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Sumario Vol. 42 - Nº 3 Julio - Septiembre 2013

Fatal Pulmonary Embolism in a Patient
with an Initial Low Clinical Probability

Eliezer San Román García, Luis Miguel Morales Pérez,
Juan Valiente Mustelier, Juan Linares Medina,

Instituto Nacional de Cardiología y Cirugía Cardiovascular.
Calle 17 Nº 702. El Vedado. (10400) La Habana, Cuba.
E mail 1     E mail 2

Recibido 30-ABR-13 – ACEPTADO después de revisión el 21-JUNIO-2013.

The authors declare not having a conflict of interest.

Rev Fed Arg Cardiol. 2013; 42(3): 209-214


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RESUMEN

El tromboembolismo pulmonar constituye una grave y frecuente urgencia cardiovascular, con una alta mortalidad y un difícil diagnóstico por la baja sensibilidad y especificidad de su presentación clínica, así como de las pruebas básicas (electrocardiograma, radiografía de tórax y gasometría), lo cual hace que presente un amplio diagnóstico diferencial. Se han creado reglas (score) de predicción clínica, sin renunciar al juicio clínico con la intención de elevar el valor de estas, incrementando el nivel de sospecha, eslabón fundamental en el diagnóstico, aunque ello no excluye la presencia de tromboembolismo. Estas reglas deben ser aplicadas de forma continua y dinámica, pues la clínica del paciente puede variar de un momento a otro. Se presenta el caso de un paciente, interpretado como un síndrome coronario agudo, que posteriormente fallece como resultado de un tromboembolismo pulmonar de ramas gruesas. Inicialmente presentaba baja probabilidad cínica, lo que varió durante el ingreso.

Palabras clave: Tromboembolismo pulmonar. Probabilidad clínica..
SUMMARY

Pulmonary embolism is a severe and frequent cardiovascular emergency, which comprises a high mortality. Although individual symptoms, signs, and findings on frequently performed tests (chest x-ray examination, electrocardiogram, and blood gases) are neither sensitive nor specific for pulmonary embolism; their combination allows an accurate risk classification of patients suspected of having this disease. Based on clinical assessment, several clinical or pretest probability scores has been developed to increase the suspicion index, a cornerstone in the diagnosis of pulmonary embolism. These models must be reviewed in a continuous and dynamic approach, because the clinical picture of the patients may change at any moment. We describe a patient initially diagnosed with an acute coronary syndrome, which developed a fatal pulmonary embolism in spite of an initial low clinical probability. This case emphasizes the relevance of subsequent assessment of the patients to determine the clinical probability to develop pulmonary embolism.

Key words: Pulmonary embolism. Clinical probability.

 

 

INTRODUCTION
Pulmonary thromboembolism (PTE) is a relatively frequent cardiovascular emergency and potentially lethal. PTE inevitably leads to acute pulmonary hypertension and may cause right ventricular insufficiency that may be reversible, but endangers the patient’s life [1].

An early and accurate diagnosis is essential, since the immediate treatment is highly effective, increasing mortality with its delay; however, this entity has shown to be hard to diagnose in most cases, and it may happen in patients with no identifiable risk, and may be missed because there is no specific clinical presentation. Thus, it forces a differential diagnosis with numerous pathologies, as in the case of acute coronary syndrome.

To strengthen the value/specificity of the clinical symptoms, scores of prediction were created, not giving up on the proper use of clinical judgment [2], and identifying a group of patients in whom this diagnosis would be more or less likely and in whom other studies would be made or not, with a greater sensibility and specificity for diagnosis, observing with the increase of the category, an increase in the prevalence of pulmonary embolism. This doesn’t allow ruling out or confirming it, but it does increase the index of suspicion, a fundamental link for diagnosis. But on occasions, as it happens in the case we present next, omitting this diagnosis as possible, even in cases of low probability, may lead to diagnostic mistakes [2].

 

CLINICAL CASE
We present a male, 72-year-old patient, white, with a personal history of type II diabetes mellitus and ischemic heart disease, with no other risk factors. He came to the emergency service of the Instituto de Cardiología y Cirugía Cardiovascular, presenting for several days before admittance, the symptom of oppressive chest pain, sometimes accompanied by a discrete “shortness of breath”, which was relieved with the sublingual administration of nitroglycerin. Nothing worth mentioning was found in the physical examination (heart rate, 82 bpm, blood pressure, 130/70 mmHg, respiratory rate: 19/min) to continue with the following supplementary tests:

Electrocardiogram (ECG): Sinus rhythm, with negative T waves in DIII and aVF, present in previous recordings, as well as negative T from V1-V4, of recent onset, which later extended until V6 (Figure 1).

Figure 1. Twelve lead electrocardiogram that shows sinus rhythm, negative T waves in DIII and aVF, and from V1 through V6.


Chest X-ray: Cardiothoracic index within normal limits. No pleuropulmonary, bone or soft parts alterations.

Arterial blood gas: PH: 7.40; PaO2: 135 mmHg; PaCO2: 2:36 mmHg; SatO2: 95%; BE: +1.5; HCO3: 23. The interpretation is non-ST elevated acute coronary syndrome (NSTEACS), so he is admitted in the Coronary Unit (CU). After several days of intensive treatment where among other medications IV unfractionated heparin (UH) was administered,due to his satisfactory evolution, he was moved outside the unit into a non-severe patients care ward. On the following day, coronary angiography was performed, presenting a single lesion of the anterior descending artery (ADA) of 30-40% stenosis in the proximal segment. Approximately 24 hours after the procedure, the patient started with symptoms similar to those causing his admittance, but more intense, characterized by oppressive pain, irradiated toward the left arm, dyspnea, anxiety, sweating, polypnea and tachycardia. The interpretation again, is that of acute coronary syndrome and he is sent to the cardiosurgical intensive care unit, where the general care for these cases is adopted, as well as the invasive monitoring relevant to all patients in a severe state. The hemodynamically unstable patient is received, with marked hypotension (BP: 70/25 mmHg), anxious, pale, sweating, with tachycardia, polypnea, with thermal gradient (cold) in both lower limbs until the thighs, as well as crepitants until the middle third of both lung fields, using the accessory muscles of breathing, saturation by pulse oxymetry that does not exceed 50%. We started with intensive treatment with anticoagulation and support with drugs that increase inotropism, as well as a proper correction of cardiac output determinants, including mechanical ventilatory support and supplementary actions were made with no improvement.

Arterial blood gas: PH: 7.30; PaO2: 58 mmHg; PaCO2: 30 mmHg; SatO2: 55%; BE: -3; HCO3: 15.

Electrocardiogram: Sinus rhythm, heart rate 60 bpm, QT 440 ms with negative T waves  in DIII, aVF and from V1-V6 (Figure 1).

Echocardiogram: It showed as relevant data the existence of pressure overload signs in the right cardiac chambers, with significant dilatation of the right atrium and ventricle (RA and RV respectively), the pulmonary artery and its main branches, as well the inferior vena cava (IVC); with absence of inspiratory collapse of the latter, abnormal movement of the interventricular septum, with marked flattening of the latter in systole and in diastole that produces the characteristic “D” shape in the short axis; tricuspid failure, as well as decrease of pulmonary acceleration time, marked hypokinesis of the RV free wall with mid-basal predominance, with preservation of the apical movement (McConnell’s sign) and signs of poor systo-diastolic right ventricular function (Figure 2).

Figure 2. Transthoracic echo: A: Parasternal long axis showing right ventricular (RV) dilatation. B: Parasternal short axis showing the “D” shape of the left ventricular and RV growth. C: Parasternal short axis of great vessels, where pulmonary artery trunk dilatation is observed, as well as in its main branches (left and right). D: Apical view of the four chambers that shows right chambers dilatation (atrium and ventricle). E: Subcostal view that shows the dilatation of the inferior vena cava (IVC). F: A type III flow in the pulmonary artery trunk is observed from the use of pulsed Doppler in a parasternal short axis view of the great vessels, with time shortening of pulmonary acceleration. G: Apical view of the four chambers that shows the presence of functional tricuspid insufficiency by the increase in right chambers pressure.

It was decided to add thrombolysis to the treatment with recombinant streptokinase, but the severity and rapid evolution into a deadly end, with cardiorespiratory arrest in electromechanic dissociation and cardiopulmonary and brain resuscitation maneuvers, prevented the onset of infusion.

An anatomopathological study was conducted (Figure 3).

Figure 3. Macroscopic image of the anatomopathological piece. The presence of thrombi are observed in both branches (right and left) of the pulmonary artery.

Although prediction models to evaluate the clinical probability of suffering pulmonary thromboembolism have been designed as pre-test prediction, they were applied to this case, with an unequivocal diagnosis of pulmonary thromboembolism in a retrospective manner to know their accuracy [8,9].

 

DISCUSSION
Pulmonary thromboembolism in most cases is a consequence of deep venous thrombosis (DVT).Eighty five to ninety percent of the thrombi come from the lower limbs, with a minor percentage remaining for other territories, such as upper limbs, right cardiac chambers, the deep pelvic venous system, renal and axillary veins, as well as thrombi associated to central catheters [1].

Although usually it is possible to detect several predisposing factors (secondary PTE), increasing the probability of PTE with the number of such factors, it may happen in a patient with no identifiable predisposing factor, as in this case.

In studies such as the International Cooperative Pulmonary Embolism Registry (ICOPER), the proportion of patients with idiopathic or unprovoked PTE was around 20%. Between the predisposing factors the following are included: age, history of previous thromboembolism, active cancer, neurological disease with limb paresis, medical pathology requiring prolonged rest in bed, such as heart failure or acute respiratory failure, congenital or acquired thrombophilia, hormone replacement therapy and oral contraceptive therapy [3]. An advanced age is controversial as independent risk factor (this would be the only identifiable factor in the patient), although it is known that the incidence of venous thromboembolism increases exponentially with it, since with age different predisposing medical and surgical pathologies arise more frequently, as well as sedentarism, which is very hard to quantify [4].

The diagnosis of PTE is complex and the clinical entities the differential diagnosis of which should be posed are numerous, since for most authors the individual clinical signs and symptoms are not very helpful, because they are not sensitive or specific, frequently being both overdiagnosed and underdiagnosed. The case we present is an example of it. The most frequent one is for dyspnea to be prevalent between the symptoms, which may even be intense, sudden or have a progressive start over weeks. The diagnosis of PTE may be reached by the absence of other causes for progressive dyspnea and not what happened with our patient, in whom “shortness of breath” was discrete, with chest pain being prevalent.

Chest pain may be pleuritic, which is usually caused by pleural irritation due to distal emboli that causes the so-called pulmonary infarction. But on occasions, as what happened with the example we showed, pain may have other characteristics. It could be oppressive, retrosternal, similar to angina, which could be a reflect of right ventricular ischemia. In the most severe cases, there may be shock and hypotension, as it finally occurred with the patient, shortly before dying.

The basic tests (electrocardiogram, chest X-ray, arterial blood gas) also have a low sensibility and specificity, and they may even be completely normal in cases of PTE, as in the present case, thus making its diagnosis more difficult.
The electrocardiographic signs of RV enlargement, as inversion of T waves in leads V1-V4 (present in 49% of the patients in the PIOPED study), QR pattern in lead V1, the classical S1Q3T3 type and complete or incomplete right bundle branch block could be helpful, especially when they have a recent onset [5]. However, these changes are infrequent (6% in the PIOPED study), are usually associated to the most severe forms of PTE, and may be found in RV enlargement by any cause. The presence in our patient of negative T from V1-V4, which later extended to V6, in a scenario where oppressive chest pain was predominant and with the history of ischemic heart disease, led to the mistaken diagnosis of non-ST elevation acute coronary syndrome (NSTEACS).

In the cases of pulmonary embolism, chest X-ray could be completely normal, as it happened in our clinical case, it is useful to rule out other causes for dyspnea and chest pain. There are some anomalies that by being present increase the probability, although they are not specific. The most frequent findings are atelectasis, pleural effusion or elevated hemidiaphragm. Other authors report pulmonary artery thickening and focal hypovolemia. Westermark’s sign (prominent pulmonary hilum with decrease of peripheral pulmonary vessels) is rare [6].

PTE is generally associated to hypoxemia and/or hypocapnia, but not always so, so normal arterial gases do not rule out its existence either. Up to 20% of the patients with PTE have normal arterial oxygen pressure (PaO2) and an alveolar-arterial oxygen gradient [D (A-a) O2] [7].

Because the high level of suspicion is the first link to the diagnosis of pulmonary thromboembolism and the great variability in its form presentation, the scant sensibility and specificity of signs and symptoms, as well as the basic tests (electrocardiogram, chest X-ray, arterial blood gas) and the use in the diagnosis of PTE of methods we often lack because of their very high cost, and existing only in some health care institutions, and at other times having them but in spite of that the patient is so severe it cannot be moved to undergo such tests, the use of prediction scores has been attempted, not giving up on a proper use of clinical judgement.

This assessment allows identifying a group of patients in whom this diagnosis would be more or less likely, in whom other studies would be made or not, with more sensibility and specificity for diagnosis; but it is important to emphasize that they increase the index of suspicion, but don’t rule out or confirm the presence of acute PTE.

The most widely used scores for clinical prediction are the Canadian Wells’ score (Table 1) and the reviewed Geneva score (Table 2). In both an outline of three categories is used (low, moderate or high clinical probability) and in the Wells’ score also an outline of two categories (probable or improbable PTE). Both scores are simple to use and are completely based on clinical variables. Whichever the score used, the ratio of patients with PTE is approximately 10% in the category of low probability, similar to our case, 30% in the moderate probability category and 65% in the high clinical probability [8-12].

Variables

Score

Predisposing factors

 

Previous DVT or PTE.

+1.5

Recent surgery or immobilization.

+1.5

Cancer.

+1

Symptoms

 

Hemoptysis

+2

Clinical signs

 

Heart rate >100 bpm.

+1.5

Clinical signs of DVT.

+3

Clinical judgment

 

Alternative diagnosis less likely than PTE.

+3

 

 

Clinical probability (3 levels)

Total

Low.

0-1

Intermediate.

2-6

High.

≥7

 

 

Clinical probability (2 levels)

Total

Improbable PTE.

0-4

Probable PTE.

>4

DVT: Deep venous thrombosis; PTE: Pulmonary thromboembolism.

Table 1. Wells' score for the clinical prediction of PTE.

 

Variables

Score

Predisposing factors.

 

Age >65 y.o.

+1

Previous DVT or PTE

+3

Surgery or fracture ≤1 month

+2

Active malignancy

+2

Symptoms

 

Unilateral pain in lower limbs.

+3

Hemoptysis

+2

Clinical signs.

 

Heart rate 75-94 bpm.

+3

Heart rate ≥95 bpm.

+5

Pain with palpation in deep veins in lower limbs and unilateral edema.

+4

 

 

Clinical probability

Total

Low

0-3

Intermediate

4-10

High

≥11

DVT: Deep venous thrombosis; PTE: Pulmonary thromboembolism.

Table 2. Reviewed Geneva Score for the clinical prediction of PTE.

 

In some studies, it was reported that one every hundred admitted patients dies for this cause and that almost two thirds of the emboli diagnosed post-mortem, were not in life [13]. Seventy five to ninety percent of the deaths occur over the first hours after the PTE occurs; the cause of death in the remaining 10-25% is probably recurrent embolisms that occur over the 2 following weeks, as it happened with our patient.

 

CONCLUSIONS
The suspicion of PTE should always be present, regardless of the clinical evaluation allowing us to classify it in low probability, since this does not rule out its presence and the evaluation of this pathology should be continuous and dynamic. The clinical case presented obtained the low probability classification in the initial evaluation, with reappearance of the symptoms days later, in which the high probability classification of PTE was clear when applying once again any of the existing scores. But not having suspected from the start about this pathology did not allow to diagnose it and to change the natural history of its pitiful evolution.

 

REFERENCES

  1. Alonso Martínez JL, Echegaray Agara M, Urbieta Echezarreta MA, et al. Embolismo pulmonar agudo. Un registro de 10 años: de mayo d 1992 a mayo de 2002. Rev Clin Esp 2004; 204: 521-7.
  2. Miniati M, Monti S, Bottai M. A structured clinical model for predicting the probability of pulmonary embolism. Am J Med 2003; 114: 173-9.
  3. Goldhaber SZ, Visani L, De Rosa M. Acute pulmonary embolism: clinical outcomes in the International Cooperative Pulmonary Embolism Registry (ICOPER). Lancet 1999; 353: 1386-9.
  4. Heit JA. Risk factors for venous thromboembolism. Clin Chest Med 2003; 24: 1-12.
  5. Geibel A, Zehender M, Kasper W, et al. Prognostic value of the ECG on admission in patients with acute major pulmonary embolism. Eur Respir J 2005; 25: 843-8.
  6. Elliott CG, Goldhaber SZ, Visani L, et al. Chest radiographs in acute pulmonary embolism. Results from the International Cooperative Pulmonary Embolism Registry. Chest 2000; 118: 33-8.
  7. Stein PD, Goldhaber SZ, Henry JW, et al. Arterial blood gas analysis in the assessment of suspected acute pulmonary embolism. Chest 1996; 109: 78-81.
  8. Wells PS, Anderson DR, Rodger M, et al. Derivation of a simple clinical model to categorize patients probability of pulmonary embolism: increasing the models utility with the SimpliRED D-dimer. ThrombHaemost 2000; 83: 416-20.
  9. Le Gal G, Righini M, Roy PM, et al. Prediction of pulmonary embolism in the emergency department: the revised Geneva score. Ann Intern Med 2006; 144: 165-71.
  10. Van Belle A, Buller HR, Huisman MV, et al. Effectiveness of managing suspected pulmonary embolism using an algorithm combining clinical probability, D-dimer testing, and computed tomography. JAMA 2006; 295: 172-9.
  11. Anderson DR, Kovacs MJ, Dennie C, et al. Use of spiral computed tomography contrast angiography and ultrasonography to exclude the diagnosis of pulmonary embolism in the emergency department. J Emerg Med 2005; 29: 399-404.
  12. Miniati M, Bottai M, Monti S. Comparison of 3 clinocal models for predicting the probability of pulmonary embolism. Medicine 2005; 84: 107-14.
  13. Cohen AT, Agnelli G, Anderson FA, et al. Venous thromboembolism (VTE) in Europe. The number of VTE events and associated morbidity and mortality. ThrombHaemost 2007; 98: 756-64.

 

Publication: September 2013

 
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