Tag: resuscitation

Intraosseous (IO) Lines/Access (2024)

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by Yousif Al-Khafaji & Mustak Dukandar

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Introduction

Obtaining intravascular access in the emergency department is one of the most essential steps in managing critically ill patients. While it is a simple step for most patients, it can be the most challenging procedure during resuscitation. The pediatric population has more body fat, making it difficult to localize their veins. In addition, they have tiny peripheral veins that easily collapse in states of shock. On the other hand, in adults, patients who are obese, those who suffer from extensive burns, or are in shock challenge the clinician in obtaining vascular access [1].

Intraosseous (IO) access involves inserting a hollow needle through the cortex of the bone and into the medullary space. This allows clinicians to infuse fluids, medication, or almost anything that can be administered through the intravenous (IV) route and achieve the same desired effect as the IV route. The IO line is merely a bridging tool to buy the clinician time to obtain IV access. In most cases, IO access is a simple procedure, and clinicians should not hesitate to insert an IO line if peripheral IV access attempts fail.

IO lines can safely remain in place for up to 24 hours and are often a bridge to either IV or Central Venous line placement.

Indications

There are clear indications for IO access. Each of these indications highlights the critical role of IO lines in emergency medicine, providing a swift and effective solution for vascular access in life-threatening situations [3]. When IV access cannot be achieved, IO access is safe, reliable, and quick. It can be accomplished in 30 to 60 seconds and even faster with an IO gun. This is especially helpful in pediatric emergencies when time is critical. 

Emergency intravascular access when other methods have failed
IO access is indicated when IV access is not achievable in critical situations, such as trauma, shock, or severe dehydration. In critically ill patients, a maximum of two failed attempts is generally considered sufficient to shift to IO access. The IO line provides a rapid and reliable alternative to IV lines for administering fluids, medications, or blood products directly into the vascular system via the bone marrow [4]. 

Cardiac arrest
During cardiac arrest, time is critical, and establishing vascular access can be challenging. IO access is often used to administer life-saving medications like epinephrine when IV access cannot be obtained quickly. It ensures the rapid delivery of drugs into circulation during resuscitation [5].

Obtaining blood for laboratory evaluation
IO access allows for the collection of blood samples for laboratory testing, including complete blood count, electrolytes, and blood gas analysis [6]. This is especially useful in emergency situations where traditional venipuncture is impractical or impossible.

Contraindications

Physicians should be aware of a couple of important complications. These contraindications emphasize the importance of careful site selection and patient evaluation before performing IO access to minimize complications and maximize the effectiveness of the procedure [1].

Fractured bone
A fracture at the intended site of IO access is an absolute contraindication. Using a fractured bone for IO infusion can result in extravasation of fluids and medications, potentially worsening the injury and causing further complications.

Infection or burn overlaying insertion site
Localized infection or burns at the insertion site pose a significant risk of introducing pathogens into the bone marrow, leading to osteomyelitis or systemic infection. These conditions are absolute contraindications for IO placement.

Prior use of the same bone for IO infusion
Repeated use of the same bone for IO access can damage the bone marrow and structure, increasing the risk of complications such as extravasation or impaired drug delivery. A different site should be chosen for subsequent IO insertions.

Osteoporosis and osteogenesis imperfecta
These conditions result in fragile bones, increasing the likelihood of fractures or other complications during needle insertion. Alternative access methods should be considered for patients with these conditions.

Administration of ultra-short-acting medications like adenosine (relative contraindication)
Medications like adenosine, which rely on rapid systemic distribution, may not be as effective when administered via IO access due to potential delayed uptake into circulation. This is a relative contraindication, depending on the clinical scenario.

Equipment and Patient Preparation

Equipment

IO Needle

  • Ranges from 15-18 gauge needles
  • Color coding is common:
    • Pink (15 mm): For patients weighing 3–39 kg
    • Blue (25 mm): For patients ≥3 kg and above
    • Yellow (45 mm): For patients ≥40 kg, excessive tissue, or dense bone sites (e.g., proximal humerus or anterior superior iliac spine)

IO Devices (to facilitate insertion)

  • Powered IO Drills (e.g., EZ-IO)
  • Manual IO Drills (e.g., Cook IO Needle or Jamshidi-type needle)

Skin Disinfectants

  • Chloraprep
  • Alcohol swabs
  • Optional: Povidine or Chlorhexidine

Syringe and Flush Materials

  • Saline flush (crystalloid solution, e.g., normal saline or lactated Ringer’s)
  • Intravenous tubing

Lidocaine 2% (without epinephrine)

  • For topical and subcutaneous infiltration in awake patients, as they may experience pain during fluid infusion rather than needle insertion.

Additional Equipment

  • Infusion pump (to regulate fluid delivery)
  • Tape (for securing the IO line)
Arrow® EZ-IO® Intraosseous Vascular Access System - adopted from https://www.teleflex.com/usa/en/product-areas/emergency-medicine/intraosseous-access/arrow-ez-io-system/use-and-application/Arrow_EZ-IO_Landmarking_Poster.pdf

Patient Preparation

  1. Informed Consent
    • Obtain informed consent by explaining the procedure, its benefits, and associated risks to the patient or their guardians. In emergency situations where consent cannot be obtained, implied consent applies.
  2. Site Selection
    • Choose the most appropriate insertion site based on the clinical scenario. Common sites include:
      • Humeral Head
      • Proximal Tibia
      • Medial Malleolus
      • Sternum
      • Distal Radius
      • Distal Femur
      • Anterior Superior Iliac Spine
    • Note: The proximal tibia and humeral head are most commonly used during cardiac arrest as these locations do not interfere with other life-saving procedures like intubation [7].
  3. Contraindication Assessment
    • Ensure there are no contraindications (e.g., fractures, infections, burns, prior IO use at the same site, or certain bone conditions) at the intended site of insertion.
  4. Site Exposure
    • Properly expose the selected insertion site to facilitate accurate placement and reduce the risk of contamination.
  5. Universal Precautions
    • Apply universal precautions, such as wearing gloves at a minimum, to maintain aseptic conditions during the procedure.
  •  
IO placement locations. IO size (color) is subject to the patients body weight.

Sites of IO insertion and some hints [8]

  1. Proximal Tibia
    • 2 finger breadths below the tibial tuberosity (1-3 cm) on the medial, flat aspect of the tibia.
    • Commonly used for ease of access, especially in emergencies.
  2. Distal Tibia
    • Medial surface at the junction of the medial malleolus and the shaft of the tibia, posterior to the greater saphenous vein.
  3. Proximal Humerus (Adults only; use the yellow needle)
    •  Preparation:
      • Keep the arm adducted and internally rotated (rest the patient’s hand on their bellybutton).
      • Slide fingers up the humerus until you feel the notch (surgical neck).
    •  Insertion:
      • Insert the IO needle 1 cm above the surgical neck into the greater tubercle.
      • Immobilize the arm to prevent displacement of the IO line (avoid shoulder abduction).
  4. Distal Femur
    • Primarily used in infants and children due to easier bone access and growth plate considerations.
  5. Pelvic Anterior Superior Iliac Spine (ASIS)
    • An alternative site, especially when lower extremity or upper extremity sites are unavailable.
  6. Sternum
    • Provides the highest flow rate of any location, making it suitable for rapid infusions during critical situations.

Procedure Steps

  1. Preparation
    • Identify the designated site using a sterile gloved finger.
    • Disinfect the overlying skin using appropriate antiseptic (e.g., chlorhexidine).
    • Administer local anesthetic if the patient is awake.
    • Ensure the stylet is properly positioned on the needle prior to insertion.
    • Prepare necessary equipment, including a 20 ml saline syringe, IV tubing, tape, medications, fluids, and infusion pump.
  2. Needle Insertion
    • Insert the needle perpendicularly through the skin down to the bone.
    • Use an IO drill or manually twist the needle clockwise with firm, gentle pressure until a “give” is felt (loss of resistance), indicating entry into the marrow.
    • Ensure the needle locks into place.
  3. Confirmation of Placement
    • The needle should stand upright without additional support if properly positioned.
    • Remove the stylet and attach a syringe.
    • Aspirate to confirm the presence of marrow or blood (not always visible).
    • Gently flush the line with saline while observing for swelling at or around the insertion site.
  4. Troubleshooting
    • If swelling occurs or the test injection fails, remove the IO needle and repeat the procedure on a different site.
  5. Securing and Using the IO Line
    • If Io works properly, stabilize the needle using tape or gauze padding as necessary.
    • Attach IV tubing to the needle hub.
    • Begin infusion of fluids, blood products, or medications.
    • If the patient is awake and experiences pain during infusion, administer lidocaine through the IO line for analgesia [2].
  •  

Complications [9]

Extravasation of Fluid

Occurs when fluid or medication leaks into surrounding soft tissues instead of the bone marrow cavity. This can cause localized swelling, tissue damage, and discomfort. Proper placement and observation for swelling during infusion are essential to avoid this complication.

Compartment Syndrome

Results from increased pressure within a muscle compartment due to extravasation of fluid. It can compromise blood flow, leading to tissue ischemia and potential necrosis. Immediate recognition and corrective action are necessary to prevent long-term damage [10].

Bone Fracture

More common in patients with pre-existing bone disorders, such as osteoporosis or osteogenesis imperfecta. Improper needle insertion technique can increase the risk of fracturing the bone at the insertion site. Physicians should be careful when inserting IO lines in small children because too much pressure during drilling may cause fractures.

Osteomyelitis

A rare but serious complication involving infection of the bone and marrow. This risk increases if aseptic technique is not followed or if there is a pre-existing infection near the insertion site.

Preventative Measures:

  • Use strict aseptic technique to minimize infection risks.
  • Properly assess the patient’s bone health and contraindications before insertion.
  • Monitor the insertion site for early signs of complications, such as swelling or pain, during and after infusion

Hints and Pitfalls

Purpose and Time Limit

  • IO access is a bridging tool used to buy time for obtaining peripheral or central IV access.
  • IO needles should not remain in place for more than 24 hours, as the risk of complications increases significantly after that time frame.

Site and Device Selection

  • Always use an uninjured limb for IO placement; if no uninjured limb is available, the sternum is preferred.
  • An IO drill or gun is recommended over manual insertion for consistent and reliable placement.
  • Needle selection must be appropriate for the selected site and the marrow cavity to ensure proper access.

Needle Placement and Security

  • IO needle displacement can sometimes occur, especially in pediatric patients with soft bones; this can be mitigated by securing the needle to the skin properly.
  • The anterior superior iliac spine may be considered as an alternative site in cases of soft bone structures.

Medication and Dosage

  • Any medication that can be administered via IV access can also be given through IO access without dose adjustment, as the bioequivalence between IO and IV routes is similar. [11,12]

Laboratory Sampling

  • Lab tests with good correlation from IO samples include hemoglobin/hematocrit, chloride, glucose, urea, creatinine, and albumin.
  • Other lab values, such as WBC, platelets, serum CO2, sodium, potassium, and calcium, may not correlate well with venous samples. [13]
  •  

Special Patient Groups

Pediatrics

  • Challenges: In pediatric patients, the bones can sometimes be too soft, which increases the risk of needle displacement even when placed correctly.
  • Recommendation: To mitigate this risk, consider using the anterior superior iliac spine as an alternative site. This site may provide a more stable placement in cases where traditional sites like the tibia are less effective.

Geriatrics

  • Challenges: Older adults often have pre-existing bone disorders such as osteoporosis, which make their bones more fragile.
  • Risks: IO insertion in such patients can lead to fractures, especially if not performed with careful technique and appropriate needle selection.
  • Recommendation: Perform a thorough assessment of bone health and use alternative vascular access methods if significant bone fragility is present.

Pregnant Patients

  • Considerations: There are no contraindications for IO insertion in pregnant women. This makes IO access a viable option during emergencies where quick vascular access is necessary.
  • Precautions: Ensure that the chosen site does not interfere with obstetric care and consider patient positioning to maintain comfort and safety during the procedure.

Authors

Picture of Yousif Al-Khafaji

Yousif Al-Khafaji

Chief Emergency Medicine Resident - Tawam Hospital, Al Ain, UAE

Picture of Mustak Dukandar

Mustak Dukandar

Tawam Hospital Emergency Department

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References

  1. Roberts and Hedges’ Clinical Procedures in Emergency Medicine and Acute Car-Elsevier (2017), chapter 25
  2. ATLS Student course manual Tenth Edition (2018). Appendix G, 351
  3. Phillips L, Brown L, Campbell T, et al. Recommendations for the use of intraosseous vascular access for emergent and nonemergent situations in various healthcare settings: a consensus paper. J Emerg Nurs. 2010;36(6):551-556. doi:10.1016/j.jen.2010.09.001
  4. Oksan D, Ayfer K. Powered intraosseous device (EZ-IO) for critically ill patients. Indian Pediatr. 2013;50(7):689-691. doi:10.1007/s13312-013-0192-z
  5. Leidel BA, Kirchhoff C, Bogner V, et al. Is the intraosseous access route fast and efficacious compared to conventional central venous catheterization in adult patients under resuscitation in the emergency department? A prospective observational pilot study. Patient Saf Surg. 2009;3(1):24. Published 2009 Oct 8. doi:10.1186/1754-9493-3-24
  6. Tallman CI, Darracq M, Young M. Analysis of intraosseous blood samples using an EPOC point of care analyzer during resuscitation. Am J Emerg Med. 2017;35(3):499-501. doi:10.1016/j.ajem.2016.12.005
  7. Wampler D, Schwartz D, Shumaker J, Bolleter S, Beckett R, Manifold C. Paramedics successfully perform humeral EZ-IO intraosseous access in adult out-of-hospital cardiac arrest patients. Am J Emerg Med. 2012;30(7):1095-1099. doi:10.1016/j.ajem.2011.07.010
  8. Day MW. Intraosseous devices for intravascular access in adult trauma patients. Crit Care Nurse. 2011;31(2):76-90. doi:10.4037/ccn2011615
  9. ACLS provider Manual Supplementary Material (2016). Intraosseous Access, 57-61
  10. Vidal R, Kissoon N, Gayle M. Compartment syndrome following intraosseous infusion. Pediatrics. 1993;91(6):1201-1202.
  11. Faga, M., & Wolfe, B. (2016). Vascular access in hospitalized patients. Hospital Medicine Clinics, 5(1), 1-16.
  12. Von Hoff, D.D., Kuhn, J.G., Burris, H.A. 3rd, & Miller, L.J. (2008). Does intraosseous equal intravenous? A pharmacokinetic study. Am J Emerg Med, 26, 31-38
  13. Miller LJ, Philbeck TE, Montez D, Spadaccini CJ. A new study of intraosseous blood for laboratory analysis. Arch Pathol Lab Med. 2010;134(9):1253-1260.

FOAM and Further Reading

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Fundamentals of Pediatric Advanced Life Support (2024)

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by Burak Çakar & Ayça Koca

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Introduction

Pediatric cardiac arrest (CA) is a rare but critical event associated with high mortality and significant risk of severe sequelae [1,2]. Unlike in adults, respiratory causes are the primary contributors to CA in children. Hypoxia and bradycardia can lead to cardiopulmonary failure, which may ultimately progress to CA.

Common causes of pediatric CA include infections (e.g., pneumonia, sepsis), trauma, asphyxia, seizures, asthma, suffocation, and sudden infant death syndrome [2]. Clinical signs of cardiopulmonary arrest include respiratory arrest, absence of a palpable pulse, muscle flaccidity, unresponsiveness, cyanosis or other discoloration, and dilated pupils. Recognizing and promptly addressing these signs is crucial for improving outcomes.

Recognition of a Critically Ill Child

Early recognition of a critically ill child is essential to implementing timely interventions that may prevent progression to CA [3]. Abnormal vital signs, relative to age-specific norms, are often the most reliable indicators of impending arrest.

Pediatric Early Warning Scores (PEWS) are recommended as a systematic tool to identify children at risk of clinical deterioration [4]. PEWS evaluates three domains: behavior, cardiovascular function, and respiratory status [5]. It incorporates vital findings such as respiratory rate, heart rate, blood pressure, oxygen saturation, temperature, level of consciousness, and capillary refill time [6]. 

Monitoring Vital Signs in Children

It is essential to recognize abnormal vital signs for early recognition of pediatric deterioration.

Blood Pressure

Systolic Hypotension is defined as a systolic blood pressure below the 5th percentile for age. The threshold for concern is when the systolic blood pressure is <70 mmHg + (2x the child’s age in years).

Respiratory Rate

Tachypnea: A respiratory rate exceeding 60 breaths per minute indicates tachypnea.
Decreased Respiratory Rate: A reduction in respiratory rate in a previously tachypneic patient could signal either improvement or fatigue. Fatigue in this context could precede respiratory failure, particularly if it occurs in conjunction with other signs of decompensation.

Temperature

Fever significantly affects physiology. For every 1°C increase in body temperature:

  • The heart rate increases by approximately 10 beats per minute.
  • The respiratory rate increases by 2 to 5 breaths per minute.

End-Tidal Carbon Dioxide (EtCO2)

Changes in EtCO2 levels are critical indicators of respiratory status. A progressive increase or decrease in EtCO2 levels can signal impending desaturation and respiratory failure.

Assessment

Given the poor outcomes associated with pediatric CA, the emphasis must be on early recognition of pre-arrest states. Identifying signs of impending respiratory failure and shock, regardless of their underlying cause, should be a primary focus [4].

Findings Preceding Cardiopulmonary Arrest

Key findings preceding cardiopulmonary arrest are categorized as follows:

  1. Airway: Signs include stridor, drooling, and retractions, which indicate significant airway obstruction or distress.

  2. Breathing: Irregular respiration, bradypnea, gasping respirations, and cyanosis are warning signs of severe respiratory compromise.

  3. Circulation: Indicators such as a capillary refill time greater than 5 seconds, bradycardia, hypotension, cool extremities, weak central pulses, and the absence of peripheral pulses suggest circulatory failure.

  4. Disability: An altered level of consciousness and decreased responsiveness point toward significant neurological impairment, often accompanying or preceding arrest.

Initial Assessment

The initial assessment begins with a first impression of the child’s general appearance, breathing pattern, and circulatory status. During the primary assessment, the ABCDE approach is followed, with immediate interventions performed at each step when abnormalities are identified. Initial management focuses on supporting airway, breathing, and circulation [7].

The clinician should rapidly assess the following:

Airway

  • Assess for patency (open, requiring maneuvers/adjuncts, partially or completely obstructed)
  • Perform cervical spine stabilization for injured children.
  • Provide 100% inspired oxygen, clear the airway (e.g., suction), apply airway maneuvers, and insert airway adjuncts if the child is unconscious.
  • Initiate chest compressions immediately if the child is unresponsive and shows no signs of life.
  •  

 Breathing

  • Evaluate respiratory rate, effort, tidal volume, lung sounds, and pulse oximetry.
  • Assist ventilation manually for patients unresponsive to basic airway maneuvers or exhibiting inadequate respiratory effort.
  • Monitor oxygenation and ventilation using pulse oximetry and ETCO₂.
  • Administer appropriate medications based on the cause of respiratory distress (e.g., albuterol for status asthmaticus, inhaled racemic epinephrine for croup).
  • Consider intubation when necessary, ensuring 100% oxygen delivery via a non-rebreather mask. Apply positive pressure ventilation with a bag-valve-mask (BVM) in cases of respiratory failure.

Circulation

  • Assess skin color and temperature, heart rate and rhythm, blood pressure, peripheral and central pulses, and capillary refill time.
  • Control hemorrhage in injured children.
  • For circulation deficiencies, monitor heart rate and rhythm, and establish vascular access for volume resuscitation or medication administration.

Disability

  • Evaluate neurological status and level of consciousness using the AVPU scale (Alert, Voice, Pain, Unresponsive) and the Glasgow Coma Scale (GCS) for trauma patients.
  • Assess pupil size and reactivity to light.
  • Check for hypoglycemia using rapid bedside glucose testing or by observing the response to empiric dextrose administration.

Exposure

  • Examine for skin findings, fever or hypothermia, and evidence of trauma.

Secondary and Tertiary Assessments

  • The secondary assessment involves a detailed head-to-toe physical examination, supplemented with a medical history.
  • The tertiary assessment focuses on identifying the underlying causes of trauma, illness, or infection through ancillary studies.

Respiratory Distress and Failure

Respiratory distress and failure are common precursors to CA in children. Early recognition of breathing difficulties is essential to improving clinical outcomes.

Respiratory distress is characterized by tachypnea, nasal flaring, retractions, and the use of accessory muscles. Additional signs include agitation, hypoxia, and abnormal breath sounds, such as stridor or wheezing. If not promptly addressed, these findings can progress to a decreased respiratory rate, respiratory fatigue, and eventual respiratory arrest.

Bradycardia

In children, bradycardia is often secondary to hypoxia. A heart rate slower than the age-appropriate normal range is indicative of bradyarrhythmia. Management focuses on optimizing oxygenation and ventilation through basic airway maneuvers.

If the heart rate remains below 60 beats per minute despite adequate oxygenation and ventilation, chest compressions should be initiated. Epinephrine (0.01 mg/kg) should be administered every 3–5 minutes. For bradycardia caused by increased vagal tone or primary atrioventricular block, atropine (0.02 mg/kg; maximum single dose 0.5 mg) is recommended [7].

Tachycardia

Tachycardia refers to a heart rate that exceeds the normal range for a child’s age, considering other factors such as physical activity or fever. The management of tachycardias depends on the child’s hemodynamic condition and rhythm [7].

Pulseless Arrest

Pediatric CAs are typically the result of cardiopulmonary distress, failure, or shock. When a child has no palpable pulse and is unresponsive, cardiopulmonary resuscitation (CPR) should be initiated.

A child with pulseless arrest will present as apneic and may exhibit gasping respirations. The rhythms associated with pulseless arrest include [2]:

Shockable rhythms: Ventricular fibrillation (VF), pulseless ventricular tachycardia (pVT).

Ventricular Fibrillation

Ventricular Tachycardia

Unshockable rhythms: Asystole, pulseless electrical activity (PEA).

Asystole

Pulseless Electrical Activity (PEA)

During CPR, reversible causes of PEA should be actively identified and addressed. The mnemonic 6H5T is useful for recalling these potential causes [2]:

  • 6 H’s:
    • Hydrogen ion (acidosis)
    • Hypoxia
    • Hypovolemia
    • Hypo- or hyper -kalemia, -calcemia, -magnesemia
    • Hypoglycemia
    • Hypo- or hyperthermia
  • 5 T’s:
    • Tension pneumothorax
    • Tamponade
    • Thrombosis (cardiac)
    • Thrombosis (pulmonary)
    • Toxic agents

By addressing these potential causes, advanced life support providers can significantly improve the likelihood of successful resuscitation.

Resuscitation

An effective resuscitation team is critical to the successful management of pediatric advanced life support (PALS). The team must perform multiple tasks simultaneously, including airway management, ventilation, vascular access, medication preparation and administration, chest compressions, monitor/defibrillator operation, recording/timing, and overall leadership.

The team leader plays a pivotal role by assigning tasks, directing team members, and modeling exemplary teamwork. In addition to medical expertise and resuscitation skills, the team must demonstrate effective communication. Key elements of effective team dynamics include:

  • Closed-loop communication
  • Clear messages
  • Defined roles and responsibilities
  • Knowing and communicating one’s limitations
  • Knowledge sharing
  • Constructive interventions
  • Reevaluation and summarization
  • Mutual respect [8]

Initiation of CPR

Timely recognition of CA, prompt initiation of high-quality chest compressions, and ensuring adequate ventilation are crucial for improving outcomes [2].

Healthcare providers should begin chest compressions promptly in any child who is unresponsive, not breathing normally, and has no signs of circulation [7, 9]. Pulse checks may be performed but should not delay the initiation of CPR for more than 10 seconds [10, 11]. Pulse palpation alone is unreliable in determining the need for compressions or confirming CA.

Since respiratory-related CA is more common in infants and children than primary cardiac causes, ensuring adequate ventilation during resuscitation is essential [2]. The recommended sequence for CPR is compressions-airway-breathing (CAB) [12].

High-quality CPR enhances blood flow to vital organs and increases the likelihood of return of spontaneous circulation (ROSC). The five key components of high-quality CPR are [2, 13]:

  • Optimal chest compression rate
  • Sufficient chest compression depth
  • Minimal interruptions in compressions
  • Complete chest recoil between compressions [7, 14]
  • Avoidance of excessive ventilation

Components of High-Quality CPR

  • Compression Rate: 100–120 compressions per minute [15–18].
  • Compression Depth:
    • At least one-third of the anterior-posterior diameter of the chest:
      • 4 cm for infants
      • 5 cm for children
      • 5–6 cm for adolescents who have reached puberty [7, 19].
    • Allow complete chest recoil after each compression.
    • Use 100% oxygen with a bag-valve-mask (BVM) during CPR.
    • Compression-Ventilation Ratios:
      • 30:2 for single rescuers.
      • 15:2 for two rescuers [7, 20].

To prevent fatigue and ensure adequate compressions, switch the person performing compressions at least every 2 minutes or sooner if necessary [7].

CPR Technique

For Infants

Single Rescuer: Use two fingers (Figure 1) or two thumbs below the nipple line (lower half of the sternum but one-finger width above the xiphisternum) [21–24].

Figure 1. Two-finger compressions

Two Rescuers: Use the two-thumb encircling hands technique (Figure 2) [25–29].

Figure 2. Thumb-encircling hands compression

If the recommended depth cannot be achieved, use the heel of one hand (Figure 3) [2, 18, 30, 31].

Figure 3. Compression with the heel of one hand

For children older than 1 year

Use either one-handed or two-handed CPR.

Perform chest compressions on a firm surface. Use a backboard or activate the bed’s “CPR mode” if available [32–35].

The Airway

Unless a cervical spine injury is suspected, the head tilt-chin lift maneuver is recommended to open the airway [36]. In trauma patients with suspected cervical spinal injury, the jaw thrust maneuver should be used. If the jaw thrust is ineffective, the head tilt-chin lift may be performed, even in cases of suspected cervical spine injury [2].

Use 100% oxygen delivered via bag-valve-mask (BVM) during CPR.

Advanced Airway Interventions During CPR

Bag-mask ventilation (BMV) is effective for most patients but requires pauses in chest compressions and carries risks of aspiration and barotrauma [2]. Advanced airway interventions, such as supraglottic airway (SGA) placement or endotracheal intubation (ETI), improve ventilation, reduce aspiration risks, and enable uninterrupted chest compressions. However, these procedures require specialized equipment and trained providers, and may be challenging for those inexperienced in pediatric intubation [2]. BMV is more reliable than advanced airway interventions during out-of-hospital pediatric CA [37–39].

For patients with advanced airway, ventilations should be asynchronous. Exceeding recommended ventilation rates can compromise hemodynamics and lower systolic blood pressure [40].

Ventilations should be tailored to age:

  • 25 breaths/min (infants)
  • 20 breaths/min (>1 year)
  • 15 breaths/min (>8 years)
  • 10 breaths/min (>12 years) [7].

Capnography should be used to confirm endotracheal tube placement and monitor for ROSC. However, ETCO₂ should not be used as a definitive quality indicator or target during PALS [7].

Drug Administration During CPR

Establish IV access as early as possible during PALS. If IV access is challenging, promptly consider intraosseous (IO) access as an alternative [7]. Drug dosing for children is typically based on weight, which can be challenging to determine in emergencies. When the actual weight cannot be obtained, various estimation methods are available [41]

The administration of vasoactive agents during CA aims to improve coronary and cerebral perfusion and increase the likelihood of ROSC. However, optimal timing and overall impact on long-term outcomes are still under investigation [42]

  • Administer epinephrine (10 mcg/kg; max 1 mg; IV or IO ) as soon as possible for non-shockable rhythms. For shockable rhythms, administer epinephrine immediately after the third shock, along with antiarrhythmic drugs. Once given, adrenaline should be repeated every 3–5 minutes until ROSC.

Antiarrhythmic drugs can reduce the risk of recurrent VF or pVT and improve the likelihood of successful defibrillation [43, 44]. Only in shockable rhythms, administer antiarrhythmic drugs immediately after the third shock, along with epinephrine.

  • Amiodarone: 5 mg/kg (max 300 mg); a second dose (max 150 mg) may follow after the fifth shock if the rhythm remains shockable.
  • Lidocaine: 1 mg/kg, as an alternative to amiodarone.

Magnesium sulfate (25–50 mg/kg) should be considered for torsades de pointes. Routine administration of sodium bicarbonate and calcium is not recommended unless specific conditions (e.g., electrolyte imbalances, drug toxicities) are present [45–48].

Flush all IV or IO resuscitation drugs with 5–10 mL of normal saline to ensure delivery to the central circulation.

Defibrillation During PALS

Shockable rhythms in children include pulseless ventricular tachycardia (pVT) and ventricular fibrillation (VF). When identified, defibrillation should be performed immediately, regardless of the ECG amplitude. If there is uncertainty about the rhythm, it should be treated as shockable to avoid delays in care. [7].

The preferred method for defibrillation during pediatric ALS is manual defibrillation, but an automated external defibrillator (AED) can be used if manual defibrillation is unavailable. Currently, self-adhesive defibrillation pads are the standard. When using these pads:

  • Chest compressionsshould continue while the defibrillator charges.
  • The pads should be placed in either the antero-lateral (AL)or antero-posterior (AP) positions:
    • AL position: One pad below the right clavicle and the other in the left axilla.
    • AP position: The front pad in the mid-chest just left of the sternum, and the back pad between the scapulae.

Avoid contact between the pads to prevent electrical arcing.

If self-adhesive pads are unavailable, paddles with gel or pre-shaped gel pads can be used as an alternative. In this case, charging should occur directly on the chest, pausing compressions during the process [7]. Pre-planning each step is critical to minimizing delays during the intervention.

Charge the defibrillator for an initial shock of 4J/kg. Avoid exceeding the maximum doses recommended for adults (typically 120–200J, depending on the defibrillator). Pause chest compressions briefly to deliver the shock, ensuring all rescuers are clear of the patient. Resume CPR immediately after the shock, minimizing the pause to under 5 seconds. Reassess the rhythm every 2 minutes and, if it remains shockable, deliver subsequent shocks at 4J/kg. For refractory VF/pVT (requiring more than 5 shocks), incrementally increase the dose up to 8J/kg (maximum 360J) [7].

CPR should continue until an organized, potentially perfusing rhythm is recognized during a rhythm check and is accompanied by signs of ROSC, identified either clinically (e.g., eye-opening, movement, normal breathing) or through monitoring (e.g., etCO2, SpO2, blood pressure, ultrasound) [7].

A summary of the fundamentals of pediatric ALS can be found in Figure 5.

Figure 5. Pediatric cardiac arrest algorithm [7] CPR: cardiopulmonary resuscitation, EMS: emergency medical services, ALS: advanced life support, VF: ventricular fibrillation, pVT: pulseless ventricular tachycardia, PEA: pulseless electrical activity, IV: intravenous, IO: intraosseous.

Post-cardiac Arrest Management

Achieving ROSC is only the first step in resuscitation. Comprehensive post-CA care is crucial to optimizing outcomes, particularly in pediatric patients. This phase focuses on treating the underlying cause of the event and preventing secondary injuries.

Key Components of Post-Cardiac Arrest Care

Targeted Temperature Management (TTM):

  • For unconscious children after ROSC, TTM helps prevent further brain injury.

Ventilation and Oxygenation:

  • Inspired oxygen should be titrated to maintain oxygen saturation (SpO₂) between 94% and 99%.
  • For intubated patients, confirm endotracheal tube (ETT) placement and monitor ventilation to avoid hyperoxia or hypoxia, as well as hypercapnia or hypocapnia.

Hemodynamic Support:

  • Prevent and treat hypotension using parenteral fluids and vasoactive medications, guided by physiologic endpoints and cardiac function.
  • Monitor for signs of recurrent shock and intervene promptly.

Glucose Management:

  • Maintain blood glucose levels below 180 mg/dL to avoid complications associated with hyperglycemia.

Seizure Management:

  • For unconscious children after ROSC, continuous electroencephalography monitoring is also recommended to detect subclinical seizures. Seizures should be monitored and treated aggressively, as they can exacerbate neurological injury.

Temperature Regulation:

  • Avoid hyperthermia (core temperature >37.5°C) using cooling measures as necessary to reduce metabolic demands and limit neuronal damage.

Summary

Pediatric CA remains a critical event with high mortality and significant morbidity. Unlike adult CA, pediatric cases are often precipitated by respiratory failure and hypoxia, highlighting the need for timely recognition and intervention. Early identification of abnormal vital signs, particularly through tools like PEWS, and a structured approach to initial assessment using the ABCDE framework are paramount in preventing CA. Furthermore, rapid and effective resuscitation, incorporating high-quality CPR, advanced airway management, and appropriate medication use, significantly improves the likelihood of survival and favorable outcomes.

Managing pediatric CA extends beyond achieving ROSC. Comprehensive post-cardiac arrest care, including targeted temperature management, optimized ventilation and oxygenation, hemodynamic support, glucose management, and seizure control, is critical to minimize secondary injuries and improve neurological recovery. Pediatric Advanced Life Support (PALS) algorithms and effective resuscitation team dynamics play essential roles in guiding care.

Ultimately, improving outcomes in pediatric CA requires a systematic approach to prevention, timely recognition, prompt intervention, and evidence-based post-resuscitation care. Continuous education, training, and adherence to updated guidelines are essential for healthcare providers to ensure the best possible outcomes for critically ill or arrested children.

Authors

Picture of Burak Çakar

Burak Çakar

Gaziantep Islahiye State Hospital, Department of Emergency Medicine, Gaziantep, Turkey

Picture of Ayça Koca

Ayça Koca

Ayça Koca is an emergency physician at Ankara University School of Medicine, Department of Emergency Medicine. She completed both her medical degree and residency at Ankara University, where she developed a deep connection to patient care and teaching. With a special interest in medical education and simulation, she is passionate about creating engaging learning experiences to support the growth and confidence of future healthcare providers.

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References

  1. López-Herce J, Del Castillo J, Matamoros M, et al. Factors associated with mortality in pediatric in-hospital cardiac arrest: a prospective multicenter multinational observational study. Intensive Care Med. 2013;39(2):309-318.
  2. Topjian AA, Raymond TT, Atkins D, et al. Part 4: Pediatric Basic and Advanced Life Support 2020 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Pediatrics. 2021;147(Suppl 1):e2020038505D.
  3. Fink EL, Prince DK, Kaltman JR, et al. Unchanged pediatric out-of-hospital cardiac arrest incidence and survival rates with regional variation in North America. Resuscitation. 2016;107:121-128.
  4. Wyckoff MH, Greif R, Morley PT, et al. 2022 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations: Summary From the Basic Life Support; Advanced Life Support; Pediatric Life Support; Neonatal Life Support; Education, Implementation, and Teams; and First Aid Task Forces [published correction appears in Resuscitation. 2024;201:110267.]. Resuscitation. 2022;181:208-288.
  5. Monaghan A. Detecting and managing deterioration in children. Paediatr Nurs. 2005;17(1):32-35.
  6. Halpern NA: Early Warning Systems for Hospitalized Pediatric Patients. Jama 2018, 319(10):981-982.
  7. Van de Voorde P, Turner NM, Djakow J, et al. European Resuscitation Council Guidelines 2021: Paediatric Life Support. Resuscitation. 2021;161:327-387.
  8. Sen IM, Kumar R, Grewal A, Singh M. A simple mnemonic to remember team tasks during cardiopulmonary resuscitation. J Anaesthesiol Clin Pharmacol. 2021;37(3):486-487.
  9. Uzun DD, Lang K, Saur P, Weigand MA, Schmitt FCF. Pediatric cardiopulmonary resuscitation in infant and children with chronic diseases: A simple approach?. Front Pediatr. 2022;10:1065585.
  10. O’Connell KJ, Keane RR, Cochrane NH, et al. Pauses in compressions during pediatric CPR: Opportunities for improving CPR quality. Resuscitation. 2019;145:158-165.
  11. Tibballs J, Weeranatna C. The influence of time on the accuracy of healthcare personnel to diagnose paediatric cardiac arrest by pulse palpation. Resuscitation. 2010;81(6):671-675.
  12. Lubrano R, Cecchetti C, Bellelli E, et al. Comparison of times of intervention during pediatric CPR maneuvers using ABC and CAB sequences: a randomized trial. Resuscitation. 2012;83(12):1473-1477.
  13. Niles DE, Duval-Arnould J, Skellett S, et al. Characterization of Pediatric In-Hospital Cardiopulmonary Resuscitation Quality Metrics Across an International Resuscitation Collaborative. Pediatr Crit Care Med. 2018;19(5):421-432.
  14. Sutton RM, Niles D, Nysaether J, et al. Quantitative analysis of CPR quality during in-hospital resuscitation of older children and adolescents. Pediatrics. 2009;124(2):494-499.
  15. Sutton RM, French B, Nishisaki A, et al. American Heart Association cardiopulmonary resuscitation quality targets are associated with improved arterial blood pressure during pediatric cardiac arrest. Resuscitation. 2013;84(2):168-172.
  16. Sutton RM, Reeder RW, Landis W, et al. Chest compression rates and pediatric in-hospital cardiac arrest survival outcomes. Resuscitation. 2018;130:159-166.
  17. Dezfulian C, Fink EL. How Bad Is It to Fail at Pushing Hard and Fast in Pediatric Cardiopulmonary Resuscitation?. Pediatr Crit Care Med. 2018;19(5):495-496.
  18. Kim MJ, Lee HS, Kim S, Park YS. Optimal chest compression technique for paediatric cardiac arrest victims. Scand J Trauma Resusc Emerg Med. 2015;23:36.
  19. Sutton RM, French B, Niles DE, et al. 2010 American Heart Association recommended compression depths during pediatric in-hospital resuscitations are associated with survival. Resuscitation. 2014;85(9):1179-1184.
  20. Wu ET, Li MJ, Huang SC, et al. Survey of outcome of CPR in pediatric in-hospital cardiac arrest in a medical center in Taiwan. Resuscitation. 2009;80(4):443-448.
  21. Clements F, McGowan J. Finger position for chest compressions in cardiac arrest in infants. Resuscitation. 2000;44(1):43-46.
  22. Finholt DA, Kettrick RG, Wagner HR, Swedlow DB. The heart is under the lower third of the sternum. Implications for external cardiac massage. Am J Dis Child. 1986;140(7):646-649.
  23. Orlowski JP. Optimum position for external cardiac compression in infants and young children. Ann Emerg Med. 1986;15(6):667-673.
  24. Phillips GW, Zideman DA. Relation of infant heart to sternum: its significance in cardiopulmonary resuscitation. Lancet. 1986;1(8488):1024-1025.
  25. Douvanas A, Koulouglioti C, Kalafati M. A comparison between the two methods of chest compression in infant and neonatal resuscitation. A review according to 2010 CPR guidelines. J Matern Fetal Neonatal Med. 2018;31(6):805-816.
  26. Lee JE, Lee J, Oh J, et al. Comparison of two-thumb encircling and two-finger technique during infant cardiopulmonary resuscitation with single rescuer in simulation studies: A systematic review and meta-analysis. Medicine (Baltimore). 2019;98(45):e17853.
  27. Lee SY, Hong JY, Oh JH, Son SH. The superiority of the two-thumb over the two-finger technique for single-rescuer infant cardiopulmonary resuscitation. Eur J Emerg Med. 2018;25(5):372-376.
  28. Pellegrino JL, Bogumil D, Epstein JL, Burke RV. Two-thumb-encircling advantageous for lay responder infant CPR: a randomised manikin study. Arch Dis Child. 2019;104(6):530-534.
  29. Tsou JY, Kao CL, Chang CJ, Tu YF, Su FC, Chi CH. Biomechanics of two-thumb versus two-finger chest compression for cardiopulmonary resuscitation in an infant manikin model. Eur J Emerg Med. 2020;27(2):132-136.
  30. Peska E, Kelly AM, Kerr D, Green D. One-handed versus two-handed chest compressions in paediatric cardio-pulmonary resuscitation. Resuscitation. 2006;71(1):65-69.
  31. Stevenson AG, McGowan J, Evans AL, Graham CA. CPR for children: one hand or two?. Resuscitation. 2005;64(2):205-208.
  32. Beesems SG, Koster RW. Accurate feedback of chest compression depth on a manikin on a soft surface with correction for total body displacement. Resuscitation. 2014;85(11):1439-1443.
  33. Fischer EJ, Mayrand K, Ten Eyck RP. Effect of a backboard on compression depth during cardiac arrest in the ED: a simulation study. Am J Emerg Med. 2016;34(2):274-277.
  34. Ruiz de Gauna S, González-Otero DM, Ruiz J, Gutiérrez JJ, Russell JK. A Feasibility Study for Measuring Accurate Chest Compression Depth and Rate on Soft Surfaces Using Two Accelerometers and Spectral Analysis. Biomed Res Int. 2016;2016:6596040.
  35. Sanri E, Karacabey S. The Impact of Backboard Placement on Chest Compression Quality: A Mannequin Study. Prehosp Disaster Med. 2019;34(2):182-187.
  36. Bhalala US, Hemani M, Shah M, et al. Defining Optimal Head-Tilt Position of Resuscitation in Neonates and Young Infants Using Magnetic Resonance Imaging Data. PLoS One. 2016;11(3):e0151789.
  37. Andersen LW, Raymond TT, Berg RA, et al. Association Between Tracheal Intubation During Pediatric In-Hospital Cardiac Arrest and Survival. JAMA. 2016;316(17):1786-1797.
  38. Hansen ML, Lin A, Eriksson C, et al. A comparison of pediatric airway management techniques during out-of-hospital cardiac arrest using the CARES database. Resuscitation. 2017;120:51-56.
  39. Ohashi-Fukuda N, Fukuda T, Doi K, Morimura N. Effect of prehospital advanced airway management for pediatric out-of-hospital cardiac arrest. Resuscitation. 2017;114:66-72.
  40. Sutton RM, Reeder RW, Landis WP, et al. Ventilation Rates and Pediatric In-Hospital Cardiac Arrest Survival Outcomes. Crit Care Med. 2019;47(11):1627-1636.
  41. Young KD, Korotzer NC. Weight Estimation Methods in Children: A Systematic Review. Ann Emerg Med. 2016;68(4):441-451.e10.
  42. Campbell ME, Byrne PJ. Cardiopulmonary resuscitation and epinephrine infusion in extremely low birth weight infants in the neonatal intensive care unit. J Perinatol. 2004;24(11):691-695.
  43. Holmberg MJ, Ross CE, Atkins DL, et al. Lidocaine versus amiodarone for pediatric in-hospital cardiac arrest: An observational study. Resuscitation. 2020;149:191-201.
  44. Valdes SO, Donoghue AJ, Hoyme DB, et al. Outcomes associated with amiodarone and lidocaine in the treatment of in-hospital pediatric cardiac arrest with pulseless ventricular tachycardia or ventricular fibrillation [published correction appears in Resuscitation. 2019;142:117-118.]. Resuscitation. 2014;85(3):381-386.
  45. Del Castillo J, López-Herce J, Cañadas S, et al. Cardiac arrest and resuscitation in the pediatric intensive care unit: a prospective multicenter multinational study. Resuscitation. 2014;85(10):1380-1386.
  46. Matamoros M, Rodriguez R, Callejas A, et al. In-hospital pediatric cardiac arrest in Honduras. Pediatr Emerg Care. 2015;31(1):31-35.
  47. Wolfe HA, Sutton RM, Reeder RW, et al. Functional outcomes among survivors of pediatric in-hospital cardiac arrest are associated with baseline neurologic and functional status, but not with diastolic blood pressure during CPR. Resuscitation. 2019;143:57-65.
  48. Lasa JJ, Alali A, Minard CG, et al. Cardiopulmonary Resuscitation in the Pediatric Cardiac Catheterization Laboratory: A Report From the American Heart Association’s Get With the Guidelines-Resuscitation Registry. Pediatr Crit Care Med. 2019;20(11):1040-1047.

Reviewed and Edited By

Picture of Elif Dilek Cakal, MD, MMed

Elif Dilek Cakal, MD, MMed

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Blood Transfusion And Its Complications (2024)

~ iEM Education Project Team ~ Leave a comment

by Yaman Hukan, Thiagarajan Jaiganesh

Authors
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You have a new patient!

A 68-year-old male with a history of controlled HTN, DM, and Ischemic heart disease presents to the Emergency Department with complaints of easy fatiguability that started 2 months ago. He reports a gradual onset of symptoms and inability to tolerate his usual morning walk. He denies chest pain or palpitations. Upon further questioning, he mentioned that he noticed his clothes getting loose, and his family noticed he had lost weight. On review of systems, he states he has bouts of diarrhea with dark stools. Upon arrival, his vitals are Temp 36.9 C, HR 105 BPM, BP 122/68 mmHg, RR 17 BPM, and SpO2 of 98% on RA.  Blood investigations reveal an Hgb level of 5.0 g/dL. Therefore, you decide to initiate a Packed RBC transfusion in the ER. One hour after starting the transfusion, you are called by the nurse as the patient is becoming distressed. You attend to the patient and notice him to be in severe respiratory distress.

What do you need to know?

Often, patients presenting to Emergency Departments require a blood transfusion. According to the National Blood Collection and Utilization survey administered by the US Department of Health and Human Services, 2019 around 1 million RBC transfusions took place in EDs across the United States [1]. The clinical conditions necessitating a blood transfusion include upper and lower gastrointestinal bleeding, traumatic shock, symptomatic anemia, etc., to name a few. Therefore, medical trainees and emergency physicians must be aware of complications that may arise from blood transfusions and manage them appropriately.

Commonly administered blood products in the emergency department (ED) include packed red blood cells (PRBCs), fresh frozen plasma (FFP), platelet concentrates, and cryoprecipitate. PRBCs are frequently used to increase oxygen-carrying capacity in patients with significant anemia or hemorrhage. FFP provides essential clotting factors, making it valuable in cases of coagulopathy or massive transfusion protocols. Platelet concentrates are utilized to manage thrombocytopenia or platelet dysfunction, while cryoprecipitate supplies fibrinogen, von Willebrand factor, and other clotting factors, supporting hemostasis in patients with severe bleeding or fibrinogen deficiency.

The choice of components should be directed by the patient’s clinical condition, rate of bleeding, cardiopulmonary status, and operative intervention, with the goal of restoring volume and oxygen-carrying capacity [2].

Administering blood and blood products to patients has resulted in numerous adverse reactions. These reactions are broadly classified as either Acute (onset within 24 hrs), such as febrile nonhemolytic reactions, or Delayed (onset beyond 24 hrs), such as delayed hemolytic reactions [3].

Data from the National Healthcare Safety Network Hemovigilance Module in the United States demonstrate that 1 in 455 blood components transfused was associated with an adverse reaction. However, the incidence of serious reactions was much lower, at 1 in 6224. Despite the relatively lower rates of serious reactions, 23 fatalities were recorded between 2013 and 2018 [4].

Severe adverse reactions result from transfusing incompatible (ABO or Rh) blood. The ABO blood group system remains of extreme importance in blood transfusions, as it is the most immunogenic of all blood group antigens [5]. The four blood groups are A, B, O, and AB.

The table shows the summary of ABO Antigens and Antibodies contained within each blood type.

 

A

B

O

AB

Antigens

A

B

None

A and B

Antibodies

Anti-B

Anti-A

Anti-A & Anti-B

None

There are several ABO blood group antigens expressed on every RBC cell. Each blood group early on during life forms antibodies against ABO antigens not found on the surface of RBCs. When an individual is transfused ABO-incompatible blood, preformed antibodies in its own serum react against the donor’s red blood cells, causing rapid acute intravascular hemolysis, a life-threatening transfusion reaction.

The second significant blood grouping system is the Rh system. The presence of Rh Antigen implies that the patient is Rh(+) (e.g., Blood group O+). Patients who are Rh(-) lack the RhD antigen. Therefore, their blood develops antibodies against Rh(+) blood groups if they are ever exposed to it. This incompatibility can lead to a hemolytic reaction, but it is much less likely than a hemolytic reaction due to ABO incompatibility. The clinical significance of the Rh system lies in the pregnancy setting when a Rh(-) mother is pregnant with an Rh(+) fetus. Upon first exposure to the positive blood from the fetus, the mother’s blood would form antibodies against Rh-blood. In case of a repeated pregnancy with Rh+ fetus, the mother’s antibodies cross the placenta and attack the RBCs of the fetus, which can lead to a condition called hemolytic disease of the newborn [6]. This is the reason why women of childbearing age should always receive O(-) blood in the setting of acute hemorrhage needing a blood transfusion, as opposed to men who may receive O(+) blood safely.

Medical History

Should a patient receiving or recently received a blood or a blood product transfusion develop new signs and symptoms, consider a transfusion reaction. Commonly encountered signs and symptoms of mild transfusion reactions include:

  • Increase in body temperature/fever,
  • Chills/Rigors,
  • Pruritis, New rash, or swelling of the mucous membranes.

Severe reactions include:

  • Difficulty in breathing,
  • Respiratory distress,
  • Altered level of consciousness,
  • Decreased urinary output.

Reaction Types

Acute Transfusion Reactions

Febrile nonhemolytic transfusion reaction

This is one of the most common transfusion reactions, occurring at a rate of around 1:900 [7]. It has been attributed to cytokines released from white blood cells and their accumulation in blood products [8].

Diagnostic criteria

  • A reaction which occurs during or within 4 hours of cessation of transfusion,

AND

  • Either Fever (> 38 C° and a change of at least 1 C° from pretransfusion value) OR Chills/Rigors is present [9].

Caution must be exercised when distinguishing between febrile nonhemolytic transfusion reactions and hemolytic reactions, which could also present with fever. Febrile nonhemolytic transfusion reaction is considered a diagnosis of exclusion [8]. In the case of first onset of a febrile reaction, a hemolytic reaction must be suspected until proven otherwise.

Allergic and anaphylactic transfusion reactions

Another very common non-infectious transfusion reaction is allergy. Allergic reactions vary in severity from mild to severe. Mild reactions are primarily characterized by itching and hives. They occur at a rate of 1:1200 transfusions. However, rates may be much higher due to underreporting [7].

On the other hand, anaphylactic reactions are typically more severe and occur at a rate of around 1:30000 blood transfusions [7]. Anaphylactic reactions are acute systemic allergic reactions characterized most significantly by hypotension and/or respiratory compromise. They typically arise abruptly within 0-4 hours of initiating the transfusion.

Allergic reactions are thought to be multifactorial in etiology, mainly caused by an antibody-mediated response to donor proteins. These reactions fall under Type 1 hypersensitivity reactions and involve pre-existing IgE antibodies [10].

The criteria for a definitive diagnosis of an allergic reaction encompasses two or more of the following during or within 4 hours of cessation of transfusion: conjunctival edema, edema of lips, tongue, and uvula; Erythema and edema of the periorbital area, generalized flushing, hypotension, localized angioedema, maculopapular rash, pruritis (itching), respiratory distress/bronchospasm, and urticaria (hives) [9].

Acute hemolytic transfusion reaction

The hemolytic transfusion reaction is perhaps the most severe and life-threatening transfusion reaction. They account for 5% of all severe adverse reactions of blood transfusions.  Reactions due to ABO incompatibility occur at a rate of 1:200000 [7]. The rate significantly increases in the setting of uncross-matched blood transfusions in bleeding patients (e.g., major trauma), where the rate reaches as high as 1:2000 [11].

Despite their relative rarity, mainly due to growing hemovigilance procedures and schemes, acute hemolytic transfusion reactions can lead to significant morbidity and mortality. Mortality rates increase with the increase in the volume of the incompatible transfused blood. However, even a volume of as low as 30 mL could lead to a severe fatal reaction [12].

Reactions due to ABO system incompatibility most often occur due to a clerical or laboratory error, including misidentification of patient or mislabelling blood samples collected from the recipient for crossmatching. The recipient’s blood contains pre-existing antibodies against ABO antigens that are not present in their blood. When incompatible blood is administered, those pre-existing antibodies attack the donor’s RBCs. Through complement activation and membrane attack complex, the donor’s RBCs are destroyed, leading to intravascular hemolysis, which subsequently gives rise to the clinical features of hemolysis, including acute tubular necrosis, renal failure, hypotension, disseminated intravascular coagulopathy (DIC), and shock [13].

The criteria for the definitive diagnosis of acute hemolytic transfusion reactions is complex and includes components that can be obtained from clinical presentation combined with laboratory studies, detailed below [9]:

Decision-Making Algorithm for Suspected Hemolytic Transfusion Reaction
1. Identify New-Onset Symptoms

Check if the patient has developed any new symptoms during the transfusion or within 24 hours of transfusion cessation. The presence of any of the following symptoms warrants further investigation:

  • Back or flank pain
  • Chills or rigors
  • Disseminated intravascular coagulation (DIC)
  • Epistaxis (nosebleed)
  • Fever
  • Hematuria (indicative of gross hemolysis)
  • Hypotension
  • Oliguria or anuria (reduced or absent urine output)
  • Pain and/or oozing at the IV site
  • Renal failure

AND

Check for Laboratory Evidence of Hemolysis
Confirm the presence of at least two of the following laboratory findings:

  • Decreased fibrinogen
  • Decreased haptoglobin
  • Elevated bilirubin
  • Elevated lactate dehydrogenase (LDH)
  • Hemoglobinemia
  • Hemoglobinuria
  • Plasma discoloration consistent with hemolysis
  • Spherocytes visible on blood film

AND EITHER

Determine the Mechanism of Hemolysis. Differentiate between immune-mediated and non-immune-mediated hemolysis.

IMMUNE-MEDIATED HEMOLYSIS

  • Perform a Direct Antiglobulin Test (DAT) to detect anti-IgG or anti-C3.
  • Conduct an elution test to detect any alloantibodies on the transfused red blood cells. If the DAT or elution test is positive, this suggests an immune-mediated HTR.

NON-IMMUNE-MEDIATED HEMOLYSIS

  • If serologic testing is negative and there is evidence of a physical cause (e.g., thermal, osmotic, mechanical, or chemical), consider a non-immune etiology. A confirmed physical cause indicates a non-immune-mediated HTR.
Transfusion related acute lung injury (TRALI)

Transfusion-related acute lung injury (TRALI) is an infrequent but incredibly serious blood transfusion reaction. Despite only occurring at the rate of 1:60000 [7], TRALI is reported to be one of the most life-threatening complications according to data from the US Food and Drug Administration, coming in 2nd place among the most fatal blood transfusion reactions in the United States between 2016 and 2020, causing 21% of reported fatalities [14].

TRALI results in a constellation of symptoms that manifest as acute respiratory distress along with hemodynamic instability and can occur with virtually all blood components. The proposed mechanism is complex and involves activation of pulmonary endothelium and polymorphonuclear leucocytes and transfusion of plasma-containing antibodies directed against antigens on the surface of those leucocytes, leading to their activation [15].

The TRALI diagnosis remains clinical and significantly overlaps with other respiratory conditions (e.g., ARDS and Transfusion-associated circulatory overload). A set of clinical features have been adopted to define TRALI, including [9]:

  • No evidence of acute lung injury prior to transfusion, AND,
  • Acute lung injury onset during or within 6 hours of cessation of transfusion, AND,
  • Hypoxemia defined by any of the following methods:
      • PaO2/FiO2 less than or equal to 300 mmHg
      • Oxygen saturation less than 90% on room air
      • Other clinical evidence

AND,

  • Radiographic evidence of bilateral infiltrates
  • No evidence of left atrial hypertension (i.e., circulatory overload)
Transfusion associated circulatory overload (TACO)

The last of the acute transfusion reactions is transfusion-associated circulatory overload (TACO), which carries the highest mortality risk among all reactions. Between 2016 and 2020, 34% of recorded fatalities due to reactions to blood transfusions were caused by TACO [14]. It is relatively more common than TRALI, occurring at an estimated rate of 1:9000 transfusions [7]. TACO can present on a spectrum of mild symptoms to life-threatening ones. Significant overlap exists between TRALI and TACO as both may cause respiratory distress and potentially lead to hemodynamic instability.

TACO is a form of volume overload leading to pulmonary edema. Patients who are older than 70 years of age, suffer from pre-existing cardiac disease, or have a history of renal dysfunction are at increased risk of developing this complication [16].

The criteria for diagnosing TACO have evolved several times over the years. Currently, establishing a definitive diagnosis would require the following [9]:

New onset or exacerbation of 3 or more of the following within 12 hours of cessation of transfusion:

At least 1 of the following two items:-

  1. Evidence of acute or worsening respiratory distress (dyspnea, tachypnoea, cyanosis, and decreased oxygen saturation values in the absence of other specific causes) and/or 
  2. Radiographic or clinical evidence of acute or worsening pulmonary edema (crackles on lung auscultation, orthopnea, cough, a third heart sound, and pinkish frothy sputum in severe cases) or both

             AND;

  • Elevated brain natriuretic peptide (BNP) or NT-pro BNP relevant biomarker
  • Evidence of cardiovascular system changes not explained by underlying medical condition (Elevated central venous pressure, evidence of left heart failure including development of tachycardia, hypertension, widened pulse pressure, jugular venous distension, enlarged cardiac silhouette, and/or peripheral edema)
  • Evidence of fluid overload

Delayed Transfusion Reactions

In addition to acute blood transfusion reactions, there are certain reactions which could appear days or weeks following blood transfusions.

Delayed hemolytic transfusion reaction

Delayed hemolytic transfusion reactions are less severe forms of hemolytic reactions in patients receiving blood transfusions. They appear to be caused by secondary (anamnestic) responses in patients who have already received transfusions. They rarely cause life-threatening or serious manifestations [17]. Those reactions may occur up to 4 weeks following the completion of the transfusion. They are less common than acute hemolytic transfusions, occurring at a rate of 1:22000 transfusions [7].

The criteria for definitive diagnosis of delayed hemolytic transfusion reactions include [9]:

Positive direct antiglobulin test (DAT) for antibodies developed between 24 hours and 28 days after cessation of transfusion

AND EITHER

  • Positive elution test with alloantibody present on the transfused red blood cells OR
  • Newly identified red blood cell alloantibody in recipient serum

AND EITHER

  • Inadequate rise of post-transfusion hemoglobin level or rapid fall in hemoglobin back to pre-transfusion levels OR
  • Otherwise, unexplained appearance of spherocytes
Transfusion associated graft vs. host disease

Transfusion-associated graft vs. host disease is an extremely rare and exceptionally dangerous complication of transfusions, occurring at a rate of 1 in every 13 million [7]. It can present any time up to 6 weeks following the transfusion. It is thought to be caused by viable lymphocytes in the donor’s blood recognizing their new host’s cells as foreign and attacking them, often leading to fatal outcomes [17].

Diagnosis is made when the following characteristics appear between 2 days to 6 weeks from cessation of transfusion [9]:

  • Characteristic rash: erythematous, maculopapular eruption centrally that spreads to extremities and may, in severe cases, progress to generalized erythroderma and hemorrhagic bullous formation.
  • Diarrhea
  • Fever
  • Hepatomegaly
  • Liver dysfunction (i.e., elevated ALT, AST, Alkaline phosphatase, and bilirubin)
  • Marrow aplasia
  • Pancytopenia

AND

  • Characteristic histological appearance of skin or liver biopsy
Post transfusion purpura

This reaction may appear up to 2 weeks post-transfusion and involves platelets [17]. Its prevalence is thought to be around 1 in 57,000 transfusions [7]. A definitive diagnosis may be reached by the following two findings [9]:

  • Alloantibodies in the patient directed against human platelet antigens (HPAs) or other platelet-specific antigens detected at or after the development of thrombocytopenia AND
  • Thrombocytopenia (i.e., decrease in platelets to less than 20% of pre-transfusion count)

Physical Examination

Transfusion reactions could manifest in several organ systems. It is important to exercise vigilance when approaching a patient with a suspected transfusion reaction, as clinical features significantly overlap between several reactions.

One unified step in the physical examination of patients with suspected transfusion reactions is to obtain a complete set of vital signs. This can provide important clues to the diagnosis. For instance, a rise in baseline temperature could indicate a Febrile nonhemolytic reaction, Acute hemolytic reaction, or even TRALI.

Hypotension is a feature of anaphylaxis or acute hemolysis. In addition, while keeping in mind that TRALI can present with either Hypotension or Hypertension, hypotension is more common in TRALI [18] and can help distinguish it from TACO, which can present with respiratory distress coupled with hypertension. Tachypnea and desaturation can be signs of respiratory distress, which would point to either TRALI or TACO as possible diagnoses. Following vitals, emphasis should be on signs relating to the suspected reactions.

Chills and rigors might be observed in acute hemolytic transfusion reaction, along with fever and hypotension. Respiratory status examination is essential and could yield signs of acute distress, including tachypnea, oxygen desaturation, use of accessory muscles, and wheezing. Patients would be anxious, with some reporting a sense of impending doom. Additionally, urine frequency and color should be observed for oliguria or dark-colored urine, pointing to acute hemolysis.

Observe any signs of maculopapular urticarial rash in suspected allergic reactions. Also, look for any signs of dyspnea, wheezing, anxiety, and angioedema. Anaphylaxis could further present with hypotension which could pose a diagnostic dilemma.

There are significant similarities between TRALI and TACO. Examination should look for dyspnea, tachypnoea, cyanosis, and decreased oxygen saturation. Furthermore, auscultation for crackles might be evidence of pulmonary edema. Orthopnea, cough, a third heart sound, and pinkish frothy sputum could all be clues leading to the diagnosis of these reactions.

Alternative Diagnoses

When new symptoms arise after blood transfusions, the diagnosis of transfusion reactions should be established. However, an extensive differential diagnosis list must be carefully formulated depending on the presentation.

In the context of transfusions, certain signs and symptoms may indicate potential complications or adverse reactions. A new rash or swelling of mucous membranes could suggest an allergic reaction, anaphylaxis, urticaria, food allergies, or angioedema. Dyspnea, or respiratory distress, may be indicative of transfusion-related acute lung injury (TRALI), transfusion-associated circulatory overload (TACO), anaphylaxis, cardiogenic pulmonary edema, acute respiratory distress syndrome, or acute chest syndrome. Hypotension could point to anaphylaxis, TRALI, septic shock, hemorrhagic shock, or neurogenic shock. Lastly, the presence of fever may indicate a febrile non-hemolytic reaction, an acute hemolytic reaction, an infection from any source, or sepsis. Identifying these symptoms promptly is essential to manage and mitigate potential adverse events during transfusions.

The table summarizes signs&symptoms and potential differential diagnoses. 

Signs and Symptoms

Differential Diagnoses

New rash, or swelling of mucous membranes

Allergic reaction, Anaphylaxis, Acute, Urticaria, Food Allergies, Angioedema

Dyspnea (Respiratory distress)

TRALI, TACO, Anaphylaxis, Cardiogenic pulmonary edema, Acute respiratory distress syndrome, Acute chest syndrome

Hypotension

Anaphylaxis, TRALI, Septic shock, Hemorrhagic shock, Neurogenic shock

Fever

Febrile nonhemolytic reaction, Acute hemolytic reaction, infection of any source, sepsis

Acing Diagnostic Testing

While most transfusion reaction diagnoses are primarily clinical, few diagnostic tests may assist clinicians in establishing a diagnosis.

  1. Visual inspection of the pre-transfusion sample for its color and any unusual clumps [19].
  2. Allergic reactions: IgA levels could also be obtained in patients with suspected IgA deficiency, although the diagnosis for moderate or severe allergic reactions is usually clinical. Eosinophilia could indicate allergic reactions but may not always be present [10].
  3. Hemolytic reactions: Elevated Lactate dehydrogenase levels (LDH) as well as indirect bilirubin levels with decreased haptoglobin levels would suggest a hemolytic reaction arising out of an ABO incompatibility. Elevated PTT and PT/INR, as well as D-Dimer coupled with decreased fibrinogen, would suggest the presence of DIC. Blood film can be examined for schistocytes or spherocytes [12]. Dark urine could suggest hemoglobinuria. Direct antiglobulin test (DAT) for anti-IgG or anti-C3 and elution test with alloantibody present on the transfused red blood cells would help.
  4. TRALI & TACO: arterial blood gas (ABG) is used to calculate the PaO2/FiO2 ratio, and Chest XR is used to evaluate the presence of bilateral infiltrates or features of pulmonary edema. Bedside ultrasound can confirm the absence of circulatory overload in TRALI, which is a distinguishing feature from TACO. Additionally, a BNP level should be obtained when evaluating for TACO.

Risk Stratification

Unfortunately, no objective risk stratification tool exists that would lead to recognizing patients with worse outcomes due to transfusion reactions.

Characteristics which place patients at increased risk of developing transfusion reactions are:

  • Previous transfusion history,
  • Abortions or termination of pregnancy history,
  • Longer blood storage time,
  • Receiving three or more units of blood [3].
  • Critically ill and surgical patients (Risk of mortality due to TRALI appears to be higher) [20].

Management

In case of transfusion reactions, the ABCDE algorithm for managing conditions in the emergency department should be followed. The airway must be assessed for patency and secured if needed, followed by addressing breathing and circulation.

The cornerstone of managing most transfusion reactions is stopping the transfusion and maintaining Intravenous access. In all reactions, the next step is to confirm the details of the transfused unit, make sure no clerical error occurred, and then report the reaction to the concerned blood bank [17].

Febrile nonhemolytic reaction:  Management of this reaction encompasses frequent monitoring of vital signs and administering antipyretics. Transfusion can be continued in stable patients with no other symptoms [12]. However, this remains a diagnosis of exclusion, and other reactions must be considered.

Mild allergic reaction: An H1 antihistamine (e.g., Diphenhydramine 25-50 mg IV) should be administered for symptom management in case of a mild allergic reaction. Restart the transfusion under direct supervision at a slower rate upon resolution of symptoms. In case of recurrence, transfusion must be suspended [17].

Anaphylaxis reaction: Manage as per standard institutional protocol or as delineated in an earlier chapter within this textbook (e.g., IM 1:1000 Epinephrine, H1 antihistamine, e.g., IV Diphenhydramine, Beta-adrenergic drugs, e.g., Salbutamol nebs in case of wheezing and/or bronchospasm, Steroids, e.g., Hydrocortisone and IV Fluids as required) [17].

Acute hemolytic transfusion reaction: The onset of hemodynamic instability will indicate an acute hemolytic transfusion reaction, and it is imperative to immediately halt the transfusions. Treatment is largely supportive. Focus on supporting the respiratory, cardiovascular, and renal systems and treating possible complications such as DIC to halt the patient’s condition [21].

Transfusion-related acute lung injury (TRALI): Similar to acute hemolytic reaction, treatment of TRALI is supportive. Most importantly, support of ventilatory status should be established with noninvasive or invasive means. Most patients who develop TRALI require ventilatory support [22]. As most patients with TRALI develop hypotension, supporting hemodynamics with IV fluids and possible vasopressors may be needed to ensure adequate organ perfusion.

Transfusion-associated circulatory overload (TACO): Since TACO reflects a volume overload status, this condition can be treated similarly to other conditions that result in volume overload. In deteriorating patients, ventilatory support may be needed through noninvasive or mechanical ventilation. Furosemide 0.5/1 mg/kg may be used. In addition, IV Nitroglycerin 50 – 100 mcg as an initial dose may theoretically have a role in clinical status improvement [16,17].

Special Patient Groups

Pregnant Patients

This patient population should always receive O(-) blood when prompt uncross-matched blood is needed for transfusion to minimize the risk of Rh(-) mothers developing antibodies against the Rh(+) fetus, leading to subsequent hemolytic disease of the newborn [5].

Geriatrics

About half of RBC units are administered to patients aged 70 and above [23]. They are frail, have various comorbid conditions, and age-related altered physiology. Clinicians must base their transfusion decisions on the risk-benefit ratio for elderly patients [24]. TACO is the most common transfusion reaction in elderly patients. It occurs at a substantially higher rate in this population compared to younger patients, and those with more comorbidities are at higher risk. Slower transfusion rates are recommended to mitigate the risk [25]. In addition, several studies have mentioned that blood transfusions in the elderly are linked to the risk of developing delirium, although the causation is unknown [26].

Pediatrics

According to a recent meta-analysis, the incidence of transfusion reactions is higher in children than in adults, including rare transfusion reactions [27], due to their size difference (volume-related) and immature liver [28].

When To Admit This Patient

It is advisable to observe patients with hemodynamic instability or severe reactions following a blood transfusion (e.g., ICU for Acute hemolytic reaction). No clear guidelines exist on the criteria for admission for patients with transfusion reactions, and the decision might need to be made on a case-by-case basis, depending on the clinician’s experience and clinical evaluation.

Revisiting Your Patient

Recall that your patient was started on a blood transfusion for a Hgb of 5.0 g/dl and then developed respiratory distress. You arrive at the room and connect to the patient on a monitor. His vitals now show a temperature of 38 C, HR of 132 BPM, RR of 35, BP of 205/120, and SpO2 of 75% on Room Air. You immediately assess the airway and note that the patient is talking clearly but cannot complete full sentences. No secretions in the oral cavity. You judge the airway to be patent and move to assess breathing. He is tachypneic and desaturating, and you immediately place him on 15L O2 via a nonrebreather mask. The patient’s SpO2 picks up to 90%. Upon chest inspection, you hear diffuse crackles. The patient is also unable to lie supine. Hypertension and tachycardia are noted, as well as elevated Jugular venous pressure.

By now, you judge the patient has developed a transfusion reaction, and you immediately order the nurse to suspend the transfusion and notify the blood bank.

An X-ray was ordered, and it showed features of pulmonary edema as well as blunting of the costophrenic angles. Arterial blood gas shows a PaO2/FiO2 ratio 190 and a lactate 4. A BNP is sent and returns at 25,000 pg/mL

Upon review of the patient, he is in significant distress despite the nonrebreather mask, so the respiratory therapist is contacted to initiate BiPAP treatment. You diagnose TACO and, in addition, start the patient on 100 mcg/min of IV Nitroglycerin and a 40 mg dose of IV Furosemide.

The patient started improving shortly after and stated that his breathing was improving. The patient was admitted to the ICU for further stabilization and management of his condition.

Author

Picture of Yaman Hukan

Yaman Hukan

Yaman Hukan is an Emergency Medicine resident at Tawam Hospital in the United Arab Emirates. He completed his bachelor's of medicine (MBBS) degree in 2018 from the University of Sharjah. He is interested in humanitarian medicine. As a medical student, he joined the Syrian American medical society (SAMS) on several of their missions to provide healthcare for Syrian refugees in Jordan. His interests also include resuscitation and toxicology, a field in which he hopes to pursue further training.

Picture of Thiagarajan Jaiganesh

Thiagarajan Jaiganesh

Dr. Jaiganesh is a Chairman and Consultant in Adult and Pediatric Emergency Medicine and serves as an Adjunct Assistant Professor at UAE University. As the former Director of the Emergency Medicine Residency Program at Tawam Hospital in Al Ain, UAE, Dr. Jaiganesh is dedicated to training the next generation of emergency medicine professionals. With a strong academic and professional background, Dr. Jaiganesh has published numerous peer-reviewed articles on emergency medicine and contributes as a Section Editor and Chapter Author for notable medical texts, including the Oxford Handbook for Medical School. A sought-after speaker, Dr. Jaiganesh has been invited to present at numerous national and international conferences and serves as an instructor in various life support courses. Additionally, Dr. Jaiganesh is an expert in medico-legal and clinical negligence matters, providing valuable insights into complex legal and ethical cases in healthcare.

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References

  1. Mowla SJ, Sapiano MRP, Jones JM, Berger JJ, Basavaraju SV. Supplemental findings of the 2019 National Blood Collection and Utilization Survey. Transfusion. 2021;61 Suppl 2(Suppl 2):S11-S35. doi:10.1111/trf.16606
  2. Kumar TA, Geet A. Blood transfusion therapy and related complication. In: Richhariya D, ed. Textbook of Emergency Medicine including intensive care and trauma. New Delhi: Jaypee brothers medical publishers; 2022: 990
  3. Gelaw Y, Woldu B, Melku M. Proportion of Acute Transfusion Reaction and Associated Factors Among Adult Transfused Patients at Felege Hiwot Compressive Referral Hospital, Bahir Dar, Northwest Ethiopia: A Cross-Sectional Study. J Blood Med. 2020;11:227-236. Published 2020 Jun 30. doi:10.2147/JBM.S250653
  4. Kracalik I, Mowla S, Basavaraju SV, Sapiano MRP. Transfusion-related adverse reactions: Data from the National Healthcare Safety Network Hemovigilance Module – United States, 2013-2018. Transfusion. 2021;61(5):1424-1434. doi:10.1111/trf.16362
  5. Dean L. The ABO Blood Group. In: internet, ed. Blood Groups and Cell Antigens. Bethesda MD: National Center for Biotechnology Information (US); 2005: 25-31
  6. Dean L. The ABO Blood Group. In: internet, ed. Blood Groups and Cell Antigens. Bethesda MD: National Center for Biotechnology Information (US); 2005: 39-44
  7. Goel R, Tobian AAR, Shaz BH. Noninfectious transfusion-associated adverse events and their mitigation strategies. Blood. 2019;133(17):1831-1839. doi:10.1182/blood-2018-10-833988
  8. Shmookler AD, Flanagan MB. Educational Case: Febrile Nonhemolytic Transfusion Reaction. Acad Pathol. 2020;7:2374289520934097. Published 2020 Jul 14. doi:10.1177/2374289520934097
  9. Division of healthcare quality promotion. National healthcare safety network biovigilance component hemovigilance module surveillance protocol. Atlanta, GA: Center of disease control and prevention; February 2023: 9-22
  10. Tobian A. Immunologic transfusion reactions. UpToDate. https://www-uptodate-com.eu1.proxy.openathens.net/contents/immunologic-transfusion-reactions?search=anaphylaxis%20transfusion&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1 . Updated on Sep 06, 2022. Accessed on March 15, 2023.
  11. Fiorellino J, Elahie AL, Warkentin TE. Acute haemolysis, DIC and renal failure after transfusion of uncross-matched blood during trauma resuscitation: illustrative case and literature review. Transfus Med. 2018;28(4):319-325. doi:10.1111/tme.12513
  12. San Miguel C. & Kaide C. Blood and Blood Components. In: Walls R., ed. Rosen’s Emergency Medicine: Concepts and Clinical Practice. Philadelphia, PA: Elsevier; 2023: 1452-1561
  13. Panch SR, Montemayor-Garcia C, Klein HG. Hemolytic Transfusion Reactions. N Engl J Med. 2019;381(2):150-162. doi:10.1056/NEJMra1802338
  14. Center for Biologics Evaluation and Research. Fatalities reported to FDA following blood collection and transfusion. United States: Food and drug administration; 2020: 4-5
  15. Otrock ZK, Liu C, Grossman BJ. Transfusion-related acute lung injury risk mitigation: an update. Vox Sang. 2017;112(8):694-703. doi:10.1111/vox.12573
  16. van den Akker TA, Grimes ZM, Friedman MT. Transfusion-Associated Circulatory Overload and Transfusion-Related Acute Lung Injury [published correction appears in Am J Clin Pathol. 2022 Nov 3;158(5):665]. Am J Clin Pathol. 2021;156(4):529-539. doi:10.1093/ajcp/aqaa279
  17. Delaney M, Wendel S, Bercovitz RS, et al. Transfusion reactions: prevention, diagnosis, and treatment. Lancet. 2016;388(10061):2825-2836. doi:10.1016/S0140-6736(15)01313-6
  18. Vlaar AP, Juffermans NP. Transfusion-related acute lung injury: a clinical review. Lancet. 2013;382(9896):984-994. doi:10.1016/S0140-6736(12)62197-7
  19. Al-Riyami AZ, Al-Hashmi S, Al-Arimi Z, et al. Recognition, Investigation and Management of Acute Transfusion Reactions: Consensus guidelines for Oman. Sultan Qaboos Univ Med J. 2014;14(3):e306-e318.
  20. Gajic O, Rana R, Winters JL, et al. Transfusion-related acute lung injury in the critically ill: prospective nested case-control study. Am J Respir Crit Care Med. 2007;176(9):886-891. doi:10.1164/rccm.200702-271OC
  21. Tobian A. Hemolytic transfusion reactions. UpToDate. https://www-uptodate-com.eu1.proxy.openathens.net/contents/hemolytic-transfusion-reactions?sectionName=DELAYED%20HEMOLYTIC%20TRANSFUSION%20REACTIONS%20AND%20DELAYED%20SEROLOGIC%20TRANSFUSION%20REACTIONS&search=blood%20transfusion%20reaction&topicRef=95132&anchor=H354791&source=see_link#H354791. Updated on Jan 05, 2022. Accessed on March 15, 2023
  22. Vlaar AP, Binnekade JM, Prins D, et al. Risk factors and outcome of transfusion-related acute lung injury in the critically ill: a nested case-control study. Crit Care Med. 2010;38(3):771-778. doi:10.1097/CCM.0b013e3181cc4d4b
  23. Bosch MA, Contreras E, Madoz P, et al. The epidemiology of blood component transfusion in Catalonia, Northeastern Spain. Transfusion. 2011;51(1):105-116. doi:10.1111/j.1537-2995.2010.02785.x
  24. Boureau AS, de Decker L. Blood transfusion in older patients. Transfus Clin Biol. 2019;26(3):160-163. doi:10.1016/j.tracli.2019.06.190
  25. Menis M, Anderson SA, Forshee RA, et al. Transfusion-associated circulatory overload (TACO) and potential risk factors among the inpatient US elderly as recorded in Medicare administrative databases during 2011. Vox Sang. 2014;106(2):144-152. doi:10.1111/vox.12070
  26. van der Zanden V, Beishuizen SJ, Swart LM, de Rooij SE, van Munster BC. The Effect of Treatment of Anemia with Blood Transfusion on Delirium: A Systematic Review. J Am Geriatr Soc. 2017;65(4):728-737. doi:10.1111/jgs.14564
  27. Wang Y, Sun W, Wang X, et al. Comparison of transfusion reactions in children and adults: A systematic review and meta-analysis. Pediatr Blood Cancer. 2022;69(9):e29842. doi:10.1002/pbc.29842
  28. Sostin N, Hendrickson JE. Pediatric Hemovigilance and Adverse Transfusion Reactions. Clin Lab Med. 2021;41(1):51-67. doi:10.1016/j.cll.2020.10.004

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Just Some Broken Ribs

Just Some Broken Ribs
~ Ibrahim Sarbay, Turkey ~ Leave a comment

The phone was ringing incessantly. I barely woke up. In my pitch dark bedroom, the ringing phone was the only light source. I slowly grabbed my phone while involuntarily rubbing my eyes. I looked at the caller I.D. It was my father. And what time was it? 1:30 am! In a typical day, this might be an early hour for me, but I was attending a local Emergency Medicine conference that day; so I went to bed early.

I cradled the phone between my ear and shoulder. My father’s voice was fussy. “Someone lies unconscious on the street,” he said hastily. “Can you come and help us?” I asked him to call for an ambulance by that time. He said that he already called. 

While I was preparing in a hurry, my heart started to beat faster and my mind swelled with CPR guidelines, syncope algorithms and my past experiences.

My home is down the block from my parents. I ran there and saw a crowd gathered around a man who was lying on the street. When I passed through I realized someone was doing CPR. I have spotted my parents standing in the crowd and my eyes met with my father. He pointed my younger brother, a trainee surgeon also lives in the same area and was taking his turn on the CPR and checking his pulse. I rushed near them and he filled me in with all they know about the citizen at that point.

The first responder to the cries of the patient’s wife was an ambulance driver with ten years of experience. He said he pulled the patient out of his vehicle. He laid down the man in his 50s suffered from heartburn for the last couple of hours and was about to go to the hospital but lost his consciousness as soon as he started the engine. Since the man wasn’t responding, the former driver started the CPR. About 3 minutes later, my brother showed up along with my father and he took the turn while they kept checking for any response. He said that the rhythm never lasted longer than 10 seconds. So I asked them to keep it up and I took my turn till the ambulance shows up.

It was clear that the patient endured a heart-related condition, probably a myocardial infarction. And I knew by experience that with a proper CPR and early defibrillation, these patients have a high chance of returning of spontaneous circulation, and survival.

The ambulance arrived in a couple of minutes. Paramedics jumped out of the vehicle and rushed to the scene and recognized that I am an Emergency Medicine resident at the State Research and Education Hospital. They let me control the situation. The first rhythm was read on the screen as ventricular fibrillation (VF) and we delivered a shock and started chest compressions again. With the equipment they’ve brought, I intubated the patient while they monitored him with the defibrillator from the ambulance. The nearest hospital was 10 minutes away, and we have shocked-compressed for at least 4 or 5 times in an ambulance moving fast. IT-WAS-HARD!

We have arrived at the hospital. After 10 minutes of additional CPR and proper mediations, spontaneous circulation of the patient returned spontaneous circulation. And a control ECG was consistent with Inferior MI. In a couple of minutes, we were in a different ambulance, headed to the nearest hospital with a coronary angiography unit and ICU.

I took a deep breath after we have delivered the patient to the ICU safe and sound. It was over, for now. One week later, he returned to his home with full recovery, without any neurological sequelae. They were very thankful.

Later on, I’ve heard many funny words people were chattering about this incident. One has particularly given me the giggle. It was coming from an ENT specialist. He said, “So that was no big deal, they probably overreacted and caused him a couple of broken ribs.”

Yeah, there were just some broken ribs… and a life saved.

Further Reading

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IV Catheters and Flow Rates

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