ATLS 10.6 QUESTIONS AND ANSWERS: EXAM GUIDE 2022/2023

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In severe TBI, ventilate with % oxygen until . Maintain an oxygen saturation of . 100%, blood gas measurements are available, >98%.

In severe TBI, set ventilation parameters to maintain a PCO2 of 35 mmHg

Barbiturates may be effective in , though should not be used in the presence of or

Reducing ICP refractory to other methods

Hypovolemia

Hypotension

Post-traumatic epilepsy occurs in approximately % of inpatients with closed head injuries and % ofinpatients with severe head injuries.

5%, 15%

Nearly % of prehospital trauma-related deaths involve brain injury.

90%

Approximately % of patients with brain injuries who receive medical attention can be categorized as having mild injuries, % as moderate, and % as severe.

75%, 15%, 10%

The primary goal of treatment for patients with suspected TBI is to:

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Prevent secondary brain injury.

The most important ways to limit secondary brain damage and thereby improve a patient's outcome areto:

1. Ensure adequate oxygenation

2. Maintain blood pressure at a level that is sufficient to perfuse the brain.

3. If neurosurgery consultation available, identify any mass lesion that requires surgical evacuation

4. If imaging and neurosurgical consultation available, rapidly obtain a computed tomographic (CT) scanof the head.

5. Transfer to head injury unit once stabilized.

When consulting a neurosurgeon about a patient with TBI, communicate the following information:

1. Patient age

2. Mechanism and time of injury

3. Patient's respiratory and cardiovascular status (particularly blood pressure and oxygen saturation)

4. Results of the neurological examination, including the GCS score (particularly the motor response), pupil size, and reaction to light

5. Presence of any focal neurological deficits

6. Presence of suspected abnormal neuromuscular status

7. Presence and type of associated injuries Results of diagnostic studies, particularly CT scan (if available)

8. Treatment of hypotension or hypoxia

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9. Use of anticoagulants

Because of the scalp's generous blood supply, what complications may arise?

Scalp lacerations can result in major blood loss, hemorrhagic shock, and even death. Patients who aresubject to long transport times are at particular risk for these complications.

What are anatomy and injury implications of the anatomy of the base of the skull?

The base of the skull is irregular, and its surface can contribute to injury as the brain moves within the skull during the acceleration and deceleration that occurs during the traumatic event.

The anterior fossa houses the , the middle fossa houses the , and the posterior fossa contains the .

frontal lobes / temporal lobes / lower brainstem and cerebellum

The meninges cover the brain and consist of three layers:

Dura mater, arachnoid mater, and pia mater

Describe the anatomy and injury implications of the dura mater:

Tough, fibrous membrane that adheres firmly to the internal surface of the skull. At specific sites, the dura splits into two "leaves" that enclose the large venous sinuses, which providethe major venous drainage from the brain.

The midline superior sagittal sinus drains into the bilateral transverse and sigmoid sinuses, which areusually larger on the right side.

Laceration of the venous sinuses can result in massive hemorrhage.

Describe the anatomy and injury implications of the meningeal arteries

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Meningeal arteries lie between the dura and the internal surface of the skull in the epidural space.

Overlying skull fractures can lacerate these arteries and cause an epidural hematoma.

The most commonly injured meningeal vessel is the , which is located over the . An expanding hematoma from injury in this location can lead to rapid deterioration and death.

Middle meningeal artery

Temporal fossa

Epidural hematomas can arise from:

Lacerations of the meningeal arteries (rapid, most common)

Injury to the dural sinuses (slow)

Skull fractures (slow)

Most epidural hematomas must be managed as....

Life-threatening emergencies that must be evaluated by a neurosurgeon as soon as possible.

Describe the anatomy and injury implications of the arachnoid mater:

Beneath the dura mater

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Thin and transparent

A potential space between the dura and the arachoid layers exists (the subdural space)

Hemorrhage into the subdural space arises from :

Bridging veins, which travel from the surface of the brain to the venous sinuses within the dura.

Describe the anatomy and injury implications of the pia mater:

Firmly attached to the surface of the brain.

CSF fills the space between the watertight arachnoid mater and the pia mater (the subarachnoid space)

Subarachnoid space cushions the brain and spinal cord.

Hemorrhage into the subarachnoid space frequently accompanies brain contusion and injuries to the basal brain.

The brain consists of the , , and .

Cerebrum, brainstem, and the cerebellum

The cerebrum is composed of the and hemispheres, separated by the .

Left, right, falx cerebri

ATLS 10.6 QUESTIONS AND ANSWERS:EXAM GUIDE 2022/2023

The left hemisphere contains the in all people and % of people.

language centers, right-handed, >85%, left-handed

The frontal lobe controls:

Executive function

Emotions

Motor function

Motor speech (dominant side)

The parietal lobe controls:

Sensory function

Spatial orientation

The temporal lobe controls:

Memory function

Olfactory function

The occipital lobe controls:

Vision

The brainstem is composed of:

Midbrain

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Pons

Medulla oblongata

The midbrain and upper pons contain:

Reticular activating system (alertness)

The medulla contains:

Cardiorespiratory centers, extending to the spinal cord.

The cerebellum is responsible for and connects to :

Coordination and balance

Spinal cord, brainstem, cerebral hemispheres

Describe the anatomy and injury implications of the ventricular system:

CSF is constantly produced within the ventricles and absorbed of the surface of the brain.

Blood in the CSF impairs reabsorption and leads to increased intracranial pressure.

Hematomas and swelling cause effacement or shifting of the normally symmetric ventricles.

The divides the intracranial cavity into the and compartments.

Tentorium cerebelli

Supratentorial and infratentorial

The midbrain passes through an opening called the

Tentorial hiatus (or notch)

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The nerve runs along the edge of the tentorium and may become compressed during

Oculomotor (III) , temporal lobe herniation

Compression of the third cranial nerve leads to Inactivity of the parasympathetic fibers that constrict the pupil, leading to unopposed sympatheticactivity and pupillary dilation (mydriasis), also called a blown pupil.

The part of the brain that usually herniates through the tentorial notch is , leading to and , and the presentation of

The uncus i.e. the medial part of the temporal lobe.

Compression of the third cranial nerve.

Compression of the efferent corticospinal (pyramidal) tract in the midbrain before it has crossed to theopposite side of the foramen magnum.

Ipsilateral mydriasis with contralateral hemiparesis

Elevation of intracranial pressure results in this physiological effect:

Reduced cerebral perfusion pressure (CPP = MAP - ICP)

The normal ICP for patients in resting state is . Pressures greater than are associated with poor outcomes.

10 mmHg

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22 mmHg

Describe the Cushing response:

The Cushing reflex (vasopressor response) is a physiological nervous system response to acute elevations of intracranial pressure (ICP) resulting in Cushing's triad of widened pulse pressure (increasingsystolic, decreasing diastolic), bradycardia, and irregular breathing.

Describe the Monro-Kellie Doctrine:

Explains intracranial pressure dynamics.

In a closed head injury, total volume of intracranial contents must remain constant.

ICP rises if intracranial contents (e.g. blood, fluid) increases.

Venous blood and CSF can be compressed out of the container, providing a degree of pressure buffering.

Very early after injury, a mass (e.g. hematoma) can displace enough venous blood and CSF to maintainadequate ICP.

Once the limit of displacement is reached, ICP increases exponentially and decompensation occurs.

Severe TBI can markedly reduce cerebral blood flow (CBF) during the first few hours after injury. How does CBF differ in those who remain comatose and those that recover?

In those that recover, CBF will increase in 2-3 days.

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In those that remain comatose, it remains below normal for days-to-weeks, leading to global cerebral ischemia.

Describe intracranial pressure autoregulation and the effects of TBI:

Pre-capillary cerebral vasculature can reflexively constrict or dilate in response to MAP changes.

A MAP of 50-150 mmHg is auto-regulated to maintain constant CBF.

Severe TBI disrupts autoregulation, and can lead to ischemia and infarction (low MAP) or cerebral edema (high MAP).

Describe intracranial chemical autoregulation and the effects of TBI:

The partial pressures of oxygen and carbon dioxide predictably cause vasoconstriction and vasodilationof the cerebral vasculature.

List major physiologic causes of secondary brain injury:

Hypotension

Hypoxia

Hypercapnia

Hypocapnia (iatrogenic)

Define mild, moderate, and severe brain injury based on the Glasgow Coma Scale (GCS).

GCS 13-15 = Mild

GCS 9-12 = Moderate

GCS ≤8 = Severe

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When there is left vs. right or upper vs. lower asymmetry in motor function, how should GCS be reported?

Use the best motor response, but record the actual responses for each side.

List the morphologies of cranial trauma:

Skull fractures (vault, basilar)

Intracranial lesions (focal, diffuse)

List the categories of skull fractures:

Cranial vault vs. skull base fractures

Linear vs. stellate

Open vs. closed

Describe the clinical signs of a basilar skull fracture:

Periorbital ecchymosis (raccoon eyes)

Retroauricular ecchymosis (Battle's sign)

CSF rhinorrhea or otorrhea

Hemotympanum

Cranial nerve VII and VIII palsy (facial paralysis, hearing loss)

Basilar skull fractures can be diagnosed using what diagnostic test?

CT scan with bone-window settings

Describe vascular injuries that can arise from skull fractures, and how they are diagnosed:

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Fractures can traverse the carotid canals and can cause dissection, pseudoaneurysm, or thrombosis.

Diagnosed via CT angiogram (CT-A) or conventional angiogram.

What skull fractures provide direction communication between the scalp and the cerebral surface?

Open fractures or compound skull fractures, when the dura is torn. What injuries are associated with linear vault fracture?

It takes considerable force to fracture the skull.

A linear vault fracture in conscious patients increases the likelihood of an ICH 400-fold. List the morphologies of intracranial brain injury categories:

Focal (subdural, epidural, intracerebral)

Diffuse (concussions, multiple contusions, hypoxic/ischemic, axonal)

Describe the mechanism of injury of severe diffuse hypoxic, ischemic brain injuries:

Prolonged shock or apnea occurring immediately after trauma will starve the brain, leading to ischemicinjury.

Initially, the brain may appear radiographically normal.

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Over time, cerebral edema will develop leading to loss of gray-white matter distinction.

Describe the injury patterns in high-velocity impact or deceleration injuries on the brain:

Shearing injuries occur at the border between gray and white matter, which present as multiplepunctate hemorrhages throughout the cerebral hemispheres.

This pattern is often characterized as diffuse axonal injury, which has variable often poor outcomes.

Epidural hematomas occur in about % of patients with brain injuries and % of patients with TBI who are comatose.

0.5%, 9%

Describe the appearance of epidural hematomas and how they most often occur:

Biconvex (lenticular, lens-shaped) as they push the adherent dura away from the inner table of the skull.

Most often in the temporal or temporoparietal regions.

Most often result from tears of the middle meningeal artery due to fracture.

Most often arterial in origin, but can result from major venous sinus hemorrhage, or bleeding from askull fracture.

Describe the classic presentation of epidural hematoma:

A lucid interval between the time of injury and neurological deterioration

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Subdural hematomas occur in approximately % of patients with severe brain injuries:

30%

Describe the appearance of subdural hematomas and how they most often occur.

Crescent-shaped (conforming to the contours of the brain).

Develop from shearing of the small surface or bridging blood vessels of the cerebral cortex.

Often accompanies severe parenchymal injury.

Cerebral contusions occur in approximately % of patients with severe brain injuries.

20-30%

Describe the appearance of cerebral contusions and how they most often occur.

Most occur in the frontal and temporal lobes, but can be anywhere in the brain.

Over hours–days, contusions evolve to form an intracerebral hematoma or a coalescent contusion.

Mass effect can develop, indicating immediate surgical evacuation in about 20% of cases.

Common presenting features in mild TBI:

Transient loss of consciousness

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Disorientation

Amnesia

Often confounded by alcohol or other intoxicants

Initial management of mild traumatic brain injury

Mechanism

Time of injury

Initial GCS

Confusion

Amnestic interval

Seizure

Headache severity

AMPLE history

Neurological examination

Anticoagulation assessment

Secondary management of mild traumatic brain injury

Serial examination until GCS 15 and no persistent memory deficit or perseveration.

Follow-up CT scan if first is abnormal or GCS remains <15.

Consider transfer if neurological status deteriorates.

Prognosis of mild traumatic brain injury:

Most have uneventful recovery.

Approximately 3% unexpectedly deteriorate, potentially resulting in severe neurological dysfunctionunless the decline in mental status is detected early.

Diagnostic workup for mild traumatic brain injury

CT scan (if CT Head rules apply)

EtOH and drug screen

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Admission criteria for mild traumatic brain injury

No CT available

CT abnormal

Skull fracture

Penetrating head injury

No reliable companion at home

Moderate-severe headache

Evidence of CSF leak

Focal neurological deficit

GCS does not return to 15 after 2 hours

Significantly intoxicated (for observation)

Disposition of minor traumatic brain injury

Home if no admission criteria, discharge with Head Injury Warning sheet and out-patient follow-up.

Medical and/or neuropsychological follow-up if at risk but no admission criteria.

Admission and/or transfer to neurosurgery if abnormal CT, abnormal examination, or if patient statusdeteriorating.

Canadian CT Head Rules

Inclusion Criteria

Glasgow Coma Scale (GCS) 13-15 and at least one of the following:

Loss of consciousness

Amnesia to the head injury event

Witnessed disorientation.

ATLS 10.6 QUESTIONS AND ANSWERS:EXAM

GUIDE 2022/2023

Exclusion Criteria

Age <16 years

Blood thinners

Seizure after injury

High risk factor (≥1) for neurosurgical intervention

GCS <15 at 2 hours post-injury

Suspected open or depressed skull fracture

Any sign of basilar skull fracture

Vomiting >2 episodes Age >65 years

Anticoagulation use Moderate risk for brain injury

Loss of consciousness >5 minutes

Retrograde amnesia >30 minutes

Dangerous mechanism (e.g. pedestrian vs. car, ejected from vehicle, fall >3 feet or 5 stairs)

Other compelling indications for CT scan (not in formal rules)

Severe headaches

Seizures

Short-term memory deficit

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Alcohol or drug intoxication

Focal neurological deficit attributable to brain

Common presenting features in moderate TBI:

Can follow simple commands

Confused or somnolent

May have focal neurological deficits such as hemiparesis

Diagnostic workup for moderate traumatic brain injury

CT scan in all cases

Type and crossmatch and coagulation studies

EtOH and drug screen

Evaluate for other injuries and investigations as appropriate

Admission criteria for moderate traumatic brain injury

All moderate TBI requires admission and observation in unit capable of close nursing observation and frequent neurological reassessment for at least the first 12 to 24 hours.

A follow-up CT scan within 24 hours is recommended if the initial CT scan is abnormal or the patient's neurological status deteriorates.

Initial management of moderate traumatic brain injury

Early neurosurgical consultation and transfer if needed

Primary survey and resuscitation

Focused neurological examination

AMPLE history

Secondary survey

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Secondary management of moderate traumatic brain injury

Serial examination

Follow-up CT scan in 12-18 hours

Urgent transfer if neurological status deteriorates.

Disposition of moderate traumatic brain injury

Admission and/or transfer to neurosurgery and/or trauma center for serial observation, CT scan, andintervention if needed

Prognosis of moderate traumatic brain injury:

Approximately 10% to 20% of these patients deteriorate and lapse into coma.

Common presenting features in severe TBI:

Unable to follow simple commands, even after cardiopulmonary stabilization.

Confused, somnolent, or comatose

Diagnostic workup for severe traumatic brain injury

Frequent serial neurological exam including GCS

CT scan in all cases once stabilized

Type and crossmatch and coagulation studies

EtOH and drug screen

Evaluate for other injuries and investigations as appropriate

Admission criteria for severe traumatic brain injury

All severe TBI requires admission and observation in unit capable of close nursing observation and frequent neurological reassessment for at least the first 12 to 24 hours.

A follow-up CT scan within 24 hours is recommended if the initial CT scan is abnormal or the patient's neurological status deteriorates.

CT scan findings of severe brain injury

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Midline shift

Loss of definition of basal cisterns

Severe skull fractures with intrusion

Initial management of severe traumatic brain injury

Urgent neurosurgical consultation and transfer

Primary survey and resuscitation

Intubation and ventilation for airway protection

Treat hypotension, hypovolemia, and hypoxia

Focused neurological exam

AMPLE history and secondary survey

Secondary management of severe traumatic brain injury

Serial examination

Neurosurgical consultation.

PaCO2 35-40 mmHg

Avoid hyperventilation in the first 24 hours as bloodflow may be critically reduced.

Mannitol and brief hyperventilation (maintain PaCO2 >25 mmHg) if deteriorates

Utilize SjO2 or PbTO2 to monitor and titrate oxygen delivery.

Hypertonic saline.

Disposition of severe traumatic brain injury

Admission and/or transfer to neurosurgery and/or trauma center for serial observation, CT scan, andintervention if needed

Priorities for the Initial Evaluation and Triage of Patients with Severe Brain Injuries

1. Primary survey and adhere to ABCDE priorities.

2. Brief neurological examination should be performed before administering drugs for intubation.

3. Once blood pressure normalized, complete a neurological examination including GCS and pupil exam.

4. If hypotension is persistent, perform the neurological exam and record the blood pressure.

5. If systolic pressure cannot be raised to >100 mmHg, determine cause of hypotension first rather than neurosurgical evaluation (e.g. FAST, DPL, laparotomy).

6. If clinical evidence of intracranial mass, then diagnostic and therapeutic burr hole or craniotomy canbe performed in the OR simultaneously.

7. If systolic pressure is resuscitated to >100 mmHg and there is evidence of intracranial mass, then CT head becomes next priority.

8. If systolic pressure is resuscitated but is trending downward (metastability), consult with trauma surgical and neurosurgical teams about CT scan before or after operative management.

Describe how cardiopulmonary success affects mortality in severe brain injury

Hypotension at admission doubles mortality rate.

Hypoxia in addition to hypotension increases relative risk of mortality by 75%.

The purpose of intubation of a comatose (GCS ≤8) patient is to:

Prevent hypoxia.

Indications for hyperventilation in severe TBI:

Acute neurologic deterioration, or

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Signs of herniation

Prolonged hyperventilation with PCO2 of is not recommended.

<25 mmHg

What oxygen saturation should be targeted in brain injury, if blood gas analysis is not available?

98%

When may hypotension be due to brain injury?

Terminal stages of medullary failure

Concomitant spinal cord injury (neurogenic shock)

Maintain systolic blood pressure at for patients years or at for patients years or older than years; this may decrease mortality and improve outcomes.

≥100 mmHg, 50-69 years

≥110 mmHg, 15-49 years or >70 years

Goals of treatment in brain injury:

Systolic blood pressure

Temperature

Glucose

Hemoglobin

ATLS 10.6 QUESTIONS AND ANSWERS:EXAM GUIDE 2022/2023

INR

Na

PaO2

PaCO2

pH

Platelets

Cranial perfusion pressure (CPP)

Intracranial pressure (ICP)

Partial pressure of brain tissue oxygen (PbTO2)

Pulse oximetry

≥100 mmHg36-38°C

4.4-10 mM/L (80-180 mg/dL)

≥70 g/L (7 g/dL)

≤1.4 135-145

≥100 mmHg

35-45 mmHg

7.35-7.45

ATLS 10.6 QUESTIONS AND ANSWERS:EXAM GUIDE 2022/2023

≥75 mmHg

≥60 mmHg

5-15 mmHg

≥15 mmHg

≥95%

The rapid, focused neurological examination in severe TBI consists of:

GCS score

Pupillary light response

Identifying focal neurological deficit

How long may a post-ictal state impair patient responsiveness?

Minutes-hours

In a comatose patient, motor responses can be elicited by:

Pinching the trapezius

Nail-bed pressure

Supraorbital ridge pressure

Which neurological exams should be deferred to the neurosurgeon, and after only what has beenexcluded?

Cervical spine trauma must be ruled out first.

Doll's-eye movements (oculocephalic testing)

Caloric testing (oculovestibular testing)

Corneal testing

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Do not use paralytic and sedating agents during the primary survey.

Long-acting

In traumatic brain injury, avoid sedation except when ....

Patient's agitated state could present a risk. Use the shortest-acting agents available when pharmacologic paralysis or brief sedation is needed for endotracheal intubation or obtaining reliablediagnostic studies.

Preferred agents to be used in analgesia and agitation in initial management:

Low doses of short-acting IV narcotics (e.g. Fentanyl), and reversed with naloxone if needed.

Short-acting IV benzodiazepines (e.g. Versed) for sedation and reversed with flumazenil if needed.

When should CT scanning of the head be considered in moderate or severe traumatic brain injury?

As soon as possible, once hemodynamically stabilized.

Whenever there is a change in the patient's clinical status.

Within 24 hours of injury if there is a subfrontal or temporal contusion.

Within 24 hours of injury if patient is on anticoagulation.

Within 24 hours of injury if patient is ≥65 years.

If patient has a known intracranial hemorrhage with a volume >10 mL.

What critical features should be identified on head CT?

Intracranial blood

Intracranial contusions

Shif t of midline structures (mass effect)

Obliteration of the basal cisterns.

A shift of often indicates need for neurosurgical evacuation of the blood clot or contusion. ≥5 mm

ATLS 10.6 QUESTIONS AND ANSWERS:EXAM GUIDE 2022/2023

What neurological harms may stem from fluid mismanagement?

Hypovolemia

Hypervolemia

Hypo-osmolality and hyponatremia

Hyperglycemia

Hyponatremia

What fluids are recommended for resuscitation in brain injury?

Ringer's lactate

Normal saline

Anticoagulation reversal

Antiplatelets (e.g., ASA, clopidogrel)

Coumadin (warfarin)

Heparin

Low molecular weight heparin, e.g., Lovenox (enoxaparin)

Direct thrombin inhibitors

dabigatran etexilate (Pradaxa)

Xarelto (rivaroxaban)

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Platelets, DDAVP

FFP, Vitamin K, PCC, Factor VIIa

Protamine sulfate

Protamine sulfate

idarucizumab (Praxbind) or PCC

PCC

Describe the relationship between ventilation, PaCO2, and vasoconstriction.

Hyperventilation drives down PaCO2 and causes cerebral vasoconstriction. Excessive hyperventilation can lead to cerebral ischemia.

If hyperventilation is required, it is preferable to keep PaCO2 at approximately . 35 mmHg (low-end of normal)

The risk of hyperventilation-associated brain injury is particular high if PaCO2 falls below 30 mmHg

Hypercarbia with PaCO2 will cause in the brain. 45 mmHg, vasodilation and increase intracranial pressure.

Describe the role of hyperventilation in management of brain injury.

Brief periods of hyperventilation, titrated to PaCO2 25-30 mmHg, may be necessary to manage acute

neurological deterioration while other treatments are initiated or surgical intervention is performed.

The most common preparation of mannitol is: 20% solution (20 g mannitol in 100 mL of solution).

Mannitol should not be given in patients with...

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Hypotension (SBP <90 mmHg), as it does not lower ICP if hypovolemic and is a potent osmotic diuretic.

Mannitol is strongly indicated if...

Acute neurological deterioration occurs - uncal herniation syndrome (dilated, fixed pupil with

contralateral hemiparesis) or loss of consciousness, and the patient is not hypovolemic.

The bolus dose of mannitol is...

1 g/kg infused rapidly over 5 minutes for acute neurological deterioration (e.g. uncal herniation).

0.25-1 g/kg to control elevated ICP.

Parameters which must be monitored when administering mannitol: ICP

Serum osmolality (<320 mOsm)

Volume status (urine output, blood pressure >90 mmHg)

Typical concentrations of hypertonic saline range from: 3%-23.4%

Hypertonic saline may be used in patients with...

Elevated ICP, and may be used in patients with hypotension because it is not a diuretic. However, inhypovolemic patients, the effect is minimal.

Disadvantages of barbiturates to reduce intracranial pressure:

Long half-life delays time in determining brain death.

Not preferred agent to induce burst suppression in status epilepticus.

Management of a patient with TBI who is seizing when long-acting paralytic wears off:

Avoid long-acting paralytic agents, as muscle paralysis confounds the neurologic examination.

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Use benzodiazepines to acutely manage seizures, as muscle relaxants mask rather than control seizures.

Three factors linked to a high incidence of traumatic epilepsy are:

Seizures occurring within the first week

Intracranial hematoma

Depressed skull fracture

True or false: Early anticonvulsants aid in improving long-term traumatic seizures.

False. They do not change long-term seizure outcomes.

Disadvantages of anticonvulsants in brain injury:

Inhibit brain recovery, so should be used only when absolutely necessary.

Anticonvulsants used in the acute phase:

Dilantin (phenytoin)

Valium (diazepam)

Ativan (lorazepam)

Cerebyx (fosphenytoin)

Dilantin (phenytoin) loading, maintenance, and titration target: 1 g IV at no faster than 50 mg/min, with typical maintenance rate of 100 mg/8 hours, to achievetherapeutic serum levels.

Control of continuous seizures may require...

General anesthesia (intravenous and inhaled anesthetics)

ATLS 10.6 QUESTIONS AND ANSWERS:EXAM GUIDE 2022/2023

Prolonged seizures lasting may cause secondary brain injury.

30-60 minutes

The most common cause of infected scalp wounds is:

Inadequate cleansing and debridement.

Methods to control scalp hemorrhage:

Direct pressure

Cauterizing

Ligating large vessels

Sutures, clips, or staples

Red flags features of scalp wounds:

Skull fracture (open or depressed)

Foreign body

CSF leakage (dural tear)

can be commonly confused with a skull fracture on examination:

Subgaleal hematoma

Skull fracture can be confirmed or excluded by:

Plain X-ray or CT scan

For patients with depressed skull fractures, a is an invaluable test because it :

CT Head

Identifies degree of depression

Evaluates for intracranial hematoma or contusion

Operative criteria for depressed skull fractures:

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Degree of depression is greater than the thickness of the adjacent skull

Fracture is open and grossly contaminated.

Less severe depressed skull fractures can often be managed by:

Closure of the overlying scalp laceration, if present.

Indications for an emergency craniotomy by non-neurosurgeon

Rapidly deteriorating patient

Austere or remote areas

After consultation with a neurosurgeon

Definitive neurosurgical care is unavailable

Decompressive craniotomy does not improve outcomes in diffuse cranial swellings

In penetrating cranial injuries, plain radiographs of the head are helpful to:

Evaluate bullet trajectory

Identify missile fragmentation

Identify large foreign bodies

Identify intracranial air

True or false: Plain radiographs of the head should be used concurrently with CT and angiography.

False. If CT or angiography is available, plain radiographs are not essential.

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CT and/or conventional angiography are recommended with any penetrating brain injury and when ...: The trajectory passes through or near the skull base or a major dural venous sinus.

Substantial subarachnoid hemorrhage or delayed hematoma should prompt consideration of what diagnostic test?

Vascular imaging

Patients with penetrating injury of the orbitofacial or pterional region(s) should undergo to identify

Angiography (conventional or CT)

Traumatic intracranial aneurysm or AV fistula

Magnetic resonance imaging (MRI) can play a role in evaluating injuries from....

Penetrating wooden and other nonmagnetic objects.

Indications for prophylactic broad spectrum antibiotics in head trauma:

Open skull fracture

Penetrating brain injury

CSF leak

Indications for early ICP monitoring:

Clinician unable to assess neurological exam accurately (e.g. intoxication, post-ictal, peripheral injuries)

Need to evacuate a mass lesion is unclear

Imaging studies suggest elevated ICP

Management of small bullet entrance wounds

Exclude major intracranial pathology.

Local wound care and closure if scalp is not devitalized.

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Management of penetrating head injuries with partially exteriorized objects (e.g. arrow, knives,screwdrivers).

Do not disturb or remove objects prematurely

Exclude vascular injury with imaging and neurosurgeon opinion

Describe burr hole craniostomy i.e. craniotomy and its indications.

Placement of a 10-15 mm drill hole in the skull

Emergently diagnoses accessible hematoma when definitive care unavailable

Indicated for patients with rapid neurological deterioration