Topic: Clinical Case Report
D'Souza, Ryan MD1; Odeyemi, Yewande MBBS1; Onigkeit, James MD1
1Department of Anesthesiology and Perioperative Medicine, Mayo Clinic, Rochester, Minnesota, USA
Introduction: Anterior spinal artery syndrome following abdominal aortic surgery is a known complication, giving rise to paraplegia, sphincter incontinence, and dissociated sensory loss.[1] It is very rare with an incidence of 0.1-0.2%.[1] Etiological factors comprise hypotension, prolonged aortic crossclamping, and embolization of the artery of Adamkiewicz. Complete recovery is uncommon.
Case presentation: A 72 year old female with a history of thoracoabdominal aortic aneurysm was admitted to the intensive care unit (ICU) after undergoing open left aorto-iliac to left renal bypass. Intra-operative course was unremarkable and anesthesia was maintained with propofol and remifentanil. Total length of surgery was eight hours and thirty minutes. Intra-operative mean arterial pressure (MAP) was over 80 mm Hg, and the lowest recorded MAP was 65 mm Hg. The patient was monitored with somatosensory and motor evoked potentials. Near-infrared spectroscopy (NIRS) was utilized and measured values between 70-79%. A total of 2.7 liters of crystalloid, 3 units of packed red blood cells, and 364 mL of autologous blood from cell salvage was given. A phenylephrine infusion was administered for the majority of the case running between 0.1 to 0.5 mcg/kg/min. Estimated blood loss was 740 mL. The lowest intra-operative hemoglobin was 7.4 g/dL.
During ICU admission, her neurologic exam revealed adequate strength bilaterally with intact sensation to touch. She was hemodynamically stable with a MAP between 70-75 mmHg, but she experienced a brief five-minute period with MAP at 67 mmHg. She was subsequently started on a norepinephrine infusion with goal MAP greater than 75 mmHg, and her neurological exam remained stable. One hour later, she experienced acute-onset paraplegia and was unable to move her lower extremities bilaterally, but reported intact sensation to touch. The NIRS device reported values at 50%. Vascular surgery was consulted, and a spinal drain was placed emergently and drained 25 mL of cerebrospinal fluid (CSF). Immediately, the patient was able to move her toes and partially flex her quadriceps bilaterally, although the strength was not at baseline. MAP was maintained above 100 mmHg and hemoglobin greater than 10 mg/dL, and a concurrent rise in NIRS oxygen saturation to a baseline of 70% was noted. The spinal drain was placed to drain at a level of 10 mmHg for 12 hours, then 15 mmHg for 12 hours, then clamped for 36 hours, and was removed when her neurological exam remained stable. Although her motor function did not return to baseline, she had 3/5 strength in her right lower extremity and 2/5 strength in her left lower extremity. An MRI of the spine revealed a subacute infarct in the distal thoracic cord extending to the conus medullaris. She was transferred to the floor where she underwent physical therapy with plans to continue care in an inpatient rehabilitation facility.
Conclusion: While our patient's spinal cord ischemia might have resolved spontaneously, we are struck by the rapidity of partial reversal of her lower extremity paralysis after emergent spinal drain placement, which is a rare phenomenon.[2, 3] The rapid improvement in neurological deficits is presumably due to the reduction in CSF pressure and subsequent increase in spinal cord perfusion pressure.[4] Because paraplegia is a devastating complication and no proven treatment exists, CSF drainage should be investigated in future trials in the setting of spinal cord ischemia.
References:
1. Aydin, A., Mechanisms and prevention of anterior spinal artery syndrome following abdominal aortic surgery. Angiol Sosud Khir, 2015. 21(1): p. 155-64.
2. Blacker, D.J., E.F. Wijdicks, and G. Ramakrishna, Resolution of severe paraplegia due to aortic dissection after CSF drainage. Neurology, 2003. 61(1): p. 142-3.
3. Killen, D.A., C.L. Weinstein, and W.A. Reed, Reversal of spinal cord ischemia resulting from aortic dissection. J Thorac Cardiovasc Surg, 2000. 119(5): p. 1049-52.
4. Coselli, J.S., et al., Cerebrospinal fluid drainage in thoracoabdominal aortic surgery. Semin Vasc Surg, 2000. 13(4): p. 308-14.
Topic: Clinical Case Report
D'Souza, Ryan MD1; Odeyemi, Yewande MBBS1; Onigkeit, James MD1
1Department of Anesthesiology and Perioperative Medicine, Mayo Clinic, Rochester, Minnesota, USA
Introduction: Anterior spinal artery syndrome following abdominal aortic surgery is a known complication, giving rise to paraplegia, sphincter incontinence, and dissociated sensory loss.[1] It is very rare with an incidence of 0.1-0.2%.[1] Etiological factors comprise hypotension, prolonged aortic crossclamping, and embolization of the artery of Adamkiewicz. Complete recovery is uncommon.
Case presentation: A 72 year old female with a history of thoracoabdominal aortic aneurysm was admitted to the intensive care unit (ICU) after undergoing open left aorto-iliac to left renal bypass. Intra-operative course was unremarkable and anesthesia was maintained with propofol and remifentanil. Total length of surgery was eight hours and thirty minutes. Intra-operative mean arterial pressure (MAP) was over 80 mm Hg, and the lowest recorded MAP was 65 mm Hg. The patient was monitored with somatosensory and motor evoked potentials. Near-infrared spectroscopy (NIRS) was utilized and measured values between 70-79%. A total of 2.7 liters of crystalloid, 3 units of packed red blood cells, and 364 mL of autologous blood from cell salvage was given. A phenylephrine infusion was administered for the majority of the case running between 0.1 to 0.5 mcg/kg/min. Estimated blood loss was 740 mL. The lowest intra-operative hemoglobin was 7.4 g/dL.
During ICU admission, her neurologic exam revealed adequate strength bilaterally with intact sensation to touch. She was hemodynamically stable with a MAP between 70-75 mmHg, but she experienced a brief five-minute period with MAP at 67 mmHg. She was subsequently started on a norepinephrine infusion with goal MAP greater than 75 mmHg, and her neurological exam remained stable. One hour later, she experienced acute-onset paraplegia and was unable to move her lower extremities bilaterally, but reported intact sensation to touch. The NIRS device reported values at 50%. Vascular surgery was consulted, and a spinal drain was placed emergently and drained 25 mL of cerebrospinal fluid (CSF). Immediately, the patient was able to move her toes and partially flex her quadriceps bilaterally, although the strength was not at baseline. MAP was maintained above 100 mmHg and hemoglobin greater than 10 mg/dL, and a concurrent rise in NIRS oxygen saturation to a baseline of 70% was noted. The spinal drain was placed to drain at a level of 10 mmHg for 12 hours, then 15 mmHg for 12 hours, then clamped for 36 hours, and was removed when her neurological exam remained stable. Although her motor function did not return to baseline, she had 3/5 strength in her right lower extremity and 2/5 strength in her left lower extremity. An MRI of the spine revealed a subacute infarct in the distal thoracic cord extending to the conus medullaris. She was transferred to the floor where she underwent physical therapy with plans to continue care in an inpatient rehabilitation facility.
Conclusion: While our patient's spinal cord ischemia might have resolved spontaneously, we are struck by the rapidity of partial reversal of her lower extremity paralysis after emergent spinal drain placement, which is a rare phenomenon.[2, 3] The rapid improvement in neurological deficits is presumably due to the reduction in CSF pressure and subsequent increase in spinal cord perfusion pressure.[4] Because paraplegia is a devastating complication and no proven treatment exists, CSF drainage should be investigated in future trials in the setting of spinal cord ischemia.
References:
1. Aydin, A., Mechanisms and prevention of anterior spinal artery syndrome following abdominal aortic surgery. Angiol Sosud Khir, 2015. 21(1): p. 155-64.
2. Blacker, D.J., E.F. Wijdicks, and G. Ramakrishna, Resolution of severe paraplegia due to aortic dissection after CSF drainage. Neurology, 2003. 61(1): p. 142-3.
3. Killen, D.A., C.L. Weinstein, and W.A. Reed, Reversal of spinal cord ischemia resulting from aortic dissection. J Thorac Cardiovasc Surg, 2000. 119(5): p. 1049-52.
4. Coselli, J.S., et al., Cerebrospinal fluid drainage in thoracoabdominal aortic surgery. Semin Vasc Surg, 2000. 13(4): p. 308-14.
Topic: Clinical Case Report
D'Souza, Ryan MD1; Odeyemi, Yewande MBBS1; Onigkeit, James MD1
1Department of Anesthesiology and Perioperative Medicine, Mayo Clinic, Rochester, Minnesota, USA
Introduction: Anterior spinal artery syndrome following abdominal aortic surgery is a known complication, giving rise to paraplegia, sphincter incontinence, and dissociated sensory loss.[1] It is very rare with an incidence of 0.1-0.2%.[1] Etiological factors comprise hypotension, prolonged aortic crossclamping, and embolization of the artery of Adamkiewicz. Complete recovery is uncommon.
Case presentation: A 72 year old female with a history of thoracoabdominal aortic aneurysm was admitted to the intensive care unit (ICU) after undergoing open left aorto-iliac to left renal bypass. Intra-operative course was unremarkable and anesthesia was maintained with propofol and remifentanil. Total length of surgery was eight hours and thirty minutes. Intra-operative mean arterial pressure (MAP) was over 80 mm Hg, and the lowest recorded MAP was 65 mm Hg. The patient was monitored with somatosensory and motor evoked potentials. Near-infrared spectroscopy (NIRS) was utilized and measured values between 70-79%. A total of 2.7 liters of crystalloid, 3 units of packed red blood cells, and 364 mL of autologous blood from cell salvage was given. A phenylephrine infusion was administered for the majority of the case running between 0.1 to 0.5 mcg/kg/min. Estimated blood loss was 740 mL. The lowest intra-operative hemoglobin was 7.4 g/dL.
During ICU admission, her neurologic exam revealed adequate strength bilaterally with intact sensation to touch. She was hemodynamically stable with a MAP between 70-75 mmHg, but she experienced a brief five-minute period with MAP at 67 mmHg. She was subsequently started on a norepinephrine infusion with goal MAP greater than 75 mmHg, and her neurological exam remained stable. One hour later, she experienced acute-onset paraplegia and was unable to move her lower extremities bilaterally, but reported intact sensation to touch. The NIRS device reported values at 50%. Vascular surgery was consulted, and a spinal drain was placed emergently and drained 25 mL of cerebrospinal fluid (CSF). Immediately, the patient was able to move her toes and partially flex her quadriceps bilaterally, although the strength was not at baseline. MAP was maintained above 100 mmHg and hemoglobin greater than 10 mg/dL, and a concurrent rise in NIRS oxygen saturation to a baseline of 70% was noted. The spinal drain was placed to drain at a level of 10 mmHg for 12 hours, then 15 mmHg for 12 hours, then clamped for 36 hours, and was removed when her neurological exam remained stable. Although her motor function did not return to baseline, she had 3/5 strength in her right lower extremity and 2/5 strength in her left lower extremity. An MRI of the spine revealed a subacute infarct in the distal thoracic cord extending to the conus medullaris. She was transferred to the floor where she underwent physical therapy with plans to continue care in an inpatient rehabilitation facility.
Conclusion: While our patient's spinal cord ischemia might have resolved spontaneously, we are struck by the rapidity of partial reversal of her lower extremity paralysis after emergent spinal drain placement, which is a rare phenomenon.[2, 3] The rapid improvement in neurological deficits is presumably due to the reduction in CSF pressure and subsequent increase in spinal cord perfusion pressure.[4] Because paraplegia is a devastating complication and no proven treatment exists, CSF drainage should be investigated in future trials in the setting of spinal cord ischemia.
References:
1. Aydin, A., Mechanisms and prevention of anterior spinal artery syndrome following abdominal aortic surgery. Angiol Sosud Khir, 2015. 21(1): p. 155-64.
2. Blacker, D.J., E.F. Wijdicks, and G. Ramakrishna, Resolution of severe paraplegia due to aortic dissection after CSF drainage. Neurology, 2003. 61(1): p. 142-3.
3. Killen, D.A., C.L. Weinstein, and W.A. Reed, Reversal of spinal cord ischemia resulting from aortic dissection. J Thorac Cardiovasc Surg, 2000. 119(5): p. 1049-52.
4. Coselli, J.S., et al., Cerebrospinal fluid drainage in thoracoabdominal aortic surgery. Semin Vasc Surg, 2000. 13(4): p. 308-14.
Topic: Clinical Case Report
D'Souza, Ryan MD1; Odeyemi, Yewande MBBS1; Onigkeit, James MD1
1Department of Anesthesiology and Perioperative Medicine, Mayo Clinic, Rochester, Minnesota, USA
Introduction: Anterior spinal artery syndrome following abdominal aortic surgery is a known complication, giving rise to paraplegia, sphincter incontinence, and dissociated sensory loss.[1] It is very rare with an incidence of 0.1-0.2%.[1] Etiological factors comprise hypotension, prolonged aortic crossclamping, and embolization of the artery of Adamkiewicz. Complete recovery is uncommon.
Case presentation: A 72 year old female with a history of thoracoabdominal aortic aneurysm was admitted to the intensive care unit (ICU) after undergoing open left aorto-iliac to left renal bypass. Intra-operative course was unremarkable and anesthesia was maintained with propofol and remifentanil. Total length of surgery was eight hours and thirty minutes. Intra-operative mean arterial pressure (MAP) was over 80 mm Hg, and the lowest recorded MAP was 65 mm Hg. The patient was monitored with somatosensory and motor evoked potentials. Near-infrared spectroscopy (NIRS) was utilized and measured values between 70-79%. A total of 2.7 liters of crystalloid, 3 units of packed red blood cells, and 364 mL of autologous blood from cell salvage was given. A phenylephrine infusion was administered for the majority of the case running between 0.1 to 0.5 mcg/kg/min. Estimated blood loss was 740 mL. The lowest intra-operative hemoglobin was 7.4 g/dL.
During ICU admission, her neurologic exam revealed adequate strength bilaterally with intact sensation to touch. She was hemodynamically stable with a MAP between 70-75 mmHg, but she experienced a brief five-minute period with MAP at 67 mmHg. She was subsequently started on a norepinephrine infusion with goal MAP greater than 75 mmHg, and her neurological exam remained stable. One hour later, she experienced acute-onset paraplegia and was unable to move her lower extremities bilaterally, but reported intact sensation to touch. The NIRS device reported values at 50%. Vascular surgery was consulted, and a spinal drain was placed emergently and drained 25 mL of cerebrospinal fluid (CSF). Immediately, the patient was able to move her toes and partially flex her quadriceps bilaterally, although the strength was not at baseline. MAP was maintained above 100 mmHg and hemoglobin greater than 10 mg/dL, and a concurrent rise in NIRS oxygen saturation to a baseline of 70% was noted. The spinal drain was placed to drain at a level of 10 mmHg for 12 hours, then 15 mmHg for 12 hours, then clamped for 36 hours, and was removed when her neurological exam remained stable. Although her motor function did not return to baseline, she had 3/5 strength in her right lower extremity and 2/5 strength in her left lower extremity. An MRI of the spine revealed a subacute infarct in the distal thoracic cord extending to the conus medullaris. She was transferred to the floor where she underwent physical therapy with plans to continue care in an inpatient rehabilitation facility.
Conclusion: While our patient's spinal cord ischemia might have resolved spontaneously, we are struck by the rapidity of partial reversal of her lower extremity paralysis after emergent spinal drain placement, which is a rare phenomenon.[2, 3] The rapid improvement in neurological deficits is presumably due to the reduction in CSF pressure and subsequent increase in spinal cord perfusion pressure.[4] Because paraplegia is a devastating complication and no proven treatment exists, CSF drainage should be investigated in future trials in the setting of spinal cord ischemia.
References:
1. Aydin, A., Mechanisms and prevention of anterior spinal artery syndrome following abdominal aortic surgery. Angiol Sosud Khir, 2015. 21(1): p. 155-64.
2. Blacker, D.J., E.F. Wijdicks, and G. Ramakrishna, Resolution of severe paraplegia due to aortic dissection after CSF drainage. Neurology, 2003. 61(1): p. 142-3.
3. Killen, D.A., C.L. Weinstein, and W.A. Reed, Reversal of spinal cord ischemia resulting from aortic dissection. J Thorac Cardiovasc Surg, 2000. 119(5): p. 1049-52.
4. Coselli, J.S., et al., Cerebrospinal fluid drainage in thoracoabdominal aortic surgery. Semin Vasc Surg, 2000. 13(4): p. 308-14.
