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Fulminating Fatal Paradoxical Fat Embolism Without Cardiac Septal Defect - Clinical And Histopathological Features

Seetharaman Hariharan*,Chalapathi Rao AdidamVenkata

*Faculty of Medical Sciences , The University of the West Indies, St Augustine, Trinidad and Tobago

Address for Correspondence:  

Seetharaman Hariharan,
Senior Lecturer
Department of Clinical Surgical Sciences
Faculty of Medical Sciences
The University of the West Indies
Eric Williams Medical Sciences Complex
Mount Hope
TRINIDAD (West Indies)
Telephone/Fax: 1 868 662 4030




Paradoxical fat embolism involving multiple organs is usually reported to have been associated with cardiac defects such as patent foramen ovale. We report a case of fat embolism syndrome following unilateral femoral and bimalleolar fracture, which rapidly progressed to death. The patient did not satisfy the required Gurd’s criteria to diagnose fat embolism syndrome clinically. At autopsy, the patient did not have any cardiac septal defects or arteriovenous malformations. But fat deposition could be demonstrated histopathologically in many organs.  The increase in the pulmonary vascular resistance would have opened the physiological anastomoses between the pulmonary arteries and veins, leading to massive embolisation of fat into the left side of the heart and dissemination to other organs. This patient did not receive PEEP during his mechanical ventilation which could have possibly physically prevented embolisation through the arteriovenous shunts. Massive paradoxical fat embolism can occur without a cardiac septal defect. Fat embolism syndrome should be suspected even when a patient does not satisfy the Gurd’s criteria.

J.Orthopaedics 2008;5(4)e8


Fat embolism syndrome is characterized by symptoms and signs involving the respiratory, haematological, dermatological and neurological systems (1). Paradoxical fat embolism is commonly reported after orthopaedic surgeries such as hip arthroplasty and placement of intramedullary rods (2-4). It has also been proposed as a cause of postoperative neurocognitive dysfunction and persistent unconsciousness after anaesthesia following orthopaedic surgery (5, 6). Massive paradoxical fat embolism has been usually reported to be associated with cardiac defects such as Patent Foramen Ovale (PFO) (7, 8). We report a patient with no such abnormality, and had fat deposition in many organs and rapidly progressed to death.

Case Report :

A 20-year-old otherwise healthy man sustained a closed comminuted fracture involving the mid-shaft of the right femur and bi-malleolar fractures of left ankle following motor vehicle accident. He was initially taken to a primary health centre and after a two-hour wait was transferred to a tertiary care centre. Because the patient was dissatisfied with the care he received in this hospital, he discharged himself in 12 hours and got admitted to another tertiary care centre. He was placed on tibial-pin traction. 24 hours following the fracture, while on the orthopaedic ward he developed tachypnoea; the pulse oximeter reading showed 94-95% oxygen saturation. At this point of time, he was fully conscious and orientated, there were no petechial spots on the skin, and his haematological and biochemical parameters were completely within the normal range. His chest radiograph did not show any changes. He was given oxygen supplementation by facemask and later by Venturi devices increasing the FiO2 until 60%. However, in a six-hour period, his tachypnoea and hypoxaemia worsened. He also had confusion at this point, which was attributed to his hypoxaemia (pulse oximeter showed 89-90% saturation). He had tachycardia in the range of 110-120 beats per minute. He was endotracheally intubated and was awaiting Intensive Care Unit (ICU) admission, hand ventilated by a physician. Patient was later provided mechanical ventilatory support in an operating room by an anaesthetic ventilator, where his condition worsened. He had a severe hypoxaemia (PaO2 of 52 mmHg with a FiO2 of 100%), but a normocarbia. He required noradrenaline infusion to maintain the mean arterial pressure. Even at this stage he did not have a low haematocrit, thrombocytopaenia or leucocytosis. He did not have any cutaneous petechial spots. However, he developed anuria and the renal biochemical parameters started to rise. He had adequate volume replacement guided by the central venous pressure but did not receive blood transfusion. Dobutamine infusion was started along with the noradrenaline because of a low value of the central venous oxygen saturation. He was continued to be ventilated in the operating room with the anaesthetic ventilator. 48 hours after the trauma, a CT scan of the head along with a spiral CT of the pulmonary vessels was requested and he was transported to the radiology suite. He had a cardiac arrest on the CT scan table and could not be successfully resuscitated.

An autopsy was performed, which revealed the following findings:

There was a closed comminuted fracture of the mid-shaft of right femur with haematoma (200 ml). Bimalleolar fractures of left ankle with swelling and contusions were present. Cyanosis was present but skin petechiae were absent. Bronchial lumen contained haemorrhagic frothy fluid. Pleural surface of lungs had petechiae. Both the lungs were heavy (> 1000 g), congested and had patchy haemorrhagic areas. Right pleural cavity contained 300 ml of straw-coloured fluid.

Histology of lung revealed clear spaces within blood vessels with displacement of red blood cells, parenchymal haemorrhages, focal pneumonic changes, and fibrinous material in the air spaces.

Most organs (lungs, brain, kidney, spleen and liver) revealed congestion and clear vacuoles in the blood vessels. Frozen section and Oil red O staining of lungs, kidneys, adrenals and brain showed fat deposition with foci of inflammatory response (Figures 1-4).

There was no evidence of PFO or any other cardiac septal defects, and there was no evidence of arteriovenous malformations in any organs studied.

Figure 1: Frozen section of the lung stained with oil red O showing multiple orange red fat globules of varying sizes in the septal vasculature

Figure 2: Frozen section of the kidney stained with oil red O showing multiple orange-red fat globules of varying sizes in the glomerular capillaries

Figure 3: Section from the adrenal gland showing cortical distended capillary containing clear refractile fat vacuoles (H&E, ×20)

Figure 4: Frozen section of brain tissue stained with oil red “O” reveals fat globule in the lumen of blood vessel (10×)

Discussion :

Although fat embolism syndrome is commonly reported in the literature, there are few reports which have histopathologically demonstrated the presence of fat in multiple organs. A recent histopathological report demonstrated fat in the lungs; however this was an artificial lung used for resuscitation of the patient (9).

Fat embolism syndrome is predominantly a clinical diagnosis. Radiological and laboratory findings are mostly inconsistent and nonspecific (10). The diagnosis may be assisted by employing the Gurd’s criteria, which include both clinical and laboratory parameters (11). At least one major criterion and two minor criteria should be satisfied to establish the diagnosis of fat embolism. However, in the present case, the only major criterion to be satisfied was hypoxaemia and the only minor criterion was tachycardia. Despite this, the patient had a fatal fat embolism and the autopsy showed systemic fat deposition.

            Multi-organ dysfunction syndrome (MODS) can be associated with Acute Respiratory Distress Syndrome, which is a common sequel to fat embolism (12). However, this is usually common in trauma involving multiple anatomical regions and the post-mortem findings of MODS is found when the patient dies after 72 hours (12). In the present case, the patient died in 48 hours following an isolated femoral and bimalleolar fracture with no other co-morbidities or cardiac abnormalities.

Reports in the literature have suggested the possibility of systemic fat embolisation through pulmonary capillaries, although this is on the basis of animal studies (13, 14). An earlier report which demonstrated the presence of veno-arterial shunts in the brain by Transcranial Doppler (TCD), proposed these shunts as a possible explanation for paradoxical cerebral fat embolism following orthopaedic surgeries (15). The study reported that some of the cerebral emboli were spontaneous and many required ‘provocation’ such as Valsalva manœuvre. The authors also opined that the small and delayed emboli through pulmonary arteriovenous shunts may be clinically insignificant (15). But the question remains that when the systemic arterial pressure is at a higher level than the venous pressure, how does large amount of fat get into the systemic arterial side in various organs to cause a massive paradoxical fat embolism?

Intrapulmonary arteriovenous shunts are known to be dormant in healthy humans, which could be recruited in certain conditions such as physical exercise (16). In the present case, the increased pulmonary vascular resistance caused by the pulmonary fat embolism would have opened the physiological pulmonary arteriovenous shunts. The higher pressure in the pulmonary arterial network relative to the pulmonary venous network would have assisted this massive embolisation to the left side of the heart and eventually to all the other organs. Although there is proposal of the mechanical theory of fat embolism (17), the feasibility of massive systemic embolisation through pulmonary arteriovenous shunts has not been widely investigated in both animal and human studies.

Another corroborative finding in the present case is that, the patient was provided mechanical ventilatory support with an anaesthetic ventilator, which had no provision of Positive End Expiratory Pressure (PEEP). PEEP and Continuous Positive Airway pressure (CPAP) are presumed to be therapeutic interventions in fat embolism (in distinction to being a supportive intervention) (18). PEEP and CPAP are well known to recruit alveoli, increase the functional residual capacity and also prevent the alveoli from collapsing thus facilitating a better gas exchange (19). Improvement in ventilation – perfusion ratio and reduction of the shunting of the deoxygenated blood to the arterial side is the well-established function of PEEP/CPAP. However, it is possible that the constant distending pressures offered by these ventilatory modes may also prevent fat emboli reaching the systemic side through both the pulmonary capillary system as well as the arteriovenous shunts. Hence in the present case, because PEEP was not provided, there could have been a massive systemic embolisation of the fat through these routes.

There are additional features, which could have contributed to the deterioration of this patient. Early fixation of the long bone fractures is known to prevent continuous embolisation (20). This was not done in this patient, which could have been another reason for continuous embolisation. In addition, transportation to various health care institutions as well as within the hospital could have aggravated the embolisation process into many organs. The patient did not also receive corticosteroids, which could have prevented rapid progression of the systemic inflammatory response.

In summary, the present report highlights the following points:

1.Fat embolism syndrome should be suspected even when a patient does not satisfy the Gurd’s criteria.

2.Massive paradoxical fat embolism can occur even without a cardiac septal abnormality or arterio-venous malformations.

3.Pulmonary arterio-venous shunts, which are otherwise physiological may open up and lead to embolisation of fat into the left side of the heart from which it may be disseminated to other organs, which needs to be further investigated.

4.Mechanical ventilation with PEEP/CPAP may ‘physically’ prevent embolisation through the above route, which also needs further investigation.

Reference :

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This is a peer reviewed paper 

Please cite as :Seetharaman Hariharan : Fulminating Fatal Paradoxical Fat Embolism Without Cardiac Septal Defect - Clinical And Histopathological Features

J.Orthopaedics 2008;5(4)e8





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