Surgical Critical Care Therapy: A Clinically Oriented Practical Approach

 This text provides a comprehensive, state-of-the art review of this field, and will serve as a valuable resource for clinicians, surgeons and researchers with an interest in surgical critical care.  The book reviews up to date data regarding the management of common problems that arise in the Surgical Intensive Care Unit. The protocols, care bundles, guidelines and checklists that have been shown to improve process measures, and in certain circumstances, are discussed in detail. The text also discusses several well designed randomized prospective trials conducted recently that have altered the way we care for surgical patients with traumatic brain injury, hemorrhagic shock, acute respiratory distress syndrome, and sepsis.  This book provides the practicing physician with a clinically oriented practical approach to handle basic and complex issues in the Surgical Intensive Care Unit.  
This text will serve as a very useful resource for physicians dealing with critically ill surgical patients. It provides a concise yet comprehensive summary of the current status of the field that will help guide patient management and stimulate investigative efforts.  All chapters are written by experts in their fields and include the most up to date scientific and clinical information. This text will become an invaluable resource for all graduating fellows and practicing physicians who are taking the surgical critical care board examinations.

• Language: English
• Publisher: Springer
• Release date: May 3, 2018
• ISBN: 9783319717128

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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 https://doi.org/10.1007/978-3-319-71712-8_1

1. Traumatic Brain Injury

Asad Azim¹   and Bellal Joseph¹

(1)

Department of Surgery, University of Arizona, Tucson, AZ, USA

Asad Azim

Email: [e-mail]

Keywords

Traumatic brain injuryDecompressive craniotomyIntracranial pressureMonitoringHyperosmolar therapy

Introduction

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 physical functions —it may or may not be associated with a diminished or altered state of consciousness. The external forces that create the injury may be the result of a variety of insults, including acceleration or deceleration, compression, penetrating objects, and complex mechanisms like blast injuries. TBI is the leading cause of death and disability among trauma patients. According to an estimate, about 2.5 million TBIs occur every year. Of those, about 50,000 people die, and approximately 80,000–90,000 survivors suffer severe lifelong neurological disabilities [1]. The external cause of injury (mechanism of injury) associated with TBI varies with age and demographics. Males aged 0–4 have the highest rates of TBI-related visits, whereas adults aged 75 years and older have the highest rate 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 than half (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 , accounting for 15% of all TBI-related ED visits (1). Motor vehicle collisions and assaults are the third and fourth 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 cortical bridging 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 with underlying 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 meningeal artery. 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 skull injury rather than brain injury, although brain injury certainly can occur with them. Morbidity and mortality associated with EDH is primarily due to the mass effect from the hematoma, which, if left 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. The positive predictive value of SAH (>1 cm) for poor outcome is 72–80%. On CT imaging, SAH appears 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. It commonly 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 heterogeneous region. This type of lesion usually occurs in coup or contrecoup injuries. It manifests in cortical tissue and can be associated with multiple microhemorrhages and small vessels that leak into brain tissue. The most common regions of the brain affected are the frontal and anterior temporal lobes. Cerebral contusions often take 12–24 h to evolve and may be absent on an initial head CT scan [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-lived impairment of neurological function that resolves spontaneously. Concussions are a clinical diagnosis as there are no CT scan findings associated with it. The key signs and symptoms of a concussion 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 from traumatic shearing forces that occur when the head is rapidly accelerated or decelerated. DAI is commonly seen in motor vehicle collisions and shaken baby syndrome. The sites frequently involved 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 standard MRI 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 to the liberation of proinflammatory cytokines and chemicals as result of primary injury that leads to cerebral edema neuronal death and disruption of the blood-brain barrier [13]. The common pathways that 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 limit primary injury, the main goals of current TBI management strategies are targeted at limiting secondary brain injury. With recent advances and better understanding of cellular and biochemical functions, it has become more clear that inadequate blood flow and substrate delivery result in exacerbation of secondary 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, a description 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. Special attention should be paid to medications with the ability to alter the neurological examination, including sedatives or psychopharmacologics, paralytics, atropine (for cardiac resuscitation), and other 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.

Neurological Assessment

An accurate neurological examination is necessary in order to make a correct diagnosis as well as to plan appropriate treatment strategies. The exam may be limited or altered by age, language, sedative or paralytic medication, alcohol intoxication, or illicit drug abuse. It is crucial to monitor trends that appear in neurological examinations overtime because they fluctuate based on the patient’s improving 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 each patient’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 pupil shows 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 be excluded as a cause of pupillary dilation. Orbital trauma can be ruled out by using direct and consensual 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 a TBI. 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 a maximum score of 15, and the most severely injured patient can get a minimum score of 3. If the patient 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 and have 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

Airway, Breathing, and Circulation

Clinicians should adhere to the basic principles of trauma resuscitation, including rapid assessment and maintenance of an airway, breathing, and circulation [18]. The maintenance of an unobstructed and clear airway is of the utmost importance as hypoxia is the most critical factor leading to adverse outcomes in TBI patients. A multicenter trial has shown that mortality rises by 17% in patients that experience hypoxic episodes following a TBI [19]. Regarding patients with a GCS <9, guidelines recommend 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 be protected.

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 of 11,000 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 hyperventilation may be an option.

Hypotension is a major secondary brain insult . Studies have shown that even a single episode of hypotension is associated with a dramatic increase in mortality in TBI patients [21]. It should be treated 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 decreased mortality and better neurological outcomes in TBI patients [22].

Radiological Assessment

Computed Axial Tomography (CT) Scan

CT scan remains the investigation of choice for patients presenting 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 also allows for a CT angiogram reconstruction in order to evaluate vasculature of the head and neck. CT scan findings after trauma include SDH, EDH, SAH, IPH, IVH, contusions, hydrocephalus, cerebral edema 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 basilar skull fracture [23].

Magnetic Resonance Imaging (MRI)

MRI scans have better parenchymal resolution and can evaluate infarction, ischemia, edema, and DAI. An MRI is also helpful to determine a ligamentous injury 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 image acquisition time, image interference by monitoring devices, and a greater cost. Although their use in the initial assessment of trauma is not routinely recommended because intracranial surgical lesions seen 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

Monitoring

Blood Pressure

Systolic blood pressure (SBP) plays a critical role in a secondary brain injury cascade after a severe TBI. TBI patients admitted with a systolic blood pressure of less than 85 mmHg have mortality rates as high as 35%, compared to only 6% in patients with a higher SBP [19]. Autoregulatory vasodilation plays a critical role in maintaining cerebral perfusion. After 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 the single most important secondary insult. In order to decrease mortality and improve clinical outcomes following 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-Kellie hypothesis . Assuming that the skull is a closed space, the hypothesis states that there is a balance between 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 clinical practice, and there are inconsistent reports about the utility of ICP monitoring on clinical outcomes and 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 severe TBI (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 on these guidelines. However, only a small subset of these patients receives ICP monitoring based on institutional 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 and clinical examination [27]. Medical management remains the standard of care for elevated ICP, with a possible role for ICP monitoring and operative intervention in a subset of patients. However, further studies 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 of cerebral 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 blood inflow 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 60 and 70 mmHg for improved survival and favorable outcomes [25]. TBI management includes CPP monitoring in the bundle of care; however, the impact of CPP-based management of TBI patients remains unclear. There is some evidence which suggests that the management of TBI patients’ using information from CPP monitoring is associated with 2-week post-injury mortality.

Treatment

Hyperosmolar Therapy

An injured brain is highly susceptible to secondary ischemia from either systemic hypotension or diminished cerebral perfusion (attributable to intracranial hypertension, cerebral edema, and inflammation). The objective of hemodynamic therapy in TBI is to ensure adequate brain perfusion and to keep intracranial pressure within normal limits. There are various methods for controlling ICP; however, one of the key pharmacological interventions is hyperosmolar therapy [24–29]. Such 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 the flow into the circulation . Another mechanism, which explains the rather more rapid action of osmolar agents, is improvement in the rheology of the blood due to plasma expansion as well as decreased hematocrit, which leads to decreased viscosity and more efficient cerebral blood flow (CBF) . It is believed that the two most commonly utilized hyperosmolar agents, that is, hypertonic saline and mannitol, 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. Although there 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 the treatment of intracranial hypertension after a TBI. Mannitol can be administered as a bolus in response 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 opinion still exists concerning the two modes of administration. Although mannitol plays a vital role in controlling ICP in severe TBI patients, its eventual diuretic effect is undesirable in hypotensive patients, and appropriate monitoring and aggressive fluid resuscitation are required to replenish fluid 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 higher than 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 resuscitation and maintenance therapy in TBI patients. Physiologically, the sodium content is what determines the amount of volume increased intravascularly during initial resuscitation. HTS was initially used 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 hemorrhagic shock and TBI, resuscitation with HTS was associated with better survival [30]. In patients with severe TBI and increased ICP or brain edema, a serum sodium level Na + up to 150–155 mEq/L may 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 is attributed to a reduction in ICP and cerebral edema, which was due to hyperosmolar effects of HTS. 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 in adverse effects [32]. Over time, HTS evolved as an alternative to mannitol in treating cerebral edema 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 osmotic diuresis, 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 , HTS has clear logistical advantages over mannitol in the treatment of TBI.

Decompressive Craniectomy (DC)

Cerebral edema can result from a combination of several pathophysiological mechanisms associated with primary and secondary injury following a TBI. As the skull is a closed cavity, increase in intracranial contents (i.e., cerebral edema) results in brain tissue displacement causing cerebral herniation ultimately leading to severe disability or death. DC is defined as the surgical removal of a portion of the skull and the opening of the underlying dura for the purpose 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 (not less than 12 × 15 or 15 cm diameter) is recommended to reduce mortality and improve neurological outcomes in patients with a severe TBI with a diffuse injury and ICP values >20 mmHg refractory to medical 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 , subdural hygromas, 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 the 1950s as a direct consequence of the space race. However, most of the studies to date have utilized whole-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 effects and 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 achieve rapid 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 brain edema. 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 Outcome Scale-Extended (GOS-E) scores among patients with therapeutic brain cooling. These findings in the interim 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 rewarming after severe TBI in children was conducted. It was also terminated early due to ineffectiveness of the therapy 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 and neurological 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 increased risk 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 is linearly responsive to PaCO2. Low PaCO2 therefore causes a decrease in CBF by cerebrovascular constriction , while a high PaCO2 increases CBF via cerebrovascular dilation. Older studies suggested that cerebral hyperemia is more common than cerebral ischemia; hence they recommended hyperventilation as a management therapy for TBI patients. However, this has been falsified by recent studies demonstrating cerebral ischemia as a major culprit, thereby changing the long-standing recommendations concerning ventilation therapy. Current guidelines state that prolonged prophylactic hyperventilation with partial pressure of carbon dioxide in arterial blood (PaCO2) of 25 mmHg or less 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. The optimal 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 in duration of mechanical ventilation. In addition, reduction in hospital and ICU length of stay was also observed in the early tracheostomy group [39]. According to Eastern Association for the Surgery of Trauma (EAST) , early tracheostomy (within 3–7 days of TBI) should be performed as it decreases the total days of mechanical ventilation and ICU length of stay [40]. However, none of the randomized clinical trials have demonstrated survival benefit of early tracheostomy [41].

Anesthetic Analgesics and Sedatives

Anesthetics , analgesics , and sedatives are widely used therapies 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, metabolic suppression, and alteration of cerebral vascular tone [42]. Anesthetic, analgesic, and sedative therapy also carries with it high morbidity. Side effects include hypotension, decreased cardiac output, as well 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 altered vascular permeability in brain edema, reduction of cerebrospinal fluid production, and attenuation of free radical production. Several randomized controlled trials demonstrated benefits with the use of methylprednisolone for 24 h; however, meta-analysis of these randomized trials failed to demonstrate any conclusive benefit of steroids in TBI. The most conclusive evidence was brought forward after the CRASH (Corticosteroid Randomization After Significant Head Injury ) trial in over 10,000 TBI patients 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 after TBI provides patients with appropriate substrates, essential nutrients, and enough calories to inhibit catabolism and promote rapid neurological recovery [46]. Based on this evidence, current BTF guidelines and the American Association of Neurological Surgeons’ (AANS) guidelines recommend initiation 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 can interfere with post-injury acute phase response , which is an immediate protective response of the body to protect primary host functions. This can lead to slower recovery and higher incidence of pneumonia in these TBI patients [47]. For optimal clinical results and rapid recovery in TBI, nutrition can be safely started after the first 24 h post-injury and should advance toward optimal nutritional goals 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 they occur 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 factors for early PTS include the following: GCS of ≤10; immediate seizures; post-traumatic amnesia lasting longer 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 nor valproic acid has shown any benefit in limiting late PTS. Levetiracetam (Keppra), a relatively newer drug, 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. This increase in sympathetic activity by surge in catecholamine has shown to be directly associated with increased mortality, lower neurological recover, and increase in hospital stay [50].Based on these findings, 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 mice demonstrated improved survival and histological recovery [51]. Several retrospective studies have shown 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 its nonselective 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 was associated 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 sympathetic hyperactivity [55].

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

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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. Coagulopathy affects up to one-third of TBI patients [56]. Mechanisms by which TBI induces coagulopathy include local and systemic inflammation, which lead to the release of tissue factor, activation of the protein C pathways, platelet dysfunction, and disseminated intravascular coagulation. Coagulopathy after TBI is a dynamic process that goes through stages of hypercoagulability and hypocoagulability ultimately leading 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 international normalized 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 also more efficient in predicting therapy for TBI-induced coagulopathy [57].

The reversal of TBI coagulopathy requires the replacement of coagulation factors. Classically, fresh frozen plasma (FFP) has been used to reverse both acquired and induced TBI coagulopathy. Studies have 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 faster time to craniotomy in all patients with TBI-induced coagulopathy. While recombinant factor VIIa has been shown as an effective therapy in reversing coagulopathy, there is no difference in its effectiveness when compared with PCC [58, 60].

Thromboembolic Events

TBI patients are at increased risk of developing deep venous thrombosis (DVT) with rates as high as 20–30% even with appropriate mechanical prophylaxis. Pharmacological prophylaxis with low molecular weight heparin is the first-line therapy to limit thromboembolic events. Due to high risk of bleeding in TBI patients, thromboprophylaxis in head-injured patients must weigh the dangers of pulmonary embolism with risk of bleeding. The challenge in deciding when to initiate pharmacologic prophylaxis lies in determining when the risk of progression of intracranial hemorrhage has become sufficiently low. American College of Surgeons Trauma Quality Improvement Program (ACS-TQIP) best practice guidelines recommend that in patient with minimal risk of progression, pharmacological prophylaxis can be started if the repeat head CT scan is stable at 24 h. For patients with moderate risk defined as subdural/epidural hematoma >8 mm or intraventricular hemorrhage >2 cm or if the progression is seen on repeat head CT at 24 hours, DVT prophylaxis should be delayed up to 72 h until the repeat head CT scan is stable. In patients with ICP monitor placement , craniotomy, or 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 evaluation and 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 been challenged for two fundamental reasons. First, the vast majority of these patients never undergo any form of neurosurgical intervention and are managed nonoperatively by the critical care surgeons in the 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 decision about neurosurgical intervention or a repeat head CT scan can be unfailingly predicted by considering the size of initial head bleed, close clinical examination, and the presence of risk factors for bleed progression, such as antiplatelet and anticoagulation medication [63]. For the abovementioned reasons, several studies have suggested that patients with TBI undergoing nonoperative management can 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 neurosurgical consultation , repeat CT scans, and hospital costs) without affecting patient care.

Table 1.2

Brain injury guidelines

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%. In brain-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 no spontaneous 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 absent uptake.

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 therapy before 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 therapy available to enhance organ donation rates following brain death.

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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 https://doi.org/10.1007/978-3-319-71712-8_2

2. Intracranial Pressure

David A. Hampton¹ and Deborah M. Stein¹  

(1)

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

Deborah M. Stein

Email: [e-mail]

Keywords

BrainTraumaPressureGuidelines

Background

Cranial injuries related to enemy combatants, hunting, or natural disasters have influenced human evolution. The ability to adequately address these injuries determined which early humans survived. Throughout Africa, Asia, and South America, archeologist have excavated skulls which have holes of various sizes across the cranium [1]. Many of these skulls had more than one hole, and many were found in various stages of healing. Trepanation , derived from the Greek trypanon meaning a borer or auger, was a procedure used to create holes in the skull to relieve pressure after injury or to release evil spirits in the mentally ill [2, 3].

The Edwin Papyrus, an Egyptian medical treatise drafted in 1600 BC by a physician working with pyramid 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, cerebral spinal fluid, and cranial injury and their associated physiologic deficit. Given its detail and utility, it was 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, athletic collision, 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 against the immobile cranium resulting in a focal injury [7–9]. Diffuse injury can occur secondary to shock waves from the initial strike or cavitation injury from a foreign body translating through the brain parenchyma [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 States service members diagnosed with a TBI [12]. In 2000 there were 1.7 million individuals in the United States who sustained a TBI. Fifty two thousand died, 275,000 were hospitalized, and 1.3 million were released from the emergency department. In total, this resulted in an estimated $60 billion economic burden [13].

TBIs are gradated into three tiers – mild, moderate, and severe – based upon the presenting Glasgow Coma Scale (GCS) (Table 2.1). The GCS is a reliable objective measure of a patients’ consciousness based upon three physical examination criteria – eye, motor, and verbal responses [14, 15]. The summation of the individual component scales ranges from 3 to 15. The TBI’s severity is based upon this composite number.

Table 2.1

Glasgow Coma Scale [14]

A mild TBI is defined as a GCS greater than or equal to 13. These patients will usually have a history of a brief loss of consciousness, amnesia to the event, confusion, and may perseverate when asked questions. Patients afflicted with a mild TBI usually do not require an inpatient admission and are managed on an outpatient basis. A moderate TBI is classified as a GCS less than 13 but greater than or equal to 9. This injury is associated with a prolonged loss of consciousness, neurologic deficits, and radiographic findings, i.e., subdural, epidural, or subarachnoid hemorrhage [16]. Unlike the mild TBI, these patients require further observation as an inpatient.

A severe TBI is classified as a GCS less than or equal to 8. These patients will usually have radiographic evidence of an intracranial hemorrhage. Additionally, depending on their level of consciousness, the patient may have an abnormal neurologic examination with respect to motor function and pupillary or other cranial nerve responsiveness. These patients are at a high risk for respiratory failure and a potentially elevated intracranial pressure (ICP) secondary to the physical insult sustained. A TBI can result in an elevated ICP secondary to cerebral edema, hyperemia, hematoma formation, presence of a foreign body, or depressed skull fracture.

Physiology

The adult cranium volume is approximately 1400–1700 mls. The intracranial contents by volume are: brain parenchyma (80%), CSF (10%), and blood (10%) [17]. The ICP generated is the force exerted by the three tissue volumes against the intracranial surface area. ICP varies by age. An adult ICP is <10–15 mmHg, while a child’s is <3–7 mmHg. The Monro-Kellie hypothesis states the volume of tissue within the cranium is conserved; therefore when one tissue volume expands, for example, secondary to brain edema, vascular injury, or outflow obstruction, an equal decrease must occur in one or both of the other two (Fig. 2.1). Compensatory mechanisms, such as the removal of CSF or blood, to relieve pressure, are the body’s immediate response. The cranium is a non-expansile vault, and the force is considered to be distributed evenly; therefore the pressure-related effects are experienced throughout the cranial vault. In the event the compensatory mechanisms fail or are inadequate, the rising pressure can result in intracranial hypertension (IC-HTN) , ICP ≥20 mmHg. Aside from the aforementioned physical changes, IC-HTN can occur or be exacerbated by seizure activity, Valsalva maneuvers, venous sinus thrombosis, systemic hypertension, or obstruction of CSF circulation.

../images/418368_1_En_2_Chapter/418368_1_En_2_Fig1_HTML.gif

Fig. 2.1

Monro-Kellie Doctrine – (a) Intracranial contents – CSF, brain parenchyma , and blood; (b, c) an increasing intracranial mass/insult results in compensatory removal of blood and CSF, reducing overall compression of the brain parenchyma in order to maintain constant intracranial volume; (d) when compensatory mechanisms are exhausted, continued increasing ICP results in brain herniation

An elevation in ICP can adversely affect cerebral blood flow (CBF) . Brain function and survival are dependent upon adequate CBF and oxygen delivery [18]. Cerebral perfusion is dependent upon the driving pressure and resistance encountered. Analogous to Ohm’s law, the current through a conductor is directly proportional to the change in voltage across it; the CBF is equal to the change in pressure across the brain [19]:

$$ \mathrm{CBF}=\frac{\mathrm{CAP}-\mathrm{JVP}}{\mathrm{CVR}} $$

(2.1)

where CAP is carotid artery pressure, JVP is jugular venous pressure, and CVR is the cerebrovascular resistance. The CBF is not typically directly measured; therefore the cerebral perfusion pressure (CPP ) is often used as an indirect surrogate. CPP is defined as:

$$ \mathrm{CPP}=\mathrm{MAP}-\mathrm{ICP} $$

(2.2)

the difference between the MAP, the forward driving pressure, and the ICP, the pressure retarding it.

Autoregulation

Cerebrovascular autoregulation maintains a constant CBF over a wide range of perfusion pressures (Fig. 2.2). This cerebral autoregulation allows for shifts in pressure without adversely affecting CBF [20, 21]. This mechanism allows for adequate oxygen and nutrients to be delivered while removing carbon dioxide and other metabolic waste products. The majority of this regulation occurs within the immense arteriolar network where the greatest changes in resistance can occur.

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Fig. 2.2

Autoregulation – The cerebral blood flow is held constant over a wide range of perfusion pressures. Elevated pressures and exhaustion of or dysfunctional compensatory mechanisms can result in cerebral edema. Conversely, a decreased cerebral perfusion pressure can result from elevated intracranial pressures and present as reduced cerebral blood flow and herniation

After an intracranial insult, autoregulation may become dysfunctional. Conditions which result in an elevated ICP will decrease the CPP and cause cerebral ischemia. Conversely, an elevated MAP can increase the CPP leading to hyperemia or worsening of cerebral edema [21–23]. Under these conditions, knowledge of the signs associated with and elevated ICP will directly affect patient outcomes.

Clinical Signs and Symptoms

In the setting of an evolving intracranial injury, clinical manifestations of the cerebral insult may develop. Commonly an elevated ICP is associated with headache, depressed consciousness, and emesis. Additionally, the compression of the brain stem will result in respiratory lability. As the CBF decreases secondary to the elevated ICP, the sympathetic nervous system will stimulate vascular alpha-1 adrenergic receptors causing an increase in systemic vascular resistance and systolic blood pressure. This response is an innate mechanism to maintain adequate CBF. However, the aortic baroreceptors will sense the new onset hypertension and stimulate the parasympathetic response, the vagus nerve, resulting in bradycardia. The constellation of bradycardia, hypertension, and respiratory lability is known as Cushing’s reflex [17, 18]. This reflex can be an early sign that the compensatory mechanisms are exhausted, and brain herniation will occur to further relieve the developing IC-HTN.

Brain herniation is classified by the structure herniating or the anatomic landmark traversed.

Subfalcine herniation is the most common form. It occurs when the frontal lobe is displaced beneath the falx cerebri resulting in contralateral hydrocephalus secondary to obstruction of the foramen of Monro and compression of the anterior cerebral artery manifesting as contralateral lower extremity weakness [24].

Central herniation occurs secondary to downward pressure resulting in bilateral uncal herniation and a lateral gaze deficit secondary to a cranial nerve VI palsy [25].

Uncal herniation , a variant of transtentorial herniation, results in the uncus and medial temporal lobe exiting through the tentorial incisura and compressing against the brain stem and tentorial edge. This can result in ipsilateral hemiparesis also known as Kernohan-Woltman notch phenomenon [24].

Tonsillar herniation occurs when the cerebellar tonsils transit below the foramen magnum. This is often caused by a posterior fossa hematoma or fourth ventricle obstruction and can result in respiratory depression, blood pressure instability, and sudden death [25].

Invasive ICP Monitors

An ICP monitor is an invasive device which helps direct patient care through maximizing the CPP , resulting in improved cerebral oxygenation and avoidance of a secondary insult to the injured brain [26]. Using the ICP, MAP, and Eq. 2.2, a clinician will be able to achieve their therapeutic goals: a ICP < 20 mmHg and a CPP between 60 and 70 mmHg [27]. Interventions to reduce a suspected elevated ICP without a monitor can potentially result in adverse outcomes. For example, hyperventilation will result in vasoconstriction and decreased intracranial volume; however prolonged hyperventilation is complicated by decreased oxygen delivery and the potential for cerebral ischemia. Given these potential complications, ancillary monitoring such as venous oxygen content (CvjO2) or brain tissue oxygenation (PbrO2) is often beneficial.

Currently an ICP monitor is recommended for patients with a post-resuscitation GCS ≤ 8 and radiographic evidence of intracranial pathology such as herniation, contusion, basal cistern compression, cerebral edema, or intracranial hemorrhage [18, 27]. Additionally, ICP monitors can be indicated for patients after a traumatic head injury with normal CT scans. In this patient population, it has been shown that individuals who meet two or more of these criteria: (1) SBP < 90 mmHg, (2) posturing on physical examination, and (3) age > 40 years old, have been found to have an intracranial hemorrhage 60% of the time [27–29].

The first ICP monitors were passive devices, U-shaped tubes directly communicating with the CSF and the atmosphere [30]. The CSF back pressure was an indirect measure of ICP. Modern ICP monitors have been engineered to utilize solid-state or fiber-optic transducers which convert changes in mechanical resistance or light reflection into an electrical signal corresponding to pressure [31]. The American National Standards Institute/Association for the Advancement of Medical Instrumentation standards require these devices to function within a range of 0–100 mmHg with a ± 2 mmHg error from 0 to 20 mmHg and a ± 10% error from 21 to 100 mmHg [32]. The invasive monitors have been designed to be placed within one of four intracranial sites:

Intraventricular  – This is the gold standard location (Fig. 2.3b). The monitor’s pressure sensing arm is inserted into the lateral ventricle. Aside from being used as an ICP monitor, it can also provide a therapeutic intervention by draining CSF to relieve pressure as needed. These devices can be complicated by infection [33, 34] and potentially misplacement due to collapsed ventricles.

Subarachnoid  – The Richmond bolt is a hollow screw placed through the skull and terminates against the dura (Fig. 2.3c). A dural puncture allows CSF and the ICP to communicate directly with the transducer. These devices have a low infection risk; however, they can become obstructed by debris. They are infrequently utilized in modern intensive care units.

Intraparenchymal  – These monitors, such as the Camino® (Integra LifeSciences Corporation), are a cable with a fiber-optic transducer tip placed within the brain’s parenchyma (Fig. 2.3d). The device is technically less challenging than the EVD to deploy and has a lower infection rate. Unlike the EVD, it is only a measurement tool and cannot be used to remove CSF. Additionally, it is dependent upon the tissue in which it is embedded.

Epidural  – This device does not enter the brain parenchyma or penetrate the dura (Fig. 2.3e). It is an optical transducer which is placed against the dura. Its accuracy is limited by the dura damping the true ICP. It is infrequently utilized, but due to low hemorrhagic complications, it may be useful in coagulopathic patients.

../images/418368_1_En_2_Chapter/418368_1_En_2_Fig3_HTML.gif

Fig. 2.3

Sagittal cross sections of the skull, brain parenchyma , and intracranial pressure monitors – (a) identification of the tissue layers from the skin to brain parenchyma, (b) intraventricular pressure transducer/extraventricular drain with sensor/drain within the lateral ventricle, (c) subdural pressure transducer with open communication between the subdural space and sensor,