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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)

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

 

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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Friday
Jul202018

Ultrasound for Critical Care Physicians: Caught in the Act

Uzoamaka Ogbonnah MD1

Isaac Tawil MD2

Trenton C. Wray MD2

Michel Boivin MD1

 

1Department of Internal Medicine

2Department of Emergency Medicine

University of New Mexico School of Medicine

Albuquerque, NM USA

 

A 16-year-old man was brought to the Emergency Department via ambulance after a fall from significant height. On arrival to the trauma bay, the patient was found to be comatose and hypotensive with a blood pressure of 72/41 mm/Hg. He was immediately intubated, started on norepinephrine drip with intermittent dosing of phenylephrine, and transfused with 3 units of packed red blood cells. He was subsequently found to have extensive fractures involving the skull and vertebrae at cervical and thoracic levels, multi-compartmental intracranial hemorrhages and dissection of the right cervical internal carotid and vertebral arteries. He was transferred to the intensive care unit for further management of hypoxic respiratory failure, neurogenic shock and severe traumatic brain injury. Following admission, the patient continued to deteriorate and was ultimately declared brain dead 3 days later. The patient’s family opted to make him an organ donor

On ICU day 4, one day after declaration of brain death, while awaiting organ procurement, the patient suddenly developed sudden onset of hypoxemia and hypotension while being ventilated. The patient had a previous trans-esophageal echo (TEE) the day prior (Video 1). A repeat bedside TEE was performed revealing the following image (Video 2).

Video 1. Mid-esophageal four chamber view of the right and left ventricle PRIOR to onset of hypoxemia.

 

Video 2. Mid-esophageal four chamber view of the right and left ventricle AFTER deterioration.

What is the cause of the patient’s sudden respiratory deterioration? (Click on the correct answer to be directed to an explanation)

  1. Atrial Myxoma
  2. Fat emboli syndrome
  3. Thrombus in-transit and pulmonary emboli
  4. Tricuspid valve endocarditis

Cite as: Ogbonnah U, Tawil I, Wray TC, Boivin M. Ultrasound for critical care physicians: Caught in the act. Southwest J Pulm Crit Care. 2018;17(1):36-8. doi: https://doi.org/10.13175/swjpcc091-18 PDF 

Monday
Jul022018

July 2018 Critical Care Case of the Month

Stephanie Fountain, MD

Banner University Medical Center Phoenix

Phoenix, AZ USA

 

Critical Care Case of the Month CME Information

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

0.25 AMA PRA Category 1 Credit(s)™

Estimated time to complete this activity: 0.25 hours 

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

Learning Objectives: As a result of 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 45-year-old man was brought to the Emergency Room by his mother complaining of weakness, dizziness, and trouble swallowing. He was also incontinent of stool and looked “sunburned”.

Past Medical History

He has a past medical history of:

  • Schizophrenia
  • Depression
  • Polysubstance abuse
  • Crohn’s disease
  • Type 2 diabetes
  • Hyperlipidemia

Medications

  • Prazosin
  • Venlafaxine
  • Risperidone
  • Buspirone
  • Oxcarbazepine
  • Gabapentin
  • Hydroxyzine
  • Lithium
  • KCL
  • Metformin
  • Atorvastatin
  • Adalimumab
  • Mesalamine
  • Prednisone
  • Ferrous sulfate

Physical Examination

  • Vitals: 80 kg / 97.3 degrees / 101 bpm / 100% 28RR  / BP 111/72 
  • The patient was toxic appearing and flushed.
  • Oriented to self only, very lethargic
  • Dry mucous membranes
  • Lungs clear to auscultation and percussion
  • Heart tachycardic but no murmurs
  • Abdomen without organomegaly, masses or tenderness
  • Extremities without edema

Which of the following should be done at this time? (Click on the correct answer to be directed to the second of six pages)

  1. Electrolytes
  2. Lumbar puncture
  3. Urine drug screen
  4. 1 and 3
  5. All of the above

Cite as: Fountain S. July 2018 critical care case of the month. Southwest J Pulm Crit Care. 2018;17(1):7-14. doi: https://doi.org/10.13175/swjpcc085-18 PDF

Saturday
Jun022018

June 2018 Critical Care Case of the Month

Stephanie Fountain, MD

Banner University Medical Center Phoenix

Phoenix, AZ USA

 

History of Present Illness

A 60-year-old native American man presented to an outside hospital with several days of nausea, vomiting and diarrhea. The patient felt weak and called emergency medical services and was taken to the emergency department.

Past Medical History

He has a history of end stage renal disease secondary to diabetes mellitus and hypertension. He received a cadaveric renal transplant in 2008 which was complicated with acute on chronic rejection and symptomatic hyponatremia.

Physical Examination

His pulse was recorded as 28 beats/min and his blood pressure was 90/60.

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

  1. Administer atropine
  2. Begin transcutaneous pacing
  3. Obtain a drug history
  4. 1 and 3
  5. All of the above 

Cite as: Fountain S. June 2018 critical care case of the month. Southwest J Pulm Crit Care. 2018;16(6):304-10. doi: http://doi.org/10.13175/swjpcc065-18 PDF 

Thursday
May312018

Fatal Consequences of Synergistic Anticoagulation

Payal Sen, MD1

Uddalak Majumdar, MD2

Patrick Rendon, MD1

Ali Imran Saeed, MD1

Akshay Sood, MD1

Michel Boivin, MD1

 

1University of New Mexico

Albuquerque, NM US

2Cleveland Clinic Foundation

Cleveland, OH USA

 

Abstract

Objective: Novel oral anticoagulants (NOACs) are increasingly being preferred by clinicians (and patients) because they have a wide therapeutic window and therefore do not require monitoring of anticoagulant effect. Herein, we describe the unfortunate case of a patient who had fatal consequences as a result of switching from warfarin to rivaroxaban.

Case Summary: A 90-year-old Caucasian woman, with atrial fibrillation on chronic anticoagulation with warfarin, was admitted to the hospital for pneumonia. She was treated with levofloxacin. In the same admission, her warfarin was switched to rivaroxaban. On Day 3 after the switch, her INR was found to be 6, and she developed a cervical epidural hematoma from C2 to C7. She ultimately developed respiratory arrest, was put on comfort care and died.

Discussion: Rivaroxaban and warfarin are known to have a synergistic anticoagulant effect, usually seen shortly after switching. Antibiotics also increase the effects of warfarin by the inhibition of metabolizing isoenzymes. It is hypothesized that these two effects led to the fatal cervical spinal hematoma. 

Conclusion: The convenience of a wide therapeutic window and no requirement of laboratory monitoring makes the NOACs a desirable option for anticoagulation. However, there is lack of data and recommendations on how to transition patients from Warfarin to NOACs or even how to transition from one NOAC to another. Care should be taken to ensure continuous monitoring of anticoagulation when stopping, interrupting or switching between NOACS to avoid the possibility of fatal bleeding and strokes.

Introduction

Novel oral anticoagulants (NOACs) are increasingly being preferred by clinicians (and patients) because they have a wide therapeutic window and therefore do not require monitoring of anticoagulant effect. They have also shown greater efficacy and safety when compared to warfarin (1). The choice among the novel oral anticoagulants depends on their different pharmacokinetic profile, patients' stroke and bleeding risk, comorbidities, drug tolerability and costs and, finally, patients' preferences (2). There is however, paucity of evidence regarding the process of switching from warfarin to a NOAC, from one NOAC to the other, and the consequent ‘synergism’ (3). Herein, we describe the unfortunate case of a patient who had fatal consequences as a result of switching from warfarin to rivaroxaban. We also wish to highlight the adverse effects that antibiotic interaction can have with both warfarin and the NOACS (4).

Case Report

A 90-year-old Caucasian woman, who resided in a nursing home was admitted to the hospital with chief complaints of fever and confusion for 2 days. She also had intermittent cough, but denied headache, blurry vision, dysuria, diarrhea and constipation. Past medical history was significant for non-valvular atrial fibrillation, for which she was on therapeutic anticoagulation with warfarin. Family history and social history were not significant. Vitals revealed a temperature of 100 F and physical exam was positive for crackles in the right lower lobe of the lung. Her white count was elevated at 16 x 103/µL, and hepatic and renal function were both normal. Chest x-ray revealed a right sided lower lobe pneumonia. She was admitted to the hospital for acute metabolic encephalopathy due to sepsis secondary to hospital associated pneumonia and was initially given a dose of vancomycin and piperacillin tazobactam, which was later narrowed to levofloxacin. 

Hospital Course

On day 2, the patient’s disorientation had improved marginally and her white count had also reduced to 11. Her INR was therapeutic on warfarin and she underwent transesophageal echocardiography and cardioversion for symptomatic atrial fibrillation with rapid ventricular rate. After a long discussion with the patient and her family, it was decided to switch from warfarin to rivaroxaban, to avoid the hassle of frequent INR monitoring. 

On Day 3, the patient suddenly developed tachypnea, hypotension and dysarthria after receiving the second dose of rivaroxaban. Rapid Response had to be called. Vitals revealed blood pressure of 92/52, respiratory rate 20, and heart rate of 84 with pulse oximetry showing 92% on 2 liters nasal cannula. 

Neurological Examination

Cognition was relatively normal. Patient was alert and oriented X 3.

Motor exam: The patient was quadriplegic.

Touch, pain, and pressure sensations were absent (0/4) below C3-C4.

Reflexes were diminished (¼) and she had absolutely no feeling of any noxious stimuli. Babinsky' s sign was negative.

Urgent Labs on Day 3 (current day)

Arterial blood gases: PaO2 of 62 on 3 liters oxygen via Nasal cannula, PaCO2 of 78.  

International Normalized Ratio (INR): 6, prothrombin time was 64.2 seconds.

Radiographic Imaging

Figure 1. Computed tomography scan of the neck revealed posterior cervical epidural hematoma (arrow) from C2 to C7 with cord compression.

 

Figure 2. Posterior epidural hematoma (arrow) extending from C2-3 through approximately C6-7, which caused significant spinal stenosis.

The patient was then rushed to the neurosurgical ICU. Neurosurgery was consulted and recommended reversing the anticoagulation and taking the patient for emergency surgical evacuation of the hematoma. However, on further discussion with the family, it was revealed that the patient’s earlier wishes had been to never be bedbound and paralyzed. Since she was a 90-year-old patient, chronically debilitated, with a do not resuscitate code status, the ultimate decision was to place her on comfort care. Patient passed away 24 hours later.

Discussion

Rivaroxaban and warfarin are known to have a synergistic anticoagulant effect, usually seen shortly after switching (5). Antibiotics also increase the effects of warfarin by the inhibition of metabolizing isoenzymes (4). It is hypothesized that these two effects led to the fatal cervical spinal hematoma. 

For decades, vitamin K antagonists like warfarin have been the agent of choice for oral anticoagulation in different clinical conditions. However, the disadvantages of warfarin are that it needs frequent INR monitoring, has a narrow therapeutic window and interacts with multiple food substances and drugs (6). Warfarin is also known to cause major bleeding. The NOACS (novel oral anticoagulants) such as the direct thrombin inhibitor dabigatran, and Factor Xa Inhibitors like rivaroxaban, edoxaban and apixaban have been developed almost fifty years after the approval of warfarin (7). These NOACS have more predictable pharmacodynamics and pharmacokinetics, fewer drug and dietary interactions and have the added advantage of not requiring frequent laboratory monitoring (7,8).  Clinicians are increasingly using these NOACS to replace Vitamin K antagonists for multiple indications like the prevention of thromboembolic complications in atrial fibrillation, treatment of Deep vein thrombosis (DVT) and pulmonary embolism (PE), and thromboprophylaxis during orthopedic surgery (9).

Rivaroxaban, which is an oxazolidinone derivative, inhibits both free Factor Xa and Factor Xa bound in the prothrombinase complex (10). It is a highly selective Factor Xa inhibitor and has high oral bioavailability, with rapid onset of action and a predictable pharmacokinetic profile across a wide spectrum of patients with respect to gender, age, weight and race (11).  There is paucity of data on how to safely switch from warfarin to rivaroxaban. Expert opinion is to switch 24 hours after INR < 3 (3). There is only one observational matched-cohort study of switching from warfarin to rivaroxaban and results supported present practices (3). It analyzed a French registry and fluindidione (not warfarin) was the Vitamin K Antagonist in about 90% of the study subjects. In another study of in silico effects, a post-switch synergistic anticoagulant effect has also been observed and a nomogram has been developed for switching to Rivaroxaban, based on INR for Caucasian and Japanese patients (5). INR is affected variably by rivaroxaban and cannot be used as a marker for its anticoagulant effect (12). Laboratory monitoring of anticoagulant effect of NOACs needs to be considered, since INR is unsuitable for this (13). 

Some of the manufacturers offer guidance relating to switching from warfarin to NOACs:

  • To apixaban: warfarin should be discontinued and apixaban started when the INR is <2.0.
  • To dabigatran: warfarin should be discontinued and dabigatran started when the INR is <2.0.
  • To rivaroxaban: warfarin should be discontinued and rivaroxaban started when the INR is <3.0.

With longer experience with these NOACs in Europe, the European Heart Rhythm Association does make slightly different recommendations than those in the United States (14). Again, looking at switching from a vitamin K antagonist to a NOAC, the group suggests:

  • The NOAC can be immediately initiated once the INR is <2.0.
  • If the INR is 2.0 to 2.5, the NOAC can be started immediately or (preferably) the next day.
  • If the INR is >2.5, use agent pharmacokinetics to estimate the time for the next INR.

As for moving from parenteral anticoagulation to a NOAC, the European recommendation is:

  • For unfractionated heparin (UFH), start the NOAC once the UHF is discontinued.
  • For low-molecular weight heparin (LMWH), start the NOAC when the next dose of LMWH would have been due.

Hence, switching vitamin K antagonists to newer direct oral anticoagulants (NOACs) is becoming routine now, since the latter are thought to have a reduced incidence of intracranial bleeding (15). This case teaches us that the synergistic effect and interactions with antibiotics should be kept in mind during switching and when possible, nomograms should be used. Further study is required regarding bridging doses, bridging periods and population-specific dosing. 

Conclusion

The convenience of a wide therapeutic window and no requirement of laboratory monitoring makes the NOACs a desirable option for anticoagulation. However, there is lack of data and recommendations on how to transition patients from a vitamin K antagonist to NOACs or even how to transition from one NOAC to another. Care should be taken to ensure continuous monitoring of anticoagulation when stopping, interrupting or switching between NOACS to avoid the possibility of fatal bleeding and strokes. Further trials are also needed to test for appropriate laboratory monitoring of the NOACs. Also, caution must be used whilst using antibiotics with the NOACs, since their interaction can often increase the efficacy of the NOACs and lead to fatal bleeding, like in our patient.

References

  1. Prisco D, Cenci C, Silvestri E, Ciucciarelli L, Di Minno G. Novel oral anticoagulants in atrial fibrillation: which novel oral anticoagulant for which patient? J Cardiovasc Med (Hagerstown). 2015 Jul;16(7):512-9. [CrossRef] [PubMed]
  2. Gallego P, Roldan V, Lip GY. Novel oral anticoagulants in cardiovascular disease. J Cardiovasc Pharmacol Ther. 2014 Jan;19(1):34-44. [CrossRef] [PubMed]
  3. Bouillon K, Bertrand M, Maura G, Blotiere PO, Ricordeau P, Zureik M. Risk of bleeding and arterial thromboembolism in patients with non-valvular atrial fibrillation either maintained on a vitamin K antagonist or switched to a non-vitamin K-antagonist oral anticoagulant: a retrospective, matched-cohort study. Lancet Haematol. 2015 Apr;2(4):e150-9. [CrossRef] [PubMed]
  4. Lane MA, Zeringue A, McDonald JR. Serious bleeding events due to warfarin and antibiotic coprescription in a cohort of veterans. Am J Med. 2014 Jul;127(7):657-663.e2. [CrossRef] [PubMed]
  5. Burghaus R, Coboeken K, Gaub T, Niederalt C, Sensse A, Siegmund HU, Weiss W, Mueck W, Tanigawa T, Lippert J. Computational investigation of potential dosing schedules for a switch of medication from warfarin to rivaroxaban-an oral, direct Factor Xa inhibitor. Front Physiol. 2014 Nov 7;5:417. [CrossRef] [PubMed]
  6. Ezekowitz MD, Aikens TH, Brown A, Ellis Z. The evolving field of stroke prevention in patients with atrial fibrillation. Stroke. 2010 Oct;41(10 Suppl):S17-20. [CrossRef] [PubMed]
  7. Mendell J, Zahir H, Matsushima N, Noveck R, Lee F, Chen S, Zhang G, Shi M. Drug-drug interaction studies of cardiovascular drugs involving P-glycoprotein, an efflux transporter, on the pharmacokinetics of edoxaban, an oral factor Xa inhibitor. Am J Cardiovasc Drugs. 2013 Oct;13(5):331-42. [CrossRef] [PubMed]
  8. Ogata K, Mendell-Harary J, Tachibana M, Masumoto H, Oguma T, Kojima M, Kunitada S. Clinical safety, tolerability, pharmacokinetics, and pharmacodynamics of the novel factor Xa inhibitor edoxaban in healthy volunteers. J Clin Pharmacol. 2010 Jul;50(7):743-53. [CrossRef] [PubMed]
  9. Bauer KA. Recent progress in anticoagulant therapy: oral direct inhibitors of thrombin and factor Xa. J Thromb Haemost. 2011 Jul;9 Suppl 1:12-9. [CrossRef] [PubMed]
  10. Roehrig S, Straub A, Pohlmann J, Lampe T, Pernerstorfer J, Schlemmer KH, Reinemer P, Perzborn E. Discovery of the novel antithrombotic agent 5-chloro-N-({(5S)-2-oxo-3- [4-(3-oxomorpholin-4-yl)phenyl]-1,3-oxazolidin-5yl}methyl)thiophene- 2-carboxamide (BAY 59-7939): an oral, direct factor Xa inhibitor. J Med Chem. 2005 Sep 22;48(19):5900-8. [CrossRef] [PubMed]
  11. Eriksson BI, Borris LC, Dahl OE, Haas S, Huisman MV, Kakkar AK, Muehlhofer E, Dierig C, Misselwitz F, Kälebo P; ODIXa-HIP Study Investigators. A once-daily, oral, direct Factor Xa inhibitor, rivaroxaban (BAY 59-7939), for thromboprophylaxis after total hip replacement. Circulation. 2006 Nov 28;114(22):2374-81. [CrossRef] [PubMed]
  12. Favaloro EJ, Lippi G. The new oral anticoagulants and the future of haemostasis laboratory testing. Biochem Med (Zagreb). 2012;22(3):329-41. [CrossRef] [PubMed]
  13. Lindahl TL, Baghaei F, Blixter IF, Gustafsson KM, Stigendal L, Sten-Linder M, Strandberg K, Hillarp A; Expert Group on Coagulation of the External Quality Assurance in Laboratory Medicine in Sweden. Effects of the oral, direct thrombin inhibitor dabigatran on five common coagulation assays. Thromb Haemost. 2011 Feb;105(2):371-8. [CrossRef] [PubMed]
  14. Heidbuchel H, Verhamme P, Alings M, Antz M, Hacke W, Oldgren J, Sinnaeve P, Camm AJ, Kirchhof P; European Heart Rhythm Association. European Heart Rhythm Association Practical Guide on the use of new oral anticoagulants in patients with non-valvular atrial fibrillation. Europace. 2013 May;15(5):625-51. [CrossRef] [PubMed]
  15. Caldeira D, Barra M, Pinto FJ, Ferreira JJ, Costa J. Intracranial hemorrhage risk with the new oral anticoagulants: a systematic review and meta-analysis. J Neurol. 2015 Mar;262(3):516-22. [CrossRef] [PubMed]

Cite as: Sen P, Majumdar U, Rendon P, Saeed AI, Sood A, Boivin M. Fatal consequences of synergistic anticoagulation. Southwest J Pulm Crit Care. 2018;16(5):289-95. doi: https://doi.org/10.13175/swjpcc058-18 PDF 

Wednesday
May022018

May 2018 Critical Care Case of the Month

Lacey Gagnon APRN, CNP
Theo Loftsgard APRN, CNP

Department of Anesthesiology and Critical Care

Mayo Clinic Minnesota

Rochester, MN USA

  

Chief Complaint

Shortness of breath

History of Present Illness

The patient is a 44-year-old woman who was admitted with a history of “pericarditis”. She has a several years history of progressive shortness of breath, abdominal distention and lower extremity edema.

Past Medical History, Social History and Family History

She has a history of obesity, poorly controlled type 2 diabetes, uterine fibroids and hypertension. She does not smoke but does have 1-2 alcoholic beverages per day. Family history is noncontributory.

Physical Examination

  • Vital signs: pulse 96 beats/min, blood pressure 110/85 mm Hg, temperature 37° C, respirations 18 breaths/min.
  • Neck: there is jugular venous distention with a positive hepatojugular reflux.
  • Lungs: rales at both bases.
  • Heart: regular rhythm without murmur.
  • Abdomen: Distended. Shifting dullness is present.
  • Extremities: 2-3 pretibial pitting edema.

Chest Radiography

Chest x-ray shows a small right pleural effusion with mild vascular congestion at the bases. Heart size is normal.

Which of the following should be performed?

  1. Abdominal CT scan
  2. Echocardiography
  3. Thoracic CT scan
  4. 1 and 3
  5. All of the above

Cite as: Gagnon L, Loftsgard T. May 2018 critical care case of the month. Southwest J Pulm Crit Care. 2018;16(5):245-51. doi: https://doi.org/10.13175/swjpcc048-18 PDF