MANAGEMENT

Hemodynamic Control

Goal: Maintain SBP >110mmHg. In polytrauma patients with ongoing bleeding, aggressively control hemorrhage using all means available and restore circulating blood volume by using blood products. Note: An SBP >90mmHg has traditionally been targeted in TBI patients, though recent literature has suggested better outcomes may occur when SBP is maintained above 110mmHg in TBI patients.10,11

- Minimum: Stop all external bleeding. Manage internal bleeding to the extent possible with available resources. Administer tranexamic acid (TXA) per TCCC guidelines. Avoid medications that may lower the blood pressure (e.g., narcotics).
- Better: If there is evidence of bleeding and no blood products are available, administer 1L 0.9% sodium chloride (NaCl). Target is an SBP >110mmHg.
- Best: If there is evidence of bleeding, transfuse whole blood or, if not available, transfuse blood products. Greater emphasis on the use of Low Titer O Whole Blood is the optimal strategy. Target is an SBP >110mmHg.

Hemodynamic Control Notes

- Do not neglect scalp bleeding. This can become a significant source of blood loss. Scalp lacerations should be sutured or stapled as soon as possible.
- Take caution if an underlying skull fracture is present or if there is obvious penetrating trauma. DO NOT tightly pack or irrigate an open head wound. Suture or staple the skin closed, if bleeding. A pressure dressing may be placed if needed to control bleeding.
- Hypotension is usually not caused by TBI except as a late finding due to herniation.12 Always look for other causes of hypotension, such as ongoing bleeding or tension pneumothorax.
- Urine output (UOP) provides an important assessment of blood supply to the organs. Monitoring continuously by a Foley catheter is ideal. If a Foley catheter is not available, monitor by a graduated cylinder. Goal UOP in a polytrauma patient is 30–50mL/h.13
- The role of TXA in TBI patients is currently under investigation in the CRASH-3 trial. Limited data suggest TXA limits ICH expansion and may improve outcomes in TBI patients.14 Until more definitive data are available, TXA can be used in TBI patients.
- Colloids (e.g., albumin) have demonstrated a trend toward worsening outcomes in brain-injured patients.15 Hetastarches are associated with coagulopathy and increased risk of kidney injury in trauma patients.
- Avoid colloids and hetastarches in TBI patients; however, they can be used if no alternative is available.
- Avoid hypotonic fluids (including lactated Ringer’s) whenever possible; they can make brain swelling worse.

Most trauma patients with moderate or severe TBI will have other traumatic injuries. A careful search for bleeding should be performed in any hypotensive trauma patient.

Brain injury with associated hemorrhagic shock is a complicated scenario with a high risk of death. Balancing hemorrhage control (which is easier with lower blood pressure) with maintaining cerebral perfusion pressure (which requires higher blood pressure) should be guided with expert teleconsultation (i.e. critical care, neurocritical care, neurosurgical) whenever possible.

Airway, Oxygenation/Ventilation Management

Goal: Manually maintain or secure the patient’s airway and avoid hypoxia, hypocapnia, or hypercapnia to reduce the risk of secondary brain injury. If GCS score is ≤8 or there is facial trauma with compromised airway, a definitive airway is most likely needed. The provider should place the type of airway (i.e. cricothyroidotomy or endotracheal tube [ETT]) that they have the most confidence in placing, based on their training and practice.

- Minimum: Nasopharyngeal airway and bag-valve-mask with PEEP valve as needed. Use supplemental oxygen, if available. Maintain SpO2 >93%.
- Better: Perform a cricothyroidotomy/ETT placement or place a supraglottic airway (e.g., laryngeal mask airway [LMA], King laryngeal tube [LT]) followed by continuous sedation and airway maintenance, supplemental oxygen via oxygen concentrator, and portable ventilator to maintain an SpO2 >95% and EtCO2 of 35-45mmHg.
- Best: Cricothyroidotomy or ETT followed by continuous sedation and airway maintenance, supplemental oxygen, portable ventilator. Targets: SpO2 >95% and EtCO2 35-45 mmHg. Check arterial blood gas results and correlate with EtCO2 within 30 minutes of intubation if laboratory capability is available. A positive end-expiratory pressure (PEEP) of 5cmH2O should be used routinely. PEEP can be safely increased up to 15cmH2O if needed to improve SpO2, but be alert for problems caused by increased intrathoracic pressure (e.g., lower blood pressure or increased ICP).16

In the JTS Traumatic Brain Injury Management and Basic Neurosurgery in the Deployed Environment CPG, a goal of >93% is recommended, However, in order to establish a safety buffer in the prolonged field care setting often characterized by equipment challenges and limited personnel, in addition to anticipated transport challenges, a goal SpO2 of > 95% for ventilated patients is recommended.

Airway Management Notes

- Patients with a GCS score ≤8 should undergo placement of an advanced airway (i.e. cricothyroidotomy or ETT) unless arrival to a higher level of care will occur in a timely manner or the airway can be manually maintained. The risk versus benefit of advanced airway placement should be carefully considered and discussed by telemedicine consultation whenever possible.
- Airway interventions may cause transient hypoxia during the procedure. Every effort should be made to optimize airway placement on the first attempt by preoxygenating with supplemental O2, selecting the most experienced provider available, and using the technique most familiar to the provider.
- Patients typically require less sedation after cricothyroidotomy than after ETT placement. This may help conserve resources if medications are limited.
- Monitor EtCO2 and adjust ventilations to achieve the target range. Avoid hyperventilation (EtCO2 <35mmHg) except in extreme cases where imminent herniation is suspected, because hyperventilation worsens cerebral ischemia. Also avoid hypoventilation (EtCO2 >45 mmHg) that will increase ICP.
- Gastric decompression with a nasogastric tube (NGT) or oral gastric tube (OGT) will decrease the risk of aspiration in unconscious patients. If patients required bag-masking, they may have a distended stomach, which, in some patients, contributes to bradycardia. NGT and OGT cannot be placed with a supraglottic airway.

ICP Management

Goal: Suspect high ICP in any head injury patient with GCS score ≤8 OR declining findings on neurologic examination (unless explained by sedation, hypotension, hypoxia, hypercarbia, high fever). Minimize factors that contribute to elevated ICP, such as pain, anxiety, and fever. Rapidly recognize and manage elevated ICP, and maintain an adequate cerebral perfusion pressure.

- Minimum: Use general measures to reduce ICP.
- Elevate head of bed (HOB) 30°–60°.
- Maintain neck in midline position.
- Maintain arterial blood oxygen saturation (SpO2) >93% (or >95% if receiving ventilatory support.)
- Maintain EtCO2 between 35mmHg and 45mmHg
- Maintain core temperature between 96°F and 99.5°F.
- Maintain SBP >100mmHg, ideally at >110mmHg.
- Prevent or rapidly manage seizure activity.
- If concerned for impending herniation (e.g., unresponsive patient with unilateral dilated pupil, presence of Cushing’s triad), ventilate the patient for no more than 20 minutes to an EtCO2 target of 35mmHg17 Seek expert consultation immediately.

The optimum duration of hyperventilation and frequency that can be repeated are not known. If performed, assess response (i.e. pupils, GCS score, and so forth). If patient responds, consider performing again if needed, guided by expert teleconsultation, if possible

- Better: Even unconscious patients may experience pain and anxiety, manifested by hypertension (i.e., SBP >160mmHg) and/or agitation. Anxiety and agitation can increase ICP. In addition to all minimum measures, ensure adequate sedation and analgesia by targeting a Richmond Agitation and Sedation Score of −1 to −2. Refer to the JTS PFC Analgesia and Sedation CPG.18
- Ketamine 20mg IV/IO
- Hydromorphone 0.5–2mg IV/IO
- Fentanyl 25–50μg IV/IO

In addition to analgesics, consider administration of a rapid-onset, short-duration anxiolytic. Midazolam 1–2mg IV/IO as needed for agitation or anxiety.

- Best: In addition to all minimum and better measures, administer osmotic therapy via peripheral intravenous (IV) or intraosseous (IO) access:
- Hypertonic saline (HTS): 3% NaCl 250mL bolus over 20 minutes; repeat every 3 hours as needed when concerned for elevated ICP.
- Mannitol can be used if there is no sign of bleeding and the SBP is >110mmHg. Mannitol 1g/kg IV/IO over 20 minutes. Repeat at 0.5g/kg IV/IO every 3 hours as needed when concerned for elevated ICP.

Seek additional medical direction as soon as possible and evacuate to neurosurgical care at the earliest opportunity.

ICP Management Notes

- ICP cannot be directly measured without advanced intracranial monitoring devices. Therefore, vigilant clinical observation and the use of noninvasive ICP assessment modalities are critical to monitoring TBI patients until neurosurgical placement of neuromonitoring devices can occur.
- HTS bolus lowers ICP and has a duration of action of approximately 3 hours.19,20
- Mannitol, although effective, has several potentially adverse complications. It is a diuretic and might lower the blood pressure. Also, after repeated use, it can cross a damaged blood–brain barrier and potentially worsen ICP.20 For these reasons, HTS is preferred to mannitol in TBI and polytrauma patients.
- Some institutions have reported ICP-lowering benefits from vertical positioning of patients, particularly when high intraabdominal or intrathoracic pressure is suspected. Lower intraabdominal and intrathoracic pressures may facilitate venous drainage from the intracranial compartment. If safe to do so, this can be attempted when other measures have failed.21

Always treat hypotension before treating elevated ICP. Cerebral blood flow is more affected by a decrease in blood pressure than an increase in ICP.

Cerebral perfusion pressure (CPP) = mean arterial pressure (MAP; mmHg) − ICP (mmHg)

Hyperventilation reduces CO2 and rapidly lowers ICP by causing cerebral vasoconstriction and decreasing the overall cerebral blood volume. However, hyperventilation also damages the brain by causing ischemia and should only be performed for brief periods. Avoid hyperventilation unless all other interventions have been ineffective.22

Although there are invasive interventions to help assess and treat elevated ICP, evacuate hematomas, and so forth, such as decompressive craniectomy, extraventricular drains, intracranial bolt monitors, and burr holes, such procedures are not recommended unless the PFC provider has training and experience in performing these procedures and is directed by expert teleconsultation.

Infection Control

Goal: Dress all wounds to prevent further exposure to environmental pathogens and administer antibiotic prophylaxis to all patients with penetrating TBI.

- Minimum: Dress all wounds to prevent further introduction of infectious materials. Optimize wound and patient hygiene to the extent possible given the environmental and situational conditions.
  - For penetrating head wounds, apply superficial dressings and seal the dressing to the extent possible.
  - Bleeding head injuries must be sutured or stapled to control bleeding.
  - DO NOT introduce any material into the wound cavity.
  - DO NOT attempt to flush the wound.
  - Antibiotics are not necessary in TBI without open or penetrating trauma.
- Better: Antibiotics should be used for open or penetrating TBI.
  - Ertapenem 1g IV/IO every 24 hours and moxifloxacin 400mg PO every 24 hours for 5 days.

Ertapenam and moxifloxacin may increase the risk of seizure and ertapenam may not penetrate an intact blood-brain barrier. This combination, while commonly available, should only be used in TBI patients when the antibiotics with proven CNS penetration are not available.

- Best: Administer CNS-penetrating antibiotics for open or penetrating TBI.
  - Ceftriaxone 2 gm IV/IO every 24 hours or cefazolin 2g IV/IO every 8 hours for 5 days. .
  - Add metronidazole 500mg IV/IO every 8 hours for 5 days for wounds that are grossly contaminated with organic debris (e.g., dirt, debris, clothing).17

Infection Control Notes

- Moxifloxacin may be replaced with levofloxacin 750 mg PO daily to provide better coverage of bacteria found in wet terrain/ jungle environment.
- If recommended antibiotics are not available or significant drug allergies are present, obtain teleconsultation to discuss alternative medications. Additional detailed recommendations may be found in Forgione, et al.23

Seizure Prophylaxis and Management

Goal: Rapidly identify and manage seizure activity in TBI patients.

- Minimum: For witnessed convulsive seizure activity, place the patient on his/her side and clear the area of any potentially harmful objects. Suction the mouth, if possible, but DO NOT attempt to place anything inside a seizing patient’s mouth. Treat any witnessed or suspected seizures with a rapid-acting benzodiazepine.
  - Midazolam 5mg IV/IO/IM every 5 minutes until seizure stops.
  - An alternate benzodiazepine can be used if available (diazepam 5mg IV every 5 minutes until seizure stops; lorazepam 4mg IV every 5 minutes until seizure stops).
- Best: For witnessed or suspected seizures, administer a rapidly acting benzodiazepine (midazolam 5mg IV/IO/intramuscularly [IM]) plus a maintenance antiepilepsy drug. Broad-spectrum IV agents such as levetiracetam (Keppra; UCB Pharma, http://www.ucb.com/) are preferred.
  - Maintenance antiepilepsy-drug dosing: Levetiracetam: 1500mg IV/IO loading dose over 15 minutes followed by maintenance dosing of 1000mg IV/IO every 12 hours.
  - Alternate maintenance antiepilepsy drugs:
    - Phenytoin (loading dose: 1.5g IV over 1 hour, then 100mg PO/IV/IO every 8 hours)
    - Phenobarbital (loading dose: 1.5g IV/IO over 1 hour, then 100mg PO/IV/IO daily). Be ready to support ventilation if phenobarbital is used.

Seizure Notes

- Not all seizures are easy to see. At times, the findings may be obvious with generalized convulsions, or they may be subtle (e.g., persistent twitching of facial muscles, fingers).
- Risk factors for seizures after TBI include: GCS score <10, skull fractures, penetrating injuries, prolonged length of coma (>24 hours).24
- Non-convulsive seizures (NCSs) should be considered in any TBI patient with a GCS score ≤8 and who does not improve with appropriate resuscitation and/or ICP management. NCSs may persist after convulsive seizures are stopped and may be associated with higher morbidity and mortality.25 The most common signs of patients with NCS are coma, delirium, agitation, aphasia (impairment of language affecting production and/or comprehension of speech, reading, and/or writing) and/or “blank staring.”
- Prompt initiation of seizure prophylaxis reduces early seizures after TBI.26 In PFC settings, where possible, an anti-epilepsy drug should be used early after injury to help prevent seizure.
- Midazolam has a high rate of seizure control and works rapidly to terminate seizure activity.27 Midazolam is preferred because it is a short-acting medication (elimination time: 2–4 hours) and will allow for more regular and comprehensive neurologic examinations. It can be given IM in patients who do not yet have IV/IO access.
- If not already placed, strong consideration should be given to placing an advanced airway (cricothyroidotomy or ETT) in any TBI patient who experiences seizures (place airway after seizures are controlled).

Fever Control

Goal: Maintain core temperature between 96°F and 99.5°F. Treat fever aggressively in TBI patients with a combination of medication, cold fluid boluses, and surface cooling techniques.

- Minimum: Ensure patient has been removed from heat or sun. Remove clothes to allow evaporative cooling, Use surface-cooling measures (e.g., evaporative heat loss by misting and fan cooling) to reduce core body temperature.
- Better: Apply cold packs to axillary regions, posterior cervical region, and the groin.
- Best: Acetaminophen 650mg every 4 hours orally (PO) or rectally as needed for rectal temperatures >99.5° Additionally, cold saline IV fluid bolus can be used for refractory fever, if available.

Fever Notes

- Fever will increase cerebral metabolism and may increase ICP.
- Although targeted temperature management (previously referred to as therapeutic hypothermia) is used to reduce ICP in a critical care setting, hypothermia is part of the “lethal triad” in trauma patients, along with coagulopathy and acidosis. Targeted temperature management strategies beyond what is outlined in TCCC should NOT be attempted in the field or Role 1 setting.
- Hypothermia prevention and management kits should continue to be used in all trauma patients. In TBI patients, however, warming measures should be avoided when the core body temperature is above the target range.

Avoid non-steroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen, naproxen, ketorolac. Although these agents can effectively lower temperature, their antiplatelet effect may increase bleeding in TBI if intracranial hemorrhage is present (e.g., epidural hematomas, subdural hematomas).

Sodium Management

Goal: Avoid hyponatremia, which can worsen brain swelling. The target serum sodium level in patients with severe TBI is slightly above normal, between 145mmol/L and 160mmol/L.

- Minimum: Avoid the administration of any free water or hypotonic fluids that will lower serum sodium levels.
- Best: Monitor serum sodium level via blood sampling. In a stable patient, check sodium level every 6 hours. In an unstable patient, or in a patient receiving HTS, check sodium level every 3 hours. Adjust fluids as needed to meet the sodium goals.

Sodium Management Notes

- Several conditions can develop rapidly in brain-injured patients that can lower serum sodium levels (e.g., cerebral salt wasting, syndrome of inappropriate antidiuretic hormone secretion) or raise serum sodium levels (e.g., diabetes insipidus). Sodium levels, fluid intake, and urine output should be monitored closely.
- If laboratory testing for serum sodium level is not available, then, as a reference, 250mL of 3% saline can be expected to raise the serum sodium level of an 80kg patient approximately 2–3mmol/L. Assuming a normal serum level of 140mmol/L before starting HTS therapy, it would take six 250mL bags of 3% HTS to raise the serum sodium to concerning levels (i.e. >160mmol/L). This is without factoring in the regulation of serum sodium by the kidneys. If patient is urinating, it will be difficult to raise serum sodium above 160mmol/L with 3% HTS. If patient is not urinating, more caution should be used because sodium levels can build up more quickly.

Obtain telemedicine consultation, preferably from a critical care or neurocritical care expert, before giving more than two 250mL boluses of 3% NaCl HTS.

BLOOD GLUCOSE CONTROL

Goal: Avoid both hypoglycemia and hyperglycemia. Target a blood glucose level of 180mg/dL via handheld glucometer.

- Minimum: Monitor for clinical signs and symptoms of hypoglycemia (e.g., sweating, confusion, tremor, generalized weakness, generalized lethargy). If patient is hungry and able to safely swallow, allow the patient to eat to avoid hypoglycemia. Avoid the administration of any substances that are excessively high in sugar or carbohydrate content to prevent hyperglycemia.
- Best: Check blood glucose level every 6 hours. If glucose level is <100mg/dL, give 20g of oral glucose (5 teaspoons of sugar or 4 teaspoons of honey) PO or by NG tube. Or administer 25g (50mL) dextrose 50% in water (D50) solution IV/IO. Recheck blood glucose in 1 hour, then continue to check every 6 hours.

Blood Glucose Control Notes

- Hypoglycemia is more harmful to the brain than hyperglycemia.
- Hyperglycemia may occur in TBI as an acute stress response or as a result of brain-induced catecholamine release. Early hyperglycemia (i.e., >180mg/dL) has been associated with poor neurologic outcome in severe TBI.28
- The treatment of hyperglycemia requires insulin. If the appropriate medications, laboratory capability, and expertise are available, hyperglycemia may be treated; however, the treatment of hyperglycemia is not covered in this CPG.