CHAPTER SYNOPSIS:

Cerebrospinal fluid (CSF) leaks are a potential complication resulting from a dural violation during spinal surgery. Persistent CSF leakage leads to either pseudomeningocele formation or a CSF fistula, which can result in poor wound healing, infection, and meningitis. Diagnosis of a CSF leak during surgery necessitates direct surgical repair of the dural violation. In instances in which the dural breach cannot be primarily closed, several techniques involving dural sealants, muscle or fat graft, or complex muscle closure can be performed to decrease the risk for forming a CSF fistula. Delayed diagnosis of a CSF leak can be occasionally managed with less invasive measures including bed rest, oversewing, subarachnoid drain placement, and percutaneous epidural blood patch. This chapter reviews the anatomy, diagnosis, and management of CSF leaks.

IMPORTANT POINTS:

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  Dural violations and CSF leaks are potential complications of spinal surgery.

  
  
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  Prompt diagnosis of a CSF leak is essential for initiating appropriate intervention and minimizing the risk for pseudomeningocele or CSF fistula formation.

  
  
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  Direct primary surgical repair of the dural violation is the ideal method for treating a CSF leak.

  
  
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  Failure of conservative or less invasive measures to treat a CSF leak necessitates reoperation for primary repair.

CLINICAL/SURGICAL PEARLS:

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  Primary closure of a dural violation requires sufficient bony removal for adequate exposure of the defect.

  
  
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  Nonabsorbable, fine suture is recommended.

  
  
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  Magnification with either a microscope or loupes facilitates visualization.

  
  
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  Patients with persistent CSF fistula often require a paraspinal muscle flap advancement to obliterate the dead space.

CLINICAL/SURGICAL PITFALLS:

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  Postoperative bed rest after treatment of a CSF leak decreases outflow of CSF through the dural suture line and facilitates adherence of soft tissue to the durotomy.

  
  
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  The use of a subfascial drain after durotomy may potentiate a myelocutaneous fistula along the drain tract and serve as a conduit for bacterial spread into the CSF space.

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ANATOMY

The central nervous system is covered by three separate membranes, known as the meninges. The dura mater is the thickest, outermost layer, and is a dense, fibrous membrane that forms a sheath about the brain and spinal cord. Intracranially, the dura is fused to the periosteum; however, at the level of the foramen magnum, the dura becomes detached from the skull and extends caudally through the spinal column to the level of the second sacral vertebra. At each spinal level, the dura evaginates through the intervertebral foramen, surrounding the nerve roots and fusing with the periosteum of the vertebrae. Outside the spinal canal, the dura becomes continuous with the epineurium around each nerve root.

The arachnoid layer is the intermediate layer closely but loosely adjoined to the dura. A potential space (known as the subdural space) exists between the dura and the arachnoid layers. The arachnoid is connected to the innermost pial layer by fine trabeculae, which creates a true space, known as the subarachnoid space. The subarachnoid space is filled with CSF, and contains large veins and arteries that supply the spinal cord. The pia is a delicate layer adherent to the brain and spinal cord, containing the plexus of small blood vessels that invest nervous tissue. The pia layer also forms 21 pairs of dentate ligaments, which are pial reflections that attach to the dura, thereby supporting the spinal cord centrally within the subarachnoid space.

Collectively, the meninges and CSF perform important protective and circulatory functions for the brain and spinal cord. CSF is a clear, colorless ultrafiltrate of blood produced by choroid plexus in the ventricular system of the brain. Approximately 125 mL CSF exists in the ventricles and the subarachnoid space (25 mL in the ventricles, 100 mL in the subarachnoid space), with about 500 mL CSF produced each day. CSF produced in the ventricular system circulates from the lateral and third ventricles of the brain to the fourth ventricle, which empties into the central spinal canal. CSF also exits the ventricular system through the foramina of Luschka and the foramen of Magendie of the fourth ventricle to fill the entire subarachnoid space. In the spinal column, the lumbar cistern is a large collection of CSF that exists between the conus medullaris (about L1) and the coccygeal ligament (about S2), in which the cauda equina is suspended. Ultimately, CSF is resorbed by small, unidirectional valves (arachnoid villi) in the dural sinuses and returned to the systemic circulation.

DIAGNOSIS

Intraoperative identification of an unintended dural tear is readily made by evidence of herniated arachnoid from a dural violation, or the rapid extravasation of CSF into the surgical field. This usually occurs immediately after a surgical maneuver, such as dissecting adherent dura from the ligamentum flavum or use of the Kerrison rongeur or high-speed drill. With loss of CSF, the thecal sac becomes notably flaccid, decreasing the tamponade effect on epidural veins and leading to increased bleeding. The site of the durotomy may be either directly visible or inaccessible if located in a far lateral recess, such as along a nerve root sleeve.

An unidentified intraoperative durotomy or an unsuccessful dural repair can result in development of a postoperative CSF fistula or pseudomeningocele. Cutaneous CSF fistulas generally occur in the immediate postoperative period, usually within 1 to 7 days. Obvious diagnosis can be made with the evidence of persistent drainage of clear or serosanguineous fluid from the surgical wound. This leakage may increase with a Valsalva maneuver or when sitting upright. CSF drainage from the wound produces a clear halo surrounding a central pink stain on a gauze dressing. Patients often will describe postural headaches, in which the pain is most severe when sitting or standing erect, and relieved by lying flat. Spinal headaches are due to a decrease in intradural CSF pressure in the cerebrospinal axis, causing traction on pain-sensitive structures such as the meninges and vessels. Intracranial hypotension from loss of CSF can theoretically also result in cerebellar tonsillar herniation, and subdural hematoma or hygroma formation. Other associated symptoms include nausea, vomiting, photophobia, vertigo, dizziness, and neck stiffness.

A postoperative pseudomeningocele is diagnosed by a visible or palpable fluctuant mass over the surgical site. Pseudomeningoceles form by the persistence of a patent durotomy leading to constant outflow of CSF. Intrathecal hydrostatic pressure forces CSF with regular pulsations into the soft-tissue muscular and subcutaneous space. An encysted, fluid-filled cavity forms, which further facilitates the pressure gradient flow of CSF from the subarachnoid space into the growing pseudomeningocele. Clinically, pseudomeningoceles can cause severe back pain. Nerve roots can evaginate through the fistulous opening, becoming entrapped or anchored, resulting in radiculopathy, weakness, or cauda equina symptoms. In the case of spinal cord herniation through a dural defect, myelopathy, paraplegia, or a Brown–Séquard syndrome may present. A ball-valve mechanism with one-way flow of CSF through the durotomy can lead to an enlarging pseudomeningocele causing cord compression.

Magnetic resonance imaging (MRI) is the diagnostic imaging modality of choice. MRI demonstrates superb visualization of the neural elements, as well as the overlying soft tissues. Presence of a CSF fistula or pseudomeningocele will reveal low signal intensity on T1-weighted images and high signal intensity on T2-weighted images, consistent with CSF. MRI is particularly advantageous for delineating the location and extent of a pseudomeningocele and may demonstrate the level of the fistulous communication. MRI may also help identify entrapped nerve roots or any areas of spinal cord compression.

MRI facilitates differentiation between a pseudomeningocele and a postoperative hematoma or abscess. Hematomas and abscesses create irregularly shaped fluid collections, whereas CSF-filled cavities tend to be regular and well circumscribed. Contrast ring enhancement is suggestive of a postoperative abscess. Signal characteristics demonstrating age-related changes in blood may also help distinguish a hematoma from CSF. Myelography with computed tomography (CT) is an additional imaging modality that can aid in the diagnosis of a CSF fistula or pseudomeningocele. Myelography may better localize the exact site of the fistulous communication as compared with MRI. CT imaging also provides better bone imaging, which may help reference the level of the durotomy and indicate a mechanism of injury, such as a fractured bone edge or spur.

Analysis of the draining fluid may identify the presence of CSF and, therefore, confirm the diagnosis of a cutaneous CSF fistula. Only a small sample of fluid is necessary (less than 1 mL). The proteins in the fluid are separated by polyacrylamide gel electrophoresis, and an antibody reaction is used to analyze the banding patterns for the presence of β1- and β2-transferrin. β2-transferrin arises by the action of cerebral neuraminidase, which is present only in the central nervous system. Importantly, β2-transferrin is noticeably absent from any other bodily fluids such as sweat or serum. Therefore, the presence of the β2-transferrin isoform indicates the presence of CSF and establishes the diagnosis of a cutaneous CSF fistula.