Introduction

This clinical case report is of an 83 years old female patient who got admitted to the hospital on August 30^th, 2020. She lives independently in her home with mobility dependent on a walking frame. The major complaints by the patient upon admission to hospital were shortness of breath and unwitnessed fall. After being admitted, her primary diagnosis came out to be a medical emergency condition known as acute pulmonary oedema which is characterized primarily by the impairment of compliance as well as gas exchange in the lungs due to fluid accumulation and secondarily by the presence of hypoxia and dyspnoea. Of other assessments of the patient upon admission i.e., COVID-swab, chest X-ray, CT scan, neurological, neurovascular, fall and risk assessments all came out to be normal. However, an analysis of blood samples’ results indicated high levels of neutrophils, lymphocytes, urea, creatinine, bilirubin, globulin and C-reactive protein.

The medical situation of the patient upon admission included initial oxygen supply to 95% at a flow rate of 8 L per minute from nasal cannula which then decreased to a flow rate of 4 L per minute. However, when the patient’s vitals were checked again, they were found to be indicative of cardiopulmonary arrest i.e., there was an increased respiratory rate of 36, abnormal blood pressure of 177/81, low body temperature of 34.4 degrees Celsius and oxygen saturation of 88%. By seeing these conditions, the blue code was called immediately accompanied with the instant infusion with glyceryl trinitrate (GTN) and 80 mg furosemide intravenous treatment by multidisciplinary team.

The past medical history of the patient includes type 2 diabetes, asthma, hypertension, hypercholesterolemia, osteoarthritis, chronic lymphoedema, arterial fibrillation, ischemic heart disease and a long standing history of dysphagia alias difficult swallowing.

Discussion

Acute pulmonary oedema, characterized by a accrual of fluids in the lungs followed by hypoxia and dyspnoea ultimately resulting in the impairment of lung compliance and effective gas exchange, is a medically emergent situation requiring immediate management (Baird, 2010). The mortality rate of patients over a period of one year after being diagnosed with acute pulmonary oedema is about 40% with most frequent causes of the disease being the ischemic heart condition and arrhythmia or arterial fibrillation, both of which have been diagnosed in the past history of this patient too. Other common factors include anemia, fluid overloading, acute valvular dysfunction, pulmonary embolus, as well as renal artery stenosis (Messerli et al., 2011; Purvey & Allen, 2017).

Congestive heart failure is often the leading cause of acute pulmonary oedema due to inefficient pumping of blood by heart as well as a reduction in the normal oxygen exchange through the lungs. Combined together, these two factors contribute towards the resulting shortness of breath. The common causes of pulmonary oedema due to heart malfunctioning include conditions causing stiffness of heart muscles and weakness of heart, narrowing of heart valves or their leakage, hypertension or sudden shoots in blood pressure and congestion or narrowing down of arteries, all of which have been already identified in the patient’s medical history (Herrero, Sanchez, & Lorente, 2018).

Evaluation

After a thorough physical and history examination, the diagnosis of cardiac ischemia is an important task which can be done either by electrocardiograms or other less specialized tests. Some of the tests which not only help in the diagnosis of the pulmonary oedema but also aid in its differentiation into the specific types. These are going to be discussed in detail in the paragraphs that follow.

The radiographic testing of the patient was done by the radiologist utilizing portable imaging for carrying out both the posteroanterior views as well as lateral views of the chest. Since there were no pleural effusions in the chest X-ray, the possibility of cardiogenic pulmonary edema was ruled out for the patient. The pathologist carried out the blood testing of the patient to assess if there is any inflammation and C-reactive protein test came high suggestive of inflammation (Assaad, Kratzert, Shelley, Friedman, & Perrino, 2018).

Echocardiography was done by the cardiologist to assist the diagnosis of the systolic dysfunction of left ventricle, if present any. Furthermore, the presence of diastolic function as well as its degree can be analyzed via the tissue Doppler imaging technique of the mitral annulus (Levis, 2011).

The whole MDT team thus worked up on the patient and the suggestive medications are given in the management section of this report. Apart from the roles just described of the cardiologist, radiologist, pathologist, pharmacist, and the general physician, some other important roles are of occupational therapist, community nurse and social workers especially after discharge. These included: occupational therapy teaching of the patient for the management of physical and cognitive problems; monitoring the oxygen stats, HR, BP, and RR as well as assessment of changes to find any respiratory compromises by the community nurse; and the provision of emotional and other physical support by a social or community health worker (Bolt, Ikking, Baaijen, & Saenger, 2019; Selby, Wang, Murray, & Lang, 2018; Steketee, Ross, & Wachman, 2017; White, Roberts, & White, 1991).

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Mechanism of lung edema development

Under normal conditions, the exchange small proteins and fluids continuously happens between intravascular environment and interstitial spaces present in the capillary endothelial cells. This fluid which has been entered in between the capillary endothelial spaces also is returned back to the systemic circulation via the lymphatic system. During all this process, the small proteins, some of the other solutes along with their respective fluids do not enter the alveolar cells of the lungs. One reason of their restriction from entry into the alveoli is the presence of a tight epithelium in these (Herrero et al., 2018).

Under pathogenic conditions, there is a generation of alveolar edema. The main mechanism of this generation of the alveolar edema is a prompt increased hydrostatic pressure of the lung capillaries. This is the main mechanism of the cardiogenic induced pulmonary oedema. However, this type of oedema is generally resolved quickly as long as the alveolar and epithelial barrier is intact and not damaged via a process known as alveolar fluid clearance (AFC). Therefore, in patients with acute pulmonary oedema, there is a loss of the barrier between alveolar cells and the epithelia cells resulting in an excess movement of fluids, proteins and solutes into the interstitial spaces and thus consequential flooding of the lung airspaces (Matthay, Folkesson, & Clerici, 2002; Ware, Fremont, Bastarache, Calfee, & Matthay, 2010).

Assessment of the patient

Initial assessment

The initial assessment and management of this patient by nursing care included the call of help by other general physicians, clinical staff and nurses. This was done by calling the blue code for this patient. Other steps included the commencement of oxygen and a definitive treatment to the patient with ongoing assessment. This was also done with oxygen supply and immediate infusion of GTN and furosemide (80 mg) intravenously. Besides these, the insertion of 16-gauge cannula was also done intravenously for further administration of drugs as required.

Examination of the patient

The physical examination of the patient is important criterion for making an instant distinction between the patients suffering from chronic or acute pulmonary oedema. Usually patients are presented with shortness of breath which can be acute when it progresses relatively faster ranging in time from minutes to hours or it can be chronic which presents itself with relatively slow progression with typical time ranges of hours to days. These two types according to their progression further depend on the underlying etiology of the disease ([Internet], 2020; Murray, 2011).

The common physical symptoms of the acute pulmonary edema include: extreme breath shortening which worsens on lying down; anxiety and sinking heart feeling also worsening on lying down; breath gasping and sweating along with dizziness; coughing accompanied sometimes with blood tinging; cold and moist skin; and chest pain. On the other hand, some of the physical indicators of chronic pulmonary oedema are different from the acute, which are: exertion; weight gain and fatigue; swelling of the lower limbs; nocturnal dyspnea and orthopnea (Murray, 2011). Since the patient had unwitnessed fall, the most common reason for this could be dizziness. Among other physical condition, shortness of breath was observed. Both of these signs indicated towards the presence of acute pulmonary oedema in the patient.

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Medical management and treatment of the patient

Pharmacological treatments of the patient

The medications prescribed by MDT were: apixaban (2.5 mg) for arterial fibrillation (non-valvular in nature); during MRG, 1 tablet each of furosemide and omlessarton was prescribed to the patient along with 1 GTN patch on daily basis; and for asthma management, salbutamol was prescribed with 2 puffs inhalation. The night medications of the patient included simvastatin (for hypercholesterolemia) and spironolactone (as a diuretic to prevent too much salt absorption in the body). Other medications on the ‘as needed’ basis included paracetamol and senna for pain relief and laxative purposes, respectively. Moreover, the case was also checked for the availability of third party information such as care planning documents, however none was given in the records.

Apart from these, the initial measurements also included oxygenation of the patient via a reservoir bag at a rate of 9 liters per minute. This initial oxygenation therapy is also a priority for patients with COPD who have a higher risk of being hyperoxic, done with continuous monitoring of subsequent oxygenation, respiratory rates, and their conscious states as well. The oxygen dose is also reduced to 2-6 liters/min in case of patient stability, as same was done for the patient too – reducing oxygenation to 4 liters/min.

Non-pharmacological treatments

The non-pharmacological treatments for the current patient will include, although not limited to: posture maintenance of the patient in an upright or sitting up position with some support. Supine posture is suggested for patients with cardiogenic shock or in case of unconsciousness – both of which were not applicable to the current patient’s scenario (Alberta; Shah, Pellicori, Cuthbert, & Clark, 2017).

Postacute care management

Postacute care management of the patient was designed to have regular follow up with the cardiologist to see and mange any further complications which may arise after the acute phase is over. There will also be an active involvement of the dietitian for the proper planning of diabetic diet for the patient as she is not taking any medications for diabetes and dietitian will make a food chart in view of the history of dysphagia (Myc et al., 2020; Sergeant & Dyson, 2018).

Social work assistance was also defined to ensure that the patient can get the appropriate medical support needed as the patient is unable to work on her own. Apart from confirming the medication and their respective dosages, the pharmacist will also participate in the better management of the patient’s medications via pharmacist interventions. Moreover, a physiotherapist will guide the patient about pulmonary physical therapies and exercises to help improve air exchange and ventilation functions. In this way, the multidisciplinary involvement of task forces will result in a better outcome of the patient health (Gai, Tong, & Yan, 2018; Purvey & Allen, 2017).

Patient / family education post discharge

A patient’s education in his/her own medical health and well-being is a crucial factor in one’s care management. For the current case, the patient was educated about the proper control of blood pressure as it can lead to various heart diseases and strokes. The patient was advised to regularly monitor the blood pressure and take prescribed medications. Moreover, being diabetic, the patient was also advised on controlling the blood glucose level (Alberta; Drugs.com).

Additional thing to teach the patient include: a familiarity with the early symptoms before the onset of the disease; in case of developing wet cough the patient should sit on the bed in such a way so as the legs are hanging from the bed side; a teaching and practice of the patient to take slow, steady and deep breaths so as to increase oxygenation; guiding the patient through the foods containing lower amounts of sodium but high amounts of potassium because she was taking furosemide in her medications (Oh & Han, 2015); and an education about regular check and balance of a healthy weight by monitoring weight on daily basis along with carrying out necessary exercises. Moreover, since the patient suffered from oedema and was on fluid restriction limitation to 1.5 L, she was advised to limit fluid intake along with a sedentary lifestyle to avoid and mange stress and pain. She was also educated about the compression stoking of the legs to improve blood flow and managing discomforting swelling in addition to the limb elevation exercises and postures to avoid accumulation of fluid in the legs  (Alberta; Cataldo, de Godoy, & de Barros, 2011; Drugs.com; Mosti, Picerni, & Partsch, 2011).

 

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