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Spinal Cord Perfusion in Clinical Anesthesia Practice
Case Context
A 39-year-old male is scheduled for microlumbar discectomy (MLD) at the L3–L4 level in the prone position.
Why Spinal Cord Perfusion MattersAlthough the surgical site lies below the conus medullaris, which typically terminates at L1–L2 in adults, adequate blood flow to the cauda equina and lower cord segments remains crucial. These regions are dependent on segmental arterial supply. The prone position alters hemodynamics by modifying venous drainage and arterial inflow, and this can compromise spinal perfusion. Hypotension, anemia, increased intrathoracic or intra-abdominal pressures are recognized risk factors. If perfusion becomes inadequate, ischemia or nerve root injury may occur (Malhotra 2020; Amiri 2019).
Spinal cord perfusion pressure is defined as the difference between mean arterial pressure (MAP) and cerebrospinal fluid pressure (CSFP), or central venous pressure (CVP) if this is higher. In the prone position, abdominal compression increases intra-abdominal pressure, which in turn raises CVP and CSFP, leading to a reduction in SCPP even when systemic MAP appears normal. Thus, maintaining spinal perfusion requires not only stable systemic blood pressure but also minimization of venous congestion (Werndle 2017; Varsos 2016).
The anterior spinal artery supplies approximately two-thirds of the spinal cord, including motor tracts and anterior horn cells. Because it is a single vessel, it is particularly vulnerable to compromise. The paired posterior spinal arteries supply the posterior one-third, mainly sensory tracts, and benefit from redundancy. Segmental radicular arteries, such as the artery of Adamkiewicz (usually arising between T8 and L1), provide critical reinforcement to the anterior spinal circulation. Below L1–L2, the cauda equina is supplied predominantly by these radicular feeders, making their integrity essential for nerve root function (Santillan 2018; Martirosyan 2011).
The anterior spinal artery and radicular arteries form a dense capillary network within the cord. The blood–spinal cord barrier, composed of endothelial tight junctions, regulates molecular entry. Neurons, especially motor neurons, are highly vulnerable to ischemia. Oligodendrocytes, responsible for myelin production, are similarly sensitive to hypoxia. Astrocytes contribute to nutrient delivery and barrier support, while microglia provide immune surveillance and respond to injury. Endothelial cells regulate vascular tone and maintain barrier integrity (Bartanusz 2011; Mautes 2000).
Spinal ischemia follows a predictable pathophysiological sequence. Hypoperfusion causes energy failure due to depletion of oxygen and glucose, reducing ATP production. Ion pump failure then disrupts sodium and potassium gradients, leading to conduction block. Excitotoxicity develops as glutamate accumulates, activating NMDA and AMPA receptors with resultant calcium influx. Mitochondrial injury follows, driven by calcium overload and generation of reactive oxygen species (ROS). Oxidative stress damages lipids, proteins, and DNA, while inflammatory cytokine release breaks down the blood–spinal cord barrier. This cascade culminates in vasogenic edema, which elevates CSFP and further reduces perfusion (Hausmann 2003; Tator 1991).
Several perioperative factors influence spinal cord perfusion. Hypotension directly lowers MAP and thereby SCPP. Anemia reduces oxygen delivery capacity, increasing ischemia risk. Hypoxemia diminishes arterial oxygen content and delivery to the cord. Abdominal compression in the prone position raises intra-abdominal pressure, which elevates CVP and CSFP, lowering SCPP. High levels of positive end-expiratory pressure (PEEP) increase intrathoracic pressure and further elevate CSFP (Kwolek 2016; Deem 1990).
To maintain optimal spinal cord perfusion, several strategies are essential. Proper positioning using chest and pelvic bolsters ensures that the abdomen is free and venous drainage is not obstructed. Hemodynamics should be optimized to maintain MAP between 70 and 80 mmHg, or above 85 mmHg in high-risk patients. Ventilation strategies should avoid high PEEP and excessive airway pressures. Oxygen delivery is improved by maintaining hemoglobin above 10 g/dL and ensuring normoxemia. Euvolemia should be preserved throughout the case (Schonfeld 1988; Bhardwaj 2002).
Different anesthetic agents influence spinal cord perfusion differently. Propofol reduces cerebral metabolic rate and preserves autoregulation but can cause hypotension. Volatile anesthetics induce vasodilation and impair autoregulation at higher MAC levels, so lower concentrations are preferable. Ketamine raises MAP and blocks NMDA receptors, but should be avoided in uncontrolled hypertension. Dexmedetomidine has anti-inflammatory and anti-excitotoxic properties but may produce bradycardia and hypotension (Bilotta 2014; Cole 2007).
Monitoring hemoglobin is essential, with values below 10 g/dL indicating reduced oxygen delivery. Elevated arterial lactate above 2 mmol/L suggests hypoperfusion. Oxygenation should be tracked with arterial saturation, with levels below 90% representing hypoxemia. Central venous oxygen saturation values below 65% indicate increased extraction or reduced delivery. Biomarkers such as neuron-specific enolase, S100β, and neurofilament light chain are being studied for detection of neuronal and axonal injury (Thelin 2017; Kuhle 2016).
Neuroprotection is achieved through maintenance of perfusion with MAP above 70–80 mmHg, optimization of oxygen delivery with adequate hemoglobin and normoxemia, and reduction of venous congestion by freeing the abdomen and maintaining neutral neck alignment. Excitotoxicity can be attenuated with low-dose ketamine or magnesium in select cases, while inflammation may be reduced by using dexmedetomidine and avoiding unnecessary steroid administration (Fehlings 2017; Kwon 2011).
Although the risk of direct cord ischemia is low at L3–L4, nerve root ischemia may occur if hypotension or venous congestion develops. The prone position reduces cardiac output by 10–20%, predisposing the patient to hemodynamic instability. Even short periods of hypotension may contribute to postoperative neuropathic symptoms.
If MAP falls below 70 mmHg, vasopressors such as phenylephrine should be administered. If somatosensory evoked potentials decline despite adequate MAP, positioning should be reassessed, PEEP reduced, and hemoglobin levels checked. If no improvement occurs, anesthetic depth may be adjusted and low-dose ketamine considered. Persistent abnormalities necessitate postoperative MRI with diffusion-weighted imaging.
Emerging research is focused on biomarkers such as neurofilament light chain and microRNAs for early ischemia detection, pharmacologic approaches including mitochondrial stabilizers and NMDA antagonists, and strategies to protect the blood–spinal cord barrier through vascular endothelial growth factor modulation and endothelial stabilizers.
For prone microlumbar discectomy, the abdomen must remain free to facilitate venous return. Mean arterial pressure should be maintained at 70–80 mmHg or higher in at-risk patients. High PEEP and elevated intrathoracic pressures should be avoided. Anemia and hypoxemia must be corrected to preserve oxygen delivery. Vigilant monitoring during induction and positioning is essential, and invasive blood pressure monitoring should be considered in high-risk or prolonged procedures.
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By RENNY CHACKOCase Context
A 39-year-old male is scheduled for microlumbar discectomy (MLD) at the L3–L4 level in the prone position.
Why Spinal Cord Perfusion MattersAlthough the surgical site lies below the conus medullaris, which typically terminates at L1–L2 in adults, adequate blood flow to the cauda equina and lower cord segments remains crucial. These regions are dependent on segmental arterial supply. The prone position alters hemodynamics by modifying venous drainage and arterial inflow, and this can compromise spinal perfusion. Hypotension, anemia, increased intrathoracic or intra-abdominal pressures are recognized risk factors. If perfusion becomes inadequate, ischemia or nerve root injury may occur (Malhotra 2020; Amiri 2019).
Spinal cord perfusion pressure is defined as the difference between mean arterial pressure (MAP) and cerebrospinal fluid pressure (CSFP), or central venous pressure (CVP) if this is higher. In the prone position, abdominal compression increases intra-abdominal pressure, which in turn raises CVP and CSFP, leading to a reduction in SCPP even when systemic MAP appears normal. Thus, maintaining spinal perfusion requires not only stable systemic blood pressure but also minimization of venous congestion (Werndle 2017; Varsos 2016).
The anterior spinal artery supplies approximately two-thirds of the spinal cord, including motor tracts and anterior horn cells. Because it is a single vessel, it is particularly vulnerable to compromise. The paired posterior spinal arteries supply the posterior one-third, mainly sensory tracts, and benefit from redundancy. Segmental radicular arteries, such as the artery of Adamkiewicz (usually arising between T8 and L1), provide critical reinforcement to the anterior spinal circulation. Below L1–L2, the cauda equina is supplied predominantly by these radicular feeders, making their integrity essential for nerve root function (Santillan 2018; Martirosyan 2011).
The anterior spinal artery and radicular arteries form a dense capillary network within the cord. The blood–spinal cord barrier, composed of endothelial tight junctions, regulates molecular entry. Neurons, especially motor neurons, are highly vulnerable to ischemia. Oligodendrocytes, responsible for myelin production, are similarly sensitive to hypoxia. Astrocytes contribute to nutrient delivery and barrier support, while microglia provide immune surveillance and respond to injury. Endothelial cells regulate vascular tone and maintain barrier integrity (Bartanusz 2011; Mautes 2000).
Spinal ischemia follows a predictable pathophysiological sequence. Hypoperfusion causes energy failure due to depletion of oxygen and glucose, reducing ATP production. Ion pump failure then disrupts sodium and potassium gradients, leading to conduction block. Excitotoxicity develops as glutamate accumulates, activating NMDA and AMPA receptors with resultant calcium influx. Mitochondrial injury follows, driven by calcium overload and generation of reactive oxygen species (ROS). Oxidative stress damages lipids, proteins, and DNA, while inflammatory cytokine release breaks down the blood–spinal cord barrier. This cascade culminates in vasogenic edema, which elevates CSFP and further reduces perfusion (Hausmann 2003; Tator 1991).
Several perioperative factors influence spinal cord perfusion. Hypotension directly lowers MAP and thereby SCPP. Anemia reduces oxygen delivery capacity, increasing ischemia risk. Hypoxemia diminishes arterial oxygen content and delivery to the cord. Abdominal compression in the prone position raises intra-abdominal pressure, which elevates CVP and CSFP, lowering SCPP. High levels of positive end-expiratory pressure (PEEP) increase intrathoracic pressure and further elevate CSFP (Kwolek 2016; Deem 1990).
To maintain optimal spinal cord perfusion, several strategies are essential. Proper positioning using chest and pelvic bolsters ensures that the abdomen is free and venous drainage is not obstructed. Hemodynamics should be optimized to maintain MAP between 70 and 80 mmHg, or above 85 mmHg in high-risk patients. Ventilation strategies should avoid high PEEP and excessive airway pressures. Oxygen delivery is improved by maintaining hemoglobin above 10 g/dL and ensuring normoxemia. Euvolemia should be preserved throughout the case (Schonfeld 1988; Bhardwaj 2002).
Different anesthetic agents influence spinal cord perfusion differently. Propofol reduces cerebral metabolic rate and preserves autoregulation but can cause hypotension. Volatile anesthetics induce vasodilation and impair autoregulation at higher MAC levels, so lower concentrations are preferable. Ketamine raises MAP and blocks NMDA receptors, but should be avoided in uncontrolled hypertension. Dexmedetomidine has anti-inflammatory and anti-excitotoxic properties but may produce bradycardia and hypotension (Bilotta 2014; Cole 2007).
Monitoring hemoglobin is essential, with values below 10 g/dL indicating reduced oxygen delivery. Elevated arterial lactate above 2 mmol/L suggests hypoperfusion. Oxygenation should be tracked with arterial saturation, with levels below 90% representing hypoxemia. Central venous oxygen saturation values below 65% indicate increased extraction or reduced delivery. Biomarkers such as neuron-specific enolase, S100β, and neurofilament light chain are being studied for detection of neuronal and axonal injury (Thelin 2017; Kuhle 2016).
Neuroprotection is achieved through maintenance of perfusion with MAP above 70–80 mmHg, optimization of oxygen delivery with adequate hemoglobin and normoxemia, and reduction of venous congestion by freeing the abdomen and maintaining neutral neck alignment. Excitotoxicity can be attenuated with low-dose ketamine or magnesium in select cases, while inflammation may be reduced by using dexmedetomidine and avoiding unnecessary steroid administration (Fehlings 2017; Kwon 2011).
Although the risk of direct cord ischemia is low at L3–L4, nerve root ischemia may occur if hypotension or venous congestion develops. The prone position reduces cardiac output by 10–20%, predisposing the patient to hemodynamic instability. Even short periods of hypotension may contribute to postoperative neuropathic symptoms.
If MAP falls below 70 mmHg, vasopressors such as phenylephrine should be administered. If somatosensory evoked potentials decline despite adequate MAP, positioning should be reassessed, PEEP reduced, and hemoglobin levels checked. If no improvement occurs, anesthetic depth may be adjusted and low-dose ketamine considered. Persistent abnormalities necessitate postoperative MRI with diffusion-weighted imaging.
Emerging research is focused on biomarkers such as neurofilament light chain and microRNAs for early ischemia detection, pharmacologic approaches including mitochondrial stabilizers and NMDA antagonists, and strategies to protect the blood–spinal cord barrier through vascular endothelial growth factor modulation and endothelial stabilizers.
For prone microlumbar discectomy, the abdomen must remain free to facilitate venous return. Mean arterial pressure should be maintained at 70–80 mmHg or higher in at-risk patients. High PEEP and elevated intrathoracic pressures should be avoided. Anemia and hypoxemia must be corrected to preserve oxygen delivery. Vigilant monitoring during induction and positioning is essential, and invasive blood pressure monitoring should be considered in high-risk or prolonged procedures.