Senior Report 7.4

Case Presentation by Dr. Erin Murphy

CC: “I’m having back pain.”

HPI: 63yo male presents to ED c/o abdominal pain & left flank pain x 2-3 days as well as cough, shortness of breath and intermittent sweating/chills. He describes the abdominal pain as diffuse, constant, achy, 10/10 in severity today and radiating to his low back. His left flank pain is sharp, constant & severe. He has nausea & vomiting today. The patient saw his PCP recently, was thought to have possible kidney stone & was prescribed Norco and Flomax. He denies urinary symptoms or diarrhea. Today, he is nauseated and has vomited several times. Denies hematemesis.

ROS:
Constitutional: +subjective chills
ENT: No sore throat
Respiratory: +difficulty breathing
Cardiovascular: No chest pain
GI: +abdominal pain, no bloody stools
GU: No hematuria
Musculoskeletal: No arthralgias
Skin: No rash
Neuro: No weakness

PMH: anxiety/panic attacks, HTN
PSH: left hand surgery
Meds: clonazepam, acetaminophen-hydrocodone, paroxetine, tamsulosin
Allergies: NKDA
Social: smokes 1ppd cigarettes, denies alcohol

Physical Exam:
Vitals: BP 169/124 Pulse 80 RR 16 Temp 36.9 oral Pulse ox 90% room air
Constitutional: obese male, moderate distress, slightly diaphoretic
HEENT: no conjunctival pallor, sclera anicteric, oropharynx is dry
Respiratory: mild tachypnea, bibasilar crackles, no wheezes
Cardiovascular: regular rate & rhythm, S1, S2, no murmurs or gallops
Abdomen: obese, soft, no abdominal tenderness
Back: no CVA tenderness
Musculoskeletal: no pedal edema
Skin: no rash
Neurologic: awake, alert & oriented x3, no focal deficits

Emergency department course:
After the patient was evaluated by the physician, he was standing up to urinate when he suddenly collapsed onto the stretcher, became unresponsive & was found to be pulseless with agonal respirations. Cardiac monitor showed PEA, patient was intubated and resuscitated per ACLS protocol and had spontaneous ROSC but remained hypotensive despite aggressive fluids & pressors. CT-abdomen/pelvis with IV contrast was obtained.

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Questions:
1. What is the above diagnosis?
a. ruptured perinephric hematoma
b. intra-abdominal abscess
c. ruptured AAA
d. spontaneous adrenal hemorrhage

2. Which of the following is NOT a risk factor for the above condition?
a. family history
b. diabetes
c. smoking
d. male gender

3. What is the next step in managing this patient?
a. Go to OR
b. CTA of abdomen and pelvis
c. bedside ultrasound of abdomen
d. angiograph

Answers & Discussion:
1) c
2) b
3) a

A true aortic aneurysm is a localized dilatation of the aorta caused by weakening of its wall; it involves all three layers (intima, media, and adventitia) of the arterial wall. This should not be confused with aortic dissections and pseudoaneurysms.

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Rosen’s 7th Ed. Figure 84-1.

Aneurysms can develop in any segment of the aorta, but most involve the aorta below the renal arteries. The diameter of the normal adult infrarenal aorta is approximately 2 cm, and a diameter of 3 cm or more defines an AAA.

An AAA is a disease of aging. The average age at the time of diagnosis is 65-70 and men are affected much more often than women. The patient often has atherosclerotic occlusive disease of other vessels. Smoking is strongly associated with AAA. A family history of an AAA is a very strong risk factor; those with an affected first-degree relative have a 10- to 20-fold increased risk of developing an AAA. Female sex, African American race, and presence of diabetes mellitus are negatively associated with AAA.

AAAs progressively enlarge, ultimately resulting in rupture of the aneurysm and fatal hemorrhage. The most important factor determining the risk of rupture is the size of the aneurysm. The rupture risk increases dramatically with increased aneurysm size, and most ruptured AAAs have diameters greater than 5 cm. Rupture of an AAA usually occurs into the retroperitoneum, where hemorrhage may be temporarily limited by clotting and tamponade at the rupture site. Of patients with ruptures, 10 to 30% have free intraperitoneal rupture, which is often rapidly fatal. Complications can also arise from intact AAAs. The walls of AAAs are often lined with clot and atheromatous material, which can embolize and occlude distal vessels.Aortic thrombosis may occur rarely. Patients can also have complications caused by impingement on adjacent structures, like vertebral body erosion.

Patients with unruptured AAA may have symptoms, such as pain in the abdomen, back, or flank; an awareness of an abdominal mass or fullness; or a sensation of abdominal pulsations. The pain associated with stable, intact aneurysms has a gradual onset and a vague, dull quality. It is usually constant but may be described as throbbing or colicky. Acute or severe pain is an ominous symptom that suggests imminent or actual aortic rupture.

The most consistent physical finding is a pulsatile, expansile abdominal mass. There is virtually no risk of causing aneurysm rupture by abdominal palpation.However, an AAA may be difficult to palpate if the patient is obese. Most intact AAAs are nontender; tenderness suggests aneurysm expansion or rupture. The classic triad of a ruptured AAA is pain, hypotension, and a pulsatile abdominal mass,many patients have only one or two components of this triad, and an occasional patient has none of the classic features. Most patients with a ruptured AAA experience pain in the abdomen, back, or flank. Pain is usually acute, severe and constant. An AAA can rupture into the gastrointestinal tract (aortoenteric fistula) or inferior vena cava (aortocaval fistula) and should be suspected in patients with suspected AAA who are presenting with GI bleed or signs & symptoms of a large AV fistula.

Because of its low sensitivity compared with CT and ultrasound, plain abdominal radiography should not be used to investigate possible AAA. AAA’s may be incidentally seen on CXR as curvilinear calcification of the aortic wall or a paravertebral soft tissue mass.

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Rosen’s 7th Ed. Figure 84-2

Ultrasonography is extremely sensitive in detecting AAAs, provided that a technically adequate study can be obtained (sometimes the aorta is not well visualized because of obesity or excess bowel gas). Ultrasonography has distinct advantages in the emergency evaluation of a patient with a possible ruptured AAA.It can be performed very rapidly at the patient’s bedside, obviating the need to take a potentially unstable patient to the radiology suite. If an aorta has a normal diameter visualized throughout its abdominal course, the patient does not have an AAA. However, ultrasonography cannot be relied on to determine whether an AAA has ruptured. The sensitivity of emergency ultrasonography in detecting extraluminal blood is very low. If ultrasonography reveals an AAA in an unstable patient, aneurysm rupture is presumed, and the patient requires immediate aneurysm repair.

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Rosen’s 7th Ed. Figure 84-3. Cross-sectional ultrasound of a 6-cm abdominal aortic aneurysm. Note mural thrombus and eccentrically shaped patent lumen.

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Probe placement.

As with ultrasonography, abdominal CT is virtually 100% accurate in determining the presence or absence of an AAA and provides accurate measurements of the aortic diameter.CT is less subject to technical problems and interpretation errors than ultrasonography and is much more sensitive in detecting extraluminal blood. IV contrast is desirable, but not essential, in emergency situations. Obtaining CT is appropriate only in hemodynamically stable patients.

The patient with a ruptured AAA is unstable until the aorta is cross-clamped in the operating room or stabilized with endovascular techniques. No patient with a known or suspected aortic rupture should be considered “stable,” regardless of the initial vital signs or initial hemoglobin level.

When the patient arrives at the ED, large-bore IV access should be established and blood sent for crossmatching. Because patients with ruptured AAAs often have large transfusion requirements, at least 6 U of blood should be made available initially, with notification to the blood bank of the potential need for significantly more.The surgical and anesthesia team should be notified immediately. The hemodynamically unstable patient in whom a ruptured AAA has been diagnosed or is strongly suspected should be taken to the operating room as soon as possible. Attempts to resuscitate hypotensive patients fully in the ED and normalize the vital signs should be avoided. If transfer is required, it should be initiated as soon as the diagnosis is known or strongly suspected. Attempts to stabilize the patient in the ED are often fruitless and waste valuable time.

The appropriate degree of preoperative volume resuscitation is controversial. No prospective studies have compared different preoperative fluid regimens in hypotensive patients with ruptured AAAs, and the optimal resuscitation strategy has not been determined. The goal is to prevent irreversible end-organ damage without over-resuscitating to the point that clots may become dislodged and worsen bleeding. Although blood pressure necessary for vital organ perfusion varies among patients, a systolic blood pressure of 80-100 mm Hg is a reasonable target.

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Key points:

  • An infrarenal diameter >3cm defines an AAA
  • Risk factors include age >65, male sex, smoking & family history
  • Risk of rupture greatest with aneurysms >5 cm
  • Acute or severe pain is an ominous symptom
  • Classic triad of a ruptured AAA = pain, hypotension & pulsatile mass
  • Maintain high clinical suspicion, especially in elderly
  • Bedside ultrasound is very effective at detection of AAA
  • Patients should be taken to OR as soon as possible

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