Jan 12, 2018 in Medicine

Acute Exacerbation of Copd Secondary Pneumonia

This is a case of a 69-year-old man admitted on 9 February 2013 at West Anaheim Medical Center for acute exacerbation of chronic obstructive pulmonary disease (COPD) caused by acute pneumonia. COPD is a lung disease, which when experienced by the patient, has progressive airflow limitation that is not completely reversible. The airflow limitation in most cases associates with an inflammatory response in the lungs from exposure to noxious particles and gases over time. Spectrum of COPD includes acute and chronic bronchitis, emphysema and asthma. Chronic bronchitis comprises of extreme sputum production during for a period of at least three months in a year for the minimum duration of two years. Emphysema is characterized by an increase of air spaces distal to terminal bronchioles, which leads to the loss of elastic tissue and damage to alveolar septal walls. Asthma known to be a reversible obstruction of airways is considered separately. However, many COPD patients have some degree of reversibility in their airways. Exacerbations of COPD are episodes of symptoms becoming more intense, which can lead to extensive morbidity and death. COPD exacerbations are linked with increased airway and systemic inflammation and physiological changes. About 10% to 15% of patients who have an obvious acute exacerbation are found to have pneumonia defined by chest imaging. When describing pneumonia, it is usually referred to as inflammation of the lung parenchyma and is most often used to describe inflammation caused by infection.

Patients with pneumonia experience fevers, more acute onset of illness, and somewhat greater severity of acute illness when compared with COPD patients without pneumonia. Most cases of COPD result because of a combination of exposure to noxious particles, fumes, and host factors. The most common cause leading to the onset of COPD is cigarette smoking. People who smoke have a much higher occurrence of COPD, a larger decline in lung function over time, and a greater COPD mortality rate. Acute exacerbations of COPD emerge throughout the course of the disease over the patient's lifetime. Exacerbations differ in severity and are triggered primarily by infections (both viral and bacterial) and airborne pollutants. This 69-year-male patient, has a long history of smoking, and has just stopped about four weeks ago, is admitted for acute exacerbation of COPD causing by acute pneumonia. The patient has a history of COPD secondary to smoking and history of cerebrovascular accident, a sudden death of some brain cells due to the oxygen deprivation when the blood flow to the brain is interrupted by a blockage or tearing of an artery.

A CVA is also referred to as a stroke. The patient begins to experience cough and obstruction of airways. He is admitted with a shortness of breath and low saturation on the February 9 2013. The patient is placed on BiPAP in the emergency room, as well as given breathing treatment, and takes antibiotics. At admission, his vital signs have the following values: blood pressure is 136/69, heart rate was 80, respiratory rate 27, and temperature 98 F. Based on the vital signs data, the patient is tachypneic and experiences hypertension. Chest auscultation reveals rhonchus, a few crackles, expiratory wheezing and intense breath sounds in the left lung. His ECG shows arterial fibrillation with rapid ventricular response. His arterial blood gas values measured with 45-50% FiO2 on a treatment are pH 7.20, PCO2 100.2, HCO-3 38.5 and PO2 78. According to his ABG values, the patient depicts an acute hypoventilation on chronic respiratory failure with mild hypoxemia. Normally with this critical value, a patient is intubated, but the physician has decided to place the patient on BiPAP with 60% FiO2, as patient is awake and well oriented with no detectable distress. Chest x-ray shows COPD and early pneumonia, which resulted in an increased white blood cells.

Based on the present findings, the patient takes antibiotics and Solu-Medrol for the treatment of pneumonia. For the symptoms of COPD, the patient undergoes breathing treatment. As mentioned before, the patient has an acute hypoventilation on chronic respiratory failure, which referred to a pH lower than 7.35, PCO2 greater than 45 mm Hg and HCO-3 greater than 26 mm Hg. After placing the patient on BiPAP with 60% FiO2, another ABG has been drawn, the result pH 7.26, PCO2 85.6, HCO-3 37.2 and PO2 141.2 has shown an improvement of patient's condition. During the course of treatment, the patient has improved and on the 02/12/13 on nasal cannular with 32% FiO2, the ABG shows a pH 7.4, PCO2 66.1, HCO-3 39.8 and PO2 77.1, which shows a fully compensated respiratory acidosis with mild hypoxemia. PCO2 and the bicarb are still elevated, normal range of PCO2 is 35-45 mm Hg and of HCO-3 is 22-26 mmol/L, although, taking into consideration of a COPD patient an elevated PCO2 and bicarb can be considered as normal. All factors in patient’s condition have improved. According to the hematology lab results, there is an elevated white blood cell count of 11.9 K/mm3, normal range is 4.5-10.5 K/mm3, which is made up by 85% of increased neutrophils and means that there is an infection. In addition, the methicillin resistant Staphylococcus aureus (MRSA) screening came back positive and there are Staph aureus bacteria found. The patient's chemical lab results are within normal range.

Patchy interstitial infiltrates in the lower lobes of lungs seen on the chest x-ray suggested pneumonia. The prescribed medications include Levalbuterol 0.63 mg Q4, Ipratropium Bromide 0.5 mg Q4, Methylprednisolone Sodium Succinate (Solu-Medrol) 60 mg Q12 and Pneumococcal Polyvalent vaccine 0.5 ml. In addition, these medicine should be taken Levofloxacin/Dextrose 750 mg daily, Ondansetron HCl 4 mg Q6, Digoxin 0.25 mg daily, Lisinopril 10 mg daily, Diltiazem HCl 240 mg daily, Hydralazine HCl 20 mg Q4, Furosemide 40 mg daily and Tamsulosin HCl 0.4 mg daily. Levalbuteral is beta-2 adrenergic bronchodilator that relaxes the muscles in the airways and increases airflow to the lungs. Ipratropium Bromide is an anticholinergic bronchodilator that is used to prevent bronchospasm, or narrowing airways in the lungs. Methylprednisolone Sodium Succinate is a corticosteroid hormone (glucocorticoid) that prevents the release of substances in the body that cause inflammation. Levofloxacin is an antibiotic that is used to treat amongst others bacterial infections that cause bronchitis or pneumonia. Ondansetron is a serotonergic antagonist that blocks the actions of chemicals in the body that can trigger nausea and vomiting. Digoxin, Lisinopril, Diltiazem, Hydralazine, Furosemide and Tamsulosin class among cardiac drugs. During the weaning process, I took care of this patient.

On  02/13/13, I assess the patient. After knocking the door and entering the room, the patient sat on the chair with a nasal cannular. Upon entrance, I introduced myself to him while informing that I was here to give him a breathing treatment. Before proceeding with the treatment, I check his identity on the bracelet. The patient is alert, oriented and no respiratory distress observed, but I note that the patient has a slight shortness of breath. I question him regarding his breathing, and the patient acknowledges of having no problem. I check on the flow meter how much O2 he is getting, it's 3lpm (32% FiO2). When I place the pulse ox on his finger, I observe that he has a good color warming skin, no edema at the extremities. The pulse ox measures a SPO2 96% and HR 91 and I count a respiratory rate of 24. The patient has blood pressure of 139/76 and a temperature of 98.4 F, the values the nurse charts indicate. I request to listen to the patient’s lungs. I hear wheezing on both lung sides. After that, I ask the patient if he prefers to take his treatment via mouthpiece or mask and he indicates he prefers to take the mask. The patient receives Levalbuterol and Ipratropium Bromide. After the treatment, I listen to his lungs again and some wheezing is detectable. I leave the patient in a stable condition. Later in the afternoon, an ABG order for the patient abounds. I explain to the patient that I need to draw some blood from him. The modified Allen's test is positive, which I performed before by picking the patient. After drawing his blood, I pressure tight on the puncture and bend his arm. I make sure that that it was not bleeding. The whole time my preceptor looks over me and my supervisor compliments me for doing a great job. Back to the patient's ABG, the result shows a normal ABG referring to a COPD patient pH 7.4, PCO2 66.1, HCO-3 39.8 and PO2 77.1, a fully compensated respiratory acidosis with mild hypoxemia. The following day, I assess the patient again in the same way, as I assessed the patient yesterday. Overall, the patient is doing well with improved breathing and no other problems observed. Later during the day, the patient is discharged.

To conclude, the patient is admitted for acute exacerbation of COPD caused by pneumonia. For the treatment of the pneumonia, the patient takes antibiotic. For the respiratory ailments, he is placed on BiPAP and later O2 delivery via nasal cannular and additional breathing treatment provided. The patient improves quickly and without further incidence. The patient recuperates from the hospital for six weeks and is discharged.

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