Resuscitation, 5, 191-195

The role of shock in the pathogenesis of fat embolism after trauma J. DURST, W. HELLER, J. HALJSDOERFER

and K. SCHMIDT

Surgical Department, University of Tuebingen, 7400 Tuebingen,Calwer Strasse 7, Federal Republic of Germany

Summary Experimental studies and pathological investigations indicate that intrusion of fat into the circulation is common after trauma. This may not have any effect unless frank hypovolaemia supervenes upon changes in the blood vessels, manifested by a deficient vasomotility in shock. After fat embolism disseminated intravascular coagulopathy may occur as a consequence of the haematological changes and disturbances of capillaries. The morphological appearance of massive post-traumatic fat embolism evolves from the compensatory effect of accumulated synergistic factors that primarily induced the changes. From this point of view fat embolism should be recognized in the additional important role of an epiphenomenon of post-traumatic shock. Historical background In man fat embolism after trauma was first described by the pathologist F. A. Zenker as early as 1862. Since then clinicians and morphologists have proposed various theories for its aetiology and pathogenesis (Sevitt, 1962; Wehner, 1968). The trend was reversed in recent years by experimental and clinical studies, which showed that the pathology of fatal fat embolism depended on the degree of traumatic shock (Bergentz, 1962; Burkhardt, 1970; Durst, Knodel, Heller, Ehlers & He&hen, 1973; Swank, Seaman, Hissen & Lint, 1966). The traditional points of view were due for revision. Pathogenesis

aud pathophysiology

of shock

Shock is believed to result in a reduction of blood flow to vital organs. The initial opening of arteriovenous junctions results in a functional redistribution of the remaining circulating blood. Vasoconstriction primarily leads to a decrease of splanchnic and renal perfusion. The abnormal flow pattern results from the activation of the sympathoadrenergic system due to the release of postganglionic adrenaline, and the maximal stimulation of the adrenals. 191

192 J. DURST AND OTHERS

Since about 80% of the volume of circulating blood is contained in venous vessels, the increase of venous sympathetic tone must lead to a shrinkage of the venous capacitance space. This mechanism prevents a decreasing venous return to the heart. The supply of intracellular oxygen to under-perfused organs will be deranged by pre- and post-capillary vasoconstrictors. Lack of adenosine diphosphate and uncoupled respiration/phosphorylation mechanisms must stop mitochondrial oxygenation and adenosine triphosphate formation. Untreated metabolic acidosis further stimulates discharge of adrenaline. A deficient vasomotor tone characterizing shock prevails (Messmer & Brendel, 197 1). Precapillary sphincters, which are refractory to endogenous catecholamines, collapse and vasoconstriction of post-capillary veins continues unabated and is refractory to pharmacological treatment. The haemodynamics are primarily affected by hypercoagulopathy (‘sludge’) induced by trauma. Decreasing pressure in the capillary bed engenders the danger of disseminated intravascular coagulation, clinically manifested by the rapid disappearance of thrombocytes and clotting factors; fibrin-rich thrombi are deposited.

Pathogenesis of post-traumatic fat embolism In pathology embolism is defined as an intravascular distribution of material foreign to the normal circulation, in which the solid embolus becomes proportional to the inner diameter of the vessel through which it has to pass. The pathophysiological effects on circulation and tissues derive from ischaemia, and morphologically the result is infarction, and clinical symptoms arise after this. Until the end of the nineteenth century fat embolism was interpreted like any other embolism. About 20 years ago the concepts were put on to a broader base. The extension of the concept beyond the embolic distribution of fat implied a multitude of contributory factors. Three main theories were held for a long time: (i) Proponents of the theory dealing with the intrusion of fat into the bloodstream believed that in burns, contusions or fractures, fat globules would be detached from cell aggregations and transported to the lungs by venous or lymphatic flow (Bschor & Haasch, 1963; Peltier, 1957; Hallgren, Kerstell, Rudenstam & Svanborg, 1966). Special anatomical conditions and the low melting point of depot fats should favour the release of liquid lipids after tissue damage. These are identified as drops of oil overlying fracture haematomas. The veins of bone form a reticular system of sinuses which cannot collapse despite their fragility. In injury, fat from adjacent cells which are separated only by thin membranes may invade the bloodstream. Studies with fluorescence microscopy support this theory (Bschor & Haasch, 1963). A review of experimental and morphological evaluations has been presented by Savitt (1962). (ii) A second theory held that there was a certain segregation of blood fat, caused by a less-stable suspension and poorer solubility of hydrophobe plasma lipids after trauma. An inhibited coagulation system as well as changes of physical characteristics of blood elements were related to the lower solubility of hydrophobe lipids (Bergen& 1962; Swank et al., 1966). (iii) An enzymatically induced segregation of plasma lipids was suggested (Schiittemeyer & Flach, 1950; Kronke, 1956). These latter theories evolved since it was evident that the existing marrow fat would not be sufficient in amount to cause fatal embolism. The theory of unstable plasma lipids was discounted after measurement of enzymes and substrates in the serum of accident victims,

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especially by comparing patients with and without histologically evident fat embolism. Furthermore, an enzymatically induced dispersal of endogenous plasma lipids was not found, even in cases of unusually severe and generalized post-traumatic fat embolism (Durst et al., 1973). As a result of experimental and clinical studies one might expect measurably altered substrate concentrations in serum of accident victims (Bergentz, 1962; Bltimel, Huth & Lasch, 1970; Burkhardt, 1970; Swank et aZ., 1966). Although substrate concentrations depend on the degree of shock, they do not appear to be related pathologically to fat embolism. In these and our own studies the decrease in non-esterified fatty acids paralleled the degree of shock (Durst & Heller, 1971; Durst et al., 1973). About 4 h after the trauma, the triglyceride concentrations were reduced at the same time as the nonesterified fatty acid changes were demonstrable. The initial disappearance of triglycerides was accompanied by a lowered thrombocyte count. Our studies showed that the serum lipids were not similar in composition to that of haematoma lipids, as we found them in fracture sites, where ester-iced fatty acids predominate. Yet in massive fat embolism, serum triglycerides and esterified fatty acids increased, and there was a definite decrease of thrombocytes. In patients with fat embolism, the triglycerides obviously reached high est concentrations when thrombocytes were at a minimum. The same applied to fatal clinically manifest fat embolism, which was confirmed by autopsy. These results lead to the conclusion that hyperlipoproteinaemia was caused by traumatically induced lipolysis. Accordingly, it was concluded that fat embolism was a result and not a cause of the above phenomena. Pathophysiology

of post-traumatic fat embolism

Evaluation of the pathogenesis of haemorrhagic shock and the causes of fat embolism led to the belief that circulating fat droplets in the blood of accident victims did not have pathophysiological consequences. The characteristic structure of the pulmonary vessels and the anatomical position of the lung may explain why this organ primarily acts like a filter in trapping blood corpuscles. An important pathophysiological effect depends less on the extent of fat invasion than on an irritation of the terminal flow region in the lung and a concomitant coagulopathy dependent upon shock. Pathological studies have also shown the frequent coincidence of high morbidity with a strikingly low mortality (Sevitt, 1962; Durst et al., 1973). The morphological picture is mainly explained by physical alterations of haematological factors. Microthrombi, fat inclusions, interstitial oedema, the presence of granulocytes and fat in the cells of the alveolar membranes are the commonest pathological findings. Gas exchange in the lung is impaired by these processes. Increasing respiratory insufficiency leads to hypoxaemia followed by hypercapnia. Metabolic acidosis characteristic of the immediate post-traumatic course is complicated by respiratory acidosis. Pathologically respiratory insufficiency may be maintained by increased dead space and diminished gaseous diffusion. Contusions of the lungs often constitute additional lesions. Atelectases cause an unequal alveolar ventilation/perfusion ratio. In addition, the alveolar surfactant preventing atelectasis may be altered by local hypoxia and the toxic products of metabolism. Transfer of oxygen across the pulmonary parenchyma is impaired, which increases detrimental shunt volume. Respiratory insufficiency, especially the extent of ventilation of the dead space, becomes of great prognostic significance in patients with haemorrhagic shock, irres-

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pective of additional injuries. If the clinical course is complicated by fat embolism, further parts of the lung may be underperfused although the ventilation is kept at a normal level. Eventually even the high pressures that are achieved by a mechanical ventilator may prove ineffective, and the patient succumbs with signs of right heart failure arising from pulmonary hypertension. In cases of severe haemorrhagic shock cerebral as well as pulmonary fat embolism may seriously affect the prognosis (Sevitt, 1962). This is observed clinically as a clouding of consciousness after a lucid interval. Irrespective of the organ affected, potentially lethal fat embolism always represents an epi-phenomenon of traumatic shock. The event comprises a strict interaction of three factors producing pathological effects: (i) trauma in combination with considerable contusion or injury to soft tissue or bone, together with compound lacerations leading to invasion of fat or marrow particles into veins; (ii) shock caused by loss of blood volume, which primarily alters the haematological balance of corpuscular and soluble components, leading to metabolic and respiratory acidosis; (iii) excessive clotting, which may be followed by disseminated intravascular coagulopathy. Therapeutic consequences Traumatic vascular fat invasion may not be preventable and no drugs are known to be effective against fat embolism. A few authors advocate treatment with stabilizers (phospholipids), which they believe reliably prevents a fatal outcome. Proof is similarly lacking for the claim that aprotinin (Trasylol) prevents fat embolism. The necessary clinical diagnostic evidence is often missing, and this should be confirmed by roentgenographic changes of the lungs, the natural history of the disease and a progressively deteriorating gas exchange. The introduction of any reliable test into the clinic would not even entail changes of treatment intended to restore the blood volume and treat the shock lung. One tries to improve the tissue perfusion by reducing the viscosity of blood with plasma substitutes, to correct metabolic and respiratory acidosis detected by blood gas analysis by infusing bicarbonate or THAM (trihydroxymethylaminomethane), and to replace fluid, depending on the urinary output and clinical biochemistry. Assisted or controlled ventilation may be life-saving, according to the experiences of the Tuebingen and other teams (Vogel, 1974). If a volume-deficient condition indicates generalized hypercoagulopathy, the patient is subjected to intravenous proteinase inhibitor treatment with Trasylol(2 x 106 i.u./24 h), which requires admission to hospital (Durst & Heller, 197 1). We found that this complication is apt to be present in all cases with fracture of the femur, severe trauma to the thorax and pelvis, and with injuries with a shock index of 1.0 or greater (Allgower, 1974). Bhimel et al. (1970) showed experimentally that Trasylol, a proteinase inhibitor, may reduce the extent of traumatically induced interstitial changes in the lungs. Lasch (1969) demonstrated an inhibition of hypercoagulopathy. On the other hand, heparin (25 000 i.u./24 h, infused intravenously) has to be considered as an ultimate remedy in lifethreatening shock where disseminated intravascular coagulation is haematologically evident. This treatment entails a high risk of bleeding into the fracture sites. Prevention and treatment of fat embolism eventually means a consequent treatment of the pathophysiological effects of shock during the clinical course of the disease. In recent years both the clinical and the forensic importance were often subject to misinterpretation (Sack & Wegener, 1968).

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AllgBwer, M. (1974) Der traumatisch-hiimorrhagische Schock. Chirurg. 45,103-106. Bergen& S. E. (1962) Studies on the genesis of posttraumatic fat embolism. Acfa Chir. Stand. Suppl. 282. Bltimel, G., Huth, K. & Lasch, H. G. (1970) Zur Beeinflussung der experimentellen Fettembolie mit Trasylol. Neue Aspekte der Trasylol-Therapie, 4, pp. 117-123. Schattauer, Stuttgart-New York: Bschor, F. & Haasch, K. (1963) Fluoreszensmikroskopische Untersuchungen an Venenblut bei traumatischer Fettembolie. Langenbacks Arch. Dtsch. Z. Chir. 302,408-422. Burkhardt, K. (1970) Untersuchungen zur Pathogenese der Fettembolie. Med. Welt. 21,1969-1976. Durst, J. & Helter, W. (1971) Prophylaxe und Therapie der posttraumatischen Fettembolie. Dtsch. med. Wschr. 96,210-212.

Durst, J., Knodel, W., Heller, W., Ehlers, Th. & Helmchen, U. (1973) Zur Lipasetheorie Krlinkes und ihrer Bedeutung ftir die Pathogenese der posttraumatischen Fettembolie. Mschr. Unfall-heilk. 76, 193-204. Hallgren, B., Kerstell, H., Rudenstam, C. M. & Svanborg, A. (1966) A method for the isolation and chemical analysis of pulmonary fat emboli. Acta Chir. Stand. 132,613-617. Kranke, E. (1956) Die Bedeutung der Lipase in der Pathogenese der traumatischen Fettembolie. Langenbecks

Arch. klin. Chir. 283,466-483.

Lasch, H. C. (1969) Schock, Hhinostase und Mikrozirkulation. Neue Aspekte der TrasyMTherapie, 3, pp. 3 l-36. Schattauer, Stuttgart-New York: Messmer, K. & Brendel, W. (1971) Pathophysiologische Aspekte des hypov?&mischen, kardiogenen und bakteriotoxischen Schocks. Med. Welt. 22,1159-l 164. Peltier, S. F. (1957) An appraisal of the problem of fat embolism. Surg. Gynec. Obstet. 104, 313-324. Sack, K. & Wegener, F. (1968) Artifizielle postmortale Fettembolie. ZbZ. allg. Path. Anat. 111, 24-31. Schtittemeyer, W. & Flach, A. (1950) Neue Untersuchungsmethode zur Diagnose der Fettembolie. Chirurg. 21,289-292. Sevitt, S. (1962) Fat Embolism, p.25, Butterworth, London. Swank, R. L., Seaman, G. V. F., Hissen, W. & Line, L. (1966) Physicochemical changes in blood induced by trauma. Surg. Gynec. Obstet. 121,251-259. Vogel, W. (1974) Die Bedeutung der disseminierten intravasalen Gerinnung in der terminalen Lungenstrombahn fiir die postoperative und posttraumatische respiratorische Insuffiiienz. Chirurg. 45,115-120.

Wehner, W. (1968) Die Fettembolie, p.28. Volk und Gesundheit, Berlin. Zenker, F. A. (1862) Beitrgge zur normalen und pathologischen Anatomie der Lunge. Cited by Sevitt, S. (1962) Fat Embolism, p.26. Butterworth, London.

The role of shock in the pathogenesis of fat embolism after trauma.

Experimental studies and pathological investigations indicate that intrusion of fat into the circulation is common after trauma. This may not have any...
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