Can’t Miss Surgical Emergencies – Part 1

Authors: Sarah Brubaker, MD (EM Resident at SAUSHEC, US Army) and Brit Long, MD (@long_brit, EM Attending Physician at SAUSHEC) // Edited by: Jennifer Robertson, MD, MSEd and Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW Medical Center / Parkland Memorial Hospital)

You are near the end of a long shift, when you get a call from paramedics. They report that they are bringing a 65-year-old male who complains of abdominal pain and syncope. Upon arrival, he is tachycardic and hypotensive. He has a visible pulsatile abdominal mass, and upon placement of the ultrasound probe, you discover a 5.5 cm abdominal aortic aneurysm (AAA). What should you do?

In this case, the answer is clear. You call vascular surgery and he goes to the operating room (OR) almost immediately. However, what should be done to stabilize the patient before he goes to surgery?  What would you have done if his presentation had been subtle?  Would you have correctly diagnosed the patient and transferred him to the operating room, or would you have misdiagnosed him with renal colic and sent him home? Some patients may, indeed, have “classic” presentations of these disease processes. On the other hand, other patients may have more subtle signs and symptoms.  Importantly, any delay in diagnosis can hinder treatment and increase morbidity and mortality.

This is the first of a two-part series on surgical emergencies. This series discusses “cannot miss” diagnoses that require immediate, or at least emergent, surgical intervention.

Case 1:

A 28-year-old female presents to the emergency department (ED) complaining of diffuse abdominal pain that is worst in right lower quadrant (RLQ). She has associated with nausea. Her vital signs are normal except a slight tachycardia to 110 beats per minute (bpm), and physical examination is remarkable for severe tenderness to palpation in the RLQ.


Epidemiology and Risk Factors

Among women presenting to the ED with vaginal bleeding or pain in the first trimester of pregnancy, the incidence of ectopic pregnancy is approximately 10% (1). In addition, ectopic implantation occurs in 2.6% of all pregnancies and is responsible for 6% of maternal deaths during early pregnancy (2). Not all ectopic pregnancies are surgical emergencies, however, rupture of an ectopic is an emergency and requires rapid resuscitation.

The incidence of ectopic pregnancy is highest in women aged 25 to 34 years. Risk factors include previous salpingitis (3-fold risk), previous ectopic pregnancy, tubal ligation, intrauterine device use, and assisted reproductive techniques (1). The risk of subsequent ectopic pregnancy after a previous one is 22%. However, it is important to note that risk factors are absent in almost ½ of patients with a diagnosed ectopic pregnancy (3-5).


An ectopic pregnancy is defined as the implantation of a gestational sac anywhere except the uterus. Approximately 93-97% of ectopic pregnancies are located in the distal portion of the fallopian tubes, but other locations include C-section scars, the cervix, ovary, and abdomen (6). Heterotopic pregnancy, or the presence of both an intrauterine and ectopic pregnancy, occurs in 0.3-0.8% of the general population and in 1-3% of women who use assisted reproduction.

Clinical presentation

The classic symptoms of ectopic pregnancy include amenorrhea for 6-8 weeks, followed by vaginal bleeding and unilateral lower abdominal pain (1). However, 15-20% of patients with symptomatic ectopic pregnancy have no missed menstrual periods (2,5), and many patients report no history of vaginal bleeding. One study demonstrated that fewer than half of women with ectopic pregnancy have the classically described symptoms of abdominal pain and vaginal bleeding (5). In fact, these symptoms are actually more consistent with miscarriage.

Pain caused by an ectopic pregnancy can be of almost any variety. However, as a general rule, localized pain is indicative of acute distension of the fallopian tube at the site of the ectopic pregnancy. Colicky pain is consistent with small-volume intraperitoneal hemorrhage. Although rupture is typically associated with longer-lasting, more generalized pain (due to hemoperitoneum), rupture may result in a decrease in or resolution of pain (4). Shoulder pain, which is seen in 10% of ectopic pregnancies, is an indicator of poor prognosis (7) because it is a late sign caused by irritation of the diaphragm from intraperitoneal blood (2).

Because the signs and symptoms of ectopic pregnancy are not sensitive or specific, one should suspect ectopic pregnancy in any woman of reproductive age with vaginal bleeding and/or abdominal pain. About 40% of patients with ectopic pregnancy have a delay in diagnosis beyond their initial visit (8,9) because 31% of women presenting symptoms during early pregnancy are initially diagnosed as pregnancy of unknown origin (i.e., positive hCG but no pregnancy detected on ultrasound).

Physical Examination

The physical examination is also non-specific, especially in early ectopic pregnancy. An adnexal mass can be palpated in 10-20% of ectopic pregnancies (1). Depending on the size of the gestational sac, there may be cervical motion tenderness, adnexal tenderness, or slight uterine enlargement. An open cervical os and heavy vaginal bleeding are more consistent with threatened or incomplete miscarriage (2).

Hypotension, tachycardia, rebound tenderness, and low-grade fever are indicative of rupture and/or hemoperitoneum. However, these are late signs that may not be present, even in significant hemoperitoneum. Thus, if a patient is hemodynamically unstable and a ruptured ectopic is suspected, emergent surgical intervention is necessary. Of note, 20% of women with ectopic pregnancies will manifest signs and symptoms warranting immediate intervention (10).  In patients with severe hypovolemia, obtain a type and crossmatch while beginning blood transfusion in the ED prior to transport to the OR.


Necessary tests include quantitative hCG, baseline hemoglobin and hematocrit, and blood type with crossmatch. If a patient is Rh negative, administer Rh immunoglobulin 50 mcg intramuscularly (IM). Patients may demonstrate minimal symptoms despite 1000-1500 mL hemoperitoneum, so a focused assessment sonography in trauma (FAST) examination is warranted in patients with suspected ectopic pregnancy. Even if a patient is hemodynamically stable, patients with a positive FAST exam will likely need operative intervention.

In patients who are hemodynamically stable but in whom ectopic is suspected, the American College of Emergency Physicians (ACEP) guidelines recommend serum quantitative b-hCG testing, followed by TVUS. TVUS has a sensitivity of 87-99% and specificity of 94-99% (11). Several studies have demonstrated that TVUS performed by an emergency physician has similar sensitivity to TVUS performed by radiology technicians and radiologists (12,13).

The risk for ectopic pregnancy increases fourfold in a b-hCG less than 1000 (1). Thus, per ACEP guidelines, it is important to perform the ultrasound if you have suspicion for ectopic pregnancy, even if the b-hCG is below the discriminatory zone (14). In addition, do not use b-hCG value to exclude the diagnosis of ectopic in patients with indeterminate ultrasound results (Level B). However, ectopic pregnancy is likely if the b-hCG is above the discriminatory zone and no intrauterine pregnancy (IUP) is visualized.


Patients who are hemodynamically stable and without suspicion for rupture can be medically managed with methotrexate in conjunction with obstetrics consultation and follow-up. If laparoscopy is needed to confirm the diagnosis, then surgical consultation is necessary.

Any hemodynamically unstable patient with a suspected or confirmed ruptured ectopic pregnancy merits immediate surgical intervention. Stabilization should be performed concomitantly with obstetrics consultation, as patients must undergo emergent laparotomy. Patients with significant anemia and/or positive FAST results also merit emergent surgical consultation, even if they are hemodynamically stable.

Case 2:

A 68-year-old male presents with vague, intermittent abdominal pain, worse in his right flank. He has a history of hypertension, hyperlipidemia, two previous myocardial infarctions, chronic obstructive pulmonary disease, and multiple previous kidney stones. His examination is only remarkable for mild diffuse abdominal tenderness.


Epidemiology and risk factors

The prevalence of abdominal aortic aneurysm (AAA) in patients over 50 years old is 1-5% (16). AAAs are rare before age 50, and the average age of diagnosis is 65-70 (17). In addition, men are affected much more commonly than women; the incidence in men is 11.3/100,000, compared to 3/100,000 in women. However, women who develop AAA are more likely to experience complications, such as rupture.

People who smoke cigarettes are 7.6 times more likely to have an AAA than those who do not smoke (18). Risk increases with a larger number of pack-years and decreases with years since quitting smoking (19). In addition, family history is an important risk factor. One study found the prevalence of AAA in patients with affected first-degree relatives to be 15-29%, compared to 2% in the control group (20). Other risk factors include hypertension, peripheral artery disease, and COPD. Interestingly, diabetes is inversely related to AAA (21).

It is important to note that risk factors are often absent, and there are few known risk factors to predict rupture. Aneurysm size is the most important prognostic factor for rupture; aneurysms greater than 5 cm are at high risk for rupture. In addition, aneurysms whose size increase in diameter greater than 5 mm in six months are also at an increased rupture risk (22). Patients with a history of AAA grafting are also at higher risk of rupture.

Ruptured AAAs are highly associated with poor clinical outcomes. AAAs that rupture outside the hospital confer a mortality of over 60%. Even patients who survive transport to the hospital and to the OR have a mortality rate of 41-50% (23).


An aneurysm is a defect that involves all three layers (intima, media, and adventitia) of the arterial wall. The infrarenal aorta, the most common location for an AAA, has a normal diameter of 2 cm and any diameter more than 3 cm is considered an aneurysm. As previously mentioned, any diameter greater than 5 cm is at increased risk for rupture and may require surgical intervention (17,19).

There are two broad categories for ruptured AAAs: intraperitoneal and retroperitoneal. Between 10 and 30% of ruptures are intraperitoneal and these are likely to result in acute decompensation and rapid death (22). These patients often die at home or en-route to the hospital.  Patients with retroperitoneal hemorrhages are more likely to survive transport to the hospital because tamponade occurs at the rupture site, which may temporize bleeding.

Clinical Presentation

The classic triad for AAA is abdominal pain, hypotension, and a pulsatile mass. However, this triad is present in only 25-50% of cases of ruptured AAA (24). Unruptured AAAs may be completely asymptomatic. Hypotension is the least reliable feature, as most ruptures are retroperitoneal and thus, hemodynamic compensation occurs through tamponade of any bleeding at the site.

Pain from an unruptured AAA is usually gradual in onset, vague, dull, and either constant or throbbing. Sudden, acute pain may indicate rupture. Approximately half of patients describe the pain as ripping or tearing in nature (19). Retroperitoneal hemorrhage can mask symptoms for several weeks to months, resulting in colicky abdominal, flank, or back pain. Pain can radiate to chest, thigh, inguinal area, or scrotum. Patients may also present with nausea, vomiting, and other gastrointestinal symptoms. In rare cases, a large intact AAA may compress and obstruct the ureters, causing urinary symptoms such as dysuria and urinary retention.

Because symptoms of AAA are nonspecific, it is important to consider ruptured AAA in any middle-aged or elderly patient with vague symptoms and/or abdominal pain. It should also be considered in patients for whom differential diagnoses include pancreatitis, cholecystitis, intestinal ischemia, diverticulitis, appendicitis, bowel obstruction, or MI. Approximately 30% of ruptured AAAs are initially misdiagnosed (22,24) and are commonly misdiagnosed as renal colic or musculoskeletal pain. 10% of ruptures present with syncope or near-syncope, so always consider AAA in patients over 50 with syncope.

Physical Examination

The classic physical examination findings for a patient with ruptured AAA are hypotension, tachycardia, a palpable abdominal mass, and a bruit heard on abdominal auscultation. However, as mentioned above, early tamponade and compensation often result in normal vital signs, despite significant rupture. Hypotension is considered the least reliable part of the triad, as it only occurs in half of patients with ruptured AAA. It is a late finding and a poor prognostic indicator.

The abdominal examination may reveal diffuse tenderness and in the setting of AAA, this indicates expansion or rupture. A bruit may be present, but this finding is neither sensitive nor specific. An AAA may be palpated above the umbilicus. One study found abdominal palpation can detect 30-60% of unruptured, intact AAAs measuring 3.0-3.9 cm; 50-70% of AAAs measuring 4.0 to 4.9 cm; and 75%-85% of AAAs 5 cm or larger (25). However, the sensitivity of abdominal palpation much lower after rupture, especially in the setting of hypotension or significant abdominal guarding. A review in 1992 found that only 39% of AAAs were palpated by clinicians, and the overall positive predictive value of a palpable abdominal mass was only 43% (20).

Perfusion distal to the AAA is usually well-maintained, but palpation of the pulses in the lower extremities must be performed to assess for involvement of the distal aortic branches. Look for femoral pulse deficits, cyanosis, and hypoperfusion.

A rectal examination with gross blood or positive hemoccult may indicate an aortoenteric fistula, especially in patients with previous surgical AAA repair (22).


If a patient presents with hypotension and a pulsatile abdominal mass, call the vascular surgeons immediately. The best imaging modality to evaluate for AAA is ultrasound (US), which is 100% sensitive. Any aortic diameter (measured from outer wall to outer wall) greater than 3 cm is an aneurysm; an aneurysm greater than 5 cm is at high risk for rupture. However, the sensitivity of ED US in detecting extraluminal blood is very low (26), so a AAA of any size in a patient with hemodynamic instability should be presumed ruptured and the patient should be sent straight to surgery.  Free intraperitoneal/retroperitoneal blood, in the presence of AAA, confirms rupture.

If the patient is hemodynamically stable, computed tomography (CT) is the diagnostic modality of choice. It is able to characterize the aneurysm and is 100% sensitive in detecting retroperitoneal hemorrhage associated with rupture (17). However, only obtain CTs in stable patients. Patients may be taken to the OR based only on strong clinical presumption or ultrasound findings.

In addition to imaging, laboratory studies are also necessary. Obtain a complete blood count (CBC), a prothrombin (PT) and partial thromboplastin times (PTT), a lactic acid level, and type/crossmatch to facilitate potential resuscitation and operative management. In addition, obtain an electrocardiogram, troponin, and renal function panel to assess for end-organ damage secondary to hypotension. Patients may present with type 2 non-ST elevation myocardial infarctions (NSTEMIs) from demand ischemia, so it is necessary to obtain an EKG and troponin. Conversely, findings consistent with an acute MI do not exclude the diagnosis of ruptured AAA. Patients may also present with respiratory failure, so chest x-ray (CXR) and venous blood gas (VBG) may be warranted.


In all patient with known or suspected ruptured AAA, establish large bore IV access, place the patient on telemetry, and obtain an EKG, CBC, lactic acid, coagulation panel, troponin, and type/crossmatch. Any such patient should be considered unstable, regardless of initial vital signs and hematocrit.

Unstable patients with a AAA of any size require emergent surgical intervention. Patients taken to the OR soon after arrival to the ED are known to have significantly higher survival rates than those in whom surgical care is delayed (27).  Patients with ruptured AAAs often require 6-10 units of blood, so call for at least 6 units of blood as early as possible. Transfusing 1:1 PRBC:FFP has been shown to lower 30-day mortality and the incidence of colonic ischemia (28). However, hypotension may slow bleeding in patients with AAA and allow local clot formation and stabilization, so avoid over-resuscitation. In addition, do not delay transport to the OR for the sake of full resuscitation. Patients with ruptured AAA are often refractory to resuscitative efforts and any delay in definitive treatment increases mortality. The only intervention known to improve mortality is surgical repair.

Case 3:

A 59 –year-old male presents with sudden onset, 10/10, sharp, left-sided chest pain that radiates to his left shoulder blade. He appears uncomfortable, diaphoretic, and tachycardic. His blood pressure is 190/110. Physical examination is otherwise unremarkable.


Epidemiology and risk factors

Although non-traumatic thoracic aortic dissection is a rare disease (its incidence is estimated at 1/100,000), it is rapidly fatal and must be expediently diagnosed and treated (29). Up to 20% of patients with aortic dissection will suffer sudden death at home (30); some studies predict an overall mortality of up to 58% (31). The majority of aortic dissections will require surgical intervention.

Males are more likely to develop aortic dissection than females. However, there is a bimodal age distribution: the first peak occurs in younger patients with connective tissue disorders, congenital bicuspid aortic valves, or vasculitis (29,32). Up to 44% of patients with Marfan syndrome may develop aortic dissection during their lifetime; pregnant women with Marfan syndrome are at increased risk. The second peak occurs in patients older than 50 years. Up to 80% of non-traumatic aortic dissections occur between 60 and 70 years old (31).

Almost all patients with aortic dissection have a history of hypertension. Other risk factors include previous cardiac surgery, documented aortic pathology, and family history of aortic dissection or AAA.


Aortic dissection occurs as a sequela of medial degeneration (which occurs in all individuals with increasing age, but more rapidly in patients with connective tissue disorders); and intimal weakening, which results from repetitive hemodynamic stress (32,33). This repetitive stress to the aortic wall results in aortic dilation, which ultimately leads to a tear in the intima that allows blood into the medial layer. This may result in the formation of a false lumen or a subintimal hematoma. The process can happen suddenly, leading to acute symptoms or sudden death; or it can have an insidious course that presents with more subtle symptoms.

There are multiple ways to classify aortic dissections, but the most popular is the Stanford classification system. A Stanford type A dissection involves the ascending aorta, while the Stanford type B dissection involves the part of the descending aorta that is distal to the left subclavian artery (29-32). Because the highest levels of shear stress occur within the first few centimeters distal to the aortic valve, type A dissections (62%) are much more common than type B (38%) (30). Approximately 90% of aortic dissections occur within the first 10 centimeters of the aortic valve (34).

Clinical Presentation

Chest or back pain is present in up to 84.8% of patients with aortic dissection (31). Although this number may seem fairly high, it is actually quite startling because 15% of dissections may present with no pain at all. However, an absence of pain does confer lower risk of dissection, with a negative likelihood ratio of 0.3 (35). The pain is classically abrupt in onset, severe in intensity, and ripping or tearing in nature. However, it may also be pleuritic, migratory, or described as“pressure” (36-38).  46% of patients describe pain that radiates to the intra- or interscapular region of the back, and 22% of patients describe abdominal pain (39).  The pain may be constant, or propagation of the dissection may lead to episodic pain with clinical deterioration as rupture becomes imminent.

Due to involvement of proximal aortic branches, up to 17% of patients may experience neurological symptoms such as focal weakness, paresthesias, or changes in mental status (36).  In addition, aortic dilation may lead to compression of the esophagus, recurrent laryngeal nerve, or superior cervical sympathetic chain, resulting in dysphagia, hoarseness, and Horner’s syndrome. Thus, always consider aortic dissection in patients with chest pain in addition to neurological complaints (35-37).

Aortic dissection must also be considered in patients who present with syncope. 12-20% of patients with aortic dissection may present with syncope, even without chest pain and/or neurological complaints.

Although ACEP guidelines do not recommend the use of any decision-making rules to risk-stratify patients (40), one should always have a high suspicion for aortic dissection in patients with chest pain. Some studies demonstrate that up to 30% of patients ultimately diagnosed with dissection are initially suspected of having acute coronary syndrome (ACS), non-dissecting aneurysms, pericarditis, pulmonary embolism, aortic stenosis, cholecystitis, or pancreatitis (29,39,41).

Physical Examination

It is especially important to fully evaluate a patient’s risk factors and history of present illness in aortic dissection, because there are often no physical examination findings (29). A patient may appear anxious, with a “sense of impending doom.” Vital signs may be normal, but tachycardia is common, and hypertension is present in 49% of patients. Dissection may result in acute-onset congestive heart failure (cardiogenic shock) or tamponade (obstructive shock), so hypotension may be present in up to 25% of patients. Notably, hypotension portends a poor prognosis (39).

Pulse deficits and a blood pressure differential between arms are classically described findings, but in reality, they are quite rare.  Normal pulses occur in 66-94% of patients (41,42).  A diastolic murmur indicating aortic insufficiency is found in up to 75% of patients with type A aortic dissection, but the presence or absence of diastolic murmur does not significantly change pretest probability of dissection.

The physical examination may reveal neurological deficits secondary to dissection into the origin of proximal aortic side branches. The deficits may be transient or sustained, and are seen in approximately 5-10% of patients with aortic dissection (36,39). The presence of pulse deficits or blood pressure differentials and neurological deficits do increase likelihood of aortic dissection.

As a whole, there are no specific examination findings that are consistently present in aortic dissection. Because the examination is often normal, you must keep high index of suspicion for aortic dissection, despite normal presenting vital signs and nonspecific examination (29). Specifically, always consider aortic dissection in the setting of syncope, shock, or chest pain plus a neurologic deficit.


An EKG, chest X-ray and basic laboratory studies should immediately be obtained in the setting of a suspected aortic dissection. However, keep in mind that they are rarely useful in making the diagnosis. The most common EKG finding is nonspecific ST/T wave changes (33). An ascending dissection compromises coronary artery supply in 2-5% of patients with acute aortic dissection (39), and thus it may lead to myocardial damage and present as a STEMI or another form of ACS. Thus, do not exclude the diagnosis of aortic dissection in the setting of ACS.

Between 12 and 37% of patients with aortic dissection have a normal chest x-ray (33). Even those with CXR abnormalities often have subtle, non-specific changes. The classic findings include widened mediastinum/aortic knob, pleural effusion (greater on the left than the right), opacification of anterior/posterior (AP) window, left apical pleural cap, indistinct/irregular aortic contour, and tracheal/esophageal deviation. The classic “mediastinal widening” lacks sensitivity, so do not depend on the CXR to rule out aortic dissection.

CT aortogram is the gold standard diagnostic modality, with a sensitivity close to 100% (31). The “triple rule out” CT (used to evaluate the coronary arteries, aorta, and pulmonary arteries) is not recommended (33). It fails to improve diagnostic yield, reduce clinical events, or diminish downstream resource use.

Although transesophogeal echocardiogram (TEE) is 86-100% sensitive (29,31), its use is decreasing because it is time consuming and often unavailable in the ED setting.

Laboratory studies have low diagnostic yield in the setting of aortic dissection, but they are useful for stabilization and preoperative purposes. Obtain a CBC, type/crossmatch, basic metabolic panel, coagulation panel, lactate, and troponin. If the diagnosis is unclear, a lipase, liver function panel, and urinalysis may be warranted to assess for other causes of the patient’s symptoms. ACEP guidelines recommend against the use of D-dimer in the setting of suspected aortic dissection (40). Its sensitivity may be as low as 50%, and its specificity is even lower, perhaps as low as 23%. Therefore, D-dimer has no role and should not be ordered.


Always begin by stabilizing the patient, using large-volume blood transfusion if necessary. Order basic laboratory tests (CBC, electrolytes, coagulation panel, troponin, lactate, EKG, and portable CXR). In an unstable patient, a type/crossmatch for at least six units of blood should be obtained. The most important treatment is surgical intervention, so involve the cardiothoracic surgeons early.

Mortality rates are as high as 1-2% per hour (29), so it is important to promptly diagnose and treat aortic dissection.  All Stanford A (ascending) dissections require prompt surgery. A randomized control trial comparing endovascular surgical repair to medical management demonstrated no benefit to surgical intervention in uncomplicated type B dissections (31). However, Stanford B dissections that are complicated by treatment-resistant hypertension, rapidly expanding aortic diameter, or hemodynamic instability also warrant emergent surgical consult. If a patient with a Stanford B dissection does not require emergent surgical intervention, then they should be admitted to an intensive care unit (ICU).

Management of aortic dissection in the ED focuses on reducing aortic shear stress. This can be achieved by reducing blood pressure and heart rate. ACEP guidelines do not establish a target heart rate or blood pressure (40). Some guidelines suggest a goal systolic blood pressure of 100-120 mmHg, while others recommend 120-130 mmHg. The first line treatment is a beta blocker, preferably esmolol or labetalol (32,33). Esmolol can be used as an initial bolus of 0.1-0.5mg/kg IV over 1 min, followed by an infusion 0.025-0.2mg/kg/min. Labetalol is given at an initial dose of 10-20mg IV, with repeat doses of 20-40 mg q10m (max 300mg). Nitroprusside can be used as an adjunct, but only after beta blocker administration. Always administer the beta blocker before the vasodilator.  If you give the vasodilator first, reflex tachycardia will increase the shear stress and worsen the dissection.


There are several disease processes that cannot be missed in the ED. A number of them require emergency surgery, and an even smaller percentage require time-sensitive surgery. The diseases discussed in this post include ruptured ectopic pregnancy, AAA, and aortic dissection.  More disease processes will be covered in a future post. You must maintain a high index of suspicion for these diseases, as delay in treatment can lead to substantial increases in morbidity and mortality. In all of these disease processes, hemodynamic instability = emergent surgical consultulation


-You must consider this diagnosis in every female with abdominal pain and/or vaginal bleeding, especially in the setting of syncope/presyncope, hemodynamic instability.

-Do not rely on b-HCG levels to exclude this diagnosis.

Transvaginal ultrasound is the preferred diagnostic modality.

-While US is relatively sensitive and specific, do not depend on the results if the results are indeterminate and your clinical suspicion is high.

-If your patient is Rh negative, remember to give 50 mcg RhoGAM before they go to surgery.


-Classic patient: Elderly man, history of smoking and/or hypertension, with abdominal pain.

-This is another diagnosis that must be considered in syncope.

-While the classic triad is hypotension, abdominal pain, and a pulsatile abdominal mass, many patients present in atypical manners, so AAA is commonly misdiagnosed as renal colic or MSK pain.

-If you have any suspicion for AAA, especially ruptured AAA, use bedside ultrasound.

-Patients with hemodynamic instability and AAA of any size require emergent surgery.

-Look for signs of rupture (e.g blood in Morison’s pouch), but remember: US is sensitive for aneurysm, but NOT aneurysmal rupture!

-If your patient is unstable, send him or her straight to the OR. If your patient is stable and you are unsure of rupture, you may opt for a CT angiogram.

-In cases of severe hemodynamic instability, you may start emergent transfusion, but the most important stabilizing measure is surgical intervention. So do not delay surgical treatment in an attempt to “stabilize” your patient before going to the OR.


Classically severe, stabbing/tearing pain that is maximal in onset.

-Look for chest pain and other symptoms (back pain, abdominal pain, extremity pain, headache, paresthesias, weakness etc.)

-Look for symptoms above and below the diaphragm, or chest pain with neurologic symptoms.

-Do not rely on chest X-ray, D dimer, or exam to rule out dissection.

CT aortogram is the study of choice.

-Treatment requires heart rate and blood pressure control.

Stanford A and complicated Type B require emergent surgical intervention.

References/Further Reading:

  1. Houry DE, Salhi BA. Acute complications of pregnancy. In: Marx JA, Hockberger RS, Walls RM, et al, eds. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 8th ed. Philadelphia, PA: Elsevier Saunders; 2014: chap 178.
  2. Crochet JR, Lori AB, Chireau MV, Does this woman have an ectopic pregnancy? The rational clinical examination systematic review. JAMA. April 2013; 309(16): 1722-1725.
  3. Dart, Robert G., Beth Kaplan, and Kalli Varaklis. Predictive value of history and physical examination in patients with suspected ectopic pregnancy. Ann Emerg Med March 1999; 33(3): 283-290.
  4. Buckley RG, King KJ, Disney JD, Gorman JD, Klausen JH. History and physical examination to estimate the risk of ectopic pregnancy: validation of a clinical prediction model. Ann Emerg Med. 1999; 34(5): 589-594.
  5. Ramakrishnan K, Scheid DC. Ectopic pregnancy: Forget the “classic presentation” if you want to catch it sooner. J Fam Pract. 2006; 55(5): 388-395.
  6. Bouyer J, Coste J, Fernandez H, Pouly JL, Job-Spira N. Sites of ectopic pregnancy: a 10 year population-based study of 1800 cases. Hum Reprod. 2002; 17(12): 3224-3230.
  7. Ferri I. Ferri’s differential diagnosis: a practical guide to the differential diagnosis of symptoms, signs, and clinical disorders. 2nd ed. Philadelphia, PA: Elsevier/Mosby; 2011.
  8. Kirk E, Papageorghiou AT, Condous G, Tan L, Bora S, Bourne T. The diagnostic effectiveness of an initial transvaginal scan in detecting ectopic pregnancy. Hum Reprod. 2007;22(11):2824-2828.
  9. Stovall TG, Kellerman AL, Ling FW, Buster JE. Emergency department diagnosis of ectopic pregnancy. Ann Emerg Med. 1990;19(10):1098-1103.
  10. Seror V, et al: Care pathways for ectopic pregnancy: A population-based cost-effectiveness analysis. Fertil Steril 2007; 87: p 737.
  11. Kirk E., and Bourne T.: Diagnosis of ectopic pregnancy with ultrasound. Best Pract Res Clin Obstet Gynaecol 2009; 23: pp. 501-508.
  12. McRae A, Murray H, Edmonds M. Diagnostic accuracy and clinical utility of emergency department targeted ultrasonography in the evaluation of first trimester pelvic pain and bleeding: a systematic review. CJEM. 2009; 11(4):355-364.
  13. Stein JC, Wang R, Adler N, et al. Emergency physician ultrasonography for evaluating patients at risk for ectopic pregnancy: a meta-analysis. Ann Emerg Med. 2010; 56(6):674-683.
  14. Kalinski MA, et al: Hemorrhagic shock from ruptured ectopic pregnancy in a patient with a negative urine pregnancy test result. Ann Emerg Med 2002; 40: 102.
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  16. Spark JI, Baker JL, Vowden P, et al. Epidemiology of abdominal aortic aneurysms in the Asian community. Br J Surg; 2001; 88:382-384.
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  18. Vardulaki KA, Walker NM, Day NE, et al. Quantifying the risks of hypertension, age, sex and smoking in patients with abdominal aortic aneurysm. Br J Surg 2000; 87:195-200.
  19. Avegno J. Gastrointestinal emergencies. In: Tintinalli J, ed. Emergency Medicine: A Comprehensive Study Guide. 7th ed. New York, NY: McGraw-Hill; 2011:chap 72.
  20. Lederle FA, Johnson GR, Wilson SE, et al. Prevalence and associations of abdominal aortic aneurysm detected through screening. Aneurysm Detection and Management (ADAM) Veterans Affairs Cooperative Study Group. Ann Intern Med 1997; 126:441-449.
  21. Blanchard JF, Armenian HK, Friesen PP. Risk factors for abdominal aortic aneurysm: results of a case-control study. Am J Epidemiol 2000; 151:575-583.
  22. Reed KC, Curtis LA. Aortic emergencies part II: Abdominal aneurysms and aortic trauma. Emergency Medicine Practice March 2006; 8(3): 1-24.
  23. Brown MJ, Sutton AJ, Bell PR, et al. A meta-analysis of 50 years of ruptured abdominal aortic aneurysm repair. Br J Surg 2002; 89:714-730.
  24. Assar AN, Zarins CK. Ruptured abdominal aortic aneurysm: a surgical emergency with many clinical presentations. Postgraduate Medical Journal 2009; 85:268-273.
  25. Fink HA, et al: The accuracy of physical examination to detect abdominal aortic aneurysm. Arch Intern Med 2000; 160: p 833-836.
  26. Hermsen K and Chong WK: US eval of abdominal aortic and iliac aneurysms and mesenteric ischemia. Radiol Clin North Am 2004; p 365-381.
  27. Hans SS, Huang RR: Results of 101 ruptured AAA repairs from a single surgical practice. Arch Surg 2003; 138; p 898-901.
  28. Mell MV, Oneil AS, Callcut RA, Acher CW. Effect of early plasma transfusion on mortality in patients with ruptured AAA. Surgery 2010; 148: p 955-962.
  29. Reed KC, Curtis LA. Aortic emergencies, part I: Thoracic dissections and aneurysms. Emergency Medicine Practice February 2006; 8(2): 1-24.
  30. Aziz S, Ramsdale DR. Acute dissection of the thoracic aorta. Hosp Med 2004; 65(3):136-142.
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