(BQ) Part 2 book Critical care emergency medicine has contents: Management after cardiac surgery, pericardial diseases, gastrointestinal bleeding, electrolyte disorders, alterations in mental status, management of acute intracranial hypertension,.... and other contents.
Critical Care Emergency Medicine Notice Medicine is an ever-changing science As new research and clinical experience broaden our knowledge, changes in treatment and drug therapy are required The authors and the publisher of this work have checked with sources believed to be reliable in their efforts to provide information that is complete and generally in accord with the standards accepted at the time of publication However, in view of the possibility of human error or changes in medical sciences, neither the authors nor the publisher nor any other party who has been involved in the preparation or publication of this work warrants that the information contained herein is in every respect accurate or complete, and they disclaim all responsibility for any errors or omissions or for the results obtained from use of the information contained in this work Readers are encouraged to confirm the information contained herein with other sources For example and in particular, readers are advised to check the product information sheet included in the package of each drug they plan to administer to be certain that the information contained in this work is accurate and that changes have not been made in the recommended dose or in the contraindications for administration This recommendation is of particular importance in connection with new or infrequently used drugs Critical Care Emergency Medicine David A Farcy, MD, FAAEM, FACEP, FCCM Medical Director of the Surgical Intensivist Program Director of Emergency Department Critical Care Mount Sinai Medical Center Miami Beach, Florida William C Chiu, MD, FACS, FCCM Associate Professor of Surgery Director, Fellowship Programs in Surgical Critical Care and Acute Care Surgery R Adams Cowley Shock Trauma Center University of Maryland School of Medicine Baltimore, Maryland Alex Flaxman, MD, MSE Director, Emergency Medicine Critical Care Emergency and Critical Care Attending St Joseph’s Regional Medical Center Paterson, New Jersey Attending Intensivist Pittsburgh Critical Care Associates, Inc Staff Intensivist Upper Allegheny Health System Olean, New York John P Marshall, MD, FACEP Chair Department of Emergency Medicine Maimonides Medical Center Brooklyn, New York New York Chicago San Francisco Lisbon London Madrid Mexico City Milan New Delhi San Juan Seoul Singapore Sydney Toronto Copyright © 2011 by The McGraw-Hill Companies All rights reserved Except as permitted under the United States Copyright Act of 1976, no part of this publication may be reproduced or distributed in any form or by any means, or stored in a database or retrieval system, without the prior written permission of the publisher ISBN: 978-0-07-163981-1 MHID: 0-07-163981-0 The material in this eBook also appears in the print version of this title: ISBN: 978-0-07-162824-2, MHID: 0-07-162824-X All trademarks are trademarks of their respective owners Rather than put a trademark symbol after every occurrence of a trademarked name, we use names in 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mechanical error by our sources, McGraw-Hill, or others, McGraw-Hill does not guarantee the accuracy, adequacy, or completeness of any information and is not responsible for any errors or omissions or the results obtained from the use of such information TERMS OF USE This is a copyrighted work and The McGraw-Hill Companies, Inc (“McGrawHill”) and its licensors reserve all rights in and to the work Use of this work is subject to these terms Except as permitted under the Copyright Act of 1976 and the right to store and retrieve one copy of the work, you may not decompile, disassemble, reverse engineer, reproduce, modify, create derivative works based upon, transmit, distribute, disseminate, sell, publish or sublicense the work or any part of it without McGraw-Hill’s prior consent You may use the work for your own noncommercial and personal use; any other use of the work is strictly prohibited Your right to use the work may be terminated if you fail to comply with these terms THE WORK IS PROVIDED “AS IS.” McGRAW-HILL AND ITS LICENSORS MAKE NO GUARANTEES OR WARRANTIES AS TO THE ACCURACY, ADEQUACY OR COMPLETENESS OF OR RESULTS TO BE OBTAINED FROM USING THE WORK, INCLUDING ANY INFORMATION THAT CAN BE ACCESSED THROUGH THE WORK VIA HYPERLINK OR OTHERWISE, AND EXPRESSLY DISCLAIM ANY WARRANTY, EXPRESS OR IMPLIED, INCLUDING BUT NOT LIMITED TO IMPLIED WARRANTIES OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE McGraw-Hill and its licensors not warrant or guarantee that the functions contained in the work will meet your requirements or that its operation will be uninterrupted or error free Neither McGraw-Hill nor its licensors shall be liable to you or anyone else for any inaccuracy, error or omission, regardless of cause, in the work or for any damages resulting therefrom McGraw-Hill has no responsibility for the content of any information accessed through the work Under no circumstances shall McGraw-Hill and/or its licensors be liable for any indirect, incidental, special, punitive, consequential or similar damages that result from the use of or inability to use the work, even if any of them has been advised of the possibility of such damages This limitation of liability shall apply to any claim or cause whatsoever whether such claim or cause arises in contract, tort or otherwise To my father Dr Jean Pierre Farcy for his love and for sharing and instilling in me the passion for medicine, to Dr Thomas M Scalea for teaching me to have compassion and to always put patients first, to Dr Amy Church and Dr John P Marshall for believing in me To my mother, Poe, Eve, Frederic, and Sarah for always being there for me, and all my patients and their families, who have helped me become a better doctor and believed in me during their most difficult moments — David A Farcy — To all those who have been influential to me: Terri, Anthony, Katherine, Victoria, and the extended Shock Trauma family — William C Chiu — To all those who helped, worked, and sacrificed, to get me to where I am: Mom, Dad, Sally, grandparents, great grandparents, cousins, aunts and uncles, great aunts and uncles, and great great uncle, this effort is for you — Alex Flaxman — To my wife, Seriti, and my three boys, Sahm, Siahvash, and Kianoosh Your love, patience, and support make everything possible — John P Marshall — This page intentionally left blank CONTENTS Contributors xi Foreword xix Preface xxi SECTION I INTRODUCTION The Emergency Department Intensivist Scott D Weingart SECTION II AIRWAY AND VENTILATORY SUPPORT Approach to the Difficult Airway Timothy B Jang and Jason C Wagner The Failed Airway 21 David R Gens, David A Farcy, and Dale J Yeatts Mechanical Ventilation 31 David A Farcy, Paul L Petersen, Dennis Heard, and Peter DeBlieux Weaning and Extubation 41 Alex Flaxman Noninvasive Ventilation 55 Brian J Wright and Todd L Slesinger Extracorporeal Cardiopulmonary Membrane Oxygenation 71 David A Farcy, David Rabinowitz, and Paola G Pieri SECTION III PULMONARY DISORDERS Acute Respiratory Failure 81 Imoigele P Aisiku Acute Respiratory Distress Syndrome (ARDS) 89 Isaac Tawil and Megan L Garcia viii CONTENTS 10 Severe Asthma and COPD 99 Michael T Dalley and Triminh Bui 11 Pulmonary Embolism 109 Rayan A Rouhizad and Beth A Longenecker SECTION IV CARDIOVASCULAR DISORDERS 12 Hemodynamic and Perfusion Monitoring 117 Elizabeth Lea Walters and H Bryant Nguyen 13 Acute Coronary Syndrome 127 John P Marshall and Jonathan Rose 14 Hypertensive Crises 139 Christopher M Perry, Qiuping Zhou, and Todd L Slesinger 15 Post-Cardiac Arrest Management 149 Alan C Heffner 16 Vasopressors and Inotropes 159 Amber Rollstin, John P Marshall, and William C Chiu 17 Management after Cardiac Surgery 167 Justin T Sambol and LaMont C Smith 18 Pericardial Diseases 181 Joseph R Shiber SECTION V GASTROINTESTINAL AND RENAL DISORDERS 19 Gastrointestinal Bleeding 195 Marie-Carmelle Elie-Turenne, Carrie A Cregar, and Selwena Brewster 20 Acute Liver Failure: How to Orchestrate Emergency Critical Care Interventions 207 Thomas H Kalb and Jennifer A Frontera 21 Acid–Base Disorders 221 Kevin M Jones and William C Chiu 22 Electrolyte Disorders 231 Kevin M Jones, Samantha L Wood, and William C Chiu 23 Acute Renal Failure and Renal Replacement Therapy 247 Alex Flaxman and Deborah M Stein SECTION VI NEUROLOGIC AND NEUROSURGICAL DISORDERS 24 Alterations in Mental Status 261 Nestor D Tomycz and David W Crippen 25 Management of Acute Intracranial Hypertension 269 Asma Zakaria and Imoigele P Aisiku CONTENTS ix 26 Stroke 275 Alex M Barrocas and Beth A Longenecker 27 Intracranial Hemorrhage 285 Alex M Barrocas and Beth A Longenecker 28 Traumatic Brain Injury and Spinal Cord Injury 293 Jason A Ellis, Kiwon Lee, and Dorothea Altschul SECTION VII HEMATOLOGIC AND ENDOCRINE DISORDERS 29 Transfusion in Critical Care 307 Julie A Mayglothling and Therese M Duane 30 Deep Venous Thrombosis 315 Amy Tortorich and David R Gens 31 Hyperglycemic Emergency 327 Grace S Lee and Shyoko Honiden 32 Glucose Management in Critical Care 333 Ari J Ciment and Joseph Romero 33 Adrenal Insufficiency 343 Evie G Marcolini and William C Chiu SECTION VIII INFECTIOUS DISORDERS 34 Approach to Fever in Critical Care 349 Marnie E Rosenthal 35 Principles of Antimicrobial Use in Critical Care 359 Anu Osinusi and Manjari Joshi 36 Sepsis and Septic Shock 371 David A Farcy, John Yashou, and Emanuel Rivers 37 Nosocomial and Health Care-Associated Pneumonia 383 Michael T McCurdy 38 Infectious Endocarditis 391 Joseph R Shiber 39 Clostridium Difficile Infection (CDI) 401 Claudio D Tuda SECTION IX TOXICOLOGIC CONDITIONS 40 Approach to Poisoning 409 Mohan Punja and Robert J Hoffman 41 The Critically Ill Poisoned Patient 419 Robert J Hoffman 286 SECTION VI NEUROLOGIC AND NEUROSURGICAL DISORDERS Figure 27–1 CT lobar hemorrhage The patient presented with sudden-onset right face, arm, and leg weakness with alteration of consciousness Coronal sequence is particularly useful at demonstrating uncal herniation extravasation into the hematoma “spot sign” on these studies Increase in ICH is seen in 38% of patients within the first hours of ictus and two thirds of those are within the first hour Hemorrhages from chronic hypertension commonly occur in the basal ganglia, thalamus, pons, and cerebellum, among other sites (Figure 27-2) These sites are supplied by perforating vessels that are susceptible to lipohyalinosis, fibrinoid necrosis, and Charcot–Bouchard microaneurysms in the setting of chronic hypertension Hemorrhages from amyloid angiopathy usually occur in a lobar distribution This disease is characterized by b-amyloid deposition in small- and medium-sized vessels, history of Alzheimer’s disease, recurrent hemorrhages (of various sorts—subdural, subarachnoid, etc.), and Apo E2 and E4 alleles A B Figure 27–2 (A and B) CT hypertensive hemorrhage Note the left basal ganglia hemorrhage encompassing the left putamen and globus pallidus Six-month follow-up CT reveals small linear cystic encephalomalacia in the site of prior hemorrhage consistent with the form of healing in the brain by cavitation The site of hypertensive hemorrhages is most commonly in the territory of perforating vessels (basal ganglia—lenticular striate arteries; pons—basilar perforators; thalamus—thalamoperforators) Hemorrhages from vasculopathy usually result from rupture of small- or medium-sized vessels History is critical in making this diagnosis as typically the hemorrhage is preceded by months of headache, and neurologic deficits such as cognitive decline and psychiatric symptoms from multiple small strokes Vasculopathy can be seen with infectious diseases such as herpes, tuberculosis, bacterial/fungal/viral vasculitis, syphilis, systemic diseases such as polyarteritis nodosa, Wegener’s granulomatosis, Churg–Strauss syndrome, systemic lupus erythematosis, rheumatoid arthritis, Sjögren’s disease, hepatitis, Behỗets disease, sarcoidosis, drug induced (cocaine), etc MEDICAL MANAGEMENT OF PATIENTS WITH ICH Airway Management Patients with ICH often deteriorate rapidly and require careful monitoring of their airway Endotracheal intubation should be performed in patient with Glasgow Coma Scale (GCS) score of or lower, or those unable to manage secretions If patients require transfer from a carefully monitored setting or to an outside facility, realize that there is the potential for these patients to suffer airway compromise and consider intubation in patients who are obtunded Rapid sequence induction should be performed prior to intubation The use of lidocaine prior to intubation has not been proven to prevent increases in ICP and is of questionable benefit.7 The preferred induction agents should be short acting and should not increase ICP Current recommendations are for the use of etomidate or propofol in the setting of acute ICH Propofol can cause a rapid decrease in blood pressure (BP), but this generally is responsive to boluses of isotonic fluids Midazolam should be avoided as it may adversely affect ICP A short-acting nondepolarizing agent such as rocuronium is preferred to the shorter-acting succinylcholine in patients at risk for increased ICP.8 The evidence is incomplete, but it does suggest that succinylcholine may increase ICP in those with a space-occupying lesion in the cranium If a decision is made to use succinylcholine, pretreatment with a “defasciculating” dose of a nondepolarizing agent such as vecuronium or pancuronium should be employed as this has been demonstrated to protect against such increases in ICP.9 There are no unique aspects to ventilator management in patients following acute ICH Hyperoxygenation is not necessary, and hyperventilation should be reserved as a temporizing measure for patients with elevations in ICP Positive end-expiratory pressure (PEEP) of up to 12 mm Hg may safely be used and will not increase ICP so long as mean arterial pressure (MAP) is maintained.10 CHAPTER 27 Blood Pressure Management There is still some controversy over definite limits at which to begin therapy for hypertension in patients following spontaneous ICH Prior literature showed possible increases in morbidity and mortality accompanying aggressive management of hypertension However, two recent trials, the INTERACT and the ATACH trials,11,12 demonstrated that it is safe to aggressively lower BP in patients with ICH The studies are not sufficient to establish parameters for BP control, nor they provide sufficient evidence to demonstrate improved outcome in patients receiving aggressive early lowering of BP As such, the American Heart Association/ American Stroke Association (AHA/ASA) continues to support the 2007 recommendations1 as follows: If systolic BP (SBP) is >200 mm Hg or MAP is >150 mm Hg, consider aggressively lowering pressure using an agent given by intravenous (IV) infusion For SBP >180 mm Hg or MAP >130 mm Hg in the setting of possible increased ICP, consider lowering BP via either continuous infusion or intermittent administration of IV medications while monitoring the ICP Consider lowering BP to 160/90 mm Hg if SBP >180 mm Hg or MAP is >130 mm Hg in patients with no evidence of increased ICP Again, continuous IV infusion or intermittent dosing of medication is appropriate The guidelines were modified to include the following in the 2009 update by the AHA/ASA: If a patient presents with an SBP of 150–220 mm Hg, it is probably safe to acutely lower the SBP to 140 mm Hg.13 In general, agents chosen for BP control in this setting should be easy to titrate and have a relatively short duration of action The most frequently recommended agents include IV nicardipine, labetalol, or esmolol Minimizing Hematoma Expansion It is widely recognized that hematoma expansion during the first hours after an ICH is predictive of poor outcome Patients with coagulopathy, be it inherent or iatrogenic, should receive agents that attempt to correct the abnormality and therefore limit hematoma size Patients who have a severe coagulation factor deficiency or severe thrombocytopenia should receive appropriate factor replacement or platelets.13 In patients who have received recombinant tissue plasminogen activator (rt-PA) and suffer symptomatic ICH, there are no solid guidelines available Current recommendations are to infuse 6–8 U of platelets as well as cryoprecipitate that contains factor VIII.14 INTRACRANIAL HEMORRHAGE 287 In patients suffering ICH who have been on heparin, reversal with protamine sulfate, mg for every 100 U of heparin given (within the first 30 minutes of heparin administration), is indicated; 0.75 mg/100 U heparin of protamine within 31–60 minutes, 0.5 mg/ 100 U heparin of protamine within 61–120 minutes, and 0.4 mg/100 U heparin of protamine at greater than hours of heparin administration, keeping in mind the half-life of heparin is hours The total dose should not exceed 50 mg, and protamine should be injected slowly by IV as rapid infusion may trigger hypotension.1 People receiving oral anticoagulants, such as warfarin, account for 12–14% of all ICH patients The current AHA/ASA guidelines for patients with elevated INR are to (1) withhold warfarin; (2) give IV vitamin K (dose: mg, slow IV)—be prepared for a possible anaphylactic response when administering IV vitamin K; (3) use either fresh frozen plasma (FFP) 15 mL/kg or prothrombin complex concentrates (PCC) 50–150 mL to provide vitamin K–dependent clotting factors PCC may hold some benefit over FFP as there is less volume loading and PCC has been shown to more rapidly improve INR However, no current studies have demonstrated improved outcome with their use and the product is far more costly Current AHA/ASA recommendations are for either product.1 There has been a great deal of interest in the use of recombinant factor VIIa in acute hemorrhage; however, in phase III trials, there was no improvement in outcome in patients with ICH receiving rVIIa and there was some increase in arterial thrombus in the treatment arm.15 Current AHA/ASA guidelines state that there is no indication for rVIIa in unselected patients, but many still contend that its use should be considered in those patients with ICH who were receiving oral anticoagulant therapy if neurosurgical intervention is a possibility Other Management Considerations It is critical to attempt to minimize secondary brain injury following ICH Studies have shown an improved outcome in these patients when managed in a specialized neuroscience intensive care unit (NICU); as such, this is the most appropriate setting for these patients whenever possible.16 Management of Increased Intracranial Pressure Patients with large intracerebral hematomas or with intraventricular involvement are at increased risk of developing increased ICP There are no techniques specific to management in the subset of patients with ICH The standard medical therapies remain 288 SECTION VI NEUROLOGIC AND NEUROSURGICAL DISORDERS unchanged: (1) the head of the bed should be maintained at 30°; (2) 20% mannitol should be infused in a dose of 1–1.5 g/kg; (3) hyperventilation may provide a temporary decrease in ICP and should be initiated with a goal toward maintaining the patient’s PCO2 at 25–30 mm Hg; (4) barbiturates, such as pentobarbital, given in 5-mg boluses every 10–15 minutes may improve ICP in intractable cases; (5) intracranial monitoring of ICP or ventriculostomy with drainage of cerebrospinal fluid (CSF) should also be considered on an individual basis.1,8 Intraventricular administration of rt-PA has been explored in patients with ICH but is still considered investigational by the AHA/ASA.1 Rigid control of glucose has been shown to be beneficial in surgical intensive care unit (SICU) patients; however, hypoglycemia must also be avoided Several studies in patients with closed head injury have demonstrated episodes of hypoglycemia and possible increased risk of mortality.17 The current AHA/ASA guidelines are for less aggressive management than the recommended tight glucose control of 80–110 mg/dL and instead call for maintenance of euglycemia and avoidance of hypoglycemia.1 Fever has been shown to worsen outcome in patients with ICH; conversely, there is no evidence demonstrating that temperature control improves outcome in these patients It is recommended that antipyretics and cooling blankets be employed to maintain euthermia.1,8 Patients with lobar ICH are at increased risk for seizure Prophylactic antiepileptic medications are not currently recommended by the AHA/ASA Treatment should begin if the patient has clinical seizures or in patients with changes in mental status who demonstrate seizure on electroencephalography (EEG) Continuous EEG monitoring should be considered in patients with mental status depression that is out of proportion to the degree of demonstrated brain injury.1 Initial management of seizures should begin with benzodiazepines such as lorazepam 0.1 mg/kg, followed by a loading dose of phenytoin or fosphenytoin (20 mg/kg).8 Patients are at increased risk for thromboembolic events while under care in the NICU It is recommended that all patients be placed in compression stockings with intermittent compression devices to the lower extremities Once bleeding has been documented to have stopped, low-dose subcutaneous low-molecular-weight heparin or unfractionated heparin may be considered for deep vein thrombosis (DVT) prevention.1 The current recommendations for surgical intervention are based largely on the STICH trial18 that did not confirm benefit for surgery in patients with superficial lobar hemorrhage The trial did demonstrate worsened outcome in patients with deeper hemorrhages undergoing surgery The current AHA/ASA guidelines are for early surgical intervention in patients with cerebellar A B Figure 27–3 (A and B) Cerebellar hemorrhage and weeks postoperative CT Note the mass effect that the hematoma causes on the fourth ventricle (fully compressed), and complete effacement of the quadrigeminal plate cistern and brainstem On the 2-week postdecompressive craniectomy follow-up CT, the fourth ventricle is again visible and the mass effect on the brainstem relieved with residual encephalomalacia in the area of hemorrhage Immediate relief of the compressive effect of the hematoma is the objective of the surgical intervention hemorrhage with rapid deterioration, brainstem compression, or hydrocephalus (Figure 27-3) Craniotomy may be considered in patients with large hemorrhages >30 mL within cm of the surface of the brain Finally, the use of minimally invasive techniques for clot evacuation is still considered investigational.1 Finally, the current AHA/ASA guidelines address the issue of mortality in patients with ICH It is well published that the majority of patients who die from ICH will so during their initial acute hospitalization Newer studies that have looked at lack of intervention (do not resuscitate [DNR] orders) in the initial phase of treatment in patients with ICH have demonstrated that “early care limitations” may be an independent risk factor for mortality in this population.19,20 The AHA/ASA now recommends that implementation of DNR orders in patients who not currently have them in place should not be initiated until the second hospital day.1 c SUBARACHNOID HEMORRHAGE SAH accounts for approximately 5% of all strokes and about 1% of all patients presenting to the emergency department with the complaint of headache While the incidence of SAH has remained relatively unchanged, mortality has significantly improved, remaining anywhere from 33% to 45%.21,22 The most common cause CHAPTER 27 of nontraumatic SAH is rupture of an intracranial aneurysm and will be the focus of this discussion Numerous other causes of SAH exist, including intracranial arterial dissection, arteriovenous malformation (AVM), dural arteriovenous fistula (AVF), infectious aneurysms, infectious endocarditis, trauma, coagulation disorders, cocaine abuse, cervical origin (from a spinal AVM or AVF), cavernous malformations, vasculitis, vasculopathy, intracranial tumor, sickle cell anemia, pituitary apoplexy, and intracranial venous sinus thrombosis to list a few for which cerebral angiography is indicated in the diagnostic evaluation Independent risk factors for the development of SAH include cigarette smoking, hypertension, cocaine, and heavy use of alcohol.23 Certain genetic syndromes are also linked to formation of aneurysm and SAH These include a1-antitrypsin deficiency, autosomal dominant polycystic kidney disease,24 type IV Ehlers–Danlos syndrome,25 and familial intracranial aneurysm syndrome (defined as first-degree relatives with $2 affected members) Patients with this disorder tend to have multiple aneurysms and a 10% risk of having an aneurysm compared with 2% in general population, and tend to suffer aneurysmal rupture at an early age Patients with a history of ruptured aneurysm have an annual rate of new aneurysm formation of 1–2%.26 The diagnosis of spontaneous SAH requires a high index of suspicion It is estimated that approximately between 5% and 12% of patients with this type of bleed remain undiagnosed.27,28 This is a dismal statistic, as failure to diagnose SAH considerably increases morbidity and mortality The most common presenting symptom of SAH is sudden onset of severe headache Patients may describe the headache as the “worst headache of my life.” Severe headache is present in up to 80% of patients with subarachnoid bleeding Patients may also present with nausea, vomiting, neck pain, or alterations in mental status or focal neurologic deficits, frequently cranial nerve palsies.21 It should be remembered that improvement of pain in response to conventional therapies used for headache control does not rule out SAH, and this thought process is a trap to be avoided Initial neurologic examination is predictive of outcome in SAH as shown by the Hunt and Hess scale where grade is asymptomatic to mild headache and nuchal rigidity; grade is moderate–severe headache, nuchal rigidity, but no neurologic deficit other than cranial neuropathy; grade is drowsiness, altered sensorium, and/or mild focal neurologic deficit; grade is stupor and/or moderate–severe hemiparesis; grade is coma/decerebrate posturing.29 The 30-day survival is 70% for grades 1–3, and 20% for grades and 5.30 Modern advancements in treatment of SAH (in 1995) including the advent of interventional neuroradiology for endovascular treatment of vasospasm have improved these figures at least INTRACRANIAL HEMORRHAGE 289 in good grades (1–3) that demonstrate 86% return to independent functioning.31 Further improvement in outcomes is expected as the technological advancements in endovascular treatments continue The diagnosis of SAH should begin with radiographic analysis Noncontrast CT remains the initial test of choice, with a sensitivity of 98–100% in the first 12 hours following SAH Sensitivity declines with time, and falls to 93% at 24 hours and to as low as 57% at days after the event.21 CTA may be helpful in identification of aneurysm and is highly sensitive for aneurysms larger than mm; however, sensitivity is low in detecting smaller aneurysms Magnetic resonance angiography (MRA) is also a helpful tool in identifying cerebral aneurysm, but again sensitivity is limited and is highest for aneurysms of >5 mm in diameter For these reasons, the gold standard used to rule out SAH in patients with suspected SAH and a nondiagnostic, noncontrast CT remains the lumbar puncture The sensitivity of this test, when properly performed and interpreted, approaches 100% with a 99% negative predictive value Tubes and should be sent for a cell count, and >400 red blood cells (RBC) (which does not decrease from tube to tube 4) and an elevated opening pressure are suggestive of SAH Finding xanthochromia is diagnostic of this disorder; however, it may take up to 12 hours for RBCs to lyse sufficiently to produce this finding There is evidence to support the use of visual inspection to make this diagnosis and suggests that spectrophotometry is not necessary to safely exclude SAH.32 TREATMENT OF ANEURYSMAL SUBARACHNOID HEMORRHAGE The object of aneurysmal SAH treatment is to prevent rerupture of the aneurysm Early treatment (within 48 hours) is recommended to prevent the 67% mortality rate associated with rebleeding.21 There is a 3–4% risk of rebleeding in the first 24 hours and 2% risk in the second day Each subsequent day carries a 0.3% risk and 15–20% risk in the first weeks If left untreated, there is a 50% risk of rerupture in the first months.33 Securing an aneurysm may be performed either by open microsurgical technique (clipping) or via endovascular technique (coiling) (Figure 27-4) The international subarachnoid aneurysm trial (ISAT) randomized 2,143 spontaneous SAH patients to clipping versus coiling within 28 days of SAH ictus Although the randomization process is heavily criticized, at year there was a 24% major disability or death in the endovascular group versus 31% in the surgical group (P 0019) At the 7-year follow-up, the mortality was significantly higher in the surgically treated group (P 03), and seizure rates were higher as well The early rebleeding risk was higher with the 290 A SECTION VI NEUROLOGIC AND NEUROSURGICAL DISORDERS B C D Figure 27–4 (A–D) CT scan demonstrates diffuse subarachnoid hemorrhage CTA demonstrates a left anterior communicating artery aneurysm pointing right and upward This is confirmed on cerebral angiography Postaneurysm coil embolization angiogram is demonstrated Note the lack of filling within the aneurysm endovascular group at the 30-day follow-up, but at years it was similar in both groups.33,34 The optimal method of treatment remains individualized for each patient depending on aneurysm morphology, location, and patient characteristics MEDICAL MANAGEMENT OF SUBARACHNOID HEMORRHAGE Patients requiring airway or ventilatory support should be managed as in the prior discussion of patients with ICH All patients with SAH are best served by admission to an NICU preferably in a facility with access to experts in neurovascular interventional care Management of patients with SAH should be set with the goals to prevent rebleeding and to limit vasospasm in the cerebral circulation BP should be maintained at normal levels in these patients until the ruptured aneurysm is secured (coiled or clipped) Appropriate analgesia may assist in this endeavor Antiemetics are indicated to prevent vomiting and subsequent increases in ICP As in ICH, hyperglycemia and hyperthermia may worsen outcome and should be avoided.21,36 The second arm of medical treatment is an attempt to prevent vasospasm and subsequent decreased cerebral blood flow Patients with vasospasm will present with new onset of focal neurologic deficits that may either resolve or continue on to permanent ischemic infarction Up to 15% of patients with episodes of vasospasm post-SAH will either suffer a stroke or die from this process in spite of maximal therapy.21 Oral nimodipine (60 mg every hours) should be started as soon as possible once the diagnosis is obtained in an effort to prevent the development of this complication, and continued for 21 days Early intervention is the key to preventing rebleeding and allowing for hypertensive/ hypervolemic therapy in the setting of arterial vasospasm Symptomatic vasospasm occurs in 20–40% of patients with aneurysmal SAH within days 5–21 Cerebral ischemia or infarction results from symptomatic vasospasm Risk factors include poor grade, thick blood on CT, sentinel bleed, fever, early angiographic spasm, volume depletion, low cardiac output, and smoking Endovascular treatment of vasospasm can reverse symptoms of delayed ischemia Treatment may consist of intra-arterial medication delivery (verapamil, milrinone, among others) and/or angioplasty, and treatment within hours of symptom onset is ideal Finally, patients with SAH are at risk for other complications, including seizure, DVT, hydrocephalus, and hyponatremia Compression stockings and intermittent compression devices should be used to prevent the development of DVT Subcutaneous administration of anticoagulants may be used once the aneurysm is safely secured (clipped or coiled) Prophylactic use of anticonvulsants remains controversial but may be considered.21 Seizures should be managed as with seizures from any cause, first with lorazepam or another benzodiazepine followed by anticonvulsants such as phenytoin or fosphenytoin.36 External ventricular drains should be placed in patients with hydrocephalus or evidence of increased ICP (i.e., Cushing’s triad or decreased sensorium with hydrocephalus seen on CT) Prior to securing the aneurysm, the ICP should be kept at the high end of normal (20 mm Hg CSF) The theory is to reduce the transdome pressure in an effort to reduce the rerupture rate Once the aneurysm is secured, the drain may be kept open to a level of 10 mm Hg CSF Finally, hyponatremia occurs in between 10% and 30% of all patients with SAH It was originally suggested that CHAPTER 27 this is a form of syndrome of inappropriate antidiuretic hormone (SIADH); however, fluid restriction and volume contraction have been shown to worsen outcome in this population Cerebral salt wasting syndrome (CSW) is most often the cause and has been postulated to be related to alterations in brain natriuretic peptide (BNP) levels CSW is differentiated from SIADH in that in CSW there is volume depletion with the loss of sodium as opposed to SIADH where there is normovolemia or hypervolemia When urine output exceeds fluid input, the diagnosis of CSW should be considered Current AHA/ASA guidelines are to maintain euvolemia, use isotonic fluids to maintain a normal fluid balance, use fludrocortisone acetate, and consider the use of 3% hypertonic saline to correct hyponatremia in these patients.21 Caution is advised not to correct hyponatremia too quickly as to cause central pontine myelinolysis; however, this is rare in patients with hyponatremia less than 24 hours’ duration This is avoided by not exceeding mEq/ 24 hours in the chronically hyponatremic patient REFERENCES Broderick J, Connolly S, Feldmann E, et al Guidelines for the management of spontaneous intracerebral hemorrhage in adults: 2007 update: a guideline from the American Heart Association/American Stroke Association Stroke Council, High Blood Pressure Research Council, and the Quality of Care and Outcomes in Research Interdisciplinary Working Group Stroke 2007;38:2001–2023 Ariesen MJ, Claus SP, Rinkel JGE et al Risk factors for intracerebral hemorrhage in the general population: a systematic review Stroke 2003;34:2060–2065 Wojak JC, Flamm ES Intracranial hemorrhage and cocaine use Stroke 1987;18:712–715 Buxton N, McConachie NS Amphetamine abuse and intracranial haemorrhage J R Soc Med 2000;93:472–477 Gorelick PB, Weisman SM Risk of hemorrhagic stroke with aspirin use: an update Stroke 2005;36;1801–1807 Steiner T, Rosand J, Diringer M Intracerebral hemorrhage associated with oral anticoagulant therapy: current practices and unresolved questions Stroke 2006;37; 256–262 Robinson M, Clancy N In patients with head injury undergoing rapid sequence intubation, does pretreatment with intravenous lingocaine/lidocaine lead to an improved neurological outcome? A review of the literature Emerg Med J 2001;18:453–457 Rincon F, Mayer SA Clinical review: critical care management of spontaneous intracerebral hemorrhage Crit Care 2008;12:237–251 Clancy M, Halford S, Walls R, et al In patients with head injuries undergoing rapid sequence intubation using succinylcholine, does pretreatment with a competitive neuromuscular blocking agent improve outcome? A literature review Emerg Med J 2001;18: 373–375 INTRACRANIAL HEMORRHAGE 291 10 Georgiadis D, Schwarz S, Baumgartner RW, et al Influence of positive end-expiratory pressure on intracranial pressure and cerebral perfusion pressure in patients with acute stroke Stroke 2001;32;2088–2092 11 Anderson CS, Huang Y, Wang JG, et al Intensive blood pressure reduction in acute cerebral haemorrhage trial (INTERACT): a randomized pilot trial Lancet Neurol 2008;7:391–399 12 Quereshi AI Antihypertensive treatment of acute cerebral haemorrhage (ATACH): rationale and design Neurocrit Care 2007;6:56–66 Results presented at International Stroke Conference, New Orleans, February 2008 13 Morgenstern LB, Hemphill JC III, Anderson C, et al Guidelines for the management of spontaneous intracerebral hemorrhage: a guideline for healthcare professionals from the American Heart Association/American Stroke Association Stroke 2010;41:2108–2129 14 Adams HP Jr, Adams RJ, Brott T, et al Guidelines for the early management of patients with ischaemic stroke: A scientific statement from the Stroke Council of the American Stroke Association Stroke 2003;34:1056–1083 15 Mayer SA, Brun NC, Begtrup K, et al Recombinant activated factor VII for acute intracerebral hemorrhage N Engl J Med 2005;352:777–785 16 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 17 Oddo M, Schmidt JM, Carrera E, et al Impact of tight glycemic control on cerebral glucose metabolism after severe brain injury: a microdialysis study Crit Care Med 2008;36:3233–3238 18 Mendelow AD, Gregson BA, Fernandes HM, et al Early surgery versus initial conservative treatment in patients with spontaneous supratentorial intracerebral haematomas in the International Surgical Trial in Intracerebral Haemorrhage (STICH): a randomised trial Lancet 2005;365:387–396 19 Zahuranec DB, Brown DL, Lisabeth LD, et al Early care limitations independently predict mortality after intracerebral hemorrhage Neurology 2007;68:1651–1657 20 Zurasky JA, Aiyagari V, Zazulia AV, et al Early mortality following spontaneous intracerebral hemorrhage Neurology 2005;64:725–727 21 Bederson JB, Connolly ES Jr, Batjer HH, et al Guidelines for the management of aneurysmal subarachnoid hemorrhage: a statement for healthcare professionals from a special writing group of the Stroke Council, American Heart Association Stroke 209;40:994–1025 22 Edlow JE Diagnosis of subarachnoid hemorrhage Are we doing better? Stroke 2007;38:1129–1131 23 Feigin VL, Rinkel GJE, Lawes CM, et al Risk factors for subarachnoid hemorrhage: an updated systematic review of epidemiological studies Stroke 2005;36: 2773–2780 24 Schievink WI, Torres VE, Piepgras DG, et al Saccular intracranial aneurysms in autosomal dominant polycystic kidney disease J Am Soc Nephrol 1992;3:88–95 25 Schievink WI, Limburg M, Oorthuis JW, et al Cerebrovascular disease in Ehlers–Danlos syndrome type IV Stroke 1990;21:626–632 292 SECTION VI NEUROLOGIC AND NEUROSURGICAL DISORDERS 26 Bederson JB, Awad IA, Wiebers DO, et al Recommendations for the management of patients with unruptured intracranial aneurysms: a statement for healthcare professionals from the Stroke Council of the American Heart Association Stroke 2000;31:2742–2750 27 Vermeulen MJ, Schull MJ Missed diagnosis of subarachnoid hemorrhage in the emergency department Stroke 2007;38:1216–1221 28 Kowalski RG, Claassen J, Kreiter KT, et al Initial misdiagnosis and outcome after subarachnoid hemorrhage JAMA 2004;291:866–869 29 Hunt WE, Hess RM Surgical risk as related to time of intervention in the repair of intracranial aneurysms J Neurosurg 1968;28:14–20 30 Longstreth WT Jr, Nelson LM, Koepsell TD, et al Clinical course of spontaneous subarachnoid hemorrhage: a population-based study in King County, Washington Neurology 1993;43:712–718 31 Le Roux PD, Elliot JP, Downey L, et al Improved outcome after rupture of anterior circulation aneurysms: a retrospective 10-year review of 224 good-grade patients J Neurosurg 1995;83:394–402 32 Dupont SA, Wijdicks EF, Manno EM, et al Thunderclap headache and normal computed tomographic results: value of cerebrospinal fluid analysis Mayo Clin Proc 2008;83(12):1326–1331 33 Naidech AM, Janjua N, Kreiter KT, et al Predictors and impact of aneurysm rebleeding after subarachnoid hemorrhage Arch Neurol 2005;62:410–416 34 Molyneux AJ, Kerr RS, Stratton I, et al International subarachnoid aneurysm trial (ISAT) of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: a randomized trial Lancet 2002;360(9342):1267–1274 35 Molyneux AJ, Kerr RS, Stratton I, et al International subarachnoid aneurysm trial (ISAT) of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: a randomized comparison of effects on survival, dependency, seizures, rebleeding, subgroups, and aneurysm occlusion Lancet 2005;366(9488):809–817 36 Suarez JI, Tarr RW, Selman WR, et al Aneurysmal subarachnoid hemorrhage N Engl J Med 2006;354: 387–396 chapter 28 Traumatic Brain Injury and Spinal Cord Injury Jason A Ellis, Kiwon Lee, and Dorothea Altschul c INTRODUCTION 293 c EPIDEMIOLOGY 293 c PATHOPHYSIOLOGY c INITIAL ASSESSMENT AND CLASSIFICATION 294 c ETIOLOGIES OF INJURY 295 295 c RADIOGRAPHIC EVALUATION c SURGICAL INDICATIONS 297 c INTENSIVE CARE MEASURES c INTRODUCTION Traumatic brain injury (TBI) and traumatic spinal cord injury (TSI) represent pathologies that result from a diverse spectrum of primary insults to the central nervous system (CNS) Nearly million cases of neurotrauma, including both TBI and TSI, occur annually in the United States making it an important public health issue.1–3 In addition to the long-term physical disabilities and the psychosocial impairments seen in neurotrauma survivors, the economic burden of TBI and TSI is significant The cost of TBI in the United States is estimated to be somewhere between $40 and $200 billion.3–6 For TSI, it is estimated that the lifetime total cost directly attributable to spinal cord injury in a 25-year-old patient may exceed $3 million.2 Advancements in our understanding of the pathophysiology of CNS injury post-trauma have led to improvements in the critical care of patients with TBI and TSI Indeed, the development of standardized guidelines for aggressive medical and surgical management of these patients has been credited for helping to improve outcomes.7,8 For severely brain- and/ or spinal cord–injured patients, it is crucial that a multidisciplinary approach be taken from the outset The foremost principle guiding the management of TBI and TSI patients is to minimize the secondary neural injury that inevitably follows a primary CNS insult Appropriate and timely emergency stabilization, criti- 297 299 cal care management, and surgical interventions are essential for delaying the progression of secondary CNS injury Toward this end, the clinician treating TBI and TSI patients must be able to assess, monitor, and treat the multitude of physiologic derangements that result from and also facilitate CNS injury In this chapter, we review the epidemiology, pathophysiology, and critical care management of TBI and TSI patients As neurosurgical intervention—whether at the bedside or in the operating room—is generally necessary for TBI and TSI patients, the surgical indications for pathology encountered in the emergency and critical care setting will also be reviewed c EPIDEMIOLOGY TRAUMATIC BRAIN INJURY The Centers for Disease Control and Prevention (CDC) estimates that 1.7 million people sustain TBI annually.1 Of this total, approximately 52,000 die, 275,000 are hospitalized, and 1.365 million are treated and released from an emergency department However, the actual number of TBI cases is uncertain as many patients either receive care in the field or not seek medical attention at all The causes of TBI in all age groups combined are: falls in 35.2%, motor vehicle accident in 17.3%, being struck in 16.5%, assault in 10%, and other or unknown causes 294 SECTION VI NEUROLOGIC AND NEUROSURGICAL DISORDERS in 21% Among all age groups, males have higher incidences of TBI and on average present with TBI about 1.4 times more frequently than females The CDC identified three age groups—children aged 0–4 years, adolescents aged 15–19 years, and adults aged 65 years and older—as most likely to sustain TBI Children aged 0–4 years had the highest rate of TBI-related emergency department visits (1,256 per 100,000 population) while hospitalization (339 per 100,000 population) and death (57 per 100,000 population) rates were highest among those 75 years and older TBI-related death rates have substantially declined in the past 30 years and can mostly be attributed to primary prevention Motor vehicle–related TBI deaths declined 22% and firearm-related TBI deaths declined 14% between 1989 and 1998.9 Recent data indicate more modest declines or relative stability in TBI mortality trends.1,10 TRAUMATIC SPINAL CORD INJURY The National Spinal Cord Injury Statistical Center (NSCISC) collects and dispenses the most comprehensive epidemiologic data on spinal cord injury in the United States They estimate the annual incidence of spinal cord injury at 40 cases per million population, representing about 12,000 new cases each year in the United States.2,11 About 80% of these injuries occur in males The most common causes of spinal cord injury include motor vehicle accident in 41.3%, fall in 27.3%, and violence in 15% Cervical spinal cord injuries are the most common comprising over 50% of lesions within the NSCISC database, followed by thoracic, lumbar, and sacral lesions Among all levels of injury, cervical lesions confer the worst prognosis with ventilator dependency having a strong negative association with survival Death in spinal cord–injured patients most commonly results from respiratory infections and septicemia associated with urinary infections and decubitus ulcers c PATHOPHYSIOLOGY An appreciation for the pathophysiologic mechanisms at work after TBI and TSI is important for the development and implementation of effective clinical therapeutic strategies Although typically treated separately, the pathophysiologies of both TBI and TSI have a number of similarities Most notably, the injury due to both TBI and TSI can be understood in terms of primary and secondary insults to neural tissue Primary injury denotes the initial mechanical damage secondary to energy transmission during impact while secondary injury results from the destructive tissue-intrinsic and body systemic response to primary injury The critical care of TBI and TSI patients is directed at minimizing secondary injury Detailed accounts of the molecular and cellular mechanisms of TBI and TSI have been given.12–15 Here we present a concise review of the pathophysiology of TBI and TSI with emphasis on delineating pathologic processes that are routinely targeted clinically BLOOD FLOW Both TBI and TSI are associated with focal and/or global hypoperfusion to the brain and spinal cord, respectively.13,14,16,17 Hypoperfusion can result from a number of mechanisms including microvascular or macrovascular damage, vasospasm, neurogenic/spinal shock, loss of autoregulation, or mechanical tissue disruption Decreased blood flow to neural tissue results in ischemia and ultimately infarction as cellular metabolic demands exhaust available resources For these reasons, it is unsurprising that reductions in cerebral blood flow (CBF) and hypotension portend a worse prognosis for TBI patients.18–23 The evidence suggests this may be true in TSI patients as well; however, further studies are warranted.24,25 Paradoxically, focally increased blood flow resulting in hyperemia may also result from acute injury to neural tissue Hyperemia is similarly as deleterious to the injured brain and spinal cord as is hypoperfusion Mechanistically, both processes result in a mismatch between blood flow and cellular metabolism Additionally, by facilitating oxidative damage to cells, promoting tissue edema, and increasing intracranial pressure (ICP), hyperemia further promotes secondary injury in the acute setting.12–14 METABOLISM Metabolic dysfunction results after TBI and TSI due to impaired delivery and/or utilization of oxygen and glucose within the injured brain and spinal cord.12–14 As neural cells depend on the production of highenergy molecules from aerobic metabolism to meet their energy requirements, even modest reductions in oxygen and glucose are poorly tolerated.12,26 The ionic fluxes associated with primary cellular injury result in the initiation of energy-dependent processes such as membrane transport in an attempt to restore homeostasis As energy stores become depleted, especially within the ischemic penumbra, cell death occurs.12 INFLAMMATION The robust inflammatory reaction seen within the damaged brain and spinal cord is a major component of both negative secondary injury processes and positive, CHAPTER 28 TRAUMATIC BRAIN INJURY AND SPINAL CORD INJURY reparative processes.12–14,26 At the site of injury, leukocyte recruitment and concurrent expression of inflammatory mediators such as TNF-a, interleukins, and complement molecules promote vascular permeability, edema, and progressive tissue damage Inhibition of this cytotoxic inflammatory milieu is a major target for the development of neuroprotective therapies EXCITOTOXICITY TBI and TSI are associated with excessive release of excitatory neurotransmitters such as glutamate in response to hypoxia.12–14,26 This in turn results in major ionic flux involving sodium, potassium, and calcium across cell membranes The accumulation of intracellular calcium in particular is associated with many toxic processes such as lipase and peroxidase activation as well as free radical generation c ETIOLOGIES OF INJURY TBI can be caused by a number of mechanisms that involve deforming brain tissue at various strain rates This may range from the relatively low strain rates imparted during simple collision to the higher rates associated with ballistic and blast mechanisms Injuries can be divided into two main categories—open (including penetrating) and closed head injuries Open head injuries involve violation of the skull and can result from foreign body (i.e., bullet, arrow, knife) entry or direct blunt force (i.e., blow from baseball bat) Closed head injury is most often caused by direct blunt force; however, primary blast– or shock wave–induced injuries are becoming increasingly prevalent in the military theater c INITIAL ASSESSMENT AND CLASSIFICATION The initial assessment of neurotrauma patients should begin with the familiar ABCs: evaluate the airway, confirm breathing with effective ventilation, and assess the circulatory status Cervical hard collar placement and 295 body immobilization on a rigid backboard is warranted for all trauma patients.27 Clinically deteriorating patients and those with a Glasgow Coma Scale (GCS) score of or less should be intubated as they are unable to adequately protect their airway Precautions such as logrolling and inline stabilization during intubation are prudent until spinal stability is verified.27 Cardiac, hemodynamic, respiratory, and pulse oximetry monitoring is necessary for all patients with moderate and severe TBI (see below) as well as in all TSI patients.16,17,28 Hypoxemia (SaO2 25 cm3 Midline shift >5 mm No high or mixed density lesion >25 cm3 a Data from Marshall L, Marshall S, Klauber M, et al A new classification of head injury based on computerized tomography J Neurosurg 1991;75(suppl):S14–S20 298 SECTION VI NEUROLOGIC AND NEUROSURGICAL DISORDERS essential for any physician caring for TBI and TSI patients Through the combined efforts of the Brain Trauma Foundation and the Congress of Neurological Surgeons, evidence-based recommendations were codified in the Guidelines for the Surgical Management of Traumatic Brain Injury.46 The specific intracranial traumatic lesions and the indications for surgery are outlined below As the indications for emergency surgery in TSI patients are not well defined, only a brief discussion will be given It is important to keep in mind that guidelines only provide recommendations for patients meeting specific criteria Thus, clinical judgment must also guide management in each unique scenario EPIDURAL HEMATOMA An acute EDH with a volume greater than 30 mL should be evacuated regardless of the patient’s GCS score In patients with GCS less than 9, pupillary abnormalities, or other focal neurologic deficits, a craniotomy for evacuation should occur as soon as possible An EDH with volume less than 30 mL, thickness less than 15 mm, and midline shift less than mm in a patient with GCS greater than and no focal deficits may be managed nonoperatively with serial head CT and close observation.47 a clinical decline by or more GCS points, hematoma evacuation as soon as possible is also indicated.48 PARENCHYMAL LESIONS Traumatic parenchymal lesions include both focal and nonfocal lesions The focal lesions occur at the site of impact (coup) or opposite the site of impact (contrecoup) and include intracerebral hematoma (ICH), contusion, and infarction Nonfocal lesions include diffuse injury typically resulting in hemispheric or global cerebral edema Patients with traumatic parenchymal mass lesions causing neurologic deterioration, refractory intracranial hypertension, or evidence of mass effect on CT should be treated surgically Similarly, any lesion greater than 50 mL should be evacuated In patients with GCS 6–8, a lesion greater than 20 mL should be evacuated if it is frontal or temporal in location and causing more than mm of midline shift and/or cisternal compression.49 Contusions commonly affecting the orbitofrontal and anterior temporal lobes must be observed with particular vigilance Delayed hematomas that can manifest or “blossom” within hours to days may require urgent craniectomy (Figure 28-1) POSTERIOR FOSSA MASS LESIONS SUBDURAL HEMATOMA An acute subdural hematoma (SDH) with thickness greater than 10 mm or midline shift greater than mm should be evacuated regardless of the patient’s GCS score If the patient is comatose (GCS 20 mm Hg or had A B A traumatic posterior fossa mass lesion should be evacuated by suboccipital craniectomy if there is radiographic evidence of mass effect or if neurologic dysfunction is referable to the lesion As neurologic decline can be precipitous in patients with these lesions, surgery should be performed as soon as possible.50 C Figure 28–1 Intracerebral hematoma expansion within bifrontal contusions This 27-year-old male patient presented with a GCS score of after being ejected head first from a motorcycle during a collision Initial noncontrast head CT was significant for bilateral frontal lobe contusions with early evidence of sulcal effacement (A) A follow-up noncontrast head CT performed hours after initial presentation showed the interval development of large bilateral intraparenchymal hemorrhages (B) The patient subsequently developed refractory intracranial hypertension necessitating performance of a bilateral frontotemporal craniectomy with duraplasty for ICP control (C) CHAPTER 28 TRAUMATIC BRAIN INJURY AND SPINAL CORD INJURY 299 DEPRESSED CRANIAL FRACTURES c INTENSIVE CARE MEASURES Closed (simple) nondepressed, typically linear, cranial fractures are not surgical lesions unless associated with an intracranial mass On the other hand, depressed cranial fractures may be managed either surgically or nonsurgically depending on the particular case Patients with open (compound) cranial fractures depressed greater than the thickness of the cranium should undergo early elevation of the bone fragments and debridement of the wound Open cranial fractures with depression less than cm and no dural penetration, significant intracranial hematoma, frontal sinus involvement, gross deformity, wound infection, pneumocephalus, or gross wound contamination may be treated nonoperatively Although not rigorously supported in the literature, closed depressed cranial fractures are often surgically treated if the extent of depression is greater than the thickness of the adjacent calvarium to effect better cosmesis and lower rates of post-traumatic seizure (PTS) and neurologic deficit Nonoperative management, however, is a treatment option in these cases.51 No discrete segregation exists between the emergency care, the surgical care, and the critical care of neurotrauma patients The intensive care management of TBI and TSI patients begins in the field with first responders and continues until the patient is stable for intensive care unit (ICU) discharge At all phases of care, the goal is to prevent additional primary injuries and to minimize the extent of secondary injury to the CNS The recommendations set forth in the Brain Trauma Foundation’s Guidelines for the Management of Severe Traumatic Brain Injury7 and in the American Association of Neurological Surgeons/Congress of Neurological Surgeons Joint Section on Disorders of the Spine and Peripheral Nerves’ Guidelines for the Management of Acute Cervical Spine and Spinal Cord Injuries56 are invaluable resources detailing medical management Additional guidelines have been released in an attempt to optimize prehospital, combat-related, and neurosurgical care These include the Guidelines for Prehospital Management of Traumatic Brain Injury,57 the Guidelines for the Field Management of Combat-Related Head Trauma,58 and the previously mentioned Guidelines for the Surgical Management of Traumatic Brain Injury.46 PENETRATING BRAIN INJURY Penetrating brain injury involves both missile and nonmissile trauma to the brain No strict guidelines dictate when surgical debridement, hematoma evacuation, and/or removal of protruding foreign body are warranted In one study of gunshot wounds to the head, it was suggested that all patients with GCS 9–15 should have aggressive surgical therapy; patients with GCS 6–8 should have surgical therapy if no transventricular, multilobar, or dominant hemisphere injury is present; and patients with GCS 3–5 should have surgical therapy only if a large extra-axial hematoma is present.52 SPINAL DECOMPRESSION AND STABILIZATION There are no well-defined indications for emergency decompression and stabilization in TSI patients.53,54 While animal studies suggest that early decompression is beneficial, the available human studies not consistently indicate improved neurologic outcomes A recent systematic review concluded that urgent decompression in patients experiencing neurologic deterioration, with bilateral locked facets in the setting of incomplete tetraplegia, or cervical cord injury may be appropriate.55 However, further studies are warranted to clarify the role of emergent surgical intervention in TSI patients BLOOD PRESSURE AND OXYGENATION As already emphasized in the section “Initial Assessment and Classification,” both hypotension (systolic blood pressure