SAEM Clinical Images Series: Blue is Bad

66 year-old-male with a history of type 2 diabetes and hypertension presented as a transfer for rapid progression of lower extremity pain, swelling, and blue-purple discoloration of the entire limb with concern for a possible necrotizing infection. His symptoms began earlier in the day and progressed over just a few hours. He had no known thromboembolic risk factors.

MSK: Swollen, tender, and blue/purple-colored right lower extremity

Complete Blood Count (CBC): WBC 8.7; Hb 15; Hct 45; Plt 172

Glucose: 472

Severe venous thromboembolism (VTE), also known as Phlegmasia Cerulea Dolens, which means “painful blue inflammation”, is commonly seen with a unilateral exquisitely tender, swollen, and bluish/purple-colored lower extremity.

Phlegmasia Cerulea Dolens has a high amputation rate secondary to venous gangrene or compartment syndrome. If no pulse is noted on exam, a high suspicion for compartment syndrome must be maintained.

Take-Home Points

  • Phlegmasia Cerulea Dolens is a rare ischemic complication of massive venous thromboembolism with amputation and mortality rates as high as 50% and 40% respectively.
  • Phlegmasia Cerulea Dolens tends to affect the iliofemoral segment of the lower extremities and is commonly associated with malignancy.
  • The preferred imaging modality is doppler ultrasound. Management includes limb elevation, IV fluids, and either systemic anti-coagulation, catheter-directed thrombolysis, and/or thrombectomy.

  • Bazan HA, Reiner E, Sumpio B. Management of bilateral phlegmasia cerulea dolens in a patient with subacute splenic laceration. Ann Vasc Dis. 2008;1(1):45-8. doi: 10.3400/avd.AVDcr07002. Epub 2008 Feb 15. PMID: 23555338; PMCID: PMC3610218.
  • Chaochankit W, Akaraborworn O. Phlegmasia Cerulea Dolens with Compartment Syndrome. Ann Vasc Dis. 2018 Sep 25;11(3):355-357. doi: 10.3400/ PMID: 30402189; PMCID: PMC6200621.
  • Gardella L, Faulk J. Phlegmasia Alba And Cerulea Dolens. 2022 Oct 3. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan–. PMID: 33085284.
  • Said A, Sahlieh A, Sayed L. A comparative analysis of the efficacy and safety of therapeutic interventions in phlegmasia cerulea dolens. Phlebology. 2021 Jun;36(5):392-400. doi: 10.1177/0268355520975581. Epub 2020 Nov 25. PMID: 33236674.
  • Schroeder M, Shorette A, Singh S, Budhram G. Phelgmasia Cerulea Dolens Diagnosed by Point-of-Care Ultrasound. Clin Pract Cases Emerg Med. 2017 Mar 13;1(2):104-107. doi: 10.5811/cpcem.2016.12.32716. PMID: 29849409; PMCID: PMC5965407.

SAEM Clinical Images Series: An Ominous Umbilical Lesion


A 54-year-old male with a past medical history of atrial flutter and alcohol use disorder presents with an umbilical wound that has been bothering him for approximately six months. There is no history of trauma, prior infection, or umbilical surgery. There is intermittent mild pain and irritation that occurs randomly. No drainage or bleeding. He admits to picking at the wound regularly. He denies fever, chills, nausea, generalized abdominal pain, diarrhea, constipation, dysuria, and hematuria. The patient drinks four or more alcoholic beverages daily and has a long-standing history of tobacco use.


Vitals: BP 105/73; HR 70; RR 16; SpO2 97% on room air; Temp 36.1°C

Constitutional: Appears stated age, resting comfortably, well-appearing.

Abdominal: Soft, flat, non-tender.

Skin: Umbilical wound characterized by a peripheral eschar and a central area of hyperpigmented and crusted tissue overlying an area of whiteish moist tissue that was uncovered by gentle cleansing. No surrounding erythema and no areas of fluctuance. No active drainage or malodor.

None available.

Sister Mary Joseph (SMJ) nodule is a rare cutaneous metastasis of gastrointestinal or genitourinary primary malignancies to the umbilicus [1,3]. They are typically firm, painful, indurated, and irregularly shaped, with sizes typically less than 2 cm [1]. They can be ulcerated or necrotic with variable presence of discharge ranging from purulent to serous or serosanguinous [1]. Sister Mary Joseph nodules typically arise late in disease and portend a poor prognosis [1]. Most primary malignancies are adenocarcinomas (75%), and pancreatic cancers represent approximately 9% of umbilical metastases [1]. Mean survival of patients with SMJ nodules is less than 12 months, and less than three in those with pancreatic primaries [1]. Prognosis is slightly less bleak if the SMJ nodule is the only metastatic site [1]. Sister May Joseph Dempsey was a nun and surgical assistant to Dr. William Mayo, the surgeon who developed the approach to umbilical hernia repair and the first to identify the connection between abdominopelvic cancers and umbilical nodules [2,3].

Abdominal CT imaging.

Our patient was discharged on the initial visit with wound care instructions. He returned to the Emergency Department two months later and was admitted for atrial flutter with rapid ventricular response and acute on chronic congestive heart failure. During that visit, the patient had a CT chest/abdomen/pelvis that demonstrated likely a pancreatic tail adenocarcinoma with metastasis to the peritoneal and abdominal walls. The patient declined any further intervention.

Take-Home Points

  • Sister Mary Joseph nodules are umbilical metastases from abdominopelvic primary malignancies.
  • Recognition of their features on clinical exam can lead to a more rapid diagnosis.
  • Prognosis is grim with an average survival of less than one year.

  1. Vekariya P, Daneti DB, Senthamizh Selvan K, Verma SK, Hamide A, Mohan P. Sister Mary Joseph Nodule as an Initial Presentation of Pancreatic Adenocarcinoma. ACG Case Rep J. 2020 Aug 25;7(8):e00453. doi: 10.14309/crj.0000000000000453. PMID: 32903972; PMCID: PMC7447472.
  2. Palazzi DL, Brandt ML. Care of the umbilicus and management of umbilical disorders. UpToDate. Updated August 27, 2021. Accessed January 2, 2022.
  3. Tso S, Brockley J, Recica H, Ilchyshyn A. Sister Mary Joseph’s nodule: an unusual but important physical finding characteristic of widespread internal malignancy. Br J Gen Pract. 2013 Oct;63(615):551-2. doi: 10.3399/bjgp13X673900. PMID: 24152477; PMCID: PMC3782795.

SAEM Clinical Images Series: Dermatology Deserving a Deeper Dive

A 22-year-old female without significant past medical history presented to the Emergency Department (ED) for a progressive rash for the past six months. She had initially complained of dry and peeling skin on bilateral hands and feet and had multiple ED and dermatology encounters where topical steroids, acyclovir, and methotrexate were prescribed with no improvement. The rash continued to progress with worsening pain and inability to flex fingers secondary to lesions and scabbing at the joints. The patient also developed painful sores in her mouth primarily involving the tongue. More concerningly, she had lost 60 pounds since the onset of the rash and mouth lesions which she attributed to the inability to eat due to significant pain. Otherwise, she denied systemic symptoms, exposures, new medications, or previous illnesses.

Vitals: Within normal limits

HEENT: Swelling, erythema, and mild desquamation of the tongue mucosa with adherent white discharge present. Lesions are limited to the surface of the tongue with no buccal involvement.

Cardiovascular/Respiratory: Heart sounds within normal limits. Bilateral breath sounds without wheezes, rales, or rhonchi.

Abdomen: Soft, non-tender and non-distended.

Skin: The patient was noted to have desquamated, scabbing and oozing lesions on bilateral palms and fingers, soles of the feet, and web spaces between toes. The patient had no observable vesicles/bullae, or target lesions. Negative Nikolsky sign.

Complete Blood Count (CBC): Mild anemia, stable from baseline.

Basic Metabolic Panel (BMP): Within normal limits.

CT Abdomen/Pelvis with contrast (relevant findings only): Large solid right retroperitoneal mass lobulated in contour with heavy coarse calcifications measuring 21.2 x 8.5 x 10.4 cm, traversing the right hemidiaphragm and extending to the right lower mediastinum. The diaphragm itself is asymmetrically thickened as compared with the contralateral left side with a small volume of adjacent retroperitoneal fluid and there is extension into the right neural foramina.

The diagnosis of paraneoplastic pemphigus (PNP) was made after skin biopsy along with the constellation of findings including desquamating cutaneous lesions, painful mucosal erosions, and large retroperitoneal mass concerning for malignancy. Skin biopsy findings in this case include a distinct suprabasilar cleft, apoptotic keratinocytes, eosinophilic spongiosis, and superficial perivascular lymphocytic infiltrate with scattered eosinophils. Focally, there was full-thickness necrosis of the epidermis and dermis.

Patients with concern for PNP without known malignancy require a full neoplastic workup. In this case, a biopsy of the retroperitoneal mass and subsequently full resection was notable for Castleman’s disease, a rare lymphoproliferative disorder. PNP is an often fatal paraneoplastic mucocutaneous blistering disease that is most commonly caused by various lymphoproliferative disorders including non-Hodgkin’s lymphoma, chronic lymphocytic leukemia (CLL), and Castleman’s disease. It is an extremely rare condition with an unknown incidence rate. The mucosal erosions present are a requirement for the diagnosis. It typically presents as an erosive stomatitis involving the tongue and is characteristically chronic, progressive, and painful. These lesions are the initial disease manifestation in almost one-half of patients with PNP and often lead to malnutrition secondary to pain with attempts at oral intake. The cutaneous lesions in the disease are widely variable in morphology and can present with tense or flaccid bullae, as well as inflammatory papules or plaques.

Take-Home Points

  • In patients with a progressive rash involving the oral mucosa that have failed multiple outpatient regimens and have findings concerning for possible systemic involvement, dermatology consultation, tissue biopsy, and body imaging are often needed to confirm a diagnosis of complicated disease processes such as paraneoplastic pemphigus (PNP).
  • Significant unintentional weight loss may be due to a variety of reasons stemming from one unifying etiology. In this case, our patient had both mouth pain limiting oral intake as well as a lymphoproliferative disorder.
  • Anhalt GJ, Kim SC, Stanley JR, Korman NJ, Jabs DA, Kory M, Izumi H, Ratrie H 3rd, Mutasim D, Ariss-Abdo L, et al. Paraneoplastic pemphigus. An autoimmune mucocutaneous disease associated with neoplasia. N Engl J Med. 1990 Dec 20;323(25):1729-35. doi: 10.1056/NEJM199012203232503. PMID: 2247105.
  • Kaplan I, Hodak E, Ackerman L, Mimouni D, Anhalt GJ, Calderon S. Neoplasms associated with paraneoplastic pemphigus: a review with emphasis on non-hematologic malignancy and oral mucosal manifestations. Oral Oncol. 2004 Jul;40(6):553-62. doi: 10.1016/j.oraloncology.2003.09.020. PMID: 15063382.
By |2023-01-02T04:44:30-08:00Jan 2, 2023|Dermatology, Heme-Oncology, SAEM Clinical Images|

SAEM Clinical Images Series: ‘Tis Not the Season to be Wheezing


A 2-year-old male with a history of solitary kidney presented with greater than one month of daily coughing, wheezing, and decreased appetite. The patient was previously seen by his primary care physician after three weeks of symptoms where he was prescribed albuterol as needed for viral bronchospasm. The patient’s wheezing did not improve after two weeks of albuterol treatment so a chest x-ray was ordered. The patient’s mother denied any fevers, vomiting, diarrhea, weight changes, or night sweats.

Vitals: BP 131/60; Pulse 148; Temp 36.7 °C (98.1 °F) (Axillary); Resp 28; Wt 15.7 kg (34 lb 9.8 oz); SpO2 95%

General: Alert; well appearing

HEENT: Pupils equally reactive to light; moist mucous membranes; nares with normal mucosa without discharge

Cardiovascular: Regular rate; regular rhythm; normal S1, S2; no murmur noted; distal pulses 2+

Pulmonary: Good aeration throughout all lung fields; clear breath sounds bilaterally; prolonged expiratory phase; stridor with agitation

Abdomen: Soft; non-tender; non-distended

White blood cell (WBC) count: 56.1/uL (Blasts 58%)

Platelets: 288/uL

Uric acid: 8.3 mg/dL

LDH: 2231 iU/LD

D-Dimer: 3.22 ug/mL

Fibrinogen: 463 mg/dL

Bronchospasm, bronchiolitis, viral infection, pneumonia, foreign body aspiration, space-occupying lesion, vocal cord dysfunction, cardiac dysfunction, and acute chest in patients with sickle cell disease.

The radiograph shown demonstrates a mediastinal mass. This patient was ultimately diagnosed with T-cell acute lymphoblastic leukemia. T-ALL can present with fatigue, fevers, weight loss, easy bleeding/bruising, paleness, or a mediastinal mass. Mediastinal masses found on chest x-ray require further evaluation to determine the diagnosis, location, and treatment. If malignancy is suspected, an oncology referral and bone marrow sample will be necessary.

Take-Home Points

  • In patients with first-time wheezing that does not improve with bronchodilator therapy, consider alternative diagnoses and further evaluation.
  • A mediastinal mass is found at the time of diagnosis in 10% to 15% of children with acute lymphoblastic leukemia.

  • Steuber, P (2021). Overview of common presenting signs and symptoms of childhood cancer.UpToDate. Retrieved January 2, 2021.2.
  • Juanpere, S., Cañete, N., Ortuño, P., Martínez, S., Sanchez, G., & Bernado, L. (2013). A diagnostic approach to the mediastinal masses. Insights into imaging, 4(1), 29–52.

SAEM Clinical Images Series: Breast Swelling

A female in her 50s with a past medical history of coronary artery disease, pacemaker placement, hypertension, and ESRD presented to the emergency department with the chief complaint of missed dialysis, breast engorgement, and an increase in vascularity in her chest and abdomen. The patient reported an increase in breast swelling and increased vascularity in her belly over the past three months. Additionally, she woke up short of breath on the morning of presentation and reported dyspnea at rest. She denied chest pain, diaphoresis, breast pain, fever, rash, trauma to the breasts, or drainage.

Vitals: T 36.9°C; HR 105; BP 109/74; RR 20; O2 sat 97% on nasal canula @ 3L

Neck: JVD

Lungs: Bilateral crackles

Chest and abdomen: Increased vascularity

Breast: Bilateral breast swelling and redness

Lower extremity: Bilateral pitting edema and varicose veins

Basic metabolic panel (BMP): K 6.9; Cr 9.53

Brain natriuretic peptide (BNP): >35,000

Troponin I: 0.1

DDX: Inflammatory carcinoma, mastitis, superior vena cava syndrome, portal hypertension, pulmonary hypertension, pulmonary embolism.

Superior vena cava (SVC) syndrome results from any condition that leads to obstruction of blood flow through the SVC. Our case was caused by complete occlusion from a thrombus and the patient presented with bilateral breast swelling, skin changes (peau d’orange), and an increase in vascularity in the abdomen and chest (caput medusa). Breast tissue largely drains into the axillary veins, and more proximally into the subclavian veins. Due to occlusion of the SVC, a complete backup of venous flow occurs, resulting in all of the noted collateral hypervascularity.  Often SVC occlusion is caused by malignancy obstructing the superior vena cava or invading the vein.

The CTA demonstrates occlusion of the superior vena cava. There are multiple varices in the chest wall and the imaged upper abdominal wall. There is also diffuse subcutaneous edema with diffuse soft tissue swelling and skin thickening of the bilateral breasts.

Take-Home Points

  • Consider superior vena cava occlusion in patients undergoing hemodialysis who present with the above physical exam findings.
  • Consider occult malignancy as the source or cause of thrombosis.
  • Be sure to fully expose your patient when appropriate and keep your differential broad.

  • Corduff N, Rozen WM, Taylor GI. The superficial venous drainage of the breast: a clinical study and implications for breast reduction surgery. J Plast Reconstr Aesthet Surg. 2010 May;63(5):809-13. doi: 10.1016/j.bjps.2009.02.055. Epub 2009 Apr 3. PMID: 19345164.
  • Friedman T, Quencer KB, Kishore SA, Winokur RS, Madoff DC. Malignant Venous Obstruction: Superior Vena Cava Syndrome and Beyond. Semin Intervent Radiol. 2017 Dec;34(4):398-408. doi: 10.1055/s-0037-1608863. Epub 2017 Dec 14. PMID: 29249864; PMCID: PMC5730434.

Are Thrombolytics Safe for Acute Ischemic Strokes in Patients on DOACs?


Direct-acting oral anticoagulants (DOACs), including apixaban, rivaroxaban, edoxaban, and dabigatran, are widely used for various indications and considered first-line therapy for prevention of acute ischemic stroke in patients with nonvalvular atrial fibrillation [1]. The management of acute ischemic stroke in patients on DOACs presents a difficult clinical scenario in the emergency department due to concern for increased risk of hemorrhage. IV thrombolytics (e.g., alteplase, tenecteplase), a mainstay in acute ischemic stroke management, are not recommended in current guidelines for patients whose last DOAC dose was within the last 48 hours [2, 3]. Therefore, patients with an acute ischemic stroke who are compliant with their DOACs are often excluded from guideline recommended therapy. Additionally, as covered in a previous ALiEM post, it is not recommended to reverse anticoagulation status in order to administer a thrombolytic.


The use of IV thrombolytics in patients on DOACs was evaluated by Kam et al in a 2022 study published in JAMA [4]. This retrospective analysis included 163,038 patients from the AHA/ASA Get With The Guidelines-Stroke registry with acute ischemic stroke who received IV alteplase within 4.5 hours of symptom onset. Of the total number of patients, only 2207 had documented use of a DOAC within the last 7 days, with 25 of these patients reporting DOAC use within 48 hours. Patients on warfarin or other anticoagulants were excluded. The primary outcome was symptomatic intracranial hemorrhage (ICH) within 36 hours of IV alteplase administration. After adjusting for clinical factors, the rate of symptomatic ICH was not significantly different between patients taking DOACs and those not on anticoagulation (3.7% vs. 3.2%, adjusted OR 0.88, 95% CI 0.70 to 1.10). However, when stratified based on time from last DOAC dose, patients who took their DOAC 0-48 hours prior had an 8% rate of symptomatic ICH compared to 3.2% among those not on DOACs. Furthermore, the rate of any alteplase complication was 12% vs. 6% in those taking DOACs within 48 hours vs. no DOAC.


  • The population at highest risk for bleeding is patients who took a DOAC within the last 48 hours, and this study only included 25 such patients.
    • A similar study tried to answer the same question for warfarin patients with an INR between 1.5-1.7. They also failed to include enough patients to make any definitive conclusions. [5]
  • Timing from the last DOAC dose was given as a range, with the majority of patients reporting use sometime within the last 7 days. It has been established in current AHA/ASA guidelines that receipt of DOACs past 48 hours prior is considered safe for thrombolytic administration, and if the included institutions were following current recommendations, thrombolytics were likely administered mostly to patients outside the 48-hour window.
  • Large potential for selection bias, since it was reported that almost 23,000 patients on DOACs from the original registry (who were otherwise eligible) did not receive thrombolytics.
  • Not clear how patients were determined to be on DOACs or if the authors were able to confirm this in unresponsive/intubated/deceased patients retrospectively. This could have resulted in DOAC patients being included in the non-DOAC group, which could have falsely evened-out the bleeding rates.

Bottom Line

  • The management of acute ischemic stroke in patients receiving prior anticoagulation presents a challenging clinical scenario.
  • Studies to date fail to include enough patients to evaluate the true risk of bleeding.
  • This study supports the current guideline recommendation to avoid alteplase in patients receiving a DOAC within 0-48 hours due to the increased risk of intracranial hemorrhage.

Want to learn more about EM Pharmacology?

Read other articles in the EM Pharm Pearls Series and find previous pearls on the PharmERToxguy site.


  1. January CT, Wann LS, Calkins H, et al. 2019 AHA/ACC/HRS focused update of the 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation. Published correction appears in Circulation. 2019;140(6):e285. Circulation. 2019;140(2):e125-e151. doi: 10.1161/CIR.0000000000000665. PMID: 30686041.
  2. Powers WJ, Rabinstein AA, Ackerson T, et al. Guidelines for the early management of patients with acute ischemic stroke: 2019 update to the 2018 guidelines for the early management of acute ischemic stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2019;50(12):e344-e418. doi: 10.1161/STR.0000000000000211. PMID: 31662037.
  3. Berge E, Whiteley W, Audebert H, et al. European Stroke Organisation (ESO) guidelines on intravenous thrombolysis for acute ischaemic stroke. Eur Stroke J. 2021;6(1):I-LXII. doi: 10.1177/2396987321989865. PMID: 33817340.
  4. Kam W, Holmes DN, Hernandez AF, et al. Association of Recent Use of Non-Vitamin K Antagonist Oral Anticoagulants With Intracranial Hemorrhage Among Patients With Acute Ischemic Stroke Treated With Alteplase. JAMA. 2022;327(8):760-771. doi:10.1001/jama.2022.0948. doi: 10.1001/jama.2022.0948. PMID: 35143601.
  5. Xian Y, Liang L, Smith EE, et al. Risks of intracranial hemorrhage among patients with acute ischemic stroke receiving warfarin and treated with intravenous tissue plasminogen activator. JAMA. 2012;307(24):2600-2608. doi:10.1001/jama.2012.6756. doi: 10.1001/jama.2012.6756. PMID: 22735429.


Primary author:

Jessica Mason, PharmD

PGY-2 Emergency Medicine Pharmacy Resident

Massachusetts General Hospital

INR reduction with FFP – How low can you go?


Bleeding patients or those undergoing procedures that are at high risk of bleeding may require correction of their INR. Multiple products can be used to achieve this, including fresh frozen plasma (FFP). FFP contains many substances, including clotting factors, fibrinogen, plasma proteins, electrolytes, and anticoagulant factors. It is sometimes said that the intrinsic INR of FFP is approximately 1.6-1.7 and that it’s not possible to achieve a lower INR. This pearl will further explore these concerns.


  • What is the INR of FFP?
    • The mean INR of FFP appears to be ~1.1 (0.9-1.3) [1,2].
    • Reports that the intrinsic INR of FFP is 1.6-1.7 may be based on the clinical experience of not being able to achieve an INR <1.6-1.7 with FFP.
  • Is it possible to “normalize” the INR with FFP alone?
    • Several studies have found that it’s difficult to achieve an INR <1.7 with only FFP [3,4]. However, other studies were able to achieve lower average INR values [2,5,6]. 
    • Overall, these studies found that there was a significantly greater decrease in INR when the pre-FFP INR was higher, but there was a much smaller decrease when the INR was closer to the normal range.
  • Why does FFP appear to have diminishing returns when the pre-FFP INR is lower?
    • The relationship between the INR and percentage of clotting factors present in the blood is not linear (see figure) [7].
    • For example: An increase of ~5% in clotting factors may decrease the INR from 3 to 2.5 but the same amount of FFP may only reduce an INR of 1.7 to 1.6.

Figure 1: Adapted from Dzik  2012 [7].

    • Additionally, the table below also demonstrates that small volumes of FFP result in large changes when the initial INR is elevated, but very large amounts of FFP are required to achieve an INR of 1.3 no matter the initial INR (see table).
Amount of FFP to Achieve a Target INR Based on Pre-FFP INR
Target INR
Initial INRVolume (L)Dose (mL/kg)Factor (%)Volume (L)Dose (mL/kg)Factor (%)Volume (L)Dose (mL/kg)Factor (%)

Table 1: Adapted from Holland 2006 [3]. Note: 1 unit of FFP is ~200-250 mL

    • Given the above data, the issue preventing the achievement of an INR <1.7 appears to be the dose/volume of FFP required and not the intrinsic INR of FFP.
  • Does the INR need to be <1.7 to achieve hemostasis?
    • Since the INR only provides limited information regarding a single aspect of anticoagulation status, complete normalization for the INR to control bleeding is usually not necessary [6].
    • An INR elevation alone does not indicate a patient is coagulopathic or at an increased risk of bleeding [7]. Additionally, an INR elevation in patients with liver dysfunction likely reflects an overall state of decreased factor production, both procoagulant and anticoagulant factors [8].
    • The target INR varies depending on multiple patient factors and planned interventions, but an INR of 1.0 is likely not necessary to prevent bleeding or achieve hemostasis.

Bottom Line

  • A unit of FFP has an INR of ~1.1, but this doesn’t mean it can easily normalize the INR.
  • There is a non-linear relationship between percentage of clotting factors and the INR, resulting in diminishing returns from each unit of FFP as the INR decreases.
  • Very large doses of FFP may be required to fully correct an elevated INR, which frequently precludes its use.
  • Complete normalization of the INR is not required to achieve hemostasis or prevent bleeding from a procedure.

Want to learn more about EM Pharmacology?

Read other articles in the EM Pharm Pearls Series and find previous pearls on the PharmERToxguy site.


  1. Holland LL, Foster TM, Marlar RA, Brooks JP. Fresh frozen plasma is ineffective for correcting minimally elevated international normalized ratios. Transfusion. 2005;45(7):1234-1235. doi: 10.1111/j.1537-2995.2005.00184.x. PMID: 15987373.
  2. Only AJ, DeChristopher PJ, Iqal O, Fareed J. Restoration of normal prothrombin time/international normalized ratio with fresh frozen plasma in hypocoagulable patients. Clin Appl Thromb Hemost. 2016;22(1):85-91. doi: 10.1177/1076029614550819. PMID: 25294634.
  3. Holland LL, Brooks JP. Toward rational fresh frozen plasma transfusion: The effect of plasma transfusion on coagulation test results. Am J Clin Pathol. 2006;126(1):133-139. doi: 10.1309/NQXH-UG7H-ND78-LFFK. PMID: 16753596.
  4. Abdel-Wahab OI, Healy B, Dzik WH. Effect of fresh-frozen plasma transfusion on prothrombin time and bleeding in patients with mild coagulation abnormalities. Transfusion. 2006;46(8):1279-1285. doi: 10.1111/j.1537-2995.2006.00891.x. PMID: 16934060.
  5. Müller MCA, Straat M, Meijers JCM, et al. Fresh frozen plasma transfusion fails to influence the hemostatic balance in critically ill patients with a coagulopathy. J Thromb Haemost. 2015;13(6):989-997. doi: 10.1111/jth.12908. PMID: 25809519.
  6. McCully SP, Fabricant LJ, Kunio NR, et al. The International Normalized Ratio overestimates coagulopathy in stable trauma and surgical patients. J Trauma Acute Care Surg. 2013;75(6):947-953. doi: 10.1097/TA.0b013e3182a9676c. PMID: 24256665.
  7. Dzik W “Sunny.” Reversal of drug-induced anticoagulation: old solutions and new problems. Transfusion. 2012;52(s1):45S-55S. doi: 10.1111/j.1537-2995.2012.03690.x. PMID: 22578371.
  8. Harrison MF. The misunderstood coagulopathy of liver disease: a review for the acute setting. West J Emerg Med. 2018;19(5):863-871. doi: 10.5811/westjem.2018.7.37893. PMID: 30202500.
By |2021-08-28T10:03:39-07:00Aug 21, 2021|EM Pharmacy Pearls, Heme-Oncology|
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