The use of streptokinase in the treatment of acute arterial occlusion after catheterization of the femoral artery in children weighing less than 10 kg

Abstracts

CONTEXTO: O tratamento da oclusão arterial aguda em menores de 5 kg tem constituído tema de discussão. OBJETIVOS: Avaliar o tratamento do quadro da oclusão arterial aguda pós-cateterismo da artéria femoral em crianças com menos de 10 kg com o uso de heparina isolada e também associada com estreptoquinase, e comparar os resultados do exame físico (como diagnóstico), da reversão da oclusão arterial, de complicações e de exames laboratoriais nos dois métodos MÉTODOS: Trinta casos de oclusão da artéria femoral foram identificados em 1.583 cateterismos em crianças no Instituto de Cardiologia de Porto Alegre, entre 1992 e 2000. Os pacientes foram divididos em dois grupos: um usou apenas heparina (14 casos), e o outro usou heparina associada com estreptoquinase (16 casos). Os exames laboratoriais (tempo de protrombina, tempo de tromboplastina parcial ativado e fibrinogênio) coletados antes e durante a infusão intravenosa foram avaliados estatisticamente, assim como o tempo de uso da medicação, as complicações e os resultados. RESULTADOS: O exame físico mostrou-se método fidedigno para avaliar a oclusão; no grupo que utilizou a associação de heparina e estreptoquinase, houve a resolução de 87% dos casos de oclusão arterial, e a principal complicação foi sangramento no sítio de punção em 56,3% dos pacientes. Os resultados apresentaram p < 0,05. Os exames laboratoriais não tiveram significado estatístico. CONCLUSÃO: A estreptoquinase associada com a heparina é mais efetiva do que a heparina isolada no tratamento da oclusão arterial aguda da artéria femoral pós-cateterismo, tanto que sua associação apresenta uma redução do risco relativo de 88% em relação à heparina isolada.

Estreptoquinase; criança; cateterismo; oclusão arterial

ORIGINAL ARTICLE

The use of streptokinase in the treatment of acute arterial occlusion after catheterization of the femoral artery in children weighing less than 10 kg

Nilo César Barbosa Mandelli^I; Cláudio Nhuch^II; Paulo Roberto Fontes^III; Haroldo Diez Paiva^IV; Raul Rossi^V; Mario Frederico Chagas Pereira^II; Silvio Perini^II

^I

^IIVascular surgeon, IC–FUC, Porto Alegre, RS, Brazil

^IIIPhysician. Associate professor, Surgery, FFFCMPA, Porto Alegre, RS, Brazil

^IVProfessor of Vascular Surgery, FFFCMPA, Porto Alegre, RS, Brazil

^VPediatric hemodynamicist, IC–FUC, Porto Alegre, RS, Brazil

^{Correspondence}

ABSTRACT

BACKGROUND: The treatment of acute arterial occlusion in children weighing less than 5 kg has been widely discussed.

OBJECTIVES: To evaluate the treatment of acute arterial occlusion after catheterization of the femoral artery in children weighing less than 10 kg using heparin alone and associated with streptokinase, and to compare the results of physical examination (such as diagnosis), reversal of the arterial occlusion, complications and laboratory tests between both methods.

METHODS: Thirty cases of femoral artery occlusion were identified among 1,583 catheterizations in children at Instituto de Cardiologia de Porto Alegre between 1992 and 2000. The patients were divided into two groups: one used heparin alone (14 cases) and the other used heparin associated with streptokinase (16 cases). The laboratory tests (prothrombin time, activated partial thromboplastin time and fibrinogen) performed before and during the intravenous infusion were statistically analyzed, as well as period of drug administration, complications and results.

RESULTS: Physical examination proved to be reliable to evaluate occlusion; in the group using heparin associated with streptokinase, there was resolution of the arterial occlusion in 87% of cases, and the main complication was bleeding at the puncture site, which was present in 56.3% of the patients. These results showed p < 0.05. Laboratory tests were not statistically significant.

CONCLUSION: Streptokinase associated with heparin is more effective on acute artery occlusions following femoral catheterization than heparin alone. Its association presents an 88% rate of relative risk reduction in relation to heparin alone.

Keywords: Streptokinase, child, catheterization, arterial occlusion.

Introduction

Acute arterial occlusion of the upper and lower limbs in children, whether iatrogenic or not, rarely leads to limb loss (2.5%).^1,2 However, it often evolves to growth deficit (Figure 1).^3–5 Surgery is the treatment of choice for acute arterial occlusions due to secondary thrombosis, caused by catheter or arterial wall lesion, but results are not satisfactory in children because of reduced vessel diameter.^6–10 For that reason, thrombolytic and anticoagulant drugs started being used through systemic approach or intraarterial direct injection.^5,8,11

Late treatment of complications caused by occlusion has become a challenge. Spinal curvatures resulting from the difference in leg length is usually repaired by wearing inner soles, orthopedic boots or surgeries.¹² Arterial reconstruction is complex, since prostheses do not follow the child's growth, veins or arteries present reduced diameters.

It is known that the systems of hemostasis and fibrinolysis in children are immature and are developed after 6 months of age. When a parallel is established between the levels of factors pro– and anticoagulants, a slight tendency to coagulation is likely to occur, and predisposition is higher in premature children and in those with associated diseases (polycythemia, respiratory, renal or hepatic failure).¹³

The most frequent iatrogenic cause is catheterization of the femoral artery using Seldinger's technique,^14–17 with the aim of performing hemodynamic study. The incidence in patients weighing less than 10 kg (from birth to 2 years) is 0.8–9%, being reduced after systemic heparinization was introduced in 1970.^5.18–25 Factors such as child weight lower than 10 kg, higher catheter diameter and longer time of procedure are related to higher incidence of complications. Another cause of arterial occlusion is the catheterization of the umbilical artery leading to thrombosis of the abdominal aorta and umbilical vein leading to thrombosis of the right atrium.^21.26

The most frequently used drugs are heparin, streptokinase, urokinase and tissue plasminogen activator (TPA).^15.27–32

This study aimed at: 1) comparing the use of heparin alone and its association with streptokinase in acute arterial occlusions in children weighing less than 10 kg; 2) studying the complications resulting from the methods; 3) assessing laboratory changes – prothrombin time (PT), activated partial thromboplastin time (APTT) and fibrinogen – in the occurrence of complications; 4) verifying whether physical examination is a reliable diagnostic method to confirm acute arterial occlusion after catheterization.

Methods

We assessed 1,583 catheterizations of the common femoral artery, performed at Instituto de Cardiologia de Porto Alegre, for the diagnosis or treatment of congenital diseases of the myocardium or thoracic aorta, in children weighing less than 10 kg, with no distinction of gender or race. Thirty cases of acute arterial occlusion were diagnosed, which were divided into two groups:

– Group 1 (GH) – patients who were given only endovenous heparin (peripheral or central vein) at 25 U/kg/h, and the study was carried out retrospectively (March 1, 1992 to October 23, 1996), including a total of 14 cases;

– Group 2 (GHS) – patients who were given endovenous heparin at 25 U/kg/h and streptokinase at 3,000 U/kg/h, in a total of 16 cases, and the study was carried out prospectively (November 1, 1996 to April 30, 2000). The study design is clinical and quasi–experimental.

Drugs were used until pulses reappeared. Limitation for the use of drugs in GH, in case the pulse had not returned, was established as improvement in perfusion of the extremity (back to normal color and warm foot, compared with the upper or contralateral limb, if it had no lesion). For the GHS, drugs were maintained for 48 hours, in case the pulse had not returned, independent of foot perfusion.

The following variables were assessed: gender, weight, age, time until post–catheterization care, audible Doppler signs before and after the end of the procedure (GHE), clinical signs and symptoms, drug dosage, time of drug use and complications after drug use. All patients were given a single dose of endovenous (peripheral or central) heparin 25 U/kg before the catheterization. Positive signs of arterial occlusion were absence of pulse in the artery in which the catheterization was performed and distally to it, foot pallor and unfixed cyanosis without edema. Doppler was positive when it presented an audible sound similar to the local sounds of normal pulse. All patients, after diagnostic suspicion of occlusion, were given heparin 25 U/kg/h for 6 hours to exclude the postexamination vasospasm. Diagnostic time of arterial occlusion was the time spent from the moment the procedure was over to the moment the vascular surgeon arrived. PT, APTT and plasminogen were collected before the infusion. Complications were classified into:

1)bleeding at the puncture site;

2)bleeding in other sites: brain, abdomen, thorax and ocular;

3)allergic reactions;

4)hypotension with shock caused by bleeding or anaphylaxis.

Contraindicative criteria for use of heparin and streptokinase were presence of cerebral congenital disease with risk of bleeding, determined active bleeding or history of anaphylaxis to heparin. To analyze the variables weight, heparin dose, PT before and after medication, APTT before and after medication, fibrinogen before and after medication, Student's t test was used; for the variables age, time until confirmation of the definitive diagnosis by the vascular surgeon and time of drug use, Mann–Whitney's test was used; for the variable race and to compare complications, Fisher's exact test was used; for the variable gender and to compare results, continuity correction was used.³³.

Results

Of all 1,583 catheterizations (GH, n = 628; GHS, n = 955), 30 (1.89%) resulted in occlusion of the femoral artery (GH, n = 14, 2.22%; GHS, n = 16, 1.67%).

Table 1 shows that there was no statistical difference between both groups as to gender, race, age, weight, diagnostic time and heparin dose. There was statistical difference in time of drug use. There were no complications in GH. In GHS, nine patients (56.25%) had bleeding at the femoral puncture site, which was solved only with prolonged compression (mean of 16 minutes, with no hypotension) of the site. Only one patient presented fibrinogen below normal (90 mg/%) in the GHS, but he did not have bleeding, showing that the examinations were not related to risk of bleeding.

All patients with occlusion had no pulse after catheterization, and audible Doppler was absent or with monophasic sound in the arteries distal to the puncture (superficial femoral, popliteal, anterior and posterior tibial). With clinical improvement, there was reappearance of pulse and audible Doppler sound equal to the non–occluded limb.

The effect of the treatment can be seen in Table 1. The risk of remaining occluded in GHS was 12.5%, and in GH 100%, with relative risk of 0.125 (IC95% 0.03–0.46) and absolute risk reduction (ARR) of 87.5%. The use of heparin + streptokinase reduced in 88% the acute arterial occlusions after femoral catheterization in children when compared with the use of heparin alone. This shows a relative risk reduction (RRR) of 88% (IC95% 54–97%). The number needed to treat (NNT) was 1.1 (IC95% 0,9–1,2), i.e., approximately for each treated patient one occlusion is avoided.

Discussion

In GH, the study was carried out retrospectively, since a new study would not be ethically acceptable, considering that there was no resolution in the clinical status of any patient (all had growth deficit).

It is known that the most efficacious treatment of non–atherosclerotic acute arterial occlusions is direct and immediate surgical intervention on the artery, repairing the lesion or removing the thrombus inside it.^1,34 Some authors have used high doses of endovenous fibrinolytics,^29.35–38 or low doses of intraarterial fibrinolytics with the aid of catheters, solving the acute occlusion. For children, surgical intervention can worsen the lesion of the arterial tree, since the diameter of these arteries is very small, especially in children weighing less than 10 kg;^5,7,8,11 when using catheters for intrathrombus injection, the new puncture may cause lesion in another artery.

The efficacy of heparin alone for the treatment of arterial occlusion was reported by Wessel,⁵ solving 50% of cases of acute arterial occlusion in children. This was not confirmed in the present study. A criticism that can be directed to that publication is the fact that postexamination arterial vasospasm was not assessed by the authors.³⁹

All patients had clinical signs (foot pallor and unfixed cyanosis without edema). Clinical symptoms were hard to be defined, due to the difficulty in communicating with the children. This shows that signs help to establish the diagnosis, but symptoms do not.^40.41

Doppler was used only in GHS patients as a method to confirm the diagnosis of acute arterial occlusion and when assessing the response to treatment through vascular physical examination of the patient. This diagnostic method showed that the physical examination can be 100% sensitive; therefore, it is sufficiently reliable for assessment before and after catheterization. It is known that, when the Doppler is positive and there is no arterial pulse, the sound listened at the Doppler is the flow coming to the occluded artery through collateral arteries, which was already confirmed by Hurowitz² in the arteriographic examination, and also confirmed by Deeg, using Doppler ultrasonography.

Time of heparin and streptokinase use is not defined in the literature. The studies using heparin do not refer to time, since its action is nor directly on the thrombus,⁵ and those using streptokinase can be exemplified by Kirk & Qureshi's study,⁴² who used it for 48 hours; however, Saxena²¹ reported its use for more than 48 hours. Kothari⁴³ relates increased time or inefficacy with low fibrinogen levels; there are reports in which the child has around 50–70% of the amount of fibrinogen and plasminogen in adults.^19,28,44–49 Corrigam^44,50 demonstrates that the child needs a concentration of streptokinase or urokinase 11 times higher and a concentration of TPA five times higher than the adult for their action. Brus,¹⁸ failing to obtain the desired effect over a 48–hour period, infused fresh plasma (providing plasminogen) and repeated the streptokinase dose for another 48 hours, thus obtaining almost 100% efficacy.

Mean time of streptokinase use in this study was 4 hours and 15 minutes, and maximum time was 48 hours. Some studies in the literature adopt a longer time of drug use to obtain a positive effect. Prichard⁵¹ used 44 hours, Ino,⁷ 48 hours, Kirk & Qureshi,⁴² a maximum limit of 44 hours, Brus,¹⁸ 120 hours, Kothari,⁴³ 48 hours, and Saxena²¹ demonstrated a time reduction of 5 hours in relation to previous studies. Time of heparin use in GH was 88 hours, and the end of the infusion occurred when there was improvement in perfusion, and not pulse reappearance. For that reason, there was an increased time of drug use.

Heparin dose in the literature²¹ ranges between 10 U/kg/h and 25 U/kg/h, continuously used. In GHS, it was used in association with streptokinase, with the aim of avoiding recurrent thrombosis,⁴³ in case of arterial endothelium lesion due to clot next to the wall or due to the puncture itself. For that reason, it was maintained for 48 hours after pulse returned and suspension of streptokinase, since the platelets, over that period of time, covered that injured area, avoiding thrombus formation.⁵² Some authors use 10 mg/kg acetylsalicylic acid instead of heparin after suspension of streptokinase. Streptokinase dose in the literature ranges from 1,000 U/kg/h to 4,000 U/kg/h, not showing a relation between dose and bleeding complication.⁴³ We used the continuous endovenous dose of 3,000 U/kg/h, according to Kothari.⁴³

In GH and GHS, all assessed patients presented altered APTT values, above normal. This result was obtained before the use of medication, since they all had used heparin during the catheterization of the femoral artery and, in case of suspicion of occlusion, the drug was maintained for another 6 hours, to dismiss diagnosis of vasospasm due to arterial puncture.³⁹ It should be remembered that there is a direct relationship between both coagulation approaches, in which the activity of the extrinsic approach is measured through PT and can sometimes be slightly altered with the use of heparin.⁵³

PT and APTT are inefficient to follow the action of streptokinase.^21.54 Fibrinogen dosage can be useful, but it does not provide the prognosis as to chance of bleeding.⁵⁴ All patients with bleeding had PT and APTT changes, as previously explained, and normal values for fibrinogen. In the literature, Prichard⁵¹ mentions the difficulty in knowing whether the laboratory tests discussed above would cause bleeding, and Kothari⁴³ reports the difficulty in establishing a relation between values of laboratory examinations and risk of bleeding, even associating the dosage of fibrin degradation products.

The major issue about using fibrinolytic drugs is their complications.^7,55–58 It was shown above that the complications resulting from the use of streptokinase are hard to be predicted by laboratory evaluation of the patient during its endovenous infusion. Because of this problem, use of medication could be contraindicated. However, in this study, there were few complications. The only registered complication was bleeding at the arterial puncture site in 56.25% of cases, which was easily solved by compressing the puncture site and suspending the medication being infused. In the literature, other sites with risk of bleeding in childhood are mentioned, such as cases of cerebral and retroperitoneal hemorrhage and in urinary and digestive systems;⁵⁹ however, the studies on use of streptokinase for occlusions after catheterization do not report cases of bleeding in sites other than the puncture site.^18.21 A severe complication such as cerebral hemorrhage, according to a 30–year review carried out by Zenz,⁵⁹ is considered very rare, around 0.4% in children aged less than 1 month. Another complication such as anaphylaxis is not found in children; digestive bleedings have only been reported in patients who used streptokinase in the treatment of renal vein thrombosis. It is worth stressing that renal and hepatic failure, when present and if associated with streptokinase, increase the chance of bleeding.⁵⁹

As to study outcome, the results were similar to those found in the literature, in which Brus¹⁸ had 85% of resolution, Kothari,⁴³ 100%, and Saxena,²⁸ 95%. The results obtained were statistically significant in relation to the resolution of occlusions and to period of time for that, with RAR of 87.5%, RRR of 87.5% and NNT of 1.1. It is concluded that the association of streptokinase with heparin in the treatment of acute arterial occlusions after catheterization in children weighing less than 10 kg and using the methodology described above solves arterial occlusions in 87.5% of cases. The complications occurred with the use of streptokinase associated with heparin are considered nonsevere, and the laboraty tests obtained from children did not prove to be useful in preventing bleeding. During the endovenous infusion of streptokinase, physical examination is a reliable method to confirm the diagnosis of acute arterial occlusion in children after catheterization.

References

Manuscript received July 24, 2006, accepted January 18, 2007.

This study was carried out at IC–FUC, Porto Alegre, RS, Brazil. It is based on a master's thesis (Surgical Clinic) developed at FFFCMPA in 2002 and presented at XXIII Congresso de Cardiologia do Rio Grande do Sul in 2003 and at 36° Congresso Brasileiro de Cirurgia Vascular in 2005.

• 1. Haimovici H. Arterial embolism of the extremities and technique of embolectomy. In: Haimovici H, Ascer E, Hollier LH, Strandness Jr. DE, Towne JB. Vascular surgery: principles and techniques. 4th ed. Massachusetts: Blackwell Science; 1996. p. 423-44.
• 2. Hurwitz RA, Franken EA Jr., Girod DA, Smith JA, Smith WL. Angiographic determination of arterial patency after percutaneous catheterization in infants and small children. Circulation. 1977;56:102-5.
• 3. Fairbairn JF. Clinical manifestations of perpheral vascular disease. Juergens JL, Spittell JR, Fairbairn JF II. Peripheral vascular disease. 5th ed. Philadelphia: WB Saunders; 1980. p. 3.
• 4. Burrows PE, Benson LN, Williams WG, et al. Iliofemoral arterial complications of balloon angioplasty for systemic obstructions in infants and children. Circulation. 1990;82:1697-704.
• 5. Wessel DL, Keane JF, Fellows KE, Robichaud H, Lock JE. Fibrinolytic therapy for femoral arterial thrombosis after cardiac catheterization in infants and children. Am J Cardiol. 1986;58:347-51.
• 6. Fogarty TJ. Rutherford RB. Vascular surgery. 4th ed. Philadelphia: WB Saunders; 1995. p. 410-4.
• 7. Ino T, Benson LN, Freedom RM, Barker GA, Airpursky A, Rowe RD. Thrombolytic therapy for femoral artery thrombosis after pediatric cardiac catheterization. Am Heart J. 1988;115:633-9.
• 8. Stanger P, Heymann MA, Tarnoff H, Hoffman JI, Rudolph AM. Complications of cardiac catheterization of neonates, infants, and children. A three-year study. Circulation. 1974;50:595-608.
• 9. Mansfield PB, Gazzaniga AB, Litwin SB. Management of arterial injuries related to cardiac catheterization in children and young adults. Circulation. 1970;42:501-7.
• 10. Mason AC, Llull R, Bentz ML. Revascularization of the upper extremity in a preterm infant: a case report and review of the literature. Ann Plast Surg. 1999;43:646-8
• 11. While JS, Talbert JL, Haller JA Jr. Peripheral arterial injuries in infants and children. Ann Surg. 1968;167:757-67.
• 12. Beaty JH. Congenital anomalies of lower extremity. In: Crenshaw AH. Campbell 's operative orthopedics. 7th ed. St. Louis: Mosby; 1987. p. 2623-780.
• 13. Corrigan JJ Jr., Sleeth JJ, Jeter M, Lox CD. Newborn's fibrinolytic mechanism: components and plasmin generation. Am J Hematol. 1989;32:273-8.
• 14. Seldinger SI. Catheter replacement of the needle in percutaneous arteriography; a new technique. Acta Radiol. 1953;39:368-76.
• 15. Tokel K, Yildirim SV, Varan B, Ekici E. Sequential balloon dilatation for combined aortic valvular stenosis and coarctation of the aorta in a single catheterization procedure: a prognostic evaluation based on long-term follow up. J Invasive Cardiol. 2006;18:65-9.
• 16. Galal MO, Schmaltz AA, Joufan M, Benson L, Samatou L, Halees Z. Balloon dilation of native aortic coarctation in infancy. Z Kardiol. 2003;92:735-41.
• 17. Saxena A, Gupta R, Kumar RK, Kothari SS, Wasir HS. Predictors of arterial thrombosis after diagnostic cardiac catheterization in infants and children randomized to two heparin dosages. Cathet Cardiovasc Diagn. 1997;41:400-3.
• 18. Brus F, Witsenburg M, Hofhuis WJ, Hazelzet JA, Hess J. Streptokinase treatment for femoral artery thrombosis after arterial cardiac catheterisation in infants and children. Br Heart J. 1990;63:291-4.
• 19. Gamba P, Pettenazzo A, Kalapurackal M, Saia SO, Guglielmi M. Primary occlusion of the iliac and femoral artery in two newborn infants: efficacy of medical treatment. J Pediatr Surg. 1993;28:735-7.
• 20. Kothari SS, Kumar RK, Varma S, Saxena A. Thrombolytic therapy in infants for femoral artery thrombosis following cardiac catheterization. Indian Heart J. 1996;48:246-8.
• 21. Saxena A, Gupta R, Kumar RK, Kothari SS, Wasir HS. Predictors of arterial thrombosis after diagnostic cardiac catheterization in infants and children randomized in two heparin dosages. Cathet Cardiovasc Diagn. 1997;41:400-3.
• 22. Richardson R, Applebaum H, Touran T, et al. Effective thrombolytic therapy of aortic thrombosis in the small premature infant. J Pediatr Surg. 1988;23:1198-200.
• 23. Strife JL, Ball WS Jr., Towbin R, Keller MS, Dillon T. Arterial occlusions in neonates: use of fibrinolytic therapy. Radiology. 1988;166:395-400.
• 24. Aydogan U. Arterial duct closure with detachable coils: application in the small child. Asian Cardiovasc Thorac Ann. 2002;10:124-8.
• 25. Agnoletti G, Bonnet C, Boudjemline Y, et al. Complications of pediatric interventional catheterisation: an analysis of risk factors. Cardiol Young. 2005;15:402-8.
• 26. Ross P Jr., Ehrenkranz R, Kleinman CS, Seashore JH. Thrombus associated with central venous catheters in infants and children. J Pediatr Surg. 1989;24:253-6.
• 27. O'Relly RA. Anticoagulants, antithrombotics and thrombolytics drugs. In: Gilman AG, Goodman LS, Rall TW, Murad F. The pharmacological basis of therapeutics. 7th ed. Macmillan; 1987. p. 878-90.
• 28. Verstraete M, Vermylen J, Amery A, Vermylen C. Thrombolytic therapy with streptokinase using a standard dosage scheme. Br Med J. 1966;1:454-6.
• 29. Deucher GP, Mickelberg A, Nunes P, Cabral CA, Degni M. Nossa experiência clínica com a fibrinoliticoterapia pela estreptocinase nas embolias e tromboses arteriais. Rev Bras Cardiovasc. 1975;11:112-7.
• 30. Albisetti M, Schmugge M, Haas R, et al. Arterial thromboembolic complications in critically ill children. J Crit Care. 2005;20:296-300.
• 31. The Thrombolysis in Myocardial Infarction (TIMI) trial. Phase I findings. TIMI Study Group. N Engl J Med. 1985;312:932-6.
• 32. Van de Werf F, Ludbrook PA, Bergmann SR, et al. Coronary thrombolysis with tissue-type plasminogen activator in patients with evolving myocardial infarction. N Engl J Med. 1984;310:609-13.
• 33. Fletcher RH, Fletcher SW, Wagner EH. Tratamento. In: Fletcher RH, Fletcher SW, Wagner EH. Epidemiologia clínica: elementos essenciais. 3Ş. ed. Porto Alegre: Artmed; 1996. p. 145-73.
• 34. Haimovici H. Acute arterial thrombosis. In: Haimovici H, Ascer E, Hollier LH, Strandness Jr. DE, Towne JB. Vascular surgery: principles and techniques. 4th ed. Massachusetts: Blackwell; 1996. p. 458-65.
• 35. Ramos AI, Ramos RF, Togna DJ, et al. Fibrinolytic therapy for thrombosis in cardiac valvular prosthesis short and long term results. Arq Bras Cardiol. 2003;81:393-8, 387-92. Epub 2003 Nov 5.
• 36. Gupta D, Kothari SS, Bahl VK, et al. Thrombolytic therapy for prosthetic valve thrombosis: short-and long-term results. Am Heart J. 2000;140:906-16.
• 37. Bolz D, Kuhne T, Jivraj R, Hammer J. Thrombolysis of prosthetic tricuspid valve thrombosis with human recombinant tissue plasminogen activator in an adolescent. Pediatr Cardiol. 2000;21:397-400.
• 38. Atiyeh BS, Hashim HA, Hamdan AM, Musharafieh RS. Local recombinant tissue plasminogen activator (rt-PA) thrombolytic therapy in microvascular surgery. Microsurgery. 1999;19:265-71.
• 39. Bergstrom K, Jorulf H. Reaction of femoral and common carotid arteries in infants after puncture or percutaneous catheterization. Acta Radiol Diagn (Stockh). 1976;17:577-80.
• 40. Pousti TJ, Wilson SE, Willams RA. Clinical examination of the vascular system. Veith FJ, Hobson RW, Williams RA, Wilson SE. Vascular surgery: principles and practice. 2nd ed. New York: McGraw-Hill; 1994. p. 74-89.
• 41. Ascer E, Gennaro M, Mohan Chittur, Veith FJ. Management of acute lower-extremety ischemia. In: Callow AD, Ernst CB. Vascular surgery: theory and practice. Connecticut: Appleton & Lange; 1995. p. 715-34.
• 42. Kirk CR, Qureshi SA. Streptokinase in management of arterial thrombosis in infancy. Int J Cardiol. 1989;25:15-20.
• 43. Kothari SS, Varma S, Wasir HS. Thrombolytic therapy in infants and children. Am Heart J. 1994;127:651-7.
• 44. Corrigan JJ Jr., Sleeth JJ, Jeter M, Lox CD. Newborn's fibrinolytic mechanism: components and plasmin generation. Am J Hematol. 1989;32:273-8.
• 45. Peters M, ten Cate JW, Jansen E, Breederveld C. Coagulation and fibrinolytic factors in the first week of life in healthy infants. J Pediatr. 1985;106:292-5.
• 46. Peters M, ten Cate JW, Koo LH, Breederveld C. Persistent antithrombin III deficiency: risk factor for thromboembolic complications in neonates small for gestacional age. J Pediatr. 1984;105:310-4.
• 47. Vergnes C, Larnaudie B, Hourdille P, Roudaut MF, Choussat A, Boisseau MR. Thrombose aortique abdominale sous-renale neonatale. Presse Med. 1985;14:492-9.
• 48. Batsford S, Brundiers M, Schweier O, Horbach E, Monting JS. Antibody to streptococcal cysteine proteinase as a seromarker of group A Streptococcal (Streptococcus pyogenes) infections. Scand J Infect Dis. 2002;34:407-12.
• 49. Nowak-Gottl U, Auberger K, Halimeh S, et al. Thrombolysis in newborns and infants. Thromb Haemost. 1999;82 Suppl 1:112-6.
• 50. Vojdani A, Bazargan M, Vojdani E, et al. Heat shock protein and gliadin peptide promote development of peptidase antibodies in children with autism and patients with autoimmune disease. Clin Diagn Lab Immunol. 2004;11:515-24.
• 51. Pritchard SL, Culham JA, Rogers PC. Low-dose fibrinolytic therapy in infants. J Pediatr. 1985;106:594-8.
• 52. Silver D, Kikta MJ. Thrombogenesis and thrombolysis. In: Haimovici H, Ascer E, Hollier LH, Strandness Jr. DE, Towne JB. Vascular surgery: principles and techniques. 4th ed. Massachusetts: Blackwell; 1996. p. 195-208.
• 53. Keller PK, Silver D. Anticoagulants: heparin and warfarin. In: Vieth FJ, Hobson RW, Williams RA, Wilson SE. Vascular surgery: principles and practice. 2nd. ed. New York: McGraw-Hill; 1994; p. 219-27.
• 54. Bovill EG, Becker R, Tracy RP. Monitoring thrombolytic therapy. Prog Cardiovasc Dis. 1992;34:279-94.
• 55. Estelles A, Aznar J, Gilabert J, Parrilla JJ. Dysfunctional plasminogen in full-term newborn. Pediatr Res. 1980;14:1180-5.
• 56. Marder VJ, Sherry S. Thrombolytic therapy: current status (1). N Engl J Med. 1988;318:1512-20.
• 57. Marder VJ, Sherry S. Thrombolytic therapy: current status (2). N Engl J Med. 1988;318:1585-95.
• 58. Reznik VM, Anderson J, Griswold WR, Segall ML, Murphy JL, Mendoza SA. Successful fibrinolytic treatment of arterial thrombosis and hypertension in a cocaine-exposed neonate. Pediatrics. 1989;84:735-8.
• 59. Zenz W, Arlt F, Sodia S, Berghold A. Intracerebral hemorrhage during fibrinolytic therapy in children: a review of the literature of the last thirty years. Semin Thromb Hemost. 1997;23:321-32.

Publication Dates

• Publication in this collection
  19 July 2007
• Date of issue
  Mar 2007

History

• Received
  24 July 2006
• Accepted
  18 Jan 2007