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Critical Care

Last 50 Critical Care Postings

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Severe Accidental Hypothermia in Phoenix? Active Rewarming Using 
   Thoracic Lavage
Left Ventricular Assist Devices: A Brief Overview
July 2019 Critical Care Case of The Month: An 18-Year-Old with
   Presumed Sepsis and Progressive Multisystem Organ Failure 
An Observational Study Demonstrating the Efficacy of Interleukin-1 
   Antagonist (Anakinra) in Critically-ill Patients with Hemophagocytic
Which Half Are You? Almost Half of Pediatric Oncologists and Intensivists
   Are Burnt Out……
Management of Refractory Hypoxemic Respiratory Failure Secondary to
   Diffuse Alveolar Hemorrhage with Venovenous Extracorporeal Membrane
Amniotic Fluid Embolism: A Case Study and Literature Review
April 2019 Critical Care Case of the Month: A Severe Drinking
Ultrasound for Critical Care Physicians: An Unexpected Target Lesion
January 2019 Critical Care Case of the Month: A 32-Year-Old Woman
   with Cardiac Arrest
The Explained Variance and Discriminant Accuracy of APACHE IVa 
Severity Scoring in Specific Subgroups of ICU Patients
Ultrasound for Critical Care Physicians: Characteristic Findings in a 
   Complicated Effusion
October 2018 Critical Care Case of the Month: A Pain in the Neck
Ultrasound for Critical Care Physicians: Who Stole My Patient’s Trachea?
August 2018 Critical Care Case of the Month
Ultrasound for Critical Care Physicians: Caught in the Act
July 2018 Critical Care Case of the Month
June 2018 Critical Care Case of the Month
Fatal Consequences of Synergistic Anticoagulation
May 2018 Critical Care Case of the Month
Airway Registry and Training Curriculum Improve Intubation Outcomes in 
   the Intensive Care Unit
April 2018 Critical Care Case of the Month
Increased Incidence of Eosinophilia in Severe H1N1 Pneumonia during 2015
   Influenza Season
March 2018 Critical Care Case of the Month
Ultrasound for Critical Care Physicians: Ghost in the Machine
February 2018 Critical Care Case of the Month
January 2018 Critical Care Case of the Month
December 2017 Critical Care Case of the Month
November 2017 Critical Care Case of the Month
A New Interventional Bronchoscopy Technique for the Treatment of
   Bronchopleural Fistula
ACE Inhibitor Related Angioedema: A Case Report and Brief Review
Tumor Lysis Syndrome from a Solitary Nonseminomatous Germ Cell Tumor
October 2017 Critical Care Case of the Month
September 2017 Critical Care Case of the Month
August 2017 Critical Care Case of the Month
Telemedicine Using Stationary Hard-Wire Audiovisual Equipment or Robotic 
   Systems in Critical Care: A Brief Review
Carotid Cavernous Fistula: A Case Study and Review
July 2017 Critical Care Case of the Month
High-Sensitivity Troponin I and the Risk of Flow Limiting Coronary Artery 
   Disease in Non-ST Elevation Acute Coronary Syndrome (NSTE-ACS)
June 2017 Critical Care Case of the Month
Clinical Performance of an Interactive Clinical Decision Support System for 
   Assessment of Plasma Lactate in Hospitalized Patients with Organ
May 2017 Critical Care Case of the Month
Management of Life Threatening Post-Partum Hemorrhage with HBOC-201 
   in a Jehovah’s Witness
Tracheal Stoma Necrosis: A Case Report
April 2017 Critical Care Case of the Month
March 2017 Critical Care Case of the Month
Ultrasound for Critical Care Physicians: Unchain My Heart
February 2017 Critical Care Case of the Month
January 2017 Critical Care Case of the Month
December 2016 Critical Care Case of the Month


For complete critical care listings click here.

The Southwest Journal of Pulmonary and Critical Care publishes articles directed to those who treat patients in the ICU, CCU and SICU including chest physicians, surgeons, pediatricians, pharmacists/pharmacologists, anesthesiologists, critical care nurses, and other healthcare professionals. Manuscripts may be either basic or clinical original investigations or review articles. Potential authors of review articles are encouraged to contact the editors before submission, however, unsolicited review articles will be considered.



Severe Accidental Hypothermia in Phoenix? Active Rewarming Using Thoracic Lavage

Michael Mozer BS1

Guy Raz, MD2

Ryan Wyatt, MD2

Alexander Toledo, DO, PharmD2

1University of New England College of Osteopathic Medicine

Biddeford, ME USA

2Department of Emergency Medicine

Maricopa Medical Center, Phoenix, AZ USA



Hypothermia can progress quickly and become life threatening if left untreated. Rewarming in the severely hypothermic patient is of critical importance and is achieved with active and passive techniques. Here we present a case of a hypothermic patient with cardiac instability for whom thoracic lavage was ultimately used. We will review the treatment of hypothermia and discuss the technical aspects our approach.

Case Presentation

A 53 year-old male with a past medical history of substance abuse, chronic hepatitis C, and poorly controlled type 2 diabetes mellitus complicated by a recent hospitalization for osteomyelitis was brought to the emergency department after being found lying on a road in a shallow pool of water in the early morning hours of a rainy day in Phoenix, Arizona. The ambient temperature that night was 39 °F (3.9 °C). Emergency Medical Services (EMS) noted a decreased level of consciousness and obtained a finger stick glucose of 15 mg/dl. EMS reported a tympanic membrane temperature of 23.9 °C. En route, the patient was administered 2mg naloxone and 25g dextrose intravenously with no improvement in his mental status. On Emergency Department (ED) arrival, the patient had a GCS of 8 (Eyes 4, Verbal 1, Motor 3) and exhibited intermittent posturing. His foot wound appeared clean and without signs of infection. The initial core temperature recorded was 25.9°C via bladder thermometer, systolic blood pressure was 92/50, and heart rate fluctuated between 50 and 90 beats per minute.

After removing wet clothing, initiation of warmed saline, and placing a forced warm air blanket on the patient, he was intubated for airway protection and vasopressors were initiated. Osborn waves were evident on the initial EKG (Figure 1).

Figure 1. Initial EKG with Osborn Waves (arrows).

A warmed ventilator circuit was initiated with only 0.5 °C increase in temperature in first 30 minutes. Despite these measures, he remained hypotensive and unstable. Significant laboratory findings were a white blood cell count of 25.5 thousand (92% neutrophils), lactic acid of 7.6, potassium of 5.8, serum creatinine of 1.05, glucose of 283, INR of 1.1, and urine drug screen positive for cocaine. Given his recalcitrance to norepinephrine and risk of death secondary to fatal dysrhythmia with temperatures below 28 °C intrathoracic lavage initiated.

The right hemithorax was selected for irrigation because left-sided tube placement can induce ventricular fibrillation in a perfusing patient (1). Using standard sterile technique, two 36 French thoracostomy tubes were placed; the first in the second intercostal space along the mid-clavicular line, and the second in the 5th intercostal space in the posterior axillary line (1-3). The tips of the thoracostomy tubes were oriented such that the anterior-superior tube was positioned near the right apex and the lateral-inferior tip was positioned low in the thoracic cavity (1,3). To maintain the temperature of the instilled fluid, a fluid warmer system (Level 1; Smiths Medical; Minneapolis, MN) was used and set to 41 °C. A Christmas tree adapter was used to connect the IV tubing to the superior thoracostomy tube, and a water seal chamber was attached to the inferior tube for passive drainage (3). Flow through the system was targeted to maintain steady passive drainage as described in the literature (1-6).

Thoracic cavity lavage with 41 °C saline was performed and the patient was transferred to the medical ICU after 3 hours in the ED. When he was transferred his core temperature was 29 °C and he remained on norepinephrine for hemodynamic instability. After 2 hours of continued rewarming in the MICU, his core temperature was 32 °C. Osborn waves evident on initial EKG were resolved (Figure 2).

Figure 2. Repeat EKG showing resolution of Osborn waves.

The patient left against medical advice from the hospital 4 days later neurologically intact and without sequela.


Hypothermia can be clinically classified as mild, moderate or severe (7). Mild hypothermia, defined as core temperatures of 32-35 °C, presents with shivering. Amnesia, dysarthria, ataxia, tachycardia, and tachypnea can also be seen (1). Moderate hypothermia, defined as core temperatures of 28-32 °C, usually can present with or without shivering. Stupor, hypoventilation, paradoxical undressing and non-fatal arrhythmias such as atrial fibrillation and junctional bradycardia may also be seen (1). Patients with severe hypothermia, generally defined as temperatures below 28 °C, can present with coma, areflexia, pulmonary edema, bradycardia, and hypotension (1). There is a significant risk of fatal cardiac dysrhythmias without rapid therapeutic rewarming (1,7,8).

Rewarming in the hypothermic patient is of critical importance and is achieved with passive and/or active techniques. Attempts to limit heat loss are often unsuccessful, especially in the absence of a normal shiver response. It however remains as the first line treatment for hypothermia (8-10). Passive rewarming is attempted by the removal of cold/wet clothing and keeping the patient covered (8-10). Active external rewarming (AER) is the next line of treatment and consist of the use of externally rewarming devices such as warmed blankets, warm environment, forced air warming (Bair Hugger; 3M; Maplewood, MN) or warm hot water bladders placed in the groin and axilla (1,7-10). Active Internal Rewarming (AIR) techniques can be used to achieve more rapid increases in core temperature and are primarily utilized in cases of cardiac instability or if AER is unsuccessful (8). When available, the method of choice for active internal rewarming (AIR) is cardiopulmonary bypass (CPB) or extracorporeal membrane oxygenation (ECMO) as they can achieve the fastest increase in core temperature (9 °C/hr and 6 °C/hr respectively) and provide cardiovascular support (1,8,11,12). Several techniques are described in the literature that can be considered if CPB or ECMO are unavailable. These include esophageal warming devices, endovascular catheters, hemodialysis, and endocavitary lavage (1,2,4-6,13-15). While no randomized controlled trials exist, several case reports and reviews have tried to compare various techniques. These sources to do not seem to favor any particular technique over another but rather reports the rates of temperature rise (1-3,5-7,13-15). Classically, lavage techniques are attempted in the thoracic cavity, the peritoneum, the bladder, the stomach, the esophagus, or the colon. These techniques are generally coupled with warm IV fluids and warming air through the ventilator to limit loss of body heat to iatrogenic procedures during the rewarming attempt (1,7). Thoracic lavage is effective with a reported rewarming rates of 3-6 °C/hr and with excellent outcomes in case reports (1,2,4-6). Here we present a case of a hypothermic patient with cardiac instability where thoracic lavage is used and discuss the technical aspects of this approach.

Our case demonstrates the efficacy of utilizing thoracic cavity lavage for rapid rewarming in patients with severe hypothermia with a pulse and at high risk of fatal cardiac arrhythmia. In multiple case reports, thoracic lavage has been used successfully in hypothermic patients who suffered complete cardiopulmonary collapse requiring CPR (2,4,5). Although warm thoracic lavage is not the treatment of choice in these circumstances, in a facility not equipped with ECMO or CPB and a patient too unstable to transfer, it seemed to us to be the best technique. Gastric, colonic, and bladder lavage offer very minimal heat transfer due to limitations in surface area (2).

Hemodialysis would have required for us to call in a technician and would have required approval by a nephrologist at our institution. Available central venous rewarming catheters require bypass of a failsafe mechanism that does not allow rewarming to be initiated below 30 °C (1). Peritoneal lavage was a plausible choice but does not directly warm the mediastinum (2). While an open mediastinal technique has been used, we did not feel it was appropriate in a patient with a concurrent pulse (1,3). Thoracic lavage is therefore an effective alternative that should be used in cases where CPB and ECMO are unavailable especially in a patient that is hemodynamically unstable and may not survive transfer. The equipment is readily available to any Emergency Medicine or Critical Care physician. In addition, this case exemplifies the positive outcomes that are associated with rapid rewarming in the hypothermic patient with a pulse. We believe our case demonstrates the efficacy of this technique for myocardial protection from hemodynamic collapse, a topic which has not been adequately studied in the literature.


  1. Brown DJ, Danzl DF. Accidental hypothermia. In: Auerbach PS, ed. Wilderness Medicine. 7th ed. St. Louis: Mosby Inc.; 2017:135-62.
  2. Plaisier BR. Thoracic lavage in accidental hypothermia with cardiac arrest--report of a case and review of the literature. Resuscitation. 2005 ;66(1):99-104. [CrossRef] [PubMed]
  3. Schiebout JD. Hypothermic Patient Management. In: Reichman EF. eds. Reichman's Emergency Medicine Procedures, 3e New York, NY: McGraw-Hill. Available at: (accessed August 02, 2019).
  4. Little G. Accidental hypothermic cardiac arrest and rapid mediastinal warming with pleural lavage: A survivor after 3.5 hours of manual CPR. BMJ Case Reports. July 2017:bcr-2017-220900. [CrossRef] [PubMed]
  5. Turtiainen J, Halonen J, Syväoja S, Hakala T. Rewarming a patient with accidental hypothermia and cardiac arrest using thoracic lavage. Ann Thorac Surg. 2014 Jun;97(6):2165-6. [CrossRef] [PubMed]
  6. Ellis MM, Welch RD. Severe hypothermia and cardiac arrest successfully treated without external mechanical circulatory support. Am J Emerg Med. 2016;34(9):1913.e5-6. [CrossRef] [PubMed]
  7. Tintinalli J, Stapczynski J, Ma O, Yealy D, Meckler G, Cline D. Tintinalli's Emergency Medicine. 8th ed. New York, NY: McGraw-Hill Education; 2016:1743-4.
  8. Brugger H, Boyd J, Paal P. Accidental Hypothermia. N Engl J Med. 2012;367(20):1930-8. [CrossRef] [PubMed]
  9. Paal P, Gordon L, Strapazzon G, et al. Accidental hypothermia-an update: The content of this review is endorsed by the International Commission for Mountain Emergency Medicine (ICAR MEDCOM). Scand J Trauma Resusc Emerg Med. 2016;24(1):111. [CrossRef] [PubMed]
  10. Zafren K, Giesbrecht GG, Danzl DF, et al. Wilderness Medical Society practice guidelines for the out-of-hospital evaluation and treatment of accidental hypothermia: 2014 update. Wilderness Environ Med. 2014 Dec;25(4 Suppl):S66-85. [CrossRef] [PubMed]
  11. Schober A, Sterz F, Handler C, et al. Cardiac arrest due to accidental hypothermia-A 20 year review of a rare condition in an urban area. Resuscitation. 2014;85(6):749-56. [CrossRef] [PubMed]
  12. Saczkowski RS, Brown DJA, Abu-Laban RB, Fradet G, Schulze CJ, Kuzak ND. Prediction and risk stratification of survival in accidental hypothermia requiring extracorporeal life support: An individual patient data meta-analysis. Resuscitation. 2018;127:51-7.[CrossRef] [PubMed]
  13. Primozic KK, Svensek F, Markota A, Sinkovic A. Rewarming after severe accidental hypothermia using the esophageal heat transfer device: a case report. Ther Hypothermia Temp Manag. 2018 Mar;8(1):62-4. [CrossRef] [PubMed]
  14. Murakami T, Yoshida T, Kurokochi A, et al. Accidental hypothermia treated by hemodialysis in the acute phase: three case reports and a review of the literature. Intern Med. 2019 Jun 7. [CrossRef]
  15. Klein LR, Huelster J, Adil U, et al. Endovascular rewarming in the emergency department for moderate to severe accidental hypothermia. Am J Emerg Med. 2017 Nov;35(11):1624-9. [CrossRef] [PubMed]

Cite as: Mozer M, Raz G, Wyatt R, Toledo A. Severe accidental hypothermia in Phoenix? Active rewarming using thoracic lavage. Southwest J Pulm Crit Care. 2019;19(2):79-83. doi: PDF 


Left Ventricular Assist Devices: A Brief Overview

Bhargavi Gali MD

Department of Anesthesiology and Perioperative Medicine

Division of Critical Care Medicine

Mayo Clinic Minnesota

Rochester, MN, USA



Second and third generation left ventricular assist devices (LVAD) have been increasingly utilized as both a bridge to transplantation and as destination therapy (in patients who are not considered transplant candidates) for advanced heart failure. Currently approximately 2500 LVADs are implanted yearly, with an estimated one year survival of >80% (1). Almost half of these patients undergo implantation as destination therapy. A recent systematic review and meta-analysis found no difference in one-year mortality between patients undergoing heart transplantation in comparison with patients undergoing LVAD placement (2).

Early LVADs were pulsatile pumps, but had multiple limitations including duration of device function, and requirement for a large external lead that increased risk of infection. Currently utilized second and third generation devices are continuous flow (first generation were pulsatile flow). Second generation devices have axial pumps (HeartMate II®). The third generation LVADs ((HeartMate III®), HVAD®) are also continuous flow, with centrifugal pumps, which are thought to decrease possibility of thrombus formation and increase pump duration in comparison to the second generation axial pumps. It is also felt that a lack of mechanical bearings contributes to this effect.

LVADs support circulation by either replacing or supplementing cardiac output. Blood is drained from the left ventricle with inflow cannula in the left ventricular apex to the pump, and blood is returned to the ascending aorta via the outflow cannula (3) (Figure 1).

Figure 1. Third generation Left Ventricular Assist Device. Heartware System ™. Continuous flow left ventricular assist device (LVAD) configuration. One of the third generation LVADs is the HeartWare System. With this device the inflow cannula is integrated into the pump. The pump is attached to the heart in the pericardial space, with the outflow cannula in the aorta. A driveline connects the device to the control unit. This control unit is attached to the two batteries. (Figure used with permission from Medtronic).

The device assists the left ventricle by the action of the axial (second generation) or centrifugal (third generation) pump that rotates at a very high speed and ejects the blood into the aorta via the outflow cannula. A tunneled driveline connects the pump to the external controller that operates the pump function. The controller connects to the power source via two cables, which can be battery or module-powered.

LVADs offload volume from the left ventricle, and decrease left ventricular work. Pulmonary pressures and the trans pulmonary gradients are also decreased by the reduced volume in the left ventricle (4). End organ perfusion is improved secondary to enhanced arterial blood pressure and micro perfusion.

There are four main parameters of pump function:

  • Pump speed: the speed at which the LVAD rotors spin, and is programmed. Measured in RPM.
  • Pump power: the wattage needed to maintain speed and flow, which is the energy needed to run the pump. Measured in Watts.
  • Pump flow: estimate of the cardiac output, which is the blood returned to the ascending aorta, and is based on pump speed and power. Measure in L/min
  • Pulsatility index (PI): a calculated value that indicates assistance the pump provides, in relation to intrinsic left ventricular A higher number indicates higher left ventricular contribution to pulsatile flow.

The cardiac output of currently utilized LVADs is directly related to pump speed and inversely related to the pressure gradient across the pump. As the pump speed is fixed, right ventricular failure can decrease the volume of blood transmitted to the pump and decrease LVAD flow (3, 4). With right ventricular failure, inotropic support may be needed to improve the LVAD pump flow. High afterload, such as may be seen with an increase in systemic vascular resistance can decrease pump flow.


Adverse events occur in more than 70% of LVAD patients in the first year (5). These complications include infections, bleeding, stroke, and LVAD thrombosis. More than 50% of patients are readmitted within the first 6 months after LVAD implantation (6).

Driveline infections are the most commonly reported LVAD infection, and are the most likely to respond to treatment (7). Pump pocket infections may require debridement plus/minus antibiotic bead placement. Bloodstream infections are less commonly reported, and more difficult to treat, and many patients are placed on chronic suppressive antibiotic therapy (7). There is a possible association between stroke and bloodstream infection, reported in some studies. Patients who were younger and had a higher body mass index were noted to have a higher incidence of LVAD infections.

Gastrointestinal bleeding is a major cause of nonsurgical bleeding, reported in almost 30% of patients after LVAD placement (1). Patients may develop acquired von Willebrand factor deficiency secondary to high shear forces in the LVAD that lead to breakdown of von Willebrand protein (6). Antithrombotic therapy is commonly instituted after LVAD implantation which also increases risk of bleeding. A high incidence of arteriovenous malformations is reported in these patients, although the etiology is not clear. Transfusion, holding antithrombotic therapy, and identifying possible sources are included in the standard approach to management.

There is a high risk of both ischemic and hemorrhagic strokes in the first year after LVAD placement (8). Surgical closure of the aortic valve and off-axis positioning of the cannulas have been suggested as altering shear forces, increasing thrombotic risk, and thus risk of stroke.  Post-surgical risks may include pump thrombosis, infections, supratherapeutic INR, and poorly controlled hypertension. Early diagnosis has led to consideration of interventions such as thrombectomy (8).

LVAD thrombosis can occur on either cannula (inflow or outflow) or the pump. Typically patients receive ongoing anticoagulation, commonly with warfarin, and antiplatelet agents, and often aspirin. Heartmate II® may have higher rate of thrombosis than HVAD or Heart Mate 3, although this is under debate (6). Thrombotic complications range in severity from asymptomatic increase in lactate dehydrogenase or plasma-free hemoglobin, to triggering of LVAD alarms, up to development of heart failure. The inflow and outflow cannulas and pump can be the site of thrombosis. Management typically involves revising the antithrombotic management. If there is no improvement or worsening, replacement of LVAD may be indicated. There is limited evidence to suggest that systemic thrombolysis may be of benefit in treating pump thrombosis, particularly in regards to the HVAD, though better data would be useful

Procedural Management

When a patient with an LVAD requires non cardiac surgery, optimal management includes having an on-site VAD technician, and close involvement of VAD cardiology and cardiac surgery in consultation. Anticoagulation will often be transitioned to heparin infusion prior to elective procedures (9). Suction events (LV wall is sucked into the inflow cannula) can occur secondary to under filled left heart, and this can become more apparent perioperatively. This can also decrease right heart contractility by moving the interventricular septum to the left, and thus decrease cardiac output. Management often involves fluid bolus. Suction events can lead to decreased flow, left ventricular damage, and ventricular arrhythmias. Hemodynamic management can be challenging with non-pulsatile flow, and placement of an arterial line can facilitate optimal management. Postoperative care in a monitored setting is beneficial in case of further volume related events and to watch for bleeding.

Emergent Complications

Arrhythmias occur in many patients after LVAD implantation. Atrial arrhythmias are reported in up to half of LVAD patients, and ventricular arrhythmias in 22-59% (10, 11).  Loss of AV synchrony can lead to decreased LV filling and subsequent RV failure. Rhythm or rate control with rapid atrial arrhythmias is necessary to decrease development of heart failure. Ventricular arrhythmias may be hemodynamically tolerated for some time secondary to the LVAD support (6).  If there is concern that the inflow cannula is touching the LV septum, as may occur with severe hypovolemia, echocardiography can help determine if volume resuscitation should be the initial step in treating ventricular arrhythmia.

If cardiac arrest occurs, the first step of cardiopulmonary resuscitation in patients with LVAD is assessment of appropriate perfusion via physical examination (12). If perfusion is poor or absent, assessment of LVAD function should take place. If the LVAD is not functioning appropriately, checking for connections and power is the next step. If unable to confirm function or restart LVAD, chest compressions are indicated by most recent guidelines from the American Heart Association. There is always concern of dislodgement of LVAD cannula or bleeding during these situations.


Currently implanted LVADS are continuous flow, and provide support via a parallel path from the left ventricle to the aorta. As the number of patients with LVADs increase all medical providers should have a basic understanding of the function and common complications associated with these devices. This will enhance the ability to initiate appropriate care.


  1. Kirklin JK, Pagani FD, Kormos RL, et al. Eighth annual INTERMACS report: Special focus on framing the impact of adverse events. J Heart Lung Transplant. 2017 Oct;36(10):1080-6. [CrossRef] [PubMed]
  2. Theochari CA, Michalopoulos G, Oikonomou EK, et al. Heart transplantation versus left ventricular assist devices as destination therapy or bridge to transplantation for 1-year mortality: a systematic review and meta-analysis. Annals of Cardiothoracic Surgery. 2017;7(1):3-11. [CrossRef] [PubMed]
  3. Lim HS, Howell N, Ranasinghe A. The physiology of continuous-flow left ventricular assist devices. J Card Fail. 2017;23(2):169-80. [CrossRef] [PubMed]
  4. Roberts SM, Hovord DG, Kodavatiganti R, Sathishkumar S. Ventricular assist devices and non-cardiac surgery. BMC Anesthesiology. 2015;15(1):185. [CrossRef] [PubMed]
  5. Miller LW, Rogers JG. Evolution of left ventricular assist device therapy for advanced heart failure: a review. JAMA Cardiol. 2018 Jul 1;3(7):650-8. [CrossRef] [PubMed]
  6. DeVore AD, Patel PA, Patel CB. Medical management of patients with a left ventricular assist device for the non-left ventricular assist device specialist. JACC Heart Fail. 2017 Sep;5(9):621-31. [CrossRef] [PubMed]
  7. O'Horo JC, Abu Saleh OM, Stulak JM, Wilhelm MP, Baddour LM, Rizwan Sohail M. Left ventricular assist device infections: a systematic review. ASAIO J. 2018 May/Jun;64(3):287-294. [CrossRef] [PubMed]
  8. Goodwin K, Kluis A, Alexy T, John R, Voeller R. Neurological complications associated with left ventricular assist device therapy. pert Rev Cardiovasc Ther. 2018 Dec;16(12):909-17. [CrossRef] [PubMed]
  9. Barbara DW, Wetzel DR, Pulido JN, et al. The perioperative management of patients with left ventricular assist devices undergoing noncardiac surgery. Mayo Clinic Proceedings. 2013;88(7):674-82. [CrossRef] [PubMed]
  10. Enriquez AD, Calenda B, Gandhi PU, Nair AP, Anyanwu AC, Pinney SP. Clinical impact of atrial fibrillation in patients with the heartmate ii left ventricular assist device. J Am Coll Cardiol. 2014 Nov 4;64(18):1883-90. [CrossRef] [PubMed]
  11. Nakahara S, Chien C, Gelow J, et al. Ventricular arrhythmias after left ventricular assist device. Circ Arrhythm Electrophysiol. 2013 Jun;6(3):648-54. [CrossRef] [PubMed]
  12. Peberdy MA, Gluck JA, Ornato JP, et al. Cardiopulmonary resuscitation in adults and children with mechanical circulatory support: a scientific statement from the American Heart Association. Circulation. 2017;135(24):e1115-e34.`[CrossRef] [PubMed]

Cite as: Gali B. Left ventricular assist devices: a brief overview. Southwest J Pulm Crit Care. 2019;19(2):68-72. doi: PDF 


July 2019 Critical Care Case of The Month: An 18-Year-Old with Presumed Sepsis and Progressive Multisystem Organ Failure 

Robert A. Raschke, MD

The University of Arizona College of Medicine – Phoenix

Phoenix, AZ USA


Critical Care Case of the Month CME Information

Completion of an evaluation form is required to receive credit and a link is provided on the last page of the activity. 

0.50 AMA PRA Category 1 Credit(s)™

Estimated time to complete this activity: 0.50 hours

Lead Author(s): Robert A. Raschke, MDAll Faculty, CME Planning Committee Members, and the CME Office Reviewers have disclosed that they do not have any relevant financial relationships with commercial interests that would constitute a conflict of interest concerning this CME activity.

Learning Objectives: As a result of completing this activity, participants will be better able to:

  1. Interpret and identify clinical practices supported by the highest quality available evidence.
  2. Establish the optimal evaluation leading to a correct diagnosis for patients with pulmonary, critical care and sleep disorders.
  3. Translate the most current clinical information into the delivery of high quality care for patients.
  4. Integrate new treatment options for patients with pulmonary, critical care and sleep related disorders.

Learning Format: Case-based, interactive online course, including mandatory assessment questions (number of questions varies by case). Please also read the Technical Requirements.

CME Sponsor: The University of Arizona College of Medicine-Tucson

Current Approval Period: January 1, 2019-December 31, 2020

Financial Support Received: None


History of Present Illness

An 18-year-old female student from Flagstaff was transferred to our hospital for refractory sepsis. She had presented with a 2 week history of fever, malaise, sore throat, myalgias, arthralgias and a rash.

PMH, SH and FH

She reported no significant past medical history or family history. She attended cosmetology school, denied smoking or drug abuse and was sexually monogamous. She had only traveled in-state, did not hike or camp and her only animal exposure was playing with her two pet Great Danes.

Physical Examination

The patient had a fever of 38.5°C. on original presentation. HEENT exam was reported as unrevealing. Lungs were clear. There were no heart murmurs and the abdominal exam was unremarkable. No joint effusions were apparent. A rash was mentioned, but not described and it apparently disappeared shortly after admission.

Initial laboratory testing was significant for WBCC of 12.1 K/mm3, creatinine of 1.5 mg/dL and AST of 45 IU/L. A rapid influenza screen, urinalysis and chest radiography were unrevealing. Blood cultures were drawn and intravenous fluids, piperacillin/tazobactam and azithromycin were administered. Over the next four days, the fever persisted and the blood cultures resulted in no growth. Serial laboratory values demonstrated progressive worsening in renal function and increasing hepatic enzymes. The patient became dyspneic and developed rales and progressive hypoxia prompting transfer.

On arrival in our ICU, the patient was alert, in mild respiratory distress and hypotensive to 78/43 mmHg, requiring immediate initiation of intravenous norepinephrine. She reported nausea and severe diffuse myalgia and arthralgia. On examination, she was ill-appearing with blood pressure 101/58 (on norepinephrine at 25 mcg/min), heart rate 104 beats/min, respiratory rate 33 breaths/min, temperature 38.8°C. She had mild oropharyngeal erythema, some shotty cervical lymph nodes, bilateral rales, mild epigastric and right upper quadrant tenderness, and a macular erythematous rash approximately 14 x 29 cm on her left forearm that disappeared within several hours.

Her ICU admission chest x-ray is shown in Figure 1.


Figure 1. Admission ICU portable chest X-ray showing bilateral areas of consolidation.

Her laboratory evaluation showed the following:

  • WBCC: 2,500/mm3 63% segs with toxic granulation/vacuolated segs
  • Hemoglobin/Hematocrit: 7.9 g/dL/26.7%
  • Platelets: 50,000/mm3
  • BUN/creatinine: 23/1.25 mg/dL
  • AST/ALT: 246/189 IU/L (normal 10-40 and 7-56)
  • PT: 20.9 sec
  • Lactate: 4.5 mmol/L
  • Urinalysis: bland sediment, without bacteria or leukocytes
  • ABG: 7.33, pCO2 34, pO2 78 (on 45% FiO2 by ventimask)
  • Transthoracic echocardiogram showed normal LV and RV size and systolic function with no vegetations
  • US abdomen showed hepatosplenomegaly, retroperitoneal lymphadenopathy, and normal kidneys and ureters.

What are diagnostic considerations at this time?  (Click on the correct answer to be directed to the second of six pages)

  1. Rocky mountain spotted fever (RMSF)
  2. Acute retroviral syndrome
  3. Still’s disease
  4. Systemic lupus erythematosus (SLE)
  5. All of the above

Cite as: Raschke RA. July 2019 critical care case of the month: an 18-year-old with presumed sepsis and progressive multisystem organ failure. Southwest J Pulm Crit Care. 2019;19(1):1-9. doi: PDF 


An Observational Study Demonstrating the Efficacy of Interleukin-1 Antagonist (Anakinra) in Critically-ill Patients with Hemophagocytic Lymphohistiocytosis

Kyle Henry MD, Banner University Medical Center

Robert Raschke MD, University of Arizona College of Medicine-Phoenix

Phoenix, AZ USA


Secondary Hhmophagocytic lymphohistiocytosis (HLH) is an underrecognized cause of multisystem organ failure (MSOF) in critically ill adults, associated with high mortality even when recommended etoposide-based treatments are administered.  Anakinra, an interleukin-1 receptor antagonist, has shown promise in treating children with HLH. This retrospective case series describes seven adult patients who presented to our ICU with a unremitting syndrome consistent with sepsis / MSOF, who were subsequently diagnosed with secondary HLH and received anakinra.   Five of seven (71%) survived.  Two non-survivors died secondary to opportunistic fungal infections. Our study contributes to mounting observational evidence regarding anakinra’s possible efficacy in critically ill adults with HLH, and also raises awareness of possible infectious complications of its use. 


Hemophagocytic lymphohistiocytosis (HLH) is a syndrome characterized by immune dysregulation, hypercytokinemia and tissue infiltration by activated cytotoxic lymphocytes and macrophages (1-3). Primary HLH is a familial syndrome in which gene mutations causing abnormalities of cytotoxic T-lymphocyte and natural killer (NK) cell function result in a systemic hyperinflammatory state. Primary HLH typically presents in the first years of life, progressing to multisystem organ failure (MSOF) and death unless successfully treated with chemotherapy and bone marrow transplantation. Secondary HLH shares clinical features with primary HLH but typically occurs later in life after an underlying illness triggers a dysregulated inflammatory response (3, 4). The diagnosis of primary or secondary HLH is made when five of eight criteria proposed by the International Histiocyte Society are met (Table 1) (5). Heterogeneous groups of patients may satisfy HLH diagnostic criteria, including those in whom HLH is triggered by sepsis, malignancy, and rheumatologic disease (4). Macrophage Activation Syndrome (MAS) is a specific HLH subcategory describing those patients with secondary HLH due to underlying rheumatologic disease (2). The clinical course of secondary HLH is highly variable, progressing relatively slowly in some patients in whom a diagnosis may be made in an outpatient oncology or rheumatology clinic (2, 4, 6-9). Other patients deteriorate rapidly and may require ICU care before the diagnosis of HLH is suspected (3). It has been increasingly recognized that subgroups of patients with HLH have distinctive clinical features, and require special treatment considerations (1, 3-5, 10).

One distinct subgroup consists of adults who present to the intensive care unit (ICU) with sepsis syndrome and MSOF with progressive deterioration despite standard therapy for sepsis (3). Life threatening manifestations in such patients suspected of experiencing HLH may force consideration of presumptive immunotherapy before all HLH diagnostic tests have resulted. Infectious and/or rheumatologic triggers for secondary HLH are eventually found in many, but a clear distinction between sepsis and HLH cannot be made in some (3, 4, 10, 11). The standard treatment protocol for HLH incorporates etoposide – a myelosuppressive chemotherapy agent generally regarded as the standard of care, but has known serious side effects, especially in the setting of hepatic or renal dysfunction typical of sepsis (5, 12). Furthermore, etoposide-based HLH treatment may cause severe immunosuppression leading to opportunistic infections. The mortality of secondary HLH in the adult ICU exceeds 50% (13-16) regardless of the underlying catalyst for the hypercytokinemia. New therapeutic options are desperately needed.

Mounting observational evidence suggests that Anakinra, a recombinant interleukin-1 receptor antagonist (IL-1Ra), may have promise in the treatment of HLH (6,17). Naturally-occurring IL-1Ra is secreted by immune cells to inhibit the pro-inflammatory effects of interleukin 1β (IL-1β) – a key cytokine in the pathogenesis of sepsis and HLH (7, 18). Anakinra was originally developed as a potential therapy for sepsis (7), but is now FDA-approved for use in rheumatoid arthritis. A single case-series describes the successful use of anakinra in critically-ill children with secondary HLH and a few case reports describe its use in critically-ill adults (6, 8, 19, 20). More recently, Wohlfarth and colleagues showed that anakinra is a reasonable option for critically ill patients adults with HLH.  At the same time Wohlfarth et al were studying these effects in an Austrian population, we demonstrated similar results in a series of adult patients in the United States who presented to the ICU with sepsis syndrome and underwent treatment with anakinra for secondary HLH.


This retrospective study was approved by our institutional review board. The setting was the medical and surgical ICU at Banner-University Medical Center Phoenix – a 72-bed ICU in a 650-bed academic tertiary referral center. We identified consecutive adult patients at least 18 years old admitted with sepsis syndrome (known or suspected infection plus acute organ system dysfunction) (21) who subsequently met five or more HLH-2004 diagnostic criteria (Table 1) and received anakinra as part of their treatment regimen between May 2013 and May 2016.

Table 1. HLH-2004 Diagnostic Criteria for Secondary HLH: At least five of eight criteria needed for diagnosis.

Clinical management of patients was not strictly protocolized, but care was provided by an academic 24/7 on-site intensivist service with strong internal consensus regarding the management of HLH. All patients had at least daily complete blood counts and basic metabolic panels. In our practice, diagnostic workup for HLH generally commences upon recognition of unremitting sepsis syndrome with MSOF and bicytopenia. Such patients underwent workup for sepsis and potential causes of secondary HLH that included at minimum: blood cultures, ferritin, fibrinogen, triglycerides, bone marrow aspiration and biopsy, PCR and/or serological testing for systemic lupus erythematosus (SLE), Epstein-Barr virus (EBV), cytomegalovirus, herpes simplex virus, human immunodeficiency virus, hepatitis viruses and coccidioidomycosis (a mycosis endemic in the region). The decision to start HLH therapy was typically based on clinical suspicion plus consistent preliminary laboratory results such as hyperferritinemia, hypofibrinogenemia and/or hypertriglyceridemia, while awaiting the complete results of bone marrow aspiration/biopsy and send-out tests such as soluble interleukin-1 receptor and NK cell functional assays. Presumptive treatment of HLH began with corticosteroids - typically intravenous dexamethasone 10mg/m2 daily. Additional therapies were added at the discretion of the intensivist with consideration of the rapidity of clinical deterioration and likely intolerance of some therapies due to kidney, liver, and/or bone marrow failure. Choice of HLH therapies was based on the HLH-1994 therapy protocol, and influenced by our prior unfavorable experience with etoposide (discussed in conclusions) and recognition of observational literature suggesting that anakinra might be efficacious in patients with secondary HLH. Anakinra was typically given in a dose of 100mg subcutaneously daily, except in patients with creatinine clearance <30ml/min who were dosed every other day.

We retrospectively performed chart reviews to abstract demographics and clinical features related to sepsis and MSOF including infections present on admission, mental status, acute respiratory failure requiring mechanical ventilation, acute renal failure requiring hemodialysis, shock requiring intravenous vasopressors, and liver injury (defined as total bilirubin >2 mg/dL and aminotransferase greater than two times upper limit of normal) (22). The sequential organ failure assessment (SOFA) score was calculated for each patient (21). HLH-2004 diagnostic criteria and the underlying disease process thought to have triggered HLH were abstracted. We documented all treatments including antibiotics and immunosuppressive therapy for HLH, including the dose and duration of anakinra. Outcomes included survival to hospital discharge, duration of fever, mechanical ventilation and renal replacement therapy and ICU length of stay indexed to the time anakinra commenced. Infectious complications occurring during admission after HLH therapy started were also documented. Simple descriptive statistics were performed.

The H Score for each patient was also calculated retrospectively. The H Score is a score used to estimate an individual's risk for having secondary HLH and was recently validated in a 147 patient cohort by Debaugnies et al. (23).


Seven patients were treated with anakinra for a diagnosis of secondary HLH in our ICU between May 2013 and May 2016. Patient ages ranged from 22-59 years – three were female. All patients initially presented to our ICU with a febrile illness consistent with sepsis and received broad-spectrum intravenous antibiotics. Microbiological testing eventually documented infections in two patients – due to influenza A and EBV, respectively. All patients were encephalopathic, five required mechanical ventilation, four required hemodialysis due to acute renal failure, four had liver injury and three required vasopressors due to shock (Table 2).

Table 2. Patient characteristics and some clinical outcomes.

The median SOFA score was 13 (range: 3-17) predicted poor outcome for the group overall (13-16). H Scores for this cohort ranged from 122-263.  HLH diagnostic criteria and presumed etiologies are listed in Table 3.

Table 3. Suspected etiology and positive HLH-2004 diagnostic criteria for secondary HLH in patients treated with anakinra: Five of eight criteria required to diagnose HLH.

Two patients were known to have SLE prior to ICU admission and four others were subsequently diagnosed with underlying autoimmune diseases demonstrating a preponderance of MAS in this cohort.  

All patients initially received corticosteroids (dexamethasone 10mg/m2 or methylprednisolone >500mg every 12 hours) followed by anakinra. Three patients also received cyclosporine, three underwent plasmapheresis and two received IVIG. Only one patient received etoposide and this was later transitioned to anakinra due to lack of response. Anakinra was started a median of seven days after ICU admission (range 2-58 days). All patients received anakinra 100mg daily, but Q48 hour dosing was used temporarily in five patients who transiently experienced creatinine clearances <30mL/min. Duration of anakinra therapy was 10-159 days - we were unable to determine duration of anakinra after discharge in one patient.

All patients appeared to clinically improve after initiation of anakinra. Of six patients experiencing fever at the time anakinra was started, five defervesced within 24 hours. In five patients that had follow-up ferritin levels within two weeks of starting anakinra, ferritin fell from a median of 7,371 ng/L (range 2,217->40,000) to 4,535 ng/L (range 2,137-26,634). Five of seven patients (71%) survived to hospital discharge with an ICU length of stay (LOS) ranging from 6-17 days and an overall LOS of 17-103 days. Once anakinra was started, liberation from the ventilator occurred within 1-3 days, transfer out of the ICU within 3-5 days, discharge from the hospital within 10-32 days and discontinuation of hemodialysis within 10-44 days.

Death in both non-survivors was due to opportunistic fungal infections - necrotizing pulmonary aspergillosis and disseminated mucormycosis (which occurred despite prophylaxis with amphotericin B).  Three other secondary infections all occurred in a single survivor: methicillin-sensitive S. aureus and E coli bacterial ventilator-associated pneumonias and C. difficile colitis all of which responded favorably to treatment while anakinra was continued.


Secondary HLH may be more common in the ICU than previously recognized (3), overlapping with and at times indistinguishable from sepsis (3, 4, 10, 11). Rapid clinical deterioration in patients with suspected HLH may force treatment decisions to be made before full diagnostic test results are available. The risk of myelosuppression due to etoposide-based HLH treatment regimens may be intolerable in critically-ill, possibly septic patients with MSOF (4, 12). A therapeutic agent with a more HLH-specific mechanism of action and better safety profile is badly needed.

Anakinra is a recombinant IL-1Ra originally investigated as a potential immune-modulatory treatment for sepsis (7). Phase I and II studies established acceptable safety for further study in sepsis, but a phase III trial failed to demonstrate an overall survival benefit (7). A post-hoc analysis of data from this trial showed that septic patients with hepatobiliary dysfunction, hypofibrinogenemia and thrombocytopenia, such as often seen in secondary HLH, had significantly improved survival if they received anakinra vs placebo (65% vs. 35% 28-day survival, p=0.0007) (7). Anakinra was later approved for use in rheumatoid arthritis (18). Observational studies suggested efficacy in adult onset Still’s disease and systemic juvenile arthritis (9, 24, 25) and in non-critically-ill patients with secondary HLH triggered by these rheumatologic diseases (9, 25, 26). Case reports described the use of anakinra in critically-ill children with secondary HLH (25, 26, 27) and Rajasekaran and colleagues published a case series describing their experience using anakinra in eight critically-ill pediatric patients with secondary HLH/sepsis syndrome (6). All eight patients survived their initial illness, and no infectious complications were attributed to anakinra.

Fourteen cases describing the use of anakinra in adults with secondary HLH have previously been published (6, 8 ,17, 19, 20, 28).  Four were due to infections (EBV, CMV, MAC, histoplasmosis, four to autoimmune disease (two with AOSD, SLE antisynthetase syndrome), two post transplantation immunosuppression, one due to acute lymphocytic leukemia and three of unknown trigger.  Twelve of 15 (80%) required life support (mechanical ventilation, hemodialysis, vasopressors).  All but two received corticosteroids and just over half IVIg.  Overall survival was 67%, and no complications of immunosuppression were reported. 

The mechanism by which anakinra might ameliorate secondary HLH is not fully elucidated. Secondary HLH (and some forms of sepsis) are characterized by high levels of circulating cytokines including interleukin-6 (IL-6), tumor necrosis factor and interferon-gamma (IFN-γ) (2, 4, 7, 18, 29) - constituting what some have called a “cytokine storm”. Many investigators believe that hypercytokinemia is pathogenic in HLH. Renal failure, cytopenia, coagulopathy and cholestasis have been associated with elevated levels of IL-6 and IFN-γ (2, 18, 28). IL-1β activates lymphocytes responsible for production of these same cytokines (2, 7, 18, 28). IL-1Ra is a competitive inhibitor of IL-1β (7, 29). Therefore IL-1 receptor antagonism by anakinra might inhibit the maladaptive hypercytokinemia characteristic of secondary HLH. This brief explanation oversimplifies a complex and poorly-understood process that requires much further research.

The observed survival rate in our adult patients treated with anakinra (71%) appears favorable compared to that described in other comparable groups of patients (13-16) with survival rates ranging from 25-41%, although we cannot definitively attribute this to treatment effect. It is notable that the majority of our patients had MAS, which has a improved prognosis compared to other forms of HLH when it presents in the outpatient setting, but similar high mortality once the patient develops MSOF and requires intensive care (13-16). This finding supports the concept that secondary HLH of any cause is related to a cytokine storm universal to all underlying catalysts, and that after a critical point the inflammatory cascade becomes increasingly difficult to reverse.

We have previously diagnosed and treated a total of 29 cases of secondary HLH in our ICU. Survival among 22 patients who did not receive anakinra was 14%. This group included eight patients who received etoposide, all of whom died or developed severe neutropenia (WBC <0.5 X 109/L) within a week of its initiation. The patient who survived etoposide did so after her regimen transitioned to anakinra. Statistical comparison of patients in our practice who did or did not receive anakinra was not undertaken due to potential bias and confounding. Controlled prospective trials are required to determine whether anakinra will improve survival of patients with secondary HLH. One such trial is currently under way ( Identifier: NCT02780583) specifically in regards to MAS.

Two of our patients died from opportunistic fungal infections. Fatal fungal infections have previously been reported to occur in patients receiving treatment for HLH who did not receive anakinra (28) and are likely a result of multiple risk factors including the underlying immune dysregulation associated with HLH, other immunosuppressive therapies and invasive procedures related to ICU care (30, 31), and therefore these infections cannot be specifically attributed to anakinra. We consider prophylactic posaconazole or amphotericin therapy in selected ICU patients at high risk for fungal infections given the evidence of invasive fungal infection prophylaxis including mucormycosis in similarly immunocompromised patients (30, 31). 


Our study contributes to mounting observational evidence supporting the hypothesis that anakinra may be efficacious in adult patients presenting to the ICU with life-threatening secondary HLH.  In our opinion, it can be considered as first line therapy, in combination with corticosteroids and IVIg, in selected patients for whom renal, hepatic and bone marrow dysfunction put them at higher risk of toxicity due to etoposide.  Vigilance is warranted in relation to opportunistic infections, particularly those due to fungi.  Prospective controlled trails are needed to definitively establish effective therapy of HLH. 


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Cite as: Henry K, Raschke RA. An observational study demonstrating the efficacy of interleukin-1 antagonist (anakinra) in critically-ill patients with hemophagocytic lymphohistiocytosis. Southwest J Pulm Crit Care. 2019;18(6):177-86. doi: PDF 

Editor's Note: The July 2019 Critical Care Case of the Month is a case presentation of HLH with 0.5 Hour CME credit. Click on the link to be directed to the case.


Which Half Are You? Almost Half of Pediatric Oncologists and Intensivists Are Burnt Out……

K. Sarah Hoehn, MD, MBe1

Manjusha Abraham, MD2

John Gaughan, PhD3

Brigham C. Willis, MD4

1Department of Pediatric Critical Care, University of Chicago Comer Children’s Hospital, Chicago IL

2Department of Pediatrics, Section of Critical Care, St. Mary’s Hospital, St Louis MO

3Biostatistics Consulting Center, Temple University School of Medicine, Philadelphia, PA

4Division of Cardiovascular Intensive Care, Department of Child Health, University of Arizona College of Medicine – Phoenix and Phoenix Children’s Hospital, Phoenix, AZ



Objective: To study the prevalence of burnout, secondary traumatic stress, and wellbeing among pediatric critical care and pediatric hematology and oncology physicians 

Design: Observational cohort study

Setting: Online survey

Patients: Active American Academy of Pediatrics (AAP) members of the section of critical care and the section of hematology and oncology

Interventions: Surveys containing three validated instruments (the Maslach Burnout Inventory, the secondary traumatic stress scale and the Personal Wellbeing Index, as well as questions on demographics and lifestyle) were emailed out via the AAP.

Measurements and Main Results: We had 231 respondents with a response rate of 15.8% among PICU physicians and 26.1% among hematology-oncology physicians. 45.9% of our participants consisted of hematology-oncology physicians and 54.1% of pediatric critical care physicians. The population was a balanced gender mix but was predominantly Caucasian (82% Caucasian and 10% Asian). The overall rate of burnout was 46.6% (47.8% among hematology-oncology physicians and 45.8% among pediatric intensivists). We found significant rates of emotional exhaustion, with 43.0% of respondents scoring high on this subscale.

The prevalence of secondary traumatic stress was 46.8% (42.5% among hematology-oncology physicians and 50.9% among pediatric intensivists). Physicians in practice over 10 to 15 years had significantly higher rates of secondary traumatic stress (p < 0.05). No other demographic or lifestyle variable was significantly associated with an increased risk of burnout or secondary traumatic stress.

Conclusion: Our study reports concerning rates of burnout and secondary traumatic stress among pediatricians in the specialties of Hematology/Oncology and Pediatric Critical Care Medicine. The results raise concern for better screening and prevention for burnout in these high risk specialties. Promoting recognition of early symptoms is crucial, as well as creating a work environment that promotes mental health.


For millennia, physicians have promised to take care of patients to the best of our abilities. In doing so, physicians make personal sacrifices and face challenging situations, including significant administrative burdens of the electronic medical record; all of which may contribute to burnout (1). This led to the AMA supporting a Charter of Physician Well Being, highlighting the importance of building resilience among physicians (2). The topic of physician burnout as one of the leading stories in 2017 (3). Physicians have a have a higher rate of burnout compared to US workers in other fields (4). Burnout has been defined as “a syndrome of emotional exhaustion and cynicism that occurs frequently among individuals who do ‘people-work’ of some kind” (5). Burnout syndrome has 3 key dimensions: emotional exhaustion, depersonalization and lack of personal accomplishment. These problems can affect not only physicians themselves but also patient care. Studies show that burnout is more common among physicians who are 11-20 years in practice (6). A German study suggests that female senior physicians having children are at the greatest risk for burnout (7).  

Along with burnout, physicians may face post-traumatic stress. It has become increasingly more evident that trauma does not only affect the individual(s) directly involved, but also others around them, including healthcare workers. Thus, the concept of secondary traumatic stress has been defined. Secondary traumatic stress (STS) is defined as “the natural, consequent behaviors and emotions resulting from knowledge about a traumatizing event experienced by a significant other. It is the stress resulting from helping or wanting to help a traumatized or suffering person” (8). STS has been studied in a variety of caregiving populations, including social workers, nurses, chaplains, and child life specialists, but there is only limited to no data on STS among pediatric physicians (9-12).

In studying the prevalence of burnout and secondary traumatic stress among physicians, we would be remiss not to also assess the overall wellbeing of these individuals. Wellbeing is defined as “a relative state where one maximizes his or her physical, mental, and social functioning in the context of supportive environments to live a full, satisfying, and productive life”.  The measurement of wellbeing in all Americans is a Healthy People 2020 objective (13).

We used standardized instruments to assess the prevalence of burnout, the prevalence of secondary post-traumatic stress, and the overall wellbeing of high-risk pediatric physicians. We hypothesized that pediatric critical care physicians and pediatric hematology/oncology physicians would have similarly high rates of burnout, STS and adverse effects on overall wellbeing.


The study was reviewed and approved by the Institutional Review Board of Kansas University Medical Center via expedited review. Four questionnaires (Maslach Burnout Scale, Secondary Traumatic Stress, Personal Wellbeing Index, demographic survey) were emailed to the section of critical care medicine and the section on pediatric hematology and oncology of the American Academy of Pediatrics. Reminders to complete the surveys were sent out at 4 and 6 weeks after the initial email. No identifiable data was recorded.

Maslach Burnout Inventory (MBI)

The Maslach Burnout Inventory (MBI) was developed to study burnout syndrome, and has 3 sub scales focusing on the areas of emotional exhaustion (EE), depersonalization (DP) and personal accomplishment (PA). It consists of 22 items on a questionnaire that uses a six point Likert scale (Appendix 1). A high degree of burnout is reflected by high scores on the emotional exhaustion and depersonalization scale in addition to low scores on the personal accomplishment scale. The MBI has been shown to have coefficient alpha between 0.70 to 0.80 in 84 different studies that used the MBI to assess burnout, indicating that the MBI has good internal consistency in low stakes testing (14). Since its initial publication in 1980, the MBI has been shown to adequately assess the presence or absence of burnout in a variety of physician groups (15-19). In our study we defined burnout as the presence of at least one of the following: EE ≥ 37 or DP ≥ 13 or PA < 31 (15).

Secondary Traumatic Stress Scale (STSS)

The Secondary Traumatic Stress Scale (STSS) was developed by Bride and colleagues (20) by using the seventeen symptoms of post traumatic stress disorder from the DSM-IV, and has seventeen items that are answered using a five point Likert type scale. It has been found to have an overall coefficient alpha of 0.94. There are three subscales and each subscale has a coefficient alpha as well: intrusion, 0.80; avoidance, 0.87; arousal 0.79.

Personal Wellbeing Index (PWI)

The Personal Wellbeing Index (PWI) scale contains 7 questions, each one addressing a quality of life domain: standard of living, achieving in life, health, relationships, safety, community-connectedness, and future security. In regards to reliability, the Cornbach alpha lies between 0.70 and 0.85 in Australia and overseas and the index has shown good test-retest reliability with an intra-class correlation coefficient of 0.84 (21).

Demographic Survey

The demographic questionnaire is a self-constructed survey with common factors (years in practice, hours of sleep at night, hours of exercise per week, healthy diet, marital status, number of children, religion) that can be associated as a risk versus protective factors for burnout, secondary traumatic stress and overall wellbeing. Each factor had a comment section for qualitative analysis.

Data Analysis

Variables measured on a continuous scale are presented as means with standard deviations. Groups were compared using the Wilcoxon rank sum test and ANOVA on ranks. Categorical measurements are presented as frequencies with percentages. Groups were compared using Fisher’s exact test and chi-square. A value of < 0.05 was considered statistically significant. All analyses were carried out using SAS V9.2 statistical software (SAS Institute, Cary, NC).



Our study population consisted of 231 participants, in which hematology/oncology physicians and pediatric critical care physicians were evenly distributed (45.89% vs 54.1%). Initially the study was sent out to 732 members of AAP section of pediatric critical care and 445 members of the AAP section of hematology and oncology. The response rate was 15.8% among PICU physicians and 26.1% among hematology and oncology physicians. We attribute our low response rate to the automated depersonalized email from a website, rather than individual requests to members. Surveys that were started but were determined to be incomplete were excluded.

The population was gender balanced (female 51.8%, male 48.2 %), but predominantly Caucasian. 82.5% identified themselves as Caucasian, 10.8% as Asian, 0.9% as African American and 5.8% as others. With regard to religion more than half identified themselves as Christians (56.1%) followed by 25.3% who chose not to specify their religion. 11.8% identified themselves as Jewish, 3.6% as Hindus and 3.2% as Muslims. Most of our participants (76.8%) were married. 35.1% had 2 children followed by 22.1% who had no children. This study group mostly consisted of physicians who were > 20 years in practice (40.6%). 75.5% sleep 5-7 hours per night and 58.4% exercise 2-3 times per week. Half of this group (53.1%) claimed to consume a healthy diet (Table 1-2).

Table 1. Demographic Characteristics (n=231)

Table 2. Habits (n=231)

Maslach Burnout Inventory

The overall burnout rate was 46.8% (45.8% among pediatric critical care physicians and 47.8% among hematology/oncology physicians) (Table 3).

Table 3: Comparison of burnout, secondary traumatic stress and wellbeing rates between pediatric critical care and hematology oncology physicians

Almost half of the participants scored high (42.9%) on the emotional exhaustion subscale and 20.2% scored high for depersonalization. 50.5% also scored high on the personal accomplishment scale. 52.4% of burned out physicians were female. One third of physicians at risk for burnout had 2 children, but the number of children did not correlate with an increased risk of burnout. No demographic factors were identified as a risk or a protective factor for the development of burnout.

Secondary Traumatic Stress Scale

STS was defined as a total score of > 38. The rate of STS was 46.7% (Table 3). A higher total STSS score was noted for physicians practicing for 10- 15 years compared to those practicing for 5-10 years (p=0.04) with a higher score on the arousal subscale (p=0.03). Physicians who followed a healthy diet had a lower total STS score (p=0.01) and a lower score on all three subscales. The same group also seems to have higher scores on the wellbeing scale (p=0.01).

Personal Wellbeing Index

A Personal Wellbeing Index score of >35 was defined as a positive score, which means that an individual was satisfied with his personal life. The overall rate of satisfaction was 95.3% (Table 3). There was no significant difference for PWI scores for critical care and hematology/oncology physicians. With regard to hours of sleep per night, there was no significant difference in burnout or STS rate. However, physicians who slept >7h had a higher score on the PWI scale compared to those who sleep 3-5h (p=0.008) and 5-7h (p=0.02). Married physicians scored higher on the wellbeing scale compared to single physicians (p=0.04). Neither the number of children nor any other lifestyle or demographic factors were associated with increased wellbeing.


Our results demonstrate high rates of burnout and secondary traumatic stress in pediatric critical care and pediatric hematology/oncology physicians. This is consistent with recent studies showing that burn out starts during pediatrics residency (18). Fields et al studied burnout rates among PICU physicians 20 years ago and found a rate of 14%, which is significantly lower than our findings. Garcia et al reported a burnout rate of 50% among general pediatricians and pediatric intensivists (19), in line with our findings.  Burn out is not unique to Americans. Other studies have reported a rate of 41% at high risk for burnout among pediatric critical care physicians in Argentina (22).  Interestingly, this study also found the highest rates among academic pediatricians working in a university setting. Comparing with other specialties, surgeons had similar rates of burnout, ranging from 39-41% (4).

Interestingly our study shows that physicians that are in practice for >20 years had higher scores on the depersonalization subscale. This is in contrast to prior studies that showed that physicians in the middle of their career (11-20 years in practice) are at the greatest risk for burnout (4). Another study by Downey et al assessed burnout among anesthesiologists and came to the conclusion that doctors who are 5-15 years in practice are at the greatest risk for burnout. In our study, physicians who are 10-15 years into their careers had higher secondary traumatic stress scores. Unfortunately, there is not much literature to compare our rates of secondary traumatic stress to and available data is mainly focused on military physicians (22).

We did find that a number of factors can mitigate burnout and STS rates. A healthy diet, sleep and religion positively influenced wellbeing and secondary traumatic stress rates. A subjectively healthy diet was associated with decreased total secondary traumatic stress scores and increased scored on the personal wellbeing scale. Consuming fruits and vegetables is associated with lower incidents of depression and higher rates of happiness and higher life satisfaction (23-25). Along with a healthy diet, more than 7 hours of sleep is also associated with physician wellbeing. It is well known that sleep deprivation is associated with decreased cognitive function, memory and reaction time (26).

Burnout poses a risk for the physician and the patient. High scores on the depersonalization and emotional exhaustion subscale are associated with alcohol abuse or dependence (27). Oreskovich et al. (28) sampled 25,073 surgeons, out of which 15.4% were identified to have an alcohol abuse disorder. Participants who were burned out (odds ratio, 1.25; P = .01) and depressed (odds ratio, 1.48; P < .001) were more likely to have alcohol abuse or dependence. Other studies have identified a correlation between burnout rates (specifically emotional exhaustion) and patient safety risks. Clinicians who scored high on the emotional exhaustion subscale of the MBI had higher standardized mortality ratios (29). A Mayo Clinic study also clearly linked burnout with self-perceived medical errors in both internal medicine residents and surgeons (30). In contrast, a recent study conducted in the adult ICU setting established that there is an increased rate of medical errors by depressed physicians, but burn out did not seem to correlate with an increase rate of medical errors (31). Another prospective cohort study done in three children’s hospitals on pediatric residents have had similar results. (32). In our study we did not measure depression or assess for medical errors related with physician burnout. More studies are needed in the future to elicit if burnout leads to an increase rate of medical errors and the potential risks for the patients.

One important limitation of this study is that it was sent to members of the American Academy of Pediatrics, where 40.63% of the physicians are >20 years in practice. This could have skewed the outcomes. One limitation in our study may be that respondents to our survey could be those who are more likely to suffer from burnout and more likely to want to report their issues, or conversely, those most severely affected may have chosen not to participate. We also did not separately analyze burnout and STS against each other, and we presumed that the similar rates were in the same respondents, but that may not be accurate.


The rates of burnout and secondary traumatic stress are high in both pediatric critical care physicians and pediatric hematologist / oncologists. It may be that lifestyle factors, such as a healthy diet, sleep and exercise may serve as protective factors and increase overall wellbeing. Further studies need to be done to assess burnout, secondary traumatic stress rates among other pediatric subspecialties and to analyze proper coping mechanisms.


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 Cite as: Hoehn KS, Abraham M, Gaughan J, Willis BC. Which half are you? Almost half of pediatric oncologists and intensivists are burnt out…… Southwest J Pulm Crit Care. 2019;18(6):167-76. doi: PDF