EM@3AM: Uterine Perforation

Authors: Nour Sino, MD (Department of Emergency Medicine, Western Michigan University Homer Stryker M.D. School of Medicine, Kalamazoo, Michigan) and Glenn Ekblad, DO, MSN, (Clinical Assistant Professor, Department of Emergency, Medicine Western Michigan University Homer Stryker M.D. School of Medicine, Kalamazoo, Michigan) // Edited by: Alex Koyfman, MD (@EMHighAK) and Brit Long, MD (@long_brit)

Welcome to EM@3AM, an emDocs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.

A 31 y/o female presents to the ED for acute lower abdominal pain that she rates at a 10/10. Six hours prior to arrival, the patient had a D&C for an elective abortion at 15 weeks gestation. She had a prior caesarean section two years ago. She has intermittent nausea but no vaginal bleeding, and she denies any recent blunt trauma.

VS: T: 98.8, HR 107, RR 20, BP 102/76, SpO2 98% on room air

Physical exam: Patient appears uncomfortable due to pain. There is tenderness to palpation in the suprapubic region, with guarding. Pelvic exam reveals scant vaginal blood and small clots present in the vaginal vault. Cervical-os is 1cm dilated, without active bleeding. There is no significant adnexal tenderness or cervical motion tenderness.

What is the diagnosis?

What is your next step for evaluation?

What is your management?

Diagnosis: Uterine Perforation

Uterine perforation is rare and usually occurs as a complication of intrauterine procedures such as IUD placement, D&C, or hysteroscopy.

– Incidence of 0.1-0.5% and seen mainly in postmenopausal women with a gynecological malignancy.5

– Risk factors for perforation include an inexperienced clinician performing intrauterine procedure, advanced age, increased parity, increased gestational age during D&C, and obesity.2

– Uterine perforation and bowel injuries are the major complications following unsafe abortions.7

– Incidence of uterine perforation with IUD insertion is 1 in 1,000 insertions.4

– The most common perforated site with D&C is the fundus, which is relatively avascular when compared to the lateral body and cervix.1

– May also occur spontaneously from a pyometrium, which is an accumulation of pus in the uterine cavity blocking drainage from the cervix.

– Complete perforation occurs through all uterine layers (endometrium, myometrium, and serosa), as compared to partial.4

– Complications include perforation into bowel wall or urinary tract (ureter and/or bladder), and hemoperitoneum.4,1

– Unrecognized uterine perforation may result in postoperative abdominal or pelvic pain beyond what is expected for post-operative recovery.3

– Differential diagnosis includes intra-abdominal pathology (abscess, infection, obstruction, etc.), PID, cystitis, torsion, stone, endometriosis, urinary retention, and uterine fibroid.8


Presentation: Heavy vaginal bleeding, abdominal distension, abdominal or pelvic pain, hematuria, nausea, and vomiting.3

Exam: Patients may present with varying symptoms and exam findings. Tachycardia, hypotension, fever, abdominal distension, rebound or guarding, abdominal tenderness, and vaginal bleeding can occur.



  • Vital signs – monitor for tachycardia, hypotension, and tachypnea suggesting shock.
  • Abdominal exam – tenderness to palpation, peritoneal signs.
  • Pelvic exam – evaluate for vaginal bleeding, adnexal tenderness, mass, foreign bodies, IUD threads, or cervical motion tenderness.
  • Laboratory studies – consider CBC, CMP, urinalysis, PT/INR and aPTT, lactic acid, pregnancy test, type and screen.
  • Hemodynamically stable patients – Pelvic U/S is the imaging modality of choice. 1,4 *Note that perforation cannot be excluded or confirmed with any imaging study. Diagnosis is made primarily on clinical suspicion.7
  • If bladder or ureter injury is suspected, evaluate with intravenous urography and/or CT urography.6



– IV fluids, antiemetics, pain control, and blood products if necessary.

– Immediately consult for surgical exploration if: patient is hemodynamically unstable, intraperitoneal contents such as bowel or omentum are found at the cervix, there is suspicion for bowel injury, lateral wall perforation with uterine vessel injury.2

– Hemodynamically stable: OB/GYN consultation; Patients with no evidence of hemorrhage can be safely monitored without surgical exploration.2  Antibiotics are not indicated unless there is suspicion for infectious process (i.e. endometritis, peritonitis).

Antibiotics (a variety of options are available):

– Peritonitis: Ceftriaxone 1g IV daily and Flagyl 500mg IV q8hrs.

– Endometritis: Post-partum: Clindamycin 900mg q8hrs and Gentamicin 1.5mg/kg q8rs; Non-pregnant inpatient: Cefoxitin 2g IV q6hrs and Doxycycline 100mg PO/IV BID OR Outpatient: Ceftriaxone 250mg IM once and doxycylcine 100mg BID.      



– Maintain a high index of suspicion for uterine perforation with recent intrauterine procedure or manipulation.

– Early OB/GYN consultation is critical.

– Surgical exploration is warranted when there is hemodynamic instability, intraperitoneal contents such as bowel or omentum are found at the cervix, suspicion for bowel injury, lateral wall perforation with uterine vessel injury.2


References/Further Reading:

  1. Seol, H. J., & Ki, K. D. (2015). Rupture of uterine serosal hematoma: Delayed complication of uterine perforation.Clinical and experimental obstetrics & gynecology,42(3), 388-389.
  2. Patounakis, G., & Schlaff, W. (2012). Management of Uterine Perforation.Postgraduate Obstetrics & Gynecology,32(23), 1-7. doi:10.1097/01.pgo.0000425901.51473.a3
  3. Lobo, R. A., Gershenson, D. M., Lentz, G. M., & Valea, F. A. (2017). Endoscopy: Hysteroscopy and Laparoscopy: Indications, Contraindications, and Complications. Comprehensive Gynecology (190-204). Philadelphia, Pennsylvania: Elsevier.
  4. Rowlands, S., Oloto, E., & Horwell, D. (2016). Intrauterine devices and risk of uterine perforation: current perspectives.Open Access Journal of Contraception,19. doi:10.2147/oajc.s85546.
  5. Kutuk, M., Ozgun, M., & Uludag, S. (2013). Spontaneous uterine perforation due to pyometra.Journal of Obstetrics and Gynaecologoy ,33(3), 322-323. http://dx.doi.org.ezproxy.med.wmich.edu/10.3109/01443615.2012.754415.
  6. Esparaz, A. M., Pearl, J. A., Herts, B. R., LeBlanc, J., & Kapoor, B. (2015). Iatrogenic Urinary Tract Injuries: Etiology, Diagnosis, and Management.Seminars in Interventional Radiology,32(2), 195–208. http://doi.org/10.1055/s-0035-1549378.
  7. Sama, C., Aminde, L., & Angwafo, F. (2016). Clandestine abortion causing uterine perforation and bowel infarction in a rural area: a case report and brief review. BMC Research Notes. 9:98. doi 10.1186/s13104-016-1926-5 https://www.ncbi.nlm.nih.gov/pubmed/26880002
  8. Hang, B., Abnormal Uterine Bleeding, Ch 96, pages 619-625, in Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, Ed by J.E. Tintinalli, et at., 8th Ed., Pub 2016, ISBN: 978-0-07-179476-3.


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Originally published at Pediatric EM Morsels on September 2, 2016, updated on July 23, 2017. Reposted with permission.

Follow Dr. Sean M. Fox on twitter @PedEMMorsels

Brief Resolved Unexplained Events

We have previously explored some issues with one of my “favorite” topics: Apparent Life Threatening Events (See ALTE and Never Trust a Neonate).  Recently, it has been recommended that the term “Apparent Life Threatening Event / ALTE” be removed from our medical lexicons.  Since we like to always stay in style and remain “hip and with it” (said in the voice of Dr. Evil), let’s review what the cool kids will be referring to in the future: Brief Resolved Unexplained Event / BRUE.


BRUE: What’s in a name?

  • We have known that the definition of an ALTE is imprecise at best.
    • This leads to challenges in studying the entity as a whole.
    • This also leads to many challenges with its evaluation and management.
    • “Life Threatening” also seems to generate confusion when the family is then told “everything is ok.”
  • Brief Resolved Unexplained Events” is the term now recommended to be used.
    • It aims to be more precise (at least it has age limits).
    • It highlights the reassuring qualities of the “typical” episode: Brief and Resolved.
    • The clinical practice guideline also defines “Lower Risk” patients.


BRUE: What is it?

  • BRUE describes an event that:
    • Occurs in a child younger than 1 year of age,
    • Lasts less than 1 minute (typically 20-30 seconds),
    • Has one or more of the following:
      • Central Cyanosis or Pallor 
        • Discoloration of face, gums and/or trunk.
        • Not acrocyanosis or only peri-oral cyanosis
        • Not rubor / redness
      • Absent, Decreased, or Irregular breathing
      • Marked change in tone (hypertonia or hypotonia)
      • Altered level of responsiveness
    • Resolves and patient returns to baseline, and
    • Has a reassuring history, physical exam, and vital signs during ED evaluation.
  • BRUE is used only when another condition cannot be discerned as the etiology of the event.
    • BRUE is still a constellation of symptoms that, in the end, may be attributed to a more specific diagnosis, but if you can be more specific at the outset, then do not label as BRUE.
      • For example, if a child has bronchiolitis and had an apneic event, that is not a BRUE… it is apnea associated with bronchiolitis.
      • Additionally, if the child a choking event, this is not a BRUE either. Maybe it is a T-E fistula…
    • A good goal is to attempt to use the H+P to determine a more precise Ddx rather than BRUE.


BRUE: Low Risk?

  • There are characteristics of patients at Lower Risk for having a serious underlying condition.
  • Lower Risk criteria:
    • Older than 60 days
    • Gestational Age 32 weeks or greater and a Postconceptional Age of 45 weeks or greater.
    • First BRUE (no previous BRUE ever and not occurring in clusters)
    • Not requiring CPR by a trained medical provider
    • NO concerning historic features 
      • See Guideline’s Table 2 for long list of features to consider [Tieder, 2016]
      • Some features not to overlook:
        • History concerning for potential Abuse.
        • Family history of sudden death in first degree relatives.
        • Social and Environmental issues
          • House mold problems (yes… mold is listed as a concerning feature)
          • Previous Child Protective Services or Law Enforcement involvement
          • Current level of concern/anxiety of family
    • NO concerning physical examination findings
      • Obviously, these children need a thorough physical exam… use your super sleuth skills.
      • Don’t overlook skin and genital exam.
  • If the patient does not meet Lower Risk criteria, then she/he is High Risk by default!


BRUE: What to do?

  • This is similar to what we would have done for ALTE.
  • There is a nice diagram in the Guideline’s… [Tieder, 2016]
  • But I’m simple so…
  • Medical Stabilization! 
    • Don’t forget, little neonates can be tricky and deceptive. Check capillary refill!
    • Check a glucose early! (I say this mostly so I don’t forget!)
  • History and Physical
    • The foundation upon which we build all medical decisions
    • Abnormal vital signs? H+P consistent with a specific diagnosis? – NOT a BRUE.
    • H+P meets BRUE criteria? No other explanation? – It’s a BRUE! (yeah)
      • Even if BRUE, consider the broad Ddx that exists
      • Try to narrow down the most likely culprits to help guide evaluation and work-up.
        • Cardiac vs Pulmonary
        • Neuro vs GI
        • Zebras vs Horses
  • Risk Stratify BRUE
    • This is simple… does the patient fit Lower Risk criteria?
      • Yes! = Lower Risk
      • No! = High Risk
    • Realize that Lower Risk does not equate to “No Risk.”
  • Disposition
    • High Risk
      • Hospitalize.
      • Base initial evaluation upon your assessment of most likely culprits on DDx.
        • Neonate doing weird things? –> LP and start antibiotics
        • “Funny” story that changes? –> Head CT and evaluate for NAT
      • We know that indiscriminate, broad work-ups are not useful.
    • Lower Risk
      • Avoid:
        • Indiscriminate labs and imaging studies – not helpful in this group either.
        • Empirically prescription of GI meds (ex, acid suppression medications) -unless you are diagnosing the episode was GER… in which case it is not a BRUE.
        • Admission solely for CardioPulmonary monitoring.
      • Do:
        • It is reasonable to obtain 12 Lead ECG.
        • Some advocate for pertussis testing.
        • Monitor the child in the ED and perform serial exams[Tieder, 2016]
          • 1-4 hours seems “reasonable” – no solid evidence
          • Establish stability of vital signs and exam.
          • May witness another event that assists in the diagnosis.
        • Educate family
          • Discuss BRUE.
          • Discuss CPR training for families.
          • Engage in shared decision making.
        • If, and only if, the stars align and the child can be discharged safely and the family is comfortable, ensure ability to bere-evaluated within the next 12-24 hours.


BRUE: What’s new?

Admittedly, this is my humble opinion (feel free to gently disagree with me… my feelings are fragile).

  • Essentially, I do not see this change in terminology as a huge alteration in my current practice.
    • I like the term BRUE as it accentuates the Brief and Resolved nature, but fear that that may also diminish provider’s vigilance.
    • “BRUE” should not equate to no concern, even though it does offer a pathway to actually discharge some.
    • Remember, being vigilant most often only requires a thorough H+P.
  • First and foremost: NEVER TRUST A NEONATE!
    • Similar to what we worried about with ALTE, BRUE in a neonate is concerning for badness!
    • Neonates are, by definition, High Risk kids in BRUE criteria.
  • Use your super sleuth skills for the history and exam – Is this a BRUE or something else that is Brewing (get it?).
  • Don’t order a million tests. Direct initial evaluation toward what your super sleuth skills have determined to be the most likely etiology of the event.
  • What’s new is the fact that there is now a guideline that supports the potential discharge of a LOWER RISK patient who has had a BRUE.
    • This does not mean all lower risk kids get to go home.
    • Part of the lower risk characteristics is the family’s perspective of the event.  It may be counterproductive to argue with a family that their CPR was not necessary and the kid is safe at home. (Yes, CPR provided by untrained personnel (ex, family) would still qualify as being Lower Risk potentially).
    • Often, the story and exam evolves… many times before your eyes… use observation in the ED in cases where you are unsure.


FOR ANOTHER PERSPECTIVE, See Dr. May’s post on St. Emlyns.



Tieder JS, Bonkowsky JL, Etzel RA, Franklin WH, Gremse DA, Herman B, Katz ES, Krilov LR, Merritt JL 2nd, Norlin C, Percelay J, Sapién RE, Shiffman RN, Smith MB; SUBCOMMITTEE ON APPARENT LIFE THREATENING EVENTS. Brief Resolved Unexplained Events (Formerly Apparent Life-Threatening Events) and Evaluation of Lower-Risk Infants. Pediatrics. 2016 May;137(5). PMID: 27244835. [PubMed] [Read by QxMD]
Tieder JS, Bonkowsky JL, Etzel RA, Franklin WH, Gremse DA, Herman B, Katz ES, Krilov LR, Merritt JL 2nd, Norlin C, Percelay J, Sapién RE, Shiffman RN, Smith MB; SUBCOMMITTEE ON APPARENT LIFE THREATENING EVENTS. Brief Resolved Unexplained Events (Formerly Apparent Life-Threatening Events) and Evaluation of Lower-Risk Infants: Executive Summary. Pediatrics. 2016 May;137(5). PMID: 27244836. [PubMed] [Read by QxMD]

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Budd Chiari Syndrome: ED Presentation, Evaluation, and Management

Authors: Rukayat Balogun, MD (Transition Year Resident, San Antonio, TX) and Josh Oliver, MD (EM Attending Physician, San Antonio, TX) // Edited by: Alex Koyfman, MD (@EMHighAK) and Brit Long, MD (@long_brit)

The views expressed are those of the authors and do not reflect the official views or policy of the Department of Defense or its Components.


A 46-year-old female presents to your ED with a complaint of abdominal pain and fullness. She said this started about two weeks ago and has been getting worse. She describes the pain as dull, achy, and constant that localizes to the right upper quadrant. Review of systems reveals a 15-pound weight gain over the same time period. Most of her family is healthy and still living, but one of her sisters takes a medication to prevent blood clots. She denies drinking alcohol. Physical exam reveals a positive fluid wave.1

What is your leading diagnosis; what should your next steps in treatment be?

Answer: Budd-Chiari syndrome


The liver is one of the most metabolically active organs in our body, and as such it is particularly susceptible to vascular insults. In Budd-Chiari syndrome (BCS), obstruction of the liver circulation usually occurs at the level of the hepatic veins and inferior vena cava.2 Presentation of the syndrome may be fulminant, acute, subacute, or chronic.2, 12 Fulminant BCS can be defined by severe and rapid onset of right upper quadrant pain, hepatomegaly, ascites, coagulopathy, and encephalopathy; it typically involves blockage of all hepatic veins at the same time.  BCS of acute onset presents similarly to fulminant but is less severe and rapid in onset as it may take weeks to develop. Encephalopathy is not characteristic of acute presentation.12 In subacute BCS, signs and symptoms will have been present for less than six months, while chronic BCS for greater than six months. Formation of collateral hepatic circulation and development of varices are signs that will only be seen in subacute and chronic forms of BCS.1 In chronic presentation, spider angiomata and palmar erythema may also be present. Keep in mind that the majority of cases will be subacute to chronic. However, it is especially important to pick up on fulminant presentations, as they can be fatal without prompt intervention.12


Epidemiological information about BCS is limited. Several studies in Europe give estimates of 0.4-0.8 patients per million per year and found it affects women more than men from ages 30-49.9,14 In contrast, a study done in Japan indicated there was a slight male predominance and an incidence of 0.2 per million in 1989.10 More recently, a Chinese study published in 2015 also demonstrated a male predominance and showed an incidence of 0.88 per million from 1990-2013.11 The pediatric population is also affected by BCS, and epidemiologic data on this population is even more scarce than in adults, though it also demonstrates a male predominance.4


Cases of BCS have been described to be primary or secondary. Primary causes are usually due to hypercoagulable states, while secondary causes are caused by extravascular obstruction or different types of liver disease. Table 1 contains a breakdown of potential causes.

In general, it is important to note that hypercoagulable states have been associated with 75% of cases of BCS and should be considered when investigating a patient presenting with this syndrome.1, 3


Presentation of patients with this syndrome will vary based on the acuity. Fulminant and acute afflictions of BCS will appear very similar to patients who are in acute liver failure. As noted in the introduction section, most cases of BCS are subacute or chronic. Be on the lookout for patients with abdominal pain, abdominal fullness, organomegaly, ascites, jaundice, and a history of hypercoagulable states in addition to changes in dietary habits, nausea, and vomiting, as these will be present in the most common BCS presentations.3


Pattern recognition is paramount in quickly diagnosing this syndrome. A patient presenting with right upper quadrant tenderness, signs of portal hypertension (e.g. ascites, abdominal varices, esophageal varices, anal varices), and liver failure may be important clues to quick diagnosis. Although it is not the job of the emergency physician to determine the exact cause of the syndrome, knowing some of the more common causes can speed up diagnosis and disposition. Presence of any of the conditions mentioned in Table 1 can also be considered risk factors for development of BCS.


Imaging: Right upper quadrant ultrasound (RUQUS) is often the first imaging modality ordered, which offers a great deal of information about hepatic vasculature. It has been estimated to have a sensitivity and specificity of 85% for diagnosing Budd-Chiari syndrome. Findings seen on RUQUS that help to support the diagnosis of BCS are formation of hepatic collaterals, obstruction or stenosis of the hepatic veins, non-visualization of the hepatic veins, diminished or absent blood flow in hepatic veins, hypertrophy of the caudate lobe of the liver, and narrowing of the inferior vena cava. Computed tomographic scanning (CT) and magnetic resonance imaging (MRI) also options for imaging that may display similar findings.

CT scan is very useful for obtaining anatomical information about the liver and its venous blood supply network. Because of the liver’s unique vascularization, the CT scan should be ordered with IV contrast, especially in the case of chronic BCS. Patchy enhancement of liver tissue (nutmeg liver; Figure 2) and hyperattenuation of regenerated nodules in the arterial phase and in the portal phase may be present.15, 16

MRI has an estimated sensitivity and specificity of 90% and is effective for assessing hepatic venous flow and for visualization of the inferior vena cava.3,8  It is more expensive than CT, time-consuming, and may not be readily available at all facilities. These reasons make MRI less appealing than RUQUS and CT for assessment of BCS.

Hepatic venography is the gold standard for diagnosis, but this should only be ordered if RUQUS, CT, and MRI are negative and clinical suspicion is high. 1, 3 Expect to see “spider web” pattern (Figure 1), which indicates formation of collateral circulation between the distal portions of the hepatic veins and the liver capsule, for confirmation of BCS on venography.3

Labs/Procedures: Patients presenting with this constellation of symptoms should be investigated with laboratory tests that focus on liver function and coagulation. Proper work up should include comprehensive metabolic panel, ammonia, coagulation panel, and complete blood count with differential. Expect the patient to have non-specific increases liver enzymes, alkaline phosphate, and bilirubin. In fulminant and acute presentations, serum aspartate and alanine aminotransferase may be more than five times the upper limit of normal. 1, 3 Mild to moderate elevations of these enzymes will be seen in subacute and chronic cases of BCS.13 A hepatitis panel and drug levels for hepatotoxic agents can also be ordered to evaluate for conditions that may mimic BCS.

In cases where abdominal compartment syndrome or spontaneous bacterial peritonitis is suspected, a diagnostic/ therapeutic paracentesis can be performed. If this procedure is performed, be sure to include serum-ascites albumin gradient, cytology, culture, and gram stain of peritoneal fluid. More specific laboratory tests (e.g. factor V Leiden, protein C, protein S, anticardiolipin, antithrombin, etc) can be deferred to the specialist or the inpatient team.

Special Populations

Pediatrics: Budd-Chiari syndrome does not discriminate, as it may also present in the pediatric population. Similar to adults, a small study conducted at a hospital in the United Kingdom suggests that hypercoagulable states are present in 66% of children presenting with this syndrome. With rapid diagnosis, treatment, and coordinated specialist care the long-term outlook is favorable, however, any delay in diagnosis can leaded to high morbidity. 4

Pregnancy: Pregnancy and the post-partum state are known risk factors for developing Budd-Chiari syndrome and may complicate existing disease in women who desire to become pregnant. For expectant mothers, an observational study showed that maternal outcome is good after the diagnosis of the syndrome. Additionally, the study found that in patients who have established Budd-Chiari syndrome, pregnancy is not contraindicated if the disease process is stable. 5


Goals of treatment may vary depending on patient presentation but should always include liver decompression to prevent further injury and reduction of ascites; in those who have an associated hypercoagulable state this should also be addressed.1 Aggressive management of fulminant presentations of Budd-Chiari syndrome may include urokinase or tissue plasminogen activator in addition to admission for surgical management.3 Patients who present acutely will likely need admission for surgical intervention (e.g. portosystemic shunt, transplant) or gastroenterology consult along with medical management. For those who present with subacute or chronic case of Budd-Chiari syndrome, they may be able to be discharged with the appropriate medical management, which includes diuretics and anticoagulants, fluid and salt restriction, and regular follow up.3, 6-8 In all cases, surgical and medical management should be tailored to the needs of the patient with the rapid achievement of the aforementioned goals in consideration. Since most cases are associated with hypercoagulable state, it is reasonable to anticoagulate patients initially as long as there are no contraindications and the patient has follow up for reassessment. The same is true of diuretics. Listed below are some of the pharmacologic options with suggested dosing for the treatment of BCS.

Urokinase 240,000U/hour for 2 hours3

Tissue plasminogen activator 0.5-1.0mg/hour for 24 hrs3, 8

Heparin titrate to INR 2-2.5 for use prior to warfarin3

Warfarin titrate to INR 2-2.53, 8

Spironolactone 100mg daily (can titrate every 3-5 days based on clinical fluid status; max dose 400mg) 6, 7

Furosemide 40mg daily (can titrate every 3-5 days based on clinical fluid status; max dose 160mg) 6, 7

Key Points

– Budd Chiari is a rare syndrome that is usually associated with a hypercoagulable state.

Paracentesis may support diagnosis and be therapeutic to the patient.

– Treatment of this syndrome can be managed medically but may require surgical intervention.

– Be wary of other serious conditions that may mimic this syndrome such as: constrictive pericarditis, tricuspid insufficiency, right atrial myxoma, congestive heart failure, hepatitis, and cholecystitis.3


References/Further Reading

  1. Raymond T. Chung MD, A. J. I. M. P., Philip C. Amrein MD, Dushyant V. Sahani MD, Joseph Misdraji MD (2006). “Case 15-2006: A 46-year-old Woman with Sudden Onset of Abdominal Distension.” New England Journal of Medicine 354(20): 2166-2175.
  2. Walter L Kemp MD, D. K. B. M., Travis G Brown MD (2008). Pathology: The Big Picture, McGraw-Hill Education.
  3. K. V. Narayanan Menon MD, V. S. M., Patric S Kamath MD (2004). “The Budd-Chiari Syndrome.” The New England Journal of Medicine 350(6): 578-585.
  4. Susana Nombre, R. K., Eirini Kyrana, Sue Height, John Karani, Pauline Kane, Nigel Heaton, Anil Dhawan (2017). “Primary Budd-Chiari Sundrom in Children: King’s College Hospital Experience.” Journal of Pediatric Gastroenterology & Nutrition 65(1): 93-96.
  5. Faisal Khan, I. R., Bill Martin, Ellen Knox, Tracey Johnston, Charlie Elliot, Will Lester, Frederick Chen, Simon Olliff, Homoyon Mehrzad, Zergham Zia, Dhiraj Tripathi (2017). “Outcomes of prenancy in patients with known Budd-Chiari Syndrome.” World Journal of Hepatology 9(21): 945-952.
  6. Justiniano Santos, R. P., Albert Pardo, Rosa Durandez, Eduard Cabre, Rosa Maria Morillas, Maria Luisa Granada, Jose Angel Jimenez, Enrique Quintero, Miquel Angel Gassull (2003). “Spironolactone alone or in combination with furosemide in treatment of moderate ascites in nonazotemic cirrhosis. A randomized comparative study of efficacy and safety.” Journal of Hepatology 39: 187-192.
  7. Runyon, B. A. (2012). “Management of Adult Patients with Ascites due to Cirrhosis.” The American Association for the Study of Liver Disease: 66-67.
  8. A.V. Kyriakidis, I. V., M. Pyrgioti (2008). “Budd-Chiari Syndrome.” Annals of Gastroenterology 21(4): 223-228.
  9. R Rajani, S. A. (2009). “Incidence and prevalence rates in Budd–Chiari syndrome.” Gut 58(6): 889.
  10. Valla, D.-C. (2008). “Budd–Chiari syndrome and veno-occlusive disease/sinusoidal obstruction syndrome.” Gut 57: 1469-1478.
  11. Wei Zhang, X., Xitong Zhang, Hongying Su, Hongshan Zhong, Jingpu Shi, and Ke Xu (2015). “Budd-Chiari Syndrome in China: A Systematic Analysis of Epidemiological Features Based on the Chinese Literature Survey.” Gastroenterology Research and Practice 2015: 1-8.
  12. Marvin H. Sleisenger, J. S. F. (1998). Gastrointestinal and Liver Disease: Pathophysiology/diagnosis/management, W.B Saunders Company.
  13. Lee Goldman MD, A. I. S. M. (2012). Goldman’s Cecil Medicine, Elsevier.
  14. Rupesh Rajani, T. M., Einar Bjonsson, Ulrika Broome, Per Sangfelt,Ake Danielsson, Anders Gustavsson, Olof Grip, Hans Svensson, Lars Loof, Sven Wallerstedt and Sven HC Almer (2009). “Budd-Chiari syndromeinSweden: epidemiology, clinical characteristics and survival-an 18-year experience.” Liver International 29(2): 253-259.
  15. Hector Ferral, G. B., Jorge Lopera (2012). “Budd-Chiari Syndrome.” American Journal of Roentgenology 199: 737-745.
  16. Giuseppe Brancatelli, V. V., Michael P. Federle, Antoine Hakime, Roberto Lagalla, Riccardo Iannaccone, Dominique Valla (2007). “Budd-Chiari Syndrome: Spectrum of Imaging Findings.” American Journal of Roentgenology 188(2): W168–W176.


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