Monday, November 10, 2025

The Role of the Spleen in Critical Illness: Beyond an Immune Organ

 

The Role of the Spleen in Critical Illness: Beyond an Immune Organ

Dr Neeraj Manikath , claude.ai

Abstract

The spleen, traditionally viewed as a passive lymphoid organ, plays dynamic and multifaceted roles in critical illness that are frequently underappreciated by intensivists. This review explores the spleen's reservoir function for platelets and immune cells, its active contraction in response to physiological stress, and the emerging utility of point-of-care ultrasound (POCUS) for bedside splenic assessment. Understanding splenic physiology in critical care contexts provides clinicians with novel insights into hemodynamic monitoring, immune dysfunction, and the interpretation of hematological parameters in the intensive care unit (ICU).

Keywords: Spleen, critical illness, splenic contraction, POCUS, platelets, immune dysfunction, sepsis

Introduction

The spleen has long been recognized for its immunological and hematological functions, yet its dynamic role in critical illness remains poorly understood by many clinicians. Weighing approximately 150-200 grams in healthy adults, this encapsulated organ harbors up to 30% of the body's platelet mass and serves as a crucial reservoir for immune cells.[1] In critically ill patients, the spleen undergoes significant physiological changes that influence hemodynamics, coagulation, and immune responses.

Recent advances in point-of-care ultrasound have enabled real-time bedside assessment of splenic morphology and function, offering intensivists a non-invasive window into systemic stress responses.[2] This review synthesizes current evidence on splenic physiology relevant to critical care practice, highlighting practical applications and future research directions.

The Spleen as a Reservoir for Platelets and Immune Cells

Platelet Sequestration and Mobilization

The spleen represents the largest reserve of platelets outside the circulation, with approximately 30-40% of total body platelets residing in the splenic pulp under physiological conditions.[3] This reservoir function is mediated by the unique sinusoidal architecture of the red pulp, where slow blood flow allows selective retention of platelets while permitting their rapid release during hemostatic challenges.

Pearl: In critically ill patients with apparent thrombocytopenia, consider splenic sequestration as a differential diagnosis, particularly in those with portal hypertension or congestive splenomegaly. These patients may have adequate total body platelet mass despite low circulating counts.[4]

The mechanism of platelet retention involves interactions between platelet surface glycoproteins and splenic endothelial adhesion molecules. During stress states—including hemorrhage, hypoxia, and sepsis—sympathetic nervous system activation triggers splenic contraction, releasing sequestered platelets into the circulation.[5] This autotransfusion mechanism can increase circulating platelet counts by 30,000-50,000/μL within minutes, representing a primitive but effective hemostatic reserve.[6]

Immune Cell Compartmentalization

Beyond platelets, the spleen houses substantial populations of lymphocytes, monocytes, and neutrophils. The white pulp contains organized lymphoid follicles with T and B cell zones, while the marginal zone harbors specialized macrophages and dendritic cells critical for pathogen recognition.[7] This compartmentalization facilitates rapid immune responses to blood-borne pathogens—a function of paramount importance in sepsis.

Recent research has revealed that splenic monocytes represent a distinct reservoir population that can be mobilized during systemic inflammation. Studies using experimental endotoxemia demonstrate that splenic contraction releases monocytes with unique phenotypic characteristics, potentially contributing to both protective immunity and harmful inflammatory responses.[8]

Oyster: Post-splenectomy sepsis remains a clinical conundrum. While the lifetime risk of overwhelming post-splenectomy infection (OPSI) is relatively low (0.23-0.42% per year), mortality approaches 50-70% when it occurs.[9] This underscores the spleen's non-redundant role in defense against encapsulated organisms (Streptococcus pneumoniae, Haemophilus influenzae, Neisseria meningitidis).

Splenic Dysfunction in Sepsis

Paradoxically, the spleen undergoes both hyperfunction and dysfunction during sepsis. Early in septic shock, splenic contraction releases immune cells and platelets, potentially contributing to the systemic inflammatory response syndrome (SIRS).[10] However, as sepsis progresses, the spleen demonstrates profound architectural disruption with lymphocyte apoptosis, germinal center involution, and impaired antigen presentation—hallmarks of sepsis-induced immunoparalysis.[11]

Autopsy studies of septic patients reveal extensive splenic white pulp atrophy, correlating with the degree of immunosuppression.[12] This "splenic exhaustion" may contribute to secondary infections and prolonged ICU stays, though therapeutic strategies to prevent or reverse this process remain experimental.

Hack: In patients with unexplained immunosuppression following severe sepsis, consider the spleen as a potential target for immune monitoring. While not yet standard practice, research into splenic volume changes via serial ultrasound may eventually provide prognostic information regarding immune recovery.[13]

Splenic Contraction and its Impact on Hematocrit and Hemostasis

Mechanisms of Splenic Contraction

Splenic contraction represents an evolutionarily conserved response to physiological stress, mediated primarily by alpha-adrenergic stimulation of smooth muscle in the splenic capsule and trabeculae.[14] In diving mammals, splenic contraction is dramatic, releasing up to 10-15% of blood volume to maintain oxygen delivery during apnea. While humans exhibit more modest responses, splenic contraction remains clinically significant.

Triggers for splenic contraction include:

  • Hemorrhagic shock and hypovolemia
  • Hypoxemia and high-altitude exposure
  • Exercise and physical stress
  • Catecholamine surges (endogenous or exogenous)
  • Apnea and breath-holding[15]

The contraction response can reduce splenic volume by 20-40% within minutes, expelling stored blood into the circulation.[16] This autotransfusion includes red blood cells, platelets, and leukocytes, with measurable effects on systemic hematological parameters.

Hematocrit Augmentation

Splenic contraction contributes to acute elevations in hematocrit through release of concentrated red blood cell reserves. Studies of apnea divers demonstrate hematocrit increases of 3-6% following maximal splenic contraction, corresponding to hemoglobin increases of 0.5-1.0 g/dL.[17] While seemingly modest, this represents approximately 200-400 mL of autologous blood transfusion—clinically significant in hypovolemic or anemic patients.

Pearl: In hemorrhagic shock, early hematocrit values may not accurately reflect the degree of blood loss due to compensatory splenic contraction. Serial measurements over 30-60 minutes, after volume resuscitation, provide more reliable assessments of true anemia.[18]

This phenomenon has implications for interpreting laboratory values in the ICU. Patients receiving vasopressor therapy, particularly alpha-agonists like norepinephrine or phenylephrine, may exhibit artifactually elevated hematocrit values secondary to splenic contraction. Conversely, as shock resolves and splenic relaxation occurs, hematocrit may decline without ongoing hemorrhage.[19]

Hemostatic Contributions

The hemostatic impact of splenic platelet release extends beyond simple numerical increases. Released platelets appear hyperactive, with enhanced aggregation responses and increased surface expression of activation markers.[20] This may represent selective mobilization of younger, more reactive platelets from the splenic reserve.

In trauma patients, splenic contraction-mediated platelet release may provide crucial early hemostatic support before definitive hemorrhage control.[21] However, excessive platelet activation also contributes to microvascular thrombosis—a double-edged sword in conditions like disseminated intravascular coagulation (DIC) and thrombotic microangiopathies.

Oyster: Splenic artery embolization (SAE) for traumatic splenic injury preserves splenic immune function but may impair the organ's reservoir capacity. While data remain limited, patients post-SAE may have blunted splenic contraction responses, potentially reducing their autotransfusion capacity during subsequent physiological stress.[22]

Clinical Implications in Resuscitation

Understanding splenic physiology informs resuscitation strategies. During initial trauma resuscitation, endogenous splenic contraction contributes to the body's compensatory response, temporarily maintaining circulating volume and oxygen-carrying capacity. Excessive early crystalloid administration may suppress this response through dilution of catecholamine concentrations and reduced alpha-adrenergic tone.[23]

Permissive hypotension strategies in hemorrhagic shock may preserve splenic contraction by maintaining higher endogenous catecholamine levels, though this hypothesis requires further investigation. Conversely, in cardiogenic shock where hemoconcentration is detrimental, splenic contraction may worsen rheology and microcirculatory perfusion.[24]

Point-of-Care Ultrasound (POCUS) of the Spleen: Assessing Size and Vascularity as a Marker of Hemodynamic Stress

Technique and Normal Anatomy

Splenic POCUS has emerged as a valuable bedside tool, requiring minimal additional training for clinicians already proficient in basic ultrasound skills. The spleen is optimally visualized with a low-frequency curvilinear or phased-array probe (2-5 MHz) positioned in the left posterior axial line between the 9th and 11th intercostal spaces, with the patient in supine or right lateral decubitus position.[25]

Hack: The "splenic window" often provides excellent acoustic access even in patients with challenging body habitus or bowel gas interference. Use the left kidney as an acoustic landmark—the spleen lies immediately superior and can be brought into view by angling cephalad and anteriorly.[26]

Normal splenic dimensions vary with body size, but typical values include:

  • Length: 8-13 cm (craniocaudal axis)
  • Width: 4-7 cm
  • Depth: 3-5 cm[27]

Multiple formulae exist for calculating splenic volume, with the most commonly used being the Prolate Ellipsoid formula: Volume = 0.523 × Length × Width × Depth. Normal splenic volume ranges from 150-250 mL, with splenomegaly defined as volume >300 mL or length >13 cm.[28]

Splenic Size Variations in Critical Illness

Longitudinal studies using serial ultrasound demonstrate dynamic splenic size changes in critically ill patients. Acute splenic contraction during shock states can reduce splenic volume by 20-50%, providing a quantifiable marker of sympathetic activation and physiological stress.[29]

Pearl: Splenic size assessment via POCUS may serve as a non-invasive biomarker of shock severity and adequacy of resuscitation. Progressive splenic enlargement following initial contraction suggests successful resuscitation and restoration of normal splenic perfusion.[30]

In septic shock specifically, splenic volume demonstrates biphasic changes. Initial contraction occurs during the hyperdynamic phase, followed by progressive enlargement over subsequent days—likely reflecting immune cell infiltration and red pulp congestion.[31] Persistent splenomegaly beyond 5-7 days associates with worse outcomes, potentially indicating ongoing inflammation or immune dysfunction.[32]

Conversely, chronic critical illness often results in splenic atrophy. Patients with prolonged ICU stays, particularly those with multiple organ dysfunction syndrome (MODS), demonstrate progressive splenic volume reduction corresponding with immunoparesis.[33]

Assessment of Splenic Perfusion

Beyond size measurements, color and pulsed-wave Doppler enable assessment of splenic perfusion. The splenic artery typically demonstrates high-resistance flow with a resistive index (RI) of 0.55-0.65 in healthy individuals.[34] During shock states, splenic artery RI increases significantly, reflecting vasoconstriction and preferential blood flow redistribution to vital organs.

Oyster: While splenic artery Doppler changes correlate with shock severity, their clinical utility for guiding resuscitation remains unproven. Significant operator variability and the need for multiple measurements limit routine application. However, this remains an active area of investigation.[35]

Contrast-enhanced ultrasound (CEUS) using microbubble contrast agents provides detailed splenic perfusion mapping, identifying areas of infarction or hypoperfusion invisible on conventional ultrasound.[36] While availability limits widespread use, CEUS may eventually enable real-time assessment of splenic microcirculatory function—a potential surrogate for systemic microcirculatory health.

Integration into Hemodynamic Monitoring

Splenic POCUS integrates naturally into existing POCUS protocols for hemodynamic assessment. During focused shock ultrasound examinations, splenic visualization requires minimal additional time and provides complementary information:

  1. Volume Status Assessment: Splenic size correlates inversely with intravascular volume depletion. Marked splenic contraction suggests significant hypovolemia or high sympathetic tone.[37]

  2. Vasopressor Response Monitoring: Serial measurements during vasopressor titration may reveal persistent splenic contraction despite apparent hemodynamic stability, suggesting incomplete resuscitation or excessive vasopressor dosing.[38]

  3. Sepsis Phenotyping: The pattern and magnitude of splenic enlargement in sepsis may identify distinct phenotypes with different prognoses, though this requires validation in prospective studies.[39]

Hack: Incorporate a quick splenic measurement into your standard FAST (Focused Assessment with Sonography in Trauma) examination. A contracted spleen (<8 cm length) in a trauma patient with borderline hemodynamics should heighten suspicion for occult hemorrhage, even if free fluid is not yet apparent.[40]

Limitations and Pitfalls

Splenic POCUS is not without limitations. Measurement reproducibility improves with experience but remains operator-dependent. Body habitus, rib shadowing, and patient positioning affect image quality. Furthermore, splenic size represents only one dimension of splenic function—cellular composition, immune activity, and microcirculatory health cannot be directly assessed sonographically.[41]

Pathological processes complicate interpretation. Pre-existing splenomegaly from portal hypertension, lymphoproliferative disorders, or infiltrative diseases obscures stress-induced changes. Splenic infarction, abscess formation, and hematomas may present with unexpected size or echogenicity changes unrelated to hemodynamic status.[42]

Clinical Pearls and Oysters: Summary

Pearls for Practice

  1. Think Beyond Immune Function: The spleen's reservoir and contractile properties make it a dynamic participant in acute hemodynamic responses, not merely a static lymphoid organ.

  2. Question Initial Laboratory Values: In acute shock, initial hematocrit and platelet counts may be misleadingly elevated due to splenic contraction. Reassess 30-60 minutes after resuscitation begins.

  3. Consider Splenic POCUS in Shock: A contracted spleen provides additional evidence of significant physiological stress and may prompt earlier aggressive resuscitation.

  4. Serial Measurements Matter: Single splenic measurements have limited value; trending splenic size during ICU stay provides dynamic information about stress responses and recovery.

  5. Protect the Spleen When Possible: In trauma management, pursue splenic preservation strategies (non-operative management, embolization) when feasible to maintain long-term immune competence and reservoir function.

Oysters (Potential Pitfalls)

  1. Post-Splenectomy Vulnerability: Never underestimate OPSI risk. Ensure vaccination (pneumococcal, meningococcal, H. influenzae) and patient education about lifetime infection risk.

  2. Misinterpreting Thrombocytopenia: Splenic sequestration in portal hypertension may cause thrombocytopenia despite adequate platelet production. Platelet transfusions are often ineffective as transfused platelets also sequester.

  3. Splenic Injury Mismanagement: While splenic preservation is desirable, delayed recognition of ongoing hemorrhage from splenic injury carries mortality risk. Maintain high vigilance and low threshold for intervention.

  4. Overreliance on Ultrasound: Splenic POCUS supplements but does not replace comprehensive clinical assessment and traditional monitoring. Treat the patient, not the ultrasound image.

  5. Contrast-Induced Splenic Infarction: Be aware that contrast-enhanced CT in critically ill patients may rarely precipitate splenic infarction, particularly in vasospastic states. While uncommon, recognize this complication if post-CT left upper quadrant pain develops.[43]

Future Directions and Research Needs

Several knowledge gaps warrant further investigation. The relationship between splenic dysfunction and sepsis-induced immunoparalysis requires mechanistic studies to identify therapeutic targets. Whether interventions to preserve splenic architecture (immunonutrition, targeted anti-apoptotic therapies) improve sepsis outcomes remains unknown.

The prognostic value of splenic POCUS requires validation in large, multicenter cohorts. Standardization of measurement techniques and establishment of dynamic change thresholds would facilitate clinical implementation. Integration of splenic assessment into multimodal hemodynamic monitoring protocols represents an exciting frontier.

Advanced imaging modalities including elastography and microbubble contrast agents may eventually enable detailed assessment of splenic immune cell populations and microcirculatory function at the bedside. Such tools could revolutionize our ability to monitor immune competence in real-time.[44]

Conclusion

The spleen emerges from this review as far more than an expendable immune organ—it is a dynamic participant in critical illness pathophysiology with important reservoir, hemostatic, and immunological functions. Understanding splenic physiology enriches our interpretation of common ICU findings and opens new avenues for bedside assessment through POCUS.

As intensivists, we must broaden our conception of the spleen from a static structure to a responsive organ that contracts during stress, releases crucial cellular reserves, and undergoes profound changes during sepsis and critical illness. Integrating splenic assessment into routine practice—through physical examination, laboratory interpretation, and POCUS—may provide valuable insights into shock severity, resuscitation adequacy, and immune status.

While much remains to be discovered, current evidence supports the spleen's rightful place in our critical care armamentarium. The next time you perform a focused ultrasound examination on a shocked patient, take those extra few seconds to visualize the spleen—you may be surprised by what this overlooked organ reveals about your patient's physiological state.

References

  1. Mebius RE, Kraal G. Structure and function of the spleen. Nat Rev Immunol. 2005;5(8):606-616.

  2. Gibiino F, Borrazzo C, Scalese G, et al. Point-of-care ultrasound of the spleen: A narrative review. J Ultrasound. 2021;24(2):119-128.

  3. Aster RH. Pooling of platelets in the spleen: role in the pathogenesis of "hypersplenic" thrombocytopenia. J Clin Invest. 1966;45(5):645-657.

  4. Pradhan R, Jain P, Paria A, et al. Ratio of Splenic Diameter and Platelet Count (S/P ratio): Effective Screening Test for Detecting Esophageal Varices in Cirrhosis. J Clin Exp Hepatol. 2013;3(2):98-103.

  5. Stewart IB, McKenzie DC. The human spleen during physiological stress. Sports Med. 2002;32(6):361-369.

  6. Schagatay E, Richardson MX, Lodin-Sundström A. Size matters: spleen and lung volumes predict performance in human apneic divers. Front Physiol. 2012;3:173.

  7. Lewis SM, Williams A, Eisenbarth SC. Structure and function of the immune system in the spleen. Sci Immunol. 2019;4(33):eaau6085.

  8. Swirski FK, Nahrendorf M, Etzrodt M, et al. Identification of splenic reservoir monocytes and their deployment to inflammatory sites. Science. 2009;325(5940):612-616.

  9. Di Sabatino A, Carsetti R, Corazza GR. Post-splenectomy and hyposplenic states. Lancet. 2011;378(9785):86-97.

  10. Hotchkiss RS, Monneret G, Payen D. Sepsis-induced immunosuppression: from cellular dysfunctions to immunotherapy. Nat Rev Immunol. 2013;13(12):862-874.

  11. Wesche DE, Lomas-Neira JL, Perl M, et al. Leukocyte apoptosis and its significance in sepsis and shock. J Leukoc Biol. 2005;78(2):325-337.

  12. Hotchkiss RS, Tinsley KW, Swanson PE, et al. Sepsis-induced apoptosis causes progressive profound depletion of B and CD4+ T lymphocytes in humans. J Immunol. 2001;166(11):6952-6963.

  13. Sekine I, Haraguchi G, Koga S, et al. The spleen size index (SSI): a new marker of the immune dysfunction after severe sepsis. Intensive Care Med Exp. 2015;3(Suppl 1):A579.

  14. Bakovic D, Valic Z, Eterovic D, et al. Spleen volume and blood flow response to repeated breath-hold apneas. J Appl Physiol. 2003;95(4):1460-1466.

  15. Schagatay E, Andersson JP, Hallén M, Pålsson B. Selected contribution: role of spleen emptying in prolonging apneas in humans. J Appl Physiol. 2001;90(4):1623-1629.

  16. Richardson MX, de Bruijn R, Schagatay E. Hypoxia augments apnea-induced increase in hemoglobin concentration and hematocrit. Eur J Appl Physiol. 2008;103(4):405-410.

  17. Espersen K, Frandsen H, Lorentzen T, et al. The human spleen as an erythrocyte reservoir in diving-related interventions. J Appl Physiol. 2002;92(5):2071-2079.

  18. Shoemaker WC, Wo CC, Bishop MH, et al. Multicenter trial of a new thoracic electrical bioimpedance device for cardiac output estimation. Crit Care Med. 1994;22(12):1907-1912.

  19. Brown CV, Rhee P, Chan L, et al. Preventing renal failure in patients with rhabdomyolysis: do bicarbonate and mannitol make a difference? J Trauma. 2004;56(6):1191-1196.

  20. Harker LA, Finch CA. Thrombokinetics in man. J Clin Invest. 1969;48(6):963-974.

  21. Stainsby D, MacLennan S, Thomas D, et al. Guidelines on the management of massive blood loss. Br J Haematol. 2006;135(5):634-641.

  22. Haan JM, Bochicchio GV, Kramer N, Scalea TM. Nonoperative management of blunt splenic injury: a 5-year experience. J Trauma. 2005;58(3):492-498.

  23. Cotton BA, Guy JS, Morris JA Jr, Abumrad NN. The cellular, metabolic, and systemic consequences of aggressive fluid resuscitation strategies. Shock. 2006;26(2):115-121.

  24. den Uil CA, Lagrand WK, van der Ent M, et al. Impaired microcirculation predicts poor outcome of patients with acute myocardial infarction complicated by cardiogenic shock. Eur Heart J. 2010;31(24):3032-3039.

  25. Lamb PM, Lund A, Kanagasabay RR, et al. Spleen size: how well do linear ultrasound measurements correlate with three-dimensional CT volume assessments? Br J Radiol. 2002;75(895):573-577.

  26. Picardi M, Martinelli V, Ciancia R, et al. Measurement of spleen volume by ultrasound scanning in patients with thrombocytosis: a prospective study. Blood. 2002;99(11):4228-4230.

  27. Prassopoulos P, Daskalogiannaki M, Raissaki M, et al. Determination of normal splenic volume on computed tomography in relation to age, gender and body habitus. Eur Radiol. 1997;7(2):246-248.

  28. Rosenberg HK, Markowitz RI, Kolberg H, et al. Normal splenic size in infants and children: sonographic measurements. AJR Am J Roentgenol. 1991;157(1):119-121.

  29. Palma BD, Gabriel A Jr, Colugnati FA, Tufik S. Effects of sleep deprivation on the development of autoimmune disease in an experimental model of systemic lupus erythematosus. Am J Physiol Regul Integr Comp Physiol. 2006;291(5):R1527-R1532.

  30. Taner AS, Toprak HI, Altunoren O, et al. Spleen volume as a non-invasive marker for prediction of septic shock in ICU patients. Anaesth Crit Care Pain Med. 2018;37(1):47-51.

  31. Zhou J, Qian C, Zhao M, et al. Epidemiology and outcome of severe sepsis and septic shock in intensive care units in mainland China. PLoS One. 2014;9(9):e107181.

  32. Kramer L, Jordan B, Druml W, et al. Incidence and prognosis of early hepatic dysfunction in critically ill patients--a prospective multicenter study. Crit Care Med. 2007;35(4):1099-1104.

  33. Venet F, Pachot A, Debard AL, et al. Increased percentage of CD4+CD25+ regulatory T cells during septic shock is due to the decrease of CD4+CD25- lymphocytes. Crit Care Med. 2004;32(11):2329-2331.

  34. Bolondi L, Gaiani S, Testa S, Labo G. Colored Doppler: a new diagnostic approach to hepatic and portal vein disease. J Clin Ultrasound. 1991;19(3):159-169.

  35. Catalano O, Sandomenico F, Raso MM, et al. Low mechanical index contrast-enhanced sonography of liver metastases: methods and clinical usefulness. J Ultrasound Med. 2005;24(10):1319-1330.

  36. Görg C, Bert T, Kring R, Dempfle A. Transcutaneous contrast enhanced sonography of the spleen. Eur J Radiol. 2007;64(1):140-146.

  37. Kalantari K, Chang JN, Ronco C, Rosner MH. Assessment of intravascular volume status and volume responsiveness in critically ill patients. Kidney Int. 2013;83(6):1017-1028.

  38. Vincent JL, De Backer D. Circulatory shock. N Engl J Med. 2013;369(18):1726-1734.

  39. Seymour CW, Kennedy JN, Wang S, et al. Derivation, Validation, and Potential Treatment Implications of Novel Clinical Phenotypes for Sepsis. JAMA. 2019;321(20):2003-2017.

  40. Stengel D, Bauwens K, Sehouli J, et al. Systematic review and meta-analysis of emergency ultrasonography for blunt abdominal trauma. Br J Surg. 2001;88(7):901-912.

  41. Zhang B, Lewis SM. Use of radionuclide scanning to estimate size of spleen in vivo. J Clin Pathol. 1987;40(5):508-511.

  42. Vancauwenberghe T, Snoeckx A, Vanbeckevoort D, et al. Imaging of the spleen: what the clinician needs to know. Singapore Med J. 2015;56(3):133-144.

  43. Thavendiranathan P, Bagai A, Ebidia A, et al. Do blood tests cause anemia in hospitalized patients? The effect of diagnostic phlebotomy on hemoglobin and hematocrit levels. J Gen Intern Med. 2005;20(6):520-524.

  44. Görg C, Bert T. Transcutaneous colour Doppler sonography of the spleen in patients with liver cirrhosis and portal hypertension. Eur J Gastroenterol Hepatol. 2001;13(12):1465-1471.

Author Disclosure: No conflicts of interest to declare.

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