Complications of brain stem surgery: Prevention and treatment

Complications of brain stem surgery: Prevention and treatment

Complications of Brain Stem Surgery: Prevention and Treatment Francesco Procaccio, MD, 2 Roberta Gambin, MD, 1 Leonardo Gottin, MD, 2 and Albino Brico...

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Complications of Brain Stem Surgery: Prevention and Treatment Francesco Procaccio, MD, 2 Roberta Gambin, MD, 1 Leonardo Gottin, MD, 2 and Albino Bricolo, MD i

With experienced neurosurgical, neuroanesthetic, and intensive care teams, postoperative recovery after brain stem surgery may be uneventful in patients without severe preoperative neurological deficits. The primary goal of postoperative intensive care is to ensure adequate monitoring and maintenance of homeostasis in an effort to prevent systemic and cerebral complications. Nevertheless, systemic complications and postoperative neurological deterioration are common. Respiratory failure, dysphagia, and pulmonary aspiration are possible life-threatening postoperative complications that may occur days or weeks after surgery. Impaired respiratory drive may result in progressive carbon dioxide retention and hypoxia, leading to respiratory arrest. GIossopharyngeal and vagal nerve dysfunction may be associated with high rates of postoperative morbidity and mortality. Damage to these nerves impairs swallowing and protective and coughing reflexes and may result in dysphagia, vocal cord paralysis, and gastric stasis. A comprehensive assessment (qualitative and quantitative) of possible swallowing deficits is important before and after extubation, particularly at early extubation trials, in an effort to prevent major postoperative complications. If a swallowing deficit is underestimated, dramatic episodes of aspiration may occur with acute respiratory failure or pulmonary edema. Continuous subclinical pulmonary inhalation predisposes the patient to sepsis and multiple organ failure. Treatment of dysphagia is complex and requires a multidisciplinary team to evaluate the most feasible therapeutic option for the patient to ensure adequate and safe separation of airways and food passages. Expert medical and nursing care consists of experienced, dedicated, and professional personnel who are aware of the strict relationship among intensive care treatment, prevention of complications, and the possibility of recovery. Copyright 9 2000 by W.B. Saunders Company

he literature documents a wide range and high incidence

T of early postoperative complications after miscellaneous neurosurgical procedures, i Intraoperative problems predispose the patient to postoperative complications, with hypotension and hypertension representing the most common events leading to cardiovascular imbalance and bleeding complications. During the initial postoperative hours, hemodynamic stability is essential. 2

From the Departments of 1Neurosurgery and 2Neuroanesthesiology, University Hospital of Verona, Verona, Italy. Address reprint requests to Francesco Procaccio, MD, Department of Anesthesia and Intensive Care, City Hospital, Piazza Stefani 1, 37124 Verona, Italy. Copyright 9 2000 by W.B. Saunders Company 1092-440)
Postoperative Complications of the Sitting Position The postoperative risks associated with the sitting position include venous air embolism, macroglossia, and pneumocephalus. 3 Direct toxicity of air bubbles on the pulmonary endothelial cells may favor clinical or subclinical pulmonary edema, a complication that may require postoperative ventilatory support. 4 Consequences of uneventful intraoperative paradoxical air embolism should be kept in mind if unexplained cardiac or neurological problems occur, with coronary and cerebral vascular beds representing a major risk. Macroglossia, resulting from venous and lymphatic drainage impairment 3 or perhaps from some neurogenic mechanism, 5 typically occurs within the first 24 hours after surgery and may cause respiratory obstruction, which tends to resolve spontaneously days or weeks later. Tension pneumocephatus with a severe increase of intracranial pressure should be considered if unexplained postoperative deterioration occurs. Neurosurgeons and neuroanesthetists, working together, can minimize air trapping by adequately managing intraoperative ventilation, brain bulk, and nitrous oxide. 3,6 Nitrous oxide should be avoided, particularly if the patient is administered anesthesia again during the postoperative period. Tension pneumocephalus has been also reported as a possible origin of venous air embolism after craniotomy closure. 7 At surgery, optimizing the semisitting position by limiting gravitational effects and flexion of the neck is fundamental in avoiding or minimizing venous air embolism, macroglossia, and pneumocephalus. Major systemic medical complications are more frequent after infratentorial than after supratentorial surgery.8 Early seizures may occur in the early postoperative period after posterior fossa surgery but are typically related to an altered metabolic or electrolytic imbalance.9 Maintenance of homeostasis is the goal of postoperative intensive care in an effort to prevent systemic and cerebral complications and to improve patient outcome. Inappropriate secretion of antidiuretic hormone and temperature should be strictly controlled, and circulatory and respiratory parameters must be monitored continuously in an intensive care setting, keeping in mind the time frame of possible secondary cerebral damage after surgery.6

Specific Complications of Brain Stem Surgery Neurological Deterioration Preoperative deficits often worsen after a posterior fossa surgical approach, l~ After brain stem surgery, specific postoperative sequelae and complications occur that may require dedicated and often prolonged intensive care. ll Postoperative

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neurological deterioration is common, relating to pre-existing deficits and surgical invasiveness. Motor disturbances of upper cranial nerves and pyramidal impairment may be transient and vary in severity and duration. Dramatic clinical situations of coma, dilated pupils, and quadriplegia have been described with good recovery. 12 Respiratory failure, cranial nerve impairment, quadriparesis, and sensitivity deficits may all occur in the acute postoperative period and resolve, completely or partially, in days, weeks, or months. 1>15 An early and complete recovery of consciousness with severe concomitant neurological deficits is frequent in the acute postoperative period, n Reversible locked-in syndrome is also possible when secondary damage of the ventral pons occurs. These severe clinical situations require nursing and medical expertise, with particular attention and sensitivity to conscious paralyzed patients who find themselves in perhaps a frightening setting of a neurointensive care unit. Transient mutism and dysarthria are described after brain stem surgery, 16according to the well-recognized phenomenon occurring in posterior fossa surgery, particularly in pediatric patients. Damage of cranial nerves V and VII may cause ocular lesions, which can be prevented with protective means or tarsorrhaphy. Clinical data on respiratory failure and loss of cranial nerve function are mostly anecdotal 12-14 and offer poor prognostic support in determining the requirement for delayed extubation, postoperative sedation, or tracheostomy. Guidelines for early versus delayed awakening from anesthesia in neurosurgical patients have been suggested, 17 but the postoperative plan for brain stem surgery should be discussed for each individual case, considering the patient's preoperative deficits, intraoperative course, direct surgical lesion, and risk of secondary cerebral damage. At times, an early unstable illusive recovery from anesthesia may precede respiratory failure and severe swallowing dysfunction, particularly when delayed ischemia and edema of the brain stem occur hours or days after surgery.

Respiratory Failure Respiratory failure may be associated with the following: (1) mechanical airway obstruction, (2) direct or secondary involvement of the respiratory control pathways and centers, and (3) damage to cranial nerves and protective reflexes. Frequent checks of the tongue, the face, and the soft palatal tissues are recommended before and after extubation. Fiberoptic endoscopy and associated skills for difficult airway management must be readily available. Complete upper airway obstruction after extubation may be due to a collapse of the extrathoracic airway, caused by impaired function of the lower cranial nerves, particularly the hypoglossal.18 Impaired respiratory drive may occur with progressive carbon dioxide retention and hypoxia leading to respiratory arrest. 14 Ventilatory failure may be prolonged for weeks: some patients may present with toss of respiratory drive during sleep (Ondine's curse) and suffer from severe complications of mechanical invasive ventilation and difficult weaning. In patients without recovery of respiratory drive, phrenic pacing is a delayed therapeutic option to be considered. ~8 Frequent respiratory physiotherapy and patient turning are mandatory to drain secretions; to maintain pulmonary volumes; and to prevent atelectasis and damage to muscles, tendons, and tissues. 156

Lower Cranial Nerve Impairment Patients with glossopharyngeal and vagal nerve dysfunction may have higher postoperative morbidity and mortality. 13 Damage to cranial nerves IX and X impairs swallowing and protective and coughing reflexes, resulting in dysphagia, vocal cord paralysis, and gastric stasis. Prevention of direct damage to cranial nerves and motor nuclei during tumor resection is the main objective to preserve protective reflexes and to minimize definitive neurological deficits. During surgery, the susceptibility of cranial nerve motor nuclei to injury differs according to tumor location as well as the cranial motor nuclei displacement pattern; such displacement patterns are understood using neurophysiological brain stern mapping in an effort to facilitate safer microsurgery. 19 Although difficult, an accurate clinical assessment of gag reflex and glottis functionality in the intubated patient is critical to prevent major postoperative life-threatening complications. If a swallowing deficit is not diagnosed or is underestimated, dramatic episodes of aspiration may occur with acute respiratory failure or pulmonary edema. Postobstructive pulmonary edema may be a consequence of bilateral vocal cord paralysis. Continuous subclinical pulmonary inhalation, caused by a swallowing impairment, predisposes the patient to sepsis and multiple organ failure. Comprehensive (qualitative and quantitative) assessment of possible swallowing deficits is important before and after extubation, particularly in early extubation trials, t7 in which a dedicated, multidisciplinary team collaborates to define a feasible postoperative management plan. 2~ Videofluoroscopy of the oral and pharyngeal stages of swallowing, direct fiberoptic laryngoscopy, and neurophysiological recordings can be used effectively. 2~

Treatment of Dysphagia Treatment of dysphagia is complex and requires a collaborative effort by intensivists, speech pathologists, radiologists, otorhinolaryngologists, and nurses. 2~ This meticulous approach may define the best therapeutic option and strategy for the individual patient: early versus delayed extubation and tracheostomy; strict parenteral feeding and gastric drainage versus enteral feeding by nasogastric tube or gastrostomy; early temporary surgical closure of the glottis versus vocal cord augmentation. In patients with aspiration, treatment is focused on the separation of airways from food passages. 2~ Tracheostomy and the positioning of a nasogastric feeding tube are the most common tools to achieve this separation2~ they are not ideal devices, however, because of the risk of tracheomalacia and an incomplete protection against aspiration. 24 In an effort to avoid tracheostomy, rehabilitation with compensatory swallowing techniques may be useful to provide long-lasting protection in fully cooperative patients or in those with mild or moderate dysphagia. 2~ Percutaneous endoscopic gastrostomy or jejunostomy may be used to provide long-term enteral feeding, even if complete protection from reflex and aspiration is not provided. 24 Vocal cord augmentation and glottic or supraglottic laryngeal closure are effective methods to avoid chronic aspiration. 2~ Vocal cord augmentation can be performed by injection of polytetrafluoroethylene (Teflon) or absorbable gelatin sponge (Gelfoam) into the larynx. 2~ Because Teflon may be difficult to PROCACClO ET AL

remove, Gelfoam injection should be performed if recovery of function is anticipated. 2~ Surgical closure of the larynx can be considered a temporary and reversible procedure, but the severity of associated side effects suggests that this procedure be limited to patients refractory to the other forms of therapy.2~

Conclusions With experienced neurosurgical, neuroanesthetic, and intensive care teams, postoperative recovery may be uneventful in patients without severe preoperative neurological deficits. In selected cases, respiratory failure, dysphagia, and pulmonary aspiration are possible life-threatening postoperative complications: meticulous prevention and prompt, aggressive treatment of systemic complications are imperative in patients with delayed neurological recovery. Expert medical and nursing care consists of experienced, dedicated, and professional personnel who are aware of the strict relationship among adequate intensive care treatment, prevention of complications, and actual possibility of recovery.

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COMPLICATIONS OF BRAIN STEM SURGERY

8. Sawaya R, Hammoud M, Schoppa D, et al: Neurosurgical outcomes in a modern series of 400 craniotomies for treatment of parenchymal tumors. Neurosurgery 42:1044-1056, 1998 9. Lee S-T, Lui T-N, Chang C-N, et al: Early postoperative seizures after posterior fossa surgery. J Neurosurg 73:541-544, 1990 10. Cochrane DD, Gustavsson B, Poskitt KP, et al: The surgical and natural morbidity of aggressive resection for posterior fossa tumors in childhood. Pediatr Neurosurg 20:19-29, 1994 11. Bricolo A, Turazzi S, Cristofori L, et al: Direct surgery for brainstem tumours. Acta Neurochir 53(suppl):148-58, 1991 12. Xu QW, Bao WM, Mao RL, et ak Surgical treatment of solid brain stem tumors in adults: a report of 22 cases, Surg Neuro148:30-36, 1997 13. Behnke J, Christen HJ, Mursch K, et al: Intra-axial endophytic tumors in the pons and/or medulla oblungata. Childs Nerv Syst 13:135-146, 1997 14. Abbott R, Shiminski-Maher T, Wisoff JH, et al: Intrinsic tumors of the medulla: surgical complications. Pediatr Neurosurg 17:239-244, 19911992 15. Heffez DS, Zinreich SJ, Long DM: Surgical resection of intrinsic brain stem lesions: an overview. Neurosurgery 27:789-798, 1990 16. Frim DM, Ogilvy CS: Mutism and cerebellar dysarthria after brain stem surgery: case report. Neurosurgery 36:854-857, 1995 17. Bruder N, Ravussin P: Recovery from anesthesia and postoperative extubation of neurosurgical patients: a review. J Neurosurg Anesthesiol 11:282-293, 1999 18. Howard R, Mahoney A, Thurlow AC: Respiratory obstruction after posterior fossa surgery. Anaesthesia 45:222-224, 1990 19. Morota N, Deletis V, Lee M, et al: Functional anatomic relationship between brain stem tumors and cranial motor nuclei. Neurosurgery 39:787-794, 1996 20. Blitzer A: Approaches to the patient with aspiration and swallowing disabilities. Dysphagia 5:129-137, 1990 21. Martens L, Cameron T, Simonsen M: Effects of a multidisciplinary management program on neurologically impaired patients with dysphagia. Dysphagia 5:147-151, 1990 22. Young EC, Durant-Jones L: Developing a dysphagia program in an acute care hospital: a needs assessment. Dysphagia 5:159-165, 1990 23. MacKay LE, Morgan AS, Bernstein BA: Swallowing disorders in severe brain injury: risk factors affecting return to oral intake. Arch Phys Med Rehabi180:365-369, 1999 24. Hensel M, Haake K, Vogel S, et al: Management of swallowing disorders and chronic aspiration by glottic closure procedure. J Neurosurg Anesthesiol 9:273-276, 1997 25. Jennings KS, Siroky D, Jackson CG: Swallowing problems after excision of tumors of the skull base: diagnosis and management in 12 patients. Dysphagia 7:40-44, 1992

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