Therapeutic apheresis is a treatment modality that processes whole blood through medical technologies for the purpose of separating it into components and removing identified pathological cellular or plasma components.[1][2][3] Pediatric therapeutic apheresis treatments includes plasma exchange, red cell exchange/depletion, stem cell collections, leukodepletion and plasma exchange with secondary plasma device.[2][3][4]

There are considerations to be made when performing apheresis in pediatric patients, with the understanding that the apheresis technology and equipment used to perform adult apheresis are also used for pediatric apheresis.[1][2][3][4] Additionally, pediatric patients require advance monitoring and clinical accommodations, due to their smaller body mass and immature body system functions, to safely perform treatments.[1][3][5]

This article addresses common considerations of apheresis when performed in the pediatric population: Central venous access, extracorporeal volume, electrolyte imbalances, monitoring of pediatric patient during treatments, as well as, adverse events and psychosocial considerations.[1]

Pediatric Consideration in Apheresis

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Central venous access used for apheresis.

Central venous catheter access: Venous access is required to perform apheresis treatments, commonly used access are central venous catheter devices.[6] The flow through a central venous catheter accommodates high blood flows[2][6] (mls/min) to achieve blood separation and remove the appropriate isolated blood component.[1][2] Pediatric considerations for central access include (but not limited to) size of veins, size of catheter for insertion, maturity of pediatric patient and the duration of treatment chronic (> 1 year) or acute (1–10 days).[2][6]

Extracorporeal volume: Apheresis equipment and tubing set used for pediatrics apheresis, exceeds a safe volume of extracorporeal blood outside of the body at any given time, especially for low weight children.[2][3] Priming the circuit prior to treatments reduces the adverse effects associated with hypovolemia, due to large volumes of blood that is extracorporeal.[2][3] Blood products used to minimize this adverse effect are: Red cells, Reconstituted blood and 5% Albumin.[3][7][8] The use of each blood product is dependent on the clinical considerations for the pediatric patient, in all cases the prime serves to reduce the hypovolemic effects a large extra-corporeal volume of the apheresis circuit places on small low weight children.[2][3][7] Listed below are blood products used to prime the circuit for pediatric apheresis:

  • Red cells: Concentrated red cells
    • Replaces the prime volume in the apheresis circuit with red cells.[3][7]
    • Reduces risk for anemia (see adverse events)
  • Reconstituted whole blood: Diluted whole blood with either saline or plasma to a hematocrit equal to patients own hematocrit.[7]
    • Replaces the prime volume in the apheresis circuit with reconstituted whole blood.[7]
    • Reduces risk for anemia (see adverse events)
  • 5% Albumin: Isotonic solutions
    • Replaces the prime volume in the circuit with 5% albumin.[3][7]
    • Reduces risk of hypotension related to hypovolemia.[7]
 
Clotting cascade. Ionized calciums role in clotting.

Electrolyte imbalances: There are large volumes of separated blood components being exchanged during an apheresis treatments, this can create electrolyte imbalances when combined with citrate as the circuit anticoagulant.[3][4][5][7][8] Electrolyte imbalances can include (but not limited to) Hypokalemia, hypocalcemia hypomagnesemia and elevated total carbon dioxide.[2][5][8] When citrate is used as regional anticoagulant in pediatric apheresis treatments, it binds to free floating calcium (ionized) to disrupt the clotting cascade (see image) leading to hypocalcemia.[2][8] In the same process it chelates magnesium and can cause hypomagnesemia.[2] The by-product of metabolizing citrate elevates carbon dioxide levels in the blood that can lead to metabolic acidosis.[5] Potassium is a plasma-bound electrolyte, and in large volumes of plasma exchange and replacement of a isotonic solution (5% albumin) can induce hypokalemia.[3] Reducing the effects these electrolyte imbalances can have on a pediatric patient receiving apheresis treatments can include: establishing acceptable blood levels prior to the start of treatment (which can vary across institutions),[7] pre blood electrolyte levels outside of this established parameter are corrected to within normal limits before treatment is initiated.[7][9] If the child is symptomatic then electrolyte management and replacement is required according to institution policy.[1][2][7][8]

Monitoring patients: Pediatric patients undergoing apheresis treatments require ongoing monitoring in relation to the electrolyte imbalances noted, and the risk of hypotension related to the large extra-corporeal volume.[2][5] This includes cardiac monitoring and close clinical observation for signs and symptoms related to adverse events (see below) by the bedside nurse, caregiver and healthcare team.[7] Close monitoring of the patient subverts the escalation of symptoms, especially for young non-verbal children.[2][7][9]

Psychosocial considerations: Children and infants can become anxious prior to and during treatments. Reducing their fears through therapeutic play, to explain the procedure and process, can alleviate some of that anxiety.[9] The cognitive development of the child is considered when implementing measures to reduce anxiety and to ensure that they are also age appropriate.[9]

Adverse Events in Pediatric Apheresis

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During apheresis treatments adverse events such as anemia, citrate toxicity, central venous catheter safety and infections are notable.[2][3][8]

Anemia: Anemia is related to numerous and/or consecutive treatments and/or large extracorporeal circuits that reduces the hemoglobin levels in pediatric patients.[2][3] Hemoglobin is responsible for oxygen transport in the blood.[2]

Pediatric considerations to reduce incidence of anemia:

  • Close monitoring of hemoglobin levels.[3]
  • Circuit primed with red cells or reconstituted whole blood.[3][7]

Citrate Toxicity: Experienced when ionized calcium levels are low due to citrate anticoagulation which binds to free calcium in the blood resulting in hypocalcemia.[1][2][5][8][9]

Pediatric considerations to reduce incidences[spelling?] of citrate toxicity:

  • Infusion of intravenous calcium during treatment.[2][7][8]
  • Adequate blood ionized calcium levels prior to treatment.[8]

Central venous catheter infections and safety: Central venous access used for treatments are at risk for central venous catheter acquired bloodstream infections.[1][10] Additionally, children are at a higher risk of dislodging indwelling central venous catheters.[6]

Pediatric consideration to reduce incidence of central line infection and dislodgement:

  • Appropriate size and type of catheter for treatment based on child's size of veins, size of catheter for insertion, maturity of pediatric patient and the duration of treatment chronic (> 1 year) or acute (1–10 days).[2][3][6]
  • Surveillance of the central venous catheter access and insertion site to note early on signs of infection or dislodgement.[10]
  • Regular central venous catheter care including: dressing changes, placing of a securement device/dressing to prevent line pulling, and central line cap changes (if used) to prevent accumulation of fluids at the entry point of the central venous catheter.[10]

See also

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References

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  1. ^ a b c d e f g h Meyer, Erin K.; Wong, Edward C.C. (2016). "Pediatric Therapeutic Apheresis: A Critical Appraisal of Evidence". Transfusion Medicine Reviews. 30 (4): 217–222. doi:10.1016/j.tmrv.2016.08.002. PMID 27555064.
  2. ^ a b c d e f g h i j k l m n o p q r s t u Kim, Yeowon A.; Sloan, Steven R. (2013). "Pediatric Therapeutic Apheresis". Pediatric Clinics of North America. 60 (6): 1569–1580. doi:10.1016/j.pcl.2013.08.006. PMID 24237988.
  3. ^ a b c d e f g h i j k l m n o p q Hans, Rekha; Prakash, Satya; Sharma, Ratti Ram; Marwaha, Neelam (2016). "Role of therapeutic apheresis in pediatric disorders". Pediatric Hematology Oncology Journal. 1 (3): 63–68. doi:10.1016/j.phoj.2016.11.002.
  4. ^ a b c Kasprisin, Duke O. (2019-08-14), "Therapeutic Apheresis in Children", Therapeutic Hemapheresis, CRC Press, pp. 73–89, doi:10.1201/9780429281099-7, ISBN 9780429281099, S2CID 204065837, retrieved 2021-11-03
  5. ^ a b c d e f Perotti, Cesare; Seghatchian, Jerard; Fante, Claudia Del (2018-06-01). "Pediatric apheresis emergencies and urgencies: An update". Transfusion and Apheresis Science. 57 (3): 339–341. doi:10.1016/j.transci.2018.05.016. ISSN 1473-0502. PMID 29784538. S2CID 29166691.
  6. ^ a b c d e Johansen, Mathias; Classen, Volker; Muchantef, Karl (2021). "Long-term IV access in paediatrics - why, what, where, who and how". Acta Anaesthesiologica Scandinavica. 65 (3): 282–291. doi:10.1111/aas.13729. ISSN 1399-6576. PMID 33147351. S2CID 226259970.
  7. ^ a b c d e f g h i j k l m n o Delaney, Meghan; Capocelli, Kelley E.; Eder, Anne F.; Schneiderman, Jennifer; Schwartz, Joseph; Sloan, Steven R.; Wong, Edward C. C.; Kim, Haewon C. (2014). "An international survey of pediatric apheresis practice". Journal of Clinical Apheresis. 29 (2): 120–126. doi:10.1002/jca.21301. ISSN 1098-1101. PMID 24105856. S2CID 43264963.
  8. ^ a b c d e f g h i Sigler, Katie; Lee, Ji; Srivaths, Poyyapakkam (2018). "Regional citrate anticoagulation with calcium replacement in pediatric apheresis". Journal of Clinical Apheresis. 33 (3): 274–277. doi:10.1002/jca.21594. PMID 29027706. S2CID 380450.
  9. ^ a b c d e MacPherson, James L.; Kasprisin, Duke O., eds. (2019-08-22). Therapeutic Hemapheresis. Boca Raton: CRC Press. doi:10.1201/9780429281099. ISBN 978-0-429-28109-9.
  10. ^ a b c Rinke, Michael L.; Heo, Moonseong; Saiman, Lisa; Bundy, David G.; Rosenberg, Rebecca E.; DeLaMora, Patricia; Rabin, Barbara; Zachariah, Philip; Mirhaji, Parsa; Ford, William J. H.; Obaro-Best, Oghale (2021). "Pediatric Ambulatory Central Line–Associated Bloodstream Infections". Pediatrics. 147 (1): e20200524. doi:10.1542/peds.2020-0524. ISSN 0031-4005. PMID 33386333. S2CID 229935127.