Geriatric Assessment 48
Running Head: ASSESSMENT OF THE GERIATRIC PATIENT
Assessment of the Geriatric Patient
Diana Stiles
Kent State University
Spring 2010
Assessment of the Geriatric Patient
Client Profile
F.B. is a 82 year old widowed female that was admitted to Altercare of Nobles Pond on 2/8/2010 for rehabilitation. She is a retired executive secretary and has two children, a son and a daughter and until her admission she lived with her son. She admitted to smoking between two to four packs of cigarettes a day for more than twenty years; quit in 1972, denies any significant alcohol use. After her knee surgery she started to have pain on her right side and trouble breathing. She sought healthcare and they found multiple pulmonary emboli.
Medical Diagnosis
Diagnoses for F.B. include multiple PE, OMD, DM, HTN, general debilitation, CAD, hyperlipidemia, hypothyroidism, GERD with severe esophagitis and stricture, osteoporosis, cholelithiosis, cholecystitis, dysphagia, major depression, general anxiety, right lower lobe pneumonia, increasing fatigue, lethargy, and temporary rehabilitation due to debilitation. Despite all of these diagnoses F.B. still believes that her health is fair to good.
Past Surgical History
F.B. also has a pretty extensive past surgical history as well. She has undergone an appendectomy, coronary artery bypass graft, PTCA with three stents, right hip fracture, left total knee replacement, remote back surgery, bilateral cataracts, remote bowel resection due to obstruction ( two resections due to ischemic disease), lumbar decompression fusion surgery, history of spinal stenosis, and a left breast biopsy that came back benign. A significant family history of diabetes and multiple cancers were also reported.
Pulmonary Embolism – PEDefinition- An occlusion of a portion of the pulmonary blood vessels by an embolus. An embolus is a clot or other plug that is carried by the bloodstream from its point of origin to a smaller blood vessel where it obstructs circulation; can be lethal depending on its size.
(Black & Hawks, 2009, p.1591).
Pathophysiology- When emboli travel to the lungs, they lodge in the pulmonary vasculature. Blood flow is obstructed, leading to decreased perfusion of the section of lung supplied by the vessel. Ventilation continues but the tissue is not perfused, leading to hypoxemia. If an embolus lodges in a large pulmonary vessel, it increases proximal pulmonary vascular resistance, causes atelectasis, and over time reduces cardiac output. Smaller vessels produce less dramatic effects, but perfusion is still altered. The arterioles constrict due to platelet degranulation, paired with a release of histamine, serotonin, catecholamines, and prostaglandins resulting in bronchial and pulmonary artery constriction. PE can lead to right sided heart failure because once the clot lodges, affected blood vessels collapse increasing pressure in the pulmonary vasculature. The increased pressure increases the workload of the right side leading to failure. A massive PE of the pulmonary artery can also result in cardiopulmonary collapse from lack of perfusion and resulting hypoxia and acidosis. (Black & Hawks, 2009, p.1591-1592).
Sx- Most common manifestations are tachypnea, dyspnea, anxiety or fretfulness, and chest pain. Hypoxemia may also be present depending on the size of the embolism. The pain experienced is pleuritic in nature, has a sudden onset, and is exacerbated by breathing. Patient may by dyspneic, have a cough, and syncope or hemoptysis may occur. Respirations usually increase; crackles and an accentuated second heart sound, tachycardia, and fever may develop.
(Black & Hawks, 2009, p. 1592).
Tx- Prompt recognition and immediate treatment are essential. Goals are to stabilize the cardiopulmonary system and reduce the threat of a further PE with anticoagulation therapy or tapping with an umbrella in the vena cava; for some the clot can be lysed. Stabilization is the first priority; hypoxemia may be reversed with low-flow via nasal cannula whereas some may require endotracheal intubation to maintain PaO2 greater than 60mm Hg. Hypotension is treated with fluids, although inotropic agents may be required if the fluids do not raise the preload enough to raise the blood pressure. Acidosis is corrected with bicarbonate. Anticoagulation begins with IV standard heparin sodium based initially on body weight and current level of anticoagulation to reduce the risk of further clots or extension of present ones; anticoagulants are administered until a therapeutic PTT time is achieved. Sodium warfarin is started 3 to 5 days before discontinuing heparin to provide a transition to oral therapy due to the difference in half lives of the two drugs. Sodium warfarin is maintained for 3 to 6 months.
(Black & Hawks, 2009, p. 1593).
Diabetes Mellitus - DM
Definition- Type 1 diabetes mellitus is the result of autoimmune beta-cell destruction, leading to absolute insulin deficiency. (Black & Hawks, 2009, p. 1062).
Pathophysiology- Diabetes does not develop in everyone who has a genetic predisposition; of those who gene markers indicate a risk, less than 1% develop it. Environmental factors are thought to play a part in the development of diabetes since incidence is increased in both spring and fall, and onset is usually coincidental with epidemics or various viral diseases. Active autoimmunity is directed against the beta cells of the pancreas and their products. ICA’s and insulin antibodies progressively decrease the effective circulating insulin level which can lead to an abrupt onset of diabetes. Hyperglycemia can result from acute illness or stress which increase insulin demand beyond the reserves of the damaged beta-cell mass. When the situation resolves, reverting back to a variable duration in which the pancreas once again manages to produce adequate amounts of insulin may take place. Compensation usually lasts 3 to 12 months and ends when the diminishing beta-cell mass cannot produce enough insulin to sustain life and then the patient becomes dependent on exogenous insulin administration to survive.
(Black & Hawks, 2009, p. 1065-1066).
Sx- An elevated glucose level, hyperglycemia, leads to frequent urination, polyuria, increased thirst or fluid intake, polydipsia, and as the disease progresses, weight loss despite drinks and increased food intake, ployphagia. (Black & Hawks, 2009, p. 1067).
Tx- Treatment includes restoring and maintaining blood glucose levels to as close to normal as possible by balancing diet, exercise, and administering oral hypoglycemic agents or insulin. Generally, if the diabetes is well managed, patients can avoid complications of hyperglycemia and hypoglycemia both. (Black and Hawks, 2009, p.1071).
Hypertension -HTN
Definition- High blood pressure. A persistent elevation of the systolic blood pressure at a level of 140mm Hg or higher and a diastolic blood pressure at a level of 90mm Hg or higher.
(Black & Hawks, 2009, p. 1290).
Pathophysiology- Any factor that produces an alteration in peripheral vascular resistance, heart rate, or stroke volume affects systemic arterial blood pressure. Four control systems play a major role in maintaining blood pressure; the arterial baroreceptor and chemoreceptors’ system; regulation of body fluid volume; the rennin-angiotension system; and vascular autoregulation. Baroreceptors monitor the level of arterial pressure and counteract increases through vasodilation and slowing of the heart rate via the vagus nerve. Chemoreceptors are sensitive to changes in the concentrations of oxygen, carbon dioxide, and hydrogen ions in the blood. A rise in blood pressure is caused by a decrease in arterial oxygen concentration or pH whereas a decrease in pressure is cause by an increase in carbon dioxide concentration. Changes in fluid volume affect systemic arterial pressure; when sodium and water levels are excessive, total blood volume increases which also increases blood pressure. Renin is an enzyme produced by the kidney that catalyzes a plasma protein substrate to split of angiotension I, which is removed by converting enzyme to the lung to form angiotension II and then angiotension III. Angiotension II and III act as vasoconstrictors and also stimulate aldosterone release, and inhibit sodium excretion which results in elevated blood pressure. (Black & Hawks, 2009, p. 1293).
Sx- In early stages of hypertension no manifestations are noted but if the condition remains untreated the blood pressure will continue to rise and eventually will warrant a trip to the physician with complaints of frequent headaches, fatigue, dizziness, palpitations, flushing, blurred or double vision, or epistaxis. A hypertension diagnosis is made after the patient has been allowed 5 minutes of resting time and at least two readings separated by at least 2 minutes with a systolic pressure of 140mm Hg or higher and a diastolic pressure of 90mm Hg or higher. Clients that fall into the prehypertensive category, systolic of 120-139mm Hg and a diastolic of 80-89mm Hg are strongly encouraged to adopt a lifestyle changes.
(Black & Hawks, 2009, p. 1295-1296).
Tx- The goal is to normalize blood pressure and reduce risk factors in an effort to control the progression of hypertension. Compliance is the most essential element in controlling and living with hypertension. For some, lifestyle changes such as a change in their diet or exercise habits are enough to bring the blood pressure down to normal, and even in patients who cannot control the blood pressure with diet and exercise alone, it can significantly reduce the number and dosage of antihypertensive medications needed. Weight also plays a role in the development of hypertension. A BMI of 27 or greater, a waist size greater than 35in for females and 40in for males, and anyone whose weight is greater than 10% over ideal, correlates closely with elevated blood pressure. For these patients a 10lb weight loss can lower the blood pressure as much as 10mm Hg and also greatly enhance the effectiveness of the antihypertensives.
(Black & Hawks, 2009, p. 1296-1297).
Medications currently ordered for FB:
Actonel (Risedronate)- 35 mg. po every week on Sundays
Alprazolam (Xanax)- 0.5 mg. po tid PRN
Amlodipine (Norvasc)- 5mg. po q day
Acetylsalicylic Acid (Asprin)- 81mg. po q day
Atenolol (Tenormin)- 50mg. po q day
Furosemide (Lasix)- 40mg po q day
20mg po q day
Iron- 325mg po q day
Isosorbide Mono ER (IMDUR)- 30mg po q day
Levalbuterol (Xoponex)- 0.63mg/3ml breathing treatment q4h
Levothyroxine (Synthroid)- 0.15mg po q day
Lisinopril (Prinivil)- 20mg po q day
Megestrol Acet. (Megace)- 40mg/ml oral suspension 10cc (400mg) po HS for 3 weeks
Metformin HCL (Glucophage)- 500mg po bid
Mirtazapine (Remeron)- 15mg po HS
Multi-vit/min- 1 tablet po q day
Novolin- sliding scale ( blood sugars - 0600 and 1600)
151-200 – 1unit
201-250 – 2 units
251-300 – 3 units
301-350 – 4 units
351-400 – 5 units
Ø 400 call MD
Omeprazole- 20mg po q day
Potassium Chl. ER (Micro-K)- 10mEq- 1 tab po bid
Simvastatin (Zocor)- 40mg po HS
Sucralfate (Carafate)- 1GM po q6h
Tramadol HCL (Ultram)- 50mg- 1-2 tab po bid PRN
Warfarin- 2.5mg po q day
Geriatric Assessment 48
Drug Name(generic/trade name) / Drug Action/
Purpose / Normal Dose
Range / Major side
Effects / Nursing Considerations
Actonel
(Risedronate) / Prevention and treatment of postmenopausal and corticosteroid –induced osteoporosis. Management of Paget’s disease of bone in patients who: have serum alkaline phosphate level of at least twice as normal, have symptoms, are at risk for complications. Increase bone mass in men with osteoporosis. It inhibits bone resorption by binding to bone hydroxyapatite, which inhibits osteoclast activity.
Route: PO
Onset: within days
Peak:30days
Duration: up to 16 months / 5mg daily before breakfast
OR
35mg once weekly
OR
75mg taken on two consecutive days for a total of two per month / skin rash, abdominal pain w/cramps, diarrhea, esophageal ulcer, gastric ulcer, nausea, headache disorder, dyspepsia, arthralgia, back pain / Administer first thing in the morning with 6-8oz of plain water, 30 min prior to any other food, meds, or drinks. Remain upright for at least 30 min after administration to help with passage to the stomach and minimize esophagus irritation. Assess patients via bone density study for a low bone mass before and during therapy. Assess serum calcium before and periodically during therapy. Hypocalcemia and vitamin D deficiency should be treated before starting therapy. May cause mild transient increase in calcium and phosphate. Assess for allergy
Alprazolam
(Xanax) / Treatment of generalized anxiety disorder. Management of anxiety with depression. It acts at many levels in the CNS to produce anxiolytic effect. May produce CNS depression. Effects may be mediated by GABA, an inhibitory neurotransmitter.
Route: PO
Onset: 1-2 hr
Peak: 1-2 hr
Duration: up to 24hr / 0.25-0.5mg 2-3 times daily / slurred speech, drowsy, sedation, dizziness / Assess orientation, mood, behavior, and degree of anxiety. Assess for drowsiness, lightheadedness, and dizziness. Assess CNS effects and risk of falls. Institute fall prevention strategies. May be given with food, give highest dose at night. Do not crush, break, or chew. Don’t drink grapefruit juice. Assess for allergy
Amlodipine
(Norvasc) / Antihypertensive. Inhibits transport of calcium into myocardial and vascular smooth muscle cells, resulting in inhibition of excitation- contraction coupling and subsequent contraction.
Route: PO
Onset: unknown
Peak:6-9 hr
Duration: 24hr / 5-10mg once daily / peripheral edema, edema, flushing, headache disorder / Assess pulse and blood pressure. Monitor I&O and daily weight. Assess for allergy
Acetylsalicylic Acid
(Aspirin) / Antiplatelet. Inflammatory disorders, mild to moderate pain or fever. Prophylaxis of transient ischemic attacks and myocardial infarction. It produces analgesia and reduces inflammation and fever by inhibiting the production of prostaglandin. Asprin only decreases platelet aggregation.
Route: PO
Onset: 5-30 min
Peak: 1-3 hr
Duration: 3-6 hr / Pain/Fever
325-1000mg q 4-6hr
Inflammation
2.4g/day
Increase to maintenance dose of 3.6-5.4g/day
Prevention of transient ischemic attacks
50-325mg/day
Prevention of MI
80-325mg/day / Gastrointestinal bleeding, dyspepsia, gastric distress, nausea, abdominal pain, anorexia, hepatotoxicity, vomiting, anemia, increased bleeding time, tinnitus, hearing loss, rash, thrombocytopenia, anaphylaxis, and laryngeal edema / Give with meals. Prolongs bleeding time for 4-7 days and, in large doses, may cause prolonged prothrombin time. Assess pain and fever. Monitor hepatic function before antirheumatic therapy begins. Assess for allergy
Atenolol
(Tenormin) / Management of hypertension. Management of angina pectoris. Prevention of myocardial infarction. It blocks stimulation of beta1-adrenergic receptors. Does not usually affect beta receptor sites.