Authors: Destiny F. Chau MD and Meera Gangadharan MD – Arkansas Children’s Hospital/ University of Arkansas for Medical Sciences, Little Rock, AR.
A 10-year-old, otherwise healthy female is undergoing aortic coarctation repair via left posterolateral thoracotomy. In addition to coarctation of the aorta, a transthoracic echocardiogram demonstrated mild left ventricular hypertrophy, normal systolic function, mildly impaired relaxation, and a bicuspid aortic valve. The surgery proceeds uneventfully with an excellent result and the patient is extubated in the operating room with spontaneous movement of all extremities and has adequate postoperative pain control. The arterial blood pressure gradually increases to 128/74. What is the MOST APPROPRIATE therapy?
Correct!
Wrong!
Question of the Week 333
Postoperative paradoxical hypertension after coarctation of the aorta repair is a common occurrence. It is immediately apparent in greater than 50% of patients following coarctation repair. This phenomenon can have an early or delayed postoperative presentation. Early presentation often is limited to the first 24 hours postoperatively. A delayed presentation typically manifests after three to five postoperative days and may be associated with abdominal pain, mesenteric arteritis, and possible bowel ischemia.
The etiology of postoperative paradoxical hypertension is likely multifactorial in origin although the exact mechanism is still uncertain. Disproportionate increases in epinephrine, norepinephrine, renin and angiotensin levels have been found following surgical repair of aortic coarctation. Proposed theories for postoperative hypertension include the following:
• The carotid and aortic arch baroreceptor set points adapt to a higher blood pressure in patients with an aortic coarctation in order to perfuse distal organs such as the kidney. This is the most likely mechanism for the immediate hypertensive response following repair.
• The release of stretch/pressure on the carotid and aortic arch baroreceptors after coarctation resection results in sympathetic nervous system activation with release of norepinephrine and hypertension.
• Activation of the renin–angiotensin–aldosterone system with a resultant increase in renin production is proposed to contribute to delayed hypertension.
Diligent and immediate antihypertensive therapy is necessary for adequate blood pressure control in order to minimize bleeding, prevent anastomotic leaks, and to counteract the clinical sequelae of delayed postoperative paradoxical hypertension.
Pharmacotherapy of postoperative paradoxical hypertension varies from institution to institution. An international survey demonstrated that the most commonly utilized first-line agents include sodium nitroprusside, esmolol, labetalol, angiotensin-converting enzyme inhibitors, and nicardipine. The selection of a particular therapeutic drug may be influenced by regional availability and cost. Some patients require several antihypertensive agents for satisfactory blood pressure control. In addition to the aforementioned drugs, dexmedetomidine may reduce the need for multiple antihypertensive agents to control blood pressure in behaviorally challenging patients. Adequate pain management is also important to minimize the hypertensive response. In this case scenario, the patient appeared comfortable, thus administering an opioid would not be the most appropriate therapeutic choice. In a retrospective study comparing patients who developed hypertension to those who did not develop hypertension in the immediate postoperative period after coarctation repair, the authors concluded that a net positive fluid balance (caused either by higher intraoperative fluid volumes or decreased urine output) contributed to an increased incidence of postoperative hypertension and longer intensive care unit stays. Despite this conclusion, survey research suggests that most institutions do not use diuretics such as furosemide in the management of hypertension in this patient population, which explains why choice D is incorrect.
References:
Fox S, Pierce WS, Waldhausen JA. Pathogenesis of paradoxical hypertension after coarctation repair. Ann Thorac Surg. 1980; 29(2): 135-141.
Rocchini AP, Rosenthal A, Barger AC, Castaneda AR, Nadas AS. Pathogenesis of paradoxical hypertension after coarctation resection. Circulation. 1976; 54(3): 382-387.
Roeleveld PP, Zwijsen EG. Treatment strategies for paradoxical hypertension following surgical correction of coarctation of the aorta in children. World J Pediatr Congenit Heart Surg. 2017; 8(3): 321-331.
Moffett BS, Penny DJ. Variability in treatment of post-coarctectomy hypertension: a multicenter study. Pediatr Cardiol. 2016; 37(4): 772-777.
Schroeder VA, DiSessa TG, Douglas WI. Postoperative fluid balance influences the need for antihypertensive therapy following coarctation repair. Pediatr Crit Care Med. 2004; 5(6): 539-541.
Sahu MK, Manikala VK, Singh SP, Bisoi AK, Chowdhury UK. Use of dexmedetomidine as an adjunct in the treatment of paradoxical hypertension after surgical repair of coarctation of the aorta in infants. Ann Card Anaesth. 2015; 18(3): 437-440.
Soliman R, Saad D. Assessment the effect of dexmedetomidine on incidence of paradoxical hypertension after surgical repair of aortic coarctation in pediatric patients. Ann Card Anaesth. 2018; 21(1): 26-33.
The etiology of postoperative paradoxical hypertension is likely multifactorial in origin although the exact mechanism is still uncertain. Disproportionate increases in epinephrine, norepinephrine, renin and angiotensin levels have been found following surgical repair of aortic coarctation. Proposed theories for postoperative hypertension include the following:
• The carotid and aortic arch baroreceptor set points adapt to a higher blood pressure in patients with an aortic coarctation in order to perfuse distal organs such as the kidney. This is the most likely mechanism for the immediate hypertensive response following repair.
• The release of stretch/pressure on the carotid and aortic arch baroreceptors after coarctation resection results in sympathetic nervous system activation with release of norepinephrine and hypertension.
• Activation of the renin–angiotensin–aldosterone system with a resultant increase in renin production is proposed to contribute to delayed hypertension.
Diligent and immediate antihypertensive therapy is necessary for adequate blood pressure control in order to minimize bleeding, prevent anastomotic leaks, and to counteract the clinical sequelae of delayed postoperative paradoxical hypertension.
Pharmacotherapy of postoperative paradoxical hypertension varies from institution to institution. An international survey demonstrated that the most commonly utilized first-line agents include sodium nitroprusside, esmolol, labetalol, angiotensin-converting enzyme inhibitors, and nicardipine. The selection of a particular therapeutic drug may be influenced by regional availability and cost. Some patients require several antihypertensive agents for satisfactory blood pressure control. In addition to the aforementioned drugs, dexmedetomidine may reduce the need for multiple antihypertensive agents to control blood pressure in behaviorally challenging patients. Adequate pain management is also important to minimize the hypertensive response. In this case scenario, the patient appeared comfortable, thus administering an opioid would not be the most appropriate therapeutic choice. In a retrospective study comparing patients who developed hypertension to those who did not develop hypertension in the immediate postoperative period after coarctation repair, the authors concluded that a net positive fluid balance (caused either by higher intraoperative fluid volumes or decreased urine output) contributed to an increased incidence of postoperative hypertension and longer intensive care unit stays. Despite this conclusion, survey research suggests that most institutions do not use diuretics such as furosemide in the management of hypertension in this patient population, which explains why choice D is incorrect.
References:
Fox S, Pierce WS, Waldhausen JA. Pathogenesis of paradoxical hypertension after coarctation repair. Ann Thorac Surg. 1980; 29(2): 135-141.
Rocchini AP, Rosenthal A, Barger AC, Castaneda AR, Nadas AS. Pathogenesis of paradoxical hypertension after coarctation resection. Circulation. 1976; 54(3): 382-387.
Roeleveld PP, Zwijsen EG. Treatment strategies for paradoxical hypertension following surgical correction of coarctation of the aorta in children. World J Pediatr Congenit Heart Surg. 2017; 8(3): 321-331.
Moffett BS, Penny DJ. Variability in treatment of post-coarctectomy hypertension: a multicenter study. Pediatr Cardiol. 2016; 37(4): 772-777.
Schroeder VA, DiSessa TG, Douglas WI. Postoperative fluid balance influences the need for antihypertensive therapy following coarctation repair. Pediatr Crit Care Med. 2004; 5(6): 539-541.
Sahu MK, Manikala VK, Singh SP, Bisoi AK, Chowdhury UK. Use of dexmedetomidine as an adjunct in the treatment of paradoxical hypertension after surgical repair of coarctation of the aorta in infants. Ann Card Anaesth. 2015; 18(3): 437-440.
Soliman R, Saad D. Assessment the effect of dexmedetomidine on incidence of paradoxical hypertension after surgical repair of aortic coarctation in pediatric patients. Ann Card Anaesth. 2018; 21(1): 26-33.
