Left Ventricular Assist Devices: A Brief Overview

Bhargavi Gali MD

Department of Anesthesiology and Perioperative Medicine

Division of Critical Care Medicine

Mayo Clinic Minnesota

Rochester, MN, USA

Introduction

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

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

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

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

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

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

There are four main parameters of pump function:

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

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

Complications

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

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

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

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

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

Procedural Management

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

Emergent Complications

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

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

Conclusion

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

References

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

Cite as: Gali B. Left ventricular assist devices: a brief overview. Southwest J Pulm Crit Care. 2019;19(2):68-72. doi: https://doi.org/10.13175/swjpcc039-19 PDF 

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 

Tracheal Stoma Necrosis: A Case Report

Stella Pak, MD

Arjan Flora, MD 

Young-Sook Yoon, MD

Department of Medicine

University of Toledo Medical Center

Toledo, OH, USA

Abstract

Acute tracheal dilatation, due to an overinflated cuff, has been reported early in the course of mechanical ventilation through an endotracheal tube. Tracheal stoma necrosis is a rare complication, but such can accompany acute tracheal dilation. Herein, we report a case of tracheal necrosis 9 days following tracheostomy placement in a 71-year old woman associated with overinflation of the tracheal tube cuff. This case report aims to 1) add to the scant body of knowledge about the diagnosis and management for the patients with tracheal stoma necrosis and 2) raise awareness for error-traps in interpreting diagnostic images, specifically satisfaction of search error, inattentional blindness error, and alliterative error.

Case Report

A 71-year-old woman with a history of chronic respiratory failure on mechanical ventilation presented to the emergency department for bleeding around the tracheostomy site. The tracheostomy was recently inserted 9 days prior to admission. A chest radiograph demonstrated left lower lobe atelectasis, pleural effusion, and cardiomegaly that was consistent with pre-existing congestive heart failure (Figure 1).

Figure 1. Chest radiograph (AP) performed during first admission.

The cuff overinflation was demonstrated as a spherical shaped hypolucent region surrounding the trachea. However, the lesion escaped attention possibly because the focus of attention was limited to the thoracic compartment. A CT of the soft tissue in the neck ruled out the possibility of hematoma or infection. However, the features suggestive of overinflation of tracheostomy tube once again escaped attention. The spherical shaped hypolucent area, representing the cuff, was 3.9 cm in the anterior-posterior axis and 3.8 cm along the right-left axis.

A fiberoptic bronchoscopy through the tracheostomy tube revealed a large blood clot obstructing the distal end of the tube. A necrotic lesion around the stoma was also found. Careful observation via the bronchoscope during the procedure revealed no tearing or rupture. The patient was conservatively treated with vancomycin and cefepime for treatment of a ventilator-associated pneumonia. The oozing of blood from the tracheostomy stopped on with conservative wound care, including cleaning and dressing. She returned back to her baseline and was subsequently discharged on 3^rd day of admission. During this first admission, a tracheostomy tube exchange was not done due to bleeding from the stoma.

The patient was readmitted 12 days after discharge for an episode of hematemesis of approximately 400 mL of bright red blood. A chest radiograph showed satisfactory position of tracheotomy tube and cardiomegaly at baseline (Figure 2).

Figure 2.  Chest radiograph (AP) after readmission.

For the third time, the features suggestive of cuff-overinflation went unnoticed, delaying accurate diagnosis and proper treatment.

As a part of the patient’s evaluation, a CT of the chest with intravenous contrast was done, revealing the overinflated cuff of the trachea tube into the soft tissue of the neck (Figure 3).

Figure 3. Thoracic CT scan showing the overinflated tracheostomy cuff in the (A) coronal, (B) sagittal, and (C) axial views.

The ovoid shaped hypolucent area, representing the cuff, was 5.3 cm in the anterior-posterior axis and 4.6 cm along the right-left axis.

The Shiley proximal tracheal tube was urgently replaced with a portex Bivona tracheal tube. The new tracheostomy tube is more extensible, soft, and longer in distal length. Postoperatively, the patient was kept ventilated in the ICU. Repeated chest CT showed the new tracheostomy tube in satisfactory position and normalization of trachea shape. She made an uneventful recovery and was discharged 8 days after the tracheotomy tube replacement.

Discussion

A case of nonfatal hemorrhage due to innominate artery erosion with soft tissue necrosis at the stoma site of a tracheostomy is presented. In this ventilator-dependent patient with a recent tracheotomy stoma creation, an overinflated cuff of a tracheotomy tube was the key culprit in the pathology. Tracheal tube cuff pressure should be monitored so that it does not exceed a reasonable estimate of capillary perfusion pressure. Cuffs with pressure over 25 mmHg can compress the surrounding soft tissue, including delicate vascular structures. The damage to the vasculature in contact with the tube can result in ischemic necrosis in the soft tissue. If left untreated, these necrotic regions can develop infection or undergo fibrosis, leading to progressive stenosis (1).

A number of cognitive errors led to multiple episodes of misdiagnosis in this patient. Satisfaction of search error is a type of false negative error caused by premature termination of search after an abnormality has been detected (2). In this patient, we readily detected several abnormalities—cardiomegaly, pulmonary atelectasis, and pleural effusion. These initial findings likely led us to subconsciously neglect later findings.

Inattentional blindness error is a false negative error caused by the psychological lack of attention on an unexpected stimulus (3). In the present case, none of the diagnostic imaging was taken to check for cuff-overinflation. The images from the first admission were ordered for a concern of NG tube malposition, infection, and hematoma. The images ordered during the second admission were ordered to check the tracheotomy tube position. The thoracic compartment (the area for the expected abnormalities) received a disproportionately large amount of attention, whereas only a scant amount of attention was paid to the neck compartment.

Alliterative error is an error caused by a preconceived notion from a previous interpretation by a colleague or oneself (4). The negative finding in the previous reports could have affected the subsequent interpretative performance.

To the best of our knowledge, there are only 3 other cases of soft tissue necrosis caused by cuff overinflation. In two of these cases, the extended trachea did not recoil back to the previous size (5, 6). In the presented case, the stretched trachea recoiled back, similar to the case described by Sachdeva and his colleagues (7). The prognostic value of this difference in recovery is unknown, but might have a significant clinical implication. To explore the clinical relevance of this finding, more data on this condition is needed.

Teaching Points

1. Careful attention should be paid to cuff inflation pressure in patients presenting with bleeding at the tracheostomy site.
2. Conscious efforts to avoid well-known errors in diagnostic image interpretation, such as satisfaction of search error, and inattentional blindness error, should be made to improve diagnostic accuracy.

References

1. De Leyn P, Bedert L, Delcroix M, et al. Tracheotomy: clinical review and guidelines. Eur J Cardiothorac Surg. 2007 Sep;32(3):412-21. [CrossRef] [PubMed]
2. Ashman CJ, Yu JS, Wolfman D. Satisfaction of search in osteoradiology. AJR Am J Roentgenol. 2000 Aug;175(2):541-4. [CrossRef] [PubMed]
3. Richards A, Hannon EM, Derakshan N. Predicting and manipulating the incidence of inattentional blindness. Psychol Res. 2010 Nov;74(6):513-23. [CrossRef] [PubMed]
4. Berlin L. Malpractice issues in radiology. Alliterative errors. AJR Am J Roentgenol. 2000 Apr;174(4):925-31. [CrossRef] [PubMed]
5. Rhodes A, Lamb FJ, Grounds RM, Bennett ED. Tracheal dilatation complicating tracheal intubation. Anaesthesia. 1997 Jan;52(1):70-2. [CrossRef] [PubMed]
6. Honig EG, Francis PB. Persistent tracheal dilatation: onset after brief mechanical ventilation with a "soft-cuff" endotracheal tube. South Med J. 1979 Apr;72(4):487-90. [CrossRef] [PubMed]
7. Sachdeva A, Pickering EM, Reed RM, Shanholtz CB. Ice cream cone sign: reversible ballooning of the trachea due to tracheostomy tube cuff overinflation. BMJ Case Rep. 2016 May 4;2016. [CrossRef] [PubMed]

Cite as: Pak S, Flora A, Yoon Y-S. Tracheal stoma necrosis: a case report. Southwest J Pulm Crit Care. 2017;14(4):172-6. doi: https://doi.org/10.13175/swjpcc032-17 PDF 

June 2016 Critical Care Case of the Month

Theodore Loftsgard APRN, ACNP

Julia Terk PA-C

Lauren Trapp PA-C

Bhargavi Gali MD

Department of Anesthesiology

Mayo Clinic Minnesota

Rochester, MN USA

Critical Care Case of the Month CME Information

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

0.25 AMA PRA Category 1 Credit(s)™

Estimated time to complete this activity: 0.25 hours 

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

Learning Objectives:
As a result of this activity I will be better able to:

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

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

CME Sponsor: University of Arizona College of Medicine

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

Financial Support Received: None

History of Present Illness

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

PMH, SH, and FH

He had the following past medical problems noted:

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

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

Physical Examination

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

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

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

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