The trusted source for
healthcare information and
Common Diagnoses Become Difficult Diagnoses When Geriatric Patients Visit the Emergency Department: Part II
While HIV infection remains predominantly a disease of younger adults, a growing number of older adults are living with HIV infection. The term "older adult" in HIV literature refers to patients 50 years and older, and roughly 10% of patients with HIV in the United States are older adults.1 The introduction of highly active antiretroviral therapy (HAART) has allowed patients to live longer with HIV infection, although not necessarily free of symptoms. Thus, by the year 2015, it is estimated that 50% of people living with HIV/AIDS will be 50 years old or older.2
The risk factors for contraction of HIV remain the same for older adults. For men, the most common risk factor is men having sex with men, followed by injection drug use and heterosexual sex. For women, heterosexual sex is the most common route of infection. Of these new cases, the rates of infection are highest for men who have sex with men and for African-Americans.3 For example, the risk for HIV infection in African-American women is as high as 21 times that for white women.4
Although not a common problem compared to other causes of infection in the elderly, HIV-related infections can easily be misdiagnosed. As a rule, older adults experience a longer delay in diagnosis of their HIV infection.5 Some of the reasons for this include that fact that older adults have many more comorbid illnesses that can be considered as a cause of the patient's symptoms. Older adults tend to progress more rapidly to AIDS from initial HIV infection as well, possibly due to the natural decline in immune function with age.6 For example, one study found that 75% of 20-29 year olds did not progress to AIDS in one year, but 55% of 50-59 year olds and 62% of those older than 60 years progressed to AIDS in one year.7
Abdominal Emergencies With Minimal Pain
Acute abdominal pain is consistently the most common chief complaint for ED visits. Unfortunately, the elderly patient with abdominal pain is both time-consuming and high risk for surgical intervention. Recent studies of elderly ED patients with acute abdominal pain have found their length of stay in the ED is roughly 20% longer than young adults with abdominal pain, nearly 60% will be admitted, and 18-33% will require surgery during the admission.8,9 Patients who were discharged were followed for two weeks, and 10% of them returned to the ED, with another 5% dying in the two weeks after their visit.9 Studies have shown that misdiagnosis rate for these patients are as high as 52%.10 In addition, the diagnosis reached in the ED when elderly patients are sent to the operating room is not correct in up to 21% of cases.8 As one might expect from these data, overall mortality for elderly patients with abdominal pain also is relatively high, with 10% of these patients not surviving to discharge.8
There is no shortage of reasons why elderly patients with abdominal pain can be difficult to diagnose in the ED. As mentioned previously, fever can be absent in up to 33% of elderly patients with significant bacterial/viral infections.11 Histories can be vague due to underlying dementia or to acute mental status changes, or elderly patients can be stoic and minimize pain. The physical exam may mislead one as to the severity of the disease as well. One recent study of elderly patients with abdominal pain found that older patients had less rigidity or rebound tenderness in the presence of peritonitis than did younger counterparts.10 Another study found only 21% of patients older than 70 years with perforated ulcer presented with abdominal rigidity.12 Medications that elderly patients commonly take can mask symptoms, such as beta-blockers masking tachycardia, chronic steroids lowering inflammatory response, or chronic narcotics blunting pain severity.
Given all these limitations in the clinical evaluation of elderly patients with acute abdominal pain, one would expect CT scanning to be a common tool used in their ED evaluation. (See Table 1.) These data support the idea that CT scan is useful in diagnosis of acute abdominal pain. As only 12% of CT scans in this study were normal, this information reinforces the fact that there is a high incidence of pathology in elderly patients with acute abdominal pain.
Bowel Obstruction. Intestinal obstruction is one of the most common diagnoses leading to surgery in elderly patients with abdominal pain and accounts for 15% of admissions overall in patients with acute abdominal pain.15 About 80% of these admissions are small bowel obstructions, and the other 20% are large bowel in origin.15 Bowel obstructions are classified as mechanical or functional (ileus), which is an important distinction. Mechanical obstructions often require surgery to prevent/treat perforation, while functional obstructions are treated medically. The two can be very hard to discern, especially in their early stages. In general, patients with obstruction tend to be sicker, have more severe symptoms, and progress more rapidly than those with ileus.16 Air-fluid levels and obliteration of the lumen are not present in ileus, and CT scan is up to 90% sensitive and specific in identifying obstruction from ileus.16
Mechanical obstructions can be complete or partial, with complete ones requiring surgical intervention while partial ones usually can be resolved medically. Obstructions are further divided as small or large bowel in origin. In general, small-bowel obstructions have benign causes while large-bowel ones are more often caused by cancer. Once blocked, the bowel dilates from accumulated liquid and increased gas production resulting from bacterial overgrowth. Dilated bowel is highly sensitive to ischemia once the luminal pressure exceeds the diastolic pressure, and if not relieved in time, perforation results. Bowel segments that are occluded at two points form closed-loop obstructions, as in an incarcerated hernia. Volvulus is another common example in which a loop of bowel is compressed at both ends of a twist. Large-bowel obstructions can form closed loops with only one pathologic obstruction if the ileocecal valve is competent. Closed-loop obstructions lead to perforation more rapidly, as the segment is blocked both proximally and distally, not allowing any outlet for accumulating liquid/gas.
Small-bowel Obstruction (SBO). In the past, incarcerated hernias were the main cause of SBO, but their incidence dropped dramatically as elective hernia repair rates rose. Now the vast majority of cases are caused by postoperative adhesions (75%), and up to 15% of patients will develop SBO within 2 years after laparotomy.18 Pelvic surgeries (gynecology, appendectomy, and colorectal) are particularly high risk for adhesions. The risk of SBO peaks in the first few years after the initial surgery but can occur many years after. The 10-year risk of SBO from adhesions is estimated to be as high as 40%.19 Other SBO causes include hernia (15%) or cancer (5-10%).15 While the overall rate of cancer is low, it rises to 50% in cases in which the patient has not had prior abdominal surgery or evidence of an incarcerated hernia.20
SBO is one of the few diseases discussed in this paper that tends to present in a similar fashion regardless of age. Most patients present with colicky abdominal pain, vomiting, distension, and obstipation (failure to pass flatus/feces). Vomiting can be less prominent with more distal obstructions. Pain can improve with bowel fatigue or as emesis relieves distension. Pain also can become intense and unrelenting after perforation. Likewise, bowel sounds can be high-pitched and hyperactive early on, but fade and ultimately disappear with bowel fatigue. Passage of stool or flatus does not rule out SBO, as luminal contents distal to the obstruction still pass normally. Some patients also have diarrhea early on, resulting from hyperperistalsis distal to the obstruction. When symptoms are mild, SBO easily can be misdiagnosed, and it is the second most common condition (behind appendicitis) with which patients who have acute abdominal pain are mistakenly discharged.21
Plain radiographs are diagnostic in 50-70% of cases, but most commonly miss closed-loop obstructions as they often lack air-fluid levels.22 Closed-loop obstructions are also difficult to detect on CT scan, and CT is only 60% sensitive for this.15 Early consultation with a surgeon is advised, as 90% of partial SBOs resolve with conservative treatment, while complete obstruction constitutes a surgical emergency.
Large-bowel Obstruction (LBO). While adhesions are the primary cause of SBO, in LBO the principle cause is colon cancer, which accounts for 60% of cases.15 Colonic volvulus causes another 10-15% of cases, and strictures from colonic diverticular disease cause another 10%.15 Acute diverticular abscesses also can cause obstruction by external compression. While cancer causes obstruction by progressive narrowing of the lumen, a volvulus occurs when a portion of the colon twists on itself. In 80% of cases, torsion of the sigmoid colon is to blame, and the remaining 20% are cecal in nature.23 Sigmoid volvulus is mostly seen in elderly patients, as it occurs in patients with an excessively dilated colon, often from chronic constipation or megacolon. Cecal volvulus is actually a torsion of the right colon and terminal ileum, but it is so named because it arises due to a abnormally mobile cecum. In contrast to sigmoid volvulus, the cecal type is most often seen in patients in their fifties.
Patients with LBO classically present with abdominal pain combined with progressive distension and obstipation. Vomiting can occur but tends to be more prominent in SBO. In LBO, up to 50% of patients have vomiting and nearly 20% report diarrhea).24 The underlying cause tends to predict the presentation, as progressive narrowing from cancer produces a gradual development of symptoms, while volvulus patients present with acute onset of pain and distension.15 As with SBO, bowel sounds are hyperactive early on, but then activity decreases with time.
Sensitivity and specificity of plain films for LBO are 84% and 72%, respectively.27 In most cases, additional imaging is required. Water-soluble contrast enema is 96% sensitive and 98% specific, while CT scan is only 90% sensitive and specific.28
Treatment is considerably different depending on the cause of the obstruction. Cancerous obstructions require partial colectomy, and cecal volvulus requires urgent surgery to untwist the bowel before infarction occurs. However, about 75% of sigmoid volvulus cases can be decompressed with simple flexible sigmoidoscopy.29 The greater the stretch of the intestinal wall, the higher the likelihood of ischemia and perforation. Critical thresholds for the cecum (12 cm) and the transverse colon (9 cm) have been suggested.16 These are not exact numbers, but when the bowel diameter approaches this range, urgent surgical consultation is recommended.
It is important to consider acute colonic pseudo-obstruction (ACPO) or Ogilvie syndrome when evaluating patients with suspected LBO. ACPO is a pseudo-obstruction without any mechanical obstruction and is seen most often in critically ill patients after recent surgery or medical illness, or in institutionalized patients.16 A large review found it was most common in post-surgical patients (23%), patients admitted with myocardial infarction (17%), or nonoperative trauma (11%).30 ACPO is more common in the elderly and presentation is similar to LBO, but the exact etiology is unclear. Up to 33% of patients diagnosed with LBO by clinical exam and plain radiographs will actually have ACPO instead.31 ACPO can only be diagnosed after exclusion of LBO, typically through contrast enema, abdominal CT scan, or colonoscopy. Colonoscopy can be both diagnostic and therapeutic, with a success rate of 80%.32 However the procedure also carries a 2% risk of perforation and is recommend only for experienced endoscopists. About 75% of ACPO cases resolve with conservative therapy, but patients with persistent symptoms or signs of perforation are treated surgically.
Diverticulits. Diverticulitis occurs in roughly 25% of patients with diverticula, and typically presents with crampy left-lower-quadrant pain and tenderness. More severe cases also can have nausea, vomiting, and fever. Elderly patients may lack leukocytosis and may have pyruia or hematouria when the colon is adjacent to the bladder, leading to misdiagnosis of renal colic or UTI. Mild cases in relatively healthy patients can be managed as an outpatient with oral antibiotics, but these patients should be given close follow-up in the next 1-2 days. The incidence of a co-existing malignancy is as high as 9%;33 therefore, all patients should be screened for colon cancer after their first episode has resolved. Abscess formation in diverticulitis is relatively common, and smaller ones can be managed with CT-guided drainage, while larger ones and patients with perforation, obstruction, peritonitis, or fistulas will require surgery. The recurrence of diverticulitis is common, and up to 62% of patients who respond to antibiotics will have a second episode; the risk of a third episode is nearly 50%.34
Cholecystitis. Acute cholecystitis remains the most common reason for abdominal surgery in the elderly,23 and the most common cause of cholecystitis is cholelithiasis. The incidence of cholelithiasis increases with age, and autopsy studies show that anywhere from 11-35% of American adults have gallstones.35 Roughly 1-3% of these people will develop acute cholecystitis.35 Not only does the incidence of cholelithiasis increase with age, but the severity of gallstone disease also increases with age. The elderly are at higher risk for complications of cholecystitis, including perforation, gangrene, ascending cholangitis, gallstone pancreatitis, and emphysematous cholecystitis.36
Elderly patients tend to present with right-upper-quadrant or epigastric abdominal pain, but up to 50% do not have nausea, vomiting, or fever.37 Even with gangrene or frank perforation, nearly 33% still present without fever.37 Elderly patients also are more likely to have these complications (empyema, gangrene, perforation, or abscess), and they were present in 40% of older patients with cholecystitis.37 Biliary colic can be difficult to distinguish from acute cholecystitis, but in general pain should not last more than 6 hours with simple colic.38 WBC is normal in up to 40% of elderly patients, and it is not unusual for liver function tests to also be normal.15 Ultrasound findings are not significantly different in the elderly, but the elderly do have an increased risk of acalculous cholecystitis in which ultrasound is only 67% sensitive.39 Acalculous cholecystitis accounts for up to 15% of cases35 and also has higher complication and mortality rates (40%).40 Radionucleotide (HIDA) scan is recommended when ultrasound is non-diagnostic and clinical suspicion is high.
Appendicitis. While appendicitis traditionally is thought of as a young patient's disease, it is the diagnosis in 5-7% of elderly patients with acute abdominal pain.41,42 While the mortality for acute appendicitis in younger patients is < 1%, elderly patients can have rates as high as 4-8%.43 Besides comorbid conditions, the high perforation rate for the elderly contributes to the elevated mortality risk. From 51-72% of elderly patients have perforation at the time of surgery44 compared to overall rates of 17-20% for younger patients. Increased rates of perforation can be linked directly to delays in presentation and atypical presentation.
One study spanning 20 years documented that in elderly patients with appendicitis, 26% presented atypically, 33% delayed seeking care, and only 46% were correctly diagnosed on admission.45 Fever was relatively rare in this study and was only seen in 37%, whereas 74% had an elevated WBC (> 10,000), 72% had anorexia, and 70% had right-lower-quadrant pain.45 Only 30% presented with all four of these findings, and they had perforation more often. Fifty percent of patients had no rebound or guarding, and 25% did not even have right lower quadrant tenderness.45 Liberal use of CT scan to rule out appendicitis in elderly patients is recommended, as the differential diagnosis is broad in these patients, they have an increased risk of rupture, and the risk with radiation exposure is much lower.
Abdominal Aortic Aneurysm (AAA). Aneurysm diameter correlates well with risk of rupture. Those less than 4 cm have an annual risk of rupture of only 1%, while in those greater than 5 cm, risk increases to 5%. For aneurysms greater than 8 cm, the risk increases to 30-40%.46
AAAs are found in roughly 5% of men 65 years and older, as detected by ultrasound;47 they are thought to occur as a result of wear and tear of the aorta and thus primarily affect the elderly. Smoking tobacco is the strongest known risk factor and is seen in 90% of patients with AAA.48 Hypertension, hyperlipidemia, and coronary artery disease are other risk factors. Positive family history carries an increased risk of 30%, and these patients tend to have aneurysms at younger ages and have increased risk of rupture.49 Men also are roughly 10 times more likely to have AAA than women.47
The vast majority of AAAs (95%) are infrarenal in location. Combined with the retroperitoneal location of the aorta slightly on the left of the vertebrae, these anatomical facts guide the symptoms that patients experience. Pain tends to be located in the left-lower abdomen or more often in the left flank, and some patients also have radiation to the left groin. Thus, the most common misdiagnosis of ruptured AAA is renal colic, followed by acute diverticulitis. The classic triad of hypotension, back pain, and pulsitile abdominal mass is seen in only 30-50% of cases.50 Further, some aneurysms produce sudden onset of severe pain as a result of rapid expansion without hemorrhage. Thus symptomatic patients with AAA who have no evidence of bleeding on CT scan should still have urgent surgical consultation, as this can be a sign of impending rupture.51 Likewise, transient bleeding can cause syncopal episodes.
CT scan and ultrasound are the two most common imaging modalities used in the ED to detect AAA. CT scan has the advantage of accurately defining the shape and extent of the aneurysm as well as aiding in pre-operative planning (i.e., relation to the renal and visceral arteries). Disadvantages include the patient having to leave the ED, which is unsafe with unstable patients, and intravenous contrast media can worsen risk of acute renal failure. When necessary, non-contrast CT scan still is adequate to detect hemorrhage. When available in the ED, bedside ultrasound can rapidly answer the question of whether an AAA is present, but it is unlikely to rule out the presence of retroperitoneal hemorrhage. In most cases, though, hypotension with presence of AAA is enough to take the patient to surgery.
Mesenteric Ischemia. Acute mesenteric ischemia is a relatively rare and very challenging diagnosis to make. As the population ages, it is becoming more common. Currently, 1-2 of every 100 admissions for abdominal pain are for mesenteric ischemia.52 The mortality ranges from 70-93%, and misdiagnosis rates are nearly as high. Of the three vessels that supply the intestine, the superior mesenteric artery (SMA) is most commonly the source of mesenteric ischemia. Arterial embolism of the SMA is the most frequent cause of mesenteric ischemia and is responsible for 50% of cases.53 Acute thrombosis of the SMA is the second most common cause of mesenteric ischemia (15-30%), and mesenteric vein thrombosis causes another 5-15%.54 Arterial embolism occurs as a result of atrial fibrillation, valvular disease, or from left ventricular thrombus. These patients have no previous history of intestinal ischemia, unlike patients with SMA thrombosis, as these clots form at areas of pre-existing atherosclerosis. Like patients with coronary disease, patients often have prodromal symptoms indicating progressive arterial narrowing, report abdominal pain with meals, and have weight loss. Mesenteric vein thrombosis occurs in patients with hypercoaguable state, and they often have history of previous deep vein thrombosis or pulmonary emboli.55
Patients classically present with sudden onset of intense abdominal pain, but in some cases the pain can be more gradual in onset. As with other ischemic pains such as testicular torsion or strangulated hernia, it is progressive and unresponsive to narcotic analgesia. The primary clue on exam is that dramatic abdominal pain is coupled with lack of abdominal tenderness, i.e., pain out of proportion to the exam. The physical exam will change with time, and when intestinal infarction develops, tenderness with peritoneal signs and bloody stools also appear. While bowel sounds are classically absent, this occurs after infarction, and nearly 75% of patients have hyperactive sounds initially.55 The best diagnostic tool is suspicion for the disease in an ill patient without other explanations for his or her condition.
Laboratory tests also are unhelpful, and while elevated serum lactate is 96% sensitive, it is a later finding.56 Plain films often are obtained to rule out free air, but early on there are no diagnostic findings. The traditional gold standard for diagnosis is standard angiography, but CT angiography is becoming more useful with the advent of multidetector row technology. Recent studies have shown the positive and negative predictive values in diagnosis of mesenteric ischemia were 90% and 98%, respectively.57 Angiography does have the advantage of providing a treatment option with localized thrombolytics and vasodilators, although the majority of patients are treated surgically. Any patients with signs of bowel infarction need emergent surgical consultation. Even when angiography is being pursued for primary treatment, surgical consultation is necessary. One study found that even a delay of 6 hours from consultation to surgery was associated with increased mortality.58
Gastrointestinal Perforation. Peptic ulcer disease is one of the most common causes of GI perforation and is estimated to cause about 50% of cases.25 The average age for perforating ulcer has increased from 41 to 62 years over the past 50 years, and thus is becoming more frequent in the elderly.59 Mortality rates for the elderly are triple those of younger patients (30% vs. 10%).60 Mortality rates also rise with delay of diagnosis; a delay of 12 hours doubles mortality, while a delay of 24 hours increases it eight-fold.61 Unfortunately, elderly patients are more likely to have less dramatic symptoms and therefore be diagnosed later, but also are less tolerant of delayed treatment.
Sudden onset of severe abdominal pain is the classic hallmark of peptic ulcer perforation in younger patients, as the gastric contents rapidly leak out into the abdomen. In only 4-6 hours the patient can be febrile, dehydrated, tachycardic, hypotensive, and have an ileus. Free air on an upright chest radiograph can make the diagnosis. As with other emergent conditions, elderly patients can present with minimal or even no abdominal pain. Increased confusion or restlessness, or abdominal distension may be the only complaints. In addition, ulcer perforation into an adjacent organ can be more subtle even in younger patients. Ulcers perforate into other organs in 20% of perforations,62 and common sites include the pancreas, omentum, hepatobiliary system, and colon. Further, elderly patients are less likely to have pain as their ulcer disease develops, and therefore history of previous ulcer symptoms may be lacking.
While the presence of free air on plain films can be diagnostic. From 40-50% of cases of ulcer perforation lack pneumoperitoneum.59 CT scan is very accurate for free abdominal air, with sensitivities near 100%, although the sensitivity for localizing the source of the perforation is much less (65%).63 Water-soluble oral contrast can be used in cases of suspected GI perforation, but barium is not safe as it causes a severe peritonitis.
Myocardial Infarction without Chest Pain
Elderly patients make up about 65% of acute myocardial infarctions (AMIs) and about 80% of deaths.64 Age is a primary risk factor for coronary disease, and while the incidence of disease is only 7% in patients younger than 40 years, for those older than 80 years, it rises to about 50% of women and 80% of men in the United States.65 One might expect elderly patients to be the most commonly missed MI patient, but studies show this is not the case. As discussed below, elderly patients often present with atypical features (no pain) and have higher mortality, but the patient sent home with MI most often is younger than 55 years, female, nonwhite, with no history of coronary disease, lacking classical MI symptoms and with no obvious ECG changes.66
Several recent studies have attempted to determine the frequency of AMI or unstable angina patients without chest pain. A 2004 study with 2588 patients presenting with acute coronary syndrome (ACS) found no chest pain in 6.2% of unstable angina patients and 9.8% of AMI patients.67 By far the most common chief complaint was dyspnea, as this was the presenting symptom in 72% of patients without chest pain, compared to only 5% of those with any chest pain.67 They also found that patients who presented without chest pain had more than double the mortality rate of those with chest pain (18% vs. 7%).67
The Global Registry of Acute Coronary Events (GRACE) examined records of 20,881 patients from 14 countries with suspected ACS.69 They confirmed that incidence of atypical presentation increases with age and was seen in 29% of those younger than 65 years, but in 43% of those older than 75 years.69 It was also more common in diabetics (32% vs. 24%). They also found that the primary chief complaint by far was dyspnea (49%), followed by diaphoresis (26%), and nausea/vomiting (24%).69
With the high frequency of atypical presentations in elderly patients, one must then rely on ECG and biomarkers to detect MI. While the ECG often is the single most important test to identify STEMI patients, ECG interpretation in the elderly is not always straightforward due to baseline pathology.
One must be careful, though, to use cardiac biomarkers appropriately. Initial cardiac enzyme levels can be highly variable, with only 21-39% of the first levels being positive in AMI.70 Despite the recommendation that cardiac biomarkers should be checked with at least two values checked over at least 6 hours (serial biomarkers), many emergency physicians often obtain only one value. This practice is contrary to stated guidelines from the American Cardiology College, the American Heart Association, and the current ACEP clinical policy on management of ACS/NSTEMI.71,72
The question then arises, what strategies should be used to evaluate for possible MI in elderly patients with vague symptoms? The first is to use the kinetics of troponin to one's advantage. While a single troponin or CK-MB alone can miss up to 74% of AMIs,73 they can be useful in the proper setting. In other words, one can safely evaluate patients who present with chest pain one or two days before with just a single troponin. ACEP guidelines also suggest using a single CK-MB or troponin drawn 8-12 hours after symptom onset, or using ED presentation time when symptom onset is unclear/unavailable.72
Negative biomarkers do not rule out the presence of coronary disease, and unstable angina is roughly 6 times more common than AMI in ED patients with chest pain.74 In addition, troponin levels can be falsely elevated in a number of conditions, such as CHF, pericarditis, end-stage-renal disease, ischemia from anemia or prolonged tachycardia, and even from laboratory error. Thus troponin levels are cardiac-specific, but not disease-specific.
The recent introduction of CT coronary angiography has added yet another option for some ED physicians. Advanced 64-slice multidetector-row CT became available in 2000 and gave the ability to perform both high-speed and high-resolution CT scanning. While these studies add another option for patient evaluation, the limits of coronary CT in ED patients need to be stressed. With current technology, vessels less than 1.5 mm in diameter are not well visualized, resulting in inadequate evaluation of 2-12% of coronary segments.75 More importantly, even if 100% of the coronary vessels were visualized, their anatomy alone does not necessarily correlate with the patient's symptoms. In other words, 20% lesions are unlikely to cause symptoms just as 90% lesions are very likely to produce chest pain. However, knowing that a right coronary lesion of 70% stenosis exists does not in itself identify that lesion as one that is responsible for causing the patient's current symptoms of ischemia. Patients with intermediate lesions on a CT scan would still need a functional study (stress test) to identify if intervention is required. Thus, knowing the patient's anatomy would undoubtedly help detect patients with very normal/abnormal vessels, but those with intermediate lesions still need further evaluation.
Ultimately, given the high frequency of atypical presentation of elderly patients for ACS and the difficulty detecting this in a timely fashion in busy EDs, the chest pain unit or 24-hour admission will be the definitive tool to accurately diagnose as many elderly patients with ACS/AMI as possible. One should maintain a low threshold for admission of elderly patients with dyspnea or other AMI equivalent symptoms.
Thoracic Aortic Dissection
While younger patients can have dissections for example a patient with Marfan's syndrome, cocaine use, or bicuspid aortic valve the average patient is a man in his 70s. Previous data show men outnumber women with this disease 5:1,76 but recent data from the International Registry of Acute Aortic Dissection (IRAD) find dissection is much more common than this in elderly women. Of patients older than 70 years with type A (proximal) dissections, 52% were women, and with type B (distal), 38% were female.77,78 Data from IRAD confirm primary risk factors include hypertension (72% of patients), atherosclerosis (31%), prior cardiac surgery (18%), and known aortic aneurysm (16%).79
Many physicians misuse the term "dissecting aneurysm" when referring to aortic dissection. An aortic dissection is a tear in the intimal surface of the vessel that allows blood to spread into the medial layer of the vessel wall and propagate longitudinally. An aneurysm is an enlargement of a vessel that occurs as a result of local weakening of the wall. Dissections nearly always arise from a normal-caliber aorta. Likewise, it is important to identify the section of the aorta where the dissection occurred, as this determines the difference between medical treatment and emergent surgery. Dissections originating in the ascending aorta (Stanford type A) are treated surgically, as they have a high risk of cardiac tamponade, aortic regurgitation, and acute myocardial infarction.80 Ascending aorta dissections represent 65% of all cases, 10% originate in the arch, 20% in the descending aorta, and 5% in the abdominal aorta.79 IRAD data show an in-hospital mortality of 56% for type A dissections that are not taken to surgery.81 In contrast, dissections arising from the arch or descending aorta (Stanford type B) are treated medically in most cases.
The classic presentation is a patient with sudden onset of severe chest pain, described as ripping or tearing, which migrates from the chest to the back and to the abdomen. The classic physical finding is a pulse deficit, defined as unilateral weakly palpated or absent pulses.82 Unfortunately, as with many conditions, the classic presentation is not the common one. The most recent IRAD data show pulse deficits are more common in any age patients with type A dissections (30%) than type B (20%), but they were less common in elderly patients compared to those younger than 70 years with either type A (24 vs. 33%) or type B (15 vs. 24%).77,78 Ultimately, thoracic aortic dissection can present with a great variety of symptoms, as any major branch of the aorta can be occluded by the dissection or adjacent structures can be compressed. Thus patients can present with neurologic complaints (syncope, stroke, paralysis from spinal cord ischemia), cardiovascular symptoms (myocardial infarction, hypertension, hypotension, aortic regurgitation), gastrointestinal complaints (hemorrhage, mesenteric ischemia), renal failure, and ischemia of limbs.83 (See Table 4.)
Clinical features that can be useful to identify patients who need imaging for aortic dissection include sudden onset of chest pain (85%) and severity of pain that is "worst ever" (90%).79 Unfortunately, classic features of ripping/tearing pain (50%) and migratory nature of pain (16-24%) are less common in patients of any age.79,84 Interestingly, while elderly patients (> 70 years) with type A dissections were found to present less often with abrupt-onset chest pain (76 vs. 88%) or migratory pain (14 vs. 12%), elderly patients with type B dissections had no differences from younger ones.77,78 Only 49% of all patients are hypertensive, and 34% have normal blood pressures on presentation.79 Back pain is common (46-64%) and may be the presenting complaint instead of chest pain.79 Syncope can be a presenting complaint in aortic dissection, but it was seen in only 13% of patients in a previous study.85 When patients do have syncope, they are more likely to have type A dissections, tamponade, or stroke.
Chest radiographs can be helpful when a widened mediastinum is found, but confirmatory imaging still is required. Diagnosis of aortic dissection can be made only with CT, TEE (transesophageal echocardiogram), angiography, or MRI. Of these, CT angiography has emerged as the test of choice. Multidetector CT scan has a 99% accuracy for diagnosis,86 and the entire aorta should be imaged whenever considering dissection. TEE is accurate but has difficulty evaluating the descending aorta and is not as readily available as CT scan.
As expected from the difficulty in diagnosing aortic dissection, misdiagnosis rates vary from 64–85% in some studies,87 and some 28% are only diagnosed by autopsy.100 The most common misdiagnosis is acute myocardial infarction (MI) or unstable angina, which has been a consistent finding for the past 40 years.88 This is understandable, as given the relative incidence of MI vs. acute dissection, one will see on average 800 MI patients for every 1 dissection.89
Increasing age correlates well with increased risk of PE. Risk rises at age 40 years, and increases further after age 60 years.92 It has been estimated that the risk of PE doubles every 10 years after age 60.93 Some or perhaps all of this increased risk is due to the higher incidence of other PE risk factors in the elderly, such as COPD, recent surgery, immobility or stroke, infection, cancer, or implantable cardiac devices and central lines.94
Clinically, acute PE can be divided into three major groups: massive PE with hemodynamic instability, small PE with minimal or no symptoms, or moderate PE with highly variable symptoms. Elderly patients with massive PE undoubtedly will be admitted even if the diagnosis is not clear in the ED. However, it should be stressed that up to 13% of patients with PE present with syncope, which is more common with massive PE.95 Thus, one should consider PE in elderly patients being evaluated for syncope. Patients with small, asymptomatic PE are unlikely to present for evaluation. Thus the rest of this section will discuss the presentation and diagnosis of moderate PE in elderly patients.
Studies that specifically evaluate the symptoms of elderly patients with PE find that older patients consistently have less-frequent symptoms compared to younger ones. PIOPED II data show that dyspnea at rest or exertion was present in 76% of those younger than 70 years, but was found in only 66% of those older than 70 years.96 Likewise, pleuritic chest pain was seen in 46% of those younger than 70 years and only 35% of patients older than 70 years.96 Cough was seen nearly as often as chest pain, as was seen in 36% of those younger than 70 years and 29% of those older than 70 years.96 Patients older than 70 years only had tachypnea (20 min or more) in 47% and tachycardia (> 100 bpm) in 23%, compared to 57% and 25% of younger patients, respectively.96 Thus, elderly patients did have fewer symptoms and underscores the limits of clinical data for diagnosis of PE.
Physical exam findings can be misleading as well. Crackles were heard on lung exam in 26% of the elderly patients with PE and would suggest pneumonia more often than PE.96 One also should not be reassured when clinical findings of DVT are absent. In one study, only 17% of patients with PE had unilateral leg swelling or signs of DVT.97
Only a few laboratory tests are helpful in the diagnosis of acute PE. Elevated D-dimer levels can be helpful in some cases to screen for PE. Most studies recommend using D-dimer only in low-probability patients in whom a negative level precludes further testing.98 Problems arise when trying to D-dimer levels in the elderly because elevations are sensitive but not specific for PE. One study found the specificity of a D-dimer level for PE in patients older than 80 years was only 10%.99 Many other conditions can cause D-dimer elevations, including acute MI, sepsis, cancer, trauma, or other inflammatory states.92 Thus, studies of D-dimer levels in elderly patients being evaluated for PE find that they are rarely negative.100
Imaging studies are the primary means to diagnose PE, and CT angiography has replaced VQ scans as the modality of choice.94 The most recent study shows CT angiography for PE has a sensitivity of 83% and a specificity of 96%).101 When combined with venous-phase imaging (CTA-CTV), these numbers increase to 90% and 95%, respectively).101 CTV involves scanning the patient's legs for DVT using the same contrast bolus. The downside for CT is that patients with renal dysfunction are not able to have the study, and elderly people are much more likely than younger patients to have underlying renal disease. Another disadvantage for CT in the past was the poor visualization of emboli in subsegmental arteries. Recent multidetector CT scans are better at diagnosing PE in these smaller arteries, with a sensitivity of 87% for CT vs. 32% with conventional angiography.102 Currently the clinical significance of these small emboli remains unclear. For younger, healthier patients, these emboli may spontaneously resolve, but patients with poor cardiopulmonary reserve or pulmonary hypertension do have increased mortality.103
1. Centers for Disease Control and Prevention. HIV/AIDS Surveillance Report, 2007. Vol. 19. Atlanta: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention; 2009: 1–63. http://www.cdc.gov/hiv/topics/surveillance/resources/reports/.
2. Brañas F, Berenguer J, Sánchez-Conde M, et al. The eldest of older adults living with HIV: Response and adherence to highly active antiretroviral therapy. Am J Med 2008;121:820– 824.
3. Hall HI, Song R, Rhodes P, et al. Estimation of HIV incidence in the United States. JAMA 2008;300:520–529.
4. McDavid K, Li J, Lee LM. Racial and ethnic disparities in HIV diagnoses for women in the United States. J Acquir Immune Defic Syndr 2006;42:101–107.
5. Luther VP, Wilkin AM. HIV infection in older adults. Clin Geriatr Med 2007;23:567–583.
6. Balslev U, Monforte AD, Stergiou G, et al. Influence of age on rates of new AIDS-defining diseases and survival in 6546 AIDS patients. Scand J Infect Dis 1997;29:337–343.
7. Hall HI, McDavid K, Ling Q, et al. Determinants of progression to AIDS or death after HIV diagnosis, United States, 1996 to 2001. Ann Epidemiol 2006;16:824–833.
8. Kizer KW, Vassar MJ. Emergency department diagnosis of abdominal disorders in the elderly. Am J Emerg Med 1998;16:357–362.
9. Lewis LM, Banet GA, Blanda M, et al. Etiology and clinical course of abdominal pain in senior patients: a prospective, multicenter study. J Gerontol A Biol Sci Med Sci 2005;60:1071–1076.
10. Laurell H, Hansson LE, Gunnarsson U. Acute abdominal pain among elderly patients. Gerontology 2006;52:339–344.
11. Liang SY, Mackowiak PA. Infections in the elderly. Clin Geriatr Med 2007;23:441–456.
12. Fenyo G. Acute abdominal disease in the elderly: Experience from two series in Stockholm. Am J Surg 1982;143:751–754.
13. Esses D, Birnbaum A, Bijur P, et al. Ability of CT to alter decision making in elderly patients with acute abdominal pain. Am J Emerg Med 2004;22:270–272.
14. Hustey FM, Meldon SW, Banet GA, et al. The use of abdominal computed tomography in older ED patients with acute abdominal pain. Am J Emerg Med 2005;23:259–265.
15. Cappell MS, Batke M. Mechanical obstruction of the small bowel and colon. Med Clin North Am 2008;92:575–597.
16. Batke M, Cappell MS. Adynamic ileus and acute colonic pseudo-obstruction. Med Clin North Am 2008;92:649–657.
17. Bugliosi TF, Meloy TD, Vukov LF. Acute abdominal pain in the elderly. Ann Emerg Med 1990;19:1383–1386.
18. Beck DE, Opelka FG, Bailey HR, et al. Incidence of small-bowel obstruction and adhesiolysis after open colorectal and general surgery. Dis Colon Rectum 1999;42:241–248.
19. Landercasper J, Cogbill TH, Merry WH, et al. Long-term outcome after hospitalization for small-bowel obstruction. Arch Surg 1993;128:765–770.
20. McCloy C, Brown T, Bolton JS, et al. The etiology of intestinal obstruction in patients without prior laparotomy or hernia. Am Surg 1998;64:19–22.
21. Brewer RJ, Golden GT, Hitsch DC, et al. Abdominal pain: an analysis of 1,000 consecutive cases in a university hospital emergency room. Am J Surg 1976;131:219–224.
22. Frager D. Intestinal obstruction role of CT. Gastroenterol Clin North Am 2002;31:777–799.
23. Martinez JP, Mattu A. Abdominal pain in the elderly. Emerg Med Clin North Am 2006;24:371–388.
24. Greenlee HB, Pienkos EJ, Vanderbilt PC, et al. Acute large bowel obstruction. Arch Surg 1974;108:470–476.
25. Hendrickson M, Naparst TR. Abdominal surgical emergencies in the elderly. Emerg Med Clin N Am 2003;21:937–969.
26. [No authors listed.] Clinical policy: Critical issues for the initial evaluation and management of patients presenting with a chief complaint of nontraumatic acute abdominal pain. Ann Emerg Med 2000;36:406–415.
27. Chapman AH, McNamara M, Porter G. The acute contrast enema in suspected large bowel obstruction: value and technique. Clin Radiol 1992;46:273–278.
28. Beattie GC, Peters RT, Guy S, et al. Computed tomography in the assessment of suspected large bowel obstruction. ANZ J Surg 2007;77:160–165.
29. Mangiante EC, Croce MA, Fabian TC, et al. Sigmoid volvulus: A four-decade experience. Am Surg 1989;55:41–44.
30. Wegener M, Borsch G. Acute colonic pseudo-obstruction (Ogilvie's syndrome): Presentation of 14 of our own cases and analysis of 1027 cases reported in the literature. Surg Endosc 1987;1:169–174.
31. Taourel P, Kessler N, Lesnik A, et al. Helical CT of large bowel obstruction. Abdom Imaging 2003;28:267–275.
32. De Giorgio R, Knowles CH. Acute colonic pseudo-obstruction. Br J Surg 2009;96:229–239.
33. Peterson MA. Disorders of the large intestine. In: Marx, JA ed. Rosen's Emergency Medicine: Concepts and Clinical Practice, 7th ed. St. Louis: Mosby; 2009: 1228–1242.
34. Dominguez EP, Sweeney JF, Choi YU. Diagnosis and management of diverticulitis and appendicitis. Gastroenterol Clin N Am 2006;35:367–391.
35. Elwood DR. Cholecystitis. Surg Clin North Am 2008;88:1241–1252.
36. Bedirli A, Sakrak O, Sözüer EM, et al. Factors effecting the complications in the natural history of acute cholecystitis. Hepatogastroenterology 2001;48:1275-1278.
37. Morrow DJ, Thompson J,Wilson SE. Acute cholecystitis: a surgical emergency. Arch Surg 1978;113:1149–1152.
38. Flasar MH, Goldberg E. Acute abdominal pain. Med Clin N Am 2006;90:481–503.
39. Shuman WP, Rogers JV, Rudd TG, et al. Low sensitivity of sonography and cholescintigraphy in acalculous cholecystitis. AJR Am J Roentgenol 1984;142:531–534.
40. Kalliafas S, Ziegler DW, Flancbaum L, et al. Acute acalculous cholecystitis, risk factors, diagnosis and outcome. Am Surg 1998;64:471–475.
41. Vissers RJ, Lennarz WB. Pitfalls in appendicitis. Emerg Med Clin N Am 2010;28:103–118.
42. Kauvar DR. The geriatric acute abdomen. Clin Geriatr Med 1993;9:547–558.
43. Gupta H, Dupuy D. Abdominal emergencies: has anything changed? Surg Clin N Am 1997;77:1245–1264.
44. Hiu TT, Major KM, Avital I, et al. Outcome of elderly patients with appendicitis. Arch Surg 2002;137:995–1000.
45. Storm-Dickerson TL, Horattas MC. What have we learned over the past 20 years about appendicitis in the elderly? Am J Surg 2003;185:198–201.
46. Brady AR, Thompson SG, Fowkes FG, et al. Abdominal aortic aneurysm expansion: risk factors and time intervals for surveillance. Circulation 2004;110:16–21.
47. Multicentre Aneurysm Screening Study Group. Multicentre aneurysm screening study (MASS): Cost-effectiveness analysis of screening for abdominal aortic aneurysms based on four year results from a randomized controlled trial. BMJ 2002;325:1135–1138.
48. 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.
49. Isselbacher EM. Thoracic and abdominal aortic aneurysms. Circulation 2005;111:816–828.
50. Banerjee A. Atypical manifestations of ruptured abdominal aortic aneurysms. Postgrad Med 1993;69:6–11.
51. Goldstone J. Aneurysms of the aorta and iliac arteries. In: Moore WS, ed. Vascular Surgery: A Comprehensive Review. 4th Ed. Philadelphia: WB Saunders; 1993: 401–421.
52. Schneider TA, Longo WE, Ure T, et al. Mesenteric ischemia: Acute arterial syndromes. Dis Colon Rectum 1994;37:1163–1174.
53. Greenwald DA, Brandt LJ, Reinus JF. Ischemic bowel disease in the elderly. Gastroenterol Clin N Am 2001;30:445–473.
54. Stoney RJ, Cunningham CG. Acute mesenteric ischemia. Surgery 1993;114:489–490.
55. Martinez JP, Hogan GJ. Mesenteric ischemia. Emerg Med Clin N Am 2004;22:909–928.
56. Murray MJ, et al. Serum D(-)-lactate levels as an aid to diagnosing acute intestinal ischemia. Am J Surg 1994;167:575–578.
57. Ozden N, Gurses B. Mesenteric ischemia in the elderly. Clin Geriatr Med 2007;23:871–887.
58. Eltarawy IG, Etman YM, Zenati M, et al. Acute mesenteric ischemia: the importance of early surgical consultation. Am Surg 2009;75:212–219.
59. Borum ML. Peptic-ulcer disease in the elderly. Clin Geriatr Med 1999;15:457–471.
60. Blomgren LG. Perforated peptic ulcer: long-term results after simple closure in the elderly. World J Surg 1997;21:412–414.
61. Wakayama T. Risk factors influencing the short-term results of gastroduodenal perforation. Surg Today 1994;24:681–687.
62. Norris JR, Haubrich WS. The incidence and clinical features of penetration in peptic ulceration. JAMA 1961;178:386– 89.
63. Chen CH. The features of perforated peptic ulcers in conventional computed tomography. Hepatogastroenterology 2001;48: 393–1396.
64. Goldberg RJ, McCormick D, Gurwitz JH, et al. Age-related trends in short and long term survival after acute myocardial infarction. Am J Cardiol 1998;82:1311–1317.
65. Williams MA, Fleg JL, Ades PA, et al. Secondary prevention of coronary heart disease in the elderly (with emphasis on patients 75 years of age): an American Heart Association scientific statement from the Council on Clinical Cardiology Subcommittee on Exercise, Cardiac Rehabilitation, and Prevention. Circulation 2002;105:1735–1743.
66. Pope JH, Aufderheide TP, Ruthazer R, et al. Missed diagnoses of acute cardiac ischemia in the ED. N Engl J Med 2000;342:1163–1170.
67. Coronado BE, Pope HJ, Griffith JL, et al. Clinical Features, Triage, and Outcome of Patients Presenting to the ED With Suspected Acute Coronary Syndromes but Without Pain: A Multicenter Study. Am J Emerg Med 2004;22:569–574.
68. Canto JG, Fincher C, Kiefe CI, et al. Atypical Presentations Among Medicare Beneficiaries With Unstable Angina Pectoris*. Am J Cardiol 2002;90:248–253.
69. Brieger D, Eagle, KA, Goodman SG, et al. Acute coronary syndromes without chest pain, an underdiagnosed and undertreated high-risk group: insights from the Global Registry of Acute Coronary Events. Chest 2004;126:461–469.
70. Lee TH, Cook EF, Weisberg M, et al. Acute chest pain in the emergency room: Identification and examination of low risk patients. Arch Intern Med 1985;145:65–69.
71. Anderson JL, Adams CD, Antman EM, et al. ACC/AHA 2007 Guidelines for the Management of Patients With Unstable Angina/Non-ST-Elevation Myocardial Infarction A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non-STElevation Myocardial Infarction). Circulation 2007;116:e148–e304.
72. Fesmire FM, Decker WW, Diercks DB, et al. Clinical policy: Critical issues in the evaluation and management of adult patients with non-ST-segment elevation acute coronary syndromes. Ann Emerg Med 2006;48:270–301.
73. Ghaemmaghami CA, Brady WJ. Pitfalls in the emergency department diagnosis of acute myocardial infarction. Emerg Med Clin North Am 2001;9:351–369.
74. Kohn MA, Kwan E, Gupta M, et al. Prevalence of acute myocardial infarction and other serious diagnoses in patients presenting to an urban emergency department with chest pain. J Emerg Med 2005;29:383–390.
75. Hoffmann MHK, Shi H, Schmitz BL, et al. Noninvasive coronary angiography with multislice computed tomography. JAMA 2005;293:2471–2478.
76. Karmy-Jones R, Simeone A, Meissner M, et al. Descending thoracic aortic dissections. Surg Clin N Am 2007;87:1047–1086.
77. Mehta RH, O'Gara PT, Bossone E, et al. Acute type A aortic dissection in the elderly: clinical characteristics, management, and outcomes in the current era. J Am Coll Cardiol 2002;40:685–692.
78. Mehta RH, Bossone E, Evangelista A, et al. Acute type B aortic dissection in elderly patients: clinical features, outcomes, and simple risk stratification rule. Ann Thorac Surg 2004;77:1622–1628.
79. Hagan PG, Nienaber CA, Isselbacher EM, et al. The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease. JAMA 2000;283:897–903.
80. Kamalakannan D, Rosman HS, Eagle KA. Acute aortic dissection. Crit Care Clin 2007;23:779–800.
81. Mehta RH, Suzuki T, Hagan PG, et al. Predicting death in patients with acute type A aortic dissection. Circulation 2002;105:200–206.
82. Isselbacher EM, Diseases of the aorta. In: Libby P, Bonow RO, Mann DL, et al, eds. Braunwald's Heard Disease: A Textbook of Cardiovascular Medicine, 8th ed. Philadelphia, PA: Elsevier; 2008: 145 –1487.
83. Hals G. Acute thoracic aortic dissection: current evaluation and management. Emerg Med Rep 2000;21:1–10.
84. Suzuki T, Mehta R, Ince H, et al. Clinical Profiles and Outcomes of Acute Type B Aortic Dissection in the Current Era: Lessons From the International Registry of Aortic Dissection (IRAD). Circulation 2003;108:312–317.
85. Nallamothu BK, Mehta RH, MD, Saint S, et al. Syncope in Acute Aortic Dissection: Diagnostic, Prognostic, and Clinical Implications. Am J Med 2002;113:468–471.
86. Hayter RG, Rhea JT, Small A, et al. Suspected aortic dissection and other aortic disorders: multi-detector row CT in 373 cases in the emergency setting. Radiology 2006;238:841–852.
87. Haro LH, Decker WW, Boie ET, et al. Initial approach to the patient who has chest pain. Cardiol Clin 2006;24:1–17.
88. Viljanen T. Diagnostic difficulties in aortic dissection. Ann Chir Gynaecol 1986;75:328–332.
89. Nallamothu BK, Eagle KA. When zebras run with horses: the diagnostic dilemma of acute aortic dissection complicated by myocardial infarction. J Interv Cardiol 2002;15:297–279.
90. Bayegana K, Domanovitsa H, Schillinger M, et al. Acute type A aortic dissection: the prognostic impact of preoperative cardiac tamponade. Eur J Cardiothorac Surg 2001;20:1194–1198.
91. Fann JI, Sarris GE, Mitchell RS, et al. Treatment of patients with aortic dissection presenting with peripheral vascular complications. Ann Surg 1990;212:705–713.
92. Tapson VF. Acute pulmonary embolism. N Engl J Med 2008;38:1037–1052.
93. Montagnana M, Favaloro EJ, Franchini M, et al. The role of ethnicity, age and gender in venous thromboembolism. J Thromb Thrombolysis 2009;June 18.
94. Goldhaber SZ. Pulmonary embolism. In: Libby P, Bonow RO, Mann DL, et al, eds. Braunwald's Heard Disease: A Textbook of Cardiovascular Medicine, 8th ed. Philadelphia, PA: Elsevier; 2008: 1863–1879.
95. Thames MD, Alpert JS, Dalen JE. Syncope in patients with pulmonary embolism. JAMA 1977;238:2509–2511.
96. Stein PD, Beemath A, Matta F, et al. Clinical characteristics of patients with acute PE: Data from PIOPED II. Am J Med 2007;120:871–879.
97. Miniati M, Prediletto R, Fromichi B. Accuracy of clinical assessment in the diagnosis of pulmonary embolism. Am J Respir Crit Care Med 1999;159:866–871.
98. Kearon C, Ginsberg JS, Douketis J, et al. An evaluation of d-dimer in the diagnosis of pulmonary embolism: A randomized trial. Ann Intern Med 2006;144:812–821.
99. Rigihini M, Goehring C, Bounameaux H, et al. Effects of age on the performance of common diagnostic tests for pulmonary embolism. Am J Med 2000;109:357–361.
100. Tardy B, Tardy-Poncet B, Viallon A, et al. Evaluation of D-dimer ELISA test in elderly patients with suspected pulmonary embolism. Thromb Haemost 1998;79:38–41.
101. Stein PD, Fowler SE, Goodman LR, et al. Multidetector computed tomography for acute pulmonary embolism. N Engl J Med 2006;354:2317–2327.
102. Kuriakose J, Patel S. Acute pulmonary embolism. Rad Clin N Am 2010;48:31–50.
103. Perrier A, Bounameaux H. Accuracy or outcome in suspected pulmonary embolism. N Engl J Med 2006;354:2383–2385.