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Fellowship Vivas – Thrombocytopenia, TAVI and TBI

Dr Swapnil Pawar November 14, 2022 228


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    Fellowship Vivas – Thrombocytopenia, TAVI and TBI
    Dr Swapnil Pawar

FELLOWSHIP PODCAST 

Written by Dr Madhuri Anupindi

 

  1. 75M has been in ICU for 4 days following MVR + CABGs, he is ventilated and shocked, requiring ongoing cardiovascular support. Over this time, his platelet count has dropped (386 pre-op 109 post bypass 151 day 1 61 on day 5). What are the likely causes of thrombocytopenia in this situation?

The likely causes of thrombocytopenia in this gentleman are via increased destruction or consumption, decreased production, dilution, sequestration or factitious.

Increased consumption or destruction:

  • Drug related: heparin, post transfusion purpura, antibiotics (ampicillin, piperacillin, vancomycin), digoxin
  • Mechanical: if mechanical heart valve, less likely to be from the bypass circuit now on day 5, if IABP is in situ
  • DIC secondary to sepsis
  • Thrombotic microangiopathy such as TTP, HUS (can occur post surgery)

Decreased production:

  • Drugs: beta lactams, linezolid
  • Infection: EBV, hepatitis, sepsis, HIV
  • Less likely an underlying co-morbidity: neoplasm, liver disease

Dilution

  • Massive transfusion
  • Haemodilution secondary to IV fluids

Sequestration:

  • Hypersplenism
  • Portal hypertension

Factitious (much less likely)

  • If collected in EDTA tube  can recollect in citrate tube
  • Traumatic venepuncture: less likely as if patient still ventilated and shocked will have arterial/central access still in situ

How would you evaluate the cause of his thrombocytopenia?

This would require obtaining further information through history, examination and investigations.

History:

  • Trajectory in ICU including symptoms/signs of other causes e.g. fever/localising symptoms for sepsis
  • Co-morbidities that may cause thrombocytopenia e.g. autoiummune conditions, neoplasms
  • Medications given: antibiotics, heparin – especially time course, transfusions, large volumes of fluid

Exam:

  • Signs of sepsis, autoimmune conditions, portal hypertension, lymphadenopathy, splenomegaly
  • Signs of bleeding, DIC, purpura
  • Signs if thrombosis: skin necrosis, leg swelling, stroke, limb ischaemia etc

Investigations:

  • Bloods:
    • Blood film: evaluate for schistocytes (suggests microangiopathic process), spherocytes (suggest immune mediated haemolytic anaemia or hereditary spherocytosis, leukoerythroblastic picture suggests infiltrative bone marrow process, leucocytosis with left shit suggests infection, immature WBCs suggest leukemia or myelodysplasia, hypersegmented neutrophils suggests megaloblastic process
    • FBC see if all cell lineages affected which is more suspicious of bone marrow issue
    • Fibrinogen, D dimer and coagulation panel: DIC screen
    • UEC and LFTs: assess for renal and liver dysfunction, some thrombocytopenic conditions are associated with renal impairment e.g. HUS/TTP
    • Depending on suspicion:
      • Infectious screen: blood culture if febrile, EBV, hepatitis, HIV serology
      • B12 level if macrocytosis
      • If intermediate or high probability of HITTS: ELISA for anti-platelet factor 4/heparin antibodies
      • Autoimmune screen: consider DS-DNA, anticardiolipin antibodies, ANCA, rheumatoid factor, cryoglobulins, complement
      • ADAMTS13 if considering TTP
    • Imaging: generally not part of work up unless evaluating for potential bleeding sites (e.g. may do CT scan), CXR potentially for septic work up
    • Other: bone marrow biopsy

You mentioned PFA antibodies for HITTS – these come back strongly positive. How does this test work?

This is an immunoassay that detects the presence of anti-platelet factor 4/heparin antibodies in the patient’s blood. It is performed by adding the patient’s serum to a plate coated with heparin-PF4 complexes. If antibodies against these complexes are present in the patient’s blood they will then bind. A second antibody to human immunoglobulin that is attached to an enzyme is then added. Following this a substrate for this enzyme is added, the product of this enzyme-substrate reaction results in a change in colour. The colour intensity is directly proportional to the degree of conjugate binding which is proportional to the amount of HIT antibody present. The colour intensity is reported as the optical density at a specific wavelength, a higher optical density represents a higher amount of antibody in the patient’s serum which is more strongly suggestive of HITTs.

What other type of test is available to diagnose HITTS and when would you perform it?

Functional assays are the other category of test available to diagnose HITTS. These assess the ability of HIT antibodies in the patient serum to activate test platelets. The main test used is a serotonin release assay which detects the release of serotonin from test platelets in the presence of patient serum and heparin. The serotonin release assay is considered the gold standard for detection of HITTS and is more specific than immunoassays. However, it is also more expensive, less easily available and takes longer to run. I would only perform it if the immunoassay result was indeterminate (depends on the optical density) or unexpected.

This patient is diagnosed with HITTs. What would your approach be if he currently required anticoagulation?

I would stop heparin, obtain baseline coagulation profile and check the UEC and LFTs to evaluate organ function. If this patient had no severe hepatic dysfunction then I would start Argatroban. It is a parenteral direct thrombin inhibitor with a short half life and its effect can be monitored by the aPTT. This is useful in the post cardiac surgery patient as can be easily titrated and ceased if required.

2.You are part of an MDT assessing high-risk cardiac surgical patients: 84F with symptomatic severe AS for an AVR. She has had CABG 10 years ago, femoro-popliteal bypass surgery 4 years ago. BG: HTN, diabetes, emphysema and CKD. What further information/investigations would you obtain and why?

I would want to obtain further information and investigations regarding her:

  • Aortic stenosis
  • Other co-morbidities
  • Functional status

in order to perform an individualised risk stratification for this patient and to assess the feasibility of performing this procedure or alternatives.

Aortic stenosis  deem the suitability for invasive surgery

  • Severity
  • Symptoms: dyspnoea, exercise tolerance, syncope, angina, arrhythmias
  • TTE results: valve size, valve area

Co-morbidities: in order to assess her risk as well as suitability for other alternative procedures

  • IHD: previous CABG details and complications, last angio/TTE (patency of grafts), any LV/RV dysfunction, use of antiplatelet agents
    • Previous scars  may not be able to do minimally invasive techniques
  • HTN: control of BP, medications, any complications from same
  • CKD: extent of CKD, cause, previous dialysis
    • UEC, imaging of renal tract
  • Emphysema: lung function tests/spirometry, number of exacerbations, exercise tolerance, use of steroids/inhalers, CXR/CT, presence and degree of pulmonary hypertension
  • Peripheral vascular disease: ?suitability of arterial access for TAVI, increased risk ischaemia
    • CTA: assess calcification of aorta and peripheral arterial cannulation sites  important for suitability of mini-sternotomy, porcelain aorta is also a contraindication to surgical AVR
    • Peripheral femoral doppler  calibre of femoral vessel
    • Mini-thoracotomy may not be an option
  • Assess for any other co-morbidities: renal function, liver function, previous strokes

Functional status and quality of life:

  • Frailty: Katz activity of daily living (independence in ADLs)
    • Muscle bulk, gait speed, weight/BMI, mobility
    • Significant risk of further deterioration post op
  • Cognition
    • MMSE: risk of cognitive impairment post op
  • Social situation and supports

What are the alternatives to performing an AVR in this patient?

The alternatives are a transcatheter aortic valve implantation (TAVI), a balloon valvuloplasty, or medical management.

  • TAVI: a large sheath is inserted usually into the femoral artery, a wire is placed through the sheath and then advanced to go across the aortic valve. This is then used to guide a replacement aortic valve to the correct position. A TAVI can also be performed via alternative approaches such as transapical in patients with unfavourable ileofemoral anatomy.
  • Balloon valvuloplasty: a balloon in inflated within the aortic valve with the aim to increase the size of the valve and therefore temporarily relieve some of the symptoms. This is a less invasive measure but does not provide a long term solution as there is early restenosis of the dilated valve. It is sometimes used as a bridge to TAVI or surgical valve replacement
  • Medical management: generally reserved for patients who are too high risk for procedures or have a life expectancy of < 1 year

What are the indications, advantages and complications of a TAVI?

Indications:

  • Patients with severe symptomatic AS who are high risk or unsuitable surgical candidates and who do not have a contraindication for TAVI. Patients should also be thought to be likely to have improvement in their quality of life post procedure.

Advantages

  • Lower rate of major bleeding and AF compared to surgical aortic valve replacement
  • Less invasive
  • Avoids complications of bypass
  • Less expensive: may also avoid ICU stay, invasive ventilation
  • Outcomes are improving over time with increased operator experience, new technology and improved patient selection

 

Complications:

  • Access related complications: bleeding, pseudoaneurysm, limb ischaemia, aortic dissection or perforation, transapical tear or rupture, ventricular perforation
  • Mechanical complications: annular rupture, transcatheter valve malpositioning, aortic regurgitation, mitral valve disruption, coronary obstruction
  • Thromboembolic complications: stroke, valve thrombosis
  • Acute kidney injury
  • Arrhythmias: AV heart block – may require PPM, new AF
  • Prosthetic valve endocarditis

 

  1. 25M cyclist admitted after a crash at 40km/hr. GCS was 4 at the scene, intubated. CTB shows petechial haemorrhages at grey-white junction but no extra-axial mass lesion. No other injuries identified imaging or clinically. Sedated with morphine and midazolam 5mg/hr. Intubated and ventilated SIMV RR 14 TV 550ml PEEP 10. Afebrile, HR 90, BP 100/55 sats 96% on fio2 0.3 etco2 40. Outline your management specific to patient’s head injury.

Management specific to the patient’s head injury would involve a targeted history, assessment of his neurology with consideration of ICP monitoring if unable to assess clinically, prevention of secondary brain injury and supportive care.

Targeted history

  • Co-morbidities, medications and allergies
  • History of the crash: confounders for neurological assessment and prognostic factors
    • Suspicion of drug use
    • In ED: GCS post resus, presence of hypotension, hypoxia, seizure activity, pupillary abnormalities
    • Treatment given: fluids, sedation, paralysis
    • Blood tests including electrolytes, BSL, organ function, blood alcohol level

Neurological assessment

  • Wean sedation (if no recent paralysis: check TOF, no other confounders (electrolytes/drugs/alcohol))  would change from midaz to propofol as shorter onset/offset
  • Discussion with neurosurgical colleagues re ICP monitoring
  • Repeat CTB after 24 hours

Prevent secondary injury

  • Sats > 92%, pao2 > 60, reduce PEEP if this level is not required as could raise ICPs
  • Paco2 < 40mmHg  correlate with ABG
  • Avoid hypotension
  • Aim Na 140 – 150
  • Glucose 6 – 10
  • Normothermia: regular paracetamol, monitor temperature
  • Levetiracetam 500mg BD for 1 week (institutional – BTF recommends phenytoin in patients where the overall benefit is thought to outweigh the risks)
  • ICP < 22mmHg (if an ICP monitor is inserted)  aim CPP 60 – 80mmHg
  • Head of bed 30 degrees
  • Avoid tight ties for ETT  tapes used in my institution
  • Avoid further bleeding: correct coagulopathy

Supportive care

  • Nutrition: NG feeds
  • PPI
  • Mechanical DVT prophylaxis initially
  • Secondary/tertiary survey

What are the guidelines for ICP monitoring in this situation?

The 4th edition BTF guidelines recommend insertion of an ICP monitor and ICP guided management in TBI patients who have a GCS of 3-8 after resuscitation and an abnormal CT scan. It is also recommended for patients with a severe TBI with a normal CT scan if => 2 of the following are present at admission: age > 40, unilateral or bilateral motor posturing, or SBP < 90mmHg. There is minimal high quality evidence assessing whether ICP guided management in patients with severe TBI improves outcome. In our current clinical environment it is considered standard of care so there is a lack of equipoise in order to perform RCTs.

When would you commence chemical DVT prophylaxis in this patient?

This patient is at high risk of DVTs just by virtue of his severe TBI. I would commence chemical DVT prophylaxis in this patient if a follow up CTB at 24 hours showed no new or progression of intracranial haemorrhage, and he had no other significant sequelae of trauma that was a contraindication to chemoprophylaxis.

List the prognostic factors for patients with traumatic brain injury?

Clinical:

  • Age > 40 years
  • Low GCS post resuscitation
  • SBP < 90mmHg
  • Hypoxia
  • Abnormal pupil size and reaction
  • Co-morbidities

Radiological:

  • CT: obliteration of 3rd ventricle/basal cistern, midline shift, SAH, petechial haemorrhage, brainstem injury, unevacuated haematoma
  • MRI: brainstem lesions, damage to splenium of corpus callosum, diffuse axonal injury

 

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