Abdominal Aortic Aneurysm: Avoiding Failure to Diagnose
By Marshall S. Salkin, MD, JD, FACEP, FCLM, Attending Physician, Emergency Department, Northwest Community Hospital, Arlington Heights, IL.
Although the morbidity and mortality associated with cerebrovascular disease and coronary artery disease have decreased precipitously over the past three decades, the incidence of abdominal aortic aneurysm (AAA) has actually increased substantially.1 AAA is now the 13th most common cause of death in this country, accounting for more than 15,000 deaths/year.2 Only one-third of patients with AAA have the classic triad of abdominal pain, shock, and a pulsatile abdominal mass.3 Because these "typical" features are frequently absent, misdiagnosis is a common problem.4 As a result, emergency physicians must be aware that leaking or ruptured AAA may present with atypical signs and symptoms frequently leading to such erroneous diagnosis as renal colic, diverticulitis, or gastrointestinal bleeding.5 Hence, any elderly patient, with or without hypotension, who presents with abdominal pain, flank pain, or back pain must be evaluated for a symptomatic AAA. (Unless specifically indicated to the contrary this discussion pertains to symptomatic AAAs only.)Anatomy of the Normal Aorta
The signs and symptoms of an AAA are, to a large extent, a reflection of the anatomy of the normal aorta. Therefore, it is important to briefly review this subject. The aorta enters the abdomen at the level of the twelfth thoracic vertebra6 and bifurcates into the common iliac arteries at the level of the umbilicus.7 It is located retroperitoneally throughout its course in the abdomen and normally does not extend to the right of the midline of the abdomen.8 The aorta is composed of three layers: the intima, media and the adventitia. Various portions of the gastrointestinal tract, venous channels, osseous structures, the ureters, nerves, and nerve roots are in close proximity to the aorta and may be involved in the pathophysiology and symptoms of an AAA. The aorta also gives off many branches while in the abdomen: the renal, superior mesenteric, inferior mesenteric, celiac, and spinal radicular arteries.9 These arteries also may be involved in the development of symptoms of an AAA.Classification of AAA
AAA are true aneurysms. That is, they contain all three layers of the normal vessel wall.10 Therefore, symptoms result from dilatation, with or without leakage or rupture, inflammation, infection, compression of surrounding structures, or peripheral embolism.11 In more than 95% of cases, AAAs arise below the origins of the renal arteries. The normal infrarenal aorta averages approximately 2.0 cm in diameter.12 The most widely used definition of an AAA is an aorta that is dilated at least 1.5 times that of the adjacent intact aorta, usually the infrarenal aorta, or any abdominal aorta with a diameter of 3.0 cm or greater.13Etiology and Pathogenesis of AAA
In the past, atherosclerosis was believed to be the primary predisposing factor in the development of AAA. However, this is no longer the case. Most patients with advanced atherosclerosis develop occlusive vascular disease and not aneurysms.14 New hypotheses regarding the formation of AAA concern collagen and elastin, which are the two main structural proteins in the abdominal aorta. Elastin maintains the normal aortic dimension and compliance of the aorta, while collagen provides the tensile strength of the aortic wall.15 The abdominal aorta contains more collagen and less elastin than the thoracic aorta, making it stiffer and less compliant. More importantly, because there is less elastin and more collagen in the wall of an AAA than in the wall of the normal abdominal aorta,16 it is predisposed to the development of an AAA by virtue of a stiffer, less compliant aortic wall. This alteration in structural proteins is also the basis for the increased incidence of AAA seen in Marfan's and Ehrlos Danlos' syndromes, connective tissues disorders that have a genetic predisposition for an increased degradation of both collagen and elastin.17 Mechanical and hemodynamic factors also contribute to the development of an AAA. As the normal arterial pressure wave is transmitted from the aortic valve distally, the systolic blood pressure and pulse pressure increase, which increases the mechanical force subjected intraluminally upon the abdominal aorta.18 In addition, the aorta normally tapers and thus decreases in cross-sectional area as it progresses distally. This feature also increases the pressure wave amplitude upon the abdominal aortic wall, predisposing to the development of AAA. To compound the problem, the abdominal aorta, unlike the thoracic aorta, is devoid of nutrient blood vessels, called vasa vasorum, and, consequently, nourishment of the abdominal aorta depends on diffusion of oxygen and other nutrients from the lumen. The process of diffusion is compromised when the vessel wall is thickened by atherosclerosis, resulting in a reduced ability of the abdominal aorta to repair itself. This, in turn, leads to dilation, and, in some cases, rupture of the aorta.19Risk Factors
Including both symptomatic and asymptomatic versions, AAA are found in 2-5% of patients 65 years or older20 and symptomatic AAA is the 10th leading cause of death for males in this age group.21 The male to female ratio is approximately 6:1. Some risk factors associated with the development of AAA include: advanced age (mean age of diagnosis is 67 years); male gender; smoking history; chronic obstructive pulmonary disease; hypertension; hyperlipidemia; diabetes; Caucasian race; and atherosclerotic vascular disease.22 In addition, there is a definite increased incidence in patients with a first-degree relative with AAA. In fact, more than one-quarter of all patients with AAA have a first-degree relative with this condition.23 There is also an increased frequency of inguinal hernias and epithelial neoplasms in patients with AAA. The association of Marfan's and Ehrlos Danlos' syndrome with AAA has already been mentioned.Factors Influencing Rupture Rates of AAA
The risk of rupture of an AAA is directly related to its size. Five percent of AAAs that are 4 cm or smaller in diameter will rupture within five years, but AAAs that are 4-5 cm in size rupture at a rate approaching 10% in five years, and those AAAs greater than 5 cm in diameter have a rupture rate of 25-40% in five years.24 More than 50% of patients with asymptomatic AAAs over 5 cm will die from rupture, whereas only 5% of patients with AAA less than 5 cm will die from this condition.25 In general, large AAAs expand more rapidly than small AAAs, which predispose them to earlier rupture. AAAs less than 4 cm in diameter grow at a rate of 0.2-0.4 cm/year, while those over 4 cm grow at a rate of 0.3-0.8 cm/year.26 For these reasons, some authors have suggested surgery for asymptomatic AAAs which are 4-5 cm, inasmuch as 60% of these AAAs will grow to greater than 5 cm within 3-5 years.27 However, a more accurate predictor of rupture than aortic diameter is the ratio of the maximum aneurysm transverse diameter to the transverse diameter of the third lumbar vertebral disc. If the ratio is greater than one, there is a very high likelihood of rupture.28Clinical Presentation of Symptomatic AAA
History
The classic triad of abdominal or back pain associated with hypotension and a pulsatile abdominal mass is present in less than half of patients with AAAs.29 There may be no hypotensive symptoms initially, as most AAAs rupture into the left retroperitoneal space and bleeding is contained by the tamponade effect of the periaortic tissues.30 If the AAA ruptures into the peritoneal cavity, the patient generally expires prior to hospital admission. Abdominal, flank, or back pain remain the most common symptoms in patients with symptomatic AAA.31 However, urologic symptoms are present in up to 10% of all patients with ruptured AAAs and may be the most frequent reason for misdiagnosis of these patients.32 Hematuria may occur from direct trauma to the ureter by the expanding or leaking AAA or from renal parenchymal damage due to vascular disruption or renal artery embolization. The back and flank pain present with AAA may be due to irritation of the retroperitoneal ureter or by direct compression of the ureter by the expanding or leaking AAA. This mechanism, as well as compression of the sensory nerves in the retroperitoneal space, may explain the testicular, perineal, and inguinal area pain experienced by some patients with AAAs.33 One study found that almost 10% of patients 65 years and older referred for evaluation of renal colic had AAAs.34 Hence, it is imperative to rule out AAAs in elderly patients who present with signs and symptoms of renal colic. Symptomatic AAAs present with neurologic symptoms ranging from frank syncope to spinal cord ischemia in up to 5% of cases.35 A history of unexplained syncope may be the only symptom of an AAA. Patients may also present with isolated lower extremity paresis or symptoms of complete spinal cord transection.36 In light of the fact that AAAs most often rupture from the left side, producing a left lower-quadrant abdominal mass, the history of tenderness in this area mass may suggest the diagnosis of diverticulitis. Indeed, in one study, 12% of all cases of symptomatic AAAs were misdiagnosed as diverticulitis.37 The erosion of an AAA into the adjacent duodenum may produce an aortoenteric fistula that presents with Chiari's triad of midthoracic pain, sentinel hemorrhage, and subsequent massive bleeding after a symptom-free interval.38 An aortovenous fistula is suggested by a very large AAA, generally over 10 cm, associated with low back pain or abdominal pain, in a patient with symptoms of high-output heart failure and distended superficial veins of the abdomen or lower extremity.39 A symptomatic AAA is also suggested by a history of atheroembolism. Peripheral emboli to the lower extremities is the initial manifestation of an AAA in up to 5% of patients and is manifested by symptoms ranging from acute ischemia of the legs to painful cyanotic toes termed the "blue-toe syndrome."40 These emboli may also involve the renal artery, leading to hematuria and renal insufficiency or mesenteric artery occlusion with symptoms of mesenteric artery ischemia. Lastly, musculoskeletal complaints with back and leg pain may be seen with AAAs. This results from expansion of the aneurysm with pressure on adjacent neurosensory structures or from vertebral body erosion.41As with any other condition, the key to diagnosis is to maintain a high index of suspicion. This is especially true of AAAs. Any elderly patient with associated risk factors who presents with abdominal, back, flank, genital, or inguinal pain, should have AAAs as part of their differential diagnosis.
Physical Exam
It is important to stress that in many cases the physical examination will not detect the presence of an AAA, and, thus, the evaluation for an AAA is often driven by the history alone. However, the following are some physical findings that may be present in patients with this condition: unexplained hypotension or alteration of level of consciousness (however, up to 70% of patients are normotensive initially due to the hematoma being tamponaded by the retroperitoneal periaortic tissue); the presence of a pulsatile abdominal mass (obesity and abdominal distention decrease the ability to appreciate this finding); an abdominal bruit (only present in a small percentage of cases); a pulsation to the right of the midline of the abdomen (a merely tortuous or prominent aorta does not present to the right of the midline); lateral displacement of the abdominal pulse wave, as opposed to the normal aorta which expands in an anterior direction;42 and/or a left lower quadrant abdominal mass with abdominal tenderness and distention (also seen with diverticulitis and other conditions not related to an AAA). As a result of these variables, abdominal examination is highly unreliable in diagnosing an AAA. However, the physical finding of absent or diminished peripheral pulses, cyanotic or blue toes, or hematuria all are strongly suggestive in a patient with a history of abdominal or back pain, or peripheral embolization from an AAA.The Laboratory
Unfortunately, laboratory studies usually do not directly aid in the diagnosis of an AAA, and, in fact, the laboratory may suggest the diagnosis of conditions not actually present. A fall in hemoglobin, often seen with abdominal pain in an AAA, may suggest the erroneous diagnosis of a GI bleed. The presence of hematuria may suggest the presence of a kidney stone and lead the physician away from the correct diagnosis. Leukocytosis, which may also be seen with an AAA, in the presence of left lower-quadrant abdominal pain or tenderness, may lead to the misdiagnosis of diverticulitis. For these reasons, the clinical laboratory should not be relied upon for the diagnosis of an AAA.Evaluation of Suspected AAA
Up to 90% of patients with AAA will have suspicious abnormalities on plain films of the abdomen, but these changes are very often not specific for AAA. Therefore, plain films should not be used to exclude the presence of an AAA. Ultrasonography is 100% sensitive in the diagnosis of AAAs, is noninvasive, and can be rapidly done at the bedside. It is the modality of choice, in some hospitals, for screening stable patients suspected of having a symptomatic AAA and for following asymptomatic AAA growth over time.43 However, it is not ideal for evaluating complications of AAA such as visceral or renal artery involvement and cannot readily distinguish between ruptured and intact AAA. Computerized tomography (CT) is able not only to measure the size of an AAA, but is more accurate than ultrasound at detecting rupture and visceral involvement and is less operator dependent. The major disadvantages of CT are expense, time requirements, and the need to transport the patient out of the ED to perform the study. However, the high resolution of the CT may make it superior to ultrasound in the assessment of the stable patient with an AAA.44 Magnetic resonance imaging (MRI) is equivalent to CT and ultrasound in assessing aortic diameter and is superior at assessing branch vessel involvement, but MRI has the disadvantages of relative high cost, lack of availability, and the need to transport the patient out of the ED.45Management
When the patient has an asymptomatic AAA, discovered coincidentally, timely diagnostic evaluation is mandatory. If the AAA is less than 4 cm by ultrasound, repeat examination should be carried out every six months. If growth exceeds 0.5 cm in six months, or symptoms from the AAA develop, surgical intervention is indicated.46 If the AAA is initially found to be greater than 5 cm in diameter, surgical resection should be carried out unless medically contraindicated, as with recent myocardial infarction, severe pulmonary insufficiency, etc. The mortality rate for elective surgical repair of an asymptomatic AAA is only 1-5%, whereas the emergent surgical mortality rate for a ruptured AAA may exceed 75% if the patient is hypotensive when surgery is undertaken.47In the symptomatic patient with a possible AAA, the management depends upon hemodynamic stability. If the patient is stable, close monitoring and aggressive fluid resuscitation in preparation for surgery are suggested. Immediate surgical consultation, intravenous lines, type and cross match, and laboratory evaluation are in order. As opposed to the use of ultrasound in the asymptomatic patient, many authors suggest CT for assessment of the stable patient with a symptomatic AAA because the CT is less operator-dependent and provides more information about the abdominal aorta, its branches, and other abdominal organs.48
In the unstable patient suspected of having an AAA, aggressive fluid resuscitation and immediate surgical repair are indicated. Once the diagnosis of a ruptured AAA in an unstable patient is considered, any delay in surgery increases the risk of death from blood loss. The only test that might be considered, if it does not delay surgery, is a bedside ultrasound.
More significantly, a recent study found that even if the diagnosis of a ruptured AAA is incorrect, in those patients brought directly to surgery with hypotension and abdominal pain, more than 75% of patients had a condition that required surgical intervention: appendicitis, perforated peptic ulcer, diverticulitis with abscess formation, etc. The fine points of differential diagnosis are not of much practical value when dealing with abdominal pain and shock, for practically all conditions that cause this picture warrant prompt abdominal exploration. This fact further emphasizes the need for rapid surgical intervention in unstable patients believed to have a symptomatic AAA.49
The mortality rate of emergent surgery for AAA is a reflection of the hemodynamic stability of the patient at the time of surgery. Patients who are not hypotensive and have small contained hematomas have an operative mortality rate less than 20%. The mortality rate for those presenting with hypotension, but who respond adequately to fluid resuscitation with good urine output and return of normal blood pressure, approaches 40%. Those whose hypotension responds inadequately to parenteral fluids have a 60% mortality rate. If in addition to lack of return of a normal blood pressure, the patient has no urine output at the time of operation, the mortality rate is 80%.50 Therefore, with a symptomatic AAA, time is of the essence. If the patient can be brought to surgery quickly before a large hemorrhage has occurred and the blood pressure falls, a low operative mortality rate results. With AAAs, low blood pressure equals low survival rates. The key to the rapid diagnosis and treatment of an AAA is to have a high index of suspicion in every elderly patient who presents with abdominal, back, or flank pain.
It should be emphasized that in many patients with symptomatic AAAs, the history alone may drive the workup.
Missed Symptomatic AAA Lawsuits
Case #1
The patient was a 64-year-old white male with a history of diabetes mellitus, hypertension, a CVA, and a CABG. He entered the ED with complaints of abdominal pain and inability to urinate for three hours. On physical examination the patient had "low midline tenderness to palpation." There is no record of the presence or absence of abdominal masses, bruits, bowel sounds, or peripheral pulses. The patient had a normal urinalysis on a catheterized specimen, but was discharged on antibiotics with a diagnosis of urinary retention and urinary tract infection. The patient expired of a ruptured AAA the following day. The case settled for $325,000.51This patient had the following risk factors for an AAA: white, hypertension, age, male sex, diabetes, and diffuse vascular disease. His admitting complaints were urinary retention and abdominal pain. In any elderly male with abdominal pain, back pain, or flank pain, the onus is on the physician to definitively and definitely rule out an AAA before the patient can be safely discharged. The diagnosis is even more assured when one adds this patient's multiple risk factors. Moreover, an unstable AAA often presents with urinary tract symptoms, and, in fact, presents specifically with urinary retention in a significant percentage of cases. The emergency physician must bear in mind that renal colic is one of the most frequent misdiagnoses in the presence of a symptomatic AAA.
In this case, there was no record of the presence or absence of abdominal masses, bruits, bowel sounds, or peripheral pulses. In the abdominal pain presentation, documentation of key elements of the history and physical examination is absolutely critical in managing this major risk in emergency practice. The emergency physician's legal duty is to provide reasonable care under the circumstances. If the diagnosis of AAA is not apparent on history and physical, then there is no legal duty to make a diagnosis. If the key elements of the history and physical are not documented, the plaintiff's attorney can use that to great advantage during deposition and trial testimony. The emergency physician should take a very disciplined approach to performing and documenting history and physical examination in abdominal pain cases.
Case #2
A 63-year-old white male entered the ED with complaints of lightheadedness and diaphoresis while having a bowel movement the prior night. This episode was followed by abdominal pain and low back pain that brought the patient to the hospital. On physical examination the patient had a blood pressure of 104/54 and left lower-quadrant tenderness to palpation. There was a slight increase in the total white blood cell count. The patient was discharged on antibiotics with a diagnosis of diverticulitis. He returned to the ED the next day, sustained a cardiac arrest and died.52AAAs often present with a history of frank syncope or some transient alteration of the level of consciousness in a patient with abdominal, flank, or back pain. In addition, since most AAAs rupture out the left side, a left lower-quadrant abdominal mass or left lower-quadrant tenderness is often found on physical examination. This leads to another frequent misdiagnosis; that of diverticulitis. It is imperative in an elderly male who presents with findings in the left lower quadrant suggestive of diverticulitis to rule out an AAA by appropriate radiographic studies.
There are several additional problems in this case. The physician apparently dismissed the importance of the episode of diaphoresis and lightheadedness. In an elderly patient, an episode of diaphoresis must be considered an indication of serious disease, and many times in AAA it indicates a hypotensive episode. The physician also dismissed the importance of the blood pressure of 104/54. This level of blood pressure must be considered low in an elderly patient unless proven otherwise. These are not subtle findings, but similar fact patterns are common in missed AAA cases.
Case #3
A 73-year-old white male with history of diabetes and hypertension entered the ED at 8:40 a.m. with the history of abdominal pain, confusion, and syncope. Admitting blood pressure was 90/50, with a hemoglobin of 10.2 g%. On physical examination the patient had tenderness to palpation in the left lower quadrant and was found to have blue toes. There was both a progressive enlargement of the abdomen and a progressive fall of hemoglobin, with a second value of 7.1 g%. In spite of these findings, the patient was not taken to surgery until 1:40 p.m., approximately five hours after his ED admission. The patient had a stormy operative and post-operative course and expired. Settlement was for $1,700,000.53Here we have an elderly white male patient with the additional risk factors of hypertension and diabetes who enters the ED with a history of syncope and abdominal pain. On physical examination he is hypotensive, has evidence of intra-abdominal pathology with left lower quadrant tenderness and progressive abdominal distention. Significantly he has evidence of peripheral embolization with the "blue toe" syndrome.
The laboratory evaluation reveals a brisk blood loss, but no site of blood loss was evident. All of these factors strongly suggest an unstable AAA. An immediate surgical consult should have been obtained and the patient taken to surgery with alacrity well before the five-hour time delay that actually occurred in this case.
This case is representative of one type of missed AAA litigation. In these cases, the diagnosis is ultimately considered or made, but there is a delay in triage or in the waiting room, a delay in obtaining diagnostic tests, or a delay in surgical consultation and definitive management in the operating room. Once the abdominal patient enters the ED, the clock starts ticking. The entire ED team needs to participate in rapid and appropriate management of these cases. Delays at any stage of the process may have to be explained in court. The emergency physician's documentation must identify efforts made to facilitate diagnosis and intervention.
Case #4
A 59-year-old Japanese male with a history of previously resected AAA entered the ED with the chief complaint of low back and rectal area pain for one hour. The physical examination was normal except for the presence of hemorrhoids. The patient was discharged without any further evaluation with the diagnosis of internal hemorrhoids. On the way home, he sustained a cardiac arrest and expired of an AAA found at autopsy. Jury verdict for the plaintiff in the amount of $55,000.54A patient with a history of a resection of an AAA who presents with the acute onset of back pain associated with rectal, perineal, or inguinal area pain must be assumed to have a recurrence of an AAA, or some complication at the graft site. It is well-known that a percentage of patients develop late complications of abdominal aortic reconstructive surgery. Therefore, this condition must be considered and evaluated before the patient can be safely discharged.
Case #5
A 68-year-old white male entered the ED with complaints of severe pain in the abdomen and back, extending to the left flank. Physical examination revealed left lower quadrant abdominal tenderness. An IVP was ordered and the patient discharged on pain medications, apparently with the diagnosis of ureteral colic. The next day, the patient returned to the ED where the diagnosis of AAA was made. The patient went to surgery but was rendered paraplegic.Jury verdict for plaintiff was in the amount of $1,300,000.55
This is another case where an AAA presented with symptoms compatible with renal colic. Hematuria, flank pain, testicular pain, etc., can all be caused by an AAA. In fact, some authorities suggest that such elderly patients be evaluated with an abdominal ultrasound, instead of an IVP, so that both the kidneys and the aorta can be examined at one time. When the patient is an elderly male, without a past history of renal pathology, who presents with symptoms suggestive of renal colic, it is imperative that an AAA be considered and evaluated, so that the true diagnosis is not overlooked.
Case #6
A 64-year-old male presented to the ED with complaints of abdominal pain. The patient was seen by a physician who noted his suspicion of an AAA but did not order any tests and referred the patient back to his own doctor. The patient saw his own physician several times and returned to the same ED several times for the same complaint, but an ultrasound was not ordered until five months later. The test revealed an AAA, but when the patient was called to inform him of the test results his family said he had died the night before from complications of the AAA. Settlement for $360,000.56This case illustrates the rather obvious point that if the diagnosis of a symptomatic AAA is entertained an immediate evaluation should be carried out. Most leaking AAAs will rupture out the left posterolateral wall of the aorta. The ensuing hemorrhage will usually be tamponaded by the periaortic retroperitoneal tissue. This stabilizes the patient's hemodynamic status and may minimize symptoms. However, the effect is transient and eventually containment will fail, and the patient will expire unless timely diagnosis and intervention occur.
Case #7
A 57-year-old male presented to the ED with complaints of abdominal pain and was diagnosed with renal colic. There were no abnormal findings on physical examination. Subsequently, the patient's pain worsened and he died of an AAA. Jury verdict for the plaintiff was for $1,200,000.57This case reflects two principals:
1. In an elderly male with symptoms of renal colic, an AAA must be excluded.
2. Many cases of AAA have no abnormal physical findings, and the diagnosis must be considered and evaluation made on the basis of history alone.
Case #8
A 55-year-old male with a history of vascular disease entered a VA hospital for "a prostate condition" on Nov. 21, 1983. He first complained of lower abdominal and low back pain on Dec. 9, 1983. From December 9 through mid-December the patient continued to complain of low back pain and also pain radiating "out to his flanks." The patient reported the pain in his back was "starting to radiate down into his sacrum" on December 23, 1983. The pain progressively increased between Dec. 23 and Jan. 4, 1984, with a progressive fall in hemoglobin during this period of time. The patient went to surgery for an AAA on Jan. 12, 1984, but expired post-operatively. Bench trial verdict found the VA doctors had breached the standard of care, however the court also found the plaintiff failed to prove that he had a better than 50% chance of survival had the diagnosis been made and surgery carried out earlier. On appeal, the court reversed the latter finding and stated the trial court erred when it entered judgment for the defendants on the ground that the patient did not have to prove a better than 50% chance of surviving had the surgery been performed sooner.58This case again demonstrates that when an elderly male with risk factors presents with abdominal and back pain, an AAA must be considered in the differential diagnosis. When, in addition, the pain radiates to the flanks and down into the pelvic area, progressively increases, and is associated with a falling hemoglobin, an even stronger case for an AAA can be made. Here, the patient was in the same VA hospital continually from November 21 to his death on January 16, and the diagnosis was not entertained until four days before his demise.
If you don't think of it, you will not diagnosis it!
Case #9
A 66-year-old male presented to the ED with complaints of abdominal pain radiating into the right testicle. The emergency physician ordered a urinalysis, blood count, and a flat plate of the abdomen. The tests were "compatible with a kidney stone," although no IVP or ultrasound of the kidneys were performed. The patient was discharged with the diagnosis of a right ureteral calculus, given pain medications, a urine strainer, and sent home. The patient had a syncopal episode driving home from the hospital. Subsequently, a diagnosis of an AAA was made and the patient went to surgery, but expired postoperatively. The jury found the emergency physician was negligent, but held that her negligence was not a proximate cause of the patient's death. That is, the jury felt that although the emergency physician had breached a standard of care (i.e., negligence), that breach did not cause injury to the patient. The injury would have occurred anyway, unrelated to the negligent conduct of the emergency physicians. Hence a defense verdict.59This is a case that easily could have gone the other way. The presence of hematuria and what looks like a stone on a KUB in an elderly patient with abdominal pain radiating into the right testicle, neither makes the diagnosis of a ureteral calculus nor excludes the diagnosis of an AAA. More definitive tests, such as an IVP or abdominal ultrasound, must be performed to diagnose a kidney stone and rule out an AAA in these cases.
Case #10
The patient was a 55-year-old male who entered the ED with complaints of a severe pain in his lower back and down into his lower abdomen. The examination was positive for a "pulsatile abdominal aorta." In spite of the absence of urinary symptoms and the presence of what the emergency physician read as a normal KUB and IVP, the patient was discharged on antibiotics, with the diagnosis of possible kidney stone or urinary tract infection. He was also given a prescription for an ultrasound of the abdomen to be performed two days later. Nine hours later the patient returned to the same ED and was seen by another physician who relied on the prior physician's interpretation of the x-rays. The second physician again discharged the patient. The following day the films were reviewed by the radiologist who reported an enlarged abdominal aorta; "probably aneurysmal dilatation." The radiologist did not contact the ED, but merely dictated his report. On return of this report to the ED, the auditing nurse noted the discrepancy, but left the report for review by the auditing physician. This physician placed the reports in the chart without further action. The patient called for the ultrasound appointment on the appropriate day, but was told that an appointment could not be made by that department until the following morning. Eventually, the patient did get his ultrasound, which showed an AAA. Stat surgery was undertaken, but before he got to surgery, the AAA ruptured, precipitating shock and difficult surgery. He died postoperatively. A substantial confidential settlement was reached.60This is the proverbial case from hell. Anything that could go wrong, did go wrong . . . in spades! However, everything flowed from the first emergency physician's mistake in discharging a 55-year-old male patient who entered with complaints of abdominal and back pain, without clearly ruling out an AAA. This was in spite of her noting a pulsatile abdominal aorta on physical examination. She also missed calcifications in the abdominal aorta on the KUB that suggested an AAA. In addition, this physician must have been thinking of an AAA as she ordered an ultrasound of the abdomen; but she ordered it as an outpatient, non-emergent exam. A symptomatic AAA is a condition that must be evaluated immediately once the diagnosis is entertained. An outpatient, non-emergent, abdominal ultrasound in a elderly patient who presents with abdominal and back pain is like an outpatient, non-emergent ECG for a patient presenting with chest pain: it is neither prudent nor reasonable and is dangerous both for the patient and the ordering physician.
Summary
The signs and symptoms of an AAA are easily confused with such disease entities as renal colic diverticulitis, GI bleed, musculoskeletal pain, etc. Failure to diagnosis an AAA may result in a disaster both for the patient and the emergency physician. Therefore the physician must have a high index of suspicion when evaluating any elderly patient with risk factors who presents with abdominal, back, or flank pain, with or without associated hypotension. These patients may present with the additional confounding findings of an unexplained drop in hemoglobin, hematuria, a left lower quadrant tender mass, or syncope. The evaluation for an AAA must be aggressively pursued in such patients with either ultrasound or CT in order to avoid the failure to diagnosis this condition. If the diagnosis is made and surgery undertaken while the patient's blood pressure is stable, the mortality rate is low. However, if the diagnosis and surgical therapy is delayed, and the hematoma no longer is contained, the blood pressure will fall, and with it the chance for a successful outcome. Hence, the reasonable and prudent emergency physician must include AAAs in the differential diagnosis whenever evaluating patients similar to those described in the previous case reports.Best, and last, suggestion: Listen to the patient! In many cases of AAAs the history alone drives the workup and makes the diagnosis.
References
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8. Ibid.
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19. Ibid.
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25. Ibid.
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29. Banerjee A, Op. cit.
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32. Marston WA, Op. cit.
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34. Phillips SM, King D. The role of ultrasound to detect aortic aneurysms in "urologic" patients. Eur J Vasc Surg 1993;7:298-300.
35. Lynch DR, Dawson TM, Raps EC, et al. Risk factors for the neurologic complications associated with aortic aneurysms. Arch Neurol 1992;49:284-288.
36. Szilagyi DE, Hageman JH, Smith RF, et al. Spinal cord damage in surgery of the abdominal aorta. Surgery 1978;83:38-56.
37. Marston WA, Op. cit.
38. Peck JJ, Eidemiller LR. Aortoenteric fistulas. Arch Surg 1992;127:1191-1193.
39. Calligaro KD, Savarese RP, DeLaurentis DA. Unusual aspects of aortovenous fistulas associated with ruptured abdominal aortic aneurysms. J Vasc Surg 1990;12: 586-590.
40. Yao JS, Op. cit.
41. Tsolakis I, Korovessis P, Spastris P, et al. Acute rupture of an aortic aneurysm mimicking the discus hernia syndrome. A case report. Int Angiol 1992;11:142-144.
42. Kiell CS, Op. cit.
43. Earnst CB, Op. cit.
44. Stanford W, Rooholamini SA, Galvin JR. Ultrafast computed tomography in the diagnosis of aortic aneurysms and dissections. J Thorac Imaging 1990;6:32-39.
45. Arlart IP, Guhl L, Edelman RR. Magnetic resonance angiography of the abdominal aorta. Cardiovas Intervent Radiol 1992;15:43-50.
46. Hollier LH, Taylor LM, Ochsner J. Recommended indications for operative treatment of abdominal aortic aneurysms. J Vasc Surg 1992;15:1046-1056.
47. Goldstone J, Op. cit.
48. Rothrock SG, Op. cit.
49. Valentine RJ, Barth MJ, Myers SI, et al. Nonvascular emergencies presenting as ruptured abdominal aortic aneurysms. Surgery 1993;113:286-289.
50. Rutherford RB, Op. cit.
51. Illinois Case, 1995. Personal communication.
52. Case currently in litigation. Personal communication.
53. Illinois Case, 1996. Personal communication.
54. Fujimoto v. Caporale, Rao and Lutheran General Hospital Lincoln Park. Case No. 89L-12319; Illinois.
55. Charles Silvio and Virginia Silvio v. White Memorial Hospital, Spectrum Emergency Care. Docket No. 90-19530, Florida.
56. Estate of Cox v. Defendants. LRP Publications No. 181105, Settlement date: May 1996, California.
57. Estate of Murphey v. Brookhaven Memorial Hospital, et al. Case No. 7591/83. LRP Publication No. 155472 Trial date: January 1995.
58. Bell v. U.S. 854 F.2d. 881 (6th Cir. 1988)
59. Bradford v. Midway Hospital et al. Case No. 8307630-HLH December 6, 1985 California
60. Emily Elliott v. Patricia Webber, et al. Hardford County Maryland Circuit Court, No. 12638 22 525
Physician CME Questions:
9. What area of the abdominal aorta is most likely to rupture in a symptomatic AAA?
a. Left posterolateral
b. Right posterolateral
c. Left anterior
d. Right anterior
10. True or False: Most AAA arise below the origins of the renal arteries.
a. True
b. False
11. Which of the following are risk factors for AAA?
a. hypertension
b. Age
c. Male gender
d. Smoking
e. All of above
12. It is generally agreed that asymptomatic AAA above what diameter should have elective surgery?
a. 2 cm
b. 3 cm
c. 4 cm
d. 5 cm
13. True or false: A plain film of the abdomen is a good screening test for an AAA?
a. True
b. False
14. What is the approximate surgical mortality rate for symptomatic AAA patients who present with, and maintain, a normal blood pressure?
a. 20%
b. 40%
c. 60%
d. 80%
A Note from the Editor . . .
As of June 1997, I have been editing the ED Legal Letter for one year. I have enjoyed the task and am beginning to get some feedback. Readers have been calling me with interesting cases and comments, and recommendations for future articles. I began with a strong clinical focus last year and intend to continue that theme in the future. I would greatly appreciate your sharing interesting lawsuits and medical legal dilemmas with me. Please contact me through American Health Consultants at (404) 262-5475. If you have a particular interest in medicine and law or an interest in writing, let me know. Thanks.djs
First Place Winner
Daniel Sullivan, MD, JD, Executive Editor, and American Health Consultants, Publisher, are pleased to announce that ED Legal Letter took first place in the Newsletter Publishers Association annual awards. The June 1996 issue, "Missed Myocardial Infarction: Minimizing the Risk," by Dr. Sullivan and Robert Zalenski, MD, won in the category of Best Single Topic Health Newsletter. American Health Consultants would like to congratulate and thank Dr. Sullivan and all who worked on this issue for an outstaning job.
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