Platelet Count and Venous Thromboembolism

Monréal, Manuel; Lafoz, E.; Casals, A; Ruiz, J.; Arias, Antonio

doi:10.1378/chest.100.6.1493

Cited by 36 publications

(9 citation statements)

References 17 publications

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“…(29) The mechanism for developing thrombocytopenia in these patients remains unclear, but the association of postoperative platelet counts with stroke after CABG surgery suggests that the reduction in platelet numbers likely occurs in a context of increased platelet reactivity. This notion is supported by the fact that in a non-cardiac surgical context, low platelet counts are predictive of deep vein thrombosis,(30,31) and that a drop in platelet numbers is a risk factor for recurrence of pulmonary embolism,(32) re-infarction after ST-elevation MI,(33) and severity of stroke. (34) In addition, a study in patients with acute coronary syndrome demonstrated that low platelet counts are associated with an increased risk for recurrent infarction, stroke, and death in drug-associated (ie, heparin, glycoprotein inhibitors) as well as drug-independent thrombocytopenia.…”

Section: Discussionmentioning

confidence: 97%

Platelet Counts and Postoperative Stroke After Coronary Artery Bypass Grafting Surgery

Karhausen

Smeltz

Akushevich

et al. 2017

Anesthesia &Amp; Analgesia

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Background Declining platelet counts may reveal platelet activation and aggregation in a postoperative prothrombotic state. Therefore, we hypothesized that nadir platelet counts after on-pump coronary artery bypass grafting (CABG) surgery are associated with stroke. Methods We evaluated 6,130 adult CABG surgery patients. Postoperative platelet counts were evaluated as continuous and categorical (mild vs. moderate to severe) predictors of stroke. Extended Cox proportional hazard regression analysis with a time-varying covariate for daily minimum postoperative platelet count assessed the association of day-to-day variations in postoperative platelet count with time to stroke. Competing risks proportional hazard regression models examined associations between day-to-day variations in postoperative platelet counts with timing of stroke (early: 0–1 days; delayed: ≥2 days). Results Median [interquartile range] postoperative nadir platelet counts were 123.0 [98.0, 155.0] × 109/L. The incidences of postoperative stroke were 1.09%, 1.50%, and 3.02% for platelet counts, >150×109/L, 100–150×109/L, and <100×109/L, respectively. The risk for stroke increased by 12% on a given postoperative day for every 30 × 109/L decrease in platelet counts (adjusted hazard ratio [HR], 1.12; 95% confidence interval [CI], 1.01–1.24; P=0.0255). On a given day, patients with moderate to severe thrombocytopenia were twice as likely to develop stroke (adjusted HR, 1.99; 95% CI, 1.18–3.34; P=0.0093) as patients with nadir platelet counts >150×109/L. Importantly, such thrombocytopenia, defined as a time-varying covariate, was significantly associated with delayed (≥2days after surgery; adjusted HR, 2.87; 95% CI, 1.49–5.55; P=0.0016), but not early postoperative stroke. Conclusion Our findings suggest an independent association between moderate to severe postoperative thrombocytopenia and postoperative stroke, and timing of stroke after CABG surgery.

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Section: Discussionmentioning

confidence: 97%

Platelet Counts and Postoperative Stroke After Coronary Artery Bypass Grafting Surgery

Karhausen

Smeltz

Akushevich

et al. 2017

Anesthesia &Amp; Analgesia

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“…A decrease in platelets, while common occurrence in a hyperinflammatory state, is also observed during acute PE due to platelet activation in the pulmonary vasculature. 30,31 Indeed, 4 of the 5 patients diagnosed with PE in our cohort had abnormal strain patterns, although the process by which pulmonary angiography was performed in our patients introduces selection bias. We also expect that pulmonary thrombosis, if leading to abnormal FWLS, would also cause a concomitant rise in pulmonary artery pressures.…”

Section: Discussionmentioning

confidence: 94%

Right Ventricular Strain Is Common in Intubated COVID-19 Patients and Does Not Reflect Severity of Respiratory Illness

Gibson

Fenza

Lang

et al. 2021

J Intensive Care Med

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Background: Right ventricular (RV) dysfunction is common and associated with worse outcomes in patients with coronavirus disease 2019 (COVID-19). In non-COVID-19 acute respiratory distress syndrome, RV dysfunction develops due to pulmonary hypoxic vasoconstriction, inflammation, and alveolar overdistension or atelectasis. Although similar pathogenic mechanisms may induce RV dysfunction in COVID-19, other COVID-19-specific pathology, such as pulmonary endothelialitis, thrombosis, or myocarditis, may also affect RV function. We quantified RV dysfunction by echocardiographic strain analysis and investigated its correlation with disease severity, ventilatory parameters, biomarkers, and imaging findings in critically ill COVID-19 patients. Methods: We determined RV free wall longitudinal strain (FWLS) in 32 patients receiving mechanical ventilation for COVID-19-associated respiratory failure. Demographics, comorbid conditions, ventilatory parameters, medications, and laboratory findings were extracted from the medical record. Chest imaging was assessed to determine the severity of lung disease and the presence of pulmonary embolism. Results: Abnormal FWLS was present in 66% of mechanically ventilated COVID-19 patients and was associated with higher lung compliance (39.6 vs 29.4 mL/cmH2O, P = 0.016), lower airway plateau pressures (21 vs 24 cmH2O, P = 0.043), lower tidal volume ventilation (5.74 vs 6.17 cc/kg, P = 0.031), and reduced left ventricular function. FWLS correlated negatively with age (r = −0.414, P = 0.018) and with serum troponin (r = 0.402, P = 0.034). Patients with abnormal RV strain did not exhibit decreased oxygenation or increased disease severity based on inflammatory markers, vasopressor requirements, or chest imaging findings. Conclusions: RV dysfunction is common among critically ill COVID-19 patients and is not related to abnormal lung mechanics or ventilatory pressures. Instead, patients with abnormal FWLS had more favorable lung compliance. RV dysfunction may be secondary to diffuse intravascular micro- and macro-thrombosis or direct myocardial damage. Trial Registration: National Institutes of Health #NCT04306393. Registered 10 March 2020, https://clinicaltrials.gov/ct2/show/NCT04306393

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“…She presented with thrombocytosis at 418 x103/uL on admission as well. Research by Monreal et al has indicated that this can often be a significant indicator for a lack of pulmonary embolism (PE) in those with venous thrombosis/thromboembolism, which was indeed true for this patient, as her thromboembolism was a dural venous sinus and leg DVT, while evidence of PE was ruled out [12]. Although high hematocrit, hemoglobin, and RBC levels are often associated with increased risk of thrombosis and thromboembolism, her hematocrit was 34.7%, just below the 36% lower limit of normal in women, hemoglobin was 11.5, again just barely below the lower limit of normal in women, and RBC of 4.26 million/mcL, which is within the normal range [13].…”

Section: Figure 3: Doppler Us Without (Left) and With Compression (Right) Suggesting Venous Thrombosismentioning

confidence: 53%

Unexpected Populations for Deep Vein Thrombosis: Presentation in an Endurance Athlete

LeBlanc¹,

Cooper²,

Chopra

2021

Cureus

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This case presents an athletic 40-year-old female marathon runner who presented with a headache secondary to dural venous sinus thrombosis and right calf deep vein thrombosis (DVT). Though this is outside of the typical image we portray of a common DVT patient, athletes too experience hypercoagulable risk factors and medical issues, just as their less in-shape peers. This patient's history of oral contraceptive use, Lynch syndrome, colon cancer, and pregnancy indicates potential risk factors for DVT. Even without these though, it is important to note that every endurance athlete experiences hemoconcentration, dehydration, and inflammation during exercise, training, and competition events. This case demonstrates the need for an increased index of suspicion in endurance athletes. The case exemplifies an all-too-frequent occurrence of allowing our differential to be skewed away from potentially life-threatening conditions like DVT, and their thrombotic sequelae, because of the "textbook population" descriptions of a given disease state. We hope this case will shed needed light on the phenomenon and lead to more controlled research on the probability and pathophysiology for thrombotic events in this broadened population so that its incidence and prevalence in endurance athletes can be accurately reported in the literature.

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Platelet Count and Venous Thromboembolism

Cited by 36 publications

References 17 publications

Platelet Counts and Postoperative Stroke After Coronary Artery Bypass Grafting Surgery

Platelet Counts and Postoperative Stroke After Coronary Artery Bypass Grafting Surgery

Right Ventricular Strain Is Common in Intubated COVID-19 Patients and Does Not Reflect Severity of Respiratory Illness

Unexpected Populations for Deep Vein Thrombosis: Presentation in an Endurance Athlete

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