Postoperative Care of the Surgical Patient With Neurological Disease
Lucia Rivera-Lara, MD Department of Anesthesiology and Critical Care Medicine, Division of Neurosciences Critical Care Medicine, Johns Hopkins University, Baltimore, Maryland
Marek Mirski, MD, PhD Department of Anesthesiology and Critical Care Medicine, Neurology and Neurosurgery, Johns Hopkins University, Baltimore, Maryland Neurosciences Critical Care Unit, Johns Hopkins Hospital, Baltimore, Maryland
The postoperative care of neurosurgical patients in Neurocritical Care Units is a field that has largely developed over the last 4 decades. The current model utilizes the combined expertise from neurology, neurosurgery, anesthesiology, and other disciplines to treat complex neurological conditions such as subarachnoid and intracerebral hemorrhage (ICH), brain tumors, spinal cord injury, intractable seizures, and stroke. In short, neurocritical care deals with any life-threatening diseases and trauma of the nervous system, including the brain, spinal cord, and peripheral nerves. Today, there are over 100 Neurocritical Care Unit’s in the United States registered with the Neurocritical Care Society (http://www.neurocriticalcare.org). The benefits of having a neuroscience specialty intensive care unit (ICU) arena staffed by specialty trained intensivists and critical care nurses include reduced in-hospital mortality and length of stay, improvement in ICU management, and significant net cost savings to a medical center, beyond the additional expense of financing a subspecialty intensivist driven ICU, of between US$800,000 and US$3,000,000.1–4 This chapter is intended for any health professional (critical care nurse, internist, anesthesiologist, and neurologist) evaluating postoperative neurological patients and consulting in their care. In addition, intensivists working in general ICU’s taking care of patients with acute brain injury may benefit.
REPRINTS: MAREK MIRSKI, MD, PHD, DEPARTMENT OF ANESTHESIOLOGY AND CRITICAL CARE MEDICINE, JOHNS HOPKINS UNIVERSITY, 1800 ORLEANS STREET, PHIPPS 455, BALTIMORE, MD 21287-7840. E-MAIL: MMIRSKI@ JHMI.EDU INTERNATIONAL ANESTHESIOLOGY CLINICS Volume 53, Number 1, 166–176 r 2015, Lippincott Williams & Wilkins
166 | www.anesthesiaclinics.com
Surgery and Neurological Disease ’
’
167
General Principles of the Postoperative Patient With Neurological Disease
It is imperative that the physician evaluates the patient immediately upon arrival to the postoperative area. The assessment should begin with the standard full clinical history (generally recorded on the preoperative evaluation), and include a comprehensive review of the type of surgery performed in the operating room, time and type of medications given, and any complications that the anesthesiologist and surgeon encountered. The general examination should initially focus on the vital signs and the cardiopulmonary system. The postoperative neurological patient requires a full neurological examination including mental status, cranial nerves, motor, sensory, and cerebellar function. It is essential to take into consideration the type of surgery performed. In the patient who undergoes an endovascular procedure, a careful watch of the groin puncture site and the distal peripheral pulses should be completed; in a patient who undergoes a carotid endarterectomy, careful measurement and assessment of the neck is warranted to detect an expanding lifethreatening hematoma as early as possible. The purpose of the postoperative assessment is to identify any deficits not present in the preoperative examination. The clinical assessment should be followed by a laboratory check of hemoglobin, electrolytes, renal function, etc. If the patient is intubated, an arterial blood gas and chest radiograph should be assessed. Any new neurological deficit must be investigated with appropriate and immediate follow-up. Typically the fastest and most readily available type of imaging for intracerebral or spinal pathology is a computed tomography (CT) of the head or spine. If the question is not answered then magnetic resonance imaging (MRI) should be considered. An electroencephalogram would be an important consideration if there were concern for seizures or subclinical status epilepticus. Furthermore, complete understanding of the physiological and neurological status of the postoperative patient is necessary to decide the disposition and further management.
’
Altered Mental Status in the Postoperative State: Delirium and Coma
Postoperative neurological patients often suffer from various degrees of altered mental status secondary to their primary neurological disease and/or as a consequence of the sedative medications they received in the operating room. www.anesthesiaclinics.com
168
’
Rivera-Lara and Mirski
Delirium is an acute and fluctuating disorder of consciousness characterized by inattention, disorganized thinking, and perceptual disturbances.5 Reported rates of delirium in critically ill patients are between 50% and 80%.6 Specific contributors to this brain dysfunction include the use of benzodiazepines in mechanically ventilated patients, anticholinergic medications, insufficient pain relief, and excessive sedation with narcotics. Therefore, optimization of sedation and analgesia is imperative in postsurgical care; the judicious use of opioids may be protective of acute brain dysfunction in patients at high risk for pain but may be detrimental if used excessively. Dexmedetomidine is perhaps an especially useful sedative in postoperative neurosurgical patients in that the agent has been shown in multiple randomized controlled trials to decrease the incidence and duration of delirium when compared with benzodiazepines and morphine. It is essential to think of delirium as a diagnosis of exclusion, which is entertained only after a thorough neurological assessment has been completed and other causes of brain dysfunction have been ruled out. In addition to delirium, coma is another common disorder in the postoperative state. Coma is defined as a complete loss of both awareness and arousal. Coma can result from primary brain injury (acute stroke, status epilepticus, etc.), and systemic metabolic derangements (hypoglycemia, septic encephalopathy, etc.; Table 1). The neurological examination is critical to uncover possible causes of coma. For example, small pupils (< 2 mm) that are minimally reactive or unreactive to light are commonly seen in patients who use opioids and in patients with a pontine lesion that interrupts descending sympathetic outflow. Dilated (> 8 mm) pupils are seen in disruption of cranial nerve III secondary to either a mesencephalic injury or a lesion of the peripheral nerve. Midsize, light-fixed pupils are due to midbrain lesions resulting potentially from transtentorial brain herniation and in severe form are frequently the first sign of loss of all brainstem reflexes (brain death). Tonic deviation of the eyes in the horizontal plane may indicate an ipsilateral hemispheric lesion affecting the frontal eye fields or a contralateral pontine lesion. Horizontal deviation can also be seen in nonconvulsive status epilepticus and may be one of the few signs to indicate the need for an urgent electroencephalogram. Further testing with neuroimaging and laboratory evaluation should follow in the unresponsive patient who lacks any localizing signs on the neurological examination. Head CT is excellent for detecting a hemorrhagic stroke, hydrocephalus, and cerebral edema. However, an acute ischemic stroke may take up to 12 to 24 hours to be evident on a head CT. In this circumstance an urgent brain MRI is justified. The initial laboratory work-up of comatose patients should include: complete blood count, full electrolyte panel, basic metabolic panel with liver function tests, thyroid function tests, urinalysis, toxicology screen, and arterial blood gas. www.anesthesiaclinics.com
Surgery and Neurological Disease
Table 1.
’
169
Major Causes of Acute Coma
Primary brain injury With/without localizing motor deficits Intracerebral hemorrhage Middle cerebral artery occlusion Brain tumor Cerebral abscess Traumatic brain injury Status epilepticus Subarachnoid hemorrhage Without localizing motor deficits Bilateral thalamic infarcts Cerebral venous thrombosis Encephalitis Gliomatosis Cerebral edema Cerebellar stroke Hypoxemic ischemic encephalopathy Subclinical status epilepticus With localizing cranial nerve deficits Basilar artery occlusion Brainstem hemorrhage Central pontine myelinolysis Systemic insults causing brain dysfunction Electrolyte derangements Hyponatremia 165 mg/dL Hypercalcemia >13 mg/dL Endocrine abnormalities Acute hypothyroidism Addison’s disease Acute panhypopituitarism Poisoning, illegal drug use Opioids Anticholinergic drugs Carbon monoxide inhalation Other metabolic derangements Hypothermia 12 h) can lead to cerebral CBV, and ICP ischemia, poor outcome ICP monitoring and CSF Risk for ventriculitis and CSF drainage overdrainage. During its placement an ICH or IVH may occur May worsen cerebral edema, Enlarges the intracranial possibly associated with space, allowing the swollen cerebral hyperemia as a cerebral hemisphere or result of elevated CPP and cerebellum to expand out of impaired cerebral normal cranial limits while autoregulation. Increases avoiding brain herniation cerebral inflammation and and brainstem compression. risk for brain infection Improves cerebral compliance and reduces ICP
CBV indicates cerebral blood volume; CPP, cerebral perfusion pressure; CSF, cerebrospinal fluid; ICH, intracerebral hemorrhage; ICP, intracranial hypertension; IVH, intraventricular hemorrhage.
www.anesthesiaclinics.com
Surgery and Neurological Disease
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173
Only half of all patients presenting in shock will be volume responsive, in terms of increasing their cardiac output in response to a fluid challenge.17 Therefore, when there is not a favorable response to a fluid challenge, other causes of hypotension must be entertained, like neurogenic, anaphylactic, cardiogenic, or obstructive shock (massive pulmonary embolism). It is essential to consider the possibility of hemorrhagic shock in the postoperative period. Patients undergoing endovascular procedures are at an increased risk of vascular injury and a retroperitoneal hematoma. Administering fluid resuscitation in a patient with massive vascular injury before reversing the vascular defect only increases mortality by causing arterial pressure to rise, which increases bleeding and promotes further exsanguination.18 Thus, surgical management of the vascular defect should be prioritized. The administration of blood products is critical in these patients with transfusion of red blood cells, plasma, and platelets in approximately 1:1:1 or 2:1:1 ratio to optimize hemostatic mechanisms. The best vasoactive drug for shock depends on the indication. In general, norepinephrine is superior to dopamine for the treatment of shock.19
’
Electrolytes and Fluid Management in Acute Brain Injury
Abnormalities in electrolytes and fluid regulation are common in postoperative patients with acute brain injury, and these patients may tolerate these disorders poorly as they may already have cerebral edema and poor intracranial compliance from the primary brain injury. Hypoosmolarity and hypovolemia are deleterious in patients with acute brain injury and can worsen cerebral edema and ischemia.20 Hypo-osmolality should be avoided. As sodium is the major determinant of serum osmolality, and hence the major determining force affecting water translocation across the blood-brain barrier, a fundamental principle is to maintain sodium at least within the normal range of 135 to 145 mmoL/L.21 Hyponatremia (sodium 40 mEq/L). Assessing the volume status is the best way www.anesthesiaclinics.com
174
’
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to distinguish them; patients with SIADH are euvolemic or hypervolemic and patients with CSW are hypovolemic. Hyponatremia should be aggressively corrected in the postoperative period of patients with acute brain injury; however, caution should be paid in patients with chronic hyponatremia developing over at least 48 hours as its rapid correction, currently considered to be if >5 to 10 mEq/d, will put the patient at risk for osmotic demyelination causing quadriplegia, coma, and pseudobulbar palsy. The management of SIADH is with fluid restriction and avoidance of free water or hypotonic fluids. The treatment of CSW is with repletion of salt and fluid to achieve normal sodium and fluid balance. Hypertonic saline, salt tablets, and fludrocortisone are options that can be implemented according to the clinical condition of the patient and sodium levels. One of the frequent causes of hypernatremia in the postoperative state is central diabetes insipidus, which is a feared complication of endoscopic pituitary surgery. Central diabetes insipidus occurs when ADH fails to be released from the hypothalamic-pituitary axis. The diagnosis is made when the patient has a sodium Z145 mmoL/L, urinary output Z250 mL/h in 2 consecutive hours and a dilute urine with a specific gravity r1.005. The treatment includes correction of the water deficit and administration of vasopressin or desmopressin. Additional electrolyte derangements include hypokalemia, which can cause rhabdomyolysis, muscle weakness, and cardiac arrhythmias. Hyperkalemia may cause arrhythmias and muscle weakness and can also alter the conduction system. Peaked T waves and shortened QT interval precede PR and QRS interval widening. Conduction abnormalities include bundle branch and atrioventricular blocks; p-wave disappearance may be followed by asystole. Hypocalcemia is frequently found in patients that were massively transfused with blood products in the operating room. Clinical manifestations of hypocalcemia include QT interval prolongation, tetany, seizures, and hypotension. Hypomagnesemia causes weakness and polymorphic ventricular tachycardia with prolonged QT interval. Therefore, electrolyte derangements can cause significant complications and should be aggressively corrected.
’
Prevention of Postoperative Neurological Injury. Which Patients are at Increased Risk?
It is specifically important to attempt to prevent neurological damage as it is most often irreversible and can lead to devastating patient disability. The key to prevention is to identify patients at increased risk and to act quickly at the mildest sign of a neurological deficit. Well-established patient factors for increased risk of complications after neurosurgery include increased age, multiple comorbidities, and www.anesthesiaclinics.com
Surgery and Neurological Disease
Table 3.
’
175
Risk Factors for Perioperative Neurological Morbidity
Preoperative Old age Obesity Multiple comorbidities Need for anticoagulation Hypertension Diabetes
Intraoperative Prolonged surgery (> 2 h) Excessive blood loss during surgery (> 1 L) Massive resuscitation Emergent surgery
history of hypertension, diabetes, and obesity.22,23 Intraoperative risk factors associated with increased postoperative morbidity include prolonged surgeries (> 2 h), excessive blood loss during surgery (> 1 L), and the need for massive resuscitation.24 Risk factors for postoperative respiratory failure include obstructive sleep apnea, obesity, chronic obstructive pulmonary disease, and smoking (Table 3). Patients who required anticoagulation to decrease their risk of stroke from atrial fibrillation, mechanical heart valves, etc. and have their anticoagulation withheld for the surgical procedure are at an increased risk of perioperative stroke. Therefore, anticoagulation should be withheld only as long as the type of surgical procedure indicates. Prediction of which patients are at risk for postoperative complications will allow for the implementation of risk reduction strategies and individually tailored management approaches including the selection of the most appropriate care setting for postoperative monitoring. ’
Conclusions
Postoperative morbidity continues to thwart the quality of recovery in patients undergoing neurosurgery. Neurological surgical morbidity affects significantly the quality of life and life expectancy of a patient. This chapter has focused on the secondary insults that must be watched and managed to mitigate postoperative adverse outcomes and mortality.
The authors declare that they have nothing to disclose.
’
References
1. Suarez JI, Zaidat OO, Suri MF, et al. Length of stay and mortality in neurocritically ill patients: impact of a specialized neurocritical care team. Crit Care Med. 2004;32: 2311–2317. 2. Mirski MA, Chang CW, Cowan R. Impact of a neuroscience intensive care unit on neurosurgical patient outcomes and cost of care: evidence-based support for an intensivist-directed specialty ICU model of care. J Neurosurg Anesth. 2001;13:83–92. www.anesthesiaclinics.com
176
’
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3. Diringer MN, Edwards DF. Admission to a neurologic/neurosurgical intensive care unit is associated with reduced mortality rate after intracerebral hemorrhage. Crit Care Med. 2001;29:635–640. 4. Pronovost PJ, Needham DM, Waters H, et al. Intensive care unit physician staffing: financial modeling of the Leapfrog standard. Crit Care Med. 2006;34:S18–S24. 5. Pandharipande P, Cotton BA, Shintani A, et al. Motoric subtypes of delirium in mechanically ventilated surgical and trauma intensive care unit patients. Inten Care Med. 2007;33:1726–1731. 6. Ely EW, Shintani A, Truman B, et al. Delirium as a predictor of mortality in mechanically ventilated patients in the intensive care unit. JAMA. 2004;291:1753–1762. 7. Weed LH. Some limitations of the monro-kellie hypothesis. Arch Surg. 1929;18: 1049–1068. 8. Czosnyka M, Pickard JD. Monitoring and interpretation of intracranial pressure. J Neurol Neurosurg Psych. 2004;75:813–821. 9. Albeck MJ, Borgesen SE, Gjerris F, et al. Intracranial pressure and cerebrospinal fluid outflow conductance in healthy subjects. J Neurosurg. 1991;74:597–600. 10. Chapman PH, Cosman ER, Arnold MA. The relationship between ventricular fluid pressure and body position in normal subjects and subjects with shunts: a telemetric study. Neurosurgery. 1990;26:181–189. 11. Miller JD, Stanek A, Langfitt TW. Concepts of cerebral perfusion pressure and vascular compression during intracranial hypertension. Prog Brain Res. 1972;35:411–432. 12. Engelhard K, Werner C, Mollenberg O, et al. Effects of remifentanil/propofol in comparison with isoflurane on dynamic cerebrovascular autoregulation in humans. Acta Anaesth Scand. 2001;45:971–976. 13. Strebel S, Lam AM, Matta B, et al. Dynamic and static cerebral autoregulation during isoflurane, desflurane, and propofol anesthesia. Anesthesiology. 1995;83:66–76. 14. Steiner LA, Czosnyka M, Piechnik SK, et al. Continuous monitoring of cerebrovascular pressure reactivity allows determination of optimal cerebral perfusion pressure in patients with traumatic brain injury. Crit Care Med. 2002;30:733–738. 15. Asgeirsson B, Grande PO, Nordstrom CH. A new therapy of post-trauma brain oedema based on haemodynamic principles for brain volume regulation. Inten Care Med. 1994;20:260–267. 16. Perel P, Roberts I, Ker K. Colloids versus crystalloids for fluid resuscitation in critically ill patients. Cochrane Database Syst Rev. 2013;2:Cd000567. 17. Michard F, Teboul JL. Predicting fluid responsiveness in ICU patients: a critical analysis of the evidence. Chest. 2002;121:2000–2008. 18. Bickell WH, Wall MJ Jr, Pepe PE, et al. Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries. NEJM. 1994;331:1105–1109. 19. De Backer D, Biston P, Devriendt J, et al. Comparison of dopamine and norepinephrine in the treatment of shock. NEJM. 2010;362:779–789. 20. Bhardwaj A. Neurological impact of vasopressin dysregulation and hyponatremia. Ann Neurol. 2006;59:229–236. 21. Bhardwaj A, Ulatowski JA. Hypertonic saline solutions in brain injury. Curr Opin Crit Care. 2004;10:126–131. 22. Zrinzo L, Foltynie T, Limousin P, et al. Reducing hemorrhagic complications in functional neurosurgery: a large case series and systematic literature review. J Neurosurg. 2012;116:84–94. 23. Patil CG, Lad SP, Harsh GR, et al. National trends, complications, and outcomes following transsphenoidal surgery for Cushing’s disease from 1993 to 2002. Neurosurg Focus. 2007;23:E7. 24. Pull ter Gunne AF, Cohen DB. Incidence, prevalence, and analysis of risk factors for surgical site infection following adult spinal surgery. Spine. 2009;34:1422–1428.
www.anesthesiaclinics.com
Lucia Rivera-Lara, MD Department of Anesthesiology and Critical Care Medicine, Division of Neurosciences Critical Care Medicine, Johns Hopkins University, Baltimore, Maryland
Marek Mirski, MD, PhD Department of Anesthesiology and Critical Care Medicine, Neurology and Neurosurgery, Johns Hopkins University, Baltimore, Maryland Neurosciences Critical Care Unit, Johns Hopkins Hospital, Baltimore, Maryland
The postoperative care of neurosurgical patients in Neurocritical Care Units is a field that has largely developed over the last 4 decades. The current model utilizes the combined expertise from neurology, neurosurgery, anesthesiology, and other disciplines to treat complex neurological conditions such as subarachnoid and intracerebral hemorrhage (ICH), brain tumors, spinal cord injury, intractable seizures, and stroke. In short, neurocritical care deals with any life-threatening diseases and trauma of the nervous system, including the brain, spinal cord, and peripheral nerves. Today, there are over 100 Neurocritical Care Unit’s in the United States registered with the Neurocritical Care Society (http://www.neurocriticalcare.org). The benefits of having a neuroscience specialty intensive care unit (ICU) arena staffed by specialty trained intensivists and critical care nurses include reduced in-hospital mortality and length of stay, improvement in ICU management, and significant net cost savings to a medical center, beyond the additional expense of financing a subspecialty intensivist driven ICU, of between US$800,000 and US$3,000,000.1–4 This chapter is intended for any health professional (critical care nurse, internist, anesthesiologist, and neurologist) evaluating postoperative neurological patients and consulting in their care. In addition, intensivists working in general ICU’s taking care of patients with acute brain injury may benefit.
REPRINTS: MAREK MIRSKI, MD, PHD, DEPARTMENT OF ANESTHESIOLOGY AND CRITICAL CARE MEDICINE, JOHNS HOPKINS UNIVERSITY, 1800 ORLEANS STREET, PHIPPS 455, BALTIMORE, MD 21287-7840. E-MAIL: MMIRSKI@ JHMI.EDU INTERNATIONAL ANESTHESIOLOGY CLINICS Volume 53, Number 1, 166–176 r 2015, Lippincott Williams & Wilkins
166 | www.anesthesiaclinics.com
Surgery and Neurological Disease ’
’
167
General Principles of the Postoperative Patient With Neurological Disease
It is imperative that the physician evaluates the patient immediately upon arrival to the postoperative area. The assessment should begin with the standard full clinical history (generally recorded on the preoperative evaluation), and include a comprehensive review of the type of surgery performed in the operating room, time and type of medications given, and any complications that the anesthesiologist and surgeon encountered. The general examination should initially focus on the vital signs and the cardiopulmonary system. The postoperative neurological patient requires a full neurological examination including mental status, cranial nerves, motor, sensory, and cerebellar function. It is essential to take into consideration the type of surgery performed. In the patient who undergoes an endovascular procedure, a careful watch of the groin puncture site and the distal peripheral pulses should be completed; in a patient who undergoes a carotid endarterectomy, careful measurement and assessment of the neck is warranted to detect an expanding lifethreatening hematoma as early as possible. The purpose of the postoperative assessment is to identify any deficits not present in the preoperative examination. The clinical assessment should be followed by a laboratory check of hemoglobin, electrolytes, renal function, etc. If the patient is intubated, an arterial blood gas and chest radiograph should be assessed. Any new neurological deficit must be investigated with appropriate and immediate follow-up. Typically the fastest and most readily available type of imaging for intracerebral or spinal pathology is a computed tomography (CT) of the head or spine. If the question is not answered then magnetic resonance imaging (MRI) should be considered. An electroencephalogram would be an important consideration if there were concern for seizures or subclinical status epilepticus. Furthermore, complete understanding of the physiological and neurological status of the postoperative patient is necessary to decide the disposition and further management.
’
Altered Mental Status in the Postoperative State: Delirium and Coma
Postoperative neurological patients often suffer from various degrees of altered mental status secondary to their primary neurological disease and/or as a consequence of the sedative medications they received in the operating room. www.anesthesiaclinics.com
168
’
Rivera-Lara and Mirski
Delirium is an acute and fluctuating disorder of consciousness characterized by inattention, disorganized thinking, and perceptual disturbances.5 Reported rates of delirium in critically ill patients are between 50% and 80%.6 Specific contributors to this brain dysfunction include the use of benzodiazepines in mechanically ventilated patients, anticholinergic medications, insufficient pain relief, and excessive sedation with narcotics. Therefore, optimization of sedation and analgesia is imperative in postsurgical care; the judicious use of opioids may be protective of acute brain dysfunction in patients at high risk for pain but may be detrimental if used excessively. Dexmedetomidine is perhaps an especially useful sedative in postoperative neurosurgical patients in that the agent has been shown in multiple randomized controlled trials to decrease the incidence and duration of delirium when compared with benzodiazepines and morphine. It is essential to think of delirium as a diagnosis of exclusion, which is entertained only after a thorough neurological assessment has been completed and other causes of brain dysfunction have been ruled out. In addition to delirium, coma is another common disorder in the postoperative state. Coma is defined as a complete loss of both awareness and arousal. Coma can result from primary brain injury (acute stroke, status epilepticus, etc.), and systemic metabolic derangements (hypoglycemia, septic encephalopathy, etc.; Table 1). The neurological examination is critical to uncover possible causes of coma. For example, small pupils (< 2 mm) that are minimally reactive or unreactive to light are commonly seen in patients who use opioids and in patients with a pontine lesion that interrupts descending sympathetic outflow. Dilated (> 8 mm) pupils are seen in disruption of cranial nerve III secondary to either a mesencephalic injury or a lesion of the peripheral nerve. Midsize, light-fixed pupils are due to midbrain lesions resulting potentially from transtentorial brain herniation and in severe form are frequently the first sign of loss of all brainstem reflexes (brain death). Tonic deviation of the eyes in the horizontal plane may indicate an ipsilateral hemispheric lesion affecting the frontal eye fields or a contralateral pontine lesion. Horizontal deviation can also be seen in nonconvulsive status epilepticus and may be one of the few signs to indicate the need for an urgent electroencephalogram. Further testing with neuroimaging and laboratory evaluation should follow in the unresponsive patient who lacks any localizing signs on the neurological examination. Head CT is excellent for detecting a hemorrhagic stroke, hydrocephalus, and cerebral edema. However, an acute ischemic stroke may take up to 12 to 24 hours to be evident on a head CT. In this circumstance an urgent brain MRI is justified. The initial laboratory work-up of comatose patients should include: complete blood count, full electrolyte panel, basic metabolic panel with liver function tests, thyroid function tests, urinalysis, toxicology screen, and arterial blood gas. www.anesthesiaclinics.com
Surgery and Neurological Disease
Table 1.
’
169
Major Causes of Acute Coma
Primary brain injury With/without localizing motor deficits Intracerebral hemorrhage Middle cerebral artery occlusion Brain tumor Cerebral abscess Traumatic brain injury Status epilepticus Subarachnoid hemorrhage Without localizing motor deficits Bilateral thalamic infarcts Cerebral venous thrombosis Encephalitis Gliomatosis Cerebral edema Cerebellar stroke Hypoxemic ischemic encephalopathy Subclinical status epilepticus With localizing cranial nerve deficits Basilar artery occlusion Brainstem hemorrhage Central pontine myelinolysis Systemic insults causing brain dysfunction Electrolyte derangements Hyponatremia 165 mg/dL Hypercalcemia >13 mg/dL Endocrine abnormalities Acute hypothyroidism Addison’s disease Acute panhypopituitarism Poisoning, illegal drug use Opioids Anticholinergic drugs Carbon monoxide inhalation Other metabolic derangements Hypothermia 12 h) can lead to cerebral CBV, and ICP ischemia, poor outcome ICP monitoring and CSF Risk for ventriculitis and CSF drainage overdrainage. During its placement an ICH or IVH may occur May worsen cerebral edema, Enlarges the intracranial possibly associated with space, allowing the swollen cerebral hyperemia as a cerebral hemisphere or result of elevated CPP and cerebellum to expand out of impaired cerebral normal cranial limits while autoregulation. Increases avoiding brain herniation cerebral inflammation and and brainstem compression. risk for brain infection Improves cerebral compliance and reduces ICP
CBV indicates cerebral blood volume; CPP, cerebral perfusion pressure; CSF, cerebrospinal fluid; ICH, intracerebral hemorrhage; ICP, intracranial hypertension; IVH, intraventricular hemorrhage.
www.anesthesiaclinics.com
Surgery and Neurological Disease
’
173
Only half of all patients presenting in shock will be volume responsive, in terms of increasing their cardiac output in response to a fluid challenge.17 Therefore, when there is not a favorable response to a fluid challenge, other causes of hypotension must be entertained, like neurogenic, anaphylactic, cardiogenic, or obstructive shock (massive pulmonary embolism). It is essential to consider the possibility of hemorrhagic shock in the postoperative period. Patients undergoing endovascular procedures are at an increased risk of vascular injury and a retroperitoneal hematoma. Administering fluid resuscitation in a patient with massive vascular injury before reversing the vascular defect only increases mortality by causing arterial pressure to rise, which increases bleeding and promotes further exsanguination.18 Thus, surgical management of the vascular defect should be prioritized. The administration of blood products is critical in these patients with transfusion of red blood cells, plasma, and platelets in approximately 1:1:1 or 2:1:1 ratio to optimize hemostatic mechanisms. The best vasoactive drug for shock depends on the indication. In general, norepinephrine is superior to dopamine for the treatment of shock.19
’
Electrolytes and Fluid Management in Acute Brain Injury
Abnormalities in electrolytes and fluid regulation are common in postoperative patients with acute brain injury, and these patients may tolerate these disorders poorly as they may already have cerebral edema and poor intracranial compliance from the primary brain injury. Hypoosmolarity and hypovolemia are deleterious in patients with acute brain injury and can worsen cerebral edema and ischemia.20 Hypo-osmolality should be avoided. As sodium is the major determinant of serum osmolality, and hence the major determining force affecting water translocation across the blood-brain barrier, a fundamental principle is to maintain sodium at least within the normal range of 135 to 145 mmoL/L.21 Hyponatremia (sodium 40 mEq/L). Assessing the volume status is the best way www.anesthesiaclinics.com
174
’
Rivera-Lara and Mirski
to distinguish them; patients with SIADH are euvolemic or hypervolemic and patients with CSW are hypovolemic. Hyponatremia should be aggressively corrected in the postoperative period of patients with acute brain injury; however, caution should be paid in patients with chronic hyponatremia developing over at least 48 hours as its rapid correction, currently considered to be if >5 to 10 mEq/d, will put the patient at risk for osmotic demyelination causing quadriplegia, coma, and pseudobulbar palsy. The management of SIADH is with fluid restriction and avoidance of free water or hypotonic fluids. The treatment of CSW is with repletion of salt and fluid to achieve normal sodium and fluid balance. Hypertonic saline, salt tablets, and fludrocortisone are options that can be implemented according to the clinical condition of the patient and sodium levels. One of the frequent causes of hypernatremia in the postoperative state is central diabetes insipidus, which is a feared complication of endoscopic pituitary surgery. Central diabetes insipidus occurs when ADH fails to be released from the hypothalamic-pituitary axis. The diagnosis is made when the patient has a sodium Z145 mmoL/L, urinary output Z250 mL/h in 2 consecutive hours and a dilute urine with a specific gravity r1.005. The treatment includes correction of the water deficit and administration of vasopressin or desmopressin. Additional electrolyte derangements include hypokalemia, which can cause rhabdomyolysis, muscle weakness, and cardiac arrhythmias. Hyperkalemia may cause arrhythmias and muscle weakness and can also alter the conduction system. Peaked T waves and shortened QT interval precede PR and QRS interval widening. Conduction abnormalities include bundle branch and atrioventricular blocks; p-wave disappearance may be followed by asystole. Hypocalcemia is frequently found in patients that were massively transfused with blood products in the operating room. Clinical manifestations of hypocalcemia include QT interval prolongation, tetany, seizures, and hypotension. Hypomagnesemia causes weakness and polymorphic ventricular tachycardia with prolonged QT interval. Therefore, electrolyte derangements can cause significant complications and should be aggressively corrected.
’
Prevention of Postoperative Neurological Injury. Which Patients are at Increased Risk?
It is specifically important to attempt to prevent neurological damage as it is most often irreversible and can lead to devastating patient disability. The key to prevention is to identify patients at increased risk and to act quickly at the mildest sign of a neurological deficit. Well-established patient factors for increased risk of complications after neurosurgery include increased age, multiple comorbidities, and www.anesthesiaclinics.com
Surgery and Neurological Disease
Table 3.
’
175
Risk Factors for Perioperative Neurological Morbidity
Preoperative Old age Obesity Multiple comorbidities Need for anticoagulation Hypertension Diabetes
Intraoperative Prolonged surgery (> 2 h) Excessive blood loss during surgery (> 1 L) Massive resuscitation Emergent surgery
history of hypertension, diabetes, and obesity.22,23 Intraoperative risk factors associated with increased postoperative morbidity include prolonged surgeries (> 2 h), excessive blood loss during surgery (> 1 L), and the need for massive resuscitation.24 Risk factors for postoperative respiratory failure include obstructive sleep apnea, obesity, chronic obstructive pulmonary disease, and smoking (Table 3). Patients who required anticoagulation to decrease their risk of stroke from atrial fibrillation, mechanical heart valves, etc. and have their anticoagulation withheld for the surgical procedure are at an increased risk of perioperative stroke. Therefore, anticoagulation should be withheld only as long as the type of surgical procedure indicates. Prediction of which patients are at risk for postoperative complications will allow for the implementation of risk reduction strategies and individually tailored management approaches including the selection of the most appropriate care setting for postoperative monitoring. ’
Conclusions
Postoperative morbidity continues to thwart the quality of recovery in patients undergoing neurosurgery. Neurological surgical morbidity affects significantly the quality of life and life expectancy of a patient. This chapter has focused on the secondary insults that must be watched and managed to mitigate postoperative adverse outcomes and mortality.
The authors declare that they have nothing to disclose.
’
References
1. Suarez JI, Zaidat OO, Suri MF, et al. Length of stay and mortality in neurocritically ill patients: impact of a specialized neurocritical care team. Crit Care Med. 2004;32: 2311–2317. 2. Mirski MA, Chang CW, Cowan R. Impact of a neuroscience intensive care unit on neurosurgical patient outcomes and cost of care: evidence-based support for an intensivist-directed specialty ICU model of care. J Neurosurg Anesth. 2001;13:83–92. www.anesthesiaclinics.com
176
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