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(Radiology. 2001;219:645-650.)
© RSNA, 2001

Pediatric Imaging

Does Umbilical Vein Catheterization Lead to Portal Venous Thrombosis? Prospective US Evaluation in 100 Neonates1

Ji Hye Kim, MD, Young Seok Lee, MD 2, Sang Hee Kim, MD, Seon-Kyu Lee, MD, Myung Kwan Lim, MD and Hyung Sik Kim, MD

1 From the Departments of Radiology (J.H.K., Y.S.L., S.K.L., H.S.K.) and Pediatrics (S.H.K.), Gachon Medical School, Ghil Medical Center, 1198 Kuwal-Dong Namdong-Gu, Incheon 405-220, Korea; and Department of Radiology, Inha University Hospital, Incheon, Korea (M.K.L.). Received January 6, 2000; revision requested February 22; final revision received September 22; accepted October 2. Address correspondence to J.H.K. (e-mail: kimjh@ghil.com).


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
PURPOSE: To establish, by means of serial ultrasonography (US), the incidence and natural history of neonatal portal venous thrombosis associated with catheterization of the umbilical vein and to evaluate the potential risk factors predisposing patients to thrombus formation.

MATERIALS AND METHODS: Neonates who had undergone umbilical vein catheterization were studied. US was performed at 2–7-day intervals, before and after the removal of the catheter, until clot resolution or hospital discharge. The presence of portal venous thrombosis and temporal evolution were noted, and various risk factors were analyzed.

RESULTS: US demonstrated clinically silent portal venous thrombosis in 43 (43%) of 100 neonates. Follow-up US revealed complete or partial resolution in 20 (56%) of 36 babies. A significant (P = .024) correlation was found between the initial size of the thrombi and spontaneous clot resolution. Statistically significant risk factors were catheterization for more than 6 days (P = .001) and transfusion (P = .019).

CONCLUSION: Portal venous thrombosis is frequently associated with the placement of an umbilical venous catheter, and spontaneous resolution is expected in many cases. The duration of catheter placement should be minimized, and US monitoring is recommended as a guide to catheter removal.

Index terms: Catheters and catheterization, complications, 957.442 • Catheters and catheterization, in infants and children, 957.126 • Portal vein, thrombosis, 957.442 • Portal vein, US, 957.1298, 957.12983 • Ultrasound (US), in infants and children, 957.1298, 957.12983


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Portal venous thrombosis is the major cause of extrahepatic portal hypertension and gastrointestinal bleeding in children, and the catheterization of the umbilical vein has been implicated as a cause (1–5). In spite of the potential hazard of thrombus formation, the umbilical venous catheter remains a usual route for the monitoring and treatment of critically ill babies. Because portal venous thrombosis seldom causes clinical problems during the neonatal period, the majority of cases remain unrecognized and are fortuitously found later (4,5). For this reason, retrospective clinical observations are insufficient to determine whether an umbilical venous catheter is substantially responsible for portal venous thrombosis.

Ultrasonography (US) is a valuable and safe screening procedure for the assessment of catheter-associated complications (6,7) and portal venous patency (8,9). Authors of prospective studies (10–12) in which US was used concluded that a properly inserted umbilical venous catheter does not lead to the development of portal venous thrombosis. However, we detected portal venous thrombosis during the course of umbilical catheterization more frequently than reported in these earlier studies. Thus, we hypothesized that short-term serial US, starting immediately after the insertion of an umbilical venous catheter, could reveal undetected portal venous thrombosis, which might have been resolved before US in the previous studies.

This prospective study was designed to establish by means of serial US the incidence and natural history of immediately developed portal venous thrombosis related to an umbilical venous catheter. In addition, we examined the potential risk factors associated with the development of portal venous thrombosis.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Patient Population
All neonates admitted to the neonatal intensive care unit at our hospital (Gachon Medical School, Ghil Medical Center, Incheon, Korea) from March 1995 to November 1995 were included in this prospective study, on the condition that an umbilical venous catheter was placed. All decisions regarding the placement of umbilical venous catheters, infusates, and the duration of catheter placement were made by the attending physicians (S.H.K.). The umbilical venous catheters were inserted by attending pediatric physicians or resident physicians with the supervision of attending staff. Polyvinyl chloride end-hole catheters (5.0-F umbilical catheter; Vycon, Ecouen, France) were used throughout the study period. After placement of the umbilical venous catheter, a radiograph was obtained to confirm the location of the catheter, and removal or repositioning was performed in those cases involving improper positioning.

If the catheters were introduced into the portal venous branch, they were removed or repositioned so they were no longer in the portal vein. Umbilical venous catheters positioned below the level of the diaphragm were not removed immediately in babies with difficult venous access. Instead, catheter duration was restricted to a minimal time, and infusion of hypertonic solutions or transfusion through the umbilical venous catheter was avoided when possible. In the cases with catheters placed beyond the right atrium, repositioning was tried by means of careful withdrawal of the catheter.

All these manipulations were performed according to the attending pediatric physician’s decision. Neonates whose catheter was removed immediately were also included in the study. Because US is not potentially harmful, and the information obtained in this study was considered to be of benefit to the babies, the institutional review board of our hospital ruled that verbal parental consent alone was acceptable.

Study Design
Gestational age, birth weight, infusates, duration of catheter use, initial location of the umbilical venous catheter tips, and major clinical problems during admission were recorded for each patient. In addition, careful attempts were made to identify septicemia by means of positive blood culture results. The absence or presence of clinical findings of acute portal obstruction, such as hepatosplenomegaly or elevation of the results of the liver function test (13), was also recorded.

US included color Doppler US scanning of the portal vein and was performed by a pediatric radiologist (J.H.K.) with a 7.5–11.3 multi-MHz linear-array transducer (Apogee RX 400; Advanced Technology Laboratories, Bothell, Wash). The diagnosis of portal venous thrombosis was made by documenting the echogenic intraluminal thrombus at gray-scale US and the absence of flow on color Doppler US images (6,8). In addition to the patency of the portal vein, morphologic changes of the liver and spleen and the presence of collateral vessels or ascites were examined. Initial US was performed within 1 week (median, 2 days) after umbilical venous catheter placement and then serially at 2–4-day intervals until the removal of the catheters. If portal venous thrombosis was not present after catheter removal, US was not performed again. In the remaining cases with portal venous thrombosis, additional studies were performed at 2–7-day intervals until clot resolution or hospital discharge. After discharge, we recommended US for the unresolved thrombi when the babies were brought to the outpatient department for follow-up examination.

In the cases with portal venous thrombosis, the location, extent, and size of the thrombus were recorded. The thrombi were classified into two groups, partial or occlusive, according to size—nonocclusive small thrombi were classified as "partial," and thrombi replacing the entire lumen were classified as "occlusive." Temporal evolution of the thrombi on follow-up studies was classified as (a) completely resolved, (b) decreased in size or extent, (c) persistent, or (d) progressive. Statistical analysis was performed to evaluate whether the size of the thrombi was related to the recanalization of the portal vein. When portal venous thrombosis was detected, the attending pediatricians decided whether to remove the catheter. Although other authors (14,15) have advocated it, we did not attempt clot resolution through intervention.

Several risk factors were identified that correlated with catheter-related thrombosis (1,3,6,15,16). Among them, the following were identified: (a) low birth weight (<1.5 kg), (b) a catheter being present for more than 6 days, (c) the infusion of calcium salt or transfusion of blood products through the catheter, and (d) sepsis. In addition, the position of the catheter tip was classified in accordance with its level of insertion (high, liver, and low). The standard landmarks used were (a) the junction between the inferior vena cava and the right atrium and (b) the lower margin of the liver.

Statistical analysis was performed according to the location of the catheter by using two sets of three variables to evaluate whether the different catheter positions were related to portal venous thrombosis. First, we compared the incidence of portal venous thrombosis between the groups with the catheter tip above (high group) and those with the catheter tip below (liver or low group) the level of the diaphragm (approximate junction of the inferior vena cava and the right atrium at conventional radiography). Second, the group with an umbilical venous catheter that traversed the liver (traverse group, liver or high) was compared with the group with an umbilical venous catheter that did not traverse the liver (nontraverse group, low). The rationale of our method to evaluate whether the different catheter levels are related to the portal venous thrombosis will be discussed later. All statistical analysis was performed by using the {chi}2 test, except in evaluations with expected counts less than 5 in a 2 x 2 table, and then the Fisher exact test was used instead. A P value less than .05 was regarded as indicating a significant difference.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
DISCUSSION
 REFERENCES
 
One hundred nine neonates were enrolled during the study period, and 199 US scans were obtained in 102 babies. Of the seven patients not examined, three died, and four were discharged before US. Among the remaining 102 patients examined, data were deleted from the analysis in two in whom the first US examination was performed more than 1 week after catheterization. Gestational ages of the neonates were 27–42 weeks (mean gestational age, 34 weeks ± 3.58 [SD]), and they weighed 0.98–5.46 kg (mean weight, 2.11 kg). Through umbilical venous catheters, the patients received blood products, calcium preparations, hyperalimentation, antibiotics, and other medications. The catheters were placed for 1–18 days (median, 4 days).

The initial location of the umbilical venous catheter tip was at or above the junction between the inferior vena cava and the right atrium (high) in 64 cases, in the liver in 12, and below the inferior hepatic margin (low) in 15. In eight cases, the umbilical venous catheter tip was mistakenly inserted into the portal vein (Fig 1a). The umbilical venous catheter was folded within the umbilical vein in one neonate. The babies’ major clinical problems included respiratory distress syndrome, sepsis, pneumonia, neonatal jaundice, congenital heart disease, and persistent fetal circulation. Blood culture examination was performed in 57 of the 100 babies, and septicemia was proved in nine of the 57.



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  		Figure 1a. Portal venous thrombosis associated with catheter malposition. (a) Anteroposterior radiograph shows the umbilical venous catheter (arrow) inserted into the portal vein from the umbilicoportal confluence. (b) Transverse US scan obtained after catheter removal reveals a partial thrombus (arrowheads) attached to the wall of the left portal vein.

 


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  		Figure 1b. Portal venous thrombosis associated with catheter malposition. (a) Anteroposterior radiograph shows the umbilical venous catheter (arrow) inserted into the portal vein from the umbilicoportal confluence. (b) Transverse US scan obtained after catheter removal reveals a partial thrombus (arrowheads) attached to the wall of the left portal vein.

 
Portal venous thrombosis was detected in 43 (43%) of the 100 neonates. In all cases, the thrombus occurred in the left intrahepatic portal vein where it is traversed by the junction of the umbilical vein and the ductus venosus (umbilicoportal confluence) (Figs 1b, 2–4). In 26 (60%) of these 43 patients, a small thrombus was attached to the catheter or partially filled the umbilicoportal confluence with a blood flow signal from the remaining patent lumen on color Doppler US images (Figs 1b, 2a). In the remaining 17 (40%), a complete thrombus occupied the entire lumen, and blood flow from the occluded portal vein was not seen (Fig 3). Extension of the thrombus into the right or main portal vein was not noted, although propagation into more peripheral branches occurred in three cases. The liver and the spleen were not enlarged, and neither ascites nor extrahepatic collateral vessels were noted in any case. There were no specific clinical findings suggesting acute portal occlusion in any of the 43 cases with portal venous thrombosis.



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  		Figure 2a. Completely resolved partial thrombosis of the portal vein. (a) Transverse color Doppler US scan shown in black and white reveals echogenic thrombus (black arrow) attached to the umbilical venous catheter (white arrow), which can be identified with an acoustic shadow (arrowheads), within the lumen of the umbilicoportal confluence. The flow signal appears in the remaining patent lumen. (b) Transverse color Doppler US scan shown in black and white obtained 7 days after the catheter was removed shows the thrombus is not visible.

 


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  		Figure 2b. Completely resolved partial thrombosis of the portal vein. (a) Transverse color Doppler US scan shown in black and white reveals echogenic thrombus (black arrow) attached to the umbilical venous catheter (white arrow), which can be identified with an acoustic shadow (arrowheads), within the lumen of the umbilicoportal confluence. The flow signal appears in the remaining patent lumen. (b) Transverse color Doppler US scan shown in black and white obtained 7 days after the catheter was removed shows the thrombus is not visible.

 


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  		Figure 3a. Occlusive portal venous thrombosis and late findings. (a) Transverse US scan shows the umbilical portion of the left portal vein is completely filled with hyperechoic thrombus (arrow). (b) Transverse US scan obtained 2 months later shows the thrombus became a linear cordlike lesion (arrow), and the patent portal lumen is not identified.

 


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  		Figure 3b. Occlusive portal venous thrombosis and late findings. (a) Transverse US scan shows the umbilical portion of the left portal vein is completely filled with hyperechoic thrombus (arrow). (b) Transverse US scan obtained 2 months later shows the thrombus became a linear cordlike lesion (arrow), and the patent portal lumen is not identified.

 


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  		Figure 4. Diagram of the neonatal umbilical and portal venous system. The umbilical vein joins the left portal vein (LPV) in the liver, which goes to the hepatic sinusoid, and a direct communication is formed between the umbilical vein and the ductus venosus, which bypasses the liver and joins the inferior vena cava (IVC). Note the umbilicoportal confluence ({bullet}) where the portal vein (PV) is traversed by the junction of the umbilical vein and the ductus venosus. LHV = left hepatic vein, RHV = right hepatic vein, RPV = right portal vein, SMV = superior mesenteric vein, SV = splenic vein.

 
Follow-up US after the detection of portal venous thrombosis was available in 36 of the 43 patients, and the total follow-up period was 2–73 days (median, 8 days). Thrombosis was monitored to complete resolution in 18 neonates, and the size of the thrombus decreased in two. The time to the detection of resolution after the removal of the catheter varied (range, 2–23 days; mean, 10 days). In the remaining 16 cases, thrombosis was persistently found in 11, and the extent or size increased in five. Recanalization occurred more frequently in cases with partial thrombi than in cases with occlusive thrombi, and a statistically significant (P = .024) relationship was found between the initial size of the thrombus and clot resolution (Table 1).


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  		TABLE 1. Initial Thrombus Size and Clot Resolution

 
In four babies with a relatively long follow-up (range, 16–73 days; mean, 45 days), the thrombus contracted to become an echogenic linear structure or disappeared, and the lumen of the portal vein became obliterated without any flow signal on color Doppler US scans (Fig 3b). In addition, the left lobe of the liver appeared shrunken compared with that in the previous scan in one case. The right and main portal veins were all intact, and splenic venous flow was preserved. We could not find any case that met the US criteria (9) of a cavernous transformation of the portal vein.

As shown in Table 2, the risk of thrombosis was significantly increased in 29 babies who had a catheter in place for more than 6 days (P = .001). Blood products added to the umbilical venous catheter infusate also significantly increased the risk of clot formation in 47 babies (P = .019). Among the three different catheter levels (high, liver, low), the incidence of portal venous thrombosis was highest in the liver, intermediate in the high, and lowest in the low group (Table 3). Between patients with the catheter tip above and those with the catheter tip below the level of the diaphragm, however, a statistically significant difference in the occurrence of portal thrombosis was not found (P = .648). Moreover, the incidence was not significantly different between the traverse and nontraverse groups (P = .264). Portal venous thrombosis was noted in five (63%) of the eight babies with the umbilical venous catheter erroneously inserted into the portal vein from the umbilicoportal confluence (Fig 1). We also detected portal thrombosis in a neonate with a folded umbilical venous catheter.


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  		TABLE 2. Significance of Risk Factors

 

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  		TABLE 3. Location of Umbilical Venous Catheter Tip and Occurrence of Portal Venous Thrombosis

 

   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
REFERENCES
 
Many investigators (1–5) believe that umbilical venous catheters and umbilical sepsis play a causative role in the development of portal venous thrombosis. This belief is based on the retrospective observation that many infants and children with extrahepatic portal hypertension have undergone catheterization of the umbilical vein during the newborn period. Our result of portal venous thrombosis development in a significant number (43%) of babies with an umbilical venous catheter partly supports this deduction. In spite of the alleged complications associated with umbilical venous catheters, authors of prospective studies (10–12) have concluded that properly inserted umbilical venous catheters did not cause portal venous thrombosis.

Among these, however, in the study of Yadav et al (10), portal venous thrombosis was alleged to occur in at least seven (32%) and possibly 12 (55%) of 22 neonates, as evidenced by the absence of splenoportal venous flow, although it was normalized by the age of 2 years. By considering that a small nonocclusive thrombus does not totally interrupt the splenoportal circulation, their real incidence might be much higher.

Guimaraes et al (12) studied the late outcome of umbilical vein catheterization in school-age patients. Doppler US revealed intact portal circulation in all 40 children except in two in whom the left portal vein was not identified. One of these latter two also had a small left hepatic lobe. Although they considered nonvisualized left portal vein as a normal variant, according to our experience, it may be a late sequela of unresolved portal venous thrombosis. None of these patients developed portal hypertension. The results of these two studies (10,12) and the current study indicate that portal venous thrombosis related to an umbilical venous catheter develops in a significant number of cases during the newborn period, but most of these thrombi resolve spontaneously and do not cause portal hypertension.

Until now, the reported incidence of catheter-related thrombosis in infants and children was 1.3%–67% (3,6,7,10–12, 16–21). The major differences among the many investigations include the prospective or retrospective nature of the study; the diagnostic method used to study the thrombus; the time schedule of examinations; and catheter variables such as size, location, and duration (Table 4). In general, prospective US examinations, starting shortly after catheterization, revealed a 17%–44% incidence of thrombosis associated with use of umbilical venous catheters, umbilical arterial catheters, or femoral venous catheters.


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  		TABLE 4. Details of Reported Catheter-related Thrombosis in Various Studies

 
In comparison with authors of other studies, Schwartz et al (11) reported a low (1.3%) incidence of portal venous thrombosis related to an umbilical venous catheter during the early infant period. When one considers the temporal evolution of the thrombi in many studies, the timing and frequency of US monitoring seems to be a key factor in terms of the reported incidence of portal venous thrombosis. As discussed in the article by Schwartz et al (11), thrombi developed during the early neonatal period but resolved before US might have missed it in their study, in which results were obtained at a median age of 2 months. In addition, controlling catheter position so that it was not allowed to terminate in the liver and using a smaller (uniformly 3.0-F) catheter possibly contributed to the lower incidence of portal venous thrombosis.

The long-term sequelae and clinical importance of thrombosis detected at US in asymptomatic neonates admittedly are not fully understood. The natural history of established thrombi has previously been addressed at postmortem examination (22) or by means of experimental work (23). US is uniquely suited for studying the in vivo evolution of thrombus; moreover, the spontaneous regression of catheter-related thrombi detected at US has been reported (7,11,13). Although our study was limited to hospital stay in most cases, clot resolution occurred in more than half of the cases within 23 days after catheter removal, and partial thrombi disappeared more frequently than did occlusive thrombi. In this respect, US monitoring for the early detection of small thrombi and prompt catheter removal could limit the propagation of thrombi and lead to rapid resolution.

Unfortunately, many patients were discharged before clot resolution was achieved, and, in four cases, recanalization was not achieved until much later. However, none of the patients exhibited clinical findings of portal hypertension. If the thrombus does not propagate into the main or right portal vein, the effect on portal obstruction is limited. Moreover, periportal collateral circulation would minimize portal obstruction. It is, therefore, presumed that even in cases of unresolved thrombosis, clinically significant portal hypertension will not develop as long as the clot remains in the left portal vein only.

Known factors associated with the initiation and propagation of thrombosis include endothelial damage during catheter placement, composition of the infusate, catheter characteristics, and the duration and location of catheter placement. Patient variables that can increase the complications caused by umbilical catheterization include low birth weight, low flow state, hypercoagulation disorder, and hypoxia (3,6,15–17,24). Clearly, the need to use umbilical venous catheters preselects those children who are critically ill and in whom many of these risk factors already coexist. When these factors occur concomitantly in a neonate who requires the insertion of an umbilical venous catheter, it is not surprising that a significant percentage develop thrombotic complications. In the current study, prolonged catheterization was the most significant risk factor; duration of umbilical venous catheter placement should be minimized.

The rationale of our classification of the catheter levels and statistical analysis originated from the idea (1,11) that portal venous thrombosis would occur less frequently if the umbilical venous catheter tip was either in the right atrium or in the inferior vena cava (high group). The greater blood flow in this region than in the portal sinus or umbilical vein (liver or low group) ensures adequate mixing of the infusates with the patient’s own blood, and the liver is not directly exposed to unphysiologic stimuli. In addition to the adverse effect of infused fluids, we also believed whether the catheter traverses the umbilicoportal confluence could influence the incidence of thrombosis, because mechanical endothelial damage and altered blood flow caused by the catheter itself in the vascular lumen also play a role in thrombus formation. Moreover, there are reports (20,25) that thrombus or fibrin sheath covering the outside of the venous catheter was present in 45%–100% of cases.

Our observation that most of the small thrombi were attached to the catheter rather than the wall of the portal vein also supports the idea that a catheter in the lumen is closely related to the initiation of thrombosis. However, a statistically significant difference was not found among the different catheter locations. Complex events during catheterization, including both the adverse effect of infusates and mechanical change caused by the catheter, probably led to thrombus formation.

Catheter malposition in the left portal vein apparently increased the occurrence of portal venous thrombosis (Table 3). Review of the anatomy of the umbilical and portal venous system (Fig 4) makes it easy to see how an umbilical venous catheter introduced into the umbilical vein could enter the portal vein. This anatomic relationship can also explain why the main site of thrombosis related to an umbilical venous catheter is the umbilicoportal confluence (the space of Rex).

The prophylactic use of heparin, thrombolytic therapy, and surgical thrombectomy have been examined as means of managing catheter-related thrombosis of the aortic branches (15,16,19). Treatment of symptomatic acute portal venous thrombosis, extending to the main portal vein, by means of regional streptokinase infusion has also been reported (14). However, there is no general guideline regarding the treatment of acute portal venous thrombosis related to an umbilical venous catheter. In contrast to the ischemic symptoms caused by thromboembolism of the arteries, portal venous thrombosis seldom causes clinical problems during the neonatal period. Moreover, many thrombosed portal veins become recanalized without any treatment (11,13), and even unresolved thrombosis is expected to remain silent if it does not propagate into other branches. Probably for these reasons, therapeutic trial is usually not performed. We recommended removal of the catheter as soon as possible after detection of the thrombus and did not try any intervention.

Our results indicate that clinically silent portal venous thrombosis is frequently associated with catheterization of the umbilical vein in critically ill neonates, and spontaneous resolution without any treatment is expected in many cases. US monitoring can facilitate early detection of small thrombi and provide a guide for catheter removal, which could limit the propagation of thrombi and lead to rapid resolution. Significant risk factors identified during this study were the extended duration of catheter presence and the need for transfusion.


   ACKNOWLEDGMENTS
 
We thank Young Chae Kim, MD, and Mi Sun Jang, MD, for their help with data acquisition. We also thank pediatric physicians Kwang Hoon Lee, MD, Dong Joon Kim, MD, Hae Joong Yoon, MD, and Eun Kyung Hwang, MD, for their help with recording patient clinical data and obtaining verbal permission from the parents.


   FOOTNOTES
 
2 Current address: Department of Radiology, Dankook University College of Medicine, ChungNam, Korea. Back

Author contributions: Guarantor of integrity of entire study, J.H.K.; study concepts, J.H.K., Y.S.L.; study design, J.H.K., Y.S.L., S.H.K.; literature research, J.H.K., Y.S.L., S.H.K., M.K.L.; clinical studies, J.H.K., S.H.K.; data acquisition, J.H.K.; data analysis/interpretation, J.H.K., Y.S.L., S.K.L.; statistical analysis, J.H.K., S.K.L.; manuscript preparation, J.H.K.; manuscript definition of intellectual content, J.H.K., Y.S.L., H.S.K.; manuscript editing, J.H.K.; manuscript revision/review, J.H.K., M.K.L., H.S.K., S.H.K.; manuscript final version approval, J.H.K., S.H.K., M.K.L.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 

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