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CASE REPORT
Year : 2020  |  Volume : 23  |  Issue : 3  |  Page : 429-433

Bleeding oesophageal varices in a 9 -year old girl as a late complication of neonatal umbilical catheterization


1 Paedaitric Surgery Unit, Department of Surgery, Nnamdi Azikiwe University Teaching Hospital, Nnewi, Anambra State, Nigeria
2 General Surgery Unit, Department of Surgery, Nnamdi Azikiwe University Teaching Hospital, Nnewi, Anambra State, Nigeria
3 Department of Paediatrics, Nnamdi Azikiwe University Teaching Hospital, Nnewi, Anambra State, Nigeria

Date of Submission22-Mar-2019
Date of Acceptance15-Oct-2019
Date of Web Publication5-Mar-2020

Correspondence Address:
Dr. J O Ugwu
Department of Surgery, Nnamdi Azikiwe University Teaching Hospital, Nnewi, P.M.B 5025, Nnewi, Anambra State
Nigeria
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/njcp.njcp_163_19

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   Abstract 


Bleeding oesophageal varices is a rare condition in children and most of them are usually of extrahepatic causes. Neonatal umbilical catheterization even though safe has been identified as a cause of portal vein thrombosis and oesophaeal varices. We report a 9-year old Nigerian girl who had massive upper gastrointestinal bleeding from oesophageal varices secondary to pulmonary vein stenosis. She had umbilical catheterization for exchange blood transfusion as a neonate. She was sequentially managed with endoscopic sclerotherapy and band ligation We seek to highlight the need for a high index of suspicion of oesophageal varices in children with upper gastrointestinal bleeding who had neonatal umbilical catheterization.

Keywords: Massive upper gastrointestinal bleeding, oesophagogastroduodenoscopy, umbilical catheterization


How to cite this article:
Ugwu J O, Emegoako C D, Ugwunne C A, Ulasi T O, Ugwu N O. Bleeding oesophageal varices in a 9 -year old girl as a late complication of neonatal umbilical catheterization. Niger J Clin Pract 2020;23:429-33

How to cite this URL:
Ugwu J O, Emegoako C D, Ugwunne C A, Ulasi T O, Ugwu N O. Bleeding oesophageal varices in a 9 -year old girl as a late complication of neonatal umbilical catheterization. Niger J Clin Pract [serial online] 2020 [cited 2020 Apr 6];23:429-33. Available from: http://www.njcponline.com/text.asp?2020/23/3/429/280020




   Introduction Top


Esophageal variceal bleeding is uncommon in children and most of the time, it is as a result of portal hypertension from portal venous obstruction rather than from chronic liver diseases.[1] The most common causes of presinusoidal portal hypertension include umbilical catheterization, omphalitis, dehydration, and neonatal sepsis.[1],[2] These would induce portal venous thrombosis and consequently stenosis over time, thereby increasing the portal venous pressure.

Portal vein thrombosis (PVT) is rare in children. It was first described by Balfour and Stewart[3] in 1868. Umbilical catheterization has been identified as a major cause of portal hypertension from PVT, however about 50% of cases of PVT have unidentified etiology.[2],[4] The umbilical vein is a common parenteral access for blood transfusions, administration of drugs, fluids and nutrition but its use can lead to complications including PVT.[2],[4],[5]

Extrahepatic portal vein obstruction is suspected in upper gastrointestinal (UGI) bleeding or unexplained splenmegaly in the absence of jaundice or other features of chronic liver diseases.[4] Massive UGI bleeding from esophageal varices in children as a late complication of neonatal umbilical catheterization poses diagnostic and treatment challenges.[1] Other common causes of massive UGI bleeding in children such as erosive esophagitis, peptic ulcer disease  Mallory-Weiss tear More Details, nonsteroidal anti-inflammatory drugs (NSAIDs)-induced gastritis, and Henoch Schonlein purpura should be excluded.[6] A high index of suspicion is required during evaluation, to facilitate early diagnosis appropriate and timely interventions.

We therefore report a case of a 9-year-old Nigerian girl who presented with massive UGI bleeding from esophageal varices. She had a history of umbilical catheterization for exchange blood transfusion during her neonatal period. She was successfully managed with UGI endoscopic interventions. This report is to highlight the need to suspect esophageal or gastric variceal bleeding from PVT in children with massive UGI, especially if they had umbilical catheterization during the neonatal period.


   Case Summary Top


A 9 –year-old girl was admitted via the Children Emergency Room with a 5-day history of abdominal pain and fever, a 2-day history of bloody vomitus, and passage of blood per rectum. Abdominal pain was of sudden onset, periumbilical, colicky, non-radiating, but did not disturb sleep. It was temporarily relieved by antacids and paracetamol. She had experienced similar episodes of abdominal pain about 2–3 monthly for about 2 years. Fever started few hours after the onset of abdominal pain and was of moderate grade, intermittent, worse during the day and temporarily relieved by paracetamol.

Three days after onset of abdominal pain and fever, patient started vomiting blood. Vomitus contained frank blood and clots, with an estimated volume of 100 mL per vomitus. The frequency of vomiting was about three times daily. There was associated passage of blood per rectum which consisted of altered blood and clots. There was history of dizziness and generalized body weakness but no fainting spells. There was no bleeding from any other parts of the body or antecedent history of trauma. There was no history of use NSAIDs. She had no abdominal swelling or jaundice. There was a history of neonatal jaundice for which she had a session of exchange blood transfusion via an umbilical catheter with feeding tube in our center shortly after birth. The duration of the catheter and whether it was used for any other purpose other than exchange of blood transfusion could not be determined from history. She had taken over-the-counter medications and visited a private hospital where antibiotics and antacids where given but with onset of bleeding was referred to our center for specialized care.

On examination, she was apprehensive, pale, anicteric, febrile with a temperature of 38°C. She was not dehydrated, no pedal edema, and no significant peripheral lymphadenopathy or stigmata of chronic liver disease. The respiratory rate was 40 cycles/min, pulse rate was 120/min, and was of low volume. Her chest was clinically clear and only the first and second heart sounds were heard.

Her abdomen was flat and moved with respiration, she had epigastric and umbilical tenderness, liver and spleen were not palpable. The kidneys were not ballotable and bowel sounds were normoactive. Rectal examination revealed good anal sphincteric tone. The rectum was empty and contained no masses. The gloved examining finger was stained with blood. Other systems were essentially normal.

A diagnosis of massive UGI bleeding was made, with differential diagnoses including peptic ulcer disease, vascular malformation, and esophageal varices.

She had a packed cell volume of 16%, hemoglobin concentration of 4.6 g/dl, and a hemoglobin genotype of AA. Other hematological indices were within normal limits. She was negative for retroviral disease and her serum electrolytes, creatinine, and blood urea were within normal limits. Abdominal radiographs were unremarkable. However, Doppler ultrasonography showed portal venous stenosis [Figure 1]. We immediately commenced her on intravenous fluids (normal saline), administered proton pump inhibitors (omeprazole), vitamin K, third generation cephalosporins (ceftriaxone), and metronidazole. A nasogastric tube was passed to monitor for spontaneous remission or rebleeds.
Figure 1: Doppler ultrasound demonstrating portal venous stenosis

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She received six units of whole blood transfusion within 3 days but despite initial efforts, the patient continued draining frank blood via the nasogastric tube and continued to pass altered blood per rectum. Due to unavailability of facilities for interventional pediatric UGI endoscopy in our center, she was referred to another hospital. There, at the hospital, UGI endoscopy confirmed the diagnosis of bleeding esophageal varices [Figure 2]. She then had sclerotherapy with hypertonic dextrose (50%) which arrested the bleeding. However, bleeding recurred 2 days later necessitating another session of endoscopy during which endoscopic band ligation (EBL) was conducted [See [Figure 3]. She has not bled again afterward. She has been followed up in the outpatient clinic for 3 months now and is scheduled for regular UGI endoscopic follow-up.
Figure 2: Endoscopic view of the esophageal varices

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Figure 3: Following endoscopic band ligation of the esophageal varices

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   Discussion Top


Umbilical vein is often a choice route for venous access in neonates. It is easily accessible and serves as a central vein at that age, hence intravenous fluid and drug administrations, exchange blood transfusion, s and parenteral nutrition can be conveniently administered through this route.[5],[7],[8]

Despite these benefits, the procedure is not without problems and complications such as catheter malpositioning, infection, retained catheter segments, extravasations, hemorrhage, arrhythmias, pericardial effusion, and thromboembolisms.[7],[8],[9] A common late sequaele of portal vein thrombosis is portal stenosis which would lead to prehepatic portal hypertension and consequently gastroesophageal varices.[2],[5]

Our index case, a 9-year-old girl had umbilical venous catheterization in the neonatal intensive care unit for exchange blood transfusion occasioned by neonatal jaundice shortly after birth. This was without any immediate or early complication. There have been previous reports of similar cases. Rogvi et al.[9] and Rahman et al.[10] had a patient each with massive UGI bleeding following umbilical catheterization during the neonatal period. The index case presented at an older age than those in their reports. Farahmand et al.[5] in a prospective study discovered two children out of 40 who had portal venous thrombosis and varices following umbilical catheterization for exchange blood transfusion for neonatal jaundice. PVT and varices were detected in these two children at 2.5 years and 1.5 years, respectively. The lower age of the patients is most likely because it was a prospective study in which the researchers prospectively conducted ultrasonographies for PVT and UGI endoscopies as part of their protocol.

The development of PVT and later hypertension following umbilical catheterization has been attributed to long duration of catheterization and poor skill of insertion.[4],[5] Obladen et al.[4] have recommended X-ray check for the position of the catheter after insertion. Intravenous heparin 0.5 iu/ml infusion via the catheter has been tried but its efficacy in preventing thrombosis is still debatable.[11] There was no check X-ray or ultrasound done on the index case and catheter was not heparinized.

Patients with varices secondary to PVT often present with UGI bleeding and splenomegaly without hepatomegaly as reported by Ferri et al.[2] and Farahmand et al.[5] We had entertained the possibilities of peptic ulcer disease, vascular malformations, and esophageal varices. Peptic ulcer disease or erosive esophagitis would present with burning epigastric pains related to meals and regurgitations, Mallory-Weiss tear follows forceful retching, and NSAID gastritis has antecedent history of intake of NSAID. Closely related to esophageal varices from PVT are varices from chronic liver diseases which often present with jaundice, hepatomegaly, spider angiomata, and varices at other areas of portosystemic anastomosis.[6] The index patient presented with massive UGI bleeding and fever but there was no jaundice, hepatomegaly, or splenomegaly. This explains why all other diagnostic investigations came out normal except the Doppler ultrasound scan which showed portal vein stenosis. [Figure 1] Doppler ultrasound scan has high diagnostic value in PVT.[2],[5] It may also be of great use in routine follow-up of patients who had umbilical catheterization at infancy for early detection of stenosis.[2] Whether this will really be of public health interest may be debatable considering the low prevalence of PVT among those who had umbilical catheterization. The few who may come down with this complication would obviously benefit from Doppler ultrasound scan which is cheap, noninvasive, and accessible.

UGI endoscopy remains the gold standard for diagnosis of esophageal and gastric varices and it serves both diagnostic, therapeutic, and follow-up purposes.[2],[5],[6] It identifies the source and grades the varices. UGI endoscopy can be carried out as an emergency or elective procedures.

Definitive treatment is often preceded by adequate resuscitation with fluids, blood transfusions, blood factor concentrates, and in some cases, vasopressors and balloon tamponades using Sengstaken–Blakemore or Minnesota tubes.[2],[6],[12] Rahman et al.[10] administered 36 sessions of blood transfusion in the management of a patient with massive UGI bleeding from esophageal varices. Ferri et al.[2] reported that 79.5% of their patients required transfusions. Our index case had six units of transfusions with fresh whole blood despite which she continued to bleed. Continuous upper bleeding in a child despite adequate resuscitation should really raise suspicion of bleeding esophageal varices especially when there is no other feature of chronic liver disease.

Options vary on the exact definitive endoscopic treatment to apply between sclerotherapy and band ligation.[2],[6],[12],[13] Both techniques have been found very useful in addressing variceal bleeding. Ferri et al.[2] carried out both EBLs and endoscopic sclerotherapy (ES) among children with PVT and varices, they reported lower complication rates in the former. Maksound et al.[12] applied sclerotherapy with good outcomes, reporting only 4.6% recurrent bleeding. The most preferred and commonly used agents for sclerotherapy are sodium tetradecyl sulphate and thanolamine oleate, others agents that have been used incude sodium morrhuate, polidocanone, and alcohol.[13],[14] Hypertonic glucose has also been used with favorable outcome as reported by Chang et al.[15] Hypertonic dextrose was used as a sclerosant in our patient because more potent agents were not available. When this failed to provide permanent relief, EBL was done and was successful.

In recalcitrant cases, shunting procedures and esophageal devascularization may be options.[6],[10] The role of non-selective B-blockers such as propranolol, in prevention of bleeding from varices rather than as a sole treatment agent has been documented. They function by reducing variceal pressures.[6] Regular follow-up with periodic endoscopies is highly recommended to monitor for recurrences.


   Conclusion Top


Neonatal umbilical catheterization though a very useful and safe procedure may lead to PVT with attendant portal hypertension and development of variceal bleeding later in life. This should be sought for during evaluation of children with massive UGI bleeding and timely endoscopic interventions have been found useful in arresting the bleeding and for follow-up too. There is also need for pediatricians to be aware of this complication and be very gentle with umbilical catheterization.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
   References Top

1.
Costaguta A, Alvarez F. Etiology and management of hemorrhagic complications of portal hypertension in children. Int J Hepatol 2012;2012:879163.  Back to cited text no. 1
    
2.
Ferri PM, Ferreira AR, Fagundes ED, Liu SM, Roquete ML, Penna FJ. Portal vein thrombosis in children and adolescents: 20 years experience of a pediatric hepatology reference center. Arq Gastroenterol 2012;49:69-76.  Back to cited text no. 2
    
3.
Balfour GW, Stewart G. Case of enlarge spleen complicated with ascites, both depending upon varicose dilatation and thrombosis of the portal vein. Edinburgh Med J 1869;14:589-99.  Back to cited text no. 3
    
4.
Obladen M, Ernst D, Feist D, Wille L. Portal hypertension in children following neonatal umbilical disorders. J Perinat Med 1975;3:101-4.  Back to cited text no. 4
    
5.
Farahmand F, Kiano MA, Alizadeh H, Mahdizadeh M, Behjati M, Khatami SF, et al. Prevalence of portal vein thrombosis following umbilical catheterization in neonatal period. Iran J Neonatol 2012;3:51-5.  Back to cited text no. 5
    
6.
Pillai RB, Tolia V. Gastrointestinal bleeding in infants and children. Therapy-London 2008;1;5:465.  Back to cited text no. 6
    
7.
Bothur-Nowacka J, Czech-Kowalska J, Gruszfeld D, Nowakowska-Rysz M, Kościesza A, Polnik D, et al. Complications of umbilical vein catherisation. Case Report. Pol J Radiol 2011;76:70.  Back to cited text no. 7
    
8.
Mutlu M, Aslan Y, Kul S, Yılmaz G. Umbilical venous catheter complications in newborns: A 6-year single-center experience. J Matern Fetal Neonatal Med 2016;29:2817-22.  Back to cited text no. 8
    
9.
Rogvi RÁ, Møller FG, Bergström A, Ifaoui IB, Jørgensen MH. [Bleeding oesophageal varices in a seven-year-old boy supposedly as a late complication to neonatal umbilical venous catheter]. Ugeskr Laeger 2016;178. pii: V03160221.  Back to cited text no. 9
    
10.
Rahman A, Khalil N, Al Thani G, Ismail A. Massive upper GI bleeding in a child. Qatar Med J 2000;2000:5.  Back to cited text no. 10
    
11.
Unal S, Ekici F, Cetin II, Bilgin L. Heparin infusion to prevent umbilical venous catheter related thrombosis in neonates. Thromb Res 2012;130:725.  Back to cited text no. 11
    
12.
Maksoud-Filho JG, Gonçalves ME, Cardoso SR, Gibelli NE, Tannuri U. Long-term follow-up of children with extrahepatic portal vein obstruction: Impact of an endoscopic sclerotherapy program on bleeding episodes, hepatic function, hypersplenism, and mortality. J Pediatr Surg 2009;44:1877-83.  Back to cited text no. 12
    
13.
Cordon JP, Torres CF, García AB, Rodriguez FG, de Parga JM. Endoscopic management of esophageal varices. World J Gastroentero 2012;4:312.  Back to cited text no. 13
    
14.
Chung JB, Nam DK, Han KH, Kim WH, Kim DY, Chon CY, et al. Endoscopic injection sclerotherapy in patients with bleeding esophageal varices: A retrospective analysis. Korean J Intern Med 1990;5:5.  Back to cited text no. 14
    
15.
Chang KY, Wu CS, Chen PC. Prospective, randomized trial of hypertonic glucose water and sodium tetradecyl sulfate for gastric variceal bleeding in patients with advanced liver cirrhosis. Endoscopy 1996;28:481-6.  Back to cited text no. 15
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]



 

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