**16. Cardiovascular**

Tachycardia is invariably present. Hemodynamic changes include: (Aebli et al., 2005; Krebs et al., 2007; Murphy et al., 1997)


Cardiovascular deterioration is often transient but can be fulminant resulting in severe cardiac failure, cardiac arrest and even death.

Other findings: Rarely severe hypocalcemia leading to tetany has been reported (Gurd & Wilson, 1974). Jaundice/icterus can be present. Hematological findings include anemia, thrombocytopenia and DIC (Dines et al., 1972; Herndon, 1975; Hulman, 1988b; McCarthy et al., 1973; Peltier, 1984; Peltier, 1988). Elevation of ESR & CRP, presence of fat globules in the urine, sputum or blood, elevation of serum lipase and phospholipase A2 have been described.

### **17. Role of bronchial alveolar lavage (BAL)**

Presence of lipid inclusions in alveolar macrophages in the BAL has been associated with various traumatic and nontraumatic conditions, especially aspiration pneumonia and lipid infusion. Quantification of cells containing fat droplets in bronchial alveolar lavage (BAL) fluid within the first 24 hours after trauma have also been shown to correlate with clinical fat embolism in some studies ) (Al-Khuwaitir et al., 2002; Chastre et al., 1990; Mellor & Soni, 2001; Mimoz et al., 1995). In the absence of an exogenous source of fat, BAL fluid that contains more than 30% macrophages laden with lipid inclusions is highly suggestive of FES.

#### **18. Imaging**

82 Pulmonary Embolism

ventilation (Bernard et al., 1994). The most "fulminant" form of FES presents as "acute cor pulmonale" with respiratory failure causing death within a matter of few hours, usually after a major trauma (Mellor & Soni, 2001; Parisi et al., 2002; Peltier, 1984; Schonfeld et al., 1983). Although frequently clinically inapparent, hypoxemia is nearly universal (Peltier et

Neurological findings are nonspecific and usually completely reversible**.** They can **r**ange from anxiety and restlessness to comatose state requiring mechanical ventilation. The early signs and symptoms are delirium, restlessness, confusion or anxiety. Diffuse encephalopathy and coma can ensue (Jacobson et al., 1986). Focal neurological deficits are common. These findings are frequently not responsive to correction of hypoxemia (Metting et al., 2009) and have infrequently been observed in absence of pulmonary

The characteristic petechial rash has been reported to be in present in about 50% to 60% of patients with FES. Upper anterior torso, axillae, neck, upper arm, conjunctivae and oral mucosa are usual sites. The rash is NOT due to thrombocytopenia but from fat emboli obstructing capillaries and causing capillary damage and subsequent hemorrhages. The

Retinopathy has been reported in up to 50% of patients (Adams, 1971). Fundoscopic findings (Kearns, 1956) include macular edema, cotton-wool spots, retinal hemorrhages and occasional fat droplets. The findings are attributed to microvascular injury in the form of microinfarcts of retina which usually disappear with possible residual

Tachycardia is invariably present. Hemodynamic changes include: (Aebli et al., 2005; Krebs

• Increase in pulmonary arterial pressure due to not only mechanical obstruction from fat

Other findings: Rarely severe hypocalcemia leading to tetany has been reported (Gurd & Wilson, 1974). Jaundice/icterus can be present. Hematological findings include anemia, thrombocytopenia and DIC (Dines et al., 1972; Herndon, 1975; Hulman, 1988b; McCarthy et

Cardiovascular deterioration is often transient but can be fulminant resulting in severe

embolism but also from pulmonary vasoconstriction.

al., 1974; A. P. Ross, 1970).

involvement.

**14. Skin** 

**15. Eye** 

scotomas.

**16. Cardiovascular** 

• Arrythmias

et al., 2007; Murphy et al., 1997)

• Reduction in cardiac output

• Reduction in systemic arterial pressure

cardiac failure, cardiac arrest and even death.

**13. Central nervous system** 

petechial rash may be the only physical sign.

The findings are nonspecific and appear after a variable lag period as related to clinical symptoms. Chest roentgenogram may reveal diffuse evenly distributed alveolar and interstitial densities suggestive of pulmonary edema or acute lung injury. Computed tomography (CT) of the chest may rarely show fat in the pulmonary artery. Multiple subcentimeter, ill-defined centrilobular and subpleural nodules can be seen in the acute phase of FES. Diffuse lung calcifications located in the branches of the pulmonary arteries have been described in the late course of FES (Hamrick-Turner et al., 1994). Ventilation perfusion scan (V/Q scan) may reveal subsegmental perfusion defects (H. M. Park et al., 1986).

Computed tomography (CT) of the brain may show nonspecific signs of cerebral edema and hemorrhagic infarcts in multiple areas (Meeke et al., 1987). Magnetic resonance imaging (MRI) of the brain and MR spectroscopy seem to be the most sensitive method in detection of cerebral emboli, but nonspecific (J. J. Chen et al., 2008; Eguia et al., 2007; Guillevin et al., 2005; Sasano et al., 2004; Satoh et al., 1997; Stoeger et al., 1998). Diffusion-weighted imaging may reveal bright spots on a dark background, a finding known as the ''Starfield pattern'' (Parizel et al., 2001). Cerebral micro-emboli can be detected in vivo after long bone fracture by transcranial Doppler (Barak et al., 2008; Forteza et al., 1999).

Transesophageal Echo (TEE) is most useful for diagnosing intra-operative FES. TEE has sensitivity of 80% and specificity of 100% in patients with fat embolism large enough to cause hemodynamic instability (Pruszczyk et al., 1997). TEE cannot reliably distinguish fat emboli from tumor emboli.

#### **19. Diagnosis**

Given the extremely heterogeneous pattern of presentation, precise diagnosis of FES remains elusive. Various diagnostic criteria have been proposed. However given the lack of gold standard diagnostic tests and lack of pathognomic signs, it is difficult to determine validity of these criteria. Therefore the diagnosis of FES is based on a constellation of clinical and laboratory findings and exclusion of other potential diagnoses (Taviloglu & Yanar, 2007).

The following diagnostic criteria are widely used.

Non-Thrombotic Pulmonary Embolism 85

2009; Kallenbach et al., 1987; Lindeque et al., 1987; Schonfeld et al., 1983). Nonetheless, prophylactic use of corticosteroids remains controversial mainly because of lack of large scale studies. The results of treatment with drugs, including clofibrate, dextran-40, ethyl alcohol, heparin, and aspirin are inconclusive (K. M. Chan et al., 1984; Gossling &

With timely supportive care and hemodynamic support, most patients with FES recover completely. Mortality rate has been variably reported to be 10 to 20% (Fabian et al., 1990;

Septic pulmonary embolism (SPE) is an uncommon but serious disorder that is often difficult to diagnose. SPE are thrombi containing microorganisms in a fibrin matrix that are mobilized via the bloodstream from an infectious nidus to get implanted into the vascular

In 1978, MacMillan et al. (MacMillan et al., 1978) studied 60 patients with SPE over a 5-year period and reported that most of SPE cases occurred in drug users. Intravenous drug abuse (IVDA-78%) and tricuspid endocarditis were identified as the embolic source in 53% of these IVDA cases (fig 2b) (MacMillan et al., 1978). However, the epidemiology and outcome of patients with SPE have changed over the past 30 years with the increased use of long term indwelling catheters and devices (pacemakers, prosthetic vascular devices) and also increase in the number of immune-compromised patients. The predominant cause of SPE in the current era is infections related to intravascular devices/catheters or soft-tissue infections. Its incidence is declining among IVDA presumably due to greater needle hygiene (Fig 2a) (Cook et al., 2005)**.** Intravascular devices are a common cause of local site infection and cause up to 50% of the nosocomial bacteremias. Central venous catheters account for 80-90%

In a large series of postmortem examinations in Japan, a total of 11,367 PE cases were identified from 396,982 postmortem examinations. In this study, the incidence of septic PE

A prerequisite for the development of SPE appears to be a heavily infected source such as long-term indwelling vascular devices, bacterial endocarditis of the right heart valves or peripheral thrombophlebitis (head and neck or pelvic infections) leading to showers of septic emboli to the lung. In the above-mentioned recent Japanese study with 247 SPE patients, fungal emboli were more common than bacterial emboli. Among the fungi, Aspergillus was the most common pathogen (20.8%) encountered preceding Mucor or Candida. Cancer was the most common predisposing factor associated with fungal SPE (63%) – Leukemia (43.2%), followed by adenocarcinoma and lymphoma. The top three infectious sources showering

Pellegrini, 1982; Peltier, 1984; Shier et al., 1977; Stoltenberg & Gustilo, 1979).

system of the lungs. The organisms can be bacteria, fungi or parasites.

**21. Prognosis** 

**23. Epidemiology** 

of these infections.

**24. Risk factors** 

was found to be 2.2% (Sakuma et al., 2007).

septic emboli were pneumonia, sepsis and infective endocarditis.

Moreau, 1974; Peltier, 1965; Peltier et al., 1974).

**22. Septic pulmonary embolism** 


Table 5. Gurd and Wilson: FES = 1 major + 4 minor + Fat microglobulinemia


Table 6. Schonfeld's criteria - FES = 5 or more points
