Tag Archives: ob-gyn

Tachycardic Arrhythmias in Pregnancy: Management

Author: Jennifer Robertson, MD, MSEd (Assistant Professor, Emory University, Atlanta GA) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

Case 1: A 37 yo G1P0 female at approximately 17 weeks gestational age presents to the emergency department (ED) with a chief complaint of a racing heart.  She denies any past medical history. Her heart rate is 180 beats per minute (bpm) but otherwise her vital signs are within normal limits. She denies chest pain. Her electrocardiogram (EKG) is shown below:

ekg1

http://emedicine.medscape.com/article/156670-overview

Case 2:  A 21 year old G1P0 female at approximately 16 weeks gestational age presents with a chief complaint of syncope. She arrives to the ED with a complaint of lightheadedness but is alert and oriented and able to converse. She does complain of some mild chest pain. Her heart rate is 160 bpm and her blood pressure is 85/60 mmHg. Her other vital signs are within normal limits.

ekg2

http://lifeinthefastlane.com/ecg-library/rvo/

Case 3: A 40-year-old G4P3 female at approximately 12 weeks gestational age presents after feeling palpitations for the last several days. She denies chest pain, syncope or shortness of breath. She denies any past medical history and denies taking any medications. Her initial heart rate is 165 bpm (irregular) and her blood pressure is 130/80 mmHg. Her EKG is shown as follows:

ekg3

http://misc.medscape.com/pi/iphone/medscapeapp/html/A156670-business.html

Introduction

Compared to the non-pregnant population, cardiac arrhythmias are rare in pregnancy, with an incidence of about 1.2 per 1000 pregnant women (1). However, they can negatively affect the health of both the mother and child, especially if they lead to hypoperfusion. Thus, emergently addressing them is important. Additionally, it is important to understand that the management of arrhythmias in pregnancy may vary considerably from the non-pregnant patient due to the potential effects of anti-arrhythmic medications and electrical therapy with sedation (2). Thus, this is a brief review of the evaluation and management of the pregnant patient who may present to the emergency department with a tachy-arrhythmia. Pathologic bradycardia is very rare in pregnancy and will not be covered in this current article (3).

General Physiology: Brief Review

Arrhythmias in pregnancy can be due to a number of causes including congenital heart disease, channelopathies, and other structural heart diseases (3). Examples include Wolff Parkinson White Disease, pulmonary hypertension, Marfan syndrome with a dilated aortic root, arrhythmogenic right ventricular dysplasia, and even coronary artery disease (4,5).  They can also be due to reasons that are commonly seen in non-pregnant patients such as idiopathic, infection/sepsis, electrolyte abnormalities, medications, toxins, pulmonary emboli and hyperthyroidism (2,6,7). Similar the general population, these causes should also be considered when evaluating for the underlying cause of the arrhythmia (6, 7).

For some pregnant patients, an arrhythmia may be recurrent from a previously diagnosed cardiac disease or a first-time presentation. Due to the many physiologic changes and stresses on the cardiovascular system, pregnancy can provoke arrhythmias in some women with undiagnosed structural heart disease (s) (4). In addition, in women with known tachy-arrhythmias, pregnancy may cause an increased risk of recurrence or worsening of the dysrhythmia (3, 7). A thorough family and personal history of structural heart disease should be obtained in addition to a family history of sudden or unexplained death (3).

Palpitations are usually benign and life threatening arrhythmias are rare in pregnant patients (1, 3, 7, 8), but evaluation for more serious arrhythmia is always necessary from an emergency medicine standpoint. As previously mentioned, assessing for underlying reversible causes such as infection, hyperthyroidism and toxins is important. However, if no underlying cause can be found and/or if the patient is unstable, then medical and/or electrical management is warranted.

Unstable Rhythms

In any unstable patient, the American Heart Association (AHA) makes the following recommendations (all Level C recommendations-consensus opinion of experts, case studies or standard of care) (9):

(a) Place the patient in the full left lateral decubitus position to relieve aortocaval compression.

(b) Administer 100% oxygen by facemask to treat and prevent hypoxemia.

(c) Ideally, intravenous (IV) access should be established above the diaphragm to ensure that medications can be adequately distributed into the circulation (not obstructed by the gravid uterus)

(d) Evaluate for any underlying causes of the patient’s symptoms.

Please review the following article for any specifics about cardiac arrest in pregnancy:

Jeejeebhoy FM, Zelop CM, Lipman S, Carvalho B, Joglar J, Mhyre JM, Katz VL, Lapinsky SE, Einav S, Warnes CA, Page RL. Cardiac Arrest in Pregnancy A Scientific Statement From the American Heart Association. Circulation 2015; 132(18):1747-73.

However, just as in non-pregnant patients with an unstable tachycardia causing hemodynamic compromise, immediate direct current (DC) cardioversion is indicated (1, 2, 10, 11). Overall, DC cardioversion has been found to be safe in all trimesters of pregnancy, but it does carry a small risk of inducing a fetal arrhythmia (3). Therefore, it is strongly recommended that when possible, cardioversion should be conducted with concurrent fetal monitoring and emergency caesarean section (C-section) availability (1, 3, 6, 12).  Women in later stages of pregnancy should have their pelvis tilted to the left to relieve compression of the vena cava, however the process, including the dosing of electricity, is otherwise the same as in non-pregnant patients (3, 7, 13). Higher doses of energy (up to 360J) in refractory cases still remains safe for both the mother and fetus (13).

Medication options for sedation (for cardioversion):

This article is also not intended to be a review of safe sedation in pregnancy. However, some excellent articles on sedation in pregnancy include:

Neuman G, Koren G. MOTHERISK ROUNDS: Safety of Procedural Sedation in Pregnancy. J Obstet Gynaecol Can 2013; 35(2):168-73.

Shergill AK, Ben-Menachem T, Chandrasekhara V, et al. Guidelines for endoscopy in pregnant and lactating women. Gastrointest Endosc. 2012; 76(1):18-24.

Stable Tachyarrhythmias

The majority of arrhythmias during pregnancy are stable and can be managed with conservative therapies (7). Medication therapy should be considered in patients who are symptomatic and/or have tachyarrhythmias that may lead to negative hemodynamic or physiologic complications (7). Of course, any significant acute hemodynamic compromise should lead the provider to consider cardioversion, as mentioned in the above section (14)

In addition, as previously discussed, a thorough history and physical should be conducted to rule out any reversible causes of the arrhythmia such as a pulmonary embolism, hyperthyroidism, hemorrhage, or infections (). A history of prior episodes and/or a history of structural heart disease are also important to obtain. Once reversible causes are ruled out and a thorough history is obtained, a primary stable arrhythmia requiring drug therapy can be considered (3).

The risk of any medication on the mother and fetus should be reviewed prior to its administration. Most antiarrhythmic medications have not been systematically studied in pregnancy and thus, all should be viewed as potentially harmful in pregnancy (6, 15). Most of these drugs are labeled as a Food and Drug Administration (FDA) category C except for amiodarone and atenolol, which are labeled as category D (16). As a review, category C means that risk cannot be ruled out and any category C medication should be used only if the potential benefits outweigh any potential risks to the fetus. Category D means that there is evidence of risk. There may be a benefit of this drug but that patients should be informed of all risks of the drug prior to giving it (16).

It should be noted that as of June 2015, the FDA initiated a change to pregnancy category labeling and that the use of letters will be phased out. In place of letters, a narrative summary based on the risk of each medication will be provided (17). Any medications submitted to the FDA after June 30, 2015 will use the new format immediately and that any prior prescription medications approved after June 2001 will have new labeling within 3-5 years (17). So as of now, most of these antiarrhythmic medications are still under the old letter category labeling but may change in the future.

Teratogenic risk is also the highest in the first eight weeks after fertilization and thus, especially careful consideration should be given to women in early pregnancy who receive drug therapy (18). This is not to say there is no risk in the other stages of pregnancy, but the risk to the fetus is significantly reduced after the first eight weeks (18).

Finally, it should be remembered that many of the physiologic changes of pregnancy will affect drug metabolism (19). Some of these changes include increased plasma volume, reduction in plasma proteins, changes in renal clearance of drugs and altered gastrointestinal absorption (7, 19). Progesterone levels also increase, which can affect hepatic metabolism (7). Thus, administering the lowest effective dose of a medication is prudent in this patient population (7).

  1. Palpitations/Premature Ventricular Contractions

Palpitations are very common during pregnancy. Along with paroxysmal supraventricular tachycardia, premature atrial and ventricular beats are the most frequently seen arrhythmias in pregnancy (3, 14). Treatment is typically not necessary but in patients with unbearable symptoms, cardioselective beta blockers can be started, but preferably after the first trimester (6).

  1. Atrioventricular (AV) Nodal Re-entrant Tachycardia (AVNRT) and AV Re-entrant Tachycardia (AVRT):

The most common supraventricular tachycardia in pregnancy is AVNRT. AVNRT occurs when there are dual AV nodal pathways (slow and fast) that form a part of a re-entry circuit. The tachycardia is initiated when a premature beat is blocked in the fast pathway but conducts over the slow pathway (20). If there is enough time for the fast pathway to recover from its refractory period, then the slow pathway impulse (initiated by the premature beat) may conduct retrogradely over the fast pathway and cause the re-entry circuit (20).

AVNRT should not be confused with AVRT, which is the second most common supraventricular tachycardia in pregnancy (21). AVRT occurs in patients with WPW. In AVNRT, the accessory pathways are located within or near the AV node, while in AVRT, the accessory pathways are located in the AV valvular rings (22). The majority of patients will have the orthodromic form with anterograde conduction through the AV conduction system and retrograde conduction via the accessory pathway, which leads to a regular, narrow complex tachycardia. On occasion, antidromic conduction can occur and cause a wide complex tachycardia (Obel et al). If there is concomitant atrial fibrillation and it is conducted via the antidromic pathway, a wide complex, irregular tachycardia can occur (22).

If AVNRT or AVRT is rapid enough, hemodynamic instability can occur and thus, cardioversion may be necessary (1, 14, 21). However, the majority of patients will not have hemodynamic instability and thus, conservative or medication therapies can be initiated.

First line therapies for stable AVNRT in pregnancy (1, 3, 4, 6, 7, 14, 23):

  1. Vagal maneuvers such as carotid massage or the Valsalva maneuver.
  2. Adenosine: safe and should be the initial drug of choice. The initial standard doses are the same as in non-pregnant patients – 6mg and 12 mg. Adenosine has a short half live and does not cross the placenta. Minor effects in the mother may include transient bradycardia and dyspnea. Note adenosine can induce bronchospasm and should be a consideration if the patient has a history of asthma.
  3. Intravenous metoprolol or propranolol can be used if adenosine is ineffective. Beta blockers are considered safe in pregnancy but they have been associated with intrauterine growth retardation. Atenolol should never be given, however as it has been associated with fetal hypotonia, neonatal respiratory depression, low birth weight and hypoglycemia.
  4. Verapamil should be considered as a third line agent if the above medications are not effective. Doses up to 10mg can be given without affecting the fetal heart rate. Watch for hypotension in the mother, however.

First line therapies for stable AVRT in pregnancy (3, 6, 7, 14, 15, 18):

  1. Vagal maneuvers
  2. Adenosine: may be used but only in regular tachycardias. Patients who have orthodromic AVRT with concomitant atrial fibrillation should not receive adenosine or any other AV nodal blocking agent as this can potentially lead to accelerated conduction through the accessory pathway and lead to dangerous ventricular tachycardias.

AV nodal blocking agents including calcium channel blockers and digoxin should also be used with caution in patients with wide complex tachycardias of unknown pathogenesis.  Just as in non-pregnant patients, procainamide is the drug of choice in these circumstances.

  1. Procainamide: IV procainamide is safe in the short-term treatment of AVRT. It should be avoided in patients with underlying structural heart disease as it can be pro-arrhythmogenic. It should not be used long term as it can cause a lupus-like syndrome.
  1. Focal Atrial Tachycardia:

Focal atrial tachycardia (FAT) is usually associated with structural heart disease and is rarely seen in pregnancy (14). FAT can be difficult to treat as many are resistant to medications and even cardioversion (7, 15). The main objective is to control the maternal heart rate so that tachycardia-induced cardiomyopathy can be prevented. Adenosine should be attempted first as it is diagnostic and may, on occasion, terminate the arrhythmia (6). If adenosine does not work, the next recommended initial therapies are beta blockers, non-dihydropyridine calcium channel blockers or digoxin. Sotalol, flecainide or propafenone can be given if the beforementioned drugs do not work. Finally, amiodarone can be given but only in severe, refractory cases (7, 15).

  1. Atrial fibrillation/Atrial Flutter:

Unless there is underlying structural heart disease or hyperthyroidism, atrial flutter and atrial fibrillation are rarely seen during pregnancy (15, 21). However, if atrial flutter (AFL) or atrial fibrillation (AF) with a rapid ventricular response is present in pregnancy, serious hemodynamic effects can occur to both mother and fetus (15). Thus, urgent treatment is important in these patients.

Therapeutic options for stable patients with AFL or AF with rapid ventricular response:

  1. DC or pharmacologic cardioversion: similar to the non-pregnant population, stable pregnant patients who have had AFL or AF for > 48 hours duration will require 3 weeks of anticoagulation and/or a transesophageal echocardiogram to evaluate for a left atrial thrombus prior to the procedure (15). However, if the duration of the arrhythmia is less than 48 hours and the patient’s CHADS2-VASC score is < 2, post-cardioversion anticoagulation may not be necessary (7, 15). In this case, the patient should receive a dose of heparin or weight adjusted low molecular weight heparin (LMWH) prior to and during cardioversion (15). For patients who require anticoagulation after cardioversion, LMWH is the drug of choice (15). Warfarin can be used in the second and third trimesters but not in the first trimester or last month of pregnancy (6, 15). As of now, given the limited research, the new oral anticoagulants should not be used in pregnant patients (6, 15).

If pharmacologic cardioversion is considered, ibutilide or flecainide can be given but only in patients with structurally normal hearts (15, 21, 24). Ibutilide is particularly useful in treating AF in patients with pre-excitation syndromes. It can prolong the QT and thus, pre-treatment with magnesium is recommended (7). Again, amiodarone can be given but only as a last resort. There is less experience with propafenone so it should be avoided unless it must be used as a last resort as well (15).

  1. Rate control: For stable patients who are not candidates for cardioversion and/or have refractory AF or AFL, rate control is recommended (6, 7, 14, 15, 25). The AHA/ACC do not define what adequate rate control in pregnancy is, nor could any other literature be found regarding a goal maternal heart rate (26).

With the exception of atenolol, beta blockers are recommended as first line rate control medications in patients with rapid AF or AFL who do not have acute heart failure (6, 7, 14, 15, 25).Metoprolol 5mg IV over 5 minutes and repeated, if necessary, is an option for initial rate control (14). Verapamil, diltiazem and digoxin are second line agents (6, 14, 15, 25). Remember that these drugs should not be given if a pre-excitation syndrome is present.

  1. Ventricular Tachycardia:

Ventricular tachycardia (VT) is rare during pregnancy and inherited disorders should be considered when asking patients about their past medical and family histories (15). Some of the more common causes of VT in pregnancy may include idiopathic right ventricular (RV) outflow tract tachycardia, long QT syndrome, valvular heart disease and hypertrophic cardiomyopathy (3, 6, 15, 27). Rarely does ischemia cause a cardiomyopathy or arrhythmias in pregnant patients but coronary artery dissection or vasospasm has been known to occur in pregnant patients (6).  Post-partum cardiomyopathy should also be ruled out in women presenting with new onset VT during the last 6 weeks of pregnancy or in the early post-partum period (15).

The most important goal for pregnant patients with VT is timely conversion back to normal sinus rhythm because eventually, poor perfusion to both mother and fetus can occur (15).Just as in unstable supraventricular rhythms, acute treatment of any unstable VT should always be treated with DC cardioversion (15). Conversely, pharmacotherapy may be considered in pregnant patients with stable VT (6, 13, 15, 27). Importantly, any pregnant patient with a wide complex tachycardia should be evaluated by obstetric and cardiology specialists (18).

Idiopathic RV outflow tract tachycardia is one of the more common types of VT seen in pregnancy. It is almost always a stable tachycardia and most of the time, it is not sustained. The recommended treatment is beta blockade or verapamil. Idiopathic LV tachycardia is not as common but it responds well to verapamil (3, 15).

In pregnant patients with stable monomorphic VT, lidocaine, procainamide, or sotalol are recommend as first line agents (3, 15, 27).

Polymorphic VT is definitely most concerning as it has a higher likelihood of converting to ventricular fibrillation (3). Long QT syndrome should be a concern in patients with polymorphic VT and thus, all medications that may prolong the QT should be eliminated. In addition, treatment should include magnesium and correction of any electrolyte disturbances (3). Magnesium should be given at a dose of 1-2 grams IV over 1-2 minutes (13). It is controversial whether pregnant patients with long QT are at risk for VT during pregnancy, but it has been demonstrated that patients with long QT are definitely at an increased risk for arrhythmias post-partum (28, 29). Thus, any post-partum patient who presents in VT should have long QT syndrome as a possible etiology of her condition.

Conclusions

While there are a few differences, the management of tachycardic arrhythmias in pregnancy is quite similar to the non-pregnant patient. DC cardioversion should always be conducted in patients with hemodynamic instability. Pharmacologic cardioversion of supraventricular and ventricular arrhythmias is possible in the stable patient. No drugs are completely safe in pregnancy, but most are rated category C in pregnancy and if the benefit exceeds the risk, then the medication may be given.  Amiodarone and atenolol are two medications that should be avoided in the pregnant patient, especially in the first trimester. Rate control with beta blockers or calcium channel blockers is an option in patients with supraventricular tachycardias who are not immediate candidates for cardioversion. Stroke risk should still be accounted for and at risk patients should be anticoagulated with LMWH or vitamin K antagonists (only in the 2nd and 3rd trimesters and not in the last month of pregnancy). Finally, close cardiac monitoring of both the mother and fetus and availability of emergency C section should be available whenever medication or cardioversion is indicated. Finally, but importantly, obstetrics and cardiology consultation is prudent whenever a pregnant patient with an abnormal tachycardic arrhythmia presents to the ED.

Case Resolution

Case 1: The patient in this case has new onset AVNRT. Her electrolytes are normal, her thyroid function is normal, and her infection workup is negative.  Since her vital signs are otherwise stable and she denies chest pain, adenosine 6mg IV push is administered. Her rhythm returns back to normal sinus rhythm and she is discharged home with close cardiology and obstetrics follow up.

Case 2: This patient has unstable ventricular tachycardia. She is immediately cardioverted with direct current. She was ultimately found to have right ventricular (RV) outflow tract tachycardia. Obstetrics and cardiology were consulted and the patient was admitted for maternal and fetal cardiac monitoring. She was eventually discharged with a beta blocker for prophylaxis and cardiology follow up.

 Case 3: The last patient has atrial fibrillation with rapid ventricular response. Her workup for infection is also negative and her thyroid function tests and electrolytes are normal. Since her symptoms had been present for several days, rate control was chosen. Metoprolol was given and she achieved adequate rate control. She was admitted for a transesophageal echo prior to cardioversion and eventually she was cardioverted back to normal sinus rhythm.

References/Further Reading

  1. Tromp CH, Nanne AC, Pernet PJ, Tukkie R, Bolte AC. Electrical cardioversion during pregnancy: safe or not? Neth Heart J 2011;19(3):134-6.
  2. Ferrero S, Colombo BM, Ragni N. Maternal arrhythmias during pregnancy. Arch Gynecol Obstet 2004; 269(4):244-53.
  3. Adamson DL, Nelson-Piercy C. Managing palpitations and arrhythmias during pregnancy. Heart. 2007; 93(12):1630-6.
  4. Newstead-Angel J, Gibson PS. Cardiac drug use in pregnancy: safety, effectiveness and obstetric implications. ExpertRev Cardiovasc Ther 2009; 7(12):1569-80.
  5. Gaiser R. Physiologic changes of pregnancy. Chestnut’s obstetric anesthesia: Principles and practice. 2009;4:15-36.
  6. Enriquez AD, Economy KE, Tedrow UB. Contemporary management of arrhythmias during pregnancy. Circ Arrhythm Electrophysiol 2014;7(5):961-7.
  7. Burkart TA, Miles WM, Conti JB. Principles of Arrhythmia Management During Pregnancy. Cardiovascular Innovations and Applications. 2016;1(2):143-55.
  8. Joglar JA, Page RL. Management of arrhythmia syndromes during pregnancy. Curr. Opin. Cardiol. 2014; 29(1):36-44.
  9. Jeejeebhoy FM, Zelop CM, Lipman S, Carvalho B, Joglar J, Mhyre JM, Katz VL, Lapinsky SE, Einav S, Warnes CA, Page RL. Cardiac Arrest in Pregnancy A Scientific Statement From the American Heart Association. Circulation. 2015;132(18):1747-73.
  10. Petrescu V, Petrescu M, Bogdan S. Arrhythmias in Pregnancy-one case report and current recommendations from a cardiological perspective. GINECO RO 2010; 6(2):124-7.
  11. Crijns HJ. Electrical cardioversion in healthy pregnant women: safe yes, but needed? NethHeartJ 2011; 19(3):105-6.
  12. Barnes EJ, Eben F, Patterson D. Direct current cardioversion during pregnancy should be performed with facilities available for fetal monitoring and emergency caesarean section. BJOG 2002; 109(12):1406-7.
  13. Trappe HJ. Emergency therapy of maternal and fetal arrhythmias during pregnancy. J EmergTraumaShock 2010; 3(2):153.
  14. Knotts RJ, Garan H. Cardiac arrhythmias in pregnancy. In Seminars in perinatology 2014 (Vol. 38, No. 5, pp. 285-288). WB Saunders.
  15. Regitz-Zagrosek V, Lundqvist CB, Borghi C, Cifkova R, Ferreira R, Foidart JM, Gibbs JS, Gohlke-Baerwolf C, Gorenek B, Iung B, Kirby M. ESC Guidelines on the management of cardiovascular diseases during pregnancy. EurHeartJ 2011:ehr218.
  16. Food and Drug Administration; Accessed Nov 15, 2016: www.fda.gov.
  17. Food and Drug Administration. Content and format of labeling for human prescription drug and biological products; requirements for pregnancy and lactation labeling. Federal registrar 2014; Vol. 79 (233): 72064-72103.
  18. Page RL. Treatment of arrhythmias during pregnancy. AmHeartJ 1995;130(4):871-6.
  19. Cox JL, Gardner MJ. Treatment of cardiac arrhythmias during pregnancy. Prog Cardiovasc Dis. 1993; 6(2):137-78.
  20. Kwaku KF, Josephson ME. Typical AVNRT—an update on mechanisms and therapy. Card Electrophysiol Rev. 2002; 6(4):414-21.
  21. Merino JL, Perez-Silva A. Tachyarrhythmias and Pregnancy.
  22. Obel OA, Camm AJ. Accessory pathway reciprocating tachycardia. EurHeartJ 1998; 19:E13-24.
  23. Elkayam U, Goodwin TM. Adenosine therapy for supraventricular tachycardia during pregnancy. Am J Cardiol 1995; 75(7):521-3.
  24. Kockova R, Kocka V, Kiernan T, Fahy GJ. Ibutilide‐Induced Cardioversion of Atrial Fibrillation During Pregnancy. J Cardiovasc Electrophysiol. 2007;18(5):545-7.
  25. Cacciotti L, Passaseo I. Management of Atrial Fibrillation in Pregnancy. J AtrFibrillation 2010;2(2).
  26. Anderson JL, Halperin JL, Albert NM, Bozkurt B, Brindis RG, Curtis LH, DeMets D, Guyton RA, Hochman JS, Kovacs RJ, Ohman EM. Management of patients with atrial fibrillation (compilation of 2006 ACCF/AHA/ESC and 2011 ACCF/AHA/HRS recommendations): a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2013;61(18):1935-44.
  27. Gowda RM, Khan IA, Mehta NJ, Vasavada BC, Sacchi TJ. Cardiac arrhythmias in pregnancy: clinical and therapeutic considerations. Int J Cardiol 2003;88(2):129-33.
  28. Meregalli PG, Westendorp IC, Tan HL, Elsman P, Kok WE, Wilde AA. Pregnancy and the risk of torsades de pointes in congenital long-QT syndrome.
    Neth Heart J. 2008; 16(12):422-5.
  29. Seth R, Moss AJ, McNitt S, Zareba W, Andrews ML, Qi M, Robinson JL, Goldenberg I, Ackerman MJ, Benhorin J, Kaufman ES. Long QT syndrome and pregnancy. J Am Coll Cardiol. 2007; 49(10):1092-8.

Pelvic Inflammatory Disease: Pearls and Pitfalls

Authors: Marina N. Boushra, MD (EM Resident Physician, Vidant Medical Center) and Cassandra Bradby, MD (EM Attending Physician, Vidant Medical Center) // Edited by: Jennifer Robertson, MD, MSEd and Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

A 24-year-old female with no significant past medical history presents to the emergency department (ED) with lower abdominal pain for five days. The pain has been associated with decreased appetite and nausea but no vomiting. It is exacerbated by sexual intercourse. Her last menstrual was period five days ago, and while she typically gets cramping, she states that this pain is more severe. Her vitals on arrival are temperature 101.2º Fahrenheit (F), heart rate (HR) 80 beats per minute (bpm), respiratory rate (RR) 14/minute, blood pressure (BP) 115/70 mmHg. Her physical examination is notable for diffuse tenderness to palpation of the abdomen, scant blood in the vaginal vault, yellow discharge from the cervical os, and severe bilateral adnexal tenderness on bimanual examination.

Background

Pelvic inflammatory disease (PID) is infection of the upper genital tract (uterus, endometrium, fallopian tubes, ovaries) in women. PID may extend to involve adjacent structures, causing periappendicitis, pelvic peritonitis, and perihepatitis (Fitz-Hugh-Curtis syndrome). The majority of PID is caused by ascending sexually-transmitted infections (STI). Neisseria gonorrhea and Chlamydia trachomatis are the most commonly implicated pathogens in PID1. However, PID can also be caused by bacterial-vaginosis related organisms or, more rarely, enteric or respiratory pathogens that have colonized the lower genital tract1. Even more rarely, a chronic form of PID may be seen with tuberculosis in endemic areas or Actinomyces in women who have intrauterine devices2,3.

Any sexually active woman is at risk for PID but women with multiple sexual partners are at the highest risk4. Other risk factors include age younger than 25 years, herpes infection, HIV infection, a partner with an STI, prior PID, or prior STI. Barrier contraception is protective5. Pregnancy also decreases the risk of PID due to the mucus plug that can prevent ascending infection from the lower to the upper genital tract. Note, however, that PID can still develop in the first 12 weeks of pregnancy6. The spectrum of PID symptoms is wide with some patients going undiagnosed until they develop sequelae such as tubal factor infertility or an ectopic pregnancy. In symptomatic patients, lower abdominal pain, typically bilateral, is often the presenting symptom1. Dyspareunia and/or an onset of pain with, or shortly after, menstruation should also raise suspicion for PID7. A history of abnormal uterine bleeding, such as menorrhagia, metrorrhagia, or post-coital bleeding, is seen in one third of patients with PID8. Physical examination typically reveals lower abdominal pain, which may be unilateral or bilateral, although diffuse abdominal pain may also be seen. Cervical motion tenderness and the classic “chandelier sign” – severe pain with cervical motion such that the patient “jumps for the chandelier” on examination – may be present. Fever, rebound tenderness, and/or hypoactive bowel sounds are indicative of more severe disease and should increase suspicion for a pelvic abscess. Associated right upper quadrant pain is concerning for Fitz-Hugh-Curtis syndrome inflammation of the hepatic capsule. The most common cause of death in PID is rupture of a tubo-ovarian abscess (TOA), which has a mortality rate of 5-10%6. Serious complications include tubal factor infertility, tubal scarring leading to ectopic pregnancy, and chronic pelvic pain.

Differential Diagnosis

The differential diagnosis for pelvic and lower abdominal pain is extremely broad and varies by age. The differential in pre-menopausal women includes ectopic pregnancy, a complicated intrauterine pregnancy, ovarian cyst, ovarian torsion, endometriosis, urinary tract pathologies, appendicitis, and irritable bowel syndrome. Laboratory evaluation should include a pregnancy test in any pre-menopausal woman. In post-menopausal women, many of the gastrointestinal and urinary pathologies are still possible but there is lower risk for ovarian torsion and endometriosis. Diagnoses such as ovarian masses, endometrial cancer, and colon cancer should be considered.

Diagnosis

There is no specific lab value, physical examination finding, or imaging study that is diagnostic of PID. The diagnosis of PID is often presumptive based on clinical findings. The clinical diagnosis is only 65-90% specific, but the addition of the criteria in Table 1 increases the specificity of the clinical diagnosis1,5,9. In patients with known or suspected PID, testing for STIs, including syphilis and HIV, should be obtained. Other helpful laboratory tests include a white blood cell count, C reactive protein (CRP), and erythrocyte sedimentation rate (ESR). A positive urinalysis does not exclude the diagnosis of PID, as inflammation in the pelvis can cause white blood cells in the urine6.

 Table 1: Findings suggestive of PID1

Oral temperature >101°F (>38.3°C)
Abnormal cervical or vaginal mucopurulent discharge
Cervical friability
Abundant white blood cells on saline microscopy of vaginal secretions
Documented infection with of N. gonorrhoeae or C. trachomatis

Imaging with pelvic ultrasound may be helpful in excluding other causes of pelvic pain, including ectopic pregnancy, ovarian cysts, and ovarian torsion. It is also helpful in the diagnosis of TOA. Computed tomography (CT) or magnetic resonance imaging (MRI) may also be used, with MRI being particularly useful in characterizing complicated soft-tissue masses as would be seen with TOA6.

Management

While the clinical diagnosis is only 65-90% specific, even minimal symptoms without an alternative diagnosis warrant antibiotic therapy to reduce the risk of potentially serious complications due to the delay of or withholding therapy1. Women with IUDs do not need to have them removed prior to the start of treatment because they are rarely the cause of PID1. If symptoms fail to improve in 48-72 hours, removal of the IUD should be considered1.

Antibiotic selection should cover for N. gonorrhea and C. trachomatis. The importance of anaerobic coverage is controversial, since no trial has demonstrated improved outcomes and there is concern that the gastrointestinal side effects associated with metronidazole will lead to noncompliance10. There is currently an ongoing study on the role of anaerobic coverage in PID (Clinical Trials.gov, identifier NCT01160640).

Anaerobic coverage should be added, however, in patients who have a history of gynecologic instrumentation in the prior two to three weeks. Possible antibiotic regimens for inpatient and outpatient management are listed in Table 2.

 There has been a trend towards outpatient management of patients with mild to moderate disease. The Pelvic Inflammation Disease Evaluation Clinical Health Trial (PEACH Trial) showed similar short-term clinical and microbiologic and long-term reproductive outcomes between the inpatient and outpatient arms of the trial, with the inpatient arm experiencing high rates of phlebitis from IV doxycycline administration12.

Table 2: Inpatient and Outpatient Treatment Regimens1

Outpatient management Ceftriaxone (250mg IM in one dose) plus doxycycline (100mg po bid for 14 days)
Cefoxitin (2g IM) with probenecid (1g orally) plus doxycycline (100mg po bid for 14 days)
Inpatient management Cefoxitin (2g IV q6 hours) plus doxycycline (100mg po bid for 14 days)
Cefotetan (2g IV q12 hours) plus doxycycline (100mg po bid for 14 days)
Clindamycin (900mg IV q8 hours) plus gentamicin (2mg/kg loading dose then 1.5 mg/kg q8 hours IV)

Indications for hospitalization and IV antibiotics include pregnancy, clinically severe disease, complicated PID (pelvic abscess), and intolerance to, noncompliance with, or failure of oral antibiotics1.

If a patient is treated as an outpatient, follow up in 72 hours should be arranged. Patient education is paramount, especially in adolescents where the risk of recurrence is higher and the time to pregnancy is shorter than in adult patients. Partner notification, evaluation and treatment should be encouraged. Patients should be educated about the use of barrier contraception and safe sex practices and instructed to remain abstinent from sexual activity until one week after the completion of treatment for them and their partner.

Pearls

  • Even though the presumptive clinical diagnosis is only 65-90% specific, symptoms suggestive of PID should be treated with antibiotics immediately to avoid the risk of serious sequelae, including permanent scarring that may lead to infertility and ectopic pregnancy.
  • Obtain a pelvic ultrasound to assess for TOA in patients with asymmetrical pelvic findings or clinical signs of toxicity.
  • Fluoroquinolones should not be used in known or suspected gonorrhea infection due to increasing rates of resistance.
  • IUDs do not need to be removed prior to treatment of PID.
  • Antibiotics should cover both gonorrhea and C. trachomatis.
  • Anaerobic coverage is only suggested if there has been recent gynecologic instrumentation.

 Pitfalls

  • Dismissing the pelvic pain associated with PID for dysmenorrhea.
  • Assuming a positive UA excludes the diagnosis of PID (beware sterile pyuria)
  • Failing to do a pelvic exam and STI testing on a woman with lower abdominal pain.

References / Further Reading

  1. Workowski KA, Bolan GA, Centers for Disease Control and Prevention. Sexually transmitted diseases treatment guidelines, 2015. MMWR Recomm Rep 2015; 64:1.
  2. Namavar Jahromi B, Parsanezhad ME, Ghane-Shirazi R. Female genital tuberculosis and infertility. Int J Gynaecol Obstet 2001; 75:269.
  3. Kim YJ, Youm J, Kim JH, Jee BC. Actinomyces-like organisms in cervical smears: the association with intrauterine device andpelvic inflammatory  Obstet Gynecol Sci. 2014 Sep;57(5):393-6.
  4. Lee NC, Rubin GL, Grimes DA. Measures of sexual behavior and the risk of pelvic inflammatory disease. Obstet Gynecol 1991; 77:425.
  5. Ross, Johnson. Pelvic Inflammatory Disease: pathogenesis, microbiology, and risk factors. UpToDate, Post TW (Ed), UpToDate, Waltham, MA. Accessed 12 October 2016.
  6. Shepherd SM, Weiss B, Shoff WH. Pelvic Inflammatory Disease in Tintinalli, Judith E., Gabor D. Kelen, and J. Stephan Stapczynski. Emergency Medicine: A Comprehensive Study Guide. New York: McGraw-Hill, Medical Pub. Division, 2016. Ch 103:668-672.
  7. Korn AP, Hessol NA, Padian NS, et al. Risk factors for plasma cell endometritis among women with cervical Neisseria gonorrhoeae, cervical Chlamydia trachomatis, or bacterial vaginosis. Am J Obstet Gynecol 1998; 178:987.
  8. Wiesenfeld HC, Sweet RL, Ness RB, et al. Comparison of acute and subclinical pelvic inflammatory disease. Sex Transm Dis 2005; 32:400.
  9. Peipert JF, Boardman LA, Sung CJ. Performance of clinical and laparoscopic criteria for the diagnosis of upper genital tract infection. Infect Dis Obstet Gynecol 1997; 5:291.
  10. Walker CK, Wiesenfeld HC. Antibiotic therapy for acute pelvic inflammatory disease: the 2006 Centers for Disease Control and Prevention sexually transmitted diseases treatment guidelines. Clin Infect Dis 2007; 44 Suppl 3:S111.
  11. Wiesenfeld, HC. Pelvic Inflammatory Disease: Treatment. UpToDate, Post TW (Ed), UpToDate, Waltham, MA. Accessed 12 October 2016.
  12. Ness RB, Soper DE, Holley RL, et al. Effectiveness of inpatient and outpatient treatment strategies for women with pelvic inflammatory disease: results from the Pelvic Inflammatory Disease Evaluation and Clinical Health (PEACH) Randomized Trial. Am J Obstet Gynecol 2002; 186:929.

Intraabdominal Catastrophes in the Pregnant Patient

Author: Liang Liu, MD (EM Chief Resident, UT Southwestern / Parkland Hospital) // Edited by: Courtney Cassella, MD (@Corablacas, EM Resident Physician, Icahn SoM at Mount Sinai) and Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

A 20-year-old female presents with abdominal pain. She is gravid 2, para 1 at 18 weeks gestation confirmed by ultrasound dating. She has had an uncomplicated pregnancy but has had one day of gradual onset abdominal pain with nausea, vomiting and anorexia. How should this patient be managed? What should be considered for the fetus?

Introduction

Though many obstetric complications occur during pregnancy, the pregnant woman is still a woman with all her other organs that can be at risk, regardless of her pregnancy status. Typically, patients with obstetric complications will complain of uterine tenderness, vaginal bleeding and may have abnormal fetal heart tones on monitoring. When signs and symptoms do not support an obstetric cause for the patient’s abdominal pain, it is imperative that the differential is still wide for all other causes.

The gravid uterus is considered an abdominal organ at 12-week gestation, and this (in conjunction to natural physiologic changes in pregnancy) can complicate and confuse presentations of non-obstetric medical emergencies.1 The expanding uterus can delay the recognition of acute pain and may mask typical findings of peritonitis. Due to a naturally occurring increase in white blood cells during pregnancy, leukocytosis no longer provides as much information in the diagnosis of acute pathology. Additionally, a relative increase in blood volume can delay the development of tachycardia and hypotension in the truly ill patient.1

Appendicitis

Source: Jang KM et al. The value of 3D T1-weight gradient-echo MR imaging for evaluation of the appendix during pregnancy: preliminary results. Acta Radiol. 2011 Ocr 1; 52(8):825-8.
Source: Jang KM et al. The value of 3D T1-weight gradient-echo MR imaging for evaluation of the appendix during pregnancy: preliminary results. Acta Radiol. 2011 Ocr 1; 52(8):825-8.

The incidence of appendicitis in young women is 1 in every 1500 regardless of pregnancy status.2 It is one of the most common indication for operative management of a non-obstetric condition in the pregnant woman with acute abdomen. Additionally, pregnancy is associated with a two to three times increased rate of appendiceal rupture when comparing pregnant to nonpregnant women.3 Perforation increases both maternal and fetal morbidity, including peritonitis, sepsis, preterm labor, and fetal demise.4 In fact, fetal morbidity and mortality rates increase from 0% to 1.5% in uncomplicated appendicitis to as high as 20% to 35% with perforation.5 This increased rate of complications can be attributed to a delay in diagnosis as many of the symptoms of appendicitis are common during pregnancy including nausea, vomiting and anorexia. Additionally, with the growth of the uterus, the appendix will also move cephalad resulting in an atypical location of pain. The gravid uterus can lift and stretch the anterior abdominal wall away from the inflamed appendix resulting in less direct contact between the area of inflammation and the peritoneum which would result in a muted guarding or rebound tenderness.1,6 Oftentimes, the inflamed appendix is actually in contact with a ureter or renal pelvis resulting in pyuria without bacteriuria and urinary symptoms.7

Though the gold standard for diagnosis of appendicitis is CT in the general population, physicians must weigh the risk of delayed diagnosis and rupture with the risk of exposing the fetus to radiation. Ultrasound, where possible, can confirm diagnosis without exposing the fetus to this risk. Like in the nonpregnant patient, diagnosis is based on first identifying the appendix, a blind ended aperistaltic tubular structure that originates from the base of the cecum. The normal appendix has a wall thickness of 2 mm or less. Appendicitis is diagnosed upon seeing an incompressible, blind ended tubular structure with wall thickness of 3 mm or more and an outer anterior-posterior diameter of 6 mm or more.8 Other findings suggestive of appendicitis include presence of fecalith, hyperechoic periappendicular fat, or a peritoneal fluid collection. However, evaluation of the compressibility of the appendix is less sensitive after 35-week gestation due to the gravid abdomen.9 If the appendix is not visualized due to operator experience, body habitus, intraluminal air or distortion of normal anatomy as seen in pregnancy, an ultrasound is equivocal for the diagnosis. MRI has also been recommended by several studies in place of CT to minimize risk of radiation exposure.1 If US is equivocal and MRI can be obtained without delaying care then proceed to MRI rather than CT.

Definitive management upon diagnosis is early appendectomy within 24 hours of diagnosis to minimize risk of perforation. Perioperative antibiotic treatment should be given in the case of acute appendicitis without peroration to cover gram negatives aerobes and anaerobes as outline in the table below.4 In the case of perforated appendicitis, patients will appear septic and an empiric broad-spectrum antibiotic selection is important and should be continued until cultures can aid in narrowing the agents.4

Cholestasis and Cholecystitis

Source: http://www.meddean.luc.edu/lumen/meded/radio/curriculum/surgery/cholecystitis_list2.htm

Progesterone during pregnancy not only slows gastric motility through smooth muscle relaxation but also causes bile stasis. 1 Additionally, elevated levels of estrogen cause aggregation of cholesterol crystals and increased bile concentration.1 Together, these two hormones result in an increased incidence of cholelithiasis and puts patients at risk for acute cholecystitis. Acute cholecystitis is the second most common surgical problem during pregnancy and has an incidence of 0.05% to 0.8%.10

Presentation of the pregnant versus the nonpregnant female with cholecystitis is identical. Laboratory values may not be useful, however, as an increase in white blood cell count, elevated amylase and elevated alkaline phosphatase are all normal during pregnancy.1 Diagnosis is with ultrasound and is confirmed with a gallbladder wall thickness greater than 3 mm, presence of pericholecystic fluid, presences of gallstones and a positive sonographic Murphy’s sign. Management of cholecystitis in pregnancy is identical to that in the nonpregnant patient: cholecystectomy or conservative management with IV fluids, supportive care, and antibiotics (ampicillin-sulbactam, piperacillin-tazobactam, ticarcillin-clavulanate OR ceftriaxone plus metronidazole).11

Pyelonephritis

Nulliparous, young pregnant women, especially in their second trimester, are at highest risk for acute pyelonephritis, and it is most often caused by Escherichia coli.12 Pregnant women are susceptible to pyelonephritis due to the ureteral dilatation that occurs early during pregnancy and persists until delivery due to increased progesterone levels that relax the smooth muscles of the ureters and the direct compression of the ureters by the uterus. This slowed peristalsis and dilatation of the ureters result in urinary stasis and places pregnant women at increased risk of kidney stone formation and infections.2 The IDSA recommends screening for bacteriuria during the early stages of pregnancy and treating for asymptomatic bacteriuria with nitrofurantoin (100 mg BID) or a cephalosporin (generally, Cephalexin 500 mg BID, even though it does not cover enterococci) for 3-7 days with confirmatory test of cure.13 Typically, imaging is not necessary but when complications of pyelonephritis are suspected, renal ultrasounds can be helpful. All pregnant females with pyelonephritis require admission for intravenous antibiotics, and all women in their third trimester with cystitis need admission due to the risk of pre‐term labor.1

Pancreatitis

Acute pancreatitis occurs in 1% of pregnant women and is often self-limited and conservatively managed.1 Presentation is identical to that in nonpregnant patients and diagnosis is based on elevated lipase and clinical picture. Most commonly, this occurs during the third trimester or immediately postpartum. It is thought that the increased incidence in the third trimester is due to increased intra-abdominal pressure by the gravid uterus on the biliary ducts.6 Ultrasound can be useful in identifying complications associated with pancreatitis including common bile duct dilation, cholelithiasis, pancreatic pseudocysts, and abscesses. Generally, a CT is not necessary unless the clinical course is complicated by suspected extensive necrotic pancreatitis or severe pancreatitis. Mainstay of management is no different than pancreatitis in the nonpregnant patient and is primarily supportive care including analgesia, antiemetics, advancing diets as tolerated and maintaining volume status with intravenous hydration.

Adnexal Torsion

Source:http://www.ovariancystmiraclereview.org/the-risks-and-complications-of-ovarian-cysts/
Source: http://www.ovariancystmiraclereview.org/the-risks-and-complications-of-ovarian-cysts/

Adnexal torsion is a rare problem but does complicate 1 in every 1,800 pregnancies.14 This is more likely during the first and early second trimester, typically involves the right side, and most commonly is due to the presence of the corpus luteum cyst.14 Presentation will be similar to that of nonpregnant patients and ultrasound is the imagining modality of choice for diagnosis. The transabdominal approach can be used initially for evaluation and becomes more useful at later stages of pregnancy as the ovaries are brought out of the pelvis by the enlarging uterus.15 A transvaginal approach may be needed if the adnexal structures are not well visualized in the transabdominal approach. Doppler flow should be used to evaluate for torsion though the presence of flow does not exclude the diagnosis. Management is surgical and requires consultation with OBGYN.

Intestinal Obstruction

Intestinal obstruction occurs in 1 in 1,500 to 3,000 pregnancies.2 Adhesions contribute to 60-70% of small bowel obstructions in pregnancy and are attributed primarily to previous abdominal procedures and prior pelvic inflammatory disease.14 Intestinal obstructions most commonly occur in the third trimester due to the mechanical effects of a rapidly growing uterus on the gastrointestinal tract.1 It is also seen immediately postpartum with the rapid decrease in size of the uterus.1 The maternal mortality rate associated with bowel obstructions during pregnancy can be as high as 6% and fetal mortality as high as 26%.1,14 This risk then increases in the third trimester with maternal mortality rate of 10-20%.1,14

Diagnosis is dependent on serial physical exams and imaging. Serial abdominal films obtained 4-6 hours apart showing air fluid levels and bowel dilatation is diagnostic for intestinal obstruction.6 Absent typical findings on plain films, a CT with contrast is needed for diagnosis in the patient with high clinical suspicion.6 Like in the nonpregnant patient, management is initially conservative: fluid and electrolyte replacement, nasogastric decompression, fetal monitoring and close monitoring.6 However, in the setting of clinical deterioration and worsening symptoms, management regardless of pregnancy status is surgical.6

HELLP Syndrome

In the second half of pregnancy, HELLP (Hemolysis, Elevated Liver enzymes and Low Platelets) syndrome, a complication of preeclampsia, can present with many of the similar symptoms as described for an acute abdomen including nausea, vomiting, and abdominal pain. While some women will have previously documented hypertension and proteinuria in previous pregnancies, 20% of pregnant women will present with HELLP syndrome as their first presentation of pre-eclampsia.16 Patients may complain of acute onset right upper quadrant or epigastric abdominal pain or have other symptoms concerning for development of eclampsia including headache, visual disturbances, altered consciousness or irritability. Workup in these patients will show elevated blood pressures, peripheral smear with schistocytes and burr cells, elevated lactate dehydrogenase, elevated liver enzymes including bilirubin and low platelets.16

Mainstays of management include blood pressure control, prevention of seizures, correction of coagulopathy and delivery of the fetus. A number of antihypertensive medications have been described in the literature for the management of preeclampsia and eclampsia including hydralazine, labetalol, sodium nitroprusside, alpha blockers, calcium channel blockers, and methyldopa.17 Hydralazine and labetalol are the most commonly used. Hydralazine is given initially as a 5 mg IV bolus then repeated at 20 minute intervals of 5 to 10 mg IV bolus depending on response until blood pressure is controlled and then repeat dosing to maintain blood pressure control every 3 hours.17 Labetalol is given as an initial 20 mg IV bolus and then doubled every 10 minutes until blood pressure controlled with a maximum dose of 220 mg.17 (Summary see Table 2.) Magnesium is also given for its vasodilatation role and to prevent seizures.17, 20 For dosing of magnesium, see Table 3.20

table-2-antihypertensives

Table borrowed directly from: Lew M, Klonis E. Emergency Management of eclampsia and severe pre-eclampsia. Emerg Med (Fremantle). 2003 Aug; 15(4):361-8.
Table directly from: Lew M, Klonis E. Emergency Management of eclampsia and severe pre-eclampsia. Emerg Med (Fremantle). 2003 Aug; 15(4):361-8.

Hepatic rupture is a rare complication in these patient, and patients will present with severe abdominal pain and in hemorrhagic shock.16 Fetal outcomes in these patients are devastating with mortality rates ranging from 40% to 60% in both the mother and the fetus regardless of gestational age due to delays in diagnosis and the critically ill state of the mother.18 Emergency laparotomy with bleeding control, termination of the pregnancy and correction of the coagulopathy is paramount in the management of these patients to save the mother’s life.19

Conclusion

Delays in care of the pregnant female with non-obstetric emergencies arise both from delays in diagnosis due to vague symptoms and atypical presentation and also from delays in obtaining appropriate and definitive diagnostic imaging. Though radiation exposure does place risk on the development of the fetus and future cancer risks of the child, a fetus absorbs 3.5 rad when exposed to a typical CT scan of the abdomen and pelvis and 0.02 to 100 mrad with conventional chest and abdomen radiographs.19 These levels are much lower than the radiation dose threshold thought to cause morbidity and mortality to the fetus.1,19 As such, with good clinical gestalt, delays in diagnosis and in obtaining definitive workup should be avoided to improve outcomes for the pregnant woman.

Take Home Points

  • The gravid uterus can mask the signs of peritoneal irritation (guarding, rigidity and rebound tenderness) by preventing the inflamed organ from contacting the peritoneum.
  • Due to increased white blood cells that naturally occur during pregnancy, leukocytosis is not helpful in identifying acute pathology.
  • A relative increase in blood volume can delay the development of tachycardia and hypotension in the truly ill patient.
  • Consider appendicitis in the patient complaining of typical signs and symptoms of appendicitis even if confounded by right middle and upper quadrant abdominal pain, pyuria, urinary symptoms and subtle signs of peritonitis.
  • HELLP syndrome is managed with blood pressure control, prevention of seizures, correction of coagulopathy, and delivery of the fetus.
  • Radiological investigations, including abdominal plain films, can be safely undertaken during pregnancy and should always be considered so as to avoid delays and failures in diagnosing potentially life-threatening conditions.

References / Further Reading

  1. Diegelmann L. Nonobstetric abdominal pain and surgical emergencies in pregnancy. Emerg Med Clin North Am. 2012 Nov;30(4):885-901. doi: 10.1016/j.emc.2012.08.012.
  2. Kilpatrick CC, Monga M. Approach to the acute abdomen in pregnancy. Obstet Gynecol Clin North Am 2007; 34: pp. 389-402
  3. Gilo NB, Amini D, Landy HJ. Appendicitis and cholecystitis in pregnancy. Clin Obstet Gynecol 2009; 52: pp. 586-596
  4. Young BC, Hamar BD, Levine D, Roqué H. Medical management of ruptured appendicitis in pregnancy. Obstet Gynecol. 2009 Aug;114(2 Pt 2):453-6. doi: 10.1097/AOG.0b013e3181998424
  5. Guttman R, Goldman R, and Koren G. Appendicitis during pregnancy. Can Fam Physician 2004; 50: pp. 355-357
  6. Augustin G, Majerovic M. Non-obstetrical acute abdomen during pregnancy. Eur J Obstet Gynecol Reprod Biol 2007; 131: pp. 4-12
  7. Kennedy A. Assessment of acute abdominal pain in the pregnant patient. Semin Ultrasound CT MR. 2000 Feb;21(1):64-77. doi:10.1016/S0887-2171(00)90014-3
  8. Wild JRL, Abdul N, Ritchie JE, Rud B, Freels S, Nelson RL. Ultrasonography for diagnosis of acute appendicitis (Protocol). Cochrane Database of Systematic Reviews 2013, Issue 2. Art. No.: CD010402. doi: 10.1002/14651858.CD010402
  9. Vissers R.J., and Lennarz W.B.: Pitfalls in appendicitis. Emerg Med Clin North Am 2010; 28: pp. 103-118
  10. Date R.S., Kaushal M., and Ramesh A.: A review of the management of gallstone disease and its complications in pregnancy. Am J Surg 2008; 196: pp. 599-608
  11. Brooks D.: Gallstone disease in pregnant women. Wolters Kluwer Health, 2012.
  12. Sharma P., and Thapa L.: Acute pyelonephritis in pregnancy: a retrospective study. Aust N Z J Obstet Gynaecol 2007; 47: pp. 313-315
  13. Nicolle LE, Bradley S, Colgan R, Rice JC, Schaeffer A, and Hooton TM. Infectious Diseases Society of America Guidelines for the Diagnosis and Treatment of Asymptomatic Bacteriuria in Adults. CID 2005; 40: pp. 643-654
  14. Cappell M.S., and Friedel D.: Abdominal pain during pregnancy. Gastroenterol Clin North Am 2003; 32: pp. 1-58
  15. Graham L.: ACOG releases guidelines on management of adnexal masses. Am Fam Physician 2008; 77: pp. 1320-1323
  16. Chandraharan, E., Arulkumaran, S. Acute abdomen and abdominal pain in pregnancy. Obstet Gynaecol Reprod Med. 2008;18: pp. 205–212.
  17. Neligan PJ and Laffey JG. Clinical review: Special populations – critical illness and pregnancy. Crit Care. 2011; 15(4): 227. Epub 2011 Aug 12. doi: 10.1186/cc10256
  18. Augustin G, Majerovic M. Non-obstetrical acute abdomen during pregnancy. Eur J Obstet Gynecol Reprod Biol. 2007 Mar;131(1):4-12. Epub 2006 Sep 18. doi: 10.1016/j.ejogrb.2006.07.052
  19. Devarajan S, Chandraharan E. Abdominal pain in pregnancy: a rational approach to management. Obstet Gynaecol Reprod Med. 2011;21:198–206. doi: 10.1016/j.ogrm.2011.04.001
  20. Lew M, Klonis E. Emergency Management of eclampsia and severe pre-eclampsia. Emerg Med (Fremantle). 2003 Aug; 15(4):361-8.
  21. Calhoun DA, Oparil S. Treatment of hypertensive crisis. N Engl J Med. 1990 Oct 25;323(17):1177-83.

 

The Bleeding Pregnant Patient in the Third Trimester: Pearls and Pitfalls

Authors: Cynthia Peng, MD (EM Resident Physician, York Hospital) and Robert Stuntz, MD (Program Director and Vice Chair of Education, York Hospital) // Edited by: Jennifer Robertson, MD, MSEd and Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

You are working in the emergency department (ED) when a 30-year-old G2P0010 female presents with painless vaginal bleeding. She is 30 weeks pregnant. Vital signs are a temperature (T) 98.7° Fahrenheit (F), a heart rate (HR) 130 beats per minute (bpm/min), blood pressure (BP) 80/40 mmHg, and a respiratory rate (RR) of 14/min. The patient’s abdomen is soft and non-tender. What are the next steps?

STABILIZE THE PATIENT, EVALUATE THE HEMORRHAGE

On average, pregnant women lose about one liter (L) of blood during birth [6]. Immediately after delivery, a pregnant patient’s blood volume requirement decreases, and thus, this one liter loss is typically well tolerated. On the other hand, this amount of blood loss would be hemodynamically significant in a third trimester pregnant patient. In the patient with significant third trimester bleeding, the initial steps in management are just as in any patient with hemorrhagic shock. These steps include judicious crystalloid volume resuscitation and early treatment with blood products (packed red blood cells (PRBC), platelets, fresh frozen plasma (FFP), and cryoprecipitate). Indications for blood transfusion include signs of hemorrhagic shock, 30-40% blood volume loss, or severe thrombocytopenia with platelets <20,000 x 109/L.

One of the most important factors to evaluate is the amount of bleeding. In extreme situations, the patient may be in hypovolemic shock. For any hemorrhage greater than 750-1500 milliliters (mL), you may see vital sign changes consistent with a Class II hemorrhage. However, the traditional classes of hemorrhage are not always reliable. Pregnancy itself can be a complicating factor, as:

  1. HR increases 10-20 bpm and reaches a maximum throughout third trimester [4].
  2. BP reaches a nadir in 2nd trimester (5-10mm Hg below baseline), but increases in the 3rd trimester.
  3. Total blood volume, plasma volume, and RBC mass increases during pregnancy, and laboratory testing reflects physiological anemia from hemodilution [4].

Historically, in a Rhesus (Rh) alloimmunized pregnancy, there was a 25-30% chance of a fetus to contract mild to moderate hemolytic disease and a 25% of hydrops fetalis [5]. With Rho (D) immune globulin (RhoGAM), the maternal sensitization process can be temporarily prevented. In Rh negative patients, RhoGAM is typically administered in the 26-28 week period, then again within three days of delivery. In the setting of third trimester bleeding with an Rh negative mother, RhoGAM should be administered if not already given. It is imperative to maintain a level of passive anti-D every 12 weeks if given before [5]. The Kleihauer-Betke (KB) test is important to quantify transplacental hemorrhage. It also helps determine if the amount of fetal to maternal hemorrhage exceeds that which can be treated with a standard 300 microgram (mcg) dose of RhoGAM. The KB test is indicated in the setting of severe vaginal bleeding (as in this case) and maternal trauma. It is an acid elution test where the adult hemoglobin is dissolved and the fetal hemoglobin remains and stains. The test is positive if >0.01mL of fetal blood is detected.

CONSIDER THE DIFFERENTIAL DIAGNOSES

The differential for third trimester bleeding includes placental abruption, placenta previa, and vasa previa. Vaginal speculum and bimanual exams are contraindicated with these diagnoses due to the risk of inciting massive hemorrhage. Therefore, always perform an ultrasound first in a third trimester bleeding patient.  Placental abruption occurs when the placenta detaches prematurely from the uterine wall, and can be seen in up to 30% of third trimester vaginal bleeding. Severe placental abruption can cause catastrophic vaginal bleeding and non-reassuring fetal heart rates. Complications of placental abruption include hypovolemic shock and disseminated intravascular coagulation (DIC) (occurs with 10-20% cases). Placenta previa (20% of cases) occurs when placental tissue covers the cervical os. At 24 weeks gestational age, placenta previa will be present in 1 in 20 pregnancies, but this typically resolves by the third trimester. Placenta previa usually presents as painless vaginal bleeding that is less severe in volume. Ultrasound is critical in differentiating between these placenta previa and placental abruption. In the absence of placenta previa or placental abruption, painless vaginal bleeding could be vasa previa. Vasa previa is a condition where the umbilical cord is trapped between the fetus and the cervix. This usually occurs in multiple gestations. If any of these diagnoses are present, an obstetrics/gynecology (OB-GYN) consultation is warranted for a possible Cesarean (C) section.  In any pregnant woman, the loss of 500 mL of bright red blood can be indicative of placental abruption [5]. These patients need to be taken to the operating room immediately. Other considerations include genital trauma and laceration, cervical cancer, cervicitis, foreign body, and bloody show.

MONITOR FOR FETAL WELLBEING

The mother is not your only patient in this setting. Remember to document a fetal heart rate, and perform constant fetal monitoring. In the setting of a 24 to 34 week gestation pregnancy, consider steroids to expedite lung maturity. Tocolytics can also be used in preterm patients with third trimester bleeding. Evidence has not shown any increased morbidity or mortality associated with tocolytic agent use [2].

Pearls:

  1. Normal physiological changes in pregnancy are important to consider. Heart rate increases by about 10-20 bpm, and peaks in the third trimester. Blood pressure may be 5-10 mm Hg lower than baseline, but usually rebounds in the third trimester.
  2. RhoGAM should be administered in any Rh-negative mother who presents with vaginal bleeding or trauma. The Kleihauer-Betke test can quantify the amount of fetal blood. The standard RhoGAM dose is 300mcg of Rho(D) immune globulin for 15mL of fetal red cells.
  3. The most concerning causes of third trimester bleeding include placental abruption, placenta previa, and vasa previa. Any pregnant woman presenting with a loss of 500cc of bright red blood should be taken to the operating room immediately, as this can be indicative of placental abruption [5].

Pitfalls:

  1. Do not perform a speculum or bimanual genital exam until after an ultrasound has been performed. This will rule out placental abruption, placenta previa, and vasa previa and decrease the chance for causing an obstetrical emergency.
  2. Do not forget the rest of your differential diagnoses. Other considerations include genital trauma and laceration, cervical cancer, cervicitis, foreign body, and bloody show.
  3. Remember, you have two patients! Do not forget to document fetal heart rate, and maintain fetal monitoring. Consider steroids and tocolytics.

References / Further Reading

[1] Balderston KD1, Towers CV, Rumney PJ, Montgomery D. Is the incidence of fetal-to-maternal hemorrhage increased in patients with third-trimester bleeding? Am J Obstet Gynecol. 2003 Jun;188(6):1615-8; discussion 1618-21.

[2] Towers CV1, Pircon RA, Heppard M. Is tocolysis safe in the management of third-trimester bleeding? Am J Obstet Gynecol. 1999 Jun;180(6 Pt 1):1572-8.

[3] Shakuntala Chhabra, Preetindar Kaur, Chandan Tickoo, Prashant Zode. Transplacental haemorrhage in women having third trimester bleeding and perinatal outcome. Open Journal of Obstetrics and Gynecology, 2011, 1, 149-152

[4] Monika Sanghavi, MD; John D. Rutherford, MB ChB, FRACP. Cardiovascular Management in Pregnancy. Circulation.2014; 130: 1003-1008

[5] Prevention of Rh D Alloimmunization. ACOG Practice Bulletin. Number 4, May 1999. Clinical management guidelines for obstetrician-gynecologists. American College of Obstetricians and Gynecologists.

[6] “3rd Trimester Bleeding.” Brookside Associates, N.D. Web. 14 June 2016

Recent Elective Abortion

Author: Courtney Cassella, MD (EM Resident Physician, Icahn School of Medicine at Mount Sinai) // Edited by: Jennifer Robertson, MD, MSEd and Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

Clinical Case / Intro

A 24-year-old female with no past medical history presents to the emergency department (ED) with two days of pelvic pain. Three days prior to presentation to the ED, the patient underwent a dilation and aspiration for termination of pregnancy. Physical exam revealed mild suprapubic tenderness to palpation, no cervical laceration, no cervical motion or adnexal tenderness, and moderate dark red blood in the vaginal vault.

In a 2015 study examining 54,911 abortions among fee-for-service California Medicare recipients, 1 of 115 women visited the emergency department for an abortion-related complication. Among these patients, one third received a pathologic diagnosis or treatment.1 This review will attempt to give a base for evaluating these post-procedure patients and provide a framework to help determine who has an abortion-related complication requiring obstetric and gynecology (OB-GYN) consultation.

Definitions and Terminology

  • Induced abortion: medical or surgical abortion
  • Early medical abortion: < 9 weeks gestational age with mifepristone, methotrexate, or misoprostol
  • Surgical abortion
    • Dilation and aspiration or curettage: < 13 weeks with suction or sharp curettage of the uterus
    • Dilation and evacuation: ≥ 13 weeks with suction and sharp curettage through a dilated cervix
  • Unsafe abortion: terminations by persons lacking necessary skill and/or in an environment lacking minimal medical standards
    • Brief note on Unsafe Abortion2-4: Globally, unsafe abortions account for 67,000 maternal deaths annually, the majority in African and Asia.3 The major complications are uterine perforation and bowel injuries. The leading cause of death is septic shock with or without hemorrhage. Although rare in the United States, given the high mortality emergency physicians should be aware of this entity.

Demographics5, 6

  • Estimated 1 million induced abortions in the US per year5
  • Method Type6
    • 5% by Early Medical < 9 weeks
    • 4% by Curettage ≤ 13 weeks
    • 7% by Curettage > 13 weeks
  • 9 abortions per 1,000 women aged 15-44 years5
    • Highest rate 23.3 per 1,000 women in the 20-24 age group6
Percentage of Total Legal Abortions by Age6
Age (years) Percent of all abortions (%)
< 15 0.4
15 – 19 12.2
20 – 29 58.2
30 – 39 25.5
≥ 40 3.7

 

Induced Abortion Complications Statistics

The complication rate of surgical abortions is 6.1%. These complications occur approximately 1 – 30 days post-procedure with a mean 5 days post-procedure.7 In a 2009 to 2010 report, the overall incidence of adverse events after medical abortion was noted to be 0.65% and major complication rates ranged from 0.1% to 0.23%.8 These complications were defined as events requiring admission, surgery, or blood transfusion.1,8,9 From 1998 to 2010, a total of 108 deaths were causally related to legal induced abortions, with a rate of 0.7 deaths per 100,000.10

Timing of Complications with Induced Abortion11

  • Immediate (within 24 hours): Bleeding, pain
    • Uterine perforation
    • Cervical lacerations
  • Delayed (between 24 hours and 4 weeks): Bleeding or Discharge
    • Retained products of conception
    • Endometritis
  • Late complications (> 4 weeks): Amenorrhea

Hemorrhage12, 13

Post-abortion hemorrhage is defined as clinical response to excessive bleeding (i.e. transfusion or admission) and/or bleeding in excess of 500 mL. 13

  • As much as 7% of women experience bleeding14
  • Risk factors
    • Unsafe abortion
    • Advanced maternal age
    • Insufficient cervical dilation
    • History of more than one cesarean delivery
    • Known bleeding disorder
  • Causes
    • Uterine atony
    • Cervical laceration
    • Uterine perforation or rupture
    • Abnormal placentation
    • Disseminated intravascular coagulation (DIC) (5%)
    • Retained products of conception
  • Key Components of the physical examination
    • Evaluate the cervix for lacerations
    • Conduct a bimanual examination to evaluate for uterine tone and location of a cervical laceration
    • Bedside ultrasound to assess for retained blood or tissue
  • Treatment13
    1. Resuscitate and transfuse as needed
    2. Evaluate for a cervical laceration and repair if found (see below)
    3. Uterine massage
    4. Urgent obstetrics/gynecology consult
    5. Consider uterotonic agents such as methergine, misoprostol, and oxytocin*
      • *Warning: Order only in consultation with OB-GYN
      • First line: Methergine 0.2mg IM or IV, repeat every five minutes, to a maximum of five doses
      • Misoprostol 800 to 1000mcg orally or rectally
      • Oxytocin 10U IM or 10-40U IV

 Cervical Laceration or Injury15

Cervical lacerations or injuries can be seen in anywhere from 0.1% to 3.3% of surgical abortions.7, 12 Most often cervical lacerations are seen as an immediate complication resulting in vaginal bleeding and therefore not as often seen in the ED.

  • Risk factors16
    • Provider inexperience
    • Abnormal uterine cavity
    • Increasing gestational age
    • Nulliparity
    • Adolescent age17
  • Treatment
    • Hemorrhage control
      • Small lacerations may be managed by applying pressure and if no resolution, hemostatic agents such as silver nitrate or Monsel’s solution can be used
      • Large lacerations must be closed with absorbable sutures
      • If hemostasis cannot be achieved vaginal packing may be employed while waiting for consultants
    • Fluids or blood products as indicated
    • Consult OB-GYN

Uterine Perforation15,18

The incidence of uterine perforation after surgical abortion varies between <0.1% and 2.3%14. Commonly, uterine perforation is recognized at the time of the procedure. However, small or partial thickness perforations may initially go unrecognized. Severe cases may cause bowel or bladder perforation.

  • Risk factors16, 19
    • Provider inexperience
    • Abnormal uterine cavity
    • Previous surgery to the cervix
    • Increasing gestational age
    • Multiparity
  • Symptoms
    • Vaginal bleeding
    • Pelvic pain or diffuse abdominal pain
    • Vaginal discharge (rare)
  • Physical examination
    • Vaginal bleeding
    • Suprapubic tenderness
    • Signs of peritonitis (late)
  • Work-up
    • Pre-operative laboratory testing
    • Abdominal x-ray (XR) to evaluate for free air
    • Computed tomography (CT) Abdomen/Pelvis with IV contrast
  • Treatment
    • Resuscitation and pain control as needed
    • Prompt OB-GYN consultation
    • Admit

Ectopic Pregnancy

It is easy to assume all women undergoing medical or surgical abortions have a confirmed intrauterine pregnancy. However, ectopic pregnancies have been found after induced abortions. In two studies, the rate of ectopic pregnancy was 0.7 and 1.77 per 1,000 women undergoing medical and early surgical abortion, respectively.8, 20 In the cases of early medical (<9 wk) or early surgical (<6 wk) abortion, a pseudogestational sacs may be confused with fetal demise of an intrauterine pregnancy. In order to avoid a catastrophic oversight, emergency physicians should risk stratify patients for ectopic pregnancy and if possible review imaging to ensure a confirmed fetal pole and gestational sac prior to the induced abortion. If there is any doubt about ectopic pregnancy radiology ultrasound should be performed.

  • Incidence of ectopic pregnancy in early medical abortion 0.7 per 1,0008
  • Incidence of ectopic pregnancy in early surgical abortion 1.77 per 1,00020
  • Risk stratify patients for ectopic pregnancy
    • Risk factors: Prior ectopic, history of tubal ligation or prior tubal surgery, history of pelvic inflammatory disease, and fertility treatment
    • See emDocs review article on “Ectopic Pregnancy” http://www.emdocs.net/ectopic-pregnancy/
  • Review pre-procedure imaging for documentation of intrauterine pregnancy

Retained Products of Conception21

Incidence of retained products of conception is 0.7% to 2.9%.7, 9 Retained products of conception can both present primarily as persistent bleeding or secondarily with an infection (see below).

  • Work-up
    • Complete blood count (CBC)
    • Coagulation panel – platelet count, prothrombin time (PT), partial thromboplastin time (PTT)
      • If abnormal obtain DIC screening
    • Blood type and screen
    • β-hCG
    • Basic metabolic panel (BMP)
    • Ultrasound
  • Treatment
    • Consult OB-GYN
    • Consider admission for dilatation and curettage if there is:
      • Evidence of infection (see below)
      • DIC
      • Retained products for more than 4 weeks

Septic abortion and Endometritis11, 21-23

  • Septic abortion – Spontaneous, medical, or surgical abortion complicated by pelvic infection infecting the products of conception (placenta and fetus)
  • Endometritis – infection of the endometrium
  • Risk Factors
    • Increasing gestational age
    • Retained products of conception
    • Delay in seeking medical attention
    • Unsafe abortion
    • Prolonged vaginal bleeding
  • Most common causes
    • Retained products of conception
    • Introduction of normal or pathologic vaginal bacteria by instrumentation
  • Symptoms
    • Fever
    • Abdominal or pelvic pain
    • Vaginal discharge or bleeding
  • Physical exam
    • Suprapubic tenderness to palpation
    • Closed os
    • Firm and tender uterus
    • Pus or foul smelling fluid from the cervix
  • Work-up
    • β-hCG
    • CBC
    • BMP
    • Lactic acid level
    • Blood type and screen
    • Blood cultures
    • Urinalysis
    • Ultrasound to evaluate for
      • Retained products of conception – thickened endometrium with echogenic contents
      • Adnexal masses
      • Free fluid in the cul-de-sac
    • Consider abdominal XR or CT for free air in the abdomen or gas in the myometrium
  • Treatment
    • Prompt obstetric consultation
    • Fluid resuscitation
    • Broad spectrum antibiotics covering normal vaginal flora and sexually transmitted diseases:
Mild

(14 days)

Doxycycline 100mg q12h AND Ceftriaxone 250mg IM
+/- Metronidazole 500mg q12h
Moderate – Severe Clindamycin 900mg IV q8h24 AND Gentamicin 5 mg/kg IV daily24
 

Doxycycline 100mg IV BID

 

AND

Ampicillin/sulbactam 3g IV q6h
OR
Cefoxitin 900mg IV q6h

 

Case Conclusion

The patient’s work-up was notable for an elevated white blood cell count, mild anemia, a plateau of β-hCG, and pelvic ultrasound consistent with retained products of conception. Obstetrics was consulted and the patient was admitted to ambulatory surgery for D&C of retained products of conception.

Summary

  • Immediate (<24 hours) complications of induced abortion include hemorrhage and pain, commonly caused by cervical laceration and uterine perforation.
  • Delayed (24 hours – 4 weeks) complications include retained products of conception and infection.
  • Key historical features to evaluate induced abortion complication risk are: prior cervical surgery, prior Caesarean section, increased gestational age, and parity.
  • Consider early OB-GYN consult in any post-abortion patient
  • Risk stratify patients for ectopic pregnancy
  • Review pre-procedure imaging for documentation of intrauterine pregnancy
  • Ultrasound is a key imaging modality for suspected delayed complications of induced abortion.
  • If you suspect septic abortion, cover for normal vaginal flora and sexually transmitted diseases

Further Reading / References

  1. Upadhyay UD, Desai S, Zlidar V, Weitz TA, Grossman D, Anderson P, et al. Incidence of emergency department visits and complications after abortion. Obstetrics and gynecology. 2015;125(1):175-183.
  2. Fawcus SR. Maternal mortality and unsafe abortion. Best practice & research Clinical obstetrics & gynaecology. 2008;22(3):533-548.
  3. Organization WH. Unsafe abortion: global and regional estimates of the incidence of unsafe abortion and association mortality in 2003. 5th ed. ed. Geneva: WHO; 2007.
  4. Sama CB, Aminde LN, Angwafo FF, 3rd. Clandestine abortion causing uterine perforation and bowel infarction in a rural area: a case report and brief review. BMC research notes. 2016;9(1):98.
  5. Jones RK, Jerman J. Abortion incidence and service availability in the United States, 2011. Perspectives on sexual and reproductive health. 2014;46(1):3-14.
  6. Pazol K, Creanga AA, Jamieson DJ, Centers for Disease C, Prevention. Abortion Surveillance – United States, 2012. Morbidity and mortality weekly report Surveillance summaries. 2015;64(10):1-40.
  7. Heisterberg L, Kringelbach M. Early complications after induced first-trimester abortion. Acta obstetricia et gynecologica Scandinavica. 1987;66(3):201-204.
  8. Cleland K, Creinin MD, Nucatola D, Nshom M, Trussell J. Significant adverse events and outcomes after medical abortion. Obstetrics and gynecology. 2013;121(1):166-171.
  9. Ireland LD, Gatter M, Chen AY. Medical Compared With Surgical Abortion for Effective Pregnancy Termination in the First Trimester. Obstetrics and gynecology. 2015;126(1):22-28.
  10. Zane S, Creanga AA, Berg CJ, Pazol K, Suchdev DB, Jamieson DJ, et al. Abortion-Related Mortality in the United States: 1998-2010. Obstetrics and gynecology. 2015;126(2):258-265.
  11. Waller N. Complications of Gynecologic Procedures. In: Tintinalli JE, Stapczynski J, Ma O, Yealy DM, Meckler GD, Cline DM, editors. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e. New York, NY: McGraw-Hill; 2016.
  12. ACOG Practice Bulletin No. 135: Second-trimester abortion. Obstetrics and gynecology. 2013;121(6):1394-1406.
  13. Kerns J, Steinauer J. Management of postabortion hemorrhage: release date November 2012 SFP Guideline #20131. Contraception. 2013;87(3):331-342.
  14. White K, Carroll E, Grossman D. Complications from first-trimester aspiration abortion: a systematic review of the literature. Contraception. 2015;92(5):422-438.
  15. Allen RH, Goldberg AB, Board of Society of Family P. Cervical dilation before first-trimester surgical abortion (<14 weeks’ gestation). SFP Guideline 20071. Contraception. 2007;76(2):139-156.
  16. Kaunitz AM, Rovira EZ, Grimes DA, Schulz KF. Abortions that fail. Obstetrics and gynecology. 1985;66(4):533-537.
  17. Cates W, Jr., Schulz KF, Grimes DA. The risks associated with teenage abortion. The New England journal of medicine. 1983;309(11):621-624.
  18. Pridmore BR, Chambers DG. Uterine perforation during surgical abortion: a review of diagnosis, management and prevention. The Australian & New Zealand journal of obstetrics & gynaecology. 1999;39(3):349-353.
  19. Grimes DA, Schulz KF, Cates WJ, Jr. Prevention of uterine perforation during curettage abortion. Jama. 1984;251(16):2108-2111.
  20. Paul ME, Mitchell CM, Rogers AJ, Fox MC, Lackie EG. Early surgical abortion: efficacy and safety. American journal of obstetrics and gynecology. 2002;187(2):407-411.
  21. Tucker R, Platt M. Obstetric and Gynecological Emergencies and Rape. In: Stone C, Humphries RL, editors. CURRENT Diagnosis & Treatment Emergency Medicine. 7e ed. New York, NY: McGraw-Hill; 2011.
  22. Lapinsky SE. Obstetric infections. Critical care clinics. 2013;29(3):509-520.
  23. Eschenbach DA. Treating spontaneous and induced septic abortions. Obstetrics and gynecology. 2015;125(5):1042-1048.
  24. Mackeen AD, Packard RE, Ota E, Speer L. Antibiotic regimens for postpartum endometritis. The Cochrane database of systematic reviews. 2015(2):CD001067.

 

 

 

 

Postpartum (within 1st month) Emergencies and their Management

Authors: Megha Rajpal, MD and Brendan Milliner, MD (EM Resident Physicians, Icahn School of Medicine at Mount Sinai) // Edited by: Jennifer Robertson, MD, MSEd and Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

 Case 1: Vaginal Bleeding

A 35-year-old female presents to the emergency department (ED) with four days of heavy vaginal bleeding.  She says she has had to change her pad once every hour.  The patient also states that she had an uncomplicated spontaneous vaginal delivery (SVD) of a full-term female one week prior to her ED presentation. She was discharged home with her baby after the delivery.  The patient denies any history of fever or pain.  On examination, she is afebrile and hemodynamically stable.  On pelvic examination, her cervical os is closed, but active bleeding is present.  There is no cervical motion tenderness or signs of trauma.

Vaginal bleeding after a SVD or Caesarean (C)-section can be normal.  However, heavy postpartum bleeding can signify more serious hemorrhage.  Postpartum hemorrhage (PPH) can be divided into two categories:

  1. Early: Early PPH is defined as heavy bleeding that occurs less than 24 hours after delivery. Most often, it is caused by uterine atony.  Other differential diagnoses of early PPH include genital tract laceration (s), retained placental parts, placenta accreta, hematomas, uterine inversion, uterine rupture, and coagulopathy.1
  2. Late: Late PPH occurs after 24 hours but no later than six weeks after delivery. Differential diagnoses of late PPH include endometritis, retained placental parts, or delayed placental site involution.1,2

Pearls:

  • Uterine atony is the most common cause of early PPH.
  • Retained placenta is a common cause of early and late PPH.

Tests to order in the ED may include:

  • Complete blood count (CBC), coagulation studies, type and screen with crossmatch if necessary.
  • Ultrasound (US) looking for retained placental tissue (r/o by demonstrating a normal uterine stripe). US is also useful to distinguish between retained tissue (echogenic) and intrauterine clot (sonolucent).  You can also visualize occult hematomas.
  • Computed tomography (CT) can help visualize a hematoma if US is non-diagnostic.

How can we manage this patient in the ED?

  • Before any orders are placed, assess the patient’s airway, breathing and circulation (ABCs). Two large bore intravenous (IV) lines should be placed, the extent of blood loss should be estimated, and the patient should be immediately.
  • If the uterus feels boggy, start with a manual massage.
  • Use medications to treat uterine atony by increasing uterine muscular tone.1,3
Drug Dose Side effects
Oxytocin (first line) 10U IM, 20-30U in 1L NS at 200cc/hr IV Hypotension, cramping
Ergonovine maleate 0.2mg intramuscular (IM) Cramping
Methylergonovine 0.2mg IM Cramping
15-methyl-prostaglandin 0.25mg IM Nausea, vomiting
  • If bleeding continues after the above therapies, look for vaginal trauma and retained placental products.
  • If uterine inversion is visualized, then the uterine anatomy should be restored manually. If any placenta is attached, then it should be removed.
  • Refractory bleeding from any source may require emergent surgical intervention or arterial embolization by interventional radiology (IR). Patients with uterine rupture require surgical intervention.  Retroperitoneal hematomas also require surgery or embolization.

Pitfalls:

  1. Failure to realize the extent of blood loss. Young women can compensate for acute blood loss Therefore, they may not develop signs of hypovolemia until later.
  2. Failure to give oxytocin for uterine atony because manual uterine massage is working. However, once massage has ceased, bleeding can resume again and can be brisk.
  3. Failure to detect vaginal lacerations. After uterine atony, lacerations are the second most common cause of PPH.

Case 2: Fever

A 30-year-old postpartum female presents to the ED complaining of fever.  She had an uncomplicated SVD of a full-term female week ago.  She was discharged home with her baby one day after the delivery.  She notes she has not been feeling well for two days and on the day of presentation to the ED, she developed a temperature of 100.9 °Fahrenheit (F).

Postpartum, or puerperal, fever can be divided into two general categories:

  1. Early puerperal fever (occurring < 48 hours after delivery): diagnoses may include uterine and/or pelvic infections, urinary tract infections (UTI) or respiratory tract infections.1
  2. Late puerperal fever (occurring > 48 hours but < 6 weeks after delivery): diagnoses may include uterine and pelvic infections, abdominal and episiotomy wound infections, breast infections, or thrombophlebitis

In a patient who has post-partum fever (PPF), a thorough history of present illness (HPI) and obstetric (OB) history should be obtained. Perform a detailed physical examination with emphasis on the genital tract, breasts, wounds, urinary, and respiratory systems.  Look for abdominal and uterine tenderness and evaluate uterine tone. Consider abscess or hematoma if an adnexal mass is palpated.

Lower abdominal pain can be from non-specific inflammation or it could be from retained placental products and persistent contractions.  Vaginal discharge could be normal or a sign of endometritis.  Abdominal tenderness, foul-smelling lochia, tachycardia, decreased bowel sounds are all non-specific.  Make sure to examine any wound sites for signs of cellulitis, necrotizing fasciitis, and dehiscence.  Mastitis can present with fever, fatigue, and upper respiratory infection symptoms so make sure to do a comprehensive physical examination, including the breasts and lungs. Septic thrombophlebitis can present with just fevers or symptoms of PE. 4

What to order in the ED?

  1. CBC, UA, blood cultures.
  2. Chest X-ray (CXR) if respiratory symptoms are present.
  3. An X-ray might demonstrate soft tissue gas if necrotizing fasciitis is present.
  4. Ultrasound can show endometrial gas
  5. CT for endometritis might show intrauterine debris or fluid in some patients.

Treatment:

Treatment of puerperal fever depends on what is suspected based on history, physical examination and primary ED workup:

Site Cause of fever Treatment
Pelvic Endometritis – most common cause Clindamycin and gentamicin or clindamycin and a third-generation cephalosporin.

Unasyn, Timentin, Zosyn, and Primaxin are all effective single, broad-spectrum antibiotics. 5

Wound infection Open and debride
Necrotizing fasciitis Surgical emergency
Pelvic abscess – US or CT to diagnose Incision and Drainage (I&D)
Septic thrombophlebitis – failure to respond to abx for endometritis Anticoagulation and antibiotics for 7-10 days.6
Urinary Pyelonephritis PO: fluoroquinolone

IV: fluoroquinolone, aminoglycoside, extended spectrum cephalosporin

Pulmonary Atelectasis or pneumonia Macrolide, fluoroquinolone
Breast Engorgement vs. mastitis (flu-like symptoms, focal erythema and tenderness) Mastitis: cover for staphylococcus with dicloxacillin or clindamycin

 

Continue breast-feeding.

Other Viral syndrome, sepsis, bacteremia Treat as clinically indicated

 

Pitfalls:

  1. Failure to consider non-gynecological sources of infection such as UTIs and pneumonia.
  2. Failure to recognize necrotizing fasciitis or call an emergent surgery consult.
  3. Failure to aggressively resuscitate and start antibiotics early.
  4. Thinking that breast pain and fever automatically equate to mastitis. Engorgement is a possibility and antibiotics are not necessary for this.

Case 3: Hypertension

A 40-year-old female presents to the ED with a chief complaint of high blood pressure. She had an uncomplicated C-section one week prior to presentation to the ED.   Her blood pressure in the ED is 190/110 and other vital signs are within normal limits.  The patient denies any other symptoms including headache, nausea, vomiting, blurry vision, chest pain, dyspnea, or focal weakness.

 Definitions:

  1. Postpartum hypertension may be defined several ways including: diastolic blood pressures of ≥ 90mmHg on two consecutive occasions at least four hours apart or a single diastolic blood pressure >110mmHg. It may also be defined as a systolic blood pressure >140mmHg or a diastolic blood pressure > 90mmHg without proteinuria with readings taken on at least two occasions, six hours apart. 7
  2. Pre-eclampsia is defined as a systolic blood pressure >140mmHg or diastolic blood pressure > 90 mmHg and proteinuria of ≥ 0.3 grams (gm) in 24-hour urine specimen. Random urine dipstick of 1+ is suggestive but not diagnostic.8 Note: while some providers continue to screen for proteinuria, others have moved away from this practice as end-organ damage can be present without proteinuria.
  3. Eclampsia is defined as a seizure in association with hypertension and proteinuria. Late postpartum eclampsia (LPPE) is defined as eclamptic seizures that occur > 48 hours after delivery but within four weeks postpartum.
  4. HELLP syndrome is defined as a hemolytic anemia with a microspherocytes or schistocytes on blood smear, elevated liver enzymes (LDH > 600 IU/L, AST > 70 IU/L, bilirubin > 1.2 mg/dL), and a low platelet count (< 100,000/mm^3).9

It is essential to remember that postpartum hypertensive disorders (the ones defined above) do not need to be a continuation of antenatal or gestational hypertensive disorders.  Post-partum hypertension can be a new diagnosis after delivery and it is important to recognize and treat high blood pressure early in order to avoid any complications that may arise from it.

Tests to obtain in the ED include:

  1. Repeat vital signs often
  2. A UA to evaluate for proteinuria
  3. CBC and peripheral blood smear to look for hemolysis, anemia, and/or thrombocytopenia
  4. A basic metabolic panel (BMP) to assess electrolytes
  5. Liver function tests
  6. Baseline magnesium level
  7. Prothrombin time (PT), Partial thromboplastin time (PTT), and fibrinogen to evaluate for disseminated intravascular coagulation (DIC)
  8. Order a CXR in any patient with pulmonary signs and symptoms, especially those who may have HELLP Syndrome
  9. Remember that a hepatic hematoma is a complication of HELLP. Therefore, if your patient with HELLP Syndrome has right upper quadrant (RUQ) pain, order a CT. Note that CT is better than US in diagnosing a hepatic hematoma.
  10. If your patient has altered mental status, hypoglycemia and drug toxicity should be ruled out. Consider ordering a head CT to rule-out intracranial pathology.  Never forget about the non-OB causes of altered mental status.
  11. One rare, but lethal, complication of eclampsia is posterior reversible encephalopathy syndrome (PRES). This syndrome presents with headache, confusion, visual changes, and seizures that can be diagnosed with magnetic resonance imaging (MRI) of the brain. White matter changes are diagnostic of PRES. A 1993 study by Raps et al demonstrated that PRES is an indicator of eclampsia, even in the absence of hypertension and proteinuria.10

Managing Post-Partum Hypertension in the ED:

If your patient has post-partum hypertension without any signs of preeclampsia, then treat if you think it is clinically warranted. An asymptomatic post-partum patient with high blood pressure does not necessarily require treatment.  In addition, there is not strong evidence to show that treating hypertension prevents pre-eclampsia.11

  1. If you choose to treat your patient, labetalol or propranolol should be given. These are preferred first line agents as they do not concentrate in breast milk. Nifedipine or verapamil can be given as second line agents if beta-blockers are contraindicated. 11,12
  2. Pre-eclampsia, unlike post-partum hypertension, requires immediate treatment. The goal is to reduce the blood pressure as soon as possible to prevent eclampsia. First line agents to manage blood pressure include labetalol 10-20 mg IV or hydralazine 5mg IV.  Magnesium sulfate (4-6 gm IV over 15 minutes followed by a drip at 2 gm/hr) should also be given as it is neuroprotective and can reduce risk of eclampsia.13
  3. For persistent seizures, give diazepam 0.1-0.3 mg/kg IV push (P), lorazepam 0.02-0.03 mg/kg IVP or Phenytoin 20 mg/kg IV as a 50 mg/min infusion.
  4. Like pre-eclampsia, the goals of treating HELLP are to control blood pressure and prevent seizures. Administer platelets if the platelet count is < 20,000/microliter (µL) or if there are overt signs of bleeding.
  5. If a ruptured hepatic hematoma is suspected on physical examination, focus on resuscitating and obtaining OB/Gynecology (GYN) consult.

Pitfall:

  1. Not recognizing and diagnosing pre-eclampsia. In one retrospective chart review of 24 women with post-partum eclampsia, 22 women had only one warning sign or symptom and 12 women had two.  Only 1/3 of these women sought medical attention for their prodromal complaints and 6/7 of these women were discharged from the ED without treatment.14

Case 4: Headache

The same patient above, instead of the complaint of high blood pressure, complains of a headache.  She reports her headache is severe, constant, and is associated with nausea and vomiting. However, she denies focal weakness, visual complaints and seizure activity.  Pre-eclampsia remains on the differential as headache can be a presenting sign for this diagnosis. However, besides pre-eclampsia, there are other causes of headache that can occur in post-partum patients.   These possible causes include central nervous system (CNS) infection, subarachnoid hemorrhage (SAH), intracranial hemorrhage (ICH), vasculitis, cerebral venous sinus thrombosis, carotid or vertebral artery dissection, ischemic stroke, post-dural puncture headache and other less emergent causes such as tension and migraine headaches.

In a retrospective review of 95 women with severe post-partum headache, 39% were diagnosed with tension headache, 24% with pre-eclampsia/eclampsia, 16% with post-dural puncture headache, 11% with migraine, and 10% with serious conditions such as ICH, mass, cerebral venous sinus thrombosis. 15 While performing the physical examination, be sure to look for meningismus, papilledema, and check reflexes.  While there are multiple etiologies of headache, the more urgent and “cannot miss” causes of headache and some of their concerning symptoms include:

  1. Pre-eclampsia: hypertension plus concerning symptoms as mentioned in the prior section. Remember patient does not need to have a history of pre-eclampsia during pregnancy to be diagnosed with it during postpartum period.
  2. Post-dural headache: constant, dull, throbbing pain exacerbated by an upright position
  3. CNS infection: fever, leukocytosis, altered mental status
  4. SAH: sudden onset headache with or without focal neurologic examination findings
  5. Cerebral venous sinus thrombosis: progressive headache with or without focal neurologic findings. Patients may or may not have signs of intracranial hypertension. Pregnancy and the puerperium are risk factors for central venous sinus thrombosis, likely due to the hypercoagulable state of pregnancy.
  6. The risk of both hemorrhagic and ischemic stroke peaks in the six weeks postpartum

Tests to order in the ED:

  1. If a post-dural headache, migraine, or tension headache is suspected, then no tests are necessary.
  2. Of course if your patient has neurologic signs, altered mental status, fever, and/or meningismus, a CT head should be obtained along with a CBC, BMP and blood cultures. A lumbar puncture (LP) with cerebrospinal (CSF) cultures should be considered if deemed safe to perform.
  3. Consider LP if meningitis is suspected
  4. If cerebral venous sinus thrombosis is suspected, MRI and magnetic resonance venography (MRV) are the gold standard diagnostic imaging modalities

ED Treatments:

  1. The recommended treatment for a post-dural headache is bed rest and analgesics. However, an epidural blood patch is definitive treatment.16
  2. Pre-eclampsia treatment as discussed above.
  3. Cerebral venous sinus thrombosis are typically treated with anti-coagulation, however neurology should be consulted.
  4. Treat SAH, migraines, and tension headaches as you would in any other patient. Note that the ergot alkaloids are contraindicated in patients who are breastfeeding.

Pitfall:

  1. Blaming a post-partum patient’s headache on recent stressors.

Case 5: Cardiomyopathy

A 38-year-old female arrives in the ED complaining of progressively worsening shortness of breath, cough, and orthopnea.  She delivered twins by C-section one week prior to presenting to the ED and she also relays a history of pre-eclampsia during the pregnancy. Her vital signs in the ED are the following: blood pressure (BP) 180/110, heart rate (HR) 125, respiratory rate (RR) 25, temperature 99°F, pulse oximetry 95% on room air (RA).  On examination, she has jugular venous distention (JVD), pulmonary rales, a S3 gallop, and bilateral lower extremity edema.  You are concerned that the patient may have peri-partum cardiomyopathy.

Peripartum cardiomyopathy is defined as the development of cardiac failure in the final month of pregnancy. Peripartum cardiomyopathy may also occur in the first five post-partum months if no other identifiable cause or history of cardiac disease can be identified.17  The majority (97%) of patients present in the first two post-partum months. The diagnosis is more common in older, multi-parous women and in patients with twin gestations.  Patients often have superimposed pre-eclampsia, obesity, or coexisting obstetric infection.18

Patients present with symptoms of left heart failure including dyspnea, orthopnea, and rales.  

Tests to consider ordering in the ED:

  1. An electrocardiogram (ECG), which may demonstrate ST-T wave changes or LV hypertrophy(LVH)
  2. A CXR may show cardiomegaly and pulmonary edema
  3. If obtained, an echocardiogram (Echo) may demonstrate four chamber enlargement and abnormalities of LV contractility.

ED Management:

  1. Treatment for peripartum cardiomyopathy is similar to that for any heart failure: oxygen as needed, diuretics when appropriate acutely, vasodilators, and arrhythmia management.

Pitfall:

  1. Shortness of breath, tachypnea, and tachycardia in a postpartum patient is concerning. A full evaluation should be conducted in the ED. Remember that anxiety is always a diagnosis of exclusion.

Summary: Common postpartum emergencies include hemorrhage, infections, hypertension, preeclampsia/eclampsia, and headache. HELLP and peripartum cardiomyopathy are rare postpartum complications.   A careful history and physical examination, knowledge of differential diagnoses, and early treatments are essential in managing the postpartum patient.

Postpartum hemorrhage requires rapid resuscitation even if signs and symptoms of shock are not initially present.  Preeclampsia and eclampsia do not always occur during pregnancy and CAN de novo in the postpartum period.  Headache is usually a common and benign complaint, but it can be a presenting symptom of preeclampsia, SAH or cerebral venous sinus thrombosis.  

 If the history and physical exam are concerning enough for one of the malignant pathologies mentioned above, admission for observation may be prudent, even with a negative ED workup. Because these patients can be complicated, consultation with OB, anesthesia, neurology, and/or cardiology is also recommended.

 References / Further reading:

  1. Mendelson MH, Lang J. “Postpartum Emergencies”. Wolfson AB (Ed.). Lippincott Williams and Wilkins. Philadelphia, PA; 2005: 522-27.
  2. Babarinsa IA, Hayman RG, Draycott TJ. Secondary post-partum haemorrhage: Challenges in evidence-based causes and management. Eur J Obstet Gynecol Reporod Biol. 2011;159:255–260.
  3. American College of Obstetricians and Gynecologists. ACOG Practice Bulletin: Clinical Management Guidelines for Obstetrician-Gynecologists Number 76, October 2006: Postpartum hemorrhage. Obstet Gynecol. 2006;108:1039–1047.
  4. Jaiyeoba O. Postoperative infections in obstetrics and gynecology. Clin Obstet Gynecol. 2012;55:904–913
  5. Mackeen AD, Packard RE, Ota E, Speer L. Antibiotic regimens for postpartum endometritis. Cochrane Database Syst Rev. 2015.
  6. Garcia J, Aboujaoude R, Apuzzio J, et al. Septic pelvic thrombophlebitis: Diagnosis and management. Infect Dis Obstet Gynecol. 2006;2006:15614.
  7. Brown MA, Hague WM, Higgins J, et al. The detection, investigation and management of hypertension in pregnancy: executive summary. Aust N Z J Obstet Gynaecol.  2000;40(2): 133-138.
  8. ACOG Practice Bulletin: Diagnosis and management of pre-eclampsia and eclampsia. Obstet Gynaecol. 2002;99(1): 159-167.
  9. Stone JH. HELLP Syndrome: Hemolysis, elevated liver enzyme, and low platelets. JAMA.  1998;280:559-562.
  10. Raps EC, Galetta SL, Broderick M, et al. Delayed peripartum vasculopathy: cerebral eclampsia revisited. Ann Neurol.  1993;33:222-225.
  11. Abalos E, Duley L, Steyn DW, et al. Antihypertensive drug therapy for mild to moderate hypertension during pregnancy. Cochrane Database Sys Rev. 2007.
  12. American College of Emergency Physicians Clinical Policies Subcommittee. Clinical policy: critical issues in the evaluation and management of adult patients with asymptomatic hypertension in the emergency department. Ann Emerg Med.  2006;47:237-249.
  13. Sibai BM. Magnesium sulfate prophylaxis in preeclampsia: evidence from randomized trials. Clin Obstet Gynecol. 2005;48:478-488.
  14. Sibai B, Schneider J, Morrison J, et al. The late postpartum eclampsia controversy. Obstet Gynecol. 1980;55:74-78.
  15. Stella CL, Jodicke CD, How HY, et al. Postpartum headache: is your work-up complete? Am J Obstet Gynecol.2007;196:318-322.
  16. Schievink WI. Spontaneous spinal cerebrospinal fluid leaks and intracranial hypotension. JAMA. 2006:295:2286-2296.
  17. Pearson G, Veille JC, Rahimtoola S, et al. Peripartum cardiomyopathy: National Heart, Lung, and Blood Institute and Office of Rare Diseases (National Institutes of Health) workshop recommendations and review. JAMA. 2000;283(9):1183-1188.
  18.  Homans D. Peripartum cardiomyopathy.  N Engl J Med.  1985;312:1432-1437

Guidelines for Imaging: Abdominal Pain in the Pediatric and Gravid Populations

Author: Geoff Jara-Almonte, MD (PEM Fellow, New York Methodist Hospital) // Edited by: Jennifer Robertson, MD, MSEd and Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

The computed tomography (CT) scan is a commonly utilized test for abdominal pain in the emergency department (ED).  CT is so ubiquitous in the evaluation of abdominal pain in the ED that it sometimes seems as though the scan is done prior to physician evaluation. But CT is not the best test for everyone as it involves a relatively large dose of ionizing radiation, which can cause harm to a developing fetus. CT is also theorized to be associated with an increased risk of cancer in children. Additionally, some specific pediatric complaints are better evaluated, at least initially, with other diagnostic studies.

Case 1: A 10 year-old previously healthy boy presents with 16 hours of abdominal pain that was initially periumbilical, but is now worse in the right lower quadrant (RLQ). His pain is also associated with nausea, vomiting and anorexia without any diarrhea.  He lies still in bed and tenses with any abdominal palpation.  He will jump up and down, but he seems to be in significant pain.

Appendicitis is a notoriously difficult-to-diagnose condition, particularly in children and pregnant patients. Missed appendicitis is the most common cause of lawsuits in cases with patients aged 6-17 years.[i]  Children, especially younger children, are more likely to present late in the course of the disease or with a perforated appendicitis.

In the case of the pediatric patient with suspected appendicitis in whom the diagnosis remains equivocal after physical exam and laboratory testing, imaging is indicated.  The American College of Radiology (ACR) recommends ultrasound of the abdomen as the most appropriate first test in evaluating appendicitis.[ii] The American College of Emergency Physicians (ACEP) recommends using ultrasound to rule-in appendicitis, and using CT of the abdomen and pelvis to exclude appendicitis.i

A positive ultrasound has a high positive likelihood ratio for the diagnosis of appendicitis.  However a negative ultrasound generally has inadequate sensitivity to rule out appendicitis, and equivocal studies or non-visualization of the appendix are common.  In the case of an equivocal ultrasound a CT is the recommended next step. Contrast is generally favored in CT for appendicitis, however, adequate studies in the pediatric population are lacking.i

Magnetic resonance imaging (MRI) has good sensitivity for appendicitis in children however it is not recommended as a routine study due to limitations including duration of study, need for sedation, and limited experience in most centers.ii

Case 1b: 26 year-old pregnant G1P0 at 14 weeks by last menstrual period (LMP) complains of lower abdominal pain, worse on the right side for the past two days.  She has had nausea and vomiting without diarrhea.  She has had no dysuria, fever, vaginal bleeding or discharge.

 The use of ionizing radiation in pregnant patients is particularly concerning because of the radiosensitivity of the developing fetus.  MRI and ultrasound are safe in pregnancy and are the favored means of abdominal imaging in pregnancy.  The ACR recommends abdominal ultrasound and/or MRI as the most appropriate tests in the pregnant patient with RLQ pain suspicious for appendicitis or acute non-localized abdominal pain and fever.ii, [iii]  ACEP’s guidelines on the evaluation of suspected appendicitis specifically exclude pregnant patients.i

The American College of Obstetrics and Gynecology (ACOG) guidelines for diagnostic imaging during pregnancy do not address specific clinical conditions or suggest any particular imaging algorithms.  ACOG recommends that when available and appropriate, ultrasound and MRI should be used preferentially. However, the society adds the following recommendation:

With few exceptions, radiation exposure through radiography, computed tomography scan, or nuclear medicine imaging techniques is at a dose much lower than the exposure associated with fetal harm. If these techniques are necessary in addition to ultra-sonography or magnetic resonance imaging or are more readily available for the diagnosis in question, they should not be withheld from a pregnant patient.[iv]

 Case 2: A 3 week-old female is brought in by her concerned parents after vomiting up “green stuff” twice this afternoon.  The patient is the product of a term pregnancy, born by normal vaginal delivery without complications. Up to this point, she has been breast feeding 15-20 minutes every two hours without any issues. 

Acute bilious vomiting in a child under a year of age should raise suspicion for malrotation with midgut volvulus.  Malrotation is a congenital condition of inappropriate fixation of the mesentery.  The bowel may rotate about the points of abnormal fixation leading to obstruction, ischemia, and necrosis of the bowel.

The presentation of midgut volvulus may include acute bilious vomiting, with or without abdominal pain. However, it may also demonstrate gradually progressive vomiting.  Abdominal tenderness and distention may or may not be present.  Plain radiographs may show a classic “double bubble sign” with gaseous distention of the stomach and duodenum and paucity of air elsewhere. However, plain films may also be show non-specific findings or be completely normal.

Some textbooks recommend a rapid abdominal x-ray as the initial study of choice for diagnosing midgut volvulus[v], however the ACR recommends an upper gastrointestinal (GI) series as the initial diagnostic study.[vi]  The GI series will show an abnormally positioned duodenum and an absent ligament of TreitzApproximately 25% of cases of malrotation are diagnosed in children over 1 year of age.  These may present with acute bilious vomiting or recurrent intermittent episodes of abdominal pain and vomiting.  CT of the abdomen and pelvis has demonstrated high sensitivity for malrotationvii but is not part of the ACR recommendations for criteria for children under 3 months; consensus guidelines are lacking for evaluation in children outside of this age group.

Case 3a: A 5 week-old infant is brought in for vomiting.  The parents report he has been vomiting after every feed for the past 5 days.  Initially, they thought he was spitting up, but now it has become projectile.  The emesis consists of milk and is non-bloody and non-bilious.  Immediately after vomiting, the patient is hungry again and tries to feed.

New onset non-bilious vomiting in the first several weeks of life should raise suspicion for hypertrophic pyloric stenosis.  This occurs more commonly in males and firstborn children. Both an upper GI series and/or abdominal ultrasound can show real-time transit through the pyloric channel.

The ACR recommends abdominal ultrasound as the most appropriate initial study for diagnosing pyloric stenosis. A thickened and elongated pylorus can be visualized on ultrasound, and real-time evaluation can demonstrate a failure to pass gastric contents.  The ACR allows that in some centers with less experience with pyloric ultrasound, or in atypical cases, upper GI series may be an appropriated first study.

Case 3b: An 11 month-old infant has had two uncharacteristic episodes of inconsolable screaming at home.  The first one lasted about 20 minutes and resolved spontaneously. After this first episode, she was fine, happy and playful. However, about 2 hours later, the patient had a second episode and thus, her parents brought her to the ED.  On the way to the ED, the crying resolved and she became once again, happy, curious, and playful.  She has had no fever, cough, vomiting, or diarrhea.  She did have a cold one week ago. 

 The history of intermittent colicky episodes of screaming are suspicious for the diagnosis of intussusception.  In the pre-verbal child, a history of abdominal pain cannot be elucidated, but parents may report drawing of the knees to the chest.  Bloody or “currant jelly” stools and vomiting are late findings as bowel ischemia and obstruction progress.  Parents may also note pallor and lethargy during these periods.  Children may have no symptoms between episodes.  The frequency and intensity of colicky episodes typically progresses.

Consensus guidelines for the best initial study in the diagnosis of intussusception are lacking.  Plain abdominal X-ray has poor sensitivity and specificity for the condition, though it is useful to rule out free air. Plain abdominal x-ray may also demonstrate a paucity of bowel gas in the RLQ or a target sign.  Abdominal ultrasound has very high (near 100%) sensitivity and specificity for intussusception.  Typically, ultrasound is the initial test of choice.  Air or contrast enema under fluoroscopic guidance can also be used to diagnose and reduce an intussusception, either as an initial study or following a diagnostic ultrasound.

References / Further Reading

[i] Howell, John M., et al. “Clinical policy: critical issues in the evaluation and management of emergency department patients with suspected appendicitis.” Annals of emergency medicine 55.1 (2010): 71-116.

[ii] American College of Radiology – ACR Appropriateness Criteria: Right Lower Quadrant Pain – Suspected Appendicitis; https://acsearch.acr.org/docs/69357/Narrative/

[iii] American College of Radiology – ACR Appropriateness Criteria: Acute (Nonlocalized) Abdominal Pain and Fever or Suspected Abdominal Abscess https://acsearch.acr.org/docs/69467/Narrative/

[iv] Guidelines for diagnostic imaging during pregnancy and lactation. Committee Opinion No. 656. American College of Obstetricians and Gynecologists. Obstet Gynecol 2016;127:e75–80.

[v] Fleisher, Gary R., and Stephen Ludwig, eds. Textbook of pediatric emergency medicine. Lippincott Williams & Wilkins, 2010.

[vi] American College of Radiology – ACR Appropriateness Criteria: Vomiting in Infants up to Three Months of Age; https://acsearch.acr.org/docs/69445/Narrative/

viiTackett JJ, Muise ED, Cowles RA. Malrotation: Current strategies navigating the radiologic diagnosis of a surgical emergency. World Journal of Radiology. 2014;6(9):730-736. doi:10.4329/wjr.v6.i9.730.

 

Ovarian Torsion: Pearls and Pitfalls

Author: Matthew Streitz, MD (EM Resident at SAUSHEC, USAF) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit, EM Chief Resident at SAUSHEC, USAF)

How many reproductive-aged women with abdominal pain does the average emergency physician see in a shift in the emergency department? The etiology of pelvic and abdominal pain in any female patient from the age of 10 to 60 years is vast and overlapping. How do you as an ED physician decide what is at the top of the differential? Is it age, pain onset, description, or quality of pain? Is she pregnant? Does she have vaginal bleeding? What are the diagnoses that cannot be missed? Most if not all would agree that list encompasses ectopic pregnancy, tubo-ovarian abscess, acute abruption, appendicitis, and ovarian torsion, the topic of this pitfall and pearls post.

Introduction

Ovarian torsion is one of the most common gynecologic emergencies encountered by Emergency Medicine physicians and remains a must not miss diagnosis. Ovarian torsion is the partial or complete rotation of the ovary on the ligamentous support (infundibulopelvic ligament and the utero-ovarian ligaments) within the abdomen, often critically limiting the blood supply to the ovary. [1] The goal of the ED physician is to diagnose torsion in a timely fashion in an attempt to preserve ovarian function and viability.

Pathogenesis

The mechanism of ovarian torsion involves the twisting of the ovary on its ligamentous support within which the blood supply rests.   The ovary is suspended within the abdomen by the suspensory ligament of the ovary, also known as the infundibulopelvic ligament, which is not a fixed structure. The length of the ligament varies with age and gets shorter as women age. [2,3] The blood supply to the ovary is found within the ligaments and includes the tubal and ovarian branches of the uterine artery.

The most likely predisposing factor for torsion in an adult woman is an adnexal mass, either a physiologic cyst or a neoplasm. The presence of an ovarian mass increases the likelihood of torsion up to a certain size of the mass. Once a mass is large enough, the incidence of torsion actually will decrease due to decreased maneuverability and possibly secondary to adhesions as is the case with malignant masses within the ovaries. In addition the right ovary is more likely to develop ovarian torsion, possibly due to the presence of the sigmoid colon on the left side.

Normal ovaries are also at risk for torsion, which is more likely to occur with premenarchal females likely secondary to anatomy. The infundibulopelvic ligament is elongated early on and shortens with age and as girls progress through puberty. [2,3]

Once the ovary has torsed the blood supply can be diminished. The likely sequence of events is due to anatomical function and development with the venous supply, or the venous outflow limited secondary to the compressibility of veins. As time progresses and the venous congestion accumulates, the swelling and enlargement of the ovary leads to arterial compression and worsening of the condition and outcome. If allowed to progress to tissue necrosis, sepsis and peritonitis can develop. This is often very late in the course of events and is rare.

Screen Shot 2016-03-07 at 9.54.28 PM

Comprehensive Gynecology, 5th Ed. Katz, et al.

Epidemiology

The true incidence of ovarian torsion is unknown. Ovarian torsion is described as the 5th leading cause of gynecologic emergencies and represents about 15% of surgically treated adnexal masses. [4] An adnexal mass, typically with a diameter of 5 cm or greater, is the greatest risk factor for torsion although in one case series the mass size associated with torsion ranged from 1 cm to 30 cm with an average size of 9.5 cm. In premenarchal females, a case series reported over 50% of girls with torsion had normal anatomy (i.e. no mass). [4,5,6,7,8,9]  Ovarian torsion can also occur in the pregnant female, with the greatest incidence between 10 and 17 weeks although possible in all three trimesters. In pregnancy the masses most likely to torse were 6 to 8 cm, with larger masses less likely to develop torsion. [7,8,9,10]

Another important population to consider the diagnosis of ovarian torsion is the patient undergoing reproductive and infertility evaluations and using ovulation induction agents. These patients are at risk for ovarian hyperstimulation syndrome, and in one case series, 8% of patients developed torsion from physiologic cysts. [11]

Other risk factors include polycystic ovarian syndrome and tubal ligation, possibly secondary to adhesions. As with any condition or disease process those with prior history are at risk for repeat occurrence. In patients with prior ovarian torsion, 11% were likely to recur, and of those, women with normal anatomy are at greater risk. [5,6]

Clinical Presentation

The classic presentation of ovarian torsion includes acute onset of moderate to severe pain with nausea and vomiting in a patient with a prior history of an adnexal mass. Nausea typically occurs at the onset of pain. Fever and chills can occur but are more likely to occur with premenarchal females since their course is typically slower at onset with later presentation to the ED for care. They are more likely to present with fever and diffuse pain, rather than focused right or left lower quadrant pain.

The most common presenting symptom is pelvic pain followed by the history of or a palpable adnexal mass on physical exam. Patients typically present 1 to 3 days after onset, although patients with intermittent torsion can present at any time. Abdominal pain can be characterized as sharp, stabbing, and colicky, and it can possibly radiate to the flank, back, or into the pelvis and upper thigh. [5,12,13]

Evaluation in the ED – History and Physical

As with the vast majority of patient encounters, the history and physical can yield significant value to the ED physician. Important questions regarding medical history include the presence of adnexal mass, gynecologic or obstetric diseases, pregnancy, ongoing infertility treatment, and prior adnexal mass. Was there a history of recent vigorous activity, which can be seen at the onset of ovarian torsion?

Physical examination should include vital signs, which can show tachycardia, hypertension, hypotension, or even fever. Abdominal and pelvic examination (speculum and bimanual) should be performed on all sexually active females and in some cases of virginal patients. In cases of adolescent females, care should be taken to fully explain the exam to alleviate concerns and to fully explain the rationale and importance of the exam in helping with the diagnosis of torsion and other etiologies of pelvic and abdominal pain. Consent should be obtained as necessary.

Laboratory and Radiologic Imaging

Laboratory testing is not especially helpful except in determining if the patient is pregnant. Hemoglobin, white blood cell count, urinalysis, type and screen, and tests for sexually transmitted infections are all common tests that are collected during an evaluation of women with abdominal and pelvic pain where torsion is a leading diagnosis.

The preferred modality of imaging in the female with pelvic and abdominal pain is ultrasound with the use of Doppler flow studies to aid in the diagnosis of ovarian torsion. Ultrasound is also helpful in ruling out other causes of pain such as tubo-ovarian abscess, appendicitis, and ectopic pregnancy. [14,15,17]

Sonographic findings associated with ovarian torsion include a rounded and enlarged ovary on the ipsilateral side with pain. Ovarian mass, heterogeneous stroma of the ovary on the side of pain as well as an abnormal location of the ovary can all be seen in ovarian torsion. [17] Ovaries with torsion can frequently be anterior to the uterus. Decreased or absent Doppler flow is also seen with ovarian torsion, and the finding of decreased flow in the setting of pelvic pain and adnexal mass is 100% sensitive and 97% specific for torsion. [16,17]

CT and MRI are helpful for determining other causes of pelvic and abdominal pain and may show signs consistent with ovarian torsion, which include an enlarged and edematous ovary, abnormal location of an ovary, pelvic free fluid, and lack of IV contrast enhancement due to the occlusion of ovarian vessels. [18]

Diagnosis of Ovarian Torsion

A definitive diagnosis of ovarian torsion is made upon direct visualization of a rotated ovary during surgical evaluation. In a patient with an adnexal mass, acute pelvic pain, and ultrasound findings consistent with torsion, the diagnosis can be presumed. If the patient underwent CT instead, the findings discussed above with a good history for torsion warrant further evaluation by Gynecology. It is important to note that the absence of an adnexal mass does not exclude torsion. All patients with pelvic pain where ovarian torsion is high on the differential should have a Gynecologic consultation and evaluation in the Emergency Department, despite what the ultrasound demonstrates.

Differential Diagnosis

In women with acute pelvic and lower abdominal pain, ectopic pregnancy, ruptured ovarian cyst, and tubo-ovarian abscess should be on the differential when a mass is present. The most important aspect of differentiating conditions includes the pregnancy test, so this should be one of the first laboratory tests obtained. This greatly changes the differential diagnosis. It is important to keep your differential broad and to include gynecologic as well as gastrointestinal causes of pain while simultaneously ruling out all of the life threats.

Management

The management of ovarian torsion is to mitigate the effects of the decreased blood flow to the ovary with reversal of the torsion.   Preservation of ovarian function and the prevention of complications including sepsis, peritonitis, and the possibility of infertility secondary to adhesions and scarring are the main goals of management. Management of fluid and electrolyte abnormalities should be addressed immediately; antibiotics in the setting of sepsis should cover anaerobes and aerobes. Adequate treatment would include broad-spectrum antibiotics, and the patient should be typed and screened or cross-matched for blood depending on the presence of hemodynamic instability and hemoglobin levels. Ultimately surgical correction is the definitive treatment, with early surgical consultation.

References / Further Reading

  1. McWilliams GD, Hill MJ, Dietrich CS 3rd. Gynecologic emergencies. Surg Clin North Am 2008; 88:265.
  2. Germain M, Rarick T, Robins E. Management of intermittent ovarian torsion by laparoscopic oophoropexy. Obstet Gynecol 1996; 88:715.
  3. Buss JG, Lee RA. Sequential torsion of the uterine adnexa. Mayo Clin Proc 1987; 62:623.
  4. Bouguizane S, Bibi H, Farhat Y, et al. [Adnexal torsion: a report of 135 cases]. J Gynecol Obstet Biol Reprod (Paris) 2003; 32:535.
  5. Houry D, Abbott JT. Ovarian torsion: a fifteen-year review. Ann Emerg Med 2001; 38:156.
  6. Tsafrir Z, Hasson J, Levin I, et al. Adnexal torsion: cystectomy and ovarian fixation are equally important in preventing recurrence. Eur J Obstet Gynecol Reprod Biol 2012; 162:203.
  7. Anders JF, Powell EC. Urgency of evaluation and outcome of acute ovarian torsion in pediatric patients. Arch Pediatr Adolesc Med 2005; 159:532.
  8. Tsafrir Z, Azem F, Hasson J, et al. Risk factors, symptoms, and treatment of ovarian torsion in children: the twelve-year experience of one center. J Minim Invasive Gynecol 2012; 19:29.
  9. Worthington-Kirsch RL, Raptopoulos V, Cohen IT. Sequential bilateral torsion of normal ovaries in a child. J Ultrasound Med 1986; 5:663.
  10. Schmeler KM, Mayo-Smith WW, Peipert JF, et al. Adnexal masses in pregnancy: surgery compared with observation. Obstet Gynecol 2005; 105:1098.
  11. Gorkemli H, Camus, M, Clasen K. Adnexal Torsion after gonadotropin ovulation induction for IVF or ICSI and its conservative treatment. Arch Gynecol Obstet 2002; 267:4.
  12. Huchon C, Panel P, Kayem G, et al. Does this woman have adnexal torsion? Hum Reprod 2012; 27:2359.
  13. Ashwal E, Hiersch L, Krissi H, et al. Characteristics and Management of Ovarian Torsion in Premenarchal Compared With Postmenarchal Patients. Obstet Gynecol 2015; 126:514.
  14. Anthony EY, Caserta MP, Singh J, Chen MY. Adnexal masses in female pediatric patients. AJR Am J Roentgenol 2012; 198:W426.
  15. Wilkinson C, Sanderson A. Adnexal torsion — a multimodality imaging review. Clin Radiol 2012; 67:476.
  16. Nizar K, Deutsch M, Filmer S, et al. Doppler studies of the ovarian venous blood flow in the diagnosis of adnexal torsion. J Clin Ultrasound 2009; 37:436.
  17. Mashiach R, Melamed N, Gilad N, et al. Sonographic diagnosis of ovarian torsion: accuracy and predictive factors. J Ultrasound Med 2011; 30:1205.
  18. Haque TL, Togashi K, Kobayashi H, et al. Adnexal torsion: MR imaging findings of viable ovary. Eur Radiol 2000; 10:1954.
  19. http://www.ncbi.nlm.nih.gov/pubmed/23810116
  20. http://www.ncbi.nlm.nih.gov/pubmed/23558274