Case Presentation by Dr. Dan Paling
History and Physical
61-year-old obese male was sent to the local Emergency Department by his primary care physician with a complaint of low back pain. He reported a history of intermittent, worsening low back pain over the past 2 months. The patient experienced pain with movement of his low back. The pain was characterized as dull, aching, and rated 6-7/10 in intensity located at the level of L3-L5. He patient denied any radiation of the pain down his legs, but admitted that sitting and standing for long periods aggravated his pain. He denied recent or remote falls and/or trauma to this region of his back. The patient denied urinary or fecal incontinence. He stated that he had similar pain about one year ago and was treated for a lumbar muscular strain. The patient felt that he has had fevers intermittently over the past 3 months for which he took acetaminophen. He denied any complaint of chest pain or shortness of breath. He also reported having occasional epigastric abdominal pain with nausea, but no vomiting. He attributed this to a history of heartburn.
Past Medical History: hypertension and peripheral artery disease. No surgical history
Medications: hydrochlorothiazide and metoprolol, but has been noncompliant.
Social History: 40-pack-year tobacco, currently smoking 4 to 5 cigarettes a day.
Physical Examination: BP is 184/112, HR 78, RR 15, Temp 38.2 (oral), O2 Sat 95% on RA.
General appearance: mild distress secondary to pain.
HEENT: AT/NC, PERRL, EOMI
CV: RRR, S1 S2, no m/r/g
Resp: CTAB/L, equal breath sounds, no wheezes or ronchi appreciated
ABD: obese, soft, diffuse tenderness to palpation worse in the umbilical region, no rebound or guarding, no CVA tenderness
Extremities: 2+ distal pulses present in all extremities, no cyanosis, clubbing, or edema
Rectal exam: guaiac negative, normal tone, no masses
Neuro: strength 5/5 bilaterally in all extremities, no sensory or motor deficits, straight leg test positive bilaterally at 60 degrees of hip flexion, reflexes 2+ b/l
Musculoskeletal: point tenderness over spinous processes of L3, L4, and L5, no soft tissue pain
WBC 21, Hb 13.6, Platelets 426, Na 134, K 4.5, Cl 102, CO2 content 23, BUN 28, Cr 1.1
ALT 35, AST 38, Alk Phos 98, Lipase 23, Lactate 0.8
Acute abdominal Series is unremarkable. No free air. No evidence of obstruction
MRI Lumbar Spine: as shown…
Interpretation: Osteomyelitis of L3 and L4 vertebral bodies. Inflammation extends into adjacent structures including the abdominal aorta. Marked dilation of the abdominal aorta at approximately 4 cm in diameter showing inflammatory changes of the vessel wall.
1. Which of the following is a modifiable risk factor for developing an abdominal aortic aneurysm?
- alcohol abuse
- diabetes mellitus
- tobacco smoking
2. Which of the following cases requires medical management ONLY?
- AAA that has enlarged from 3.0 to 3.7cm over the past 6 months
- AAA that has enlarged from 4.7 to 5.0cm in the past 6 months
- 55 YOM with newly diagnosed symptomatic 4.5cm infrarenal AAA
- 65 YOM with asymptomatic 5.7cm infrarenal AAA
- 71 YOM with ruptured 5.0cm AAA exhibiting good mentation and stable vital signs
3. Which is the most important predictor of AAA rupture?
- advanced age
- aneurysm diameter
- expanding AAA
- family history of AAA rupture
- female gender
Abdominal Aortic Aneurysm (AAA) is a potentially life-threatening condition that is frequently diagnosed incidentally when working up various abdominal complaints, and is often undiagnosed until the time of rupture. It is important for EM physicians to know that elderly white males are at the highest risk of having an AAA. High risk patients complaining of abdominal or back pain should receive a bedside ultrasound to screen for the possibility of AAA as the cause of their clinical presentation.
Managing patients with an AAA in the emergency department is primarily focused on heart rate and blood pressure control as well as appropriate surgical consultation. Once an AAA is diagnosed (normally with u/s), a CT angiogram should be performed to determine the AAA’s location and potential involvement with other vessels including the SMA, IMA, renal and iliac arteries. Patients with asymptomatic AAAs less than 5.5 cm can be watched and followed by a vascular surgeon. The patient should undergo abdominal ultrasonography every 6 to 12 months to assess the extent of further dilation if the aneurysm is less than 5.5 cm, is completely infrarenal, and only involves the aorta.
A CT angiogram should be performed every 6 to 12 months in patients with SMA, renal and/or iliac artery involvement.
Symptomatic patients may present with vague or sharp abdominal pain, low back pain, and/or the sensation of an abdominal pulsation. Patients with AAA not complaining of pain may present with syncope, nausea, vomiting, or early satiety. Patients with AAA that complain of abdominal tenderness (usually epigastric) are likely to have an expanding or infected AAA. These patients should receive an immediate surgical consultation as rupture can be spontaneous and imminent. Blood pressure control is the goal in these patients. Intravenous beta blockers are the drug of choice for acutely reducing blood pressure and heart rate. Goals of treatment include a heart rate of 55 to 65 bpm and a systolic blood pressure of 100 to 120mmHg or a MAP of 60 to 65 mmHg. If this SBP range is not achieved with a beta blocker alone and the patient has good mentation, nitroprusside can be added at 0.5mcg/kg/min until the blood pressure is controlled.
A ruptured AAA can present similarly to a myocardial infarction with syncope, hypotension, epigastric pain, nausea, vomiting, and diaphoresis. As many as 30% of AAAs are misdiagnosed on presentation, therefore ED physicians should have a high level of suspicion in patients with h/o AAA or that fall into the high risk categories (ie., white males of advanced age, patients with MCTD (spell out), or smokers with PVD). Rapid diagnosis, resuscitation and surgical consultation are required for treating these patients.
Answers to Questions
- “(e) tobacco smoking” is the correct answer. There are several risk factors, both unmodifiable and modifiable, for developing an AAA. Smoking is the leading modifiable risk factor. It is hypothesized to increase a patient’s risk by 8-fold over a nonsmoker of similar age and comorbidities. (c) stress and (d) insomnia are not risk factors for the development of an AAA. (a) alcohol abuse and (b) diabetes mellitus are modifiable risk factors for the development of many other disorders including cardiovascular disease, but have not been linked to an increased incidence of AAA.
- “(b) AAA that has enlarged from 4.7 to 5.0cm in the past 6 months” is the correct answer. Many AAAs are medically managed while being monitored by a vascular surgeon. Asymptomatic AAAs that are less than 5.5cm in diameter are managed medically until they become (a) symptomatic (regardless of size), (b) rapidly expanding (>0.5 cm in a 6 month period), (c) larger than 5.5 cm in diameter, or (e) ruptured, at which time surgical intervention is necessary.
- “(b) aneurysm diameter” is the correct answer. The three main predictors of AAA rupture are size (aneurysm diameter), (c) rapid expansion (>0.5cm in 6 month period), and (e) female gender (18 vs 12% in males with aneurysms > 5.5cm), but the most important predictor for AAA rupture is aneurysm diameter. (d) Family history of AAA rupture and (a) advanced age are risk factors for AAA development, not rupture.
- AAA rupture is misdiagnosed in nearly 30% of patients upon presentation. Have a high level of clinical suspicion for the high risk groups!
- Heart rate (<65 bpm) and systolic blood pressure (100 to 120 mmHg) control are the keys to managing symptomatic / acutely expanding AAAs. Intravenous beta blockers are the drug of choice for HR and BP control.
- Patients should be counseled on smoking cessation and proper follow-up once an AAA is diagnosed.
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