OBJECTIVE: To investigate the causes, treatment options and outcomes of immune thrombocytopenia (ITP) patients with splanchnic venous thrombosis (SVT). METHODS: The clinical diagnosis, treatment and outcomes data of one 26-year-old male ITP patient with SVT as initial manifestation were collected. The possible causes and treatment options of the patients were discussed through literatures review. RESULTS: The result of blood routine tests of the patient showed that Plt（17-38）×10 CONCLUSION ITP combined with large scale of SVT is rare, and it is difficult to cure. It should be pay more attention to the possible thrombosis risk triggered by a transiently increased EOS in the blood stream. Promptly etiological treatment and the balance between anticoagulant therapy and bleeding risks should be taken in clinical practice.
Aged, 80 and over ; Anticoagulants/therapeutic use* ; Heparin, Low-Molecular-Weight ; Humans ; Male ; Purpura, Thrombocytopenic, Idiopathic/complications* ; Splanchnic Circulation ; Venous Thrombosis

The incidence of cerebral palsy has not decreased despite advances in neonatal care. Preterm infants are at a high risk of cerebral palsy. Moreover, preterm infants might experience permanent neurological sequelae due to injury in the preterm brain. Although the etiology of preterm brain injury is not fully understood, preterm brain injury is strongly associated with abnormal cerebral perfusion and oxygenation. Monitoring systemic blood pressure or arterial oxygen saturation using pulse oximetry is not enough to guarantee proper cerebral perfusion or oxygenation. Early detection of improper cerebral perfusion can prevent irreversible cerebral damage. To decrease brain injury through the early detection of under-perfusion and deoxygenation, other diagnostic modalities are needed. Near-infrared spectroscopy can continuously and noninvasively monitor regional oxygen saturation (rSO₂), which reflects the perfusion and oxygenation status of tissues at bedside. Near-infrared spectroscopy represents a balance between tissue oxygen supply and demand. Cerebral rSO₂ monitoring has been used most frequently in neonatal cardiac surgery to monitor cerebral oxygenation and prevent hypoxic damage or shock. Recently, cerebral, renal, or splanchnic rSO₂ in neonates is frequently monitored. The progression of a disease, brain injury, and death can be prevented by detecting changes in rSO₂ values using near-infrared spectroscopy. In this article, the basic principles, usefulness, and applications of near-infrared spectroscopy in neonates are discussed.
Blood Pressure ; Brain ; Brain Injuries ; Cerebral Palsy ; Cerebrovascular Circulation ; Humans ; Incidence ; Infant, Newborn ; Infant, Premature ; Oximetry ; Oxygen ; Perfusion ; Shock ; Spectroscopy, Near-Infrared ; Splanchnic Circulation ; Thoracic Surgery

PURPOSE: To investigate the hemodynamic risk factors for necrotizing enterocolitis (NEC), we analyzed the characteristics of descending aorta (DA) blood flow in preterm neonates, who later developed NEC. METHODS: This was an observational case-control study on 53 preterm neonates at a tertiary referral center. Clinical and echocardiographic data were collected from 23 preterm neonates with NEC (NEC group), and compared with those of 30 preterm neonates without NEC (control group). Echocardiography was done at a median (interquartile range) of 5 (3–9) days after birth and 2 (1–2.5) days before the diagnosis of NEC. RESULTS: Basic clinical characteristics including gestational age, birth weight, Apgar score, breast feeding status, use of umbilical catheters, and mode of invasive ventilator care were similar between the groups. Compared with the control group, the lowest diastolic velocity of DA was significantly decreased, whereas the diastolic reverse flow and the ratio of diastolic reverse to systolic forward flows were significantly increased in the NEC group. In addition, the resistive index (RI) of DA was significantly increased in the NEC group and showed a positive association with the development of NEC. Multivariate logistic regression analysis showed that increasing RI of DA was an independent risk factor for the development of NEC (P=0.008). CONCLUSION: Significant changes in DA flow characteristics including decreased diastolic velocity and increased diastolic reverse flow along with increased peripheral vascular resistance were observed before the development of NEC in preterm neonates. These findings may help clinicians stratify in advance neonates at a risk of developing NEC and may help improve outcomes in these neonates.
Aorta, Thoracic* ; Apgar Score ; Birth Weight ; Breast Feeding ; Case-Control Studies ; Catheters ; Critical Care ; Diagnosis ; Echocardiography ; Enterocolitis, Necrotizing* ; Gestational Age ; Hemodynamics ; Humans ; Infant, Newborn* ; Logistic Models ; Parturition ; Risk Factors ; Splanchnic Circulation ; Tertiary Care Centers ; Vascular Resistance ; Ventilators, Mechanical

In cirrhotic patients undergoing liver transplantation, reperfusion of a liver graft typically increases portal venous blood flow (PVF) because of a decrease in resistance in the liver graft to the PVF and underlying hyperdynamic splanchnic circulation, which develops due to liver cirrhosis complicated by portal hypertension and persists even after successful liver transplantation. If the liver graft has enough capacity to accommodate the increased PVF, the shear stress inflicted on the sinusoidal endothelial cells of the graft promotes hepatic regeneration; otherwise, small-for-size syndrome (SFSS) develops, leading to poor graft function and graft failure. In particular, a partial graft transplanted to patients undergoing living donor liver transplantation has less capacity to accommodate the enhanced PVF than a whole liver graft. Thus, the clinical conditions that the partial graft encounters determine either hepatic regeneration or development of SFSS. Consistent with this, this review will discuss the two conflicting effects of portal hyperperfusion (hepatic regeneration vs. portal hyperperfusion injury) on the partial grafts in cirrhotic patients suffering from hyperdynamic splanchnic circulation, in addition to normal physiology and pathophysiology of hepatic hemodynamics.
Endothelial Cells ; Hemodynamics ; Humans ; Hypertension, Portal ; Liver Cirrhosis ; Liver Regeneration ; Liver Transplantation ; Liver* ; Living Donors ; Physiology ; Regeneration* ; Reperfusion ; Splanchnic Circulation* ; Transplants*

OBJECTIVEBased on the observation that coagulation necrosis occurs in the majority of neonatal necrotizing enterocolitis (NEC) patients, it is clear that intestinal ischemia is a contributing factor to the pathogenesis of NEC. However, the published studies regarding the role of intestinal ischemia in NEC are controversial. The aim of this paper is to review the current studies regarding intestinal microcirculatory dysfunction and NEC, and try to elucidate the exact role of intestinal microcirculatory dysfunction in NEC.

DATA SOURCESThe studies cited in this review were mainly obtained from articles listed in Medline and PubMed. The search terms used were "intestinal microcirculatory dysfunction" and "neonatal necrotizing enterocolitis".

STUDY SELECTIONMainly original milestone articles and critical reviews written by major pioneer investigators in the field were selected.

RESULTSImmature regulatory control of mesentery circulation makes the neonatal intestinal microvasculature vulnerable. When neonates are subjected to stress, endothelial cell dysfunction occurs and results in vasoconstriction of arterioles, inflammatory cell infiltration and activation in venules, and endothelial barrier disruption in capillaries. The compromised vasculature increases circulation resistance and therefore decreases intestinal perfusion, and may eventually progress to intestinal necrosis.

CONCLUSIONIntestinal ischemia plays an important role through the whole course of NEC. New therapeutic agents targeting intestinal ischemia, like HB-EGF, are promising therapeutic agents for the treatment of NEC.

Endothelin-1 ; physiology ; Endothelium, Vascular ; physiopathology ; Enterocolitis, Necrotizing ; drug therapy ; etiology ; pathology ; Heparin-binding EGF-like Growth Factor ; Humans ; Infant, Newborn ; Intercellular Signaling Peptides and Proteins ; therapeutic use ; Intestines ; blood supply ; Ischemia ; complications ; Microcirculation ; physiology ; Nitric Oxide ; physiology ; Splanchnic Circulation

Gastrointestinal ischemia happens by splanchnic artery stenosis, thrombus, or physiological vasoconstriction during a low-blood-stream state. However, even if arterial stenosis exists in the upper gastrointestinal tract, ischemic injury is very rare due to rich collateral circulation. The authors experienced 92-year-old female patient with vomiting, epigastric pain, and hematemesis. An electrocardiogram showed paroxysmal atrial fibrillation. The patient had diffuse and segmental mucosal edema, erythema, and hemorrhage in the second part of the duodenum on esophagogastroduodenoscopy (EGD). On abdomen computed-tomography angiography, stenosis of the celiac and superior mesenteric arteries was observed, and segmental concentric wall thickness was seen from the proximal second portion of the duodenum to the proximal jejunum. The patient was treated with PPI and fluid therapy for one week. At follow-up EGD, the mucosa had improved compared with the previous EGD examination. In conclusion, ischemic injury rarely affects the duodenum and jejunum; however, it can develop in the presence of inducing factors.
Abdomen ; Angiography ; Arteries ; Atrial Fibrillation ; Collateral Circulation ; Constriction, Pathologic ; Duodenitis ; Duodenum ; Edema ; Electrocardiography ; Endoscopy, Digestive System ; Enteritis ; Erythema ; Female ; Fluid Therapy ; Follow-Up Studies ; Hematemesis ; Hemorrhage ; Humans ; Ischemia ; Jejunum ; Mesenteric Artery, Superior ; Mucous Membrane ; Splanchnic Circulation ; Thrombosis ; Upper Gastrointestinal Tract ; Vasoconstriction ; Vomiting

Portal hypertension (PHT) is associated with hemodynamic changes in intrahepatic, systemic, and portosystemic collateral circulation. Increased intrahepatic resistance and hyperdynamic circulatory alterations with expansion of collateral circulation play a central role in the pathogenesis of PHT. PHT is also characterized by changes in vascular structure, termed vascular remodeling, which is an adaptive response of the vessel wall that occurs in response to chronic changes in the environment such as shear stress. Angiogenesis, the formation of new blood vessels, also occurs with PHT related in particular to the expansion of portosystemic collateral circulation. The complementary processes of vasoreactivity, vascular remodeling, and angiogenesis represent important targets for the treatment of portal hypertension. Systemic and splanchnic vasodilatation can induce hyperdynamic circulation which is related with multi-organ failure such as hepatorenal syndrome and cirrhotic cadiomyopathy.
Collateral Circulation/physiology ; Endothelial Cells/metabolism ; Hemodynamics ; Hepatic Stellate Cells/metabolism ; Hypertension, Portal/*etiology ; Liver Circulation/physiology ; Liver Cirrhosis/*etiology ; Splanchnic Circulation/physiology

Animals ; Extremities ; blood supply ; Heparin ; pharmacology ; Male ; Mesentery ; blood supply ; Microcirculation ; drug effects ; Rats ; Rats, Wistar ; Reperfusion Injury ; Splanchnic Circulation ; drug effects

Acute Disease ; Animals ; Female ; Hypoxia ; physiopathology ; Male ; Microcirculation ; physiology ; Rats ; Splanchnic Circulation ; physiology ; Superoxide Dismutase ; blood

Renal dysfunction in patients with chronic liver disease encompasses a clinical spectrum of hyponatremia, ascites, and hepatorenal syndrome. Clinical observation has suggested that patients with cirrhosis have hyperdynamic circulation, and recent studies strongly suggest that peripheral arterial vasodilatation and subsequent development of hyperdynamic circulation are responsible for disturbances in renal function. Arterial vasodilatation predominantly occurs in the splanchnic vascular bed, and seems to precede an increase in blood flow in the splanchnic circulation. Nitric oxide plays a central role in progressive vasodilatation, as evidenced by in vivo and in vitro studies. Renal dysfunction negatively affects the prognosis of patients with cirrhosis, as hyponatremia, ascites, and azotemia are associated with increased rate of complications and mortality. Recent advances in understanding the pathophysiology of renal dysfunction have enabled clinicians to develop new diagnostic criteria and therapeutic recommendations. Hepatorenal syndrome is regarded as a potentially reversible disorder, as systemic vasoconstrictors with concomitant albumin administration are emerging as a promising management option, especially in terms of providing bridging therapy for patients awaiting liver transplantation.
Ascites ; Azotemia ; Fibrosis ; Hepatorenal Syndrome ; Humans ; Hyponatremia ; Liver ; Liver Cirrhosis ; Liver Diseases ; Liver Transplantation ; Nitric Oxide ; Prognosis ; Splanchnic Circulation ; Vasoconstrictor Agents ; Vasodilation