Pulmonary thromboembolism (PTE) is a serious and often fatal condition that occurs due to partial or complete embolic occlusionof pulmonary arteries or its branches due to thrombi originating from the venous system or right side of the heart (3,4,5). The incidence of PE ranges from 39 to 115 per 100,000 populations annually (6). Pulmonary embolism acutely has been reported to have variable mortality rates as low as 2% in normotensive patients without right ventricle (RV) dysfunction, and as high as 95% in patients who present with cardiac arrest (7,8). The typical clinical manifestations of PE include dyspnea (more than 50%), pleural pain (39%), cough (23%), retrosternal pain (15%), fever (10%), hemoptysis (8%), syncope (less than 5%), unilateral limb swelling (24%), and unilateral limb pain (6%) (9).

A 66-year-old female with a history of hypertension, diabetes mellitus Type II, and 14 days post-bilateral knee arthroplasty was admitted to the ER with progressive lethargy for 5-6 days and worsening shortness of breath over the past day. She was on rivaroxaban, aspirin, and clopidogrel. On examination, she was obese (BMI: 44.1 kg/m²), conscious but dyspneic, with vital signs showing severe hypertension (BP: 196/125 mmHg), tachypnea (RR: 32/min), and severely low oxygen saturation (50% on room air). Bilateral lower limb edema was noted.

Initial oxygen supplementation through a non-rebreather mask failed, and a trial of non-invasive ventilation was unsuccessful in improving her saturation and tachypnea. After consulting with her family, she was intubated and placed on mechanical ventilation. Lab results showed an elevated white blood cell count (23.3 x 10³/μL), predominantly neutrophils (17.73 x 10³/μL), elevated D-dimer (8.03 mg/L), and an extremely high B-type natriuretic peptide (32446.2 pg/mL). Troponin I was normal, and renal function tests showed elevated creatinine (155.59 μmol/L).

Despite being sedated and paralyzed on controlled mode of mechanical ventilation on 100% FiO2, her oxygen saturation remained critically low (<40%), and then further she started to become hypotensive, requiring high doses of norepinephrine (1200 mcg/h).  ECG showed normal sinus rhythm ( Figure 1), and  POCUS ECHO revealed no significant findings. Based on her clinical signs, the provisional diagnosis included heart failure as Pro Bnp was high and pulmonary embolism (PE)  due to her recent history of bilateral knee arthroplasty and High D- Dimer. However, she lacked classic signs of PE, such as tachycardia, right ventricular strain on echo, even no S1Q3T3 changes in ECG .The patient's condition was rapidly deteriorating, and a CTPA could not be performed as she was hemodynamically very unstable. Apart from the surgical history and an elevated D-dimer, there was no strong evidence to confirm a diagnosis of pulmonary embolism and patient was on rivaroxaban, aspirin, and clopidogrel which also went against the diagnosis of Pulmonary embolism. Given the complexity of the situation the decision was made to thrombolyse the patient but it was a difficult decision , as the patient was also on blood-thinning medications, which significantly increased the risk of bleeding. Despite the lack of clear evidence, after carefully weighing the risks and discussing the situation with the patient's relatives,informed  consent was obtained, and thrombolysis was administered(Intra VenousTenecteplase 50 mg was given) . Within two hours, her oxygen saturation improved to above 90% on the ventilator. A subsequent CTPA confirmed  bilateral pulmonary embolism involving both pulmonary arteries, with signs of right ventricular strain and associated pulmonary hemorrhage(Figure 2 and 3)

The patient was transferred to the ICU for close monitoring, where she was kept on mechanical ventilation (PAC mode, FiO2: 100%) and heparin infusion, adjusted based on APTT levels. On day 1, she showed signs of improvement. A detailed echocardiogram revealed  dilated right atrium, right ventricle, and pulmonary artery, moderate tricuspid regurgitation, and pulmonary hypertension.

On day 2, with improved hemodynamics, she was extubated and placed on non-invasive ventilation. Blood tests revealed severe anemia (6.2 g/dL), for which she received 2 units of packed red blood cells. On day 3, her oxygen saturation remained stable, and she transitioned to oral rivaroxaban for anticoagulation. After two days in the ward, she was discharged home in stable condition.

Figure 1 

                                                                  Figure 2

When considering bilateral Total knee Arthroplasty (TKA), the decision to perform simultaneous bilateral TKA or staged procedures depends on several factors, including the risk of complications like pulmonary embolism (PE). Some studies suggest a higher perioperative risk of PE with simultaneous bilateral TKA compared to unilateral procedures (10,11).

Acute PE severity primarily depends on its hemodynamic impact, often resulting in pulmonary hypertension and right ventricular (RV) overload. As pulmonary vascular resistance increases, the RV can dilate and eventually fail, potentially causing sudden death through pulseless electrical activity or asystole. A gradual decline in RV output can lead to reduced left ventricular filling, hypotension, and shock. RV overload and reduced coronary flow may also cause RV ischemia or infarction, exacerbating the situation.(12)

In this case, the ECG did not show any specific signs of pulmonary embolism (PE), such as the S1Q3T3 pattern although it is not highly sensitive or specific,found in only 10 % of the cases (13,14,15) . Tachycardia, commonly seen in PE(16), was also absent in our patient. The bedside echocardiogram initially did not reveal any significant changes, but after thrombolysis, there were noticeable changes suggestive of PE. D-dimer levels were elevated, though not excessively, and Pro-BNP was high, indicating possible heart failure.

CT pulmonary angiography (CTPA) is considered the gold standard for diagnosing PE, but due to the patient's critical condition, we could not proceed with this test. The patient was also on rivaroxaban, clopidogrel, and aspirin, which increased the risk of bleeding. Despite this, the decision to administer thrombolysis was made.

The patient, had the predisposing factors for PE broadly fitting in  Virchow’s triad of blood stasis, endothelial injury, and enhanced blood coagulability. A few days post-bilateral total knee arthroplasty, exhibited risk factor for pulmonary embolism (PE), including increasing dyspnea. With a Wells score of 6, PE was highly likely. Given the progressive deterioration and clinical signs, the patient likely had a massive/high-risk PE, as per AHA/ESC classification. Immediate chemical thrombolysis was initiated before performing CTPA due to the critical hemodynamic status which in our case proved to be crucial and highly effective resulting in significant hemodynamic improvement.It was a life saving step.

This situation highlights the importance of clinical judgment, even in an era dominated by advanced diagnostic tools and artificial intelligence. In some cases, technology cannot replace the need for quick, informed decision-making to save a life. The choice to administer thrombolysis was difficult, as it carried the risk of bleeding, and without definitive proof of PE, it could have been hard to justify afterward if things would have gone otherwise. However, in emergency medicine, swift decisions often need to be made under pressure. Communication with the patient's family is vital. By keeping them informed and engaged, the decision-making process becomes smoother, fostering confidence for both the family and the doctor. This collaboration is crucial for achieving the best possible outcome for the patient, particularly in challenging circumstances.

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