Neurologic Injury: Prevention and Initial Care



During the evaluation and observation of the TBI patient, repeated neurologic monitoring includes the vital signs with special attention to extremes in blood pressure. Hypotension may result in secondary injury, whereas hypertension, not always associated with bradycardia, can be a sign of impending cerebral herniation. If ICP rises, cerebral autoregulation elevates MAP to maintain an adequate CPP.


A rapid neurologic assessment includes level of consciousness and ability to speak or understand language by assessing the ability to follow simple commands or to at least mimic clear hand signals. The GCS score (Table 117.1), first developed and introduced in 1974 to help monitor the depth and duration of impaired consciousness, provides a standard, rapid, and reproducible score utilizing eye opening, verbal output, and motor movement (68). The severity of head injury based on the GCS has been divided into three categories: (i) Mild or minor: GCS 13 to 15; (ii) Moderate: GCS of 9 to 12, and (iii) Severe: GCS of 8 or less. Interrater variability is usually minimal, but can exist (69).


A patient’s best GCS score following adequate fluid resuscitation and stabilization is predictive of outcome (70). A GCS of 3, reflecting no eye opening or motor movement to pain and no verbal output, has a 65% mortality compared to mortality of 10% to 15% in patients with a GCS of 7 to 13 (71). Additionally, when measured repetitively without effects of pharmacologic sedation or hemodynamic or pulmonary instability, a decreasing score can portend poor outcome (71,72).


Vision is assessed by asking the patient to count fingers placed in the right or left visual field with one eye covered, or to mimic finger movements. In patients with a lower level of consciousness, vision is assessed by blinking to a visual threat. Pupillary response to light (cranial nerves [CN] II, III), corneal reflex (CN V, VII), and gag and cough (CN IX, X) responses assess cranial nerve and brainstem function. Oculocephalic maneuvers (CN III, VI, VIII) should not be performed in patients who have a risk of cervical spine fracture. Ice water caloric response (CN III, VI, VIII) can be performed if the tympanic membranes are intact: the head of the bed (HOB) should be kept at 30 degrees, and 60 to 90 mL of ice water is instilled into the otic canal. A normal response is a slow lateral deviation to the side stimulated with ice water and nystagmus with the fast phase to the opposite side; absence of this response may be caused by medications or brainstem injury.


Motor response is assessed by verbal commands to move the limbs. In patients with lower levels of consciousness, motor responses are elicited by painful stimuli delivered to the sternum or fingernail bed. During painful stimulation, the examiner should also reassess facial movement for asymmetry. If flexion is noted, pain is applied to the supraorbital ridge or by trapezius squeeze to test for localization. In the lower extremities, it is important to recognize a triple flexion response, which is described by the flexion of the ankle, knee, and hip. The triple reflex is a spinal reflex to painful stimulation of the legs or feet. It is stereotyped in appearance, independent of the location of pain delivery on the lower extremity, and does not reflect brainstem or upper spinal cord function. Patients who are brain dead or who have higher complete spinal cord lesions can triple-flex lower extremities.


Laboratory evaluation of patients with head injury includes complete blood count with platelet counts, activated partial thromboplastin time (aPTT), prothrombin time (PT), electrolytes with blood urea nitrogen, creatinine, glucose, and liver function tests to assess for liver dysfunction which may impair clotting ability. Thrombin time or ecarin clotting time has recently been added by some to trauma-related admission panels due to new oral anticoagulants that are not reflected by the PT and aPTT (73). A toxicology screen including a blood alcohol level is essential to assist in evaluating for other causes of altered mental status and to determine whether delirium tremens may be a factor in the following days of ICU care. Arterial blood gas (ABG) and lactic acid levels help assess volume status and whether ventilation is adequate.


Imaging

The initial imaging, often coupled with the neurologic examination, determines the need for acute neurosurgical intervention. Neurosurgical guidelines have been established for focal intracranial lesions (74–76). Noncontrast head CT is the fastest, most widely available noninvasive imaging technique to determine this. All patients with altered mental status and/or focal neurologic findings should have an initial CT scan performed. In minor head injury, a CT scan may not be necessary if the examination is normal and the GCS is 15, unless the patient is older than 60 years, has a headache, emesis, drug or alcohol intoxication, deficits in short-term memory, physical evidence of trauma above the clavicles, coagulopathy, or seizures (77).


Evolving Injury and Repeat Head CT

Progressive intracranial hemorrhage consistent with an evolving contusion is seen in 14% to 38% of patients (57,78,79). Although worsening CT findings does not necessarily require treatment, up to 54% of patients may require neurosurgical intervention including ICP monitoring or craniotomy subsequent to the findings on a repeat scan (53,80–85). A significant risk factor is early initial imaging within 2 hours of injury (54,78,85,86). Often community standards are to repeat a CT scan within 12 to 24 hours of the initial imaging.


In stable patients without clinical neurologic deterioration, the utility of repeat imaging is debated and many believe it is unnecessary since it is unlikely that neurosurgical intervention will be required (54,82,85,86). Other independent risk factors for progression include associated tSAH, SDH, older age, and prolonged partial thromboplastin (53,57,78,85,86). A large initial contusional or IPH size and effacement of cisterns are strongly predictive of failure of nonoperative management (57).


TREATMENT


Following immediate impact and anatomic damage, secondary damage at the cellular level from inflammation, edema, free radicals, and excitatory neurotransmitters can worsen outcome. Contributing factors include hypoxemia, hypotension, seizures, fever, and intracranial hypertension. Immediate postinjury care focuses on the prevention of these problems.


Hypoxemia and Respiratory Management

Hypoxemia, defined as a PaO2 less than 60 mmHg or O2 saturation less than 90%, can independently increase mortality from 27% to 50% and increase poor outcome from 28% to 71% (87,88). Early intubation can prevent aspiration and minimize hypoxic and hypercapnic events (89), and is recommended by the Eastern Association for the Surgery of Trauma (EAST) (90), Advanced Trauma Life Support (ATLS) guidelines from the American College of Surgeons (91), and the Brain Trauma Foundation Traumatic Brain Injury prehospital guidelines (92). A GCS of 8 or less is the usual threshold for endotracheal intubation.


There are caveats to intubation of which the practitioner should be aware. In the prehospital setting, rapid sequence intubation has been associated with increased mortality (93–95). This may be a result of decreased cerebral perfusion due to hyperventilation-induced hypocapnia. Positive pressure ventilation may cause hypotension in a hypovolemic patient if central venous return is impeded by high intrathoracic pressures (96). Intubation is a high-risk procedure which may cause secondary neurologic injury. Sedative/hypnotic medications and bag/mask ventilation with positive pressure ventilation contribute to hypotension and hypercapnia and hypocapnia, respectively, during induction. In addition, direct laryngoscopy causes a marked, transient increase in ICP. Intravenous lidocaine may blunt this ICP response (97,98).


Hyperventilation with resultant hypocapnia causes cerebral vasoconstriction and a reduction in CBF (99–101). Prolonged hypocapnia appears to slow neurologic recovery (102). Prophylactic hyperventilation of PaCO2 less than 35 mmHg should be avoided, although PaCO2 as low as 30 mmHg may be necessary for brief periods for immediate treatment of intracranial hypertension. Options to identify cerebral ischemia in the setting of hyperventilation include the use of jugular venous oxygen saturation, arterial jugular venous oxygen content differences, brain tissue oxygen monitoring or CBF monitoring (103).


To achieve adequate ventilation, positive end-expiratory pressure (PEEP) may be necessary. PEEP affects CPP and ICP when the lung is compliant and the chest wall is not. The high lung compliance allows for an increased intrathoracic volume which, in the setting of a low compliant chest wall, increases intrathoracic pressures. The high intrathoracic pressure decreases cerebral venous outflow, which will increase ICP (104,105). Additionally, if intrathoracic pressure is elevated, cardiac venous return is diminished and results in lowered MAP and CPP.


Pulmonary infections were seen in 41% of patients registered in the TCDB and were an independent predictor of unfavorable outcome (106). Bedside management includes adequate pulmonary toilet and strategies such as elevation of the HOB to decrease the risk for ventilator-associated pneumonia (VAP). In patients with intracranial hypertension, during endotracheal suctioning, adequate sedation is necessary to prevent an increase in ICP (107).


Neurogenic Pulmonary Edema

In addition to hypoventilation and aspiration from poor airway protection, a less frequently recognized cause of hypoxemia following TBI is neurogenic pulmonary edema (NPE) (108), resulting from central sympathetic stimulation. Pretreatment with adrenergic-blocking agents prevents experimental NPE (109). Experimental lesions in the hypothalamus (110), bilateral nucleus tractus solitarius (111), and the ventrolateral medulla (112) can produce NPE. TBI causes a sympathetic discharge, which increases systemic and pulmonary vascular pressures; the resultant increase in pulmonary capillary pressure increases the hydrostatic pressure and causes pulmonary capillary injury. This, in turn, causes leakage of fluid and protein and pulmonary hemorrhages (113–115).


Clinical signs include dyspnea, tachypnea, tachycardia, and chest pain if the patient is awake; rales are present on chest auscultation. Laboratory results show hypoxemia and a mild leukocytosis, with chest radiograph showing a bilateral alveolar filling process (116). Pulmonary capillary wedge pressures and pulmonary artery pressures can be elevated or normal. There are two distinct forms of NPE: the classic form appears early, within minutes to a few hours after acute brain injury; a delayed form of NPE slowly progresses over 12 to 72 hours following injury. Treatment is supportive and often requires supplemental oxygen and positive pressure ventilation. Dobutamine may be effective by decreasing cardiac afterload and increasing cardiac contractility (117).


Hypotension

Hypotension, defined as SBP less than 90 mmHg, independently worsens mortality (118,119). The TCDB reports hypotension was present in 29% of patients and doubled mortality from 27% to 55% (106,118). In patients whose SBP were less than 90 mm Hg, mortality was 65% independent of age, admission GCS motor score, hypoxia, or associated severe extracranial trauma. Adequate fluid resuscitation with euvolemia is essential. Independent of ICP, MAP, or CPP, a negative fluid balance of approximately 600 mL was associated with poorer outcome (120). Guidelines recommend adequate fluid resuscitation and have been updated to recommend SBP 100 mm Hg or greater in patients 50 to 69 years old and 110 mm Hg or greater in patients 15 to 49 or greater than 70 years old. Blood pressure support to maintain SBP greater than 90 mmHg (67). Once an ICP monitor is placed, the optimal blood pressure is determined by that required to keep the CPP 60 to 70 mmHg (67).


Contraction Band Necrosis

Following head trauma, SAH, seizures, or stroke, patients may have cardiogenic shock with global hypokinesis associated with transient cardiac dysrhythmias and repolarization changes (121–124). Dysrhythmias may include supraventricular tachycardias, sinus bradycardia, atrioventricular (AV) block, AV dissociation, nodal rhythms, and paroxysmal ventricular tachycardia. These changes are cerebrally mediated and are recognized as myofibrillar degeneration (also known as contraction band necrosis [CBN] or coagulative myocytolysis). The histologic appearance of CBN contrasts to the coagulation necrosis seen with ischemic injury where there are cytoplasmic degenerative changes with cloudy swelling, hyaline droplets, and fatty change. With CBN, the myocardium instead shows loss of definition of the linear arrangement of myofibrils and the appearance of prominent dense eosinophilic transverse bands (contraction bands), and intervening granularity throughout the cytoplasm (125). This injury pattern was first described with pheochromocytoma and has been associated with the administration of catecholamines, including cocaine abuse (126,127). It is postulated that centrally mediated sympathetic or exogenous catecholamine stimulation of the myocardium results in cellular calcium overload and results in the formation of the contraction bands (128). CBN is predominantly located in the subendocardium with the cardiac conducting system, which results in the associated arrhythmias (129).


In CBN, cardiac enzymes are often elevated and may be difficult to differentiate from an acute coronary syndrome. However, the treatment for CBN is vastly different and typically includes observation for dysrhythmias and blood pressure support in contrast to reperfusion therapy with an acute ischemic myocardial infarction. Clinical differentiation typically relies on the recognition of patients with higher risk for coronary artery disease such as older age, hypertension, diabetes, and hyperlipidemia rather than a young patient with massive head injury.


Posttraumatic Vasospasm

Following TBI, posttraumatic vasospasm can occur in as many as 24% to 36% of adults and children (130–132) and causes focal ischemia with lateralizing neurologic deficits such as hemiparesis and aphasia between 2 to 37 days following injury (132–134). In patients with severe TBI, small studies have reported incidences as high as 82% (135). Explosive blast TBI is especially associated with early cerebral edema and cerebral vasospasm (136). Disruption of cerebrovascular tone may be a result of inflammatory and other vascular changes (137). Some mechanisms include an increased expression of an inducible isoform of nitric oxide synthase (138) and a hypercontraction-induced phenotypic switch that potentiates vascular remodeling (139). Transcranial Doppler, while reasonably specific, is not a sensitive test for vasospasm. If vasospasm is suspected, cerebral angiography can confirm the diagnosis. The effectiveness of treatment of posttraumatic vasospasm with modalities used following aSAH (e.g., hypervolemic, hypertensive therapy, or nimodipine) has not been assessed.


Hyperthermia

Hyperthermia accelerates neuronal injury by increasing basal energy requirements (neuronal discharges), excitatory neurotransmitters, free radial production, calcium-dependent protein phosphorylation, ICAM-1 and inflammatory responses, DNA fragmentation, and apoptosis, causing blood–brain barrier changes as seen by extravasation of protein tracers (140,141). Despite this, multiple TBI studies of prophylactic moderate hypothermia (32° to 33°C) and their meta-analyses have not shown improved outcome (142–144). This may be due to significant intercenter variability in the management of MAP, CPP, fluids, and vasopressors (145,146).


In the individual patient, therapeutic hypothermia lowers ICP by reducing the cerebral metabolic rate 7% for each degree Celsius decrease. This treatment can be lifesaving and result in reasonable neurologic recovery (144,147). Pentobarbital coma and/or neuromuscular blockade (NMB) may be necessary to achieve cooling without shivering. Various techniques for intravascular and topical cooling are available. Although complications of hypothermia can include increased risk of cardiac dysrhythmias, hypotension, bradycardia, thrombocytopenia, and pneumonia, in studies evaluating hypothermia in cardiac arrest patients, there was no statistical increase in these adverse events (148,149).


Hyperglycemia

Hyperglycemia can cause brain tissue acidosis (150), and early hyperglycemia has been associated with worsened neurologic outcome following TBI (151,152). Persistent hyperglycemia following severe TBI in one study was an independent risk factor of mortality with a 4.9 times increase in risk of death (153). It is not fully understood whether the hyperglycemia is causative or is a marker for severity of injury and subsequent poor outcome; however, control of hyperglycemia following TBI is theoretically reasonable.


In the ICU setting, where glycemic control often uses insulin infusion or injection, patients with acutely altered mental status should be urgently evaluated for hypoglycemia.


Coagulopathy

Brain is rich in tissue thromboplastin and following head injury, increased tissue thromboplastin activity in the frontal, parietal, and temporal lobes activates the coagulation cascade and causes a disseminated intravascular coagulopathy (DIC) (154). The TCDB reported that 19% of patients were coagulopathic (106). In children, the incidence of coagulopathy increased with worsening severity of head injury reflected by the head Abbreviated Injury Scale score and was as high as 40% (155). Although initial evaluation may show thrombocytopenia in 14% and coagulopathy in 21% of TBI patients, in ensuing days, DIC can be seen in 41% to 60% of patients with blunt brain injury (156,157). It is more common in patients with penetrating head trauma (158).


Abnormalities in PT, PTT, or platelet count have been associated with 55% of patients who have progressive intracranial hemorrhage after TBI (159,160). Associated coagulopathy and thrombocytopenia increases mortality in TBI (156,157,160,161). Some centers are using thromboelastometry and portable coagulometers to detect coagulopathy in the ED. Typically, fresh frozen plasma is transfused for an elevated aPTT or a PT international ratio (INR) of 1.5 or more. Current European guidelines for TBI patients recommend transfusion of platelets for values below 100,000 cells/μL or for patients receiving antiplatelet agents (162). Other alternatives such as activated factor VII or prothrombin complex concentrate (PCC) may be effective emergently (158); PCC is recommended in the European guidelines for emergency reversal of vitamin K-dependent and oral antifactor Xa agents such as rivaroxaban, apixaban, or edoxaban (162).


Intracranial Pressure Monitoring and Management

Normal ICP is less than 10 mmHg; the TCDB reports that 72% of patients with severe TBI had ICPs above 20 mmHg (163). Since multiple studies show worsened outcome with ICP above 20 to 25 mmHg, published guidelines use this as the threshold to treat (65).



FIGURE 117.1 Algorithm for management of intracranial hypertension. CI, cardiac index L/min/m2; pRBC, packed red blood cells; SR, suppression ratio.


Maneuvers for management of ICP begin with those with fewer potential side effects and progress to more invasive treatments with higher complication risk (Fig. 117.1). Elevation of the head of bed to more than 30 to 45 degrees not only decreases the risk of VAP but can facilitate cerebral venous drainage and lower ICP. In orthostatic, hypovolemic patients, however, head of bed elevation can lower MAP; adequate fluid resuscitation is necessary. Adequate pain therapy with opioids and adequate sedation with sedative-hypnotics decrease ICP. Constant infusion may be hemodynamically better tolerated than bolus administration. Prophylactic or sustained hyperventilation of PaCO2 less than 35 mmHg may be harmful and should be avoided (101–104). In the situation of impending herniation or refractory intracranial hypertension, decreasing PaCO2 to 30 mmHg for transient “rescue” therapy will give the practitioner time to initiate other maneuvers to lower ICP.


Osmotic therapy is a mainstay in ICP management. Mannitol and hypertonic saline are both effective (164–166). However, repetitive dosing by the above agents may eventually shift fluid into the injured brain across the damaged blood–brain barrier and thereby increase the volume of injured brain and elevate ICP (167–169). To avoid this, osmotic therapy, similar to hyperventilation, might be best used as rescue therapy until more definitive therapy is implemented. Doses of 0.25 to 1 g/kg of mannitol are effective. The lower dose drops ICP and may decrease the risk of vasogenic edema seen with multiple dosing (167). High serum concentrations of mannitol may cause renal failure. Maximal mannitol dosing traditionally has been when serum osmolarity reaches 320 mOsm/kg, but with the increased use of hypertonic saline, an osmolar gap is now being used. The difference of measured to calculated serum osmolarity is a surrogate marker for mannitol concentration as an “unmeasured” osmole. A rising osmolar gap of greater than 10 from baseline may be a better indicator of maximized mannitol administration (170,171). Hypertonic saline may be more effective and have a longer duration of action on lowering ICP than mannitol (169,172,173). Usual doses include 250 mL of 3% or 30 mL of 23% saline which have equimolar amounts of sodium chloride (174). The concentration used usually depends on volume status, with the lower volume 23% saline used when the patient is hypervolemic. Osmotic therapy is best administered through a central venous access as it may sclerose veins. When deciding which osmotic agent to use, elevated ICP with low fluid status would be best treated with hypertonic saline. Studies evaluating the prophylactic use of hypertonic saline compared to conventional fluids for prehospital or ED resuscitation have not shown outcome improvement (175,176).


NMB lowers ICP by decreasing muscle tone, especially during shivering. Shivering increases the metabolic rate and generates carbon dioxide. After administering NMB, an ABG analysis should be obtained to ensure that the PaCO2 has not dropped below 35 mmHg; minute ventilation should be adjusted accordingly. Rapid increases in PaCO2 may result in rebound vasodilation and ICP elevation. Ventilator manipulation should be performed in small increments when adjusting to increase the PaCO2. NMB also assists in cooling the patient. As noted above, hypothermia is useful in refractory intracranial hypertension. Temperatures of 32° to 33°C can be well tolerated. On a cautionary note, the combination of NMB and cooling appears to put the patient at high risk for pneumonia, as they are unable to effectively clear secretions; empiric pulmonary toilet with frequent suctioning is often necessary.


Barbiturate-induced coma, using either thiopental or pentobarbital infusion, lowers the cerebral metabolic rate; this results in lowered cerebral blood volume and ICP. Thiopental in long-term infusion, because of its lipophilicity, may take over a week to clear after the infusion is stopped. For pentobarbital, 20 mg/kg is given as a slow loading dose followed by a maintenance infusion of 1 mg/kg/hr; the loading dose may significantly lower MAP. Often fluids and vasopressor administration may be necessary. Electroencephalography (EEG) is critical to titrating the dose during barbiturate coma. Although the infusion can be titrated to ICP effect, once the EEG is isoelectric, there is little to be gained in the way of ICP control by increasing the infusion; at this point, worsening side effects result from increased drug. These include hypotension from peripheral vasodilation, decreased cardiac inotropy, and ileus; cough reflex is diminished and decreased bronchociliary activity and slowed leukocyte chemotaxis increase the risk for pneumonia. A benefit of barbiturate coma is a quiescent hypothalamus that no longer modulates body temperature. Hypothermia can often be achieved without the need for NMB since shivering is diminished.


Loop diuretics have been used to help manage ICP by decreasing CSF production in the choroids plexus (177). Loop diuretics will decrease volume status, thus unless the patient is hypervolemic, CSF diversion is a more effective method of lowering ICP.


Other therapy for refractory intracranial hypertension requires neurosurgical intervention. Placement of an EVD allows for CSF drainage. Hemicraniectomy may be life-saving and a viable option depending on the patient; case series of 19, 23, and 51 children at three different centers had mortalities of 30% to 31.4%. Favorable outcome with return to school and functional independence was reported in 68% to 81%; 18% to 21% were severely disabled and dependent on caregivers (178–180). In a randomized trial of adults with diffuse brain injury, early bilateral frontotemporoparietal decompressive craniectomy decreased ICP and the ICU length of stay, but was associated with worsened neurologic outcome (181).


Brain Tissue Oxygenation

To monitor and help prevent the secondary damage seen with hypoxic brain injury, new modalities to evaluate cerebral oxygenation have been developed. Jugular bulb oximetry (SjvO2) is a global measure of the balance between oxygen delivery to the brain and oxygen consumption. Local brain tissue partial pressure oxygen (PbtO2) can be measured either by a quenching process by fluorescence or by a polarographic Clark-type microcatheter. An increase in cerebral oxygen delivery is reflected by increases in SjvO2 and PbtO2. Oxygen delivery to the brain is manipulated by increases in blood pressure, cardiac output, and red blood cell transfusion (182). Normobaric hyperoxia has not shown to improve cerebral oxygen metabolism on PET imaging, and the use of 100% oxygen is not supported by the available literature (183). Optimal SjvO2 is generally accepted as 50% oxygen saturation (103,184). The optimal PbtO2 is not fully established but guidelines currently recommend higher than 15 mmHg (103). Various studies show worsened outcome in patients with mean PbtO2 less than 15 mmHg; other thresholds include 25 mmHg (185–188). Mortality was significantly decreased and functional outcomes improved in one study comparing 25 patients treated by traditional ICP/CPP-guided therapy to 28 patients with therapy targeted to a PbtO2 greater than 25 mmHg (189); however, other studies have not shown improvement in outcome (190–192). Cerebral microdialysis evaluating the biochemical byproducts of ischemia such as increased lactate and glutamate and lactate–pyruvate ratio is another potential technology to assist bedside care, but has not yet reached practical clinical use (193).


At the time of this writing, an evaluation of 31 adult neurocritical care units in the United Kingdom managing TBI patients showed that 100% of units followed ICP; 97% monitored CPP with 25 of 31 units using a CPP target of 60 to 70 mmHg; PbtO2 was utilized in 26% of units, cerebral microdialysis in 13%, and SjvO2 was used in only one unit (194). No unit was using near-infrared spectroscopy, a modality developed to measure cerebral oximetry as a measure of perfusion.


Antibiotic Prophylaxis

Fractures of the skull base and severe facial trauma can result in a CSF leak. Various studies report incidences of 2.6% to 4.6% of all patients with basilar or facial fractures (195,196). In one study, otorrhea was three times more common than rhinorrhea (195). Approximately 50% of CSF leaks stop within 5 days (197); the risk of bacterial meningitis is approximately 12% to 21%. Studies conflict as to whether prophylactic antibiotics decrease the risk of infection and meta-analyses suggest no benefit, hence, there are no guidelines or recommendations regarding antibiotics in this setting (197–199); constant surveillance for meningitis is essential.


In the setting of CSF leak, if the spine is stable and blood pressure is adequate, the HOB should be elevated to facilitate leak closure. Stool softeners help avoid vigorous Valsalva maneuvers that may worsen the leak. Neurosurgical intervention with CSF diversion (i.e., lumbar drain or EVD) or surgical closure may be necessary if the leak persists. Following penetrating head trauma, a CSF leak is the primary predictor of intracranial infection. Infection is seen in 38% to 63% of CSF leaks after military-related penetrating cerebral injury (200–202). Current recommendations advise treatment for 5 to 14 days with empiric broad-spectrum antibiotics immediately following penetrating brain injury (202–205).


For clean neurosurgical procedures, such as twist drill craniostomy for EVD or ICP monitor placement, burr holes, or craniotomy, guidelines have been established by the Surgical Infection Prevention and Surgical Care Improvement Projects that recommend an intravenous first-generation cephalosporin within 1 hour prior to surgical incision (206).


Posttraumatic Seizures

Early posttraumatic seizures occur within 7 days of injury; 3% to 6% of patients with closed head injury suffer early posttraumatic seizures, compared to 8% to 10% with penetrating brain injury (207–209). Late posttraumatic seizure by definition manifests at least 7 days postinjury and is seen in 30% of patients with penetrating brain injury; these late posttraumatic seizures may occur up to 5 years after injury. There is adequate evidence to recommend antiseizure medications, for example, phenytoin and carbamazepine, for the first week after closed and penetrating brain injury to prevent early posttraumatic seizures (210–213). Of note, valproate showed no benefit for seizures following brain injury and had a trend to higher mortality (214). Levetiracetam, compared to phenytoin, shows equal efficacy in post-TBI seizure prevention (215,216) and has fewer complications, such as hypotension, and does not require monitoring of therapeutic levels, although dosing should be adjusted in renal failure. There is no evidence that continuing prophylactic antiseizure medications beyond a week prevents late posttraumatic seizures, and it is not recommended for closed or penetrating head injury beyond 7 days of injury (210,213).


Thromboprophylaxis

In the general postoperative neurosurgical population, the risk for deep venous thrombosis (DVT) is 3% to 14% (217–220); following major head injury, the risk for DVT is as high as 54% (221). The BTF recommends the use of graduated compression stockings or intermittent pneumatic compression (IPC) stockings in combination with low–molecular-weight (LMWH) or low-dose unfractionated heparin (LDUH) with the warning that this may result in intracranial hemorrhage expansion; there were no specific recommendations for a preferred agent, dose, or timing of treatment (222). The American College of Chest Physicians (ACCP) 9th edition has similar recommendations for major trauma patients with TBI, ASCI, or spinal surgery for trauma (Grade 2C). The Neurocritical Care Society recommends initiating LMWH or UFH for VTE prophylaxis within 24-48 hours of presentation or 24 hours after craniotomy (223). If LMWH and LDUH are considered contraindicated, mechanical prophylaxis, preferably with IPC devices, should be utilized until the risk of bleeding diminishes and contraindication to chemoprophylaxis resolves (Grade 2C). Inferior vena cava (IVC) filters are not considered acceptable primary prophylaxis in trauma patients (Grade 2C) (220).


Nutrition

Following severe TBI, patients enter a hypermetabolic, catabolic state with rapid weight loss associated with a negative nitrogen balance and protein wasting. In experimental models of TBI, 3 hours after injury morphologic changes are seen in the gut mucosa that include shedding of epithelial cells, fracture of villi, focal ulcers, fusion of adjacent villi, mucosal atrophy, and edema in the villous interstitium and lamina propria. On electron microscopy, there is a loss of tight junctions between enterocytes, damage of mitochondria and endoplasm, and apoptosis of epithelial cells (224). These changes in gut permeability increase bacteria translocation and endotoxin, which increases the risk of the systemic inflammatory response; the amino acids arginine and glutamine modulate gut permeability.


Early parenteral or enteral nutrition within 24 to 72 hours can speed neurologic recovery and decrease disability and mortality (225–228). Early enteral feeding may have benefit over parenteral feeding by protecting against intestinal apoptosis and atrophy (229) and decreasing infection clinically (230). Early enteral nutrition with glutamine and probiotics may decrease the infection rate and length of ICU stay (231,232). There is some theoretical concern that glutamine should not be used in brain injury patients due to the potential increase in cerebral glutamate with neuroexcitatory properties and cell damage, although there are no data to date to support this concern.


Fasted TBI patients lose nitrogen at a rate that reduces weight by 15% per week. Replacement of resting energy expenditure (REE) by 100% to 140%, with 15% to 20% nitrogen calories may reduce nitrogen loss; therefore, BTF guidelines recommend that full (100% REE) nutritional replacement be achieved within 7 days after injury (233). An Institute of Medicine (IOM) report was more aggressive and recommended the provision of early (i.e., within 24 hours of injury) nutrition of more than 50% of total energy expenditure and 1 to 1.5 g/kg protein for the first 2 weeks after injury (232,234).


Stress Gastritis

Stress gastritis was seen in 91% of 44 comatose mechanically ventilated patients within 24 hours of head injury; lesions were most commonly seen in the fundus and body of the stomach (235). Mucosal ulceration is typically prevented by maintaining intraluminal pH above 5 or by H2 receptor blockade (236). In TBI patients, stress ulcer bleeding prophylaxis with proton pump inhibitors or H2 antagonists is recommended. Neither is recommended over the other, but the practitioner should be aware that one retrospective study in neurosurgery patients showed a statistically significant increased incidence of thrombocytopenia of 50 patients on famotidine compared to 98 of those not treated (34% vs. 11.2%) (237).


Prognosis

Survivors of TBI variably suffer from long-term cognitive, motor, sensory, and emotional deficits. These manifest as weakness, incoordination, emotional lability, impulsivity, and difficulty with vision, concentration, memory, judgment, and mood. Nearly 5.3 million in the United States live with disabilities as a result of TBI (14). When the postresuscitation GCS is not complicated by medications or intubation, approximately 20% of patients with GCS 3 will survive and 8% to 10% will have moderate to good recovery such that they are able to live independently (238). Despite this, 34% to 47% of “minor” head injury patients cannot return to work or their previous lifestyle (239,240). Independent predictors of outcome include older age at time of injury, the postresuscitation Glasgow coma score, injury severity score (ISS), pupillary response on admission, and CT scan findings of diffuse edema, tSAH, SDH, partial obliteration of the basal cisterns, or midline shift (241–246). The TCDB reports a postresuscitation mortality rate of severe TBI patients of 76% and 18%, for patients with postresuscitation GCS of 3 and 6 to 8, respectively. Overall mortality was 36% in 746 patients (42). In another study of 1,311 head-injured patients, the highest mortality was associated with spinal cord injury, obstructed airway, difficulty breathing, and shock, although none of these was independently predictive of survival when adjusted for GCS (247). There are on-going trials to find medications to improve outcome following TBI; studies to date, with agents such as free radical scavengers (248) and progesterone (249) have been unsuccessful.


ACUTE SPINAL CORD INJURY


Pathophysiology

Primary spinal cord injury results from cord compression from discs, bone, ligament, or hematoma, or from distractional forces such as flexion, extension, dislocation, or rotation, which cause shearing of the neuronal axons or vasculature with intramedullary hemorrhage. Similar to head injury, the spinal cord undergoes both primary and secondary injury. Secondary injury can result from additional mechanical injury if the spine is manipulated when it is unstable or as a result from systemic and local vascular insults, which may be a result of hypotension, electrolytes changes, edema, and excitotoxicity (250).


Diagnosis

Examination

The physical examination includes a general examination to survey for other injuries; the quality of the patient’s breathing should be assessed to ensure adequate ventilatory effort. The neurologic examination should include a mental status evaluation as concomitant head injury may occur. A complete cranial nerve examination assesses for evidence of cranial neuropathies or nystagmus suggestive of brainstem or cerebellar ischemia that may result from vertebral artery injury. In 1982, the American Spinal Injury Association (ASIA) developed the International Standards for Neurological Classification of Spinal Cord Injury (ISNCSCI) (Fig. 117.2) (251) to improve precision in determining the level and extent of neurologic injury for the National SCI Statistical Center Database (252). These have been updated since that time, have good interrater reliability (253,254), and are recommended as the preferred neurologic examination tool (255). The ASIA Impairment Scale standardizes language used to describe severity SCI (Table 117.2) (251). The single neurologic level of injury is defined as the most caudal segment of the cord with intact sensation and antigravity muscle function strength.




FIGURE 117.2 International Standards for Neurological Classification of Spinal Cord Injury (ISNCSCI). (From American Spinal Injury Association. International Standards for Neurological Classification of Spinal Cord Injury, revised 2011; Atlanta, GA. Updated 2015. Courtesy of the American Spinal Injury Association.)


Radiologic Evaluation

No cervical radiologic evaluation is recommended in an awake, alert, nonintoxicated trauma patient who has no neck pain or tenderness and is neurologically normal unless there are significant associated injuries that would interfere with the history and physical examination. In this setting, cervical immobilization can be discontinued without imaging. However, in patients with neck pain or tenderness, a high-quality cervical spine CT should be performed. The CT scan is better than MRI for evaluating bones; however, for ligamentous injury, dynamic flexion/extension radiographs in an awake patient are preferred. Alternatively, an MRI within 48 hours of injury can also detect ligamentous injury (256). Newer-generation CT scanners are sensitive, and routine three-view (anteroposterior, lateral, and odontoid) cervical spine radiographs are not recommended unless high-quality CT imaging is not available. In obtunded patients, again, high-quality cervical CT is recommended to rule out clinically significant injury (257). However caution is taken before removing and immobilizing collar since an obtunded patient cannot report pain associated with ligamentous injury and instability. Options to remove the collar include: (1) waiting until the patient is awake and asymptomatic; (2) a normal MRI obtained within 48 hours of injury (although this is considered level III evidence with limited or conflicting data); (3) at the discretion of the treating physician (256) or 4) more recent guidelines recommend the removal of the collar following a normal high quality CT scan defined as 3 mm slices or less (258).








TABLE 117.2 American Spinal Injury Association Impairment Scale

MRI is recommended for patients with cervical fracture-dislocation injuries if they cannot be examined during closed reduction. An MRI is performed to evaluate for disrupted or herniated intervertebral discs, which are found in up to 33% to 50% of patients with facet subluxation injuries (259). MRI is also recommended for patients with occipital condyle fractures to assess the integrity of the craniocervical ligaments (260).


Treatment

Immobilization

If the unstable spine is manipulated, 3% to 25% of spinal cord injuries may occur after the initial traumatic event. Additionally, nearly 20% of ASCIs include multiple noncontiguous vertebral levels (261,262). For this reason, early management of patients with SCI includes immediate prehospital immobilization of the entire spine with a rigid cervical collar with supportive blocks for head immobilization on a rigid backboard with straps (263). To prevent decubitus ulcers, it is recommended that the patient be transferred off the hard board as soon as possible; if the patient is awaiting transfer to another institution, they should be removed during the interim and replaced on the board for actual transport. Padded boards or bean bag boards are recommended to reduce pressure to the occiput and sacrum. Current recommendations advise against the use of sandbags and tape (264).


Hemodynamic Support

Systemic hypotension, which contributes to secondary spinal cord injury, can result from trauma-related hypovolemia and from neurogenic shock (265–267). Neurogenic shock is defined as the loss of sympathetic innervation that causes loss of peripheral vasoconstriction and cardiac compensatory mechanisms of tachycardia and increased stroke volume and cardiac output. In experimental models, microvascular spasm, thrombosis, and rupture will disrupt spinal cord vascular autoregulation and make the spinal cord more susceptible to systemic hypotension. This worsens spinal cord ischemia several hours after injury (267). MAP augmentation to 85 to 90 mmHg for 5 to 7 days after injury has been shown to reduce morbidity and mortality and shorten length of stay and are recommended by the recent 2013 guidelines (268–272).


Treatment typically includes volume resuscitation with crystalloid or red blood cell transfusion if the patient is anemic. Volume-resistant hypotension is fivefold more common among patients with complete spinal cord injury above the thoracic sympathetic innervation (269); vasoactive medications such as norepinephrine, dopamine, and phenylephrine may be required. In the subset of patients requiring vasopressors and inotropes, central venous catheters and invasive monitoring with arterial catheters should be used.


Surgical Intervention

The timing of surgical decompression, reduction of bony structures, and fusion in the treatment of ASCI have been debated. Earlier “practice options” included surgical intervention on patients with incomplete injury with persisting compression from dislocation with bilateral locked facets, burst fracture, or disc rupture, especially in patients with neurologic deterioration (273). Recent data suggest that early surgery, within 24 hours, has a beneficial effect on motor recovery (274) and current guidelines from 2013 are more definitive regarding recommendations with the goal of decompression of the spinal cord with restoration of the spinal canal (275). Recommendations include early (as rapidly as possible after injury) closed reduction of cervical spinal fracture/dislocation injury (259), and early reduction of fracture-dislocation injuries in the setting of acute traumatic central cord syndrome (CCS) with surgical decompression of the compressed spinal cord, particularly if the compression is focal and anterior (276). Overall, early surgery, possibly because of the ability to mobilize the patient earlier, appears to shorten hospital length of stay and reduce pulmonary complications (273,274,277–279).


Pharmacologic Intervention

Following ASCI, a cascade of biochemical processes is activated that produces excitatory amino acids, calcium fluxes, free radicals, acidosis, protein phosphorylation, phospholipases, and apoptosis, which can further injure surrounding tissue (267). Pharmacologic agents targeted to interrupt this cascade may provide neuroprotection by preventing secondary injury; however, similar to TBI, no agent has yet shown benefit (280).


Naloxone, GM-1 ganglioside, and methylprednisolone have undergone randomized clinical trials to examine their effects following spinal cord injury. After multiple trials evaluating the use of methylprednisolone (281–284), based on the lack of class I or class II evidence of benefit and inconsistent class III data, current neurosurgical and ATLS guidelines do not recommend the use of methylprednisolone after ASCI (91). Guidelines note that there are class I, II, and III evidence that high-dose steroids are associated with harmful side effects including pneumonia, gastrointestinal hemorrhage, sepsis and result in longer hospital stays, and death (281,285–287).


Pulmonary Support

The most common cause of death in patients with spinal cord injury is due to pneumonia, pulmonary emboli, and septicemia (22). In patients with tetraplegia, pneumonia and other respiratory complications occur in 40% to 70% of patients (288,289); aggressive pulmonary toilet is, therefore, essential.


Patients with high-level cervical injuries (C3–5) may fatigue over the first few hours to days. Pulmonary compromise can also be seen in patients with lower cervical cord injuries. Although diaphragmatic innervation arises from the cervical levels of three through five (C3–5), an effective cough and deep inspiration requires intercostal musculature and thoracic innervation to splint the chest wall while the diaphragm descends. Additionally, patients who are smokers with increased pulmonary secretions or those who have aspirated fluid such as blood, water, or stomach contents may have difficulty clearing their airway and should be monitored closely for failing pulmonary reserve.


Bedside evaluation with deep inspiration will frequently show a “functional flail chest,” wherein, with deep inspiration, the diaphragm descends, the abdomen rises, but the chest wall does not rise, but collapses or is immobile. Of the pulmonary function tests, vital capacity (VC) appears to be the single global measure of ventilatory status that best correlates with other pulmonary function tests (290). Serial measurements of bedside VC can indicate the need for elective endotracheal intubation if the VC is less than 20 mL/kg or decreasing rapidly. Hypoxia and hypercapnia are late signs of respiratory failure, and intubation should not await these findings.


Associated Vascular Injury

Blunt cervical spinal trauma can result in vascular injury and cause cerebral ischemia (291). Incidence varies from 0.03% to 4.8% and likely depends on the screening method (292–294). Mortality ranges from 23% to 28%, while 48% to 58% of survivors have significant neurologic deficits (295). The most common mechanism of blunt cerebrovascular injury (BCVI) is MVC, followed by falls, and pedestrian and motorcycle crashes. Many institutions use modifications of the Denver Screening Criteria for BCVI based on risk factors to determine whom to screen (296). Risk factors include cervical fractures with subluxation or with a fracture through the transverse foramen, displaced or complex midface or mandibular fracture (LeForte II or III), a basilar skull fracture involving the carotid canal or sphenoid sinus, near-hanging resulting in cerebral hypoxia, and cervical vertebral body fraction or distraction injury, a seatbelt sign or tissue injury of the anterior neck, and massive epistaxis or a cervical hematoma (292). Suspicion should be high if the patient develops a lateralizing neurologic deficit with an initially normal CT scan, or evidence of a recent ischemic stroke on cerebral imaging. CT angiography (CTA) is sensitive for BCVI and has taken the place of conventional cerebral angiography as the recommended screening tool unless CTA is not available or endovascular treatment is anticipated (297–300). In a patient with a vertebral subluxation or complete spinal cord injury, MRI is the recommended diagnostic modality (300).


A grading system of injury has been described by Biffl (301) (Table 117.3). Fifty-seven percentage of grade I injuries heal spontaneously in 10 days independent of therapy (302); therefore, they can be treated with aspirin. Retrospective studies of grade II through IV injuries show no difference between antiplatelet agent or heparin therapy although heparinization increases hemorrhage risk (303,304). Current recommendations suggest individualized therapy dependent on the vascular injury, associated injuries, and the risk of hemorrhage. Options include no treatment, antiplatelet therapy, or anticoagulation. No recommendations regarding endovascular therapy can yet be made (300).


Thromboprophylaxis

DVT detection with 131I-fibrinogen scans of patients with ASCI and paralysis ranges as high as 100% (305). Recommended diagnostic tests include: duplex Doppler ultrasound, impedance plethysmography, venous occlusion plethysmography, venography, and the clinical examination (306).








TABLE 117.3 Grading Scale for Blunt Cervical Vascular Injury

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Feb 26, 2020 | Posted by in CRITICAL CARE | Comments Off on Neurologic Injury: Prevention and Initial Care

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