, lethargy, and fatigue are the result of decreased tissue perfusion from altered alveolar gas exchange. Diminished cough, gag, and swallow reflexes resulting from altered levels of consciousness can contribute to aspiration risk. • Breath sounds Adventitious breath sounds such as wheezing, rhonchi, crackles, and rales may be audible on lung assessment as a result of bronchospasm and/or fluid and exudates filling the alveoli. • Peripheral pulses and skin temperature and color Diminished tissue perfusion causes blood to be shunted away from peripheral areas to the main core body organs. Peripheral pulses diminish, and skin becomes moist and pale. Peripheral cyanosis (bluish color to the nailbeds) is a late sign of tissue hypoxia. • Respiratory secretions Purulent and/or bloody secretions may result from a buildup of exudate in the alveoli. • Laboratory testing • Sputum microbiology Culture and sensitivity reports indicate the offending organism and list the antibiotics to which the organism is sensitive. • Arterial blood gases Bacterial respiratory infections may initially cause primary respiratory alkalosis (increased pH, decreased CO2) due to increased respiratory rate. As the condition progresses, a primary respiratory acidosis will occur (decreased pH, increased CO2). • Intake and Output Insensible losses from fever and tachypnea along with decreased intake from malaise and increased work of breathing can lead to more serious tachycardia and dehydration. -Treatment • The treatment of pneumonia is dependent on the type of pneumonia, an early diagnosis, and the overall health of the patient. Uncomplicated pneumonias can be effectively treated in the outpatient setting. More severe cases require hospitalization and supportive care. Because pneumonia may result in hypoxia, administration of oxygen to reverse or prevent hypoxia is an essential first step. In the case of patients with chronic lung pathology, high concentrations of oxygen can depress the drive to breathe. Those patients require careful monitoring while receiving oxygen. Ensuring adequate hydration is also an important intervention to support the patient's cardiovascular status and assist in thinning respiratory secretions for easy expectoration. • Administer humidified oxygen as ordered. Oxygen administration helps maintain adequate oxygen levels. Humidification of respiratory tract mucous membranes helps liquefy secretions to facilitate expectoration. Careful administration should be given to the patient with chronic lung pathology in whom the drive to breathe comes from decreased oxygen levels. • Administer antibiotics as ordered. Prompt administration of antibiotics to defeat the offending organism is the definitive treatment of choice. • Pulmonary hygiene: • Incentive spirometry • Coughing and deep breathing • Postural drainage • Vibration/percussion • Early mobility • Pulmonary hygiene is done in an effort to mobilize respiratory secretions and allow expectoration. This reduces the incidence of atelectasis and worsening pneumonia in hospitalized patients. • Patient positioning Elevating the head of the bed to 30 degrees prevents aspiration of colonized nasopharyngeal secretions and gastric contents and facilitates lung expansion. Side-to-side turning assists with alveolar recruitment strategies to ensure maximum ventilation-perfusion. For infiltrates of only one lung, when turning, preferentially position patient with the good lung down to maximize perfusion to the functional alveolar units. • Monitor intake and output. Optimal fluid balance assists with thinning respiratory secretions for ease of expectoration and maintains adequate tissue perfusion/oxygenation. • Ensure adequate nutritional support. Adequate caloric intake is necessary for cellular recovery. Small, frequent meals that are high in protein and vitamins are recommended. Assess cough, gag, and swallow reflexes prior to offering food and drink. If reflexes are impaired, maintaining NPO status or initiating enteral feedings via feeding tube may be required until a formal swallow evaluation can be obtained and the degree of aspiration risk can be determined. • Activity grouping Approach activities of care with intervals of rest. Fatigue and decreased tissue oxygen delivery limit activity tolerance. - Medications • Bronchodilator therapy with albuterol (short-acting selective beta-2 adrenoceptor agonist) or Combivent (slow-onset anticholinergic agent) delivered either by aerosol nebulization or by metered-dose inhaler will open swollen and narrowed airways and promote ease of breathing. Antibiotic therapy, the definitive treatment, is based on the offending organism, and initially, broad-spectrum antibiotics are initiated promptly. For HAP, antibiotic treatment is empiric—treatment based on clinical experience before the exact offending organism is identified. Because Pseudomonas aeruginosa is the major pathogen associated with HAP, initial treatment is focused on that organism.

Sickle cell anemia

-Diagnosis • Vital signs Tachycardia and tachypnea are a result of the sickling of RBCs that causes a decreased oxygen-carrying capacity of the hemoglobin molecules. It is also as a result of the decreased life span and increased destruction of RBCs. • Fatigue, pallor, and shortness of breath Fatigue, pallor, and shortness of breath worsen with increasingly decreased levels of hemoglobin and RBCs causing inadequate tissue perfusion and hypoxia. • Pain, swelling in joints and extremities Pain is caused by tissue hypoxia and clumping of cellular debris, particularly in the joints, bones, chest, and abdomen, leading to vaso-occlusion. • Jaundice The decreased life span of RBCs in people with SCD and the increased destruction of those RBCs may cause an increase in serum bilirubin, leading to jaundice. • Hand-foot syndrome Multiple episodes of crises and bone infarctions may lead to uneven growth of the fingers and toes. • Clinical manifestations of infection Fever may be present without infection. However, infection must be ruled out. X-rays to eliminate pneumonia or osteomyelitis may be necessary. Any skin lesions must be assessed for infection. Dental hygiene should not be overlooked as a source of infection. • Hemoglobin and serum bilirubin levels The sickled RBCs have decreased hemoglobin levels, and increased hemolysis of RBCs elevates serum bilirubin. • Serum iron, vitamin B12, and folate levels Because of the lower-socioeconomic status of a large percentage of African descendants globally, malnutrition is a concern. Frequently, patients with SCD also have decreased levels of iron, vitamin B12, and folic acid. These deficiencies complicate the anemia and need to be corrected. • Psychosocial issues Patients with SCD may have anger and/or depression in response to chronic disease. Frequent absences from work may interfere with employment, leading to feelings of guilt or anger. -Treatment • Administer oxygen. Oxygen assists in decreasing hypoxia and minimizing the severity of the crisis. • Provide aggressive hydration. Aggressive hydration increases blood volume (easing clumping of debris in capillaries) and flushes the kidneys, minimizing the risk for renal failure. • Administer pain medication. Administering analgesia, usually opiates, helps manage the pain caused by vaso-occlusion. • Administer blood transfusions. Blood transfusions may be needed in cases where the anemia is profound to improve oxygen delivery to the tissues. • Administer antipyretics. Antipyretics help reduce fever if present and decrease the fluid loss associated with temperature elevation and increased metabolic rate. • Provide supportive measures. A sickle cell crisis can be frightening to all involved, the individual with SCD as well as the family. The nurse needs to provide emotional support and be cognizant of the possible need for counseling. Contact additional resources if needed.

Rhinitis

-Diagnosis • Vital signs Temperature elevation may indicate the presence of infection. Elevations in heart rate and blood pressure may be related to the medication used to treat symptoms. • Peak flow rate and spirometry (if acute asthma exacerbation also present) Assessment of peak flow rate and spirometry may indicate the severity of exacerbation and response to therapy. • Nasal drainage Nasal drainage should be thin and clear. Yellow or green indicates infection. -Treatment and management of rhinitis are dependent on the cause. Diagnosis is based on history and symptoms. Obtaining a history of the onset of symptoms that focuses on the pattern, seasonal aspects, environmental exposures to allergens in the home or work, and precipitating factors serves as the basis of determining treatment. If rhinitis is the result of a viral cause, medication to relieve symptoms may be prescribed. In patients with allergic rhinitis, allergy testing may be indicated, followed by a desensitizing regimen. Referral to an ear, nose, and throat specialist for assessment of nasal polyps, nasal septal deviation, and hypertrophy of the nasal turbinate or sinus tumors may be indicated. Avoidance of exposure to known allergens at home, at work, or in the environment will assist in limiting symptoms. Effective management of asthma and obstructive sleep apnea (OSA), which can coexist or be complicating respiratory conditions, is often dependent on adequate and appropriate management of rhinitis. Asthma and rhinitis can both be triggered in response to allergens. Nasal inflammation as seen in rhinitis increases upper airway resistance, leading to OSA. Pharmacological management in allergic and nonallergic rhinitis is aimed at symptom relief. The use of oral antihistamines, nasal spray antihistamines and corticosteroids, and decongestant medications can assist in the relief of symptoms (Table 25.1). Prescription and over-the-counter (OTC) antihistamines are the most common treatment of rhinitis symptoms of sneezing, rhinorrhea, and pruritus. Sedation, performance impairment, and anticholinergic effects such as dry mouth and eyes, constipation, and increased heart rate are common side effects of first-generation antihistamines. Second-generation OTC antihistamines such as loratadine (Alavert, Claritin) have less or no tendency to cause sedation. Long-term use of nonsedating antihistamines in rare cases results in mild acute liver injury. Intranasal corticosteroid is the most effective treatment of allergic rhinitis and related symptoms when used on a regular basis. As-needed use of these nasal sprays can also be effective in relieving symptoms. There is no systemic effect from the use of intranasal corticosteroid medication. Intranasal sprays that contain antihistamines are effective at symptom relief and can work within minutes, whereas an intranasal corticosteroid may take days or weeks to provide full symptom relief. Antihistamine nasal sprays can result in systemic effects. These sprays are sometimes used in combination. Saline nasal sprays can be effective in relieving symptoms such as nasal congestion and sinus pressure-related effects. They moisten dry nasal mucous membranes to remove or reduce nasal plugs. Saline nasal sprays have no negative effects as can be seen with antihistamine or decongestants. Decongestant medications can reduce nasal congestion and obstruction. Oral decongestants contain pseudoephedrine and phenylephrine, which reduce nasal congestion. Side effects of these medications include insomnia, irritability, and palpitations. The use of these medications should be avoided unless nasal antihistamines and a corticosteroid have been ineffective. They should also be avoided in patients with a history of cardiac disease, hypertension, glaucoma, cerebrovascular disease, and cardiac dysrhythmias because of the vasoconstriction caused by these medications. Decongestant nasal sprays such as oxymetazoline (Afrin) should only be used for a few days at a time because overuse may cause rebound congestion (severe congestion). If infectious rhinitis is present, the administration of antibiotics is required, with the selection of the antibiotic based on patient history, allergies, and the severity of the infection.

Atherosclerosis/Arteriosclerosis

-Diagnosis ■ Assessments • Complete patient history and cardiovascular assessment There is a genetic and environmental link to cardiovascular disease. Patients with a family history of cardiovascular disease have a higher prevalence of the traditional cardiovascular risk factors highlighting opportunities for prevention. • Assess blood pressure (BP) in both arms Hypertension is a strong risk factor for atherosclerotic disease. • Palpate pulses at all the major sites on the body and note any differences. Carotid arteries are palpated one at a time. Weak pulses may suggest poor flow through the artery. Palpate the carotids one at a time so as not to risk blocking flow to the brain. • Auscultate for bruits A bruit is a turbulent, swishing sound that can be soft or loud in pitch. It is heard as a result of blood trying to pass through a narrowed artery. Bruits often occur in the carotid, aortic, femoral, and popliteal arteries. A bruit is considered abnormal, but it does not indicate the severity of the disease. • Fasting lipid profile Low-density lipoprotein cholesterol (LDL-C) High LDL-C levels indicate an increased risk for atherosclerosis. Target LDL-C level is less than 100 mg/dL for healthy adults. High-density lipoprotein cholesterol (HDL-C) Low HDL-C levels indicate an increased risk for atherosclerosis. The target HDL-C level is greater than 40 mg/dL. • Triglyceride levels Triglyceride levels may be elevated with atherosclerosis. Elevated triglycerides are considered a marker for other lipoproteins. A level of 150 mg/dL or above indicates hypertriglyceridemia. • Homocysteine Homocysteine is a sulfur-containing amino acid derived from dietary protein. High serum levels of homocysteine may block production of nitric oxide on the vascular endothelium, making the cell walls less elastic and permitting plaque to build up. • Glycosylated hemoglobin A1c (HgbA1c) Hyperglycemia is a risk for the development of atherosclerosis. An HgbA1c of greater than 7% may indicate poor glycemic control. -Treatment Identifying and controlling risk factors for the development of atherosclerosis are the basis of medical management. A decrease in serum LDL-C levels leads to a reduction in the risk of atherosclerotic cardiovascular disease. Medications used to lower lipid levels are the primary treatment modality. Anticoagulation is also used to decrease clot formation. Medication therapy is similar to that for coronary artery disease and is outlined in Table 30.2 in Chapter 30. Other options include modification in dietary habits, smoking cessation, and lifestyle modifications including an exercise and stress reduction plan. • Administer medications as ordered such as: • Antihypertensive medication • Lipid-lowering therapy including statin therapy There is a direct relationship between hypertension and increased cholesterol levels and atherosclerosis.

Respiratory complications

Chest x-rays are normally a first-line diagnostic test for patients with respiratory complaints because they are widely available and relatively inexpensive.

Respiratory acidosis

PaCO2: greater than 45 mm Hg pH: less than 7.35 HCO3: greater than 26

Respiratory alkalosis

PaCO2: less than 35 mm Hg pH: greater than 7.45 HCO3: less than 22