Physical Examination in the Intensive Care Unit: Opinions of Physicians at Three Teaching Hospitals

Rodrigo Vazquez, MD¹

Cristina Vazquez Guillamet, MD¹

Mohamed Adeel Rishi, MD²

Jorge Florindez, MD⁴

Priya S Dhawan, MD³

Sarah E. Allen, MD¹

Constantine A Manthous, MD⁵

Geoffrey Lighthall MD, PhD⁶

Affiliations: University of New Mexico School of Medicine¹ Albuquerque NM. McNeal Hospital², Berwyn Il. Mayo Clinic Arizona³, Scottsdale AZ. Bridgeport Hospital⁴, Bridgeport CT. Yale School of Medicine⁵, New Haven CT. Stanford University School of Medicine⁶, Stanford CA.

Study Sites: Stanford University Medical Center, Stanford CA. McNeal Hospital, Berwyn Il and Bridgeport Hospital, Bridgeport CT.

Abstract

Purpose: Technological advances in intensive care unit may lead physicians to question or omit portions of the physical exam. Our goal is to assess the opinions of intensive care unit physicians about physical examination in modern day medicine.

Methods: Subjects included physicians on medical intensive care unit teams at one university hospital and two university-affiliated teaching hospitals. Participants responded to an interview divided into two sections: (1) A semi-structured interview including open-ended questions on the management of four critical care scenarios and on the utility of physical exam; (2) Multiple-choice questions about physical exam.

Main Results: The response rate was 100%. A total of 122 individuals, 16(13%) attendings, 24(20%) fellows and 82(67%) residents, responded. Half 61 (50%) considered physical examination to be of limited utility in the intensive care unit. Fifteen percent of answers to the clinical scenarios were reasoned based on physical examination. Most extended the definition of physical examination to include data derived from monitoring 119(97%), life support 121(99%) and bedside imaging devices 112(92%). Residents 45(37%), students 35(29%) and nurses 35(29%) were recognized as the team members who examine patients the most.

Conclusion: Physical examination was considered useful by half of the physicians. Percussion is the least appreciated component. The role of nurses examining patients is recognized. A new definition of physical examination that extends beyond the patient to include monitoring, life support and bedside imaging is proposed to revitalize bedside clinical medicine.

For accompanying editorial click here.

Introduction

Physical examination is one of the mainstays of clinical activities at the bedside. The many maneuvers and signs of the physical exam were developed and described over the last two centuries when most patients presented in advanced states of disease with obvious physical examination findings (1). In the last few decades, advances in fields of imaging, laboratory and bedside monitoring technologies have increased expectations for early and accurate diagnoses, often before physical exam findings become apparent (2).

In Critical Care Units (ICU) patients have severe presentations of diseases, making it likely to encounter diagnostic physical examination findings; however ICUs have easy access to imaging and automated physiologic measurements that may lead physicians to question, or omit portions, of the physical examination.

In this context, we sought the opinions of physicians working in intensive care units about physical examination in modern day medicine.

Material and Methods

The study was divided into two sections. The first is based on mixed methods analysis (qualitative and quantitative) of semi-structured interviews with open-ended questions. The second is based on the quantitative analysis of multiple-choice questions.

Setting

The study was conducted in 2011, in three ICUs in three states.  One of three hospitals (Stanford) was a 32-bed closed medical-surgical unit in a university medical center hospital. The other two hospitals were 16-17 bed closed medical units at university-affiliated community teaching hospitals. All three hospitals had postgraduate residencies in Internal Medicine and Pulmonary and Critical Care Medicine, and were equipped with electronic medical records systems and computer acquisition and storage of bedside data. At the time of the study, Stanford had begun an initiative to increase the use and appreciation of physical examination in its medical school (3). No other confounding variables were apparent. The Investigational Review Boards of each center approved the protocol independently and waived the need for written consent.

Eligible subjects included residents, critical care fellows, and attending physicians on ICU rotations. Investigators approached all candidates for possible participation; subjects were informed that the study would evaluate their approach to diagnosis and treatment of ICU patients but not about its specific focus on physical examination.

Data collection

Demographic data collected included age, gender, type of specialty and subspecialty training, and level of training.

First section

Semi-structured interviews on how four hypothetical ICU clinical vignettes would be managed; questions were chosen by consensus of the authors and responses were open-ended.

Subjects were presented with this introductory statement: “I’m going to present you with four clinical scenarios. I would like you to explain how you would manage these clinical scenarios in real life. This is not an exam. We are just interested in how physicians practice.” The following four case scenarios were then introduced: “You have to manage an Intensive Care Unit patient with: 1) hypoxemia, 2) hypotension, 3) dyspnea and 4) oliguria. What would you do?”

After discussing management of the case scenarios, subjects were then asked: “What’s your opinion about the utility of physical exam in the ICU?”

Second section

Multiple-choice questions were then asked of each subject:

- How frequently do you examine your patients? Answer choices (or options): “Always, sometimes, never”

-Who do you think examines their patients the most? Answer choices: “Attendings, fellows, residents, students or nurses”

 -Which data obtained at the bedside should be included in an updated definition of physical exam in the ICU? Inspection? palpation? percussion? auscultation? venous lines? arterial line data? ventilator data?, bedside ultrasonography? Answer options: “Strongly agree, agree, disagree, strongly disagree”

The interview was pilot tested in six subjects to verify subjects had a clear understanding of the questions. Investigators performing the interviews were the same within each center and were trained prior to subject enrollment. Investigators read the questions in the same order. Subsequent questions were not revealed until the previous question had been answered. Responses were recorded and transcribed.

Analysis

Data analysis used a mixed-methods approach for the first section. The transcriptions were analyzed looking for key actions or ideas around which the rest of the response was organized, we called these “codes”. For example if an individual answered: “I would auscultate the lungs, order an arterial blood gas and a chest radiograph ” the codes would be lung auscultation, arterial blood gas and chest radiograph. After analyzing all the answers we decided to group “codes” into categories and report them as percentages of all the answers provided, four clinical scenarios per each of the 122 participants. For the previous example the categories would include: auscultation, laboratory test and radiology.

Mention of the physical exam was categorized as: a) mentions physical examination (e.g. “ I would examine the patient…”), b) mentions physical examination or the intention to go to the bedside, c) describes a reasoned physical examination (e.g.“ I would auscultate the lungs, if I heard wheezes then I would…”).

Illustrative comments were highlighted. The findings of each interviewer were checked against each other. In case of discrepancy, answers were compared to reach a consensus.

The analysis of the second section was quantitative.

We used the statistical package Stata 11. Chi² was used to compare rates. Factorial logistic regression and logistic regression were used to evaluate categorical and continuous data when appropriate. A p -value of <0.05 was considered significant.

Results

A total of 122 individuals were approached for study participation and all agreed to participate. The subjects included 16 (13%) attendings, 24 (20%) fellows and 82 (67%) residents. The average age was 32 years (range 24-65). There were 79 (65%) males. Most respondents had Internal Medicine training 116 (95%) and had attended medical school in the US 76 (62%).

First section

Clinical scenarios

Categories identified during the responses to the clinical scenarios are summarized in Table 1.

We report mention of the physical exam in three not mutually exclusive categories: a) mentions physical examination (e.g. “ I would examine the patient…”), b) mentions physical examination or the intention to go to the bedside, c) describes a reasoned physical examination (e.g.“ I would auscultate the lungs, if I heard wheezes then I would…”).

Answers to “What’s your opinion about the utility of physical exam in the ICU?” The physical exam was considered to be of “limited utility” by 61(50%) of the respondents. Table 2 includes answers that illustrate opinions for and against the utility of the physical exam.

According to the respondents, the components of the physical exam that remain useful in the intensive care unit are: a) general appearance; b) the neurological exam; c) abdominal exam since there are no adequate monitoring devices; d) anterior auscultation of the chest to detect pneumothoraces, effusions or cardiac murmurs; and e) examination of the skin.

Second section, multiple-choice questions

A. How frequently do you examine your patients?

Figure 1. Histogram with the percentages of each of the possible answers to question: How frequently do you examine your patients?

B. Who do you think examines patients the most? (Figure 2).

Figure 2. Histogram with the percentages for each of the possible answers to question: Who do you think examines patients the most?

C. Which data obtained at the bedside should be included in an updated definition of physical exam in the ICU?

At least 90% of the respondents agreed to include data obtained through inspection 112 (100%), auscultation 118 (97%), data from ventilators 121 (99 %), arterial lines 120 (98%), central lines 118 (97%), and bedside ultrasound 112(92%). Palpation 107(88%) and percussion 79 (65%) did not exceed the 90% threshold.

Besides the intergroup comparisons noted above, there were no statistically significant differences between responses based on level of training, age, gender, location of medical school training or hospital (p>0.05).

Discussion

We report the opinion of 122 physicians with regard to physical examination in the intensive care unit and the way they reported using the physical exam in four hypothetical clinical scenarios. We found that half of the physicians reported they considered physical exam useful, but only 15 percent mentioned physical exam in deducing answers to the clinical scenarios. Percussion was the least appreciated component of the physical exam. There was generalized agreement that the inclusion of data derived from bedside imaging, monitoring, and life support devices into an updated definition of physical examination would be valuable. Nurses and students were recognized as the team members who examined their patients the most. Study participants provided explanations behind their opinions.

The findings that only 50% of the physicians found the standard physical examination to be useful, and that only 15 % mentioned the physical exam in deducing their case scenario answers suggests a low appreciation for the standard physical exam. Available literature on the utility of the physical exam supports our current study findings. In one study the time spent at the bedside during clinical rounds was down to 11% from an historical 75%, with most of the time spent in hallways or conference rooms (4,5). In an ethnographic study, residents felt it was unnecessary to examine their patients in the ICU as long as they had monitoring and a good nurse (6).

Perceptions from patients and the general public support our findings that use of the physical exam is low. In a questionnaire to ambulatory patients, 56 patients perceived 113 omissions in their physician visit, the most common omissions being those related to what they felt were missed portions of the physical examination (7). Mass media has produced the following headlines: Physician revives a dying art: the physical; Is physical exam facing extinction? and Not on the Doctors’ checklist but touch matters (8-10).

Comments by our study participants help explain these findings. Participants had more confidence in the accuracy of data provided by monitoring devices and imaging than in findings of their physical exams.  Some participants mentioned that it was difficult to convince peers to change management based on physical examination findings alone. Participants also reported there was lack of role modeling physicians performing physical exams.

Attending and fellow physicians were perceived as the team members who examine their patients the least; Attending and fellows validated this perception in reporting examining their patients sometimes or never in more than half of the cases.

An alternative explanation for this perception about the senior team members could be related to differences in diagnostic reasoning between trainees and more experienced physicians (11). Students and residents probably relay more in hypothetic deductive reasoning and collect larger amounts of data, including a more detailed physical examination, to reach a diagnosis. As they become more experienced and start working as fellows and attendings the use of short cuts, heuristics, increases and they reach a diagnosis with smaller amounts of data. Time constraints also make them relay in the information relayed by more junior team members.

Whatever the reason for this perception about senior team members may be, it explains, at least in part, the atrophy of physical examination skills during residency training (12), and feeds a downward spiral with graduates that examine their patients less and less.

Residents, nurses and students on the other hand were recognized as the ones who examined their patients the most. This observation expands the role of nurses in the ICU, and if confirmed by others could change the allocation of responsibilities in the multidisciplinary ICU team.

Although until now our discussion portrays the current poor standings of physical examination in the ICU, we also found hope.

Despite the small proportion of participants basing their reasoning on physical examination during the clinical scenarios, most responses included going to the bedside and almost all participants agreed on extending the physical examination beyond the patient to include data derived from monitoring, life support and bedside imaging devices.

Just as Laennec revolutionized bedside diagnosis with the introduction of the stethoscope (13), a new standardized definition of physical examination including these new bedside diagnostic tools, has the potential to greatly enrich clinical medicine and would reflect the practice of modern medicine better (14,15). Critical care medicine is in a privilege position to lead this conceptual change and spread it to other specialties.

Our study has several limitations. First of all, it describes opinions and behaviors in theoretical scenarios and the answers provided may not correlate with true physician practices. The order and choice of the clinical scenarios and questions may have biased the respondents negatively against the physical exam. In support of our results, once the participants learned about the focus of the study one would have expected an attempt to offer better impressions of themselves with an “over reporting” bias towards the physical examination. However, our results pointed in the opposite direction. It does not correlate the use of physical examination to outcomes.

In regards to the composition of the respondents, residents conformed the great majority. Although one could argue that this limits the generalizability of the results, the proportion of residents, fellows and attending physicians mimics that found in the ICU teams at the participating institutions. Our findings may not be generalized to hospitals in areas with limited resources.

Finally its main limitation and at the same time its main virtue is the generation of new questions that will require new studies with direct observation of team practices and their correlation to patient outcomes.

Conclusion

Physical examination was considered useful by half of the physicians. Percussion is the least appreciated component. The role of nurses examining patients is recognized. A new definition of physical examination that extends to include monitoring, life support and bedside imaging is proposed to revitalize bedside clinical medicine.

Conflict of interests: The authors declare that they have no conflict of interest.

References

1. Walker HK, Hall WD, Hurst JW, Walker HK. The origins of the history and physical examination 3rd ed. Boston, MA: Butterworths; 1990.
2. Berenguer J, Bruguera M, Gervas J, et al. The Physician of the Future. El Metge del Futur. Fundacion Educaion Medica, Barcelona, Spain; 2009. Available at: http://www.econ.upf.edu/~ortun/publicacions/MedicoDelFuturo.pdf (accessed 1/6/15).
3. Verghese A, Horwitz RI. In praise of the physical examination. BMJ. 2009;339:b5448. [CrossRef] [PubMed]
4. LaCombe MA. On bedside teaching. Ann Intern Med. 1997;126(3):217-20. [CrossRef] [PubMed]
5. Miller M, Johnson B, Greene HL, Baier M, Nowlin S. An observational study of attending rounds. J Gen Intern Med. 1992;7(6):646-8. [CrossRef] [PubMed]
6. Bosk CL. Forgive and remember: managing medical failure. 2nd ed. Chicago, IL. University of Chicago Press; 2003. [CrossRef]
7. Kravitz RL, Callahan EJ. Patients' perceptions of omitted examinations and tests: A qualitative analysis. J Gen Intern Med. 2000;15(1):38-45. [CrossRef] [PubMed]
8. Knox R. The Fading Art Of The Physical Exam. National Public Radio. 2010. Available at: http://www.npr.org/player/v2/mediaPlayer.html?action=1&t=1&islist=false&id=129931999&m=129984296 (accessed 1/6/15).
9. Ofri D. Not on the doctor's checklist but touch matters. The New York Times. August 2, 2010.
10. Grady D. Physician revives a dying art: the physical. The New York Times. October 11, 2010. Available at: http://www.nytimes.com/2010/10/12/health/12profile.html?pagewanted=all&_r=0 (accessed 1/6/15).
11. Sackett DL, Tugwell P, Guyatt GH. Clinical epidemiology: a basic science for clinical medicine, 2nd ed. Boston: Little, Brown; 1991.
12. Mangione S, Nieman LZ. Cardiac auscultatory skills of internal medicine and family practice trainees. A comparison of diagnostic proficiency. JAMA. 1997;278(9):717-22. [CrossRef] [PubMed]
13. Laennec R. Traite de l’auscultation mediate. Bull Acad Natl Med. 1819;151:393-398.
14. COBATRICE Domain 2: diagnosis: assessment, investigation, monitoring and data interpretation. Available at: http://www.cobatrice.org/Data/ModuleGestionDeContenu/PagesGenerees/en/02-competencies/0B-diagnosis/8.asp (accessed 1/6/15).
15. American Association of Chest Physicians. Critical care ultrasonography. http://www.chestnet.org/Education/Advanced-Clinical-Training/Certificate-of-Completion-Program/Critical-Care-Ultrasonography (accessed 1/6/15).

Reference as: Vazquez R, Vazquez Guillamet C, Adeel Rishi M, Florindez J, Dhawan PS, Allen SE, Manthous CA, Lighthall G.  Physical examination in the intensive care unit: opinions of physicians at three teaching hospitals. Southwest J Pulm Crit Care. 2015;10(1):34-43. doi: http://dx.doi.org/10.13175/swjpcc165-14 PDF

Analysis of a Fatal Left Ventricular Assist Device Infection: A Case Report and Discussion

Neal Stuart Gerstein, MD FASE¹

Henry G. Chou, MD²

Andrew Lewis Dixon, MD¹

¹Department of Anesthesiology & Critical Care Medicine

University of New Mexico

Albuquerque, NM

²Department of Anesthesiology

Cedars-Sinai Medical Center

Los Angeles, CA

Introduction

Left ventricular assist device (VAD) therapy is an increasingly utilized treatment as a bridge to heart transplantation or as long-term destination therapy. Recent reports show there is a 22% - 32% incidence of VAD-associated infections with staphylococci and nosocomial gram-negative bacilli being the most common causative organisms (1,2). These organisms are often found in intensive care units, where they have the highest proportion of resistance, thus exposing already critically ill patients to the possibility of resistant organism VAD-associated infections (3). Mortality rates exceed 60% when sepsis develops in a patient with a continuous flow left VAD and infection is the number one cause of death in those awaiting cardiac transplantation (4,5). With continued left VAD use clinicians will likely see multidrug-resistant (MDR) or even pandrug-resistant organism VAD-associated infections. Clinicians need to be prepared to manage such an intimidating entity.

Case Report

We report a case of a 25 year-old male with a pandrug-resistant Pseudomonas aeruginosa VAD-associated infection. The patient’s medical history is significant for a diagnosis of idiopathic dilated cardiomyopathy refractory to maximal medical therapy requiring implantation of a HeartMate II (Thoratec Co., Pleasanton, CA, USA) continuous flow left VAD (Figure 1).

Figure 1. HeartMate II^® left VAD schematic (reprinted with the permission of Thoratec Co., Pleasanton, CA, USA).

His course was complicated with multiple hospital admissions for recurrent VAD-associated infections and numerous episodes of P. aeruginosa bacteremia that had been treated with a multitude of antipseudomonal antibiotics. He presented to our hospital for management of severe volume overload in the setting of VAD-associated infections. Transesophageal echocardiography demonstrated a left ventricular ejection fraction of 24% with severe left and right ventricular dilatation. Chest x-ray revealed cardiomegaly and multiple devices including the left VAD (Figure 2).

Figure 2. Chest X-ray demonstrating an enlarged cardiac silhouette, the HeartMate II axial pump (*) with inflow (down arrow, ↓) and outflow (up arrow, ↑) cannulas, biventricular pacer with leads in right atrium (A), coronary sinus (B), and right ventricle (C) (dashed arrows).

Blood cultures revealed MDR P. aeruginosa; except for showing intermediate sensitivity to tobramycin there was resistance to all antimicrobials tested. In vitro synergy testing revealed modest bacterial inhibition when only colistin, fosfomycin, imipenem, and tobramycin were combined. After maximizing medical therapy, multiple left VAD pocket washings and implantation of tobramycin beads followed. Intraoperative findings included an encapsulated infection around the driveline and obvious infection of the left VAD pocket. Repeat blood cultures showed P. aeruginosa had developed resistance to all antimicrobials including tobramycin. Subsequently the left VAD was explanted and the patient was transitioned to an extracorporeal membrane oxygenator (ECMO) in attempt to clear the infection. He was then transitioned to a TandemHeart (CardiacAssist Inc., Pittsburgh, PA, USA), a percutaneous LVAD, as he was not dependent on ECMO for oxygenation. He was able to clear the bacteremia after removal of the infected HeartMate II while on colistin, fosfomycin, tobramycin, azithromycin and rifampin, but was not able to clear the remaining left VAD pocket infection, which again spread systemically. Despite maximal medical and surgical interventions, he died from profound septic shock and multisystem organ failure. To date this is the first known case of a pandrug-resistant P. aeruginosa VAD-associated infection reported in the literature.

Discussion

P. aeruginosa organisms have intrinsic resistance to numerous broad spectrum antibiotics, and can easily develop acquired resistance to most if not all available antimicrobial agents (3). Risk factors for the development of pandrug-resistant P. aeruginosa include previous treatment with antipseudomonal antibiotics and prolonged treatment times. Given our patient had multiple P. aeruginosa infections, treated with multiple rounds of antipseudomonal antibiotics, it is not surprising that pandrug-resistance developed. Few therapeutic options are available for treatment and no new agents are available to evade the known resistance mechanisms. Treatment can be optimized using synergistic combination therapy, which may be the only medical management option in patients with pandrug-resistant P. aeruginosa infections. Some have suggested that rifampin in combination with colistin may be a promising approach (3). Some experts recommend in vitro synergy testing when an organism is resistant to currently recommended antibiotic regimens (6,7). However, a recent review of antibiotic therapy for gram-negative infections describes the utility of in vitro synergy testing equivocal in the context of Pseudomonas infection (8). We managed our patient with combination therapy; however, not until pandrug-resistant P. aeruginosa was isolated did we introduce rifampin in combination with colistin.

A recent review of VAD-associated infections showed the majority were managed without surgical intervention; only 13% required surgical debridement and only in cases of severe infection and/or failed conservative treatment was left VAD explantation required. Since this case there has been a proposed algorithm for management of VAD-associated infections (2); our management, though prior to published guidelines, was in step with the algorithm. Of note, there was no discussion of explanting an left VAD to ECMO to aid in clearing a resistant infection. We felt this was a rational option given our inability to clear the infection. It is unclear as to exactly why our patient was never able to fully clear his infection. Given the patient’s other pre-existing extensive cardiac hardware (i.e. implanted pacer), it is possible that he remained colonized even after maximal surgical and medical therapy. Though speculative, it is possible that removing all foreign material may have allowed for complete infection clearance.

Aside from aggressive medical and surgical management, systolic heart failure with VAD-associated infections may be effectively managed with heart transplantation (9). Our consensus was that this option was neither in the best interest of the patient nor the best use of available resources given the severity of his condition.

Conclusion

Clinicians will continue to see VAD-associated infections with resistant organisms. To minimize adverse outcomes, including VAD-associated infection, prudent patient selection and timing of VAD placement is paramount, as VAD’s placed in critically ill patients have been consistently associated with adverse outcomes (10).

References

1. Gordon RJ, Weinberg AD, Pagani FD, Slaughter MS, Pappas PS, Naka Y, Goldstein DJ, Dembitsky WP, Giacalone JC, Ferrante J, Ascheim DD, Moskowitz AJ, Rose EA, Gelijns AC, Lowy FD. Prospective, multicenter study of ventricular assist device infections. Circulation. 2013;127:691-702. [CrossRef] [PubMed]
2. Nienaber JJ, Kusne S, Riaz T, Walker RC, Baddour LM, Wright AJ, Park SJ, Vikram HR, Keating MR, Arabia FA, Lahr BD, Sohail MR. Clinical manifestations and management of left ventricular assist device-associated infections. Clin Infect Dis. 2013;57:1438-48. [CrossRef] [PubMed]
3. Zavascki AP, Carvalhaes CG, Picao RC, Gales AC. Multidrug-resistant Pseudomonas aeruginosa and Acinetobacter baumannii: resistance mechanisms and implications for therapy. Expert Rev Anti Infect Ther. 2010;8:71-93. [CrossRef] [PubMed]
4. Topkara VK, Kondareddy S, Malik F, Wang IW, Mann DL, Ewald GA, Moazami N. Infectious complications in patients with left ventricular assist device: etiology and outcomes in the continuous-flow era. Ann Thorac Surg. 2010;90:1270-7. [CrossRef] [PubMed]
5. Bartoli CR, Demarest CT, Khalpey Z, Takayama H, Naka Y. Current management of left ventricular assist device erosion. J Card Surg. 2013;28:776-82. [CrossRef] [PubMed]
6. Balaji V, Jeremiah SS, Baliga PR. Polymyxins: Antimicrobial susceptibility concerns and therapeutic options. Indian J Med Microbiol. 2011;29:230-42. [CrossRef] [PubMed]
7. Martis N, Leroy S, Blanc V. Colistin in multi-drug resistant Pseudomonas aeruginosa blood-stream infections: a narrative review for the clinician. J Infect. 2014;69:1-12. [CrossRef] [PubMed]
8. Tamma PD, Cosgrove SE, Maragakis LL. Combination therapy for treatment of infections with gram-negative bacteria. Clin Microbiol Rev. 2012;25:450-70. [CrossRef] [PubMed]
9. Prendergast TW, Todd BA, Beyer AJ, 3rd, Furukawa S, Eisen HJ, Addonizio VP, Browne BJ, Jeevanandam V. Management of left ventricular assist device infection with heart transplantation. Ann Thorac Surg. 1997;64:142-7. [CrossRef] [PubMed]
10. Lietz K, Long JW, Kfoury AG, Slaughter MS, Silver MA, Milano CA, Rogers JG, Naka Y, Mancini D, Miller LW. Outcomes of left ventricular assist device implantation as destination therapy in the post-REMATCH era: implications for patient selection. Circulation. 2007;116:497-505. [CrossRef] [PubMed] 

Reference as: Gerstein NS, Chou HG, Dixon AL. Analysis of a fatal left ventricular assist device infection: a case report and discussion. Southwest J Pulm Crit Care. 2015;10:16-20. doi: http://dx.doi.org/10.13175/swjpcc139-14 PDF 

January 2015 Critical Care Case of the Month: Who's Your Momma?

Carlos Hartmann, MD

Layth Al-Jashaami, MD

Timothy T. Kuberski, MD

Department of Medicine

Maricopa Integrated Health Services

Phoenix, AZ USA

History of Present Illness

A 39-year-old Hispanic woman was admitted complaining of shortness of breath and bilateral lower extremity edema. She was felt to be in acute hypoxic respiratory failure.

Past Medical History

• Systemic lupus erythematosus
• Congestive heart failure with an ejection fraction of 40%
• End-stage renal disease on dialysis secondary to lupus nephritis

Medications

• Rituximab 550 mg once a week
• Prednisone 40 mg daily
• Plaquenil 200 mg twice a day

Physical Examination

The patient was tachypneic in obvious respiratory distress. She was afebrile. Crackles at the bases. Heart was tachycardic. There was 3+ bilateral pitting pretibial edema.

Laboratory

CBC: Hemoglobin 7.8 g/dL, WBC 11 X 10⁹ cells per liter, differential: neutrophils 98%, eosinophils 0%, lymphocytes 1%.

Electrolytes: Potassium 5.8 mEq/L, sodium 143 mEq/L, creatinine 3.3 g/dL, BUN 98 mg/dL.

Brain naturetic peptide: 4055 pg/ml.

Imaging

Admission chest x-ray showed cardiomegaly and bilateral interstitial prominence suggestive of congestive heart failure.

Which of the following are appropriate initial management? (Click on the correct answer to proceed to the 2nd of 4 panels)

1. Bronchoscopy with bronchoalveolar lavage
2. Hemodialysis
3. Increased methylprednisolone for a potential lupus "flare"
4. 1 and 3
5. All of the above 

Reference as: Hartmann C, Al-Jashaami L, Kuberski TT. January 2015 critical care case of the month: who's your momma? Southwest J Pulm Crit Care. 2015:10(1):11-15. doi: http://dx.doi.org/10.13175/swjpcc145-14 PDF

Brief Review: Delirium

Evan D. Schmitz, MD

Jack B. Vu, MD

University of Washington

Seattle, WA

A significant number of patients develop a decline in cognitive function while hospitalized. Delirium in the intensive care increases mortality and healthcare costs and should be recognized and treated promptly (1,2). 

This is a brief review of delirium and important treatment options such as early percutaneous tracheostomy, neuroleptics, propofol, daily awakenings and reorientation by all team members. We recommend neither neuroimaging nor neurology consultation unless physical exam suggests an acute cerebral vascular accident or status epilepticus as the majority of these patients require no neurologic intervention and may be harmed by transportation to obtain additional testing.

The DSM-5 defines delirium as a disturbance in attention (reduced ability to direct, focus, sustain, and shift attention) and awareness (reduced orientation to the environment). The disturbance develops over a short period of time (usually hours to a few days), represents a change from baseline attention and awareness, and tends to fluctuate in severity during the course of a day. Delirium may also be a disturbance in cognition (memory deficit, disorientation, language, visual spatial ability, or perception).

The leading cause of delirium in the intensive care unit is metabolic encephalopathy caused by the patient’s primary disease and exacerbated by treatment with life saving measures such as intubation with mechanical ventilation. The required anesthesia and analgesia during intubation contribute to worsening delirium. The quicker the patient is extubated, the better is the overall prognosis. Delirium makes it more difficult to extubate the patient, independent of the disease process as the clinician is uncertain if the patient will be able to protect their airway and breathe on their own. This is further compounded by the increasing need for nursing during this critical period. There are numerous studies showing the benefits of sedation vacation and reorientation by nursing. If you were to speak with nurses they will tell you how difficult it is dealing with a delirious patient as the patient can become combative and difficult to console. As hospitals continue to cut back on nurses, nursing aids, respiratory therapists and sitters, it becomes increasingly more difficult to care for these patients.

Nursing is one of the most dangerous careers according to the U.S. Bureau of Labor (3). Delirium is directly responsible for traumatic injuries nurses suffer from combative patients while caring for the critically ill. It is therefore understandable why a majority of nurses are concerned when they are told to extubate these delirious patients.

We make it a point to educate nurses that they should extubate the patient as soon as possible. Once a plan is established, including neuroleptics to control agitation, it is important that the physician conducts bed rounds on the patient multiple times during the day. The physician should also explain to the nocturnal staff the importance of avoiding re-intubation, as these delirious patients do respond to neuroleptics and redirection. We only recommend extubation if the whole team is on board.

We have been performing percutaneous tracheostomies since 2006 and have noticed a significant decrease in ventilator days and duration of delirium in those patients receiving this surgery. Once a percutaneous tracheostomy is placed, a patient can be ventilated with minimal or no sedatives which allows improvement in their cognitive function.

Immediately after paralytics have worn off after performing a bedside percutaneous tracheostomy, we stop all sedatives and narcotics to allow the patient to regain consciousness. We use neuroleptics to treat delirium while awaiting for the return of cognitive function. With a tracheostomy in place, the respiratory therapists and nurses appear much more comfortable allowing patients to recover without giving any narcotics or sedatives resulting in a much faster recovery. Patients with neurological impairment, including delirium, demonstrate tachypnea out of proportion to their respiratory needs. Recognition of this type of breathing pattern is important. Educating the staff about this type of breathing pattern also helps nurses and respiratory therapists to cope with the resultant high minute ventilation. If there are periods of apnea with irregular periods of hyperventilation, the breathing pattern is called Biot’s breathing (4).

Once placed, percutaneous tracheostomy as opposed to endotracheal intubation, requires neither anesthetic nor analgesic. Since the tracheostomy is usually placed between the first and second tracheal cartilaginous rings, the vocal cords are free from damage including swelling that occurs with endotracheal tubes. Endotracheal tubes are very uncomfortable and analgesia and anesthesia are required to keep patients comfortable. This can cause delirium. The incidence of tracheal stenosis does not appear to be greater with percutaneous tracheostomy as opposed to endotracheal intubation.

Percutaneous tracheostomy can be performed safely at the bedside in the intensive care unit. As long as one physician is controlling the airway while performing direct visualization via bronchoscopy and the other is performing the percutaneous tracheostomy, any adverse complications can be managed promptly. Remember to place a sign in the patient’s room warning staff not to replace the tracheostomy if it were to fall out within the first seven days and to call a code for prompt intubation. This will avoid misplacement which can lead to death.

Although we are not recommending tracheostomy just for the treatment of delirium, we do recommend early tracheostomy within a few days as opposed to waiting to perform a tracheostomy when anticipated ventilation is longer than ten days. Most of our colleagues who perform percutaneous tracheostomy agree (Schmitz ED, unpublished observations.

Haloperidol (Haldol®) has been around for decades. Haloperidol is a butyrophenone antipsychotic which acts primarily by blocking postsynaptic mesolimbic dopaminergic D2 receptors in the brain. This results in depression of the reticular activating system (5).

As opposed to sedatives and analgesics, haloperidol does not suppress intellectual function or cause respiratory failure. It appears underutilized because of concern about prolonging the QT interval and increasing the risk for a cardiac arrhythmia (6). Although it is true that neuroleptics can prolong the QT interval, the fear associated with this rare phenomenon inhibits the use of the most effective treatment for delirium we have at our disposal. 

Newer antipsychotics such and olanzapine, risperidone and ziprasidone may be used as well, but they also have been associated with inducing cardiac arrhythmias. These drugs appear to have less extrapyramidal side effects caused by the excitatory actions of unopposed cholinergic neurons. These newer antipsychotics block the serotonin receptor 5HT and to a lesser extent D2, and therefore, they decrease the likelihood of acute dystonic reactions, pseudo-parkinsonism, akathisia and tardive dyskinesia (7).

We have had great success with intravenous haloperidol. We recommend starting with a 5-10 mg intravenously and repeating this dose every 15 minutes until the patient’s agitation is controlled. We then schedule haloperidol intravenously as needed. Depending on which newer neuroleptics are available, we schedule these drugs until the patient recovers from their delirium. We have also had success with sublingual or intramuscular olanzapine 10 mg every 8 to 12 hours. Much higher doses, greater than 200 mg a day, have been reported in hospice patients without adverse cardiac effects (8).

Prior to instituting neuroleptics, ensure that the patient’s electrolytes are normal which will decrease the likelihood of an arrhythmia. Try to avoid haloperidol in patients with Parkinson’s disease because it diminishes the availability of dopamine.

An additional measure to decrease the risk and length of delirium is by using propofol and fentanyl for sedation rather than a benzodiazepine. Recent studies have shown that using propofol instead of a benzodiazepine decreases mortality, ventilator days and delirium (9). The elderly and those with liver impairment appear to benefit the most from propofol because of the faster metabolism of this class of drug. Side effects such as hypotension can be easily managed with fluids and a low dose of norepinephrine.

Renal failure is common in critically ill patients. It is important to monitor patients closely for signs of uremic encephalopathy which occurs when patients are unable to adequately excrete nitrogenous waste and other factors (10).

Nitrogen is excreted by the kidneys as urea and ammonium. Amino acids are catabolized by transamination which is the process of transferring their alpha-amino group to alpha-ketoglutarate which produces glutamate. The two most important are alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Alpha-ketoglutarate is an essential intermediate substrate in the citric acid cycle (11).

Glutamate can be oxidized to form free ammonia or it can combine with ammonium in the presence of ATP to form glutamine in the muscle, liver and nervous system providing a nontoxic storage and transport form of ammonia. 

In renal failure hyperammonemia occurs leading to tremors, slurring of speech and blurring of vision. In the presence of elevated ammonia, alpha-ketoglutarate combines with ammonia to form glutamate. Glutamate accumulates which causes cytotoxicity to nerve cells and death via NMDA-type synapses which mediate calcium influx (5). As the concentration of alpha-ketoglutarate declines, the brain cannot produce the energy it needs through the citric acid cycle which can lead to coma and death.

Although drugs used to treat hyperammonemia in patients with liver failure such as neomycin, lactulose and rifaximin will help decrease the amount of urea and ammonia reabsorbed in the intestines, in patients with renal failure, dialysis is imperative to recovery. After only one treatment with dialysis, the cognitive improvement is profound. As the acute kidney injury resolves, dialysis is no longer necessary.

It is unclear whether antiepileptics can also help with delirium. Valproic acid may inhibit glutamates action on the NMDA receptor. Glutamate mediated neuronal excitotoxicity has been postulated as a cause of nerve cell death. Antiepileptics may be beneficial at attenuating the deleterious effects of glutamate in the brain.

Delirium can also be caused by too much serotonin. Medications such as serotonin re-uptake inhibitors (SSRIs), linezolid, metoclopramide, fentanyl and baclofen can cause the serotonin syndrome. Patients typically exhibit some type of clonus (12). We recommend stopping all antidepressants in critically ill patients exhibiting signs of delirium. After the delirium subsides, resuming the SSRI appears appropriate. Depression is common as patients recover from their critical illness and the addition of an SSRI may be beneficial prior to transfer out of the intensive care unit.

By adhering to the above recommendations, you will be able to recognize delirium and institute effective lifesaving treatments. Patients and their family members will be grateful as they will be able to communicate with their loved ones once again. Nurses will also be happier as they will suffer less emotional and physical trauma. This will lead to a faster patient recovery and a shorter length of hospitalization.

References

1. Yamaguchi T, Tsukioka E, Kishi Y. Outcomes after delirium in a Japanese intensive care unit. Gen Hosp Psychiatry. 2014;36(6):634-6. [CrossRef] [PubMed]
2. Hsieh SJ, Soto GJ, Hope AA, Ponea A, Gong MN. The Association Between ARDS, Delirium, and In-hospital Mortality in ICU Patients. Am J Respir Crit Care Med. 2014 Nov 13. [Epub ahead of print] [CrossRef] [PubMed]
3. U.S. Department of Labor, Bureau of Labor Statistics. Lost-worktime injuries and illnesses: characteristics and resulting time away from work 2010. Available at: http://www.bls.gov/news.release/osh2.nr0.htm (accessed 12/22/14).
4. Wijdicks EF. Biot's breathing. J Neurol Neurosurg Psychiatry. 2007;78(5):512-3. [CrossRef] [PubMed]
5. Waxman SG. Clinical Neuroanatomy. 25th edition. New York, NY: McGraw Hill Medical; 2003.
6. Hatta K, Kishi Y, Wada K, Odawara T, Takeuchi T, Shiganami T, Tsuchida K, Oshima Y, Uchimura N, Akaho R, Watanabe A, Taira T, Nishimura K, Hashimoto N, Usui C, Nakamura H. Antipsychotics for delirium in the general hospital setting in consecutive 2453 inpatients: a prospective observational study. Int J Geriatr Psychiatry. 2014;29(3):253-62. [CrossRef] [PubMed]
7. Howland RD. Phamacology. 3rd edition. Philadelphia. Lippincott, Williams & Wilkins. 2003. Howland RG. Pharmacology. 3rd edition. Philadelphia, PA: Lippincott, Williams and Wilkins; 2006.
8. Bascom PB, Bordley JL, Lawton AJ. High-dose neuroleptics and neuroleptic rotation for agitated delirium near the end of life. Am J Hosp Palliat Care. 2014;31(8):808-11. [CrossRef] [PubMed]
9. Lonardo NW, Mone MC, Nirula R, Kimball EJ, Ludwig K, Zhou X, Sauer BC, Nechodom K, Teng C, Barton RG. Propofol is associated with favorable outcomes compared with benzodiazepines in ventilated intensive care unit patients. Am J Respir Crit Care Med. 2014;189(11):1383-94. [CrossRef] [PubMed]
10. Scaini G, Ferreira GK, Streck EL. Mechanisms underlying uremic encephalopathy. (10) Rev Bras Ter Intensiva. 2010;22(2):206-211. [CrossRef] [PubMed]
11. Champe PC, Harvey RA. Biochemistry. 2nd edition. Philadelphia:JB Lippincott-Raven;1994.
12. Boyer EW, Shannon M. The serotonin syndrome. N Engl J Med. 2005;352(11):1112-20. [CrossRef] [PubMed] 

Reference as: Schmitz ED, Vu JB. Brief review: delirium. Southwest J Pulm Crit Care. 2014;9(6):343-7. doi: http://dx.doi.org/10.13175/swjpcc166-14 PDF

Ultrasound for Critical Care Physicians: Lung Sliding and the Seashore Sign

Spencer M. Lee, MD

Gregory T. Chu, MD

Banner Good Samaritan Medical Center

Phoenix, AZ

A 70-year-old Native American woman was having increasing difficulty with ventilation. She had an extensive past medical history including quadriplegia after a motor vehicle accident in 2009, chronic mechanical ventilation since the accident, end-stage renal disease, and diabetes mellitus. A feeding tube had recently been inserted. A portable chest radiograph was performed (Figure 1).

Figure 1. Portable chest radiograph.

A lung ultrasound was performed (Figure 2).

Figure 2. Lung ultrasound of the left lung (upper panel) and of the right lung (lower panel).

M-mode images of the ultrasound are shown in Figure 3.

Figure 3. M-mode image of the left lung (panel A on left) and the right lung (Panel B on right).

Which of the following are true regarding the images presented? (Click on the correct answer to procced to the next and final panel)

1. The chest x-ray shows the feeding tube in the right lung
2. The M-mode image shows the seashore sign on the left suggestive of a pneumothorax
3. The ultrasound shows an absence of lung sliding on the right suggestive of a pneumothorax
4. 1 and 3
5. All of the above

Reference as: Lee SM, Chu GT. Ultrasound for critical care physicians: lung sliding and the seashore sign. Southwest J Pulm Crit Care. 2014;9(6):337-40. doi: http://dx.doi.org/10.13175/swjpcc163-14 PDF

December 2014 Critical Care Case of the Month: Weak for Weeks

Bhupinder Natt MD¹

Shadi Koleilat MD²

Janet Campion MD¹

¹Division of Pulmonary, Allergy, Critical care and Sleep Medicine

²Department of Neurology

University of Arizona Medical Center

Tucson, AZ

History of Present Illness

A 65 year old woman presents with weakness involving both upper and lower extremities that is intermittent over the last 3 months, but in the last 2 weeks she has also noticed increasing neck weakness, droopy eyelids and increased drooling. Prior to this she was able to walk without difficulty and ride a recumbent bike for 20 minutes, but now is having difficulty walking on her own. She denies fevers, weight loss, shortness of breath, chest pain, palpitations, LE edema, joint pain, rash, any recent or current GI/GU symptoms and no new medications.

Past Medical History, Social History, and Family History

The patient has a past history of hypertension, hyperlipidemia, diabetes mellitus Type II, GERD, obstructive sleep apnea (compliant with BiPAP), atrial fibrillation and hypothyroidism. She has a 40 pack-year history of tobacco use. Family history is noncontributory.

Medications

• Dabigatran 75mg BID
• Esomeprazole 20 mg BID
• Furosemide 30 mg BID
• Insulin glargine 50 Units BID and Lispro per sliding scale
• Levothyroxine 88 mcg per day
• Losartan 50 mg QD,
• Pregabalin 75 mg BID
• Rosuvastatin 40 mg per day

Physical Examination

Vital signs: Afebrile. Pulse 86, respiratory rate 20, PaO2 92% on room air

General: Awake, fully oriented, dysarthric speech.

HEENT: Non-icteric, ears, nares, oropharynx unremarkable; there is no neck LAD, elevated JVP or thyromegaly.

Respiratory: Normal breath sounds, no wheeze or rhonchi.

CVS: Irregularly irregular rhythm, no murmurs. Peripheral vascular exam normal.

Abdomen: Obese, soft, non-tender with normal bowel sounds. No organomegaly appreciable.

Extremities: Trace pedal edema, normal muscle bulk and tone.

CN: Ptosis bilaterally, no nystagmus, reactive pupils, extra-ocular muscles intact, sensation intact, weak cheek puff, symmetric palate excursion, normal tongue protrusion.

Motor: Neck flexion and extension 4-/5, bilateral pronator drift, no focal lower extremity weakness, no muscle atrophy, no tremors or fasciculations.

Sensation: Intact to light touch hands and feet.

Reflexes: 2+ and symmetric throughout.

Gait: Wide-based and slow, can only walk short distances before experiencing bilateral leg weakness.

Laboratory: Normal electrolytes, complete blood count, and liver function tests. Creatinine mildly elevated at 2.1 mg/dL.

EKG

Atrial Fibrillation.

What is the most likely diagnosis? (Click on the correct answer to proceed to the next panel)

1. Guillain-Barré syndrome (GBS)
2. Hypothyroidism
3. Lambert-Eaton myasthenic  syndrome (LEMS)
4. Motor neuron disease (ALS)
5. Myasthenia gravis crisis

Reference as: Natt B, Koleilat S, Campion J. December 2014 critical care case of the month: weak for weeks. Southwest J Pulm Crit Care. 2014;9(6):302-8. doi: http://dx.doi.org/10.13175/swjpcc141-14 PDF

Ultrasound for Critical Care Physicians: Now My Heart Is Full

Sapna Bhatia M.D.

Rodrigo Vazquez-Guillamet M.D.  

Division of Pulmonary, Critical Care and Sleep Medicine

University of New Mexico School of Medicine

Albuquerque, NM

A 65 year old woman with a history of hypertension and a recent diagnosis of multiple myeloma was admitted to the ICU with septic shock due to Morganella morganii bacteremia. She was treated with cefepime, levophed and dobutamine. During treatment she developed symptoms and a chest x-ray compatible with congestive heart failure. A transthoracic echo is shown below (Figures 1 and 2).  

Figure 1. Parasternal long echocardiogram of the patient.   

Figure 2. Apical four-chamber echocardiogram of the patient.

Additionally a spectral pulsed-wave Doppler study of the mitral inflow velocities is presented (Figure 3).

Figure 3. Pulsed-wave spectral Doppler velocities of the mitral-valve inflow of the patient. 

What is the best explanation for the findings seen in on the echocardiogram? (Click on the correct answer to proceed to the next panel and explanation)  

1. Cardiac amyloidosis
2. Hypertensive heart disease
3. Hypertrophic cardiomyopathy
4. Stress (Takotsubo) cardiomyopathy

Reference as: Bhatia S, Vazquez-Guillamet R. Ultrasound for critical care physicians: now my heart is full. Southwest J Pulm Crit Care. 2014;9(5):291-4. doi: http://dx.doi.org/10.13175/swjpcc154-14 PDF 

November 2014 Critical Care Case of the Month: I Be Gaining on My Addiction

Nathaniel R. Little, MD

Carolyn H. Welsh, MD

University of Colorado and the Eastern Colorado Veterans Affairs Medical Center

Department of Medicine

Division of Pulmonary Sciences and Critical Care Medicine

Denver, CO

History of Present Illness

A 33 year-old man came by ambulance to the Emergency Department for progressive altered mental status and bizarre behavior. Per history from his significant other, the patient had a long-standing history of heroin addiction and diazepam abuse. Despite multiple failed attempts at prior detoxification, he had recently resolved to “take matters into his own hands.”

The patient had informed his girlfriend that he quit heroin “cold turkey” 3 days prior to admission. On the first day after his last heroin use, he was communicative, energetic, and appeared normal. On the second day, he was increasingly introspective, somnolent, and mute. He spent the majority of the day in bed, and had tremors of all extremities. On the third day, he experienced increased arousal, with auditory and visual hallucinations. His speech was “very technical and scientific” with episodes of “waxing philosophic.” Given increasingly erratic behavior, worsening tremors, and inability to ambulate; emergency services were called for transport to the hospital.

Past Medical History, Social history and Family History:

The patient had a history of heroin and diazepam addiction, with failed attempts at cessation. He carried prior diagnoses of depression and anxiety, with a history of suicide attempts in his youth. He took no prescribed medications. He was employed as a software engineer. Aside from daily intravenous heroin use, he did not smoke nor drink alcohol. Family history was non-contributory.

Physical Examination:

On admission , he was hypothermic (35.8 C), hypotensive (BP = 81/48), and bradycardic (HR =41). Respiratory rate and oxygen saturations were normal. He was pale, diaphoretic, altered, and responsive only to internal stimuli. Additional findings included nystagmus, with oral exam showing dry mucus membranes. Per cardiovascular exam, he had profound bradycardia, with diminished radial and dorsalis pedis pulses. His extremities were cool to the touch. Pulmonary and abdominal exams were normal. On neurologic evaluation, the patient demonstrated a Glasgow Coma Score of 9, opened eyes only to command, demonstrated mumbled speech, and had tongue fasiculations. He was able to move all extremities, but with severe ataxia. Deep tendon reflexes were normal.

Laboratory Studies:

Complete Blood Count: White blood cell count (WBC) 9.0 x 1000 cells/µL, hemoglobin 14.5 g/dL, hematocrit 43.0, platelets 220,000 cells/µL

Chemistry: Sodium 150 meq/L, potassium 3.6 meq/L, chloride 113 meq/L, bicarbonate (CO2) 25 meq/L, blood urea nitrogen (BUN) 31 mg/dL, creatinine 1.14 mg/dL, glucose 114 mg/dL, magnesium 1.6 meq/L, phosphorus 4.1 mg/dL, creatinine kinase 33.

Toxicology Screen: Urine drug screen positive only for benzodiazepines, negative for opiates.

Urine: trace ketones, otherwise unremarkable.

Imaging:

Figure 1. Admission AP of chest.

The patient’s clinical presentation thus far is most consistent with what type of shock: (click on the correct answer to proceed to the next panel)

1. Cardiogenic
2. Distributive
3. Hypovolemic
4. Neurogenic
5. Obstructive
6. Both 1 and 3
7. All of the above

Reference as: Little NR, Welsh CH. November 2014 critical care case of the month: I be gaining on my addiction. Southwest J Pulm Crit Care. 2014:9(5):257-63. doi: http://dx.doi.org/10.13175/swjpcc146-14 PDF

Clinical Performance Of An Automated Systemic Inflammatory Response Syndrome (SIRS) / Organ Dysfunction Alert: A System-Based Patient Safety Project

Robert A Raschke, MD, MS

Huw Owen-Reece, MBBS

Hargobind Khurana, MD 

Robert H Groves Jr, MD

Steven C Curry, MD

Mary Martin, PharmD

Brenda Stoffer

Suresh Uppalapu, MD 

Heemesh Seth, DO

Nithya Menon, MD 

Banner Good Samaritan Medical Center, Phoenix Arizona

Abstract

Objective: We have employed our electronic medical record (EMR) in an effort to identify patients at the onset of severe sepsis through an automated analysis that identifies simultaneous occurrence of systemic inflammatory response syndrome (SIRS) and organ dysfunction. The purpose of this study was to determine the positive predictive value of this alert for severe sepsis and other important outcomes in hospitalized adults.

Design: Prospective cohort.

Setting: Banner Good Samaritan Medical Center, Phoenix AZ

Patients: Forty adult inpatients who triggered alert logic within our EMR indicating simultaneous occurrence of SIRS and organ dysfunction.

Interventions: Interview of bedside nurse and chart review within six hours of alert firing to determine the clinical event that triggered each alert.

Results: Eleven of 40 patients (28%) had a major clinical event (immediately life-threatening illness) associated with the alert firing. Severe sepsis or septic shock accounted for four of these – yielding a positive predictive value of 0.10 (95%CI: 0.04-0.23) of the alert for detection of severe sepsis. The positive predictive value of the alert for detection of major clinical events was 0.28 (95%CI: 0.16-0.43), and for detecting either a major or minor clinical event was 0.45 (95%CI: 0.31-0.60). Twenty-two of 40 patients (55%) experienced a false alert.

Conclusions: Our first-generation SIRS/organ dysfunction alert has a low positive predictive value for severe sepsis, and generates many false alerts, but shows promise for the detection of acute clinical events that require immediate attention. We are currently investigating refinements of our automated alert system which we believe have potential to enhance patient safety.

Introduction

Severe sepsis is defined as systemic inflammatory response syndrome (SIRS) of infectious etiology with secondary organ dysfunction. It is estimated that 750,000 patients suffer severe sepsis annually in the United States - 3 cases per 1000 population (1). Mortality has fallen over the past several decades, but ranges from 20-30% in recent studies (1,3). Results of recent treatment trials for severe sepsis are consistent with the hypothesis that early diagnosis and treatment are important (2,3), but reliable systems for early recognition of severe sepsis in hospitalized patients are not widely available.  

We have sought to improve patient safety at our institution by using our integrated electronic medical record (EMR) to identify patients at the onset of severe sepsis through a logic algorithm that analyzes vital signs and laboratory data. This logic function identifies patients with simultaneous systemic inflammatory response syndrome (SIRS) and organ dysfunction, but cannot distinguish whether an acute infection is the cause of these findings. The purpose of this study was to determine what clinical events – infectious or non-infectious - actually cause the vital sign and laboratory changes that trigger this alert, and what the positive predictive valve of the alert is for detecting the onset of severe sepsis in hospitalized adult patients.

Methods

This was a prospective cohort study carried out at Banner Good Samaritan Medical Center – a 700-bed University-affiliated teaching hospital in Phoenix AZ. It was part of an ongoing quality improvement project and was thereby exempted from IRB approval. The SIRS / organ dysfunction alert logic was developed at Banner Health using Cerner Discern Expert^®, Cerner Corporation, North Kansas City MO, USA. The logic function monitored the EMR for standard SIRS criteria and laboratory evidence of organ dysfunction with thresholds consistent with standard definition of severe sepsis (Table 1) (4,5).

Table 1. Specific criteria for the logic function of our SIRS/organ failure alert. 

When any single criterion for SIRS was met, the program searched the prior 6 hours for the most recent vital signs, and the prior 30 hours for the most recent white blood cell count. If a second SIRS criterion was met, the program identified the patient as exhibiting SIRS, but did not trigger an alert. When any single laboratory criterion for organ dysfunction was met (table 1), the program identified the patient as suffering organ dysfunction. If criteria for SIRS and organ dysfunction overlap in any 8 hour window, the alert fired, triggering a real-time notification in the Cerner Millenium^® EMR alerting clinicians to the possibility of severe sepsis or septic shock. The alert has been in clinical application since 2010. 

We sampled 40 non-consecutive inpatients in the first three months of 2014 by a nonrandom method blinded to the patient’s clinical condition. On days of data collection, all alerts that had fired within the prior 6 hours were reviewed, regardless of patient location or diagnosis. The patient bedside was visited by a physician researcher during the six-hour window after alert firing and the nurse interviewed in order to determine the circumstances that caused the alert to fire. The patient might be briefly examined if necessary to confirm the nursing impression. Chart review was also performed to assist in this determination. Demographics, admission diagnosis, vital signs and laboratory data that triggered the alert logic, and any treatment the associated clinical event required were also recorded. Chart review was repeated 48 hours later to review microbiological test results and physician progress notes that might shed further light on the clinical event that triggered the alert.

The “clinical event” associated with each alert was defined as the most likely acute explanation for the vital sign and laboratory abnormalities that triggered the alert. A clinical event might be an acute illness, such as pneumonia with septic shock, or a non-illness event, such as initiation of dialysis. Clinical events could include the illness that necessitated admission if the alert fired within 24 hours of admission, or secondary illnesses - for instance, a catheter-associated blood stream infection.

The severity of clinical events related to alert firings were classified into three tiers. 

1. Major clinical events were acute life-threatening illnesses that required emergent resuscitation with any one or more of the following: >1 L intravenous fluid resuscitation, vasopressor infusion, >2 units of packed red blood cell transfusion, endotracheal intubation, advanced cardiac life support, or emergent surgical intervention.
2. Minor clinical events were acute non-life-threatening illnesses that required urgent treatments not included in the definition of major clinical events above.
3. False alerts were said to have occurred when no acute illness was recognized in temporal relationship to the alert firing. 

The positive predictive value of the alert for detecting severe sepsis, major clinical events, and major or minor clinical events were calculated, with 95% confidence intervals.

Results

Nineteen women and 21 men, with ages ranging from 22 to 103 years were included. Twenty-two of forty (55%) were in the ICU at the time the alert fired, and 18 on the floors. Vital signs and laboratory values that triggered the alert logic are listed in Table 2. 

Table 2. SIRS / organ dysfunction alert trigger criteria in forty patients. 

Eleven of 40 patients (28%) had a major clinical event associated with the alert firing – two of these occurred outside the ICU. Severe sepsis or septic shock accounted for four of these major clinical events – yielding a positive predictive value of 0.10 (95%CI: 0.04-0.23) of the alert for detection of severe sepsis or septic shock. The seven remaining patients with major events suffered acute pulmonary edema, pulmonary embolism, ischemic bowel, pancreatitis, acute cardiogenic shock, acute right heart failure secondary to pulmonary hypertension, and an incarcerated enteric hernia. The positive predictive value of the alert for detection of major clinical events was 0.28 (95%CI: 0.16-0.43).

Major clinical events were clearly recognized before the alert fired in nine of 11 cases, as evidenced by the patient having been admitted or transferred to the intensive care unit specifically for the event of interest, and/or having received treatment such as intubation or initiation of intravenous vasopressors before the alert fired. In two cases, the alert fired at about the same time that treatment of the acute clinical event commenced, and it was unclear what role it played in clinical recognition of the event.

Seven of 40 patients (17%) had a minor clinical event associated with the alert firing. These included two patients with anemia, and one each with hypotension from an antihypertensive medication, dialysis disequilibrium, post-operative pain, dehydration, and paroxysmal atrial fibrillation. The positive predictive value of the alert for detecting either a major or minor clinical event was 0.45 (95%CI: 0.31-0.60).

Twenty-two of 40 patients (55%) were not experiencing any identifiable acute illness that could explain the alert firing - these were considered false alerts. Aberrant vital signs triggered false alerts during dialysis (2), turning or sitting-up post-operative patients (2), an endoscopy procedure, and a family argument. Other false alerts were attributable to the pharmacological effect of calcium channel blocker, oximeter malfunction, error in vital sign entry, and widely discrepant blood pressures between right and left arms. The remaining false alerts were triggered by slightly abnormal vital signs with no identifiable cause.

Four patients (10%) did not survive to discharge – two had major clinical events, one a minor clinical event and one a false alert – in the later two cases, the cause of death was unrelated to the clinical event that triggered the alert.  

We examined alert triggering criteria to better understand how the discriminant ability of the alert might be improved. We noted that 15 of 40 (37%) alerts triggered with respiratory rates of 21 or 22 bpm, however these included six alerts associated with major clinical events. Twelve of 40 (30%) alerts triggered with heart rates in 91-95 bpm range, including two alerts associated with major clinical events. Laboratory results contributed to 31 of 40 alert firings – but in 12 cases they were stable or improving at the time they triggered the alert. In no case was a stable or improving laboratory value associated with a major clinical event.

Discussion

It’s important to study the effects of any quality improvement project in order to determine whether it is having the desired results. Our small pilot study suggests that our first-generation SIRS/organ dysfunction alert has a low positive predictive value for severe sepsis, and generates many false alerts. This is partially a reflection of the low specificity of SIRS criteria for sepsis (6). The high number of false positive alerts has led to alert-fatigue among physicians and nurses providing bedside patient care – a phenomenon which is not unique to our institution (7).  

Our alert demonstrated greater potential utility to detect acute clinical deterioration than to detect sepsis. Buck and colleagues (7) used an EMR-based logic system to activate a sepsis alert similar to ours, and observed similar results in that only 17% of alert patients had a sepsis-related discharge diagnosis, but 40% had a major illness which required urgent intervention. We have used the results of our study to re-task future iterations of our alert to detect acute clinical deterioration rather than sepsis.

Other researchers provide guidance in this regard. Vital sign and laboratory result criteria similar to the ones used in our study have been previously shown to predict in-hospital cardiac arrest (8), predict 30-day mortality (9), generate early warning scores to detect acute clinical deterioration (9), and activate medical emergency teams (8,10). A recent large study by Churpek and colleagues (11) validated a risk stratification tool that utilized vital signs, laboratory findings and demographics to predict the combined outcome of cardiac arrest, ICU transfer or death on the wards. The model yielded notable discriminant accuracy with an area under the receiver operating curve (AUROC) of 0.77.

We are currently investigating revisions in our alert logic to improve detection of acute clinical deterioration. The alert logic now trends laboratory values associated with organ dysfunction. We are studying whether adding a reflex serum lactate to the automatic alert response might help identify patients who are acutely deteriorating (12).   

Our study has many apparent weaknesses, but it should be noted that it was carried out originally only to provide data to help guide local efforts to improve patient safety. In this regard, it succeeded in guiding our (and perhaps other’s) future efforts in what will more likely be a useful direction.

We failed to clearly determine what role our automated alert played in bedside decision-making. In most cases, clinicians were already evaluating or treating the clinical event that triggered the alert before the alert fired. However, we feel that a safety net is a wise precaution even in a high-reliability system. It should also be noted that our institution has medicine and surgery residency teaching programs, a critical care fellowship, 24/7 in-house intensivist coverage, and remote video ICU coverage. The benefit of EMR-based automated alerts is likely to be amplified in less well-staffed institutions. Refined versions of EMR-based automated alerts, such as the ones we are currently investigating, have potential to enhance patient safety. 

References

1. 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;29:1303-10. [CrossRef] [PubMed]
2. Rivers E, Nguyen B, Havstad S, Ressler J, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med. 2001;345:1368-77. [CrossRef] [PubMed]
3. The ProCESS investigators. A randomized controlled trial of protocol-based care for early septic shock. N Engl J Med. 2014;370(18):1683-93. [CrossRef] [PubMed]
4. Levy MM, Fink MP, Marshall JC, Abraham E, Angus D, Cook D, Cohen J, Opal SM, Vincent JL, Ramsay G. International Sepsis Definitions Conference. Crit Care Med. 2003;31(4):1250-6. [CrossRef] [PubMed]
5. Dellinger RP, Levy MM, Rhodes A, et al, Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012. Crit Care Med. 2013;41(2):580. [CrossRef] [PubMed]
6. Pittet D, Range-Frausto S, Tarara LN, et al. Systemic inflammatory response syndrome, sepsis, severe sepsis and septic shock: incidence, morbidities and outcomes in surgical ICU patients. Intensive Care Med. 1995;21:302-9. [CrossRef] [PubMed]
7. Buck KM. Developing an early sepsis alert program. J Nurs Care Qual. 2014;29(2):124-32. [CrossRef] [PubMed]
8. Hodgetts TJ, Kenward G, Ioannis G, et al. The identification of risk factors for cardiac arrest and formulation of activation criteria to alert a medical emergency team. Resuscitation. 2002;54:125-31. [CrossRef] [PubMed]
9. Goldhill DR, McNarry AF. Physiological abnormalities in early warning scores are related to mortality in adult inpatients. Br J Anaesth. 2004;92:882-4. [CrossRef] [PubMed]
10. Kenward G, Castle N, Hodgetts T, Shaikh L. Evaluation of a medical emergency team one year after implementation. Resuscitation. 2004;61:257-63. [CrossRef] [PubMed]
11. Churpek MM, Yuen TC, Winslow C, et al. Multicenter development of validation of a risk stratification tool for ward patients. Am J Respir Crit Care Med. 2014;190:649-55. [CrossRef] [PubMed]
12. Bakker J, Nijsten MWN, Jansen TC. Clinical use of the lactate monitoring in critically-ill patients. Ann Intensive Care. 2013;3:12-20. [CrossRef] [PubMed] 

Reference as: Raschke RA, Owen-Reece H, Khurana H, Groves RH Jr, Curry SC, Martin M, Stoffer B, Uppalapu S, Seth H, Menon N. Clinical performance of an automated systemic inflammatory response syndrome (sirs) / organ dysfunction alert: a system-based patient safety project. Southwest J Pulm Crit Care. 2014;9(4):223-9. doi: http://dx.doi.org/10.13175/swjpcc121-14 PDF

October 2014 Critical Care Case of the Month: A Skin Rash in the ICU

Robert A. Raschke, MD

Banner Good Samaritan Medical Center

Phoenix, AZ

History of Present Illness

A 28 year old man was admitted to an outside hospital with an ethylene glycol overdose in an apparent suicide attempt. At that time the patient was delirious and vomiting. He had a severe metabolic acidosis and a creatinine of 2.1 mg/dL. He was intubated, a nasogastric tube was placed, and he was transferred to the toxicology service.

PMH, FH, SH

There was no significant past medical history. Family history was noncontributory. He was a nonsmoker who recently had a fight with his girlfriend prompting the suicide attempt.

Physical Examination

Vital signs were stable and he was sedated and nasally intubated receiving mechanical ventilation. There were no other significant findings on physical examination

Which of the following can be used for ethylene glycol poisoning? (Click on the correct answer to proceed to the next of 5 panels)

1. Ethanol
2. Fomezipole
3. Hemodialysis
4. Pyridoxine
5. All of the above

Reference as: Raschke RA. October 2014 critical care case of the month: a skin rash in the ICU. Southwest J Crit Care Med. 2014;9(4):208-13. doi: http://dx.doi.org/10.13175/swjpcc110-14 PDF

Ultrasound for Critical Care Physicians: A Tempting Dilemma

Issam Marzouk MD

Lana Melendres MD

Michel Boivin MD

Division of Pulmonary, Critical Care and Sleep

Department of Medicine

University of New Mexico School of Medicine

MSC 10-5550

Albuquerque, NM 87131 USA

A 46 year old woman presented with progressive severe hypoxemia and a chronic appearing pulmonary embolus on chest CT angiogram to the intensive care unit. The patient was hemodynamically stable, but had an oxygen saturation of 86% on a high-flow 100% oxygen mask. The patient had been previously investigated for interstitial lung disease over the past 2 year, this was felt to be due to non-specific interstitial pneumonitis. Her echocardiogram findings are as presented below (Figures 1 and 2).

Figure 1. Parasternal long axis view. Upper panel: static image. Lower panel: video.

 

Figure 2. Apical four chamber view. Upper panel: static image. Lower panel: video

The patient had refractory hypoxemia despite trials of high flow oxygen and non-invasive positive pressure ventilation. She had mild symptoms at rest but experienced severe activity intolerance secondary to exertional dyspnea. Vitals including blood pressure remained stable and normal during admission and the patient had a pulsus paradoxus measurement of < 10 mmHg. She had previously had an echocardiogram 6 months before that revealed significant pulmonary hypertension.

What would be the most appropriate next step regarding management of her echocardiogram findings? (click on the correct answer to move to the next panel)

1. Diagnostic pericardiocentesis
2. Urgent therapeutic pericardiocentesis
3. Avoid pericardiocentesis at this time
4. Urgent thrombolysis with tissue plasminogen activator

Reference as: Marzouk I, Melendres L, Boivin M. Ultrasound for critical care physicians: a tempting dilemma. Southwest J Pulm Crit Care. 2014;9(3):193-6. doi: http://dx.doi.org/10.13175/swjpcc128-14 PDF

September 2014 Critical Care Case of the Month: Bad Case of Colic

Sherry Andrews MD

Eyad Almasri MD

Pulmonary and Critical Care

UCSF Fresno

Fresno, CA

History of Present Illness:

A 70 year old man with a past medical history of chronic kidney disease, bipolar disorder, benign prostatic hypertrophy, hypertension and diabetes presented to the emergency department with constipation associated with bloating for 15 days. He denies flatus. He tried over the counter laxatives (polyethylene glycol) with no relief. He has no recent history of colonoscopy or recent antibiotic use. He denies chills, diarrhea, dysuria, fever, hematochezia, hematuria, melena, nausea or vomiting. In the emergency department, he is tachypneic with a grossly distended abdomen.

Past Medical History:

• Diabetes
• Hypertension
• Chronic kidney disease
• Bipolar disorder
• Benign prostatic hypertrophy
• Hyperlipidemia

Past Surgical History:

• Cholecystectomy 2012

Medications:

• Aspirin 81 mg daily
• Furosemide 20 mg daily
• Quetiapine 300 daily
• Doxazosin- 4 mg daily
• Clonazepam 1 mg – twice daily as needed
• Simvastatin 20 mg – daily
• Pioglitazone 15 mg daily

Social History:

He is a retired farm laborer and worked in a cannery. He is married and has two adult children.

He was a former smoker and quit in 2010 He denies any alcohol or illicit drug use

Physical Exam:

• Vital signs – Temperature 37.2 °C, heart rate 84 beats/min, respiratory rate 18-24 breaths/min, blood pressure 121/83 mmHg, SpO2 94 % on 4 L NC 
• General – Average build, well-nourished, in mild distress
• HEENT – Unremarkable
• Neck - Supple, no jugular venous distention
• Chest – Decreased breath sounds right base more than left base
• Heart - Regular rate, normal S1/S2, no murmur
• Abdomen – hypoactive bowel sounds, soft, distended, non-tender to palpation but diffusely tympanic.
• Neurological - Appropriately moves all 4 extremities, CN II-XII grossly intact
• Extremities - No edema
• Skin - No rash or palpable nodules

Laboratory:

• CBC: WBC 6.4 X 10³ /μL, hemoglobin 15.3 g/dL, hematocrit 45%, Platelets 121,000 /μL.
• Chemistries: Na⁺ 141 mmol/L, K⁺ 4.5 mmol /L, Cl^- 105 mmol /L, CO₂ 25 mmol /L, blood urea nitrogen (BUN) 24 mg/dL, creatinine 1.2 mg/dL, glucose 95 mg/dL, calcium 9.9 mg/dL, albumin 4.2 g/dL, liver function tests within normal limits. hemoglobin A1C 5.1%. lactic acid 1.8 mmol/L
•  Coagulation: Prothrombin time (PT) 16.6 sec, international normalized ratio (INR) 1.3

Radiography:

A CT scan abdomen and pelvis was done and a representative coronal view is shown in Figure 1.

Panel 1. Coronal cut of computed Tomography (CT) of the abdomen and pelvis on admission.

Which of the following are characteristics of acute colonic pseudo-obstruction (Ogilvie’s syndrome)? (Click on the correct answer to proceed to the next panel)

1. Antibiotics and abnormal bacterial overgrowth are implicated in the pathogenesis
2. Immediate surgical decompression is required
3. It is a complication of inflammatory bowel disease
4. It occurs in the absence of an anatomic lesion that obstructs the flow of intestinal contents

Reference as: Andrews S, Almasri E. September 2014 critical care case of the month: bad case of colic. Southwest J Pulm Crit Care. 2014;9(3):151-9. doi: http://dx.doi.org/10.13175/swjpcc094-14 PDF 

Life Threatening Zygomyces Infection of the Gastrointestinal Tract

Mohanad Al-Qaisi, MD¹

Charles Stauffer, MD¹

Gerges Makar, MD¹

Tim Kuberski, MD²

¹Department of Medicine, Maricopa Medical Center, Phoenix, Arizona

²Department of Medicine, Infectious Diseases, Maricopa Medical Center, Phoenix, Arizona

Abstract

A 25 year old diabetic woman was admitted into the Intensive Care Unit because of ketoacidosis, hypotension and upper gastrointestinal bleeding. Emergency endoscopic biopsy of the upper gastrointestinal tract demonstrated invasive, non-septate fungal hyphae suggestive of either a Zygomyces or Basidiobolus. Amphotericin B was not used because of its ineffectiveness against Basidiobolus and her renal failure. In addition, first generation antifungal azoles were not used because of their ineffectiveness against Zygomyces. The patient responded to medical therapy and the broad-spectrum azole antifungal posaconazole which has activity against both Basidiobolus and Zygomyces. The patient recovered from her critical illness and on follow up was without residual problems.

Introduction

Zygomyces are a group of fungi which include Mucor, Rhizopus and Absidia, the more common pathologic fungi in the order of Mucorales. As a group, these fungi are characterized by having non-septate hyphae and cause aggressive angioinvasion in certain immunosuppressed settings like ketoacidosis (1). We present a patient who presented with a life-threatening septic syndrome, ketoacidosis and gastrointestinal bleeding due to an infection by an unknown non-septate hyphal fungus, eventually identified as Rhizopus species. On presentation the patient was critically ill and admitted to the Intensive Care Unit. Her early course was complicated by a therapeutic antifungal dilemma which could influence her survival.

Case Report

A 25 years old woman with diabetes was admitted to the Intensive Care Unit with septic syndrome and diabetic ketoacidosis. She was hypotensive, blood pressure was 75/42 mmHg, heart rate 147/min, temperature 38.7 C. Pertinent blood testing revealed the following; glucose 623 mg/dl, creatinine 2.15 mg/dl, bicarbonate 13.6 mmol/L, lactic acid 6.8 mmol/L, WBC 9200/ μL, hemoglobin 7.4 gm/ dl. She was treated aggressively with intubation, mechanical ventilation, vasopressors and continuous renal replacement therapy (CRRT). Her diabetes was treated conventionally. Her course was complicated by a drop in hemoglobin from 11.4 to 7.0 gm/ dl despite transfusions. Her stool was found to be hemoccult positive.

Upper endoscopy showed multiple ulcers involving the gastric body extending onto the cardia which was covered with coffee ground exudate. Biopsies were obtained and showed a "fungus" with non-septate hyphae on preliminary histopathology and amphotericin B was initiated empirically. She continued to experience significant hematemesis and hypotension requiring multiple transfusions (4 units). The amphotericin B was discontinued because of progressive azotemia. Upon review of the pathology from the stomach biopsy, the possibility was raised that she might have either a Basidiobolus or Zygomyces infection (Figure 1).

Figure 1 illustrates the difference in appearance of non-septate hyphae between fungi in tissue in vivo and on culture in vitro. (A) Fungal culture (in vitro) showing the non­ septate hyphae. (B) GMS stain of the stomach tissue from the patient (in vivo) showing fungus fragments having broad, irregular, non-septate hyphae, arrow. The hyphae morphology becomes distorted with angioinvasion and tissue necrosis.

The patient was started empirically on oral posaconazole 400 mg twice daily which theoretically would be effective for both fungi. Within a few days the ketoacidosis resolved, the gastrointestinal bleeding stopped and she was discharged a few days later. After her discharge a Rhizopus species was cultured and identified as the causative agent.

Discussion

The therapeutic dilemma in the treatment of this patient was related to the inability to differentiate between two potential fungal pathogens, Zygomyces or Basidiobolus on the basis of only tissue pathology. Under ideal circumstances the histopathology might differentiate the two, however trying to distinguish between the two can be difficult because both have non-septate hyphae, are morphologically similar, and can involve the stomach. Based on morphology the differentiation between Basidiobolus and Rhizopus is subtle. For Basidiobolus the hyphal elements typically show "sparse" septation while Rhizopus hyphal elements show "infrequent" septation. There was an added problem in that confirmatory cultures can take weeks before a specific identification can be made. Zygomyces infections tend to be rapidly destructive, but are rare to involve the gastrointestinal tract (1). In contrast, Basidiobolus rananum is endemic to Arizona and generally known to primarily cause gastrointestinal infections (2). That organism however, usually causes an indolent process and is less likely to be fatal. However, there is a case report of angioinvasive disease with basidiobolomycosis reminiscent of mucormycosis in diabetics (3). Epidemiological studies on Basidiobolus suggest that the common risks for this infection include living in Arizona, having diabetes and use of medications that suppress stomach acids (2).

A high index of suspicion in our patient with some of these risk factors made Basidiobolus a consideration. Importantly, the antifungal treatment of Basidiobolus is different than for the Zygomyces (i.e., Rhizopus). Basidiobolus is known to be resistant to amphotericin B and the preferred treatment is itraconazole (2).

Our patient initially received a few doses of amphotericin B empirically because of the report of a non-septate "fungus" on biopsy. Amphotericin B is the drug of choice for Zygomyces, but not for Basidiobolus (4). Notably itraconazole is not effective for the Zygomyces. The treatment decision was made to use posaconazole because of its broad spectrum antifungal activity that would have activity against both Zygomyces and Basidiobolus. In addition, there is a report of posaconazole being used successfully to treat gastrointestinal basidiobolomycosis (5). Of the Zygomyces, Rhizopus is the most common cause of human infections, more than Mucor. Certainly correcting the ketoacidosis and gastrointestinal bleeding contributed to her improvement, but the mortality rate in diabetic patients with Zygomyces involving the gastrointestinal tract is about 85% (6). The patient appeared to be effectively treated based on the therapeutic antifungal decision while the patient was critically ill. She was seen in follow up several weeks later without any obvious residual effects. Her response to posaconazole suggests it would be an effective consideration in places like Arizona where Basidiobolus and Zygomyces could be in the differential.

References

1. Chayakulkeeree M, Ghannoum MA, Perfect JR. Zygomycosis: the re-emerging fungal infection. Eur J Clin Microbiol Infect Dis. 2006;25(4):215-29. [CrossRef] [PubMed]
2. Vikram HR, Smilack JD, Leighton JA, Crowell MD, De Petris G.. Emergence of gastrointestinal basidiobolomycosis in the united states, with a review of worldwide cases. Clin Infect Dis. 2012;54(12):1685-91. [CrossRef] [PubMed]
3. Bigliazzi C, Poletti V, Dell'Amore D, Saragoni L, Colby TV. Disseminated basidiobolomycosis in an immunocompetent woman. J Clin Microbiol. 2004;42(3):1367-9. [CrossRef] [PubMed]
4. Guarro J, Aguilar C, Pujol I. In-vitro antifungal susceptibilities of Basidiobolus and Conidiobolus spp. strains. J Antimicrob Chemother. 1999;44(4):557-60. [CrossRef] [PubMed]
5. Rose RR, Lindsby MD, Hurst SF, Paddock CD, Damodaran T, Bennett J. Gastrointestinal basidiobolomycosis treated with posaconazole. Med Mycol Case Rep. 2012;2:11-4. [CrossRef] [PubMed]
6. Roden MM, Zaoutis TE, Buchanon WL, Knudsen TA, Sarkisova TA, Schaufele RL, Sein M, Sein T, Chiou CC, Chu JH, Kontoyiannis DP, Walsh JT. Epidemiology and outcome of zygomycosis: a review of 929 reported cases. Clin Infect Dis. 2005;41(5):634-53. [CrossRef] [PubMed]

Reference as: Al-Qaisi M, Stauffer C, Makar G, Kuberski T. Life threatening zygomyces infection of the gastrointestinal tract. Southwest J Pulm Crit Care. 2014;9(2):133-6. doi: http://dx.doi.org/10.13175/swjpcc090-14 PDF 

Ultrasound For Critical Care Physicians: Where Did the Bubbles Go?

A 35-year-old woman with factor V Leiden deficiency on chronic anticoagulation therapy and a history of multiple deep vein thrombosis, pulmonary embolism and transient ischemic attacks presented for an evaluation of dyspnea. An echocardiogram with agitated saline contrast (bubble study) was performed (Figure 1).

Figure 1. Apical 4 chamber video taken from bubble study.

What is the best explanation for the findings in the video?

1. Intra-atrial right to left shunting
2. Normal bubble study
3. Pulmonary arterial-venous malformation
4. Ventricular septal defect

Reference as: Natt B, Snyder L, Lax D. Ultrasound for critical care physicians: where did the bubbles go? Southwest J Pulm Crit Care. 2014;9(2):91-3. doi: http://dx.doi.org/10.13175/swjpcc100-14 PDF

August 2014 Critical Care Case of the Month: The Beans Are Done

Theodore Loftsgard RN, CNP

Zanele Manaka R.R.T., C.R.T.

Jocelyn Coy R.N.

Jared J. Jones, Pharm.D., R.Ph.

Division of Critical Care

Mayo Clinic

Rochester, Minnesota

Case Presentation

A 68-year-old woman was admitted to the ICU due to acute renal failure in setting of ovarian cancer recurrence.

She reports a two week history of abdominal pain with increased, loose ileostomy output, nausea, one episode of vomiting of food returns, and profound increasing generalized weakness. She states she has been voiding urine in normal frequency. She took her most recent dose of Xarelto 20mg the evening prior to presentation.

On ICU arrival, she was alert and oriented but pale and underweight with dry mucous membranes. She reported 2/10 generalized abdominal pain. Her blood pressure was stable. 

PMH

March 2013: Diagnosed with stage IIIC metastatic ovarian cancer.  She underwent extensive abdominal surgery including radical hysterectomy, diverting loop ileostomy and cholecystectomy.  Final pathology: grade 3 serous carcinoma involving omentum, descending colon, cecum and terminal ileum, both ovaries with implants on bilateral tubes and uterine serosa, right pelvic side wall, right diaphragm, 3 right paraaortic lymph nodes, and gallbladder. 

April 2013: She developed thrombus of the bilateral peroneal veins, left posterior tibial vein, and right soleal veins and was started on Lovenox She was recently transitioned to rivaroxaban (Xarelto).

February 2014: abdominal ultrasound showed numerous small, hypoechoic nodules and lesions throughout the liver which were worrisome for metastatic disease. She presented to the clinic today for a second opinion.

Current Medications

1. Fentanyl 100 mcg/hr patch 72 hour 1 patch transdermally every 3 days
2. Ibuprofen PRN
3. Oxycodone PRN
4. Rivaroxaban (Xarleto®) 20 mg daily
5. Sertraline (Zoloft®) 25 mg daily

Past Medical/Surgical History

    Past Medical History   

1. Craniocervical dystonia receives Botox injections.
2. Ovarian cancer

    Past Surgical History  

1. Appendectomy at 8 years old.
2. Tonsillectomy.
3. Laparoscopy in 1983 for infected Dalkon Shield.
4. L5 bulging disk surgery in the 1990s.
5. Total abdominal hysterectomy, bilateral salpingo-oophorectomies, cholecystectomy, lymphadenectomy, and tumor debulking for ovarian cancer March 2013.

Physical Exam

Vital signs: height 164.3 cm, weight 42.90 kg, BSA(G) 1.40 M², BMI 15.892 Kg/M², temperature 36.4 °C, respiratory rate 13 breaths/minute, blood pressure 148/77 mmHg.  pulse 64/minute.  SpO2 98% on room air.

Heart: S1, S2 with no murmur, click, rub. Sinus rhythm, rate 64, no ectopy.

Lungs: Respirations symmetrical and easy with bilateral breath sounds clear to auscultation.

Abdomen: Slightly firm, nondistended, mild tenderness to palpation, bowel sounds present. Ostomy pink with dark brown liquid output in bag.

Electrocardiogram

Figure 1. ICU admission electrocardiogram.

Ultrasonography

Figure 2. Panel A: Static image from abdominal ultrasound of inferior vena cava. Panel B: Static image from abdominal ultrasound showing longitudinal axis of left kidney. Panel C: Static image from abdominal ultrasound showing longitudinal axis of right kidney. Lower panel: movie of ultrasound of inferior vena cava.

Which of the following is (are) true? (Click on the correct answer to proceed to the next panel)

1. The electrocardiogram shows tall, peaked T waves
2. The inferior vena cava is collapsed suggesting volume depletion
3. There is hydronephrosis of the left kidney
4. There is hydronephrosis of the right kidney
5. All of the above

Reference as: Loftsgard TO, Manaka Z, Coy J, Jones JJ. August 2014 critical care case of the month: the beans are done. Southwest J Pulm Crit Care. 2014;9(2):72-82. doi: http://dx.doi.org/10.13175/swjpcc087-14 PDF

Ultrasound for Critical Care Physicians: Cardiogenic Shock-This Is Not a Drill

Ramakrishna Chaikalam, MD 

Shozab Ahmed, MD

Division of Pulmonary, Critical Care and Sleep

University of New Mexico

Albuquerque, NM

A 45-year-old woman with no significant past history developed gradual onset of shortness of breath and cough over 1 week. She presented to the emergency department. Her initial chest x-ray showed an enlarged heart and bilateral pulmonary edema. The patient became progressively hypotensive and hypoxic and was intubated. Transthoracic echocardiography is shown below (Figure 1).

Figure 1. Transthoracic echocardiogram in the para-sternal long axis view of the heart.

What intra-cardiac device in the left ventricle is pictured on the image? (Click on the correct answer to proceed to the next panel)

1. Amplatz closure device of atrial septal defect
2. Extracorporeal membrane oxygenator (ECMO) cannula
3. Impella device
4. Intra-aortic balloon pump
5. Pacemaker lead

Reference as: Chaikalam R, Ahmed S. Ultrasound for critical care physicians: cardiogenic shock-this is not a drill. Southwest J Pulm Crit Care. 2014;9(1):27-9. doi: http://dx.doi.org/10.13175/swjpcc091-14 PDF

July 2014 Critical Care Case of the Month: There Is Still a Role for Physical Examination

Robert A. Raschke, MD 

Banner Good Samaritan Medical Center

Phoenix, AZ

History of Present Illness

A 90-year-old woman was the seatbelt-restrained driver in a low speed frontal motor vehicle collision with airbag deployment, after she accidentally hit the gas instead of the brake. In the emergency room, the patient’s main complaint was right shoulder pain. On ER physical exam, she had sternal ecchymosis consistent with “seatbelt sign”. Her right shoulder was said to be tender, but the mechanism of injury to the right shoulder was unclear since her drivers-side seatbelt would been in contact with her left rather than right shoulder. Her right upper extremity was said to be “weak secondary to pain”. Further neurological examination was noted to be difficult due to “patient crying out in pain and anxiety”, but it was noted that she could lift both legs off the bed. Her left knee was echymotic. Cardiac auscultation revealed irregularly irregular rhythm.

PMH

• Chronic atrial fibrillation
• Coronary artery disease
• Hypertension

Medications

• Warfarin
• Aspirin
• Clonidine
• Metoprolol

Labs performed in the emergency room showed an INR 1.9. Radiographs demonstrated a normal right shoulder and a left patellar fracture. CT scans of the cervical spine and chest showed no bony abnormalities. An incidental 4 cm thoracic aortic aneurysm was noted. CT of the brain showed periventricular white matter hyperlucencies consistent with small vessel disease. The patient became a bit drowsy after receiving narcotic analgesia in the emergency room and was transferred to the medical ICU for management of pain and delirium.

ICU Physical Examination

In the medical ICU the patient was alert, and seemed much younger than 90 years of age, with a sharp wit. She complained of 10/10 shoulder pain at rest which occasionally made her wince, cry out in pain and move her shoulder – however, she said there was no position in which her shoulder did not hurt. There were no ecchymosis of the shoulder, and it could be passively abducted and rotated without worsening the pain. The initial neurological examination was cursory and unrevealing because the patient was distracted by pain, and her left leg was immobilized.  A short time later the nurse reported that she felt the patient’s right leg was weak and the neurological exam was repeated. Strength in the patient’s right leg was 1/5, her left leg was immobilized, but ankle extension was 5/5. She could not cooperate well with strength testing of her painful right arm, but her right grip was 2/5 with a normal strength in her left arm and hand. Toes were down-going and reflexes were generally hypoactive. She was not aphasic. Neurology was consulted.

Which of the following is true in regards to this patient’s neurological findings? (Click on the correct answer to proceed to the next panel)

1. A cervical spinal cord injury could explain these findings
2. A seat belt injury of the left carotid artery could have resulted in traumatic dissection and subsequent stroke
3. Right hemiparesis without aphasia could represent a lacunar stroke
4. They might represent a cardio-embolic stroke related to her history of atrial fibrillation
5. All of the above

Reference as: Raschke RA. July 2014 critical care case of the month: there is still a role for physicial examination. Southwest J Pulm Crit Care. 2014;9(1):8-14. doi: http://dx.doi.org/10.13175/swjpcc086-14 PDF

Ultrasound For Critical Care Physicians: Neutropenic Patient With Fever and Shortness of Breath

Erik Kraai MD

Michel Boivin MD

Division of Pulmonary / Critical Care and Sleep

University of New Mexico

Albuquerque, NM

A 63 year old female with a history of acute myelogenous leukemia presents with shortness of breath, fever and hypotension to the ICU. She is in septic shock on norepinephrine, and has been treated on the oncology unit with vancomycin, cefepime, acyclovir and voriconazole. She has been neutropenic for 1 month. The patient develops a progressive right lower chest opacity. This opacity has progressed in spite of antibiotics and antifungals. The portable AP chest radiograph is presented below (Figure 1). 

Figure 1. Portable AP of chest.

An ultrasound of the right chest was performed for further evaluation of the opacity (figure 2). 

Figure 2. Ultrasound of right hemithorax.

Question: What pathology does the ultrasound reveal in the right hemithorax? (Click on the correct answer to proceed to the next panel)

1. Air filled cavity
2. Chest wall abscess
3. Fractured ribs
4. Pleural effusion and suspected empyema
5. Simple consolidation

Refernece as: Kraai E, Boivin M. Ultrasound for critical care physicians: neutropenic patient with fever snd shortness of breath. Southwest J Pulm Crit Care. 2014;8(6):330-3. doi: http://dx.doi.org/10.13175/swjpcc073-14 PDF

June 2014 Critical Care Case of the Month: Acute Exacerbation in Cystic Fibrosis

Seongseok Yun, MD PhD¹ 

Juhyung Sun, BS²

Laura Howe, MD¹

Roberto Bernardo, MD¹

Sepehr Daheshpour, MD¹

Department of Medicine¹

College of Medicine²

University of Arizona

Tucson, AZ 85724

History of Present Illness

A 28 year-old woman with a history of cystic fibrosis, presented with worsening shortness of breath and cough associated with productive secretions. She was diagnosed with cystic fibrosis when she was 14 months old, and has a history of multiple inpatient admissions for acute pulmonary exacerbation of cystic fibrosis. Her most recent hospitalization was a month prior to this admission, and sputum culture demonstrated methicillin-resistant Staphylococcus aureus, multidrug-resistant Pseudomonas aeruginosa, and Achromobacter xylosoxidans. She was treated with linezolide, meropenum, colistin, and azithromycin with significant symptom improvement, then, discharged home with ciprofloxacin, linezolide and zosyn. However, she developed worsening respiratory distress again and came back to hospital. In the emergency department she required 10 L/min of oxygen to maintain an SpO₂ above 90 %.

PMH

• Cystic fibrosis
• Seizure
• Kidney stone
• Portacath placement
• Gastrostomy tube placement

Medications

• Azithromycin 500 mg 3 times a day
• Dornase alpha 1 mg/ml nebulizer twice a day     
• Fluticasone-salmeterol 500-50 mcg/dose inhaler twice a day
• Lipase-protease-amylase 21,000-37,000-61,000 unit 4 caps a day
• Cholecalciferol  2,000 unit capsule daily
• Ferrous sulfate 325 mg PO twice a day
• Ascorbic acid 250 mg PO twice a day
• Oxycodone-acetaminophen  10-325 mg 4 times a day as needed

Social History

• No smoking
• No alcohol use
• No recreational drug use

Physical Examination

Vital signs: Temperature 37.3 °C, heart rate 114 beats/min, respiratory rate 20-24 breaths/min, blood pressure 99/69mmHg, SpO2 88-90 % on 10 L NC

General: Alert and oriented X 3, acutely distressed, tachypneic and dyspneic

Skin: Diaphoretic. No rash or lesions.

HEENT: Unremarkable.

Respiratory: Diffuse rales in all lung fields, no wheezing, no stridor

CVS: Tachycardic, regular rhythm, no murmur.

Abdomen: Soft, non-tender, no tenderness, no guarding, no hepato-splenomegaly, PEG tube placed

Lymphatics: No cervical or axillary lymphadenopathy

Extremities: No clubbing, no cyanosis, no peripheral edema, normal tone, normal range of movement

Neurological: Normal speech, no focal neurologic deficit, CN exam within normal range

Laboratory

CBC: WBC 11.9X 10³ /μL, Hb 9.8 g/dL, Hct 30.7%, Platelets 356,000 /μL.

Chemistries: Na⁺ 137 meq/L, K⁺ 4.1 meq/L, Cl^- 107 meq/L, CO₂ 22 mmol/L, blood urea nitrogen (BUN) 13 mg/dL, creatinine 0.7 mg/dL, glucose 106 mg/dL, calcium 8.0 mg/dL, albumin 2.6 g/dL, liver function tests within normal limits.

Prothrombin time (PT) 14.0 sec, international normalized ratio (INR)1.1, partial thromboplastin time (PTT) 37.2sec

Pulmonary Function Test

FVC 48 % (1.95 L), FEV₁ 36 % (1.25 L), FEF_25-75 14 % (0.55 L/sec)

Radiography

An old chest x-ray and thoracic CT scan were reviewed (Figure 1).

Figure 1. Previous PA (Panel A), lateral (Panel B) chest x-ray and representative image from the thoracic CT scan (Panel C).

Which of the following are findings of cystic fibrosis on chest x-ray? (Click on the correct answer to move to the next panel)

1. Bronchiectasis
2. Hyperinflation
3. Lobar collapse
4. Prominent pulmonary arteries
5. All of the Above

Reference as: Yun S, Sun J, Howe L, Bernardo R, Daheshpour S. June 2014 critical care case of the month: acute exacerbation in cystic fibrosis. Southwest J Pulm Crit Care. 2014;8(6):305-19. doi: http://dx.doi.org/10.13175/swjpcc047-14 PDF

Ultrasound for Critical Care Physicians: Really, At Her Age?

A 71 year old woman presented with dyspnea since late 2013 and denies a prior history of dyspnea. She had a cardiac pacemaker placed in 2008 for sick sinus syndrome. Her physical exam was unremarkable and her SpO2 was 96% on room air. However,  it decreased to 84% with exercise. Chest x-ray and pulmonary function testing were unremarkable (a DLco was unable to be performed). A transthoracic echocardiogram was performed (Figure 1).

Figure 1. Movie with Doppler flow of transthoracic echocardiogram. 

Which of the following best explains the patient's dyspnea and hypoxia? (Click on the correct answer to proceed to the next panel)

1. Cardiac tamponade
2. Decreased cardiac contractility
3. Intracardiac shunt
4. Mitral insufficiency
5. Ventilation perfusion mismatch from COPD

Reference as: Wesselius LJ. Ultrasound for critical care physicians: really, at her age? Southwest J Pulm Crit Care. 2014;8(5):278-9. doi: http://dx.doi.org/10.13175/swjpcc061-14 PDF