|Year : 2020 | Volume
| Issue : 3 | Page : 120-123
Clinical profile of patients presenting to the emergency department with acute pulmonary edema
Fathima S Nissar, Manna Maria Theresa, TP Sreekrishnan, BS Dhanasekaran, KP Gireesh Kumar
Department of Emergency Medicine, Amrita Institute of Medical Science, Kochi, Kerala, India
|Date of Submission||05-Feb-2020|
|Date of Acceptance||25-Mar-2020|
|Date of Web Publication||09-Oct-2020|
Dr. Manna Maria Theresa
Department of Emergency Medicine, Amrita Institute of Medical Science, Kochi, Kerala
Source of Support: None, Conflict of Interest: None
Objective: The objective is to study the clinical profile of patients presenting to an emergency department with acute pulmonary edema. Materials and Methods: This is a prospective, observational study performed in 100 patients presenting to the Emergency Department of Amrita Institute of Medical Sciences (Kochi) with acute pulmonary edema. Patients were selected according to the inclusion and exclusion criteria. The variables analyzed were age, sex, comorbidities, ABG, cardiac enzymes, NT-prob-type natriuretic peptide, chest X-ray, electrocardiogram, and clinical outcome. Results: Of the 100 patients, 64% were male and 36% were female. Age group affected were between 51 and 70 years (52 patients) and between 71 and 90 years (32 patients). Data analysis revealed that the cause of pulmonary edema in 63 patients was cardiogenic and 37 patients was chronic kidney disease. Conclusion: In this study, the incidence was more in males, nearly twice that of females. The most commonly affected age group was between 51 and 70 years of age (52%). We found that the most common cause of pulmonary edema was congestive heart failure (63%) followed by chronic kidney diseases (37%). Moreover, the most common ABG finding was high anion gap metabolic acidosis, mostly lactic acidosis.
Keywords: Acute pulmonary edema, emergency department, pro-BNP
|How to cite this article:|
Nissar FS, Theresa MM, Sreekrishnan T P, Dhanasekaran B S, Gireesh Kumar K P. Clinical profile of patients presenting to the emergency department with acute pulmonary edema. Amrita J Med 2020;16:120-3
|How to cite this URL:|
Nissar FS, Theresa MM, Sreekrishnan T P, Dhanasekaran B S, Gireesh Kumar K P. Clinical profile of patients presenting to the emergency department with acute pulmonary edema. Amrita J Med [serial online] 2020 [cited 2020 Oct 30];16:120-3. Available from: https://www.ajmonline.org.in/text.asp?2020/16/3/120/297549
| Introduction|| |
Cardiogenic pulmonary edema is one of the most common and fatal causes of acute respiratory failure, and it mostly results in acute decompensated heart failure (ADHF). The clinical features are dyspnea associated with the rapid accumulation of fluid within the lung's interstitial and alveolar spaces, because of acutely elevated cardiac filling pressures.,
ADHF is most commonly developed because of impaired left ventricular systolic and/or diastolic function, with or without coronary artery disease or valve abnormalities. Noncardiogenic causes of pulmonary edema include primary fluid overload conditions (e.g. due to blood transfusion), severe hypertension, renal artery stenosis, and severe renal disease.,
Noncardiogenic pulmonary edema is a clinical syndrome associated with diffuse filling of the alveolar spaces with fluid in the absence of elevated pulmonary capillary wedge pressure. A focused history, physical examination, echocardiography, laboratory analysis, and direct measurement of the pulmonary capillary wedge pressure can be used to distinguish cardiogenic from noncardiogenic pulmonary edema, as well as from other causes of acute respiratory distress. Some of the causes are as follows:
- Acute respiratory distress syndrome
- Exposure to some chemicals (ammonia)
- Multi-organ dysfunction – Congestive heart failure, kidney failure, or liver injury
- Near drowning
- Reaction to certain medications
- Drug overdose.
“Flash” pulmonary edema is a dramatic form of cardiogenic alveolar pulmonary edema. In “flash” pulmonary edema, the underlying pathophysiologic principles, etiologic triggers, and initial management strategies are similar to those of less severe ADHF, but there is a greater degree of urgency to the implementation of initial therapies and the search for triggering factors. Often, “flash” pulmonary edema is associated with sudden rise in the left-sided intracardiac filling pressures in the setting of hypertensive emergency, acute ischemia, new-onset tachyarrhythmia, and obstructive valvular disease. In addition to standard therapies for cardiogenic pulmonary edema, combined venous, and arterial vasodilators should be added.,
| Materials and Methods|| |
Study type and size
This is a prospective, observational study performed in 100 patients visiting the Emergency Department of Amrita Institute of Medical Sciences (AIMS, Kochi) with acute pulmonary edema within 6 months (June 2019–December 2019). Patients were selected according to the inclusion and exclusion criteria.
The variables included for the study are age, values of ABG, NT prob-type natriuretic peptide (BNP), cardiac enzymes, findings of the chest X-ray and electrocardiogram (ECG), and the clinical outcome.
- Age – More than 30 years
- Patients presenting with acute onset breathlessness.
- Patients on mechanical ventilator.
| Results|| |
In this study, 64 patients were male and 36 were female. The incidence was more in the age group of 51–70 years (52 patients). The rest of the age distribution were 32 patients in the age group of 71–90 years and 16 patients in the age group of 30–50 years.
Of the 100 patients, 63 patients had congestive heart failure and 37 were suffering from chronic kidney diseases.
The pH was in the normal range in 35 patients, <7.35 in 41 patients, and >7.45 in 24 patients.
In 56 patients, the lactate value was in the range between 2.5 and 4; in two patients, it was between 0.5 and 2; and in the rest, it was below 0.5.
Twenty-three patients needed bilevel positive airway pressure (BiPAP) support initially for varying periods, and the rest were managed with high-flow oxygen through non-rebreathing mask.
The pro-BNP values were higher than 145 pg/ml in 52 patients. In the remaining 48 patients, it was <125 pg/ml.
All the study patients needed intensive care unit (ICU) care. The mortality rate was 3%.
Distribution of age
The incidence of pulmonary edema was most common (52%) in the age group of 51–70 years followed by the age group between 71 and 90 years (32%) and between 30 and 50 years (16%) [Figure 1].
Distribution of gender
The incidence is more in males – 64% [Figure 2].
Distribution of pH
The pH was <7.35 (acidosis) in 41% of patients and >7.45(alkalosis) in 24% of the patients. In the rest, it was in the normal range [Figure 3].
Distribution of lactate
In 56% of the patients, the lactate value was in the range between 2.5 and 4; in 2%, it was between 0.5 and 2, and in the rest, it was below 0.5 [Figure 4].
Distribution of causes
In 63% of the patients, the pulmonary edema was because of congestive heart failure, and the rest was chronic kidney disease [Figure 5].
Distribution of the need for mechanical ventilatory support
Twenty-three percent of the patients needed noninvasive ventilator support with BiPAP, while the rest were managed with high-flow oxygen administration with nonrebreathing mask [Figure 6].
Distribution of disposal
Ninety-seven percent of the patients needed ICU care and the mortality rate was 3% [Figure 7].
Distribution of pro-B-type natriuretic peptide
The pro-BNP value was higher than 145 pg/ml in 52% of the patients. It was <125 pg/ml in the remaining 48% of the patients [Figure 8].
| Discussion|| |
This is a prospective, observational study done on 100 patients presented to the Emergency Department, AIMS, with acute pulmonary edema. The incidence was more in males – 64%, maximum in the age group – between 51 and 70 years – 52%. In 63% of the patients, the pulmonary edema was due to congestive heart failure, and in the rest, it was because of chronic kidney diseases.
Regarding the ABG analysis values, the pH was normal in 35% of the patients; <normal in 41%, and >normal in 24%. Of 100 patients included in the study, 42% had serum lactate values in between 0.5 and 2.5 mmol/L, 2% had lactate value <0.5 mmol/L, and 56% had lactate value >2.5 mmol/L. High anion gap metabolic acidosis, mostly lactic acidosis, was the common ABG finding.
The proBNP and renal function test values helped us to narrow down the cause ofbreathlessness/pulmonary edema – Whether cardiac or renal.
A normal BNP level is about 98% accurate in ruling out the diagnosis of heart failure as the cause for pulmonary edema. This warrants to find the other causes of breathlessness and fluid overload such as chronic kidney diseases. In this study, proBNP was >145 pg/ml in 48% and <125 pg/ml in 52% of the patients.
Twenty-three percent of the patients needed BiPAP, whereas the rest of the patients were managed with oxygen administration through nonrebreathing mask with the flow rate of 15 L/min. All the patients were admitted in the ICU for management. Three percent was the mortality rate.
| Conclusion|| |
From the study, it was found that the cardiogenic causes are more than noncardiogenic causes. The congestive heart failure ranks number one followed by chronic kidney diseases which cause the pulmonary edema. Cardiomyopathy, chronic hypertension, valvular, and ischemic heart diseases are few to name the common intrinsic causes of cardiac failure. The incidence is more in males, twice that of females; the most commonly affected age group was between 51 and 70 years (52%) while the least commonly affected age group was between 30 and 50 years (16%). Normal proBNP values were found to be useful in the exclusion of the presence of cardiac failure. High anion gap metabolic acidosis, mostly lactic acidosis, was the common ABG finding. Nearly one-quarter of the patients needed BiPAP assistance in their initial management. The ECG, echocardiogram, cardiac enzyme studies, X-ray chest, and renal function tests are few diagnostic tools to mention in the study.
We would like to thank Dr. T. P. Sreekrishnan, Department of Emergency Medicine, Amrita Institute of Medical Science, Kochi.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Baird A. Acute pulmonary oedema – Management in general practice. Aust Fam Physician 2010;39:910-4.
Ware LB, Matthay MA. Clinical practice. Acute pulmonary edema. N
Engl J Med 2005;353:2788-96.
Chua TP, Coats AJ. The lungs in chronic heart failure. Eur Heart J 1995;16:882-7.
Szidon JP. Pathophysiology of the congested lung. Cardiol Clin 1989;7:39-48.
West JB, Mathieu-Costello O. Vulnerability of pulmonary capillaries in heart disease. Circulation 1995;92:622-31.
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8]