HIT and heparin alternatives

Took care of a patient who came to OR for a redo-sternotomy and triple valve replacement on ECMO.

Scroll down to see how we managed the patient’s possible HIT.  The patient had a low score on her 4Ts assessment.  Therefore, we opted to move forward before the functional assay came back with results as the patient was in dire need of triple valve replacement.

 


HIT Basics

Heparin Induced Thrombocytopenia and Cardiac Surgery: A Comprehensive Review. J Blood Disord Transfus 2011, S2.

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From https://www.omicsonline.org/open-access/heparin-induced-thrombocytopenia-and-cardiac-surgery-a-comprehensive-review-2155-9864-S2-003.pdf

The goals of treatment for HIT are threefold: Interrupt the pathological immune response, inhibit the uncontrolled generation of thrombin, and minimize the complications.

Cessation of heparin alone does not sufficiently reduce the risk of thrombosis. The next step in management targets the uncontrolled generation of thrombin with the use of direct thrombin inhibitors (DTIs).  Argatroban is preferred in patients with renal insufficiency, whereas lepirudin is the drug of choice for patients with liver disease.  Bivalirudin is another hirudin analog that differs from lepirudin in that it is hemodialyzable and primarily undergoes enzymatic elimination. Its half-life is the shortest, 20-25 minutes, making bivalirudin the safest option since there are no reversal agents available.

All three agents can be monitored using the activated partial thromboplastin time (aPTT) to levels of 1.5 to 2.0 above baseline. Once the platelet count has increased to a minimum of 150,000/µL bridging therapy to warfarin is essential for the safe transition from DTIs.

Iloprost is a prostacyclin analogue that reversibly inhibits platelet aggregation.  Plasma exchange was successful in reducing anti-P4/heparin antibodies and allowed for the restoration of a normal platelet count, essentially reversing the disease.

A-suggested-approach-to-diagnosis-and-initial-management-of-patients-with-suspected-HIT
From https://www.researchgate.net/figure/A-suggested-approach-to-diagnosis-and-initial-management-of-patients-with-suspected-HIT_fig1_236255402

HIT/HITT and alternative anticoagulation: current concepts. BJA: British Journal of Anaesthesia, Volume 90, Issue 5, 1 May 2003, Pages 676–685.

Heparin-induced thrombocytopenia and cardiac surgery. Curr Opin Anaesthesiol, 2010; 23:74–79.

Perioperative care in cardiac anesthesia and surgery.  Chapter 19: HIT and heparin alternatives.  

Handbook of patient care in cardiac surgery. Chapter 2: Operative management.


Prostacyclins in Cardiac Surgery: Coming of Age.  Seminars in Cardiothoracic and Vascular Anesthesia 22(3):108925321774929 · December 2017.

Intraoperative infusion of epoprostenol sodium for patients with heparin-induced thrombocytopenia undergoing cardiac surgery. The Japanese Journal of Thoracic and Cardiovascular Surgery. Volume 54, Issue 8, pp 348–350.

Cardiac Surgery With Cardiopulmonary Bypass in Patients With Type II Heparin-Induced Thrombocytopenia. Ann Thorac Surg 2001;71:678–83.

HIT and urgent open heart surgery: a sticky situation. Grand Rounds, Hematology. UW 2015. 


Screen Shot 2018-12-19 at 8.45.41 PM
From https://www.omicsonline.org/open-access/percutaneous-coronary-intervention-in-patients-with-heparin-inducedthrombocytopenia-case-report-and-review-of-literature-2329-6607-1000202.php?aid=82752

Bivalirudin for Cardiopulmonary Bypass in the Setting of Heparin-Induced Thrombocytopenia and Combined Heart and Kidney Transplantation— Diagnostic and Therapeutic Challenges. Journal of Cardiothoracic and Vascular Anesthesia 31 (2017) 354–364.

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From https://www.jcvaonline.com/article/S1053-0770(16)30273-7/fulltext

Cardiac Bypass Surgery in the Setting of Heparin Induced Thrombocytopenia.  BIDMC guidelines.

Anticoagulation during Cardiopulmonary Bypass in Patients with Heparin-induced Thrombocytopenia Type II and Renal Impairment Using Heparin and the Platelet Glycoprotein IIb–IIIa Antagonist Tirofiban. Anesthesiology 2 2001, Vol.94, 245-251. 

Management of anticoagulation in patients with subacute heparin-induced thrombocytopenia scheduled for heart transplantation. BLOOD, 15 NOVEMBER 2008 VOLUME 112, NUMBER 10; 4024-4027.

Screen Shot 2018-12-19 at 8.56.04 PM
From http://www.bloodjournal.org/content/bloodjournal/112/10/4024.full.pdf?sso-checked=true

 

What we did:

  • Prior to giving heparin, we started alprostadil (PGE1) infusion at 1mcg/min and increased the doseage as tolerated to 5mcg/min.  We did offset the hypotension with levophed and vasopressin.
  • We gave our routine dose of heparin.
  • No heparin resistance noted.  Because this would be a long pump run, we opted to give an antifibrinolytic infusion as well as bolus.
  • This patient required higher than normal amounts of pressors and ultimately received methylene blue to help with vasoplegia.
  • We reversed the heparin with protamine and stopped the PGE1 at that time.
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ERAS for Cardiac Surgery

ERAS for cardiac surgery. #eras #pain #multimodal #opioids #surgery #cardiac #perfusion #perfusionist

I have been utilizing ERAS in general surgery, OB, and ortho cases.  Diving into one of my more tricky populations, I opted to see what ERAS practices are out there for cardiac surgery.  Careful what you look for my friends.  There’s actually a good amount of information out there!

ACCRAC podcast: ERAS for Cardiac Surgery

ERAS Cardiac Consensus Abstract – April 2018

Enhanced recovery after surgery pathway for patients undergoing cardiac surgery: a randomized clinical trial. European Journal of Cardio-Thoracic Surgery, Volume 54, Issue 3, 1 September 2018, Pages 491–497, https://doi.org/10.1093/ejcts/ezy100

** Audio PPT ** American Association for Thoracic Surgery: Enhanced Recovery After Cardiac Surgery. April 2018

The impact of enhanced recovery after surgery (ERAS) protocol compliance on morbidity from resection for primary lung cancer.  The Journal of Thoracic and Cardiovascular Surgery. April 2018Volume 155, Issue 4, Pages 1843–1852. 

Enhanced Recovery for Cardiac Surgery. J Cardiothorac Vasc Anesth. 2018 Jan 31. pii: S1053-0770(18)30049-1. DOI: https://doi.org/10.1053/j.jvca.2018.01.045

ERAS
From Journal of Anesthesiology

Enhanced Recovery After Cardiac Surgery Society

My blog posts:

Key Points

  • Level 1 (Class of recommendation=Strong Benefit):
    • Tranexamic acid or epsilon aminocaproic acid should be administered for on-pump cardiac surgical procedures to reduce blood loss.
    • Perioperative glycemic control is recommended (BS 70-180; [110-150]).
    • A care bundle of best practices should be performed to reduce surgical site infection.
    • Goal-directed therapy should be performed to reduce postoperative complications.
    • A multimodal, opioid-sparing, pain management plan is recommended postoperatively
    • Persistent hypothermia (T<35o C) after CPB should be avoided in the early postoperative period. Additionally, hyperthermia (T>38oC) should be avoided in the early postoperative period.
    • Active maintenance of chest tube patency is effective at preventing retained blood syndrome.
    • Post-operative systematic delirium screening is recommended at least once per nursing shift.
    • An ICU liberation bundle should be implemented including delirium screening, appropriate sedation and early mobilization.
    • Screening and treatment for excessive alcohol and cigarette smoking should be performed preoperatively when feasible.
  • Level IIa (Class of recommendation=Moderate Benefit)
    • Biomarkers can be beneficial in identifying patients at risk for acute kidney injury.
    • Rigid sternal fixation can be useful to reduce mediastinal wound complications.
    • Prehabilitation is beneficial for patients undergoing elective cardiac surgery with multiple comorbidities or significant deconditioning.
    • Insulin infusion is reasonable to be performed to treat hyperglycemia in all patients in the perioperative period.
    • Early extubation strategies after surgery are reasonable to be employed.
    • Patient engagement through online or application-based systems to promote education, compliance, and patient reported outcomes can be useful.
    • Chemical thromboprophylaxis can be beneficial following cardiac surgery.
    • Preoperative assessment of hemoglobin A1c and albumin is reasonable to be performed.
    • Correction of nutritional deficiency, when feasible, can be beneficial.
  • Level IIb (Class of recommendation=Weak Benefit)
    • A clear liquid diet may be considered to be continued up until 4 hours before general anesthesia.
    • Carbohydrate loading may be considered before surgery.

 

ERAS for cardiac surgery. Journal of Cardiothoracic and Vascular Anesthesia

IABP

There’s always a good reason to review the physiology and reasons for placement of an Intra Aortic Balloon Pump (IABP).  We come across these a couple of times a month in our cardiac patients.  They’re a great temporary measure to stabilizing and treating the patient.

Contemporary Clinical Niche for Intra-Aortic Balloon Counterpulsation in Perioperative Cardiovascular Practice: An Evidence-Based Review for the Cardiovascular Anesthesiologist. JCVA, February 2017. Volume 31, Issue 1, Pages 309–320.

gr5
From JCVA, Feb 2017.

One of the best explanations that I have ever seen for the IABP is from Dr. Rishi Kumar.  He’s a board certified anesthesiologist and is ICU fellowship trained and is pursuing a cardiac anesthesia fellowship as well.  This lovely human is no joke.  I’ve read his blog and his instagram posts, and he’s a wonderful teacher and mentor to those he reaches.  Please click his link for an entry regarding IABPs on his blog.

RKMD.com: Intra-Aortic Balloon Pump, Arterial Line, and EKG Waveforms. April 2018.

iabp-inflate-deflate-600x570

iabp-ekg-arterial-line-waveforms-aligned-600x559

 

TEE for placement of IABP

Anesthesia & Analgesia, July 2011. Vol 113, No. 1.

  • Want the tip 1-2 cm from left subclavian artery (LSCA)
  • X-plane aortic arch down to descending aorta to see the left subclavian artery
  • Visible during systole when the IABP balloon is deflated

Good visualization of the LSCA

A Novel Technique for Intra-aortic Balloon Positioning in the Intensive Care Unit.  J Extra Corpor Technol. 2012 Sep; 44(3): 160–162.

 

Mr. Chill

CPR training
Image via Wikipedia

Feb 17, 2011

Today was an ordinary day.  Come in for a minimally invasive aortic valve and call it a day.  However, that case was cancelled secondary to UTI.  So, I opted to get involved in a different case…. an epicardial lead placement.  This was a gentleman I’ll refer to as Mr. Chill.  He was getting an epicardial lead placement b/c he was in heart failure and was going to undergo CRT.  He already had RA/RV leads and AICD.  He was a rather obese gentleman (280lb, 5’6″).  He had a history of amphetamine induced cardiomyopathy with an EF of 18%, inferior wall infarct and ant-sept wall infart, LV dilatation.  There was noted coronary sinus stenosis hence the need to abandon a coronary sinus lead and just go for the epicardial lead that would be placed via thoracotomy.  Aside from his heart history, he also had DM, HTN, AFib, sleep apnea (not using CPAP).  He’s on a whole host of meds… preop echo showed EF20%, severely decreased LV systolic function, hypokinesis of LV/RV, mild MR/TR, mod pulm HTN.

I met Mr. Chill in the pre-op holding area while a resident and CRNA were attempting to place PIV.  I took a look and you really can’t see anything.  So, while they were bringing the U/S, I was able to get a 22G PIV — not worthy of cardiac surgery…but worthy for induction.  A right radial a-line was placed with some difficulty (imagine poor EF…difficult to feel pulsatility anywhere).  The AICD rep was supposed to be available, but was running late so we were given the green light to go back to the OR.  The reason he earned the name Mr. Chill was b/c he was very relaxed and very interactive with us during PIV and a-line.  Every now and then he’d doze off, but then we’d say his name and he’d wake back up and interact with us.  I’m thinking that’s probably a combo of his OSA and his low flow state.

We brought him back to the OR, placed monitors on him.  The EKG appeared to be a wide complex regular sinus rhythm…someone who appeared to have a LBBB.  His a-line was reading 110-110SBP.  We were pre-oxygenating him for awhile.  Induction: lido 100mg, fentanyl 150mcg, etomidate 20mg, roc 70mg…after induction he stayed in the SBP90s.  Slowly, he started to drift down while taking over mask ventilation.  Luckily, he was an easy mask.  Now his SBP 80s, we intubate with a L DLT.  Confirmed with ETCO2.  SBP hanging in the 70s…multiple boluses of phenylephrine (total 600mcg), ephedrine (30mg), epi (100mcg) the SBP would go up to low 80s, but come back down to 70s.  We checked the DLT via FOI…it seemed a bit deep, therefore we pulled it back.  Still, we weren’t happy with it and his SBP was sagging, therefore, we took out the DLT and reintubated with an 8.0ETT.  Pt was oxygenating well as the SpO2 read 96-98%.  Then, his radial aline went to 60s. We cycled NIBP that showed 50s/20s.  Then the art line went flat.  We started CPR, 1mg EPI followed by atropine.  With CPR, the arterial trace looked good reading a pressure in the 80s.  PEA was suspect…we ran serial ABG, got femoral access.  We came out of it.  First ABG showed CO2 70s…ETCO2 was in the 40s.  We hyperventilated him and started him on an epi infusion.  The AICD rep interrogated his AICD…and we found out that the patient had 4 episodes of VT that was treated by overpacing from the AICD (not shocks).  This occurred in the pre-op area prior to going back to the OR and lasted for 35 seconds total.

We cancelled the case and took the patient to the SICU.

Things I took away from this case:

1) Always have the AICD rep interrogate prior to going to OR.  Period.  It doesn’t matter if everyone in the OR wants you to go… it’s worth waiting.  Obviously, Mr. Chill didn’t show any signs of VT to us b/c we were with him in the pre-op area.  There were no shocks delivered from the AICD.  Had I known he had 4 consecutive VT episodes that were worthy of AICD treatment via pacing, I’d have cancelled the case prior to going back to the OR.  Done!

2)  With an EF hanging around 10%, this guy is probably living off his sympathetic tone.  Do NOT give fentanyl, even if you think he may get tachycardic from the intubation.  Give it as it’s needed…even though it’s “cardiac stable”.  No one is stable with an EF10%.  The last thing I want to do is decrease any tone that may be supporting him. (Sure, maybe it’s a placebo for me… so be it!)

3) This guy’s PEA was most likely caused by hypercarbia.  He had a history of OSA and would intermittently fall asleep in the pre-op holding area… he may have been hypoventilating.  We didn’t see it on the ETCO2 trace while masking him b/c he probably has a large A-a gradient (ETCO2 registered on our monitors was 45).  His lungs are getting well ventilated…but his circulation time is so slow that he’s underperfused.  Dead space… and a lot of it.

4) For a guy like this, make sure surgeon and perfusionist are present in the room on induction.  They were present here…just an FYI.

5) R2 pads are always good to have in place, just in case.  Yes, this guy has an AICD… but at some point the treatment/shock mode will be turned off for the surgery.

6) Go with your gut instinct.  If your gut is telling you that he needs some beta activity to get the heart jumpy enough to tolerate induction… then do it.

7) Be a calm, cool cucumber during the resuscitation.  Our team did a fabulous job of communicating and getting things done… all b/c of clear, concise communication.  It really does make a difference.

8) Debrief.  This helps get everything on the table and brainstorm what could have been done differently or better.  We’re all colleagues; no one has room  to pass judgment.  Ever. (If they do, take’em out back and kick ’em in the shins!)