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. S E T I A D H A R M A and T. H I M A W A N
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 tim e; 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 the complication of disseminated in travascular coagulation (D IC ). DIC processes may occur mostly in chil dren with shock, haemorrhagic, sep tic as well as anaphylactic and burns (Hardaway, 1966). In certain condi tions of bacterial or viral infections (M cKay and Margaretten, 1967), in premature newborns suffering from respiratory distress syndrome — RDS — (Swyer, 1971; Weissbach et al., 1973), and in many other patho logical circumstances which have been extensively reviewed by Abildgaard (1969), Karpatkin (1971), M cKay (1965),, and Rodriquez-Erdmann (1965), this pathological in travascular clotting mechanism was noted; in typhoid fever DIC is not uncommon (Setiadharma and Kho, 1973).
Four children, comprising 3 males and 1 female, whose ages ranged from 3 to 12 years, w ere studied. They were transferred to the Depar tment of Child Health o f Sumber Waras Hospital, Jakarta, due to fe ver, diarrhoea, vomiting and abdomi nal pain of several days duration. A ll patients were severely ill on ad mission and had some degree of cir culatory failure (cold extremities, excessive transpirations, reduced systolic and diastolic pressures) and dehydration. N o neurological abnor malities were noted on admission. Torniquet test was applied to all pa tients. The following coagulation studies were perform ed: platelet count, prothrombin time according to the one-stage method o f Lynch (1989), fibrinogen concent,ration of the iblood according to the method of Stirland (1956), the clotting time according to the method o f Lee and White (1913), and the bleeding time done by the method of Duke (Owen, 1969).
Four patients, 3 males and 1 fe male, varying in ages from 3 to 12 years, showing the shock syndrome in gastroenteritis aeeompained by DIC are reported. A ll patients had some degree of circulatory failure with
developing thrombocytopenia,
prolonged prothrombin time as well as partial thromboplastin time, and a decreased content of fibrinogen in the blood several days after hospi talization. These are valuable mea sure fo r detecting DIC.
A ll patients were treated with antibiotics parenterally followed by oral administration: Pat. 1 with ampiciilin 50 mg./kg. body weight d aily; chloramphenicol 50 mg./kg. body weight daily given to Pats. 2 and 4; Pat. 3 with tetracycline 40 mg./kg. body weight daily. The treatment of shock was intensively carried out by infusion of Ringer’s lactate solution,
D.I.C. IN GASTROENTERITIS
plasma "volume expanders, and blood transfusion (to Pats. 1 and 3), besi des the commonly used saline, glu cose, and electrolytes solutions. Cor ticosteroids were administered to 3 patients: Celestone was given intra venously in a dosage of 0.25 mg./kg. body weight daily; heparin 1 mg./ kg. ¡body weight intravenously was given to Pats. 1 and 2 every 4 hours for 2 and 8 days, respectively. Tables 1 and 2 showed the clinical features, therapy and laboratory examinations respectively of the pa tients on admission and during hos pitalization. A ll patients showed a significant drop of platelets several days after hospitalization (Table 3). The partial thromboplastin time of 3 patients showed a prolongation several days after admission; in Pat. 3 it was already prolonged on the first day of hospitalization (56 se conds). The fibrinogen content of the blood was determined based upon the probability of intravascu lar clotting (Table 4). The clotting time varied from 7 to more than 15 minutes in 3 patients, while in Pat. 2 it was not measured. The bleeding time was abnormal in Pats. 1 and 4 (more than 15 minutes), in Pat. 3 it was 5 minutes on admission, while Pat. 2 showed a normal value (2’30” ) on the 4th day of hospitalization. Haematemesis and melaena were in Pats. 1 and 3 ; haematomas on the sites of injections were noted in Pat. 1. Torniquet tests were negative in
241
all patients except one (Pat. 1). Fecal culture revealed Vibrio E ltor positi ve in Pat. 3, and Salmonella typhosa was confirmed positive in the blood of Pat. 4. Hospital course: * Patient 1 died on the 6th day o f hospitalization after one d!ay of heparinization; probable cause o f death was profuse bleeding as indicated by the fall o f the hemo globin content of 11 gm. % on admis sion to 6.5 gm% on the 5th day of hospitalization, although blood trans fusion had been given. * In Pat. 2 (female, 3 years old) the fibrinogen content was still low (84 mg. % ) after heparin administration, although the blood platelet count and prothrombin time were increasing, respectively 336,000 per cu.mm. and 64%. This patients died on the 14th day of hospitalization. * Patient 3 (male, 12 years old) with positive Eltor in the fecal culture showed a significant drop o f platelet count (19,020 per cu.mm.) on the 4th day o f hospitalization. Heparin was not yet administered as the pa tient died due to irreversible circular tory failure on the day when DIC was detected. * Patient 4 (male, 8 years old), con firmed typhoid fever by blood cul ture, did show thrombocytopenia of 78,000 cu.mm. on admission and a progressive reduction of 36,000 blood platelets/cu.mm. on the 2nd day of hospitalization, Hypofibrinogenaemia
242
S. SETIADARMA AND T. HIMAWAN
of 44 m g.% on the 2nd. day after ad mission was noted. Both bleeding and clotting time were prolonged (more than 15 minutes). The patient did not show any signs of bleeding on the skin. The Rumpel-Leede test was negative. Celestone was added to the intravenous fluid and electro lytes administration. Heparinization was not performed in this case. The patient recovered after 16 days of hospitalization.
red and fragmented red blood cells, possibly caused by the passing of the erythrocytes through the meshes of intravascular fibrin (Rudenberg et ah, 1968). Blood clotting defects may be deficiency of multiple coagulation factors (factors n, V, V III, IX, X, X I). These factors m ay become re duced to levels inadequate for hae mostasis because they are being used up more rapidly than they can be pro duced.
Discussion
Disseminated intravascular coa gulation may (develop 'in any se verely M child, mostly in those Showing the shock syndrome. :T he recognition p f DIC process is ve ry important as ¡an early success ful diagnosis and treatment Ito prevent death, although the morta lity rate still remains high. The authors are convinced o f the impor tant role of shock as a trigger me chanism in the development o f DIC as intravascular clotting is frequen tly associated with endotoxin shock. Experimentally, according to Mason et all (1970), endotoxin has been shown to activate Hageman factor (factor X IH , also called the fibrin stabilizing enzyme) and destroy pla telets (Cohen et ah, 1965). Weil and Shubin (1967) stated that the me chanism of endotoxin shock was a reaction in the plasma o f a sensitized antigen with an antibody and a bac terial endotoxin, resulting in the pro duction o f histamin, slow reactive substance A, and bradykinin. These -
The patients presented were in shock: reduced systolic and diasto lic blood pressures, cold extremities, and excessive transpiration. DIC was diagnosed on the following cri teria: Shock aceompained by a sud den drop o f previously normal blood platelet count (McKay, 1965), pro longed prothrombin and partial th romboplastin time, reduced fibrino gen level in the blood, and alterations o f the red blood cells. These are valuable measures fo r the early de tection of DIC. Other coagulation studies (BraticMikes and Miikes, 1973) and the presence of fibrin split products (F S P ) are found to be non-reliable indicators, as this latter matter is also found in other circumstances without the occurence of DIC, e.g. in renal and hepatic disorders, th rombotic thrombocytic purpura (H a thaway, 1970). Peripheral blood smear examinations may show bur
D.I.C. IN GASTROENTERITIS
substances w ill lead to arteriolar di latation, venular constriction, in creased capillary permeability, and consequently arterial hypotension. Decreased cardiac output accompa nied by simultaneous opening of all capillaries at one time results in ex tremely slow capillary blood flow. This slow blood flow results in hypoxaemia and enhances lactic acid formation resulting in acidosis. As slow circulating acid blood is hypercoaguable (Hardaway et al., 1962), there w ill be a vicious cycle of shock and the development of intravascular clotting defects. Hypofibrinogenaemia, frequently found in DIC (McKay, 1965), was noted in our patients. The most im portant management is the adminis tration of proper antibiotics for the underlying diseases (Karpatkin, 1971), and the treatment of shock. Corticosteroids have played an im portant role in the management of shock in general, especially in endo toxin shock. Abildgaard (1969) sug gested that corticosteroids should be added to the treatment of the shock syndrome, especially if heparin was given. Heparin may be a useful thera peutic agent in the treatment, o f DIC,
243
but it must (be given as early as pos sible. Corrigan and Jordan (1970) showed that heparinization may cor rect. the coagulation abnormalities occuring in DIC, but the mortality rate still remains high for patients with the shock syndrome. The control of DIC does not. increase survival, and it seems that heparin may not be the most important factor in aboli shing intravascular clotting. The role of heparin therapy in treating this condition awaits further studies. In conclusion, the following sug gestions to the severely ill patients with the shock syndrome can be re commended : 1. estimation of thrombocytes and, if possible, coagulation factors ; 2. treatment of shook with adequate fluids and electrolytes intrave nously, plasma volume expanders, and/or blood transfusions; 3. vasoactive agents such as E ffortil; 4. administration of corticosteroids in high doses; 5. heparin 1 mg./kg. body weight intravenously every 4 hours ; and, 6. proper antibiotic therapy fo r the underlying disease.
S. SETIADARMA AND T. HIMAWAN
244 T A B I jB 1 :
Climcai features and therapy of Gastroenteritis with D IO .
BS.
Blood pressure
|
90/70
¡os.
u.
SA.
90/00
90/30
90/60
Fever
4*
+
4"
+
Vomiting
4*
—
+
—
Diarrhoea
4*
+
+
+
Abdominal pain
+
—
4-
+
Haematemesis
+
‘
—
+
—
Melaana
+
■ —
+
—
Haematoma
+
—
—
—
Petechia©
—
— -
—
—
Rumpel-Leede
+
—
—
—
Corticosteroids
+
—
+
+
Heparim
4-
+
—
—
Antibiotics
+
+
+
+
Died
+
+
+
__
TABLE 2 :
Peripheral Mood examinaticms, fecal and blood cultures of patients with D IC in Gastroenteritis.
A g e (in years) Haemoglobin (g m .% ) Haematocrit (vol.% ) W.B.C./cu.mm. Cultures: Fecal Blood
BS.
OS.
4 11 36 4,300
3 12 42 7,000
— -
—
—
—
U.
12 16.5 42 21,000
V. Eltor —
SA.
8 11.8 35 4,500
—
S. Typhosa
D.X.C. IN GASTROENTERITIS
TABLE 3 :
Patients
245
Thrombocytopenia, in patients with Gastroenteritis with DIC.
Number of platelets/cu. mm. on admission
after admission
occurence in days after admission
1.
BS
156,000
4,000
3
2.
OS
156,000
96,000
3
3.
U
300,000
19,000
4
4.
SA
78,000
36,000
2
TABLE 4 :
Hypofibrinogenaemia in Gastroenteritis with DIO.
Fibrinogen concentration in mg. % Patients on admission
after admission
occurence in days after admission
1.
BS
not done
1Í8
3
2.
OS
not done
95
4
3.
U
84
10
13
4
44
2
4.
SA
472 not done
REFERENCES 1. A B IL D G A A R D , C.F.: Recognition, and treatment of intravascular coagulation. J. Pediatr., 74 : 164 (1969). 2. B R A T IC -M IK E S, V. and M IK ES, A.: Laboratory screening for Disseminated Intravascular Coagulation. Abstract Se cond Haematol. Meeting, Vienna, p. 277 (1973). 3. C O H E N , P. B R A U N W A L D , J. and G A R D N E R , F.H.: Destruction of canim and rabbit platelets following intrave nous administration of carbon particles endotoxin, J. Lab. clin. Med. 66 : 263
(1965), cited from (1973).
GERARD
et al.
4. C O R R IG AN, J.J. and JORDAN, C.M.: Heparin therapy in septicemia with dis seminated intravascular coagulation N. Engl. J. Med. 283 : (1970). 5. GER AR D , P.: J. Pediatr. 82 : 780 (1973).
purpura.
6. H A R D A W A Y , R.M.: Syndromes of Dis seminated Intravascular Coagulation, (Thomas, Springfield, HI. 1966). 7. H A R D A W A Y , R.M. et al.: Studies on the role of intravascular coagulation in
S. SETIADARMA AND T. HIMAWAN
246
blood coagulation: haemorrhagic syn dromes caused by consumption of blood-clotting factors (consumption coagulopathies). N . Eng. j . Med. 273 •. 1370 (1965).
irreversible hemorrhagic shock. Ann. Surg. 155 : 241 (1962). 8.
H A T H A W A Y , W .E .: Care of the cri tically ill child: the problem of Disse minated intravascular Coagulation, Pediatrics 5 : 771 (1970).
10. DEE, R.I. and W H IT E , P.D.: A clinical study of the coagulation time of blood. A m . J. Med. Sci. 145 : 495 (1913). 11. U Y N C H , M.J.: Medical Daboratory Technology and) Clinical Pathology (Saunders, Philadelphia 1969). 12. M ASO N , J.W. jKDEEBERG, U.; DOD A N , R. and OODMAN, R. W .: Plasma kalllikfeim and Hageman factor in Gram-negative bacteria. Ann. intern. Med. 73 : 545 (19701).
18. R U B E N B E R G , M.D. et a l.: Microangi opathic haemolytic anaemia: the expe rimental production of haemolysis and red-cell fragmentation by defibrination in !vivo. Brit. J. Haematol. 14 : 627 (1968). 19. S E T IA D H A R M A , S. and KHO, D.K.: Disseminated intravascular coagulation in typhoid fever in childhood. South east Asian J. trop. Med. Publ. Hlth. 4 : 461 (1973). 20.
STIR D AND , R.M.: A rapid method of estimating fibrinogen. Dancet 672 (1965).
21.
S W Y E R , P.R.: The clinical features and management of the seriously ill newborn, in JO N ES and O W E N -TH O M A S ’ Care of the critically ill child, p. 198 (Arnold, Dondon 1971).
13. M cK A Y, D.G.: Disseminated Intrava scular Coagulation; an intermediary mechanism of disease. (Hoeber, N ew • Y ork 1965). 14. M cK AY, D.G. and M A R G A R E T T E N , W .: Disseminated intravascular coagu lation in viral diseases. Arch, intern. Med. 120 : 129 (1967). 15. O W E N , C.A. et al.: The Diagnosis of Bleeding Disorders ( Churchill, Dondon 1969).
22. W E ID , MH. and S H U B IN , H.: D iag nosis and treatment of shock (Williams and Wilkins, Baltimore 1967).
16. QUICK, A .J.: Determination of proth rombin. Am. J. Med. Sci. 190 : 501 (1935).
23. W E IS S B A C H , G. et al.: Fibrinolysis and consumption coagulopathy in new borns with respiratory distress syndro me (R D S ). Abstracts Second Haema tol. Meeting, Vienna, p. 267 (1973).
17. R O D R IQ U E Z -E R D M A N N , F.: Bleed ing due to increased intravascular
239
From, the Department of Child Health, Sumber Waras Hospital, University of Tarumanegara, Jakarta, Ihdoinesia
Disseminated Intravascular Coagulation in Gastroenteritis
by
8. S E T I A D H A R M A and T. H I M A W A N
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 tim e; 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 the complication of disseminated in travascular coagulation (D IC ). DIC processes may occur mostly in chil dren with shock, haemorrhagic, sep tic as well as anaphylactic and burns (Hardaway, 1966). In certain condi tions of bacterial or viral infections (M cKay and Margaretten, 1967), in premature newborns suffering from respiratory distress syndrome — RDS — (Swyer, 1971; Weissbach et al., 1973), and in many other patho logical circumstances which have been extensively reviewed by Abildgaard (1969), Karpatkin (1971), M cKay (1965),, and Rodriquez-Erdmann (1965), this pathological in travascular clotting mechanism was noted; in typhoid fever DIC is not uncommon (Setiadharma and Kho, 1973).
Four children, comprising 3 males and 1 female, whose ages ranged from 3 to 12 years, w ere studied. They were transferred to the Depar tment of Child Health o f Sumber Waras Hospital, Jakarta, due to fe ver, diarrhoea, vomiting and abdomi nal pain of several days duration. A ll patients were severely ill on ad mission and had some degree of cir culatory failure (cold extremities, excessive transpirations, reduced systolic and diastolic pressures) and dehydration. N o neurological abnor malities were noted on admission. Torniquet test was applied to all pa tients. The following coagulation studies were perform ed: platelet count, prothrombin time according to the one-stage method o f Lynch (1989), fibrinogen concent,ration of the iblood according to the method of Stirland (1956), the clotting time according to the method o f Lee and White (1913), and the bleeding time done by the method of Duke (Owen, 1969).
Four patients, 3 males and 1 fe male, varying in ages from 3 to 12 years, showing the shock syndrome in gastroenteritis aeeompained by DIC are reported. A ll patients had some degree of circulatory failure with
developing thrombocytopenia,
prolonged prothrombin time as well as partial thromboplastin time, and a decreased content of fibrinogen in the blood several days after hospi talization. These are valuable mea sure fo r detecting DIC.
A ll patients were treated with antibiotics parenterally followed by oral administration: Pat. 1 with ampiciilin 50 mg./kg. body weight d aily; chloramphenicol 50 mg./kg. body weight daily given to Pats. 2 and 4; Pat. 3 with tetracycline 40 mg./kg. body weight daily. The treatment of shock was intensively carried out by infusion of Ringer’s lactate solution,
D.I.C. IN GASTROENTERITIS
plasma "volume expanders, and blood transfusion (to Pats. 1 and 3), besi des the commonly used saline, glu cose, and electrolytes solutions. Cor ticosteroids were administered to 3 patients: Celestone was given intra venously in a dosage of 0.25 mg./kg. body weight daily; heparin 1 mg./ kg. ¡body weight intravenously was given to Pats. 1 and 2 every 4 hours for 2 and 8 days, respectively. Tables 1 and 2 showed the clinical features, therapy and laboratory examinations respectively of the pa tients on admission and during hos pitalization. A ll patients showed a significant drop of platelets several days after hospitalization (Table 3). The partial thromboplastin time of 3 patients showed a prolongation several days after admission; in Pat. 3 it was already prolonged on the first day of hospitalization (56 se conds). The fibrinogen content of the blood was determined based upon the probability of intravascu lar clotting (Table 4). The clotting time varied from 7 to more than 15 minutes in 3 patients, while in Pat. 2 it was not measured. The bleeding time was abnormal in Pats. 1 and 4 (more than 15 minutes), in Pat. 3 it was 5 minutes on admission, while Pat. 2 showed a normal value (2’30” ) on the 4th day of hospitalization. Haematemesis and melaena were in Pats. 1 and 3 ; haematomas on the sites of injections were noted in Pat. 1. Torniquet tests were negative in
241
all patients except one (Pat. 1). Fecal culture revealed Vibrio E ltor positi ve in Pat. 3, and Salmonella typhosa was confirmed positive in the blood of Pat. 4. Hospital course: * Patient 1 died on the 6th day o f hospitalization after one d!ay of heparinization; probable cause o f death was profuse bleeding as indicated by the fall o f the hemo globin content of 11 gm. % on admis sion to 6.5 gm% on the 5th day of hospitalization, although blood trans fusion had been given. * In Pat. 2 (female, 3 years old) the fibrinogen content was still low (84 mg. % ) after heparin administration, although the blood platelet count and prothrombin time were increasing, respectively 336,000 per cu.mm. and 64%. This patients died on the 14th day of hospitalization. * Patient 3 (male, 12 years old) with positive Eltor in the fecal culture showed a significant drop o f platelet count (19,020 per cu.mm.) on the 4th day o f hospitalization. Heparin was not yet administered as the pa tient died due to irreversible circular tory failure on the day when DIC was detected. * Patient 4 (male, 8 years old), con firmed typhoid fever by blood cul ture, did show thrombocytopenia of 78,000 cu.mm. on admission and a progressive reduction of 36,000 blood platelets/cu.mm. on the 2nd day of hospitalization, Hypofibrinogenaemia
242
S. SETIADARMA AND T. HIMAWAN
of 44 m g.% on the 2nd. day after ad mission was noted. Both bleeding and clotting time were prolonged (more than 15 minutes). The patient did not show any signs of bleeding on the skin. The Rumpel-Leede test was negative. Celestone was added to the intravenous fluid and electro lytes administration. Heparinization was not performed in this case. The patient recovered after 16 days of hospitalization.
red and fragmented red blood cells, possibly caused by the passing of the erythrocytes through the meshes of intravascular fibrin (Rudenberg et ah, 1968). Blood clotting defects may be deficiency of multiple coagulation factors (factors n, V, V III, IX, X, X I). These factors m ay become re duced to levels inadequate for hae mostasis because they are being used up more rapidly than they can be pro duced.
Discussion
Disseminated intravascular coa gulation may (develop 'in any se verely M child, mostly in those Showing the shock syndrome. :T he recognition p f DIC process is ve ry important as ¡an early success ful diagnosis and treatment Ito prevent death, although the morta lity rate still remains high. The authors are convinced o f the impor tant role of shock as a trigger me chanism in the development o f DIC as intravascular clotting is frequen tly associated with endotoxin shock. Experimentally, according to Mason et all (1970), endotoxin has been shown to activate Hageman factor (factor X IH , also called the fibrin stabilizing enzyme) and destroy pla telets (Cohen et ah, 1965). Weil and Shubin (1967) stated that the me chanism of endotoxin shock was a reaction in the plasma o f a sensitized antigen with an antibody and a bac terial endotoxin, resulting in the pro duction o f histamin, slow reactive substance A, and bradykinin. These -
The patients presented were in shock: reduced systolic and diasto lic blood pressures, cold extremities, and excessive transpiration. DIC was diagnosed on the following cri teria: Shock aceompained by a sud den drop o f previously normal blood platelet count (McKay, 1965), pro longed prothrombin and partial th romboplastin time, reduced fibrino gen level in the blood, and alterations o f the red blood cells. These are valuable measures fo r the early de tection of DIC. Other coagulation studies (BraticMikes and Miikes, 1973) and the presence of fibrin split products (F S P ) are found to be non-reliable indicators, as this latter matter is also found in other circumstances without the occurence of DIC, e.g. in renal and hepatic disorders, th rombotic thrombocytic purpura (H a thaway, 1970). Peripheral blood smear examinations may show bur
D.I.C. IN GASTROENTERITIS
substances w ill lead to arteriolar di latation, venular constriction, in creased capillary permeability, and consequently arterial hypotension. Decreased cardiac output accompa nied by simultaneous opening of all capillaries at one time results in ex tremely slow capillary blood flow. This slow blood flow results in hypoxaemia and enhances lactic acid formation resulting in acidosis. As slow circulating acid blood is hypercoaguable (Hardaway et al., 1962), there w ill be a vicious cycle of shock and the development of intravascular clotting defects. Hypofibrinogenaemia, frequently found in DIC (McKay, 1965), was noted in our patients. The most im portant management is the adminis tration of proper antibiotics for the underlying diseases (Karpatkin, 1971), and the treatment of shock. Corticosteroids have played an im portant role in the management of shock in general, especially in endo toxin shock. Abildgaard (1969) sug gested that corticosteroids should be added to the treatment of the shock syndrome, especially if heparin was given. Heparin may be a useful thera peutic agent in the treatment, o f DIC,
243
but it must (be given as early as pos sible. Corrigan and Jordan (1970) showed that heparinization may cor rect. the coagulation abnormalities occuring in DIC, but the mortality rate still remains high for patients with the shock syndrome. The control of DIC does not. increase survival, and it seems that heparin may not be the most important factor in aboli shing intravascular clotting. The role of heparin therapy in treating this condition awaits further studies. In conclusion, the following sug gestions to the severely ill patients with the shock syndrome can be re commended : 1. estimation of thrombocytes and, if possible, coagulation factors ; 2. treatment of shook with adequate fluids and electrolytes intrave nously, plasma volume expanders, and/or blood transfusions; 3. vasoactive agents such as E ffortil; 4. administration of corticosteroids in high doses; 5. heparin 1 mg./kg. body weight intravenously every 4 hours ; and, 6. proper antibiotic therapy fo r the underlying disease.
S. SETIADARMA AND T. HIMAWAN
244 T A B I jB 1 :
Climcai features and therapy of Gastroenteritis with D IO .
BS.
Blood pressure
|
90/70
¡os.
u.
SA.
90/00
90/30
90/60
Fever
4*
+
4"
+
Vomiting
4*
—
+
—
Diarrhoea
4*
+
+
+
Abdominal pain
+
—
4-
+
Haematemesis
+
‘
—
+
—
Melaana
+
■ —
+
—
Haematoma
+
—
—
—
Petechia©
—
— -
—
—
Rumpel-Leede
+
—
—
—
Corticosteroids
+
—
+
+
Heparim
4-
+
—
—
Antibiotics
+
+
+
+
Died
+
+
+
__
TABLE 2 :
Peripheral Mood examinaticms, fecal and blood cultures of patients with D IC in Gastroenteritis.
A g e (in years) Haemoglobin (g m .% ) Haematocrit (vol.% ) W.B.C./cu.mm. Cultures: Fecal Blood
BS.
OS.
4 11 36 4,300
3 12 42 7,000
— -
—
—
—
U.
12 16.5 42 21,000
V. Eltor —
SA.
8 11.8 35 4,500
—
S. Typhosa
D.X.C. IN GASTROENTERITIS
TABLE 3 :
Patients
245
Thrombocytopenia, in patients with Gastroenteritis with DIC.
Number of platelets/cu. mm. on admission
after admission
occurence in days after admission
1.
BS
156,000
4,000
3
2.
OS
156,000
96,000
3
3.
U
300,000
19,000
4
4.
SA
78,000
36,000
2
TABLE 4 :
Hypofibrinogenaemia in Gastroenteritis with DIO.
Fibrinogen concentration in mg. % Patients on admission
after admission
occurence in days after admission
1.
BS
not done
1Í8
3
2.
OS
not done
95
4
3.
U
84
10
13
4
44
2
4.
SA
472 not done
REFERENCES 1. A B IL D G A A R D , C.F.: Recognition, and treatment of intravascular coagulation. J. Pediatr., 74 : 164 (1969). 2. B R A T IC -M IK E S, V. and M IK ES, A.: Laboratory screening for Disseminated Intravascular Coagulation. Abstract Se cond Haematol. Meeting, Vienna, p. 277 (1973). 3. C O H E N , P. B R A U N W A L D , J. and G A R D N E R , F.H.: Destruction of canim and rabbit platelets following intrave nous administration of carbon particles endotoxin, J. Lab. clin. Med. 66 : 263
(1965), cited from (1973).
GERARD
et al.
4. C O R R IG AN, J.J. and JORDAN, C.M.: Heparin therapy in septicemia with dis seminated intravascular coagulation N. Engl. J. Med. 283 : (1970). 5. GER AR D , P.: J. Pediatr. 82 : 780 (1973).
purpura.
6. H A R D A W A Y , R.M.: Syndromes of Dis seminated Intravascular Coagulation, (Thomas, Springfield, HI. 1966). 7. H A R D A W A Y , R.M. et al.: Studies on the role of intravascular coagulation in
S. SETIADARMA AND T. HIMAWAN
246
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