What does anesthesia in a head trauma patient need to manage?

Patients with severe traumatic brain injury (TBI) often have other visceral, pulmonary, extremity, or spinal cord trauma, so management is often complex and requires a multidisciplinary combination of treatments
.

Anesthesiologists are involved in the treatment of TBI patients in many cases, and surgery and anesthesia can cause new secondary damage to damaged brain tissue due to hypotension, hypoxemia, hypocapnicsia/hypercapnia, fever, hypoglycemia/hyperglycemia, and/or increased intracranial pressure, which may adversely affect
outcomes.

This time will discuss the intraoperative anesthesia management of patients with acute TBI, summarize the knowledge, strengthen the intraoperative management of such patients, and hope that as an anesthesiologist, patients will have a better management and prognosis in anesthesia
.

Anesthesia management

Anesthesia Management Goals—Anesthesia management objectives for patients with TBI include:

●Beneficial for early cerebral decompression
in patients with dilated intracranial hematomas.

●Maintenance of CPP for the treatment of increased intracranial pressure
.

●Avoid secondary injuries, including hypotension, hypoxemia, hypocapnic and hypercapnic acidemia, hypoglycemia and hyperglycemia, seizures, and coagulation
.

● Adequate analgesia and amnesia
.

●Assist doctors with early postoperative neurological assessments
.

Monitoring — All anesthesia patients should monitor items, including ECG, noninvasive blood pressure, pulse oximetry, carbon dioxide monitoring, and body temperature
.
Additional intraoperative monitoring in patients with TBI includes:

●Arterial catheterization – A ductus arteriosus should be inserted to continuously monitor blood pressure and facilitate blood sample collection
.
The arterial sensor should be zeroed at the level of the external auditory canal to ensure accurate assessment of cerebral perfusion, especially if
the patient's head is above the heart level.
It should be noted that surgery should not delay the removal of rapidly expanding intracranial hematomas
for indwelling the arteriosus.

●Intracranial pressure monitoring – Intracranial pressure monitoring devices are often required in TBI patients, and intracranial pressure should be monitored continuously during patient transport in order to rapidly treat increased intracranial pressure
.

Intravenous access — Intraoperative blood loss should be established based on surgical planning, anticipated intraoperative blood loss, and estimated preoperative blood loss
.
Even simple head trauma, scalp wounds, scalp incisions, and intracranial hemorrhage can cause major blood
loss.

Patients with TBI may have a central venous catheter (CVC) indwelling to establish reliable intravenous access and give vasopressors
.
However, rapid expansion of intracranial hematomas cannot be delayed in order to insert CVC, and CVCs are generally not inserted prior to cerebral decompression
.
CVC can be established after cerebral decompression surgery to facilitate subsequent ICU therapy or extracranial surgery
in TBI patients.

Selection of anesthetics — Anesthetic drugs used to induce and maintain general anesthesia and their dosages must maintain hemodynamic stability, ensure cerebral perfusion, and avoid increased intracranial pressure and secondary brain injury
.
There are currently no data to suggest that any particular anesthetic is associated with the outcome of TBI
.

Pre-anesthesia medication – Patients who may have increased intracranial pressure are advised not to administer pre-anesthesia medication
.

Rapid sequence induction and intubation (RSII)

• Fentanyl 2-4 μg/kg intravenously, or refentanyl 1-3 μg/kg intravenously

• Lidocaine 1-1.
5 mg / kg intravenously

• Propofol 1.
5-2 mg / kg, administered intravenously, the dose is adjusted according to the patient's condition

•Etomidate 0.
2-0.
6 mg/kg, given intravenously, can be used in patients with hypotension before induction

• Succinylcholine 1-1.
5 mg / kg; Patients may have non-depolarizing neuromuscular blocking agents (NMBA) given doses of demuscular fibrillation at increased intracranial pressure, such as rocuronium bromide 2 mg, citreconium 1.
5 mg, or vicuronium bromide 0.
3 mg, followed by succinylcholine 1.
5 to 2 mg/kg, all intravenously
.

When patients have contraindications to succinylcholine, intravenous rocuronium bromide 1 mg/kg is replaced

●Anesthesia maintenance

•Minimum alveolar concentration (MAC) less than 1 isoflurane or sevoflurane, or propofol 70-140 μg/(kg·min), preferably adjusted according to the results of EEG monitoring after treatment

•Low-dose ketamine (dosage up to 10 mg/h) or dexmedetomidine [0.
2-0.
6 μg/(kg·h)] can be used as an adjunct to anesthesia

• Fentanyl is given every 1-2 hours 1-2 μg/kg, or refentanyl 0.
05-0.
3 μg/(kg·min), depending on the hemodynamic state, using higher doses when NMBA is not used

• Gradually adjust the dose of rocuronium bromide/vicuronium bromide to four strings (train-of-four, TOF) stimuli causing 1-2 tremors, provided that there are no contraindications to neuromonitoring

Airway management— Many patients with severe TBI have an endotracheal catheter
inserted before entering the operating room.
If the patient requires simultaneous induction anesthesia and airway management, the following principles should be followed:

●Cervical spine injury – Until cervical spine injury is definitively ruled out, it should be assumed that patients with severe TBI have an injury
.
Cervical spine injuries have been reported to occur in patients with severe head trauma in 4% to 8%, and are mostly mechanically unstable and associated with SCI [1].

Airway management must minimize the mobility of the cervical spine to avoid SCI
.

●Risk of aspiration – Patients with TBI should be assumed to be gastric satiety and therefore at risk of aspiration of
gastric contents.
The need for RSII
should be based on the expected degree of difficulty in airway management and other patient factors.

●Neuromuscular blockers – NMBAs are routinely given after anesthesia induction for endotracheal intubation and as needed during maintenance anesthesia as appropriate
.
RSII is most commonly used in succinylcholine or rocuronium
bromide.

Hemodynamic management—Fluids, blood products, vasopressors, and inotropics should be used with caution in the hemodynamic management of patients with TBI
.
The goal of intraoperative hemodynamic management is to adequately maintain CBF to avoid secondary injury
.
CBF is difficult to measure at the bedside, and CPP can be used as an alternative indicator: CPP = MAP–ICP, episodes of hypotension (low MAP), increased intracranial pressure, and/or decreased CPP can all lead to secondary brain injury and worsen clinical outcomes [2-3].

Target intracranial and cerebral perfusion pressure — guidelines published in 2017 recommending the maintenance of the ICP

Target blood pressure — The perioperative goal of patients with severe TBI is primarily to avoid hypotension because observational data suggest that hypotension leads to adverse neurologic outcomes
.
We agree with the Brain Trauma Foundation guidelines [6] to target blood pressure:

●Systolic blood pressure in patients aged 50-69 years≥ 100 mmHg

●Systolic blood pressure in patients aged 15-49 years or > 70 years ≥ 110 mmHg

The incidence of hypotension in emergency craniotomy in adults with TBI ranges from 32 to 65 percent [11,12].

Patients with intraoperative hypotension who develop intraoperative hypotension after craniotomy are more likely to die, develop persistent vegetative status, or have disability [10
].
The duration of intraoperative hypotension is negatively associated
with neurologic outcomes.

Intraoperative fluid management— Normal blood volume should be maintained in patients with TBI by means of a sugar-free isotonic crystal solution at the appropriate temperature [13-15].

The role of colloidal fluids is still controversial, and we do not use albumin in patients with TBI to avoid increased intracranial pressure due to colloidal changes in patients with changes in the blood-brain barrier
.
There are currently no data supporting or opposing the use of starch colloids
in TBI patients.
We don't use starch for the same reasons as albumin, and starch colloids have the potential to alter clotting function
.

Blood transfusions — The optimal intraoperative transfusion strategy for patients with TBI is uncertain
.
Anemia theoretically causes secondary brain injury by reducing oxygen delivery to brain tissue and is associated with poor outcomes [16,17
].
However, the current literature assessing the effect of blood transfusion on outcomes in patients with TBI does not support the use of relaxed transfusion thresholds (i.
e.
, higher target levels of Hgb
).
In a randomized trial of 200 patients with moderate to severe TBI, a relaxed transfusion threshold (target > 10 g/dL) did not improve outcomes after six months compared to the threshold of 7 g/dL and increased the incidence of thromboembolic adverse events [18].

Vasoactive agents — Vasoactive agents
are often used during anesthesia to obtain targeted blood pressure.
The brain-physiological effects of these drugs are very complex and are related
to baseline blood pressure, the state of the cerebrovascular self-regulatory mechanism, the drug's own mechanism of action, and the magnitude of blood pressure changes.
In addition, patients with moderate to severe TBI may present with cardiac dysfunction
.
When selecting vasopressors or inotropic agents, the resulting mild to moderate decrease in left ventricular ejection fraction should be taken into account [19,20
].

Vasopressors — The available evidence does not confirm which vasopressor is more appropriate in patients with TBI
.
Vasopressors
should be selected according to patient factors and clinical circumstances.

●Phenylephrine – The effect of phenylephrine on CBF is controversial
.
The drug may reduce brain oxygenation
, at least in some cases.
However, phenylephrine may be the most commonly infused vasopressor in surgery and is effective in increasing MAP and CPP [21
].

●Other vasopressors – Small randomized trials have compared norepinephrine and dopamine in patients with TBI
.
In one study of 20 patients with TBI in ICUs, intracranial pressure after dopamine use was higher than norepinephrine in the same MAP [22].

In another study of 10 TBI patients, there was no difference in the effects of norepinephrine and dopamine on CBF or intracranial pressure, but the hemodynamic effects of norepinephrine were more stable [23].

Vasodilators — In the case of adequate maintenance of MAP, vasodilators (i.
e.
, sodium nitroprusside, nitroglycerin, hydralazine, and calcium channel blockers) dilate cerebrovascular vessels, increase CBF, and thereby increase intracranial pressure
.
Therefore, patients with increased intracranial pressure should be used with
caution.

β receptor blockers—β receptor blockers reduce CBF and cerebral metabolic rate (CMR), but may also have no effect on both [24].

The use of β blockers to protect nerves after TBI has been proposed, but evidence of long-term benefit is lacking [25].

Intraoperative ventilation and oxygenation — Patients with TBI should target arterial partial oxygen pressure (PaO2)>60 mmHg [26,27], and partial pressure of carbon dioxide (PCO2) of 35 to 38 mmHg, unless therapeutic hyperventilation
is required.

●Oxigenation – Hypoxemia is associated with increased mortality and worse neurological outcomes in patients with TBI [28-30].

We agree with the Brain Trauma Foundation's recommendation to maintain PaO2 > 60 mmHg and peripheral oxygen saturation > 90% [26].

●Ventilation – Ventilation should be guided based on PCO2 in blood gas analysis rather than end-expiratory partial pressure of carbon dioxide (ETCO2
).
Although the correlation is generally good, there are many factors that can cause significant differences, such as age, lung disease, and position during surgery [31,32].

Patients with TBI should avoid hypercapnia as much as possible, as elevated PCO2 increases CBF and may increase intracranial pressure
.

Hyperventilation should only be used
when needed.
For example, in the presence of cerebral edema, hyperventilation and the resulting CBF drop may be required to reduce brain tissue tone, thereby reducing intracranial pressure or improving field exposure
.
However, vasoconstriction due to hyperventilation may cause ischemia, especially high-risk brain tissue after TBI
.
Multiple studies using multiple methods have found evidence that hyperventilation to PCO2 is 25-30 mmHg to cause ischemia in damaged brain tissue [33-35].

Therefore, if hyperventilation is required in multimodal processing aimed at reducing brain tissue tone, we limit the hyperventilation time so that PCO2 is between
30-35mmHg.

Temperature Management — The goal of temperature management is to maintain a normal intraoperative body temperature
.

Blood glucose management— In patients with TBI who require craniotomy, the incidence of intraoperative hyperglycemia is 15 to 20 percent [36,37
].
Both hyperglycemia and hypoglycemia can worsen outcomes in patients with severe TBI, but optimal blood glucose goals are uncertain and strict glycemic control is controversial
.
We monitor blood glucose during surgery and keep it at 80-180 mg/dL
.

Intraoperative glucocorticoid use — glucocorticoids are usually given during craniotomy during elective neurosurgery, but routine use is not recommended in patients with TBI [38]; Several large studies have found that glucocorticoids are harmful in patients with moderate to severe TBI
.

Author: Zhang Ziyin, The First Affiliated Hospital of Guangzhou University of Chinese Medicine