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Thrombocytopenia in the Intensive Care Unit Joshua Laing UND Medical Student.

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Presentation on theme: "Thrombocytopenia in the Intensive Care Unit Joshua Laing UND Medical Student."— Presentation transcript:

1 Thrombocytopenia in the Intensive Care Unit Joshua Laing UND Medical Student

2 Outline Case StudyCase Study Role of plateletsRole of platelets Thrombocytopenia in the ICUThrombocytopenia in the ICU HITTSHITTS

3 The Curious Case of Barry Bareblood 47 year old farmer47 year old farmer Nil PMHxNil PMHx 13/7: R homonymous hemianopia, headache, sweats ED ?Low platelet count as refused LP 15/7: native aortic valve endocarditic Cx by septic emboli ICU Commenced on fluclox, rifampicin, fusidic acid DC MSSA native valve endocarditis/bacteremia

4 The Plot (doesnt) Thicken 25/7: Post-mechanical AVR ICU Brain – L occipitoparietal, R frontal infarctsBrain – L occipitoparietal, R frontal infarcts Seizures: leviteracetam, clonazepam, propofol, topiramate Heart – coronaries NAD, AVR, systolic dysfunctionHeart – coronaries NAD, AVR, systolic dysfunction Infective endocarditis: fluclox, rifampicin, fusidic acid, cirpofloxacin, vancomycin, meropenem. Lungs – effusions, haemorrhageLungs – effusions, haemorrhage Trache, mechanical ventilation GI – PR haemorrhage, oesophageal legionsGI – PR haemorrhage, oesophageal legions Kidneys: infarct/abcessesKidneys: infarct/abcessesHaemofiltration Spleen: infarctsSpleen: infarcts Liver – US: structurally normal, synthetic dysfunction (albumin, coags)Liver – US: structurally normal, synthetic dysfunction (albumin, coags) Blood – coagulopathy, HITTS +ve, bleeds, clots.Blood – coagulopathy, HITTS +ve, bleeds, clots. Heparin changed to danaparoid. Lepirudin.

5 Recent Thrombocytopenic Episode 28/8: platelets 13, INR 1.4, APTT 69, Hb 7728/8: platelets 13, INR 1.4, APTT 69, Hb 77 Symptomatically: reduced GCS, bleeds, ooze. Possible causes: -Bleeding -Haemodilution -Haemofilter -Sepsis -DIC -Nutritional deficiency -Liver dysfunction -HITTS -Drug induced: antituberculosis, quinidine, thiazides, penicillins, sulphonamides, anticonvulsants (leviteracetam), rifampicin.

6 Platelets Normal count range 150-450 x 10^9/LNormal count range 150-450 x 10^9/L Produced by megakaryocytes, about 30 to 50k/ul per dayProduced by megakaryocytes, about 30 to 50k/ul per day –Production can be increased 8x during stress –Young platelets have much greater function –Average platelet survival is 8-10 days –Up to 1/3 of platelets reside in spleen – but this can be much higher in splenomegaly.

7 Thrombocytopenia Strictly defined as a platelet count of <150k/ulStrictly defined as a platelet count of <150k/ul Distinguish fromDistinguish from –Defective platelet function (eg: Bernard- Soulier, aspirin usage, and uremia) –Clotting factor deficiencies (eg: hemophilia) Symptoms – include petichiae, purpura, conjunctival hemorrhage, mucocutaneous bleedingSymptoms – include petichiae, purpura, conjunctival hemorrhage, mucocutaneous bleeding

8 Differential Diagnosis Decreased ProductionDecreased Production –Marrow disease: Aplastic anemia, infiltration –Production impairment: drugs, HIV –Poor maturation Decreased SurvivalDecreased Survival –Immunologic destruction – ITP, HIT, drug, infxn –Nonimmune destruction – DIC, TTP/HUS Sequestration – splenomegaly (liver disease)Sequestration – splenomegaly (liver disease) Dilutional – severe bleedingDilutional – severe bleeding

9 Differential Diagnosis Thrombocytopenia in Primary CareThrombocytopenia in Primary Care –Most common: platelet clumping, wrong patient, or chronic ITP –Need to r/o HIV and occult liver disease –In pregnancy ?gestational thrombocytopenia –In those age >60 ?myelodysplastic disorder –May be congenital in those with longstanding thrombocytopenia

10 Thrombocytopenia in the ICU Systematic Review: The Frequency and Clinical Significance of Thrombocytopenia Complicating Critical Illness Background: The epidemiology of thrombocytopenia in critically ill patients has not been well characterized. The objective of this study was to systematically review the prevalence, incidence, and consequences of, and risk factors for, thrombocytopenia among critically ill patients.Background: The epidemiology of thrombocytopenia in critically ill patients has not been well characterized. The objective of this study was to systematically review the prevalence, incidence, and consequences of, and risk factors for, thrombocytopenia among critically ill patients. Results: We identified 24 studies (12 prospective) enrolling 6,894 patients from medical, surgical, mixed, or trauma ICUs. Prevalent thrombocytopenia (on ICU admission) occurred in 8.3% to 67.6% of patients; incident thrombocytopenia (developing during the course of the ICU stay) occurred in 13.0% to 44.1% of patients. High illness severity, sepsis, and organ dysfunction often correlated with thrombocytopenia. Only one study using multivariate analysis examined whether thrombocytopenia was associated with major bleeding, but it found no association. Six out of eight studies using multivariate analysis found that thrombocytopenia increased the risk of death.Results: We identified 24 studies (12 prospective) enrolling 6,894 patients from medical, surgical, mixed, or trauma ICUs. Prevalent thrombocytopenia (on ICU admission) occurred in 8.3% to 67.6% of patients; incident thrombocytopenia (developing during the course of the ICU stay) occurred in 13.0% to 44.1% of patients. High illness severity, sepsis, and organ dysfunction often correlated with thrombocytopenia. Only one study using multivariate analysis examined whether thrombocytopenia was associated with major bleeding, but it found no association. Six out of eight studies using multivariate analysis found that thrombocytopenia increased the risk of death. Conclusions: The frequency of thrombocytopenia during critical illness varies widely, based on case mix and definition. After confounding factors are adjusted for, thrombocytopenia appears to increase the risk of death. CHEST 2011; 139(2):271–278Conclusions: The frequency of thrombocytopenia during critical illness varies widely, based on case mix and definition. After confounding factors are adjusted for, thrombocytopenia appears to increase the risk of death. CHEST 2011; 139(2):271–278

11 Differential Diagnosis Thrombocytopenia in the ICU is usually due to an underlying medical condition:Thrombocytopenia in the ICU is usually due to an underlying medical condition: –Sepsis – 52% –DIC – 25% –Drug Induced – 10% –Blood loss – 8% –HIT – 1% –Hematologic Malignancy - excluded Levi M et al. Coagulation abnormalities in critically ill patients. Critical Care 2006, 10:222.

12 Other Contributors in the ICU Massive blood transfusionMassive blood transfusion Post-transfusion purpuraPost-transfusion purpura Cardiopulmonary resuscitationCardiopulmonary resuscitation Cardiopulmonary bypassCardiopulmonary bypass Adult respiratory distress syndromeAdult respiratory distress syndrome Pulmonary embolismPulmonary embolism Use of intravascular cathetersUse of intravascular catheters Solid organ allograft rejectionSolid organ allograft rejection

13 Suggested Diagnostic Approach Levi M et al. Coagulation abnormalities in critically ill patients. Critical Care 2006, 10:222. Abnormal Pt/Ptt? yes no Bleed? no +d-dimer, Fibrinogen Or DIC score? no yes Platelet lossDIC Possibly: Sepsis Mild DIC Cirrhosis (Next Slide)

14 Suggested Diagnostic Approach Heparin? yes no HIT panel Positive? no yes Schistocytes? yes no Levi M et al. Coagulation abnormalities in critically ill patients. Critical Care 2006, 10:222. Other drugs? yes no Anti- plt Abs? yes Bone Marrow Biopsy HIT TTP/HUS Drug-induced ITP ?Malignancy

15 Heparin-Induced Thrombocytopenia ( Heparin-Induced Thrombocytopenia (HITS) Up to 5% chance with UFH, 1% with LMWHUp to 5% chance with UFH, 1% with LMWH Can occur with heparin flushes, cathetersCan occur with heparin flushes, catheters Immune reaction occurring 7-10 days after RxImmune reaction occurring 7-10 days after Rx Distinguish types of HITDistinguish types of HIT –Type 1 – rapid onset, clinically insignificant (clumping) –Type 2 – onset in 5-14 days, severe thrombosis Verify HIT 2 with PF4 antibody testVerify HIT 2 with PF4 antibody test Anticoagulate with Lepirudin, Argatroban, or bivalirudin (direct thrombin inhibitors)Anticoagulate with Lepirudin, Argatroban, or bivalirudin (direct thrombin inhibitors) Avoid coumadin and platelet transfusion until platelet recoveryAvoid coumadin and platelet transfusion until platelet recovery Monitor platelets after heparinMonitor platelets after heparin

16 Thrombocytopenia in IE Initial observation: 9/24 patients developed thrombocytopeniaInitial observation: 9/24 patients developed thrombocytopenia Co-occurring hypocomplementaemiaCo-occurring hypocomplementaemia In Staph. aureus IE thrombocytopenia and hypocomplementaemia, occurring early in the course of the disease, may be due to a non- immune interaction of Staph. cell wall products (Protein A) with immunoglobulin, complement components, and thrombocytes.In Staph. aureus IE thrombocytopenia and hypocomplementaemia, occurring early in the course of the disease, may be due to a non- immune interaction of Staph. cell wall products (Protein A) with immunoglobulin, complement components, and thrombocytes. OConnor, DT et al. (1978). Activation of the alternate complement pathway in Staph. aureus infective endocarditis and its relationship to thrombocytopenia, coagulation abnormalities, and acute glomerulonephritis. Clin. exp. Immunol.

17 References UpToDateUpToDateEtc.


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