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Respiratory Distress

      Dr. Liza Gonen: This is the case of an 80-year-old woman who presented to the Emergency Department (ED) with respiratory distress. The patient had a 112 pack-year smoking history but endorsed no medical problems and had not sought medical care for the past 20 years. She woke up that morning acutely short of breath and walked out onto her front stoop to “get some air” when concerned neighbors noticed her struggling to breathe and called 911. On arrival to the ED, the patient was afebrile, heart rate 92 beats/min, blood pressure 220/100 mm Hg, respiratory rate 30 breaths/min, and oxygen saturation 84% on room air, improved to 98% on continuous positive airway pressure (CPAP) ventilation. Head, ears, eyes, nose, and throat examination revealed equal and reactive pupils. The cardiac examination showed a regular tachycardia with no murmurs noted. There were crackles throughout bilateral lung fields and bilateral lower extremity edema. The abdomen was soft and non-tender, without palpable mass. Extremities were soft, without edema or tenderness. Neurological examination revealed normal strength and sensation of all extremities.
      Dr. Tim Tan: This sounds like a case of acute decompensated heart failure. What was the initial management strategy for this patient?
      Dr. Gonen: The clinical examination suggestive of volume overload and hemodynamic abnormalities did suggest decompensated heart failure. We approached acute blood pressure management with a continuous nitroglycerin infusion followed by diuresis with 80 mg of intravenous (i.v.) furosemide. Of note, the initial electrocardiogram (ECG) did not reveal any acute ischemic changes, which was reassuring, as occlusion of the proximal left anterior descending or left main coronary artery can present with this clinical picture but would be expected to cause marked ischemia on ECG. With this patient's significant smoking history, however, we also considered undiagnosed chronic obstructive pulmonary disease. We treated her concurrently with solumedrol 125 mg i.v. and in-line nebulized albuterol and ipratropium. Initial laboratory assessment values were notable for a compete blood count with a white blood count of 13 k/mm3 with a 93% neutrophil predominance, hematocrit 46%, and platelets 160 k/mm3. The coagulation panel revealed a partial thromboplastin time of 24.3 s, prothrombin time 12.8 s, and an international normalized ratio of 1.0. Chemistries revealed blood urea nitrogen 48 mg/dL, creatinine 1.43 mg/dL, and normal electrolytes. The brain natriuretic peptide was 3208 pg/mL, and the troponin T was negative. Initial chest X-ray study revealed a right lower lobe infiltrate, and the patient was given i.v. levofloxacin to cover for community-acquired pneumonia.
      Dr. Will Tollefson: How did she respond to the initial treatment?
      Dr. Gonen: Initially, the patient diuresed approximately 1 L and was weaned off of the nitroglycerin infusion. She was taken off the CPAP and was able to maintain her oxygenation on 2 L of supplemental oxygen via nasal cannula. Before planned admission to the Medical Service, the patient began to complain of weakness of her legs.
      Dr. Sarah Frasure: Were there any neurologic findings?
      Dr. Gonen: On repeat physical examination, despite having walked out of her apartment to her front stoop just a few hours earlier, the patient could no longer move her toes or plantarflex or dorsiflex her ankles. She could, however, still extend her legs at the knee. She also reported bilateral numbness from mid-thigh distally. Within several minutes she was unable to extend or flex either of her knees. She became incontinent of urine and on rectal examination was found to have absent rectal tone. The lower extremities remained edematous to the mid-tibia, and no dorsalis pedis or posterior tibial pulses were palpable. Femoral pulses could not be identified either by palpation or by Doppler.
      Dr. Jonathan Elmer: The absence of pulses certainly argues for a vascular process. How was the patient managed?
      Dr. Gonen: Given the new high clinical concern for an acute vascular emergency, a stat computed tomography (CT) aortogram was ordered and Vascular Surgery was consulted. The CT aortogram revealed an acute abdominal aortic occlusion at the level of the L4 vertebra (Figure 1, Figure 2). The patient was started on intravenous heparin bolus and infusion, and taken emergently to the operating room. The surgeons performed a right axillofemoral bypass, right femoral-femoral bypass, right superficial femoral artery thrombectomy, and right profunda femoris artery thrombectomy. The patient had a complicated post-operative course including lower-extremity compartment syndrome requiring bilateral four-quadrant fasciotomies, rhabdomyolysis, and intensive care unit delirium. She was discharged to rehab on hospital day 14 with bilateral foot drops, but otherwise neurologically intact.
      Figure thumbnail gr1
      Figure 1Aorta appears normal at the level of the renal arteries.
      Figure thumbnail gr2
      Figure 2Complete occlusion of the abdominal aorta (arrow) at the level of the L4 vertebra.
      Dr. David Brown: This case illustrates the importance of reevaluating your patients when the clinical examination changes. This is a rare diagnosis and one that can easily be missed if one does not think to check for distal pulses. Can you discuss acute aortic occlusion?
      Dr. Gonen: Acute occlusion of the abdominal aorta is a rare but potentially catastrophic vascular emergency, most often occurring in elderly patients with cardiac disease. Mortality has been as high as 75% in some series, and ED management consists of prompt recognition and surgical referral because outcomes are time dependent for surgical intervention (
      • Surowiec S.
      • Isiklar H.
      • Sreeram S.
      • Weiss V.J.
      • Lumsden A.B.
      Acute occlusion of the abdominal aorta.
      ). Unfortunately, because the most conspicuous presenting symptoms are often neurologic deficits, correct diagnosis may be delayed if the symptoms are attributed to a primarily neurologic rather than vascular etiology.
      Acute occlusion can be the result of in situ thrombosis, saddle embolism, thrombosis of an abdominal aortic aneurysm, aortic dissection, or traumatic aortic hematoma (
      • Frost S.
      • Jorden R.
      Acute abdominal aortic occlusion.
      ). Obstruction typically occurs below the level of the renal arteries and can occur in patients even without underlying atherosclerotic disease (
      • Frost S.
      • Jorden R.
      Acute abdominal aortic occlusion.
      ). It is a distinct entity from Leriche syndrome, which is a progressive disease of the distal aorta and iliac vessels caused by atherosclerotic build-up associated with exertional symptoms of claudication. Paradoxically, if pre-existing atherosclerotic disease is present, the degree and severity of presenting symptoms in acute occlusion may actually be lessened due to prior development of collateral circulation (
      • Frost S.
      • Jorden R.
      Acute abdominal aortic occlusion.
      ).
      Dr. Eric Nadel: Can you discuss the presenting symptoms for acute aortic occlusion and how this syndrome can cause neurologic deficits?
      Dr. Gonen: The symptoms are often a direct function of ischemia to the lower extremities or the spinal cord. The presenting symptoms are typically a variable combination of pulselessness with pain, pallor, paresthesia, or paralysis. The physical examination will be marked by absence of pulses in the lower extremities, including absence of femoral pulses, which is a critical and diagnostic finding for this condition (
      • Surowiec S.
      • Isiklar H.
      • Sreeram S.
      • Weiss V.J.
      • Lumsden A.B.
      Acute occlusion of the abdominal aorta.
      ). The skin may be cool, pale, and waxy, with cyanosis being a late finding because skin can withstand ischemia for as long as 24 h (
      • Surowiec S.
      • Isiklar H.
      • Sreeram S.
      • Weiss V.J.
      • Lumsden A.B.
      Acute occlusion of the abdominal aorta.
      ). The muscles may begin to feel doughy in 8–10 h as cellular swelling and necrosis begins to take effect (
      • Frost S.
      • Jorden R.
      Acute abdominal aortic occlusion.
      ). The neurologic symptoms can be a fairly abrupt flaccid paralysis of the lower extremities if infarction of the spinal cord occurs, or more commonly, and as seen in our patient, a progressive ascending weakness of the lower extremities due to ischemia of the cauda equina and spinal nerves themselves (
      • Meagher A.P.
      • Lord R.S.
      • Graham A.R.
      • Hill D.A.
      Acute aortic occlusion presenting with lower limb paralysis.
      ). Whereas the superior spinal cord has a robust vascular supply, the distal thoracolumbar spinal cord often has only paired posterolateral arterial trunks and a single anterior median longitudinal trunk, typically arising from a single aortic branch known as the artery of Adamkiewicz. This anterior system supplies the ventral two-thirds of the spinal cord, often including all but the dorsal columns. Interruption of this vascular supply would cause flaccid paraplegia associated with loss of pain and temperature sensation, but with intact proprioception and vibratory sensation. Although the artery of Adamkiewicz typically arises above the level of the L1 vertebra and the renal arteries, superior to and typically unaffected by acute aortic occlusion, the origin may be variable (
      • van Zyl H.P.
      Paralysis: a rare presentation of abdominal aortic aneurysm thrombosis.
      ). Therefore, patients still may present with an acute flaccid paralysis if the origin of this artery is occluded (
      • Surowiec S.
      • Isiklar H.
      • Sreeram S.
      • Weiss V.J.
      • Lumsden A.B.
      Acute occlusion of the abdominal aorta.
      ,
      • van Zyl H.P.
      Paralysis: a rare presentation of abdominal aortic aneurysm thrombosis.
      ). When occlusion occurs infrarenally, flow obstruction to the iliac and femoral arteries causes an ischemic neuropathy of the cauda equina and large spinal nerves. Whereas spinal cord infarction occurs within 60 min and is almost always irreversible, peripheral nerves can withstand ischemia for up to 12–24 h and some degree of recovery is likely with timely intervention (
      • Surowiec S.
      • Isiklar H.
      • Sreeram S.
      • Weiss V.J.
      • Lumsden A.B.
      Acute occlusion of the abdominal aorta.
      ).
      Dr. Tan: Were the patient's respiratory symptoms related to her aortic occlusion?
      Dr. Gonen: Occasionally, abrupt occlusion of the aorta can also cause marked hemodynamic changes associated with the rapid increase in afterload. Patients can present in acute decompensated heart failure with pulmonary edema and respiratory distress, as found in our patient (
      • Psathas E.D.
      • Bourantas C.V.
      • Parthenis D.G.
      • Verikokos C.
      • Geraqotou T.
      • Kouraklis G.
      Acute respiratory distress as an initial presentation of acute aortic occlusion.
      ). These respiratory symptoms can also be a distraction from the primary vascular process, leading practitioners towards premature closure, which occurred in our patient as well, and may even delay the patient's ability to report the associated lower extremity symptoms for several hours into the ED stay (
      • Psathas E.D.
      • Bourantas C.V.
      • Parthenis D.G.
      • Verikokos C.
      • Geraqotou T.
      • Kouraklis G.
      Acute respiratory distress as an initial presentation of acute aortic occlusion.
      ).
      Dr. Nadel: How is acute aortic occlusion managed in the ED?
      Dr. Gonen: Once acute abdominal aortic occlusion is suspected, emergent surgical consultation should be initiated in parallel with emergent imaging of the abdominal aorta. Although absence of both femoral pulses is diagnostic, the surgical management strategies will depend on the etiology of the obstruction, its extent, and the surrounding anatomy (
      • Frost S.
      • Jorden R.
      Acute abdominal aortic occlusion.
      ). Bedside ultrasound or abdominal ultrasound in Radiology can yield some of this information, but CT aortogram or intraoperative angiography is often preferred, and this choice depends on the preference of the surgeon as well as the capabilities of the institution. Systemic anticoagulation with i.v. heparin should be initiated immediately to prevent proximal and distal propagation of the occlusion (
      • Frost S.
      • Jorden R.
      Acute abdominal aortic occlusion.
      ). After revascularization, patients are at risk for the sequelae of ischemia-reperfusion injury. These include compartment syndromes, myoglobinuria, and renal failure, and metabolic abnormalities such as lactic acidosis and hyperkalemia. Post-operatively, patients are best monitored in the intensive care unit setting.

      References

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