ISSN: 2451-0637
Archives of Medical Science - Civilization Diseases
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1/2016
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abstract:
Letter to the Editor

What can hide a neonatal sepsis with subsequent foot amputation?

Paola Di Filippo
,
Alessandra Scaparrotta
,
Raffaella Basilico
,
Sabrina Di Pillo
,
Piernicola Pelliccia
,
Francesco Chiarelli

Arch Med Sci Civil Dis 2016; 1: e10–e15
Online publish date: 2016/04/27
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Portal vein thrombosis (PVT) is defined as a partial or complete obstruction of the extrahepatic portal vein, due to the presence of a thrombus in the vessel lumen and documented by radiological imaging [1, 2]. It is one of the most common vascular disorders of the liver. Large cohort studies have reported a global prevalence of 1%, but in some risk groups it can be up to 26%. The most frequent causes are cirrhosis, hepatobiliary malignancy, abdominal infectious, inflammatory diseases and myeloproliferative disorders (MPD) [3]. Myeloproliferative disorders are recognized to be among the principal causes of PVT in non-cirrhotic patients [1]. The natural history of PVT results in portal hypertension leading to splenomegaly and formation of portosystemic collateral blood vessels and esophageal, gastric, duodenal, and jejunal varices [3]. Portal vein thrombosis is the leading cause of variceal bleeding in children [4]. Diagnosis of PVT is made by imaging, mainly Doppler ultrasonography [3].
A 10-year-old child attended our Pediatric Department in October 2014 for recurrent vomiting from about 3 months; the child had vomiting 1–2 days/week (10–15 episodes/day). The episodes were not associated with abdominal pain or fever or other symptoms. His mother reported weight loss of 1 kg in the last month, but the child continued to feed regularly, without rejection of particular foods.
His past medical history was characterized by foot amputation during the neonatal period because of a sepsis and consequent disseminated intravascular coagulation. The patient had no history of hematemesis, jaundice, abdominal distension or abdominal pain. There was no family history for coagulation disorders.
At admission the complete blood count was normal and the inflammatory markers were negative. Metabolic parameters were within normal limits (Table I). Aminoacidemia and aminoaciduria were normal. Celiac disease, food allergy and acute gastroenteritis were excluded.
A neurological study was performed to exclude a central cause of vomiting: the electroencephalogram was normal, and the brain magnetic resonance imaging (MRI) documented no encephalic abnormalities.
The child was also evaluated in the gastroenterological field. Abdominal ultrasound was performed, revealing: liver left lobe mild atrophy; thrombosis of the portal vein left branch with left hepatic artery hypertrophy (Figures 1 A and 1 B); perihepatic and perigastric collateral circulation...


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