2018 surgical critical care therapy a clinically oriented practical approach

For example,several well-designed randomized prospective trials have recently altered the way we care for surgical patients presenting with traumatic brain injury, hemorrhagic shock, acu

Ali Salim, Carlos Brown, Kenji Inaba and Matthew J Martin

Surgical Critical Care Therapy

A Clinically Oriented Practical Approach

Library of Congress Control Number: 2018935893

© Springer International Publishing AG, part of Springer Nature 2018

This work is subject to copyright All rights are reserved by the Publisher, whether the whole or part

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The field of surgical critical care is constantly expanding, evolving, and undergoing rapid change.Providers are experiencing increasing volumes of complex surgical cases and clinically challengingpostoperative patients from a wide variety of surgical subspecialties With the introduction of newtechnologies, less invasive surgery, balanced resuscitation strategies, and an aging population,

updating and communicating improved care techniques for the critically ill surgical patient are

crucial As providers, our goal is to deliver optimal, evidence-based care supported by relevantpolicies and data; however, there is no comprehensive source that provides concise and practicalguidance to intensivists and multidisciplinary ICU team members

The Surgical Critical Care Therapy textbook will provide a comprehensive, state-of-the-art

review of the field and will serve as a valuable resource for clinicians, surgeons, and researcherswith an interest in surgical critical care The chapters focus on the management of common problemsand critical decision-making scenarios that arise in the Surgical Intensive Care Unit For example,several well-designed randomized prospective trials have recently altered the way we care for

surgical patients presenting with traumatic brain injury, hemorrhagic shock, acute respiratory distresssyndrome, and sepsis The protocols, care bundles, guidelines, and checklists that show improvedprocess measures and patient outcomes will be discussed in detail throughout the book

We hope that this textbook will help guide patient management and stimulate future investigativeefforts Each chapter is written by widely recognized and established experts in the field who sharenumerous tips and wisdom gained over the course of their careers We also believe that this textbookwill become an invaluable resource for residents preparing for their in-service exams or the criticalcare portions of their general surgery board exams and for all fellowship-trained intensivists who aretaking the surgical critical care board examinations

We wish to thank the professional editorial efforts of Springer and to acknowledge our peers andfamily members for their support throughout this project Without the help of so many, this projectcould not have been brought to fruition

Carlos Brown Kenji Inaba Matthew J Martin

Ali Salim Austin, TX, USA, Los Angeles, CA, USA, Tacoma, WA, USA, Boston, MA, USA

1 Traumatic Brain Injury

Asad Azim and Bellal Joseph

2 Intracranial Pressure

David A Hampton and Deborah M Stein

3 Spinal Cord Injury

Michael Hernon and George Kasotakis

4 Analgesia, Sedation, and Delirium in the ICU

Douglas R Oyler and Andrew C Bernard

5 Alcohol Withdrawal

Uzer Khan and Alison Wilson

6 Brain Death Evaluation and Determination

Anupamaa Seshadri and Ali Salim

7 Management of the Potential Organ Donor

Margaret K M Ellis, Mitchell B Sally and Darren J Malinoski

8 Care of the Postop Craniectomy/​Craniotomy Patient

Filip Moshkovsky, Maureen Mercante and Mark Cipolle

9 Arrhythmia Evaluation and Management in the Surgical ICU

Benjamin L Davis and Martin A Schreiber

13 Care for the Postoperative Cardiac Surgery Patient

Andrew S Kaufman, Philip S Mullenix and Jared L Antevil

14 Targeted Temperature Management After Cardiac Arrest

Cindy H Hsu and Hasan B Alam

15 Assessment and Management of Acute Respiratory Distress in the ICU

Bishwajit Bhattacharya and Kimberly Davis

16 Noninvasive Ventilation

Eric Bui

17 Conventional Mechanical Ventilation

Elizabeth Warnack and Marko Bukur

18 Advanced Modalities and Rescue Therapies for Severe Respiratory Failure

Charles S Parsons and Charles H Cook

19 Acute Respiratory Distress Syndrome (ARDS)

Trista D Reid and David A Spain

20 Care of the Postoperative Pulmonary Resection Patient

John Kuckelman and Daniel G Cuadrado

21 Stress Gastritis and Stress Ulcers:​ Prevention and Treatment

Lisa M Kodadek and Christian Jones

22 Nutritional Support in the Surgical Critical Care Patient

Matthew J Martin, Joseph V Sakran and Robert G Martindale

23 Intra-abdominal Hypertension and Abdominal Compartment Syndrome

Javid Sadjadi and Gregory P Victorino

24 Acute Liver Failure

Amar Gupta and Chad G Ball

25 Acute Pancreatitis

Peter Fagenholz and Marc de Moya

26 Management of the Post-op Abdominal Catastrophe and Open Abdomen

Priya S Prakash and Patrick M Reilly

27 Acute Kidney Injury

Ian J Stewart and Joseph J DuBose

28 Renal Replacement Therapy:​ A Practical Approach

Craig R Ainsworth and Kevin K Chung

29 Management of Common Urologic Conditions Among the Critically Ill

E Charles Osterberg

30 Venous Thromboembolism, Prophylaxis, and Treatment (Including Fat Embolism Syndrome)

Franz S Yanagawa and Elliott R Haut

31 Blood Products and Transfusion Therapy in the ICU

Damon Forbes

32 Damage Control Resuscitation

Kyle J Kalkwarf and John B Holcomb

33 Anticoagulants and Antiplatelet Agents

Dave D Paskar and Sandro B Rizoli

34 Laboratory Assessment of Coagulation

Hunter B Moore, Eduardo Gonzalez and Ernest E Moore

35 Coagulopathies and Hypercoagulable States

Aaron Strumwasser and Erin Palm

36 Antibiotic and Antifungal Therapy in the ICU

Mitchell J Daley, Emily K Hodge and Dusten T Rose

37 SIRS/​Sepsis/​Septic Shock/​MOSF

Thomas J Herron and David J Ciesla

38 CLABSI

Tarek Madni and Alexander L Eastman

39 Catheter-Associated Urinary Tract Infections

Stephanie Nitzschke

40 Ventilator-Associated Pneumonia

Dina M Filiberto and Martin A Croce

41 Fungal, Viral, and Other Oddball Infections and the Immunosuppressed​ Patient

Sameer A Hirji, Sharven Taghavi and Reza Askari

42 Postoperative Intra-abdominal Infection

Paul B McBeth and Andrew W Kirkpatrick

43 New Fever in the Surgical Intensive Care Unit Patient

Evan Ross, Deidra Allison, Athena Hobbs and Ben Coopwood

44 Glycemic Control in Critically Ill Surgical Patients

Brian C Beldowicz, Jeremiah J Duby, Danielle Pigneri and Christine S Cocanour

45 Adrenal Insufficiency

Ellie Cohen and Walter L Biffl

46 Thyroid Hormone Abnormalities

James M Bardes and Elizabeth Benjamin

47 Intravenous Fluids

Peter Rhee and Paul M Evans

48 Sodium and Potassium Abnormalities

Caroline Park and Daniel Grabo

49 Other Electrolyte Abnormalities

Galinos Barmparas and George Paul Liao

50 Acid-Base Disorders

Jack Sava and Robel Beyene

51 Cirrhosis and End-Stage Liver Disease

James M Tatum and Eric J Ley

52 Obesity in Critical Care

Julietta Chang and Stacy Brethauer

53 Care of the Elderly Critical Care Patient

Christos Colovos, Nicolas Melo and Daniel Margulies

54 Burns

Gary Vercruysse

55 Care of the Patient with Liver Failure Requiring Transplantation

Caroline Park and Damon Clark

56 Care of the Critically Ill Pregnant Patient

Alexandra Edwards and Wendy F Hansen

57 Unique Aspects of Surgical Critical Care for Children

Jamie Golden, Aaron R Jensen, David W Bliss and Jeffrey S Upperman

58 Palliative Care in the Surgical Intensive Care Unit

Kathleen O’Connell and Zara Cooper

59 Ethics in Critical Care

Jessica Ballou and Karen J Brasel

60 Biostatistics and Research Design for Clinicians

Tarsicio Uribe-Leitz, Alyssa Fitzpatrick Harlow and Adil H Haider

61 Organizational Innovation in Surgical Critical Care

Brian C Beldowicz and Gregory J Jurkovich

62 Billing

R Lawrence Reed II

63 Tracheostomy in the ICU

Maher M Matar, Stephen A Fann and Bruce A Crookes

64 Feeding Gastrostomy Tubes

Brittany K Bankhead-Kendall and Jayson Aydelotte

65 Central Line Placement

Marc D Trust and Pedro G R Teixeira

66 Pulmonary Artery Catheter

Matthew J Eckert and Matthew J Martin

67 Extracorporeal Membrane Oxygenation:​ How Do We Do It?​

Pablo G Sanchez and Aaron M Cheng

68 Ultrasound Imaging for the Surgical Intensivist

Charity H Evans and Samuel Cemaj

69 Intra-aortic Balloon Pump

Daniel Dante Yeh

Index

Craig R Ainsworth

Burn Intensive Care Unit, Burn Center, US Army Institute of Surgical Research, Brooke Army

Medical Center, JBSA Fort Sam Houston, TX, USA

Uniformed Services University of the Health Sciences, Bethesda, MD, USA

Division of Trauma, Emergency Surgery and Surgical Critical Care, Los Angeles County and

Univeristy of Southern California Medical Center, Los Angeles, CA, USA

Galinos Barmparas

Department of Surgery, Division of Acute Care Surgery and Surgical Critical Care, Cedars-Sinai

Medical Center, Los Angeles, CA, USA

Brian C Beldowicz

Department of Surgery, Division of Trauma, UC Davis Health, Acute Care Surgery and Surgical

Critical Care, Sacramento, CA, USA

Elizabeth Benjamin

Division of Trauma, Emergency Surgery and Surgical Critical Care, Los Angeles County and

Univeristy of Southern California Medical Center, Los Angeles, CA, USA

Section of General Surgery, Trauma and Surgical Critical Care, Department of Surgery, Yale School

of Medicine, New Haven, CT, USA

Walter L Biffl

Scripps Memorial Hosptial La Jolla, San Diego, CA, USA

David W Bliss

Department of Surgery, Keck School of Medicine of the University of Southern California, Division

of Pediatric Surgery, Children’s Hospital Los Angeles, Los Angeles, CA, USA

Department of Surgery, Bellevue Hospital Center, New York, NY, USA

Division of Trauma and Surgical Critical Care, New York University School of Medicine, New York,

NY, USA

Samuel Cemaj

Department of Surgery, University of Nebraska Medical Center, Omaha, NE, USA

Department of Medicine, Brooke Army Medical Center, JBSA-Fort Sam Houston, TX, USA

Uniformed Services University of the Health Sciences, Bethesda, MD, USA

Section of General Surgery, Trauma and Surgical Critical Care, Department of Surgery, Yale School

of Medicine, New Haven, CT, USA

Marc de Moya

Division of Trauma, Acute Care Surgery, Medical College of Wisconsin, Froedtert Hospital,

Milaukee, WI, USA

Joseph J DuBose

Division of Vascular Surgery, David Grant Medical Center, Travis AFB, CA, USA

Jeremiah J Duby

Department of Pharmacy Services, UC Davis Health, Sacramento, CA, USA

Touro University, College of Pharmacy, Vallejo, CA, USA

UCSF School of Pharmacy, San Francisco, CA, USA

Alexander L Eastman

Department of Surgery, Division of Burns, Trauma, and Critical Care, University of Texas

Southwestern, Dallas, TX, USA

Department of Surgery, Keck School of Medicine of the University of Southern California, Division

of Pediatric Surgery, Children’s Hospital Los Angeles, Los Angeles, CA, USA

Wendy F Hansen

Department of Obstetrics and Gynecology, University of Kentucky College of Medicine, Lexington,

KY, USA

Alyssa Fitzpatrick Harlow

Center for Surgery and Public Health (CSPH), Brigham and Women’s Hospital, Boston, MA, USA

Department of Surgery, Keck School of Medicine of the University of Southern California, Division

of Pediatric Surgery, Children’s Hospital Los Angeles, Los Angeles, CA, USA

Department of Surgery, Cedars-Sinai Medical Center, Los Angeles, CA, USA

George Paul Liao

Department of Surgery, Division of Acute Care Surgery and Surgical Critical Care, Cedars-SinaiMedical Center, Los Angeles, CA, USA

Tarek Madni

Department of Surgery, Division of Burns, Trauma, and Critical care, University of Texas

Southwestern, Dallas, TX, USA

Department of Surgery, University of Colorado Denver, Denver, CO, USA

Department of Surgery, Denver Health, Denver, CO, USA

Revenue Cycle Services, IU Health, Department of Surgery, IU Health Methodist Hospital,

Indianapolis, IN, USA

Trista D Reid

Division of General and Acute Care Surgery, UNC Department of Surgery, University of North

Carolina at Chapel Hill, Chapel Hill, NC, USA

Patrick M Reilly

Department of Surgery, Division of Trauma, Surgical Critical Care, and Emergency Surgery,

Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA

Peter Rhee

Division of Acute Care Surgery, Department of Surgery, Grady Memorial Hospital, Atlanta, GA,USA

Department of Surgery, Acute Care Surgery Division, University of Rochester Medical Center,

Rochester, NY, USA

Department of Surgery, Keck School of Medicine of the University of Southern California, Division

of Pediatric Surgery, Children’s Hospital Los Angeles, Los Angeles, CA, USA

Department of Surgery, Bellevue Hospital Center, New York, NY, USA

Division of Trauma and Surgical Critical Care, New York University School of Medicine, New York,

NY, USA

Alison Wilson

WVU Critical Care and Trauma Institute, Department of Surgery, Ruby Memorial Hospital, WVU

Medicine, Morgantown, WV, USA

Franz S Yanagawa

Department of Surgery, Johns Hopkins University School of Medicine, Baltimore, MD, USA

Daniel Dante Yeh

Department of Surgery, Ryder Trauma Center, Miami, FL, USA

© Springer International Publishing AG, part of Springer Nature 2018

Ali Salim, Carlos Brown, Kenji Inaba and Matthew J Martin (eds.), Surgical Critical Care Therapy , 71712-8_1

https://doi.org/10.1007/978-3-319-1 Traumatic Brain Injury

Traumatic brain injury (TBI) is a non-degenerative, non-congenital disruption of brain function from

an external force that leads to a permanent or a temporary impairment of cognitive and/or physicalfunctions —it may or may not be associated with a diminished or altered state of consciousness Theexternal forces that create the injury may be the result of a variety of insults, including acceleration ordeceleration, compression, penetrating objects, and complex mechanisms like blast injuries TBI isthe leading cause of death and disability among trauma patients According to an estimate, about 2.5million TBIs occur every year Of those, about 50,000 people die, and approximately 80,000–90,000survivors suffer severe lifelong neurological disabilities [1] The external cause of injury

(“mechanism of injury”) associated with TBI varies with age and demographics Males aged 0–4have the highest rates of TBI-related visits, whereas adults aged 75 years and older have the highestrate of TBI-related hospitalizations and deaths (1) Falls are the leading mechanism of injury of TBI,accounting for 40% of all TBI-related emergency department (ED) visits (2) They cause more thanhalf (55%) of all TBIs among children aged 0–14 years and 81% of all TBIs among adults aged

65 years and older The second leading mechanism of injury is unintentional blunt trauma , accountingfor 15% of all TBI-related ED visits (1) Motor vehicle collisions and assaults are the third andfourth leading mechanisms of injury, accounting for 14% and 10% of TBI-related ED visits,

respectively [2]

Types of Primary Injuries

Various types of primary TBI are summarized below

Subdural Hematoma (SDH): SDH is the most common type of traumatic brain lesion and occurs

in about 20–40% of severely head-injured patients SDH originates in the space between the

dura and the arachnoid matter of the meninges [3] It results from damage and tearing of corticalbridging veins, which drain the cerebral cortical surface into the dural venous sinuses The

presentation can be acute, subacute, or chronic Patients have variable loss of consciousness(LOC) On CT imaging, SDH appears to be crescent-shaped It tends to be associated withunderlying cerebral injury and thus usually has a poor prognosis [4]

Epidural Hematoma (EDH): EDH is a form of intracranial bleed between the dura mater and the

inner table of the skull It results from tearing of arterial dural vessels, i.e., middle meningealartery The most common site is temporal, where the bone is very thin and susceptible to

fracture On CT imaging, EDH appears to be lenticular-shaped EDH is usually due to skullinjury rather than brain injury, although brain injury certainly can occur with them Morbidity andmortality associated with EDH is primarily due to the mass effect from the hematoma, which, ifleft unchecked, can lead to brain herniation [5]

Subarachnoid Hemorrhage (SAH): SAH results from disruption of small pial vessels between

the subarachnoid and the pia mater of the meninges Trauma is the most common cause of SAH.Patients with traumatic SAH have 70% higher risk of developing cerebral contusion and 40%higher risk of developing subdural hematoma [6] SAH is a marker of the severity of TBI Thepositive predictive value of SAH (>1 cm) for poor outcome is 72–80% On CT imaging, SAHappears as hyper-attenuating material filling the subarachnoid space [7]

Intraparenchymal Hemorrhage (IPH): This is a form of intracerebral bleed in which there is

bleeding within the brain parenchyma IPH , along with cerebral edema, may disrupt and

compress adjacent brain tissue, constituting an immediate medical emergency On CT imaging,IPH appears as the accumulation of blood within different intracranial spaces, most commonly

as a lobar hemorrhage [8]

Intraventricular Hemorrhage (IVH): IVH refers to bleeding into the ventricular system of the

brain, where cerebrospinal fluid is produced and circulates toward the subarachnoid space Itcommonly results from an intracerebral hemorrhage with ventricular reflex On CT imaging,blood appears as hyper-dense material in the ventricles that is best seen in the occipital horns.Blood in ventricular system also predisposes these patients to post-traumatic hydrocephalus.IVH is also a marker of severity of injury and is associated with adverse outcomes [9]

Cerebral Contusion: Contusion is bruising of brain tissue often caused by a blow to the head.

When this happens, the blood-brain barrier loses its integrity, thereby creating a heterogeneousregion This type of lesion usually occurs in coup or contrecoup injuries It manifests in corticaltissue and can be associated with multiple microhemorrhages and small vessels that leak intobrain tissue The most common regions of the brain affected are the frontal and anterior temporallobes Cerebral contusions often take 12–24 h to evolve and may be absent on an initial head CTscan [10]

Cerebral Concussion: This is the most common type of TBI It occurs with a head injury caused

by acceleration/deceleration forces or contact forces It can result in rapid-onset, short-livedimpairment of neurological function that resolves spontaneously Concussions are a clinicaldiagnosis as there are no CT scan findings associated with it The key signs and symptoms of aconcussion are confusion and amnesia [11]

Diffuse Axonal Injury (DAI): A DAI is the most common and devastating type of TBI, resulting

from extensive damage to white matter tracts over a widespread area This injury develops fromtraumatic shearing forces that occur when the head is rapidly accelerated or decelerated DAI iscommonly seen in motor vehicle collisions and shaken baby syndrome The sites frequentlyinvolved in DAI are the frontal and the temporal lobes CT imaging usually appears normal.Newer imaging modalities, such as diffusion tensor imaging, are more sensitive than a standardMRI for detecting a white matter tract injury [12].

Secondary Brain Injury

Secondary brain injury is a consequence of pathological processes set in motion at the time of

primary insult Mechanism behind secondary brain injury is complex It is purposed that it is due tothe liberation of proinflammatory cytokines and chemicals as result of primary injury that leads tocerebral edema neuronal death and disruption of the blood-brain barrier [13] The common pathwaysthat contribute to this damage are the liberation of excitatory amino acids, platelet-activating factors,and oxygen free radicals and ubiquitous nitric oxide radicals [14] While little can be done to limitprimary injury, the main goals of current TBI management strategies are targeted at limiting secondarybrain injury With recent advances and better understanding of cellular and biochemical functions, ithas become more clear that inadequate blood flow and substrate delivery result in exacerbation ofsecondary injury [15] Hence, ensuring adequate nutritional supply and avoiding hypoxia and

hypotension can help limit secondary brain injury and enhance neuronal recovery [16]

Emergency Management

History and Physical Examination

A history and physical examination should be obtained, including the events preceding a trauma, adescription of the actual event, and complete description of the patient’s neurological status History

of medications as well as medications given in the prehospital setting should be determined Specialattention should be paid to medications with the ability to alter the neurological examination,

including sedatives or psychopharmacologics, paralytics, atropine (for cardiac resuscitation), andother mydriatics (for evaluation of ocular trauma) Primary and secondary surveys should be

performed thoroughly evaluating for systemic injuries Open lacerations and a vigorous scalp

hemorrhage may lead to hypovolemia

or declining condition The accuracy and completeness of a neurological exam is based on the

alertness and cooperativeness of the patient The extent of the examination must be tailored to eachpatient’s neurological ability

Pupillary Response : Documenting pupillary abnormality is important, and it has a high

diagnostic and prognostic utility [17] Pupillary asymmetry is defined as a difference of >1 mm

between the pupils A dilated pupil is defined as a diameter of a pupil >4 mm A fixed pupilshows no response to bright light Orbital trauma, hypotension, and hypoxia are common causes

of pupillary dilation Hypoxia and hypotension should be corrected before herniation can beexcluded as a cause of pupillary dilation Orbital trauma can be ruled out by using direct andconsensual response for each pupil

Glasgow Coma Scale (GCS): An important component of a primary survey is to obtain an

accurate GCS It has become the standard for the objective measurement of the severity of aTBI A GCS assesses a patient’s neurological status based on three components: motor function,verbalization, and eye opening (Table 1.1) A patient who is neurologically intact can receive amaximum score of 15, and the most severely injured patient can get a minimum score of 3 If thepatient is intubated, the verbal component is given a score of “q,” and the overall score is

annotated with a “T.” A GCS 13–15 defines a mild TBI—such patients are usually awake andhave no focal deficits A GCS 9–12 is considered a moderate TBI, in which patients have

altered sensorium and focal neurological deficits Patients with a GCS 3–8 have a severe TBI.Usually, they will not follow commands, and they fit the criteria of comatose state [17]

Table 1.1 Glasgow Coma Scale

6 Obeys command – –

5 Localizes to pain Oriented –

4 Withdraws to pain Confused Spontaneously

3 Flexes arm Words/phrases To voice

2 Extends arm Makes sounds To pain

1 No response No response Remain closed

Airway, Breathing, and Circulation

Clinicians should adhere to the basic principles of trauma resuscitation, including rapid assessmentand maintenance of an airway, breathing, and circulation [18] The maintenance of an unobstructedand clear airway is of the utmost importance as hypoxia is the most critical factor leading to adverseoutcomes in TBI patients A multicenter trial has shown that mortality rises by 17% in patients thatexperience hypoxic episodes following a TBI [19] Regarding patients with a GCS <9, guidelinesrecommend that skilled personnel should intubate them by rapid sequence induction During

intubation, the cervical spine should be considered injured until proven otherwise, and it must beprotected

Once the airway is secured, the patient must be ventilated appropriately to maintain normocarbia(PaCO2 35–40 mmHg) Monitoring of oxygen saturation and capnography is recommended in

severely injured patients to avoid unrecognized hypoxemia or changes in ventilation A study of11,000 TBI patients showed that both hypo- and hypercarbia were associated with increased

mortality in TBI patients [20] In patients with signs of brain herniation, transient hyperventilationmay be an option

Hypotension is a major secondary brain insult Studies have shown that even a single episode ofhypotension is associated with a dramatic increase in mortality in TBI patients [21] It should betreated with appropriate fluid resuscitation and blood products to achieve euvolemia Recent studies

have shown that maintaining systolic blood pressure above 100 mmHg is associated with decreasedmortality and better neurological outcomes in TBI patients [22].

Radiological Assessment

Computed Axial Tomography (CT) Scan CT scan remains the investigation of choice for patientspresenting with head trauma In a single, rapid pass, without patient repositioning, scans of the head,neck, chest, abdomen, and pelvis can be performed Additionally, administration of contrast alsoallows for a CT angiogram reconstruction in order to evaluate vasculature of the head and neck CTscan findings after trauma include SDH, EDH, SAH, IPH, IVH, contusions, hydrocephalus, cerebraledema or anoxia, skull fractures, ischemic/infarction (if >12 h old), and mass effect resulting in

midline shift Indications for an initial post-traumatic head CT scan include GCS ≤14,

unresponsiveness, focal deficit , amnesia for the injury, altered mental status, and signs of basilarskull fracture [23]

Magnetic Resonance Imaging (MRI) MRI scans have better parenchymal resolution and canevaluate infarction, ischemia, edema, and DAI An MRI is also helpful to determine a ligamentousinjury of the spine or a traumatic cord injury It is generally performed after the initial trauma

evaluation and resuscitation have been completed MRIs have limited availability, slower imageacquisition time, image interference by monitoring devices, and a greater cost Although their use inthe initial assessment of trauma is not routinely recommended because intracranial surgical lesionsseen on an MRI can also be identified on a CT scan [24], their use in the ICU setting can play a

crucial role in evaluating DAI

Intensive Care Unit Management

disruption of cerebral autoregulation, which is a common event following severe TBI, cerebral

perfusion relies on SBP Hence, a low SBP leads to cerebral ischemia, which is recognized as thesingle most important secondary insult In order to decrease mortality and improve clinical outcomesfollowing a TBI, SBP should be maintained at ≥100 mmHg for patients 50–69 years old or at

≥110 mmHg for patients 15–49 years old or over 70 years old (5)

Intracranial Pressure (ICP) The concept of intracranial pressure is based on the Monro-Kelliehypothesis Assuming that the skull is a closed space, the hypothesis states that there is a balancebetween brain, blood volume, and CSF Increase in the volume of one constituent (e.g., cerebral

edema) or an addition of a constituent (i.e., hemorrhage or tumor) mandates a compensatory decrease

in other constituents in order to maintain ICP The management of raised ICP varies greatly in clinicalpractice, and there are inconsistent reports about the utility of ICP monitoring on clinical outcomesand survival of TBI patients According to the recently updated Brain Trauma Foundation (BTF 4th

Edition 2016) guidelines, ICP monitoring should be performed in all salvageable patients with severeTBI (GCS 3–8) and an abnormal head CT, a normal head CT scan with a SBP of ≤90 mmHg,

posturing, or age ≥40 years [25] Studies have shown that treating ICP above 22 mmHg is

recommended to reduce overall mortality [26] Moreover, management of severe TBI using

information from ICP monitoring is associated with reduced in-hospital and 2-week post-injury

mortality A vast majority of patients with severe TBI meet the criteria for ICP monitoring based onthese guidelines However, only a small subset of these patients receives ICP monitoring based oninstitutional guidelines A prospective multicenter controlled trial performed in Ecuador

demonstrated that there is no difference in clinical outcomes in patients who underwent ICP

monitoring compared to those who were managed with an established protocol of neuroimaging andclinical examination [27] Medical management remains the standard of care for elevated ICP, with apossible role for ICP monitoring and operative intervention in a subset of patients However, furtherstudies are required to better define subset of patients requiring ICP monitoring

Cerebral Perfusion Pressure Monitoring (CPP) A traumatically injured brain is at a high risk of

a local cerebral ischemia around the area of primary insult as well as global ischemia due to loss ofcerebral circulation In such a situation, maintaining adequate cerebral perfusion is of prime

importance CPP is defined as the pressure gradient across the cerebral vascular bed between bloodinflow and outflow It is calculated as the difference between mean arterial pressure (MAP) and ICP.Studies have shown that a CPP of less than 50 mmHg is associated with a high risk of cerebral

ischemia and secondary brain injury The BTF guidelines recommend a target CPP value between 60and 70 mmHg for improved survival and favorable outcomes [25] TBI management includes CPPmonitoring in the “bundle” of care; however, the impact of CPP-based management of TBI patientsremains unclear There is some evidence which suggests that the management of TBI patients’ usinginformation from CPP monitoring is associated with 2-week post-injury mortality

therapies reduce ICP by two distinct methods One commonly accepted mechanism is via

establishment of an osmolar gradient across the blood-brain barrier , with the gradient favoring theflow into the circulation Another mechanism, which explains the rather more rapid action of osmolaragents, is improvement in the rheology of the blood due to plasma expansion as well as decreasedhematocrit, which leads to decreased viscosity and more efficient cerebral blood flow (CBF) It isbelieved that the two most commonly utilized hyperosmolar agents, that is, hypertonic saline andmannitol, utilize both mechanisms [29]

Mannitol: Mannitol is a naturally occurring sugar alcohol used clinically for its osmotic diuretic

properties It has been accepted as an effective tool for reducing intracranial pressure Althoughthere has never been a randomized comparison of mannitol with a placebo, both the BTF and the

European Brain Injury Consortium identify level II and III evidence to support its use for thetreatment of intracranial hypertension after a TBI Mannitol can be administered as a bolus inresponse to raised ICP or as a continuous drip in a prophylactic fashion [29] Studies have

shown that bolus infusion is superior to continuous therapy ; however, a difference of opinionstill exists concerning the two modes of administration Although mannitol plays a vital role incontrolling ICP in severe TBI patients, its eventual diuretic effect is undesirable in hypotensivepatients, and appropriate monitoring and aggressive fluid resuscitation are required to replenishfluid loss and to maintain SBP within target limits Clinicians should be cautious, however,

because mannitol therapy can accumulate in extracellular space if the infusion rates are higherthan the excretion of the drug This leads to a phenomenon known as the “rebound effect ”

movement of water back into the brain

Hypertonic Saline : While hyperosmolar therapy has been utilized to reduce elevated

intracranial pressure and edema in TBIs for nearly five decades, the use of hypertonic saline(HTS) as a hyperosmolar agent has only recently become a popular choice for both resuscitationand maintenance therapy in TBI patients Physiologically, the sodium content is what determinesthe amount of volume increased intravascularly during initial resuscitation HTS was initiallyused as a volume expander in the resuscitation of patients with hemorrhagic shock on the

battlefield as a low-volume resuscitation fluid It was observed that in patients with hemorrhagicshock and TBI, resuscitation with HTS was associated with better survival [30] In patients withsevere TBI and increased ICP or brain edema, a serum sodium level Na + up to 150–155 mEq/Lmay be acceptable [31] At our institution, the serum Na + should be maintained below

158 mEq/L Further studies on animal and humans revealed that this decrease in mortality isattributed to a reduction in ICP and cerebral edema, which was due to hyperosmolar effects ofHTS There is no consensus about the exact makeup of HTS Concentrations of 3%, 5%, 7.2%,10%, and 23.4% have all been referred to in the literature The most commonly used

concentration of HTS is 3%, though, recently, 5% saline has become more prevalent In

comparison with 3% HTS , studies have demonstrated that 5% HTS has a sustained higher

serum osmolarity and serum sodium concentration within the first 72 h, without any increase inadverse effects [32] Over time, HTS evolved as an alternative to mannitol in treating cerebraledema and raised ICP following a TBI HTS has been shown to have more profound and

sustained effects on ICP, immune modulation, neurological recovery, and survival Moreover,known adverse effects of mannitol, like renal injury, worsening of heart failure, and osmoticdiuresis, make HTS a better contender for hyperosmolar therapy for the management of TBI.Although there is not enough evidence to support its definitive superiority over mannitol , HTShas clear logistical advantages over mannitol in the treatment of TBI

Decompressive Craniectomy (DC) Cerebral edema can result from a combination of severalpathophysiological mechanisms associated with primary and secondary injury following a TBI Asthe skull is a closed cavity, increase in intracranial contents (i.e., cerebral edema) results in braintissue displacement causing cerebral herniation ultimately leading to severe disability or death DC isdefined as the surgical removal of a portion of the skull and the opening of the underlying dura for thepurpose of relieving elevated ICP A lot of controversy exists regarding the role of DC in the

management of severe TBI due to variation in surgical techniques, timing, and the patient population

in the recent literature published in the last decade According to current BTF guidelines, bifrontal

DC is not recommended to improve outcomes as measured by the Glasgow Coma Outcome

Scale-Extended (GOS-E) score at 6 months post-injury However, a large frontotemporoparietal DC (notless than 12 × 15 or 15 cm diameter) is recommended to reduce mortality and improve neurologicaloutcomes in patients with a severe TBI with a diffuse injury and ICP values >20 mmHg refractory tomedical treatment [25] A recent randomized controlled trial of DC for refractory traumatic

intracranial hypertension (RESCUEicp Trial) [33] has shown that it is associated with lower

mortality but higher rates of a vegetative state at 6 months In contrast to a DC as a last-tier therapy,

an early DC as a primary treatment has the advantage of rapid ICP control of elevated ICP; there is,however, increased risk of a number of potential complications that include infections , subduralhygromas, hydrocephalus, syndrome of trephined, and cerebral infarction [34]

Prophylactic Hypothermia Suspended animation, the ability to put a person’s biological

processes on hold, has long been a staple of science fiction Interest in the field blossomed in the1950s as a direct consequence of the space race However, most of the studies to date have utilizedwhole-body cooling, and this technique is associated with an increased risk of adverse effects,

including coagulopathy, hypotension, and infections in patients [35] In order to minimize such effectsand gain maximum benefits of therapeutic hypothermia, a novel method of selective brain cooling(SBC) has been devised It uses bilateral common carotid artery (CCA) cooling cuffs that can achieverapid reductions in core brain temperature without significant changes in normal body temperature[36] Potential neuroprotective effects of SBC are mediated by reducing the hemoglobin

accumulation, inhibition of injury-mediated upregulation of HO-1, which, in turn, ameliorates brainedema Compared to standard therapy , a recent international, multi-institutional, randomized

controlled trial (Eurotherm 3235) that examined the effects of titrated therapeutic hypothermia (32–35°C) as a treatment for raised ICP demonstrated worse outcomes with lower Glasgow OutcomeScale-Extended (GOS-E) scores among patients with therapeutic brain cooling These findings in theinterim analysis were considered harmful, and the trial was stopped in 2014 [37] Another multi-institutional trial to access the utility of therapeutic hypothermia for 48–72 h with slow rewarmingafter severe TBI in children was conducted It was also terminated early due to ineffectiveness of thetherapy as compared to a standard treatment [38] Therefore, in keeping with the results of these

randomized trials, the previously ascertained therapeutic benefit of hypothermia on mortality andneurological outcome in TBI patients is minimal, and recommendations for its use cannot be made

Ventilation Therapy Severe TBI patients require airway protection because they are at increasedrisk of aspiration or compromised respiratory drive In addition to normal ventilation, which is

currently the goal for severe TBI patients, sometimes these patients may require transient

hyperventilation to treat intracranial hypertension and cerebral herniation Under normal

circumstances, PaCO2 is a strong determinant of CBF, and a range between 20 and 80 mmHg CBF islinearly responsive to PaCO2 Low PaCO2 therefore causes a decrease in CBF by cerebrovascularconstriction , while a high PaCO2 increases CBF via cerebrovascular dilation Older studies

suggested that cerebral hyperemia is more common than cerebral ischemia; hence they recommendedhyperventilation as a management therapy for TBI patients However, this has been falsified by recentstudies demonstrating cerebral ischemia as a major culprit, thereby changing the long-standing

recommendations concerning ventilation therapy Current guidelines state that prolonged prophylactichyperventilation with partial pressure of carbon dioxide in arterial blood (PaCO2) of 25 mmHg orless is not recommended Hyperventilation can be used as a temporizing measure to reduce elevated

ICP; however, it should be avoided during first 24 h post-injury when CBF is typically reduced Theoptimal timing for tracheostomy has been controversial A common perception is that early

tracheostomy may reduce the necessity for mechanical ventilation In a prospective randomized

clinical trial of trauma patient, early tracheostomy (within 7 days) was associated with reduction induration of mechanical ventilation In addition, reduction in hospital and ICU length of stay was alsoobserved in the early tracheostomy group [39] According to Eastern Association for the Surgery ofTrauma (EAST) , early tracheostomy (within 3–7 days of TBI) should be performed as it decreasesthe total days of mechanical ventilation and ICU length of stay [40] However, none of the randomizedclinical trials have demonstrated survival benefit of early tracheostomy [41]

Anesthetic Analgesics and Sedatives Anesthetics , analgesics , and sedatives are widely usedtherapies in acute TBI as either prophylaxis or to control ICP and seizures Barbiturates have

historically been used to control ICP, presumably by preventing unnecessary movements, metabolicsuppression, and alteration of cerebral vascular tone [42] Anesthetic, analgesic, and sedative therapyalso carries with it high morbidity Side effects include hypotension, decreased cardiac output, aswell as increased intrapulmonary shunting, which leads to hypoxia and decreased cerebral perfusion.For these reasons, high-dose barbiturates (barbiturate coma) should not be initiated unless

hemodynamic stability is insured in victims of refractory intracranial hypertension following TBI[43]

Steroids Steroids were introduced in the early 1960s as a treatment for brain edema [44]

Experimental evidence accumulated indicates that steroids were useful in the restoration of alteredvascular permeability in brain edema, reduction of cerebrospinal fluid production, and attenuation offree radical production Several randomized controlled trials demonstrated benefits with the use ofmethylprednisolone for 24 h; however, meta-analysis of these randomized trials failed to demonstrateany conclusive benefit of steroids in TBI The most conclusive evidence was brought forward afterthe CRASH (Corticosteroid Randomization After Significant Head Injury ) trial in over 10,000 TBIpatients that demonstrated an 18% higher risk of death 2 weeks post-injury in patients who were

randomized to receive corticosteroids for 48 h [45]

Nutrition Following TBI there is a cascade of inflammatory cytokines released into the blood

stream that initiates rapid catabolism and increased energy expenditure Therefore, TBI patients

require appropriate nutritional support at the right time for optimal recovery Nutritional support afterTBI provides patients with appropriate substrates, essential nutrients, and enough calories to inhibitcatabolism and promote rapid neurological recovery [46] Based on this evidence, current BTF

guidelines and the American Association of Neurological Surgeons’ (AANS) guidelines recommendinitiation of enteral nutrition within 72 h and full nutritional replacement by the seventh day [25].Recent studies have shown that initiation of tube feeds as early as within the first 24 h of injury caninterfere with post-injury acute phase response , which is an immediate protective response of thebody to protect primary host functions This can lead to slower recovery and higher incidence ofpneumonia in these TBI patients [47] For optimal clinical results and rapid recovery in TBI, nutritioncan be safely started after the first 24 h post-injury and should advance toward optimal nutritionalgoals over the next 48–72 h

Seizure Prophylaxis Acute symptomatic seizures occur as a result of severe TBI Post-traumatic

seizures (PTS) are classified as “early” when they occur within 7 days of injury and “late” when theyoccur after 7 days of injury Rate of PTS in patients with severe TBI is as high as 12%, whereas rate

of subclinical seizures detected by electroencephalography is as high as 20–25% [48] Risk factorsfor early PTS include the following: GCS of ≤10; immediate seizures; post-traumatic amnesia lastinglonger than 30 min; a linear or depressed skull fracture; a penetrating head injury; subdural, epidural,

or intracerebral hematoma; cortical contusion; age ≤65 years; and chronic alcoholism The BTF

recommends use of phenytoin to decrease the incidence of early PTS; however, neither phenytoin norvalproic acid has shown any benefit in limiting late PTS Levetiracetam (Keppra), a relatively newerdrug, has recently gained popularity for seizure prophylaxis for various pathologies , including TBI[49] However, current evidence is insufficient to recommend for or against its use over other

available agents

Beta Blocker

Animal model studies of TBI have shown an increase in sympathoadrenal activity after TBI Thisincrease in sympathetic activity by surge in catecholamine has shown to be directly associated withincreased mortality, lower neurological recover, and increase in hospital stay [50].Based on thesefindings, beta blockers have been studied as a potential therapeutic option after brain injury In a

murine model of TBI, propranolol was administrated after induction of TBI Propranolol-treated micedemonstrated improved survival and histological recovery [51] Several retrospective studies haveshown an independent association of beta blockers with survival [52, 53] Despite optimistic results,early beta-blockade use is not indicated routinely Propranolol may be the ideal agent because of itsnonselective inhibition and its lipophilic properties allowing it to penetrate the blood-brain barrier

In a randomized placebo controlled clinical trial, early administration of propranolol after TBI wasassociated with improved survival after controlling for confounding factors, demonstrating its

potential role in TBI [54] Another randomized placebo controlled trial is currently ongoing to

evaluate the role of beta blockers in traumatic brain injury by decreasing adrenergic or sympathetichyperactivity [55]

Most of the modern ICUs utilize guidelines for the management of TBI and ICP Figure 1.1 showsthe intracranial pressure monitoring guidelines which is implemented at our level I trauma center

Fig 1.1 Intracranial pressure monitoring guidelines SaO2, oxygen saturation; SBP, systolic blood pressure; PCO2, partial pressure of

carbon dioxide; GCS, Glasgow Coma Scale; HO, house officer; CPP, cerebral perfusion pressure; ICP, intracranial pressure; ETT, endotracheal tube

Complications

Coagulopathy TBI is often associated with disturbances in the coagulation profile Coagulopathyaffects up to one-third of TBI patients [56] Mechanisms by which TBI induces coagulopathy includelocal and systemic inflammation, which lead to the release of tissue factor, activation of the protein Cpathways, platelet dysfunction, and disseminated intravascular coagulation Coagulopathy after TBI is

a dynamic process that goes through stages of hypercoagulability and hypocoagulability ultimatelyleading to a state of bleeding diathesis [56] TBI coagulopathy is diagnosed with traditional measures

of coagulation, such as prothrombin time, activated partial thromboplastin time, and internationalnormalized ratio It has also been shown that development of coagulopathy after TBI is associated

with higher mortality In recent years, viscoelastic tests such as thromboelastography (TEG) and

rotational thromboelastometry (ROTEM) have been frequently used to assess TBI coagulopathy

These coagulation tests are both more sensitive and specific than conventional assays They are alsomore efficient in predicting therapy for TBI-induced coagulopathy [57]

The reversal of TBI coagulopathy requires the replacement of coagulation factors Classically, freshfrozen plasma (FFP) has been used to reverse both acquired and induced TBI coagulopathy Studieshave demonstrated that prothrombin complex concentrate (PCC) , when used in conjunction with FFP,

is associated with complete and more rapid reversal of coagulopathy, without any increase in

complications compared to FFP alone [58, 59] PCC, in conjunction with FFP, also leads to a fastertime to craniotomy in all patients with TBI-induced coagulopathy While recombinant factor VIIa hasbeen shown as an effective therapy in reversing coagulopathy, there is no difference in its

effectiveness when compared with PCC [58, 60]

evidence of progression at 72 h, IVC filter placement should be considered [61]

Role of Acute Care Surgeon in Acute Management of TBI

Traditionally, patients with a suspected TBI are first seen by trauma surgeons for initial evaluationand receive an initial head CT scan, followed by neurosurgical consultation, regardless of the

severity of injury, clinical presentation, or associated risk factors Recently, this approach has beenchallenged for two fundamental reasons First, the vast majority of these patients never undergo anyform of neurosurgical intervention and are managed nonoperatively by the critical care surgeons inthe ICU [62] Indiscriminate use of repeat imaging in these patients results in unwarranted expenditure

of valuable human and financial resources Second, because TBI is a clinical diagnosis, the decisionabout neurosurgical intervention or a repeat head CT scan can be unfailingly predicted by consideringthe size of initial head bleed, close clinical examination, and the presence of risk factors for bleedprogression, such as antiplatelet and anticoagulation medication [63] For the abovementioned

reasons, several studies have suggested that patients with TBI undergoing nonoperative managementcan be reliably followed for any sign of neurological decline without a routine repeat head imaging[64, 65] Some institutes have developed their own guidelines to manage TBI patients based on well-

known risk factors for neurosurgical consultation, such as the use of antiplatelet/anticoagulant

medications, intoxication, and clinical examination The Brain Injury Guidelines (BIG) (Table 1.2.)formulated at the University of Arizona demonstrated safe and effective management of TBI patients.Based on BIG, a subset of TBI patients with minimal injury can be managed reliably via neuro-

examination without the need for neurosurgical consultation or repeat head CT scans [66] This

practice has resulted in a significant reduction in the use of valuable resources (such as neurosurgicalconsultation , repeat CT scans, and hospital costs) without affecting patient care

Table 1.2 Brain injury guidelines

Neurologic examination Normal Normal Abnormal

Skull Fracture No Non-displaced Displaced

IPH ≤4 mm, 1 location 3–7 mm, 2 locations ≥8 mm, multiple locations

BIG brain injury guidelines , CAMP Coumadin, Aspirin, Plavix, EDH epidural hemorrhage, IVH

intraventricular hemorrhage, IPH intraparenchymal hemorrhage, LOC loss of consciousness, NSC neurosurgical consultation, RHCT repeat head computed tomography, SAH subarachnoid hemorrhage,

SDH subdural hemorrhage

Brain Death and Organ Donation

“Brain death” denotes the absence of any neurological activity in a patient whose core temperature is

>32.8 C, whose mental status is not impacted by sedating or paralyzing medications, who is

completely resuscitated with a SBP >90 mmHg, and whose oxygen saturations are above 90% Inbrain-dead patients, pupils are fixed and dilated; there are no observable corneal oculocephalic,oculovestibular, gag, or cough reflexes [67] No movement to deep central or peripheral pain and nospontaneous breathing is seen on disconnection from the ventilator with PaCO2 > 60 mmHg (i.e.,apnea test) If the brain death protocol is equivocal, one can perform secondary tests, such as a

cerebral angiography to show absence of CBF or a cerebral ribonucleotide angiogram to show absentuptake

In 1999, TBI was the cause of brain death for more than 40% of the individuals from whom

organs were procured Many efforts have been made to date to improve organ donation rates

following brain death Administration of levothyroxine (T4) after brain death has emerged as one of

the most effective therapies It has led to an increase in both the quantity and quality of organs

available for transplantation More recent studies have shown that initiation of levothyroxine therapybefore declaration of brain death further increases the yield of organ donation in such individuals.Currently, administration of T4 alone, or in combination with corticosteroids, is the prime therapyavailable to enhance organ donation rates following brain death

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32 Joseph B, et al The physiological effects of hyperosmolar resuscitation: 5% vs 3% hypertonic saline Am J Surg 2014;208(5):697– 702.

38 Adelson PD, et al Comparison of hypothermia and normothermia after severe traumatic brain injury in children (cool kids): a phase

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43 Roberts DJ, et al Sedation for critically ill adults with severe traumatic brain injury: a systematic review of randomized controlled trials Crit Care Med 2011;39(12):2743–51.

Jones KE, et al Levetiracetam versus phenytoin for seizure prophylaxis in severe traumatic brain injury Neurosurg Focus.

55 Patel MB, et al Decreasing adrenergic or sympathetic hyperactivity after severe traumatic brain injury using propranolol and

clonidine (DASH after TBI study): study protocol for a randomized controlled trial Trials 2012;13(1):177.

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62 Patel NY, et al Traumatic brain injury: patterns of failure of nonoperative management J Trauma Acute Care Surg 2000;48(3):367– 75.

Brown CV, et al Does routine serial computed tomography of the head influence management of traumatic brain injury? A

prospective evaluation J Trauma Acute Care Surg 2004;57(5):939–43.

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© Springer International Publishing AG, part of Springer Nature 2018

Ali Salim, Carlos Brown, Kenji Inaba and Matthew J Martin (eds.), Surgical Critical Care Therapy , 71712-8_2

https://doi.org/10.1007/978-3-319-2 Intracranial Pressure

David A Hampton1

and Deborah M Stein1

R Adams Cowley Shock Trauma Center, University of Maryland Medical Center, Baltimore,

The Edwin Papyrus, an Egyptian medical treatise drafted in 1600 BC by a physician working withpyramid construction teams, describes numerous injuries sustained by the workforce [1, 4] The

document details 48 cases of which 27 were related to head trauma The Papyrus was the first

descriptive medical documentation of cranial structures, the meninges, the brain’s surface, cerebralspinal fluid, and cranial injury and their associated physiologic deficit Given its detail and utility, itwas believed the Papyrus was later utilized as a textbook for military trauma [1]

Traumatic Brain Injury

In modern times, cranial injuries commonly occur after a motor vehicle accident, assault, athleticcollision, or ground level fall [5, 6] The sudden acceleration and deceleration resulting in

translational and rotational forces moving the brain within the cranial vault causes it to impact againstthe immobile cranium resulting in a focal injury [7–9] Diffuse injury can occur secondary to shockwaves from the initial strike or cavitation injury from a foreign body translating through the brainparenchyma [10, 11] This injury pattern is commonly known as a traumatic brain injury (TBI) TBI

is the signature injury of the recent Middle East conflicts As of 2016, there were 357,000 United