Angioedema Case Studies

Physical Examination: General: The patient is an alert, oriented male appearing his stated age. He appears to be in moderate distress. Vital signs: blood pressure 132/78 and pulse 68 and regular. Temperature is 38.56 oC (101.4 oF). HEENT:Normocephalic, atraumatic. Pupils were equal, round, and reactive to light. Ears are clear. Throat is normal. Neck: The neck is supple with no carotid bruits. Lungs: The lungs are clear to auscultation and percussion. Heart: Regular rate and rhythm. Abdomen:Bowel sounds are normal. There is rebound tenderness with maximal discomfort on palpation in the right lower quadrant. Extremities: No clubbing, cyanosis, or edema.

Mr. Howard, a 57-year-old man, had a 3-month history of progressive typical anginal chest pain. He reported that the symptoms first occurred with heavy exertion and involved what he described as“heaviness” in his chest. The symptoms were promptly relieved with rest. Over the past weeks, he had been experiencing increasingly frequent episodes of chest pain and diaphoresis. The episodes had become more prolonged, and he had experienced one episode of pain occurring at rest after a heavy meal. Mr. Howard was moderately obese and had a 20-year history of hypertension, which was being treated. Other risk factors in Mr. Howard’s history include hypercholesterolemia (350 mg/dL), which he was attempting to treat with dietary modifications, and a 30-year two-pack-a-day smoking history which continued up to the present time. Mr. Howard previously had surgery for a bilateral inguinal hernia repair, cholecystectomy, and arthroscopic surgery on his left knew. He also gave a history of problems with gastric reflux and was currently taking cimetidine (Tagamet).

Hypertension. His blood pressure is great here in the office. I will have him continue with his same medication and I will continue to follow along and he was asked also monitor for signs of hypotension and I did review with him what to be monitoring for.

Mr. S is a 29-year-old male with past medical history of (PMH) hypertension (HTN) and obesity who presented to local emergency room (ER) with headache and chest and back pain. Mr. s had been seen at urgent care three days prior for a headache and near syncope and was told to hold his metoprolol due to bradycardia. Due to health insurance related problem, he has been off amlodipine and lisinopril for a month.

“The patient is Adam Rudd, a 78 y/o white male with a history of hypertension. He has been diagnosed with hypertension past 15 years and is on anti-hypertensive medications and aspirin. He is very weak and short of breath. He is accompanied with his longtime friend Jennifer, who reports that Rudd was looking very weak and was complaining of severe headache and blurred vision before coming to the hospital. He is 5’9” and weighs 270 lb. Vital signs recorded were: oral temperature 98.20 F, BP 224/120 mm Hg with a heart rate of 102 beats/minute and respiration of 24 breaths per minute. The pulse oximetry reading was 94% on room air. He is complaining of severe headache and blurred vision. Rudd said that he did not take his antihypertensive medication or aspirin since he ran out of pills. He has not been taking his medication for past 15 days. He reports no known allergies to any medications or other substances.”

An elderly male with congestive heart failure was brought to a clinic because he was experiencing atrial fibrillation and had a ventricular response of 110 beats/min with palpitations and shortness of breath1. Medications that he was taking includes angiotensin-converting enzyme inhibitor, Lisinopril, Carvediol, Digoxin, and Furosemide1. His left ventricular ejection fraction has been reduced to 25%1. Further examinations showed that he had edema in his legs and crackles at the base of his lungs1. He was then told to increase the dosage of Furosemide by taking the drug twice daily instead of once, and doubling the dose per administration1. One week later, the electrocardiogram revealed that he had ventricular arrhythmias such as premature

Patient A.S. is 87-year-old female with a diagnosis of Acute onset chronic systolic heart failure, Afib, CHF, and hypothyroidism. She has a past medical history of Hypertension, diabetes mellitus, CAD (Stent 2001). The patient was admitted to Lutheran Augustana Center on January 4, 2016 and was evaluated for therapy on January 5, 2016. Her current medications include Albuterol and Ipratropium via nebulizer to address shortness of breath. A combination of drugs to treat the symptoms of congestive heart failure and other comorbid diagnosis include: Eliquis, Furosemide, hydralazine, and metoprolol. Other medications include Synthroid to treat hypothyroidism, Tradjenta for hyperglycemia, and Zocor for hyperlipidemia. The patient also presented with skin problems. She has bilateral ecchymosis in her lower extremities and abdomen. Lotrisone lotion was prescribed for atopic dermatitis. Edema was also present in her lower extremities.

Together ACE inhibitors and ARB’s work to lower heart rate and blood pressure by inhibiting the RAS (renin-angiotensin system) in the sympathetic nervous system. This “fight or flight” system is activated by the heart when it senses the inability of the ventricles to pump blood, in which cardiac output and blood pressure are decreased. These medications act by blocking this system and therefore decreasing blood pressure and heart rate (Markaity, 2012). Commonly used ACE inhibitors include: enalapril (Vasotec), benazepril (Lotensin), lisinopril (Prinivil, Zestril) and captopril (Capoten). Commonly used ARBs include: losartan (Cozaar), Candesartan (Atacand), Valsartan (Diovan) (heart.org).Common side effects of ACE inhibitors and ARBs are: dry cough, dizziness, hypotension and hyperkalemia. Renal function tests and serum potassium levels should be monitored periodically. ACE inhibitors and ARBs have a label of pregnancy category D while in the second and third trimesters

The study shows that disease-modifying medications were prescribed significantly more often in 2000 than in 1995, particularly in patients younger than 65 and in those aged 75 to 84 (Saczynski et al., 2009, p. 3). The study indicates that Beta-blockers and ACE inhibitors have been shown to improve survival and reduce hospitalizations in patients with Heart Failure. The second article mentioned about the elderly patients who have CHF not on or under dosage of Angiotensin Converting Enzyme (ACE) inhibitors. According to this article ACE inhibitors should be given for patients diagnosed asymptomatic left ventricular systolic dysfunction (LVSD) (EF<40%) and symptomatic heart failure with systolic dysfunction associated with other heart problems such as myocardial infarction, pulmonary hypertension. The suggested dosage for the CHF patients mentioned in the article and due to age-related changes in pharmacokinetic drugs, it also recommended the initial dosage must be half the standard dose and gradual increase after assessing renal function. After studying a group of elderly CHF patients revealed that higher or standard dose of ACE inhibitors reduce the risks of major clinical events. Results from the research display a decrease of hospitalizations due to cardiovascular reason, heart failure, and ischemic events in the standard-dose group. The study also found out that the adverse effects of high doses can be managed by reducing the dosage or by changing

Usually angiotensin has an effect on the body to increase blood pressure, increase blood volume and increase pressure in the kidney. As the ACE inhibitor lowers the amount of angiotensin, this causes the blood vessels to become wider and there is an increase in the amount of urine produced by the kidneys. The result of this is the blood pressure goes down, blood volume decreases and decreases pressure in the kidneys. The decrease of angiotensin levels by ACE inhibitors also causes a drop in noradrenalin and aldosterone levels, which helps to reduce blood pressure. Another effect ACE inhibitors have is to increase bradykinin which also causes the blood vessels to widen with a further decrease in blood pressure. Examples of ACE inhibitors include; Lisinopril (Prinivil), Captopril (Capoten) and Enalapril

The last visit I had with the patient on June 7th, I elected to start him on antihypertensive therapy. He was given a prescription for Zestoretic 10/12.5 mg one p.o. to take daily. He says that he did take one as recommended. That same day in the afternoon, he noted that he was short of breath in the afternoon. He says that he attributed it to the work that he was doing out in the yard and later that day, it seemed to resolve. A few days later, he had the same thing happen again. He eventually went on to see Dr. Lilly on June 25th. Please see that note for complete details. She did have him go through a series of testing, including laboratory studies, which were normal

The patient is a 64-year-old female who was noted to have elevated blood pressures. She had been on atenolol in the past, but got some hair thinning with it. She was willing to try it again, from her physical appointment in April 2015. This time however, she felt very fatigued and groggy on it. We, therefore, switched her to losartan 50 mg, which she was taking a half a tablet per day. With taking this, however, she states she started feeling more anxious and had more difficult time sleeping. She stopped it on her own. She has been checking her blood pressures at home and they have ranged in the 120's/60s to 80s.

ACE inhibitors such as Captopril block activity of the enzyme ACE and therefore the conversion of angiotensin I to angiotensin II (the most bio active product of the RAAS), thus inhibiting the actions of angiotensin II and leading to decreased aldosterone production, decrease blood volume and reduced hypertension. ACE inhibitors also work to decrease fibroblast activity as a protective measure against remodelling of the left ventricle (19). Side effects of ACE inhibitors include a dry cough due to the inhibition of bradykinin break down, hypotension and hyperkalemia (due to higher levels of potassium reuptake). ACE inhibitors are currently one of the drugs of choice to treat patients with HF.

Angioneurotic edema, also called angioedema, is the rapid swelling of the dermis, subcutaneous tissue, mucosa and submucosal tissues. Angioedema is classified as either hereditary or acquired. Acquired angioedema is usually caused by allergy to food or drugs. Common food or food additive agents include artificial food coloring, seafood, chocolate, nuts, strawberries, tomatoes and eggs. Hereditary edema is caused by a genetic mutation inherited in an autosomal dominant form. The great majority of cases of angioedema can be diagnosed based on the history and physical examination alone. Symptoms of angioedema include swelling of the skin of the face, normally around the mouth as well as the tongue. The swelling can be itchy or painful. In severe

Patient is a 45 yo male; 5’7”, 221 lbs who entered the emergency room at 6:30 am on 9/7/14 with severe chest pain (onset at 6:00 am) radiating to his arm, L arm numbness and nausea and vomiting. Past medical history reported by wife includes peptic ulcer, tobacco use (1-2ppd for 27 years), elevated blood pressure (controlled by lopressor). Wife did not know of any family history but reports patient’s father is deceased, died at 42 in his sleep. Mother alive and with high blood pressure.