**1.5.1 Clinical**

Intravascular catheters are responsible for more than 80% of venous thrombotic complications.Signs and symptoms of catheter-related thrombosis vary from diminished blood flow through the cateter to tenderness and swelling of the affected extremity or swelling of the neck and head associated with superior vena cava syndrome. Although clinically apparent thrombi occur in less than 5% of neonates with a central line. (Beardsley, 2007).

Renal vein thrombosis (RVT) is the most common form of non-catheter-related thrombosis (Nathan et al., 2003). Risk factors for RVT include maternal diabetes, dehydration, infection, asphyxia, polycythemia, prematurity,critical illness, femoral CVL and male gender (chest,913,veldman). Approximately 80% present within the first month and usually within

Venous Thromboembolism in Neonates, Children and

clinical practice.

Patients with Chronic Renal Disease – Special Considerations 41

VTE. Valuable and comprehensive evidence-based clinical practice guidelines have been developed by the American College of Chest Physicians (ACCP) on antithrombotic therapy in neonates and children (Monagle et al, 2008). Their recommendations are necessarily based on extrapolation of principles of therapy from adult guidelines, limited clinical information from registries, individual case studies and knowledge of current common

The following is the summary of the recommendations of the ACCP 2008 on Anticoagulation and Trombolytic Therapy for neonates with VTE: We suggest that central venous lines (CVL) or UVCs associated with confirmed thrombosis be removed, if possible, after 3 to 5 days of anticoagulation (Grade 2C).It is a weak recommendation. We suggest either initial anticoagulation, or supportive care with radiologic monitoring (Grade 2C); however, we recommend subsequent anticoagulation if extension of the thrombosis occurs during supportive care (Grade 1B). It is a strong recommendation. We suggest anticoagulation should be with either of the following: (1) LMWH given bid and adjusted to achieve an anti-FXa level of 0.5–1.0 U/mL: or (2) UFH for 3 to 5 days adjusted to achieve an anti-FXa of 0.35 to 0.7 U/mL or a corresponding APTT range, followed by LMWH. We suggest a total duration of anticoagulation of between 6 weeks and 3 months (Grade 2C). We suggest that if either a CVL or a UVC is still in place on completion of therapeutic anticoagulation, a prophylactic dose of LMWH be given to prevent recurrent VTE until such time as the CVL or UVC is removed (Grade 2C). We recommend against thrombolytic therapy for neonatal VTE unless major vessel occlusion is causing critical compromise of organs or limbs (Grade 1B). We suggest that if thrombolysis is required the clinician use tPA and supplement with plasminogen fresh frozen plasma) prior to commencing therapy (Grade 2C). For neonates or children with unilateral renal vein thrombosis (RVT) in the absence of renal impairment or extension into the inferior vena cava, we suggest supportive care with monitoring of the RVT for extension or anticoagulation with UFH/LMWH or LMWH in therapeutic doses; we suggest continuation for 3 months (Grade 2C). For unilateral RVT that extends into the inferior vena cava, we suggest anticoagulation with UFH/LMWH or LMWH for 3 months (Grade 2C). For bilateral RVT with various degrees of renal failure, we suggest anticoagulation with UFH and initial thrombolytic therapy with TPA, followed by anticoagulation with UFH/LMWH (Grade 2C).Remark: LMWH therapy

requires careful monitoring in the presence of significant renal impairment.

the prevention of this disease in high risk individuals and groups of patients.

Pulmonary embolism and Deep Vein Thrombosis are a wide spectrum of a single disease defined as Venous Thromboembolism, and it occurs for the first time in approximately 100 persons per 100,000 each year in the United States and rises exponentially from less than 5 cases per 100,000 persons at 15 years and less to approximately 500 cases per 100,000

An understanding of the risk factors for venous thrombosis is necessary in order to increase

The major risk factors for thrombosis include endogenous pattern characteristics like obesity and genetic factors, and triggering factors such as surgery, immobility or pregnancy. Venous thrombosis tends to occur due to additive effects of endogenous, genetic and environmental

**2. Venous thromboembolism and chronic kidney disease** 

persons at age 80 years (White, 2003; Ageno, 2006; Heit, 2008).

risk factors present simultaneously (Cushman, 2007).

the first week of life and it is likely that a number of these :events initially develop antenatally. (Monagle et al., 2008; Veldman, 2008). Presenting symptoms and clinical findings are different in neonates and older patients and are influenced by the extent and rapidity of thrombus formation. Neonates usually have a flank mass, hematuria, proteinuria, thrombocytopenia and nonfunction of the involved kidney. (Nathan et al., 2003). Approximately 25% of cases are bilateral and 52-60% are reported to have evidence of extension into the inferior vena caval (IVC). (Monagle et al., 2008). Overall survival following neonatal RVT is generally favorable. Four small cohort studies with variable follow-up reported 81-100% of neonates survived. Clinical sequelae included chronic renal impairment and hypertension. (Monagle et al., 2008)

Thombosis of the inferior vena cava can present with signs resembling obstruction of the renal vein (hematuria and retroperitoneal mass); however, these will occur bilaterally when the inferior vena cava is affected. In addition, the lower limbs may be edematous and, if blood flow is susbstantially impared, the child may be in respiratory distress and may have high blood pressure. (Veldman, 2008)

Signs of impared liver function, hepatomegaly and splenomegaly should raise the suspicion of portal vein thrombosis (PVT); however, only about 10% of children with PVT develop acute clinical symptoms (Veldman, 2008).
