Platelet Transfusion Summary

February 20th, 2010 by peter_lunny No comments »

Platelet Transfusions

Ira Shulman, MD

Background:

Close to 3 million platelet transfusions in the U.S. every year

“Single donor” platelets (apharesis platelets) used at LAC-USC rather than the former “six pack” (pooled platelet concentrates) to reduce infection risks

Transfusion Guidelines:

Platelet transfusion guidelines to treat bleeding or to prevent bleeding in thrombocytopenia

Expected rise in platelet count after transfusion is based on weight

70kg (150lb) – 1 apharesis pack (450 billion platelets) à expected increase ~ 30,000

More if a smaller patient, less if a larger patient (may require 2 apharesis packs)

Post-count should be obtained 30 minutes after transfusion

May be blunted by DIC, SIRS, or other inflammatory responses

ABO compatibility

Typing of platelets isn’t necessary for transfusion, however:

Compatibility improves incremental rise in platelet counts & long-term outcome

Platelet transfusion NOT recommended in:

ITP (Idiopathic thrombocytopenic purpura) – not recommended unless actively, significantly bleeding.

Autoantibody will destroy transfused platelets. Massive transfusion may be a temporizing measure.

PTP (Post-transfusion purpura) – Rare condition caused by autoantibody formed in females days after PRBC transfusion.

Platelet counts drop. Treatment is IVIG. Transfusion of platelets not indicated as counts will improve.

HIT (Heparin induced thrombocytopenia) – Caused by antibody formed against heparin-platelet factor IV complex. Platelets

may actually increase risk of thrombotic event.

TTP (Thrombotic thrombocytopenic purpura) – platelets may increase microthrombotic event.

Risks of platelet transfusion:

Platelet transfusions are discouraged because of limited resources & other risks

Riskiest blood product transfused

TRALI (Transfusion Related Acute Lung Injury)

Acute onset of respiratory failure with hypoxemia; higher risk in SIRS/sepsis

CXR: bilateral infiltrates, haziness

#1 cause of transfusion death

1 in 5,000 transfusions, 5% death rate

TRALI theories:

Donor has anti-HLA antibodies in plasma at time of donation à recipient with same antigen on WBCs. As blood products are stored, bioactive lipids are released & activate neutrophils on capillary endothelium

TRALI is most associated with apharesis platelet transfusion from female donors

Male blood products are safer because less WBC antibodies formed

Hemostatic Resuscitation

LAC-USC data: Patients requiring >10 units PRBC in 12hrs, aggressive plasma & platelet support have better outcomes

However, if patients require < 10 units PRBC in 12-24hrs, plasma & platelet transfusion may cause more harm (higher risk of ARDS & complications) and no gain in outcomes

What if you don’t know?

If patient on anti-coagulation, begin with aggressive plasma/platelet transfusion

If not, after 6 units PRBC given à move on to plasma/platelet transfusion

Up to 25% of massively injured trauma victims are already coagulopathic by the time they reach the ED (due to activation of

thrombin, Protein C & massive fibrinolysis)

 

Some Changes…

February 16th, 2010 by admin No comments »

Okay crew.   Unless you’re asleep at the scalpel, you’ve already noticed things look a bit different on your myMacombER site.

This site has transitioned to a blog style format.   There will be an event calendar and other relevant links shown on this site.

If you’re looking for the Tintinalli / lecture archive files, click the ‘Document Library’ tab at the top of this page and you can still get there.

-Dave Poskevich

 

ANAPHYLAXIS

February 12th, 2010 by peter_lunny No comments »

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ANAPHYLAXIS:

Epidemiology

Incidence- likely under-reported because no set definition

Pathophysiology

Sensitization-exposure leads to Ig-E antibodies on mast

cells and basophils

Re-exposure-cross-linking of antibodies causes release of

active mediators

Histamine, cytokines, leukotrienes…


Classification

Gell-Coombs classification

See Chart (Am Fam Physician 2003;68:1781-90)

Anaphylactoid reaction

Immediate systemic reaction that mimics anaphylaxis but→ no Ig-E antibodies

Can occur on first exposure

Reactions dependent on systemic exposure

Example: radiographic contrast

Acute treatment similar to true anaphylaxis

Clinical Symptoms (4 organ sx)

Respiratory-upper or lower

Cardiovascular-entire spectrum

Gastrointestinal- N/V/D, wide variety sx

Skin-we associate with anaphylaxis but skin findings absent 10%

Definition

No good definition→we know it when we see it

Spectrum

Urticaria, Angioedema

versus non-specific rash?

Anaphylaxis (at least 1 out of 2: )

Respiratory difficulty→throat, posterior pharynx, larynx

Hemodynamic instability

Etiology

Foods→most common

Early life: allergens that are outgrown (eggs, milk, soy)

Later life: peanuts, treenuts, fish, shellfish

If these occur in early life→ tend to not outgrow

Medications→antimicrobials, NSAIDS, ASA, any

Exercise induced→ ½ are food induced

Idiopathic→20%

Other→Hymenoptera, latex, blood components, beer, others

Differential diagnoses

Scombroid poisoning: 30 min after spoiled fish (tuna, mackerel, mahi-mahi), N/V/D, urticaria

Treatment→antihistamines

Angioedema:

Hereditary→C1 esterase inhibitor replacement, FFP; (not associated with urticaria)

ACE-inhibitor induced→ manage airway + usual treatment

Severe Asthma

Panic disorders

Treatment Recommendations (J Allerg Clin Immunol 2005;115:S483-523)

Oxygen

IV Fluids

Epinephrine (1st line agent)

Route

IV→ virtually all adverse outcomes in literature are from IV use

i ↑adverse effects when given too rapidly, too concentrated, or too high of a dose

ii Reserve for sickest patients (true shock, not responsive to IM)

IM vs SQ→ more rapid peak plasma concentrations with IM use in children and adults

i Adults-J Allergy Clin Immunol. 2001;108:871– 873;   Children: J Allerg Clin Immunol 1998;101:33

ii SQ absorption decreased in shock states

iii Epinephrine is vasoconstrictor→ decreases its own absorption

iv Limitations of recommendations→need study with both injections in thigh, studies done with

patient not in anaphylaxis

Recommendations: IM is better than SQ, regardless of age

Dose

IM Dose

i Adults IM: 0.3-0.5 mg IM of 1:1000 repeat q 5-15 min

ii Pediatrics IM: 0.01 mg/kg to max 0.3 mg 1:1000 IM repeat q 5-15 min

IV Dose: 0.1mg IV = 100 mcg IV = 1ml of 1:10,000 (need to dilute to 10 or

100ml→see below!)

i Dilution options: go to http://emrap.tv/

(a) Option #1: add 1ml of 1:10,000 solution to 9ml NS →10 ml of

1:100,000 dilution (10mcg/ml) over 5-10 min →10-20mcg/min

(b) Option #2: add 1ml of 1:10,000 (crash cart epi) to 100ml NS and run

over 5-10min→ (1mcg/ml) = 10mcg/min

(c) Compare to epinephrine gtt→1-4 mcg/min

(d) Pediatrics: 0.1mcg/kg/min (diluted to 1:100,000 solution) and titrate to

response

Epinephrine gtt: same dilution as option #2→(1mcg/ml), to run at 1-4

ml/min (1-4 mcg/min)

Safety?

IV→ virtually all adverse outcomes in literature are from IV use

IM/SQ→not too bad

Caution: elderly, hypertensive, CAD

Contraindications?

No absolute contraindications

β –blockers:

i Anaphylaxis may be worse

(a) relative state of hypoadrenergic;

(b) β –receptors are blocked (Epi won’t work on β receptors→unopposed α blockade)

ii Recommendations:

(a) ½ dose of epinephrine→ evaluate for response

(b) Glucagon (bypass β receptor altogether→ still stimulates cAMP)

(i) Dose: Glucagon 1-2 mg IV q 5-10min

(ii) Adverse effects: Nausea/Vomiting

Epinephrine allergy

i Not true allergy, likely preservative allergy→ MBS, sulfite

ii Recommendation: Sulfite-free epinephrine?

Antihistamines (2nd line agent)

H1 blockers

Diphenhydramine→works well, can give IV

Non-sedating H1 blockers?→not available for IV use

H2 blockers

Benefit over H1 blockers alone

Low adverse effects (except possibly cimetidine→CYP450)

Corticosteroids

Delayed effect of corticosteroids?

May prevent recurrent anaphylaxis

No role in acute management?? (J Allerg Clin Immunol 2005;115:S483-523)

Effects never been validated in placebo controlled studies, effects extrapolated from asthma

Inhaled β2 agonist (albuterol)→if bronchospasm

Remove source: venom sac! Stop antibiotics

Vasopressin?

AHA Summary of treatment recommendations (Circulation 2005;112;IV-143-IV-145)

Click on this: http://circ.ahajournals.org/cgi/content/full/112/24_suppl/IV-143

Special Case: Cardiac Arrest

Aggressive fluid resuscitation (4-8L)

High dose epinephrine IV: 1mg→3mg→5mg then start infusion at 4-10mcg/min

Antihistamine IV

Steroids IV

Prolonged CPR→effective CPR may maintain O2 delivery until catastrophic effects of anaphylaxis resolve

Airway management

RSI normal way vs

Supraglottic device (LMA, Combitube)→less increasing edema without endotracheal tube in?

Angioedema ?→ consider nasotracheal intubation (prepare for cric)

Disposition

Mild Urticaria (no respiratory compromise/hemodynamic instability)→Home

Severe anaphylaxis (intubated, epinephrine gtt)→ICU

Anaphylaxis that improves?

Recurrent anaphylaxis?

Biphasic or multiphasic form of anaphylaxis

Reappearance of allergic phenomenon after resolution of original symptoms

As high as 20% and as long as 72 hours after initial event! (see chart below)

Hong Kong study (Journal of Emergency Medicine, Vol. 28, No. 4, pp. 381–388, 2005)

i Biphasic symptoms in 5% of 282 patients

ii 3 patients with stable VS on presentation→ developed hypotension or severe dyspnea on

recurrence

Corticosteroids do not prevent this phase from recurring

Observation?→ no firm established criteria

Mild sx→ several hours, 4hours

Severe sx → observe x 24hours or admit

High risk features for fatal anaphylaxis

Specific allergens: peanuts, treenuts

H/O Asthma

Discharge planning

Reliable caretaker?

Access to 911?

H1/H2 blocker

Corticosteroids x 3-5 days

Self-injectable epinephrine

i Underprescribed→ should be given to all true anaphylaxis,

maybe multiple

ii EpiPen and EpiPen Jr

iii Twinject→can administer 2 doses

iv Education: YouTube?

Adverse Drug Reactions

Define: All non-therapeutic consequences of drug, excluding treatment failure, poisonings or drug abuse.

Allergic ADRs: 5-25% of ADRs

Type 1 Hypersensitivity→ small fraction of allergic ADRs

Is patient having a true ADR?

Non-allergic ADRs: N/V/D, weakness, non-specific rash (urticaria vs routine maculopapular eruption)???