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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5573_Библиотеки_им_академика_М_И_Перельмана.pdf
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L. V. JuradoHernández and T. A. Allison
area of exion, (b) utilizing a dedicated line for infusion, (c) rotating the infusion
site every 2–4days for prolonged infusions, (d) scheduled monitoring of the line to
ensure that it is functioning, and (e) scheduled monitoring of the sites for any
changes in color, swelling, or tenderness.
There is no clear short-term benet or documented evidence for long-term outcomes with the titration of continuous HTS infusions to a sodium goal. Currently,
the primary advantage of utilizing a sodium goal is to reduce the risk of adverse
events. The quality of evidence evaluating the risk of AKI associated with HTS is
low. Due to the uncertain association, literature and guidelines recommend monitoring serum sodium and chloride concentrations while the patient is receiving
HTS. The 2020 NCS Guidelines for the Acute Treatment of Cerebral Edema in
Neurocritical Care Patients recommend an upper sodium limit of 150–160mEq/L
and an upper chloride limit of 110–115 mEq/L to limit the risk of AKI [23].
Furthermore, hypernatremia (above 150 mEq/L) has been associated with an
increase in mortality in TBI patients [54–56]. This further suggests that HTS should
only be administered for the treatment of elevated ICP and not to target a specic
serum sodium level [57].
Large-volume administration of HTS can produce a metabolic acidosis due to
hyperchloremia and volume expansion. It leads to volume expansion of the extracellular uid and intravascular volume with bicarbonate-poor intracellular uid,
reducing the serum bicarbonate and resulting in a temporary decline in
pH.Additionally, hyperchloremia is associated with AKI [58–61]. In order to alleviate the acid-base disturbances observed with a high-chloride load, buffered sodium
solutions are used. Buffered sodium solutions can contain sodium acetate, sodium
bicarbonate, or sodium lactate with or without sodium chloride. Buffered sodium
solutions require compounding, and there is no standard formulation. This results in
solutions with different concentrations and osmolarities, which has led to the recommendation that pharmacists formulate the admixture using milliequivalents of
sodium rather than grams so that the osmolarity of the solution matches that of commercially available hypertonic sodium chloride solutions [62].
A signicant concern with the use of HTS is overcorrection of the serum sodium
concentration, leading to osmotic demyelination syndrome (ODS). ODS is most
likely to occur in patients with extremely low serum sodium levels (<120mEq/L)
[63]. Osmotic demyelination syndrome has been reported in normonatremic
(>135mEq/L) patients, though not when being treated for cerebral edema. HTS
should be administered cautiously, and serum sodium concentrations should be
monitored.
16.5.2 Sedation andAnalgesia
The use of sedation and analgesia has many purposes in ICU patients, including
limiting the stress response to critical illness, providing anxiolysis, facilitating
mechanical ventilator support and tolerance, and enabling ICU care. In the critically
16
raumatic Brain Injury
T
407
ill patient, pain arises from different sources and is subjective. TBI patients may
experience moderate-to-severe pain at rest depending on the extent of their injuries,
though they may also experience pain during routine care in the ICU.In patients
who are able to self-report pain, the 0–10 numeric rating scale, administered either
verbally or visually, is considered a valid and feasible pain scale. Validated pain
scales, such as the behavioral pain scale (BPS) or the critical care pain observation
tool (CPOT), allow clinicians to assess pain in patients that are unable to self-report
it [64].
In the TBI patient, sedation and analgesia are used to provide adequate conditions that favor recovery of brain tissue and prevent secondary neuronal injury [65].
Because pain and agitation can lead to increases in ICP, intravenous sedation and
analgesia are considered rst-line therapy. Other neurological conditions TBI
patients may experience, including status epilepticus and paroxysmal sympathetic
hyperactivity (PSH), utilize sedation and analgesia as mainstays of therapy.
Sedation and analgesia are believed to be benecial in managing elevated ICP
through three mechanisms [66]. First, they decrease cerebral metabolic rate of oxygen (CMRO2), subsequently leading to a reduction in CBF with a comparable
decrease in cerebral blood volume. Based on the Monro-Kellie hypothesis, the
reduction in cerebral blood volume will lead to a reduction in ICP. Second, sedation
and analgesia reduce pain and agitation, which decreases the incidence of arterial
hypertension and an associated increase in ICP. Third, analgesia reduces agitation
and coughing associated with intolerance of the endotracheal tube. This reduces the
intrathoracic pressure, leading to increased jugular venous outow and decreased
ICP. Table16.4 gives a more complete summary of the physiologic effects of sedative and analgesic agents.
The neurological examination is the gold standard for monitoring TBI patients.
Sedation and analgesia may impair the ability to get an accurate assessment of the
patient’s neurological status. It is often a balancing act between maintaining adequate
sedation and analgesia as well as being able to assess the patient accurately.
Additionally, agents may have side effects such as reducing CPP. The ideal agent for
Table 16.4 Systemic and cerebral physiologic effects of sedative and analgesic agents
HR CO SVR MAP ICP CPP CBF CMRO
Barbiturates ↑ ↓ ↑↓ ↓↓ ↓↓ ↓ ↓↓ ↓↓
Benzodiazepines ↔⎕↑ ↓↔⎕ ↓↔⎕ ↓ ↓ ↓ ↓ ↓
Dexmedetomidine ↓ ↓ ↔⎕↑ ↓ ↓? ↓? ↓↓ ↔⎕
Etomidate ↔⎕ ↔⎕ ↔⎕ ↔⎕ ↓ ↔⎕ ↓ ↓
Ketamine ↑ ↑ ↑ ↑ ↑ ↔⎕ ↑↑ ↔⎕
Opioids ↓ ↔⎕ ↓↔⎕ ↓ ↓↔⎕ ↓↔⎕ ↔⎕ ↓
Propofol ↔⎕ ↓ ↓↓ ↓↓ ↓↓ ↓ ↓↓ ↓↓
↓, decrease; ↑, increase; ↔⎕ no change, HR heart rate, CO cardiac output, SVR systemic vascular
resistance, MAP mean arterial pressure, ICP intracranial pressure, CPP cerebral perfusion
pressure, CBF cerebral blood ow, CMRO
Adapted from Rhoney DH, Parker D.Use of sedative and analgesic agents in neurotrauma patients
on cerebral physiology. Neurol Res 2001;23;237–59
, cerebral metabolic rate of oxygen
2
2
408
a TBI patient would include (1) a quick onset and offset to allow for frequent neurological exams, (2) reduced ICP by cerebral blood volume reduction or cerebral vasoconstriction, (3) reduced CBF and CMRO2 while maintaining coupling of the two, (4)
maintained cerebral autoregulation, (5) allowing usual cerebral vascular reactivity to
changes in PaCO2, and (6) minimal cardiovascular depressant effects [65].
L. V. JuradoHernández and T. A. Allison
16.5.3 Barbiturate Coma
Barbiturates have been recommended to treat high and refractory ICP since the
early 1980s [67, 68]. Barbiturates are thought to be neuroprotective through depression of cerebral metabolism and oxygen consumption. They may also lead to higher
brain oxygenation with lower cerebral blood ow secondary to improving coupling
of regional blood ow to metabolic demands. Additionally, this leads to decreased
ICP from decreased cerebral blood volume. Other brain-protective mechanisms
include inhibition of oxygen radical-mediated lipid peroxidation [69–71].
Despite the perceived benets of barbiturates, the literature has not demonstrated
a mortality benet [72–74]. Furthermore, numerous complications occur with their
use, including severe hypotension, decreased gastrointestinal motility, and increased
incidence of infections. Currently, high-dose barbiturate administration is recommended to control elevated ICP refractory to maximum standard medical and surgical treatment [13]. However, hemodynamic stability is essential before and during
barbiturate therapy. Due to the high incidence of hypotension, many patients will
require a vasopressor and uid support during barbiturate therapy.
16.6 Nonpharmacological Treatments
16.6.1
The standard posture for critically ill patients is a semi-recumbent position with
head elevation at an angle of 30°. This position has been shown to reduce the frequency and risk of nosocomial pneumonia, especially in patients who receive
enteral nutrition [75]. Several studies have demonstrated the benets of elevating
the head of the bed for lowering ICP in TBI patients [76–78]. One recent study
showed that changing stable TBI patients from a head elevation of 30° to 15° and
then to 0° resulted in a gradual increase in ICP. However, brain oxygenation and
brain circulation were improved [79]. This study did not assess clinical outcomes
resulting from these changes. Currently, there is limited evidence to recommend an
ideal head position. Based on other perceived benets, such as lowering the risk of
nosocomial pneumonia, head elevation should be maintained at 30° and then individualized to the patient’s needs.
Body/Head
Position
16 Traumatic Brain Injury
409
16.6.2 Temperature Management
The United States Centers for Disease Control and Prevention denes fever in
hospital- acquired infections as a measured temperature of greater than
38 °C. Similarly, the Society of Critical Care Medicine and Infectious Diseases
Society of America dene fever as a temperature equal to or greater than 38.3°C
[80]. Fever is observed in 20–50% of TBI patients, with nearly 90% having at least
one episode within 7days of hospitalization [81]. High fever (>39.0°C) within 72h
of the injury has been associated with six times the mortality of afebrile patients,
while even low-grade fever (38–39°C) has been associated with increased mortality
[82]. Fever burden, particularly early after TBI, is associated with poor prognosis
[83]. Every 1 °C increase in temperature has been associated with a 2.2-fold
increased risk of adverse outcomes. Further, a 0.5°C rise in temperature can lead to
a series of secondary injuries and neuron death [84].
While infection is the most common cause of fever, many causes in TBI patients
exist including disruption of the hypothalamic set point by endogenous pyrogens
released from injured neurons [85]. Through several complex mechanisms, fever
can lead to cerebral edema and potentially a decrease in CPP [85, 86]. Fever
increases the cerebral metabolic rate for oxygen and glucose, which can lead to an
increase in CBF and eventually an increase in CBV and ICP [87]. Fever in TBI
patients can lead to secondary injury including ischemic neuronal injury, mitochondrial dysfunction, reactive oxygen species, and thereby neuronal death.
Temperature in TBI patients should be maintained at normothermia (37.5°C) to
lessen the risk of secondary brain injury and elevated ICPs. First-line treatment of
fever includes scheduled acetaminophen 650mg every 4h (4000mg maximum in
24h). Second-line therapy includes applying an external cooling blanket and ice
packs to the axilla, groin, and neck if temperature remains >37.5 °C. Third-line
therapy includes administration of cold IV uids and 0.9% sodium chloride in
500–1000mL if temperature remains elevated despite previous therapies. Fourthline therap
patients or esophageal cooling in intubated patients, is often reserved for those who
cannot tolerate the additional volume. Once intravascular cooling is initiated, other
external cooling methods can be [88] removed. The devices are regulated to a core
body temperature that is measured by a bladder thermistor or esophageal temperature probe.
Aggressive fever control to maintain normothermia can lead to shivering.
Shivering increases the patient’s metabolic rate, which can have detrimental effects
on oxygenation and ICP, making it challenging to achieve goal temperatures [88].
Shivering can be scored at the bedside by using the Bedside Shivering Assessment
Scale (BSAS), with scores of 0=no shivering, 1=mild shivering localized to neck
and/or thorax, 2= moderate shivering with gross movement of upper extremities,
and 3=severe shivering that involves gross movements of the trunk and upper and
lower extremities [88]. The goal BSAS is a score of ≤1. Medications to prevent
shivering as well as counter warming during the cooling period have been
y, which includes intravascular or external cooling in non-intubated
410
L. V. JuradoHernández and T. A. Allison
protocolized to minimize shivering. Medications are given in a stepwise approach
with the goal to maximize one agent prior to moving to the next; see Table16.5.
16.6.3 Prophylactic Hypothermia
Prophylactic hypothermia is believed to be neuroprotective through several mechanisms
including reduced ICP, reduced CMRO2, reduced CBF, and maintenance of the BBB
function. Additionally, it is thought to limit secondary brain injury by reducing the
inammatory response and biochemical cascade early after TBI [13, 89–91].
Nevertheless, there are signicant risks associated with the use of prophylactic hypothermia including seizures and myoclonus and effects on the immune system leading to
an increase in infections, predominantly pneumonia, coagulopathy, and ventricular ectopic beats [92]. Electrolyte disturbances, particularly hypokalemia and hyperkalemia, are
common. Hypokalemia can lead to ventricular arrhythmias, cardiac arrest, and death. If
prophylactic hypothermia is used, the pharmacist should participate in the development
of an electrolyte protocol specic to the cooling and rewarming phases.
Prophylactic hypothermia for TBI has been studied since the 1990s in 14 randomized controlled trials with different TBI patient populations, outcomes, and
cooling devices. Currently, the evidence is inconsistent and does not support
improved morbidity and mortality. Prophylactic hypothermia is not recommended
because of these ndings as well as the increased risks associated with it [13].
Table 16.5 Medications used for management of shivering
Step Intervention Dose
1 Buspirone and magnesium sulfate
infusion
2 Dexmedetomidine infusion or
fentanyl infusion or meperidine
3 Propofol infusion Initiate at 20mcg/kg/min; titrate to effect (max dose
4 Vecuronium or rocuronium Vecuronium: 0.1mg/kg IV as needed based on
BSAS bedside shivering assessment scale, PRIS propofol-related infusion syndrome, TOF train of
four, CrCl creatinine clearance, ESRD end stage renal disease
Adapted from: Choi HA, Ko S-B, Presciutti M.Prevention of shivering during therapeutic temperature modulation: the Columbia anti-shivering protocol. Neurocrit Care. 2011;14:389–94
Buspirone: 30mg Q8h
15mg Q8h if CrCl <50mL/min
Avoid use in CrCl <20mL/min or ESRD
Magnesium: Start at 0.5mg/h; titrate by 0.25g/h
Q4h, to goal magnesium level (3–3.5mg/dL)
Start at 0.25mg/h if CrCl </=30mL/min
Dexmedetomidine: Initiate at 0.2mcg/kg/h, titrate
every 15min to effect. Max dose 1.4mcg/kg/h
Fentanyl: Initiate at 25mcg/h
Meperidine: 12.5–75mg IM or IV Q4h as needed
75mcg/kg/min); monitor patients for PRIS at higher
doses
BSAS score and TOF monitoring
Rocuronium:1–1.2mg/kg IV as needed based on
BSAS score and TOF monitoring
()
..
01
()
raumatic Brain Injury
16
T
16.7 Adjunct Therapies
411
16.7.1
Seizure
Prophylaxis
Patients with severe TBI have a high risk of seizures [13, 93]. Seizures usually occur
in the area of the brain where scarring has developed secondary to the injury [94].
Post-traumatic seizures (PTSs) are classied as early (occurring within 7days of
injury) or late (occurring after 7days of injury). Post-traumatic epilepsy (PTE) is
dened as recurrent seizures more than 7days following injury. Table 16.6 highlights risk factors for PTS and PTE. The rate of clinical PTS has been reported to be
as high as 12–25%, including subclinical seizures detected on electroencephalography [95]. Early PTS is associated with higher mortality, longer hospital length of
stay, and non-home discharge [96]. PTE doubles the rate of unfavorable outcomes
at 2years and increases the risk of unexpected death by a factor of 30 [5, 97, 98].
The BTF Guidelines recommend the use of anticonvulsants following TBI to
prevent the occurrence of PTS. Phenytoin is recommended in the guidelines; however, the use of levetiracetam is increasing for this indication. Currently, there is a
lack of comparative studies to recommend one agent over another. Table16.7 compares the dosing and monitoring of the two agents.
Total phenytoin levels must be adjusted for hypoalbuminemia and renal dysfunction. The formula for dose adjustment that most accurately predicts adjustment
based on albumin and renal dysfunction is the Winter-Tozer equation [101, 102]:
Predicted free phenytoin measured total PHTalbumin=
×+/.02 0.
10
×
Adverse events with phenytoin are predominantly concentration related. Adverse
events associated with total concentrations less than 40mcg/mL include nystagmus,
blurred vision, diplopia, ataxia, slurred speech, and lethargy, while coma and death are
associated with concentrations greater than 40mcg/mL.Other concerns include cardiovascular collapse, extravasations and purple glove syndrome, Stevens- Johnson
syndrome/toxic epidermal necrolysis, drug interactions, and enteral tube feed
Table 16.6 Risk factors for PTS and PTE after TBI [95, 99, 100]
PTS PTE
Age ≤65years
Cortical contusion
Chronic alcoholism
Epidural hematoma
Glasgow coma scale (GCS) score ≤10
Intracerebral hemorrhage
Immediate seizures
Linear or depressed skull fracture
Penetrating head injury
Post-traumatic amnesia >30min
Subdural hematoma
Acute intracerebral hematoma
Age >65years
Cortical contusion
Early PTS
History of depression
Post-traumatic amnesia >24h
Severe TBI
412
Table 16.7 Comparison of phenytoin and levetiracetam for seizure prophylaxis [13, 110, 112, 114]
Phenytoin Levetiracetam
Loading dose 20mg/kg IV×1 (max 2000mg) NA
Maintenance
dose
Duration 7days 7days
Monitoring Total 10–20mg/L
GT gastric tube, IV intravenous, PO oral, SR sustained release
5mg/kg/day or 100mg IV/PO/GT every 8h or 300mg
SR capsules PO daily
Free 1–2mg/L
L. V. JuradoHernández and T. A. Allison
500–1000mg every
12h
May be given IV/
PO/GT
NA
interactions. Phenytoin can produce cardiovascular collapse when infused too quickly
[103]. However, this is thought to be due to the diluent, which contains propylene
glycol. Patients develop hypotension and bradyarrhythmias [104]. Phenytoin is a
Vaughan-Williams class 1B antiarrhythmic. However, it has quick on-off kinetics at
the sodium channel, making it less arrhythmogenic compared with agents with slow
on-off kinetics, such as the class IC agents. Additionally, phenytoin can cause signicant tissue damage when extravasation occurs. It leads to a purplish-black discoloration accompanied by edema and pain distal to the site of injection. On rare occasions,
it may progress to necrosis, ischemia, vascular compression, or compartment syndrome requiring surgical interventions. It is termed purple glove syndrome (PGS)
because of its appearance. The pathophysiology is not well understood, and several
mechanisms have been proposed [105]. Phenytoin comes in a highly alkaline
(pH = 12) solution, and it has been proposed that it may induce vasoconstriction
resulting in leaking of the solution into surrounding interstitial soft tissue spaces. This
is usually followed by damage to vascular endothelial integrity, promoting further
leakage of phenytoin solution into adjacent interstitial soft tissue spaces. It has also
been proposed that mixing of the highly alkaline solution with the more neutral pH of
the blood may produce precipitation of phenytoin that may obstruct the vein and lead
to phenytoin backup and leakage into soft tissue interstitial spaces and the development of PGS. Finally, IV phenytoin solution contains sodium hydroxide, propylene
glycol, and ethanol, all of which are known tissue irritants that can cause damage in
extravasations. In order to reduce the risk of extravasation, phenytoin should be
administered through an 18-gauge peripheral IV catheter or larger or via a central line.
Additionally, the nurse should check the patency of the line prior to infusion. Phenytoin
should never be infused through lines in the hands or feet.
Fosphenytoin is a water-soluble prodrug of phenytoin. It has several advantages
over phenytoin. It may be administered intravenously or intramuscularly. The maximum recommended infusion rate is 150 mg / min vs. 50mg/min for phenytoin. The
prodrug has an 8–15-min half-life of conversion to phenytoin. Due to this conversion
time, the time to therapeutic levels is the same between agents [106–108]. It is often
preferred over phenytoin due to better tolerance at the infusion site, lower risk of cardiac arrhythmias or hypotension, and lower risk of PGS [109]. However, fosphenytoin
is converted to phenytoin and can cause similar electrocardiography (ECG) changes.
16 Traumatic Brain Injury
413
Additionally, it has been theorized to have direct effects on calcium equilibrium due
to its metabolism to phenytoin and an inorganic phosphate. The inorganic phosphate
binds with cations and leads to a reduction in both total and ionized calcium concentrations. The subsequent hypocalcemia has the potential to produce various cardiac
arrhythmias. Continuous ECG monitoring, particularly during the loading dose, is
recommended for both agents due to the potential for bradyarrhythmias.
Despite the knowledge that phenytoin interacts with enteral tube feeds for over
40years, the mechanism of the interaction remains poorly understood. It is thought
that phenytoin adheres to the plastic tubing or there is a physical incompatibility
with the enteral feed. Regardless, phenytoin serum levels can be reduced by 50–75%
when it is administered via the enteral feeding tube. Recommendations to overcome
this issue include (1) ush tube before and after phenytoin administration and (2)
hold tube feeds 1–2h before and after each dose. Due to the complications of holding tube feeds and adjusting rates to ensure adequate nutrition, a reasonable option
is to empirically increase the dose from 100mg every 8h to 200mg every 12h.
The use of levetiracetam for seizure prophylaxis is increasing due to a favorable
adverse effect prole, more predictable pharmacokinetics making the need for therapeutic drug monitoring less burdensome, and similar clinical efcacy to phenytoin
and valproic acid in status epilepticus. Currently, the ideal dose of levetiracetam for
seizure prophylaxis is unknown. Recent evidence recommends lower doses due to
the nding of no difference between higher and lower dosing regimens [110].
Intravenous levetiracetam is well tolerated when diluted in 100mL of 0.9% sodium
chloride and 5% dextrose and infused over 15–60min. Recently, rapid IV push
administration of undiluted drug at doses as high as 4500mg has been shown to be
safe and well tolerated [111, 112]. Administration of undiluted drugs can lead to a
reduction in the time to administration secondary to delays in ordering and preparation and allowing for the drug to be stored on the unit in medication-dispensing units.
Adverse effects most often frequently observed with levetiracetam include psychiatric and behavioral symptoms [113]. Twenty to thirty-ve percent of adults
treated with levetiracetam for epilepsy experience behavioral adverse events.
Specically, patients experience greater irritability, aggression, depressive mood,
and anxiety compared to other antiepileptics. Approximately 18% of patients will
require cessation or dose reduction due to behavioral adverse effects. Additional
adverse effects include psychotic symptoms, paranoid ideation, and hallucinations.
16.7.2 Venous Thromboembolism (VTE) Prophylaxis
The incidence of VTE in TBI patients is up to 54% in patients who do not receive prophylaxis and 25% in patients who are placed on sequential compression devices (SCDs)
alone [115, 116]. The incidence of VTE increases with the severity of TBI.As such,
surveillance protocols are recommended in high-risk patients to ensure early detection
and intervention. Low-molecular-weight heparin (LMWH) or low-dose unfractionated
heparin (UFH) may be used in combination with mechanical prophylaxis.
414
L. V. JuradoHernández and T. A. Allison
Low-molecular-weight heparin is the preferred agent in trauma patients with
injury severity score (ISS) >10 per the Western Trauma Association (WTA) guidelines [117]. Enoxaparin 40mg twice daily is considered the standard dose in most
trauma patients, while the recommended dose for patients greater than 65years old,
with weight less than 50kg, or who have a creatinine clearance (CrCl) of 30–60mL/
min is 30mg subcutaneously (SC) twice daily. Additional enoxaparin weight-based
dosing regimens exist. Anti-Xa levels should be monitored in patients on enoxaparin who are underweight, in females with less than 50kg total body weight, in those
with BMI greater than 40, in acute renal failure patients, in those at increased risk
of bleeding, or in those who were initiated on weight-based doses. The recommended timing for anti-Xa levels is 4h after the third dose. Most agree that the goal
range for prophylaxis is 0.2–0.4units/mL.Once in the goal range, anti-Xa levels
should be rechecked if renal function declines.
Unfractionated heparin is recommended in patients with a CrCl less than 30mg/
dL or in renal failure. Dosing is 5000units SC every 8h if the body mass index
(BMI) is less than 40 or 7500units and SC Q8H if the BMI is greater than 40 and
CrCl is less than 30mL/min [13, 117, 118].
Pharmacological prophylaxis for VTE prophylaxis can be initiated safely 24h after
injury in most TBI patients with a stable head CT.However, there are several risk stratication scoring systems used to guide surveillance and prophylaxis in polytrauma and
TBI patients. The risk for thromboembolism in trauma patients is assessed using the
Greeneld Risk Assessment Prole. Risk factors are divided into categories: underlying
conditions, iatrogenic factors, injury-related factors, and age. The maximum score is 14.
A score of 5 or more has been shown to increase the DVT risk threefold; pharmacologic
VTE prophylaxis should be initiated [119]. The Trauma Embolic Scoring System
(TESS) is another VTE risk stratication scoring system for polytrauma patients determined by ve clinical variables: age, Injury Severity Score (ISS), BMI, ventilator days,
and presence of a lower extremity fracture [120]. A score of 0–2 indicates no risk, a
score of 3–6 is low risk, and a score of 7–14 is considered moderate to high risk. This
tool has been shown to be a useful clinical decision-making tool in predicting VTE in
military trauma patients [121]. The Parkland Protocol is an algorithm for VTE prophylaxis specically in TBI patients. It straties patients into categories for spontaneous
progression of hemorrhage and provides recommendations on starting VTE prophylaxis
[122]. In low-
risk TBI patients, enoxaparin is started 24h post-injury; in moderate-risk
TBI patients, enoxaparin is initiated 72h post-injury; and in high-risk TBI patients, a
prophylactic inferior vena cava (IVC) lter is recommended.
16.7.3 Antibiotic Prophylaxis
The infection rate in patients with intracranial pressure monitors has been reported
to be as high as 27% [123]. These infections are associated with high morbidity and
mortality, longer intensive care unit and hospital stay, and increased healthcare costs
[124–126].
16 Traumatic Brain Injury
415
Methods to prevent external ventricular drain (EVD) infections include disinfection of the skin, pre- and postoperative prophylaxis, shortening the duration of EVD
use, antibiotic-impregnated shunts, prolonged prophylactic antibiotics, or combinations of these in protocols [126, 127]. Published protocols from some institutions
have demonstrated rates as low as 0%. In patients with EVDs, systemic prophylactic
antibiotics can prevent infection. The Neurocritical Care Society Consensus
Statement on Insertion and Management of EVDs recommends to administer one
dose of antimicrobials prior to EVD insertion and not continuing antibiotics for the
duration of EVD placement [128].
For neurosurgery procedures, CSF-shunting procedures, the recommended regimen is cefazolin 2g IV×1 or 3g IV×1 for patients weighing ≥120kg. Redosing
of cefazolin if surgery continues longer than 4h from the preoperative dose is recommended. Alternative agents for patients allergic to β-lactam antibiotics include
vancomycin 15mg/kg IV×1 or clindamycin 900mg IV×1. Redosing of clindamycin if surgery continues longer than 6h from the preoperative dose is recommended.
The recommended duration of postoperative antimicrobials is a single dose or continuation for less than 24h [129]. There is insufcient data to recommend continuation of antibiotics beyond 24h postoperatively in patients with craniectomy or
additional doses beyond the perioperative dose in patients with indwelling devices
[123, 128, 130].
16.7.4 Stress Ulcer Prophylaxis (SUP)
Stress ulcers are supercial ulcers in the upper gastrointestinal (GI) tract that may
develop during hospitalization and in the ICU setting [131, 132]. Stress ulcers
develop because of either hypersecretion of acid or impaired mucosal protection
secondary to GI tract hypoperfusion, mucosal ischemia, or disruption. Additionally,
TBI patients are at an increased risk for developing gastric stress ulcers during their
hospital stay because of increased ICP and overstimulation of the vagus nerve,
which can lead to excess production of gastric acid as well as general hypoperfusion
of the gut due to the stress of critical illness [133–135].
Stress ulcers in critically ill patients can be divided into four categories, including asymptomatic stress ulceration, stress ulceration with occult bleeding, stress
ulceration with overt bleeding, and stress ulceration with clinically signicant
bleeding [131, 136, 137]. The incidence of asymptomatic stress ulceration in critically ill patients who do not receive prophylaxis may exceed 75%, while stress
ulceration leading to clinically signicant bleeding affects approximately 1–3% of
patients in the ICU [138, 139]. Stress ulceration can lead to an increased length of
stay as well as serious complications including perforation, hemorrhagic shock, and
death. Stress ulcer management should focus on prevention.
Multiple risk factors have been linked to the risk of stress ulceration. Patients are
considered to be at very high risk for developing a stress ulcer with clinically signicant bleeding if they have either prolonged mechanical ventilation beyond 48h