Subdural hematoma induced by cerebrospinal fluid drainage

A 50-year-old man underwent replacement of the descending thoracic aorta for a DeBakey type III-b chronic dissecting aortic aneurysm. During the surgery, lumbar cerebrospinal fluid (CSF) drainage with a 10 cm H₂O pop-off pressure was used to protect against spinal cord ischemia. During cardiopuhnonary bypass, the patient’s pupils were isocoric, but anisocoric at end of the operation. As computed tomography of the brain showed right subdural hematoma, neurosurgical drainage was instituted emergently. Although some neurological deficit remained, the patient recovered well and was discharged. This case provides a strong reminder that CSF drainage for spinal cord protection against ischemia might induce subdural hematoma, which can be catastrophic during an operation for thoracoabdominal aortic aneurysm.     

Subdural hematoma after thoracoabdominal aortic aneurysm repair: an underreported complication of spinal fluid drainage?

OBJECTIVE: Cerebrospinal fluid (CSF) drainage is a commonly used adjunct to thoracoabdominal aortic aneurysm (TAAA) repair that improves perioperative spinal cord perfusion and thereby decreases the incidence of paraplegia. To date, little data exist on possible complications, such as subdural hematoma caused by stretching and tearing of dural veins, should CSF drainage be excessive. We reviewed our experience with patients in whom postoperative subdural hematomas were detected. METHODS: The records of 230 patients who underwent TAAA repair at the Johns Hopkins Hospital between January 1992 and February 2001 were reviewed. RESULTS: Eight patients had subdural hematomas (3.5%). The four men and four women had a mean age of 60.6 years; two of these patients had a connective tissue disorder. All patients had lumbar drains placed before surgery, including one patient who underwent an emergency operation for rupture. Drains were set to allow drainage for CSF pressure greater than 5 cm H(2)O in all but one patient set for 10 cm H(2)O; spinal cooling was not performed in any patient. All drains were removed on the third postoperative day. In patients in whom subdural hematomas developed, the mean amount of CSF removed after surgery was 690 +/- 79 mL, which was significantly greater than the amount drained from patients in whom subdural hematomas did not develop (359 +/- 24 mL; P =.0013, Mann-Whitney U test). Six patients had postoperative subdural hematomas detected during hospitalization (mean postoperative day, 9.3; range, 2 to 16), and two patients were seen in delayed fashion after discharge from the hospital at 1.5 and 5 months. Four patients died of the subdural hematoma (50%); only one of these patients had neurosurgical intervention. All four survivors responded to neurosurgical intervention and are neurologically healthy. Two patients, both of whom were seen in delayed fashion, needed a lumbar blood patch. Multivariate logistic regression identified the volume of CSF drained as the only variable predictive of occurrence of subdural hematoma (P =.01). CONCLUSION: Subdural hematoma is an unusual and potentially catastrophic complication after TAAA repair. Prompt recognition and neurosurgical intervention is necessary for survival and recovery after acute presentation. Epidural placement of a blood patch is recommended if a chronic subdural hematoma is detected. Care should be taken to ensure that excessive CSF is not drained perioperatively, and higher (10 cm H(2)O) lumbar drain popoff pressures may be necessary together with meticulous monitoring of patient position and neurologic status.     

Spinal subdural hematoma following intracranial aneurysm surgery: four case reports

Four patients presented with rare spinal subdural hematoma (SDH) occurring after intracranial aneurysm surgery and manifesting as postoperative back pain. Magnetic resonance imaging performed from 4 to 11 days after the operation showed acute or subacute thoracolumbar SDH. No patient had risk factors for bleeding at this site (e.g., lumbar puncture, coagulation abnormality). Overdrainage of the cerebrospinal fluid (CSF) was performed for brain retraction during the operation in all four cases. Computed tomography performed during the postoperative period showed a suspicious tentorial subdural hemorrhage in Case 1 and an interhemispheric subdural hemorrhage in Case 3. All four patients received conservative management and their lumbago improved. We hypothesize that CSF hypotension due to overdrainage of CSF and downward migration of intracranial SDH under the influence of gravity were involved in the formation of spinal SDH.     

Reversal of twice-delayed neurologic deficits with cerebrospinal fluid drainage after thoracoabdominal aneurysm repair: a case report and plea for a national database collection

Delayed neurologic deficits are an uncommon yet devastating complication of thoracoabdominal aortic aneurysm repair. The mechanisms involved in the development of delayed spinal cord ischemia remain ill defined. We report a case of complete reversal of delayed neurologic deficits with postoperative cerebrospinal fluid (CSF) drainage. After a thoracoabdominal aneurysm extent I repair, the patient experienced delayed paraplegia at 6 hours and again at 34 hours after the operation, with elevated CSF pressure (>10 mm Hg) on both occasions. Prompt CSF decompression completely reversed the neurologic deficits within hours after onset. The findings in this case further support the role of CSF drainage in spinal cord protection for patients who undergo thoracoabdominal aneurysm repair and make a plea for a national database collection.     

Treatment of delayed-onset neurological deficit after aortic surgery with lumbar cerebrospinal fluid drainage

OBJECTIVE: The phenomenon of delayed neurological deficit after thoracoabdominal aortic aneurysm repair was first reported in the late 1980s. The mechanism may be reduced collateral circulation during periods of hypotension, cord edema, or reperfusion injury. Few patients with delayed-onset neurological deficit have recovered from this devastating complication. The experience with six patients treated with lumbar cerebrospinal fluid (CSF) drainage is reported. METHODS: Five patients underwent thoracoabdominal aortic aneurysm repair. Before and immediately after the operation, the patients exhibited no abnormalities in motor or sensory function. Patients presented between 12 and 40 hours postoperatively with rapid motor and sensory loss in their lower extremities. Hypotensive events immediately preceded the onset of deficit in five patients. The sixth patient experienced an acute onset of back pain and was found to have thrombus without evidence of dissection in the descending aorta. RESULTS: Patients were treated with volume expansion and vasoactive drugs to achieve a mean arterial pressure of more than 70 mm Hg. Lumbar CSF drainage was instituted promptly in four patients; all displayed marked neurological improvement. Two patients underwent CSF drainage several hours after the onset of symptoms and did not improve. The duration of CSF drainage ranged from 15 to 72 hours, with a goal of maintaining the lumbar CSF pressure at less than 10 mm Hg. CONCLUSION: The efficacy of CSF drainage may relate to reducing CSF pressure, which may increase spinal cord perfusion. Rapid initiation of CSF drainage with aggressive support of blood pressure may result in neurological improvement in some patients.     

Prolonged loss of leg myogenic motor evoked potentials during thoracoabdominal aortic aneurysm repair, without postoperative paraplegia

No postoperative paraplegia occurred in a patient whose leg myogenic motor evoked potentials (mMEPs) disappeared during thoracoabdominal aortic aneurysm repair. A 69-year-old man underwent resection and repair of a type III (Crawford classification) thoracoabdominal aneurysm. An epidural catheter was placed into the epidural space for epidural cooling, and a Swan-Ganz catheter was placed into the subarachnoid space for cerebrospinal fluid (CSF) drainage. Continuous CSF pressure and temperature measurement was carried out the day before surgery. The mMEPs gradually disappeared 10 min after proximal double aortic clamping and complete aortic transection. Selective perfusion of intercostal arteries was started about 20 min after the loss of the mMEPs, but the mMEPs were not restored. Possibly, spinal cord hyperemia, induced by selective perfusion of the intercostal vessels, narrowed the subarachnoid space so that CSF could not be satisfactorily drained during surgery. The spinal cord hyperemia may have decreased spinal function and suppressed the leg mMEPs. The persistence of the loss of mMEPs was undeniably due to the influence of the anesthetic agent or a perfusion disorder in the lower-extremity muscles. Of note, moderate spinal cord hypothermia and postoperative CSF drainage probably resulted in improved lower-limb motor function.     

Correlations of Cerebrospinal Fluid Pressure with Hemodynamic Parameters During Thoracoabdominal Aortic Aneurysm Repair

Central venous pressure (CVP) has long been thought to correlate with cerebrospinal fluid (CSF) pressure during thoracoabdominal aortic aneurysm repair. We examined hemodynamic factors during thoracoabdominal aortic aneurysm surgery to determine their relationship with CSF pressure and aortic cross-clamping. Hemodynamic parameters and CSF pressure were measured in 124 patients at six different stages during repair of descending thoracic or thoracoabdominal aortic aneurysms: skin incision, left lung collapse, pump on, aortic clamp on, aortic clamp off, and pump off. Stepwise multiple regression analysis was used for statistical analysis. CVP was a weak predictor for CSF pressure at the beginning of surgery and when the pump was initiated. At the onset of left lung collapse, cardiac output correlated with CSF pressure. There were no predictors during aortic cross-clamping. Model r2 values were low, ranging 0.03-0.15. We found no hemodynamic predictors of CSF pressure throughout the period of aortic cross-clamping during descending thoracic or thoracoabdominal aortic aneurysm surgery. Model r2 values were low, indicating generally poor prediction of CSF pressure.     

Cerebral epidural hematoma following cerebrospinal fluid drainage during thoracoabdominal aortic repair

Cerebrospinal fluid (CSF) drainage is a common adjunct to thoracoabdominal aortic aneurysm (TAAA) repair. CSF drainage may improve perioperative spinal cord perfusion and thereby decrease the incidence of paraplegia or paraparesis. Complications of CSF drainage may arise. We present a case of cerebral epidural hematoma (EDH), possibly arising from excessive CSF drainage, during thoracoabdominal aortic repair.     

Reversal of delayed-onset paraparesis after revision thoracic endovascular aortic repair for ruptured thoracic aortic aneurysm

Thoracic endovascular aortic repair (TEVAR) is an important surgical option for the emergency treatment of ruptured thoracic aortic aneurysms, but is associated with a risk of spinal cord ischemia (SCI). Although risk factors for the development of SCI have been well described, the effectiveness of treatment to increase spinal cord perfusion pressure remains incompletely understood. We report the successful treatment of delayed-onset paraparesis after revision TEVAR for acute descending thoracic aortic rupture with the combined use of blood pressure augmentation and cerebrospinal fluid drainage. The clinical manifestations, pathophysiology, and management of SCI after TEVAR are reviewed.     

Spinal subdural hematoma: a sequela of a ruptured intracranial aneurysm?

BACKGROUND: A case of spinal subdural hematoma (SSDH) following subarachnoid hemorrhage (SAH) because of a ruptured internal carotid aneurysm is described. Such a case has never been reported. CASE DESCRIPTION: A 52-year-old woman underwent a craniotomy for a ruptured internal carotid aneurysm. A computed tomography scan showed that SAH existed predominantly in the posterior fossa and subdural hematoma beneath the cerebellar tentorium. Intrathecal administration of urokinase, IV administration of fasudil hydrochloride, and continuous cerebrospinal fluid (CSF) evacuation via cisternal drainage were performed as prophylactic treatments for vasospasm. On the sixth postoperative day, the patient complained of severe lower back and buttock pain. Magnetic resonance imaging showed a subdural hematoma in the lumbosacral region. Although the mass effect was extensive, the patient showed no neurologic symptoms other than the sciatica. She was treated conservatively. The hematoma dissolved gradually and had diminished completely 15 weeks later. Her pain gradually subsided, and she was discharged 7 weeks later without any neurologic deficit. CONCLUSION: Although the exact mechanism of SSDH in this case is unclear, we speculate that this SSDH was a hematoma that migrated from the intracranial subdural space. Low CSF pressure because of continuous drainage and intrathecal thrombolytic therapy may have played an important role in the migration of the hematoma through the spinal canal. It is important to recognize the SSDH as a possible complication of the SAH accompanied with intracranial subdural hematoma.     

Postoperative rupture of an untreated aneurysm on the 3rd day after subarachnoid hemorrhage surgery

A 58-year-old male presented with severe consciousness disturbance and left hemiparesis. Computed tomography (CT) revealed subarachnoid hemorrhage (SAH) and acute subdural hematoma caused by a ruptured right middle cerebral artery aneurysm. The aneurysm was clipped and the hematoma was evacuated. The patient had almost recovered without new neurological deficits on the next day. Arterial systolic blood pressure was postoperatively controlled within 120 to 150 mmHg. Continuous ventricular and cisternal drainage from the level 10 cm above the external auditory meatus was performed to drain bloody cerebrospinal fluid and prevent vasospasm. Three days after surgery, the patient suddenly lapsed into a coma. CT demonstrated diffuse SAH and bilateral intraventricular hemorrhage caused by rupture of an anterior communicating artery aneurysm. Neck clipping was performed immediately. Unfortunately, the patient died of primary damage due to SAH 3 days after the second surgery. In this case, cisternal drainage was probably important in the aneurysm rupture because of decreased intracranial pressure and change in the perianeurysm environment. Postoperative management of patients with residual untreated aneurysms must consider the possibility that cisternal drainage may result in higher transmural pressure, leading to rupture of the untreated aneurysms.     

Strategies for prevention from spinal cord ischemia during thoracic endovascular aortic repair

Spinal cord ischemia (SCI) is one of the most serious complications in patients who undergo thoracic endovascular aortic repair (TEVAR). The incidence of SCI after TEVAR has been supposed to be lower than the one after traditional open surgical repair. However, not a few cases regarding SCI after TEVAR have been reported recently. Since the detailed mechanism of the SCI is still not fully understood, preventive strategies against SCI including preoperative identification of critical segmental artery (CSA) applying the artery of Adamkiewicz, preservation of the CSA, motor evoked potential (MEP) monitoring, and cerebrospinal fluid (CSF) drainage are routinely performed during TEVAR in our practice.     

Intracerebellar hematoma following thoracoabdominal aortic repair: an unreported complication of cerebrospinal fluid drainage.

Cerebrospinal fluid (CSF) drainage is a routinely used adjunct in thoracoabdominal aortic aneurysm (TAAA) surgery which may reduce the incidence of perioperative paraplegia by improving the spinal cord perfusion. However, a small but evident complication rate of lumbar drainage should be considered. We present two rare cases of intracerebellar hematoma possibly due to excessive CSF drainage after TAAA repair.     

Paraplegia following elective endovascular repair of abdominal aortic aneurysm: reversal with cerebrospinal fluid drainage.

Paraplegia secondary to spinal cord ischaemia is a rare but devastating complication of abdominal aortic aneurysm repair. We report a case of paraplegia following elective endovascular repair of an infrarenal aortic aneurysm. A cerebrospinal fluid (CSF) drain was immediately inserted and resulted in full neurological recovery. This case highlights the fact that endovascular techniques are prone to similar complications as open surgery, and the importance of prompt cerebrospinal fluid drainage in cases of spinal cord ischaemia.     

Changes in Cerebrospinal Fluid Pressure and Lactate Concentrations during Thoracoabdominal Aortic Aneurysm Surgery

Background: Although ischemic injury to the spinal cord is a well-known complication of aortic surgery, no metabolic markers have been identified as predictors of an adverse outcome. This study evaluated the effect of cerebrospinal fluid (CSF) drainage, with and without distal femoral perfusion or moderate hypothermia on blood and CSF lactate concentrations and CSF pressure during thoracoabdominal aortic aneurysm surgery.

Methods: Three nonconcurrent groups of patients were studied prospectively: patients with normal body temperature (35 degrees Celsius) but without distal femoral bypass (n = 6), patients with normal body temperature with bypass (n = 7), and patients with hypothermia (30 degrees Celsius) and bypass (n = 8). In all patients, CSF pressure was recorded before, during, and after aortic cross-clamping. During the surgical repair, CSF drainage was performed using a 4-Fr intrathecal silicone catheter. Blood and CSF lactate concentrations were measured throughout the operation.

Results: Significant increases in blood (490%) and CSF (173%) lactate concentrations were observed during and after thoracic aortic occlusion in patients with normothermia and no bypass (P < 0.02 and 0.05, respectively). Distal perfusion attenuated the increase in both blood and CSF lactate (P < 0.01), and a further reduction was achieved with hypothermia of 30 degrees Celsius (P < 0.001). Patients who became paraplegic showed a greater increase in CSF lactate concentrations after aortic clamp release compared with those who suffered no neurological damage (275% vs. 123% of baseline; P < 0.05). Increased CSF pressure of 42-60% (P < 0.005) was noted soon after thoracic aortic occlusion, both with and without distal femoral bypass.     

Reversal of paraparesis after thoracic aneurysm repair by cerebrospinal fluid drainage

PURPOSE: To describe a case of reversal of delayed paraparesis, after an elective type I thoracoabdominal aortic aneurysm (TAAA) repair, via cerebrospinal fluid (CSF) drainage. CLINICAL FEATURES: A 75-yr-old woman developed paraparesis 13 hr after type I TAAA repair. The patient had been given combined regional and general anesthesia. There was no cerebrospinal fluid drain inserted at the time of surgery. The patient was hemodynamically stable throughout the procedure and was transported to the intensive care unit with trachea intubated and lungs ventilated. She demonstrated some initial lower limb paraparesis but had good recovery of limb function three hours after cessation of the epidural infusion. However, five hours and forty-five minutes after stopping the epidural, she was again paraparetic. Peripheral nerve injury, prolonged effects of epidural local anesthetic, and epidural hematoma were ruled out as precipitating factors. Cord ischemia was considered possible and a CSF catheter was inserted. Immediate improvement was seen upon catheter insertion and commencement of drainage, beginning with movement in the left toes and foot. Drainage was performed when the CFS pressure became > 15 mmHg. Motor function in the lower limbs continued to improve with each drainage extending to complete recovery after 40 hr. She was discharged home 11 days after surgery with no neurological deficit. CONCLUSION: Drainage of CSF was useful in treating a case of post-TAAA neurologic deficit.     

Somatosensory evoked potentials and spinal cord perfusion pressure are significant predictors of postoperative neurologic dysfunction

Paraplegia after thoracoabdominal aneurysm repair can occur in 3% to 40% of patients. This study investigated the efficacy of cerebrospinal fluid (CSF) drainage to protect the spinal cord during aortic cross-clamping (AXC) and the interrelationship between drainage, spinal cord perfusion pressure (SCPP), and changes in somatosensory evoked potentials (SEP) in a canine model of spinal cord ischemia. SCPP was defined as the mean distal aortic pressure minus the CSF pressure. In the experimental group, CSF was drained before AXC. SEP changes were quantitated as time to latency increase of 10% (L-10) and time to complete SEP loss. Drainage of CSF had no significant effect on the distal aortic pressure but significantly increased SCPP from 9.4 to 21.8 mm Hg and decreased the incidence of postoperative neurologic injury. Ischemic SEP changes were highly significant predictors of postoperative neurologic injury, occurring more than two times earlier in the paralyzed and paraparetic animals. Dogs without neurologic injury had significantly higher SCPP, delayed L-10 time, and delayed SEP loss.     

A case report of a patient who developed hemiparaplegia with multiple cerebral infarction during thoracoabdominal aortic aneurysm repair

To protect the spinal cord during thoracoabdominal aortic aneurysm repair, motor evoked potentials (MEP) monitoring and cerebrospinal fluid drainage are often employed. Herein, we report a case, where intraoperative diminishment of motor evoked potentials was accompanied by multiple cerebral infarction. A 63-year-old man underwent elective surgery for both thoracoabdominal aortic aneurysm and abdominal aortic aneurysm. He had a past history of cerebral infarction, resulting in Wernicke aphasia but no paralysis. Preoperative magnetic resonance angiography and echocardiography revealed occlusion of the intercostal and lumbar arteries, mild aortic regurgitation, and atherosclerotic lesions at the aortic arch as well as descending aorta. Anesthesia and muscular relaxation were maintained with fentanyl, propofol, and continuous administration of vecuronium at 0.5 mg x kg(-1) x h(-1). The thoracoabdominal aortic aneurysm was repaired under distal aortic perfusion with femorofemoral bypass. After terminating the bypass, we found that the MEP at the lower limb had disappeared. Although we reconstructed intercostal arteries under mild hypothermia and partial bypass, the amplitude of MEP remained very low. Suspecting spinal cord ischemia, we performed cerebrospinal fluid drainage immediately after the operation. On the postoperative day 4, when we stopped the cerebrospinal fluid drainage and propofol administration, his level of consciousness was poor and brain CT revealed multiple cerebral infarction. On the postoperative day 30, he was discharged from an intensive care unit with complications of hemiplagia and paraplegia. Although cerebrospinal fluid drainage may be recommended to protect spinal cord during thoracoabdominal aortic aneurysm repair, we should consider performing brain CT to exclude a risk of brain herniation secondary to cerebrospinal fluid drainage if there is a possibility of cerebral incidents.     

Spinal cord injury after thoracic endovascular aortic aneurysm repair

Purpose

Thoracic endovascular aortic aneurysm repair (TEVAR) has become a mainstay of therapy for aneurysms and other disorders of the thoracic aorta. The purpose of this narrative review article is to summarize the current literature on the risk factors for and pathophysiology of spinal cord injury (SCI) following TEVAR, and to discuss various intraoperative monitoring and treatment strategies.

Source

The articles considered in this review were identified through PubMed using the following search terms: thoracic aortic aneurysm, TEVAR, paralysis+TEVAR, risk factors+TEVAR, spinal cord ischemia+TEVAR, neuromonitoring+thoracic aortic aneurysm, spinal drain, cerebrospinal fluid drainage, treatment of spinal cord ischemia.

Principal findings

Spinal cord injury continues to be a challenging complication after TEVAR. Its incidence after TEVAR is not significantly reduced when compared with open thoracoabdominal aortic aneurysm repair. Nevertheless, compared with open procedures, delayed paralysis/paresis is the predominant presentation of SCI after TEVAR. The pathophysiology of SCI is complex and not fully understood, though the evolving concept of the importance of the spinal cord’s collateral blood supply network and its imbalance after TEVAR is emerging as a leading factor in the development of SCI. Cerebrospinal fluid drainage, optimal blood pressure management, and newer surgical techniques are important components of the most up-to-date strategies for spinal cord protection.

Conclusion

Further experimental and clinical research is needed to aid in the discovery of novel neuroprotective strategies for the protection and treatment of SCI following TEVAR.

     

Intracranial hemorrhage associated with cerebrospinal fluid drainage during thoraco-abdominal aortic surgery

A 69-year-old woman underwent thoraco-abdominal aortic aneurysm repair with cerebrospinal fluid drainage (CSFD). The initial CSF pressure was elevated to approximately 25 cmH₂O, and clear CSF was continuously drained at a rate of 30 ml/h with the drainage level at 10–20 cmH₂O. The CSF became bloody when cardiopulmonary bypass was terminated. The total volume of CSF drained was approximately 300 ml at the conclusion of the 638 min operation. Three hours later, she suffered a series of generalized seizures because of intracranial hemorrhage (ICH). It was suggested that excessive drainage of CSF was associated with ICH. Meticulous control of drainage volume combined with standard pressure-based management may be the key to avoiding these complications.