Table of Contents  
REVIEW ARTICLE
Year : 2015  |  Volume : 2  |  Issue : 3  |  Page : 101-104

A Brief Review of Deep Vein Thrombosis in Pediatric Patients


1 Department of Vascular Surgery, Citizens Hospital, Serilingampally, Hyderabad, Telangana, India
2 Department of Vascular Surgery, Bidar Medical College, Karnataka, India

Date of Web Publication8-Oct-2015

Correspondence Address:
Abhijit S Nair
Department of Vascular Surgery, Citizens Hospital, Serilingampally, Hyderabad, Telangana
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0972-0820.166935

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  Abstract 

Deep vein thrombosis (DVT) that develops in a hospitalized pediatric patient can has serious consequences. Prophylactic strategies with unfractionated or low molecular weight is not practised in children like it is practised by clinicians in adults. It is important to identify high-risk pediatric patient who has risk factors for developing DVT, so as to prevent in-hospital morbidity, mortality and increased hospital stay.

Keywords: Deep vein thrombosis, heparin, pediatrics, pulmonary embolism


How to cite this article:
Nair AS, Kamtikar S. A Brief Review of Deep Vein Thrombosis in Pediatric Patients. Indian J Vasc Endovasc Surg 2015;2:101-4

How to cite this URL:
Nair AS, Kamtikar S. A Brief Review of Deep Vein Thrombosis in Pediatric Patients. Indian J Vasc Endovasc Surg [serial online] 2015 [cited 2019 Aug 22];2:101-4. Available from: http://www.indjvascsurg.org/text.asp?2015/2/3/101/166935


  Introduction Top


Deep vein thrombosis (DVT) is relatively uncommon in hospitalized children but in certain group of pediatric patients, the chances are significantly high. If identified on time and if proper therapeutic measures are started, the chances of DVT manifesting as pulmonary thromboembolism can be prevented. DVT contributes to a significant morbidity and increases the cost of treatment and hospital stay. If DVT is not detected and venous thromboembolism (VTE) develops, it can be life-threatening. In this article, we've described risk factors and reviewed relevant literature to highlight the importance of identifying high risk pediatric patients who are susceptible for DVT and to initiate prophylactic measures to avoid occurrence of DVT in such patients.

DVT is an entity which is well described in pediatric patients but still protocols are not well established for preventive prophylaxis in many medical centers. The incidence of DVT is low in children as compared to adult patients in the perioperative period or during their stay in the Intensive Care Unit (ICU). The reasons for this reasonably low incidence is decreased capacity to generate thrombin, increased capacity of α2 macroglobulin to inhibit thrombin and enhanced anti-thrombotic potential by vessel wall. The National Hospital Discharge Survey published by Stein et al. estimated the incidence of pediatric VTE as 5 per 10,000 per year.[1] However, Raffini et al. reported a dramatic increase in the incidence of DVT in pediatric patients after retrospectively review the discharge summary of 35–40 children hospitals over 6 years. Most of the patients were either having malignancy or complex medical conditions leading to hospitalization. During this period, the annual rate of VTE increased by 70% (from 34 to 58 cases per 10,000 hospital admissions).[2]


  Predisposing Factors Top


The factors predisposing to DVT in pediatric age group are presence of central venous catheter (especially femoral route), congenital heart disease, decreased intravascular volume status, obesity, immobilization, infection. Presence of neonatal septicemia and perinatal asphyxia is the predisposing factors in neonates. Maternal risk factors such as diabetes mellitus and toxemia of pregnancy are predisposing factors for neonatal DVT [3] [Figure 1].
Figure 1: Factors leading to deep vein thrombosis in a hospitalized pediatric patient

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The high incidence age groups of DVT are hospitalized neonates and adolescents, teenage girls on oral contraceptives and early pregnancies, patients with sickle cell anemia, nephritic syndrome, anti-phospholipid antibody syndrome, and liver failure. Pediatric oncology patients (hematological, soft tissue, or visceral) have a greater susceptibility for DVT. Wilms tumor and leukemias are the common malignancies were DVT may be encountered. Children with brain malignancies have less chances of DVT.[4]

Branchford et al. identified 78 pediatric patients with thromboembolism over 7 years of observation. After data analysis they found that mechanical ventilation, systemic infection and hospitalization more than 5 days was responsible for the cases of thromboembolism.[5]

Immunosuppression due to malignancy and chemotherapy predisposes a child to infections leading to hospitalization and immobilization. Such patient has indwelling lines (central venous catheters [CVCs], peripherally inserted CVCs, chemoport ) that predisposes a child to DVT. Male et al. conducted a prospective, multicenter, cohort study in general pediatric population requiring CVC to assess whether the location, type, size, and duration of CVC was associated with VTE.

They found that the incidence of VTE was increased in the presence of femoral and subclavian catheters compared to brachial and jugular catheters. In their review, the VTE was independent of the type of CVC (i.e. PICC, tunneled, untunneled) and duration of catheter in situ. Only the location of the catheter was responsible for the susceptibility to DVT.[6]

Worly et al. suggested to avoid femoral CVC as far as possible due to possible DVT in pediatric patients. However if other CVCs are not possible or are contraindicated, then DVT prophylaxis should be considered as per institutional protocol.[7] An indwelling CVC along with the medications that are administered through it causes endothelial damage leading to thrombosis in the lumen of vessel thereby predisposing to thromboembolic events.[8] Tshifularo et al. did a retrospective review of children <13 years of age with VTE between 1993 and 2009 to identify an association of known risk factors in children with VTE. They felt that children with femoral venous access or chronic infective states (TB/HIV) makes them more susceptible to venous thrombosis.[9]

Sandoval et al. retrospectively studied the incidence, risk factors and treatment patterns for DVT in a single tertiary care hospital over 14 years by evaluating 358 children.

They felt that patients with thrombophilia or lower extremity disease and patients with severe medical conditions requiring prolonged ICU stay and presence of femoral venous access were the candidates in whom DVT prophylaxis should be considered.[10] Congenital conditions such as factor V Leiden mutation, prothrombin gene mutation, deficiencies of antithrombin III, protein C and S, increased homocysteine, and lipoprotein (a1) predisposes a child for DVT. The hemostatic mechanisms are not optimal in neonates hence the predisposition to thrombosis is more in susceptible patients. The embolus in a pediatric patient could be air, an infected material or a metastatic tissue from a primary source. Still, a thrombus is the most common material.[11],[12]

Prophylaxis for DVT is usually not practiced in pediatric medical or surgical patients with the exception of patients with malignancy or at times after cardiac surgeries.

Perioperatively, this is usually not practiced due to the risk of bleeding. This is because the incidence of DVT is very low in this age group. This is the reason why there is a delay in the diagnosis and initiation of therapeutic anticoagulation which at times can prove fatal.[13] The presentation is usually after a pulmonary thromboembolic event in the form of cough, breathlessness, pleuritic chest pain, fever, and in rare cases hemoptysis. Edematous, painful, discoloration should alert a physician. DVT is also possible in the upper limbs. When present it is associated with swelling, pain, discoloration, superior vena cava syndrome, chylothorax, chylopericardium. Absence of blood on aspiration should raise the suspicion of thrombosis in the lumen of a central venous catheter.[14]


  Diagnosis Top


Venography is considered the gold standard in diagnosing DVT.[15] But as a routine, ultrasound is used for screening as it can be done bedside, is noninvasive and can be repeated as many times as required, with no hazards of radiation exposure. When pulmonary thromboembolism is suspected, a chest radiograph is usually nonspecific. A 12 lead electrocardiogram usually shows sinus tachycardia with nonspecific ST changes. A two-dimensional echocardiogram can detect right ventricular dilatation or dysfunction. Pulmonary angiography is considered as the gold standard for diagnosing pulmonary thromboembolism, but it is usually reserved for unusual cases. A spiral computed tomography scan with intravenous contrast gives all the necessary information.


  Management Top


Once diagnosis is made, anticoagulation should be initiated. Unfractionated heparin (UFH) is the drug of choice. 75–100 U/kg bolus followed by 18–20 U/kg infusion is usually followed. Currently, low molecular weight heparin (LMWH) is used frequently in pediatric patients due to their predictable mode of action, ease of administration and no frequent monitoring practices. Enoxaparin 1–1.5 U/kg subcutaneously twice daily is the dosing practiced at many centers.[16],[17] American College of Chest Physicians has provided clinical evidence based guidelines for management of thrombosis in neonates and pediatric patients. Although they've mentioned that the evidence remains weak, wherever indicated UFH or LMWH (enoxaparin) should be used. When UFH is used, APTT has to be monitored and while using LMWH a target range of 0.5–1.0 units/ml of anti-Xa should be achieved 4–6 h after the subcutaneous infection. The management of these patients should be done in consultation with a neonatologist or pediatric intensivist and a hematologist.[18] Stine et al. retrospectively, reviewed 7 patients with DVT diagnosed between 5 years (1999–2009) in a pediatric hemato-oncology hospital who were treated with enoxaparin 1–1.5 mg/kg two times daily till clot resolution to maintain anti-Xa level of 0.5–1.5 IU/ml. Thereafter, it was decreased to once daily. All 7 patients had resolution of thrombosis in 1–2 months of treatment.

Few of them required blood and platelet transfusion support, but the ongoing treatment was not interrupted.[19]

Vitamin K antagonists (warfarin, acenocoumarin) is usually started after a few days of overlap with UFH under strict monitoring for bleeding. Anticoagulation is usually continued for 3–6 months. In patients with existing thrombotic disease, a longer duration of treatment is required. Thrombolysis is done in the life-threatening situations where patients present with pulmonary embolism requiring invasive ventilation and vasopressor support. Agents used are urokinase, streptokinase, and rTPA.


  Prognosis Top


The prognosis is variable. Patients with a background of malignancy, severe systemic infections, and cardiac disease have a poor prognosis in established DVT. Early diagnosis and prompt initiation of treatment can avoid the life-threatening thromboembolic phenomenon. The patients should be admitted and monitored in an intensive care setup or a high dependency unit.


  Conclusion Top


The index of suspicion for DVT in hospitalized children should be very high.

Appropriate diagnostic tests should be done to confirm or rule out a thrombosis whenever a child is encountered in an ICU who has predisposition to DVT, prophylactic strategies should be initiated. Pediatric Departments should have policies for recognizing high risk patients or a checklist to find a susceptible patient. A Cardiovascular or Vascular Surgeon can be involved in situ ations where surgical intervention is likely. A checklist for identifying high risk pediatric patients susceptible for DVT can be prepared which will help in identifying patients at risk who deserve prophylaxis. Every pediatric department should have protocols in place for DVT prophylaxis and treatment in place. Never hesitate to involve a specialist (Hematologist, Vascular Surgeon) whenever in doubt.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Stein PD, Kayali F, Olson RE. Incidence of venous thromboembolism in infants and children: Data from the National Hospital Discharge Survey. J Pediatr 2004;145:563-5.  Back to cited text no. 1
    
2.
Raffini L, Huang YS, Witmer C, Feudtner C. Dramatic increase in venous thromboembolism in children's hospitals in the United States from 2001 to 2007. Pediatrics 2009;124:1001-8.  Back to cited text no. 2
    
3.
Levy ML, Granville RC, Hart D, Meltzer H. Deep venous thrombosis in children and adolescents. J Neurosurg 2004;101 1 Suppl: 32-7.  Back to cited text no. 3
    
4.
Vu LT, Nobuhara KK, Lee H, Farmer DL. Determination of risk factors for deep venous thrombosis in hospitalized children. J Pediatr Surg 2008;43:1095-9.  Back to cited text no. 4
    
5.
Branchford BR, Mourani P, Bajaj L, Manco-Johnson M, Wang M, Goldenberg NA. Risk factors for in-hospital venous thromboembolism in children: A case-control study employing diagnostic validation. Haematologica 2012;97:509-15.  Back to cited text no. 5
    
6.
Male C, Kuhle S, Mitchell L. Diagnosis of venous thromboembolism in children. Semin Thromb Hemost 2003;29:377-90.  Back to cited text no. 6
    
7.
Worly JM, Fortenberry JD, Hansen I, Chambliss CR, Stockwell J. Deep venous thrombosis in children with diabetic ketoacidosis and femoral central venous catheters. Pediatrics 2004;113 (1 Pt 1):e57-60.  Back to cited text no. 7
    
8.
Gutierrez JA, Bagatell R, Samson MP, Theodorou AA, Berg RA. Femoral central venous catheter-associated deep venous thrombosis in children with diabetic ketoacidosis. Crit Care Med 2003;31:80-3.  Back to cited text no. 8
    
9.
Tshifularo N, Arnold M, Moore SW. Thromboembolism and venous thrombosis of the deep veins in surgical children – An increasing challenge? J Pediatr Surg 2011;46:433-6.  Back to cited text no. 9
    
10.
Sandoval JA, Sheehan MP, Stonerock CE, Shafique S, Rescorla FJ, Dalsing MC. Incidence, risk factors, and treatment patterns for deep venous thrombosis in hospitalized children: An increasing population at risk. J Vasc Surg 2008;47:837-43.  Back to cited text no. 10
    
11.
Gerotziafas GT. Risk factors for venous thromboembolism in children. Int Angiol 2004;23:195-205.  Back to cited text no. 11
    
12.
Male C, Julian JA, Massicotte P, Gent M, Mitchell L, PROTEKT Study Group. Significant association with location of central venous line placement and risk of venous thrombosis in children. Thromb Haemost 2005;94:516-21.  Back to cited text no. 12
    
13.
Anton N, Massicotte MP. Venous thromboembolism in pediatrics. Semin Vasc Med 2001;1:111-22.  Back to cited text no. 13
    
14.
Chan AK, Deveber G, Monagle P, Brooker LA, Massicotte PM. Venous thrombosis in children. J Thromb Haemost 2003;1:1443-55.  Back to cited text no. 14
    
15.
Nevin MA. Pulmonary embolism, infarction, and hemorrhage. In: Kliegman RM, Jenson HB, Behrman RE, Stanton BF, editors. Nelson Textbook of Pediatrics. 18th ed. Philadelphia: Thomas Press; 2007. p. 1826-8.  Back to cited text no. 15
    
16.
Leary SE, Harrod VL, de Alarcon PA, Reiss UM. Low-dose systemic thrombolytic therapy for deep vein thrombosis in pediatric patients. J Pediatr Hematol Oncol 2010;32:97-102.  Back to cited text no. 16
    
17.
Tousovska K, Zapletal O, Skotakova J, Bukac J, Sterba J. Treatment of deep venous thrombosis with low molecular weight heparin in pediatric cancer patients: Safety and efficacy. Blood Coagul Fibrinolysis 2009;20:583-9.  Back to cited text no. 17
    
18.
Monagle P, Chan AK, Goldenberg NA, Ichord RN, Journeycake JM, Nowak-Göttl U, et al. Antithrombotic therapy in neonates and children: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest 2012;141 2 Suppl:e737S-801S.  Back to cited text no. 18
    
19.
Stine KC, Saylors RL, Saccente CS, Becton DL. Treatment of deep vein thrombosis with enoxaparin in pediatric cancer patients receiving chemotherapy. Clin Appl Thromb Hemost 2007;13:161-5.  Back to cited text no. 19
    


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