Positioning and Sterile Preparation

The operating room must be kept warm to avoid hypothermia. All prep solutions are warmed to body temperature. The infant is intubated in the lateral position or supine with a doughnut-sponge on the back to accommodate the sac. The pelvis is propped up with a horizontal roll to render the lumbar spine hyperlordotic and give maximum relaxation of the skin and soft tissues. The membranous portion of the sac, containing the exposed neural placode, is irrigated profusely with antibiotic-reinforced saline (betadine compounds have been shown to be neurotoxic), and the surrounding skin scrubbed with the usual antiseptic agents.

Opening the Sac

Magnification is used from the very beginning. The sac is entered through the diaphanous leptomeningeal membrane halfway between the margin of healthy skin and the edge of the placode (eFig. 60-4). Neural tissue of the placode is recognizable by its pink, felty surface, transverse wrinkles, and a straight, longitudinal median raphe (Fig. 60-1A) and since the epithelialized membrane itself is relatively avascular, any substantial bleeding from the cut edges signifies breaching of the neural tissue (Fig. 60-1B). Bleeding is controlled with a pair of ultrafine irrigating bipolar cautery forceps. After the initial gush of CSF and collapse of the cyst, the edge of the neural placode is gently flipped up to identify the ventral nerve roots. Several crossing blood vessels may have to be coagulated to free the placode margins. The pearly epithelium must be meticulously trimmed circumferentially from the placode to avoid later occurrence of inclusion dermoid cyst. At the caudal extreme of a terminal placode, the epithelial membrane may remain thin, or one may encounter a band-like thickening probably representing remnant of the medullary cord that must be divided to free the tip. At the rostral extreme of the placode, careful incision of the epithelium–neural tissue junction on both sides exposes the delicate bevel-shaped transition between the neurulated cylindrical spinal cord and the un-neurulated, flat placode (eFig. 60-5). At the apex of the bevel, the central canal of the normal cord can be seen unfurling into the median raphe of the placode, from which CSF sometimes slowly oozes.

FIGURE 60-1 A, Open myelomeningocele with a terminal neural placode. Note longitudinal median raphe on the neural placode. Small arrowheads outline margin of placode. Glistening leptomeningeal membrane stretches between placode and skin. Large arrowheads outline skin edge. Triangular end of the sac is toward the anus. B, Cutting into the leptomeningeal membrane just outside the margin of the placode. C, Neural placode after dural edges from all sides have been defined and dissected free, ready for dural closure. D, Closed dural tube. Paraspinous muscles and periosteum of bifid neural arch are exposed on each side of the closed dural tube. Anus to the right of picture.

Handling the Neural Placode

The neural placode is always handled gently with jeweler’s micro-forceps. If the placode is pliable and thin enough, it is rolled on itself and sewn up with 8-0 nylon sutures through the delicate pial edges (eFig. 60-6). There is no evidence that this improves neurologic function, but it reduces the “sticky” surface from a flat plate to a seam and theoretically lessens the chances of later tethering. If the placode is too thick or too stiff, it should not be forced to roll up for fear of strangulation. Also, tugging too hard on the proximal spinal cord will cause ascension of the neurologic level. In addition, the caudal end of the placode must be checked for the presence of a neurulated cord in the rare case of a segmental placode (see below).

Paradoxically, small and compact neural placodes are likely functional and therefore should be treated with extreme care, whereas large, thin, and “spread-out” placodes commonly found in middle to high thoracic lesions are usually nonfunctional. It is sometimes advisable to cordectomize these large placodes, for whilst they do not convey volitional movements, the decentralized neuronal pools within them can produce pathologically hyperactive local reflexes underlying high-pressured, spastic bladders and prominent ureteral reflux. Reflux is less prevalent when the bladder is rendered flaccid following elimination of this type of placode.

Dural Closure

The margins of the dural flaps are created by sharply incising the ventral dura from the lumbosacral fascia and periosteum (Fig. 60-1C and eFig 60-7; see also eFig. 60-4A and B), and a new dural tube is reconstructed in the midline (Fig. 60-1D). One aims to obtain as capacious a dural sac as possible commensurate with the size of the placode, the theory being if the placode passively flops freely within a large CSF space, it is less likely to adhere to the dorsal dura. This is almost always achievable with the patient’s own dura, even if some of the periosteum overlying the bifid neural arches have to be mobilized with the dura proper to enlarge the sac. In the rare event of insufficient dura, bovine pericardium can be used as a graft because its texture is compatible with newborn dura and because it seldom has suture-hole leakage of CSF. At the end of closure, the suture line is tested with a Valsalva maneuver held at a pressure of 30 to 35 cm of H₂O for 10 seconds.

Skin and Myofascial Closure

The true size of the skin defect is only apparent after completely excising the epithelialized membrane back to full thickness skin. Defects up to 5 or 6 cm diameter can usually be closed primarily after the subcutaneous layer is mobilized a short distance centrifugally, just enough to reduce the tension on the skin edges. The subdermal layer is closed with interrupted absorbable sutures, and the skin with fine nylon sutures. A number of surgical techniques have been developed to minimize suture line tension in large defects. Lateral relaxing incisions with bipedicle flap closure in the midline have been effective,¹¹ but the relaxing incisions themselves then require skin grafting at the same time or at a later date. Complex multiple rotation skin flaps have also been tried, but this necessitates extensive skin undermining and still does not altogether eliminate all tension spots. For impossibly large defects, I favor using composite skin–muscle (myocutaneous) flaps. There are three advantages to this technique. Cadaver vaso-latex studies show that a rich vascular anastomosis exists in the skin overlying the gluteus maximus and the latissimus dorsi muscles on each side and across the midline; the muscles themselves are supplied by the gluteal and thoracodorsal arteries, respectively. As long as these arterial pedicles are preserved, blood supply to the lumbosacral skin is well maintained when the four muscles are apposed in the midline, even if the short paraspinous arterial perforators deep to the muscle are taken.¹² Secondly, because there is no undermining of the subcutaneous tissues, the skin tension is mostly absorbed by the muscle closure. Finally, this method results in a triple-layered (muscle, subcutaneous tissue, and skin) closure with extra insurance against CSF leak. The flaps survival rate even for enormous defects is greater than 92% with this technique, and the blood loss and extra anesthetic time are quite acceptable.¹²

It is important to avoid large wound seroma or hematoma, which increases skin tension and prevents flap adherence to the underlying tissue from which revascularization for the flap must be derived. If the flaps are large and “wet,” a small drain without negative suction may be left in for 24 hours. Suction drains may perpetuate a CSF fistula and are best avoided.

Early Complications (First Postoperative Week)

The operative mortality for children undergoing repair of an ONTD should be close to 0.^13–15 The most common cause of postoperative death is related to hindbrain dysfunction (73%),^10,16 but this seldom occurs acutely in the first week of life. Most of the immediate complications pertain to the wound itself.

Wound Dehiscence

A study of the nutritional status of newborn infants who have had myelomeningocele surgery using body weight, nitrogen balance, serum protein, and total lymphocyte count as parameters, showed that these neonates undergo an initial period of severe catabolic changes that do not readjust themselves for as long as 1 month after surgery. This nonspecific catabolic response is caused by rises in circulating levels of ACTH, cortisol, thyroxin, growth hormone, and antidiuretic hormone, stimulated by the extreme stress of surgery, general anesthesia, and blood transfusion.⁸ During this period, the resistance to infection is lowered, and all anabolic processes, including wound healing, are temporarily slowed. This metabolically unstable time also coincides with feeding difficulties caused by hydrocephalus, postoperative ileus, neurogenic dysphagia (due to brainstem compression), and prematurity. It is no surprise that wound dehiscence is the single most common complication during the first postoperative week.⁸

Local factors, mostly avoidable, also contribute to this problem. A large sac means higher wound tension and precarious blood supply. An untreated kyphus adds stretching to the suture line and aggravates the local ischemia. Any additional external pressure caused by a tight dressing or improper patient positioning also interferes with healing.

It is common to see erythema along an 8- to 10-mm strip on either side of the suture line, particularly in areas of high tension. Sometimes the skin flaps may even look deep red to dusky as a result of venous stasis. These color changes often pass after a few days. When there is necrosis, the intensely dark red skin edges will turn black, but the necrosis may be limited to the epidermis, and the dermis and subdermis may survive, which should make adequate coverage. If full-thickness necrosis occurs, the blackness extends farther laterally. The junction between dead and viable skin demarcates, and the surrounding skin becomes erythematous and edematous. The sloughing skin edge also begins to pull away from the sutures, and serous exudate from subjacent fat necrosis seeps from the exposed subcutaneous tissues. Demarcation and sloughing are usually complete by the 7th or 10th day.

Sloughing of only the epidermis in small areas requires only simple dressing changes because the wound eventually epithelializes over the underlying dermal and subdermal layers. Skin grafting is unnecessary. If the skin necrosis is full thickness but there is healthy muscle underneath, the wound edges should be carefully debrided back to bleeding skin. It may then be dressed for second intention healing from below, but this will take some time and delay CSF shunting. A faster way would be partial-thickness skin grafting, which should take well over a well vascularized bed. If full thickness necrosis exposes the dural tube, some measure of immediate coverage must be instituted to prevent desiccation and meningitis. This usually means a more radical and extensive flap rotation or even pediculated full thickness skin flap grafting.¹⁷

Finally, parenteral or enteral hyperalimentation should be set up to ensure adequate nutrition.

Wound Infection

Considering how badly the exposed neural placode is contaminated during and shortly after birth, it is surprising how rarely wound (extradural) infections occur after closure of an ONTD. The wound infection rate is about 1.5% to 2.5%, which is only moderately higher than clean neurosurgical procedures.⁸ However, if one counts the intradural infections, the infection rate rises to 7% to 10% even for early closure.^15,18

The initial period of obligatory catabolism in these infants lowers both their cellular and humoral defenses. In as much as the infant must depend on transplacentally acquired maternal antibodies during the first 3 months of life, and IgA does not cross the placenta well, infections from enteric bacteria are particularly common. Chief among local predisposing factors to infection is a large sac with redundant, folded membranes. It is virtually impossible to sterilize all the creases and folds of the wobbly sac and the placode is therefore recontaminated during surgery. During closure, the contaminated placode is put inside a closed intradural space, which explains why intradural infection is more common than extradural infection.

Systemic signs of sepsis due to gram-negative meningitis are usually present 1 to 3 days after closure. In neonates, these early signs tend to be nonspecific, such as poor feeding, lethargy, or an ashen complexion. It is more common to see hypothermia than pyrexia, and the systemic white blood cell count often drops below 4000/mm.³ If the dural sac is well invested with a myocutaneous coverage, an intradural abscess may eventually form without any external signs. It is important to obtain CSF for culture from a ventricular tap if there is clinical suspicion of sepsis, for the long-term prognosis of gram-negative ventriculitis in the newborn depends almost solely on the promptness of diagnosis and treatment.

If the infection is confined to the extradural space, the wound will become red and fluctuant on day 5 to 7. The surrounding skin will also appear edematous but, unlike CSF infection, there is often no systemic signs of sepsis and the infant may continue to feed and move normally. A red, fluctuant wound should be diagnostically aspirated for purulent material. An abscessed wound must be opened immediately, widely debrided, irrigated with antibiotic solution, and reclosed over suction drains. Associated vascular occlusion and myonecrosis may require refashioning of a new myocutaneous closure. Depending on whether the CSF indices indicate intradural infection, the dura may have to be opened to rule out an intradural abscess. The patient is then put on broad spectrum, CSF-penetrating antibiotics.

Cerebrospinal Fluid Leak

The dura nearest its lateral margin may be severely attenuated in large myelomeningocele defects. This plus the often tense and precarious myocutaneous closure makes large lesions particularly prone to leak CSF. Also, the timing of the slowly climbing CSF pressure happens to coincide with weakening of the tenuous suture line, around the 5th to 8th postoperative day. A small amount of transdural CSF leak probably occurs through the suture holes in most cases, considering the thinness of the newborn dura. The appearance of slight fluctuance under the skin flaps during the first few postoperative days is likely due to a combination of CSF and blood. As long as the skin closure holds, and there is no outward leak of CSF, there is no risk of infection. This small amount of seepage is self limiting. A large transdural leak causes a tense subcutaneous accumulation that will eventually threaten the viability of the suture line. When CSF actually breaks through the skin barrier, the risk for gram-negative infection rapidly rises, and treatment must be promptly initiated.

A shunt is effective in preventing CSF leak but is not recommended after the leak has sprung, especially if the leak has already breached the skin closure. Even a low pressure shunt maintains a constant lumbar CSF pressure of 5 to 6 cm H₂O, still considerably higher than that in the subcutaneous pocket, which is near atmospheric. The preferential passage of CSF is still out through the back wound and not through the shunt. If a CSF leak persists in the presence of a shunt, the latter becomes infected sooner or later. The external ventricular drain (EVD) is a much better means of decompression after a substantial leak has already existed. The drainage chamber can be lowered to subzero pressure to siphon CSF away from the back wound. With elimination of outward leak, the probability of infection is mitigated. The skin edges can now be oversewn, and the infant may have to be sedated to minimize the milking action of muscles overlying the thecal sac. Many leaks can be successfully managed by such measures without a reoperation. If the leak persists post-EVD, the wound needs to be explored to close the dural defect.

Dorsal Lipoma

The lipoma–cord interface is entirely on the dorsal surface of the lumbar spinal cord, sparing the distal conus (Fig. 60-2A). The junctional demarcation between lipoma, cord, and pia, the fusion line, can always be traced neatly along a roughly oval track, separating fat from the dorsal root entry zone (DREZ) and dorsal nerve roots laterally (Fig. 60-2B and eFig 60-10). The lipoma therefore never contains nerve roots. The lipomatous stalk runs through an equally discrete dorsal dural defect to blend with extradural fat. The uninvolved conus often ends in a thickened filum terminale.

FIGURE 60-2 A, Dorsal lipoma on MRI. Sagittal image shows intact conus caudal to lipoma stalk. Axial images: upper shows site of lipoma attachment to cord; lower shows free conus just caudal to the level of lipoma attachment. B, Intraoperative picture shows neat oval fusion line around lipoma–cord interface on a horizontal plane. Note intact conus and caudal sacral roots. C, Transitional lipoma. Left: Sagittal MRI shows lipoma begins dorsally but involves entire conus. Ventral side of neural placode is free of fat. Right: Plane of the fusion line begins dorsally and then cuts obliquely toward the tip of the conus. The array of DREZ and dorsal roots is also forced to slant dorsoventrally. D, Transitional lipoma. Intraoperative picture showing massive lipoma but very distinct dorsoventral fusion line separating fat from the DREZ and dorsal roots, which always lie lateral and ventral to the fusion line. The ventral side of placode is always free of fat in a regular transitional lipoma. DREZ, dorsal root entry zone.

Transitional Lipoma

The rostral portion of this type is identical to that of a dorsal lipoma, with a discrete fusion line and easily identifiable DREZ and dorsal roots. Unlike the dorsal type, however, which always spares the conus, the transitional lipoma then plunges caudally to involve the conus as the plane of the fusion line cuts ventrally and obliquely towards the tip of the conus likened to making a slanting, beveled cut on a stick (Fig. 60-2C). The lipoma–cord interface thus created may be undulating and tilted so that the neural placode is rotated to one side or even spun into a parasagittal edge-on orientation, but the neural tissue is always ventral to it and the DREZ and the nerve roots are predictably localizable lateral and ventral to the fusion line and therefore do not course through the fat (Fig. 60-2D). There may or may not be a discrete filum. The dorsal dural defect extends to the caudal end of the thecal sac and may be much larger on the biased side.

Terminal Lipoma

Unlike the dorsal and transitional types, terminal lipomas insert into the caudal extremity of the conus without blending with the spinal cord or its root entry zones. All the sacral roots unmistakably leave the conus rostral to the lipoma, and in most cases the conus itself looks normal. The dural sac and the dorsal myofascial coverings are intact. The lipoma either replaces the filum entirely, or is separated from the conus tip by a short, thickened filum (Fig. 60-3A and B).

FIGURE 60-3 A, Terminal lipoma. Drawings showing insertion of fat directly on the end of the conus, which is itself intact. Resection plane is right through a clear transition plane. Typical MR appearance is shown at right. B, Intraoperative pictures for terminal lipoma. Top shows the typical terminal lipoma. Middle shows separation of “hitch-hiker” nerve roots from lipoma. Lower shows conus after transaction through separation plane. C, Choatic lipoma. Intraoperative picture showing fat ventral to placode and on one of the sacral roots (arrow). Note absence of discrete fusion line. D, Lipomyelomeningocele with the lipoma stalk, cerebrospinal fluid sac, and part of the conus extending out of the spinal canal through a dorsal defect.

Chaotic Lipoma

This previously undescribed type is so named because it does not “follow the rules” of either the dorsal, transitional, or terminal lipoma. It begins dorsally in an orderly fashion as in a dorsal or transitional lipoma, but its caudal portion is ventral to the neural placode and does engulf neural tissue and nerve roots (eFig. 60-11). The fusion line may be distinct rostrally but quickly becomes blurred distally, and the location of the DREZ and nerve roots is less predictable. The moniker “chaotic” depicts the sometimes confusing blend of the ventral fat and neural placode, and the often impossible task of separating fat from neural tissue at surgery (Fig. 60-3C). Chaotic lipomas are uncommon but are characteristically seen with sacral agenesis.

The literature^30,31 describes one other lipoma type, the lipomyelomeningocele, in which part of the distal conus extends into the extraspinal compartment, dragging with it a small collar of dural sac (Fig. 60-3D). The basic structure is either that of a transitional or a dorsal lipoma. Accordingly, we choose to classify this type as either a transitional or dorsal lipoma with a descriptive qualifier of “extraspinal extension.”

Embryogenesis of Dorsal and Transitional Lipomas

In the embryo, a progressive disparity exists between the spinal cord and vertebral column as a result of the faster growth rate of the latter.^32–35 The caudal end of the cord ascends gradually from opposite the coccyx in the 30-mm human embryo to the L₁–L₂ level at birth.^34–37 Proper ascent of the cord requires a well-formed neural tube and a smooth pia-arachnoid covering. If during early development a dorsal defect exists in the dura (duraschisis) and neural tube (myeloschisis), mesodermal elements from the surrounding mesenchyme will enter the dural sac and form attachment with the sliding neural tube in the form of a fibro-fatty stalk, resulting in its entrapment. This theory features a fundamental defect in neural tube closure during primary neurulation (secondary neurulation does not involve dorsal neural fold closure), and thus applies only to the dorsal and transitional lipomas (see below). It is compatible with the observation that these two types of lipomas are always associated with neural arch defects.

The embryologic error leading to the mesodermal invasion of the neural tube probably lies in premature disjunction between the cutaneous and neural ectoderms^38–40; that is, the separation of one from the other occurs before the converging neural folds fuse with each other. This allows the paraxial mesenchyme to roll over the still gaping neural folds and enter the central canal. Once contact between mesenchyme and ependymal neuroectoderm is made, further closure of the neural tube is permanently prevented and a segmental dorsal myeloschisis is created (eFig. 60-12A and B). Alternatively, the fault may lie in a delay in neural folds fusion secondary to an insufficiency of the paraxial mesoderm in impelling their dorsal convergence,^41–47 so that ectodermal disjunction again precedes neural folds fusion. Lastly, faulty fusion of the neural folds due to metabolic disturbance of the cell membrane-bound glycosaminoglycans, which are vital to cell–cell recognition and adhesion,^48–51 could likewise reverse the temporal relationship between disjunction and neural folds fusion.

Experimental studies show that the pluripotent mesenchyme forms derivatives according to the inductive properties of the adjacent neuroectoderm (eFig. 60-12C).^6,9 The ependymal side of the neural tube induces mesenchyme to form fat, muscles, collagen, and occasionally bone and cartilage, whereas the outer surface of the neural tube induces the formation of meninges.⁵² However, no dura can now form over the dorsal opened portion of the neural tube, and the dural defect neatly surrounds the evolving lipomatous stalk, which tethers the neural tube to the subcutaneous adiposity. In like manner, deficiencies in the overlying myofascial layers (from myotomal mesoderm) and neural arches (from scleromesoderm) also neatly surround the lipomatous stalk (eFig. 60-12D).

Within the neural tube, the intramedullary fat and muscles fuse with the developing alar and basal plates. Since the dorsal root ganglions develop from neural crest cells at the outer aspect of the neural fold lateral to the site of failed fusion, the dorsal nerve roots grow outward ventrolateral to, but never traverse, the lipomatous stalk. The DREZ must correspondingly lie very near, but always lateral to, the exact junctional boundary between lipoma and spinal cord. This boundary, called fusion line, is of tremendous surgical significance^22,53,54 (eFig. 60-12D). Meanwhile, the cutaneous ectoderm, long detached from the neuroectoderm, heals over in the dorsal midline to form wholesome skin over the subcutaneous lipoma.

The genesis of a dorsal lipoma perfectly exemplifies mistimed disjunction during primary neurulation. Its fibro-fatty stalk always involves cord segments above the conus, which mainly forms from secondary neurulation. Furthermore, failure of primary neural tube closure appears to be segmental, normal closure takes place “business-as-usual” immediately following the abnormal event. This “square pulse” nature is illustrated by the fact that the sharp fusion line between fat, spinal cord, and pia-arachnoid can be neatly traced circumferentially around the lipomatous stalk^53–55 (see Fig. 60-2B and eFig. 60-10). Dorsal lipomas therefore result from a segmental closure abnormality involving only primary neurulation. They are found in less than 15% of spinal cord lipomas in our series.^22,26

In transitional lipoma, the myeloschisis involves much more than an isolated segment of the primary neural tube. Even though its rostral part resembles the dorsal lipoma, the involvement of the whole of the caudal spinal cord means that not only primary but also secondary neurulation have been profoundly disturbed by the mesodermal invasion. This is supported by the observations that in many transitional lipomas the filum is incorporated into the distal fat, and within the lipomas are often spaces resembling the vacuoles within the secondary neural tube. Also, while the rostral part of the transitional lipoma is always dorsal and aptly reflects premature disjunction of primary neurulation, the distal part sometimes involves both the dorsal and ventral aspects of the conus, a situation compatible with misguided mesenchymal inclusion during the much less orderly events of secondary neurulation. Intramedullary mesenchyme may migrate within the neural tube after invasion and travel caudally across the boundary from the primary to the secondary neural canal, since the two neural canals are in continuity.⁵⁶ In fact, the hypothesis that the rostral part of the transitional lipoma arises from aberrant primary neurulation (involving only the dorsal cord) and the caudal lipoma arises from abnormal condensation of the secondary neural cord (affecting more ventral aspects of the conus) furnishes at least one explanation for the dorsoventral obliquity of the lipoma–cord interface.

Embryogenesis of Chaotic Lipomas

Chaotic lipomas do not quite fit into either the dorsal or transitional schema. They often do not have a distinct dorsal part with the symmetry of a dorsal lipoma, and the lipoma–cord interface is irregular and ill-defined, with fat running through the neural placode to the ventral side in large and unruly measures. Even in the context of the less orderly transitional lipoma, the interplay between lipoma and cord in this type of lesion seems to be in constant chaos.

This degree of anatomic unpredictability in chaotic lipoma and its strong association with caudal agenesis (82% in our series²²) suggest that the embryogenetic error occurs during the early stage of secondary neurulation as part of the general failure of the caudal cell mass (eFig. 60-13).^57,58 Secondary neurulation comprises three distinct stages: (1) condensation of neural material from the caudal cell mass to form the solid medullary cord, (2) intrachordal cavitation of the medullary cord^56,58,59 and its integration with the primary neural tube, and (3) partial degeneration of the cavitary medullary cord through massive apoptosis to result in the thin filum terminale.^34,56 It is possible that formation of the chaotic lipoma involves the entanglement of lipogenic mesenchymal stem cells with cells from the caudal cell mass during aberrant condensation of the medullary cord, forming an inseparable mixture of neural tissue and fat, with nerve roots projecting out haphazardly.²²

Embryogenesis of Terminal Lipoma

Terminal lipomas result from abnormal secondary rather than primary neurulation, as evidenced by the unexcepted rule that the lumbar and upper sacral cord segments, products of primary neurulation, are never affected in a terminal lipoma. Furthermore, dorsal myeloschisis and duraschisis, both hallmarks of failed (primary) neural fold fusion, are never seen. Lastly, the terminal lipoma either replaces or forms part of a thickened filum, which temporally places the pathogenetic process at secondary neurulation. The fact that the distal conus in terminal lipomas always remains fat-free argues against an abnormal condensation phase during early secondary neurulation. On the other hand, the terminal lipoma often contains (disorganized) spinal cord elements and ependymal tubules,^60,61 which suggests rather an incomplete or ineffective degeneration phase at late secondary neurulation.

Step 1. Exposure

The skin and soft tissue incision should go straight through the subcutaneous lipoma if one is present. Removing this will leave behind a large subdermal space into which CSF could collect under tension and consequently hinder wound healing. Frequently a discrete fatty stalk connects the subcutaneous with the intraspinal lipoma through a defect in the lumbodorsal fascia. This stalk is continuous with the spinal cord and should not be tugged on during fascial dissection.

The upper extent of the bony exposure should include one level above the rostral end of the lipoma. This reveals for proper orientation the “last” normal set of nerve roots and DREZ before starting lipoma resection. Wide laminectomy is essential to afford full access to the lateral edges of the dural sac (see below). Visualization of the normal dura rostral to any lipoma gives a depth perspective as to how far out neural tissue and CSF sac might have extruded beyond the plane of the dura. The heavy bulk of extradural fat could then be safely lopped off to give room for intradural dissection and lighten the tug on the conus.

Step 2. Detachment of Lipoma from Dura

The dura rostral to the lipoma is opened in the midline. For dorsal lipoma, the dural incision is carried circumferentially around the discrete lipoma stalk and then down the middle again to expose the conus (eFig. 60-10