- Email: [email protected]
Delayed paradoxical herniation after a decompressive craniectomy: case report
Available online at www.sciencedirect.com
Surgical Neurology 69 (2008) 293 – 296 www.surgicalneurology-online.com
Technique
Delayed paradoxical herniation after a decompressive craniectomy: case report Marcelo Duarte Vilela, MD4 Department of Neurological Surgery, Harborview Medical Center, University of Washington, Seattle, WA 98104, USA Received 2 May 2006; accepted 4 January 2007
Abstract
Background: Paradoxical herniation can occur as a complication of lumbar puncture in patients who had a decompressive craniectomy. The supposed mechanism is the development of a negative pressure gradient that allows the brain to shift toward the infratentorial space with subsequent herniation. Trendelenburg position plus early cranioplasty has been the suggested treatment to eliminate the gradient. Case Description: A 53-year-old woman had a decompressive hemicraniectomy for SAH-related swelling. A lumbar puncture was performed on postoperative day 5 to rule out infection. She remained neurologically stable until 6 weeks later, when she deteriorated because of a paradoxical herniation. Head positioning and cranioplasty were only temporarily helpful. She developed a second episode of decline a few days later due to an extraaxial CSF collection. A lumbar blood patch plus drainage of the collection successfully allowed full neurologic recovery. Conclusions: Cranioplasty and head positioning alone might not be sufficient to eliminate the negative pressure gradient. A blood patch should be part of the management of paradoxical herniation. D 2008 Elsevier Inc. All rights reserved.
Keywords:
Lumbar puncture; Decompressive craniectomy; Paradoxical herniation; Blood patch; Cranioplasty
1. Introduction Lumbar puncture is known to be hazardous in the face of elevated ICP combined with mass effect and/or brain shift [22]. In addition, a lumbar puncture with persistent CSF leakage or continuous spinal CSF drainage can lead to a negative pressure gradient between the intracranial space and spinal canal with displacement of the intracranial structures toward the infratentorial compartment and foramen magnum, even in patients with normal ICP [4,10,15]. Paradoxical herniation is the herniation of a craniectomized, decompressed brain with subsequent brainstem compression and neurologic deterioration after a lumbar puncture Abbreviations: CSF, cerebrospinal fluid; CT, computerized tomography; ICP, intracranial pressure; IV, intravenous; GOS, Glasgow outcome scale; MRI, magnetic resonance imaging; SAH, subarachnoid hemorrhage. 4 Tel.: +1 206 744 9330; fax: +1 206 744 9944. E-mail address: [email protected]. 0090-3019/$ – see front matter D 2008 Elsevier Inc. All rights reserved. doi:10.1016/j.surneu.2007.01.027
[12,17]. The effects of gravity and atmospheric pressure combined with a negative pressure in the spinal canal allow the brain to shift toward the infratentorial compartment, causing herniation and neurologic dysfunction. There are only a few cases of paradoxical herniation reported in the literature [12,17]. The recommended management has been to position the patient’s head down, administer IV fluids, and perform an early cranioplasty [17]. Our objective is to present a case that is noteworthy because of the following reasons: it shows that this management strategy is not always effective and although a lumbar blood patch has been suggested by others [12], this was the first occasion that it was actually done, with full neurologic recovery and an excellent outcome. 2. Case report A 53-year-old woman was admitted with a diagnosis of SAH due to an anterior communicating artery aneurysm
294
M.D. Vilela / Surgical Neurology 69 (2008) 293 – 296
Fig. 1. A: Head CT done on postoperative day 23 showing mild hydrocephalus and a subgaleal collection but no shift. B: Head CT done on postoperative day 43 demonstrating a markedly sunken brain with midline shift. C: Complete resolution of midline shift after cranioplasty.
rupture. After 12 hours postictus, clipping using a pterional approach was performed. A large prophylactic decompressive hemicraniectomy and a right frontal ventriculostomy were also done in the same sitting, because of severe brain swelling. On postoperative day 5, because of a sustained high-grade fever, a lumbar puncture using a 20-gauge spinal needle was done to rule out meningitis. The opening pressure was 12 cm H2O, only 5 mL of CSF was sent for analysis and the closing pressure was 11 cm H2O. Over the next 2 weeks, her course was complicated by cerebral salt wasting syndrome and cerebral vasospasm requiring angioplasty, but both eventually resolved without major deficits. On the fourth postoperative week, the patient was mildly somnolent and confused. A head CT scan showed only a subgaleal CSF collection but no shift (Fig. 1A). The patient thereafter slowly improved with some difficulties with mobilization and apathy. The craniectomy defect was slightly depressed on inspection. During the following week, she would alternate between periods of drowsiness and alertness, with no obvious explanation. On postoperative day 43, she was found to be stuporous, not following commands, had sluggish pupils, left hemiparesis, and a depressed, tender craniectomy defect on exam. A head CT showed a markedly sunken brain with midline shift (Fig. 1B). The bed was immediately placed in the Trendelenburg position, which resulted in some improvement of the mental status. She was shortly thereafter taken to the operating room for an emergent cranioplasty. The following morning she was fully awake, conversing, with no neurologic deficits. A head CT showed complete resolution of the midline shift (Fig 1C). On postoperative day 5, she started complaining of mild headaches and on the following day lethargy and left hemiparesis were again present. A head CT demonstrated a large extraaxial collection, with midline shift (Fig. 2A). The patient was immediately taken to the operating room for drainage of this fluid collection. A burr hole was made in the superior temporal region and a large epidural CSF collection was found and drained. A presumptive diagnosis of a persistent spinal CSF leak was made and a lumbar blood patch was done at the same
sitting. A head CT scan done a few days later showed complete resolution of the epidural collection and shift (Fig. 2B). Further follow-up scans demonstrated no recurrence of the epidural collection. Three months later, a ventriculoperitoneal shunt was inserted for symptomatic normal pressure hydrocephalus. The patient is doing very well 12 months after the aneurysm clipping, with a GOS of V and return to full activities. 3. Discussion Lumbar puncture is well known to be hazardous in the presence of a high ICP combined with mass effect and/or brain shift [22]. The phenomenon of downward herniation not associated with high ICP and/or shift has been reported after lumbar puncture or placement of a lumbar drain [4,9,10,15,19], following lumbar spinal surgery with a persistent CSF leak [2] or spontaneous spinal CSF leaks [3,16]. The mechanism is the occurrence of a negative pressure gradient between the intracranial and the spinal compartments due to persistent CSF leakage, which causes spinal and intracranial hypovolemia [10,15]. Characteristically, the ICP is low [3,15]. The intracranial contents bsink down,Q with herniation of the cerebral hemispheres and diencephalon toward the posterior fossa and the displace-
Fig. 2. A: Head CT showing a large extraaxial fluid collection, with striking shift. B: Head CT demonstrating resolution of the CSF collection.
M.D. Vilela / Surgical Neurology 69 (2008) 293 – 296
ment of the brainstem and cerebellum toward the foramen magnum [2-4,16]. Symptoms include deterioration of the level of consciousness, dilated or asymmetric pupils, extensor posturing, dysphagia, extraocular movement palsies, nystagmus, incoordination, absent gag reflex, and death [4,9,10,15,19]. The diagnosis of spontaneous leaks is supported by the finding of pachymeningeal enhancement, subdural fluid collections, pituitary hyperemia, venous engorgement, and downward brain displacement on brain MRI scans [16]. In addition, spinal MRI or nuclear medicine scans can be helpful in establishing the diagnosis, but CT myelography best demonstrates the anatomical location of the spinal leak [16]. Decompressive craniectomies have been done more frequently in the past decades because of their known benefits in treating cerebral herniation and intracranial hypertension, due to several different conditions [1,5-8, 11,13,14,18,20]. Paradoxical herniation has been referred to as the herniation of a brain that has been decompressed surgically [12,17], without any extraaxial collection that could account for the herniation. The postulated mechanism is the combination of the effects of gravity and the atmospheric pressure on the decompressed brain plus the presence of a negative pressure in the spinal canal, which creates a gradient and leads to brain shifting [12,17]. There are only a few cases of paradoxical herniation reported in the literature. Schwab et al [17] reported 4 patients who presented with a sunken brain on inspection, evidence of neurologic deterioration and intracranial shift after a lumbar puncture was performed. Oyelese et al [12] reported a patient that developed a paradoxical herniation with irreversible neurologic deterioration and death 4 days after a lumbar puncture was performed. Schwab et al [17] managed their patients by positioning the head down, administering IV fluids, and doing an early cranioplasty, with good results. The patient reported by Oyelese et al [12] died before any specific treatment could be instituted. Because paradoxical herniation is caused by a negative pressure gradient between the intracranial space and spinal canal, its management involves eliminating the gradient. We initially managed our patient with the same approach advocated by Schwab et al [17]. Interestingly, this strategy was only temporarily effective in this patient. A few days after the cranioplasty, a new episode of neurologic deterioration associated with a large extraaxial CSF fluid collection occurred. This extraaxial collection led to the assumption that a gradient was still present, despite the cranioplasty. Extraaxial CSF collections have been reported to develop as a complication of lumbar punctures or lumbar drainage, in an attempt to normalize the CSF volume/ pressures in the cranial/spinal compartments [15]. Although the diagnosis of a delayed spinal CSF leak was presumptive, it appeared to be the most likely explanation for the persistence of the gradient and for the development of this new epidural CSF collection.
295
Spinal MRI has been shown to be effective in demonstrating spinal leaks after lumbar puncture [21], and it is possible that an MRI would have helped establishing the diagnosis in this patient. However, it was not contemplated because the patient presented with a recurrent picture of neurologic deterioration due to cerebral herniation and an MRI would have delayed the treatment, with a possible unfavorable outcome. It is well known that a blood patch is quite effective in stopping a postlumbar puncture CSF leak [16,21]. A blood patch as part of the treatment of a paradoxical herniation has been suggested by Oyelese et al [12]; unfortunately, their patient died before it was carried out. Although their article was published after this patient was treated, their suggestion and reasoning further supports the use of a blood patch in the setting of a paradoxical herniation. In this patient, a lumbar blood patch was performed as soon as the postulation of a spinal CSF leak was made. It actually proved to be very successful in preventing reaccumulation of the extraaxial CSF collection and additional episodes of neurologic deterioration, allowing full recovery. 4. Conclusion The data presented suggest that management with Trendelenburg position plus a cranioplasty might not be sufficient to eliminate the negative gradient in all cases of paradoxical herniation. A blood patch should be strongly considered for all cases. Acknowledgments I gratefully thank Dr Robert Goodkin, MD, for his review and suggestions. References [1] Albanese J, Leone M, Allez JR, Kaya JM, Antonini F, Alliez B, Martin C. Decompressive craniectomy for severe traumatic brain injury: evaluation of the effects at one year. Crit Care Med 2003;31: 2535 - 8. [2] Andrews R, Koci TM. Cerebellar herniation and infarction as a complication of occult postoperative lumbar dural defect. AJNR Am J Neuroradiol 1995;16:1312 - 5. [3] Binder DK, Dillon WP, Fishman RA, Schmidt MH. Intrathecal saline infusion in the treatment of obtundation associated with spontaneous intracranial hypotension: technical case report. Neurosurgery 2002; 51:830 - 7. [4] Bloch J, Regli L. Brainstem and cerebellar dysfunction after lumbar spinal fluid drainage: case report. J Neurol Neurosurg Psychiatry 2003;74:992 - 4. [5] Carter BS, Ogilvy CS, Candia GJ, Rosas HD, Buonanno F. One-year outcome after decompressive surgery for massive nondominant hemispheric infarction. Neurosurgery 1997;40:1168 - 75. [6] Ebel H, Kuchta J, Balogh A, Klug N. Operative treatment of tentorial herniation in herpes encephalitis. Childs Nerv Syst 1999;15:84 - 6. [7] Harscher S, Reichart R, Terborg C, Hagemann G, Kalff R, Witte OW. Outcome after decompressive craniectomy in patients with severe ischemic stroke. Acta Neurochir (Wien) 2006;148:31 - 7.
296
M.D. Vilela / Surgical Neurology 69 (2008) 293 – 296
[8] Heuer GG, Smith MJ, Elliot JP, Winn HR, LeRoux PD. Relationship between intracranial pressure and other clinical variables in patients with aneurysmal subarachnoid hemorrhage. J Neurosurg 2004;101: 408 - 16. [9] Klimo Jr P, Kestle JR, MacDonald JD, Schmidt RH. Marked reduction of cerebral vasospasm with lumbar drainage of cerebrospinal fluid after subarachnoid hemorrhage. J Neurosurg 2004;100: 215 - 24. [10] Komotar RJ, Mocco J, Ransom ER, Mack WJ, Zacharia BE, Wilson DA, Naidech AM, McKhann II GM, Mayer SA, Fitzsimmons BFM, Connoly Jr ES. Herniation secondary to critical postcraniotomy cerebrospinal fluid hypovolemia. Neurosurgery 2005; 57:286 - 92. [11] Mori K, Nakao Y, Yamamoto T, Maeda M. Early external decompressive craniectomy with duroplasty improves functional recovery in patients with massive hemispheric embolic infarction: timing and indication of decompressive surgery for malignant cerebral infarction. Surg Neurol 2004;62:420 - 9. [12] Oyelese AA, Steinberg GK, Huhn SL, Wijman CAC. Paradoxical cerebral herniation secondary to lumbar puncture after decompressive craniectomy for a large space-occupying hemispheric stroke: case report. Neurosurgery 2005;57:594 - 7. [13] Rutigliano D, Egnor MR, Priebe CJ, McCormack JE, Strong N, Scriven RJ, Lee TK. Decompressive craniectomy in pediatric patients with traumatic brain injury with intractable elevated intracranial pressure. J Pediatr Surg 2006;41:83 - 7. [14] Sahuquillo J, Arikan F. Decompressive craniectomy for the treatment of refractory high intracranial pressure in traumatic brain injury. Cochrane Database Syst Rev 2006;25(1):CD003983. [15] Samadani U, Huang JH, Baranov D, Zager EL, Grady MS. Intracranial hypotension after intraoperative lumbar cerebrospinal fluid drainage. Neurosurgery 2003;52:148 - 52. [16] Schievink WI. Spontaneous spinal cerebrospinal fluid leaks and intracranial hypotension. JAMA 2006;295:2286 - 96. [17] Schwab S, Erbguth F, Aschoff A, Orberk E, Spranger M, Hacke W. Paradoxe herniation nach entlastungstrepanation. Nervenarzt 1998; 69:896 - 900 [German]. [18] Smith ER, Carter BS, Ogilvy CS. Proposed use of prophylactic decompressive craniectomy in poor-grade aneurysmal subarachnoid hemorrhage patients presenting with associated large sylvian hematomas. Neurosurgery 2002;51:117 - 24. [19] Snow RB, Kuhel W, Martin SB. Prolonged lumbar spinal drainage after the resection of tumors of the skull base: a cautionary note. Neurosurgery 1991;28:880 - 2. [20] Taylor A, Butt W, Rosenfeld J, Shann F, Ditchfield M, Lewis E, Klug G, Wallace D, Henning R, Tibballs J. A randomized trial of very early decompressive craniectomy in children with traumatic brain injury and sustained intracranial hypertension. Childs Nerv Syst 2001;17:154 - 62. [21] Vakharia SB, Thomas PS, Rosenbaum AE, Wasenko JJ, Fellows DG. Magnetic resonance imaging of cerebrospinal fluid leak and tamponade effect of blood patch in postdural puncture headache. Anesth Analg 1997;84:585 - 90. [22] Van Crevel H, Hijdra A, de Gans J. Lumbar puncture and the risk of herniation: when should we first perform CT? J Neurol 2002;249: 129 - 37.
Commentary The report is instructive and sounds like a great neurosurgery board question. The author reports yet another complication that may accompany the management of aneursymal SAH. Paradoxical herniation is a rare event, probably occurring in more circumstances than the literature suggests and usually responding to the simple expedient of bed rest in the Trendelenburg position. The situation reported here developed in response to the communicating hydrocephalus while the excess fluid was drained into the spinal epidural space, thus making the simple expedient ineffective. I suspect the blood patch would not have been effective without the cranioplasty. The author is congratulated on the clever management just when we thought neurosurgery was getting easier. Harry O. Cole, MD Neurosurgical Associates Chesterfield, MO 63017, USA
In this case report, Dr Vilela details a case of delayed, downward herniation after a lumbar puncture. The patient had previously undergone a decompressive craniectomy. The negative pressure gradient was initially temporized by performing a cranioplasty and altering the patient’s head position. Ultimately, a simple blood patch was required to reverse the negative pressure gradient. This case is unusual and underscores the complexities of CSF dynamics. Cerebrospinal fluid dynamics can be clearly altered by an SAH, decompressive craniectomy, and lumbar puncture. Neuroimaging may be useful in detecting abnormalities in such complicated cases. Restoration of CSF flow and normalization of pathologic pressure gradients are the goal for such patients. Achieving these goals may require surgical intervention (eg, shunt placement, cranioplasty, or blood patch). The case report by Dr Vilela brings attention to a rare but noteworthy neurosurgical phenomenon. Jason P. Sheehan, MD Department of Neurosurgery University of Virginia, Charlottesville VA 22908, USA
Surgical Neurology 69 (2008) 293 – 296 www.surgicalneurology-online.com
Technique
Delayed paradoxical herniation after a decompressive craniectomy: case report Marcelo Duarte Vilela, MD4 Department of Neurological Surgery, Harborview Medical Center, University of Washington, Seattle, WA 98104, USA Received 2 May 2006; accepted 4 January 2007
Abstract
Background: Paradoxical herniation can occur as a complication of lumbar puncture in patients who had a decompressive craniectomy. The supposed mechanism is the development of a negative pressure gradient that allows the brain to shift toward the infratentorial space with subsequent herniation. Trendelenburg position plus early cranioplasty has been the suggested treatment to eliminate the gradient. Case Description: A 53-year-old woman had a decompressive hemicraniectomy for SAH-related swelling. A lumbar puncture was performed on postoperative day 5 to rule out infection. She remained neurologically stable until 6 weeks later, when she deteriorated because of a paradoxical herniation. Head positioning and cranioplasty were only temporarily helpful. She developed a second episode of decline a few days later due to an extraaxial CSF collection. A lumbar blood patch plus drainage of the collection successfully allowed full neurologic recovery. Conclusions: Cranioplasty and head positioning alone might not be sufficient to eliminate the negative pressure gradient. A blood patch should be part of the management of paradoxical herniation. D 2008 Elsevier Inc. All rights reserved.
Keywords:
Lumbar puncture; Decompressive craniectomy; Paradoxical herniation; Blood patch; Cranioplasty
1. Introduction Lumbar puncture is known to be hazardous in the face of elevated ICP combined with mass effect and/or brain shift [22]. In addition, a lumbar puncture with persistent CSF leakage or continuous spinal CSF drainage can lead to a negative pressure gradient between the intracranial space and spinal canal with displacement of the intracranial structures toward the infratentorial compartment and foramen magnum, even in patients with normal ICP [4,10,15]. Paradoxical herniation is the herniation of a craniectomized, decompressed brain with subsequent brainstem compression and neurologic deterioration after a lumbar puncture Abbreviations: CSF, cerebrospinal fluid; CT, computerized tomography; ICP, intracranial pressure; IV, intravenous; GOS, Glasgow outcome scale; MRI, magnetic resonance imaging; SAH, subarachnoid hemorrhage. 4 Tel.: +1 206 744 9330; fax: +1 206 744 9944. E-mail address: [email protected]. 0090-3019/$ – see front matter D 2008 Elsevier Inc. All rights reserved. doi:10.1016/j.surneu.2007.01.027
[12,17]. The effects of gravity and atmospheric pressure combined with a negative pressure in the spinal canal allow the brain to shift toward the infratentorial compartment, causing herniation and neurologic dysfunction. There are only a few cases of paradoxical herniation reported in the literature [12,17]. The recommended management has been to position the patient’s head down, administer IV fluids, and perform an early cranioplasty [17]. Our objective is to present a case that is noteworthy because of the following reasons: it shows that this management strategy is not always effective and although a lumbar blood patch has been suggested by others [12], this was the first occasion that it was actually done, with full neurologic recovery and an excellent outcome. 2. Case report A 53-year-old woman was admitted with a diagnosis of SAH due to an anterior communicating artery aneurysm
294
M.D. Vilela / Surgical Neurology 69 (2008) 293 – 296
Fig. 1. A: Head CT done on postoperative day 23 showing mild hydrocephalus and a subgaleal collection but no shift. B: Head CT done on postoperative day 43 demonstrating a markedly sunken brain with midline shift. C: Complete resolution of midline shift after cranioplasty.
rupture. After 12 hours postictus, clipping using a pterional approach was performed. A large prophylactic decompressive hemicraniectomy and a right frontal ventriculostomy were also done in the same sitting, because of severe brain swelling. On postoperative day 5, because of a sustained high-grade fever, a lumbar puncture using a 20-gauge spinal needle was done to rule out meningitis. The opening pressure was 12 cm H2O, only 5 mL of CSF was sent for analysis and the closing pressure was 11 cm H2O. Over the next 2 weeks, her course was complicated by cerebral salt wasting syndrome and cerebral vasospasm requiring angioplasty, but both eventually resolved without major deficits. On the fourth postoperative week, the patient was mildly somnolent and confused. A head CT scan showed only a subgaleal CSF collection but no shift (Fig. 1A). The patient thereafter slowly improved with some difficulties with mobilization and apathy. The craniectomy defect was slightly depressed on inspection. During the following week, she would alternate between periods of drowsiness and alertness, with no obvious explanation. On postoperative day 43, she was found to be stuporous, not following commands, had sluggish pupils, left hemiparesis, and a depressed, tender craniectomy defect on exam. A head CT showed a markedly sunken brain with midline shift (Fig. 1B). The bed was immediately placed in the Trendelenburg position, which resulted in some improvement of the mental status. She was shortly thereafter taken to the operating room for an emergent cranioplasty. The following morning she was fully awake, conversing, with no neurologic deficits. A head CT showed complete resolution of the midline shift (Fig 1C). On postoperative day 5, she started complaining of mild headaches and on the following day lethargy and left hemiparesis were again present. A head CT demonstrated a large extraaxial collection, with midline shift (Fig. 2A). The patient was immediately taken to the operating room for drainage of this fluid collection. A burr hole was made in the superior temporal region and a large epidural CSF collection was found and drained. A presumptive diagnosis of a persistent spinal CSF leak was made and a lumbar blood patch was done at the same
sitting. A head CT scan done a few days later showed complete resolution of the epidural collection and shift (Fig. 2B). Further follow-up scans demonstrated no recurrence of the epidural collection. Three months later, a ventriculoperitoneal shunt was inserted for symptomatic normal pressure hydrocephalus. The patient is doing very well 12 months after the aneurysm clipping, with a GOS of V and return to full activities. 3. Discussion Lumbar puncture is well known to be hazardous in the presence of a high ICP combined with mass effect and/or brain shift [22]. The phenomenon of downward herniation not associated with high ICP and/or shift has been reported after lumbar puncture or placement of a lumbar drain [4,9,10,15,19], following lumbar spinal surgery with a persistent CSF leak [2] or spontaneous spinal CSF leaks [3,16]. The mechanism is the occurrence of a negative pressure gradient between the intracranial and the spinal compartments due to persistent CSF leakage, which causes spinal and intracranial hypovolemia [10,15]. Characteristically, the ICP is low [3,15]. The intracranial contents bsink down,Q with herniation of the cerebral hemispheres and diencephalon toward the posterior fossa and the displace-
Fig. 2. A: Head CT showing a large extraaxial fluid collection, with striking shift. B: Head CT demonstrating resolution of the CSF collection.
M.D. Vilela / Surgical Neurology 69 (2008) 293 – 296
ment of the brainstem and cerebellum toward the foramen magnum [2-4,16]. Symptoms include deterioration of the level of consciousness, dilated or asymmetric pupils, extensor posturing, dysphagia, extraocular movement palsies, nystagmus, incoordination, absent gag reflex, and death [4,9,10,15,19]. The diagnosis of spontaneous leaks is supported by the finding of pachymeningeal enhancement, subdural fluid collections, pituitary hyperemia, venous engorgement, and downward brain displacement on brain MRI scans [16]. In addition, spinal MRI or nuclear medicine scans can be helpful in establishing the diagnosis, but CT myelography best demonstrates the anatomical location of the spinal leak [16]. Decompressive craniectomies have been done more frequently in the past decades because of their known benefits in treating cerebral herniation and intracranial hypertension, due to several different conditions [1,5-8, 11,13,14,18,20]. Paradoxical herniation has been referred to as the herniation of a brain that has been decompressed surgically [12,17], without any extraaxial collection that could account for the herniation. The postulated mechanism is the combination of the effects of gravity and the atmospheric pressure on the decompressed brain plus the presence of a negative pressure in the spinal canal, which creates a gradient and leads to brain shifting [12,17]. There are only a few cases of paradoxical herniation reported in the literature. Schwab et al [17] reported 4 patients who presented with a sunken brain on inspection, evidence of neurologic deterioration and intracranial shift after a lumbar puncture was performed. Oyelese et al [12] reported a patient that developed a paradoxical herniation with irreversible neurologic deterioration and death 4 days after a lumbar puncture was performed. Schwab et al [17] managed their patients by positioning the head down, administering IV fluids, and doing an early cranioplasty, with good results. The patient reported by Oyelese et al [12] died before any specific treatment could be instituted. Because paradoxical herniation is caused by a negative pressure gradient between the intracranial space and spinal canal, its management involves eliminating the gradient. We initially managed our patient with the same approach advocated by Schwab et al [17]. Interestingly, this strategy was only temporarily effective in this patient. A few days after the cranioplasty, a new episode of neurologic deterioration associated with a large extraaxial CSF fluid collection occurred. This extraaxial collection led to the assumption that a gradient was still present, despite the cranioplasty. Extraaxial CSF collections have been reported to develop as a complication of lumbar punctures or lumbar drainage, in an attempt to normalize the CSF volume/ pressures in the cranial/spinal compartments [15]. Although the diagnosis of a delayed spinal CSF leak was presumptive, it appeared to be the most likely explanation for the persistence of the gradient and for the development of this new epidural CSF collection.
295
Spinal MRI has been shown to be effective in demonstrating spinal leaks after lumbar puncture [21], and it is possible that an MRI would have helped establishing the diagnosis in this patient. However, it was not contemplated because the patient presented with a recurrent picture of neurologic deterioration due to cerebral herniation and an MRI would have delayed the treatment, with a possible unfavorable outcome. It is well known that a blood patch is quite effective in stopping a postlumbar puncture CSF leak [16,21]. A blood patch as part of the treatment of a paradoxical herniation has been suggested by Oyelese et al [12]; unfortunately, their patient died before it was carried out. Although their article was published after this patient was treated, their suggestion and reasoning further supports the use of a blood patch in the setting of a paradoxical herniation. In this patient, a lumbar blood patch was performed as soon as the postulation of a spinal CSF leak was made. It actually proved to be very successful in preventing reaccumulation of the extraaxial CSF collection and additional episodes of neurologic deterioration, allowing full recovery. 4. Conclusion The data presented suggest that management with Trendelenburg position plus a cranioplasty might not be sufficient to eliminate the negative gradient in all cases of paradoxical herniation. A blood patch should be strongly considered for all cases. Acknowledgments I gratefully thank Dr Robert Goodkin, MD, for his review and suggestions. References [1] Albanese J, Leone M, Allez JR, Kaya JM, Antonini F, Alliez B, Martin C. Decompressive craniectomy for severe traumatic brain injury: evaluation of the effects at one year. Crit Care Med 2003;31: 2535 - 8. [2] Andrews R, Koci TM. Cerebellar herniation and infarction as a complication of occult postoperative lumbar dural defect. AJNR Am J Neuroradiol 1995;16:1312 - 5. [3] Binder DK, Dillon WP, Fishman RA, Schmidt MH. Intrathecal saline infusion in the treatment of obtundation associated with spontaneous intracranial hypotension: technical case report. Neurosurgery 2002; 51:830 - 7. [4] Bloch J, Regli L. Brainstem and cerebellar dysfunction after lumbar spinal fluid drainage: case report. J Neurol Neurosurg Psychiatry 2003;74:992 - 4. [5] Carter BS, Ogilvy CS, Candia GJ, Rosas HD, Buonanno F. One-year outcome after decompressive surgery for massive nondominant hemispheric infarction. Neurosurgery 1997;40:1168 - 75. [6] Ebel H, Kuchta J, Balogh A, Klug N. Operative treatment of tentorial herniation in herpes encephalitis. Childs Nerv Syst 1999;15:84 - 6. [7] Harscher S, Reichart R, Terborg C, Hagemann G, Kalff R, Witte OW. Outcome after decompressive craniectomy in patients with severe ischemic stroke. Acta Neurochir (Wien) 2006;148:31 - 7.
296
M.D. Vilela / Surgical Neurology 69 (2008) 293 – 296
[8] Heuer GG, Smith MJ, Elliot JP, Winn HR, LeRoux PD. Relationship between intracranial pressure and other clinical variables in patients with aneurysmal subarachnoid hemorrhage. J Neurosurg 2004;101: 408 - 16. [9] Klimo Jr P, Kestle JR, MacDonald JD, Schmidt RH. Marked reduction of cerebral vasospasm with lumbar drainage of cerebrospinal fluid after subarachnoid hemorrhage. J Neurosurg 2004;100: 215 - 24. [10] Komotar RJ, Mocco J, Ransom ER, Mack WJ, Zacharia BE, Wilson DA, Naidech AM, McKhann II GM, Mayer SA, Fitzsimmons BFM, Connoly Jr ES. Herniation secondary to critical postcraniotomy cerebrospinal fluid hypovolemia. Neurosurgery 2005; 57:286 - 92. [11] Mori K, Nakao Y, Yamamoto T, Maeda M. Early external decompressive craniectomy with duroplasty improves functional recovery in patients with massive hemispheric embolic infarction: timing and indication of decompressive surgery for malignant cerebral infarction. Surg Neurol 2004;62:420 - 9. [12] Oyelese AA, Steinberg GK, Huhn SL, Wijman CAC. Paradoxical cerebral herniation secondary to lumbar puncture after decompressive craniectomy for a large space-occupying hemispheric stroke: case report. Neurosurgery 2005;57:594 - 7. [13] Rutigliano D, Egnor MR, Priebe CJ, McCormack JE, Strong N, Scriven RJ, Lee TK. Decompressive craniectomy in pediatric patients with traumatic brain injury with intractable elevated intracranial pressure. J Pediatr Surg 2006;41:83 - 7. [14] Sahuquillo J, Arikan F. Decompressive craniectomy for the treatment of refractory high intracranial pressure in traumatic brain injury. Cochrane Database Syst Rev 2006;25(1):CD003983. [15] Samadani U, Huang JH, Baranov D, Zager EL, Grady MS. Intracranial hypotension after intraoperative lumbar cerebrospinal fluid drainage. Neurosurgery 2003;52:148 - 52. [16] Schievink WI. Spontaneous spinal cerebrospinal fluid leaks and intracranial hypotension. JAMA 2006;295:2286 - 96. [17] Schwab S, Erbguth F, Aschoff A, Orberk E, Spranger M, Hacke W. Paradoxe herniation nach entlastungstrepanation. Nervenarzt 1998; 69:896 - 900 [German]. [18] Smith ER, Carter BS, Ogilvy CS. Proposed use of prophylactic decompressive craniectomy in poor-grade aneurysmal subarachnoid hemorrhage patients presenting with associated large sylvian hematomas. Neurosurgery 2002;51:117 - 24. [19] Snow RB, Kuhel W, Martin SB. Prolonged lumbar spinal drainage after the resection of tumors of the skull base: a cautionary note. Neurosurgery 1991;28:880 - 2. [20] Taylor A, Butt W, Rosenfeld J, Shann F, Ditchfield M, Lewis E, Klug G, Wallace D, Henning R, Tibballs J. A randomized trial of very early decompressive craniectomy in children with traumatic brain injury and sustained intracranial hypertension. Childs Nerv Syst 2001;17:154 - 62. [21] Vakharia SB, Thomas PS, Rosenbaum AE, Wasenko JJ, Fellows DG. Magnetic resonance imaging of cerebrospinal fluid leak and tamponade effect of blood patch in postdural puncture headache. Anesth Analg 1997;84:585 - 90. [22] Van Crevel H, Hijdra A, de Gans J. Lumbar puncture and the risk of herniation: when should we first perform CT? J Neurol 2002;249: 129 - 37.
Commentary The report is instructive and sounds like a great neurosurgery board question. The author reports yet another complication that may accompany the management of aneursymal SAH. Paradoxical herniation is a rare event, probably occurring in more circumstances than the literature suggests and usually responding to the simple expedient of bed rest in the Trendelenburg position. The situation reported here developed in response to the communicating hydrocephalus while the excess fluid was drained into the spinal epidural space, thus making the simple expedient ineffective. I suspect the blood patch would not have been effective without the cranioplasty. The author is congratulated on the clever management just when we thought neurosurgery was getting easier. Harry O. Cole, MD Neurosurgical Associates Chesterfield, MO 63017, USA
In this case report, Dr Vilela details a case of delayed, downward herniation after a lumbar puncture. The patient had previously undergone a decompressive craniectomy. The negative pressure gradient was initially temporized by performing a cranioplasty and altering the patient’s head position. Ultimately, a simple blood patch was required to reverse the negative pressure gradient. This case is unusual and underscores the complexities of CSF dynamics. Cerebrospinal fluid dynamics can be clearly altered by an SAH, decompressive craniectomy, and lumbar puncture. Neuroimaging may be useful in detecting abnormalities in such complicated cases. Restoration of CSF flow and normalization of pathologic pressure gradients are the goal for such patients. Achieving these goals may require surgical intervention (eg, shunt placement, cranioplasty, or blood patch). The case report by Dr Vilela brings attention to a rare but noteworthy neurosurgical phenomenon. Jason P. Sheehan, MD Department of Neurosurgery University of Virginia, Charlottesville VA 22908, USA