A 64-year-old male with a past medical history significant for hypertension, heart failure with reduced ejection fraction, myocardial infarction 2 years prior, and chronic kidney disease presents to the ICU following open AAA repair. He was restarted on his home medications on postoperative day 1. Three days later, his vitals and pertinent laboratory values include: blood pressure 150/100 mm Hg, heart rate 94 bpm, potassium 2.9 mmol/L, serum creatinine 2.6 mg/dL. The following electrocardiogram is obtained 24 hours after admission:
Which of the following medications was the patient most likely taking before surgery?
Correct Answer: B
Digoxin is one of the oldest medications used to treat heart failure with reduced ejection fraction. Digoxin should be used with caution secondary to its narrow therapeutic window and significant risk of toxicity. Digoxin binds to the K+ site of the Na+/K+ adenosine triphosphate-ase pump and inhibits the ion transport, thus secondarily increasing intracellular calcium resulting in an ionotropic effect. Digoxin also has a stimulating effect on both sympathetic and parasympathetic tone with the latter being responsible for its chronotropic effects. Hypokalemia increases the risk of digoxin toxicity secondary to its interaction with the Na+/K+ ATPase pump. A number of other factors can also increase the risk of digoxin toxicity including hypomagnesaemia, hypercalcaemia, myocardial ischemia, hypoxemia, and acid-base disturbances. In addition, renal impairment can prolong the half life of digoxin, therefore increasing the risk of toxicity.
The electrocardiogram above shows characteristic ST segment downsloping depression as well as a shortened QT interval. However, a number of atrial and ventricular arrhythmias are possible with digoxin toxicity. Increased automaticity (atrial fibrillation/ flutter) with AV block, ventricular tachycardia, fibrillation and ectopy, and bradycardia can be seen.
Symptoms of acute digoxin toxicity include nausea, vomiting, diarrhea, hyperkalemia, lethargy, and confusion. The initial GI symptoms occur early at 2 to 4 hours post ingestion, with cardiovascular complications occuring later at 8 to 12 hours. Chronic digoxin toxicity typically has a more insidious onset and is often related to concurrent illness i.e. impaired renal function. The features are similar to acute toxicity with the addition of visual disturbances (reduced vision, yellow halos, and altered color perception) The treatment of digoxin toxicity is with Digoxin-specific Fab antibody fragments, which bind to molecules of digoxin, making them unavailable for binding at their site of action. Digoxin has a narrow therapeutic index and patients must be monitored closely to detect signs of toxicity in the setting of electrolyte, acid-base disturbances, and in renal impairment.
Which of the following findings on physical examination are most likely observed in post-thoracic aortic aneurysm repair spinal cord infarction?
Correct Answer: D
The most common clinical presentation of a spinal cord infarction is anterior spinal artery syndrome. The anterior spinal cord is at higher risk of ischemia because of its vascular anatomy; it is supplied by a single artery with few collaterals unlike the posterior cord, which is supplied by two arteries. An infarct of the anterior spinal cord presents as loss of motor function and pain/ temperature sensation, with sparing of proprioception and vibratory sense below the level of the lesion. The acute stages are characterized by flaccidity and loss of deep tendon reflexes; spasticity and hyperreflexia develop over ensuing days and weeks. In rare cases, the paralysis may affect one leg more than the other and may be asymmetric, depending on the collateral network integrity.
It is important to distinguish spinal cord infarction from other etiologies of postoperative neurologic deficits. Vascular occlusion (C) is a surgical emergency. It presents with lack of peripheral pulse, severe pain, and temperature change in addition to the motor deficit. The patient complains of paresthesia, which is not characteristic for anterior spinal cord syndrome. Spinal cord compression from hematoma or abscess is an important category to exclude as these often require prompt diagnosis and emergent surgical decompression (D). The clinical presentation can occur abruptly and mimic SCI. This diagnostic consideration mandates urgent magnetic resonance imaging of the spinal cord in all patients presenting with possible spinal cord infarct.
It is important to identify the cause of a postoperative neurologic deficit to avoid delay in treatment for etiologies requiring urgent intervention such as spinal cord compression or vascular occlusion.
Which of the following potential complications IS NOT paired correctly with the corresponding classification of aortic dissection?
Correct Answer: A
There are two main classification systems for thoracic aortic dissections, the Stanford classification and the DeBakey classification. Stanford Type A includes all dissections involving the ascending aorta regardless of the extent or site of origin. Stanford Type B includes all dissections distal from the left subclavian artery.
Stanford classification is focused on anticipated treatment of the dissection. Type A dissection accounts for about 60% of all dissections and mandates early surgical repair, as any delay carries a 2% increase in mortality for every hour delayed. Additionally, postponing repair increases the risk for developing life-threatening complications of proximal dissection, which include rupture into the pericardial sac with resulting cardiac tamponade, severe aortic regurgitation, and coronary artery occlusion from extension of the dissection flap into the coronary arteries with subsequent myocardial infarction. Type B dissections account for about 40% of aortic dissections and require medical management focused on decreasing the shear stress on the aortic wall, via reduction in both heart rate and arterial pressure. Surgical repair is indicated if there is severe compression of the true lumen or critical branches arising from the false lumen with signs of hypoperfusion to the lower extremities, visceral organs, and/ or kidneys.
The DeBakey classification takes into account the site of origin of the dissection and the extent of the dissection distally. Type I originated in the ascending aorta and propagates to the descending aorta. Type II originates within and is confined to the ascending aorta. Type III originates below the left subclavian artery and extends distally or, more rarely, retrogrades into the arch and ascending aorta.
By understanding these classification systems, the potential branch vessels that could be compromised by a dissection flap can be identified. Ischemic bowel is due to occlusion of visceral vessels branching off of the descending aorta and thus would not be affected in a DeBakey type II dissection, which is limited to the ascending aorta (A). Acute myocardial infarction can result from intimal flap dissection into a coronary artery. Cerebrovascular accident is a potential complication of dissections involving the carotid arteries. The aortic valve can also be compromised when a proximal dissection flap prolapses through the valve in diastole.
There is an uncommon form of aortic dissection, which originates as type III DeBakey, with subsequent retrograde (proximal) propagation to the aortic arch and ascending aorta. This scenario is not appropriately addressed by the DeBakey and Stanford classification systems. If the proximal propagation is confined within the aortic arch, then it is still considered type B. If the dissection involves the aorta proximal to the brachiocephalic trunk, then it is Stanford Type A.
There are two main systems for classifying aortic dissections; it is important to understand the dissection type as the complications vary. Beyond identifying branch vessels at risk of compromise based on dissection type, determining site of origin and propagation of the dissection is important as it effects management.
A 65-year-old male is admitted to the ICU with confusion, headache, nausea, vomiting, and hypertension. He underwent right carotid endarterectomy 8 hours ago. The first set of vital signs obtained in the ICU showed blood pressure 171/94 mm Hg, heart rate 84 bpm, respiratory rate 22 per minute, and oxygen saturation 96% on room air.
Which of the following IS NOT recommended as treatment for his complication?
Cerebral hyperperfusion syndrome is relatively a rare following carotid endarterectomy or carotid stenting (incidence 0.74%-1.16%). The pathophysiology of hyperperfusion injury is not completely understood, but it is believed that impaired autoregulation due to baroreceptor dysfunction, hypertension, and increased blood flow to the ipsilateral hemisphere play a significant role. It is reversible if recognized early but can progress to unilateral cerebral edema or intracerebral hemorrhage, which significantly increases morbidity and mortality. Several imaging modalities are useful in the identification of cerebral hyperperfusion syndrome. Transcranial Doppler is noninvasive and provides real-time information. It will demonstrate increased flows when compared to preoperative values. CT or magnetic resonance imaging can detect areas of ischemia, edema, and intracerebral hemorrhage. Magnetic resonance perfusion study measures cerebral blood flow and may demonstrate interhemispheric differences in flow/ volume.
The mainstay of treatment is strict blood pressure control postoperatively (C). Hyperperfusion can be seen even in the setting of normotension in some patients. Medication selection is important as those with vasodilatory effects, which further increase cerebral blood flow, can worsen outcomes. Thus, antihypertensive agents that possess negative inotropic effects would be an appropriate first line therapy. There is no indication for prophylactic use of antiepileptic medications in cerebral hyperperfusion syndrome (D).
Although their benefit for treating cerebral hyperperfusion syndrome specifically is unclear, osmotic agents such as hypertonic saline and mannitol should be considered in the setting of symptomatic cerebral edema (A/B).
Cerebral hyperperfusion syndrome is an uncommon but potentially serious complication following carotid endarterectomy and stenting. Care should be taken to minimize precipitating factors such as uncontrolled hypertension.
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