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14. COMPLICA TIONS Allan D. Levi and Roberto C. Heros omplications form a very significant element of the Oral Board Examination. In fact, the scoring system gives a grade for “the handling of com plications relevant to the neurosurgical treatment of your cases” (see chapter 1). The good news is that there really is a limited number of complications in neurosurgery, and if up front you have an answer for most complications, you will be ahead of the game. Again, we would emphasize that complications are expected on the Oral Board Examination, and when you get them, it does not mean that you are handling the case poorly. When complications ensue, and they will, be ready to jump into the fray. Come in and see the patient, lay hands on, express your concern. Do not send your resident or nurse practitioner or delay the visit until Monday if the problems are occurring on the weekend. T o assist with board preparation, we have compiled some of the more common complications seen in neurosurgery so that you can make a well- defined plan when hearing them on your examination. This way, you can easily respond without generating too much stress. 1. Postoperative neuropathic pain 2. Postoperative wound infection 3. Cerebrospinal fluid (CSF) leak 4. C5 nerve palsy 5. Postoperative cranial or spinal hematoma 6. Hyponatremia 7. V asospasm 8. Intraoperative aneurysm rupture— open or endovascular 9. Major arterial injuries with cranial and spinal surgery 10. Uncontrolled intracranial pressure 11. Brain swelling during operative exposure 12. Esophageal injury POSTOPERA TI v E NEUROPA THIC PAIN Postoperative neuropathic pain is associated with injury or irritation typically to a peripheral nerve. Such injuries can give rise to paresthesias, numbness, tingling, or electrical sensation. The pain associated with these nerve injuries is often unrelenting. It is typically described as burning. Neuropathic pain is typically not responsive to antiin flammatory agents or steroids and is poorly responsive to opioids. Managing a neuropathic patient after cervical, lum bar, or peripheral nerve surgery is a very important com ponent of the Oral Board Examination. It is clear that the primary line agents are antiepileptics, such as gabapentin (Neurontin) and pregabalin (Lyrica). Start with a low dose of gabapentin, such as 300 mg given orally three times daily, raising the dose until the patient achieves pain relieve or cannot tolerate side effects that can be common. They include drowsiness and peripheral extremity edema. Ruling out a surgical etiology for neuropathic pain such as a resid ual disk or constriction of the nerve by a band or hematoma is always important in the workup. Occasionally, when all conservative treatments fail, consideration is given to a spinal cord stimulator or a peripheral nerve stimulator. POSTOPERA TI v E WOUND INf ECTIONS How to manage postoperative wound infections is a com mon question on the Oral Board Examination. Infections can occur after either cranial or spinal procedures. An

n all conservative treatments fail, consideration is given to a spinal cord stimulator or a peripheral nerve stimulator. POSTOPERA TI v E WOUND INf ECTIONS How to manage postoperative wound infections is a com mon question on the Oral Board Examination. Infections can occur after either cranial or spinal procedures. An 168 • G OODMAN ’S N EUROSURGERY O RAL B OARD R E v IEW aggressive stance is usually needed. The typical presentation is that of drainage, fever, pain, and wound redness. The differential diagnosis is often spinal fluid leak. Ancillary test ing, such as laboratory data to look at the white blood cell count, erythrocyte sedimentation rate (ESR), and C- reactive protein, is always helpful. With possible spine infections, it is important to distinguish between a superficial infection or stitch granuloma in which there is typically no systemic symptoms and a deep infection that often presents with fever, pain, and mal aise. Deep infections require irrigation and debridement supplemented by intravenous (IV) antibiotics. T ypically, a minimum of a 2- week course of IV antibiotics for a deep infection is required, although there are many subtle fac tors involved in the final decision of how long to administer the antibiotics. In the presence of spinal instrumentation with an acute infection, the hardware can be left in, but the wound will require irrigation and debridement and removal of all necrotic material, placement of drains, and typically 6 weeks of IV antibiotics. If the patient presents with a chronic wound infection, and particularly if there is an associated osteomyelitis, the instrumentation frequently needs to be removed. For cranial wound infections, the bone flap frequently needs to be removed, particularly if there is pus under the bone flap or any erosion of the bone suggestive of osteomyelitis. This is followed by irrigation and debridement, evacuation of an epidural abscess, and removal of devitalized wound edges. Drains form an important part of the treat ment to prevent reaccumulation of infected fluids leading to a potential recurrent abcess. The patient will need the infection completely eradicated before reconsideration of cranioplasty because obviously the previously infected bone flap cannot be used and should have been discarded. A minimum waiting time of 3 months, but preferably 6 months, before performing cranioplasty is necessary. Postoperative meningitis is another important consid eration for any cranial or spinal intradural procedure or in cases in which CSF drains are used. It is critical to sample CSF if meningitis is suspected to look for an elevated white blood cell count with elevated percentage of neutrophils, a reduction in glucose below 50% of serum value, and ele vated protein. Whenever a wound infection, whether cranial or spinal, is suspected, it is important not to start the patient on antibiotics and to let the situation define itself. If a “real” wound infection exists, it will declare itself with obvious signs such as swelling, redness, drainage, or systemic symptoms related to a deep wound infection. Antibiotics should not be started until cultures are obtained at surgery. Starting antibiotics empirically, before open surgical treatment of the infection, can result in a partially treated infection that becomes a chronic problem with possible development of a deeper infection, such as meningitis or osteomyelitis. In addition, if the patient has been taking antibiotics before the wound is opened and cultured, frequently the causative organism cannot be recovered at culture and the patient needs to be unnecessarily treated empirically with broadspectrum antibiotics, which is not satisfactory.

such as meningitis or osteomyelitis. In addition, if the patient has been taking antibiotics before the wound is opened and cultured, frequently the causative organism cannot be recovered at culture and the patient needs to be unnecessarily treated empirically with broadspectrum antibiotics, which is not satisfactory. CEREBROSPINAL f LUID LEAK CSF leak again is a very common complication presented on the Oral Board Examination. Spinal CSF leaks may present with positional headache or simply as an obvious clear liquid escaping from the wound or possibly a pseudomeningocele with a bulging wound (Figure 14.1). Postoperative imaging, including MRI, can help define the borders of the spinal fluid leak, and very rarely a myelogram is required to determine the area where the leakage is emanating from. The incidence of CSF leaks after spinal surgery is in the range of Figure 14.1 A large dorsal pseudomeningocele is seen after resection of a large lumbosacral schwannoma. The arrow points to the dural defect.

fluid leak, and very rarely a myelogram is required to determine the area where the leakage is emanating from. The incidence of CSF leaks after spinal surgery is in the range of Figure 14.1 A large dorsal pseudomeningocele is seen after resection of a large lumbosacral schwannoma. The arrow points to the dural defect. COMPLICA TIONS • 169 about 3%. It is certainly more common after revision sur geries. Minimally invasive surgeries have a similar incidence, but the likelihood that they will present with symptoms is less because the spinal fluid leak is contained by the muscles, which are still firmly attached to the spine, and there is no potential space for the CSF to collect into. The manage ment often is multi- tiered; one can consider a blood patch, especially if it is a post– lumbar puncture headache. This works less frequently for a postoperative CSF leak. Often, what is required is to reexplore the wound and consider direct repair with sutures. Occasionally, indirect repair with glue needs to be done often to supplement the repair with a lumbar or cervical CSF drainage to help offset the pres sure with the repair. Thoracic CSF leaks are certainly more difficult to treat because the negative intrathoracic pressure encourages CSF to leak in to the chest cavity; these leaks often require the adjunct of a cervical CSF drain (Farhat et al., 2011). With postoperative cranial CSF leaks, one must always consider the issues of CSF drainage into air cells, such as the mastoid air cells after posterior fossa craniotomy or the frontal sinus air cells after an anterior fossa craniotomy. In these cases, one may encounter CSF from the wound, lowpressure headaches, or leakage of spinal fluid from the nose. Direct dural repair is often required in complex anterior skull base cases, and the use of a vascularized galeal flap may be required. Again, supplementation with a lumbar CSF drain may be important, particularly if there is no focal tumor mass effect or raised intracranial pressure. Chronic problems with CSF leakage may be related to increased intracranial pressure and may require the placement of a ventriculoperitonal shunt. C5 NER v E PALSY C5 nerve palsy is another complication that can occur after cervical spinal surgery. It can happen either with anterior approaches, including anterior cervical discectomy or cor pectomy, or posterior approaches, including a cervical laminectomy, cervical laminoplasty, or cervical laminectomy and fusion. The important issue is to obtain a correct diagnosis. T ypically, the weakness involves the deltoid supraspinatus and infraspinatus muscles and results in the inability to adduct the arm and often in weakness of the biceps muscles, which are also innervated by the C5 nerve root. The other important issue has to do with the onset of the symptoms; usually, if the onset is immediately after surgery, and par ticularly if it is complete, the prognosis is less certain and less favorable. T ypical onset is in a delayed fashion, and this occurs in between 3% and 8% of posterior cervical pro cedures. The prognosis for delayed palsy is certainly bet ter, and often the recovery is complete. It is important in the diagnostic workup to rule out structural causes such as a hematoma or a disk fragment, and if there are none, the treatment is conservative with physical therapy when appropriate. If there is a severe injury and no hope for recovery through regeneration, one can consider a nerve transfer. This may involve a spinal accessory– to– suprascapular nerve transfer to reanimate the supraspinatus and infraspinatus muscles, and using a branch of the radial nerve to the long head of the triceps to the axillary nerve to reinnervate the deltoid.

e for recovery through regeneration, one can consider a nerve transfer. This may involve a spinal accessory– to– suprascapular nerve transfer to reanimate the supraspinatus and infraspinatus muscles, and using a branch of the radial nerve to the long head of the triceps to the axillary nerve to reinnervate the deltoid. POSTOPERA TI v E CRANIAL OR SPINAL HEMA TOMA Postoperative hematomas can occur after cranial neurosurgery in any number of locations: intralesional, intracerebral, subdural, and epidural (Figure 14.2). Application of epi dural tack- up stitches lets your examiner know that you are thinking of prevention. In each case, consider antiplatelet agents and anticoagulants as potential risk factors for the development of a postoperative hematoma. Patients will typically present with pain, new or worsening neurolo- gical deficit, or reduced level of consciousness. Confirmation of the diagnosis is done with a CT scan of the brain, if time permits, and prompt evacuation is the typical trajectory. Post operative spinal hematomas can occur in an immediate or delayed fashion. Severe pain associated with wors ening neurological symptoms is the typical presentation. An intended (e.g., intradural procedure) or inadvertent durotomy may increase the potential for development of a hematoma. Postoperative wound drains should theo retically reduce the risk for hematoma formation. Again, confirmation of the diagnosis with spinal MRI or CT and surgical evacuation of the hematoma are required. HYPONA TREMIA Hyponatremia is one of the most commonly encountered neurosurgical complications. It can result in a decreased level of consciousness as well as exacerbation of previously existing focal neurological deficits and, when severe (sodium level usually less than 120 mEq/ L), can also result in sei zures. W e teach our residents a very simple scheme to work

ommonly encountered neurosurgical complications. It can result in a decreased level of consciousness as well as exacerbation of previously existing focal neurological deficits and, when severe (sodium level usually less than 120 mEq/ L), can also result in sei zures. W e teach our residents a very simple scheme to work 170 • G OODMAN ’S N EUROSURGERY O RAL B OARD R E v IEW up hyponatremia. Whenever hyponatremia develops, the urine sodium level and renal function (blood urea and nitrogen and creatine) should be checked. If the urine sodium level is low (usually less than 10 mEq/ L), sodium depletion should be suspected. This can be due to some diuretics, vomiting, diarrhea, ascites, pleural effusion, or nasogas tric suction. If the urine sodium is high (usually more than 60 mEq/ L) and renal function is impaired, pathologic sodium loss in the urine, such as occurs with chronic renal failure or in the subacute phase of acute nephropathy, is the probable diagnosis. On the other hand, if renal function is normal, despite low serum sodium and high urinary sodium, the diagnosis is usually either a syndrome of inappropriate antidiuretic hormone (SIADH) secretion or cerebral salt wasting secondary to excess natriuretic hormone as seen after subarachnoid hemorrhage (SAH). The basic differ ence between these two conditions is that in inappropriate ADH secretion, total extracellular volume and intravascu lar volume are increased, whereas in cerebral salt wasting, they are decreased. The problem is that it is difficult to tell this difference, and there are no quick and easy laboratory tests that can give us an answer. For practical purposes, if the patient has had an SAH, the diagnosis is almost certainly cerebral salt wasting. In the absence of SAH, the over whelming likelihood is that the diagnosis is inappropriate ADH secretion. This difference is very important because in the former condition, the treatment is replenishment of intravascular volume, which is best accomplished with col loid infusion, such as Albumisol. Replenishing the intravascular volume suppresses ADH secretion and gradually leads to restoration of sodium homeostasis. With the syndrome of inappropriate ADH secretion, on the contrary, the treatment is volume restriction, which should be very strict (total fluids for 24 hours of less than 1 L/ day and in severe cases of hyponatremia less than 600 mL/ day). This can be accompanied by administration of sodium tablets when the patient is eating, and when the hyponatremia is severe, hypertonic (3%) saline can be administered. It is very important not to correct the sodium too rap idly or the patient can develop central pontine myelinoly sis, especially when the sodium is corrected by more than 25 mEq/ L in less than 48 hours. Patients will present with flaccid quadriplegia, locked- in syndrome, cranial nerve abnormalities, and mental status changes. Brainstem MRI will demonstrate high signal intensity within the pons and possibly also in the thalamus. Many patients have a preexisting history of alcoholism or malnutrition. INTRAOPERA TI v E BRAIN SWELLING During a craniotomy, one may encounter uncontrolled brain swelling (Figure 14.3). Considerations include the development of an intracerebral hematoma, such as from a ruptured aneurysm or a remote epidural or subdural hematoma, even potentially contralaterally situated; venous outflow obstruction (e.g., internal jugular vein); vasodilation of Figure 14.2 A large postoperative spinal epidural hematoma was diagnosed on postoperative day 2 after resection of a large intradural disk was resected after a T12 to L2 laminectomy. The hematoma can be seen to dissect under the caudal lamina, and hence the laminectomy had to be extended.

jugular vein); vasodilation of Figure 14.2 A large postoperative spinal epidural hematoma was diagnosed on postoperative day 2 after resection of a large intradural disk was resected after a T12 to L2 laminectomy. The hematoma can be seen to dissect under the caudal lamina, and hence the laminectomy had to be extended. Figure 14.3 Massive brain swelling leads to brain herniation during a craniotomy for aneurysmal rupture and ultimately death despite the attempted ventriculostomy just to the midline of the dural opening.

jugular vein); vasodilation of Figure 14.2 A large postoperative spinal epidural hematoma was diagnosed on postoperative day 2 after resection of a large intradural disk was resected after a T12 to L2 laminectomy. The hematoma can be seen to dissect under the caudal lamina, and hence the laminectomy had to be extended. Figure 14.3 Massive brain swelling leads to brain herniation during a craniotomy for aneurysmal rupture and ultimately death despite the attempted ventriculostomy just to the midline of the dural opening. COMPLICA TIONS • 171 cerebral vessels from systemic hypercarbia due to anesthetic considerations; or progressive brain edema especially after trauma. A common example is uncontrolled brain swelling after removal of a subdural hematoma. Management pearls include elevating the head of the bed (anti- T rendelenburg position), making sure that neck rotation has not kinked the internal jugular vein, particu larly in the park- bench position, ensuring that ventilatory pressures are not elevated by speaking to anesthesia, and measuring end- tidal Pco 2. Employing measures to reduce intracranial pressure, including inducing hyperventilation to attain P co 2 (30– 35  mm Hg), giving mannitol (1 mg/ kg IV bolus), and finally considering CSF drainage through a lumbar drain or ventriculostomy or draining CSF from an available operative cistern. All maneuvers are critical to avoid having herniated brain compress against the edge of the craniotomy wound and thereby lacerating the brain with further impairment of venous outflow. If all else fails, one may need to enlarge the craniotomy and consider aborting the procedure and many times avoid replacing the bone flap until the swelling subsides. A dramatic onset of brain swelling can occur when a large venous sinus is accidentally occluded during a craniotomy. This occasionally happens when the sinus is lacerated and vigorous bleeding develops, and in an attempt to stop the bleeding, the surgeon “packs” the area with Gelfoam or Surgicel. If this packing protrudes into the lumen of the sinus, it can occlude it, which may result in an immediate severe increase in venous pressure and progressive brain swelling. The correct way of handling a sinus laceration during craniotomy is first to elevate the head of the bed and then to place a strip of Gelfoam over the laceration, taking care to avoid any intraluminal obstruction by the Gelfoam. By placing a patty over the strip of Gelfoam, the bleeding almost always stops, particularly after some head elevation. At this point, under relaxed circumstances, the surgeon can proceed to repair the sinus in a variety of ways as necessary, although usually the bleeding simply stops and the Gelfoam strip can be left in place after removing the covering patty. v ASOSPASM V asospasm is, of course, a common sequela of SAH. V asospasm (constriction of the large conductive arteries along the base of the brain) may be clinically asymptomatic or lead to severe neurological deficits and even death. One peculiarity of vasospasm is that it develops in a delayed fashion, and we can predict with relative accuracy, immediately after SAH, whether the patient is going to have severe vasospasm or not. A simple CT scan tells us how much blood there is in the subarachnoid space, and we have learned from Fisher and others, 1980 that there is a direct corre lation with the thickness of the blood clot along the basal subarachnoid spaces and the development of vasospasm. This gives us a chance to treat the patient prophylactically. Essentially all SAH patients are treated with oral nimodipine, but this does not really prevent the development of vasospasm, although it does have a beneficial effect on outcome.

ood clot along the basal subarachnoid spaces and the development of vasospasm. This gives us a chance to treat the patient prophylactically. Essentially all SAH patients are treated with oral nimodipine, but this does not really prevent the development of vasospasm, although it does have a beneficial effect on outcome. For now, the only important prophylactic treatment in patients who have a high likelihood of developing vaso spasm is to treat them with some degree of hypervolemia, or at the very minimum to avoid hypovolemia, which develops in these patient almost routinely for a variety of reasons (e.g., frequent blood drawing, supine diuresis, decreased red blood cell production). Certainly, hypotension should be avoided, and some degree of artificial hypertension can be safely induced if the aneurysm has been secured. When the clinical effects of vasospasm become manifest, the treatment with “the 3 Hs” (hemodilution, hypertension, and hypervolemia) is indicated and should be established early on. When the patient does not improve, repeat angiography and consideration of endovascular chemical vasodilation and mechanical angioplasty should be considered. INTRAOPERA TI v E ANEURYSM RUPTURE— OPEN OR ENDO v ASCULAR A key to open aneurysm surgery is proximal control. Ophthalmic artery aneurysm exposure will require prep ping the neck for possible temporary internal carotid artery ligation. Proximal control is also key to more dis tal intracranial aneurysms. It is important to be prepared in advance with blood (2– 4 U packed red blood cells) in the operating room, cell saver, and two large- bore suckers so that you can clear the blood quickly to dissect around the bleeding aneurysm and identify the neck. When bleed ing occurs, the goal is to achieve proximal and, if neces sary, distal control with temporary clips and to control the bleeding with a strategically placed patty on the bleeding point and gentle pressure with a sucker while the neck is dissected. Avoid the temptation to put multiple large clips into the area of brisk bleeding because you will likely injure the parent vessel. Consideration of adenosine administra tion to temporarily stop the heart can be considered as a last ditch effort. Above all, the surgeon must remain cool and poised, which will ensure maximal efficiency of the entire surgical team.

clips into the area of brisk bleeding because you will likely injure the parent vessel. Consideration of adenosine administra tion to temporarily stop the heart can be considered as a last ditch effort. Above all, the surgeon must remain cool and poised, which will ensure maximal efficiency of the entire surgical team. 172 • G OODMAN ’S N EUROSURGERY O RAL B OARD R E v IEW MAJOR ARTERIAL INJURIES WITH CRANIAL AND SPINAL SURGERY Some of the common scenarios in which large arterial ves sels can be injured in neurosurgery include carotid artery injury with transsphenoidal surgery; vertebral artery injury with posterior cervical surgery, with instrumentation placed at C2 and with lateral dissection over the posterior arch of C1; and aortic injury and its branches with posterior lum bar spinal surgery. The key elements are recognition, repair when possible, blood volume replacement, and follow- up angiography to diagnose and possibly treat endovascularly, usually with a stent, by embolizing the area of injury or sacrificing the parent vessel. If there is an injury to the vertebral artery with C2 screw placement, it is important to place the screw to tamponade the vessel and not to put a screw on the other side because bilateral vertebral artery injuries can be lethal, whereas unilateral injuries are surprisingly well tolerated. Do not entertain drilling the bone of C2 to expose the artery and repair it because the patient will bleed out before you accomplish this goal. Common error in judgment leading to vertebral artery injury with C2 pars screws placement is lateral or low trajectory with the drill. A  similar event can happen dur ing an anterior cervical discectomy and fusion with a lateral bite within the foramen or during exposure of the longus colli. Postoperative angiography is important to confirm that the vessel is occluded and not partially injured, which can lead to pseudoaneurysm formation, arteriovenous fis tula, or a source of emboli (Figure 14.4). In the case described in this chapter, the ipsilateral vertebral artery will need to be sacrificed by endovascular occlu sion, provided there is good flow from the contralateral vertebral artery. When the vertebral artery is injured with open dissection over the arch of the atlas, arterial control can be quickly obtained with rapid dissection. When the injury is caused by sharp dissection, which we always recommend in this area, it can frequently be repaired primarily; however, blunt injuries and injuries caused by monopolar dissection usually cannot be repaired and require sacrifice of the artery. Carotid artery injuries with transsphenoidal surgery are seen particularly when there is medial bowing of the carotid siphon into the sella or simply errors in judgment as to the location of the midline. T amponade the vessel intraopera tively with a Cottonoid and consider immediate angiogra phy for possible repair or sacrifice of the vessel. Endovascular treatment options include vessel sacrifice, coil embolization (with or without stent assistance), and endoluminal reconstruction. Delayed complications such as pseudoaneurysm formation and rupture are common without treatment. Finally, a simple lumbar laminectomy and discectomy can result in death after a ventral and lateral bite with the pituitary rongeurs that avulse a segmental branch from the aorta or iliac artery. Again, recognition is the most impor tant issue. Intraoperative hypotension and tachycardia can signify a large retroperitoneal hematoma. When this is recognized intraoperatively, the best course of action is to rapidly close the incision temporarily with two or three through- and- through stitches, to turn the patient over, and to start preparing the abdomen while an emergency call to a vascular or general surgeon is placed.

ge retroperitoneal hematoma. When this is recognized intraoperatively, the best course of action is to rapidly close the incision temporarily with two or three through- and- through stitches, to turn the patient over, and to start preparing the abdomen while an emergency call to a vascular or general surgeon is placed. Prompt recognition in these cases can save a life. Postoperatively, the presence of abdominal bruising (Grey T urner sign), a low hemoglobin level, and signs of shock indicates the need to rush the patient back to the operating room to deal with bleeding arterial vessel through a retroperitoneal approach. A BC D Figure 14.4 A– D: A large left cerebellar infarct is seen on postoperative day 2 after an occipital cervical fusion. Patient complained of nystagmus and left arm dysmetria. Postoperative angiography demonstrates complete occlusion of the left vertebral artery on lateral (B) and anteroposterior (C) views with filling of the contralateral superior cerebellar artery, anterior inferior cerebellar artery, and posterior inferior cerebellar artery with right vertebral artery injection.

ysmetria. Postoperative angiography demonstrates complete occlusion of the left vertebral artery on lateral (B) and anteroposterior (C) views with filling of the contralateral superior cerebellar artery, anterior inferior cerebellar artery, and posterior inferior cerebellar artery with right vertebral artery injection. COMPLICA TIONS • 173 ESOPHAGEAL f ISTULA One has to be cognizant of the potential complication of an esophageal fistula after anterior cervical spinal surgery. T ypically, these patients present with wound drainage, subcutaneous emphysema, pain, difficulty swallowing, and fever. The diagnosis can be confirmed with laboratory work, including white blood cell count ,erythrocyte sedimentation rate, C- reactive protein and finally, further investigations may include barium swallow and rigid esophagoscopy. It is a very important diagnosis to make and treat early and aggressively because progression to mediastinitis can be lethal. Patients require an otolaryngology consultation and exploration of the esophagus along with these colleagues. T reatment options include simple repair of a small esop3ageal perforation or a more radical repair including the placement of a muscle flap, such as a sternocleidomastoid or pectoralis major muscle. Part of the treatment often requires resting the esophagus, which would involve either a parentral or enterostomy feeding. A rarer complication is a tracheoesophageal fistula. This is usually a delayed complication that frequently manifests as regurgitation and coughing up of food. The usual causes are excessive intraoperative pressure by a retractor on both the trachea and the esophagus or electrical burn to both structures, usually caused by a poorly insulated monopolar electrocoagulation tip. BIBLIOGRAPHY Farhat HI, Elhammady MS, Levi AD, Aziz- Sultan MA. Cervical sub arachnoid catheter placement for continuous cerebrospinal fluid drainage: a safe and efficacious alternative to the classic lumbar cis tern drain. Neurosurgery. 2011;68(1):52– 56. Fisher CM, Kistler JP, Davis JM. Relation of cerebral vasospasm to sub arachnoid hemorrhage visualized by computerized tomographic scanning. Neurosurgery. 1980;6(1):1– 9. Levi AD, Dickman CA, Sonntag VK. Management of postoperative infections after spinal instrumentation. J Neurosurg . 1997;86(6): 975– 980. McMahon P, Dididze M, Levi AD. Incidental durotomy after spinal surgery:  A  prospective study in an academic institution. J Neurosurg Spine. 2012;17(1):30– 36 Navarro R, Javahery R, Eismont F, et  al. The role of the sternocleido mastoid muscle flap for esophageal fistula repair in anterior cervical spine surgery. Spine. 2005;30(20):E617– E622.