Pericardiocentesis and pancreatic aspiration needle biopsy in coagulopathic and thrombocytopenic cirrhotic patient

We report on the case of a 40-year-old patient with coagulopathic alcoholic cirrhosis who underwent ultrasound-directed pericardiocentesis and fine-needle aspiration biopsy of the pancreas after receiving recombinant human factor VIIa (rhFVIIa). The infusion of rhFVIIa rapidly corrected her coagulopathy and made it possible to perform both procedures. The marked changes produced in the prothrombin time and international normalized ratio as a result of the infusion of rhFVIIa are presented. As a result of these changes in coagulation status, both procedures were performed safely, and the patient's clinical management and subsequent care plan were defined.     

Hematologic effects of recombinant factor VIIa combined with hemoglobin-based oxygen carrier-201 for prehospital resuscitation of swine with severe uncontrolled hemorrhage due to liver injury

The combination of traumatic injury, hemorrhage, and fluid resuscitation results in consumption and dilution of coagulation factors, adversely impacting hematology outcome in trauma patients. The hemostatic effects of escalating doses of recombinant factor VIIa added to hemoglobin-based oxygen carrier-201 were assessed as prehospital fluid resuscitation in swine with severe uncontrolled hemorrhage. Swine underwent liver injury causing severe uncontrolled hemorrhage and shock. During a 4-h prehospital phase, either hypotensive or tachycardic, or both, animals were resuscitated with hemoglobin-based oxygen carrier-201 without (0x) or with escalating doses of recombinant factor VIIa [90 microg/kg (1x), 180 microg/kg (2x), or 360 microg/kg (4x)]. The animals received one initial full dose of 10 ml/kg at 15 min and up to four doses of 5 ml/kg thereafter. From 4 to 72 h (hospital phase), animals received either transfusions or isotonic saline or both as needed. Hematology profile (complete blood count), thromboelastography, in-vitro bleeding (platelet function analyzer), and coagulation (prothrombin time) were measured and the results were compared using mixed statistical models. In all groups, dilutional coagulopathy was evidenced by reduced hematocrit, platelets, and thromboelastography-maximum amplitude, and increased platelet function analyzer closure time and thromboelastography-reaction time. During the prehospital phase, hemoglobin-based oxygen carrier-201 restored hemoglobin in all groups. Recombinant factor VIIa decreased prothrombin time in recombinant factor VIIa groups compared with the hemoglobin-based oxygen carrier-201 group (P < 0.01). Unexpectedly, increasing recombinant factor VIIa dosage tended to increase fluid requirement (P > 0.05). Compared with hemoglobin-based oxygen carrier, 1x recombinant factor VIIa tended to decrease blood loss, lactate and thromboelastography-reaction time at 24 h but the 4x group increased these parameters. Platelets and thromboelastography-maximum amplitude decreased (P < 0.01) with the 4x group. In swine with severe uncontrolled hemorrhage, prehospital resuscitation with escalating doses of recombinant factor VIIa in combination with hemoglobin-based oxygen carrier-201 did not change survival or hemostasis. However, there were trends toward possible benefits of low recombinant factor VIIa doses, whereas high recombinant factor VIIa doses adversely affected hemostasis.     

Recombinant activated factor VIIa in uncontrolled bleeding: a haemostasis laboratory study in non-haemophilia patients.

Extensive surgery and massive tissue trauma are often associated with severe bleeding. We present retrospective data on the use of recombinant factor VIIa in haemostatic emergencies in13 non-hemophilia patients with uncontrolled bleeding. Recombinant factor VIIa was administered in doses ranging from 16 mug/kg bodyweight to 60 microg/kg bodyweight. Blood loss during 24 h before and after the infusion was registered, showing that 10 out of 13 patients (77%) had a 70% or greater reduction in transfusion requirement decreasing significantly in mean from 28.1 to 9.9 red blood cell units. Coagulation parameters were studied in blood samples collected 10 min before and 10-15 min after the injection of recombinant factor VIIa. Factors VII:C, II:C, and X:C increased significantly while the activated partial thromboplastin time, platelet numbers, and concentration of fibrinogen and D-dimers were unchanged. The dose of rFVIIa correlated significantly with the rise in factor X:C and inversely with transfusion requirements. Dynamic clot velocity of whole blood was recorded before and after rFVIIa infusion in four patients. Judged from red blood cell usage no improvement in haemostasis was seen in one patient suffering thrombocytopenia and low fibrinogen. This patient died 6 h after recombinant factor VIIa infusion, and three other patients died before 1 month. None of the fatalities appeared to be related to recombinant factor VIIa usage. No thromboembolic complications were seen. In conclusion, 12 out of 13 patients survived the first 24 h after treatment with relatively low doses of recombinant factor VIIa for large-scale bleeding. Recombinant factor VIIa was well tolerated and safe in these non-hemophilia patients. With quite low doses of recombinant factor VIIa (相似文献   

Partial splenic embolization as a preoperative treatment for refractory idiopathic thrombocytopenic purpura

A 53-year-old woman presented with idiopathic thrombocytopenic purpura (ITP) that was refractory to corticosteroid therapy. Her bleeding had worsened gradually due to prolonged thrombocytopenia, but her low platelet count after high-dose intravenous gamma globulin therapy contraindicated a splenectomy. We therefore decided to perform a partial splenic embolization (PSE). The patient's platelet count increased gradually thereafter, allowing us to safely perform a splenectomy. We concluded that PSE is a useful preoperative procedure, especially for patients with ITP that is refractory to high-dose intravenous gamma-globulin therapy. Moreover, it is possible to predict the effects of a splenectomy preoperatively if the PSE procedure is used.     

Therapeutic factors considered according to the preoperative splenic volume for a prolonged increase in platelet count after partial splenic embolization for liver cirrhosis

Purpose  

Infarcted splenic volume has been identified as the predictive factor for a prolonged increase in platelet count after partial splenic embolization (PSE). However, despite enough infarcted splenic volume, some patients show only a slight increase in platelet counts after PSE because of rapid regrowth of the noninfarcted splenic parenchyma within several months post-PSE. The purpose of this study was to determine the therapeutic factors based on the preoperative splenic volume for a prolonged increase in platelet counts after PSE.     

Near-fatal uterine hemorrhage during induction chemotherapy for acute myeloid leukemia: a case report of bilateral uterine artery embolization

Severe transfusion-dependent uterine hemorrhage is a relatively uncommon complication of induction chemotherapy for acute myeloid leukemia (AML). Even less common is the failure of systemic conjugated estrogens in this setting. We report a case of life-threatening uterine hemorrhage in a 38-year-old woman in the setting of transfusion-refractory thrombocytopenia after completing induction chemotherapy for AML. She experienced dramatic breakthrough uterine hemorrhage despite multiple platelet transfusions, conjugated estrogens, recombinant factor VIIa, epsilon-aminocaproic acid, and intracavitary thrombin-soaked gauze tamponade. At the point of near-exsanguination in the setting of hypotension, hematocrit of 14%, and a platelet count of 3,000/microL, she underwent bilateral uterine artery embolization which proved immediately successful. We review the literature and indications for this procedure in the oncologic patient care setting.     

The effect of an adrenaline infusion on the splenic blood flow and intrasplenic platelet kinetics

The effect of an adrenaline infusion on the venous platelet count, splenic blood flow and intrasplenic platelet kinetics was investigated in seven healthy male volunteers by using 111In-labelled platelets and dynamic gamma camera scintigraphy. The infusions were administered in two different doses, 0.2 microgram/kg/min and 0.1 microgram/kg/min, respectively. Regardless of the given dose, adrenaline was found to markedly decrease the splenic blood flow, decrease the exchangeable splenic platelet pool size and to prolong the intrasplenic platelet transit time. In response to the higher dose of adrenaline the splenic blood flow was 1.3 +/- 0.5 (SD) % of total blood volume per min and the intrasplenic platelet transit time 17.3 +/- 2.3 (SD) min. In contrast, after termination of infusion, the splenic blood flow was 7.0 +/- 2.1 (SD) % of total blood volume per min and the intrasplenic platelet transit time was 11.5 +/- 1.5 (SD) min. The present results firmly demonstrate that the splenic blood flow is the immediate variable governing the size of the exchangeable splenic platelet pool, and that the adrenaline-induced depletion of the splenic platelet pool is a consequence of the splenic blood flow reduction. Finally, the splenic perfusion appears to be a major determinant of the intrasplenic platelet transit time.     

The effect of an isoprenaline infusion on the splenic blood flow and intrasplenic platelet kinetics

The effect of a constant isoprenaline infusion on the venous platelet count, splenic blood flow and intrasplenic platelet kinetics was investigated in 6 healthy male volunteers. The study was carried out using autologous 111In-labelled platelets and dynamic gamma camera imaging of the initial distribution of radiolabelled platelets between blood and splenic platelet pool. The isoprenaline infusions were administered i.v. over 30 min in a dose of 0.03 micrograms/kg/min. These infusions significantly increased the splenic blood flow and the size of the exchangeable splenic platelet pool. Concomitantly, there was a decrease of labelled as well as unlabelled platelets in the peripheral blood. The intrasplenic platelet transit time was not affected. Before start of infusion, the splenic blood flow was 6.1 +/- 2.9 (SD) % of total blood volume/min and the splenic platelet pool size 34 +/- 9 (SD) %. During infusion the corresponding values were 8.7 +/- 3.9 (SD) and 41 +/- 11 (SD), respectively. It is concluded that an i.v. infusion of isoprenaline enhances splenic pooling of platelets as a result of an increase in splenic blood flow.     

Predictive factors for platelet increase after partial splenic embolization in liver cirrhosis patients

BACKGROUND AND AIM: Partial splenic embolization (PSE) is often performed for improving thrombocytopenia in cirrhotic patients. We investigated the largely unclear predictive factors for platelet increase at both 1 month and 1 year after PSE. METHODS: Aimed at increasing the platelet count, PSE was performed in 42 cirrhotic patients with thrombocytopenia (platelets < 80 x 10(4)/mL) caused by hypersplenism. The clinical data were analyzed to clarify the predictive factors for platelet increase at 1 month (n = 42) and 1 year (n = 38) after PSE. RESULTS: The mean splenic infarction ratio was 76.7% +/- 11.2%. The platelet count increased to 259% +/- 112% and 228% +/- 75% of the pretreatment values at 1 month and at 1 year after PSE, respectively. Stepwise multiple linear regression analysis showed that the infarcted splenic volume had a positive independent association with the increase in platelet count at both 1 month (P = 0.00004) and 1 year (P = 0.005) after PSE (increase in platelet count (x10(4)/mL): at 1 month = 0.752 + 0.018 x infarcted splenic volume (mL), R(2) = 0.344; at 1 year = 2.19 + 0.01 x infarcted splenic volume (mL), R(2) = 0.203). Receiver operating characteristic analysis yielded a cut-off value of 388 mL of infarcted splenic volume for achieving an increase of 5.0-8.0 x 10(4)/mL in platelet count at 1 year. CONCLUSIONS: PSE can reduce the platelet pool and induce an increase in platelet count. This increase is greatly dependent on the infarcted splenic volume.     

Partial splenic embolization for hypersplenism in cirrhosis: A long-term outcome in 62 patients

BackgroundAlthough partial splenic embolization (PSE) has been widely used for treatment of leucocytopaenia and thrombocytopaenia in cirrhosis, only few studies on the correlation between splenic infarction rate and long-term outcome of partial splenic embolization have been reported so far.AimTo evaluate long-term results of partial splenic embolization with different infarction rates in cirrhotic patients with hypersplenism.MethodsSixty-two consecutive patients with hypersplenism in cirrhosis received partial splenic embolization. According to the splenic infarction rate after partial splenic embolization, the patients were divided into three groups: more than 70% in group A (n = 12), 50–70% in group B (n = 34), and less than 50% in group C (n = 16). The post-partial splenic embolization following-up time was 5 years.ResultsBefore partial splenic embolization, there were no significant differences among the three groups with respect to sex, age, splenic volume, Child-Pugh class, oesophageal varices, and peripheral blood cell counts. After partial splenic embolization, the short- and long-term outcomes of leucocyte and platelet counts showed significant difference among the three groups (P < 0.001). In groups A and B, the leucocyte and platelet counts after partial splenic embolization remained significantly higher than those before partial splenic embolization for 2 weeks to 5 years (P < 0.05), the post-partial splenic embolization leucocyte and platelet counts was even higher in group A than in group B; while in group C, leucocyte and platelet count improvement only lasted for 6 months after partial splenic embolization. No significant changes were observed concerning blood red cell counts and liver function parameters after partial splenic embolization among the three groups. Severe complications occurred in six patients (50%) in group A and three patients (8.8%) in group B (P < 0.05), while in group C, no severe complications developed.ConclusionsIn partial splenic embolization, the splenic infarction rate should be limited to 50%–70% in order to ensure the long-term efficacy in alleviating hypersplenism and reduce complications.     

The role of thrombopoietin in the thrombocytopenia of patients with liver cirrhosis

OBJECTIVES: Thrombocytopenia is a common disorder among cirrhotics that has been traditionally explained by splenic platelet pooling and destruction. Thrombopoietin (TPO), the main stimuli for thrombopoiesis is produced primarily in the liver and degraded by circulating platelets, but its role in the thrombocytopenia of liver cirrhosis is not well understood. The main goal of this study is to clarify the role of TPO in the pathogenesis of thrombocytopenia in cirrhosis. METHODS: The relation among TPO, platelet count, spleen size, portal hypertension, and liver function was studied in 33 cirrhotic patients before and after either partial splenic embolization or liver transplantation. RESULTS: Cirrhotics with thrombocytopenia had lower serum TPO levels than healthy controls (median values (interquartile range: ICR) were 120.7 (42.0-191.6) vs 756.4 (527.0-965.1) pg/mL, respectively; p<0.001). Among cirrhotics with thrombocytopenia, serum TPO was related to spleen size (rho=-0.387, p=0.046), but not to platelet count as occurs physiologically. After partial splenic embolization, TPO and platelet count increased significantly and the physiological relation between TPO and platelet count was restored (rho=-0.665, p=0.026). Similar results were observed after liver transplantation. CONCLUSIONS: Our results suggest that besides impaired production in the failing liver, an increased TPO degradation by platelets sequestered in the congested spleen may contribute to thrombocytopenia in cirrhotic patients.     

Factor-VIII Activity and Antigen, Platelet Count and Biochemical Changes after Adrenoceptor Stimulation

Adrenaline, isoprenaline and salbutamol were administered by intravenous infusion to human subjects. Isoprenaline was covered with practolol in an attempt to reduce the unpleasantness of the circulatory effects. Changes were recorded in pulse rate and blood pressure, and in blood levels of factors V, VIII, X, XI and XII, platelet count, lactate, pyruvate, potassium and free fatty acids. Factor VIII was studied by clotting assays, by reactions with two rabbit antisera and two human antibodies, and by desulphated agarose chromatography. At the rate at which they were administered, all three drugs increased the pulse rate by 20–40 beats/min. Factor VIII rose c. 2.5 x with adrenaline but only c. 1.5 x with isoprenaline and salbutamol; but other clotting factors did not alter. Chromatography provided no evidence of a change in the size of the molecule carrying factor-VIII clotting activity. The rate of clearance of the heightened plasma activity could not be shown to differ from that of 'ordinary'factor VIII infused into haemophiliacs. The platelet count rose after adrenaline, fell after salbutamol and did not change significantly after isoprenaline. Among the biochemical responses, the only significant difference between the drugs was that lactate rose after adrenaline and salbutamol but did not change after isoprenaline.
The rise in factor-VIII clotting activity after adrenaline is considered to represent a real increase in blood concentration, presumably by release of additional factor VIII from stores. The evidence suggests that this could be classified as a β₂ effect; and that the quantity which can be released is unrelated to the current plasma level. The rise in platelet count produced by adrenaline may be the resultant of an α-mediated rise due to contraction of the exchangeable splenic pool and a β₂-mediated fall, the α effect predominating.     

Recombinant coagulation factor VIIa: from the concept to clinical application in hemophilia treatment in 2000

The development of factor VIII and factor IX concentrates markedly improved the management of hemophilia A and B and made home therapy possible. However, treatment of hemophilic patients with acquired inhibitors remained difficult. The preparation of prothrombin complex concentrates, nonactivated or activated, addressed this difficult clinical problem, but their use was associated with serious side effects. Factor VIIa was found to be a safer treatment modality. Factor VIIa per se is inactive and needs tissue factor (TF) to become biologically active. TF serves as the receptor for factor VIIa. TF is expressed from vessel walls only upon injury. Treatment of inhibitor patients with plasma-derived factor VII was found to be successful. This led to the development of recombinant factor VIIa, which was also found to be successful in managing hemophilia patients with inhibitors. Up to this point, large numbers of patients have been treated and few serious side effects have been noted. Because of its unique effects on the hemostasis system, recombinant factor VIIa will be useful for other indications as well, including patients with congenital factor VII deficiency, patients with bleeding and liver function impairment, patients with quantitative and qualitative platelet defects, and individuals who have sustained multiple trauma. The development of recombinant factor VII is reviewed in detail.     

Modulation of endothelial cell inflammatory integrins and stress markers with rh-factor VIIa in patients with advanced chronic hepatitis C

Summary. Individuals with chronic hepatitis C (CHC) progress to cirrhosis and hepatic cancer. Individuals with advanced CHC are coagulopathic and can manifest fibrinolysis. The coagulopathy is a consequence of hepatocytic dysfunction. The fibrinolysis represents a response to local endothelial cell injury, and is of a low-grade. Based upon this hypothesis, the effect of the infusion of recombinant human factor VIIa (rh-FVIIa) on endothelial cell inflammatory integrins and measures of endothelial stress were determined in 17 individuals with advanced CHC. Immediately prior to the infusion of rh-FVIIa, the plasma levels of tissue factor (TF), Thrombomodulin (TM), human soluble ICAM-1 (hs-ICAM-1), human soluble VCAM-1 (hs-VCAM-1), human soluble L-Selectin (hs-L-Selectin), the prothrombin time and the activated partial thromboplastin time were determined. The same parameters were assayed at 5, 10, 30, 120, 240 and 360 min after infusion. TF and TM levels were very high at baseline consistent with a vascular endothelial stress response. Similarly hs-ICAM-1, hs-VCAM-1 as well as L-Selectin levels were increased. Thirty minutes after the infusion, a marked reduction in ICAM-1 and VCAM-1 and to a lesser degree L-Selectin levels was observed. This reduction persisted for 360 min. No change in measures of fibrinolysis [plasminogen activator inhibitor-1 (PAI-1), total tissue factor pathway inhibitor (t-TFPI), activated tissue factor pathway inhibitor (TFPIa), d-dimers (DD), FSP and fibrinogen levels] occurred. In addition, no change in plasma Annexin-V was observed. Based upon these data it can be concluded that: (1) rh-FVIIa corrects the coagulopathy seen in advanced CHC; (2) reduces endothelial cell injury and/or stress as evidenced by the TF, TM, hs-ICAM-1 and hs-VCAM-1 levels in plasma; (3) these changes in coagulation occurred without inducing a propagated vascular thrombosis.     

Treatment of factor XI inhibitor using recombinant activated factor VIIa

A 30-year-old female with severe factor XI deficiency of 0-2% acquired factor XI inhibitor following many infusions for fresh frozen plasma (FFP) for surgical procedures starting at 4 years of age. Seven months before this inhibitor was diagnosed, surgery was complicated by prolonged bleeding resistant to FFP, requiring epsilon aminocaproic acid (EACA) and surgical packing. The inhibitor was measured at 2.2 Bethesda units, 7 months since the last FFP. The inhibitor was confirmed as specific anti-XI and anti-XIa binding by patient's IgG to immobilized factor XI and factor XIa from whole plasma and purified IgG. For repair of a painful anterior cruciate ligament (ACL) defect she was given recombinant factor VIIa (rVIIa) at 90 mug kg(-1), starting one-half hour preoperatively and continued every 2 h for 8 h when haemostasis was complete. Thereafter the rVIIa was given every 3 h for two doses, and then every 4 h for four doses at which time she was discharged on EACA which was continued for 6 days. There was excellent haemostasis during and following the surgery. There was no evidence of consumptive coagulopathy, with no change in the fibrinogen, platelet count, or D-D dimer; and no increase of platelet factor 4, beta-thromboglobulin, or prothrombin fragment F 1.2. The thrombin-antithrombin complex increased over baseline after 24 h. There was no postoperative deep vein thrombosis or pulmonary embolus. In this patient with a factor XI inhibitor, the recombinant factor VIIa was effective and safe, ensuring adequate haemostasis with no thrombotic complications. This product which was designed for patients with inhibitors to factor VIII or factor IX, and factor VII deficiency, has now been given successfully to four patients with factor XI inhibitors.     

Partial splenic embolization.

Partial splenic embolization (PSE) is a non-surgical procedure developed to treat hypersplenism as a result of hepatic disease and thus avoid the disadvantages of splenectomy. A femoral artery approach is used for selective catheterization of the splenic artery. Generally, the catheter tip is placed as distally as possible in an intrasplenic artery. After an injection of antibiotics and steroids, embolization is achieved by injecting 2-mm gelatin sponge cubes suspended in a saline solution containing antibiotics. PSE can benefit patients with thrombocytopenia, esophagogastric varices, portal hypertensive gastropathy, encephalopathy, liver dysfunction, splenic aneurysm, and splenic trauma. The contraindications of PSE include secondary splenomegaly and hypersplenism in patients with terminal-stage underlying disease; pyrexia or severe infections are associated with a high risk of splenic abscess after PSE. Complications of PSE include daily intermittent fever, abdominal pain, nausea and vomiting, abdominal fullness, appetite loss, and postembolization syndrome. Decreased portal-vein flow and a rapid increase in the platelet count after excessive embolization may cause portal-vein or splenic-vein thrombosis.     

Splenic artery aneurysm presenting as a submucosal gastric lesion: A case report

We are reporting the rare case of splenic artery aneurysm of 4 cm of diameter presenting as a sub mucosal lesion on gastro-duodenal endoscopy. This aneurysm was treated by endovascular coil embolization and stent graft implantation. The procedure was uneventful. On day 1, the patient presented an acute severe epigastric pain and cardiovascular arrest. Abdominal computed tomography scan showed an active leak of the intravenous contrast dye in the peritoneum from the splenic aneurysm. We performed an emergent resection of the aneurysm, and peritoneal lavage. Postoperatively, hemorrhagic choc was refractory to large volumes replacement, and intravenous vaso-active drugs. On day 2, he presented massive hematochezia. We performed a total colectomy with splenectomy and cholecystectomy for ischemic colitis, with spleen and gallbladder infarction. Despite vaso-active drugs and aggressive treatment with Factor VIIa, the patient died after uncontrolled disseminated intravascular coagulation.     

Correction of both prothrombin time and primary haemostasis by recombinant factor VII during therapeutic alcohol injection of hepatocellular cancer in liver cirrhosis.

We evaluated the efficacy of recombinant factor VII to correct impaired haemostasis in a patient with liver cirrhosis requiring an invasive procedure. A test intravenous bolus of 80 microg/kg of recombinant factor VII was given to a Jehovah's Witness, with a solitary 4.4-cm hepatocellular carcinoma and underlying hepatitis C virus cirrhosis, in an attempt to correct his haemostatic disorders and safely inject the tumour with alcohol. An extensive portal block had precluded consideration of liver transplantation. Haemostasis was evaluated by clotting assays, bleeding time and thromboelastography 10 min before and 10 min and 1, 2, 4, 8 and 24 h after factor VII infusion. Parameters of both coagulation (prothrombin time) and platelet function (bleeding time and the alpha and ma parameters of thrombelastography) were improved 10 min after factor VII infusion; improvements lasted 4 to 8 h or more. Platelet count did not change and there was no evidence of disseminated intravascular coagulation. The improvements in haemostatic parameters correlated significantly with the increases in factor VII plasma concentrations (p<0.04). Factor VII clearance was 25.1 U/h/kg and its half-life was 5.8 h. The same dose of recombinant factor VII was given to the patient 1 week later, just before the alcohol injections. The patient had no subsequent bleeding or other complication, with no change in haemoglobin levels over 24 h. Thus, recombinant factor VII represents a therapeutic advance, as it can correct fully both coagulation and platelet function defects in cirrhosis and allow invasive procedures to be performed safely.     

Emergency caesarean section and symptomatic immune thrombocytopenic purpura

A 24-year-old woman presented in labour with profound purpuric bleeding due to idiopathic immune thrombocytopenia. She was assessed as requiring immediate caesarean section for cephalopelvic disproportion and foetal distress. In view of her platelet count of 21 x 10(9)/L she was prepared with intravenous methylprednisolone, isovolaemic plasma exchange, and infusion of 400 mg/kg of gammaglobulin and 5 x 10(11) allogeneic platelets. Six hours after commencing the procedure, at a time when her platelet count was 97 x 11(9)/L, she went uneventful operation and with no further therapy this level subsequently reached 175 x 10(9)/L, at which time an uneventful operation was performed. The mother and her normal, full-term infant have been discharged; both are well and at follow-up have normal platelet counts. This experience illustrates that major surgery can safely be undertaken in severely thrombocytopenic patients, even as an emergency procedure, using this regimen.     

Evaluation of the effect of partial splenic embolization on platelet values for liver cirrhosis patients with thrombocytopenia

AIM： TO investigate the effect of partial splenic embolization （PSE） on platelet values in liver cirrhosis patients with thrombocytopenia and to determine the effective embolization area for platelet values improvement.
METHODS： Blood parameters and liver function indicators were measured on 10 liver cirrhosis patients （6 in Child-Pugh grade A and 4 in grade B） with thrombocytopenia （platelet values 〈 80 × 10^3/μL） before embolization. Computed tomography scan was also needed in advance to acquire the splenic baseline. After 2 to 3 d, angiography and splenic embolization were performed. A second computed tomography scan was made to confirm the embolization area after 2 to 3 wk of embolization. The blood parameters of patients were also examined biweekly during the 1 year follow-up period. RESULTS： According to the computed tomography images after partial splenic embolization, we divided all paUents into two groups： low （〈 30%）, and high （≥ 30%） embolization area groups. The platelet values were increased by 3 times compared to baseline levels after 2 wk of embolization in high embolization area group. In addition, there were significant differences in platelet values between low and high embolization area groups. GPT values decreased significantly in all patients after 2 wk of embolization. The improvement in platelet and GPT values still persisted until 1 year after PSE. In addition, 3 of 4 （75%） Child-Pugh grade B patients progressed to grade A after 2 mo of PSE. The complication rate in 〈 30% and ≥30% embolization area groups was 50% and 100%, respectively. CONCLUSION： Partial splenic embolization is an effective method to improve platelet values and GPT values in liver cirrhosis patients with thrombocytopenia and the ≥ 30% embolization area is meaningful for platelet values improvement. The relationship between the complication rate and embolization area needs further studies.