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A 25-year-old apparently normal man, nonsmoker, presented to the ED with history of high-grade fever for 8 days that was associated with headache, body ache, and cough with minimal white mucoid expectoration and streaky hemoptysis, which progressed to severe breathlessness at rest and orthopnea for the last 2 days. It was not associated with chest pain, reduced urine output, or jaundice.
On initial evaluation, he was conscious and oriented, severely dyspneic at rest with a respiratory rate of 38/min, pulse rate if 136/min, regular BP of 98/70 mm Hg, and oxygen saturation of 88% on room air. Chest examination showed bilateral inspiratory crackles and absence of wheeze or stridor. Arterial blood gas revealed respiratory alkalosis with hypoxemia with wide P(A-a)O2 gradient of 98.8 mm Hg and Pao2/Fio2 of 116 mm Hg. Baseline blood investigation showed a hemoglobin level of 14 gm%, total leukocyte count of 7,400 cells, platelet count of 1,24,000 cells/μL. Serum procalcitonin was <0.1 pg/mL, and his renal and liver parameters were within normal limits. Figure 1 shows the chest radiograph.
On further evaluation, he was found to be positive for dengue NS1 antigen and IgM antibody. He was admitted initially in the medicine department with a provisional diagnosis of dengue fever with moderate ARDS and later was intubated and started on mechanical ventilator because of worsening hypoxemia. He was then referred to our ICU for further treatment.
On evaluation from our ICU, his ventilatory parameters showed evidence of reduced lung compliance. Lung ultrasonography showed normal lung sliding with bilateral extensive B lines and minimal bilateral pleural effusion.
Video of bedside critical care echocardiogram is shown in Video 1.
Question: What does the echocardiogram show, and what is the likely cause of hypoxemic failure?
Answer: Transthoracic echocardiogram in parasternal long axis view shows evidence of thickened mitral valve leaflets with reduced diastolic opening and doming, which is suggestive of mitral stenosis. The adjacent lung parenchyma shows increased B lines due to interstitial edema. These B lines could be due to cardiogenic pulmonary edema (due to the mitral stenosis and excessive fluid administration) or due to noncardiogenic pulmonary edema (due to ARDS); both these condition likely coincided in the patient
Patient did not respond to conservative treatment and failed initial attempts of weaning from the ventilator. Cardiology consultation was sought; after ruling out significant mitral regurgitation and possibility of left atrial clot, he underwent a percutaneous mitral balloon valvulotomy.
The procedure was followed by improvement in the hemodynamics and oxygen status and with clinical and radiologic improvement (Fig 2). He was soon weaned off the mechanical ventilator.
This was a case of an apparently normal male patient who presented with acute febrile illness with viral prodrome that progressed to acute hypoxemic respiratory failure. The patient was positive for dengue fever. He was treated initially as a case of ARDS complicating dengue fever. However, the treatment changed after critical care ultrasonography and echocardiography revealed a hitherto undiagnosed cardiac valvular abnormality. We present this case to emphasize the usefulness of incorporating ultrasonography and echocardiography in the initial assessment for guiding therapy and monitoring critically ill patients. Critical care ultrasonography combined with critical care echocardiography has now become an integral part in the assessment and treatment of critically ill patients. It is an easy, noninvasive, and portable technique devoid of radiation exposure, and it is universally available in most of the current ICUs (Discussion Video).
In younger patients, the common causes of acute respiratory failure are pneumonia, ARDS, cardiogenic pulmonary edema, sepsis and asthma.
In such cases, critical care echocardiography can be used not only to detect the presence of cardiogenic pulmonary edema but also to look for various potential causes like left ventricular systolic function, right ventricular dilatation, valvular abnormality, pericardial effusion, and the presence of intracardiac masses.
Mitral stenosis usually presents with dyspnea on exertion and/or reduced exercise tolerance.
But because of the slow progression of disease, some patients with severe mitral stenosis fail to recognize the symptoms. However, symptoms can be precipitated by sudden changes in heart rate, volume status, and cardiac output. In the patient, the tachycardia associated with high-grade fever and the probable fluid overload due to IV fluid therapy may have been the reasons behind the acute decompensation. The availability of ultrasonography and echocardiography helped us in identifying the mitral stenosis.
In the treatment of severe mitral stenosis, medical therapy is often ineffective. Definitive therapy entails percutaneous mitral balloon valvulotomy in patients with suitable morphologic mitral valve characteristics; if not, a surgical repair is needed.
Percutaneous mitral balloon valvulotomy leads to a significant immediate decrease in the left atrial pressure, mean mitral gradient, and pulmonary artery systolic pressure with corresponding increase in mitral valve area and improved ventricular function.
In general, percutaneous mitral balloon valvulotomy is a safe procedure with a high success rate, particularly if the patients have chosen to have optimal valve morphology as determined by echocardiography score. In the patient, the value morphology was deemed suitable; after the procedure, the patient had significant hemodynamic improvement and could be weaned successfully from mechanical ventilation.
B-lines in lung ultrasound scans can be seen in cardiogenic pulmonary edema and ARDS; echocardiography may help in differentiating them, or it may reveal an associated cardiac contribution to respiratory failure.
A patient with a previously undiagnosed valvular disease may be diagnosed in the ICU by the use of bedside echocardiography.
Weaning from mechanical ventilation is difficult in patients who have valvular disease with cardiovascular dysfunction.
Treatment of the underlying valvular disease allows prompt improvement in the hemodynamics and assists in weaning and extubating patients.
Transthoracic echocardiogram in parasternal long axis view shows evidence of thickened mitral valve leaflets with reduced diastolic opening and doming, which is suggestive of mitral stenosis. The adjacent lung parenchyma shows increased B lines due to interstitial edema. These B lines could be due to cardiogenic pulmonary edema (due to the mitral stenosis and excessive fluid administration) or due to noncardiogenic pulmonary oedema (due to ARDS); both these condition likely coincided in the patient.
Apical four-chamber view of transthoracic echocardiogram shows grossly dilated left atrium and thickened mitral valve leaflet with doming and markedly reduced movement and failure of opening during diastole. There was no significant mitral regurgitation and no evidence of pericardial effusion or LV dysfunction.