Post lumbar puncture spinal subarachnoid hematoma causing paraplegia: a short report

A 53 year old male underwent total excision of a large sphenoidal wing meningioma. Patient was treated with cephalosporins and phenytoin for postoperative meningitis. Three weeks after surgery, a follow up lumbar puncture was done. The patient became paraplegic over a few hours. Imaging of the dorsolumbar spine and other investigations demonstrated a large intraspinal hematoma caused by thrombocytopenia which was probably drug induced. After normalising the platelet count surgical evacuation of the spinal subarachnoid hematoma was done. Relevant literature is reviewed.     

CSF RBC count in successful first-attempt lumbar puncture: the interest of atraumatic needle use

The objective of this study is to analyze CSF red blood cell (RBC) count from first-attempt lumbar punctures and to analyze parameters associated with first-attempt lumbar punctures and hemorrhagic lumbar puncture. This is a prospective analysis of consecutive patients who underwent lumbar puncture for any reason other than suspected acute subarachnoid hemorrhage. Analyzed parameters were the following: age, indication for lumbar puncture, aPTT ratio, PTT, platelet count, patient’s position, needle type (atraumatic/standard), needle diameter, person performing lumbar puncture (medical student/resident/attending physician), number of lumbar levels punctured, necessity of needle repositioning, CSF RBC and white blood cell count, and protein level. Lumbar puncture resulting in RBC count > 5 RBC/mm² was classified as hemorrhagic lumbar puncture (different cut-offs were studied: > 5/> 10/> 100/> 500/> 1000 RBC). In total, 169 elective lumbar punctures in 165 different patients were included. First-attempt lumbar puncture occurred in 22% > 5 RBC, in 19.5% > 10 RBC, in 4.5% > 100 RBC, in 3% > 500 RBC, and 1.5% > 1000 RBC count. First-attempt lumbar puncture was associated with non-hemorrhagic lumbar puncture for each of the RBC count cut-offs (OR for non-hemorrhagic lumbar puncture in first-attempt lumbar puncture 2.8, 95% CI 1.4–5.7). The presence of a hemorrhagic disorder (concerning cerebral amyloid angiopathy in all patients) and higher aPTT ratio were associated with hemorrhagic lumbar puncture. Atraumatic needle use was associated with non-hemorrhagic lumbar puncture for RBC count cut-offs ≤ 5 and ≤ 10 RBC (OR for non-hemorrhagic lumbar puncture in atraumatic needle use 2.5 [95% CI 1.3–4.8] and 2.2 [95% CI 1.1–4.4], respectively). First-attempt lumbar puncture and hemorrhagic lumbar puncture were not associated with other parameters. Slightly elevated CSF RBC count after first-attempt lumbar puncture occurs relatively frequently, but is even more frequent in non-first-attempt lumbar puncture. Atraumatic needle use is associated with non-hemorrhagic lumbar puncture.     

The biological significance of platelet volume: its relationship to bleeding time, platelet thromboxane B2 production and megakaryocyte nuclear DNA concentration

Bleeding time, platelet thromboxane B2 production and megakaryocyte nuclear DNA concentration were measured in rabbits recovering from thrombocytopenia caused by a single injection of anti-platelet serum. Similar measurements were made on rabbits in a steady state of normal platelet production. The effects of a sustained state of thrombocytopenia on megakaryocyte DNA concentration were investigated by repeated daily injections of anti-platelet serum. It is shown that bleeding time depends on both platelet count and mean platelet volume. Furthermore changes in mean platelet volume appear to play a more important role in haemostasis than changes in platelet count. The mean megakaryocyte nuclear DNA concentration is significantly increased after 24 hours of thrombocytopenia and continues to increase as thrombocytopenia is sustained. Thromboxane B2 production/unit volume of platelet is increased in platelets produced after 24 hours of thrombocytopenia compared with platelets produced in normal steady state function. As a consequence platelets produced in response to thrombocytopenia not only have a larger mean platelet volume but are also more reactive. Mean platelet volume, as well as platelet count, should be considered as an index of haemostasis and its dysfunction, thrombosis.     

A case of myasthenia gravis complicated by cyclic thrombocytopenia]

A 47-year-old woman with myasthenia gravis for last 11 years was admitted because of relapsed muscle weakness, hypermenorrhea and thrombocytopenia. Physical and neurological examinations revealed diplopia, proximal muscle weakness and purpuras on the left arm and bilateral legs. Repeated hematological examinations revealed cyclic fluctuation of platelet counts which spontaneously changed from the nadir levels of 12-27 x 10(3)/microliters to the peak levels of 150-400 x 10(3)/microliters. The platelet count reached a nadir at the onset of menstruation. Platelet-associated IgG (PAIgG) was within normal level when platelet count was at an increasing phase. Survival time of autologous platelets was normal when platelet count was at an increasing phase. Megakaryocytes in the bone marrow were apparently normal at the nadir phase. The patient's serum obtained at the nadir of platelet count significantly suppressed megakaryocyte colony forming unit (Meg-CFU) formation in comparison with that after the stabilization of platelet count, suggesting that this cyclic thrombocytopenia was secondary to cyclic hypoproduction of megakaryocytes caused by a suppressive factor. On the other hand muscle weakness showed no cyclic fluctuation. Administration of 60 mg/day prednisolone stabilized the platelet count at about 280 x 10(3)/microliters, abolished hypermenorrhea and gradually improved muscle weakness. These findings suggested autoimmune mechanism in the production of a Meg-CFU-suppressive factor might be involved in the pathogenesis of thrombocytopenia.     

Post-DDAVP thrombocytopenia in type 2B von Willebrand disease is not associated with platelet consumption: failure to demonstrate glycocalicin increase or platelet activation

Thrombocytopenia is frequently reported in type 2B von Willebrand disease (vWD), and thought to be related to the abnormally high affinity of 2B von Willebrand factor (vWF) for platelet GPIb-IX. To gain an insight into the nature of this thrombocytopenia, we measured plasma glycocalicin (GC) levels (as a marker of platelet turnover), and platelet surface expression of the alpha granule protein P-selectin (as a marker of platelet activation) in 9 patients with type 2B vWD before, and in 4 patients also following the infusion of 1-desamino-8-d-arginine vasopressin (DDAVP). Three patients presented a persistent decrease of platelet counts in the resting condition. GC levels were within the normal range, regardless of the platelet counts, in all but one patient who presented, on the other hand, a normal platelet count. Moreover, platelets expressed normal amounts of P-selectin on their surface, regardless of platelet counts. These findings suggest that the thrombocytopenia observed in type 2B vWD is not due to platelet activation and subsequent consumption in circulation. Despite a significant, albeit transient, decrease in platelet count, DDAVP did not induce an increase in plasma GC levels, nor enhance P-selectin expression. These observations indicate that the acute post-DDAVP thrombocytopenia in type 2B vWD is not related to platelet activation and consumption. We advance that the post-DDAVP 2B vWF is hemostatically more active, and able to induce agglutination but not aggregation of circulating platelets. This would explain both the prompt recovery of basal platelet counts after the post-DDAVP decrease, and the lack of reported thrombotic complications in this disorder. Therefore, even though 2B vWF is characterized by an enhanced affinity for the platelet surface, its binding to platelet GPIb-IX in the soluble phase is not able to induce true platelet aggregation: vWF thus appears to be mainly an adhesive protein, rather than an aggregating agent.     

Autologous platelet-labeling in thrombocytopenia

Field studies performed with peripheral platelets obtained from 6 male volunteers aged 23 to 29 years revealed an extraordinary dependence of labeling efficiency on incubation time and platelet concentration after 111In-oxine platelet labeling. Since the monitoring of in vivo-platelet function in patients with thrombocytopenia may cause problems due to insufficient labeling results and homologous platelets may show a different in vivo behaviour to autologous ones, we have searched for the minimal amount of platelets necessary to allow appropriate labeling and imaging in patients with thrombocytopenia. In 15 patients with untreated thrombocytopenia aged 14 to 79 years demonstrating a mean peripheral platelet count of 2.509 +/- 1.45 x 10(4) cells/microliters autologous 111In-oxine platelet labeling was performed. The results indicate that approximately 1 x 10(8) (concentrated) platelets/ml are necessary to obtain an adequate labeling efficiency and recovery. This platelet concentration can be easily achieved by drawing one more Monovette of whole blood per each 5 x 10(4) platelets/microliter peripheral platelet count less than 2 x 10(5)/microliter. It is concluded, that calculation of the required number of platelets in advance, variation of the blood volume drawn and the volume of incubation buffer allow informative, qualitative and quantitative results using autologous platelets. The method presented effectively circumvents the requirement of homologous platelets for radiolabeling in thrombocytopenia.     

Spinal subarachnoid hematoma after lumbar puncture in a patient with leukemia: report of a case and review of the literature

Acute myeloradicular compression due to a spinal subarachnoid hematoma (SSAH) after lumbar puncture (LP) is an extremely rare complication. Several risk factors have been involved in the production of these hematomas, mainly the presence of hemostasis disorders in the patient. We report the case of a 20-year-old man with leukemia and thrombocytopenia (26,000 platelets/mm(3)) who, after undergoing a LP, developed paraparesis and became unable to stand. A magnetic resonance disclosed the presence of a ventral intradural hematoma from D12 to L4. An emergency decompressive laminectomy was performed and a hematoma located in the subarachnoid space was partially removed. On the fourth postoperative day, the patient was able to walk without assistance, but one month later, he died because of systemic complications of his disease. Only 26 cases of SSAH after LP have been found in the literature review we have performed. In most of them, the following common features have been observed: association with anticoagulant therapies, association with thrombocytopenia, delayed onset of compressive myeloradicular syndrome, need of surgical treatment, good functional outcome in half of patients, and short life expectancy for patients with previous serious illness. Risk for developing a SSAH after LP could be high in leukemia patients with a tendency to have severe thrombocytopenia (perhaps less than 25,000 platelets/mm(3)).     

Valproic acid and thrombocytopenia in children: A case-controlled retrospective study

Thrombocytopenia in association with valproic acid (VPA) therapy has been reported in patients of various ages with incidences ranging from 1 to 32%. To evaluate this association in a pediatric population, we retrospectively studied 167 children treated with VPA at our institution between 1989 and 1993. Ninety-one patients on VPA monotherapy and 76 on VPA polytheraphy (VPA plus 1 to 3 other antiepileptic drugs) were compared with 92 age- and sex-matched control patients treated with antiepileptic drugs other than VPA. Study variables included patient age, most recent platelet count, VPA dose, dose/kg, and serum VPA level. Thrombocytopenia, defined as a platelet count <200 × 10³/mm³, was present in 21.6% of the children treated with VPA (26.4% in those on VPA monotherapy and 15.8% in those on VPA polytherapy) but in only 5.4% of controls untreated with VPA. Serum VPA level was the highest risk factor for the development of thrombocytopenia in these patients (P = .0001) and greater age also independently predicted thrombocytopenia. The dose of VPA or dose/kg were not independent predictors of thrombocytopenia (P = .0025). The degree of thrombocytopenia was mild among these patients, reflected in the absence of significant difference in mean platelet count between the three groups and the absence of any bleeding complication or excessive bruising. We conclude from these findings that the risk for children developing severe thrombocytopenia with bleeding complications while taking VPA is low and that mild thrombocytopenia does not necessarily mandate discontinuing the drug. Because higher serum VPA levels do predict thrombocytopenia, platelet counts should be closely monitored after dose escalation in such patients.     

Acute Ischemic Stroke Revealing ChAdOx1 nCov-19 Vaccine-Induced Immune Thrombotic Thrombocytopenia: Impact on Recanalization Strategy

Vaccine-induced immune thrombotic thrombocytopenia is a rare syndrome following the ChAdOx1 nCov-19 or Ad26.COV2.S vaccine. Reported patients developed mainly venous thrombosis. We describe a case of a young healthy women suffering from acute ischemic stroke due to large vessel occlusion without cerebral venous thrombosis 8 days after vaccination and its consequences on recanalization strategy.Considering the thrombocytopenia, intravenous thrombolysis was contraindicated. She underwent mechanical thrombectomy with complete recanalization and dramatically improved clinically. Positive detection of anti-PF4-heparin-antibodies confirmed vaccine-induced immune thrombotic thrombocytopenia diagnosis.In case of acute ischemic stroke after recent ChAdOx1 nCov-19 or Ad26.COV2.S vaccine, platelet count should be systematically checked before giving thrombolysis, and direct mechanical thrombectomy should be proposed in patients with large vessel occlusion.     

比阿培南联合腰穿治疗开颅术后颅内感染的疗效及安全性分析

目的分析比阿培南联合腰穿治疗神经外科开颅术后颅内感染患者的疗效及安全性。方法将40例神经外科开颅术后颅内感染患者分为治疗组和对照组各20例。治疗组使用比阿培南联合腰穿治疗,对照组使用头孢吡肟联合腰穿治疗,分别观察2组治疗前后体温(T)、白细胞总数(WBC)、脑脊液有核细胞数(TC-BF)、脑脊液葡萄糖(GLU)、脑脊液总蛋白(TPC3)、药物不良反应及实验室检查结果。结果治疗组总有效率95.0%(19/20),对照组为85.0%(17/20);2组治疗后体温均有明显改变,血液及脑脊液相关指标(WBC、TC-BF、GLU、TPC3)治疗前后均有显著改善(P0.05),但治疗组临床有效治疗时间优于对照组(P0.05);2组治疗前后药物不良反应及实验室检查结果差异有统计学意义(P0.05)。结论比阿培南联合腰穿治疗神经外科开颅术后颅内感染患者可显著改善患者的血液及脑脊液指标,比头孢吡肟联合腰穿治疗时间明显缩短,不良反应少。     

Clinical features of heparin-induced thrombocytopenia including risk factors for thrombosis. A retrospective analysis of 408 patients

Immune mediated heparin induced thrombocytopenia (HIT) is a prothrombotic adverse effect of heparin. However, only a subgroup of patients with HIT develops thromboembolic complications. We aimed to identify risk factors for developing HITassociated thrombosis. We analyzed a registry of patients with clinical suspicion of HIT who tested positive using a sensitive functional assay. Patient information was obtained by a standardized questionnaire. By multivariate analysis the association of age, gender, type of patient population, and magnitude of the platelet count decline with the frequency, type (venous or arterial), and temporal pattern of thrombotic events was assessed. In 408 HIT patients we observed predominance of venous thrombosis (2.4:1), with 40% of patients developing a pulmonary embolism. However, in the subgroup of post-cardiovascular surgery patients there was predominance of arterial thrombosis (1:8.5). The type of arterial thrombosis (limb artery thrombosis > thrombotic stroke > myocardial infarction) was the converse of that observed with typical atherothrombotic clots in non-HIT populations. In 59.8% of patients HIT-related thrombosis manifested either on the same day a platelet count decrease >50% was documented (26.3%) or before the decrease in platelet counts (33.5%). The most important risk factors for thrombosis were orthopedic/trauma surgery and the magnitude of platelet count decrease. HIT-associated thrombosis occurs in a considerable proportion of patients before platelet counts decrease by more than 50%.     

A family having type 2B von Willebrand disease with an R1306W mutation: Severe thrombocytopenia leads to the normalization of high molecular weight multimers

In type 2B von Willebrand disease (2B VWD), abnormal von Willebrand factor (VWF) spontaneously binds to platelets. This leads to the clearance of the high molecular weight multimers (HMWM) of VWF and results in thrombocytopenia. Herein we report a family of 2B VWD with an R1306W mutation which caused thrombocytopenia with giant platelets. The most important finding in this study is dynamic changes in VWF values in association with platelet counts. When the proband (2 years of age) had severe thrombocytopenia, his HMWM were normal, however, hematological examination showed a low level of VWF and a lack of HMWM after platelet count recovered. His affected sister also exhibited similar phenomenona. These results suggest that the severe thrombocytopenia leads to decreased clearance of VWF HMWM and restoration of VWF HMWM in plasma. We must consider 2B VWD in the case of recurrent thrombocytopenia following infection or other stress condition.     

1-Desamino-8-D-arginine vasopressin (DDAVP) infusion in type IIB von Willebrand's disease: shortening of bleeding time and induction of a variable pseudothrombocytopenia

We have investigated the effects of 1-desamino-8-D-arginine vasopressin (DDAVP) infusion on platelet count and bleeding time in 4 patients with type IIB von Willebrand's disease (vWd). Three of four patients showed a normalization of the bleeding time within 1 h after the infusion, while bleeding time was not modified in the fourth. In accordance with the literature, thrombocytopenia was observed after DDAVP infusion, but this thrombocytopenia was due to the anticoagulants used for blood collection. In two patients (F.I., G.F.) no thrombocytopenia was observed when platelets were counted by fingerstick method but there was a 20% platelet decrease in blood samples collected in sodium citrate and a 50% decrease in samples collected in EDTA. Dramatic falls in platelet counts (70-95%) were observed in the additional two patients (C.A., D.Z.) after DDAVP infusion, when both sodium citrate or EDTA were used as anticoagulants. In the latter two patients there was also a 50% decrease in platelet count when the fingerstick method was used. The decrease in the patient's platelet count in EDTA samples after DDAVP infusion could be prevented, in part, by the previous additions of an anti GPIb monoclonal antibody and an anti GPIIb-IIIa monoclonal antibody. Thus, the thrombocytopenia observed in the four IIB vWd patients studied after DDAVP infusion seems to be, at least partially, a pseudothrombocytopenia depending on the calcium concentration in the blood samples and the availability of GPIb and GPIIb-IIIa receptors. These findings and the normalization of the bleeding time observed in three of the four patients has led us to reconsider the possible use of DDAVP in the treatment of our IIB vwd patients.     

Treatment of ChAdOx1 nCoV-19 Vaccine-Induced Immune Thrombotic Thrombocytopenia Related Acute Ischemic Stroke

Recently cases of vaccine-induced immune thrombotic thrombocytopenia (VITT) and thrombosis following the adenoviral vector vaccine against the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) were reported. A mechanism similar to heparin-induced thrombocytopenia was proposed with antibodies to platelet factor 4 (PF4). Vaccine related arterial thrombosis in the brain is rare but life-threatening and optimal treatment is not established. We report clinical, laboratory, imaging findings and treatment in a 51-year-old female presenting with acute left middle cerebral artery (MCA) occlusion 7 days after the first dose of ChAdOx1 nCoV-19 vaccine. Due to low platelet count and suspicion of VITT she was not eligible for intravenous thrombolysis (IVT) and proceeded to mechanical thrombectomy (MER) with successful recanalization four hours after onset of symptoms. Treatment with intravenous immunoglobulin (IVIG) and heparin pentasaccharide fondaparinux was initiated. Presence of anti-PF4 antibodies was confirmed. The patient improved clinically with normalization of platelet count. Clinicians should be alert of VITT in patients with acute ischemic stroke after ChAdOx1 nCov-19 vaccination and low platelet counts. MER showed to be feasible and effective. We propose considering MER in patients with VITT and large vessel occlusion despite thrombocytopenia. High-dose IVIG should be started immediately. Alternative anticoagulation to heparin should be started 24 hours after stroke onset unless significant hemorrhagic transformation occurred. Platelet transfusion is contraindicated and should be considered only in severe hemorrhagic complications. Restenosis or reocclusion of the revascularized artery is possible due to the hypercoagulable state in VITT and angiographic surveillance after the procedure is reasonable.     

Platelet kinetics and scintigraphic imaging in thrombocytopenic malaria patients

Thrombocytopenia is a common occurrence in acute malaria. It is attributed, among other factors, to excessive splenic platelet pooling and a shortened platelet lifespan. The aim of our study was to evaluate the platelet kinetics and sequestration site by isotopic studies in uncomplicated malaria-induced thrombocytopenia. Seven thrombocytopenic malaria patients (74,000+/-36,000 platelets/ micro l) were included in the study. Autologous (111)In-labeled platelet scintigraphy was performed up to 96 hours (h) post injection (p.i.) to evaluate the platelet sequestration site. Late sequestration for the spleen (S) and the liver (L) was analyzed according to the following activity ratios: S (spleen count on the last day of the platelet lifespan / spleen count at 30 min) and L (liver count on the last day of the platelet lifespan / liver count at 30 min). Additionally, platelet survival studies were performed. A normal late sequestration (S: 0.95+/-0.06 and L: 1.04+/-0.08; normal values, S and L: 1+/-0.2.) was observed in all of our patients. The platelet lifespan was reduced (1 to 4 days; normal range, 7-9 days), recovery was normal (mean, 63+/-6%; normal range, 55-75%), and the turnover rate was enhanced (mean, 95,000+/-80,000/ micro l/day; normal value, 35,000+/-4,500/ micro l/ day). According to the results of scintigraphy, the sequestration site by uncomplicated malaria-induced thrombocytopenia appears to be non-splenic and/or hepatic, yet diffuse.     

Interactions of liposomes and platelets

Rats were injected intravenously with liposomes of various compositions and sizes and blood platelet count measured. It was found that negatively-charged liposomal systems produced a transient reduction in platelet count in the first 5 minutes after injection which recovered by 60 minutes post-injection. This effect was most striking for multilamellar vesicles (MLV's) containing phosphatidylglycerol (PG). Dose levels of 25 mg/kg of MLV's containing 10 mole% PG caused the platelet count to drop from a control value of 1,086 +/- 21 X 10(9)/l to 193 +/- 14 X 10(9)/l by 2 minutes post-injection, an 82% decline. This thrombocytopenic effect was observed to diminish as vesicle size or vesicle dose was decreased. Positively-charged liposomes produced a less pronounced transient reduction in platelet count while neutral liposomes caused only a mild, transient platelet decline. This transient thrombocytopenic effect was not blocked by common anticoagulants and fibrinolytic agents but was prevented by liposomal pretreatment. Radiolabeled platelet studies revealed that transient sequestration of platelets occurs in the liver and spleen 2 minutes after PG:EPC:CHOL MLV injection with a normalization of platelet distribution by 60 minutes post-injection. In vitro studies, using an automated blood counter, suggest a transient association of liposomes and platelets occurring following injection. Liposomally-induced transient thrombocytopenia suggests a role for platelets in the biodistribution of liposomes.     

Heparin-induced thrombocytopenia: diagnosis and management

Heparin-induced thrombocytopenia (HIT) is an immune reaction in response to platelet factor 4-heparin complexes, which results in increased platelet activation and thrombocytopenia beginning on the 4th-5th day after heparin exposure induced by IgG antibody production. Platelet activation can lead to arterial thrombosis, but more commonly platelet microparticle formation contributes to venous thrombosis. Accurate diagnosis of HIT is based on the presence of clinical features, including a 50% fall in platelet count, appropriate timing of thrombocytopenia, development of new thrombosis despite thrombocytopenia and heparin therapy, and the absence of a more likely cause of thrombocytopenia. Documentation of an anti-PF4-heparin antibody is necessary, but is not sufficient to make the diagnosis since antibody formation occurs in a variety of clinical settings without the development of thrombocytopenia or thrombosis. Once HIT is suspected or confirmed, all forms of heparin should be discontinued and an alternative form of anticoagulation should be administered until the platelet count recovers. Treatment options include intravenous administration of argatroban, lepirudin, and bivalirudin; subcutaneous administration of fondaparinux has also been described. Warfarin therapy, if indicated, should be avoided until platelet recovery. Re-exposure to heparin can be avoided by use of alternative anticoagulants for most circumstances. Heparin-induced thrombocytopenia (HIT) has been the focus of increasing attention over the past 15-20 years. As interventions for HIT are developed, there is a need to accurately diagnose the condition, which can be challenging especially in severely ill patients.     

Platelets, alcohol consumption, and onset of brain infarction.

OBJECTIVES: Previous investigations have suggested that recurrent rebound thrombocytosis after alcohol misuse may be a factor in the pathogenesis of thromboembolic disease. Alcohol consumption, platelet count, and platelet function were examined among patients of working age with brain infarction. METHODS: Platelet count and risk factors for stroke were studied in 426 stroke patients and 157 control patients in hospital. The measures were platelet count obtained within four days after the stroke onset, in vitro adenosine diphosphate induced platelet aggregation, associated thromboxane B2 formation, and urinary excretion of 11-dehydrothromboxane B2. RESULTS: After adjustment for sex, age, cardiac disease, diabetes, and alcohol intake, hypertension (OR 3.4, 95% confidence interval (95% CI) 2.0-6.0) and current smoking (OR 2.1, 95% CI 1.4-3.3) were associated with an increased risk for brain infarction. Platelet count shortly after the onset of disease was higher in the stroke patients than in the controls (OR 1.05/10(10)/1 platelets; 95% CI 1.02-1.09). The patients with brain infarction who were heavy alcohol drinkers (n = 144) showed both thrombocytosis (OR 2.30, 95% CI 0.82-6.44) and thrombocytopenia (OR 3.20, 95% CI 1.19 to 8.59) more often at the onset of the stroke than the other patients with brain infarction. The thromboxane variables showed inconsistent associations with the onset of stroke. There was no consistent platelet abnormality among alcohol misusers at the onset of ischaemic brain infarction. CONCLUSIONS: Alcohol induced thrombocytopenia and rebound thrombocytosis were both often seen at the onset of brain infarction in patients who were heavy alcohol drinkers. Therefore, other mechanisms which could contribute to the high frequency of recurrences of ischaemic stroke among heavy drinkers should be investigated.     

Sodium valproate and thrombocytopenia.

Thrombocytopenia has been occasionally reported in patients on sodium valproate. Here is reported a 6-year-old boy on this drug who was found to have thrombocytopenia 6 months after initiation of administration and it was progressive up to 16 months. Though the medication was continued because of its efficacy, platelet count gradually recovered to the normal level spontaneously. Throughout the course, no hemorrhagic tendency was observed clinically. It was suggested that platelet count should be monitored periodically, but that the presence of thrombocytopenia itself does not serve as an absolute indication for discontinuing the drug.     

Effects of intra-arterial cannulation on blood platelet consumption in rats

Experimental arterial thrombosis has been induced by an indwelling cannula in the abdominal aorta of rats. The involvement of blood platelets was studied by the determination of the blood platelet count and the survival of ⁵¹Cr labeled platelets. Cannulation transformed the platelet disappearance patterns from linear to curvi linear and exponential curves. The blood platelet consumption rate increased 2–3 fold immediately after cannulation and remained at that level for at least 8 days. The consumption rate was higher when longer cannulae were used. Initially the increased blood platelet consumption was not compensated by an increase in platelet production, this resulted in a decreasing platelet count. After 3 to 7 days a long lasting steady state thrombocytopenia was achieved, under these circumstances the platelet turnover in cannulated and normal rats was the same. Withdrawal of the cannula normalized the platelet consumption within a few hours, leading to a linear disappearance pattern of the residual labeled platelets. The platelet count was readily restored to normal values via a rebound overshoot.