ABCDE…F nel paziente ustionato

Spinto dalla recente partecipazione in qualità di discente, ad un corso formativo strutturato per medici e infermieri, per eseguire l’assistenza e la rianimazione di base nell’adulto e nel bambino ustionato nelle prime ore successive al trauma (ABLS – Advanced Burn Life Support – basato su linee guide proposte dall’ American Burn Association organizzato da F. D’asta), mi sono […]

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Ultrasound Leadership Academy: Basic Cardiac

By Michael Macias

By Michael Macias

Welcome to the Ultrasound Leadership Academy (ULA) summary blog series. This week, we summarize basic cardiac ultrasound. The ULA is essentially an online advanced ultrasound education experience put on by the team from Ultrasound Podcast which brings cutting edge learning to emergency medicine personnel through a variety of interactive platforms including video lectures, google hangouts with experts, simulation, live conferences and real time scanning with a pocket-sized ultrasound device known as a Vscan.

Over the next year I will be posting summaries of the key learning points from my experience. If you want to learn more about the program you can visit Ultrasound Leadership Academy or Ultrasound Podcast to see more from the hosts of this awesome program.


Cardiac ultrasound has become an essential component to our beside ultrasound curriculum in EM. It is fast, can identify key lesions that may require intervention, and is something that can be learned and implemented without significant training. Literature has shown that EM physicians can recognize pericardial effusions with a 96% sensitivity, grossly assess LV function (normal, moderately depressed or severely reduced) at a similar level to cardiologists, and even predict ROSC during cardiac arrest with a sensitivity of 91.6%, with bedside cardiac ultrasound. Not only this but it can even be useful in helping with diagnostic uncertainty in the dyspneic patient and assessing for suspected wall motion abnormalities if occult ACS is a concern. ACEP has provided EM physicians with the following goals for cardiac ultrasound below:

  • Assessment of the presence of pericardial effusion
  • Assessment of global cardiac systolic function
  • Identification of marked RV/LV enlargement
  • Intravascular volume status 
  • Guidance of pericardiocentesis
  • Confirmation of transvenous pacing wire placement 

This post will focus on the key cardiac views, the pertinent anatomy and useful pearls to get started in assessment of cardiac function. 


  • Probe: Phased array (small footprint, low frequency)
  • Probe Indicator: The probe indicator is moved to the right side of the screen 
  • Positioning: Left lateral decubitus is ideal to improve acoustic window
  • Views: Subcostal, parasternal long axis, parasternal short axis, apical 



This is your go to window for pericardial effusion. Remember you are looking anteriorly between the liver and anterior cardiac surface for fluid.

  • Your probe indicator is pointed at the patient's left shoulderHold the probe on the top surface to allow the probe to lie flat on the patient; If you are fanning too posteriorly you will miss your view. 
  • Be sure to use the liver as an acoustic window here. 
  • Once you obtain a good subcostal 4 chamber view, twist probe 90 degrees towards patient's head (you will be sagittal at this point) to obtain subcostal long axis view and IVC longitudinally. This view will be useful for assessing volume status. 



In this view you will observe approximately 90% of cardiac pathology so pay attention! Use this view to assess LV function, compare chamber sizes, and localize effusions.

  • Use the 3rd or 4th intercostal space and point the indicator at the patient's right shoulder
  • The RVOT, aortic root and LA should all be approximately equal in size (~2cm) if you draw a straight line through them in this view.
  • The anterior mitral valve leaflet should almost touch the septum during diastole, this will tell you the patient has a normal EF. (More on this here.)
  • Make sure to look posteriorly to identify the descending thoracic aorta which is useful landmark when assessing location of an effusion (more on this later).


Parasternal Short at Cardiac Base
Parasternal Short at Cardiac Base Parasternal Short at Papillary Muscles
Parasternal Short at Papillary Muscles Coronary Artery Territories
Coronary Artery Territories Parasternal Short at Mitral Valve
Parasternal Short at Mitral Valve

To get to the parasternal short, simply rotate the probe 90 degrees, from the probe indicator pointed at the patient's right shoulder, to their left shoulder. You will then fan the probe from the base of the heart to the apex to obtain different cross sectional views. 

  • This view is important for visualization of how the RV and LV function interdependently. You will be able to assess for increased right sided pressures and wall motion abnormalities.
  • Point towards the base of the heart to assess the RV inflow/outflow; Look for the 'Mercedes Benz' sign in the center which represents the 3 leaflets of the aortic valve.
  • Point over the mitral valve and you will see what appears to be a 'fish mouth' coming out straights towards you.
  • Fan further towards the left hip to view the papillary muscles. Notice the RV crescent shape overlying the round LV; A flattened septum is concerning for RV overload.  



This can be a more challenging view but once obtained if adds quite a bit more information to your cardiac assessment. You will be able to assess cardiac function (EF), wall motion, diastology and valve abnormalities using this view. 

  • Your probe is placed at the PMI: the probe indicator pointed towards the patient's left axilla. Left lateral decubitus will be extremely helpful for this view. 
  • The probe needs to be as flat to patient surface as possible to obtain view of all four chambers.
  • Be sure to glance at the ratio of the RV to LV diameter which should be <0.6. Greater than this should raise suspicion for RV overload or PE.
  • If you are confused about which ventricle is which, look at the septum, the tricuspid valve inserts more apically than the mitral valve, making the LV appear longer than the RV. 


Intraventricular Dependence
Intraventricular Dependence Tamponade Physiology
Tamponade Physiology Pericardial Effusion
Pericardial Effusion

You are looking for an anechoic stripe surrounding the cardiac muscle. Subcostal is the most sensitive but parasternal long axis can also be used. You can grade pericardial effusions based on size ( <0.5 cm = small, > 2.0 cm = large) however rate of accumulation is more critical to possible hemodynamic compromise. You want to know if there is tamponade physiology!

  • Tamponade clinically can appear as hemodynamic compromise with associated pericardial effusion (don't forget Beck's classic triad is hypotension, distended neck veins and muffled heart sounds)
  • On your PSLA view, identify the descending thoracic aorta (DTA). If you have an effusion visible, identify if anterior to DTA (pericardial) or posterior to DTA (pleural). 
  • Echo Findings of tamponade:
    • RV collapse in diastole: More specific for tamponade than RA collapse but less specific 
      • Think of the man 'jumping on the trampoline' where the trampoline is the RV.
      • One easy way to determine if RV collapse is truly during systole is to use M-mode via PSLA. Look for RV free wall collapse when mitral valve is open. 
    • RA collapse in systole 
      • More difficult to see as the RA is often not visualized but is usually impressive when it's there. 
    • MV/TV inflow variation: With a pericardial effusion, the ventricles take on more interdependence (see image above) since they now have a limited space to expand from external fluid compression. 
      • Normal respiratory variation in LV flow will be exaggerated in tamponade resulting in pulsus paradoxus. This can be visualized by ultrasound using pulse wave doppler gate at the mitral valve or tricuspid valve. Normal change in flow is 15% at MV, 25% at TV. Any more than this is concerning for tamponade. 
    • IVC Collapse
      • Obtain a subcostal long axis view  to assess for a distended, non collapsible IVC which would suggest high filling pressures and possible tamponade. 






More Resources:

Previous Posts: 

Acute Aortic Dissection

Author: Jennifer Robertson, MD (Attending Physician – EM, Cleveland Clinic) // Editor: Alex Koyfman, MD

General Info
Aortic dissection is a life-threatening yet infrequent diagnosis, estimated at about three cases in every 100,000 person years (1,2). Because of its low frequency and emergency nature, large randomized controlled trials are difficult to conduct (3). Thus, the International Registry of Acute Aortic Dissection (IRAD) was established in 1996 to obtain up-to-date data on patients with acute aortic dissection. Currently, 30 large referral centers in 11 countries participate. Most novel research on aortic dissection is based on IRAD data.

Aortic dissection is defined as disruption of the layers of the aorta. On occasion, the dissection may originate from a penetrating atherosclerotic ulcer or from an intramural hematoma (4,5). However in 90% of patients, dissection occurs from a primary tear in the intima (4). Blood then travels through the media, resulting in separation of the layers and a false lumen. Under high blood pressure, the dissection can then propagate along the entire length of the aorta (4,6) and hypoperfusion can occur, usually by obstruction of the true lumen (6,7).

Although not present in most patients with dissection, aneurysm is a known risk factor (4). Other risk factors include family history of aneurysm, hypertension, old age, atherosclerosis, Marfan Syndrome, Turner Syndrome, Ehlers-Danlos syndrome, bicuspid aortic valve, and history of aneurysmal or dissection repair (4,6,8,9,10). Cocaine use and even heavy weight lifting are also risk factors (4).

By definition, the diagnosis of acute aortic dissection is made within 2 weeks after initial symptoms while chronic aortic dissection is made after 2 weeks (6). Generally, dissections are classified by their location. Two well-known classification schemes include the Stanford and DeBakey systems. In the Stanford classification, type A includes the ascending aorta and type B does not. The DeBakey classification includes types 1 through 3 with type 1 involving the entire aorta, type 2 involving the ascending aorta and type 3 involving the descending aorta. Classification is important as it helps determine surgical or medical management (4).

Recap Basics
The diagnosis of aortic dissection requires a high level of suspicion (4). Symptoms of dissection may be similar to other conditions such as acute coronary syndrome, pleurisy, and even stroke (6). The diagnosis should be considered in any patient with syncope, chest pain, back pain, abdominal pain, and/or unexplained neurologic deficits (4).

Pain is the most common symptom and 90% of patients present with back and/or chest pain (4). The pain is typically described as sharp, ripping, or tearing and can migrate as the dissection progresses. In a 2002 review article by Klompas, 274 articles were identified to evaluate for signs and symptoms of acute aortic dissection (11). The sensitivity of any pain was 90% while pain of sudden onset had 84% sensitivity. A pulse deficit, as well as focal neurologic deficits, was also supportive of the diagnosis (11). “Painless” dissection can also occur but is rarer and occurs in patients with heart failure, syncope, or neurologic symptoms (4). Heart failure is related to severe aortic regurgitation and syncope may occur due to aortic rupture or hemopericardium with cardiac tamponade (12). Vascular compromise can occur in any junctional vessel causing syndromes such as acute myocardial infarction, paraplegia, mesenteric ischemia, and limb ischemia (6).

Physical exam can also vary. Most patients with type B dissection are hypertensive upon presentation, while many with type A dissections are normotensive. (6). Based on IRAD data of 591 patients with type A dissection, 32% were hypertensive, 45% normotensive and 14% hypotensive (13). On the other hand, of 384 patients with type B dissection, 69% were hypertensive and only 3% were hypotensive (9). Interestingly, in both type A and type B dissections, pulse deficits were found to be uncommon and only found to be present in about one quarter of patients (9,13). An adequate vascular exam is still necessary, however, and should be done on all patients with suspected aortic dissection (4).

Any suspicion of aortic dissection should prompt clinicians to initiate work-up immediately. An initial chest x-ray may provide some clues as it may show abnormal aortic contour, pleural effusion, intimal calcification, or wide mediastinum. However, it is important to note that chest x-rays are normal in 12 to 15% of patients with dissection (4). Thus, a negative x-ray does not exclude dissection. Additionally, electrocardiography (EKG) is also usually normal or non-specific (6). However, per current American Heart Association (AHA) and American College of Cardiology Foundation (ACCF) guidelines, an EKG should always be obtained as myocardial infarction is more common than dissection and any EKG abnormalities should be treated as a primary cardiac event 4).

Overall, the presentation of thoracic aortic dissection is inconsistent, and cannot be ruled out based on medical history, examination, EKG, or plain radiography findings. Thus, if aortic dissection is suspected at all, clinicians should initiate more definitive testing such as computed tomographic (CT) imaging, magnetic resonance imaging, or transesophageal echocardiography (TEE) (4,6). All three imaging studies have high sensitivity and specificity in diagnosing aortic dissection (4,14).

The death rate in acute dissection is as high as 1% per hour in the first 24 hours (4,15). Treatment must, thus, be immediately initiated. Early management includes controlling blood pressure and heart rate, which decreases aortic wall pressure. Intravenous beta blockers such as esmolol, metoprolol or labetalol, should be initiated and titrated to a heart rate less than 60 bpm and a systolic blood pressure of 100 to 120 mmHg (4,6,16). If patients have contraindications to beta blockade, non-dihydropyridine calcium channel blockers may be used instead (4). Beta blockers should also be used cautiously in acute aortic regurgitation. If systolic blood pressure remains greater than 120 mmHg after adequate beta blockade or rate control, then vasodilators should be administered (4). Agents such as nicardipine, nitroglycerin and sodium nitroprusside may be used (4,16). If vasodilators are used, it is important to note that they should never be given prior to beta blockade as this can lead to reflex tachycardia and greater aortic wall stress.

If the patient is hypotensive, medical management is limited, as surgery is really what is required (4). One should always immediately administer fluids. Although vasopressors can be added to maintain adequate perfusion, they can increase aortic stress and worsen the clinical picture. Per the AHA/ACCF, any hypotension or shock in acute dissection really suggests need for immediate operative management (4).

All patients should be transferred to tertiary care centers where staff is experienced in managing aortic dissections. Type A dissections should be evaluated more urgently for surgical repair as immediate life threatening complications such as rupture can occur. Per AHA guidelines, type b dissections can be managed medically unless life threatening complications such as hypoperfusion, enlarging aneurysm or progress occur (4). Regardless of location, however, the AHA does recommend surgical consultation for all aortic dissections, regardless of location (4).

What’s New
Although not new, one topic that remains a source of debate is the use of D-dimer and its role in the diagnosis, namely the rule out of, aortic dissection (please go here for extended discussion: While many studies have shown a high sensitivity of D-dimer in ruling out dissection, especially in the first 24 hours, (9,17,18), others have shown conflicting data (19,20,21). In order to rule out an aortic dissection with a negative d-dimer, the pre-test probability has to be very low. D-dimer may be useful to rule out the diagnosis in low-risk patients (18) but currently, there are no validated scoring systems, such as the Well’s score for pulmonary embolism, that can determine patients’ pre-test probability (4,22,23). However, in 2010, the AHA/ACCF did publish a risk scoring system called the aortic dissection risk score (ADD) that divides patients into low, intermediate, and high risk of aortic dissection (4). The full algorithm can be viewed in the article by Hiratzka et al, but essentially it helps clinicians risk-stratify patients. Recent research has found this risk score to be highly sensitive (95%) for detecting aortic dissection (24).

Most recently, other studies have evaluated the aortic dissection detection (ADD) risk score and its combined use with d-dimer for ruling out aortic dissection. Nazerian et al published data in 2014 that evaluated the ADD risk score plus D-dimer to help rule out aortic dissection. They found that D-dimer 5.5 cm Is Not a Good Predictor of Type A Aortic Dissection: Observations from the International Registry of Acute Aortic Dissection (IRAD). Circulation 2007;116:1120-1127.
14) Shiga T, Wajima Z, Apfel CC, et al. Diagnostic Accuracy of Transesophageal Echocardiography, Helical Computed Tomography, and Magnetic Resonance Imaging for Suspected Thoracic Aortic Dissection: Systematic Review and Meta-analysis. Arch Intern Med 2006;166:1350-1356.
15) Trimarchi S, Eagle K, Nienaber CA, et al. Role of Age In Acute Type A Aortic Dissection Outcome: Report from the International Registry of Acute Aortic Dissection (IRAD). J Thorac Cardiovasc Surg 2010;140:784-9.
16 Tsai TT, Nienaber CA, Eagle KA. Acute Aortic Syndromes. Circulation 2005; 112: 3802-3813.
17) Shimony A, Filion K, Mottillo S, et al. Diagnosis of Acute Aortic Dissection By D-Dimer: A Meta-Analysis. Can J Cardiol 2010; 26: 60D.
18 Marill KA. Serum D-Dimer is a Sensitive Test for the Detection of Acute Aortic Dissection: A Pooled Meta-Analysis. J Emerg Med 2008; 34(4): 367-376.
19) Paparella D, Malyndi PG, Scrascia G, et al. D-Dimers Are Not Always Elevated In Patients with Acute Aortic Dissection. J Cardiovasc Med 2009; 10 (2): 212-214.
20) Wieganda J, Kollerb M, Bingissera R. Does Negative D-Dimer Test Rule Out Aortic Dissection? Swiss Med Wkly 2007; 137: 462.
21 Sutherland A, Escano TP, Coon TP. D-Dimer as the Sole Screening Test for Acute Aortic Dissection: A Review of the Literature. Ann Emerg Med 2008 ;52:339-343.
22) Wells PS, Anderson DR, Rodger M, et al. Derivation of a Simple Clinical Model To Categorize Patients Probability of Pulmonary Embolism: Increasing the Models Utility with the SimpliRED D-Dimer. J Thromb Haemost 2000; 83 (3): 416-420.
23) Brown MD, Newman DH. Can a Negative D-Dimer Result Rule Out Acute Aortic Dissection? Ann Emerg Med 2011; 58 (4): 375-76.
24) Rogers AM, Hermann LK, Booher AM, et al. Sensitivity of the Aortic Dissection Detection Risk Score, a Novel Guideline-Based Tool for Identification of Acute Aortic Dissection at Initial Presentation: Results From the International Registry of Acute Aortic Dissection. Circulation 2011;123:2213-2218.
25) Nazerian P, Morello F, Vanni S, et al. Combined Use of Aortic Dissection Detection Risk Score and D-Dimer in the Diagnostic Workup of Suspected Acute Aortic Dissection. Int J Cardiol 2014; 175 (1): 78-82.
26) Nazerian P, Morello F, Vanni S, et al. Combined Use of a Standardized Risk Score and D-Dimer to Rule Out Acute Aortic Dissection in the Emergency Department. Eur Heart J 2013; 34 (suppl 1): 5939.
27) Bayes AA, Cochon L. 133 Improved Rule-Out Diagnostic Gain with a Combined Aortic Dissection Detection Risk Score and D-Dimer Bayesian Decision Support Scheme. Ann Emerg Med 2014; 64 (4): S48.

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Dan Hasse – Echocardiographic Evaluation of Right Ventricular (RV) Dysfunction

Dr. Hasse is a man of many talents. Trained in emergency medicine, surgical critical care, critical care medicine, and understands the value of Point of Care Ultrasound (POCUS). This week he’s addressing the often under appreciated and under recognized importance of RV dysfunction. Done a TAPSE of the RV lately? If not, take notes and…

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Caso 156: Metástasis pulmonares; RX: “suelta de globos”

Mujer de 72 años con disnea progresivamente en aumento de dos semanas de evolución asociada a hematuria sin clínica miccional.


Exploración general: PA 134/70 mmHg. Fc 96 lpm. Tª 36.4ºC. SO2 80% (aire ambiente) Fr 28 rpm. Taquipnea sin tiraje con buena respuesta a O2 en ventimax al 31% -> SO2 93%.

Rx de Tórax: múltiples nódulos pulmonares en ambos campos pulmonares.

Gasometría Arterial basal: pH 7.35, pO2 42, pCO2 35, Bicarbonato 19, SO2 80.

-> Severa Insuficiencia respiratoria parcial (pO2 baja con pCO2 normal).

Llama la atención una Rx tan horrible con clínica de disnea de tan solo 2 semanas.

Se realiza Angi TC Torácico que no evidencia imagen de TEP y objetiva múltiples lesiones nodulares, de distribución difusa en ambos campos pulmonares, de tamaño comprendido entre 1 y 3.5 cm, compatibles con METÁSTASIS PULMONARES.

Comentario: se le llama NÓDULO a una lesión < de 3 cm. MASA si es > de 3 cm. Múltiples nódulos o masas (“suelta de globos”) sugieren METÁSTASIS de un origen a determinar.

En este caso los cortes bajos del TC evidenciaban un riñón derecho patológico y se amplió el estudio TC a abdomen y pelvis -> Lesión vegetante de 2.5 cm en vejiga con atrapamiento ureteral e hidronefrosis derecha.

La paciente queda ingresada con sospecha de MTX pulmonares 2ªs a CANCER de vejiga.

Biopsia de vejiga: Carcinoma papilar uretelial de bajo grado.

Citología de esputo: frotis positivo para células malignas concordante con carcinoma pobremente diferenciado. En la IHQ:  Positivo (+): CK 7 y P 63; Negativo (-): CK 20, TTF1, Sinaptofisina y Calretitina.

Comentado el caso con oncología se decide quimioterapia paliativa con CDDP-Gemcitabina que se suspende por Neutropenia + trombocitopenia. De forma asociada, la paciente presenta edema en EII por lo que se realiza Ecodopler que confirma TVP de dicha pierna izquierda. Se inicia anticoagulación con Innohep/24h + media de compresión fuerte.

Comentario: está suficientemente demostrada la asociación del tabaquismo con el cáncer de pulmón y con el de vejiga. En el caso que aquí se presenta me gustaría aclarar que la paciente no era fumadora en su juventud ni en su etapa adulta, empezó a fumar recientemente: 1 cigarro/día, desde hace 5 años.

Ojito con la HEMATURIA: frecuentemente se asocia a cistitis de gente joven; en los pacientes de más edad -> pensar en neoplasia. El diagnóstico tardío, como en este caso, tiene severas implicaciones en el pronóstico de dicha enfermedad.







Damage Control Resuscitation

Massive Transfusion


Damage Control Resuscitation has been the hot topic to discuss in the adult trauma bays.  Naturally, this conversation has been also heard more commonly during pediatric trauma resuscitations.  What is it and does it really apply to kids?  Great questions!  Fortunately, a nice review article was published last month (Hughes, Ped EM Care: 2014) that I encourage you all to read… but I’ll do my best to recap.


Damage Control Resuscitation

  • Strategies applied to caring for hemorrhagic shock in the severely traumatized patient.
    • Fortunately, the vast majority of your pediatric trauma patients will NOT fit into this category.
    • Intended for patients in whom severe hemorrhage necessitates transfusions of large-volumes of blood products.
  • Aimed at helping to avoid or diminish the Lethal Triad of Trauma Management: Acidosis, Hypothermia, Coagulopathy.
    • The traditional approach of giving large volumes of isotonic saline can exacerbate all of these conditions.
    • Even large volumes of PRBCs can lead to electrolyte changes (ex, hyperKalemia) and coagulopathy.
  • Has three core concepts:
    • Acute Coagulopathy of Trauma
    • Permissive Hypotension
    • Massive Transfusion & Hemostatic Resuscitation


Acute Coagulopathy of Trauma

  • The vast majority of healthy children do not require Coagulation studies prior to surgery (ex, the patient with appendicitis), unlike the adult population.
  • Interestingly though, it has been found that pediatric trauma patients can present with acute coagulopathy associated with their trauma.
    • This is distinct from the coagulopathy that can develop during the resuscitation due to administered therapies.
    • Theories = tissue factor release, Protein C activation, Hyperfibrinolysis.
    • Also studies that show association with Traumatic Brain Injury and acute coagulopathy.
  • This does not mean that ever kid in a car crash needs 1,000 labs looking for coagulopathy, though!


Permissive Hypotension

  • We all know that any hypotension that occurs during medical resuscitations is associated with higher mortality, but can hypotension be “ok” in trauma?
  • Observations that patients with uncontrolled hemorrhage may have worsening shock after IV fluids seem counterintuitive.
    • Perhaps the increased volume and/or pressure leads to a tenuous clot being dislodged.
    • Perhaps the increased volume further dilutes the already over-utilized coagulation factors.
    • Perhaps there is some other inflammatory change or cellular structure alteration (ex, swelling) as a result of the IV fluids.
  • The practice of Permissive Hypotension is the plan of tolerating below normal BPs and limiting IV fluids until definitive management of the bleeding can be performed (surgery or embolization).
    • What is the goal BP?  Dunno.
    • Ideally, you need to still maintain enough end-organ perfusion pressure to keep the vital organs alive.
  • It works in animals and some adults. How about kids?
    • While we are all mammals, pediatric patients may not benefit as much from this management strategy as adults or other studied animals.
    • Children are able to tolerate hypovolemia much better than adults.
      • Kids can compensate for up to 45% of blood volume loss prior to becoming hypotensive.
      • If you already have a child that is hypotensive, you are in the very deep dark woods.
    • Children are often have head injuries, which don’t respond well to hypotension.
    • There have been no pediatric studies that demonstrate utility in permissive hypotension in pediatric trauma patients to date.


Massive Transfusion Protocols & Hemostatic Resuscitation

  • Refers to the use of Fresh Frozen Plasma and Platelets along with Packed Red Blood Cells in ratios to approximate whole blood.
  • The best ratio is not known, but often protocols use 1:1:1.
  • Does it work in children?
    • Cases reports of non-traumatic, intra-operative hemorrhage being successfully managed with massive transfusion protocols.
    • No studies of pediatric trauma patients show any mortality benefit from massive transfusion protocols to date.


First do no harm!

  • Massive Transfusions have been associated with cardiac arrest in pediatric patients.
  • Transfusion-Associated Hyperkalemic Cardiac Arrest (TAHCA) is rare, but can occur.
  • Possible strategies to reduce the risk of TAHCA:
    • Use fresher RBCs for massive transfusions
    • Use Large Bore PERIPHERAL IVs instead of central lines (remember there is more resistance in a long central line)
    • Check for and correct electrolyte abnormalities frequently.


Hughes NT1, Burd RS, Teach SJ. Damage control resuscitation: permissive hypotension and massive transfusion protocols. Pediatr Emerg Care. 2014 Sep;30(9):651-6; quiz 657-8. PMID: 25186511. [PubMed] [Read by QxMD]

Lee AC1, Reduque LL, Luban NL, Ness PM, Anton B, Heitmiller ES. Transfusion-associated hyperkalemic cardiac arrest in pediatric patients receiving massive transfusion. Transfusion. 2014 Jan;54(1):244-54. PMID: 23581425. [PubMed] [Read by QxMD]

Parker RI. Transfusion in critically ill children: indications, risks, and challenges. Crit Care Med. 2014 Mar;42(3):675-90. PMID: 24534955. [PubMed] [Read by QxMD]

Nosanov L1, Inaba K, Okoye O, Resnick S, Upperman J, Shulman I, Rhee P, Demetriades D. The impact of blood product ratios in massively transfused pediatric trauma patients. Am J Surg. 2013 Nov;206(5):655-60. PMID: 24011571. [PubMed] [Read by QxMD]

Chidester SJ1, Williams N, Wang W, Groner JI. A pediatric massive transfusion protocol. J Trauma Acute Care Surg. 2012 Nov;73(5):1273-7. PMID: 23064608. [PubMed] [Read by QxMD]

Chidester SJ1, Williams N, Wang W, Groner JI. A pediatric massive transfusion protocol. J Trauma Acute Care Surg. 2012 Nov;73(5):1273-7. PMID: 23064608. [PubMed] [Read by QxMD]

Dehmer JJ1, Adamson WT. Massive transfusion and blood product use in the pediatric trauma patient. Semin Pediatr Surg. 2010 Nov;19(4):286-91. PMID: 20889085. [PubMed] [Read by QxMD]

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