Intravascular coagulation in a case of Clostridium perfringens septicaemia: treatment by exchange transfusion and heparin.

Abstract

Clostridium perftingens (Cl. welchii) infection following an abortion has always been associated with a very high mortality, often as great as 80% (Toombs and Michaelson, 1928 ;Hill, 1936;Russell and Roach, 1939; Butler, 1945). Although the use of antibiotics in addition to antitoxin might have been expected to reduce the death rate, the fatality rate recorded by Mahn and Dantuono (1955) differed little from that of previous reports. Immediate hysterectomy (Decker and Hall, 1966), hyperbaric oxygen (Brummelkamp et al., 1963 i McAllister et al., 1963Brummelkamp, 1965), and exchange transfusion (Bessis, 1949 ;Funck-Brentano et al., 1965) (1951). Fibrinogen catabolism was measured, using fibrinogen prepared by the method of Regoeczi and Walton (1967) and iodinated by the 13"I monochloride method of McFarlane (1963). The fractional catabolic rates of fibrinogen and the relative partition of the protein between the intravascular and the extravascular compartments were calculated by the method of Matthews (1957).Fibrin split products were assayed in the serum by agar-gel immunodiffusion (Ouchterlony, 1958) and by the tanned-redcell haemagglutination inhibition assay, using rabbit anti-human fibrinogen antiserum (Merskey et al., 1966 (Fig. 1).

Fibrinogen Catabolism in Microangiopathic Haemolytic Anaemia

“…The association of raised levels of serum fibrin split products and states of intravascular coagulation is documented (Mersky et al, 1966). Furthermore, in the case reported by Rubenberg, Baker, McBride, Sevitt and Brain (1967), an undoubted state of intravascular coagulation, which followed massive intravascular haemolysis due to Clostridium perfringens septicaemia, was associated with both an increase in the fractional catabolic rate of 1311-fibrinogen and the presence of high levels of fibrin split products in the serum.…”

Microangiopathic Haemolytic Anaemia: the Experimental Production of Haemolysis and Red‐Cell Fragmentation by Defibrination in Vivo

“…The conversion of fibrinogen to fibrin is the end result of intravascular coagulation from whatever cause, i.e. obstetrical defibrination (McKay, Merrill, Weiner, Hertig and Reid, 1953 ;Vassalli, Morris and McCluskey, 1963 ;Willoughby, 1966), the release of tissue thromboplastins from normal or tumour tissue (Godal and Abildgaard, 1963 ;Miller and Davison, 1967), as a result of antigen-antibody reactions (Gerber, 1936;Robbins and Stetson, 1959) and the release of red-cell thromboplastins from enzymatically damaged red blood cells (Rubenberg, Baker, McBride, Sevitt and Brain, 1968).…”

Intravascular coagulation

“…These reports include the use of heparin for purpura fulminans (Hjort, Rapaport & Jorgensen, 1964), the haemolyticuraemic syndrome (Moncrieff & Glasgow, 1970), Clostridium perfringens septicaemia (Rubenberg et al, 1967), and virus infections (McKay & Margaretten, 1967) Dennis et al (1967) of thirty-one patients with malaria due to drug-resistant strains of Plasmodium falciparum showed many with signs of intravascular coagulation due to haemolysis. Heparin combined with antimalarials gave a more rapid control of the infection than antimalarial drugs used alone.…”

“…These reports include the use of heparin for purpura fulminans (Hjort, Rapaport & Jorgensen, 1964), the haemolyticuraemic syndrome (Moncrieff & Glasgow, 1970), Clostridium perfringens septicaemia (Rubenberg et al, 1967), and virus infections (McKay & Margaretten, 1967) as well as the studies already referred to in acute hepatic necrosis. McGehee, Rapaport & Hjort (1967) carefully investigated nineteen patients with acute meningococcal infection.…”