Paediatrica Indonesiana 15 : 239 — 246. Sept. — Qkt. 1975. 239 From, the Department of Child Health, Sumber Waras Hospital, University of Tarumanegara, Jakarta, Ihdoinesia Disseminated Intravascular Coagulation in Gastroenteritis by 8. SETIADHARMA and T. HIMAWAN Abstract Four children, 3 males and 1 female, varying in ages from 3 to 12 years, showing the shock syndrome in gastroenteritis accompanied by in­ travascular coagulation (DIC) are reported. A ll patients developed pro­ gressive thrombocytopema, prolonged prothrombin time as well ¡as par­ tial thromboplastin time; and a decreased content of fibrinogen in the Mood several days after hospitalization was observed. The diagnosis and treatment of DIC are also discussed. Received 30th. Nov. 1974. 240 S. SETIADARMA AND T. HIMAWAN Introduction Report of cases A n y severely ill child may develop Four children, comprising 3 males the complication of disseminated in­ and 1 female, whose ages ranged travascular coagulation (DIC). DIC from 3 to 12 years, were studied. processes may occur mostly in chil­ They were transferred to the Depar­ dren with shock, haemorrhagic, sep­ tment of Child Health of Sumber tic as well as anaphylactic and burns Waras Hospital, Jakarta, due to fe­ (Hardaway, 1966). In certain condi­ ver, diarrhoea, vomiting and abdomi­ tions of bacterial or viral infections nal pain of several days duration. (McKay and Margaretten, 1967), in A ll patients were severely ill on ad­ premature newborns suffering from mission and had some degree of cir­ respiratory distress syndrome — culatory failure (cold extremities, RDS — (Swyer, 1971; Weissbach et excessive transpirations, reduced al., 1973), and in many other patho­ systolic and diastolic pressures) and logical circumstances which have dehydration. No neurological abnor­ been extensively reviewed by Abil- malities were noted on admission. dgaard (1969), Karpatkin (1971), Torniquet test was applied to all pa­ McKay (1965),, and Rodriquez-Er- tients. The following coagulation dmann (1965), this pathological in­ studies were performed: platelet travascular clotting mechanism was count, prothrombin time according noted; in typhoid fever DIC is not to the one-stage method of Lynch uncommon (Setiadharma and Kho, (1989), fibrinogen concent,ration of 1973). the iblood according to the method of Stirland (1956), the clotting time Four patients, 3 males and 1 fe ­ according to the method of Lee and male, varying in ages from 3 to 12 White (1913), and the bleeding time years, showing the shock syndrome done by the method of Duke (Owen, in gastroenteritis aeeompained by 1969). DIC are reported. A ll patients had All patients were treated with some degree of circulatory failure antibiotics parenterally followed by with developing thrombocytopenia, oral administration: Pat. 1 with am- prolonged prothrombin time as well piciilin 50 mg./kg. body weight daily; chloramphenicol 50 mg./kg. body as partial thromboplastin time, and weight daily given to Pats. 2 and 4; a decreased content of fibrinogen in Pat. 3 with tetracycline 40 mg./kg. the blood several days after hospi­ body weight daily. The treatment of talization. These are valuable mea­ shock was intensively carried out by sure for detecting DIC. infusion of Ringer’s lactate solution, D.I.C. IN GASTROENTERITIS 241 plasma "volume expanders, and blood all patients except one (Pat. 1). Fecal transfusion (to Pats. 1 and 3), besi­ culture revealed Vibrio Eltor positi­ des the commonly used saline, glu­ ve in Pat. 3, and Salmonella typhosa cose, and electrolytes solutions. Cor­ was confirmed positive in the blood ticosteroids were administered to 3 of Pat. 4. patients: Celestone was given intra­ Hospital course: * Patient 1 died on venously in a dosage of 0.25 mg./kg. the 6th day of hospitalization after body weight daily; heparin 1 mg./ one d!ay of heparinization; probable kg. ¡body weight intravenously was cause of death was profuse bleeding given to Pats. 1 and 2 every 4 hours as indicated by the fall of the hemo­ for 2 and 8 days, respectively. globin content of 11 gm. % on admis­ Tables 1 and 2 showed the clinical sion to 6.5 gm% on the 5th day of features, therapy and laboratory hospitalization, although blood trans­ examinations respectively of the pa­ fusion had been given. tients on admission and during hos­ * In Pat. 2 (female, 3 years old) the pitalization. A ll patients showed a fibrinogen content was still low (84 significant drop of platelets several mg. %) after heparin administration, days after hospitalization (Table 3). although the blood platelet count and The partial thromboplastin time of prothrombin time were increasing, 3 patients showed a prolongation respectively 336,000 per cu.mm. and several days after admission; in Pat. 64%. This patients died on the 14th 3 it was already prolonged on the day of hospitalization. first day of hospitalization (56 se­ conds). The fibrinogen content of * Patient 3 (male, 12 years old) with the blood was determined based positive Eltor in the fecal culture upon the probability of intravascu­ showed a significant drop of platelet lar clotting (Table 4). The clotting count (19,020 per cu.mm.) on the time varied from 7 to more than 15 4th day of hospitalization. Heparin minutes in 3 patients, while in Pat. was not yet administered as the pa­ 2 it was not measured. The bleeding tient died due to irreversible circular time was abnormal in Pats. 1 and 4 tory failure on the day when DIC (more than 15 minutes), in Pat. 3 was detected. it was 5 minutes on admission, while * Patient 4 (male, 8 years old), con­ Pat. 2 showed a normal value (2’30” ) firmed typhoid fever by blood cul­ on the 4th day of hospitalization. ture, did show thrombocytopenia of Haematemesis and melaena were 78,000 cu.mm. on admission and a in Pats. 1 and 3 ; haematomas on the progressive reduction of 36,000 blood sites of injections were noted in Pat. platelets/cu.mm. on the 2nd day of 1. Torniquet tests were negative in hospitalization, Hypofibrinogenaemia 242 S. SETIADARMA AND T. HIMAWAN of 44 m g.% on the 2nd. day after ad­ red and fragmented red blood cells, mission was noted. Both bleeding possibly caused by the passing of the and clotting time were prolonged erythrocytes through the meshes of (more than 15 minutes). The patient intravascular fibrin (Rudenberg et did not show any signs of bleeding ah, 1968). Blood clotting defects may on the skin. The Rumpel-Leede test be deficiency of multiple coagulation was negative. Celestone was added factors (factors n, V, VIII, IX, X, to the intravenous fluid and electro­ X I). These factors may become re­ lytes administration. Heparinization duced to levels inadequate for hae­ was not performed in this case. The mostasis because they are being used patient recovered after 16 days of up more rapidly than they can be pro­ hospitalization. duced. Discussion Disseminated intravascular coa­ gulation may (develop 'in any se­ The patients presented were in verely M child, mostly in those shock: reduced systolic and diasto­ Showing the shock syndrome. :The lic blood pressures, cold extremities, recognition pf DIC process is ve­ and excessive transpiration. DIC ry important as ¡an early success­ was diagnosed on the following cri­ ful diagnosis and treatment Ito teria: Shock aceompained by a sud­ prevent death, although the morta­ den drop of previously normal blood lity rate still remains high. The platelet count (McKay, 1965), pro­ authors are convinced of the impor­ longed prothrombin and partial th­ tant role of shock as a trigger me­ romboplastin time, reduced fibrino­ chanism in the development of DIC gen level in the blood, and alterations as intravascular clotting is frequen­ of the red blood cells. These are tly associated with endotoxin shock. valuable measures for the early de­ Experimentally, according to Mason tection of DIC. et all (1970), endotoxin has been Other coagulation studies (Bratic- shown to activate Hageman factor Mikes and Miikes, 1973) and the (factor XIH, also called the fibrin presence of fibrin split products stabilizing enzyme) and destroy pla­ (FSP) are found to be non-reliable telets (Cohen et ah, 1965). Weil and indicators, as this latter matter is Shubin (1967) stated that the me­ also found in other circumstances chanism of endotoxin shock was a without the occurence of DIC, e.g. reaction in the plasma o f a sensitized in renal and hepatic disorders, th­ antigen with an antibody and a bac­ rombotic thrombocytic purpura (Ha­ terial endotoxin, resulting in the pro­ thaway, 1970). Peripheral blood duction of histamin, slow reactive smear examinations may show bur­ substance A, and bradykinin. These - D.I.C. IN GASTROENTERITIS 243 substances will lead to arteriolar di­ but it must (be given as early as pos­ latation, venular constriction, in­ sible. Corrigan and Jordan (1970) creased capillary permeability, and showed that heparinization may cor­ consequently arterial hypotension. rect. the coagulation abnormalities oc- Decreased cardiac output accompa­ curing in DIC, but the mortality rate nied by simultaneous opening of all still remains high for patients with capillaries at one time results in ex­ the shock syndrome. The control of tremely slow capillary blood flow. DIC does not. increase survival, and This slow blood flow results in hy- it seems that heparin may not be poxaemia and enhances lactic acid the most important factor in aboli­ formation resulting in acidosis. As shing intravascular clotting. The role slow circulating acid blood is hyper- of heparin therapy in treating this coaguable (Hardaway et al., 1962), condition awaits further studies. there will be a vicious cycle of shock In conclusion, the following sug­ and the development of intravascular gestions to the severely ill patients clotting defects. with the shock syndrome can be re­ Hypofibrinogenaemia, frequently commended : found in DIC (McKay, 1965), was 1. estimation of thrombocytes and, noted in our patients.