**27. Diagnosis**

88 Pulmonary Embolism

clinician into thinking about a diagnosis of SPE. Other pulmonary complications of SPE include pleural effusion, empyema, and rupture of subpleural lesions leading to

Lemierre's syndrome usually occurs in previously healthy adolescent or young adults, generally presenting with high grade fever (39-41C) and rigors. History is usually significant for sore throat, tooth ache, odynophagia, dysphagia and chest pain in the week preceding the presentation. On examination the patient appears ill, may have signs of periodontal disease, the tonsils are usually inflamed with exudates and peritonsillar abscesses releasing foul-smelling pus. ''The diagnosis of this infection may be suggested by the peculiar odour—like Limburger or overripe Camembert cheese—of pus produced by it.''(Alston, 1955). Signs of internal jugular vein thrombosis may be present in 26–45% of cases. Features suggestive of the development of internal jugular vein thrombophlebitis include neck pain and stiffness, cervical lymphadenopathy often in the anterior triangle and more characteristically a tender (normally unilateral) swelling at the angle of the jaw-

anterior to, and parallel with, the sternomastoid muscle (Riordan & Wilson, 2004).

spontaneous pneumothorax.

Fig. 4. Clinical manifestations of SPE

Clinical and radiological features at presentation are usually nonspecific and the diagnosis is frequently delayed (Huang et al., 1989). Radiographic findings, predisposing background or illness, and clinical evidence of infection usually are clues to the diagnosis. Blood cultures, chest CT and echocardiography are valuable when evaluating a patient with suspected SPE. Basic laboratory testing provides some clues to diagnosis. Patients typically have a neutrophil predominant leucocytosis. Liver function tests are abnormal in approximately

50% of patients. C-reactive protein is invariably raised. Microbiology: The diagnosis of bacteremia or fungemia is confirmed by recovery of the same species of micro-organisms from the peripheral blood cultures and from quantitative cultures obtained from the source of SPE. Pus drained from any site should be sent for culture, including catheter tip, localized abscesses in the neck, empyema, septic arthritis, bone, and soft tissue abscesses.

Chest radiograph findings are usually nonspecific with a spectrum of radiological abnormalities. The usual findings include patchy air space opacities simulating nonspecific broncho-pneumonia, multiple ill-defined nodules (usually 1-3 cm) in various stages of cavitation with irregular thick walls or wedge-shaped densities of varying sizes located peripherally abutting the pleura. Other x-ray features also include blunting of the costophrenic angle, indicating small pleural effusions or empyema.

Computed tomography (CT) of the chest: Common findings are patchy consolidation with air bronchograms, nodules in various stages of cavitation (predominant in the lower lobes), wedge-shaped peripheral lesions abutting the pleura with or without extension into the pleural space - pleural effusion/empyema, and hilar or mediastinal lymphadenopathy. The *"feeding vessel sign"* has been considered highly suggestive (although not pathognomonic) of septic PE and consists of a distinct vessel leading directly into the center of a nodule (Fig 5). This sign may represent hematogenous spread to the lungs and may also be seen in metastasis. The prevalence of this sign varies from 67–100% in various series and the heterogeneous sub pleural wedge-shaped opacities are seen in 70–75% of patients (Kwon et al., 2007). Multi-detector CT is faster and superior to the classical CT technology for detection of this sign (Dodd et al., 2006).

Fig. 5. The "Feeding vessel" sign and multiple peripheral cavitating lesions suggestive of SPE

1941).

**30. Epidemiology and risk factors** 

**31. Clinical features** 

Non-Thrombotic Pulmonary Embolism 91

subsequently by Steiner and Lushbaugh in 1941 as an autopsy series (Steiner & Lushbaugh,

The true incidence of AFE remains unknown and is variably reported in literature. The incidence of AFE has been estimated to be in 1 in 8000 to 80000 deliveries with reported mortality rates in older reports as high as 60%. However, more recent data suggest lower mortality rates ranging between 27-37% (Clark et al., 1995; Morgan, 1979; Tuffnell, 2005). For unknown reasons, the incidence of AFE is much higher in North America, around 1 in 15000 deliveries, Australia -1 in 30000 deliveries (C. L. Roberts et al., 2010), United Kingdom – 1 in

AFE usually occurs during immediate postpartum period. Data from a national registry revealed that AFE occurred during labor but before delivery in 70% of cases and during caesarean section in 19% (Clark et al., 1995). Although, reported as early as second trimester, the diagnosis in cases occurring as late as 36 h postpartum has been described (Devriendt et al., 1995). AFE following trans-abdominal amniocentesis is very rare (Hasaart & Essed, 1983). It has been estimated that AFE accounted for 12% of all maternal deaths related to legally induced abortion since 1972 (Grimes & Schulz, 1985; Guidotti et al., 1981). It is seldom associated with (surgical) manipulation during caesarean section (Laforga, 1997), curettage (Grimes & Cates, 1977), cervical suture removal (Margan et al., 1984) or repair of an incompetent cervix (Margan et al., 1984), or after car or motor vehicle accidents (Olcott et al., 1973). Large fetal size, use of oxytocics and vaginal prostaglandins, advanced gestational age, amnio-infusion or complicated labor have all been implicated (Maher et al., 1994; Morgan, 1979). In reality, specific risk factors have not been conclusively identified. Logistic regression identified advanced maternal age, placental pathologies and caesarean deliveries in a large population-based cohort study (Abenhaim et al., 2008). Maternal age below 20

Pathophysiology: The pathogenesis of AFE remains poorly understood. The detection of fetal tissue in maternal pulmonary artery is not pathognomonic. In fact, there is no clear temporal relationship between entry of amniotic fluid in to maternal circulation and symptom onset. The "antigenic" nature of AF along with pulmonary eosinophilic infiltrates, elevated antitryptase activity suggestive of mast cell degranulation has resulted in some authors to propose "Anaphylactoid syndrome of Pregnancy" as an alternative name to AFE. Autopsy findings frequently reveal disseminated intravascular coagulation (DIC). Isolated

Hemodynamic Effects: A biphasic pattern of hemodynamic changes have been favored in most recent descriptions. The "acute phase" comprising of acute elevation of pulmonary arterial pressure ("acute Cor Pulmonale"), followed by left ventricular dysfunction/failure.

AFE is a diagnosis of exclusion. It typically occurs during labor and delivery or in the immediate postpartum period, although it can occur as late as 48 hours postpartum. About 70% of cases occur before delivery (range, 63–76%). The symptoms are often sudden and protean. AFE is typified by maternal collapse associated with breathlessness, cyanosis, cardiac dysrhythymia, hypotension and then haemorrhage associated with DIC. Clark et al,

DIC may herald AFE. Amniotic fluid accelerates clot initiation and propagation.

50000 (Abenhaim et al., 2008; Knight et al., 2010; Kramer et al., 2006).

years and dystocia has been associated with lower incidence of AFE.


Table 7. Characteristics of SPE

Echocardiography is an important tool in evaluating patients for endocarditis. Transesophageal echocardiography (TEE) increases the sensitivity of detecting vegetations from 75 to 95 percent while maintaining the specificity of 85 to 98 percent and is thus, superior to the transthoracic technique (TTE) in delineating vegetations, abscesses and leaflet perforations in the heart (Dodd et al., 2006).
