Dr. Patrick- The document you are looking for, "Guidelines for the Management of Severe Head Injury," is available from the A.A.N.S., at the address listed below. You can request paper or CD-ROM format, although I recommend the book. It is essentially a series of chapters outlining n evidence-based rationale ("Standards", Guidelines", and "Options") for various interventions in the management of head trauma. The most elaborate and valuable part of the publication is the "evidentiary table" which lists the appropriate studies used for each subject evaluation, as well as a consensus classification on the "quality" of each study. I have excerpted some introductory information, and the statements of guidelines from each of the chapters below. I highly recommend contacting the A.A.N.S. to obtain the complete work, with the evidentiary tables. Thank you for your interest. Cameron Brennan, M.D. C.U.M.C.-New York Hospital The American Association of Neurological Surgeons 22 South Washington Street Park Ridge, Illinois 60068-4287 Guidelines for the Management of Severe Head Injury: Excerpts from the Original Text Note: This material is protected by copyright against duplication and distribution without permission from the publishers. Degrees of Certainty: Standards: represent accepted principles of patient management that reflect a high degree of clinical certainty . Guidelines: represent a particular strategy or range of management strategies that reflect a moderate clinical certainty . Options: are the remaining strategies for patient management for which there is unclear clinical certainty . Note that the term "guidelines" is used both in a global sense, i.e., clinical practice guidelines, as well as in a more specific sense, as noted above. Classification of Evidence: When assessing the value of therapies or interventions, the available data is classified into one of three categories according to the following criteria * : Class I evidence: Prospective randomized controlled trials (PRCT)-the gold standard of clinical trials. However, some may be poorly designed, lack sufficient patient numbers, or suffer from other methodological inadequacies. Class II evidence: Clinical studies in which the data were collected prospectively, and retrospective analyses which were based on clearly reliable data. Types of studies so classified include: observational studies, cohort studies, prevalence studies, and case control studies. Class III evidence: Most studies based on retrospectively collected data. Evidence used in this class indicates clinical series, databases or registries, case reviews, case reports, and expert opinion. Technology Assessment: The assessment of technology, such as intracranial pressure monitoring devices, does not lend itself to classification in the above-mentioned format. Thus, for technology assessment the devices were evaluated in terms of their accuracy, reliability, therapeutic potential, and cost effectiveness. Correlation Between Evidence and Recommendations: Standards are generally based on Class I evidence. However, strong Class II evidence may form the basis for a standard, especially if the issue does not lend itself to testing in a randomized format. Conversely, weak or contradictory Class I evidence may not be able to support a standard. Guidelines are usually based on Class II evidence or a preponderance of Class III evidence. Options are usually based on Class III evidence and are clearly much less useful except for educational purposes and in guiding future studies. THE INTEGRATION OF BRAIN-SPECIFIC TREATMENTS INTO THE INITIAL RESUSCITATION OF THE SEVERE HEAD INJURY PATIENT A. Standards There are insufficient data to support a treatment standard for this topic. B. Guidelines There are insufficient data to support a treatment standard for this topic. C. Options The first priority for the head -injured patient is complete and rapid physiologic resuscitation. No specific treatment should be directed at intracranial hypertension in the absence of signs of transtentorial herniation or progressive neurologic deterioration not attributable to extracranial explanations. When either signs of transtentorial herniation or progressive neurologic deterioration not attributable to extracranial explanations are present, however, the physician should assume that intracranial hypertension is present and treat it aggressively. Hyperventilation should be rapidly established. The administration of mannitol is desirable , but only under conditions of adequate volume resuscitation. Sedation and neuromuscular blockade can be useful in optimizing transport of the head injury patient. However, both treatments interfere with the neurological examination. In the absence of outcome-based studies, the choice of sedative is left to the physician. Neuromuscular blockade should be employed when sedation alone proves inadequate and short-acting agents should be used when possible. RESUSCITATION OF BLOOD PRESSURE AND OXYGENATION A. Standards There are insufficient data to support a treatment standard for this topic. B. Guidelines Hypotension (systolic blood pressure < 90 mm Hg) or hypoxia (apnea or cyanosis in the field or a PaO 2 < 60 mm Hg) must be scrupulously avoided, if possible, or corrected immediately. C. Options The mean arterial pressures should be maintained above 90 mm Hg throughout the patient's course to attempt to maintain cerebral perfusion pressure (CPP) 70 mm Hg. INDICATIONS FOR INTRACRANIAL PRESSURE MONITORING A. Standards There are insufficient data to support a treatment standard for this topic. B. Guidelines Intracranial pressure (ICP) monitoring is appropriate in patients with severe head injury with an abnormal admission CT scan. Severe head injury is defined as a Glasgow Coma Scale score (GCS) of 3-8 after cardiopulmonary resuscitation. An abnormal CT scan of the head is one that reveals hematomas, contusions, edema, or compressed basal cisterns. ICP monitoring is appropriate in patients with severe head injury with a normal CT scan if two or more of the following features are noted at admission: age over 40 years, unilateral or bilateral motor posturing, systolic blood pressure < 90 mm Hg. ICP monitoring is not routinely indicated in patients with mild or moderate head injury. However, a physician may choose to monitor ICP in certain conscious patients with traumatic mass lesions. INTRACRANIAL PRESSURE TREATMENT THRESHOLD A. Standards There are insufficient data to support a treatment standard for this topic. B. Guidelines Intracranial pressure (ICP) treatment should be initiated at an upper threshold of 20-25 mm Hg. C. Options Interpretation and treatment of ICP based on any threshold should be corroborated by frequent clinical examination and cerebral perfusion pressure (CPP) data. RECOMMENDATIONS FOR INTRACRANIAL PRESSURE MONITORING TECHNOLOGY The assessment of ICP monitoring technology does not lend itself to classification of evidence as in other guideline sections. Thus, the ICP devices were evaluated in terms of their accuracy, reliability, therapeutic potential, and cost effectiveness. In the current state of technology the ventricular catheter connected to an external strain gauge is the most accurate, low cost, and reliable method of monitoring intracranial pressure (ICP). It also allows therapeutic cerebrospinal fluid (CSF) drainage. ICP transduction via fiberoptic or strain gauge devices placed in ventricular catheters provide similar benefits, but at a higher cost. Parenchymal ICP monitoring with fiberoptic or strain gauge catheter tip transduction is similar to ventricular ICP monitoring, but has the potential for measurement drift. Subarachnoid, subdural, and epidural monitors (fluid coupled or pneumatic) are currently less accurate. GUIDELINES FOR CEREBRAL PERFUSION PRESSURE A. Standards There are insufficient data to support treatment standards for this topic. B. Guidelines There are insufficient data to support treatment guidelines for this topic. C. Options Cerebral perfusion pressure (CPP) should be maintained at a minimum of 70 mm Hg. Scientific Foundation: The rationale for attempting to optimize CPP arises from the increasing evidence that CBF is typically very low following traumatic brain injury, and in many cases, may be near the ischemic threshold. 4,5,15,17,28 CBF in the vicinity of posttraumatic contusions and subdural hematomas is reduced even further than global CBF. 24,32 Low CBF values may be due to compression of cerebral vessels from mass lesions, but also may be related to reduced cerebral metabolism in comatose patients 26 or to posttraumatic vasospasm, as has been documented in as many as 40% of these patients.34 While there is debate about the absolute CBF value below which irreversible ischemia will occur, it is apparent from histologic analysis of the brains of those who die following traumatic brain injury (TBI) that ischemia is very common. 13,14,31 The adverse consequences of failure to maintain an adequate CPP following severe TBI are well described. Several studies document worsened clinical outcomes in TBI patients who have had hypotensive episodes (systolic blood pressure<90 mm Hg) during the first several hours or days after their injury. 8,27 A significant inverse relationship between outcome and elevated ICP has been reported,1,21 and hypotension has been shown to cause an increase in ICP in those with intact cerebral vascular autoregulation. 2,3 There is experimental evidence that a decline in blood pressure is responsible for a sudden increase in ICP (plateau waves), and that such waves can be aborted by increasing the blood pressure. 29 There also is evidence that autoregulatory vasodilation in response to hypotension may be as high as 65% above baseline vessel diameters. 16 It has been argued that the hypertensive therapy needed in some head-injured patients to maintain an adequate CPP can cause an increase in ICP and poor outcome. 22,33 The effect of artificial blood pressure elevation on ICP and CBF has been systematically studied in patients with severe TBI. Bauma and Muizelaar studied 35 patients and found that elevation of the mean arterial blood pressure from 92±10 mm Hg to 123±8 mm Hg led to only a slight (insignificant) increase in ICP in those patients with intact autoregulation (less than 1% change in CBF). 2 In the group with defective autoregulation, as defined by a 53±20% increase in CBF, there was actually a significant decrease in the mean ICP. In 14 patients with severe TBI, Bruce et al. found that artificially increasing the systolic blood pressure by 30 mm Hg caused an average increase in ICP of only 4 mm Hg, and in 3 cases the ICP actually decreased. 6 In a subgroup of these patients with defective autoregulation, as defined by an increase of CBF of 7 ml/100 g/min or more with the increased blood pressure, ICP increased by only 3 mm Hg or less in 4 patients, though it increased by 13 and 27 mm Hg in the other two. These studies clearly demonstrate that ICP usually changes very little when blood pressure is increased by as much as 30 mm Hg in head-injured patients, and this is true regardless of the status of autoregulation. Since loss of autoregulation is defined as an increase in CBF when the blood pressure is increased, there is no direct relationship between CBF and ICP. Thus, moderate increases in blood pressure, as might be induced to maintain an adequate CPP, should not be expected to cause an increase in ICP in most TBI patients. THE USE OF HYPERVENTILATION IN THE ACUTE MANAGEMENT OF SEVERE TRAUMATIC BRAIN INJURY A. Standard In the absence of increased intracranial pressure (ICP), chronic prolonged hyperventilation therapy (PaCO2 of 25 mm Hg or less) should be avoided after severe traumatic brain injury (TBI). B. Guidelines The use of prophylactic hyperventilation (PaCO2 = 35 mm Hg) therapy during the first 24 hours after severe TBI should be avoided because it can compromise cerebral perfusion during a time when cerebral blood flow (CBF) is reduced. C. Options Hyperventilation therapy may be necessary for brief periods when there is acute neurologic deterioration, or for longer periods if there is intracranial hypertension refractory to sedation, paralysis, cerebrospinal fluid (CSF) drainage, and osmotic diuretics. Jugular venous oxygen saturation (SO2), arterial-jugular venous oxygen content differences (AVdO2), and CBF monitoring may help to identify cerebral ischemia if hyperventilation, resulting in PaCO2 values less than 30 mm Hg, is necessary. THE USE OF MANNITOL IN SEVERE HEAD INJURY A. Standards There are insufficient data to support a treatment standard for this topic. B. Guidelines Mannitol is effective for control of raised intracranial pressure (ICP) after severe head injury. Limited data suggest that intermittent boluses may be more effective than continuous infusion. Effective doses range from 0.25g-1gm/kg body weight. C. Options 1. The indications for the use of mannitol prior to ICP monitoring are signs of transtentorial herniation or progressive neurological deterioration not attributable to systemic pathology. (However, hypovolemia should be avoided by fluid replacement.) 2. Serum osmolarity should be kept below 320 mOsm when there is concern for renal failure. 3. Euvolemia should be maintained by adequate fluid replacement. A Foley catheter is essential in these patients. THE USE OF BARBITURATES IN THE CONTROL OF INTRACRANIAL HYPERTENSION A. Standards There are insufficient data to support a treatment standard for this topic. B. Guidelines High-dose barbiturate therapy may be considered in hemodynamically stable salvageable severe head injury patients with intracranial hypertension refractory to maximal medical and surgical intracranial pressure (ICP) lowering therapy. THE ROLE OF GLUCOCORTICOIDS IN THE TREATMENT OF SEVERE HEAD INJURY A. Standards The use of glucocorticoids is not recommended for improving outcome or reducing intracranial pressure (ICP) in patients with severe head injury. B. Guidelines None. C. Options None. CRITICAL PATHWAY FOR THE TREATMENT OF ESTABLISHED INTRACRANIAL HYPERTENSION A critical pathway, developed by consensus, is presented in Figure 1. We developed a treatment algorithm for established intracranial hypertension wherein the order of steps is determined by the risk: benefit ratio of individual treatment maneuvers. The considerations involved are outlined in the chapter specific to each step. As discussed in the section on intracranial pressure (ICP) treatment threshold, the absolute value defining unacceptable intracranial hypertension is unclear. Although a general threshold of 20-25 mm Hg has been presented, there will be situations where such pressures are too high as well as instances where higher ICP values are acceptable. These considerations are relevant to the decision to pursue any step in the escalated treatment of ICP. This critical pathway is a committee consensus and, therefore, must be viewed as Class III ("expert opinion") evidence. As such, it should be interpreted as a framework that may be useful in guiding an approach to treating intracranial hypertension. It can and should be modified in an individual case by any circumstances unique to the patient as well as by the response of the ICP to individual treatment steps. NUTRITIONAL SUPPORT OF BRAIN-INJURED PATIENTS A. Standards There are insufficient data to support a treatment standard for this topic. B. Guidelines Replace 140% of resting metabolism expenditure in non-paralyzed patients and 100% resting metabolism expenditure in paralyzed patients using enteral or parenteral formulas containing at least 15% of calories as protein by the seventh day after injury. C. Options The preferable option is use of jejunal feeding by gastrojejunostomy due to ease of use and avoidance of gastric intolerance. Scientific Foundation: Three randomized (Class I) studies have evaluated relationship of level of caloric intake to patient outcomes. 14,31,39 Rapp showed that the consequence of severe undernutrition for a two-week period after injury was an increased mortality rate as compared to full replacement of measured calories by seven days. 31 In a subsequent study of brain injured patients, Young et al. showed that with full replacement at three days after injury in the early group (fed parenterally) as opposed to nine days after injury in the late feeding group (fed enterally), there were no changes in morbidity. 39 Patient outcome was better at three months but not at six months. Hadley randomized 45 patients with severe head injury to receive enteral or parenteral nutrition. While caloric intake between groups was not significantly different, the parenteral group had significantly better nitrogen intake. 14 To achieve full caloric replacement by seven days after injury, nutritional replacement is usually begun no later than 72 hours after injury. This is so because 2-3 days are required to gradually increase feedings to full replacement whether feeding is by jejunal or gastric route.3,6,13,33,39 Intravenous hyperalimentation must also be started at levels below resting metabolism expenditure and advanced over three days. Whichever method is used in order to achieve full replacement , feedings are usually begun within 72 hours of injury. THE ROLE OF ANTI-SEIZURE PROPHYLAXIS FOLLOWING HEAD INJURY A. Standards Prophylactic use of phenytoin, carbamazepine, or phenobarbital is not recommended for preventing late posttraumatic seizures (PTS). B. Guidelines None. C. Options It is recommended as a treatment option that anticonvulsants may be used to prevent early posttraumatic seizures in patients at high risk for seizures following head injury. Phenytoin and carbamazepine have been demonstrated to be effective in preventing early posttraumatic seizures. However, the available evidence does not indicate that prevention of early posttraumatic seizures improves outcome following head injury. Excerpts: Certain risk factors have been identified that place head-injured patients at increased risk for developing PTS. 8,11 These risk factors include: Glasgow Coma Scale score < 10 Cortical contusion Depressed skull fracture Subdural hematoma Epidural hematoma Intracerebral hematoma Penetrating head wound Seizure within 24 hours of injury