Tag Archives: heme/onc

WARFARIN REVERSAL – When and How?

10 Jul
submitted by Amit Kumar, M.D. 
 
SERIOUS LIFE-THREATENING BLEEDING:
-Hold warfarin
-Vit K 10mg IV infusion over 20-60minsholygrail018
-PCC. Dosing based on weight and INR. Typical for INR >6: 50 U/kg. Re-check INR 30 mins post-admin.
-Transfusions: RBC, Platelets (if <50,000), FFP (15-30cc/kg; if PCC unavailable)
-Other agents: TXA/aminocaproic acid (anti-fibrinolytic), DDAVP (for platelet dysfunction)
 
URGENT SURGERY/PROCEDURE:
-Hold warfarin. Vit K + PCC, as above
 
SURGERY/PROCEDURE after 24H:
-Hold warfarin. Vit K 1-2mg
 
MINIMAL BLEEDING:
-Clinical judgement: withhold warfarin vs hold warfarin + Vit K vs more aggressive reversal (like above)
-Weigh pros/cons of current bleeding vs thromboembolic risk
 
NO BLEEDING:
-INR >9:  Vit K 2.5-5mg PO. Will reduce INR over 24-48 h. Can re-start warfarin (maybe reduced dose) when INR therapeutic
-INR 5-9: Hold warfarin temporarily (1-2 doses) +/- Vit K 1-2.5mg (elderly with slower clearance, prior bleeding)
-INR <5: Hold next dose of warfarin
 
SUPERWARFARIN POISONING:
-Often found in rodenticides, laced street-drugs. Accidental vs suicide attempt.
-Usually requires massive doses of Vit K (50-800mg/d) for months-years, based on repeat assays and coagulation studies
————————————————————————————————–
PCC pearls:
-If 4-factor PCC missing, use 3-factor PCC + FFP (to supplement factor VII)
-PCC dose based on units of factor IX activity
-PCC advantage over FFP: more rapid admin (doesn’t have to be thawed), faster INR reversal, lower risks for volume overload or TRALI
 
References:
“Paper Chase 1- PCC vs. FFP.” Review. Audio blog post. Www.emrap.org. EM:RAP, Dec. 2013. Web. <https://www.emrap.org/episode/december2013/paperchase1pcc>. Episode 147
 
Advertisements

WBC – too high or too low?

23 Oct
RAPID FIRE PEARLS:
 
WBC TOO HIGH (Hyperleukocytosis):
 
  • WBC > 50k (often >100k)
  • usually with AML or CML with blast crisis
  • symptoms usually pulm or neuro – due to white cells plugging microvasculature and/or tissue hypoxemia with cytokine damage
 
Treatment:
  • call oncology (need chemo or leukopheresis)
  • IV fluids
  • antibiotics
  • only chemo improves mortality
 
 
WBC TOO LOW (neutropenia):
 
  • fever is sometimes the earliest/only symptoms (due to muted inflamm response)
  • neutropenia = ANC < 1500 cells/uL
  • severe neutropenia = ANC < 500
 
ANC = WBC count X (%PMNs + %Bands)
 
Management:
  • IV antibiotics
  • IV Fluids
  • pan infectious workup (blood cx’s, urine, etc)

 

SLIGHT TANGENT, since we’re talking about low immune response…
10 second version:
absolute lymphocyte count = ALC 
ALC < 2500 (95% sensitive for CD4 <200)
ALC < 800 (91% specific for CD4 <200)
 
 
 There you go.  
 

SVC Syndrome

27 Aug

RAGING HYPOTHETICAL:

Your next patient is a 70 yo M with neck swelling and syncopal episode, who said he “felt like couldn’t breathe” when bending forward, then passed out. 

Vital Signs – WNL

Physical exam – Awake, ambulating male with chest wall venous distention, b/l neck swelling, facial plethora when leaning forward and trace peripheral, LE edema. 

 

WHAT DOES THAT MEAN?svc

Superficial venous distention in superior vena cava syndrome  —>

 

 

Imaging – In ED, CT chest and neck (w/ contrast) to evaluate for obstructing mass (e.g. something compressing the SVC)

 

Etiology – In the preantibiotic era, syphilitic thoracic aortic aneurysms, were frequent causes of the SVC syndrome.  More recently, intrathoracic malignancy is responsible for 60 to 85 % of cases of SVC syndrome.  Non-small cell lung cancer (NSCLC) is the most common, accounting for 50 %  of all cases.

Clinical Manifestations – Interstitial edema of the head and neck is visually striking, but generally of little clinical consequence.  However, edema may narrow the lumen of the nasal passages and larynx –> dyspnea, stridor, cough, hoarseness, and dysphagia.  Cerebral edema can also occur (not awesome).

Cardiac output may be diminished transiently by acute SVC obstruction, but, within a few hours, blood return is reestablished by increased venous pressure and collaterals. Hemodynamic compromise, if present, more often results from mass effect on the heart than from SVC compression.

 

Submitted by Christina Brown.

 

References: Up to Date: malignancy related SVC syndromeWilson LD, Detterbeck FC, Yahalom J. Clinical practice. Superior vena cava syndrome with malignant causes. N Engl J Med 2007; 356:1862.SCHECHTER MM. The superior vena cava syndrome. Am J Med Sci 1954; 227:46.Yellin A, Rosen A, Reichert N, Lieberman Y. Superior vena cava syndrome. The myth–the facts. Am Rev Respir Dis 1990; 141:1114.Rice TW, Rodriguez RM, Light RW. The superior vena cava syndrome: clinical characteristics and evolving etiology. Medicine (Baltimore) 2006; 85:37.Chee CE, Bjarnason H, Prasad A. Superior vena cava syndrome: an increasingly frequent complication of cardiac procedures. Nat Clin Pract Cardiovasc Med 2007; 4:226.picture

Catheter-related upper extremity DVT

26 Mar

QUICK PEARLS:

The majority (70-80%) of thrombotic events in the upper extremity deep veins (subclavian, axillary, brachial) occur in the presence of IV catheters.

 

Any catheter has the potential to cause thrombosis. Think about PIV, PICC, tunneled and non-tunneled central catheters, ports and pacemakers.

 

In addition to the classic risk factors that you commonly consider for DVT (prior surgery, malignancy, h/o DVT, etc.), specifically catheter-associated thrombosis is more likely with:

large-diameter catheters (more likely to have stagnate blood v. free flowing)

PICC as compared to centrally placed catheters

-catheter malposition (In one study, DVT developed in 46% of patients whose catheter tip was in the innominate vein or junction of the immoninate vein with the SVC, compared with 6% of patients with a properly positioned catheter)

-chemical irritation (potassium chloride, antibiotics such as vancomycin, diazepam, hypotonic and hypertonic electrolyte solutions)

 

Clinical presentation: inability to withdraw blood, phlebitis, extremity edema

 

Diagnosis is made with Doppler ultrasound.

 

Treatment involves observation, anticoagulation to prevent embolization, and removal of the catheter. Prophylactic systemic anticoagulation is not routinely recommended in this population.

 

Submitted by K Estes.

 

References:  Luciani, et. Al. Catheter-related upper extremity deep venous thrombosis in cancer patients: a prospective study based on Doppler US. Radiology. 2001;220(3):655. PMID 11526263

Uptodate.com; picture

TTP: quick review

27 Oct

TTP is thrombotic thrombocytopenic purpura, characterized by a pentad (FATRN)

  • Fever,
  • Anemia (microangiopathic hemolytic),
  • Thrombocytopenia,
  • Renal dysfunction,
  • Neurologic dysfunction (that may be transient)

All of these are present only 1/3 of the time.

 

TTP occurs usually in adults and rarely in children, while HUS is more common from age 6 mos to 5 years.

TTP is a hematologic emergency with 100% mortality if untreated, and 10-20% if treated- bad stuff.

 

– If TTP is suspected, steroids should be started, give FFP, and consult hematology for plasma exchange therapy.

 

Why FFP?

As in treatment of hereditary angioedema which lacks C1 esterase, in TTP the protease ADAMTS13 (aka vWF-cleaving protease) is qualitatively or quantitatively absent, but this is found in FFP.

 

Avoid platelet transfusion unless there is bleeding that will kill the patient before TTP does, as platelet replacement may exacerbate the thrombus formation.

 

– All of the pentad are cause by the effects of large, uncleaved vWF monomers clumping with platelets, causing unstable thrombi that transiently cause vessel occlusions, leading to renal and neurologic dysfunction, the shearing of RBCs in the small vessels, and low platelets.

 

– So what causes TTP anyway?

It is associated with HIV, flu vaccination, acute pancreatitis, and often medication use including Plavix, flouroquinolones, resperdol, valacyclovir, and infliximab, among others.

 

References: Koyfman A. Thrombotic Thrombocytopenic Purpura.[Review] Pediatric Emergency Care. 27(11):1085-1088, November 2011.; uptodate.com; picture

ITP (quick hits)

20 Jun

2 requirements:

  • isolated thrombocytopenia
  • absence of another cause.

 

pathogenesis of immune thrombocytopenia (ITP)

  • increased platelet destruction
  • inhibition of megakaryocyte platelet production via IgG autoantibodies, often directed against platelet membrane glycoproteins such as GPIIb/IIIa.

 

Symptoms:

  • range from bleeding diatheses to petechiae.
  • Gingival bleeding,
  • GI bleeding,
  • epistaxis

 

Order CBC along with smear to assess for other causes. HIV and HCV testing is recommended as well.

 

For severe thrombocytopenia and/or bleeding, emergent hem consultation is warranted.

For less severe sx, non urgent f/u.

 

Submitted by J. Rothstein.

 

References: uptodate.com; picture

carbon monoxide testing

13 May

RAGING HYPOTHETICAL:

Your next patient is a 30 yo who is brought in by EMS after being pulled out of a burning apartment building.  They’re awake, but complaining of a headache, and of course, you’re worried about carbon monoxide. 

How do you want to test for this, and what number/percent are you ok with?

 

CARBON MONOXIDE TESTING (QUICK PEARLS):

2 most commonly found options in the ED: co-oximetry & serum carboxyhemoglobin testing

 

noninvasive pulse co-oximetry (similar to your pulse-ox, but for CO)

  • via some small studies: mean absolute error of 3.15% (vs. serum testing)
  • frame of reference: mean absolute variation between various blood gas analyzers – 2.4%

 

carboxyhemoglobin testing

  • relationship between COHb levels and poisoning severity is generally poor
  • no clinically relevant difference between arterial and venous COHb levels
    • 95% of samples range between 2.4% and -2.1% of each other
  • COHb level > 3% in non-smokers or > 10% in smokers suggests an abnormal CO exposure

 

References: EBMedicine article, picture