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L. V. JuradoHernández and T. A. Allison
or the presence of coagulopathy [140, 141]. Patients are at high risk if they have two
of the following risk factors: GCS <10, head or spinal cord injury, high-dose corticosteroids (>250mg/day of hydrocortisone or equivalent), history of GI bleeding
within 1year, hypotension, ICU admission >1week, ileus, major surgery, multipleorgan failure, myocardial infarction, renal or hepatic failure, sepsis, severe burns
(>35% body surface area), solid-organ transplant, and trauma [131, 137, 140–142].
The Surviving Sepsis Campaign guidelines recommend the use of a proton pump
inhibitor (PPI) or histamine 2-receptor antagonist (H2RA) for stress ulcer prophylaxis [143]. Both medication classes lead to the inhibition of gastric acid secretion
and an increase in gastric pH.Proton pump inhibitors block the hydrogen-potassium
ATPase pump, while H2RAs bind to the histamine-2 receptor on parietal cells and
inhibit the pathway histamine utilizes to stimulate proton pump activity. Sucralfate
has also been used for SUP; however; it requires gastric access. The use of sucralfate is limited in the ICUs, as many have moved to jejunal nutrition to reduce aspiration. The choice of agent can vary per institution and patient population and should
take into account administration, adverse effects, drug interactions, and cost. Many
institutions will elect to administer pantoprazole orally or intravenously and lansoprazole enterally as a suspension. Compared to cimetidine and ranitidine, famotidine has a longer duration of action and fewer drug interactions involving the
cytochrome P-450 hepatic enzyme system [144]. Combined with this and its general tolerability, famotidine is frequently the preferred H2RA.Table16.8 highlights
the dosing of agents used for stress ulcer prophylaxis.
Despite the benets of these agents in preventing stress ulcers, concerns regarding the association between non-judicious acid suppression and increased risk of
bacterial infections, particularly pneumonia and Clostridioides difcile, exist. The
risk of infection is thought to be higher with the PPIs than the H2RAs. Additionally,
both classes of agents have been associated with thrombocytopenia in case reports
and case series. However, larger analyses were not able to conrm this concern. In
most of the reports describing thrombocytopenia, patients had additional risk
Table 16.8 Stress ulcer prophylaxis agents [135, 137, 140, 144]
H 2-receptor antagonists
Cimetidine 400mg PO Q6H
Famotidine 20mg PO/NG/IV Q12H
Ranitidine 150mg PO/IV Q12H
Proton pump inhibitors
Esomeprazole 40mg PO/IV Q24H
Lansoprazole 30mg NG Q24H
Omeprazole 40mg PO/NG Q24H
Pantoprazole 40mg PO/IV/NG Q24H
Gastrointestinal protectant
Sucralfate 1g PO/NG Q6H
IV intravenously, NG nasogastrically, PO orally
Q24H
(CrCl <50mL/min)
Q24H
(CrCl <50mL/min)
16 Traumatic Brain Injury
factors that could have caused or contributed to the development of thrombocytopenia. As such, the risks and benets need to be considered. Therapy should be initiated and discontinued as applicable to the clinical situation. The pharmacist can
play an important role in managing appropriate stress ulcer therapy.
417
16.7.5 Tranexamic Acid
Tranexamic acid (TXA) is a synthetic lysine analogue that competitively inhibits
the conversion of plasminogen to plasmin. This reduces the proteolytic action of
plasmin on brin clots, resulting in an inhibition of brinolysis [145, 146]. It has
been shown to reduce surgical bleeding and decrease mortality in patients with
extracranial bleeding [147, 148]. Intracranial bleeding starts at the moment of
impact and can continue for several hours after injury [149, 150]. Increased brinolysis is often observed in TBI patients and predicts hemorrhagic expansion [151]. It
has been proposed that early administration of TXA could prevent or decrease hemorrhagic expansion and therefore herniation and death.
The CRASH-3 trial concluded that the risk of death was reduced with early
tranexamic acid use in patients with mild-to-moderate head injury. TXA should be
administered as a loading dose of 1g over 10min, started within 3h of injury, followed by a continuous infusion of 1g over the next 8h. However, the use of TXA
in isolated TBI remains controversial due to several questions regarding the effect
size, mortality only being observed in subgroups, quality of survival, mid-study
protocol changes, safety, and other concerns about CRASH-3 and TXA use in general [152, 153]. A subsequent meta-analysis of 9 studies including CRASH-3 data
concluded that in acute TBI patients, TXA may decrease hematoma expansion but
probably has no effect on mortality or disability [154]. If TXA is to be considered,
it is recommended to use it in moderate TBI patients with GCS 9–12 and preserved
pupillary reactivity. What is likely to have more of an impact is limiting secondary
brain injuries by preventing hypotension, hypoxemia, and pyrexia insults [7,
153, 155].
16.7.6 Glucose Targets
Acute hyperglycemia after TBI is common and has been associated with poor outcomes [156–158]. An early surge in sympathetic activity leads to an increase in
systemic circulating catecholamines. The degree of sympathoadrenal response
appears to increase linearly with the severity of the brain injury [159]. The catecholamine surge occurs within minutes of the insult and may be transient, while the
circulating glucose surge that follows soon after is sustained. Studies indicate that
hyperglycemia is harmful because it contributes to anaerobic metabolism in the
brain, resulting in brain tissue lactic acidosis and secondary neuronal injury
418
L. V. JuradoHernández and T. A. Allison
[160–162]. However, data also suggests that moderate hyperglycemia may be necessary during acute TBI because glucose is the only energy source for the brain, and
its utilization signicantly increases to meet energy demands immediately following injury [163, 164]. It is unclear as to what level of hyperglycemia should be
treated and if it will improve or worsen outcomes.
Tight glycemic control has been shown to increase global glucose uptake and
increase cerebral metabolic distress after TBI [165]. Additionally, reduced CSF
microdialysis levels of glucose after TBI have been demonstrated [166, 167].
Persistent low levels of glucose independently predict poor outcomes. Decreases in
microdialysis glucose levels can be due to several causes, including brain ischemia,
herniation, and seizures. Given that these processes could be occurring and that the
brain has an increased need for glucose, it is reasonable to assume that a reduction
in glucose supply would be harmful.
The BTF Guidelines do not provide a specic recommendation for glycemic
control due to insufcient evidence. The 2024 Society of Critical Care Medicine
Guidelines on Glycemic Control for Critically Ill Children and Adults state that
“analysis from neurological ICUs yielded comparable ndings, and these
patients should be managed like unselected patients.” The guidelines recommend treating persistent hyperglycemia greater than or equal to 180mg/dL in
critically ill adults. For the acute management of hyperglycemia, the guideline
suggests using an IV insulin infusion vs. subcutaneous insulin. The recommended target glucose ranges are 140–200mg/dL vs. 80–139mg/dL in order to
decrease the risk of hypoglycemia. While managing hyperglycemia with an IV
insulin infusion, ≤1 h, continuous, or near-continuous glucose monitoring
should occur.
16.7.7 Steroids
The only level 1 recommendation in the BTF Guidelines is against the use of
steroids for improving outcomes or reducing ICP. In severe TBI, high-dose
methylprednisolone was associated with increased mortality. Since the 1950s,
glucocorticoids have been used to provide symptomatic relief to patients with
brain tumors. A large portion of patients will experience symptomatic edema,
which often produces a mass effect larger than the tumor [168]. This mass
effect can lead to headaches and neurological deficits. Based on the benefits
observed in patients with brain tumors in the perioperative phase, their use
became common in other neurosurgical procedures and in the treatment of
TBI.A systematic review in 1997 showed no benefit for improving outcomes
in TBI patients; however, the authors recommended a larger trial to confirm
these results [169].
The Corticosteroid Randomization After Signicant Head Injury (CRASH) trial
was an international, multicenter, randomized controlled trial of methylprednisolone in patients with TBI. The trial evaluated 10,008 adult hospitalized patients
16 Traumatic Brain Injury
within 8h of injury with a GCS <14. Patients received methylprednisolone 2g IV
followed by 0.4mg/h for 48h or placebo. The study was stopped early due to the
increased risk of death in the steroid group [125, 167]. Six-month follow-up conrmed a higher risk of death.
419
16.8 Complications
16.8.1 Paroxysmal Sympathetic Hyperactivity
Paroxysmal sympathetic hyperactivity (PSH) is a syndrome that occurs in 8–10% of
patients with TBI and is characterized by episodes of hypertension, tachypnea,
hyperthermia, diaphoresis, and dystonic posturing [170, 171]. These episodes may
last from minutes to hours and can occur several times a day or, in refractory cases,
nearly continuously. It is associated with greater morbidity, increased healthcare
costs, longer hospitalizations, and worse outcomes. Uncontrolled symptoms can
lead to secondary brain injury from hypertension, hyperthermia, cardiac damage,
and death [172]. Detailed descriptions of the time course of PSH are difcult to nd
in the literature. One study showed that the rst episode occurred on average
5.9±3.7days after injury [173]. It may persist into the rehabilitation phase and may
last for weeks to months after the injury. In severe cases, it may persist for more than
1year [173, 174].
Signicant risk factors for developing PSH after TBI include the severity of the
initial brain injury, younger age, and male gender. Most agree that PSH is caused by
a functional disconnection leading to unbalanced activation of brainstem systems
controlling the autonomic nervous system. PSH can be caused by different mechanisms of injury in different locations, explaining the variability in symptoms and
severity. Regardless of the lesion location, the nal common pathway is an imbalance of adrenergic outow.
Symptom-based ndings are used for the early identication of PSH. As such,
PSH is frequently only recognized once the patient begins to awaken. Diagnosis is
often one of exclusion and recognition of a recurring pattern. An expert consensus
group proposed the use of the PSH assessment measure (PSH-AM) tool shown in
Table16.9, which is a clinical scoring system used for probabilistic diagnosis [171].
There are two components in the PSH-AM tool; the clinical feature scale (CFS)
assesses the severity of clinical features and motor activity, and the diagnosis likelihood tool (DLT) measures the presence of compatible features of PSH. Combined
scores indicate the diagnostic likelihood of PSH as unlikely, possible, or probable.
This assessment tool should be used on a daily basis in the ICU and through the
rehabilitation phase.
Management of PSH requires a combination of pharmacological and nonpharmacological treatment modalities. The etiology of PSH is not well understood,
which makes treatment difcult. Therapy focuses on the control of symptoms. A
combination of medications from different classes is tried based on symptoms and
420
Table 16.9 PSH assessment measure tool
Clinical feature scale (CFS)
0 1 2 3 Score
Heart rate <100 100–119 120–139 ≥140
Respiratory rate <18 18–23 24–29 ≥30
Systolic blood pressure <140 140–159 160–179 ≥180
Temperature <37 37–37.9 38–38.9 ≥39.0
Sweating Nil Mild Moderate Severe
Posturing during episodes Nil Mild Moderate Severe
CFS subtotal
Severity of clinical features Nil 0
Diagnosis likelihood tool (DLT): Score 1 point for each feature present
Clinical features occur simultaneously
Episodes are paroxysmal in nature
Sympathetic over-reactivity to normally non-painful stimuli
Features persist for ≥3 consecutive days
Features persist for ≥2weeks post-brain injury
Features persist despite treatment of alternative differential diagnoses
Medication administered to decrease sympathetic features
≥2 episodes daily
Absence of parasympathetic features during episode
Absence of other presumed causes of features
Antecedent acquired brain injury
DLT subtotal
CFS+DLT total
PSH diagnostic likelihood Unlikely <8
Adapted from Baguley IJ, Perkes IE, Fernandez-Ortega F.Paroxysmal sympathetic hyperactivity
after acquired brain injury: consensus on conceptual denition, nomenclature, and diagnostic criteria. J Neurotrauma.2014;31:1515–1520
L. V. JuradoHernández and T. A. Allison
Mild 1–6
Moderate 7–12
Severe ≥13
Possible 8–16
Probable >17
individualized to the patient. Pharmacological management of PSH focuses on
symptom management, prevention of symptoms, and treatment of refractory issues.
Optimizing outcomes with medications and minimizing side effects are important.
A combination of short-acting medications for termination of symptoms should be
used with long-acting agents to prevent symptoms. Intravenous medications and
continuous infusions should be added for refractory symptoms. Table 16.10 highlights the commonly used medications used to treat PSH and the symptoms they
treat via their proposed mechanism.
Symptoms are often triggered by minimal external stimuli from routine patient
care. Because of this, patients can be placed on minimal stimulation protocols to
reduce the number of times interventions are performed.
16
raumatic Brain Injury
T
Table 16.10 Medications used for treatment of paroxysmal sympathetic hyperactivity [170, 172]
Medication Symptoms treated
Clonidine Hypertension α-Agonist
Dexmedetomidine Hypertension, agitation, tachycardia α-Agonist
Propranolol Hypertension, tachycardia, fever β-Blocker
Dantrolene Muscle rigidity, posturing Calcium ion
Bromocriptine Dystonia, fever, posturing Dopamine agonist
Gabapentin Spasticity, allodynic response GABA agonist
Benzodiazepines Agitation, hypertension, tachycardia,
Baclofen (oral and
intrathecal)
Morphine Tachycardia, peripheral vasodilation,
posturing
Pain, clonus, rigidity GABA
allodynic response
Proposed
mechanism
blocker
GABA
μ-Opiate agonist
agonist
A
agonist
B
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16.8.2 Infections inTBI Patients
Patients with TBI can be hospitalized for long periods, and they are exposed to
nosocomial infections due to the need for mechanical ventilation and urinary catheters [175–177]. Nosocomial infections affect approximately 30% of patients in the
ICU, while they affect up to 50% of TBI patients [178–180]. Infections can develop
in severe TBI patients due to extracranial injuries; however, the TBI injury can contribute to infections due to its ability to cause immunosuppression [181, 182].
Infections of concern in TBI patients include those related to the EVD, ventriculitis, and meningitis. Reported ventriculostomy-related infection (VRI) rates are as
high as 32%; however, rates of less than 10% are most often reported [128, 183,
184]. Empiric therapy for healthcare-associated ventriculitis and meningitis includes
vancomycin plus an anti-pseudomonal β-lactam (cefepime, ceftazidime, or meropenem) per the 2017 IDSA guidelines [185]. In patients with allergies to β-lactams
who are not able to tolerate meropenem or if it is contraindicated, ciprooxacin or
aztreonam is recommended. In patients with infections due to Candida species,
liposomal amphotericin B combined with 5-ucytosine is recommended initially;
once clinical improvement is demonstrated, therapy may be changed to uconazole
based on susceptibilities.
When treating infections in the neuro ICU, the possibility of neurotoxicity with
β-lactams should be considered. Patients should be monitored for decreased levels
of consciousness, nonconvulsive status epilepticus, myoclonus, and new-onset psychiatric disorders [186, 187]. Beta-lactams competitively inhibit the gammaaminobutyric acid A (GABAA) receptor, which could lead to the neurotoxicity
[188–190]. However, higher serum concentrations of β-lactams have been associated with neurotoxicity, predominantly in the setting of renal failure [191]. Of the
β-lactams, cefepime is most often associated with neurotoxicity [191–196].
Cefepime-induced neurotoxicity has been associated with supratherapeutic levels as
422
well as total exposure, dened by duration of therapy [191]. Risk factors associated
with β-lactam neurotoxicity include age, baseline cognitive dysfunction, inappropriate dosing, and kidney dysfunction [197]. Because of the risk of neurotoxicity
with any of the β-lactam, appropriate dose adjustments should be made in patients
with renal dysfunction. Additionally, patients should be monitored for signs of
neurotoxicity.
L. V. JuradoHernández and T. A. Allison
16.8.3 Central Fever
Fever affects approximately 70% of critically ill patients at some point during their
hospital admission. In neuro ICU patients, only 50% of fevers are associated with
an infection [198]. Fever in brain injury patients leads to larger infarct size in ischemic stroke patients, poorer outcomes in the acute phase of brain injury, and
increased mortality [199].
Central or neurogenic fever is a noninfectious source of fever in TBI patients.
Studies have reported the incidence ranges from 4% to 37% in TBI survivors
[200, 201]. It is likely the result of an injury to the hypothalamus leading to a
disruption in the hypothalamic set point temperature and an abnormal increase
in body temperature. It is often characterized by bradycardia, lack of perspiration, high temperatures, and a plateau-like temperature curve that persists for
days to weeks [200, 202]. However, others report that it results in high temperatures, tachycardia, hyperhidrosis, hypertension, and sometimes seizures [200,
202–204].
There are several etiologies of fever in ICU patients, including infection, venous
thromboembolism, medications, surgery, atelectasis, and PSH. Diagnosis of central
fever is a diagnosis of exclusion. Antipyretic medications including acetaminophen
and nonsteroidal anti-inammatory drugs (NSAIDs) often do not provide adequate
temperature control [205]. When these agents fail to control the temperature, external cooling devices or endovascular cooling catheters may be tried [198]. Case
reports discuss the potential benets of bromocriptine, propranolol, and baclofen
for the treatment of central fever [201, 206–210]. However, further evaluation of
these agents for this indication is needed.
16.8.4 Sodium andWater Disorders
Patients may experience one of the three sodium/water disorders after a TBI.Diabetes
insipidus (DI) is on the opposite spectrum of syndrome of inappropriate antidiuretic
hormone secretion (SIADH) with regard to renal handling of water. SIADH and
cerebral salt wasting (CSW) syndrome appear clinically similar and are often misdiagnosed for the other. However, SIADH is a “water” issue, while CSW is a
“sodium” issue.
16 Traumatic Brain Injury
423
16.8.4.1 Diabetes Insipidus
Diabetes insipidus (DI) is characterized by polyuria (>50mL/kg per 24 h), hypotonic urine (<300mOsm/kg), and polydipsia [211, 212]. Because patients are often
unable to sense or respond to thirst, polydipsia is absent. Serum sodium levels are
often elevated due to the lack of compensation with uid intake. There are four etiologic categories of DI, including central (or neurogenic) DI, nephrogenic DI, primary polydipsia, and gestational DI. Primary polydipsia and gestational DI are
outside the scope of this review.
Nephrogenic DI is due to a renal insensitivity to the antidiuretic effect of normal
levels of antidiuretic hormone or arginine vasopressin (AVP). There are genetic causes;
however, medications and electrolyte disturbances (hypercalcemia or hypokalemia) are
the most common causes of nephrogenic DI in the ICU.Up to 20% of patients who take
lithium long-term will develop nephrogenic DI. Other agents reported to cause DI
include demeclocycline, ooxacin, foscarnet, clozapine, and orlistat [211, 213].
Central DI, the most common etiology for DI in the ICU, is due to a loss of production of AVP.Several cerebral diseases, such as tumor, granulomatosis, or meningitis, can lead to a loss of ADH secretion. However, the most common cause is
injury to the posterior pituitary or hypothalamic median eminence. This may be due
to a TBI, pituitary surgery, or cerebral edema/herniation.
Treatment of DI primarily consists of (1) replacing AVP to prevent ongoing renal
water loss and (2) replacing water loss to correct hypernatremia. In the case of
medication-induced nephrogenic DI, the offending medication should be identied
and immediately discontinued.
16.8.4.2 Syndrome ofInappropriate Antidiuretic Hormone
Secretion (SIADH)
SIADH accounts for one-third of all hyponatremia cases [214]. It occurs when
secretion of AVP continues inappropriately with normal or decreased plasma osmolality. SIADH is considered a euvolemic hypotonic hyponatremic state. Diagnostic
criteria include (1) serum sodium level of <135 mEq/L, (2) urine osmolality
>100 mOsm/kg, (3) urine sodium concentration >20–30 meq/L, (4) clinical
euvolemia or hypervolemia, (5) absence of other potential causes, and (6) normal
renal function and absence of diuretic use [215].
Treatment of SIADH most commonly includes uid restriction, treatment of
underlying pathology, hypertonic saline, loop diuretics, desmopressin, and vasopressin receptor antagonists or “vaptans.” Previously, drugs that cause DI such as
demeclocycline and lithium were used to manage SIADH. However, this is not recommended due to the adverse effects of these medications. Choice of treatment is
determined by symptoms of hyponatremia and underlying conditions. Patients
exhibiting mild-to-moderate symptoms may require uid restriction and treatment
of underlying pathology. Patients with severe symptoms such as seizures or severe
somnolence will require hypertonic saline.
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The speed at which the sodium is corrected depends on whether the hyponatremia is considered acute (<24–48h) or chronic (>48h). An increase of 4–6mEq/L
of the serum sodium is sufcient to reverse the serious manifestations of hyponatremia including brain herniation and neurological damage. If there is any question as
to whether or not the hyponatremia is acute or chronic, chronic correction recommendations should be followed. Minimum correction of sodium should be no more
than 4–8mEq/L per day, and no more than 4–6mEq/L per day if there is a concern
for osmotic demyelination syndrome. Previously, it was recommended that the limit
should not exceed 10–12mEq/L per 24-h period [215]. However, many now advocate increasing the serum sodium to no more than 8mEq/L in a 24-h period [216].
16.8.4.3 Cerebral Salt Wasting Syndrome
Cerebral salt wasting (CSW) syndrome is a loss of sodium and water in the urine
leading to a decrease in intravascular volume and hyponatremia. It is often associated with neurological disorders including SAH, head injury, and neurosurgical procedures. Differentiating CSW from SIADH is almost impossible.
Volume restriction, which is commonly done in SIADH, can be detrimental in
neurological conditions, particularly in SAH patients. For this reason, most neurological ICU patients with hyponatremia are managed with various concentrations of
sodium chloride or balanced sodium solutions depending on the serum sodium level
and perceived intravascular volume.
16.9 Conclusion
Traumatic brain injury is a potentially devastating disease that is complicated by
secondary injuries. Complications lead to further increases in morbidity and mortality. Patients with TBI should be treated in a dedicated neuro ICU in order to improve
outcomes.
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