Reduced platelet function in subarachnoid hemorrhage

1986 ◽  
Vol 64 (6) ◽  
pp. 907-910 ◽  
Author(s):  
Sotirios A. Tsementzis ◽  
Jaswinder S. Gill ◽  
Edward R. Hitchcock ◽  
Jennifer A. Hartley ◽  
Surinder K. Gill ◽  
...  
Keyword(s):  
Platelet Count ◽  
Subarachnoid Hemorrhage ◽  
Platelet Aggregation ◽  
Platelet Function ◽  
Maximum Rate ◽  
Adenosine Diphosphate ◽  
Platelet Adhesiveness ◽  
Content Type ◽  
Aneurysmal Rupture ◽  
Fine Print

✓ The hypothesis that abnormalities of platelet function may relate to the occurrence or recurrence of subarachnoid hemorrhage (SAH) has been examined. Seventy patients with SAH and 65 control individuals were studied. The adenosine diphosphate (ADP) threshold for secondary platelet aggregation was significantly higher in the SAH group than in the controls. In tests using 4.0 µg/ml ADP, the percent platelet aggregation (at 2 minutes) and the maximum rate of platelet aggregation (over 20 seconds) were significantly lower in the SAH patients. There was no difference in total platelet count between the two groups. Platelet adhesiveness was lower in the SAH patients when compared to controls. Circulating microaggregates did not differ between the two groups. The results indicate that reduced platelet function does relate to SAH and may either contribute to aneurysmal rupture in cases of SAH or be a consequence of it.

Reduced platelet aggregability and thromboxane release after rebleeding in patients with subarachnoid hemorrhage

1991 ◽  
Vol 74 (1) ◽  
pp. 21-26 ◽  
Author(s):  
Seppo Juvela ◽  
Marrku Kaste
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Platelet Aggregation ◽  
Platelet Function ◽  
Statistical Significance ◽  
Adenosine Diphosphate ◽  
Blood Samples ◽  
Content Type ◽  
Platelet Aggregability ◽  
Before And After ◽  
Fine Print

✓ Serial blood samples were obtained from 80 patients with subarachnoid hemorrhage (SAH) to study adenosine diphosphate-induced platelet aggregation and associated thromboxane B2 release. The goal of the investigation was to detect whether reduced platelet function is involved in rebleeds. Seventeen patients (21%) suffered a rebleed, six of those experiencing their first rebleed within 24 hours after SAH. Therefore, most platelet function studies were performed after rebleeds. Thromboxane release was lower in patients with rebleeds than in the others, both before and after rebleeding, although statistical significance was reached only in samples collected after rebleeds. Patients rebleeding within 24 hours after SAH had lower platelet aggregability (p = 0.037) than patients without a rebleed in the samples taken within 3 days after SAH. The results suggest that reduced platelet aggregability and thromboxane release are involved in rebleeds following primary SAH.

Disturbance Of Platelet Function In The Nephrotic Syndrome

1981 ◽  
Author(s):  
E Walter ◽  
D Deppermann ◽  
K Andrassy ◽  
E Weber
Keyword(s):  
Nephrotic Syndrome ◽  
Platelet Count ◽  
Platelet Aggregation ◽  
Kidney Function ◽  
Platelet Function ◽  
Platelet Adhesiveness ◽  
Spontaneous Aggregation ◽  
Spontaneous Platelet Aggregation ◽  
Platelet Functions

Thromboembolic phenomena often (30 %) complicate the nephrotic syndrome. It was therefor investigated, wether disturbed platelet functions play a role in this disease.28 normals, 34 patients with nephrotic syndrome and 18 of them with impaired kidney function were tested. In 20 patients the measurements were repeated after administration of aspirin plus dipyridamo1e.Patients with nephrotic syndrome showed in comparison to normals the following changes: 1. increased platelet count (p < 0.01), 2. enhanced platelet adhesiveness (Wright-test: p < 0.001), 3. increased spontaneous aggregation (PAT I: p < 0.001; PAT III: p < 0.01), 4. enhanced PF 4-activity (heparin neutralisation: p < 0.001), 5. elevated β TG-levels only in impaired kidney function. There was no difference in the reaction of platelets against ADP as well as collagen. The changes in platelet function correlated with the severity of the nephrotic syndrome (proteinurea, hypalbuminaemia, hyperlipo- proteinaemia). After aspirin plus dipyridamole administration spontaneous platelet aggregation and adhesiveness were normalized.There is a disturbance of platelet function in patients with nephrotic syndrome, which can be reversed with antiaggregating agents.

scholarly journals Influence of Hepatocellular Carcinoma on Platelet Aggregation in Cirrhosis

Cancers ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1150
Author(s):  
Alberto Zanetto ◽  
Marco Senzolo ◽  
Elena Campello ◽  
Cristiana Bulato ◽  
Sabrina Gavasso ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Platelet Count ◽  
Platelet Aggregation ◽  
Platelet Function ◽  
Adenosine Diphosphate ◽  
Compensated Cirrhosis ◽  
Impedance Aggregometry ◽  
Child Class ◽  
Von Willebrand ◽  
Willebrand Factor

Hyper-functional platelets are being proposed as a potential therapeutic target in multiple cancers. Whether this can be considered in patients with cirrhosis and hepatocellular carcinoma (HCC) is unknown as their platelet function has not yet been investigated. We evaluated platelet function in cirrhosis patients with HCC. Patients with cirrhosis with and without HCC were prospectively recruited. Platelet aggregation, a marker of platelet function, was assessed by impedance aggregometry with adenosine diphosphate (ADP), arachidonic acid (ASPI), and thrombin (TRAP) stimulation. Plasmatic levels of Von Willebrand factor antigen (VWF) were also determined. One-hundred patients were recruited (50 cirrhotics with and 50 without HCC). Cirrhosis severity by Child class and platelet count were comparable between cirrhotics with and without HCC. Cirrhotics with HCC had higher ADP- (45 vs. 28; p < 0.001), ASPI- (47 vs. 28; p < 0.001), and TRAP- (85 vs. 75; p = 0.01) induced platelet aggregation than cirrhotics without HCC, all indicative of platelet hyper-function. The relatively increased platelet aggregation in patients with HCC was confirmed after adjusting the analysis for platelet count/severity of thrombocytopenia. Levels of VWF were higher in patients with vs. without HCC (348 vs. 267; p = 0.006), particularly in compensated cirrhosis. In patients with cirrhosis, HCC is associated with increased platelet aggregation and higher VWF. The clinical implications of these findings deserve further investigation.

Aspirin and delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage

1995 ◽  
Vol 82 (6) ◽  
pp. 945-952 ◽  
Author(s):  
Seppo Juvela
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Cerebral Infarction ◽  
Platelet Function ◽  
Delayed Cerebral Ischemia ◽  
Aneurysm Rupture ◽  
Content Type ◽  
Reduced Risk ◽  
Fine Print

✓ This follow-up study was designed to evaluate whether the use of aspirin either before or after aneurysm rupture affects the occurrence of delayed cerebral ischemia. Aspirin inhibits platelet function and thromboxane production and has been shown to reduce the risk of various cardiovascular and cerebrovascular ischemic diseases. Following admission, the patients in this study were interviewed regarding their use of aspirin and other medicines prior to and after hemorrhage, and their urine was screened qualitatively for salicylates. Patient outcome and the occurrence of hypodense lesions consistent with cerebral infarction on follow-up computerized tomography (CT) were studied prospectively up to 1 year after hemorrhage. Of 291 patients, 31 (11%) died because of the initial hemorrhage and 18 (6%) died due to rebleeding within 4 days after hemorrhage. Of the remaining 242 patients, 90 (37%) had delayed cerebral ischemia, which caused a permanent neurological deficit or death in 54 patients (22%). Of 195 patients undergoing follow-up CT, 85 (44%) had cerebral infarction that was not seen on the CT scan obtained on admission. Those who had salicylates in the urine on admission had a relative risk of 0.40 (95% confidence interval (CI), 0.15 to 1.10) of delayed ischemia with fixed deficit and a risk of 0.40 (95% CI, 0.18 to 0.93) of cerebral infarction compared with patients who did not have salicylates in their urine. This reduced risk of ischemic complications with aspirin use was restricted to those patients who used aspirin before hemorrhage, when the risk of ischemia was 0.21 (95% CI, 0.03 to 1.63) and the risk of infarct was 0.18 (95% CI, 0.04 to 0.84) compared with those who had not used aspirin. The reduced risk of cerebral infarction remained significant after adjustment for several potential confounding factors (adjusted risk 0.19; 95% CI, 0.04 to 0.89). These observations suggest that platelet function at the time of subarachnoid hemorrhage may be associated with delayed cerebral ischemia after aneurysm rupture.

Decrease in platelet count as an independent risk factor for symptomatic vasospasm following aneurysmal subarachnoid hemorrhage

2005 ◽  
Vol 102 (5) ◽  
pp. 882-887 ◽  
Author(s):  
Yutaka Hirashima ◽  
Hideo Hamada ◽  
Masanori Kurimoto ◽  
Hideki Origasa ◽  
Shunro Endo
Keyword(s):  
Platelet Count ◽  
Subarachnoid Hemorrhage ◽  
Blood Cells ◽  
White Blood Cells ◽  
Experimental Studies ◽  
Content Type ◽  
Symptomatic Vasospasm ◽  
Cell Counts ◽  
Fisher Grade ◽  
Fine Print

Object. Increased platelet consumption is expected in patients with cerebral vasospasm, according to data from clinical and experimental studies. The authors investigated sequential changes in platelet counts in patients with subarachnoid hemorrhage (SAH) and the difference in platelet consumption between patients with and those without symptomatic vasospasm (SV). Variables related to platelet count as well as other clinical and radiological variables were analyzed as independent predictors of SV. Methods. One hundred consecutive patients who had undergone surgery within 48 hours after SAH onset were entered in the study. Clinical and radiological variables and blood cell counts, including red blood cells, white blood cells, and platelets, after SAH were retrospectively examined. Twenty of these variables were entered into univariate and multivariate analyses to determine predictors for SV. After SAH, the platelet count decreased to a minimum and then increased rapidly to levels greater than those recorded on admission. This change was specific to SAH, and platelet consumption was more severe in patients with SV than in those without. There were three independent predictors of SV: a ratio of the lowest platelet count and the admission count greater than 0.7 (odds ratio [OR] 0.322, 95% confidence interval [CI] 0.124–0.834, p = 0.0196) and a history of hypertension (OR 0.338, 95% CI 0.126–0.906, p = 0.0311) were negatively significant (that is, decreases the occurrence of SV), and a Fisher Grade 3 (OR 4.42, 95% CI 1.48–13.2, p = 0.0077) was positively significant (that is, increases the occurrence of SV). Conclusions. The association between a decrease in platelet count and the occurrence of SV indicates the important role of platelets in the pathophysiology of vasospasm following SAH.

Heparin-induced thrombocytopenia and thrombosis following subarachnoid hemorrhage

2000 ◽  
Vol 93 (1) ◽  
pp. 136-139 ◽  
Author(s):  
Ian F. Parney ◽  
David E. Steinke
Keyword(s):  
Platelet Count ◽  
Subarachnoid Hemorrhage ◽  
Large Body ◽  
Artery Aneurysm ◽  
Left Middle Cerebral Artery ◽  
Cerebral Angiogram ◽  
Related Disorder ◽  
Heparin Induced Thrombocytopenia ◽  
Content Type ◽  
Fine Print

U The authors present a case of heparin-induced thrombocytopenia and thrombosis (HITT) that occurred after aneurysmal subarachnoid hemorrhage (SAH), and they review the relevant literature. An immune-mediated syndrome, HITT is characterized by moderate thrombocytopenia and paradoxical vascular thromboses. Although it has been estimated in prospective studies that HITT occurs in between 1 and 3% of patients receiving heparin, it is underrecognized in the neurosurgical literature. In the present case, a 49-year-old woman underwent clipping of a right posterior communicating artery aneurysm after suffering a Hunt and Hess Grade III SAH. She had an uncomplicated postoperative course with good clip positioning and no vasospasm observed on a cerebral angiogram obtained on Day 7.On Day 23, the patient developed a right hemiparesis and experienced a grand mal seizure. A head computerized tomography scan revealed a hemorrhagic infarct in the left middle cerebral artery distribution. Repeated cerebral angiograms did not show vasospasm. She was thrombocytopenic (platelet count as low as 46 × 109/L on Day 28 compared with 213 × 109/L on Day 1) and had been receiving heparin flushes to maintain intravenous catheter patency. An assay for HITT-associated antibodies was positive. The heparin flushes were discontinued and the platelet count recovered (121 × 109/L). She improved neurologically, but was left with a significant right hemiparesis at discharge. This patient had assay-proven heparin-induced thrombocytopenia despite minimal exposure to heparin. Because there was no evidence of vasospasm or other factors to account for her delayed hemorrhagic infarction, an HITT-related disorder seemed most likely. Despite a large body of literature describing HITT in nonneurosurgical patients, only three previous neurosurgical cases have been published. This case report may serve to heighten awareness of this disorder.

Experimental cerebral vasospasm

1974 ◽  
Vol 41 (3) ◽  
pp. 285-292 ◽  
Author(s):  
Hajime Nagai ◽  
Yoshiaki Suzuki ◽  
Mitsuo Sugiura ◽  
Satoshi Noda ◽  
Hideo Mabe
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Posterior Communicating Artery ◽  
Content Type ◽  
Aneurysmal Rupture ◽  
Experimental Subarachnoid Hemorrhage ◽  
Fine Print

✓The authors describe a model for making an experimental subarachnoid hemorrhage that closely simulates human aneurysmal rupture. A needle previously inserted into the posterior communicating artery is subsequently withdrawn by traction on a thread. Using this model they demonstrate biphasic spasm by measurement of cerebral blood flow and angiography after rupture of the artery; the early spasm lasted 60 minutes and the late spasm began 3 or 4 hours after subarachnoid hemorrhage and continued for several days. The authors discuss the pathogenesis of early and late spasm.

Acute microvascular platelet aggregation after subarachnoid hemorrhage

2005 ◽  
Vol 102 (6) ◽  
pp. 1094-1100 ◽  
Author(s):  
Fatima A. Sehba ◽  
Gulam Mostafa ◽  
Victor Friedrich ◽  
Joshua B. Bederson
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Platelet Aggregation ◽  
Subsequent Increase ◽  
Platelet Surface ◽  
Content Type ◽  
Acute Cerebral Ischemia ◽  
Vessel Structure ◽  
Surface Receptor ◽  
Platelet Aggregates ◽  
Fine Print

Object. The mechanisms underlying acute cerebral ischemia after subarachnoid hemorrhage (SAH) are not well established. Platelets aggregate within major cerebral vessels hours after SAH, but this has not been studied in the microvasculature. Platelet aggregates within the microvasculature could mechanically obstruct the lumen and initiate events that injure vessel structure. In the present study the authors examined the hypothesis that platelets aggregate within the cerebral microvasculature acutely after SAH. Methods. Subarachnoid hemorrhage was induced in the rat by using the endovascular perforation model. The animals were killed between 10 minutes and 48 hours after SAH. Immunostaining for the platelet surface receptor glycoprotein (GP)IIb/IIIa, which mediates platelet aggregation, was used to detect platelet aggregation. Sham-operated animals were used as controls. The GPIIb/IIIa immunoreactive platelet aggregates were abundant in the microvasculature of the basal and frontal cortex, striatum, and hippocampus 10 minutes after SAH. These aggregates decreased in number from 1 to 6 hours post-SAH and then increased to a peak at 24 hours. No immunoreactive aggregates were observed 48 hours after SAH. Conclusions. The data indicate that widespread platelet aggregation occurs very rapidly in response to SAH followed by a decrease within 6 hours and a subsequent increase 24 hours after SAH. Microvascular platelet aggregates may contribute to decreased cerebral blood flow and ischemic injury after SAH via a number of mechanisms.

Oral Contraceptives and Platelet Function

1972 ◽  
Vol 28 (02) ◽  
pp. 213-220 ◽  
Author(s):  
L Mettler ◽  
Meseck B. Selchow
Keyword(s):  
Platelet Count ◽  
Oral Contraceptive ◽  
Platelet Aggregation ◽  
Platelet Function ◽  
Oral Contraceptives ◽  
Platelet Adhesiveness ◽  
Predisposing Factor ◽  
Platelet Counts ◽  
Contraceptive Therapy ◽  
Oral Contraceptive Therapy

SummaryPlatelet function was studied in women receiving two oral oestrogen-progestagen compounds (Neogynon and Noracyclin-22). Platelet count, adhesiveness, spreading, aggregation (PAT) and thromboelastography (TEG) were studied twice monthly for six months in 186 cycles. Platelet counts in rotated plasma were decreased in both groups. A significant increase in non-spread platelets was found in the Neogynon group only. PAT-degrees were significantly increased in both groups. Platelet adhesiveness and thromboelastographic measurements were not affected. Increased platelet aggregation during oral contraceptive therapy is regarded as a predisposing factor to thrombosis.

The Effect of Dimethyl Sulfoxide on In Vitro Platelet Function

1976 ◽  
Vol 36 (01) ◽  
pp. 221-229 ◽  
Author(s):  
Charles A. Schiffer ◽  
Caroline L. Whitaker ◽  
Morton Schmukler ◽  
Joseph Aisner ◽  
Steven L. Hilbert
Keyword(s):  
Platelet Count ◽  
Platelet Aggregation ◽  
Dimethyl Sulfoxide ◽  
Platelet Function ◽  
Platelet Volume ◽  
Short Term ◽  
Platelet Factor ◽  
Short Term Exposure ◽  
Structural Abnormalities

SummaryAlthough dimethyl sulfoxide (DMSO) has been used extensively as a cryopreservative for platelets there are few studies dealing with the effect of DMSO on platelet function. Using techniques similar to those employed in platelet cryopreservation platelets were incubated with final concentrations of 2-10% DMSO at 25° C. After exposure to 5 and 10% DMSO platelets remained discoid and electron micrographs revealed no structural abnormalities. There was no significant change in platelet count. In terms of injury to platelet membranes, there was no increased availability of platelet factor-3 or leakage of nucleotides, 5 hydroxytryptamine (5HT) or glycosidases with final DMSO concentrations of 2.5, 5 and 10% DMSO. Thrombin stimulated nucleotide and 5HT release was reduced by 10% DMSO. Impairment of thrombin induced glycosidase release was noted at lower DMSO concentrations and was dose related. Similarly, aggregation to ADP was progressively impaired at DMSO concentrations from 1-5% and was dose related. After the platelets exposed to DMSO were washed, however, aggregation and release returned to control values. Platelet aggregation by epinephrine was also inhibited by DMSO and this could not be corrected by washing the platelets. DMSO-plasma solutions are hypertonic but only minimal increases in platelet volume (at 10% DMSO) could be detected. Shrinkage of platelets was seen with hypertonic solutions of sodium chloride or sucrose suggesting that the rapid transmembrane passage of DMSO prevented significant shifts of water. These studies demonstrate that there are minimal irreversible alterations in in vitro platelet function after short-term exposure to DMSO.

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