The Younger Patient

There are several modified versions of the Glasgow Coma Scale for application to infants and children ( Tables 44.2, 44.3, 44.4, 44.5, 44.6 ).12–16 There is no consensus opinion recommending one system over another, and the pediatric scales are likely subject to more intraobserver variability than is the adult scale. The neonate and infant can be observed for spontaneous facial and limb movements, eye opening and extraocular muscle function, respiratory pattern, and vocal output. With respect to motor function, the detection of asymmetry is the most important abnormal finding, alerting the clinician to a possible hemiparesis.17 Responses can be elicited with tactile or noxious stimuli, and the character of cry can also be assessed. Pupillary response and other brainstem reflexes can be tested. The ability to palpate an open fontanel cannot be overemphasized as a means of directly and rapidly providing a gross clinical assessment of intracranial pressure (ICP), with descriptions such as “flat,” “soft,” “full,” “bulging,” or “tense” being often utilized. Table 44.7 lists several findings that may be considered abnormal in older children and adults but normal in patients younger than 2 years of age.

The Older Patient

The neurologic assessment of older children and adolescents follows that used with adults. Typically, the level of alertness is assessed first, concurrent with notation of the presence or absence of spontaneous or purposeful movements. If they eyes are not spontaneously open, the ability of the patient to open his or her eyes to vocal or noxious stimuli is observed. Orientation and verbal responses are then gauged. The ability to follow commands can be graded, with a midline command (e.g., tongue protrusion) considered simpler or more primitive than a lateralizing command (e.g., the showing of two fingers). Having the patient touch the opposite ear with a specified finger, such as the thumb, is useful as a more complex three-step midline-crossing command. If the patient is not conscious, testing of the brainstem reflexes, including pupillary response and corneal and gag reflexes, is mandatory. Likewise the motor response to noxious stimuli and assessment of long-tract signs, including tone and deep tendon and plantar reflexes, is basic to the evaluation of an unconscious patient. The Glasgow Coma Scale can be useful under these conditions ( Table 44.3 ). Though initially validated as a prognosticator for head-injured patients,12,13 the scale has found widespread utility in the evaluation of neurologically compromised patients regardless of etiology.

Often the postoperative neurologic examination is tailored to the surgery performed. The examiner may pay closer attention to tests for ataxia, dysarthria, voice quality, and tongue deviation in patients who have undergone posterior fossa surgery. The visual fields may warrant closer inspection after cases of suprasellar or hypothalamic tumor surgery, whereas after supratentorial tumor resection the examiner may focus more on tests of motor function. In all cases, it is the early detection of neurologic deterioration through regular examination that offers the patient the best chance of optimizing outcome ( Table 44.7 ).

Temperature

Younger patients can experience wide fluctuations in core temperature; esophageal or rectal probes are commonly used. Both elevated and depressed temperatures can affect the level of consciousness and the neurologic exam, and patients with compromised cerebral function are likely more sensitive to these changes ( Table 44.8 ).18 The definition of hypothermia varies from source to source, ranging from below 32.2°C19 to 35°C20 to any temperature significantly below 37°C.21 It may occur following general anesthesia, especially after prolonged surgery, and is seen commonly, with untoward effects resulting if the problem is not addressed. Prolongation of emergence secondary to hypothermia can delay the subsequent detection of a deficit; shivering and rewarming can increase oxygen consumption and potentially exacerbate an hypoxemia; and the pressure of air trapped intracranially can increase as the air warms.22 Arrhythmias, dehydration, and lactic acidosis can also result if hypothermia goes untreated.23 Hypothermia can also be seen with posterior hypothalamic dysfunction following resection of tumors near this region, such as gliomas or craniopharyngioma,19,22,24 or as a syndrome associated with agenesis of the corpus callosum (Shapiro syndrome).25 Therapy generally consists of use of heat lamps, blankets, humidified oxygen, and, if necessary, warmed intravenous fluids. Hypothermia is one of the major causes of postoperative morbidity in infants and neonates and as such is aggressively treated as outlined.

Postoperative fevers in children are common. Temperatures above 38.5°C often occur within the first 24 to 48 hours after surgery, typically a self-limiting stress-induced pyretic response. Though commonly attributed to atelectasis, and there is some controversy regarding this contention,26,27 a diagnostic workup during this period is generally of low yield. There is little agreement and wide variation in the literature as to the incidence of postoperative fever, ranging from 14 to 91%.28 An incidence of 73% and 76% has been reported after pediatric orthopedic and craniosynostosis surgeries,29,30 respectively, and as high as 82% after hemispherectomy. A true infectious source was found in only 1 to 6%,29–31 though up to 14% in the immunocompromised postsurgical child.32 A survey of nosocomial infection in the PICU found bloodstream, pulmonary, urinary tract, and surgical sites to be the predominant sources.33 Meningitis is always a concern in the postoperative patient for whom another source cannot be found, and the workup may eventually lead to a lumbar puncture for cerebrospinal fluid (CSF) evaluation. Drug-induced fever by phenytoin is a well-known phenomenon,19,34 usually diagnosed by exclusion, as is tumor fever.26 Fevers secondary to anterior hypothalamic dysfunction (neurogenic or central) are usually high, approaching 40°C.19 The postictal state is also commonly associated with elevated temperature.

Recent studies in pediatric traumatic brain injury have found that fever increased both length of stay and risk for lower hospital discharge Glasgow Coma Scale score.35,36 Fever can negatively affect the neurologic status of a patient, even leading to coma if greater than 42°C,37 and is known to increase CO₂ concentration and cerebral blood flow (CBF), which can exacerbate increased ICP.38,39 Hence, a search for a treatable source is typically initiated, guided by clinical status and the timing of fever onset relative to surgery. Every attempt should be made to aggressively lower the temperature below 38.5°C23 with cooling blankets or more aggressive measures, if antipyretics and source-specific treatment plans are not effective.

Heart Rate and Blood Pressure

Close continuous monitoring of the heart rate and arterial blood pressure is absolutely essential in the postoperative patient. Changes can indicate a physiological response to several potentially dangerous situations, prompting imaging studies, more invasive monitoring, or therapeutic interventions. Therefore, fluctuations must be correlated with the clinical status to help determine the best course of action. The development of sinus tachycardia may result from inadequate analgesia, agitation, fever, hypovolemia, or increased ICP.40,41 Primitive cardiovascular autonomic control in infants and young children translates to a predominance of parasympathetic tone and decreased sympathetic tone.40 This can result in an exaggerated vagotonic response and reflex bradycardia in several situations, including hypoxia, laryngotracheal stimulation, gastroesophageal reflux, as well as increased ICP as part of the Cushing reflex ( Table 44.9 ).

The combination of hypertension and bradycardia, along with irregular respiration, in association with increased ICP, was described by Cushing at the turn of 20th century.42,43 In the postoperative setting, these signs should raise concerns about the possibility of an expanding intracranial mass lesion, such as hemorrhage or edema. Local pressure on the brainstem may also manifest in a Cushing reflex, as later work demonstrated the reflex to be secondary to pressure-sensitive areas in the dorsal brainstem at the pontomedullary junction, along the floor of the fourth ventricle.44 In children, the hypertension component of the reflex may be absent or not clinically obvious, and brady-cardia alone should likewise raise suspicions of increased ICP.19 Similarly, isolated hypertension in the absence of bradycardia has also been noted in children with high ICP.45

Although hypertension most commonly occurs secondary to pain, it should be controlled because the risk of hemorrhage into the tumor resection bed is increased with higher pressures. Simple maneuvers, such as analgesia or sedation, may be successful, and acetaminophen with or without codeine is usually sufficient. If sedating agents are used, they should be reversible (e.g., morphine). However, the use of antihypertensive agents may be necessary. This may not be straightforward in a patient with increased ICP because overly aggressive lowering of the pressure may compromise cerebral perfusion. Adrenergic receptor antagonists, such as labetalol, are often preferred over direct vasodilators, such as nitroprusside, as the latter may negatively affect ICP.46 Continuous labetalol infusion has been found to be safe and efficacious in the management of hypertensive crisis in children under 24 months of age.47 Infusions of calcium channel antagonists, such as nicardipine and clevidipine, are also particularly effective in the pediatric population at providing controlled hypotension during surgery as well as management of hypertension after surgery.48,49

Hypotension must quickly be corrected to avoid compromise of systemic and cerebral perfusion. Loss of blood must be ruled out as an etiologic factor ( Table 44.10 ). Although ongoing, hemodynamically significant blood loss after brain tumor surgery is rare, inadequate resuscitation from intraoperative blood loss is one of the most common causes of serious morbidity and even mortality in young postoperative patients. In procedures with significant blood loss, the hematocrit is measured immediately following surgery, and usually every 6 hours for the next 24 hours. It is difficult to resuscitate a patient once the hematocrit falls below 17%. Additional causes of hypotension in the postoperative patient include fluid depletion and hypovolemia, which can result from diuretic or mannitol use during treatment for increased ICP; diabetes insipidus (DI) following resection of tumors near the pituitary gland; vasodilatation secondary to fever or sepsis; and adrenal insufficiency secondary to inadequate exogenous glucocorticoid coverage. The latter occurs in steroid-dependent patients who are unable to mount an appropriate perioperative stress response.50

Knowledge of the blood pressure is crucial in the management of increased ICP and cerebral perfusion. Cerebral perfusion pressure (CPP) is the difference between the systemic mean arterial blood pressure (MAP) and ICP:

CPP = MAP – ICP

Thus, it can be appreciated how fluctuations in blood pressure can affect the CPP and, through complex interactions soon to be discussed, the ICP as well. Therapeutic modalities aimed at manipulating these interactions are increasing, and blood pressure will likely take on even greater significance as our sophistication increases.

Respiratory Rate

Following resection of a brain tumor, patients may experience depressed respiratory drive secondary to pharmacological influences or central impairment of brainstem autonomic centers. The resultant hypercarbia and hypoxemia can increase cerebral blood volume (CBV) and CBF and potentially increase ICP.45,51 So-called pneumotactic nuclei within the pontine tegmentum appear to coordinate respiration and circulation.52,53 Compression syndromes here may contribute to a decline in respiratory function.52 The main areas of autonomic coordination of inspiration and expiration are within the reticular formation of the medulla oblongata.52,53 Sudden mass effect on these medullary centers, as in a cerebellar hemorrhage following posterior fossa surgery, can cause sudden respiratory standstill without warning.52

Hyperventilation can be associated with fever and sepsis, anxiety, drugs, and brainstem lesions. Theories include interference with cortical inhibitory influences normally exerted on the brainstem respiratory centers,54 and stimulation of these centers by either drugs54 or local pH changes secondary to brainstem tumor metabolism.55,56 The therapeutic use of hyperventilation and hypocarbia to vasoconstrict cerebral arteries, decrease CBV, and therefore lower ICP has long been known. However, there is a rationale for avoiding hyperventilation in the tachypneic patient and intervening as necessary. The danger of prolonged hyperventilation is attributed to the ability of the cerebral vasculature to adapt to the chronically low arterial partial pressure of carbon dioxide (PaCO₂) and eventually vasodilate back to the baseline vessel diameter despite the low PaCO₂.57 If the lower PaCO₂ is elevated back to normal, the vessels will react to the “new” hypercarbic stimulus and vasodilate further. This increases CBV and ICP.51

Historically, certain classic changes in respiratory patterns were used to help localize lesions in the brains of comatose patients ( Table 44.11 ). In the postoperative setting they would indicate serious neurologic decline if acute. Cheyne-Stokes respirations follow a crescendo-decrescendo hyperventilation pattern interspersed with apnea, the result of abnormally heightened dependence on CO₂ drive. It always implies bilateral damage, seen with widespread cortical injury, such as infarctions, deeper thalamic dysfunction (most likely),55 or any bilateral descending pathway disturbance from forebrain to upper pons. Metabolic disturbance can underlie the pattern, and it may provide a warning of impending transtentorial herniation.37

The following patterns can occur with brainstem injury, such as expanding posterior fossa lesions. Apneustic breathing is characterized by long end-inspiratory pauses, possibly alternating with prolonged end-expiratory pauses. Damage is localized to the mid- or caudal level pons, specifically to the pneumotactic centers involved with the coordination of respiration mentioned earlier.14 Cluster breathing appears as clusters of breaths with brief apneic pauses in between. It may result from low pontine or high medullary lesions.55 Ataxic breathing has a completely irregular pattern of deep or shallow inspiratory gasps with intermittent apnea. It is seen in agonal patients, heralds complete respiratory failure, and indicates damage to the dorsomedial aspect of the medulla.37,55

Respiratory irregularities can aid in the early identification of problems with airway maintenance, which may be compromised in any patient with a depressed level of consciousness. The tongue may fall back against the pharynx and partially or completely occlude the airway. Lower cranial nerve dysfunction after brainstem tumor surgery can also compromise airway integrity in terms of swallowing difficulties.22 Oropharyngeal or nasopharyngeal airways may avoid intubation in patients with partial airway obstruction, but concerns about aspiration may yield to endotracheal intubation.58 Such decisions should be individualized to the patient and overall clinical status, keeping in mind that, after blood loss and hypothermia, aspiration is the next greatest cause of morbidity in pediatric postoperative patients. Arriving at a diagnosis entails, in succession, direct observation, obtaining worsening arterial blood gas values and relative hypoxemia, and noting the development of fluffy infiltrates on chest radiographs, more commonly on the right side if unilateral.59

Indications

There are several indications to monitor ICP following surgery for brain tumors, most based on the premise that increases are detectable prior to the development of neurologic symptoms and signs45 ( Table 44.14 ). If the child required ICP monitoring prior to surgery, the monitor should be left in place postoperatively until normalization of ICP is verified. Likewise, if a child did not require an ICP monitor preoperatively, then it is usually not necessary to place one after uncomplicated supratentorial or infratentorial tumor surgery. However, observations of brain swelling intraoperatively or concerns regarding the risk of brain swelling due to prolonged retraction for example should lead to ICP monitor placement prior to leaving the operating room. Inability to reliably follow the neurologic status of a child requires ICP monitor placement. This may be secondary to prolonged surgery and inability to extubate, or to a requirement for heavy sedation or paralysis. Mechanically ventilated patients with high mean airway pressures, raised not only by positive endexpiratory pressure (PEEP) but also by peak airway pressure or inspiratory time, can transmit pulmonary pressures to the CSF column (via the vertebral venous plexus) and to the jugular vein (through the superior vena cava).81 These patients are at risk for development or exacerbation of increased ICP and should be monitored. ICP should also be followed in patients who deteriorate neurologically, especially if found to have edema on CT.

Position and Elevation of Head

The effectiveness of this simplest of maneuvers in lowering an increased ICP has long been known. The effect is so rapid that a brief lowering of the head of the bed is frequently done to ensure that a recently placed ICP monitor is functioning properly. The rationale is that facilitating cerebral venous outflow into the systemic circulation lowers cerebral venous blood volume and therefore reduces ICP. Likewise, jugular venous outflow can be impeded by head rotation; therefore, a neutral midline position should always be maintained, and the use of constricting endotracheal tube tape should be avoided.101–103

However, concerns regarding the possibility of head elevation causing a decrease in CPP have been raised. Several studies have not found a significant drop in CPP unless the head is elevated more than 30 degrees,104,105 whereas others have provided evidence that CPP is maximal when patients are flat (zero degrees) despite a higher ICP in this position.106,107 In addition, the ICP will increase in up to one third of adults when the head is elevated, likely due to activation of the vasodilatation cascade as a result of decreased CPP.51 A study that measured CBF concluded that head elevation to 30 degrees reduced ICP in the majority of patients without significantly compromising mean CPP or CBF, yet a significant decrease in CBF occurred in 23% of patients.108 Some groups therefore favor the supine position due to the belief that it optimizes CPP.109 Others have suggested that optimal head positioning should be established individually in patients with high ICP owing to an unpredictable response.110

There are few objective data addressing this issue specifically in children. In one study, newborn infants had significantly lower ICP at 30 degrees, as compared with the flat or dependent head positions.111 We currently maintain a head elevation of 30 degrees in postoperative patients at risk for or with evidence of increased ICP, while recognizing that decreases in blood pressures are less likely in patients with adequate volume status. Head-of-bed elevation has also been implemented in care bundles shown to reduce the incidence of ventilator-associated pneumonia in pediatric ICU care.112