Massive pleural effusion masquerading as acute pulmonary thromboembolism – An unreported entity

Sir,

Acute pulmonary embolism (APE) is a common, potentially life-threatening condition. APE can produce several abnormalities on Electrocardiogram (ECG) like, right axis deviation (RAD), T wave inversion in right-sided precordial leads, and S1Q3T3 pattern. These changes reflect the severity of pulmonary hypertension. Early recognition of these findings may alter the estimated pre-test probability of pulmonary embolism (PE) and prompt more aggressive treatment before hemodynamic instability ensues. However, these changes are not sensitive or specific and can rarely be associated with other non-thromboembolic clinical conditions like right-sided pneumothorax, severe bronchospasm, and lobar pneumonia. Herein, we present an unusual case of right-sided massive pleural effusion, where S1Q3T3 was a red herring. This, to the best of our knowledge, is first report of right-sided massive pleural effusion presenting with S1Q3T3 changes in ECG.

CASE SUMMARY

A 22-year-male patient, non-smoker, no known co-morbidity, reported to our Accident and Emergency department with complaints of progressively worsening breathlessness and right-sided pleuritic chest pain over four days duration. He denied any history of fever, palpitation or syncope. There was no history of recent travel, sick contacts, smoking or illicit drug use.

Upon physical examination, the patient appeared to be in severe respiratory distress. He had tachycardia with a heart rate of 124 beats per minute, oxygen saturation of 83% on room air and 92% on a 6-liter nasal mask and was afebrile. His accessory muscles of respiration were recruited, but palpation of the chest did not elicit any tenderness. On auscultation, breath sounds were absent in the right infra-scapular, inter-scapular, infra-axillary, and mammary regions. The rest of the physical examination was unremarkable.

The patient’s arterial blood gas values were pH 7.45, pO₂ 64 mm of Hg, and pCO₂ 27.8 mm of Hg. ECG taken in the emergency room revealed S1Q3T3 [Figure 1], and chest radiograph showed massive right-sided pleural effusion [Figure 2a]. The patient had persistent tachycardia and hypoxia, with increasing oxygen requirement, and he was transferred to the respiratory intensive care unit (RICU). The patient’s symptoms, together with the ECG findings of tachycardia and S1Q3T3 led us to suspect pulmonary embolism, and therefore to request a computed tomography pulmonary angiogram (CTPA), which ruled out pulmonary embolism, and a large right-sided pleural effusion was noted [Figure 2b and c]. A Doppler of the lower extremity was negative for deep vein thrombosis. A 2-D echocardiogram (2-D Echo) showed normal ejection fraction, normal diastolic function, and mildly elevated pulmonary artery pressure.

Figure 1.

Electrocardiograph showing Tachycardia and S1Q3T3 pattern

Figure 2.

(a) Chest radiograph showing massive pleural effusion on right side of hemithorax. (b and c) Contrast enhanced computed tomography of chest showing right sided massive pleural effusion and normal pulmonary circulation

On further evaluation, he was found to have hyperbilirubinemia with normal liver enzymes. (USG) Ultrasound abdomen done showed cholelithiasis without cholecystitis. MRCP was done, but there was no evidence of choledocholithiasis. An intercostal drain (ICD) was placed in the fourth intercostal space in the right hemithorax, and therapeutic thoracocentesis was done for right-sided pleural effusion. Pleural fluid analysis showed exudative fluid with neutrophil predominance. He underwent thoracoscopic pleural biopsy, and its histopathology revealed necro-inflammatory tissue with fibroblastic proliferation with no evidence of malignancy or tuberculosis. He was managed conservatively with antibiotics and supportive medications, and the patient responded well to the management. The ECG showed reversal of S1Q3T3 once right-sided pleural effusion was drained in our patient [Figure 3].

Figure 3.

Repeat electrocardiograph showing reversal of S1Q3T3 after drainage of pleural fluid

DISCUSSION

McGinn and White had first described the S1Q3T3 pattern in 1935 with these subsequent voltage criteria in acute pulmonary embolism: S wave in the lead I, Q- wave in lead III, and amplitude of more than 0.15 mV with the T-wave inversion in the lead III. There can also be late inversion of the T-wave in lead III, and S-wave in lead I with right QRS axis deviation.[1] In the presence of these changes and suggested clinical settings, an early diagnosis of pulmonary embolism can be made. The incidence of S1Q3T3 is reported to be between 12% and 50% in acute pulmonary embolism and is non-specific. The presence of this ECG abnormality doesn’t confirm pulmonary embolism.[2]

S1Q3T3 has been reported in the presence of several other non-thromboembolic conditions, like right-side pneumothorax,[3] aortic intramural hematoma with extension to pulmonary artery,[4] acute bronchospasm,[5] and lobar pneumonia.[6] Spontaneous or COPD associated right sided pneumothorax can cause various ECG changes including prolonged QT interval, right axis deviation, peaked P waves in II, III and aVF and S1Q3T3 on ECG. The mechanism includes air between the heart and ECG leads and increased pulmonary capillary wedge or central venous pressure.[3] Asthma exacerbation especially acute bronchospasm can cause various ECG abnormalities like tachycardia, P pulmonale, right bundle branch block, ST elevation and even S1Q3T3 changes. However, the incidence of S1Q3T3 changes in asthma exacerbation is very rare and the mechanism includes dynamic hyperinflation which can lead to increased right ventricular load and elevated pulmonary artery pressure. These changes can get accentuated due to volume overload conditions especially during pregnancy.[5] Lobar pneumonia can also give rise to various ECG abnormalities which can be non-specific like sinus tachycardia, atrial fibrillation, conduction abnormalities, ST-segment abnormalities including S1Q3T3 changes. The incidence of S1Q3T3 is generally around 3% and presence of T wave changes in these patients indicate a poor prognosis.

In our case, the typical S1Q3T3 pattern was thought to indicate acute pulmonary embolism; however, the same was subsequently ruled out by CTPA. It has been hypothesized that S1Q3T3 sign is rarely present in patients with ventilation-perfusion (VQ) mismatch like pneumonia.[7] This pattern reflects a right axis deviation (RAD) state so, the right ventricle appears projected more anteriorly and to the right of the left ventricle which moves posteriorly.[1] Alternately, pleural effusions might change ECG vectors through physical shifts in the position of the heart within the chest. The large volume of conductive fluid could change the flow of current through thoracic contents, altering the axis on the surface ECG, even while the heart retains its normal axis.[8] A similar mechanism is invoked to explain the left axis deviation, sometimes seen in emphysema.

CONCLUSION

S1Q3T3 changes in ECG, at times, can be a red herring. Several clinical conditions other than PTE can present with these non-specific electrical changes on surface ECG. However, emergency and critical care physicians should keep a low threshold for considering the diagnosis of PE while interpreting electrical changes in ECG. APE is common; however, being a fatal disease warranting early diagnosis and treatment to prevent mortality. S1Q3T3 is not sensitive or specific to PE but is indicative of RV dysfunction associated with acute PE. Hence, emergency care physicians should demand more sensitive tests to rule out PE before considering alternative diagnoses like massive pleural effusion or pneumothorax.

Statement of ethics

The patient had given written informed consent to publish their case and the study protocol was approved by the departmental and institute’s committee of medical research

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.