Example Of Case Study Oedema

Lungs: Demonstrate good air entry. Faint end-expiratory wheeze throughout all lung fields. No rales or rhonchi. Symmetric chest expansion. Breathing nonlabored.

A 68 year old male presented to the emergency department at 0800 hours via ambulance after experiencing chest discomfort and intermittent palpitations since 0500 hours. Prior to presentation, the patient stated he

I was well versed with the patient’s medical history and current treatment, as I was the Long Call IM PGY – II Resident who supervised the medical intern when this patient was being downgraded from the ICU to the medical floor on 5/20/17 (and even suggested to the medical intern to add in her notes that the patient would benefit from statins, ACE inhibition and Spironolactone given CAD, CVA and HFrEF (LVEF < 35%.) The medical team subsequently started the patient on Atorvastatin 40 MG PO QHS, Lisinopril 10 MG PO QD and Spironolactone 12.5 MG PO QD.

The presence of fluid in the alveolar space could potentially cause the lung capacity to be effected as well.

D.Z.is a 65-year-old man admitted to medical ward with an exacerbation of chronic obstructive pulmonary disease (COPD; emphysema). Past medical history (PMH) indicates hypertension (HTN), well managed with enalapril (Vasotec) past six years, diagnosis (Dx) of pneumonia yearly for the past three years. D.Z. appears cachectic with difficulty breathing at rest. Patient reports productive cough with thick yellow-green sputum. He seems anxious and irritable during subjective data collection. He states, he has been a 2-pack-a-day smoker for 38 years. He complains of (c/o) insomnia and

A.O. is an 89-year-old woman with a long history of systolic heart failure secondary to a large left ventricular infarct when she was in her 70s. She had poor activity tolerance and required assistance with activities of daily living. Even minimal activity was associated with moderately severe dyspnea and exertional chest pain, which was relieved by rest. A.O. also exhibited marked pedal edema bilaterally. She is being treated with digitalis, furosemide (Lasix), KCl, and sublingual nitroglycerin.

Another Consultation Report dated 12/06/2016, indicated that the claimant presented with exacerbation of COPD, acute bronchitis, and pseudomonas aeruginosa. The CT scan of the chest revealed bilateral lower lobe atelectatic changes, fibrosis, and a small 1 cm left lower lobe nodular density. A pulmonary consultation was recommended. His blood pressure was 142/79 mmHg. The physical examination revealed bilateral decreased breath sounds and scattered wheezes. His glucose was 189. DuoNeb, IV Solu-Medrol, and IV antibiotics were prescribed.

Mr BW was a 74-year-old man who had a fall due to a new onset of seizures, which resulted, to a direct impact of his head on the ground while at home. While at the hospital, MR BW underwent a CT and MRI brain scan and showed a haematoma, which resulted to commencing of the patient on Keppra and Bezodiapenes. Moreover, Mr BW also developed a sudden onset of pleuretic chest pain, which was confirmed by CTPA as a small pleural effusion on the left lungs; while there was also pulmonary embolism on both upper and lower lobes of the left lung. Due to the development of a provoked pulmonary embolism, patient commenced on Clexane injection. In September 2015, an elective open abdominoperineal resection was performed on Mr BW, which resulted to prolonged stay in the hospital due to delayed wound healing.

Pleural effusion is the accumulation of fluid in the pleural space. This may lead to the accumulation of fibrous tissue and the fluid will move towards the dependant area and collapse the adjacent lung.

You had a recent episode of lower leg edema (swelling) which your primary care physician prescribed Lasix (medicine to get rid of fluid). You vital signs were within normal limits and there was no oxygen saturation (rest) provided. Your electrocardiogram (recording of your heart activity) was Sinus (normal). In emergency room you received 30 milligram of Lovenox (blood thinner) and Methylprednisolone (medicine to help with breathing). You were admitted, started on aspirin, Cardiac enzymes (test) were done and your first troponin (test) was negative (no other results provided). You were continued on Prednisone (medicine) 10 milligram daily; restarted on Coumadin (blood thinner), Diltiazem (medicine), and a low salt diet was recommended as well as you received Albuterol via a nebulizer (breathing treatment) every 4 hours. Your pulmonary (breathing specialist) consult states that the shortness of breath was most likely due to deconditioning (changes in body with inactivity), obesity (over weight), and less likely due to Sarcoidosis (inflammatory disease). Chest pain syndrome was musculoskeletal (muscle-bone) in origin as it was reproducible (pain present when area is pushed

is Pneumonia. This is based on the patient’s subjective and objective data. The collaborative diagnosis to address this problem is Pneumonia r/t immobilization; r/t pleural effusion, and r/t debilitation (Carpenito, 2013, p. 859-860). The nursing goal for this patient on the day of care is to control and reduce the complication of pneumonia (Carpenito, 2012, p. 860). The nurse will monitor the patient’s respiratory status while assessing for sign and symptoms of infection, and inflammation (Carpenito, 2012, p.

A 63-year-old Caucasian male presented to the hospital for one-week symptoms of exertional dyspnea and lower extremity muscle weakness. CT/Thorax demonstrated bilateral pleural effusions with subcutaneous edema in the thorax and abdomen. Total creatinine phosphokinase level was 3,227 units/L and aldolase

A: Janie is a 60 year old Female with PMH of A-Fib, COPD, Hypothyroidism, HTN, Lung Cancer and recently diagnosed Pulmonary Embolism. Janie presents to ER for evaluation on SOB, cough with greenish sputum, sore thoart, hoarseness and generalized weakness. Janie lives at home with her husband, use to smoke ½ pack per week, but quit many years ago, denies alcohol or drugs. Family history is non-contributory. Allergies: NKDA. Differential diagnosis includes worsening Lung Ca, PE, COPD and CHF. Janie uses home O2 at 4 L/NC. V/S: T=98.7, HR=89, R=16, B/P=132/56, O2 sats=100% on 4L/NC, Pain=6/10. Labs: WBC=7.6, H&H=8.5/27, Na=141, Troponin=0.08/0.06, BNP=495, INR=4.2, UA=3+ protein, 1+ blood and 6-10 RBC. CXR: Impression:1). COPD with nonspecific coarsening of the basilar interstitium. 2). Mild cardiomegaly with borderline cardiac compensation. 3). Right

Imagine waking up in the morning to the discomfort of not being able to take a proper ventilation. Horrible, right? This is what people who have pleural effusions feel. I chose to do my paper on pleural effusions. Pleural effusions are a collection of fluid in the pleural space, the cavity surrounding the lungs. Typically, there is 10 mL of fluid in this space to lubricate the pleura, however when disrupted by diseases such as pneumonia, pulmonary embolisms, congestive heart failure, or cancer, fluid begins to third space and collect in abnormal amounts. The biggest challenge then becomes dyspnea and tachypnea. This is because the extra fluid decreases pressure making it difficult for the lung to fully expand. Pleural effusions

Emphysema Emphysema is a condition in which there is over-inflation of structures in the lungs known as alveoli or air sacs. This over-inflation results from a breakdown of the walls of the alveoli, which causes a decrease in respiratory function (the way the lungs work) and often, breathlessness. Early symptoms of emphysema include shortness of breath and cough. Emphysema and chronic bronchitis together comprise chronic obstructive pulmonary disease (COPD).