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 Critical Care

Last 50 Critical Care Postings

(Click on title to be directed to posting, most recent listed first, CME offerings in Bold)

August 2017 Critical Care Case of the Month
Telemedicine Using Stationary Hard-Wire Audiovisual Equipment or Robotic 
   Systems in Critical Care: A Brief Review
Carotid Cavernous Fistula: A Case Study and Review
July 2017 Critical Care Case of the Month
High-Sensitivity Troponin I and the Risk of Flow Limiting Coronary Artery 
Disease in Non-ST Elevation Acute Coronary Syndrome (NSTE-ACS)
June 2017 Critical Care Case of the Month
Clinical Performance of an Interactive Clinical Decision Support System for
   Assessment of Plasma Lactate in Hospitalized Patients with Organ
   Dysfunction
May 2017 Critical Care Case of the Month
Management of Life Threatening Post-Partum Hemorrhage with HBOC-201 
   in a Jehovah’s Witness
Tracheal Stoma Necrosis: A Case Report
April 2017 Critical Care Case of the Month
March 2017 Critical Care Case of the Month
Ultrasound for Critical Care Physicians: Unchain My Heart
February 2017 Critical Care Case of the Month
January 2017 Critical Care Case of the Month
December 2016 Critical Care Case of the Month
Ultrasound for Critical Care Physicians: A Pericardial Effusion of Uncertain 
   Significance
Corticosteroids and Influenza A associated Acute Respiratory Distress 
   Syndrome
November 2016 Critical Care Case of the Month
October 2016 Critical Care Case of the Month
September 2016 Critical Care Case of the Month
Ultrasound for Critical Care Physicians: Unraveling a Rapid Drop of 
   Hematocrit
Fluid Resuscitation for Septic Shock – A 50-Year Perspective:
   From Dogma to Skepticism
August 2016 Critical Care Case of the Month
Ultrasound for Critical Care Physicians: Complication of a Distant
   Malignancy
July 2016 Critical Care Case of the Month
Ultrasound for Critical Care Physicians: Now My Heart Is Still 
   Somewhat Full
June 2016 Critical Care Case of the Month
May 2016 Critical Care Case of the Month
Design of an Electronic Medical Record (EMR)-Based Clinical Decision
Support System to Alert Clinicians to the Onset of Severe Sepsis
April 2016 Critical Care Case of the Month
Ultrasound for Critical Care Physicians: Two’s a Crowd
March 2016 Critical Care Case of the Month
February 2016 Critical Care Case of the Month
Ultrasound for Critical Care Physicians: Hungry Heart
January 2016 Critical Care Case of the Month
Ultrasound for Critical Care Physicians: The Pleura and the Answers that 
   Lie Within
December 2015 Critical Care Case of the Month
Ultrasound for Critical Care Physicians: 50 Ways to Line Your Liver
November 2015 Critical Care Case of the Month
Ultrasound for Critical Care Physicians: The Martian
October 2015 Critical Care Case of the Month: A Moldy But Gooey
Ultrasound for Critical Care Physicians: Shortness of Breath
September 2015 Critical Care Case of the Month: If You Don't Look, 
   You Won't Find 
August 2015 Critical Care Case of the Month: A Diagnostic Branch 
   of Medicine
Ultrasound for Critical Care Physicians: Take a Deep Breath
July 2015 Critical Care Case of the Month: An Unusual Presentation 
June 2015 Critical Care Case of the Month: Just Ask the Nurse
Acute Pregabalin Withdrawal: A Case Report and Review of the Literature
Organ Failure in Acute Pancreatitis and Its Impact on Outcome in Critical
   Care

 

For complete critical care listings click here.

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

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Wednesday
Aug022017

August 2017 Critical Care Case of the Month

Kolene E. Bailey, MD1

Carolyn Welsh, MD1,2

 

Pulmonary Sciences and Critical Care Medicine

1University of Colorado Anschutz Medical Campus and 2VA Eastern Colorado Health Care System

Denver, CO USA

 

Critical Care Case of the Month CME Information

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

0.25 AMA PRA Category 1 Credit(s)™

Estimated time to complete this activity: 0.25 hours 

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

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

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

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

CME Sponsor: University of Arizona College of Medicine

Current Approval Period: January 1, 2017-December 31, 2018

Financial Support Received: None

 

History of Present Illness

The patient is a 26-year-old woman with who was admitted to the hospital for second cycle of chemotherapy for a large mediastinal synovial sarcoma diagnosed 2 months prior to admission. Symptoms started 6 months prior to presentation with cough. She related the cough to her cigarette smoking and quit. Upon persistence of symptoms, she was evaluated by her physician who ordered imaging. Work-up revealed a large 12 x 14cm synovial sarcoma with internal necrosis that encased the subclavian artery, and descending thoracic aorta, inseparable from pericardium and left atrium. It also encased the pulmonary veins, pulmonary arteries, and airways. Malignancy was complicated by extensive left upper extremity DVT for which she has been on anticoagulation since her last admission, SVC syndrome, and severe mucositis.

Past Medical History, Family History, and Social History
She has a past medical history significant for malignant melanoma surgically resected 7 years previously, as well as generalized an anxiety disorder.

Her family history includes a maternal grandfather with esophageal cancer and maternal great-grandmother with pancreatic cancer. She is single and lives with her parents. She is a former 8 pack year smoker, and daily edible marijuana user. She worked as a hairdresser, but is now unable to work.

Current Medications:

  • Escitalopram (Lexapro) 10mg PO daily
  • Dalteparin
  • Oxycontin 10mg PO BID + Oxycodone 5-10mg PO Q4H PRN pain
  • Antiemetics: Compazine PRN, Ondansetron PRN, dexamethasone 4mg BID for 3 days following chemotherapy
  • Lorazepam 1mg PO Q4H PRN anxiety
  • Pegfilgastrim after chemotherapy
  • Senna 3 tabs in AM, 2 tabs in PM

Hospital Course

After starting cycle #2 of chemotherapy (doxorubicin, ifosfamide, and mesna), she experienced significant nausea and anxiety and was prescribed scheduled ondansetron/dexamethasone, prochlorperazine, promethazine and lorazepam. The night of hospital day #2, her providers noticed altered mental status and unusual behavior. They asked her draw a clock which is shown (Figure 1).

Figure 1. Clock drawn by patient.

What is on your differential diagnosis for this patient’s altered mental status? (Click on the correct answer to proceed to the second of five pages)

  1. Delirium
  2. Ifosfamide-induced encephalopathy
  3. Toxic-metabolic encephalopathy secondary to the medications received
  4. 1 and 3
  5. All of the above

Cite as: Bailey KE, Welsh C. August 2017 critical care case of the month. Southwest J Pulm Crit Care. 2017;15(2):61-6. doi: https://doi.org/10.13175/swjpcc094-17 PDF

Thursday
Jul272017

Telemedicine Using Stationary Hard-Wire Audiovisual Equipment or Robotic Systems in Critical Care: A Brief Review

Nidhi S. Nikhanj, MD1,2

Robert A. Raschke, MD1,2

Robert Groves, MD1,2

Rodrigo Cavallazzi, MD3

Ken S. Ramos, MD1

 

1Arizona College of Medicine-Phoenix

Phoenix, AZ USA

2Banner University Medical Center-Phoenix

Phoenix, AZ USA

3University of Louisville School of Medicine

Louisville, KY USA

 

A shortage of critical care physicians in the United States has been widely recognized and reported (1). Most intensive care units (ICUs) do no not have a formally-trained intensivist in their staff despite compelling evidence that high-intensity intensivist staffing leads to better patient outcomes (1,2). Critical care telemedicine is one potential solution that has expanded rapidly since its inception in 2000 (3). In its simplest form, telemedicine leverages audiovisual technology and the electronic medical record to provide remote two-way communication between a physician and a patient. Current telemedicine models differ by the type of hardware facilitating remote audiovisual interaction, the location of the provider, and the type of patient-care service provided. We collectively have experience with several of these models and feel that future telemedicine programs will likely integrate the most advantageous aspects of each with an increasing role for telemedicine robotics.

The dominant current model for providing critical care telemedicine in large healthcare systems utilizes stationary hard-wired audiovisual equipment linking each ICU room to a centralized control location (4). Typically, this control center provides surveillance of a large number of patients using computerized decision support software linked to the EMR – a single physician can cover approximately 100 patients with the appropriate support infrastructure. This model also provides the ability to remotely “round” on ICU patients and to quickly respond to questions posed by nursing or medical emergencies across a broad geographic range. This approach requires a high up-front capital cost approximated at 50-100K per hospital bed covered (5).

Data supporting the benefit of this model of ICU telemedicine has been mixed, but several considerations are important in appraising the literature. A double-blinded RCT for ICU telemedicine intervention is not feasible. Heterogeneity in clinical workflows and staffing models across the country should be considered when assessing the internal validity and generalizability of published studies. For instance, Thomas and colleagues concluded that a telemedicine ICU service resulted in no overall improvement in mortality or length of stay (LOS) (6), but the tele-intensivists in the study were limited by only being allowed to intervene in the care of less than a third of the study patients. Nassar and colleagues published a negative study in a healthcare system in which resident and attending physicians were already available in-house for overnight patient care (7). Likely, the potential benefit of a telemedicine program can be optimized in a clinical setting in which other physicians are not physically available at the locality 24/7 and telemedicine intensivists are allowed to appropriately intervene when indicated.

Despite these difficulties, there is a growing body of evidence that suggests a centralized telemedicine ICU model is effective in a number of areas including: improvements in compliance with evidence based practices (8, 9), increased job satisfaction of ICU nurses (10) and reduction in the cost of care of the sickest patients in the institutional setting (11). Other studies suggest that a telemedicine platform can reduce mortality and LOS by allowing for earlier intensivist involvement, promoting adherence to best practices, shortening alarm response times and improving access to ICU performance data that can be used to drive continuous quality improvement (12,13).

Commercially available telemedicine robots are mobile units equipped with a digital camera, microphone and monitor screen that provides two-way audiovisual communications with the control center via a wireless internet connection (14). Telemedicine robots can be operated with much lower initial capital costs - for instance, an ICU group at a large acute care hospital might provide coverage at a rural healthcare setting using a single robot (15). Such a system can be used for daily rounding or for reactive consultation. Like hard-wired systems, telemedicine robots have been shown to be well accepted by providers (16) and patients (17), and their use has been associated with reduced ICU length-of-stay and decreased delay in response to clinical events by the physician (18).

Telemedicine robotic systems have several disadvantages – they do not provide large-scale EMR surveillance leveraging computerized decision support logic and they are significantly less efficient than hard-wired systems for high-volume patient care since they have to physically relocate from patient room to patient room.  However, unique capabilities of telemedicine robots are being developed that cannot be duplicated by hard-wired systems. Telemedicine robots can be equipped with a digital stethoscope (19). They can perform physical examination elements that require tactile communication – such as the determination of the Glasgow coma scale (20). A robotic arm can be used to remotely perform point-of-care ultrasonography. This has been successfully operationalized for cardiac, abdomino-pelvic, and vascular indications (21,22). Telemedicine robots have been developed that can place peripheral or central venous catheters (23). The development of surgical robots that incorporate tomographic capability and that can perform battlefield stabilization procedures in either autonomous or teleoperative modes (24) provide a glimpse of the potential for telemedicine robots in the ICU.

Although healthcare systems currently implementing telemedicine services will likely choose either a hard-wired or a robotic model – largely based on cost and the volume of required services - we believe the optimal telemedicine system of the future will and should incorporate both technologies. Real-time data acquisition coupled with ready access to timely interventions constitute the basis for faster deployment of precision health care strategies in the ICU setting.

References

  1. Kelley MA, Angus D, Chalfin DB, Crandall ED, et al. The critical care crisis in the United States: A report from the profession. Chest. 2004;125:1514-7. [CrossRef] [PubMed]
  2. Pronovost PJ, Angus DC, Dorman T, Robinson KA, et al. Physician staffing patterns and clinical outcomes in critically ill patients. JAMA. 2002;288:2151-62. [CrossRef] [PubMed]
  3. Rosenfeld BA, Dorman T, Breslow MJ, et al. Intensive care unit telemedicine: alternate paradigm for providing continuous intensivist care. Crit Care Med. 2000;28:3925-31. [CrossRef] [PubMed]
  4. Kahn JM, Cicero BD, Wallace DJ, Iwashyna TJ. Adoption of intensive care unit telemedicine in the United States. Crit Care Med. 2014;42:362-8. [CrossRef] [PubMed]
  5. Kumar G, Falk DM, Bonello RS, et al. The costs of critical care telemedicine programs: A systematic review and analysis. Chest. 2013;143:19-29. [CrossRef] [PubMed]
  6. Thomas EJ, Lucke JF, Wueste L. Association of telemedicine for remote monitoring of intensive care patients weith mortality, complications and length of stay. JAMA. 2009;302:2671-78. [CrossRef] [PubMed]
  7. Nassar BS, Vaughan MS, Jiang L, Reisinger HS, et al. Impact of an intensive care unit telemedicine program on patient outcomes in an integrated health care system. JAMA Intern Med. 2014;174:1160-7. [CrossRef] [PubMed]
  8. Ventataraman R, Ramakrishnan N. Outcomes related to telemedicine in the intensive care Unit. Crit Care Clinics 2015;31:225-37. [CrossRef] [PubMed]
  9. Youn BA. ICU process improvement using telemedicine to enhance compliance and documentation for the ventilator bundle. Chest. 2006;130:(meeting abstracts) 226S-c.
  10. Hoonakker PL, Carayon P, McGuire K, et al. Motivation and job satisfaction of tele-ICU nurses. J Crit Care. 2013;28:890-901. [CrossRef] [PubMed]
  11. Franzini L, Sail KR, Thomas EJ, et al. Costs and cost-effectiveness of a telemedicine intensive care unit program in six intensive care units in a large health care system. J Crit Care. 2011;26:329e1-6. [CrossRef] [PubMed]
  12. Lilly CM, Cody S, Zhao H. Hospital mortality, length of stay and preventable complications among critically ill patients before and after tele-ICU reengineering of critical care processes. JAMA. 2011;305:2175-83. [CrossRef] [PubMed]
  13. Lilly CM, Zubrow MT, Kempner KM, Reynolds H, et al. Critical Care telemedicine: Evolution and state of the art. Crit Care Med. 2014;42:2429-36. [CrossRef] [PubMed]
  14. Chung KK, Grathwohl KW, Poropatich RK, Wolf SE, et al. Robotic telepresence: Past present and future. Journal of Cardiothoracic and Vascular Anesthesia. 2007;21:593-6. [CrossRef] [PubMed]
  15. Murray C, Ortiz E, Kubin C. Application of a robot for critical care rounding in small rural hospitals. Crit Care Nurs Clin North Am. 2014;26:477-85. [CrossRef] [PubMed]
  16. Reynolds EM, Grujovski A, Wright T, Foster M, Reynolds HN. Utilization of robotic remote presence technology within North American intensive care units. Telemedicine and e-health. 2012;18:507-15. [CrossRef] [PubMed]
  17. Sucher JF, Todd SR, Jones SL, Throckmorton T, et al. Robotic telepresence: A helpful adjunct that is viewed favorably by critically ill surgical patients. Am J Surg. 2011;202:843-7. [CrossRef] [PubMed]
  18. Vespa PM, Miller C, Hu X, Nenov V, et al. Intensive care unit robotic telepresence facilitates rapid physician response to unstable patients and decreased cost in neurointensive care. Surgical Neurology. 2007;67:331-7. [CrossRef] [PubMed]
  19. Lakhe A, Sodhi I, Warrier J, Sinha V. Development of digital stethoscope for telemedicine. J Med Eng Technol. 2016;40:20-4. [CrossRef] [PubMed]
  20. Adcock AK, Kosiorek H, Parich P, Chauncey A, Wu Q, Demaerschalk BM. Reliability of robotic telemedicine for assessing critically ill patients with the full outline of unresponsiveness score and Glasgow coma scale. Telemed J E Health. 2017 Jan 13. [CrossRef] [PubMed]
  21. Avgousti S, Panayides AS, Jossif AP, Christoforou EG, et al. Cardiac ultrasonography over 4G wireless networks using a tele-operated robot. Healthc Technol Lett. 2016;3:212-7. [CrossRef] [PubMed]
  22. Georgescu M, Sacccomandi A, Baudron B, Arbeille PL. Remote sonography in routine clinical practice between two isolated medical centers and the university hospital using a robotic arm: A 1-year study. Telemed J E Health. 2016;22:276-81. [CrossRef] [PubMed]
  23. Kobayashi Y, Hong J, Hamano R, Okada K, Fujie MG, Hashizume M. Development of a needle insertion manipulator for central venous catheterization. Int J Med Robot. 2012;8(1):34–44. [CrossRef] [PubMed]
  24. Garcia P, Rosen J, Kapoor C, Noakes M, et al. Trauma Pod: a semi-automated telerobotic surgical system. Int J Med Robot. 2009;5:136-46. [CrossRef] [PubMed]

Cite as: Nikhanj NS, Raschke RA, Groves R, Cavallazzi R, Ramos KS. Telemedicine using stationary hard-wire audiovisual equipment or robotic systems in critical care: a brief review. Southwest J Pulm Crit Care. 2017;15(1):50-3. doi: https://doi.org/10.13175/swjpcc087-17 PDF

Tuesday
Jul112017

Carotid Cavernous Fistula: A Case Study and Review

Iaswarya Ganapathiraju, OMS-IV1

Douglas T Summerfield, MD2

Melissa M Summerfield, MD2

 

1Des Moines University College of Osteopathic Medicine

Des Moines, IA USA

2Mercy Medical Center North Iowa and North Iowa Eye Clinic

Mason City, IA USA

 

Abstract

Carotid cavernous fistulas are rare complications of craniofacial trauma, resulting in abnormal connections between the arterial and venous systems of the cranium. The diagnosis of carotid cavernous fistulas and other injuries as a result of trauma can be confounded by the traumatized patient’s inability to communicate their symptoms to their physician. The following case study demonstrates the importance of a thorough physical exam in caring for such patients and serves to remind physicians to have a low threshold for consultation when managing numerous injuries following trauma.

Introduction

Carotid cavernous fistulas (CCFs) are aberrant connections between the carotid arterial system and the cavernous sinus, which form as complications of craniofacial trauma, or are congenital or spontaneous in nature (1). They occur in up to 3.8% of patients with basilar skull fractures and are more common with middle fossa fracture (2). Prompt diagnosis and treatment of CCF is necessary as approximately 20 – 30% of carotid cavernous fistulas lead to vision loss if not addressed appropriately (3)/\The following is a case study of a patient who presented with multiple traumatic injuries including CCF with subsequent discussion of the typical presentation, diagnosis, and treatment of direct CCF.  

Case Presentation

A 64-year-old woman with a therapeutic INR on Coumadin for atrial fibrillation sustained a fall down a flight of stairs. She was found unresponsive the next day by her relatives and was subsequently brought to the emergency department for evaluation. A maxillofacial CT showed a nondisplaced right maxillary wall fracture and nondisplaced zygomatic arch fracture, as well as a subtle inferotemporal orbital fracture, none of which was determined to require immediate treatment by the otolaryngology service. Further imaging included a CT of the head which revealed a large subdural hematoma, a superotemporal hematoma, and subfalcine herniation. She was taken to the OR for emergent craniotomy and evacuation of the hematoma before transfer to the critical care unit. In the CCU, she remained intubated and sedated but her condition improved until extubation on hospital day 3. She continued to have swelling surrounding both eyes during this time, but physical exam showed pupils which were equal, round, and reactive to light.

On day 6 of her stay, the patient was noted to have waxing and waning confusion and slightly increased oxygen requirement. Thus, she was re-intubated and sedated for “agitation” and “hypoxic respiratory failure.” Physical exam on the next day was notable for pupillary anisocoria with the right pupil at 1 mm diameter and left at 2.5 mm. There was a poor pupillary light reaction bilaterally. Neurology was consulted and recommended repeat imaging and EEG. Repeat CT and MRI of the brain showed no evidence of herniation, and EEG was negative for seizure-like activity. The anisocoria was thought to be from mass effect of the temporal lobe on cranial nerve III. The patient’s condition continued to deteriorate; physical exam elicited grimace to painful stimuli and the patient was able to open her eyes but did not track movement or follow commands. She was subsequently noted to have a left orbit that became harder to compress with ballottement test compared to the right, so Ophthalmology was consulted.

An ophthalmologic exam showed extensive chemosis of the left eye compared to the right with conjunctival hemorrhage in bilateral eyes (Figure 1).

Figure 1. Ophthalmologic exam revealed chemosis, exophthalmos, and a mid-dilated, fixed pupil of left eye compared to right.

Ocular tonometry revealed a pressure of 14 mmHg in the right eye and 53 mmHg in the left. There was a mid-dilated, fixed pupil on the left. The differential at this point included traumatic acute angle closure glaucoma versus a retroorbital process. The patient was started on timolol, pilocarpine, and dorzolamide eye drops for intraocular pressure control. An orbital CT was obtained, which showed an engorged superior ophthalmic vein on the left with a new 4 mm proptosis of the left eye (Figure 2) when compared to previous imaging.

Figure 2. A: CT scan showed proptosis of 4 mm of left eye compared to right eye. B: Enlarged left ophthalmic vein also noted on CT scan (arrow).

This raised concern for traumatic carotid cavernous fistula. A CTA obtained the following morning confirmed this suspicion (Figure 3).

Figure 3. A: Reconstructed coronal CT coronal angiogram showing enlarged left cavernous sinus, confirming diagnosis of carotid cavernous fistula. B-E: Static coronal images from CT angiogram with major arteries labeled. F: Video of CT angiogram.

The patient was transferred to an outside facility for surgical management, which consisted of angiography and embolization via coiling of her CCF.

Discussion

Carotid cavernous fistulas are abnormal connections that form between the cavernous sinus and the internal or external carotid arteries, or branches of the internal or external carotid arteries. They are divided into direct and indirect variants per Barrow classification (Table 1, Figure 4).

ICA = Internal carotid artery ECA = External carotid artery

Figure 4. A: The normal eye: superior ophthalmic vein draining into cavernous sinus and internal and external carotid arteries traversing the cavernous sinus. B: Barrow Classifications for types of carotid cavernous fistulas: Type A: direct connection between internal carotid artery and cavernous sinus. Type B: connection between dural branches of internal carotid artery and cavernous sinus. Type C: connection between dural branches of external carotid artery and cavernous sinus. Type D: connection between dural branches of both internal carotid artery and external carotid artery and the cavernous sinus.

Types B through D are commonly termed ‘indirect’ or ‘dural’ fistulas. These can develop spontaneously as a result of hypertension and are the more common presentation of CCF. More specifically, type B is a connection between the dural branches of the ICA and the cavernous sinus, type C is a connection between the dural branches of the external carotid artery (ECA) and the cavernous sinus, and type D connects the dural supply of both the ICA and ECA and the cavernous sinus (1). Type A, or a ‘direct’ CCF, is a connection between the intracavernous internal carotid artery (ICA) and the cavernous sinus. Direct CCF is a rare ocular complication that forms most commonly as a result of craniofacial trauma, but can also be due to aneurysmal rupture or spontaneous development. This is also the most dramatic presentation of CCF and was the case in our patient.

Prompt identification and management of CCF is necessary to prevent associated morbidity and mortality. The presentation of CCF depends mainly on the drainage of the fistula. Anterior-drainage of fistulas through the superior ophthalmic vein produces symptoms of exophthalmos, proptosis, acute chemosis or swelling/edema of conjunctiva, and headache, all of which are more common in direct CCFs. The backup of drainage can result in a secondary angle closure with extremely high intraocular pressure. Posterior-drainage of fistulas into the superior and inferior petrosal sinuses tend to lack the aforementioned features of orbital congestion, but can produce painful cranial neuropathy of the trigeminal, facial, or ocular motor nerves. Failure to identify and appropriately treat posterior-draining fistulas can lead to eventual reversal of flow and development of anterior drainage (4).

The signs of CCF are not visible on neuroimaging at a patient’s presentation and generally develop over the first week a patient is admitted.  Clinical signs which may prompt further investigation and repeat imaging include chemosis, increasing exophthalmos, pain, and increased intraocular pressure. Often, the tools for checking intraocular pressure are not available in an ICU setting. In the absence of signs of a ruptured globe, an intensivist could palpate the orbit over a closed eye (as occurred in this case). If there is asymmetry in resistance to palpation, this should incite an ophthalmologic consult to consider a retro-orbital process.

Repeat neuroimaging is likely to be done in these cases, but it is important to order the right test. Radiologic signs of CCF include proptosis and asymmetric enlargement of a cavernous sinus or superior ophthalmic vein and would be noted on an orbital or maxillofacial CT. A head CT might miss these signs, so it is important to obtain imaging dedicated to examining the retro-orbital space. To confirm the diagnosis of CCF, one must then obtain a CT angiogram, which will show the aberrant connections between the intracranial vessels. Upon confirming a diagnosis of CCF, the preferred mode of management is endovascular obliteration using an arterial or venous approach as it has been shown to be safe and effective, and confers long-term cure in most cases (5).

A previous review of 16 cases of carotid cavernous fistulas treated with transarterial embolization with detachable balloon show satisfactory results, defined as resolution of CCF without residual disability, in 11 cases and resolution but with residual disability in 5 cases. The most common of the disabilities in these cases was vision impairment, as seen in 4 out of the 5 cases. In addition, 14 out of the 16 cases resolved with preserved internal carotid artery flow (1). As a result, transarterial embolization with detachable balloon (TAEDB) has been established as the preferred method of treatment for carotid cavernous fistulas (6). Other options for treatment include neurosurgery and stereotactic radiosurgery when endovascular approach is not feasible.

Our patient presented with several traumatic injuries following a fall down a flight of stairs and was unable to contribute to history-taking. Detection and treatment of the CCF that she later developed was complicated by several factors. The true exophthalmos of the affected eye was partially masked by the fact that she had an inferotemporal orbital fracture of the opposite eye, which was incorrectly thought to be enophthalmic. Additionally, her altered mental status and subsequent re-intubation limited her ability to vocalize the pain which would have been present in her affected eye due to tremendously increased intraocular pressure.

From a critical care physician perspective, part of the key to her diagnosis was her re-intubation. The patient developed severe agitation requiring sedation without other more typical reasons for intubation such as hypoxia, tachypnea, or dyssynchronous breathing. We suspect this agitation was likely secondary to pain from the rapidly increasing pressure in her affected eye which became symptomatic just prior to her worsening mental status. Her physical exam was ultimately crucial to the detection of her CCF, specifically chemosis, exophthalmos, and increased intraocular pressure in the affected eye. These signs led to the subsequent ophthalmologic consultation, imaging, and eventually the diagnosis of CCF.

An important lesson learned from this patient’s management is having a low threshold for consultation when the clinical picture does not match diagnostic workup. In our case, the patient’s clinical condition changed but repeat workup including EEG and MRI of the head was negative. Previous imaging had revealed right-sided facial fractures, yet her new findings, including increased resistance to palpation of the orbit and chemosis, were largely left-sided. In situations when the cause of a patient’s deteriorating condition is unclear and there is incongruity between the physical exam and diagnostic workup, it is imperative to obtain further consultation. In our case, the ophthalmic exam gave the clues for further workup and the ultimate diagnosis.

In conclusion, this patient’s case is a good study in the classic presentation of direct CCF in association with craniofacial trauma, and also illuminates the difficulty in detection of orbital injuries in a trauma patient who cannot vocalize the symptoms they are experiencing. The lesson learned from her presentation is to have a low threshold for ophthalmologic consultation for unexplained changes in ophthalmic condition and discrepancies between clinical presentation and diagnostic findings.

References 

  1. Barrow DL, Spector RH, Braun IF, Landman JA, Tindall SC, Tindall GT. Classification and treatment of spontaneous carotid-cavernous sinus fistulas. J Neurosurg. 1985 Feb;62(2):248-56. [CrossRef] [PubMed]
  2. Liang W, Xiaofeng Y, Weiguo L, Wusi Q, Gang S, Xuesheng Z. Traumatic carotid cavernous fistula accompanying basilar skull fracture: a study on the incidence of traumatic carotid cavernous fistula in the patients with basilar skull fracture and the prognostic analysis about traumatic carotid cavernous fistula. J Trauma. 2007 Nov;63(5):1014-20. [CrossRef] [PubMed]
  3. Doran M. Carotid-Cavernous Fistulas: Prompt Diagnosis Improves Treatment. American Academy of Ophthalmology. https://www.aao.org/eyenet/article/carotid-cavernous-fistulas-prompt-diagnosis-improv. Published March 18, 2016. Accessed July 11, 2017.
  4. Miller NR. Diagnosis and management of dural carotid-cavernous sinus fistula. Neurosurg Focus. 2007;23(5):E13. [PubMed]
  5. Gupta AK, Purkayastha S, Krishnamoorthy T, Bodhey NK, Kapilamoorthy TR, Kesavadas C, Thomas B. Endovascular treatment of direct carotid cavernous fistulae: a pictorial review. Neuroradiology. 2006 Nov;48(11):831-9. [CrossRef] [PubMed]
  6. Lewis AI, Tomsick TA, Tew JM Jr, Lawless MA. Long-term results in direct carotid-cavernous fistulas after treatment with detachable balloons. J Neurosurg. 1996 Mar;84(3):400-4. [CrossRef] [PubMed]

Cite as: Ganapathiraju I, Summerfield DT, Summerfield MM. Carotid cavernous fistula: a case study and review. Southwest J Pulm Crit Care. 2017:15(1):32-8. doi: https://doi.org/10.13175/swjpcc083-17 PDF 

Sunday
Jul022017

July 2017 Critical Care Case of the Month

Robert A. Raschke, MD

Banner University Medical Center Phoenix

Phoenix, AZ USA

 

Critical Care Case of the Month CME Information

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

0.25 AMA PRA Category 1 Credit(s)™

Estimated time to complete this activity: 0.25 hours 

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

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

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

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

CME Sponsor: University of Arizona College of Medicine

Current Approval Period: January 1, 2017-December 31, 2018

Financial Support Received: None

 

History of Present Illness

A 62-year-old man was brought to the Emergency Department with an altered mental status after a neighbor found him unresponsive. Medications the paramedics found in his home were cyclobenzaprine, duloxetine, gabapentin, levothyroxine, ibuprofen, and tramadol.

Past Medical History, Social History and Family History

He had a past medical history of neck and back pain and hypothyroidism. He lived alone. There was a history of a C3-4 anterior cervical discectomy in 2010. Other history including family history was unobtainable.

Physical Examination

  • Vital Signs: HR 61 beats/min, BP 86/50 mm Hg, RR 8 breaths/min, T 32.2º C
  • General: arousable but did not answer questions. He had multiple tattoos. No needle track marks are identified.
  • HEENT: pupils were small but reacted to light.
  • Lungs: clear to auscultation.
  • Heart: regular rhythm without murmur.
  • Abdomen: soft without organomegaly or masses.
  • Neurology: he moved all 4 extremities but minimally. Plantar reflexes were downgoing.

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

  1. Administer naloxone
  2. CT scan of the head
  3. Obtain a blood glucose
  4. 1 and 3
  5. All of the above

Cite as: Raschke RA. July 2017 critical care case of the month. Southwest J Pulm Crit Care. 2017;15(1):7-14. doi: https://doi.org/10.13175/swjpcc081-17 PDF

Tuesday
Jun132017

High-Sensitivity Troponin I and the Risk of Flow Limiting Coronary Artery Disease in Non-ST Elevation Acute Coronary Syndrome (NSTE-ACS)

Ali Abdul Jabbar, MD 1,3,4

Omar Mufti, MD1

Sayf Altabaqchali, MD RPVI4

Chowdhury Ahsan, MD PhD2

Mohanad Hasan, MD2

Ronald Markert, PhD1

Bryan White, MD1

George Broderick, MD1

 

1Cardiology Division, Department of Internal Medicine, Wright State University Boonshoft School of Medicine, Dayton, Ohio.

2Cardiology Division, Department of Internal Medicine, University of Nevada School of Medicine, Las Vegas, Nevada.

3Department of Cardiovascular Medicine, University of Toledo Health Science Campus, Toledo, Ohio.

4Department of Cardiology, Ochnser Heart and Vascular Institute, New Orleans, Louisiana.

 

Abstract

Background: In acute coronary syndrome, elevated troponins are associated with worse clinical outcomes. We examined the relationship between the level of troponin elevation and the presence of a flow-limiting lesion for patients with no history of coronary disease admitted with NSTE-ACS.

Methods: From January of 2010 until April of 2013, 561 patients received coronary angiography for new-onset NSTE-ACS. The Mann-Whitney Test, chi-square test, and Spearman correlation were used to examine relationships. Inferences were made at the 0.05 level of significance. The independent samples t test and the chi square test were used to identify predictors of LV systolic dysfunction- LVSD.

Results: The 430 patients with a flow-limiting coronary lesions had a higher troponin I level than the 131 patients without obstructive coronary disease (5.69 ng/ml vs. 2.85 ng/ml, p=0.002). Further, within troponin categories, those in the greater than 5.0 ng/ml group were more likely to have angiographically significant CAD than those in the less than 0.5 ng/ml group (p=0.012). Elevated troponins were also associated with increased thrombus burden, worse systolic function, higher complexity of the lesions, and worse post intervention TIMI flow. Cardiac troponin >5ng/ml [odds ratio=2.13 (95%CI=1.22 to 3.70) p=0.008] and DM [odds ratio=1.74 (95%CI=1.02 to 2.97) p=0.042] were independent predictors of LVSD. Advanced LM disease and age were marginally significant.

Conclusion: The degree of cardiac troponin I elevation should be incorporated into the risk stratification models of NSTE-ACS to promptly triage high-risk patients to early invasive strategies and tailored anticoagulant therapy to reduce troponin elevation and improve myocardial perfusion.

Background

Cardiac troponin is the main biomarker of myocardial ischemia. In acute coronary syndrome, elevated troponin levels are associated with complex obstructive coronary anatomy and impaired myocardial tissue perfusion. Elevated troponins can identify high-risk patients with non-ST elevation acute coronary syndrome (NSTE-ACS), who may benefit from early invasive management. However, the degree of troponin elevation has not been incorporated in risk stratification models for NSTE-ACS. To triage patients for conservative versus invasive management strategies, we need to define the significance of the magnitude of troponin elevation following NSTE-ACS (1).

NSTE-ACS is the most common form of acute coronary syndrome. Troponin elevation signifies a delayed presentation in ST elevation MI not so for NSTE-ACS. The determination of ischemic injury timing becomes more challenging when NSTE-ACS patient present with variable levels of troponin elevation.

Thus, we examined the relationship between troponin levels and the extent of coronary disease and myocardial dysfunction, as assessed by coronary angiography, in a subset of patients with no history of coronary disease admitted with NSTE-ACS.

Methods

Study design

This is a retrospective study of a cohort admitted to a university-affiliated teaching hospital with highly specialized cardiovascular care over a period of 40 months. The data for this study were obtained from the National Cardiovascular Data Registry (NCDR) database and electronic chart review of study participants.

Serum cardiac troponin levels were measured using a high-sensitivity enzyme-linked immune-absorbent assay kit (VITROS® Troponin I ES Assay, © Ortho Clinical Diagnostics, Johnson & Johnson -Hong Kong- Ltd. 2003-2014). A level greater than 0.033 ng/ml is considered above the reference range and represents a positive test value. The highest troponin I level prior to coronary angiography was used in the analyses.

Selection of study participants

The study investigated the association of cardiac troponin I levels and the presence of a flow-limiting coronary arterial lesion; a flow-limiting lesion was defined as an angiographically significant coronary lesion warranting percutaneous and/or surgical revascularization. The study only included patients with new-onset (de novo) NSTE-ACS. Patients with a history of coronary artery disease, heart failure, and cardiac bypass were excluded.

Study Objectives and Data Analysis

In addition to determining the association between cardiac troponin I levels and the presence of flow-limiting coronary artery disease, the study also examined the relationship between cardiac troponin I levels and various other factors, including vascular anatomy, lesion complexity, success of percutaneous intervention (based on the post-intervention Thrombolysis In Myocardial Infarction - TIMI - study grading system of the coronary blood flow), and incidence of Left Ventricular Systolic Dysfunction (LVSD), defined by an ejection fraction of less than 40% on left ventriculogram, in de-novo NSTE-ACS patients.

Means and standard deviations are reported for continuous variables, and counts and percents for categorical variables. The independent samples Mann-Whitney Test (two groups), Kruskal-Wallis Test (three groups), one-way analysis of variance (ANOVA) with Least Significance Difference post hoc test, chi square test, and Spearman correlation were used to examine relationships. Inferences were made at the 0.05 level of significance with no corrections for multiple comparisons. Multivariable logistic regression was used to determine if troponin is an independent risk factor for LVSD. Analyses were conducted using IBM SPSS Statistics 22.0 (IBM, Armonk, NY).

Results

Baseline characteristics

From January 2010 through April 2013, 561 patients received coronary angiography for new onset NSTE-ACS. Of this total, 485 (86.5%) had left ventricular functional assessment at the time of cardiac catheterization. All patients were managed invasively.

Patients were divided into three groups according to the degree of troponin I elevation (mild <0.5 ng/ml [n = 167], moderate 0.5-5 ng/ml [n = 263], and high >5 ng/ml [n = 131]).  Table 1 shows that age differed among the three groups (p = 0.008): the moderate group was older than the mild group (mean age = 66.3±13.9 vs. 62.2±12.5) but not the high groups (64.1±13.3).  

Table 1. Characteristics of troponin groups.

Abbreviations - GFR: glomerular filtration rate; PCI: percutaneous coronary artery intervention; IABP: intra-aortic balloon pump; UH: unfractionated heparin; LMWH: low molecular weight heparin

a The moderate group was older than the mild group (mean age = 66.3±13.9 vs. 62.2±12.5) but not the high group (64.1±13.3).

bPatients were more likely to be Caucasian as troponin categories increased (66.5% for the <0.5 ng/ml group, 78.2% for the 0.5-5 ng/ml group, 81.5% for the >5.0 ng/ml group) and less likely to be African American as troponin categories increased (32.3% for the <0.5 ng/ml group, 21.0% for the 0.5-5 ng/ml group, 17.7% for the >5.0 ng/ml group); p value for chi square test excludes Asians and Hispanics due to low counts.

cThe moderate and high groups had a higher euroscore than the mild group (mean euroscore = 5.44±3.3 and 5.98±6.1 vs. 4.38±2.8).

dPatients were more likely to receive unfractionated heparin as troponin categories increased (63.4% for the <0.5 ng/ml group, 69.7% for the 0.5-5 ng/ml group, 84.2% for the >5.0 ng/ml group).

Patients were more likely to be Caucasian as troponin categories increased (66.5% for the <0.5 ng/ml group, 78.2% for the 0.5-5 ng/ml group, 81.5% for the >5.0 ng/ml group) and less likely to be African American as troponin categories increased (32.3% for the <0.5 ng/ml group, 21.0% for the 0.5-5 ng/ml group, 17.7% for the >5.0 ng/ml group).

The moderate and high groups had a higher euro-score than the mild group (mean euro-score = 5.44±3.3 and 5.98±6.1 vs. 4.38±2.8 p = 0.003). Patients were more likely to have been treated with unfractionated heparin as troponin levels increased (63.4% for the <0.5 ng/ml group, 69.7% for the 0.5-5 ng/ml group, 84.2% for the >5.0 ng/ml group (p = 0.01).

Primary outcomes

Patients with flow-limiting coronary lesions (n = 430) had higher mean troponin I levels than patients without obstructive coronary disease (n = 131) [5.69±12.57 ng/ml vs. 2.85±5.76 ng/ml, p = 0.002]. More importantly, the proportion of patients with angiographically significant CAD increased as troponin levels increased (70.7% for the <0.5 ng/ml group, 77.2% for the 0.5-5 ng/ml group, 83.2% for the >5.0 ng/ml group (p = 0.038) (Figure 1).

Figure 1. Troponin groups and the presence of flow-limiting CAD.

Secondary outcomes

Elevated troponin levels were associated with increased thrombus burden (8.34±15.44 ng/ml for patients with intracoronary thrombus vs 5.29±13.11 ng/dl for those without thrombotic lesions, p = 0.001), worse systolic function (6.62+9.77 ng/dl for those with LVEF <40% compared to 4.42+8.70 ng/dl for those with preserved LV function, p=0.003), higher complexity of the lesions (patients with high - type C – lesions, per AHA/ACC classification, had mean troponin level of 8.38±17.71 ng/ml vs 3.44±7.7 ng/ml for those with non-high - type C - lesions, p < 0.001), and worse TIMI flow (patients with TIMI grade 0 flow post-intervention had mean troponin of 49.1±71.99 ng/ml vs 5.16±10.41 ng/ml for those with TIMI grade 3 flow, p = 0.017) post intervention.

Patients with LVSD were more likely to be older, have diabetes (DM), have more advanced left main coronary disease, and have cardiac troponin levels greater than 5 ng/ml. When the statistically significant predictors for LVSD (p<0.05) from the univariate analysis were entered into a multivariable logistic regression model of analysis, cardiac troponin levels > 5ng/ml [odds ratio = 2.13 (95%CI = 1.22 to 3.70) p = .008] and DM [odds ratio = 1.74 (95%CI = 1.02 to 2.97) p = .042] were found to be independent predictors for LVSD (Table 2). Age and left main coronary disease almost reached statistical significance.

Table 2. Independent predictors of LVSD.

Discussion

The classic definition of myocardial infarction (MI) by the World Health Organization (WHO) is based on symptoms, electrocardiographic abnormalities, and elevated cardiac enzymes. However, over the past decade the Global MI Task Force has integrated new elements to the definition of MI based on the mechanisms of myocardial injury. Obstructive coronary lesion is the most clinically relevant form of injury and results in troponin release (2,3).

Routine detection of troponin levels using high sensitivity assays that yield a continuous gradient in apparently normal subjects makes it difficult to differentiate myocardial necrosis related to plaque rupture in ACS patients from necrosis in non-ACS patients. Newby et al. discussed the impact of improved test sensitivity on the interpretation of cardiac troponin and emphasized the value of pretest probability when interpreting troponin elevation (3).

The major findings of the present study were: 1) obstructive coronary lesions (flow-limiting) related myocardial injury resulted in greater troponin elevation when compared to other etiologies of myocardial injury, 2) in the context of a flow-limiting coronary artery disease, the degree of troponin elevation implies high-risk features for invasively managed NSTE-ACS patients related to their vascular anatomy, lesion complexity, and the eventual success of percutaneous intervention, and 3) regardless of the mechanism of troponin release, a high level of troponin I was an independent predictor of LVSD in de novo NSTE-ACS patient population.

Troponin I and the presence of hemodynamically significant (flow-limiting) coronary artery disease

Troponin I is independently associated with in-hospital mortality in NSTE-ACS patients. Antman et al. reported that short-term mortality increases with rising levels of cardiac troponin I, and the highest increment in mortality was observed when levels are > 5 ng/ml (4). Additionally, Kleiman et al. (5) demonstrated that invasive management could improve mortality risk in a NSTE-ACS subset of patients with positive cardiac biomarkers.

Interestingly, analyses from the ACTION Registry (NCDR published data) indicate that single vessel flow-limiting coronary artery disease was the most common finding identified by cardiac angiography, and that percutaneous coronary artery intervention was the most common mode of treatment in invasively managed NSTE-ACS patients (6,7). We previously reported that the likelihood of hemodynamically significant coronary artery disease in invasively managed NSTE-ACS patients when the troponin level is more than 5 ng/ml was significantly higher than that in individuals with a lower troponin level (8).

Concern about elevated troponin was reflected in the guidelines that recommend incorporating risk stratification models (TIMI risk score, Grace risk score, or PURSUIT risk model) to the management strategy for NSTE-ACS patients (9). However, none of these models has integrated the additive value of the degree of troponin elevation in their risk-score calculation (10-12).

Being closely associated with mortality and the presence of flow-limiting coronary artery disease, the degree of cardiac troponin elevation should be scored properly in risk stratification modules and contemplated in the timing for invasive management of those presenting with NSTE-ACS.

Troponin I and percutaneous coronary artery interventions in NSTE-ACS

In the setting of ACS, elevated troponin is associated with impaired myocardial tissue perfusion and lower rate of coronary recanalization after percutaneous coronary intervention (13-18). Troponin elevation also signifies adverse short and long-term prognosis in this patient population (19-22). Similarly, in our study, we observed that elevated troponin was associated with increased thrombus burden, worse systolic function, higher complexity of the lesions, and worse post intervention TIMI flow.

Subgroup analysis of ACS clinical trials showed that elevated troponin identified a subset of NSTE-ACS patients who would derive benefit from the addition of antithrombotic therapy and intravenous anti-platelet therapy to a conventional regimen. This is gained via reduction of thrombus formation at the culprit lesion and facilitation of distal micro-thrombi resolution (23-26).

The current guidelines identify the value of elevated troponin when choosing anti-thrombotic therapy, with or without invasive strategy. However, there is no consensus regarding a clinically relevant level of troponin that will provide the most benefit to invasively managed NSTE-ACS patients.

Predictors of left ventricular systolic dysfunction (LVSD) in NSTE-ACS:

Ischemic cardiomyopathy is the main etiology for LVSD in the United States and North America. The development of LVSD following ACS significantly worsens short- and long-term prognosis (17,27,28).  

We targeted patients with no prior history of coronary artery disease, heart failure or cardiac surgery who were referred for coronary angiograms for a new diagnosis of NSTE-ACS to assess the predictors of LVSD. Cardiac troponin I levels >5 ng/ml were the most important predictor of LVSD following a new onset NSTE-ACS in patients with no prior history of coronary artery disease (Table 2).

The previous ACC/AHA (2012-2013) guidelines recommended early invasive strategy in NSTE-ACS patients with a systolic ejection fraction of less than 40% (9). The timing of this recommendation was revised in the most recent guidelines (29).

Using clinical characteristics and risk factors at admission to identify risk of heart failure influences therapeutic decisions and permits an individualized approach to each patient. LVSD is a major concern among invasively managed ACS patients and imposes a large economic burden on the health care system. Troponin level could be used as a cost-effective tool to stratify patients who are at risk of LVSD, allowing appropriate early measures to improve their outcome.

Troponin I and Early versus Delayed Intervention in NSTE-ACS

The optimal timing of angiography has not been conclusively established in NTE-ACS (29). In earlier randomized trials, better outcomes were obtained with an early invasive strategy in patient with troponin I elevation when compared to those with normal troponin levels (30). In other reports, investigators found that early invasive intervention was not superior to a delayed invasive approach in NSTE-ACS patients for the prevention of death or myocardial infarction, even in those with positive cardiac biomarkers (31, 32).

The most notable beneficial effect of an invasive versus a conservative strategy in the management of NSTE-ACS patients was demonstrated in the reduction of recurrent MI, although the effect on mortality was seen in high-risk patients only (29,33).  Prospective trials to determine a clinically relevant troponin level that will determine the timing of an invasive strategy and its impact on patients’ outcomes are yet to be conducted (1).

Study Limitations

Our cohort study is subject to the standard bias associated with retrospective observations including selection bias, incomplete records, and loss of patients’ long-term follow-up.

The results of our study were derived from a single-center using a particular assay kit for serum troponin testing; thus, generalizability is a concern. Follow-up of cardiac events, recurrent hospitalizations, and long-term adverse events was beyond the scope of our study.

Conclusion

The degree of cardiac troponin I elevation should be incorporated into the risk stratification models of NSTE-ACS to promptly triage high-risk patients to early invasive strategies and tailored anticoagulant therapy to reduce troponin elevation and improve myocardial perfusion.

Acknowledgement

The authors of the study would like to thank Melissa Hodges (Cardiac Clinical Nurse Specialist) for her help with data abstraction.

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Cite as: Abdul Jabbar A, Mufti O, Altabaqchali S, Ahsan C, Hasan M, Markert R, White B, Broderick G. High-sensitivity troponin i and the risk of flow limiting coronary artery disease in non-ST elevation acute coronary syndrome (NSTE-ACS). Southwest J Pulm Crit Care. 2017;14(6):296-307. doi: https://doi.org/10.13175/swjpcc059-17 PDF