Anaesth. Tntens. Care (l!176), 4, 53

THE FAT EMBOLISM SYNDROME, RESULTS OF A THERAPEUTIC REGIME A. B. BAKER* University of Queensland, Royal Brisbane Hospital, Brisbane SUMMARY

Results of a therapeutic regime for the fat embolism syndrome are presented. The basis of this regime is to prevent hypoxia by use of oxygen and if necessary intermittent positive pressure ventilation. Prophylactic oxygen therapy in patients likely to develop the fat embolism syndrome is suggested. The fat embolism syndrome has been variously defined clinically and scientifically and has been well reviewed by Ross (1970). At the Royal Brisbane Hospital this diagnosis has been applied to patients suffering from orthopaedic injuries, with chest X-ray evidence of pulmonary oedema, hypoxia whilst breathing air, and characteristic petechiae over the axillary, pectoral, infra-orbital and the sUb-conjunctival areas. Urine and sputum are not always inspected for fat globules as this is regarded as an unreliable test (Ross 1970). Treatment for this syndrome is varied and includes corticosteroids both low dosage (Ashbaugh and Petty 1966) and high dosage (Fischer et al. 1971), ethanol (Hermann 1932), heparin (Sage and Tudor 1958), Rheomacrodex (Evarts 1970) clofibrate (Cole 1971) and Trasylol (Morl1967). Recently, more emphasis has been placed on the prevention of hypoxia and the role of oxygen therapy (Cole 1974). Since ]969 in the Royal Brisbane Hospital, oxygen therapy with or without intermittent positive pressure ventilation (IPPV) has been the mainstay of therapy for the fat embolism syndrome together with correction of shock and fluid, electrolvte and acid-base disturbances. " METHODS

A retrospective survey was carried out for the years 1969-74 of all patients admitted to the

* Reader in Anaesthesia, Department of Surgery, University of Queensland. Address for reprints: Prof. A. B. Baker, Department of Anaesthesia, ·Cniversity of Otago, Dunedin, Kew Zealand.

Respiratory Unit, Royal Brisbane Hospital, with the fat embolism syndrome. These patients were referred when their orthopaedic surgeon entertained diagnosis of fat embolism either from clinical signs, X-ray evidence or blood gas results. The most common presenting sign was confusion or coma and this agrees with the findings of Ross (1970). TABLE

Patients with Fat Embolism Syndrome

Year 1969 1970 1971 19n

1973 1974

Number and Treatment 2 Trachy. + 1 E.T.T. -1 1 Trachy. + 3 E.T.T. + 4 No E.T.T. 1 Trachy. 3 E.T.T. + 2 Trachy. + 1 E.T.T. + 2 No E.T.T. 5 E.T.T. + 1 E.T.T. 3 No E.T.T. 1 Trachy. + 5 No E.T.T.

Vent. Vent. Vent. Vent.

Disorientated or Unconscious when Breathing Air

Died 1

2 1 1 1 3 1 3 2 1

-

1 1 -

Vent. Vent. '"ent.

3 -

Vent.

I

-

-

5 1 -

-

1

'"ent. -

1

-

Key: Trachy.=tracheostomy "ent. = mechanical ventilation E.T.T.=endotracheal tube

Whilst all patients were treated with external immobilization of fractures, only half of the patients had internal fixation of their fracture prior to the development of the fat embolism syndrome.

Anaesthesia and Intensive Care, Vol. IV, No. 1, February, 1970

54

A. B. RESCLTS

There \Vere :3;) patients of whom seven died. Tahle I shows the results broken down into separate years, and Tahle :2 shows those patients who died. Although it is well recognized (Cole J 9Uri) that the fat embolism syndrome may follow burns, soft tissue injury, septicaemia, diabetes and pancreatiti,.;, no case which could TABLE :! Deaths from Fat h'lIlbolis1I1 Syndlnme

I

!,

I

!

Suryival Tin1c Year, .\gc I Sex I' from Dia, gnosis ; I (])ays) I

I

I

iBIl!;-1-71- V!,---s---i I BiO

I I'

~,: 'l~I' 11

I

HOur:,' only

11

_ IIl71

:!:!

i F

I:! hours

I ,:!3

UlH

F

1\l

:\1

31

1\1

Hours only

Cause of Death Pneumonia and cardiac failure

PI~~~~l~~?~pathY and Pneumonia and cardiac failure Pncul11onopathyand hypoxia i'neul11onopathyand hypoxia Pncnlllonopathyand hypoxia PnculI1onopathyand hypoxia Liver and n'nal failure

be attributed to such causes has been recorded in the Respirator\' Cnit, I\m'al Brisbane Hospital, since it opened in 19:i(j, ' DISCl'SSIO,'\

It has been said; "it appears that early correction of hypoxaemia and the use of general re,.;piratory care prevent many people dying of rt'spiratory failure" (in the fat embolism ,.;~:ndrollle) (Cole HI7.!) but there are very fc\\' reporb of the sole use of oxygen in the therapy of fa t CIll boli";lll (Ledingham d ai, 1H7 .!), The largt' number of therapeutic regime,.; are noteworth\' for their diversity rather than their scientIfic appraisal. 1n fac:t, the only controllcd therapeutic trial in the fat embolisl11 s\'ndrome was Cl "tudy on clofibrate (Cole \!I 7 I ), 'and thi" ,.;howcd that the drug had no effect on the paticnt's course of illncss, Thc earlier that ox\'gcn therapy is instituted in the s\'nclrolllt', the hetter the ovcrall response, bccause: hypo.'\ia itself compounds capillary damage in the lungs, brain and heart, ,H the Ho\'al Brisbane lIospital, patient:; arc being gi\'en' ox\'gen earl\, in the orthopaedic wards prior to tra'lsfcr to th'e

BAKER

Respiratory l'nit. This early therapy with is thought to be the main factor in reduction of mortality, It is a strong clinical impression that whenever patients are diagnosed at a late stage or not treated with oxygen then the\' are more severe in their manifestation and tak-e longer to recover. The mortalit\' of the fat embolism syndrome has been quoted as low as 1 U per cent in ten unconscious patients (Ross HJ70) and as high as Kt) per cent in i57 unconscious patients (Sevitt HW2), In this series, seven patients died out of :22 severely disorientated or unconscious patients, However, this may be slightly misleading as with earlier diagnosis and oxygen therapy there may be fewer patients se\'erely affected, In the last three years of the series ] H72-7 -t, the death rate in 20 patients was 5 per cent, or 10 per cent of those severely disorientated or unconscious (1 0 patients)~on('e again suggesting that early diagno;ois and therapy have lessened the severity of the syndrome. \Vith treatment aimed at preventing hypoxia « ti() mm Hg arterial p(2) and maintaining fluid, electrolyte and acid-base balance, the overall mortality in a six year series with ;);) patients was 20 'per cent. '.rhe last three years of the series with 20 patients showed an overall mortality of 5 per cent and this reduction ma\' be due to earlier oxygen therapy. ~o steroids, heparin, Trasylol, Rheomacrodex or ethanol were given to patients in this series, because it is believed that there is no evidence that the\' provide a better prognosis and also because it Is belie\'ecl they all exhibit harmful side effects in the intensive care situation, Steroids wC'aken resistance to infection and predispose patients to gastrointestinal haemorrhage and tracheal fistulae; heparin predisposes to bleeding and may perhaps worsen the syndrome by rclea,.;e of free fatty acids; Trasylol bas been implicated in the production of pneull1onopathy' (Lcwi~ 197.!); Rheomacrodex has caused acute renal failure; and ethanol predisposes to cerebral clouding and excitability difficult to clistingui,.;h from the cerebral effects of the fat embolism s\'mlrome itself. Also, though most patients exhibited tliromboC\topenia and mild coagUlation defects tberap\' wa,.; never instituted, and in no ca"e \\'a,.; deatb thougbt to be due to disseminated intra\'a,.;cular coagUlation though it ha,.; lJt'en argued that the lung' pathol()gv is a manifestation of disseminated intravascular coagulation (Bradford et ai, I H70), The importance of fracture imlllobiliz~ltion is difficult to a,.;scs,.; as it is used in the gem'ral ()x~'gen

FAT

EMBOLISM

55

REFERENCES nursing management of the patient and for pain D. G., and Petty, T. L. (1966) : " The Use relief. Mobile fractures are thought to increase .'\shbaugh, of Corticosteroids in the Treatment of Respiratory the likelihood of fat embolism, but whether by Failure Associated with Massive Fat Embolism ", Surg. Gynec. Obstet., 123, 493. direct embolization or indirectly due to free D. S., Foster, R R, and Nossel, H. L. fatty acid release by increased catecholamines Bradford, (1970): "Coagulation Alterations, Hypoxaemia and Fat Embolism in Fracture Patients ", J. due to pain is unknown. Trauma, 10, 307. Although cerebral disturbance is very Cole, W. G. (1971) : "Clofibrate and Fat Embolism: common no specific therapy is thought necessary A Double Blind Trial of the Effects of Clofibrate on Sequelae to Injury", Brit. Med. j., 4, 148. for cerebral oedema. Steroids are specifically W. G. (1974): "Fat Embolism-A Current not used for this confusion state as their Cole,Concept ", Med. J. Aust., 1,535. usefulness in cerebral oedema is debated, they Cole, \V. R. (1965): "Traumatic Pulmonary Fat exhibit other adverse effects, and trial has shown Embolism", J. Coli. Radial. A ust., 9, 228. that the patients respond to the oxygen therapy. Evarts, L. 1\1. (1970) : " The Fat Embolism SyndromeA Review", Surg. Clin. N. Amel'., 50, 493. In fact there is no good evidence that cerebral Fischer, J. E., Turner, R. H., Herndon, J. H., and oedema occurs in this syndrome except after l{iseborough, E. J. (1971): "Massive Steroid Therapy in Severe Fat Embolism ", Surg. Gynec. long hypoxic episodes. Early treatment with Obstet., 132, 667. oxygen should thus markedly reduce the L. G. (1932) : " Effects of Dextrose-alcohol incidence of confusion states associated with the Hermann, Mixture upon Pulmonary Fat Embolism ", Proc. fat embolism syndrome. Soc. Exp. Bioi., 30, 558. I. McA., Mone, J. G., Finlay, \V. E. 1., These results and the reduction in mortality, Ledingham, and Kerr, J. W. (1974): "Treatment of Fat suggest the prophylactic use of oxygen by mask Embolism ", Scientific Abstracts, First World Congress on Intensive Care, p. 122. in patients thought to be at risk from the fat em bolism syndrome; that is, those patients Lewis, M. L. (1974): "Trasylol for Pancreatitis ", 1"led. j., 2, 741. with fractures particularly of femur and tibia ;\lorl,Brit. F. K. (1967): "Fcttembolic und Proteinasenbut also those with pelvic fractures (Ross 1970). hemmer ", Med. Welt., 35, 1997. Such therapy maintained for 48 hours may Ross, A. P. J. (1970) : "The Fat Embolism Syndrome: with special reference to the Importance of reduce the incidence of the fat embolism Hypoxia in the Syndrome ", Ann. Ray. Call. syndrome. Increased inspired oxygen can lead Surg. Engl., 46, 159. to oxygen toxicity but it is suggested that the Sage, R H., and Tudor, R. \V. (1958) : " Treatment of Fat Embolism with Heparin ", Brit. NIed. j., 1. inspired level be kept to 30-40 per cent so that 1160. the arterial p02 is not above 200 mm Hg. Such Sevitt, S. (1962): Fat Embolism. Butterworths: a level has not been known to cause pulmonary London. oxygen toxicity at normal pressures (Winter Winter, P. M., and Smith, G. (1972) : " The Toxicity of Oxygen ", Anesthesiology, 37, 210. and Smith 1972).

A l1aestizesia and In/ensivl' Care, Vol. IV, iVu. 1, February, 1I171j