Protean manifestations of pylethrombosis. A review of thirty-four patients

C. L. Witte, M. L. Brewer, Marlys H Witte, G. B. Pond

Research output: Contribution to journalArticle

96 Citations (Scopus)

Abstract

Thirty-four adult patients with portomesenteric venous occlusion (PVO) were reviewed. In 11 with hepatic cirrhosis, PVO was usually heralded by worsening ascites often with varix hemorrhage; mortality was high. Four with isolated portal block had varix hemorrhage without ascites. All of these patients survived despite recurrent hematemesis when portal decompression was not feasible in two patients. Eight others (5 agnogenic and 3 with hypercoagulability), experienced sudden abdominal pain with a clot typically propagated into mesenteric tributaries with ileojejunal infarctions; survival was related to the promptness of operation and the extent of bowel ischemia. Of five patients with intraabdominal sepsis and pylephlebitis, only one survived. In the final six patients, PVO occurred with intraabdominal carcinoma. Five had progressive ascites, cachexia, and an early death. Imaging techniques included plain and contrast roentgenograms, ultrasonography, and for definitive diagnosis direct portography (operative or splenoportogram), indirect portography (splanchnic arteriovenogram), and computed tomography. Thirteen of 34 patients had ascites, and in nine of 11 patients examined, protein concentration of ascitic fluid was extremely low (< 0.6 g/dl). Clinical presentation of PVO varies, depending on acuteness and extent of visceral venous blockade, severity of portal hypertension, auxiliary venous collateralization, and regional lymph flow. Inciting factors include endothelial damage and blood hypercoagulability from trauma, infection, stagnant circulation, blood dyscrasia, and malignancy. Improved imaging now allows early diagnosis.

Original languageEnglish (US)
Pages (from-to)191-202
Number of pages12
JournalAnnals of Surgery
Volume202
Issue number2
StatePublished - 1985

Fingerprint

Ascites
Portography
Thrombophilia
Varicose Veins
Hemorrhage
Hematemesis
Cachexia
Viscera
Blood Circulation
Ascitic Fluid
Portal Hypertension
Lymph
Decompression
Liver Cirrhosis
Infarction
Abdominal Pain
Early Diagnosis
Ultrasonography
Sepsis
Ischemia

ASJC Scopus subject areas

  • Surgery

Cite this

Witte, C. L., Brewer, M. L., Witte, M. H., & Pond, G. B. (1985). Protean manifestations of pylethrombosis. A review of thirty-four patients. Annals of Surgery, 202(2), 191-202.

Protean manifestations of pylethrombosis. A review of thirty-four patients. / Witte, C. L.; Brewer, M. L.; Witte, Marlys H; Pond, G. B.

In: Annals of Surgery, Vol. 202, No. 2, 1985, p. 191-202.

Research output: Contribution to journalArticle

Witte, CL, Brewer, ML, Witte, MH & Pond, GB 1985, 'Protean manifestations of pylethrombosis. A review of thirty-four patients', Annals of Surgery, vol. 202, no. 2, pp. 191-202.
Witte, C. L. ; Brewer, M. L. ; Witte, Marlys H ; Pond, G. B. / Protean manifestations of pylethrombosis. A review of thirty-four patients. In: Annals of Surgery. 1985 ; Vol. 202, No. 2. pp. 191-202.
@article{6834b3e968db4ed885e83d3b22ab88d9,
title = "Protean manifestations of pylethrombosis. A review of thirty-four patients",
abstract = "Thirty-four adult patients with portomesenteric venous occlusion (PVO) were reviewed. In 11 with hepatic cirrhosis, PVO was usually heralded by worsening ascites often with varix hemorrhage; mortality was high. Four with isolated portal block had varix hemorrhage without ascites. All of these patients survived despite recurrent hematemesis when portal decompression was not feasible in two patients. Eight others (5 agnogenic and 3 with hypercoagulability), experienced sudden abdominal pain with a clot typically propagated into mesenteric tributaries with ileojejunal infarctions; survival was related to the promptness of operation and the extent of bowel ischemia. Of five patients with intraabdominal sepsis and pylephlebitis, only one survived. In the final six patients, PVO occurred with intraabdominal carcinoma. Five had progressive ascites, cachexia, and an early death. Imaging techniques included plain and contrast roentgenograms, ultrasonography, and for definitive diagnosis direct portography (operative or splenoportogram), indirect portography (splanchnic arteriovenogram), and computed tomography. Thirteen of 34 patients had ascites, and in nine of 11 patients examined, protein concentration of ascitic fluid was extremely low (< 0.6 g/dl). Clinical presentation of PVO varies, depending on acuteness and extent of visceral venous blockade, severity of portal hypertension, auxiliary venous collateralization, and regional lymph flow. Inciting factors include endothelial damage and blood hypercoagulability from trauma, infection, stagnant circulation, blood dyscrasia, and malignancy. Improved imaging now allows early diagnosis.",
author = "Witte, {C. L.} and Brewer, {M. L.} and Witte, {Marlys H} and Pond, {G. B.}",
year = "1985",
language = "English (US)",
volume = "202",
pages = "191--202",
journal = "Annals of Surgery",
issn = "0003-4932",
publisher = "Lippincott Williams and Wilkins",
number = "2",

}

TY - JOUR

T1 - Protean manifestations of pylethrombosis. A review of thirty-four patients

AU - Witte, C. L.

AU - Brewer, M. L.

AU - Witte, Marlys H

AU - Pond, G. B.

PY - 1985

Y1 - 1985

N2 - Thirty-four adult patients with portomesenteric venous occlusion (PVO) were reviewed. In 11 with hepatic cirrhosis, PVO was usually heralded by worsening ascites often with varix hemorrhage; mortality was high. Four with isolated portal block had varix hemorrhage without ascites. All of these patients survived despite recurrent hematemesis when portal decompression was not feasible in two patients. Eight others (5 agnogenic and 3 with hypercoagulability), experienced sudden abdominal pain with a clot typically propagated into mesenteric tributaries with ileojejunal infarctions; survival was related to the promptness of operation and the extent of bowel ischemia. Of five patients with intraabdominal sepsis and pylephlebitis, only one survived. In the final six patients, PVO occurred with intraabdominal carcinoma. Five had progressive ascites, cachexia, and an early death. Imaging techniques included plain and contrast roentgenograms, ultrasonography, and for definitive diagnosis direct portography (operative or splenoportogram), indirect portography (splanchnic arteriovenogram), and computed tomography. Thirteen of 34 patients had ascites, and in nine of 11 patients examined, protein concentration of ascitic fluid was extremely low (< 0.6 g/dl). Clinical presentation of PVO varies, depending on acuteness and extent of visceral venous blockade, severity of portal hypertension, auxiliary venous collateralization, and regional lymph flow. Inciting factors include endothelial damage and blood hypercoagulability from trauma, infection, stagnant circulation, blood dyscrasia, and malignancy. Improved imaging now allows early diagnosis.

AB - Thirty-four adult patients with portomesenteric venous occlusion (PVO) were reviewed. In 11 with hepatic cirrhosis, PVO was usually heralded by worsening ascites often with varix hemorrhage; mortality was high. Four with isolated portal block had varix hemorrhage without ascites. All of these patients survived despite recurrent hematemesis when portal decompression was not feasible in two patients. Eight others (5 agnogenic and 3 with hypercoagulability), experienced sudden abdominal pain with a clot typically propagated into mesenteric tributaries with ileojejunal infarctions; survival was related to the promptness of operation and the extent of bowel ischemia. Of five patients with intraabdominal sepsis and pylephlebitis, only one survived. In the final six patients, PVO occurred with intraabdominal carcinoma. Five had progressive ascites, cachexia, and an early death. Imaging techniques included plain and contrast roentgenograms, ultrasonography, and for definitive diagnosis direct portography (operative or splenoportogram), indirect portography (splanchnic arteriovenogram), and computed tomography. Thirteen of 34 patients had ascites, and in nine of 11 patients examined, protein concentration of ascitic fluid was extremely low (< 0.6 g/dl). Clinical presentation of PVO varies, depending on acuteness and extent of visceral venous blockade, severity of portal hypertension, auxiliary venous collateralization, and regional lymph flow. Inciting factors include endothelial damage and blood hypercoagulability from trauma, infection, stagnant circulation, blood dyscrasia, and malignancy. Improved imaging now allows early diagnosis.

UR - http://www.scopus.com/inward/record.url?scp=0021826669&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0021826669&partnerID=8YFLogxK

M3 - Article

VL - 202

SP - 191

EP - 202

JO - Annals of Surgery

JF - Annals of Surgery

SN - 0003-4932

IS - 2

ER -