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Biomedical subjects

C L Witte

Publications and source records attributed to C L Witte.

At least 91 records · Page 5Linked to original sources
PubMed1985

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

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 infarction; 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 (less than 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.

Abdominal Neoplasms↗
PubMed1985

Retroperitoneal nodal aplasia, asplenia, chylous effusion and lymphatic dysplasia: an acquired immunodeficiency syndrome?

Two adult patients (one in Italy and the other in the USA) are described with similar findings of paraaortic nodal aplasia, asplenism, multiple serous and chylous effusions, and retroperitoneal lymphatic dysplasia. Although the clinical courses are incomplete, this unusual constellation of signs in the setting of normal peripheral lymph trunks suggest an acquired rather than inborn anomaly and possibly a variant acquired immunodeficiency syndrome.

Acquired Immunodeficiency Syndrome↗
PubMed1984

AIDS in 1968.

Explore the source record for details and available documents.

Acquired Immunodeficiency Syndrome↗
PubMed1984

Cystic hygroma reconsidered: hamartoma or neoplasm? Primary culture of an endothelial cell line from a massive cervicomediastinal hygroma with bony lymphangiomatosis.

A young woman presented with massive enlargement of a giant cervicomediastinal cystic hygroma, which communicated in part with the thoracic duct and was associated with generalized bony lymphangiomatosis. Modern imaging and sophisticated intraoperative physiologic monitoring made one-stage resection feasible. Tissue culture of explants of the hygroma yielded a primary endothelial cell line still surviving after 18 months, which, like the cyst-lining endothelium in the original resected specimen, reacted positively for Factor VIII-associated antigen. These findings, in conjunction with the histologic picture, support the notion that cystic hygroma represents an expanding proliferating endothelial growth process and not simply a sequestered lymphatic receptacle.

Adult↗
PubMed1984

Choledochal obstruction by cystic duct stone. Mirizzi's syndrome.

Two patients with high-grade common bile duct obstruction from an impacted cystic duct stone are described. A low-lying cystic-choledochal duct juncture or contiguity of a large cystic duct with the common hepatic duct are usual preexisting anatomic conditions. Known as Mirizzi's syndrome, this uncommon phenomenon needs to be considered when clinical and intraoperative findings indicate obstruction of the common bile duct by stone, but bidirectional exploration of the common bile duct or location of an elusive calculus after choledochotomy proves unexpectedly difficult.

Aged↗
PubMed1984

Spontaneous iron overload in alpha-thalassemic mice.

Because clinical disorders of spontaneous iron overload have no experimental counterpart, we studied iron distribution (atomic absorption analysis) and intestinal absorption (59Fe) in mice with hereditary alpha-thalassemia. Mice heterozygous for a radiation-induced alpha-Hb gene deletion exhibit a mild hemolytic anemia, like the human condition, with microcytosis, reticulocytosis, splenomegaly, and chemical evidence of defective alpha-chain synthesis. Quantitative iron determination showed that total iron content in spleen, liver, and kidney, but not heart or lung, of adult alpha-thalassemic mice was greater (P less than .05) than that in unaffected littermates. Iron concentration was also increased in liver (P less than .001), spleen (P = .025), kidney (P = .058), and heart (P = .010); in general, the greater the iron concentration in liver, the greater that in spleen (r = .39, P = .009), kidney (r = .70, P less than .001), and heart (r = .46, P less than .001). In mice examined 8 months postoperatively, splenectomy, as compared to sham operation, significantly raised iron content in extrasplenic tissues, but did not affect total body iron. At 10-11 weeks of age, but no longer at 12-14 weeks, thalassemic mice showed higher rates of iron absorption than age-matched controls. Thus, alpha-thalassemic mice display an early occurring iron absorption defect, leading to a modest, sustained, nonprogressive iron overload, and thereby represent a valuable model for exploring disorders of iron homeostasis.

Animals↗
PubMed1983

Transcapillary water and protein flux in the canine intestine with acute and chronic extrahepatic portal hypertension.

Intestinal transcapillary water and total protein flux were determined in dogs with chronic extrahepatic portal hypertension after construction of an aortic-portal shunt combined with hilar portal vein constriction and compared to acute portal vein constriction. Measurements were made of thoracic duct lymph flow, portal venous pressure, and total protein concentration in plasma, thoracic duct lymph, intestinal and liver lymph. From these data and calculations based on the dual visceral origin of thoracic duct lymph from liver and intestine, intestinal transcapillary water flux in chronic extrahepatic portal hypertension (portal venous pressure = 21.4 +/- 2 mm Hg; mean +/- SEM), increased 5-fold (93 +/- 12 from 17 +/- 4 microliters/min/kg, P less than 0.001), while intestinal total protein flux expressed as protein clearance (intestinal transcapillary water flux X intestinal lymph/plasma total protein concentration) was unchanged (13 +/- 3 from 10 +/- 2 microliters/min per kg; P greater than 0.4), a finding supported by unaltered whole body plasma albumin "leak rate" (83 +/- 16 from 80 +/- 2 microliters/min per kg; P greater than 0.9). In acute portal vein constriction (portal venous pressure = 26 +/- 1 mm Hg) intestinal transcapillary water flux was similarly increased (58 +/- 16 from 9 +/- 2; P less than 0.014) but intestinal total protein flux was increased 3-fold (16 +/- 4 from 5 +/- 2; P less than 0.032). Calculated permeability surface area product and protein reflection coefficient (cross-point method) increased similarly in both preparations. In accord with earlier findings in patients with hepatic cirrhosis, chronic elevation in portal pressure increased intestinal transcapillary water flux but not total protein flux.

Animals↗
PubMed1983

A rational approach to serious blunt hepatic injury.

Based on our cumulative experience in patients with serious blunt liver trauma, hepatic resection is seldom necessary where cross-clamping the hepatoduodenal ligament (portal triad) effectively stops parenchymal hemorrhage. Oversewing or "hemo-clipping" of intrahepatic disrupted vascular tributaries combined, when appropriate, with lobar hepatic arterial ligation and transposition of an omental pedicle graft into the "fracture" defect is usually sufficient treatment. On the other hand, avulsion of hepatic veins and/or tears of the retrohepatic vena cava require major hepatic resection primarily for exposure. But even in conjunction with internal vena caval bypass shunts, the mortality with this injury remains high.

Adolescent↗
PubMed1983

Splanchnic circulatory and tissue fluid dynamics in portal hypertension.

Bleeding esophagogastric varices and ascites are the most serious complications of portal hypertension. Rupture of varices develops because of progressively rising portal pressure as rapid splanchnic blood flow combines with increasing portal vascular resistance (active congestion). The greater the restriction to transhepatic portal venous flow, the less the increment in splanchnic blood flow required to generate a venous pressure ultimately exceeding the bursting tension of thin-walled varices. Ascites, on the other hand, represents an imbalance of hydrodynamic forces in the microcirculation of the liver and digestive tract. Large amounts of fluid are driven out of the vascular space into visceral tissues. When the rate of lymph return to the systemic venous circulation fails to keep pace with increased capillary filtration, peritoneal transudation ensues. A complex sequence of events is then set into motion leading to renal salt and water retention. Plasma volume is restored, but at the same time hepatosplanchnic lymph formation is aggravated and a vicious cycle is thereby created. Treatment depends on reduction of lymph formation by indirect (dietary restriction of salt and water and diuretic drugs) or direct (portasystemic shunt) portal decompression or, alternatively, on acceleration of an already rapid lymph return (peritoneovenous shunt) to match the high rate of lymph production.

Ascites↗
PubMed1983

Preservation of the spleen.

Because the spleen can no longer be considered readily dispensable, a variety of alternatives to total splenectomy (splenic repair, partial resection, autotransplantation, ischemic therapy, reticuloendothelial blockade and irradiation) have been developed to preserve functioning remnants in trauma and hypersplenism. It remains unclear how much spleen adequately protects against OPSI or under persistent workload stimulus leads to recurrence of hypersplenism.

Humans↗
PubMed1983

Circulatory dynamics of the spleen.

Circulatory dynamics are examined in terms of the open and closed circulation, pathologic changes in blood dyscrasia and portal hypertension, and the rationale of circulatory control (ischemic therapy) in treatment of hypersplenism.

Angiography↗