which of the following findings would be least suggestive of the presence of high-energy trauma?

Standing Didactics Activeness

Traumatic brain injury (TBI) due to caput trauma is a common presentation in emergency departments and unremarkably accounts for more than ane million visits annually. Information technology is a common cause of expiry and disability among children and adults. Traumatic brain injury is classified equally mild, moderate, or severe, based on the Glasgow Coma Scale (GCS) score. This activity reviews the evaluation and direction of head trauma and highlights the part of interprofessional team members in collaborating to provide well-coordinated care and enhance outcomes for affected patients.

Objectives:

• Summarize the incidence of head trauma.

• Explain how to classify traumatic brain injury.

• Depict how to evaluate a patient with a head injury.

• Explain the importance of improving coordination amongst the interprofessional team to enhance treat patients affected past head trauma.

Access free multiple choice questions on this topic.

Introduction

Traumatic brain injury (TBI) is a common presentation in emergency departments, which accounts for more than one million visits annually. It is a common crusade of expiry and disability amid children and adults.[i]

Based on the Glasgow Coma Scale (GCS) score, it is classified equally:

• Mild = GCS thirteen to 15, also chosen concussion

• Moderate = GCS nine to 12

• Severe = GCS iii to viii

Etiology

The leading causes of head trauma are (1) motor vehicle-related injuries, (2) falls, and (iii) assaults.[2][three] Based on the mechanism, head trauma is classified as (1) blunt (the about common machinery), (2) penetrating (most fatal injuries), (3) boom. About severe TBIs outcome from motor vehicle collisions and falls.

Epidemiology

Caput trauma is more common in children, adults up to 24 years, and those older than 75 years.[4][5][6] TBI is iii times more common in males than in females. Although only x% of TBI occurs in the elderly population, it accounts for up to 50% of TBI-related deaths.

Pathophysiology

The post-obit concepts are involved in the regulation of claret flow and should be considered.

i) Monroe-Kellie Doctrine

• Related to the understanding of intracranial pressure (ICP) dynamics.

• Any individual component of the intracranial vault may undergo alterations, but the total volume of intracranial contents remains constant since the space inside the skull is fixed. In other words, the encephalon has a compensatory mechanism to maintain an equilibrium thereby maintaining normal intracranial pressure.

• According to this, the deportation of cerebrospinal fluid (CSF) or blood occurs to maintain normal ICP. A rise in ICP will occur when the compensatory mechanisms are wearied.

ii) Regulation of Cognitive Claret Menstruum (CBF) (Autoregulation)

• Under normal circumstances, the brain maintains CBF via automobile-regulation which maintains equilibrium between oxygen delivery and metabolism.

• Autoregulation adjusts Cerebral perfusion pressure level (CPP) from 50 to 150 mm Hg. Beyond this range, autoregulation is lost, and blood menstruum is but dependent on blood force per unit area.

• Astringent brain injury may disrupt the autoregulation of CBF.

3) Cerebral Perfusion Force per unit area (CPP)

• The departure between the mean arterial force per unit area (MAP) and the ICP (CPP = MAP – ICP)

• Target CPP is 55 mm Hg  to sixty mm Hg

• An increase in ICP tin subtract the CPP

• A decrease in ICP may meliorate CPP

• Remember, lowering MAP in a hypotensive patient may lower CPP.

• A minimum CPP should be maintained to avoid cerebral insult. Information technology is age-dependent and is as follows: Infants - 50 mm Hg, Children - 60 mm Hg, and Adults - lxx mm Hg.

• CBF is quite sensitive to oxygen and carbon dioxide.

• Hypoxia causes vasodilation and therefore increases CBF and may worsen ICP.

• Hypercarbia also results in vasodilation and can alter ICP via effects on cerebrospinal fluid (CSF) pH and increases CBF.

4) Mean arterial pressure (MAP)

• Maintain = 80 mm Hg

• sixty mm Hg = cognitive vessels maximally dilated

• < sixty mm Hg = cognitive ischemia

• > 150mmHg =  increased ICP

5) Intracranial pressure (ICP)

• An increase in ICP can decrease CPP.

• ICP is dependent on the volume of the following compartments:

• Brain parenchyma (< 1300 mL)

• Cerebrospinal fluid (100 - 150 mL)

• Intravascular claret (100 - 150 mL)

• Cushing reflex (hypertension, bradycardia, and respiratory irregularity) due to an increase in ICP

• Normal ICP is age-dependent (developed younger than ten years quondam, child three-vii years old, infant one.5-6 years old)

• > 20 mm Hg= increased morbidity and mortality and should be treated. It is perchance more than of import to maintain an adequate CPP.

TBI can be classified as chief injury and secondary injury:

Principal Injury

Chief injury includes injury upon the initial impact that causes deportation of the brain due to direct impact, rapid acceleration-deceleration, or penetration. These injuries may crusade contusions, hematomas, or axonal injuries.

• Contusion (trample on the brain parenchyma)

• Hematoma (subdural, epidural, intraparenchymal, intraventricular, and subarachnoid)

• Lengthened axonal injury (stress or damage to axons)

Secondary Injury/Secondary Neurotoxic Cascade

Secondary injury consists of the changes that occur after the initial insult. It tin be due to:

• Systemic hypotension

• Hypoxia

• Increase in ICP

After a master encephalon injury, a cascade of cellular and biochemical events occurs which include the release of glutamate into the presynaptic space resulting in activation ofN-methyl-D-aspartate, a-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid, and other receptors. This ionic shift may activate cytoplasmic and nuclear enzymes, resulting in mitochondrial damage, and prison cell decease and necrosis.

Encephalon Herniation

Herniation occurs due to increased ICP. The following are the types of herniations.

1) Uncal transtentorial

• The uncus is theabout medial portion of the hemisphere, and the commencement construction to shift below the tentorium.

• Compression of parasympathetic fibers running with the tertiary cranial nervus

• Ipsilateral fixed and dilated pupil with contralateral hemiparesis

2) Central transtentorial

• Midline lesions, such as lesions of the frontal or occipital lobes or vertex

• Bilateral pinpoint pupils, bilateral Babinski signs, and increased musculus tone. Fixed midpoint pupils follow along with prolonged hyperventilation and decorticate posturing

3) Cerebellar tonsillar

• Cerebellar tonsils herniate in a downwardly direction through the foramen magnum

• Compression on the lower brainstem and upper cervical spinal cord

• Pinpoint pupils, flaccid paralysis, and sudden death

4) Upwardly posterior fossa/cerebellar herniation

• The cerebellum is displaced in an up direction through the tentorial opening

• Cohabit downward gaze with an absenteeism of vertical eye movements and pinpoint pupils

History and Physical

A proficient history concerning the mechanism of injury is important. Follow advanced trauma life back up protocol and perform primary, secondary, and third surveys. Once the patient is stabilized, a neurologic test should exist conducted. CT scan is the diagnostic modality of choice in the initial evaluation of patients with caput trauma.

The GCS is used to describe the level of consciousness. Patients who are intubated are only evaluated for motor scores and eye-opening and the suffix T is added to the concluding score. The maximal GCS score is 10T and the lowest is 2T.

Nomenclature of TBI is every bit follows:

• Clouding of consciousness, where in that location is a mild deficit in processing by the encephalon. It may persist for many months and the patient may have a loss of recent memory, but long-term memory remains intact.

• Lethargy is a state of depressed alacrity and tin can result in an disability to perform tasks that are unremarkably done without any effort. The patient may be aroused by stimuli but then settles back into a state of inactivity. Awareness of the environment is nowadays.

• Obtundation is a state of decreased alertness and awareness. The patient will briefly reply to stimuli and just follow uncomplicated commands, but will not be enlightened of the surroundings.

• Stupor is when the patient cannot communicate lucidly and requires painful stimuli to exist aroused. One time the stimulation is withdrawn, the patient returns to the inactive state.

• Coma is when the patient is not able to reply to whatsoever type of stimuli.

Evaluation

CT scan is required in patients with head trauma

• Moderate (GCS score ix to 12)

• Severe (GCS score < 8)

For patients who are at low risk for intracranial injuries, there are 2 externally validated rules for when to obtain a head CT scan after TBI.[vii][viii]

It is important to sympathise that no individual history and concrete exam findings tin eliminate the possibility of intracranial injury in head trauma patients.

Skull x-rays are merely used to assess for foreign bodies, gunshots or stab wounds

New Orleans Criteria

• Headache

• Airsickness (whatever)

• Age > 60 years

• Drug or alcohol intoxication

• Seizure

• Trauma visible higher up clavicles

• Short-term memory deficits

Canadian CT Caput Rule

• Dangerous machinery of injury

• Vomiting = two times

• Age > 65 years

• GCS score < xv, 2-hours mail service-injury

• Whatsoever sign of basal skull fracture

• Possible open or depressed skull fracture

• Amnesia for events thirty minutes before injury

Level A Recommendation

With the loss of consciousness or posttraumatic amnesia only if one or more of the following symptoms are nowadays:

• Headache

• Vomiting

• Age > threescore years

• Drug or alcohol intoxication

• Deficits in brusk-term retention

• Physical findings suggestive of trauma above the clavicle

• Posttraumatic seizure

• GCS score < xv

• Focal neurologic arrears

• Coagulopathy

Level B Recommendation

Without loss of consciousness or posttraumatic amnesia if 1 of the following specific symptoms presents:

• Focal neurologic deficit

• Airsickness

• Severe headache

• Age > 65 years

• Physical signs of a basilar skull fracture

• GCS score < 15

• Coagulopathy

• Unsafe machinery of injury

• Ejection from a motor vehicle (such every bit Pedestrian struck or a fall from a height > three feet or five stairs)

The hazard of intracranial injury when clinical decision dominion results are negative is less than ane%.

For children, Pediatric Emergency Care Applied Research Network (PECARN) decision rules exist to rule out the presence of clinically important traumatic brain injuries. Still, this rule applies merely to children with GCS > 14.

Treatment / Management

The most important goal is to prevent secondary brain injuries. This can exist achieved by the following:

• Maintain airway and ventilation

• Maintain cerebral perfusion pressure level

• Forbid secondary injuries (by recognizing and treating hypoxia, hypercapnia, or hypoperfusion)

• Evaluate and manage for increased ICP

• Obtain urgent neurosurgical consultation for intracranial mass lesions

• Identify and treat other life-threatening injuries or conditions (if they exist)

A relatively college systemic blood pressure is needed:

• Increment in intracranial pressure

• Loss of autoregulation of cerebral circulation

Priorities remain the same:  the ABC also applies to TBI. The purpose is to optimize perfusion and oxygenation.[i][9][x]

Airway and Breathing

Identify any condition which might compromise the airway, such as pneumothorax.

For sedation, consider using short-acting agents having minimal effect on blood pressure or ICP:

• Consecration agents:  Etomidate or propofol

• Paralytic agents: Succinylcholine or Rocuronium

Consider endotracheal intubation in the post-obit situations:

• Inadequate ventilation or gas exchange such as hypercarbia, hypoxia, or apnea

• Severe injury (GCS score of = 8)

• Disability to protect the airway

• Agitated patient

• Demand for patient send

The cervical spine should be maintained in-line during intubation.

Nasotracheal intubation should be avoided in patients with facial trauma or basilar skull fracture.

Targets:

• Oxygen saturation > 90

• PaO2 > 60

• PCO at 35 - 45

Circulation

Avoid hypotension. Normal blood pressure may not be adequate to maintain adequate period and CPP if ICP is elevated.

Target

• Systolic claret force per unit area > 90 mm Hg

• MAP > eighty mm Hg

Isolated head trauma ordinarily does not cause hypotension. Look for another cause if the patient is in shock.

Increased ICP

Increased ICP tin can occur in caput trauma patients resulting in the mass occupying lesion. Utilise a team approach to manage impending herniation.

Signs and symptoms:

• Change in mental status

• Irregular pupils

• Focal neurologic finding

• Posturing: decerebrate or decorticate

• Papilledema (may not be apparent with a rapid height of ICP)

CT scan findings:

• Attenuation of sulci and gyri

• Poor gray/white matter demarcation

General Measures

Head Position: Raise the caput of the bed and maintain the caput in midline position at thirty degrees: potential to improve cerebral blood menstruation by improving cognitive venous drainage.

Lower cerebral blood volume (CBV) tin can lower ICP.

Temperature Control: Fever should exist avoided as it increases cerebral metabolic need and affects ICP.

Seizure prophylaxis: Seizures should be avoided as they can besides worsen CNS injury by increasing the metabolic requirement and may potentially increase ICP. Consider administering fosphenytoin at a loading dose of 20mg/kg.

Only use an anticonvulsant when it is necessary, as it may inhibit brain recovery.

Fluid management: The goal is to achieve euvolemia. This volition help to maintain adequate cerebral perfusion. Hypovolemia in caput trauma patients is harmful. Isotonic fluid such as normal saline or Ringer Lactate should be used. Also, avoid hypotonic fluid.

Sedation: Consider sedation every bit agitation and muscular activity may increment ICP.

• Fentanyl: Prophylactic in intubated patients

• Propofol: A short-acting amanuensis with practiced sedative backdrop, the potential to lower ICP, possible risk of hypotension and fatal acidosis

• Versed: allaying, anxiolytic, possible hypotension

• Ketamine: Avoid every bit it may increase ICP.

• Musculus relaxants: Vecuronium or Rocuronium are the best options for intubation; Succinylcholine should not be used as ICP may rise with fasciculations.

 ICP monitoring:

• Severe head injury

• Moderate head injury with increased risk factors such as abnormal CT scan finding

• Patients who cannot be evaluated with serial neurological examination

• ICP monitoring is often done in patients with severe trauma with a GCS of less than 9. The reference range for normal CIP is 2-fifteen mmHg. In add-on, the waveform of the tracing is of import.

Hyperventilation:

Normocarbia is desired in most head trauma patients. The goal is to maintain PaCO betwixt 35-45 mmHg. Judicious hyperventilation helps to reduce PaCO2 and causes cerebral vasoconstriction. Beware that, if farthermost, it may reduce CPP to the point that exacerbation of secondary encephalon injury may occur. Avoid hypercarbia: PaCO > 45 may cause vasodilatation and increases ICP.

Mannitol:

A strong osmotic diuretic with net intravascular volume loss

Reduces ICP and improves cerebral blood flow, CPP, and encephalon metabolism

Expands plasma volume and tin can improve oxygen-carrying capacity

The onset of action is within 30 minutes

Elapsing of activity is from ii to eight hours

Dose is 0.25-ane g/kg (maximum: four g/kg/twenty-four hours)

Avoid serum sodium > 145 m Eq/50

• Serum sodium > 145 m Eq/50

• Serum osmolality > 315 mOsm

Relative contraindication:  hypotension does not lower ICP in hypovolemic patients.

Hypertonic saline:

May be used in hypotensive patients or patients who are non adequately resuscitated.

The dose is 250 mL over xxx minutes.

Serum osmolality and serum sodium should be monitored.

Hypothermia may be used to lower cerebral metabolism only it is of import to be aware that hypothermia also makes the patient susceptible to infections and hypotension.

Mild Head Trauma

The bulk of caput trauma is mild. These patients can be discharged following a normal neurological examination as there is minimal chance of developing an intracranial lesion.

Consider observing at least iv to 6 hours if no imaging was obtained.

Consider hospitalization if these other risk factors are present:

• Bleeding disorder

• Patient taking anticoagulation therapy or antiplatelet therapy

• Previous neurosurgical procedure

Provide strict return precautions for patients discharged without imaging.

Differential Diagnosis

• Anterior apportionment stroke

• Brain metastasis

• Cognitive aneurysm

• Confusional states and astute memory disorders

• Emergent management of subarachnoid bleeding

• Epileptic and epileptiform encephalopathies

• Frontal lobe syndromes

• Generalised tonic-clonic seizures

• Hydrocephalus

• Prion-related diseases

• Psychiatric disorders associated with epilepsy

• Subdural empyema

• Temporal lobe epilepsy

Prognosis

The outcomes after head trauma depend on many factors. The initial GCS score does provide some information on the outcome; the motor score is nigh predictive of outcome. Patients with a GCS of less than 8 at presentation accept high mortality. Advanced age, comorbidity, respiratory distress, and a comatose state are also associated with poor outcomes.

Complications

• Deep vein thrombosis rates are higher in caput trauma patients

• Neurological deficits

• CSF leak

• Hydrocephalus

• Infections

• Seizures

• Cerebral edema

Pearls and Other Issues

Hyperglycemia may worsen the effect.

An elevated temperature may increase ICP and worsen outcomes.

• Increment metabolic demand

• Increase glutamate release

A prolonged seizure may worsen secondary encephalon injuries.

Enhancing Healthcare Team Outcomes

Head trauma is a major public health problem accounting for thousands of admissions each year and costing the healthcare system billions of dollars. The majority of patients with head trauma are seen in the emergency section; the caput injury is often associated with other organ injuries as well. The intendance of a patient with caput trauma is past an interprofessional team that is defended to managing head trauma patients.

Well-nigh patients require admission and monitoring in an ICU setting. The outcome of these patients depends on the severity of the head trauma, initial GCS score, and whatever other organ injury. Information indicate that those patients with an initial GCS of 8 or less accept a mortality charge per unit of 30% within 2 weeks of the injury. Other negative prognostic factors include advanced age, elevated intracranial force per unit area, and the presence of a gross neurologic arrears on presentation. ICU nurses play a vital role in the managing of these patients; from providing basic medical care, monitoring, DVT and ulcer prophylaxis and monitoring the patient for complications and reporting concerns to the team. The dietitian manages the diet and physical therapists provide bedside exercises to prevent muscle wasting.

Patients with a GCS less than ix often require mechanical ventilation, tracheostomy, and a feeding tube. With prolonged hospital stay, there are prone to pressure ulcers, aspiration, sepsis, failure to thrive and deep vein thrombus. Patients deemed to exist brain expressionless are assessed by the entire squad that includes specialists from the finish of life care.

Recovery in near patients tin can take months or even years. Even those who are discharged ofttimes have residuum deficits in executive function or neurological deficits. Some require speech communication, occupational and physical therapy for months. In addition, the social worker should assess the home environment to make certain information technology is safety and offers amenities for the disabled person. Only through such a squad approach can the morbidity of caput trauma exist lowered.

Outcomes

Unfortunately, despite the instruction of the public, many young people nevertheless lead a lifestyle that predisposes them to caput injury. Young people nevertheless potable and drive, text while driving, abuse alcohol and illicit drugs, and are often involved in high-risk sporting activities, which makes them susceptible to caput trauma.[eleven][12]

Review Questions

Figure

Abusive Caput Trauma/Shaken Baby Syndrome/Subdural hematoma (arrow), bleeding betwixt the dura mater of the meninges and the encephalon, commonly occurs in SBS/Calumniating head trauma. Contributed past Wikimedia Eatables ( Public Domain)

Figure

Original description: Figure ii. CT and enhanced gradient echo T2 star-weighted angiography (ESWAN) images of the encephalon of a 54-year-quondam homo who experienced a traumatic brain injury. An axial head CT epitome displays right frontotemporal SAH (Fisher grade (more...)

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Source: https://www.ncbi.nlm.nih.gov/books/NBK430854/

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