Critical Care

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.

Rick Robbins, M.D. Rick Robbins, M.D.

Ultrasound for Critical Care Physicians: A Pericardial Effusion of Uncertain Significance

Brandon Murguia  M.D.

Department of Medicine

University of New Mexico School of Medicine

Albuquerque, NM USA

A 75-year-old woman with known systolic congestive heart failure (ejection fraction of 40%), chronic atrial fibrillation on rivaroxaban oral anticoagulation, morbid obesity, and chronic kidney disease stage 3, was transferred to the Medical Intensive Care Unit for acute hypoxic respiratory failure thought to be secondary to worsening pneumonia.

She had presented to the emergency department 3 days prior with shortness of breath, malaise, left-sided chest pain, and mildly-productive cough over a period of 4 days. She had mild tachycardia on presentation, but was normotensive without tachypnea, hypoxia, or fever. Routine labs were remarkable for a leukocytosis of 15,000 cells/μL. Cardiac biomarkers were normal, and electrocardiogram demonstrated atrial fibrillation with rapid ventricular rate of 114 bpm. Chest x-ray revealed cardiomegaly and left lower lobe consolidation consistent with bacterial pneumonia. Patient was admitted to the floor for intravenous antibiotics, cardiac monitoring, and judicious isotonic fluids if needed.

On night 2 of hospitalization, the patient developed respiratory distress with tachypnea, pulse oximetry of 80-85%, and increased ventricular response into the 140 bpm range. The patient remained normotensive. A portable anterior-posterior chest x-ray showed cardiomegaly and now complete opacification of the left lower lobe. She was transferred to the MICU for suspected worsening pneumonia and congestive heart failure.

Upon arrival to the intensive care unit, vital signs were unchanged and high-flow nasal cannula was started at 6 liters per minute. A focused point-of-care cardiac ultrasound (PCU) was done, limited in quality by patient body habitus, but nonetheless demonstrating the clear presence of a moderate pericardial effusion on subcostal long axis view.

Figure 1: Subcostal long axis view of the heart.

What should be done next regarding this pericardial effusion? (Click on the correct answer for the answer and explanation)

  1. Observe, this is not significant.
  2. Additional echocardiographic imaging /evaluation.
  3. Immediate pericardiocentesis.
  4. Fluid challenge.

Cite as: Murguia B. Ultrasound for critical care physicians: a pericardial effusion of uncertain significance. Southwest J Pulm Crit Care. 2016;13(5):261-5. doi: https://doi.org/10.13175/swjpcc127-16 PDF

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Rick Robbins, M.D. Rick Robbins, M.D.

Corticosteroids and Influenza A associated Acute Respiratory Distress Syndrome

Philippe R. Bauer, MD, PhD

Vivek N. Iyer, MD, MPH

 

Pulmonary and Critical Care Medicine

Mayo Clinic

Rochester, MN USA

 

Abstract

The use of corticosteroids remains controversial in influenza infection, especially with lower respiratory tract infection. We present a case of moderate acute respiratory distress syndrome (ARDS) associated with influenza A that showed a dramatic improvement with combined corticosteroids and antiviral therapy. Host defense against virus infection consists of both innate and adaptive immune responses. An exuberant immune response to the primary pathogen leads to ‘collateral’ lung damage resulting in ARDS.  The use of corticosteroids to modulate this excessive immune response, although intuitive, has been associated with increased mortality when administered early in the course of severe influenza A pneumonia. The administration of corticosteroids in this case was associated with a dramatic and unequivocal improvement. This unique case highlights the potential benefits of corticosteroids use in influenza A associated ARDS and may challenge clinicians to rethink current recommendations that specifically discourage corticosteroids use in patients with Influenza A associated ARDS.   

Introduction

The impact of corticosteroids on clinical outcome in patients with influenza A associated respiratory failure is unclear (1). Retrospective studies suggest an adverse effect from early parenteral corticosteroids use in patients with pandemic influenza infection. On the other hand, in immunosuppressed patients, high dose corticosteroid given at the time of diagnosis of influenza was associated with a reduced risk for mechanical ventilation, without increased adverse effects other than delayed viral clearance. In general, the effect of corticosteroids on acute respiratory distress syndrome (ARDS) is controversial and its use is not routinely recommended. The adjunctive use of prednisone during the early phase of community-acquired pneumonia may actually reduce the development of ARDS (2). In severe influenza, early corticosteroids showed no evidence of benefit and suggested potential harm (3). We present a case of moderate ARDS associated with influenza A that showed a dramatic and unequivocal improvement after initiation of corticosteroids.

Abbreviations:

APACHE: Acute Physiology and Chronic Health Evaluation

ARDS: Acute Respiratory Distress Syndrome

ICU: Intensive Care Unit

PCR: Polymerase Chain Reaction

SOFA: Sequential Organ Failure Assessment

Case Report

A 62-year old male, nonsmoker, with a history of hypertension, dyslipidemia and depression, presented in March 2014 with chills, fever and nonproductive cough; he was initially treated for ‘bronchitis’ as an outpatient with levofloxacin. He had not received the influenza vaccine. Three days later, he developed acute hypoxemic respiratory failure with bilateral pulmonary infiltrates and was hospitalized elsewhere. Influenza testing was negative and he was started on piperacillin/tazobactam and azithromycin. He was transferred to our facility the next day because of worsening respiratory status. Initial heart rate was 80 bpm, blood pressure was 120/60 mm Hg, respirations was 22/min, and temperature was 37.7 ºC. The Acute Physiology and Chronic Health Evaluation (APACHE) IV score was 55 and the Sequential Organ Failure Assessment (SOFA) score was 8. His presentation was consistent with moderate ARDS with a PaO2/FiO2 ratio of 143, a chest radiograph showing bilateral pulmonary infiltrates (Figure 1) and no evidence of heart failure confirmed by bedside echocardiogram.

Figure 1. Bilateral pulmonary opacities consistent with moderate ARDS (PaO2/FiO2 ratio 143).

Nasal swab was again negative for influenza by polymerase chain reaction (PCR). Leukocyte count was 4.4 x 109/L with lymphopenia (0.22 x 109/L), hemoglobin was 11.7 g/dL, and platelet count was 216 x 109/L. Sodium was 134 mmol/L, creatinine was 1 mg/dL and AST was 142 U/L. He was initiated of high flow nasal oxygen, and vancomycin and oseltamivir were added. Due to the severity of his condition, he was also started on methylprednisolone (125 mg intravenously every 8 hours). After a brief trial of noninvasive ventilation, he was intubated, sedated, paralyzed and placed on a low tidal volume strategy with an initial PEEP of 15 cm H2O and a FiO2 of 0.7. A broncho-alveolar lavage, performed post intubation about 16 hours after admission to our facility, showed 35% alveolar macrophages, 8% lymphocytes and 57% neutrophils and was positive for influenza A by PCR; cultures were negative for other organisms. Other tests including HIV, RSV, Mycoplasma, Legionella and urine for Streptococcus antigen were all negative. The patient improved rapidly. He was extubated two days later, and continued on prednisone (40 mg daily) for five more days when he was dismissed home without any need for supplemental oxygen, although the chest radiograph continued to show infiltrates.

Discussion

This case illustrates a patient with delayed diagnosis and treatment of influenza A associated with moderate ARDS who made a rapid and complete recovery with antiviral, antibiotic and adjunctive high dose corticosteroid therapy. 

The diagnosis of influenza A in this case meets all criteria established by Clinical Practice Guidelines of the Infectious Diseases Society of America (4). Rapid influenza testing lack sensitivity and false negative are not infrequent. ARDS is a well-defined complication of influenza infection. While the administration of corticosteroids appeared to temporally co-relate with clinical improvement, a causal link cannot be established definitively. The role of immunosuppression in influenza associated ARDS is very controversial with conflicting evidence from prospective (supportive) and retrospective (against) studies. For example, the combined use of sirolimus and prednisone was associated with significantly improved oxygenation as well as reduced organ dysfunction in mechanically ventilated patients with severe H1N1 respiratory failure (5). On the other hand, retrospective studies have shown increased mortality with the early use of high dose corticosteroids in severe influenza A pneumonia and respiratory failure. Furthermore, corticosteroids are now rarely used in ARDS and only sparingly given in case of refractory septic shock. The immune response to influenza infection depends on the virus, the host and the host response to infection. Host defense against virus infection consists of both innate and adaptive immune responses. An excessive immune response may result in ‘collateral damage’ and critical respiratory illness which may be ameliorated by the use of systemic corticosteroids. On the other hand, suppression of the host immune system may enhance viral replication and prolong critical illness. As a result of these conflicting data, major societies have been unable to firmly recommend for or against corticosteroids therapy in Influenza A associated respiratory failure.

In conclusion, we report on a case of Influenza A with ARDS and rapid improvement on corticosteroids. We have reviewed the current uncertainty surrounding the use of corticosteroids in this setting and leave open the possibility for careful consideration of this adjunctive therapy in other cases. Randomized trials are needed to further delineate the potential benefit of corticosteroids in severe influenza infection.

References

  1. Rodrigo C, Leonardi-Bee J, Nguyen-Van-Tam J, Lim WS. Corticosteroids as adjunctive therapy in the treatment of influenza. Cochrane Database Syst Rev. 2016 Mar 7;3:CD010406. [CrossRef] [PubMed]
  2. Blum CA, Nigro N, Briel M, et al. Adjunct prednisone therapy for patients with community-acquired pneumonia: a multicentre, double-blind, randomised, placebo-controlled trial. Lancet. 2015 Apr 18;385(9977):1511-8. [CrossRef] [PubMed]
  3. Brun-Buisson C, Richard JC, Mercat A, Thiébaut AC, Brochard L; REVA-SRLF A/H1N1v 2009 Registry Group. Early corticosteroids in severe influenza A/H1N1 pneumonia and acute respiratory distress syndrome. Am J Respir Crit Care Med. 2011 May 1;183(9):1200-6. [CrossRef] [PubMed]
  4. Harper SA, Bradley JS, Englund JA, et al. Seasonal influenza in adults and children--diagnosis, treatment, chemoprophylaxis, and institutional outbreak management: clinical practice guidelines of the Insert LinkInfectious Diseases Society of America. Clin Infect Dis. 2009 Apr 15;48(8):1003-32. [CrossRef] [PubMed]
  5. Wang CH, Chung FT, Lin SM, Huang SY, Chou CL, Lee KY, Lin TY, Kuo HP. Adjuvant treatment with a mammalian target of rapamycin inhibitor, sirolimus, and steroids improves outcomes in patients with severe H1N1 pneumonia and acute respiratory failure. Crit Care Med. 2014 Feb;42(2):313-21. [CrossRef] [PubMed]

Cite as: Bauer PR, Iyer VN. Corticosteroids and influenza A associated acute respiratory distress syndrome. Southwest J Pulm Crit Care. 2016;13(5):248-51. doi: https://doi.org/10.13175/swjpcc102-16 PDF

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Rick Robbins, M.D. Rick Robbins, M.D.

November 2016 Critical Care Case of the Month

Richard A. Robbins, MD

Phoenix Pulmonary and Critical Care Research and Education Foundation

Gilbert, AZ USA

 

History of Present Illness

A 45-year-old Iraqi War Veteran was seen in the outpatient clinic after referral for COPD based on abnormal blood gases. He denies any dyspnea or cough.

PMH, SH and FH

He has a history of a lower back injury and uses a motorized wheelchair. His pain is managed with morphine sulfate ER 60 mg daily and morphine sulfate 10 mg every 4 hours as needed for breakthrough pain.

He does not smoke cigarettes but does use marijuana for pain. He denies alcohol abuse.

Physical Examination

Physical examination shows a lethargic man in a wheelchair who intermittently falls asleep during questioning and examination. When aroused he is oriented to time, place and person and frequently mentions that his pain is a 10. His vital signs are normal expect his SpO2 is 75% on room air. His lungs were clear and his heart had a regular rhythm without murmur. His pupil size is approximately 2 mm bilaterally and muscle strength is difficult to determine due to his inability to remain alert or fully cooperate.

Radiography

A chest x-ray had been performed about a week previously (Figure 1).

Figure 1. Initial chest x-ray.

Spirometry had been performed earlier in the day (Figure 2).

Figure 2. Spirometry.

Which of the following are indicated at this time? (Click on the correct answer to proceed to the second of four pages)

  1. Arterial blood gases (ABGs)
  2. Immediate intubation
  3. Intensive care unit (ICU) admission
  4. 1 and 3
  5. All of the above

Cite as: Robbins Ra. November 2016 critical care case of the month. Southwest J Pulm Crit Care. 2016;13(5):196-201. doi: http://dx.doi.org/10.13175/swjpcc103-16 PDF

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Rick Robbins, M.D. Rick Robbins, M.D.

October 2016 Critical Care Case of the Month

Stephanie Fountain, MD

Banner University Medical Center Phoenix

Phoenix, AZ USA

 

Critical Care Case of the Month CME Information

Members of the Arizona, New Mexico, Colorado and California Thoracic Societies and the Mayo Clinic are able to receive 0.25 AMA PRA Category 1 Credits™ for each case they complete. Completion of an evaluation form is required to receive credit and a link is provided on the last panel of the activity. 

0.25 AMA PRA Category 1 Credit(s)™

Estimated time to complete this activity: 0.25 hours 

Lead Author(s): Stephanie Fountain, MD.  All 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 this activity I will be better able to:

  1. Correctly interpret and identify clinical practices supported by the highest quality available evidence.
  2. Will be better able to establsh the optimal evaluation leading to a correct diagnosis for patients with pulmonary, critical care and sleep disorders.
  3. Will improve the translation of the most current clinical information into the delivery of high quality care for patients.
  4. Will integrate new treatment options in discussing available treatment alternatives 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: University of Arizona College of Medicine

Current Approval Period: January 1, 2015-December 31, 2016

Financial Support Received: None

 

A 27-year-old Caucasian man with past medical history of opioid abuse (reportedly sober for 10 years on buprenorphine), post traumatic stress disorder, depression and anxiety presented to the emergency department complaining of dysarthria after taking diphenhydramine and meclizine in addition to his prescribed trazodone and buprenorphine to try to sleep. He was discharged to home after his symptoms appeared to improve with intravenous fluid.

He returned to the emergency department the following afternoon with worsening dysarthria, dysphagia, and subjective weakness. The patient was non toxic appearing, afebrile, vital signs were stable and his strength was reported as 5/5. Computed tomography  of his head did not show any evidence of acute intracranial abnormality. Given his ongoing complaints, he was admitted for observation to the general medicine wards.

That night a rapid response was initiated when the nurse found the patient to be unresponsive, but spontaneously breathing. The patient’s clinical status did not change with naloxone administration. An arterial blood gas obtained demonstrated a profound respiratory acidosis with a pH of 7.02 and a pCO2 of 92. He was emergently intubated. A chest x-ray was performed (Figure 1).

Figure 1. Panel A: admission portable chest x-ray. Panel B: chest -ray immediately after intubation. 

Which of the following are present on his chest X-ray? (Click on the correct answer to proceed to the second or four panels)

  1. Left lung atelectasis
  2. Left pleural effusion
  3. Right mainstem intubation
  4. 1 and 3
  5. All of the above

Cite as: Fountain S. October 2016 critical care case of the month. Soutwest J Pulm Crit Care. 2016:13(4):159-64. doi: http://dx.doi.org/10.13175/swjpcc095-16 PDF

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Rick Robbins, M.D. Rick Robbins, M.D.

September 2016 Critical Care Case of the Month

Clement U. Singarajah, MD

Samir Sultan, DO

Phoenix VA Medical Center

Phoenix, AZ USA

 

Critical Care Case of the Month CME Information

Members of the Arizona, New Mexico, Colorado and California Thoracic Societies and the Mayo Clinic are able to receive 0.25 AMA PRA Category 1 Credits™ for each case they complete. Completion of an evaluation form is required to receive credit and a link is provided on the last panel of the activity. 

0.25 AMA PRA Category 1 Credit(s)™

Estimated time to complete this activity: 0.25 hours 

Lead Author(s): Clement U. Singarajah, MD.  All 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 this activity I will be better able to:

  1. Correctly interpret and identify clinical practices supported by the highest quality available evidence.
  2. Will be better able to establsh the optimal evaluation leading to a correct diagnosis for patients with pulmonary, critical care and sleep disorders.
  3. Will improve the translation of the most current clinical information into the delivery of high quality care for patients.
  4. Will integrate new treatment options in discussing available treatment alternatives 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: University of Arizona College of Medicine

Current Approval Period: January 1, 2015-December 31, 2016

Financial Support Received: None

 

Clinical History

A 66-year-old man was admitted to the ICU in complete heart block with borderline hypotension. After cardiology consultation, a decision was made to place an urgent transvenous pacer. The transvenous pacer was place without use fluoroscopy from an right internal jugular venous (IJV) approach using real time ultrasound by two very experienced operators. The ultrasound confirmed right  IJV placement and the pacer was found to capture and pace appropriately without any complications. A post placement CXR was obtained (Figure 1).

 Figure 1. Portable chest x-ray after RIJV transvenous pacer (TVP).

What does the chest x-ray show? (Click on the correct answer to proceed to the second of five panels)

Cite as: Singarjah CU, Sultan S. September 2016 critical care case of the month. Southwest J Pulm Crit Care. 2016;13(3):108-13. doi: http://dx.doi.org/10.13175/swjpcc079-16 PDF

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Rick Robbins, M.D. Rick Robbins, M.D.

Ultrasound for Critical Care Physicians: Unraveling a Rapid Drop of Hematocrit

Deepti Baheti, MBBS

Pablo Garcia, MD

 

Department of Internal Medicine and LifeBridge Critical Care

Sinai Hospital of Baltimore.

Baltimore, MD USA

 

An 85-year-old woman was admitted to our hospital with complaints of shortness of breath on exertion. Her medical history was significant for hypertension, pulmonary embolism and stage III chronic kidney disease. She was diagnosed with severe decompensated pulmonary hypertension and started to improve with diuretics. While hospitalized, she suffered an asystolic arrest and was successfully resuscitated. As a result of chest compressions, the patient developed multiple anterior rib fractures. Within a few days of recovering from her cardiac arrest, she was anticoagulated with enoxaparin as a bridge to warfarin for her prior history of pulmonary embolism. Five days after initiation of enoxaparin and warfarin, she was noted to have an acute drop in her hemoglobin from 8 g/dl to 5 g/dl. A thorough physical examination revealed a large area of swelling in her left anterior chest wall. Point-of- care ultrasound was utilized to image this area of swelling centered at the 3rd intercostal space between the mid-clavicular and anterior axillary line (Figures 1 and 2).

Figure 1. Ultrasound image of the chest wall in the sagittal plane.

 

Figure 2. Ultrasound image of the chest wall in the transverse plane.

What is the cause of this patient’s acute anemia? (Click on the correct answer for an explanation)

Cite as: Baheti D, Garcia P. Ultrasound for critical care physicians: unraveling a rapid drop of hematocrit. Southwest J Pulm Crit Care. 2016;13(2):84-7. doi: http://dx.doi.org/10.13175/swjpcc078-16 PDF 

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Rick Robbins, M.D. Rick Robbins, M.D.

Fluid Resuscitation for Septic Shock – A 50-Year Perspective: From Dogma to Skepticism

Robert A. Raschke, MD

Arooj Kayani, MD 

Samir Sultan, DO

Stephanie Fountain, MD

Moustafa Abidali, DO

Kyle Henry, MD

 

Banner University Medical Center Phoenix

Phoenix, AZ USA 

 

Few clinicians would challenge the contention that fluid resuscitation of sepsis improves tissue perfusion thereby protecting end-organs from injury. This is an underlying tenet of current Surviving Sepsis Campaign (SSC) recommendations (1) and Center for Medicare and Medicaid Services (CMS) mandate that hospitals report sepsis bundle compliance as a measure of healthcare quality.  It has persisted for decades despite the lack of convincing empirical evidence that fluid resuscitation improves clinical outcomes. To the contrary, large randomized controlled trials have shown that aggressive intravenous fluid resuscitation prolongs the need for mechanical ventilation (2) and increases mortality in some patients (3) – more on these studies later.  Furthermore, the pathophysiological rationale commonly used to explain why fluid resuscitation ought to be beneficial has been challenged by a growing body of evidence.  This article started as a journal club held by our Pulmonary Critical Care fellows, but we expanded the scope to review other related studies over the past 50 years that challenge the current accepted paradigm of aggressive fluid resuscitation of sepsis and septic shock.

The positive results of River’s early goal-directed therapy (EGDT) trial in the early 2000s (4) were inexplicable to many that followed previous literature. EGDT required aggressive fluid resuscitation to achieve a central venous pressure (CVP) >8-12 cmH2O, culminating in a mean positive fluid balance >13 L at 72 hours. But it had been recognized for decades that CVP could not reasonably be used in this manner. In 1965, Dr. Max Weil (considered by some the founder of critical care medicine) made the observation that the CVP is primarily an index of right ventricular function rather than an index of volume status (5). The widely-held concept (which has persisted since 1965) that low venous pressure indicates low blood volume was developed using data from normal subjects and was not valid in critical illness. Elevated CVP reflects incompetence of the heart to accept the blood returned to it. As such, CVP ought to be used primarily to limit over-resuscitation rather than to indicate when more fluids are needed (5).

These early observations and decades of corroborating evidence were set-aside for yet another decade as EGDT was systematically endorsed. Near the peak of enthusiasm for EGDT, a meta-analysis of 24 studies demonstrated no significant relationship between CVP and blood volume (r2=0.02) or fluid responsiveness (r2=0.03) (6). A graph from that article based on 1500 simultaneous measurements of CVP and blood volume graphically illustrates the apparent lack of any association, supporting Dr Weil’s clinical observations from over 40 years earlier (Figure 1). 

 

Figure 1. Graph of simultaneous measurements of blood volume and central venous pressure (CVP) in a heterogenous cohort of 188 ICU patients demonstrating no association between these two variables (r=0.27) (6).

Nevertheless, EGDT was avidly endorsed by authoritarian professional organizations and immense time and effort expended on national and international efforts to promote it’s systematic implementation. Several observational studies showed that systematic implementation of EGDT in healthcare institutions decreased sepsis mortality (7,8). However,  the use of historical controls in these studies allowed other simultaneous changes in ICU practice and the Hawthorne effect to potentially confound their results.

In 2006, the ARDS clinical trials network published a multi-center controlled trial that randomized 1000 patients with acute lung injury to liberal or conservative fluid management (2). Approximately 70% of the patients in the study satisfied current criteria for sepsis (were classified as having sepsis or pneumonia with acute organ system dysfunction). Critical appraisal of the study revealed that >90% of screened patients were excluded, complicated fluid management protocols were unlikely to be practical for routine use and the study was not blinded. But the study methodology was otherwise essentially sound. Liberal fluid management achieved a more positive fluid balance over the first 7 days (+6992 +/-502 mL vs. -136 +/- 491 mL p<0.001), but failed to reduce the incidence of shock or acute renal failure requiring dialysis. It was instead associated with significantly prolonged ventilator dependence (12.1 vs. 14.6 ventilator-free days, p<0.001) and prolonged ICU length-of-stay (11.2 vs. 13.4 ICU-free days, p<0.001).  These results seemed contrary to those of Rivers and we struggled at the time to reconcile the two. Our shared impression at journal club is that aggressive fluid resuscitation followed by permissive hypervolemia, such as seen in the liberal fluid management arm of this study, is still common in current practice. This study suggests that this approach significantly prolongs recovery from acute lung injury. 

Maitland’s study of fluid boluses in African children in 2011 is remarkable as the only large prospective randomized controlled trial (RCT) to study the clinical effect of early fluid resuscitation in patients with severe infections (3). The study randomized children with high fever and clinical evidence of impaired perfusion to three groups: 5% albumin bolus, normal saline bolus or no bolus. The safety monitoring committee ended the study after 3141 of 3600 projected patients had been enrolled, based on evidence that administration of either type of fluid bolus significantly increased mortality (RR 1.45 95%CI: 1.13-1.86 p=0.003). Methodology was limited by available healthcare infrastructure. Although the proportion of patients with sepsis cannot be calculated, 39% had a lactate >5 mmol/L. The study had reasonable internal validity, but significant challenges to external validity – the mean patient age was 23 months, and 57% had malaria.  However, the authors noted: “The excess mortality with fluid resuscitation was consistent across all subgroups, irrespective of physiological derangement (whether or not the patient was in shock) or underlying microbial pathogen, raising fundamental questions about our understanding of the pathophysiology of critical illness.” The authors speculated that the neuro-hormonal vasoconstrictor response to shock might confer protection by reducing perfusion to non-vital tissues and that rapid reversal with fluid resuscitation could therefore be harmful. This specific hypothesis was supported by a post-hoc analysis that showed that the increased mortality associated with fluid boluses could not be explained by an increase in pulmonary or cerebral edema.  Although the generalizability of this study is limited, there is no comparable RCT of fluid boluses in any other group of patients to refute it’s findings.

The review of resuscitation fluids by Myberg and Mythen in 2013 (9) emphasized ongoing uncertainty and reasoned against a protocolized approach driving aggressive fluid resuscitation stating “the requirements for and response to fluid resuscitation vary greatly during the course of any critical illness. No single physiological or biochemical measurement adequately reflects the complexity of fluid depletion or the response to fluid resuscitation.”  They reviewed observational evidence that the development of positive fluid balance and elevated CVP were associated with increased mortality in patients with sepsis. They pointed out that intravenous fluids should be considered as a drug with potentially serious side effects: interstitial edema - and in the case of normal saline, hyperchloremic acidosis and acute kidney injury. They recommended modest amounts of balanced isotonic salt solutions guided by clinical consideration of multiple individual patient factors, cautioned against continuing fluid resuscitation after the first 24 hours of illness and encouraged early initiation of norepinephrine.

Myberg’s review was published about the time that the results of three randomized controlled trials, which cumulatively enrolled 4201 patients at 138 emergency departments and ICUs internationally conclusively refuted any clinical benefit of EGDT (10-12). Shortly thereafter, CMS paradoxically mandated monthly sepsis bundle compliance reporting as a measure of healthcare quality, strongly incentivizing hospitals to systematically institute sepsis bundles, even though they had just been proven to be ineffective.

We greatly enjoyed the review of fluid therapy in sepsis by Marik and Bellomo (13). They argue that the standard pathophysiological explanation for the theoretical benefit of fluid resuscitation in sepsis is contradicted by a growing body of evidence. Septic shock is not characterized by hypovolemia but rather by vasoplegia and injury to the endothelial glycocalyx. Resultant microvascular permeability and propensity to interstitial edema impairs organ function. As such, restoration of vascular tone (including that of capacitance veins) is the preferred initial intervention to restore perfusion. Elevating the CVP > 8 cm H2O with fluid boluses does not reliably improve preload and cardiac output as commonly supposed. Instead, it most often overfills the heart, inducing acute diastolic dysfunction in a majority of patients. This paradoxically reduces stroke volume and moves the patient onto the flat portion of the Frank Starling curve mitigating any potential augmentation of cardiac fluid by further fluid administration. Elevated CVPs in this setting are not an indication of successful fluid resuscitation but rather a sign of cardiac incompetence to accommodate iatrogenic hypervolemia. Cardiac natriuretic peptides released in response to cardiac overfilling cleave glycoproteins that make up the endothelial glycocalyx further injuring it. Venous back-pressure worsens organ perfusion and increases interstitial edema, particularly affecting the kidneys. However, cellular hypoxia and bioenergetics failure does not occur and is not the cause of lactic acidosis in septic shock as is often supposed. Elevated lactate levels are instead caused by bioenergetic-coupling of epinephrine-induced stimulation of Na/K ATPase activity to aerobic glycolysis. The critical level of oxygen delivery below which oxygen consumption falls is almost never associated with septic shock, and increasing oxygen delivery has been not been shown to improve oxygen consumption or lower lactate levels. Attempts to specifically increase oxygen delivery in sepsis have in fact worsened survival. 

Furthermore, only a minority of patients with sepsis respond with increased stroke volume after a fluid bolus. Hemodynamic improvements seen in “fluid responders” return to baseline within an hour. 95% of administered fluid is rapidly sequestered in tissues where it contributes to organ dysfunction. Goal-directed fluid administration achieves only a transient hemodynamic improvement in a minority of patients at the cost of accumulating injurious tissue edema in all. Analysis of five serial randomized controlled trials that ultimately disproved the efficacy of EGDT shows that sepsis mortality has been fallen significantly over the past 15 years in association with a tendency towards significantly more conservative fluid management (approx. 13L/72hrs vs. 6L/72 hours) suggesting that a more conservative approach to fluid resuscitation may explain improved survival (Figure 2).

Figure 2. Fluid administerered between enrollment and 72 h and 90-day mortality in the control arm of the early goal directed therapy (EGDT) studies performed between 2001 and 2015. APACHE II=APACHE II severity of illness scoring system.

Marik and Bellomo (13) recommend early administration of norepinephrine, which can be safely administered via a well-functioning peripheral intravenous catheter and cautious administration of small volume fluid boluses (200-500 mL) only in patients in whom passive leg raise (a reversible fluid bolus) can be demonstrated to augment stroke volume. They argue that CVP, central venous oxygen saturation and lactate should not be used to guide fluid management, and should in fact not even be measured.

Taken individually, each of these studies seems anomalous in the context of our preconceived notion that aggressive fluid resuscitation must be beneficial. Taken together, they comprise a cohesive argument that ought to change our bedside care.  There certainly isn’t any convincing or enduring empirical evidence that aggressive fluid resuscitation of sepsis is clinically beneficial. There is only flawed pathophysiologic rationale and dogma. The common practice of aggressive fluid resuscitation followed by prolonged permissive hypervolemia should be actively avoided. As we struggle to comply with a CMS mandate regarding sepsis bundle compliance in the face of overwhelming evidence that it doesn’t work, we recommend a focus on early administration of appropriate antibiotics and maintenance of adequate perfusion pressure with vasopressors – the only bundle components likely to be associated with improved patient outcomes.

References

  1. Dellinger RP, Levy MM, Rhodes A, et al. ; Surviving Sepsis Campaign Guidelines Committee including The Pediatric Subgroup. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock, 2012. Intensive Care Med. 2013 Feb;39(2):165-228. [CrossRef] [PubMed]
  2. National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome (ARDS) Clinical Trials Network, Wiedemann HP, Wheeler AP, Bernard GR, et al. Comparison of two fluid-management strategies in acute lung injury. N Engl J Med. 2006 Jun 15;354(24):2564-75. [CrossRef] [PubMed]
  3. Maitland K, Kiguli S, Opoka RO, et al. Mortality after fluid bolus in African children with severe infection. N Engl J Med. 2011 Jun 30;364(26):2483-95. [CrossRef] [PubMed]
  4. Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med. 2001 Nov 8;345(19):1368-77. [CrossRef] [PubMed]
  5. Weil MH, Shubin H, Rosoff L. Fluid repletion in circulatory shock. JAMA. 1965;192:84–90. [CrossRef] [PubMed]
  6. Marik PE, Baram M, Vahid B. Does central venous pressure predict fluid responsiveness? A systematic review of the literature and the tale of seven mares. Chest. 2008 Jul;134(1):172-8. [CrossRef] [PubMed]
  7. Ferrer R, Artigas A, Levy MM, et al. Improvement in process of care and outcome after a multicenter severe sepsis educational program in Spain. JAMA. 2008 May 21;299(19):2294-303. [CrossRef] [PubMed]
  8. Rhodes A, Phillips G, Beale R, et al. The Surviving Sepsis Campaign bundles and outcome: results from the International Multicentre Prevalence Study on Sepsis (the IMPreSS study). Intensive Care Med. 2015 Sep;41(9):1620-8. [CrossRef] [PubMed]
  9. Myburgh JA, Mythen MG. Resuscitation fluids. N Engl J Med. 2013 Sep 26;369(13):1243-51. [CrossRef] [PubMed]
  10. ProCESS Investigators, Yealy DM, Kellum JA, Huang DT, et al. A randomized trial of protocol-based care for early septic shock. N Engl J Med. 2014 May 1;370(18):1683-93. [CrossRef] [PubMed]
  11. ARISE Investigators; ANZICS Clinical Trials Group, Peake SL, Delaney A, Bailey M, et al. Goal-directed resuscitation for patients with early septic shock. N Engl J Med. 2014 Oct 16;371(16):1496-506. [CrossRef] [PubMed]
  12. Mouncey PR, Osborn TM, Power GS, et al. Trial of early, goal-directed resuscitation for septic shock. N Engl J Med. 2015 Apr 2;372(14):1301-11. [CrossRef] [PubMed]
  13. Marik P, Bellomo R. A rational approach to fluid therapy in sepsis. Br J Anaesth. 2016 Mar;116(3):339-49. [CrossRef] [PubMed] 

Cite as: Raschke RA, Kayani A, Sultan S, Fountain S, Abidali M, Henry K.  Fluid resuscitation for septic shock – a 50-year perspective: from dogma to skepticism. Southwest J Pulm Crit Care. 2016;13(2):65-70. doi: http://dx.doi.org/10.13175/swjpcc073-16 PDF 

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Rick Robbins, M.D. Rick Robbins, M.D.

August 2016 Critical Care Case of the Month

Jillian L. Deangelis, APRN, CNP

Theodore Loftsgard APRN, ACNP

 

Department of Anesthesiology

Mayo Clinic Minnesota

Rochester, MN USA

 

Critical Care Case of the Month CME Information

Members of the Arizona, New Mexico, Colorado and California Thoracic Societies and the Mayo Clinic are able to receive 0.25 AMA PRA Category 1 Credits™ for each case they complete. Completion of an evaluation form is required to receive credit and a link is provided on the last panel of the activity. 

0.25 AMA PRA Category 1 Credit(s)™

Estimated time to complete this activity: 0.25 hours 

Lead Author(s): Jillian L. Deangelis, MS, APRN, CNP.  All 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 this activity I will be better able to:

  1. Correctly interpret and identify clinical practices supported by the highest quality available evidence.
  2. Will be better able to establsh the optimal evaluation leading to a correct diagnosis for patients with pulmonary, critical care and sleep disorders.
  3. Will improve the translation of the most current clinical information into the delivery of high quality care for patients.
  4. Will integrate new treatment options in discussing available treatment alternatives 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: University of Arizona College of Medicine

Current Approval Period: January 1, 2015-December 31, 2016

Financial Support Received: None

 

History of Present Illness

The patient is a previously healthy, albeit anxious, 15-year-old girl seen by her primary care physician. She has had several months of general malaise and ongoing fatigue and an increased frequency in night terrors over the past few weeks. Her family attributes this to stress of school and her new job. She was noted to have lost 3 kg in the previous nine weeks.

PMH, SH, and FH

Her PMH was unremarkable. She is a student and denies smoking, drinking or drug abuse. Her family history is noncontributory.

Physical Examination

  • Vital signs: BP 100/60 mm Hg, P 90 beats/min and regular,  R 16 breaths/min, T 100.8 ºF, BMI 15.  
  • Diffuse, non-tender lymphadenopathy through the submandibular and upper anterior cervical chains.
  • Lungs: clear
  • Heart: regular rhythm without murmur.
  • Abdomen: slightly rounded and firm.

Which of the following are diagnostic considerations at this time? (Click on the correct answer to proceed to the second of seven panels)

  1. Anorexia nervosa
  2. Lymphoma
  3. Mononucleosis
  4. Teenage adjustment disorder
  5. All of the above

Cite as: Deangelis JL, Loftsgard T. August 2016 critical care case of the month. Southwest J Pulm Crit Care. 2016;13(2):46-53. doi: http://dx.doi.org/10.13175/swjpcc056-16 PDF

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Rick Robbins, M.D. Rick Robbins, M.D.

Ultrasound for Critical Care Physicians: Complication of a Distant Malignancy

S. Cham Sante M.D.1

Michel Boivin M.D.2

 

Department of Emergency Medicine1

Division of Pulmonary, Critical care and Sleep Medicine2

University of New Mexico School of Medicine

Albuquerque, NM USA

 

An 82-year-old woman with prior medical history of stage IV colon cancer and chronic obstructive pulmonary disease presented to the medical intensive care unit with newly diagnosed community acquired pneumonia and acute kidney injury. The patient presented with acute onset of shortness of breath, nausea, generalized weakness, bilateral lower extremity swelling and decreased urine output. She was transferred for short term dialysis in the setting of multiple electrolyte abnormalities, including hyperkalemia of 6.4 mmol/l, as well as a creatinine of 6.5 mg/dl. The following imaging of the right internal jugular vein was performed with ultrasound during preparation for placement of a temporary triple lumen hemodialysis catheter.

Figure 1. Panel A: Transverse ultrasound image of the right neck. Panel B: Longitudinal ultrasound image of the right neck, centered on the internal jugular vein.

Based on the above imaging what would be the best location to place the dialysis catheter? (Click on the correct answer for an explanation and discussion)

Cite as: Sante SC, Boivin M. Ultrasound for critical care physicians: complication of a distant malignancy. Southwest J Pulm Crit Care. 2016;13(1):27-9. doi: http://dx.doi.org/10.13175/swjpcc055-16 PDF

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Rick Robbins, M.D. Rick Robbins, M.D.

July 2016 Critical Care Case of the Month

Warren Carll, DO

Susanna Tan, MD

Shannon Skinner, MD

 

Maricopa Integrated Health System

Phoenix, AZ USA

 

Critical Care Case of the Month CME Information

Members of the Arizona, New Mexico, Colorado and California Thoracic Societies and the Mayo Clinic are able to receive 0.25 AMA PRA Category 1 Credits™ for each case they complete. Completion of an evaluation form is required to receive credit and a link is provided on the last panel of the activity. 

0.25 AMA PRA Category 1 Credit(s)™

Estimated time to complete this activity: 0.25 hours 

Lead Author(s): Warren Carll, DO.  All 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 this activity I will be better able to:

  1. Correctly interpret and identify clinical practices supported by the highest quality available evidence.
  2. Will be better able to establsh the optimal evaluation leading to a correct diagnosis for patients with pulmonary, critical care and sleep disorders.
  3. Will improve the translation of the most current clinical information into the delivery of high quality care for patients.
  4. Will integrate new treatment options in discussing available treatment alternatives 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: University of Arizona College of Medicine

Current Approval Period: January 1, 2015-December 31, 2016

Financial Support Received: None

 

History of Present Illness

The patient is a 20-year-old man with admitted to Maricopa Integrated Health System unconscious after being found down on a hiking trail.

Past Medical History

Hypertension and morbid obesity.

Physical Examination

  • Vital signs: BP 90/60 mm Hg, P 128 beats/min, Respiration 28 breaths/min, T 105.8º F, SpO2 98% on 2 L/min by NC.
  • General: he is unresponsive to verbal stimuli but withdraws from pain
  • Neck: there is no jugular venous distention. Thyroid is not palpable.
  • Lungs: clear
  • Heart: Regular tachycardia without murmur
  • Abdomen: Obese but soft without organomegaly or tendernesses
  • Extremities: apparent burns over both lower extremities

Which of the following should be done initially? (Click on the correct answer to proceed to the second of five panels)

  1. Cool the patient as quickly as possible
  2. Cool the patient slowly to prevent cerebral edema
  3. Aggressively administer normal saline to correct hypotension
  4. 1 and 3
  5. All of the above

Cite as: Carll W, Tan S, Skinner S. July 2016 critical care case of the month. Southwest J Pulm Crit Care. 2016;13(1):9-14. doi: http://dx.doi.org/10.13175/swjpcc046-16 PDF 

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Rick Robbins, M.D. Rick Robbins, M.D.

Ultrasound for Critical Care Physicians: Now My Heart Is Still Somewhat Full

Krystal Chan, MD

Bilal Jalil, MD

 

Department of Internal Medicine

University of New Mexico School of Medicine

Albuquerque, NM USA

 

A 48-year-old man with a history of hypertension, intravenous drug abuse, hepatitis C, and cirrhosis presented with 1 day of melena and hematemesis. While in the Emergency Department, the patient was witnessed to have approximately 700 mL of hematemesis with tachycardia and hypotension. The patient was admitted to the Medical Intensive Care Unit for hypotension secondary to acute blood loss. He was found to have a decreased hemoglobin, elevated international normalized ratio (INR), and sinus tachycardia. A bedside echocardiogram was performed.

 

Figure 1. Apical four chamber view of the heart.

 

Figure 2. Longitudinal view of the inferior vena cava entering into the right atrium.

 

What is the best explanation for the echocardiographic findings shown above? (Click on the correct answer for an explanation and discussion)

  1. Atrial Fibrillation
  2. Atrial Myxoma
  3. Cardiac Lymphoma
  4. Tricuspid Valve Endocarditis
  5. Tumor Thrombus

Cite as: Chan K, Jalil B. Ultrasound for critical care physicians: now my heart is still somewhat full. Southwest J Pulm Crit Care. 2016;12(6):236-9. doi: http://dx.doi.org/10.13175/swjpcc054-16 PDF 

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Rick Robbins, M.D. Rick Robbins, M.D.

June 2016 Critical Care Case of the Month

Theodore Loftsgard APRN, ACNP

Julia Terk PA-C

Lauren Trapp PA-C

Bhargavi Gali MD

 

Department of Anesthesiology

Mayo Clinic Minnesota

Rochester, MN USA

 

Critical Care Case of the Month CME Information

Members of the Arizona, New Mexico, Colorado and California Thoracic Societies and the Mayo Clinic are able to receive 0.25 AMA PRA Category 1 Credits™ for each case they complete. Completion of an evaluation form is required to receive credit and a link is provided on the last panel of the activity. 

0.25 AMA PRA Category 1 Credit(s)™

Estimated time to complete this activity: 0.25 hours 

Lead Author(s): Theodore Loftsgard, APRN, ACNP.  All 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 this activity I will be better able to:

  1. Correctly interpret and identify clinical practices supported by the highest quality available evidence.
  2. Will be better able to establsh the optimal evaluation leading to a correct diagnosis for patients with pulmonary, critical care and sleep disorders.
  3. Will improve the translation of the most current clinical information into the delivery of high quality care for patients.
  4. Will integrate new treatment options in discussing available treatment alternatives 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: University of Arizona College of Medicine

Current Approval Period: January 1, 2015-December 31, 2016

Financial Support Received: None

 

History of Present Illness

A 64-year-old man underwent three vessel coronary artery bypass grafting (CABG). His intraoperative and postoperative course was remarkable other than transient atrial fibrillation postoperatively for which he was anticoagulated and incisional chest pain which was treated with ibuprofen. He was discharged on post-operative day 5. However, he presented to an outside emergency department two days later with chest pain which had been present since discharge but had intensified.

PMH, SH, and FH

He had the following past medical problems noted:

  • Coronary artery disease
  • Coronary artery aneurysm and thrombus of the left circumflex artery
  • Dyslipidemia
  • Hypertension
  • Obstructive sleep apnea, on CPAP
  • Prostate cancer, status post radical prostatectomy penile prosthesis

He had been a heavy cigarette smoker but had recently quit. Family history was noncontributory.

Physical Examination

His physical examination was unremarkable at that time other than changes consistent with his recent CABG.

Which of the following are appropriate at this time? (Click on the correct answer to proceed to the second of four panels)

  1. Chest x-ray
  2. Electrocardiogram (ECG)
  3. Troponins
  4. 1 and 3
  5. All of the above

Cite as: Loftsgard T, Terk J, Trapp L, Gali B. June 2016 critical care case of the month. Southwest J Pulm Criti Care. 2016 Jun:12(6):212-5. doi: http://dx.doi.org/10.13175/swjpcc043-16 PDF

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Rick Robbins, M.D. Rick Robbins, M.D.

May 2016 Critical Care Case of the Month

Layth Al-Jashaami, MD

Yousef Usta, MD

Negin N. Blattman, MD

Rakesh Nanda, MD 

 

Phoenix VA Health Care System

650 E Indian School Road

Phoenix, Arizona, 85012 USA

 

Critical Care Case of the Month CME Information

Members of the Arizona, New Mexico, Colorado and California Thoracic Societies and the Mayo Clinic are able to receive 0.25 AMA PRA Category 1 Credits™ for each case they complete. Completion of an evaluation form is required to receive credit and a link is provided on the last panel of the activity. 

0.25 AMA PRA Category 1 Credit(s)™

Estimated time to complete this activity: 0.25 hours 

Lead Author(s): Layth Al-Jashaami, MD.  All 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 this activity I will be better able to:

  1. Correctly interpret and identify clinical practices supported by the highest quality available evidence.
  2. Will be better able to establsh the optimal evaluation leading to a correct diagnosis for patients with pulmonary, critical care and sleep disorders.
  3. Will improve the translation of the most current clinical information into the delivery of high quality care for patients.
  4. Will integrate new treatment options in discussing available treatment alternatives 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: University of Arizona College of Medicine

Current Approval Period: January 1, 2015-December 31, 2016

Financial Support Received: None

 

History of Present Illness

A 50-year-old African American woman presented with weakness, altered mental status and constipation of 12 days duration. She was complaining of abdominal distension with diffuse pain and bloating. She denied melena, hematochezia or hematemesis. She had a history weight loss, anorexia and fatigue which had evolved over the past few months leading to recent severe weakness and inability to get out of bed.

Past Medical History, Social History and Family History

Her past medical history included HIV infection with AIDS and noncompliance with her antiretroviral medications. Her most recent CD4 count was <20 cells/uL and viral load of 554,483 copies/mL.

Physical Examination

Vital signs: Blood pressure, 120/80 mmHg, heart rate, 105/min, temperature, 98.6° and respiratory rate, 20/min.

General: Physical examination showed a lethargic female who was poorly responsive to questioning.

Abdomen: Distended, tympanic abdomen with hypoactive bowel sounds and diffuse tenderness.

Radiography

Plain x-ray examination of the abdomen on admission is shown in Figure 1.

Figure 1. Admission x-ray of the abdomen.

Which of the following are possible causes of the patient's complaints, physical findings and abdominal x-ray findings? (Click on the correct answer to proceed to the second of six panels)

  1. Electrolyte disturbances
  2. Use of anticholinergic drugs
  3. Use of narcotics
  4. 1 and 3
  5. All of the above

Cite as: Al-Jashaami L, Usta Y, Blattman NN, Nanda R. May 2016 critical care case of the month. Southwest J Pulm Crit Care. 2016 May;12(5):171-9. doi: http://dx.doi.org/10.13175/swjpcc038-16 PDF

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Rick Robbins, M.D. Rick Robbins, M.D.

Design of an Electronic Medical Record (EMR)-Based Clinical Decision Support System to Alert Clinicians to the Onset of Severe Sepsis

Stephanie Fountain, MD

James Perry III, MD

Brenda Stoffer

Robert Raschke, MD

 

Banner University Medical Center Phoenix

Phoenix, AZ, USA

 

Abstract

Background: The aim of our study was to design an electronic medical record ­based alert system to detect the onset of severe sepsis with sensitivity and positive predictive value (PPV) above 50%.

Methods: The PPV for each of seven potential criteria for suspected infection (white blood cell count (WBCC) >12 or <4 x 109 /L, immature granulocyte count >0.1 K/uL or immature granulocyte % >1%, temperature >38 C. or <36 C. or the initiation of broad­spectrum antibiotics) was determined by chart review of 160 consecutive patients who had evidence of organ system failure (as defined by standard criteria)plus at least one of the proposed criteria. Then, using only criteria with calculated PPV >50%, the charts of sixty consecutive patients who met CMS criteria for severe sepsis were reviewed to calculate the sensitivity of organ dysfunction plus any one of the suspected infection criteria.

Results: Four proposed criteria for suspected infection had PPV >50%: WBCC >12 x 10 9 /L (69%; 95%CI:53­84%), Temperature >38C. (84%; 95%CI:68­100%), Temperature <36C. (57% 95%CI:36­78%), and initiation of antibiotics (70% 95%CI:56­84%). These four criteria were present in 53/60 of the patients with severe sepsis by CMS criteria, yielding a sensitivity of 88.3% (95%CI: 80.2­96.4%). Alert criteria were satisfied before the onset of severe sepsis in 25/53 cases, and within 90 minutes afterwards in 28/53 cases.

Conclusions: Our criteria for suspected infection plus organ dysfunction yields reasonable sensitivity and PPV for the detection of severe sepsis in real­time.

Editor's Note: For accompanying editorial click here

Introduction

The American College of Chest Physicians and the Society for Critical Care Medicine define sepsis as a systemic inflammatory syndrome in response to infection and defined sepsis as “severe” when associated with acute organ dysfunction (1,2). The incidence of severe sepsis varies depending on the method of data abstraction from 300 to >1,000 per 100,000 person-years with an in-hospital mortality of 14.7% to 29.9% (3). Severe sepsis was estimated to cost U.S. healthcare system more than $24 billion in 2007 (4). The incidence and mortality of severe sepsis is expected to continue to rise (3-6).

Early recognition of severe sepsis and rapid implementation of standardized treatment bundles is associated with improved patient outcomes (7-12), but compliance rates with standardized time-sensitive treatment bundles for severe sepsis are generally in the 30% range (13). One reason may be that clinicians do not always recognize the onset of severe sepsis and therefore don’t have the opportunity to initiate all the elements required for bundle compliance in time. Therefore, a system that could alert providers to the onset of severe sepsis could help them achieve bundle compliance.

Clinical Decision Support Systems (CDSSs) use innovative software incorporated into electronic medical records (EMRs) to augment the awareness and expert knowledge of clinicians by providing pertinent and timely information at the point of care. CDSSs are adept at performing surveillance of electronic data to identify patients with vital signs and laboratory findings consistent with clinical deterioration. Several researchers have previously attempted to identify patients with severe sepsis in real-time with EMR-based CDSSs, but these systems suffered poor positive predictive value (PPV) and uncertain sensitivity (14,15). The PPV of a CDSS surveillance alert is important because it is inversely related to the proportion of false alerts. False alerts lead to clinician alert fatigue and subsequent disregard of alert recommendations (16,17).  High sensitivity is another important operating characteristic, but sensitivity is typically only achievable at the cost of reducing PPV. 

The goal of this pilot study was to develop criteria that could be used in a CDSS to identify patients at the onset of severe sepsis in real-time in order to alert clinicians. We chose to operationalize severe sepsis as organ system dysfunction due to infection, without requiring systemic inflammatory response syndrome, since a recent study that showed that the requirement of SIRS in the definition of severe sepsis excludes 1-in-8 patients suffering organ system dysfunction due to infection (18).  Organ dysfunction already has a standard definition based on laboratory results and vital signs (2) that are  discrete and easily extracted from the EMR by CDSS logic, but suspected infection does not.   Thus, a specific aim of this study is to determine optimal EMR-based criteria to define suspected infection in relation to the diagnosis of severe sepsis.  Our hypothesis was that we could identify a set of criteria for suspected infection which would have acceptable sensitivity and PPV for severe sepsis when combined with standard organ system dysfunction criteria.      

Methods

We chose seven potential criteria to identify suspected infection: the presence of a white blood cell count (WBCC) >12 x 109/L or <4 x 109/L, immature granulocyte count >0.1 K/uL or immature granulocyte % >1%, temperature >38 C. or <36 C. or the initiation of broad-spectrum antibiotics (piperacillin/tazobactam, third or fourth-generation cephalosporin, aminoglycoside, carbapenem, or vancomycin).  Organ system dysfunction was identified in the EMR as previously described and delineated in table 1.  

Table 1. Suspected infection and organ dysfunction criteria.

Our study occurred in two phases.  In the first, we tested individual criteria related to suspected infection in order to determine which had PPV >50% and were therefore incorporated into the second phase of the study.  In the second phase, we combined those accepted criteria for suspected infection with organ system dysfunction criteria and calculated the sensitivity for the diagnosis of severe sepsis as defined by Centers for Medicare and Medicaid (CMS).

Phase 1.  We used Cerner Discern® to access clinical data in our Cerner Millennium® EMR (Cerner Corporation, North Kansas City MO, USA) in order to identify a retrospective cohort of 160  Banner Health inpatients who satisfied any one of the seven potential suspected infection criteria plus one organ system dysfunction criteria (Table 1) within an eight-hour window.

The cohort consisted of four groups of forty patients each based on the type of suspected infection criteria present: abnormal WBCC, abnormal temperature, elevated immature granulocytes and initiation of antibiotics.  Patients were also selected so that half met criteria in the emergency department and half on the hospital wards.  Patient selection was otherwise consecutive. Chart reviews were performed by physician research staff to determine whether each patient was suffering the onset of severe sepsis at the time suspected infection and organ dysfunction criteria were satisfied. Such patients were considered to be true positive for the purposes of calculating PPVs. We decided a-priori that individual criteria that did not achieve at least 50% PPV would not be used in our final list of accepted criteria for suspected infection to be used in phase 2 of our study. We also compared PPV for each criteria between emergency department patients and inpatients.

Phase 2. The charts of sixty consecutive patients who met CMS criteria for severe sepsis in Banner Health were reviewed to calculate sensitivity of the combination of any one of the suspected infection criteria accepted in phase 1, plus one organ system dysfunction criteria occurring together within a six-hour window. The gold standard for the diagnosis of severe sepsis, and the time of onset of severe sepsis, were determined using CMS criteria by trained Banner Health data extraction staff for the primary purpose of regulatory reporting to CMS. The chart of each patient identified with severe sepsis by CMS methodology was reviewed to determine how many exhibited criteria for suspected infection and organ system dysfunction within 8 hours before, or 90 minutes after the onset of severe sepsis determined by CMS methodology.  [The rationale for this time window was that a hypothetical alert triggered by these criteria would only be valuable if it identified patients before, or shortly after the onset of severe sepsis].  We considered these to be true positive for the purposes of calculating sensitivity.

Results

Phase 1: PPVs with 95% confidence intervals for each of the potential criteria for suspected infection are listed in Table 2 below.

Table 2. PPV and 95% CI for individual suspected infection criteria (when found in temporal association with organ system dysfunction) for the clinical diagnosis of severe sepsis.

Only WBCC had a significantly different PPV when used in the emergency department vs the inpatient wards:  84% vs 50% (p=0.03).   

Immature granulocytes and WBCC <4 x 109/L had PPV <50% and could be excluded from the set of accepted criteria with no loss of sensitivity. The set of accepted criteria include: WBCC >12 x 109/L. temperature >38 or <36 and initiation of antibiotics. Finding any one of these accepted criteria in association with organ system dysfunction yielded a PPV of 70% (95%CI: 61-78%) for the diagnosis of severe sepsis.  

In 35/115 cases in which patients with one of these accepted criteria for suspected infection were not suffering an infection (false positive) the actual diagnoses included: cardiovascular diseases (s/p coronary artery bypass, myocardial infarction, cardiogenic shock), post-operative state, endocrinological disorders (hypothyroidism, diabetic ketoacidosis, adrenal failure), central nervous system pathology (intracranial hemorrhage, subarachnoid hemorrhage, seizure), obstetrical complications (placenta previa, spontaneous hemorrhage), and gastrointestinal hemorrhage.

Conclusions

Our data suggests that the best criteria set for suspected infection are likely to be: WBCC >12 x 109/L, temperature >38 or <36 C. or initiation of broad spectrum antibiotics. The PPV of this set of criteria is likely to be >60%.  Leukopenia, and elevated immature granulocyte counts each had poor PPV and their exclusion would not significantly diminish the sensitivity of the set of criteria. 

Compared to other alert systems, this logic is novel for its abandonment of the use of SIRS criteria and the inclusion of antibiotic initiation. It could be argued that initiation of antibiotics should not be used to identify suspected infection because the clinician starting antibiotics is obviously already aware of infection.  However, unpublished analysis of 323 Banner health patients who qualified for severe sepsis by CMS criteria showed that 76% of those who failed bundle compliance received appropriate and timely antibiotics, but failed other important aspects of care, such as getting blood cultures before starting antibiotics and assessing lactate concentration. This suggests that a severe sepsis alert, triggering when a clinician enters an order for antibiotics could potentially assist the clinician in ordering other bundle elements. Exclusion of antibiotic initiation from our accepted criteria would have reduced the sensitivity of our alert logic to 75%.

The operating characteristics of our CDSS compares favorably to four previously published severe sepsis surveillance CDSSs which utilized SIRS criteria (see table 3 below). 

Table 3. Operating characteristics of CDSSs designed to provide surveillance for severe sepsis.

One of the strengths of this alert logic is that is it widely generalizable. It only includes data that is collected on most, if not all, hospitalized patients. It does not require additional tests or measurements that may limit its utility to a smaller patient population. It does not require physicians or ancillary staff to perform additional tasks or deviate from their standard workflow. Another strength of this logic is that it was created within the software program Cerner Discern® in our Cerner Millennium® EMR, one of the most widely used EMRs across the country. This would potentially allow seamless integration into any hospital system using this software, improving patient care and fulfilling “meaningful use” mandate of the Affordable Care Act.  However, our study is only a small pilot study. These results will need further validation using a larger data set. Further studies are needed to show whether a CDSS using these criteria can improve clinical outcomes of patients with severe sepsis.

Refenences

  1. Geroulanos S, Douka ET. Historical perspective of the word "sepsis". Intensive Care Med. 2006 Dec;32(12):2077. [CrossRef] [PubMed]
  2. Bone RC, Balk RA, Cerra FB, Dellinger RP, Fein AM, Knaus WA, Schein RM, Sibbald WJ. Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. The ACCP/SCCM Consensus Conference Committee. American College of Chest Physicians/Society of Critical Care Medicine. Chest. 1992 Jun;101(6):1644-55. [CrossRef] [PubMed]
  3. Gaieski DF, Edwards JM, Kallan MJ, Carr BG. Benchmarking the incidence and mortality of severe sepsis in the United States. Crit Care Med. 2013 May;41(5):1167-74. [CrossRef] [PubMed]
  4. Lagu T, Rothberg MB, Shieh MS, Pekow PS, Steingrub JS, Lindenauer PK. Hospitalizations, costs, and outcomes of severe sepsis in the United States 2003 to 2007. Crit Care Med. 2012 Mar;40(3):754-61. [CrossRef] [PubMed]
  5. Dombrovskiy VY, Martin AA, Sunderram J, Paz HL. Rapid increase in hospitalization and mortality rates for severe sepsis in the United States: a trend analysis from 1993 to 2003. Crit Care Med. 2007 May;35(5):1244-50. [Pubmed]
  6. Angus DC, Linde-Zwirble WT, Lidicker J, Clermont G, Carcillo J, Pinsky MR. Epidemiology of severe sepsis in the United States: analysis of incidence, outcome, and associated costs of care. Crit Care Med. 2001 Jul;29(7):1303-10. [CrossRef] [PubMed]
  7. Miller RR 3rd, Dong L, Nelson NC, Brown SM, Kuttler KG, Probst DR, Allen TL, Clemmer TP; Intermountain Healthcare Intensive Medicine Clinical Program. Multicenter implementation of a severe sepsis and septic shock treatment bundle. Am J Respir Crit Care Med. 2013 Jul 1;188(1):77-82. [CrossRef] [PubMed]
  8. Levy MM, Rhodes A, Phillips GS, Townsend SR, Schorr CA, Beale R, Osborn T, Lemeshow S, Chiche JD, Artigas A, Dellinger RP. Surviving Sepsis Campaign: association between performance metrics and outcomes in a 7.5-year study. Intensive Care Med. 2014 Nov;40(11):1623-33. [CrossRef] [PubMed]
  9. Levy MM, Dellinger RP, Townsend SR, Linde-Zwirble WT, Marshall JC, Bion J, Schorr C, Artigas A, Ramsay G, Beale R, Parker MM, Gerlach H, Reinhart K, Silva E, Harvey M, Regan S, Angus DC. The Surviving Sepsis Campaign: results of an international guideline-based performance improvement program targeting severe sepsis. Intensive Care Med. 2010 Feb;36(2):222-31. [CrossRef] [PubMed]
  10. Dellinger RP, Levy MM, Rhodes A, et al. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock, 2012. Intensive Care Med. 2013 Feb;39(2):165-228. [CrossRef] [PubMed]
  11. Levy MM, Pronovost PJ, Dellinger RP, Townsend S, Resar RK, Clemmer TP, Ramsay G. Sepsis change bundles: converting guidelines into meaningful change in behavior and clinical outcome. Crit Care Med. 2004 Nov;32(11 Suppl):S595-7. [CrossRef] [PubMed]
  12. ProCESS Investigators, Yealy DM, Kellum JA, Huang DT, Barnato AE, Weissfeld LA, Pike F, Terndrup T, Wang HE, Hou PC, LoVecchio F, Filbin MR, Shapiro NI, Angus DC. A randomized trial of protocol-based care for early septic shock. N Engl J Med. 2014 May 1;370(18):1683-93. [CrossRef] [PubMed]
  13. Gao F, Melody T, Daniels DF, Giles S, Fox S. The impact of compliance with 6-hour and 24-hour sepsis bundles on hospital mortality in patients with severe sepsis: a prospective observational study. Crit Care. 2005;9(6):R764-70. [CrossRef] [PubMed]
  14. Tafelski S, Nachtigall I, Deja M, Tamarkin A, Trefzer T, Halle E, Wernecke KD, Spies C. Computer-assisted decision support for changing practice in severe sepsis and septic shock. J Int Med Res. 2010 Sep-Oct;38(5):1605-16. [CrossRef] [PubMed]
  15. Umscheid CA, Betesh J, VanZandbergen C, Hanish A, Tait G, Mikkelsen ME, French B, Fuchs BD. Development, implementation, and impact of an automated early warning and response system for sepsis. J Hosp Med. 2015 Jan;10(1):26-31. [CrossRef] [PubMed]
  16. Guidi JL, Clark K, Upton MT, et al. Clinician Perception of the Effectiveness of an Automated Early Warning and Response System for Sepsis in an Academic Medical Center. Ann Am Thorac Soc. 2015 Oct;12(10):1514-9. [CrossRef] [PubMed]
  17. Shapiro NI, Howell MD, Talmor D, et al. Implementation and outcomes of the Multiple Urgent Sepsis Therapies (MUST) protocol. Crit Care Med. 2006 Apr;34(4):1025-32. [CrossRef] [PubMed]
  18. Kaukonen KM, Bailey M, Pilcher D, Cooper DJ, Bellomo R. Systemic inflammatory response syndrome criteria in defining severe sepsis. N Engl J Med. 2015 Apr 23;372(17):1629-38. [CrossRef] [PubMed]
  19. Alsolamy S, Al Salamah M, Al Thagafi M, et al. Diagnostic accuracy of a screening electronic alert tool for severe sepsis and septic shock in the emergency department. BMC Med Inform Decis Mak. 2014 Dec 5;14:105. [CrossRef] [PubMed]
  20. Amland RC, Lyons JJ, Greene TL, Haley JM. A two-stage clinical decision support system for early recognition and stratification of patients with sepsis: an observational cohort study. JRSM Open. 2015 Oct 8;6(10):2054270415609004. [CrossRef] [PubMed]
  21. Semler MW, Weavind L, Hooper MH, et al. An Electronic Tool for the Evaluation and Treatment of Sepsis in the ICU: A Randomized Controlled Trial. Crit Care Med. 2015 Aug;43(8):1595-602. [CrossRef] [PubMed]
  22. Nelson JL, Smith BL, Jared JD, Younger JG. Prospective trial of real-time electronic surveillance to expedite early care of severe sepsis. Ann Emerg Med. 2011 May;57(5):500-4. [CrossRef] [PubMed]

Cite as: Fountain S, Perry J III, Stoffer B, Raschke R. Design of an electronic medical record (EMR)-based clinical decision support system to alert clinicians to the onset of severe sepsis. Southwest J Pulm Crit Care. 2016 Apr;12(4):153-60. doi: http://dx.doi.org/10.13175/swjpcc021-16 PDF

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Rick Robbins, M.D. Rick Robbins, M.D.

April 2016 Critical Care Case of the Month

Samir Sultan, DO

Banner University Medical Center Phoenix

Phoenix, AZ

 

Critical Care Case of the Month CME Information

Members of the Arizona, New Mexico, Colorado and California Thoracic Societies and the Mayo Clinic are able to receive 0.25 AMA PRA Category 1 Credits™ for each case they complete. Completion of an evaluation form is required to receive credit and a link is provided on the last panel of the activity. 

0.25 AMA PRA Category 1 Credit(s)™

Estimated time to complete this activity: 0.25 hours 

Lead Author(s): Samir Sultan, DO.  All 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 this activity I will be better able to:

  1. Correctly interpret and identify clinical practices supported by the highest quality available evidence.
  2. Will be better able to establsh the optimal evaluation leading to a correct diagnosis for patients with pulmonary, critical care and sleep disorders.
  3. Will improve the translation of the most current clinical information into the delivery of high quality care for patients.
  4. Will integrate new treatment options in discussing available treatment alternatives 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: University of Arizona College of Medicine

Current Approval Period: January 1, 2015-December 31, 2016

Financial Support Received: None

 

History of Present Illness

The patient is a 22-year-old African-American man who was initially seen following a rapid response team called to the neonatal intensive care unit for a seizure. He was visiting his newborn child. The nurses described the seizure as tonic-clonic which resolved spontaneously without treatment before the rapid response team arrived.

Past Medical History, Family History and Social History

The patient has a past medical history of a brain aneurysm treated by coil embolization 2 years earlier. He had no complications of the embolization including seizures. Family history is unremarkable. He smokes 1-2 cigars per day but does not drink alcohol.

Physical Examination

He was drowsy when initially seen but the drowsiness resolved in about 5 minutes. The physical examination was unremarkable and there were no focal neurologic signs.

What should be next? (Click on the correct answer to proceed to the second of seven panels)

  1. CT scan of the head
  2. Phenytoin administration
  3. Metabolic screening (BUN, glucose and electrolytes)
  4. 1 and 3
  5. All of the above

Cite as: Sultan S. April 2016 critical care case of the month. Southwest J Pulm Crit Care. 2016 Apr;12(4): . doi: http://dx.doi.org/10.13175/swjpcc033-16 PDF 

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Rick Robbins, M.D. Rick Robbins, M.D.

Ultrasound for Critical Care Physicians: Two’s a Crowd

A 43 year old previously healthy woman was transferred to our hospital with refractory hypoxemia secondary to acute respiratory distress syndrome (ARDS) due to H1N1 influenza. She had presented to the outside hospital one week prior with cough and fevers. Chest radiography and computerized tomography of the chest revealed bilateral airspace opacities due to dependent consolidation and bilateral ground glass opacities. A transthoracic echocardiogram at the time of the patient’s admission was reported as not revealing any significant abnormalities.

At the outside hospital she was placed on mechanical ventilation with low tidal volume, high Positive end-expiratory pressure (20 cm H20), and a Fraction of inspired Oxygen (FiO2) of 1.0. Paralysis was later employed without significant improvement.

Upon arrival to our hospital, patient was severely hypoxemic with partial pressure of oxygen / FiO2  (P/F) ratio of 43. She was paralyzed with cis-atracurium and placed on airway pressure release ventilation (APRV) with the following settings (pressure high 28 cm H2O, pressure low 0 cm H2O, time high 5.5 sec, time low 0.5 sec). The patient remained severely hypoxemic with on oxygen saturation in the high 70 percent range.

A bedside echocardiogram was performed (Figures 1 and 2).

Figure 1. Subcostal long axis echocardiogram.

 

Figure 2. Subcostal short axis echocardiogram

What abnormality is demonstrated by the short and long axis subcostal views? (Click on the correct answer for an explanation)

Cite as: Abukhalaf J, Boivin M. Ultrasound for critical care physicians: two's a crowd. Southwest J Pulm Crit Care. 2016 Mar;12(3):104-7. doi: http://dx.doi.org/10.13175/swjpcc028-16 PDF

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Rick Robbins, M.D. Rick Robbins, M.D.

March 2016 Critical Care Case of the Month

Theo Loftsgard APRN, ACNP

Joel Hammill APRN, CNP

 

Mayo Clinic Minnesota

Rochester, MN USA

 

Critical Care Case of the Month CME Information

Members of the Arizona, New Mexico, Colorado and California Thoracic Societies and the Mayo Clinic are able to receive 0.25 AMA PRA Category 1 Credits™ for each case they complete. Completion of an evaluation form is required to receive credit and a link is provided on the last panel of the activity. 

0.25 AMA PRA Category 1 Credit(s)™

Estimated time to complete this activity: 0.25 hours

Lead Author(s): Theo Loftsgard APRN, ACNP.  All 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 this activity I will be better able to:

  1. Correctly interpret and identify clinical practices supported by the highest quality available evidence.
  2. Will be better able to establsh the optimal evaluation leading to a correct diagnosis for patients with pulmonary, critical care and sleep disorders.
  3. Will improve the translation of the most current clinical information into the delivery of high quality care for patients.
  4. Will integrate new treatment options in discussing available treatment alternatives 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: University of Arizona College of Medicine

Current Approval Period: January 1, 2015-December 31, 2016

Financial Support Received: None

 

History of Present Illness

A 58-year-old man was admitted to the ICU in stable condition after an aortic valve replacement with a mechanical valve.

Past Medical History

He had with past medical history significant for endocarditis, severe aortic regurgitation related to aortic valve perforation, mild to moderate mitral valve regurgitation, atrial fibrillation, depression, hypertension, hyperlipidemia, obesity, and previous cervical spine surgery. As part of his preop workup, he had a cardiac catheterization performed which showed no significant coronary artery disease. Pulmonary function tests showed an FEV1 of 55% predicted and a FEV1/FVC ratio of 65% consistent with moderate obstruction.

Medications

Amiodarone 400 mg bid, digoxin 250 mcg, furosemide 20 mg IV bid, metoprolol 12.5 mg bid. Heparin nomogram since arrival in the ICU.

Physical Examination

He was extubated shortly after arrival in the ICU. Vitals signs were stable. His weight had increased 3 Kg compared to admission. He was awake and alert. Cardiac rhythm was irregular. Lungs had decreased breath sounds. Abdomen was unremarkable.

Laboratory

His admission laboratory is unremarkable and include a creatinine of 1.0 mg/dL, blood urea nitrogen (BUN) of 18 mg/dL, white blood count (WBC) of 7.3 X 109 cells/L, and electrolytes with normal limits.

Radiography

His portable chest x-ray is shown in Figure 1.

Figure 1. Portable chest x-ray taken on admission to the ICU. 

What should be done next? (Click on the correct answer to proceed to the second of five panels)

  1. Bedside echocardiogram
  2. Diuresis with a furosemide drip because of his weight gain and cardiomegaly
  3. Observation
  4. 1 and 3
  5. All of the above

Cite as: Loftsgard T, Hammill J. March 2016 critical care case of the month. Southwest J Pulm Crit Care. 2016;12(3):81-8. doi: http://dx.doi.org/10.13175/swjpcc018-16 PDF

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Rick Robbins, M.D. Rick Robbins, M.D.

February 2016 Critical Care Case of the Month

Thomas M. Stewart, MD

Bhargavi Gali, MD 

 

Department of Anesthesiology

Mayo Clinic Minnesota

Rochester, MN USA

  

Case Presentation

A 32 year-old, previously healthy, female hospital visitor had been participating in a family care conference regarding her critically ill grandmother admitted to the cardiac intensive care unit. During the care conference, she felt unwell and had some mild chest discomfort; she collapsed and cardiopulmonary resuscitation (CPR) was initiated (1). Upon arrival of the code team, she was attached to the monitor and mask ventilation was initiated. Her initial rhythm is shown in Figure 1.

Figure 1. Initial rhythm strip.

In addition to DC cardioversion which of the following should be administered immediately? (Click on the correct answer to proceed to the second of four panels)

  1. Lidocaine
  2. Magnesium sulfate
  3. Procainamide
  4. 1 and 3
  5. All of the above

Cite as: Stewart TM, Gali B. February 2016 critical care case of the month. Southwest J Pulm Crit Care. 2016;12(2):41-5. doi: http://dx.doi.org/10.13175/swjpcc011-16 PDF 

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Rick Robbins, M.D. Rick Robbins, M.D.

Ultrasound for Critical Care Physicians: Hungry Heart

A 31-year-old incarcerated man with a past medical history of intravenous drug use and hepatitis C, presented with a one week history of dry, non-productive cough, orthopnea and exertional dyspnea. He denied current intravenous drug use, and endorsed that the last time he used was before he was incarcerated over 3 years ago, his last tattoo was in prison, 6 months prior. He was found to have an oxygen saturation of 77% on room air, fever of 40º C, heart rate of 114 bpm, and blood pressure of 80/50 mmHg. The patient had a leukocytosis of 14 x109/L, and a chest x-ray demonstrating patchy airspace disease. Blood cultures were sent and he was treated with antibiotics and vasopressors for septic shock. The patient was intubated for acute hypoxemic respiratory failure secondary to multifocal pneumonia. A bedside transthoracic echocardiogram was performed. 

Figure 1. Apical four chamber view echocardiogram with color Doppler over the mitral valve.

 

Figure 2. Right Ventricular (RV) inflow view echocardiogram from same patient

 

What is the likely diagnosis supported by the echocardiogram? (Click on the correct answer for an explanation)

Cite as: Villalobos N, Stoltze K, Azeem M. Ultrasound for critical care physicians: hungry heart. Southwest J Pulm Crit Care. 2016;12(1):24-7. doi: http://dx.doi.org/10.13175/swjpcc007-16 PDF

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Rick Robbins, M.D. Rick Robbins, M.D.

January 2016 Critical Care Case of the Month

Sandra L. Till, DO

Banner University Medical Center Phoenix

Phoenix, AZ USA  

History of Present Illness

The patient is an 18-year-old woman who was driving to high school on a frontage road when she fell asleep at the wheel and her car rolled over. She was wearing her seatbelt but there was no airbag deployment. She did not lose consciousness and she was responsive and answering questions at the scene. She self-extricated from the vehicle. She had left arm pain with a boney deformity and she walked to the ambulance that transferred her to the hospital emergency department (ED).

Upon arrival in the ED she appeared pale and had difficulty breathing. In addition to her arm pain with an obvious left humeral fracture she also complained of upper abdominal and anterior chest pain. O2 saturation was initially 90% but declined to 70%.

Which of the following should be ordered immediately? (Click on the correct answer to proceed to the second of six panels)

  1. Begin intravenous lines with large bore needles
  2. X-ray of humerus
  3. Hemoglobin and hematocrit
  4. 1 and 3
  5. All of the above

Cite as: Till SL. January 2016 critical care case of the month. Southwest J Pulm Crit Care. 2016;12:6-12. doi: http://dx.doi.org/10.13175/swjpcc151-15 PDF 

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